The case against sugar isn’t closed. But we do have astonishing new evidence

    5 November 2015

    My Spectator Health colleague Christopher Snowdon has strongly criticised Professor Robert Lustig’s case series, published last week, about the effects of reducing fructose in the diet. The study had no control group, he says, and relied on information provided by participants about their daily diet — its conclusions are therefore useless. I beg to differ.

    On its own, the study doesn’t prove anything. It doesn’t prove that sugar is the cause of obesity. That caveat aside, the results were astonishing.

    To recap: over the course of nine days, volunteers were encouraged to follow their previous dietary patterns, with the proviso that fructose, as a percentage of total calories, was not to exceed 14 per cent. Overall the amount of carbohydrates in the diet was to remain the same as was the calorie content. Participants were guided as to what to eat and supplied with food by the research team.

    What happened? Researchers noted highly statistically significant decreases in LDL (‘bad cholesterol’), triglycerides and insulin levels. Glucose tolerance (the ability of the body to handle a glucose load, a marker for impending or current diabetes) improved too. Blood pressure, another important marker, was also seen to improve.

    Were such changes to be sustained over the long-term we are talking about a significant decrease in the development of subsequent diabetes, heart attacks, strokes and, potentially, cancer.

    What makes this even more interesting is the fact that, in patients like these, the most spectacular biochemical effects are usually seen when a low-carbohydrate diet is followed, something this protocol certainly wasn’t.

    An average of 0.6kg weight was lost, even though participants were eating with the goal of weight maintenance. In the absence of a caloric deficient, most participants lost weight. (It should be clarified, though, that this loss was not fat loss and could simply have been a transient event.)

    The study, of course, has far from proved direct causality; no one is pretending that fructose is behind the obesity epidemic in isolation. But it seems to show quite spectacularly that, without any other intervention, a substitution of a carbohydrate found in almost all processed foods with another can be associated with significant changes in health parameters in unhealthy children and young adults.

    The potential ramifications of such a substitution are huge if the study is replicated, something mandatory before any concrete claims can be made or clinical practice changed. Nevertheless, more evidence has been supplied that the traditional paradigm requires further reappraisal.

    The case is still open about the consumption of excess refined sugar. But this study is an interesting piece of evidence.