In particular, exposure to high levels of childhood adversity is linked to reduced cardiovascular acute stress reactivity , but its relationship with acute stress recovery is less well-investigated. Moreover, while processes by which stress “gets under the skin” and contribute to disease development are unlikely to occur during only one developmental period, studies have not yet considered the joint roles of childhood and adulthood stressors on cardiovascular acute stress response. Evaluating relations between stressor exposure and health-relevant biological processes at multiple times in the life course may provide insight into whether and how developmental timing affects the stress-health association. As not all stressful exposures are avoidable, identifying modifiable, positive psychosocial resources that limit the effects of stress on pathophysiological processes may inform interventions targeting downstream diseases. Meta-analytic studies have linked lower cardiovascular acute stress reactivity and slower recovery to higher levels of psychosocial stressor exposure and subsequent cardiovascular health . Growing evidence further supports an association of childhood adversity with lower acute stress reactivity as assessed by cardiovascular and cortisol markers . In a prospective study, higher early adversity levels were associated with reduced BP acute stress reactivity at age 32,snap clamps ABS pvc pipe clip which in turn was linked to worse self-rated health and higher inflammation levels at age 45.
These findings were replicated in a cross-sectional adult sample . Across studies, effect sizes of psychosocial adversity tend to be larger for BP than HR, and fewer studies consider acute stress recovery than reactivity as an outcome. Despite common references to the acute stress response as being “exaggerated” or “blunted,” no clinical threshold or normative data underlie such classifications; rather, they are based on within-study comparisons of individual responses, resulting in limited cross-study generalizability. Nonetheless, individual differences in cardiovascular reactivity consistently predict health outcomes across diverse populations . Closely related to BP is baroreflex sensitivity , an understudied hemodynamic marker that may be sensitive to the effects of psychosocial stressors and predicts cardiovascular health . Upon detecting BP changes, arterial baroreceptors maintain BP homeostasis by altering inter beat intervals . Baroreflex inhibition during stress may be adaptive given it seems to enhance biological readiness for the challenge, facilitate task engagement, and filter environmental distraction . Initial evidence links lower resting BRS to chronic stress , post-traumatic stress disorder , and anxiety , but whether higher psychosocial stressor exposure influences BRS acute stress response is unknown. Given findings suggesting acute stress response in BP versus HR is more closely related to both psychosocial stressors and future cardiovascular health, and initial evidence hinting at connections between chronic stressor exposure and BRS, in this study we examined hemodynamic acute stress response in relation to psychosocial stressors. Positive psychosocial resources, such as optimism, are associated with salubrious health outcomes and may mediate or moderate associations between psychosocial stressor exposure and health.
Rigorous epidemiologic evidence has prospectively linked optimism to reduced risk of cardiovascular events , even after adjusting for psychological distress. Cardiovascular acute stress response may be one mechanism underlying cardioprotective effects of optimism, but findings on associations of optimism with cardiovascular acute stress reactivity and recovery are inconclusive . A key limitation is the predominant use of small undergraduate samples, which limits the generalizability of findings to middle-aged and older populations. Optimism may have “stress-buffering” properties by serving as a resource bank, or reserve capacity, that dampens the potentially harmful impact of stressors on health . For example, Boylan et al. reported that low childhood socioeconomic status was associated with weaker cardiovascular acute stress recovery only among individuals with lower, but not higher, optimism levels. Alternatively, early adversity may elevate risks for poor health by hindering the accrual of optimism and other health-promoting resources from a young age ; this suggests a mediating rather than moderating role for optimism, although they are not mutually exclusive. Optimism’s role in linkages between early adversity and later cardiovascular health is largely uninvestigated.Allostasis theory posits abnormal patterns of physiological acute stress response as the sequelae of cumulative stressor exposure , yet studies rarely considered if childhood and adulthood stressors synergistically influence hemodynamic acute stress response. Such synergistic effects are commonly evaluated with a cumulative scoring approach that sums total adversity exposure across one’s lifetime . This approach may obscure differing effects in direction or magnitude of childhood versus adulthood stressors. The current study addressed the following questions on the developmental timing of stressor exposure in relation to hemodynamic acute stress response: Does early adversity leave a residue above and beyond the more proximal influence of adulthood stressors? Does early adversity sensitize individuals resulting in stronger effects of adulthood stressors ? Alternatively, are the effects of early adversity and adulthood stressors additive?
Using data from a national adult sample, we evaluated lifespan patterns of childhood and adulthood stressors in relation to hemodynamic acute stress reactivity and recovery, and the role of optimism in the associations. We hypothesized greater childhood adversity exposure would be independently associated with lower hemodynamic acute stress reactivity and slower recovery, beyond any hemodynamic effects of adult stressors. We expected stress buffering by optimism, with greater attenuation of the association of lifespan stressor exposure with acute stress response among more versus less optimistic adults. Given evidence suggesting stressor exposure can erode accrual of psychosocial resources, we also evaluated the indirect association from life course stressor exposure via optimism to acute stress response. Our study used data from the same parent study described in two recent reports examining related questions. Bourassa et al. considered linkages among early adversity , BP and HR acute stress reactivity, and health-related outcomes. Keogh et al. tested depression as a mediator of the association between childhood abuse and neglect and cardiovascular acute stress reactivity. Our study extends prior work by: broadening the conceptualization of childhood stressors to include negative life events beyond abuse, neglect, and SES; testing synergistic effects of childhood and adulthood stressor exposure; considering acute stress recovery as well as reactivity; adding BRS as a novel marker of acute stress response; and testing the role of optimism in the association between lifespan stressor exposure and adulthood acute stress response.Hemodynamic acute stress response was operationalized as reactivity and recovery scores for SBP, DBP, and BRS from the psychophysiology protocol. A healthy pattern of acute stress response is generally characterized by a moderate increase in BP from baseline to stressor presentation, followed by a BP decrease to baseline levels during the recovery period. For BRS, a healthy response involves a decline from baseline to stressor due to stress-related BRS inhibition, followed by an increase during the recovery period signaling an end of the inhibition response. Following standard practice and given no baseline differences in the physiological parameters by stressor exposure categories, we calculated a reactivity score for each physiological parameter in each stressor task by subtracting the parameter value obtained at baseline from the value obtained in the stressor task, and averaging reactivity scores across stressor tasks. Positive reactivity scores represent an increase in the parameter from baseline to the cognitive stressor task periods. Recovery scores for SBP and DBP were calculated by subtracting BP during recovery from BP obtained in the stressor task,greenhouse snap clamps and then averaging recovery scores across stressor tasks. To facilitate interpretation, we calculated the BRS recovery score by subtracting BRS in each stressor period from BRS obtained in the recovery period and then averaging the two scores. Positive BRS recovery scores represent a BRS increase from stressor to recovery, consistent with termination of baroreflex inhibition. In the Biomarker Project, 71% of participants had data on all six hemodynamic acute stress response variables, 12% had data on 4–5 variables, 7% had data on 1–3 variables, and 11% had no data on these variables.All covariates were self-reported and assessed during the MIDUS II interview or survey unless otherwise indicated. They were selected based on their role as potential confounders in the exposure-outcome relations.
Covariates included age at the Biomarker Project visit, sex , race , highest education level , current use of BP-altering medications at the Biomarker Project , and lifetime chronic diseases . Following prior work in this sample , depression status was assessed at the Biomarker Project with the depressive affect sub-scale of the Center for Epidemiologic Studies Depression Scale . Our manipulation check for the psychophysiology protocol considered participant stress ratings “at the moment” on a scale from 1 to 10 during each protocol period.We examined distributions of demographics, health variables, and optimism by lifespan stressor exposure profiles using one-way analysis of variance and χ2 tests. To test hypotheses regarding associations of lifespan stressor exposure with hemodynamic acute stress response, we used ordinary least squares regression with acute stress reactivity and recovery in SBP, DBP, and BRS as outcomes in separate models. We entered the main effects of lifespan stressor exposure categories while considering two levels of covariate of adjustment: Model 1 adjusted for demographics . Model 2 added chronic diseases and BP-altering medications as potential health confounders. To test the stress buffering hypothesis, we added the main effect of optimism and the interaction between optimism and each lifespan stressor exposure profile . Exploratory analyses evaluated the role of optimism in the associations between life course stressor exposure and acute stress response. For each acute stress response outcome, we specified a path model comprising the direct effects of each lifespan stressor exposure profile on the outcome and all indirect effects via optimism. Paths predicting optimism adjusted for demographics and chronic diseases; paths predicting acute stress response variables additionally adjusted for BP-altering medications. Each indirect effect was computed as the product of its component paths . Models used maximum likelihood estimation and missing covariate data were handled using multiple imputations with 30 imputed datasets. We conducted five sets of sensitivity analyses. First, we compared stress ratings during the cognitive stressors to those during the baseline and recovery periods as a manipulation check. Second, we examined intraclass correlations of the acute stress response for evidence of clustering due to twin or sibling status, as defined by ICC . .05. ICCs were 37.4%, 40.3%, 24.5%, 13.2%, ,1%, and ,1% for reactivity and recovery in SBP, DBP, and BRS, respectively. To account for familial clustering in SBP and DBP outcomes, we re-estimated the main effects and interaction of lifespan stressor exposure and optimism using multilevel regression with multiple imputations. Because the multilevel regression results were highly similar to those from main analyses, we report findings without adjustment in the Results section for simplicity. Third, because lifespan stressor exposure was operationalized using binary variables for childhood trauma, cNLEs and aNLEs, and specific cutpoints have not been validated, we ran OLS regression using continuous stressor variables to test the total versus unique effects of childhood and adulthood stressor exposure , and to evaluate the additive versus multiplicative effects of childhood and adulthood stressors. Fourth, in light of ongoing debate regarding the dimensionality of dispositional optimism and evidence suggesting a stronger association of pessimism than optimism with physical health outcomes , we re-estimated the main effects of lifespan stressor exposure and optimism by replacing the LOT-R total score with optimism and pessimism subscale scores . Fifth, given Keogh et al.’s findings suggesting depressive affect mediated the association between early adversity and reduced cardiovascular reactivity , we re-estimated the indirect effects via optimism in the path models while further adjusting for an indirect path via depressive affect.In a large, national sample of middle-aged and older adults, high exposure to psychosocial stressors in childhood was associated with lower BP reactivity and slower recovery from acute stressors, above and beyond the influence of adulthood stressors. Irrespective of childhood adversity exposure, associations of adulthood stressor exposure with BP acute stress response were not evident. Our study provides initial evidence linking persistent stressor exposure across childhood and adulthood to slower BRS recovery. While we found little support for a stress-buffering role of optimism, in exploratory analyses greater lifespan stressor exposure was indirectly linked to lower BP reactivity and slower BP recovery through lower optimism levels. Our findings contribute knowledge on the developmental timing of stressor exposure and on the role of optimism in the association between early adversity and hemodynamic acute stress response. High childhood exposure alone and persistent stressor exposure were both associated with lower reactivity and slower recovery in BP.