Causal Connections between Socio-Economic Status and Health: Reciprocal Effects and

Mediating Mechanisms
Author(s): Mesfin Samuel Mulatu and Carmi Schooler
Source: Journal of Health and Social Behavior, Vol. 43, No. 1 (Mar., 2002), pp. 22-41
Published by: American Sociological Association
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Causal Connections between Socio-economic Status and

Health: Reciprocal Effects and Mediating Mechanisms*
MESFIN SAMUEL MULATU
CARMI SCHOOLER
National Instituteof Mental Health

Journalof HealthandSocialBehavior2002,Vol43 (March):22-41

Using structural equation modeling techniques on data from a nationally representative longitudinal survey, we first explored the reciprocal relationships
between socio-economic status (SES) and health status. Wethen estimated the
degree to which health-related lifestyles/behaviors and psychosocial distress
are mediating mechanisms of these relationships. As predicted, SES positively
affects health, and health positively affects SES. Although the causal path from
SES to health is stronger than the reverse, these findings confirmed the hypothesis that both social causation and health selection contribute to social inequalities in health. In terms of the mediating mechanisms through which SES and
health affect each other, more than a third of the overall SES-health relationship
was accountedfor by health-related lifestyles/behaviors and psychosocial distress. A notable part of the effect of SES on health is due to differences in psychological distress, with the effects of health-related lifestyles/behaviors being
much smaller. On the other hand, in terms of the effects of health on SES, differences in weight and sleeping behavior are more important than psychological distress.
One of the most consistent social epidemiological finding is the inverse relationship
between socioeconomic status (SES) and
health:The lower the SES, the higher the incidence and prevalenceof health problems, disease, and death. This inverse SES-healthrelationship is found not only in the more developed and industrial countries of North
* Thedatacollectionforthisstudywassupported
by
the National Instituteon Aging throughIntraY02AG-1-0168entitled"Social
AgencyAgreement

Environments and Psychological Functioning in

Older People."We would like to thank the staffs of
the Cygnus Corporationand the National Opinion
Research Center for their efforts on the survey.
ArthurKorotkin,then of the Cygnus Corporation,
was gracious and helpful well beyond the call of
duty. We are grateful to Leslie Caplan, Melvin
Kohn, and Gary Oates for their very helpful comments on earlier versions of this article. Address
correspondence to Mesfin Mulatu, PhD, MPH,
Section on Socio-EnvironmentalStudies, NIMH,
Room B1A-14, Federal Building, Bethesda, MD
20892-9005. Electronic mail may be sent to
Mesfin.Mulatu@nih.gov

America and western Europe, but also in

developing countries such as Costa Rica,
Hungary,Nigeria, and SouthAfrica (Adler and
Ostrove 1999; Marmot 1999; Marmot et al.
1997; Robert and House 2000). The negative
relationship between SES and health is also
found whethersocial inequalityis measuredat
an individuallevel or at the level of neighborhood, community, or even society (Kawachi
1999; Kennedy et al. 1998). This relationship
is so regularlylinearthat it has been described
as a gradientin which health status apparently
improveswith every incrementin SES (Adler
and Ostrove 1999; Marmot 1999).
The very consistency and regularityof the
SES-healthrelationshipleads to a sociological
conundrum:Exactly what is it about SES that
underlies the relationship?Although there is
compelling evidence for the "social causation"
hypothesis according to which SES affects
health status, there is also some evidence supportingthe alternative"social drift,"or "health
selection,"hypothesis that causally links poor
health statusto subsequentlower levels of SES
22

EXPLAININGTHE SES AND HEALTHCONNECTIONS

(Adler and Ostrove 1999). For both the social

causation and social drift hypotheses, there is
the furtherquestion of the natureof the proximal mediating mechanisms through which
SES either affects or is affected by health.
Thus, although the SES-health status relationship seems well established, we are left with
the conundrumof its causes - a conundrumthe
difficulty of whose solution would seem to be
made even greater by the apparentgradientlike natureof the relationships.Teasingout the
mechanismsunderlyingthis persistentassociation between SES and health remains an
importantchallenge for both public policy and
scientific reasons (Adler and Ostrove 1999).
Severalsocial, psychological, and biological
mechanisms have been hypothesizedto underlie the SES-health relationship. One set of
hypotheses centers on the ways that SES may
influence health status through its effect on
shaping the individual's day-to-day lifestyle
and health-affecting behaviors (e.g., Lynch,
Kaplan, and Salonen 1997; Kaplan et al.
1996). Among these potentially SES-related
health-affecting lifestyles/behaviors are patterns of diet, sleep, exercise, smoking, drinking, and drug use. Health-related lifestyles/
behaviors and health status may affect one
anotherthroughdirect,indirect,and interactive
mechanisms. In terms of direct effects, health
related lifestyles/behaviors may affect health
by acting on biologic systems or their functioning. A reciprocal direct effect through
which level of health may affect motivation
and capacity to engage in positive health-related behaviors is also possible. In terms of indirect effects, health-relatedlifestyles/behaviors
may indirectly affect health status through
their potentialimpact on SES, which may then
affect health levels. For example, alcohol or
sleeping problemsmay lead to poorjob performance, which might then result in lowered
SES. In addition,it is plausiblethatpsychological characteristics(e.g., relatively high levels
of intellectual functioning) that may predispose individuals to engage in positive healthrelated lifestyles/behaviors may also make
them more likely to achieve higher SES levels
and, as a result, become healthier. Thus, a
majorpurpose of the presentpaper is to elucidate such linkages between SES, health-related
lifestyles/behaviors,and health outcomes.
Another pathway through which SES and
health are hypothesizedto influence each other
is by way of SES differences in exposure to

23

psychological stress and distress. As in the

case of the other potentially explanatoryvariables, both direct and indirect effects have
been proposedto link psychological distressto
SES and health. Both cross-sectional and longitudinal studies indicate that lower SES people tend to have higher levels of anxiety,
depression, or hopelessness (Fiscella and
Franks 1997; Lewis et al. 1998). Nonetheless,
the nature of the causal role of psychological
distress on the SES-healthstatus relationships
remains open to question. There is, however,
some evidence suggesting that some forms of
psychological distress lead to lower SES,
although much of the evidence for this causal
path comes from instances where the distress
is severe enough (e.g., schizophrenia) or
occurs early enough in life (e.g., duringchildhood or adolescence) to hinder status attainment. On the other hand,there is evidence for
the hypothesis that SES is related to psychological vulnerabilityto stress, lower SES individuals being more negatively affected by a
given level of stress (Gallo and Matthews
1999). This psychological vulnerabilitymay in
turntranslateto physical vulnerability.Support
for the existence of such a causal chain is
found in evidence that, even where stress levels are controlled,lower SES people tend to be
more vulnerablethan higher SES ones to psychological distress (e.g., anxiety, depression,
and hostility), and that such psychological disturbancesaccount, at least in part, for the disproportionateburden of disease among them
(Gallo and Matthews 1999). The question of
the potential reciprocal causal connections
among psychological distress, SES, and health
remainsunresolved.
An obvious way in which SES may affect
health is through differences in occupational
conditions;the job demandsand conditions of
workers in different positions in the occupational hierarchymay differentiallyaffect their
health. Studies have clearly shown that job
conditions such as high work strain,poor work
support, low control in the work place, job
insecurity, repetitive work, and exposure to
uncomfortableworking conditions are associated with elevated risks of health problems,
including a general worsening of self-rated
health and an increase in specific illnesses
such as coronaryheart disease (e.g., Borg and
Kristensen 2000; Bosma et al. 1997).
Unfortunately,although we are well aware of
the potential effects of work conditions on

24

JOURNALOF HEALTHAND SOCIALBEHAVIOR

health,because of the combinedeffects of limitationsin the size of our availablesample and

the very high level of intercorrelations
between our indexes of SES and occupational
conditions, we have not been able to carry out
analyses that reliably disentangle the causal
connections among SES, job-conditions, and
health.Hence, the centralfocus of this paperis
limited to the effects of non-occupational
facets of SES on health outcomes.
In the presentpaper,we used data from two
waves of an extensive longitudinal study
(Kohn and Schooler 1983; Schooler and
Mulatu 2001; Schooler, Mulatu, and Oates
1999) to reexamine the relationshipsbetween
SES and health. The nature of our data also
permitted us to use various forms of causal
structural equation modeling to specifically
test a number of the above hypotheses about
the causal mechanisms underlying the SEShealth relationship.In orderto do this we estimatedfive sets of models hypothesizingdifferent causal relationships.First, we estimated a
model to test the degree to which the correlation between SES and health was due to the
effect of SES on health and how much was due
to the reciprocal effect of health on SES.
Although many of the investigatorsview their
findings as providing evidence that the SEShealth relationshipis due to the effect of SES
on health (Power,Matthews,and Manor 1998),
some studies have shown evidence for the
reverse effect of levels of health on SES (van
de Mheen et al. 1998). To our knowledge, no
studieshave used structuralequationmodeling
to test reciprocal effects models that simultaneously estimate the effects of both possible
causal directions.
Second, given the findings that different
indexes of SES relateto levels of health differently (Adler and Ostrove 1999; Marmotet al.
1997), we estimated a model to test the
hypotheses that particularcomponentsof SES
(i.e., education, income) have independent
effects on health status over and above their
combined effects. We focused particularlyon
the effects of income and educationbecause it
is plausible that income and education may
each independently provide individuals with
resourcesthat enable them to select and carry
out health promoting actions (e.g., locate and
employ effective doctors, select and adhereto
healthfuldiets).
Third, we tested whether the outcomes of

health-related lifestyles/behaviors such as

smoking, exercise, sleep, and observed weight
influence the SES-health relationship. We
hypothesized that health-related lifestyles/
behaviorswould relate to both SES and health
and that controllingfor their effects would significantly reduce the SES-healthgradient.
Fourth,we hypothesized that psychological
distress, as reflected by self-reportedlevels of
anxiety and self-deprecation,would have significant negativereciprocalcausal connections
with both SES andhealthand thus help explain
some of the SES-healthrelationship.Thus, we
tested a model that has three-way reciprocal
effects among SES, health, and psychological
distress.
Finally, we tested a model that combined
effects of statisticallysignificanthealth-related
lifestyle/behavioralfactors and psychological
distress on SES and health. Figure 1 presents
our general model, which shows the hypothesized relationshipsbetween our latentconcepts
of interest.
METHOD
Respondents
The male participants were a subsample,
interviewedin 1974, of a nationallyrepresentative sample of employed men first interviewed in 1964 for the Kohn and Schooler
(1983) study of the psychological effects of
occupationalconditions.The 1964 sample was
an area probability sample, drawn by the
National Opinion Research Center of males
over 16 years of age who were then currently
employed at least 25 hours per week in nonmilitary occupations.From an initial selection
of 4,105 men, a reasonablyrepresentativesample of 3,101 (76%) completedthe interviews.
In 1974, the National Opinion Research
Center, in carrying out the follow-up survey
for Kohn and Schooler (1983), interviewed a
representativesample of approximatelyonefourth of the 1964 respondentswho were less
than 65 years old at that time. Of the 883 men
who were randomlyselected for the follow-up
study,National Opinion Research Center succeeded in locating 820 (93%). Of the 785 men
who were still alive, National Opinion
Research Center actually interviewed 687
(88%). Assessment of the generalizability of

THESES ANDHEALTH
CONNECTIONS
EXPLAINING

25

FIGURE 1. The General SES-Health Reciprocal Effects and Mediating Mechanisms Model

this subsample revealed no demographicdifferences between the men who were interviewed and those who were randomlyexcluded from the 1974 study.
In 1974, the wife of every male respondent
who was then married was also targeted for
interview.Interviewswere conductedwith 555
women, 90 percent of the 617 eligible. They
ranged in age from 21 to 65 years. Besides
sampling issues arising from the lack of independence of the women's sample, we face two
issues of generalizability.First, the women's
sample did not have adequaterepresentationof
the younger and older women because it consisted of women who were marriedto men who
were at least 26 years old and no older than 65
at the time of the 1974 survey.A second problem of generalizability is whether the results
based on marriedwomen would generalize to
those never married and previously married.
For the present study, generalizations about
women can most confidently be made to (1)

those who were married in 1974 to men

between 26 and 65 years of age who had been
working in 1964 and (2) quite plausibly to
other women in the same cohort.
In preparationfor the 1994/1995 follow-up,
we succeeded in locating 95 percent (650) of
the 687 households that took part in the 1974
survey. The present analyses included all
respondents for which there were relevant
1974 and 1994/1995 data. Of the 687 men
interviewedin 1974, 647 (94.2%) were located
in 1994/1995; of these, 192 (29.7%) had died
and 18 (2.8%) were disabled.Of the remaining
437 cases, 352 (80.5%) were interviewed,and
the other 85 cases (19.5%) were not interviewed because they refusedoutrightor proved
to be unavailableafter three contacts.The parallel numbers for the 555 women who were
interviewedin 1974 were: 510 (91.9%) found,
of these 56 (11.0%) had died and 12 (2.3%)
were disabled.Of the remaining442 cases, 355
(80.3%) were interviewed, and the other 87

26

JOURNALOF HEALTHAND SOCIALBEHAVIOR

(19.7%) cases were not interviewedbecause of

refusal or unavailability.
The total sample for the present analyses
contained 351 men and 356 women. The
respondentsrangedin age from 41 to 88 years
with a mean of 64.0 (SD = 9.5). There were
661 European Americans, 40 African
Americans, and 6 respondents from other
racial or ethnic origins. Their median level of
educationwas high school graduatewith some
technical schooling. Two hundred forty-two
(34.2%) worked for pay both in 1974 and
1994/1995. In orderto determinehow our current sample might be different from the 1974
sample, from which it was derived, we performed a series of logistic regressionanalyses.
Participants'1974 socio-demographiccharacteristics, including age, gender, race, education, occupational status, family income, and
working status were used to predict whether
therewere differences:(1) betweenthe respondents who were or were not located and (2)
among those located, between those interviewed and not interviewed.
There were only two statisticallysignificant
socio-demographic predictors of whether or
not 1974 participantswere located (X2[df= 7,
N = 1,242] = 17.92.14, p = .01). The results
suggested that those we had located in
1994/1995 were younger and less likely to be
AfricanAmericansthanwere those we had not
located. Beyond these differences, those who
were not located tended to be similar in their
1974 characteristicsto those we had found. In
terms of who was interviewed, participants
who were interviewedin 1994/1995 were more
likely to be male, younger, educated,
employed, and less likely to be African
Americansthan those we did not interview(X2
[df= 7, N = 1,157] = 169.79, p < .001). All in
all, the differenceswe found between those we
did and did not locate and re-interviewsuggest
that we should temper the generalizationswe
make from these data with the acknowledgment that female, older, unemployed,less educated people, and African Americans may be
underrepresentedin our sample.

logical effects of occupationalconditions, but

also on a general review of other researchrelevant to understandinghow older individuals
react psychologically to their environments.
The interviews were carried out by the
National Opinion Research Center and the
Cygnus Corporation (Rockville, Maryland),
all of the interviewersbeing trainedand supervised by the Center.It took an average of 3.5
hours to complete an interview. Respondents
were paid $50.
Measures

Socio-economic status. Both 1974 and

1994/1995 SES factors were measuredby levels of education, family income, and occupational status (Hollingsheadand Redlich 1958).
Education in both 1974 and 1994/1995 was
coded from 1 (primary grade level) to 9
(advanced degree). In 1974, reported family
income was coded from 1 (less than $3,000) to
14 ($75,000 or more). In 1994/1995, reported
family income was coded from 1 (up to
$1,500) to 32 (above 870,000). In both 1974
and 1994/1995, occupationallevel was coded
using the Hollingshead rating scale
(Hollingshead and Redlich 1958; from 1 =
unskilled to 7 = managerialand professional).
If the respondents were married and both
worked,we used the highest occupationalstatus of the couple based on the assumptionthat
when the occupational status of the spouses
differ,the families' social status is likely to be
heavily influenced by the status of the highest
ranking spouse (e.g., in the case of company
president/secretary).If the respondents were
marriedand one of the partnersdid not work,
the occupationalstatus of the working partner
was used for both. If the respondents were
unemployed during the time of the interview,
the occupation status of their last job was
coded. It should be noted that the
Hollingshead'sscheme of coding occupational
status has been found reasonableand strongly
correlated to other occupational status measures (Schooler and Schoenbach 1994).
Health status. Our 1974 Health factor was
based on two indicators. The first indicator
Data Collection
was derivedfrom the question, "Haveyou had
Our data are derived from a subset of ques- any seriousphysical illness or injurywithin the
tions from a much largerinterview.This inter- past one year?"Respondentswere asked to list
view was based not only on the earlier Kohn up to three illnesses and then asked to rate the
and Schooler (1983) research on the psycho- degree of impact of each health problem on

27

EXPLAININGTHE SES AND HEALTHCONNECTIONS

their lives on a four point scale (1 = not much

at all to 4 = a great deal). A single indicator
was createdby summingup the impactratings.
The second indicatorwas based on the question, "Atthe presenttime, do you have a physical health condition that limits your activities?" Based on the informationgatheredduring the interview, trained coders then rated
whether the respondent's:(1) emotional/psychological wellbeing was affected; (2) future
was threatened;(3) ability to workwas limited;
(4) ability to stand,walk, bend, or sit was limited, or (5) ability to think or concentratewas
limited by the health condition identified. The
ratings (0 = no limitationor impact, 1 = probable limitationor impact,and 2 = definite limitationor impact)were summedacross the five
categories to create the indicator with values
rangingfrom 0 to 10.
Our 1994/1995 Healthfactorwas based on a
previous analysis (Mulatuand Schooler 1999)
and was indicatedby three variables:the number of physical illnesses the respondent was
diagnosedwith at the time of the interview,the
numberof types of prescriptionmedicationthe
respondent took within the 24-hour period
prior to the interview, and the respondents'
self-rateddegree of health as comparedto age
peers (1 = extremely poor to 7 = extremely
good). The negative health indicatorsboth in
1974 and 1994/1995 were reverse scored to
reflect absence of health problems.
Health-related lifestyles/behaviors. Four
health-relatedlifestyles/behaviorswere used in
this study: aerobic exercise, diet (as reflected
by judged weight), smoking, and sleep. Both
1974 and 1994/1995 Exercise factors were
measuredby two indicators:the frequency of
exercise in a month and the numberof types of
sport activities in which one frequently
engaged. Our 1974 and 1994/1995 Weightfactors were each based on a single-indicator
interviewers' rating of the weight of the
respondentson a five-point scale: 1 = skinnyto
5 = obese. Smoking was measuredonly in the
follow-up study.This 1994/1995 Smoking factor was indexed by the averagenumberof cigarettes smoked daily and whether or not the
respondents smoked during the interview
(coded as 1 = did not ask and did not smoke, 2
= asked but did not smoke, 3 = asked and
smoked, and 4 = did not ask but did smoke).
Finally, both 1974 and 1994/1995 Sleep factors were each indexedby a single variablethat

measured the total hours of sleep the respondents had in a typical day.
Psychological distress. Symptoms of anxiety and self-deprecation were measured by
standarditems adaptedby Kohn and Schooler
(1983) from popularlyused assessment instruments. Eleven indicators(e.g., "How often do
you feel uneasy about something without
knowing why?") measured both 1974 and
1994/1995 Anxiety factors.Each indicatorwas
ratedon five point scale in 1974 and on a seven
point scale in 1994/1995 (1 = never to 5 or 7 =
always). Similarly, our 1974 and 1994/1995
Self-Deprecation factors were based on five
indicators (e.g., "How frequentlydo you feel
downcast or dejected?")rated on a five point
scale in 1974 (1 = never to 5 = always) and on
a seven point scale in 1994/1995 (1 = never to
7 = always).
Demographic characteristics. Measures of
age, gender (1 = male, 2 = female), and race (1
= EuropeanAmerican,2 = AfricanAmerican);
were also included.'
Data AnalyticProcedures
The structuralequation models were estimated on covariancematricesusing the recently releasedMplus version 2 modeling program
(Muthenand Muthen2001). Figure 1 presents
our general model and the hypothetical relationships that were expected. We followed a
strategyof testing the componentsof the generalmodel before testing it in its entirety.Thus,
our first model (core SES-healthmodel) postulated reciprocal effects between 1994/1995
SES and 1994/1995 Health, and longitudinal
paths from 1974 SES and 1974 Health to their
correspondingfactors in 1994/1995, and paths
to 1994/1995 SES and 1994/1995 Health from
age, gender, and race. Subsequent analyses
built on this core SES-healthmodel by including health-relatedlifestyles/behaviorsor psychological distress, or both, and reciprocal
effects among these mediating factors, SES,
and health status in 1994/1995.
In all ourmodels, residualsbetween endogenous concepts thatwere reciprocallyconnected
and errors between similar indicators across
time (e.g., between 1974 and 1994/1995 levels
of education) were allowed to correlate. In
addition, other error correlations were also
allowed if the modification indices suggested
that model fitness would improve and if such

28

JOURNALOF HEALTHAND SOCIALBEHAVIOR

correlationsare theoreticallyplausible. In subsequentre-estimations,we excluded,in a stepby-step manner, non-significant paths from

backgroundvariables,non-significantresidual
correlations,and, finally, non-significantpaths
from substantive predictors (e.g., 1994/1995
health-related lifestyle/behavioral factors) to
the outcome constructs(i.e., 1994/1995 health
status or SES). In the results section, we present in detail the findings of the model estimations after all of the above adjustmentswere
made.
We identifiedthese non-recursivemodels by
estimatingthe reciprocaleffects only "contemporaneously"and by not simultaneouslytesting for cross-lagged effects. The exclusion of
these cross-lagged effects provides instruments to identify the model. This approachfollows that of Kohn and Schooler (1983, chapter
6) and Schooler,Mulatu,and Oates (1999); for
general discussions of it, see Heise (1975) and
Kohn and Slomczynski (1990, pp. 130-31).
The consequenceof this modelingprocedureis
that for each pair of variablesinvolved in a reciprocal relationship,the observed concurrent
effect of one variable on the other is actually
the sum of the true contemporaneouseffect
and the omitted cross-lagged effect. Thus,
when we test a model thatonly examines "contemporaneous" effects, without modeling
lagged effects, we can reasonablyassume that
the effects we find significant are real,
although we cannot assess how much of the
effect is actually contemporaneousand how
much is actuallylagged. What is certainis that
any significant reciprocal paths between our
measuresof the complexityof leisure activities
and cognitive functioning represent the total
effect of each type of measure on the other
over the two time periods.
Three indices of model goodness-of-fit
availablein Mplusversion 2 were used. (1) The
X2statistic divided by the degrees of freedom
was used to evaluatehow closely the expected
covariancematrix derived from the estimated
model fits the actually observed matrix. A
X2/dfratioof 2 or less indicatesa very good fit,
although some have considered values less
than 5 as acceptable (Bollen and Long 1993;
Hayduk 1987). (2) The ComparativeFit Index
(CFI), which is a measureof how much better
the proposed model fits the observed data
comparedto a baseline, usually a null, model
(Bentler 1990) was also used. The CFI is consideredparticularlyappropriatefor small sam-

ples and multiple-groupmodels (Bentler 1990;

Hu and Bentler 1995). Scores of above .90 on
this index are considered acceptable (Hu and
Bentler 1995). (3) The Root Mean Square
Errorof Approximation(RMSEA), which is a
measure of residual variance adjusted for the
degrees of freedom (Steiger 1990), was also
included. A RMSEA less than .05 is considered to representa good fit, although values
less than .08 are also taken as indicative of an
appropriatemodel (Browneand Cudeck 1993).
RESULTS
Properties of MultipleIndicatorFactors
Our causal models include variables measuredby single indicators,as well as latentfactors based on multiple indicators.The singleindicator-basedvariables (i.e., age, race, gender, weight, and sleep) for which we could not
use structuralequationmodeling to adjust for
measurementerror,were assumed to be measured error free. On the other hand, for latent
factors indexed by two or more indicators,
such as SES, Health, Anxiety, SelfDeprecation,Smoking, and Exercise, structural equationmodeling could be used to develop
measurementmodels so that the effects of the
measurement errors could be accounted for.
For ease of presentation, in this section we
describethe developmentand propertiesof the
measurementmodels for each set of multiple
indicator-based latent factors separately,
althoughall of our final measurementparameters were estimatedas part of full-information
structuralequationmodels in which all of the
measurementand causal parametersare estimated simultaneously.
In our development of a measurement
model for 1974 and 1994/1995 SES, SES was
indexed by three variables in both time periods. This two-factor measurementmodel fit
the data well (X2[df = 5, N = 706] = 13.27; p
= .02; RMSEA = .02; CFI = .99). In our measurement model for the latent concept for
health status,Health,was indexedby two variables in 1974 and threevariablesin 1994/1995.
This measurementmodel also showed a very
good fit to the data (X2 [df = 4, N = 705] =
4.86; p = .31; RMSEA = .02; CFI = .99). A
third measurement model was estimated for
the health-related lifestyles/behaviors. This
model includedlatentfactorsindexedby single

29

EXPLAININGTHE SES AND HEALTHCONNECTIONS

indicators (e.g., 1974 and 1994/1995 Weight

and Sleep) and those indexedby multiple indicators (e.g., 1994/1995 Smoking, 1974 and
1994/1995 Exercise). Here again, the measurement model showed very good fit to the data
(X2 [df = 16, N = 690] = 28.54; p = .03;

Distress factors in 1974 and 1994/1995. This

model also had a good fit to the data (X2[df=
430, N = 706] = 734.80, p < .001; RMSEA =

.03; CFI = .95), and provides a theoretically

parsimonious model. In both analyses, all of
the variables loaded statistically significantly
RMSEA = .03; CFI = .99). In all of these mea- on theirrespective factors.Table2 presentsthe
surementmodels, the loading of the indices on loadings of the indicators on their respective
their respective latent factor was statistically first-orderfactors from the subsequentlyestisignificant at least at the p < .01 level. Table 1 mated full-informationmodels.
presents these indices and their loadings from
the subsequently estimated full-information
models.
Confirmingthe SES and HealthAssociation:
A fourthmeasurementmodel was estimated The Core Model
that included the two psychological distress
factors measured similarly in both 1974 and
Our initial task was to confirm that our data
1994/1995: Anxiety (indexed by eleven items) show the expected relationshipsbetween SES
and Self-Deprecation(indexed by five items). and health, and to examine the nature and
The initial four factor model fit the data quite extent of the reciprocalrelations between the
well (X2 [df = 429, N = 706] = 707.69, p < two factors.The proposedcore model estimat.001; RMSEA = .03; CFI = .96). It gave evi- ed (1) reciprocal effects between 1994/1995
SES and 1994/1995 Health, (2) longitudinal
dence, however, of very strong correlations
between 1974 Anxiety and 1974 Selfpaths from 1974 SES and 1974 Health to their
Deprecation (r = .72, p < .001) and between
counterpartsin 1994/1995, and (3) paths from
the corresponding factors in 1994/1995 (r = age, gender, and race to 1994/1995 SES and
.69, p < .001). We therefore estimated another 1994/1995 Health. We also estimated signifimeasurement model in which the first-order cant residual correlations between the
factors of Anxiety and Self-Deprecation
1994/1995 latent concepts and theoretically
reflected separate second-order Psychological
plausible correlationsof indicator errors.The
TABLE 1. Standardized Factor Loadings of Indicators of Health, SES, Exercise, and Smoking from
Combined Full-Information Model
Factorsand Indicators
1974 Health
Serious illnesses or injuriesa
Extent of functionallimitationsdue to healtha
1994/1995 Health
Numberof diagnoses made by doctorsa
Self-ratedhealth relativeto peers
Types of prescriptionmedicationsa
1974 SES
Yearsof education
Occupationalstatus
Familyincome
1994/1995 SES
Yearsof education
Occupationalstatus
Family income
1974 Exercise
Number of sports/exerciseactivities
Frequencyof participationin those activities
1994/1995 Exercise
Number of sports/exerciseactivities
Frequencyof participationin those activities
1994/1995 Smoking
Averagenumberof cigarettessmoked daily
Extent of smoking duringthe interview
Note: All factor loadings are statisticallysignificant at least at p < .01.
a Reverse scored items.

StandardizedCoefficient
.39
.64
.86
.53
.64
.71
.77
.63
.71
.68
.55
.85
.45
.99
.65
.95
.76

30

JOURNAL OF HEALTH AND SOCIAL BEHAVIOR

TABLE 2. Standardized Factor Loadings of Indicators of Anxiety and Self-Deprecation from

Combined Full-Information Model
StandardizedCoefficients

Factorsand Indicators
Anxiety
1. Feels aboutto go to pieces
2. Feels downcastand dejected
3. Feels anxious and worrying
4. Feels uneasy without knowing why
5. Feels restless that he/she cannot sit still
6. Feels unable to get rid of some ideas
7. Feels bored with everything
8. Feels powerless to get what he/she wants
9. Feels guilty for having done somethingwrong
10. Feels that the worldjust isn't understandable
11. Feels not much purpose in being alive
Self-Deprecation
1. Wishes he/she could have more respect for self
2. Thinks that he/she is no good at all
3. Feels useless at times
4. Wishes he/she could be as happy as others
5. Feels uncertainabout many things
Note: All factor loadings are statisticallysignificant atp < .01.

1974
.59
.68
.48
.45
.47
.47
.57
.58
.39
.45
.51

1994/1995
.75
.75
.62
.57
.50
.48
.67
.69
.21
.55
.65

.52
.64
.61
.39
.34

.69
.74
.70
.58
.39

pendenteffects of the two indexes of SES, two

separate models were estimated that added
paths from 1994/1995 family income and levIn subsequentmodeling, we excluded non- els of educational attainment,respectively,to
significant paths from demographicfactors to 1994/1995 Health in the core model. In both
1994/1995 SES and 1994/1995 Health, and models, the addedpaths from 1994/1995 famadded two errorcorrelationssuggested by the ily income (y = .03, p > .10) and from
modification indices: between age and the part 1994/1995 levels of education( = .04, p > .10)
of 1994/1995 family income not explained by to 1994/1995 Health did not reach statistical
SES and between 1974 extent of functional significance. In both cases, the reciprocal
limitations due to health and family income. effects between 1994/1995 SES and
This re-specified model (see Figure 2), which 1994/1995 Health remained significant and
fit the data much better than the original one were identical with the findings of the earlier
(X2 [df = 41, N = 705] = 84.56, p < .001; core SES-healthmodel. These results suggest
RMSEA = .04; CFI = .99), demonstrated the that education and income levels did not have
existence of significant reciprocal effects independenteffects on health statusaside from
between 1994/1995 SES and 1994/1995 those of SES.
Health. In doing so it confirmed the hypotheses that health is both affected by and affects
SES, while indicatingthat SES had a stronger Impactsof Health-RelatedLifestyles/
Behaviors on SES and Health
effect on health than health had on SES.2
initial estimation indicated a reasonablywell-

fitting model (X2 [df= 56, N = 699] = 272.24,

p < .001; RMSEA = .07; CFI = .95).

Independent Effects of SES Components on

Health
As we noted in the introduction, it is plausible that apart from being indexes of SES, both
income and education may each independently
facilitate individuals' abilities to take health
maintaining and improving actions. To test the
possibility that the SES-health status relationship is in large part the function of the inde-

We also tested the hypothesis that the SEShealth reciprocalrelationshipswe found are a
function of health-relatedlifestyle/behavioral
differences. Finding reductions in the magnitudes of the direct causal paths between SES
and health status when health-related
lifestyles/behaviors are modeled as affecting
both has importantimplications.From a theoretical perspective, such findings would suggest that among the mechanisms through
which SES and health status affect each other

CONNECTIONS
THESES ANDHEALTH
EXPLAINING

31

Note: x2 (df = 41, N = 705) = 84.56,p < .001; RMSEA = .04; CFI = .99.

**p < .01; ***p < .001.

FIGURE 2. The Core SES-Health Reciprocal Effects Model

are their respective effects on health-related

and behaviors. Our SESlifestyles
lifestyles/behaviors-healthmodel had the following open parameters.As in our core SEShealth model, we included reciprocal effects
between 1994/1995 SES and 1994/1995
Health. In addition, with the exception of
1994/1995 Smoking factor, for which we did
not have earlier data, we posited reciprocal
paths between our other 1994/1995 healthrelated lifestyle/ behavioral factors (Exercise,
Weight, and Sleep) and 1994/1995 SES and
1994/1995 Health. In the case of 1994/1995
Smoking, we estimated a path from it to
1994/1995 Health and another path from
1994/1995 SES to it. Paths from age, race, and
gender to 1994/1995 health-relatedlifestyles
and behaviors were added. Residual correlations between health-related lifestyle/behavioral factors were also allowed. In our initial
estimation attempt,we found the model to fit
the data quite well (X2 [df = 178, N = 674] =
316.07, p < .001; RMSEA = .03; CFI = .98).
The re-estimatedfinal model (see Figure 3),
which included significant paths and residual
correlations and excluded the non-significant
ones, fit the data very well (X2[df = 200, N =

674] = 342.66, p < .001; RMSEA = .03; CFI =

.97). Although this re-specified model showed
no appreciable improvement in the global
model fit statistics comparedto the one before
re-specification, it providedimprovedspecific
parameterfit statistics and clearer results. As
shown in Figure 3, the results of this analysis
indicate that 1994/1995 SES and 1994/1995
Healthcontinuedto have significant reciprocal
causal connections, as they had in the earlier
models in which the health-related
lifestyles/behaviors were not included. The
magnitudesof these causal connections, however, appearedto be slightly weakened by the
impact of lifestyle/behavioral factors (i.e.,
from P = .24 to P = .22 in the path from
1994/1995 SES to 1994/1995 and from P = .14
to P = .09 in the reverse path), the reduction
being by about 8 percent and 33 percent
respectively. The findings indicate that
1994/1995 Sleep had significant reciprocal
relationships with both 1994/1995 SES and
1994/1995 Health. Higher levels of 1994/1995
Weight, which was significantly increased by
lower 1994/1995 SES, significantly decreased
the levels of 1994/1995 Health. The reverse
effect from 1994/1995 Health to 1994/1995

32

JOURNAL OF HEALTH AND SOCIAL BEHAVIOR

Note: Z2(df= 200, N = 674) = 342.66,p < .001; RMSEA = .03; CFI = .97.
* p < .05; ** p < .01; *** p < .001.
FIGURE 3. The SES-Health Lifestyles/Behaviors-Health Model

Weight was not significant; neither was the

path from 1994/1995 Weight to 1994/1995
SES. Interestingly, 1994/1995 SES also had
significant impacts on all of the other
1994/1995 health-relatedlifestyles/behaviors.
All in all, the findings from this analysis
indicate that althoughthere is a web of causal
interconnectionsamong the SES, health, and
the health-related lifestyle/behavioral factors
in our model, these lifestyle/behavioralfactors
playedat best a moderatepartin explainingthe
SES-healthrelationship.The partthat they did
play seemed to be concentratedon explaining
the causal path from health to SES.
Impacts of Psychological Distress on SES and
Health

Psychological distressassociatedwith lower

SES has been considered anothermechanism
by which SES has its impacts on health status.
We used two measures of psychological distress, Anxiety and Self-Deprecation, to test
whether or not such mechanisms underlie the
SES-health status relationshipin our data. As
indicated earlier, because of the strong intercorrelationbetween the two factors, we created a second order factor: Psychological
Distress. Following a strategy parallel to that
used in the preceding model, we specified a
three-way reciprocal effects model among
1994/1995 SES, 1994/1995 Health, and
1994/1995 Psychological Distress. As before,
paths from age, race, and gender to the
1994/1995 latent factors were included;residual correlations between endogenous factors

EXPLAINING
THESES ANDHEALTH
CONNECTIONS
were also allowed. Here again, our initial estimate of this model indicateda very good fit to
the data (X2[df= 919, N = 699] = 1,469.18, p
< .001; RMSEA = .03; CFI = .95).
When we re-estimatedthe model using our
usual procedure of excluding, one at a time,
the smallest (1) non-significantresidualcorrelations, (2) non-significant paths from demographiccharacteristicsto 1994/1995 latentfactors, and (3) non-significantpaths to and from
1994/1995 latent factors, our final model of
SES-Psychological Distress-Health (see
Figure4) showeda very good fit to the data(X2
[df = 884, N = 705] = 1,415.07, p < .001;
RMSEA =.03; CFI = .95). The improvementin
model fit was marginally significant using a
one-tailed test. The findings indicated that

33

even when Psychological Distress was included as a potentialcause of each, 1994/1995 SES
and 1994/1995 Health continued to significantly affect each other. The direct effect of
SES on health, however, was reduced by 33
percent from what it was in the core model
(from P = .24 to P = .16), while the magnitude
of the effect of health on SES remainedessentially unchanged(from P = .14 to P = .13). The
resultsalso indicatethat 1994/1995 Healthand
1994/1995 Psychological Distress had significant negative reciprocaleffects on each other.
There was also a marginallysignificant negative causal path from 1994/1995 SES to
1994/1995 Psychological Distress. The overall
patternof results suggests thata notablepartof

Note:X2(df = 884, N = 705) = 1,415.07,p< .001;RMSEA= .03; CFI = .95.

ap < .10; *p < .05; **p < .01; ***p < .001.
FIGURE 4. The SES-Psychological Distress-Health Model

34

JOURNALOF HEALTHAND SOCIALBEHAVIOR

the effect of SES on healthis mediatedthrough and concurrentlyestimatedthem in one model.

In this model, we estimated the effects of the
SES differencesin Psychological Distress.
two sets of mediating mechanisms by including only statistically significant paths and
CombinedImpacts of MediatingFactors on
residualcorrelationsfrom the models that sepSES and Health
arately examined the effects of health-related
lifestyles/behaviorsand psychological distress,
In order to assess the degree to which the whose findings were presentedin the two predifferenttypes of variablesserve as the mech- vious sections.
The combinedmodel (see Figure 5) showed
anisms through which SES and health status
affect each other, we combined health-related a very good fit to the data (X2[df= 1,378, N =
lifestyles/behaviorsand psychological distress 699]) = 2,051.53,p < .001; RMSEA = .03; CFI

Note: X2(df = 1,378, N = 674) = 2,051.53,p < .001; RMSEA = .03; CFI = .95.
ap < .10; *p < .05; **p < .01; ***p < .001.
FIGURE 5. The Combined SES-Mediators-Health

Model

35

EXPLAININGTHE SES AND HEALTHCONNECTIONS

= .95). It demonstratedthe existence of significant reciprocal effects between 1994/1995

Health and 1994/1995 SES and between
1994/1995
Health
and
1994/1995
Psychological Distress. Other significant reciprocal paths included those between
1994/1995 Sleep and 1994/1995 Health and
between 1994/1995 Sleep 1994/1995 and SES.
There were also statistically significant paths
from 1994/1995 SES to 1994/1995 Weightand
from 1994/1995 Weight to 1994/1995 Health.
Regardlessof the additionof both health-related lifestyles/behaviorsand psychological distress variables, the reciprocal paths between
1994/1995 SES and 1994/1995 Health
remainedstatisticallysignificant. However,the
inclusion of these factors reduced the magnitude of the path from 1994/1995 Health to
1994/1995 SES by 36 percent and the reciprocal path from 1994/1995 SES to 1994/1995
Healthby about46 percent(see Table3). These
reductionssuggest that a notableproportionof
the overall SES-healthrelationshipis mediated
throughthese factors. Furthermore,as can be
seen from Table 3, the relatively small further
reduction(from 3 = .24 to P = .22) in the SES
to Health path when the health-related
lifestyles/behaviorswere addedas comparedto
that when Psychological Distress was added
(from P = .24 to P = .16) as mediatingmechanisms suggests that much of the effect of SES
on ill healththatwe have foundmay be an indirect result of differences in Psychological
Distress. In contrast, health-relatedlifestyles/
behaviorsaccounted for a largerproportionof
the path fromHealthto SES when comparedto
Psychological Distress. In any case, no matter
what the relative effects of psychological distress and health-relatedlifestyles/ behaviorson
health are, the continued significance, despite
decreases in magnitude, of the reciprocal
effects between 1994/1995 SES and 1994/
1995 Health shows that the SES-health relationship is far from completely explained by

the differences we have examined in healthrelated lifestyles/ behaviorsand psychological

distress.
Impacts of Sample Compositionand Gender
Differences
In our study, the issues of sample composition and genderdifferencesmay be interrelated.
It is conceivablethatourresultscould havebeen
affectedby the fact thatthe women in our sample were not randomly and independently
selected, but were the wives of the men in the
original 1964 Kohn and Schooler sample. A
substantiveconsequence of this featureof our
sampleis thatthe responsesof the husbandsand
theirwives may reflect characteristicscommon
to the couple. It is also possible that,aside from
samplingissues, gender differencescould exist
thatdifferentiallyaffectthe SES-healthrelationships.We dealtwith these issues by carryingout
two types of analyses: (1) single-groupmenonly analyses, and (2) multi-group analyses
comparingmen andwomen. Giventhatthe men
were a nationalrepresentativeand independently selected sample,the men-onlyanalysesdealt
with concerns about the degree to which the
results based on our combined sample of men
andwomen could havebeen affectedby the fact
thatthe women in our samplewere not selected
independentlyfrom the men. The mutli-group
analyses explored the potential gender differences by testing whetherthe model parameters
were the same for men and women. In both sets
of analyses,two of ourpreviousmodels werereestimated:the core SES-healthmodel (Figure2)
and the combinedSES-mediators-health
model
5).
(Figure
The results of the men-only models were
remarkablysimilar to the results of the core
SES-health reciprocal effects model reported
in Figure2. All significant paths, includingthe
SES-healthreciprocaleffects, remainedsignif-

TABLE3. Summary of the Impacts of Health-RelatedLifestyles/Behaviorsand Psychological

Distresson the SES-HealthRelationships
Direction of Path
Models
SES-> Health
Core SES-healthmodel
.24
Core model + health lifestyles/behaviors
.22
Core model + psychological distress
.16
Core model + health lifestyles/behaviors+ psychological distress
.13
Note: The numbersin the table are standardizedcoefficients and are statisticallysignificant at p < .05.

Health-> SES
.14
.09
.13
.09

36

JOURNALOF HEALTHAND SOCIALBEHAVIOR

icant. The combined SES-mediators-health

model for men, however,revealedsome differences from what was reported in Figure 5.
Three previously significant paths became
non-significant: one path from 1994/1995
Psychological Distress to 1994/1995 Health (5
= -.05, p > .10) and two paths from 1994/1995
SES to 1994/1995 Psychological Distress (P =
-.04, p > .10) and 1994/1995 Weight(P = -.04,
p > .10). Despite these differences, all other
parametersremainedsignificant including the
reciprocal SES-health effects, suggesting that
our central findings were robust even in this
much reducedsample.
The re-estimation of the core SES-health
and the combined SES-mediators-healthmodels as multi-groupmodels comparingmen and
women showed that (1) the models fit the data
as well as the models estimated in the single
group analyses with our total sample, and (2)
that the main SES-health reciprocal effects
remained significant with only minor differences being found between men and women.
Only three gender differenceswere identified,
one in the core SES-healthmodel and two in
the combined SES-mediators-healthmodel.
The core SES-health multi-group analysis
indicatedthat the path from age to 1994/1995
Health was statistically different in the two
groups. Relaxing the equality constraint as
suggested by the modification indices indicated thatthe effect of age on healthfor women (y
-.35, p < .001) was greaterthanthat for men
(y = -.20, p < .001). The re-estimated combined SES-mediators-healthmodel indicated
that the paths from 1994/1995 Sleep to
1994/1995 Health and from 1994/1995 SES to
1994/1995 Weightwere significantly different
for men than for women. We subsequently
relaxed these paths and re-estimated the
model. Although both are in the same direction, the path from 1994/1995 Sleep to
1994/1995 Health remained significant for
men (P = .58, p < .001) but not for women (P
= .21, p > .10). In contrast, the path from
1994/1995 SES to 1994/1995 Weight continued to be significant for women (P = -.28, p <
.001) but not for men (1 = .02, p > .10), a finding consistent with the men-only analysis. No
other differenceswere found.
All in all, our supplementaryanalyses dealing with the issues of sample composition and
gender differences indicate the fact that our
primary analyses that combined the two genders did not unduly affect the findings. These

analyses also suggest that the two genders did

not differ greatly in terms of the SES-health
relationship and its determinants.Our confidence in this latter conclusion has to be tempered,however,by the caveatthatthe sampling
procedures used may have served to reduce
potentialgender differencesin our sample.
DISCUSSIONSAND CONCLUSIONS
The centralgoals of this paperhave been to
determineif SES and health are causallyreciprocally connected and, if so, to examine the
degreeto which health-relatedlifestyles/behaviors and psychologicaldistressserve as mediating mechanisms underlying the persistently
reported, gradient-like, relationship between
SES and health. Consistentwith the literature
(Adler and Ostrove 1999; Marmot 1999;
Marmotet al. 1997), our core structuralequation modeling based analyses confirmed the
existence of a relationshipbetween SES and
health.Unlike most studiesthatonly focused on
a unidirectionalrelationshipbetween SES and
health, our analyses also established that the
SES-healthrelationshipis the result of a reciprocal causal connection between the two. The
significantand substantialcausalpathwe found
from SES to health in our core model provides
empirical evidence for the "social causation"
hypothesisthat SES differencesin health-relevant life circumstancescause SES disparitiesin
health.This hypothesishas been the most consistentlyadvocatedin the literature(Adler and
Ostrove 1999; Marmot 1999), even though the
direction of the actual causal connection
between SES and healthhas generallynot been
put to the test. In fact, althoughnot as strongas
the reciprocalpathfromSES to health,ourfinding of a significant causal path from health to
SES provides evidence for the alternative
"social drift"hypothesis that, over time, sickness resultsin a loss, and good healthin a gain,
in SES. Otheravailableevidence for this effect
is primarilybased on studies that linked childhood and adolescent illnesses to their subsequent SES impacts (Koivusilta, Rimpela, and
Rimpela 1998; van de Mheen, et al. 1998). Our
findings suggest that the effects of adults'
health on their SES shouldnot be dismissed as
unimportant.
Our other analyses centered on explicating
some of the specific ways that SES and health
affect each other. We did this by determining

EXPLAININGTHE SES AND HEALTHCONNECTIONS

the degree to which a range of potentially

health-relevant lifestyles/behaviors and psychological characteristicsserved as the proximal mediating mechanisms through which
SES affects and is affectedby health.We found
that some health-related lifestyles/behaviors
(i.e., sleep, weight) and psychological distress
do in fact serve as mechanisms underlying
both reciprocal causal connections between
SES and health. In terms of the magnitudeof
the "social causation" path from SES to
Health, controlling the effect of our set of
health-relatedlifestyles/behaviors led to an 8
percentreductionin path size, controllingpsychological distress to a 33 percent reduction,
and controllingboth to a 46 percentreduction.
In terms of the reciprocal "social drift" path
from Health to SES, controlling the effects of
health-relatedlifestyles/ behaviors led to a 36
percentreductionin path size, controllingpsychological distress to a 7 percent reduction,
and controllingboth to a 36 percentreduction.
Despite these reductions, none of which
exceeded 50 percent, both reciprocal paths
remainedsignificant, suggestingthatthe mediating factors we examined do not come close
to completely accountingfor the health disparities among people in differentsocial strata.
Further analyses cast doubt on another
potential explanation of the SES-health relationship-the possibility that education and
income, aside from serving as indexes of SES,
may directly enable individualsto act in ways
that would improve or maintain their health
(e.g., make appropriately informed health
decisions; buy effective, but expensive medicines). When we added direct independent
paths to Health from these two SES indicators
in our core model containingreciprocalcausal
paths between SES and Health, neither of the
additionalpaths was significant. Thus, neither
educationnor income would seem to independently impacthealth over and above the effects
they have as componentsof SES.
Health-relatedlifestyles/behaviorshad both
direct and indirect effects on the SES-health
relationship.Their overall effect, however, is
much greaterin explainingthe causalpath from
healthto SES than from SES to health.Among
the four lifestyle/behaviors included in this
study,neitherexercisenor smokingdemonstrated the expected independenteffects on health.
On the otherhand,both sleeping little andbeing
overweighthad significantnegative impactson
health.These findings are consistentwith liter-

37

aturesuggestingthat sleep loss and being overweightmay contributeto the incrementof"allostaticload"andthusthe developmentof adverse
health conditions such as diabetes and hypertension (VanCauterand Spiegel 1999).
Because levels of SES have significant
causal links with both the amountof sleep and
weight, partof the total effect of SES on health
occurred indirectly through these two healthrelated lifestyle/behaviors. Similarly, part of
the total effect of health status on SES
occurred indirectly. Health had a significant
positive effect on sleep; high levels of sleep
were, in turn, unexpectedly associated with
lowered SES. We should note that our finding
of an inverse relationship between SES and
amount of sleep should be taken cautiously
since earlier studies have speculated that the
health-compromisingeffects of SES are partly
due to deficiencies in the quantityand quality
of sleep among lower SES individuals (Van
Cauterand Spiegel 1999).
Psychological distress, as expected, was
inverselyand reciprocallyconnected to health,
thus confirming the supposition that distress
contributesto ill health, as does ill health to
psychological distress. The fact that the effect
of health status on psychological distress was
substantiallygreaterthan the reverse suggests
that the bruntof the effect is from ill health to
psychological distress. As shown by the
notable reductionin the size of the path from
SES to healthwhen psychological distresswas
includedin the model, distressplays a remarkably significant part in mediating the SEShealth relationship.The marginal finding that
low SES leads to psychological distress not
only suggests an indirect mechanism through
which SES influences health status,but it also
provides further evidence that differences in
socio-economic status lead to differences in
psychological distress.
Variousissues aboutthe generalizabilityand
conclusivenessof our findings can be raised.In
terms of our full 1994/1995 sample,as we have
noted,female, older,unemployed,less educated
people, and AfricanAmericansmay be underrepresentedcomparedto theirrepresentationsin
the earlierwaves of the study.Ourmethodological approachmitigates the potentialeffects of
this sample bias in several ways. Because our
analyses are essentially longitudinalones that
examinehow the individual'sSES affects and is
affectedby his or her healthover time, the individual. in a sense. serves as his or her own con-

38

JOURNALOF HEALTHAND SOCIALBEHAVIOR

trol. Ourfindings are thereforeprobablygeneralizable to the extent that there are no interactions involving the variablesbiasing who was
re-interviewedin 1994/1995 and the relationshipsbetweenhealthand SES, ourtwo variables
of central concern. In addition, although age,
race,andgenderwere includedas controlsin all
of our models, these variableshad only very
limited significant effects on SES and health,
of these
suggesting that under-representation
characteristicsin our sample would not greatly
distortthe generalizabilityof our findings.
Several other characteristicsof our sample
represent potential further limitations to the
generalizabilityof the study.Oursample is relatively small, and this may have led to the
underestimation of the significance of the
impact of marginallypowerful,but still potentially significant, mediatingvariables.In addition, the 1994/1995 interviews obviously
excluded those who were medically incapacitated or those who died, implying that data
analyzed for this study came from those who
were relatively healthier, and as a result the
findings may have underestimatedthe relationships between the variables of interest.
Furthermore,as we have noted earlier, our
couple-based sampling procedure may have
affected the generalizability of our overall
findings. Our supplementary analyses have
suggestedthatthis is not the case, althoughthe
possibility remains that differences between
the gendersmay have been underestimated.
There are also non-sampling based limitations to our study.Some of our latent concepts
were not measured optimally-particularly
those indexed by error-free single variables
and even possibly those factors indexed by
only two indicators.It is conceivablethat some
of our non-significantfindings may be due, at
least in part, to imprecision in the measurement of our factors.A furtherlimitationis that
we cannot assess how much of any significant
effect we found between SES and health is
actually contemporaneousand how much is
actually lagged. It is also the case that the
twenty-yeargap between the times of our two
survey waves is unusually long. On the one
hand,the length of this gap makes the longitudinal componentof any causal connectionswe
find impressively enduring.On the other, it is
possible that othercausal connectionsfound in
previous studies (e.g., between exercise and
health), but not in this study, would have

emerged if the period between the two survey

waves had been shorter.
Perhapsthe most serious limitation is that
severaltheoreticallysignificantmediatorsof the
relationshipbetween SES and health were not
included in our analyses. The most striking
omission, given thatthe datafor this studywere
derived from an interview focusing on the
effects of occupationalconditions,is our omission of considerationof the partthatSES differences in such conditionsmay play in explaining
SES differencesin health. As we noted in the
introduction,high intercorrelationsamong our
range of occupationaland SES variablesseem
to have played a part in stoppingus from successfully estimating the structural equation
models necessaryto assurethatwe havereliably
disentangledthe causalinterconnectionsamong
SES,job-conditions,and health.3
We have also not been able to include other
potentialmediatorsof the SES-healthrelationship because we do not have the data to do so.
The omissions include, among others, diet,
drinking and health care seeking behaviors,
and psychosocial and health resourcessuch as
social capital and access to health care services-factors that have previously been found
to contribute to social inequalities in health
(Borg and Kristensen 2000; Kawachi, et
al.1997; Lantz, et al. 1998; Lynch, et al. 1996;
Power,Matthews,and Manor 1998).
Despite all of these potential limitations in
our dataand analyses, we have reachedseveral
importantconclusions. First, we have shown
that the SES and health relationshipis reciprocal, and not simply unidirectional,althoughthe
causal path from SES to health is strongerthan
the reverse. Second, we have identified some
importantmechanismsthroughwhich at least a
third of these reciprocals effect takes place.
Partof the effect of health on SES seems to be
due to SES differences in weight and sleeping
behavior.A notablepartof the effect of SES on
health arises from SES differences in psychological distress. Importantquestions remain.
Finding ways to reduce SES based health
inequalities presents a conundrumof an even
greatermagnitudethan coming to a full understanding of the causal patternsunderlyingthe
SES-healthrelationship.
NOTES
1. Six cases whose race was neitherEuropean

THESES ANDHEALTH
CONNECTIONS
EXPLAINING
nor African American were coded missing
and were excluded from analyses involving
race.
2. We have also estimatedwhat we considered
a less satisfactory cross-lagged effects
model that estimates a path from 1974 SES
to 1994/1995 Health and anotherpath from
1974 Health to 1994/1995 SES. The results
of this model were similarto those reported
in our core SES-healthmodel, and indicated that the cross-lagged path from 1974
SES to 1994/1995 Health(P = .23,p < .001)
was still strongerthanthe cross-laggedpath
from 1974 Health to 1994/1995 SES (P=
.04, p < .05).
3. We tried to test the hypothesis that occupational conditions serve as a mediating
mechanism through which SES affects
health using data from the 242 of the
respondentswho worked in both 1974 and
1994/1995. The effects of several occupational conditions-including substantive
complexity, routinization, closeness of
supervision,job pressures,job security,and
heaviness/dirtinessof the job-were examined (see Kohn and Schooler 1983 for complete descriptionof the measurementof this
variable).When we used structuralequation
modeling procedures parallel to those we
used to asses the effects of health-related
lifestyles/behaviors and psychological distress, our SES-occupational conditionshealth models showed distinct symptomsof
multicolinearity between the measures of
SES and occupational conditions. The
effects of this multicolinearitywere clearly
aggravated by the low ratio between the
large numbers of measurementand causal
parametersthat had to be simultaneously
estimatedand the relativelysmall portionof
our sample appropriatefor these analyses.
By accepting some tenable, but not necessarily correct assumptions, we could estimate simpler models that tested the effects
of occupational conditions on health. By
doing so, we found some evidence of such
effects, particularly a positive effect on
1994/1995
Health
of
1994/1995
Work-an
SubstantivelyComplex
occupational conditionthathas been shown to have
a wide range of notable psychological
effects (Kohn and Schooler 1983; Schooler,
Mulatu, and Oates 1999). Nevertheless, no
model that we could estimate allowed us to
assess the degree to which occupational

39

conditions affect the SES-healthreciprocal

relationshipswith a comfortablyacceptable
degree of confidence.
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THESES ANDHEALTHCONNECTIONS
EXPLAINING

41

Mesfin Samuel Mulatu is a visiting research fellow at the Section on Socio-EnvironmentalStudies,

National Instituteof Mental Health. His currentresearchinterestsinclude examiningthe psychosocial, cultural and environmentalbases of health and disease, HIV/AIDS-relatedsexual risk and preventivebehaviors particularlyamong youth and adults in sub-SaharanAfrica (Ethiopia,Mali), and cross-culturalissues
in mental health researchand services.
Carmi Schooler is Chief of the Section on Socio-EnvironmentalStudies of the National Instituteof Mental
Health. His sociological researchcenters on the cross-culturalexaminationof the psychological effects of
social structurallydeterminedenvironmentalconditionsthroughoutthe life course. He is presentlyinvolved
in analyzingthe dataof a thirtyyear longitudinalstudy focussing on the effects of cognitivelycomplex, selfdirectedoccupationalconditions in the US and carryingout the datacollection phase of a comparablestudy
in ruralMali. This latter study extends the range of dependentvariablesto include psychiatricillness and
AIDS relatedknowledge and behavior.