Does Metabolic Syndrome Predict Heart Disease?

Metabolic syndrome or syndrom X (recently refered to as Xyndrome) is the combination of abdominal obesity, high trigylcerides, low HDL cholesterol, high blood pressure and elevated levels of fasting blood glucose. This concept has been widely promoted as helping to clinically identify individuals at increased risk for heart disease.

While the concept appears intuitively sound (as all five components of this syndrome have been individually associated with increased cardiovascular risk), there is a continuing debate on whether the concept of this “syndrome” is any better in identifying individuals at risk for heart disease than looking at each individual risk factor on its own.

To address the issue of whether or not the “metabolic syndrome” is indeed a risk factor for heart disease, Naveed Sattar and colleagues from University of Glasgow examined the relationship between the metabolic syndrome and incident cardiovascular disease and type 2 diabetes in in 4812 non-diabetic individuals aged 70-82 years from the Prospective Study of Pravastatin in the Elderly at Risk (PROSPER). They corroborated these data in a second prospective study (the British Regional Heart Study [BRHS]) of 2737 non-diabetic men aged 60-79 years. (The Lancet)

In PROSPER, metabolic syndrome was not associated with increased risk of cardiovascular disease over 3.2 years but was associated with a 4-fold increased risk of diabetes. In contrast elevated fasting glucose alone was associated with an 18-fold increased risk for diabetes.

Likewise, in BRHS, metabolic syndrome was only modestly associated with incident cardiovascular disease despite a strong association with diabetes.

Importantly, in both studies, body-mass index or waist circumference, triglyceride, and glucose cutoff points were also not associated with risk of cardiovascular disease, but all five components were associated with risk of new-onset diabetes.

The authors conclude that while metabolic syndrome and its components are associated with type 2 diabetes, they only have a weak to no association with vascular risk in elderly individuals. Their recommendation is that the clinical focus should remain on establishing optimum risk algorithms for each individual risk factor rather than lumping them together as a putative “syndrome”.

Obviously, one could argue that there may still be some use for the concept of the metabolic syndrome in younger individuals, but, as discussed in this paper, the same group (and others) have also not found the metabolic syndrome to be a strong predictor of heart disease in younger individuals.

Irrespective of whether or not the concept of the metabolic syndrome is helpful, it should be remembered that obesity treatment is the only intervention that can simultaneously have beneficial effects on all five components of this syndrome. Thus, while conventional care continues to aggressively target the individual risk factors, only aggressive obesity treatment will indeed improve all features of this putative syndrome.

Unfortunately, with the exception of obesity surgery, we still lack outcome studies confirming that obesity treatment will indeed decrease cardiovascular mortality.

Remember, the assumption that losing weight (without surgery) will save lives is not based on hard evidence from randomised controlled trials. My guess is that till we have better data on this issue, physicians, payers and policy makers will continue to question the benefits of tackling obesity with the same resources and enthusiasm as for other chronic diseases.

Edmonton, Alberta