International Journal of Behavioral Medicine (2023) 30:801–813

https://doi.org/10.1007/s12529-022-10141-2

FULL LENGTH MANUSCRIPT

Early Life SES, Childhood Trauma Exposures, and Cardiovascular

Responses to Daily Life Stressors in Middle‑aged Adults
Kristina D. Dickman1 · Elizabeth Votruba‑Drzal1 · Karen A. Matthews1,2,3 · Thomas W. Kamarck1,2

Accepted: 8 November 2022 / Published online: 22 November 2022

© International Society of Behavioral Medicine 2022

Abstract
Background Dysregulation in physiological responses to stress may provide a mechanism through which low socioeconomic
status (SES) in childhood negatively impacts health. Evidence linking early life SES to physiological stress responses is
inconsistent. Exposure to childhood trauma may be an important source of heterogeneity accounting for mixed findings.
Guided by the adaptive calibration model, we examined whether childhood SES and childhood trauma jointly predict ambu-
latory measures of cardiovascular responses to daily life stressors.
Method A sample of 377 healthy, middle-aged adults (62% female, 80% White, 64% college-educated, Mage = 52.59 ± 7.16)
completed a 4-day ecological momentary assessment protocol that measured task strain, social conflict, and ambulatory
systolic and diastolic blood pressure (SBP and DBP, respectively) at hourly intervals throughout the day. Average ambulatory
blood pressure responses to stress were calculated by regressing momentary SBP and DBP on momentary measures of stress
within the multilevel models. Early life SES and childhood trauma were measured retrospectively by self-report questionnaire.
Results Multilevel models controlling for momentary influences on blood pressure and age, sex, and race showed no main
effects of early life SES or childhood trauma on ambulatory measures of cardiovascular responses to daily life stress. An
interaction emerged for DBP responses to social conflict, where individuals raised in middle SES families who experienced
trauma showed a blunted response relative to those who did not (𝛾14 =−0.93, 95% CI: [−1.62, −0.24], p = .008). There was
no significant SES-trauma interaction in predicting SBP responses to social conflict or blood pressure responses to task strain.
Conclusion Results do not provide support for our predictions that were derived from the adaptive calibration model, but
do suggest that the impacts of early childhood experiences on cardiovascular responses may vary by type of daily stress
experience.

Keywords Childhood trauma · Socioeconomic status · Early life adversity · Cardiovascular reactivity · Ecological
momentary assessment

Introduction Galobardes and colleagues found that individuals of lower

early life SES were at greater risk of premature mortality
Socioeconomic status (SES) is a salient predictor of health than their higher SES peers, regardless of their SES in adult-
inequalities. Accumulating evidence suggests that chil- hood [2]. Similarly, low SES in childhood places individu-
dren raised in lower SES households show greater physical als at a modestly increased risk for cardiovascular disease
health risk as adults [1]. In a large review of the literature, (CVD), independent of adult SES [3].
Psychosocial factors such as increased stress or stress
* Kristina D. Dickman vulnerability may provide one path through which early life
kdd41@pitt.edu SES may affect health. Low SES environments are associ-
ated with greater risks of familial conflict, harsh and incon-
1
Department of Psychology, University of Pittsburgh, sistent parenting, neighborhood crime and violence, and
Pittsburgh, PA, USA
socioeconomic uncertainty and worry [4]. Many physiologi-
2
Department of Psychiatry, University of Pittsburgh, cal systems are relatively plastic in early life, and exposure to
Pittsburgh, PA, USA
psychosocial stressors during this period may alter nervous,
3
Department of Epidemiology, University of Pittsburgh, endocrine, and immune systems in persistent and permanent
Pittsburgh, PA, USA

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802
ways [5]. The form that these alterations take may vary as a
function of early life environmental exposure.
Individual differences in the patterning of physiological
stress responding may form as an adaption to social and
physical conditions present during development. The adap-
tive calibration model (ACM) posits, in part, that individu-
als adapt optimal stress response systems dependent on the
safety and predictability of their childhood environments [6].
For an individual reared in a relatively safe and supportive
environment, a moderately active physiological reactivity
profile would allow the individual to respond adequately to
emergencies, while also preserving energy for long-term
fitness. However, in accordance with this model, a dan-
gerous or unpredictable environment may cause an indi-
vidual to adopt a highly reactive stress response profile, as
this would increase the individual’s ability to respond to
short-term danger. In this environment, an individual may
be better served placing resources into short-term growth
and maintenance activities, as longer-term reproductive fit-
ness is uncertain. Individuals reared in very traumatic or
persistently stressful environments, however, may adopt an
unresponsive approach towards acute stressors, as constant
activation of the stress response system may incur greater
physiological costs with few benefits. In these cases, a pro-
file characterized by physiological withdrawal may be the
optimal strategy because of the frequency and severity of
expected stressors and the resource economization associ-
ated with withdrawal. The ACM asserts that physiological
stress reactivity develops as a direct consequence of the
stability and safety of one’s early life environment along
with one’s own available resources. Both of these provide a
context for helping the organism predict the likely balance
of demands for both acute adaptation and long-term fitness.
As alluded to in the above model, one metric of physi-
ological dysregulation is the level of (either exaggerated or
blunted) cardiovascular response to stress. The reactivity
hypothesis asserts that prolonged or exaggerated cardiovas-
cular reactivity (CVR) to psychological stress promotes the
development of CVD, in part, due to structural and func-
tional changes in the coronary arteries that may accompany
frequent or prolonged hemodynamic responses [7]. Empiri-
cally, exaggerated and prolonged CVR to acute cognitive
or social stressors have been linked with several adverse
health outcomes including CVD risk and early mortality [8,
9]. More recently, blunted CVR to acute stressors has been
linked with adverse health outcomes including obesity and
depression [10]. While early life SES consistently relates
with disease, the connection between SES and cardiovascu-
lar stress responding is inconclusive.
Lower early life SES, typically measured by parental
education and income, has been linked with both exagger-
ated and blunted cardiovascular reactivity to stress. To our
knowledge, at least ten studies have investigated childhood
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International Journal of Behavioral Medicine (2023) 30:801–813
SES in relation to CVR [11–20]. Of these, five reported an
inverse relationship, or exaggerated CVR in relation to lower
SES [11–15]. Two studies identified reduced reactivity in
relation to lower early life SES [16, 17]. The remaining three
studies found either null or contradictory effects [18–20].
We hypothesize that these mixed findings may be explained
by heterogeneity in sample characteristics — namely, expo-
sure to additional forms of childhood adversity. While it is
possible that the mixture of results linking SES and car-
diovascular reactivity suggests no overall relationship, it is
also possible that this relationship is moderated by a third
variable, such as exposure to adverse childhood experiences.
A parallel and growing line of research demonstrates
more consistent associations between childhood adversity,
a general term that describes exposure to harmful experi-
ences such interpersonal stress, material deprivation, abuse,
and/or neglect, and CVR to laboratory stressors. With only
a couple of exceptions [21, 22], the majority of work in this
area finds that children with more exposure to adverse life
events demonstrate lower CVR to acute stressors than their
peers without adversity exposure [23]. Overall, growing evi-
dence suggests an inverse relationship where greater child-
hood adversity relates with blunted responses to acute stress.
Exposure to a materially disadvantaged SES background
is one type of childhood adversity. While increased child-
hood trauma, also a form of adversity, is more prevalent
among low SES environments, exposure to trauma is not
limited to lower SES households [24]. To date, the litera-
tures linking early life SES with cardiovascular reactivity
and childhood adversity with cardiovascular reactivity have
remained largely independent of one another. Given the
mixed evidence linking early life socioeconomic disadvan-
tage with elevated [11–15], blunted [16, 17], and equivalent
[18–20] cardiovascular reactivity, it might be that differential
exposure to childhood trauma is an important source of vari-
ability causing these two stress-related profiles to emerge.
As described above, the ACM posits that early environ-
mental influences may predispose the organism to adopt
different patterns of stress responding, with moderately
demanding environments shaping a stress reactive response
pattern, and extreme conditions eliciting an unemotional,
or blunted, stress response profile [6]. We drew from the
ACM to generate a priori predictions on how childhood
trauma and SES may interact. We hypothesized that child-
hood surroundings with few material resources but nontrau-
matic psychosocial environments may serve as moderately
demanding and encourage heightened reactivity to stress. At
the same time, the double burden of material disadvantage
and childhood trauma exposure might create a more persis-
tently stressful developmental context, which promotes the
unemotional, or blunted, stress response profile. We hypoth-
esized that these two domains of early life stress should be
particularly susceptible to this type of synergy, as they might
International Journal of Behavioral Medicine (2023) 30:801–813
be seen to capture heightened demands (i.e., stress/trauma)
and decreased psychosocial or material resources during the
childhood period. The unbalanced experience of demands
and resources may thus increase the early life stress bur-
den and constrain stress coping [25]. Therefore, it may be
that links between low early life SES and cardiovascular
responses to stress depend on exposure to childhood trauma,
where low SES individuals with a history of childhood
trauma demonstrate blunted cardiovascular reactivity and
low SES individuals with no history of childhood trauma
demonstrate exaggerated cardiovascular reactivity relative
to their high SES counterparts.
A variety of composite measures are utilized to assess the
prevalence of adversity. The present study uses the child-
hood trauma questionnaire [26] to retrospectively assess
exposure to experiences of abuse and neglect prior to the
age of 18. This measure of childhood adversity is specifi-
cally designed to capture trauma experiences, in contrast to
indices such as the Adverse Childhood Experience Ques-
tionnaire [27], which concurrently assesses other forms of
adversity including household dysfunction.
Most of the previous work on the topic of childhood
adversity and cardiovascular stress reactivity has centered on
reactivity defined in the laboratory. In contrast, the current
study uses ecological momentary assessment (EMA), a data
collection method in which information on an individual’s
current state is gathered as it occurs in the natural environ-
ment [28]. Methodologically, there are three advantages of
using EMA to investigate SES and trauma differences in
cardiovascular stress responding. First, momentary meas-
ures of stress may provide a more representative depiction
of daily life experiences than global self-report assessments.
Second, if we assume that low SES individuals may be less
comfortable than their more affluent counterparts in a for-
mal laboratory setting, EMA may permit us to assess stress
responses in a manner that is more equivalent across the
SES gradient. Research shows that individuals from lower
SES backgrounds perceive greater discrimination in medical
settings compared to their higher SES peers [29], although
no study to our knowledge has explored this phenomenon in
laboratory stress paradigms. Third, psychosocial factors and
health risks measured through EMA protocols may be more
strongly associated with markers of disease than those meas-
ured using global retrospective self-reports. The Karasek job
strain model posits that environments high in psychologi-
cal demands but low in decision control are associated with
elevated cardiovascular risk [30]. Work from this laboratory
has shown that EMA measures of job strain prospectively
predicted intima-medial thickness, a measure of preclinical
vascular disease, while traditional self-report measures of
job strain did not [31, 32]. EMA measures of social con-
flict have likewise been linked with risk of atherosclerosis
and coronary heart disease [32–34]. In the current study, we
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selected two EMA-based measures of stress — task strain
and social conflict — which reflect diverse thematic content
and have previously been shown relevant to cardiovascular
disease risk. Use of EMA in the current study may allow
us to measure stress responsivity while avoiding potential
SES-driven confounds that may arise from participating in
a laboratory setting.
To our knowledge, this interaction between early life SES
and childhood trauma on cardiovascular reactivity has yet
to be examined in a single study. Furthermore, while these
individual associations have been studied in the laboratory,
the current study is, to our knowledge, the first to examine
the association between early life SES and cardiovascular
stress response in daily life and only the second to do so for
childhood trauma [22]. The present report assesses whether
childhood SES and the presence or absence of childhood
trauma associate with the effect of daily life stress on con-
currently assessed ambulatory blood pressure (ABP), and
whether the two interact in this relationship. Daily stress
was operationalized as social conflict and task strain, two
areas of stress that relate to risk for cardiovascular disease
in epidemiological studies [31–34]. It was hypothesized
that early life SES would not directly relate to cardiovascu-
lar responses to stress, but that history of trauma exposure
would relate with decreased (i.e., blunted) stress responses.
It was predicted that trauma and early life SES would inter-
act to predict stress responses. Specifically, it was expected
that lower early life SES individuals with a history of child-
hood trauma would exhibit blunted ABP stress responses
when compared to low early life SES individuals without
a trauma history and that low SES individuals with no his-
tory of childhood trauma would show exaggerated responses
relative to those of high early life SES and those without a
trauma history.
Methods
Participants
Participants were drawn from the Study of Health and Inter-
actions in the Natural Environment (SHINE). This study
recruited 391 healthy adults aged 40 to 65 from the Pitts-
burgh area between 2014 and 2018. Exclusionary criteria
included a history of cardiovascular disease, schizophrenia
or bipolar disease, chronic hepatitis, renal failure, neuro-
logical disorder, lung disease requiring drug treatment, or
stage 2 hypertension, use of insulin, glucocorticoid, antiar-
rhythmic, antihypertensive, lipid-lowering, psychotropic,
autonomically active, or prescription weight loss medica-
tions, and current pregnancy. The study was approved by
the University of Pittsburgh Institutional Review Board.
All participants were administered informed consent before
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804
enrollment and were compensated between $350 and $400
for their participation.
From the original sample of 391, 8 individuals were
removed due to missing trauma history data, 5 for incom-
plete parental education data, and 1 for having less than
two ABP observations. The final analytic sample was
composed of 377 healthy adults. The final analytical sam-
ple was 62% female and 20% BIPOC. Participants were,
on average, middle-aged (Mage = 52.59 ± 7.16), overweight
(MBMI = 28.0 ± 5.37), and well-educated (64% had received
at least a bachelor’s degree).
Procedure
Individuals completed a total of four laboratory visits, each
lasting 3–4 h. In visit 1, participants provided demographic
information and verified their study eligibility. At visit 2,
participants completed questionnaires not relevant to this
study. At visit 3, participants were trained to participate in
ambulatory monitoring procedures. All participants were
instructed on use of several devices including an automated
blood pressure cuff (Oscar 2 oscillometric monitor, Suntech
Medical Inc, Morrisville, NC) and an electronic diary. Train-
ing visits lasted approximately 4 h and participants demon-
strated device comprehension prior to use in daily life. The
participants then completed a 7–10-day EMA protocol. Four
of these days constituted “full monitoring” days in which
participants responded to hourly surveys and obtained hourly
blood pressure readings. On the “partial monitoring” days,
participants responded to morning and evening question-
naires. Participants then returned to the laboratory for visit
4, where they completed questionnaires including the Child-
hood Trauma Questionnaire.
Measures
Socioeconomic Status Participants completed a self-report
demographic questionnaire which probed their parents’ edu-
cation levels, current household income, and current educa-
tion level. Parental education was separately assessed for
each individual’s mother and father, and was scored on a
12-point scale ranging from 1 = less than eighth grade to
12 = MD, PhD, JD, PharmD. Early life SES was conceptual-
ized as the highest level of education level achieved by the
most-educated parent. This metric is more easily recalled
than other childhood SES measures (e.g., parental income)
and is recommended for use in retrospective studies with
adult samples [35]. While parental education represents
only one marker of early life socioeconomic disadvantage,
it predicts adult health outcomes above and beyond adult
education levels [36] and explains unique variance in adult
health outcomes controlling for family income [37]. Based
on reports of parental education, individuals were divided
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International Journal of Behavioral Medicine (2023) 30:801–813
into three dummy-coded early life SES groups: low (high
school degree or less), middle (some college experience
but no 4-year degree), and high (at least a college degree).
A categorical classification strategy was selected to allow
for non-equivalent differences between education groups
and the potential for non-linear associations between early
life SES and cardiovascular reactivity. Three groups were
selected a priori based on examination of sample size dis-
tributions. Thirty-four percent of the sample grew up in a
“low SES” household, 29% in a “middle SES” household,
and 37% in a “high SES” household.
Childhood Trauma During visit 4, participants completed
the Childhood Trauma Questionnaire-Short Form (CTQ) to
retrospectively assess the presence and severity of childhood
trauma [26]. An example question is “People in my family
hit me so hard that it left me with bruises or marks,” rated on
a Likert scale from 1 (never) to 5 (very often true). The scale
provides five subscores: physical abuse, emotional abuse,
sexual abuse, emotional neglect, and physical neglect. The
five CTQ trauma exposure types have been found to have
good criterion-related validity [33]. In this study, clinical
cut points as introduced by Walker et al. (1998) were used to
designate the presence of each trauma exposure as follows:
physical abuse ≥ 8, emotional abuse ≥ 10, sexual abuse ≥ 8,
emotional neglect ≥ 15, physical neglect ≥ 8 [38]. Presence
of childhood trauma was scored dichotomously, where child-
hood trauma exposure was endorsed when a participant
scored at or above clinical threshold on any one subscale
and absence of childhood trauma exposure occurred when
participants scored below all clinical thresholds. These cut
points have been previously used in middle-aged samples
similar to ours [39, 40].
Ambulatory Blood Pressure Ambulatory blood pressure
(ABP) was assessed at consistent, hourly intervals across
the waking period of each monitoring day. Both systolic
(SBP) and diastolic (DBP) readings were gathered. In
accordance with the SunTech Oscar 2 user manual, ABP
readings associated with an error code (e.g., leaky cuff, low
battery) were deleted prior to analyses. In accordance with
criteria put forth by Marler, Jacob, Lehoczky, and Shap-
iro (1988), ABP readings were removed as invalid when-
ever SBP < 70 mmHg or > 250 mmHg, DBP < 45 mmHg
or > 150 mmHg, or SBP/DBP < [1.065 + (0.00125 × DBP)]
or > 3 [41].
Daily Life Stressors After each ABP measurement, partici-
pants completed an ambulatory interview on an electronic
diary. The diary presented between 49 and 58 multiple
choice questions regarding recent stressors and social inter-
actions. Using these diary questions, two types of life stress-
ors were measured: task strain and social conflict.
International Journal of Behavioral Medicine (2023) 30:801–813
Task Strain On each interview, participants were asked to
“think about mental and physical activity in the past 10 min,”
then to indicate the degree of psychological demand asso-
ciated with this activity (i.e., “working hard?”, “working
fast?”, juggling “several tasks at once?”), and the relative
control associated with the activity (i.e., “felt in command,”
“handled [themselves] well?”). Of note, this measure of con-
trol is distinct from and more general than the measure of
decision latitude previously used in our laboratory [32, 42].
Items were scored on a 1–10 Likert scale. Situations rated
above the sample median in demand and below or equal to
the sample median in control were coded “1” as instances
of task strain. All other situations (those low in demand and
those high in control) were coded “0” as instances absent of
“task strain.”
Social Conflict Participants documented their most recent
social interaction, and whether that interaction was marked
by conflict (“someone was insensitive to you,” “someone
interfered with your efforts,” and “someone made you
tense”). These three items were designed to capture both
obvious and subtle instances of social conflict, and were
scored on a 10-point Likert scale. Only interactions which
occurred within the 10 min preceding ABP readings were
included in the analyses. Social conflict was operationalized
as the mean of the items. This calculation of a continuous
social conflict score is consistent with prior work out of our
laboratory [33].
Covariates
Time‑Dependent Covariates In the hourly interview, par-
ticipants reported their current posture (standing, sitting, or
lying down), temperature comfort (comfortable, too hot, or
too cold), speaking status (speaking or not speaking), self-
report physical activity (limited, light, moderate, or vigor-
ous), and recent consumption of food, alcohol, or caffeine
(yes or no). Participants used the electronic diary to report
each time they smoked a cigarette or other nicotine exposure.
Timestamped self-reports of smoking that occurred within
10 min of a ABP measurement were marked (cigarette used
or no cigarette used). These variables have previously been
associated with acute ABP changes [36], and were included
as covariates in the analyses involving stress-related changes
in ABP.
Between‑Subject Covariates In addition to the momentary
covariates, self-reported race, sex, age, and body mass index
(BMI) were included as between-person covariates. Race,
sex, and age were assessed in the demographic questionnaire
obtained in visit 1. BMI was calculated using measurements
of height and weight collected by trained research staff at
visit 1. Race (black, indigenous, people of color (BIPOC)
805
vs white) and sex (male vs female) were dichotomized. Age
and BMI were added as continuous variables.
Plan of Analysis
Analyses were performed utilizing R Statistical Software
[43]. Separate one-way ANOVA and χ2 analyses were used
to test differences between high, middle, and low early life
SES groups for demographic characteristics. Multilevel
modeling (MLM) procedures were used to test the study
hypotheses. MLM corrects for nested data structures, repre-
sents within-person changes over multiple time points, and
models how individuals differ in these changes. All analy-
ses were run using the “nlme” statistical package for linear
and nonlinear mixed effects models [44] in R software 3.5.1.
using log-likelihood methods, or “ML,” for estimating fixed
and random effects simultaneously. All models were run
with a continuous AR1 autocorrelation structure that cor-
rects for correlated error between adjacent timepoints. As
recommended by the multivariate literature, task strain and
social conflict were both person-centered prior to analy-
ses [45]. This process created two variables for each stress
measure: within-person measures of stress added at level 1,
and between-person measures of stress added at level 2. All
independent variables, including covariates, were centered
on within-person means (level-1 variables) or on between-
person means (level-2 variables) prior to statistical modeling.
Analyses were performed separately for each measure of
stress and each blood pressure outcome, such that a total
of four models were fit to assess the impact of early life
SES and childhood trauma on SBP reactivity to task strain,
DBP reactivity to task strain, SBP reactivity to social con-
flict, and DBP reactivity to social conflict. For each of the
aforementioned models, analyses followed five hierarchical
steps. First, unconditional multilevel models predicting ABP
by participants were estimated to inspect the variance in
ABP accounted for by within and between-person differ-
ences. In step two, time-varying covariates were added as
fixed effects and fixed and random effects of person-centered
stress (either task strain or social conflict) were added to
test the acute effect of stress on ABP and whether these
associations vary between people. In step three, all level-2
predictors and covariates were added as main effects, and
early life SES and childhood trauma were added as cross-
level interactions to assess the effects of early life SES and
childhood trauma on ABP reactivity. In step four, two-way
interactions between early life SES and childhood trauma on
ABP were added as fixed effects in order to provide a com-
parison to test significance for a fifth model step. In step five,
the three-way cross-level interaction terms between early
life SES, childhood trauma, and the within-person effect of
stress were added. The fully identified (step five) models are
depicted in Electronic Supplementary Materials 1.
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806 International Journal of Behavioral Medicine (2023) 30:801–813

Model comparisons occurred between each step using
likelihood ratio tests (L.ratio). The results of the third and
fifth steps were interpreted to test the study hypotheses.
In models where the 3-way interaction terms significantly
increased variance explained (significant L.ratio between
steps 4 and 5), simple slopes were investigated by re-cen-
tering the reference groups for early life SES and childhood
trauma and examining the relevant 2-way interactions [46].
Planned Exploratory Analyses For models in which a
significant three-way interaction appeared, exploratory
analyses examined whether types of childhood trauma
interact differently with early life SES to predict CVR.
McLaughlin, Sheridan, and Lambert suggest that threat
(e.g., abuse experiences) and deprivation (e.g., neglect
experiences) may represent distinct dimensions of early
life trauma and differentially impact downstream physiol-
ogy [47]. Based off their theory, childhood trauma was
divided into four distinct groups: history of abuse only,
history of neglect only, history of both abuse and neglect,
or no trauma history. Exploratory analysis involved fitting
an MLM almost equivalent to that of the analogous step 5.
Sensitivity Analyses Controlling for Adult SES To evaluate
whether any observed associations between early life SES,
childhood trauma, and CVR persist after controlling for
adult SES, we repeated the main analyses controlling for
adult education (dummy coded into HS degree or less, some
college, college degree, and advanced degree) and income
level.
Results
Table 1 provides descriptive characteristics of the final ana-
lytic sample. Overall, the sample was 62% female and 20%
BIPOC. Sixty-four percent had received at least a bachelor’s
degree and, in total, 42% of the sample reported exposure to
childhood trauma. Rates of childhood trauma endorsed in the
present sample align with previous reports using the CTQ
and Walker et al.’s (1998) cutoffs in similar middle-aged
samples, which range from 38 to 48% exposure to any child-
hood trauma [39, 40]. There were no significant differences
in trauma history, biological sex, or adult income between
the three early life SES groups. There was a significant dif-
ference in age (F(2,374) = 3.05, p = 0.049), where the middle
SES group was marginally younger than the low and high
SES groups; a significant difference in adult educational
obtainment (F(2,371) = 13.29, p < 0.001), where the low and
middle early life SES groups had less adult education than
the high SES group; a significant difference in race (χ2 (2,
N = 377) = 9.82, p = 0.007), where the middle SES group had

Table 1  Descriptive characteristics by early life SES (mean ± standard deviation or %)

Variable Low SES (n = 128) Middle SES (n = 108) High SES (n = 141) Total sample (n = 377)

Age* 53.85 ± 6.75 51.85 ± 7.45 52.01 ± 7.19 52.59 ± 7.16

Sex (female) 66% 62% 57% 62%
Race*
White 80% 70% 87% 80%
Black 18% 30% 10% 18%
Asian 2% 2% 4% 3%
American Indian 1% 1% 0% 1%
Childhood trauma
No history 63% 51% 60% 58%
Abuse only 11% 19% 14% 15%
Neglect only 8% 6% 7% 7%
Abuse and neglect 19% 24% 18% 20%
(Adult) education*
High school 9% 6% 4% 6%
Some college 42% 31% 18% 30%
College degree 28% 32% 36% 32%
Advanced degree 21% 31% 42% 32%
(Adult) income 7.83 ± 3.89 7.33 ± 3.49 8.50 ± 4.02 7.94 ± 3.85
Body mass index* 28.3 ± 6.15 28.8 ± 5.09 27.1 ± 4.68 28.0 ± 5.37

An adult household income score of 7 corresponds with $65,000–79,999/year, a score of 8 corresponds with $80,000–94,999/year, and a score
of 9 corresponds with $95,000–109,999/year. Participants were allowed to select multiple racial identities. An * depicts significant (p < .05)
overall difference between low, middle, and high SES groups

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International Journal of Behavioral Medicine (2023) 30:801–813
a higher proportion of BIPOC than the low and high SES
groups; and a significant difference in BMI (F(2,373) = 3.59,
p = 0.029), where the middle early life SES group had a
larger average BMI than the high early life SES group.
Individuals completed an average of 46 ambulatory
measurements over the course of the 4 days (range: 9–67).
On average, 27 of these occurred within 10 min of a social
interaction (range: 2–57), judged to be the average duration
over which social interaction effects on ABP might persist.
In total, task strain analyses included 17,263 observations,
and social conflict analyses included 10,017 observations.
In-depth output for the hypothesis-testing model steps (steps
3 and 5) is depicted in Tables 2 and 3. Relevant parameters
for steps 1 through 5 are provided in-text. Full output for all
steps can be viewed on our OSF page at osf.io/2y376/.
SBP Response to Task Strain The unconditional model dem-
onstrated that 60.0% of the variance in SBP occurs at the
between-person level. Step two indicated significant influence
of momentary factors on SBP (L.ratio = 1116.46, p < 0.001).
A significant fixed effect of within-person task strain emerged
such that, after controlling for time-varying covariates, pres-
ence of task strain associated with a 1.30 mmHg increase in
SBP, on average (𝛾10 = 1.30, 95% CI: [0.72, 1.89]). There
was also a significant random effect of task strain on SBP
(τ11 = 3.04, 95% CI: [1.14, 8.11]), indicating that people vary in
SBP response to task strain. The addition of level-2 covariates
and two-way cross level interactions in step three explained
additional variance (L.ratio = 114.28, p < 0.001). However,
no significant interaction effects emerged between childhood
SES and task strain reactivity (𝛾11 = 0.62, 95% CI: [−0.87,
2.10]; 𝛾12 = 1.28, 95% CI: [−0.07, 2.63]) or childhood trauma
and task strain reactivity (𝛾13 =−0.91, 95% CI: [−2.07, 0.25]).
Three-way interactions were added to the model in step five
and compared to step four. No overall three-way interaction
emerged (L.ratio = 1.83, p = 0.40).
DBP Response to Task Strain The unconditional model
demonstrated that 53.9% of the variance in DBP occurs
at the between-person level. Step 2 indicated significant
influence of momentary factors on DBP (L.ratio = 1633.92,
p < 0.001). A significant fixed effect of within-person task
strain emerged such that, after controlling for time-varying
covariates, a 1-point increase in task strain was associated
with a 0.84-mmHg increase in DBP, on average (𝛾10 = 0.84,
95% CI: [0.41, 1.27]). Likewise, there was a significant
random effect of task strain on DBP (τ11 = 2.93, 95% CI:
[1.56, 5.49]). The addition of level-2 covariates and two-
way cross-level interactions in step three increased vari-
ance explained (L.ratio = 85.96, p < 0.001). However, no
cross-level interactions emerged between early life SES and
within-person task strain (𝛾11 = 0.26, 95% CI: [−0.84, 1.37];
𝛾12 = 0.29, 95% CI: [−0.72, 1.31]) or between childhood
807
trauma and within-person task strain ( 𝛾13 =−0.51, 95%
CI: [−1.38, 0.35]). There was no increase in variance
explained when three-way interactions were added in step
five (L.ratio = 0.30, p = 0.86).
SBP Response to Social Conflict The unconditional model
demonstrated that 59.6% of the variance in SBP occurs
at the between-person level. The second step of mod-
eling explained a significant increase in SBP variance
(L.ratio = 513.90, p < 0.001). A significant fixed effect of
within-person social conflict emerged such that, after con-
trolling for time-varying covariates, a 1-point increase in
social conflict associated with a 0.44-mmHg increase in
SBP, on average (𝛾10 = 0.44, 95% CI: [0.24, 0.64]). A sig-
nificant random effect of social conflict on SBP (τ11 = 0.46,
95% CI: [0.14,1.52]) indicated that individuals vary in their
relationship between social conflict and SBP. The addition
of level-2 covariates and two-way cross-level interactions
in step three significantly increased variance explained
(L.ratio = 104.96, p < 0.001). However, no cross-level inter-
actions emerged between early life SES and within-person
social strain (𝛾11 = 0.40, 95% CI: [−0.09, 0.89]; 𝛾12 =−0.20,
95% CI: [−0.65, 0.26], respectively) or between child-
hood trauma and within-person social strain ( 𝛾13 =−0.07,
95% CI: [−0.47, 0.32]). There was no increase in variance
explained when three-way interactions were added in step
five (L.ratio = 0.14, p = 0.93).
DBP Response to Social Conflict The unconditional model
demonstrated that 54.1% of the variance in DBP occurs
at the between-person level. The second step of mod-
eling explained a significant increase in DBP variance
(L.ratio = 752.96, p < 0.001). A significant fixed effect of
within-person social conflict emerged such that, after con-
trolling for time-varying covariates, a 1-point increase in
social conflict associated with a 0.25-mmHg increase in
DBP, on average (𝛾10 = 0.25, 95% CI: [0.11, 0.39]). A sig-
nificant random effect of social conflict on DBP (τ11 = 0.21,
95% CI: [0.08,0.61]) indicated that individuals vary in their
relationship between social conflict and DBP. The addition
of level-2 covariates and two-way cross-level interactions
in step three significantly increased variance explained
(L.ratio = 84.94, p < 0.001). However, no significant inter-
actions emerged between early life SES and within-person
social strain (𝛾11 = 0.23, 95% CI: [−0.12, 0.57]; 𝛾12 = 0.03,
95% CI: [−0.30, 0.35], respectively) or between childhood
trauma and within-person social strain (𝛾13 =−0.18, 95% CI:
[−0.46, 0.10]). The addition of three-way interactions in step
five caused a significant increase in variance explained, indi-
cating a significant three-way interaction between early life
SES, childhood trauma, and DBP response to social conflict
(L.ratio = 6.93, p = 0.031; see Fig. 1). The model showed,
specifically, a three-way interaction term between childhood
13
808 International Journal of Behavioral Medicine (2023) 30:801–813

Table 2  Early life SES, childhood trauma, and blood pressure reactivity to task strain
SBP DBP
Step 3 Step 5 Step 3 Step 5

Fixed effects
Intercept,𝛾00 135.4 (1.66)*** 136.5 (1.88)*** 80.44 (1.08)*** 81.33 (1.18)***
Level-1 variables
Posture standing,𝛾20 3.39 (0.25)*** 3.40 (0.25)*** 3.33 (0.17)*** 3.33 (0.17)***
Posture laying,𝛾30 −7.30 (0.50)*** −7.29 (0.50)*** −7.64 (0.35)*** −7.64 (0.35)***
Talking,𝛾40 2.11 (0.24)*** 2.11 (0.24)*** 1.91 (0.17)*** 1.91 (0.17)***
Physical activity,𝛾50 2.23 (0.21)*** 2.23 (0.21)*** 1.08 (0.15)*** 1.08 (0.15)***
Recent meal,𝛾60 1.15 (0.24)*** 1.15 (0.24)*** −0.22 (0.17) −0.23 (0.17)
Caffeine,𝛾70 0.05 (0.30) 0.05 (0.30) −0.02 (0.21) −0.02 (0.21)
Temperature hot,𝛾80 1.05 (0.49)* 1.04 (0.49)* 0.15 (0.34) 0.15 (0.34)
Temperature cold,𝛾90 3.15 (0.53)*** 3.16 (0.53)*** 1.33 (0.37)*** 1.33 (0.37)***
Alcohol,𝛾100 −0.33 (0.61) −0.34 (0.61) −0.51 (0.42) −0.51 (0.42)
Smoking status,𝛾110 −0.06 (0.69) −0.06 (0.69) 0.14 (0.48) 0.14 (0.48)
Task strain,𝛾10 0.98 (0.56)† 1.39 (0.64)* 0.86 (0.42)* 0.87 (0.48)†
Level-2 variables
Child ­SESmiddle,𝛾01 −0.01 (2.00) −0.97 (2.67) −0.41 (1.25) −1.06 (1.67)
Child ­SEShigh,𝛾02 1.29 (1.88) −0.63 (2.39) 0.63 (1.18) −1.08 (1.48)
Childhood trauma,𝛾03 0.45 (1.60) −2.17 (2.76) −0.36 (1.00) −2.57 (1.73)
Child ­SESmiddle*child trauma,𝛾04 2.62 (4.02) 1.89 (2.52)
­ EShigh*child trauma,𝛾05
Child S 5.01 (3.80) 4.50 (2.38)†
Task strain (person means),𝛾06 6.29 (2.97)* 6.02 (2.97)* 4.88 (1.87)** 4.62 (1.86)**
Race,𝛾07 −6.87 (1.99)*** −6.94 (1.99)*** −5.52 (1.25)*** −5.57 (1.25)***
Age,𝛾08 0.50 (0.11)*** 0.51 (0.11)*** 0.16 (0.07)* 0.16 (0.07)*
Sex,𝛾09 −8.72 (1.61)*** −8.64 (1.62)*** −5.55 (1.02)*** −5.45 (1.02)***
BMI,𝛾010 1.05 (0.15)*** 1.04 (0.15)*** 0.47 (0.09)*** 0.46 (0.09)***
Cross-level interaction variables
Task strain*child ­SESmiddle 𝛾11 0.62 (0.76) −0.08 (0.99) 0.26 (0.57) 0.42 (0.75)
Task strain*child ­SEShigh,𝛾12 1.28 (0.69)† 0.59 (0.86) 0.29 (0.52) 0.19 (0.65)
Task strain*child trauma,𝛾13 −0.91 (0.59) −2.13 (1.10)† −0.51 (0.44) −0.52 (0.82)
Task strain*child ­SESmiddle*child trauma,𝛾14 1.47 (1.54) −0.32 (1.15)
Task strain child ­SEShigh*child trauma,𝛾15 1.90 (1.43) 0.26 (1.07)
Random effects
Intercept,𝜏00 219.60 218.54 86.57 85.74
Task strain slope,𝜏11 2.64 2.36 2.87 2.86
Level 1, Var within person,𝜎 2 184.37 184.42 83.77 83.77
Log-likelihood −69,162.96 −69,161.33 −62,791.57 −62,789.64
L.ratio test (compared to step 2 or 4) 114.28*** 1.83 85.96*** 0.30

Step 3 refers to the model in which level-1 predictors and covariates were added as main effects, and childhood trauma and early life SES were
added as cross-level interactions. Step 5 refers to the model including the three-way cross-level interaction terms between early life SES, child-
hood trauma, and the within-person effect of task strain. An † depicts p < 0.10, an * indicates p < 0.05, an ** indicates p < 0.01, and an *** indi-
cates p < 0.001. All random effects are significantly different from zero

trauma, middle early life SES (compared to low SES), and
the influence of social conflict on DBP (𝛾14 =−0.93, 95% CI:
[−1.62, −0.24], p = 0.008).
Analysis of simple slopes demonstrated significant dif-
ferences in DBP response for individuals from middle early
life SES, where those without a history of childhood trauma
showed significantly greater DBP response than those
with a history of childhood trauma ( 𝛾13 =−0.66, 95% CI:
[−1.17, −0.15]). There were no childhood trauma differences
in DBP response for the individuals from high or low SES
upbringings (𝛾13 =−0.21, 95% CI: [−0.66, 0.24]; 𝛾13 = 0.23,

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International Journal of Behavioral Medicine (2023) 30:801–813 809

Table 3  Full early life SES, childhood trauma, and blood pressure reactivity to social conflict
SBP DBP
Step 3 Step 5 Step 3 Step 5

Fixed effects
Intercept,𝛾00 137.8 (1.69)*** 139.0 (1.91)*** 81.94 (1.06)*** 82.90 (1.20)***
Level-1 variables
Posture standing,𝛾20 3.33 (0.33)*** 3.33 (0.33)*** 3.27 (0.23)*** 3.27 (0.23)***
Posture laying,𝛾30 −7.43 (0.80)*** −7.43 (0.80)*** −7.85 (0.56)*** −7.83 (0.55)***
Talking,𝛾40 1.83 (0.29)*** 1.83 (0.29)*** 1.72 (0.20)*** 1.72 (0.20)***
Physical activity,𝛾50 1.85 (0.29)*** 1.85 (0.29)*** 0.89 (0.20)*** 0.89 (0.20)***
Recent meal,𝛾60 1.16 (0.32)*** 1.16 (0.32)*** −0.11 (0.23) −0.11 (0.23)
Caffeine,𝛾70 −0.23 (0.40) −0.23 (0.40) 0.06 (0.28) 0.06 (0.28)
Temperature hot,𝛾80 1.00 (0.64) 1.00 (0.64) −0.06 (0.44) −0.04 (0.44)
Temperature cold,𝛾90 3.39 (0.75)*** 3.39 (0.75)*** 1.36 (0.52)** 1.37 (0.52)**
Alcohol,𝛾100 0.76 (0.77) 0.77 (0.77) 0.57 (0.52) 0.60 (0.52)
Smoking status,𝛾110 −0.37 (0.95) −0.37 (0.95) 0.02 (0.66) 0.04 (0.66)
Social conflict,𝛾10 0.42 (0.18)* 0.38 (0.21)† 0.25 (0.13)† 0.10 (0.14)
Level-2 variables
Child ­SESmiddle,𝛾01 −0.58 (2.04) −1.85 (2.72) −0.67 (1.28) −1.32 (1.70)
Child ­SEShigh,𝛾02 1.07 (1.91) −0.98 (2.41) 0.58 (1.20) −1.32 (1.51)
Childhood trauma,𝛾03 0.42 (1.64) −2.54 (2.81) −0.43 (1.03) −2.80 (1.76)
Child ­SESmiddle*child trauma,𝛾04 3.31 (4.09) 1.90 (2.65)
Child ­SEShigh*child trauma,𝛾05 5.38 (3.87) 4.95 (2.42)*
Social conflict (person means),𝛾06 0.57 (0.75) 0.50 (0.75) 0.76 (0.47) 0.68 (0.47)
Race,𝛾07 −7.36 (2.01)*** −7.44 (2.01)*** −6.08 (1.04)*** −6.11 (1.27)***
Age,𝛾08 0.51 (0.11)*** 0.52 (0.11)*** 0.18 (0.07)* 0.18 (0.07)**
Sex,𝛾09 −8.03 (1.64)*** −7.96 (1.65)*** −5.46 (1.04)*** −5.34 (1.04)***
BMI,𝛾010 1.07 (0.15)*** 1.06 (0.15)*** 0.49 (0.09)*** 0.49 (0.09)***
Cross-level interaction variables
Social conflict*child S ­ ESmiddle 𝛾11 0.40 (0.25) 0.47 (0.34) 0.23 (0.18) 0.64 (0.23)**
Social conflict*child S ­ EShigh,𝛾12 −0.20 (0.23) −0.15 (0.29) 0.03 (0.16) 0.17 (0.20)
Social conflict*child trauma,𝛾13 −0.07 (0.20) 0.03 (0.34) −0.18 (0.14) 0.23 (0.24)
Social conflict*child S ­ ESmiddle*child trauma,𝛾14 −0.17 (0.51) −0.93 (0.35)**
Social conflict*child ­SEShigh*child trauma,𝛾15 −0.15 (0.48) −0.39 (0.33)
Random effects
Intercept,𝜏00 221.99 220.86 87.38 86.44
Social conflict slope,𝜏11 0.39 0.38 0.21 0.18
Level 1, Var within person,𝜎 2 188.21 188.23 85.08 85.08
Log-likelihood −40,550.17 −40,549.05 −36,785.98 −36,780.32
L.ratio test (compared to step 4) 104.98*** 0.14 84.94*** 6.93*

Step 3 refers to the model in which level-1 predictors and covariates were added as main effects, and childhood trauma and early life SES were
added as cross-level interactions. Step 5 refers to the model including three-way cross-level interaction terms between early life SES, childhood
trauma, and the within-person effect of social conflict. An † depicts p < 0.10, an * indicates p < 0.05, an ** indicates p < 0.01, and an *** indi-
cates p < 0.001. All random effects are significantly different from zero

95% CI: [−0.23, 0.69], respectively). For individuals without
a history of childhood trauma, those from a middle early life
SES showed higher DBP response than those from a low
early life SES (𝛾11= 0.61, 95% CI: [0.15, 1.06]) and margin-
ally higher response than those from a high early life SES
(𝛾 = −0.40, 95% CI: [−0.85, 0.06]). Among the individuals
exposed to childhood trauma, there were no significant SES-
driven differences in DBP response.
Exploratory Analyses Since the middle SES group had a
greater proportion of BIPOC than the other two SES groups
(see Table 1), an exploratory analysis was run where race

13
810
Fig. 1  DBP reactivity to social
conflict
was substituted in for early life SES in the fully identified
model to explore the interaction between race, childhood
trauma, and DBP reactivity to social conflict. No signifi-
cant interaction emerged (𝛾 = 0.12, 95% CI: [−0.60, 0.84],
p = 0.74), suggesting that the observed effect of early life
SES and childhood trauma on DBP response to social strain
is not driven by racial differences. However, it should be
noted that this analysis may have been underpowered to
detect small interaction effects.
An additional exploratory analysis probed the heterogene-
ity within the middle early life SES group, which was com-
prised of parents who had completed technical degrees and
those who had initiated but not completed college. The latter
may be indicative of contexts (e.g., mental health struggles,
unexpected life events, earlier age of childbirth), which may
uniquely impact early life environments. The fully identified
model investigating DBP response to social conflict was re-
run with middle early life SES separated into the two afore-
mentioned sub-categories. The model demonstrated similar
three-way interactions for both middle SES groups, although
the latter did not reach statistical significance (𝛾 = −1.01,
p = 0.011; 𝛾 = −0.94, p = 0.068, respectively).
As initially proposed, the model for which a three-way
interaction emerged between early life SES, childhood
trauma, and DBP response to social conflict was broken
down by type of childhood trauma (neglect only, abuse only,
both neglect and abuse, and none). No significant independ-
ent three-way interaction terms emerged between any trauma
group, social conflict, and middle SES.
Sensitivity Analysis Controlling for Adult SES The inclusion
of adult education and income as covariates did not alter
13
International Journal of Behavioral Medicine (2023) 30:801–813
our interpretation of the results (see Electronic Supplemen-
tary Materials 2 and 3). There were no main effects of early
life SES or childhood trauma on ABP response to social
conflict or task strain. As before, an interaction emerged
between early life SES, childhood trauma, and DBP response
to social conflict (L.ratio = 6.46, p = 0.039).
Discussion
The present study examined the impact of early life SES
and childhood trauma on cardiovascular response to daily
life social conflict and task strain in healthy mid-life adults.
Results are in line with expectations and previous literature
demonstrating no effect of early life SES on cardiovascu-
lar reactivity [18–20], but differ from other studies which
demonstrate both inverse and positive associations between
early life SES and cardiovascular reactivity [11–17]. A
recent meta-analysis probing the relationship between gen-
eral SES (whether that be adult or child) and cardiovascular
reactivity does not show clear evidence that SES is related
to laboratory measures of reactivity, although the relation-
ship between SES and cardiovascular reactivity may vary by
stressor type and high SES may be linked with faster recov-
ery to laboratory stress [48]. The present study differed from
the majority of previous work [23] in that we found no main
effects of childhood trauma on cardiovascular response to
stress in daily life. Rather, results provide little evidence that
exposures to childhood trauma may interact with early life
SES to predict stress responsivity. The observed interactions,
however, were inconsistent and not aligned with predictions.
The present study observed an interaction effect between
childhood trauma and early life SES in only one out of the
International Journal of Behavioral Medicine (2023) 30:801–813
four domains tested. In the models investigating cardiovas-
cular response to social conflict, the middle childhood SES
group who had not experienced childhood trauma showed
greater diastolic blood pressure response than their lower
and higher early life SES peers (Fig. 1). Likewise, among the
middle SES individuals, those with a history of childhood
trauma showed significantly lower DBP reactivity to social
conflict than those without a history of childhood trauma.
No significant interactions appeared when investigating SBP
response to social conflict. Unlike the measure of social con-
flict, neither model investigating ABP response to task strain
demonstrated a significant three-way interaction between
childhood trauma, early life SES, and task strain response.
The fact that the interaction effect was most pronounced in
the middle SES group departs from expectations derived from
the adaptive calibration model. We had predicted that the low
early life SES group would show marked trauma-dependent
disparities in reactivity, rather than the middle early life SES
group. The unexpected observed findings are not explained
by either race differences between early life SES groups or
heterogeneity within the middle SES group. A recent p-curve
meta-analysis conducted by Hosseini-Kamkar et al. may help
interpret these results [49]. Researchers found evidence for
an inverted U-shaped relationship between severity of adver-
sity and cortisol stress reactivity, where exposure to trauma
was related to blunted reactivity while low/medium adversity
was inconsistently related to hyper-reactivity. It may be that
growing up in a “middle” SES home without experiences of
trauma prompts hyper-reactivity to stress, while growing up in
a “middle” SES home with trauma exposure prompts blunted
reactivity. This possibility, however, is speculative. Overall,
it is not clear what characteristics of this group made them
apparently more vulnerable to the effects of early childhood
trauma in terms of its association with stress reactivity. Future
research may need to incorporate additional and more sensitive
measures of early life SES (e.g., measures of income as well
as education) in order to better characterize the early socioeco-
nomic situation. SES indicators represent unique concepts and
predict independent variance in health outcomes [35].
Likewise, relationships between childhood socioeco-
nomic disadvantage and trauma and cardiovascular reactiv-
ity in the present study differ slightly by the type of daily
life stressor encountered, with some effects present for
responses involving social conflict. It may be that sensitiv-
ity to naturalistic social stressors is influenced by the early
life environment, while sensitivity to nonsocial, or task,
stressors is not. Some evidence suggests that individuals
who perceive themselves to be of lower social standing show
greater neural activity in the face of negative social evalu-
ation than their peers of higher social standing [50], and
are more likely to perceive social threat during ambiguous
social situations [11]. It may be that individuals from a lower
SES background place greater emphasis on social resources
811
due to decreased availability of physical resources [51], thus
prompting greater reactivity to social conflict.
Contrary to much of the prior work done in a laboratory
setting, the present study did not observe an overall effect of
childhood trauma on cardiovascular response to daily stress. To
our knowledge, the present study is the second empirical work
to investigate the link between childhood trauma and ambula-
tory cardiovascular responses to daily stress. The first, which
investigated the impact of childhood bereavement on SBP
response to daily life stress over the course of 24 h, likewise
observed no differences in cardiovascular response by childhood
bereavement, a type of early life adversity [22]. It may be that
the “blunting” effect of early life adversity only manifests when
measuring cardiovascular reactivity to acute laboratory stress,
and not in relation to daily life stress in the natural environment.
Daily life stressors differ from those manipulated in a labora-
tory setting. Laboratory stress paradigms require participants
to perform relatively atypical tasks, such the preparation and
delivery of a speech or the public performance of mathematical
operations [52]. Daily life stressors, on the other hand, often
involve routine or more familiar tasks and commonly take place
with known individuals, such as coworkers, family, or spouses.
These daily life stressors may be deemed as less foreign, and
thus less threatening than those manufactured in the laboratory.
In line with the ACM, it may be that individuals reared in trau-
matic environments develop blunted physiological reactions to
foreign/atypical stressors (such as those in laboratory settings)
but not to daily hassles, more predictable, or previously encoun-
tered stressors. Our understanding of the relationships between
adverse childhood experiences and physiological reactivity
would be strengthened by further investigation of various types
and domains of stressors.
The present study has several strengths worth mentioning.
First, as the first investigation to synthesize the literatures link-
ing childhood trauma and SES to cardiovascular reactivity,
results provide a practical test of the adaptive calibration model
as it applies to early life social contextual factors and socioeco-
nomic disadvantage. Likewise, the present study investigated
cardiovascular response to two common stressors: social and
task strain, allowing us to compare effects across two different
stressor domains. Additionally, the present analysis utilized an
EMA design to investigate stress reactivity in the natural envi-
ronment. This momentary assessment of stress provided for
more frequent and real-time depictions of daily life experiences
than global self-report assessments, and the assessment of stress
reactivity in a manner potentially more equivalent across the
SES gradient.
Despite the strengths of the present study design, key limita-
tions are worth noting. First, the present work utilized parental
education to measure early life SES. Future work should incor-
porate additional indicators of early life SES such as family
income or wealth, to better characterize socioeconomic cir-
cumstances in childhood. Likewise, the present study grouped
13
812
individuals whose parents had college degrees and those with
advanced degrees into one “high” early life SES group due
to sample size constraints. There may be differences between
these two groups that could impact their association with car-
diovascular stress responding. This may be a domain for future
exploration. Second, although inclusion of two distinct domains
of stress (task strain and social conflict) is a key strength of
the study, not all domains of daily stress are captured by these
indices. Third, given the complexity of the models, the present
analyses may have been underpowered to detect small interac-
tion effects. Fourth, the present study recruited a sample of
healthy, middle-aged adults who were higher SES than the
national average and primarily white. These factors limit the
generalizability of the study and contribute to a body of lit-
erature normed on white individuals. While use of EMA is a
key strength of the study, we lack comparable laboratory meas-
ures of stress reactivity. Although we have previously shown
moderate links between blood pressure responses to laboratory
stressors and ambulatory measures of the type used here [53],
it is unknown whether SES and trauma associations with stress
reactivity in natural settings differ from those in the laboratory.
Overall, the present work integrates literatures on early
life SES and childhood trauma with respect to their joint
influence on physiological reactivity. Neither early life SES
nor childhood trauma independently predicted cardiovascu-
lar responses to daily life stress. Likewise, across most of the
measures in this study, we could not confirm that childhood
SES and trauma interact to predict cardiovascular reactivity
in adulthood. Although not consistent with our predictions,
some of the findings here point to the possibility that social
contextual factors may moderate effects of early life SES
on stress response systems. Future research should continue
to explore the nature of economic and social influences in
childhood that trigger changes in stress responding, how
stress responding differs by type of stressor and environ-
ment in which stressors occur (i.e., laboratory or daily life),
and the development of these effects across the life span.
Supplementary Information The online version contains supplemen-
tary material available at https://d​ oi.o​ rg/1​ 0.1​ 007/s​ 12529-0​ 22-1​ 0141-2.
Acknowledgements We would like to express our gratitude to the par-
ticipants who committed their time and shared their daily life experiences
with us over the course of this study. We would also like to acknowledge
Dr. Barbara Anderson for her contribution to data collection.
Funding This research is funded by the Heart Lung and Blood Institute
(4T32HL007560) and the National Institutes of Aging (AG041778).
Declarations
Ethnical Approval All procedures performed in studies involving
human participants were in accordance with the ethical standards of
the institutional and/or national research committee and with the 1964
Helsinki declaration and its later amendments or comparable ethical
standards.
13
International Journal of Behavioral Medicine (2023) 30:801–813
Informed Consent Informed consent was obtained from all individual
participants included in the study.
Conflict of Interest The authors declare no competing interests.
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