The Great Cholesterol Myth (17 page)

Basically, she wasn’t bought or influenced by or beholden to anyone in the heart disease–cholesterol–statin drug establishment. She had no preconceived ideas, either positive or negative, about what she’d find. Her research for the next few years was motivated primarily by two things: one, helping her husband get well, and two, her lifelong interest in biology and nutrition.

And let’s remember that we’re talking about someone whose ability to understand systems, theory, statistics, interpretation, experimental bias, confounding variables, and all the rest of the esoterica associated with evaluating studies is nothing short of world-class.

Here’s what Seneff told us about statin drugs when we contacted her for this book: “Statin drugs are toxic. I liken them to arsenic, which will slowly poison you over time.” (P.S.: Seneff’s husband terminated his statin therapy, and all of his symptoms disappeared. Needless to say, he switched to a different doctor.)

Seneff has become one of the most respected and outspoken critics of the cholesterol hypothesis, and she is quite vocal about her opposition to statin drugs, which she believes are the next medical tragedy waiting to happen.

Let’s be clear: Although Seneff and other independent researchers are pretty unequivocal in their negative appraisal of statin drugs, we are a little more moderate. (Just a little.) Neither of us, especially Steve, believes that statin drugs are all bad. As mentioned earlier, Steve still prescribes them very occasionally, in certain limited circumstances (to middle-aged men who have already had a heart attack and are at very high risk for another). Even Duane Graveline, M.D., perhaps the most outspoken critic of statins on the planet and author of
Lipitor: Thief of Memory
, lists low-dose statin therapy as one possible option for “high-risk” people.

Statin drugs do some good in some circumstances, but their benefits, and the circumstances in which they are appropriate, are much more limited than the pharmaceutical companies would have us believe. Further-more, any good they may accomplish has little to do with cholesterol lowering, as you will soon see.

Statin drugs are anti-inflammatory. They lower C-reactive protein (a protein in the blood that’s an excellent measure of systemic inflammation), and they decrease blood viscosity (meaning they make the blood flow more easily). Any of the benefits, however mild they are in reality and however overstated they are in promotional materials, are almost definitely related to these other two effects, not to the drugs’ fairly meaningless ability to lower cholesterol.

(In fact, when you finish reading this section, you may find that you agree with a growing number of health professionals who think that statin drugs would be even
more
effective if they
didn’t
lower cholesterol. But we digress.)

If you still doubt that the cholesterol-lowering effect of statins is the least important thing they do, put on your detective hat for a moment, and consider the following:

Prior to the introduction of statin drugs in the 1990s,
*
there were a number of studies done in which cholesterol was successfully lowered by other drugs, notably the class of drugs known as
fibrates
, the go-to treatment for high cholesterol prior to the near-universal switch to statins in the last decade of the twentieth century. These drugs actually lowered cholesterol quite well, thank you very much. If lowering cholesterol does in fact prevent heart attacks or strokes, then we should see a significant reduction in heart attacks and strokes anytime we successfully lower it, regardless of the particular drug (or diet) used to accomplish this.

But investigations of the cholesterol-lowering studies prior to the mainstream use of statin drugs showed quite the opposite. And there’s proof, all cataloged, collected, and assembled in one place, thanks to a man named Russell Smith.

Back in the late 1980s, Russell Smith, Ph.D., an American experimental psychologist with a strong background in physiology, math, and engineering, decided to write the most comprehensive and critical review of the diet–heart disease literature yet seen. Published in two volumes that spanned more than six hundred pages and contained three thousand references, it was titled
Diet, Blood Cholesterol, and Coronary Heart Disease: A Critical Review of the Literature
.

In the vast majority of studies reviewed, there was no difference in the number of deaths between the group that lowered its cholesterol and the group that didn’t.

Then in 1991, together with Edward Pinckney, M.D., an editor of four medical journals and former coeditor of the
Journal of the American Medical Association
, Smith published a summary of this massive work in a book called
The Cholesterol Conspiracy
.

Among many other things, Smith and Pinckney reviewed all of the cholesterol-lowering trials that had been done prior to 1991. The studies found that using drugs to lower cholesterol was quite effective—at lowering cholesterol. The problem was that they weren’t much good for anything else. If cholesterol lowering was in fact the holy grail of preventing heart disease and death, then we would expect the research to show a reduction in heart attacks, strokes, and deaths when cholesterol was effectively lowered, wouldn’t we?

Let’s see what Smith and Pinckney had to say about that:

“Drugs were used to lower blood cholesterol levels in twelve trials (i.e., studies). Eight of these trials were both randomized and blinded.
*
Of the eight that met this standard, total deaths in six trials were the same or greater in the treatment group than in the control group. For the remaining four trials (either nonrandomized or unblinded), there were no differences between the treatment group and the control group.”

Translated into clear English: In the vast majority of the studies reviewed, there was no difference in the number of deaths between the group that lowered its cholesterol and the group that didn’t. In fact, in a few cases, more people died in the group that lowered its cholesterol.

Okay, so much for ten out of those twelve trials—pretty dismal results. But what about the remaining two trials?

In these two trials, there were fewer deaths in the group treated with cholesterol-lowering drugs than in the control group. These two studies, accounting for only a sixth of the total number of drug studies conducted, the rest of which showed no benefit, were
exactly the ones the cholesterol establishment seized on as “proof” of the link between cholesterol and heart disease. “However,” reported Smith and Pinckney, “one of these trials was conducted by a pharmaceutical company, which evaluated its own cholesterol-lowering drug.
¹
The second trial involved an estrogen drug that produced more harm than good in three other trials.
²
Therefore, both of these trials are suspect.”

Scorecard: Out of twelve studies, ten showed no benefit; the two that did were both questionable.

Choosing one or two studies that show a positive result and burying the ones that don’t is a well-documented tactic of the pharmaceutical industry. It’s akin to finding two white checkers in a bucket of black ones and then holding up the white ones and claiming they’re proof that all checkers are white.

Back to the scorecard.

Smith and Pinckney now turned their attention to sixteen randomized and blinded studies that looked at the combined effect of drugs and diet on lowering cholesterol. “The total numbers of all-cause deaths in the treatment groups were the same as or greater, statistically speaking, than those in the control groups for fourteen of those trials,” they wrote. “The total numbers of coronary heart disease deaths in the treatment groups were the same as or greater than those in the control groups for fifteen of these trials. And the total number of nonfatal coronary heart disease events in the treatment groups were the same as those in the control groups for fifteen trials.”

Did your eyes just glaze over? No problem. Allow us to translate. If you define “benefit” as a lower amount of fatal or non-fatal heart attacks, a whopping fifteen out of sixteen studies showed exactly zero benefits from lowering cholesterol. Whoops.

The authors of this exhaustive review of the literature summed up their findings thusly:

“In effect, the clinical trial data overwhelmingly demonstrated no benefits of cholesterol-lowering for either coronary heart disease deaths, nonfatal coronary heart disease events, or all-cause deaths.”

So prior to the introduction of statin drugs, it was overwhelmingly clear that lowering cholesterol by itself did virtually nothing to prevent a single death or even to affect coronary heart disease in any meaningful way. Therefore, if any positive effects were to be seen in the studies using the new statin drugs (as opposed to the old cholesterol-lowering drugs), these beneficial effects couldn’t possibly be due to lowered cholesterol.

As Smith and Pinckney conclusively demonstrate, all thirty or so studies completed prior to 1990 showed that you could lower cholesterol to your heart’s content without adding a single day to your life. John Abramson, M.D., a professor of medicine at Harvard Medical School and the author of
Overdosed America
, recently summed up the problem perfectly in the medical journal
The Lancet
: “You can lower cholesterol with a drug, yet provide no health benefits whatsoever. And dying with corrected cholesterol is not a successful outcome.”

Let’s review: Lowering cholesterol, as the thirty-some odd studies prior to 1990 showed, accomplishes nothing (except, of course, lowering cholesterol). If
there’s a benefit to statin drugs at all, that benefit has to be coming from something
other
than their ability to lower cholesterol.

Now, one might reasonably argue,
so what
? Suppose you’re right that the ability of statin drugs to lower cholesterol is irrelevant, but suppose they do a lot of good anyway? Why not just use them for their other benefits?

Good question. But to answer it, we need to know two things: One, just how great a benefit do we actually
see
with statin drugs? And two, what are the side effects?

In simple terms, we’d want to know: What are we risking, and what are we getting?

Only when we know the answers to these two questions can we make a smart decision about whether to go on a statin drug (or any drug, for that matter). We want to know what the risks are so we can calculate whether those risks are worth taking, which means we have to know exactly what we’re likely to gain. For example, if your risk in taking a drug was a one in one hundred chance of getting a mild tummy ache, but the potential benefit was lowering your risk of cancer by 25 percent, you would probably take that drug in a heartbeat. Why? Because the potential benefit is so great and the potential downside is so small. On the other hand, if the risk of taking a drug was a 40 percent chance of hair loss, and the potential benefit was shortening the length of a cold by a few hours, you might decide that the benefit is way too insignificant to justify even the possibility of going bald!

With that in mind, let’s take a look at the side of statin drugs you probably don’t know about. (No surprise here—this is not exactly the data that manufacturers of these drugs are dying to publicize.)