1. Feeding and Obesity Dr.Dlair Maroof

2. Feeding Stretch receptors in the stomach activate sensory afferent pathways in the vagus nerve and inhibit food intake. Peptide YY (PYY), cholecystokinin (CCK),and insulin are gastrointestinal hormones that are released by ingestion of food and suppress further feeding. Ghrelin is released by the stomach, especially during fasting, and stimulates appetite. Leptin is a hormone produced in increasing amounts by fat cells as they increase in size; it inhibits intake.

4. The usual tight regulation of the size of the adipose organ indicates that neural or humoral signals from the adipose organ are transmitted to the brain, which in turn regulates food seeking and consumption, and energy expenditure
Fat deposition results from the discrepancy between fat consumption and energy expenditure and maximum weight gain being achieved in middle age.
Bodily fat is stored as triglycerides in adipose tissue, which is distributed under the skin and in the breasts, buttocks, thighs, and abdomen. Adipose tissue accounts, on average, for 26 to 42% of the weight.

5. Obesity
Definition and Measurement
Obesity is a state of excess adipose tissue mass. Although often viewed as equivalent to increased body weight, this need not be the case—lean but very muscular individuals may be overweight without having increased adiposity.
Obesity is more effectively defined by assessing its linkage to morbidity or mortality.
The distribution of adipose tissue in different anatomic depots also has substantial implications for morbidity. Specifically, intraabdominal and abdominal subcutaneous fat have more significance than subcutaneous fat present in the buttocks and lower extremities.

6. Although not a direct measure of adiposity, the most widely used method to gauge obesity is the body mass index (BMI), which is equal to weight/height2 (in kg/m2).
Other approaches to quantifying obesity include anthropometry (skin-fold thickness), densitometry (underwater weighing), CT or MRI, and electrical impedance.

7. Clinical features
Two distinct phenotypes are apparent:
Abdominal obesity (apple shaped) which is a stronger predictor of developing coronary heart disease, associated with insulin resistance and type 2 diabetes mellitus
Generalized obesity (pear shaped): fat is distributed in the hips and thighs Specifically, intraabdominal and abdominal subcutaneous fat have more significance than subcutaneous fat present in the buttocks and lower extremities.

8. Abdominal fatness can be assessed by waist circumference or the circumference of the waist divided by the hips (WHR).
determining the waist-to-hip ratio, with a ratio 0.9 in women and 1.0 in men being abnormal.
a waist circumference greater than 102 cm for men and 88 cm for women is considered high risk. These values lose their validity in patients with a BMI 35 kg/m2.
They vary according to ethnicity; an Asian female a waist circumference >80 cm and in an Asian male a value >90 cm are abnormal.
Although computed tomography (CT) and magnetic resonance imaging (MRI) are more accurate, they are too expensive to be performed for this purpose alone.

9. Aetiology
Until recently, obesity was considered to be the direct result of a sedentary lifestyle plus chronic ingestion of excess calories.
Although these factors are undoubtedly the principal cause in some cases, there is evidence for strong genetic influences on the development of obesity.
As much as 40–70% of obesity may be explained by genetic influences.

10. Behavioral factors
The prevalence of obesity has been increased over the last 20 years in developed countries
The major factor leading to obesity is decreased overall physical activity rather than simply increased food intake
High content of fat in diets, as most of the fat is stored rather than being consumed in energy expenditure
Snaking and loss of formalized meal patterns
Consumption of energy dense meals( often high in fat and sugar and low in bulk
Alcohol consumption, by providing substantial energy
Giving up smoking; Nevertheless the risk of smoking is so substantial that a weight gain of approximately 11 kg negates the benefit of giving up smoking 20 cigarette per day

11. genetic factors
Five genes affecting control of appetite have been identified and result in obesity.
One gene codes leptin and another for the leptin receptor in the brain. The other three genes affect brain pathways downstream from the leptin receptor.
Most human obesity undoubtedly develops from the interactions of multiple genes, environmental factors, and behavior.
Mutation of melanocortin-4receptor accounts for 5% of severe early onset obesity (prader-willi syndrome)
Mutation sites
Proenzyme convertase 1
Agouti related peptide

12. Endocrine factors Drug treatments
POTENTIALLY REVERSIBLE CAUSES OF WEIGHT GAIN
Endocrine factors
Hypothyroidism
Hypothalamic tumours or injury
Cushing's syndrome
Insulinoma
Drug treatments
Tricyclic antidepressants
Corticosteroids
Sulphonylureas
Sodium valproate
Oestrogen-containing contraceptive pill
β-blockers

13. Obesity Class BMI(kg/m2)
CLASSIFICATION OF OVERWEIGHT AND OBESITY BY BMI
  Obesity Class BMI(kg/m2)
Underweight  <18.5
Normal  –24.9
Overweight  25().0–29.9
ObesityI –34.9
ObesityII –39.9
Extreme obesityIII ≥40
Overweight for Americans is defined as a BMI between 25 and 29.9 kg/m2 and obesity is defined as a BMI of 30 kg/m2 or more.
For Asians, overweight is a BMI between 23 and 29.9 kg/m2 and obesity a BMI >30 kg/m2

14. Pathophysiology of obesity and complications

15. Complications of weight gain
Type 2 diabetes mellitus
Hypertension
Stroke
Hyperlipidemia
Coronary artery disease
Gall stone
Increased risk of certain cancers
Breathlessness and reparatory distress
Menstrual abnormality and hirsutisim
Pregnancy related complications
Weight related musculoskeletal disorders and arthritis
Stress incontinence
Obstructive sleep apnea
psychological consequences on the individual and the society
Risk of death increases with increasing weight, the only medical benefit of obesity is in osteoporosis where bone density increases in response to excess weight

16. Metabolic syndrome ”syndrome X “ any three of five risk factors
Defining level
Abdominal obesity(waist circumference)
Men
women
>102 cm
>88 cm
triglycerides
>1.7 mmol/L
HDL cholesterol
<1.0 mmol/L
<1.3 mmol/L
Blood pressure
>130/>85 mmHg
Fasting blood glucose
>110 mg/dl