Diet-Heart Hypothesis
The diet-heart hypothesis, also known as the lipid hypothesis, proposes that there is a direct relationship between dietary fat intake, particularly saturated fat and cholesterol, and the development of heart disease. It suggests that consuming high amounts of these fats leads to an increase in blood cholesterol levels, specifically low-density lipoprotein (LDL) cholesterol, which in turn contributes to the formation of atherosclerotic plaques in the arteries. Some consider this hypothesis nothing more than wishful thinking.
Recent History
January 1, 1991
George Mann hosted a small meeting of researchers with alternative views.
The AHA and NHLBI together also administered the vast majority of grants for all cardiovascular research. By the mid-1990s, the NHLBI’s annual budget had reached $1.5 billion, with most of those funds going to heart disease research; the AHA, meanwhile, was devoting about $100 million a year toward original research. These two pots of money dominated the field. The NIH or AHA financed virtually all the American-led studies we will discuss in this book. The only other significant source of research funding came from the food and drug industries, which researchers tried to avoid for the obvious reason of avoiding any conflict of interest or even the appearance of one. As George Mann wrote in 1991, when he hosted a small meeting of researchers with alternative views, “This was a daunting task, because we cannot obtain federal funding, and we must not accept food industry funding lest we be seen as speaking for a vested interest.”
- Nina Teicholz - Page 70
January 1, 1991
Framingham publishes new findings and the predictive power of total cholesterol was not nearly as strong as study leaders had originally thought.
However, thirty years later, in the Framingham follow-up study—when investigators had more data because a greater number of people had died—it turned out that the predictive power of total cholesterol was not nearly as strong as study leaders had originally thought. For men and women with cholesterol between 205 and 264 milligrams per deciliter (mg/dL), no relationship between these numbers and heart disease risk could be found. In fact, half of the people who had heart attacks had cholesterol levels below the “normal” level of 220 mg/dL. And for men aged forty-eight to fifty-seven, those with cholesterol in the midrange (183–222 mg/dL) had a greater risk of heart attack death than those with higher cholesterol (222–261 mg/dL). Total cholesterol turned out not to be a reliable predictor for heart disease after all.
Because the Framingham leaders had been trumpeting total cholesterol as the best possible risk factor for heart disease for so many years, they did not take great pains to publicize these weaker follow-up numbers when they came out in the late 1980s. (Soon they would be shifting the conversation over to cholesterol subfractions, known as high-density lipoprotein [HDL] and low-density lipoprotein [LDL], which could now be measured and whose predictive powers showed more promise, although even aspects of these subfractions turned out to be disappointing in the end, as we’ll see in Chapters 6 and 10.)
The Framingham data also failed to show that lowering one’s cholesterol over time was even remotely helpful. In the thirty-year follow-up report, the authors state, “For each 1% mg/dL drop of cholesterol there was an 11% increase in coronary and total mortality [italics added].” This is a shocking finding, the very opposite of the official line on cholesterol lowering. Yet this particular Framingham finding is never discussed in scientific reviews, even though many large trials have found similar results.
Other important findings from Framingham have also been ignored, including—notably—those on dietary risk factors, which were examined in the part of the study that Mann conducted. Together with a dietician, Mann spent two years collecting food-consumption data from one thousand subjects, and when he calculated the results in 1960, it was very clear that saturated fat was not related to heart disease. Concerning the incidence of coronary heart disease and diet, the authors concluded, simply, “No relationship found.”
http://revisionisthistory.com/episodes/20-the-basement-tapes
January 1, 1997
MRFIT’s follow-up findings delivered more bad news: at the sixteen-year follow-up to the study in 1997, the treatment group was found to have higher rates of lung cancer even though 21 percent of them had quit smoking, compared to only 6 percent of the controls.
MRFIT triggered widespread comment and criticism in the research community, but after much hand-wringing, its failure did not generate a change of course or even a serious reevaluation of the direction of heart disease research. And that was true even after MRFIT’s follow-up findings delivered more bad news: at the sixteen-year follow-up to the study in 1997, the treatment group was found to have higher rates of lung cancer even though 21 percent of them had quit smoking, compared to only 6 percent of the controls.
When I asked Stamler about this apparent paradox, he took it straight on. “I don’t know! That could be a chance finding. . . . It’s just one of those findings. Troublesome. Unexpected. Not explained. Not rationalized!” (Stamler meets even the most timid challenge to his ideas with enthusiasm, delivered through an earthy Chicago accent. One colleague described him in his nineties as “frail but on fire.”)
