Pinel basics ch10

Copyright © 2007 by Allyn and Bacon

Chapter 10Hunger, Eating, and Health

Why Do Many People Eat Too Much?

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Control of Eating

Is there a “set point” for the body’s energy reserves that determines when we eat?

The prevalence of eating disorders suggests that this may not be the case Over half of the adult population in the

U.S. meets clinical criteria for obesity 3% of U.S. adolescents suffer from

anorexia nervosa


Process of Digestion

Purpose of eating is to provide the body with energy

Digestion – breaking down food and absorbing its constituents

3 forms of energy Lipids (fats)Amino acids (proteins)Glucose (carbohydrates)



Energy

Delivered as lipids, amino acids, and glucose

Stored as fats, glycogen, and proteins Most stored as fats. Why? More economical

1 gram of fat stores 2X as much energy as 1 gram of glycogen

Fat does not attract and hold much water


Energy Metabolism

Chemical changes that make energy available for use – 3 phases:Cephalic – preparationAbsorptive – energy absorbedFasting – withdrawing energy from

reserves, ends with next cephalic phase


Energy Metabolism

Controlled by 2 pancreatic hormones Insulin – high during cephalic phase

Allows body cells to use glucose Promotes formation of glycogen, fat, and protein Promotes storage of energy

Glucagon – high during cephalic and absorptive phases Promotes the release of free fatty acids and their

conversion to ketones – making stored energy available



Set-Point Assumption

Despite lack of evidence, most believe that hunger is a response to an energy need; we eat to maintain an energy setpoint

A negative feedback system – eating is turned “on” when energy is needed, “off” when setpoint is reached



What’s the set-point?

If we eat to maintain an energy homeostasis, what is monitored?

Glucostatic theories – glucose levels Lipostatic theories – fat stores Glucose levels determine when we eat, fat

stores determine amount of consumption over long-term (explaining why weight tends to be constant)


Problems with Set-Point Theories

Epidemic of eating disorders Contrary to evolutionary pressures that

favored energy storage for survival Reductions in blood glucose or body fat do

not reliably induce eating Do not account for the influence of

external factors on eating and hunger


Positive-Incentive Perspective We are drawn to eat by the

pleasure of eating – we evolved to crave food

Multiple factors interact to determine the positive-incentive value of eating

Accounts for the impact of external factors on eating behavior


Factors That Determine What We Eat

Adaptive species-typical preferencesSweet and fatty foods – high energySalty – sodium-rich

Adaptive species-typical aversionsBitter – often associated with toxins

Learned preferences and aversions


Factors That Influence When We Eat We tend to get hungry at mealtime As mealtime approaches, the body

enters the cephalic phase leading to a decrease in blood glucose

Pavlovian conditioning of hunger demonstrated experimentally


Factors That Influence How Much We Eat Satiety – stops a meal, “being full” Satiety signals – food in gut and

glucose in the blood can induce satiety signals

Signals depend on both volume and nutritive density (amount and calories)


Factors That Influence How Much We Eat Change nutritive density >

rats will adjust volume consumed to compensate

Can’t compensate if change is too extreme

Will increase caloric intake if palatability is increased (contrary to set-point theories)



Sham Eating

Subject chews and swallows, but food then leaves the body

No energy consumed Sham fed rats initially eat the same

amount as they ate before, demonstrating the power of experience on meal size


Factors That Influence How Much We Eat Appetizer effect – small amounts of food

may increase hunger Due to cephalic-phase responses?

Social influencesEven rats eat more when in a group

Sensory-specific satietyEat more with a cafeteria diet – satiety is

largely taste-specific


Sensory-specific Satiety

Tasting a food immediately decreases the positive-incentive value of similar tastes and decreases the palatability of all foods ~ 30 min later

Adaptive – encourages a varied diet


Physiological Research on Hunger and Satiety

Role of blood glucose levels Myth of hypothalamic centers Role of the GI tract Hunger and satiety peptides Serotonin and satiety


Role of Blood Glucose Levels in Hunger and Satiety Blood glucose drops prior to a meal as

preparation to eat – not a cue to eat Serving a tasty meal leads to eating

without a drop in glucose Premeal drops in glucose appear to be a

response to the intention to eat (and the resulting increase insulin), not its cause

No meal > glucose levels return to normal



Myth of Hypothalamic Hunger and Satiety Centers

Experiments suggested 2 hypothalamic centersVentromedial (VMH) – a satiety centerLateral (LH) – a hunger center

Lesion VMH > hyperphagia Lesion LH > aphagia and adipsia



Effect of bilateral VMH lesions


Myth of Hypothalamic Hunger and Satiety Centers

VMH lesion rats maintain a new higher weight

LH lesion rats will recover if kept alive by tube feeding

Hypothalamus – regulates energy metabolism


Myth of Hypothalamic Hunger and Satiety Centers VMH lesions increase blood insulin

Lipogenesis (fat production) increasesLipolysis (fat breakdown) decreasesAll calories are quickly stored so the rat must

eat more to meet immediate needs Same results seen with lesions of

noradrenergic bundle or paraventricular nuclei


Location of hypothalamic nuclei that impact feeding behavior


Role of the Gastrointestinal Tract in Satiety

Cannon and Washburn (1912)Studies suggested stomach contractions

led to hunger, distension to satiety But – hunger is still experienced with

no stomach Blood-borne satiety signals?




Satiety Peptides

Several gut peptides bind to receptors in the brain and decrease meal size

Must 1st establish that peptide does not merely create illness

CCK causes nausea at high doses, but suppresses food intake at doses insufficient to induce taste aversions


Hunger Peptides

Peptides that increase appetite tend to be synthesized in the hypothalamus

Many different signals control eating Hypothalamus plays a central role –

microinjections of some peptides have major effects on eating


Serotonin and Satiety

Serotonin agonists consistently reduce rats’ food intakeEven intake of palatable food is affected Reduces amount eaten per mealPreferences shift away from fatty foods

Similar effects seen in humans


Set-Point Assumptions about Body Weight and Eating Variability of body weight

Would your weight stay the same if you ate whenever you were motivated to?

Set points and healthFree-feeding does not lead to optimum healthPositive effects seen with caloric-restriction

Diet-induced thermogenesis – changes in body fat lead to changes in energy use


Settling-point Model

Body weight drifts around a natural settling point – “the level at which the various factors that influence body weight achieve an equilibrium.”

A loose kind of homeostatic regulation

The leaky-barrel model



Why Is There an Epidemic of Obesity? Evolution favored preferring high calorie

food, eating to capacity, storing fat, & using energy efficiently

Cultural practices and beliefs promote consumption

Such as?



Mutant Obese Mice and Leptin

ob/ob mice are 3X normal weightEat more and convert calories to fat more

efficiently than controlsLack leptin, a hormone produced by fat cells

Leptin – a negative feedback fat signalLeptin levels and fat deposits are correlated Injections decrease eating and body fat in

ob/ob miceReceptors for leptin in the brain


Insulin: Another Negative Feedback Signal Like leptin,

levels correlated with body fatreceptors found in the brainreduces eating at levels too low to be aversive

or to affect blood glucose Insulin deficiency leads to hyperphagia,

but not obesity – food not converted to fat in the absence of insulin


Serotonergic Drugs and the Treatment of Obesity Leptin and insulin produce long-term satiety

signals based on fat stores Serotonin appears to increase short-term satiety

signals associated with the consumption of a meal- decrease: urge to eat high-calorie foods consumption of fat intensity of hunger size of meals number of snacks and bingeing


Anorexia Nervosa

Why would a disorder of undereating develop?

Can this be explained by the theories presented in this chapter?

Pinel basics ch10

Health & Medicine

satiety blood glucose

energy storage

energy setpoint

energy digestion

energy homeostasis

meal glucose levels

stored energy available

energy consumed sham