Barry Lewis

Quotes

Thinking back on this, this has been an exciting field from the very beginning. But the controversies were disproportionate, I think, to the quality of the evidence. For some reason the diet-lipid area was strongly antigenic to the medical and scientific community for a long time. If you think how readily people have accepted, for example, the risk of smoking, a very close analogy….or even overweight, physical activity. But the… risk factors for heart disease were a struggle to get across and I suppose the penny should have dropped for me as a junior doctor working in Capetown with John Brock and seeing the ethnic disparity in heart disease. But the penny did drop in the case of Ancel Keys and he very early came to Capetown…

I enjoyed the subject from the very beginning. And, of course, it was Ancel Keys who saved me from a life as an endocrinologist and I might as well tell the anecdote again. I think you may know it personally. He was the guest of John Brock in Capetown. I think it was his first visit there and Ancel was due to give a lecture that evening. The lecture theatre, which was a large one, was packed. People were sitting in the aisles. It was somebody with something new to say. But it was by then late, very late because he and John Brock had been touring the cape vineyards and that resulted in a certain amount of delay. And when they arrived there was a further delay because I remember how difficult John Brock found it [after some hours at the wineries] to pronounce Laboratory of Physiological Hygiene… a neurological test. Ancel finally gave a talk, which was early in his own researches… which galvanized me personally.

Resistance to the diet-heart idea

But the opposition was already so massive. Capetown followed suit immediately. Even cardiologists there stopped using butter 40 years ahead of the rest of them. But… just after I came to London to do my specialist exams… I remember how hostile even Goodwin was in those days. It has to have been emotive, in that every time a negative case was demolished a new negative case would spring forward. First we heard that cholesterol was the consequence of heart disease. [Then] we heard that cholesterol was an ‘epiphenomenon.’ We heard it was a non-causal association and then the epidemiology crushed that, as well as many early trials [having] suggested it was causal. But these were dismissed because they were small, not state-of-the-art design, not powerful, etc. And it was then said, “Well, total mortality doesn’t fall, so this can’t be a serious finding.” And then as soon as total mortality was clearly, if not significantly reduced in the trials after about 1985-1990, we had that wealth of counter arguments to do with the dangers of a low serum cholesterol level. Yes, about half the epidemiology – in our school of epidemiology – did show that low serum cholesterol levels were associated with a rise in total mortality. Some of them showed an excess of cancer. Some of them showed an excess of respiratory illness, traumatic death, suicide. There was nothing very consistent about the non-cardiovascular excess deaths. It was biologically implausible even when it happened because you could look at Chinese persons with serum cholesterol levels of 100 or 110 and… And, of course, now in the 90s we have these large-scale statin trials in none of which has there been an excess of non-cardiovascular mortality.

Joint Recommendations

And I think I chaired that initial committee (ESC Joint Recommendations) in the late 80s and there have been four generations of guidelines since. The guidelines are difficult because now they have assimilated the basic epidemiological recognition that risk factors are graded without a threshold and [yet] they keep trying to pinpoint cutoff points for blood pressure, for cholesterol. The trials show what the epidemiology shows and especially the newest trials in the last six months or a year. There is no lower threshold. The lower the better for cholesterol and there is a wide range for blood pressure. And I don’t quite know how to teach clinicians how to handle that situation because if you are literal- minded you have to say we’ll give everybody a diet and the maximum tolerated dose of statin. There are people saying that. There’s another design we’ve both thought about – the poly pill. At least it marries the idea that risk factors are widely distributed within a population and everybody needs multi-risk factor reduction, but the idea of exposing everybody over age 50 to the side effects of the six drugs. Perhaps you’re not aware that within the last month the first major statin, synthestatin, has become an over-the-counter drug in this country.

Low Fat?

The conventional wisdom now is to lower carbohydrate intake – ‘higher carbohydrate intake is bad for you.’ There’s talk about the metabolic syndrome. There’s talk about high glycemic-index carbohydrates. I can’t assimilate all this. But if you take this triangle, that is, if you have to give less fat, then [they say] you must give more carbohydrate, which is one of Scott Grundy’s debating points. It just ain’t true, because you don’t have to keep that triangle the same size. You can reduce calorie intake and most people would benefit by a reduction in calorie intake. You can give less fat and the same amount of carbohydrate and protein.