CHAPTER 107: SOCIAL DETERMINANTS OF CARDIOVASCULAR DISEASE

Cardiovascular disease (CVD) is the number one cause of death around the globe, now accounting for about one in three deaths.¹ More than 80% of these CVD deaths take place in low- and middle-income countries.² Although mortality from CVD in the United States has been declining since the 1970s, heart disease is still the leading cause of death in America as well, accounting for approximately 31.3% of deaths in 2011.³ The US decline in CVD mortality has been attributed to advances in prevention, diagnosis, and treatment. However, if current trends prevail, the prevalence of CVD in the United States is expected to rise 10% between 2010 and 2030.⁴ This projected rise in CVD prevalence is attributed to a number of factors: an aging populace, an increase in major risk factors (hypertension, lack of physical activity, obesity, and diabetes), and growing socioeconomic inequality that accentuate the deleterious social determinants of health. Further, the clinical advances made in the diagnosis, treatment, and prevention of CVD have not been equally available to all individuals throughout our society.⁵ The United States is one of the richest nations in the world and spends more per capita on health care than any other nation, and yet America has one of the shortest life expectancies at birth of any industrialized nation, ranking 27th out of 34 Organization for Economic Cooperation and Development countries.⁶

This chapter, unlike preceding chapters that have primarily focused on clinical issues and proximal determinants of CVD, explores the social determinants of CVD that operate at the population level. As the World Health Organization (WHO) Commission on Social Determinants of Health noted in its report, “heart disease is caused not by a lack of coronary care units but by the lives people lead, which are shaped by the environments in which they live.”⁷ The broader social context in which individuals lead their lives has a major impact on health status and ultimately on longevity. CVD is at heart a “lifestyle” disease, driven by our contemporary way of life, marked as it is by the overconsumption of highly processed foods, little physical activity, obesity, use of tobacco products, and elevated levels of chronic stress. But CVD is also a disease propelled by deeply entrenched social inequalities. Decades of research have yielded a large body of literature that clearly exposes the numerous societal factors that have a profound impact on the development of CVD and significantly contribute to the disparities in health and longevity among various populations and subpopulations. This chapter explores the role that social determinants of health play in driving CVD.

Definitions

WHO defines social determinants of health as “the circumstances in which people grow, live, work, and age, and the systems put in place to deal with illness. The conditions in which people live and die are, in turn, shaped by political, social, and economic forces.”⁷ This broad definition recognizes that the social determinants of health are multifactorial, deeply interrelated, complex, and driven by a multitude of forces, including social, cultural, economic, and political forces.

Although every individual is affected by the society in which he or she lives, some are more burdened than others by social and economic disadvantages, which in turn can result in health disparities. Health disparities are defined as “differences that occur by gender, race or ethnicity, education or income, disability, geographic location, or sexual orientation.”⁸ With respect to differences in health outcomes, the term refers to those outcomes that persist despite controlling for access to care and patient clinical factors. These outcome disparities signal the effects of institutional barriers, provider barriers (such as cultural insensitivity, language barriers, unconscious bias, or frank racism), and patient issues (such as cultural beliefs, health literacy, adherence, and trust of the medical profession).⁹ The term health disparities not only typically connotes that the observed differences are unnecessary and avoidable, but that they are unjust as well. Some prefer to use the term health inequalities rather than health disparities to highlight the injustice of the observed differences in health status and health outcomes that characterize our society, while others use the two terms interchangeably.¹⁰

Given the complexity of our social environments and the myriad factors and forces that combine and interact to give rise to them, it is challenging to identify concisely and measure accurately the full range of the social determinants of health. Nevertheless, decades of research have given us important insights into key determinants of health and how they interact to create health disparities.

The Socioeconomic Gradient of Heart Disease

Public health experts have long recognized that social factors play a role in determining health status. Rudolf Virchow, the 19th century German physician and public health activist, queried: “Do we not always find the diseases of the populace traceable to defects in society?”

Virchow went on to identify lack of education, unemployment, poverty, and political disenfranchisement as drivers of disease.¹¹ The 19th century saw the rise of sanitary campaigns, which focused on the connections between people’s living conditions and their sickness. During the latter half of the 20th century, the scientific evidence linking the social determinants of health with disease prevalence and health outcomes rapidly accumulated up to the present day, when the study of social disadvantage and its effects on health is an extensive and penetrating focus of inquiry and policy action.

Heart disease is considered a disease of affluence. It has emerged in both developed and developing countries as industrialization and urbanization have homogenized patterns of consumption and lifestyle practices. Evidence shows that the rise and fall in the prevalence of CVD varies according to a country’s stage of economic development.¹² And while the poorest regions of the world still see relatively low rates of CVD, regions within developing countries that are marked by increasing wealth and adoption of the “Western” lifestyle have seen a rapid rise in heart disease. The epidemiologic transition we are witnessing in developing countries has been compressed into a few decades, whereas the epidemic of heart disease observed in Western developed nations took place over the course of a century.¹³ The swift pace of economic globalization and the rapid diffusion of the Western lifestyle are thought to be powerful drivers of the present-day, expanding global epidemic of heart disease.¹⁴

Evidence also reveals a gradient of heart disease not only across countries according to the stage of development, but also within societies. Inequalities in the distribution of heart disease change according to the stage of epidemiologic transition reached by a country.¹⁵ Early in the transition, individuals in the higher socioeconomic positions are usually the first to adopt a lifestyle (eg, physical inactivity, smoking, poor diet) that leads to the development of CVD risk factors (eg, hyperlipidemia, hypertension, obesity, metabolic syndrome, diabetes) and the development of the disease itself. However, in the later stages of the transition, these individuals are the first to experience a reduction in behavioral risk factors and a decline in the prevalence of the disease. In the most advanced economies, as the epidemic has matured, the socioeconomic gradients of heart disease and risk factors have reversed over time, and heart disease has become more prevalent among people in lower socioeconomic positions. As countries develop—both developed and developing nations—the social pattern converges to a more homogeneous one, as the disadvantaged socioeconomic position progressively becomes a systematic risk factor for heart disease.¹⁵ The landmark Whitehall study, led by Sir Michael Marmot, conducted on over 17,500 male British civil servants in the 1970s, revealed the pervasive effects of social gradient on health. It showed that occupational grade has a powerful effect on health and longevity. In the Whitehall study, those at the lowest occupational grades had the worst health (heavier weight, more tobacco use, less exercise, and higher blood pressure and blood glucose) and highest CVD mortality (three to six times the mortality of men in the highest grade). Health and longevity improved at each successive level of occupational grade, up to the very highest level (Fig. 107–1).¹⁶

As the later stages of socioeconomic development in a nation are reached, the relationship between low socioeconomic status (SES) and the behavioral risk factors for heart disease also becomes more homogeneous; the relationship becomes more consolidated and consistent across individual-level and area-level indicators.¹⁷ For example, tobacco use is more prevalent almost everywhere in the lower socioeconomic groups than in the higher socioeconomic groups.¹⁸ It is important to note, however, that while behavioral risk factors for heart disease become more common among less privileged groups than privileged groups in both affluent and less affluent societies as they develop, evidence indicates that conventional risk factors account for only a small proportion of the observed social gradient in heart disease.¹⁹ Additional findings from the Whitehall study, which investigated mortality from coronary heart disease over a 25-year period, showed that traditional coronary heart disease risk factors accounted for less than one-third of the social gradient in mortality.¹⁹ These findings stimulated further investigations of additional factors that could explain the other two-thirds of the observed social gradient of heart disease.

The Growth and Evolution in Health Disparities Research

Over the past several decades, investigators from a wide range of disciplines, in their exploration of the social determinants of health, have looked critically at several distinct areas of interest, asking more complex questions as the field has evolved.²⁰ First, poverty was explored as a categorical determinant of health; it was approached from a threshold framework. Researchers found that the greatest drop in mortality occurred as income increased at the lowest levels of income. However, even as income increased to ever higher levels, mortality continued to decline. Researchers then examined the graded associations between socioeconomic resources and health status across the entire SES hierarchy, exploring the linkage between SES position—indicated by education, occupational status, and/or income—and social disadvantage related to race/ethnicity and sex. The next focus of inquiry moved to exploring the mechanisms by which various social determinants resulted in poor health outcomes. SES is now recognized as only one key factor among many. It is the intersection and interaction of these myriad factors that constitutes social disadvantage, whereby the whole is greater than the sum of the parts in creating a stressful social context in which an individual is born, lives, and falls ill. We have now moved into an era in which researchers are teasing out the complexity of the multilevel effects of the range of social determinants of health, from individual characteristics to numerous aspects of the environment. Given the complexity of social context, there are methodologic challenges in establishing causality between the various factors and health status. Nevertheless, over the past 25 years, we have witnessed an explosion in research focused specifically on health disparities, and we now have a better understanding of the biology of disadvantage.

As part of this research endeavor, the Institute of Medicine (IOM), at the request of the US Congress, undertook a review of more than 100 studies in order to assess the extent of racial and ethnic disparities in health care, explore contributing factors, and recommend policies to eliminate the inequities. Published in 2002, the IOM report stated the following: “Racial and ethnic minorities tend to receive a lower quality of healthcare than non-minorities, even when access-related factors, such as patients’ insurance status and income, are controlled. The sources of these disparities are complex, are rooted in historic and contemporary inequities, and involve many participants at several levels” and “studies of racial and ethnic differences in cardiovascular care provide some of the most convincing evidence of healthcare disparities.”⁹

The IOM report received widespread media coverage and deepened national concern. In 2005, the WHO, acting on the global stage, set up an independent Commission on the Social Determinants of Health, with the mission to link knowledge to action and assist countries around the world in addressing health inequities. Although much has been done in the intervening years and progress has been made in some areas, the issue of racial and ethnic disparities remains a difficult and complex problem to address. According to the US Agency for Healthcare Research and Quality’s 2014 National Healthcare Quality and Disparities Report, regarding the situation in the United States, “disparities in quality and outcomes by income and race and ethnicity are large and persistent, and were not, through 2012, improving substantially.”²¹ Over the past decade, few health disparities have been eliminated in the United States, despite the issue having been on the national agenda.^21,22

The Major Social Determinants of Cardiovascular Disease

Among the major social determinants of health are SES, race/ethnicity, sex, the environment (including social relationships, neighborhood physical and social environments, and work environment), and access to care (Table 107–1). There is a substantial body of literature on each of these social determinants of health and also on theories of how they interact to maintain health or contribute to illness. It is beyond the scope of this chapter to explore each in detail; salient points regarding each will be briefly explored in relation to the current status of cardiovascular health in the United States.

Socioeconomic Status

One of the most studied and important social determinants of health is SES, which is defined as a “multidimensional concept comprising measures of resources such as income, wealth, and educational credentials, and the access to goods, services, and knowledge that these resources afford those who have them.”²³ It is challenging to investigate SES, as it comprises a number of domains. Nevertheless, it has been most commonly measured using educational attainment, income, threshold poverty status, and/or occupational grade level. Decades of research have taught us that the effects of SES are substantial and occur at all levels of the socioeconomic gradient. Thousands of studies now document an association between higher educational attainment or higher income and better health and longevity. An international study of the United States and 11 other Western nations showed that in all countries total CVD mortality is higher among individuals with lower educational level or lower occupational class, although the magnitude of the association varied across countries.²⁴

The effects begin early in life and extend across the lifespan. Children of parents of low SES—children who thus start out in life with few material or psychosocial resources—experience greater morbidity and mortality. A systematic review of the 40 studies revealed robust data that establish an association between parental SES, poor childhood circumstances, and increased CVD risk, although findings sometimes varied among specific outcomes, socioeconomic measures, and sex.^25,26 In part, the effect of low SES in childhood is mediated through its effect on adult health behaviors and the subsequent development of conventional risk factors for CVD.^27,28 Health behaviors that are associated with CVD risk are more common among individuals in lower socioeconomic groups than those in higher socioeconomic groups (see later section, Health Behaviors).

SES is also related to, among other issues, the type of the neighborhoods in which people live and their work environments, as well as to insurance status and the ability to access health care. Over the course of the lifespan, there is a dynamic relationship between SES and health, whereby those in the higher socioeconomic groups have greater access to numerous resources, including economic, social, cultural, physical, and medical resources, that interact to promote health and well-being.

Race/Ethnicity

Racial and ethnic minority populations are disproportionately burdened with more illness, premature death, and disability, and often suffer higher mortality than whites (see Chapter 109).^*10,29 It is CVD that accounts for the largest proportion of inequality in life expectancy between blacks and whites: in the United States, blacks are two to three times more likely to die of heart disease than whites.³ Blacks and other ethnic minorities tend to have more CVD risk factors and a greater prevalence of disease, and they experience greater premature CVD death than whites.^30,31 Racial and ethnic minorities are less likely to have health insurance,³² face greater barriers in accessing health care, and often receive lower quality care.^9,33 Even when minority patients have the same type of health insurance as whites, evidence reveals they tend to receive lower quality of care.^9,33 A number of studies have documented the race-based invasive procedural gap. Data from the CRUSADE^† Quality Improvement and National Registry of Myocardial Infarction registries reveal racial and ethnic (as well as sex-based) differences in comorbidities, evidence-based therapies and procedures, and prolonged time to reperfusion.^31,34,35 For example, African American and Hispanic patients have been shown to have longer delays to reperfusion, with door-to-balloon times ≤ 90 minutes observed in 83% of white patients compared with 75% and 76% of black and Hispanic patients, respectively.³¹ However, the gap may be narrowing; one study found that, although small differences in door-to-balloon times persist among different races/ethnicities, the proportion achieving door-to-balloon times ≤ 90 minutes has increased substantially for all patients over time.³⁵ Black patients have been found to be transferred more slowly to revascularization hospitals after acute myocardial infarction than white patients. One-year mortality for black patients with acute myocardial infarction was shown to be 12% to 35% higher than those for white patients, even after adjusting for SES, age, sex, comorbidity, and severity of illness.³⁶ Studies also show that blacks are less likely to receive longitudinal guideline-compliant care; they are less likely to have consistently controlled blood pressure or to achieve low-density lipoprotein treatment goals than non-Hispanic whites.^{31,37,38,39,40}

SES, which varies considerably by race and ethnicity in the United States, contributes to these health disparities. Black and Hispanics are disproportionately represented among the lower socioeconomic groups and face numerous obstacles in gaining access to high-quality education, employment, adequate income, and housing. However, although SES across racial/ethnic groups explains some portion of observed health disparities, it does not account for all of it. Racial disparities in health persist at every level of SES. SES is only part of the multifaceted context that constitutes social disadvantage. The social construct of race and racism—prejudice, stereotyping, and discrimination—comprises multiple dimensions of social inequality and ongoing injustices that intersect and interact in complex ways, giving rise to powerful impacts on health and well-being.

Sex

CVD disease is the leading cause of death in women in the United States, and it kills more women than the next three leading causes of death combined (see Chapter 108).³ Significant disparities exist in cardiovascular risk factors, treatment, and outcomes based on sex.³ Scientific evidence shows that women receive less significant treatment for CVD risk factors,^41,42 are often not treated according to recommended guidelines for a number of CVD diagnoses,⁴³ have lower long-term adherence with statins⁴⁴ and antihypertensive medications,⁴⁵ are given significantly lower priority for emergent ambulance service than men,⁴⁶ undergo fewer invasive procedures (eg, percutaneous coronary intervention and bypass surgery),^47,48 are more likely to experience a delay in door-to-balloon times,^49,50 suffer greater in-hospital mortality after myocardial infarction when aged <55 years,^51,52 experience greater long-term mortality after myocardial infarction,^53,54 and are significantly less likely to be referred to cardiac rehabilitation.⁵⁵ Further, women continue to be underrepresented in clinical trials, and publications often lack sex-stratified analyses, which limits the ability to identify sex differences and provide evidence-based care that ensures safety and efficacy by sex.⁴⁷ (US legislation that requires sex-specific analysis is expected to improve these sex inequities in biomedical research.) Although biology may underlie some of these observed differences, sex bias is thought to play a substantial role in creating these health disparities.

It is important to note that sex intersects with other social determinants of health, most importantly, race and ethnicity. Almost 50% of African American women in the United States have some form of CVD.³ Comparisons of the risk factor burden according to sex and ethnicity show that black women have the greatest burden of risk factors.⁵⁶ For example, they have a 46.1% prevalence of hypertension compared with 30.1% in non-Hispanic white women and 29.9% in Hispanic women,^‡ and they are more likely to have metabolic syndrome than white women.³ Black women are less likely to receive evidence-based therapies and have higher CVD mortality than white women (248.6/100,000 vs 188.1/100,000).³

Hispanics, the largest minority in the United States, have a higher prevalence of several cardiovascular risk factors than non-Hispanic whites. Notably, Hispanic women have twice the prevalence of diabetes as white women (about 12% vs 6%) and often face the challenge of low SES and poor access to health care, and yet Hispanics have lower mortality than non-Hispanic whites. This has been called the “Hispanic paradox” and has been confirmed by recent cardiovascular data.⁵⁷ Further studies are needed to identify the mechanisms mediating this protective cardiovascular effect in Hispanics.

Clinicians need to recognize that there is compelling evidence regarding the ongoing sex disparities that powerfully impact cardiovascular outcomes in women, especially among specific subpopulations who are also burdened with racial and ethnic inequalities.

Environment

Social Relationships

In a provocative article published in 1988 on the link between social relationships and mortality, the authors proposed a causal association and declared, “Social relationships, or the relative lack thereof, constitute a major risk factor for health—rivaling the effect of well-established health risk factors such as cigarette smoking, blood pressure, blood lipids, obesity and physical activity.”^58,59 The body of evidence accumulated since then consistently shows that a dearth of social relationships is linked to the development and progression of heart disease.^60,61,62,63 Small social networks, poor functional support, loneliness, and/or a sense of poor emotional support all have been shown to increase the risk for cardiac events.^64,65 A gradient relationship has been observed between the degree of reduced social support and the likelihood of adverse cardiac events.⁶⁶

A meta-analysis of 148 studies involving 308,849 participants from North America (51%), Europe (37%), Asia (11%), and Australia (1%) determined the extent to which social relationships influenced the risk for mortality. Investigators found that individuals with adequate social relationships experienced a 50% greater likelihood of survival compared to those with poor or insufficient relationships during an average follow-up time of 7.5 years.⁵⁹ The effect remained after controlling for age, sex, initial health status, follow-up period, and cause of death. Given the magnitude of the effect, the investigators make a compelling case for adding social relationship factors to the list of major conventional risk factors for morbidity and mortality, along with smoking, physical inactivity, poor nutrition, and obesity.

Although “social relationships” is a concept that is difficult to define concisely and various methods have been used to measure it, three major components are consistently evaluated: “(a) the degree of integration in social networks,⁶⁷ (b) the social interactions that are intended to be supportive (ie, received social support), and (c) the beliefs and perceptions of support availability held by the individual (ie, perceived social support).”⁵⁹ All three have been shown to be associated with morbidity and mortality, although they may exert their effects on health through different mechanisms, including cognitive, affective, and behavioral pathways. For example, one study⁶⁸ investigated interactions between social support and sleep in the prediction of inflammation in prehypertensive and hypertensive individuals at high risk for CVD. It found that social support moderated the association between sleep and circulating levels of both interleukin-6 and C-reactive protein, such that poor sleep appeared to confer a risk of increased inflammation only in those participants who also reported low social support. The same relationship was observed for tumor necrosis factor-α in women. Studies have also shown that the salutary—or deleterious—effects of social relationships start early in life. For example, one study found that greater emotional and instrumental support in childhood was associated with less biologic dysregulation in midlife, even after accounting for socioeconomic disadvantage in childhood and other potential confounders.⁶⁹

Neighborhood Environment

Over the past two decades, neighborhoods and residential areas have become an intense focus of research, because they have the capacity to affect individuals through various factors, including social influences, multiple aspects of the built environment, and potential exposures to myriad hazards.⁷⁰ Where one lives is strongly determined by socioeconomic position and race/ethnicity, and thus neighborhood is deeply interrelated with the other determinants of health and is an important contributor to health disparities. However, attributes of the neighborhoods themselves can promote and maintain health or promote illness and disease, independent of the socioeconomic position of individuals. The effects of these community-level factors often operate over the course of a lifetime, starting in childhood and lasting into old age. Today, the study of neighborhood health effects is multifaceted and complex, with investigative methodologies and techniques having become more sophisticated and nuanced as the field has developed.

In one of the seminal studies investigating neighborhoods and CVD, researchers examined the relation between characteristics of four neighborhoods in four different states and the incidence of coronary heart disease. After controlling for income, education, and occupation, data revealed that living in a disadvantage neighborhood was associated with a 70% to 90% higher risk of coronary heart disease in whites and a 30% to 40% higher risk in blacks compared with high-income persons in the most advantaged neighborhoods.⁷¹ Other subsequent studies have found a similar association between neighborhood SES and cardiovascular health,^71,72 conventional risk factors for CVD including hypertension⁷³ and diabetes,⁷⁴ mortality after myocardial infarction,⁷⁵ and all-cause mortality.^76,77,78,79

Other studies have explored how health behaviors may be influenced by place of residence. Poorer neighborhoods tend to have fewer health-promoting community resources, including healthy food options, parks and recreational facilities, built walkable areas, and accessible transportation. Compared to moderate- or high-income communities, the poorest neighborhoods have fewer supermarkets and fruit and vegetable markets, but more liquor stores.⁸⁰ Adverse social environments are thought to influence health behaviors deleteriously.⁸¹ Increasing evidence reveals the association between neighborhood built environment and health behaviors, such as physical activity levels^82,83 and eating patterns,^84,85,86,87 and obesity rates in the community.^88,89,90 Higher levels of crime add to the adverse social environment and may affect people’s level of outdoor physical activity.^91,92

Environmental exposure is an important, but underappreciated, risk factor for the development of CVD,⁹³ and is a particularly salient issue for those living in low-quality neighborhoods. Individuals in highly urbanized, densely populated, and poor residential areas are exposed to a number of environmental health threats, including toxic chemicals, biologic agents, noise and congestion, and air pollution, which is now identified as the world’s largest single environmental health risk (see Chapter 110).⁹⁴ The burgeoning field of environmental justice^§ research focuses on a number of critical issues, including proximity to potentially harmful locations and fair remediation procedures of hazardous sites. It also explores whether some populations face higher exposures to contaminants than others, and whether exposure levels have larger impacts on some groups more than on others.⁹⁵ Given the widespread prevalence of environment exposures, policy interventions that target the reduction of such threats can have a substantial impact on cardiovascular health.

Work Environment

A large body of literature substantiates that people with better jobs enjoy better health. Research over the past several decades has focused on the relationship between CVD health and a number of workplace factors, including the role of status in a hierarchical setting, the role of psychosocial stress on the job, the effects of physical and chemical hazards exposures in the workplace, the role of work organizational structure, and role of job insecurity and job loss in a changing global economic environment.⁹⁶ Also under intense investigation is whether the observed correlations are causal, and if so, via what mechanisms.

The most widely studied factor has been psychosocial work stress, which has been associated with CVD in a number of studies.^97,98,99 There are two main epidemiologic models of psychosocial job stress in the literature: job strain (high demands and low control) and effort-reward imbalance (high effort, low reward, and overcommitment). Both models have been shown to significantly predict myocardial infarction and CVD mortality.^{100,101,102,103} The INTERHEART study, the largest case-control study of its kind, compared 15,000 patients with myocardial infarction and 15,000 healthy controls,¹⁰⁴ and found that job strain doubled the risk of coronary heart disease, with a stronger effect in men than women.¹⁰⁵ However, subsequent studies have found a smaller risk,¹⁰⁶ with similar effects between sexes.^107,108 A more recent meta-analysis of 13 published and unpublished cohort studies found that job strain is associated with a small, but consistent, increased risk (1.2-1.3 times) of an incident event of CVD.⁹⁸ This association is apparent across strata of sex, age, SES status, and region, and after adjustments for SES status, as well as lifestyle and conventional risk factors. Another meta-analysis of seven cohort studies comprising 102,128 men and women showed that the risk of coronary artery disease was highest among subjects who reported both job strain and an unhealthy lifestyle; those with job strain and a healthy lifestyle had half the rate of disease.¹⁰⁹ These data suggest that people with job strain—notably hard to eliminate—may be able to substantially reduce their risk of coronary artery disease by adopting a healthy lifestyle.

Long working hours have also been implicated in the risk of CVD.⁹⁹ In two meta-analyses of published cohort studies, the relative risk of coronary heart disease was about 1.4 in employees working long hours compared to those working standard hours.^110,111 A systematic review and meta-analysis of published and unpublished data for almost 604,000 individuals found that working more than 55 hours per week was associated with an increase in risk of incident coronary heart disease (relative risk, 1.13) and incident stroke (relative risk, 1.33).¹¹² The researchers found a dose-response association for stroke.

Job insecurity and job loss have also been associated with increased risk of CVD. A meta-analysis of 13 cohort studies revealed a modest association between perceived job insecurity and incident coronary heart disease, partly attributable to poorer socioeconomic circumstances and less favorable risk factor profiles among people with job insecurity.¹¹³ In a prospective cohort study of 13,451 US adults, researchers found that unemployment status, multiple job losses, and short periods without work are all significant risk factors for acute cardiovascular events. Risks for acute myocardial infarction were particularly elevated within the first year of unemployment (hazard ratio, 1.27; 95% CI, 1.01-1.60) but not thereafter. Results were robust after adjustments for multiple clinical, socioeconomic, and behavioral risk factors.¹¹⁴

Access to Care

Unequal access to healthcare is a key social determinant of health and one of the important drivers of health disparities. As of 2014, after the Patient Protection and Affordable Care Act’s major coverage provisions went into effect, 32 million Americans still lacked health insurance,¹¹⁵ with most of them disproportionately drawn from racial and ethnic minorities and living at the lowest income levels. Hispanics and blacks have significantly higher uninsured rates (20.9% and 12.7%, respectively) compared with whites (9.1%).¹¹⁶ Data reveal that uninsured US adults are less likely to receive medical care, including screening for CVD risk factors.^{117,118,119,120} US adults without health insurance coverage are, perhaps as a result, also less likely to have ideal cardiovascular health, as measured by seven factors (blood pressure, body mass index, cholesterol, fasting blood glucose, smoking status, physical activity, and dietary intake).¹²¹ Numerous studies have found an association between lack of insurance and all-cause mortality.^122,123 Specifically, lack of insurance is associated with an increased risk of stroke and CVD death.¹²⁴

However, insurance is only part of the equation. Even among those who are insured, there are disparities in the quality of healthcare according to income. Those at the lowest SES levels experience gaps in access to care and quality services. Clinicians are less likely to refer low-income patients for diagnostic testing and treatment for heart disease.^{120,125,126,127} Compared with individuals with private insurance, Medicaid beneficiaries reported more barriers (unable to get through on telephone, unable to obtain appointment soon enough, long wait in the physician’s office, limited clinic hours, lack of transportation) to timely primary care and had higher associated emergency room utilization.¹²⁸ Barriers to specialty care exist as well. A study of community health centers revealed that referrals to off-site specialty services are frequently needed, yet medical directors reported major problems obtaining access to specialized medical and mental health services for uninsured patients and Medicaid recipients.¹²⁹ Given the structural barriers in the healthcare system, expanding Medicaid eligibility or other forms of insurance coverage alone is insufficient to improve healthcare access for disadvantaged groups.¹³⁰

Other barriers include lack of proximity to heart centers, transportation issues, lack of flexibility in work schedules, low Medicaid payment rates, health literacy issues, language and cultural barriers, patient beliefs, and perceived racial bias. A review of the literature on the effects of interpersonal and institutional racism and discrimination occurring within healthcare settings revealed that up to 52% of African Americans, 13% of Latinos, and 6% of whites reported receiving biased treatment based on their race or ethnicity.¹³¹ Health care providers’ racial and ethnic attitudes are a factor in creating health disparities. According to the IOM’s Unequal Treatment report, “research to date demonstrated that healthcare providers’ diagnostic and treatment decisions, as well as their feelings about patients, are influenced by patients’ race or ethnicity and stereotypes associated with them … [al]though myriad sources contribute to these disparities, some evidence suggests that bias, prejudice and stereotyping on the part of healthcare providers may contribute to differences in care.”⁹ Studies reveal that clinicians, similar to the general population, display substantial bias and prejudice in their implicit (unconscious) attitudes.^132,133,134

The sources of disparities embedded in the healthcare system are complex and involve participants and factors that operate at many levels of the system. A comprehensive, multilevel strategy is needed to eliminate healthcare disparities.

We have presented evidence in this chapter that clearly establishes the strong correlation between social disadvantage and ill health. The central question, then, is how does social disadvantage mediate the development of disease? In other words, what is the biology of disadvantage?²⁰ Based on accumulating evidence, myriad investigators have proposed a number of different mediating pathways by which numerous social factors interact to produce poor health outcomes. Figure 107–2 shows a simplified model of how personal characteristics (race, ethnicity, sex, and SES) may interact with a variety of social stressors and environmental factors to influence health behavior, psychological reactions, and biological substrates, which, in concert with other factors such as access to healthcare, ultimately determine health outcomes.

Psychosocial Factors

Researchers have come to appreciate the role that psychosocial risk factors play in mediating CVD. The emerging field of behavior cardiology has divided psychosocial factors into two broad categories, emotional factors and chronic stressors: “Emotional factors include affective disorders such as major depression and anxiety disorders as well as hostility and anger. Chronic stressors include factors such as low social support, low SES, work stress, marital stress, and caregiver strain.”⁶⁵ A vast body of literature now links emotional states—depression, anxiety, and hostility/anger—with increased cardiovascular risk, a worse cardiometabolic profile, adverse outcomes, and mortality.^135,136 A meta-analysis of the association between perceived stress and incident coronary heart disease found that high perceived stress is associated with a moderately increased risk of incident coronary heart disease.¹³⁷

Multiple Risk Exposure

One proposed pathway that may explain the link between social determinants and health is the concept of multiple risk exposure.¹³⁸ Socially disadvantaged individuals are particularly exposed to multiple, clustered psychosocial and physical stressors, either sequentially or simultaneously, while concurrently having fewer resources to cope. The stressors that accompany deprivation, many of them discussed earlier, include adverse circumstances in childhood; low educational attainment; poverty, financial worry, and low social status; racial discrimination; poor housing; work strain and job insecurity; crowded and unsafe neighborhoods; exposure to toxins, pollutants, noise, and congestion; early pregnancy; family conflict and divorce; incarceration; and lack of quality health care, among others. The frequency and intensity of exposure to these stressors and related emotional responses are thought to constitute the primary pathway of how social disadvantage is biologically linked to CVD. Evidence reveals a strong dose-response relationship for most psychosocial risk factors, with data suggesting that adverse clinical effects may begin to occur with even minimal levels of distress.⁶⁶ A meta-analysis of 10 large, community-based cohort studies, each of which assessed psychological distress by using the 12-item General Health Questionnaire, found that even minor elevations in General Health Questionnaire-12 scores were associated with a 25% increase in cardiac mortality.¹³⁹

Allostatic Load and Chronic Stress

Allostatic load (AL) is a useful heuristic model that helps conceptualize how chronic stress drives pathophysiologic mechanisms. Cumulative chronic stress is thought to lead to long-term dysregulation of allostasis, through activation of the sympathetic nervous system and hypothalamic-pituitary axis, which promotes maladaptive wear-and-tear on the brain and body that, in turn, compromises resiliency.¹⁴⁰ Evidence is accumulating that shows individuals of low SES have higher AL scores (indicating greater dysregulation and increased vulnerability to disease) than individuals in high SES groups. One investigation studied AL scores based on 10 biomarkers and examined cardiovascular/diabetes-related mortality disparities between blacks and whites. Researchers found that black men and women had higher AL scores than whites, and they concluded that AL burden partially explains higher mortality among blacks, independent of SES and health behaviors.¹⁴¹ This may be one of the mechanisms through which racism and discrimination exert their destructive effects. Discrimination is a source of acute and chronic stress for many oppressed group members.^{142,143,144,145}

Another study looked at whether greater life-course SES adversity experience was associated with higher scores on a multisystem AL index of physiologic function in adulthood.¹⁴⁶ Based on 24 biomarkers from 7 different physiologic systems, researchers found that greater SES adversity experience at each phase of, and cumulatively across, the life course was associated with higher AL scores, even when adjusted for a wide array of health status, behavioral, and psychosocial factors.

SES adversity experience may accumulate throughout life and have a negative impact on multiple organ systems in adulthood, especially the cardiovascular system.^146,147,148 Numerous studies in the literature now document the deleterious effects of chronic stress on the cardiovascular system, including activation of the inflammatory response, endothelial dysfunction, thrombosis, vascular hyperactivity, and metabolic disturbances.^{149,150,151,152,153}

Health Behaviors

Deleterious health behaviors (eg, smoking, inactivity, poor diet, medication nonadherence) increase the risk of CVD. Correspondingly, alterations in these behaviors reduce the risk of developing the disease and its associated morbidity and mortality (see Chapter 111).³ A body of literature also firmly establishes that socioeconomic gradients exist for major health behaviors over the course of the lifespan. That is, smoking, inactivity, poor diet, and medication nonadherence tend to be more prevalent among people in lower SES groups,^{154,155,156,157,158,159} and these individuals, in turn, tend to have more cardiovascular risk factors, including hypertension, lipid abnormalities, obesity, insulin resistance, and diabetes mellitus.

For example, tobacco use—the health behavior that accounts for the greatest number of premature deaths, 480,000 in the United States alone in 2014¹⁶⁰—was equally prevalent among all socioeconomic groups in the United States 50 years ago, but now is more common among people with less education and lower incomes.¹⁶¹ According to the most recent American Heart Association (AHA) statistics, between 2003 and 2012, obesity decreased among those of higher SES, but increased among those of lower SES.³

Children in lower socioeconomic groups have a steeper weight gain trajectory from birth, with a strong socioeconomic gradient in the prevalence of child and adult obesity.¹⁶² It appears the die is cast early in life, as childhood SES has been shown to account for both the uptake of unhealthy behaviors and subsequent health risk in the adult years. For example, a long-term British cohort study of 2132 individuals that determined risk of death between the ages of 26 and 66 years found that childhood and adult SES accounted for a significant portion of health inequalities observed in death risk. The investigators concluded that the combination of material and psychosocial conditions in childhood was almost as powerful as smoking in accounting for the inequality in adult mortality seen in the cohort. These effects of early life circumstances were seen to continue far into adulthood and to influence mortality by their impact on smoking and other health behaviors.¹⁶³

Health behaviors vary according to race and ethnicity as well as SES. Compared with non-Hispanic whites, nonwhite groups—blacks, Hispanics, and Native Americans—tend to have more unfavorable health behaviors, including smoking, physical inactivity, unhealthy eating habits, obesity, medication nonadherence, and lower health care use.^{153,164,165,166,167,168,169,170} For example, non-Hispanic blacks (41.4%) and Hispanics (42.9%) are less likely to meet current aerobic physical activity guidelines than non-Hispanic whites (53.4%).³ High rates of obesity are found among all racial/ethnic groups, but in particular among American Indians and Alaska Native populations, of whom 39.4% are obese compared with 24.3% of non-Hispanic whites.¹⁷¹ Numerous studies have documented that nonwhites are significantly less likely to adhere to CVD medications, including statins, antihypertensives, and heart failure regimens.^{44,172,173,174,175,176} A number of factors, including patient self-efficacy and depression, patient-provider communication, trust in physicians, and health care system–related factors, have been shown to be associated with medication nonadherence.^177,178,179 Furthermore, studies have shown that medication nonadherence mediates the association between ethnicity and CVD outcomes.¹⁸⁰

Differences in health behaviors are seen among racial and ethnic minorities. This presents the opportunity to focus interventions to promote behavioral change among high-risk populations. However, although differences in health behaviors account for some of the observed socioeconomic gradient in CVD, they do not account for all of it.

If the major determinants of health are socially driven, then policy initiatives—both health policy and wider social and economic policy—are critical to improving health outcomes and reducing health disparities. In response to the continuing challenge posed by the reality of entrenched health disparities, broad, intensive, well-coordinated efforts are now under way to address this most urgent and complex issue. There is still a profound mismatch between the evidence that documents the human toll and economic burden posed by CVD and the efforts aimed at addressing it.¹⁸¹ More must be done to galvanize the effort.

Comprehensively speaking, initiatives to address the CVD epidemic must entail addressing individual-level actions, health care systems, and population-wide efforts. Proximate risk factors for CVD (genomic, biologic, and behavioral) must be addressed at the individual level, and diagnosis and treatment of CVD must always receive high priority. Within this context, individual-level approaches should target high-risk individuals, especially those who are socially disadvantaged. But individual-level approaches are not enough. Public policy initiatives are needed that focus on improving access to health insurance. Further, barriers to access to care, which are multiple, need to be addressed systemically across the health care system. Evidence suggests that performance measure-based quality improvement, provider cultural competency training, team-based care, and patient education are effectively strategies in mitigating disparate CVD care and may improve outcomes.³¹ The American College of Cardiology’s Coalition to Reduce Racial and Ethnic Disparities in Cardiovascular Disease Outcomes (CREDO) is predicated on these strategies. CREDO seeks to provide cardiologists and other clinicians who treat patients with CVD with evidence-based tools and information to reduce health disparities. Although access to medical care and quality of treatment are critical, it has been estimated that only 10% of premature mortality is due to shortfalls and failures of health care.

Public policy needs to address the social, environmental, and economic conditions that contribute to the development of illness. Two broad types of policies will make a difference in promoting health and reducing disparities: (1) policies that reduce inequalities between the socioeconomic classes, and (2) policies that buffer the adverse consequences of living at the lowest socioeconomic levels.¹⁸² Policies that reduce inequalities include those that address educational attainment, job training, income and occupational status, and wealth distribution. Policies that buffer the adverse consequences of low SES include those that address affordable housing, the built environment, workplace issues, occupational safety, exposure to toxins, and interventions that promote healthier behaviors. The AHA has endorsed changing the social context so that individuals will make healthy decisions by default. In the AHA’s view, this shift potentially has the greatest impact on population-wide health promotion and risk reduction.⁵ Societal-level approaches also include public policies aimed at the agriculture, food, and tobacco industries, as well as at changes in urban planning and efforts to contain environmental pollution. Future research is needed to discover which of the social factors can be modified, as well as how findings can best be formulated into policies that have the greatest impact on promoting health, preventing CVD and reducing disparities in the most disadvantaged populations.

Importantly, many public and private actors are engaged in addressing the social determinants of health; the US federal government, state governments, many foundations, nonprofit and community-based organizations, and a number of professional medical societies have initiated programs to reduce health disparities. Although it is beyond the scope of this chapter to enumerate the various initiatives under way, of note are the activities of the US federal government. The US Department of Health and Human Services’ (DHHS) Office of Minority Health, established in 1986, is charged with improving the health of racial and ethnic minority populations through the development of health policies and programs to eliminate health disparities. The Affordable Care Act of 2010¹⁸³ extended the reach of this federal initiative by establishing Offices of Minority Health within six federal agencies.^** The Affordable Care Act also elevated the National Institute on Minority Health and Health Disparities (NIMHD) to an institute level at the National Institutes of Health. The mission of NIMHD is to lead scientific research to improve minority health and eliminate health disparities. To accomplish this, NIMHD (1) plans, coordinates, reviews and evaluates minority health and health disparities research and activities of the National Institutes of Health; (2) conducts and supports research in minority health and health disparities; (3) promotes and supports the training of a diverse research workforce; (4) translates and disseminates research information; and (5) fosters innovative collaborations and partnerships.¹⁸⁴

In 2011, the DHHS published its “Action Plan to Reduce Racial and Ethnic Health Disparities.”¹⁸⁵ The goals of the plan are to (1) transform healthcare; (2) strengthen the nation’s health and human services infrastructure and workforce; (3) advance the health, safety, and well-being of the American people; (4) advance scientific knowledge and innovation; and (5) increase the efficiency, transparency, and accountability of DHHS programs. Figure 107–3 shows the overarching priorities and goals of the DHHS Disparities Action Plan. Table 107–2 enumerates the plan’s strategies. The DHHS Disparities Action Plan was developed in concert with the National Partnership for Action’s (NPA) 2011 National Stakeholder Strategy for Achieving Health Equity (available at http://minorityhealth.hhs.gov/npa). The NPA Stakeholder Strategy, which proposes a comprehensive, community-driven approach to reduce health disparities, resulted from a public-private collaboration that solicited broad community input with the assistance of state and local government and federal agencies. It reflects the commitment of thousands of people across the country representing myriad sectors. The DHHS Disparities Action Plan builds on the goals and objectives previously articulated in Healthy People 2020 (available at http://www.healthypeople.gov/) to reduce health disparities, and it leverages a number of important provisions of the Affordable Care Act and other cutting-edge DHHS initiatives.¹⁸⁶

CVD is the leading cause of death worldwide, including in the United States. Epidemiologic trends document enduring patterns of inequalities. Complex interrelated social factors drive these inequalities and the resulting health disparities. But health disparities are neither inevitable nor immutable.^187,188 In our efforts to reduce the profound human toll and vast economic burden posed by CVD, we urgently need to broaden our notion of what constitutes “intervention.” Focusing on health as a problem of the individual, as clinical medicine does, is insufficient. Heath care providers and organizations need to further extend their responsibility for reducing disparities, and specifically target high-risk populations with culturally sensitive interventions. We must continue to examine what has been called the “causes of the causes,”¹⁸⁹ and develop evidence-based public policy—including health, social, development, and economic policy—that prioritizes the social determinants of health. In the end, this will not only have major ramifications on the health status of vast populations around the world and reduce morbidity and premature mortality, especially from CVD, but it will also drive development and prosperity across the globe and address one of the major social justice issues of our time.