ARE YOU TYPE A OR TYPE B?
Sometimes research ideas and theories emerge from seemingly trivial observations. In the 1950s, cardiologist Meyer Friedman was looking over his waiting room furniture, which consisted of upholstered chairs with armrests. Friedman decided to have these chairs reupholstered. When the man doing the reupholstering came to the office to do the work, he commented on how the chairs were worn in a unique manner—the front edges of the cushions were worn down, as were the front tips of the arm rests. It seemed like the cardiology patients were tapping or squeezing the front of the armrests, as well as literally sitting on the edge of their seats (Friedman & Rosenman, 1974). Were cardiology patients somehow different than other types of patients? If so, how?
After researching this matter, Friedman and his colleague, Ray Rosenman, came to understand that people who are prone to heart disease tend to think, feel, and act differently than those who are not. These individuals tend to be intensively driven workaholics who are preoccupied with deadlines and always seem to be in a rush. According to Friedman and Rosenman, these individuals exhibit Type A behavior pattern; those who are more relaxed and laid-back were characterized as Type B (Figure). In a sample of Type As and Type Bs, Friedman and Rosenman were startled to discover that heart disease was over seven times more frequent among the Type As than the Type Bs (Friedman & Rosenman, 1959).
The major components of the Type A pattern include an aggressive and chronic struggle to achieve more and more in less and less time (Friedman & Rosenman, 1974). Specific characteristics of the Type A pattern include an excessive competitive drive, chronic sense of time urgency, impatience, and hostility toward others (particularly those who get in the person’s way).
An example of a person who exhibits Type A behavior pattern is Jeffrey. Even as a child, Jeffrey was intense and driven. He excelled at school, was captain of the swim team, and graduated with honors from an Ivy League college. Jeffrey never seems able to relax; he is always working on something, even on the weekends. However, Jeffrey always seems to feel as though there are not enough hours in the day to accomplish all he feels he should. He volunteers to take on extra tasks at work and often brings his work home with him; he often goes to bed angry late at night because he feels that he has not done enough. Jeffrey is quick tempered with his coworkers; he often becomes noticeably agitated when dealing with those coworkers he feels work too slowly or whose work does not meet his standards. He typically reacts with hostility when interrupted at work. He has experienced problems in his marriage over his lack of time spent with family. When caught in traffic during his commute to and from work, Jeffrey incessantly pounds on his horn and swears loudly at other drivers. When Jeffrey was 52, he suffered his first heart attack.
By the 1970s, a majority of practicing cardiologists believed that Type A behavior pattern was a significant risk factor for heart disease (Friedman, 1977). Indeed, a number of early longitudinal investigations demonstrated a link between Type A behavior pattern and later development of heart disease (Rosenman et al., 1975; Haynes, Feinleib, & Kannel, 1980).
Subsequent research examining the association between Type A and heart disease, however, failed to replicate these earlier findings (Glassman, 2007; Myrtek, 2001). Because Type A theory did not pan out as well as they had hoped, researchers shifted their attention toward determining if any of the specific elements of Type A predict heart disease.
Extensive research clearly suggests that the anger/hostility dimension of Type A behavior pattern may be one of the most important factors in the development of heart disease. This relationship was initially described in the Haynes et al. (1980) study mentioned above: Suppressed hostility was found to substantially elevate the risk of heart disease for both men and women. Also, one investigation followed over 1,000 male medical students from 32 to 48 years. At the beginning of the study, these men completed a questionnaire assessing how they react to pressure; some indicated that they respond with high levels of anger, whereas others indicated that they respond with less anger. Decades later, researchers found that those who earlier had indicated the highest levels of anger were over 6 times more likely than those who indicated less anger to have had a heart attack by age 55, and they were 3.5 times more likely to have experienced heart disease by the same age (Chang, Ford, Meoni, Wang, & Klag, 2002). From a health standpoint, it clearly does not pay to be an angry young person.
After reviewing and statistically summarizing 35 studies from 1983 to 2006, Chida and Steptoe (2009) concluded that the bulk of the evidence suggests that anger and hostility constitute serious long-term risk factors for adverse cardiovascular outcomes among both healthy individuals and those already suffering from heart disease. One reason angry and hostile moods might contribute to cardiovascular diseases is that such moods can create social strain, mainly in the form of antagonistic social encounters with others. This strain could then lay the foundation for disease-promoting cardiovascular responses among hostile individuals (Vella, Kamarck, Flory, & Manuck, 2012). In this transactional model, hostility and social strain form a cycle (Figure).
For example, suppose Kaitlin has a hostile disposition; she has a cynical, distrustful attitude toward others and often thinks that other people are out to get her. She is very defensive around people, even those she has known for years, and she is always looking for signs that others are either disrespecting or belittling her. In the shower each morning before work, she often mentally rehearses what she would say to someone who said or did something that angered her, such as making a political statement that was counter to her own ideology. As Kaitlin goes through these mental rehearsals, she often grins and thinks about the retaliation on anyone who will irk her that day.
Socially, she is confrontational and tends to use a harsh tone with people, which often leads to very disagreeable and sometimes argumentative social interactions. As you might imagine, Kaitlin is not especially popular with others, including coworkers, neighbors, and even members of her own family. They either avoid her at all costs or snap back at her, which causes Kaitlin to become even more cynical and distrustful of others, making her disposition even more hostile. Kaitlin’s hostility—through her own doing—has created an antagonistic environment that cyclically causes her to become even more hostile and angry, thereby potentially setting the stage for cardiovascular problems.
In addition to anger and hostility, a number of other negative emotional states have been linked with heart disease, including negative affectivity and depression (Suls & Bunde, 2005). Negative affectivity is a tendency to experience distressed emotional states involving anger, contempt, disgust, guilt, fear, and nervousness (Watson, Clark, & Tellegen, 1988). It has been linked with the development of both hypertension and heart disease. For example, over 3,000 initially healthy participants in one study were tracked longitudinally, up to 22 years. Those with higher levels of negative affectivity at the time the study began were substantially more likely to develop and be treated for hypertension during the ensuing years than were those with lower levels of negative affectivity (Jonas & Lando, 2000). In addition, a study of over 10,000 middle-aged London-based civil servants who were followed an average of 12.5 years revealed that those who earlier had scored in the upper third on a test of negative affectivity were 32% more likely to have experienced heart disease, heart attack, or angina over a period of years than were those who scored in the lowest third (Nabi, Kivimaki, De Vogli, Marmot, & Singh-Manoux, 2008). Hence, negative affectivity appears to be a potentially vital risk factor for the development of cardiovascular disorders.