Copyright © 2009 by Allyn & Bacon Why Do Many People Eat Too Much? Chapter 12 Hunger, Eating, and Health
Copyright © 2009 by Allyn & Bacon 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
Copyright © 2009 by Allyn & Bacon 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)
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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
Copyright © 2009 by Allyn & Bacon Three Phases of Energy Metabolism Energy metabolism: Chemical changes t hat 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
Copyright © 2009 by Allyn & Bacon 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
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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
Copyright © 2009 by Allyn & Bacon 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
Copyright © 2009 by Allyn & Bacon 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
Copyright © 2009 by Allyn & Bacon 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
Copyright © 2009 by Allyn & Bacon 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
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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
Copyright © 2009 by Allyn & Bacon 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
Copyright © 2009 by Allyn & Bacon Location of hypothalamic nuclei that impact feeding behavior Myth of Hypothalamic Hunger and Satiety Centers (continued)
Copyright © 2009 by Allyn & Bacon 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?
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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
Copyright © 2009 by Allyn & Bacon 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
Copyright © 2009 by Allyn & Bacon 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
Copyright © 2009 by Allyn & Bacon 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
Copyright © 2009 by Allyn & Bacon 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
Copyright © 2009 by Allyn & Bacon The five stages of a typical weight-loss program.
Copyright © 2009 by Allyn & Bacon 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)
Copyright © 2009 by Allyn & Bacon 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
Copyright © 2009 by Allyn & Bacon 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
Copyright © 2009 by Allyn & Bacon 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
Copyright © 2009 by Allyn & Bacon 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