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-- Eli Ipp, M.D.

With billions of dollars spent on attempts to lose weight and a new book appearing on the shelves of bookstores each month promising a better approach to weight loss, obesity and its management are clearly among our society's most important health and aesthetic preoccupations. While obesity per se is an important risk factor for a number of different disease processes, it has become apparent in recent years that the site of adipose tissue accumulation may be as important a risk factor as how much fat a person has -- perhaps more important.

This discussion will focus on the clinical phenomenon of abdominal obesity and will reveal that there are many unanswered questions. This topic was chosen because of its clinical importance and its potential for providing us with better understanding of obesity and its complications. In the future, from time to time, important updates on our knowledge in this area will be added to this discussion. Be on the lookout for these and feel free to post your own comments at the left

What Are the Diseases Which Are Influenced by Body Fat Distribution?

In numerous epidemiological studies, distribution of adiposity in the upper body or abdominal region has been associated with numerous disease processes:

1. Impaired glucose tolerance
2. Insulin resistance, fasting hyperinsulinemia
3. Hypertriglyceridemia, hypercholesterolemia and low HDL cholesterol
4. Diabetes mellitus
5. Coronary artery disease
6. Hypertension
7. Hyperuricemia
8. Stroke

This results in increased overall mortality. Although abdominal obesity is often accompanied by whole body obesity, the former has been shown to be an independent risk factor for increased mortality.

When Did We Become Aware of This Phenomenon?

As early as 1956, Dr. Vague, a French physician, noted that adipose tissue was distributed differently in women and men. He coined the terms 'android' and 'gynoid' for the respective patterns of upper body or abdominal, versus lower body or gluteo-femoral, fat accumulation. Furthermore, he observed that there was an increased association of android, i.e. abdominal obesity, with diabetes mellitus, coronary artery disease and gout. Little further progress was made in exploring or understanding this information until the 80's, when investigators began to explore the metabolic implications in more detail.

Where Does One Measure Abdominal Obesity?

The classical anthropometric measurement of upper and lower body obesity is the Waist-Hip-Ratio (WHR). This crude measurement of waist and hip, using the simplest of methods -- a tape-measure -- and expressed as a ratio, has been shown in numerous cross-sectional and longitudinal epidemiological studies to be positively correlated with the disorders mentioned above. The waist is measured at its narrowest point and the hip circumference at its widest, while standing. Attempts to standardize and render this measurement more accurate have been developed in recent years. CT scans of the abdominal region and MRI evaluation of intra-abdominal adipose depots are the most accurate quantitative methods and have been used in metabolic studies with small numbers of subjects. These methods are too expensive and cumbersome for clinical purposes or epidemiological studies, which still use the WHR as the method of choice. Normal values depend on age and technique of measurements; increased risk is considered to occur with a WHR >0.8 for females and >0.95 for males.

How Do Abdominal or Gluteofemoral Patterns of Adipose Tissue Distribution Occur?

There appear to be two major influences upon the accumulation of fat in these areas, genetic and hormonal. Identical twin studies and other population studies indicate an estimated 20-50 % genetic influence upon body fat distribution. The genes responsible for this have not been identified. That hormonal factors play a role was suggested from the outset because of the role of gender in determining the site of fat deposition as originally described by Vague. Estrogen and prolactin appear to play a role in fat deposition in the gluteo-femoral region. Testosterone may influence the accumulation of abdominal fat. Corticosteroids may also contribute to abdominal fat stores, with Cushings syndrome providing the most extreme clinical example. Upper body obesity is part of the typical clinical picture of adrenal glucocorticoid secretion in Cushings syndrome, designated as the 'centripetal' distribution of adiposity.

Why Is an Elevated WHR a Risk Factor?

The mechanisms for the deleterious influence of abdominal obesity are unclear at this time, although some intriguing hypotheses have been suggested. Most important is the concept that all adipose tissue is not uniform in its metabolic characteristics. Striking metabolic differences have been demonstrated between gluteo-femoral and intra-abdominal adipocytes. Fat cells derived from the intra-abdominal region tend to be more susceptible to lipolysis; they respond more vigorously to the lipolytic influence of catecholamines and respond less well to the effects of insulin to inhibit lipolysis. It is thought that this critical difference may explain many of the associations of disease with an elevated WHR. Increased lipolysis results in an increase in free fatty acids (FFA) flux. FFA, while an important metabolic fuel, are also thought to be the villains in a number of metabolic scenarios. These include FFA inhibition of glucose utilization, which may cause insulin resistance and glucose intolerance, hyperinsulinemia and increased hepatic glucose production, a typical finding in Type II diabetes mellitus. FFA also stimulate the synthesis of triglycerides in the liver, VLDL (very-low density lipoprotein) and also LDL production. Thus, it is reasoned that the higher the rate of lipolysis, the more likely an association with these metabolic disorders.

What to Do?

The influence of diet, drugs and exercise to diminish abdominal obesity has been evaluated in separate studies. Diet appears to influence all body fat depots, although some studies seem to indicate a greater degree of weight loss from the abdominal region in those subjects who start out with an increased upper body obesity. Exercise has been shown in some studies to have a beneficial effect upon abdominal weight loss. Little information is available on the effects of weight reduction drugs at this time. On the other hand, people with predominant gluteofemoral fat accumulation may be counseled that the problem is more aesthetic than health-related.

Conclusions

It is probably still too early for all patients to be evaluated for abdominal obesity, though weight and body mass index (BMI) should be part of an initial physical evaluation. When specific therapies become available, the rationale will be clearer. At this time, more studies are needed to evaluate whether it is possible to specifically target abdominal weight loss. Nor is it known if successful intervention in the long-term will alter the natural history of high risk in subjects with abdominal obesity. However, until then, it is prudent to offer diet and exercise as methods to reduce abdominal fat and thus try to influence the high risk course of the disease. As an adjunct to counseling for obesity management, measurement of the waist- hip-ratio should be performed; patients should be informed as to the significance of an elevated WHR as further encouragement to lose weight. It is anticipated that further research in this area may provide important clues in the pathogenesis of obesity and its relationship to its concomitant metabolic disorders.