12.3-Stress and Illness

Psychophysiological Disorders

If the reactions that compose the stress response are chronic or if they frequently exceed normal ranges, they can lead to cumulative wear and tear on the body, in much the same way that running your air conditioner on full blast all summer will eventually cause wear and tear on it. For example, the high blood pressure that a person under considerable job strain experiences might eventually take a toll on his heart and set the stage for a heart attack or heart failure. Also, someone exposed to high levels of the stress hormone cortisol might become vulnerable to infection or disease because of weakened immune system functioning (McEwen, 1998).

Physical disorders or diseases whose symptoms are brought about or worsened by stress and emotional factors are called psychophysiological disorders. The physical symptoms of psychophysiological disorders are real and they can be produced or exacerbated by psychological factors (hence the psycho and physiological in psychophysiological). A list of frequently encountered psychophysiological disorders is provided in Table 14.3.

In addition to stress itself, emotional upset and certain stressful personality traits have been proposed as potential contributors to ill health. Franz Alexander (1950), an early-20th-century psychoanalyst and physician, once postulated that various diseases are caused by specific unconscious conflicts. For example, he linked hypertension to repressed anger, asthma to separation anxiety, and ulcers to an unconscious desire to “remain in the dependent infantile situation—to be loved and cared for” (Alexander, 1950, p. 102). Although hypertension does appear to be linked to anger (as you will learn below), Alexander’s assertions have not been supported by research. Years later, Friedman and Booth-Kewley (1987), after statistically reviewing 101 studies examining the link between personality and illness, proposed the existence of disease-prone personality characteristics, including depression, anger/hostility, and anxiety. Indeed, a study of over 61,000 Norwegians identified depression as a risk factor for all major disease-related causes of death (Mykletun et al., 2007). In addition, neuroticism—a personality trait that reflects how anxious, moody, and sad one is—has been identified as a risk factor for chronic health problems and mortality (Ploubidis & Grundy, 2009).

Below, we discuss two kinds of psychophysiological disorders about which a great deal is known: cardiovascular disorders and asthma. First, however, it is necessary to turn our attention to a discussion of the immune system—one of the major pathways through which stress and emotional factors can lead to illness and disease.

Stress and the Immune System

In a sense, the immune system is the body’s surveillance system. It consists of a variety of structures, cells, and mechanisms that serve to protect the body from invading toxins and microorganisms that can harm or damage the body’s tissues and organs. When the immune system is working as it should, it keeps us healthy and disease free by eliminating bacteria, viruses, and other foreign substances that have entered the body (Everly & Lating, 2002).

Stressors and Immune Function

The question of whether stress and negative emotional states can influence immune function has captivated researchers for over three decades, and discoveries made over that time have dramatically changed the face of health psychology (Kiecolt-Glaser, 2009). Psychoneuroimmunology is the field that studies how psychological factors such as stress influence the immune system and immune functioning. The term psychoneuroimmunology was first coined in 1981, when it appeared as the title of a book that reviewed available evidence for associations between the brain, endocrine system, and immune system (Zacharie, 2009). To a large extent, this field evolved from the discovery that there is a connection between the central nervous system and the immune system.

Some of the most compelling evidence for a connection between the brain and the immune system comes from studies in which researchers demonstrated that immune responses in animals could be classically conditioned (Everly & Lating, 2002). For example, Ader and Cohen (1975) paired flavored water (the conditioned stimulus) with the presentation of an immunosuppressive drug (the unconditioned stimulus), causing sickness (an unconditioned response). Not surprisingly, rats exposed to this pairing developed a conditioned aversion to the flavored water. However, the taste of the water itself later produced immunosuppression (a conditioned response), indicating that the immune system itself had been conditioned. Many subsequent studies over the years have further demonstrated that immune responses can be classically conditioned in both animals and humans (Ader & Cohen, 2001). Thus, if classical conditioning can alter immunity, other psychological factors should be capable of altering it as well.

Hundreds of studies involving tens of thousands of participants have tested many kinds of brief and chronic stressors and their effect on the immune system (e.g., public speaking, medical school examinations, unemployment, marital discord, divorce, death of spouse, burnout and job strain, caring for a relative with Alzheimer’s disease, and exposure to the harsh climate of Antarctica). It has been repeatedly demonstrated that many kinds of stressors are associated with poor or weakened immune functioning (Glaser & Kiecolt-Glaser, 2005; Kiecolt-Glaser, McGuire, Robles, & Glaser, 2002; Segerstrom & Miller, 2004).

When evaluating these findings, it is important to remember that there is a tangible physiological connection between the brain and the immune system. For example, the sympathetic nervous system innervates immune organs such as the thymus, bone marrow, spleen, and even lymph nodes (Maier, Watkins, & Fleshner, 1994). Also, we noted earlier that stress hormones released during hypothalamic-pituitary-adrenal (HPA) axis activation can adversely impact immune function. One way they do this is by inhibiting the production of lymphocytes, white blood cells that circulate in the body’s fluids that are important in the immune response (Everly & Lating, 2002).

Some of the more dramatic examples demonstrating the link between stress and impaired immune function involve studies in which volunteers were exposed to viruses. The rationale behind this research is that because stress weakens the immune system, people with high stress levels should be more likely to develop an illness compared to those under little stress. In one memorable experiment using this method, researchers interviewed 276 healthy volunteers about recent stressful experiences (Cohen et al., 1998). Following the interview, these participants were given nasal drops containing the cold virus (in case you are wondering why anybody would ever want to participate in a study in which they are subjected to such treatment, the participants were paid $800 for their trouble). When examined later, participants who reported experiencing chronic stressors for more than one month—especially enduring difficulties involving work or relationships—were considerably more likely to have developed colds than were participants who reported no chronic stressors (Figure 14.15).

Figure 14.15 This graph shows the percentages of participants who developed colds (after receiving the cold virus) after reporting having experienced chronic stressors lasting at least one month, three months, and six months (adapted from Cohen et al., 1998).

In another study, older volunteers were given an influenza virus vaccination. Compared to controls, those who were caring for a spouse with Alzheimer’s disease (and thus were under chronic stress) showed poorer antibody response following the vaccination (Kiecolt-Glaser, Glaser, Gravenstein, Malarkey, & Sheridan, 1996).

Other studies have demonstrated that stress slows down wound healing by impairing immune responses important to wound repair (Glaser & Kiecolt-Glaser, 2005). In one study, for example, skin blisters were induced on the forearm. Subjects who reported higher levels of stress produced lower levels of immune proteins necessary for wound healing (Glaser et al., 1999). Stress, then, is not so much the sword that kills the knight, so to speak; rather, it’s the sword that breaks the knight’s shield, and your immune system is that shield.

DIG DEEPER

Stress and Aging: A Tale of Telomeres

Have you ever wondered why people who are stressed often seem to have a haggard look about them? A pioneering study from 2004 suggests that the reason is because stress can actually accelerate the cell biology of aging.

Stress, it seems, can shorten telomeres, which are segments of DNA that protect the ends of chromosomes. Shortened telomeres can inhibit or block cell division, which includes growth and proliferation of new cells, thereby leading to more rapid aging (Sapolsky, 2004). In the study, researchers compared telomere lengths in the white blood cells in mothers of chronically ill children to those of mothers of healthy children (Epel et al., 2004). Mothers of chronically ill children would be expected to experience more stress than would mothers of healthy children. The longer a mother had spent caring for her ill child, the shorter her telomeres (the correlation between years of caregiving and telomere length was r = -.40). In addition, higher levels of perceived stress were negatively correlated with telomere size (r = -.31). These researchers also found that the average telomere length of the most stressed mothers, compared to the least stressed, was similar to what you would find in people who were 9–17 years older than they were on average.

Numerous other studies since have continued to find associations between stress and eroded telomeres (Blackburn & Epel, 2012). Some studies have even demonstrated that stress can begin to erode telomeres in childhood and perhaps even before children are born. For example, childhood exposure to violence (e.g., maternal domestic violence, bullying victimization, and physical maltreatment) was found in one study to accelerate telomere erosion from ages 5 to 10 (Shalev et al., 2013). Another study reported that young adults whose mothers had experienced severe stress during their pregnancy had shorter telomeres than did those whose mothers had stress-free and uneventful pregnancies (Entringer et al., 2011). Further, the corrosive effects of childhood stress on telomeres can extend into young adulthood. In an investigation of over 4,000 U.K. women ages 41–80, adverse experiences during childhood (e.g., physical abuse, being sent away from home, and parent divorce) were associated with shortened telomere length (Surtees et al., 2010), and telomere size decreased as the amount of experienced adversity increased (Figure 14.16).

Figure 14.16 Telomeres are shorter in adults who experienced more trauma as children (adapted from Blackburn & Epel, 2012).

Efforts to dissect the precise cellular and physiological mechanisms linking short telomeres to stress and disease are currently underway. For the time being, telomeres provide us with yet another reminder that stress, especially during early life, can be just as harmful to our health as smoking or fast food (Blackburn & Epel, 2012).

Cardiovascular Disorders

The cardiovascular system is composed of the heart and blood circulation system. For many years, disorders that involve the cardiovascular system—known as cardiovascular disorders—have been a major focal point in the study of psychophysiological disorders because of the cardiovascular system’s centrality in the stress response (Everly & Lating, 2002). Heart disease is one such condition. Each year, heart disease causes approximately one in three deaths in the United States, and it is the leading cause of death in the developed world (Centers for Disease Control and Prevention [CDC], 2011; Shapiro, 2005).

The symptoms of heart disease vary somewhat depending on the specific kind of heart disease one has, but they generally involve angina—chest pains or discomfort that occur when the heart does not receive enough blood (Office on Women’s Health, 2009). The pain often feels like the chest is being pressed or squeezed; burning sensations in the chest and shortness of breath are also commonly reported. Such pain and discomfort can spread to the arms, neck, jaws, stomach (as nausea), and back (American Heart Association [AHA], 2012a) (Figure 14.17).

Figure 14.17 Males and females often experience different symptoms of a heart attack.

A major risk factor for heart disease is hypertension, which is high blood pressure. Hypertension forces a person’s heart to pump harder, thus putting more physical strain on the heart. If left unchecked, hypertension can lead to a heart attack, stroke, or heart failure; it can also lead to kidney failure and blindness. Hypertension is a serious cardiovascular disorder, and it is sometimes called the silent killer because it has no symptoms—one who has high blood pressure may not even be aware of it (AHA, 2012b).

Many risk factors contributing to cardiovascular disorders have been identified. These risk factors include social determinants such as aging, income, education, and employment status, as well as behavioral risk factors that include unhealthy diet, tobacco use, physical inactivity, and excessive alcohol consumption; obesity and diabetes are additional risk factors (World Health Organization [WHO], 2013).

Over the past few decades, there has been much greater recognition and awareness of the importance of stress and other psychological factors in cardiovascular health (Nusair, Al-dadah, & Kumar, 2012). Indeed, exposure to stressors of many kinds has also been linked to cardiovascular problems; in the case of hypertension, some of these stressors include job strain (Trudel, Brisson, & Milot, 2010), natural disasters (Saito, Kim, Maekawa, Ikeda, & Yokoyama, 1997), marital conflict (Nealey-Moore, Smith, Uchino, Hawkins, & Olson-Cerny, 2007), and exposure to high traffic noise levels at one’s home (de Kluizenaar, Gansevoort, Miedema, & de Jong, 2007). Perceived discrimination appears to be associated with hypertension among African Americans (Sims et al., 2012). In addition, laboratory-based stress tasks, such as performing mental arithmetic under time pressure, immersing one’s hand into ice water (known as the cold pressor test), mirror tracing, and public speaking have all been shown to elevate blood pressure (Phillips, 2011).

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 14.18). 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).

Figure 14.18 (a) Type A individuals are characterized as intensely driven, (b) while Type B people are characterized as laid-back and relaxed. (credit a: modification of work by Greg Hernandez; credit b: modification of work by Elvert Barnes)

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 14.19).

Figure 14.19 According to the transactional model of hostility for predicting social interactions (Vella et al., 2012), the thoughts and feelings of a hostile person promote antagonistic behavior toward others, which in turn reinforces complimentary reactions from others, thereby intensifying ones’ hostile disposition and intensifying the cyclical nature of this relationship.

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.

Depression and the Heart

For centuries, poets and folklore have asserted that there is a connection between moods and the heart (Glassman & Shapiro, 1998). You are no doubt familiar with the notion of a broken heart following a disappointing or depressing event and have encountered that notion in songs, films, and literature.

Perhaps the first to recognize the link between depression and heart disease was Benjamin Malzberg (1937), who found that the death rate among institutionalized patients with melancholia (an archaic term for depression) was six times higher than that of the population. A classic study in the late 1970s looked at over 8,000 manic-depressive persons in Denmark, finding a nearly 50% increase in deaths from heart disease among these patients compared with the general Danish population (Weeke, 1979). By the early 1990s, evidence began to accumulate showing that depressed individuals who were followed for long periods of time were at increased risk for heart disease and cardiac death (Glassman, 2007). In one investigation of over 700 Denmark residents, those with the highest depression scores were 71% more likely to have experienced a heart attack than were those with lower depression scores (Barefoot & Schroll, 1996). Figure 14.20 illustrates the gradation in risk of heart attacks for both men and women.

Figure 14.20 This graph shows the incidence of heart attacks among men and women by depression score quartile (adapted from Barefoot & Schroll, 1996).

After more than two decades of research, it is now clear that a relationship exists: Patients with heart disease have more depression than the general population, and people with depression are more likely to eventually develop heart disease and experience higher mortality than those who do not have depression (Hare, Toukhsati, Johansson, & Jaarsma, 2013); the more severe the depression, the higher the risk (Glassman, 2007). Consider the following:

• In one study, death rates from cardiovascular problems was substantially higher in depressed people; depressed men were 50% more likely to have died from cardiovascular problems, and depressed women were 70% more likely (Ösby, Brandt, Correia, Ekbom, & Sparén, 2001).
• A statistical review of 10 longitudinal studies involving initially healthy individuals revealed that those with elevated depressive symptoms have, on average, a 64% greater risk of developing heart disease than do those with fewer symptoms (Wulsin & Singal, 2003).
• A study of over 63,000 registered nurses found that those with more depressed symptoms when the study began were 49% more likely to experience fatal heart disease over a 12-year period (Whang et al., 2009).

The American Heart Association, fully aware of the established importance of depression in cardiovascular diseases, several years ago recommended routine depression screening for all heart disease patients (Lichtman et al., 2008). Recently, they have recommended including depression as a risk factor for heart disease patients (AHA, 2014).

Although the exact mechanisms through which depression might produce heart problems have not been fully clarified, a recent investigation examining this connection in early life has shed some light. In an ongoing study of childhood depression, adolescents who had been diagnosed with depression as children were more likely to be obese, smoke, and be physically inactive than were those who had not received this diagnosis (Rottenberg et al., 2014). One implication of this study is that depression, especially if it occurs early in life, may increase the likelihood of living an unhealthy lifestyle, thereby predisposing people to an unfavorable cardiovascular disease risk profile.

It is important to point out that depression may be just one piece of the emotional puzzle in elevating the risk for heart disease, and that chronically experiencing several negative emotional states may be especially important. A longitudinal investigation of Vietnam War veterans found that depression, anxiety, hostility, and trait anger each independently predicted the onset of heart disease (Boyle, Michalek, & Suarez, 2006). However, when each of these negative psychological attributes was combined into a single variable, this new variable (which researchers called psychological risk factor) predicted heart disease more strongly than any of the individual variables. Thus, rather than examining the predictive power of isolated psychological risk factors, it seems crucial for future researchers to examine the effects of combined and more general negative emotional and psychological traits in the development of cardiovascular illnesses.

Asthma

Asthma is a chronic and serious disease in which the airways of the respiratory system become obstructed, leading to great difficulty expelling air from the lungs. The airway obstruction is caused by inflammation of the airways (leading to thickening of the airway walls) and a tightening of the muscles around them, resulting in a narrowing of the airways (Figure 14.21) (American Lung Association, 2010). Because airways become obstructed, a person with asthma will sometimes have great difficulty breathing and will experience repeated episodes of wheezing, chest tightness, shortness of breath, and coughing, the latter occurring mostly during the morning and night (CDC, 2006).

Figure 14.21 In asthma, the airways become inflamed and narrowed.

According to the Centers for Disease Control and Prevention (CDC), around 4,000 people die each year from asthma-related causes, and asthma is a contributing factor to another 7,000 deaths each year (CDC, 2013a). The CDC has revealed that asthma affects 18.7 million U.S. adults and is more common among people with lower education and income levels (CDC, 2013b). Especially concerning is that asthma is on the rise, with rates of asthma increasing 157% between 2000 and 2010 (CDC, 2013b).

Asthma attacks are acute episodes in which an asthma sufferer experiences the full range of symptoms. Asthma exacerbation is often triggered by environmental factors, such as air pollution, allergens (e.g., pollen, mold, and pet hairs), cigarette smoke, airway infections, cold air or a sudden change in temperature, and exercise (CDC, 2013b).

Psychological factors appear to play an important role in asthma (Wright, Rodriguez, & Cohen, 1998), although some believe that psychological factors serve as potential triggers in only a subset of asthma patients (Ritz, Steptoe, Bobb, Harris, & Edwards, 2006). Many studies over the years have demonstrated that some people with asthma will experience asthma-like symptoms if they expect to experience such symptoms, such as when breathing an inert substance that they (falsely) believe will lead to airway obstruction (Sodergren & Hyland, 1999). As stress and emotions directly affect immune and respiratory functions, psychological factors likely serve as one of the most common triggers of asthma exacerbation (Trueba & Ritz, 2013).

People with asthma tend to report and display a high level of negative emotions such as anxiety, and asthma attacks have been linked to periods of high emotionality (Lehrer, Isenberg, & Hochron, 1993). In addition, high levels of emotional distress during both laboratory tasks and daily life have been found to negatively affect airway function and can produce asthma-like symptoms in people with asthma (von Leupoldt, Ehnes, & Dahme, 2006). In one investigation, 20 adults with asthma wore preprogrammed wristwatches that signaled them to breathe into a portable device that measures airway function. Results showed that higher levels of negative emotions and stress were associated with increased airway obstruction and self-reported asthma symptoms (Smyth, Soefer, Hurewitz, Kliment, & Stone, 1999). In addition, D’Amato, Liccardi, Cecchi, Pellegrino, & D’Amato (2010) described a case study of an 18-year-old man with asthma whose girlfriend had broken up with him, leaving him in a depressed state. She had also unfriended him on Facebook , while friending other young males. Eventually, the young man was able to “friend” her once again and could monitor her activity through Facebook. Subsequently, he would experience asthma symptoms whenever he logged on and accessed her profile. When he later resigned not to use Facebook any longer, the asthma attacks stopped. This case suggests that the use of Facebook and other forms of social media may represent a new source of stress—it may be a triggering factor for asthma attacks, especially in depressed asthmatic individuals.

Exposure to stressful experiences, particularly those that involve parental or interpersonal conflicts, has been linked to the development of asthma throughout the lifespan. A longitudinal study of 145 children found that parenting difficulties during the first year of life increased the chances that the child developed asthma by 107% (Klinnert et al., 2001). In addition, a cross-sectional study of over 10,000 Finnish college students found that high rates of parent or personal conflicts (e.g., parental divorce, separation from spouse, or severe conflicts in other long-term relationships) increased the risk of asthma onset (Kilpeläinen, Koskenvuo, Helenius, & Terho, 2002). Further, a study of over 4,000 middle-aged men who were interviewed in the early 1990s and again a decade later found that breaking off an important life partnership (e.g., divorce or breaking off relationship from parents) increased the risk of developing asthma by 124% over the time of the study (Loerbroks, Apfelbacher, Thayer, Debling, & Stürmer, 2009).

Tension Headaches

A headache is a continuous pain anywhere in the head and neck region. Migraine headaches are a type of headache thought to be caused by blood vessel swelling and increased blood flow (McIntosh, 2013). Migraines are characterized by severe pain on one or both sides of the head, an upset stomach, and disturbed vision. They are more frequently experienced by women than by men (American Academy of Neurology, 2014). Tension headaches are triggered by tightening/tensing of facial and neck muscles; they are the most commonly experienced kind of headache, accounting for about 42% of all headaches worldwide (Stovner et al., 2007). In the United States, well over one-third of the population experiences tension headaches each year, and 2–3% of the population suffers from chronic tension headaches (Schwartz, Stewart, Simon, & Lipton, 1998).

A number of factors can contribute to tension headaches, including sleep deprivation, skipping meals, eye strain, overexertion, muscular tension caused by poor posture, and stress (MedicineNet, 2013). Although there is uncertainty regarding the exact mechanisms through which stress can produce tension headaches, stress has been demonstrated to increase sensitivity to pain (Caceres & Burns, 1997; Logan et al., 2001). In general, tension headache sufferers, compared to non-sufferers, have a lower threshold for and greater sensitivity to pain (Ukestad & Wittrock, 1996), and they report greater levels of subjective stress when faced with a stressor (Myers, Wittrock, & Foreman, 1998). Thus, stress may contribute to tension headaches by increasing pain sensitivity in already-sensitive pain pathways in tension headache sufferers (Cathcart, Petkov, & Pritchard, 2008).

REGULATION OF STRESS

As we learned in the previous section, stress—especially if it is chronic—takes a toll on our bodies and can have enormously negative health implications. When we experience events in our lives that we appraise as stressful, it is essential that we use effective coping strategies to manage our stress. Coping refers to mental and behavioral efforts that we use to deal with problems relating to stress, including its presumed cause and the unpleasant feelings and emotions it produces.

Control and Stress

The desire and ability to predict events, make decisions, and affect outcomes—that is, to enact control in our lives—is a basic tenet of human behavior (Everly & Lating, 2002). Albert Bandura (1997) stated that “the intensity and chronicity of human stress is governed largely by perceived control over the demands of one’s life” (p. 262). As cogently described in his statement, our reaction to potential stressors depends to a large extent on how much control we feel we have over such things. Perceived control is our beliefs about our personal capacity to exert influence over and shape outcomes, and it has major implications for our health and happiness (Infurna & Gerstorf, 2014). Extensive research has demonstrated that perceptions of personal control are associated with a variety of favorable outcomes, such as better physical and mental health and greater psychological well-being (Diehl & Hay, 2010). Greater personal control is also associated with lower reactivity to stressors in daily life. For example, researchers in one investigation found that higher levels of perceived control at one point in time were later associated with lower emotional and physical reactivity to interpersonal stressors (Neupert, Almeida, & Charles, 2007). Further, a daily diary study with 34 older widows found that their stress and anxiety levels were significantly reduced on days during which the widows felt greater perceived control (Ong, Bergeman, & Bisconti, 2005).

DIG DEEPER

Learned Helplessness

When we lack a sense of control over the events in our lives, particularly when those events are threatening, harmful, or noxious, the psychological consequences can be profound. In one of the better illustrations of this concept, psychologist Martin Seligman conducted a series of classic experiments in the 1960s (Seligman & Maier, 1967) in which dogs were placed in a chamber where they received electric shocks from which they could not escape. Later, when these dogs were given the opportunity to escape the shocks by jumping across a partition, most failed to even try; they seemed to just give up and passively accept any shocks the experimenters chose to administer. In comparison, dogs who were previously allowed to escape the shocks tended to jump the partition and escape the pain (Figure 14.22).

Figure 14.22 Seligman’s learned helplessness experiments with dogs used an apparatus that measured when the animals would move from a floor delivering shocks to one without.

Seligman believed that the dogs who failed to try to escape the later shocks were demonstrating learned helplessness: They had acquired a belief that they were powerless to do anything about the noxious stimulation they were receiving. Seligman also believed that the passivity and lack of initiative these dogs demonstrated was similar to that observed in human depression. Therefore, Seligman speculated that acquiring a sense of learned helplessness might be an important cause of depression in humans: Humans who experience negative life events that they believe they are unable to control may become helpless. As a result, they give up trying to control or change the situation and some may become depressed and show lack of initiative in future situations in which they can control the outcomes (Seligman, Maier, & Geer, 1968).

Seligman and colleagues later reformulated the original learned helplessness model of depression (Abramson, Seligman, & Teasdale, 1978). In their reformulation, they emphasized attributions (i.e., a mental explanation for why something occurred) that lead to the perception that one lacks control over negative outcomes are important in fostering a sense of learned helplessness. For example, suppose a coworker shows up late to work; your belief as to what caused the coworker’s tardiness would be an attribution (e.g., too much traffic, slept too late, or just doesn’t care about being on time).

The reformulated version of Seligman’s study holds that the attributions made for negative life events contribute to depression. Consider the example of a student who performs poorly on a midterm exam. This model suggests that the student will make three kinds of attributions for this outcome: internal vs. external (believing the outcome was caused by his own personal inadequacies or by environmental factors), stable vs. unstable (believing the cause can be changed or is permanent), and global vs. specific (believing the outcome is a sign of inadequacy in most everything versus just this area). Assume that the student makes an internal (“I’m just not smart”), stable (“Nothing can be done to change the fact that I’m not smart”) and global (“This is another example of how lousy I am at everything”) attribution for the poor performance. The reformulated theory predicts that the student would perceive a lack of control over this stressful event and thus be especially prone to developing depression. Indeed, research has demonstrated that people who have a tendency to make internal, global, and stable attributions for bad outcomes tend to develop symptoms of depression when faced with negative life experiences (Peterson & Seligman, 1984).

Seligman’s learned helplessness model has emerged over the years as a leading theoretical explanation for the onset of major depressive disorder. When you study psychological disorders, you will learn more about the latest reformulation of this model—now called hopelessness theory.

People who report higher levels of perceived control view their health as controllable, thereby making it more likely that they will better manage their health and engage in behaviors conducive to good health (Bandura, 2004). Not surprisingly, greater perceived control has been linked to lower risk of physical health problems, including declines in physical functioning (Infurna, Gerstorf, Ram, Schupp, & Wagner, 2011), heart attacks (Rosengren et al., 2004), and both cardiovascular disease incidence (Stürmer, Hasselbach, & Amelang, 2006) and mortality from cardiac disease (Surtees et al., 2010). In addition, longitudinal studies of British civil servants have found that those in low-status jobs (e.g., clerical and office support staff) in which the degree of control over the job is minimal are considerably more likely to develop heart disease than those with high-status jobs or considerable control over their jobs (Marmot, Bosma, Hemingway, & Stansfeld, 1997).

The link between perceived control and health may provide an explanation for the frequently observed relationship between social class and health outcomes (Kraus, Piff, Mendoza-Denton, Rheinschmidt, & Keltner, 2012). In general, research has found that more affluent individuals experience better health mainly because they tend to believe that they can personally control and manage their reactions to life’s stressors (Johnson & Krueger, 2006). Perhaps buoyed by the perceived level of control, individuals of higher social class may be prone to overestimating the degree of influence they have over particular outcomes. For example, those of higher social class tend to believe that their votes have greater sway on election outcomes than do those of lower social class, which may explain higher rates of voting in more affluent communities (Krosnick, 1990). Other research has found that a sense of perceived control can protect less affluent individuals from poorer health, depression, and reduced life-satisfaction—all of which tend to accompany lower social standing (Lachman & Weaver, 1998).

Taken together, findings from these and many other studies clearly suggest that perceptions of control and coping abilities are important in managing and coping with the stressors we encounter throughout life.

Social Support

The need to form and maintain strong, stable relationships with others is a powerful, pervasive, and fundamental human motive (Baumeister & Leary, 1995). Building strong interpersonal relationships with others helps us establish a network of close, caring individuals who can provide social support in times of distress, sorrow, and fear. Social support can be thought of as the soothing impact of friends, family, and acquaintances (Baron & Kerr, 2003). Social support can take many forms, including advice, guidance, encouragement, acceptance, emotional comfort, and tangible assistance (such as financial help). Thus, other people can be very comforting to us when we are faced with a wide range of life stressors, and they can be extremely helpful in our efforts to manage these challenges. Even in nonhuman animals, species mates can offer social support during times of stress. For example, elephants seem to be able to sense when other elephants are stressed and will often comfort them with physical contact—such as a trunk touch—or an empathetic vocal response (Krumboltz, 2014).

Scientific interest in the importance of social support first emerged in the 1970s when health researchers developed an interest in the health consequences of being socially integrated (Stroebe & Stroebe, 1996). Interest was further fueled by longitudinal studies showing that social connectedness reduced mortality. In one classic study, nearly 7,000 Alameda County, California, residents were followed over 9 years. Those who had previously indicated that they lacked social and community ties were more likely to die during the follow-up period than those with more extensive social networks. Compared to those with the most social contacts, isolated men and women were, respectively, 2.3 and 2.8 times more likely to die. These trends persisted even after controlling for a variety of health-related variables, such as smoking, alcohol consumption, self-reported health at the beginning of the study, and physical activity (Berkman & Syme, 1979).

Since the time of that study, social support has emerged as one of the well-documented psychosocial factors affecting health outcomes (Uchino, 2009). A statistical review of 148 studies conducted between 1982 and 2007 involving over 300,000 participants concluded that individuals with stronger social relationships have a 50% greater likelihood of survival compared to those with weak or insufficient social relationships (Holt-Lunstad, Smith, & Layton, 2010). According to the researchers, the magnitude of the effect of social support observed in this study is comparable with quitting smoking and exceeded many well-known risk factors for mortality, such as obesity and physical inactivity (Figure 14.23).

Figure 14.23 Close relationships with others, whether (a) a group of friends or (b) a family circle, provide more than happiness and fulfillment—they can help foster good health. (credit a: modification of work by Nattachai Noogure; credit b: modification of work by Christian Haugen)

A number of large-scale studies have found that individuals with low levels of social support are at greater risk of mortality, especially from cardiovascular disorders (Brummett et al., 2001). Further, higher levels of social supported have been linked to better survival rates following breast cancer (Falagas et al., 2007) and infectious diseases, especially HIV infection (Lee & Rotheram-Borus, 2001). In fact, a person with high levels of social support is less likely to contract a common cold. In one study, 334 participants completed questionnaires assessing their sociability; these individuals were subsequently exposed to a virus that causes a common cold and monitored for several weeks to see who became ill. Results showed that increased sociability was linearly associated with a decreased probability of developing a cold (Cohen, Doyle, Turner, Alper, & Skoner, 2003).

For many of us, friends are a vital source of social support. But what if you found yourself in a situation in which you lacked friends or companions? For example, suppose a popular high school student attends a far-away college, does not know anyone, and has trouble making friends and meaningful connections with others during the first semester. What can be done? If real life social support is lacking, access to distant friends via social media may help compensate. In a study of college freshmen, those with few face-to-face friends on campus but who communicated electronically with distant friends were less distressed that those who did not (Raney & Troop-Gordon, 2012). Also, for some people, our families—especially our parents—are a major source of social support.

Social support appears to work by boosting the immune system, especially among people who are experiencing stress (Uchino, Vaughn, Carlisle, & Birmingham, 2012). In a pioneering study, spouses of cancer patients who reported high levels of social support showed indications of better immune functioning on two out of three immune functioning measures, compared to spouses who were below the median on reported social support (Baron, Cutrona, Hicklin, Russell, & Lubaroff, 1990). Studies of other populations have produced similar results, including those of spousal caregivers of dementia sufferers, medical students, elderly adults, and cancer patients (Cohen & Herbert, 1996; Kiecolt-Glaser, McGuire, Robles, & Glaser, 2002).

In addition, social support has been shown to reduce blood pressure for people performing stressful tasks, such as giving a speech or performing mental arithmetic (Lepore, 1998). In these kinds of studies, participants are usually asked to perform a stressful task either alone, with a stranger present (who may be either supportive or unsupportive), or with a friend present. Those tested with a friend present generally exhibit lower blood pressure than those tested alone or with a stranger (Fontana, Diegnan, Villeneuve, & Lepore, 1999). In one study, 112 female participants who performed stressful mental arithmetic exhibited lower blood pressure when they received support from a friend rather than a stranger, but only if the friend was a male (Phillips, Gallagher, & Carroll, 2009). Although these findings are somewhat difficult to interpret, the authors mention that it is possible that females feel less supported and more evaluated by other females, particularly females whose opinions they value.

Taken together, the findings above suggest one of the reasons social support is connected to favorable health outcomes is because it has several beneficial physiological effects in stressful situations. However, it is also important to consider the possibility that social support may lead to better health behaviors, such as a healthy diet, exercising, smoking cessation, and cooperation with medical regimens (Uchino, 2009).

DIG DEEPER

Coping with Prejudice and Discrimination

While having social support is quite beneficial, being the recipient of prejudicial attitudes and discriminatory behaviors is associated with a number of negative outcomes. In their literature review, Brondolo, Brady, Pencille, Beatty, and Contrada (2009) describe how racial prejudice and discrimination serve as unique, significant stressors for those who are the targets of such attitudes and behavior. Being the target of racism is associated with increased rates of depression, lowered self-esteem, hypertension, and cardiovascular disease.

Given the complex and pervasive nature of racism as a stressor, Brondolo et al. (2009) point out the importance of coping with this specific stressor. Their review is aimed at determining which coping strategies are most effective at offsetting negative health outcomes associated with racism-related stress. The authors examine the effectiveness of three coping strategies: focusing on racial identity to handle race-related stress, anger expression/suppression, and seeking social support. You’ve learned a bit about social support, so we’ll focus the remainder of this discussion on the potential coping strategies of focusing on racial identity and anger expression/suppression.

Focusing on racial identity refers to the process by which a person comes to feel as if he belongs to a given racial group; this may increase a sense of pride associated with group membership. Brondolo et al. (2009) suggest that a strong sense of racial identity might help an individual who is the target of racism differentiate between prejudicial attitudes/behaviors that are directed toward his group as a whole rather than at him as a person. Furthermore, the sense of belonging to his group might alleviate the distress of being ostracized by others. However, the research literature on the effectiveness of this technique has produced mixed results.

Anger expression/suppression refers to the options available as a function of the anger evoked by racial prejudice and discrimination. Put simply, a target of racist attitudes and behaviors can act upon her anger or suppress her anger. As discussed by Brondolo et al. (2009), there has been very little research on the effectiveness of either approach; the results are quite mixed with some showing anger expression and others showing anger suppression as the healthier option.

In the end, racism-related stress is a complex issue and each of the coping strategies discussed here has strengths and weaknesses. Brondolo et al. (2009) argue that it is imperative that additional research be conducted to ascertain the most effective strategies for coping with the negative outcomes that are experienced by the targets of racism.

Stress Reduction Techniques

Beyond having a sense of control and establishing social support networks, there are numerous other means by which we can manage stress (Figure 14.24). A common technique people use to combat stress is exercise (Salmon, 2001). It is well-established that exercise, both of long (aerobic) and short (anaerobic) duration, is beneficial for both physical and mental health (Everly & Lating, 2002). There is considerable evidence that physically fit individuals are more resistant to the adverse effects of stress and recover more quickly from stress than less physically fit individuals (Cotton, 1990). In a study of more than 500 Swiss police officers and emergency service personnel, increased physical fitness was associated with reduced stress, and regular exercise was reported to protect against stress-related health problems (Gerber, Kellman, Hartman, & Pühse, 2010).

Figure 14.24 Stress reduction techniques may include (a) exercise, (b) meditation and relaxation, or (c) biofeedback. (credit a: modification of work by “UNE Photos”/Flickr; credit b: modification of work by Caleb Roenigk; credit c: modification of work by Dr. Carmen Russoniello)

One reason exercise may be beneficial is because it might buffer some of the deleterious physiological mechanisms of stress. One study found rats that exercised for six weeks showed a decrease in hypothalamic-pituitary-adrenal responsiveness to mild stressors (Campeau et al., 2010). In high-stress humans, exercise has been shown to prevent telomere shortening, which may explain the common observation of a youthful appearance among those who exercise regularly (Puterman et al., 2010). Further, exercise in later adulthood appears to minimize the detrimental effects of stress on the hippocampus and memory (Head, Singh, & Bugg, 2012). Among cancer survivors, exercise has been shown to reduce anxiety (Speck, Courneya, Masse, Duval, & Schmitz, 2010) and depressive symptoms (Craft, VanIterson, Helenowski, Rademaker, & Courneya, 2012). Clearly, exercise is a highly effective tool for regulating stress.

In the 1970s, Herbert Benson, a cardiologist, developed a stress reduction method called the relaxation response technique (Greenberg, 2006). The relaxation response technique combines relaxation with transcendental meditation, and consists of four components (Stein, 2001):

1. sitting upright on a comfortable chair with feet on the ground and body in a relaxed position,
2. a quiet environment with eyes closed,
3. repeating a word or a phrase—a mantra—to oneself, such as “alert mind, calm body,”
4. passively allowing the mind to focus on pleasant thoughts, such as nature or the warmth of your blood nourishing your body.

The relaxation response approach is conceptualized as a general approach to stress reduction that reduces sympathetic arousal, and it has been used effectively to treat people with high blood pressure (Benson & Proctor, 1994).

Another technique to combat stress, biofeedback, was developed by Gary Schwartz at Harvard University in the early 1970s. Biofeedback is a technique that uses electronic equipment to accurately measure a person’s neuromuscular and autonomic activity—feedback is provided in the form of visual or auditory signals. The main assumption of this approach is that providing somebody biofeedback will enable the individual to develop strategies that help gain some level of voluntary control over what are normally involuntary bodily processes (Schwartz & Schwartz, 1995). A number of different bodily measures have been used in biofeedback research, including facial muscle movement, brain activity, and skin temperature, and it has been applied successfully with individuals experiencing tension headaches, high blood pressure, asthma, and phobias (Stein, 2001).