1. OBESITY
Presented By:
Ms. Tasneem Navagharwala
Registered Dietician

2. DEFINITION
• The term obesity has been derived from the Latin word “obseus”
which means to eat excessively.
• Obesity is commonly known as a condition in which excessive
fat is stored in the body.
• It can be defined as deviation of 10% or more than the IBW.
• It is considered as the “New World Syndrome” and is already
creating enormous socio economic & public health burden in
poor nations.

3. • Obesity is a disease of multiple etiologies characterized by an excess
accumulation of adipose tissues due to enlargement of fat cell size
(hypertrophic obesity) or an increase in fat cell number (hyper plastic
obesity) or combination of both.
• This pathologic enlargement of fat cells in turn produces altered levels
of many peptides & nutrient signals that are responsible for the disease
we call obesity. (Mishra et al 2003)
• The genetic make up of human beings which reflects a long history of
relative scarcity of food stuff has run into an age of surfeit and many
people cannot readily adapt.
• Thus, increased food intake does not signal satiety and there is a
gradual increase in energy stores as intake of energy outpaces the
need as we grow older.

4. INCIDENCE OF OBESITY IN CHILDREN
• If both parents are lean= 9-14%
• If 1 parent is obese= 41-50%
• If both parents are obese= 66-80%

5. BODY FAT PERCENTAGE IN HUMANS
• At Birth= 12%
• At 6 months of age= 25%
• Pre-pubertal age= 15-18%
• At 18 yrs of age: Boys= 15-18%
Girls= 20-25%
• Adults= 30-40%

6. BODY FAT CONTENT
• According to Mishra et al (2002) Indians
have shorter height, lower BMI but higher
body fat content.
• Studies have shown that Indian babies have
more body fat compared to Caucasian
babies, even the small for gestational age
Indian babies have more fat (Matarell et al,
2004; Mishra et al, 2006)
• Excess fat in Indians generate more
inflammatory molecules which significantly
contributes to heart diseases and Diabetes.
(Joglekar et al 2003)

7. Hyperplasia Vs Hypertrophy
• No. of fat cells is genetically determined in an infant.
• During critical periods of growth, the body has the potential to accumulate an
excess no. of fat cells.
Hyperplasia occurs in 3 periods of life:
1. During last 3 months of fetal development
2. First 3 yrs of life
3. Adolescence
After 18 yrs of age, fat cell size & no. increase until adulthood. Once the no. is
fixed, they continue to grow in size indefinitely.
Hypertrophic obesity correlates with metabolic disorders
Hyperplasic obesity is usually present in individual with BMI> 40kg/m2

8. PREVALENCE OF OBESITY
• Obesity has reached epidemic proportions globally, with more than
1 billion overweight adults - at least 300 million of them clinically
obese.
• It is a major contributor to the global burden of chronic disease and
disability (WHO, 2006).
• According to Nutrition foundation of India, 2008; the states that have
high prevalence of obesity are:
STATE MALES FEMALES
PUNJAB 30.3 % 37.5 %
KERALA 24.3 % 34 %
GOA 20.8 % 27 %

9. Comparative statistics between Asian Indians in US and Asian Indians
in Indian rural and urban areas(Mishra R, Mishra .A. et al 2008).
Variable AI (US) AI(urban) AI(rural)
Overweight 73 65 32
/obesity
Abdominal 23 39 8
obesity.
• According to the above table the prevalence of over weight /obesity in Asian
Indians in US is 73% compared to Asian Indians in Indian urban and rural
areas which is 65% and 32% respectively.
• However the prevalence of abdominal obesity is highest amongst Asian Indian
from urban area i.e. 39% compared to Asian Indians in US and Asian Indian in
rural areas i.e. 23% and 8% respectively.

10. PREVALENCE UNDER DIFFERENT
CATEGORIES
• URBAN VS RURAL= 64% vs. 36%
• SOCIO-ECONOMIC CLASS: High > Middle> Lower. (Slum= negligible)
• GENDER: Females (30-33%) vs. Males (19-21%)
• AGE: obesity increases with age
– Incidence more at adolescence, both girls & boys, and in women after
45 yrs
• TYPE OF OBESITY: Central obesity more in males, generalized obesity
more in females

11. ASSESSMENT OF OBESITY
• BMI
• Waist Circumference
• WHR
• Body fat percentage (DEXA)

12. Consensus Statement for Asian Indans
a. BMI is the most researched measure of generalized obesity and should
continue to be used using Asian Indian-specific cut-offs as described later.
b. Waist circumference should be used as a measure of abdominal obesity
with Asian Indian specific cut-offs.
c. Both BMI and WC should be used together (with equal importance) for
population- and clinic-based metabolic and cardiovascular risk stratification.

13. CUT OFFS FOR BMI & BODY FAT %
Normal BMI: 18.0-22.9 kg/m2
Overweight: 23.0-24.9 kg/m2
Obesity: >25 kg/m2
Body fat Percentage:
25% in men and 30% in women

14. CUT OFFS FOR WAIST
CIRCUMFERENCE
Methodology of WC Measurement:
WC should be measured using non-stretchable flexible tape in horizontal
position, just above the iliac crest, at the end of normal expiration, in the fasting
state, with the subject standing erect and looking straight forward and observer
sitting in front of the subject.
• WC Cut-offs for Asian Indians:
– Action level 1: Men: 78 cm, women: 72 cm. Any person with WC above
these levels should avoid gaining weight and maintain physical activity to
avoid acquiring any of the cardiovascular risk factor.
– Action level 2: Men: 90 cm, women: 80 cm. Subject with WC above this
should seek medical help so that obesity-related risk factors could be
investigated and managed.

15. ETIOLOGY OF OBESITY
1. Hypothalamic Obesity
2. Endocrine Obesity
3. Genetic Obesity
4. Dietary Obesity
5. Inactivity
6. Drug induced Obesity
7. Essential Obesity

16. HYPOTHALAMIC OBESITY
Rare syndrome that can be caused by
• Tumor
• Trauma
• Inflammatory disease
• Surgery in the posterior fosse
• Increased intracranial pressure
Symptoms present in 1 of the 3 patterns:
1. Headache, vomiting, diminished vision.
2. Impaired endocrine function(Amenorrhea, impotency, diabetes
insipidus, thyroid or adrenal insufficiency)
3. Neurologic & physiologic derangements(coma, convulsions,
somnolence, hypo/hyperthermia)

17. ENDOCRINE OBESITY
1. Cushing Syndrome
2. Insulinoma
3. Hypothyroidism
4. GH Deficiency
5. Castration
6. PCOS (Stein-levinthal Syndrome)
7. Pregnancy
8. Oral Contraceptives
9. Menopause

18. ENDOCRINE OBESITY: Cushing Syndrome
• Cushing's syndrome is a hormone disorder caused by high levels of cortisol in
the blood.
• A common clinical feature of Cushing’s Disease is progressive central obesity,
usually involving the face, neck (leading to a buffalo hump), trunk, abdomen.
• The extremities are usually spared and are often wasted.
• In contrast to adults, nearly all children with Cushing’s disease have generalized
obesity accompanied by a decrease in linear growth.
• Thus, any child whose weight increases and whose stature remains static when
compared with normal growing children of the same age should be evaluated for
Cushing’s disease.
• The differential diagnosis of obesity and Cushing’s disease is clinically important
in making decisions about therapy and may require consultation with an
endocrinologist.

19. CUSHING’S SYNDROME

20. ENDOCRINE OBESITY: Insulinoma
• An insulinoma is a tumour of the pancreas that is derived from beta cells and
secretes insulin.
• The secretion of insulin by insulinomas is not properly regulated by glucose and the
tumours will continue to secrete insulin causing glucose levels to fall further than
normal.
• As a result patients present with symptoms of low blood glucose (hypoglycemia),
which are improved by eating.
• Sudden weight gain (the patient can become massively obese) is sometimes seen.
• The diagnosis of an insulinoma is usually made biochemically with low blood glucose,
elevated insulin, proinsulin and C-peptide levels and confirmed by localising the
tumour with medical imaging or angiography.
• The definitive treatment is surgery.

21. INSULINOMA- LOW BLOOD
GLUCOSE

22. ENDOCRINE OBESITY: Hypothyroidism
• Patients with hypothyroidism frequently gain weight because of a
generalized slowing of metabolic activity, and some of this gain is
fat.
• The weight gain, however, is usually modest, and marked obesity is
uncommon.
• It is common particularly in older woman, in this group, TSH test is
available for diagnosis.

23. ENDOCRINE OBESITY: GH Deficiency
• LBM is decreased & Fat mass is increased in adults who are
deficient in GH as compared with those having normal GH
secretion.
• GH replacement therapy reduces body fat, especially visceral.
• The gradual decline in GH with age may be 1 reason for the
increase in visceral fat with age.

24. ENDOCRINE OBESITY: Castration
• Castration is any action, surgical, chemical, or otherwise, by which a
male loses the functions of the testicles or a female loses the
functions of the ovaries.

25. ENDOCRINE OBESITY: PCOS
• Nearly 50% of the women with PCOS are obese.
• Features: Oligomenorrhea, hirsutism, polycystic ovaries.
• Insulin resistance is present.
• LH is generally increased.
• Ovarian overproduction of testosterone (probably through
stimulation of the ovary by insulin like Growth factor1)

26. ENDOCRINE OBESITY: Pregnancy
• Pregnancy is often an important event in the weight gain history of
women.
• It may leave a legacy of increased weight.

27. ENDOCRINE OBESITY: Oral
Contraceptives
• Use of OC pills may initiate weight gain in some women, although
this effect is diminished with low dose estrogen pills.

28. ENDOCRINE OBESITY: Menopause
• Weight gain & changes in fat distribution also occur after
menopause.
• The decline in estrogen & progesterone secretion during
menopause alters fat-cell biology, resulting in increased central fat
deposition.

29. GENETIC OBESITY
1. Laurence-Moon-Biedl Syndrome
2. Hyperostosis frontails interna
3. Alstrom’s Syndrome
4. Prader-Willi Syndrome

30. GENETIC OBESITY:
Laurence-Moon-Biedl Syndrome
In 1866 Laurence and Moon described a disease characterized by
adiposity, genital dystrophy, retinitis pigmentosa, and mental
deficiency, affecting four members of one family.
It is a rare autosomal recessive genetic disorder associated with
• Retinitis pigmentosa
• Spastic paraplegia
• Hypogonadism
• Mental retardation

31. Laurence-Moon-Biedl
Syndrome

32. GENETIC OBESITY: Hyperostosis frontails
interna
• Thickening of the inner table of the frontal bone, which may be
associated with hypertrichosis and obesity.
• It is characterised by benign overgrowth of the inner table of the
frontal bone; may be a part of Morgagni syndrome.
• Visible by x-ray
• The etiology is unknown.
• It most commonly affects women near menopause.
• The condition is generally of no clinical significance and an
incidental finding.

33. GENETIC OBESITY: Alstrom’s Syndrome
• Alstrom's syndrome (AS) is a rare autosomal recessive disease
characterized by multiorgan dysfunction.
• The key features are childhood obesity, blindness due to congenital
retinal dystrophy, and sensorineural hearing loss.
• Associated features: hyperinsulinemia, early-onset type 2 diabetes,
and hypertriglyceridemia.
• Thus, AS shares several features with the common metabolic
syndrome.
• It is among the rarest genetic disorders in the world, as currently it
has only 266 reported cases in medical literature and over 501
known cases in 47 countries.

34. Alstrom’s Syndrome

35. GENETIC OBESITY: Prader-Willi Syndrome
• It is a rare genetic disorder in which seven genes on chromosome
15q are deleted or unexpressed on the paternal chromosome
• Obesity in childhood, adolescence & adulthood.
• Excess fat, especially in the central portion of the body.

36. DIETARY OBESITY
• The amount of energy intake relative to energy expenditure is
crucial in the development of obesity, also the composition of the
diet may play an important role in the pathogenesis of obesity.
1. Frequency of eating
2. Night eating Syndrome
3. Binge-eating disorder

37. DIETARY OBESITY
Weight gain due to:
• High total energy intake
• High carbohydrate diet, especially refined CHOs & simple sugars
• High Glycemic Index & Glycemic Load
• High fat diet, especially saturated fat
• Low protein Diet
• Low Calcium Diet
• Alcohol Intake: Especially Beer & WC
*Smoking Cessation: Weight gain is very common among people who stop
smoking, maybe caused by nicotine withdrawal. A gain of 1-2kgs in the first few
weeks after a patient stops smoking is often followed by an additional gain of 2-3
kgs over the next 4-6 months. Average weight gain is 4-5 kgs but can be much
greater.

38. DIETARY OBESITY: Frequency of eating
• The relationship between the frequency of meals & development of
obesity is unsettled.
• There are many studies which show that overweight persons eat
less often than normal weight persons.
• The frequency of eating does change glucose & lipid metabolism.
• When normal weight persons eat several small meals a day, their
cholesterol & blood glucose levels are lower.

39. DIETARY OBESITY: Night eating Syndrome
• It is defined as the consumption of >25% (and usually >50%) of
energy between the evening meal & the next morning.
• Common pattern of disturbed eating in the obese.
• May be a component of sleep apnea, in which daytime somnolence
& nocturnal wakefulness are common.

40. DIETARY OBESITY: Binge-eating disorder
• It is a psychiatric illness characterized by uncontrolled episodes of
eating that usually occur in the evening.
• The patient may respond to treatment with drugs that modulate
serotonin reuptake. (Sibutramine is a serotonin reuptake inhibitor,
leads to weight loss)

41. PHYSICAL INACTIVITY
• Physical inactivity represents more than an absence of activity; it
refers to participation in physically passive behaviors such as TV
viewing, reading, working at a computer, talking on the telephone,
driving a car, meditation or eating.
• A sedentary lifestyle lowers energy expenditure and promotes
weight gain.
• In an affluent society, energy-sparing devices in the workplace and
at home reduce energy expenditure even further and may enhance
the tendency to gain weight.

42. DRUG INDUCED OBESITY
• Several drugs can cause weight gain.
• The degree of weight gain is generally not sufficient to cause massive obesity, except
occasionally in those patients treated with high dose corticosteroids.
• Antipsychotics (Phenothiazines & butyrophenones) often cause weight gain.
• Antidepressant (amitriptyline) likely to cause wt gain & increase CHO preference.
• Antiepileptic (Valproate) causes wt gain in half of the patients who receive it.
• Steroid: Glucocorticoids cause fat accumulation. (Prednisone dose >=10mg/day)
• Steroid: Progestins used in breast cancer & AIDS increase appetite & causes wt gain. The
increase in weight is fat.
• Serotonin antagonist (Cyproheptadine) is associated with wt gain.
• Weight gain occurs in diabetic patients treated with insulin, sulfonylureas or
thiazolidinediones.