In the late 20th century, medical focus shifted from treating cardiovascular disease to preventing it in those at risk. In 1998, while I was still in medical school, researchers published a formula, based on the major independent cardiac risk factors that had been identified — family history, smoking, diabetes, high serum cholesterol, and hypertension — to calculate a patient’s risk of getting heart disease within 10 years. Today, we know that programs targeting such risk factors improve public health. For example, a recent 12-year study of 20,000 Swedish men showed that almost four out of five heart attacks could be prevented through lifestyle changes, such as a healthy diet, moderate alcohol consumption, no smoking, increased physical activity, and maintaining a normal body weight. Men who adopted all five changes were 86 percent less likely to have a heart attack than those who did not.
Much of this science first came to be understood through the famous Framingham Heart Study, in which investigators monitored about 5,000 residents of Framingham, Massachusetts, for 20 years, beginning in 1948. Its findings were massively influential in identifying risk factors—indeed, Framingham researchers introduced the term “risk factor” in 1961. But even then, the researchers recognized the lack of diversity in the study population as a major limitation. The results for the mostly white subjects do not seem to apply equally to nonwhite ethnic groups. In 1959, for instance, the first study showing an increased risk of premature heart disease in Indian males was published in the American Heart Journal. These men had four times the rate of heart disease compared with men living in Framingham, despite having lower rates of hypertension, smoking, and high cholesterol and more often consuming a vegetarian diet. Over the past half-century, the average age at which a first heart attack occurs has increased by 10 years in the United States but decreased by about 10 years in India. South Asians will soon make up over half of the world’s cardiac patients. What is it about South Asian genetics or environments that leads to so much heart disease? We need a Framingham-type study to answer this question.
Today, a massive amount of epidemiological data associates heart disease with chronic emotional disorder — or disruption of the metaphorical heart.
But there are almost certainly cardiovascular risk factors that Framingham investigators did not identify. Some of these factors are likely in the “psychosocial” domain that Framingham investigators decided to ignore when the National Heart Institute (NHI) took over the study in the early 1950s. For example, consider heart disease in Japanese immigrants. Coronary artery disease is relatively rare in Japan; however, its rate is almost double in Japanese immigrants who settle in Hawaii and triple in those who settle in the mainland United States. Part of the explanation might be that Japanese immigrants adopt unhealthy American habits, like a sedentary lifestyle or a diet rich in processed foods. Still, Framingham risk factors do not fully explain the disparity.
In the early 1970s, Sir Michael Marmot and his colleagues at the UC Berkeley School of Public Health studied nearly 4,000 middle-aged Japanese men living in the San Francisco Bay Area. They found that immigrants who stayed true to their Japanese roots (as evidenced in surveys by their ability to read Japanese, the frequency with which they spoke Japanese, the frequency with which they had Japanese co-workers, and so on) had a much lower prevalence of heart disease, even when they matched Americans in terms of serum cholesterol and blood pressure, than immigrants who were more integrated into their new culture. “Traditional” Japanese immigrants had coronary disease rates in line with their homeland counterparts. “Westernized” immigrants had a prevalence that was at least three times higher. “Retention of Japanese group relationships is associated with a lower rate of coronary heart disease,” the authors concluded. And so, acculturation, they declared, is a major risk factor for coronary disease in immigrant populations.
If cutting traditional cultural ties increases the risk of heart disease, then psychosocial factors must play a role in cardiovascular health. Today, we know this to be true in many strata of human society. For example, American blacks in poor urban centers have a much higher prevalence of hypertension and cardiovascular disease than other groups. Some have proposed genetics to be the deciding factor; however, this is an unlikely explanation, because American blacks have hypertension at much higher rates than their West African counterparts. Moreover, hypertension pervades other segments of American society in which poverty and social ills are rampant.
Peter Sterling, a neurobiologist at the University of Pennsylvania, has written that hypertension in such communities is a normal response to what he calls “chronic arousal,” or stress. In small preindustrial communities, he writes, people tend to know and trust one another. Generosity is rewarded; cheating tends to be punished. When this milieu is disrupted, as in migration or urbanization, there is often an increased need for vigilance. People become estranged from their neighbors. Communities become diverse and more mistrustful. Physical and social isolation often results. Add in poverty, fragmented families, and joblessness, and you get extremely stress-prone populations. The chronic arousal triggers release of hormones, such as adrenaline and cortisol, that tighten blood vessels and cause retention of salt. These in turn lead to long-term changes, like arterial-wall thickening and stiffening, that increase the blood pressure that the body tries to maintain.
In Sterling’s formulation, nothing is broken (except perhaps “the system”). The body is responding exactly in the way it should to the chronic fight-or-flight circumstances in which it finds itself. Just as acute psychological disruption can bring on a cardiac event, Sterling’s theories suggest that chronic, low-level stress may be equally harmful. His theories put psychosocial factors front and center in how we think about and approach heart problems. They show that chronic heart disease is inextricably linked to the state of our neighborhoods, jobs, and families. Heart disease, in this conception, is no longer strictly biological; it is cultural and political as well. Improving our social structures and relationships becomes not only a quality-of-life issue but also a public health concern.
The harmful cardiovascular effects of chronic arousal apply to traditionally white communities, too. One example is the Whitehall study, also conducted by Marmot, of 17,000 male workers in the British civil service. In this study, early death and poor health were found to increase stepwise from the highest to the lowest levels of the civil service hierarchy. Messengers and porters had nearly twice the death rate of higher-ranking administrators, even after accounting for differences in smoking, plasma cholesterol, blood pressure, and alcohol consumption. None of these civil servants were poor, in the usual sense. They all enjoyed clean water, plenty of food, and proper toilet facilities. The main ways they differed were in occupational prestige, job control, and other gradients of the social hierarchy. Marmot and his co-workers concluded that emotional disturbance, because of financial instability, time pressures, lack of advancement, and a general dearth of autonomy, drives much of the difference in survival.
Nothing is broken (except perhaps “the system”). The body is responding exactly in the way it should to the chronic fight-or-flight circumstances in which it finds itself.
Lower socioeconomic classes are not the only ones susceptible to stress-induced heart problems. Recent research has focused on the association of “negative affectivity” traits, such as depression, anxiety, and anger, with heart disease. The strongest evidence has emerged for depression, which seems to be an independent risk factor for coronary artery disease and increases the risk of poor outcomes, including death, after a heart attack. How does depression affect heart health? Possible mechanisms include elevating blood pressure, causing vascular inflammation, disturbing autonomic nervous system function, and increasing blood clotting. Also probably playing a role are unhealthy behaviors associated with depression, such as physical inactivity, smoking, and failure to take medications or adhere to medical advice. Today, a massive amount of epidemiological data associates heart disease with chronic emotional disorder — or disruption of the metaphorical heart. For example, individuals in unhappy marriages are at a much higher risk for heart disease than those in more joyous unions. The risk of myocardial infarction and death increases dramatically in the year following a broken romance.
We paid little attention to “psychosocial” factors during my cardiology fellowship. The focus of our seminars was on pressure-volume loops, cardiac work cycles, resistance of fluid-filled pipes, and capacitance of fluid-filled chambers. We concentrated on clinical trial design, biological mechanisms, and understanding the heart as a machine. As with most academic training programs, the fact that there was an emotional world that could damage (or heal) this pump was largely ignored.
Ironically, the view that heart disease results from unfulfilled social or psychological needs was widely accepted in primitive societies. That is almost certainly how people thought about heart disease in rural Punjab in the 1950s, when my grandfather died suddenly at the age of 57. A few hours after suffering a snake bite, neighbors brought in the corpse of the shiny black cobra they claimed had bit him. My grandfather took one look at it and went pale. “How can I survive this?” he said, before slumping to the floor, dead. But at the hospital, a doctor found that it was a heart attack, not venom, that had killed him.
That doctor did not know about the damaging effects of cholesterol and hypertension. (Framingham results had not yet been broadly disseminated.) He would have explained my grandfather’s heart attack as the result of a sudden emotional shock (as when your neighbors bring a dead cobra into your home while you are having lunch with your family), or the years of social and financial struggle he endured after the Partition of India, or the loss of social connectivity that resulted from the fracturing and large-scale displacement of communities that had lived together for centuries, and in a sense they would have been right. Stress-induced surges of adrenaline can cause a stable atherosclerotic plaque to fissure and rupture, forming a thrombosis that can acutely block the artery and stop blood flow, thus causing a heart attack. Starved for oxygen, tissue begins to die. Irreversible cellular injury occurs within 20 minutes. And then, frequently, death.
Medicine today conceptualizes the heart as a machine. With advances in technology, perhaps this was inevitable. Drugs and devices have been responsible for much of the improvement in cardiovascular mortality over the past 50 years.
However, this narrow focus on biological mechanisms has hurt patients. We have overused stents and pacemakers. We have moved away from the emotional heart to a narrow focus on the biomechanical pump. The American Heart Association still does not list emotional stress among the key modifiable risk factors for heart disease — perhaps in part because serum cholesterol is so much easier to reduce than emotional and social disruption. We need a better way, one that recognizes the power and importance of emotions that the heart — the metaphorical heart — was believed to house for millennia. Though we know today that the heart is not the repository of the affections, it nevertheless remains the physiological canvas upon which our emotions are most easily written.