PS263: Chapter 12 – Hunger, Eating and Health
Average American consumes 3,800 calories a day (2x the daily requirement)
Many people believe that hunger & eating are normally triggered when the
body’s energy resources fall below a prescribed optimal level or, set point.
Purpose of hunger = increase the probability of eating, the primary purpose
of eating = supply the body with molecular building blocks & energy to live
Digestion, Energy Storage & Utilization
Digestion: Gastrointestinal process of breaking down food & absorbing its
constituents into the body (7 steps of digestion; page 300) – food has not
been consumed until it has been digested; broken down and absorbed.
Energy is delivered to the body in 3 forms: 1) lipids (fats), 2) amino acids
(breakdown products of proteins), 3) glucose (simple sugar that is the
breakdown product of complex carbs; sugars & starches)
Body uses energy continuously – consumption is intermittent; must store
energy for use in intervals between meals: fats, glycogen and proteins.
o Glycogen: Largely stored in liver & muscles; readily convert to glucose
o Fats: The primary energy source: a gram of fat can store twice as
much as a gram of glycogen & it attracts and holds a lot of water.
Three phases of energy metabolism (chemical changes by which energy is
made available for an organisms use)
1. Cephalic Phase: Preparatory phase; often begins with the sight, smell or even
just the thought of food & it ends when the food is absorbed to bloodstream.
2. Absorptive Phase: Period during which the energy absorbed into the
bloodstream from the meal is meeting the body’s immediate energy needs.
3. Fasting Phase: Period during which all of the unstored energy from the
previous meal has been used and the body (extreme weight gain = 1+3 no 2)
During cephalic & absorptive, pancreas releases a great deal of insulin:
1. Promotes use of glucose as the primary source of energy by the body.
2. Promotes the conversion of blood borne fuels to forms that can be stored.
3. Promotes the storage of glycogen in liver & muscle, fat in adipose tissue &
proteins in muscle.
In cephalic it lowers levels of blood borne fuels (glucose) anticipating influx
In absorptive is minimizes the increasing levels by utilizing & storing them.
Fasting phase is characterized by high levels of glucagon and low insulin –
without insulin glucose has difficulty entering – saves glucose for the brain,
and promoted conversion of glycogen into glucose (gluconeogenesis)
o High levels of fasting-phase glucagon promotes the release of free fatty
acids from adipose tissue (use as primary fuel)
o Also promote the conversion of free fatty acids to ketones: used by
muscles as a source of energy during the fasting phase.
Theories of Hunger
Set-Point Assumption: After a meal, a person’s energy resources are assumed
to be near their set point and to decline thereafter as the body uses energy to
fuel its physiological processes. – When the level of the body’s energy
resources falls far enough below set point a person becomes motivated by PS263: Chapter 12 – Hunger, Eating and Health
hunger to initiate another meal. Meal continues according to set-point, until
the energy level returns to the set point and the person feels satiated.
o Assume that hunger & earing work the same as a thermostat
o Set-point mechanism defines the set point, the detector mechanism
detects deviations from the set point, the effector mechanism acts to
eliminate the deviations.
All set-point systems are negative feedback systems: in which feedback
changes in one direction to elicit compensatory effects in the opposite
direction – they maintain homeostasis (stable internal environment)
Glucostatic Theory: Eating is regulated by a system designed to maintain
blood glucose set point – we become hungry when our blood glucose levels
drop below their set point & we become satiated when eating returns our
blood levels to set point - glucose = brains primary fuel. (short-term)
Lipostatic Theory: Every person has a set point for body fat & deviations
from this set point; body weights of adults are relatively constant (long-term)
There is an epidemic of obesity & overweight – shouldn’t happen in set-point:
1. Set point theories of hunger/eating are inconsistent with basic eating-related
evolutionary pressures – inconsistency & unpredictability (need to store fat)
2. Set point theories of hunger and eating predictions have not been confirmed.
3. Set point theories of hunger & eating are deficient because they fail to
recognize the major influences on hunger & eating of such factors: taste, etc.
Positive-Incentive Theory: Humans & other animals are not normally driven
to eat by internal energy deficits but are drawn to eat by the anticipated
pleasure of eating, the anticipated pleasure of a behavior = positive incentive
value; degree of hunger you feel depends on all factors together.
Factors determining: What, When & How much we Eat
Preference & Aversion: Animals prefer tastes with an infusion of calories and
avoid tastes that make them ill. Humans learn from conspecifics & culture.
Vitamins & Minerals: When an animal is deficient in sodium it develops an
immediate & compelling preference for sodium salt, but deficient in vitamins
& minerals must learn to consume foods rich in missing nutrients (positive)
o Nutrients do not play a part in hunger; they play a role in health.
Number of times humans eat per day depends on cultural norms, work
schedules, family routines (3 meals vs. all day snacking), when hungry times.
o Malaise: headache, nausea, & inability to concentrate
Premeal Hunger: Strong, unpleasant feelings of hunger you may experience
at meal times is not cries out for food – they are sensations of your body’s
preparations for the expected homeostasis-disturbing meal; expectation.
Pavlovian Conditioning: Hunger is caused by expectation not deficit
Satiety - Motivational state that causes us to stop eating a mean when food is
remaining – plays a major role in determining how much we eat.
Satiety Signals: Food in the guy & glucose entering the blood can induce
signals that inhibit consumption; they depend on both volume & nutritive
density (calories per unit volume of food) PS263: Chapter 12 – Hunger, Eating and Health
Sham Eating: Satiety signals from the gut/blood are not necessary to
terminate a meal – food is chewed & not swallowed, passed out tube.
Appetizer Effect: If appetizers served you will notice small amounts of food
consumed before a meal actually increase hunger – elicits cephalic phase.
Social & Size: The larger the serving, the more we are inclined to eat –
depends on eating alone or with others.
Cafeteria Diet: Diet of highly palatable foods - # of tastes available.
Sensory-Specific Satiety: The fact that a consumption of a particular food
produces increased satiety for foods of the same taste than for other foods.
1. Encourages the consumption of a varied diet – without = no variation.
2. Encourages animals that have access to a variety of foods to eat a lot.
Physiological Research on Hunger & Satiety
Ventromedial Hypothalamus: 1940 discovered that large bilateral
electrolytic lesions to the ventromedial hypothalamus produce hyperphagia
(excessive eating) & obesity in rats.
1. Dynamic Phase = Begins as soon as the subject regains consciousness after
the operation, characterized by several weeks of excessive eating & weight.
2. Static Phase = Consumption gradually declines to a level sufficient to
maintain a stable level of obesity – animal maintains its new body weight.
Lateral Hypothalamus: 1951, bilateral electrolytic lesions to the lateral
hypothalamus produce aphagia (complete cessation of eating)