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Obesity - A Global Epidemic

Written by Dr. Engela Honey
Department of Human Genetics, University of Pretoria , South Africa

 

Obesity/overweight in adults and children is becoming a worldwide health problem and the incidence has increased markedly over the past decade. The World Health Organisation recognises obesity as a global epidemic and it is now regarded as a disease. It is estimated that 97 million or 55% of the USA adult population is overweight or obese and worldwide it affects 300 million people of whom 194 million have diabetes. By 2025 the number of obese people is expected to soar to 333 million. This was discussed at a recent Obesity conference. In Britain more women are obese than men and Kuwaitian citizens are among the most obese individuals in the world. Statistics for children are also alarming and studies have shown that half of overweight children become overweight adults and that children of obese parents may become obese themselves.

Obesity is defined as a Body Mass Index (BMI) (body weight in kilogram divided by the square of height in meters) equal or more than 30. Overweight individuals have a BMI of 25 to 29. Hypertension, elevated cholesterol and Type II diabetes is more common in overweight individuals than in the normal population and they also experience more arthritis and joint and mobility problems. The so-called metabolic syndrome with increased risk for heart attacks due to increased accumulation of fat in the abdomen, resistance to insulin and low HDL (good) cholesterol are also more common in obese individuals. There is some indication that the immune system may also be altered, which make obese individuals more susceptible for infection and disease. Obese adolescents may develop a negative self-image, which could persist into adulthood.

The increase in obesity rates has been attributed to the increased availability of food with a high caloric content and a decreased level of physical activity. Fast food, soft drinks, television and computer games are implicated as causes. When energy expenditure is less than intake, energy will be stored as triglyceride in the adipose (fat) tissue. Leptin (a hormone) secreted by the adipocyte (fat cell) controls food intake by stimulation receptors in the hypothalamus informing the brain of the fat store level and via the secretion of other hormones control appetite. Other hormones identified in this regulation are neuropeptide Y, ghrelin, insulin and cholecystokinin. A leptin deficiency could be the cause of obesity. The so-called Syndrome X. Research has suggested the involvement of genetic factors in the susceptibility to the development of obesity with convincing evidence from twin studies by comparing identical twins to non-identical twins. A lot of research on this subject is currently undertaken and hopefully would give insight into new therapies for controlling weight gain.

Obesity is some of the cardinal features of numerous genetic syndromes (at least 25) of which Prader-Willi syndrome is one of the commonest with an incidence of 1 in 20 000. Other syndromes identified and genetically mapped are Cohen (short stature, large central incisors), Alström (blindness, deafness and diabetes) and Bardet-Biedl (blindness and extra fingers and toes) syndromes. Other medical causes are hypothyroidism (under-active thyroid gland), a growth hormone deficiency and brain lesions involving the hypothalamus and pituitary gland. It might also be due to certain drugs such as steroids (cortisone) or chemotherapy. If a medical cause is suspected a specialist medical professional and a dietician should address the problem. Medical causes however are the minority and the most causes are due to excess behavioural and social energy intake associated with reduced energy expenditure.

The management consists of caloric restriction (diet), physical activity, lifestyle changes and behavioural therapies as in Prader-Willi syndrome. Prevention however is better than cure and adequate information should be given to families regarding the risk factors for obesity and the preventative strategies.

References:

1. Reuters Health Information 2004.

2. Endocrinology and Metabolism Clinics of North America 1996/2003.

3. Nelson’s textbook of Paediatrics.

4. Nursing Standard Jan 2004.

5. Circulation Sept 2003