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Psychosom Med. Author manuscript; available in PMC 2014 September 01.
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Psychosom Med. 2013 September ; 75(7): 658–669. doi:10.1097/PSY.0b013e31829bbc89.
Stress-Induced Inflammatory Responses in Women: Effects of

Race and Pregnancy
Lisa M. Christian, PhD1,2,3,4, Ronald Glaser, PhD2,5, Kyle Porter, MAS6, and Jay D. Iams,
MD3
1Department of Psychiatry, The Ohio State University Wexner Medical Center
2The Institute for Behavioral Medicine Research, The Ohio State University Wexner Medical
Center
3Department of Obstetrics and Gynecology, The Ohio State University Wexner Medical Center
4Department of Psychology, The Ohio State University
5MolecularVirology, Immunology and Medical Genetics, The Ohio State University Wexner
Medical Center
6Center for Biostatistics, The Ohio State University
Abstract
Objective—African Americans experience preterm birth at nearly twice the rate of Whites.
Chronic stress associated with minority status is implicated in this disparity. Inflammation is a key
biological pathway by which stress may affect birth outcomes. This study examined effects of race
and pregnancy on stress-induced inflammatory responses.
Methods—Thirty-nine women in the 2nd trimester of pregnancy (19 African American; 20
White) and 39 demographically similar nonpregnant women completed an acute stressor (Trier
Social Stress Test). Psychosocial characteristics, health behaviors, and affective responses were
assessed. Serum interleukin(IL)-6 was measured via high sensitivity ELISA at baseline, 45
minutes, and 120 minutes post-stressor.
Results—IL-6 responses at 120 minutes post-stressor were 46% higher in African Americans
versus Whites (95%CI:8%-81%; t(72)=3.51, p=.001). This effect was present in pregnancy and
nonpregnancy. IL-6 responses at 120 minutes post-stressor tended to be lower (15%) in pregnant
versus nonpregnant women (95%CI:-5%-32%; p=0.14). Racial differences in inflammatory

responses were not accounted for by demographics, psychological characteristics, health
behaviors, or differences in salivary cortisol across the study session. Pregnant Whites showed
lower negative affective responses than nonpregnant women of either race (ps≤.007).
Conclusion—This study provides novel evidence that stress-induced inflammatory responses
are more robust among African American women versus Whites during pregnancy and
nonpregnancy. The ultimate impact of stress on health is a function of stressor exposure and
physiological responses. Individual differences in stress-induced inflammatory responses represent
Address correspondence and reprint requests to Lisa M. Christian, PhD, The Ohio State University Wexner Medical Center, Institute
for Behavioral Medicine Research, Room 112, 460 Medical Center Drive, Columbus, Ohio 43210. [email protected] Phone:
614-293-0936.
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Christian et al. Page 2
a clear target for continued research efforts in racial disparities in health during pregnancy and
nonpregnancy.
Keywords
women; pregnancy; pregnant; race; racial disparities; inflammation; inflammatory response;
interleukin-6; IL-6; proinflammatory cytokines; preterm birth; stress; trier social stress test; acute
stressor; affective responses; cortisol
Introduction
Preterm birth affects 12-13% of births in the US and is a leading cause of infant mortality (1,
2). The estimated societal economic burden is at least $26.2 billion per year, or $51,600 per
preterm infant (1). In the US, the preterm birth rate is approximately 18% among African
American women and 10.5-11.5% among non-Hispanic White, Asian, and Hispanic women
(3). Although numerous explanations have been forwarded, demographic characteristics and
health behaviors do not adequately account for this racial disparity. Associations between
race and preterm birth, as well as low birth weight, and infant mortality remain after
accounting for indicators of socioeconomic status including educational attainment, income,
and occupational status (4-8).
Because traditional explanations have failed to adequately explain the racial disparity in
preterm birth, theories have increasingly focused on understanding the health implications of
chronic stress associated with minority status (1, 9-13). Supporting the conceptualization of
minority status as a chronic stressor, perceived racial discrimination has repeatedly been
linked to increased risk of preterm delivery and low birth weight (12, 14-18). These
relationships remain after accounting for traditional behavioral risk factors, suggesting a role
for more direct physiological links between stress and preterm birth.
Inflammation is a key biological pathway by which psychological stress may affect birth
outcomes. Available data suggest that healthy pregnancy elicits mild elevations in both pro-
and antiinflammatory serum cytokine levels and that exaggerated increases in circulating
inflammatory markers are predictive of greater risk of spontaneous preterm delivery (19-24).
Moreover, successful pregnancy in humans has been associated with attenuated
proinflammatory cytokine production in response to in vitro immune challenges, with the
most marked changes in the 3rd trimester (25-29). This adaptation may be critical in
preventing rejection of the fetus by the maternal immune system and protecting the fetus
from excessive maternal inflammatory responses to infectious agents (30, 31). Failure to
demonstrate attenuation of inflammatory responses has been reported among women who
subsequently experience miscarriage or deliver small for gestational age babies (27) as well
as in nonpregnant women with a history of recurrent spontaneous miscarriage versus women
with a history of successful pregnancy (32). Thus, factors influencing appropriate adaptation
of inflammatory responses may affect risk of adverse pregnancy outcomes.
Psychosocial factors including perceived stress, stressful life events, depressive symptoms,
and trauma have been associated with higher circulating inflammatory markers including
interleukin(IL)-6, tumor necrosis factor(TNF)-α, and IL-1RA (33-38) as well as exaggerated
inflammatory responses to in vivo and in vitro immune challenges in pregnant women (39,
40). Linking such effects to birth outcomes, in a study of 173 women followed across
pregnancy, an association between prenatal stress and gestational age at birth was mediated
by levels of circulating inflammatory markers (41).

Notably, we know of no studies examining inflammatory responses to acute psychological

stress in pregnancy, or the extent to which psychosocial factors modify this response. Data
in nonpregnant adults show that interleukin(IL)-6 responses to acute stressors are delayed
and extended as compared to responses of the sympathetic nervous system and

hypothalamic-pituitary-adrenal (HPA) axis. Increases in IL-6 from baseline have been
observed beginning at 30-45 minutes post-stressor with continuing increases at final follow-
up timepoints of up to two hours post-stressor (42, 43). Thus, exposure to elevated
inflammatory markers may be considerable in duration among individuals who experience
frequent stressors in daily life.
Prior studies show that African American race and greater exposure to racial discrimination
predict greater cardiovascular reactivity to a variety of acute stressors (44-48). In addition,
stressors of a racially provocative nature elicit stronger cardiovascular responses among
African Americans than do stressors that are racially neutral (49). Thus, race is a factor
which may affect not only frequency of stressor exposure (particularly racial
discrimination), but also the magnitude of physiological response to stressors. The extent to
which race modifies inflammatory responses to acute stress is not known. However, other
sociodemographic factors indicative of chronic stress including low socioeconomic status
and clinical depression have been associated with exaggerated stress-induced IL-6 responses
(43, 50, 51).
In sum, given the growing literature linking both stressor exposure and inflammation to
racial disparities in adverse pregnancy outcomes, examination of effects of race and
pregnancy on stress-induced inflammatory responses is warranted. The first goal of this
study was to examine the effect of race on stress-induced inflammatory responses. It was
hypothesized that during pregnancy and nonpregnancy African American women would
exhibit more robust stress-induced IL-6 responses than their White counterparts. The second
goal of this study was to examine the effect of pregnancy on stress-induced inflammatory
responses. It was hypothesized that pregnant women would show attenuation of IL-6
responses as compared to nonpregnant women and that this attenuation would be more
notable among Whites versus African Americans. Finally, in exploratory analyses, we
examined associations between cortisol and inflammatory responses to determine whether
pregnancy or race-related differences in cortisol may mediate the hypothesized differences
in IL-6 response.
Methods
Participants
Participants included 40 pregnant women (20 African American; 20 White) who were
assessed during the second trimester of pregnancy (21-24 weeks gestation) and 40
nonpregnant control participants matched for age, race, parity, and income. Study visits
were conducted between August 2009 and November 2011. The study was approved by the
Ohio State University Biomedical Sciences Institutional Review board (IRB). Women were
recruited from the Ohio State University Wexner Medical Center General Prenatal Clinic,
which serves a racially diverse group of primarily socioeconomically disadvantaged women.
In addition, women were recruited from the general community of Columbus, Ohio. Blood
sampling was unsuccessful for two women (one nonpregnant African American, one
pregnant African American). Thus, the final sample included 78 women (39 pregnant and 39
nonpregnant).
In terms of the trimester of assessment, we focused on the 2nd trimester rather than the 1st
trimester because a primary goal was to examine differences in stress reactivity due to
pregnancy status; more significant adaptations in cardiovascular, neuroendocrine and

immune function are evidenced by the 2nd trimester than in the 1st trimester. We chose to
focus on the 2nd rather than 3rd trimester for two reasons. First, increasing evidence suggests
that stressors which occur earlier in pregnancy are more likely to have detrimental effects
(e.g., 52). However, research to date has focused almost exclusively on stress reactivity
during the third trimester (53). Second, assessment in the 2nd trimester avoids systematic
exclusion of women who may go on to deliver preterm during the 3rd trimester.
Women were ineligible if they reported current tobacco use or chronic health problems
which affect immune, endocrine, or cardiovascular function including cancer, diabetes,
chronic hypertension, gestational hypertension, preeclampsia, or anemia at the time of
screening. In addition, women were excluded if they were taking anti-depressants, anti-
anxiety medications, or mood stabilizers. If a woman reported antibiotic use, she was
scheduled at least two weeks following usage.
Women were excluded if they reported consuming more than 300mg of caffeine per day.
Women reporting use of any recreational drugs (e.g., marijuana, cocaine,
methamphetamines) in the previous 6 months were excluded. Women were excluded if they
were obese, defined as a pre-pregnancy (if pregnant) or current (if nonpregnant) body mass
index (BMI) ≥ 30 (kg/m2). Because the racial disparity in preterm birth most clearly affects
US-born African American women, women who were not US-born were ineligible.
Women were not eligible as nonpregnant control participants if they had given birth within
the past 6 months or were currently breastfeeding. Among the pregnant participants, women
were excluded if they had multifetal gestation or known fetal anomaly. Because previous
pregnancy has been associated with more significant physiological changes in subsequent
pregnancy [208], pregnant participants with at least one previous live birth were targeted.
Pregnancy timing in terms of maternal age varies considerably with sociodemographic
factors such as income and marital status. Thus, to provide ideal demographic matching,
nonpregnant women with a prior live birth were also targeted. In the final sample, 76 of 78
(97.4%) women had a prior live birth (38 pregnant and 38 nonpregnant). Two nulliparous
women were included due to mistaken endorsement of a prior live birth by one nonpregnant
woman at the time of screening who was subsequently matched with a pregnant nulliparous
woman.
Study Visit Overview

All study sessions were conducted in the afternoon, beginning at 12:00 pm. Upon arrival to
the Ohio State University Clinical Research Center, participants provided informed consent
and were given a standardized lunch to ensure a euglycemic state. Following lunch, a
catheter was inserted into an antecubital vein to allow for serial blood sampling and baseline
questionnaires were completed assessing mood. Following a 20 minute acclimation/rest

period, baseline blood samples were obtained. Next, the Trier Social Stress Test (TSST) was
initiated. Serum samples were collected at 45 minutes and 120 minutes following the
conclusion of the TSST for assessment of circulating IL-6. Across the course of the 4.5 hour
study protocol, a total of 122 mL of blood was drawn. Saliva samples were collected by
salivette at 25 minutes prior to stressor initiation and at 0, 15, 30, 45, 60, and 90 minutes
post-stressor.
Laboratory Stressor: The Trier Social Stress Test (TSST)

This commonly used and well-validated laboratory stressor reliably evokes physiological
reactivity as well as increases in self-reported stress (54-57). The TSST is a 20-minute task
which requires participants to make a speech and perform mental arithmetic in front of an
“audience” of 2-3 evaluators. For this study, the audience was composed of two female

evaluators, one African American and one white. The participant was told to imagine that
she had applied for a job and been invited to an interview by the selection committee. She
was informed that she would be given 10 minutes to prepare a speech about why she would
be best for the job and 5 minutes to talk with the committee, followed by a second
experimental task. Following the speech, the participant completed a 5 minute mental
arithmetic task involving serial subtraction. The difficulty of the subtraction task was
adjusted each minute on the basis of the participant’s performance during the previous
minute to improve the equivalence of the stress task across participants as described
elsewhere (42, 58). To enhance the evaluative aspect of the task, the speech and math tasks
were videotaped and participants were informed that these would be used for later
“behavioral analysis”.
Psychosocial Measures
Questionnaires were used to assess various psychological constructs as well as subjective
responses to the stressor in order to determine the similarity between groups on these
factors. All questionnaires, with the exception of the baseline Positive and Negative Affect
Scale (PANAS), were completed post-stressor. The Experiences of Discrimination Scale
was administered after the final blood draw to ensure that racial differences in recall of
potentially stressful events did not differentially affect inflammatory responses.
The Positive and Negative Affect Scale (PANAS) was administered three times to measure
transient affective responses to the stressor: at the conclusion of the acclimation/rest period,
immediately upon conclusion of the stressor, and at 120 minutes post-stressor. With
excellent norms and strong reliability and validity, this is an excellent self-report measure of
transient affective states (59).
Depressive symptoms were assessed with the Center for Epidemiological Studies
Depression Scale (CES-D). This measure is brief and shows good reliability and validity
(60, 61). Further, CES-D scores during pregnancy are associated with negative outcomes
including restricted fetal growth (62), spontaneous preterm birth (63), and impaired
neuromotor performance among neonates (64). A cut-off of ≥ 16 is commonly used to
indicate clinically meaningful depressive symptoms.
The state subscale of the State-Trait Anxiety Inventory (STAI) includes 20 items which
measure state anxiety (65). This measure shows good internal consistency and test-retest
reliability (66).
The 14-item version of the Perceived Stress Scale (PSS), also widely used and well-
validated, was used to measure the subjective experiences of stress and coping with stress
during the past month (67). The PSS measures a construct that is independent of depressive
symptomatology (67). Demonstrating predictive validity in pregnant populations, the PSS
has been associated with maternal neuroendocrine function (68, 69) and risk of bacterial
vaginosis (70).
The Cook-Medley Hostility Scale is a 50-item set of true-false items which sum to yield a
hostility score (71). A subset of 13 items measure cynical hostility. The scale has good
internal consistency and test-retest reliability (72). Hostility tends to be positively correlated
with perceived racism (73, 74) and has been associated with stronger cardiovascular
reactions to stress (75, 76).
Social support was measured using the Multidimensional Scale of Perceived Social Support
(MSPSS). This 12-item measure assesses support from family, friends, and a significant
other. It has been validated for use among pregnant women (77, 78).

The short form of the Childhood Trauma Questionnaire (CTQ-SF) is a 28-item self-
report measure of childhood or adolescent abuse and neglect (79, 80). This scale shows
measurement invariance across diverse samples and good criterion-related validity among
adolescents in relation to corroborative data (79). Standard cut-offs on the CTQ were used to
classify women as having experienced or not experienced childhood abuse in the form of
emotional abuse, physical abuse, and/or sexual abuse (81).
Sleep quality was assessed with the Pittsburgh Sleep Quality Index (PSQI). This scale has
good diagnostic sensitivity and specificity in distinguishing good and poor sleepers (82). A
score > 5 is indicative of clinically disturbed sleep.
The Experiences of Discrimination (EOD) scale is a 9-item measure assessing the

occurrence and frequency of discrimination due to race/ethnicity. Specifically, participants
indicate whether they have experienced discrimination over their lifetime (Yes or No) in the
following settings: 1) at school, 2) getting hired or getting a job, 3) at work, 4) getting
housing, 5) getting medical care, 6) getting service in a store or restaurant, 7) getting credit,
bank loans or a mortgage, 8) on the street or in a public setting, 9) from the police or in the
courts. For items endorsed, participants rate the frequency of this occurrence: once, 2-3
times, or 4+ times. This scale has high test-retest reliability and predictive validity for health
outcomes in Black adults (83-85). Moreover, validation studies indicate that scores are not
related to social desirability (83).
Health Behaviors
As described, women reporting tobacco use at the time of screening were excluded from
participation. Exercise was operationalized as the frequency of engaging in vigorous
physical activity long enough to build up a sweat with a range of “less than once per month”
to “more than once per week”. Prenatal vitamin use was defined as never, some days (1-3
days per week), most days (4-6 days per week) and every day (7 days per week).
Interleukin-6
Serum was prepared from clotted blood samples from all participants at each of the three
assessment time points (baseline, 45 minutes post-stressor, and 120 minutes post-stressor).
Serum levels of IL-6 were measured using ultra-sensitive kits from Meso Scale Discovery.
All samples were batched and assayed on kits from the same lot. The lower limit of
detection was 0.61 pg/ml. All samples were above the limit of detection. Inter- and intra-
assay coefficients of variation were 10.65% and 10.66%, respectively.
Salivary Cortisol
Saliva was collected via salivette at seven timepoints: 25 minutes prior to the stressor
(baseline), immediately upon completion of the stressor, and at 15, 30, 45, 60, and 90
minutes post-stressor. Determinations are made using the Cortisol Coat-A-Count RIA kit
(Siemens Medical Solutions Diagnostics, 5700 West 9th Street, Los Angeles, Ca. 90045).
Intra-assay coefficient of variation was 4.3% and inter-assay coefficient of variation was
5.2%. The sensitivity of the assay was 0.025 μg/dl. Assays were counted and calculated on
the Packard Cobra II Gamma Counter (PerkinElmer, 710 Bridgeport Avenue, Shelton, Ct.
06484).
Statistical Analyses
Summary statistics were reported as mean and standard deviation for continuous variables
and frequency and percentage for categorical variables. Participants were grouped into four
categories based on race and pregnancy status. Demographic variables, health behaviors,

and psychosocial assessments were compared using analysis of variance for continuous
outcomes, chi-squared or Fisher’s exact tests for categorical outcomes, and the
nonparametric Jonckheere-Terpstra (JT) test for ordered categorical outcomes. Differences
by pregnancy and race overall and also between each pair of race/pregnancy subgroups were
tested.
Linear mixed models were used to test for differences in stress responses across race and
pregnancy. Outcome variables were IL-6, salivary cortisol, and PANAS positive and
negative affect. The distributions of IL-6 and salivary cortisol measures were right-skewed;
thus, IL-6 and salivary cortisol measures were log-transformed to better satisfy the normality
assumptions of the mixed model analyses. For each model, the independent fixed effects
were the fully saturated interactions and main effects for race, pregnancy, and time. For IL-6
and PANAS positive/negative, models were fit to the change scores at the two post-stressor
time points, controlling for the baseline value of the outcome variable by including it as a
covariate. With the inclusion of the baseline covariate, this model yields equivalent p-values
whether post-scores or change scores are modeled; the change score outcomes are preferred
as they yield estimates directly indicating change from baseline. As a sensitivity analysis, we
also evaluated IL-6 with the baseline level included as a dependent variable along with the
two post-stressor time points. For salivary cortisol, since there were six follow-up time
points instead of two, the baseline value was included as a dependent variable at time = 0
and subsequent time points were tested against the baseline parameter estimate. A random
subject effect was also included in each model, accounting for the correlation across time
within a subject. Parameter contrasts were set up in SAS® PROC MIXED to test race and
pregnancy effects at each time point. The contrasts produce a one degree of freedom test
with a t-statistic. Marginal distributions of race and pregnancy were used as the coefficients
for interaction terms including race or pregnancy, as appropriate.
To assess the association of cortisol with change in IL-6, the area under the curve (AUC) for
salivary cortisol from 25 minutes pre-stressor to 90 minutes post-stressor was calculated for
each participant using the trapezoidal rule. Correlations between cortisol area under the
curve and IL-6 change from baseline at 45 and 120 minutes were calculated.
The study was powered based on enrolling 40 pregnant and 40 nonpregnant women (50%
African American and 50% White), which would yield greater than 90% power to detect the
expected effect sizes of 1 standard deviation in terms of Cohen’s d for pregnancy and race
effects on IL-6 responses.
Results
Demographic Characteristics
Women did not significantly differ by race or pregnancy status in age, education, income,
nulliparity, or BMI (based on pre-pregnancy weight for pregnant women; Table 1).
Nonpregnant women were less likely to be married than pregnant women (X2(1) = 8.67, p
= .003). This effect was driven by nonpregnant African Americans who were less likely to
be married than pregnant White (X2(1) = 11.3, p = .001) or pregnant African American
women (X2(1) = 5.7, p = .017).
Inflammatory Responses to Acute Stress

Baseline IL-6 levels were significantly lower in pregnant White versus nonpregnant White
women (t(74) = 2.54, p = .013). Linear mixed model results demonstrated that, controlling
for baseline IL-6, African American women exhibited significantly greater IL-6 increases at
120 minutes post-stressor as compared to Whites (t(72) = 3.51, p = .001). Controlling for

baseline, IL-6 levels at 120 minutes post-stressor were 46% higher among African American
women (95% CI: 18% to 81%; Fig 1).
Model contrasts demonstrated that nonpregnant African Americans showed significantly

greater inflammatory responses at 120 minutes post-stressor than either pregnant (t(72) =
3.50, p = .001) or nonpregnant (t(72) = 2.26, p = .027) Whites. Pregnant African American
women had significantly greater inflammatory responses than pregnant Whites (t(72) = 2.67,
p = .009). Thus, effects of race were observed in pregnancy as well as nonpregnancy. In a
sensitivity analysis modeling IL-6 at baseline, 45 minutes, and 120 minutes, the race by time
interaction was significant (F(2,146) = 5.15, p=.007). In terms of pregnancy effects,
controlling for baseline, IL-6 levels at 120 minutes post-stressor tended to be lower (15%) in
pregnant versus nonpregnant women (95% CI: -5% to 32%; p = .14).
Salivary Cortisol
At baseline, cortisol was significantly higher in pregnant women than in nonpregnant
women (t(72) = 15.30, p < .001; Fig 2). A non-significant trend was seen for lower baseline
cortisol among African Americans versus Whites (t(72) = 2.65, p = .11). Across all
participants combined, salivary cortisol was significantly lower than baseline immediately
post-stressor (t(72) = 2.03, p = .046) and at 30, 45, 60, and 90 minutes post-stressor (30
minutes: t(72) = 3.08, p = .003; 45 minutes: t(72) = 4.82, p < .001; 60 minutes: (t(72) = 5.99,
p < .001; 90 minutes: t(72) = 9.70, p < .001). There were no significant increases from
baseline in cortisol in any of the groups. There were no significant differences in estimated
slopes for linear change in salivary cortisol from 25 minutes pre-stressor to 90 minutes post-
stressor with the exception of a flatter cortisol slope among nonpregnant African-Americans
compared to pregnant (t(73) = 2.26, p = .027) and nonpregnant (t(73) = 2.05, p = .044)
Whites.
The AUC of cortisol across the study session was marginally higher among Whites versus
African Americans (t(75) = 1.77, p = .080) and significantly higher among pregnant versus
nonpregnant women (t(75) = 4.45, p <.001). In the overall sample, total salivary cortisol
(AUC) was not associated with the change from baseline in IL-6 at 45 (r = 0.14, p =.22) or
120 (r = −0.03, p = .81) minutes post-stressor. Moreover, after controlling for cortisol AUC,
race remained significantly associated with change in IL-6 at 120 minutes post-stressor
(t(71) = 3.95, p< .001).
Subjective Responses to Acute Stress

At baseline (prior to stressor onset), pregnant women reported significantly less positive
affect as measured by the PANAS as compared to nonpregnant women (t(74) = 12.6, p < .
001). Controlling for baseline, positive affect did not differ based on race or pregnancy
status immediately post-stressor (race: t(74)=0.10, p = .92; pregnancy: t(74) = 0.22, p = .82)
or at 120 minutes post-stressor (race: t(74) = 1.86, p = .067; pregnancy: t(74) = 1.33, p = .19;
Fig 3).
Women did not differ in negative affect at baseline on the basis of either race or pregnancy
status (race: t(74) = 0.06, p = .95; pregnancy: t(74) = 0.98, p = .33). Immediately post-
stressor, pregnant women had a significantly lower increase in negative affect than
nonpregnant women (t(74) = 7.65, p = .007; Fig 4). This effect was driven by pregnant
Whites who had lower increases in negative affect than both nonpregnant African
Americans (t(74) = 2.76, p = .007) and nonpregnant Whites (t(74) = 2.94, p = .004), while
pregnant African Americans did not differ significantly from either nonpregnant African
Americans (t(74) = 1.11, p=.27) or nonpregnant Whites (t(74) = 0.95, p=.35). The race by

pregnancy interaction was not significant immediately post-stressor (t(74) = 1.38, p=0.17).
Women did not differ in negative affect at 120 minutes post-stressor.
Health Behaviors
Health behaviors are presented in Table 2. Participation in vigorous activity was
significantly greater among Whites versus African Americans (JT, Z = 2.35, p = .019) and in
nonpregnant versus pregnant women (JT, Z = 3.20, p = .001). These differences were driven
by nonpregnant White women, who reported taking part in vigorous activity significantly
more frequently than each of the other 3 groups (ps < .003). Observed differences in
inflammatory responses did not change after controlling for physical activity. Groups did not
differ in smoking status or prenatal vitamin use (between pregnant groups).
Psychosocial Factors
In terms of psychosocial factors, 26.9% of women overall scored at or above a clinical cut-
off of 16 on the CES-D indicating significant depressive symptoms. The mean state anxiety
score (STAI) was 35.12 which is the 56%ile for women in this age range (86). The mean
perceived stress score (PSS) was 17.92 (SD = 6.52), which is also slightly higher than a
mean of 16.14 (SD=7.56) among women in a population-based sample of women (87). The
overall mean total score on the social support measure (MSPSS) was 5.59 (SD = 1.06)
which is slightly less than that reported in a prior study of pregnant women (Mean = 6.01;
SD = 0.90) (77). In the overall sample, 56.4% were classified as poor sleepers on the basis
of a score of > 5 on the PSQI. In addition, 52.5% met criteria for childhood abuse on the
basis of scores on the CTQ.
Analyses were conducted to psychosocial factors based on race and pregnancy status
assessed (Table 3). Women did not differ by race or pregnancy status in the proportion of
women with CES-D > 16 or the proportion reporting childhood abuse (all X2 (1) < 1.89, ps
> .17), or in state anxiety as measured by the STAI (both t(74) > 0.53, ps > .60) . Perceived
support in total (t(74) = 2.26, p = .026) and from a significant other (t(74) = 2.67, p = .009)
was greater in pregnant versus nonpregnant women. African American women reported
greater racial discrimination both in terms of the number of situations (JT, Z = 2.70, p = .
007) and total frequency (JT, Z = 2.52, p = .012). Among African American women greater
racial discrimination was not significantly related to scores on the CES-D, STAI, or MSPSS
(ps ≥ .39). The correlation between the PSS and EOD scores in terms of number of
situations (r = .26, p = .11) and total frequency (r = .32, p = .056) approached statistical
significance. Observed racial differences in inflammatory responses did not change when
controlling for social support or racial discrimination in separate models.
Discussion
The first goal of this study was to examine effects of race on inflammatory responses to
acute stress. As hypothesized, African American women exhibited greater serum IL-6
responses to the stressor as compared to Whites. Model contrasts demonstrated that this
effect of race was significant during both pregnancy and nonpregnancy. This effect was not
accounted for by demographic variables or health behaviors.
Notably, African Americans and Whites were similar in all psychosocial variables measured
with the exception of greater reported experiences of discrimination among African
Americans. The relationship between race and inflammatory responses remained after
controlling for perceived racial discrimination, indicating exposure to racism as measured by
this scale did not account for observed racial differences. Despite this result, the potential
role for racial discrimination in the observed effects cannot be discounted. It is of note that a

relatively high percentage of White women in the current study (42.5%) reported
experiencing racial discrimination in one or more major life situation. However, the
qualitative experience and social implications of racial discrimination among Whites versus
African Americans differ (88). Thus, a simple comparison or statistical control for frequency
of exposures among Whites versus African Americans may not meaningfully capture the
psychosocial impact of such exposures. Moreover, this study did not have adequate
statistical power to compare inflammatory responses among African Americans on the basis
of the severity of perceived racial discrimination. Within group variability may ultimately be
more meaningful with regard to physical health effects of racial discrimination. For
example, our prior work shows that among pregnant African Americans, those reporting
greater racial discrimination have higher Epstein Barr Virus antibody titers, indicating
poorer cellular immune function (89). Finally, it is also possible that a different measure of
racial discrimination may provide more predictive value in this context.
These data have implications for understanding biological mechanisms by which racial
minority status may confer increased risk of adverse birth outcomes. The majority of studies
to date have focused on stressor exposure and/or subjective experiences of stress in
predicting preterm birth. However, the ultimate physical impact of stress on health is a
function of exposure as well as physiological response. As reviewed, inflammatory
processes are implicated in adverse birth outcomes including preterm birth (9). Therefore,
more robust and extended inflammatory responses may confer increased risk of adverse
birth outcomes, particularly among women who experience more frequent acute stressor
exposure. Moreover, prior data show that upon repeated exposures to an acute laboratory
stressor, habituation of cortisol and blood pressure reactivity is evidenced, but stress-induced
elevations in IL-6 remain similar (42). Therefore, the experience of continued or repeated
psychosocial stressors may confer considerable exposure to inflammatory markers.
An exploratory aim of this study was to examine the correspondence between cortisol and
stress-induced IL-6 responses. Baseline and cortisol AUC was higher among pregnant
versus nonpregnant women, as expected. Compared to Whites, African Americans showed a
trend toward lower baseline cortisol (p = .11) and lower cortisol AUC (p = .080). The study
protocol was conducted in the early afternoon. Prior data show that, compared to Whites,
African Americans have lower cortisol levels in the morning/early afternoon and higher
levels in the evening resulting in a flatter diurnal slope (90, 91). Thus, these data are
consistent with prior studies. Cortisol AUC was not associated with IL-6 responses in the
overall sample, and the noted racial differences in IL-6 responses were not modified by
inclusion of cortisol AUC in the model.
Some prior data suggests that activity of the HPA axis is inversely associated with IL-6
responses to acute stress (92), although other studies have found this relationship to be
inconsistent (42). It is important to consider that although cortisol has robust anti-
inflammatory effects on cytokine-producing cells, extended exposure to elevated levels of
glucocorticoids (GC), such as that seen in conditions of repeated or chronic stress, may
produce GC insensitivity at the level of both cytokine producing cells and the HPA axis (93,
94). GC insensitivity is marked by a diminished ability of the HPA axis and cytokine
producing cells to respond to cortisol, resulting in more sustained HPA axis responses and
greater production of inflammatory markers. Thus, in the context of GC resistance, the
expected inverse relationship between cortisol and inflammatory markers may be
diminished or eliminated. Therefore, without knowledge of GR function or typical cortisol
exposure (i.e., measurement of the complete diurnal slope), the lack of association between
IL-6 and salivary cortisol responses in the current study is difficult to interpret.

Of note, in this study, no significant cortisol increases were seen in response to the stressor.
Due to typical diurnal decline in cortisol, effects of stress on cortisol responses are less
apparent without the use of a non-stressor control day, particularly when measurement
occurs in the afternoon (95). In the absence of stress-induced cortisol increases, stressor
exposure may slow the downward diurnal cortisol slope, but this effect within subjects is not
quantifiable without comparison to a non-stress day. In addition, prior studies show that
cortisol reactivity to acute stressors is less robust among women than men (96). Thus, these
factors may explain the lack of increase in cortisol in response to the stressor.
The current study included 39 pregnant women, among whom only two (5.1%) delivered
preterm (one African American; one White). This preterm birth rate is lower than in the US
population overall and reflects the exclusion of women with high risk health conditions
(e.g., hypertension) and health behaviors (e.g., smokers). Thus, this study was not
appropriately powered to detect potential associations between inflammatory responses to
acute stress and birth outcomes. This is a clear direction for future studies.
Although the focus of the current study was on pregnancy, the evidenced effect of race on
inflammatory responses has implications for health outcomes well beyond pregnancy. In
particular, there are substantial racial disparities in cardiovascular diseases (97). Black
women as well as men experience greater prevalence, earlier disease onset, and greater
cardiovascular mortality compared to White individuals of the same age (98). Inflammation
is an established mechanistic factor in cardiovascular disease risk (99, 100). Moreover, it has
been demonstrated that stress-induced increases in IL-6 predict ambulatory blood pressure
three years later (101). The current data provide novel evidence of racial differences in
stress-induced inflammatory responses. Attention is needed regarding the potential role of
inflammatory responses to acute stress in racial disparities in cardiovascular disease risk.
In terms of pregnancy status, contrary to prediction, there was no significant difference

between pregnant women, who were assessed in the 2nd trimester of pregnancy, and
nonpregnant women in terms of inflammatory responses, although there was a trend toward
this effect (p=0.14). IL-6 increases in response to the stressor were 15% lower in pregnant
versus nonpregnant women (95% CI: −5% to 32%). This effect size translates to a Cohen’s
d of .17 which is a small effect. Prior data in humans and animals indicate that inflammatory
responses to both in vivo and in vitro biological challenges (e.g., lipopolysaccharide) are
attenuated in pregnancy (25-29). It has been postulated that this attenuation of inflammatory
responses represents an adaptive mechanism by which the fetus is protected from excessive
maternal responding. Following from this argument, adaptation of the inflammatory
responses to psychological challenge may be similarly beneficial. Data from a larger cohort
would provide greater statistical power to determine if this effect is present.
Prior data has shown that negative affective responses to a speech task are associated with
the magnitude of inflammatory response (102). In the current study, there was no main
effect of race on negative affective responses. However, pregnant White women reported
significantly smaller increases in negative affect than did nonpregnant Whites or
nonpregnant Blacks. Prior evidence suggests that stressors are experienced as less stressful
during pregnancy versus nonpregnancy. For example, upon exposure to an earthquake,
women rated the experience as more stressful in earlier versus later stages of pregnancy and
showed increasingly shorter gestation upon earlier exposure (52). It is notable that, in the
current sample, pregnant African American women did not show attenuation of negative
affective responses compared to nonpregnant African Americans.
The current study used the Trier Social Stress Test (TSST). The TSST is mild stressor
designed to be similar to stressors such as public speaking that most people encounter at

some time in their daily life. It has previously been used with women during pregnancy and
postpartum (e.g., 103, 104). However, the vast majority of previous studies of reactivity to
psychological stressors during pregnancy have used tasks such as mirror tracing, Stroop
selective attention tasks, and cold pressor tasks (for review see 53, 105). Due to its similarity
to naturally occurring stressors, the TSST arguably provides a stronger approximation of
reactivity to everyday psychological stressors than these other types of tasks. In addition,
evidence suggests pregnant women exhibit significantly higher reactivity to public speaking
as compared to other types of acute stressors (106). Therefore, use of the TSST in this study
provides both strong external validity and improved power to detect effects of the stressor
on physiological parameters of interest relative to other stressors.
This study included assessment of IL-6 at 45 minutes and 120 minutes post-stressor, given
that inflammatory responses to laboratory stressors are delayed (107). Although these are
appropriate sampling timepoints, longer follow-up would provide valuable data regarding
the full duration and magnitude of inflammatory marker exposure in different groups. This
should be considered in future studies. In addition, this study included assessment of
pregnant women in the second trimester. It has been hypothesized that stress responsivity is
progressively attenuated as pregnancy progresses (105). Longitudinal assessment during
each trimester of pregnancy and/or cross-sectional studies with demographically matched
groups of women during each trimester would provide valuable data regarding the
adaptation of inflammatory responses across the course of gestation. Relatedly, in the
nonpregnant control group, effects of menstrual cycle phase were not assessed. Prior data
indicate that menstrual cycle phase does not appreciably alter heart rate, blood pressure,
catecholamine, lipid, or inflammatory cytokine responses to acute stress (108, 109), but does
alter cortisol responses (110).
Women with a previous live birth were targeted for recruitment and comprised 76/78
(97.4%) of the final sample. This strengthens the study design because available data
suggest that physiological adaptation to pregnancy may be greater during subsequent versus
initial pregnancy (111). In addition, recruitment of nonpregnant controls with a prior live
birth provided a sample with the best demographic equivalence to pregnant participants in
terms of women experiencing motherhood at a given stage of life. Although this study
design was chosen based on these empirical considerations, results may differ among
women who are nulliparous.
This study included stringent inclusion/exclusion criteria. All women were normal weight,
generally healthy, and denied use of recreational drugs or smoking at the time of eligibility
screening. However, we did not confirm drug or smoking status via objective measures (e.g.,
serum cotinine). Self-reported smoking likely underestimates true smoking behavior,
particularly among pregnant women (112). These stringent inclusion/exclusion requirements

increase homogeneity within groups, increasing statistical power. However, as noted earlier,
these criteria also exclude women at greatest risk for adverse birth outcomes. Moving
forward, future studies should endeavor to include women with more diverse health
behaviors and demographic characteristics to provide power to examine inflammatory
responses in relation to birth outcomes and typify the mediating and moderating role of the
factors in predicting stress-induced inflammatory responses.
This study was powered to detect effects of race and pregnancy status. Psychological data
(e.g., hostility, depressive symptoms, etc.) were collected to determine the comparability of
groups in factors which may affect physiological responses to acute stress. However, this
sample size did not permit analyses of meditational or moderation effects of these constructs
(e.g., if hostility, sleep quality, or other factors differentially affected inflammatory
responses by race or pregnancy status). In addition, we did not conduct clinical interviews to

determine history of clinical depression. Future research should aim to examine such
psychological mediators and moderators.
In sum, this study provides novel data regarding inflammatory responses to acute stress
among women on the basis of race and pregnancy status. These data represent a promising
direction in delineating pathways by which stress may affect pregnancy outcome and fetal
development. Although numerous studies demonstrate a link between various psychosocial
stress exposures and pregnancy outcomes, comparatively few have focused on 1) biological
mechanisms underlying these links or 2) individual differences in responses to stress. In
addition, these results may possibly have relevance beyond pregnancy for racial disparities
in diseases with an inflammatory component, particularly cardiovascular diseases. As the
ultimate impact of stressor exposure is a function of not only the occurrence of the stressor
but also the individual response to the stressor, focus on individual differences in stress-
induced inflammatory responses represents a clear target for continued research efforts.
Acknowledgments
We appreciate the contributions of Clinical Research Assistants Colleen Sagrilla, Kelly Marceau, and Rebecca
Long to data collection. We would like to thank our study participants. We also thank the staff at the OSU Clinical
Research Center and Wexner Medical Center Prenatal Clinic.
Role of the Funding Sources This study was supported by NICHD (HD061644, LMC and HD067670, LMC). The
project described was supported by the Ohio State University Clinical Research Center, funded by the National
Center for Research Resources, Grant UL1RR025755 and is now at the National Center for Advancing
Translational Sciences, Grant 8UL1TR000090-05. The content is solely the responsibility of the authors and does
not necessarily represent the official views of the National Center for Research Resources or the National Institutes
of Health. NIH had no further role in study design; in the collection, analysis and interpretation of data; in the
writing of the report; and in the decision to submit the paper for publication. Lisa Christian had full access to all of
the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis.
Abbreviations
IL-6 Interleukin-6
ELISA Enzyme-linked Immunosorbent Assay
TNF-α Tumor Necrosis Factor-α
IL-1RA Interleukin-1 Receptor Antagonist
BMI Body Mass Index
TSST Trier Social Stress Test
PANAS Positive and Negative Affect Scale
CES-D Center for Epidemiological Studies Depression Scale

STAI State-Trait Anxiety Inventory
PSS Perceived Stress Scale
CTQ-SF Childhood Trauma Questionnaire- Short Form
PSQI Pittsburgh Sleep Quality Index
EOD Experiences of Discrimination Scale
MSPSS Multidimensional Scale of Perceived Social Support
AUC Area under the curve

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Fig 1. Inflammatory Responses to the Trier Social Stress Test in Pregnant and Nonpregnant
Women
Controlling for baseline, IL-6 levels at 120 minutes post-stressor were 46% higher in
African Americans versus Whites (95% CI: 18% to 81%; t(72) = 3.51, p = .001). This effect
of race was significant during pregnancy and nonpregnancy. Note: Data are pictured in raw
values. Analyses were conducted using log-transformed values.

Fig 2. Cortisol Responses to the Trier Social Stress Test in Pregnant and Nonpregnant Women
At baseline, cortisol was significantly higher in pregnant women than in non-pregnant

women (t(72) = 15.30, p < .001). A non-significant trend was seen for lower baseline
cortisol among African Americans versus Whites (t(72) = 2.65, p = .11). The AUC of
cortisol across the study session was significantly higher among pregnant versus non-
pregnant women (t(75) = 4.45, p <.001) and marginally lower among African Americans
versus Whites (t(75) = 1.77, p = .08). Note: Data are pictured in raw values. Analyses were
conducted using log-transformed values.

Fig 3. Changes in Positive Affect in Response to the Trier Social Stress Test
Pregnant women reported significantly less positive affect at baseline as compared to non-
pregnant women (F(1,74) = 12.6, p < .001). Controlling for baseline positive affect, positive
affect immediately post-stressor or 120 minutes post-stressor did not differ based on race or
pregnancy status (ps ≥ .06).

Fig 4. Changes in Negative Affect in Response to the Trier Social Stress Test
Women did not differ in negative affect at baseline based on either race or pregnancy status.
Immediately post-stressor, pregnant women had a significantly lower increase in negative
affect than nonpregnant women (t(74) = 7.65, p = .007). This effect was driven by pregnant
Whites who had lower increases in negative affect than either nonpregnant African
Americans or nonpregnant Whites (ps ≤ .01).

Table 1
Demographic Characteristics
Nonpregnant Nonpregnant Pregnant Pregnant

White African American White African American
(n=20) (n=19) (n=20) (n=19)
Age [Mean (SD)]1 24.85 (3.10) 23.16 (4.20) 23.90 (3.21) 23.68 (3.56)
Marital Status [n (%)]*2
Married 5 (25%) 1 (5%) 11 (55%) 7 (37%)
In a relationship 11 (55%) 7 (37%) 8 (40%) 12 (63%)
Single 4 (20%) 11 (58%) 1 (5%) 0 (0%)
Education [n (%)]3
High school graduate or less 6 (30%) 9 (47%) 9 (45%) 5 (25%)
Some college 6 (30%) 7 (37%) 7 (35%) 9 (47%)
College degree (2 or 4 yr) 8 (40%) 2 (11%) 4 (20%) 4 (21%)
Income [n (%)]3
<$15,000 7 (35%) 8 (42%) 8 (40%) 9 (47%)

$15,000-29,999 7 (35%) 6 (32%) 6 (30%) 6 (35%)
≥ $30,000 6 (30%) 5 (26%) 6 (30%) 4 (21%)
Nulliparous# [n(%)]2 0 (0%) 1 (5%) 0 (0%) 1 (5%)
BMI†[Mean (SD)]1 24.13 (3.88) 23.57 (3.48) 24.32(2.72) 23.57 (3.70)
1
Analysis of variance, 2-tailed
2
Chi-square test
3
Jonckheere-Terpstratest, 2-tailed
*
nonpregnant African American women were significantly less likely to be married than pregnant White (X2(1) = 11.3, p = .001) or pregnant
AfricanAmerican women (X2(1) = 5.7, p = .017).
#
women with prior pregnancies were targeted for recruitment; see methods
†
based on pre-pregnancy weight for pregnant women; obese women (BMI ≥ 30) were excluded from participation

Table 2
Health Behaviors

(n=20) (n=19) (n=20) (n=19)
Smoking Status 1
Current 0 (0%) 0 (0%) 0 (0%) 0 (0%)
Past 8 (40%) 4 (21%) 9 (45%) 4 (21%)
Never 12 (60%) 15 (79%) 11 (55%) 15 (79%)
Prenatal Vitamin Use 2 n/a n/a
Never 8 (40%) 5 (26%)
Some days (1-3/week) 4 (20%) 2 (11%)
Most days (4-6/week) 5 (25%) 2 (11%)
Every day (7 days/week) 3 (15%) 10 (53%)
Exercise # 2
Less than once per month 0 (0%) 3 (16%) 8 (40%) 9 (47%)
Once per month 1 (5%) 2 (11%) 0 (0%) 2 (11%)
2-3 times per month 2 (10%) 7 (37%) 5 (25%) 3 (16%)
Once per week 7 (35%) 4 (21%) 3 (15%) 2 (11%)
More than once per week 10 (50%) 3 (16%) 4 (20%) 3 (16%)
1
Chi-square test
2
Jonckheere-Terpstrates (JT)t, 2-tailed
#
Participation in vigorous activity was significantly greater among Whites versus AfricanAmericans (JT, p = .019) and in nonpregnant versus
pregnant women (JT, p = .001). These differences were driven by nonpregnant White women, who reported taking part in vigorous activity
significantly more frequently than each of the other 3 groups (ps < .003).

Table 3
Psychological Functioning

(n=20) (n=19) (n=20) (n=19)
Depressive Symptoms 1
CES-D ≥ 16; n (%) 6 (30%) 7 (36.8%) 3 (15.0%) 5 (26.3%)
Anxiety 2
State Anxiety [STAI; Mean (SD)] 35.25 (13.14) 36.26 (10.40) 34.80 (8.82) 34.17 (9.46)
Perceived Stress 2
PSS Score; Mean (SD) 17.79 (7.6) 19.72 (6.24) 17.10 (6.56) 17.21 (5.66)
Impaired Sleep Quality 1
PSQI Score > 5 11 (55%) 13 (68%) 11 (55%) 9 (45%)
Social Support [Mean (SD)] #2
Total MPSSS 5.22 (1.02) 5.44 (1.16) 5.81 (1.14) 5.92 (0.83)
Family Support 5.40 (1.64) 5.43 (1.20) 5.66 (1.59) 5.75 (1.59)
Friend Support 4.94 (1.24) 5.55 (1.27) 5.52 (1.37) 5.74 (1.07)
Significant Other Support 5.33 (1.84) 5.33 (1.98) 6.25 (1.22) 6.28 (0.91)
Hostility 2
Cook-Medley Score; Mean (SD) 19.40 (7.44) 22.05 (7.74) 20.10 (7.91) 20.42 (6.69)
Childhood Trauma 1
Abused; n (%) 10 (50%) 12 (63.2%) 8 (40%) 11 (57.9%)
Racial Discrimination ^ 3
EOD Score Situations
0 12 (60%) 6 (32%) 11 (55%) 7 (37%)
1-2 7 (35%) 7 (37%) 7 (35%) 5 (26%)
>2 1 (5%) 6 (32%) 2 (10%) 7 (37%)
EOD Score Frequency

0 12 (60%) 6 (32%) 11 (55%) 7 (37%)
1-5 6 (30%) 7 (37%) 7 (35%) 4 (21%)

6-10 1 (5%) 2 (11%) 0 (0%) 7 (37%)
>10 1 (5%) 4 (21%) 2 (10%) 1 (5%)
1
Chi-square test
2
Analysis of variance, 2-tailed
3
Jonckheere-Terpstratest, 2-tailed
#
Perceived support was significantly greater among pregnant versus nonpregnant women in total (t(74) = 2.26, p = .026) and from a significant
other (t(74) = 2.67, p = .009).
^
Racial discrimination was significantly greater among African Americans versus Whites in terms of both the number of situations (Jonckheere-
Terpstra (JT), p = .007) and total frequency of discrimination (JT, p = .012) as reported on the EOD.

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Psychosom Med. 2013 September ; 75(7): 658–669. doi:10.1097/PSY.0b013e31829bbc89.

Stress-Induced Inflammatory Responses in Women: Effects of

versus nonpregnant women (95%CI:-5%-32%; p=0.14). Racial differences in inflammatory

Psychosom Med. Author manuscript; available in PMC 2014 September 01.

Notably, we know of no studies examining inflammatory responses to acute psychological

and extended as compared to responses of the sympathetic nervous system and

Psychosom Med. Author manuscript; available in PMC 2014 September 01.

Study Visit Overview

questionnaires were completed assessing mood. Following a 20 minute acclimation/rest

Laboratory Stressor: The Trier Social Stress Test (TSST)

Psychosom Med. Author manuscript; available in PMC 2014 September 01.

Psychosom Med. Author manuscript; available in PMC 2014 September 01.

The Experiences of Discrimination (EOD) scale is a 9-item measure assessing the

Psychosom Med. Author manuscript; available in PMC 2014 September 01.

Inflammatory Responses to Acute Stress

Psychosom Med. Author manuscript; available in PMC 2014 September 01.

Model contrasts demonstrated that nonpregnant African Americans showed significantly

Subjective Responses to Acute Stress

Psychosom Med. Author manuscript; available in PMC 2014 September 01.

Psychosom Med. Author manuscript; available in PMC 2014 September 01.

Psychosom Med. Author manuscript; available in PMC 2014 September 01.

In terms of pregnancy status, contrary to prediction, there was no significant difference

Psychosom Med. Author manuscript; available in PMC 2014 September 01.

particularly among pregnant women (112). These stringent inclusion/exclusion requirements

Psychosom Med. Author manuscript; available in PMC 2014 September 01.

CES-D Center for Epidemiological Studies Depression Scale

Psychosom Med. Author manuscript; available in PMC 2014 September 01.

Psychosom Med. Author manuscript; available in PMC 2014 September 01.

1110. [PubMed: 17712652]

Saunders; Philadelphia: 1992.

Psychosom Med. Author manuscript; available in PMC 2014 September 01.

elevated blood pressure on responses to stress. Hypertension. 1987; 10(6):555–63. [PubMed:

Psychosom Med. Author manuscript; available in PMC 2014 September 01.

psychobiological stress responses in a laboratory setting. Neuropsychobiology. 1993; 28:76–81.

Psychosom Med. Author manuscript; available in PMC 2014 September 01.

Psychosom Med. Author manuscript; available in PMC 2014 September 01.

responses to psychosocial stress in human pregnancy. Journal of Clinical Endocrinology and

Psychosom Med. Author manuscript; available in PMC 2014 September 01.

Psychosom Med. Author manuscript; available in PMC 2014 September 01.

Psychosom Med. Author manuscript; available in PMC 2014 September 01.

At baseline, cortisol was significantly higher in pregnant women than in non-pregnant

Psychosom Med. Author manuscript; available in PMC 2014 September 01.

Psychosom Med. Author manuscript; available in PMC 2014 September 01.

Psychosom Med. Author manuscript; available in PMC 2014 September 01.

Nonpregnant Nonpregnant Pregnant Pregnant

Marital Status [n (%)]*2

Married 5 (25%) 1 (5%) 11 (55%) 7 (37%)

In a relationship 11 (55%) 7 (37%) 8 (40%) 12 (63%)

Single 4 (20%) 11 (58%) 1 (5%) 0 (0%)

High school graduate or less 6 (30%) 9 (47%) 9 (45%) 5 (25%)

Some college 6 (30%) 7 (37%) 7 (35%) 9 (47%)

College degree (2 or 4 yr) 8 (40%) 2 (11%) 4 (20%) 4 (21%)

<$15,000 7 (35%) 8 (42%) 8 (40%) 9 (47%)

$15,000-29,999 7 (35%) 6 (32%) 6 (30%) 6 (35%)

≥ $30,000 6 (30%) 5 (26%) 6 (30%) 4 (21%)

Nulliparous# [n(%)]2 0 (0%) 1 (5%) 0 (0%) 1 (5%)

BMI†[Mean (SD)]1 24.13 (3.88) 23.57 (3.48) 24.32(2.72) 23.57 (3.70)

Psychosom Med. Author manuscript; available in PMC 2014 September 01.