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3
Framing the Question
T
he chapters that follow in this part of the report (Chapters 4-8)
present a systematic examination of potential explanations for the
pervasive U.S. health disadvantages documented in Part I. A number
of factors distinguish the United States from other countries, but their con-
tribution to the nation’s health is unclear. For example, the United States
has a very large economy and a large geographic footprint. At 3.7 million
square miles, its land mass is much larger than any other high-income coun-
try but Canada (United Nations, 2012b) and it encompasses large rural
expanses, although comparable cross-national data on the urban-rural mix
are limited.1 The United States is also a much younger nation than most
1
According to the OECD, fully 78 percent of the U.S. land mass is “predominately rural”
(defined as more than 50 percent of the population living with fewer than 150 inhabitants
per square kilometer). An even larger proportion of the land mass is predominately rural in
some other peer countries, including Austria (79 percent), Norway (84 percent), Australia
(85 percent), Sweden (90 percent), Finland (93 percent), and Canada (96 percent). Compared
with Americans, larger proportions of the populations of Austria, Sweden, Denmark, Finland,
and Norway live in predominately rural areas. Among 13 peer countries for which data were
available, the United States had the third lowest percentage (3.8 percent) of people living in
“remotely rural” areas, defined as having to drive more than 60 minutes to reach a locality
with more than 50,000 inhabitants (OECD, 2011d). These definitions differ from those com-
monly used in the United States to define rural areas, such as those developed by the U.S.
Office of Management and Budget and the U.S. Census Bureau, which themselves are not
entirely consistent (Aron, 2006).
95
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96 U.S. HEALTH IN INTERNATIONAL PERSPECTIVE
of its wealthy European counterparts. However, there is little empirical
evidence to link these distinctive conditions to adverse health outcomes.2
The panel recognized the need to identify and organize the leading
factors that could plausibly contribute to cross-national health differences,
which naturally led to the question of what factors affect health in the
first place. This chapter begins by examining the determinants of health
and then turns to two issues that helped us frame our approach in looking
for potential explanations for the U.S. health disadvantage: the need for a
social-ecological perspective that reflects both upstream and downstream
influences on health and the need for a life-course perspective that considers
influences over time. These concepts were instrumental in persuading the
panel to map out a systematic approach to examining the role of health sys-
tems (Chapter 4), individual behaviors (Chapter 5), social factors (Chapter
6), the environment (Chapter 7), and policies and social values (Chapter 8).
THE DETERMINANTS OF HEALTH
Attempting to explain the cause(s) of the U.S. health disadvantage leads
one to the question of what causes health and disease, a topic that social
epidemiologists and other social scientists have studied for decades. Some
factors are innate biological characteristics, such as age, sex, and genes, that
generally cannot be modified.3 Age and other standard sociodemographic
factors are highly predictive of health outcomes but, as documented in
Part I, the U.S. health disadvantage persists even after adjusting for these
factors.
Both the general public and policy makers often assume that health is
determined primarily by health care (Robert and Booske, 2011). Thus, it
is reasonable to wonder if the U.S. health disadvantage reflects a deficiency
in the U.S. health care system. For example, in contrast to many other
countries, a large proportion of the U.S. population is uninsured (National
Center for Health Statistics, 2012). But even if health care plays some role,
decades of research have documented that health is determined by far
more than health care. The seminal article by McGinnis and Foege (1993)
highlighted the important role of health behaviors. By some estimates,
approximately 40 percent of all deaths in the United States are associated
2
Subsequent parts of this report do discuss the role of rural conditions in the United States
in contributing to health disadvantages, such as access to medical care.
3
Although it is possible that differences in population gene pools or other innate biological
characteristics contribute to observed cross-national health differences, these and other non-
modifiable risk factors receive little emphasis in this report due to their unlikely contributory
role. However, Chapter 6 does address the important topic of gene-environment interactions
and the potential role of epigenetics as a causal pathway for social and environmental influ-
ences on health.
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FRAMING THE QUESTION 97
with four health behaviors: tobacco use, unhealthy diet, physical inactivity,
and problem drinking (Mokdad et al., 2004, 2005).
Yet health care and health-related behaviors are still not the whole
story and raise a bigger question: Why are adverse behaviors or deficiencies
in health care more common in the United States than in peer countries?
Analytic disciplines often draw from different theoretical traditions to
answer this question. For example, the behavioral sciences have developed
elegant theoretical frameworks for understanding the complex influences
on human behavior (Glanz et al., 2008), and economists have proposed
human capital models to explain the tradeoffs people make to optimize
their “health capital” (Galama and Kapteyn, 2011).
The fact remains that the U.S. health disadvantage is pervasive, cut-
ting across multiple population subgroups and diverse health outcomes
(as different as chronic diseases and injuries). This pervasiveness highlights
the need to look beyond individual behaviors and choices by examining
systemic processes that may influence multiple health outcomes through
various specific and often interrelated pathways. Two conceptual models
that are useful in framing these more distal, or upstream, health influences
are the social-ecological framework and a life-course framework.
THE SOCIAL-ECOLOGICAL FRAMEWORK
Extensive research documents the behavioral and biological conse-
quences of income, occupation, education, and social and physical envi-
ronments (see, e.g., Adler and Stewart, 2010; Braveman et al., 2011b;
Commission on the Social Determinants of Health, 2008; Kawachi et
al., 2010). In a knowledge economy, education is the main pathway for
economic security, and socioeconomic conditions influence the ability of
individuals and families to make healthier choices and to live in health-
ier neighborhoods. The environment influences one’s ability to engage
in healthy behaviors, receive health care, and protect oneself from direct
environmental threats. Enhanced recognition that “place matters” has per-
meated both research and public policy discourse (see California Newsreel,
2008). Television, advertising, and other media also influence health and
health-related behaviors, negatively or positively, for example, by promot-
ing (un)healthy foods and (un)safe sex (Center on the Developing Child
at Harvard University, 2010; Grier and Kumanyika, 2008; Harris et al.,
2009).
All the determinants of health noted above—health care, health behav-
iors, neighborhood conditions, education, and income—are shaped by both
public- and private-sector policies. Decisions made by government officials,
business leaders, voters, and other stakeholders affect access to health care,
the location of supermarkets, school lunch menus, crime rates, public trans-
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98 U.S. HEALTH IN INTERNATIONAL PERSPECTIVE
portation, toxic waste sites, employment opportunities, and the quality of
schools (Institute of Medicine, 2011d). Environmental factors and policies
can affect everyone in the population and can influence multiple disease
processes, thereby having consequences for multiple outcomes and offering
a potential explanation for the recurring patterns observed in Part I.
The multifactorial nature of social-ecological influences on health
has long been recognized (see Evans and Stoddart, 1990; Dahlgren and
Whitehead, 1991). Many diagrammatic representations of the social-
ecological model have appeared in reports of the Institute of Medicine (e.g.,
2003, 2011e), in the conceptual framework developed by the World Health
Organization (WHO) Commission on Social Determinants of Health, and
in a schematic for public outreach developed by the Robert Wood Johnson
Foundation Commission to Build a Healthier America (Braveman and
Egerter, 2008). Figure 3-1 shows one such model, which was adopted for
Healthy People 2020, the federal government’s national health objectives
(U.S. Department of Health and Human Services, 2012a). All such mod-
els show (with nesting concentric circles or boxes with multiple arrows)
connections between individuals, families, and communities, and the bio-
logical, physical, social, and economic environments that surround them.
They all emphasize the existence of proximate, or “downstream,” health
FIGURE 3-1 Model to achieve Healthy People 2020 overarching goals.
SOURCE: Secretary’s Advisory Committee on Health Promotion and Disease Pre-
FIG3-1.eps
vention Objectives for 2020 (2008, p. 7).
bitmap
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FRAMING THE QUESTION 99
influences (e.g., smoking) that are shaped by distal, or “upstream,” factors
(e.g., social norms regarding smoking, tobacco regulations). The models all
attempt to highlight societal policies, cultures, and values as the important
upstream context for conditions that promote, or undermine, good health
downstream.4
Adverse conditions may also affect some population groups more than
others,5 thereby contributing to health disparities among vulnerable groups
and, possibly, to the health disadvantage experienced in aggregate by the
U.S. population (Bleich et al., 2012). The panel focused on its charge to
examine and explain cross-national differences in health, not the causes of
health differences (or disparities) within countries. Yet we recognize that
the two might be interconnected in ways that the field is only beginning to
understand. Within-country health disparities may contribute to aggregate
cross-national health differences if the former are more pronounced in
one country than in another; however, they cannot explain all of the U.S.
health disadvantage. The evidence reviewed in Part I suggests that differ-
ences persist even among similarly advantaged groups. Understanding why
advantaged populations in the United States appear to be less healthy than
their counterparts in other countries led the panel to explore upstream
processes that affect everyone, including national policies and other aspects
of American life.
A LIFE-COURSE PERSPECTIVE
The complex relationships just described are in play at any given
moment of time, but they also play out over time. For example, the absence
of green space today may be the product of zoning decisions two decades
ago. Such influences also extend over a person’s lifetime: that is, the
upstream-downstream continuum can also be a temporal experience for
an individual. An individual’s struggle through middle age with exertional
angina from coronary artery disease may have originated in adolescence
with the adoption of cigarette smoking, perhaps as a coping mechanism
for a stressful childhood (Richter et al., 2009) or simply because the family
lived in a poor neighborhood where smoking was the norm. In turn, the
family’s move into that poor neighborhood may have resulted from finan-
cial setbacks that occurred before the child was born. Health trajectories
unfold not only over a lifetime, but also across generations as people are
4
Policy is typically portrayed as the outer ring of models with concentric circles or as the far
left-hand starting point of left-to-right logic models of influences on health outcomes.
5
Such effects would be heightened if adverse conditions are more prevalent, more adverse,
or have stronger effects in these populations.
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100 U.S. HEALTH IN INTERNATIONAL PERSPECTIVE
subject to changing health influences stemming from family, neighborhood,
and public policies.
This continuum of influences offers a potentially important systemic
explanation for the higher prevalence of disorders (e.g., obesity, cardio-
vascular disease), violence (e.g., homicide), and risk factors documented in
Part I. Over the past several decades, a great deal of social and biomedical
sciences research has been devoted to looking across individuals’ life spans
in an effort to better understand developmental and health trajectories over
time and, more specifically, how characteristics and experiences early in life
may influence health and biobehavioral pathways much later in life (Billari,
2009; Braveman and Barclay, 2009; Braveman et al., 2011b; Gluckman and
Hanson, 2006; Halfon and Hochstein, 2002; Keating and Hertzman, 1999;
Kuh and Ben-Shlomo, 2004; Lynch and Davey Smith, 2005; Mayer, 2009;
Palloni et al., 2009; Pollitt et al., 2005; Power and Hertzman, 1997). The
life-course framework casts health as a developmental process influenced by
multiple nested social, environmental, and biological spheres that continu-
ally interact over the course of one’s life and shape the quality and nature
of each person’s growth, health, and development (Halfon and Hochstein,
2002).
Biological, physical, and social influences over the life course can exert
both positive and negative effects on health trajectories. As one study
explained, health early in life “lay(s) out the foundation for a life time of
well-being” (Center on the Developing Child at Harvard University, 2010,
p. 1). Conversely, harmful experiences early in life “are built into our bod-
ies and significant adversity early in life can produce biological ‘memories’
that lead to lifelong impairments in both physical and mental health”
(p. 3). The same DNA can be expressed differently during development as
an outcome of adaptive responses and may be modified over time.
Ontogeny—the development or course of development of an individual
organism—involves the development of both organ systems and personality.
“Developmental plasticity” refers to how the fetus, child, and adolescent are
sensitive to the physical environment and to interaction with other human
beings. As noted in Chapter 2, the acquisition of certain cognitive traits and
abilities, such as social skills, impulse control, self-image, motivation, and
self-discipline, may occur during critical “transition periods” (Viner, 2012).
Although protective factors during these sensitive periods can foster resil-
ience and healthy development, harmful exposures may cause an individual
to adapt abnormally or in unhealthy ways (Gluckman and Hanson, 2006).
These patterns may be relevant to understanding some of the health prob-
lems documented in Part I that are more common among American youth
than among their peers in other countries. Although research in genetics,
molecular biology, developmental neurobiology, psychology, economics,
and sociology is only beginning to elucidate the causal pathways that link
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FRAMING THE QUESTION 101
early experiences with later disease, at least five general causal pathways
have emerged as potentially important.
First, much of the association between early and adult health condi-
tions results from the persistence of material, social, and cultural conditions
over time. Children who grow up in poverty not only endure immediate
health risks such as poor nutrition and exposure to lead, allergens, and
other pollutants, but they are also more likely to face poverty and its
consequences as adults (Case and Paxson, 2010, 2011; Case et al., 2005;
Currie and Widom, 2010; Delaney and Smith, 2012; Isaacs et al., 2008).
To the extent that such exposures remain stable across the life course,
disadvantages during childhood and adolescence will persist later in life.
Accordingly, poor health status early in life is associated with poor health
status during adulthood (Kuh and Ben-Shlomo, 2004; Power et al., 1991;
Wadsworth, 1991).
Second, biological exposures during early life, notably to certain infec-
tious diseases—from human papilloma virus to HIV—can produce clini-
cal complications later in life (Elo and Preston, 1996; Finch, 2010; Fong,
2000).
Third, adverse experiences and stimuli can result in biological embed-
ding6 (Hertzman, 2000). For example, Barker and colleagues were among
the first to hypothesize that nutritional status in utero and during infancy
and early childhood can cause organ damage that is responsible for hyper-
tension, heart disease, metabolic syndrome, insulin resistance, obesity,
and diabetes much later in life (Barker, 1998, 1999; Barker et al., 1993;
Godfrey, 2006; Hales et al., 1991; Ravelli et al., 1998). Similarly, other
investigators have documented associations between early life conditions
(e.g., social class, income, nutrition, infections) and subsequent mortality
and morbidity from diabetes, cancer, disabilities, and drug use (Freedman
et al., 2008; Galobardes et al., 2008; Kuh and Ben-Shlomo, 2004; Kuh et
al., 1997; Maty et al., 2008; Mayer, 2009; Palloni, 2006; Palloni et al.,
2009; Turrell et al., 2007; Wadhwa et al., 2009; Warner and Hayward,
2006). Research on developmental plasticity is examining the mechanisms
through which social and environmental exposures become biologically
embedded or reversed during critical periods (Gluckman and Hanson,
2006; Gluckman et al., 2008, 2010). For example, sustained stress is
thought to affect the brain and the neuroendocrine and immune systems
(see Chapter 6).
Fourth, the relatively new field of epigenetics (see Chapter 6) has
documented gene-environment interactions, in which permanent changes in
6
Embedding is a process that leaves signatures in the brain and other organ systems that
may remain latent for many years and then become manifest and influence adult physical and
mental health.
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102 U.S. HEALTH IN INTERNATIONAL PERSPECTIVE
gene expression, triggered by environmental cues, are thought to precipitate
chronic conditions (Sandoval and Esteller, 2012) and may be inherited by
offspring (Gluckman and Hanson, 2006; Institute of Medicine, 2006b).
Fifth, adversities during childhood and adolescence may cultivate dys-
functional traits (such as poor self-control, limited social skills, lack of per-
severance and resilience, and shortsightedness), maladjusted personalities,
and susceptibility to antisocial behavior (Caspi, 2000; Caspi and Moffit,
1995; Center on the Developing Child at Harvard University, 2010; Dozier
and Peloso, 2006; Elder and Shanahan, 2007; Felitti et al., 1998; Knudsen
et al., 2006; Trzesniewski et al., 2006). Stress may alter gene expression
in ways that predispose children to specific behavioral phenotypes (Caspi
et al., 2002, 2003; Taylor et al., 2006). These traits may in turn influence
physical activity, diet, and risky behaviors (e.g., smoking, substance abuse,
unprotected sex) (Richter et al., 2009) and they may exacerbate propensi-
ties for self-abuse, mental illness,7 suicide, violence, unintended pregnancy,
obesity, and diabetes (Dong et al., 2004; Edwards et al., 2003; Felitti et al.,
1998; Guyer et al., 2009; Hillis et al., 2004; Horwitz et al., 2001; National
Research Council and Institute of Medicine, 2000; Schilling et al., 2007;
Shonkoff et al., 2009).8 As noted in Chapter 2, adolescence is especially
critical in shaping cognitive and social skills that fuel success in education,
careers, and parenting9 (Bowles et al., 2005; Heckman, 2007).
Life circumstances provide an essential context to properly interpret
bivariate correlations between health and observed predictors, such as edu-
cation or income. For example, educated adults may not necessarily experi-
ence better health as a direct result of what they have learned in school: the
benefits may come from early experiences that foster self-efficacy, a desire to
succeed in various endeavors—education among them—and an interest in
good health (Pampel et al., 2010; Ross and Wu, 1995). On similar grounds,
these factors may be relevant in understanding the evidence in Part I regard-
ing the inferior health status and higher risk exposure of young people in
the United States compared with those in other high-income countries.
Higher rates of obesity, adolescent pregnancy, motor vehicle deaths, and
7
Mental illness has other innate causes and can only partially be attributed to childhood
experiences.
8
Adults with cardiovascular disease, lung disease, depression, alcoholism, and mental disor-
ders are more likely to report a history of child abuse (Anda et al., 2006; Caspi and Moffitt,
1995; Danese et al., 2007; Moffitt et al., 1992). Longitudinal studies of humans in particular
situations (orphaned children, children living in refugee camps) and animals (McEwen, 2000;
Zhang et al., 2005) suggest that inadequate maternal attachment and disruptions in protective
adult behavior can trigger responses like those observed with child abuse, albeit less extreme
(Thompson et al., 2002).
9
Thus, adverse conditions during early childhood can breed adverse conditions in subse-
quent generations.
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FRAMING THE QUESTION 103
homicide may have a common explanation in the life experiences of the
victims.
In short, existing research points to a variety of pathways that could
link early childhood exposures and late adult conditions (e.g., diabetes,
cardiovascular disease). The same pathways might also explain correlations
between health status across contiguous stages of the life cycle, spanning
shorter time intervals, such as between infancy and early childhood or
between adolescence and young adulthood.
However, early life experiences are hardly the only influences on health
and mortality later in life. It is important to differentiate between the
health trajectories experienced by individuals and the epidemiologic trends
observed in populations over time. For the latter, “period effects” can play
a major role in explaining cross-national differences. For example, increases
in smoking during the first half of the 20th century and in obesity in the
second half were largely period effects that touched adults of all age groups
and eventually extended to adolescents and children as well. Similarly, U.S.
tobacco control efforts designed to reduce smoking among adults, which
achieved success from the 1960s onward (see Chapter 5), benefited people
of all ages.
The panel was acutely aware of one of the most well-known and vexing
challenges when studying nonmedical influences on health, that of describ-
ing and empirically demonstrating causal pathways between a given health
factor and a biological health outcome. In other words, how do the condi-
tions presented by family, community, and national environments get under
a person’s skin to affect health? And how do these conditions affect people
differently? Even twins do not experience the same health development
trajectories over time (Madsen et al., 2010). Unlike the study of clinical
interventions or biological effects, research on social, environmental, and
policy factors involves more multidisciplinary and varied methodologi-
cal approaches, including different notions in the epistemology of what
constitutes “evidence” (Anderson and McQueen, 2009; Braveman et al.,
2011c; McQueen, 2009; Rychetnik et al., 2002; Victora et al., 2004).10 As
the Measurement and Evidence Knowledge Network (Kelly et al., 2006, p.
33) of the WHO Commission on the Social Determinants of Health noted:
The data and evidence which relate to social determinants of health come
from a variety of disciplinary backgrounds and methodological tradi-
tions. The evidence about the social determinants comprises a range of
ways of knowing about the biological, psychological, social, economic
and material worlds. The disciplinary differences arise because social his-
tory, economics, social policy, anthropology, politics, development studies,
10
The limitations of randomized controlled trials are discussed in Chapter 6.
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104 U.S. HEALTH IN INTERNATIONAL PERSPECTIVE
psychology, sociology, environmental science and epidemiology, as well as
biology and medicine, may all make contributions. Each of these has its
own disciplinary paradigms, arenas of debate, agreed canons and particu-
lar epistemological positions. Some of the contributions of these disciplines
are highly political in tone and intent.
CONCLUSIONS
The panel used both a social-ecological framework and a life-course
perspective in determining what factors to consider in search of an explana-
tion for the U.S. health disadvantage. Many theories or constructs could be
pursued, but the panel identified five domains of particular interest that set
the agenda for the next five chapters (see Figure 3-2).
We begin with health systems and individual behaviors, both of which
can have important proximate influences on health, and are addressed in
Chapters 4 and 5, respectively. The social-ecological model emphasizes
that interactions with health systems, individual behaviors, and disease
processes themselves are shaped by social factors and the environment.
Chapters 6 and 7, respectively, examine their potential contributory role in
the U.S. health disadvantage. Finally, Chapter 8 addresses how all these fac-
tors might be influenced at the macro level by the societal context of life in
America, ranging from life-style to policies, governance, and social values.
Health Systems
(Chapter 4)
Social Factors Mortality
(Chapter 6) (Chapter 1)
and and
Environmental Morbidity
Individual
Factors (Chapter 2)
Behaviors
(Chapter 7)
(Chapter 5)
Policies and Social Values (Chapter 8)
FIGURE 3-2 Panel’s analytic framework for Part II.
FIG3-2.eps
redrawn, but corrections not yet provided
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FRAMING THE QUESTION 105
Once again, we emphasize that the division of topics across the follow-
ing chapters is not meant to imply that these categories of health influences
operate independently or contribute in a simple additive fashion to the U.S.
health disadvantage. The key dynamic trajectories of health, risk factors,
socioeconomic circumstances, and physical and institutional environments
are all integrally linked and cannot be decomposed in a reductionist fash-
ion. As the following chapters make clear, these synergistic interactions are
central to understanding the U.S. health disadvantage.
