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The Pittsburgh Common Cold Studies: Psychosocial predictors of susceptibility to respiratory infectious illness

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This article provides a selected overview of 20 years of research on the role of psychosocial factors in susceptibility to upper respiratory infections. We present evidence from our laboratory that psychological stress is associated with increased risk for developing respiratory illness for persons intentionally exposed to a common cold virus, that the longer the duration of the stressor the greater the risk, and that stress association with susceptibility may be mediated by stress-induced disruption of the regulation of proinflammatory cytokines. We further provide evidence that social relationships (social integration and social support) are also associated with risk for respiratory illness: Social integration is associated with reduced risk irrespective of stress level and social support protects persons from the pathogenic influences of stress. Finally, we report recent evidence that lower levels of early childhood socioeconomic status (SES) are associated with greater risk of viral-induced illness during adulthood, independent of adult SES.
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KEYNOTE PRESENTATION AT THE EIGHT INTERNATIONAL
CONGRESS OF BEHAVIORAL MEDICINE
Mainz, Germany August 25–28, 2004
The Pittsburgh Common Cold Studies: Psychosocial Predictors
of Susceptibility to Respiratory Infectious Illness
Sheldon Cohen
This article provides a selected overview of 20 years of research on the role of
psychosocial factors in susceptibility to upper respiratory infections. We present evi-
dence from our laboratory that psychological stress is associated with increased risk
for developing respiratory illness for persons intentionally exposed to a common cold
virus, that the longer the duration of the stressor the greater the risk, and that stress
association with susceptibility may be mediated by stress-induced disruption of the
regulation of proinflammatory cytokines. We further provide evidence that social re-
lationships (social integration and social support) are also associated with risk for re-
spiratory illness: Social integration is associated with reduced risk irrespective of
stress level and social support protects persons from the pathogenic influences of
stress. Finally, we report recent evidence that lower levels of early childhood socio-
economic status (SES) are associated with greater risk of viral-induced illness during
adulthood, independent of adult SES.
Key words: psychoneuroimmunology, socioeconomic status, stress buffering, social
integration, social rank, social support, infectious illness susceptibility, respiratory
infections, common cold, influenza, cytokine regulation, cortisol regulation
Over the last 20 years, our laboratory has been inter-
ested in the extent to which social and psychological
factors may influence susceptibility to infectious ill-
ness. In particular, we have employed a unique pro-
spective design in which healthy participants are evalu-
ated on psychosocial factors and then intentionally ex-
posed to a virus that causes a mild cold. After exposure
to the virus, participants are carefully monitored (in
quarantine) for the development of a clinical illness as
defined by the presence of both biologically verified
infection and symptom expression. Approximately
one-third of the participants we expose to a virus de-
velop a clinical cold. The question we pose is whether
we can predict from baseline psychosocial measures
who will become ill.
The primary focus of this article is our work on psy-
chological stress, social network composition, and
childhood socioeconomic status (SES) as predictors of
susceptibility to colds and flu. A summary of the stud-
ies we discuss is provided in Table 1. Other factors we
have studied include sociability (Cohen, Doyle,
Turner, Alper, & Skoner, 2003a), social rank (Cohen,
1999; Cohen, Line et al., 1997), and both positive and
negative emotional styles (Cohen, Doyle, Turner,
Alper, & Skoner, 2003b; Feldman, Cohen, Doyle,
Skoner, & Gwaltney, 1999).
International Journal of Behavioral Medicine
2005, Vol. 12, No. 3, 123–131
Copyright © 2005 by
Lawrence Erlbaum Associates, Inc.
123
Sheldon Cohen, Department of Psychology, Carnegie Mellon
University.
This article is based on a Keynote Address delivered at the Eighth
International Congress of Behavioral Medicine in Mainz, Germany.
The work was supported by grants from the U.S. National Institute of
Allergies and Infectious Diseases (AI23072) and the U.S. National In-
stitute of Mental Health (NIMH: MH47234; MH50429), a Senior Sci-
entist Award to Dr. Cohen from the NIMH (MH00721), and supple-
mental funds from the John D. and Catherine T. MacArthur
Foundation Network on Socioeconomic Status and Health. The prep-
aration of this article was facilitated by the PittsburghNIH Mind-Body
Center (HL65111 and HL65112). Weare indebted to our staff and the
volunteers for their contributions to the research and to Ellen Conser
and Jeffrey Best for their assistance in preparing this manuscript.
Correspondence concerning this article should be addressed to
Sheldon Cohen, Department of Psychology, Carnegie Mellon Uni-
versity, 5000 Forbes Avenue, Pittsburgh, PA 15213. E-mail:
scohen@cmu.edu
Psychological Stress
and Susceptibility to Colds
Invasion of the body by a disease-causing agent is
not sufficient cause for disease. Disease occurs when
the immune system is compromised or unable to rec-
ognize the foreign material. When we began our work
in the mid-1980s, evidence was accumulating that sug-
gested that psychological stress could alter immune re-
sponse in humans (e.g., review by Herbert & Cohen,
1993); however, it was still unclear whether stress ef-
fects on immunity were of the quality or quantity nec-
essary to influence the body’s ability to fight infectious
disease (Cohen & Williamson, 1991; Laudenslager,
1987; O’Leary, 1990). Our work on stress and colds
addressed two primary issues in this regard: (a) Does
psychological stress increase susceptibility to infec-
tious illness? and (b) How could stress “get under the
skin” to influence our host resistance? We begin by de-
scribing a series of studies designed to answer these
questions.
Stress Predicts Susceptibility
to the Common Cold
In our first viral-challenge study (VCS1), we admin-
istered three questionnaires to assess psychological
stress at baseline: a stressful life events scale, perceived
stress scale, and negative affect scale. Participants were
then exposed to one of five viruses that cause a common
cold and monitored closely for infection and illness. We
standardized the stress scores within each of the three
scales and added them together to create a stress index.
We found that the higher the score on the stress index,
the greater was the probability of developing a clinical
cold following viral exposure (Cohen, Tyrrell, & Smith,
1991, 1993). As apparent from Figure 1 (collapses
across viruses), this was a graded relation with every in-
crease in stress associated with an increase in risk.
Moreover, the association occurred for all of the five vi-
ruses tested (three rhinovirus types, respiratory
syncytial virus, and a corona virus). This association oc-
curred independent of immunity to the virus at baseline
as assessed by the amount of specific antibody to the
challenge virus. It was also independent of age, sex, edu-
cation, allergic status, body mass index, and season of
the year. Finally, we examined whether we could ex-
plain the association between stress and colds by
stress-related health behaviors (smoking, alcohol con-
sumption, sleep quality, exercise, diet) or nonspecific
quantitative measures of immune function (white blood
cell counts and total immunoglobulin levels). None of
the hypothesized mediators we assessed were able to ex-
plain the relation.
The Type of Stressor Matters
The second study (VCS2) focused on identifying the
types of stressful life events that were associated with in-
creased susceptibility to infectious illness (Cohen et al.,
1998). Using an intensive stress interviewtechnique, we
demonstrated that there were two types of stressful life
events strongly associated with greater susceptibility:
enduring (1-month or longer) interpersonal problems
with family and friends and enduring problems related
to work (under- or unemployment). Moreover, across all
types of events, the longer the stressful life event lasted,
the greater was the risk for developing a clinical illness
(Figure 2). These effects held across two rhinoviruses
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Table 1. Designs, Viruses Used, Psychological Predictor Variables Included, and Sample Sizes for Studies Discussed in This
Article
Code Format Virus Psych Var N
VCS 1 Viral-Challenge RV, RSV, CV Stress 420
VCS2 Viral-Challenge RV Stress, soc network 276
VCS3 Viral-Challenge Influenza A Stress 55
VCS4 Viral-Challenge RV Stress 334
EPIS Epidemiological None Ill child 50
ANEXS Animal Exper. None Stress, affiliation 43
Note. CV = corona virus; RSV = respiratory synctial virus; RV = rhinovirus; Psych Var = psychological variable; soc network = social network.
Figure 1. Increases in psychological stress are associated with
increases in risk for developing a cold after exposure to a cold
virus.
Note. The data are from “Psychological Stress and Susceptibility
to the Common Cold,” by S. Cohen, D. A. Tyrrell, & A. P. Smith,
1991, New England Journal of Medicine, 325, p. 609.
we administered (RV39 & Hanks) and were equal for
persons with and without prior immunity (specific anti-
body) to the challenge virus.
Finally, we examined the possibility that health be-
haviors, endocrine response (24-hour urine epineph-
rine, norepinephrine, and cortisol), or markers of im-
mune status (natural killer cell cytotoxicity and white
blood cell counts assessed at baseline) might constitute
the pathways through which psychosocial factors influ-
ence susceptibility.Interestingly, we found that many of
the proposed mediators were associated with suscepti-
bility to clinical illness as predicted. Nonsmoking, regu-
lar exercise, and greater sleep efficiency (percent of time
in bed sleeping) were all associated with less suscepti-
bility to developing a cold (Cohen, Doyle, Skoner,
Rabin, & Gwaltney, 1997; Cohen, Tyrrell, Russell,
Jarvis, & Smith, 1993), and higher 24-hour urinary epi-
nephrine and norepinephrine were both associated with
greater susceptibility (Cohen, Doyle, et al., 1997).
However, these effects appeared to be relatively inde-
pendent of the associations between psychological
stress and susceptibility, and hence our data did not sup-
port these factors as contributors to the pathways linking
psychosocial factors and disease resistance. Neither the
immune measures nor the 24-hr urine cortisols were as-
sociated with susceptibility to clinical illness. In short,
although we replicated and extended the association be-
tween psychological stress and disease resistance we
found in the original study, we were still unable to iden-
tify any mediating pathways.
Stress Association with Colds
is Mediated by Cytokine Regulation
Up until this point, the major outcome in our studies
had been whether persons exposed to a virus develop a
clinical illness (both infection and symptoms). More re-
cently,we became interested in the possibility that stress
influences resistance to respiratory infectious illness
through its influence on proinflammatory cytokines.
Proinflammatory cytokines are produced in response to
infection and are thought to trigger the symptoms that
are associated with upper respiratory viral infections. To
address the role of cytokines, we altered our challenge
model to focus on illness expression among infected
persons. We selected only persons without previous ex-
posure to the virus (no antibody to the challenge virus at
study onset) and we chose to use an influenza A virus
that results in infection in 98% or more of participants
without previous exposure. We then examined the ex-
tent to which psychological stress predicted illness ex-
pression among the infected participants.
Our hypothesis was that stress may interfere with
the body’s ability to turn off cytokine production. Ap-
propriate regulation would allow the production of
enough cytokine to help rid the body of the virus but
not so much that it produced a massive symptomatic
response. If stress short-circuited the body’s ability to
turn off cytokine release, then it could trigger a severe
symptomatic response. In a study of an influenza virus,
we assessed the potential role of infection-induced lo-
cal (in nasal secretions) release of the proinflammatory
cytokine interleukin-6 (IL-6) as a mediator of the asso-
ciation between stress and illness expression (VCS3;
Cohen, Doyle, & Skoner, 1999). After completing a
measure of psychological stress (Perceived Stress
Scale, PSS), 55 participants were experimentally in-
fected with an influenza A virus. They were then moni-
tored in quarantine for 8 days (baseline and 7 days after
inoculation) for upper respiratory symptoms, mucus
production, and levels of IL-6 in their nasal secretions.
Analyses controlled (covaried) for age, gender, ethnic-
ity, body mass, and season. The results for mucus
weights and IL-6 are presented in Figures 3 and 4.
Higher psychological stress assessed prior to the viral
challenge was associated with greater symptom scores,
greater mucus weights, and higher IL-6 lavage concen-
trations in response to infection. (Stress was not associ-
ated with basal levels of cytokines.) The IL-6 response
was temporally related to both markers of illness ex-
pression, and mediation analyses indicated that these
data were consistent with IL-6 acting as a major path-
way through which stress was associated with in-
creased symptoms of illness (Cohen et al., 1999).
However, this is a correlational analysis, and this pat-
tern of data is also consistent with rises in IL-6 occur-
ring in response to tissue damage associated with ill-
ness symptoms.
Chronic Stress Influences
Cortisol Regulation
How could stress interfere with the body’s ability to
turn off the proinflammatory cytokine response? A
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THE PITTSBURGH COMMON COLD STUDIES
Figure 2. Increases in the duration of stressful events are asso-
ciated with increased risk for developing a cold after exposure to
a cold virus.
Note. Figure reprinted from “Types of Stressors that Increase Sus-
ceptibility to the Common Cold in Adults,” by S. Cohen et al., 1998,
Health Psychology, 17, p. 219. Copyright ©1998 by the American
Psychological Association. Reproduced with permission.
likely culprit is the hormone cortisol. Cortisol release
is triggered by psychological stress. Moreover, one of
the functions of cortisol is to regulate (turn off)
cytokine production. This picture is complicated, how-
ever, under chronic stressful conditions, because a
feedback system often turns off the release of cortisol
when there is too much in circulation. Moreover, re-
ceptors for cortisol on immune cells downregulate
(turn in and become less sticky) when flooded with
cortisol. In short, chronic stress may impair the im-
mune system’s capacity to respond to hormonal signals
that terminate inflammation (Avitsur, Stark, &
Sheridan, 2001; Stark et al., 2001).
To investigate this hypothesis, we studied a group of
50 healthy adults—25 parents of a young child with
cancer and 25 matched control parents of healthy chil-
dren (EPIS; Miller, Cohen, & Ritchey, 2002). We
chose parents of cancer patients because they were ex-
periencing a chronic and extremely stressful life event.
When compared to control parents, parents of cancer
patients reported more psychological distress and had
lower cortisol levels (most notable during the morning
hours). We also treated a blood sample from each par-
ticipant with dexamethasone (dex)—a synthetic
glucocorticoid (cortisol-like substance)—and then
stimulated the cells to produce cytokine. When we
added the dex to the blood samples from control sam-
ple, as expected, their cells produced less IL-6 than
cells that were not treated with dex. The dex was turn-
ing off the cells’ production of cytokine. When we
added dex to the blood samples from the parents of
cancer patients, the dex was significantly less effective
in turning off cytokine production. These findings sug-
gest that prolonged stress alters the course of inflam-
matory disease by decreasing cortisol’s effectiveness
in regulating proinflammatory cytokine response. This
is consistent with our finding in VCS3 that stress was
associated with increased production of IL-6 (suggest-
ing decreased effectiveness of cortisol) and increased
illness expression.
In sum, our work on stress and upper respiratory
symptoms has led us to a somewhat unexpected con-
clusion. Stress effects may not be due to stress-elicited
suppression of immune function. Instead, chronic
stress may influence resistance to respiratory viruses
by interfering with the immune system’s ability to re-
spond to hormonal signals that turn off the release of
proinflammatory cytokines. Consequently, persons
under stress produce too much cytokine (the immune
system overresponds) that in turn triggers and prolongs
the symptoms of upper respiratory infections.
Social Environments
and Susceptibility to Colds
In VCS2, we found that enduring interpersonal
problems with family and friends were associated with
greater susceptibility to disease. Interpersonal conflict
was presumed to be detrimental to health because it is a
potent source of psychological stress (Cohen, 2004;
Rook, 1984). However, there is also substantial evi-
dence that our social networks can be beneficial to our
health. We have distinguished between two types of
models that describe how social relationships might
benefit health outcomes: the stress-buffering model
and the main effect model (Cohen, 1988, 2004; Cohen
126
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Figure 4. Increases in perceived stress (low = below median
and high = above median) are associated with greater produc-
tion of IL–6 in nasal secretions among participants infected with
an influenza A virus. Viral inoculation occurred at the end of day
0. SEs are indicated.
Note. Figure reprinted from “Psychological Stress, Cytokine Pro-
duction, and Severity of Upper Respiratory Illness,” by S. Cohen, W.
J. Doyle, & D. P. Skoner, 1999, Psychosomatic Medicine, 61, p. 178.
Copyright © 1999 by the American Psychosomatic Society. Repro-
duced with permission.
Figure 3. Increases in perceived stress (low = below median
and high = above median) are associated with greater produc-
tion of mucus (mucus weights) among participants infected with
an influenza A virus. Viral inoculation occurred at the end of day
0. SEs are indicated.
Note. Figure reprinted from “Psychological Stress, Cytokine Pro-
duction, and Severity of Upper Respiratory Illness,” by S. Cohen, W.
J. Doyle, & D. P. Skoner, 1999, Psychosomatic Medicine, 61, p. 177.
Copyright © 1999 by the American Psychosomatic Society. Repro-
duced with permission.
& Wills, 1985). The stress-buffering model suggests
that the benefits of social relationships derive from
their role in protecting people from the pathogenic in-
fluences of stress. The main effect model predicts that
the social environment’s influence on health is inde-
pendent of current stress level.
We have also emphasized the need to distinguish
between different conceptions of social networks and
supports (Cohen, 1988, 2004; Cohen & Wills, 1985).
The relevant literature consists primarily of studies us-
ing limited numbers of structural measures of social
groups such as network size and social integration and
those using functional measures of social support such
as availability or receipt of emotional, informational,
and tangible support. Correlations between and within
structural and functional groupings of measures tend to
be small to moderate (Cohen, 1991). The two measures
with the most consistent relations with health are so-
cial integration (having a diverse social network; e.g.,
being married, belonging to church and social groups,
having close family and friends) and social support
(the availability of social resources to help one cope in
stressful situations). Social integration has consistently
been associated with more positive health outcomes ir-
respective of whether persons are facing adversity or
not, whereas measures of social support tend to be ben-
eficial only in the presence of stress (Cohen, 2004; Co-
hen & Wills, 1985). In the following, we discuss some
of our research on the role of social integration and so-
cial support in susceptibility to colds as well as in
changes in physiological mechanisms that play a role
in host resistance.
Social Integration is Associated
with Greater Resistance to Disease
There is substantial evidence that those who are so-
cially integrated, that is, those having multiple social
roles (e.g., marriage, work, neighbors, friends, social
groups, religious groups) are healthier and live longer
than those who are not (Berkman, 1995; Cohen, 2004;
Cohen, Gottlieb, & Underwood, 2000; Helgeson, Co-
hen, & Fritz, 1998; Seeman, 1996). Unfortunately, the
mechanisms linking diverse networks to a broad range
of diseases have not been identified. Infectious agents
have recently been implicated in the development of a
range of diseases not traditionally thought to have in-
fectious etiologies such as coronary artery disease
(Gupta & Camm, 1998), asthma (Kraft, Cassell, Pak,
& Martin, 2002), and some cancers (Butel, 2000). We
hypothesized that persons who had multiple social
roles might be less susceptible to infectious disease
and that this increase in host resistance might help ex-
plain associations between social integration and total
morbidity and mortality. In VCS2, we assessed the role
of social integration in susceptibility (Cohen, Doyle, et
al., 1997). We used a scale we developed, the Social
Network Index (Cohen, 1991), at baseline to assess so-
cial integration—the number of social roles (domains)
in which a person has social contacts. As described ear-
lier, participants were subsequently exposed to one of
two rhinovirus types.
The results are depicted in Figure 5. Greater num-
bers of social roles were associated with less suscepti-
bility to clinical illness. This association occurred irre-
spective of the challenge virus. It was also independent
of the stress associations reported previously. There
were also no stress-by-social integration interactions
and hence no evidence for a stress-buffering effect of
social network diversity (not even a supportive pat-
tern). Moreover, mere numbers of people in the social
network (independent of roles) were not associated
with disease susceptibility. The association between
social networks and colds was unaffected by the addi-
tion of controls (covariates) for age, sex, season, body
mass index, education, race, and immunity to the virus
at baseline as assessed by specific antibody to the chal-
lenge virus.
Social Support Buffers the Effects
of Stress on Disease
The previously described work focused on social in-
tegration, which is expected to have a direct effect (irre-
spective of stress level) on immunity and health. As
noted earlier, we hypothesize that social support influ-
ences health through a different pathway (i.e., by pro-
tecting people from the potentially detrimental influ-
ences of stress; Cohen, 1988, 2004; Cohen & Wills,
1985). We were interested in experimentally manipulat-
ing chronic stress and obtaining objective measures of
social interaction. To accomplish these goals, we con-
ducted the next study with nonhuman primates. This
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THE PITTSBURGH COMMON COLD STUDIES
Figure 5. Greater numbers of social roles are associated with a
lower risk for developing a cold among persons exposed to a cold
virus.
Note. Data from “Social Ties and Susceptibility to the Common
Cold,” by S. Cohen, W. J. Doyle et al., 1997, Journal of the American
Medical Association, 277, p. 1943.
study addressed the question of whether close relation-
ships buffer the effects of chronic stress on cellular im-
mune response (ANEXS; Cohen, Kaplan, Cunnick,
Manuck, & Rabin, 1992). There, 43 male cynomolgus
monkeys were randomly assigned to stable or unstable
social conditions for 26 months. Animals in the stable
social condition remained in a cage with the same four
animals over the course of the entire study. Those in the
unstable condition were rotated every month so that at
least three animals with whom they had not been housed
in the previous month were substituted for animals pre-
viously in the cage. The proportion of time spent in
affiliative behaviors was assessed by observations made
twice weekly. T-cell immune response (mitogen stimu-
lated proliferation) was assessed weekly for 3 weeks im-
mediately following the 26 months of manipulation. Al-
though immune response was relatively suppressed
among animals in the unstable social condition, this sup-
pression occurred primarily among animals with low
levels of affiliation (stress by affiliation interaction; Fig-
ure 6). A similar stress-buffering analysis wasapplied in
our study of parents of cancer patients (EPIS; Miller et
al., 2002). In that case, we found that parents of children
with cancer who reported the availability of material aid
were protected from stress-associated effects (showed
little glucocorticoid resistance; Figure 7). Both studies
are consistent with the hypothesis that social support op-
erates as a stress-buffer, protecting people (and mon-
keys)fromthe potential pathogenicinfluences of stress.
Childhood SES and Susceptibility
to the Common Cold
SES during childhood as measured by living condi-
tions, family income, and parental education and em-
ployment has been repeatedly associated with adult
health status (Aber, Bennett, Conley, & Li, 1997;
Gissler, Rahkonen, Jarvelin, & Hemminki, 1998; Nel-
son, 1992; Roberts & Power, 1996). Lower childhood
SES has been reported to be a risk factor for mortality
(Davey-Smith, Hart, Blane, Gillis, & Hawthorne,
1997; Davey-Smith, McCarron, Okasha, & McEwen,
2001; Nystrom, 1994; Vagero & Leon, 1994) primarily
resulting from cardiovascular disease (Davey-Smith,
Hart, Blane, & Hole, 1998; Frankel, Davey-Smith, &
Gunnell, 1999; Heslop, Davey-Smith, Macleod, &
Hart, 2001) but also from respiratory disease, stroke,
and stomach and lung cancer (Davey-Smith et al.,
1998). There is also evidence relating lower childhood
SES to increased risk for adult cardiovascular disease
(Poulton, Caspi, Milne, Thomson, Taylor, Sears, et al.,
2002; Wannamethee, Whincup, Shaper, & Walker,
1996), chronic bronchitis (Marmot, Shipley, Brunner,
& Hemingway, 2001), and periodontal disease
(Poulton et al., 2002).
As mentioned earlier, infectious agents have re-
cently been implicated in the development of a range of
diseases not traditionally thought to have infectious
etiologies. Hence, an association between childhood
SES and adult host resistance would suggest a hypo-
thetical pathway through which childhood experiences
might influence a broad range of health outcomes. To
pursue this possibility, we conducted a preliminary
study using the viral-challenge paradigm to determine
if childhood SES is associated with adult susceptibility
to infectious illness, and, if so, whether the effect is
limited to a critical period of low SES exposure, can be
undone by changes in childhood SES, and is explained
by adult SES.
In VCS4, prior to being exposed to the virus, we
had volunteers report their own and their parents’
level of education and the ages during their childhood
when their parents owned their homes (Cohen, Doyle,
Turner, Alper, & Skoner, 2004). Volunteers’ current
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Figure 6. Chronic stress (unstable social environment) inter-
acts with affiliation in predicting cellular immune response in
cynomolgus macaques.
Note. Data from “Chronic Social Stress, Affiliation and Cellular
Immune Response in Nonhuman Primates,” by S. Cohen et al., 1992,
Psychological Science, 3, p. 303.
Figure 7. Stress (child with cancer of matched control) and in-
strumental social support interact in predicting the ability of
dexamethasone to suppress IL–6 production.
Note. Data from “Chronic Psychological Stress and the Regulation
of Pro-Inflammatory Cytokines: A Glucocorticoid Resistance
Model,” by G. E. Miller et al., 2002, Health Psychology, 21, p. 537.
home ownership was recorded from real estate re-
cords. Subsequently, they were given nasal drops
containing one of two rhinoviruses and monitored in
quarantine for infection and signs and symptoms of a
common cold. For both viruses, susceptibility to
colds decreased with the number of childhood years
during which their parents owned their home (odds
ratios by tertiles adjusted for demographics, body
mass, and season and prechallenge viral-specific im-
munity were 3.7 for fewest years, 2.6 the mid tertile
of number of years, and 1 for the most years). This
decreased risk was attributable to both lower risk for
infection and lower risk for illness in infected partici-
pants (Figure 8). Moreover, those whose parents did
not own their home during their early life but did dur-
ing adolescence were at the same increased risk as
those whose parents never owned their home. These
associations were independent of parent education
level and of adult education, home ownership, and
personality characteristics. Finally, we assessed the
role of home ownership at different ages by creating
ownership variables based on 2-year intervals starting
from 1–2. As apparent from Figure 9, the largest as-
sociations occurred early in life. The later the experi-
ence with parental home ownership, the less its asso-
ciation with disease risk. These data suggest that very
early (or possibly even prenatal) experiences are re-
sponsible for the association of childhood SES and
susceptibility to colds as adults.
In short, a marker of low income and wealth during
early childhood was associated with decreased resis-
tance to upper respiratory infections in adulthood.
Higher risk was not ameliorated by higher SES during
adolescence and is independent of adult SES. Our on-
going work is looking more closely at the nature of
childhood environments that might influence adult
health (social and physical environments, parental be-
haviors, etc.) and attempting to identify specific as-
pects of immunity and behavior that might mediate
these associations. We are also exploring alternative
explanations for the association such as parental age,
family stability, and single parent households.
Summary
This article provided an overview of three of the ar-
eas of research we have pursued. In our early work, we
found that psychological stress was associated with
129
THE PITTSBURGH COMMON COLD STUDIES
Figure 8. Adjusted (for standard controls) incidences of infection (a) and clinical illness among infected volunteers (b) decrease as a
function of years of parental home ownership (tertiled).
Note. Figure reprinted from “Childhood Socioeconomic Status and Host Resistance to Infectious Illness in Adulthood,” by S. Cohen et al.,
2004, Psychosomatic Medicine, 66, p. 556. Copyright ©2004 by the American Psychosomatic Society. Reproduced with permission.
Figure 9. Adjusted effect size (regression coefficient) forthe as-
sociations between parental home ownership and adult suscepti-
bility to colds decrease with age of exposure.
Note. Figure reprinted from “Childhood Socioeconomic Status and
Host Resistance to Infectious Illness in Adulthood,”by S. Cohen et al.,
2004, Psychosomatic Medicine, 66, p. 556. Copyright © 2004 by the
American Psychosomatic Society. Reproduced with permission.
greater susceptibility to colds and influenza, that this
risk increased with the duration of major stressful
events, and that the increased risk is probably attribut-
able to stress-induced and endocrine mediated disrup-
tion of the regulation of proinflammatory cytokines. In
our work on social environments, we found that social
integration predicted susceptibility with persons with
more diverse social networks less susceptible to dis-
ease. This association occurred independently of pre-
vious exposure to the challenge-viruses as indicated by
baseline viral-specific antibody. Moreover, support
and affiliative behaviors operated as stress-buffers,
protecting (in this case) animals from stress-triggered
immunosuppression and humans from stress-triggered
insensitivity to hormonal control of cytokine produc-
tion. Finally, we discussed our preliminary work on the
potential role of childhood SES in adult susceptibility.
We found not only that parental home ownership pre-
dicted susceptibility during childhood but that very
early childhood exposure was the most critical. In fact,
exposure during adolescence did not contribute much
and (when SES in adolescence was greater than it was
in childhood) did not buffer the effects of early expo-
sure. The association between childhood SES and
adult susceptibility was not mediated by current (adult-
hood) SES.
In sum, we have been fortunate to have the opportu-
nity to work with a paradigm that allowed us to inten-
tionally expose people to an infectious virus and objec-
tively determine their host resistance to disease. This
work has been exceptionally exciting in two ways.
First, it has demonstrated that a wide range of different
social and psychological factors are likely to influence
our ability to fight off infectious illness. Second, it has
allowed us to begin to understand the psychological
and biological mechanisms that are responsible for
these effects.
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Adverse socioeconomic circumstances in childhood have been related to increased cardiovascular disease (CVD) risk in adulthood in most, but not all, studies.1 The findings of such studies can be difficult to interpret given the association of childhood social circumstances with social conditions and behavioural risk factors for CVD in adulthood. Statistical adjustment for these, however, generally indicates an important additional contribution of childhood socioeconomic background.2 In this study we investigate the association between childhood circumstances and CVD mortality among male former students of Glasgow University, who will have experienced a relatively homogeneous and privileged adulthood social environment. Students attending the University of Glasgow between 1948–68 were invited to participate in a medical examination carried out by the student health department.3 Data collected included sociodemographic data, details of health behaviours and measured blood pressure. Participants were traced through the National Health Service Central Register. Full details are reported elsewhere.3The social class of the fathers of …
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We report the first experimental study of the effect of long-term (over 2 years) exposure to a stressor on cellular immune response. Forty-three male cynomolgus monkeys were randomly assigned to stable or unstable social conditions for 26 months. The proportion of time spent in affiliative behaviors was assessed by observations made twice weekly. T-cell immune response (mitogen-stimulated cell proliferation) was assessed weekly for 3 weeks immediately following the 26-month manipulation. The possibility that affiliative behavior represents an attempt to cope with social stress was supported by greater affiliation among animals in the unstable condition than in the stable condition. Animals in the unstable condition also demonstrated relatively suppressed immune response. More affiliative animals showed enhanced immune response, with the beneficial effects of affiliation occurring primarily among unstable animals. The data are interpreted as consistent with the stress-buffering hypothesis; that is, affiliation protects animals from the potentially pathogenic influences of chronic social stress.