Carbohydrate, not fat, consumption is linked with increased risk of metabolic syndrome

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In recent years there has been increasing awareness regarding a condition known a ‘metabolic syndrome’. While its precise definition varies a bit, the main feature of metabolic syndrome is excess weight around the midriff (abdominal obesity), coupled with other unwanted findings such as raised levels of sugar and/or blood fats known as triglycerides, raised blood pressure, and low levels of ‘healthy’ HDL cholesterol. Those suffering from metabolic syndrome have been found to be at significantly enhanced risk of conditions such as type 2 diabetes and heart disease.

What causes metabolic syndrome has been a subject of some debate, and the focus here has naturally been on diet and exercise. Traditionally, as far as nutrition is concerned, the emphasis has been (rather predictably) on fat. Basically, the concept here is that eating a lot of fat is most likely to make us fat, and therefore increase our risk of the excess weight that is the hallmark of metabolic syndrome.

However, this proposed mechanism does not quite make sense when one considers the fact that a key biochemical imbalance in metabolic syndrome is raised levels of the hormone insulin. Insulin is primarily secreted in response to rising levels of sugar in the bloodstream, which comes, essentially, from the eating of either sugar and/or starch. Eating fat, on the other hand, does not cause insulin levels to rise. Despite these plain biochemical facts, individuals with metabolic syndrome are often advised to eat a low-fat, high-carb diet.

In a study published recently in the Journal of the American Geriatrics Society, researchers based in London, UK, went about assessing risk factors, including diet, for metabolic syndrome in a group of men aged 60-79 years [1].

Two factors associated with an enhanced risk of metabolic syndrome included physical inactivity and smoking.

When the researchers analysed the dietary data they found that fat intake was NOT associated with metabolic syndrome risk.

However, a high-carbohydrate diet was found to be associated with increased risk of metabolic syndrome. In this study, a high-carbohydrate diet was defined as one in which more than 57 per cent of calories come from carbohydrate. It should perhaps be noted that we are very often encouraged to ensure that 60 per cent or more of our calories are carb-based.

A study of this nature (known as an ‘epidemiological’ study) cannot prove that eating an excess of carbohydrate causes metabolic syndrome. The fact that carbs cause insulin secretion means there is a plausible biological mechanism which could explain this association.

This study also assessed the impact of lifestyle modification on metabolic syndrome risk. Compared to individuals whose weight did not change, those who lost weight in the preceding 2-4 years had about half the risk of metabolic syndrome. What this study suggests is that lifestyle modification is likely to protect against metabolic syndrome, even relatively late in life.

Those wanting to prevent or even reverse metabolic syndrome might look to take some regular activity. Personally, I recommend daily walking. In addition, it would seem sensible for individuals to control their intake of carbohydrates that tend to boost blood sugar and insulin levels. Foods with added sugar will generally do this, as will starchy carbohydrates such as bread (even wholemeal bread), potato, rice, and many breakfast cereals.

In finding a link between carbohydrate intake and metabolic syndrome this recent study has merely helped to confirm what is blindingly obvious to anyone with even a rudimentary knowledge of biochemistry. My hope, though, is that it might help ease the grip of doctors and scientists who seem to cling tenaciously to the notion that metabolic syndrome and related ills (including diabetes) are down to fat.


1. Wannamethee SG, et al. Modifiable lifestyle factors and the metabolic syndrome in older men: effects of lifestyle changes. Journal of the American Geriatrics Society. 2006;54(12):1909-14

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