Published on

In today's society, leanness is often equated with beauty, success, fitness, and self-control. Obesity, on the other hand, is considered as undesirable as leanness is desirable, for reasons that are often more related to cosmetic concerns than to actual or potential medical complications.

Published in: Health & Medicine


  1. 1. NEUROPSYCHIATRIC & PSYCHOLOGICAL ASPECTS OF OBESITY Windsor University School of Medicine Psychiatry RotationConsultant Psychiatrist – Dr. Sharon Halliday Presentation by: OLADAPO SAMSON OLUWABUKOLA 30TH JULY, 2012
  2. 2. Overview In todays society, leanness is often equated with beauty, success, fitness, and self-control. Obesity, on the other hand, is considered as undesirable as leanness is desirable, for reasons that are often more related to cosmetic concerns than to actual or potential medical complications.
  3. 3. Definition of terms Obesity – is simply, excess body fat; consequences depend not only on the absolute amount but also on the distribution of the fat. Complications include cardiovascular disorders, diabetes mellitus, many cancers, cholelithasis, fatty liver and cirrhosis, osteoarthritis, reproductive disorders in men and women, psychological disorders, and premature death. Diagnosis is based on Body Mass Index (BMI) – calculated from height and weight; and waist circumference. BP, fasting plasma glucose, lipid levels should be measured. Treatment includes physical activity, dietary and behavioral modification, and sometimes drug or surgery.
  5. 5. Relevant Anatomy The adipocyte, which is the cellular basis for obesity, is increasingly found to be a complex and metabolically active cell. At present, the adipocyte is being perceived as an endocrine gland with several peptides and metabolites that may be relevant to the control of body weight, and these are being studied intensively. The ongoing flurry of investigation into the intricacies of adipocyte metabolism has not only improved our understanding of the pathogenesis of obesity but has also offered several potential targets for therapy. Among the products of the adipocyte involved in complex intermediary metabolism are cytokines, tumor necrosis factor-alpha (TNF- α), interleukin 6, lipotransin, monocyte chemo-attracting protein-1 (MCP- 1), plasminogen activator inhibitor-1 (PAI-1), adipocyte lipid-binding protein, acyl-stimulation protein, prostaglandins, adipsin, perilipins, lactate, leptin, adiponectin, mon obutyrin, and phospholipid transfer protein.
  6. 6. Relevant Anatomy Among critical enzymes involved in adipocyte metabolism are endothelial-derived lipoprotein lipase (lipid storage), hormone-sensitive lipase (lipid elaboration and release from adipocyte depots), acyl- coenzyme A (acyl-CoA) synthetases (fatty acid synthesis), and a cascade of enzymes (beta-oxidation and fatty acid metabolism). Another area of active research is investigation of the cues for the differentiation of preadipocytes to adipocytes. With the recognition that this process occurs in white and brown adipose tissue, even in adults, its potential role in the development of obesity and the relapse to obesity after weight loss has become more important than before.
  7. 7. Incidence The prevalence of obesity worldwide is increasing, particularly in the industrialized nations of the Northern hemisphere, such as the United States, Canada, and most countries of Europe. Available data from the Multinational Monitoring of Trends and Determinants in Cardiovascular Disease (MONICA) project suggest that at least 15% of men and 22% of women in Europe are obese. Prevalence of obesity in the US is high and is increasing, particularly among children and adolescents. Prevalence is more than twice as high at age 55 as at age 20. Obesity is twice common among women in a lower socioeconomic group as among those in a higher group.
  8. 8. Incidence Prevalence among black and white men does not differ significantly, but it is higher among black women than white women. More than 50% of black women greater than 40 years are obese; greater than 80% are overweight In the US, obesity and its complications cause as many as 300,000 premature deaths each year, making it second only to cigarette smoking as a preventable cause of death. Within societies where food is scarce, obesity is more prevalent in the wealthier groups. However, in areas of relative affluence and/or westernized lifestyles, obesity is more prevalent in the lower socio- economic classes; this social gradient is particularly strong in the case of female obesity.
  9. 9. Risk factors Obesity occurs basically as a result of metabolic (energy) imbalance that is, when you eat and drink more calories than you burn through exercise and normal daily activities. Your body stores these extra calories as fat. Obesity usually results from a combination of causes and contributing factors, including: Genetics. Your genes may affect the amount of body fat you store and where that fat is distributed. Genetics may also play a role in how efficiently your body converts food into energy and how your body burns calories during exercise. Even when someone has a genetic predisposition, environmental factors ultimately make you gain more weight. Inactivity/sedentary lifestyle. If youre not very active, you dont burn as many calories. With a sedentary lifestyle, you can easily take in more calories every day than you burn off through exercise and normal daily activities.
  10. 10. Risk factors Familial predisposition. Obesity tends to run in families. Thats not just because of genetics. Family members tend to have similar eating, lifestyle and activity habits. If one or both of your parents are obese, your risk of being obese is increased. Quitting smoking. Quitting smoking is often associated with weight gain. And for some, it can lead to a weight gain of as much as several pounds a week for several months, which can result in obesity. In the long run, however, quitting smoking is still a greater benefit to your health than continuing to smoke. Pregnancy. During pregnancy a womans weight necessarily increases. Some women find this weight difficult to lose after the baby is born. This weight gain may contribute to the development of obesity in women.
  11. 11. Risk factors Unhealthy diet and eating habits. Having a diet thats high in calories, eating fast food, skipping breakfast, consuming high-calorie drinks and eating oversized portions all contribute to weight gain. Social and economic issues. Certain social and economic issues may be linked to obesity. You may not have safe areas to exercise, you may not have been taught healthy ways of cooking, or you may not have money to buy healthier foods. In addition, the people you spend time with may influence your weight — youre more likely to become obese if you have obese friends or relatives. Medical problems. Obesity can rarely be traced to a medical cause, such as Prader-Willi syndrome, Cushings syndrome, polycystic ovary syndrome, and other diseases and conditions. Some medical problems, such as arthritis, can lead to decreased activity, which may result in weight gain. A low metabolism is unlikely to cause obesity, as is having low thyroid function.
  12. 12. Risk factors Certain medications. Some medications can lead to weight gain if you dont compensate through diet or activity. These medications include some antidepressants, anti-seizure medications, diabetes medications, antipsychotic medications, steroids and beta blockers. Age. Obesity can occur at any age, even in young children. But as you age, hormonal changes and a less active lifestyle increase your risk of obesity. In addition, the amount of muscle in your body tends to decrease with age. This lower muscle mass leads to a decrease in metabolism. These changes also reduce calorie needs and can make it harder to keep off excess weight. If you dont control what you eat as you age, youll likely gain weight. Lack of sleep. Not getting enough sleep at night can cause changes in hormones that increase your appetite. You may also crave foods high in calories and carbohydrates, which can contribute to weight gain.
  13. 13. Etiology Almost all cases of obesity result from a combination of genetic predisposition and a chronic imbalance between energy intake, energy utilization for basic metabolic processes, and energy expenditure from physical activity. The etiology of obesity is far more complex than the simple paradigm of an imbalance between energy intake and energy output. Although this concept allows easy conceptualization of the various mechanisms involved in the development of obesity, obesity is far more than simply the result of too much eating and/or too little exercise.
  14. 14. Etiology – Biological Genetic factor – heritability of BMI is about 66%. Genetic factors may affect the many signaling molecules and receptors used by parts of the hypothalamus and GI tract to regulate food intake . Rarely, obesity results from abnormal levels of peptides that regulate food intake (e.g. leptin) or abnormalities in their receptors (e.g. melanocortin-4 receptor) Genetic factors also regulate energy expenditure, including BMR, diet-induced thermogenesis, and non-voluntary activity- associated thermogenesis. Genetic factors may have a greater effect on the distribution of body fat, particularly abdominal fat than on the amount of body fat.
  15. 15. Etiology – Biological Certain medications. Some medications can lead to weight gain if you dont compensate through diet or activity. These medications include some antidepressants, anti-seizure medications, diabetes medications, antipsychotic medications, steroids and beta blockers. Medical problems. Obesity can rarely be traced to a medical cause, such as Prader-Willi syndrome, Cushings syndrome, polycystic ovary syndrome, and other diseases and conditions. Some medical problems, such as arthritis, can lead to decreased activity, which may result in weight gain. A low metabolism is unlikely to cause obesity, as is having low thyroid function.
  16. 16. Etiology – Psychological At least 2 pathologic eating patterns may be associated with obesity  Binge eating disorder is consumption of large amounts of food quickly with a subjective sense of loss of control during the binge and distress after it. This disorder does not include compensatory behaviors, such as vomiting. Prevalence is 1 to 3% among both sexes and 10-20% among people entering weight reduction programs. Obesity is usually severe, large amounts of weight are frequently gained or lost, and pronounced psychologic disturbances are present.  Night-eating syndrome consists of morning anorexia, evening hyperphagia, and insomnia. At least 25-50% of daily intake occurs after the evening meal. About 10% of people seeking treatment for severe obesity may have this disorder. Rarely, a similar disorder is induced by use of a hypnotic such as zolpidem.  Eating Disorders Not Otherwise Specified (EDNOS), probably contribute to excess weight gain in more people. For example nocturnal eating contributes to excess weight gain in may people who do not have night-eating syndrome.
  17. 17. Etiology – Social Social factors in Etiology include: Level of activity Behaviour Race, sex, and age factors Ethnic and cultural factors Socioeconomic status Dietary habits Smoking cessation
  18. 18. Pathogenesis
  19. 19. Pathways regulating food intake Preabsorptive and postabsorptive signals from the GI tract and changes in plasma nutrient levels provide short-term feedback to regulate food intake: GI hormones (eg, glucagon-like peptide 1 [GLP-1], cholecystokinin [CCK]) reduce food intake. Ghrelin, secreted primarily by the stomach, increases food intake. Leptin, secreted from adipose tissue, informs the brain as to how much fat is stored; high leptin levels correlate with increased body fat. The hypothalamus integrates various signals involved in the regulation of energy balance and then activates pathways that increase or decrease food intake: Neuropeptide Y (NPY), agouti-related peptide (ARP), α-melanocyte- stimulating hormone (α-MSH), cocaine- and amphetamine-related transcript (CART), orexin, and melanin-concentrating hormone (MCH) increase food intake. Corticotropic hormone (CRH) and urocortin decrease it.
  20. 20. Pathophysiology
  21. 21. Pathophysiology  Obesity is an exaggeration of normal adiposity and is a central player in the pathophysiology of diabetes mellitus, insulin resistance, dyslipidemia, hypertension, and atherosclerosis, largely due to its secretion of excessive adipokines.  Obesity is a major contributor to the metabolic dysfunction involving lipid and glucose, but on a broader scale, it influences organ dysfunction involving cardiac, liver, intestinal, pulmonary, endocrine, and reproductive functions.  Inflammatory, insulin-resistant, hypertensive, and thrombotic- promoting adipokines, which are atherogenic, are counterbalanced by anti-inflammatory and anti-atherogenic adipocyte hormones such as adiponectin, visfatin, and acylation-stimulating protein, whereas certain actions of leptin and resistin are pro- atherogenic.
  22. 22. Pathophysiology  The changes in adipocyte activity can be considered genetic and/or environmental. Overeating or experimental obesity studies have found that most of these changes can be included with deliberate overeating to achieve excess body fat.  Although leptin increases in overweight and obesity, it appears to decrease function. For, example, the hypothalamus becomes resistance to leptin. Thus, the signal for satiety is not recognized; neither are the signals for other endocrine functions which affect the  Hypothalamic-pituitary-adrenal axis  Hypothalamic-pituitary-thyroid axis  Hypothalamic-pituitary- gonadal axis  The leptin resistance may be found more in the central nervous system than in the peripheral organs (pancreas, liver & muscle).
  23. 23. Clinical Features Most patients recognize their own problems, although often they are unaware of the main foods that cause obesity. Many symptoms are related to psychological problems or social pressure, such as the woman who cannot find fashionable clothes to wear. In most patients, the presentation of obesity is straightforward, with the patient indicating problems with weight or repeated failure in achieving sustained weight loss. In other cases, however, the subject may present with complications and/or associations of obesity. When asking a patient about his or her history, investigate whether the rest of the patients family has weight problems, inquire about the patients expectations, and estimate the patients level of motivation. Also, determine if any of the comorbidities related to obesity, including the following have occurred:
  24. 24. Clinical Features  Respiratory - Obstructive sleep apnea, greater predisposition to respiratory infections, increased incidence of bronchial asthma, and Pickwickian syndrome (obesity hypoventilation syndrome)  Malignant - Association with endometrial, prostate, colon, breast, gall bladder, and, possibly, lung cancer  Psychologic - Social stigmatization and depression  Cardiovascular - Coronary artery disease, essential hypertension, left ventricular hypertrophy, cor pulmonale, obesity-associated cardiomyopathy, accelerated atherosclerosis, and pulmonary hypertension of obesity  Central nervous system (CNS) - Stroke, idiopathic intracranial hypertension, and meralgia paresthetica
  25. 25. Clinical Features  Obstetric and perinatal - Pregnancy-related hypertension, fetal macrosomia, and pelvic dystocia  Surgical - Increased surgical risk and postoperative complications, including wound infection, postoperative pneumonia, deep venous thrombosis, and pulmonary embolism  Pelvic - Stress incontinence  Gastrointestinal (GI) - Gall bladder disease (cholecystitis, cholelithiasis), nonalcoholic steatohepatitis (NASH), fatty liver infiltration, and reflux esophagitis  Orthopedic - Osteoarthritis, coxa vera, slipped capital femoral epiphyses, Blount disease and Legg-Calvé-Perthes disease, and chronic lumbago
  26. 26. Clinical Features  Metabolic -Type 2 diabetes mellitus, insulin resistance, hyperinsulinemia, and dyslipidemia (characterized by high total cholesterol, high triglycerides, low high-density lipoprotein, normal or elevated low-density lipoprotein)  Reproductive - Anovulation, early puberty, infertility, hyperandrogenism and polycystic ovaries (in women), and hypogonadotropic hypogonadism (in men)  Cutaneous - Intertrigo (bacterial and/or fungal), acanthosis nigricans, hirsutism, and increased risk for cellulitis and carbuncles  Extremity - Venous varicosities, lower extremity venous and/or lymphatic edema  Miscellaneous - Reduced mobility and difficulty maintaining personal hygiene
  27. 27. Differential diagnosis – Medical Diabetes mellitus, type 2 Fatty liver Hiatal hernia Polygenic hypercholesterolemia Hypertension Hypothyroidism Insulinoma Kallmann syndrome and idiopathic hypogonadotropic hypogonadism Generalized lipodystrophy Polycystic ovarian disease (Stein-Leventhal syndrome) Cushing syndrome Adiposa dolorosa (Dercum disease) Partial lipodystrophies associated with localized lipohypertrophy Acromegaly Ascites Cushing Syndrome
  28. 28. Differential diagnosis – Psychiatric Primary Depression (Depression not secondary to Obesity) Fatigue
  29. 29. Investigations Full lipid panel  At minimum, test fasting cholesterol, triglycerides, and high-density lipoprotein cholesterol (HDL-C) levels. These levels may be normal, or the typical dyslipidemia associated with cardiometabolic syndrome may be found. This dyslipidemia is characterized by reduced HDL-C and elevated fasting triglyceride concentrations; however, increased low- density lipoprotein cholesterol (LDL-C) and normal to marginally increased total cholesterol are not uncommon among obese individuals. Hepatic panel  This test is expected to yield normal results, but findings may be abnormal (eg, elevated transaminase levels in the setting of NASH or fatty infiltration of the liver).
  30. 30. Investigations Thyroid function tests  The results are typically normal, but checking them to detect primary hypothyroidism (characterized by increased serum thyrotropin and normal or reduced levothyroxine and/or triiodothyronine levels) is worthwhile.  Screening with a serum thyrotropin level is usually sufficient. Of importance, hypothyroidism itself rarely causes more than mild obesity. 24-Hour urinary free-cortisol test  This test, used for screening purposes, is needed only when Cushing syndrome or other hypercortisolemic states are clinically suspected. Approximately 4% of patients with Cushing syndrome have normal urinary free-cortisol values.
  31. 31. Investigations Fasting glucose and insulin test  Obesity is associated with insulin resistance and increased fasting insulin and c-peptide serum levels; however, insulin levels are normal in many persons who are obese. In persons with impaired fasting glucose, the fasting plasma glucose level is higher than 100 mg/dL. Histological findings  Hypertrophic obesity characterized by enlarged fat cells is typical of android abdominal obesity. Hypercellular obesity is more variable than hypertrophic obesity. Hypercellular obesity is typical of obesity with an onset in childhood or adolescence, but it is also invariably found in subjects with severe obesity.
  32. 32. Investigations Evaluation of degree of fat  Among the various procedures relevant to the treatment of patients who are obese are those to estimate percent body fat and the degree of visceral and subcutaneous fat. Procedures used for measuring total body fat include the BMI, caliper-derived measurements of skin-fold thickness, dual-energy X-ray absorptiometry (DEXA), bioelectrical impedance analysis, ultrasonography to determine fat thickness, and underwater weighing. The criterion standard techniques for measuring visceral fat are MRI and CT scanning. Cheaper techniques for direct measurement of visceral fat include abdominal ultrasonography and abdominal bioelectrical impedance.
  33. 33. Diagnosis Diagnostic criteria include:  BMI  Body Fat percentage  Waist circumference  Sometimes body composition analysis
  34. 34. Body Mass Index (BMI) In adults, BMI, defined as weight (kg) divided by the square of the height (m2), is used to screen for overweight or obesity. BMI of 25 to 29.9 kg/m2 indicates overweight; BMI ≥ 30 kg/m2 indicates obesity
  35. 35. Body Mass Index (BMI) BMI (kgm-2) Definition <18.5 Underweight 18.5-24.9 Ideal Weight 25-29.9 Overweight 30-39.9 Obese 40-49.9 or 35-49.9 with Morbidly Obese obesity-related comorbidity 50-59.9 Super Obese 60-69.9 Super Super Obese >70 Hyper Obese
  36. 36. Body Mass Index (BMI) Limitations of BMI  Not a direct measure of adiposity  No account of fat distribution  No account of duration of obesity  Inaccurate at extremes of height  Inaccurate with extremes of lean body mass (e.g. athletes, elderly)  Waist or collar circumference more predictive of cardio- respiratory co-morbidity
  37. 37. Body Fat Percentage The body fat percentage can be indirectly estimated by using the Deurenberg equation, as follows: Body fat percentage = 1.2(BMI) + 0.23(age) - 10.8(sex) - 5.4, with age being in years and sex being designated as 1 for males and 0 for females. This equation has a standard error of 4% and accounts for approximately 80% of the variation in body fat. For men, a percentage of body fat greater than 25% defines obesity, with 21-25% being borderline. For women, over 33% defines obesity, with 31-33% being borderline.
  38. 38. Waist circumference The waist circumference that increases risk of complications due to obesity varies by ethnic group and sex:  White men: > 93 cm (> 36.6 in), particularly > 101 cm (> 39.8 in)  White women: > 79 cm (> 31.1 in), particularly > 87 cm (> 34.2 in)  Asian Indian men: > 78 cm (> 30.7 in), particularly > 90 cm (> 35.4 in)  Asian Indian women: > 72 cm (> 28.3 in), particularly > 80 cm (> 31.5 in)
  39. 39. Body Composition Analysis Body composition—the percentage of body fat and muscle—is also considered when obesity is diagnosed. Although probably unnecessary in routine clinical practice, body composition analysis can be helpful if clinicians question whether elevated BMI is due to muscle or excessive fat. The percentage of body fat can be estimated by measuring skin-fold thickness (usually over the triceps) or determining mid upper arm area. Other indices used to estimate the degree and distribution of obesity include the 4 standard skin thicknesses (ie, subscapular, triceps, biceps, suprailiac) and various anthropometric measures, of which waist and hip circumferences are the most important.
  40. 40. Body Composition Analysis Android  Central distribution  High intra-peritoneal fat content  Increased neck circumference  Waist-hip ratio >0.8 women, >1.0 men  Increased morbidity (airway, CVS, metabolic, su rgical) Gynaecoid  Peripheral sites (arms, legs, buttocks)
  41. 41. Complications of Obesity Complications of obesity include the following: Metabolic syndrome Diabetes mellitus Cardiovascular disease Nonalcoholic steatohepatitis (fatty liver) Gallbladder disease Gastroesophageal reflux Obstructive sleep apnea Reproductive system disorders Many cancers Osteoarthritis Social and psychologic problems
  42. 42. Treatment Treatment includes:  Nutrition management  Physical activity  Behavioral therapy  Drugs (eg, sibutramine , orlistat)  Bariatric surgery
  43. 43. Nutrition Management Nutrition: A normal eating pattern is important. People who miss breakfast tend to passively consume too many calories later in the day. Patients should eat small meals and avoid or carefully choose snacks. Low-fat (particularly very low saturated fat), high- fiber diets with modest calorie restriction (by 600 kcal/day) and substitution of some protein for carbohydrate appear to have the best long-term outcome. Fresh fruits and vegetables and salads should be substituted for refined carbohydrates and processed food, and water for soft drinks or juices. Alcohol consumption should be limited to moderate levels. Foods with a low glycemic index and marine fish oils or monounsaturated fats derived from plants (e.g., olive oil) reduce the risk of cardiovascular disorders and diabetes. Low-fat dairy products are also part of a healthy diet. Patients need an adequate amount of vitamin D, preferably obtained by exercising outdoors in the sunshine. Use of meal replacements has proven efficacy; use can be ongoing or intermittent. Diets that require unusual eating habits should be avoided. They are unlikely to be maintained, and weight increases when patients resume previous poor eating habits. Diets of < 1200 kcal/day cannot be sustained, but such diets are sometimes needed to achieve rapid short-term weight loss (eg, to prepare for surgery, to lessen obstructive sleep apnea). Diets of < 800 kcal/day do not produce greater weight loss and are less well tolerated.
  44. 44. Physical activity Exercise increases energy expenditure, BMR, and diet-induced thermogenesis. Exercise also seems to regulate appetite to more closely match caloric needs. Other benefits include  Increased insulin sensitivity  Improved lipid profile  Lower BP  Better aerobic fitness  Improved psychologic well-being Strengthening (resistance) exercises increase muscle mass. Because muscle tissue burns more calories at rest than does fat tissue, increasing muscle mass produces lasting increases in BMR. Exercise that is interesting and enjoyable is more likely to be sustained. A combination of aerobic and resistance exercise is better than either alone.
  45. 45. Behavioral Therapy Behavioral therapy aims to improve eating habits and physical activity level. Rigid dieting is discouraged in favor of healthy eating. Common- sense measures include the following:  Avoiding high-calorie snacks  Choosing healthful foods when dining out  Eating slowly  Substituting a physically active hobby for a passive one Social support, cognitive therapy, and stress management may help, particularly during the lapses usually experienced during any long-term weight loss program. Self-monitoring is useful, and maintenance of a diet diary is particularly effective.
  46. 46. Biological Therapy Drugs may be used if BMI is > 30 or if BMI is > 27 and patients have complications (eg, hypertension, insulin resistance). Most weight loss due to drug treatment is modest (5 to 10%) at best and occurs during the first 6 mo; not all patients benefit. Drugs are more useful for maintaining weight loss but must be continued indefinitely for weight loss to be maintained. Premenopausal women taking systemically acting drugs for weight control should use contraception. Sibutramine – is a centrally acting appetite suppressant that produces dose-related weight loss. The usual starting dose is 10 mg po once/day; the dose can be decreased to 5 mg or increased to 15 mg. Common adverse effects are headache, dry mouth, insomnia, and constipation; the most common serious one is hypertension. Cardiovascular disorders, particularly poorly controlled hypertension, are contraindications.
  47. 47. Biological Therapy Orlistat – inhibits intestinal lipase, decreasing fat absorption and improving blood glucose and lipids. Because orlistat is not absorbed, systemic effects are rare. Flatus, oily stools, and diarrhea are common but tend to resolve during the 2nd yr of treatment. A dose of 120 mg po tid should be taken with meals that include fat. A vitamin supplement should be taken at least 2 h before or after taking orlistat. Malabsorption and cholestasis are contraindications; irritable bowel syndrome and other GI disorders may make orlistat difficult to tolerate. Orlistat is available Over-the- counter, OTC. Other OTC weight-loss drugs are not recommended. Some (eg, caffeine, ephedrine, guarana, phenylpropanolamine) may be marginally effective, but their adverse effects outweigh their advantages. Others (eg, brindleberry, l-carnitine, chitosan, pectin, grapeseed extract, horse chestnut, chromium picolinate, fucus vesiculosus, ginkgo biloba) have not been shown to be effective and may have adverse effects.
  48. 48. Bariatric surgery Bariatric surgery is the surgical alteration of the stomach, intestine, or both to cause weight loss. This is the most definitive and effective treatment for the morbidly obese patient.
  49. 49. Prevention Regular physical activity and healthy eating improve general fitness, can control weight, and help prevent obesity and diabetes mellitus. Even without weight loss, exercise decreases the risk of cardiovascular disorders. Dietary fiber decreases the risk of colon cancer and cardiovascular disorders. Sufficient and good-quality sleep, management of stress, and moderation of alcohol intake are also important.
  50. 50. Prognosis Untreated, obesity tends to progress. The probability and severity of complications are proportional to the absolute amount of fat, the distribution of the fat, and absolute muscle mass. After weight loss, most people return to their pretreatment weight within 5 yr, and accordingly, obesity requires a lifelong management program similar to that for any other chronic disorder.
  52. 52. Introduction When considering psychological aspects of obesity, it is currently believed that most psychological disturbances are more likely to be consequences rather than causes of obesity. It is clear that there are some well-defined psychiatric conditions that can be considered causal, e.g. binge-eating disorder. However, the traditional view that obesity is a psychopathology manifested as overeating has now been largely replaced with the idea that genetic predisposition is to a large extent driving the overconsumption.
  53. 53. Relationship With Spouse? Childhood? Mood?Job? Education?Interpersonal RelationshipRelationship? with Mother? Friends?
  54. 54. Psychological issues Studies have shown that, on the average, an obese individual will have issues concerning the following:  Poor childhood interaction  Education  Job  Interpersonal relationship  Mood swings  Friends  Relationship with mother  Relationship with spouse
  55. 55. Psychological issues One of the most compelling illustrations of the psychological implications of obesity (14), was based on interviews of morbidly obese subjects after they had lost weight by surgical means. Their results were dramatic. Most patients reported that they would prefer to be normal weight with a major handicap (deaf, dyslexic, diabetic, legally blind) than to be obese again. In contrast, research on other handicaps has indicated a strong tendency for people to evaluate their own handicap as less disabling than other handicaps, e.g. blind individuals would often prefer to be blind, etc. Thus obesity, as perceived by obese individuals themselves, is an extremely serious handicap, although it is not generally recognized as such.
  56. 56. Present cultural disposition of the body Lean, thin body  Self-discipline, achievement of cultural ideal Fat, chubby body  Ultimate failure publicly displayed for all to see and judge
  57. 57. Social Discrimination Though might seems unremarkable, comparing the obese general population with the prevalence of discrimination, but when compared with other forms of discrimination, such as race and age, it becomes thoughtful.  Reported experiences of weight discrimination among adults = 12% (Andreyeva, Puhl, & Brownell, 2008)  It is the 4th most prevalent form of discrimination  Rates similar to race (11%) & age (14%) discrimination  Rates are higher among obese women as compared to men Weight discrimination in the workplace is often largely ignored, but it’s a serious issue and one that’s been in the news recently after a Texas hospital said it would require new employees to have a body mass index of less than 35. (That’s about 245 lb. for a man of 5 ft. 10 in., and 195 lb. for a 5-ft. 2-in. woman.) Read more: overweight-could-earn-you-a-lower-salary/#ixzz21vhbi6HU
  58. 58. Weight Bias Negative attitudes affecting interactions Stereotypes leading to:  Stigma  Rejection  Prejudice  Discrimination Verbal, physical and relational forms Subtle and overt expressions
  59. 59. Dieting relationship trap Because of social as well as medical pressures to be thin, obese patients turn to health professionals for support and advice about losing weight. However, they may encounter what has been termed "dieting relationship trap" with negative undercurrents.This situation has been described by Garrow as follows: "The patient is initially pleased to find a doctor or dietician who is willing and able to help with sensible dietary advice.. Both parties may underestimate the time it will take to achieve adequate weight loss, and the difficulty of sustaining dietary compliance over a period of many months … Inevitably the time comes when the patient returns having not lost weight …Obese patients usually suffer from low self-esteem ... When they perceive that they have failed, they are precipitated into an agony of self-reproach ... and virtually invite the health carer to discharge them … The correct response is to identify factors which precipitated the problem, to provide encouragement, not criticism. The wrong response is to fix the blame for failure on the patient ... On the other hand..there is little to be gained from monthly meetings at which ... the difficulty of dieting is agreed ... but nothing is done to increase the chance of success next time."
  60. 60. Social Realities of Weight Bias Overweight people are one of the last socially acceptable targets for bias and discrimination (Puhl & Brownell, 2001) WHY?   Body as controllable, malleable  Attributions  Perceived social consensus
  61. 61. Body as Controllable and Malleable Weight loss strengthens weight control beliefs among participants (Blaine, DiBlasi, & Connor, 2002)
  62. 62. Attributions  Internal and Controllable  Lack willpower  Lack motivation  Lazy  Don’t care ―Ideology of blame‖ (Crandall, 1994)  Deserve psychological, social, and physical consequences The perception of obesity as a condition that one brings on oneself creates little sympathy towards the obese.
  63. 63. Perceived Social Consensus Perceptions of other people’s stereotypical beliefs (Puhl, Schwartz, & Brownell, 2005), leading to:  Stigma  Rejection  Discrimination  Prejudice
  64. 64. Psychoanalytic Thought of the obese Oral-stage fixation Survey found psychoanalysts commonly linked weight gain in obese patients to:  Disappointment in love relationships  Fear of competition  Fear of heterosexuality  Inability to deal with negative affect  Feelings of being unloved/un-loveable
  66. 66. Introduction Researchers have used more traditional psychometric instruments for assessment of mental health and psychological functioning in obese individuals and compared them with healthy reference populations (17). In this way, it was observed that severely obese Swedish men and (particularly) women, scored markedly worse on a mental well-being measure and had more anxiety and depressive symptoms. Furthermore, the general mental state of obese subjects was poorer than that of patients with rheumatoid arthritis, intermittent claudication, cancer survivors with no recurrence and spinal cord- injured persons several years after injury. Anxiety and depressive symptoms showed similar patterns in comparisons with chronically diseased and injured patients.
  67. 67. Introduction Neuropsychiatric co-morbidities associated with obesity include:  Macular degeneration  Alzheimers disease  Depression or Depressive illness. Depression, Alzheimer’s disease and Macular Degeneration are found in obese people. Several studies have shown that there is an increased risk of depression, psychological and emotional distress, poor coping abilities and low self-esteem. Women are particularly affected. Obese adolescents who binge-eat are more likely to have high levels of psychological distress.
  68. 68. Obesity and Depression Depression  Depression is a mental condition characterized by loss of pleasure in enjoyable activities, and states of pessimism and intense sadness. Depression is commonly measured through an individuals response to surveys. Depressive symptoms are not measured over a period of time but reflect the individuals feelings at that point in time, leading to an inefficiency in this method of measurement. Studies that use suicide to reflect depression are subject to bias due to the variety of conditions that may lead to suicide, such as obesity, gender or circumstance. Obesity  Obesity can be defined as an excess of body fat. It is commonly measured through the Body Mass Index (BMI), which compares a persons weight and height. A BMI greater than 30kg/m2 indicates obesity, while a BMI between 25-30kg/m2 signals overweight. World obesity is increasing at an alarming rate, so much so that the phrase ’obesity epidemic’ has become common. In Australia, the 1999-2000 Australian Diabetes Obesity and Lifestyle Study found that 60% of Australians over 25 years were overweight, and 21% of those were obese. Obesity leads to conditions such as heart disease, stroke and diabetes, resulting in a lower life expectancy.
  69. 69. Obesity and Depression By looking at both obesity and depression through an evolutionary perspective both could be viewed as adverse effects of an evolutionary response. In the case of obesity as human beings are bodies evolved to survive in an environment in which we led a very active lifestyle. Because of this the human body functions best when it gets regular exercise. In today’s world there is no longer a need to hunt or run from predators. This causes humans to be far more sedentary which can lead to weight gain and in many cases obesity (Eaton, B. S. 2002). In the case of depression one theory is that depression helps human beings un attach themselves from unreachable achievements. This could lead humans to not take risks that could potentially harm them in some way (Nesse, M. R. 2000). There is a positive correlation between obesity and depression!
  70. 70. Obesity and Depression Depression has been associated with obesity, but it has not yet been proven that one causes the other. In fact, it is incredibly difficult to do so because the relationship is complicated by other factors, such as socioeconomic class and genetic make up. To determine if depression leads to obesity or vice versa, large population studies need to be carried out over a period of time. Northern Finland recently published results of a study that followed a 1966 birth cohort to assess the chance of obesity and depression in young adults (up to the age of 31 years). Results indicated that teenage obesity increases the chance of suffering depression as a young adult. Similarly, depression and obesity can occur at the same time in females in adulthood and adolescence. Abdominal obesity was found to be a strong predictor of depression.
  71. 71. Depression resulting in obesity? Depression can result in dietary behaviors which may lead to obesity. Binge eating or comfort eating may result from depression, which is also associated with increased alcohol unhealthy food consumption.
  72. 72. Obesity resulting in depression? Poor diets, particularly ones low in folic acid, are associated with depression. Social stigma associated with obesity may lead to depression later in life, especially in young women. This may be emphasized in social groups in which there are lower rates of obesity.
  73. 73. Obesity, Depression and Race African American women appear, on average, to be more satisfied with their bodies, to have less desire to be thin, and to have less fear of fat than do White women. However, other data suggest that the association between obesity and self-esteem is the same between these races.
  74. 74. References Psychosocial aspects of obesity: Individual and societal perspectives By Lauren Lissner The Pathophysiology of Obesity and Its Clinical Manifestations Richard N. Redinger, MD 2010/psychology/jaramillo%20-%20obesity%20and%20depression.pdf depression/111#C2 The Merck Manual, Professional Edition.