Can Vitamin Deficiencies cause heart disease?
Would you believe vitamin deficiencies can cause cardiovascular
disease? This is what Dr. Kilmer McCully would have you believe and
what he has been trying to get the medical world to believe for the
last 36 years.
Finally the medical world is listening. Why wouldn’t they listen
before? Why are they listening now? And what made Kilmer McCully come
up with such an outlandish idea in the first place?
The Origin of the Homocysteine Theory
Forty-one years ago Kilmer McCully was a pathologist at
Massachusetts General Hospital in Boston and assistant professor of
pathology at Harvard Medical School.
At Massachusetts General in 1968, he learned of the case of a boy
with a rare genetic disease who died of a stroke at the age of 8. He
decided to investigate the pathology of the case because of the unusual
feature of death in childhood from a disease usually attributed to
aging. What he found were changes in the artery walls that looked very
similar to the arteriosclerosis, or hardening of the arteries, that he
had found in many of the elderly patients he saw during his residency.
The disease this child had was homocystinuria (pronounced
HO-mo-SIS-at-NURE-ee-a), a rare genetic disease affecting one in
200,000 Americans. It is a disease in which homocysteine
(HO-mo-SIS-teen), an amino acid that is a normal part of the body’s
chemistry, rises to astronomical levels because of an inherited enzyme
defect.
McCully believed that homocysteine was the cause of
arteriosclerosis in the disease of homocystinuria and that elevated
homocysteine can cause arteriosclerosis in people without
homocystinuria as well. But what could cause elevated homocysteine
levels in people who do not have genetic enzyme deficiencies? The
answer: vitamin deficiencies. The enzymes that rid the body of
homocysteine are activated by coenzymes. These coenzymes are vitamins –
vitamin B6, folic acid and vitamin B12.
If any of these vitamins are deficient or lacking, the enzymes will
not be able to function optimally even if there is no inherited enzyme
defect, and, as a consequence homocysteine will rise above normal
levels.
McCully reasoned that if severely high levels of homocysteine
resulting from a genetic defect could destroy a child’s arteries,
milder but more chronic elevations resulting from a vitamin deficient
diet could cause cardiovascular disease in adults.
The standard American diet is just such a vitamin B deficient diet.
This is the essence of the homocysteine theory, which McCully published
in 1969.
Reaction to the Homocysteine Theory
The vast majority of the medical community ignored it. Their
reasoning? What relevance could a rare genetic disease that causes the
death of one in 200,000 Americans have to a disease that causes the
death of one in two? And besides, everyone knew that the problem was
cholesterol, not some cockamamie amino acid that nobody had ever heard
of. McCully spent the next 10 years trying to prove his theory.
He injected rabbits with homocysteine and within weeks found
arteriosclerotic plaques in their coronary arteries. Researchers in
Japan repeated his experiment and confirmed it. Similar experiments
with baboons by other researchers yielded similar results. McCully also
did studies of the cells and tissues from children with homocystinuria
to find out how excess homocysteine can damage arteries and lead to the
formation of blood clots.
Nevertheless, the theory was not accepted.. And it is
understandable. After all, the idea of taking vitamins to prevent and
treat arteriosclerosis does sound farfetched. In fact, “crazy” was the
technical term used to describe it by one eminent expert in the
cholesterol field who was quoted in Time magazine during this period.
The director of the arteriosclerosis center at MIT attacked
McCully’s ideas as “errant nonsense” and “a hoax that is being
perpetrated on the public.” McCully lost grant funding, lost staffers
and eventually lost his job at Massachusetts General Hospital as well
as at Harvard Medical School. The two appointments go hand in hand, and
both formally ended in January 1979. He was given the explanation, “We
feel you haven’t proved your theory.”
The Breakthrough Study
In 1981, McCully succeeded in finding a job at the Veterans Affairs
Medical Center in Providence, RI, and there he continued pursuing his
theory. But he labored in obscurity – until 1992. In 1992, the
Physicians Health Study was published. This was a study whose subjects
were 15,000 doctors.
New research tests for measuring small amounts of homocysteine in
the blood had become available. These new tests made it possible for
the researchers to determine whether men with high homocysteine levels
at the start of the study were more likely to get heart attacks than
men with low homocysteine levels.
They were. Men with homocysteine levels in the top 5 percent of the
group (levels of 15 micromoles or higher) had more than three times the
heart attack risk as those in the bottom 90 percent, independent of
other risk factors. This study marked a turning point in the story of
the homocysteine theory for a number of reasons.
First, it was a “human” study. As McCully pointed out in his book,
The Homocysteine Revolution, “While studies with experimental animals,
cell cultures and biochemical pathways are of theoretical interest to
medical experts and investigators, only with successful human studies
do results begin to convince the skeptics.”
Second, it was the first prospective study in the field – the men
were healthy at the time the blood was drawn and some time in the
future developed heart disease.
Third, it was a study involving a large number of subjects (15,000)
over an extended period of time (five years) . And finally, it came out
of a prestigious and highly renowned institution, the Harvard School of
Public Health, a branch of the same institution that had fired McCully
13 years earlier for failing to prove his theory. I think if Kilmer
McCully had been Jackie Gleason, he would have said, “How sweet it is.”
Conclusive Studies
Since the Physicians Health Study, there has been an explosion of
studies on homocysteine, the overwhelming majority of them showing a
strong correlation between homocysteine and heart disease. In fact,
homocysteine is now considered by many scientists in the field to be as great a risk factor for heart disease smoking or high cholesterol.
However, none of these studies has proven a cause and effect
relationship between homocysteine and cardiovascular disease. To do
that requires a large clinical trial to see if lowering homocysteine
levels results in a lower rate of heart attacks and strokes. Such
trials are very expensive and have not been undertaken thus far because
there was and is no commercial incentive to study homocysteine.
The way to reduce it – modifying lifestyle and diet – are cheap
and not patentable. But evidence has reached such a critical mass that
there are now about 17 studies under was to determine the benefits of
lowering homocysteine levels. The studies are being financed by the
National Institutes of Health.
These studies should provide evidence for the effects of
homocysteine-lowering therapy on cardiovascular risk within a few
years. However, the circumstantial evidence is so strong that most
researchers in the field say it would be prudent not to wait until the
verdict is in before lowering homocysteine levels.
Find out if your level is too high and, if it is, how to lower it
by simple, natural means in next week’s article, “Can Three B Vitamins
A Day Keep A Heart Attack Away?”
Mary Lou Williams, M. Ed., is a lecturer and writer in the field of
nutrition. She welcomes inquiries. She can be reached at (239)
267-6480.