Here’s a provocative article at the British Medical Journal on cardiovascular outcomes and diet. Now, I free admit that the BMJ has a tendency towards controversialism, but I’m hardly in a position to throw stones. The author, Aseem Malhotra, says “Saturated fat is not the issue”.
Human lipidology is a very complex field, and anyone who tells you that they have the definite answers needs to be treated with caution. As has been well documented, the consensus advice about dietary fats of all kinds has varied quite a bit, and I don’t think it’s anywhere near settling down. The role of pharmaceutical intervention isn’t settled, either, despite the huge success of the statin drugs. There’s room to argue about their broad effects on cardiovascular morbidity and mortality, and how much of it is mechanism-based:
A meta-analysis of predominantly industry sponsored data reported that in a low risk group of people aged 60-70 years taking statins the number needed to treat (NNT) to prevent one cardiovascular event in one year was 345. The strongest evidence base for statins is in secondary prevention, where all patients after a myocardial infarction are prescribed maximum dose treatment irrespective of total cholesterol, because of statins’ anti-inflammatory or pleiotropic (coronary plaque stabilising) effects. In this group the NNT is 83 for mortality over five years. This doesn’t mean that each patient benefits a little but rather that 82 will receive no prognostic benefit. The fact that no other cholesterol lowering drug has shown a benefit in terms of mortality supports the hypothesis that the benefits of statins are independent of their effects on cholesterol.
You can go on from this to wonder how things are going to work out if any of the HDL-raising therapies ever make it into the general population. Do we know what we’re doing there, or are we only going to find out after twenty years in the real world? On saturated fat, Malhotra says that he’s not convinced by the standard recommendations, either:
Saturated fat has been demonised ever since Ancel Keys’s landmark “seven countries” study in 1970. This concluded that a correlation existed between the incidence of coronary heart disease and total cholesterol concentrations, which then correlated with the proportion of energy provided by saturated fat. But correlation is not causation. Nevertheless, we were advised to cut fat intake to 30% of total energy and saturated fat to 10%.” The aspect of dietary saturated fat that is believed to have the greatest influence on cardiovascular risk is elevated concentrations of low density lipoprotein (LDL) cholesterol. Yet the reduction in LDL cholesterol from reducing saturated fat intake seems to be specific to large, buoyant (type A) LDL particles, when in fact it is the small, dense (type B) particles (responsive to carbohydrate intake) that are implicated in cardiovascular disease.
I find this sort of thing very interesting, both as an issue in itself, and for what it says about our knowledge of medicine and human biology. You’d think that there would be nothing more well worked-out than the role of different kinds of diets in heart disease, but the closer you look, the messier the situation is. There are big public health issues here, both the obvious primary ones, and the secondary issue of causing people to become frustrated and cynical about big dietary recommendations in general.