Chapter 12: Hunger, Eating, and Health

Digestion, Energy Storage, and Energy Utilization

Digestion and Energy Storage in the Body
Digestion
• Gastrointestinal process of breaking down food and absorbing its
constituents into the body
• The work of breaking down the food we ingest is done by the
constituents of our gut microbiome (bacteria & other organisms
that live inside our gastrointestinal tract)
Energy Storage in the Body
• Digestion à energy delivered to the body in 3forms:
o Lipids (fats)
o Amino acids (breakdown products of proteins)
o Glucose (breakdown product of complex carbohydrates –
starches & sugar)
• Body’s consumption of energy is intermittent, therefore the
body must store energy for use in the intervals between meals
o Most of the body’s stored energy are fats
• Why is fat the preferred way of storing energy?
o Glycogen – largely stored in the liver and muscles, might be expected to be the body’ preferred mode since it is readily
converted to glucose – body’s main directly utilizable source of energy
o A gram of fat can store almost twice as much as energy as a gram of glycogen
o Glycogen attracts and holds substantial quantities of water. Consequently, if all your fat calories were stored as
glycogen, you would likely weigh well over 275 kilograms
Three Phases of Energy Metabolism
• Energy metabolism: chemical changes by which energy is made available for an organism’s use
• Cephalic phase: reparatory phase; begins with the sight, smell, or even just the thought of food and ends when food starts
to be absorbed into the bloodstream
• Absorptive phase: period during which the energy absorbed into the bloodstream is meeting the body’s immediate energy
needs
• Fasting phase: unstored energy from the previous meal has been used up and the body’s withdrawing energy from its
reserves to meet its immediate energy requirements; ends with the beginning of cephalic phase
• During periods of rapid weight gain, people often go directly from one absorptive phase into the next cephalic phase,
without experiencing an intervening fasting phase
• The flow of energy during these phases is controlled by two pancreatic hormones: (1) insulin and (2) glucagon
• Cephalic and absorptive phase: high levels of insulin and low levels of glucagon
• Insulin: Promotes use of glucose as primary source of energy
o Promotes conversion of of bloodborne fuels to forms that can be stored: glucose glycogen and fat & amino acids à
protein
o Promotes storage of glycogen in liver and muscle, fat in adipose tissue, proteins in muscle
• Cephalic: Lower levels of bloodborne fuels, primary glucose, in anticipation of the impending influx
• Absorptive: Minimize increasing levels of bloodborne fuels by utilizing and storing them
• Fasting phase: high levels of glucagon & low levels of insulin
o Without high levels of insulin, glucose has difficulty entering the body cells, thus, it stops being the body’s primary fuel
à saves the glucose to enter most brain cells
o Low levels of insulin promote conversion of glycogen and protein to glucose (gluconeogenesis)
o High levels of fasting phase promote release of free fatty acids from adipose tissue and their use as the body’s primary
fuel. Also stimulates conversion of free fatty acids to ketones which are used by muscles during fasting phase.
o After a prolonged period of time without food, brain also uses ketones thus conserving body’s resources of glucose.
Theories of Hunger and Eating: Set Points vs. Positive Incentives
Set-Point Assumption
• After a meal à energy resources are near their set point it’ll decline as the body uses energy to fuel its physiological
processes à f body’s energy falls below the set point, the person is motivated by hunger
• The meal continues according to this, until the energy level returns to its set points and the person feels satiated (full)
• All set-point systems have three components: (1) set-point mechanism – defines the set-point, (2) detector mechanism –
detects the variations from the set-point, and (3) effector mechanism – acts to eliminate the deviations
• All set-point systems are negative feedback systems – systems in which feedback from changes in one direction elicit
compensatory effects in the opposite direction. Common for mammals since they act to maintain homeostasis –stable
internal environment critical for mammals’ survival
• Set-point systems combine negative feedback with a set point to keep an internal environment fixed at a prescribed point
o It seemed necessary when the adult human brain was assumed to be immutable: because the brain couldn’t change,
energy resources had to be highly regulated. However, now we know that brain is plastic there is no longer a logical
imperative for the set-point regulation of eating
Glucostatic Theory
• 1940s and 1950s à “What is monitored?” They speculated about the nature of the regulation
• Glucose levels determine when we eat
o Below set-point à hungry
o Set-point à satiated
• Glucose is primarily the brain’s fuel
Lipostatic Theory
• Body fats determine how much we eat over long term
• Set-point for body fats à deviations from this leads to compensatory adjustments in level of eating à returns levels of
body fat in set-point
• Support: body weights of adults stay relatively constant
Problems with set-point theories of hunger and eating
• Epidemic of obesity and overweight
• They are contrary to evolutionary pressures favouring energy storage for survival
• Reductions in blood glucose do not reliably induce eating
• They failed to account influences of external factors such as taste, learning, and social influences
Positive-Incentive Perspective
• Humans and animals are drawn to eat by the anticipated pleasure of eating
o Anticipated pleasure of a behavior à positive-incentive value
• Major tenet of this perspective
o Eating is controlled in much the same way as sexual behavior. We engage in sexual behavior because we evolved to
crave it.
o Evolutionary pressures of unexpected food shortages have shaped us to take advantage of good food when it is present
and eat it.
• Multiple factors interact to determine the positive-incentive value of eating
o Flavour of the food you’re likely to consume
o What you have learned about the effects of this food
o Amount of time since you last ate
o Type and quantity of food in your gut
• This does not single out one factor as the major determinant of hunger and ignore the others

Factors That Determine What, When, and How Much We Eat

Factors That Influence What We Eat
Learned Taste Preferences and Aversions
• Learned to prefer tastes that are followed by an infusion of calories, and they learn to avoid tastes that are followed by
illness
Learning to eat vitamins and minerals
• Deficient in sodium à immediate and compelling preference for the taste of sodium salt
• Deficient in some vitamin or mineral other than sodium must learn to consume foods that are rich in the missing nutrient
by experiencing their positive effects
o Vitamins and minerals other than sodium normally have no detectable taste in food
• Why are dietary deficiencies so prevalent in our society?
o Manufacturers produce foods that have the tastes we prefer but lack many of the nutrients we need to maintain our
health
Factors That Influence When We Eat
Premeal Hunger
• We tend to get hungry at mealtime
• Before a meal body’s energy reserves are in homeostatic balance, After meal major homeostasis-disturbing influx of
fuels into the blood stream
• When the usual meal time approaches, the body enters the cephalic phase, leading to a decrease in the blood glucose level
• Meal time hunger is because of the expectation of food and not energy deficit
Pavlovian Conditioning of Hunger
• Hunger is caused by expectation of food and not by energy deficit
• Weingarten (1983, 1984, 1985) – presented rats with 6 meals per day at irregular intervals, and signalled delivery of foods
with a buzzer-light conditional stimulus. This procedure was continued for 11 days. Despite the fact that the subjects were
never deprived the rats started to eat each time the buzzer and light were presented – even if they had recently completed
a meal
Factors That Influence How Much We Eat
• Satiety: motivational state that causes us to stop eating a meal when there is food remaining
Satiety Signals
• Food in the gut and glucose in the blood can induce satiety signals
• These signals depend on both the volume and the nutritive density (calories per unit volume) of
the food
Sham Eating
• Indicates that satiety signals from the gut or blood are not necessary to terminate a meal.
• Because sham eating adds no energy to the body, set-point theories predict that all sham-eaten
meals should be huge but this is not the case. If it includes their usual diet or if it is familiar, they eat a normal sized meal
Appetizer Effect and Satiety
• Small amounts of food consumed before a meal increases hunger this is effective since it elicits cephalic-phase responses
Serving Size and Satiety
• The larger the serving, the more we tend to eat
Social Influences and Satiety
• People consume more when eating with others.
Sensory Specific Satiety
• As you eat one food, the positive-incentive value of all foods declines slightly, but the positive-incentive value of that
particular food plummets. As a result, you become satiated on that food and stop eating it. However, if another food is
offered to you, you will often begin eating again.
• Booth (1981) - As soon as the food was consumed; there is a decrease in the positive-incentive value of similar tastes and a
decrease in the palatability of all foods 30 minutes later.
• Rolls suggested that sensory-specific satiety has 2 kinds of effects: (1) relatively brief effects that influence the selection of
foods within a single meal, and (2) relatively enduring effects that influence the selection of foods from meal to meal.
• Some foods resistant to long lasting sensory-specific satiety: Rice, bread, potatoes, sweets, and green salads (they can be
eaten everyday with only a slight decline in their palatability)
• Phenomenon of sensory-specific satiety has 2 adaptive consequences:
o Encourages consumption of a varied diet
§ If there were no sensory-specific satiety, then a person would tend to eat their preferred food and nothing else, and
result would be malnutrition.
 o Encourages animals that have access to a variety of foods to eat a lot

Physiological Research on Hunger and Satiety

Role of Blopd Glucose Levels in Hunger and Satiety
• Campfiled and Smith (1990): rats were housed with free access to water and food, and their blood glucose levels were
continually monitored. 10 minutes before a meal was initiated, the levels quickly dropped about 8 percent.
• The blood glucose drops prior to a meal as preparation to eat. Intention to start eating triggers the decline in blood
glucose.
• Four relevant observations:
o Glucose decline occurs suddenly, just before eating begins – this is not consistent with the idea the glucose decline
reflects the gradual decline in the body’s energy
o Eliminating premeal drop in blood glucose does not eliminate the meal
o If an expected meal is not served, blood glucose soon returns to its previous level
o Glucose levels in the extracellular fluid surrounding CNS neurons stay relatively constant, even when blood glucose
levels drop
Myth of Hypothalamic Hunger and Satiety Centers
• Experiments in the 1950s suggested that eating behavior is controlled by two different
regions of the hypothalamus:
o Ventromedial hypothalamus (VMH): satiety center
o Lateral hypothalamus (LH): feeding center
VMH Satiety Center
• Large bilateral electrolytic lesions to the VMH produce hyperphagia (excessive eating) and
extreme obesity in rats.
• VHM Syndrome has 2 phases:
o Dynamic Phase
§ Begins as soon as the subject regains consciousness after the operation is
characterized by several weeks of grossly excessive eating and rapid weight gain.
o Static Phase
o Consumption gradually declines to a level just sufficient to maintain a stable level of
obesity
§ Animal maintains its new body weight
§ If a rat in this phase, is deprived of food until it has lost a substantial amount of weight it will regain the lost weight
once the deprivation ends.
LH feeding center
• Bilateral electrolytic lesions to the lateral hypothalamus produce aphagia – a complete cessation of eating
• 2 important features of LH Syndrome
o Aphagia was acompanied by adipsia – a complete cessation of drinking.
o LH-lesioned rats partially recover if they are kept alive by tube feeding
Reinterpretation of the effects of VMH and LH lesions
• VMH is not a satiety center
o Primary role of the hypothalamus is the regulation of energy metabolism and not the regulation of eating; VHM-
lesioned animals overeat because they become obese
§ Bilateral VMH lesions increase blood insuoin levels, which increases lipogenesis (the production of body fat) and
decreases lipolysis (the breakdown of body fat to utilize forms of energy)
§ Because the calories ingested by VMH-lesioned rats are converted to fat at a high rate, the rats must keep eating to
ensure that they have enough calories in their blood to meet their immediate energy requirements
o Many of the effects of VMH Lesions are not attributable to VMH damage
§ VMH lesions may non-specifically destroy other brain regions such as the ventral noradrenegic bundle and the
paraventricular nuclei
§ Ventral noradrenergic bundle: courses past the VMH; damaged by large electrolytic VMH lesions
• Bilateral lesions of the noradrenergic bundle (e.g., Gold et al., 1977) or the paraventricular nuclei (Leibowitz,
Hammer, & Chang, 1981) produce hyperphagia and obesity, just as VMH lesions do.
• LH is not a feeding center: focus on the analysis of the effects of bilateral lesions
o LH lesions produce a wide range of severe motor disturbances and a general lack of responsiveness to sensory input
Modern research on the role of hypothalamic nuclei in hunger and satiety
• Certain neurons with the paraventricular nucleus of the hypothalamus have been shown to act as nutrient sensors that can
influence feeding and satiety
• Several distinct neuronal populations within the arcuate nucleus of the hypothalamus have been shown to either:
o Control the metabolism of adipose tissue
o Reduce feeding
o Increase feeding
Role of the Gastrointestinal Tract in Satiety
• Cannon and Washburn (1912): Washburn swallowed an empty balloon tied to the end of a thin tube. Cannon pumped
some air into the balloon and connected the end of the tube to a water-filled glass U-tube so that Washburns’s stomach
contractions produced a momentary increase in the level of the water at the other end of the U-tube. Washburn reported
a “pang” of hunger each time a large stomach contraction was recorded
o Hunger is the feeling of contractions caused by an empty stomach, whereas satiety is the feeling of stomach distention
• Human patients whose stomach had been surgically removed and whose esophagus had been hooked up directly to their
duodenum continued to report feelings of hunger and satiety and continued to maintain their normal body weight by
eating more meals of smaller size
• 1980s: gastrointenstinal tract is the source of satiety signals
o Koopmans (1981): transplanted an extra stomach and length of intestine into rats and then joined the major arteries
and veins of the implants to the recipients’ circulatory systems
o Food injected injected into the transplanted stomach and kept there by a noose around the pyloric sphincter decreased
eating in proportion to both its caloric content and volume
§ GI tract satiety signal reached the brain through the blood
§ Because nutrients are not absorbed from the stomach, the bloodborne satiety signal could not have been a nutrient
§ It had to be some chemical or chemicals that were released from the stomach in response to the caloric value and
volume of the food
Hunger and Satiety Peptides
• Peptides: short chain of amino acids that can function as hormones and neurotransmitters; chemicals released by GI tract
• Gibbs, Young, and Smith (1973): injected CCK (Cholecystokinin) into hungry rats and found that they ate smaller meals
o Circulating gut peptides provide the brain with information about the quantity and nature of food in the GI Tract and
that this information plays a role in satiety
• Satiety peptides: decrease appetite
o CCK, bombesin, glucagon, alpha-melanocyte-stimulating hormone, somatostatin
o Must first establish that peptide does not merely create illness
o CCK induces illness: when they are administered to rats after they have eaten an unfamiliar substance, it induced a
conditioned taste aversion for that substance, and CCK induces nausea in human
• Hunger peptides: increase appetite
o Synthesized in the brain, particularly in the hypothalamus
o Most widely studied: neuropeptide Y, galanin, orexin-A, and ghrelin
• Discovery of these peptides has had two major effects on the search for the neural mechanisms of hunger and satiety:
o Sheer number of these peptides indicates that the neural system that controls eating likely reacts to many different
signals (not just glucose and fat)
o Renewed interest in the role of the hypothalamus in hunger and eating
§ Interest was further stimulated by the discovery that microinjection of gut peptides into some sites in the
hypothalamus can have major effects on eating
Serotonin and Satiety
• 3 major properties;
o Caused caused the rats to resist intake of highly palatable cafeteria diets
o Reduced the amount of food eaten per meal
o Associated with a shift in food preferences away from fatty foods
• These suggest that serotonin might be useful in combating obesity in humans
Prader-Willi Syndrome: Patients with Insatibale Hunger
• Results from an accident of chromosomal replication
• Experiences insatiable hunger, little or no satiety, and an exceptionally slow metabolism
• Weak muscles, small hands and feet, feeding difficulties in infancy, tantrums, compulsivity and skin picking
• If left untreated, most patients become extremely obese, and they often die in early adulthood from diabetes, heart
disease, or other obesity-related disorders.
• Genetic cause: accident of reproduction that deletes or disrupts section of chromosome 15 coming from the father

Body-Weight Regulation: Set-Point vs. Settling Points

Set-Point Assumptions about Body Weight and Eating
Variability of body weight
• It is virtually impossible for an adult to gain or lose large amounts of weight but that’s not the case
• Set-point theories suggests that the best method of maintaining a constant body weight is to eat each time there is a
motivation to eat since the theory itself states that the main function of hunger is to defend the set-point
Set-points and health
• Each person’s set point is optimal for that person’s health
• Tenet: Ad Libidum (free-feeding) levels of consumption are unhealthy
o People living in Okinawa eat so few calories that their eating habits become a concern of health officials
o Lower death rate than the rest of Japan
o Slow down the aging process
o Calorie restriction in mammalian species
o One group is allowed to eat as much as they choose while other groups consumption was reduced results of the
latter: improved numerous indices of health and increased longetivity
• Caloric restriction has been shown to reduce seizure susceptibility in human epileptics and improve memory in elderly
Regulation of body weight by changes in the efficiency of energy utilization
• Diet-induced thermogenesis: mechanism by which the body adjusts the efficiency of its energy utilization in response to its
level of body fat
o Increases in the levels of body fat, increases body temperature requiring additional energy to maintain them, making
weight-loss diets gradually less effective (obese rats on cafeteria diet)
o Level of body fat declines, person starts to use more energy resources more efficiently, which limits further weight lost;
weight gain is limited by a proggresive decrease in the efficiency of energy utilization
§ Initially low calorie diets produce substantial weight loss, though week after week it diminishes until an equilibrium
is maintained and little or no further weight loss occurs
• Basal metabolic rate: rate at which energy is utilized to maintain bodily processes when resting
Set Points and Settling Points in Weight Control
• Settling point: the level at which the various factors that influence body weight achieve an equilibrium
o As body-fat levels increase, changes occur that tend to limit further increases until a balance is achieved between all
factors that encourage weight gain and all those that discourage it
• Settling point model
o Body weight tends to drift around a natural settling point – the level at which the various factors that influence body
weight achieve an equilibirum
o Body weight remains stable as long as there are no long term changes in the factors that influence it
o It provides a loose kind of homeostatic regulation
§ Without a set-point mechanism or mechanism to return body weight to a set point
• Leaky-barrel model

• Advantage: it is more consistent with data rather than the body-fat set-point model, does so more parsimoniously