intro & etiology of obesity

OBESITY

Presented By:Ms. Tasneem Navagharwala

Registered Dietician

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.

• 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.

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%

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%

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)

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 development2. First 3 yrs of life3. 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 disordersHyperplasic obesity is usually present in individual with BMI> 40kg/m2

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 %

Comparative statistics between Asian Indians in US and Asian Indians in Indian rural and urban areas(Mishra R, Mishra .A. et al 2008).

Variable Variable AI (US)AI (US) AI(urban)AI(urban) AI(rural)AI(rural)

Overweight Overweight /obesity /obesity

7373 6565 3232

Abdominal Abdominal obesity.obesity.

2323 3939 88

• 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.

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

ASSESSMENT OF OBESITY

• BMI• Waist Circumference• WHR• Body fat percentage (DEXA)

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.

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

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.

ETIOLOGY OF OBESITY

1. Hypothalamic Obesity

2. Endocrine Obesity

3. Genetic Obesity

4. Dietary Obesity

5. Inactivity

6. Drug induced Obesity

7. Essential Obesity

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)

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

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.

CUSHING’S SYNDROME

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.

INSULINOMA- LOW BLOOD GLUCOSE

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.

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.

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.

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)

ENDOCRINE OBESITY: Pregnancy

• Pregnancy is often an important event in the weight gain history of women.

• It may leave a legacy of increased weight.

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.

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.

GENETIC OBESITY

1. Laurence-Moon-Biedl Syndrome

2. Hyperostosis frontails interna

3. Alstrom’s Syndrome

4. Prader-Willi Syndrome

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

Laurence-Moon-Biedl Syndrome

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. 

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.

Alstrom’s Syndrome

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.

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

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.

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.

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.

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)

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.

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.