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 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 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?