We customarily use stress as a variant or shortened form for distress. However, it can also refer to pleasurable stimuli or events, which Selye labeled “eustress”. Winning a race or an election can be just as stressful as losing, or even more so. Sudden death can follow news of the unexpected death of a loved one, but also occurs in healthy young brides overcome by joy and excitement on their wedding day. Thus, stress is not a useful word for scientists, because, it often cannot be adequately defined, much less measured. Nevertheless, it somehow best embraces the variegated phenomena that fall under the broad heading of mind-body relationships, and will not likely be replaced by any other word or phrase that is more meaningful.

The verb “cause”, presents similar semantic problems. Exactly what do we mean when we say that something causes something else. At the crux of this issue, is the tendency to confuse cause, as it relates to a specific diagnosis, rather than the various manifestations of that disorder. For example, it’s essential to have a very clear definition of coronary heart disease, and not to use this term to refer to associated symptoms and signs, such as angina, or elevated blood pressure and cholesterol levels. Clinical diagnoses such as hypertension, stroke, and heart attack, are not specific diseases but descriptions. Essential hypertension is simply the observation of a persistently elevated blood pressure that can have many different origins. Unless you can be certain of the source of hypertension in any given patient, you do not know its cause, and this also applies to coronary heart disease, cancer and other diseases.


While it is obvious that every disease must have a cause or possibly causes, it is essential to distinguish this sharply from contributing factors. Effective prevention and proper treatment of any disease depends upon identifying its specific causa vera , or “true cause”. The germ theory, Koch’s postulates, and the discovery of vitamin deficiency disorders contributed tremendously to our understanding of what a true cause really means. It’s impossible to develop tuberculosis without being infected by the tubercle bacillus, or to develop scurvy unless there is a lack of vitamin C. During the last century, it was generally believed that the cause of tuberculosis was close, unsanitary living conditions. Support for this came from the observation that when such situations were corrected, the incidence of tuberculosis was dramatically reduced. This belief persisted until Koch identified the tubercle bacillus as the causa vera, which was probably the first demonstration of a specific relationship between a microorganism and an infectious disease. For prevention and treatment of tuberculosis to be completely effective, it is necessary to eradicate the tubercle bacillus, rather than associated findings, signs and symptoms, such as unsanitary living conditions, fever, and hemoptysis. With respect to coronary heart disease, this also applies to hypertension, elevated blood cholesterol, cigarette smoking, and stress, which are difficult to prove as a causa vera since coronary disease can occur in their absence .

It is also very important to emphasize that the presence of the causa vera does not always guarantee that disease will result. Exposure to the tubercle bacillus or Hepatitis A virus does not always result in clinical illness, even when infection can be confirmed by immunologic testing. This is an important consideration for those interested in stress related disorders, since in many instances, the mechanism of action may be mediated by lowering host resistance. Sir William Osler believed that stress played such an important role in tuberculosis, that it was more important to know what went on in a man’s head than in his chest, to predict its clinical course. Active infectious bacteria and viruses can be cultured from many individuals who show no evidence of illness due to their presence. In one well-documented study, several hundred volunteers received nasal drops containing large doses of one of five respiratory viruses. Stress levels were evaluated by scores obtained from combining three standard measures that included severity of current negative emotions as well as life change events over the preceding year. Infection rates, as assessed by specific antiviral antibodies ranged from 75-90 percent, but clinical colds occurred in much less than half of these. The startling finding was that rates for both laboratory evidence of infection and clinical colds correlated precisely with the magnitude of psychological stress scores for each of the viruses. Would we be correct in concluding, therefore, that these colds were caused by stress?

We need to agree on what “cause” really signifies. If we say A causes B, does it mean that you can’t have B unless you have A? Does it mean that every time you have A, B will result? If we were to ask the general public or even physicians, what causes heart attacks, the answers would most likely be severe coronary atherosclerosis, high cholesterol levels, hypertension, cigarette smoking, strong family history, diabetes, and some might suggest stress or Type A behavior. However, heart attacks, can occur in the absence of all of these. Therefore. it is critical and crucial to make a sharp distinction between true causes, as opposed to associated findings, especially with respect to coronary heart disease.

Exactly what does coronary heart disease mean?

The term is often used interchangeably with, or to signify, angina, coronary insufficiency, myocardial infarction, coronary occlusive disease, sudden arrhythmogenic death, specific electrocardiographic alterations, findings on various imaging procedures, etc., etc. However, it’s possible to have electrocardiographic changes consistent with significant coronary ischemia without any signs or symptoms suggesting such a problem. It’s also possible to have extensive occlusive coronary atherosclerosis in the absence of any relevant signs, symptoms, or even electrocardiographic findings. Anginal pain may be due to coronary vasospasm without significant obstructive disease, coronary occlusion can occur without myocardial infarction, and myocardial infarction can occur without a coronary occlusion. Stress related sudden death due to ventricular fibrillation is often not associated with evidence of either acute coronary occlusion or myocardial infarction. However, all of the above are often referred to as evidence of “coronary heart disease” and/or are automatically assumed to be due to advanced coronary atherosclerosis.

Most often, coronary heart disease is used as a synonym for coronary atherosclerosis, but this is also incorrect. Is coronary atherosclerosis the same as atherosclerosis elsewhere in the body? Is atherosclerosis a distinct and specific disease? If so, then its true cause should be able to be identified as having been present in every individual or animal with atherosclerosis, as we could demonstrate for the tubercle bacillus and tuberculosis. In addition, the occlusive atherosclerotic lesions seen in familial hyperlipoproteinemia, or in animals fed high cholesterol diets are quite different from the atherosclerotic plaque commonly associated with coronary morbidity. They do not have the characteristic foam cells and other distinctive inflammatory stigmata. It has been suggested that in certain patients, various microorganisms can cause coronary heart disease by promoting the development of inflammatory atherosclerotic lesions. Indeed, some authorities view atherosclerosis as a chronic, low grade arterial infection which is aggravated by hypercholesterolemia and other risk factors. They suggest that there are probably multiple potential infectious pathogens and routes of transmission that might initiate atherosclerosis, including numerous viruses that produce clinically silent infections in animals. Pathways for transmission to humans might be via food, which could account for the parallel increases of meat consumption and mortality from coronary heart disease seen in the U.S. during the middle third of this century. Atherosclerotic plaque may result from infection with cytomegalovirus and other herpesviruses, based on antibody studies and transplant atherosclerosis findings. A Finnish study suggests that a strain of chlamydia encountered in common upper respiratory infections may also be involved. Researchers found that 60% of heart attack patients had antibodies to this strain of chlamydia, which is spread by droplet infection, in contrast to only 20% of a control group. Coronary heart disease is a very imprecise and inappropriate measure of the severity of coronary atherosclerosis. Another common and major error is coronary heart disease “risk factors” as causes of coronary atherosclerosis and heart disease rather than merely statistical associations and “risk markers”.

This also applies to stress, which can promote all the risk factors for CHD. Stress can contributes significantly to hypertension, elevated serum lipids, diabetes and cigarette smoking. An increased incidence of coronary morbidity and mortality ias associated with such psychosocial stresses as poverty, loneliness, rapid sociocultural change, crowding, and having little control over one’s life, especially in the workplace. Similarly, there is a wealth of literature linking stressful emotions such as depression, suppressed anger and hostility to various coronary events. And there can be little doubt that stress can precipitate angina, congestive failure and sudden death. There is also support from the salubrious cardioprotective benefits afforded by various stress reduction approaches, and the buffering benefits of a strong social support system, firm faith, and other examples of eustress. Thus, there is a great deal of evidence to support the contention that stress can contribute to coronary heart disease. However, evidence is quite different than proof, and contribute is quite different than cause. See Stress and Heart Disease, Type A Behavior and Heart Disease.

Does stress cause cancer is even more of a difficult question to answer because it is impossible to state when cancer begins as opposed to its clinical detection, which makes it impossible to establish a convincing temporal relationship. See Stress and Cancer. While there is little doubt that cigarette smoking can cause lung cancer, it often takes decades to develop to the time it is diagnosed, during which air pollution and other contributing factors may play a role, and malignancies of the lung can arise in non smokers not exposed to any of these. However, the same is not true for stress and Graves’ disease, where there is often a clear cut time relationship, especially in animals.

Can Stress Cause Coronary Heart Disease, Cancer – Or Anything Else?” Proving this will be impossible, until we can all agree on exactly what these terms mean. Unfortunately, we don’t know what “stress” is, it’s often not clear what “cause” means, or what “coronary heart disease” really refers to. At present, I suspect the safest answer is “perhaps”, since, like other risk factors, stress could play a contributory role in certain patients. At some future date, we may have the tools and skills to demonstrate this more conclusively to the satisfaction of the scientific community. Until then, all we can say is that the evidence for “stress” as a cause of coronary disease is as strong as any other proposed non heritable “risk factor”. More importantly, association should never be confused with causation. “Risk marker” would be a more appropriate description of well over 200 “risk factors” such as a deep earlobe crease, premature baldness, abdominal obesity and even smoking, hypertension and cholesterol, especially since their reduction or even eradication does not significantly reduce the incidence of coronary morbidity or mortality.