Donette Steele, M.A. / Clinical Psychology

Motivation and Regulation

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CHAPTER 6

Motivation and the Regulation of Internal States

 

Motivation and Homeostasis

Hunger: A Complex Drive

Obesity

Anorexia and Bulimia

 

Motivation
and Homeostasis

            Motivation, which literally means “to set in motion,” refers to the set of factors that initiate, sustain, and direct behaviors.

            An instinct is a complex behavior that is automatic and unlearned, and occurs in all the members of a species.

       Examples: migration and maternal behavior.

 

Motivation
and Homeostasis

             According to drive theory, the body maintains a condition of homeostasis, in which any particular system is in balance or equilibrium.

        Any departure from homeostasis, such as depletion or nutrients or a drop in temperature, produces an aroused condition or drive, which impels the individual to engage in appropriate action such as eating, drinking, or seeking warmth.

             Incentive theory recognizes that people are motivated by external stimuli, not just internal needs.

             Arousal theory says that people behave in ways that keep them at their preferred level of arousal.

Motivation
and Homeostasis

            To sustain life a number of conditions, such as body temperature, fluid levels, and energy reserves, must be held within a fairly narrow range, which requires a control system.

            Control systems have a set point, which is the point of equilibrium the system returns to.

       All animals have to maintain internal temperature within certain limits in order to survive, and they operate more effectively within an even narrower range; this is their set point.

Motivation
and Homeostasis

            The “thermostat” is located in the preoptic area of the hypothalamus, which contains separate warmth-sensitive and cold-sensitive cells.

       Some of these neurons respond directly to the temperature of the blood flowing through the area.

       Other  neurons receive input from temperature receptors in other parts of the body, including the skin.

 

 

 

 

Motivation
and Homeostasis

            Osmotic thirst occurs when the fluid content decreases inside the cells.

       This happens when the blood becomes more concentrated than usual, usually because the individual has not taken in enough water to compensate for food intake.

       As a result, water is drawn from the cells into the bloodstream by osmotic pressure.

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

       This can be due to sweating, vomiting, and diarrhea.

Motivation
and Homeostasis

             The reduced water content of cells that contributes to osmotic thirst is detected primarily in areas bordering the third ventricle, particularly in the OVLT (organum vasculosum lamina terminalis).

             The OLVT communicates the water deficit to the median preoptic nucleus of the hypothalamus, which initiates drinking.

             The reduced blood volume in the heart that accompanies volemia is signaled by the vagus to the NST (nucleus of the solitary tract) in the medulla.

              Hypovolemia is detected by the receptors located where the large viens enter the atrium of  the heart –  These receptors respond to stretching of the vascular  alls by the volume of blood passing through

             From there the signal goes to the median preoptic area of the hypothalamus.

 

Motivation
and Homeostasis

            Lowered blood volume is also detected by receptors in the kidneys, which trigger release of the hormone renin.

            Renin increases production of the hormone angiotensin II.

            Angiotensin II circulating in the blood stream informs the brain of the drop in blood volume.

            It stimulates the SFO (subfornical organ), a structure bordering the third ventricle and one of the areas that is unprotected by the blood-brain barrier.

Hunger: A Complex Drive

            The simplest form of dietary selection involves distinguishing between foods that are safe and nutritious and those that are either useless or dangerous.

            In humans, all taste experience is a result of just five taste sensations: sour, sweet, bitter, salty, and the more recently discovered umami.

       Umami is often described as “meaty” or “savory.”

 

            Taste receptors are located on taste buds, which in turn are found on the surface of papillae

            Papillae are small bumps on the tongue and elsewhere in the mouth.

            Taste neurons travel through the thalamus to the insula, the primary gustatory (taste) area in the frontal lobes.

 

 

 

            Sensory-specific satiety means that the more a particular food an individual eats, the less appealing the food becomes.

            Sensory-specific satiety is the brain’s way of encouraging you to vary your food choices, which is necessary for a balanced diet.

            Sensory-specific satiety takes place in the NST.

 

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

            Learned taste preference is a preference not for the nutrient itself, but for the flavor of a food that contains a needed nutrient.

 

            Digestion begins in the mouth, where food is ground fine and mixed with saliva.

            Saliva provides lubrication and contains an enzyme that starts the breakdown of food.

            Digestion proceeds in the stomach as food is mixed with the gastric juices hydrochloric acid and pepsin.

            The partially processed food is then released gradually so the small intestine has time to do its job.

 

 

            Digesting primarily occurs in the small intestines, particularly the initial 25 cm called the duodenum.

       Carbohydrates are metabolized into simple sugars, particularly glucose.

       Proteins are converted to amino acids.

       Fats are transformed into fatty acids and glycerol. 

            The area postrema is one of the places in the brain that is outside the blood-brain barrier, so toxins can activate it to induce vomiting.

 

 

            For a few hours following a meal our body lives off the nutrients arriving from the digestive system; this period is called the absorptive phase.

       The pancreas starts secreting insulin, a hormone that enables body cells to take up glucose for energy and certain cells to store excess nutrients.

       Some of the glucose is converted to glycogen and stored in a short-term reservoir in the liver and muscles.

       Any remaining glucose is converted into fats and stored in fat cells, also known as adipose tissue.

 

            Eventually the glucose level in the blood drops and the body must fall back on its energy stores, which is why this is called the fasting phase.

       The pancreas ceases secretion of insulin and starts secreting the hormone glucagon, which causes the liver to transform stored glycogen back into glucose.

 

            The lateral hypothalamus initiates eating and controls several aspects of feeding behavior as well as metabolic responses.

            The PVN (paraventricular nucleus) initiates eating, though less effectively than the lateral hypothalamus, and regulates metabolic processes such as body temperature, fat storage, and cellular metabolism.

            The arcuate nucleus is a vital hypothalamic structure for monitoring the body’s nutrient condition.

 

            NPY (neuropeptide Y), which is released from the PVN and lateral hypothalamus because of signals from the arcuate nucleus, dramatically increases eating while reducing metabolism.

            Rats injected with NPY double their rate of eating and add six fold to their weight. Their weight is three times greater than their increase in food intake so this suggests NPY inhibits metabolism.

            .

 

 

 

             The best known of the satiety signals is CCK (cholecystokinin), a peptide hormone that is released as food passes into the duodenum.

        CCK detects fats and causes the gall bladder to inject bile into the duodenum, which breaks down the fat so it can be absorbed.

             Another appetite-suppressing peptide hormone that is released in the intestines in response to food is PYY (peptide YY3-36).

        PPY is carried by the blood stream to the arcuate nucleus, where it inhibits the NPY-releasing neurons.

        Its non-neural route to the brain means that its action is too slow to limit the current meal; instead it decreases calorie intake by about a third over the following 12 hours.

 

Hunger: A Complex Drive

            Fat cells secrete a hormone that inhibits eating called leptin.

       The amount of leptin in the blood is proportional to body fat.

       Leptin helps regulate meal size, but it does so in response to long-term stores of fat rather than the nutrients contained in the meal.

 

Obesity

            According to the National Health and Nutrition Examination Surveys, the adult obesity rate in the U.S. has doubled since 1980.

            Obesity is most important because of its health risks.

       As overweight and obesity increase, so does the incidence of a variety of diseases, including diabetes, heart disease, high blood pressure, stroke, and colon cancer.

       Obesity is also linked to cognitive decline and risk of Alzheimer’s disease.

Obesity

            BMI (body mass index) is calculated by dividing the person’s weight in kilograms by the squared height in meters.

            Both adoption studies and twin studies demonstrate the influence of heredity on body weight.

       Adopted children show a moderate relationship with their biological parents’ weights and BMIs, but little or no similarity with their adoptive parents.

 

Obesity

            In the average sedentary adult, about 75% of daily energy expenditure goes into resting or basal metabolism, the energy required to fuel the brain and other organs and to maintain body temperature.

       The remainder is spent about equally in physical activity and in digesting food.

Obesity

            The standard treatment for obesity, of course, is dietary restriction.

       Dieters who exercise lose more weight than dieters who do not exercise.

            Another option in the treatment of obesity is medication.

       However, it has not been a particularly promising alternative.

       Lack of effectiveness is one problem and, because the drugs manipulate metabolic and other important systems, they often have adverse side effects.

Obesity

             The approval of dexfenfluramine in 1996 was the first by the FDA in 20 years.

        But just a year later, both it and the older fenfluramine were withdrawn from the market by the manufacturer after reports they caused heart valve leakage.

             In June 2007, the FDA denied approval of rimonabant, which blocks the endogenous cannabinoid receptors that are responsible for the “marijuana munchies” and produces five percent weight losses.

        The panel was concerned by reports linking the drug to increased psychiatric problems, including suicide.

Obesity

             Even the two approved drugs have their problems:

             Orlistat (Xenical) causes cramping and severe diarrhea because it blocks water absorption.

             Sibutramine (Meridia) has been linking to a number of deaths due to cardiovascular problems.

             Sibutramine blocks norepinephrine and serotonin reuptake and acts as an appetite suppressant.

        Drugs that block serotonin reuptake reduce carbohydrate intake.

             The experimental drug C75 reduces fat storage by oxidizing fatty acids.

        At the same time, it reduces appetite by interfering with NPY production.

 

 

 

Anorexia and Bulimia

             Anorexia nervosa is known as the “starving disease” because the individual restricts food intake to maintain weight at a level so low that it is threatening to health.

             There are two subgroups of anorexics.

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

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

             The anorexic individual’s unwillingness to eat does not necessarily imply lack of hunger.

        NPY levels are high and leptin levels are low.

Anorexia and Bulimia

            Bulimia nervosa also involves weight control, but the behavior is limited to 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.

            Their ghrelin levels between meals are a third higher than in controls, decrease less following a meal.

            In addition, PYY levels do not rise as much following a meal.

Anorexia and Bulimia

             Because of the role serotonin has in eating and in obesity, as well as in depression, researchers have suspected that anorexics and bulimics have lower than normal serotonin activity.

             Bulimics do have reduced levels in their cerebrospinal fluid of the serotonin metabolic by-product 5-HIAA.

             Besides depression, bulimics have an increased rate of anxiety, alcoholism, and other drug abuse, and impulsive behavior, including stealing and sexual activity.

             All these characteristics are associated with low serotonin activity.

 

RECAP 

Prader‑Willi syndrome, the result of a "genetic accident" on chromosome 15, results in uncontrollable eating and extreme obesity

 

Motivation and Homeostasis: Motivation, the set of factors that initiate, sustain, and direct behaviors, is a concept that is imposed on behavior

 

 Theoretical Approaches to Motivation

 

Instinct theory

 

An instinct is a complex behavior that is automatic and unlearned

 

Early theorists identified numerous human instincts; contemporary theory gives them less importance or denies them altogether

 

Drive theory

 

Homeostasis: Any departure will produce a drive ; May not apply to all kinds of motivation

 

Incentive theory: Behavior is motivated by external stimuli

 

Arousal theory: Behavior maintains the individual's preferred level of Arousal

 

Brain state theory gives more importance to the brain in drives than the Condition of the tissues

 

 Simple Homeostatic Drives

 

 A control system detects departures from homeostasis and signals actions to return condition to the set point

 

Temperature Regulation

 

Homoeothermic animals regulate body temperature by manipulating their environment

 

Endothermic animals are able to regulate body temperature internally

 

The preoptic area of the hypothalamus, with its warm‑sensitive and cold‑sensitive cells, is the most important brain area in temperature regulation 

 

Thirst

 

Osmotic thirst, due to reduced fluid content in cells, is detected primarily around the third ventricle, particularly in the OVLT

 

Hypovolemic thirst is due to a loss of extracellular water and reduced blood volume

 

Detected by baroreceptors in the heart, signaled to hypothalamus by vagus nerve

Detected by baroreceptors in the kidneys, signaled to subfornical organ by angiotensin

 

The satiety mechanism (which stops drinking before tissue needs are satisfied) probably involves water receptors in the stomach and liver

 

Hunger: A Complex Drive

 

The Role of Taste

 

The primary tastes of sweet, salty, and umami often identify nutritious foods, sour is associated with spoiled foods and bitter often indicates

toxic substances

 

Sensory‑Specific Satiety:

 

Varying the Choices encourages a varied diet

 

The more of something you eat, the less appealing it becomes

 

A selection of different foods increases appetite

 

Learned Taste Aversion: Avoiding Dangerous Foods

 

Conditioned aversion after getting sick helps avoid dangerous foods

 

May help avoid non‑nutritious foods

 

Learned Taste Preferences: Selecting Nutritious Foods

 

Conditioned to taste of food when the food makes the individual feel better

 

Role in human behavior is unclear

 

Regulating Food Intake

 

The Digestive Process

 

1. In the mouth, saliva provides lubrication and an enzyme that begins digestion

2. The stomach mixes food with hydrochloric acid and pepsin

3. Toxic substances are detected in the stomach and the area postrema

4. Most digestion occurs in the small intestine, especially the duodenum

 

5. Carbohydrates are converted to simple sugars, proteins to  amino acids, and fats to fatty acids and glycerol

 

6. Breakdown products are transported to the liver via the  hepatic portal vein

 

During The Absorptive Phase

1.  Blood sugar levels rise

2.  Autonomic activity shifts from sympathetic to parasympathetic

3.  Insulin secretion increases, enabling cells to take up glucose

4.  Excess glucose is converted to glycogen and stored in the liver or converted to fat and stored in  adipose tissue (fat cells)

 

During The Fasting Phase

 

1.  Blood sugar levels drop

2.  Autonomic activity shifts from parasympathetic to sympathetic

3.  Insulin secretion stops, glucagon secretion begins

4.  Stored fat is broken down to fatty acids and glycerol

5.  Muscle proteins are broken down into amino acids (emergency situations)

 

Signals that Start a Meal

 

1. Glucoprivic hunger is triggered by low blood glucose level

 

2. Lipoprivic hunger results from low fatty acid in the blood

 

3. Information travels via the vagus nerve to the medulla and the paraventricular nucleus

    of the hypothalamus

 

4. The PVN releases neuropeptide Y (NPY), which stimulates eating

 

Signals that End a Meal

 

1.  Stretch receptors in the. stomach send a signal via the vagus to the PVN

2.  Cholecystokinin released in the duodenum signals the PVN via the vagus

3.  Nutritional content of the food, detected in the liver, affects meal size

 

Long ‑Term Controls

 

1) The hormone leptin is secreted by fat cells

 

    Low leptin triggers NPY release in the PVN

    High leptin reduces NPY release

 

2) Insulin level also signals fat level and regulates NPY release

 

Eating Disorders

 

Obesity increases health risks, including susceptibility to several diseases,

as the body mass index (BMI) exceeds approximately 26

 

The Myths of Obesity:

 

Research has not indicated that obesity is due

to inadequate impulse control, maladaptive eating style, or learned overindulgence

 

The Contribution of Heredity

 

Correlations are high among relatives, low between children and their adoptive parents

 

Mice with the oblob genes do not produce leptin; dbldb mice are insensitive to it

 

Heredity influences meal size and frequency, energy intake, activity, metabolic rate, and nutrient proportions in the diet

 

Obesity and Reduced Metabolism

1. Basal metabolism rate (BMR) is one explanation for weight gain

2. Body defends weight by shifting BMR, but defends against loss more than gain

3. Defense aggressiveness varies among individuals

4. Set point may shift higher after prolonged weight gain 

5.  Set point may be altered by dieting and lead to more weight gain over time 

 

Treating Obesity

1. Dietary restriction is typically effective only if combined with exercise

2. Medication

 

Currently approved medications suppress appetite by inhibiting norepinephrine and serotonin reuptake

 

Serotonin reuptake inhibiters work only in carbohydrate cravers (who experience mood improvement from carbohydrates, which increase serotonin levels)

 

Leptin administration may be effective for some individuals

 

The experimental fatty acid synthase inhibitor C75 reduced food intake 90% in mice

 

Anorexia and Bulimia

 

Anorexia involves restricting food intake to a point that is threatening to health

 

Purgers binge on food then purge by vomiting or using laxatives

 

Restrictors restrict food intake to reduce calories

 

Bulimia nervosa involves bingeing and purging

 

Environmental and Genetic Contributions

 

Western culture encourages unreasonable slimness in women

 

Twin studies and the comorbidity of neurotransmitter‑based disorders in relatives indicate a genetic contribution

 

The Role of Serotonin

 

Bulimics have reduced serotonin activity, and antidepressants that increase serotonin activity reduce binge eating

 

Anorexics commonly have reduced serotonin activity while they are underweight, but this may be due to starvation.  The heart is a particular risk and death by heart attack may occur

 

Purgers vs. Restrictors

 

Purgers are impulsive, socially outgoing, emotionally responsive, sexually active, typical of low serotonin activity

 

Purgers do not show the same increases in serotonin as restrictors after recovery

 

Cryproheptadine reduces serotonin and aids restrictors, but impairs purgers' treatment

 

Purging anorexics are more like bulimics in personality and physiology

 

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