The most harmful industrial food-processing technique is thought to be hydrogenation, a procedure designed to transform polyunsaturated plant oils into compounds resembling animal fats (see box, page 8). The problem is that hydrogenated oils contain large quantities of toxic trans fatty acids (TFAs), ubiquitous in processed foods of all kinds.

Enig believes it's not animal fats, but hydrogenated oils and their TFAs that are primarily responsible for the rise in heart disease, a conclusion at least partially endorsed by a recent top-level survey. Nine months ago, researchers at the Harvard School of Public Health reported on their analysis of at least a decade's worth of data on trans fats intake and heart disease, and dropped a bombshell on both the food industry and CHD research.

"TFAs have a major role in heart disease," announced survey director Professor Walter Willetts. "The magnitude of the association with CHD is considerably stronger than for satura-ted fat." TFAs, he showed, have particularly nasty effects: raising triglycerides and 'bad' LDL cholesterol; reducing 'good' HDL cholesterol; and causing inflammation in the arteries-all of which are known to provoke CHD (N Engl J Med, 2006; 354: 1601-13).

What's more, there's now objective physical evidence of the damage TFAs can do to the arteries. In a little-publicized study, British researchers examined the arteries of people who had died of CHD, and found the tell-tale fatty deposits on the artery walls.

But their analyses of these deposits were another blow to the high-fat-CHD theory as it was revealed that the plaques contained no saturated fats at all and hardly any cholesterol, but were filled with masses of polyunsaturated fats and TFAs (Lancet, 1994; 344: 1195-6)-findings that have been confirmed by researchers in Poland (Eur J Nutr, 2004; 43: 313-8).

There's one more crucial piece of the jigsaw. After some painstaking detective work in the heart-disease research archives, Dr Enig discovered that, until the mid-1980s, researchers didn't discriminate between saturated fats and TFAs, lumping them both together in their diet analyses (J Am Coll Nutr, 1990; 9: 471-86). "Thus, historically, natural saturated fats have been tarred with the black brush of un-natural hydrogenated vegetable oils," she says.

So, the circle can now be squared, and puzzling paradoxes answered. Why do so many recent studies find no correlation between high saturated-fat intake and CHD, or why do many populations with high fat intakes have such little heart disease? The answer is simple: no TFAs = no CHD . . . QED.

Tony Edwards