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 HANDBOOK OF AGING
AND THE SOCIAL SCIENCES
EIGHTH EDITION
 THE HANDBOOKS
OF AGING
Consisting of Three Volumes

Critical comprehensive reviews of research knowledge,

theories, concepts, and issues

Editors-in-Chief
Laura L. Carstensen
and
Thomas A. Rando

Handbook of the Biology of Aging, 8th Edition

Edited by Matt Kaeberlein and George M. Martin

Handbook of the Psychology of Aging, 8th Edition

Edited by K. Warner Schaie and Sherry L. Willis

Handbook of Aging and the Social Sciences, 8th Edition

Edited by Linda K. George and Kenneth F. Ferraro
HANDBOOK OF AGING
AND THE SOCIAL
SCIENCES
EIGHTH EDITION
Edited by

Linda K. George and Kenneth F. Ferraro

Associate Editors

Deborah Carr, Janet M. Wilmoth, and Douglas A. Wolf

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 Dedications

To my awesome siblings, Kathie, Kent, and Karen,

who have known and loved me longer than anyone.
—LKG

To Linda C. Ferraro, my gracious wife: Many women do noble things,

but you surpass them all (Proverbs 31.29).
—KFF
 Foreword
The near-doubling of life expectancy in the
20th century represents extraordinary oppor-
tunities for societies and individuals. Just as
sure, it presents extraordinary challenges. In
the years since the last edition of the Handbook
of Aging series was published, the United States
joined the growing list of “aging societies”
alongside developed nations in Western Europe
and parts of Asia; that is, the U.S. population
has come to include more people over the age
of 60 than under 15 years of age. This unprec-
edented reshaping of age in the population will
continue on a global scale and will fundamen-
tally alter all aspects of life as we know it.
Science is responsible for the extension of
life-expectancy and science is now needed more
than ever to ensure that added years are high
quality. Fortunately, the scientific understanding
of aging is growing faster than ever across social
and biological sciences. Along with the phe-
nomenal advances in the genetic determinants
of longevity and susceptibility to age-related
diseases has come the awareness of the critical
importance of environmental and psychologi-
cal factors that modulate and even supersede
genetic predispositions. The Handbooks of Aging
series, comprised of three separate volumes, the
Handbook of the Biology of Aging, the Handbook
of the Psychology of Aging, and the Handbook of
Aging and the Social Sciences, is now in its eighth
edition and continues to provide foundational
knowledge that fosters continued advances in
the understanding of aging at the individual
and societal levels.
xi
Attention to the science of aging involves a
concomitant increase in the number of college
and university courses and programs focused
on aging and longevity. With this expansion
of knowledge, the Handbooks play an increas-
ingly important role for students, teachers
and scientists who are regularly called upon
to synthesize and update their comprehen-
sion of the broader field in which they work.
The Handbook of Aging series provides knowl-
edge bases for instruction in these continually
changing fields, both through reviews of core
and newly emerging areas, historical synthe-
ses, methodological and conceptual advances.
Moreover, the interdisciplinary nature of aging
research is exemplified by the overlap in con-
cepts illuminated across the Handbooks, such
as the profound interactions between social
worlds and biological processes. By continu-
ally featuring new topics and involving new
authors, the series has pushed innovation and
fostered new ideas.
One of the greatest strengths of the chapters
in the Handbooks is the synthesis afforded by
preeminent authors who are at the forefront of
research and thus provide expert perspectives
on the issues that current define and challenge
each field. We express our deepest thanks to
the editors of the individual volumes for their
incredible dedication and contributions to the
series. It is their efforts to which the excellence
of the products is largely credited. We thank
Drs. Matt Kaeberlein and George M. Martin
editors of the Handbook of the Biology of Aging;
xii Foreword
Drs. K. Warner Schaie and Sherry L. Willis, edi-
tors of the Handbook of the Psychology of Aging;
and Drs. Linda K. George and Kenneth F.
Ferraro, editors of the Handbook of Aging and the
Social Sciences. We would also like to express
our appreciation to our publishers at Elsevier,
whose profound interest and dedication has
facilitated the publication of the Handbooks
through their many editions. And we continue
to extend our deepest gratitude to James Birren
for establishing and shepherding the series
through the first six editions.
Thomas A. Rando
Laura L. Carstensen
Stanford Center on Longevity,
Stanford University
 Preface
Social science scholarship on aging is
alive and well. Although the last edition of
the Handbook of Aging and the Social Sciences
appeared only 5 years ago, the growth of
research since then on aging individuals, popu-
lations, and as a dynamic culmination of the life
course has been extraordinary. There are many
reasons for this stunning growth in the quantity
and quality of aging research. Infrastructure
and the methodological tools necessary for rig-
orous, sophisticated research have increased
and become widely available to the scientific
community. In the social sciences, the increase
in data sources covering significant portions of
the life course from a broad spectrum of socie-
ties, the increased coupling of social and bio-
logical data, and statistical advances have been
especially important. New, energetic cohorts of
scholars have posed fresh, innovative research
questions to the field and demonstrated the
importance of those questions for a deeper
understanding of aging. And, of course, the
complexities of population dynamics, cohort
succession, and policy changes modify the
world and its inhabitants in ways that must
be vigilantly monitored so that aging research
remains relevant and accurate.
This is the eighth edition of the Handbook
of Aging and the Social Sciences and we have
endeavored to do justice to the research topics
and questions that, in our judgment, represent
both foundational, classic, and ever-important
topics critical to aging research in the social
sciences and emerging and timely topics that
xiii
expand the field in exciting ways. This edition
of the Handbook includes 23 chapters. Seventeen
of these chapters address topics that did not
appear in the seventh edition; most of them
address topics that did not appear in any pre-
vious edition of the Handbook. Of the six topics
covered in this edition that also appeared in the
seventh edition, four were written by different
authors.
Because each edition of the Handbook
includes chapters that differ from the previous
edition, each edition is a stand-alone volume.
Thus, chapters in the seventh edition, as well
as even earlier ones, remain important compila-
tions of aging research.
Just as the majority of chapters in this edi-
tion of the Handbook address new topics, most
of the chapter authors also are new to this edi-
tion. Specifically, of the 47 chapter authors who
contributed to this edition, 40 of them did not
participate in the previous edition. Most of the
new chapter authors are well-established schol-
ars, but they are also relatively young. Without
question, they will be among the premier schol-
ars of aging for decades to come and it has been
a great pleasure to include their impressive
contributions to this edition of the Handbook.
Unlike the Handbook of the Biology of Aging
and the Handbook of the Psychology of Aging,
this Handbook is intended to cover a spec-
trum of disciplines. As a result, the chapters
in this volume were written by scholars that
include demographers, economists, epidemi-
ologists, gerontologists, political scientists,
xiv Preface
psychologists, social workers, sociologists, and
statisticians. Likewise, chapters address topics
at the micro- and macro-levels, as well as top-
ics that address the intersection of individual
and aggregate factors. The result is a rich array
of topics and perspectives that cover much,
though by no means all, of the landscape of
aging research in the social sciences.
Chapter authors were asked to contribute
scholarly reviews of their topics, devoting spe-
cial attention to what is new and exciting (theo-
retically, methodologically, and substantively)
and to priority issues for future research. They
meticulously crafted chapters that stand as
exemplary reviews of the state-of-the-science
and point the way to exciting ways to advance
the field. We found reading these chapters and
corresponding with the authors to be enlighten-
ing and we stand in awe of the knowledge and
insights that the authors generously shared.
We also owe huge debts of gratitude to our
Associate Editors: Deborah Carr, Janet Wilmoth,
and Doug Wolf. They were involved in every
part of this Handbook, including selection of top-
ics and authors, providing feedback to chapter
authors, and writing superb chapters themselves.
As a group, they beautifully buttressed us in
areas where our knowledge was less extensive
than theirs and provided insights and sugges-
tions that improved the volume in multiple ways.
Cohort succession signifies the entrance
of fresh, new generations, but also brings the
exit of those who created the world that new
cohorts enter. Bob Binstock was the senior
editor of the seven previous editions of the
Handbook of Aging and the Social Sciences. Bob
died in 2011. Bob was, without question, the
guiding spirit and the meticulous work-horse
of the Handbook of Aging and the Social Sciences
series. And this was but one of his monu-
mental contributions to aging research and
policy. Linda George had the privilege of co-
editing the third through seventh editions of
the Handbook with Bob. They had a wonderful
working partnership that she will always treas-
ure. She agreed to serve as senior editor of this
edition only if she succeeded in recruiting a co-
editor in whose intelligence, research contribu-
tions, service to the field, and judgment she had
total trust. Ken Ferraro was her choice and he
graciously accepted the call. Her choice could
not have been better. How fortunate she’s been
to work with two remarkable men who did
their share of the work and more.
This Handbook is intended to serve as a use-
ful resource, an inspiration to those searching
for ways to contribute to the aging enterprise,
and a tribute to the rich bodies of scholar-
ship that comprise aging research in the social
sciences.
Linda K. George and Kenneth F. Ferraro
 About the Editors
Linda K. George is professor of Sociology
at Duke University where she also serves
as associate director of the Duke University
Center for the Study of Aging and Human
Development. She is a fellow and past presi-
dent of the Gerontological Society of America
(GSA). She is former chair of the Aging and
Life Course Section and the Sociology of Mental
Health Section of the American Sociological
Association (ASA). She is former editor of the
Journal of Gerontology, Social Sciences. She is
currently associate editor of Social Psychology
Quarterly and former associate editor of
Demography. She is the author or editor of 8
books and author of more than 250 journal arti-
cles and book chapters. She co-edited the third,
fourth, fifth, sixth, and seventh editions of the
Handbook of Aging and the Social Sciences. Her
major research interests include social fac-
tors and illness, stress and social support, and
mental health and well-being across the life
course. Among the honors she has received
are Phi Beta Kappa, the Duke University
Distinguished Teaching Award, the Mentorship
Award from the Behavioral and Social Sciences
Section of GSA, the Dean’s Mentoring Award
from the Graduate School of Duke University,
the Kleemeier Award from the GSA, and the
Matilda White Riley Award from the ASA.
Kenneth F. Ferraro is distinguished profes-
sor of Sociology and founding director of the
Center on Aging and the Life Course at Purdue
University. He is the author of over 100 peer-
reviewed articles and 2 books and has edited 4
editions of Gerontology: Perspectives and Issues.
His recent research focuses on health inequality
over the life course. Current projects examine the
xv
early origins of adult health, health disparities,
and the health consequences of obesity. With
interests in how stratification processes unfold
over the life course, he has developed cumula-
tive inequality theory for the study of human
development, aging, and health. A fellow of
the Gerontological Society of America (GSA),
he formerly edited Journal of Gerontology: Social
Sciences and chaired the Behavioral and Social
Sciences section of GSA. He also is a member of
the honorary Sociological Research Association
and former chair of the Section on Aging
and Life Course of the American Sociological
Association (ASA). GSA has honored him with
the Distinguished Mentor Award, Richard
Kalish Innovation Publication Award, and the
Best Paper Award for Theoretical Developments
in Social Gerontology. ASA honors from the
Section on Aging and the Life Course include
Outstanding Publication Award and Matilda
White Riley Distinguished Scholar Award.
Deborah Carr is professor of Sociology at
Rutgers University where she also is a faculty
member at the Institute for Health, Health Care
Policy & Aging Research, and holds a second-
ary appointment at the School of Social Work.
She is a fellow of the Gerontological Society
of America (GSA) and a member of the hon-
orary Sociological Research Association. She
is the 2014–15 chair of the Aging and Life
Course Section of the American Sociological
Association (ASA). She is editor of the Journal of
Gerontology: Social Sciences for the 2015–18 term
and formerly served as deputy editor of Journal
of Marriage and Family, and Social Psychology
Quarterly. She is the author or editor of five
books including the Encyclopedia of the Life
xvi About the Editors
Course and Human Development (Cengage, 2009).
She has authored 70 journal articles and more
than 2 dozen book and encyclopedia chap-
ters. She is an investigator on several major
studies of aging and the life course including
the Midlife in the United States (MIDUS) and
Wisconsin Longitudinal Study (WLS), and is
chair of the Board of Overseers of the General
Social Survey (GSS). Her major research inter-
ests include stress, health and well-being over
the life course. Her specific research projects
focus on death, dying and bereavement; fami-
lies and health; and the psychosocial conse-
quences of body weight over the life course.
Janet M. Wilmoth received a Ph.D. in
Sociology and Demography, with a minor
in Gerontology, from the Pennsylvania State
University. She is professor of Sociology at
Syracuse University where she also serves as
the director of the Aging Studies Institute, sen-
ior research affiliate in the Center for Policy
Research, and senior fellow in the Institute for
Veterans and Military Families. She is a fellow
of the Gerontological Society of America (GSA),
current secretary/treasurer of GSA’s Behavioral
and Social Science Section, and past secretary/
treasurer of the Section on Aging and the Life
Course of the American Sociological Association
(ASA). She has authored of over 50 articles
and book chapters, and co-edited Gerontology:
Perspectives and Issues (third and fourth editions)
and Life Course Perspectives on Military Service.
Her research examines older adult migration and
living arrangements, health status, and finan-
cial security, and explores how military service
shapes various life course outcomes related to
marriage and family, economic well-being, health
conditions, and disability. She has received sev-
eral teaching awards, including the School of
Liberal Arts Excellence in Education Award at
Purdue University and the Chancellor’s Award
for Public Engagement and Scholarship-Faculty
and Staff Inspiration at Syracuse University.
Douglas Wolf is the Gerald B. Cramer
Professor of Aging Studies and a professor
of Public Administration and International
Affairs at the Maxwell School of Citizenship
and Public Affairs at Syracuse University.
Previously he was a senior research associate
and director of the Population Studies Center
at the Urban Institute, and was a research sci-
entist at the International Institute of Applied
Systems Analysis in Laxenburg, Austria. His
research focusses mainly on family and house-
hold demography, late-life disability, and
informal care and its consequences for care
providers and care receivers. His research has
been published in demography, gerontology,
public policy, economics, health, and evalua-
tion journals. He has served on the editorial
boards of Demography, Journal of Gerontology:
Social Sciences, Journal of Marriage and the Family,
Journal of Population Aging, Population Research
and Policy Review, and Demographic Research,
and as director of the Center for Aging and
Policy Studies at Syracuse University. At pre-
sent he is a co-investigator for the National
Health and Aging Trends Study (NHATS), a
longitudinal study that collects data on a sam-
ple of Medicare beneficiaries ages 65 and older.
 List of Contributors
Carol S. Aneshensel Department of Community
Health Sciences, University of California, Los
Angeles, Los Angeles, CA, USA
Jacqueline L. Angel The University of Texas at
Austin, Austin, TX, USA
Daniel Béland Johnson-Shoyama Graduate School
of Public Policy, University of Saskatchewan,
Saskatoon, Saskatchewan, Canada
Rebecca Benson The University of Texas at Austin,
Austin, TX, USA
Yoav Ben-Shlomo School of Social and Community
Medicine, University of Bristol, Bristol, UK
Suzanne M. Bianchi Department of Sociology
and California Center for Population Research,
University of California-Los Angeles, Los Angeles,
CA, USA
Lisa M. Brown Palo Alto University, Palo Alto, CA,
USA
Kevin E. Cahill Sloan Center on Aging & Work
at Boston College, Chestnut Hill, MA, USA
Deborah Carr Department of Sociology and
Institute for Health, Health Care Policy and Aging
Research, Rutgers University, New Brunswick, NJ,
USA
Benjamin Cornwell Department of Sociology,
Cornell University, Ithaca, NY, USA
Eileen M. Crimmins Davis School of Gerontology,
University of Southern California, Los Angeles,
CA, USA
Kenneth F. Ferraro Center on Aging and the
Life Course, Purdue University, West Lafayette,
IN, USA
Kathryn A. Frahm School of Aging Studies,
University of South Florida, Tampa, FL, USA
Vicki A. Freedman Institute for Social Research,
University of Michigan, Ann Arbor, MI, USA
xvii
Joseph E. Gaugler Center on Aging, School of
Nursing, University of Minnesota-Twin Cities,
Minneapolis, MN, USA
Linda K. George Center for the Study of Aging and
Human Development, Duke University, Durham,
NC, USA
Michael D. Giandrea US Bureau of Labor Statistics,
Office of Productivity and Technology, Washington,
DC, USA
Megan Gilligan Human Development and Family
Studies, Iowa State University, Ames, IA, USA
Emily A. Greenfield School of Social Work Affiliate
of the Institute for Health, Health Care Policy, &
Aging Research Rutgers, The State University of
New Jersey, New Brunswick, NJ, USA
Zoya Gubernskaya Department of Sociology,
University at Albany, State University of New
York, Albany, NY, USA
Frederick Harig Department of Community Health
Sciences, University of California, Los Angeles, Los
Angeles, CA, USA
R. David Hayward School of Public Health,
University of Michigan, Ann Arbor, MI, USA
Robert B. Hudson School of Social Work, Boston
University, Boston, MA, USA
Neal Krause School of Public Health, University of
Michigan, Ann Arbor, MI, USA
Diana Kuh MRC Unit for Lifelong Health and
Ageing and MRC National Survey of Health
and Development, University College London,
London, UK
Andrew S. London Department of Sociology,
Aging Studies Institute, Center for Policy Research,
and Institute for Veterans and Military Families,
Syracuse University, Syracuse, NY, USA
xviii List of Contributors
Elizabeth Luth Department of Sociology and
Institute for Health, Health Care Policy and Aging
Research, Rutgers University, New Brunswick, NJ,
USA
Scott M. Lynch Department of Sociology, Duke
University, Durham, NC, USA
Marilyn Moon American Institutes for Research,
Washington, DC, USA
Nancy Morrow-Howell George Warren Brown
School of Social Work, Washington University,
St. Louis, MO, USA
Stipica Mudrazija University of Southern
California, Los Angeles, CA, USA
Karl Pillemer Department of Human Development,
Cornell University, Ithaca, NY, USA
Amélie Quesnel-Vallée Department of Epide-
miology, Biostatistics, and Occupational Health;
Department of Sociology; Centre for Population
Dynamics, McGill University, Montréal, QC,
Canada
Joseph F. Quinn Department of Economics, Boston
College, Chestnut Hill, MA, USA
Sandra Reiter-Campeau Faculty of Medicine,
Université de Montréal, Montréal, QC, Canada
Karen A. Roberto Center for Gerontology and The
Institute for Society, Culture and Environment,
Virginia Tech, Blacksburg, VA, USA
Liana C. Sayer Sociology Department and
Maryland Population Research Center, University
of Maryland, College Park, MD, USA
Markus H. Schafer Department of Sociology,
University of Toronto, Toronto, ON, Canada
J. Jill Suitor Department of Sociology, Center on
Aging and the Life Course, Purdue University,
West Lafayette, IN, USA
Miles G. Taylor Pepper Institute on Aging and
Public Policy, Florida State University, Tallahassee,
FL, USA
Judith Treas Department of Sociology, Center for
Demographic & Social Analysis, University of
California, Irvine, Irvine, CA, USA
Sarinnapha M. Vasunilashorn Beth Israel
Deaconess Medical Center, Harvard Medical
School, Brookline, MA, USA
Richard G. Wight Department of Community
Health Sciences, University of California, Los
Angeles, Los Angeles, CA, USA
John B. Williamson Department of Sociology,
Boston College, Chestnut Hill, MA, USA
Andrea Willson Department of Sociology, Social
Science Centre, The University of Western Ontario,
London, ON, Canada
Janet M. Wilmoth Department of Sociology,
Aging Studies Institute, Center for Policy Research,
and Institute for Veterans and Military Families,
Syracuse University, Syracuse, NY, USA
Douglas Wolf Aging Studies Institute, Syracuse
University, Syracuse, NY, USA
 C H A P T E R

1
Aging and the Social Sciences:
Progress and Prospects
Linda K. George1 and Kenneth F. Ferraro2
1
Center for the Study of Aging and Human Development, Duke University, Durham, NC, USA
2
Center on Aging and the Life Course, Purdue University, West Lafayette, IN, USA

O U T L I N E

Theoretical and Conceptual Developments 4 Emerging Themes in Aging Research 9

Cumulative Advantage/Disadvantage Increased Attention to Cohort Analysis 9
Theory 5 The Effects of Social and Economic
Cumulative Inequality Theory 6 Disruptions on Aging 10
Gradual, Incremental Cultural Change 12
Methods and Data 6
Data Developments 6 What Aging Research Contributes to
Statistical Sophistication 8 the Social Sciences: The Big Picture 16
References 20

“The only constant is change.” This quote,
heard frequently today, is attributed to
Heraclitis of Ephesus, a Greek philosopher who
lived from approximately 535 BC to 475 BC.
One wonders what it was about life at about
500 years before the birth of Christ that led
Heraclitis to that conclusion. Was the pace of
social change so rapid that it led to this infer-
ence? Was it the rhythms of nature that trig-
gered this observation? Or, perhaps, was it the
flow of everyday life that convinced Heraclitis
that he was not the same person today that he
was yesterday or would be tomorrow? At any
rate, it is clear that humans have long been
aware that change is ubiquitous.
Scholars of aging arguably devote more
of their intellectual activity to studying and
understanding change than those in any other
field. Aging itself is change – some of it eas-
ily observable; some of it occurring at the cel-
lular and molecular levels and requiring years
or even decades to be measurable and the

L.K. George & K.F. Ferraro (Eds) DOI: http://dx.doi.org/10.1016/B978-0-12-417235-7.00001-9

Handbook of Aging and the Social Sciences, Eighth edition. 3 © 2016
2015 Elsevier Inc. All rights reserved.
4 1. Aging and the Social Sciences: Progress and Prospects
fodder for scientific inquiry. Aging individu-
als are embedded in macro-, meso-, and micro-
environments in which change also is omni-
present. And a fundamental assumption of the
social sciences is that those constantly changing
environments affect the ways in which people
age. Thinking seriously about the complex-
ity of change leads to the conclusion that con-
siderable audacity and fortitude are required
to study aging and lay claim to understand-
ing or explaining its dynamics. And yet that is
precisely what aging researchers do.
Audacity and fortitude also are required
in any attempt to summarize the state-of-the-
science with regard to social science aging
research. Yet, the goal of this chapter is to pro-
vide a partial summary of the state-of-the-field.
More specifically, the purpose of this chapter
is to review, in broad brush, recent theoreti-
cal, methodological, and selected substantive
developments in aging research in the social
sciences. We used the approximate dates of
1996–2015 as the focus of this review. This is an
arbitrary window of time, but we believe that it
is a reasonable temporal scope for summarizing
current significant issues in aging research.
The chapter is organized into four sections.
The first section reviews theoretical and con-
ceptual developments in the field; the second
provides an update of advances in data, meth-
ods, and statistical techniques that have become
central in aging research. The third and long-
est section reviews three thematic topics that
have emerged as cutting-edge issues in social
research on aging and the life course. In the
concluding section, we briefly comment upon
the broader issue of how aging research con-
tributes to major issues and assumptions in the
social sciences.
Considerable subjectivity was employed
in developing this chapter, especially in iden-
tifying emerging substantive issues. It is pos-
sible to produce a veritable “laundry list” of
recent and emerging themes in aging research.
We selected only three, with the unifying
I. THEORY AND METHODS
theme being “big picture” influences on aging.
Undoubtedly, other scholars would have
selected other developments in the field. Other
scholars may disagree with our labeling these
research topics as “recent” or “new.” This is
inevitable. Nonetheless, we hope that this
chapter captures much of the theoretical, meth-
odological, and substantive “action” of the past
two decades in social science research on aging.
THEORETICAL AND CONCEPTUAL
DEVELOPMENTS
Arguably, the biggest “story” in aging
research for the past several decades has been
developments in, advances in, and the greatly
increased volume of research that incorporates
the life course perspective. The life course per-
spective is not a theory per se; rather, it is a set
of five principles that contextualize individual
lives in a number of ways (Elder, Johnson, &
Crosnoe, 2003). The principle of life span devel-
opment states that human development and
aging are lifelong processes – that patterns
observable over time link distal and proximal
events and experiences across the life course.
The principle of agency focuses on the ways that
individuals construct their own lives by the
choices they make within the opportunities and
constraints of their environments. The prin-
ciple of time and place states that human lives
develop in historical and geographic contexts
that strongly affect the opportunities and con-
straints available. The principle of timing states
that the effects of events and other experiences
vary, depending on the individuals’ ages or
life stages. Finally, the principle of linked lives
focuses on the social networks and relation-
ships that also structure the opportunities and
constraints available to individuals. Although
temporality, especially biographical and histori-
cal time, is widely viewed as the hallmark of
the life course perspective, context is its major
foundation.
 Theoretical and Conceptual Developments
Questions arise at times about the rela-
tionships between life course research and
gerontological research, especially whether ger-
ontological theory and research will be or have
been eclipsed by the life course perspective. In
order to document its strengths, life course schol-
ars sometimes critique gerontological research
that does not incorporate one or more princi-
ples of the life course perspective. Nonetheless,
multiple research questions appropriately focus
on late life and need not incorporate explicit
life course principles (e.g., studies of variability
within the older population, studies that examine
the effects of interventions or policies on older
adults). Virtually all studies of older adults, how-
ever, should recognize that research participants
are members of cohorts measured at specific his-
torical times – and therefore it cannot be assumed
that the findings will generalize to other cohorts
and historical contexts.
Because the life course perspective is not a
theory, its principles need to be incorporated
and tested in conjunction with established theo-
ries. This cross-fertilization of life course prin-
ciples with mainstream social science theories
has expanded rapidly. Several examples provide
illustrations of this cross-fertilization but do not
comprise a comprehensive inventory of relevant
topics. Life course principles of life span devel-
opment, agency, timing, and linked lives have
been incorporated in stress process theory. This
research has provided important knowledge
about the persistent effects of early severe trauma
on the mental health and well-being of older
adults (e.g., Danese & McEwen, 2012; Shaw &
Krause, 2002). Another profitable area of research
focuses on the ways in which educational
achievements and occupational choices in young
adulthood affect financial security in later life
(Cahill, Giandrea, & Quinn, 2006). And perhaps
no topic has been more thoroughly investigated
than the effects of childhood conditions (trau-
matic events, persistent poverty, and poor health)
on morbidity and mortality in middle and late
life (for a review, see Chapter 5, this volume).
I. THEORY AND METHODS
5
Cumulative Advantage/Disadvantage
Theory
If there has been a bona fide theory based on
the life course perspective, specifically the prin-
ciple of life span development, it is cumula-
tive advantage/disadvantage theory (CA/DT).
The major hypothesis of CA/DT was devel-
oped by Robert Merton (1968), who called it the
Matthew Effect, based on a verse in the Gospel
of Matthew (13:12). The Matthew Effect refers to
a pattern in which those who begin with advan-
tage accumulate more advantage over time and
those who begin with disadvantage become
more disadvantaged over time (Dannefer, 1987;
O’Rand, 1996). The result is ever-widening dif-
ferences between the advantaged and disadvan-
taged. This simple theory has been supported
in many domains of life (Rigney, 2010). When
applied to trajectories of advantage and disad-
vantage over long periods of time, CA/DT is
obviously compatible with the life course per-
spective. And research on life course patterns
often finds support for CA/DT.
Nonetheless, as Rigney’s review of research
(2010) documents, CA/DT does not always
apply. A key example is late life health.
Individuals who begin adulthood in excel-
lent health do not become healthier over time
with physical and mental well-being peak-
ing at the end of life. These early advantaged
individuals are likely, on average, to have bet-
ter health than persons who entered adulthood
with poor health or experienced health prob-
lems as young adults. But their trajectory of
health is not monotonic improvement over the
life course. As a consequence, aging research-
ers often label their theoretical foundation as
cumulative disadvantage theory.
There is increasing and appropriate rec-
ognition that CA/DT is oversimplified. CA/
DT posits two trajectories when, in fact, phe-
nomena of interest are typically character-
ized by multiple trajectories. Depending on
the phenomenon under investigation, two of
6 1. Aging and the Social Sciences: Progress and Prospects
the trajectories may resemble straightforward
cumulative advantage and disadvantage, but
there will be other meaningful trajectories as
well. Despite its shortcomings as a universally
applicable theory, CA/DT has been tremen-
dously useful in emphasizing the importance
of early social status and cohort membership on
life course trajectories and has generated a large
volume of important research.
Cumulative Inequality Theory
To capture more of the contingencies
involved in how status and life experience
influence the aging process, cumulative ine-
quality theory (CIT) integrates elements from
multiple conceptual approaches, most nota-
bly but not limited to: life course perspective
(Elder, 1998), CA/DT, and stress process theory
(Pearlin, Schieman, Fazio, & Meersman, 2005).
Formulated in five axioms and 19 proposi-
tions, the theory builds upon but is distinctive
from prior approaches in several ways (Ferraro,
Shippee, & Schafer, 2009).
First, CIT prioritizes perceptions of the aging
experience while juxtaposing the systemic
generation of inequality with human agency
(Schafer, Ferraro, & Mustillo, 2011). Social struc-
tures constrain choices, and both influence
aging. Second, rather than assume inexorable
effects of early disadvantage, CIT specifies that
exposures to risks and resources also shape
life trajectories. Indeed, the timely activation
of resources may nullify or compensate for the
effects of negative exposures. Third, the influ-
ence of family lineage is emphasized in the
theory, noting the roles that genes and environ-
ment have on status differentiation. It calls for
more attention to the intergenerational trans-
mission of risks and resources. Finally, the the-
ory integrates selection processes into the study
of inequality. Given that inequality itself is an
engine of mortality and other forms of nonran-
dom selection, failure to consider selection pro-
cesses may lead to misrepresenting inequality
I. THEORY AND METHODS
in later life (i.e., typically underestimating
inequality).
Several longitudinal studies testing elements
of the theory reveal the importance of inter-
generational influences on health outcomes –
ranging from adult depression (Goosby, 2013)
to myocardial infarction (Morton, Mustillo, &
Ferraro, 2014) – but also how those health risks
may be amplified or diminished by resources
and lifestyle choices. Indeed, in a study of racial
disparities in health, Kail and Taylor (2014,
p. 805) reported that “mobilizing financial
resources into insurance coverage is protective”
against functional limitations. Other studies
testing elements of the theory reveal that both
psychosocial resources and how one interprets
life experiences are consequential to status
attainment and health (Wickrama & O’Neal,
2013; Wilkinson, Shippee, & Ferraro, 2012).
The emerging picture from empirical tests of
the theory is that there are powerful systemic
influences on exposure to risk, opportunity,
and inequality but that these influences on
well-being in later life are often contingent on
how the exposures are interpreted and whether
resources can be activated to address them.
METHODS AND DATA
Data Developments
One of the greatest boons to aging research
has been the proliferation of longitudinal
data sets covering long periods of time. The
increased availability of high-quality data sets
in the past two decades or so has transformed
aging research. Space limitations preclude a
description of all the valuable longitudinal data
sets available. Several major differences in data
sources, however, will be reviewed. With few
exceptions, we focus on data sets with three
or more times of measurement, which is the
minimum number of data points for modeling
trajectories.
 Methods and Data
Age Ranges and Times of Measurement. Some
studies were designed to focus on the dynamics
of late life; others followed samples from young
adulthood to late life; and still others recruit age-
heterogeneous samples at baseline and follow
them for significant periods of time. The Health
and Retirement Study (HRS), for example, was
originally designed to follow individuals from
late middle-age until very old age or death.
Additional cohorts have been added during the
past two decades, however, resulting in some
cohorts entering the study relatively early in
adulthood (Institute for Social Research, 2014a).
The Wisconsin Longitudinal Study (WLS), in
contrast, recruited participants during their
senior year of high school in 1957 and contin-
ues to collect data. Last surveyed in 2011, study
participants were approximately 72 years old
(University of Wisconsin, 2014). The Americans
Changing Lives (ACL) study began in 1986 and
recruited a sample of adults age 25 and older
(Institute for Social Research, 2014b).
The intervals between measurements also
vary across data sources. The HRS began data
collection of its original cohort in 1992 and
interviews participants every 2 years. The WLS
includes seven times of measurement to date
and the intervals between them range from 7 to
17 years. The ACL has four times of measure-
ment at intervals ranging from 8 to 10 years.
Some studies also oversample specific sub-
groups of interest, which can enhance oppor-
tunities for analyses based on middle and late
life. The ACL, for example, oversampled both
African Americans and adults age 60 and older.
Academic versus Government Sponsorship.
Virtually all large-scale longitudinal stud-
ies are funded by government agencies. The
distinction here is between studies that were
funded via grants to academic institutions
and studies carried out by government agen-
cies. The HRS, WLS, and ACL are examples of
studies designed and conducted by universi-
ties and funded by federal grants. Examples of
government-conducted longitudinal studies
I. THEORY AND METHODS
7
include the Second Longitudinal Study of Aging
(LSOA-II) (CDC, 2014b) and the Medicare
Current Beneficiary Survey (MCBS) (CMS,
2014). Virtually all federally funded longitudi-
nal studies focus on health. The data sets also
include, to varying degrees, information about
social, economic, and psychological charac-
teristics of study participants. In general, data
sources that are funded by grants to academic
institutions include richer social science content
than those conducted by government agencies.
National versus Regional/Local Samples. All
the longitudinal data sources mentioned above
were designed to be based on nationally repre-
sentative samples. Data sets based on regional
or local samples also offer important research
opportunities. The Established Populations for
Epidemiologic Studies of the Elderly (EPESE)
is an example of data collected at the local or
regional level that has made important contri-
butions to aging research (ICPSR, 2014). The
EPESE Program included local/regional data
collected from adults age 65 and older at four
sites: East Boston, MA, USA; New Haven, CT,
USA; Iowa and Washington Counties, IA, USA;
and central North Carolina, USA. The research
design included four in-person interviews over
a 10-year period, with brief telephone inter-
views administered in the years between the
in-person interviews. A common set of sur-
vey questions were asked at each site, supple-
mented with site-specific interview content.
A few years later, the Hispanic EPESE was
added, with the same basic research design
(Sociometrics, 2014). The sample included
Hispanic older adults, both native and for-
eign-born, living in five southwestern states.
Hundreds of scientific articles have been pub-
lished using data from one or more EPESE sites,
testifying to the value of non-national samples.
Other longitudinal studies based on local/
regional samples yielded important findings as
well (e.g., Alameda County Study).
Merging Survey and Administrative Data.
Another trend during the past two decades has
8 1. Aging and the Social Sciences: Progress and Prospects
been merging survey data from older adults
with federal and, occasionally, state adminis-
trative data. Merging data from these sources
greatly expand the research questions that can
be addressed. The most frequently used admin-
istrative data base is the National Death Index
(NDI), which includes data from death certifi-
cates in all 50 US states. Investigators routinely
use the NDI to determine study participants’
mortality status and date of death and can use
the NDI Plus for cause-of-death data. Although
not every name submitted to the NDI can be
definitively matched, the overall accuracy of
the NDI is excellent (e.g., Lash & Silliman,
2001). The other major administrative data set
often merged with longitudinal survey data is
Medicare claims data, which include detailed
information about the use and costs of inpatient
and outpatient health care (CDC, 2014a). Most
major longitudinal studies use the NDI and
many (e.g., the HRS and EPESE) also obtain
Medicare claims data.
Biomarker, Genetic, and Physical Performance
Data. Another important trend in longitudinal
studies of aging is the collection of biological
and physical performance data. Advances in
data collection methods now allow biological
data to be easily obtained via non- or minimally
invasive methods, including buccal swabs for
DNA and urine and saliva samples for selected
biomarkers. Highly trained interviewers often
collect blood samples; measure height, weight,
waist circumference, and blood pressure; and/
or administer physical performance tests. To
date, the genetic and biomarker data typically
have been collected at a single point in time. An
exception is the National Social Life, Health, and
Aging Project (NSHAP; NORC, 2014). To date,
NSHAP has collected two waves of data and
biomeasures were collected at both test dates,
permitting longitudinal analyses spanning about
5 years. This trend will undoubtedly continue
in other longitudinal studies, resulting in multi-
ple waves of biological and genetic data that are
linked to rich survey and administrative data.
I. THEORY AND METHODS
Non-US Databases. An important and rela-
tively new resource for research on aging is the
availability of large-scale longitudinal studies
conducted in countries other than the United
States. Especially rich data are available from
Europe and the Pacific Rim. European exam-
ples include the English Longitudinal Study
of Ageing (ELSA) and the Survey of Health,
Ageing, and Retirement in Europe (SHARE).
The ELSA began in 2002, conducts interviews
biannually, and has completed six waves of
data, with a seventh in progress (ELSA, 2014).
SHARE also interviews participants biannu-
ally; it began in 2004 and five waves are com-
plete. SHARE’s baseline sample included older
adults from 11 countries. By Wave 5, 15 coun-
tries had participated (SHARE, 2014). Both the
ELSA and SHARE are modeled on the HRS
in design and content. Two studies from the
Pacific Rim are especially rich in times of meas-
urement. The Australian Longitudinal Study
of Aging (ALSA) began in 1992 and completed
12 times of measurement (Luszcz et al., 2014).
The Chinese Longitudinal Healthy Longevity
Study (CLHLS) has conducted six waves to
date (1998, 2000, 2002, 2005, 2008–2009, and
2014) and focuses on the oldest-old (Chinese
Longitudinal Healthy Longevity Survey, 2014).
All four of these data sets include biomarker
and physical performance tests at one or more
times of measurement.
Statistical Sophistication
The statistical armamentarium for analysis
of three or more waves of longitudinal data
has grown in volume and sophistication over
the past two decades. The concept of trajec-
tory – a distinct temporal pattern observed over
multiple times of measurement – has become a
staple of aging research. Some studies include
multiple times of measurement over a rela-
tively short period of time, permitting estima-
tion of fine-grained trajectories (e.g., patterns
of onset, stability, and recovery of disability).
 Emerging Themes in Aging Research
Other studies examine long-term trajectories
of stability and change, such as those hypoth-
esized in CA/DT theory. A variety of statistical
techniques can be used to model trajectories, as
reviewed in Chapter 2 of this volume.
Structural equation modeling remains an
important analytic tool for analysis of longitu-
dinal data. Its unique characteristics include the
option of estimating reciprocal relationships
between variables over time, production of dis-
tinct measurement and explanatory models,
the ability to correct for unreliability of meas-
urement, and estimation of direct and indirect
effects of explanatory variables on the outcome
of interest.
Multilevel modeling is now frequently used
to jointly examine the effects of individual-level
and aggregate contextual variables on out-
comes of interest. These models have proven
especially useful in studies examining the
effects of environmental characteristics on out-
comes of interest. In many of these studies the
research question focuses on whether environ-
mental characteristics are related to outcomes
of interest after the effects of individual charac-
teristics are statistically controlled (e.g., is liv-
ing in a high-poverty neighborhood associated
with mortality after individual poverty status is
taken into account?). It also is possible to esti-
mate interactions between individual-level and
contextual variables. In aging research, most
multilevel studies examine the effects of neigh-
borhood characteristics on health and quality of
life. Chapter 16 reviews this research.
EMERGING THEMES IN AGING
RESEARCH
In this section, three topical areas of aging
research are briefly reviewed. Although there
have been notable advances on dozens of
research topics, we focus on emerging themes
not covered in detail in one of the chapters in
this volume. In addition, we selected three
I. THEORY AND METHODS
9
research themes that focus on the effects of
macro-level characteristics of social structure
that have potentially important implications
for aging and/or older adults. Of course, some
of the topics are mentioned in the chapters that
follow, but we think these emerging themes
nonetheless merit additional consideration.
Increased Attention to Cohort Analysis
The term “cohort,” of course, refers to a set
of people who experience the same event at
the same time. Although any event can define
a cohort, social scientists typically use the
term to refer to birth cohorts – to people born
at the same or approximately the same time –
and that is how the term is used here. Norman
Ryder’s classic article (1965) was the first sys-
tematic consideration of cohort as a social,
rather than simply actuarial, phenomenon. For
Ryder, cohort differences are evidence of social
change. In his words, “cohorts do not cause
change; they permit it. If change does occur, it
differentiates cohorts from one another, and
the comparison of their careers becomes a way
to study change” (p. 844). Ryder hypothesized
that four types of circumstances were most
likely to differentiate cohorts. First, cohort
size is important – very large and very small
cohorts experience different structural oppor-
tunities and constraints from each other and
from cohorts of more usual sizes. Second, major
social and historical events cause significant
differences across cohorts. Ryder posited that
societal disruptions had the strongest and most
lasting effects on cohorts who were adolescents
or young adults at the time of the events. Thus,
although all cohorts experience the disruptive
event, it is the young who are permanently
changed by it (a line of reasoning compatible
with the life course principle of timing). Third,
wide variations in the influx of migrants to a
society can change the character of a cohort
and differentiate it from those before and after
it. A variant of this, with the same result, is
10 1. Aging and the Social Sciences: Progress and Prospects
widespread migration from rural to urban
areas. Fourth, Ryder believed that technologi-
cal innovation was a primary trigger for cohort
differentiation – and argued that technological
advances were most targeted at and welcomed
by adolescents and young adults.
To support the claim that cohort analysis has
become increasingly popular in aging research,
we conducted an informal analysis of journal
articles published between 1970 and the first
half of 2014. We used the Web of Science core
collection and narrowed the search to journal
articles categorized as falling under at least
one of three topics: gerontology, geriatrics, and
sociology (aging was not a topic offered). Using
these criteria, Web of Science identified 7 635
articles in which the word “cohort” appeared
in the title or abstract. Examining the distri-
bution of these articles by date of publication
is illuminating. Less than half a percent of the
titles appeared between 1970 and 1979 and
slightly more than 1% were published between
1980 and 1989. About 16.5% were published in
the 1990s and approximately 39.5% were pub-
lished between 2000 and 2009. In the interval
between 2010 and June 30, 2014, 41.8% of the
articles were published. Even we were sur-
prised to find that the largest percentage of
articles appeared in the most recent four and a
half years. There are obvious limitations to this
analysis (e.g., we cannot know whether inves-
tigators simply began to use the term “cohort”
more frequently in article titles and abstracts).
Nonetheless, if the trend observed in this
highly unsophisticated analysis is generally
accurate, explicit attention to cohorts is increas-
ingly common in research on aging.
Most studies of cohort differences in later life
examine health outcomes. Examples include
cohort differences in the relationship between
education and health (Lynch, 2006), in depres-
sion during late life (Yang, 2007), in the extent
to which segregated southern schools partially
account for Black–White health disparities in
late life (Frisvold & Golberstein, 2013), and in the
I. THEORY AND METHODS
relationship between women’s labor market par-
ticipation and health (Pavalko, Gong, & Long,
2007). Cohort analysis is valuable for outcomes
other than health as well, such as the discrep-
ancy between chronological and “felt” age (Choi,
DiNitto, & Kim, 2014) and patterns of gradual
retirement (Giandrea, Cahill, & Quinn, 2009).
Although there are significant exceptions,
few studies either empirically test or even
speculate about the specific social changes that
trigger cohort differences. As a result, cohort
analysis often appears simply descriptive. But
the best cohort studies are those that not only
describe cohort differences, but also attempt
to explain the reasons for them. Frisvold and
Golberstein’s (2013) study of how segregated
schools and their subsequent demise are asso-
ciated with cohort differences in race dispari-
ties in health is an example of a study that
aims to explain cohort differences and not sim-
ply describe them. The increased attention to
cohort differences is an important contribution
to aging and life course research. The contribu-
tions of cohort analysis could be even greater
if this research routinely addressed potential
explanations for cohort differences.
The Effects of Social and Economic
Disruptions on Aging
Social and economic disruptions have long
been of interest in the social sciences. Major
shocks to social structure provide a rare oppor-
tunity to not only study the consequences of
and responses to significant disruptions, but
also to highlight social arrangements before
the disruptions that were not fully understood.
Large-scale events typically receive substan-
tial attention by both scientists and the general
public. Much less attention has been paid to the
differential implications of these disruptions for
population subgroups, including older adults.
Recently, however, the implications of large-
scale social and economic changes for older
adults have received increased attention.
 Emerging Themes in Aging Research
The Great Recession
Perhaps no social and economic disrup-
tion in the past quarter century generated
more scholarly and public attention than the
Great Recession that began in 2008 and contin-
ues to shape the lives of the citizens of many
countries, including the United States. No
age group has been unaffected by the conse-
quences of this major disruption, but there are
reasons to believe that older adults are suf-
fering at least as much as their younger coun-
terparts. As a New York Times headline stated,
“In Hard Economy for All Ages, Older Isn’t
Better…. It’s Brutal” (New York Times, 2013). A
growing body of research addresses the effects
of this cataclysm on older adults. Several top-
ics on the consequences of the Great Recession
have received empirical attention. First and of
obvious concern is whether the increased rates
of unemployment in the population at large
affected older adults. There appears to be both
good and bad news on that front. On the posi-
tive side, older adults (variously defined as
those age 55, 60, and 65 and older) have lower
rates of unemployment than any age group –
indeed, rates of unemployment are strongly
and inversely related to age (US Bureau of
Labor Statistics, 2013). On the other hand,
between 2008 and 2010, the unemployment rate
of older adults roughly quadrupled and has
declined little since then. In addition, the length
of time between job loss and reemployment is
significantly longer for older adults than their
younger counterparts and many older adults
opt out of job seeking after a relatively short
period of unemployment. A second important
issue is whether the Great Recession altered the
plans of those nearing retirement. It is too early
to know definitively the extent to which per-
sons at or nearing conventional retirement ages
are postponing retirement, but there is strong
evidence that these individuals report that
they plan to retire later than they had intended
prior to the Great Recession (e.g., McFall, 2011).
Chapter 14 describes the impact of long-term
I. THEORY AND METHODS
11
macroeconomic trends on the labor force par-
ticipation of older adults and reviews in detail
the economic and labor force consequences of
the Great Recession.
The consequences of the Great Recession
are not limited to purely economic issues. A
small base of research on the mental health
consequences of the Great Recession is emerg-
ing, almost none of which focuses on older
adults. Cagney and colleagues, however,
report that increases in neighborhood foreclo-
sures are associated with increases in depres-
sive symptoms among older adults in NSHAP,
controlling on demographic characteristics,
socioeconomic status (SES), and physical func-
tioning (Cagney, Browning, Iveniuk, & English,
2014). The spillover from the Great Recession
also may affect the family lives of older adults.
Livingston and Parker (2010) report that
between 2007 and 2009 the number of older
adults with custodial care of grandchildren
increased by nearly 20%, although these grand-
parents are a small proportion of the older
population.
Hurricane Katrina and Other Disasters
Natural disasters are another form of dis-
ruption and have received increased attention
in aging research. According to the Centers for
Disease Control and Prevention, “In Louisiana
during Hurricane Katrina, roughly 71% of the
victims were older than 60 and 47% were over
the age of 75” (CDC, 2013, p. 1). Given these
large percentages, it would be logical to assume
that older victims received a significant por-
tion of the publicity, aid, and health monitor-
ing in the aftermath of Katrina. There is little
evidence, however, to support that assumption.
Public discourse about Katrina gave little atten-
tion to age groups other than displaced chil-
dren. No local or regional disaster plans
included procedures for transferring residents
out of nursing homes – and residents of those
homes fared especially badly (CDC, 2013).
Some research examined the effects of Katrina
12 1. Aging and the Social Sciences: Progress and Prospects
on mental health, the coping strategies used by
older victims, and the ways that family support
did or did not ease the trauma of older victims
(e.g., Cherry et al., 2010; Henderson, Roberto, &
Kamo, 2010; Kamo, Henderson, & Roberto,
2011; and for a review of research on the effects
of disasters on older adults, see Chapter 18).
The examples above illustrate the increased
attention paid to events that threaten preexist-
ing structural arrangements and their conse-
quences for older adults. We applaud this trend
and encourage broader attention to major social
disruptions – for the United States as a whole,
such as the Great Recession, and for specific
regions or cities, such as Hurricane Katrina.
Gradual, Incremental Cultural Change
Not all consequential social changes take
the form of sudden social disruptions; gradual
and/or incremental cultural changes also can
have important implications for older adults.
In fact, social scientists are probably more
likely to miss or understudy the effects of more
gradual social change than sudden disruptions.
The history of aging research reveals numer-
ous gradual changes, the significance of which
was not recognized until a critical mass of older
adults was affected. Family care for impaired
older adults has occurred at least since the
beginning of recorded history. Nonetheless, it
was not until the vast majority of adults lived
until late life and gradual social changes (e.g.,
women’s labor force participation, intergen-
erational geographic mobility) made family
caregiving difficult for a significant proportion
of older spouses and adult children that the
concept of caregiver burden became a topic of
scientific interest. Indeed, the term “caregiver”
did not appear in public discourse until the
1980s. Similarly, the transition from defined
benefit to defined contribution pension plans
was underway for a decade or so before the
implications of this transition for the financial
security of retired adults became an issue in
I. THEORY AND METHODS
aging research. A gradual societal change that
has received significant recent attention is the
health effects of income inequality.
Income Inequality and Health
Income inequality refers to the size of the
gap between the richest and poorest members
of society – the wider the gap, the greater the
inequality. Although there are gaps between the
bottom and top of the income ladder in all soci-
eties, the size of the gap varies widely across
countries and over time. The United States has
higher income inequality than any other devel-
oped country in the world and the gap between
the richest and the poorest has widened sub-
stantially over a relatively short period of time
in the United States, with no apparent end in
sight (The Economist, 2013). The implications
of income inequality for economic growth,
social cohesion, and health are now “hot
topics” in the social sciences, politics, and pub-
lic discourse.
Conceptual and Methodological Issues. The out-
comes of income inequality for which there has
been substantial research include rates of labor
force participation, workers’ earnings, eco-
nomic growth, general trust, civic engagement,
life expectancy, and other health indicators. For
decades, most economists argued that the net
effects of economic inequality (both income and
wealth inequality) are beneficial. Mainstream
economic theory posited that income inequal-
ity motivates workers to increase their job skills
and productivity in order to climb the economic
ladder. In turn, more productive workers not
only increase their own incomes, but also spur
economic growth for the society as a whole. In
contrast, Marxian theorists and other social sci-
entists argued that because income inequality
concentrates capital in their control, the very
rich are motivated to cut labor costs as much
as possible. As a result, increasing income ine-
quality depresses workers’ wages and increases
unemployment. Quite recently, economists
have found, using data from the United States,
 Emerging Themes in Aging Research
that high levels of income inequality suppress
rather than facilitate economic development
(Stiglitz, 2012), necessitating that economic the-
ory recognize that there is a threshold beyond
which high income inequality has negative
effects on nations’ economic growth.
The potential link between income inequal-
ity and health is especially important for
older adults. Research examining the relation-
ships between income inequality and health
is voluminous and inconsistent. Some studies
report significant correlations between income
inequality and a variety of health outcomes.
Other studies, however, report nonsignificant
relationships.
Four aspects of research design may account
for much of the inconsistency in previous stud-
ies of income inequality and health. These
methodological issues largely result from theo-
retical ambiguity about the expected relation-
ships between income inequality and health.
First, is the selection of control variables. In
order to isolate the effects of income inequal-
ity on health, researchers have controlled on a
variety of other structural characteristics. The
most important of these is economic growth,
typically measured as Gross Domestic Product
(GDP). Strong and robust relationships between
economic growth and multiple indicators of
population health have been observed for dec-
ades (e.g., Easterlin, 1974). If income inequal-
ity is to continue to receive scientific attention,
it must be significantly related to health with
GDP taken into account. Research findings
demonstrate that relationships between income
inequality and multiple outcomes are substan-
tially reduced if GDP is controlled. In most
instances, coefficients for income inequality
remain statistically significant; in others, they
do not. Other frequently used control variables
include proportion of GDP spent on social and
health programs, political regime, and wom-
en’s rights. The general hypothesis underly-
ing inclusion of these characteristics is that
income inequality may be compensated for by
I. THEORY AND METHODS
13
government policies that redistribute resources
from the rich to the poor. In general, the more
control variables measuring economic growth
and welfare state benefits that are included
in analyses, the more that the net effects of
income inequality are reduced. Theoretically, it
is not clear whether these structural character-
istics should be conceptualized as control vari-
ables, included to test whether the relationships
between income inequality and health are spu-
rious, or as mediators of those relationships.
A second important decision in research
on income inequality is whether to model the
effects of income inequality on health (or other
outcomes) solely at the aggregate level or to
use multilevel models that incorporate both
individual and aggregate predictors of health.
Multilevel models are generally viewed as
superior to aggregate-only models because
the former allow researchers to determine if
income inequality is significantly related to
health once individual-level predictors are
taken into account. Most attention in multi-
level models has focused on whether coeffi-
cients for income equality are significant net
of individual-level income. Again, research
findings have been inconsistent. Another, less
recognized advantage of multilevel models is
the ability to test whether income inequality
interacts with individual-level characteristics to
exacerbate or reduce disparities across popula-
tion subgroups. Although arguments favoring
multilevel models are strong, the underlying
issue is theoretical. Do we expect high levels of
income inequality to harm individual health,
population health, or both? It is possible that
high levels of income inequality harm popu-
lation health, but not individual-level health
(or vice versa). This could happen if elevated
income inequality has small effects on multiple
risk factors for mortality and morbidity and it is
the cumulative or aggregated strength of these
multiple small effects that links high income
inequality to poorer population health. Choice
of the level of the health outcome should be
14 1. Aging and the Social Sciences: Progress and Prospects
based on theoretical grounds. If the outcome
of interest is an indicator of population health,
aggregate-only models are appropriate.
A third decision that investigators face is the
choice of a unit of analysis. Most early studies
compared the relationships between income
inequality and potential outcomes using the
nation state as the unit of analysis. An increas-
ing number of studies, however, use units of
analysis that are smaller than countries, includ-
ing states or provinces, metropolitan areas, and
neighborhoods. The choice of a unit of analy-
sis is undoubtedly determined in part by data
availability (e.g., if county-level data are not
available for important variables, another unit
of analysis for which data are available must be
used). There are countervailing advantages and
disadvantages to country versus smaller units
of analysis.
The disadvantage of country-level variables
is that they include a great deal of unmeasured
heterogeneity both within and across coun-
tries. Economic conditions and public policies
often differ substantially across geographic
units within a country, and ignoring that vari-
ability may mask relationships that would
be observed with smaller units of analysis.
Unmeasured heterogeneity is undoubtedly
even greater across countries, with cultural
preferences and unique aspects of national his-
tory ignored. The advantages of country-level
analyses are that results presumably apply to
the population as a whole and many structural
characteristics are, by definition, nationally
homogeneous (e.g., GDP, political structure).
The advantage of using smaller units of analy-
sis in the same country is that some important
structural characteristics are national and, thus,
constants that need not be included in predic-
tive models, thus permitting fine-grained anal-
yses of other structural characteristics. This also
is the primary disadvantage of small units of
analysis – if the effects of income inequality dif-
fer primarily across countries but are homoge-
neous within countries, important information
I. THEORY AND METHODS
about the effects of income inequality will be
missed. Again, theory should provide guidance
about the most appropriate unit of analysis, but
there is little evidence of that in extant research.
Fourth and finally is the question of whether
geographic units are the optimal basis for study-
ing the effects of income inequality on health
and other outcomes. Although the vast majority
of income equality research is based on compar-
isons across geographic units, other strategies
are available. Zheng and George (2012) argue
that the best way to study income inequality is
to relate time-based trajectories of inequality to
health. Time-based analyses permit investiga-
tors to determine whether patterns of increas-
ing (or decreasing, although to our knowledge,
decreasing levels of income inequality have
never been observed) income inequality are
associated with worse health. Using time-based
trajectories, the temporal order between changes
in income inequality and changes in health and
the lag times between changes in income ine-
quality and changes in health can be observed.
Lag time is important, but theory to date has
not addressed this issue. Cross-sectional studies,
while plentiful, are of dubious value. It is highly
unlikely that increases in income inequality trig-
ger immediate changes in health. Because the
lag times between changes in income inequality
and changes in health are unknown, trajectory
analyses could shed light on that dynamic.
Income Inequality, Aging, and Health. The
vast majority of research in this field focuses
on the relationship between income inequal-
ity and mortality. Other studies examine self-
rated health, physical functioning/disability,
and mental health. Because older adults have
higher rates of death and disability, and are
more likely than their younger counterparts to
rate their health as fair or poor, studies based
on age-heterogeneous samples are clearly rel-
evant to the older population. Mental disorders
are less common in later life than in middle
or young adulthood, however, and are not
reviewed here. Space limitations preclude an
 Emerging Themes in Aging Research
extensive review of the voluminous literature
linking income inequality and health.
Mortality is the health outcome most fre-
quently related to income inequality. Most stud-
ies report a positive and significant relationship
between income inequality and mortality rates
at the aggregate level, especially in the United
States (e.g., Kaplan, Pamuk, Lynch, Cohen, &
Belfour, 1996 – a study of US states; Ross et al.,
2000 – a study of US states and Canadian prov-
inces, with a significant relationship observed
only in the United States). Some aggregate stud-
ies report that income inequality is associated
with mortality rates with median income and/
or poverty rates also controlled (e.g., Kawachi &
Kennedy, 1997 – a study of US states; Wilkinson
& Pickett, 2008 – a study of US states). Other
studies report no significant relationship
between income inequality and mortality at the
aggregate level (e.g., Beckfield, 2004 – a study
of 115 countries). As noted above, an impor-
tant issue in multilevel studies is whether this
relationship remains robust with individual-
level income statistically controlled. Results are
inconsistent, with some studies reporting that
the income inequality–mortality link remains
strong and significant (e.g., Lochner, Pamuk,
Maduc, Kennedy, & Kawachi, 2001 – a study
of US states; Shi & Starfield, 2001 – a study of
US metropolitan areas) and others reporting
that the association is rendered nonsignificant
(e.g., Fiscella & Franks, 1997 – a study of US
communities).
Because fewer studies examine health out-
comes other than mortality, it is difficult to
summarize the pattern of results. Studies of
the relationship between income inequality
and self-rated health report inconsistent rela-
tionships. This is especially true of multilevel
studies that include individual-level as well
as aggregate predictors. The single multilevel
study of physical functioning reported a sig-
nificant and positive relationship between
increasing income inequality and both physical
functioning and activity limitations (Zheng &
I. THEORY AND METHODS
15
George, 2012 – a temporal study of the US pop-
ulation between 1984 and 2007).
Few multilevel studies examined interac-
tions between income inequality and indi-
vidual-level predictors, but this appears to be
worth additional effort. Diez-Roux, Link, and
Northridge (2000) examined the relationship
between income inequality and cardiovascular
disease in a multilevel study. The unit of anal-
yses was US states. The direct effect of income
inequality was significant and in the expected
direction for women, but not men. The inter-
action between income inequality and individ-
ual-level income was strong and significant.
As expected, the combination of high income
inequality and low personal income predicted
cardiovascular disease. In contrast, Sturm and
Gresenz (2002), in a multilevel study of income
inequality and number of chronic physical ill-
nesses, tested the same interaction and it was
not significant. To evaluate whether rising
income inequality contributes to status-based
health disparities, Zheng and George (2012)
examined interactions between income ine-
quality and family income, education, employ-
ment, marital status, gender, and race-ethnicity.
Coefficients for the first four variables were sta-
tistically significant and in the predicted direc-
tion. That is, the protective effects of individual
income, education, employment, and marriage
strengthened as income inequality increased.
The interaction between income inequality and
gender also was significant, with rising income
inequality having stronger negative effects on
physical functioning for men than for women.
These results suggest that increasing income
quality may exacerbate SES- and gender-based
health disparities, although there was no evi-
dence of elevated risk for racial and ethnic
minorities once SES indicators were taken into
account.
Two relatively recent reviews reach simi-
lar conclusions to those referenced above. The
first is a literature review based on 168 pub-
lished analyses of the relationships between
16 1. Aging and the Social Sciences: Progress and Prospects
income inequality and multiple health out-
comes (Wilkinson & Pickett, 2006). The authors
conclude that 70% of the studies totally or par-
tially support the hypothesis that high income
inequality is associated with poorer health. They
also found that studies based on larger geo-
graphic units of analysis were more likely to
support the hypothesis that income inequality
is positively related to worse health than those
based on small areas. They suggest that studies
that sample small areas are “too small to reflect
the scale of social class differences in a society”
(p. 1768). The second review reports the results
of a meta-analysis based on 28 studies that
cumulatively included more than 61 million
respondents (Kondo et al., 2009). The health out-
comes examined were mortality and self-rated
health. The results suggested that income
inequality is significantly related to both mor-
tality and self-rated fair/poor health in the
expected direction, although the size of the coef-
ficient is modest. Kondo et al. also observed
significant relationships between specific study
characteristics and the odds of a negative
association of income inequality with health.
Specifically, results were stronger and larger in
studies characterized by higher levels of income
inequality, longer duration of follow-up, that
used data from 1990 and later, and explicitly
modeled time lags. In line with the conclusions
of both reviews, other studies have empirically
examined the effects of size of the geographic
unit of analysis, time lags, and income inequality
thresholds (Blakely, Kennedy, Glass, & Kawachi,
2000; Kondo, van Dam, Sembajwe, Kawachi, &
Yamagata, 2012), demonstrating that these study
characteristics strongly affect the size and signifi-
cance of relationships between income inequal-
ity and health outcomes.
Income inequality is only one example of a
wide range of patterns of gradual social change
that may affect population health as a whole
and the health of older adults in particular.
Examples of other gradual social trends that
I. THEORY AND METHODS
may be worth examining include the increas-
ing age at first marriage in the United States,
which has implications for the aging of those
cohorts and their parents (US Census Bureau,
2012), the steadily increasing proportion of the
population, including the older population,
living in near poverty (Heggeness & Hokayem,
2013), and the increasing income residential
segregation in the United States (Fry & Taylor,
2012). The effects of these cumulative small
social changes are easily overlooked. And yet
a core premise of social science research is that
the larger environment substantially deter-
mines the opportunities and constraints within
which societal members live their lives. We sug-
gest that these kinds of structural changes merit
closer scrutiny from social scientists.
WHAT AGING RESEARCH
CONTRIBUTES TO THE SOCIAL
SCIENCES: THE BIG PICTURE
Opportunities for innovative and rigorous
aging research have never been better. A prolif-
eration of data sets in which large numbers of
individuals are followed over long periods of
time became available in the past two decades.
The ability to merge survey data and other data
sources (including, but not limited to Medicare
files, Census data, and the NDI) also has broad-
ened the range of research questions that can be
addressed. High-quality data sources are avail-
able for a growing number of countries other
than the United States. Statistical techniques
designed for multiple times of measurement
and multiple levels of analysis are now read-
ily available in standard statistical packages.
Obviously, advances in these and other com-
ponents of the infrastructure on which aging
research rests will continue in the future. But
plenty of exciting research questions can be
addressed with the resources available now.
 What Aging Research Contributes to the Social Sciences: The Big Picture
Aging research is important for many rea-
sons, ranging from answering basic questions
about relatively regular patterns of human
development across adulthood to understand-
ing the importance of age structures for social
institutions to providing data that guide the
development of social/health interventions and
public policy. Recently and across many dis-
ciplines, the term “big questions” has enjoyed
considerable popularity. The phrase “big ques-
tions” appears to have originated in philoso-
phy as shorthand for describing the discipline’s
content and scope (Solomon & Higgins, 2013).
Now, however, multiple disciplines are asking
their practitioners what big questions they
want to answer and how much progress has
been made in answering them (e.g., Keeler,
2010; Sussman, 2010). Like other research fields,
it may be worthwhile to ask ourselves whether
research on aging can or does address big ques-
tions. This is not the venue for a comprehensive
list of the big questions that aging research can
or does address. We will, however, suggest one
big question to which aging research makes sig-
nificant contributions.
For most social science disciplines, a core
question has always been: What mechanisms
allow societies to survive? Alternatively, what
mechanisms convince societal members to cre-
ate and sustain societies, even when those
mechanisms require members to sacrifice some
of their own resources, gains, and autonomy?
This is a big question that social scientists have
tried to answer for more than a century.
Many of the founding fathers of sociol-
ogy and anthropology looked for answers to
the big question of societal order and stabil-
ity. Durkheim’s comparison of mechanical
and organic solidarity outlined two modes of
sustaining societal order and stability (1997).
Similarly, Weber’s writings on rationalization
and bureaucracy focused on forms of organiza-
tion that yielded stability and order in increas-
ingly diverse societies (Ritzer & Stepinsky,
I. THEORY AND METHODS
17
2012). In anthropology, Levi-Strauss (1966)
posited that although societies vary widely
in the structural arrangements that they use
to achieve solidarity and stability, all humans
share the same underlying patterns of thought.
Consequently, no matter how much structural
arrangements appear to differ across societies,
the functions that they serve are the same.
During the first half of the twentieth cen-
tury, issues of stability and order were gener-
ally studied under the theoretical umbrella
of structural functionalism. It is not surpris-
ing that structural functionalism focused on
the cultural tools and practices that promoted
order and stability – that was precisely the pur-
pose of inquiries in that tradition. Nonetheless,
structural functionalism was heavily criticized
for neglecting conflict, innovation, inequal-
ity, and social change. These criticisms led to
countervailing theories and research and by the
middle of the twentieth century research based
on structural functionalist theory had declined
substantially.
But social solidarity and order are issues
that are too fundamental to lay fallow forever.
And no scholar played a larger role in bringing
these issues back to the forefront of the social
sciences than Pierre Bourdieu and his theory
of social reproduction. Bourdieu’s theory and
research is far-ranging and discussion here will
focus on his contribution to understanding the
stability of social systems. More specifically, he
studied the reproduction of social stratification
or, as he preferred to call them, status hierar-
chies. Bourdieu acknowledged the importance
of economic capital in reproducing status hier-
archies, but argued that a focus solely on mate-
rial resources is incomplete. He argued for the
importance of social capital, cultural capital,
and even physical/bodily capital in sustaining
stratification systems over long periods of time
(Bourdieu, 1977). Much of his research focused
on the role of education in social reproduc-
tion of social classes. Buttressing his belief that
18 1. Aging and the Social Sciences: Progress and Prospects
much more than financial capital is involved
in this process, his research focused on cultural
capital, especially the arts, in reproducing social
stratification (Bourdieu, 1984).
Literally hundreds of studies using the
social reproduction framework have been pub-
lished in the last several decades. As might be
expected, a disproportionate number of them
focus on education and the failure of schools
to generate as much upward mobility for dis-
advantaged students as would be desirable
(Aschaffenburg & Maas, 1997; Collins, 2009).
The scope of social reproduction studies, how-
ever, is quite large and ranges from research
on the effects of economic growth in develop-
ing countries (Boughey, 2007) to the failure of
politics to break patterns of social reproduction
(Ruckert, 2010) to feminist critiques of the per-
sistence of traditional family roles (Chodorow,
1978).
It is interesting to note that the valence of
social scientists’ views of social reproduc-
tion changed quite dramatically over time.
Durkheim and later scholars who relied on
structural functionalism began with the prem-
ise that stability and order are problems that
societies must resolve to survive. Identifying
social processes that promoted stability and
social integration was viewed as a testimony to
the power of “social facts” to create order out
of potential chaos. In short, structural func-
tionalists generally view social institutions
and the social arrangements that sustain them
favorably. Scholars using the framework of
social reproduction tend to take the opposite
view. Many studies purport to demonstrate
that schools perpetuate social hierarchies rather
than reduce them through upward mobility.
The social reproduction of inequality is viewed
as problematic. Scholars in this tradition clearly
favor social institutions that do not reproduce
established social hierarchies.
A case also can be made that social reproduc-
tion is at the heart of several major theories of
aging. Continuity theory, which emerged as
I. THEORY AND METHODS
a response to and critique of disengagement
theory, is essentially a theory of social repro-
duction (Atchley, 1999). It posits that as older
adults experience age-related transitions such
as retirement and widowhood, they sustain as
many roles and activities that they valued prior
to the transitions as possible – in essence, they
reproduce the same parameters of their lives
that they had previously. Socio-emotional selec-
tivity theory (SST) is similar, in some ways, to
continuity theory. According to SST, as aging
adults experience declines in their capacities,
they express the highest levels of life satisfac-
tion if they release less important roles, rela-
tionships, and activities and invest mainly
in those that are most meaningful for them
(Lockenhoff & Carstensen, 2004). Again, the
emphasis of this theory is on continuity or sta-
bility of meaningful engagement. Cumulative
advantage/disadvantage theory (C/AD) also
focuses on stability across individuals over
time and, thus, the social reproduction of social
stratification. For economic outcomes, C/AD
hypothesizes that the rich literally get richer
and the poor get poorer. For health outcomes
there is no expectation that health improves
throughout adulthood, but those who begin
adulthood in better health are expected to
maintain better health over time than their less
advantaged peers. This is a social reproduction
scenario.
The valence of aging and life course schol-
ars who document social reproduction is more
mixed than was the case historically. Both
the disengagement/continuity theory debate
and SST focused on identifying the conditions
under which older adults are satisfied with
their lives. Research based on continuity theory
and SST suggests that forms of social reproduc-
tion are associated with subjective perceptions
of life quality. Given the research questions
asked, there is no reason to view these social
reproduction processes as anything but posi-
tive. Researchers documenting the cumula-
tive effects of advantage and disadvantage are
 What Aging Research Contributes to the Social Sciences: The Big Picture
generally less happy with findings that point
to the maintenance and the accumulation of
resources and deficits due to stratification.
Despite the assumption of objectivity in science,
it is clear that social scientists (with the possi-
ble exception of economists) dislike inequality
and the social arrangements that reproduce or
increase it.
Whether one views it as a necessary require-
ment for societal survival or a means of perpet-
uating inequality (or both), evidence leaves no
doubt that social reproduction exists and oper-
ates in many areas of life. We suggest, however,
that excessive attention to social reproduc-
tion and stability promotes an unrealistic and
incomplete view of the dynamics of time and
aging. This chapter began with reference to the
adage that “the only constant is change.” At
the same time that we are persuaded by rigor-
ous evidence of social reproduction, most of
us believe that adage. Everything that we see,
hear, and experience tells us that change is a
frequent, if not constant, dynamic in the world
and in our lives. Thus, science needs to focus on
change as well as stability.
We hope to make a case for increased atten-
tion to individual and social change. The
study of individual change is well established
in aging research. There may be a tendency to
interpret findings from the perspective of stabil-
ity rather than change – to focus on the stability
of physical, emotional, and cognitive capaci-
ties across the life course and to miss the pro-
cesses that permit stability in outcomes (such
as life satisfaction) despite substantial change
in objective circumstances. Overall, however,
aging research in the social sciences is atten-
tive to individual-level change and, as a result
of recent statistical advances, trajectories of
change over substantial periods of time.
The study of social change and its relation-
ships with aging is much less explored. Social
scientists are cognizant of cohort changes, but
are too satisfied with labeling them, rather than
explaining them. The three topics that we chose
I. THEORY AND METHODS
19
to discuss as recent advances in aging research
all focus on social change – in the forms of
cohort differences; sudden large-scale changes
in the basic infrastructure of society or gener-
ated by natural or man-made disasters; and
gradual changes that creep up and culminate in
changes that no one “saw coming.” Social sci-
entists should be heavily invested in studying
social change, as well as social stability. Aging
researchers should examine how age and age
structures affect broad social changes and the
consequences of social change for aging adults.
The antecedents and consequences of social
change are a “big question” for social scientists.
They subsume multiple more specific research
questions such as “What kinds and degrees of
social change trigger meaningful cohort differ-
ences?” and “How and under what conditions
does social change alter the well-being of older
adults?” Aging and life course researchers are
arguably in one of the best positions of all social
scientists to tackle questions about social change
because they already study individual change
and know the tools needed to study change at
all levels of aggregation. Advancing our under-
standing of social change also would contrib-
ute to the social sciences more broadly because
social change has widespread implications for
individuals, social institutions, and societies.
Most importantly, aging research has the poten-
tial to balance the current emphasis on social
reproduction with recognition of the prevalence
and importance of social change.
Yes, aging and life course research is alive
and well. Important contributions to our
understanding of aging and the social contexts
within which it unfolds have been impressive
over the past two decades or so. There are also,
however, important research questions yet to
be addressed. Opportunities to generate new
understandings of aging, older adults, and an
aging population are plentiful. We invite fresh
attention to research opportunities that have
the potential to optimize the aging experience
in spite of current inequalities.
20 1. Aging and the Social Sciences: Progress and Prospects
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 C H A P T E R

2
Trajectory Models for Aging Research
Scott M. Lynch1 and Miles G. Taylor2
1
Department of Sociology, Duke University, Durham, NC, USA 2Pepper Institute on Aging and
Public Policy, Florida State University, Tallahassee, FL, USA

O U T L I N E

Growth Modeling in a Nutshell 25 Data Structure and Method 43

Measurement of Time 44
Latent Class Modeling in a Nutshell 31
Importance of Assumptions 46
Latent Class Growth Analysis 38 Extraction of Classes and Inclusion
of Covariates 47
Growth Mixture Modeling 39
Conclusion 49
Important Issues in the Implementation
of Trajectory Methods 43 References 50

Life course research investigates how human
lives and events unfold over time, at both the
individual level and larger levels, such as within
families or nations (Elder, 1985). At the individ-
ual level, life course research is concerned with
the development of individuals as they age,
as well as with between-person differences in
development. Such differences often exist across
sexes, races, socioeconomic classes, and other
characteristics. Importantly, the birth cohort to
which an individual belongs plays an impor-
tant role in shaping development, as do period
events (e.g., economic depression). Trajectory
methods have emerged over the last several
decades as important tools for investigating life
course dynamics, including between-person dif-
ferences in development (George, 2009).
Trajectories are simply patterns in values of
variables across time. Based on this broad defi-
nition, the term “trajectory modeling” refers to a
number of qualitatively different methods used
to model an even greater number of social phe-
nomena. For example, one may be interested
in trajectories of unemployment rates, stock
market closing values, or other macro-level
phenomena, either for a single case (e.g., the
United States) or for multiple cases (e.g., states
or nations). Alternatively, one may be interested

L.K. George & K.F. Ferraro (Eds) DOI: http://dx.doi.org/10.1016/B978-0-12-417235-7.00002-0

Handbook of Aging and the Social Sciences, Eighth edition. 23 © 2016
2015 Elsevier Inc. All rights reserved.
24 2. Trajectory Models for Aging Research
in trajectories of income or health at the individ-
ual level. In some cases, one may use the term
“trajectory” to refer to the timing and ordering
of life events: school completion, employment,
marriage, childbearing, retirement, and death.
In this chapter, we will restrict our discus-
sion of trajectory models to two broad classes –
growth curve models (Bollen & Curran, 2006;
Meredith & Tisak, 1990) and latent class mod-
els (Clogg, 1995; Goodman, 1974; Lazarsfeld &
Henry, 1968) – and two of their generalizations,
including latent class growth models (Nagin
& Odgers, 2010) and growth mixture models
(Muthén, 2004; Muthén & Muthén, 2000). While
our discussion of these models can easily extend
to macro-level units like states and countries,
we will focus our discussion on individual-level
characteristics. Following our exposition of each
of these methods, we discuss a variety of issues
relevant to consider when using them in the face
of untestable assumptions.
Due to space constraints, we will exclude
the latter type of trajectory models mentioned
above involving sequences of different types
of life events. That is, we will focus only on
models of repeated measures (i.e., levels) of the
same phenomenon, not the timing and pattern
of multiple and qualitatively distinct events like
school completion, employment, and marriage
(i.e., transitions). Recent extensions of the soft-
ware and methods we will discuss can allow
transitions between states, but handling multi-
ple, distinct types of transitions is still difficult
within the framework we discuss. Models that
handle sequences of different events are more
commonly called “sequence analyses” (see
Barban & Billari, 2012) and historically have
required specialized software.
For the purpose of illustrating trajectory
methods, we rely on a subset of data from the
Health and Retirement Study (HRS), a panel
study of adults over age 50 in the United States.
Details about the study design can be found
elsewhere (RAND HRS Data, Version M.,
2013). Our key outcome measure is the body
I. THEORY AND METHODS
mass index (BMI), a commonly used measure
of weight per height (kg/m2) that is currently
the focus of much attention in public health
research and the media (National Institutes
of Health, 1998). BMI is a good measure with
which to illustrate trajectory methods for two
reasons. First, BMI is not highly volatile across
adulthood for most individuals. While it tends
to increase or decrease over age, it does not
often change in a dramatic or erratic way.
Second, BMI can be treated as both continuous
and categorical, with well-established catego-
ries. Specifically, a BMI under 20 is considered
underweight; a BMI between 20 and 25 is con-
sidered normal weight; a BMI between 25 and
30 is considered overweight; and a BMI above
30 is considered obese, with BMIs over 30 often
further subdivided into two or more obesity
classes. The continuous version of BMI is ide-
ally suited for growth modeling, while the cat-
egorical version of BMI is most amenable to
latent class methods, as we will discuss.
We restrict the sample to members of the
arbitrarily chosen 1951 birth cohort who were
interviewed in the 2004, 2006, 2008, and 2010
waves of the study. We further restrict the
sample to blacks and whites, to those who
survived the entire time period of observa-
tion, and to those with complete information
on BMI, sex, race, region of birth (south versus
elsewhere), and years of schooling. There are
two main approaches to trajectory modeling
– multivariate methods and hierarchical meth-
ods – and both can handle missing data, albeit
in somewhat different fashions. However, the
main focus of this chapter is not on the intrica-
cies of the methodology. Thus, we simplify our
discussion by eliminating data missing due to
both item nonresponse and attrition, although
we discuss missing data handling, including
attrition, briefly later in the chapter. The result-
ing analytic sample size was n = 353, a sample
large enough to illustrate all ideas in the chap-
ter but small enough for the construction of
readable figures. We note at the outset that we
 Growth Modeling in a Nutshell
do not focus on any substantive aspect of BMI.
BMI tends to decline substantially for some at
the very oldest ages as bone density and muscle
mass decline; however, our sample is restricted
to ages younger than 60.
GROWTH MODELING IN
A NUTSHELL
Figure 2.1A shows BMI measures for four
sample members, each measured on four
25
occasions. A natural first effort at modeling
these data might involve an ordinary least
squares (OLS) regression model. Figure 2.1B
shows the prediction line. The line appears to
fit the data fairly well, with an intercept of 26.8
and a slope of 1.18 BMI units. Note that time is
measured as 0, 1, 2, and 3, reflecting waves since
baseline. Thus, the average sample member
gained 3*1.18 = 3.54 BMI units across the sur-
vey period. In other words, the average sample
member started the survey period overweight
and became slightly obese over the 6 years.

(A) (B)
40

40
3 3
1 1
35

35
3 3
3 3
3 1 3 1
30

30
4 4
4 4
BMI

BMI
4 4 4 4
1 1
25

25
1 1
2 2
2 2
2 2 2 2
20

20
15

15

2004 2006 2008 2010 2004 2006 2008 2010

Year Year
(C) (D)
40

3
45

1
35

3
3
3 1
30

4
35

4
BMI

BMI

4 4
1
25

1
25

2
2
2 2
20
15

15

2004 2006 2008 2010 2004 2006 2008 2010

Year Year

FIGURE 2.1 Plots of individual patterns in BMI across time. Panel A shows measures for four persons (1–4); panel B
shows the best-fitting single regression line for these four cases; panel C shows individual-specific regression lines for these
four cases; panel D shows regression lines for 35 sample members.

I. THEORY AND METHODS

26 2. Trajectory Models for Aging Research
There are at least two, now widely recog-
nized, shortcomings of this modeling strat-
egy. First, given that the data come from a
panel, the OLS regression model is inappro-
priate because the errors are not independent
within individuals. Thus, standard errors of
the parameter estimates are biased downward,
rendering t-tests invalid. Second, the OLS
model estimates the average age pattern for
the four individuals instead of the age pattern
for any single individual, but the average age
pattern may not reflect the actual experience of
any real person.
Example 2.1
An alternative approach to modeling these
data might be to estimate a separate OLS
regression model for each person (Bollen
& Curran, 2006). Figure 2.1C illustrates the
results of this strategy. As the figure shows,
while the single regression line for the sample
had a positive slope, the slopes of the individ-
ual lines are not uniformly positive. Instead,
two individuals have regression lines with
steeper positive slopes than the average, and
two have lines with negative slopes. The inter-
cepts vary as well. Thus, of the four persons,
one was obese at baseline and became heavier
over the study period; one was obese at base-
line but lost weight across time to end slightly
overweight (BMI > 25); one began as nor-
mal weight but gained considerable weight
and was obese by the end of the period; and
one began as normal weight but lost weight
to become nearly underweight by the end of
the period. In short, the single OLS regres-
sion model missed considerable heterogeneity
across the sample. Figure 2.1D expands Figure
2.1C in showing estimated OLS regression
lines for 35 sample members (a 10% subsam-
ple). As the figure shows, there is substantial
variation in the intercepts and slopes – that is,
trajectories.
I. THEORY AND METHODS
Figure 2.2 shows a scatterplot of the inter-
cepts and slopes obtained from estimating OLS
regression models for all sample members.
The mean intercept and mean slope for the
sample are indicated by dashed reference lines.
The mean BMI at baseline was just under 30,
and the mean rate of change in BMI was just
above 0. The histogram above the scatterplot
shows the distribution of intercepts for the
sample, while the histogram to the right of the
scatterplot shows the distribution of slopes for
the sample. The figure reveals the consider-
able heterogeneity that a single OLS regression
summary would fail to capture. Furthermore,
the correlation between intercepts and slopes is
negative and moderate, as the dotted reference
line in the scatterplot shows: those with higher
baseline BMIs tend to experience less growth,
or even decline, in BMI over time, while those
with lower baseline BMIs tend to experience
greater growth in BMI over time.
This process of estimating an OLS regres-
sion model to capture individual-level patterns
over time illustrates the key concept underlying
growth modeling. Whereas the OLS regression
model posits a single value for the inter-
cept and slope, a growth model (GM) posits a
unique intercept and slope for each individual
as shown in Eqs. (2.1) and (2.2), respectively:
OLS: yit 5b01b1tit 1eit (2.1)
GM : yit 5 b0 i1 b1itit 1 eit (2.2)
In Eq. (2.1), yit is the outcome for individual i at
time t, b0 is the intercept (the value of y when
t = 0), b1 is the slope across time, tit is the time of
measurement of y, and eit is an error term that
is assumed to follow the usual assumptions that
it is normally distributed, homoscedastic, and
independent across observations. Note that the
subscripting of t implies that individuals do not
need to be measured at the same time nor on
the same number of occasions.
 Growth Modeling in a Nutshell 27

5
0
Slopes
–5
–10

20 30 40 50 60 70
Intercepts

FIGURE 2.2 Scatterplot and histograms of unique individual intercepts and slopes estimated via OLS regression for all
sample members. Histogram at top shows distribution of intercepts; histogram at side shows distribution of slopes. Dashed
vertical and horizontal lines represent means of intercepts and slopes (respectively). Diagonal dotted reference line reflects
correlation between intercepts and slopes.

Equation (2.2) shows the extension of the
model to include individual-specific intercepts
(b0i) and slopes (b1i). Equation (2.3) shows that
this model can be rewritten as an OLS regres-
sion model with a common intercept and slope
(denoted here as b00 and b10 – the second sub-
script of 0 reflects a common intercept for
the sample), but with unit-specific “random
effects” (ui and vi) that allow individual devia-
tions from the average:
yit 5(b001 ui )1(b101 vi )tit 1 eit
Estimating this model via OLS is problem-
atic, however, because OLS can estimate an
average intercept and slope only; thus, ui and
vi are relegated to the error term as shown in
Eq. (2.4), making it both autocorrelated (due
to cross-time commonality reflected in ui) and
heteroscedastic across time (because part of the
error is a function of time: vitit):
yit 5 b001b10tit 1(eit 1ui1vitit ) (2.4)
The model is therefore generally estimated
as a hierarchical model, with probability dis-
(2.3) tributions assigned to the random effects at a
second level (i.e., “Level 2”). Specifically, u and
v are usually assumed to be multivariate nor-
mally distributed with a mean vector of 0 and

I. THEORY AND METHODS

28 2. Trajectory Models for Aging Research

a covariance matrix of Σ, which contains both Given that each individual has a unique
the variances of u and v and the covariance of u intercept and slope via the random effects u
with v. and v, we can evaluate whether fixed indi-
The normality assumption is a crucial one. vidual-level characteristics, like sex, race,
While the assumption reduces the number birth region, and education, “explain” some
of parameters to be estimated compared to of the variance in them. Figure 2.3 illustrates
the individual-specific OLS regression model this idea. The figure replicates the scatterplot
approach, it does so by imposing a specific from Figure 2.2 but limits the points to black
form for the collection of intercepts and slopes. females and white females all of whom were
At the same time, the specification of a specific born in the south. As the figure shows via the
distribution for the random effects – and the horizontal and vertical reference lines for the
estimation of the associated parameters – ena- mean intercepts and slopes for each group,
bles the random effects approach to make out- black women tend to have much higher base-
of-sample inferences regarding the population. line BMI, while white women tend to have a
Implications of this assumption are discussed much larger growth rate. In fact, white women
subsequently. have positive average growth in BMI over
4

B
2

W W
B B B
B W
W W
B W
W B W
WW B
BMI growth

B
W B B
W
W B
W W WW
W W W B
WW B
0

W W W B
B
W B W
W B
W W B
B W
W B
W B

W
–2

B
–4

20 25 30 35 40 45 50
Baseline BMI

FIGURE 2.3 Scatterplot of intercepts and slopes from individual-level OLS regression models for black (B) and white
(W) women born in the south. Vertical reference lines show the mean intercepts for blacks (solid line) and whites (dashed
line); horizontal reference lines show the mean slopes.

I. THEORY AND METHODS

 Growth Modeling in a Nutshell 29
time, while black women have negative aver- TABLE 2.1 Results of Growth Modeling Via Two
age growth (i.e., they experience decline on Strategies: Separate OLS Regression Models Versus One
SEM-Based Multivariate Model
average).
In order to capture covariate differences in Intercepts (baseline) Slopes (growth)
intercepts and slopes, we can conduct a second-
OLS MODELING APPROACH
stage (or level) OLS model by regressing the
unique intercepts (b0i) and slopes (b1i) on (time Stage 1
invariant) covariates X, as shown in Eq. (2.5): Mean 29.16 0.195

b0 i5b001Xi γ1ui (2.5a) Variance 53.7 1.15

Correlation (b0i,b1i) −0.28

b1i5b101Xiδ1vi (2.5b) Stage 2

In this equation, the ui and vi are not the same Intercept 34.86 (1.98)*** 0.16 (0.30)
as before: they have become residual terms Male 0.72 (0.78) −0.06 (0.12)
that reflect unobserved heterogeneity that Black 2.28 (1.02)* −0.05 (0.15)
remains in individual intercepts and slopes
after extracting similarities that exist among South −1.16 (0.87) −0.13 (0.13)
those who share values of X (e.g., race, sex). ui Education −0.46 (0.14)** 0.01 (0.02)
and vi remain as random effects because they Correlation (b0i,b1i) −0.28
are assumed to follow a probability distribu-
tion, similar to the typical OLS error term, ei. R2 0.046 0.010
In contrast, X are fixed covariates, and so b00, MULTIVARIATE GROWTH APPROACH
b10, γ, and δ are called “fixed effects.” That is,
Model 1 (unconditional)
these coefficients are assumed not to vary. For
this reason, the model is sometimes referred to Mean 29.16 (0.39) 0.196 (0.057)
as a “mixed model,” or a “random coefficient Variance 50.5 (4.03) 0.40 (0.13)
model” (Raudenbush, 2001). Furthermore,
Correlation (b0i,b1i) −0.21
the model is often considered a special type of
“hierarchical model,” with Eq. (2.2) represent- Model 2 (conditional)
ing level 1, and Eqs. (2.5a) and (2.5b) represent- Intercept 34.90 (1.96)*** 0.13 (0.29)
ing level 2 (Raudenbush & Bryk, 2002). Finally,
Male 0.71 (0.77) −0.07 (0.12)
it is important to note that, because there are
two levels of error terms, or “variance compo- Black 2.24 (1.02)* 0.003 (0.15)
nents,” all growth models are hierarchical mod- South −1.18 (0.86) −0.13 (0.13)
els by common statistical terminology. Thus,
Education −0.46 (0.14)*** 0.01 (0.02)
the terms “growth model” and “hierarchical
growth model” are interchangeable, with the Correlation (b0i,b1i) −0.21
latter containing some redundancy.
Note: Standard errors shown in parentheses. Growth modeling
Table 2.1 presents the results of two sets of approach estimates standard errors for all parameters, including
models. The upper half of the table shows the variances.
# p < 0.1, *p < 0.05, **p < 0.01, ***p < 0.001.
results of following the strategy of estimating
the two OLS regression models. The lower half
of the table shows the results of estimating the

I. THEORY AND METHODS

30 2. Trajectory Models for Aging Research
model as a single, two-level hierarchical model
using structural equation modeling (SEM) soft-
ware, Mplus (Geiser, 2013; Muthén & Muthén,
1998–2012).
In the Stage 1 OLS analyses, regression mod-
els were estimated for each sample member as
described above. The mean intercept obtained
from these regressions was 29.16, with a vari-
ance of 53.7. The mean slope was 0.195, with a
variance of 1.15. The correlation between inter-
cepts and slopes was −0.28.
In the Stage 2 OLS analyses (i.e., a separate,
second set of models), these intercepts and
slopes were regressed on covariates in two
regression models (one each). In the first model,
the intercept for the intercept (b00) – that is, the
intercept for the baseline BMI – was 34.86. Males
have higher BMIs at baseline than females
(γ1 = 0.72; p > 0.05), blacks have higher base-
line BMIs than whites (γ2 = 2.28; p < 0.05), and
persons born in the south have lower baseline
BMIs than those born elsewhere (γ3 = −1.16; p >
0.05). Finally, those with greater schooling have
lower BMIs at baseline than those with less,
with each year of schooling reducing baseline
BMI by γ4 = 0.46 units. Race and education were
the only significant predictors of baseline BMI.
In short, if we wish to predict an individual’s
BMI, we would use Eq. (2.5a) tailored to this set
of covariates. All in all, these covariates explain
4.6% of the variance in the collection of BMI
intercepts, indicating that the residual variance,
var(ui), is 95.6% of the total variance of 53.7.
In the second Stage 2 model, the intercept for
the slope (b10) – that is, the value of the slope
for those with all covariate values set to 0 –
was 0.195, indicating that the average sample
member saw an increase in BMI of 0.195 units
per study wave. No covariates had significant
effects on the BMI slope, but the coefficients
(δ) for males, blacks, and persons born in the
south were negative, while the coefficient for
education was positive. The R-square for the
model predicting BMI slopes was small at 1%.
I. THEORY AND METHODS
In short, growth in BMI was not predicted well
by this set of covariates.
The bottom half of the table replicates the
top half but in a growth modeling framework.
Model 1 was an “unconditional” model, mean-
ing that covariates were not included; this
model corresponds to the Stage 1 model in the
top half of the table. The estimated mean inter-
cept and slope were almost identical to those
obtained via the OLS approach. The variances,
however, were substantially smaller (e.g., 50.5
for the SEM-based approach versus 53.7 for
OLS-based approach for the intercept param-
eter). The reason for this difference is that the
OLS modeling approach fits the individual tra-
jectories better, because it does not assume any
distribution for the collection of intercepts and
slopes together. That is, since the intercepts
and slopes are estimated as n separate regres-
sion models, there is no assumption regard-
ing the combined distribution of intercepts and
slopes. In contrast, because the growth mod-
eling approach simultaneously estimates all
intercepts and slopes under the assumption
that the distribution of them is normal, there are
larger, time-specific individual deviations of the
observed measures from the individual trajecto-
ries. Thus, there is greater measurement error at
level 1 and less variance in the random effects.
The bottom quarter of the table shows the
results of the growth modeling approach for the
conditional growth model, that is, the model in
which covariate influences on the growth param-
eters are simultaneously estimated with the
variance in those parameters themselves. These
results are very similar to those obtained via the
second-stage OLS regression model. However,
the coefficients and standard errors differ slightly,
with the estimates obtained via growth being bet-
ter in a statistical sense, because simultaneous
estimation of the level 1 and 2 equations is more
efficient, and the standard errors do not suf-
fer from heteroscedasticity and autocorrelation
implicit under the OLS approach.
 Latent Class Modeling in a Nutshell
LATENT CLASS MODELING
IN A NUTSHELL
As shown in the previous section, growth
modeling assumes a particular parametric shape
for all individuals’ trajectories over time. In the
example above, while each individual had his/
her own unique intercept and slope, all trajec-
tories were assumed to be linear. Deviations
of time-specific values of BMI for individuals
are assumed to be either measurement error in
BMI, as captured by eit, or fluctuations from the
trajectory because of time-specific “shocks” that
“bump” an individual off his/her linear trajec-
tory. Equation (2.2) can be modified to include
such shocks, which account for some of the indi-
vidual time-specific error represented by eit:
yit 5b0 i1b1itit 1(Zitφ1eit ) (2.6)
In Eq. (2.6), Zit is a time-specific variable (or
vector) that has an effect (ϕ) on yit (see Bollen
& Curran, 2006, p. 192). As an example of such
a time-specific “shock,” consider that an indi-
vidual could have surgery that results in sig-
nificant weight loss that is reflected in a single
survey wave but which does not alter his/her
fundamental, long-term BMI trajectory. That is,
once the individual recovers, s/he regains the
lost weight and continues on his/her trajec-
tory established by prior and subsequent BMI
measures.
A traditional latent class model applied to
repeated measures does not assume a paramet-
ric (e.g., polynomial) trajectory shape (Collins
& Lanza, 2010). Instead of assuming that indi-
vidual deviations from a parametric trajec-
tory are attributable to shocks or measurement
error, a latent class approach assumes that such
deviations may be meaningful, at least insofar
as enough sample members experience similar
such deviations that, together, they may consti-
tute a separate “class” of individuals.
I. THEORY AND METHODS
31
Example 2.2
Before advancing to more sophisticated
latent class methods, consider the BMI data
for the first study wave. Figure 2.4A shows a
histogram of the data (solid line). We could
assume that BMI follows a normal distribution;
the figure shows the histogram for the best-
fitting normal distribution superimposed over
the observed data (dashed line). As the figure
shows, the fit is not very good.
A better fit might be obtained by assuming
that the observed BMI distribution has arisen
from two types of individuals whose BMIs
come from two different normal distributions.
Perhaps some people have a propensity for
heaviness and some have a propensity for nor-
mal weight. Thus, the observed distribution
of BMI is a “mixture” of a normal distribution
with a smaller mean and one with a greater
mean, with both distributions also possibly
having different variances. Figure 2.4B shows
the best-fitting set of two normal distributions.
The mean of the heavier BMI distribution was
38.86, and its variance was 97.85. The mean of
the lighter BMI distribution was 26.93, and its
variance was 18.51. The two distributions do
not initially appear to fit the data particularly
well, but this is only because the distributions
have not been adjusted for the relative pro-
portions of individuals in the population who
come from each group. In fact, an estimated
82% of the population belongs to the lighter
distribution, while 18% belongs to the heavier
distribution.
Figure 2.4C shows the combined mixture
distribution; that is, the single distribution
implied by the two normal distributions shown
in Figure 2.4B when the component distribu-
tions are scaled for their relative proportions of
members in the population. Figure 2.4D shows
the results of a model that assumes there are
three BMI classes in the population. As the fig-
ure suggests, and various measures of fit (not
32 2. Trajectory Models for Aging Research

(A) (B)

0.08

0.08
Density

Density
0.04

0.04
0.00

0.00
20 30 40 50 60 70 20 30 40 50 60 70
BMI BMI

(C) (D)
0.08

0.08
Density

Density
0.04

0.04
0.00

0.00

20 30 40 50 60 70 20 30 40 50 60 70
BMI BMI

FIGURE 2.4 Histograms of observed wave 1 BMI (solid lines) with additional histograms superimposed (dashed lines).
Panel A shows the best-fitting normal distribution, based on the mean and variance of BMI. Panel B shows the best-fitting
set of two normal distributions. Panel C shows the best-fitting two-component mixture distribution based on the distribu-
tions in panel B. Panel D shows the best-fitting three-component mixture distribution.

shown) indicate, the fit is not substantially n  K 

better than the two-class model. This mixing of
multiple distributions is the key concept under-
lying latent class models.
Latent class models exploit the law of total
probability, such that the probability for an
individual’s value on a variable of interest is
conditional on the latent class to which s/he
belongs. Thus, the generic likelihood function
for a latent class model is:
L(Y )5∏∑ f ( yi|ck ) f (ck ) (2.7)

i51  k51

In Eq. (2.7), Y is the complete vector of observed
responses (y1, …, yn), and the likelihood func-
tion is simply the product over individuals, as
usual. Each individual’s contribution to the
likelihood is the sum in parentheses: it is the
probability density function for yi conditional

I. THEORY AND METHODS

 Latent Class Modeling in a Nutshell
on the membership in each class, ck, f(yi|ck),
multiplied by the probability of class member-
ship, f(ck). This probability of class membership
is what differentiates Figure 2.4B from 2.4C: it
represents the proportion of individuals in the
population that belong in each class.
The conditional density, f(yi|ck), may be con-
tinuous, as in the example above, or discrete,
as we will discuss. The density f(ck) is gener-
ally discrete in latent class modeling, meaning
that the number of classes, k = 1, …, K, is dis-
tinct and finite. In statistics, this type of model
is called a “finite mixture” model, with f(ck)
being the “mixing” distribution, and f(yi|ck)
being the “mixture component” distributions
(Land, 2001). The parameters for the compo-
nent distributions are unique within a class. In
other words, what distinguishes the classes are
the values of the parameters – like the mean
and variance in the example above – in f(yi|ck).
Thus, f(yi|ck) is often generically denoted:
f(yi|ck, θk), where θk is the unique parameter vector
associated with class ck.
Membership of individuals in each class is
generally unknown, but probabilities of an indi-
vidual’s (i) membership in each class (ck) can be
computed once the parameters of the mixture
component distributions and the overall sample
proportions in each class have been estimated,
by using Bayes’ Rule (see Lynch, 2007):
f ( yi|ck ) f (ck )
p(i ∈ ck ) ≡ p(ck | yi )5 K
(2.8)
∑ k51 f ( yi|ck ) f (ck )
These probabilities are commonly referred to
as “posterior probabilities of class member-
ship” and can be used to assign an individual
to a class deterministically by simply assigning
an individual to a class based on the class for
which s/he has the highest posterior probabil-
ity of being a member. This assignment process
embodies one of the two key assumptions of
latent class models: that there is no variation
I. THEORY AND METHODS
33
of observations within a latent class. In other
words, although individuals have varying
probabilities of being in their most likely class,
the characteristics of each class are considered
identical across the individuals within the
class. We discuss both the deterministic assign-
ment to class and variability in y within classes
subsequently.
Once class membership has been estab-
lished, researchers usually engage in a second-
stage analysis in which a multinomial logit
model is estimated to determine whether
covariates predict class membership. In the
growth modeling example from the previ-
ous section (a one-class model), we found that
males, whites, those from the south, and those
with greater education had lower estimated
baseline values of BMI. Here we found that
there were two latent classes for wave 1 BMI,
with 82% of the sample in the lighter class and
18% in the heavier class. After assigning class
membership deterministically as described
above, we estimated a logistic regression model
with these covariates predicting member-
ship in the two latent classes. The results (not
shown in a table) were similar to those obtained
via the growth model: men, southerners, and
those with greater education were less likely to
be in the heavier class (OR = 0.80, p > 0.05;
OR = 0.48, p < 0.1; OR = 0.69, p < 0.1, respec-
tively), and blacks were more likely to be in the
heavier class (OR = 1.96, p < 0.1).
Extending the latent class model to handle
more than one outcome variable is straight-
forward, involving simply expanding the
likelihood function shown in Eq. (2.7) by incor-
porating additional product terms:
n J  K 
L(Y )5∏∏∑ f ( yij|ck ) f (ck ) (2.9)
 
i51 j51 k51
With this extension, there are still K latent
classes, but now each of the n sample members
34 2. Trajectory Models for Aging Research
is measured on J variables, with yij being the ith
person’s response on the jth variable.
The second key assumption that underlies
latent class analysis is apparent from this set
of products: individual responses to items are
considered independent, conditional on latent
class membership. In other words, once an
individual’s class membership is established,
his response to variable a (i.e., yia) is unrelated
to his response to variable b (i.e., yib). This is
called the “conditional independence assump-
tion” and can be relaxed but generally is not
(Vermunt & Magidson, 2002).
The collection of J variables could be mul-
tiple measures of a single theoretical con-
struct, such as happiness. In that case, latent
class analysis can be viewed as an alterna-
tive to factor analysis that clusters individuals
with similar patterns of response, rather than
clustering variables based on their intercor-
relations. Thus, latent class is akin to K-means
clustering but has a stronger statistical justi-
fication underlying it, given that its founda-
tion is based on probability theory (Magidson
&Vermunt, 2002).
The collection of J variables could, alterna-
tively, be repeated measures of a single item,
like BMI. In that case, the latent classes that
emerge from the analysis will represent the
common patterns observed in the variable
over time: trajectories. Unlike linear or other
polynomial growth models, which assume a
common average trajectory shape for all indi-
viduals, latent class models of repeated meas-
ures allow for very different, non-smooth
shapes across classes. Thus, latent class mod-
eling is sometimes referred to as a “nonpara-
metric” method. Furthermore, the data may be
continuous or fundamentally dichotomous or
categorical, unlike in the growth model, which
assumes either (1) that the observed data are
continuous or (2) that the observed categori-
cal/dichotomous data are simply limited meas-
ures of a continuous latent variable (Muthén &
Asparouhov, 2006).
I. THEORY AND METHODS
Example 2.3
To illustrate this repeated measure latent
class model, suppose our BMI data were dichot-
omized at each wave so that individuals were
observed to be obese or not. In that case, there
would be 24 = 16 possible trajectories of BMI,
ranging from stable-obese to stable nonobese.
We may hypothesize that these stable trajecto-
ries are the only two that exist in the popula-
tion, and we may estimate a series of latent class
models in order to evaluate that hypothesis.
We estimated three latent class (LC) models –
with two, three, and four latent classes – and
used the Bayesian Information Criterion (BIC) to
determine the best-fitting model. Although all of
the analyses discussed here rely on multiple test
statistics to determine overall and relative model
fit (Geiser, 2013), the BIC is the most commonly
used measure to compare LC models, with
the smallest BIC indicating the “best” model
(Nylund, Asparouhov, & Muthén, 2007). Here a
three-class model was found to fit the data best.
Given the dichotomous nature of the data in this
example, the key model parameters are thresh-
olds on a latent logistic distribution that assign
probabilities of obesity to each wave of measure-
ment for those belonging to the class. Table 2.2
presents the results of the analyses and clarifies
these ideas.
The upper half of the table presents the
probabilities that an individual in a given class
is obese at each wave of the study. Class 1 is
characterized by having members with low
probabilities of obesity at each wave: the prob-
abilities that a member is obese at each wave are
0.018, 0.009, 0, and 0.037, respectively. We might
therefore call this class a stable nonobese class.
In contrast, for members of class 3, the prob-
abilities exceed 0.98 that they are obese at every
wave. Thus, we might call this class a stable-
obese class. Members of class 2 have a modest
probability of being obese at wave 1 (0.321), but
relatively high probabilities of being obese at
subsequent waves (>0.6). We might be inclined
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Glycosuria, tests for, 422.
Glycosuria, toxic, 419.
Glycosuria, pancreatic, 420.
Glycosuria, pathological, 417.
Glycosuria, physiological, 416.
Gnathitis, 19.
Gout, 430.
Gongylonema in gullet, 93.
Grass staggers, 124.
Green potatoes, poisoning by, 286.
Growth, sugar in relation to, 428.
Gullet, inflammation of, 86.
Gullet, spasm of, 90.
Gut tie in ox, 357.

Hæmoglobinæmia, 437.
Hæmoglobinuria, 437.
Hemorrhagic gastro-enteritis in dogs, 252.
Hair and bristle balls, dog and pig, 322.
Hair balls in intestines, 320.
Hair balls in intestines, horse, 320.
Hair balls in stomach, 187.
Hard palate, congestion of, 19.
Hare lip, 49.
Harvest bug on lips, 7.
Helebore poisoning, 285.
Helleborus niger poisoning, 285.
Hepatic abscess, 495.
Hepatic congestion, 483.
Hepatic congestion in dog, 486.
Hepatic congestion in solipeds, 484.
Hepatic hemorrhage, 487.
Hepatic inflammation, 490.
Hepatic steatosis, 508.
Hepatitis, 490.
Hepatitis, infective, 498.
Hepatitis, parenchymatous, 491.
Hepatitis, suppurative, 495.
Hernia, 371.
Hernia, mesenteric, 368.
Hernia of reticulum, 367.
Hernia, omental, 368.
Hernia, pelvic, 357.
Hernia, phrenic, 359.
Hernia through foramen of Winslow, 370.
Honey dew, poisoning by, 292.
Horsetail poisoning, 286.
Hydrochloric acid and gastro-enteritis, 266.

Icterus, 457.
Icterus, from lupin poison, 476.
Icterus nouveaux nés, 473.
Impacted cloaca, 209, 319.
Impacted rumen, 108.
Impaction of colon in solipeds, 203.
Impaction of large intestine, soliped, 197.
Impaction of omasum, 123.
Indigestion, acute gastric in solipeds, 150.
Indigestion, gastric, in carnivora, 158.
Indigestion, gastric, in swine, 159.
Indigestion in abomasum, 135.
Indigestion in fourth stomach in sucklings, 136.
Indigestion, ingluvial, 94.
Indigestion, intestinal, 193.
Indigestion, intestinal in birds, 209.
Indigestion, intestinal, in solipeds, 197.
Indigestion with impaction, in dog, 205.
Indigestion, tympanitic, of rumen, 96.
Ingluvial indigestion, 94.
Intestinal atony, 314.
Intestinal calculi, 323.
Intestinal congestion, from verminous embolism, 210.
Intestinal congestion in solipeds, 220.
Intestinal indigestion in birds, 209.
Intestinal indigestion with impaction, 197.
Intestinal invagination, 344.
Intestinal obstruction in birds, 209.
Intestinal obstruction in dog, 205.
Intestinal pain, 308.
Intestinal strangulations, 356.
Intestinal tympany, 193.
Intestine, abscess of, 336.
Intestine, dilation of, 340.
Intestine, hyperplasia of, 378.
Intestine, rupture of, 332.
Intestines, foreign bodies in, 328.
Intestines, hair balls in, 320.
Intestines, strangulation of, by ovarian ligament, 380.
Intestine, stricture of, 342.
Intestine, tumors of, 374.
Intestine, ulceration of, 338.
Intestine, volvulus of, 351.
Intussusception, 344.
Invagination of bowel, 344.
Iodine poisoning, 276.
Iodism, 276.
Iron, poisoning by, 279.

Jaundice, 457
Jaundice, catarrhal, 463.
Jaundice, catarrhal, in dogs, 467.
Jaundice from ferments in fodder, 476.
Jaundice from lupins, 476.
Jaundice from obstruction, 458.
Jaundice from poisons, 459.
Jaundice in cattle, 472.
Jaundice in new born, 473.
Jaundice without bile obstruction, 459.
Juniperus sabina, poisoning, 286.

Kidney, degeneration of, 431.

Laburnum poisoning, 286.

Laceration of intestine, 332.
Lambs, infective gastro-enteritis in, 138.
Lampas, 19.
Lathyris, poisoning by, 286.
Leather in stomach, 188.
Lips, actinomycosis of, 7.
Lips, epithelioma of, 6.
Lips, indurated, 5.
Lips, inflammation of, 5.
Lips, polypi on, 6.
Lips, treatment of inflammation of, 5.
Lips, trombidiosis of, 7.
Lips, warts on, 6.
Lips, wounds of, 5.
Lipoma of intestine, 374, 377.
Lipoma of Liver, 533.
Lipoma of stomach, 191.
Liver abscess, 495.
Liver, actinomycosis of, 536.
Liver, acute yellow atrophy of, 491.
Liver, amyloid, 511.
Liver, brown atrophy of, 513.
Liver and circulatory disorders, 431.
Liver and gastro-intestinal disease, 431.
Liver and kidney disease, 431.
Liver and nervous disease, 431.
Liver and respiratory disorders, 431.
Liver and skin diseases, 432.
Liver, as a destroyer of toxins, 415.
Liver, calcareous nodules in, 534.
Liver, chronic atrophy of, 507.
Liver congestion in dog, 486.
Liver congestion in horse, 484.
Liver, congestion of, 483.
Liver, cirrhosis of, 502.
Liver disease, secondary results of, 430.
Liver, diseases of, 407.
Liver, effect on leucocytes, 409.
Liver, effect on red globules, 409.
Liver, fatty degeneration, 508.
Liver, fibroid degeneration, 502.
Liver, foreign bodies in, 525.
Liver, functional diseases, treatment, 432.
Liver, functional disorders, 416.
Liver, infective inflammation of, 498.
Liver, inflammation of, 490.
Liver, metabolism in, 410.
Liver, parasites of, 537.
Liver, pigmentation of, 513.
Liver, rupture of, 487.
Liver, sanguification in, 408.
Liver, steatosis of, 508.
Liver, tumors in, 527.
Liver, yellow atrophy of, 476.
“Loco” weeds, poisoning by, 287.
Lupinosis, 476.
Lupinosis in solipeds, 482.
Lymphadenoma of liver, 529.
Lymphadenoma of the spleen, 563.

Maize, poisoning by damaged, 289.

Male fern poisoning, 286.
Marsh’s test for arsenic, 271.
Maxillitis, 44.
May apple, poisoning by, 286.
Meadow saffron poisoning, 284.
Melanoma of gullet, 93.
Melanoma of liver, 528.
Melanoma of spleen, 562.
Melanosis in pancreas, 544.
Melia azedarach, poisoning by, 286.
Melilot poisoning, 286.
Mellituria, 416.
Mercurialis annua poisoning, 286.
Mercurialism, 32.
Mercurial poisoning, 274.
Mercurial stomatitis, 32.
Mercury, test for, 275.
Mesenteric hernia, 368.
Metabolism in liver, 410.
Meteorism, gastric, 150.
Meteorism of the intestines, 193.
Meteorism of rumen, 96.
Microbes in gastro-enteritis, 144.
Milk in infective gastro-enteritis of sucklings, 141.
Milk of woman, and animals, 143.
Marc, stomatitis from, 27.
Monocercomonas gallinæ, 71.
Moulds, poisoning by, 289, 290.
Mouldy bread, poisoning by, 296.
Mouth, diseases of, 4.
Mouth, functional disorders, 4.
Mouth, general inflammation of, 8.
Mouth, injuries to, 4.
Muguet, 27, 36.
Muriatic acid and gastro-enteritis, 266.
Mustard, poisoning by, 287.
Musty grain, poisoning by, 290, 296.
Myoma of intestine, 375.
Myxoma of intestine, 375.

Narcissus poisoning, 284.

Nails in stomach, 188.
Necrobiosis of liver, 498.
Needles in stomach, 188.
Neoplasms of intestine, 374.
Nervous ergotism, 298.
Neuralgic colic, 309.
Nitrate of soda poisoning, 268.
Nitric acid and gastro-enteritis, 266.
Nux vomica, poisoning by, 286.

Oat-hair balls in stomach, 187.

Obesity, 427.
Œnanthe crocata, poisoning by, 286.
Œsophagean tumors, 93.
Œsophagismus, 90.
Œsophagus, paralysis of, 92.
Œsophagus, spasm of, 90.
Omasum, impaction of, 123.
Omasum, inflammation of, 131.
Omasum, tumors of, 133.
Omental hernia, 368.
Osteomalacia, 78.
Ovarian ligament, strangulation of intestine by, 380.
Oxalic acid and gastro-enteritis, 266.
Oxalic acid diathesis, 430.
Oxytropis, poisoning by, 287.

Palatitis, 19.
Pancreas, diseases of, 537.
Pancreas, foreign bodies in, 542.
Pancreatic abscess, 541.
Pancreatic calculi, 543.
Pancreatic tumors, 544.
Pancreatitis, catarrhal, 538.
Pancreatitis, interstitial, 540.
Pancreatitis, suppurative, 541.
Paper-ball in stomach, 188.
Papilloma of gullet, 93.
Papilloma of omasum, 133.
Papilloma of stomach, 191.
Paralysis of gullet, 92.
Paralysis of rectum, 371.
Paralysis of the pharynx, 83.
Paralysis of tongue, 37.
Parasites of liver, 537.
Parasites of rumen and reticulum, 122.
Parasites of spleen, 564.
Paris green poisoning, 269.
Parotid gland, inflammation of, 41.
Parotitis, 41.
Pecking feathers, 76.
Pelvic hernia in ox, 357.
Perforating ulcer of stomach, 179.
Perihepatitis, 500.
Perisplenitis, 554.
Peritonitis, 380.
Peritonitis, chronic, 392.
Peritonitis, general causes, 380.
Peritonitis in birds, 399.
Peritonitis in carnivora, 397.
Peritonitis, infection of, 385.
Peritonitis in ruminants, 395.
Peritonitis in solipeds, 383.
Peritonitis, traumatic, 383.
Pharyngeal abscess, 58.
Pharyngitis, catarrhal, 49.
Pharyngitis, chronic, 73.
Pharyngitis, microbes in, 50, 56.
Pharyngitis, phlegmonous, 54.
Pharyngitis, pseudomembranous, 60.
Pharyngitis, pseudomembranous, in birds, 67.
Pharyngitis, pseudomembranous, in cattle, 63.
Pharyngitis, pseudomembranous, in dogs, 66.
Pharyngitis, pseudomembranous, in sheep, 64.
Pharyngitis, pseudomembranous, in solipeds, 61.
Pharynx, paralysis of, 83.
Pharynx, tumors of, 84.
Phenol poisoning, 281.
Phlegmonous gastritis in horse, 162.
Phosphatic calculi in stomach, 188.
Phosphorus poisoning, 272.
Phrenic hernia, 359.
Phytolacca, poisoning by, 286.
Pica, 76.
Pins in stomach, 188.
Pip in birds, 18.
Plants, paralyzing element in, 95.
Playthings in stomach, 188.
Podophyllum, poisoning by, 286.
Poisoning by acetic acid, 266.
Poisoning by aconite, 286.
Poisoning by acorns, 286.
Poisoning by aloes, 286.
Poisoning by American water hemlock, 285.
Poisoning by ammonia, 264.
Poisoning by anemone, 286.
Poisoning by antimony, 273.
Poisoning by army worm, 288.
Poisoning by arsenic, 269, 271.
Poisoning by artichokes, 286.
Poisoning by astragalus, 287.
Poisoning by azedarach, 286.
Poisoning by bacteria, 289.
Poisoning by barium, 279.
Poisoning by bluestone, 276.
Poisoning by box leaves, 284.
Poisoning by brine, 268.
Poisoning by bromine, 276.
Poisoning by bryony, 286.
Poisoning by buckwheat, 286.
Poisoning by cantharides, 288.
Poisoning by carbolic acid, 281.
Poisoning by castor seeds, 282.
Poisoning by chickweed, 286.
Poisoning by chromium, 280.
Poisoning by cicuta maculata, 285.
Poisoning by cicuta virosa, 286.
Poisoning by clematis, 286.
Poisoning by cockroach, 288.
Poisoning by colchicum autumnale, 285.
Poisoning by conium maculatum, 286.
Poisoning by copper, 276.
Poisoning by creosote, 282.
Poisoning by croton seeds or oil, 283.
Poisoning by cryptogams, 290, 292.
Poisoning by daffodils, 284.
Poisoning by digitalis, 286.
Poisoning by ergot, 289.
Poisoning by euphorbia, 283.
Poisoning by fungi, 289, 291.
Poisoning by galega, 286.
Poisoning by giant fennel, 286.
Poisoning by honey dew, 292.
Poisoning by horsetail, 286.
Poisoning by iodine, 276.
Poisoning by iron, 279.
Poisoning by laburnum, 286.
Poisoning by lathyrus, 286.
Poisoning by lolium temulentum, 286.
Poisoning by male fern, 286.
Poisoning by melilot, 286.
Poisoning by mercurialis annua, 286.
Poisoning by mineral acids, 266.
Poisoning by moulds, 289, 290.
Poisoning by muriatic acid, 266.
Poisoning by mustard, 287.
Poisoning by nitrate of soda, 268.
Poisoning by nitric acid, 266.
Poisoning by nux vomica, 286.
Poisoning by œnanthe crocata, 286.
Poisoning by oxalic acid, 266.
Poisoning by oxytropis, 287.
Poisoning by Paris green, 269.
Poisoning by phosphorus, 272.
Poisoning by phytolacca, 286.
Poisoning by podophyllum, 286.
Poisoning by poppy, 286.
Poisoning by potash, 265.
Poisoning by potatoe beetle, 288.
Poisoning by potatoe tops, 286.
Poisoning by ranunculus, 284.
Poisoning by resinous plants, 286.
Poisoning by rhododendron, 286.
Poisoning by ryegrass, 286.
Poisoning by salts of mercury, 274.
Poisoning by saltpeter, 268.
Poisoning by savin, 286.
Poisoning by silver, 278.
Poisoning by smut, 289.
Poisoning by snapdragon, 286.
Poisoning by soda, 265.
Poisoning by sodium chloride, 267.
Poisoning by spoiled potatoes, 296, 300.
Poisoning by spurge laurel, 283.
Poisoning by spurry seeds, 286.
Poisoning by St. John’s wort, 286.
Poisoning by strychnia, 286.
Poisoning by sulphur, 275.
Poisoning by sulphuric acid, 266.
Poisoning by tares, 286.
Poisoning by tartar emetic, 273.
Poisoning by tobacco, 286.
Poisoning by toxins in food and water, 292.
Poisoning by trefoil, 286.
Poisoning by vetches, 286.
Poisoning by veratrum viride, 285.
Poisoning by white vitriol, 277.
Poisoning by yew, 286.
Poisoning by zinc, 277.
Poisoning, chronic, by arsenic, 271.
Poke root, poisoning by, 286.
Polypi on lips, 6.
Poppy poisoning, 286.
Postpharyngeal abscess, 58.
Potash and gastro-enteritis, 265.
Potato beetle, poisoning by, 288.
Potato tops, poisoning by, 286.
Pseudomembranous enteritis in birds, 226.
Pseudomembranous enteritis in cattle, 223.
Pseudomembranous enteritis in dogs, 225.
Pseudomembranous enteritis in sheep, 224.
Pseudomembranous enteritis in solipeds, 221.
Pseudomembranous pharyngitis in cattle, 62.
Pseudomembranous pharyngitis in dogs, 66.
Pseudomembranous pharyngitis in pigeons and chickens, 67.
Pseudomembranous pharyngitis in sheep, 64.
Pseudomembranous pharyngitis in solipeds, 61.
Pseudomembranous pharyngitis in swine, 65.
Ptomaines and toxins of brine, 268.
Ptyalism, 39.

Rank vegetation as a cause of stomatitis, 9.

Rape cake, stomatitis from, 27.
Ranunculus poisoning, 284.
Rectum, paralysis of, 371.
Red dysentery in cattle, 258.
Resinous plants, poisoning by, 286.
Rhododendron, poisoning by, 286.
Ricinus communis poisoning, 282.
Reticulum, hernia of, 367.
Reticulum, tumors of, 122.
Retropharyngeal abscess, 58.
Rumen, actinomycosis of, 123.
Rumen, balls of vegetable fibre in, 116.
Rumen, foreign bodies in, 118.
Rumen, gaseous fermentation in, 96.
Rumen, hair balls in, 116.
Rumen, impacted, 108.
Rumen, inflammation of, 114.
Ruminitis, 114.
Rumenotomy, 113.
Rumen, overloaded, 108.
Rumen, parasites of, 122.
Rumen, puncture of, 104.
Rumen, tumors of, 122.
Ruminants, chronic gastric catarrh in, 171.
Ruminants, cryptogamic poisoning in, 295.
Ruminants, impaction of colon in, 203.
Rupture of intestine, 332.
Rupture of stomach, solipeds, 182.
Ryegrass poisoning, 286.

Saccharine diabetes, 416.

Sacculated bowel, 340.
Saliva, excessive secretion, 39.
Salivary calculus, 40.
Salivary ducts, dilation of, 40.
Salivary fistula, 40.
Salivary glands, diseases of, 38.
Salivary glands, surgical lesions, 46.
Saliva, suppression of, 38.
Salivation, 5, 39.
Salivation, mercurial, 32.
Saltpeter poisoning, 268.
Sand and gravel in stomach, 188.
Sarcoma in liver, 527, 531.
Sarcoma of intestine, 374, 377, 379.
Sarcoma of omasum, 133.
Sarcoma of spleen, 562.
Sarcoma of stomach, 191.
Savin poisoning, 286.
Schweinsberg disease, 503, 504.
Sclerostoma equinum, 210.
Scouring, 303.
Sequestrum in spleen, 564.
Silver salts, poisoning by, 278.
Smut, poisoning by, 289.
Snapdragon poisoning, 286.
Soda in gastro-enteritis, 265.
Sodium chloride, poisoning by, 267.
Soft palate, injuries to, 48.
Solipeds, acute catarrhal gastritis in, 160.
Solipeds, chronic gastric catarrh in, 170.
Solipeds, cryptogamic poisoning in, 290.
Solipeds, phlegmonous gastritis in, 162.
Solipeds, toxic gastritis in, 164.
Spanish flies, poisoning by, 288.
Spasm, intestinal, 308.
Spasmodic colic, 309.
Spirillum Metchnikowi, 256.
Spiroptera in gullet, 93.
Spleen, abscess of, 557.
Spleen, amyloid degeneration of, 563.
Spleen, anæmia of, 546.
Spleen, chronic congestion of, 550.
Spleen, diseases of, 545.
Spleen, foreign bodies in, 558.
Spleen, gangrene of, in swine, 564.
Spleen, glander nodules in, 564.
Spleen, hyperæmia of, 547.
Spleen, infarction of, 555.
Spleen, parasites of, 564.
Spleen, rupture of, 559.
Spleen, tubercles in, 564.
Spleen, tumors, of, 562.
Splenic hemorrhagic infarction, 555.
Splenic hypertrophy, 550, 551, 552, 553.
Splenic hypertrophy in dogs, 553.
Splenic hypertrophy in ruminants, 552.
Splenic hypertrophy in solipeds, 551.
Splenic hypertrophy in swine, 553.
Splenitis, 554.
Spurge laurel poisoning, 283.
Spurry seeds, poisoning by, 286.
Staggers, 124.
Stale fish, poisoning by, 302.
St. John’s wort, poisoning by, 286.
Stomach, bristle balls in, 116.
Stomach, dilatation of, 180.
Stomach, feather concretions in, 116.
Stomach, foreign bodies in, 187.
Stomach, hair balls in, 116.
Stomach, perforating ulcer of, 179.
Stomach, puncture of, 156.
Stomach, rupture of, solipeds, 182.
Stomach staggers, 124.
Stomach, torsion of, in dog, 184.
Stomach, tumors of, 191.
Stomach, tympany of, 150.
Stomach, ulceration of, 175.
Stomatitis, aphthous, 21.
Stomatitis, catarrhal in birds, 18.
Stomatitis, follicular, 21.
Stomatitis from buccal fermentation, 10.
Stomatitis from caustics, 35.