copyright © 2009 by allyn & bacon why do many people eat too much? chapter 12 hunger, eating,...

Copyright © 2009 by Allyn & Bacon

Why Do Many People Eat Too Much?

Chapter 12Hunger, Eating, and Health


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 The average American consumes 3,800 calories

per day – about twice the average requirement


Digestion, Energy Storage, and Energy Utilization

Purpose of eating is to provide the body with molecular building blocks and energy

Digestion – breaking down food and absorbing its constituents

Energy storage in the body Lipids (fats) Amino acids (proteins) Glucose (carbohydrates)


Energy Storage in the Body

Energy delivered to the body as lipids, amino acids, and glucose

Stored as fats, glycogen, and proteins Fats are most efficient for energy storage

One gram of fat stores twice as much energy as one gram of glycogen


Three Phases of Energy Metabolism

Energy metabolism: Chemical changes that make energy available for use

Cephalic phase – preparation for eating Absorptive phase – energy absorbed Fasting phase

Withdrawing energy from reserves Ends with next cephalic phase


Three Phases of Energy Metabolism (continued)

Controlled by two pancreatic hormones Insulin – high during cephalic and

absorptive phases triggers glucose use as fuel by body cells triggers conversion of bloodborne energy to fat,

glycogen, and protein triggers energy storage in adipose cells, liver, and

muscles Glucagon – high during fasting phase

triggers change of stored energy to usable fuel: fat to free fatty acids and then ketones; protein to glucose


Hunger and Eating: Set Points vs. Positive Incentives

The Set-Point Assumption: Despite lack of evidence, most believe that

hunger is a response to an energy need; we eat to maintain an energy set point Glucostatic and lipostatic theory

Positive Incentive Theory


Problems with Set-Point Theo-ries of Hunger and Eating

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


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

Must decrease blood glucose by 50% to trigger feeding

Premeal glucose infusions often do not suppress eating

Reduced blood glucose may contribute to hunger, but changes in blood glucose do not prevent hunger or satiety


Myth of Hypothalamic Hunger and Satiety Centers Experiments suggested two hypo-

thalamic centers Ventromedial (VMH) – a satiety center Lateral (LH) – a hunger center

Lesions of VMH produce hyperphagia Lesions of LH produce aphagia and

adipsia


Myth of Hypothalamic Hunger and Satiety Centers (continued)

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 (continued)

VMH lesions increase blood insulin Lipogenesis (fat production) increases Lipolysis (fat breakdown) decreases All 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

Myth of HypothalamicHunger and SatietyCenters (continued)


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?


Hunger and Satiety Peptides

Gut peptides that decrease meal size: cholecystokinin (CCK), bombesin, glucacon,

alpha-melanocyte-stimulating hormone, somatostatin

Must first 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 Usually synthesized in the

hypothalamus – neuropeptide Y, galanin, orexin-A, ghrelin

Many different signals control eating (not just glucose and fat)

Hypothalamus plays a central role – microinjections of some peptides have major effects on eating


Serotonin and Satiety

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

Similar effects seen in humans


Serotonin and Satiety: Prader-Willi Syndrome

Possible key to understanding neural basis of obesity

Symptoms Food-related: insatiable appetite, extremely slow

metabolism; eventual death in adulthood from obesity-related diseases

Other symptoms: weak muscles, small hands and feet, triangular mouth, stubbornness, feeding difficulties in infancy, tantrums, compulsivity, skin picking

Damage or absence of a section of chromosome 15


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

calorie food, eating to capacity, storing fat, and using energy efficiently

Cultural practices and beliefs promote consumption


The five stages of a typical weight-loss program.


Why Do Some People Be-come Obese and Some Not?

Energy input differences Craving for high-calorie foods Cultural norms Large cephalic-phase response to sight and

smell of food Energy output differences

Exercise Diet-induced thermogenesis NEAT (nonexercise activity thermogenesis)


Leptin and the Regulation of Body Fat

Leptin – a negative feedback fat signal Hormone released by fat cells Leptin receptors found in the brain

ob/ob mice are three times normal weight Homozygous for a mutant gene ob Lack leptin Eat more, and store fat more efficiently than

controls Human leptin research

However, most obese humans have high leptin levels. Leptin injections help the few ob/ob humans


Insulin, Leptin, and the Arcuate Melanocortin System

Insulin brain levels reflect visceral fat; leptin levels reflect subcutaneous fat

Both insulin and leptin receptors found in the arcuate nucleus of the hypo-thalamus


Serotonergic Drugs and the Treatment of Obesity

Serotonin appears to increase short-term satiety signals associated with the consumption of a meal and decrease… urge to eat high-calorie foods consumption of fat intensity of hunger size of meals number of snacks and bingeing

Early serotonin agonists produced heart disease in some patients, was withdrawn, and not yet replaced


Anorexia Nervosa and Bulimia Nervosa

Anorexia Voluntary self-starvation Fatal in 10% of patients

Bulimia – bingeing and purging Similar symptoms, difficult to distinguish

Distorted body image Strike educated, affluent young females Associated with obsessive-compulsive disorder

and depression

copyright © 2009 by allyn & bacon why do many people eat too much? chapter 12 hunger, eating,...

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