Brain Mechanisms
 

• One promising theory of hunger implicated the brain's hypothalamus as the neural basis for eating.  Separate hypothalamic centers were thought to regulate   ingestion (hungry)  and the discontinuation of eating (satiety)
• the brain region known as the lateral hypothalamic area was identified as the "hunger center".
• ventromedia nuceus of the hypothalamus (VMH) was the "satiety center"
• hyperphagia- when VMH-lesioned subjects tend to eat excessively; animals may increase to three times their normal weight  The animal’s weight eventually levels off, and the animal may actually show an indifference to food unless it is a preferred source.  The hypothalamic lesions adjust a homeostatic center up or down.

Hormonal Mechanisms
 

• the pancreas and live are crucial to maintaining proper glucose balance.
• pancreas secretes a hormone called insulin that facilitates the transfer of glucose from the blood into cells throughout the body.
• liver stores glucose in reserve in the form of glycogen
• glucagon- a hormone produced by the pancreas, serves to convert glycogen back to glucose, when it is needed.
• everything in the way of blood sugar gets transferred to cells or remains in the liver.  The result is a low level of glucose in the blood.  Today there is widespread agreement that low blood glucose level is an important physiological stimulus for hunger.

Short-Term and Long-Term Cues
 

• Short-term cues consist primarily of the properties of food that may determine meal size and frequency
• taste
• smell
• texture
• temperature of food placed in mouth
• immediate chemical changes in the gastrointestinal tract and endocrine system
• Long term cues such as body fat that regulate overall body weight.  The most popular present-day account of hunger and weight control relates to the notion of set point.  Set point is the idea that each of us has an established body fat level that remains fixed and that resists attempts to alteration.  When fat deposits drop below set individual levels, hunger occurs and consequently we eat more.  Shout we try to shift this set point, metabolic adjusts would occur to prevent it.

Eating Disorders

• Obesity- Evidence exists that environmental factors play a major role for the 25 to 45% of adults in the United States who are clinically overweight.
• Advertisements- children view and average of 222 junk-food commercials every Saturday morning
• Schachter’s hypothesis- the eating behavior of obese people is under the control of external factors, like sight, smell, and taste of food.
• Dieting
• People diet because not being thin may be interpreted as a public statement of weak will power.
• A statement released by the National Center for Health Statistics in 1992 indicates that only 10% of American dieters who lose 25 lb. or more will keep the weight off for as long as 2 years.
• Anorexia Nervosa- eating disorder characterized by self-imposed starvation
• anorexia commonly develops when there is no obvious incentive to lose eight.  People who are already too thin see themselves as overweight and needing to diet.
• physical symptoms include: tooth loss, hormonal imbalances and weakness
• many clinical psychologists believe that disorder  arises from an unstable self-concept
• is most common in young women ( about 85% of cases are adolescent females from white, middle- and upper-middle-class backgrounds)
• Bulimia Nervosa- eating disorder in which a person eats large amounts of food, only to vomit or otherwise purge the system; results in extreme weight loss.  Is most common on college campuses.  Symptoms include: discoloration of teeth, esophageal hernias, and laceration of the gastrointestinal track.