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Chapter 12 Hunger, Eating, and Health Why Do Many People Eat Too Much? This multimedia product and its contents are protected under copyright law. The following are prohibited by law: • any public performance or display, including transmission of any image over a network; • preparation of any derivative work, including the extraction, in whole or in part, of any images; • any rental, lease, or lending of the program. 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 Digestion and Energy Flow • 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 to the body 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 • Cephalic phase – preparation • Absorptive phase – energy absorbed • Fasting phase – – 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 anticipated pleasure of eating – we have 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 preferences – Sweet and fatty foods – high energy – Salty – sodium-rich • Adaptive species-typical aversions – Bitter – 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 • Sham eating – satiety signals are not necessary for meal termination – Demonstrates the role experience plays in meal termination Factors That Influence How Much We Eat • Appetizer effect – small amounts of food may increase hunger – Due to cephalic-phase responses? • Social influences – Even rats eat more when in a group • Sensory-specific satiety – Eat more with a cafeteria diet – satiety is largely tastespecific 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 • 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 2 hypothalamic centers – Ventromedial (VMH) – a satiety center – Lateral (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) 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 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 • Gut peptides that decrease meal size: – Cholecystokinin (CCK), bombesin, glucagon, alphamelanocyte-stimulating horming, somatostatin • 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 • Usually synthesized in the hypothalamus neuropeptide Y, galanin, orexinA, ghrelin • 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 intake – Even intake of palatable food is affected – Reduces amount eaten per meal – Preferences 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 health – Free-feeding does not lead to optimum health – Positive 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 weight – Eat more and convert calories to fat more efficiently than controls – Lack leptin, a hormone produced by fat cells • Leptin – a negative feedback fat signal – Leptin levels and fat deposits are correlated – Injections decrease eating and body fat in ob/ob mice – Receptors for leptin in the brain Insulin: Another Negative Feedback Signal • Like leptin, – levels correlated with body fat – receptors found in the brain – reduces 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?