Hunger, eating & health


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Hunger, eating & health

  1. 1. Hunger, Eating & HealthAyoma, Karla CaressaBajana, SheemaGaldo, GenevaTecson, Louis Marie
  2. 2. Digestion- is the mechanical and chemical breaking down of food into smaller components, to a form that can be absorbed, for instance, into a blood stream. Digestion is a form of catabolism; a break-down of macro food molecules to smaller ones.
  3. 3. Steps in DigestionTeeth- Digestion starts here. It’s job is to start tearing and crushing the food down into small enough pieces so that it can fit down our throats.Saliva- This helps soften the food in the mouth so that it is easier to swallow. Saliva is also the first of several chemicals that start to break down foods into simpler forms.
  4. 4. • Tongue- The tongue is a muscle that works with the food and saliva to form a "ball" that can be swallowed.• Esophagus- The esophagus is simply a transportation tube from the mouth to the stomach. When we swallow, what we are really doing is closing a trap door in our throat called the epiglottis. This sends food down the esophagus and prevents food from going down the trachea (or windpipe) and into our lungs.
  5. 5. • Stomach- The first stop after the esophagus is the stomach. Once the food gets to the stomach, it uses chemicals to try to make the food tinier• Liver/Gall Bladder- At this point, our food is hit with more chemicals. The liver makes a chemical called bile but bile is not stored in the liver. Instead it is stored in the gall bladder. When the gall bladder mixes bile with our food, it does an important job: breaking down the fat (from milk, butter, cheeses) into tiny droplets. This fat will supply us with much energy later.
  6. 6. • Large Intestine- Whatever the body cannot put to use is sent to the large intestine. Many plants, for example, contain cellulose which cannot be digested. The big job of the large intestine is to remove water. Water has been necessary up until now but it is no longer needed and in the large intestine water is sent into the blood stream . Food spends about 12 hours in the large intestine where it become feces and later leaves the body through the anal opening.
  7. 7. • Pancreas- The pancreas also adds a digestive chemical as the food leaves the stomach. This digestive juice works on breaking down the carbohydrates (from breads, potatoes, etc.) and the proteins (from meats, cereals, peanut butter).• Small Intestine- The small intestine is a tube that is about 22 feet long! This is where the real digestion takes place. As the food passes through, it is mixed with the new chemicals and soon our "food" is now digested small enough to be put to use by the body.
  8. 8. Energy Storage in the Body Energy is delivered to the body in three forms – Lipids (fats) – Glucose (simple sugar) – Amino Acids (breakdown product of proteins) Energy is stored in three forms: - fats - glycogen - proteins
  9. 9. Metabolism – Is the totality of an organism’s chemical reactions – Arises from interactions between moleculesEnergy Metabolism - the chemical changes by which energy is made available for an organism’s use
  10. 10. Three Phases of Energy• Cephalic Phase – preparatory phase; Often begins with the sight, smell or thought of food and ends when the food is being absorbed in the bloodstream.• Absorptive Phase – energy absorbed in the blood stream from the meal is meeting the body’s energy needs.• Fasting Phase – unstored energy form the previous meal has been used and the body is withdrawing energy from it’s reserves
  11. 11. Three components of the set pointsystems1. Set point mechanism – defines the set point2. Detector mechanism – detect deviation form the set point3. Effector mechanism – acts to eliminate the deviations• All set-point systems are negative feedback systems
  12. 12. Theories of Hunger and EatingSet point Assumption People attribute hunger to the presence of energy deficit and they view eating as the means by which the resources of the body are returned to their optimal level
  13. 13. • Glucostatic Theory– we become hungry when our blood glucose levels drop significantly below their set point and that we become satiated when eating returns our blood glucose levels to their set point.• Lipostatic Theory – every person has a set-point for body fat, and deviations from this set point procedure compensatory adjustments in the level of eating that return level of body fat to their set point.
  14. 14. Problems with Set-Point Theories ofHunger and Eating1. Inconsistent with basic eating-related evolutionary pressures2. Major predictions of the set-point theories of hunger and eating have not been confirmed.3. Set-point theories of hunger and eating are deficient because they fail to recognize the major influences on hunger and eating of such important factors as taste, learning, and social influences.
  15. 15. Factors that determine what we eatLearned taste preference and aversion Prefer tastes that are followed by an infusion of calories, and they learn to avoid tastes that are followed by illnessLearning to eat vitamins and minerals Dietary deficiencies influence diet selection
  16. 16. Positive-Incentive Perspective- Humans and animals are not normally driven to eat by internal energy deficits but are drawn to eat by the anticipated pleasure of eating* the anticipated pleasure of behavior is called positive-incentive value
  17. 17. Factors that influence when we eatPremeal Hunger provide compelling support for hungerPavlovian Conditioning of Hunger hunger is cause by expectation of food, not by energy deficit
  18. 18. Factors that influence how much we eatSatiety Signals Food in the gut and glucose entering the blood can induce satiety signals, which inhibit subsequent consumption.Sham eating satiety signals are not necessary to terminate a meal.Serving size and satiety the larger the servings, the more we tend to eat
  19. 19. Social Influences and Satiety depends on whether we are eating alone or with othersSensory-Specific Satiety the number of different tastes available at each meal has a major effect on meal size.Appetizer Effect and Satiety small amounts of food consumed before meal actually increase hunger rather than reducing it
  20. 20. Role of Blood Glucose Levels in Hunger and Satiety• It is a simple matter to construct a situation in which drops in blood glucose levels do not precede eating• The usual premeal decrease in blood glucose seem to be a response to the intention to start eating, not the other way around• If an expected meal is not served, blood glucose levels soon return to their previous homeostatic level
  21. 21. • The glucose levels in the extra-cellular fluids that surrounds CNS neurons stay relatively constant, even when blood glucose levels drop• Injections of insulin do not reliably induce eating unless the injections are sufficiently great to reduce blood glucose levels by 50% and large premeal infusions of glucose do not suppress eating
  22. 22. Myth of Hypothalamic Hunger and Satiety Centers Two different regions of the hypothalamus:Satiety by the Ventromedial Hypothalamus Large bilateral electrolytic lesions to the ventromedial hypothalamus produce hyperphagia (excessive eating) and extreme obesity in rats.
  23. 23. VMH Syndrome has 2 different phasesDynamic Phase Begins as soon as the subject regains consciousness after operation, characterized by several weeks of grossly excessive eating and rapid weight gain.Static Phase After dynamic phase, consumption gradually declines to a level that is sufficient to maintain a stable level of obesity
  24. 24. Feeding by the Lateral Hypothalamus Produce aphagia – a complete cessation of eating. It is the feeding center.2 important features of LH syndrome found that aphagi was accompanied by adipsia – a complete cessation of drinking & LH-lesioned rats partially recover if they are kept alive by tube feeding.
  25. 25. Reinterpretation of the Effects of VHM and LH Lesions• The VHM-lesioned animals become obese because they overeat, hoewever, the evidence suggests the converse – that they overeat because they become obese• LH Lesions produce a wide range of severe motor disturbances and a general lack of sensory input of which food and drink are but two examples.
  26. 26. Role of Gastrointestinal Tract in Satiety• The role of gastrointestinal tract in hunger and satiety quickly waned with the discovery that human patients whose stomachs had been surgically removed and whose esophagus had been hooked up directly to their duodenums continued to report feelings of hunger and satiety and continued to maintain their normal body weights by eating more meals of smaller size.
  27. 27. Hunger and Satiety Peptides• Circulating gut peptides provide the brain with information about the quantity and nature of food in the gastrointestinal tract and that this information plays a role in satiety.• Peptides can function as satiety signals• Satiety peptides (peptides that decrease appetite)
  28. 28. Serotonin and Satiety• Serotonin agonists consistently reduced rat’s food intake.• Serotonin agonists have been shown to reduce hunger, eating, and body weight under variety of conditions• Satiety-inducing effects of serotonin have three major characteristics: – Overcome the powerful attraction of highly palatable cafeteria diets – Reduce the amount of food that is consumed – Associated with a shift in food preferences away form fatty foods
  29. 29. Body Weight Regulations: Set Points VS. Settling PointsVariability of Body Weight Set point theories of body weight regulation suggest that the best method of maintaining a constant body weights is to eat each time there is a motivation to eat because the main function of hunger is to defend the set pointSet Points and Health each person’s set point Is optimal for that person’s health – or at least not incompatible with good health
  30. 30. Regulation of Body Weight by Changes in the Efficiency of Energy Utilization How much a person eats plays a role in his or her body weight. The body controls its fat levels, to a large degree, by changing the efficiency with which it uses energy.
  31. 31. Set Points and Settling Points in Weight Control• Settling Point – the level at which the various factors that influence body weight achieve an equilibrium.• Settling-point model – provides loose kind of homeostatic regulation. Body weight remains stable as long as there are no long term changes in the factors that influence it.
  33. 33. Statistics• A survey by the National Statistics Coordination Board (NSCB) as of 2008 showed that 26.6% of Filipino adults are overweight, higher than 16.6% in 1993.• Of the number, 5.2% are obese.• Among children aged 5 to 10 years old, 6.6% are overweight against only 5.8% during the last survey in 2003.
  34. 34. • The rise comes despite a reported drop in Filipinos food intake to 861 grams per day in 2008 from 803 grams in 1993, said Candido Astrologo Jr. of the NSCB during a seminar for health journalists in Quezon City recently.• However, Astrologo said the question that should be asked is not how much food Filipinos eat, but what kind.• He said households nutrition habits are changing. According to him, consumption of meat and poultry has been on the rise, contributing to obesity.
  35. 35. Human Obesity: Causes, Treatments, and Mechanisms• QUESTION: Are obese people more susceptible to health problems even if their blood pressure and blood cholesterol levels are within the healthy range?
  36. 36. Human Obesity: Causes, Treatments, and Mechanisms• ANSWER: Yes.• A recent study of over 17,000 people found that those who are obese have a significantly higher risk of mortality even if their blood pressure and blood cholesterol levels are normal.
  37. 37. Why is there an epidemic of Obesity?• Inconsistent food supplies were one of the main threats to survival. As a result, the fittest individuals were those who preferred high- calorie foods, ate to capacity when food was available, stored as many excess calories as efficiently as possible. Individuals who did not have these characteristics were unlikely to survive a food shortage, and so these characteristics were passed on to future generations.
  38. 38. Why is there an epidemic of Obesity?• The development of numerous cultural practices and beliefs that promote consumption has augmented the effects of evolution.
  39. 39. Why do some people become obese while others do not?• Those who are obese are those whose energy intake has grossly exceeded their energy output; those who are slim are those whose energy intake has not grossly exceeded their energy output. This serves to emphasize that two kinds of individual differences play a role in obesity: those that lead to differences in energy input and those that lead to differences in energy output.
  40. 40. Factors that lead some people to eat more than others who have comparable access to food• Some people consume more energy because they have strong preferences for the taste of high-calorie foods• Some consume more because they were raised in families and/or cultures that promote excessive eating
  41. 41. Factors that lead some people to eat more than others who have comparable access to food• Some consume more because they have particularly large cephalic-phase responses to the sight or smell.
  42. 42. • Differences in basal metabolic rate• Ability to react to fat increases by diet-induced thermogenesis• NEAT – nonexercise activity thermogenesis *generated by activities such as fidgeting and the maintenance of posture and muscle tone
  43. 43. Why are weight-loss programs typically ineffective?Most weight-loss programs are unsuccessful inthe sense that, as predicted by the settling-pointmodel, most of the lost weight is regained oncethe dieter stops following the program.
  44. 44. • The key to permanent weight loss is a permanent lifestyle change.• Any healthy person who consistently eats a nutritional low-calorie diet will have no problems with obesity.• Exercise has many health-promoting effects; however, despite the general belief that exercise is the most effective method of losing weight, several studies have shown that it often contributes little to weight loss.
  45. 45. • About 80% of the energy you expend is used to maintain the resting physiological processes of your body and to digest your food.
  46. 46. Leptin and the Regulation of Body FatFat is more than a passive storehouse of energy; it actively releases a peptide hormone called leptin.
  47. 47. Obese Mice and the Discovery of Leptin• In 1950, a spontaneous genetic mutation occurred in the mouse colony being maintained in the Jackson Laboratory at Bar Harbor, Maine.• The mutant mice were homozygous for the gene (ob), and they were grossly obese, weighing up to three times as much as typical mice.• These mutant mice are commonly referred to as ob/ob mice.
  48. 48. Obese Mice and the Discovery of Leptin• Ob/ob mice eat more than control mice; they convert calories to fat more efficiently; and they use their calories more efficiently.• It was hypothesized by Coleman that ob/ob mice lack a critical hormone that normally inhibits fat production and maintenance.
  49. 49. Hypothesis• Perhaps leptin is a negative feedback signal that is normally released from fat stores to decrease appetite and increase fat metabolism. Could leptin be administered to obese humans to reverse the current epidemic of the problem?
  50. 50. Leptin as a Treatment for Human Obesity• The early studies of leptin seemed to confirm the hypothesis that it could function as an effective treatment for obesity.• Receptors for leptin were found in the brain, and injecting it into ob/ob mice reduced both their eating and their body fat.
  51. 51. Leptin as a Treatment for Human Obesity• However, when research on leptin turned from obese mice to obese humans, the program ran into two major snags.• First, obese humans--- unlike ob/ob mice--- were found to have high, rather than low, levels of leptin.• Second, injections of leptin did not reduce either the eating or the body fat of obese humans.
  52. 52. This is what kidswith a leptindeficiency lookslike.
  53. 53. Leptin, Insulin and the Arcuate Melancortin System• Leptin was not the first peptide hormone to be discovered that seems to function as a negative feedback signal in the regulation of body fat.• More than 25 years ago, Woods and colleagues suggested that the pancreatic peptide hormone insulin serves such a function.
  54. 54. Leptin, Insulin and the Arcuate Melancortin System• The suggestion that insulin serves as a negative feedback signal for body fat regulation was viewed with skepticism.• How could the level of insulin on the body, which goes up and then comes back down to normal following each meal, provide the brain with information about gradually changing levels of body fat?
  55. 55. Leptin, Insulin and the Arcuate Melanocortin System• It turns out that insulin does not readily penetrate the blood-brain barrier, and its levels in the brain were found to stay relatively stable.• Brain levels of insulin were found to be positively correlated with levels of body fat.
  56. 56. Why are there two fat feedback signals?• Leptin levels are more closely correlated to subcutaneous fat (fat stored under the skin)• Insulin levels are more closely correlated to visceral fat (fat stored around the internal organs of the body cavity)Each fat signal provides different information.Visceral fat is more common in males and posesthe greater threat to health.
  57. 57. • Arcuate nucleus – location for receptors for both peptide hormones• Located in two classes of neurons:1) Neurons that release neuropeptide Y (the gut hunger peptide)2) Neurons that release melanocortins (class of peptides that includes the gut satiety peptide *alpha melanocyte stimulating hormone*)
  58. 58. Serotonergic Drugs and the Treatment of Obesity• Serotonin agonists have been shown to reduce food consumption in both human and nonhuman subjects, they have considerable potential in the treatment of obesity.• Serotonin agonists produce long-term satiety signals based on fat stores.• They seem to increase short-term satiety signals associated with consumption of a meal.
  59. 59. Anorexia and Bulimia NervosaAnorexia Nervosa - a disorder of under consumption -it is a very serious condition because it can lead to death - there is a particular high rate of suicide among anorexics.
  60. 60. Anorexic food behavior Signs and Symptoms• Dieting despite being thin• Obsession with calories, fat grams, and nutrition• Pretending to eat or lying about eating• Preoccupation with food• Strange or secretive food rituals
  61. 61. Anorexic appearance and body image signs and symptoms• Dramatic weight loss• Feeling fat, despite being underweight• Fixation on body image• Harshly critical of appearance• Denial that you’re too thin
  62. 62. Purging signs and symptoms• Using diet pills, laxatives, or diuretics• Throwing up after eating• Compulsive exercising
  63. 63. Major risk factors for anorexia nervosa• Body dissatisfaction• Strict dieting• Low self-esteem• Difficulty expressing feelings• Perfectionism• Troubled family relationship• History of physical or sexual abuse• Family history of eating disorders
  64. 64. Tips for helping a person with anorexia• Think of yourself as an “outsider.”• Be a role model• Take care of yourself• Don’t act like a food police• Avoid threats, scare tactics, angry outbursts, and put-downs
  65. 65. Bulimia Nervosa - a disorder characterized by periodic bingening ( eating huge amounts of food in a short period of time ) - followed by efforts to immediately eliminate the consumed calories form the body by voluntary purging; excessive use of laxatives, enemas or diuretics; or by extreme exercise
  66. 66. Binge eating signs and symptoms• Lack of control over eating• Secrecy surrounding eating• Eating unusually large amounts of food• Disappearance of food• Alternating between overeating and fasting
  67. 67. Purging signs and symptoms• Going to the bathroom after meals• Using laxatives, diuretics, or enemas• Smell of vomit• Excessive exercising
  68. 68. Physical signs and symptoms• Calluses or scars on the knuckles or hands• Puffy “chipmunk” cheeks• Discolored teeth• No underweight• Frequent fluctuations in weight
  69. 69. Relation between Anorexia and Bulimia Nervosa• Anorexics often require treatment for reduced metabolism, bradycardia (slow heart rate), hypotension (low blood pressure), hypothermia (low body temperature), and anemia (deficiency of red blood cells)• In contrast, bulimics often require treatment for irritation and inflammation of the esophagus, vitamin and mineral deficiencies, electrolyte imbalance, dehydration, and acid reflux.
  70. 70. Relation between Anorexia and Bulimia NervosaBoth anorexia and bulimia nervosa begin withan obsession about body image and slimnessand extreme efforts to lose weight. Bothanorexics and bulimics attempt to lose weightby strict dieting, but bulimics are less capable ofcontrolling their appetites and thus enter into acycle of starvation, bingeing, and purging.
  71. 71. Relation between Anorexia and Bulimia NervosaBoth have a distorted body image, seeingthemselves as much fatter and less attractivethat they are in reality.Both show the same pattern of distribution inthe population. Although their overall incidencein the population is low, estimates for Americanadults are 0.6% and 1.0% for anorexia andbulimia, respectively.
  72. 72. Relation between Anorexia and Bulimia NervosaBoth conditions occur more commonly amongeducated females in affluent cultural groups,Both anorexia and bulimia are highly correlatedwith OCD and depression.Neither disorder responds well to existingtherapies. Short-term improvements arecommon, but relapse is usual.
  73. 73. STATISTICS• It is estimated that 8 million Americans have an eating disorder – seven million women and one million men• One in 200 American women suffers from anorexia• Two to three in 100 American women suffers from bulimia• Nearly half of all Americans personally know someone with an eating disorder (Note: One in five Americans suffers from mental illnesses.)• An estimated 10 – 15% of people with anorexia or bulimia are males
  74. 74. Steps to Anorexia and bulimia nervosa recovery• Admit you have a problem• Talk to someone• Stay away from people, places, and activities that trigger your obsession with being thin• Seek professional help
  75. 75. ACCESS TO TREATMENT• Only 1 in 10 people with eating disorders receive treatment• About 80% of the girls/women who have accessed care for their eating disorders do not get the intensity of treatment they need to stay in recovery – they are often sent home weeks earlier than the recommended stay
  76. 76. • Treatment of an eating disorder in the US ranges from $500 per day to $2,000 per day. The average cost for a month of inpatient treatment is $30,000. It is estimated that individuals with eating disorders need anywhere from 3 – 6 months of inpatient care. Health insurance companies for several reasons do not typically cover the cost of treating eating disorders• The cost of outpatient treatment, including therapy and medical monitoring, can extend to $100,000 or more
  77. 77. ADOLESCENTS• Anorexia is the 3rd most common chronic illness among adolescents• 95% of those who have eating disorders are between the ages of 12 and 25• 50% of girls between the ages of 11 and 13 see themselves as overweight• 80% of 13-year-olds have attempted to lose weight
  78. 78. Some celebrities that suffer from Anorexia and Bulimia Nervosa
  79. 79. In 2006, the troubled actress admitted to suffering from bulimia in an interview with Vanity Fair. She didnt go into much detail, as people withbulimia find it difficult totalk about their illness...
  80. 80. Fresh from waging war against the Disney Channel for making a joke abouteating disorders in one of its shows, Demi came out with a blog on Seventeen magazines website entitled "My Battle With EatingDisorders," in which she talksabout her own struggles withthe disease and offers sound advice to others who are going through it as well.
  81. 81. Diana, Princess of Wales, literally married her Prince at the age of 20 and 750 million people worldwide watched the event. Unfortunately, the pressures ofconstantly being in the public eyeput a strain on Diana that led her to depression and bulimia as a way of coping. Diana claimed inan interview that sometimes she would binge and then vomitdaily, depending on the pressures that she was dealing with. Shecalled it her “escape mechanism” and dealt with it for many years before she finally was able to overcome her bulimia.