Endocrine, Nutritional, and Metabolic Diseases

During the study period (1990–2017), trends in mortality from ENM diseases were largely similar among working-age males and females within each age group (Figure 9-1). Among younger working-age adults (25–44) mortality from these diseases increased slowly throughout the 2000s and 2010s, with the largest increases occurring among Black males. Among older working-age adults (45–64), Whites experienced gradual increases in mortality from ENM diseases throughout the period, while trends among Blacks and Hispanics were marked by decreasing mortality in the 2000s and a subsequent leveling off and/or increase during the 2010s. In every age group, the largest increase in ENM mortality in the 2010s occurred among Black males.

FIGURE 9-1

Mortality rates (deaths per 100,000 population) from endocrine, nutritional, and metabolic diseases among U.S. working-age males and females (ages 25–64), 1990–2017, by sex, age, and race and ethnicity. NOTE: Each panel shows mortality (more...)

Differences between White and Hispanic adults in ENM mortality were minimal among those ages 25–54. Among older adults (ages 55–64), Hispanics experienced higher mortality than their White counterparts in the 1990s, but this gap began to narrow in the 2000s and had disappeared by the end of the study period primarily because of declining ENM mortality among Hispanics. Although working-age Blacks experienced larger changes in mortality from ENM diseases over time, these changes preserved the sizable racial inequalities in mortality from these diseases as the rates for Blacks remained roughly twice those for Whites and Hispanics throughout the period (Figure 9-1).

Working-age adults living in large central metropolitan areas (hereafter referred to as “large central metros”) generally experienced lower mortality from ENM diseases relative to those in less-populated areas throughout the study period (Figure 9-2). Mortality in nonmetropolitan areas (hereafter referred to as “nonmetros”) was not always the highest, but it increased more rapidly (or decreased more slowly) than in other areas throughout the 1990s. By 2000–2002, mortality from ENM diseases was highest in nonmetros, and this continued to be the case throughout the remainder of the study period among all working-age adults except Black males ages 25–44. The largest increases among these younger Black males occurred in small and medium metropolitan areas (hereafter referred to as “small/medium metros”). The net result was that disparities across metropolitan areas widened over time, particularly among Whites and Blacks.

FIGURE 9-2

Mortality rates (deaths per 100,000 population) from endocrine, nutritional, and metabolic diseases among U.S. working-age males and females (ages 25–64), 1990–1993 through 2015–2017, by metropolitan status. NOTE: Mortality rates (more...)

At the state level, mortality from ENM diseases increased among males in all but two states (New Jersey and Vermont) and the District of Columbia, with particularly large increases in several Southern and Western states and in South Dakota (Figure 9-3). Among females, the rates increased in 38 states. There was very little change in the rates across the Northeastern states, but small increases occurred across most of the Midwest and West, and comparatively large increases occurred in several Southern states, most notably West Virginia, Mississippi, Arkansas, Kentucky, and Oklahoma. Among both males and females, there were relatively large declines in the District of Columbia.

FIGURE 9-3

Mortality rates (deaths per 100,000 population) from endocrine, nutritional, and metabolic diseases among U.S. working-age males and females (ages 25–44), 1990–1992 and 2015–2017, by region and state. NOTE: Mortality rates are (more...)

Hypertensive Heart Disease

White adults across all working ages experienced increased mortality from hypertensive heart disease during the study period, while the trends among Hispanic and Black adults differed by age and sex (Figure 9-4). Although rates of mortality due to hypertensive heart disease were lower among younger (ages 25–44) than older (ages 45–64) adults, they increased slowly in this younger age group throughout the period among White and Black males and females and Hispanic males, with the largest increases occurring in the early 2000s and the most recent period, from 2012–2014 to 2015–2017; the increases were greater among males than females and among Blacks in this age group. Mortality rates among Hispanic females in all age groups remained stable over the study period. Older Black females ages 55–64 were the only group of working-age adults to experience declining mortality from hypertensive heart disease over the period, although these declines slowed in the 2010s and trended slightly upward after 2012. Among Black males ages 45–64 and Black females ages 45–54, mortality due to hypertensive heart disease showed small fluctuations during the 1990s and 2000s before stagnating (Black females) or increasing slightly (Black males) in the 2010s.

FIGURE 9-4

Mortality rates (deaths per 100,0000 population) from hypertensive heart disease among U.S. working-age males and females (ages 25–64), 1990–2017, by sex, age, and race and ethnicity. NOTE: Each panel shows mortality rates for non-Hispanic (more...)

Throughout the study period, working-age mortality from hypertensive heart disease was more than three times higher among Blacks than among Whites and Hispanics. Because mortality increased more quickly among younger (ages 25–44) Black adults than among their White and Hispanic peers, the mortality gap widened in this age group. However, the Black–White mortality gap narrowed slightly among older working-age adults (ages 45–64), as mortality increased among Whites but declined or stagnated among Blacks. While working-age White and Hispanic adults experienced similar mortality rates throughout the period, the mortality rates in 1990–1993 were slightly higher among Hispanic adults in every age group, but by 2015–2017, the rates were slightly higher among White adults.

While the substantive differences are not large, interesting patterns emerge when these trends are examined separately by metropolitan status (Figure 9-5). Mortality from hypertensive heart disease in large central metros was highest in 1990–1993 but increased less than in other areas, while mortality in nonmetros increased more rapidly. In 1990–1993, large central metros had the highest mortality from hypertensive heart disease among White adults and nonmetros the lowest, the exception being White females ages 25–44, among whom mortality did not differ by metropolitan status. During the 2010s, however, mortality from hypertensive heart disease increased sharply in nonmetro areas, while large central metros experienced much smaller increases. By 2015–2017, mortality from hypertensive heart disease among working-age Whites was highest in nonmetros and lowest in large central metros. The exception was mortality among older White males (ages 45–64), which ended the period with little difference across metro status because mortality in nonmetros did not increase as sharply in this population.

FIGURE 9-5

Mortality rates (deaths per 100,000 population) from hypertensive heart disease among U.S. working-age males and females (ages 25–64), 1990–1993 through 2015–2017, by metropolitan status. NOTE: Mortality rates are shown for those (more...)

The same trends occurred among working-age Black males (higher mortality in large central metros in 1990–1993 and smaller increases, or larger decreases, over time than in other areas), reducing the gap in mortality by metro size. Among older Black females, the overall declines in mortality from hypertensive heart disease that occurred in the 1990s and 2000s were driven primarily by decreasing mortality in large central metros; mortality stagnated or increased elsewhere. Despite the favorable trends in large central metros; mortality remained highest in these areas for most working-age Blacks. The exception was younger working-age Black females, among whom mortality from hypertensive heart disease increased within small/medium metros and large fringe metropolitan areas (hereafter referred to as “large fringe metros”), but decreased within both nonmetros and large central metros in the 2010s.

Mortality from hypertensive heart disease among older working-age Hispanics (ages 45–64) deviated from the overall trend among older males and females. Among older Hispanic males, mortality increased most rapidly in large fringe metros; by 2015–2017, the mortality rates were similar in large central metros and large fringe metros and lower in nonmetros and small/medium metros. Among older Hispanic women, mortality from hypertensive heart disease remained steady throughout the study period, a pattern driven by mortality trends in large central metros. Outside of large central metros, mortality in this population increased between 1990 and 2017. Even with these increases, however, mortality from hypertensive heart disease remained relatively low among Hispanic men and women.

At the state level, mortality from hypertensive heart disease increased among males in every state (Figure 9-6), a pattern of state-level consistency found for only two other causes of death (drug poisoning and liver cancer). Mortality among females increased in every state but New York (where the rate of mortality from hypertensive heart disease, the highest in the Northeast region, remained virtually unchanged). The largest increases and highest mortality rates occurred in several Southern states (notably Oklahoma, Mississippi, Arkansas, and Kentucky). In contrast, mortality from hypertensive heart disease changed comparatively little in the Northeast. Although increases among both males and females were small in the District of Columbia, it maintained the highest rate of mortality from hypertensive disease for males and the second highest for females (after Oklahoma) in 2015–2017.

FIGURE 9-6

Mortality rates (deaths per 100,000 population) from hypertensive heart disease among U.S. working-age males and females (ages 25–44), 1990–1992 and 2015–2017, by region and state. NOTE: Mortality rates are shown for 1990–1992 (more...)

Ischemic Heart Disease and Other Circulatory System Diseases

By far the largest contributor to the recent plateau in all-cause mortality among working-age adults was the slowing pace of improvements in mortality from ischemic heart disease and other circulatory diseases. The remarkable declines in mortality from these diseases seen throughout the 1990s and 2000s stalled in the 2010s (Figure 9-7).¹ Working-age Blacks had much higher rates of mortality from ischemic heart disease and other circulatory diseases relative to their White and Hispanic counterparts, although they also experienced the largest reductions between 1990 and 2017. The more rapidly declining death rates among Blacks reduced the mortality gap between them and both Hispanics and Whites over time. Although Hispanic adults had lower mortality from these diseases relative to White or Black adults, the trends among Whites and Hispanics were similar over time. The flattening of the mortality trend in ischemic heart disease and other circulatory diseases after 2010 was similar across all working-age adults.

FIGURE 9-7

Mortality rates (deaths per 100,000 population) from ischemic heart disease and other circulatory system diseases among U.S. working-age males and females (ages 25–64), 1990–2017, by sex, age, and race and ethnicity. NOTE: Each panel shows (more...)

Perhaps because ischemic heart disease and other circulatory diseases are a leading cause of death, differences in mortality from this category of causes by metropolitan status (Figure 9-8) largely mirror the patterns noted earlier for all-cause mortality. That is, mortality from ischemic heart disease and other circulatory diseases was highest in nonmetros and lowest in large central metros throughout the study period. Among working-age White adults, disparities between large central metros and nonmetros widened, just as they did for all-cause mortality. They widened among younger working-age White adults (ages 25–44) because mortality decreased in large central metros but increased elsewhere, particularly in nonmetros. Mortality also declined among older working-age Whites (ages 45–64), but these declines were largest within large central metros and smallest within nonmetros. Among younger working-age Blacks and Hispanics, the mortality gap by metropolitan status was steady throughout the period until 2010, when it widened among Hispanics.

FIGURE 9-8

Mortality rate (deaths per 100,000 population) from ischemic heart disease and other diseases of the circulatory system among U.S. working-age males and females (ages 25–64), 1990–1993 through 2015–2017, by metropolitan status. (more...)

Between 1990 and 2017, working-age mortality from ischemic heart disease and other circulatory diseases declined in every state (Figure 9-9). The District of Columbia experienced the largest absolute and relative declines. In general, the largest declines occurred in Northeastern states and the smallest in several Western and Southern states. As of 2015–2017, the South accounted for 8 of the 10 states with the highest rates of male mortality from these diseases (the two other states were Nevada and Missouri); all 10 states with the highest female rates were in the South. This was the case despite the comparatively large declines in mortality that occurred in the South over the study period.

FIGURE 9-9

Mortality rates (deaths per 100,000 population) from ischemic heart disease and other diseases of the circulatory system among U.S. working-age males and females (ages 25–44), 1990–1992 and 2015–2017, by region and state. NOTE: (more...)

Summary of Trends

Cardiovascular disease (CVD) was the leading cause of death among working-age males and Black females throughout the study period, and the second leading cause of death (after cancer) among White and Hispanic females. Mortality from CVDs declined substantially throughout the 1990s and 2000s among working-age adults, particularly Black males and females. These improvements were due primarily to steady reductions in death rates from ischemic heart disease and other circulatory diseases during the 1990s and 2000s. However, these mortality reductions in ischemic heart disease and other circulatory diseases masked concerning trends in mortality due to hypertensive heart disease and ENM diseases that were rising among young adults, White adults, and Hispanic males during the 1990s and 2000s. These countervailing mortality forces ended when reductions in cardiovascular mortality among all population groups stalled in the 2010s. From 2009–2011 to 2017, mortality from ischemic heart disease and other circulatory system diseases remained largely unchanged among U.S. working-age adults (though see footnote 1 above). At the same time (after 2010), mortality from hypertensive heart disease increased among younger (ages 25–44) working-age adults (except Hispanic females), White working-age adults, and older (ages 55–64) working-age adults, and remained steady among other working-age adults, while mortality due to ENM diseases increased among all working-age adults, particularly Blacks.

These troubling changes in cardiometabolic mortality were particularly pronounced in the South and in areas outside of large central metros, which, along with the Northeast, generally experienced the most favorable trends in cardiometabolic mortality. As a result of these trends, the gap in mortality by metropolitan size grew over time, particularly among White working-age adults.

The contribution of cardiometabolic mortality to the recent rise in all-cause working-age mortality was therefore due to the net increases in mortality from cardiometabolic diseases after 2010, when mortality declines in ischemic heart disease and other circulatory system diseases stalled and no longer offset the rising rates of mortality from ENM diseases and hypertensive heart disease. These trends in cardiometabolic mortality are likely related; that is, the factors causing the rise in mortality from ENM diseases and hypertensive heart disease may also be related to the recent slowdown in reductions in mortality from ischemic heart disease and other circulatory diseases. Moreover, the magnitude of the long-term decline in mortality from ischemic heart disease and other circulatory diseases has masked the significant implications of the recent stagnation in this trend since 2010. For example, recent research by Mehta, Abrams, and Myrskylä (2020) demonstrates that the slowing pace of decline in cardiovascular mortality was an important factor in the longer-term stagnation in U.S. life expectancy, playing a much larger role since 2010 relative to other causes of death, including drug-related causes. These authors show that drug-related mortality contributed to the shorter-term decline in life expectancy over 2014–2017, whereas stagnation in mortality due to CVD contributed to the longer-term flattening trend in life expectancy. In simulations of life expectancy at age 25, the authors found that the gains in life expectancy would have been greater by a factor of 4 for males and 8 for females if mortality from CVD had continued its rate of decline after 2010, compared with no increase in drug-related deaths since 2010. Their findings indicate that the slowdown in progress in CVD has been more consequential for U.S. life expectancy relative to increasing drug-related mortality. Similarly, Masters, Tilstra, and Simon (2018) found that without “cohort-based increases in metabolic disease mortality risk, the recent increases in middle-age U.S. White women’s overall mortality rates likely would not have occurred” (p. 87). Indeed, the stalling reductions in mortality from CVD among U.S. working-age adults will likely continue to shape U.S. mortality trends in the future (more on this below).

Turning next to explanations for the related trends in mortality from ENM diseases, hypertensive heart disease, and ischemic heart disease and other circulatory diseases between 1990 and 2017, three important themes are relevant. First, the obesity epidemic, fueled by expanding obesogenic environments, has been a major cause of increasing disease, affecting multiple body systems and leading to deaths from hypertension, diabetes, stroke, and CHD (Mensah et al., 2017). Second, while declining smoking rates and medical advances over the past 50 years have greatly lowered mortality due to CVD, declines in smoking have slowed, and the contributions of further medical innovation have had less impact in recent years. Third, cardiometabolic diseases may be rising as a result of other social, economic, and cultural changes that have undermined economic security, intergenerational mobility, and social support networks, which in turn have led to increased chronic stress among the working-age population. The next section presents the committee’s assessment of the evidence related to each of these explanations.

Rising Rates of Obesity

Prevalence and Subgroup Differences

The most important trend potentially explaining the rise in working-age mortality due to ENM diseases and hypertensive heart disease and the stagnation in improvements in mortality due to ischemic heart disease and other diseases of the circulatory system is the increased prevalence of obesity in the U.S. population (Lloyd-Jones et al., 2016; Mensah et al., 2017; Sidney et al., 2016). This report uses the Centers for Disease Control and Prevention’s (CDC’s) definition of obesity as weight that is higher than what is considered a healthy weight for a given height based on body mass index (BMI). BMI is calculated as weight in kilograms divided by height in meters squared, rounded to one decimal place. Obesity in adults is indicated when BMI is greater than or equal to 30 as a measure of abnormal or excessive fat accumulation that presents a risk to health (Hales et al., 2020). Rates of obesity began to rise in the early 1980s, a trend that has continued as a period-based phenomenon affecting children and adults of all ages (Reither, Hauser, and Yang, 2009). The prevalence of obesity among U.S. adults nearly tripled, increasing rapidly from the late 1970s through the early 2000s, with sustained but less rapid increases since then. The age-adjusted prevalence of adult obesity, defined as the percentage of adults ages 20–74 with a BMI of 30 kg/m² or above, was 42.4 percent in 2017–2018 compared with 15.0 percent in 1976–1980 (Fryar, Carroll, and Ogden, 2018; Hales et al., 2020).

Obesity rates vary by age, sex, race, ethnicity, and socioeconomic status. Older adults tend to have higher rates of obesity relative to younger adults (ages 20–39), although age differences in obesity have diminished as its prevalence has increased over time (Fryar, Carroll, and Ogden, 2018; Hales et al., 2020). Black women have higher obesity rates than Black men, but there are no significant differences in prevalence between men and women among White, Asian, or Hispanic adults (Hales et al., 2020). In 2017–2018, 56.9 percent of Black women were obese, compared with 41.1 percent of Black men. Overall, obesity rates are highest among Blacks (49.6%), followed by Hispanics (44.8%), Whites (42.2%), and Asians (17.4%).

Rates of obesity have increased in a similar fashion among adults in all income categories, as shown in Figure 9-10, and higher-income populations consistently have lower rates of obesity relative to those with lower income. Working-age adults with a college degree have a lower prevalence of obesity compared with their less-educated peers (Figure 9-11), although this pattern is not consistent by race and ethnicity and sex. For example, Black men show no difference in rates of obesity by educational attainment (Ogden et al., 2017).

FIGURE 9-10

Obesity rates by income measured as percentage of poverty in each respective period, among U.S. adults, 1960–2016 (obesity defined as body mass index [BMI] >30). NOTE: Data are from the National Health and Nutrition Examination Survey (more...)

FIGURE 9-11

Obesity prevalence by educational attainment for men and women, 2011–2014 (obesity defined as body mass index [BMI] >30). SOURCE: Prevalence of Obesity Among Adults, by Household Income and Education—United States, 2011–2014, (more...)

Given differentials in obesity by socioeconomic status, some research has examined whether obesity explains differentials by socioeconomic status in the recent rise in working-age mortality. The evidence to date suggests that changes in obesity are not exerting differential impacts on working-age mortality by socioeconomic subgroups of the population. Cutler, Meara, and Richards-Shubik (2011) show that changing rates of obesity were not responsible for widening educational differences in mortality among U.S. adults (ages 25–74) between the 1970s and early 2000s. And Geronimus and colleagues (2019) demonstrate that changes in mortality at working ages (25–64) due to CVD and diabetes between 1990 and 2015 were highly similar for low- and high-educated Black and White men and women. Together, these studies suggest that changes in obesity, while clearly contributing to working-age mortality for key causes of death over the past 25 years, has had little impact on socioeconomic disparities in those trends.

Diminishing Returns of Medical Advances

Starting in the late 1960s, there was a remarkable turnaround in the century-long trend of increasing cardiovascular mortality in the United States. By the 1970s, death rates due to CVD, and in particular CHD and stroke, were in sharp decline, registering a 70 percent decline by 2010 (Mensah et al., 2017). Medical innovations in drug development and prevention, treatment, and control of chronic diseases, together with increasing knowledge about the health effects of cigarette smoking, fueled this decline. Studies suggest that medical advances and surgical treatments explain about 47 percent of the decline, while reductions in major risk factors (e.g., smoking, poor diet, lack of physical activity) explain approximately 44 percent (Ford et al., 2007; Mensah et al., 2017).

The 1964 Surgeon General’s Report on Smoking and Health publicized the dangers of cigarette smoking, triggering a series of tobacco control efforts that successfully reduced tobacco use (see Chapter 11). The benefits of treating moderate hypertension were demonstrated in the early 1970s, and the benefits of lowering cholesterol emerged in the early 1980s, leading to the establishment of the first standards and targets for blood pressure and cholesterol management in 1987 (Mensah et al., 2017). By the late 1980s, powerful new drugs for managing blood pressure (e.g., angiotensin-converting enzyme inhibitors and beta-adrenergic blocking agents) and cholesterol (e.g., statins) also contributed to lowering CVD mortality. Furthermore, the late 1980s introduced thrombolysis² and angioplasty as standard treatments for acute myocardial infarction, stroke, and pulmonary embolisms. Coronary stents were approved by the FDA in the 1990s and widely used thereafter.

As discussed previously, the 21st century brought a slowdown in the impact of medical advances in treating CVD (Mensah et al., 2017). The new century saw some additional clinical trials of statin drugs, a focus on treating isolated systolic hypertension³ in the elderly, and a lowering of blood pressure targets to increase blood pressure control, but innovations after 2000 had a smaller impact relative to those in prior decades. Stagnation in improvements in CVD mortality became evident after 2010, garnering public attention (e.g., Bever, 2019; McKay and Winslow, 2016; Painter, 2019) and stimulating research to find an explanation (Ma et al., 2015; Mensah et al., 2017; Shah et al., 2019; Sidney et al., 2016). Several explanations for the diminishing returns of medical advances in lowering CVD mortality after 2010, detailed in the next section, have been proposed: more incremental development of medical innovations, rising obesity that blunted the impact of medical advances, and differential delivery of or access to the medical advances that enabled the reductions in CVD mortality.

International data do not support the explanation that a lack of medical innovations after 2010 is responsible for the stalling improvements in CVD. The flattening of the CVD mortality trend in the United States after 2010 has occurred in other industrialized countries as well (Case and Deaton, 2017; Lopez and Adair, 2019; Ma et al., 2015; Preston, Vierboom, and Stokes, 2018; Shah et al., 2019; Sidney et al., 2016). International comparisons are shown in Figure 9-12 (adapted from Mehta, Abrams, and Myrskylä, 2020). Although all of the 10 countries with high life expectancy in this figure experienced flattening trends in CVD mortality after 2010, the United States has not kept pace with the reductions in CVD mortality seen in these other countries, suggesting that other factors specific to the United States have been stalling continued improvements. Prime among those factors is obesity and its cardiometabolic consequences, which, as noted above, typically lag obesity exposure (Mensah et al., 2017; Olshansky et al., 2005). Preston, Vierboom, and Stokes (2018) estimate that rising levels of BMI during 1988–2011 reduced life expectancy at age 40 by .9 years in 2011 and have reduced the impact of many beneficial factors working to improve mortality, such as declining smoking rates and medical advances that include pharmacological treatments for several obesity-related chronic conditions, such as hypertension, hyperglycemia, and dyslipidemia. Indeed, the cardiometabolic consequences of the obesity epidemic were beginning to emerge in data in 2009 showing an increase in the prevalence of high blood pressure and cholesterol, a decrease in physical activity, and an increase in BMI and high blood glucose (Mannsverk et al., 2016; McEwen et al., 2011; Pilkerton et al., 2015). Thus, the slowdown in improvements in mortality, particularly CVD mortality, in the past decade may be due to the lagged cardiometabolic consequences of the obesity epidemic, now under way for more than 30 years.

FIGURE 9-12

Death rates for cardiovascular disease (CVD) in the United States and selected peer countries, 1999–2017. NOTES: Age-standardized death rates (per 100,000 person-years) for CVD from 1999 to 2017. Gray shaded lines are trends for individual U.S. (more...)

Another factor unique to the U.S. context that may explain the diminishing returns of medical advances in reducing CVD mortality is the persistent racial, ethnic, and socioeconomic disparities in chronic health conditions and control of chronic conditions related to cardiometabolic mortality that slow continued gains once those most at risk or those with greater health care access are treated. When new pharmaceuticals and other therapeutic treatments to control hypertension and heart disease were developed, delivery of these treatments was naturally targeted to those with the highest levels of disease (e.g., the highest levels of cholesterol or blood pressure), sharply reducing CVD mortality in the 1970s and 1980s (Weisfeldt and Zieman, 2007). Treating those with more moderate or mild cardiometabolic conditions, by contrast, results in marginal gains in improvement of CVD mortality, so that progress slowed after 2000.

In addition, many individuals may not be receiving or correctly using medications that are effective in controlling hypertension, diabetes, and heart disease, and many may be struggling to discontinue tobacco use. Research has shown that poor adherence to treatment results from a variety of barriers, including those experienced by patients (Ho, Bryson, and Rumsfeld, 2009; Rashidi et al., 2020) and those introduced by the health care system (Banerjee et al., 2016). Baroletti and Dell’Orfano (2010) divide the barriers faced by patients into three categories: socioeconomic (e.g., lack of adequate health care coverage, unemployment, poverty, concerns about cost), communication related (e.g., inadequate instructions, language barriers, mental illness), and motivational (e,g., not appreciating the gravity of these conditions or benefits of treatment, fears and concerns, and cultural beliefs) (Baroletti and Dell’Orfano, 2010). Understanding the barriers faced by patients and designing solutions to overcome those barriers is thus a priority for the control of cardiometabolic mortality and chronic diseases more generally.

When cardiovascular treatments were first introduced and when the dangers of smoking were first recognized decades ago, individuals with greater access to care, higher education, and other socioeconomic advantages were more likely to receive care and to quit smoking (Hiscock et al., 2012; Kanjilal et al., 2006; Ma et al., 2005; Sterling et al., 2019; U.S. Department of Health and Human Services [HHS], 2011). Much of the progress in lowering CVD mortality in prior decades may reflect the widespread uptake of these interventions among these more advantaged population groups, but adults who faced greater barriers to care may have been left behind. People of color and those of lower socioeconomic status face greater barriers to adherence to treatment targets and have higher rates of tobacco use (Cokkinides et al., 2008; Kiefe et al., 2001). The field of implementation science (also known as translational and health services research) studies interventions to close this gap between recommended care and the care actually received by individuals, especially members of vulnerable groups (Bauer et al., 2015; University of Washington, n.d.). The magnitude of this gap first became apparent in 2003, when a classic study documented that U.S. adults received only 54.9 percent of recommended care (McGlynn et al., 2003).

That gap has persisted, especially among marginalized populations that have limited access to care and live in settings that make adherence difficult. For example, fewer than half of U.S. adults (44%) with hypertension have achieved optimal blood pressure control (Dorans et al., 2018), and slightly more than half (55%) who could benefit from lipid-lowering agents are currently taking that medicine (Mercado et al., 2015). Disparities in the prevalence of chronic diseases mirror disparities in control of those diseases. In 2015–2016, for example, Blacks had higher rates of hypertension (57.3%) but lower rates of blood pressure control (37.2%) relative to Whites (43.8% and 45.7%, respectively) (Dorans et al., 2018). Moreover, individuals with hypertension, hyperlipidemia (high cholesterol levels), and insulin resistance may be asymptomatic and escape detection. This is the case especially among younger adults, who get fewer regular medical checkups and have less access to screenings for disease at work or in other community settings (Zhang and Moran, 2017). National estimates show that three-quarters of young adults ages 24–32 with measured hypertension were unaware of their condition (e.g., had not received a medical diagnosis), and two-thirds with measured diabetes were similarly unaware (Nguyen et al., 2011, 2014).

It is well documented that both research to identify strategies for reducing these disparities in care and the evidence-based programs and policies that emerge from translational research have been less heavily funded relative to investments in new drugs and technologies (Dzau and Balatbat, 2019; Woolf, 2008). This imbalance is counterproductive with respect to reducing mortality. For example, improving adherence to older-generation treatments can save more lives than developing newer agents with incrementally greater efficacy (Woolf and Johnson, 2005). Thus, after years of declining CVD mortality due to the broad uptake of pharmacotherapy and smoking cessation among advantaged populations, the recent decline in the pace of progress may reflect the failure to invest adequately in closing the prevention and treatment gap among high-risk populations. If so, a resurgence in progress in lowering CVD mortality in the United States could be stimulated by more robust efforts to help these populations overcome socioeconomic and environmental barriers to receiving effective cardiovascular treatments and successfully discontinue tobacco use.

A closer look at tobacco use is illuminating. The reduction in U.S. smoking first occurred among men in the early 1950s and later among women beginning in the late 1970s, producing a substantial decrease in mortality for U.S. adults (Cutler, 2008; Wang and Preston, 2009). Following the U.S. Surgeon General’s Report on Smoking and Health (1964), cigarette smoking rates declined 67 percent, from 42.6 percent in 1965 to 13.7 percent in 2018 (American Lung Association, n.d.; Creamer et al., 2019). However, an array of new tobacco products, including e-cigarettes, has entered the market in the past decade, with 19.7 percent of U.S. adults reporting use of any tobacco product in 2018 (Creamer et al., 2019). That prevalence is even higher among males, adults less than 65 years old, non-Hispanic American Indians/Alaska Natives, those with a high school education or less, those with an annual household income of less than $35,000, and those with a disability or serious psychological distress (Creamer et al., 2019).

The educational disparities in the reduction of smoking are especially noteworthy. While smoking declined for all groups, greater progress occurred among adults with more education (Figure 9-13). Studies by Cutler, Meara, and Richards-Shubik (2011) and Montez and Zajacova (2013) show that reductions in smoking behavior have been greater among the highly educated than among the less educated. Over the period 1974–2016, the smoking rate declined by 76 percent among people with a college degree but by just 35 percent among those with only a high school degree. Yet despite this widening educational disparity in smoking, only a modest portion of the widening educational difference in U.S. adult mortality in recent decades is attributable to smoking because widening educational disparities in other trends (e.g., use of drugs) were more important contributors. Further research is needed to address the barriers to smoking cessation faced by populations that continue to smoke at higher rates, but whether interventions to overcome these barriers can refuel the decline in smoking and reductions in CVD mortality remains to be seen.

FIGURE 9-13

Trends in smoking by education among adults ages 20–74, 1974–2016. NOTES: The years shown in this figure are those for which data have been published. Data for 1992 and later are not strictly comparable with data for earlier years because (more...)

Social, Economic, and Cultural Change

Social, economic, and cultural shifts over the past 50 years have profoundly changed the family, work, and community environments of daily life in America, and the possibility that these shifts may have contributed to cardiometabolic morbidity and mortality cannot be dismissed. Changes in family structure and rising family instability over the past 50 years have been well documented (Cavanagh and Fomby, 2019; Cherlin, 2009). Since the 1970s, increases in divorce, cohabitation, and nonmarital childbearing have greatly altered the family contexts in which children are raised and the financial and social capital to which they have access (Bianchi, 2011; Casper and Bianchi, 2001; Cherlin, 2009; McLanahan and Sandefur, 1994; Sayer, Bianchi, and Robinson, 2004). During this period, families were affected by macroeconomic changes that included the loss of manufacturing jobs, which provided employment opportunities for many low-educated and unskilled males, and the growth of the service sector, which employed largely females and more highly educated individuals. Single mothers were now able to support a family on their own—albeit at much-reduced wages and earnings relative to a two-worker family—and the economic status of men, especially those with less education and fewer job skills, suffered (Oppenheimer, 2000, 2003). The rise in family instability, combined with additional economic distress caused by the Great Recession, permeated entire family systems and disrupted the family-based safety net on which many working-age adults once relied. Communities hardest hit by the decline in manufacturing—especially in the textile, mining, and steel industries—experienced widespread unemployment, economic insecurity, diminished access to health care, and increasing individual- and familial-level stress. Recent cohorts of middle- and working-class young adults now face the realization that they will not live a better life than their parents, as the American Dream of intergenerational mobility has drastically declined (Cherlin, 2014; Chetty et al., 2017).

These shifts coincided with other social and cultural changes in American life. Jobs now required increasing educational credentials, resulting in rapidly increasing college enrollments but also burdening many young people, especially those lacking a 4-year degree, with college debt that caused both their finances and their careers to suffer (Velez and Woo, 2017; Wei and Horn, 2013). The digital era ushered in new lifestyles featuring ubiquitous, multiplatform, and uninterrupted access to online, electronic, and digitally streamed information and introduced new forms of social interaction and network formation (IOM and NRC, 2015). Individuals without the skills to access these forms of communication remained isolated from job opportunities and social interaction. Almost all forms of daily activity at work, at home, and in social groups were being accomplished at a faster pace than in prior generations (Tapscott, 2008; Vogels, 2019). The speed and volume of information in daily life created new stresses for those managing work, home, and family responsibilities and new forms of trauma related to body image, bullying, and other adverse experiences (McEwen and McEwen, 2017).

These daily, gradual, and long-term influences from the social and physical environments have contributed to cardiometabolic morbidity and mortality risks through multiple pathways, including the influence of financial hardships on health care access and affordability and on adverse living and work conditions that affect endocrine and cardiovascular diseases (Lian, 2018; Steptoe and Kivimäki, 2013). For example, job loss means loss of health insurance, and financial strains put out-of-pocket costs for health care (and other household needs, such as housing, food, and transportation) out of reach. Individuals with chronic conditions and comorbidities cannot afford prescription medications, blood glucose testing, or doctor’s appointments, and economic pressures force many families to resort to consuming inexpensive, calorie-dense foods; to live in unhealthy housing and neighborhoods; and to work in jobs that discourage physical activity. Job loss, family breakdowns, and economically depressed neighborhoods increase social isolation and erode social supports that are vital to health and longevity (House, Landis, and Umberson, 1988; Yang et al., 2016).

These cascading and multiplicative social, economic, and cultural changes have led to increasing levels of chronic stress with known adverse effects on cardiometabolic health. For example, adults who experience social isolation and workplace stress have a 1.5-fold and 1.3-fold increased risk, respectively, of CHD (Steptoe and Kivimäki, 2013). Numerous studies with rigorous repeated cross-sectional or longitudinal designs have found that chronic exposure to low socioeconomic status is associated with increased risk of the metabolic syndrome (Elovainio et al., 2011; Loucks et al., 2007; Manuck et al., 2010; Ramsay et al., 2008). Analyses of other stressors, including loneliness (Whisman, 2010), marital stress (in women but not men) (Whisman, Uebelacker, and Settles, 2010), and workplace stress (Chandola, Brunner, and Marmot, 2006), have found a longitudinal association with the onset of the metabolic syndrome, even after controlling for socioeconomic status. Chronic stress and psychological distress are also associated with the components of the metabolic syndrome, such as higher waist circumference (central obesity); high BMI (general obesity); and dyslipidemia, indicated by higher triglycerides and lower HDL cholesterol (Chandola et al., 2008; Kivimäki et al., 2009). Several meta-analyses likewise have found an association between stress and obesity (Nyberg et al., 2012; Wardle et al., 2011).

The increasing daily stresses that characterize contemporary society are felt more intensely among certain population groups. Racial/ethnic discrimination, lack of educational opportunities and economic advancement, and incarceration are the norm rather than the exception for some of the nation’s most vulnerable groups. Additional stresses associated with social and economic inequality and exposure to structural racism and microaggression have been widely documented and are associated with higher rates of cardiometabolic disease and other adverse health outcomes (Chetty et al., 2020; Gee and Ford, 2011; Link and Phelan, 1995; Phelan and Link, 2015; Williams, 1999; Williams, Lawrence, and Davis, 2019). The stresses associated with the increased pace of daily life may be especially acute for younger adults who came of age in the digital era but lack financial or career stability (IOM and NRC, 2015). As discussed earlier, two decades of research has documented that exposure to adverse childhood experiences, including poverty, leaves a lifelong imprint on the brain and body and undermines long-term health, increasing the incidence of substance abuse, heart disease, diabetes, and poor health behaviors (Flaherty et al., 2013; McEwen and McEwen, 2017; Su et al., 2015).

Chronic stress can cause both biological and behavioral responses that affect health. Repeated activation of the stress response system keeps levels of stress hormones elevated, which in turn increases levels of blood glucose, inhibits insulin production to prevent glucose from being stored, increases glucose intolerance, contributes to the buildup of fat tissue and weight gain, increases pulse rate and blood pressure, and damages blood vessels and arteries (Lupien et al., 2006; McEwen and Lasley, 2002; Seeman et al., 1997). Stress may also induce unhealthy coping behaviors, such as smoking, alcohol and drug abuse, and unhealthy eating habits that may affect cardiometabolic risks and help explain observed mortality trends (Geronimus et al., 2010; Jackson, Knight, and Rafferty, 2010). For example, the stress hormone cortisol triggers cravings for high-fat, sugary, and salty foods (Chao et al., 2017; Tryon et al., 2013), and the extra calories consumed as a result are converted to fat deposits that increase the risk of heart disease, diabetes, high blood pressure, and stroke.

Chronic stress can bring on feelings of despair and hopelessness. When individuals lack hope for their future and feel that they have nothing to lose, they may engage in unhealthy and risky behaviors because they are apathetic about their health or the risk of premature death (Gaydosh et al., 2019; Goldman, Glei, and Weinstein, 2018; Harris, Duncan, and Boisjoly, 2002). To the extent that despair and hopelessness are associated with chronic stress, an increase in those feelings may also play a role in increasing rates of obesity, hypertension, stroke, and diabetes, although as detailed in Chapter 7, the evidence that rates of despair have increased or are responsible for the increase in working-age mortality is inconclusive.

Substantial research has documented these profound shifts in U.S. social and economic conditions since the 1970s (Cherlin, 2014; McLanahan and Sandefur, 1994; Wilson, 1987) and accompanying cultural changes in American work and home lives in the digital era, but the ways in which such macro-level long-term changes affect cardiometabolic mortality are difficult to ascertain. Research is only beginning to illuminate how daily adverse environmental exposures that chronically activate the brain’s stress management system can lead to dysregulation of individual and multiple body systems, including the immune, metabolic, and cardiovascular systems, involved in predisease pathways (Hertzman and Boyce, 2010; McEwen and Lasley, 2002; NRC, 2001). Whether such long-term shifts that have occurred over decades and are codependent and synergistic can lead to population-level changes in cardiometabolic mortality is unknown, and the research tools in the form of data, study design, and methodology with which to address this broad and important question are not yet available. There is more evidence, however, for how certain population groups are more vulnerable to adverse social and economic changes and the associated biological consequences of chronic stressors, and this avenue of research may be more fruitful in policy and programmatic efforts to reduce such disparities and thereby achieve health equity within American society.