Hunger, Eating, and Health PDF

Hunger, Eating, and Health ​ The remaining waste is turned into poop and Why Do Many People Eat Too Much? removed from the body through the anus. 𝐃𝐢𝐠𝐞𝐬𝐭𝐢𝐨𝐧, 𝐄𝐧𝐞𝐫𝐠𝐲 𝐒𝐭𝐨𝐫𝐚𝐠𝐞, 𝐚𝐧𝐝 𝐄𝐧𝐞𝐫𝐠𝐲 𝐔𝐭𝐢𝐥𝐢𝐳𝐚𝐭𝐢𝐨𝐧 Energy Storage in the Bod...

Hunger, Eating, and Health ​ The remaining waste is turned into poop and Why Do Many People Eat Too Much? removed from the body through the anus. 𝐃𝐢𝐠𝐞𝐬𝐭𝐢𝐨𝐧, 𝐄𝐧𝐞𝐫𝐠𝐲 𝐒𝐭𝐨𝐫𝐚𝐠𝐞, 𝐚𝐧𝐝 𝐄𝐧𝐞𝐫𝐠𝐲 𝐔𝐭𝐢𝐥𝐢𝐳𝐚𝐭𝐢𝐨𝐧 Energy Storage in the Body The primary purpose of hunger is to increase the probability Three main types of energy of eating, and the primary purpose of eating is to supply the body with the molecular building blocks and 1. Fats (Lipids) – Found in foods like oils, butter, and nuts. energy it needs to survive and function (see Blackburn,2001). 2. Amino Acids – Come from proteins like meat, fish, and beans. Digestion ​ Digestion is the gastrointestinal process of breaking 3. Glucose – A type of sugar from carbohydrates like bread, down food and absorbing its constituents into the rice, and pasta.​ body. ​ Energy is stored in three forms Steps in Digestion ​ Fat – The main way our body stores energy. ​ Glycogen – Stored in the liver and muscles, but in 1. Chewing (Mouth) – Chew food into smaller pieces and mix small amounts. it with saliva, which makes it easier to swallow and starts ​ Proteins – Stored in muscles but mainly used for breaking it down. body functions, not energy. 2. Swallowing (Esophagus) – The food moves down a tube called the esophagus and enters your stomach. Why Fat is the Best Energy Storage? 💡 Fat is better than glycogen because: 3. Stomach – Your stomach stores the food and uses acid to break it down further, especially proteins. 4. Small Intestine (Duodenum) – ✔ Fat stores twice as much energy as glycogen. ​ Food moves into the duodenum (the first part of the ✔ Glycogen holds water, making it heavy and bulky. If our small intestine). body stored all energy as glycogen, we would weigh over ​ Here, most of our nutrients are absorbed into our 600 pounds (275 kg)​ blood. 5. Digestive Enzymes (Pancreas and Gallbladder) – Three Phases of Energy Metabolism​ ​ The pancreas and gallbladder release special juices that 1. Cephalic Phase break down food completely: ​ The cephalic phase is the preparatory phase; it often ​ Proteins turn into amino acids (used to build begins with the sight, smell, or even just the thought muscles). of food, and it ends when the food starts to be ​ Carbohydrates turn into simple sugars (used for absorbed into the bloodstream. energy). ​ These nutrients go into the bloodstream and travel 2. Absorptive Phase to the liver. ​ The absorptive phase is the period during which the 7. Fat Digestion – energy absorbed into the bloodstream from the meal is meeting the body's immediate energy needs. The liver makes bile, which is stored in the gallbladder. 3. Fasting Phase Bile helps break fat into tiny droplets. ​ The fasting phase is the period during which all of Instead of going into the blood, fat is sent to the lymphatic the unstored energy from the previous meal has system for processing. been used and the body is withdrawing energy from its reserves to meet its immediate energy 8. Large Intestine & Waste Removal – requirements. ​ The large intestine absorbs water and minerals from leftover food. How Does Body Control Energy? 𝐓𝐡𝐞𝐨𝐫𝐢𝐞𝐬 𝐨𝐟 𝐇𝐮𝐧𝐠𝐞𝐫 𝐚𝐧𝐝 𝐄𝐚𝐭𝐢𝐧𝐠: 𝐒𝐞𝐭 𝐏𝐨𝐢𝐧𝐭𝐬 ​ 𝐯𝐞𝐫𝐬𝐮𝐬 𝐏𝐨𝐬𝐢𝐭𝐢𝐯𝐞 𝐈𝐧𝐜𝐞𝐧𝐭𝐢𝐯𝐞𝐬 ​ During the three phases of energy metabolism is controlled by two pancreatic hormones: insulin and Set-Point Assumption glucagon. ​ Hunger and eating are thought to be controlled by a "set ○​ In the Cephalic and Absorptive Phases point" of energy (body fat or glucose). The body regulates hunger to return to this "optimal" energy level. Insulin is high, which helps your body use and store energy. It helps your body use glucose (from food) How it works as the main energy source. ​ After eating, energy levels are assumed to be at the It stores extra energy by turning glucose into set point. glycogen (stored in muscles and liver) and ​ Energy levels drop over time, causing hunger to fat into fat storage. return when energy falls too low. ​ Eating continues until energy returns to the set point. Insulin lowers the glucose levels in your blood when food is coming in, and then helps store it for later when you're eating. Components of Set-Point Systems ○​ In the Fasting Phase 1. Set-Point Mechanism - Defines the ideal energy level. Glucagon is high, and insulin levels drop. 2. Detector Mechanism - Detects changes in energy levels. Without insulin, your body stops using glucose as the main energy source and 3. Effector Mechanism - Initiates eating or stops eating to saves it for the brain. return to set point. Your body converts stored energy (like Negative Feedback - Adjustments are made to bring energy glycogen and fat) into glucose to keep levels back to the set point. everything working. Glucagon also helps release fatty acids from fat stores, turning them into energy. Glucostatic and Lipostatic Theories After a long time without food, your body ​ Glucostatic Theory - Hunger is driven by low blood makes ketones (from fatty acids) to keep glucose levels. Eating restores glucose to its set muscles and even your brain running.​ point. ​ Lipostatic Theory - Hunger is driven by low body fat. Eating restores fat to its set point. Why Does This Matter? ​ When you eat, your body is focused on using and storing energy. Combination Theory ​ When you haven’t eaten for a while, your body switches to using stored energy to keep things Both theories interact: running until you eat again. ​ This balance between insulin and glucagon helps ​ Glucostatic - Short-term regulation (meal initiation your body stay energized and functioning, whether and termination). you're eating or fasting. ​ Lipostatic - Long-term regulation (maintaining body fat). Problems with Set-Point Theories 𝐅𝐚𝐜𝐭𝐨𝐫𝐬 𝐓𝐡𝐚𝐭 𝐃𝐞𝐭𝐞𝐫𝐦𝐢𝐧𝐞 𝐖𝐡𝐚𝐭, 𝐖𝐡𝐞𝐧, ​ 𝐚𝐧𝐝 𝐇𝐨𝐰 𝐌𝐮𝐜𝐡 𝐖𝐞 𝐄𝐚𝐭 Obesity Epidemic - Set-point theories struggle to explain the rise in obesity and overweight, as these theories assume This section describes major factors that commonly stable body weight regulation. determine what we eat, when we eat, and how much we eat. Notice that energy deficits are not included among these factors. Positive-Incentive Perspective Factors That Determine What We Eat ​ Humans and animals eat not because of an internal ​ Most humans have a special fondness for sweet, energy deficit, but because of the pleasure of eating fatty, and salty tastes. This species-typical pattern of human taste preferences is adaptive because in nature sweet and fatty tastes are typically characteristic of high-energy foods that are rich in Evolutionary Basis vitamins and minerals, and salty tastes are characteristic of sodium-rich foods. ​ Like sexual behavior, eating is driven by craving and the opportunity to gain pleasure from food, shaped ​ bitter tastes, for which most humans have an by evolution and the need to maintain energy levels. aversion, are often associated with toxins. Superimposed on our species-typical taste preferences and aversions, each of us has the ability to learn specific taste preferences and aversions. Factors Influencing Hunger 1.​ Learned Taste Preferences and Aversions ​ Animals learn to prefer tastes that are followed by an ​ Hunger is influenced by a variety of factors, not just infusion of calories, and they learn to avoid tastes energy levels: that are followed by illness (e.g., Baker & Booth, 1989; Lucas & Sclafani, 1989; Sclafani, 1990). * Food Flavor - Pleasant tastes increase hunger. ​ Similarly, in humans, many food preferences are * Learning - Previous experiences with food and cultural culturally specific. For example, in some cultures, influences matter. various nontoxic insects are considered to be a delicacy. Galef and Wright (1995) have shown that * Time Since Last Meal - The longer it's been since you ate, rats reared in groups, rather than in isolation, are the hungrier you might feel. more likely to learn to eat a healthy diet. * Social Influences - Eating with others or seeing others eat 2.​ Learning to Eat Vitamins and Minerals can trigger hunger. ​ How do animals select a diet that provides all of the vitamins and minerals they need? ​ To answer this question, researchers have studied Flexibility how dietary deficiencies influence diet selection. Two patterns of results have emerged: one for ​ Unlike set-point theories, positive-incentive theories sodium and one for the other essential vitamins recognize that many factors interact to influence and minerals. hunger, acknowledging that eating is not rigidly controlled by a single factor like energy deficits. Factors That Influence When We Eat ​ Collier and his colleagues (see Collier, 1986) found that most mammals choose to eat many small meals (snacks) each day if they have ready access to a continuous supply of food. ​ The number of times humans eat each day is influenced by cultural norms, work schedules, family routines, personal preferences, wealth, and a variety of other factors.  1.​ Premeal Hunger 6.​ Sensory-Specific Satiety ​ The number of different tastes available at each ​ According to Woods, the key to understanding meal has a major effect on meal size. hunger is to appreciate that eating meals stresses ​ In one study of sensory-specific satiety (Rolls et the body. Before a meal, the body's energy reserves al.,1981), human subjects were asked to rate the are in reasonable homeostatic balance; then, as a palatability of eight different foods, and then they ate meal is consumed, there is a homeostasis-disturbing a meal of one of them. influx of fuels into the bloodstream. The body does what it can to defend its homeostasis. 𝐏𝐡𝐲𝐬𝐢𝐨𝐥𝐨𝐠𝐢𝐜𝐚𝐥 𝐑𝐞𝐬𝐞𝐚𝐫𝐜𝐡 𝐨𝐧 𝐇𝐮𝐧𝐠𝐞𝐫 𝐚𝐧𝐝 𝐒𝐚𝐭𝐢𝐞𝐭𝐲 2.​ Pavlovian Conditioning of Hunger ​ Role of Blood Glucose Level in Hunger and Satiety ​ In a classic series of Pavlovian conditioning experiments on laboratory rats, Weingarten (1983, Role of glucose in the regulation of eating in 1984, 1985) provided strong support for the view that 1990’s following the development of methods of continually hunger is often caused by the expectation of food, monitoring blood glucose levels. not by an energy deficit. Classic experiment of Campfield and Smith (1990) Factors That Influence How Much We Eat Rats were housed individually with free access to mixed diet and water and there blood glucose levels were continually The motivational state that causes us to stop eating a meal monitored via chronic intravenous catheter (i.e., a when there is food remaining is satiety. hypodermic needle located in a vein). 1.​ Satiety Signals ​ Food in the gut and glucose entering the blood can In this situation, baseline blood glucose levels rarely induce satiety signals, which inhibit subsequent fluctuated more than 2%. However, about 10 minutes consumption. These signals depend on both the before a meal was initiated, the levels suddenly dropped volume and the nutritive density (calories per unit about 8% (see Figure 12.7). volume) of the food. 2.​ Sham Eating ​ The study of sham eating indicates that satiety Do the observed reductions in blood glucose before a meal signals from the gut or blood are not necessary to lend support to the glucostatic theory of hunger? I think not​ terminate a meal. ​ 5 REASONS: 1.​ It is a simple matter to construct a situation in which drops in blood glucose levels do not precede eating (e.g., Strubbe & Steffens, 1977) for example, by unexpectedly serving a food with a high positive-incentive value.​ 2.​ The usual pre meal decreases in blood glucose seem to be a response to the intention to start eating, not the other way round. The pre-meal decreases in blood glucose are typically preceded by increases in blood insulin levels, which indicates that the decreases do not reflect gradually declining 3.​ Appetizer Effect and Satiety energy reserves but are actively produced by an ​ If appetizers are served, you will notice that small increase in blood levels of insulin (see Figure 12.7).​ amounts of food consumed before a meal actually increase hunger rather than reducing it. This is the 3.​ If an expected meal is not served, blood glucose appetizer effect. levels soon return to their previous homeostatic 4.​ Serving Size and Satiety level. ​ Many experiments have shown that the amount of consumption is influenced by serving size (Geier, 4.​ The glucose levels in the extracellular fluids that Rozin, & Doros, 2006). The larger the servings, the surround CNS neurons stay relatively constant, even more we tend to eat. when blood glucose levels drop (see Seeley & 5.​ Social Influences and Satiety Woods2003). ​ Feelings of satiety may also depend on whether we are eating alone or with others.  5.​ Injections of insulin do not reliably induce eating the regulation of energy metabolism, not the regulation of unless the injections are sufficiently great to reduce eating. The initial interpretation was that VMH-lesioned blood glucose levels by 50% (see Rowland, 1981), animals become obese because they overeat; however, the and large premeal infusions of glucose do not evidence suggests the converse that they overeat because suppress eating (see Geiselman, 1987). they become obese. Bilateral VMH lesions increase blood insulin levels, which Myth of Hypothalamic Hunger and Satiety Centers increases lipogenesis (the production of body fat) and decreases lipolysis (the breakdown of body fat to utilizable In the 1950s, experiments on rats seemed to suggest that forms of energy). Both are likely to be the result of the eating behavior is controlled by two different regions of the increases in insulin levels that occur following the lesion. hypothalamus: satiety by the ventromedial hypothalamus Because the calories ingested by VMH-lesioned rats are (VMH) and feeding by the lateral hypothalamus (LH) see converted to fat at a high rate, the rats must keep eating to Figure 12.8. This theory turned out to be wrong, but it ensure that they have enough calories in their blood to meet stimulated several important discoveries. their immediate energy requirements (e.g., Hustvedt & Løvø, 1972); they are like misers who run to the bank each time VHM SATIETY CENTER they make a bit of money and deposit it in a savings account from which withdrawals cannot be made. In 1940, it was discovered that large bilateral electrolytic lesions to the ventromedial hypothalamus produce The second line of evidence that undermined the theory of a hyperphagia (excessive eating) and extreme obesity in rats VMH satiety center has shown that many of the effects of (Hetherington & Ranson, 1940). VMH lesions are not attributable to VMH damage. A large fiber bundle, the ventral noradrenergic bundle, courses past This VMH syndrome has two different phases: dynamic and the VMH and is thus inevitably damaged by large electrolytic static. VMH lesions; in particular, fibers that project from the nearby paraventricular nuclei of the hypothalamus are damaged 1.​ Dynamic - as soon as the subject regains (see Figure 12.10). Bilateral lesions of the Noradrenergic consciousness after the operation, is characterized bundles (e.g., Gold et al., 1977) or the paraventricular nuclei by several weeks of grossly excessive eating and (Leibowitz, Hammer, & Chang,1981) produce hyperphagia rapid weight gain. and obesity, just as VMH lesions do.​ ​ 2.​ STATIC - after that, consumption gradually declines Most of the evidence against the notion that the LH is a to a level that is just sufficient to maintain a stable feeding center has come from a thorough analysis of the level of obesity; effects of bilateral LH lesions. Early research focused exclusively on the aphagia and adipsia that are produced by LH FEEDING CENTER LH lesions,but subsequent research has shown that LH lesions produce a wide range of severe motor disturbances In 1951,Anand and Brobeck reported that bilateral and a general lack of responsiveness to sensory input (of electrolytic lesions to the lateral hypothalamus produce which food and drink are but two examples). Consequently, aphagia, a complete cessation of eating. the idea that the LH is a center specifically dedicated to feed- ing no longer warrants serious consideration. Even rats that were first made hyperphagic by VMH lesions were rendered aphagic by the addition of LH lesions. Anand and Brobeck concluded that the lateral region of the Role of the gastrointestinal tract in satiety hypothalamus is a feeding center. Teitelbaum and Epstein (1962) subsequently discovered two important features of In the 1980s, there was a resurgence of interest in the role of the LH syndrome. the gastrointestinal tract in eating. It was stimulated by a series of experiments that indicated that the gastrointestinal ​ tract is the source of satiety signals. First, they found out that the aphagia was accompanied by adipsia, a complete cessation of drinking. Second, they Because the transplanted stomach had no functional nerves, found that LH-lesioned rats partially recover if they are kept the gastrointestinal satiety signal had to be reaching the alive by tube feeding. First, they begin to eat wet, palatable brain through the blood. And because nutrients are not foods, such as chocolate chip cookies soaked in milk, and absorbed from the stomach, the bloodborne satiety signal eventually they will eat dry food pellets if water is could not have been a nutrient. It had to be some chemical concurrently available. or chemicals that were released from the stomach in response to the caloric value and volume of the food which Reinterpretation of the effects of VMH and LH Lesions leads us nicely into the next subsection. The theory that the VMH is a satiety center crumbled in the face of two lines of evidence. One of these lines showed that the primary role of the hypothalamus is Hunger and satiety peptides the Prader-Willi patient acts as though he or she is starving. Other common physical and neurological symptoms include Soon after the discovery that the stomach and other parts of weak muscles, small hands and feet, feeding difficulties in the gastrointestinal tract release chemical signals to the infancy, tantrums, compulsivity, and skin picking. If untreated, brain, evidence began to accumulate that these chemicals most patients become extremely obese, and they often die in were peptides, short chains of amino acids that can function early adulthood from diabetes, heart disease, or other as hormones and neurotransmitters obesity-related disorders. There has been considerable support for the hypothesis that peptides can function as satiety signals (see Gao & Horvath, Prader willi syndrome the case of miss A. 2007; Ritter, 2004). Miss A. was born with little muscle tone. Because her Several hunger peptides (peptides that increase appetite) sucking reflex was so weak, she was tube fed. By the time have also been discovered. These peptides tend to be she was 2 years old, her hypotonia (below-normal muscle synthesized in the brain, particularly in the hypothalamus. tone) had resolved itself, but a number of characteristic deformities and developmental delays began to appear. The discovery of the hunger and satiety peptides has had two major effects on the search for the neural mechanisms of At 3 1/2 years of age, Miss A. suddenly began to display a hunger and satiety. First, the sheer number of these hunger voracious appetite and quickly gained weight. Fortunately, and satiety peptides indicates that the neural system that her family maintained her on a low-calorie diet and kept all controls eating likely reacts to many different signals food locked away. (Nogueiras & Tschöp, 2005; Schwartz & Azzara, 2004), not just to one or two (e.g.,not just to glucose and fat). Miss A. is moderately retarded, and she suffers from psychiatric problems. Her major problem is her tendency to Second, the discovery that many of the hunger and satiety have tantrums any time anything changes in her environment peptides have receptors in the hypothalamus has renewed (e.g., a substitute teacher at school). Thanks largely to her interest in the role of the hypothalamus in hunger and eating family and pediatrician, she has received excellent care, (Gao & Horvath, 2007; Lam, Schwartz, & Rossetti, 2006; which has minimized the complications that arise with Luquet et al., 2005). Prader-Willi syndrome most notably those related to obesity and its pathological effects. Serotonin and satiety The monoaminergic neurotransmitter serotonin is another 𝐁𝐨𝐝𝐲 𝐖𝐞𝐢𝐠𝐡𝐭 𝐑𝐞𝐠𝐮𝐥𝐚𝐭𝐢𝐨𝐧: 𝐒𝐞𝐭 𝐏𝐨𝐢𝐧𝐭𝐬 𝐯𝐞𝐫𝐬𝐮𝐬 𝐒𝐞𝐭𝐭𝐥𝐢𝐧𝐠 𝐏𝐨𝐢𝐧𝐭𝐬 ​ chemical that plays a role in satiety. The initial evidence for this role came from a line of research in rats. In these Set-Point Assumptions about Body Weight and Eating studies, serotonin produced satiety was found to have three major properties (see Blundell & Halford, 1998): 1.​ Variability of Body Weight ​ Set-point theories of body weight regulation + It caused the rats to resist the powerful attraction of suggest that the best method of maintaining highly palatable cafeteria diets. a constant body weight is to eat each time there is a motivation to eat, because, + It reduced the amount of food that was consumed according to the theory, the main function of during each meal rather than reducing the number of hunger is to defend the set point. However, meals (see Clifton, 2000). many people avoid obesity only by resisting their urges to eat.​ + It was associated with a shift in food preferences away from fatty foods. 2.​ Set Points and Health ​ One implication of set-point theories of body This profile of effects suggested that serotonin might be weight regulation is that each person’s set useful in combating obesity in humans. Indeed, serotonin point is optimal for that person's health or at agonists (e.g., fenfluramine, dexfenfluramine, fluoxetine) least not incompatible with good health. This have been shown to reduce hunger, eating, and body weight is why popular psychologists commonly under some conditions (see Blundell & Halford, 1998). Later advise people to listen to the wisdom of their in this chapter, you will learn about the use of serotonin to bodies and eat as much as they need to treat human obesity (see De Vry & Schreiber, 2000). satisfy their hunger.​ 3.​ Regulation of Body Weight by Changes in the Prader willi syndrome patients with insatiable hunger Efficiency of Energy Utilization ​ As a person's level of body fat declines, that Prader-Willi syndrome, which results from an accident of person starts to use energy resources more chromosomal replication, experiences insatiable hunger, little efficiently, which limits further weight loss or no satiety, and an exceptionally slow metabolism. In short, (see Martin, White, & Hulsey, 1991);  conversely, weight gain is limited by a 𝐇𝐮𝐦𝐚𝐧 𝐎𝐛𝐞𝐬𝐢𝐭𝐲: 𝐂𝐚𝐮𝐬𝐞𝐬, 𝐌𝐞𝐜𝐡𝐚𝐧𝐢𝐬𝐦𝐬, 𝐚𝐧𝐝 𝐓𝐫𝐞𝐚𝐭𝐦𝐞𝐧𝐭𝐬 progressive decrease in the efficiency of energy utilization.​ Who Needs to Be Concerned about Obesity? ​ Diet-induced Thermogenesis. The relation between obesity and poor health has been ○​ The mechanism by which the body repeatedly documented. adjusts the efficiency of its energy utilization in response to its levels of a.​ Individuals who are only a bit overweight run a body fat​ greater risk of developing health problems. b.​ Obese women are at increased risk of having infants ​ Basal Metabolic Rate with health problems. ○​ The rate at which energy is utilized to maintain bodily processes when Rates of obesity are increasing in most parts of the world. resting For example, it has been estimated that over one-third of the Set-Points and Settling Points in Weight Control children born in the United States in 2000 will eventually develop diabetes, and 10% of these will develop related ​ According to the settling-point model, body weight life-threatening conditions.​ remains stable as long as there are no long-term changes in the factors that influence it; and if there are such changes, their impact is limited by negative Why Is There an Epidemic of Obesity? feedback. In the settling-point model, the negative feedback merely limits further changes in the same During the course of evolution, inconsistent food supplies direction, whereas in the set-point model, negative were one of the main threats to survival. As a result, the feedback triggers a return to the set point. fittest individuals were those who preferred high-calorie foods, ate to capacity when food was available, stored as ​ Leaky Barrel Model many excess calories as possible in the form of body fat, and used their stores of calories as efficiently as possible. These characteristics are passed onto future generations. We live in an environment in which an endless variety of foods of the highest positive-incentive and caloric value are readily and continuously available. The consequence is an appallingly high level of consumption.​ Why Do Some People Become Obese While Others Do Not? Those who are obese are those whose energy intake has ​ 4 key Facts of Weight Regulation exceeded their energy output; those who are sl are those whose energy intake has not exceeded their energy output 1.​ Body weight remains relatively constant in (Nestle, 2007). many adult animals. 2.​ Many adult animals experience enduring Differences in Consumption changes in body weight. 3.​ If a subjects intake of food is reduced, There are many factors that lead some people to eat more metabolic changes that limit the loss of than others who have comparable access to food. weight occur; the opposite happens when the subject overeats. a.​ strong preference for the taste of high-calorie foods 4.​ After an individual has lost a substantial b.​ raised in family/culture that promotes excessive amount of weight (by dieting, exercise, or eating the surgical removal of fat), there is a c.​ particularly large cephalic-phase responses to the tendency for the original weight to be sight or smell of food regained once the subject returns to the previous eating-and energy-related lifestyle. Difference on Energy Expenditure Leptin, Insulin, and the Arcuate Melanocortin System People differ markedly from one another in the degree to More than 25 years ago, Woods and colleagues (1979) which they can dissipate excess consumed energy. suggested that pancreatic peptide hormone insulin serves a function such as leptin. 1.​ Difference in basal metabolic rate 2.​ Ability to react to fat increases by diet-induced ​ Brain levels of insulin were found to be positively thermogenesis correlated with levels of body fat (Seeley et al., 3.​ NEAT, or nonexercise activity thermogenesis 1996). ​ Receptors for insulin were found in the brain (Baura Genetic Difference et al., 1993). ​ Infusions of insulin into the brains of laboratory Over 100 human chromosome loci (regions) have already animals were found to reduce eating and body been linked to obesity Although it is proving difficult to weight (Campfield et al., 1995; Chavez, Seeley, & unravel the various genetic factors that influence variations in Woods, 1995). body weight, single gene mutations have been linked to pathological conditions that involve obesity.​ Receptors for both peptide hormones are located in many parts of the nervous system, but most are in the hypothalamus, particularly in one area: the arcuate nucleus. Why Are Weight-Loss Programs Typically Ineffective? They are located in two classes of neurons: neurons that release neuropeptide Y (the gut hunger peptide that was Most of the lost weight is regained once the dieter stops discussed), and neurons that release melanocortins, a class following the program and the original conditions are of peptides that includes the gut satiety peptide reestablished. α-melanocyte-stimulating hormone (alpha-melanocyte-stimulating hormone). This neuron has The key to permanent weight loss is a permanent lifestyle been the focus of most because injections of this hormone change. have been shown to suppress eating and promote weight loss Several studies have shown that exercise often contributes little to weight loss.​ Leptin as Treatment for Human Obesity Receptors for leptin were found in the brain, and injecting it Leptin and the Regulation of Body Fat into ob/ob mice reduced both their eating and their body fat (Seeley & Woods, 2003). Fat actively releases a peptide hormone called leptin. When research on leptin turned from ob/ob mice to obese ​ Obese Mice and the Discovery of Leptin. humans, the program ran into two major snags. In 1950, a spontaneous genetic mutation occurred in the 1.​ Obese humans were found to have high, rather than mouse colony maintained in the Jackson Laboratory at Bar low, levels of leptin. Harbor, Maine. The mutant mice are commonly referred to as 2.​ Injections of leptin did not reduce either the eating or ob/ob mice, and weigh thrice as much as typical mice. They the body fat of obese humans.​ eat more than control mice; they convert calories to fat and use calories more efficiently. Coleman (1979) hypothesized ​ The Case of the Child with No Leptin​ that ob/ob mice lack a critical hormone that normally inhibits fat production and maintenance. In 1994, Friedman and his colleagues found out that because of their mutation, they Treatment of Obesity ob/ob mice lack leptin. This led to a hypothesis: Perhaps leptin is a negative feedback signal that is normally released Serotonergic Agonists from fat stores to decrease appetite and increase fat metabolism. Serotonin agonists have been shown to reduce food consumption in both human and nonhuman subjects; they Could leptin be administered to obese humans to reverse the have considerable potential in the treatment of obesity. They current epidemic of obesity?​ have been found in various studies of obese patients to ​ reduce the following: the urge to eat high-calorie foods, the ​ consumption of fat, the subjective intensity of hunger, the ​ size of meals, the number of between-meal snacks, and bingeing.​ ​ Gastric Surgery Gastric bypass is a surgical treatment for extreme obesity that involves short-circuiting the normal path of food through the digestive tract so its absorption is reduced. An alternative is the adjustable gastric band procedure, which involves surgically positioning a hollow silicone band around the stomach to reduce the flow of food through it; the circumference of the band can be adjusted by injecting saline into the band through a port that is implanted in the skin. 𝐀𝐧𝐨𝐫𝐞𝐱𝐢𝐚 𝐚𝐧𝐝 𝐁𝐮𝐥𝐢𝐦𝐢𝐚 𝐍𝐞𝐫𝐯𝐨𝐬𝐚 Anorexia nervosa is a disorder of underconsumption. Anorexics eat so little that they experience health threatening weight loss and despite their emaciated appearance, they often Clinical perceive themselves as fat. Anorexia nervosa is a serious condition; In approximately 10% of diagnosed cases, complications from starvation result in death, and there is a high rate of suicide among anorexics. Bulimia nervosa is a disorder characterized by periods of not eating interrupted by bingeing(eating huge amounts of food in short periods of time) followed by efforts to immediately eliminate the consumed calories from the body by voluntary purging (vomiting) ; by excessive use of laxatives, enemas, or diuretics; or by extreme exercise. Bulimics may be obese or of formal weight. If they are underweight,they are diagnosed as bingeing anorexics. Relation between Anorexia and Bulimia The following are other similarities that support the view that anorexia and bulimia are variants of the same disorder ​ Both anorexics and bulimics tend to have distorted body images, seeing themselves as much fatter and less attractive than they are in reality. ​ In practice,many patients seem to straddle the two diagnoses and cannot readily be assigned to one or the other categories and many patients flip-flop between the two diagnoses as their circumstances change. ​ Anorexia and bulimia show the same pattern of distribution in the population. Although their overall incidence in the population is low,both conditions occur more commonly among educated females in affluent cultural groups. ​ Both anorexia and bulimia are highly correlated with obsessive-compulsive disorder and depression. ​ Neither disorder responds well to existing therapies. Short-term improvements are common,but relapse is usual.