Fats & Protein vs. Carbohydrates (Part 6)

[Guest guest]

THE OILING OF AMERICA (part 6)

The problem with the 40 years of NHLBI-sponsored research on lipids,

cholesterol and heart disease was that it had not produced many

answers—at least not many answers that the NHLBI was pleased

with.

The ongoing Framingham Study found that there was virtually no

difference in coronary heart disease " events " for individuals

with cholesterol levels between 205 mg/dL and 294 mg/dL—the vast

majority of the US population. Even for those with extremely high

cholesterol levels—up to almost 1200 mg/dL, the difference in CHD

events compared to those in the normal range was trivial.29 This did

not prevent Dr. Kannel, then Framingham Study Director, from

making claims about the Framingham results. " Total plasma

cholesterol " he said, " is a powerful predictor of death

related to CHD. "

It wasn't until more than a decade later

that the real findings at Framingham were published—without

fanfare—in the Archives of Internal Medicine, an obscure journal.

" In Framingham, Massachusetts, " admitted Dr. Castelli,

Kannel's successor " the more saturated fat one ate, the more

cholesterol one ate, the more calories one ate, the lower

people's serum cholesterol. . . we found that the people who ate

the most cholesterol, ate the most saturated fat, ate the most

calories weighed the least and were the most physically

active. " 30 NHLBI's Multiple Risk Factor Intervention Trial

(MRFIT) studied the relationship between heart disease and serum

cholesterol levels in 362,000 men and found that annual deaths from

CHD varied from slightly less than one per thousand at serum

cholesterol levels below 140 mg/dL, to about two per thousand for

serum cholesterol levels above 300 mg/dL, once again a trivial

difference. Dr. La of the American Heart Association

claimed that the curve for CHD deaths began to " inflect "

after 200 mg/dL, when in fact the " curve " was a very

gradually sloping straight line that could not be used to predict

whether serum cholesterol above certain levels posed a significantly

greater risk for heart disease. One unexpected MRFIT finding the

media did not report was that deaths from all causes—cancer,

heart disease, accidents, infectious disease, kidney failure,

etc.—were substantially greater for those men with cholesterol

levels below 160 mg/dL.31

LIPID RESEARCH CLINIC TRIAL

What was needed to resolve the validity of the lipid hypothesis once

and for all was a well-designed, long-term diet study that compared

coronary heart disease events in those on traditional foods with

those whose diets contained high levels of vegetable oils—but the

proposed Diet-Heart study designed to test just that had been

cancelled without fanfare years earlier. In view of the fact that

orthodox medical agencies were united in their promotion of

margarine and vegetable oils over animal foods containing

cholesterol and animal fats, it is surprising that the official

literature can cite only a handful of experiments indicating that

dietary cholesterol has " a major role in determining blood

cholesterol levels. " One of these was a study involving 70 male

prisoners directed by Fred Mattson32—the same Fred Mattson who

had pressured the American Heart Association into removing any

reference to hydrogenated fats from their diet-heart statement a

decade earlier. Funded in part by Procter and Gamble, the research

contained a number of serious flaws: selection of subjects for the

four groups studied was not randomized; the experiment inexcusably

eliminated " an equal number of subjects with the highest and

lowest cholesterol values; " twelve additional subjects dropped

out, leaving some of the groups too small to provide valid

conclusions; and statistical manipulation of the results was shoddy.

But the biggest flaw was that the subjects receiving cholesterol did

so in the form of reconstituted powder—a totally artificial diet.

Mattson's discussion did not even address the possibility that

the liquid formula diet he used might affect blood cholesterol

differently than would a whole foods diet when, in fact, many other

studies indicated that this is the case. The culprit, in fact, in

liquid protein diets appears to be oxidized cholesterol, formed

during the high-temperature drying process, which seems to initiate

the buildup of plaque in the arteries.33 Powdered milk containing

oxidized cholesterol is added to reduced fat milk—to give it

body—which the American public has accepted as a healthier choice

than whole milk. It was purified, oxidized cholesterol that

Kritchevsky and others used in their experiments on vegetarian

rabbits.

The NHLBI argued that a diet study using whole foods and involving

the whole population would be too difficult to design and too

expensive to carry out. But the NHLBI did have funds available to

sponsor the massive Lipid Research Clinics Coronary Primary

Prevention Trial in which all subjects were placed on a diet low in

cholesterol and saturated fat. Subjects were divided into two

groups, one of which took a cholesterol-lowering drug and the other

a placebo. Working behind the scenes, but playing a key role in both

the design and implementation of the trials, was Dr. Fred Mattson,

formerly of Procter and Gamble.

An interesting feature of the study was the fact that a good part of

the trial's one-hundred-and-fifty-million-dollar budget was

devoted to group sessions in which trained dieticians taught both

groups of study participants how to choose " heart-friendly "

foods—margarine, egg replacements, processed cheese, baked goods

made with vegetable shortenings, in short the vast array of

manufactured foods awaiting consumer acceptance. As both groups

received dietary indoctrination, study results could support no

claims about the relation of diet to heart disease. Nevertheless,

when the results were released, both the popular press and medical

journals portrayed the Lipid Research Clinics trials as the long-

sought proof that animal fats were the cause of heart disease.

Rarely mentioned in the press was the ominous fact that the group

taking the cholesterol-lowering drugs had an increase in deaths from

cancer, stroke, violence and suicide.34

LRC researchers claimed that the group taking the cholesterol-

lowering drug had a 17% reduction in the rate of CHD, with an

average cholesterol reduction of 8.5%. This allowed LRC trials

Director Basil Rifkind to claim that " for each 1% reduction in

cholesterol, we can expect a 2% reduction in CHD events. " The

statement was widely circulated even though it represented a

completely invalid representation of the data, especially in light

of the fact that when the lipid group at the University of land

analyzed the LRC data, they found no difference in CHD events

between the group taking the drug and those on the placebo.

A number of clinicians and statisticians participating in a 1984

Lipid Research Clinics Conference workshop, including Oliver

and Krommel, were highly critical of the manner in which the

LRC results had been tabulated and manipulated. The conference, in

fact, went very badly for the NHLBI, with critics of the lipid

hypothesis almost outnumbering supporters. One participant, Dr.

Beverly Teter of the University of land's lipid group, was

delighted with the state of affairs. " It's wonderful' "

she remarked to Basil Rifkind, study coordinator, " to finally

hear both sides of the debate. We need more meetings like this "

His reply was terse and sour: " No we don't. "