Psychiatry Update 4

Series Editor: Michelle B. Riba

Mashal Khan
Jonathan Avery Editors

From Stigma
to Support
A New Vision for Alcohol Use Disorder
Treatment and Recovery
Psychiatry Update

Volume 4

Series Editor
Michelle B. Riba, University of Michigan, Department of Psychiatry,
University of Michigan Eisenberg Family Depression Center, Ann Arbor, USA
Psychiatry Update encompasses psychiatric topics that inform diagnoses,
treatments, and advances in research. The editors and authors are leaders in their
fields who bring the latest ideas, conceptual frameworks, and controversies to us in
an easy-to-read and practical format.
Mashal Khan • Jonathan Avery
Editors

From Stigma to Support

A New Vision for Alcohol Use Disorder
Treatment and Recovery
Editors
Mashal Khan Jonathan Avery
Department of Psychiatry Department of Psychiatry
Weill Cornell Medical College Weill Cornell Medical College
New York, NY, USA New York, NY, USA

ISSN 2524-8316     ISSN 2524-8324 (electronic)

Psychiatry Update
ISBN 978-3-031-73552-3    ISBN 978-3-031-73553-0 (eBook)
https://doi.org/10.1007/978-3-031-73553-0

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Contents

1 
Historical and Cultural Perspectives on Alcohol Use ����������������������������   1
Christine Collins and Christine LaGrotta
2 
The Science of Addiction: How Alcohol Affects the Brain ��������������������   9
Abdo Semaan
3 
Co-occurring Disorders: Mental Health and Alcohol Use �������������������� 21
Nicholas Romano and Rachel Luba
4 
The Impact of Alcohol Use on Physical Health �������������������������������������� 41
Nia Harris
5 
Alcohol Use Disorder, Alcohol-­Associated Liver Disease,
and Liver Transplantation������������������������������������������������������������������������ 53
Elora Basu and Akhil Shenoy
6 Alcohol Withdrawal Syndrome���������������������������������������������������������������� 65
Amanda Ramsdell and Stephanie Chiao
7 
Pharmacotherapies for Alcohol Use Disorder ���������������������������������������� 77
Evguenia Makovkina
8 
Behavioral Therapies for Alcohol Use Disorder�������������������������������������� 93
Katherine Pruzan
9 
Technology-Assisted Treatment of Alcohol Use Disorder���������������������� 109
Daniel Cabrera and Mashal Khan
10 
Alcoholics Anonymous, SMART Recovery, and Other Support
Systems for Alcohol Recovery ������������������������������������������������������������������ 117
Abdallah Tom and Kate Fruitman
11 
Building a Life in Recovery: Aftercare and Relapse Prevention ���������� 143
Maximilliam A. Cabrera and Bernadine H. Han

v
vi Contents

12 
Stigma and Alcohol Use Disorder: Overcoming
Societal Attitudes���������������������������������������������������������������������������������������� 153
Michael Woods and Jonathan Avery
13 Physicians and Alcohol������������������������������������������������������������������������������ 163
Jeffrey A. Selzer and Robyn L. Hacker
14 
Advocacy and Policy: Improving Access to Treatment
and Recovery Support Services���������������������������������������������������������������� 179
Abdallah Tom, Charalambia Louka, and Sanya Virani
15 
The Future of Alcohol Use Disorder Treatment and Research�������������� 189
A. Benjamin Srivastava and Jonathan M. Wai

Index������������������������������������������������������������������������������������������������������������������ 205
Historical and Cultural Perspectives
on Alcohol Use 1
Christine Collins and Christine LaGrotta

1.1 History of Alcohol Consumption

1.1.1 Mesopotamia and Egypt

Alcohol consumption dates back thousands of years to ancient times. Early grain
farming approximately 10,000 years ago in the Near East resulted in the beginnings
of beer which became a large part of the economic system in Mesopotamia and
Egypt [1]. Evidence has shown that in Predynastic Egypt, many types of beer had
been brewed in large quantities. There is iconographic evidence of the connection
between baking bread and brewing, with traces of bakeries being found near brew
sites. Six vats were capable of producing up to 1100 liters per day of beer, suggest-
ing that brewing was being done at the community level, as these quantities far
exceeded the quantity needed for a household. It was also thought that much of the
brewing was done by women. Throughout the later Predynastic era, it was thought
that Egyptian elites helped to define themselves by craft brewing [2].
In ancient Egypt, Osiris, the god of wine, was worshipped throughout the coun-
try, while many other gods were local or familial, showing the value placed on wine.
It was also thought that this god is the one who invented beer. Both beer and wine
were defied and offered to gods, and there was even a god whose hieroglyph was a
wine press. A ritual in ancient Egypt involved storing alcoholic beverages in the
tombs of those who had died so that they could use the alcohol in the afterlife [3].

C. Collins
Department of Psychiatry and Neuroscience, Lindner Center of HOPE/University of
Cincinnati College of Medicine, Mason, OH, USA
e-mail: [email protected]
C. LaGrotta (*)
Department of Addiction Psychiatry, James J. Peters Bronx VA Medical Center, Icahn School
of Medicine at Mount Sinai, New York, NY, USA

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2024 1

M. Khan, J. Avery (eds.), From Stigma to Support, Psychiatry Update 4,
https://doi.org/10.1007/978-3-031-73553-0_1
2 C. Collins and C. LaGrotta

The evidence for alcoholic beverages in ancient Mesopotamia is not as strong as

that for Egypt; however, there is circumstantial evidence present. Ceramic vessels
that are shaped as though they hold alcohol have been found (Fig. 1.1). In the 1990s,
an analysis of residues found in storage vessels in Mesopotamia contained tartaric
acid. This indicates that the vessels contained a grape product, which was thought
to be wine. Analysis of another jug showed that it had contained beer. However, the
origin of the grapes in Greater Mesopotamia does remain a topic of debate [2].

1.1.2 Ancient Greece

In about 2000 BC, wine-making started in what is now Greece and gained popular-
ity to become a commonly brewed beverage by about 1700 BC. The first alcoholic
beverage to obtain widespread popularity in this region was mead (made from
honey and water). Alcohol served many functions, including being part of religious
rituals, as part of meals, and used for medicinal purposes [3]. In ancient Greece,
drinking wine out of a shared bowl at parties or symposia became popular [4].
More contemporary writers have found that the Greeks had rules stressing mod-
erate drinking and praised a temperate demeanor. They often mixed their wine with
water and, in general, tended to avoid an excess of consumption. That being said,

Fig. 1.1 Uruk-period

spouted vessels (Joffee [2])
1 Historical and Cultural Perspectives on Alcohol Use 3

intoxication did happen at banquets and festivals, or in the cult of Dionysus, where
intoxication was thought to bring people closer to their god [3].
Dionysus, alternatively called Bacchus (Fig. 1.2), is best known as the Greek god
of wine-making. He also played other roles, such as being a god of fertility, fruitful-
ness, theatre, ecstasy, and abandon. He was the son of an immortal god (Zeus) and
a mortal princess (Semele) and served as a link between humans and divinity.
According to the story, Zeus was tricked into burning Semele while she was preg-
nant with Dionysus, but Zeus rescued him and implanted him into his thigh until he
was born [6]. He was a paradox of a god, and his association with wine also embod-
ies this paradox. The paradox of wine is that it both intoxicates but also has medici-
nal properties, “it brings liberation and ecstasy, yet, like any initiatory experience, it
also introduced the risks of losing hold of identity and control” [7].

1.1.3 Ancient Rome

Due to the climate of the Italian peninsula, the Roman Empire (along with ancient
Greece) was more suitable for growing grapes and thus producing wine, rather than
the production of beer (as was done in much of the rest of the ancient world). Wine
became an important product in Mediterranean trade, so much so that the trade of

Fig. 1.2 Dionysus or

Bacchus, god of wine
(Marie-Lan Nguyen [5])
4 C. Collins and C. LaGrotta

wine in ancient Rome has become known as “wine imperialism.” In addition to trad-
ing grapes and wine, by the beginning of the Christian era, the Romans started to
plant vineyards in France, England, and other parts of central and eastern Europe [6].
Though only wine, and not beer, was consumed in ancient Rome, the quality of
wine varied immensely. Poorer Romans and Roman soldiers drank posca, a mixture
of water and sour wine (spoiled wine that had not turned into vinegar). When Roman
soldiers were sick or injured, however, they were able to have wine made from fresh
grapes. Slaves and farmworkers were given Lora, a beverage made from soaking the
seeds, skins, and vine matter left over from wine-making. The result was a dilute
and thin beverage, likely with low alcohol content. At the top of the social scale,
Romans consumed wine that was full of flavor and color and had a higher alcohol
content [6].
Beginning in the fifteenth century, distillation was refined, and the formation of
higher-concentration alcoholic beverages began, including brandy, rum, and whisky.
These products were further used to barter slaves used in global exploration and
discovery of new land, such as that of North America.

1.2 History of Abuse and Withdrawal

Across history, alcohol has served a variety of purposes, including roles in religious
ceremonies, nutrition, and medical functions such as providing antiseptic and anal-
gesia benefits, promoting relaxation and social connection, and enhancing pleasure
[4]. With the widespread use of alcohol by many different cultures and for various
reasons, problematic use developed. By 1784, Benjamin Rush described what we
now recognize as alcohol addiction as an uncontrollable, overwhelming, and irre-
sistible desire to consume alcohol. Separately, Pearson and Sutton identified and
described delirium tremens in 1813 [8]. Later on, craving and withdrawal symptoms
were recognized as important aspects of addiction and contributed to the develop-
ment of the temperance movements in the United States, which led to prohibition.

1.2.1 Cultural Perspectives

Clinical cultural competence and cultural humility (Table 1.1) have been identified
as essential for healthcare providers to provide high-quality, comprehensive clinical
care to all patients. These skills involve the ability of the clinician to interact with

Table 1.1 Alcohol use in ancient cultures

Mesopotamia Egypt Greece Rome
• Less strong • Beer brewed in • Wine (no beer) • Wine became important
evidence large quantities near • Moderate in the Mediterranean trade
• Alcohol storage bakeries drinking • Variable quality of wine
vessels found • Osiris was the • Dionysus was based on class
God of wine God of wine-making
1 Historical and Cultural Perspectives on Alcohol Use 5

and engage knowledgeably with people across cultures and the lifelong process for
self-reflection, critique, and identifying one’s own personal biases to acknowledge
the complexities of intersecting identities with an ongoing curiosity [9]. As such, it
is imperative for clinicians assessing and managing individuals with alcohol use
disorder and other addictions to be aware of cultural influences in the development
and treatment of individuals affected by these disorders. While it is important to
have a basic background understanding of cultural variables and ethnic patterns
involved in alcohol use, it is equally important to exercise caution to avoid general-
ization, which may lead to stereotyping, ultimately confounding understanding and
leading to strained therapeutic relationships. It is also critical to identify sociodemo-
graphic variables overlaying cultural influences such as age, gender, and socioeco-
nomic status, adding to the complexity of alcohol and other substance use.
There are several definitions that should be reviewed when discussing cross-­
cultural sensitivity and cultural competence (Table 1.2). Culture is the way of life of
a group of people, encompassing various factors, including material environment,
social organization, symbols, status, language, technology, style of child-raising,
worldview, and citizenship [1]. Cultures typically hold rules or traditions surround-
ing substance use. Ethnicity involves people within a diverse culture who share a
common background, such as identity with a nation, language of origin, religious
practices or faith background, or family rituals. Ethnic groups may vary greatly in
their use of alcohol and other substances. Subculture refers to a distinct grouping
within a culture which share major sociocultural characteristics. In the case of peo-
ple with substance use disorders, certain subcultures arise linked to using in specific
contexts or seeking help, such as drinking at a specific college party house or having
an affiliation with a recovery group. People can belong to more than one ethnicity
and/or subculture whose expectations and norms may conflict. Cross-cultural refers

Table 1.2 Definition of terms pertaining to culture

Important definitions in studying culture
Term Definition
Culture Way of life of a group of people
Ethnicity People within a diverse culture who share a common background
Subculture To a distinct grouping within a culture which share major sociocultural
characteristics
Cross-cultural Comparing characteristics across different cultural groups
Norm Behaviors within a culture viewed in a positive or negative way
Identity How persons view themselves based on their group affiliations
Cultural The ability to function effectively within a culture
competence
Cultural humility The ability of the clinician to interact with and engage knowledgeably
with people across cultures
Clinical cultural Lifelong process for self-reflection, critique, and identifying one’s own
competence personal biases to acknowledge the complexities of intersecting identities
with an ongoing curiosity
Acculturation Individuals adapt certain values of the host culture while retaining the
values of their culture of origin
Enculturation A process of teaching children to be culturally competent
6 C. Collins and C. LaGrotta

to comparing characteristics across different cultural groups. Norms are behaviors

within a culture viewed positively or negatively; ideal norms refer to how a person
is judged as should behave, and a behavior norm is how people in a group actually
behave, regardless of the ideal. An ideal norm of an ethnic group may promote
drinking, such as the use of wine in Catholic mass or Jewish Passover, or may forbid
its use, such as in Islam. Norm conflicts that arise may lead to more excessive or
problematic substance use in an individual. Identity is how persons view themselves
based on their group affiliations. Exploring a person’s identity during a substance
use assessment may help a clinician gain insight to utilize motivational enhance-
ment better. Cultural competence is the ability to function effectively within a cul-
ture by communicating appropriately with others; avoiding interpersonal,
professional, or legal problems; and developing an identity consistent with cultural
expectations. Acculturation is a social learning process whereby individuals adapt
certain values of the host culture while retaining the values of their culture of origin.
Depending on the ethnic group and the extent of recent migration, acculturation
may increase both risk factors and protective factors for developing an addiction [1].
Enculturation is a process of teaching children to be culturally competent [10].
Estimating the prevalence of substance use in an ethnic group involves a careful
consideration of study design, including determining possible confounders such as
population selection, language barriers, timing, and response bias. Biological and
psychological factors influence the development of alcohol and other substance
addictions. For instance, approximately 50% of northeast Asians have a deficiency
in the liver enzyme aldehyde dehydrogenase 2, involved in the metabolism of alco-
hol. Having this deficiency is protective against developing alcoholism [1, 11].
Cultures that foster shame and guilt may promote alcohol abuse, whereas those that
value responsibility to others, interdependence, and group achievement, as seen in
many Asian cultures, are considered protective [1].

1.3 Clinical Relevance

Understanding a patient’s cultural background starts with properly gathering a cul-

tural history. This will allow the clinician to better understand the patient’s view of
the world, the meaning of their illness, and the expected recovery process [1]. A
cultural assessment involves first asking about the ethnic origins of the patient’s
parents and grandparents, including birthplace, living situation growing up, primary
language learned at home, roles and affiliations in their community, educational
experience, and marital and family life. The next step consists of assessing the
patient’s overall enculturation into their ethnic group of origin. Having a parent who
actively misused substances may have disturbed the development of a healthy iden-
tity and cultural competence. Living in an unfamiliar culture outside of one’s origin
may increase stress and precipitate alcohol and other substance misuse [10]. Lastly,
it is important to assess a person’s substance use in the context of enculturation.
Gathering such information may involve questions pertaining to how substance use
was viewed growing up and the context in which it began. For instance, did their
1 Historical and Cultural Perspectives on Alcohol Use 7

parents drink alcohol growing up, and was it excessive or problematic? How and
when did the patient first get introduced to alcohol, and what was their experience
like? Did they use it to cope with stress and anxiety early on in life or in the context
of developing skills like forming relationships and acquiring social skills [10]? If so,
alcohol and other drug use may lead to loss of social coping and eventual loss of
social status, including those related to marriage, job, living situation, and friend-
ships. Furthermore, young adults who fail to advance in these social constructs may
be more likely to find connections in alcohol and other drug addiction subcultures,
which tend to impose less stringent values and expectations. As addiction pro-
gresses, social connections are strained, and the individual eventually loses mem-
bers of their normal social plexus which must be reconstructed during recovery and
provides an opportunity for supportive intervention. An important step for those
seeking recovery is to remove active problematic drinkers and substance users from
their social plexus and replace them with individuals who are committed to their
sobriety. Living in a therapeutic community or recovery house may help to foster
social plexus reconstruction during recovery. Helpful strategies which may be use-
ful in reconstructing one’s social plexus include joining a group whose members are
also looking for new associates (such as a mutual help group or 12-step group);
joining a group with shared interests or a charitable organization; volunteering at a
school, hospital, or nursing home; or going back to school or starting a new job with
new associates. The person in recovery likely will also work to rebuild strained
relationships with family and friends, which involves a long and challenging pro-
cess of rebuilding trust.
Treatment geared toward specific cultures, ethnicities, nationalities, and reli-
gious groups may aid in recovery from alcohol and other substance use disorders.
Such participation may provide the person in recovery with a stable and sober envi-
ronment, meaningful work, emotional support, and the opportunity to build a new
identity as a person in recovery. Clinicians should be careful not to recommend
treatment at odds with an individual’s culture or identity. For instance, if a person is
turned off by the “Higher Power” of Alcoholics Anonymous, an alternative recom-
mendation for mutual help groups might be SMART Recovery [10].

References
1. el-Guebaly N. Chapter 4. Cross cultural aspects of addiction. In: Galanter M, Kleber HD,
Brady KT, editors. Textbook of substance abuse treatment. APA; 2015. p. 59–70.
2. Joffe AH. Alcohol and social complexity in ancient western Asia. Curr Anthropol.
1998;39(3):297–322. https://doi.org/10.1086/204736.
3. Hanson DJ. Preventing alcohol abuse. Praeger; 1995.
4. Hanson D. Chapter 1. Historical evolution of alcohol consumption in society. In: Boyle P,
Boffetta P, Lowenfels AB, et al., editors. Alcohol: science, policy and public health. Oxford
Academic; 2013. p. 3–12.
5. Nguyen M-L. Dionysus or Bacchus, god of wine, II century Roman statue of Dionysus, after
a Hellenistic model, ex-collection Cardinal Richelieu, Louvre.
6. Phillips R. Alcohol: a history. Chapel Hill, NC: The University of North Carolina Press; 2019.
8 C. Collins and C. LaGrotta

7. NatGeoUK. Dionysus, Greek God of wine and revelry, was more than
just a “Party God”. National Geographic. 2022 May 25. Available
from: www.nationalgeographic.co.uk/history-­and-­civilisation/2022/05/
dionysus-­greek-­god-­of-­wine-­and-­revelry-­was-­more-­than-­just-­a-­party-­god
8. Mann K, et al. One hundred years of alcoholism: the twentieth century. Alcohol Alcohol.
2000;35(1):10–5. https://doi.org/10.1093/alcalc/35.1.10.
9. Khan S. Cultural humility vs. competence — and why providers need both. HealthCity.
2021 Mar 9. Available from: https://healthcity.bmc.org/policy-­and-­industry/
cultural-­humility-­vs-­cultural-­competence-­providers-­need-­both
10. Westermeyer JJ, Warwick M. Chapter 37. Cultural issues in addiction medicine. In: Ries
RK, Fiellin DA, Miller SC, Saitz R, editors. The ASAM principles of addiction medicine.
Lippincott Williams and Wilkins; 2014. p. 555–60.
11. Li TK. Pharmacogenetics of responses to alcohol and genes that influence alcohol drinking. J
Stud Alcohol. 2000;61(1):5–12. https://doi.org/10.15288/jsa.2000.61.5.
The Science of Addiction: How Alcohol
Affects the Brain 2
Abdo Semaan

2.1 Introduction

Alcohol use disorder (AUD) is a significant public health concern in the United
States, impacting around 16 million individuals and contributing to the annual loss
of 85,000 Americans [1]. Historically, healthcare providers have conceptualized
alcohol addiction as a moral failing rather than a medical condition. Recent advances
in neuroscience have the potential to shift this perspective by providing a neurobio-
logical framework that challenges outdated views and promotes a more empathic
approach to AUD [2].
At the core of this neurobiological understanding of AUD is a three-stage addic-
tion cycle: binge/intoxication, withdrawal/negative affect, and preoccupation/antic-
ipation [3]. Each stage engages distinct brain areas: the basal ganglia, the extended
amygdala, and the prefrontal cortex (see Table 2.1). In the binge/intoxication phase,
there is an increased dopaminergic response within the basal ganglia to alcohol-­
related cues, a process known as “incentive salience.” This phase also initiates a
complex interaction between increasing desire and diminishing rewards from alco-
hol consumption [4]. Next, in the withdrawal/negative affect stage, the extended
amygdala becomes engaged, triggering stress pathways and leading to withdrawal
symptoms and a lower pleasure baseline [5]. Finally, the preoccupation/anticipation
stage sees the impairment of the prefrontal cortex. This impairment results in
reduced impulse control and emotional regulation, crucially contributing to the
emergence of cravings and perpetuating the addictive cycle’s repetitive nature [6].
The risk for developing AUD encompasses a complex interplay of genetic, epi-
genetic, and psychological factors. Genetically, specific individuals are predisposed
to AUD due to their variations in alcohol metabolism (see Table 2.2) and reward
circuit-related genes [7]. Environmental factors can also predispose to AUD via

A. Semaan (*)
New York-Presbyterian/Weill Cornell Medical Center, New York, NY, USA
e-mail: [email protected]

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2024 9

M. Khan, J. Avery (eds.), From Stigma to Support, Psychiatry Update 4,
https://doi.org/10.1007/978-3-031-73553-0_2
10 A. Semaan

Table 2.1 Neuroadaptations of the addiction cycle

Primary
Stage of addiction brain region Primary changes
1. Binge/intoxication Basal Incentive salience: Increased dopamine release related to
stage ganglia reward-associated cues [4]
2. Withdrawal/ Extended Withdrawal symptoms: Emotional and physical
negative affect stage amygdala withdrawal symptoms due to decreased baseline
dopamine and increased stress neurotransmitters [5]
3. Preoccupation/ Prefrontal Executive dysfunction: Impaired decision-making,
anticipation stage cortex increased impulsivity, and cravings [6]

Table 2.2 Basics of alcohol metabolism

Enzyme Substrate End products Key facts
Alcohol Ethanol Acetaldehyde Predominantly found in the liver. Variants of
dehydrogenase ADH genes can influence the rate of alcohol
(ADH) metabolism, affecting individual tolerance
and risk of alcoholism [7]
Aldehyde Acetaldehyde Acetic acid Important in the second step of ethanol
dehydrogenase processing. ALDH2 deficiency leads to the
(ALDH) accumulation of acetaldehyde, causing
flushing and other adverse reactions to
alcohol [8]
Catalase Ethanol Acetaldehyde Plays a minor role in alcohol metabolism,
less significant compared to ADH and
ALDH
CYP2E1 Ethanol Acetaldehyde Involved in the microsomal ethanol
oxidizing system (MEOS). More active in
chronic alcoholics, contributing to tolerance
and liver damage due to the production of
reactive oxygen species [9]

epigenetic modifications. For instance, exposure to trauma can trigger epigenetic

changes that strengthen stress pathways, which increases vulnerability to AUD [10].
In addition, psychological factors, including pre-existing mental health conditions
such as anxiety, depression, and stress-related disorders, significantly increase the
risk of developing AUD [11]. These conditions may lead individuals to self-­medicate
with alcohol, setting a pathway toward addiction.
AUD’s signs and symptoms are diverse, spanning physical, psychological, and
social domains of life [12]. This complexity necessitates efficient diagnostic tools
such as the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition,
Text Revision (DSM-5-TR) (see Table 2.3) [13]. At the same time, the Addictions
Neuroclinical Assessment (ANA) provides an alternative diagnostic instrument that
utilizes deeper neurobiological insights [14]. The ANA hopes to facilitate more tar-
geted treatment and help shift perceptions of AUD toward a more empathetic and
scientific understanding of the disease.
2 The Science of Addiction: How Alcohol Affects the Brain 11

Table 2.3 DSM-5-TR criteria for AUD [13]

1. Alcohol taken in larger amounts or over a longer period than intended
2. Persistent desire or unsuccessful efforts to cut down or control alcohol use
3. A great deal of time is spent in activities necessary to obtain, use, or recover from alcohol’s
effects
4. Craving or a strong desire or urge to use alcohol
5. Recurrent alcohol use resulting in a failure to fulfill major role obligations at work, school, or
home
6. Continued alcohol use despite having persistent or recurrent social or interpersonal problems
caused or exacerbated by alcohol
7. Important social, occupational, or recreational activities are given up or reduced because of
alcohol use
8. Recurrent alcohol use in situations in which it is physically hazardous
9. Alcohol use is continued despite knowledge of having a persistent or recurrent physical or
psychological problem that is likely to have been caused or exacerbated by alcohol
10. Tolerance, as defined by either a need for markedly increased amounts of alcohol to achieve
intoxication or desired effect or a markedly diminished effect with continued use of the same
amount of alcohol
11. Withdrawal, as manifested by either the characteristic withdrawal syndrome for alcohol (or
a closely related substance, such as a benzodiazepine), is taken to relieve or avoid withdrawal
symptoms

2.2 How Alcohol Affects the Brain

2.2.1 Basics of the Addiction Cycle

Extensive research conducted by neuroscientists has culminated in a well-­established

neurobiological model of addiction. The model is characterized by a repetitive cycle
of three stages (see Fig. 2.1): intoxication/binge, withdrawal/negative affect, and
preoccupation/anticipation. The duration of this cycle varies significantly among
individuals, ranging from daily occurrences to several months. Additionally, the
intensity of each stage differs from person to person. A common aspect of the cycle
is to intensify over time, resulting in escalating biological, psychological, and social
damage. Prior to delving into these neurobiological stages in greater detail, it is
essential first to examine four key behaviors central to the addiction cycle: impulsiv-
ity, positive reinforcement, negative reinforcement, and compulsivity.

2.2.2 Four Key Behaviors

In the initial stages of alcohol exposure, impulsivity often plays a pivotal role [16].
Given alcohol’s disinhibitory properties, it naturally elicits euphoria or pleasure
upon use for most individuals. This initial experience positively reinforces alcohol
use, increasing the likelihood of repeated consumption. Alternatively, some indi-
viduals turn to alcohol to alleviate negative emotions like depression or anxiety. In
these cases, the temporary relief from these feelings serves as a negative reinforce-
ment for further alcohol use. Importantly, positive and negative reinforcements can
12 A. Semaan

Fig. 2.1 The three stages

of the addiction cycle and
their respective primary
impacted brain
regions [15]

come from social factors rather than just the direct effects of alcohol. For example,
positive social reinforcement might occur through peer approval after succumbing
to peer pressure to try alcohol at a party. Conversely, negative social reinforcement
can happen when alcohol use alleviates social isolation, such as visiting a bar for
a drink.
As alcohol use continues, tolerance develops, leading to a diminished response
to the substance over time [17]. This tolerance often results in escalated or more
frequent alcohol use to achieve the initially experienced effects. Tolerance also
alters an individual’s emotional baseline, making them more prone to negative emo-
tions in the absence of alcohol. The diminished baseline leads to a persistent state of
withdrawal, characterized by low mood, anxiety, and physical symptoms, which
further drive alcohol use.
Over time, this pattern of increasing alcohol use to avoid withdrawal symptoms
transitions from an impulsive to a compulsive behavior. This shift marks a signifi-
cant loss of executive control over alcohol use and is a defining characteristic of
addiction. Compulsivity also underlines the difficulties faced by those in the addic-
tion cycle when trying to reduce or abstain from alcohol use.

2.2.3 The Intoxication/Binge Stage

The onset of the intoxication/binge stage in the addiction cycle of AUD starts with
alcohol consumption, a substance recognized for its ability to induce a positive
hedonic response. Under normal conditions, reward circuits maintain a baseline
hedonic tone via the basal ganglia [18]. A vital component of this baseline tone
comes from the midbrain’s tonic release of dopamine into the striatum and
2 The Science of Addiction: How Alcohol Affects the Brain 13

prefrontal cortex. This tonic dopamine release primarily influences high-affinity D2

receptors and, to a lesser extent, D1 receptors. Specific signaling molecules, such as
endocannabinoids, opioids, and gamma-aminobutyric acid (GABA), regulate this
dopaminergic tone. Upon the introduction of alcohol, there is an amplification of
dopaminergic transmission that specifically stimulates D1 receptors, resulting in the
typical feeling of elation commonly associated with the initial intake of alcohol [19].
The binge/intoxication stage engages two pivotal neural circuits in the brain’s
reward system: the mesolimbic and nigrostriatal pathways. The mesolimbic path-
way, encompassing the ventral tegmental area, nucleus accumbens, and ventrome-
dial striatum, plays a vital role in the reward and positive reinforcement experienced
by alcohol. Meanwhile, the nigrostriatal pathway, which involves the dorsolateral
striatum, is critical to regulating habitual motor behaviors and functions [20]. The
co-activation of these pathways creates a link between the pleasurable experience of
consuming alcohol and the behavior of seeking this pleasure.
As the addiction cycle continues, there is a shift in dopamine cell firing patterns
from the basal ganglia. This evolution results in heightened dopamine responses to
environmental cues linked to alcohol, like particular social environments or places,
rather than to the alcohol directly [4]. This shift, known as incentive salience, culti-
vates strong motivational urges. It is noteworthy that this altered pattern of dopa-
mine release may persist even when an individual’s tolerance to alcohol decreases.
Understanding incentive salience is critical in the approach to AUD as it under-
scores the importance of altering the environments associated with alcohol use.

2.2.4 The Negative Affect/Withdrawal Stage

The withdrawal/negative affect stage of the addiction cycle in AUD encompasses

both acute and post-acute withdrawal experiences. This stage is characterized neu-
robiologically by two primary adaptations. The first occurs within the reward sys-
tem, resulting in altered dopaminergic, GABAergic, and glutaminergic tone. The
dopaminergic tone is diminished, which manifests as reduced pleasure from natural
rewards such as food and sex. Consequently, this can lead to decreased satisfaction
in personal and professional relationships.
Simultaneously, there is a crucial shift in the balance between glutamatergic and
GABAergic neurotransmission within the reward system. Chronic alcohol exposure
induces an increase in glutamatergic tone and a reduction in GABAergic tone [21].
This shift leads to neurochemical imbalance, favoring excitation over inhibition.
The increased glutamatergic activity contributes to heightened neural excitability,
which underlies key withdrawal symptoms, such as restlessness, anxiety, and agita-
tion. This imbalance not only makes the experience of withdrawal particularly chal-
lenging but also decreases the individual’s tolerance for stress, complicating
recovery efforts.
The second key neuroadaptation involves the heightened activation of stress cir-
cuits in the extended amygdala, also called the “anti-reward” system [22]. This anti-­
reward system includes neural circuits from the shell of the nucleus accumbens, the
14 A. Semaan

bed nucleus of the stria terminalis (BNST), and the amygdala’s central nucleus
(CeA). The intensified anti-reward system positively modulates the hypothalamic-­
pituitary-­adrenal (HPA) axis and increases the release of stress mediators like
corticotropin-­releasing factor (CRF), dynorphin, orexin, and norepinephrine (NE).
Notably, the brain possesses a buffering mechanism against the anti-reward system,
which involves cannabinoid, nociceptive, and neuropeptide Y transmission [23–25].
Alterations in this buffering system can also predispose individuals to the
risk of AUD.
Clinically, an overactive anti-reward system manifests as irritability, anxiety, and
dysphoria, driving the chronic withdrawal symptoms seen in AUD. This withdrawal
sets the stage for further binge/intoxication through negative reinforcement.
Ultimately, it leads to a cycle where using alcohol to mitigate withdrawal symptoms
leads to exacerbated withdrawal during subsequent periods of abstinence.

2.2.5 The Preoccupation/Anticipation Stage

The preoccupation/anticipation stage is the last phase in the addiction cycle of AUD,
occurring during periods of abstinence. The length of this stage varies, tending to be
shorter in more severe cases of AUD. The hallmark of this stage is an intense preoc-
cupation with alcohol, which is also known as “cravings.” The primary brain region
affected by this stage is the prefrontal cortex (PFC), which generally controls the
capacity to plan, manage tasks, and regulate thoughts, emotions, and impulses.
To understand the role of the PFC in AUD, researchers have characterized a “Go
system” and a “Stop system” [26]. The Go system involves decisions requiring sig-
nificant attention and planning, mainly active in initiating goal-directed behaviors.
This system includes the dorsolateral prefrontal cortex and the anterior cingulate.
Neuronal firing in the Go system is highly responsive to alcohol-associated cues in
individuals with AUD. Increased activity in the Go system circuits stimulates the
nucleus accumbens, enhancing the urge to consume alcohol in the presence of
alcohol-­related environmental cues (incentive salience). The Go system also plays a
role in stimulating habitual response systems in the dorsal striatum, often promoting
more impulsive alcohol use.
On the other hand, the Stop system works by inhibiting the Go system’s activity.
It includes circuits in the orbitofrontal and ventrolateral prefrontal cortex and regu-
lates the dorsal striatum and nucleus accumbens, diminishing impulsivity and the
effects of incentive salience [27]. The Stop system also modulates stress and emo-
tional systems in the extended amygdala. A reduction in the Stop system’s activity
can result in increased stress circuitry activity in the extended amygdala, elevating
the risk of relapse into alcohol use [28].
2 The Science of Addiction: How Alcohol Affects the Brain 15

2.3 Etiology of Alcohol Use Disorder

2.3.1 Genetic Risk

Genetics’ role in AUD development is notably complex and multifaceted. Evidence

supports that individuals with a family history of AUD are more likely to develop
the disorder themselves [29]. The implicated genes are generally associated with
alcohol metabolism (seen in Table 2.2) or the integral neural circuits found in the
addiction cycle [30].
Turning our focus to alcohol metabolism, genetic variations profoundly influ-
ence the activity of enzymes like alcohol dehydrogenase (ADH), aldehyde dehydro-
genase (ALDH), cytochrome P450 2E1 (CYP2E1), and catalase [7]. These genetic
differences dictate how an individual processes alcohol, thereby affecting their risk
for AUD. For instance, certain genetic variations can cause a rapid conversion of
alcohol to acetaldehyde, a toxic by-product, which may lead to adverse reactions
and discourage excessive alcohol consumption. Oppositely, other genetic profiles
may result in a more efficient metabolism of alcohol, increasing the likelihood of
binge consumption and increasing the risk of AUD.
Genetic variations in receptors for neurotransmitters such as dopamine, GABA,
and opioid peptides can influence AUD risk. These neurotransmitters and peptides
are essential in the reward and reinforcement mechanisms that underpin the addic-
tion cycle in AUD. For instance, genetic mutations related to the mu-opioid receptor
(OPRM1) gene affect the rewarding and reinforcing properties of alcohol consump-
tion [31]. In particular, the A118G genetic variation of the OPRM1 gene is linked to
heightened feelings of euphoria in response to alcohol. Additionally, this genetic
variation can serve as an indicator of an amplified responsiveness to naltrexone
for AUD.

2.3.2 Epigenetic Risk

Epigenetics plays a pivotal and complex role in the etiology of AUD, acting as a
regulatory layer that modulates gene expression in response to various environmen-
tal factors and stressors. Unlike the fixed blueprint of genetics, epigenetic mecha-
nisms, such as DNA methylation and histone modifications, are dynamic processes.
Epigenetics serves as a bridge between an individual’s genetic makeup and their
environmental experiences.
Adverse childhood experiences (ACEs), trauma, and chronic stress can result in
significant epigenetic modifications [32]. These modifications typically alter gene
expression in stress response pathways, potentially increasing sensitivity to alco-
hol’s effects and thereby raising the risk of AUD. Moreover, epigenetic mechanisms
can transform social and cultural influences into biological consequences, altering
the likelihood of developing AUD [33]. For instance, in cultures where early-age
alcohol consumption is accepted, epigenetic and molecular alterations occur that
may predispose to the addiction cycle [34].
16 A. Semaan

2.3.3 Psychological Risk

Specific psychological factors, including mental health disorders, do contribute to

the risk of developing AUD. For example, individuals struggling with mental health
disorders such as anxiety, depression, bipolar disorder, and PTSD may resort to
alcohol as a form of self-medication to seek temporary relief from their psychiatric
symptoms. However, this self-medicating behavior can aggravate the mental health
condition and lead to a deeper reliance on alcohol. The relationship between mental
health disorders and AUD is bidirectional, with each potentially exacerbating the
other [35].

2.4 Diagnosis of Alcohol Use Disorder

2.4.1 
DSM-5-TR Diagnostic Criteria

The diagnosis of AUD is complex, involving behavioral, psychological, and neuro-

biological factors. Traditionally, the medical community has relied on the DSM for
the diagnosis of AUD. Per the DSM-5-TR, an individual must exhibit at least 2 of
11 specified criteria within 12 months [13]. These criteria encompass a range of
behaviors and consequences related to alcohol consumption, as elaborated in
Table 2.3.

2.4.2 Utilizing the Addiction Cycle

Despite the advancements in the neurobiology of addiction, there have been chal-
lenges in translating that knowledge into clinical utility. This issue partly arises
from the reliance on the above DSM criteria for diagnosing substance use disorders,
which, while comprehensive, often do not sufficiently incorporate the neuroscience
aspects of addiction [36].
The National Institute of Mental Health (NIMH) initiated the Research Domain
Criteria (RDoC) project to address the limitations of the DSM. This project aimed
to fund research that adopts a neuroscience-driven perspective to understand psy-
chiatric conditions [37]. Inspired by the RDoC framework, researchers developed
the Alcohol Addiction RDoC [38]. A significant outcome of this neuroscience-­
focused research is the creation of the Addictions Neuroclinical Assessment (ANA)
[14]. The ANA aims to enhance the diagnosis and treatment of alcohol addiction by
utilizing a more in-depth understanding of the underlying neurobiological mecha-
nisms driving addiction.
2 The Science of Addiction: How Alcohol Affects the Brain 17

2.4.3 Addictions Neuroclinical Assessment

The ANA represents a significant evolution in translating addiction research into

clinical practice, integrating three neurofunctional domains: incentive salience,
negative emotionality, and executive dysfunction. These domains reflect the stages
of the addiction cycle, including binge/intoxication, withdrawal/negative affect, and
preoccupation/anticipation.
Regarding the neurofunctional domains, the one tied to the binge/intoxication
stage is incentive salience. This domain highlights how the brain becomes more
attuned to alcohol-related cues, such as the people, places, and things they associate
with alcohol. This domain can be addressed by modifying the patient’s environ-
ment, such as with an admission to a rehabilitation facility [39]. The negative emo-
tionality domain is indicative of withdrawal experiences and is marked by heightened
anxiety and diminished pleasure from non-substance activities. This domain is man-
aged by targeting neurotransmitter imbalances during withdrawal with GABAergic
agents. Lastly, the executive dysfunction domain encompasses impairment of cog-
nitive processes like attention, planning, and behavioral flexibility.
The ANA utilizes a blend of neuroimaging, genetic testing, questionnaires, and
clinical interviews to provide a comprehensive understanding of an individual’s
alcohol addiction [14]. The ANA’s comprehensive approach underlines the neces-
sity of capturing multidimensional information to deepen our understanding of
addiction and refine diagnostic and treatment methodologies.

2.5 Conclusion

As we conclude this chapter, it is evident that the neurobiological understanding of

AUD has improved with time. This enhanced perspective frames AUD as a chronic,
relapsing condition marked by distinct neuroadaptations. These adaptations propel
an individual into a relentless cycle of seeking alcohol despite harmful conse-
quences. The addiction cycle includes three stages: intoxication/binge, withdrawal/
negative affect, and preoccupation/anticipation—each modulating specific neural
pathways and brain regions, thereby reinforcing the grip of addiction. It is vital to
understand that genetic, epigenetic, and psychological factors influence predisposi-
tion to this addiction cycle.
In the realm of assessment for AUD, it is pivotal to appreciate the multifaceted
signs and symptoms that span the physical, psychological, and social aspects of life.
Regarding diagnostic instruments, the traditional DSM-5-TR criteria provide a basis
for diagnosing and assessing the severity level of AUD. However, the advent of the
ANA marks a significant leap forward. The ANA prioritizes a neurobiological per-
spective, focusing on three key brain domains affected by addiction: incentive
salience, negative emotionality, and executive dysfunction. This approach enhances
diagnostic precision and opens new avenues for targeted treatment strategies.
Most importantly, understanding the neurobiology of addiction may lessen the
negative attitudes those with AUD face from providers [40]. When clinicians view
18 A. Semaan

addiction as a treatable medical condition akin to diabetes or hypertension, they can

offer more empathic and suitable care. Incorporating this perspective, along with
comprehensive addiction training, can destigmatize AUD and enhance patient
outcomes.

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Co-occurring Disorders: Mental Health
and Alcohol Use 3
Nicholas Romano and Rachel Luba

3.1 Introduction

This chapter will focus on co-occurring psychiatric conditions and mental health in
the context of alcohol use disorder (AUD). First, we will provide an overview of the
most-prevalent co-occurring psychiatric conditions and diagnostic considerations.
Second, we will discuss the pathophysiology of AUD and comorbid psychiatric
conditions. Third, we will discuss medications and psychotherapy approaches tar-
geting AUD with comorbid psychiatric conditions. Finally, we will conclude with
future directions for the study and treatment of AUD and comorbid psychiatric
conditions.

3.2 Prevalence and Epidemiology

In the United States, approximately 29.5 million people aged 12 or above met past-­
year criteria for alcohol use disorder (AUD) in 2022, and globally, an estimated 95
million people experience AUD [1, 2]. Annually, about 140,000 deaths in the United
States are attributable to alcohol use [3]. Alcohol overdose or poisoning accounts
for 32% of alcohol-related deaths, and 22.5% of alcohol-related deaths are due to
suicide [3]. Psychiatric comorbidity refers to the presence of one or more

N. Romano (*)
Department of Psychiatry, New York Presbyterian Weill Cornell Medicine,
New York, NY, USA
e-mail: [email protected]
R. Luba
Department of Psychiatry, Columbia University Irving Medical Center, New York, NY, USA
e-mail: [email protected]

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2024 21

M. Khan, J. Avery (eds.), From Stigma to Support, Psychiatry Update 4,
https://doi.org/10.1007/978-3-031-73553-0_3
22 N. Romano and R. Luba

psychiatric conditions in an individual, either simultaneously or sequentially. AUD

often co-occurs with other psychiatric conditions [4]. Estimates from national
comorbidity surveys suggest that compared to those without AUD, individuals with
AUD are significantly more likely to meet criteria for another substance use disor-
der, a personality disorder, major depressive disorder, attention deficit hyperactivity
disorder (ADHD), bipolar disorder, generalized anxiety disorder, and PTSD [5–11].
Comorbidity increases the risks associated with AUD and may lead to more serious
consequences in both the psychiatric disorder and the alcohol use disorder, includ-
ing relapse, hospitalizations, violence, incarceration, homelessness, failure in work
and school, medical sequelae, and treatment non-adherence [11, 12].
A recent series paper from Castillo-Carniglia and colleagues succinctly summa-
rizes findings on psychiatric comorbidity in the context of AUD from nearly 150
studies [5]. Key findings will be presented here with most to least-frequent comor-
bid diagnoses presented in order. Prior work suggests that comorbid substance use
disorders may be the most common co-occurring diagnosis in individuals with
AUD. Specifically, 40.6% of men and 47.1% of women with AUD have a lifetime
SUD diagnosis, and individuals with an SUD diagnosis in adolescence are 3.5 to
3.96 times more likely to have an AUD onset in early adulthood. Further, among
those with an SUD diagnosis, 47.3% have a comorbid AUD diagnosis. ADHD is the
second most common comorbid condition with AUD, with 33% of adults and
19.9–23.6% of adolescents with AUD meeting criteria for ADHD. Individuals diag-
nosed with ADHD are 1.35 to 1.74 times more likely to be diagnosed with AUD [5].
Prevalence rates for MDD vary by study, with a wide range of estimates published.
A median estimate from 35 studies presented by Castillo-Carniglia and colleagues
suggests nearly 30% of individuals with MDD have a lifetime history of AUD and
37% of those with a lifetime history of AUD meet the criteria for MDD. Notably,
estimates range from 4 to 22% when examining the prevalence of MDD in those
with a past-year AUD diagnosis. Longitudinal studies suggest that those with AUD
are two to three times as likely to be diagnosed with MDD. Anxiety disorders also
commonly co-occur with AUD, with 19.4% of those with AUD having any lifetime
anxiety disorder and 20–40% of those diagnosed with an anxiety disorder meeting
criteria for AUD. Examination of specific anxiety disorders suggests that among
those with AUD, lifetime social phobia is most common, followed by generalized
anxiety disorder and then panic disorder. Women with AUD have higher rates of all
anxiety disorders compared to men with AUD [5]. In those diagnosed with PTSD,
approximately an estimated 30–55% evidence a lifetime AUD diagnosis. Conversely,
among those diagnosed with AUD, 10% of men and 26% of women demonstrate
lifetime PTSD diagnoses. The odds of developing PTSD among those with AUD are
estimated between 0.70 and 1.35, while the odds of developing AUD among those
with PTSD are between 4.10 and 5.43 [5].
Prevalence estimates for AUD comorbid with personality disorders vary widely,
and there aren’t clear longitudinal association studies examining this overlap.
Antisocial personality disorder is estimated to occur in 18% of individuals with
AUD based on a pooled estimate from 16 studies, with a wide range from 1 to 52%
across studies. The prevalence of comorbid borderline personality disorder and
3 Co-occurring Disorders: Mental Health and Alcohol Use 23

Table 3.1 Prevalence estimates of specific comorbidities

Comorbidity Prevalence estimates [5]
AUD + SUD 40.6% of males
47.1% of females
AUD + mood disorder 37% of adults
AUD + anxiety 19.4%
AUD + PTSD 10% of males
26% of females
AUD + personality disorder 18–21% of adults
AUD + schizophrenia 3.8% of adults
Note: Prevalence estimates reflect the estimated percentage of individuals with AUD that also meet
criteria for each indicated comorbid diagnosis

AUD is also difficult to conclude, given estimates range from 6 to 66% across exist-
ing studies and an estimated median prevalence of 21% [5]. Notably, among those
diagnosed with antisocial or borderline personality disorder, lifetime AUD diagno-
ses are 77% and 52%, respectively. Compared to other psychiatric comorbidities
examined, schizophrenia co-occurs with AUD relatively rarely, with 3.8% of those
with AUD diagnosed with schizophrenia. However, among those with schizophre-
nia, an estimated 20.6% meet criteria for AUD [5] (Table 3.1).

3.3 Assessment and Diagnostic Considerations

When assessing individuals with co-occurring disorders, one goal is to be mindful

of under-diagnosis of a psychiatric or AUD: treatment of the AUD will not necessar-
ily also treat the mood disorder, for example. Both co-occurring disorders should be
treated simultaneously when diagnosed. Another goal is to avoid over-diagnosis by
considering the time course of which alcohol can induce psychiatric symptoms and
make the diagnoses once the individual is no longer undergoing withdrawal [13].
For instance, it may be necessary to wait several months to make a psychiatric diag-
nosis in individuals with alcohol-induced psychoses. Further, individuals with
chronic alcohol or other substance use disorders, chronic mental illness, and medi-
cal comorbidities may have further diagnostic challenges [13]. Nonetheless, it is
more likely that individuals will have co-occurring diagnoses, rather than etiologi-
cal disorders where the treatment of one disorder resolves the next. Therefore, co-­
occurring diagnoses should also be treated concurrently.
A complete assessment with screening for co-occurring psychiatric, alcohol, and
other substance use disorders is warranted, in addition to consideration of medical
comorbidities and at-risk behaviors, including self-harming behaviors and violence.
The evaluator should ascertain the scope of the disorders, including its interpersonal
and environmental impacts, to inform and guide treatments and recovery while also
considering the individual’s motivation for change. Further, assessments of indi-
viduals with co-occurring psychiatric and AUD should ideally be serially and longi-
tudinally utilizing multiple information sources, including individual interviews,
collateral, physical examination, and laboratory testing [13].
24 N. Romano and R. Luba

Differentiating whether the psychiatric symptoms or disorder(s) exist either

before or upon cessation of alcohol use proves difficult given the bi-directionality of
the psychiatric and AUD, each influencing the other. Moreover, there are overlap-
ping symptoms among many psychiatric disorders and AUD, in addition to whether
the individual is intoxicated or in withdrawal from alcohol and at different periods
of abstinence from alcohol.
An individual may present intoxicated on alcohol, in withdrawal from alcohol, or
in varying lengths of abstinence. Psychiatric symptoms may, therefore, be the result
of or exacerbated by the presence or absence of alcohol (Reference: Absolute
Addiction Psychiatry Review). Some of the presenting symptoms, including mood
instability and anxiety, may be due to the alcohol itself and may, therefore, resolve
upon cessation and continued abstinence from alcohol [13]. In these contexts, it
would be important to consider a diagnosis of a substance-induced psychiatric dis-
order, as outlined in the DSM-V, including substance-induced mood, anxiety, or
psychotic disorders, among others.
Light consumption of alcohol is associated with a slight euphoria or “buzz,”
whereas moderate to heavy use may be associated with depression, suicidal think-
ing, or violent behavior [11]. Over time and with prolonged consumption of alco-
hol, the rate of anxiety and dysphoria in the individual increases [11]. With prolonged
and heavy use, an individual may also develop a physiological dependence on alco-
hol that increases the risk of experiencing an alcohol withdrawal syndrome. Alcohol
withdrawal is associated with a hyperadrenergic state characterized by a variety of
clinical signs and symptoms, including severe anxiety, agitation, insomnia, malaise,
hallucinations, and delusions, among other life-threatening conditions [11]. Alcohol
withdrawal is to be discussed in greater detail elsewhere in this text (see Chap. 6).
Following acute alcohol withdrawal, some individuals experience ongoing mood
instability, fatigability, insomnia, hostility, as well as reduced sexual interest [11].
For example, symptoms of anxiety that occur while an individual is experiencing
an alcohol withdrawal syndrome could indeed be attributed to alcohol withdrawal
and would be expected to resolve once the withdrawal subsides [13]. Yet, if symp-
toms of anxiety are part of a primary psychiatric disorder, the symptoms would
likely persist beyond alcohol intoxication and withdrawal and may hinder the treat-
ment of AUD [13].

3.4 Pathophysiology of AUD and Other

Psychiatric Conditions

In assessing and treating AUD comorbid with other psychiatric conditions, it is

important to consider the pathophysiology or directionality of comorbid conditions.
On the one hand, the presence of psychiatric disorders may increase the risk of
exposure to alcohol and the subsequent risk of the development of an
AUD. Alternatively, it is possible that AUD, like other substance use disorders, may
induce and/or exacerbate psychiatric symptoms and disorders. Mechanisms under-
lying AUD and comorbid psychiatric conditions remain under study, with some
3 Co-occurring Disorders: Mental Health and Alcohol Use 25

developmental or genetic pathways more clearly elucidated than others. Two pre-
dominant theories outline the development and maintenance of AUD comorbid with
other psychiatric conditions. The common liability pathway proposes that co-­
occurring psychiatric conditions are a result of shared underlying vulnerabilities
activated by environmental, genetic, and epigenetic factors (and their interactions)
and that the order of onset of co-occurring disorders has no causal role [5, 14, 15].
Alternately, some propose that comorbidity develops sequentially, with one disor-
der directly predicting or contributing to the development of another and especially
in the context of substance use, certain types of substance use initiation typically
preceding heavier, more problematic patterns of use (The Gateway Hypothesis)
[16]. Merging of these models acknowledges common underlying vulnerabilities
while also reflecting evidence that there are reinforcing and reciprocal causal rela-
tionships between comorbid conditions [5]. For instance, while a shared underlying
vulnerability paired with adverse environmental influences may contribute to the
development of both AUD and depression, the developmental and sequential course
of disorder development is also important. AUD preceding the onset of depression
may present a different clinical picture than depression preceding the onset of AUD,
and this trajectory can and should inform clinical decision-making and outcomes.
In the context of AUD comorbid with other substance use disorders, the evidence
does support a common sequential and temporal order of drug use initiation across
cultures where alcohol use onset precedes the initiation of other drug use. Still, the
sequence of alcohol and drug use is influenced by social context, drug availability,
and social norms. Thus, it appears likely that access and exposure to early alcohol
or other drug use increase the probability of exposure or access to other drugs, sug-
gesting that the gateway hypothesis may be more salient in predicting drug initia-
tion rather than problematic drug use itself [5, 17–19]. Further, cross-reinforcement
and cross-tolerance support a reciprocal relationship between alcohol and other
drug use in the context of SUD where (1) one substance often enhances motivation
for another by acting on shared neurobiological reward mechanisms (cross-­
reinforcement) or (2) repeated co-use of more than one substance contributes to
tolerance and escalation of use of both substances due to pharmacological effects
(cross-tolerance) [5, 20–22].
Prospective data supports early-onset ADHD as a risk factor in the development
of AUD and a causal connection in the development of this comorbidity [5, 23, 24].
Children and adolescents diagnosed with ADHD are 1.35 to 1.74 times more likely
to develop AUD later in life than those without ADHD. There is also evidence of
increased odds of a mutation in the D4 dopamine receptor in those with ADHD,
which alters the effect of alcohol on the dopamine system and appears to make the
effect of alcohol similar to stimulant medications used to treat ADHD [5, 25], per-
haps altering its reinforcement and use in those with ADHD. Executive functioning
differences in those with AUD are also strongly implicated in the initiation and
maintenance of alcohol use [5, 26].
Examinations of directionality in the development and maintenance of AUD
with comorbid depression support the onset of alcohol use to relieve depressive
symptoms as well as the onset of depressive symptoms in response to the sequelae
26 N. Romano and R. Luba

of AUD, making it difficult to disentangle directionality and support the common

liability pathway. Genetic evidence supports common genetic pathways in the
development of both disorders separately and in combination, and gene-­environment
studies support the role of shared common genetic risk factors activated by environ-
mental or socio-cultural factors [5, 27–34].
Available evidence supports genetic and environmental components in the etiol-
ogy of AUD comorbid with anxiety disorders, with evidence suggesting shared
genetic mechanisms underlying each disorder and an increased risk of this comor-
bidity in individuals with a family history of either disorder [35–37]. Though evi-
dence supports a common pathway where social anxiety tends to precede AUD [38,
39] and the use of alcohol to regulate anxiety symptoms as a risk factor for the
development of AUD [40], contradictory findings suggest that when controlling for
other risk factors (depression, social support), the longitudinal association between
anxiety symptoms and AUD is weak [41]. Therefore, more research is needed to
elucidate the mechanisms underlying the comorbidity of AUD and anxiety disor-
ders, with an emphasis on longitudinal outcomes.
Though there is certainly a need for additional research, there does appear to be
evidence that, in many cases, AUD develops after the onset of PTSD [42, 43]. In a
longitudinal analysis of outcomes among veterans, there was no significant relation-
ship between alcohol use prior to deployment and the etiology of PTSD. There was,
however, a significant relationship between PTSD symptoms and the development
of AUD symptoms [44]. Additional work suggests that while many experience an
increase in alcohol consumption following a traumatic event, the development of
AUD is largely attributable to risky patterns of alcohol use prior to trauma exposure
[45]. There is, therefore, growing attention to shared causal pathways in the devel-
opment of this comorbidity, such that early-life stressors, exposure to interpersonal
violence, and early adversity are common predictors of both PTSD and AUD.
The common liability pathway is also supported when considering AUD comor-
bid with personality disorders, particularly through behavioral disinhibition.
Specifically, the high impulsivity and low harm avoidance that characterize behav-
ioral disinhibition increase the likelihood of early alcohol use. In one longitudinal
study in Sweden, low-risk aversion and high sensation seeking in late childhood
greatly increased the risk of alcohol misuse in adulthood. Additional evidence
points to a mediating effect, whereby psychosocial correlates of personality disor-
ders (viz., social and academic difficulties, family dysfunction, and deviant peer
groups) increase the risk for AUD [46–50].

3.5 Pharmacotherapy Approaches Targeting AUD

and Other Psychiatric Conditions

The treatment of co-occurring disorders can be challenging, particularly since the

treatment of psychiatric and alcohol use disorders is often offered separately or
consecutively, thereby impeding on access to care and perpetuating the fragmenta-
tion of services, culminating in treatment non-adherence and worse outcomes [11].
3 Co-occurring Disorders: Mental Health and Alcohol Use 27

Importantly, the integration and simultaneous treatment of co-occurring psychiatric

and substance use disorders, including AUD, are necessary. FDA-approved medica-
tions for AUD include disulfiram (Antabuse), naltrexone (reVia), acamprosate
(Campral), and long-acting naltrexone (Vivitrol) [11]. Pharmacotherapies for AUD
are discussed extensively in the chapter on pharmacotherapies (see Chap. 7). Here,
we focus on unique considerations for the pharmacological treatment of AUD and
comorbid psychiatric conditions. Though there is evidence that adequate treatment
of AUD helps to alleviate mood or anxiety symptoms associated with alcohol with-
drawal, for some these symptoms persist, termed “subacute withdrawal.” [11]
Controlled trials of pharmacotherapies to address subacute withdrawal symptoms
suggest that a minority of patients experiencing subacute withdrawal have symp-
toms reflective of diagnosable psychiatric conditions and most post-withdrawal
depression symptoms remit without specific treatment when abstinence from alco-
hol is maintained [51, 52]. In a meta-analysis of co-occurring SUD and depression,
eight included studies focused on alcohol use disorder and demonstrated a signifi-
cant benefit of medication versus placebo to treat depressive symptoms [53].
Findings also suggest that a 1-week period of abstinence prior to diagnosis of
depression was associated with a more robust antidepressant effect. Comparisons of
antidepressant within this meta-analysis suggest that tricyclic or other antidepres-
sants performed somewhat better than SSRIs. Finally, those who experienced a
moderate medication effect also demonstrated moderate reductions in substance
use, while smaller antidepressant effects were associated with no notable reductions
in substance use. A large randomized controlled trial comparing sertraline (200 mg),
naltrexone (100 mg), sertraline (200 mg) + naltrexone (100 mg), and placebo sug-
gests that across 14 weeks, combined treatment contributed to the most robust
effects on abstinence and depression remission, supporting combined treatment
with naltrexone and sertraline for those with comorbid AUD and depression [54].
Additional considerations in the treatment of AUD with comorbid depression
include attention to the potential for SSRIs to exacerbate the tremor, anxiety, and
insomnia associated with physiological dependence and recent alcohol withdrawal
[11]. Further, in one recent systematic review of research with over 100,000 patients
with comorbid AUD or another SUD and depression, antidepressants (primarily
SSRIs) combined with psychotherapy appeared to be the most efficacious treatment
option [55].
The pharmacological treatment of ADHD comorbid with AUD has been impacted
by provider reluctance around psychostimulant use among those with an SUD, even
though psychostimulants are considered the first-line treatment for ADHD [56].
Still, this reluctance is not necessarily consistent with available data, which suggests
moderate reductions in substance use, reductions in ADHD symptoms, and greater
retention in treatment with moderate doses of psychostimulants for those with
comorbid SUD and ADHD [56–59]. Prior work also suggests the potential for
effective treatment of ADHD in adolescence to reduce the risk of later SUD or AUD
[56, 57]. As more work is needed, especially focusing on the use of psychostimu-
lants for AUD with ADHD, attention to ADHD symptom severity, use of
28 N. Romano and R. Luba

extended-­ release psychostimulant formulations, and consideration of the risk-­

benefit analysis are necessary to guide clinical decision-making [56, 59–63].
Concurrent pharmacological treatment of AUD and anxiety symptoms depends
on the nature of anxiety symptoms and the timing of treatment. It is common (and
beneficial with regard to treatment retention) [64] to offer benzodiazepines for anxi-
ety in the context of alcohol withdrawal symptoms. On the other hand, long-term
use of benzodiazepines in those with a history of AUD is less common, often due to
concerns for the development of sedative use disorder in these patients. Though
some research purports that the risk of sedative use disorder in those with a history
of AUD is somewhat low [65, 66], there is evidence that the risks of comorbid seda-
tive and alcohol use disorders carry a risk of increased depressive symptoms and
treatment complications [51, 67]. Given there are pharmacokinetic and pharmaco-
dynamic differences across benzodiazepines, some research favors use of chlordiaz-
epoxide, clorazepate, oxazepam, or halazepam [65, 68, 69] over diazepam,
lorazepam, and alprazolam (which appear to have a higher potential for misuse)
[68]. When considering the treatment of an anxiety disorder (distinct from alcohol
withdrawal-related anxiety), there is support for the use of buspirone, a non-­
benzodiazepine medication. Though not thought to have acute anxiolytic or rein-
forcing effects, findings from three out of four placebo-controlled trials support
buspirone as superior to placebo with regard to treatment retention, anxiety symp-
tom management, and alcohol use [70, 71].
A systematic review examining nine randomized controlled trials focused on
medication treatment in individuals with comorbid AUD and PTSD suggests weak
and/or contradictory results for one medication that effectively addresses this
comorbidity [72]. Of nine included studies, four utilized medications considered
first-line for PTSD (SSRIs sertraline and paroxetine) [73–75], four employed medi-
cations specifically for AUD (naltrexone in two studies, naltrexone and disulfiram in
one study, and topiramate in the fourth study) [74, 76–78], and three tested medica-
tions with the potential to concurrently address AUD and PTSD (prazosin in two
studies and aprepitant in one study) [79–81]. The authors of this systematic review
conclude that there is inconsistent or weak evidence to support the combined phar-
macological treatment of AUD comorbid with PTSD. Still, there is evidence that
clinicians can safely deploy medications to treat one condition within this comor-
bidity (e.g., naltrexone for AUD or sertraline for PTSD), though effects on the non-­
treated condition are likely to be minimal. In these cases, it seems that combined
delivery of pharmacotherapy with behavioral treatments is most prudent, given that
reviewed studies with strong behavioral components had the strongest effects [72].
More work, specifically large randomized controlled trials, is needed to further
explore this comorbidity and effective pharmacotherapies.
Research on pharmacological approaches for AUD with comorbid SUD remains
limited and difficult to integrate given extensive methodological differences across
trials, diverse combinations of medications and psychotherapies, and no FDA-­
approved pharmacotherapies for many substance use disorders to date [82].
Research on combined treatments for AUD and cocaine use disorder suggests a
benefit of disulfiram in reducing alcohol and cocaine use and increasing treatment
3 Co-occurring Disorders: Mental Health and Alcohol Use 29

retention, with results sustained at 12-month follow-up [83, 84]. There are mixed
findings regarding the use of naltrexone for AUD with comorbid cocaine use with
several studies finding no apparent benefit of naltrexone over placebo for those with
AUD and cocaine [stimulant] use disorder [85, 86]. One randomized controlled trial
did find a benefit of naltrexone for this subpopulation but only at doses of 150 mg
and only among men [87, 88]. In addressing AUD with comorbid opioid use disor-
der (OUD), existing work suggests that efforts to prioritize OUD and stabilize
patients on methadone or buprenorphine appear to be the most beneficial approach
to addressing alcohol use. Achieving and maintaining adequate doses of methadone
or buprenorphine is associated with reductions in opioid and alcohol use [82, 89]
and alcohol-related acute events [90]. The addition of disulfiram may be beneficial
for those with AUD and OUD, but again, this should be considered secondary to
medications for opioid use disorder (MOUD) stabilization, and the evidence base
remains limited [91]. A secondary analysis of the pivotal trial comparing buprenor-
phine to naltrexone for OUD [92] examined whether there was a benefit of naltrex-
one for individuals with AUD and OUD. Findings suggest that drinking was reduced
for those on buprenorphine and naltrexone, and the hypothesis that naltrexone
would be superior to buprenorphine with regard to alcohol use was not supported
[93]. Clinical practice guidelines suggest limiting use of naltrexone in individuals
with AUD and OUD to those who have demonstrated abstinence from opioid use for
a “clinically appropriate time” and those who wish to abstain from opioid use and
abstain from or reduce alcohol use. In such cases, use of long-acting formulations is
preferable [94]. Given notable heterogeneity across existing trials, more work is
needed to understand pharmacotherapy approaches for AUD with comorbid SUD,
especially given the prevalence of this comorbidity and risk for poorer treatment
outcomes.
Research on the pharmacological treatment of comorbid bipolar disorder and
AUD is somewhat limited. There is some evidence that this comorbidity carries a
risk of rapid cycling and a greater likelihood of mixed or dysphoric manic and/or
greater overall bipolar disorder severity [95]. As there are difficulties in effectively
conducting randomized controlled trials of medications for this population, further
work is needed. To date, one pilot study and one well-controlled trial suggested that
the use for those with bipolar disorder and AUD on lithium, the addition of dival-
proex sodium, was associated with significant reductions in heavy drinking days
compared to placebo. However, this medication did not appear to confer improve-
ments in manic or depressive symptoms compared to placebo [96, 97].

3.6 Psychotherapy Approaches Targeting AUD and Other

Psychiatric Conditions

Though behavioral treatments of AUD are covered elsewhere in this text (see Chap.
8), we will briefly summarize available data on behavioral treatments or psycho-
therapy approaches to treating AUD with comorbid psychiatric conditions. A sys-
tematic review on the treatment of AUD suggests that while there are clear bolstering
30 N. Romano and R. Luba

effects of adding pharmacotherapy to psychotherapy for AUD, the effects of adding

pharmacotherapy to psychotherapy are more subtle. Still, this systematic review
excluded trials examining psychiatric comorbidity in the context of AUD, and such
work generally remains limited [98]. While there are compelling findings noted
below in considering the potential bolstering effects of psychotherapy to treat AUD
with comorbid psychiatric conditions, methodological variability across psychoso-
cial treatments has made it quite challenging to assess these potential benefits or
establish concrete treatment guidelines [99].
To date, the largest body of research on this topic focuses on AUD with comorbid
depression. A meta-analysis of 12 studies combining cognitive behavioral therapy
(CBT) with motivational interviewing (MI) in individuals with MDD and clinical or
subclinical AUD suggests small but significant effects of this combination com-
pared to treatment as usual (TAU) [100]. The numbers needed to treat (NNT) analy-
sis in this study found a higher NNT for CBT/MI compared to a meta-analysis of
antidepressants for MDD and AUD [53]. Interestingly, compared to TAU, CBT/MI
was associated with reductions in depressive symptoms, and this effect remained
stable at 12-month follow-up, while the effect of CBT/MI on alcohol use appeared
to get stronger over time. This “sleeper effect” suggests that stabilization of depres-
sive symptoms with CBT/MI may precede marked changes in alcohol use perhaps
explained by general improvements in functioning because of reduced depression
or a generalization of CBT/MI skills toward alcohol-related concerns [100]. The
combination of pharmacotherapy and CBT for AUD and depression has also been
linked with more pronounced reductions in alcohol use and depressive symptoms
and increased treatment retention compared with either CBT or pharmacotherapy
alone [56, 101–104]. Consensus on the value of combined behavioral and pharma-
cological treatments for AUD comorbid with other psychiatric conditions is limited
by a smaller number of clinical trials to date.
A recent meta-analysis of 11 studies integrating behavioral treatments to concur-
rently treat SUD and comorbid anxiety disorders suggests a benefit for integrated
treatment compared with behavioral treatments targeting SUD alone. This review
found that overall, integrated treatments produce superior outcomes compared to
SUD treatment alone with regard to SUD outcomes and anxiety symptom severity.
Effect size estimates were small to moderate but considered clinically significant
[105]. Three studies included in this review focused specifically on alcohol use. The
first compared community-based AUD treatment with progressive muscle relaxation
to community-based AUD treatment with CBT for anxiety and found that the latter
group demonstrated significantly greater improvements in alcohol use and a slight
advantage with regard to anxiety reductions (notably, both groups experienced sig-
nificant reductions in anxiety) [106]. The second study compared behavioral treat-
ments following a stabilization period on pharmacotherapy (naltrexone, acamprosate,
or their combination). This work found that compared to TAU (counseling), a behav-
ioral treatment integrating CBT for AUD, anxiety, and/or depression contributed to
greater improvements in nearly all alcohol outcomes, though there were no signifi-
cant differences in anxiety outcomes [107]. The third trial compared relapse preven-
tion alone to relapse prevention paired with anxiety-focused CBT and provided
participants with optional pharmacotherapy. All patients were already abstinent from
3 Co-occurring Disorders: Mental Health and Alcohol Use 31

alcohol at the time of treatment enrollment. Contrary to the study noted above, this
trial found that integrated treatment was associated with significant reductions in
anxiety symptoms but no significant between-group differences with regard to alco-
hol relapse rate [108]. Thus, though existing research supports integrated behavioral
treatments for SUD and anxiety broadly, more work is needed to clarify discrepant
findings for integrated behavioral treatments for AUD and anxiety.
A recent meta-analysis examined integrated treatments for comorbid SUD and
PTSD across 36 trials. Findings suggest that trauma-focused psychotherapy paired
with pharmacotherapy produced more marked reductions in PTSD severity com-
pared to treatment as usual. Notably, some of the most compelling findings for SUD
outcomes were for studies targeting AUD. Findings suggested that compared to
TAU, trauma-focused psychotherapy combined with pharmacotherapy for AUD
significantly reduced alcohol use severity, with a large effect size observed and sus-
tained treatment effects at 12-month follow-up [109].
As noted above, summarizing the literature on combined interventions for AUD
with comorbid SUD is challenging due to the complexity and heterogeneity of study
designs and psychotherapies utilized (which are primarily delivered alongside phar-
macotherapies). Some work suggests that as with other comorbidities, combining
CBT with pharmacotherapies bolsters the effects of CBT. For instance, in a study of
CBT combined with naltrexone or disulfiram for individuals with AUD and cocaine
[stimulant] use disorder, CBT combined with either medication was associated with
more robust reductions in alcohol and cocaine use compared with CBT alone [110].
Contingency management and 12-step facilitation have demonstrated mixed results
in addressing AUD with comorbid cocaine use, and some work suggests a benefit of
contingency management in the context of AUD with comorbid opioid use, but this
work remains limited [82, 91]. A recent meta-analysis examining 60 studies includ-
ing 10,444 participants found that in the context of MOUD, contingency manage-
ment (compared to MOUD only) is associated with increased abstinence and
medication adherence and reduced stimulant, cigarette, and polysubstance use.
Unfortunately, this study did not specifically explore AUD-related outcomes, limit-
ing generalizability to those with AUD and OUD. Though integrated behavioral
treatments for AUD with comorbid SUD appear intuitive, existing trials are limited
and make it difficult to reach firm conclusions on the best approach for those with
AUD and other SUD. Still, bolstering effects of psychotherapy when combined with
pharmacotherapy appear a consistent theme across psychiatric comorbidity, and an
integrative approach appears to have more benefits than risks. Future work should
determine which psychotherapies are most likely to benefit those with AUD and
SUD, especially when combined with available FDA-approved medications.
There are limited trials examining behavioral interventions targeting AUD with
comorbid ADHD or bipolar disorder. Existing work supporting the utility of behavioral
interventions paired with psychostimulants to offer long-term management of ADHD
[111–113] would suggest that where available, behavioral treatment for ADHD may
complement or bolster the effects of pharmacotherapy for AUD, but more specifically
exploring this combination is needed. Further, though quite limited, some work sug-
gests combining CBT and pharmacotherapy to treat comorbid AUD and bipolar disor-
der, with major gaps in the literature on this topic noted [114] (Table 3.2).
32 N. Romano and R. Luba

Table 3.2 Summary of research on pharmacotherapies and psychotherapies for observed

comorbidities
Comorbidity Pharmacotherapy outcomes Psychotherapy outcomes
AUD + SUD Disulfiram is associated with Psychotherapy (CBT, contingency
some benefit for co-occurring management, and 12-step facilitation)
AUD and cocaine [stimulant] appears to bolster the effects of
use disorder, though effects are pharmacotherapies for comorbid
inconsistent [82–84] AUD + SUD [82, 91, 110]
Optimizing methadone or CBT + naltrexone or disulfiram
buprenorphine for those with contributes to more robust outcomes
AUD and opioid use disorder for those with AUD and cocaine use
appears to be the most valuable disorder compared to CBT alone
first step in managing AUD
with comorbid OUD [82, 89,
90]. The use of disulfiram is
recommended for those who
continue to experience AUD
symptoms after MOUD
stabilization [91]
AUD + ADHD Psychostimulants contribute to Behavioral
reductions in AUD and ADHD interventions + psychostimulants may
symptoms and increased bolster the effects of psychostimulants
treatment retention [56–59] for ADHD in the context of AUD
*extended-release [111–113]. More work is needed
psychostimulants may be
preferred [56, 59–63]
AUD + mood Antidepressants are associated SSRIs + psychotherapy contributes to
disorder with reductions in mood most robust outcomes [55]
symptoms for those with AUD CBT + MI is superior to TAU [100]
and MDD. Those with more CBT + MI is associated with greater
robust medication effects reductions in depression and alcohol
experience more robust use compared to TAU. Effects on
reductions in alcohol use. alcohol use appear to lag effects on
Tricyclics may be preferable to depressive symptoms [53]
SSRIs [53] Pharmacotherapy + CBT contributes
Sertraline + naltrexone to more marked reductions in alcohol
performs better than either use and depression than either
medication alone for those with treatment alone [56, 101–104]
AUD and depression [54]
Lithium + divalproex sodium
associated with reductions in
alcohol use for those with AUD
and bipolar disorder [96, 97]
AUD + anxiety Buspirone contributes to Integrated treatments produce superior
reductions in anxiety and outcomes compared to SUD treatment
alcohol use and increased alone [92]
treatment retention [70, 71] Mixed findings regarding whether
In considering integrated behavioral treatments
benzodiazepines, consider contribute to reductions in alcohol use
those with lower potential for and anxiety [106], alcohol use only
misuse (chlordiazepoxide, [107], or anxiety only [108]
clorazepate, oxazepam,
halazepam) [65, 68, 69]
(continued)
3 Co-occurring Disorders: Mental Health and Alcohol Use 33

Table 3.2 (continued)

Comorbidity Pharmacotherapy outcomes Psychotherapy outcomes
AUD + PTSD Inconsistent and/or weak Trauma-focused
evidence for pharmacotherapies psychotherapy + pharmacotherapy
alone [72] contributes to more marked reductions
in PTSD symptoms and alcohol use
than TAU [109]
AUD + personality More research is needed More research is needed
disorder
AUD + schizophrenia More research is needed More research is needed

3.7 Conclusions and Future Directions

Psychiatric comorbidity is prevalent among individuals with AUD, with the highest
prevalence being for other substance use disorders, ADHD, depression, and anxiety
disorders. Comorbid AUD and psychiatric disorders increase an individual’s risks
for consequences from both the alcohol and psychiatric disorders, whether due to
the psychiatric symptoms inducing or perpetuating AUD or vice versa. Although
evidence of the mechanisms underlying AUD and comorbid psychiatric conditions
are ongoing, research has emphasized the important contributions of genetic, epi-
genetic, environmental, and psychosocial factors to the development and mainte-
nance of psychiatric disorders comorbid with AUD while also considering the
presence of common underlying vulnerabilities among them. Further, such mecha-
nisms may differ among psychiatric conditions comorbid with AUD, though more
research is needed. Diagnostically, it may prove challenging to distinguish between
overlapping symptoms of an AUD and other psychiatric disorder while also delin-
eating their chronology. Nonetheless, the co-occurring diagnoses should be treated
concurrently utilizing both pharmacologic and psychotherapeutic approaches that
target both. Future directions include further elucidation of the underlying patho-
physiologic mechanisms of AUD comorbid with other psychiatric disorders, in
addition to a need for randomized controlled trials to further outline pharmacologic
combinations, effective psychotherapies and moderators, and mediators of out-
comes relevant to the concurrent treatment of AUD with psychiatric comorbidity.
Further work that can address implementation challenges to the delivery of pharma-
cotherapy, psychotherapy, and integrated treatment is essential.

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The Impact of Alcohol Use on Physical
Health 4
Nia Harris

4.1 Introduction

Alcohol use has been steadily increasing in recent years. Importantly, alcohol use
disorders (AUD) are one of the most common forms of substance use disorders,
affecting approximately 30 million people according to the 2021 National Survey
on Drug Use and Health [1]. Despite this, alcohol is one of the easiest to access
substances, and its use is widely socially accepted. Collectively, the sequelae from
AUD and alcohol misuse serve as a far-reaching problem.
Alcohol use has a vast impact on physical health. These effects include a combi-
nation of direct toxicity as well as indirect predisposal to adverse consequences.
Notably, alcohol use has a well-documented causal relationship to numerous medi-
cal conditions and is reported to be implicated in up to 40% of medical hospitaliza-
tions [2]. Moreover, excessive alcohol use is thought to account for approximately
28 billion dollars of healthcare costs per year [3]. Here, we will review the effects
of alcohol on various organ systems.

4.2 Physical Health

Alcohol use is associated with numerous short- and long-term health risks. The
short-term health risks result from the immediate effects associated with alcohol
intoxication that increase the risk of many harmful health conditions. Alcohol poi-
soning, for example, is defined as the direct result of drinking large amounts of
alcohol in a short period of time and is considered a medical emergency that may
impact multiple organ systems [4]. Some other short-term health effects include
increased risk of motor vehicle crashes, drowning, falls, and other injuries, as well

N. Harris (*)
New York-Presbyterian/Weill Cornell Medical Center, New York, NY, USA
e-mail: [email protected]

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2024 41

M. Khan, J. Avery (eds.), From Stigma to Support, Psychiatry Update 4,
https://doi.org/10.1007/978-3-031-73553-0_4
42 N. Harris

as increased risk of various types of violence [5]. Additionally, increased risky sex-
ual behaviors, miscarriages, still births, and fetal alcohol spectrum disorders are
risks that have several outcomes that may impact future health [6]. Conversely, the
long-term health risks are not associated with acute intoxication, but rather are asso-
ciated with impact of alcohol use over a chronic period. These include the impact of
alcohol on various organ systems including cardiovascular, immune, and gastroin-
testinal, among others (see Table 4.1). Moreover, long-term risks also include
increased risk of mental health conditions, social problems, relationship difficulties,
and other comorbid substance use disorders [5]. The impact of alcohol on long-term
physical health risks will be the focus of this chapter.
There are many broad mechanisms through which alcohol has a chronic impact
on physical health. Some of the most common pathways involve effects on neu-
rotransmitter balance, vitamin metabolism, and electrolyte derangement (see
Table 4.2), many of which impact multiple organ systems. Here, we will review the
major health systems associated with alcohol use as well as conditions that may

Table 4.1 Impact of alcohol by organ systems

Medical conditionsa Mechanism
Neurological health
1. Alcohol withdrawal syndrome 1. Imbalance in gamma-amino butyric acid (GABA)-
(+/− delirium tremens) mediated inhibition and glutamate-mediated excitation
2. Wernicke encephalopathy/ 2. Vitamin deficiency (thiamine and vitamin B12)
subacute degeneration 3. Hypokalemia, metabolic alkalosis, and GI hemorrhage
3. Hepatic encephalopathy contribute to hyperammonemia
Cardiovascular health
1. Angina 1. Coronary vasospasm
2. Cardiomyopathy 2. Myocyte loss, decrease of contractile proteins, calcium
3. Myocardial infarction dysregulation
3. Coronary insufficiency
Respiratory health
1. Acute respiratory distress 1.–3. Weakening of respiratory muscles, depression of
syndrome mucociliary function, decrease of normal respiratory
2. Acute respiratory failure defenses
3. Respiratory infection (e.g.,
aspiration pneumonia)
Gastrointestinal health
1. Cancers of GI tract (various) 1. Mediated my mucosa [7]
2. Pancreatitis 2. Premature intracellular digestive enzyme activation [8]
3. Alcoholic liver disease 3. Toxic effects on hepatocytes, immune response [9]
Musculoskeletal health
1. Myopathy 1.–2. Toxicity to myocytes [10]
2. Rhabdomyolysis 3. Traumatic falls, bone loss
3. Avascular necrosis
Hematologic/immune health
1. Anemia 1.–3. Hypocellular bone marrow production, impact on
2. Thrombocytopenia clotting factors, impaired ciliary function
3. Various infections
Adapted from Mannelli & Pae, [2]
a
We have listed three examples per health system, which is not an exhaustive all-inclusive list
4 The Impact of Alcohol Use on Physical Health 43

Table 4.2 Impact of alcohol by mechanism

Mechanism Organ system (s) impacted (condition example)
Neurotransmitter imbalance Central nervous system (CNS; alcohol
withdrawal syndrome)
Vitamin metabolism CNS (subacute degeneration), gastrointestinal
(GI), heme (anemia)
Electrolyte derangement (e.g., Most if not all organ systems impacted
hypoglycemia, hypokalemia)
Tissue integrity Cardiovascular (cardiomyopathy),
musculoskeletal (myopathy)

result. We will also review the primary mechanism of alcohol’s impact involved in
a select number of various conditions (approximately two per system).

4.2.1 Neurotransmitter Balance

Alcohol has a profound impact on neurotransmission. Without the influence of alco-

hol, GABA, an inhibitory neurotransmitter, and glutamate, an excitatory neurotrans-
mitter, are in a state of homeostasis [11]. Acutely, alcohol attenuates the action of
GABA, an inhibitory neurotransmitter, which in turn leads to decreased CNS excit-
ability. Alcohol simultaneously decreases glutamate, which reduces CNS excitatory
tone [11]. Low GABA levels in the prefrontal cortex are associated with poor impulse
control, impaired executive function, and disinhibition commonly associated with
relaxation and euphoria [12]. Chronic, regular alcohol use leads to downregulation,
or decreased number, of GABA receptors and upregulation, or increased number of
glutamate receptors as well as increased glutamate production, of more glutamate to
maintain homeostasis [11]. Clinically, this translates into needing a larger alcohol
requirement to achieve the same level of euphoria. In the setting of abrupt cessation
in the context of chronic use, CNS inhibition is reduced, and glutamate’s excitatory
effects are unopposed. Clinically, this translates into tremors, tachycardia, sweating,
and other symptoms seen with alcohol withdrawal [13]. Alcohol also contributes to
the release of dopamine [14]. Moreover, dopamine is increased in withdrawal states
and contributes to hallucinations and hyper arousal [11].

4.2.2 Vitamin Metabolism

Chronic alcohol use contributes to poor vitamin absorption and intake, which col-
lectively leads to a range of medical conditions. Some of the most implicated vita-
mins in chronic alcohol use are vitamin B12, folate, and thiamine. Conditions that
arise from vitamin B12, thiamine, and folate deficiency will be the focus of this
chapter, though it is worth noting that alcohol can contribute to the impaired metab-
olism of other vitamins as well.
44 N. Harris

4.2.3 Vitamin B12 and Folate

Vitamin B12 and folate are closely linked and are crucial vitamins involved in the
methionine and folate cycles [15]. Vitamin B12 deficiency is largely caused by mal-
absorption [15]. Folate deficiency is caused by insufficient intake and absorption,
reduced liver uptake and storage, and increased urine folate secretion [15].
Deficiency in either of these vitamins can lead to impairment in cellular metabo-
lism, DNA synthesis, methylation, and mitochondrial metabolism [15]. Clinically
vitamin B12 or folate deficiency can manifest in megaloblastic anemia (secondary
to impaired erythrocyte DNA synthesis), pancytopenia, or neurological changes,
though most patients do not present with the latter [16]. Vitamin B12 can addition-
ally cause glossitis, whereas folate deficiency tends to cause oral ulcers [17].

4.2.4 Thiamine

Thiamine is another B vitamin commonly deficient in patients who consume chronic

amounts of alcohol. Thiamine deficiency arises from inadequate nutrition, decreased
absorption in GI tract, and impaired thiamine utilization in cells [18]. In affluent
countries where people on average receive adequate nutritional thiamine, alcohol
use is the most common cause of thiamine deficiency [19]. Important enzymes
involved in the breakdown of carbohydrates (e.g., pyruvate dehydrogenase and
alpha-ketoglutarate) are thiamine dependent which further depletes the already sub-
optimal thiamine supply. Thiamine deficiency results in conditions that affect the
heart and CNS system (e.g., Wernicke–Korsakoff syndrome; [18]).

4.2.5 Electrolyte Derangement

Alcohol contributes to electrolyte and metabolic derangement through a range of

different mechanisms (see Tables 4.3 and 4.4). Alcohol can contribute to direct tis-
sue or organ damage [20]. Moreover, alcohol-related metabolic derangements are
made more severe by malnutrition [21]. Patients who consume chronic amounts of
alcohol have lower serum concentrations of potassium, magnesium, bicarbonate,
calcium, and phosphate as well as a lower arterial pH values [22]. Hypomagnesemia
is the most common electrolyte derangement in patients with alcohol use disorders
[20]. Alcohol also impacts fluid balance by suppressing anti-diuretic hormone
(ADH) and may result in syndrome of inappropriate antidiuretic hormone secretion,
as well as impacting pH balance [21].
4 The Impact of Alcohol Use on Physical Health 45

Table 4.3 Impact of alcohol on kidneys and electrolytes

Acute electrolyte and
acid base Chronic electrolyte and Acute kidney
abnormalities acid base abnormalities injury Chronic kidney injury
Hypomagnesemia Hypokalemia Pre-renal Renal tubular
azotemia dysfunction
Hypophosphatemia Hyponatremia (beer Myoglobinuric Depressed renal
potomania) renal failure ammoniagenesis
secondary to renal
tubular damage
Hyponatremia Hypomagnesemia Acute tubular Hepato-renal syndrome
necrosis
Hypokalemia Hypocalcemia Moonshine
nephropathy (lead
toxicity)
Metabolic acidosis Hypophosphatemia
Respiratory alkalosis Metabolic acidosis mixed
with volume contracted
metabolic alkalosis
Adapted from [20]

Table 4.4 Effects of alcohol on electrolyte derangement

Electrolyte
abnormality Mechanism
Water diuresis Suppression of ADH
Hypomagnesaemia Increased magnesium excretion, inappropriate magnesiuria
(hypophosphatemia, acidemia), transcellular shift, respiratory alkalosis,
poor oral intake, diarrheal loss, magnesuric effect of alcohol
Hypokalemia Hypomagnesemia-induced inappropriate kaliuresis, respiratory alkalosis,
beta-adrenergic stimulation, hyperinsulinemia
Hypocalcemia Impaired secretion of parathyroid hormone, end organ unresponsiveness
to parathyroid hormone
Hypophosphatemia Poor oral intake, respiratory alkalosis, hyperinsulinemia, GI losses,
inappropriate phosphaturia
Metabolic acidosis Insulin deficiency with excess glucagon
Adapted from [20]

4.3 Neurological Health

Alcohol is a CNS depressant that causes many immediate and long-term detrimen-
tal effects on physical health. A hallmark of the chronic impact of alcohol, not sur-
prisingly, is impaired cognition. As mentioned previously, the process through
which alcohol impacts neurological health is multifactorial. Alcohol has down-
stream effects on neurotransmitter balance, especially GABA and glutamate [11].
This is implicated in alcohol withdrawal syndrome and delirium, among other con-
ditions. Additionally, alcohol has effects on vitamin absorption (namely folate and
other B vitamins; [23]), which in turn impacts enzymes involved in Krebs cycle,
pentose phosphate pathway, as well as myelination [15, 18]. These disrupted
46 N. Harris

pathways have numerous downstream effects and conditions. Moreover, alcohol has
effects on electrolyte derangement via direct and indirect impact on the liver and
kidney, all of which can consequently lead to a range of CNS conditions. We will
now expand on the mechanistic specifics for some of these conditions.

4.3.1 Delirium

Importantly, when evaluating mental status changes in patients with history of

chronic alcohol use, delirium should always remain on the differential. Delirium is
commonly multifactorial. It may be in the context of acute alcohol (or other sub-
stance) intoxication or withdrawal, medications, or medical comorbidities, among
other causes. Delirium involves alterations of a range of neurotransmitters. If delir-
ium is diagnosed, it is imperative to identify and treat the underlying cause.
Moreover, use of antipsychotics in the treatment of delirium should be avoided
when possible if alcohol withdrawal is suspected given their impact on lowering the
seizure threshold. Of note, alcohol withdrawal will be covered in detail in a separate
chapter (Chap. 6).

4.3.2 Wernicke Encephalopathy

Wernicke encephalopathy arises from deficiency in thiamine [24]. Importantly, thia-

mine is a crucial vitamin involved in cell metabolism and functioning of brain cells
[24]. The classic findings in a patient with Wernicke encephalopathy include mental
status changes, ocular dysfunction, and gait apraxia. Notably, however, these three
findings are only present in about 10% of cases [25]. Approximately 80% of patients
with untreated Wernicke encephalopathy develop Korsakoff syndrome (also termed
Wernicke–Korsakoff syndrome), which is characterized by memory impairment
associated with confabulation [25]. Optimal treatment involved high dose parenteral
thiamine administration [26].

4.4 Cardiovascular Health

There remains controversy in the literature regarding the impact of alcohol on car-
diovascular health. Reported outcomes vary based on amount of alcohol consumed,
pattern of consumption, outcome being studied, and type of beverage consumed
[27, 28]. Low to moderate alcohol consumption is reported to be more protective
than life-long abstinence [29]. Namely, low to moderate alcohol consumption con-
tributes to reducing the concentrations of intermediate biomarkers of inflammation,
oxidation, and coagulation and improves lipid profile, which may collectively con-
tribute to decreased risk of cardiovascular events [29]. Chronic heavy and binge
consumption of alcohol, however, is reported to be harmful to cardiovascular health
at all levels [30].
4 The Impact of Alcohol Use on Physical Health 47

Alcohol has acute and chronic toxic effects on the tissue integrity of cardiac
myocytes. Acutely, consuming large volumes of alcohol promotes inflammation of
the myocardium leading to increased troponin concentration in serum as well as
tachyarrhythmias, such as atrial fibrillation and ventricular fibrillation [31]. Chronic
alcohol consumption leads to myocyte structural changes as well as mitochondrial
damage, oxidative stress injury, and apoptosis, which collectively lead to myocar-
dial dysfunction [31]. When such dysfunction occurs in the absence of coronary
artery disease, it is referred to as alcohol-induced cardiomyopathy (ACM; [31]).
Diagnosis of ACM relies on a thorough history. The most important factor of
course is a significant history of chronic alcohol intake. ACM is characterized by
dilation and impaired contraction of one or both myocardial ventricles [32].
Diastolic dysfunction is the earlier sign and is observed in 30% of cases [31].
Patients may also present with systolic dysfunction [31]. Palpitations and syncopal
episodes can occur secondary to tachyarrhythmias seen in ACM. Myocardial infarc-
tion results from compromised cardiac muscle integrity due to insufficient oxygen
supply [31]. Symptoms of ACM are non-specific and are like that observed in other
types of heart failure [32]. Early diagnosis is imperative to prevent progression of
heart failure.

4.5 Gastrointestinal Health

Alcohol has a widespread impact on the gastrointestinal tract. These effects span
from the entry point of the GI tract at the oral cavity, to the liver and pancreas, to the
rectum, and everywhere in between. Alcohol may cause direct damage to mucosal
tissue, impaired gastric motility, and impaired vitamin and nutrient absorption,
among other factors [33]. The relationship between alcohol and GI health may addi-
tionally be impacted by medication interactions, foods and beverages, and other
substances. Alcohol has been recognized as an important risk factor for cancers of
the upper GI tract for years [7], especially when combined with tobacco use [34].
Alcohol consumption should be considered as a possible differential and requires a
thorough substance use history.

4.5.1 Alcoholic Liver Disease

Alcoholic liver disease encompasses a spectrum of conditions, ranging from mild to

life threatening. The first major impact that alcohol has on liver functioning occurs
via impairment of fat mobilization and breakdown, often referred to as hepatic ste-
atosis or fatty liver [9]. Next, stored free fatty acids promote oxidative stress and
subsequent hepatocyte apoptosis [9]. This process activates Kupffer cells which in
turn produce pro-inflammatory cytokines [9]. Following this, hepatic stellate cells
become active and deposit fibrotic tissue [35]. Most individuals who consume more
than 40 g of alcohol per day develop hepatic steatosis; however, only a small
48 N. Harris

percentage of these individuals go on to develop more advanced liver disease [36].

Early diagnosis is the key to prevent progression of disease.

4.5.2 Pancreatitis

Alcohol consumption is a well-documented modifiable risk factor for pancreatitis

and has been found linked to both the acute and chronic forms of pancreatitis [37].
The mechanism through which alcohol causes pancreatitis is thought to be multifac-
torial. Ethanol induces stimulation of pancreatic digestive enzymes (e.g., pancreatic
amylase) which leads to autodigestive and classical symptoms associated with pan-
creatitis [8]. Additionally, ethanol metabolites, such as acetaldehyde, have direct
toxic effects of pancreatic acinar cells and interfere with secretagogue secretion
[38]. Alcohol also contributes to pancreatitis via effects on impaired pancreatitis
blood flow and hypoxia [39]. Moreover, chronic alcohol exposure accelerates pan-
creatic necrosis [40]. Collectively, alcohol has a multitude of direct and indirect
toxic effects on the pancreas that contribute to pancreatitis.

4.6 Hematologic Health

As discussed previously, alcohol consumption is a modifiable risk factor for liver

disease and is associated with various types of hematologic disorders, especially
anemias and thrombocytopenia. Alcohol is a well-known toxin to the bone marrow
[41]. Moreover, the impact of alcohol on secondary malnutrition that arises second-
ary to vitamin deficiency (namely folate and vitamin B12 malabsorption) further
exacerbates alcohol-induced anemia [41]. Alcohol consumption is associated with
increased risk of anemia of chronic disease, macrocytic anemia, and aplastic anemia
and has a converse relationship with iron deficiency anemia [41, 42]; see Table 4.5).
Ioannou et al. [42] found that consumption of more than two drinks/day decreased
risk of iron deficiency anemia and risk of iron overload. Of note, however, in the
setting of alcoholic gastritis and GI bleeding, iron deficiency anemia may result
from blood loss [42]. Similar to anemia, thrombocytopenia can arise from the direct
toxic effects that alcohol has on the bone marrow as well as secondary to chronic

Table 4.5 Alcohol-induced hematologic conditions

Anemia Alcohol-mediated mechanism
Iron deficiency anemia GI bleeding (e.g., from variceal bleed, ruptured ulcer, etc.)
Anemia of chronic Reduced erythropoiesis resultant from toxicity to bone marrow
disease
Megaloblastic anemia Impaired DNA synthesis resultant from vitamin B12/folate deficiency
Aplastic anemia Previous hepatitis infection
Thrombocytopenia Reduce thrombopoiesis resultant from toxicity to bone marrow;
resultant from chronic liver disease
Adapted from Gonzales et al. (2009)
4 The Impact of Alcohol Use on Physical Health 49

liver disease [43]. As discussed the direct and indirect effects of alcohol are
far-reaching.

4.7 Other Health Systems

Alcohol has a wide impact on several separate health systems apart from those pre-
viously discussed. Our walking, our breathing, and our ability to fight off infections
are all impacted by alcohol. Acute and chronic consumption of alcohol negatively
impacts anabolic and catabolic skeletal muscular signaling and contributes to
myopathy and other muscular disorders [10]. Moreover, alcohol contributes to
decreased bone formation rate and poses as a risk factor for osteoporosis [44].
Chronic alcohol consumption, additionally, impedes the respiratory protective
mucociliary clearance system, a defense that moves mucus and pathogens up and
out of the lower airways [45]. Moreover, decreased consciousness that results from
acute intoxication promotes aspiration of oral secretions and increases risk of lower
airway infections, which further increases risk of infection [46]. Not surprisingly,
alcohol is a known risk factor for acute respiratory distress syndrome [47] and a
range of other infections [48].

4.8 Other Factors

It is worth noting that there are other factors to consider when discussing the impact
of alcohol on physical health. Alcohol, which is a sedative substance, interacts with
several medications. The combination of alcohol with other medications can worsen
underlying conditions, precipitate adverse side effects (e.g., when combined with
disulfiram), and of course contribute to delirium, among other issues.
Patients with substance use disorders have a high risk of comorbid mental and
medical conditions making them among the sickest patients we treat. Despite this,
they historically receive sub-optimal care [49]. This is due to many factors, includ-
ing provider bias and access to healthcare. It is important to think about all of these
factors in order to optimize care. While there are many factors that should be con-
sidered, this section will focus on discussing the role provider bias plays in the
physical health of patients with substance use disorders and substance misuse.
The medical community has exceedingly worse attitudes toward patients with
substance use disorders than patients with medical or psychiatric disorders [50, 51].
Stigma interferes with help-seeking behavior among those with substance use dis-
orders [52] and may serve to increase substance use and other high-risk behaviors
[53]. The role of racial bias is an important aspect of stigma that has been well
studied. Acevedo et al. [49] found that black individuals with substance use disor-
ders were less likely to meet treatment initiation criteria compared to white indi-
viduals. Moreover, racially/ethnically minoritized populations are less likely to
receive widely accepted minimal levels of outpatient substance use disorder treat-
ment than their white counterparts [54]. Despite all of this, however, we (the
50 N. Harris

medical community) continue to serve as part of the problem! In order to start

addressing the full impact of alcohol on physical health, we should first take stock
of our own biases and the pitfalls in the system that prevent our patients from suc-
ceeding. Only then can our patients receive optimal care.

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Alcohol Use Disorder,
Alcohol-­Associated Liver Disease, 5
and Liver Transplantation

Elora Basu and Akhil Shenoy

5.1 Alcohol Use Disorder (AUD) and Alcohol-Associated

Liver Disease (ALD)

AUD contributes to a variety of health problems with alcohol-associated liver dis-

ease (ALD) being the most common reason for early mortality worldwide [1]. In the
United States, 100,000 people die annually from liver disease with alcohol respon-
sible for 46% of these deaths (NIAAA). The incidence of ALD has been rising with
overall increase in the prevalence of AUD, particularly among young people and
women [2].
The risk of (ALD) rises proportionally with heavy and daily consumption of
alcohol, and higher quantity and frequency of alcohol use are independent risk fac-
tors for the development of ALD [3]. A standard drink is 14 g of alcohol, and low
risk drinking typically entails no more than one drink daily in women and no more
than two drinks daily in men. Heavy alcohol use (>3 drinks on any day or >7/week
for women and >4 drinks on any day or >14/week for men), defined by the NIAAA,
begins to put individuals at risk for ALD. It is estimated that about 10–20% of those
with heavy alcohol use may go on to develop alcohol-associated cirrhosis or alcohol-­
associated hepatitis (AH) which are types of ALD [4]. A reduction in WHO alcohol
risk level of “very high” levels of drinking (>4 daily drinks for women and >7 daily
drinks for men) down to low-risk drinking levels leads to an 83% reduction in risk
for liver disease.
ALD, histologically, consists of a spectrum of disease stages and varying degrees
of liver injury. There are direct and indirect mechanisms by which alcohol

E. Basu (*)
New York Presbyterian—Weill Cornell Medicine, New York, NY, USA
e-mail: [email protected]
A. Shenoy
Columbia University Irving College of Physicians and Surgeons, New York, NY, USA
e-mail: [email protected]

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2024 53

M. Khan, J. Avery (eds.), From Stigma to Support, Psychiatry Update 4,
https://doi.org/10.1007/978-3-031-73553-0_5
54 E. Basu and A. Shenoy

contributes to liver damage. Direct pathogenesis involves increasing levels of acet-

aldehyde and other pro-inflammatory changes upon heavy alcohol consumption that
become toxic to hepatocytes [5]. Indirectly, acetaldehyde forms protein adducts that
can trigger an immune response and promote inflammation. ROS can cause lipid
peroxidation, DNA damage, and mitochondrial dysfunction, leading to cell death
and consequent fibrosis [6]. Also, indirectly, alcohol-induced inflammation can
recruit immune cells such as neutrophils, macrophages, and T cells, which release
proinflammatory cytokines and contribute to liver damage [6]. Alcohol can also
alter the gut microbiota composition and function, leading to dysbiosis and increased
intestinal permeability, which can facilitate the translocation of bacterial products
such as lipopolysaccharide (LPS) into the liver and trigger an inflammatory
response [7].
In response to injury, fibrogenesis occurs to control tissue damage. Steatosis,
typically the first form of injury to occur, consists of fatty changes to liver tissue.
Even from steatosis, only about 20% of patients advance to more severe forms of
ALD, including fibrosis and cirrhosis, though the rate of progression may be slowed
by abstinence [5]. Cirrhosis is an advanced fibrotic process whereby liver structure
is no longer preserved. Regenerative nodules and fibrous septa develop, represent-
ing a premalignant condition.
Decompensated cirrhosis signifies symptomatic disease, manifesting as signs of
portal hypertension including esophageal varices, ascites, hepatic encephalopathy,
or jaundice, among other symptoms [8]. At any stage of ALD, patients can develop
an inflammatory process known as alcohol-associated hepatitis (AH), though it is
most likely to occur in cirrhotic patients and manifests as jaundice with signs of
liver failure [5, 9]. Ultimately, cirrhosis may progress to hepatocellular carcinoma
(HCC), which is the sixth most common cancer worldwide [10]. Alcohol was linked
to about 46% of all liver cancer-related deaths in 2022, and those with alcohol-­
associated HCC tended to have more advanced disease due to limited screening and
later diagnoses compared to other causes of liver disease [11] (CDC).
The progression of ALD can be compounded by various other factors including
genetics, female sex, obesity, and other sources of liver injury such as diabetes and
hepatitis C [12]. Genetic variation in alcohol metabolism can lead to great acetalde-
hyde production in susceptible individuals, and other genetic polymorphisms of
ALD are the same for fatty liver disease, what is now called metabolic dysfunction-­
associated steatotic liver disease (MASLD). Female sex is an additional risk factor
possibly due to sex differences in enzyme distribution and body habitus. It is impor-
tant to note that any prior injury to the liver, including daily excessive acetamino-
phen use, can increase the risk for ALD.
In recent years hepatologists have been studying the rising use of alcohol and
AUD rates and its impact on ALD. Recent trends follow increasing use among older
adults, women, minorities, and patients of lower socioeconomic status [13].
Moreover, alcohol use increased several fold across many countries during the
COVID-19 pandemic, with a national increase of 107% in the rate of adding patients
with acute alcohol-associated hepatitis to the liver transplant waiting list and 210%
of liver transplantation compared to pre-pandemic rates [11, 14]. All clinicians
5 Alcohol Use Disorder, Alcohol-Associated Liver Disease, and Liver Transplantation 55

seeing patients with heavy alcohol use will need to work together to prevent and
manage AUD and ALD.

5.2 Screening and Diagnosis of AUD and ALD

All clinicians should screen for patterns of unhealthy alcohol use [15]. Clinicians
should feel capable to address both should they coexist, suggesting that interdisci-
plinary models of care are beneficial when taking care of this type of patient.
Screening for AUD helps identify those at highest risk for ALD. General AUD
screening tools can be adopted for use in medical and liver clinics [9]. These include
AUDIT (Alcohol Use Disorders Identification Test, composed of ten questions);
AUDIT-C (consumption, three questions); CAGE (Cutting down, Annoyance by
criticism, Guilty feeling, Eye-opener); and CIWA-Ar to assess withdrawal [16–18].
In addition to outpatient providers, emergency room and inpatient clinicians also
have the opportunity to employ these scales and initiate conversations about treat-
ment options.
The AUD diagnosis can be made with DSM-5 criteria alongside ALD and other
comorbid problems. The clinician can type the AUD as mild (2–3 criteria), moder-
ate (4–5 criteria), or severe (>6 criteria) [19]. As one may imagine, screening may
be challenging due to patients’ tendencies to underreport or minimize alcohol use,
often due to shame or stigma. While toxicology results through urine ethyl gluco-
nide and blood phosphatidylethanol are very useful in corroborating the last alcohol
use and perhaps the level of drinking, these tests have not been validated for screen-
ing for AUD and ALD [20]. The American Society of Addiction Medicine and
American Psychiatric Association posit that biomarkers should be a catalyst for
positive discussions with the patient toward recovery, rather than a tool used nega-
tively [21].
The diagnosis of ALD is typically clinical based on history, physical exam, and
certain laboratory studies. Jaundice, ascites, edema, and hepatic encephalopathy
can be the overt signs of decompensated liver disease. ALD is often only diagnosed
after a patient has become cirrhotic, given the challenging nature of diagnosis and
the delay in seeing a hepatologist [9]. Blood tests such as international normalized
ratio (INR), elevated bilirubin, decreased albumin, and platelet count suggest intrin-
sic liver tissue injury and may represent advanced ALD. In fact, these latter criteria
are considered in the scoring tools for short-term mortality: Model for End-Stage
Liver Disease, Child–Turcotte–Pugh Score, Maddrey’s Discriminant Function
(MDF), and Glasgow AH score, among others [21]. The MELD is used most often
in risk stratification among the pre-transplant population and plays a role in consid-
eration of transplant [22].
Tests such as gamma-glutamyl transpeptidase (GGT), mean corpuscular volume,
and aspartate aminotransferase (AST) may suggest ALD over other liver disease but
are not confirmatory. Metabolites of alcohol such as ethyl glucuronide and ethyl
sulfate can be measured in urine, with relatively high sensitivity and specificity [21].
Phosphatidylethanol (PEth) is also a useful alcohol-related biomarker, as it is
56 E. Basu and A. Shenoy

unaffected by age, body mass index (BMI), sex, and kidney or liver disease [23].
ALD can be distinguished from other liver disease through biopsy and pathologic
study. Though liver biopsy is the gold standard for a definitive diagnosis of fibrosis
and/or cirrhosis, other tools have come into favor given the potential complications
and invasive nature of the procedure [5]. A non-invasive, but not specific for ALD,
test to assess fibrosis is transient elastography (TE) [5]. TE measures liver stiffness,
which is representative of the degree of fibrosis, and can be performed with ultra-
sound or MRI studies [24]. Other non-specific fibrosis markers include the enhanced
liver fibrosis (ELF) test and fibrosis 4 (Fib4) test, which compile laboratory data to
estimate fibrosis [5].
Standard practice is to also screen and diagnose other common comorbid condi-
tions with AUD and ALD. National data have shown significant associations with
AUD and other substance use disorders, major depressive disorder, bipolar disorder,
and borderline and antisocial personality disorder [25]. Like other patterns of addic-
tion, chronic AUD can alter one’s brain state, specifically reward and motivation
pathways, stress response, and executive functioning [19]. Nutritional problems and
vitamin deficiencies are common in both AUD and ALD. Cognitive disorders such
as Wernicke–Korsakoff dementia and sensory-motor neuropathies associated with
AUD will need to be tested for alongside overt and covert hepatic encephalopathy
seen in ALD. Moreover, hepatic encephalopathy and depression share a number of
clinical signs such as psychomotor retardation and can be difficult to distinguish.
Tobacco and other substance use disorders are often comorbid with AUD and may
impact the ALD. Addressing comorbid psychiatric illness and substance use disor-
ders should also further improve the treatment of AUD and ALD.

5.3 Treatment of AUD in ALD

Treatment for AUD in ALD entails both pharmacologic and nonpharmacologic

strategies, aimed overall at decreasing alcohol use, with the eventual goal of absti-
nence and relapse prevention [9]. Regarding medication-assisted treatment (MAT),
we will focus on the three FDA-approved medications for AUD in the United States:
acamprosate, disulfiram, and naltrexone (Table 5.2) (cite). Medications often used
off-label for AUD treatment include topiramate, gabapentin, baclofen, nalmefene,
ondansetron, and varenicline [19].
Of the FDA-approved medications, acamprosate and oral naltrexone have clini-
cally significant effects to treat AUD compared to placebo based on clinical trial
data. These medications are poorly studied in liver disease patients, though the
European Association for the Study of the Liver recommends acamprosate due to
minimal impact on liver function [26]. Among other medications, baclofen has been
studied and demonstrated some success within an alcohol-related cirrhosis popula-
tion to promote abstinence and prevent relapse [27, 28].
Detoxification and rehabilitation centers also focus on pharmacologic and non-
pharmacologic strategies to aid in AUD treatment. Detoxification is more focused
on MAT and symptomatic treatment of withdrawal, while rehabilitation aims to use
5 Alcohol Use Disorder, Alcohol-Associated Liver Disease, and Liver Transplantation 57

Table 5.2 Medications for AUD (FDA approved and off-label)

Safety
Medication Mechanism of action Dose Adverse effects considerations
Naltrexone Opioid antagonist Oral: 50 mg Hepatotoxicity Contraindicated in
that reduces alcohol daily injectable: (rare), nausea, acute hepatitis or
cravings and 380 mg headache, liver failure due to
euphoria by blocking intramuscularly dizziness, risk of
opioid receptors monthly fatigue hepatotoxicity.
Caution in renal
impairment. Not
recommended in
concurrent HE
Acamprosate Modulates glutamate 666 mg three Diarrhea, Requires dose
neurotransmission, times daily insomnia, adjustment in renal
restoring balance anxiety, muscle impairment
between neuronal weakness (creatinine
excitation and clearance ≤30 mL/
inhibition min). Generally
safe for liver but
avoid in severe
renal impairment
Disulfiram Inhibits aldehyde 250–500 mg Hepatotoxicity, Contraindicated in
dehydrogenase, daily neuropathy, severe hepatic and
causing unpleasant psychiatric renal impairment
effects when alcohol symptoms
is consumed
Gabapentin Modulates GABA 300–600 mg Dizziness, Adjust dose in renal
activity, reducing three times daily fatigue, ataxia, impairment.
alcohol cravings and edema Generally
withdrawal well-tolerated but
symptoms limited data on use
in liver disease
Topiramate Enhances GABA 25–300 mg daily Cognitive Limited data on use
activity and inhibits impairment, in severe liver
glutamate receptors, dizziness, disease; caution
reducing alcohol weight loss advised in renal
consumption and impairment
cravings
Baclofen GABA receptor 5–10 mg three Drowsiness, Generally safe in
agonist, reduces times daily, dizziness, liver disease; can be
alcohol cravings titrated up to weakness, used in patients
30–80 mg daily fatigue with liver cirrhosis.
Requires caution in
renal impairment
and dose adjustment
may be needed

both medication and therapy modalities to heal and enact further change on the path
to recovery [21]. Other medical management to consider involves optimizing nutri-
tion, eliminating tobacco use, and, specifically with ALD patients, treatment of
infections and complications of portal hypertension [15]. Corticosteroids are often
58 E. Basu and A. Shenoy

used as short-term therapy in patients with severe ALD, though use is limited by
infection risk and other adverse side effects [9].
The mainstay of nonpharmacologic strategies for AUD treatment is therapy and
psychosocial interventions [9]. Motivational interviewing is a form of counseling
utilized to identify a patient’s goals and strengthen motivation toward achieving
those goals. In the case of AUD, the goal would be to reduce alcohol consumption
or to achieve abstinence. A more specific form of treatment is called motivation
enhancement therapy (MET), which consists of techniques curated to patient assess-
ment in order to better evoke change [9]. Cognitive behavioral therapy (CBT),
focused on relapse prevention, is aimed at identifying high-risk situations and
employing coping skills. Strategies include managing cravings, addressing self-­
harm, anger management, drink and drug refusal skills, and leading a balanced life-
style, among other skills [19]. Finally, peer support groups, such as Alcoholics
Anonymous (AA), are a well-established source of psychological support for those
with AUD; AA employs a 12-step facilitation model to target changes in behav-
ior [29].
Those with ALD are a sicker, more medically complex population, often unable
to adhere to the full gamut of interventions due to repeated hospitalizations and
medical comorbidities. ALD patients have typically also been excluded from stud-
ies assessing pharmacologic management of AUD [21]. A systematic review dem-
onstrated that in those with ALD, a combination of psychosocial and medical
interventions improved abstinence rates compared to standard medical care [30].

5.4 Risk Factors for Relapse in Transplant Patients

Relapse can be a nebulous term to define but is generally characterized as falling

back into prior patterns of drinking after a period of abstinence. A lapse or slip is
usually a brief period of alcohol use, without returning to prior use patterns [29].
Relapse can be expected in the chronic course of AUD and should be met with sup-
port and reasonable goal setting. Prospective studies have demonstrated that relapse
assessment based solely on self-report can fail to capture true relapse rates. In fact,
the sum of self-report, screening tools such as AUDIT, laboratory testing, and col-
lateral information from friends and family is likely necessary to best estimate inci-
dence of relapse [31].
We can risk-stratify patients based on variables known to be associated with
relapse. Based on cohort data, certain demographics, such as age >50, were associ-
ated with a greater relapse risk post-transplant, and women were more likely than
men to relapse while on the transplant list [29, 32]. Regarding alcohol use, contin-
ued alcohol use after diagnosis of ALD was associated with relapse, as well as fewer
months of sobriety pre-transplant. Family history of AUD was also associated with
relapse post-transplant. Psychiatric illness and other substance use increased rates
of relapse post-transplant, as well as medical factors such as noncompliance and
poor health status [33]. Finally, socioeconomics played a role in relapse, with
employment immediately prior to transplant and lack of spouse or social support
contributing to relapse risk [29, 34].
5 Alcohol Use Disorder, Alcohol-Associated Liver Disease, and Liver Transplantation 59

Scoring instruments to quantify relapse can also assist with risk stratification and
subsequent tailored interventions. The High-Risk Alcohol Relapse (HRAR) scale
and the Alcohol Relapse Risk Assessment (ARRA) are validated scoring tools
designed to predict patients at high risk of relapse [29, 35, 36]. Prospective data
using these scales is limited and would aid in further characterizing and managing
risk factors for relapse. Overall, any given risk factor cannot definitively predict
relapse in AUD patients, and we must take an individualized, harm-reduction
approach to address relapse.

Pearls
• Clinicians should approach relapse by addressing modifiable and unmodi-
fiable risk factors with patients, such as age, social supports, socioeco-
nomic status, psychiatric illness, and other substance use.
• Medications can be a useful component of a relapse prevention strategy
and can be more widely trialed in clinical settings.
• An individualized approach embedded within a multidisciplinary care
model is helpful to normalize relapse and support patients suffering
from AUD.

Pitfalls
• Relapse is difficult to predict, and no specific risk factor is independently
causative of relapse.
• Placing negative perceptions or blame on a patient for relapse can be stig-
matizing, especially given the medical and psychosocial vulnerabilities of
AUD/ALD patients.

5.5 Liver Transplantation and Post-liver Transplant

Management of AUD

Liver transplantation (LT) evaluation is often started with new-onset decompen-

sated cirrhosis (indicated by ascites, encephalopathy, varices, and/or jaundice),
spontaneous bacterial peritonitis, HCC, or a MELD score greater than 21 [21]. A
comprehensive evaluation for liver transplant includes several components: history-­
taking, collateral-gathering, cognitive testing, confirming an alcohol use disorder
diagnosis, gauging motivation for change and relapse risk, and assessing social sup-
ports [37]. Additionally, AASLD guidelines recommend that potential LT candi-
dates be seen by a psychiatrist for evaluation and subsequent planning of treatment
course [21]. Multidisciplinary care is thus required prior to making a determination
about listing a patient for LT.
Historically, LT centers nationally required ALD patients to be abstinent for
6 months to be eligible for transplant. Few ALD patients were referred for
60 E. Basu and A. Shenoy

transplant, although it was known that patient survival rates for ALD versus other
etiologies of liver disease are similar [38, 39]. This period of abstinence was justi-
fied with rationale such as allowing time for liver recovery and assessing patient
motivation to remain abstinent and prevent relapse [21]. There was a level of hesi-
tancy to list ALD patients for transplant, given the general stigma and attitudes
toward this patient population [40]. Data has shown, however, that the 6-month
period is not a sufficient predictor of post-LT relapse rates [41]. In fact, abstinence
itself is not a treatment for substance use and does not imply that patients have
internalized skills and strategies to abstain from drinking long term [42].
Consequently, the emphasis on a specific abstinent period prior to LT evaluation
has decreased in recent years. Given the risk of relapse and its negative effect on
graft function and long-term survival post-LT, the emphasis has been placed on
reducing risk of post-LT relapse.
As mentioned previously, risk factors for AUD relapse include but are not limited
to age, employment, social supports, cigarette smoking, continued substance use,
and psychiatric comorbidities. An interesting consideration is the role of substance
use treatment; data has shown that patients who received substance use treatment
pre-LT did not significantly differ in relapse rates compared to patients without
treatment. However, patients who receive treatment both pre- and post-LT did have
significantly lower relapse rates [35]. These data suggest that a multidisciplinary
care model to address patient needs beyond just medical follow-up, even after trans-
plantation, is the best strategy to mitigate relapse risk.
In fact, integrated care has been shown to benefit patients post-liver transplant.
For instance, one retrospective analysis demonstrated that having an alcohol addic-
tion unit embedded within a liver transplant center, as opposed to evaluation by
addiction psychiatrists unaffiliated with the LT center, significantly reduced relapse
risk post-liver transplant [43].

5.6 Conclusions and Future Directions

Patients with AUD and ALD are psychologically and medically vulnerable. The
risk of ALD can be mitigated by alcohol cessation and management of the
AUD. Clinicians should focus on medical and therapeutic interventions to
decrease alcohol use, emphasize abstinence, and minimize relapse risk. An inte-
grated care model with primary care, hepatologists, and psychiatrists/addiction
specialists is key to improving outcomes for patients with AUD. If alcohol cessa-
tion does not lead to liver recovery, liver transplantation for ALD is a viable and
potentially successful option. Alcohol-related liver disease is the most common
indication for transplant presently; clinicians should adopt a stigma-free treatment
approach to this vulnerable and medically as well as psychiatrically tenuous
population.
5 Alcohol Use Disorder, Alcohol-Associated Liver Disease, and Liver Transplantation 61

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Alcohol Withdrawal Syndrome
6
Amanda Ramsdell and Stephanie Chiao

6.1 Pathophysiology and Clinical Dangers Related

to Alcohol Withdrawal Symptom

As described throughout this book, the prevalence of risky alcohol use and alcohol
use disorders is common within the United States and globally. The absolute health
impacts and healthcare cost of alcohol-related health complications are large and
concerning, with estimations of the overall cost to the healthcare system and econ-
omy of $250 million in 2010 [1]. One such health-related adverse outcome from
alcohol use is the development of a potentially lethal withdrawal state. The immedi-
ate clinical dangers of alcohol withdrawal are addressed in this chapter, which range
from mild symptoms of anxiety and restlessness to the more severe complications
of seizure and even death if not diagnosed properly and treated adequately. The
consequences of alcohol withdrawal are pertinent not only to providers aiming to
care for patients attempting detoxification as a treatment for alcohol use disorder but
also for providers caring for patients in settings in which alcohol consumption is
unintentionally stopped abruptly and withdrawal can unexpectedly precipitate (i.e.,
patients hospitalized for other indications, including elective surgeries). It is diffi-
cult to estimate the extent of the impact that alcohol withdrawal has on our society
as a whole, as not all people seek treatment for symptoms related to alcohol with-
drawal. However, some have extrapolated that up to two million people in the United
States experience alcohol withdrawal to some extent each year [2].

A. Ramsdell (*)
Department of Medicine, Division of General Internal Medicine, Section of Hospital
Medicine, Weill Cornell Medicine, New York, NY, USA
e-mail: [email protected]
S. Chiao
Department of Medicine, Division of General Internal Medicine, Section of Hospital
Medicine, Weill Cornell Medicine, New York, NY, USA
Department of Psychiatry, Division of Addiction Psychiatry, Weill Cornell Medicine,
New York, NY, USA
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2024 65
M. Khan, J. Avery (eds.), From Stigma to Support, Psychiatry Update 4,
https://doi.org/10.1007/978-3-031-73553-0_6
66 A. Ramsdell and S. Chiao

In a state of equilibrium, the brain balances both neuro-excitatory and neuro-­

inhibitory transmitters. Pathology can develop when either of these states predomi-
nates. Alcohol produces a neuro-inhibitory effect by amplifying the effects of
gamma-aminobutyric acid or GABA neurotransmitter (a neuro-inhibitory transmit-
ter) at the GABA (A) receptors and downregulating the effects of the N-methyl-b-­
aspartate or NMDA receptors, where glutamate acts (a neuro-excitatory transmitter).
When a person becomes chemically dependent on alcohol, the brain compensates
for these consistent effects of alcohol, and therefore, abrupt cessation leads to
upregulation of glutaminergic activity at the NMDA receptor and a lack of
GABAergic activity at the GABA (A) receptors, all contributing to a pathologic
excitatory state. Symptoms of alcohol withdrawal, which are outlined in the
CIWA-Ar scale (discussed below), include nausea, anxiety, diaphoresis, agitation,
and auditory and visual hallucinations, among other excitatory features. Severe
alcohol withdrawal syndrome, though variably defined, may include at its extremes
seizure activity and potential death [2]. It has been hypothesized that recurrent epi-
sodes of this excitation state, or withdrawal, may predispose individuals to with-
drawal episodes of increased severity and more likelihood of seizure and other
adverse outcomes, sometimes called “the kindling effect” [3] (Fig. 6.1).
The estimated prevalence of alcohol dependence among hospitalized patients on
non-psychiatry services varies with studies citing between 6 and 20% over the past
few decades, depending on care setting [5, 6]. Thus, it is imperative for a wide range
of healthcare providers to be able to assess risk for alcohol withdrawal, identify
emerging signs of withdrawal, and appropriately manage withdrawal to avoid seri-
ous complications related to this syndrome, including death. Though the prevalence
of alcohol withdrawal cases varies by region and study, it has been cited that of
people with AUD presenting for clinical trials, over 30% are found to have alcohol
withdrawal symptoms [7]. Another study assessed patients presenting to the
Emergency Department with acute trauma and a documented Clinical Institute
Withdrawal Assessment for Alcohol-revised score (CIWA-Ar) which found over
half (52%) showed severely elevated CIWA-Ar score of >20 and 24% of these
patients are progressing to delirium tremens, which if untreated can be fatal in up to
15% of patients [8].
In assessing risk, we recommend screening patients for risky alcohol use, assess-
ing frequency and quantity of alcohol consumption and, importantly, the timing of
the last alcohol intake, which is especially important when caring for patients in a
facility or inpatient setting. Daily consumption, quantity per day, emerging signs of
withdrawal in the setting of an elevated ethanol level, prior history of severe with-
drawal, delirium tremens, and seizure are some risk factors for a severe course.
Special populations, including the geriatric population, with underlying cognitive
impairment or those with other concurrent substance use may present with confu-
sion or other signs of delirium prior to the typical autonomic activity changes.
Symptoms, which are additionally outlined in the CIWA scale (discussed below),
include nausea, tremors, diaphoresis, anxiety, agitation, tactile disturbances, audi-
tory and visual disturbances, headache, and confusion. Given the potentially deadly
consequences of severe withdrawal, there have been efforts to further identify and
6 Alcohol Withdrawal Syndrome 67

a c

b d

Fig. 6.1 Valenzuela [4]

predict patients most at risk. While prior episodes of alcohol withdrawal syndrome
are the strongest predictor of severe alcohol withdrawal, there are ongoing efforts to
better identify and inform providers’ clinical decisions. Currently patients with a
personal prior history of withdrawal should be monitored closely for withdrawal
symptoms and escalation [9].
68 A. Ramsdell and S. Chiao

6.2 Treatment Approaches for Alcohol Withdrawal

Syndrome: Symptom-Triggered Strategies vs.
Standing Regimens

Understanding the roles of both excitatory and inhibitory neurotransmitters in

regard to alcohol’s effects on the brain allows us to identify and comprehend the
symptoms of alcohol withdrawal when alcohol is abruptly stopped. If a person has
become chemically dependent and experiences alcohol cessation, this produces the
uninhibited excitatory state that results in symptoms ranging from anxiety and rest-
lessness to extreme hypertension, diaphoresis, and even seizure. One commonly
used tool to determine severity of withdrawal is the revised Clinical Institute
Withdrawal Assessment for Alcohol (CIWA-Ar), a validated 10-point scale, which
can be used for both initially gauging withdrawal severity and subsequently assess-
ing response to treatment. The ten symptoms assessed clearly demonstrate the
neuro-excitatory state of withdrawal and include a spectrum of the following cate-
gories: nausea and vomiting, tremor, paroxysmal sweats, anxiety, agitation, tactile
disturbances, auditory disturbances (including hallucinations), visual disturbances,
headache, and orientation or clouding of the sensorium (see Fig. 6.2) [10]. CIWA-Ar
scoring of less than 8 is considered mild, 9–15 is moderate, and over 15 is consid-
ered severe withdrawal, information that can help inform treatment plans.
As discussed later in this chapter, benzodiazepines have been the mainstay of
alcohol withdrawal treatment since initial evidence in the 1960s. Today, providers
choose in general between scheduled pharmacologic approaches and those which
use the CIWA-Ar in a more symptom-triggered way, meaning dosing medications
based on occurrence of withdrawal symptoms and their severity. Symptom-triggered
approaches, using the CIWA-Ar scale, came into favor in various settings where
randomized controlled trials showed efficacy of treating withdrawal and, impor-
tantly, a reduction in the amount of benzodiazepine used and drastically shortened
length of treatment [11, 12]. In choosing an approach for an individual patient, it is
important to understand the context and population of these studies and how they
apply to your own practice setting. For example, these symptom-triggered cited
studies excluded any acute medical or psychiatric condition or comorbidity, concur-
rent benzodiazepine, opioid or stimulant use, and any cognitive dysfunction and
took place in a medical detoxification unit, not a general medicine inpatient setting.
Saitz et al. additionally excluded patients with any history of seizure.
Therefore, for patients with medical complexity, concurrent opioid or other sub-
stance use, cognitive impairment, or any risk of delirium, it is reasonable to consider
a scheduled treatment approach with individualization based on response rather
than a solely symptom-triggered approach as outlined by these studies, in which
logistics and challenges of the emergency room and general medicine inpatient
units were limited or absent. In fact, initial retrospective studies utilizing chart
reviews of patients with alcohol withdrawal in medicine inpatient settings, as well
as psychiatric inpatients and alcohol detoxification studies, with similar exclusion
criteria found that of 172 charts identified with alcohol withdrawal, 132 were
excluded due to being medically complicated, with 64% of these exclusions based
6 Alcohol Withdrawal Syndrome 69

Fig. 6.2 The revised Clinical Institute Withdrawal Assessment for Alcohol Scale (CIWA-Ar) [10]
70 A. Ramsdell and S. Chiao

on additionally active medical comorbidities, having a severe liver disease or a his-

tory of withdrawal seizure, which should be noted prior to applying this to every
setting [13]. The challenges of the treatment settings should be considered to create
realistic planning for addressing withdrawal. Recently, in 2024, a multicenter, retro-
spective cohort study of medically complex patients with alcohol withdrawal on
medical or surgical wards suggested improved outcomes using strategies consistent
with ASAM’s practice guidelines, emphasizing using long-acting benzodiazepines
with a symptom-triggered approach [14]. In the future, randomized controlled trials
enrolling medically complex patients could help clarify best practices and eliminate
confounders.
Additional limitations to accurately using a symptom-triggered approach include
staffing, particularly nursing staffing ratios (i.e., how many patients are assigned per
nurse at any given time), staff training and experience, and any alternative diagnoses
that may independently affect the score. A nurse who is inexperienced in taking care
of patients with alcohol withdrawal or who is taking care of numerous complex
patients may have varying success in accurately using the CIWA-Ar score, and there
may be inter-operator variations, leading to over- or under-scoring. Other physio-
logic states, including sepsis, thyrotoxicosis, stimulant use, or medications, such as
beta-blockers, will additionally change a patient’s experience of symptoms and may
inaccurately change the CIWA-Ar score, making it uninterpretable. Important to
note additionally is that a patient must be cognitively intact and without confusion
or any signs of delirium in order to reliably report symptoms. Therefore, for patients
who are unable to interact with the care team to provide accurate symptom reports,
providers cannot safely rely on the CIWA-Ar scale and symptom-triggered
approaches alone. Despite these important caveats, the CIWA-Ar score provides
important information to the provider regarding withdrawal severity and is an
important tool in triaging patients for appropriate monitoring and treatment.

6.3 Various Pharmacologic Approaches to Treating

Alcohol Withdrawal

As mentioned above, if alcohol withdrawal symptoms are recognized, they should

be promptly addressed using a mainstay of pharmacologic therapy to improve
symptoms and prevent seizure, delirium, and death if not treated. Every 5 years, the
American Society of Addiction Medicine provides updated guidance on evidence-­
based treatment for various clinical states related to substance use disorders, includ-
ing specifically alcohol withdrawal [15]. Knowing the basic mechanisms by which
neurotransmitter imbalance leads to the over-excitatory withdrawal state and symp-
toms gives logical insights into therapeutic approaches. For example, medications
such as benzodiazepines and neuroleptics, like gabapentin, act on the GABA (A)
activity in a similar fashion to alcohol and can thus be used to reverse the immediate
effects of alcohol cessation in patients who are alcohol dependent [15].
Compared to placebo, benzodiazepines have a clearly documented efficacy as
compared to placebo in treating alcohol withdrawal and in severe cases improving
6 Alcohol Withdrawal Syndrome 71

mortality and are the most widely accepted strategy for treatment. However, there
are limited head-to-head comparisons for different classes of medications to address
withdrawal [16]. Meta-analysis shows that sedative-hypnotic (i.e., benzodiazepine)
treatment practices compared to neuroleptic treatment (i.e., antipsychotics) pro-
duces a favorable mortality benefit and thus early on became standard of practice to
treat alcohol withdrawal syndrome [17]. Benzodiazepines have been the mainstay
of treatment approaches both in outpatient and inpatient settings for decades and are
typically the basis for what are called symptom-triggered protocols.
Benzodiazepines have the most robust data supporting their use as first-line
agents to address alcohol withdrawal, driven by their efficacy at preventing seizure
and delirium [18]. There is no particular benzodiazepine that is more effective than
others, though providers may consider risk factors for oversedation, liver function,
onset of action, and half-life to help guide their approach [19]. It is preferred to start
with and use one agent, when possible, to avoid unintentional “stacking” and
oversedation while addressing withdrawal symptoms. New data suggests that better
outcomes, including length of stay and complicated withdrawal event, are associ-
ated with long-acting benzodiazepines such as diazepam and chlordiazepine as
compared to lorazepam, though providers should take a patient’s individual charac-
teristics into consideration when treating [14].
While benzodiazepines are the preferred agent to address withdrawal in moder-
ate to severe cases and prevent life-threatening complications, such as seizures,
there have been various attempts to reduce the overall benzodiazepine needs and
create more benzo-sparing approaches. Alternative agents, namely, gabapentin and
carbamazepine, are used both in monotherapy regimens for mild withdrawal and as
adjuncts in benzodiazepine-sparing strategies. We discuss here both approaches that
may help further prevent complications and are deemed safe to use concurrently to
address withdrawal and approaches that aim to treat symptoms only and may mask
withdrawal symptoms and should be avoided.
One such approach is the use of standing gabapentin, which can be used as
monotherapy in mild withdrawal or as adjuvant treatment to reduce overall as
needed benzodiazepine use in symptom-triggered protocols. Given the pharmacol-
ogy of gabapentin and its safety profile, this provides additional GABAergic sup-
port and safely helps prevent withdrawal and seizure. Alternatively, for patients with
mild withdrawal, carbamezapine can be considered for monotherapy, with close
monitoring for any escalation of symptoms.
For cases of severe withdrawal or for patients who require prohibitive doses of
benzodiazepine, providers commonly consider adding adjunct medications such as
carbamazepine, gabapentin, or valproic acid (caution is required with pregnancy
and/or liver disease). For those with inadequate symptom reduction while on benzo-
diazepine, one can also consider transitioning to an alternative agent, such as
phenobarbital.
A common, non-evidence-based, and potentially dangerous approach that we do
not recommend is to address specific symptoms that compose the withdrawal syn-
drome and help gauge severity. For example, providers may attempt to treat nausea
with antiemetics as needed and not directly provide more benzodiazepine support to
72 A. Ramsdell and S. Chiao

treat the underlying cause of nausea, which is likely withdrawal. In only treating the
symptom of nausea, one potentially artificially reduces the CIWA-Ar score, making
the patient’s withdrawal appear less severe but without reducing the likelihood of
escalation or seizure. Similarly, there have been attempts to treat hallucinations with
antipsychotics, which can be a sign of severe withdrawal and potential delirium
tremens, a condition that needs to be aggressively addressed with benzodiazepines
to treat the underlying cause, alcohol withdrawal. Antipsychotics may acutely
sedate the patient and give the appearance of clinical improvement but do not
address withdrawal itself, leaving the patient at increasing risk of withdrawal
complications.
As part of managing the withdrawal state, care teams should also carefully assess
the volume status, electrolyte disturbances, and the nutritional status of patients
experiencing withdrawal. Patients are at higher risk for Wernicke’s encephalopathy,
and all patients presenting to the ED and/or inpatient setting should receive at least
100 mg IV thiamine prior to any glucose-containing fluids as a preventative mea-
sure. For patients experiencing any confusion, providers should have a low thresh-
old to empirically treat with high-dose intravenous thiamine for possible Wernicke’s
encephalopathy. Teams should take standard hospital precautions in regard to pre-
venting delirium, reducing harm if seizures occur, and preventing falls.

6.4 Ambulatory Approaches to Alcohol

Withdrawal Treatment

Safe and effective ambulatory withdrawal treatment requires careful assessment to

determine the appropriate level of care. The appropriate care setting is determined
by the severity of the withdrawal syndrome, the risks of severe or complicated with-
drawal, and other factors related to the living environment where the patient is resid-
ing and recovering [15]. In general, those with severe withdrawal presentations who
are at risk for complications such as seizures, delirium tremens, or other medical or
psychiatric complications should be treated as inpatients. These can include indi-
viduals with significantly abnormal laboratory results suggestive of medical com-
plexity and risk, a history of withdrawal seizures, a long history of large amounts of
alcohol use, poorly controlled or severe medical or psychiatric problems, and con-
current withdrawal from or dependence on other substances [20]. Those with sig-
nificant alcohol cravings have also been shown to be more likely to return to drinking
or be lost to follow-up during detoxification and may benefit from a higher level of
care [21].
Absent indications for inpatient treatment, ambulatory treatment is the preferred
setting for most patients. Patients with mild alcohol withdrawal can usually be man-
aged in an ambulatory setting that does not have extensive onsite monitoring, such
as a physician’s office or by a home health agency, and this is often significantly less
disruptive and costly to patients [22]. Patients with moderate withdrawal and even
some with uncomplicated severe withdrawal can be managed in an ambulatory set-
ting with extended onsite monitoring capabilities, such as a day hospital or
6 Alcohol Withdrawal Syndrome 73

addiction treatment facility. These can include patients with moderate to severe
anxiety and moderate to severe tremors but not confusion, hallucinations, or sei-
zures [15]. In circumstances with experienced clinicians and sufficiently close mon-
itoring, patients with concurrent withdrawal from other substances or with remote
histories of complicated withdrawal can be considered for ambulatory treat-
ment [15].
For effective ambulatory treatment, patients must have access to safe housing
and transportation, be able to tolerate oral medications and be able to comply with
regular evaluations and communicate their symptoms to providers, and in some
cases, they may require a caregiver who can stay with them [20]. Patients must also
be able to reliably adhere to recommendations about medications and abstinence, as
the combination of alcohol and medications such as benzodiazepines can be immi-
nently dangerous.
As with inpatient settings, benzodiazepines are first-line treatment. However,
there are additional risks with benzodiazepines in the outpatient setting, such as
risks of misuse, diversion, and alcohol-drug toxicity. These risks may be managed
by prescribing limited doses or more frequent monitoring. Additionally, non-­
benzodiazepine medications can be maximized, minimizing the need for benzodiaz-
epine exposure. Carbamazepine and gabapentin are often suitable monotherapy
options, particularly for mild and moderate withdrawal.
Various benzodiazepine dosing regimens may be appropriate, including front-­
loading, symptom-triggered, or scheduled approaches. A symptom-triggered
approach would require regular and reliable assessment of signs and symptoms,
often requiring a healthcare professional or a caregiver who has received sufficient
guidance. With a scheduled approach, frequent monitoring is also required to make
dose adjustments. For those with more severe withdrawal, a front-loading strategy
has been recommended [15]. On the other hand, for patients with mild withdrawal
who are at low risk for developing complications, pharmacotherapy may not be
needed at all. For those with some risk factors for developing worsening symptoms,
a low threshold for prescribing medications is reasonable, given the lack of continu-
ous monitoring.

6.5 Initiation of Medications for Alcohol Use Disorder:

Timing and Other Considerations

A withdrawal event can serve as an important opportunity to discuss long-term

medications to treat alcohol use disorder. The American Society of Addiction
Medicine emphasizes one goal of alcohol detoxification treatment being “to prepare
a patient for ongoing treatment of dependence on alcohol” [2]. All patients admitted
to the hospital who are treated for alcohol withdrawal should be offered additional
treatment options for AUD, including medications, which are described elsewhere
in this book. Contrary to prior thought, initiation of AUD treatment should not nec-
essarily be delayed until days after the withdrawal period or after discharge from the
hospital. Additionally, those patients with alcohol dependence who have withdrawal
74 A. Ramsdell and S. Chiao

symptoms are more at risk for returning to alcohol use after periods of cessation and
should be offered evidence-based medication and therapeutic modalities to support
them in their treatment goals [23]. Therefore, we consider the event of a hospital
admission to be an important opportunity to explore options for alcohol use disorder
treatment, including pharmacologic support and initiation.

6.6 Conclusion

The health and cost burdens of the complications of alcohol use disorder, including
alcohol withdrawal syndrome, remain high worldwide [1, 6]. It is imperative that
both addiction medicine providers and medical professionals in all fields be aware
of the symptoms and health consequences to alcohol withdrawal as patient can
experience withdrawal both in the context of intended detoxification protocol and
unintentionally through the unplanned abrupt cessation of alcohol in other circum-
stances (i.e., emergency hospitalizations or surgeries). With the guidance of several
professional societies, the landscape for options of approaching alcohol cessation
have evolved, both in pharmacological options and treatment settings (inpatient vs.
outpatient) with the goals of reducing harm and allowing greater access to care for
more patients [15]. Given the life-threatening nature of untreated withdrawal, symp-
toms should be identified early and managed adequately in the appropriate setting,
depending on severity. Evolving approaches to adequate withdrawal treatment
should continue to critically assess the existing data and assess their generalizabil-
ity. In caring for patients who experience withdrawal, providers should additionally
see this as an opportunity to discuss long-term treatment options for AUD and pro-
vider initiation or connection to continued care.

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Pharmacotherapies for Alcohol Use
Disorder 7
Evguenia Makovkina

Key Points
• There are three FDA-approved medications for alcohol use disorder: acampro-
sate, disulfiram, and naltrexone.
• There is strong evidence for using naltrexone to curb alcohol use and help pre-
vent craving in withdrawal. Naltrexone is typically well-tolerated in both the oral
and long-acting injectable formulations.
• Acamprosate is contraindicated in people with severe kidney impairment, and
naltrexone is contraindicated in people with severe liver impairment. There have
not been head-to-head trials comparing the efficacy of these two medications.
• The disulfiram-alcohol reaction can be severe, even fatal, and is dependent on the
amount of alcohol consumed. The ideal candidate for disulfiram is a reliable,
highly motivated person with a goal of abstinence. Supervised administration of
disulfiram has the greatest benefit.
• Gabapentin, topiramate, and baclofen all function within the GABAergic sys-
tem, with additional neurotransmitters implicated downstream depending on
each mechanism. These three off-label medications are helpful in reducing nega-
tive physiologic symptoms commonly experienced in alcohol recovery.

7.1 Introduction

Alcohol use disorder (AUD) is highly prevalent worldwide [1] yet significantly
undertreated [2]. In 2021, 10.6% of Americans aged 12 or older (29.5 million peo-
ple) were estimated to have been diagnosed with AUD in the past 12 months [3];
however, approximately 7% of those with a lifetime history of AUD and only 3.1%
of those with a 12-month history of AUD receive any kind of treatment [4]. The rate

E. Makovkina (*)
NewYork-Presbyterian Weill Cornell, New York, NY, USA
e-mail: [email protected]

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2024 77

M. Khan, J. Avery (eds.), From Stigma to Support, Psychiatry Update 4,
https://doi.org/10.1007/978-3-031-73553-0_7
78 E. Makovkina

of medication-assisted treatment is even lower. In a 2019 survey, only 1.6% of

patients diagnosed with AUD reported treatment with one of the FDA-approved
medications [5].
The underutilization of medications is likely related to several factors. There are
gaps in proficiency among medical professionals in treating alcoholism, lack of
information and/or confidence in the treatments [6], and, undoubtedly, stigma [7]. A
study comparing treatment rates from 1991–1992 and 2001–2002 found that while
rates of depression treatment increased with time, rates of treatment for alcoholism
slightly decreased [4] despite adequate access to healthcare among most excessive
drinkers [8]. This discrepancy highlights a gap between available treatments and
their use in individuals with AUD.
There are currently three pharmaceutical agents approved by the US Food
and Drug Administration (FDA) for alcohol use disorder: acamprosate, disulfi-
ram, and naltrexone. Other agents are used off-label. Though the effect of some
of these medications is modest, medication-assisted treatment has a large evi-
dence base and is a first-line treatment for alcohol use disorder. The COMBINE
(Combined Pharmacotherapies and Behavioral Interventions for Alcohol
Dependence) study, a large randomized controlled trial conducted in 2006,
showed equally good clinical outcomes among individuals treated with naltrex-
one alone, a combination of naltrexone and a combined behavioral intervention,
and the behavioral intervention alone [9]. As always, multimodal treatment,
which includes the use of psychotherapeutic and psychosocial interventions
(i.e., motivational interviewing and community-­based groups), is important for
recovery.
In this chapter, we review the medications that have been shown to be helpful for
supporting individuals with a goal of recovery from alcohol, both with a harm
reduction and abstinence-focused approach. This chapter focuses on each medica-
tion’s therapeutic effects, mechanism of action, possible side effects, contraindica-
tions, and other considerations for clinical use. This chapter also reviews the
emerging evidence for new pharmacological agents.

7.2 FDA-Approved Agents

Even after a prolonged recovery period from alcohol, the brain circuitry of
someone with a pre-existing addiction to alcohol is primed for relapse. This
priming occurs at the level of neuroadaptation in the brain as well as the level of
psychological classical conditioning of stimuli associated with alcohol [10].
Generally, relapse occurs when people seek out a positive reward from drinking
or drink to avoid a negative consequence of alcohol withdrawal or abstinence. It
is helpful to think of the medications used in AUD treatment as either curbing
the positive reward or pleasure of drinking or making the absence of alcohol less
unpleasant (Table 7.1).
7 Pharmacotherapies for Alcohol Use Disorder 79

Table 7.1 FDA-approved and off-label agents for alcohol use disorder (AUD)
Reduce positive Reduce negative effects of Reduce
reward of prolonged withdrawal or craving for
alcohol abstinence alcohol
FDA-approved medications for
the treatment of alcohol use
disorder
Acamprosate – Yes Yes
Disulfiram Yes – –
Naltrexone Yes – Yes
Non-FDA-approved
medications for alcohol use
disorder
Gabapentin – Yes Yes
Topiramate – Yes Mixed results
Baclofen – Yes Yes
Novel and emerging
therapeutics
PDE-4 inhibitors ? ? ?
5-HT3 receptor antagonists ? ? ?
Psychedelics ? ? ?

7.3 Acamprosate

7.3.1 Therapeutic Effects

While some individual studies—such as the COMBINE trial from 2006—do not
show any significant benefits of acamprosate in AUD compared to placebo [9], a
recent meta-analysis of 95 randomized controlled trials (RCTs) concluded that there
is moderate strength evidence for using acamprosate in AUD [11]. Acamprosate has
been shown to reduce rates of return to drinking and reduce the number of drinking
days in people with AUD, according to a recent meta-analysis of several [11]. The
number needed to treat (NNT) for acamprosate to prevent one person from return-
ing to drinking is 12 [11].

7.3.2 Mechanism

While the exact mechanism is unclear, it is known that acamprosate acts on the
GABAergic system, which is responsible for neuronal inhibition, and glutamatergic
system, which is responsible for neuronal excitation, in the central nervous system.
Acamprosate likely interacts with these two systems because it structurally resem-
bles both GABA and glutamate [10]. Acamprosate increases activity in the
GABAergic system and reduces overstimulation of glutamate activity through indi-
rect modulation of the N-methyl d-aspartate (NMDA) receptor complex [10]. By
reducing glutamate overstimulation, acamprosate reduces cravings associated with
alcohol-related cues and helps prevent relapse.
80 E. Makovkina

7.3.3 Dose Range

666 mg, by mouth (PO), three times per day (TID).

For people with moderate kidney impairment: 333 mg PO TID.

7.3.4 Potential Side Effects

Gastrointestinal distress (diarrhea), CNS effects (nervousness), and fatigue are the
most common side effects.

7.3.5 Contraindications and Other Considerations

Acamprosate is renally cleared and excreted into urine as an unchanged drug. Thus,
acamprosate is contraindicated in people with severe kidney impairment (creatinine
clearance ≤30 mL/min). Individuals with moderate kidney impairment (CrCl
30–60 mL/min) require a dose adjustment (333 mg three times a day). Kidney func-
tion should be obtained at baseline prior to starting acamprosate and monitored as
clinically necessary.
Since acamprosate is not metabolized by the liver, it is a good option for people
with comorbid alcohol dependence and hepatic impairment. Acamprosate is dosed
three times per day, making it a less convenient choice than other available medica-
tions, which are dosed once a day.

7.4 Disulfiram

7.4.1 Therapeutic Effects

Disulfiram was the first medication approved by the FDA to treat AUD in 1951 [12].
It works by negatively reinforcing abstinence through the disulfiram-ethanol reac-
tion, which causes unpleasant symptoms when alcohol is consumed concurrently
while taking disulfiram. Evidence for disulfiram’s efficacy in AUD has been mixed,
as only results from open-label studies have shown potential benefits [13]. One pos-
sible explanation for this is that the full impact of the psychological mechanism of
disulfiram, which produces negative reinforcement, can only be evaluated in open-
label studies [13].
Nevertheless, the most recent practice guideline from the American
Psychiatric Association recommends that disulfiram be offered to people with
moderate to severe AUD (level 2C recommendation) who have a goal of achiev-
ing abstinence, prefer disulfiram, or cannot use or have not responded to acam-
prosate or naltrexone, are capable of understanding the possible risks of alcohol
consumption while taking disulfiram, and have no other contraindications to
disulfiram [14].
7 Pharmacotherapies for Alcohol Use Disorder 81

7.4.2 Mechanism

The main mechanism of action is irreversible inhibition of the enzyme aldehyde

dehydrogenase, which blocks the metabolism of acetaldehyde to acetone [15].
Acetaldehyde is a toxic metabolite of alcohol that causes highly unpleasant physi-
ological symptoms when its breakdown is inhibited: sweating, headache, nausea,
vomiting, and tachycardia. Through classical conditioning, disulfiram creates a link
between alcohol consumption and these unpleasant physical sensations, ultimately
acting as a deterrent to alcohol use. The severity of the reaction usually corresponds
to the amount of alcohol consumed [16].
Disulfiram is more likely to successfully deter someone from drinking when it is
taken daily; thus, regular adherence to the medication and high motivation for absti-
nence are important to its success. A meta-analysis of 22 randomized controlled
trials for disulfiram vs a placebo showed that supervised administration of disulfi-
ram by a family member or other was associated with significant advantage over
placebo, while unsupervised administration of disulfiram did not reach significant
benefit over the control [13].

7.4.3 Dose Range

250–500 mg PO daily.

7.4.4 Potential Side Effects

The most common side effects in the absence of alcohol are headache, fatigue, and
dermatitis. Some people report experiencing a bitter or metallic taste in their mouth
when taking disulfiram [16].
Severe forms of the disulfiram-ethanol reaction—confusion, myocardial infarc-
tion, cardiac arrhythmia, psychosis, seizure, hepatitis, or even death—have been
reported but are rare. Due to the risk of hepatitis, checking baseline liver function
tests and repeating them every 6 months are recommended.

7.4.5 Contraindications and Other Considerations

People with a history of clinically significant coronary artery disease or psychosis

should not be treated with disulfiram because of the potential severity of the
disulfiram-­ethanol reaction. Disulfiram can react with ethanol up to 14 days after
last taking disulfiram. Waiting at least 12–48 h from last alcohol consumption
before starting disulfiram is recommended [16]. Metronidazole should not be used
within 14 days of taking disulfiram due to a drug interaction which can increase the
risk of psychosis [16, 17].
82 E. Makovkina

7.5 Naltrexone

7.5.1 Therapeutic Effects

Naltrexone is used to reduce the pleasurable effects of alcohol when it is consumed

while taking naltrexone. Importantly, naltrexone also reduces craving for alcohol
when not drinking. Some people take naltrexone daily to prevent cravings while absti-
nent, and some people take it as needed on days when they expect to drink to reduce
the number of drinks they have. The number needed to treat (NNT) to prevent some-
one from returning to drinking is approximately 20 for oral naltrexone at a 50 mg
daily dose [18]. The long-acting intramuscular formulation has been shown to be
effective in reducing heavy drinking days compared to placebo [19].
A meta-analysis of 64 randomized placebo-controlled trials showed that naltrex-
one may be more helpful for reducing overall number of drinks and preventing
heavy drinking while acamprosate may be more helpful for maintaining abstinence
[20]. While naltrexone can be used safely without prior detoxification from alcohol,
this meta-analysis also concluded that detoxification prior to initiation of either nal-
trexone or acamprosate led to better outcomes [20].

7.5.2 Mechanism

Naltrexone is an opioid receptor antagonist which has the highest affinity for the mu
opioid receptor. It is thought to reduce craving for alcohol and reduce overall con-
sumption by blocking the reinforcing effects of endogenous opioids in the mesolim-
bic dopaminergic system [21]. It exists in two forms: oral tablets and long-acting
intramuscular injection.
A randomized controlled trial conducted in 2015 tested whether a polymorphism
(Asn40Asp) in the μ-opioid receptor gene (OPRM1) mediates the treatment
response to naltrexone with respect to return to heavy drinking [22]. The study did
not find a difference in treatment response to oral naltrexone between groups strati-
fied by this genetic polymorphism.

7.5.3 Dose Range

Oral formulation: 50–100 mg/day, can start with 25 mg/day to reduce the risk of
nausea and increase the dose when tolerated.
Long-acting injectable (LAI) formulation: 380 mg every 4 weeks administered
to the gluteal muscle.

7.5.4 Potential Side Effects

Nausea is the most common side effect and occurs in approximately 33% of people
taking LAI or oral naltrexone [UpToDate]. Nausea can be prevented by starting at a
low dose of naltrexone (25 mg daily) and titrating it up slowly to a therapeutic dose.
7 Pharmacotherapies for Alcohol Use Disorder 83

For the LAI formulation, pain or induration at the injection site is common. Other
common side effects include headache, abdominal pain, and diarrhea. These side
effects often subside after continued use of the medication. Naltrexone can tran-
siently elevate serum transaminase levels.

7.5.5 Contraindications and Other Considerations

Naltrexone is metabolized by the liver and contraindicated in people with acute

hepatitis and fulminant liver failure [14]. It is important to check markers of liver
function prior to initiating naltrexone and every 6 months during treatment.
Because naltrexone is an opioid receptor antagonist, at least 7–10 days between
last opioid administration and naltrexone initiation should pass to prevent precipi-
tating opioid withdrawal. Naltrexone should be stopped at least 72 h prior to receiv-
ing opioids to prevent opioid withdrawal [UpToDate].

7.6 Non-FDA Approved Agents

7.6.1 Gabapentin

7.6.1.1 Therapeutic Effects

Gabapentin is an antiepileptic approved for partial-onset seizures, post-herpetic
neuralgia, and restless legs syndrome; it is used off-label in AUD. Because of its
anxiolytic and sedative effects, it can be particularly helpful for treating prolonged
withdrawal symptoms. A meta-analysis of seven randomized controlled trials look-
ing at the use of gabapentin in AUD showed that the most significant benefit is in
reduction of the percentage of heavy drinking days [23].

7.6.1.2 Mechanism
Gabapentin is thought to decrease the release of excitatory neurotransmitters,
such as glutamate, and modulate GABAergic activity, which likely contributes to
stabilizing hyperexcitable neurons in the central nervous system. It does this by
binding a subunit of the voltage-gated calcium channels in the brain and spinal
cord [24].

7.6.1.3 Dose Range

300–1800 mg/day in three divided doses.

7.6.1.4 Potential Side Effects

At the higher end of the dose range, gabapentin can cause ataxia, dizziness, somno-
lence, ataxia, and peripheral edema [25].

7.6.1.5 Contraindications and Other Considerations

Dose adjustment is required for people with renal impairment. Avoid abrupt discon-
tinuation as there is evidence of withdrawal syndrome [26]. Case reports of people
84 E. Makovkina

who develop a dependence or addiction to gabapentin typically take high does and
have history of other substance use disorder (>3000 mg/day) [26].

7.6.2 Topiramate

7.6.2.1 Therapeutic Effects

Topiramate is an anticonvulsant with indications for seizure prophylaxis, migraine
prophylaxis, and weight management. It has a moderate effect on reducing alcohol
consumption [27]. A meta-analysis of seven randomized controlled trials explored
topiramate’s impact on abstinence from alcohol, heavy drinking, craving, and
c-­
glutamyltranspeptidase (GGT) outcomes [27]. Topiramate’s impact on these
parameters was significant on abstinence, heavy drinking, and GGT (listed from
highest magnitude of effect to lowest, respectively) [27]. It also concluded that the
magnitude of therapeutic impact of topiramate was similar if not greater than the
effects of naltrexone and acamprosate in AUD. Topiramate’s effect on craving did
not reach significance in this meta-analysis; however one study looking at craving
in response to alcohol-related cues did show a significant decrease [28]. This
double-­blinded randomized controlled study which compared topiramate to placebo
showed reduced craving and reduced brain activity on fMRI in response to cues
associated with alcohol [28].

7.6.2.2 Mechanism of Action

Topiramate is thought to impact alcohol consumption by modulating GABA and
glutamate. It enhances the inhibitory effects of gamma-aminobutyric acid
(GABA) and decreases excitatory glutamate transmission by interacting with
the AMPA/kainate receptors [28, 29]. One of the ways in which topiramate
reduces heavy drinking is thought to be by decreasing alcohol-associated dopa-
mine release in the mesolimbic system, thereby lessening the reward of drinking
alcohol [28].

7.6.2.3 Dose Range

Most people achieve therapeutic benefit at 200–300 mg/day. Starting at 25–50 mg/
day and increasing gradually by 50 mg/day each week are recommended to reduce
the risk of side effects.

7.6.2.4 Potential Side Effects

The most common side effects include paresthesias, dizziness, drowsiness, diffi-
culty concentrating, weight loss, and ocular effects (myopia, secondary angle-­
closure glaucoma).
Topiramate causes non-anion gap metabolic acidosis through inhibition of the
enzyme carbonic anhydrase, which over time may predispose adults and children to
nephrolithiasis. Overall, people taking topiramate are 2–4 times more likely to
develop kidney stones [30, 31].
7 Pharmacotherapies for Alcohol Use Disorder 85

7.6.2.5 Contraindications and Other Considerations

Topiramate is contraindicated in people taking medications that cause metabolic
acidosis. People with a creatinine clearance below 70 mL/min would benefit from a
reduced dose [32].

7.6.3 Baclofen

7.6.3.1 Therapeutic Effects

Baclofen, a muscle relaxant primarily used to treat spasticity, has potential thera-
peutic effects in the treatment of alcohol use disorder (AUD). There have been
mixed results published. A randomized, placebo-controlled trial of 180 veterans
taking 30 mg baclofen daily for 12 weeks did not show significant impact on absti-
nence, reduction of alcohol use, or craving [33]. However, a more recently pub-
lished meta-analysis of 13 randomized controlled trials concluded that treatment
with baclofen was associated with significant improvement in time to relapse and
likelihood of maintaining abstinence [34].

7.6.3.2 Mechanism of Action

Baclofen is an agonist at the gamma-aminobutyric acid type B (GABA-B) receptor
[34]. Since the GABA-B receptor is implicated in dopamine modulation, it is
hypothesized that by activating GABA-B receptors, baclofen causes downstream
effects in the mesolimbic system that reduce the rewarding effects of alcohol [35].
Baclofen’s muscle relaxant and other GABAergic properties likely help with physi-
ologic aspects of prolonged withdrawal.

7.6.3.3 Dose Range

30–80 mg/day in divided doses, typically titrated slowly from a low starting dose
(5 mg TID) to prevent adverse effects and assess patient’s tolerance and response
with each dose increase.

7.6.3.4 Potential Side Effects

CNS effects (drowsiness, dizziness, confusion, slurred speech), nausea, vomiting,
headache, and hypotonia are common adverse effects [33].
Abrupt withdrawal of baclofen has been associated with altered mental status,
muscle rigidity, tachycardia, fever, insomnia, confusion, psychosis, and agitation
[36, 37].

7.6.3.5 Contraindications and Other Considerations

As baclofen is excreted primarily unchanged by the kidneys, checking baseline kid-
ney function and monitoring throughout treatment is advised. Given the high likeli-
hood of CNS effects and its propensity to cause altered mental status and, rarely,
psychosis if withdrawn abruptly, it should be used cautiously in older people and
those with a history of severe mental illness.
86 E. Makovkina

7.7 Novel and Emerging Therapeutics

7.7.1 Phosphodiesterase Inhibitors

7.7.1.1 Therapeutic Effects

There are ongoing studies exploring cyclic nucleotide phosphodiesterase (PDE)
inhibitors as potential therapeutic targets for AUD. This group of agents was first
implicated in the neurobiology of alcohol and nicotine addiction through genetic-­
wide association studies [38]. Preclinical studies have shown decreased alcohol-­
seeking behavior in rats treated with a selective PDE-4 inhibitor, rolipram [39]. A
recent study also showed decreased alcohol intake and binge-like behavior in mice
with alcohol dependence when treated with apremilast, a PDE-4 inhibitor that is
already FDA-approved for Behçet disease, psoriasis, and psoriatic arthritis [40].

7.7.1.2 Mechanism of Action

PDE-4 is an enzyme that catalyzes the breakdown of cyclic AMP (cAMP), thereby
playing a role in regulating intracellular levels of cAMP, a signaling molecule
involved in various cellular processes [41]. Preclinical studies link PDE-4 to neuro-
nal activation in the nucleus accumbens (NAc), a key brain region in the reward
pathway implicated in addictions [40]. Clinical trials are necessary to evaluate the
safety and efficacy of these potential medications.

7.7.2 5-HT3 Receptor Antagonists

7.7.2.1 Therapeutic Effects

There are four 5-HT3 receptor antagonists currently approved in the United States:
ondansetron, granisetron, dolasetron, and palonosetron. The main indication of this
class of medications is the prevention of chemotherapy-induced nausea and vomit-
ing. Serotonergic medications have been investigated for the treatment of AUD
because preclinical studies have shown that serotonin signaling is implicated in the
rewarding, addictive aspects of alcohol use [42]. Prior studies have shown that dif-
ferent drug mechanisms acting on serotonin signaling have produced different ther-
apeutic effects in two subtypes of AUD. SSRIs, for example, may be helpful for
people with late-onset alcoholism and comorbid depression, while the 5-HT3 antag-
onist ondansetron has shown promise for people with early-onset alcoholism [43].
This differential therapeutic response is thought to be linked to polymorphisms in
the genes encoding the serotonin transporter (5-HTT) protein and certain serotonin
receptor subunits (HTR3A and HTR3B) [44, 45].
A randomized trial of 283 participants showed that people with the LL homozy-
gous genotype in a promoter region of the gene encoding 5-HTT drank less on aver-
age and had a higher percentage of days abstinent in response to low-dose
ondansetron (4 μg/kg twice daily) compared to the other two genotype groups [45].
A later study with a naturalistic design confirmed this differential treatment response
to low-dose ondansetron based on genotype [46]; however a more recent
7 Pharmacotherapies for Alcohol Use Disorder 87

randomized controlled study failed to replicate a therapeutic response in partici-

pants stratified by ondansetron-responsive and ondansetron-nonresponsive geno-
types in the genes encoding 5-HT3R and 5-HTT [47]. Nevertheless, the existing
data on ondansetron response based on genotype supports further investigation and
a personalized pharmacogenetic approach to AUD treatment.

7.7.2.2 Mechanism of Action

Ondansetron is the most commonly studied 5-HT3 receptor antagonist for the treat-
ment of AUD. It acts as a selective antagonist at the 5-HT3 receptor in both the
central and peripheral nervous systems. Blockade of the 5-HT3 receptor is thought
to be helpful in people with certain polymorphisms in the 5-HTT gene promotor
region because they have a relative hyposerotonergic state due to upregulation of
postsynaptic 5-HT receptors [45].

7.7.3 Psychedelic Drugs

7.7.3.1 Therapeutic Effects

The group of classic psychedelics, also referred to as serotonergic hallucinogens,
includes ayahuasca, DMT, lysergic acid diethylamide (LSD), mescaline, and psilo-
cybin [48]. Historically, psychedelics were first studied in the context of AUD in the
1950s–1970s, during the “psychedelic era.” Research into the clinical benefits of
psychedelics was quiescent until a resurgence of interest in the last decade. There
are many ongoing trials looking into the clinical benefit of psychedelics, though
none are yet FDA-approved treatments.
The studies investigating psychedelic drugs for alcohol dependence appear
promising. A double-blinded randomized trial of 93 participants, published in 2022,
showed a decrease in the study group who received both manualized psychotherapy
and 2 days of psilocybin compared to an active placebo, diphenhydramine [49]. The
psilocybin study group achieved a significantly lower percentage of heavy drinking
days during the 32-week follow-up period [49].
A meta-analysis of 6 randomized controlled trials, examining a total of 536
pooled participants across the 6 studies, identified statistically significant odds of
LSD being beneficial for decreasing alcohol use [50]. Although the results are
promising, the sample sizes in existing trials are limited, and there is more research
on tolerability and safety to be done before psychedelics becomes a widely accepted
treatment.

7.7.3.2 Mechanism of Action

Most psychedelics act on the serotonin 2A receptors (5-HT 2A) in the brain [48];
however the exact mechanism in relation to alcohol use disorder is unknown. The
potential side effects of the serotonergic hallucinogens are hypertension, severe
anxiety, or psychosis [49]. Given their hallucinogenic properties, the risk of worsen-
ing psychosis in people with unstable, primary psychosis would likely outweigh the
benefit of using a psychedelic drug for AUD, but this risk remains to be studied.
88 E. Makovkina

7.8 Conclusion

Supporting individuals in recovery from alcohol use disorder (AUD) through phar-
macological interventions remains a critical, yet underutilized, approach despite the
availability of effective FDA-approved medications. This chapter has summarized
the therapeutic effects, mechanisms of action, side effects, and other considerations
for using these FDA-approved treatments clinically, underscoring each medica-
tion’s role in preventing and mitigating setbacks for individuals in recovery.
Integrating pharmacotherapy with a multifaceted approach of psychotherapeutic
and psychosocial interventions remains as important as ever for a disorder that has
far-reaching impact on an individual’s social, professional, cognitive, and physio-
logic capacities.
The exploration of novel therapeutics and off-label agents holds promise for
expanding treatments for AUD. Emerging evidence for the efficacy of these off-­
label treatments, alongside potential future candidates like PDE inhibitors, 5-HT3
receptor antagonists, and certain hallucinogens, reflects a growing understanding of
the neurobiological underpinnings of AUD and new approaches to address them. As
research continues to evolve, these developments could lead to more personalized
and effective treatment strategies for individuals suffering from AUD.

Clinical scenario Answer and discussion

You are asked to assist in the treatment of a Acamprosate is the most appropriate
hospitalized patient with AUD and recommendation due to active liver dysfunction.
fulminant liver failure secondary to Acamprosate is not metabolized by the liver and
alcoholic hepatitis. The patient has is renally cleared as unchanged drug. Given this
significantly elevated liver transaminases patient’s intact kidney function, they should be
and evidence of hepatic dysfunction. Renal prescribed the full dose, 666 mg PO three times a
function is normal. Comorbidities include day. Naltrexone is contraindicated here due to
hypertension and CAD with history of stent recent hepatitis and liver dysfunction. Disulfiram
placement. The patient achieves is not an ideal choice due to history of clinically
detoxification from alcohol in the hospital significant CAD, but could be considered after
over the course of 1 week and they are hospitalization depending on psychosocial
motivated to maintain abstinence from factors, reliability, and motivation for abstinence
alcohol
Which medication for AUD would you
recommend starting while the patient is
hospitalized?
A patient with AUD presents for evaluation Depending on the degree of kidney impairment,
to your outpatient clinic. They have a gabapentin could be used at a reduced dose to
history of type 2 diabetes complicated by address both the neuropathic pain and help with
mild kidney disease and sciatica requiring recovery from alcohol. Acamprosate could also
opioids for pain relief as needed. Hepatic be used, at a reduced dose if necessary depending
function is normal. They recently stopped on kidney function. Naltrexone is contraindicated
drinking, would like to maintain abstinence due to ongoing opioid use
from alcohol, and are seeking a medication
to assist them in reaching this goal
Which medication(s) would you
recommend?
7 Pharmacotherapies for Alcohol Use Disorder 89

Clinical scenario Answer and discussion

A patient with alcohol dependence and Naltrexone is the best choice given the patient’s
frequent binge drinking presents to your goal of reducing their alcohol intake and pattern
clinic for evaluation of low mood and of binge drinking. Disulfiram and acamprosate
episodes of aggressive behavior when would be less helpful here given the patient is not
intoxicated. They are considering reducing interested in abstinence at this time. Since the
their alcohol intake and would like to try patient plans to continue drinking, other
drinking alcohol in moderation. They have medications like gabapentin or baclofen may
no medical comorbidities; liver and kidney compound the CNS effects of alcohol (sedation,
function are normal dizziness) so are less likely to be helpful
Which medication would you recommend?

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Behavioral Therapies for Alcohol Use
Disorder 8
Katherine Pruzan

8.1 Introduction

Several years ago, I returned to my graduate school for an alumni panel on career
trajectories post-graduation. I spent my portion of the panel discussing how reward-
ing and interesting my clinical work is, with my practice primarily focused on help-
ing individuals who are considering changing their relationship with substances.
After the panel, a former professor approached, asked me when I would leave my
current position, and reflected on how burned out I must have been working with
“that population.” As helping professionals, we’re not immune to the internalization
of societal stigma and can activate stigma and shame through explicit messaging as
my former professor shared, as well as through more implicit cues we might send to
our clients. Indeed, research has suggested that individuals who have had more
encounters with the substance use treatment system experience higher levels of
stigma-related rejection [1, 2]. Additionally, practitioners across a range of health-
care settings have negative attitudes toward people with substance misuse issues,
with behavioral healthcare workers in the substance use treatment field typically
reporting fewer negative attitudes [3].
Some of this stigma from the treatment field may be related to a relative lack of
familiarity with substance use treatment due to a lack of learning opportunities dur-
ing graduate studies [4, 5]. There are a number of efficacious approaches available
for treating alcohol use issues, all of which rely on learning principles. Some
approaches, such as Relapse Prevention, were developed specifically for substance
use issues [6], while others, such as Dialectical Behavior Therapy, have been
adapted from their original focus to work with substance use issues [7]. They align
in a foundation of building an understanding of the pathways leading to and main-
taining problematic substance use for the individual client and differ in focus on

K. Pruzan (*)
The Center for Motivation and Change, New York, NY, USA
e-mail: [email protected]

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2024 93

M. Khan, J. Avery (eds.), From Stigma to Support, Psychiatry Update 4,
https://doi.org/10.1007/978-3-031-73553-0_8
94 K. Pruzan

ways the client and provider can work together to forge a different pathway. This
chapter provides an overview of several evidence-based approaches for working
with individuals with alcohol use issues.

8.2 Motivational Interviewing

Motivational Interviewing (MI) is a counseling style meant to help resolve an indi-

vidual’s ambivalence about behavioral change and move them toward a commit-
ment to make changes [8]. It does this by eliciting the individual’s own reasons for
making changes and explicitly avoiding situations where the clinician is advocating
for change. MI outlines four tasks: engaging, focusing, evoking, and planning.
During these tasks, the clinician builds rapport through a collaborative, autonomy-­
reinforcing relationship with the client (engaging), helps focus the goals of the work
together by identifying changes the client is considering (focusing), elicits from the
client their own reasons for making a change (evoking), and then provides guidance
as needed for how the client might achieve those changes (planning). MI outlines
four core skills utilized for this work, using the acronym OARS: open-ended ques-
tions, affirmations, reflections, and summary statements. The clinician uses these
types of verbalizations to highlight and further explore client change talk.
Since its development, MI has been consistently found to be significantly better
than no intervention and equally as effective as other psychosocial interventions for
substance use issues during the intervention as well as at short- and middle-term
follow-ups (see, e.g., [9]). It is effective in reducing substance use issues in adoles-
cents [10], and there is evidence that it is particularly effective as an approach with
minority populations [11].
MI can be utilized as a means of enhancing motivation in preparation for a more
skills-based intervention, during various points of treatment to increase and main-
tain motivation, or as a standalone intervention. Since it is set up to elicit from the
individual their own reasons for making change and is guided by a non-judgmental,
accepting, and collaborative stance, MI is a counseling style that is highly consistent
with the goals of combatting individual shame and societal stigma related to sub-
stance misuse.

8.3 Cognitive-Behavioral Approaches

8.3.1 Relapse Prevention

Cognitive-behavioral approaches represent a second wave of treatment options

developed within the behavioral school of treatment [12]. These approaches high-
light the role of cognitions and recognize the interplay between the world of thoughts
and reinforcement principles in shaping and sustaining behaviors. Marlatt [13]
sought to apply this theory to substance use issues, specifically focusing on a stance
that would be non-shaming and non-catastrophizing of slips through what he would
8 Behavioral Therapies for Alcohol Use Disorder 95

term a Relapse Prevention (RP) model. The substance abuse treatment world had,
up to this point, focused on the physiological impact of substances as rendering the
individual incapable of controlling themselves [6]. Interwoven with this was a moral
model that viewed those with substance use issues as lacking willpower or having
another characterological shortcoming. While this more biologically oriented dis-
ease model was less judgmental of the individual, it included a stance on the need
for total abstinence and constant vigilance against the possibility of any slips, view-
ing those as inevitably leading back to uncontrollable use.
Marlatt [13] worked to create the middle-ground concept of “lapse” as a brief
instance of reintroduction of a substance that can be coped with and contained
before it becomes an ongoing relapse. He studied and understood relapses within a
social learning framework and worked to identify the precursors to relapses as well
as the positive and negative consequences of them. This specifically identified indi-
viduals as separate from their behaviors and created the framework for understand-
ing substance misuse as making sense within a learning and reinforcement context.
Marlatt and colleagues then worked to develop an understanding of the types of
situations that were likely to lead to an initial lapse [13] as well as a treatment
approach that could be used to “cope ahead” of and in the moment with high-risk
scenarios, as well as lapses themselves [6].
Substance misuse is seen as an overlearned and maladaptive response to cues
from the internal and/or external environment [6]. RP identifies the individual as
having the ability to learn and implement healthier responses, thus providing a path
forward that both acknowledges the individual’s role in implementing change while
also identifying building mastery over slips as a non-shameful step in that process.
Relapse is viewed as a process, beginning before the first use with factors that
may or may not seem obviously tied to the likelihood of future lapse [14]. More
distal antecedents may precede a lapse, with a more covert tie-in to the lapse.
Proximal antecedents to the lapse are more immediately related, both in time and
directness. The relapse process then continues post-use, with the possibility of posi-
tive reinforcement in the short term, along with a decreased sense of self-efficacy
for meeting one’s substance use goals. Lower self-efficacy of the ability to cope,
along with an expectation of a positive outcome of substance use, is predicted to
increase the likelihood of a lapse [15]. The RP program thus aims to build aware-
ness of distal and proximal triggers, teach coping skills for them, and increase self-­
efficacy through successive efforts to cope differently with high-risk situations,
along with working to contain lapses if they happen [15].
The RP school also introduced the concept of the Abstinence Violation Effect
(AVE; [15]), hypothesized to lead to an increased likelihood that a slip will lead to
a full-blown relapse. AVE indicates that cognitive processes, such as attributions
about the reasons for a slip and emotional reactions to a slip, have the potential
impact of accelerating the pathway from slip to full relapse. AVE factors tend to
align with a belief in a disease model of addiction, namely, that attributions for a slip
are identified as internal to the person, stable, global, and largely uncontrollable.
Adherence to the disease model as an explanation for substance misuse has been
found to add to the power of the Relapse Prevention model for predicting lapses [16].
96 K. Pruzan

Treatment within a relapse prevention model starts with an assessment that iden-
tifies the various antecedents, or triggers, likely to lead to substance use [6]. Once
high-risk situations are identified, the therapist works to help the client more finely
tune their radar to these warning signals and build skills to more effectively cope
with them when they arise, as outlined in Table 8.1. RP has been assessed to be
effective in reducing substance use [17], particularly alcohol use [18].

8.3.2 Community Reinforcement Approach

The Community Reinforcement Approach (CRA) is a cognitive behavioral inter-

vention that draws heavily on operant reinforcement principles [19]. It was devel-
oped by Hunt and Azrin [20], initially for inpatient clients with alcohol use issues,
and outperformed 12-step based treatment as usual in those settings when looking
at drinking outcomes. It has since been found effective in treating outpatient clients
with alcohol issues [21] and unhoused clients with alcohol issues [22]. It has also
been found effective for individuals with cocaine use [23] and opiate use issues
[24], particularly when combined with contingency management techniques. It has
also been adapted to work with adolescents, with positive outcomes [25] and across
races and genders of adolescent clients [26].
CRA is a structured but highly flexible approach that recognizes that the indi-
vidual’s environment, or the community around them, has the capacity to reinforce
behaviors that compete with substance use [27]. A number of structured sessions
exist within CRA, but not all sessions will be utilized with each client. The clinician
has latitude to pick and choose based on an individual client’s needs, with just a few

Table 8.1 Relapse prevention skills and techniques [6, 14]

• Psychoeducation: Provide psychoeducation to counteract any misconceptions about the
impact of substances
• Enhancing self-efficacy: “Chunk” behavior changes into more manageable pieces,
acknowledging areas of mastery of new skills
• Lapse management strategies: Cope ahead/plan for future lapses so they are contained,
including leaving the lapse situation, deciding ahead who to reach out to for help, and other
coping skills that could be used
• Cognitive restructuring: Help clients change their attributions about lapses to ones that are
more realistic and provide clients with a road map for moving forward
• Lifestyle changes: Help increase engagement in competing, positive behaviors, provide
balance of “shoulds vs wants” in a client’s life, and teach skills in related areas such as
relaxation training and time management techniques
• Stimulus control techniques: Eliminate or reduce exposure to frequently triggering
situations
• Urge management techniques: Teach clients to predict high-risk situations, accept urges as a
normal part of the process, build awareness of urges as a conditioned response to a substance-­
related stimulus, teach urge-surfing to ride out those urges rather than interrupt them with use
• Relapse road map: The above techniques are combined to create a map of high-risk
situations and potential alternative responses so that clients have a plan for each stage of the
potential relapse timeline
8 Behavioral Therapies for Alcohol Use Disorder 97

sessions being required as parts of the protocol. CRA allows for flexibility of goals
related to substances, not requiring abstinence as a target [19] due to the belief that
positive outcomes can occur at any level of decreased substance use and increased
engagement with other prosocial behaviors. This non-shaming, motivationally
based stance helps invite individuals into treatment to work toward increased health
and prosocial engagement. CRA guides the individual in identifying behaviors that
compete with substance use and will be reinforcing to the person. It offers skills
development in a number of life areas, such as career exploration, to further increase
the likelihood that the individual will receive environmental reinforcement for non-­
using behaviors.
At the core of CRA are Functional Analyses of the individual’s use and prosocial
behaviors [27]. For the Functional Analysis of Use, the clinician and client together
identify the behavioral markers of use, such as time of day, quantity, and length of
time typically spent in using behavior. They explore internal and external triggers
preceding use and then move on to discuss positive and negative consequences asso-
ciated with use. This exercise provides a road map for understanding life areas
where skills are needed, what kinds of reinforcers might motivate the client toward
healthier behaviors, and how the environment might be enlisted to support this. For
example, an individual might identify drinking as occurring following isolation and
feelings of loneliness and notes that in the short term, these feelings subside, while
in the longer term, the person feels guilty for neglecting existing relationships when
drinking and recognizes that this leads to increased feelings of loneliness. This pro-
vides a road map to focus on increasing time spent with others. The means to follow
this “road map” are developed through the components of CRA, as seen in Table 8.2.

Table 8.2 Skill areas of the community reinforcement approach [27]

• Communication: Help clients communicate in clear, positive ways that are more likely to
receive reinforcement from those around them
• Problem solving: Teach clients how to define and brainstorm around a problem, engage in a
potential solution, and then assess efficacy. This conveys a sense of curiosity as well as a
non-shaming stance that some efforts might later be viewed as not worth continuing
• Substance refusal skills: Teach clients strategies for refusing drinks or substances when
offered, in ways that will promote respect for the clients’ boundaries
• Job/career: Work with clients on job hunting, resume writing, and interviewing skills. Some
versions of CRA have offered a drop-in job hunting group
• Social/recreational engagement: Help identify and engage in opportunities for socially and
recreationally positive experiences. Some implementations of CRA have included a drop-in
social club to encourage sober, prosocial engagements
• Relationship therapy: CRA recognizes a romantic partner as a source of potential positive
reinforcers to encourage reductions in use. These relationships may also be stressed due to past
use. Relationship therapy uses a modified Happiness Scale to identify life areas to address with
the couple to build positivity between them and increase communication and collaborative
problem solving
• Relapse prevention: Develop skills to cope ahead for high-risk situations and contain lapses
if they occur
• Monitored disulfiram: CRA has included monitored disulfiram, particularly when there is a
concerned significant other in the client’s life to act as a caring monitor. Skills are taught to
help this monitoring process be smooth and collaborative, rather than shaming
98 K. Pruzan

The Functional Analysis of Pro-Social Behavior is similarly set up but explores the
antecedents and consequences of a pro-social behavior that competes with sub-
stance use. This is meant to identify ways to increase engagement in this behavior.
Clinicians working within a CRA framework typically suggest a period of
“sobriety sampling” to clients [27]. This is a period of abstinence from substance
use, recognizing that committing to long-term abstinence may be daunting. CRA
approaches sobriety sampling as a motivational tool that provides the opportunity to
collaborate around the length of sobriety sampling. It is meant to help the client
experience positive reinforcers they can access without substances in the picture,
and they can then use this to assess their longer-term goals related to the substance.
CRA also utilizes a Happiness Scale, or Likert scale gauging happiness in sev-
eral life areas, to identify components of life where the client would like to make
some gains [27]. This includes areas such as finances and social life, for example.
The Happiness Scale results, along with information gleaned from the Functional
Analyses, provide information for the client and therapist to collaborate around
goals for both substance use and other life areas. CRA then provides skills training
in the areas that are relevant to the client, as outlined in Table 8.2.
Although somewhat outside the scope of this chapter, CRA has been extended
for work with family members of treatment-refusing substance users, an approach
called Community Reinforcement and Family Training (CRAFT; [28]). CRAFT
teaches concerned significant others (CSOs) skills to help their loved one experi-
ence a different set of reinforcers for non-use behaviors as compared with use
behaviors, with the goal of motivating substance users to seek treatment. There are
areas of skill overlap with the CRA approach, including communication and
problem-­solving skill training. CRAFT has been found to compare favorably to
both Johnson Institute Interventions and 12-step based family work [29]. Families
using the CRAFT approach are able to engage their loved one in treatment at rates
ranging from approximately 65% to 75% depending on the study [28]. Like CRA,
CRAFT is grounded in an MI-informed, non-shaming, non-confrontational stance
toward the substance user.

8.3.3 Contingency Management

Contingency Management (CM) also utilizes operant conditioning to increase rein-

forcement for abstinence. In contrast to CRA, which relies on changing social and
environmental reinforcers, CM focuses on providing tangible, material rewards that
are built into the treatment program itself. These rewards are tied to objective mea-
sures of abstinence. CM principles require that abstinence can be reliably detected.
Reinforcers are provided when abstinence is documented and withheld when use is
detected [30]. For CM to be optimally effective, reinforcers should be presented
immediately following verification of abstinence and occur frequently within the
course of treatment. There is also evidence that escalation of reinforcers, or increas-
ingly higher amounts for longer periods of abstinence, can increase effectiveness of
CM [31, 32]. Reinforcement typically takes the form of monetary rewards, vouchers
8 Behavioral Therapies for Alcohol Use Disorder 99

that can be used to obtain items, a grab bag set-up where clients draw from a bowl
that contains a number of reinforcements, or treatment-related changes with posi-
tive salience, such as more days of medication to take home at once.
CM is efficacious in retaining clients in treatment (see, e.g., [30, 33]) and increas-
ing abstinence during treatment for clients with both drug use [34, 35] and alcohol
use [30] issues and has been associated with decreased substance use in adults with
serious mental illness [36]. It has also been shown to be associated with increased
rates of longer-term abstinence when paired with CBT-based treatment [33, 34]. An
important critique of CM from research findings is that the effects of CM alone
appear to wane over time once the period of reinforcement ends [37].
CM is not nearly as widely utilized as would be expected by its effectiveness.
CM is hindered by concerns about costs for reinforcers, efforts required of pro-
grams to organize and maintain abstinence verification and reinforcers, and societal
stigma that questions the idea of providing reinforcers for abstinence [38]. There are
workarounds for the first two hurdles. Prizes can be used as reinforcers, and grab
bag set-ups have been found to be effective [30]. Grab bags or vouchers can be
implemented with prizes at a variety of price points, as well as sourced from com-
munity donations [38]. There is also evidence suggesting that changing from con-
sistent reinforcement to an intermittent reinforcement schedule later in treatment
can still be effective for encouraging continued abstinence [33]. Systems can be
streamlined and built into existing community treatment structures to minimize
additional costs associated with staff time. Smartphone-based platforms have been
utilized to automate much of the process of verified toxicology testing and provision
of reinforcers [39].
In the more recent treatment and research context of greater consideration of
non-abstinence based and/or harm reduction approaches, it is also worth consider-
ing some of the challenges posed by attempting to set up an easy, verifiable, real-­
world CM treatment where reinforcers could be offered for moderation or reductions
in use. Since CM requires verification of changes to substance use, it would be
onerous under current toxicology options to reliably measure reductions to use
rather than abstinence.

8.3.4 Guided Self-Change

The Guided Self-Change (GSC) approach was developed by Sobell and Sobell [40]
as a blend of Motivational Interviewing and cognitive-behavioral approaches,
guided by the recognition that many problem drinkers have less intensive problems
with alcohol and may be better served by less intensive interventions. This approach
incorporates building self-efficacy and providing choice of goals to the client, with
the belief that these would increase client motivation to engage in a change process
[41]. This is informed by the awareness that one size doesn’t fit all and provides the
option of low-risk drinking and harm reduction as options for clients to pursue. This
can help lower the stigma attached to seeking help and encourage those contemplat-
ing their substance use to begin an exploratory change process. While originally
100 K. Pruzan

Table 8.3 Guided self-­change session content [41]

• Session 1:
   – Personalized feedback from TLFB, discussion of self-­monitoring logs
   – Evaluate client goals: Abstinence or low-risk drinking
   – Decisional balance exercise: Pros/cons of drinking
• Session 2:
   – Review self-monitoring log
   – Identify triggers
   – Discuss high-risk situations and confidence navigating them
• Session 3:
   – Review self-monitoring log
   – Discuss new strategies for high risk situations
• Session 4:
   – Review self-monitoring log
   – Personalized feedback about changes during treatment
   – Revisit goals and decisional balance exercise

developed for problem drinkers [40], it has since been extended for use with clients
with non-severe drug use issues [42, 43]. Studies have found it to be positively
impactful post-treatment on both proportion of days abstinent and as average drinks
on drinking days (see, e.g., [42]).
GSC is set up as four semi-structured sessions and can be delivered in group or
individual formats [41]. The assessment session includes a Timeline Follow Back
(TLFB) which is a self-report in calendar format of an individual’s substance use in
the period prior to treatment engagement [44]. Information from this tool is utilized
to provide personalized feedback about a client’s substance use to help clients iden-
tify change goals [41]. Clients complete logs of their use over the course of treat-
ment, including urges to use and the settings where use and urges occur. This
provides assessment points for change as well as increased awareness of risky situ-
ations and emotions. Sessions proceed as outlined in Table 8.3.

8.4 Dialectical Behavior Therapy

Dialectical Behavior Therapy (DBT) was originally developed to treat clients pre-
senting with chronic suicidality and self-injury [45]. Dialectics refer to two seem-
ingly opposing ideas that can be true at the same time [45]. This includes ideas such
as radical acceptance of the individual’s current state of being while also holding
true and important the hope for making changes to improve one’s life. DBT empha-
sizes a broad goal of building a life worth living, as well as more targeted goals
related to reducing problematic and self-harming behaviors [7]. It is grounded in the
idea that individuals can experience emotions as overwhelming and may engage in
maladaptive coping strategies in an effort to avoid these painful experiences [7].
DBT focuses on mindfulness, distress tolerance, and emotion regulation skills to
decrease impulsive behaviors that are driven by these intense emotions, as well as
interpersonal effectiveness skills to help them access more reinforcing social inter-
actions [45]. DBT is also specifically focused on a non-shaming, non-judgmental
8 Behavioral Therapies for Alcohol Use Disorder 101

stance toward individuals experiencing intense life difficulties, as it recognizes that

such individuals have a history of invalidation of their experiences by the people
and systems they’ve encountered [45]. This is particularly aligned with the increas-
ing awareness in the SUD treatment world that shame-based approaches and socio-
cultural stigma about addiction disincentivize people from seeking help.
DBT is well-positioned to help address substance use issues, given both a high
degree of co-occurrence of borderline personality disorder and substance use [46],
as well as the understanding that substance misuse can arise from emotion-based
impulsivity [47] and other difficulties with emotion regulation (DER; see, e.g., [48,
49]). Research findings have supported the use of DBT to address substance use
issues, both in populations with [50] and without (see, e.g., [51–53]) borderline
personality disorder. The research literature on DBT for substance use disorder
(DBT-SA) is, however, limited by a lack of large RCTs and a need for studies com-
paring DBT to other evidence-based interventions for SUD [54]. Despite this, pre-
liminary evidence across a variety of settings and studies indicates that DBT can be
an effective treatment for SUD [54].
The positive impact of DBT is partially based on improvements to emotion regu-
lation following DBT treatment [54]. This is achieved through skills training that
addresses emotion dysregulation and its impact on impulsive decisions, such as
using substances that function to help cope with and avoid emotions [51]. Negative
urgency, or acting rashly in response to negative emotions [55], is particularly asso-
ciated with poor treatment outcomes for SUDs [56]. Mindfulness, emotion regula-
tion, and distress tolerance skills taught in DBT help individuals sit with and more
healthily cope with intense emotions. Healthier coping also affords individuals a
greater opportunity for positive reinforcement from individuals and systems around
them, further increasing the likelihood of future positive experiences and emotions
and creating a positive feedback loop for the individual [45].
Standard, treatment adherent DBT as originally outlined by Linehan [45] for the
treatment of those with chronic suicidality or self-injury is comprised of five treat-
ment components: weekly individual therapy with a DBT provider, weekly DBT
skills training group (DBT-ST), availability of 24-h phone consultation with a DBT
therapist, case management, and a consultation team meant to support the therapist
[57]. Since the positive impact of DBT on stand-alone SUD appears to be within the
realm of acquisition of self-regulation skills [52], multiple studies have looked at
the DBT skills group (DBT-ST) alone as a treatment for SUD (see, e.g., [51, 52])
with positive results. Table 8.4 outlines DBT-ST to address alcohol use issues.
Dialectical abstinence is one of the key constructs in DBT for substance misuse
[7]. It requires that the therapist ask the client to immediately stop substance use and
maintain a goal of abstinence (the change component of the dialectic) while also
validating the possibility that lapses can occur and don’t mean that the therapeutic
work is ineffective (the acceptance component of the dialectic; [46]). This stance is
based in the DBT belief that substance use interferes with an individual’s ability to
build a life worth living and acquire skills to more effectively cope with emotion
dysregulation. Dialectical abstinence can feel in opposition to other evidence-based
understandings of substance misuse if nuance isn’t well-conveyed by the therapist,
102 K. Pruzan

Table 8.4 DBT-ST for alcohol use issues, session breakdown ([52], p. 6)
• Sessions 1–2: Dialectical abstinence
• Sessions 3–6: Path to “clear mind”
• Sessions 7–18: Mindfulness skill building
• Sessions 19–24: Distress tolerance skill building
• Sessions 25–36: Emotion regulation skill building

since there is evidence that many individuals can make significant health gains with-
out maintaining complete abstinence from alcohol [41].
Additionally, DBT-SA utilizes some language that could be viewed as aligned
with a more shaming stance toward substance use issues, particularly the use of the
constructs “addict mind,” defined as a mental state focused on and influenced by
substance use, and “clean mind,” the state of being abstinent from substances and
feeling like future substance difficulties are not possible ([7], pp. 42). DBT uses
these terms to come to the concept of “clear mind,” which is abstinence while also
maintaining awareness of and vigilance against future substance use and issues. The
terms “clean” and “addict” run the risk of triggering internalized stigma and feel-
ings of shame and are among terms recognized as potentially perpetuating stigma
[58]. While DBT utilizes these terms to provide contrast and clarify the “clear
mind” construct, it is important to remember that providers of evidence-­based
approaches as well as their clients come to the room with their own biases and inter-
nalized societal stigmas and the language used by a treatment approach has the
possibility of activating these biases.

8.5 Mindfulness-Based Interventions

8.5.1 Mindfulness-Based Relapse Prevention

Marlatt and Gordon [6] set the stage for future mindfulness-based interventions for
substance use issues with the addition of Urge Surfing in Relapse Prevention, as a
coping strategy for cravings. This early prelude touches on the core components of
mindfulness as applied to behavioral health, including increased awareness of the
present moment while cultivating a non-judgmental stance toward whatever
thoughts, feelings, and sensations arise [59]. This early work was later formalized
into Mindfulness-Based Relapse Prevention (MBRP; [60]) which, along with DBT
and Acceptance and Commitment Therapy (ACT), comprises the third-wave CBT
treatments used with substance use issues. MBRP has been associated with fewer
heavy drinking days post-treatment than traditional CBT-based treatment [61, 62],
improvements in mood and anxiety in substance abusing populations [63], and
increased perceived self-efficacy related to substance abuse goals [64].
The mechanisms through which MBRP achieves these gains are still under
investigation. There have been consistent findings for the bottom-up benefits of
mindfulness, such that increased mindfulness helps reduce reactivity to craving-­
related cues [62, 65] as opposed to a top-down mechanism of action where increased
8 Behavioral Therapies for Alcohol Use Disorder 103

mindfulness would lead to more ability to exert conscious control over one’s behav-
iors and impulses. Consistent evidence has been found for gains in the sub-construct
Acting with Awareness as predicting reductions in drinking-related problems
[66–68]. Evidence related to the sub-construct of Non-Judgment has been mixed,
with some studies finding increases in Non-Judgment as associated with decreases
in problematic substance use [68] and lessening of the impact of cravings [65],
while other studies have found mixed results including variability of association by
substance [66] and Non-Judgment as a significant positive predictor of drinking-­
related problems [67].
MBRP strives to set up a treatment that is “inclusive, just, and nonpunitive” in its
approach to working with individuals with substance use disorders ([60], p. 7). It is
therefore explicitly aligned with a destigmatizing, non-shaming stance. MBRP is
set up as an eight-session group treatment, ideally run by two co-facilitators who
both have their own daily mindfulness practice. It aims to increase awareness of
body, thoughts, and behaviors; identify and interrupt automatic behaviors to increase
behavioral choice; cultivate an attitude of curiosity, openness, and acceptance
toward discomfort; and increase compassion toward self [60]. Daily practice by
group members is encouraged. Sessions cover the content outlined in Table 8.5.

8.5.2 Acceptance and Commitment Therapy

Acceptance and Commitment Therapy (ACT) is a third-wave behavioral treatment

grounded in mindfulness, with the goals of creating a robust life while accepting the
pain that happens along the way [69]. ACT is based on Relational Frame Theory
(RFT; [70]) and views human cognitions as a type of learned behavior, with the
degree to which individuals get stuck on particular thoughts as the point of interven-
tion, rather than challenging the thoughts themselves [12]. ACT believes that
becoming unstuck from thoughts (including learned self-narratives) helps to engage
in behaviors leading to a more robust life. It does this by helping the individual be
willing to engage in the full range of human emotional experiences, without feeling
pulled into experiential avoidance, or the desire to get rid of uncomfortable thoughts
or feelings [69]. ACT views trying to control or get rid of these uncomfortable inner
experiences as the starting point of an ongoing internal struggle. This struggle is
defined by avoidance of the full range of human experiences and adoption of a more

Table 8.5 MBRP sessions ([60], p 30)

• Automatic pilot and mindful awareness
• A new relationship with discomfort
• From reacting to responding
• Mindfulness in challenging situations
• Acceptance and skillful action
• Seeing thoughts as thoughts
• Supporting and sustaining well-being
• Social support and continuing practice
104 K. Pruzan

Table 8.6 ACT treatment processes [12, 69]

• Cognitive defusion: Learning to unhook from our thoughts, seeing them as pieces of
language rather than imperatives we must follow
• Acceptance: Approaching our inner experiences with an attitude of openness and curiosity,
making room for them without trying to control them
• Contact with the present moment: Being fully present in the moment as one is living it
• Self as context: Cultivating and accessing a more transcendent, observing sense of self that
holds the essence of the individual, rather than the transient thoughts, feelings, and sensations
that are not the core of the person
• Values: Identifying and anchoring behaviors to what is meaningful
• Committed action: Setting goals and engaging in behaviors aligned with one’s values.

rigid, potentially maladaptive set of behaviors to try to control emotions and

thoughts. Substance use and abuse is one way that people try to avoid or control
uncomfortable inner experiences. ACT seeks to address this through six processes,
as outlined in Table 8.6.
ACT addresses experiential avoidance, which is a style that can lead people to
seek out substances to facilitate that avoidance. Studies have found that beliefs
about the need to control thoughts predicted alcohol use at follow-up from a CBT-­
based treatment [71]. ACT has also been found to reduce cravings [72] and feelings
of shame [73, 74] for individuals with substance use issues. ACT-based treatments
have been found to be better than waitlist controls and as effective as other CBT-­
based active treatments [75] in decreasing substance use. ACT also tends to provide
longer-term benefits on broader quality of life measures when compared with other
active treatments. More RCTs are needed, particularly specific to alcohol use disor-
der being treated in outpatient settings to understand differences between treatments.

8.6 Conclusion

A variety of efficacious behavioral treatment options exist for clients with alcohol
use issues. Evidence suggests that all behavioral treatments described in this chapter
lead to reductions in alcohol use. Approaches such as Motivational Interviewing,
Relapse Prevention, and Guided Self-Change were developed for use with clients
with substance use concerns and have been well-researched with these populations.
These treatments heavily focused on teaching clients skills for identifying and cop-
ing with potentially triggering situations, thoughts, and emotions. Third-wave
approaches, such as MBRP, DBT, and ACT, include an emphasis on mindfulness,
acceptance, and non-attachment to intense emotions. Approaches such as DBT and
ACT were developed for different clinical targets and have since been extended to
work with clients with substance use concerns. More research is needed to clarify
the components and mechanisms of these two approaches that lead to improvements
in alcohol use outcomes. A motivation-enhancing therapeutic stance is recom-
mended when engaging in all approaches, whether using MI as a standalone treat-
ment or as a means of augmenting and maintaining engagement in another treatment.
8 Behavioral Therapies for Alcohol Use Disorder 105

All of the described approaches have the potential to help decrease the shame
associated with alcohol use issues through their focus on individualization of treat-
ment and building skills that work for the individual. MBRP, DBT, and ACT have
an explicit focus on non-judgment, though the language used in DBT-SA has the
potential to activate internalized stigma and shame related to substance use.
Practitioners are advised to build awareness of their own biases, implicit or explicit,
when engaging in any of the described treatments.

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Technology-Assisted Treatment
of Alcohol Use Disorder 9
Daniel Cabrera and Mashal Khan

9.1 Introduction

Alcohol use disorder affects 29.5 million people ages 12 and older in the United
States as of 2022, as per data from the National Institutes of Alcohol Abuse and
Alcoholism. Current treatments include psychosocial and pharmacological inter-
ventions, both which have been validated by multiple studies [1, 2]. However, one
limitation to treatment of this potentially fatal illness is access, which is limited to
about 10% of people suffering with AUD [3]. Emerging technologies such as mobile
health applications, web-based platforms, and wearable technology offer a large
opportunity for far-reaching interventions that could improve access to delivery of
care or as adjunct treatment [4]. Additionally, interventions that include neuromod-
ulation can offer additional tools in the treatment of AUD. In this chapter, we focus
on current technological tools specifically for alcohol use disorder (Table 9.1).

9.2 Part 1: Mobile Health Applications

As smart phones become more ubiquitous, there is an increasing number of applica-

tions tailored for health purposes. In the past decade, there has been an increasing
amount of mobile health applications targeting substance use disorder (SUD), and
many of them have evidence that they can assist in the treatment of alcohol use
disorder (AUD) [16]. Kruse et al. describe the current landscape of mobile apps and
break down whether they have been peer reviewed and describe each study, starting
with a study showing that mobile apps can be used in the sensitive period after leav-
ing active treatment for AUD. The authors in the study showed that with a mobile
app called A-CHESS, participants showed sustained participation, paving the way

D. Cabrera (*) · M. Khan

NewYork-Presbyterian-Weill Cornell Medical Center, New York, NY, USA
e-mail: [email protected]

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2024 109
M. Khan, J. Avery (eds.), From Stigma to Support, Psychiatry Update 4,
https://doi.org/10.1007/978-3-031-73553-0_9
110 D. Cabrera and M. Khan

Table 9.1 Summary of technological interventions for AUD

Peer
Technology Type Aim reviewed
ACHESS App Relapse prevention [5]
PEAR reset-O App CBT in conjunction with treatment [6]
CBT4CBT App CBT for SUD [7]
Drinkers’ checkup App Assess readiness for change and identify ([8]
those who can benefit from treatment
Therapeutic App Interactive multimedia modules based on [9]
Education System community reinforcement
Motiv8 Web Smoking cessation using home monitoring [10]
system
AA App/web Meeting schedules, sobriety tracker, and the [11]
Big Book
SMART Web Self-assessment tools with feedback to [12]
resolve ambivalence
Soberlink Hardware Breathalizer feedback for monitoring [13]
Transdermal Alcohol Hardware Perspired alcohol as feedback for intake [14]
Sensor monitoring
FibroScan Ultrasound Imaging to provide feedback on liver [15]
changes related to AUD

for a plethora of new applications to come [5]. Additionally, a large study looking at
the facilitators and barriers of substance use applications using the A-CHESS app
identified key strategies to implement mobile phone interventions in the community
setting [17]. Currently, apps for AUD focus on CBT, gamification, progress track-
ing, in-the-moment support for cravings, and anonymous forums/support groups.
Current mobile apps have diverse purposes and tools; most of them include at
least one of the following: abstinence tracker, which counts abstinence time, often
in days or hours, and this can help with motivation and provide feedback on current
progress toward sobriety. Informative content often will have text, video, or audio
that can teach the science behind addiction and recovery. Peer support is in the form
of public forum or messaging service that prevents isolation and allows connection
to others in the recovery community, e.g., 12-step groups, social networks, etc.
Habit tools are often based on principles from cognitive behavioral therapy (CBT)
with the aim to help build new, healthier habits and change habits associated with
alcohol use. An additional feature is relapse prevention to help manage cravings real
time. Apps will sometimes include a directory, usually listing or showing a map of
local treatment or peer support groups, based on the user’s location.
The current mobile app landscape for AUD includes the only FDA-approved
PEAR reset-O, which is designed to be used in conjunction with traditional treat-
ment [18]. The company behind this app bankrupted and the app was sold to another
company. While only one mobile app has been FDA approved, the National
Institutes on Drug Abuse (NIDA) and the Substance Abuse and Mental Health
Services Administration (SAMHSA) have endorsed the following applications:
CBT4CBT, which uses CBT skills training for SUD and has been validated in mul-
tiple studies [7]. Drinkers’ checkup is a validated, evidence-based, computer-based,
9 Technology-Assisted Treatment of Alcohol Use Disorder 111

brief motivational intervention that assesses alcohol use, alcohol-related problems,

and readiness to change, provides personalized normative feedback, and identifies
those who might benefit from alcohol treatment [8]. Therapeutic Education System
(TES) consists of web-based interactive multimedia modules based on community
reinforcement and has been validated to improve abstinence rate and treatment
adherence [9]. Considering the large comorbidity of nicotine and alcohol use [19],
apps that target nicotine use can also be useful in mitigating alcohol use. Programs
such as MOTIV8 provide a web-based contingency management for smoking ces-
sation that includes support groups and biological verification of breath carbon
monoxide samples, while Project Quit provides aid with smoking cessation.

9.3 Part 2: Online Platforms for AUD

The technologies and services offered via the Internet with the aim of assisting
treatment and recovery broadly focus on one of the following categories: online
mutual aid service, peer recovery services, artificial intelligence-based therapies
and interventions, web-based contingency management models, forums/support
groups/social networks, and multimedia resources. Some of these services will pro-
vide telehealth synchronous services, which provide feedback when the user
engages, versus asynchronous which will give feedback when the provider is
available.
Alcoholics anonymous (AA) 12-step program has an AA meeting guide website
with an accompanying app. This website contains meeting schedules by specific
area and sobriety tracker, and you can read/take notes on the Big Book. Another
web-based resource is Self-Management and Recovery Training (SMART)
Recovery [12]. SMART recovery features alcohol self-assessment tools with feed-
back to resolve ambivalence, a cost-benefit analysis (CBA) tool is one of the princi-
pal skills learned in SMART recovery groups, and this decision-making tool helps
with ambivalence about relapsing. The website also contains cognitive behavioral
and motivational exercises to help people achieve and maintain sobriety and educa-
tional modules on alcohol.
Web-based resources offer benefits of peer engagement, such as diversity of
available support groups or 12-step meetings, convenience of remote access, 24/7
access to peers through social media platforms, increased anonymity, opportunity to
globally expand social network of recovery-oriented peers, and decreased percep-
tions of stigma. On the other hand, the limitations include but are not limited to
perception of social disconnectedness on virtual platforms, inequity in access to
technology, and fatigue associated with excessive videoconferencing.
With the advent of machine learning (ML) and artificial intelligence (AI), the
possibility of gaining new insights from large amounts of data has become more
attainable. These new tools have also proven to be useful in the treatment of AUD. In
a recent review, the authors show how using ML you can integrate multiple inputs
such as brain imaging, behavior assessment tools, memory-based activities, and
clinical data to better understand the complexity of SUD [20]. In addition to
112 D. Cabrera and M. Khan

providing better understanding, ML and AI can be used to predict relapse and harm-
ful alcohol use after liver transplant [21, 22]. Interestingly, to fill in a health gap by
training AI to develop a chatbot that can use personalized data to provide recovery
consultation in alcohol users, authors found promising data from a pilot study point-
ing to the usefulness of this technology in the treatment of AUD [23]. The studies
mentioned above open the option of having AI-based “therapist” that can not only
predict relapse but also provide treatment that is personalized and targeted for the
user’s specific needs.

9.4 Part 3: Hardware

As wearable technologies and different gadgets have become mainstream, a grow-

ing number of people use these products for health and wellness purposes [24].
One of the technologies that has been proposed for AUD is soberlink, which is a
monitoring system to measure alcohol content in human breath as a proxy for intox-
ication and blood alcohol levels (BAC). While this technology seems promising and
their website has anecdotal recounts of its usefulness, there are no studies validating
the use in treatment of AUD. There is currently an ongoing study looking at the
effectiveness of such interventions [13].
Another type of technology that was developed in the recent years are wearable
transdermal alcohol sensors that measure alcohol vapor excreted by the skin as
proxy for BAC and thereby intoxication. In one study, these types of sensors were
tested and found to be approachable and user friendly; however, they also have large
variability in readings that brings up the issue of validity and accuracy [25].
Furthermore, a recent review describes that while these sensors’ measurement posi-
tively correlates with BAC or breath alcohol content, there is a wide range in sensi-
tivity and specificity [14], which highlights the lack of consistency as a barrier for
widespread use of these technologies.
The above interventions focus on measurement of BAC to provide the user of
direct feedback of alcohol use and potentially motivate to limit intake. Alternatively,
ultrasound technology to assess hepatic fibrosis [26], which is a direct consequence
of AUD, has been shown to be a non-invasive tool to inform liver changes as a func-
tion of alcohol use [15]. This ultrasound technology could in theory further motivate
alcohol users by showing them concrete physical changes as a consequence of alco-
hol intake.
One could argue that FibroScan technology could aid in advancing stages of
change in individuals with AUD. A study looking at association with stages of
change and medical comorbidities, among other outcomes, found that there is sig-
nificant association of comorbidities and stage of change in alcohol dependence
syndrome [27]. The ability to show negative changes in the liver due to alcohol
consumption adds another powerful tool in the motivational arsenal for providers to
aid individuals who are in the early stages of change and mitigate further injury.
9 Technology-Assisted Treatment of Alcohol Use Disorder 113

9.5 Part 4: Neuromodulation

So far, the interventions discussed in this chapter have focused on non-invasive

approaches. In this section, we will discuss current neuromodulation approaches for
AUD. Transcranial magnetic stimulation (TMS) works by using electromagnetic
induction to depolarize neurons. A recent review looks at different studies targeting
two subcortical regions—the medial prefrontal cortex (MPFC) and the dorsolateral
prefrontal cortex (DLPC) [28]. In this review, they describe current studies using
TMS and describe promising outcomes, such as improvement in cravings or changes
on imaging; however, the variability in parameters for delivery of this treatment has
room for optimization. Additionally, they also present data on studies on transcra-
nial direct current stimulation (tDCS), in which a small current is passed between
two electrodes placed on the head of the participant. This technique shows promise
with some studies suggesting improvement in cravings. Another study looking at
the behavioral effects of tDCS found decreased cravings and increased executive
function in the intervention group as compared to sham [29].
The specific mechanism for how TMS produces the changes in behavior has yet
to be fully elucidated. A recent study by Addolorato et al. [30] elegantly shows that
after rTMS to the DLPC, there is a reduction of dopamine transporter (DAT) in the
striatum, which at baseline showed higher density in participants with AUD. While
this is small study, the mechanistic understanding of these interventions builds a
foundation for well-informed future studies.
A more invasive but also promising intervention for AUD is deep brain stimula-
tion (DBS). DBS has been shown to improve symptoms in Alzheimer’s disease,
obsessive compulsive disorder, and chronic pain (reviewed in [31]). DBS involves a
surgical procedure in which electrodes are implanted in the brain. Several studies
have shown that active stimulation of the nucleus accumbens leads to decrease in
alcohol intake and cravings [32].

9.6 Future Considerations

In the current chapter, we explore current mobile health apps, web-based platforms,
hardware, and neuromodulation tools in the treatment of AUD (Fig. 9.1). Many of
the above have evidence to back up as useful treatment for AUD and have narrowed
the gap between available resources and high demand for treatment. However, as
technology advances, it will be interesting to see how the use of data with machine
learning or artificial intelligence will shape the new landscape of technology in the
AUD. These tools not only provide for additional resources for providers in the
United States but also are options in countries where resources are scarce and
demand is high. One emerging technology that also promises to have a large impact
in AUD and the field of addiction is virtual reality (VR). Virtual reality allows for
highly immersive experiences that can allow for the user to be exposed to different
environmental cues, and this is starting to show important progress not only in treat-
ment but also giving researchers new protocols to implement new approaches to
114 D. Cabrera and M. Khan

Fig. 9.1 Interventions for AUD. In the lower part of the figure are traditional approaches to
AUD. On the top part of the figure are the technological approaches summarized in this chapter

SUD [33]. Technology and medicine continue to create innovative approaches to

complex illness, such as AUD, and the field is ready for new interventions that will
have dramatic effects in millions of patients afflicted by alcohol use and other
substances.

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Alcoholics Anonymous, SMART
Recovery, and Other Support Systems 10
for Alcohol Recovery

Abdallah Tom and Kate Fruitman

10.1 Strength in Unity: Exploring Non-pharmacological

Interventions for Alcohol Use Disorder Treatment

Alcohol Use Disorder, a prevalent chronic condition, affects over 29.5 million indi-
viduals aged 12 and above in the United States alone. On a global scale, it consti-
tutes 5% of the burden of disease and contributes to 3.8% of annual global deaths,
with 88,000 fatalities recorded in the United States [1–4]. Extending beyond medi-
cal and psychiatric realms, the repercussions of alcohol use disorder extend into
individuals’ families, communities, and society, incurring an estimated societal cost
of $250 billion [5]. Addressing Alcohol Use Disorder necessitates a multifaceted
approach, incorporating pharmacological, behavioral, and combined interventions.
Pharmacological measures aim to promote complete abstinence, reduce alcohol
consumption, or prevent end-organ damage [6]. Non-pharmacological options
encompass individual or group-level interventions targeting maladaptive behaviors,
environmental triggers, and community-based support. Categorically, non-­
pharmacological interventions can be classified into Mutual Aid Organizations and
Peer Recovery Specialists. Given the chronic nature of Alcohol Use Disorder, the
need for longitudinal support, and the desire for community and interpersonal con-
nectedness, non-pharmacological therapeutic modalities are the cornerstone of
management [7]. Individuals grappling with Alcohol Use Disorder often navigate
tumultuous interpersonal relationships, resulting in feelings of ostracization and
exacerbating associated stigma [8]. This underscores the pivotal role played by
community-based support, which varies in scope, theory, practice, and implementa-
tion [9].
In delving into non-pharmacological interventions, it is crucial to first delineate
the available resources. These interventions focus on community and peer-based

A. Tom · K. Fruitman (*)

NewYork-Presbyterian Hospital/Weill Cornell, New York, NY, USA
e-mail: [email protected]; [email protected]

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2024 117
M. Khan, J. Avery (eds.), From Stigma to Support, Psychiatry Update 4,
https://doi.org/10.1007/978-3-031-73553-0_10
118 A. Tom and K. Fruitman

support, emphasizing destigmatization, the exchange of lived experiences, behav-

ioral modifications, and skills training to address triggers such as people, places,
and things [10]. These interventions can be broadly categorized into Mutual Aid
Organizations and trained Peer Recovery Specialists. Mutual Aid Organizations
(MAOs), also known as Mutual Help Organizations, consist of groups of at least
two people with similar problems or experiences providing mutual support [11, 12].
Conversely, trained Peer Recovery Specialists (PRS) comprise individuals who
have recovered from substance use disorders and are trained in peer support and
advocacy. In essence, Mutual Aid Organizations follow a bidirectional support
structure, while trained Peer Recovery Specialists operate in a unidirectional man-
ner [13].

10.2 Alcoholics Anonymous

10.2.1 Navigating the Twelve Steps: An Introduction

to Alcoholics Anonymous

Individuals grappling with Alcohol Use Disorder and those traversing the path of
recovery often yearn for connection and community support [14]. In many instances,
the burden of silence weighs heavily, exacerbated by the prevalent stigma, creating
a sense of isolation [15]. The presence of robust support systems can significantly
influence an individual’s journey, playing a pivotal role in recovery through mutual
support and influence [16]. At the core of non-pharmacological behavioral interven-
tions lies community support, with a primary embodiment being Mutual Aid
Organizations (MAOs), also known as Mutual Aid Organizations. MAOs can
broadly be categorized into three groups: Twelve Step, Secular Non-Twelve Step,
and Religious Organizations. Twelve-step programs, such as Alcoholics Anonymous
(AA), have paved the way for a diverse spectrum of mutual aid groups: those exem-
plifying Secular Non-Twelve Step programs like SMART Recovery and Women for
Sobriety and others such as moderation management [17, 18].
Today, Alcoholics Anonymous stands as one of the oldest and most prevalent
support structures for individuals combating Alcohol Use Disorder. Its impact has
extended globally, influencing peer-led mutual support beyond alcohol-related con-
cerns [19]. This non-professional, apolitical fellowship welcomes individuals fac-
ing Alcohol Use Disorder, maintaining a commitment to participant anonymity. As
of 2021, there are over 120,000 AA groups globally, spanning multiple languages
and boasting almost two million participants [20]. How did AA originate, and what
characterizes these essential support structures?
10 Alcoholics Anonymous, SMART Recovery, and Other Support Systems… 119

10.2.2 Dawn of Sobriety: Tracing the Roots and Birth

of Alcoholics Anonymous

Alcoholics Anonymous (AA) had its roots in Akron, Ohio, in 1935, founded by Dr.
Robert Smith and William Wilson, commonly known as Bill [19]. Bill, a Vermont
native and World War I veteran, had experienced a worsening Alcohol Use Disorder
impacting his social life, relationships, and career as a stockbroker throughout the
1920s. Multiple admissions to Towns Hospital in 1934, where he encountered Dr.
William Silkworth, played a crucial role in shaping his understanding of alcoholism
as a medical condition rather than a moral failure [21, 22]. During said hospitaliza-
tions he was introduced to the concept of alcoholism as a disease of the mind by Dr.
William Silkworth, which could “no more be defeated by will power than tubercu-
losis [21, 23].” Dr. Silkworth emphasized that alcohol misuse is not a moral failure,
but rather due to an underlying medical condition, he played a crucial role in chang-
ing the rhetoric. He conceptualized alcohol as a disease of the mind and compared
it to allergies to promote complete abstinence: “the action of alcohol on these
chronic alcoholics is a manifestation of an allergy…these allergic types can never
safely use alcohol in any form at all [24].” Dr. Silkworth has been credited with
influencing Wilson’s understanding of alcohol use disorder.
Another influential figure in Bill’s recovery was Edwin “Ebby” Thatcher, whom
Bill met in 1934 between his third and fourth hospitalizations. Thatcher introduced
Bill to the Oxford Group, a fellowship founded by Lutheran minister Frank Buchman
in 1921. Initially, an agnostic, Bill struggled with the religious undertones of the
Oxford Group, but Thatcher and the group played a pivotal role in Bill’s spiritual
awakening and journey to sobriety. Thatcher later became Bill’s first sponsor, con-
tributing to the foundation of AA [21, 22]. Based on experiences with Dr. Silkworth
and Thatcher, Bill conceptualized alcohol use disorder’s threefold nature: physical,
mental, and spiritual [21]. Bill had his last alcoholic drink on December 11th, 1934.
In the year preceding his meeting with Dr. Smith, Bill actively participated in the
Oxford Group and collaborated with Towns Hospital to assist individuals suffering
from Alcohol Use Disorder. In the year preceding his meeting with Dr. Smith, Bill
actively participated in the Oxford Group and collaborated with Towns Hospital to
assist individuals suffering from Alcohol Use Disorder. While in Akron, Ohio, on an
unsuccessful business trip in the spring of 1935, Wilson was fearful of relapsing.
Learning from his experience with the Oxford Group, he said “I need a drunk to
work with” [21]. He began contacting people in the phonebook. This eventually
connected to Dr. Robert Smith, an Akron based surgeon, by one of the leaders of the
Akron Oxford Group.
Dr. Smith, introduced to the Oxford Group 2 years prior, had struggled with
alcoholism for years. After meeting Bill in May 1935, Dr. Smith had his last alco-
holic drink on June 10th, 1935, marking the founding day of AA, to alleviate stress
before performing surgery. The success with Dr. Smith prompted Bill to stay in
Akron, where the two worked tirelessly to develop strategies for spreading their
approach to help others with Alcohol Use Disorder. Bill’s encounter with another
individual, Bill Dotson, at Akron’s City Hospital on June 26th, 1935, furthered their
120 A. Tom and K. Fruitman

efforts. Dotson, after being worked with closely, achieved sobriety, marking a piv-
otal moment in the birth of AA [25, 26].

10.2.3 The Birth of the First AA Group

Dr. Smith, Bill, and Dotson formed the first AA group on July 4th, 1935. Prior to
their meeting, recognizing the need to share their approach, Bill and Dr. Smith con-
tacted Akron City Hospital, where they were introduced to Bill Dotson, admitted
with delirium tremens and was restrained after physically assaulting two nurses
[23]. In the 6 months prior to his hospitalization, Dotson was hospitalized eight
times for alcoholism. Dr. Smith and Wilson first met Dotson on June 26th, 1935,
and continued to work with him during his hospitalization. They shared their jour-
neys with alcohol use, how they achieved sobriety, and the role of spirituality in
recovery with the belief that there is a higher power. Dotson’s journey of sobriety,
shared on July 4th, 1936, became the foundation of AA as they decided to work
together on their sobriety rather than separately. Dotson remained sober for 19 years
until his death [23].
In the subsequent years, Bill eventually returned to New York City. Along with
Dr. Smith, he began to share their success with others in their respective cities, and
by 1937, around 40 individuals had achieved sobriety [24]. To reach a broader audi-
ence, Bill and Dr. Smith authored “Alcoholics Anonymous” in 1939, commonly
known as “The Big Book.” The book has multiple editions published over the years
with updates to personal stories [24]. This marked the beginning of AA’s exponen-
tial growth, nationally and internationally. By the turn of the millennium, AA
boasted approximately one million members, laying the groundwork for other
recovery groups, including Narcotics Anonymous.

10.2.4 Navigating Sobriety with the Twelve Steps and Traditions

of Alcoholics Anonymous

“The Big Book” delved into the 12-step program for managing Alcohol Use
Disorder, rooted in the tenets of the Oxford Group, united under the umbrella of
“Unity, Service, and Recovery” [19]. Inspired by the Oxford Group but distinct in
its focus on spirituality over religiosity, AA set itself apart by emphasizing individ-
ual autonomy and lacking hierarchy [19].
The foundational principles of Alcoholics Anonymous (AA) are encapsulated in
the 12 steps, as outlined in Table 10.1. Initially published in “The Big Book,” these
steps serve as the spiritual underpinning for AA programs. Emphasized and taught
in AA group meetings, the 12 steps become integral practices in members’ lives.
AA fosters a sense of community and fellowship through frequent meetings, con-
ducted in various locations accommodating different group types: open, closed,
speaker, discussion, the Big Book, and step [24]. Open groups welcome all indi-
viduals, while closed groups specifically cater to those grappling with alcoholism.
10 Alcoholics Anonymous, SMART Recovery, and Other Support Systems… 121

Table 10.1 The 12 steps of Alcoholics Anonymous and analysis of each step
Step Principle [27] Analysis [28]
1 We admitted we were powerless over Honesty: Admitting to self that they are
alcohol—That our lives had become an alcoholic, rejecting denial
unmanageable
2 Came to believe that a Power greater than Spirituality: Believing in a higher power
ourselves could restore us to sanity as a source of motivation
3 Made a decision to turn our will and our lives Belief: Personal belief in a higher power
over to the care of God as we understood in a spiritual sense rather than religious
Him
4 Made a searching and fearless moral Self-discovery: Capitalizing on strengths
inventory of ourselves and working on weakness
5 Admitted to God, to ourselves, and to another Vulnerability: Sharing with others your
human being the exact nature of our wrongs admittance of being an alcoholic
6 Were entirely ready to have God remove all Readiness: Being open to changing
these defects of character behaviors and habits
7 Humbly asked Him to remove our Humility: Accepting to change behavior
shortcomings and habits
8 Made a list of all persons we had harmed and Acknowledgement: Recognizing the
became willing to make amends to them all damage done to one’s community
9 Made direct amends to such people wherever Reconciliation: Making amends with
possible, except when to do so would injure those harmed
them or others
10 Continued to take personal inventory and Reflection: Reflecting on actions and
when we were wrong promptly admitted it taking responsibility for wrong doings
11 Sought through prayer and meditation to Connection: Connecting to a higher
improve our conscious contact with God as power and fellow alcoholics. Some refer
we understood Him, praying only for to GOD as “Group Of Drunks” or “Good
knowledge of His will for us and the power to Orderly Direction”
carry that out
12 Having had a spiritual awakening as the result Maintenance and service: Committing to
of these steps, we tried to carry this message maintaining sobriety, working with others
to alcoholics and to practice these principles to maintain theirs, and sharing the
in all our affairs principles with others

Speaker meetings involve a designated individual delivering a talk, discussion

groups center around group dialogues on AA-related topics, the Big Book groups
explore readings from the AA book, and Step groups delve into specific steps from
the 12-step program [24].
With no formal organizational hierarchy and a foundation built on fellowship,
Alcoholics Anonymous developed the 12 traditions to provide guidance on logisti-
cal matters. These traditions serve as a compass, steering the course for the group’s
collective function and behavior.
While the 12 steps of Alcoholics Anonymous (AA) illuminate the spiritual path-
ways to sobriety, the 12 traditions serve as the organizational framework, ensuring
sustainability and emphasizing fellowship and purpose (Table 10.2).
122 A. Tom and K. Fruitman

Table 10.2 The 12 traditions of Alcoholics Anonymous

Tradition Principle [29]
1 Our common welfare should come first; personal recovery depends upon AA unity
2 For our group purpose, there is but one ultimate authority—A loving God as He may
express Himself in our group conscience. Our leaders are but trusted servants; they
do not govern
3 The only requirement for AA membership is a desire to stop drinking
4 Each group should be autonomous except in matters affecting other groups or AA as
a whole
5 Each group has but one primary purpose—To carry its message to the alcoholic who
still suffers
6 An AA group ought never endorse, finance, or lend the AA name to any related
facility or outside enterprise, lest problems of money, property, and prestige divert us
from our primary purpose
7 Every AA group ought to be fully self-supporting, declining outside contributions
8 Alcoholics Anonymous should remain forever non-professional, but our service
centers may employ special workers
9 AA, as such, ought never be organized; but we may create service boards or
committees directly responsible to those they serve
10 Alcoholics Anonymous has no opinion on outside issues; hence the AA name ought
never be drawn into public controversy
11 Our public relations policy is based on attraction rather than promotion; we need
always maintain personal anonymity at the level of press, radio, and films
12 Anonymity is the spiritual foundation of all our traditions, ever reminding us to
place principles before personalities

10.2.5 Companionship in Alcoholics Anonymous

Encompassing fellowship, companionship, and a dedicated pathway to recovery,

Alcoholics Anonymous operates 118,000 groups in 180 countries, serving over two
million individuals [25]. A study at Stanford University revealed that attending AA
groups correlates with both short- and long-term sobriety, as well as reduced alco-
hol consumption [25, 26]. Research further indicates that AA is more likely to result
in sobriety compared to therapy [25]. Despite its founding in 1935, it wasn’t until
2020 that research data highlighted its effectiveness. Earlier studies evaluating AA’s
effectiveness were inconclusive and lacked statistical significance [30]. An impact-
ful meta-analysis published in the Cochrane Library, involving 27 studies and
10,565 participants, concluded that AA is effective in promoting and maintaining
sobriety at 12, 24, and 36 months. Moreover, AA was found to be more effective
than other interventions, including cognitive behavioral therapy [31].
Alcoholics Anonymous lacks hierarchical structure and is built on companion-
ship. The only requirement for joining AA is “the desire to stop drinking” [32].
Consequently, AA boasts diverse membership from all walks of life, united by a
shared problem. The core purpose of AA is to remain sober and assist others in
achieving sobriety through the “24-hour plan” [32]. Rather than committing to life-
long abstinence, the 24-hour plan focuses on taking sobriety 1 day at a time, foster-
ing realistic and attainable goals. As mentioned earlier, AA meetings come in
various types, offering regular gatherings where members can share struggles and
10 Alcoholics Anonymous, SMART Recovery, and Other Support Systems… 123

experiences, forge connections, and benefit from sponsors who aid in maintaining
sobriety. Members are paired with sponsors, experienced volunteers in AA, who
provide guidance, support, and serve as personal mentors. The sponsor-sponsee
relationship is pivotal in AA, offering assistance through the 12 steps, sharing per-
sonal experiences, offering encouragement during challenging times, and evaluat-
ing a sponsee’s progress. Confidentiality and trust form the bedrock of this
relationship.

10.3 Self-Management and Recovery Training (SMART)

10.3.1 Introduction

Criticism of Alcoholics Anonymous (AA) often centers around its adherence to a

spiritual and religious approach and the 12-step model, which may not resonate
with everyone seeking help for alcohol addiction. Critics of Alcoholics Anonymous
found the reference to “God” and using the male pronoun “Him” unsettling.
Additionally, they fundamentally disagreed with the principles of powerlessness
and surrender preached by AA and the view of alcoholism as a disease. Some indi-
viduals find fault in the lack of scientific evidence supporting the effectiveness of
AA, as well as concerns about anonymity and the organization’s structure [33]. In
response to these critiques, alternative recovery programs like SMART Recovery
were established. Self-Management and Recovery Training (SMART Recovery)
offers a scientific and secular approach to addiction recovery, focusing on self-­
empowerment and evidence-based techniques. By incorporating cognitive-­
behavioral strategies, motivational enhancement, and life-balance principles,
SMART Recovery provides a viable alternative for those who seek a more individu-
alized and scientific pathway to overcoming alcohol addiction [34].
In response to the said criticism, secular mutual aid organizations saw a rise in
the 1980s–1990s. In 1986, Jack Trimpey, a California-based Social Worker, founded
Rational Recovery Systems (RR). RR is a mutual aid organization that offered an
alternative understanding of addiction and challenged the traditional recovery mod-
els such as Alcoholics Anonymous [34]. As opposed to the disease framework of
addiction and necessary surrender to a higher power in recovery seen in Alcoholics
Anonymous, Rational Recovery argued that addiction is a learned behavior that can
be unlearned through self-recovery, personal responsibility, and empowerment,
through primarily utilizing Rational Emotive Behavior Therapy. Rational Recovery
contributed significantly to changing the narrative surrounding substance use to a
secular, self-directed approach, individual agency, personal responsibility, and
behavioral modification. It paved the way for other secular mutual aid organizations
that incorporate scientific theories and practices such as SMART Recovery. Both
SMART Recovery and Rational Recovery focus on personal empowerment and
maladaptive behavioral modification. However, SMART Recovery emphasized the
utilization of scientifically backed approaches to abstinence through therapeutic
124 A. Tom and K. Fruitman

modalities such as motivational, cognitive, and behavioral treatment strategies

delivered through community programs [35].

10.3.2 The Evolution of Self-Management and Recovery Training

(SMART Recovery)

SMART Recovery was established in response to a need for secular and scientific
mutual aid organizations in Mentor, Ohio. At its inception, it was referred to as the
“Rational Recovery Self Help Network” when affiliated with Rational Recovery
Systems. In 1994, it branched off and operated under “SMART Recovery” [36].
Prior to that in 1991, Trimpey invited nationwide addiction specialists to Dallas,
Texas, to further expand his work of mutual aid organizations. A year later in
Sacramento, California, the invitees met to establish a nonprofit to further expand
mutual aid organizations, while “mutually supporting” Trimpey continued his for-­
profit work [36]. It was started by a group of mental health professionals including
physicians, psychologists, and social workers, many of whom were members of
Rational Recovery [37]. Two of the leading figures were Drs. Joseph Gerstein and
Thomas Horvath [34, 37, 38]. Dr. Gerstein is a Massachusetts-based physician and
retired Clinical Assistant Professor of Medicine, who played a vital role in the intro-
duction of Rational Recovery in Boston prior to establishing SMART. Dr. Horvath
is a clinical psychologist, and following active duty as a Navy psychologist, he
founded Practical Recovery in 1985. Dr. Gerstein went on to become the founding
president of the Alcohol and Drug Abuse Self-Help Network, which is also known
as SMART recovery [37].
In 1993 in Boston, Massachusetts, the group that initiated Rational Recovery
Self Help Network established their first board of directors with Dr. Gerstein as the
president. Shortly thereafter in 1994 due to increased tension with Trimpey, the
name was changed to “Alcohol and Drug Abuse Self-Help Network” [35]. And
2 months later, “SMART recovery” was established. The main tension points
between the two groups were attributed to their approach to recovery. While the
then Rational Recovery Self Help Network focused on Cognitive Behavioral
Therapeutic Principles, Rational Recovery Systems proceeded in a different direc-
tion [36].
In order to establish themselves as a non-profit organization, SMART Recovery
opened a central office in Beachwood, Ohio, that was later moved to Mentor, Ohio,
in close proximity to staff members. In its first decade, SMART recovery focused
on ensuring their sustainability through organizational development while continu-
ing their work in the community. Groups were initially led by professionals before
implementing the “Peer Professional Partnership.” They were able to achieve nota-
ble milestones. Initiatives included the commencement of the SMART Recovery
News and Views newsletter in 1994 and its introduction to the federal women’s
prison in Danbury, CT. The foundational document, SMART Recovery Purposes
and Methods, was ratified in 1995, coinciding with the establishment of the organi-
zation’s first website. Subsequent years saw developments such as training grants,
10 Alcoholics Anonymous, SMART Recovery, and Other Support Systems… 125

international expansion into Australia and the UK, the creation of online meetings,
and the publication of the SMART Recovery Handbook in 2004. Strategic goals
were set in 2000, focusing on marketing, facilitator support, Internet presence, fun-
draising, and the initial development of SMART Recovery Therapy. These mile-
stones laid the foundation for SMART Recovery’s growth and impact [36, 39].
In SMART Recovery’s second decade, the organization focused on building
international reach through additional licensing agreements, international opera-
tions, and translation of the handbook into eight different languages [38]. National
efforts were directed toward expanding local reach included publishing more writ-
ten works and videos, marketing initiatives, and an annual participant survey. Given
SMART Recovery’s core principle of adhering to scientific data, policy positions
were established regarding medications and the disease concept, updating the stance
to accept appropriate medication use and acknowledging diverse beliefs about
addiction as a disease. This shift paralleled SMART Recovery’s approach to indi-
vidual beliefs in a higher power, considering it a personal matter for each
participant.

10.3.3 SMART Recovery Meetings Framework

SMART Recovery imparts recovery tools grounded in evidence-based practices

from addiction treatment literature or other tools granted that they emphasize self-­
empowerment and suitability for nonprofessional volunteer-led mutual aid groups.
As such, SMART recovery is malleable and adapts to ongoing scientific research.
The foundation, articulated in SMART Recovery’s second decade, remains
unchanged. The approach adapts with evolving scientific evidence, drawing inspira-
tion from CBT and motivational interviewing through a 4-point framework [34, 40]:

1. “building and maintaining motivation”

2. “coping with urges”
3. “managing thoughts, feelings, and behaviors”
4. “living a balanced life”.

SMART Recovery meetings follow a structured format: “Welcome, Check-In,

Agenda Setting, Discussion, Pass the Hat/Pass the Brochure, Announcements, and
Check-Out [41].” The Check-Out allows participants to share the most meaningful
aspects of the meeting. Importantly, not all steps need to be completed in chronol-
ogy, as the approach is tailored to individual needs. The four points provide a frame-
work for the tools used in SMART recovery. SMART Recovery continues to evolve
in response to ongoing research in addiction treatment and recovery.
SMART Recovery implements the above tools through various methods, includ-
ing their integration into meetings and worksheets designed for participant use.
Accessible online at no cost, the SMART Recovery toolbox features resources such
as worksheets based on CBT principles [42] (Table 10.3).
126 A. Tom and K. Fruitman

Table 10.3 Summary of SMART Recovery tools and descriptions based on “SMART Recovery:
Self-Empowering, Science-Based Addiction Recovery Support” by Drs. Horvath and Yeterian
Tool [34] Description [34]
Stage of change How ready am I to change?
Change plan worksheet What do I want to change? Why? How much? How will I do it?
What might get in the way?
Cost–benefit analysis What are the costs and benefits of addiction, and of recovery?
What conclusions do I draw after listing and comparing them?
ABC of REBT for urge When I have a craving, what irrational beliefs do I typically have
coping (e.g., craving makes me use, I can’t stand having a craving so I
need to use)?
ABC of REBT for What irrational beliefs do I have about myself, others, or life and
emotional upsets the world in general? Can I perceive how these beliefs lead to
unnecessary emotional upset?
Destructive imagery and I can expose the faulty thinking and misleading images that give
self-talk awareness and rise to my cravings and vigorously counter-attack with an
refusal method assertion of thoughts and images consistent with my long-term
interests
Brainstorming In a meeting, all participants freely express any idea about a
particular issue. Only after ideas are collected does discussion and
evaluation of the ideas begin
Role-playing and In a meeting, an expected difficult encounter is re-created for a
rehearsing participant to allow for practicing a constructive response
Hierarchy of values What do I say is most important to me? Based on how I behave,
what in fact appears to be most important to me? How different is
what I say and what I do? What do I want to do about any
discrepancies?

10.3.4 Evolution of SMART Recovery

Since its inception in 1994, SMART Recovery (Self-Management and Recovery

Training) has undergone substantial development, expanding both its organizational
structure and the array of resources and support it provides for individuals grappling
with addictive behaviors. Emphasizing self-empowerment and principles rooted in
cognitive-behavioral therapy, SMART Recovery established a Central Office in
Mentor, Ohio, staffed by part-time employees and volunteers [43]. This hub serves
to coordinate activities, conduct facilitator training, create program materials, orga-
nize meetings, and manage administrative tasks. The Central Office not only facili-
tates resource development and updates based on feedback but also disseminates
information online, reaching a broader global audience [44].
Operated by volunteers, SMART Recovery fosters a sense of community and
belonging through its volunteer framework. Volunteers, who may or may not be
individuals in recovery, participate in various facets of organizational development,
including public awareness and advocacy efforts to enhance understanding of
SMART Recovery and its alternative approaches to overcoming addiction-related
stigma [43].
In its early years, SMART Recovery concentrated on refining its program,
grounding it in cognitive-behavioral principles and other evidence-based practices.
10 Alcoholics Anonymous, SMART Recovery, and Other Support Systems… 127

Founded by Drs. Joe Gerstein and Tom Horvath, the organization sought to estab-
lish a framework that prioritizes self-empowerment, personal responsibility, and
practical skills for managing addictive behaviors.
Over time, SMART Recovery has evolved into a global community of peer sup-
port, hosting over 3000 programs across 35 countries. Guided by scientifically
based principles and personalized goals, the organization’s global reach expanded,
especially with the surge in online presence prompted by the COVID-19 pandemic.
SMART Recovery meetings, lasting 60–90 min and facilitated by trained leaders,
incorporate motivational interviewing and cognitive-behavioral techniques, provid-
ing participants with a comprehensive and supportive approach to recovery.

10.3.5 The Impact of SMART Recovery

The introduction of the Peer Alternatives in Addiction (PAL) study sheds light on
the research gap surrounding mutual aid alternatives for individuals with alcohol
use disorders (AUDs). While 12-step groups like Alcoholics Anonymous (AA) are
widely available and appear effective, not all individuals find them appealing, lead-
ing to low sustained involvement. Secular mutual aid alternatives such as Women
for Sobriety (WFS), LifeRing Secular Recovery (LifeRing), and SMART Recovery
(Self-Management and Recovery Training) present potential alternatives, especially
for those who do not resonate with the spiritual aspects of 12-step groups [45].
The spotlight has predominantly shone on Alcoholics Anonymous (AA), leaving
fewer comprehensive assessments of the efficacy and effectiveness of SMART
Recovery. A study conducted in 2014 provided a glimpse into the landscape, reveal-
ing that a noteworthy 19–25% of participants grappling with significant alcohol use,
sourced through Craigslist, had engaged with a non-AA mutual aid support group,
including SMART Recovery [45].
Cross-sectional studies, although limited, shed light on the motivations behind
participants gravitating toward non-AA mutual aid groups, such as SMART
Recovery. The secular approach to treatment and the sense of community appear to
be key factors attracting individuals to these alternatives [46–48]. However, the
comparative effectiveness of different support systems for alcohol recovery remains
a nuanced area. Some studies suggest no statistical difference in efficacy between
various support systems, including both traditional and alternative approaches [45].
Nevertheless, a noteworthy finding emerges—those who engage in these support
systems for a more extended period exhibit an increased likelihood of achieving
sobriety [45]. This underscores the significance of individual preferences, empha-
sizing the importance of aligning support systems with individual needs and prefer-
ences in the pursuit of successful recovery.
The PAL study, conducted longitudinally over a 1-year period, focuses on the
comparative efficacy of Women for Sobriety, LifeRing, SMART Recovery, and
12-step groups. The study aims to understand whether the benefits of mutual aid
group involvement for substance use outcomes are equivalent across these groups.
It also explores whether differences in alcohol recovery goals contribute to varying
128 A. Tom and K. Fruitman

outcomes. The study’s design includes baseline, 6-month, and 12-month surveys,
examining membership characteristics and relationships between group involve-
ment and substance use outcomes [45]. The study found strong associations between
higher group involvement and positive outcomes, though no statistical difference
was found between different forms of support systems.
The PAL study’s exploration is particularly crucial given the limited research on
secular alternatives. Existing cross-sectional studies and a few observational studies
suggest that individuals are drawn to non-12-step mutual aid groups due to their
secular approach. While inconclusive, this trial highlights the need for further
research on SMART and other alternatives [45].

10.4 Other Support Systems for Alcohol Recovery

10.4.1 LifeRing Secular Recovery

LifeRing Secular Recovery (LifeRing) is an abstinence-based MAO born from

Secular Organizations for Sobriety and Save Ourselves (both utilizing the acronym
SOS) [12, 33, 40]. Founded in 1986 by James Christopher, SOS was established to
provide a secular, humanist alternative to AA [12, 33]. Notably, following a legal
dispute regarding its name, the largest chapter of SOS, led by Martin Nicolaus,
changed its name to LifeRing Secular Recovery (LifeRing) [12, 33, 49].
The LifeRing philosophy has three fundamental principles: sobriety, secularity,
and self-help [40]. Similar to the traditional 12-step model, LifeRing encourages
complete abstinence. However, in contrast to AA, LifeRing is a secular organization
that emphasizes reliance on the effort of individuals as opposed to the divine [40,
50]. As such, the guiding principle of “self-help” encourages members to take con-
trol of their substance use by emphasizing personal strengths and motivations as
opposed to the “powerlessness” and surrender to a “higher power” described in AA
teachings [40]. In their personalized path to recovery, members empower their
“sober self” and weaken their “addict self” through the three principles of recogni-
tion (reflecting on the positive qualities and strengths of the “sober self”), activation
(speaking in groups about decisions and issues that arise in everyday life), and mas-
tery (empowerment of members to participate in self-treatment) [40]. All leadership
within LifeRing is nonprofessional and peer-driven, including meeting facilitators
or convenors, who are individuals who have at least 1 year of sobriety [40, 47].
A membership study of LifeRing conducted in 2005 demonstrated that members
were largely white (80%) and well-educated (83% had attended some college or
junior college [51]. Notably, more than half of participants (59%) reported no reli-
gious participation in church, synagogue, temple, etc. within the past year) [51].
A subsequent study, published in 2016, evaluated LifeRing participation in
Canada, specifically in the Greater Victoria Area [47]. The study, which includes
data from 50 participants, examined how group cohesion and alliance with the
meeting convenor could relate to participation in the group and satisfaction with
LifeRing [47]. The authors found that group cohesion was positively associated
10 Alcoholics Anonymous, SMART Recovery, and Other Support Systems… 129

with active participation, such as speaking within the group [47]. This finding sug-
gests that members who experience the group as cohesive and supportive are more
likely to share personal experiences in group [47]. However, active participation in
the group was not associated with group satisfaction, highlighting that participants
may experience satisfaction not only through sharing with the group but also
through listening to the experiences and narratives of peers [47]. Notably, the
authors found that while alliance with convenors was associated with satisfaction
with the group, group cohesion did not correlate to satisfaction [47]. These findings
highlight the importance of appropriate training for convenors, perhaps mirroring
the data substantiating the efficacy of trained peer recovery specialists (PRS) in the
care of patients with SUDs [52].
While there is substantial literature characterizing outcomes of patients engaged
in 12-step work, there is a smaller body of work delineating the experiences of
members in non-12-step alternatives. A 2007 study of 12-step groups and non-12-­
step groups (SOS, SMART Recovery, and WFS) examined the relationship of reli-
giosity and group participation to days of sobriety [53]. The authors, Atkins and
Hawdon, found that active involvement in support groups (defined as attendance,
participation in discussion, time spent with members), regardless of the type of
group, resulted in greater number of days sober [53]. In addition, the respondents’
level of religiosity did not correlate with remaining sober, but did dictate their pat-
tern of participation in groups [53]. While increased religiosity significantly
improved participation in 12-step programs, increased religiosity was associated
with decreased participation in SOS [53]. As such, when clinicians or peers refer
patients to MAOs, attention must be paid to the individual’s baseline religiosity, as
it can guide appropriate group placement.
In concordance with the findings of Atkins and Hawdon, a 2018 study by Zemore
and colleagues similarly found that there is a strong association between increased
group involvement and improved SUD outcomes (such as alcohol abstinence),
regardless of group affiliation [45]. Although the study suggests equivalent efficacy
between 12-step and non-12-step groups, evidence demonstrates that participants
with a LifeRing affiliation had lower odds of total abstinence at the time of follow-
­up when compared to 12-step members [45]. However, this effect was largely driven
by differences in recovery goals, with LifeRing members being less likely to endorse
a recovery goal of lifetime abstinence [45]. This finding speaks to the variability in
recovery goals present among group members, even within organizations advocat-
ing for abstinence [33].

10.4.2 Women for Sobriety

Founded in 1975 by Jean Kirkpatrick, Women for Sobriety (WFS) created a space
uniquely designed for women in recovery [12, 33, 54]. Kirkpatrick observed that
women with AUD frequently struggled with feelings of guilt and shame and there-
fore developed WFS on the principle of instilling confidence in members. Rejecting
the AA dogma that preaches powerlessness and humility, WFS has Thirteen
130 A. Tom and K. Fruitman

Statements of Acceptance that are centered on bolstering self-efficacy [12, 33, 54].
Unlike AA, WFS inspired members to conceptualize their sobriety as a personal
achievement, discouraging sponsors or lifelong dependency on the organization
[12]. However, there are several notable similarities to the AA model. WFS encour-
ages abstinence and similarly champions peer-based support as integral to recovery
[12, 33, 54]. Although there is limited empirical evidence documenting the efficacy
of the WFS model, the PALS study (a longitudinal examination of various MAOs)
found that WFS was equally as effective as other MAO organizations [45].

10.4.3 Moderation Management

As societal awareness of the consequences of alcohol dependency heightened and

abstinence-based community support systems increased, there was a shift from
alcohol dependence to nondependent problem drinking behaviors [55]. Due to rela-
tive infrequency of health and psychosocial consequences among the latter popula-
tion, it is often underserved, receives relatively less attention, and has limited
structural support systems. In response to the increased demand for structural sup-
port, Moderation Management (MM) was established in 1994 by Audrey Kishline
with the aim of promoting moderate alcohol use through principles of harm reduc-
tion [18, 56]. Moderation Management (MM) is a secular peer-run nonprofit orga-
nization built on principles of Cognitive Behavioral Therapy and the Behavioral
Self-Control Framework, providing a space for individuals to explore their relation-
ship with alcohol and set personalized moderation goals [12, 57–59].
Audrey Kishline did not align with the prevailing disease model of alcohol mis-
use, having stated that abstinence negatively impacts her self confidence [12].
However, less than a decade following the establishment of Moderation Management,
Kishline shared with members in 2000 that she will be joining peer-led groups pro-
moting sobriety while continuing to support Moderation Management, stating that
abstinence is the best way forward for her [57]. Three months later while under the
influence of alcohol, she killed a 12-year-old girl and her father in a motor vehicle
accident [12]. She served 3.5 years of her 4.5 year sentence and was released in
2003 [12, 60]. During the following 11 years, prior to her death by suicide at age 59,
she continued her commitment and support for moderation management and
authored a book with the victims’ wife and mother [12, 58, 60].
Despite these challenges and criticism received, MM persisted to provide a space
and community for individuals who want to moderate their alcohol use or are unsure
if they want to abstain from or moderate their alcohol use. MM operates on a frame-
work that emphasizes moderated alcohol use as a viable alternative to abstinence,
drawing upon principles of Cognitive Behavioral Therapy and the Behavioral Self-­
Control Framework [12, 59]. At its core, MM offers individuals the opportunity to
set their own goals for moderate alcohol consumption within a supportive peer envi-
ronment. This framework is not mandated, but participants are encouraged to abide
by it to gain the confidence needed to moderate alcohol use by engaging with a set
10 Alcoholics Anonymous, SMART Recovery, and Other Support Systems… 131

of tools, limits, and guidelines developed from the work of Dr. Martha Sanchez-­
Craig, a psychologist and substance misuse researcher [59, 61].
Central to MM’s approach is members’ autonomy to set their own personal mod-
eration goal [59, 62]. MM describes a “moderate drinker” as someone who:

• “considers an occasional drink to be a small, though enjoyable, part of life

• has hobbies, interests, and other ways to relax and enjoy life that do not
involve alcohol
• usually has friends who are moderate drinkers or nondrinkers
• generally has something to eat before, during, or soon after drinking
• usually does not drink for longer than an hour or two on any particular occasion
• usually does not drink faster than one drink per half-hour
• usually does not exceed the 0.055% BAC moderate drinking limit
• feels comfortable with his or her use of alcohol (never drinks secretly and does
not spend a lot of time thinking about drinking or planning to drink) [63]”

Moderation Management offers flexibility to its participants through personally

set goals, encouragement of following the set limits and guidelines, and engaging
with peers. Individuals interested in joining Moderation Management are expected
to participate in an in-person or virtual “Newcomers Meeting” to learn about MM
and keep a diary to track alcohol consumption, situation, outcome, and associated
behaviors [64]. Participants are encouraged to follow a 9-step guide, rooted in CBT
principles, to facilitate their moderation journey [65]. The recommendations are
expected to empower participants, and they do not necessarily have to be done in the
specified order:

1. “Attend meetings or on-line groups and learn about the program of Moderation
Management
2. Abstain from alcoholic beverages for 30 days and complete steps three through
six during this time
3. Examine how drinking has affected your life
4. Write down your life priorities
5. Take a look at how much, how often, and under what circumstances you had
been drinking
6. Learn the MM guidelines and limits for moderate drinking
7. Set moderate drinking limits and start weekly “small steps” toward balance and
moderation in other areas of your life
8. Review your progress and update your goals
9. Continue to make positive lifestyle changes and attend meetings whenever you
need ongoing support or would like to help newcomers [63].”

In order to assist prospective members with moderation, MM introduced a set of

32 tools with the aim of behavioral modification such as “The Delay Tool” where
participants are encouraged to begin drinking an hour later than they normally
would and “The Divorce Tool” where participants are encouraged to substitute
132 A. Tom and K. Fruitman

alcohol with alternative items or behaviors in trigger situations [66]. In addition to

the above definition of a “moderate drinker” and the 9-step guidelines, the frame-
work for MM also includes set limits:

• “Strictly obey local laws regarding drinking and driving

• Do not drink in situations that would endanger yourself or others
• Do not drink every day. MM suggests that you abstain from drinking alcohol at
least 3 or 4 days per week
• Women who drink more than 3 drinks on any day, and more than 9 drinks per
week, may be drinking at harmful levels
• Men who drink more than 4 drinks on any day, and more than 14 drinks per
week, may be drinking at harmful levels [63]”

To support members in their moderation goals, MM offers a range of resources,

including in-person and online peer-led support groups, online forums, around the
clock chat rooms, and an app called “ABSTAR,” for setting and sharing personal
goals, tracking alcohol use, and holding oneself and others accountable [67]. The
online resources allow for informal peer support, engagement, and an opportunity
to learn from others’ experiences. Members whose moderation is a challenge are
recommended to explore abstinence-based peer support groups such as SMART
Recovery [59].
In the 1990s, following the establishment of Moderation Management, contro-
versy regarding its utility was prevalent among researchers and leading figures,
describing it as “dangerous temptation to alcoholics [68].” They would often argue
that it’s ineffective, and individuals who misuse alcohol cannot control their alcohol
use. Kishline’s vehicular homicide while under the influence years after launching
Moderation Management and the lack of data on efficacy further added to the skep-
ticism [68]. Relative to other mutual aid organizations, data on Moderation
Management continues to be scarce. A study conducted in 2004 aiming to under-
stand the demographic distribution of MM attendees found that most attendees were
middle aged, identified as female, were college educated, and belonged to upper-­
middle socioeconomic class, and the overwhelming majority was White [69]. On
average at baseline, members of MM consumed less alcohol and had less socioeco-
nomic consequences of alcohol misuse compared to assessing members of
Alcoholics Anonymous [68, 69]. Though data into safety and efficacy remains
scarce, MM remains a significant player in the landscape of alcohol use support
organizations [68]. Proponents of MM emphasize its potential to positively impact
the lives of its members and draw parallels to the broader harm reduction frame-
work [70].

10.4.4 Online Engagement with Mutual Aid Organizations

In a 2021 review of online digital recovery support services, Bergman and Kelly
define the existing landscape of virtual substance use support [71]. They propose
10 Alcoholics Anonymous, SMART Recovery, and Other Support Systems… 133

that existing services can be characterized according to four criteria: service type,
platform type, points of access, and the responsible organizations/individuals.
Service types encompass synchronous (real-time) and asynchronous interactions,
including video-based recovery support meetings, akin to in-person MAO meetings.
Alternatively, other service types may include recovery-focused discussion boards,
chat groups, and social network activities. These services are accessible through
various platforms, including video conferencing technology (e.g., Zoom), recovery-­
specific social networking sites (e.g., InTheRooms), or general-interest social net-
working sites (e.g., Instagram). Access points range from websites and smartphone
apps to telephonic services, especially for those with limited Internet availability.
Organizations overseeing these services vary from volunteer-moderated forums,
established MAOs such as AA, or private companies.
In a study conducted prior to the COVID-19 pandemic (2017), a survey of a
nationally representative sample of adults in the United States in recovery from a
SUD demonstrated that 11% of patients utilized at least one form of online technol-
ogy to remain abstinent or decrease substance use [72, 73]. When specifically exam-
ining peer support utilization, 4.1% attended virtual MAO meetings (e.g., AA,
SMART Recovery), 4.9% utilized a general-interest social network site (e.g.,
Facebook), and 3% used recovery-specific social network sites (e.g., InTheRooms.
com) [72].
With regard to MAO activity, there is pre-pandemic literature documenting the
long-standing practice of using devices to augment face-to-face meetings. For
example, AA members utilized mobile devices, video-chat, and virtual messaging
platforms to connect with peers outside of official gatherings [74, 75]. In a random-
ized control trial of SMART Recovery meeting attending, including both online and
in-person options, and a virtual cognitive-behavioral intervention for SUDs, authors
found that participation in online SMART Recovery meetings was positively asso-
ciated with the proportion of days abstinent within a 3-month follow-up [39, 76].
Moreover, data from a qualitative study of SMART Recovery participants utilizing
a digital platform to monitor substance use outcomes demonstrated that members
found digital monitoring to be a positive addition to in-person weekly group meet-
ings [77].
Utilizing the data from the previously discussed PAL data, a longitudinal study
of participants in various MAO groups, Timko and colleagues assessed the charac-
teristics of attendees and specifically the association of online meeting attendance
with substance use outcomes [78]. In this nationally representative sample of in-­
person participants of AA, Smart Recovery, WfS, or LifeRing, approximately two-­
thirds engaged in at least one online meeting. Participants who engaged in online
groups were more likely to utilize more than one type of MAO and at baseline felt
less efficacious about their ability to maintain abstinence from alcohol. Notably,
individuals who engaged in online meetings were less likely than in-person-only
participants to be abstinent at baseline. However, at the 12-month follow-up time-
point, there were no longer group differences in abstinence. The authors therefore
suggested that online participation may be helpful to individuals who are earlier in
134 A. Tom and K. Fruitman

their recovery process and may require more frequent and varied support to main-
tain sobriety.
When considering the various platforms on which patients can access MAO
meetings and other peer-based recovery services, there are studies characterizing
the utilization of recovery-specific social networks sites such as InTheRooms [79].
Through this platform, members can access virtual meetings, interact with peers
through live video conferencing, and post on discussion groups [79, 80]. One 2017
study found that participants interacted with the platform for an average of 30 min
per day, several times per week [79]. The features users most commonly engaged
with included virtual video meetings and brief daily meditations [79]. Another 2017
study specifically exploring virtual group engagement via InTheRooms found that
while most participants preferred a combination of in-person and videoconference
group attendance, some members exclusively accessed 12-step meetings through
the digital platform [80]. Both studies concluded that participants overall endorsed
perceived benefit from virtual InTheRooms engagement [79, 80]. Bergman and col-
leagues found that 83% of participants agreed that InTheRooms increased their
motivation for recovery and/or abstinence self-efficacy, and more than half of par-
ticipants reported that the platform decreased their cravings for drugs and/or alcohol
[79]. Similarly, Rubya and Yarosh found that participants perceived online meetings
“almost as useful” as face-to-face meetings [80]. However, the authors posited that
virtual engagement offered the convenience of remote participation and an increased
volume of offered meetings [80].
Notably, the COVID-19 pandemic accelerated the shift of peer-support meetings
to virtual platforms [13, 71]. For instance, following the onset of social-distancing
measures during the pandemic, SMART Recovery collaborated with governments
internationally to ensure the expedient provision of online groups [81]. One study
of SMART Recovery participants in Australia demonstrated that the COVID-19
pandemic saw the rise of online groups from 6 pre-pandemic to 132 [35]. In this
study, 91% of participants with both in-person and online experience found that
virtual meetings were “equivalent or better” [35]. Apart from a study of participants
in Narcotics Anonymous, which demonstrated that most members had a successful
transition to online meetings during the pandemic, there is limited data delineating
the role of the COVID-19 pandemic on MAO participation and its downstream
impact on SUD treatment outcomes [82].

10.5 Peer Recovery Specialists

While the extensive body of literature discussed in the present chapter explores the
utility of MAOs in the delivery of substance use treatment, it also highlights the
importance of engagement with peers during the recovery process. Although MAOs
have historically been responsible for the organization and delivery of peer support,
there is now growing appreciation for the role of peer recovery specialists (PRS) in
SUD treatment [52, 83, 84]. PRS are individuals in various stages of recovery with
experiential knowledge about life with an addiction. The peer specialist model
10 Alcoholics Anonymous, SMART Recovery, and Other Support Systems… 135

differs from mutual-help sponsorship, notably, in that the PRS is providing unidi-
rectional support to the client based on their training and lived experience, as com-
pared to the bidirectional support offered by participation in MAOs. PRS have been
successfully integrated in a variety of settings, including hospitals, emergency
rooms, jails, SUD treatment centers, and outpatient community environments [84].
Moreover, these programs have been demonstrated to be effective in improving both
connection to SUD outpatient treatment following detoxification and adherence to
SUD treatment following hospital discharge [29, 30]. Unsurprisingly, PRS can help
patients with SUD re-integrate into sober and protective support networks and
increase patient perceptions of “belonging” within a community [85].
Although a review of the extensive literature delineating the benefits of PRS is
outside the scope of this chapter, it is important to highlight the potential role of
PRS in strengthening mutual aid participation. Individuals in recovery often work to
disentangle from maladaptive relationships and triggering social settings, leaving
patients with SUD limited interpersonal support [86, 87]. Therefore, PRS are
uniquely positioned to leverage their experiential knowledge of recovery and their
own participation in treatment to help clients integrate into supportive and sober
communities, such as MAOs [87, 88]. PRS can speak to their experiences with
MAO participation and facilitate connection to groups, serving as a liaison between
medical or correctional environments and supportive community treatment options
[84, 87, 88]. Although there is limited quantitative evidence delineating the fre-
quency and success of connections to MAOs, specifically, there is data substantiat-
ing the role of PRS in improving treatment retention and improved relationships
with both providers and social supports [88].

10.6 Future Directions

There are various research questions within the study of mutual aid for alcohol use
that remain unanswered. For instance, a 2021 review article published by Zemore
and colleagues discussed the racial/ethnic disparities in MAO group participation
among patients with SUD [89]. The authors posited that racial/ethnic minority
groups experience barriers to engagement with mutual aid, including discrimination
among members and the concern that Christian-centric teachings are inconsistent
with personal beliefs. While some organizations have created culturally adapted
groups in an effort to contextualize a 12-step framework within culturally respon-
sive themes, not all individuals have access to these meetings or find groups that
appropriately represent their cultural/ethnic identities. In a review of 19 studies of
racial/ethnic differences in MAO participation, Zemore and colleagues found that
the studies were mostly outdated and lacking adequate representation of diverse
populations. Limited data existed for racial/ethnic minority groups beyond Black
and Latinx populations, emphasizing the need for more comprehensive research on
immigrants, women, adolescents, and various ethnic subgroups. Notably, while
studies generally did not strongly indicate racial/ethnic disparities in MAO partici-
pation, six studies highlighted Latinx-White disparities, particularly among Latinx
136 A. Tom and K. Fruitman

immigrants, emphasizing potential gaps in recovery-related services for the Latinx

population. The authors concluded that the paucity of literature discussing dispari-
ties in MAO participation among minority populations warrants further attention.
With regard to additional areas of future research, there is increasing awareness
of the utility of medication-assisted treatments for AUD, such as naltrexone (36).
Despite this, there exists limited available data concerning the perspectives and atti-
tudes of AA members toward medication-assisted treatment. Notably, AA does not
have an official stance on the use of medication [63]. However, individual AA mem-
bers may have various opinions on the role of medication in recovery. Notably,
some members view medication as a “crutch” that is contradictory to fundamental
AA tenants, while others perceive medication to be effective at treating the “symp-
tom,” but ultimately unable to address the root cause of problematic drinking [90,
91]. An article, derived from an anonymous survey conducted among AA members
in 2000, revealed that while over half of the sample had positive attitudes toward
relapse-prevention medications, almost a third of participants felt pressured to dis-
continue their medication during meetings [92]. Given the mounting evidence for
the use of medication to improve SUD outcomes, a more recent and comprehensive
study is necessary to examine the beliefs held by AA members [93]. Such a study is
essential for a deeper understanding of how MAOs, like AA, can adapt in response
to the evolving landscape of AUD treatment.

10.7 Conclusion

Alcohol misuse and Alcohol Use Disorder present substantial global and public
health challenges, with the latter contributing to 5% of the global burden of disease.
Beyond healthcare, it poses a significant social challenge, amounting to $250 billion
in societal costs. Addressing these challenges effectively and equitably requires a
multifaceted approach that encompasses both pharmacological and medical man-
agement alongside community-based and behavioral interventions. This chapter has
explored various modalities of peer support, ranging from participation in Mutual
Aid Organizations (MAOs), both in-person and virtual, to engagement with Peer
Recovery Specialists (PRS). Within MAOs, differences were drawn between Twelve
Step, Secular Non-Twelve Step, and Religious Organizations, underscoring the
diverse resources available for individuals seeking support. Additionally, the chap-
ter touched upon the significance of online engagement and the role of PRS in pro-
viding personalized support. It is evident that no one-size-fits-all, as individuals
navigating recovery have diverse needs and preferences. The long-standing tradi-
tion of integrating individuals at various stages of recovery within the Substance
Use Disorder (SUD) treatment framework underscores the importance of commu-
nity involvement in fostering resilience and enhancing outcomes [12, 33].
10 Alcoholics Anonymous, SMART Recovery, and Other Support Systems… 137

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Building a Life in Recovery: Aftercare
and Relapse Prevention 11
Maximilliam A. Cabrera and Bernadine H. Han

11.1 Defining Recovery

Recovery is often conceptualized by both patients and treaters as the final stage of
treatment in alcohol and other substance use disorders. While even healthcare pro-
fessionals may feel helpless or ineffective when it comes to addiction [1–3], studies
have shown that most people with a history of substance use disorders—75%
according to the 2018 National Survey on Drug Use and Health—eventually recover
[4, 5]. Many individuals manage this without treatment, even with a history of
severe substance use, and most individuals with severe substance use are likely to
“grow out” of these behaviors before reaching age 40 [6].
While recovery is a worthy goal, the focus on an endpoint—one that often
implies abstinence—may add an intimidating or discouraging element to what may
be more usefully conceptualized as an ongoing process of growth and change. As
are the experiences of use, misuse, and disordered use of substances, the process of
recovery can be affected, often profoundly, by stigma and shame. Alcohol, in par-
ticular, carries unique social and cultural characteristics among other substances of
abuse. Its combination of legality and widespread social acceptance, its well-known
and potentially fatal medical consequences, and its prevalent use and availability are
not approximated by another substance. These characteristics contribute to a recov-
ery experience that may differ from recovery from other substances. Individuals
who are actively drinking may fear or encounter judgment from family, social con-
tacts, and healthcare professionals [1–3] around their use. Similarly, those who are
actively seeking change in their drinking patterns may also fear and encounter judg-
ment around being someone who needs to stop, being someone who conspicuously
declines a drink, or being someone whom others might see as not being able to

M. A. Cabrera · B. H. Han (*)

New York Presbyterian Hospital–Weill Cornell Medicine, New York, NY, USA
Columbia University Center for Psychoanalytic Training and Research, New York, NY, USA
e-mail: [email protected]

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2024 143
M. Khan, J. Avery (eds.), From Stigma to Support, Psychiatry Update 4,
https://doi.org/10.1007/978-3-031-73553-0_11
144 M. A. Cabrera and B. H. Han

“handle their liquor.” Such anxieties can present significant psychological barriers
to one’s readiness to change, particularly among those individuals for whom alcohol
has been a prominent part of their social and professional activities. Beyond a
change in their drinking patterns, the first steps toward recovery may often feel as
much like defeat as the beginning of a positive change.
Recovery itself, historically defined by abstinence, has become a more ambigu-
ous term. The literature reflects various approaches to defining recovery from alco-
hol use disorder, often balancing the practical goal of allowing for measurable
research and clinical outcomes while acknowledging the substantial positive
changes that can be made to one’s life even without abstinence [7, 8]. In 2012, the
Substance Abuse and Mental Health Services Administration encompassed well-
ness, autonomy, and purpose in defining recovery as “a process of change through
which individuals improve their health and wellness, live a self-directed life, and
strive to reach their full potential.” The National Institute on Alcohol Abuse and
Alcoholism created a definition that better defines research outcomes and practi-
cally incorporates remission of DSM-5 criteria for alcohol use disorder along with
cessation of heavy drinking [9]. Redefining recovery using a criterion of cessation
of heavy drinking rather than complete abstinence was specifically informed by
harm reduction principles, an important approach to decreasing stigma among indi-
viduals struggling with and recovering from alcohol use disorders. We agree with a
perspective on recovery that combines an individual’s pursuit of a meaningful life,
remission from symptoms of alcohol use disorder, and cessation of heavy drinking.
That someone has not fully attained each of the three criteria does not exclude them
from being in recovery. Rather, we focus on a holistic process of improving one’s
life and functioning overall (Fig. 11.1).

Fig. 11.1 Defining

recovery. Our definition
focuses on the process of
improving one’s life and Pursuit of a
functioning meaningful life

Remission from
symptoms of
alcohol use
disorder

Cessation of
heavy drinking
11 Building a Life in Recovery: Aftercare and Relapse Prevention 145

11.2 Recovery and Meaning

It is in the process of engaging a patient toward recovery that we can discover with
them the important roles that alcohol (or other substances) played in their life. This
discovery also helps us recognize what our patient may fear will be missing and
what anxieties arise as they imagine their life without alcohol. As we all do, our
patients with alcohol use disorder may experience themselves at times to be inade-
quate, deficient, or lacking. Alcohol may temporarily quell difficult emotions,
bestow otherwise unfindable confidence, and dissolve interpersonal discomforts. In
repeatedly providing these functions over time, alcohol may have become the pri-
mary option among an increasingly limited range of alternatives available for the
patient who struggles to manage uncomfortable self-states or relationship chal-
lenges. Alcohol may take on a talismanic quality, or it may be a crutch; either way,
it comes to represent that without which the individual may feel they cannot meet
their life’s challenges. In this way, alcohol may fill in experiences of emptiness that
someone feels in various aspects of their life—family, intimacy, professional, spiri-
tual, or other areas—that fail to provide a greater sense of meaning and purpose.
Recovery will thus be a holistic endeavor that often benefits from a multi-faceted
approach to change. It is an ongoing process of creating the internal and external
structures that can both stabilize one’s response to painful and challenging experi-
ences and also provide new possibilities for coping and growing.
The role that alcohol plays in an individual’s life is similarly a variable of increas-
ing interest in the research literature. Studies have consistently found that the pres-
ence of meaning in a person’s life is inversely correlated with the severity of one’s
alcohol use disorder [10–12]. In contrast, searching for meaning in one’s life is
positively related to the severity of one’s alcohol use disorder. That is to say, lacking
meaning and having to search for it predict that an individual will experience a more
severe alcohol use disorder. Csabonyi and Philips [11] have likened this void of
meaning to Victor Frankl’s concept of an “existential vacuum” [13], creating a pain
for which alcohol offers a temporary remedy.
As we noted earlier, meaning can be derived from various areas of one’s life, and
it may come in different forms. We suggest that while not predicated on personal
accomplishment, meaning arises from a clear sense that one is actively engaged in
both their external and internal worlds, as well as the feeling that they are being
meaningfully engaged with in return. Individuals recovering from substance use
disorder may find meaning through the communal and spiritual components of
12-step programs such as Alcoholics Anonymous (AA) [14], which offer a way to
connect more deeply both to others and to oneself. Some may find this fulfillment
through different communities. Similarly, maintaining stable housing, deepening
and trusting in healthy relationships, exploring one’s faith, and engaging in purpose-
ful activity are all examples of ways to cultivate meaning [15]. These aspects of
meaningful experience inform the development of a comprehensive aftercare plan
and the supports that may benefit the individual who is working toward recovery.
Meaning also has a role when viewing how alcohol use fits into a patient’s life.
A psychodynamic approach proposed by Khantzian [16] organizes substance use
146 M. A. Cabrera and B. H. Han

disorders as disorders of emotions, of relations with oneself and others, and of self-­
care. Individuals who are susceptible to a substance use disorder often experience
themselves or their internal state as “too much” or “too vacuous.” Substances such
as alcohol can then play the role of numbing negative feelings or stimulating posi-
tive ones, depending on the amount consumed. At low doses, alcohol can promote
positive feelings and social connectedness, while at higher doses, its depressant
effects can be used as a sedative and an escape. These differing effects offer a way
to understand alcohol’s role in managing both one’s disordered self-experiences and
one’s fraught and difficult relationships. In more severe alcohol use disorders, a lack
of self-care is evident in one’s continued use despite medical consequences, whether
obvious (such as a hangover or withdrawal) or more easily kept far from one’s
awareness (such as worsening liver disease).
Another helpful theory in understanding the role and meaning of substances gen-
erally, and alcohol in particular, considers their function in the patient’s mind as an
internal object [17]. As the internal representations of others in an individual’s
mind, objects play a powerful role in our experiences of both ourselves and others.
Alcohol may play the role of an ever-soothing, ever-present object, thus providing
“a constant sense of being accompanied.” Even despite repeated negative conse-
quences, this experience can also cultivate a deep sense of comfort for someone who
may have returned to alcohol again and again when they felt alone. For such indi-
viduals, alcohol may supply a concrete and external sense of presence. Though
imperfect, this presence may have proven to be a dependable one, substituting for
what failed to become internalized from their parental or other caregiving objects
earlier in development. This model complements both the contemporary trends in
research identifying the hunger for substances among those who are searching to fill
a meaningful lack, as well as AA’s maxim that encourages participants to “rely on
people, not alcohol.”

11.3 Models of Relapse

Our current models of relapse describe the not infrequent return to use that typifies
periods of recovery. We will highlight three models here that are helpful in inform-
ing relapse prevention approaches (Fig. 11.2):

1. Marlatt and Gordon [18] outlined a cycle of lapse, relapse, and prolapse, in
which lapse refers to the first use of a substance (i.e., alcohol) after a period of
abstinence. Relapse indicates the period during which an individual has returned
to use after their initial lapse, while prolapse refers to the behavior change in the
direction of recovery and in the individual’s response to relapse, whether it be
abstinence or moderation. We also adapt these definitions to include moderated
and harm reduction approaches to heavy drinking, where lapse and relapse refer
to periods of heavy or uncontrolled drinking that may break patterns of more
moderated intake.
11 Building a Life in Recovery: Aftercare and Relapse Prevention 147

Lapse, Relapse, Cognitive-

Dynamic
and Prolapse behavioral

The first Abstinence-

Distal risk
return to a violation
factors
substance effect

Period of
Proximal risk
return to a
factors
substance

Behaviors
External
away from use
factors
of a substance

Fig. 11.2 Models of relapse. The three models of relapse presented with related concepts

2. The cognitive-behavioral model hinges on the significant impact of the absti-

nence violation effect (AVE) on relapse. Itself shaped by the influence of inter-
nalized stigma on the individual’s experience of recovery; AVE is the affective
and cognitive experience that an individual might have after breaking their own
rigid rules around recovery. While its name indicates abstinence as a treatment
focus, the AVE experience may also extend to moderation goals—not only
drinking when they were “supposed to be” abstinent but also drinking more
when they were only supposed to have one, for example. The AVE feeds an
experience of shame and guilt that runs the risk of ongoing relapse and unhealthy
or uncontrolled use. Examining a patient’s sense of failure over one night of
heavy drinking can be an important strategy both to mitigate the repercussions of
this episode and to build a sense of agency in affecting the circumstances that
might lead to future return to unwanted drinking. In looking more closely at the
contributing circumstances to the patient’s “rule-breaking,” we can work with
the patient to uncover the various personal, interpersonal, and environmental
contributors to their return to heavy drinking and create strategies to anticipate
and manage them in the future.
3. Witkiewitz and Marlatt [19] proposed a dynamic model that acknowledges the
complexity and randomness that underlie relapse. Recognizing the interplay of
stable background contributions from distal risk factors (such as family history
or years of use) with the more unpredictable and acute effects of proximal risk
factors (such as intense emotions or self-defeating thought processes) can
become a useful exercise for individuals in recovery, providing an ongoing
source of learning and self-understanding. This model accounts for the potential
profound effects of minor factors (e.g., passing a liquor store) that may have
contributed to a return to drinking while also identifying concrete affective,
behavioral, cognitive, and physical targets for ongoing treatment.
148 M. A. Cabrera and B. H. Han

11.4 Principles of Relapse Prevention

Relapse prevention begins with a collaborative assessment of the patient’s high-risk

situations for relapse. Triggers and their influence may vary significantly from per-
son to person, and a thorough assessment will also explore factors of personality
(e.g., distress tolerance, impulsivity), relationships (e.g., losses, high-conflict sup-
ports), environment (e.g., housing status, employment), and physiological/psychiat-
ric conditions (e.g., insomnia, anxiety, withdrawal).
Much of the work of relapse prevention focuses on personal factors of the indi-
vidual, i.e., the intrapersonal determinants (see Table 11.1), that play a significant
role in their ability to manage and respond to triggers to use. Many of these factors
may vary depending on the status of and strains imposed by other intra- or interper-
sonal factors. Changes in an individual’s outcome expectancies—i.e., one’s hopes
and expectations for what drinking will do or affect how one feels—can often pro-
vide a barometer for the sense of stress that a patient is experiencing. Alcohol may
be seen as repellent and disgusting when one is feeling more motivated for change
and sobriety, but it may seem to offer a tempting promise of relief after a fight with
a loved one. Exploring these outcome expectancies helps individuals gain insight
into both the vulnerabilities that lead to shifts in their own perception and more
expectable patterns of consequences.
Outcome expectancies strongly color an individual’s motivation—both their
motivation to change and their motivation to use. Motivational enhancement tech-
niques explore individuals’ ambivalence toward change and aim to increase their
ambivalence toward use by clarifying their values and how they might conflict with
their behaviors. High motivation to change is supported by building and strengthen-
ing one’s coping abilities. Coping involves both avoidance coping, through distrac-
tion, and approach coping, which relies on an individual’s abilities to confront,
accept, and reframe difficulties as they arise. Coping may be most helpful in manag-
ing one’s emotional states, which may have been regulated previously through alco-
hol alone. Developing an improved capacity for emotional regulation will directly
affect one’s feeling of self-efficacy, which is their sense that they can respond to a
situation in the way that they want. One’s self-efficacy can provide an important
sense of ability in responding to cravings, which are defined as the cognitive experi-
ence of wanting to drink. Medications, mindfulness, and coping skills can all con-
tribute to improved management of cravings, even without making them disappear.
It is not unusual for individuals with years of sobriety to continue to experience
cravings; many may have learned to approach these cravings with curiosity, helping

Table 11.1 Intrapersonal Outcome expectancies

determinants of relapse Motivation: For change vs. use
prevention Coping: Avoidance and approach
Emotional states
Self-efficacy
Cravings
11 Building a Life in Recovery: Aftercare and Relapse Prevention 149

them discover what emotional, interpersonal, or other needs may be arising for them
in the moment to trigger the craving.

11.5 Relapse Prevention Strategies

Relapse prevention (RP) has been demonstrated to be significantly better than pla-
cebo at treating alcohol use disorder, to mitigate the effect of relapse, and to increase
the duration of the positive effects of treatment [20]. Additional benefits have been
found for individuals who also suffer from comorbid psychiatric illness and in those
for whom substance use is more impairing affectively and physiologically [20].
Various supports can be incorporated into aftercare treatment to address these fac-
tors in different ways, including medications, AA, focused psychotherapies such as
DBT, and social work or vocational support. Relapse prevention uses cognitive-­
behavioral techniques to address self-defeating or maladaptive thought patterns,
expectations of positive experiences from returning to or continuing unhealthy use,
and management of negative affect states that may arise during periods of drinking.
Addressing interpersonal functioning has important benefits in relapse prevention
and may involve couples or family therapy. Building tools to manage unhealthy
social pressures and high-conflict relationships is central to relapse prevention
treatment.
Relapse prevention strategies target reductions in returns to drinking or heavy
drinking and the risk of sustained relapse. As a cognitive-behavioral approach, RP
focuses on the dynamic and fluid aspects of relapse risk and aims to help patients
develop insight by drawing connections between their thoughts, feelings, and life
circumstances as they relate to alcohol use. In developing this understanding,
patients can develop their cognitive and behavioral coping skills to create a greater
sense of self-awareness and self-efficacy when finding themselves in high-risk situ-
ations. Such situations often demand effective communication, and RP prioritizes
the development of communication skills that allow patients to build a healthy and
supportive social network while reducing contact with those who might impose
increased pressure to drink. Likewise, managing difficult emotional states, cravings
to drink, and unhelpful cognitive patterns are crucial treatment goals of RP. Role-­
playing, practicing a “script,” and brainstorming coping techniques in session are all
helpful approaches to building a sense of self-efficacy.
Working with the patient to bring awareness to their overall habits of health,
wellness, and meaning can also help them recognize the role of alcohol in their life
as a system versus an isolated behavior. This approach can facilitate the develop-
ment of new sources of aliveness, meaning, and connection that will further reduce
the importance of alcohol in their life. As with all substance treatment, there is no
treatment without engagement. Facilitating safety and openness with a nonjudg-
mental attitude fosters a positive therapeutic alliance and remains the basis of RP
and all treatment approaches.
150 M. A. Cabrera and B. H. Han

11.6 Conclusion

Recovery is not so much an endpoint as it is a process of improving one’s life and

overall functioning. Meaning plays a crucial role in an individual’s path to recovery
in different ways—meaning ascribed to alcohol, and the meaning one feels in their
connectedness with the world. Different models of relapse can be helpful in concep-
tualizing an individual’s recovery, whether as a linear journey, as a series of behav-
iors resulting from maladaptive thought patterns, or as part of a dynamic system of
factors and mitigators. Assessing a patient’s personality, environment, and physio-
logical/psychiatric conditions, as well as their expectancies, motivation for change,
and coping skills, is a key part of any Relapse Prevention approach. Medications,
mutual help, focused psychotherapies, and vocational supports can all be helpful
tools to facilitate an individual’s journey toward recovery.

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Stigma and Alcohol Use Disorder:
Overcoming Societal Attitudes 12
Michael Woods and Jonathan Avery

12.1 The Role Stigma Plays in Patients with AUD

Stigma in addiction can be defined as negative attitudes toward people suffering

from substance use disorders (SUDs) that ultimately impact the physical, psycho-
logical, social, and professional well-being of those individuals [1]. SUDs and AUD
have been identified by the World Health Organization as the first and fourth most
stigmatized medical condition worldwide, respectively [2]. In terms of AUD, stigma
has been found to both contribute to undertreatment and worsen physical and men-
tal health outcomes in this patient population [3] (see Fig. 12.1). Stigma against
patients with AUD can be seen in the language medical providers use when talking
about AUD, in the framework that the medical community uses to think about
addiction, and in the negative attitudes providers possess toward this patient
population.
Language plays an influential role in the generation of stigma. Smith et al. con-
tend that stigmatizing language shares certain characteristics that aim to distinguish
groups of people and to place personal responsibility for those individuals being in
a particular group [4]. Stigmatizing language is seen in many specialties within
medicine. For example, early on during the HIV epidemic, societal views toward the
illness were influenced by media reports labeling it as “the gay plague.” Such reports
placed blame on gay men and labeled them as the party responsible for the growth
of the epidemic [5]. Language used in the media to describe psychiatric illnesses
has had a similar effect. For example, patients suffering from certain mental ill-
nesses are often labeled as “maniacs, hysterics, lunatics,” which language ultimately
creates the false notion that psychiatric patients are violent people who are a danger
to society [6]. Language can have the same effect when used in reference to patients

M. Woods (*) · J. Avery

Department of Psychiatry, Weill Cornell Medicine – New York-Presbyterian,
New York, NY, USA
e-mail: [email protected]

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2024 153
M. Khan, J. Avery (eds.), From Stigma to Support, Psychiatry Update 4,
https://doi.org/10.1007/978-3-031-73553-0_12
154 M. Woods and J. Avery

Fig. 12.1 Stigma

feedback loop

Table 12.1 Number needed to treat (NNT) for medications used to treat chronic illnesses
Medication Chronic illness NNT
Naltrexone [33] AUD 12 (to return to heavy drinking)
Acamprosate AUD 9 (to return to any drinking)
[34]
ACE-I [35] Hypertension (HTN) 81 (to prevent non-fatal MI)
Metformin [36] Diabetes mellitus 14 (to prevent DM)
(DM)
Statins [37] Hyperlipidemia (HLD) 53 (to prevent heart attack in moderate-risk
patients)

with AUD. Specifically, when providers use language such as “alcohol abuser,” it
implies that patients have control over their illness and maintain responsibility for
their level of consumption [7]. In all three of these examples, the implications set
forth by using specific language contributed to stigma and discrimination toward
specific groups of people by inaccurately placing blame and responsibility on them
for merely having medical illnesses.
One issue that contributes to further stigmatization is that providers often forget
that AUD is a chronic illness with evidence-based treatment options (see Table 12.1).
Diseases like hypertension, diabetes, and hypercholesterolemia are screened at most
outpatient primary care visits. Most physicians fail to screen for AUD, however, on
the basis that such screening is not worth the time or effort [8]. One study even
found that most providers believed there was no adequate treatment for patients
with AUD in a primary care setting. Part of this belief might be a result of the fact
that 40–60% of patients that are treated for AUD or SUDs end up relapsing within
1 year [8]. This, in fact, would imply that addiction treatment is acute and curable,
rather than chronic and relapsing-remitting. Shifting expectations of addiction
12 Stigma and Alcohol Use Disorder: Overcoming Societal Attitudes 155

treatment and reminding providers to view it as a chronic medical illness will ulti-
mately lower the perception that treating patients with AUD is “a waste of time” [8].
Stigma can also be seen in how providers think about patients with AUD. Studies
have shown that attitudes of providers toward individuals diagnosed with AUD
might be worse than those toward those diagnosed with other medical and psychiat-
ric conditions [9]. These negative attitudes result in reductions in empathy displayed
toward patients during medical encounters and decreased personalization of patient
care [10]. Consequently, patients in this population end up experiencing worse treat-
ment outcomes [11]. Researchers have also documented that concerns about privacy
and being stigmatized often lead to patients opting to not disclose their alcohol use
and to not seek out treatment at all to avoid being labeled as “an addict” [12].
Patients not feeling comfortable speaking to their providers about their AUD, cou-
pled with providers failing to screen patients for AUD, partly explain why this ill-
ness is so vastly undertreated when compared to other chronic medical illnesses.

12.2 Understanding Where Negative Attitudes Come From

It has been established that AUD is prevalent, that there are many treatment options
available for patients, and that compared to other chronic diseases, it is undertreated.
This begs the question: why do providers have negative attitudes toward patients
with AUD? The answer to this question is, in part, due to lack of training in treating
AUD and lack of understanding of the science of addiction (see Table 12.2).
While there has been an effort to increase education for clinicians surrounding
the diagnosis and treatment of SUDs, research has demonstrated that physicians
often fail to identify AUD, particularly in its early stage, and feel ill-equipped to do
so due to inadequate training and perceived lack of skill [13]. Patients suffering
from AUD also have multiple medical and psychiatric comorbidities and sequelae
associated with their AUD. Thus, physicians in all specialties are likely to encounter
a patient with AUD. This places physicians in a position to prevent the progression
not only of the medical and psychiatric sequelae but also of the AUD itself.
Unfortunately, due to the lack of adequate understanding by many medical profes-
sionals about how to diagnose and treat patients with AUD, these patients remain
undertreated.
Another possible explanation for the existence of stigma in addiction is provid-
ers’ lack of understanding of the science behind it. Traditionally, two models have
been used for centuries to understand addiction: the moral model and the disease
model. More recently, a third model has been developed and is now widely used as
a framework for addiction: the biopsychosocial model. Despite the extensive

Table 12.2 Some factors Clinical experience primarily with individuals with severe
that worsen clinicians’ AUD
attitudes toward individuals Lack of exposure to individuals in recovery
with AUD Perception of alcohol misuse as a moral failing
156 M. Woods and J. Avery

knowledge that exists about the science of addiction, many providers still see addic-
tion as a moral failing and completely within an individual’s control [1]. Below is a
summary of the three models that exist in today’s literature about the nature of
addiction: the moral model, the disease model, and the biopsychosocial model [15].

12.3 Medical Models of Addiction

12.3.1 The Moral Model

The moral model frames addiction as a failure of morality or personal responsibility

[16]. It creates shame and embarrassment for the patient and ultimately decreases
the probability that they will seek treatment, as it is not viewed as a neurobiologi-
cally based illness. Rather, patients are perceived as dangerous and blameworthy,
partly because of the illicit nature of certain substances and the loss of control that
results from acute intoxication [16].

12.3.2 The Disease Model

The disease model, on the other hand, frames addiction as a brain-based illness that
is based on biology, genetics, and neuroscience [17]. This framework considers
addiction to be a brain disease that causes patients with SUDs to have little choice
when seeking and/or using substances [18]. There has been extensive research in the
neurobiology of addiction that indicates that it is a brain-based illness, rather than a
moral failing on the patient’s part. While each substance acts differently on the
brain, and each person has a different set of genetics and environmental influences
that might influence his or her addiction, there is a fundamental similarity that all
types of addiction share. That is the change in an individual’s reward circuit in the
brain [14]. Alcohol (as well as other substances) increases dopamine in the nucleus
accumbens, which alters the connection between the limbic system (where reward
and pleasure are implicated) and the prefrontal cortex (where decision-making and
planning occur). Patients with alterations in this circuit are more likely to engage in
riskier behaviors to achieve a desired goal, such as drinking alcohol [14]. Viewing
addiction within the framework of the disease model, rather than the moral model,
has concrete effects on stigma. One study aimed to assess lawyers’ and doctors’
views of the disease model and how it relates to their attitudes toward patients with
SUDs. This study found that rejecting the disease model of addiction was associated
with more negative attitudes toward individuals with SUDs. Moreover, doctors were
more likely to view these patients as having “control” than lawyers were, highlight-
ing the stigma that exists in the medical field relative to another professional
field [18].
12 Stigma and Alcohol Use Disorder: Overcoming Societal Attitudes 157

12.3.3 The Biopsychosocial Model

While the disease model has helped reduce stigma toward patients with AUD by
providing an alternative to the moral model, it does run the risk of being reduction-
istic and possibly reducing hope that patients have any control over their own recov-
ery [1]. The most recent model developed, called the biopsychosocial model,
recognizes addiction as a brain-based disease that also incorporates one’s psychol-
ogy and environment when thinking about how addiction ultimately develops in that
person [19]. Considering AUD from the context of the biopsychosocial model
allows for a more holistic and nuanced understanding of how a patient experiences
addiction.
Let’s consider a patient, who we will call AB, as an example of someone with
AUD. AB presents to his primary care physician with right upper quadrant abdomi-
nal pain. He is found to have elevated liver enzymes and, upon further questioning,
says he has increased his alcohol intake from three beers nightly to ten beers nightly.
He says that both his father and uncle have AUD and have been to inpatient rehabili-
tation facilities on multiple occasions. When asked about why he drinks every eve-
ning, he says that it helps him feel better about work-related stress, where he often
feels he is not good enough at his job. He also experiences financial stress and wor-
ries that if he does not get promoted, he will not be able to provide for his family.
While he finds that alcohol relieves his stress, he has tried to cut down because he
does not like his behavior while intoxicated around his wife and children. Despite
attempts to reduce his intake, AB has not been able to cut down. Patient AB’s case
can be used to illustrate how the biopsychosocial model can formulate a patient with
AUD holistically. From a biological perspective, there are multiple factors to con-
sider in AB. Firstly, AB might have a genetic predisposition for addiction as evi-
denced by two family members having AUD. Secondly, he likely is experiencing
tolerance for alcohol given his increase in consumption. Thirdly, he could be expe-
riencing withdrawal upon cessation/reduction of alcohol use given his difficulty
cutting down. From a psychological perspective, AB seems to be using alcohol as a
way to improve his insecurity about feeling inadequate at his job. Socially, AB
seems to have financial stressors that are contributing to his alcohol use. While uti-
lizing the disease model over the moral model helps reduce stigma, the biopsycho-
social model takes the medical model one step further by also considering how risk
factors from a larger psychological and social context might be contributing to a
patient’s addiction.

12.4 Does Medical Training Increase or Decrease Stigma?

While it might make sense that with more medical training, providers might be less
likely to possess stigma toward patients with AUD, there is evidence to suggest the
opposite: stigma may increase as medical training progresses. One study
158 M. Woods and J. Avery

investigated how psychiatry residents’ attitudes toward patients with SUDs changed
throughout their residency training, and it found that they actually worsen over time
[20]. The authors suggest that one possible reason for this might be lack of exposure
to individuals in recovery [20]. Providers often encounter patients with AUD in
acute settings where they might be intoxicated, not interested in treatment, and in
need of urgent psychiatric or medical services. These repeated, negative experiences
might, over time, taint a provider’s view about what addiction looks like, as those in
recovery or further along in the treatment process might not present in these acute
settings [1]. Another issue is that medical schools might not emphasize education in
addiction during training, and thus, providers report feeling uncomfortable in their
abilities to treat patients with AUD [21]. Furthermore, while the high rates of relapse
for addiction are comparable to other chronic illnesses, treatment of these relapses
tends to be in the form of brief, episodic interventions rather than long-term disease
management the way it might be for other chronic illnesses [22]. Ultimately, inad-
equate training results in inadequate treatment for patients with AUD.

12.5 Lack of Insurance Coverage for Treatment of AUD

While treatment for AUD does exist, one major barrier worth mentioning is diffi-
culty accessing treatment due to lack of insurance coverage [22]. Insurance compa-
nies are expected to cover addiction treatment, yet many patients with AUD still
face high costs and lack of coverage. AUD is covered less adequately than other
healthcare services, and patients with AUD face greater difficulty accessing in-­
network treatment than other types of medical treatment, which ultimately leads to
higher out-of-pocket costs [23]. The Mental Health Parity and Addiction Equity Act
of 2008 requires coverage for mental health and SUDs to be equal to the coverage
of other medical conditions [24]. Additionally, the Patient Protection and Affordable
Care Act of 2010 required covered plans to offer SUD benefits as an Essential
Health Benefit [25]. While both programs ultimately led to increased treatment of
mental health disorders, addiction treatment did not see a comparable change. This
disparity is, in large part, due to the perception that addiction treatment is too expen-
sive despite the fact that untreated addiction is far more expensive to society than
the treatment itself [26].

12.6 How to Tackle Stigma in Patients with AUD

While tackling the problem of stigma in addiction is difficult, there are many
changes that can start the process (see Table 12.3). One way is through medical
education. One study aimed to improve internal medicine residents’ attitudes with
an educational seminar that incorporated perspectives from patients with various
forms of addiction, including AUD. This study noted that most addiction medicine
12 Stigma and Alcohol Use Disorder: Overcoming Societal Attitudes 159

Table 12.3 Strategies to Increase awareness of negative attitudes

improve clinicians’ attitudes Provide forums to discuss common attitudes
toward individuals with AUD Continue to increase and improve addiction treatment options
Intervene at all levels of professional training development

curricula focus on knowledge and skill-based content, rather than stigma. They
found that exposing medical residents to personal experiences of patients with AUD
improved their attitudes toward this patient population, and this finding was sus-
tained 6 months following the study [27]. Another study found that being aware of
the negative attitudes that providers have toward patients with AUD can be helpful
for early trainees [28]. Ballon and Skinner created a curriculum for an addiction
rotation that made trainees aware of the stigma that exists in addiction, offered
didactics about the illness and treatment options, and fostered discussions where
students had the opportunity reflect on their experiences treating patients with
addiction. The results of this study demonstrated that these actions helped curb the
worsening of attitudes that takes place over time in a provider’s medical training
[29]. In addition to these studies, a recently published Letter to the Editor in
Academic Psychiatry discusses the use of affective computing and emotional artifi-
cial intelligence by medical students to help improve empathetic communication
toward patients with SUDs [30]. The article discusses the creation of a computer-
ized program that records students interacting with virtual patients with SUDs and
then simultaneously analyzes their facial expressions to provide feedback in real
time. This research is ongoing and aims to reduce stigma in future providers.
Another important change that can be used to combat stigma in addiction is
changing language used when referring to patients with AUD. Researchers demon-
strated this in a study where therapists were asked to make treatment recommenda-
tions after reading a clinical vignette. Half of the participants were assigned a
description of the patient using the terminology “substance abuser,” and the other
half were given the same vignette but with the terminology “person with a substance
use disorder.” Those who received the vignette with “substance abuser” were more
likely to recommend punitive interventions than medical ones [31]. The difference
in the above phrases has to do with how one views addiction: as a moral failing that
one is responsible for or as a disease with which one is afflicted.
One aspect of stigma that is critical to consider is how it might differ across dif-
ferent cultures. For example, a Letter to the Editor in Academic Psychiatry dis-
cussed how cultural views in the Middle East and North Africa influence the
perception of patients with SUDs [32]. It offers possible methods to reduce stigma
through narrative storytelling, where patients with SUDs engaged with medical stu-
dents in the region to discuss how stigma impacts their recovery and treatment.
While there was not enough data in the study to adequately measure changes in
attitudes after this intervention, the article suggests replicating this study with more
participants to support their qualitative finding that this method of education helped
reduce stigma toward patients with SUDs.
160 M. Woods and J. Avery

12.7 Conclusion

AUD is a prevalent, chronic medical illness that can be treated effectively by a num-
ber of therapeutic modalities. Treatment is critical, given the myriad of medical and
psychiatric comorbidities and sequelae that result from untreated AUD. Despite
this, AUD is significantly undertreated when compared to other chronic diseases.
This may be due to the stigma patients with AUD face in the medical community.
While AUD is a disorder of addiction, and often falls under the purview of psychia-
try, patients end up seeing providers across all specialties due to the aforementioned
sequelae. It is thus critical that addiction education, including education about
stigma, begins early in medical training so that patients with AUD interfacing with
providers across all specialties feel comfortable seeking treatment.

12.8 Didactic Component

1. Figure 12.1 [1] illustrates the stigma feedback loop. Stigma toward patients with
addiction might lead to sub-optimal care. This, in turn, worsens treatment out-
comes, which mistakenly leads some providers to believe addiction treatment is
not efficacious, thus increasing stigma.

2. Table 12.1 illustrates the number needed to treat (NNT) for various medications
used to treat common chronic illnesses. Notably, medications used to treat AUD
have lower NNTs in the above table, when compared to HTN, DM, and HLD.

3. Table 12.2 [1] illustrates several factors that contribute to the worsening of clini-
cians’ attitudes toward individuals with AUD.

4. Table 12.3 [1] illustrates possible strategies to improve clinicians’ attitudes

toward patients with AUD.

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editors. Disability and culture: universalism and diversity. Seattle: Hofgrebe & Huber; 2001.
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Physicians and Alcohol
13
Jeffrey A. Selzer and Robyn L. Hacker

13.1 Alcohol in Medicine

Alcohol1 has a long presence in the history of medicine. For centuries, medicinal
claims have been made for alcohol [1]; it has been used as a digestive aid, as a seda-
tive for mothers during labor, and as an anesthetic during surgery [2]. It is still
widely used as an antiseptic in hand sanitizers, an important component of patient
safety in healthcare settings.
Beyond medicinal use, health benefits, particularly related to moderate alcohol
consumption, have also been reported. What was once believed to be a benefit to
cardiovascular health is no longer clear with closer scrutiny and reanalysis [3].
Confounding variables such as other positive health practices in moderate drink-
ers [4] as well as past histories of problematic drinking in those cross-sectionally
abstinent at a later time complicate correlations previously reported. The World
Health Organization has concluded that there may be no safe dose of alcohol [5].
Given this, questions about the personal consumption of alcohol in any quantity by
medical students, physician trainees, and physicians are justified. Although
physicians’ attitudes toward patients with alcohol use disorders have been studied,

1
In this chapter, the term “alcohol” means ethyl alcohol.

J. A. Selzer (*)
New York State Committee for Physician Health, Albany, NY, USA
Northwell Health Physician Resource Network, New Hyde Park, NY, USA
Department of Psychiatry, Donald and Barbara Zucker School of Medicine at Hofstra/
Northwell, Hempstead, NY, USA
Department of Psychiatry, Albert Einstein College of Medicine, Bronx, NY, USA
e-mail: [email protected]
R. L. Hacker
Department of Psychiatry, University of Colorado School of Medicine, Aurora, CO, USA

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2024 163
M. Khan, J. Avery (eds.), From Stigma to Support, Psychiatry Update 4,
https://doi.org/10.1007/978-3-031-73553-0_13
164 J. A. Selzer and R. L. Hacker

there is little information about physician attitudes toward physicians’ personal use
of alcohol.
Physicians do safety-sensitive work. Safety-sensitive jobs are ones where
impaired performance can result in incidents which affect the health and safety of
others. In the case of physicians, impairment, the loss of ability to practice with
reasonable skill and safety due to illness [6], can affect the health and safety of
patients. Impairment due to alcohol and other drug use is a frequent cause of licens-
ing action by state medical boards (SMB), and, in most states, physicians are man-
dated to report impaired physician colleagues to SMB. Physicians who work in
settings which implement pre-employment drug testing as part of federal drug-free
workplace standards typically are not subject to alcohol testing because alcohol is
legal for adult consumption and testing for alcohol is not mandated in federal pre-­
employment regulations. The extent to which screening for alcohol use with the
possibility of brief intervention and referral for treatment (SBIRT) occurs for physi-
cians during the pre-employment process or at subsequent points in their careers is
unknown. For-cause testing, defined as testing prompted by a reasonable cause to
suspect impairment, often includes breath or blood testing for alcohol, given the
correlation between alcohol concentrations in these matrices and impairment.
Alcohol is also a part of the medical culture for celebratory events. Beyond a
tradition of reward with alcohol after completion of exams and clinical rotations
among medical students and physician trainees, they were once invited to what was
termed “liver rounds” in physician training settings. At these events, alcohol was
freely available, and its use was often encouraged and modeled by physician teach-
ers. Newer evidence about alcohol’s negative impacts on health at any dose might
prompt a reassessment of the role of alcohol in medical celebrations. Given the
tradition of alcohol use in celebratory medical events, organized medicine may be
promoting a culture of alcohol consumption and over-consumption. To the extent
that alcohol has become a means for medical students, physician trainees, and phy-
sicians to relieve stress inherent in medical training and practice, it has also become
part of medical culture.

13.2 Alcohol Curriculum in Medical School and Residency

and Fellowship Training Programs

The curriculum related to alcohol is set by medical student and physician trainee
accreditation organizations, the Liaison Committee on Medical Education and the
Accreditation Council for Graduate Medical Education, respectively. It is not clear
to what extent this curriculum focuses on personal alcohol use by physicians and
trainees as well as alcohol use by patients, even in the context of increased attention
to the well-being of medical students and residents. Medical schools and residency
and fellowship training programs need to publicize clear pathways to access confi-
dential help if alcohol use is causing problems in a student or physician trainee’s
personal or professional life. A study of medical student handbooks showed high
rates of failure to comply with standards set by the Association of American Medical
13 Physicians and Alcohol 165

Colleges for providing information on help for personal substance use problems [7].
Concerns may vary by specialty, too; given relatively high rates of substance use
disorders (SUD), particularly opioid and sedative-hypnotic use disorders, in anes-
thesiologists, specific prevention curriculum has been developed and implemented
for anesthesiology residents [8]. It is unclear what impact this curriculum has had
on anesthesiologist substance use or whether alcohol use has been given sufficient
attention given concerns regarding other drugs to which anesthesiologists have
unique access. There is a need for alcohol and other substance misuse prevention
interventions for physicians at every point in their professional life cycle and a cor-
responding need to develop a better evidence base for such interventions.

13.3 Alcohol Use Epidemiology in Physicians

A recent review of the epidemiology of problematic drinking in physicians con-

cluded that studies which should be informative are hampered by lack of consis-
tency in definitions and interpretation of the results of standardized instruments.
These instruments which rely on self-report may also not give an accurate picture of
the true prevalence in physicians when compared with other data sources [9]. An
understanding of these limitations needs to inform conclusions about the validity of
the following studies.
Available studies conclude that as is true in the general population, alcohol is the
drug most used by medical students, physician trainees, and physicians. High rates
of binge drinking, as defined by the National Institute on Alcohol Abuse and
Alcoholism (NIAAA),2 have been found in medical students and physician trainees.
Most medical students drink regularly, and approximately one third binge drink
[10], although in a study of Florida medical schools, 70% of students reported binge
drinking [11].
A study of primary care residents found 49% engaged in binge drinking, and for
18% this occurs monthly [12]. The authors of this study recommend that personal
alcohol use surveys be implemented as well as SBIRT training in primary care resi-
dencies. Binge drinking is associated with experiences of belittlement and harass-
ment in medical students [13], and students whose Alcohol Use Disorders
Identification Test (AUDIT) scores place them in the range of DSM-IV diagnoses of
alcohol abuse or dependence were more often depressed or experiencing burn-
out [14].
Because binge drinking is defined as a threshold measure, we do not know how
much of what is categorized as binge drinking may, in fact, be “extreme binge (or
“high-intensity”) drinking,” defined as twice the gender-specific binge drinking
threshold [15]. Screening for binge drinking could help identify students and

2
A pattern of drinking in which males have five or more standard drinks and females have four or
more standard drinks in a drinking episode lasting about 2 h. The resulting blood alcohol content
(BAC) levels are typically 0.08.
166 J. A. Selzer and R. L. Hacker

physician trainees who would benefit from more specific diagnostic interviews and
further intervention.
More data are available for physicians whose drinking is “hazardous” or places
them “at risk” compared with data available for physicians with alcohol use disor-
ders [9]. A study of surgeons [16] using self-reported AUDIT scores found a point
prevalence rate for alcohol abuse or dependence of 13.9% for male surgeons and
25.6% for female surgeons. In addition, as with medical students, surgeons with an
alcohol use disorder were more likely to be depressed or experiencing burnout; they
were also more likely to report a major medical error in the 3-month period before
completing the survey. The same findings were replicated in a study of physicians
from a variety of specialties, including greater numbers of female physicians diag-
nosed with alcohol abuse or dependence [17]. Suicide is reported to be more com-
mon for women compared with male physicians although rates are higher than for
the general population across genders [18]. Given rates of problematic alcohol use
reported by female physicians, alcohol may be a contributing factor to elevated
suicide rates in female physicians as much as it may for women in the general popu-
lation [19].
Physicians are fearful of coming forward for help related to problems with alco-
hol due to privacy concerns and the possibility of negative professional conse-
quences, including the possibility of disciplinary action because of asking for help
[20]. This fear is present in medical students and physician trainees who also fear
negative professional consequences if identified as a person who had or has prob-
lems with alcohol. Newer evidence is encouraging that medical students and resi-
dents are making better use of mental health resources [21]; however, it is likely that
the large gap between need for treatment and provision of treatment noted in the
general population is present in the physician population, even for those who have
mental health insurance coverage [22].
Given fears about help-seeking, raising awareness about the extent and conse-
quences of alcohol misuse in physicians may not be sufficient as a preventative
measure. Medical students, physician trainees, and physicians can be offered anon-
ymous screening opportunities such as those provided by the AUDIT website [23].
This could be followed by facilitated access to confidential Screening, Brief
Intervention, and Referral to Treatment (SBIRT). The evidence for the effectiveness
of SBIRT is better for alcohol than it is for other drugs [24]. Brief interventions for
individuals whose goal is to drink more safely may include moderation manage-
ment [25], an approach which may be supported by digital therapeutics [26].
Whatever brief intervention is offered, follow-up with reassessment is advisable.

13.4 Assessment and Treatment of Alcohol Use Disorder

If a diagnostic interview results in a diagnosis of an alcohol use disorder, or if col-

lateral history obtained from others indicates there is good reason to suspect that an
individual has an alcohol use disorder, a prompt, comprehensive assessment is
advantageous. Impairment is defined by the Federation of State Medical Boards
13 Physicians and Alcohol 167

Studies of alcohol use in physicians

Study
subjects and
study Study method Important findings
Medical students
Ayala et al. Survey of 855 medical 33.8% reported binge drinking in past 2 weeks;
(2017) [10] students from 49 students reported serious consequences of substance
medical schools use; 40% unaware of relevant school policies
Merlo et al. 1137 medical students 70% endorsed binge drinking; 70% felt they would
(2017) [11] from 9 Florida medical benefit from mental healthcare and 39.8% accessed
schools who completed help
a questionnaire
Frank et al. Surveys at start of first Students who reported the highest rates of harassment
(2006) [13] year, before clinical and belittlement were more likely to binge drink as
rotations, and during well as feel depressed and suicidal
final year for 2316
students in 16 medical
schools
Jackson et al. 4402 medical students 32.4% met criteria for alcohol abuse/dependence (did
(2016) [14] throughout the USA not report % in either diagnosis); alcohol diagnosis
surveyed with validated associated with burnout, depression, being unmarried,
tools including the and higher school debt
AUDIT-C
Physician trainees
Greene et al. 221 primary care 49% reported binge drinking in previous year, 18% at
(2017) [12] residents (family or least once per month; resident confidence in SBIRT
internal medicine) did not vary by personal drinking history
surveyed as part of an
SBIRT training program
Physicians
Oreskovich 7197 surgeons surveyed Alcohol abuse/dependence point prevalence rate of
et al. (2012) with validated tools 13.9% in males and 25.6% in females (did not report
[16] including the AUDIT-C % in either diagnosis); alcohol diagnoses more likely
in surgeons who were depressed or burned out
(especially in domains of emotional exhaustion and
depersonalization); surgeons with an alcohol
diagnosis more likely to report a “major medical
error” in the 3 months prior to the survey
Oreskovich 7288 US physicians Although misuse of prescription drugs or use of
et al. (2015) from all specialty illegal drugs was rare, alcohol abuse/dependence
[17] disciplines surveyed point prevalence rate of 12.9% in males and 26.7% in
with validated tools females (did not report % in either diagnosis); alcohol
including the AUDIT-C diagnosis associated with burnout, depression,
suicidal ideation, lower career satisfaction, and recent
medical errors

(FSMB) as “the inability of a physician to provide medical care with reasonable

skill and safety due to illness or injury [27].” The FSMB further states that the defi-
nition applies not only to licensed physicians “but also medical students, residents
and fellows, and those seeking licensure.” Although not every case of alcohol use
disorder results in impairment, when impairment is suspected, it is especially
168 J. A. Selzer and R. L. Hacker

prudent to ask the individual to stop working until an assessment can be completed.
Diagnosis and treatment needs should be clarified, and treatment implemented, if
indicated. Asking a medical student, physician trainee, or physician to stop working
until the assessment can be completed may not only protect the safety of patients; it
may also protect the student’s, trainee’s, or physician’s career.
A comprehensive evaluation is best performed by an addiction specialist physi-
cian or other licensed expert addiction clinician (e.g., PhD psychologist) who does
not have a treating relationship with the individual needing assessment and may
therefore provide an independent medical evaluation (IME). Whoever undertakes to
complete this evaluation needs to understand which professional consultations will
be a necessary part of the process. To preserve the privacy of personal medical infor-
mation, it is best that the evaluator maintain confidentiality and not report the find-
ings of an IME directly to a state medical board (SMB), unless the request for an
evaluation comes from the SMB and a release of information is in place and current.
A concerned, empathic division head, training program director, or physician col-
league may unwittingly collect “smoking guns” when intervening with a physician
of concern; this can compel direct reporting to the SMB because the findings are
learned outside of a confidential, protected relationship. An experienced evaluator
has an appreciation for the sensitivity involved in this type of assessment and
thoughtfully considers who has a need to know the findings and which findings to
share. Reporting responsibilities should also be made clear to the student, physician
trainee, or physician at the beginning of the assessment process. It is good practice
for the evaluator to obtain consent from the examinee for anyone who provides or
receives information related to the IME. For example, if a physician is referred by
an institution with an employee health service (EHS), the evaluator may be asked to
disclose diagnostic information to the EHS. However, the EHS may maintain the
confidentiality of this diagnostic information from the rest of the institution. All par-
ties involved must understand the regulations which govern confidentiality and
reporting responsibilities within their respective states.
A comprehensive evaluation should result in diagnostic clarification, recommen-
dations for a treatment plan if indicated, and determination about whether the
referred individual should be allowed to return to work after completion of the ini-
tial assessment, after successful treatment and/or after re-assessment.
The following are components of high-quality IMEs:

1. Context for evaluation: Provides clarity on what led the individual to the evalu-
ator; include both events and behaviors.
2. Psychiatric history: Details historical and present psychiatric symptoms, diag-
noses, and treatment. It should include medications and types of psychotherapy,
duration of treatments, and response to treatments.
3. Assessment of substance use and substance use disorders: A comprehensive
substance use history from initial use to present, including all substances used
and inquiry about substances to which physicians have unique access such as
propofol, is necessary to obtain an accurate clinical picture. Standardized,
structured assessment tools such as the Addiction Severity Index [28] and the
13 Physicians and Alcohol 169

Structured Clinical Interview for DSM [29] can help obtain and organize this
information. This section should also include a review of current and previous
SUD treatment, types of treatment including medications, and treatment
settings.
4. Medical history: A comprehensive medical history including current personal
health practices and medical consequences of substance use is important.
5. Family history: A comprehensive family history of substance use disorders,
other psychiatric illnesses, past and present interpersonal family dynamics, cul-
tural practices, and perceptions of help seeking provide context for the
evaluation.
6. Professional history and current functioning: Details the individual’s training
and past and present work experiences. Important historical points are periods
where work, education, or training was interrupted and if the individual was
ever placed on remediation or probation. An examination of personal satisfac-
tion with their professional responsibilities and an assessment for burnout is
pertinent.
7. Social functioning and network: This section should include relationship his-
tory, status of significant relationships—supportive and unsupportive—social
support and social activities, social stressors, usual leisure activities/hobbies,
spiritual life, and engagement with mutual support communities.
8. Legal/regulatory involvement: Review legal/regulatory involvement with col-
lateral contacts and through searches on pertinent websites (e.g., those main-
tained by SMBs).
9. Mental status exam: Provides data on the individual’s appearance, behavior,
motor activity, speech, mood, affect, and thought processes observed through-
out the evaluation period.
10. Psychological and neuropsychological tests: While not included in all assess-
ments, they are often recommended for people in safety-sensitive occupations.
They can provide more objective data about personality constructs, cognitive
performance, motivation for change, and response style. Medical students, phy-
sician trainees, and physicians are highly intelligent, and their strong verbal
intellectual abilities can mask mild to moderate cognitive deficits in domains
commonly impacted by harmful alcohol use. Test results, whenever possible,
should be compared to sample norms with similar education level and age as
the individual being evaluated. In addition, the specialty of the person being
evaluated should be considered in test interpretation.
11. Laboratory tests: These are important to assess substances used and their medi-
cal consequences, such as liver disease in the case of alcohol. Biomarkers for
alcohol use such as phosphatidyl ethanol and ethyl glucuronide are useful to
corroborate self-reports of both reported use and abstinence.
12. Collateral information: Should be obtained from multiple sources (e.g., treat-
ment providers, family and friends, colleagues, oversight organization) and
used to corroborate self-report data across the other components of the
IME. Without the inclusion of collateral information, evaluators are more likely
to make inaccurate conclusions and to complicate the return-to-work process.
170 J. A. Selzer and R. L. Hacker

13. Diagnostic impression: Presents the formal diagnoses and specific diagnostic
criteria met to justify the diagnosis.
14. Recommendations: Include recommendations about specific types and antici-
pated duration of treatment and the level of care in which treatment should
occur [30]. This section should also include whether examinees can safely
return to work or what is needed prior to that occurring. For all individuals,
recommendations for appropriate toxicology testing are helpful.

A tradition of physicians being sent to specialized inpatient or residential pro-

grams for evaluation and initial treatment persists. This tradition is based on a belief
that clinicians with extensive experience working with physicians perform better
assessments and that a multidisciplinary assessment, which is easier to obtain in a
multidisciplinary setting, adds significant value to the evaluation. It is also believed
that removing physicians from their typical environment helps them focus on them-
selves and their personal needs and to engage in the assessment and subsequent
treatment process if treatment is indicated. Furthermore, it provides the opportunity
to observe the individual outside of the examination room. Part of assessment and
initial treatment at specialized treatment programs may come from interactions with
peer physicians also in treatment for SUD, particularly from group therapy interac-
tions. This tradition is often viewed as part of what has become known as the
Physician Health Program (PHP) model [31].
PHPs emerged in the 1970s as a pathway for physicians impaired by SUDs to
obtain evaluation and treatment through a confidential and non-disciplinary path-
way. PHPs were established as part of a movement within the American Medical
Association (AMA) to identify and assist “The Sick Physician,” physicians impaired
by “psychiatric disorders, including alcoholism and drug dependence” [32]. To bal-
ance the important goals of protecting the public’s “assurance of competent care to
patients by physicians” and providing “the effective treatment and rehabilitation of
the physician-patient so that he can be restored to a useful life,” the AMA recom-
mended that state medical societies establish programs to identify and treat impaired
physicians.
PHPs currently operate in 47 states, the District of Columbia, and in Canadian
provinces. Confidentiality for participants is seen as a critical factor not only to
encourage self-referral but to encourage physicians to refer colleagues to PHPs.
PHPs typically do not provide treatment but rather provide a case management
function. An important feature of PHPs is the central role they play in monitoring
response to treatment and in attesting to a PHP participant’s fitness to practice on an
ongoing basis. The relationship between a PHP and the SMB varies by state, par-
ticularly with respect to what the PHP is expected to report to the state and which
circumstances require reporting. In some states, the PHP is operated by the
SMB. Even in states with SMBs which offer complete confidentiality for compliant
participants, participant non-compliance may require the PHP to report the partici-
pant to the SMB. SMBs in many states have enough confidence in PHPs that refer-
rals are often made from the board to the PHP for monitoring. Physicians who have
suspended or revoked medical licenses due to impairment as a type of professional
13 Physicians and Alcohol 171

misconduct also enroll in PHPs to benefit from PHP advocacy at license restoration
hearings; the foundation of this advocacy is the PHPs assessment of the physician’s
fitness for duty based on evaluations informed by monitoring over time.
The success of the PHP model was evaluated in an influential study of 16 PHPs
by McLellan et al. [33]. The methodology involved a retrospective record review of
outcomes for PHP participants. Because monitoring agreements were typically for
5 years, objective evidence of abstinence through continuous toxicology monitoring
could be obtained. The final sample included 802 physicians and, for those who
completed 5 years of monitoring, 78% never had a positive urine test over the 5-year
monitoring period. These impressive results are among the best reported in the SUD
treatment literature. The study also reported other positive outcomes including a
much lower rate of license action taken against those participants who completed
their PHP agreements.
Important limitations inherent in this retrospective study must be noted, however.
It is after all a study of physicians who entered PHPs, and this may have introduced
a sampling bias which excluded more severely ill physicians or those without the
resources to enter the PHP model of care at the time of the study (e.g., residential
treatment). It was not clear how diagnoses were made, and it is possible that bias
influenced decisions whether to diagnose a substance use disorder to keep the physi-
cian in treatment. The monitoring requirements, including the frequency of toxicol-
ogy testing and circumstance of collection, varied by PHP. Some of the outcomes,
including harm to patients by participants, were based on PHP reports; it was
unclear how or if PHPs reliably learned of this information. Although there are other
data which suggest that outcomes after 5 years of abstinence are good [34], there is
no follow-up of the study sample after PHP participation ended. Additionally, the 16
PHPs who provided data for the study may not be representative of all PHPs operat-
ing at the time of the study, and the ability to provide data may be a characteristic of
a more effective PHP. Finally, the study cannot evaluate which components of the
PHP model were important for the reported outcomes. For example, it is possible
that toxicology testing with removal from work as a contingency for positive tests
was the component of this model. If so, residential assessment and treatment, ongo-
ing treatment with fellow physicians, and even participation with a PHP may be less
important, but we do not know.
For a variety of reasons, PHPs may not be attractive to physicians. PHPs are
often perceived as being intertwined with SMBs, the 5-year monitoring agreements
are often perceived as onerous and excessive, and physicians may feel the experi-
ence is more coercive than voluntary or collaborative. Furthermore, physicians may
be opposed to their work settings making regular reports to a PHP, let alone know
they are PHP participants. In states where physicians treating physicians for alcohol
use disorder are not required to report physician patients to the state medical board,
the option of receiving treatment from a physician outside of a PHP may be more
attractive. No data are available on the treatment of medical students, physician
trainees, or physicians under the care of physicians or other mental health providers
outside of PHPs. It is possible that many physicians have received successful treat-
ment by an addiction specialist physician or other licensed expert addiction
172 J. A. Selzer and R. L. Hacker

clinician who understands not only the importance of toxicology monitoring but
also the importance of developing some means of monitoring the professional per-
formance of a physician patient. It is notable that both the American Society of
Addiction Medicine (ASAM) [35] and the Federation of State Medical Boards
(FSMB) [6] consider this an alternative to PHPs in their policy statements although
both are clear on the benefits and special expertise of PHPs. It is also possible that
harmful alcohol use or mild cases of alcohol use disorder may be treated success-
fully in office-based practices of generalist physicians with an interest in preventing
or treating alcohol use disorders. If PHPs were the only confidential option for phy-
sicians seeking help for alcohol use disorders, some physicians would never come
forward, and some colleagues would never make a referral. Physicians with histo-
ries of multiple relapses, alcohol-related impairment at work, and involvement with
regulatory authorities due to alcohol are more likely to benefit from the expertise
and credibility of PHPs rather than a sole practitioner with a less structured approach.
Anyone who treats medical students, physician trainees, and physicians with alco-
hol use disorders should understand and consider when referral to the state PHP is
in the best interest of their patient.
Given awareness of the fear of disclosure requirements, there is a growing call
for reform of medical licensing and credentialing forms which ask applicants ques-
tions regarding past episodes of illness and treatment related to mental health [36]
rather than whether the applicant is currently in good health. The Lorna Breen
Heroes Foundation [37], created in response to the suicide of emergency room phy-
sician Lorna Breen by her family, has emphasized the need to remove questions in
licensing and credentialing applications which compel physicians to report a history
of mental illness (including alcohol use disorder) or its treatment regardless of the
physician’s current health status. Two “non-reporting safe haven options” suggested
by the foundation in response to questions about mental health status are attestation
that the physician is “under treatment and in good standing with a recognized physi-
cian health program or other care provider (italics added).” Concern about intrusive
questions deterring physicians from asking for help also prompted the Lorna Breen
Foundation to suggest that physicians be asked either (1) “Are you currently suffer-
ing from any condition for which you are not being appropriately treated that
impairs your judgment or that would otherwise adversely affect your ability to prac-
tice medicine in a competent, ethical and professional manner?” or (2) no questions
at all about illness as alternatives to the preceding safe haven options.
There is no reason to believe that physician patients would not benefit from the
components of treatment that have been beneficial to other patients with alcohol use
disorders and identified by the NIAAA as indicators of quality treatment [38]. This
would include a variety of psychosocial therapies (including family therapy and
therapies focused on traumatic experiences if indicated) and medications for alco-
hol use disorder. Although not treatment, mutual support groups such as AA have a
good evidence base for helping people with alcohol use disorders [39, 40]. Treatment
approaches which facilitate mutual support group involvement would be expected
to have better outcomes [41]. Finally, clinicians who care for medical students, phy-
sician trainees, and physicians with alcohol use disorder should have a thorough
13 Physicians and Alcohol 173

appreciation for the unique, inherent stresses in these patients’ professional and
personal lives.

13.5 Assessing Fitness to Return to Work

When a medical student, physician trainee, or physician is formally removed from

practice due to harmful alcohol use or the development of an alcohol use disorder,
they are commonly required to obtain clearance from a healthcare provider to return
to work. In brief, a treating or evaluating health care provider must attest that the
individual is not presently impaired and can safely practice. In some cases, the sig-
nature of a treating provider is sufficient; however, in many cases a formal fitness-­
for-­duty evaluation and return-to-work plan will be required by an oversight
organization (e.g., school, training site, employer, physician health program,
or SMB).
Fitness-for-duty evaluations are comprehensive and ought to incorporate ele-
ments of the IME described above. When an IME has already been completed, the
evaluator making a determination regarding return to work will review the previous
IME and update all sections/gather new information from the date of the first IME
to the present. Each of the sections will focus on progress toward stable remission.
If initial cognitive testing was performed and impairment was indicated, additional
testing should be conducted. With time to heal, the brain can recover functionality.
It is generally recommended that at least 4–6 weeks of sobriety have been obtained
before cognitive testing is completed for this purpose. The more time passed
increases baseline stabilization of cognitive performance. The goal of testing at the
time of fitness-for-duty evaluation is to determine whether any problems are present
or persist that indicate the individual is impaired and unable to safely return to work.
If cognitive impairment is present following a period of sustained recovery, a return
to work will, at a minimum, be delayed providing more time to improve brain func-
tion. In the worst-case scenario, the damage done may be permanent and result in
impairments which do not permit safe return to medical practice. Determinations on
what constitutes impairment can also vary by specialty and work context. For exam-
ple, a surgeon with borderline motor speed dexterity or visuospatial skill ability
presents more risk to their patients than a psychiatrist with this same performance.
While the goal is to get people back to work, when a PHP is involved, a return to
work plan is best made in the context of a partnership between the worksite and the
PHP. The evaluator and/or treating provider may make best-case scenario recom-
mendations for a safe return to work; however, the final return to work plan is a
negotiation between the PHP, the participant, and the workplace, whose job is to
integrate the return to work recommendations within the unique work environment
for the medical student, physician trainee, or physician. For example, if the evalua-
tor’s recommendations are not manageable within the specific workplace, the work-
place can suggest alternative recommendations for PHP consideration. The PHP
and workplace collaborate to find a realistic return-to-work plan that prioritizes the
individual’s recovery needs while balancing professional responsibilities. Ideally,
174 J. A. Selzer and R. L. Hacker

the return-to-work plan includes an incremental progression in both hours worked

(e.g., starting part time without on-call duties) and responsibilities (e.g., a surgeon
may progress from surgery with peer oversight to independent surgeries).
Securing open releases of information to communicate with the workplace or
training environment, particularly with supervisors, is necessary to get the individ-
ual back to work with appropriate support in the quickest time. Communication
from the worksite primarily involves return-to-work considerations and perfor-
mance at work after the individual returns to work. Importantly, the return-to-work
process should be individualized and specific to the circumstances of the individual,
their history, progress, and current presentation. The worksite can provide valuable
information to treating clinicians and reassurance that the individual is in good
health to the PHP. Creating a credible worksite monitoring system for a solo practi-
tioner requires ingenuity.
In evaluating fitness to return to work and remain at work, PHPs monitor for
abstinence from alcohol and other substances which are not prescribed as part of
medical treatment. This may result from agreements with SMBs that confidentiality
for practicing physicians can only be maintained if this standard is upheld. To moni-
tor alcohol abstinence, laboratory testing must include metabolites of alcohol such
as ethyl glucuronide, ethyl sulfate, and phosphatidyl ethanol. The advantage of
these metabolites is the longer window of detection than that provided for in breath,
blood, or urine testing for alcohol. Medical students, physician trainees, and physi-
cians treated outside of PHPs may not be held to an abstinence standard or moni-
tored for drug use as rigorously as PHP participants. A survival analysis of 11
alcohol and 9 tobacco treatment studies concludes “that 100 days of uninterrupted
abstinence represents an important treatment milestone, and any patient who has
managed to achieve this milestone likely also possesses the ability to remain absti-
nent for 1 year or longer [42].” Given this finding, 3 months of abstinence before
returning to work may be prudent (Fig. 13.1).
Clinicians who provide treatment outside of PHPs should clearly communicate
to the people they treat what circumstances could prompt referral to PHP or even
reporting to the SMB (e.g., an impaired physician who refuses to stop working).
State laws vary in the requirements on treating clinicians for reporting impaired
physicians. Practicing while impaired is an unacceptable treatment outcome, and
knowledge that a physician is practicing while impaired poses an ethical dilemma
for the treating clinician. The challenges of monitoring impairment at work without
ongoing communication with a worksite monitor may be considerable. Here too,
there may be an advantage to PHP monitoring over individual treating clinician
monitoring, particularly in cases where treating clinicians have no means of moni-
toring work performance.
13 Physicians and Alcohol 175

Fig. 13.1 Return to work

flowchart for a PHP
participant

13.6 Monitoring the Health of Physicians in Remission

from Alcohol Use Disorders

Ongoing monitoring of the health of physicians who are in stable remission from
alcohol use disorder is prudent given the risk of recurrence. PHPs often offer con-
tinuing monitoring after completion of an initial agreement for participants who feel
it would be beneficial. Often these agreements for continued monitoring after
176 J. A. Selzer and R. L. Hacker

successful completion of the initial agreement allow for more flexibility and imple-
mentation of participant preferences (such as a reduction in toxicology collection
schedules). Ongoing care, including monitoring for recurrence, may also take place
outside of a PHP in whatever setting a physician patient prefers to receive good care.

13.7 Conclusions

Alcohol has a long history in medicine due to its extensive role in producing morbid-
ity. It has also been employed by physicians for purported medicinal properties.
Alcohol is the most used and misused drug by medical students, physician trainees,
and physicians despite growing evidence that any use of alcohol may have harmful
health effects. Alcohol misuse in this population has been associated with burnout,
depression, and self-reports of medical errors. Stigmatizing attitudes toward patients
with alcohol use disorders may be internalized and contribute to the reluctance of
medical students, physician trainees, and physicians to come forward to ask for help;
it is clear that fear of professional consequences also contributes to this reluctance.
Given the safety-sensitive nature of a physician’s work, it is important that physi-
cians who present with concerns related to alcohol have a thorough evaluation with
emphasis on the possibility that alcohol has caused impairment. PHPs have been
involved in helping physicians recover from alcohol use disorders for 50 years.
Although the outcomes of PHPs have been among the best reported in addiction
medicine, prospective research with better methodology is necessary to validate
these findings. There is a pressing need for research on prevention as well as best
treatment practices for helping medical students and physicians at every point in
their professional life cycles. Medical schools, post-graduate training programs, and
professional medical organizations can all play a role in raising awareness about
alcohol-related problems in the medical profession and in helping members of the
profession who need help.

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Advocacy and Policy: Improving Access
to Treatment and Recovery Support 14
Services

Abdallah Tom, Charalambia Louka, and Sanya Virani

14.1 Unraveling Alcohol’s Effects and Charting

the Advocacy-Regulation Nexus

Alcohol use disorder (AUD) exerts a profound global impact, affecting 283 million
adults and contributing to three million deaths worldwide. Its prevalence is notably
prominent in the European Region and the Region of the Americas, where its bur-
den is estimated at 5% of the global burden of disease [1]. In the United States, the
gravity of the issue is starkly evident, with 28.6 million adults grappling with
AUD. Alarmingly, it ranks as the fourth leading cause of death, accounting for
approximately 140,000 fatalities annually [2, 3].
Alcohol consumption and dependence are intricately linked to a myriad of
adverse physical health, mental health, and societal outcomes, precipitating severe
illness, morbidity, and mortality. Diseases arising from alcohol use, whether through
direct physiological impact or indirect ramifications, can be systematically classi-
fied into seven categories: “Infectious disease, Cancer, Diabetes, Neuropsychiatric
disease, Cardiovascular disease, Liver and pancreas disease, and Unintentional and
intentional injury [4].”
This pervasive influence positions alcohol as a major contributor to the global
burden of disease, implicated in over 30 distinct conditions and serving as a direct
catalyst for numerous others [5]. According to the World Health Organization, the
health repercussions of alcohol consumption have now surpassed those associated
with unsafe water and sanitation, hypertension, hypercholesterolemia, or even
tobacco use [4].

A. Tom · C. Louka
New York-Presbyterian Hospital/Weill Cornell Medicine, New York, NY, USA
e-mail: [email protected]
S. Virani (*)
University of Massachusetts Chan Medical School, Worcester, MA, USA

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2024 179
M. Khan, J. Avery (eds.), From Stigma to Support, Psychiatry Update 4,
https://doi.org/10.1007/978-3-031-73553-0_14
180 A. Tom et al.

Despite these dire consequences, only a mere 4.6% of individuals afflicted by

AUD receive the requisite treatment, and, concerningly, many do not recognize the
need for such intervention [6]. This somber reality underscores the critical impor-
tance of informed and effective policy development, alongside strategic advocacy
and legal framework, to tackle this burgeoning public health crisis through compre-
hensive treatment and management of alcohol use disorders, emphasizing the intri-
cate interconnection between health initiatives and broader societal well-being.
Unfortunately, access to care has often been hindered by stigma, the political land-
scape, and deeply entrenched sociocultural norms.
The exploration of the correlation between AUD and associated diseases has
been instrumental in formulating safe alcohol consumption guidelines. These guide-
lines extend beyond mitigating the adverse health effects on heavy alcohol consum-
ers; they also serve as a protective measure for those in close proximity,
acknowledging the substantial social harms associated with excessive alcohol
consumption.

14.2 The History of Shaping Alcohol Policies

in the United States

Alcohol use-related policies and advocacy have held substantial public health sig-
nificance for the past eight decades, coinciding with the establishment of the
Quarterly Journal of Studies on Alcohol. This pioneering journal was the first to
delve into the role of public policy in alcohol use management [7]. Over the years,
policies have primarily targeted primary interventions to avert the negative health
consequences of alcohol use, incorporating authoritative measures to control sales,
distribution, and production. Examples include policies dictating the minimum
drinking age and taxation [8]. Regulations concerning alcohol use disorders began
gaining attention post the Prohibition Era (1920–1933), but during this period,
many policies were founded on hypotheses and influenced by varying political cli-
mates across states. Subsequent studies examined the impact of these regulations.
Although alcohol research gained momentum from the 1950s to the 1980s, it wasn’t
until the 1980s that significant, impactful changes occurred, partly attributed to
advances in population health statistical models [8] (Fig. 14.1).
Before the European colonization of the modern-day United States, alcohol use,
in the form of locally produced “weak” beers and other fermented beverages like
wine, was reserved for ceremonial occasions and was not a prominent cultural phe-
nomenon among native tribes [9]. With the colonization of the Northern Eastern
region by Puritan settlers from England in the 1600s, fermented and distilled bever-
ages became integral to society. At that time, fermented beverages were abundant in
Europe and considered safer due to frequently contaminated water supplies. As a
melting pot of cultures, alcohol use customs were imported from different regions,
with early Puritan colonists crafting their own fermented drinks. By the mid-1600s,
rum imported from the Caribbean gained popularity among colonists [10].
Consequently, alcohol became widely available to individuals of all ages, and
14 Advocacy and Policy: Improving Access to Treatment and Recovery Support… 181

Fig. 14.1 Timeline of the history of alcohol and associated regulatory and legal policies. Created
and designed by Abdallah Tom, MD

consuming alcohol, even with breakfast, became a cultural norm by the 1770s [11].
On average, individuals consumed 3.5 gallons of alcohol per year [11]. With the
disruption caused by the American Revolution in 1775 and the cessation of British
alcohol supplies, colonies in Kentucky and Ohio began local alcohol production,
leading to the birth of bourbon. Due to local production and water contamination
concerns, whiskey became a safer and more affordable choice than coffee or milk
[11]. By the 1830s, the average American over the age of 15 consumed 7.1 gallons
of alcohol per year, a stark contrast to today’s average of 2.5 gallons per year [10].
In the modern-day United States, diverse regions and colonies embraced various
practices surrounding alcohol use, but a commonality prevailed: widespread alcohol
consumption. In Massachusetts, efforts to reduce alcohol use included ministers
declaring “public drunkenness” as a sin, while others advocated for complete absti-
nence [11]. The Washington Temperance Society, established in Washington DC in
1840, championed teetotalism, amassing over 100 thousand signatories to prohibit
alcohol and raising awareness about its societal and personal consequences [12].
Simultaneously, Massachusetts banned the sale of alcohol in quantities >15 gallons,
and various states sought to limit alcohol production, sale, and distribution [11].
President Wilson’s temporary prohibition during World War I in 1917 influenced the
introduction of the 18th Amendment in 1920, nationally prohibiting alcohol with
the enactment of the Volstead Act [13, 14].
Alcohol-related laws in the United States were significantly shaped by cultural
norms, advocacy groups, and lobbyists, including religious institutions, temperance
societies, the Anti-Saloon League, and the impact of the industrial revolution.
Alcohol was viewed as the root cause of crime and social corruption, while the
182 A. Tom et al.

industrial revolution advocated for prohibition to increase production and prolong

working hours [15]. Notably, Iowa sold its prisons on the eve of the Volstead Act’s
passage, anticipating decreased crime and violence [10]. The prohibition era was
seen as successful by some, with reduced public intoxication, alcohol-related
arrests, and a 30% decrease in alcohol consumption. However, it predominantly
limited alcohol consumption among middle and lower socioeconomic populations,
leading to the rise of speakeasies and an increase in deaths from poorly produced
moonshine [16]. Enforcing the Volstead Act faced challenges, including financial
limitations, 300 million dollars to implement, and a decrease in state tax revenue
from alcohol sales, impacting public services [17]. “Bootlegging,” the illegal pro-
duction and sale of alcoholic beverages, flourished, leading to increased organized
crime, epitomized by figures like Al Capone during the prohibition era.
Opposition to federal prohibition led to movements aiming to reverse the 18th
US amendment in the late 1920s, with some arguing it imposed “rural Protestant”
values on “urban America.” The prohibition era concluded in 1933 during the Great
Depression, with the adoption of the 21st amendment, titled “Repeal of Prohibition
Amendment,” rescinding the 18th amendment during Franklin D. Roosevelt’s presi-
dency. Subsequently, alcohol regulations were then left to the discretion of indi-
vidual states [18]. The subsequent increase in alcohol production and sales
contributed to economic recovery during the Great Depression, boosting tax reve-
nues and employment rates [14].
The historical trajectory of alcohol in the United States underscores the profound
impact of advocacy and policy development in regulating its consumption. Lobbying
and policy formulation have been pivotal, driven by political, religious, and per-
sonal interests. The 18th and 21st amendments, marking the start and end of the
prohibition era, were outcomes of lobbying movements. The lasting impact of leg-
islation on alcohol sale, distribution, and consumption is evident, with some states
maintaining their prohibition for decades after the 21st Amendment’s repeal [14].
After these pivotal moments, various laws and regulations were introduced to cur-
tail alcohol misuse.

14.3 Current Landscape of Alcohol Use Disorder

Legislations/Disparities

Advocacy and policy development have been an integral part of regulating alcohol
consumption for over a century. Today, there are several national institutions
addressing advocacy, policy, and disparities surrounding the regulation of alcohol
use. Current trends of alcohol use adverse effects underscore the importance of
continued advocacy to enhance access to and provide equitable healthcare services.
Between 2015 and 2019, alcohol misuse led to “more than 140,000 deaths and 3.6
million years of potential life lost [19].” Among adults between the ages of 20 and
49, alcohol accounted for one in five deaths, decreasing the average life expectancy
of those affected by 26 years [19, 20]. The grave burden of the consequences of
14 Advocacy and Policy: Improving Access to Treatment and Recovery Support… 183

alcohol misuse sheds light on the importance of continued research-based advocacy

and resulting policy development.
Many organizations exist nationally to address the needs of those suffering from
alcohol use disorders: National Institute on Alcohol Abuse and Alcoholism
(NIAAA), Alcohol Justice, The National Voice on Fetal Alcohol Spectrum Disorders
(FASD), and Mothers Against Drunk Driving (MADD). The NIAAA, for one, was
developed in 1970 under the Comprehensive Alcohol Abuse and Alcoholism
Prevention, Treatment, and Rehabilitation Act of 1970, with the aim of developing
research, training, and health programs focused on alcohol use disorder [21]. Since
its inception, it has conducted extensive research on underlying genetic mecha-
nisms, neuromodulatory correlates, and novel treatments of AUD. More patient-­
facing organizations such as FASD provide support groups for recovering mothers
with AUD and aid in connecting mothers and children with fetal alcohol syndromes
to medical care [22]. MADD was created in 1980 by two victims of car accidents
involving intoxicated drivers. The organization advocates for stricter judicial sys-
tems against intoxicated drivers and provides support resources for those who have
been involved in such accidents [23].
Broader national organizations and agencies also play a part by allocating
resources specifically to alcohol use disorder. These include the Substance Abuse
and Mental Health Services Administration (SAMHSA) and the American Academy
of Addiction Psychiatry (AAAP), among others. SAMSHA was established by
Congress in 1992 to research substance use disorders and develop services to help
those in need [24]. Over the decades, some of these efforts have included funding
research and policy grants, publishing informational pamphlets and guides on epi-
demiology of alcohol use and treatment, and providing a large database of treatment
resources, one of which includes a national telephone helpline [25]. The AAAP,
which was formed in 1985, has worked toward providing equitable and accessible
substance use treatment by training healthcare providers, providing public educa-
tion, and advocating for greater insurance parity [26]. The AAAP’s work in forming
extensive education and training programs helped propel addiction psychiatry into
a well-established and fundamental clinical field [27]. The Center for Disease
Control (CDC) now aids in initiatives such as surveilling national alcohol use pat-
terns, funding state and regional public health efforts to prevent excessive alcohol
use, and encouraging partnership between national leadership and local health com-
munities [28].

14.4 Alcohol Use Disorder Treatment and the US

Healthcare System

In the United States, AUD treatment is costly. A 2019 nationwide survey conducted
by the Recovery Centers of America estimated that, on average, general outpatient
substance use services cost $91 per day and intensive outpatient services cost $300
per day. Programs providing a higher level of care, such as detoxification services
and residential programs, cost an average of $650 per day [29]. The financial burden
184 A. Tom et al.

of seeking and obtaining treatment for alcohol use disorders can be prohibitive for
many (Table 14.1).
In the 1950s, with the advent of deinstitutionalization and the restructuring of the
US mental healthcare system, came the inclusion of mental health coverage by
insurance plans [30]. In the 1960s, President John F. Kennedy signed the Community
Mental Health Act, a precursor to parity that helped fund new inpatient and outpa-
tient psychiatric centers and spread mental health awareness [31]. Still, mental
health benefits were not covered by insurance plans in the same way that physical
health benefits were. In 1996, the Mental Health Parity Act (MHPA) was passed,
outlining that health plans could not set annual or lifetime dollar limits on mental
health benefits that were less favorable than general health limits [32]. While an
important step in the right direction, this act was limited in scope. It was not until
2008, when President George W. Bush signed the Paul Wellstone and Pete Domenici

Table 14.1 Table outlines categories of costs associated with the treatment of alcohol use disor-
der (AUD) in the United States
Category Description
Direct treatment cost
Outpatient services Counseling sessions
Medication management
Group therapy sessions
Medical check-ups
Inpatient services Residential treatment programs
Detoxification services
24/7 medical supervision
Medications Prescribed medications for treatment
Medications to manage withdrawal symptoms
Therapy and counseling Individual counseling sessions
Family therapy sessions
Cognitive-behavioral therapy (CBT)
Hidden costs
Loss of productivity Missed workdays due to treatment
Impact on career advancement
Legal consequences Legal fees for DUI or other alcohol-related offenses
Fines and court costs
Social and relationship costs Strained relationships with family and friends
Impact on social life and events
Creation and delivery of services
Workforce training Training healthcare providers for AUD treatment
Research and development Investment in developing new treatment methods
Administrative costs Overhead costs for running treatment facilities
Staff salaries and benefits
Geographic access
Transportation Cost of transportation to treatment facilities
Accessibility to public transportation
Rural vs. urban disparities Limited treatment options in rural areas
Greater availability in urban areas
Insurance coverage Out-of-pocket expenses after insurance coverage
Varied coverage based on insurance plans
Availability of affordable insurance plans
14 Advocacy and Policy: Improving Access to Treatment and Recovery Support… 185

Mental Health Parity and Addiction Equity Act (MHPAEA) that complete coverage
parity between mental health and physical services came into play [30]. The
MHPAEA was also the first act to include parity of substance use services.
In 2010, the Affordable Care Act (ACA) was enacted, and substance use treat-
ment benefits were expanded: substance use treatment could be included as an
“essential benefit,” parity was extended to small group and individual healthcare
plans, and protections were laid forth for patients with pre-existing conditions [33].
In 2014, eligibility criteria under the ACA were expanded, theoretically increasing
the number of covered Americans. A study by Saloner et al. investigated the out-
comes of the 2014 ACA expansion in a population of 19,243 US adults with sub-
stance use disorders; it was found that there were significant reductions in the
uninsured rate in those with substance use disorders but that the utilization of sub-
stance use treatment did not actually change [34]. It was theorized that this discrep-
ancy could be because of other persisting barriers, such as stigma, scarcity of
substance use disorder providers, and a lack of perceived need for services [34].
Further studies have elucidated that while insurance policy does indeed have the
potential to increase economic access to substance use treatment, a lack of infra-
structure and resources may pose a bottleneck effect [35]. This highlights a need for
more insurance and policy-based initiatives to help patients circumvent the ongoing
barriers to alcohol use disorder treatment.

14.5 Future Directions

Despite the many efforts put forth by government agencies, advocacy groups, and
healthcare organizations to address the growing problem of alcohol use disorder in
the United States, there is much more work to be done. The State Health Access
Data Assistance Center (SHADAC) at the University of Minnesota has suggested
that in light of the public alarm surrounding the USA’s opioid epidemic, alcohol-­
related deaths may actually be as high in number [36]. Alcohol-related deaths can
be hard to define and quantify due to the broad spectrum of acute and chronic dis-
eases that heavy alcohol use can lead to, but there are a set of these (such as alcohol
poisoning and alcoholic liver disease) that the CDC defines as attributable to alco-
hol [37]. SHADAC has estimated that from 2006 to 2019, the USA has experienced
416,000 opioid-related deaths and 414,000 alcohol-related deaths [36]. The disease
burden of alcohol, however, is estimated to be much greater than this.
There are many avenues which continue to address the alcohol use disorder epi-
demic from a policymaking and advocacy standpoint. The World Health Organization
(WHO) outlines some of these areas of focus to include awareness and commitment
of national leadership, response by health organizations, accountability at the com-
munity level, laws against drunk driving, regulation of marketing and distribution of
alcoholic beverages, and medical monitoring and surveillance [38]. SAMSHA sug-
gests similar actionable measures and calls for more public funding, research, edu-
cation, and cooperation between governmental agencies, communities, and
healthcare providers [39].
186 A. Tom et al.

Technology’s influence in the current climate can be leveraged to aid in such

future directions. It has been shown that digital communications and media cover-
age can allow the public to interact more openly with policymakers and vice versa
[40]. There is also growing evidence that telehealth, remote monitoring, and digital
health interventions are effective in detection and treatment of substance use disor-
ders [41]. In this new digital age, it will be important to set forth clear regulations to
ensure that clinical technologies meet the same quality and standards as in-­
person care.

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The Future of Alcohol Use Disorder
Treatment and Research 15
A. Benjamin Srivastava and Jonathan M. Wai

15.1 Introduction

Currently, three medications are approved by the US Food and Drug Administration
(FDA) for the treatment of alcohol use disorder: disulfiram, naltrexone, and acam-
prosate. The availability of these medications notwithstanding, significant limita-
tions remain. Disulfiram, which has only been shown to separate from placebo in
open-label trials [1] requires the patient to be motivated for abstinence and compli-
ant with treatment [2]. Acamprosate similarly has been shown to improve absti-
nence, though evidence from clinical trials is mixed [3]. However, abstinence may
not be a reasonable or attainable goal for many patients with AUD, whereas reduc-
tion in heavy drinking may be a more attainable yet still clinically meaningful out-
come [4, 5]. Naltrexone, available in both oral and long-acting injectable, has been
shown to reduce heavy drinking, though effect sizes remain low [6, 7]. Thus, novel
therapeutics are needed for both reduction in heavy drinking and abstinence.
Disulfiram acts principally through non-CNS mechanisms, and though it does
inhibit dopamine-β-hydroxylase to prevent the conversion of dopamine to norepi-
nephrine, circumstantial evidence suggests that this had limited implications for the
treatment of substance use disorders [8, 9]. Naltrexone and acamprosate are thought
to act principally through modulating distinct neurotransmitter systems. Decades of
work in neuroscience, however, has led to a conceptualization of substance use dis-
orders, including AUD, as manifestations of dysfunctions in underlying neural cir-
cuitry [10]. One such heuristic is to examine substance use disorders in terms of

A. B. Srivastava (*)
Department of Psychiatry, Columbia University Irving Medical Center, New York, NY, USA
e-mail: [email protected]
J. M. Wai
Department of Psychiatry, Columbia University Irving Medical Center, New York, NY, USA
New York State Psychiatric Institute, New York, NY, USA
e-mail: [email protected]

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2024 189
M. Khan, J. Avery (eds.), From Stigma to Support, Psychiatry Update 4,
https://doi.org/10.1007/978-3-031-73553-0_15
190 A. B. Srivastava and J. M. Wai

three phases, including binge/intoxication (broadly localized to the dorsal striatum),

withdrawal/negative affect (broadly localized to the extended amygdala), and pre-
occupation/anticipation (broadly localized to the prefrontal cortex and insula and
their modulatory effects on regions associated with craving including the orbital
frontal cortex, ventral striatum, and anterior cingulate cortex) [10].
Given the limitations of currently available FDA-approved medical treatments
for AUD, more treatments are clearly needed. In this chapter, we review the phar-
macological developments and future directions for medications to treat AUD. In
addition, we review novel device-based and brain stimulation treatments for AUD.

15.2 Novel Pharmacologic Treatments and Targets

15.2.1 Pregabalin

Like gabapentin, pregabalin is voltage-gated calcium channel (VGCC) inhibitors

FDA-approved for the treatment of neuropathic pain and epilepsy. While both were
synthesized as structural analogues to γ-aminobutyric acid (GABA), neither binds
to the GABA receptors and instead binds to the presynaptic α 2δ-1 subunit of the
VGCC [11]. Pregabalin may increase L-glutamate decarboxylase, the enzyme that
synthesizes GABA, thereby increasing GABA concentration. Because of a favor-
able pharmacokinetic profile for pregabalin, including faster absorption and time to
peak plasma concentrations with pregabalin compared with gabapentin [12],
improvements in anxiety symptoms when compared with naltrexone in the treat-
ment of AUD [13], and efficacy and accepted use for the treatment of generalized
anxiety disorder in Europe [14], Mariani and colleagues conducted an open-label
pilot study using pregabalin (titrated to 600 mg/day) for the treatment of alcohol use
disorder (n = 18) for 8 weeks. Mean heavy drinking days per week decreased, as did
the proportion of heavy drinking days, and the proportion of abstinent days increased
[15, 16]. A pilot RCT comparing pregabalin to placebo was started in 2021
(NCT04322305). Similar to gabapentin as suggested by recent work [17], pregaba-
lin may target the withdrawal/negative affect circuitry.

15.2.2 Hallucinogens: LSD, Psilocybin, Ketamine, and MDMA

Lysergic acid diethylamide (LSD) was first synthesized by Albert Hofmann in 1938
while working for Sandoz, a pharmaceutical company. LSD binds as a partial agonist at
the 5-HT2A serotonin receptor and as an agonist at the 5-HT1A, 5-HT2C, and 5-HT2B
receptors. LSD is also an agonist at D1, D2, and D4 dopamine receptors (for reviews see
[18, 19]). Much of the earlier research on LSD was performed in the 1960s and 1970s
(in the context of “psychedelic assisted psychotherapy”) and included recent meta-anal-
yses (6 RCTs, 536 total participants) showing a beneficial effect of LSD on alcohol
misuse [20]. A multicenter RCT in Switzerland comparing high dose (150 μg or 250 μg)
or low dose (10 μg) LSD to placebo for the treatment of AUD over the course of
20 weeks is estimated to begin recruitment within the next year (NCT05474989).
15 The Future of Alcohol Use Disorder Treatment and Research 191

Psilocybin is an indolamine that primarily functions as a 5HT2A-receptor partial

agonist that has been investigated as a therapeutic agent for treatment-resistant
depression, obsessive-compulsive disorder, tobacco use disorder, and AUD. In a
seminal RCT conducted by Bogenshutz and colleagues, 95 participants with AUD
were randomized to receive either psilocybin or diphenhydramine in the context of
12 weeks of manualized psychotherapy that included elements from motivational
interviewing and cognitive behavioral therapy. Participants received the medication
at weeks 4 and 8 in the context of an 8-h session with a therapist. After 32 weeks,
participants randomized to psilocybin showed a significantly lower percentage of
heavy drinking days compared with participants randomized to diphenhydr-
amine [21].
The therapeutic of serotonergic hallucinogens has been hypothesized to relate to
the idea of a spiritual experience reflected in the writings of William James [22] and
the philosophy of Alcoholics Anonymous (AA) and other 12-step programs (for
review, see [23]). Galanter and colleagues recently performed an experiment in
which sober members of AA underwent fMRI scanning and were exposed to alco-
hol cues with instructions to either recite AA prayers, read irrelevant news, or view
passively. When the prayer condition was contrasted with passive + news condi-
tions, the dorsolateral prefrontal cortex, an area implicated in cognitive control pro-
cesses [24] was activated [25]. More recently, Pagni and colleagues showed that in
participants with AUD receiving psilocybin, PFC activation was enhanced. These
findings provide circumstantial evidence that psychedelics may target circuitry
involved in preoccupation/anticipation.

15.2.3 Ketamine

Ketamine is a noncompetitive antagonist of the N-methyl-d-aspartate (NMDA)

receptor. Originally developed as an anesthetic, following a pivotal trial in 2000
demonstrating a rapid relief of depressive symptoms [26], ketamine had demon-
strated efficacy in the treatment of a number of other psychiatric disorders including
eating disorders, anxiety disorders, and substance use disorders. An intranasal for-
mulation has been FDA approved for treatment-resistant depression (for review see
[27]). In an RCT conducted by Dakwar and colleagues, 40 participants with AUD
were randomized to receive one infusion of either ketamine or midazolam during
the second week of a 5-week treatment course of motivational enhancement ther-
apy. Compared with midazolam, ketamine treatment was associated with increased
likelihood of abstinence, reduced proportion of heavy drinking days, and longer
time to relapse [28]. In another RCT, 96 participants with AUD were randomized to
receive either (1) three weekly infusions of ketamine and mindfulness-based relapse
prevention therapy, (2) three weekly infusions of saline and mindfulness-based
relapse prevention therapy, (3) three weekly ketamine infusions and alcohol educa-
tion (a control therapy condition), and (4) three weekly saline infusions and alcohol
education. Across therapy conditions, ketamine treatment was associated with a sig-
nificantly greater percentage of days abstinent at 6-month follow-up then saline
192 A. B. Srivastava and J. M. Wai

infusions. There was not a significant difference in the percentage of days abstinent
when comparing ketamine + mindfulness-based relapse prevention with ket-
amine + alcohol education [29].
Mechanistically, alcohol is a potent inhibitor of the NMDA receptor, and altera-
tions in NMDA-R function may be relevant in the development of AUD. Thus, ket-
amine, to the extent that it has shown some efficacy in the treatment of AUD, may
serve to correct this dysregulation. In a study examining resting state functional
connectivity changes in participants with treatment-resistant depression undergoing
96-h ketamine infusions, ketamine treatment was associated with increased con-
nectivity between limbic structures and cognitive control centers in the prefrontal
cortex [30]. Thus, ketamine may function to modulate systems implicated in the
preoccupation/anticipation phase.

15.2.4 MDMA

3,4-Methylenedioxymethamphetamine (MDMA) is a phenylethylamine that acts on

a variety of neurotransmitters with properties including monoamine (serotonin and
dopamine) release, alpha-2 receptor agonism, and oxytocin release [31]. Given that
MDMA has shown promise for enhancing openness and therapeutic alliance during
psychotherapy [32], MDMA has been investigated for therapeutic purposes in post-­
traumatic stress disorder (PTSD) and, in a phase 3 randomized controlled trial, was
shown to reduce PTSD symptoms [33]. Recently, participants with AUD receiving
recovery-based psychotherapy and MDMA were shown to reduce drinking without
significant adverse effects [34]. Given the comorbidity between PTSD and AUD,
MDMA may be a particularly useful therapeutic agent [35]. An open-label study
(NCT05943665) and a randomized controlled trial (NCT05709353) examining
MDMA-assisted psychotherapy in participants with comorbid AUD and PTSD are
currently ongoing.
The promising results of hallucinogens notwithstanding, important caveats
remain. First, blinding (and by extension, finding an adequate placebo) remains a
challenge. Second, given that all of these medications have been tested in the con-
text of psychotherapy (and for psilocybin and LSD, 8-h sessions), questions of scal-
ability and feasibility of implementation in heterogenous clinical settings remain
[18, 36]. Resolving these issues will be crucial for advancing these medications
through the FDA approval process and, ultimately, clinical use.

15.2.5 Glucagon Like Peptide-1 Receptor Agonists

Glucagon like peptide-1 receptor agonists (GLP1-Ras) are a class of medications

FDA approved for the treatment of type 2 diabetes mellitus. Mechanistically, GLP1-­
Ras delay gastric emptying, stimulate insulin secretion, and inhibit glucagon release,
thus lowering blood sugar. They have also been shown to decrease food intake, and
a formulation of the GLP1-Ra semaglutide (Weygovy®) has been approved for
15 The Future of Alcohol Use Disorder Treatment and Research 193

weight management in obesity [37]. Because of evidence showing that GLP1-Ras

reduces alcohol consumption in rodent models of AUD (for review see [38]), an
RCT evaluating the efficacy of exenatide, a first generation GLP-1RA, was con-
ducted. Exenatide treatment, when compared with placebo, was not associated with
changes in heavy drinking, though it was associated with reduction in alcohol-cue
evoked activity in the ventral striatum. These results suggest that GLP1-RAs may
modulate circuitry associated with preoccupation/anticipation. Exploratory analy-
ses showed that heavy drinking was significantly reduced in obese (BMI > 30) par-
ticipants [39].
Importantly, exenatide has 53% sequence homology to human GLP-1 [40],
whereas semaglutide has 94% sequence homology to human GLP-1 [41]. As such,
when semaglutide was compared head to head in an RCT with exenatide in partici-
pants with Type 2 diabetes mellitus, semaglutide was superior in terms of improved
glycemic control and weight loss [42]. Investigating semaglutide may confer a simi-
lar advantage over exenatide in the treatment of AUD, and it may work particularly
well for patients with AUD and comorbid obesity. Several RCTs investigating the
efficacy of semaglutide in AUD (NCT05892432, NCT05520775, NCT06015893)
are registered. An additional trial (NCT05895643), in which semaglutide is being
investigated for the treatment of AUD in patients with comorbid obesity, is underway.

15.2.6 Alpha-1 Antagonists: Prazosin and Doxazosin

Because early abstinence in AUD is characterized by mood dysregulation and stress,

alpha-1 antagonists have been proposed as therapeutic agents for AUD, with the
proposed therapeutic effects being a restoration of brain homeostasis and thus stress
reduction [43]. A recent meta-analysis showed that prazosin/doxazosin was associ-
ated with reduced drinking, but not abstinence [44]. Recent data from an RCT of
prazosin that included fMRI sessions at pre- and post-treatment showed that alcohol
withdrawal predicted disrupted cortical-striatal response to alcohol cues, and prazo-
sin reversed this alcohol-related cortico-striatal dysfunction [45]. Collectively these
results suggest that prazosin may work through both negative affect and preoccupa-
tion/anticipation-related mechanisms.

15.3 Device-Based Interventions

Neuromodulation with devices uses electricity or pharmacologic agents to stimulate

or deliver a drug to neural targets that are believed to have abnormal activity in a
disease process. Unlike oral or intravenous medications, neuromodulation aims to
target specific neural circuits with the hope of producing clinical effects without
exposing the entire body to a therapeutic intervention. Commonly used noninvasive
neuromodulation methods, which either apply electricity directly to the scalp or
induce a magnetic pulse using electromagnetic coils, include transcranial magnetic
stimulation (TMS), transcranial direct current stimulation (tDCS), and
194 A. B. Srivastava and J. M. Wai

electroconvulsive therapy (ECT). Invasive forms of neuromodulation require a sur-

gical procedure to apply an electrode to the brain or a nerve and include deep brain
stimulation (DBS) and vagal nerve stimulation (VNS). Given the better safety pro-
file and accessibility of noninvasive neuromodulation, especially modalities that
don’t require general anesthesia such as TMS and tDCS, these forms of stimulation
have a greater body of literature investigating their efficacy (for review see, [46]).
In the field of neuromodulation using brain stimulation, there are several impor-
tant “dosing” considerations which include the number and frequency of sessions,
the frequency and intensity of the stimulation pulses, the type of device delivering
the stimulation, and the neural structures that are targeted. Structural targets are
most commonly cortical regions closer to the scalp due to these superficial regions
being more easily reachable noninvasively [47]. Evidence for the dysfunction of
these targets come from multimodal methods of brain imaging and are often struc-
tures that involve the limbic system or cognitive control [10]. The cognitive control
circuit includes projections from the dorsolateral prefrontal cortex to the dorsal
striatum, while the limbic circuit includes projections from the medial prefrontal
cortex to the ventral striatum [48]. By manipulating the stimulation parameters of
the device in use, clinicians can aim to either facilitate or inhibit activity in the tar-
geted region, which may also lead to downstream modulation of associated regions.
As a newer form of interventional treatment, studies vary greatly in quality and
sample size, as well as in methodologies. Given the different approaches used to
apply treatment and the outcomes assessed, meta-analyses have yielded mixed
results when considering all neuromodulation studies. A vast majority of studies
have targeted the left or right dorsolateral prefrontal cortex (DLPFC), based on the
efficacy of earlier studies using TMS to treat depression [47]. However, there is
growing evidence that modulation of the frontopolar cortex may also play an impor-
tant role in treating addiction across substances [49].
Neuromodulation generally requires repeated administrations to produce a clini-
cally meaningful effect. While a number of earlier studies used only one session of
neuromodulation, clinical interpretation of these findings is difficult as only one ses-
sion would likely not lead to a sustained clinical response. This chapter will primar-
ily review treatments using TMS and tDCS, which have the greatest body of literature.
Similar to medication trials, studies providing the highest of level of evidence are
double-blind, randomized, placebo-controlled trials. With neuromodulation, a sham
intervention that mimics the experience of an active treatment but does not actually
stimulate the intended brain region or nerve takes the place of a placebo control.

15.3.1 TMS

When used clinically, TMS is administered in repeated pulses at specific frequen-

cies as repetitive TMS (rTMS). rTMS protocols with FDA approval use either high
frequency (>5 Hz) or theta-burst stimulation (TBS), which uses three pulses at
50 Hz repeated at 5 Hz and results in a greatly reduced stimulation time [50]. These
stimulation frequencies facilitate cortical excitability, while low frequency (<1 Hz)
or continuous theta-burst stimulation inhibits cortical excitability. Modulation of
15 The Future of Alcohol Use Disorder Treatment and Research 195

cortical excitability is hypothesized to be from induction of long-term potentiation

(faciliatory) or long-term depression (inhibitory) [51].
The shape of the TMS coil will also determine the location and depth of stimula-
tion. While there are numerous TMS coil geometries under study, only a few have
obtained FDA clearance for treatment of psychiatric disorders. Figure-8 coils use a
two-dimensional geometry and have a more superficial penetration depth. Coils
using more complex three-dimensional geometries can achieve a greater penetra-
tion depth, and these include the different H-coils, as well as a double cone coil
(Fig. 15.1). The Figure-8 coil can only penetrate 1–2 cm into the brain, while differ-
ent variations of the H-coil can penetrate up to 4–5 cm (also called deep TMS) [52].
Considering all the coil geometries, rTMS is currently FDA approved for major
depressive disorder, major depressive disorder with comorbid anxiety, obsessive-­
compulsive disorder, and smoking cessation [53]. Most effective TMS trials and all
methods that are FDA approved use high-frequency rTMS or TBS, both of which
lead to increased excitability and long-term potentiation.
While there are different methods used to determine the treatment stimulation
intensity, a common method used is to first determine the stimulator output required
to cause a muscle twitch when stimulating over a region of the motor cortex, either
by recording motor-evoked potentials or by visual observation. The treatment inten-
sity is then set as percentage of this motor threshold, usually between 80 and 120%
[54]. rTMS is usually administered daily, 5 days a week for 2–4 weeks. Newer
approaches may administer TMS multiple times daily [55], which can deliver an
equivalent number of total pulses over fewer days. rTMS interventions are also
more effective when combined with a concomitant behavioral intervention. In stud-
ies with alcohol and tobacco, a drug cue procedure was used, while TMS was
administered [56, 57]. Sham protocols may use a second coil which mimics the
sound and superficial sensation of rTMS, but does not actually stimulate the brain.

a b c

Fig. 15.1 An illustration depicting. (a) rTMS using the Figure-8 coil and H4-coil. There are also
several other H-coils with different coil geometries; (b) tDCS with the anode placed over the right
DLPFC and cathode over the left DLPFC with the external current stimulator; (c) surgical place-
ment of a DBS system with the electrodes contacting the bilateral nucleus accumbens (only one
shown) and the pulse generator which would be implanted under the clavicle. Reproduced with
permission from Mehta et al. [46]
196 A. B. Srivastava and J. M. Wai

Clinical trials on the effects of rTMS in AUD have most frequently used craving
scales or measures of alcohol consumption as primary outcomes. The first sham-­
controlled trial to study the effects of rTMS on AUD was published by Mishra et al.
in 2010, showing that high-frequency (10 Hz) rTMS stimulating the right DLPFC
over 10 days reduced alcohol cravings scores. Overall, the effects of rTMS to the
right or left DLPFC have been mixed, with some studies finding a reduction in crav-
ing scores [58–62] and decreased alcohol consumption [63–65], but with others
finding no significant effect on alcohol craving [66–68] or consumption [67]. Other
studies that have targeted the dorsal mPFC or used an H-coil, which provides both
a greater depth and total area of stimulation, appears more likely to decrease craving
and alcohol consumption [57, 58, 69]. Interestingly, while high-frequency rTMS to
the insula has been shown to be effective and has gained FDA approval for the treat-
ment of nicotine addiction, a recent trial showed that it had no effect in AUD [70].

15.3.2 tDCS

Transcranial direct current stimulation uses electrodes placed directly on the scalp
to produce continuous low-amplitude (0.5–2.0 mA) electrical currents [71]. tDCS
electrodes can either be anodal to increase cortical excitability or cathodal to
decrease cortical excitability, with current flowing from the anode to the cathode.
The placement of the electrodes, referred to as tDCS “montages,” varies depending
on the desired structures for stimulation. Unlike rTMS, the current is not strong
enough to cause depolarization, but instead changes the membrane potentials of
neurons. Stimulation durations are often performed daily over a period of days or
weeks and occurs for usually 10–20 min at a time. Sham protocols are easily pro-
duced by strategies such as ramping up the initial stimulation and then gradually
decreasing it until it turns off. tDCS has not been FDA cleared for the treatment of
any medical condition at this time. However, there are several studies registered
with the FDA that are currently in process.
While studies are mixed, trials placing the cathode over the left DLPFC and
anode over the right DLPFC have shown to be most effective at decreasing alcohol
craving and relapse [72–74]. Other montages that have reversed the anode and cath-
ode placement over the right and left DLPFC or have targeted other areas have more
negative or mixed results [75–79], with one study even reporting a trend toward
increasing relapse [75].

15.4 Special Considerations for Neuromodulation

to Treat AUD

As chronic substance use, especially with alcohol, is associated with cortical atro-
phy, the stimulation depth and ability to reach cortical structures are important con-
siderations when selecting a neuromodulation modality. For rTMS, while the
stimulation intensity is calibrated at the motor cortex, treatment stimulation is
15 The Future of Alcohol Use Disorder Treatment and Research 197

usually delivered to other areas of the brain which may have a different scalp-to-
cortex distance, thereby decreasing the effective intensity of the stimulation.
Due to seizures limited to the time of stimulation being the main risk of rTMS,
treatment candidates should ideally not be actively binge-drinking. However, the
risk of TMS-induced seizures in the general treatment population is exceedingly
low at <0.02/1000 sessions when TMS is administered within safety guidelines to
individuals without an elevated risk of seizure [80]. In patients with elevated risk
factors, the seizure rate increased to 0.33/1000 sessions. There are no specific safety
measures that need to be taken that differ from standard TMS precautions (e.g.,
elevated risk in patients with alcohol or benzodiazepine withdrawal) [81]. rTMS is
absolutely contraindicated in patients with ferromagnetic implanted devices in the
head, such as cochlear implants of metal aneurysm clips, or magnetically sensitive
implants in the neck or torso such as implanted pacemakers and vagus nerve stimu-
lators. Side effects are usually self-limited and mild, with scalp pain and discomfort
or headaches being the most common side effects, present in 40% of patients [82].
tDCS is exceedingly safe, with the main side effects being local skin irritation or
injuries from excessive stimulation and impedance.

15.5 Other Neuromodulation Methods

There is a paucity of evidence for the efficacy of other neuromodulation methods for
AUD. However, there are a few other methods which warrant discussion.
While ECT has not been specifically studied as a treatment for AUD, it is often
used in the treatment of depression in individuals with comorbid AUD. A comorbid
AUD was found to predict a better response to ECT in one study [83], although two
other studies which included patients with all substance use disorders did not find
improved outcomes in this population [84, 85].
DBS involves a surgical procedure that inserts electrodes to directly contact and
stimulate specified brain regions, with a battery implanted under the clavicle. DBS
uses high frequencies >100 Hz, which causes an inhibitory effect similar to ablation
when used in movement disorders [86]. Given the highly invasive nature of this
intervention, there are limited studies with small sample sizes. For AUD, the bilat-
eral nucleus accumbens is targeted, based on the incidental finding of a patient
treated with DBS for severe anxiety who had greatly reduced his alcohol use despite
ongoing severe psychiatric symptoms. Most trials have been open label, while one
used a 6-month delay prior to turning on the device. All studies found that DBS
reduced alcohol craving and consumption after treatment [87–90].
Cranial electrical stimulation (CES) is similar to tDCS, but unlike tDCS which
uses a continuous direct current, CES uses a variable waveform that produces an
alternating current. Although there are CES devices that are FDA cleared for the
treatment of insomnia, depression, or anxiety, these devices were marketed prior to
the congressional Medical Device Amendments Act in 1976, and devices that have
been subsequently cleared by the FDA obtained approval due to being substantially
equivalent to the older existing devices with FDA clearance. More recent rials using
198 A. B. Srivastava and J. M. Wai

CES to reduce drinking have been negative [91], as have studies using CES to treat
depression [92]. Thus, despite several of these devices being FDA cleared to market
for the treatment of psychiatric disorders, the level of supporting evidence for their
efficacy remains quite low.

15.6 Conclusion

Newer, circuit-based treatments such as rTMS and pharmacotherapies that may tar-
get specific brain systems hold promise, and several placebo-controlled trials have
already demonstrated their efficacy. For example, GLP-1 receptor agonists and
serotonergic hallucinogens may work through targeting circuits related to incentive
salience, whereas pregabalin may work through targeting circuits involved in with-
drawal and negative affect. There is already one FDA indication that rTMS has for
treating addiction (smoking cessation), and there are an increasing number of larger,
sham-controlled positive trials using rTMS. While these new treatment modalities
may not yet be ready for regular clinical use, clinicians should be aware that they
may soon be and that some patients may already be receiving off-label treatments
with these approaches. Rigorous clinical trials are needed to determine for which
specific patients circuit-based interventions may work.

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Index

A Alcohol use disorder (AUD), 21, 41, 58, 60,

Abstinence, 143, 144, 146, 147 77, 109, 117, 154, 155, 157, 158,
Abstinence violation effect (AVE), 147 179, 180, 189, 196
Academic psychiatry, 159 acamprosate, 79, 80
Acamprosate, 79, 80 addiction cycle, 9, 12
mechanism, 79 alcohol affects the brain
therapeutic effects, 79 addiction cycle, 11, 13
Acceptance and commitment therapy binge/intoxication stage, 13
(ACT), 103 intoxication/binge stage, 12
Addiction, 156 key behaviors, 11–12
cycle, 12 preoccupation/anticipation stage, 14
medical models, 156, 158 withdrawal/negative affect, 13
moral model, 154 alcohol metabolism, 10
Adverse childhood experiences (ACEs), 15 assessment, 23, 166–169
Advocacy, 180–182 baclofen, 85
Affordable Care Act (ACA), 185 behavioral therapies
Alcohol, 163 cognitive-behavioral approaches, 95, 99
dependence, 66, 73 dialectical behavior therapy, 101
metabolism, 10 mindfulness-based interven-
Alcohol-associated liver disease (ALD), 53 tions, 102–104
Alcohol consumption, 179 motivational interviewing, 94
abuse and withdrawal, 4 cardiovascular health, 46, 47
clinical relevance, 6, 7 diagnosis of, 16–17, 23, 24, 55
cultural perspectives, 5, 6 didactic component, 160
history disulfiram, 80, 81
Greece, 2, 3 DSM-5-TR criteria, 11
Mesopotamia and Egypt, 1, 2 epidemiology, 22, 23
Rome, 4 epigenetics, 15
Alcohol dehydrogenase (ADH), 15 etiology, 26
Alcoholic liver disease, 47 FDA-approved, 79
Alcoholics anonymous (AA), 111, 119, 120, 5-HT3 receptor antagonists, 86
123, 145 gabapentin, 83
companionship, 122, 123 gastrointestinal health, 47
navigating sobriety, 120 genetics’ role, 15
roots and birth, 119 genetic variations, 15
Alcohol relapse risk assessment (ARRA), 59 hardware, 112
Alcohol-related liver disease (ALD), 53–58 health of physicians, 175

© The Editor(s) (if applicable) and The Author(s), under exclusive license to Springer 205
Nature Switzerland AG 2024
M. Khan, J. Avery (eds.), From Stigma to Support, Psychiatry Update 4,
https://doi.org/10.1007/978-3-031-73553-0
206 Index

Alcohol use disorder (AUD) (Cont.) Clinical Institute Withdrawal Assessment for
hematologic health, 48 Alcohol (CIWA-Ar), 68
insurance coverage, 158 Cognitive behavioral therapy (CBT),
medications, 57 30, 58, 110
mobile health applications, 109 Community reinforcement approach
naltrexone, 82, 83 (CRA), 96–98
neurological health, 45, 46 Concerned significant others (CSOs), 98
off-label agents, 79 Contingency management (CM) techniques,
online platforms, 111 96, 98, 99
pathophysiology, 24–26 Cost-benefit analysis (CBA), 111
pharmacotherapy, 27–29, 32–33 Cranial electrical stimulation (CES), 197
phosphodiesterase inhibitors, 86, 87 Cultural competence, 6
physical health, 41–44 Cultural humility, 4
prevalence, 22
primary care setting, 154
progression, 54 D
psychedelic drugs, 87 DBT skills training group (DBT-ST), 101
psychological factors, 16 Deep brain stimulation (DBS), 113
psychotherapy, 30–33 Delirium, 46
screening, 55 Diagnostic instrument, 10
signs and symptoms, 10 Dialectical behavior therapy
stigma, 153, 155, 159 (DBT), 100–102
treatment, 56 Disease model, 156
United States, 182–184 Disulfiram, 81
Alcohol withdrawal syndrome Dopamine transporter (DAT), 113
ambulatory approaches, 72, 73 Dorsolateral prefrontal cortex (DLPC), 113
pathophysiology and clinical dan- DSM-5-TR criteria, 11
gers, 65, 66
pharmacologic approaches, 70–72
treatment approaches, 68, 70 E
Aldehyde dehydrogenase (ALDH), 15 Electrolyte derangement, 44
Alpha-1 antagonists, 193 Employee health service (EHS), 168
prazosin, 193 Environment, 148
American Academy of Addiction Psychiatry Epigenetics, 15
(AAAP), 183
American Medical Association (AMA), 170
Ancient, 1, 4 F
Artificial intelligence (AI), 111 5-HT3 receptor antagonists, 86
Aspartate aminotransferase (AST), 55 Food and Drug Administration (FDA), 189
Attention deficit hyperactivity disorder
(ADHD), 22
G
GABAergic agents, 17
B Gabapentin, 83
Baclofen, 85 Gamma-aminobutyric acid type B
Biopsychosocial model, 157 (GABA-B), 85
Blood alcohol levels (BAC), 112 Gamma-glutamyl transpeptidase (GGT), 55
Brain stimulation, 190, 194 Gastrointestinal health, 42
Glucagon like peptide-1 receptor agonists
(GLP1-Ras), 192
C Go system, 14
Cardiovascular health, 42 Greece, 2
Chronic alcohol exposure, 13 Guided self-change (GSC), 99, 100
Index 207

H O
Hallucinogens, 191 Opioid use disorder (OUD), 29
Hardware, 112
Healthcare disparities, 182
Health legislation, 183 P
Hepatocellular carcinoma (HCC), 54 Pancreatitis, 48
Peer alternatives in addiction (PAL), 127
Peer recovery specialists (PRS), 134, 135
I Personality, 148
Independent medical evaluation (IME), 168 Physician fitness for duty, 171
Physician health program (PHP), 170,
172, 173
K Physician impairment, 164
Ketamine, 191 Physician recovery, 173
Physicians, 164, 166, 167
Physician trainees, 163, 164, 166
L Physiological/psychiatric conditions, 148
LifeRing secular recovery (LifeRing), Pregabalin, 190
128, 129 Psychedelic drugs, 87
Lipopolysaccharide (LPS), 54 Public health, 180, 183
Liver transplantation (LT), 59
Lysergic acid diethylamide (LSD), 87
R
Rational recovery systems (RR), 123
M Recovery, 143–145
Machine learning (ML), 111 Relapse, 146‑149
Meaning, 145, 146 Relapse prevention (RP), 93, 95, 96,
Medial prefrontal cortex (MPFC), 113 148, 149
Mental Health Parity Act (MHPA), 184 Relationships, 148
Metabolic dysfunction-associated steatotic Remission, 144
liver disease (MASLD), 54 Repetitive TMS (rTMS), 194–197
Mindfulness-based relapse prevention, Respiratory health, 42
102, 103 Rome, 4
Moderation management (MM), 130–132
Moral model, 156
Motivational interviewing (MI), 94 S
Musculoskeletal health, 42 Self-Management and Recovery Training
Mutual aid organizations (MAOs), 118, (SMART) recovery, 124–126
133, 134 State Health Access Data Assistance Center
(SHADAC), 185
State medical board (SMB), 164, 168
N Stigma, 153
Naltrexone, 82 Substance Abuse and Mental Health Services
National Institute on Alcohol Abuse and Administration (SAMHSA),
Alcoholism (NIAAA), 165, 183 110, 183
Neuroadaptations, 10, 13 Substance use disorders (SUDs), 153, 165
Neurological health, 42
Neuromodulation, 113, 193, 194
Neurotransmitter balance, 43 T
N-methyl D-aspartate (NMDA), 79 Theta-burst stimulation (TBS), 194
Number needed to treat (NNT), 154 Thiamine, 44
208 Index

3,4-methylenedioxymethamphetamine V
(MDMA), 192 Vitamin B12, 44
Timeline Follow Back (TLFB), 100 Voltage-gated calcium channel (VGCC), 190
Topiramate, 84
Transcranial direct current stimulation (tDCS),
113, 193, 196 W
Transcranial magnetic stimulation Wernicke encephalopathy, 46
(TMS), 113 Women for Sobriety (WFS), 129