The complexity of gender differences in health (i.e., men's lower life expectancy and women's greater morbidity) extends beyond notions of either social or biological disadvantage. Gaps remain in understanding the antecedents of such differences and the issues this paradox raises regarding the connections between social and biological processes. Our goals in this analytic essay are to make the case that gender differences in health matter and that understanding these differences requires an explanation of why rational people are not effective in making health a priority in their everyday lives. We describe some salient gender health differences in cardiovascular disease, immune function and disorders, and depression and indicate why neither social nor biological perspectives alone are sufficient to account for them. We consider the limitations of current models of socioeconomic and racial/ethnic health disparities to explain the puzzling gender differences in health. Finally, we discuss constrained choice, a key issue that is missing in the current understanding of these gender differences, and call on the social science community to work with biomedical researchers on the interdisciplinary work required to address the paradoxical differences in men's and women's health.
IT has long been established that women live longer than men, yet they have higher morbidity rates. Men experience more life-threatening chronic diseases and die younger, whereas women live longer but have more nonfatal acute and chronic conditions and disability. Furthermore, although men's and women's overall rate of serious mental illness are similar, the most common mental health disorders differ by gender. There is considerable evidence that both biological systems and social processes underlie these perplexing patterns, but what is missing in our understanding of these gender differences is an explanation of how the social and biological factors combine to produce these paradoxical differences in health for men and women.
Our primary goals in this article are to make the case that gender differences in health matter and that understanding these differences requires an explanation of why rational people are not effective in making health a priority in their everyday lives. We describe some salient gender health differences and indicate why neither social nor biological perspectives alone are sufficient to account for them, then we consider the limitations of current models of racial/ethnic and socioeconomic health disparities to fully explain gender differences. Last, we discuss a key issue, constrained choice, that is missing in the current understanding of gender differences in health, and we call on the social science community to work with biomedical researchers on the interdisciplinary research that is required to address the paradoxical differences in men's and women's health.
The Gender and Health Paradox
As noted above, differences in men's and women's physical health are paradoxical. Women live longer than men, yet they have higher morbidity rates and in later years a diminished quality of life. In fact, although the size of the gender gap and pattern of longevity varies considerably by country, women outlive men in every region and almost every country of the world (United Nations, 2000). Although many reasons for the variation have been identified, biological theories are not considered a sufficient explanation for the cross-national differences.
Since the turn of the 20th century, American women's life expectancy has exceeded men's, with women experiencing lower mortality rates in every age group and for most of the age-adjusted leading causes of death. Although life expectancy has been increasing for both men and women, the gender gap in the United States, currently 5.4 years, has been closing since 1980 when men's gains began to exceed women's owing in large part to men's decreasing mortality from cardiovascular disease (CVD) and cancer (Centers for Disease Control and Prevention [CDC], 2000; National Center for Health Statistics [NCHS], 2003).
The paradox of men's higher mortality and lower morbidity compared with women can be explained by gender differences in age-related patterns of disease, including women's increased risk for CVD after menopause (Verbrugge & Wingard, 1987). Although the three leading age-adjusted causes of death are the same for men and women (heart disease, cancer, and stroke), men have more life-threatening chronic diseases at younger ages, including coronary heart disease, cancer, cerebrovascular disease, emphysema, cirrhosis of the liver, kidney disease, and atherosclerosis. In contrast, women face higher rates of chronic debilitating disorders such as autoimmune diseases and rheumatologic disorders as well as less life-threatening diseases such as anemia, thyroid conditions, gall bladder conditions, migraines, arthritis, and eczema. Women also have more acute conditions such as upper respiratory infections, gastroenteritis, and other short-term infectious diseases (NCHS, 2003).
In contrast to the paradoxical gender differences in physical health, men's and women's overall mental health is similar, but specific conditions differ by gender. Women experience substantially higher rates of depression and anxiety disorders than men, whereas men have higher rates of substance abuse, antisocial behavior, and suicide (Kessler et al., 2003a,b).
Below we examine three reference conditions—CVD, immune function and disorders, and depression—that exhibit substantial gender differences. Although our examination is not exhaustive, it paints a more complex portrait of specific patterns of gender differences in health than previously articulated. Later we will consider some of the primary social and biological explanations of these patterns.
Even though the prevalence and age-adjusted death rate of CVD are greater in men than in women, more women ultimately die of the disease because of their greater life expectancy, the older age at onset, and the range of CVD risk factors associated with aging. For example, in terms of total deaths since 1984, CVD has claimed the lives of more females than males (NCHS, 2003). Crimmins and colleagues (2002) provide interesting data on life expectancy by estimating years lived with and without disease by birth cohorts of men and women over the life course. Because more women survive to older ages, the gender difference in years lived with disease is even greater than years of life expectancy. For example, a cohort of women will experience 70% more years of life after age 65 with hypertension than a similar sized birth cohort of men. Likewise, a group of older women also will spend more years with CVD than will older men. Thus, the modal patient undergoing treatment for CVD and hypertension is likely to be a woman beyond middle age.
Throughout most of the last two decades, clinical researchers focused on explaining the earlier onset of CVD in men and the biological mechanisms that contribute to men's lower average in life expectancy. This research emphasis, reflected in large single-sex longitudinal clinical trials directed at prevention of CVD in men, contributed over time to significant reductions in male mortality from CVD and helped to narrow the gender gap in longevity. While the life-expectancy gender gap is narrowing, the CVD mortality gap continues to widen (NCHS, 2003).
A confluence of factors in recent decades, including the women's health movement, led to substantial increases in women's inclusion in research and in turn to dramatic changes in knowledge and understanding regarding women's risk of CVD, but little insight into the antecedents of gender differences in risk. In 1991, the Women's Health Initiative (WHI), the largest preventive study of its kind in the United States, was launched to address this gender gap. Although the WHI represented a huge step forward in gathering scientific evidence regarding women's health, it did not, for example, question the basic physiological explanations of role of hormones in women's extensive CVD mortality. For example, the study did not draw on a broader interdisciplinary model and instead was designed to test prevailing biomedical explanations, based on prior hypothesis and findings primarily from observational studies that indicated protective effects of estrogen and diet in preventing the development of CVD.
Ironically, the primary clinical trial arm of the planned 15-year hormone replacement therapy (HRT) intervention was halted in 2002 after a mean of 5.2 years of follow-up. The data and safety and monitoring board recommended stopping the trial because HRT failed to protect against CVD and women receiving the estrogen/progesterone combination were also found to have an increased risk of invasive breast cancer and other negative health effects (Fletcher & Colditz, 2002; Rossouw et al., 2002). Although the lessons that will be learned ultimately from these developments are yet to be determined, it is clear that investigations involving only women—or only men—are still valuable. However, as such, single-sex studies cannot address the larger issue of gender differences.
Immune Function and Disorders
Researchers and clinicians are challenged and perplexed by the sex-linked patterns of immune function and disease. Women have a greater risk of autoimmune disorders and a higher risk of genetic immune suppression disorders than men; for example, the female/male ratio for autoimmune thyroid disorders is 15:1, systemic lupus 9:1, and rheumatoid arthritis 3:1 (Office for Research on Women's Health, 1992). Much of the disability women experience from rheumatologic and thyroid disorders especially in middle and older ages is attributable to autoimmune disease (CDC, 2000).
Females of most, if not all, species generate a more robust immune response after challenge with an infectious agent and respond to natural and vaccine exposures by producing substantially more antibodies than males. Women's different and somewhat more intense immune response provides them with higher levels of passive immunity during pregnancy and the ability to pass on a substantial level of protective antibodies to infants during breast feeding (Grossman, Roselle, & Mendenhall, 1991; Hegde, 1991). But, pregnancy exacerbates the course of some autoimmune diseases (e.g., lupus), while it improves the course of others (e.g., rheumatoid arthritis). In other words, women's more robust immune systems appear to put them at greater risk of disorders in which their own immune system attacks their bodies.
Sex hormones also tend to modulate the immune response: What biologists refer to as distinct immune hormonal environments contribute to some of the sex differences in the prevalence of autoimmune disorders. In addition, men and women tend to develop different autoimmune conditions. While the origin of these differences appears to be primarily biological, some physicians believe that gender, and in particular the stress process (Pearlin, 1989), also affect autoimmune disease incidence and severity (Legato, 2002; Lockshin, Gabriel, Zakeri, & Lockshin, 1999). A rapidly developing research literature suggests that social/emotional factors combine with biological processes to affect health (see, e.g., Cacioppo et al., 2002; Kiecolt-Glaser, McGuire, Robles, & Glaser, 2002a; Seeman & McEwen, 1996; Seeman, Singer, Rowe, Horwitz, & McEwen, 1997).
Various possible pathways have been described through which psychological factors impact on immune function (Kiecolt-Glaser, McGuire, Robles, & Glaser, 2002b). For instance, positive relationships seem to improve function, while discordant relationships seem to have a negative impact. Even though acute and chronic stressors may operate through different physiologic pathways, coping resources such as social support mediate the impact of both (Baron, Cutrona, Hicklin, Russell, & Lubaroff, 1990; Cohen & Herbert, 1996). Although there is some debate about the type and number of social ties by gender and their impact on men's and women's health, new work on gender and stress reactivity suggests that women may actually respond to stress by “tending and befriending” rather than men's tendency to “fight or flight” (Taylor, Klein, Lewis, Gruenewald, Gurung, & Updegraff, 2000).
The World Health Organization (WHO) ranks major depression as one of the most burdensome diseases in the world (WHO, 2002). Moreover, a growing body of research links depression with physical health, further illustrating the complexity of assessing the antecedents of gender differences in health.
Women's rates of depressive disorders are between 50% and 100% greater than men's (Kessler et al., 2003a; Mirowsky & Ross, 2003). These differences occur in both treated and community samples (Nolen-Hoeksema, 1987, 1990). The National Comorbidity Survey Replication substantiated women's higher lifetime rates of major depressive disorder (Kessler et al., 2003a,b). It is now well established that women's higher rates of depression reflect a real gender difference in health rather than an artifact of help-seeking behavior or willingness to report symptoms (Mirowsky & Ross, 1995; Nazroo, Edwards, & Brown, 1998).
Until the recent men's health movement, women's disproportionate depression rates generated the erroneous impression that men were comparatively immune to depression (Courtenay, 2000a,b). The underdiagnosis of depression in men has been attributed to clinicians' failure to recognize symptoms, to men's unwillingness to seek help for such feelings, and to their tendency to cope with the feelings through drinking, drug use, and other private activities or actions (Chino & Funabiki, 1984; Nolen-Hoeksema, 1987, 1990).
The gender difference in the prevalence of depression occurs at all ages. The risk for depressive disorders begins to rise in midpuberty and persists through the mid-50s; however, the gender gap appears to be the greatest during reproductive years (Bebbington, 1996; Piccinelli & Wilkinson, 2000). There is some controversy about the determinants of gender differences and discrepancy between cross-sectional and longitudinal findings regarding the course of depressive disorders. Although men and women differ in the age and rates of onset (young males have higher rates until early adolescence), cross-sectional studies indicate that once major depression develops, the course is similar for both genders. The continuing debate about the course of depressive illness in women compared with men does not alter the consistently higher lifetime prevalence rates for women or the fact that depressed women also are more likely than are men to have comorbid anxiety, while men are more likely to have comorbid substance abuse or dependence (Endicott, 1998; Gregory & Endicott, 1999; Kessler et al., 2003a). A recent review of research on gender differences in depression concluded that while there are some psychosocial risk factors contributing to women's higher rates, the determinants of these differences remain unclear because models combining developmental physiological and psychosocial processes are lacking (Piccinelli & Wilkinson, 2000).
Prevailing Explanations for the Paradoxical Gender Differences in Health
Many of the biological explanations of women's greater longevity emphasize the health advantages that accrue from different hormones and physiological systems that facilitate pregnancy and childbirth—advantages that have long been hypothesized to lower women's risk of coronary heart disease prior to menopause. However, results from several recent clinical trials of HRT are challenging that assumption (Fletcher & Colditz, 2002; Liddle, 2003). In addition, the hypothesized advantages are not consistent with women's higher morbidity compared with men.
One could easily imagine that evolutionary selection factors would produce strong women whose ability to bear children also provided advantages in terms of both morbidity and mortality. Such evolutionary arguments build from the premise that natural selection favors individuals that produce more offspring, as their genes are more highly represented in subsequent generations of members of a species. The theory of natural selection and its impact on the prevalence and distribution of specific genes are at the core of biology. Although the evidence supporting explanations of the effects of natural selection on survival through reproductive ages is strong, the evidence is much weaker when it comes to explaining differences in men's and women's longevity well beyond prime reproductive age. Purely biological explanations, including the strong pursuit to identify the genetic basis of disease, still fall short of fully explaining the gender paradox of morbidity and mortality.
However, numerous interdisciplinary biomedical studies indicate that there are interactions between the cardiovascular system, immune functioning, and psychological processes (see, e.g., Hemingway & Marmot, 1999; Kiecolt-Glaser et al., 2002a; Lovallo, 1997). For instance, considerable evidence links clinically diagnosed major depression with increased mortality in general and CVD in particular. Although these studies do not show that depression is a predictor of mortality per se, symptoms of depression are associated with poor health and functional status, as well as increased disability, health care utilization, and cost of health services. A 13-year prospective study showed 4.5 times greater risk of a heart attack among those with major depression (Pratt, Ford, Crum, Armenian, Gallo, & Eaton, 1996). In another study, mortality was four times higher among depressed heart attack patients (Frasure-Smith, Lesperance, & Talajic, 1995). A prospective study of a large cohort of White women aged 67 years or older found that depressive symptoms were associated with increased rates of cardiovascular mortality (Whooley & Browner, 1998).
Depression is also associated with immune function and disease severity by magnifying pain and disability (Staats, 1999). Pain and depression can amplify each other: Pain increases heart rate and blood pressure; it enhances secretion of stress-related hormones including catecholamines and cortisol; and it deregulates a range of immunological activities (Kiecolt-Glaser, Page, Marucha, MacCallum, & Glaser, 1998). Thus, gender differences in mental health may contribute in unknown ways to gendered patterns of physical health (McDonough & Walters, 2001) and vice versa.
Purely social explanations of gender differences in health emphasize men's and women's social position and their differential access to protective resources (including income, education, safe parks, and other areas in which to exercise) as well as their exposure to a range of environmental factors that negatively affect health (including exposure to toxins and other social and behavioral risk factors such as domestic violence, crime, smoking, poor diet). Social position mediates access to the positive and negative social and environmental factors that occur at the individual, household, community, and society levels. For example, gender differences in income may result from a variety of factors over the life course including social role-related expectations and activities, occupational choice, opportunities for employment and advancement, work-related skills and experience, as well as access to job benefits including health insurance, pensions, and other retirement income. Women are also more likely to be single parents and thus have a lower income per capita. Although the impact of income on health would be expected to be the same for men and women, the levels of income may vary by gender for a variety of reasons other than the job one currently has or pay inequity. For instance, welfare and income entitlements such as Social Security are, in fact, tied to both one's own employment and income history and that of one's spouse.
Other risk and protective factors may differ by gender in both exposure and their impact on health. For example, toxin exposure may be related to patterns of employment (e.g., asbestos exposure leading to mesothelioma) and social roles (e.g., industrial or household use of pesticides or other chemicals or to exposure to second-hand smoke). Furthermore, exposure to a specific toxin may result either in somewhat different rates of the same problems (e.g., lung cancer) or in different health problems for men and women (e.g., breast or prostate cancer). Moreover, other resources that vary on average by gender such as education may provide additional knowledge, opportunity, and income with which to avoid multiple risk factors. Clearly, the distribution and use of toxins are regulated by social policy, but so, too, is education. Thus, in addition to being an individual resource, education is also a product of both governmental policies and community choices and priorities.
Sociological theory offers considerable insight into women's greater morbidity and the gendered patterns of psychological disorders. But for the most part, sociologists and other social scientists have not fully examined the diverse antecedents of gender differences in mortality or the types and prevalence of diseases. Instead, the research on social determinants has concentrated on socioeconomic position, a “fundamental social cause” as theorized by Link and Phelan (1995), focusing on a causal chain whereby unequal distribution of social and economic resources and related variation in exposure to stress lead to health disparities (Berkman & Kawachi, 2000; House & Williams, 2000; Phelan, Link, Diex-Roux, Kawachi, & Levin, 2004). Moreover, applying the implicit logic of disadvantage, a majority of mental health studies have concentrated on explaining women's higher levels of depression, but not men's higher levels of substance abuse and antisocial behaviors. Thus, sociological explanations of gender differences in health examine variation in gender roles and identities, the ways in which racial and socioeconomic inequality contributes to differences in men's and women's exposure to stressors, the meaning and impact of particular stressful events and coping resources, and the physical and psychological consequences of each of these factors.
Do Models of Racial and Socioeconomic Disparities Adequately Explain the Gender Health Paradox?
Clearly, racial and SES (socioeconomic status) disparities overlay the gender differences in health. Although gender differences in morbidity and mortality vary across racial/ethnic and socioeconomic groups, they also persist within each of these groups (NCHS, 1998; Rieker & Bird, 2000; Williams, 2002, 2003). Moreover, explanations of racial and socioeconomic disparities focus in large part on the multiple and cumulative consequences of poverty and discrimination, among other factors (Brunner & Marmot, 1999; House & Williams, 2000; Phelan et al., 2004; Smaje, 2000). These factors are critical to understanding racial/ethnic and socioeconomic variation in morbidity and mortality among men and among women, but they cannot fully explain women's greater longevity and men's earlier deaths and only partially explain women's pattern of greater morbidity relative to men.
Unlike racial/ethnic and socioeconomic disparities in health, men's and women's social and economic needs can and do differ in part because of biological and longevity differences in their lives. For example, because women are more likely to become single parents, caregiver to an aging spouse, widowed, and to live well into their 80s and beyond, they also have different social and economic needs and thus may not be served equally well by social policies designed to ignore these differences. In fact, a wide range of social and economic policies, including but not limited to those directly aimed at public health and health care, can create or exacerbate differences in health status and behaviors between gender groups as they do with racial and economic groups (see, e.g., Graham, 2004).
What Is Missing in Our Understanding of Gender Differences in Health?
A growing body of research indicates that the complexity of the gender health differences extends beyond narrow concepts of the relative disadvantage or advantage of men's and women's biology or the social organization of their lives. Consequently, we need a model of men's and women's health that takes into account factors other than inequality of resources, discrimination, and other unfair treatment, to understand what aspects of the broader array of differences in men's and women's lives contribute to the morbidity/mortality paradox.
Treating gender as a fundamental cause sheds little light on how social factors contribute to the gender health paradox, including whether and how they affect or interact with biological processes. We cannot simply substitute gender for race or socioeconomic status in existing models of health disparities because they are not constructed to capture the complex way in which men and women are advantaged and disadvantaged in both mortality and morbidity. Such models are based on the implicit hypothesis that the health effects produced by inequality and discrimination go in the same direction for biological and social factors. While most models of social determinants of health incorporate biological processes, only recently have researchers begun to simultaneously assess these interdisciplinary factors (see e.g., Sen, George, & Ostlin, 2002). The issue in the case of racial/ethnic and socioeconomic disparities is how to parcel out the social and biological antecedents, assuming that they do not confound each other, as may well occur with gender differences in either morbidity or mortality. For example, men's general economic advantages would not on the face of it be likely to explain their earlier mortality compared to women (although socioeconomic status might partially explain the mortality difference between White and African American men). If social factors contribute to gender differences in ways that extend beyond inequality, models of gender differences need to capture the specific processes and pathways that lead to health outcomes. Although researchers have examined some of the pathways through which social factors might differentially affect men's and women's health (including positive and negative health behaviors, exposure to stressors, and coping styles), for the most part, this approach has not been used to explain gender differences in health.
There is no comprehensive social framework for considering the influence of multiple levels of social factors, including individual agency or choice, on gender differences in health. Such a framework also needs to incorporate contextual effects at the levels of family, community, and social policy in ways that extend beyond models of gender inequality and inequity. This approach would also facilitate the broader integration of social and biological processes and contribute to a better understanding of differences in men's and women's health.
What Is Needed To Gain a Better Understanding of Gender Differences in Health?
Toward a Sociology of Constrained Choice
Nearly two decades ago, Verbrugge and Wingard (1987) pointed out that neither a strictly biomedical interpretation of the data nor one based solely on social factors adequately explains why the health of men and women differs in such obvious ways. Considerable evidence suggests that both biological systems and social processes underlie these perplexing patterns.
An explanation of how such factors combine to produce the paradoxical gender differences is still missing from our understanding of men's and women's health. We call on social scientists and biomedical researchers to work together to meet the challenge of developing models that capture the ways in which the gender health paradox differs from socioeconomic and racial/ethnic health disparities. To encourage this new direction, we are developing a model of health determinants that includes the concept we refer to as constrained choice, which we elaborate in chapter 2 of our book, Gender and Health: The Effects of Constrained Choices and Social Policies (Bird & Rieker, in preparation). This concept builds on the argument that Boudon (2003) and Light and Hughes (2001) make, distinguishing sociology of choice from economic models of rational choice theory.
Not all of the constraints that affect everyday choices and opportunities to make health a priority are the same for men and women. We contend that to explain gender differences, models of health determinants need to be modified to include these constrained choices. We are not posing constrained choice as a deviation from an idealized notion of “free” choice; rather, we are describing a process by which choices are made. We draw on the prevailing public health understanding of health disparities, which emphasizes the role of personal choices and health behaviors in enhancing or diminishing an individual's ability to live a long and healthy life.