1. Chapter 12 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. 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)

5. 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

6. 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

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

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

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 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

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
Sham eating – satiety signals are not necessary for meal termination
Demonstrates the role experience plays in meal termination

18. 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

19. 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

20. 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

21. 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

22. 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

24. Effect of bilateral VMH lesions

25. 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

26. 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

27. Location of hypothalamic nuclei that impact feeding behavior

28. 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?

30. 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

31. 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

32. 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

33. 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

34. 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

36. 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?

38. 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

39. 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

40. 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

41. Anorexia Nervosa Why would a disorder of undereating develop?
Can this be explained by the theories presented in this chapter?