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.

1. NEUROPSYCHIATRIC &
PSYCHOLOGICAL ASPECTS OF
OBESITY
Windsor University School of
Medicine
Psychiatry Rotation
Consultant Psychiatrist – Dr. Sharon Halliday
Presentation by:
OLADAPO SAMSON OLUWABUKOLA
30TH JULY, 2012

2. Overview
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.

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.

4. AN OVERVIEW OF
OBESITY

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. 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. 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. 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. 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 you're not very active, you don't
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. Risk factors
 Familial predisposition. Obesity tends to run in families. That's 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 woman's 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. Risk factors
 Unhealthy diet and eating habits. Having a diet that's 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 — you're 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, Cushing's 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. Risk factors
 Certain medications. Some medications can lead to weight gain if you
don't 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 don't control what you eat as you age, you'll 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. 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. 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. Etiology – Biological
 Certain medications. Some medications can lead to weight gain
if you don't 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, Cushing's
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. 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. 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. Pathogenesis

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. Pathophysiology

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. 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. 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 patient's family has weight problems, inquire about the
patient's expectations, and estimate the patient's level of motivation.
Also, determine if any of the comorbidities related to obesity, including
the following have occurred:

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. 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. 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. 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. Differential diagnosis – Psychiatric
 Primary Depression (Depression not secondary to Obesity)
 Fatigue

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. 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. 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. 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. Diagnosis
 Diagnostic criteria include:
 BMI
 Body Fat percentage
 Waist circumference
 Sometimes body composition analysis

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. 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. 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. 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. 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. 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. 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. 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. Treatment
 Treatment includes:
 Nutrition management
 Physical activity
 Behavioral therapy
 Drugs (eg, sibutramine , orlistat)
 Bariatric surgery

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. 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. 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. 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. 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. 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. 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. 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.

51. PSYCHOLOGICAL
ASPECTS OF OBESITY

53. 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.

54. Relationship
With Spouse?
Childhood?
Mood?
Job?
Education?
Interpersonal
Relationship
Relationship?
with Mother?
Friends?

55. 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

56. 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.

57. 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

58. 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: http://moneyland.time.com/2012/05/02/why-being-
overweight-could-earn-you-a-lower-salary/#ixzz21vhbi6HU

59. Weight Bias
 Negative attitudes affecting
interactions
 Stereotypes leading to:
 Stigma
 Rejection
 Prejudice
 Discrimination
 Verbal, physical and relational
forms
 Subtle and overt expressions

60. 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."

61. 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

62. Body as Controllable and Malleable
 Weight loss strengthens weight control
beliefs among participants (Blaine, DiBlasi, &
Connor, 2002)

63. 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.

64. Perceived Social Consensus
 Perceptions of other people’s
stereotypical beliefs
(Puhl, Schwartz, &
Brownell, 2005), leading to:
 Stigma
 Rejection
 Discrimination
 Prejudice

65. 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. NEUROPSYCHIATRIC
ASPECTS OF OBESITY

67. 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.

68. Introduction
 Neuropsychiatric co-morbidities associated with obesity include:
 Macular degeneration
 Alzheimer's 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.

69. 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 individual's response to surveys. Depressive symptoms are not
measured over a period of time but reflect the individual's 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 person's 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.

70. 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!

71. 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.

72. 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.

73. 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.

74. 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.

75. References
 http://www.clinicaladvances.com/article_pdfs/gh-article-200711-redinger.pdf
 http://emedicine.medscape.com/article/123702-overview
 Psychosocial aspects of obesity: Individual and societal perspectives By Lauren Lissner
 The Pathophysiology of Obesity and Its Clinical Manifestations Richard N. Redinger, MD
 http://www.usfsm.edu/academics/cas/capstone/2009-
2010/psychology/jaramillo%20-%20obesity%20and%20depression.pdf
 http://www.virtualmedicalcentre.com/healthandlifestyle/obesity-and-
depression/111#C2
 http://ajph.aphapublications.org/doi/pdf/10.2105/AJPH.90.2.251
 The Merck Manual, Professional Edition.