Finally, the general pattern of abnormalities in the insulin resistant group is a highly atherogenic risk profile, in support of the contention that this syndrome is a precursor of cardiovascular disease. Stout presented convincing experimental and clinical arguments that hyperinsulinemia could be involved in the pathogenesis of CHD. Results from Helsinki Policemen Study, Paris Prospective Study & the Busselton Study support this hypothesis.
In fact, the network of connections among these 6 conditions may be an amplification of normal physiological functions. The physiological basis of several such relationships is well established. Eg. A rise in plasma glucose levels can result from tissue refractoriness to insulin action on glucose uptake; hyperglycemia then elicits a heightened insulin response, which in turn is a stimulus for hepatic VLDL-TG production. Also, hyperinsulinemia may raise BP by renal sodium conservation and adrenergic activation.
One practical corollary of these findings is that diagnosing any one of these 6 conditions should be sufficient indication to screen for the other 5. Eg. in hypertensive patients, it is reasonable to check glucose and lipid profile for better evaluation of CHD risk.