Neural Control Of Food Intake PDF

NEURAL CONTROL OF FOOD INTAKE NEURAL CONTROL OF FOOD INTAKE IS A COMPLEX PROCESS IT INVOLVE MULTIPILE NEURAL AND CHEMICAL SYSTEM We eat food when we are hungry and select the food of our interest based on our appetite. The sensation of hunger is associated with a craving for food and several...

NEURAL CONTROL OF FOOD INTAKE NEURAL CONTROL OF FOOD INTAKE IS A COMPLEX PROCESS IT INVOLVE MULTIPILE NEURAL AND CHEMICAL SYSTEM We eat food when we are hungry and select the food of our interest based on our appetite. The sensation of hunger is associated with a craving for food and several other several physiologic effects, such as rhythmical contractions of the stomach and restlessness, which cause the person to search for an adequate food supply. A person’s appetite is a desire for food, often of a particular type, and is useful in helping to choose the quality of the food to be eaten. If the quest for food is successful, the feeling of satiety occurs.  ROLE OF HYPOTHALAMUS Hypothalamus Contains hunger and satiety Centres. Several neuronal centres of the hypothalamus participate in the control of food intake. The lateral nuclei of the hypothalamus serve as a feeding centre, It initiates eating stimulation of this area causes an animal to eat voraciously. (Hyperphagia) Hyperphagia – Excessive eating from excess hunger or increased appetite. Conversely, destruction of the lateral hypothalamus causes lack of desire for food and progressive inanition, a condition characterized by marked weight loss, muscle weakness, and decreased metabolism  The ventro-medial nuclei of the hypothalamus serve as the satiety centre. This inhibit eating behaviour when we are full. Electrical stimulation of this region can cause complete satiety, and even in the presence of highly appetizing food, the animal refuses to eat (aphagia) Aphagia – failure to eat when hungry caused by damage to the LH. Conversely, destruction of the ventro-medialnuclei causes voracious and continued Eating until the animal becomes extremely obese, sometimes as large as four times normal The paraventricular, dorsomedial, and arcuate nuclei of the hypothalamus also play a major role in regulating food intake. For example, lesions of the paraventricular nuclei often cause excessive eating, whereas lesions of the dorsomedial nuclei usually depress eating behaviour. The arcuate nuclei are the sites in the hypothalamus where multiple hormones released from the gastrointestinal tract and adipose tissue converge to regulate food intake as well as energy expenditure.. These nuclei of the hypothalamus also influence the secretion of several hormones that are important in regulating energy balance and metabolism, including those from the thyroid and adrenal glands, as well as the pancreatic islet cells. The hypothalamus receives neural signals from the gastrointestinal tract that provide sensory information about stomach filling, chemical signals from nutrients in the blood (glucose, amino acids, and fatty acids) that signify satiety, signals from gastrointestinal hormones, signals from hormones released by adipose tissue, and signals from the cerebral cortex (sight, smell, and taste) that influence feeding behavior The hypothalamic feeding and satiety centres have a high density of receptors for neurotransmitters and hormones that influence feeding behaviour. NEURAL CENTRES THAT INFLUENCE MECHANICAL PROCESS OF FEEDING If the brain is sectioned below the hypothalamus but above the mesencephalon, the animal can still perform the basic mechanical features of the feeding process. It can salivate, lick its lips, chew food, and swallow. Therefore, the actual mechanics of feeding are controlled by centers in the brain stem. Neural centers higher than the hypothalamus al play important roles in the control of feeding, particularly in the control of appetite.  These centers include the 1. Amygdala. 2. prefrontal cortex, which are closely coupled with the hypothalamus. Destructive lesions in the amygdala have demonstrated that some of its areas increase feeding, whereas others inhibit feeding. “psychic blindness”: destruction of the amygdala on both sides of the results in loses or at least partially loses the appetite control that determines the type and quality of food it eats. PHYSIOLOGY ASSIGNMENT DELNA MARTIN 2ND UG INTEGRATED PSYCHOLOGY Hormones That Regulates The Quantity Of Food Intake (Effect of Cholecystokinin, Peptide YY, GLP, Ghrelin ) Role Of Hormones In The Regulation Of Food Intake  Besides neural centres in the brain, hormones also play significant roles in the regulation of food intake. Gastrointestinal Hormonal Factors supress feeding. There are 2 groups of hormones. Increased food intake – orexigeniv, Decreased food intake - Hypophagia 1.GHRELIN  GHRELIN Often referred to as the “hunger hormone,” ghrelin is produced in the stomach and increases appetite. When the stomach is empty, ghrelin levels rise, signaling to the brain that it’s time to eat. After eating, ghrelin levels decrease, helping to reduce hunger. 2.GLUCOGON LIKE PEPTIDE – 1 (GLP -1 )  Glucagon-Like Peptide-1 (GLP-1):  GLP-1 is an incretin hormone secreted by L-cells in the small intestine in response to food intake, particularly carbohydrates and fats. It has a more prominent role in appetite regulation:   - **Central Appetite Suppression**: GLP-1 acts on receptors in the hypothalamus and brainstem to suppress appetite. It stimulates pro-opiomelanocortin (POMC) neurons, promoting satiety.   - **Slowing Gastric Emptying**: GLP-1 slows the rate at which the stomach empties food into the intestine, prolonging the feeling of fullness.  - **Insulin Secretion and Blood Glucose Regulation**: By enhancing insulin secretion and reducing glucagon release, GLP-1 indirectly supports energy homeostasis.  - **Therapeutic Uses**: GLP-1 receptor agonists (e.g., liraglutide, semaglutide) are used in diabetes and obesity treatments to reduce food intake and promote weight loss.  - **GLP-1** plays a more robust role in reducing food intake through central appetite regulation and delayed gastric emptying. 3.CHOLECYSTOKININ ( CCK )  Cholecystokinin (CCK) is a peptide hormone primarily produced in the small intestine that plays a critical role in regulating food intake. It is released in response to the presence of nutrients, especially fats and proteins, in the stomach. CCK functions as a satiety signal by interacting with receptors in the gut and brain to reduce food consumption. Here’s how it works:   1. **Gastrointestinal Action**: When food enters the small intestine, CCK is secreted by enteroendocrine cells. It stimulates the release of digestive enzymes from the pancreas and bile from the gallbladder, aiding in nutrient digestion.   2. **Satiety Signal**: CCK activates vagal afferent nerves that communicate with the hypothalamus and brainstem, areas responsible for regulating hunger. This signaling induces feelings of fullness, reducing meal size.  3. **Short-term Regulation**: CCK acts acutely during a meal, signaling the body to stop eating. It does not regulate long-term energy balance.   Studies indicate that administering exogenous CCK reduces food intake in both animals and humans. However, the effectiveness of CCK as a satiety signal is influenced by factors such as food composition and individual differences in receptor sensitivity.  4.PEPTIDE YY  Peptide YY (PYY) is a gut hormone secreted by L-cells in the distal small intestine and colon in response to food intake. It plays a crucial role in regulating appetite and food consumption, contributing to short-term satiety. Here’s how it affects food intake:   1. **Postprandial Release**: PYY is released into the bloodstream shortly after eating, with levels peaking approximately 1–2 hours post-meal. The amount released depends on the caloric content and macronutrient composition of the meal, with fat and protein eliciting stronger responses.   2. **Central Satiety Signals**: PYY acts on the hypothalamus and brainstem, regions involved in appetite control, to suppress hunger. It inhibits the activity of the orexigenic (appetite-stimulating) neuropeptide Y/agouti-related protein (NPY/AgRP) neurons and activates anorexigenic (appetite-reducing) pro-opiomelanocortin (POMC) neurons.  3. **Slow Gastric Emptying**: PYY also reduces gastric motility and slows gastric emptying, enhancing the sensation of fullness and prolonging satiety.   4. **Reduced Food Intake**: Studies show that administration of exogenous PYY reduces appetite and subsequent food intake in both humans and animals.   PYY’s effects are an integral part of the body’s mechanisms for maintaining energy balance and preventing overeating. Disruptions in its function or levels have been implicated in conditions like obesity and eating disorders. CONCLUSION  In conclusion, hormones play a significant role in regulating food intake, influencing appetite, satiety, and energy balance. Hormones like ghrelin (which stimulates hunger), leptin (which signals satiety), insulin, and cortisol interact with the brain and digestive system to maintain homeostasis. Disruptions in hormonal signaling can lead to overeating, altered metabolism, and weight gain or loss. Understanding the relationship between hormones and food intake is crucial for managing conditions like obesity, diabetes, and eating disorders, and can help in developing more effective dietary and therapeutic strategies. THANK YOU.....  PHYSIOLOGY Submitted by:- Jes Mariya Jose REGULATION OF FOOD INTAKE The complex physiological, psychological, and environmental processes that control the amount and timing of food consumption, maintaining energy homeostasis and overall health. The regulation of food intake involves a complex interplay between various physiological ,psychological , and environmental factors. Regulation of food intake 1. Short term regulation. The immediate physiological, psychological, and environmental mechanisms that control food consumption over a short period (minutes to hours), influencing appetite, satiety, and eating behavior. 2. Intermediate term regulation. The physiological mechanisms that control food consumption over a period of hours to days, involving changes in hormone levels, nutrient storage, and energy balance to maintain homeostasis. 3. Long term regulation. The physiological mechanisms that control food consumption over an extended period (days to weeks, months, or even years), involving adjustments in energy balance, body weight, and body composition to maintain overall health and homeostasis. EFFECT OF BLOOD CONCENTRATIONS OF GLUCOSE ON HUNGER AND FEEDING Glucose and Hunger: When blood glucose levels drop, the body perceives this as a signal to eat. This is because glucose is the primary source of energy for the brain and other vital organs. As glucose levels decrease, the brain releases hormones such as ghrelin, which stimulates appetite and increases food intake. 2. Glucose and Satiety: On the other hand, when blood glucose levels rise after a meal, the body releases hormones such as insulin, which helps to regulate glucose uptake and storage. As glucose levels increase, the brain also releases hormones such as leptin, which suppresses appetite and increases feelings of fullness and satiety. 3. Implications for Feeding Behaviors: The relationship between blood glucose concentrations and hunger/satiety signals can have important implications for feeding behaviors. For example, individuals with diabetes or those who experience frequent fluctuations in blood glucose levels may experience increased hunger and food cravings, leading to overeating or poor food choices.  EFFECT OF BLOOD CONCENTRATIONS OF AMINO ACID ON HUNGER AND FEEDING Amino Acids and Hunger: Amino acids, particularly essential amino acids (EAAs), play a crucial role in regulating hunger and satiety. When blood amino acid levels drop, the brain receives signals to increase food intake. This is because amino acids are essential for protein synthesis and other vital functions. 2. Implications for Feeding Behaviors: The relationship between blood amino acid concentrations and hunger/satiety signals has important implications for feeding behavior's.For example: Amino acid supplements, particularly leucine, may help regulate appetite and food intake in certain populations (e.g., athletes, elderly). Amino acid imbalances or deficiencies (e.g., in individuals with liver disease or malabsorption) may lead to increased hunger and food cravings. The gut-brain axis and amino acid sensing may play a role in the development of eating disorders, such as anorexia nervosa. EFFECT OF BLOOD CONCENTRATIONS OF LIPIDS ON HUNGER AND FEEDING 1.Fatty Acids and Hunger: Fatty acids, especially oleic acid, have been shown to suppress appetite and reduce food intake. When fatty acid levels are high, the brain receives signals to decrease hunger and increase feelings of fullness. 2.Cholecystokinin (CCK) and Fatty Acids: The hormone CCK is released in response to fatty acid ingestion and plays a key role in regulating appetite and satiety. CCK signals the brain to reduce food intake and increase feelings of fullness. 3. Gut-Brain Axis and Lipid Sensing: The gut and brain communicate through various signaling pathways, including the gut-brain axis. Lipid-sensing mechanisms in the gut, such as fatty acid receptors, detect changes in blood lipid levels and send signals to the brain to regulate appetite and food intake. 4. Implications for Feeding Behaviors: The relationship between blood lipid concentrations and hunger/satiety signals has important implications for feeding behaviors. For example: - High-fat diets may lead to increased feelings of fullness and reduced hunger due to the suppressive effects of fatty acids on appetite. - Abnormalities in lipid metabolism or fatty acid sensing may contribute to eating disorders, such as obesity or anorexia nervosa. - Certain lipid-lowering medications may affect hunger and satiety signals, leading to changes in food intake and body weight. IMPORTANCE OF DUAL REGULATORY SYSTEM Importance of Both Systems: 1. Flexibility and Adaptability: Having both systems allows for flexibility and adaptability in response to changing energy needs and environmental conditions. 2. Prevention of Overeating and Undereating: The combination of long-term and short-term systems helps prevent overeating and undereating, reducing the risk of obesity, malnutrition, and other health problems. 3. Optimal Nutrient Intake: Both systems work together to ensure optimal nutrient intake, supporting overall health and well-being.  CONCLUSION ▪ The regulation of hunger and feeding is a complex process involving blood concentrations of glucose, amino acids, and lipids, which signal the brain to initiate or terminate food intake. Glucose regulates hunger and satiety through insulin and glucagon, amino acids stimulate appetite through the mTOR pathway, and lipids suppress appetite through cholecystokinin (CCK). A dual regulatory system, comprising long-term and short-term mechanisms, maintains energy homeostasis and optimizes nutrient intake. Understanding these relationships can inform the development of novel therapeutic strategies for managing eating disorders and metabolic diseases, highlighting the importance of continued research into the intricate interactions between nutrient concentrations, hunger, and feeding. THANK YOU SHORT TERM REGULATION OF FOOD INTAKE AND TEMPERATURE REGULATION OF FOOD INTAKE REGULATION OF FOOD INTAKE Here we are looking at Regulation of the short term regulation, quantity of food can be which is concerned divided into short term primarily with regulation and long preventing over eating term regulation at each meal NUCLEI LATERAL NUCLEI ---- Feeding centre WHICH ARE IMPORTANT FOR VENTROMEDIAL NUCLEI --- -- Satiety centre REGULATION OF FOOD INTAKE ARCUATE NUCLEUS NUCLEI WHICH ARE IMPORTANT FOR REGULATION OF FOOD INTAKE NUCLEI WHICH ARE IMPORTANT FOR REGULATION OF FOOD INTAKE NUCLEI WHICH ARE IMPORTANT FOR REGULATION OF FOOD INTAKE NUCLEI WHICH ARE IMPORTANT FOR REGULATION OF FOOD INTAKE SHORT TERM REGULATION OF FOOD INTAKE SHORT TERM REGULATION OF FOOD INTAKE SHORT TERM REGULATION OF FOOD INTAKE SHORT TERM REGULATION OF FOOD INTAKE TEMPERATURE REGULATION OF FOOD INTAKE TEMPERATURE REGULATION OF FOOD INTAKE TEMPERATURE REGULATION OF FOOD INTAKE THANK YOU OBESITY TREATMENT MEGHA S NAIR OBESITY Obesity can be defined as an excess of body fat.A better way to define obesity is to actually measure the percentage of total body fat. Obesity is usually defined as 25% or greater total body fat in men and 35% or greater in women. Obesity results from greater energy intake than energy expenditure. When greater quantities of energy (in the form of food) enter the body than are expended, the body weight increased,and most of the excess energy is stored as fat. Therefore excessive adiposity (obesity) is caused by excess energy intake in excess of energy output.  TREATMENT Treatment of obesity depends on decreasing energy input below energy expenditure and creating a sustained negative energy balance until the desired weight loss is achieved. This means either reducing energy intake or increasing energy expenditure. Treatment for obesity typically involves a combination of lifestyle changes, behavioural modifications and sometimes medication or surgery. LIFESTYLE CHANGES Dietary modifications Eat a balanced diet with plenty of fruits, vegetables, whole grains, and lean protein sources. Sleep and Stress Management. Aim for 7-9 hours of sleep per night and engage in stress reducing activities like yoga, meditation, or deep breathing exercise. Increased Physical Activity Aim for atleast 150 min of moderate intensity aerobic exercise, or 75 min of vigorous intensity aerobic exercise, or a combination of both, per week. The more exercise one gets, the greater the daily energy expenditure and the more rapidly the obesity disappears. Ie, forced exercise is often an essential part of treatment. To decrease energy intake, most reducing diet are designed to contain large quantities of “bulk”, which is generally madeup of non nutritive cellulose substances. This bulk distends the stomach and thereby partially appears hunger.  BEHAVIORAL MODIFICATION Keep a food diary Record your eating habits to identify patterns and areas for improvement. Eat slowly and mindfully Pay attention to your hunger and fullness cues to avoid overeating Use a pedometer or fitness tracker Monitor your physical activity levels to stay motivated. MEDICATIONS Amphetamines Mostly used which directly inhibit the feeding centres in brain Sibutramine It is a sympathomimetic that reduces food intake and increases energy expenditure. Orlistat It is a drug works by altering lipid metabolism. It is a lipase inhibitor, reduces the intestinal digestion of fat. This causes a portion of the ingested fat to be lost in the feces and therefore reduces energy absorption. However, fecel fat loss may cause unpleasant gastrointestinal side effects, as well as loss of fat soluble vitamins in the feces.  Phentermine-topiramate (Qsymia) Suppresses appetite and increases feelings of fullness. Liraglutide( Saxenda) Injected medication that helps reduce hunger and increase feeling of fullness. Bupropion – naltrexone (contrave) Combination medication that suppresses appetite and increases feeling of fullness. The danger in using these drugs is that they simultaneously overexcite the CNS, making the person nervous and elevating the blood pressure. Also, a person soon adapts to the drugs, so that weight reduction is usually no greater than 5 to 10%. SURGERY Gastric bypass surgery It involves construction of a small pouch in the proximal part of the stomach that is then connected to the jejunum with a section of small bowel of varying length, the pouch is seperated from the remaining part of the stomach with staples. Gastric banding surgery. It invoves placing an adjustable band around the stomach near its upper end, this also creates a small pouch that restricts the amount of food that can be eaten at each meal.  Sleeve gastrectomy Removes a large portion of the stomach, reducing food intake. Bilio-pancreatic diversion with duodenal switch Restricts food intake and reduces nutrient absorption. Although these surgical procedures generally produce substantial weight loss in obese patients, they are major operations, and their long term effects on overall health and mortality are still uncertain.  CONCLUSION Its essential to consult with a healthcare professional before starting any weightloss programme. THANKYOU OBESITY- CAUSES Presented by Mariya Saju  What is Obesity? Obesity is a medical condition characterized by an excessive accumulation of body fat that can negatively affect health. A common method to estimate body fat is by calculating the Body Mass Index (BMI): BMI = Weight in kg / Height² in m²  Body Mass Index BMI = Weight (kg) / Height² (m²). BMI between 25 and 29.9 kg/m² is classified as overweight. BMI greater than 30 kg/m² is classified as obese. BMI is not a direct measure of body fat (adiposity). Some individuals, like those with high muscle mass, may have a high BMI but not be obese. Obesity is better defined by measuring total body fat: Men: Obesity = body fat ≥ 25%. Women: Obesity = body fat ≥ 35%. Body fat percentage provides a more accurate assessment of obesity, differentiating fat mass from muscle mass. Methods for Measuring Body Fat Skinfold thickness measurements. Bioelectrical impedance. Underwater weighing. These methods are rarely used in clinical practice because BMI is easier and quicker to calculate.  Obesity occurs when energy intake exceeds energy expenditure. Excess calories consumed are stored in the body as fat. When people consume more food energy than they burn through activities and metabolism, the body converts the extra energy into fat. For every 9.3 calories of excess energy, the body stores 1 gram of fat. Fat is mainly stored: In subcutaneous tissue (under the skin). In the intraperitoneal cavity (around organs like the liver).  Adipocyte Changes in Childhood vs. Adulthood Childhood: Excess energy intake in children leads to hyperplastic obesity. Characterized by an increased number of adipocytes (fat cells) with only small increases in adipocyte size. Adulthood: Obesity in adults primarily results from an increase in adipocyte size, referred to as hypertrophic obesity. Adults do not significantly increase the number of adipocytes. Studies show that new adipocytes can form from pre-adipocytes (precursors of fat cells) at any age.In adults, obesity involves both an increase in number and an increase in size of adipocytes. Extremely obese individuals may have up to four times as many adipocytes as lean individuals. Each adipocyte in obese individuals can store twice as much fat as those in lean individuals. When obesity stabilizes, energy intake equals energy expenditure.  Causes of Obesity: The causes of obesity are complex. Although genes play an important role in determining food intake and energy metabolism, lifestyle and environmental factors may play the dominant role in many obese people. The rapid increase in the prevalence of obesity in the past 20 to 30 years emphasizes the importance of lifestyle and environmental factors. Genetic changes could not have occurred so rapidly. 1.Sedentary Lifestyle Regular physical activity and physical training are known to increase muscle mass and decrease body fat mass. Inadequate physical activity is typically associated with decreased muscle mass and increased adiposity. Example: Studies have shown a close association between sedentary behaviors, such as prolonged television watching, and obesity. About 25-30% of the energy used each day by the average person goes into muscular activity. In a laborer, as much as 60-70% of energy is used in this way.  2. Abnormal Feeding Behavior Although powerful physiologic mechanisms regulate food intake, environmental and psychological factors can cause abnormal feeding behavior, excessive energy intake, and obesity. Psychological factors may contribute to obesity in some people: For example, people often gain large amounts of weight during or after stressful situations, such as the death of a parent, a severe illness, or even mental depression. It seems that eating can be a means of releasing tension.  3. Childhood Over-nutrition One factor that may contribute to obesity is the prevalent idea that healthy eating habits require three meals a day and that each meal must be filling. Many young children are forced into this habit by overly solicitous parents, and the children continue to practice it throughout life. The rate of formation of new fat cells is especially rapid in the first few years of life. The greater the rate of fat storage, the greater the number of fat cells. The number of fat cells in obese children is often as much as three times that in normal children. It has been suggested that over-nutrition of children, especially in infancy and, to a lesser extent, during the later years of childhood, can lead to a lifetime of obesity.  4.Neurogenic Abnormalities Lesions in the ventromedial nuclei of the hypothalamus cause an animal to eat excessively and become obese. People with hypothalamic tumors that encroach on the hypothalamus often develop progressive obesity, demonstrating that obesity in humans too can result from damage to the hypothalamus.  5.Genetic Factors Obesity definitely runs in families. It has been difficult to determine the precise role of genetics in contributing to obesity because family members generally share many of the same eating habits and physical activity patterns. Current Evidence: 20-25% of cases of obesity may be caused by genetic factors. Genes contribute to obesity by causing abnormalities in: Pathways that regulate feeding centers. Energy expenditure and fat storage. Monogenic (Single-Gene) Causes of Obesity: Monogenic (Single-Gene) Causes of Obesity: Mutations of MCR-4 (most common monogenic form of obesity discovered so far). Congenital leptin deficiency caused by mutations of the leptin gene (very rare). Mutations of the leptin receptor (also very rare). All these monogenic forms of obesity account for only a very small percentage of obesity. Likely, many gene variations interact with environmental factors to influence the amount and distribution of body fat. EATING DISORDERS NAFIA. K MSC INTEGRATED PSYCHOLOGY  BULIMIA Bulimia or Bulimia nervosa is an eating disorder. It was named and first described by the British psychiatrist Gerald Russell in 1979. Bulimia is characterized by binge eating followed by purging. Binge eating refers to eating a large amount of food in a short amount of of time. Purging refers to the attempts to get rid of the food consumed. This may be done by vomiting or taking laxatives. Other efforts to lose weight may include the use of diuretics, stimulants, water fasting, or excessive exercise. Most people with bulimia are at a normal weight. The forcing of vomiting may result in thickened skin on the knuckles and breakdown of the teeth. Bulimia is frequently associated with other mental disorders such as depression, anxiety, and problems with drugs or alcohol. There is also a higher risk of suicide and self harm.  Other risk factors for the disease include psychological stress, cultural pressure to attain a certain body type, poor self-esteem, and obesity. diagnosis based on a person's medical history Cognitive behavioural therapy is the primary treatment for bulimia. Antidepressants of the selective serotonin reuptake inhibitor (SSRI) or tricyclic antidepressant classes may have a modest benefit. globally, bulimia is estimated to affect 3.6 million people. ANOREXIA Anorexia Nervosa, commonly referred to as anorexia, is a severe eating disorder characterized by a distorted body image and an intense fear of gaining weight. Individuals struggling with anorexia restrict their food intake to an extreme degree, resulting in significant weight loss and potentially life-threatening health consequences. Symptoms of Anorexia Nervosa include restrictive eating patterns, significant weight loss, fatigue, hair loss, dry skin, , and poor wound healing. Individuals with anorexia often experience social withdrawal, obsessive behaviors, and denial of the eating disorder. The fear of gaining weight can lead to purging, and excessive exercise.  The causes of Anorexia Nervosa are complex.sociocultural factors, psychological factors, and environmental factors all contribute to the development of anorexia. Other factors such as pain and nausea also cause a person to consume less food. Anorexia nervosa is a abnormal psychic state in which a person loses all desire for food and even becomes nauseated by food. As a results severe inanition occurs. INANITION Inanition is opposite of obesity and characterized by extreme weight loss. It can be caused by inadequate availability of food or by pathophysiologic conditions that greatly decrease the desire of food. Including psychogenic disturbances, hypothalamic abnormalities and factors released from peripheral tissues. The consequences of inanition are organ damage, immune system suppression, hair loss, Skin problems, poor wound healing etc....  Treatments of inanition includes nutritional support, fluid replacement, and medications etc.... The reduced desire for food may be associated with causing serious weight loss. EATING DISORDERS Cachexia Cachexia is a metabolic disorder of increased energy expenditure leading to weight loss greater than that caused by reduced food intake alone. Anorexia and cachexia often occur together in many types of cancer or in the “wasting syndrome “ observed in patients with acquired immunodeficiency syndrome (AIDS) and chronic inflammatory disorders. Almost all types of cancer cause both anorexia and cachexia and more than half of cancer patients develop anorexia –cachexia syndrome during the course of their disease  Central neural and peripheral factors are believed to contribute to cancer – induced cachexia. Several inflammatory cytokines, including tumor necrosis factor –a, interleukin-6 , interleukin -1b,and a proteolysis-inducing factor, have been shown to cause cachexia.  Pica Pica is a psychological disorder characterized by an appetite for substance that are largely non- nutritive, such as ice, hair, drywall or paint; sharp objects ,metal, stones or soil ,glass, feces and chalk. For these actions to be considered pica, they must persist for more than one month at an age where eating such objects is considered developmentally inappropriate , not part of culturally sanctioned practice and sufficiently severe to warrant clinical attention.  It can lead to intoxication in children , which can result in an impairment of both physical and mental development. In addition , it can also lead to surgical emergencies due to an intestinal obstruction as well as more subtle symptoms such as nutritional deficiencies and parasitosis. Pica has been linked to other mental and emotional disorders. Stressors such as emotional trauma , maternal deprivation, family issues, parental neglect , pregnancy , and a disorganized family structure are strongly linked to pica as a form of comfort.