Obesity Clinical, Surgical and Practical Guide, 2nd Edition ISBN 3031624904, 9783031624902 Entire Book Download
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Obesity
Clinical, Surgical and Practical Guide
Second Edition
Editor
Shamim I. Ahmad
Nottingham, UK
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It was the year 2015 when I realized that the number of obese people on the
street has increased in comparison with the people say for 10 years ago. My
research survey then confirmed that the obesity has gone up not only from
what I observed on the street but it is going up globally with a high rate. I
then decided and proposed my publisher about writing a book on obesity,
and this was approved. I then invited my co-author Dr. Khalid Imam to join
me in publishing a book, and in 2016, Springer published our first book on
obesity, and the title of the book is Obesity a Practical Guide.
We, as editors invited at global level those scientists working on obe-
sity to participate with their high quality research, esteemed knowledge and
superior publication abilities to contribute a chapter (or more) for our book.
Sixty-seven authors and co-authors contributed toward the book resulting in
27 chapters. Every chapter covers different aspects of obesity, comprehen-
sively, and with best quality.
Then in 2022, I approached again to the same publisher proposing three
different titles to be selected one of them for the next forthcoming publica-
tion. I was advised to work on a book “Obesity—edition 2”. It was said that
this second edition would be most appropriate because the rate the obesity
is continuously increasing and may not be that far that in certain population
this disease may slip on where 50% of the people may be suffering from
this disease.
On this occasion, due to my sub-editor’s other commitments, I was to
take-up solo this challenge. About deciding its title I noted that a number of
important chapters were missing or taken lightly in the first book. I focused
on them, and the title selected for this book is Obesity: Clinical, Surgical
and Practical Guide.
The contents of this book have been divided into 7 parts, and chapters are
numbered from 1 to 21.
In many parts of the world, obesity now has taken the form of epidemic,
and both developed and developing nations are becoming concerned about
it. The World Health Organization (WHO) predicted that by 2025, 167 mil-
lion adults and children will be affected due to this disease. Moreover, it
vii
viii Preface
found that various inflammatory disorders are developed in fatty people due
to the elevated level of inflammatory mediators, playing the cabalistic role
in the development of the disease. Especially factors, such as leptin, plas-
minogen activator inhibitor-1, and adiponectin, and these contribute to car-
cinogenesis and carcinogenic progression. Also cytokines in obese adipose
tissue promote the spread of tumor cells, leading to metastasis.
The same authors in Chap. 17 have presented a detail analysis of genetic
variants connected to obesity—thus included in this part.
Genetic variation significantly affects how individuals respond to an
“obesogenic” environment. Genetics of obesity is divided into subgroups
like monogenic, syndromic, and polygenic or common obesity based on
genetic aetiology. As yet eleven genes have been identified as causative
agent of monogenic obesity. These include POMC, LEP, LEPR, PCSK1,
and MC4R. Polygenic obesity is linked with mutations in TFAP2B,
CYP27A1, IFNGR1, PARK2, UCP2 and UCP3, ADRB1-3, SLC6A14,
NPY, MC3R, and FTO. Studies of these candidate gene genome-wide
association studies (GWAS) have been playing important roles for study-
ing polygenic obesity. Also the GWAS study has played important roles
to determine the association between SH2B1, FTO, MC4R, KCTD15,
NEGR1, and TMEM18 genes with the pathogenesis of obesity.
In Chap. 4, the studies of T. Tabassum and S. Khan although found that
the obesity-linked leptin is positively correlated with cancer progression in
some cancers, yet the information remains unclear whether the defect is in
the genome or in the signaling pathways. To put more light on this infor-
mation, they incorporated two most important common gynaecological can-
cers literature searches, found both in vivo patient and animal models. This
review offers up-to-date and cohesive views of both upstream and down-
stream pathways of leptin in gynaecological cancers. The understanding
of the pathogenesis will tie together all current evidence of similarities or
differences in how leptin affects major types of cancers in women with the
hope of designing better therapeutic strategies in the future for those obese/
overweight women with cancers.
In Chap. 5, G. Seravalle and G. Grassi have critically analyzed the occur-
rence of hypertension in obese people and this is what they have said: Obesity
pandemic worldwide affecting the obese people to suffer from hypertension
and to the cardiovascular morbidity leading to a significant increased pressure
to hospitals and cost increased to the healthcare system. Several pathophysi-
ological mechanisms have been discovered to prevail both in obesity and obe-
sity-induced hypertension. These include the increase in adrenergic tone and
impairment in reflex mechanisms, renal hyperfiltration, activation of rennin-
angiotensin-aldosterone system, endothelial dysfunction, and increase in oxi-
dative stress.
In Chap. 6, P. Ginod and M. Dahan described and highlighted the links
between polycystic ovary syndrome (PCOS), obesity in women, and adverse
obstetrics outcomes, which has only recently started to be studied.
It is claimed that the obesity induces gynaecologic and obstetric compli-
cations throughout women’s reproductive life spans. Also PCOS appears to
be a risk factor for obstetrical complications, problematic reproductive and
x Preface
pregnancy outcome, and PCOS remains a risks factor for infertility. Indeed,
PCOS patients with or without obesity present specific obstetrics complica-
tions likely linked to altered endometrial function mediated by hyperandro-
genism, hyperinsulinism, and insulin resistance.
In Chap. 7, T. Barber and his co-authors discussed aspects of PCOS, in
that there is a close association between female obesity and the development
of hyperandrogenism, insulin resistance, and cardiometabolic dysfunction.
These clinical features are most notable in women with PCOS. The under-
lying mechanisms are changes in adipose-related enzyme activities and the
effects of hyperinsulinemia as a co-gonadotrophin within the ovarian theca
cells. Hyperinsulinemia also increases adrenal androgen production and the
pituitary release of luteinizing hormone and suppresses the hepatic produc-
tion of sex hormone binding globulin, thereby increasing the free androgen
index. The development of hyperandrogenemia likely promotes a prepon-
derance of visceral adipose tissue with its attendant effects on enhanced
insulin resistance and cardiometabolic risk.
Further it is proposed that female obesity with hyperandrogenism and
cardiometabolic dysfunction can be controlled by effective and sustained
weight loss. In some women this strategy may be combined with the anti-
androgen therapy and/or metformin.
Chapter 8 by N. C. C. Tapia is on non-alcoholic steatohepatitis which is
one of the earliest diseases first described in 1980. Then in 2020, its name
was changed to Metabolic Associated Fatty Liver Disease (MAFLD).
Patients with MAFLD are older, have a higher body mass index, and higher
proportions of metabolic comorbidities. Also MAFLD has been shown to be
associated with a higher risk of diabetes, chronic kidney disease, and cardio-
vascular disease. The association of fatty liver disease with obesity and/or
type-2 diabetes mellitus has been well established.
Scientists and researchers are still remaining to find a suitable ‘cure’ for
obesity which is easy to be implemented by most people. This is evident
from the fact that most people who lose weight regain their obesity within a
few years. Despite this fact, non-fattening diet and regular exercise remains
the best alternative to control obesity. My search reveals that the only
weight loss drug approved by the Food and Drug Administration (FDA) for
long-term use is orlistat. Yet it remains a contradicted issue based on the
claim that this medicine can make people to eat less or make less of the
energy from food to be absorbed by their elementary canals.
In Chap. 9, T. Lopez and co-authors indicate that the prevalence of over-
weight and obesity worldwide has seen a significant increase since 1980,
with rates approximately doubling. Currently, more than one-third of the
global population is classified as overweight or obese and if the current
trends persist, it is projected that 57.8% of the world’s population will be
overweight or obese by the year 2030. As a consequence of this escalating
trend, anesthesiologists, critical care physicians, and emergency physicians
Preface xi
of adipose tissue which changes in obesity, and this poses a health risk.
Hypertrophy, infiltration of immune cells, hypoxia, and fibrosis as micro-
environmental changes have been occurring as a result of excessive lipid
accumulation of adipocytes. Obesity-associated inflammation basically
depending on microenvironmental changes of adipose tissue, but when die-
tary polyphenols are present they can modify adipose tissue microenviron-
ment against obesity.
Various polyphenols are secondary plant metabolites, characterized as a
phenolic compound. Polyphenols-associated obesity via anti-inflammatory
roles are flavonoids, phenolic acids, and non-flavonoids. The anti-obesity
effects of polyphenols via anti-inflammatory pathways have been studied
with the cell culture (3T3-L1 adipocytes) and animal (C57BL/6J mice).
Resveratrol and catechins, these two polyphenols have drawn more atten-
tion of the researchers and extensive studies carried out. In spite of these
studies there is lack of clinical studies to demonstrate the anti-inflammatory
response of those polyphenols.
Chapter 16 by M. A. de Souza Pinhel and co-authors took an unusual
path and presented the truth about the influence of endocrine disruptors on
obesity and that what can be done.
Endocrine disruptor can be defined as an exogenous substance or mixture
with the potential to disrupt hormonal regulation, the normal endocrine sys-
tem, and consequently causes adverse health effects in humans. Among var-
ious toxicological mechanisms of action, non-essential heavy metals have
been considered as endocrine disruptors (EDs) through interference with the
adipose tissue metabolism.
One of the known risk factor for a number of chronic conditions is obe-
sity which is triggered by the disruption of adipose tissue homeostasis and
has been proven to favor a pro-oxidative and pro-inflammatory environment.
Human exposure to heavy metals such as arsenic, cadmium, and lead has
been associated with metabolic alterations, especially because they induce
oxidative stress by inhibiting the activity of superoxide dismutase, reduc-
ing antioxidants, or binding to -SH groups of proteins. Also addresses the
main elements recognized as EDs and how they can alter genetic and epi-
genetic mechanisms, creating a risk scenario for obesity and associated
comorbidities.
Chapter 17: This chapter by Md. S. Hossen and the co-authors with the title
“Genetics Variants Connected to the Obesity” has been combined with Chap. 3.
and adipokines. Patients with obesity are additionally more prone to comor-
bidities that exacerbate the clinical course of COVID-19, comprising of
type-2 diabetes mellitus, cardiovascular disease, and lung disease. Lastly,
patients with obesity are at a heightened risk of clinically severe illness and
mortality from COVID-19.
and emotional aspects associated with the surgery and post-bariatric surgery
periods, contributes to the success of the treatment, a better quality of life,
and the well-being of this population.
xvii