Summary¹

The past century has witnessed remarkable advances in life expectancy in the United States and throughout the world. In 2010, however, progress in life expectancy in the United States began to stall, despite continuing to increase in other high-income countries. Alarmingly, U.S. life expectancy fell between 2014 and 2015 and continued to decline through 2017, the longest sustained decline in life expectancy in a century (since the influenza pandemic of 1918–1919). The recent decline in U.S. life expectancy appears to have been the product of two trends: (1) an increase in mortality among middle-age and younger adults, defined as those ages 25–64 years (i.e., “working age”), which began in the 1990s for several specific causes of death (e.g., drug- and alcohol-related causes and suicide); and (2) a slowing of declines in working-age mortality due to other causes of death (mainly cardiovascular diseases) after 2010.

STUDY PURPOSE, APPROACH, AND SCOPE

Explaining why mortality has been rising among working-age adults is not straightforward. Mortality is the final result of both acute events and cumulative, long-term processes involving the interaction of social, behavioral, economic, environmental, and biological factors that develop and unfold over the life course. Establishing the complex relationships among these explanatory factors poses methodological challenges that are

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¹ This summary does not include reference citations. Citations supporting the content herein are provided in the body of the report.

complicated by issues of data availability and quality, as well as measurement. Studies in the early 2010s indicated that midlife mortality was rising primarily among middle-age non-Hispanic White (White) adults, particularly women, those with a high school degree or less, and those living in rural areas. More recent research, however, has documented this trend among most racial/ethnic groups and in most areas of the country. In some ways, these trends have exacerbated long-standing mortality divides, such as disparities between those of high and low socioeconomic status and metropolitan versus nonmetropolitan populations. These mortality disparities are important in their own right, signaling the effects of deepening inequality across many facets of American life, but they also help elucidate the underlying processes that have generated the recent increases in working-age mortality.

A full understanding of the rise in working-age mortality requires focusing beyond the factors that are most proximate to specific causes of death (e.g., behavior, psychological factors, health care utilization). One must also look upstream to the macrostructural factors (e.g., public policies, macroeconomic trends, social and economic inequality, technology) that may affect the health of Americans in multiple ways and through multiple pathways that flow through local community contexts and intersect with individuals’ lives. To that end, the National Institute on Aging and the Robert Wood Johnson Foundation asked the National Academies of Sciences, Engineering, and Medicine to conduct a consensus study to identify the key drivers of increasing midlife mortality and concomitant widening social differentials; elucidate modifiable risk factors that could alleviate poor health in midlife, as well as widening health inequalities; identify key knowledge gaps and make recommendations for future research and data collection to fill those gaps; and explore potential policy implications. In response, the National Academies convened the Committee on High and Rising Midlife Mortality Rates and Socioeconomic Disparities in 2019 to carry out this work.

The committee’s first task was to review what is known about trends in working-age mortality in order to establish the contributions of specific causes of death to overall changes in mortality over time, and about disparities in mortality rates by age, sex, race and ethnicity, socioeconomic status, and geography. This review revealed wide variations across studies in the tabulation and presentation of causes of death, as well as in the age and racial/ethnic groups and time periods included in the analyses, which made differences across studies difficult to interpret. Comparisons across studies were also complicated by methodological differences, such as whether mortality rates were adjusted to account for changes in the age distribution of the population over time. To supplement this literature review and obtain a comprehensive and consistent understanding of mortality trends and

disparities, the committee performed its own independent analyses of working-age mortality over the 1990–2017 period based on restricted-access National Vital Statistics death certificate data files. These analyses examined overall trends in mortality and disparities in those trends by age group, sex, race and ethnicity, and geography (metro status, states).

Although the committee also recognized the need to stratify data by socioeconomic status, the data required to do so were found to be lacking. The committee had concerns about the quality of data on educational attainment in vital statistics records and the total absence of data on income in death certificate records. Accordingly, the committee did not examine disparities in working-age mortality by socioeconomic status in its analyses, but instead relied on a thorough review of previous research on mortality differentials by education and income.

TRENDS IN WORKING-AGE MORTALITY

Although recently identified, increasing mortality among U.S. working-age adults is not new. The committee’s analyses confirmed that a long-term trend of stagnation and reversal of declining mortality rates that initially was limited to younger White women and men (ages 25–44) living outside of large central metropolitan areas (seen in women in the 1990s and men in the 2000s) subsequently spread to encompass most racial/ethnic groups and most geographic areas of the country. As a result, by the most recent period of the committee’s analysis (2012–2017), mortality rates were either flat or increasing among most working-age populations. Although this increase began among Whites, Blacks consistently experienced much higher mortality. These long-standing racial disparities are discussed in greater detail below. Over the 1990–2017 period, disparities in mortality between large central metropolitan and less-populated areas widened (to the detriment of the latter), and geographic disparities became more pronounced. Mortality rates increased across several regions and states, particularly among younger working-age adults, and most glaringly in central Appalachia, New England, the central United States, and parts of the Southwest and Mountain West. Mortality increases among working-age (particularly younger) women were more widespread across the country, while increases among men were more geographically concentrated.

Regarding socioeconomic status, the committee’s literature review revealed that a large number of studies using different data sources, measures of socioeconomic status, and analytic methods have convincingly documented a substantial widening of disparities in mortality by socioeconomic status among U.S. working-age Whites, particularly women, since the 1990s. Although fewer studies have examined socioeconomic disparities in working-age mortality among non-White populations, those that have

done so show a stable but persistent gap in mortality among Black adults that favors those of higher socioeconomic status.

As noted earlier, the recent increase in all-cause mortality among U.S. working-age adults is due to both rising mortality from several causes of death and slowing progress in lowering mortality from other leading causes of death. The committee identified three categories of causes of death that were the predominant drivers of trends in working-age mortality over the period: (1) drug poisoning and alcohol-induced causes, a category that also includes mortality due to mental and behavioral disorders, most of which are drug- or alcohol-related; (2) suicide; and (3) cardiometabolic diseases. The first two of these categories comprise causes of death for which mortality increased, while the third encompasses some conditions (e.g., hypertensive disease) for which mortality increased and others (e.g., ischemic heart disease) for which the pace of declining mortality slowed. This report examines most closely the explanations for mortality trends in these three categories of causes of death to identify the key drivers of and modifiable factors in the recent overall rise in working-age mortality.

Other causes of death also contributed to increasing mortality during the 1990–2017 period, although few of these causes made meaningful individual contributions to the alarming mortality increases seen since 2010. Taken together, however, their combined impact was not trivial and therefore should not be ignored, and potential explanations for these increases are addressed briefly in this report. Four of these causes in particular—liver cancer, nervous system diseases, homicides, and transport injuries—merit further attention because their contributions to rising mortality were not negligible. Although the committee of necessity focused its attention on the major drivers of increasing working-age mortality—drugs, alcohol, suicides, and cardiometabolic diseases—it encourages the research community to seek explanations for increases in working-age mortality due to other causes of death identified in this report. Of particular importance is identifying factors contributing to the large and persistent racial/ethnic disparities in working-age mortality trends, such as the rise in homicides and transport injuries among Black and Hispanic men or the delayed reductions in mortality from HIV/AIDS among older Blacks.

Drug- and Alcohol-Related Deaths

Collectively, drugs and alcohol were responsible for more than 1.3 million deaths—approximately 8 percent—among the working-age (ages 25–64 years) population between 1990 and 2017. These substance-related deaths were major contributors to the rise in working-age mortality, and they are not abating. Drug poisoning deaths have been rising for more than three decades and represent the single largest contributor to the rise

in mortality rates among U.S. working-age adults (except among older Hispanic adults ages 45–64). While drug-related mortality rates increased in every U.S. state over the study period, the increases were most pronounced in Appalachia, New England, and the industrial Midwest. The largest increases occurred among Whites (particularly men) and older Black men. Among working-age Whites, increases in mortality due to drug poisoning were largest among younger men (ages 25–44), those with a high school degree or less, and those living in large metropolitan areas. In contrast, among working-age Blacks, mortality increased most among older men (ages 55–64) in large central metropolitan areas. While the committee’s review of the literature showed that there was no difference in drug poisoning mortality by educational attainment among Blacks, increasing mortality due to drug poisoning among lower-educated individuals was responsible for most of the growing mortality gap by educational attainment among working-age Whites. The rate of alcohol-induced deaths also increased among Whites during the entire study period, and although the rate of such deaths declined among Blacks and Hispanics throughout the 1990s and early 2000s, that trend ceased in the late 2000s, and alcohol-induced deaths increased in these populations in the 2010s.

The rise in drug poisoning deaths is well studied, and research has yielded several plausible explanations for the trend. Although explanations for rising alcohol-related mortality have been less thoroughly investigated, similar supply-and-demand factors underlie both sets of trends. Sparked by the introduction of OxyContin^® in 1996, the country’s drug overdose crisis represents a “perfect storm” resulting from the flooding of the market with highly addictive yet deadly prescription and illicit drugs and the underlying and growing demand for and vulnerability to substances that might possibly bring relief, albeit temporary, from physical and/or mental pain.

On the supply side, weak governmental oversight combined with actions in the 1990s and 2000s by the pharmaceutical industry (manufacturers, distributors, pharmacies), pain control advocacy groups (often funded by pharmaceutical companies), and physicians to fuel a massive increase in opioid prescribing, which was followed by a rise in prescription opioid misuse, addiction, and overdose. While opioid-based pain relievers have an appropriate role in treating pain among those suffering from cancer, pharmaceutical companies expanded production and marketing of these drugs throughout the 1990s and 2000s for large populations with noncancer pain and made misleading claims about the drugs’ safety and lack of addictiveness. With encouragement from pain control advocacy groups and pharmaceutical companies, physicians and other health care providers significantly increased their opioid prescribing.

Collectively, these forces resulted in saturation of the United States with 76 billion opioid pills just between 2006 and 2012; no other country

approached this level of opioid prescribing. Throughout the 2000s, as policy makers, state health officials, and physicians began to recognize the dangers of opioids and prescribing of the drugs subsequently declined, prescription opioids became less available and grew more expensive. This transition created a “thick market” for heroin, lowering its price and introducing it to a new clientele. Thus emerged a second wave of the opioid crisis, in which the consolidation of the heroin supply chain in Mexico and the much more widespread availability of heroin in the United States led to an increase in heroin overdose deaths. The third wave of the crisis began in the early 2010s, when drug suppliers and dealers began mixing heroin and other drugs (e.g., cocaine) with fentanyl and fentanyl derivatives that were inexpensive but extremely potent opioids with high overdose risk. Fentanyl deaths surpassed those involving heroin in August 2016 and continued to climb even as overall overdose mortality began to level off.

Demand-related explanations for the three-decade surge in drug overdose deaths focus on why certain subpopulations and geographic areas may have been more vulnerable than others to the increased availability of opioids and other drugs. Physical pain may have been one such contributor. Millions of Americans experience chronic pain, and some evidence suggests that the prevalence of physical pain may have increased in recent decades. Although, as noted earlier, adults with non-cancer-related pain were infrequently prescribed opioids before the mid-1990s, high and possibly increasing levels of physical pain may over time have expanded demand for OxyContin and similar products that flooded the market after 1996.

Mental illnesses and substance use disorders are closely intertwined, as are adverse childhood experiences and adult substance use. However, ongoing population surveys addressing adult mental illness and existing research on temporal trends in the prevalence of adverse childhood experiences provide insufficient evidence regarding their potential contribution to the increase in drug overdoses.

“Despair” has been among the more controversial potential explanations for the rise in substance-related deaths. Despair signifies hopelessness, which is a feature of depression and other affective disorders but is not itself a formal mental health diagnosis. The notion that the past 30-year rise in working-age mortality is partly due to increasing psychological distress among working-age adults with lower education is appealing because it accords with long-term economic, family, and social changes that have increased disconnection from the people, activities, and institutions that provide support and give people purpose and meaning. While the committee could find no causal studies on the effects of changing psychological health on U.S. substance use and mortality trends, there is ample empirical support for the hypothesis that psychological health has been worsening among U.S.

working-age adults and that proxies for despair (e.g., hopelessness, sadness, worry) are connected to substance use. Ultimately, measuring despair and determining causality remain key challenges for understanding the true role of despair in contemporary mortality trends. Qualitative research, which provides compelling evidence for the role of increasing despair in substance use and overdose, can offer insights for demographers, economists, and epidemiologists who seek to develop and test strong measures of despair.

Protracted long-term structural changes in and stressors to the U.S. economy, along with acute “shocks” (e.g., the Great Recession of 2007), have had differential effects on population subgroups and geographic areas. These long-term macroeconomic trends may partly explain the geographic patterns observed in drug poisoning mortality, such as the disproportionate impact in rural areas and the industrial Midwest, which have suffered losses in manufacturing and mining jobs. The distribution of industry and occupations is uneven across the country: macro-level economic trends and policy changes have brought prosperity to some places (e.g., high-tech and finance-dominant urban hubs) and decimation to others (e.g., Appalachia, the Rust Belt). The decline and transformation of industries that once provided “good” jobs for adults with only a high school education have eroded the social fabric and economic vitality of communities that once depended on those industries. The decline in opportunities among adults with less than a college education has been especially devastating and may have contributed to the rise in drug poisoning and alcohol-related deaths in this population.

The relationship between economic conditions and mortality, however, is complex, and the evidence is mixed on the causal effect of relatively short-term economic changes on substance-related mortality. Quasi-experimental studies suggest that mortality rates increase in response to specific economic forces—such as job loss, plant closings, and disruption from foreign trade—but there is less evidence about broader economic forces, such as technological advances that replace workers and general economic trends related to productivity. Other studies have found that opioid supply availability has a larger effect on drug-related mortality relative to changes in specific economic factors. The best interpretation of current knowledge about the broader relationship between economic well-being and mortality suggests that economic hardship is associated with higher mortality, especially in the context of widespread availability of potent and life-threatening medications. However, the overall impact of the direct economic shocks that have been examined (i.e., short-term changes in economic circumstances) appears to be modest.

Suicide

Suicide was among the 10 leading causes of death at ages 25–64 in 2015–2017 when life expectancy was declining, and it accounted for 569,099 deaths in the working-age population during the 1990–2017 study period. Historically, suicide mortality has been substantially higher among men than women and among Whites than Blacks and Hispanics. The same was true between 1990 and 2017, when significant increases in suicide rates occurred mainly for Whites, and White men in particular. At the beginning of the period, suicide rates differed little by metropolitan status among White adults, but over time, the rates increased more slowly in large central metropolitan areas than in less-populated areas, widening an urban–rural gap in suicide mortality. In line with this differential, suicide rates are higher in Western states, especially those with large rural populations.

Potential causes of rising suicide rates among Whites are complex, involving multiple factors that operate independently and interactively across societal, community, and individual levels. Unfortunately, a paucity of research examines differences by race and ethnicity, estimates causal impacts, or attempts to explain change in suicide mortality. As a result, understanding of why suicide rates have increased among working-age Whites during this period is mainly inferential.

Research on suicide trends tends to focus on explanations in four general areas: economic factors; social engagement, religious participation, and social support; access to lethal means; and mental and physical health. Some of the stronger evidence is related to the role of economic conditions. Periods of economic downturn, wage stagnation, weak safety nets, and increasing foreclosure rates are associated with rising suicide mortality in national and state-level studies. In addition, deteriorating economic conditions among those without a college degree may be an important factor explaining rising suicide mortality among Whites, especially White men. There is evidence that social support from embeddedness in formal institutions (e.g., church, school), community organizations, or stable interpersonal relationships that buffer the risks of self-harm has declined in recent decades, and that this decline has been more prominent among lower-educated Whites.

Although access to lethal means of suicide is associated with suicide, changes in access do not appear to provide an explanation for rising suicide mortality among Whites. Suicide mortality by firearms rose over the period 1990–2017, but its contribution to the rise in overall suicide mortality declined as suicides by other means increased more rapidly. While there is evidence that firearm-related suicide rates are higher in states with looser gun regulations and greater gun ownership and are higher in

nonmetropolitan than in large metropolitan areas, the proportion of all suicide deaths related to firearms declined from 1990 to 2017.

Important predisposing factors related to suicide mortality are life-course traumas and stressors, especially those that occur early in life, such as adverse childhood experiences, and mental illness. Not surprisingly, those with a history of mental illness have a much higher risk of suicide, and Whites tend to report more history with mental illness relative to other racial/ethnic groups. Comorbidities related to physical illnesses, disabilities, and drug and alcohol use also contribute to levels of mental illness and pain, all of which increase the risk of suicide.

Cardiometabolic Diseases

Deaths due to cardiometabolic diseases encompass the following cause-of-death categories: endocrine, nutritional, and metabolic (ENM) diseases (e.g., thyroid conditions, diabetes, hyperlipidemia, obesity); hypertensive heart disease (e.g., heart disease caused by prolonged exposure to high blood pressure); and ischemic heart disease and other diseases of the circulatory system (e.g., reduced blood supply to the heart, including atherosclerosis and coronary heart disease, stroke, and other cardiovascular conditions). Collectively, cardiometabolic diseases were responsible for more than 4.8 million deaths among the U.S. working-age (25–64 years) population between 1990 and 2017. ENM diseases accounted for 703,247 deaths, hypertensive heart disease for 360,309 deaths, and ischemic heart disease and other diseases of the circulatory system for the largest share of 3,782,186 deaths.

The contribution of cardiometabolic mortality to the recent rise in working-age mortality is complex and involves several countervailing trends. Death rates due to ENM diseases and hypertensive heart disease generally increased during 1990–2017, especially starting in 2010, and while there have been significant long-term reductions in mortality from ischemic heart disease and other diseases of the circulatory system, much of that progress appears to have stalled since 2010. The combination of these trends operated to increase all-cause mortality after 2010 because the slowdown in mortality declines from ischemic heart disease and other circulatory diseases no longer offset the rise in mortality from ENM diseases and hypertensive heart disease.

Within the working-age population, certain subgroups experienced greater relative increases in mortality due to ENM diseases and hypertensive heart disease over the study period and slower declines in mortality from ischemic heart disease and other circulatory diseases starting in 2010. These subgroups include younger adults (ages 25–44) of all racial/ethnic groups, White men and women, Black men (in the recent decade), and

those living in rural areas. These troubling changes in cardiometabolic mortality were most pronounced in the South and outside of large central metropolitan areas. Large central metropolitan areas and the Northeast generally experienced the most favorable trends in cardiometabolic disease mortality. As a result, the gap in mortality by metropolitan status grew over time, particularly among White working-age adults.

The literature provides three potential explanations for the trends in cardiometabolic mortality: the obesity epidemic; diminishing returns of medical advances; and social, economic, and cultural changes. The increased prevalence of obesity and its lagged cardiometabolic consequences are the most important. Substantial evidence shows that obesity increases the risks of hypertension, stroke, coronary heart disease, and diabetes, driving up death rates due to ENM diseases and hypertensive heart disease and slowing declines in mortality due to ischemic heart disease and other circulatory diseases. Obesity rates began to rise in the early 1980s and remain high today as a period-based phenomenon that has affected children and adults of all ages. But its cardiometabolic consequences have occurred in a cohort fashion. More recent cohorts—those born in the 1970s, 1980s, and 1990s—have been exposed for their entire lives to “obesogenic environments,” defined as the conditions in which people live that encourage sedentary lifestyles and unhealthy diets and discourage or prevent people from adopting and maintaining healthier behaviors. These cohorts have been more affected by the obesity phenomenon because of their earlier life exposure and longer durations at risk relative to prior cohorts.

While the proximate causes of obesity involve health behaviors (diet, physical activity) that produce an imbalance between calories consumed and expended, obesogenic environments are a contributing factor. Substantial evidence documents how physical environments have become increasingly obesogenic—from urban landscapes more conducive to automobiles than pedestrians to the proliferation of fast food restaurants that encourage the consumption of inexpensive, calorie-dense foods. However, further research is needed to disentangle the complex pathways by which changing environments have led to the rise in the prevalence of obesity that, in turn, has fueled the changing trends in cardiometabolic mortality.

Medical advances in drug development and prevention, treatment, and control of chronic diseases, together with major reductions in tobacco use, played a large role in producing the long-term decline in mortality due to ischemic heart disease and other circulatory diseases that took place from 1970 to 2010. Progress may have stalled after 2010 because medical advances reached a point of diminishing returns. Medical advances also may be having less impact because their benefits are being offset by the lagged cardiometabolic consequences of rising obesity that are now affecting rates of diabetes, hypertension, and cardiovascular disease and because

many people who would benefit from cardiovascular treatments, especially those at greatest risk, face barriers to accessing services and adhering to treatment.

The social, economic, and cultural changes that have occurred over the past 50 years represent a natural progression that all advanced societies around the world have experienced. Those changes have increased the pace and efficiency of work and social interactions, but have also necessitated greater education, training, and technological skills to keep up with the faster pace of life, workplace demands, and dwindling opportunities for social mobility. Especially in the United States, these shifts have marginalized those without the necessary education and job skills, limiting not only their socioeconomic status and ability to live in healthy environments but also their access to health care, thereby increasing the daily stresses of life. Chronic stress can itself take a biological and emotional toll, disrupting and damaging endocrine, metabolic, and cardiovascular systems and increasing mortality risks. Yet while research has established links between chronic stress and cardiovascular disease, direct evidence that long-term social, economic, and cultural changes played a causal role in recent changes in cardiometabolic mortality is lacking.

RACIAL/ETHNIC, SOCIOECONOMIC, AND GEOGRAPHIC DISPARITIES

The committee’s analysis and review of research revealed large, and in some cases widening, racial/ethnic, socioeconomic, and geographic disparities in working-age mortality. While the explanations for these disparities are often specific to certain causes of death, the committee identified common underlying themes that affected population subgroups at different time periods or in different contexts.

The first of these themes is the role of adverse economic trends (e.g., stagnant wages, collapse of job sectors, unemployment) that affected certain geographic areas and population subgroups more so than others. The loss of manufacturing and mining jobs in the industrial Midwest and Appalachia in the 1970s led to a long-term economic decline, often concentrated among the largely White families and communities in these areas. Declining economic conditions tend to weaken societal institutions, community resources, family bonds, social networks, and access to health care—all of which could help explain disparities in working-age mortality according to race and ethnicity, socioeconomic status, and geography.

A second theme is socioeconomic inequality, which could help explain the pace and timing of rising 21st century working-age mortality, as well as the long-standing racial/ethnic disparities in mortality that have persisted throughout U.S. history. Unequal access to societal opportunities and

resources to climb the social ladder create gradients in health and explain mortality disparities both across and within social groups, including racial/ethnic disparities. As a result of the legacy and persistence of structural racism in the United States, Blacks and other minority groups have experienced long-standing socioeconomic inequalities that have compromised their health and produced much higher mortality rates in these groups relative to Whites, a pattern borne out in the data reviewed by the committee. Nonetheless, with the growing importance of education within U.S. society and the need for academic credentials to obtain well-paying technical and professional jobs, socioeconomic inequality has also deepened among Whites, widening socioeconomic disparities in White mortality.

A third theme that emerges in explaining the trends and disparities in working-age mortality is vulnerability, which mediates the degree to which adverse economic conditions and socioeconomic inequality make particular groups more susceptible than others to morbidity and mortality risks. As a result of educational, job, and housing discrimination, for example, Blacks tend to work and live in segregated and often disadvantaged neighborhoods, increasing their exposure to obesogenic, unsafe, and low-resource environments that limit access to medical and behavioral health services and increase mortality risks. Such vulnerability plays a prominent role in today’s drug overdose crisis, described earlier as a “perfect storm” in which the flooding of the market with highly addictive and deadly drugs occurred as the population was growing more vulnerable to emotional and physical pain, heightening demand for these products. Declining economic conditions, socioeconomic inequality, and vulnerability are themes that help in understanding how the different and changing social, economic, and geographic contexts of population subgroups may explain recent trends in working-age mortality.

IMPLICATIONS FOR RESEARCH AND POLICY

From a historical perspective, the rise in U.S. working-age mortality and recent resulting declines in life expectancy are relatively new phenomena. As this report documents, because the rise in working-age mortality was specific to certain causes of death but with varying patterns by age, sex, race and ethnicity, socioeconomic status, and geography, existing research into these complex and multilayered patterns is sparse, and research attempting to better understand the explanations for these changing patterns is nascent. Much remains to be learned, therefore, and the committee proposes numerous research efforts to generate better evidence that can serve as a basis for evaluating and refining salient policies. These recommendations span multiple levels and modes of analysis (individual, institutional, societal, and cross-national; quantitative and qualitative); address a variety of disparities

(socioeconomic, racial/ethnic, geographic); encompass a range of causes of death and related factors (drug poisoning; alcohol-related deaths; suicide; cardiometabolic diseases; mental illness; obesity; adverse childhood experiences; psychosocial indicators, such as stress, despair, hopelessness, coping, and resilience; long-term economic changes; social factors, such as family structure, community support, and religiosity); and propose numerous improvements to the data infrastructure that supports this research.

The committee also grappled with how the evidence detailed in this report suggests the need for policy changes with the potential to curb the increase and/or narrow disparities in rates of working-age mortality in the coming years. The committee stresses the immense challenge of predicting policy impacts in this area of science. Studies of mortality trends and patterns, especially at the national level, rely almost exclusively on observational data and federal statistics. As a result, causal evidence in this area is limited, and controlled experiments are difficult if not infeasible. Moreover, as discussed throughout the report, the key hypothesized influences on patterns and trends in working-age mortality are numerous and operate concomitantly at multiple levels. Many of the proposed drivers operate across the life course and/or across decades—in either period or cohort fashion—to influence current patterns and trends. This report therefore focuses on an exceptionally complex set of patterns, trends, and explanations for which clear or simple solutions are lacking.

Nonetheless, despite this complexity and the necessary reliance on observational and administrative data, the committee emphasizes the urgency of policy action in the face of a population health crisis that is claiming the lives of people in the prime of their lives (a crisis that has been exacerbated by the COVID-19 pandemic). Like the phenomena driving the crisis, policy responses need to be multilevel, focusing not only on the immediate causes of these deaths, such as drugs and obesity, but also on the upstream “causes of the causes,” such as living conditions that increase the vulnerability of communities, families, and individuals to premature mortality. The committee accordingly offers policy recommendations regarding obesity prevention programs, interventions to target the substance use and overdose crisis at multiple levels on both the supply and demand sides, and the expansion of Medicaid under the Affordable Care Act. The committee also presents broader policy conclusions regarding the need to balance the rights of the food industry, advertisers, grocers, and restaurants to enjoy free market competition against the public health imperative to limit the promotion and consumption of foods and beverages that contribute to obesity; the need to revitalize the communities hit hardest by the overdose crisis by addressing the larger economic and social strains and dislocations that made those communities vulnerable in the first place; and the importance of dismantling structural racism and discriminatory policies of exclusion so as

to reduce and ultimately eliminate inequalities that continue to drive racial/ethnic disparities in health and mortality in the United States.

The United States is losing far too many lives far too early. While it is clear that the research base for understanding the nature of this complex problem needs to be strengthened, the rise in working-age mortality threatens the future of the nation’s families, workforce, economy, and national security. It therefore constitutes a crisis that requires action even if the evidence is imperfect or only suggestive of causal effects and solutions. In taking this action, it will be essential to remain cognizant of the potential for unintended consequences—even for policies that are well intended and carefully designed to account for potential risks—and thus to continue to monitor outcomes, generate better evidence, and adjust policies over time.