The body mass index (BMI) is the current accepted medical technique for assessing the degree to which a subject is overweight, and by extrapolation their risk of cardiovascular disease. The Worlds Health Organisation (WHO) has BMI classifications for normal weight, overweight and obese, based on these measurements. However, the BMI is seriously flawed because adiposity does not increase cardiovascular risk unless it is present as visceral fat in a central location. Such central adiposity causes disease because it is an outward manifestation of an inward metabolic dysfunction. Termed the metabolic syndrome, this spectrum of metabolic aberrations that result from the overloading of the liver with fructose, is characterised by non-alcoholic fatty liver, insulin resistance, deleterious blood lipid changes and fat deposition around and in the organs of the viscera. In contrast to central adiposity, subcutaneous and peripheral fat are outward manifestations of the normal storage of lipids and their presence in no way interferes with metabolic regulation.
The deleterious effects of central adiposity are well reported in the nutritional literature in a range of subjects of different ages. For example, in one study published in the American Journal of Clinical Nutrition1, researchers assessed the relationship of body fat distribution to glucose and insulin responses in 355 school-age children. The researchers reported that the peripheral and central fat were both correlated with fasting glucose and one hour glucose following a glucose tolerance test. However, only central adiposity was correlated to the one hour insulin response following the oral glucose tolerance test. Interestingly the association was true irrespective of race, sex, age or the actual degree of total adiposity present. This therefore supports other data to show that relatively thin and normal weight individuals can still show symptoms of the metabolic syndrome despite no outward appearance of being overweight. The results also support the contention that metabolic syndrome in Western nations develops from an early age.
Central obesity is associated with detrimental changes to blood lipids and glucose homeostasis. That peripheral and subcutaneous adipose tissue is not associated with these metabolic changes highlights the dichotomy between fat storage in these two locations. Further, assessing weight through use of the BMI is of limited scope because it does not include an accurate representation of body fat topography required to ascribe risk. Visceral fat accumulates due to consumption of a low quality diet, characterised by a low fibre to starch ratio and insufficient micronutrients. Evidence from the nutritional literature shows that reversal of central adiposity is possibly only through consumption of a high quality diet characterised by a high fibre to starch ratio and which contains a high density of micronutrients. Considering that a 500 mL can of sugar sweetened energy drink can contain as much as 80 grams of sucrose, it is of no surprise that diets containing such products soon result in the early stages of metabolic syndrome amongst young adults and children.
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