Hunger & Eating Flashcards
Energy stored in the body
¢Energy delivered to the body as lipids, amino acids, and glucose
¢Stored as fats (85%), glycogen (0.5%), and proteins (14.5%)
Glycogen in liver and muscle most directly usable
¢Fats are most efficient for energy storage
One gram of fat stores twice as much energy as one gram of glycogen
Fat does not attract and hold as much water as glycogen, and so provides denser energy storage
Hunger and Eating: Set Points vs. Positive Incentives
The Set-Point Assumption:
¢Despite lack of evidence, most believe that hunger is a response to an energy need; we eat to maintain an energy set point
¢Typical assumption: Eating works like a thermostat, a negative feedback system – turns on when energy is needed, off when set point is reached.
Glucostatic and Lipostatic Set-Point Theories of Hunger
> . If we eat to maintain an energy level (homeostasis), what is monitored? (c. 1940s and 1950s)
¢Glucostatic theories – glucose levels determine when we eat
. Short-term control
¢Lipostatic theories – fat stores determine how much we eat over long term (explaining why weight tends to be constant)
. Longer-term control
Problems with Set-Point Theories of Hunger and Eating
¢“Epidemic” of eating disorders
40 – 50% of us have excessive body fat
¢Contrary to evolutionary pressures that favoured energy storage for survival
>. To survive we need a system that prevents energy deficits, not one that responds to them
¢Reductions in blood glucose or body fat do not reliably induce eating
>. Insulin injections can induce eating, but supraphysiological, and the majority of us have excess body fat
¢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
>. Same as sex
>. Availability and anticipation - take advantage of good food when it is present, and eat it
¢Multiple factors (internal and external) interact to determine the positive-incentive value of eating
¢Accounts for the impact of external factors on eating behaviour
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 >. Rats learn to prefer diets with vitamins, foods they smell in mother’s milk or other rats’ breaths
Factors That Influence When We Eat
¢We tend to get hungry at mealtimes
>. But, animals generally choose to snack unless there is a cost to food access
¢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
>. Weingarten and Kulikovsky (1989)
>. Rats beginning sham eating eat normal-sized meal if food is familiar
>. Previous experience…
¢Appetiser effect – small amounts of food may increase hunger
>. Due to cephalic-phase responses?
Serving size
¢Social influences
>. Rats eat more when in a group
•Some sex (situational?) effects
¢Sensory-specific satiety
>. Eat more with a cafeteria diet – satiety is to a degree taste-specific
Sensory-Specific Satiety
¢Tasting a food immediately decreases the positive-incentive value of similar tastes and decreases the palatability of all foods about 30 minutes later
>. Even a liquid meal – taste buds and beyond
¢Adaptive – encourages a varied diet
¢Some foods are relatively resistant to sensory-specific satiety: rice, bread, potatoes, sweets, and green salads
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
>. Surprise highly palatable meal – eat but no drop in blood glucose
>. Insulin triggers – not a gradual decline
>. Return to normal without a meal…
¢Must decrease blood glucose by 50% to trigger feeding
¢Pre-meal 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
Hypothalamic Hunger and Satiety Centres
> . Ventromedial (VMH) – a satiety centre
. Lateral (LH) – a hunger centre
¢Lesions of VMH produce hyperphagia
¢Lesions of LH produce aphagia and adipsia
¢VMH lesion rats maintain/defend a new higher weight
¢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 – so “eat because they are fat”
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?
>. Koopmans’ (1981) - extra stomach, blood vessels etc connected, but not nerves
>. Signal had to be chemical from stomach, not nutrient
Hunger and Satiety Peptides
¢Must be signals from the gut…
¢Gut peptides that decrease meal size:
>. cholecystokinin (CCK), bombesin, glucagon, alpha-melanocyte-stimulating hormone, somatostatin
¢Must be sure 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 synthesised in the hypothalamus – neuropeptide Y, galanin, orexin-A, ghrelin
¢Many different signals influence eating (not just glucose and fat)
¢Hypothalamus plays a central role – microinjections of some peptides can have major effects on eating
Set-Point Assumptions about Body Weight and Eating
¢Variability of body weight
>. According to the set-point assumption, it should be very difficult to gain weight
¢Set points and health
>. Free-feeding does not lead to optimum health
>. Positive effects seen with caloric restriction
•In animals, and humans – notably Okinawa (20-40% fewer calories than other Japanese)
