Stress and Heart Disease
The relationship between stress, heart disease and sudden death has been recognized since antiquity. The incidence of heartattacks and sudden death have been shown to increase significantly following the acute stress of natural disasters like hurricanes, earthquakes and tsunamis and as a consequence of any severe stressor that evokes “fight or flight’ responses. Coronary heart disease is also much more common in individuals subjected to chronic stress and recent research has focused on how to identify and prevent this growing problem, particularly with respect to job stress. In many instances, we create our own stress that contributes to coronary disease by smoking and other faulty lifestyles or because of dangerous traits like excess anger, hostility, aggressiveness, time urgency, inappropriate competitiveness and preoccupation with work. These are characteristic of Type A coronary prone behavior, now recognized to be as significant a risk factor for heart attacks and coronary events as cigarette consumption, elevated cholesterol and blood pressure. While Type A behavior can also increase the likelihood of these standard risk factors, its strong correlation with coronary heart disease persists even when these influences have been excluded. However, there is considerable confusion about how to diagnose and measure Type A behavior and numerous misconceptions about which components are the most as indicated in the Interview with Dr. Ray Rosenman, one of the co-authors of the Type A behavior concept. The following discussion is designed to clarify these and other aspects of the role of emotions and behavior in heart disease and how this may relate to the explosive increase in job stress. References have also been provided to obtain additional details on items that may be of special interest.
The appreciation that different emotions could have powerful influences on the heart and the recognition of some intimate but poorly understood mind-heart connection is hardly new. Aristotle and Virgil actually taught that the heart rather than the brain was the seat of the mind and soul and similar beliefs can be found in ancient Hindu scriptures and other Eastern philosophies. Some 2000 years ago, the Roman physician Celsus unwittingly acknowledged this mind-heart relationship by noting that “fear and anger, and any other state of the mind may often be apt to excite the pulse.” Our earliest uses of the word heart clearly indicate its conceptualization as the seat of one’s innermost feelings, temperament, or character. Broken-hearted, heartache, take to heart, eat your heart out, heart of gold, heart of stone, stouthearted, are just a few of the words and phrases we still use that vividly symbolize such beliefs.
William Harvey, who discovered that the circulation of the blood around the body through vessels was due to the mechanical action of the heart also recognized that the heart was more than a mere pump. As he wrote in 1628, “every affection of the mind that is attended either with pain or pleasure, hope or fear, is the cause of an agitation whose influence extends to the heart.”(Harvey, 1628) During the 18th century, John Hunter, who elevated surgery from a mechanical trade to an experimental science, suffered from angina, and being a keen observer complained, “my life is in the hands of any rascal who chooses to annoy and tease me.” He turned out to be somewhat of a prophet, since it was a heated argument with a colleague that precipitated his sudden death from a heart attack. (Home, 1796) Napoleon’s favorite physician, Corvisart, wrote that heart disease was due to “the passions of the mind”, among which he included anger, madness, fear, jealousy, terror, love, despair, joy, avarice, stupidity, and ambition.
With respect to personality and Type A behavioral traits, Von Düsch, a 19th century German physician, first noted that excessive involvement in work appeared to be the hallmark of people who died from heart attacks. (Von Düsch, 1868) He did not imply that job stress was the culprit, but rather that such individuals seemed to be preoccupied with their work and had few outside interests. Over 100 years ago, Sir William Osler, an astute clinician, succinctly described the coronary-prone individual as a “keen, and ambitious man, the indicator of whose engines are set at ‘full speed ahead”. (Osler, 1892) He later wrote that he could make the presumptive diagnosis of angina based on the appearance, demeanor and mannerisms of the patient in the waiting room and how he entered the consultation room. (Osler, 1910) In the 1930s, the Menningers suggested that coronary heart patients tended to be very aggressive. (Menninger & Menninger, 1936) Flanders Dunbar, who introduced the term “psychosomatic” into American medicine, characterized the coronary prone individual as being authoritarian with an intense drive to achieve unrealistic goals. (Dunbar, 1943) Kemple also emphasized fierce ambition and a compulsive striving to achieve power and prestige. (Kemple, 1945) A half century ago, Stewart Wolf described what he called the “Sisyphus” reaction”. (Wolf, 1955) In Greek mythology, Sisyphus, the king of Corinth, was doomed by the gods to a life of constant struggle by being condemned to roll a huge marble bolder up a hill, which, as soon as it reached the top, always rolled down again. Wolf characterized people who were coronary prone as constantly striving against real but often self-imposed challenges, and even if successful, not being able to relax or enjoy the satisfaction of achievement.
In 1959, a paper by Meyer (Mike) Friedman and Ray Rosenman appeared in the Journal of the American Medical Association entitled “Association of specific overt behavior patterns with blood and cardiovascular findings: Blood cholesterol level, blood clotting time, incidence of arcus senilis and clinical coronary artery disease.” (Friedman & Rosenman, 1959) The subtitle linking specific behavioral traits with things like blood cholesterol, clotting time, arcus senilis and coronary disease that had no apparent relationship to each other must have seemed strange to many readers. Neither of these two cardiologists had any expertise in psychology, which may have been fortuitous, since they had no preconceived notions. What they did have was an unusual combination of curiosity, diagnostic acumen and a bio-psychosocial approach to the patient as a person, rather than someone to be treated in a cookbook fashion based on laboratory tests, symptoms or signs.
As noted, psychiatrists and others interested in psychosomatic disorders had previously described certain personality characteristics in heart attack patients. However, it was not possible to prove that these had any causal relationship since such idiosyncrasies could have resulted from the illness rather than vice versa. Friedman and Rosenman were the first to explain why specific behaviors could cause heart attacks and contribute to coronary artery disease. The term “Type A” was not mentioned in this initial paper but emerged the following year in an article describing how this type of “overt pattern behavior A” could be detected by a “new psycho-physiological procedure” (Friedman& Rosenman, 1960) Rosenman was subsequently able to show the predictive value of this technique so that coronary prone patients could be identified and hopefully treated to prevent future problems. (Rosenman et al. 1964).
At the time, animal studies had led to the widespread assumption that heart attacks were due to occlusion of a coronary artery by atherosclerotic deposits resulting from elevated blood cholesterol levels. This, in turn, was primarily the consequence of increased fat and cholesterol intake. Support for this was reinforced by research showing that the significant variation in mortality rates from coronary heart disease in different countries showed a clear correlation with fat consumption. The greater the amount of saturated fat and cholesterol in the average diet the higher the blood cholesterol and death rate from heart disease in that country. However, Friedman and Rosenman could not confirm this close relationship with serum cholesterol and high fat diet in their heart attack patients and looked for other possible contributing factors. They were intrigued by the observation that two-thirds of the heart attacks in the United States occurred in men, while in Mexico the incidence was equal between men and women. The same equal split appeared to exist in southern Italy but not in northern Italy, where the ratio was four men to one woman. This disparity was obviously not due to any difference in diet or other environmental factor, and on further analysis appeared to be related more to social, cultural, and behavioral attitudes that might best come under the heading of “maleness.”
Such individuals exhibited certain characteristic activity patterns, including.
- Self-imposed standards that are often unrealistically ambitious and pursued in an inflexible fashion. Associated with this are a need to maintain productivity in order to be respected, a sense of guilt while on vacation or relaxing, an unrelenting urge for recognition or power, and a competitive attitude that often creates challenges even when none exist.
- Certain thought and activity styles characterized by persistent vigilance and impulsiveness, usually resulting in the pursuit of several lines of thought or action simultaneously.
- Hyperactive responsiveness often manifested by a tendency to interrupt or finish a sentence in conversation, usually in dramatic fashion, by varying the speech, volume, and/or pitch, or by alternating rapid bursts of words with long pauses of hesitation for emphasis, indicating intensive thought. Type A persons often nod or mutter agreement or use short bursts of laughter to obliquely indicate to the speaker that the point being made has already been anticipated so that they can take over.
- Unsatisfactory interpersonal relationships due to the fact that Type As are usually self-centered, poor listeners, often have an attitude of bravado about their own superiority, and are much more easily angered, frustrated, or hostile if their wishes are not respected or their goals are not achieved.
- Increased muscular activity in the form of gestures, motions, and facial activities such as grimaces, gritting and grinding of the teeth, or tensing jaw muscles. Often there is frequent clenching of the fist or perhaps pounding with a fist to emphasize a point. Fidgeting, tapping the feet, leg shaking, or playing with a pencil in some rhythmic fashion are also common.
- Irregular or unusual breathing patterns with frequent sighing, produced by inhaling more air than needed while speaking and then releasing it during the middle or end of a sentence for emphasis.
It was also noted that coronary prone patients tend to be very competitive and often overly aggressive. They are usually in a hurry and consequently eat, talk, walk and do most other activities at a more rapid pace. Type A’s are generally more concerned with the quantity rather than the quality of their work, try to do too many things at once, are frequently preoccupied with what they are going to do next, and tend to have few interests outside their work. (Rosch 1983a).
How the Type A coronary prone behavior hypothesis evolved is a fascinating story, especially since it began because of an interest in cholesterol metabolism rather personality characteristics. As Ray Rosenman explained to me in a recent interview (Rosch, 2004),
“Mike and I were partners in our San Francisco clinical practice across the street from Mount Zion Hospital and Medical Center. Our Harold Brunn Institute for Cardiovascular Research building adjoined the hospital and following early hospital rounds we spent full mornings in the research lab and afternoons in the office. By 1950, although fat and cholesterol had long been fed to rabbits to produce vascular lesions, little was known about where plasma cholesterol came from or how it was metabolized. We also noted that this type of vascular damage was quite different from that seen in patients with coronary artery disease. We obtained Public Health Service and other grants to begin animal studies and Mike was able to solve many fundamental aspects of cholesterol metabolism. I was later able to delineate the mechanisms underlying low and high plasma cholesterol respectivelyi in hypothyroidism and hyperthyroidism and what caused elevated lipids in patients with nephrosis. Around 1952, because of our growing interest in cholesterol, we obtained blood samples from private patients at every visit for (no-cost) accurate analyses at our research lab. We soon realized that that there were surprising fluctuations in their cholesterol levels that were unrelated to diet or weight, and had little relationship to subsequent coronary events.
We subsequently recognized and reported serious errors and omissions in papers by Keys and others about the contribution of diet to plasma cholesterol. The prevailing dogma, which still persists, was that coronary heart disease was due to elevated cholesterol, which in turn resulted from increased dietary fat intake. Our own and other data that Keys had ignored in reaching his conclusions did not support this and reinforced our belief that socioeconomic influences played a more important role in the increased incidence of coronary disease as well as gender differences.ii
A discerning secretary in our office practice told us that in contrast to our other patients, those with coronary disease were rarely late for appointments and preferred to sit in hard-upholstered chairs rather than softer ones or sofas. These chairs also had to be reupholstered far more often than others because the front edges quickly became worn out. They looked at their watches frequently and acted impatient when they had to wait, usually sat on the edges of waiting room chairs and tended to leap up when called to be examined. Her astute observations significantly reinforced our own awareness of similar behaviors in our coronary patients, then mainly males, that you summarized so well over two decades ago.” (Rosch 1983 a)
Ray also told me that when he asked patients about what they thought had caused their heart problems diet or cholesterol was hardly ever mentioned. Occupational pressures and other sociocultural stresses headed the list. Some spouses had spontaneously volunteered the opinion that their husband’s heart attack was directly due to excessive involvement in work related activities. When Rosenman and Friedman subsequently asked the wives, relatives, friends and co-workers of heart attack patients to list possible contributing factors, they were surprised at how often their assessment similarly ranked job stress right at the top. The cluster of behaviors and activity patterns previously described that also emerged from these sources was far more common in males than female. It was also was evident that the current marked increased incidence of coronary disease had occurred mainly in men without any significant change in their diet, increased prevalence of diabetes, hypertension or other risk factors. Even when combined, the standard Framingham coronary risk factors of smoking, hypertension and cholesterol accounted for only about one third of coronary disease patients in prospective studies. It became increasingly clear that these risk factors were merely markers that might predict coronary events but did not cause them. As one authority noted in an extensive review,
“The best combinations of the standard risk factors fail to identify most new cases of coronary disease . . .. And, whereas simultaneous presence of two or more risk factors is associated with extremely high risk of coronary disease, such situations only predict a small minority of cases . . . . . A broad array of recent research studies point with ever increasing certainty to the position that certain psychological, social and behavior conditions do put persons at higher risk of clinically manifest coronary disease.” (Jenkins 1971)
For example, despite the fact that standard risk factor levels were the same, there were striking geographic differences in the prevalence and incidence of coronary disease in diverse populations in Northern vs. Southern Europe and the U.S. vs. Mexico. These disparities were not due to any dietary differences and on closer analysis, seemed related more to what might be viewed as a “macho” attitude and personality. I was curious as to why it was decided to label this kind of behavior as “Type A” and Ray explained,
“While we were doing prevalence studies in male and female subjects we realized it was necessary to do a prospective study. (Rosenman & Friedman 1961) I submitted a grant proposal that was twice rejected, and then successfully modified by a suggestion from the Public Health Service Director that we term the two behavior types as ‘Type A and Type B’. After a site visit the grant was approved for two years. The methodology of the Western Collaborative Group Study, including the Structured Interview (SI) for assessing behavior patterns was described in my first follow-up paper. ( Rosenman, Friedman, Straus et al. 1966) Later site visits led to grant extensions for long-term follow-up, largely due to the efforts of the remarkable Dr. Stewart Wolf. We became good friends many years later through you, your annual Congress and other activities of the American Institute of Stress.”
The 1974 best seller Type A Behavior And Your Heart (Friedman and Rosenman 1974) stimulated studies by others and Type A soon became part of vernacular speech. The significant contribution of Type A behavior to coronary heart disease (CHD) was subsequently acknowledged by a committee of authorities assembled by the National Institutes of Health (The Review Panel 1981), who noted,
The Review Panel accepts the available body of scientific evidence as demonstrating that Type A behavior . . . is associated with an increased risk of clinically apparent CHD in employed, middle-aged U.S. citizens. This increased risk is greater than that imposed by age, elevated levels of systolic blood pressure, serum cholesterol, and smoking and appears to be of the same order of magnitude as the relative risk associated with the latter three of these other factors [p.1200]
However, the initial support and enthusiasm waned following several studies that failed to confirm the opinion of the NIH expert panel. One problem was that like stress, Type A meant different things to different people. More importantly, researchers also used different assessment or measurement methods so it is not surprising that they reached conflicting conclusions.
It is evident from their initial publications that Friedman and Rosenman were careful to emphasize that Type A was an “overt behavior pattern”. What they meant by this were observable traits and characteristics that could be readily detected by others, such as the vocal stylistics, breathing patterns, facial grimaces, body movements, hyperresponsiveness and accelerated pace of activities previously described. In their extensive study of employees of several large Western corporations, Rosenman and colleagues were able to predict susceptibility to coronary disease by behavioral characteristics such as a tense, alert and confident appearance; strong voice, clipped, rapid and emphatic speech, laconic answers; evidences of hostility, aggressiveness and impatience, and frequent sighing during questioning. As they noted, (Rosenman, Friedman, Straus et al 1964):
Before and during the personal interview, the following observations upon each subject were made and recorded by the interviewer. (1) Degree of mental and emotional alertness (minimal, average, extreme), (2) Speed of locomotion (minimal, average, extreme), (3) Body restlessness (none, average, extreme), (4) Facial grimaces (scowls, teeth-clenching and tic in which teeth are clenched and masseter muscles are tensed, (5) Hand movements (fist-clenching, gestures made with extraordinary vigor, e.g. desk-pounding). [p.122]
The actual responses to the questions were not particularly important since the major purpose of the interview was to elicit and systematically observe the stress-related body language and speech. In clinical practice, accurate assessment of Type A behavior requires a structured personal interview by a trained investigator using standardized challenges to elicit these tell tale characteristics. For example, one such challenge might be conducted as follows:
The investigator begins the interview by asking the following question in a deliberate and painfully slow, monotonous manner. “Mr. Smith, (two second pause), most people, when they go to work during the week – that is, Monday through Friday-, get up early (two second pause), – say around 6:30 to 7 AM. That is probably because it necessary to provide enough time for them to shower, brush their teeth, (two second pause) and so forth, get dressed, have something to eat, and then they travel by car, bus or train so they can get to work by a certain time (two second pause), which is often between 8:30 and 9 AM. Now, in your case* (three second pause), what time do you usually get up (two second pause) during the week, that is Monday through Friday? How do you travel to work and what time do you usually get there? Unknown to the subject, the interviewer starts a stopwatch as noted by the asterisk above after asking ” Now in your case”. A flaming Type A would interrupt almost immediately before the question was finished to quickly explain his usual daily routine. In contrast, a Type B would listen to the entire recitation, reflect for a few moments, and then slowly respond with something like “Well, on Mondays, I tend to get up at 6 or a little later but on other days it is usually closer to 7 ” and continue on with a leisurely narration of possible variations on subsequent weekday habits.
Again, the interviewer is not as interested in the content of the response as much as the manner in which it is conveyed and how the subject acts during the interview with respect to facial expressions, gestures, evidence of impatience, time urgency, and other typical Type A traits. Each of these has a certain value and is rated as to severity to obtain a final assessment. Interviews are videotaped so that several reviewers can carefully review the responses and reach agreement on the significance of each component. These Type A characteristics have been described in detail to emphasize that this complex behavioral pattern can only be accurately assessed by personal observation of the subject by an investigator who has been trained to elicit and evaluate typical responses. Type A behavior is almost impossible to detect in someone who is very sick, bored, depressed, or frightened, such as in a patient recently hospitalized for a heart attack or some other serious medical condition. Reliable ratings therefore require considerable expertise, making large-scale studies quite time consuming and costly.
As a consequence, a variety of questionnaires have been devised to detect such aspects of Type A behavior as competitiveness, ambition, impatience, hostility, preoccupation with work, or a constant sense of time urgency. The Thurstone Temperament Survey’s Activity Schedule and Gough Adjective Check List measure only selective Type A behaviors. Others like the Jenkins Activity Survey, Framingham Type A, Vickers and Bortner Scales were designed to duplicate the structured interview. However self-reports fail to capture the stylistics and psychomotor behaviors that are essential to the construct of Type A and its assessment. Self-report questionnaires were rarely validated by those who used them in so many published Type A studies, which also led to considerable confusion in this field. Such questionnaires assess different behavioral characteristics and the subject’s perception of attitudes, attributes, and activities and show poor correlation among themselves or with the results of a properly conducted structured interview. The most commonly used instrument, the Jenkins Activity Survey, detects three main behavioral syndromes: (1) hard-driving temperament, (2) job involvement, and (3) speed and impatience. (Jenkins 1965) Although the three scores derived correlate with the total evaluation, they are not necessarily related to one another, and the overall accuracy is only about 70% when compared with a structured personal interview. (Jenkins, Rosenman, Zyzanski 1974) It should be emphasized in evaluating any self-administered questionnaire that Type A individuals are often unaware of many of their behavioral patterns or will deny them. No single Type A individual should be expected to exhibit all of the above characteristics, and conversely, some Type A characteristics are often found in Type B’s. Contrary to popular opinion, there is no rating scale for Type B behavior or definition other than the relative absence of Type A traits.
As our understanding and ability to measure Type A improves, it is possible that certain components such as time urgency, latent hostility, aggressiveness, or authoritarianism may be found to have a greater predictive significance for coronary heart disease. In particular, it has been proposed that “hostility” correlates best with coronary disease. (Williams 1984) This conclusion is based on responses to the Minnesota Multiphasic Personality Inventory (MMPI), a 566-item questionnaire developed in 1937 that rapidly became the gold standard for psychological testing of hundreds of thousands of college students and prospective employees. For example, by analyzing responses to various MMPI questions that comprised a subscale, one could screen for tendencies to such undesirable things as schizophrenia, depression, paranoia and introversion. About 50 years ago, two psychologists, Cook and Medley, selected 50 items to group into what they called a hostility (Ho) subscale that could differentiate between teachers who were most likely to have good or poor rapport with students. Redford and colleagues showed that a follow-up of individuals who scored high on Ho scale ratings had significantly higher mortality rates from coronary heart disease. They also reported that the Ho rating scale could be further separated into subscales that measure cynicism and paranoid alienation. However, neither the Ho nor either of its subscales measures anger, irritability or aggression, which are the hallmarks of hostility. Rather, they are more apt to reflect neuroticism and psychopathologic traits that are not predictive of coronary disease.
Like Type A, hostility is best evaluated by observation, rather than self-report questionnaires such as the MMPI and hostility ratings obtained by personal observation do not correlate well with Ho scale measurements. Subjects with high Ho scores also tend to have high scores on the Jenkins Activity Survey speed and impatience and hard driving temperament subscales. Thus, the Ho scale may simply be measuring certain aspects of Type A coronary-prone behavior but labeling it as something else. I have had occasion to ask both Mike Friedman and Ray Rosenman whether any particular Type A trait was most useful in predicting the likelihood of a coronary event or was it the presence of many that was more important. As emphasized in the original papers, Friedman was most impressed with time urgency, and referred to Type A as “the hurry sickness”. Ray Rosenman agreed that there was little doubt that the increased incidence of coronary disease had occurred in association with a faster pace of living, but for him, the cardinal Type A characteristic was constant competitiveness. Even when playing games against children, Type A’s frequently remain fiercely competitive and hate to lose.
As previously proposed, I believe it is quite plausible that Type A is a self-perpetuating behavior due to stress induced adrenaline addiction. (Rosch 1989) It is possible that other stress-related neurohumoral secretions such as serotonin, dopamine or beta-endorphin also have the potential for inducing addiction. Support for this comes from Solomon’s “opponent-process theory of acquired motivation”, which basically asserts that man is by nature susceptible to various habits and addictions that provide a sense of pleasure. (Solomon 1977) However, when deprived of the thing that is craved, an opposing emotional state often results. The exhilarating feeling of being in love changes to melancholy if one is deprived of any contact with their beloved. People who are hooked on skydiving may become severely depressed if the weather interferes with their activities for a few days. Similarly, withdrawal from cigarettes, alcohol, narcotics, tranquilizers, or recreational drugs often produces an emotional state directly opposite from the pleasurable sensations those substances induce.
Type A’s who have become addicted to surges of their stress related hormonal secretions might unconsciously seek ways to induce their associated “highs”. That could come in the form of constructing contests and challenges, like getting to the airport shortly before takeoff to avoid waiting, turning a car trip into a race by predicting specific times at which check points must be reached, purposely leaving a desk untidy or room untidy, or delaying an assignment to the last minute-just so there will be some sort of time urgent, last-minute challenge. When deprived of such stimuli, Type A’s are apt to be irritable and depressed. Thus, recuperating from a heart attack by spending two weeks on a deserted tropical beach might be perfect for many patients but a dangerous prescription for some Type A’s, who would likely be agitated within an hour if they were unable to get back to their work or contact their office to see what was going on.
It has long been recognized that severe or sudden emotional stress could result in a heart attack or sudden death. Walter Cannon at Harvard first delineated the mechanisms responsible for this in the early part of the last century. (Cannon 1914) Cannon’s studies demonstrated that responses to the stress of acute fear resulted in a marked increase in sympathetic nervous system activity and an outpouring of sympathin (adrenaline) that prepared the animal for lifesaving “fight or flight.” His later studies of the mechanism of “bone pointing” or “voodoo” death also implicated excess secretion of hormones from the adrenal medulla into the blood stream as the most likely cause of fatal arrhythmia. (Cannon 1942) Hans Selye’s formulation of the stress concept in the late 1940’s provided further insight into the role of pituitary and adrenal cortical hormones in mediating damaging cardiovascular responses to stress.
His subsequent research included the experimental production of “metabolic cardiac necroses,” in which direct biochemical injury to heart muscle rather than occlusion of the coronary vessels was the causative factor. (Selye 1958) Since then, it has been observed that stress can cause accelerated atherosclerosis and coronary occlusion that is associated with elevated cholesterol, triglycerides, and free fatty acids, increased fibrinogen, haptoglobin, plasma seromucoids, platelet aggregation and adhesiveness, polycythemia, and accelerated blood clotting. We have also become increasingly aware of the important role of stress-induced coronary vasospasm in the production of clinical symptoms and disease. (Gersh et al 1981) Even more significant has been the identification of myocardial infarction in the absence of significant coronary occlusion due to excessive release of norepinephrine at myocardial nerve endings. This has been shown to produce a specific type of microscopic myocardial damage that appears to be identical in laboratory animals as well as humans who have succumbed to sudden cardiac death as a result of an acutely stressful situation. (Cebelin, Hirsch 1981) There is also abundant evidence that severe and acute emotional stress following an earthquake or other natural disaster or the loss of a loved one can result in hypertension, a heart attack or sudden death (Rosch 1994a, 1994b).
As emphasized, conventional dogma postulates that heart attacks are due to elevated cholesterol, which in turn is due to a high fat diet, a premise that presumably was proven by Ancel Key’s seven-country study that allegedly showed this close correlation. (Keys 1970, 1980) However, we now know that Keys conveniently hand picked these from a list of many more countries in an effort to support the fatty dietcholesterolheart attack hypothesis. Had he included all the data available to him he would have confirmed that these associations were weak, absent, and in some instances inverse. (Jacobs et al 1992) The Framingham study was largely responsible for the belief that cholesterol, cigarettes and hypertension caused heart attacks but if this was true, then removing these “risk factors” should reduce the incidence of coronary events. (Rosch 1983b)
In 1982, the disappointing results of the seven-year, $115 million MRFIT study were published in the Journal of the American Medical Association. MRFIT is an acronym for Multiple Risk Factor Intervention Trail, which was designed to show the beneficial effect of stopping smoking and lowering cholesterol and blood pressure. (Multiple Risk Factor Intervention Trial Group 1982) However, patients in whom these desired results were achieved did not receive any significant protection. In fact, a subset of hypertensives treated with diuretics had a higher incidence of heart attacks than controls, possibly because they caused hypokalemia, which potentiated damaging adrenergic effects and risk for sudden death. (Rosch 1983b) In contrast, over the same period, two other studies designed to reduce the likelihood of recurrent heart attacks were so successful that they were halted prematurely so that controls would not be denied the benefit of intervention. One was a trial using techniques to reduce Type A coronary prone behavior. (Thoresen, Friedman et al. 1982), (Friedman, Thoresen et al 1982) The other was an NIH sponsored study of almost 4,000 patients in which it was found that after only two years the administration of propanolol (Inderal) had reduced mortality by 26%. (Beta-Blocker Heart Attack Study Group 1981), (Beta-blocker heart attack trial 1982) Both trials strongly suggest that stress-related sympathetic nervous system drive and catecholamine secretion are the major culprits in coronary heart disease. Behavioral modification is aimed at turning off the epinephrine-norepinephrine spigot, and propanolol and other beta-blockers blunt the damaging effects of such agents on the cardiovascular system. These cardioprotective effects have been so well documented that it has been suggested that beta-blockers be administered to all heart-attack patients provided there are no contraindications. (Kahn 1983)
Numerous surveys confirm that occupational pressures are far and away the leading source of stress for American adults and that job stress has escalated progressively over the past four decades. (Rosch 2001) While the causes for this vary with occupations and positions, most contributors fall into the following categories:
How Work And Tasks Are Designed – Heavy workload; infrequent rest breaks; long work hours and shift work; hectic and routine tasks that: have little inherent meaning, do not allow workers to utilize their skills, and most importantly, provide little sense of control.
Management Style – Lack of participation by workers in decision-making; poor communication in the organization; lack of company policies that take employees’ family and personal obligations into consideration.
Interpersonal Relationships – Poor social environment and lack of support or help from co-workers and supervisors.
Vague Or Changing Job Description – Conflicting or uncertain job expectations; too much responsibility; too many hats to wear; too many superiors, co-workers or customers making very different demands.
Concerns About Employment Or Career – Job insecurity and lack of opportunity for advancement, or promotion; rapid changes for which workers are unprepared due to unanticipated downsizing, mergers and hostile acquisitions.
Environmental Concerns – Unpleasant or dangerous physical conditions in the workplace such as crowding, noise, air pollution, or failure to address ergonomic problems.
Discrimination – Lack of opportunity for advancement or promotion because of age, gender, race, religion, or disability despite legislation designed to prevent this.
Violence, Physical And Verbal Abuse – An average of 20 workers a week are murdered and 18,000 are physically abused in the U.S. but the number may be higher since many such crimes are not reported. Homicide has become the second leading cause of workplace deaths overall and ranks first for females.
The relationship between job stress and illness was recognized 300 years ago by Bernardo Ramazzini, who described in detail the diseases of people engaged in 40 different kinds of work and urged his fellow physicians to question their patients about their occupations. (Ramazzini 1713) While the major focus was on physical hazards such as “sharp and acid particles” in the air at certain work environments, he was well aware of the role of personal habits, behavior and psychosocial factors in causing illness and emphasized the importance of prevention. The clear link between job stress and cardiovascular disease was scientifically demonstrated 15 years ago by Karasek and Theorell (Karasek and Theorell 1990) and has since been confirmed by numerous other investigators using their demand/control model and it is essential to emphasize the importance of this approach.
While there are numerous claims that certain occupations are extremely stressful and therefore more likely to cause heart disease, these are usually self-serving and designed to obtain higher wages or more benefits for members by unions and organizations and are based on anecdotal self -report questionnaires rather than objective scientific studies. Various rankings of the “most” and “least” stressful jobs are also misleading since job stress is entirely dependent on the person/environment fit as assessed by the perception of having little control but significant demands. Some Type A’s thrive in the pressure cooker of life in the fast lane, having numerous responsibilities and doing several things at once – provided they feel in control. This would overwhelm others who are content to do dull, dead end assembly line duties that present no challenge since they are well within their capabilities. Conversely, this could be very stressful for a Type A because of the perception of having no control over what is going on. Although Type A’s tend to be preoccupied with work-related activities it is a common misconception that they are under more stress than others or that their exaggerated cardiovascular reactivity to challenges leads to sustained hypertension and coronary disease. In point of fact, Type A’s rarely perceive stress and never admit to being stressed although they are notorious for causing stress in others. (Rosenman 1990, 1993)
Stress is difficult for scientists to define since it is a subjective phenomenon that differs for each of us and we all respond to stress differently. Things that are distressful for some people can be pleasurable for others or have little significance either way, as can be readily illustrated by observing passengers on a steep roller coaster ride. Some are crouched down in the back seats with their eyes shut, jaws clenched, white knuckled as they clench the retaining bar. They can’t wait for the ride in the torture chamber to end and get on solid ground to scamper away. But up front are the thrill seekers, yelling and relishing every abrupt plunge, and who race to get on the very next ride! And in between, you may find a few with an air of nonchalance that seems to border on boredom. So, was the roller coaster ride stressful?
The roller coaster is a useful analogy that helps to explain stress. What distinguished the riders in the back from those up front was the sense of control they had over the event. While neither group had any more or less control their perceptions and expectations were quite different. Although stress is difficult to define, all of our clinical and experimental research confirms that the perception of having no control is always distressful – and that’s what stress is all about. Many times we create our own stress because of faulty perceptions. You can teach people to move from the back of the roller coaster to the front and nobody can make you feel inferior unless you allow them to. Stress is an unavoidable consequence of life but there are some stresses you can do something about and others that you can’t hope to avoid or control. The trick is in learning to distinguish between the two so that you don’t waste your time and talent, like Don Quixote, tilting at windmills you can never conquer. The best way to accomplish this is in learning how to correct faulty perceptions and develop a better sense of control over your activities at work as well as at home. This will not only improve your quality of life but also help protect you from coronary heart disease and other stress-related disorders.
Beta-Blocker Heart Attack Study Group (1981) Beta-blocker heart attack trial. JAMA 246:2073-2074,
Beta-Blocker Heart Attack Study Group (1982) Beta-blocker heart attack trial. JAMA 247:1701-1714.
Cannon, W. J. (1914) The emergency function of the adrenal medulla in pain and the major emotions. Am J Physiol 33:356-372.
Cannon, W. J. (1942) “Voodoo” death. Am Anthropol 44:169-181
Cebelin, M. S. & Hirsch, C. S. (1981) Human stress cardiomyopathy: Myocardial lesions in victims of homicidal assaults without internal injuries. Hum Pathol 2:123-132.
Dunbar, H. F. (1943) Psychosomatic Diagnosis. New York: Hoeber and Harper.
Friedman, M. & Rosenman, R. H. (1959) Association of specific overt behavior patterns with blood and cardiovascular findings: Blood cholesterol level, blood clotting time, incidence of arcus senilis and clinical coronary artery disease. JAMA 169: 1286-1296.
Friedman, M. & Rosenman, R. H. (1960) Overt behavior pattern in coronary artery disease: Detection of overt pattern behavior A in patients with coronary artery disease by a new psycho-physiological procedure. JAMA 173: 1320-1325.
Friedman, M. & Rosenman, R. H. (1974) Type A Behavior and Your Heart. New York: Knopf.
Friedman M., Thoresen, C. E., Gill, J. J., Ulmer, D., Thompson, L., Powell, L. et al. (1982) Feasibility of altering Type A behavior pattern after myocardial infarction. Recurrent coronary prevention project study: Methods, baseline results and preliminary findings. Circulation 66:83-92.
Gersh, B. J., Bassendine, M. F., Forman, R, & Walls, R. S. (1981) Case report: Coronary artery spasm and myocardial infarction in the absence of angiographically demonstrable obstructive coronary disease. Mayo Clin Proc 56:700-708.
Harvey, W. (1628) Anatomica de Motu Cordis [On the Movement of the Heart And Blood in Animals] quoted in Willius FA and Keyes TE (1941) Classics in Cardiology, p.15. New York: Dover.
Home, E. (1796) “A short account of the Author’s Life.” A Treatise on theBlood, Inflammation and Gunshot Wounds, by J. Hunter. Philadelphia: T. Bradfors.
Jacobs, D., Blackburn, H., Higgins, M., Reed, D., Iso, H., McMillan, G., Neaton, J. et al. (1992) Report of the conference on low blood cholesterol: mortality associations. Circulation 86:1046-60.
Jenkins, C. D., Friedman, M. & Rosenman, R. H. (1965) The Jenkins Activity Survey for Health Prediction, Chapel Hill: University of North Carolina.
Jenkins, C. D., Rosenman, R. H. & Zysanski, S. J. (1974) Prediction of clinical coronary heart disease by a test for the coronary-prone behavior pattern. NEJM, 290:1272-1275.
Jenkins, C. D. (1971) Psychological and social precursors of coronary disease. [First of two parts] NEJM 282:244-254.
Karasek, R. A. & Theorell, T. (1990) Healthy Work: Stress, Productivity, and the Reconstruction of Working Life. New York: Basic Books.
Khan, A. H. (1983): Beta-adrenoceptor blocking agents: Their role in reducing chances of recurrent infarction and death. Arch Intern Med 143:1759-1762.
Kemple, C. (1945) Rorschach method and psychosomatic diagnosis: Personality traits in patients with rheumatic disease, hypertensive cardiovascular disease, coronary occlusion and fracture. Psychosomatic Medicine, 7:85-89.
Keys, A. (1970) Coronary heart disease in seven countries. Circulation; 41 (suppl 1):1-211.
Keys, A. (1980) Seven countries: a multivariate analysis of death and coronary heart disease. London: Harvard University Press.
Menninger, K. A. & Menninger, W. C. (1936) Psychoanalytic observations in cardiac disorders. American Heart Journal, 11:10-21.
Multiple Risk Factor Intervention Trial Research Group. (1982) Multiple risk factor intervention trial: Risk factor changes and mortality results. JAMA 248:1465-1477.
Osler, W. (1892) Lecture on angina pectoris and allied states. New York. Appleton.
Osler, W. (1910) The Lumleian lectures on angina pectoris. Lancet, 1:839-844.
Ramazzini, B. (1713) Translation of the Latin text of De Morbus Artificum Diatriba of 1713, published under the auspices of the NY Academy of Medicine 1964. New York: Havner Press.
Review Panel on Coronary-Prone Behavior and Coronary Heart Disease: A critical review. (1981) Circulation, 63:1199-1215.
Rosch, P. J. (1983 a) Stress and Cardiovascular Disease Comprehensive Therapy, 9:6-13.
Rosch, P. J. (1983 b) Stress, cholesterol and coronary heart disease. Lancet, 2:851-852.
Rosch, P. J. (1989) “Stress Addiction”: Causes, Consequences, And Cures. pp. 189-202
in F. Flach (Ed). Stress and its Management (pp189-202) New York: Norton
Rosch, P. J. (1994a) Does Stress Cause Hypertension? Stress Medicine, 10:141-143.
Rosch, P. J. (1994b)Can Stress Cause Coronary Heart Disease? Stress Medicine, 10:207-210
Rosch, P. J. (2001) Health And Stress: The Newsletter of the American Institute of Stress. No. 3
Rosch, P. J. (2004) Health And Stress: The Newsletter of the American Institute of Stress. No. 10.
Rosenman, R. H. (1990). Cardiovascular Reactivity: Physiological or Psychological? In: R. Schmidt (Ed). Theoretical and Applied Aspects of Health Psychology. (pp. 78-94). London: Harwood.
Rosenman, R. H. (1993) Relationships of Type A Behavior Pattern with Coronary heart Disease. In J. Goldberger & S. Breznitz (Eds.), Handbook of Stress-Theoretical and Clinical Aspects. (pp. 185-204). New York: Free Press
Rosenman, R. H. & Friedman M. (1961). Association of a specific overt behavior pattern in females with blood and cardiovascular findings. Circ., 24:1173-84
Rosenman, R. H., Friedman, M., Strauss, R., Wurm, M., Kositchek, R., Hahn, W. & Werthessen, N. T. (1964) A predictive study of coronary heart disease. JAMA 189:15-22
Rosenman, R. H., Friedman, M., Straus, R., Wurm, M., Jenkins, C. D., Messinger, H. B., et al. (1966) Coronary Heart Disease in the Western Collaborative Group Study: A follow-up experience of two years. JAMA, 195: 86-92.
Selye, H. (1958) The Chemical Prevention of Cardiac Necroses. New York: Ronald Press.
Solomon, R. L. (1977) An opponent-process theory of acquired motivation: IV. The affective dynamics of addiction. In J. D. Maser& M. Seligman (Eds.), Psychopathology: Experimental Models (pp. 66-103). San Francisco: W.H. Freeman Co.
Thoresen, C. E. Friedman, M. Gill, J. J. & Ulmer, D. (1982) The recurrent coronary prevention project: Some preliminary findings. Acta Med Scandinav (Suppl.) 660:172-192.
Von Düsch, T. (1868) Lehrbuch der Herzkrankheiten, Leipzig, Verlag von Wilhelm Engelman
Williams, R. (1989) The Trusting Heart: Great News About Type A Behavior. New York: Random House.
Wolf, S. (1955) Psychosomatic aspects of industrial medicine. South Med J, 4:79.
Wolf , S. G. (1960) Modern Concepts of Cardiovascular Disease. In H. Lewis, H. Griswold & H. Underwood (eds) Stress and Heart Disease.(pp. 559-603). New York: American Heart Association.
Click here to view a Power Point presentation by Dr. Paul Rosch:
(the file is quite large and might take a moment to load)