Pinel basics ch10

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Pinel basics ch10

  1. 1. Chapter 10 Hunger, Eating, and Health Why Do Many People Eat Too Much? <ul><li>This multimedia product and its contents are protected under copyright law. The following are prohibited by law: </li></ul><ul><li>any public performance or display, including transmission of any image over a network; </li></ul><ul><li>preparation of any derivative work, including the extraction, in whole or in part, of any images; </li></ul><ul><li>any rental, lease, or lending of the program. </li></ul>
  2. 2. Control of Eating <ul><li>Is there a “set point” for the body’s energy reserves that determines when we eat? </li></ul><ul><li>The prevalence of eating disorders suggests that this may not be the case </li></ul><ul><ul><li>Over half of the adult population in the U.S. meets clinical criteria for obesity </li></ul></ul><ul><ul><li>3% of U.S. adolescents suffer from anorexia nervosa </li></ul></ul>
  3. 3. Process of Digestion <ul><li>Purpose of eating is to provide the body with energy </li></ul><ul><li>Digestion – breaking down food and absorbing its constituents </li></ul><ul><li>3 forms of energy </li></ul><ul><ul><li>Lipids (fats) </li></ul></ul><ul><ul><li>Amino acids (proteins) </li></ul></ul><ul><ul><li>Glucose (carbohydrates) </li></ul></ul>
  4. 5. Energy <ul><li>Delivered as lipids, amino acids, and glucose </li></ul><ul><li>Stored as fats, glycogen, and proteins </li></ul><ul><li>Most stored as fats. Why? </li></ul><ul><li>More economical </li></ul><ul><ul><li>1 gram of fat stores 2X as much energy as 1 gram of glycogen </li></ul></ul><ul><ul><li>Fat does not attract and hold much water </li></ul></ul>
  5. 6. Energy Metabolism <ul><li>Chemical changes that make energy available for use – 3 phases: </li></ul><ul><ul><li>Cephalic – preparation </li></ul></ul><ul><ul><li>Absorptive – energy absorbed </li></ul></ul><ul><ul><li>Fasting – withdrawing energy from reserves, ends with next cephalic phase </li></ul></ul>
  6. 7. Energy Metabolism <ul><li>Controlled by 2 pancreatic hormones </li></ul><ul><li>Insulin – high during cephalic phase </li></ul><ul><ul><li>Allows body cells to use glucose </li></ul></ul><ul><ul><li>Promotes formation of glycogen, fat, and protein </li></ul></ul><ul><ul><li>Promotes storage of energy </li></ul></ul><ul><li>Glucagon – high during cephalic and absorptive phases </li></ul><ul><ul><li>Promotes the release of free fatty acids and their conversion to ketones – making stored energy available </li></ul></ul>
  7. 9. Set-Point Assumption <ul><li>Despite lack of evidence, most believe that hunger is a response to an energy need; we eat to maintain an energy setpoint </li></ul><ul><li>A negative feedback system – eating is turned “on” when energy is needed, “off” when setpoint is reached </li></ul>
  8. 11. What’s the set-point? <ul><li>If we eat to maintain an energy homeostasis, what is monitored? </li></ul><ul><li>Glucostatic theories – glucose levels </li></ul><ul><li>Lipostatic theories – fat stores </li></ul><ul><li>Glucose levels determine when we eat, fat stores determine amount of consumption over long-term (explaining why weight tends to be constant) </li></ul>
  9. 12. Problems with Set-Point Theories <ul><li>Epidemic of eating disorders </li></ul><ul><li>Contrary to evolutionary pressures that favored energy storage for survival </li></ul><ul><li>Reductions in blood glucose or body fat do not reliably induce eating </li></ul><ul><li>Do not account for the influence of external factors on eating and hunger </li></ul>
  10. 13. Positive-Incentive Perspective <ul><li>We are drawn to eat by the pleasure of eating – we evolved to crave food </li></ul><ul><li>Multiple factors interact to determine the positive-incentive value of eating </li></ul><ul><li>Accounts for the impact of external factors on eating behavior </li></ul>
  11. 14. Factors That Determine What We Eat <ul><li>Adaptive species-typical preferences </li></ul><ul><ul><li>Sweet and fatty foods – high energy </li></ul></ul><ul><ul><li>Salty – sodium-rich </li></ul></ul><ul><li>Adaptive species-typical aversions </li></ul><ul><ul><li>Bitter – often associated with toxins </li></ul></ul><ul><li>Learned preferences and aversions </li></ul>
  12. 15. Factors That Influence When We Eat <ul><li>We tend to get hungry at mealtime </li></ul><ul><li>As mealtime approaches, the body enters the cephalic phase leading to a decrease in blood glucose </li></ul><ul><li>Pavlovian conditioning of hunger demonstrated experimentally </li></ul>
  13. 16. Factors That Influence How Much We Eat <ul><li>Satiety – stops a meal, “being full” </li></ul><ul><li>Satiety signals – food in gut and glucose in the blood can induce satiety signals </li></ul><ul><li>Signals depend on both volume and nutritive density (amount and calories) </li></ul>
  14. 17. Factors That Influence How Much We Eat <ul><li>Change nutritive density > rats will adjust volume consumed to compensate </li></ul><ul><li>Can’t compensate if change is too extreme </li></ul><ul><li>Will increase caloric intake if palatability is increased (contrary to set-point theories) </li></ul>
  15. 19. Sham Eating <ul><li>Subject chews and swallows, but food then leaves the body </li></ul><ul><li>No energy consumed </li></ul><ul><li>Sham fed rats initially eat the same amount as they ate before, demonstrating the power of experience on meal size </li></ul>
  16. 20. Factors That Influence How Much We Eat <ul><li>Appetizer effect – small amounts of food may increase hunger </li></ul><ul><ul><li>Due to cephalic-phase responses? </li></ul></ul><ul><li>Social influences </li></ul><ul><ul><li>Even rats eat more when in a group </li></ul></ul><ul><li>Sensory-specific satiety </li></ul><ul><ul><li>Eat more with a cafeteria diet – satiety is largely taste-specific </li></ul></ul>
  17. 21. Sensory-specific Satiety <ul><li>Tasting a food immediately decreases the positive-incentive value of similar tastes and decreases the palatability of all foods ~ 30 min later </li></ul><ul><li>Adaptive – encourages a varied diet </li></ul>
  18. 22. Physiological Research on Hunger and Satiety <ul><li>Role of blood glucose levels </li></ul><ul><li>Myth of hypothalamic centers </li></ul><ul><li>Role of the GI tract </li></ul><ul><li>Hunger and satiety peptides </li></ul><ul><li>Serotonin and satiety </li></ul>
  19. 23. Role of Blood Glucose Levels in Hunger and Satiety <ul><li>Blood glucose drops prior to a meal as preparation to eat – not a cue to eat </li></ul><ul><li>Serving a tasty meal leads to eating without a drop in glucose </li></ul><ul><li>Premeal drops in glucose appear to be a response to the intention to eat (and the resulting increase insulin), not its cause </li></ul><ul><li>No meal > glucose levels return to normal </li></ul>
  20. 25. Myth of Hypothalamic Hunger and Satiety Centers <ul><li>Experiments suggested 2 hypothalamic centers </li></ul><ul><ul><li>Ventromedial (VMH) – a satiety center </li></ul></ul><ul><ul><li>Lateral (LH) – a hunger center </li></ul></ul><ul><li>Lesion VMH > hyperphagia </li></ul><ul><li>Lesion LH > aphagia and adipsia </li></ul>
  21. 27. Effect of bilateral VMH lesions
  22. 28. Myth of Hypothalamic Hunger and Satiety Centers <ul><li>VMH lesion rats maintain a new higher weight </li></ul><ul><li>LH lesion rats will recover if kept alive by tube feeding </li></ul><ul><li>Hypothalamus – regulates energy metabolism </li></ul>
  23. 29. Myth of Hypothalamic Hunger and Satiety Centers <ul><li>VMH lesions increase blood insulin </li></ul><ul><ul><li>Lipogenesis (fat production) increases </li></ul></ul><ul><ul><li>Lipolysis (fat breakdown) decreases </li></ul></ul><ul><ul><li>All calories are quickly stored so the rat must eat more to meet immediate needs </li></ul></ul><ul><li>Same results seen with lesions of noradrenergic bundle or paraventricular nuclei </li></ul>
  24. 30. Location of hypothalamic nuclei that impact feeding behavior
  25. 31. Role of the Gastrointestinal Tract in Satiety <ul><li>Cannon and Washburn (1912) </li></ul><ul><ul><li>Studies suggested stomach contractions led to hunger, distension to satiety </li></ul></ul><ul><li>But – hunger is still experienced with no stomach </li></ul><ul><li>Blood-borne satiety signals? </li></ul>
  26. 34. Satiety Peptides <ul><li>Several gut peptides bind to receptors in the brain and decrease meal size </li></ul><ul><li>Must 1 st establish that peptide does not merely create illness </li></ul><ul><li>CCK causes nausea at high doses, but suppresses food intake at doses insufficient to induce taste aversions </li></ul>
  27. 35. Hunger Peptides <ul><li>Peptides that increase appetite tend to be synthesized in the hypothalamus </li></ul><ul><li>Many different signals control eating </li></ul><ul><li>Hypothalamus plays a central role – microinjections of some peptides have major effects on eating </li></ul>
  28. 36. Serotonin and Satiety <ul><li>Serotonin agonists consistently reduce rats’ food intake </li></ul><ul><ul><li>Even intake of palatable food is affected </li></ul></ul><ul><ul><li>Reduces amount eaten per meal </li></ul></ul><ul><ul><li>Preferences shift away from fatty foods </li></ul></ul><ul><li>Similar effects seen in humans </li></ul>
  29. 37. Set-Point Assumptions about Body Weight and Eating <ul><li>Variability of body weight </li></ul><ul><ul><li>Would your weight stay the same if you ate whenever you were motivated to? </li></ul></ul><ul><li>Set points and health </li></ul><ul><ul><li>Free-feeding does not lead to optimum health </li></ul></ul><ul><ul><li>Positive effects seen with caloric-restriction </li></ul></ul><ul><li>Diet-induced thermogenesis – changes in body fat lead to changes in energy use </li></ul>
  30. 38. Settling-point Model <ul><li>Body weight drifts around a natural settling point – “the level at which the various factors that influence body weight achieve an equilibrium.” </li></ul><ul><li>A loose kind of homeostatic regulation </li></ul><ul><li>The leaky-barrel model </li></ul>
  31. 40. Why Is There an Epidemic of Obesity? <ul><li>Evolution favored preferring high calorie food, eating to capacity, storing fat, & using energy efficiently </li></ul><ul><li>Cultural practices and beliefs promote consumption </li></ul><ul><li>Such as? </li></ul>
  32. 42. Mutant Obese Mice and Leptin <ul><li>ob/ob mice are 3X normal weight </li></ul><ul><ul><li>Eat more and convert calories to fat more efficiently than controls </li></ul></ul><ul><ul><li>Lack leptin, a hormone produced by fat cells </li></ul></ul><ul><li>Leptin – a negative feedback fat signal </li></ul><ul><ul><li>Leptin levels and fat deposits are correlated </li></ul></ul><ul><ul><li>Injections decrease eating and body fat in ob/ob mice </li></ul></ul><ul><ul><li>Receptors for leptin in the brain </li></ul></ul>
  33. 43. Insulin: Another Negative Feedback Signal <ul><li>Like leptin, </li></ul><ul><ul><li>levels correlated with body fat </li></ul></ul><ul><ul><li>receptors found in the brain </li></ul></ul><ul><ul><li>reduces eating at levels too low to be aversive or to affect blood glucose </li></ul></ul><ul><li>Insulin deficiency leads to hyperphagia, but not obesity – food not converted to fat in the absence of insulin </li></ul>
  34. 44. Serotonergic Drugs and the Treatment of Obesity <ul><li>Leptin and insulin produce long-term satiety signals based on fat stores </li></ul><ul><li>Serotonin appears to increase short-term satiety signals associated with the consumption of a meal- decrease: </li></ul><ul><ul><li>urge to eat high-calorie foods </li></ul></ul><ul><ul><li>consumption of fat </li></ul></ul><ul><ul><li>intensity of hunger </li></ul></ul><ul><ul><li>size of meals </li></ul></ul><ul><ul><li>number of snacks and bingeing </li></ul></ul>
  35. 45. Anorexia Nervosa <ul><li>Why would a disorder of undereating develop? </li></ul><ul><li>Can this be explained by the theories presented in this chapter? </li></ul>

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