Sociology Essay 221
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CHAPTER 3. UNDER OUR SKIN: HOW AND WHY STRESS AFFECTS OUR PHYSICAL HEALTH
Can stress kill? Popular culture would certainly have us believe so. Classic film buffs may recall the scene from when Charlotte Vale, a quiet spinster who blossoms into a world-travelingNow, Voyager sophisticate, has a heated argument with her disapproving mother, who promptly dies of a heart attack. A similar fate struck Horace Giddens in A frail man with a serious heartLittle Foxes. condition, Horace suffered a heart attack after a vicious spat with his contemptuous wife, Regina. Such dramatic depictions are not limited to the silver screen. On the small screen, ’The Simpsons Homer Simpson collapsed from a heart attack after his cruel and enraged boss Mr. Burns threatened to fire him from his job at a nuclear power plant.
These melodramatic scenes suggest that stressful encounters may be lethal (often instantaneously), yet we all can think of more gradual or subtle instances in which a friend or family member took ill after a long period of duress. In , we met Naomi, who suffered a minor stroke just weeksChapter 1 after the one-two punch of her husband’s and mother’s deaths. Or Marisol, the twenty-year-old college student who was burning the candle at both ends—working, volunteering, helping her mother with child care, and struggling with a difficult academic course load—before succumbing to the flu during final exams.
Is it really as simple as “shock” or “wear and tear” hurting our hearts and running down our immune systems? Dozens of biological studies document direct linkages between exposure to stress in laboratory settings and physical symptoms such as elevated heart rate, spikes (or drops) in cortisol levels, and susceptibility to colds and infections. Social scientists, by contrast, argue that stress—whether struggles with a daunting college curriculum or the strains of caregiving—is tightly interwoven with other health risks in our lives. As such, it’s much harder to conclude that stress alone “causes” our health problems.
Let’s suppose that Naomi was a lifelong smoker who upped her habit to two packs a day as a way to calm her nerves during her decade-long stint as a family caregiver. Or that she hadn’t gone to the doctor for an annual physical exam in years, because she couldn’t take the time away from her round-the-clock caregiving demands. Or that she had lost her health insurance coverage to pay for doctor’s visits now that her husband was too ill to work (and the family lost health benefits). Now let’s imagine that Marisol slept only four hours a night, and subsisted on energy drinks and sugary cereals, overwhelmed by her college classes and other obligations. Is it really the stressors per se that caused their ailments, or might unhealthy behaviors, lack of time for self-care, or limited access to medical care also have contributed to these women’s health woes?
Most stressors do not affect our physical health instantaneously or directly. Rather, stress often is associated with other behaviors and experiences that may compromise our health. A stressor may trigger subsequent changes in our social lives—whether shifts in our relationships, daily routines, or health behaviors—that may threaten our physical health and vigor. In this chapter, I provide an overview of the diverse ways that researchers study the linkages between stress and physical health. I then review social and biological explanations for why and how stress affects health—whether directly or indirectly. Importantly, no single explanation is sufficient to explain the stress-health connection, because our minds, bodies, and social worlds are interconnected in complex ways.
Stress and Physical Health: How Do We Study It?
Stress is associated with a broad range of health outcomes, including mortality risk and nearly every possible physical symptom or condition, including headaches, heart disease, diabetes, risk of infection, colds, and even how quickly our wounds heal. Most research on the physical health effects of stress relies either on surveys or laboratory designs, although a handful of fascinating studies also
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rely on chance events or disasters. Each approach sheds light on different aspects of the stress-health connection.
Survey Approaches to Understanding Stress and Health
Survey studies draw on questionnaire data provided by hundreds if not thousands of individuals who report on major stressful events such as divorce or job loss, chronic strains such as caregiving or job stress, and even indicators of early life strains such as exposure to child abuse or poverty. Some surveys include a daily diary component, which asks respondents to report on hassles and uplifts experienced throughout their day for a number of consecutive days or weeks.
Most surveys also obtain extensive measures of self-reported physical health. Rather than directly capturing measures such as current heart rate, most surveys ask people to describe how good their overall health is, with response categories such as excellent, very good, good, fair, or poor. Some surveys obtain detailed illness checklists, which ask respondents to indicate which of a dozen or two health conditions they have been diagnosed with—such as cancer, heart disease, hypertension, or arthritis. Similarly, symptom checklists capture the number of times in the past week (or sometimes longer) that someone has experienced a dozen or so different health symptoms, ranging from headaches to stomach aches to excessive sweating. Many survey investigators track their research subjects over long periods of time, often until old age. At each follow-up interview, health information is obtained so that researchers can track whether the study participant’s health has changed in response to a stressor that occurred between the interviews.
As part of this follow-up, researchers might learn that a participant has died since the last wave of their survey. The investigators may then obtain information on the person’s age and cause of death. These data can be obtained from a death certificate; this information helps researchers explore whether people reporting the highest level of stress in surveys are most likely to die prematurely or from particular causes. For example, one study of nearly ninety thousand adults in the United Kingdom found that persons reporting high levels of psychological distress in a survey went on to have higher overall death rates and higher rates of death due to heart disease compared to persons with less stressful lives. Survey studies also may ask about health behaviors, including drinking, smoking, exercise, and diet; health behaviors are an important mechanism that might link stress to health.
Over the past two decades, a growing number of population-based surveys have obtained biological indicators of health (or “biomarkers”) in addition to self-reported measures. In such cases, the research team members who administer the survey may also draw blood, obtain a saliva sample, or take a blood pressure reading on their study participants. The most common way to obtain a biological measure today is through the collection of saliva samples; the investigator may ask a research subject to drool into a test tube or to chew on a piece of cotton that absorbs the saliva. Researchers prefer to collect saliva rather than blood because it is less intrusive, meaning that it is less physically and psychologically distressing to research subjects. These newly collected biological data can then be analyzed as another indirect indicator of one’s health.
For example, researchers who collect information on a survey participant’s blood pressure and other physiological indicators such as cholesterol or the “stress hormone” cortisol can then calculate a person’s score on the allostatic load scale. Neurophysiologist Bruce McEwen developed the concept and measure of allostatic load (AL), which refers to a collection of symptoms and conditions that indicate accumulated wear and tear on one’s body. Persons who score high on the AL index have been found to have a heightened risk of early mortality and illnesses such as heart disease and diabetes. Thus, this measure helps researchers to understand the ways that physiological responses to chronic stress may hurt one’s health and shorten one’s life span.
Stress researchers who use survey data and either self-reported health measures or biomarkers typically investigate the long-term or cumulative effects of stress, rather than its immediate and instantaneous effects. For instance, a team of researchers who work on the Midlife Development in
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the United States (MIDUS) study, a sample survey of more than three thousand adults, found that persons who were poor when growing up (e.g., were on welfare or recalled high levels of financial stress in their families) went on to have higher AL scores in adulthood, compared to their peers who grew up without such financial strain. Another study from the MIDUS found that parents who were raising children with major mental illnesses or developmental conditions such as autism had higher scores on the AL scale. These patterns reveal the long-term “wear and tear” on multiple physiological systems of managing difficult childrearing demands for years on end.
Laboratory-Based Studies of Stress and Health
Surveys can provide us rich information on stressors spanning multiple domains—from work to family to finances—and can capture stressors dating back to our earliest years of life. However, surveys have important limitations, including recall bias. Some survey participants may not be able to accurately recall the distant past, or may even report distorted memories. An adult who is currently depressed may recall their childhood as gray and gloomy, marred by poverty, loneliness, and a lack of emotional support from parents. However, these memories may not reflect the realities of one’s childhood, but rather one’s current mood state that darkens and alters one’s memories.
Another limitation is that it is very difficult to ascertain causation using survey data. A researcher may find a strong correlation (i.e., statistical association) between a recent job loss and headaches, yet there may be other competing explanations for the association. For instance, a worker with persistent debilitating headaches may be frequently absent from work and may be the first to be fired when a boss needs to downsize the company. Social scientists recognize that laboratory-based experiments are the scientific “gold standard” in trying to understand causation. In an experiment, a researcher will typically expose a study participant to a stressor and then measure some biological indicator, such as blood pressure, before and after the stressor. If the indicator changes, then the change can be attributed to the lab-induced stressor. In other cases, the experimenter may randomly assign one half of study participants to a stressful condition and the other half to a neutral condition. If the two groups of study participants then differ on a biological or health outcome, the researcher can plausibly attribute the difference to the stressful condition. Experiments, like surveys, have many shortcomings. They often focus on artificial stressors, such as arguments triggered in the lab, rather than real-world stressors. Still, laboratory-based studies can help us to understand some general principles about stress and health.
The most common approach to inducing stress in a laboratory setting is creating what scientists call a “social evaluative threat.” A research subject will perform some task and will then be evaluated publicly by others. For example, one commonly used protocol is the Trier Social Stress Test (TSST). Subjects are required to deliver a public speech in front of a “team of experts” (who often are research staff masquerading as “experts”) after having a period of five minutes to prepare. At the end of the speech, the research participants are asked to serially subtract numbers as quickly and accurately as possible. They might be told, “Please start at 100, and count backwards by 7.” Each time the participant makes a mistake, he or she is stopped and asked to start over from the initial number. Understandably, we would all be a bit stressed out from giving a public talk and then performing a tricky math exercise in front of a team of so-called experts! The researchers examine whether this stressful experience affects subjects’ physical well-being by taking saliva samples when the study respondents first arrive at the lab (i.e., baseline), immediately after the speech and math performance, and then several times afterward.
This study design has been used many times, and consistently shows that salivary cortisol levels show a two- to fourfold increase above one’s initial level within a half hour after the stressful lab tasks have been completed. Cortisol, as described in , is a stress hormone. Although smallChapter 2 increases in cortisol levels can be good for us in the short term by boosting our memory and immune function, persistently high levels are linked with health-depleting physical responses, including suppressed thyroid function, blood sugar imbalances, high blood pressure, lowered immune
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responses, slowed wound healing, and even a decrease in bone density and muscle tissue. High levels of stress-induced cortisol rises also are linked with abdominal adiposity or “belly fat,” which in turn increases our risk of heart attack, stroke, and metabolic syndrome. Although it would be a stretch to say that a stressful lab activity such as doing a math test heightens our risk of heart attack, lab-based studies do provide important insights into the physiological mechanisms linking daily stress and health.
Some skeptical readers may be rolling their eyes, thinking that a math test or public speaking exercise in a laboratory setting doesn’t even begin to capture what the real stressors in our lives are like. Rather, the stressors that affect us most may be the ones that are most salient or meaningful to us, such as problems with our marriages, jobs, or health. Lab-based stress researchers, typically psychologists, recognize that more realistic stressors may be a better way to examine linkages between stress and physiological response, and have devised other innovative designs to address these concerns.
One common strategy is for researchers to bring into the laboratory a couple, usually married or in a long-term dating relationship, and then provoke an argument between the partners. A fight with one’s long-time love would certainly be more personally salient than would a one-time math exercise. Researchers typically assess the partners’ cortisol levels before and after the spat, as a way to track physiological response to stress. In other cases, the investigators may give the subjects a small wound or injection at the beginning of the study, and then examine how quickly the wound heals under the stressful condition of the marital spat.
For example, a team of researchers at Ohio State University brought into their laboratory forty-two healthy married couples, whose ages ranged from twenty to eighty. When the study started, the researchers gave each spouse a small (and relatively painless) cut on his or her forearm. Some study participants were then told to discuss a potentially contentious topic with their spouse, such as in-law woes or financial worries. The researchers found that the couples with the most heated arguments had significantly slower wound healing, evidenced by how quickly the small forearm cut healed. Most subjects healed within five days, but those who had a heated discussion with their spouse took one full day more to heal. The researchers also obtained information on how the couple interacted during the argument. They videotaped the arguments and rated how “hostile” the exchanges were; those couples rated as being hostile toward one another took fully seven days to heal. Taken together, these studies show that an acute stressor, such as a one-time argument, can impair one’s immune system, the biological system linked to wound healing. The study also showed that chronic strain, measured as a hostile interactional style between spouses, slowed the healing process even more.
Quasi-Experimental Designs: Tracking the Health Effects of Chance Events
Skeptical readers, once again, may question whether a lab-induced lovers’ spat really qualifies as “stress.” Others may question whether experimental designs are adequate to capture major life stressors, such as disaster and trauma. It would clearly be unethical (and impossible) to randomly assign one-half of subjects to a tragic situation, and the other half to a pleasant or neutral situation. However, researchers can sometimes capitalize on “chance events” or unexpected tragedies to explore their impact on physical health. Although these study designs are imperfect and researchers cannot definitively ascertain whether the distressing event “causes” health declines, such studies can provide valuable information on some aspects of health, specifically heart attack risk, in the face of major events.
Extensive international data reveal an increased risk of cardiovascular problems (including heightened blood pressure, heart rate, and heart attack risk) shortly after an earthquake. Earthquakes are unique disasters because they come unexpectedly and suddenly. In addition to the initial stress of the physical destruction, survivors face subsequent chronic stressors, including forced relocation; lack of electricity, water, and telephone service; and decreased access to food. Although psychological distress would certainly increase in such situations, evidence suggests that heart health also suffers.
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During a 1999 earthquake in Taiwan, twelve people in the local area were already part of a study in which their heart rates were being monitored. The monitors documented that in the minutes before and after the earthquake struck, the subjects’ heart rates increased substantially.
Similar patterns were found following the Hanshin-Awaji earthquake Japan in 1995, when blood pressure levels spiked and remained high, even at night when the subjects were sleeping. The number of heart attack patients and subsequent deaths recorded at local hospitals were also detected following the 2004 Central Niigata earthquake in Japan, and the 1994 Northridge, California, quake. However, some earthquakes, such as the 1989 Loma Prieta quake in California, have not been linked with increased risks of heart attack. Researchers point out that there is great variety in the stressfulness of even seemingly devastating events like earthquakes. Some are lower on the Richter scale and less destructive than others, while earthquakes that strike at night are more disruptive and disorienting than those that strike during the day.
Taken together, these survey, laboratory, and chance event studies show that both acute and chronic stressors may trigger physiological responses that are linked to illness risk. Although short-term physical reactions to stress, such as a cortisol spikes, may be adaptive and may help people to flee or adapt to the initial shock, the persistent consequences of stress exposure can be much more severe. As internationally renowned stress researcher Robert Sapolsky has observed, “Stress-related disease emerges, predominantly, out of the fact that we so often activate a physiological system that has evolved for responding to acute emergencies, but we turn it on for months on end, worrying about mortgages, relationships and promotions” (1998).
The Stress-Health Connection: Social Science Explanations
Social scientists, including sociologists, psychologists, and epidemiologists, generally believe that the stress in our daily lives can take a harsh toll on our physical health, even if it takes months or years for these effects to come to fruition. These explanations for stress affects our physical well-beingwhy tend to focus on our thoughts, behaviors, emotions, social ties, and social resources—rather than on biology alone. Taken together, social science perspectives suggest that reducing stress in our lives may indeed improve our health, yet it is equally important to repair the social contexts that give rise to stress and to our personal or interpersonal responses to the stress.
Drowning Our Sorrows: The Role of Health Behaviors
A stressful encounter may make our heart race and palms sweat, but stress also makes us behave in ways that hurt (or protect) our health. Think about how you deal when you’ve had a stressful day at the office, heard bad news, or gone through a heart-wrenching breakup. Do you seek comfort with a glass of wine and a cigarette? Unwind in a yoga class? Work out your frustrations with an invigorating run in the park? Devour a pint of Ben & Jerry’s while watching your favorite guilty pleasure reality show? The ways that people alter their behaviors in response to chronic and acute stressors partly explain why some get sick and others don’t. Health behaviors, including smoking, alcohol consumption, exercise, eating habits, and drug use, are associated with our risk of illness and death, and play a critical role in linking social stress to physical health.
Most Americans rely on healthy strategies to manage stress. The American Psychological Association (APA) conducts an annual survey of more than one thousand American adults, and finds that the most popular strategies for managing stress are listening to music, exercising or taking a walk, spending time with family and friends, and reading—with more than 40 percent of Americans using these stress management tactics in 2010.
Yet a significant minority also turns to unhealthy behaviors, such as overeating or eating unhealthy foods (34 percent), drinking alcohol (19 percent), or smoking (16 percent). The APA report is
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consistent with scientific studies showing that stress is associated with consuming higher-fat diets, eating fast-food meals, smoking, failed attempts to quit smoking, more frequent and heavier alcohol use, and skipping exercise. When our nerves are frayed and our minds are racing with troubling thoughts, “self-medication” might seem like a sensible and soothing quick fix. Scientists have documented that nicotine, the addictive drug component of cigarette smoke, helps to calm people’s nerves by altering activity in parts of the brain that control negative emotions such as anger. Alcohol (in moderation) relaxes or dilates our blood vessels, and takes the pressure off our hearts. A glass of wine or a beer also might help us forget our troubles (temporarily) because ethanol, the main psychoactive ingredient in alcoholic beverages, is a psychoactive drug. After a few drinks, we experience mild euphoria and loss of inhibition, as alcohol impairs the regions of the brain that control our actions and emotions.
Caffeine provides us with a short-term energy boost that may help us to survive a major work deadline or an intense exam week. Likewise, sugar is the basic source of energy in the foods and beverages we consume, so it can give us both energy and a quick mood lift. The desire to console ourselves with high-fat “comfort” foods when we’re stressed out is perfectly natural, from an evolutionary perspective. When our bodies are under constant stress, we physiologically need high-energy foods to help us persist and weather these challenges. Stress also triggers hormonal changes that make us crave high-fat, high-salt dishes. Some studies also show that we crave foods such as macaroni and cheese or meatloaf when we’re sad, stressed, or anxious because these foods remind us of a more peaceful time or place, when we felt safe, secure, and loved.
While alcohol, cigarettes, sugary or fatty foods, and caffeine might help us to feel better in the short term when we’re stressed, in the longer term, these vices may elevate our risk of diseases including heart disease, diabetes, liver disease, high blood pressure, and some cancers. Some health behaviors may create more stress in our lives, which may kick off a vicious circle of taking on even more unhealthy behaviors. Heavy drinkers may have more frequent marital feuds and shakier employment prospects than nondrinkers or abstainers, which in turn may drive them to drink even more. Obesity, which is a consequence of consuming more calories than we burn off through physical activity, increases one’s risk of weight-related discrimination and teasing, which in turn may trigger more stress-related eating. While some mood-enhancing behaviors may feel good in the short term, their longer-term health consequences can be dire.
What’s more, people who are under the most intense stress also are most likely to turn to unhealthy practices such as smoking, or to say that they’re “too busy” or “don’t have enough time” to exercise, eat healthy meals, or catch up on their sleep. For example, the 2012 APA study showed that family caregivers were much more likely than noncaregivers to overeat, or to eat unhealthy foods. These behaviors may partly account for family caregivers’ elevated risk of heart disease, stroke, and even premature death. One study by Ohio State University researchers Ronald Glaser and Janice Kiecolt-Glaser found that adult children caring for their aged parents with Alzheimer’s disease, and mothers caring for terminally ill young children, ultimately died four to eight years younger than their counterparts not providing such care. Ironically, those who provide care for others often lack the time to engage in self-care or other practices that keep them healthy and rejuvenated.
Nudging and Nagging: The Role of Significant Others
Stress drives many people to take on new or ramp up old unhealthy behaviors and eschew healthy ones. While it’s easy to blame these self-destructive coping patterns on lack of willpower, that would be an incomplete and inaccurate characterization. Part of the reason why major life stressors such as divorce, widowhood, and unemployment are linked to unhealthy behaviors is that stressed people often lose the significant others or structural supports that helped them to stay healthy, sober, drug-free, or physically fit. Let’s consider the case of marriage and marital dissolution. Academic studies show that married people (and especially happily married people) have better physical health and longer lives than their unmarried peers. Yet the health benefits of marriage are larger for men
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than for women, because women typically play the role of health protector in marriage. Women may nudge their husbands to take their daily medication, eat healthy meals, and curb their drinking. When a marriage ends, whether through death or divorce, a man often loses his helpmate and “nurse.”
That’s part of the reason why epidemiologic studies show that men are more likely than women to experience downturns in physical health when they divorce or become widowed. Widowers are more likely than married men to die of accidents, alcohol-related deaths, lung cancer, or heart disease during the first six months after their wives die. However, they are no more likely than their married counterparts to die from other causes that are less closely linked to health behaviors, such as stomach cancer or respiratory disease. While romantic movies tell us that widowers may “die of a broken heart” shortly after their wives pass away, due to the stress and emotional drain of the loss, that’s only part of the story. Widowers lose not only a lifelong partner but also their wives’ reminders to wear a seatbelt, to take their blood pressure medication, and to eat the salad rather than the sixteen-ounce steak for dinner.
Our social ties protect our physical health in another way: social roles such as spouse, worker, and parent impose a sense of obligation, responsibility, and routine into everyday life. These routines and obligations also encourage and promote healthy behaviors. Having a job to report to every morning at 9 a.m. lessens the chances that one will go on an alcohol-frenzied bender the night before. The flip side, however, is that when these roles disappear—whether through job loss, divorce, or death of one’s child—the very forces that supported our health behaviors slip away as well. For instance, upon having a child, young men and women who were previously reckless may abandon their “wild” pasts and adopt healthy lifestyles.
Sociologists Deborah Carr, Tetyana Pudrovska, Corinne Reczek, and Debra Umberson (2012) have found that single men who were big drinkers and carousers would give up their evenings at the bar when they married. Their wives would often put their foot down and demand that their husbands grow up, while some men decided on their own that their bar-hopping days were over. Yet when these marriages ended, the men (and some women) cranked up their drug use and drinking, often to dull the pain of the loss or to find emotional support with their old drinking buddies. As Jeffrey, a fifty-seven-year-old divorced participant in the study, said, “As a musician, I guess from the age of sixteen on I was experimenting with drugs . . . marijuana, alcohol, and cocaine. I think after my divorce I went back and just got way in over my head. . . . It didn’t really turn to real abuse until after the divorce. It was part of my lifestyle at that time.” Although Jeffrey eventually made his way into treatment and got clean, his case vividly shows how the stressful loss of an important role, for instance, being spouse, may trigger a return to one’s old self-destructive ways.
A Hard Day’s Night: Stress and Sleep
Sleep (or lack thereof) has recently been identified as a critical link between stress and physical health. Sleep problems, which include taking a long time to fall asleep, waking up throughout the night, getting too few hours of sleep, and waking up feeling tired, have been rising steadily in the United States. A 2013 Harris Poll of more than one thousand American adults found that 83 percent say they don’t get a good night’s sleep on a consistent basis. Severe sleep disorders are less common, but have risen steadily over the past decade. According to the Centers for Disease Control, 10 percent of Americans now have chronic insomnia, and 4 percent have used sleeping medication in the past week. Researchers have recently started to pay greater attention to sleep problems, because inadequate sleep has been linked to the onset and progression of many diseases and health conditions, including diabetes, heart disease, high blood pressure, depression, and abdominal adiposity.
Not all sleep problems are due to stress, of course. Some are due to obesity-related sleep apnea, electronic late-night distractions such as smart phones and 24/7 access to media, a spouse’s snoring, a child’s nightmares, or an overly energetic pet’s desire for nighttime feedings. Yet on the whole, personal and environmental stressors are the most common threats to a good night’s sleep. The 2013 Harris Poll found that “stress and anxiety” was the top reason people gave for their sleep problems.
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Another 47 percent said that they couldn’t turn off their anxious thoughts, which caused them to toss and turn or to wake up repeatedly. People who live in unsafe, loud neighborhoods tend to have more difficulty falling asleep and staying asleep, compared to people living in more bucolic and peaceful neighborhoods.
While stress can trigger sleep problems, sleep problems, in turn, can trigger secondary stressors. The vexing cycle of stress and sleep troubles can be difficult to break. Sleep deprivation impairs our performance on complex tasks and compromises our alertness, memory, and ability to think clearly and process information. Not surprisingly, automobile accidents and occupational injuries are linked to sleepiness behind the wheel or on the job. Sleep troubles may also threaten our relationships, either because we’re tired, irritable, and may mistreat our loved ones, or because one partner’s sleeping patterns may contribute to the other partner’s sleep troubles.
For young people today, especially some college students, there’s a new wrinkle in the stress-sleep-health cycle: increased reliance on “smart drugs” or “study drugs” such as Adderall and Ritalin. College students, especially those who feel intense pressure to get good grades while juggling other work and extracurricular activities, are turning to “cognitive enhancers.” These amphetamine-based drugs, historically prescribed for attention deficit disorder, are now the rage on many college campuses. An estimated 25 percent of students have taken these drugs; the short-term payoff is that the drugs are believed to enhance cognitive function and enable stressed-out students to study for hours with full concentration without getting fatigued. However, scientists have found that these “smart drugs” increase the brain chemical dopamine, raise students’ heart rates, and can lead to severe sleep deprivation. The drugs also can be addictive, further contributing to the cycle of school stress, self-medication, and sleep deprivation. Although it’s too soon to tell what the long-term consequences are for young people’s health, researchers say that at the very least, racing heart rates and sleep deprivation may take a toll in the short term.
The Mind-Body Connection
Chapter 2 described how difficult periods take a toll on our emotional well-being. Yet the mind and the body are closely interconnected, so the psychological reactions we have to stress (such as depression, grief, anxiety, and anger) may in turn affect our physical health. The Buddhist tradition regards the body and the mind as mutually dependent, while folk wisdom tells us that “it’s not what you eat, it’s what’s eating you” that makes people ill. Scientific evidence, too, shows that the mind and the body are mutually influential. At the most basic level, persons who are depressed and have a difficult time getting motivated may be less likely to engage in protective health behaviors, to sleep regularly, to seek out medical care when needed, or to engage in self-care. Mental health symptoms such as anger, hostility, or withdrawal from others may build a barrier between the stressed-out individuals and the friends and family who could help them to work through their stress.
Emerging scholarship argues that mental health conditions, especially depression, can “cause” physical health conditions. For example, the American Psychological Association (2007) recently published a report titled , which emphasizedContributions Toward Evidence-Based Psychocardiology how depression and hostility could contribute to heart disease by increasing stress hormones. However, most researchers find two other arguments are far more plausible. First, if risk of depression and chronic illness are correlated, it’s more likely that the depression is a result—rather than the cause—of the chronic illness. Health psychologist Howard Leventhal and colleagues have found that the tasks of managing one’s illness, whether regularly seeking treatments, altering one’s diet and lifestyle, or giving up vigorous activities one once liked to do, may depress one’s mood.
Second, if depression and chronic illness co-occur, it’s possible that the association is spurious. That is, both conditions may result from a shared set of triggers, such as persistent poverty that makes one feel consistently demoralized and hopeless yet at the same time prevents one from eating healthy foods, buying a gym membership, paying for hypertension medications, or seeing regular care from a personal physician—all of which may conspire to increase one’s risk of heart disease. No one would
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refute that problems of the mind and of the body are closely intertwined, yet there is far less agreement about which came first. However, most scholars recognize that many stress-related physical and mental health concerns are deeply rooted in social and economic inequalities.
Social Class: The Fundamental Cause behind the Stress-Health Link?
One of the most well-established findings in epidemiological studies is the “social class gradient” in health. Regardless of what health outcome is considered, including frequency of headaches, muscle pain, diabetes risk, cancer, disability, or death, those with fewer social and economic resources fare worse than those with richer resources. The social class gradient in health may partly explain the linkage between stress and physical health; as sociologist Leonard Pearlin’s stress process model tells us, not all people are equally likely to be exposed to stress. Those possessing the fewest social and economic resources, whether education, wealth, income, occupational status, or a safe and secure living space, are at the greatest risk of just about every work-, family-, and social-network-related stressor, and these stressors in turn may compromise health.
Sociologists Bruce Link and Jo Phelan (2010) developed fundamental cause theory (FCT) to explain the steep social class gradient in health. Social-class-based disparities in physical health are stark; for example, people at the top of the income ladder in the United States live seven years longer, on average, than those on the lower rungs. Fundamental cause theory argues that these stark health disparities exist because social class encompasses a sweeping array of resources, including money, knowledge, power, and beneficial social connections that may affect health in powerful ways. The uneven distribution of stress throughout the social hierarchy contributes to the class gradient in health. Lower socioeconomic status (SES) increases one’s risk of stressful life events, ranging from divorce to job loss to crime victimization, and one’s chronic stressors, including poor, overcrowded and unsanitary living conditions; persistent economic strain; and discrimination. Social class also is associated with having fewer coping resources, including supportive social ties, effective problem-solving strategies, and the financial means to escape a distressing situation.
One study by epidemiologist Sandro Galea and colleagues examined social factors related to adult mortality from 1980 to 2007; some of the most “lethal” social factors they identified sit at the intersection of poverty and stress. They estimated that 133,000 deaths in the United States in 2000 could be attributed to poverty, and that a whopping 176,000 deaths could be blamed on racial segregation, whereas car accidents accounted for just 119,000 deaths. Of course, it is difficult to prove the bold claim that the stress of living in a racially segregated, poor, or social isolated neighborhood will “kill.” However, scholars working in the tradition of fundamental cause theory draw our attention to the ways that stress and economic inequality are inextricably tied, and to how the two adversities heighten one’s risk of multiple physical and mental health woes.
The Stress-Health Connection: Physiological Pathways
Our social environments and resources clearly contribute to the stress-health link. Yet since the 1980s, many scientists have started to cast a spotlight on biological rather than social explanations for the stress-health connection. In the past three decades, a tidal wave of articles has been published on the biological pathways linking stress to health. This rise is due, in part, to technological advances in how efficiently we can measure physiological responses to stress. Scientists working in the fields of psychoneuroimmunology are better equipped than ever before to evaluate the brain’s responses to stress, while biological scientists can quickly measure and assess physiological responses in heart rate, cortisol levels, and breathing. While this explosion of scholarship is new, it shares its fundamental roots with the earliest research on stress, conducted by endocrinologist Hans Selye.
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Early Writings of Selye
Selye viewed physical distress as an automatic response to any environmental stressor. In response to stress, the body would pass through the three distinct stages of alarm, resistance, and exhaustion. In the alarm stage, the autonomic nervous system is stimulated, sympathetic nervous system activity is suppressed, and muscle tone decreases. In the resistance stage, the body tries to maintain a high level of functioning in order to survive the threat. In the final exhaustion stage, endocrine activity is heightened, and high levels of cortisol start to take their toll on the body’s circulatory, digestive, immune, and cardiovascular systems. Human energy and resources are depleted, and permanent damage to the body might result from the cumulative wear and tear.
In the six decades since the publication of Selye’s path-breaking work, scientists working in fields ranging from genetics to psychophysiology to neuroscience have elaborated on the biological pathways linking stress to physical health conditions. While Selye assumed that all stressors affect physical functioning, contemporary research sheds light on why some health conditions, especially heart disease, are susceptible to particular types of stressors. A full explication of the physiological pathways linking stress to health is complicated and beyond the scope of this slim book; however, in the next few paragraphs I provide a brief overview of the ways that key biological systems, including the central nervous, cardiovascular, and immune systems, respond to stress, and how these responses may carry long-term implications for our risk of disease and death.
Physiological responses to stress involve the direct stimulation of the central nervous system (CNS) and a hormonal relay system among three organs: the adrenal glands, located at the top of each kidney; the hypothalamus; and the pituitary gland, located in the brain. Both the CNS and the hypothalamic-pituitary-adrenal (HPA) axis play a critical role in linking stress with physical health. Most research on social stress and health has focused on the cardiovascular and immune systems because they are closely related to the progression of common diseases, including heart disease, stroke, and pneumonia.
Stress and Cardiovascular Health
Stress researchers are particularly concerned about heart disease because it is the leading cause of death in the United States and in most wealthy developed nations today. Of the roughly 2.5 million deaths in the United States in 2010, about 600,000 were due to heart disease. Stress is clearly implicated as a risk factor for heart disease and stroke—although the association may not be as direct as films like might lead us to believe. Our personal reactions to stress account in largeNow, Voyager part for the stress-heart disease link. High stress reactivity increases vascular inflammation, which leads to a buildup of plaque in our arteries (i.e., atherosclerosis). When our arteries are “clogged” with plaque buildup, our blood flows less freely and increases our risk of myocardial infarction (i.e., heart attack) and stroke. Stress and stress reactivity also increase our production of platelets. Platelets are a type of blood cell, and their main purpose is to prevent us from bleeding. Platelet activation releases substances into the blood stream that adhere to (or “stick to”) our arteries, which leads to plaque buildup; as such, it may contribute to our risk of heart disease.
Evidence linking stress to heart disease is compelling and abundant. The INTERHEART study, a study of psychosocial stress and heart attack risk among twenty-five thousand people in fifty-two countries, found that people who reported “permanent” stress at work or home had roughly twice the risk of developing an MI (myocardial infarction) compared to those who did not experience comparable stress. These effects were generally consistent across geographic regions, by ethnicity, and gender. Studies have also identified particular stressors that are especially closely tied to heart disease. One stressful aspect of work—facing high demands but having little control over one’s work environment—is a widely documented predictor of heart troubles, including high blood pressure. Working under relentless time pressures is highly distressing, as we all know. However, the pressure to get our work done while having little control over when, how, and with whom we do our work is a
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particularly devastating combination. Yet not all people are equally likely to develop heart disease in the face of stress. As we will see in , those with the highest levels of stress reactivity, or whoChapter 4 respond strongly to stress, are more likely to develop heart disease in the face of stress.
Stress and Immune Function
Marisol, the overworked and exhausted college student we met earlier in this book, fell sick with the flu after juggling multiple school, family, and work activities. One explanation for Marisol’s plight is that her immune system succumbed to the chronic stressors in her life. The immune system protects our bodies from foreign materials, such as viruses and bacteria, by releasing into our circulatory system both white blood cells and antibodies. (An antibody is a protein produced by the body’s immune system when it detects harmful substances.) When we’re under extreme stress, as Marisol was, our immune responses falter, making the body less able to defend itself against harmful foreign materials.
Stress increases our risk of viral infections such as the flu and colds. Most of this evidence comes from laboratory studies, similar to the ones described earlier in this chapter. In studies of the immune system, researchers typically ask healthy volunteers to answer questions about the stress in their lives, and then inoculate them with a virus. Researchers typically track their subjects for several days, and find that those subjects who had been exposed to the highest levels of stress—whether reported on their questionnaires or induced in the lab (such as a math test)—showed evidence of increased susceptibility to upper respiratory infection.
Recent work on stress and immune function further shows that cortisol plays a critical role in the stress-infection link. Stress researcher and psychologist Sheldon Cohen has conducted many studies showing how we get common colds after bouts of stress. His work shows that prolonged exposure to stress lessens our immune cells’ capacities to respond to hormonal signals that normally regulate inflammation. In turn, those with the inability to regulate the inflammatory response are more likely to develop colds when exposed to a virus. It’s not just colds that we’re at risk of, however. Inflammation plays a role in many diseases, such as cardiovascular, asthma and autoimmune disorders.
Mounting research also shows that stressors dating back to our earliest years may have powerful long-term effects on inflammation and ultimately on our disease risk. Adults who had been the victims of psychological, sexual, or physical abuse in childhood or who grew up with a problem-drinker parent have elevated levels of three body chemicals that are markers of inflammation: interlukin-6 (IL-6), C-reactive protein (CRP), and fibrinogen. Children who grew up in impoverished households also show higher levels of persistent and multiple infections over the life course. While the bulk of evidence suggests that the wear and tear of multiple stressors and cumulative adversities undermine our immune function, some scholars have recently posited that some young people growing up under conditions of stress and adversity may be particularly resilient in the case of infection. Likewise, children who grow up in relatively stress-free and peaceful environments may not “toughen up” to illness or infection. The “hygiene hypothesis” holds that those who face few pathogenic challenges in early life may have poorly regulated inflammatory and immune responses later in life. Although evidence is preliminary, such findings are provocative in that they provide evidence of resilience in the face of adversity, a topic we will delve into more fully in .Chapter 4
In sum, scientists working in a range of different methods and disciplines agree that stress takes a toll on our physical well-being, although experts vary in how much stock they place in social versus biological explanations for the stress-health link. Most scientists recognize, however, that we need to pay careful attention to both social and biological pathways if we really want to understand human health and well-being. Answering the questions of why and how stress affects health is the first critical step on the path to interventions and solutions. As will show, scientists’ theories andChapter 5
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empirical findings help us to figure out whether the best way to protect against stress-related health woes is through prescribing a medication, offering medical care and counseling, or altering the social structure that gives rise to health-depleting stressors.
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