© 2000, Lauren A. Colby. Version 2.5
Chapter 12: Smoking and Heart Attacks
For many years, anti-smoking activists have insisted that smoking "causes" heart attacks. In truth, there is no scientific evidence to support such a claim.
As early as the 1950's government scientists began conducting studies in Framingham, MA., to assess the "risk factors" which lead to heart attacks and stroke. Early on, they identified three such risk factors: Smoking, high blood pressure and cholesterol. As the years have gone by, however, other researchers have identified still other risk factors. Taking estrogen pills has been identified as a risk factor in women 36 . Male pattern baldness has been identified as a risk factor in men 37 . Vitamin and mineral deficiencies have been blamed for heart attacks, as well as eating fatty foods and drinking too much alcohol.
There are other obvious risk factors: 100% of all heart attack victims breathed air during the time prior to their heart attack. 90% drove automobiles. 95% paid income taxes.
I am, of course, citing these "other obvious risk factors" in jest, to illustrate the absurdity of "risk factor" analysis. If everything is a risk factor, then nothing is a risk factor, because there is no conceivable way of determining whether (a) a particular heart attack or stroke was caused by one of the risk factors and (b) if it was caused by a risk factor, which one.
Risk factor studies are, by their very nature, biased by the opinions of the people who conduct such studies. That's because the researchers must select the factors that they consider risky, before the study ever begins.
Consider this: It is a known fact that exercise sometimes causes heart attacks. I say "known fact" advisedly, because there are many newspaper accounts of athletes and others, dying from heart attacks brought on by exercise. A few years ago, my Congressman, Goodloe Byron, dropped dead of a heart attack while jogging on the C&O Canal. He'd been warned by his doctor that he had a weak heart and should not over-exercise, but he disregarded the doctor's advice. Also, a few years ago, Nelson Rockefeller suffered a fatal heart attack rhile exercising in bed in the company of two nubile young women.
Yet, nobody has ever conducted a study to determine how many heart attacks are caused by exercise. Why not? The answer, of course, lies in the conventional wisdom that "exercise is good for you". Researchers don't conduct studies to link exercise with disease because everybody knows that exercise doesn't cause disease, so there's no point in conducting such a study.
On August 18, 1995, the Wall Street Journal reported on an epidemiological study in England by anti-smoking activist Richard Peto, which claimed that in people aged 30 to 49, smokers have a heart attack risk 2.4 times that of non smokers. For that study to be meaningful, however, Peto would have had to also study a multitude of other risk factors. Smokers tend to be from the lower socio-economic strata of society, and people with low SES tend to be fat and work at hard manual labor (the "exercise factor", again). They may consume too much alcohol and eat diets deficient in the vitamins and minerals which some experts claim are protective against heart disease.
Peto selected smoking as the risk factor to be studied because he believed smoking causes heart attacks. But he might just as well have selected SES, obesity, alcohol consumption, cholesterol, estrogen consumption, diet, baldness, ear creases, etc. Even if he'd studied all of these risk factors, he might still miss the right one, because the real cause of heart attacks may be something that nobody's even remotely considered. After all, we now know that most stomach ulcers are caused by bacteria and can be treated with antibiotics; yet, until just a few years ago, every responsible physician in the world would have dismissed such a notion as total nonsense.
Just recently, researchers have suggested that the true cause of heart attacks may be surplus iron in victim's diets. This iron, they suggest, oxidizes cholesterol and deposits harmful plaque deposits on the artery walls 38
In earlier chapters, I discussed the flaws in the 1950's and 60's studies that attempted to link smoking to cancer and other diseases. Not the least of these flaws was the self-selection of the participants and the failure to establish adequate controls. Take, for example, Doll's famous (or infamous) study of British doctors. In 1951, Doll wrote to 59,600 physicians in the United Kingdom, asking them to fill out questionnaires and become part of his study group, but only 40,70l of the physicians responded 39 . Thus, the participants selected themselves. Furthermore, all of the participants were from the same highly select, elite profession, i.e., medicine. There was no control group, representing the population at large.
In the mid 1970's, some researchers decided to do a study on the effects of smoking cessation as well as other "healthy behaviors". They sought to avoid the flaws that had plagued other epidemiological studies and, to that end, they sought to study groups that were not self selected, but rather were selected, at least in part, on a random basis. The study group was called the "Multiple Risk Factor Intervention Trial (MRFIT) Research Group".
12,866 high risk men, aged 35 to 57 years, were randomly assigned to one of two groups. One group was treated to a special intervention program, consisting of drug-care treatment for hypertension, counseling to stop cigarette smoking, and dietary advice for lowering blood cholesterol (I will call this the "special intervention" or"SI group"). The other group, which I will call the "control group", was left to smoke, eat, and have high blood pressure, without intervention.
The MRFIT Research Group rendered its first report in 1982, reflecting an average follow-up time of 7 years. To the disappointment of the researchers, there was no statistically significant difference between the mortality in the SI group, from that in the control group - despite the fact that, as a result of the nagging, the participants in the SI group significantly "improved" their health habits, i.e., stopped smoking, and lowered their blood pressure and cholesterol levels 40
In 1990, the MRFIT group produced another report, reflecting 10.5 years of research, using the same two groups. This time, the results appeared to show a statistically significant reduction in coronary heart disease (CHD) in the intervention group, but this was attributed not to smoking cessation, but rather to reduction in hypertension 41 . It turned out that there were more deaths from ischemic heart disease in the SI group than in the control group (96 vs. 86 deaths). Moreover, there were more deaths from cancer of the respiratory and intrathoracic organs in the SI group than in the control group (66 vs. 55) 42.
It is amusing to read the explanations of the health establishment for the discrepancies reflected in the MRFIT study. One group of writers tried to explain the higher incidence of lung cancer in the SI group by pointing out that all of the deaths from primary lung cancer reflected in the 10.5 year trial involved smokers or ex-smokers; there were no primary lung cancer deaths among "never-smokers" 43 . These writers apparently forgot that the participants in both groups were selected because they were adjudged to be at "high risk", i.e., smokers and ex smokers. We could hardly expect to find any lung cancer deaths involving "never smokers" in a group that didn't have any "never smokers"!
The MRFIT study is not the only study to use intervention to try to reduce coronary heart disease (CHD) and cancer, by nagging people to improve their health habits. The World Health Organization conducted a massive study. It involved 63,733 men aged 49 to 59 in 44 factories in Britain, Belgium, Italy, Poland and Spain. The authors estimated that, as a result of smoking cessation and other improved health measures, they managed to reduce the risk of heart attack by 14% in the group as a whole and 24% in a high risk sub-group. Unfortunately, there was no equivalent reduction in the number of heart attacks 44 .
In 1982, Rose, Hamilton, Colvell and Shipley reported on a 10 year follow up study of middle aged smokers, thought to be at high risk for cardiorespiratory disease. The smokers were divided into two groups: a control group who were allowed to continue to smoke and an intervention group (a "SI" group) who were encouraged to give up smoking. The intervention was very successful. In fact, in the SI group of 714 men, the naggers succeeded in reducing the rate of cigarette consumption by half.
As in other studies, however, the results were negative. In fact, 17.2% of the 714 men in the intervention group died during the study period, as compared to 17.5% of the 731 men in the control group - an insignificant difference. There was also no significant difference in lung cancer. There were 25 cases in the control group and 22 in the intervention group. Interestingly, however, there was a statistically significantly greater rate of "all other cancers" in the intervention group than in the control group45 So nagging people to quit smoking - even successful nagging doesn't reduce the rate of either cancer or heart attack.
Perhaps the final word on smoking and heart attacks came in 1998, when the results of a massive study, financed by the World Health Organization, were released. The Monica Study, which assessed 21 countries over ten years, found the incidence of heart disease dropping across Europe, Australia, and North America. But scientists could find no statistical correlation between the reduction and changes in obesity, smoking, blood pressure or cholesterol levels. They didn't look at antibiotic use but maybe they should have, because at least one recent study showed that a course of treatment with antibiotics appears to protect against heart attacks, suggesting that, like stomach ulcers, they may be caused by bacteria.