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Prepared by Grant McLaren, Department of Psychology, Edinboro University of Pennsylvania FOUNDATIONS OF BEHAVIORAL NEUROSCIENCE 9 TH EDITION This multimedia product and its contents are protected under copyright law. The following are prohibited by law: any public performance or display, including transmission of any image over a network, preparation of any derivative work, including the extraction, in whole or in part, of any images, any rental, lease or lending of the program Copyright © 2014 Pearson Education, Inc. All Rights Reserved
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Chapter 11 Ingestive Behavior Copyright © 2014 Pearson Education, Inc. All Rights Reserved
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Physiological Regulatory Mechanisms Drinking Some Facts About Fluid Balance Two Types of Thirst Eating: Some Facts about Metabolism What Starts a Meal? Signals from the Environment Signals from the Stomach Metabolic Signals
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Copyright © 2014 Pearson Education, Inc. All Rights Reserved What Stops a Meal? Gastric Factors Intestinal Factors Liver Factors Insulin Long-Term Satiety: Signals from Adipose Tissue
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Copyright © 2014 Pearson Education, Inc. All Rights Reserved Brain Mechanisms Brain Stem Hypothalamus Obesity Possible Causes Treatment
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Copyright © 2014 Pearson Education, Inc. All Rights Reserved Anorexia Nervosa/Bulimia Nervosa Possible Causes Treatment
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Ingestive Behaviors Learning Objectives 1. Explain the characteristics of a regulatory mechanism. 2. Describe the fluid compartments of the body. 3. Explain the control of osmometric thirst and volumetric thirst and the role of angiotensin. 4. Describe characteristics of the two nutrient reservoirs and the absorptive and fasting phases of metabolism. 5. Discuss the signals from the environment, the stomach, and the metabolism that begin a meal. 6. Discuss the long-term and short-term factors that stop a meal. 7. Describe research on the role of the brain stem and hypothalamus in hunger and satiety. 8. Discuss the social and physiological factors that contribute to obesity. 9. Discuss surgical, behavioral, and pharmacological treatments for obesity. 10. Discuss the physiological factors that may contribute to anorexia nervosa and bulimia nervosa. Copyright © 2014 Pearson Education, Inc. All Rights Reserved
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Physiological Regulatory Mechanisms homeostasis (home ee oh stay sis) The process by which the body’s substances and characteristics (such as temperature and glucose level) are maintained at their optimal level. ingestive behavior (in jess tiv) Eating or drinking. Copyright © 2014 Pearson Education, Inc. All Rights Reserved
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Physiological Regulatory Mechanisms system variable A variable that is controlled by a regulatory mechanism, for example, temperature in a heating system. set point The optimal value of the system variable in a regulatory mechanism. correctional mechanism In a regulatory process, the mechanism that is capable of changing the value of the system variable. Copyright © 2014 Pearson Education, Inc. All Rights Reserved
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Physiological Regulatory Mechanisms negative feedback A process whereby the effect produced by an action serves to diminish or terminate that action; a characteristic of regulatory systems. satiety mechanism A brain mechanism that causes cessation of hunger or thirst, produced by adequate and available supplies of nutrients or water. Copyright © 2014 Pearson Education, Inc. All Rights Reserved
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Drinking Some Facts About Fluid Balance intracellular fluid The fluid contained within cells. extracellular fluid All body fluids outside cells: interstitial fluid, blood plasma, and cerebrospinal fluid. intravascular fluid The fluid found within the blood vessels. Copyright © 2014 Pearson Education, Inc. All Rights Reserved
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Drinking Some Facts About Fluid Balance isotonic Equal in osmotic pressure to the contents of a cell. A cell placed in an isotonic solution neither gains nor loses water. hypertonic The characteristic of a solution that contains enough solute that it will draw water out of a cell placed in it, through the process of osmosis. hypotonic The characteristic of a solution that contains so little solute that a cell placed in it will absorb water, through the process of osmosis. Copyright © 2014 Pearson Education, Inc. All Rights Reserved
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Drinking Some Facts About Fluid Balance hypovolemia (hy poh voh lee mee a) Reduction in the volume of the intravascular fluid. Copyright © 2014 Pearson Education, Inc. All Rights Reserved
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Drinking Two Types of Thirst The term thirst means different things in different circumstances. Its original definition referred to a sensation that people say they have when they are dehydrated. Because we do not know how other animals feel, thirst simply means a tendency to seek water and to ingest it. Copyright © 2014 Pearson Education, Inc. All Rights Reserved
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Drinking Osmometric Thirst osmometric thirst Thirst produced by an increase in the osmotic pressure of the interstitial fluid relative to the intracellular fluid, thus producing cellular dehydration. osmoreceptor A neuron that detects changes in the solute concentration of the interstitial fluid that surrounds it. Copyright © 2014 Pearson Education, Inc. All Rights Reserved
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Drinking Osmometric Thirst Investigators placed a micropipette against the membranes of individual osmoreceptors and found that the application of pressure or suction could alter the membrane potential of the cells. For example, if a cell was exposed to a hypertonic solution, the cell lost water and its membrane potential fell. If pressure was then applied, the volume of the cell increased and the membrane potential returned to normal. Copyright © 2014 Pearson Education, Inc. All Rights Reserved
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Drinking Osmometric Thirst A functional imaging study by Egan et al. (2003) found that the human AV3V also appears to contain osmoreceptors. The investigators administered intravenous injections of hypertonic saline to normal subjects while their brains were being scanned. They observed strong activation of several brain regions, including the AV3V and the anterior cingulate cortex. Copyright © 2014 Pearson Education, Inc. All Rights Reserved
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Drinking Volumetric Thirst volumetric thirst Thirst produced by hypovolemia. Volumetric thirst occurs when the volume of the blood plasma— the intravascular volume—decreases. Loss of blood causes pure volumetric thirst. From the earliest recorded history, reports of battles note that the wounded survivors called out for water. Copyright © 2014 Pearson Education, Inc. All Rights Reserved
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Drinking Volumetric Thirst Role of Angiotensin renin (ree nin) A hormone secreted by the kidneys that causes the conversion of angiotensinogen in the blood into angiotensin. angiotensin (ann gee oh ten sin) A peptide hormone that constricts blood vessels, causes the retention of sodium and water, and produces thirst and a salt appetite. Copyright © 2014 Pearson Education, Inc. All Rights Reserved
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Drinking Volumetric Thirst Role of Angiotensin subfornical organ (SFO) A small organ located in the confluence of the lateral ventricles, attached to the underside of the fornix; contains neurons that detect the presence of angiotensin in the blood and excite neural circuits that initiate drinking. Copyright © 2014 Pearson Education, Inc. All Rights Reserved
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Drinking Volumetric Thirst Role of Angiotensin median preoptic nucleus A small nucleus situated around the front of the anterior commissure; plays a role in thirst stimulated by angiotensin. Copyright © 2014 Pearson Education, Inc. All Rights Reserved
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Eating: Some Facts About Metabolism glycogen (gly ko jen) A polysaccharide often referred to as animal starch; stored in liver and muscle; constitutes the short-term store of nutrients. insulin A pancreatic hormone that facilitates entry of glucose and amino acids into the cell, conversion of glucose into glycogen, and transport of fats into adipose tissue. glucagon (gloo ka gahn) A pancreatic hormone that promotes the conversion of liver glycogen into glucose. Copyright © 2014 Pearson Education, Inc. All Rights Reserved
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Eating: Some Facts About Metabolism triglyceride (try gliss er ide) The form of fat storage in adipose cells; consists of a molecule of glycerol joined with three fatty acids. glycerol (gliss er all) A substance (also called glycerine) derived from the breakdown of triglycerides, along with fatty acids; can be converted by the liver into glucose. fatty acid A substance derived from the breakdown of triglycerides, along with glycerol; can be metabolized by most cells of the body except for the brain. Copyright © 2014 Pearson Education, Inc. All Rights Reserved
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Eating: Some Facts About Metabolism Figure 11.11 reviews what I have said so far about the metabolism that takes place while the digestive tract is empty, which physiologists refer to as the fasting phase of metabolism. A fall in blood glucose level causes the pancreas to stop secreting insulin and to start secreting glucagon. The absence of insulin means that most of the cells of the body can no longer use glucose; thus, all the glucose present in the blood is reserved for the central nervous system. Copyright © 2014 Pearson Education, Inc. All Rights Reserved
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Eating: Some Facts About Metabolism fasting phase The phase of metabolism during which nutrients are not available from the digestive system; glucose, amino acids, and fatty acids are derived from glycogen, protein, and adipose tissue during this phase. absorptive phase The phase of metabolism during which nutrients are absorbed from the digestive system; glucose and amino acids constitute the principal source of energy for cells during this phase, and excess nutrients are stored in adipose tissue in the form of triglycerides. Copyright © 2014 Pearson Education, Inc. All Rights Reserved
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What Starts a Meal? Regulation of body weight requires a balance between food intake and energy expenditure. If we ingest more calories than we burn, we will gain weight. Assuming that our energy expenditure is constant, we need two mechanisms to maintain a relatively constant body weight. One mechanism must increase our motivation to eat if our long- term nutrient reservoir is becoming depleted, and another mechanism must restrain our food intake if we begin to take in more calories than we need. Copyright © 2014 Pearson Education, Inc. All Rights Reserved
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What Starts a Meal? Signals from the Environment Although an empty stomach is an important signal, many factors start a meal, including the sight of a plate of food, the smell of food cooking in the kitchen, the presence of other people sitting around the table, or the words “It’s time to eat!” Copyright © 2014 Pearson Education, Inc. All Rights Reserved
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What Starts a Meal? Signals from the Stomach An empty stomach and upper intestine provide an important signal to the brain that it is time to start thinking about finding something to eat. Recently, researchers discovered one of the ways this signal may be communicated to the brain. The gastrointestinal system (especially the stomach) releases a peptide hormone called ghrelin (Kojima et al., 1999). Copyright © 2014 Pearson Education, Inc. All Rights Reserved
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What Starts a Meal? Signals from the Stomach ghrelin A peptide hormone released by the stomach that increases eating; also produced by neurons in the brain. duodenum The first portion of the small intestine, attached directly to the stomach. Copyright © 2014 Pearson Education, Inc. All Rights Reserved
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What Starts a Meal? Metabolic Signals glucoprivation A dramatic fall in the level of glucose available to cells; can be caused by a fall in the blood level of glucose or by drugs that inhibit glucose metabolism. lipoprivation A dramatic fall in the level of fatty acids available to cells; usually caused by drugs that inhibit fatty acid metabolism. Copyright © 2014 Pearson Education, Inc. All Rights Reserved
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What Starts a Meal? Metabolic Signals hepatic portal vein The vein that transports blood from the digestive system to the liver. Copyright © 2014 Pearson Education, Inc. All Rights Reserved
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What Starts a Meal? Metabolic Signals To summarize: The brain contains detectors that monitor the availability of glucose (its only fuel) inside the blood–brain barrier, and the liver contains detectors that monitor the availability of nutrients (glucose and fatty acids) outside the blood–brain barrier. Copyright © 2014 Pearson Education, Inc. All Rights Reserved
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What Stops a Meal? There are two primary sources of satiety signals—the signals that stop a meal. Short-term satiety signals come from the immediate effects of eating a particular meal, which begin long before the food is digested. These signals do not control the beginning and end of a particular meal, but they do, in the long run, control the intake of calories by modulating the sensitivity of brain mechanisms to the hunger and satiety signals that they receive. Copyright © 2014 Pearson Education, Inc. All Rights Reserved
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What Stops a Meal? Gastric Factors The stomach apparently contains receptors that can detect the presence of nutrients. Of course, this study indicates only that the stomach contains nutrient receptors; it does not prove that there are not detectors in the intestines as well. Copyright © 2014 Pearson Education, Inc. All Rights Reserved
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What Stops a Meal? Intestinal Factors The intestines do contain nutrient detectors. Studies with rats have shown that afferent axons arising from the duodenum are sensitive to the presence of glucose, amino acids, and fatty acids (Ritter et al., 1992). In fact, some of the chemoreceptors found in the duodenum are also found in the tongue. These axons may transmit a satiety signal to the brain. Copyright © 2014 Pearson Education, Inc. All Rights Reserved
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What Stops a Meal? Intestinal Factors cholecystokinin (CCK) (coal i sis toe ky nin) A hormone secreted by the duodenum that regulates gastric motility and causes the gallbladder (cholecyst) to contract; appears to provide a satiety signal transmitted to the brain through the vagus nerve. Copyright © 2014 Pearson Education, Inc. All Rights Reserved
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What Stops a Meal? Intestinal Factors Investigators have discovered another chemical produced by cells in the gastrointestinal tract that serves as an additional satiety signal. This chemical, peptide YY 3–36 (let’s just call it PYY) is released by the small intestine after a meal in amounts proportional to the calories that were just ingested. Copyright © 2014 Pearson Education, Inc. All Rights Reserved
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What Stops a Meal? Liver Factors Satiety produced by gastric factors and duodenal factors is anticipatory; that is, these factors predict that the food in the digestive system will, when absorbed, eventually restore the system variables that cause hunger. Copyright © 2014 Pearson Education, Inc. All Rights Reserved
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What Stops a Meal? Liver Factors Not until nutrients are absorbed from the intestines can they be used to nourish the cells of the body and replenish the body’s nutrient reservoirs. The last stage of satiety appears to occur in the liver, which is the first organ to learn that food is finally being received from the intestines. Copyright © 2014 Pearson Education, Inc. All Rights Reserved
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What Stops a Meal? Insulin The absorptive phase of metabolism is accompanied by an increased level of insulin in the blood. Insulin permits organs other than the brain to metabolize glucose, and it promotes the entry of nutrients into fat cells where they are converted into triglycerides. Insulin is a peptide and would not normally be admitted to the brain. However, a transport mechanism delivers it through the blood–brain barrier, and it reaches neurons in the hypothalamus that are involved in regulation of hunger and satiety. Copyright © 2014 Pearson Education, Inc. All Rights Reserved
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What Stops a Meal? Long-Term Satiety: Signals from Adipose Tissue In most people, body weight appears to be regulated over a long- term basis. If an animal is force-fed so that it becomes fatter than normal, it will reduce its food intake once it is permitted to choose how much to eat (Wilson et al., 1990). The discovery of a long-term satiety signal from fat tissue came after years of study with a strain of genetically obese mice. Copyright © 2014 Pearson Education, Inc. All Rights Reserved
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What Stops a Meal? Long-Term Satiety: Signals from Adipose Tissue ob mouse A strain of mice whose obesity and low metabolic rate are caused by a mutation that prevents the production of leptin. leptin A hormone secreted by adipose tissue; decreases food intake and increases metabolic rate, primarily by inhibiting NPY-secreting neurons in the arcuate nucleus. Copyright © 2014 Pearson Education, Inc. All Rights Reserved
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Brain Mechanisms Brain Stem decerebration A surgical procedure that severs the brain stem, disconnecting the hindbrain from the forebrain. Copyright © 2014 Pearson Education, Inc. All Rights Reserved
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Brain Mechanisms Hypothalamus Discoveries made in the 1940s and 1950s focused the attention of researchers interested in ingestive behavior on two regions of the hypothalamus: the lateral area and the ventromedial area. For many years investigators believed that these two regions controlled hunger and satiety, respectively; one was the accelerator, and the other was the brake. Copyright © 2014 Pearson Education, Inc. All Rights Reserved
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Brain Mechanisms Hypothalamus Role in Hunger melanin-concentrating hormone (MCH) One of two peptide neurotransmitters found in a system of lateral hypothalamic neurons that stimulate appetite and reduce metabolic rate. Copyright © 2014 Pearson Education, Inc. All Rights Reserved
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Brain Mechanisms Hypothalamus Role in Hunger neuropeptide Y (NPY) A peptide neurotransmitter found in a system of neurons of the arcuate nucleus that stimulate feeding, insulin and glucocorticoid secretion, decrease the breakdown of triglycerides, and decrease body temperature. Copyright © 2014 Pearson Education, Inc. All Rights Reserved
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Brain Mechanisms Hypothalamus Role in Hunger arcuate nucleus A nucleus in the base of the hypothalamus that controls secretions of the anterior pituitary gland; contains NPY-secreting neurons involved in feeding and control of metabolism. Copyright © 2014 Pearson Education, Inc. All Rights Reserved
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Brain Mechanisms Hypothalamus Role in Hunger paraventricular nucleus (PVN) A nucleus of the hypothalamus located adjacent to the dorsal third ventricle; contains neurons involved in control of the autonomic nervous system and the posterior pituitary gland. agouti-related protein (AGRP) A neuropeptide that acts as an antagonist at MC-4 receptors and increases eating. Copyright © 2014 Pearson Education, Inc. All Rights Reserved
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Brain Mechanisms Hypothalamus Role in Satiety CART Cocaine- and amphetamine-regulated transcript; a peptide neurotransmitter found in a system of neurons of the arcuate nucleus that inhibit feeding. -melanocyte-stimulating hormone ( -MSH) A neuropeptide that acts as an agonist at MC-4 receptors and inhibits eating. Copyright © 2014 Pearson Education, Inc. All Rights Reserved
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Brain Mechanisms Hypothalamus Role in Satiety melanocortin-4 receptor (MC-4R) A receptor found in the brain that binds with -MSH and agouti-related protein; plays a role in control of appetite. Copyright © 2014 Pearson Education, Inc. All Rights Reserved
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Obesity Obesity is a widespread problem that can have serious medical consequences. In the United States, approximately 67 percent of men and 62 percent of women are overweight, defined as a body mass index (BMI) of over 25. Obesity is also increasing in developing countries as household incomes rise. For example, over a 10-year period, the incidence of obesity in young urban children in China increased by a factor of eight. Copyright © 2014 Pearson Education, Inc. All Rights Reserved
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Obesity Possible Causes It appears genetic differences—and their effects on development of the endocrine system and brain mechanisms that control food intake and metabolism—appear to be responsible for the overwhelming majority of cases of extreme obesity. Changes in the gene pool cannot account for this increase; instead, we must look to environmental causes that have produced changes in people’s behavior. Copyright © 2014 Pearson Education, Inc. All Rights Reserved
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Obesity Possible Causes Body weight is the result of the difference between two factors: calories consumed and energy expended. If we consume more calories than we expend as heat and work, we gain weight. If we expend more than we consume, we lose weight. Copyright © 2014 Pearson Education, Inc. All Rights Reserved
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Obesity Possible Causes Differences in body weight—perhaps reflecting physiological differences in metabolism, activity levels, or appetite—have a strong hereditary basis. Twin studies suggest that between 40 percent and 70 percent of the variability in body fat is due to genetic differences. Twin studies have found also strong genetic effects on the amount of weight that people gain or lose when they are placed on high- or low-calorie diets. Copyright © 2014 Pearson Education, Inc. All Rights Reserved
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Obesity Possible Causes Thus, heredity appears to affect people’s metabolic efficiency. However, until recently, variations in only two genes were found to cause obesity in humans: the gene for the MC4 receptor and the FTO gene (fat mass and obesity related gene), which codes for an enzyme that acts in hypothalamic regions related to energy balance, such as the PVN, and the arcuate nucleus. Copyright © 2014 Pearson Education, Inc. All Rights Reserved
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Obesity Possible Causes However, these genes are very rare, so none of them can account for the prevalence of obesity in the general population. The high level of heritability of obesity must be explained, then, as the additive effects of a large number of genes, each of which has a small effect on BMI. In any event, we cannot blame the current epidemic of obesity and type 2 diabetes on genetics. Copyright © 2014 Pearson Education, Inc. All Rights Reserved
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Obesity Treatment Obesity is extremely difficult to treat; the enormous financial success of diet books, health spas, and weight reduction programs attests to the trouble people have in losing weight. More precisely, many programs help people to lose weight initially, but then the weight is quickly regained. Copyright © 2014 Pearson Education, Inc. All Rights Reserved
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Obesity Treatment Whatever the cause of obesity, the metabolic fact of life is this: If calories in exceed calories out, then body fat will increase. Because it is difficult to increase the “calories out” side of the equation enough to bring an obese person’s weight back to normal, most treatments for obesity attempt to reduce the “calories in.” Copyright © 2014 Pearson Education, Inc. All Rights Reserved
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Obesity Treatment Surgeons have become involved in trying to help obese people lose weight. The procedures they have developed (called bariatric surgery, from the Greek barys, “heavy,” and iatrikos, “medical”) are designed to reduce the amount of food that can be eaten during a meal or interfere with absorption of calories from the intestines. Bariatric surgery has been aimed at the stomach, the small intestine, or both. Copyright © 2014 Pearson Education, Inc. All Rights Reserved
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Obesity Treatment The most effective form of bariatric surgery is a special form of gastric bypass called the Roux-en-Y gastric bypass, or RYGB. The jejunum (the second part of the small intestine, immediately “downstream” from the duodenum) is cut, and the upper end is attached to the stomach pouch. Digestive enzymes that are secreted into the duodenum pass through the upper intestine and meet up with the meal that has just been received from the stomach pouch. Copyright © 2014 Pearson Education, Inc. All Rights Reserved
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Obesity Treatment Suzuki et al. (2005) found that rats that sustained a RYGB procedure (but not rats that received sham surgery) ate less, lost weight, and showed decreased ghrelin levels and increased PYY levels. Figure 11.25 shows the effects of RYGB surgery in two strains of rats: normal rats and those from a strain that was bred for overeating and obesity (Shin et al., 2011). As you can see, even normal rats continue to gain weight when they are housed in a cage with food always available, but the obesity surgery suppressed weight gain in both strains of animals. Copyright © 2014 Pearson Education, Inc. All Rights Reserved
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Anorexia Nervosa/Bulimia Nervosa anorexia nervosa A disorder that most frequently afflicts young women; exaggerated concern with being overweight that leads to excessive dieting and often compulsive exercising; can lead to starvation. bulimia nervosa Bouts of excessive hunger and eating, often followed by forced vomiting or purging with laxatives; sometimes seen in people with anorexia nervosa. Copyright © 2014 Pearson Education, Inc. All Rights Reserved
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Anorexia Nervosa/Bulimia Nervosa Possible Causes Anorexia is a serious disorder. Five to 10 percent die of complications of the disease or of suicide. Many anorexics suffer from osteoporosis, and bone fractures are common. When the weight loss becomes severe enough, anorexic women cease menstruating. Copyright © 2014 Pearson Education, Inc. All Rights Reserved
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Anorexia Nervosa/Bulimia Nervosa Possible Causes Many researchers and clinicians have concluded that anorexia nervosa and bulimia nervosa are symptoms of an underlying mental disorder. However, evidence suggests just the opposite: that the symptoms of eating disorders are actually symptoms of starvation. Copyright © 2014 Pearson Education, Inc. All Rights Reserved
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Anorexia Nervosa/Bulimia Nervosa Possible Causes The fact that anorexia nervosa is seen primarily in young women has prompted both biological and social explanations. Most psychologists favor the latter, concluding that the emphasis that most modern industrialized societies places on slimness— especially in women—is responsible for this disorder. Another possible cause could be the changes in hormones that accompany puberty. Copyright © 2014 Pearson Education, Inc. All Rights Reserved
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Anorexia Nervosa/Bulimia Nervosa Treatment Anorexia is very difficult to treat successfully. Cognitive behavior therapy, considered by many clinicians to be the most effective approach, has a success rate of less than 50 percent and a relapse rate of 22 percent during a one-year treatment period. Copyright © 2014 Pearson Education, Inc. All Rights Reserved
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Anorexia Nervosa/Bulimia Nervosa Treatment Researchers have tried to treat anorexia nervosa with many drugs that increase appetite in laboratory animals or in people without eating disorders. For example, antipsychotic medications, drugs that stimulate adrenergic 2 receptors, L -DOPA, and THC (the active ingredient in marijuana). Unfortunately, none of these drugs has been shown to be helpful (Mitchell, 1989). Copyright © 2014 Pearson Education, Inc. All Rights Reserved
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