Donette Steele, M.A. / Clinical Psychology

Motivation and Regulation

Motivation and the Regulation of Internal States
Chapter 6

 

Motivation and homeostasis

 

Hunger: a complex drive

 

Obesity

 

Anorexia and bulimia

Motivation and Homeostasis

 

Prader-Willi Syndrome

 

      Result of a genetic accident on chromosome 15

      Uncontrollable hunger and extreme obesity

 

 

 

 

Motivation and Homeostasis

      Motivation means “to set in motion;” it refers to the factors that initiate, sustain, and direct behaviors.

      Theoretical Approaches to Motivation

      Instinct: a complex behavior that is automatic and unlearned, and occurs in all members of a species, such as maternal behavior.

  Instincts account for few if any behaviors in humans.

      Drive theory:  The body maintains homeostasis—equilibrium—in its systems.

  Departure from homeostasis produces an aroused condition, or drive, impelling the individual to engage in appropriate action.

 

      Incentive theory: People are motivated by external stimuli, or incentives, not just internal needs.

  Incentives include money, grades, the smell of food.

      Arousal theory: People behave in ways that keep them at their preferred level of arousal.

  This is a factor, for example, in the characteristic of sensation seeking.

      In response to challenges to drive theory, psychologists have shifted to an emphasis on drives as states of the brain rather than as conditions of the tissues.

Motivation and Homeostasis

      Simple Homeostatic Drives: A “control system” maintains conditions around a set point.

      Temperature Regulation

  Ectotherms, such as reptiles, cannot regulate body temperature internally.

  Endotherms regulate their body temperature by dilating or constricting blood vessels, adjusting metabolism, sweating, etc.

  Warmth-sensitive and cold-sensitive cells in the preoptic area of the hypothalamus receive input from the blood and the skin.

  The preoptic area initiates temperature regulating responses.

 

Motivation and Homeostasis

      Thirst is more complicated in that it involves two kinds of deficits and two different systems.

  Osmotic thirst occurs when the fluid content decreases inside the cells. Water is drawn from cells into the bloodstream, usually to compensate for food intake.

  Detected in the hypothalamus by the OVLT (near 3rd ventricle).
  The OVLT signals the median preoptic nucleus to initiate drinking.

      Thirst is more complicated in that it involves two kinds of deficits and two different systems.

 

 

  Hypovolemic thirst occurs when blood volume drops, due to a loss of extracellular water.

Caused by sweating, vomiting, diarrhea, blood loss, etc.
  Lowered blood volume is detected by receptors in the heart and in the kidneys.
  Information from the heart is relayed by the vagus nerve to the nucleus of the solitary tract and to the median preoptic nucleus.
  The kidneys release the hormone renin;
     which increases production of angiotensin II;
     which stimulates the subfornical organ;
     which signals the median preoptic nucleus.
 
 

      Hunger: Feeding behavior must provide energy for fuel and for maintaining body temperature, as well as material needed for growth and repair.

     Five primary tastes help select safe and nutritious foods.

  Naturally sweet foods tend to be nutritious.

  Salty foods provide ions necessary for neural transmission.

  Sour foods may be spoiled, and bitter foods may be toxic.

  Umami taste may help select proteins.

     Receptors in the tongue’s taste buds send signals to the insula (the primary gustatory cortex), and to the nucleus of the solitary tract (NST).

 

Hunger: A Complex Drive

Papilla with Taste Buds
Figure 6.4

Hunger: A Complex Drive

      Sensory-specific satiety occurs when a food becomes less appealing as the individual consumes more.

  This encourages variation in food choices for a balanced diet.

  This type of satiety involves the NST in the medulla.

     Learned taste aversion is the avoidance of foods associated with illness or poor nutrition.

  Examples: bait shyness, avoidance of a nutrient-deficient diet

      Learned taste preference is a preference for the flavor of a food that contains a needed nutrient.

  This ability is often counteracted by the distraction of tasty, high-calorie foods not found in nature.

Hunger: A Complex Drive

      Digestion

      Digestion begins in the mouth, where an enzyme in saliva starts the break down of food.

      In the stomach, food is mixed with hydrochloric acid and pepsin to further digest food.

      Most of digestion takes place in the small intestine, particularly in the duodenum (initial 25 cm).

      The products of digestion (glucose, amino acids, fatty acids and glycerol) are absorbed through the intestinal walls.

      These nutrients are transported to the liver by the hepatic portal vein.

 

The Digestive System

Figure 6.6

Hunger: A Complex Drive

      The feeding cycle has two phases:

     During the absorptive phase, the body uses the nutrients arriving from the digestive system.

  Rising glucose levels activate the parasympathetic system, which promotes the release of insulin.

  In cells outside the nervous system, insulin receptors activate glucose transporters to carry glucose into the cells.

  The transporters in the nervous system do not require insulin; this gives the brain priority access to glucose.

  Nutrients are also stored for future use during this phase.

  Glucose is stored as glycogen in the liver and muscles.
  Excess glucose is converted into fats and stored in adipose tissue.

Hunger: A Complex Drive

      During the fasting phase glucose levels have fallen, and the body must rely on stored nutrients.

  The sympathetic nervous system promotes the release of glucagon, which converts the liver’s glycogen to glucose.

  Because insulin levels are low, this glucose is available only to the brain.

  Glucagon, secreted by the pancreas, breaks stored fat down into fatty acids and glycerol.

  Fatty acids are used by the muscles and organs.
  Glycerol is converted to glucose for the brain.

Hunger: A Complex Drive

      Cycles of feeding and fasting are mostly choreographed by:

 

      Signals That Start a Meal

      There are three major signals for hunger:

  glucose deficit, which triggers glucoprivic hunger;

  a deficit in fatty acids, which  triggers lipoprivic hunger;

  release of ghrelin as the stomach empties.

      The first two signals  are carried by the vagus nerve to the NST (nucleus of the solitary tract) in the medulla.

      Ghrelin reaches the NST via the bloodstream.

 

      The NST then communicates this information to the arcuate nucleus in the hypothalamus.

      The arcuate nucleus sends neurons to the lateral hypothalamus and the PVN.

      These neurons release neuropeptide Y and agouti-related protein (AgRP),

  which excite the lateral hypothalamus and the PVN to increase eating and reduce metabolism.

      Signals That End a Meal

     Satiety signals are essential to end a meal long before the nutrients reach the body’s tissues.

     Stretch or volume receptors in the stomach signal meal size.

     The stomach and intestines release different peptides in response to different types of food, and at least some of them act as signals in the brain.

     The best known of these peptides is cholecystokinin (CCK), which is released as food passes into the duodenum.

It detects fats and aids in fat digestion by causing the gall bladder to release bile.

CCK stimulates the vagus nerve; the signal travels to the NST and from there to the hypothalamus to decrease eating.

Hunger: A Complex Drive

      Long-term control of appetite is also essential.

      The intestines release PYY (Peptide YY3-36), which is carried by the bloodstream to the arcuate nucleus where it inhibits NPY-releasing neurons.

      Fat cells release leptin.

  Leptin provides a fat level/body weight monitor.

  Along with insulin, it inhibits hunger-inducing AgRP.

  It also activates POMC/CART, substances that reduce feeding by inhibiting the PVN.

  It helps regulate meal size on a long-term basis.

 

 

 

Hunger Control Signals And Brain Centers

Obesity

      Obesity:

     is defined as a BMI (body mass index) of 30 or higher.

       (over 40: morbidly obese; 25-29 overweight)

     has doubled in the U.S. since 1980 and has become a global epidemic;

     is associated with a variety of diseases, including diabetes, heart disease, high blood pressure, stroke, and colon cancer;

     is also linked to temporal lobe shrinkage, cognitive decline, and risk of Alzheimer’s disease;

     threatens to reduce average lifespan.

       (Caloric restriction increases lifespan, and research is focused on drugs that accomplish the same thing.)

 

      The Contribution of Heredity

      The heritability of obesity ranges from 50-90%.

      Adopted children’s weight and BMIs are moderately related to those of their biological parents, but have little similarity with those of their adoptive parents.

      Around 200 genes have been implicated in obesity; two dozen of these are specific to humans. Examples:

  Obesity (ob) gene on chromosome 4

  Diabetes (db) gene on chromosome 6

  Mutations in the MC4R gene

  FTO gene (A allele)

 

     Obesity and Reduced Metabolism

      Basal metabolic rate (BMR):

is the energy required to fuel the brain and body and maintain temperature;

  accounts for 75% of energy expenditure in the average sedentary person.

      In a study of women on a restricted diet, the 1/3 who failed to lose weight had lower BMRs.

      Heredity accounts for 40% of a person’s BMR.

      The body will “defend” its weight by shifting metabolism.

This defense is less for weight gain than for weight loss.

Prolonged weight gain may shift the set point higher.       

      Spontaneous activity may be as important as BMR in resisting obesity.

Obesity

      Treating Obesity

      Dietary restriction works, especially when coupled with exercise to burn calories and adjust metabolism.

      Medication has not produced encouraging results.

  Drugs that inhibit serotonin reuptake (Ex: sibutramine) reduce carbohydrate intake, but only in people with carbohydrate craving.

  Leptin reduces weight only in the 5%-10% who are leptin deficient.

  Orlistat (blocks fat absorption) and exenatide (increases insulin) have significant side effects, and PYY may be ineffective.

 

 

 

Obesity

      Another approach is to treat obesity as an addiction.

  Obese people share several characteristics with addicts.

  They have reduced numbers of dopamine D2 receptors and associated decreases in prefrontal metabolism.

  Peptides that induce eating target dopamine neurons.

  Anti-addiction drugs are showing effectiveness in weight loss.

 

 

Obesity

      Gastric bypass surgery is an option for the morbidly obese.

  Weight loss averages 25% after 10 years, compared to 5%-10% with dieting and, most often, relapse within a year.

  Reduces ghrelin and increases PYY and GLP-1, reducing hunger.

  Benefits include reduced mortality and many health improvements.

 

 

      Anorexia nervosa is known as the “starving disease.”

      The individual restricts food intake to maintain weight at a level so low that it is threatening to health.

      Restrictors rely only on reducing food intake to control their weight.

      Purgers restrict their calorie intake, but they also resort to purging, by vomiting or using laxatives.

      The anorexic individual may actually be battling hunger; NPY and ghrelin levels are high and leptin levels are low.

 

      Bulimia nervosa also involves weight control, by bingeing and purging.

      If the bulimic restricts food intake, it is only for a few days at a time, and restricting takes a backseat to bingeing and purging.

      Forty-four percent overeat, but most are of normal weight.

      Bulimics also may be battling hunger:

  ghrelin levels decrease less following a meal; between meals they are a third higher than in controls;

  PYY levels rise less following a meal.

 

      Environmental contributions play a role in anorexia and bulimia.

  One factor is the emphasis on thinness, as seen in the Fiji study.

  The incidence is higher in females, who experience more pressure.

      Genetic influence is suggested by:

  shared disorders in relatives and

  comorbidity with obsessive-compulsive disorder (anorexia) and depression (bulimia).

     Both anorexics and bulimics show alterations in serotonin levels.

     Serotonin is low in bulimics; antidepressants, which increase serotonin activity, provide some symptom improvement.

     Serotonin is low in purging anorexics while ill and rises to normal after weight gain. Their personality characteristics suggest low serotonin, and drugs that reduce serotonin impair treatment.

     Restricting anorexics have high serotonin after weight gain, which is typical of people with obsessive-compulsive disorder.

     But dopamine may also be involved. Olanzapine, an anti-schizophrenic drug that blocks dopamine receptors, produces some benefit.         

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