Open Heart (40 page)

“Sometimes nothing happens—even severe blockages cause at most only three out of every ten heart attacks—and sometimes the obstruction reaches a point where it interferes with the amount of blood flowing through the passageway of the artery. And when the heart is under stress because the oxygen it needs exceeds the ability of the blocked coronary artery to supply it—you're exerting yourself more than usual: swimming, walking fast, playing tennis—this
imbalance causes the symptoms of angina pectoris. But the most dangerous thing that can occur is for the atheroma to rupture into the blood vessel itself, causing a clot to form.

“This is the same kind of clot you get when your skin is cut—it's nature's way of healing us—and when these atheroma rupture, their surfaces are very sticky, and platelets bind to them. But the clot closes off the artery and the coronary artery becomes occluded. Suddenly, an area of heart muscle is starved of oxygen, and if this is not relieved quickly enough, that area of the heart dies—in other words, a heart attack occurs. If the area is large enough, you don't survive it.”

Rich talks about the experiment he and his research team performed, in collaboration with the local coroner's office and pathology researchers, in which they studied the hearts and arteries of people who had died in automobile accidents, and compared them with the hearts and arteries of people who had died of heart attacks.

“What we found,” he says, “was that the people who died of heart attacks had huge collections of macrophages—white blood cells—in their atheroma. More importantly, these macrophages secreted substances with the fancy term of
matrix metalloproteinases
, which are enzymes that digest proteins.

“What these enyzmes were doing was digesting away tissue that contained the fatty deposits, thus weakening the walls of the arteries, and making them susceptible to rupture. And we found something else that was fascinating—and totally unexpected. When we looked at other arteries in the patients whose atheroma had ruptured—at the arteries that had
not
ruptured—we found the same collection of lesions containing macrophages and metalloproteinases.

“Yet this was not the case in those people with atheroma where
no
rupture had occurred. This strongly suggests that the process is systemic—in other words, that the inflammatory process is not taking place only in the one susceptible atheroma.

“Add to this recent studies that have shown that people with elevated levels of C-reactive protein—which are nonspecific markers of inflammation circulating in the blood—are much more susceptible to heart attacks, and that high levels of C-reactive protein, even
in the absence of high cholesterol, are fairly reliable indicators of heart disease and of potential heart attacks, and you can see why infectious and inflammatory disease explanations make sense.
^*
In addition, it now seems that aspirin and the statins, which we thought were effective against coronary heart disease because they reduced clotting and/or lowered cholesterol, may owe a large part of their effectiveness to the fact that they reduce inflammation.

“All of which suggests that there is some kind of total body inflammatory process involved in triggering heart attacks, and that this process is triggered for reasons no one understands.”

My researches confirm much of what Rich tells me. Ewald's hypotheses about the infectious causes of heart disease, along with evidence that he and other evolutionary biologists present—that there are significant associations between atherosclerosis and both
Chlamydia pneumoniae
and gingivitis (
Porphyromonas gingivalis);
that treatment of bypass patients with antibiotics improves their recovery; and that an inflammatory hypothesis makes sense since it does not specify whether the atherosclerotic damage is caused directly by the infectious organism or indirectly through the organism's
stimulation of
an inflammatory response—these arguments are reiterated, reinforced, and expanded upon in an abundance of medical journal articles.

Here, for example, is the simple declarative sentence with which Dr. Russell Ross begins a January 1999 article in the
New England Journal of Medicine:
“Atherosclerosis is an inflammatory disease.”
^*

After taking us through a substantial body of evidence to support this proposition, Ross concludes that “atherosclerosis is clearly an inflammatory disease, and does not result simply from the accumulation of lipids.

“If we can selectively modify the harmful components of inflammation in the arteries and leave the protective aspects intact,” he adds, “we may create new avenues for the diagnosis and management of disease in the 50 percent of patients with cardiovascular disease who do not have hypercholesterolemia.”

“From a clinical standpoint, chronic inflammation, as evidenced by elevated levels of C-reactive protein, has been shown to be directly
associated with the development as well as progression of coronary artery disease,” Dr. Joseph Muhlestein writes in an article published a year later, in January 2000.
^*

After reviewing research from a sizable number of studies linking various infectious diseases to coronary artery disease, Muhlestein concludes that “the infectious agents with the most evidence to support a causative role in atherosclerosis” include
Chlamydia pneumoniae
, cytomegalovirus (a member of the herpesvirus genus),
Helicobacter pylori
(implicated in causing peptic ulcer disease), and several bacterial agents (including
Porphyromonas gingivalis
) associated with periodontal disease.

Although we may, thanks to the research that lends these propositions their plausibility, be getting closer to understanding the underlying cause or causes of atherosclerosis, what we do
not
know, Rich maintains, is still infinitely greater than what we do know.

He remains highly skeptical of anyone who claims to know, definitively, what can either cause or cure coronary heart disease, and outraged by the ways those claiming such knowledge go directly to the consumer with sales pitches for their products, as in the extensive campaigns to sell us cholesterol-lowering medications.

“I mean, why don't they just put the stuff in the well water and be done with it?” he asks at one point, and here again, everything I read lends credence to his skepticism.

Is Zocor really going to help me “live a longer healthier life”? Has Pravachol really been “proven to help prevent heart attacks in people with high cholesterol or heart disease”? Should I, like Dan Reeves, make taking Zocor “an important part of my game plan”—and will it not only lower my cholesterol by 29 to 45 percent, but enable me to “stay beautiful on the inside”?

In an article in
Science
(March 30, 2001), Gary Taubes, a three-time winner of the Science-in-Society Award from the National Association of Science Writers, reassesses much of what we know about the relation of a diet high in fat to cholesterol and heart disease, and demonstrates that “by the 1970s, each individual step of this chain from fat to cholesterol to heart disease had been demonstrated beyond reasonable doubt, but the veracity of the chain
as a whole
had never been proven” (italics in original).

Nor has it been proven since. In 1991, a study funded by the U.S. Surgeon General's Office determined that cutting fat consumption in the United States would delay forty-two thousand deaths each year. The key word, however, as Taubes points out, is
delay
.

“To be precise,” he explains, “a woman who might otherwise die at 65 could expect to live two extra weeks after a lifetime of avoiding saturated fat.
^*
If she lived to be 90, she could expect 10 additional weeks.”

The proposition that reducing fat consumption, whether by diet or drugs, prevents heart disease and leads to longer, healthier lives is, at best, inconclusive, and at worst, as many medical experts maintain, the result of an enormous, often greed-inspired hoax. Rich talks frequently (and is writing about) what he considers unethical collusion between doctors, hospitals, and pharmaceutical firms.
^*
(Corroborating what he has witnessed firsthand, an article in the January 2, 2002, issue of the
Journal of the American Medical Association
reports that nearly nine out of ten medical experts who write guidelines for treating conditions such as heart disease, depression, and diabetes have financial ties to the pharmaceutical industry, and that these ties are rarely if ever disclosed; moreover, approximately six out of every ten medical experts have financial ties to companies whose medications they either considered or recommended in the guidelines they wrote.)

Although more than 80 percent of the money spent on the promotion of prescription drugs is still directed to health-care professionals, annual spending on direct-to-consumer advertising for prescription drugs tripled between 1996 and 2000, when it went from 791 million dollars (9 percent of annual spending), to just under 2.5 billion dollars (16 percent).
^*

Taubes reviews not only the research concerning the relation of dietary fat to heart disease, but the history of the ways in which the general public, encouraged by drug companies, politicians, and the media, has come to accept as axiomatic what has never been proven.

Despite the existence of many trials that “showed no evidence that men who ate less fat lived longer or had fewer heart attacks,” Taubes cites
Time
magazine, for example, declaring, in its headline to a feature story (on the magazine's cover, below a plate of bacon
and eggs arranged so as to resemble a doleful face, “CHOLESTEROL: AND NOW THE BAD NEWS”)—“Sorry, It's True. Cholesterol Really Is a Killer.”
^*

“Snatching victory from the jaws of defeat of the verdict of the [cholesterol] trials,” James LeFanu, a London physician and author (a regular columnist for the London
Times
, and
Daily
and
Sunday Telegraph
), writes in an examination of the subject in his book,
The Rise and Fall of Modern Medicine
, “dozens of expert committee reports had persuaded most people that ‘Western food is the chief reason for our modern epidemic of heart disease.'
^*
This in turn had been the Trojan Horse by which millions had been prescribed cholesterol-lowering drugs.”

LeFanu subjects the claims of the pharmaceutical industry to close analysis—in one instance, when they assert that according to a “landmark study” there is “conclusive proof” that taking the drug cholestyramine reduces the chances of dying from a heart attack by 25 percent, he sorts through the data of a seven-year study used in support of such a claim.

“After seven years…thirty out of the 1,900 taking cholestyramine had had a fatal heart attack compared to thirty-eight of the similar number in the control group,” he informs us.
^*
“This indeed can be interpreted as ‘reducing the chances of dying from a heart attack by 25 percent…' But put another way, almost 2,000 men took cholestyramine for seven years to increase their chances of not having a heart attack by less than half of 1 percent. This seems a modest enough achievement, except that overall cholestyramine made no difference at all, as the total number of deaths in the ‘intervention' and ‘control' groups were exactly the same, with the modest reduction in heart disease mortality in those taking cholestyramine being balanced by an increased risk of death ‘from other causes.'”

“It is much easier to promote a drug on the grounds that it reduces the ‘risk of a heart attack by 25 percent,'” LeFanu observes, “than by pointing out that ruining one's meals with cholestyramine for seven years increases one's chances of not having a heart attack by 0.5 percent, at the price of chronic bowel symptoms, depression and increased risk of death from other causes.”

The enormous number of studies on the relation of dietary fat to
heart disease validate Rich's assertion: that while reducing cholesterol levels, especially LDL (the so-called bad cholesterol), for individuals who have already had heart disease, or are considered to be at high risk for heart disease, is probably wise, there is a distinct absence of evidence to persuade one that otherwise healthy individuals with normal or borderline cholesterol levels need to take what will, in most instances, become lifetime medications.

“The ideal way to treat atherosclerosis,” Rich says, “would be to give patients a pill that would be a medical roto-rooter and ream out the blocked arteries. But we don't have that pill, and we won't have it, if ever, for a good while. In the meantime, we have millions of people taking these medications because Dan Reeves or their doctors tell them to—and taking these meds is not like taking an antibiotic for an infection.

“You take an antibiotic for ten days to two weeks and the bug is killed and that's the end of it,” Rich goes on. “Yes, when you need these cholesterol meds, of course you should take them. But these are lifetime medications, remember, and every pill that has ever been manufactured by humankind has its own side effects, and nobody really knows what the effects of these medications will be in your body over the course of a lifetime.”

While Rich is exceptionally knowledgeable about the many useful technologies available for the treatment of heart disease (and is himself responsible for the early and ongoing development of several of these technologies, including nuclear cardiology, cardiac electrophysiology, angioplasty, and the use of calcium channel-blocker drugs to treat coronary artery spasm and hypertension), in recent years he has become more attuned to, and passionate about, the role that non-technological elements play in the healing process.

Increasingly, his life, and his work, have become informed by a range of activities—daily meditation, reading and study of Eastern thought and philosophy (especially, as with Arthur, the writings of the Dalai Lama), and his own writing—that explore experiences that cannot be fully understood or explained rationally.