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Chapter 10
Internal Regulation
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Temperature Regulation
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Temperature affects many aspects of behavior.
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Temperature regulation is vital to the normal functioning of many behavioral processes.
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Homeostasis refers to temperature regulation and other biological processes that keep certain
body variables within a fixed range.
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Temperature Regulation
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A set point refers to a single value that the body works to maintain.
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Examples: Levels of water, oxygen, glucose, sodium chloride, protein, fat and acidity in
the body.
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Processes that reduce discrepancies from the set point are known as negative feedback.
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Allostasis refers to the adaptive way in which the body changes its set point in response to
changes in life or the environment.
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Temperature Regulation
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Temperature regulation is one of the body’s biological priorities.
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Uses about two-thirds of our energy/ kilocalories per day.
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Basal metabolism is the energy used to maintain a constant body temperature while at rest.
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Temperature Regulation
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Temperature Regulation
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Mammals evolved to have a constant temperature of 37˚ C (98˚ F).
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Muscle activity benefits from being as warm as possible and ready for vigorous activity.
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Proteins in the body break their bonds and lose their useful properties at higher
temperatures.
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Reproductive cells require cooler temperatures.
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Temperature Regulation
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Body temperature regulation is predominantly dependent upon areas in the preoptic area/
anterior hypothalamus (POA/AH).
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The POA/AH partially monitors the body’s temperature by monitoring its own temperature.
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Heating the POA/AH leads to panting or shivering; cooling leads to shivering.
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Cells of the POA/AH also receive input from temperature sensitive receptors in the skin.
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Temperature Regulation
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Bacterial and viral infections can cause a fever, part of the body’s defense against illness.
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Bacteria and viruses trigger the release of leukocytes which release small proteins called
cytokines.
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Cytokines attack intruders but also stimulate the vagus nerve.
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The vagus nerve stimulates the hypothalamus to initiate a fever.
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Some bacteria grow less vigorously in warmer than normal body temperature.
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However, a fever of above 39˚ C (103˚ F) does the body more harm than good.
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Thirst
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Water constitutes 70% of the mammalian body and must be regulated within narrow limits.
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The concentrations of chemicals in water determines the rate of all chemical reactions in the
body.
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Water can be regulated by several mechanisms:
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Conserving by excreting concentrated urine.
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Decreasing sweat and other autonomic responses.
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Drinking more water than we need and excreting the rest.
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Thirst
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Vasopressin is a hormone released by the posterior pituitary which raises blood pressure by
constricting blood vessels.
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helps to compensate for the decreased water volume.
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Vasopressin is also known as an antidiuretic hormone (ADH) because it enables the kidneys to
reabsorb water and excrete highly concentrated urine.
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Thirst
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Two different kinds of thirst include:
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Osmotic thirst – a thirst resulting from eating salty foods because the level of
intracellular fluid decreases.
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Hypovolemic thirst – a thirst resulting from loss of fluids due to bleeding or sweating – a
decrease in extracellular fluid level.
Each kind of thirst motivates different kinds of behaviors.
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Thirst
The brain detects osmotic pressure from:
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Receptors around the third ventricle.
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The OVLT (organum vasculosum laminae terminalis) and the subfornical organ (detect
osmotic pressure and salt content).
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Receptors in the periphery, including the stomach, which detect high levels of sodium.
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Thirst
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Hypovolemic thirst is thirst associated with low volume of body fluids.
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Triggered by the release of the hormones vasopressin and angiotensin II, which constrict
blood vessels to compensate for a drop in blood pressure.
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Angiotensin II stimulates neurons in areas adjoining the third ventricle.
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Neurons in the third ventricle send axons to the hypothalamus where angiotensin II is also
released as a neurotransmitter.
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Thirst
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Animals with osmotic thirst have a preference for pure water.
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Animals with hypovolemic thirst have a preference for slightly salty water as pure water dilutes
body fluids and changes osmotic pressure.
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Sodium-specific hunger, a strong craving for salty foods.
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develops automatically to restore solute levels in the blood.
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Hunger
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Animals vary in their strategies of eating, but humans tend to eat more than they need at the
given moment.
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A combination of learned and unlearned factors contribute to hunger.
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Hunger
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At the age of weaning, most mammals lose the intestinal enzyme lactase, which is necessary for
metabolizing lactose.
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Lactose is the sugar found in milk.
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Milk consumption after weaning can cause gas and stomach cramps.
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Declining levels of lactase may be an evolutionary mechanism to encourage weaning.
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Hunger
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Most human adults have enough lactase to consume milk and other dairy products throughout
the lifetime.
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Nearly all people in China and surrounding countries lack the gene that enables adults to
metabolize lactose.
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Only small quantities of dairy products can be consumed.
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Hunger
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A carnivore is an animal that eats meat and necessary vitamins are found in the meat consumed.
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Herbivores are animals that exclusively eat plants.
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Omnivores are animals that eat both meat and plants.
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Herbivores and omnivores must distinguish between edible and inedible substances to find
sufficient vitamins and minerals.
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Selecting foods to eat is usually accomplished via imitation of others.
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Hunger
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Other strategies of selecting food include:
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Selecting sweet foods and avoiding bitter foods.
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Preferring things that taste familiar.
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Learning from consequences that happen after a food is consumed.
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A conditioned taste aversion is a distaste for food that develops if the food makes one ill.
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Hunger
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The brain regulates eating through messages from the mouth, stomach, intestines, fat cells and
elsewhere.
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The desire to taste and other mouth sensations, such as chewing, are also motivating factors in
hunger and satiety.
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Sham feeding experiments, in which everything an animals eats leaks out of a tube connected to
the stomach or esophagus, do not produce satiety.
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Hunger
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The main signal to stop eating is the distention of the stomach.
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The vagus nerve conveys information about the stretching of the stomach walls to the brain.
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The splanchnic nerves convey information about the nutrient contents of the stomach.
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The duodenum is the part of the small intestine where the initial absorption of significant
amounts of nutrients occurs.
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Distention of the duodenum can also produce feelings of satiety.
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The duodenum also releases the hormone cholecystokinin (CCK), which helps to regulate hunger.
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Hunger
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Cholecystokinin (CCK) released by the duodenum regulates hunger by:
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Closing the sphincter muscle between the stomach and duodenum and causing the
stomach to hold its contents and fill faster.
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Stimulating the vagus nerve to send a message to the hypothalamus that releases a
chemical similar to CCK.
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Hunger
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Glucose, insulin, and glucagon levels also influence feelings of hunger.
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Most digested food enters the bloodstream as glucose, an important source of energy for the
body and nearly the only fuel used by the brain.
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When glucose levels are high, liver cells convert some of the excess into glycogen and fat cells
convert it into fat.
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When low, liver converts glycogen back into glucose.
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Hunger
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Insulin is a pancreatic hormone that enables glucose to enter the cell.
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Insulin levels rise as someone is getting ready for a meal and after a meal.
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In preparation for the rush of additional glucose about to enter the blood, high insulin levels let
some of the existing glucose in the blood to enter the cells.
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Consequently, high levels of insulin generally decrease appetite.
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Hunger
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Glucagon is also a hormone released by the pancreas when glucose levels fall.
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Glucagon stimulates the liver to convert some of its stored glycogen to glucose to replenish low
supplies in the blood.
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As insulin levels drop, glucose enters the cell more slowly and hunger increases.
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Hunger
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Long-term hunger regulation is accomplished via the monitoring of fat supplies by the body.
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The body’s fat cells produce the peptide leptin, which signals the brain to increase or decrease
eating.
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Low levels of leptin increase hunger.
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High levels of leptin do not necessarily decrease hunger.
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Most people are obese because they are less sensitive to leptin.
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Some people are obese because of a genetic inability to produce leptin.
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Hunger
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Information from all parts of the body regarding hunger impinge into two kinds of cells in the
arcuate nucleus.
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The arcuate nucleus is a part of the hypothalamus containing two sets of neurons:
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neurons sensitive to hunger signals.
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neurons sensitive to satiety signals.
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Hunger
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Ghrelin is released as a neurotransmitter in the brain and a hormone in the stomach
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Neurons of the arcuate nucleus specifically sensitive to hunger signals receive input from:
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The taste pathways.
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Axons releasing the neurotransmitter ghrelin.
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also acts in the stomach to trigger stomach contractions.
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Hunger
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Input to the satiety-sensitive cells of the arcuate nucleus include signals of both long-term and
short-term satiety:
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Distention of the intestine triggers neurons to release the neurotransmitter CCK.
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Blood glucose and body fat increase blood levels of the hormone insulin.
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Some neurons release a smaller peptide related to insulin as a transmitter.
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Leptin provides additional input.
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Hunger
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Input from the hunger-sensitive neurons of the arcuate nucleus is inhibitory to both the
paraventricular nucleus and the satiety-sensitive cells of the arcuate nucleus itself.
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inhibitory transmitters include GABA, neuropeptide Y (NPY), and agouti-related peptide
(AgRP).
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Neuropeptide Y (NPY) and agouti-related peptide (AgRP) are inhibitory transmitters that block
the satiety action of the paraventricular nucleus and provoke overeating.
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Hunger
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Damage to the ventromedial hypothalamus that extends to areas outside can lead to overeating
and weight gain.
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Those with damage to this area eat normal sized but unusually frequent meals.
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Increased stomach secretions and motility causes the stomach to empty faster than usual.
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Damage increases insulin production and much of the meal is stored as fat.
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Hunger
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People with a mutated gene for the receptors melanocortin overeat and become obese.
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Melanocortin is a neuropeptide responsible for hunger.
Prader-Willis syndrome is a genetic condition marked by mental retardation, short stature, and
obesity.
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Blood levels of the peptide ghrelin is five times higher than normal.
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Hunger
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Although a single gene can not be identified, a genetic influence has been established in many
factors contributing to obesity.
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Monozygotic twins resemble each other more the dizygotic twins in factors contributing to
obesity.
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Examples: how much stomach distention influences the ending of eating, how much one
overeats when food tastes good.
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Hunger
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Obesity can also be a function of genes interacting with changes in the environment.
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Example: Diet changes of Native American Pimas of Arizona and Mexico.
Obesity has become common in the United States and has increased sharply since the 1970’s.
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Attributed to life-style changes, increased fast-food restaurants, increased portion sizes,
and high use of fructose in foods.
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Hunger
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Weight-loss is often difficult and specialist rarely agree.
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Plans should include increased exercise and decreased eating.
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Some appetite-suppressant drugs such as fenfluramine and phentermine block reuptake of
certain neurotransmitters to produce brain effects similar to that of a completed meal.
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Hunger
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Sibutramine has replaced fenfluramine and decreases meal size and binge eating by bloking
reuptake of serotonin and norepinephrine
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“Orlistat” is drug that prevents the intestines from absorbing fats.
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Gastric bypass surgery is the removal or sewing off of part of the stomach.
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Decreased stomach size allows greater distention of the stomach to produce satiety.
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Hunger
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Anorexia nervosa is an eating disorder associated with an unwillingness to eat as much as
needed.
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Genetic predisposition is likely.
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no clear link has been established
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Associated with a fear of becoming fat and not a disinterest in food.
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Biochemical abnormalities in the brain and blood are probably not the cause, but a result of the
weight loss.
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Hunger
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Bulimia nervosa is an eating disorder in which people alternate between extreme dieting and
binges of overeating.
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Some force vomiting after eating.
Associated with decreased release of CCK, increased release of ghrelin, and alterations of
several other hormones and transmitters.
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May be the result and not the cause of the disorder.
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Reinforcement areas of the brain also implicated.