Obesity should be considered a chronic disease due to its associated risks. Apart from cardiovascular diseases, hypertension, diabetes and dyslipideamia, obesity has also been implicated in the development of degenerative bone diseases, obstructive sleep apnoea, gallbladder disease and some cancers such as colorectal malignancy.

Obesity implies an excess of body fat, which can be measured accurately by sophisticated methods including underwater weighing and electrical bioimpedence. On average, fat accounts for approximately 20% of total body mass in men and 25% in women. In clinical practice, body weight (BW) measurements give the most convenient indication of obesity. Conventionally, overweight is defined as > 10% excess with ideal body weight (BW) as > 85th percentile of normal distribution of body weight. Severe obesity is defined as > 20%.excess of IBW as > 95th percentile of normal distribution of body weight.

  • Obesity is a chronic disease of a strong familial component.
  • Obesity increases one's risk of developing conditions such as high blood pressure, diabetes (type2), heart disease, stroke, gallbladder disease and cancer of the breast, prostate and colon.
  • Persons with obesity are victims of unemployment and other discrimination, and are penalized for their condition despite many federal and state laws and policies.

  • Genes

    Some individuals have a genetic tendency to gain weight and store fat. Although not everyone with this tendency will become obese, some persons without predisposition do become obese. Several genes have been identified as contributors to obesity, and researches are constructing a human obesity gene map in hope of finding genetic targets in humans that may lead to the development of new treatments.

  • Environment

    An environment that promotes healthy weight is one that encourages consumption of nutritious foods in reasonable portions and regular physical activity. A healthy environment is important for all individuals to prevent and treat obesity and maintain weight loss. Healthy environments can be created at home, school, work, and beyond. Identifying and consciously avoiding high-risk situations in the environment can assist in weight and control efforts.

  • Behavior

    Adopting healthy habits for lifelong weight control purposes includes regular physical activity and nutritious eating. Specific behavioral strategies for weight loss and maintenance include: logging and tracking diet and exercise patterns in a diary, eating a low calorie diet, limiting the amount of calories from fat, expending calories routinely through exercise, monitoring weight regularly, setting realistic goals, and developing a social support network.

Body weight is mainly determined by caloric intake, energy expenditure and basal metabolic rate. Obesity is occasionally a presenting feature of an endocrine as metabolic disorder. However, in the majority of subjects, obesity is a consequence of energy imbalance due to excessive energy intake and inadequate energy expenditure. Increased food intake, particularly dietary fat, is the most often cause of excessive energy input while reduced energy expenditure is usually due to a sedentary lifestyle with inadequate physical activity. Basal metabolic rate is individualized and can be increased by excessive hormones, such as thyroxine and catecholamines. Our satiety which determines the amount of food intake, is under complex hormonal influences, especially the corticotrophin and sympathetic nervous systems. Neurotransmitters such as seratonine and dopamine have been shown to suppress appetite while neuropeptide Y is a potent stimulator of appetite. Excessive caloric intake is stored as triglyceride in adipose tissue, which secretes the hormone, leptin. The latter enhances hiplysis to re-set the balance and feeds back to the hypothalamus to reduce food intake and thereby prevent incessant weight gain. Leptin is a protein and its shynthesis in adipocytes is regulated by the obesity gene. Mutations in the obesity gene may lead to either leptin deficiency or leptin resistance. Such mutations have been found to be associated with obesity in some animal and human studies although conclusive evidence is still awaited.

It has been observed a clustering of elevated plasma insulin concentration, obesity, hypertension, dyslipidaemia, and hyperglycaemia, and described the syndrome of insulin resistance. Impaired insulin - stimulated glucose uptake by peripheral tissues can lead to impaired glucose tolerance and, eventually lead to diabetes in some subjects. Associated hyperinsulineaemia has stimulatory effects on the adrenergic and rennin-aldosterone systems and promotes renal tubular sodium and water reabsorption. These factors may contribute to elevation of blood pressure. In normal subjects, insulin inhibits lipolysis and production of very low density lipoprotein (VLD2) cholesterol and promotes the catabolism with VLDL-C to high density lipoprotein cholesterol (HDL-C). Hence, insulin resistance is associated with dyslipidaemia, characterized particularly by increased triglycerides and VLDL-C, and reduced HDL-C. Increasing evidence points to obesity, particularly visceral obesity, as an important linking factor in this multiplaceted metabolic syndrome. Hormonal abnormalities such as age-related decreases in growth hormone and female sex steroids, and increased cortisel levels due to psychosocial stress, can all enhance the deposition of visceral fat. Fat depots within the peritoreal cavity are more responsive to catecholamine - stimulated lipolysis than subcutaneous fat with increased formation of free fatty acids (FFA). In the presence of excess FFA, insulin becomes less effective at promoting glucose uptake at various tissue sites, including liver, muscle and adipose tissue, for energy production or storage. Insulin resistance increases by 30 to 40% when body weight increases by 35 to 40% compared with IBW. Exercise and weight reduction can improve insulin sensitivity.

Obesity often represents positive energy homestasis due to an imbalance between dietary intake and energy expenditure. Hence, lifestyle and behavioral modification remain the main stays for weight reduction. Pharmacotherapy is indicated when the above measures have failed in subjects for whom obesity poses significant health risks especially in the presence of cardiovascular risks or complications. Most studies have shown that without effective lifestyle modification many subjects regain their weight upon cessation of anti-obesity medication. Drugs can be classified as : anorexic agents, drugs that decrease energy storage, and drugs that increase energy expenditure. Anorexic agents usually act centrally on the noradrenergic as serotonergic systems. Drugs that mimic serotonine suppress appetite and lead to reduced food intake. D-dexfenfluramine, a serotonine uptake inhibitor, has been shown to be effective in reducing weight and is generally well tolerated. However, it has recently been withdrawn due to reported side effects including pulmonary hypertension and cardiac valvular lesions. Fluoxetine is an antidrepessant agent that may have a centrally acting serotoninergic anti-obesity effect. Phentermine, diethylpropion and mazindol are centrally acting noradrenergic anorexic agents which modulate feeding by sitmulating release of catecholamines from storage sites in the central nervous system. Sibutramine is a mixed serotoninergic and noradrenergic reputable inhibitor which suppresses appetite. It has a B3 - adrenergic agonistic effect and theoretically stimulates thermogenesis.

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