UltraFit Magazine - Issue 107, Page 20

by Paul Taylor

The usual way of classifying obesity is by Body Mass Index (weight in kilos, divided by height in metres, squared). It is generally accepted that a BMI of more than 30 puts you in the obese bracket. A recent study in the US (1) showed that the prevalence of obese people in the US doubled from 1986 to 2000. In addition, the prevalence of the morbidly obese (BMI > 40) quadrupled from 1 in 200 adults to 1 in 50. The prevalence of the super obese (BMI > 50) quintupled!

While these statistics are extremely alarming, there may be a more clinically meaningful way to assess body composition. Most allied health professionals are aware of the limitations of BMI. Although it is a very easy, non-invasive way to estimate body composition, we need to consider its accuracy and the implications. For instance, many bodybuilders fall into the obese bracket when measured by BMI, despite having less than 10% body fat. Are they as at risk as someone with the same BMI, but 40% body fat?

Getting to the Core of the Problem

More than 50 years ago, the French physician Dr Jean Vague noted that complications in his obese patients had more to do with where the fat was deposited than how much was deposited. Dr Vague is credited with developing the terms ‘android’ and ‘gynoid’ obesity. Android is the high-risk type of obesity typically found in males where the fat is deposited centrally, hence the term ‘central obesity’ (apple shape). Gynoid is a low-risk type of obesity typically found in females where the fat is deposited in the gluteofemoral region, ie. the buttocks and thighs (pear shape). This concept of apple-shaped and pear-shaped obesity has been around for more than half a century, but it is only recently that researchers have uncovered mechanisms underlying the health risks of differing fat deposition sites.

The more dangerous android (central) obesity is also referred to in clinical circles as visceral obesity, since the fat surrounds our viscera, or internal organs. A 2001 review published in the British Medical Journal (3) makes a convincing case for why we should add waist circumference to our standard list of measures when conducting health/fitness assessments, arguing that excess visceral fat is the culprit, rather than simply being overweight. In this review, the authors explain how visceral obesity is closely related to the development of Type 2 diabetes, primarily through the mechanisms of insulin resistance and glucose intolerance that result in elevated levels of blood insulin and blood sugar. It is not the total amount of body fat that creates this problem, but rather the location of the fat.

Earlier studies by these authors compared two groups of obese individuals: those with excess visceral fat, versus those with excess subcutaneous fat deposits (between the muscles and the skin). Whereas both groups had similar BMI levels, those with the high accumulation of visceral fat had the highest glycaemic and insulinemic responses to an oral glucose challenge. In other words, when they were given a sugary drink, their body responded with an unhealthy response that resulted in excess production and release of insulin into the bloodstream, without lowering the high blood sugar level. Individuals with this characteristic response are at the highest risk of developing Type 2 diabetes, the Metabolic Syndrome and subsequent cardiovascular complications.

How Do We Measure Visceral Fat?

Considerable research over the past 25 years has addressed this issue. The best way is by using highly sophisticated and expensive techniques, such as Dual-Energy X-ray Absorptiometry (DEXA), Computerised Tomography (CT scans) and Magnetic Resonance Imaging (MRI). Due to the expense and scarcity of these machines, a number of estimations have been used, such as skinfolds, bio-electrical impedance, waist circumference (WC) and waist-to-hip ratio (WHR). While the first two have been discounted due to their lack of accuracy, a debate has raged as to whether waist circumference or waist-to-hip ratio is more appropriate, and both are still widely used.

In 1994, however, Dr Pouliot and colleagues (3) demonstrated that waist circumference was a better measure of abdominal visceral adipose tissue than the commonly used waist-tohip ratio in a mixed sample of men and women (n = 151). In addition, they found that higher WC levels were associated with an increased risk of premature atherosclerosis and cardiovascular disease. The validity of the WC as an indicator of abdominal visceral obesity has been confirmed by multiple studies using DEXA, CT scans and MRI.

Where Does Metabolic Syndrome Come into it?

Metabolic Syndrome, also known as Syndrome X, or the insulin resistance syndrome, represents a cluster of health risk factors present at one time in an individual. The definition varies between countries and organisations, but it generally involves raised levels of plasma lipids (cholesterol and triglycerides), glucose, blood pressure risk factors and abdominal obesity. The International Diabetes Federation has just proposed a new definition, namely if someone has abdominal obesity (94cm for Australians, 90cm for Asians) as well as two of the following: pre-diabetes or diabetes, high blood pressure and high cholesterol.

This clustering of multiple interrelated risk factors dramatically raises overall risk for an individual to develop conditions such as diabetes, cardiovascular disease or even premature death. As such, it is much more clinically meaningful than obesity, particularly as it appears to be the waist circumference, rather than BMI, that poses the greater health risk.

What Can be Done to Prevent or Treat Metabolic Syndrome?

Alarmingly, it is estimated that 25% to 30% of Australians have Metabolic Syndrome. The most sensible approach to reversing Metabolic Syndrome is weight reduction, exercise and sensible nutrition (especially reductions in saturated fat and high-GI carbohydrates). Evidence of the success of this approach is provided by the Diabetes Prevention Program (DPP), a large randomised controlled trial designed to study the impact of lifestyle and pharmacological intervention (the drug Metformin) on the prevention of diabetes among subjects with impaired glucose tolerance (4). Interestingly, 53% of the subjects actually met the criteria for Metabolic Syndrome and therefore this study also served as a data source for the impact of lifestyle and drug intervention on Metabolic Syndrome.

After 3.2 years of follow-up, the lifestyle intervention (which consisted of an intensive lifestyle regimen designed to induce 7% weight loss and 150 minutes of exercise per week) was effective at preventing or delaying the onset of diabetes for 58% of the subjects, compared with 31% among those subjects who were treated with Metformin. The prevalence of Metabolic Syndrome was also significantly reduced from 51% to 43% in the intensive lifestyle intervention group.

This result is all the more impressive as, during the course of the study, the prevalence actually increased among the control subjects from 55% to 61%. In the drug treatment group, the results remained unchanged. The change in prevalence among members of the lifestyle intervention group amounts to a 41% reduction relative to the control group and a 29% reduction compared with the Metformin group. Hence, the impact of a moderate amount of weight loss and an increase in physical activity is not only effective in reducing the incidence in diabetes, but also is more effective in reducing other components of the Metabolic Syndrome.

It is clear that the best strategy in combating Metabolic Syndrome is to try to reduce all the risk factors, and aggressive lifestyle intervention is appropriate for most people. Unfortunately, some people may need medication to control diabetes, cholesterol and blood pressure, in addition to measures to reduce weight. Some hope for those with higher levels of risk may be offered by a new drug called Rimonabant, as recent reports in The Lancet suggest that this may substantially reduce all the risk factors associated with the Metabolic Syndrome. However, it should be remembered that every drug has side-effects, whereas lifestyle changes do not. Finally, for those of us who are complacent, remember that prevention is better than cure!

References

1. Strum, R. Increases in clinically severe obesity in the US, 1986-2000. Archives of Internal Medicine 163:2146-2148, 2003
2. Despres, J P. Treatment of obesity: Need to focus on high-risk abdominally obese patients. BMJ 322:716-720, 2001
3. Pouliot, M C. et al. Waist circumference and abdominal sagittal diameter: Best simple anthropometric indices of abdominal visceral tissue accumulation and related cardiovascular risk in men and women. The American Journal of Cardiology 73(7): 460-468, 1994
4. Knowler, W C et al. Diabetes Prevention Research Group. New England Journal of Medicine 346: 393-403, 2002