Number range CHAPTER

**Population Health: Challenges for Science and Society**

David Mechanic, PhD

Rutgers, The State University of New Jersey

Presented at the

Matilda White Riley Annual Lecture in the

Behavioral and Social Sciences

National Institutes of Health

Bethesda, MD

May 22, 2006

**Population Health: Challenges for Science and Society**

I am very much honored to be asked to deliver the first Matilda White
Riley Annual Lecture in the Behavioral and Social Sciences. Matilda was
a dear friend, and inspiration. She was untiring in seeking to convey
the complexities of social and personal development and the role of
social structures in shaping opportunities and adversities for health
and welfare. She understood that the study of aging was not the study of
old age but, in contrast, the unfolding of bio-social processes from
birth or even before, shaped by social stratification. Matilda
encouraged investigators to examine not only age but also cohorts and
how unique historical experiences shaped their welfare. Her
extraordinary energy was fueled by her optimism about the potentialities
of the social and behavioral sciences to improve peoples' lives.

Today I address an emerging revitalization of a broad perspective on the
determinants of population health and its value in helping to solve
existing and future health problems (Exhibit 1). I begin by discussing
the importance of social selection, and then illustrate how varying
influences from early nutrition to broad social factors affect
population health and social disparities. I conclude with some thoughts
on intervention strategies.

Studies of population health depend substantially on epidemiological
inquiries of different cohorts under varying social and environmental
circumstances and careful theory and hypotheses are essential. In this
era of computer power and data mining, there is much descriptive
epidemiology that is atheoretical, and often lacks even biological and
psychosocial plausibility. Such work has rightfully earned a compromised
reputation. Alvan Feinstein has noted that such efforts are unable to
distinguish truth from false alarms and contribute to an epidemic of
apprehension.^1^ Underlying many false results is failure to deal
realistically with the influence of social selection. In population
health research, where randomized controlled trials are usually
impossible, impractical or unethical, we depend on longitudinal studies
using multivariate statistical designs, instrumental variables as
commonly used in economics, or on natural experiments when such
opportunities become available. Taking account of selection biases is
imperative but it is important as well to understand how selection
processes shape health outcomes.

**Some Reflections on Social Selection**

Social selection is inextricably associated with the influences of
social stratification and with the incentives and opportunities it
provides in shaping individual identity, motivation, and life chances.
It is in the context of particular cultures, and class, race, gender,
and age groups, that norms operate; aspirations, expectations, and
obligations become established; and individual behavior is influenced.
Social structures not only shape the norms and expectations but also
make possible the resources, skills, training, and networks that allow
individual and group adaptation. People are not simply preprogramed,
directed by the forces in their environment, or influenced by random
forces. They play active roles in shaping opportunities and their
futures by geographic mobility, assortative mating, educational
attainment, occupational selection, decisions about family formation,
and much more. Individuals with varying characteristics and inclinations
elicit more and less social support, select more or less appropriate
mates, selectively avoid dangers or expose themselves to risk, and
differentially seek opportunities to promote health and welfare. Some of
these selective propensities such as cognitive capacity, temperament, or
physical robustness may be substantially preprogramed; other
propensities are shaped early in life by culture, nurture, and
schooling; still others influenced by the accidents of birth in
particular cultures, families, and historical periods and environmental
exposures over the life course.

Howard Schuman and Jacqueline Scott^2^ have illustrated nicely how
historical experience in adolescence and early adulthood shape
collective memory and social consciousness (Exhibit 2). A probability
sample of 1410 American respondents age 18 or older were asked in 1985
in an open-ended survey format to name "national world events or
changes" over the past 50 years that seem especially important. Eight
events were mentioned by at least 5% of respondents -- World War II, the
Vietnam War, space exploration, the Kennedy assassination, civil rights,
the threat of nuclear war, communication/transportation, and depression,
with the two wars by far the most dominant in respondent consciousness.
The salience of each event depended on the age of the respondent and the
occurrence of the event during the formative years of adolescence and
early adulthood. Exhibit 2 provides an example of how the salience of
the two wars were associated with age of respondent. Almost half of
respondents age 60-64 spontaneously reported World War II as a major
event, having experienced this event 40-45 years earlier when they were
approximately between the ages of 15 and 24; relatively few mentioned
the Vietnam War despite its recency. In contrast, the Vietnam War was
more salient for younger age cohorts between ages 24 and 39. It has been
hypothesized that early exposure of age cohorts to a wide range of
environmental influences including nutrition, infection, economic
privation, and social disruption have important consequences throughout
the life course.^3-5^

Influences on the life course and health, involve opportunities and
constraints at many levels -- from biology to society. These influences
interact in complex ways that pose challenges for understanding and
control. In illustrating the population health perspective I draw on
conceptions of important determinants that function in varying ways from
very early life to later in the life course. I begin with a large body
of work on early influences and the importance of fetal nutrition.

**The Importance of Fetal Nutrition**

An influential hypothesis associated with David Barker and his
colleagues^6^ is that fetal under nutrition in middle to late gestation
and in early life, leading to disproportionate fetal and infant growth,
is a precursor of coronary heart disease, stroke, high blood pressure
and type II diabetes in later life. Exhibit 3 shows higher mortality
rates for heart disease later in life among low birthweight male babies
in Hertfordshire and those of low weight at one year. In a more recent
example, Barker and his colleagues report on 8760 people born in
1934-1944 in Helsinki who attended child welfare clinics (Exhibit 4).
The sample included 444 individuals who either died of coronary heart
disease or who were admitted to the hospital with this condition.^7^
Those who were later hospitalized or died due to coronary heart disease
were small at birth, thin at age two, but had a rapid increase of their
Body Mass Index between ages two and 11. Exhibit 4 shows Z score means
for height, weight, and BMI for boys which represents the reported
growth patterns of those with coronary heart disease in this sample. In
each case they are below average for the first two years, and have
accelerated weight gain and BMI after age two. The researchers speculate
that this pattern of growth is linked to insulin resistance, a precursor
of coronary heart disease.

The Barker hypothesis has encouraged much research investigation, and
has its strong proponents and also critics. Animal experimentation in a
variety of species are consistent with the hypothesis that fetal
nutrition can alter physiology so as to increase susceptibility to later
disease, although there are important species variations.^8^ Also,
natural experiments based on the Dutch famine in 1944-45,^9,\ 10^ and,
more recently, the Chinese famine of 1959-61,^11^ support a link between
fetal under nutrition and some neurodevelopmental disorders. Barker has
suggested a number of pathways for how early nutrition might affect
varying disease states by influencing the formation of number of cells
in key organs in adaptations to protect brain development; by
differential settings of hormones and metabolism; or by introducing
vulnerabilities to adverse environments in later development.^12^

Skeptics observe that RCTs of maternal dietary supplements in pregnancy
have had only small effects on birthweight. Moreover, even the very
extreme nutritional conditions in Holland and China, were associated
only with modest observed effects. As Jane Harding observes, the biology
involved is complex and maternal and fetal nutrition are separable
issues depending on transfer capacity.^13^ Influences include placental
surface area and specific nutrient transporters.

Many social scientists have an instinctive skeptical response to the
focus on prenatal determinants, knowing that fetal nutrition is
inevitably confounded with many unmeasured social class, environmental,
and contextual variables, and may not have major causal significance.
But understanding the relation between early nutrition and physical
development, the mothers' nutritional history and development,
uteroplacental blood flow, placental function, and fetal metabolism,^14^
in conjunction with other influences, should contribute to a better
understanding of the pathways to endpoints of interest.

Using the Helsinki data, Barker and his colleagues examined the
interactions between body size at birth, growth, father's occupational
status at birth, and education, occupational status, and income in adult
life in relation to hospitalization or mortality from coronary heart
disease. Exhibit 5 shows the association with parental social class and
educational and social class attainment.^15^ The resulting story is
complicated, with low rates of fetal and infant growth, low educational
attainment, and low occupational status each having independent
associations with coronary disease. Infant growth was retarded in
families of low occupational status, and subsequent educational
attainment also was less. The educational level attained was associated
with hospitalization and mortality beyond associations due to poor
infant growth. The researchers suggest that social class factors play an
important role by altering the conditions for growth and, thus, disease
risk. They also speculate that deficient fetal and infant growth
increase susceptibility to the effects of poor living standards.

**Fundamental Causes**

While Barker and colleagues view fetal and infant growth as fundamental
to what follows, Bruce Link and Jo Phelan approach related questions
through the lens of social class as a fundamental cause.^16,\ 17^ In
doing so, they seek to understand why when risk factors for disease and
mortality, associated with social class, are overcome or change, the
observed relationship between social class and mortality remains robust
and has even strengthened over time (Exhibit 6). They argue that it is
the money, other resources, knowledge, social networks, and influence,
associated with social class, that allow people to shield themselves
from adversities and take positive action to prevent or ameliorate a
wide range of threats to health.

If this is to be more than an interesting argument it has to generate
important implications that are testable and refutable. Link and Phelan
extrapolate that if the resources that social class provides really
protect against disease and death, we would expect its effects to be
linked to the preventability of varying causes of death. Using the
National Longitudinal Mortality Study, a prospective data set linking
samples of the Current Population Surveys to the National Death Index,
and physician ratings of preventability of mortality, they found that
the social class-mortality relationship was much stronger in the case of
highly preventable conditions, for example, cerebrovascular disease,
chronic obstructive pulmonary disease, and cancer of the trachea,
bronchus and lung, in contrast to low preventable conditions, such as
cancer of the pancreas, breast and prostate or multiple sclerosis.^18^
Exhibits 7 and 8 show the relationship between educational level and
preventability of mortality for the age groups 25-44 and 45-65. Both
exhibits show a large gradient for preventable conditions in relation to
education but much less so for diseases difficult to prevent.

One challenge to the fundamental cause hypothesis, and a view sometimes
heard from physicians and others, is that the key factor underlying the
relationships between social class and disease and mortality outcomes is
intelligence or cognitive ability. Barker and colleagues (2001) note,
for example, that intelligence may reflect childhood fitness related to
long-term health.^19^ Gottfredson^20^ has contended this much more
directly, arguing that intelligence is the fundamental cause underlying
both better health outcomes and higher socioeconomic status.

Link and his colleagues used two major longitudinal data sources -- the
Wisconsin Longitudinal Study and the Health and Retirement Survey --
that make it possible to examine cognitive capacity in relation to
mortality and life-threatening illnesses.^21^ They find that both SES
and cognitive ability are associated with mortality and other health
outcomes. However, analyses from both studies indicate that controlling
for cognitive ability only modestly modifies the SES/health link and it
remains statistically significant. In contrast, controlling for SES
reduces the effects of cognitive ability to nonsignificance.

The concept of fundamental causes has implications for how we understand
and address major health problems. It is conventional in most medical
and epidemiological studies to conceive of factors such as social class
as crude proxies, providing clues to the real causal factors more
proximal to disease and mortality such as biological and behavioral risk
factors. Within this view, social class is primarily important because
of its associations with many other factors that play a more immediate
role in disease processes. Preventive efforts are then focused on these
specific risk factors. Persons high on risk factors certainly have a
higher propensity for disease and death, but most disease in populations
occur among persons who are in the normal range of recognized risk
factors. This commonly results in proposals to intervene medically at
lower risk thresholds with more and more individuals near or at normal
range, for example in such areas as blood pressure and cholesterol
control. The [British Medical Journal]{.underline}, (Exhibit 9) without
tongue in cheek, published several papers in June 2003 suggesting a
strategy of reducing cardiovascular disease and mortality with a
polypill, containing a statin, three hypertensives, folic acid, and
aspirin, taken by everyone with pre-existing cardiovascular disease and
everyone over age 55.^22,\ 23^ One implication of the risk factor
approach would be to have everyone medicated.

An alternative approach is to focus relatively greater resources on
modifying factors that affect the rate of incidence in populations.
Interventions to modify incidence will impact statistical lives
significantly but not necessarily identifiable individuals, a barrier
that contributes to the political difficulty of gaining support for such
initiatives.^24^ Efforts to affect incidence include such traditional
public health measures as water and food safety and initiatives to limit
the spread of infectious disease and avoid epidemics, to those more
contentious such as control of environmental pollutants, income supports
and gun safety.

The approach to motor vehicle safety, and its success, attests to the
value of a broad population effort to address the range of factors
beyond those specific to individuals that affect the occurrence of
injury and death. The story is a remarkable one with a significant fall
in deaths per miles driven and absolute deaths despite a sharp upward
trend in miles driven^25,\ 26^ (Exhibits 10 and 11). These changes are
attributable to many factors including the design of highways, vehicle
construction and safety features, traffic enforcement, and increased
control of intoxicated drivers. The public health model, focusing on the
agent (in this case the vehicle), and the driving environment, as well
as the attributes of individual drivers, applied so successfully to
automobile safety, has broad potentialities for reducing incidence of
many types of morbidity and promoting population health.

**Health Disparities**

One important implication of the Link/Phelan hypothesis is that needed
health actions that depend on the decisions, active motivation and
resources of each individual will inevitably lead to social disparities
in health outcomes because those with more resources, knowledge,
networks, and influence will be better positioned to take advantage of
new knowledge and technologies and new biomedical advances.

Eliminating health disparities is one of the major overarching goals of
America's health objectives for the year 2010.^27^ There are significant
disparities across all indices of social stratification and in relation
to a great variety of outcome measures including the prevalence of
disease, access to treatment, the quality of care, and mortality.
Disparities by race are of particular concern because they are typically
large, and relate to America's legacy of slavery, racism, and
discrimination. As the nation has focused on racial disparities, much
policy discussion, and its representation in the public arena and in the
media, has centered on lack of progress in eliminating disparity ratios
and even loss of ground. It is obviously desirable to eliminate such
disparities. Nevertheless, a misunderstanding of the implications of
disparity ratios, in contrast to numbers of lives saved or diseases
prevented, could mislead us in how we prioritize initiatives to improve
population health.

If the ability to take advantage of new advances in prevention and
treatment depend on money, knowledge, social networks, and other
resources, as the fundamental cause hypothesis postulates, then many new
biomedical and technological advances will contribute to disparities to
the extent that these personal resources are needed to maximize the
opportunity.^28^ Differences in infant mortality, an important aspect of
overall variations in average length of life, illustrates some of these
issues.

It is commonly suggested that the poor showing of American infant
mortality rates relative to other developed nations is largely explained
by the racial heterogeneity of the United States, and particularly the
black/white disparity,^29^ but as Exhibit 12 shows, the US disadvantage,
if the comparison is restricted to the US white population, is still
large relative to many other countries.^30^ Exhibit 13 describes changes
in black and white infant mortality between 1950 and 1995, a period in
which the percent disparity more than doubled. Most important is the
dramatic improvement in infant mortality rates for both blacks and
whites. With one exception, 1960, absolute reduction in rates per 1000
live births were greater among blacks than whites. (This is presented
more clearly in Exhibit 14). Comparing 1950 to 1996, almost 50% more
black infant than white infant deaths were prevented. Relatively poor
overall rates, and especially the seeming stabilization of the black
infant mortality rate at 13-14, however, should be a continuing cause of
concern and study, and the development of new thoughtful targeted
interventions.

Prematurity and low birthweight remain the strongest predictors of
neonatal death, and are highly associated. Prematurity is the more
meaningful measure but involves large measurement error and, thus,
birthweight, which is more reliably measured, is commonly used as a
proxy. Birthweight is substantially associated with infant mortality for
individuals in specific population groups but the causal relevance of
birthweight for understanding differences in mortality across
populations is less clear.^31^ The various risk factors for low
birthweight and infant mortality are similar. Most of these factors
disadvantage black births including births to teenage mothers, unmarried
mothers, high parity, and low educational level. Black mothers are also
likely to have more medical risks, gain less weight during pregnancy,
and receive less prenatal care. They are slightly more likely to have
had birth complications and a previous pregnancy loss.^32^ While smoking
and substance use are also associated with lower birthweight and other
risk factors, black mothers are less likely to smoke than white mothers.
For reasons, not well understood, black infants, while having a much
higher risk of low birthweight than white infants, are more likely to
survive at very low birthweight, providing support for the view that
prematurity and not birthweight is of more causal importance.

If a child's later health is established for her in part in utero and
very early in life as Barker suggests, and is associated with her
mother's health during pregnancy, which in turn is affected by early
influences, then preventing prematurity and ensuring infant health is a
multi-generational challenge. This requires thinking about interventions
much more broadly than through the traditional focus on prenatal care
where research has been unable to substantiate many of the optimistic
claims.^33^

**Reflections on Population Health Interventions**

Initiatives at the population level are typically based on the premise
that wise social policies can substantially improve health and welfare.
Demonstrating such specific effects is difficult given the multiplicity
of relevant factors and possible alternative interpretations. Some
skepticism is important because commonly accepted interpretations of
many health trends, for example, the dramatic fall in cardiovascular
disease in recent decades attributed to changes in health behavior, on
closer examination do not fit the data in any convincing way.^34^
Nevertheless, research across a wide range of contexts suggests some of
the pathways through which social location affects life chances, health,
and longevity.

In the time that remains I focus on ways in which social structures,
culture, and other non medical determinants may shape health and
longevity. Non medical interventions are typically more controversial
because they often clash with ideological perspectives, and economic and
religious interests. Nevertheless, if we are to take understanding of
social structures seriously, we must attend to how the resources
associated with social hierarchies, and the influence of social
position, affect life chances, health, and longevity.

Many efforts in public health and medicine to change health behavior in
positive directions, commonly successful in the short term, either fail
or have modest effects in the longer run. They fail in part because they
require continued individual awareness and motivation that are difficult
to sustain given the structure of peoples' lives, work, and the
environment. This is evident across a range of initiatives such as
improving nutrition, increasing exercise, and other positive health
behaviors. Good health behavior that flows naturally from everyday
patterns of activity is more readily sustained than artificial
interventions imposed on already complex lives.

Lets return for a moment to the earlier discussion of historical trends
in black/white infant mortality. Prior to 1965, the black population in
the south was particularly disadvantaged by exclusion from segregated
public hospitals. In 1963, a US Appeals Court invalidated a "separate
but equal" clause in funding for hospital construction, followed by
Title VI of the 1964 Civil Rights Act, and Implementation of Medicare in
1966, requiring that hospitals eligible for federal reimbursement not
discriminate.^35^ This had a dramatic effect, particularly in the rural
South, in opening hospital access previously unavailable to many black
patients and providing access to treatment for gastroenteritis,
influenza, and pneumonia, the major causes of black infant deaths.^36^
In Mississippi, for example, black postneonatal mortality fell 50%
between 1965 and 1971. The period, 1965-1975, saw not only a large drop
in black infant deaths but also a large reduction in the disparity
between black and white infant deaths. Opening public hospitals to
blacks helped equalize a vital health resource.

While earlier improvements in infant mortality were substantially
related to living conditions and access to basic health care, in more
recent years advanced medical technology has had a more important role,
especially high risk obstetrics and neonatal intensive care, and
pulmonary surfactant therapy for the treatment of respiratory distress
syndrome in preterm infants. Following the introduction of surfactant
therapy, deaths from this cause declined substantially.^37^

The single most important cause of postneonatal mortality and
black/white disparities is Sudden Infant Death Syndrome (SIDS). Having
infants sleep on their side or back was seen as an effective
intervention and believed to account for substantial reduction in SIDS
rates.^38^ There have been large reductions in having infants sleep in
prone position in all groups, but African Americans and mothers with
less education have been most likely to retain or readopt the prone
position over time and are least likely to use the supine
position.^39-41^ This has been of major concern since supine positioning
is now believed to reduce SIDS risk as compared with either prone or
side positioning.^42^ The specific factors accounting for these
differences - whether in access to information, comprehension, or other
barriers are unclear.

Social and behavioral scientists, epidemiologists and medical
historians, aware of the large and persistent relationship between
social class and mortality around the world and over time, have long
been intrigued by the fact that some very poor nations and regions have
maintained low mortality over extended periods of time, while other
countries many times more affluent have done relatively poorly.
Generalization based on such selective comparisons among countries
varying in national development, politics, culture, and geographic
circumstances must be considered cautiously, and even skeptically, but,
nevertheless, can provide helpful insights. Three factors beyond
sufficient subsistence resources stand out. Educational attainment,
whatever the context, offers advantages in longevity both within and
across nations. Some poor regions, such as Kerala in India, despite a
low per capita income, has achieved an impressively high level of
literacy among men and women, in the vicinity of 90%^43^ and relatively
low mortality. However, Kerala has a long history of public policy
relating to education, community medical care, public support of food
distribution, and public and political activism, that makes it difficult
to separate education and literacy from other complex influences.

Educational attainment has had an important place in theories of social
development, modernization, and determinants of health.^44^ It
potentially creates opportunities through varied pathways including
increased cognitive complexity, knowledge, coping capacities, and access
to better jobs and higher incomes.^45,\ 46^ It also empowers individuals
and encourages civil engagement. A second, related factor, seen to
promote better health and reduced infant and child mortality is personal
empowerment, and especially the education and empowerment of women.
Women in most societies are the family caretakers, preparers of meals,
and monitors of family health. Poor countries with better health have
better educated women, and women more empowered and engaged in their
communities. John Caldwell has observed that countries with a high
proportion of females in primary school in 1960 had the lowest infant
mortality rates and the highest expectation of life at birth in 1982
among countries studied.^47^ In contrast, richer countries with poor
infant mortality experience often are those that have discouraged female
education, contact between the sexes, and female social participation
outside the household.

A third factor that differentiates poor countries with favorable
mortality from those with poorer health experience is accessibility to
basic primary health care services. Much of the impact of medical care
involves basic preventive services that are cost-effective, and often
inexpensive. Countries that make access to these resources universal,
and distribute them fairly, have lower mortality, and presumably better
health. It is ironic that the United States, with by far the most
expensive, and arguably, the most technically sophisticated health care
system in the world, has 46 million people uninsured, and significant
barriers to many of these basic cost-effective services.

In considering initiatives in the United States involving nonmedical
determinants, education is likely to be key. Improving access to high
quality education establishes the conditions for improved life chances
by empowering people to seek and assess information, engage in their
communities, and attain occupations and incomes that make a better life
possible. Education also influences additional factors important to
health outcomes such as self-efficacy, the ability to deal with complex
cognitive challenges, coping effectiveness, and the probability of more
control over work and other important life circumstances. It gives
individuals the tools to continue to learn and adapt to changing social
and technical circumstances. Also, in contrast to the challenges of
income redistribution, support for education is strong across the
ideological spectrum and there is broad agreement that it is a valuable
end in itself and worthy of investment.

Issue of income and income distribution, whether in the form of income
transfers, or access to basic supports in such forms as housing, food
stamps, and health insurance, are more contentious scientifically and
politically. While income clearly has a role in health outcomes, the
marginal value of additional income beyond some subsistence threshold
remains debatable. The evidence suggests that social class, whether
measured by education, income, or occupation, is associated with health
outcomes that follow a social gradient,^48^ but it is also clear that
the largest health disparities are evident at the lowest income
levels.^49^ Advancing the economic security of the entire population
obviously has merit, but transfers to the most impoverished part of the
income distribution are likely to have largest health impact.

Behrman, Sickles and Taubman estimated hazard models for mortality
between 1969 and 1979 among a national random sample who were ages 58-63
in 1969.^50^ Using linked data from the Retirement History Survey and
Social Security records, they found that additional Social Security or
pension benefits for men lowered the hazard of death. SSI, which
provides income support to the disabled and the poorest poor, had an
estimated effect on mortality five times greater than Social Security
benefits overall. Similarly, Social Security income, SSI, and pension
income were all associated with lower mortality among women.

Exhibit 15 describes data on US mortality from 1900 to 1995 presented by
House and Arno,^51^ stratified by age group. Mortality in the age group
75-84 dropped more dramatically over time than for other age groups,
beginning in the late 1930s, and then again in the early 1970s. These
descriptive data are open to alternative explanations, and cannot prove
the case, but major events in these two time periods were clearly
important in the lives of the elderly and contributed importantly to the
reduction of poverty. The passage of the Social Security Act in 1935
gave elderly citizens who had high rates of impoverishment and privation
important subsistence income; the Social Security Amendments in 1972
were said to "set the terms of Social Security politics for the rest of
the century."^52^ These Amendments not only raised basic benefits by 20%
but also established a new system for automatic adjustments.

. . . . . . . . .

These reflections covered a broad range and sought to capture some of
the complexities and interconnections that make scientific understanding
of human health challenging. Through the support, largely of NIH
agencies, we have developed improved and sophisticated representative
data sets, longitudinal as well as cross-sectional, that allow us to
monitor the health of the nation and to begin to unravel underlying
pathways. We have developed much more powerful tools for collecting and
analyzing these data. We have become more open and increasingly more
skillful in understanding the interplay of biosocial processes.
Biomedical advances have brought many human improvements and promise
even more, but it is evident that the future of the nation's health will
depend as much or more on how we use our knowledge to better structure
social arrangements consistent with our aspirations and ideals.

Matilda White Riley passionately believed that her work, and the
scientific work of her colleagues, would contribute importantly to the
quality of all stages of the life course, meaningful productivity, and a
better life for all. Thus, I am grateful to have had the opportunity to
speak to these issues at this event honoring her memory.

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27\. U.S. Department of Health and Human Services, [Tracking Healthy
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28\. David Mechanic, "Disadvantage, Inequality and Social Policy,"
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30\. National Center for Health Statistics, op cit., Tables 19 (page
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33\. Robert L. Goldenberg and Dwight J. Rouse, "Prevention of Premature
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34\. Reuel A. Stallones, "The Rise and Fall of Ischemic Heart Disease,"
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35\. David B. Smith, [Health Care Divided: Race and Healing A
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36\. Douglas V. Almond, Kenneth Y. Chay and Michael Greenstone, [Civil
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37\. W. Parker Frisbie, et al., 2004, op cit., Page 775.

38\. Paul H. Wise, "The Anatomy of a Disparity in Infant Mortality,"
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39\. Samuel M. Lesko, Michael J. Corwin, Richard M. Vezina, et al.,
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40\. Marian Willinger, Howard J. Hoffman, Kuo-Tsung Wu, et al., "Factors
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41\. Harold A. Pollack and John G. Frohna, "Infant Sleep Placement After
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42\. Michael H. Malloy, "Effectively Delivering the Message on Infant
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43\. Amartya K. Sen, [Inequality Reexamined]{.underline} (Cambridge, MA:
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44\. David Mechanic, "Promoting Health: Implications for Modern and
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45\. David Mechanic, "Socioeconomic Status and Health: An Examination of
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46\. David Mechanic, "Education, Parental Interest and Health
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47\. John C. Caldwell, "Routes to Low Mortality in Poor Countries,"
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48\. Michael Marmot and Richard G. Wilkinson, eds., [Social Determinants
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49\. Hugh Gravelle, "How Much of the Relation Between Population
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51\. Reported in James S. House and David R. Williams, "Understanding
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52\. Edward D. Berkowitz, [Robert Ball and the Politics of Social
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12.