Pinel basics ch10

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  • 1. Chapter 10 Hunger, Eating, and Health Why Do Many People Eat Too Much?
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  • 2. 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
  • 3. Process of Digestion
    • 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)
  • 4.  
  • 5. Energy
    • Delivered 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
  • 6. Energy Metabolism
    • Chemical changes that make energy available for use – 3 phases:
      • Cephalic – preparation
      • Absorptive – energy absorbed
      • Fasting – withdrawing energy from reserves, ends with next cephalic phase
  • 7. 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
  • 8.  
  • 9. 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
  • 10.  
  • 11. 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)
  • 12. 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
  • 13. Positive-Incentive Perspective
    • We are drawn to eat by the pleasure of eating – we 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
  • 14. 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
  • 15. 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
  • 16. 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
    • Signals depend on both volume and nutritive density (amount and calories)
  • 17. Factors That Influence How Much We Eat
    • Change nutritive density > rats will adjust volume consumed to compensate
    • Can’t compensate if change is too extreme
    • Will increase caloric intake if palatability is increased (contrary to set-point theories)
  • 18.  
  • 19. Sham Eating
    • Subject chews and swallows, but food then leaves the body
    • No energy consumed
    • Sham fed rats initially eat the same amount as they ate before, demonstrating the power of experience on meal size
  • 20. 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
  • 21. 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
  • 22. 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
  • 23. 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
    • Serving a tasty meal leads to eating without a drop in glucose
    • Premeal drops in glucose appear to be a response to the intention to eat (and the resulting increase insulin), not its cause
    • No meal > glucose levels return to normal
  • 24.  
  • 25. 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
  • 26.  
  • 27. Effect of bilateral VMH lesions
  • 28. 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
  • 29. 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
  • 30. Location of hypothalamic nuclei that impact feeding behavior
  • 31. 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?
  • 32.  
  • 33.  
  • 34. Satiety Peptides
    • Several gut peptides bind to receptors in the brain and decrease meal size
    • Must 1 st 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
  • 35. Hunger Peptides
    • Peptides that increase appetite tend to be synthesized in the hypothalamus
    • Many different signals control eating
    • Hypothalamus plays a central role – microinjections of some peptides have major effects on eating
  • 36. 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
  • 37. 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
  • 38. 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
  • 39.  
  • 40. 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?
  • 41.  
  • 42. 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
  • 43. 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
  • 44. 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
  • 45. Anorexia Nervosa
    • Why would a disorder of undereating develop?
    • Can this be explained by the theories presented in this chapter?