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. Author manuscript; available in PMC: 2018 Oct 1.
Published in final edited form as: Biol Psychol. 2017 Sep 14;129:207–230. doi: 10.1016/j.biopsycho.2017.08.058

Psychosocial Functioning and the Cortisol Awakening Response: Meta-analysis, P-curve Analysis, and Evaluation of the Evidential Value in Existing Studies

Ian A Boggero a, Camelia E Hostinar b, Eric A Haak a, Michael L M Murphy c, Suzanne C Segerstrom a
PMCID: PMC5673546  NIHMSID: NIHMS906138  PMID: 28870447

Abstract

Cortisol levels rise immediately after awakening and peak approximately 30-45 minutes thereafter. Psychosocial functioning influences this cortisol awakening response (CAR), but there is considerable heterogeneity in the literature. The current study used p-curve and metaanalysis on 709 findings from 212 studies to test the evidential value and estimate effect sizes of four sets of findings: those associating worse psychosocial functioning with higher or lower cortisol increase relative to the waking period (CARi) and to the output of the waking period (AUCw). All four sets of findings demonstrated evidential value. Psychosocial predictors explained 1%-3.6% of variance in CARi and AUCw responses. Based on these effect sizes, cross-sectional studies assessing CAR would need a minimum sample size of 617-783 to detect true effects with 80% power. Depression was linked to higher AUCw and posttraumatic stress to lower AUCw, whereas inconclusive results were obtained for predictor-specific effects on CARi. Suggestions for future CAR research are discussed.


The replication crisis in psychology has raised questions about the best methods to promote confidence in scientific findings. Some have suggested that “meta-analysis provides the best foundation for progress, even for messy applied questions” (Cumming, 2008, p. 292), because aggregating across studies reduces noise. Others have noted that publication bias and questionable research practices in individual studies can skew meta-analytic results (Simmons, Nelson, & Simonsohn, 2011), proposing additional ways to analyze the evidential value of a set of findings (Simonsohn, Nelson, & Simmons, 2014; van Aert, Wicherts, & van Assen, 2016). Research on relations between hormones and behavior can be particularly “messy” and vulnerable to inconsistency. The literature on psychosocial functioning and the cortisol awakening response (CAR) has more than doubled in the last six years, but heterogeneity in published findings has partially obscured the nature and direction of these effects. The present study aims to assess the evidential value of the published literature linking psychosocial functioning to the CAR.

Cortisol is a steroid hormone involved in glucose regulation and metabolism that is frequently labeled a stress hormone because its levels change markedly in response to stressors (see Sapolsky, 2004 for a review). Cortisol levels rise steeply immediately after awakening in the morning and peak approximately 30-45 minutes thereafter; from there, they slowly decrease throughout the day. This early peak in cortisol is known as the CAR (Pruessner, 1997). The CAR is responsive to stress perception and anticipation of daily stressors, making it particularly interesting to psychologists (Fries, Dettenborn, & Kirschbaum, 2009).

A meta-analysis of 62 studies revealed considerable heterogeneity in findings linking psychosocial functioning to the CAR (Chida & Steptoe, 2009). For instance, CAR measures were negatively correlated with depression in one study (O'Donnell et al., 2008) but positively correlated in another (Mommersteeg et al., 2006). Heterogeneity in the literature linking psychosocial functioning to the CAR is the rule rather than the exception; in fact, in four of seven types of psychosocial predictors, studies showing both positive and negative associations exist (Chida & Steptoe, 2009). Heterogeneity may result from inconsistency in how the CAR is measured (Stadler et al., 2016) and from small sample sizes (N < 100) that are characteristic of the literature. With small sample sizes, observed effects may misestimate both the size and the direction of any true underlying effect (Gelman & Carlin, 2014). Misestimations of direction are unlikely to be detected because there are no norms for the CAR, making it impossible to tell whether CAR values represent hyporesponsiveness, normal responses, or hyperresponsiveness.

To further complicate matters, different researchers operationalize and measure the CAR differently. Most researchers quantify the dynamic increases that occur during the first waking hour (CARi). Others compute the area under the curve relative to the waking period (AUCw) to quantify total cortisol output, although this is not strictly a measure of CAR because it is influenced by cortisol levels prior to awakening and not entirely by dynamic increases in cortisol that happen post-wakening (Stadler et al., 2016). In studies in which both CARi and AUCw were measured, their relationships to measures of psychosocial functioning were not the same (e.g., Bhattacharyya et al., 2008; Chida & Steptoe, 2009; Ellenbogen et al., 2006; Mommersteeg et al., 2006; Sonnenschein et al., 2007; Whitehead et al., 2007), suggesting possible measure-dependent effects.

Yet another source of heterogeneity in the literature emerges from specific subytpes of psychosocial predictors having unique associations with the CAR. Chida and Steptoe (2009) described seven different types of psychosocial predictors: job stress, general life stress (non-work-related), depression, anxiety (including neuroticism and negative affect), fatigue/burnout/exhaustion, posttraumatic stress, and positive psychosocial traits. These different predictors may have different relationships with the CAR. For example, AUCw was positively related to general life stress but negatively related to posttraumatic stress (Chida & Steptoe, 2009). Similarly, CARi was positively correlated with job stress and general life stress but negatively correlated with fatigue, burnout, or exhaustion and not reliably associated with positive affect. Meta-analytic findings, therefore, suggest that psychosocial predictors can be related to higher or lower CAR, depending on the nature of the predictor.

Meta-analysis is designed to aggregate across individual findings and extract the commonalities from the idiosyncrasies. The latest meta-analysis on psychosocial functioning and CAR was a step in the right direction (Chida & Steptoe, 2009). However, a potential problem with meta-analysis is the file drawer problem, where studies are “filed away” unpublished if they fail to find statistically significant relationships. When studies are statistically significant, they make their way into the literature. Over time, this practice artificially inflates Type I error and may make it appear that relationships exist when in reality they do not (Rosenthal et al., 1979). To the degree that a meta-analysis includes a disproportionate number of Type I errors, its results – although superior to individual findings – may nonetheless be biased.

New statistical tools allow researchers to test a set of findings for evidential value in less biased ways. Specifically, p-curve analysis is based on the mathematical principle that if the null hypothesis is true, the probability of a p-value falling within a range of possible values is the same for all bins of the same size (Simonsohn, Nelson, & Simmons, 2014a, 2014b, 2015). Thus, given that the null hypothesis is true (i.e., studies lack evidential value), the probability of p falling between .01 - .02 is equal to the probability of it falling between .02 - .03, .03 -.04, or .04 - .05. In this case, a curve of all the significant p-values within a set of findings (i.e., a p-curve) will be flat. However, if a set of findings contains evidential value, more significant p-values from that set will fall in the .01 - .02 and .02 - .03 bins than in the .03 - .04 and .04 - .05 bins, and the p-curve will be positively skewed. Thus, by assembling the p-values for any set of significant findings and calculating the slope of that line, evidential value can be determined (Simonsohn et al., 2014a, 2014b, 2015). Moreover, if one knows all the p-values from a set of findings, one can approximate the distribution used to obtain those p-values, resulting in an unbiased estimate of effect size (Simonsohn et al., 2014a). This point estimate can then be compared to a meta-analytic point estimate to assess for systematic bias in the literature.

The Current Study

Although the extant literature suggests that psychosocial functioning and the CAR are associated, the nature of these associations remains unclear. In some studies, psychosocial variables were related to higher CAR and in other studies, to lower CAR (Chida & Steptoe, 2009). Moreover, the relationship between psychosocial functioning and the CAR may not be the same for different measures of the CAR, and may not be consistent for all psychosocial predictors. The current study aims to clarify the following questions regarding the relationships between psychosocial functioning and the CAR by combining p-curve and meta-analytic techniques: First, do the sets of findings associating psychosocial functioning to higher or lower CAR differ in evidential value? Second, what is the effect size for each of these sets of findings? Third, is there evidence of systematic bias in the extant literature? A secondary aim of the study was to examine predictor-specific effects.

Methods

Data Sources and Study Selection

The current study updated the literature testing relationships between psychosocial functioning and the CAR. It included studies previously reviewed by Chida and Steptoe (2009) and added new findings from the past six years. Methods for updating the literature were based on those described by Chida and Steptoe (2009). Articles were identified using the search terms “cortisol” and “awakening” and “response” simultaneously (thus allowing the terms to be out of order) using the Endnote X7.2 (Thompson Reuters) software to search across the following databases: Medline, PsycINFO, Pubmed, and Web of Science. The search terms were allowed to appear in “Any field” for the Pubmed and PsycINFO databases, or in “Title/Keywords/Abstract” for Web of Science and Medline. Articles that were duplicates across these databases, published in foreign language journals, dissertations, conference abstracts, and letters to the editor were removed at a first pass. Reference sections of the identified articles were searched for other relevant articles. To avoid overlap with the previous meta-analysis, the search dates for the updated literature were restricted to articles published between October 1, 2008 and July 1, 2015. Inclusion criteria required articles to (1) be written in English, (2) be published in a peer-reviewed journal, (3) include at least one measure of psychosocial functioning, and (4) include at least one measure of the CAR. Articles were excluded if the population of interest had medical conditions/disorders known to influence cortisol, including pregnant or post-partum women, chronic pain disorders, circadian rhythm disorders, endocrine disorders, hormonal treatments, diabetes, cardiovascular disease, or other medical conditions. Biological predictors of the CAR (genetics or gene × environment interactions, family history of psychopathology, sleep patterns and disorders, chronotype), as well as intervention studies or effects of laboratory manipulations, were also excluded. Studies including participants with intellectual or developmental disabilities, dementia, or other cognitive impairments were excluded because there was insufficient research to synthesize these studies separately. Lastly, studies focusing on within-subject psychosocial changes were excluded because the current study focused on individual differences instead of intraindividual shifts, and there has recently been a thorough review on within-subject effects on the CAR (Law, Hucklebridge, Thorn, Evans, & Clow, 2013).

Where different articles reported on the same cohort (e.g., from large publicly available datasets), they were treated as multiple findings from the same study. In cases where articles met inclusion criteria but provided insufficient data for analysis, the corresponding authors were contacted. Of 32 authors contacted, 19 responded, and 17 provided additional data. In total, 159 articles met criteria for the updated literature review. These were combined with 54 articles from the Chida and Steptoe (2009) analysis. Thus, the current study included 709 findings from 212 articles. Figure 1 provides a flowchart of the included articles.

Figure 1. Flow Chart of Articles Included in Study.

Figure 1

Data Abstraction

The following information was abstracted for each article added in the current study: title, author, publication year, sample size, psychosocial predictor measurement method, CAR formula used, test statistic, statistic pertaining to psychosocial functioning/CAR relationship, and information to compute quality score (described below). Suitable formulas for CARi included the mean cortisol value post-awakening minus the wakening value (MINC), the absolute increase in cortisol as indexed by the maximum value minus the minimum value (AINC), the absolute cortisol values where the effect size was assessed through repeated-measures analysis (ACOR), the slope of the CAR curve (slope), or the ratio of cortisol values at wakening to 30 minutes post wakening (T0/T1 ratio). For AUCw, the overall volume of cortisol released during the waking period as indexed by the total area under the curve was used.

A quality score for each study was computed based on whether the studies controlled for each of the following: (1) age, (2) gender, (3) smoking status, (4) medications that influenced cortisol, (5) weekday versus weekend collection days (6) waking time, and (7) adherence to protocol. Moreover, (8) clear instructions for collection had to be provided to participants. A point was awarded for each of these eight criteria that was explicitly described in the article, leading to a total research quality score ranging from 0 to 8. Data abstraction for the articles in the current study was done by one of the first three authors (IB, CH, EH) and double-checked by another of these authors. A randomly selected subset of 15 articles were independently coded by all three authors, and there was high corroboration on the data that were extracted (>90% agreement on each variable). Discrepancies were settled by group discussions among authors. For articles published before 2009, data were drawn from the Chida and Steptoe (2009) meta-analysis (Table 1, pp. 268-272).

Table 1. Descriptive Statistics of Findings in Meta-Analysis.

Number of Articles 212
Number of Findings 709
Number of Independent Findings 186
Mean Sample Size of Studies 244.95 (SD: 520.68; Med: 74; Range: 11 – 4,364)
Mean Number of Days Sampled 2.04 (SD: 1.31; Med: 2; Range: 1 – 9)
Mean Quality Score of Studies 6.08 (SD: 1.64; Med: 6; Range: 1 – 8)
Total Number of Findings for each Predictor Type
 Job Stress 64
 General Life Stress 221
 Depression 118
 Anxiety/Neuroticism/Negative Affect 91
 Fatigue/Burnout/Exhaustion 37
 Posttraumatic Stress 56
 Positive Psychosocial Traits 122

Data Analysis

To test for evidential value, p-curves were computed for the following four sets of associations: (1) worse psychosocial functioning with higher CARi, (2) worse psychosocial functioning with lower CARi, (3) worse psychosocial functioning with higher AUCw, and (4) worse psychosocial functioning with lower AUCw. A p-curve-derived estimate of effect size was computed from each of the four p-curves. Next, meta-analysis was used to estimate effects for these four categories, and these meta-analytic estimates were compared to the p-curve-derived estimate of effect size. Details for these procedures are discussed below.

P-curve analysis for evidential value

To compute p-curves, directionality for all predictors was changed so that higher values reflected worse psychosocial functioning. P-curve analyses requires that all findings be independent of one another. If more than one significant relationship was reported from the same sample, or if samples were partially overlapping (i.e., females only in one effect, and males and females in another), the effect with the largest sample size was chosen for inclusion in the p-curve. T-values and degrees of freedom (n-2) from significant findings were entered into a publicly available p-curve calculator provided by Simonsohn and colleagues (2013; Version 4.05; http://www.p-curve.com/). To test for evidential value, the p-curve calculator estimated the probability of obtaining that p-value if the null were true. Flat curves (neither right nor left skewed) indicated that findings lacked evidential value or were underpowered to detect evidential value. These alternatives were differentiated by testing the set of findings against a null of 33% power as outlined by Simonsohn et al. (2014); if significant, findings could be assumed to lack evidential value; otherwise, evidential value could not be confirmed or denied.

P-curve analysis for estimates of effect size

Using R syntax, significant p-values of a set of findings were used to estimate the effect size of those findings (see Simonsohn et al., 2014b for the syntax). P-curve-derived effect size estimates for each of the four sets of findings were computed. Only significant, findings could be assumed findings from independent samples were entered. Effect sizes were computed in Cohen's d and were then converted into r using the formula r = d/√(d2 +4).

Meta-analysis

Methods described by Chida and Steptoe (2009) were followed to allow for the aggregation of their findings with findings retrieved for the current study. Meta-analytic estimate of effect sizes were transformed into the correlation coefficient r. When multiple estimates of the same correlation were provided, associations adjusted for covariates were included. Bivariate correlations were used when there was no covariate adjustment for analyses involving the CAR, or when there was insufficient information to extract an effect size from the covariate-adjusted analyses. Because variance of correlation coefficients depended strongly on sample size (Borenstein, Hedges, Higgins, & Rothstein, 2009), the r values derived from each study were transformed to Fisher's z and analyses were conducted on these values. The z values were later back-transformed into r values to facilitate interpretation of the meta-analytic findings.

The effect sizes were aggregated using the Comprehensive Meta-Analysis software version 2.2.064. Each random-effects model yielded an aggregate weighted effect size r ranging in value from -1.00 to 1.00, interpreted the same way as a correlation coefficient. Each r statistic was weighted before aggregation by multiplying its value by the inverse of its variance; this procedure enabled larger studies to contribute to effect size estimates to a greater extent than smaller ones. 95% confidence intervals were computed to assess whether aggregate effect sizes were statistically significant. A heterogeneity coefficient was used to determine whether the studies yielded consistent findings. Publication bias was assessed using Egger's unweighted regression asymmetry test, which tests the asymmetry of the funnel plot of effect sizes plotted by sample size (Egger, Smith, Schneider, & Minder, 1997).

Because several studies included multiple psychosocial predictors of the CAR, analyses were conducted by including all the effect sizes. To address concerns regarding the non-independence of effects drawn from the same sample, the same analyses were conducted again by selecting a single effect size at random from each study, and also by combining all the effect sizes from any study into a single average. Results did not differ with these approaches; thus, reported results include all effect sizes.

Analyses for predictor-specific effects

Chida and Steptoe (2009) described seven categories of psychosocial predictors that have been associated with the CAR: job stress, general life stress, depression, anxiety, fatigue/burnout/exhaustion, posttraumatic stress, and positive psychosocial traits. Because there were not enough significant p-values to compute independent p-curves by directionality and predictor type, p-values for both directions were entered simultaneously for each predictor. Thus, these p-curves tested whether there was evidential value for each predictor being associated with the CAR. Meta-analysis described the nature and directionality of the relationships.

Results

Study Characteristics and Quality

Table 1 reveals that studies were, on average, of medium to high quality, although quality scores varied considerably. The average number of sampling days was just over two days. The most frequently assessed psychosocial predictors were those assessing general life stress, depression, positive psychosocial traits, and anxiety/neuroticism/negative affect. Details for each of the studies are provided in Table 2.

Table 2. Effect Size and Study Details of all Findings included in the Meta-Analysis.

No Author Year OutcomeTYPE* N r Measure±
1a Adam 2006 DepressionDE 52 .01 AINC
1b Adam 2006 Trait angerAX 52 .21 AINC
1c Adam 2006 Trait anxietyAX 52 -.10 AINC
Figfig Adam et al 2006 FatigueFA 156 -.06 AINC
2b Adam et al 2006 LonelinessGL 156 .14 AINC
2c Adam et al 2006 Loss of controlGL 156 .17 AINC
2d Adam et al 2006 Low liveliness/energyDE 156 .00 AINC
2e Adam et al 2006 SadnessDE 156 .13 AINC
2f Adam et al 2006 Tense/angryGL 156 .01 AINC
2g Adam et al 2006 ThreatGL 156 .19 AINC
3a Alderling et al 2006 Job stress (females)JS 169 .00 AINC
3b Alderling et al 2006 Job stress (males)JS 87 .00 AINC
4 Aubry et al 2010 Remitted depressionDE 90 .27 AINC
5a Baes et al 2014 Childhood trauma and depressionDE 23 -.14 AUCg
5b Baes et al 2014 DepressionDE 30 -.19 AUCg
6a Barnett et al 2005 Poor marital qualityGL 75 .24 AINC
6b Barnett et al 2005 Poor marital qualityGL 75 .23 AUCg
7 Bhagwagar et al 2003 Past depressionDE 62 .32 AUCg
8 Bhagwagar et al 2005 DepressionDE 60 .28 AUCg
9a Bogg et al 2015 ConscientiousnessPO 960 -.02 AINC
9b Bogg et al 2015 NeuroticismAX 960 .00 AINC
10a Bosch et al 2009 Cognitive-affective symptoms (females)DE 795 .00 AUCi
10b Bosch et al 2009 Cognitive-affective symptoms (males)DE 785 -.08 AUCi
10c Bosch et al 2009 Somatic symptoms (females)DE 795 -.03 AUCi
10d Bosch et al 2009 Somatic symptoms (males)DE 785 .09 AUCi
10e Bosch et al 2009 Depressive symptomsDE 1580 -.01 AUCi
11 Bouma et al 2009 Depressed moodDE 568 -.05 AINC
12a Camfield et al 2013 Perceived stressGL 138 -.14 AUCi
12b Camfield et al 2013 High stress (vs low stress)GL 94 .22 AUCi
13 Chan et al 2007 NeuroticismAX 65 -.09 AUCg
14 Chui et al 2014 Cumulative depressive symptomsDE 50 -.18 AINC
15 Clingerman et al 2013 Work stressJS 28 .42 AINC
16 Cropley et al 2015 Work-related ruminationJS 108 -.19 AINC
17a Daubenmier et al 2014 AnxietyAX 43 .35 AINC
17b Daubenmier et al 2014 Negative affectAX 43 .35 AINC
17c Daubenmier et al 2014 Perceived stressGL 43 .44 AINC
17d Daubenmier et al 2014 RuminationAX 43 .42 AINC
18a Dedovic et al 2010 High-risk subclinical depressionDE 36 -.43 AUCi
18b Dedovic et al 2010 Subclinical depressionDE 50 -.30 AUCi
19a De Kloet et al 2007 PTSD symptomsPT 47 -.37 AUCi
19b De Kloet et al 2007 PTSD symptomsPT 47 -.49 AUCg
20 De Vente et al 2003 BurnoutFA 45 -.34 ACOR
21 De Vugt et al 2005 Caregiver stressGL 98 -.21 AINC
22a Diaz et al 2013 Competition stress (day 1)GL 11 .06 AUCi
22b Diaz et al 2013 Competition stress (day 1)GL 11 .10 AUCg
22c Diaz et al 2013 Negative mood (day 1)AX 11 -.55 AUCi
22d Diaz et al 2013 Negative mood (day 1)AX 11 -.59 AUCg
22e Diaz et al 2013 Competition stress (day 2)GL 9 .24 AUCi
22f Diaz et al 2013 Competition stress (day 2)GL 9 .34 AUCg
22g Diaz et al 2013 Negative mood (day 2)AX 11 -.70 AUCi
22h Diaz et al 2013 Negative mood (day 2)AX 11 -.90 AUCg
23a Dienes et al 2013 At-risk for depression (vs. control)DE 42 -.06 AINC
23b Dienes et al 2013 Depressed status (vs. control)DE 37 .17 AINC
24a Dietrich et al 2013 Aggression (mean scales)GL 361 .07 AUCi
24b Dietrich et al 2013 Aggression (mean scales)GL 361 .00 AUCg
24c Dietrich et al 2013 AggressionGL 357 .03 AUCi
24d Dietrich et al 2013 AggressionGL 1580 .01 AUCg
24e Dietrich et al 2013 Proactive aggressionGL 361 .00 AUCi
24f Dietrich et al 2013 Reactive aggressionGL 361 .09 AUCi
24g Dietrich et al 2013 Delinquent behaviorGL 235 .00 AUCi
24h Dietrich et al 2013 Delinquent behaviorGL 1578 -.04 AUCg
24i Dietrich et al 2013 AnxietyAX 364 .01 AUCi
24j Dietrich et al 2013 AnxietyAX 364 .02 AUCg
24k Dietrich et al 2013 DepressionDE 361 .07 AUCg
24l Dietrich et al 2013 DepressionDE 361 .12 AUCi
24m Dietrich et al 2013 Anxious/depressedDE 789 -.02 AUCi
24n Dietrich et al 2013 Anxious/depressedDE 1582 .04 AUCg
25a Doane et al 2010 Interpersonal stressGL 108 -.04 AINC
25b Doane et al 2010 Trait lonelinessGL 108 -.08 AINC
26a Doane et al 2011 DepressionDE 735 -.01 AINC
26b Doane et al 2011 Negative emotionalityAX 735 .01 AINC
27 Doane et al 2015 Childhood traumaPT 82 .13 AUCi
28a Donoho et al 2011 Cumulative stressGL 23 .00 AINC
28b Donoho et al 2011 Family stressGL 23 -.03 AINC
28c Donoho et al 2011 Peer stressGL 23 .00 AINC
28d Donoho et al 2011 Personal stressGL 23 -.04 AINC
28e Donoho et al 2011 School stressGL 23 .13 AINC
29a Drake et al 2015 Concurrent coping efficacyPO 70 .04 AINC
29b Drake et al 2015 Concurrent lonelinessGL 70 -.09 AINC
29c Drake et al 2015 Past coping efficacyPO 70 .19 AINC
29d Drake et al 2015 Past lonelinessGL 70 -.07 AINC
30a Duan et al 2013 AnxietyAX 63 -.30 AINC
30b Duan et al 2013 AnxietyAX 63 .04 AUCg
30c Duan et al 2013 Perceived stressGL 63 -.30 AINC
30d Duan et al 2013 Perceived stressGL 63 -.05 AUCg
30e Duan et al 2013 Test anxiety (vs. control)AX 63 -.35 AINC
30f Duan et al 2013 Test anxiety (vs. control)AX 63 -.07 AUCg
31a Ebrecht et al 2004 LonelinessGL 24 .00 AUCg
31b Ebrecht et al 2004 OptimismPO 24 .00 AUCg
31c Ebrecht et al 2004 Perceived stressGL 24 .00 AUCg
31d Ebrecht et al 2004 Poor social supportGL 24 .00 AUCg
31e Ebrecht et al 2004 Self-esteemPO 24 .00 AUCg
32a Edwards et al 2003 Perceived stressGL 26 .37 AUCg
32b Edwards et al 2003 Perceived stressGL 26 .00 MINC
33 Eek et al 2006 Perceived stressGL 381 .00 AINC
34a Ellenbogen et al 2006 Daily hasslesGL 57 .02 AINC
34b Ellenbogen et al 2006 Daily hasslesGL 57 .14 AUCg
34c Ellenbogen et al 2006 DepressionDE 57 -.02 AINC
34d Ellenbogen et al 2006 DepressionDE 57 .09 AUCg
34e Ellenbogen et al 2006 InternalizingDE 57 .08 AINC
34f Ellenbogen et al 2006 InternalizingDE 57 .05 AUCg
34g Ellenbogen et al 2006 Major life eventsGL 57 -.09 AINC
34h Ellenbogen et al 2006 Major life eventsGL 57 -.11 AUCg
34i Ellenbogen et al 2006 Negative affectAX 57 .07 AINC
34j Ellenbogen et al 2006 Negative affectAX 57 .10 AUCg
34k Ellenbogen et al 2006 Positive affectPO 57 .05 AINC
34l Ellenbogen et al 2006 Positive affectPO 57 .17 AUCg
34m Ellenbogen et al 2006 Social problemsGL 57 .16 AINC
34n Ellenbogen et al 2006 Social problemsGL 57 .07 AUCg
34o Ellenbogen et al 2006 State anxietyAX 57 .02 AINC
34p Ellenbogen et al 2006 State anxietyAX 57 -.07 AUCg
35a Ellenbogen et al 2009 Parental functioningPO 43 -.13 AUCi
35b Ellenbogen et al 2009 Parental controlPO 43 -.22 AUCi
35c Ellenbogen et al 2009 Parental neuroticismAX 43 .03 AUCi
35d Ellenbogen et al 2009 Parental structurePO 43 -.35 AUCi
35e Ellenbogen et al 2009 Parental supportPO 43 -.07 AUCi
36a Eller et al 2006 Job stress (low control), malesJS 28 .00 AINC
36b Eller et al 2006 Job stress (high demand), malesJS 28 -.02 AINC
36c Eller et al 2006 Job stress (ERI model), malesJS 28 .00 AINC
36d Eller et al 2006 Job stress (over-commitment), malesJS 28 .03 AINC
36e Eller et al 2006 Time pressure, malesJS 28 .00 AINC
36f Eller et al 2006 Job stress (low control), femalesJS 47 .01 AINC
36g Eller et al 2006 Job stress (high demand), femalesJS 52 .00 AINC
36h Eller et al 2006 Job stress (ERI model), femalesJS 53 .15 AINC
36i Eller et al 2006 Job stress (over-commitment), femalesJS 50 .00 AINC
36j Eller et al 2006 Time pressure, femalesJS 55 .31 AINC
37a Eller et al 2011 Job controlPO 70 .05 AINC
37b Eller et al 2011 Job demandsJS 70 .04 AINC
37c Eller et al 2011 Job effortJS 70 .06 AINC
37d Eller et al 2011 Job effort-reward imbalanceJS 70 -.04 AINC
37e Eller et al 2011 Job rewardPO 70 -.04 AINC
37f Eller et al 2011 Job strainJS 70 .01 AINC
37g Eller et al 2011 Life events (past year)GL 70 -.02 AINC
38a Endrighi et al 2011 DepressionDE 422 .01 AINC
38 Endrighi et al 2011 OptimismPO 422 -.11 AINC
39a Engert et al 2011 Anxiety symptomsAX 58 .28 AINC
39b Engert et al 2011 Depressive symptomsDE 58 .33 AINC
39c Engert et al 2011 Low early-life parental careGL 58 .34 AINC
39d Engert et al 2011 Self-esteemPO 58 -.24 AINC
40a Fairchild et al 2008 Adolescent-onset CD (vs. control)GL 116 -.27 AUCi
40b Fairchild et al 2008 Early-Onset CD (vs. control)GL 134 -.33 AUCi
41a Fekedulegn et al 2012 Percent of hours on midnight shiftJS 65 -.32 AUCg
41b Fekedulegn et al 2012 Percent of hours on midnight shiftJS 65 -.04 AUCi
42 Franz et al 2013 Childhood disadvantageGL 727 .06 AINC
43a Freitag et al 2009 ADHD (vs. control)GL 121 .20 MINC
43b Freitag et al 2009 ADHD + CD (vs. control)GL 91 .11 MINC
43c Freitag et al 2009 ADHD + ODD (vs. control)GL 118 .20 MINC
43d Freitag et al 2009 ADHD with anxiety (vs. control)GL 106 .17 MINC
43e Freitag et al 2009 ADHD without anxiety (vs. control)GL 155 .20 MINC
44a Garcia-Banda et al 2014 NeuroticismAX 118 .04 AINC
44b Garcia-Banda et al 2014 NeuroticismAX 118 .02 AUCg
45a Gartland et al 2014 Daily negative affectAX 64 .00 AUCi
45b Gartland et al 2014 Daily positive affectPO 64 .00 AUCi
45c Gartland et al 2014 Hassle appraisalGL 64 .00 AUCi
46a Gonzalez-bono et al 2011 Caregiver burdenGL 38 .00 AINC
46b Gonzalez-bono et al 2011 CaregivingGL 70 -.27 AINC
46c Gonzalez-bono et al 2011 Psychopathology of care recipientGL 38 -.50 AINC
46d Gonzalez-bono et al 2011 Schizophrenia symptoms of care recipientGL 38 -.35 AINC
47a Gonzalez-Cabrera et al 2014 Perceived stressGL 36 .01 AINC
47b Gonzalez-Cabrera et al 2014 State anxietyAX 36 .24 AINC
47c Gonzalez-Cabrera et al 2014 Trait anxietyAX 36 .28 AINC
48a Gostisha et al 2014 Callous-unemotional traitsGL 50 .28 Slope
48b Gostisha et al 2014 Psychopathy symptomsGL 50 .37 Slope
48c Gostisha et al 2014 Stress exposureGL 50 .35 Slope
49 Grant et al 2009 Social isolationGL 145 .20 AINC
50a Greaves-Lord et al 2007 Current anxietyAX 376 .00 AUCg
50b Greaves-Lord et al 2007 Persistent anxietyGL 354 .13 AUCg
51a Grossi et al 2005 Burnout, malesFA 29 .00 MINC
51b Grossi et al 2005 Burnout, malesFA 29 .00 AUCg
51c Grossi et al 2005 Burnout, femalesFA 35 .00 MINC
51d Grossi et al 2005 Burnout, femalesFA 35 .26 AUCg
52 Gustafsson et al 2010 Acumulated life adversityGL 130 .31 AINC
53 Gustafsson et al 2012 Cumulation of temporary employmentJS 755 .08 AINC
54 Hansen et al 2011 BullyingGL 1717 -.03 30min
55a Harris et al 2007 Job stress (DC model)JS 44 .17 AUCi
55b Harris et al 2007 Job stress (ERI model)JS 39 -.11 AUCi
55c Harris et al 2007 Poor social supportGL 42 .27 AUCi
55d Harris et al 2007 VitalityPO 42 -.32 AUCi
55e Harris et al 2007 Well-beingPO 42 -.19 AUCi
56a Hartman et al 2013 Externalizing (checklist)GL 211 .03 AUCi
56b Hartman et al 2013 Externalizing (checklist)GL 211 .00 AUCg
56c Hartman et al 2013 Externalizing (self-report)GL 211 .01 AUCi
56d Hartman et al 2013 Externalizing (self-report)GL 211 -.09 AUCg
56e Hartman et al 2013 Internalizing (checklist)DE 211 -.03 AUCi
56f Hartman et al 2013 Internalizing (checklist)DE 211 .03 AUCg
56g Hartman et al 2013 Internalizing (self-report)DE 211 .10 AUCi
56h Hartman et al 2013 Internalizing (self-report)DE 211 .13 AUCg
56i Hartman et al 2013 Internalizing × Externalizing (checklist)DE 211 .02 AUCi
56j Hartman et al 2013 Internalizing × Externalizing (checklist)DE 211 .07 AUCg
56k Hartman et al 2013 Internalizing × Externalizing (self-report)DE 211 .03 AUCi
56l Hartman et al 2013 Internalizing × Externalizing (self-report)DE 211 .17 AUCg
57a Hartwig et al 2013 Alexithymia (high vs. low)GL 78 -.34 AUCi
57b Hartwig et al 2013 AlexithymiaGL 78 -.29 AUCi
58a Heaney et al 2010 AnxietyAX 24 .46 AINC
58b Heaney et al 2010 DepressionDE 24 .59 AINC
59 Heim et al 2009 FatigueFA 237 -.17 AUCg
60a Hek et al 2013 Anxiety disorder (vs. control)AX 1788 -.05 AINC
60b Hek et al 2013 Anxiety disorder (vs. control)AX 1788 -.04 AUCg
61a Hibel et al 2014 Job strainJS 56 .05 AINC
61b Hibel et al 2014 Parenting stressGL 56 .06 AINC
62a Hicks et al 2011 Attachment anxietyAX 39 .14 AINC
62b Hicks et al 2011 Attachment avoidanceGL 39 -.15 AINC
62c Hicks et al 2011 Daily conflictGL 39 -.37 AINC
62d Hicks et al 2011 Morning negative affectAX 39 -.06 AINC
62e Hicks et al 2011 Night negative affectGL 39 .21 AINC
63a Hill et al 2013 AgreeablenessPO 92 -.08 AUCi
63b Hill et al 2013 AgreeablenessPO 92 -.03 AUCg
63c Hill et al 2013 ConscientiousnessPO 92 -.16 AUCi
63d Hill et al 2013 ConscientiousnessPO 92 .03 AUCg
63e Hill et al 2013 ExtraversionPO 92 .13 AUCi
63f Hill et al 2013 ExtraversionPO 92 .24 AUCg
63g Hill et al 2013 NeuroticismAX 92 -.03 AUCi
63h Hill et al 2013 NeuroticismAX 92 -.11 AUCg
63i Hill et al 2013 OpennessPO 92 .08 AUCi
63j Hill et al 2013 OpennessPO 92 .06 AUCg
64a Holleman et al 2012 Decision latitudeJS 1048 -.05 AUCi
64b Holleman et al 2012 Decision lattitudeJS 1048 -.05 AUCg
64c Holleman et al 2012 Job demandsJS 1048 -.03 AUCi
64d Holleman et al 2012 Job demandsJS 1048 .02 AUCg
64e Holleman et al 2012 Job insecurityJS 1048 .03 AUCi
64f Holleman et al 2012 Job insecurityJS 1048 .00 AUCg
64g Holleman et al 2012 Job strainJS 1048 -.01 AUCi
64h Holleman et al 2012 Job strainJS 1048 .01 AUCg
64i Holleman et al 2012 Negative life eventsGL 1680 -.02 AUCi
64j Holleman et al 2012 Negative life eventsGL 1680 .02 AUCg
64k Holleman et al 2012 Social supportPO 1048 .01 AUCi
64l Holleman et al 2012 Social supportPO 1048 .03 AUCg
64m Holleman et al 2012 Physical abusePT 1680 -.02 AUCi
64n Holleman et al 2012 Physical abusePT 1680 -.01 AUCg
64o Holleman et al 2012 Emotional abusePT 1680 .01 AUCi
64p Holleman et al 2012 Emotional abusePT 1680 .04 AUCg
64q Holleman et al 2012 Sexual abusePT 1680 -.01 AUCi
64r Holleman et al 2012 Sexual abusePT 1680 .00 AUCg
64s Holleman et al 2012 Trauma indexPT 1680 .00 AUCi
64t Holleman et al 2012 Trauma indexPT 1680 .02 AUCg
65a Hoyt et al 2015 High-arousal negative affectPO 315 .00 ACOR
65b Hoyt et al 2015 High-arousal positive affectPO 315 -.05 ACOR
65c Hoyt et al 2015 Low-arousal negative affectPO 315 .01 ACOR
65d Hoyt et al 2015 Low-arousal positive affectPO 315 .04 ACOR
66a Imeraj et al 2012 ADHD + ODD (vs. controls)GL 66 .05 AINC
66b Imeraj et al 2012 ADHD only (vs. controls)GL 66 -.16 AINC
67 Isaksson et al 2013 ADHDGL 308 -.04 AINC
68a Isaksson et al 2015 ADHDGL 185 -.16 AINC
68b Isaksson et al 2015 Perceived stressGL 185 .00 AINC
69a Izawa et al 2007 Writing graduation thesisGL 12 .00 AUCi
69b Izawa et al 2007 Writing graduation thesisGL 12 .50 AUCg
70a Jabben et al 2011 Bipolar depressionDE 1571 -.75 AUCi
70b Jabben et al 2011 Bipolar depressionDE 1571 .14 AUCg
70c Jabben et al 2011 Unipolar depressionDE 1571 -.68 AUCi
70d Jabben et al 2011 Unipolar depressionDE 1571 .09 AUCg
71 Jarcho et al 2013 DepressionDE 49 -.04 AINC
72 Jobin et al 2014 Perceived stress and pessimismGL 135 .22 AINC
73a Johnson et al 2008 Abuse chronicityPT 52 -.21 AUCi
73b Johnson et al 2008 Abuse chronicityPT 52 -.26 AUCg
73c Johnson et al 2008 DepressionDE 52 .28 AUCi
73d Johnson et al 2008 DepressionDE 52 .08 AUCg
73e Johnson et al 2008 Posttraumatic stress disorder symptomsPT 52 .34 AUCi
73f Johnson et al 2008 Posttraumatic stress disorder symptomsPT 52 .31 AUCg
74a Johnson et al 2014 Affective empathyPO 57 .26 AINC
74b Johnson et al 2014 Blame externalizationGL 57 -.26 AINC
74c Johnson et al 2014 Carefree nonplanfulnessGL 57 -.24 AINC
74d Johnson et al 2014 Cognitive empathyPO 57 .05 AINC
74e Johnson et al 2014 ColdheartednessGL 57 .00 AINC
74f Johnson et al 2014 FearlessnessGL 57 .00 AINC
74g Johnson et al 2014 Impulsive nonconformityGL 57 .00 AINC
74h Johnson et al 2014 Machavellian egocentricityGL 57 -.26 AINC
74i Johnson et al 2014 Proactive physical aggressionGL 57 .00 AINC
74j Johnson et al 2014 Proactive relational aggressionGL 57 .00 AINC
74k Johnson et al 2014 Prosocial behaviorPO 57 .26 AINC
74l Johnson et al 2014 Psychopathy (total score)GL 57 .00 AINC
74m Johnson et al 2014 Reactive physical aggressionGL 57 -.26 AINC
74n Johnson et al 2014 Reactive relational aggressionGL 57 .00 AINC
74o Johnson et al 2014 Social potencyPO 57 .34 AINC
74p Johnson et al 2014 Stress immunityPO 57 .00 AINC
75a Kallen et al 2008 Anxiety, femalesAX 46 .29 AINC
75b Kallen et al 2008 Anxiety, malesAX 53 .00 AINC
76a Kaplow et al 2013 Anxiety after parental lossAX 38 -.29 AINC
76b Kaplow et al 2013 Avoidant coping after parental lossGL 38 -.37 MINC
76c Kaplow et al 2013 Depression after parental lossDE 38 -.24 AUCi
76d Kaplow et al 2013 Maladaptive grief after parental lossDE 38 -.16 AINC
76e Kaplow et al 2013 Parental maladaptive griefDE 38 -.21 AUCi
76f Kaplow et al 2013 PTSD after parental lossPT 38 -.26 AINC
77 Karhula et al 2015 Job strainJS 95 -.20 AINC
78a Keeshin et al 2014 PTSD symptomsPT 24 -.41 AINC
78b Keeshin et al 2014 Sexual abusePT 36 .03 AINC
79a Kim et al 2015 Physical victimization, malesPT 122 .06 ACOR
79b Kim et al 2015 Physical victimization, femalesPT 122 -.04 ACOR
79c Kim et al 2015 Psychological victimization, malesPT 122 .01 ACOR
79d Kim et al 2015 Psychological victimization, femalesPT 122 .01 ACOR
79e Kim et al 2015 Relationship satisfaction, malesPO 122 .00 ACOR
79f Kim et al 2015 Relationship satisfaction, femalesPO 122 .00 ACOR
80 Klaassens et al 2009 TraumaPT 20 -.02 AUCg
81a Klaassens et al 2010 Work traumaPT 882 -.01 AUCi
81b Klaassens et al 2010 Work traumaPT 62 -.26 AUCg
82a Klein et al 2012 Cognitive intrusionsAX 38 -.06 AUCg
82b Klein et al 2012 Job-stressJS 38 .35 AUCg
82c Klein et al 2012 Mental distance from workJS 38 -.08 AUCg
83a Klein et al 2014 Care-related stressorsGL 158 -.03 Slope
83b Klein et al 2014 Duration of careGL 158 -.01 Slope
83c Klein et al 2014 Noncare-related stressorsGL 158 .02 Slope
83d Klein et al 2014 Positive eventsPO 158 .05 Slope
84a Kliewer et al 2006 InternalizingDE 78 .00 ACOR
84b Kliewer et al 2006 Major life eventsGL 78 .05 ACOR
84c Kliewer et al 2006 Peer victimizationGL 78 -.10 ACOR
84d Kliewer et al 2006 Witnessed violence, malesPT 45 .00 ACOR
84e Kliewer et al 2006 Witnessed violence, femalesPT 33 -.09 ACOR
85 Knack et al 2011 Peer victimizationGL 107 -.20 Slope
86 Kuehl et al 2015 Major depressive disorderDE 85 -.08 AUCg
87 Kuehner et al 2011 NeuroticismAX 66 -.12 AUCi
88a Kuhlman et al 2015 Current depressionDE 121 .04 AINC
88b Kuhlman et al 2015 Emotional abusePT 121 .17 AINC
88c Kuhlman et al 2015 Non-intentional traumaPT 121 .16 AINC
88d Kuhlman et al 2015 Physical abusePT 121 .10 AINC
89 Kumari et al 2009 FatigueFA 4364 -.01 AINC
90 Kumari et al 2013 Maternal separationGL 3712 .04 AINC
91a Lac et al 2012 Anxiety and depressionDE 69 .17 AUCi
91b Lac et al 2012 AnxietyAX 69 .23 AUCi
91c Lac et al 2012 Bullied at workGL 69 -.11 AUCi
91d Lac et al 2012 DepressionDE 69 .06 AUCi
91e Lac et al 2012 StressGL 69 .08 AUCi
92a Laceulle et al 2014 AssertivenessPO 343 .01 AINC
92b Laceulle et al 2014 Excitement seekingGL 343 -.03 AINC
92c Laceulle et al 2014 HostilityGL 343 .03 AINC
92d Laceulle et al 2014 ImpulsivenessGL 343 -.01 AINC
92e Laceulle et al 2014 Self-disciplineGL 343 -.11 AINC
92f Laceulle et al 2014 VulnerabilityGL 343 .02 AINC
93a Lai et al 2005 Negative affectAX 80 .00 AUCg
93b Lai et al 2005 OptimismPO 80 -.31 AUCg
93c Lai et al 2005 Positive affectPO 80 .00 AUCg
94a Lai et al 2010 HumorPO 45 -.02 AUCi
94b Lai et al 2010 HumorPO 45 -.32 AUCg
94c Lai et al 2010 Self-esteemPO 45 .20 AUCi
94d Lai et al 2010 Self-esteemPO 45 .06 AUCg
95a Lai et al 2012 Social network cultivationPO 78 .22 ACOR
95b Lai et al 2012 Social network emotional supportPO 78 .02 ACOR
95c Lai et al 2012 Social network sizePO 78 .02 ACOR
96a Lamers et al 2013 Atypical depressionDE 665 .08 AUCi
96b Lamers et al 2013 Atypical depressionDE 665 -.09 AUCg
96c Lamers et al 2013 Melancholic depressionDE 654 .09 AUCi
96d Lamers et al 2013 Melancholic depressionDE 654 .16 AUCg
97a Langelaan et al 2006 BurnoutFA 45 .00 AUCi
97b Langelaan et al 2006 Work engagementPO 51 .00 AUCi
98a Laudenslager et al 2009 PTSD symptomsPT 42 -.12 AINC
98b Laudenslager et al 2009 PTSD symptomsPT 17 .07 AINC
99a Lederbogen et al 2010 Depressive symptomsDE 718 .04 AINC
99b Lederbogen et al 2010 Social supportGL 718 -.04 AINC
99c Lederbogen et al 2010 Subjective health (mental symptoms)GL 718 .05 AINC
99d Lederbogen et al 2010 Subjective health (physical symptoms)GL 718 .02 AINC
100a Leggett et al 2014 AngerGL 164 .00 Slope
100b Leggett et al 2014 Depressive moodDE 164 -.20 Slope
101 Liao et al 2012 Job strainJS 1988 .01 AINC
102a Lindholm et al 2012 Severe stressPT 131 .19 T1/T0
102b Lindholm et al 2012 Shift workJS 131 .45 T1/T0
103 Lovell et al 2011 Perceived stressGL 32 -.16 AINC
104a Lovell et al 2012 Social support appraisalPO 45 .17 AINC
104b Lovell et al 2012 Social support belongingPO 45 .20 AINC
104c Lovell et al 2012 Social support self-esteemPO 45 .35 AINC
104d Lovell et al 2012 Social support tangiblePO 45 .11 AINC
105a Lovell et al 2015 AnxietyAX 18 -.13 AINC
105b Lovell et al 2015 Caregiving for child with autism or ADHDGL 57 -.03 AINC
105c Lovell et al 2015 DepressionDE 18 -.07 AINC
105d Lovell et al 2015 Perceived stressGL 18 -.40 AINC
106a Lu et al 2013 Childhood traumaPT 48 .34 AINC
106b Lu et al 2013 Childhood traumaPT 48 .32 AUCg
107 Madsen et al 2012 NeuroticismAX 48 .31 AINC
108a Maina et al 2009 Job strain (group 1)JS 68 .00 AUCg
108b Maina et al 2009 Job strain (group 2)JS 36 .32 AUCg
108c Maina et al 2009 Job effort (group 1)JS 68 .00 AUCg
108d Maina et al 2009 Job effort (group 2)JS 36 -.32 AUCg
108e Maina et al 2009 Job reward (group 1)PO 68 .23 AUCg
108f Maina et al 2009 Job reward (group 2)PO 36 .00 AUCg
108g Maina et al 2009 Job effort-reward imbalance (group 1)JS 68 -.23 AUCg
108h Maina et al 2009 Job effort-reward imbalance (group 2)JS 36 .00 AUCg
109a Maina, Palmas et al 2009 Decision latitude at workPO 36 .00 AUCi
109b Maina, Palmas et al 2009 Decision latitude at workPO 36 .00 AUCg
109c Maina, Palmas et al 2009 Psychological demands at workJS 36 .00 AUCi
109d Maina, Palmas et al 2009 Psychological demands at workJS 36 .00 AUCg
110a Mangold et al 2010 High trauma exposure (vs moderate)GL 59 -.13 AINC
110b Mangold et al 2010 Moderate/high trauma exposure (vs. low)GL 59 -.42 AINC
111a Mangold et al 2011 Depressive symptomatologyDE 55 -.32 AINC
111b Mangold et al 2011 Emotional abusePT 55 -.28 AINC
111c Mangold et al 2011 General traumasPT 55 -.34 AINC
111d Mangold et al 2011 Physical abusePT 55 -.25 AINC
111e Mangold et al 2011 Sexual abusePT 55 -.23 AINC
112 Mangold et al 2012 High acculturation and neuroticismAX 30 -.52 ACOR
113 Marchand et al 2014 BurnoutFA 401 -.13 AINC
114a Marsman et al 2012 Perceived parental rejectionGL 1594 -.03 AUCi
114b Marsman et al 2012 Perceived parental rejectionGL 1594 -.04 AUCg
114c Marsman et al 2012 Perceived parental warmthPO 1594 -.03 AUCi
114d Marsman et al 2012 Perceived parental warmthPO 1594 -.08 AUCg
115 Meinlschmidt et al 2005 Early loss eventPT 95 -.29 AINC
116a Mello et al 2015 Physical punishmentPT 113 -.24 AUCg
116b Mello et al 2015 Working on the streetsJS 113 .22 AUCg
117a Merwin et al 2015 Parental hostilityGL 149 -.26 AUCi
117b Merwin et al 2015 Parental hostilityGL 149 -.13 AUCg
118a Mikolajczak et al 2010 HappinessPO 41 -.38 Slope
118b Mikolajczak et al 2010 NeuroticismAX 41 .53 Slope
118c Mikolajczak et al 2010 Perceived stressGL 41 -.55 Slope
119a Mommersteeg et al 2006 DepressionDE 34 .04 AUCi
119b Mommersteeg et al 2006 DepressionDE 34 -.10 AUCg
119c Mommersteeg et al 2006 Depression + burnoutDE 73 .10 AUCi
119d Mommersteeg et al 2006 Depression + burnout DE 73 .10 AUCg
119e Mommersteeg et al 2006 ExhaustionFA 34 -.14 AUCi
119f Mommersteeg et al 2006 ExhaustionFA 34 -.09 AUCg
119g Mommersteeg et al 2006 Exhaustion + burnoutFA 73 -.05 AUCi
119h Mommersteeg et al 2006 Exhaustion + burnoutFA 73 -.02 AUCg
119i Mommersteeg et al 2006 NeuroticismAX 34 .04 AUCi
119j Mommersteeg et al 2006 NeuroticismAX 34 -.14 AUCg
119k Mommersteeg et al 2006 Neuroticism + burnoutAX 72 -.12 AUCi
119l Mommersteeg et al 2006 Neuroticism + burnoutAX 72 -.07 AUCg
120a Mossink et al 2015 Current-day negative affectAX 55 -.03 AINC
120b Mossink et al 2015 Current-day negative memory biasAX 55 -.23 AINC
120c Mossink et al 2015 Current-day positive affectPO 55 .07 AINC
120d Mossink et al 2015 Prior-day negative affectAX 55 .21 AINC
120e Mossink et al 2015 Prior-day negative memory biasGL 55 .04 AINC
120f Mossink et al 2015 Prior-day positive affectPO 55 -.16 AINC
120g Mossink et al 2015 Prior-day sadnessDE 55 .29 AINC
121 Moya-Albiol et al 2010 BurnoutFA 64 -.60 AINC
122 Nagy et al 2015 NightmaresGL 188 -.19 AUCg
123a Nelemans et al 2014 DepressionDE 184 .16 AUCg
123b Nelemans et al 2014 Generalized anxiety disorderAX 184 .08 AUCg
123c Nelemans et al 2014 Panic disorderAX 184 .13 AUCg
123d Nelemans et al 2014 Separation anxiety disorderAX 184 .19 AUCg
123e Nelemans et al 2014 Social anxiety disorderAX 184 .04 AUCg
124 Neu et al 2014 Life stressGL 52 -.16 AINC
125 Neylan et al 2005 PTSD symptomsPT 30 -.51 AUCg
126 Nicolson et al 2000 ExhaustionFA 59 .11 AINC
127 O'Donnell et al 2008 DepressionDE 542 -.03 AINC
128a O'Connor et al 2009 Educational attainmentPO 118 .21 AUCi
128b O'Connor et al 2009 Perceived stressGL 118 -.22 AUCi
129a Okamura et al 2011 Loneliness, weekendsGL 90 .20 AINC
129b Okamura et al 2011 Loneliness, workdaysGL 90 .00 AINC
130a Olsson et al 2010 Burnout (fatigue group)FA 36 .14 AUCg
130b Olsson et al 2010 Burnout (controls)FA 16 .07 AUCg
130c Olsson et al 2010 Depressive symptoms (fatigue group)DE 36 .08 AUCg
130d Olsson et al 2010 Depressive symptoms (controls)DE 16 -.10 AUCg
130e Olsson et al 2010 Stress-related fatigueFA 55 .35 AUCg
131 Ong et al 2011 Spousal lossGL 44 .09 AINC
132a Oosterholt et al 2015 Clinical burnoutFA 62 -.12 AINC
132b Oosterholt et al 2015 Clinical burnoutFA 62 -.30 AUCg
132c Oosterholt et al 2015 Non-clinical burnoutFA 59 -.16 AINC
132d Oosterholt et al 2015 Non-clinical burnoutFA 59 -.29 AUCg
133 Oskis et al 2011 Anxious attachmentAX 60 -.39 MINC
134a Oskis et al 2015 Active emotional support from motherPO 55 -.20 AINC
134b Oskis et al 2015 AngerGL 55 -.05 AINC
134c Oskis et al 2015 Confiding in motherPO 55 -.16 AINC
134d Oskis et al 2015 Constraints on closenessPT 55 .08 AINC
134e Oskis et al 2015 Fear of rejectionGL 55 -.37 AINC
134f Oskis et al 2015 Fear of separationGL 55 -.26 AINC
134g Oskis et al 2015 High desire for companyGL 55 -.20 AINC
134h Oskis et al 2015 MistrustGL 55 .23 AINC
135 Osterberg et al 2009 BurnoutFA 221 .02 AINC
136a Peng et al 2014 Dysfunctional attitudesGL 109 .09 AINC
136b Peng et al 2014 DepressionDE 109 -.10 AINC
136c Peng et al 2014 Childhood neglect (vs control)PT 51 .18 AINC
136d Peng et al 2014 Childhood neglect (continuous)PT 109 .26 AINC
136e Peng et al 2014 Depression + child neglect (vs. control)DE 57 .35 AUCi
136f Peng et al 2014 Depression w/o child neglect (vs. control)DE 59 -.34 AINC
137a Pinna et al 2014 Chronicity of abusePT 104 .09 AUCi
137b Pinna et al 2014 Chronicity of abusePT 104 -.26 AUCg
137c Pinna et al 2014 Comorbid PTSD and depressionDE 67 .02 AUCi
137d Pinna et al 2014 Comorbid PTSD and depressionDE 67 .32 AUCg
137e Pinna et al 2014 DepressionDE 104 .65 AUCi
137f Pinna et al 2014 DepressionDE 104 .07 AUCg
137g Pinna et al 2014 PTSDPT 104 .60 AUCi
137h Pinna et al 2014 PTSDPT 104 .29 AUCg
138a Platje et al 2013 AggressionGL 425 .10 AUCi
138b Platje et al 2013 AggressionGL 425 .04 AUCg
138c Platje et al 2013 Rule breakingGL 425 .12 AUCi
138d Platje et al 2013 Rule breakingGL 425 .10 AUCg
139a Polk et al 2005 State negative affectAX 301 -.04 AINC
139b Polk et al 2005 State positive affectPO 298 -.02 AINC
139c Polk et al 2005 Trait negative affect, malesAX 143 .27 AINC
139d Polk et al 2005 Trait negative affect, femalesAX 158 -.08 AINC
139e Polk et al 2005 Trait positive affectPO 298 -.08 AINC
140 Portella et al 2005 NeuroticismAX 30 .38 AUCi
141 Pruesnner et al 1999 Perceived stressGL 66 .07 ACOR
142a Pruessner et al 2003 Chronic stressAX 39 .31 AUCg
142b Pruessner et al 2003 Depressive symptomsDE 39 .30 AUCg
143a Quevedo et al 2012 Adolescent negative life eventsGL 159 .00 ACOR
143b Quevedo et al 2012 Adverse early-life rearingGL 159 -.20 ACOR
143c Quevedo et al 2012 Family negative life eventsGL 159 -.15 ACOR
144a Quirin et al 2008 Attachment anxietyAX 48 -.40 AINC
144b Quirin et al 2008 Self-esteemGL 48 -.21 AINC
144c Quirin et al 2008 Social stressGL 48 .22 AINC
145a Rademaker et al 2009 CooperativenessPO 107 .07 MINC
145b Rademaker et al 2009 CooperativenessPO 107 -.18 AUCg
145c Rademaker et al 2009 Harm avoidanceGL 107 .22 MINC
145d Rademaker et al 2009 Harm avoidanceGL 107 .24 AUCg
145e Rademaker et al 2009 Novelty seekingPO 107 .08 MINC
145f Rademaker et al 2009 Novelty seekingGL 107 .04 AUCg
145g Rademaker et al 2009 PersistencePO 107 .05 MINC
145h Rademaker et al 2009 PersistencePO 107 -.11 AUCg
145i Rademaker et al 2009 Reward dependenceGL 107 .15 MINC
145j Rademaker et al 2009 Reward dependenceGL 107 -.05 AUCg
145k Rademaker et al 2009 Self-directednessPO 107 .30 MINC
145l Rademaker et al 2009 Self-directednessPO 107 .10 AUCg
145m Rademaker et al 2009 Self-transcendencePO 107 .05 MINC
145n Rademaker et al 2009 Self-transcendencePO 107 .05 AUCg
146a Rane et al 2012 Caregiver burdenGL 33 .19 AUCi
146b Rane et al 2012 Caregiver distressGL 33 -.06 AUCi
146c Rane et al 2012 Caregiver stressGL 58 .00 AUCi
146d Rane et al 2012 CaregivingGL 58 -.29 AUGg
147a Ranjit etal 2009 High cynical hostility (vs. low) GL 936 -.01 AINC
147b Ranjit etal 2009 High cynical hostility (vs. mid) GL 936 .00 AINC
147c Ranjit etal 2009 Mid cynical hostility (vs. low) GL 936 -.01 AINC
148a Rhebergen et al 2015 Depression diagnosisDE 363 -.12 AUCi
148b Rhebergen et al 2015 Depression diagnosisDE 363 .05 AUCg
149a Rickenbach et al 2014 Daily stressGL 73 -.01 AINC
149b Rickenbach et al 2014 Depressed affectDE 73 -.11 AINC
149c Rickenbach et al 2014 Functional healthpo 73 .07 AINC
149d Rickenbach et al 2014 Life stressorsGL 73 .10 AINC
150 Roberts et al 2004 Chronic fatigueFA 91 -.20 AUCi
151a Rohleder et al 2004 PTSD symptomsPT 25 -.58 AUCg
151b Rohleder et al 2004 PTSD symptomsPT 25 -.40 MINC
152a Ruhe et al 2015 DepressionDE 111 -.02 AINC
152b Ruhe et al 2015 DepressionDE 111 -.08 AUCg
153 Ruiz-Robledillo et al 2013 Caregiving for offspring with AspergerGL 107 .21 AUCi
154a Ruiz-Robledillo et al 2014 Caregiver burden (non-supported)GL 12 -.59 AUCi
154b Ruiz-Robledillo et al 2014 Caregiver burden (supported)GL 12 .61 AUCi
154c Ruiz-Robledillo et al 2014 Institutional supportGL 36 .42 AUCi
155a Ruiz-Robledillo et al 2014 ResiliencePO 67 -.06 AUCi
155b Ruiz-Robledillo et al 2014 ResiliencePO 67 -.57 AUCg
156a Ruiz-Robledillo & Moya 2014 Caregiving burdenGL 68 .11 AUCi
156b Ruiz-Robledillo & Moya 2014 General mental healthPO 68 .23 AUCg
156c Ruiz-Robledillo & Moya 2014 Emotional intelligence attentionPO 68 -.09 AUCi
156d Ruiz-Robledillo & Moya 2014 Emotional intelligence attentionPO 68 .04 AUCg
156e Ruiz-Robledillo & Moya 2014 Emotional intelligence clarityPO 68 -.21 AUCi
156f Ruiz-Robledillo & Moya 2014 Emotional intelligence clarityPO 68 -.50 AUCg
156g Ruiz-Robledillo & Moya 2014 Emotional intelligence repairPO 68 .02 AUCi
156h Ruiz-Robledillo & Moya 2014 Emotional intelligence repairPO 68 -.32 AUCg
157a Saridjan et al 2014 ExternalizingGL 296 -.01 AINC
157b Saridjan et al 2014 InternalizingDE 295 -.07 AINC
158a Schlotz et al 2004 Chronic worryAX 219 .16 MINC
158b Schlotz et al 2004 Job stressJS 219 .16 MINC
159 Schulz et al 1998 Job stressJS 85 .29 ACOR
160a Shibuya et al 2014 AnxietyAX 18 .42 AINC
160b Shibuya et al 2014 ConfusionGL 18 .57 AINC
160c Shibuya et al 2014 DepressionDE 18 .47 AINC
160d Shibuya et al 2014 FatigueFA 18 .48 AINC
161a Sjögren et al 2006 DepressionDE 257 -.06 AINC
161b Sjögren et al 2006 ExhaustionFA 257 -.01 AINC
161c Sjögren et al 2006 HopelessnessDE 257 -.05 AINC
161d Sjögren et al 2006 Job stressJS 257 -.06 AINC
161e Sjögren et al 2006 Poor social supportGL 257 -.04 AINC
161f Sjögren et al 2006 Self-esteemPO 257 .08 AINC
161g Sjögren et al 2006 Well-beingPO 257 .06 AINC
162 Sjodin et al 2012 Noise annoyance at workJS 101 -.19 AINC
163 Sjors et al 2012 BurnoutFA 241 -.04 AINC
164a Sjors et al 2014 Work stressJS 180 -.01 AUCi
164b Sjors et al 2014 Work stressJS 180 -.02 AUCg
164c Sjors et al 2014 Overall stressGL 180 -.14 AUCi
164d Sjors et al 2014 Overall stressGL 180 -.13 AUCg
164e Sjors et al 2014 Home stressGL 180 -.12 AUCi
164f Sjors et al 2014 Home stressGL 180 -.20 AUCg
164g Sjors et al 2014 Home stress, malesGL 86 .00 AUCg
164h Sjors et al 2014 Home stress, femalesGL 94 -.23 AUCg
165 Sjors et al 2015 Exhaustion FA 220 -.15 AINC
166a Sladek et al 2015 Daily social connectionPO 71 .13 AINC
166b Sladek et al 2015 Depressive symptomsDE 71 -.17 AINC
166c Sladek et al 2015 LonelinessGL 71 -.23 AINC
167a Smeets et al 2007 Continuous sexual abuse memoryPT 15 .00 AUCi
167b Smeets et al 2007 Recovered sexual abuse memoryPT 16 .00 AUCi
167c Smeets et al 2007 Repressed sexual abuse memoryPT 17 .00 AUCi
168a Smyth et al 2015 Trait well-beingPO 44 -.19 AUCg
168b Smyth et al 2015 Trait well-beingPO 44 -.07 MINC
169a Sonnenschein et al 2007 General exhaustionFA 42 -.13 AUCi
169b Sonnenschein et al 2007 General exhaustionFA 42 .06 AUCg
169c Sonnenschein et al 2007 State exhaustionFA 42 -.37 AUCi
169d Sonnenschein et al 2007 State exhaustionFA 42 -.27 AUCg
170a Stafford et al 2013 Divorced status <3 yearsGL 2229 .00 AINC
170b Stafford et al 2013 Divorced status >3 yearsGL 2229 -.04 AINC
170c Stafford et al 2013 Long-term living aloneGL 2229 .00 AINC
170d Stafford et al 2013 Newly living aloneGL 2229 .00 AINC
170e Stafford et al 2013 Reduction in social networkGL 2229 .00 AINC
170f Stafford et al 2013 Single, never married statusGL 2229 .00 AINC
170g Stafford et al 2013 Small social networkGL 2229 .00 AINC
170h Stafford et al 2013 Widowed <3 yearsGL 2229 .00 AINC
170i Stafford et al 2013 Widowed >3 yearsGL 2229 .04 AINC
171a Stalder et al 2011 Difficulties in emotion regulationGL 43 .22 AUCi
171b Stalder et al 2011 Perceived stressGL 43 .29 AUCi
172 Stawski et al 2013 Frequent daily stressorsGL 1694 -.05 AUCg
173 Steinheuser et al 2014 Urban upbringingGL 116 -.18 ACOR
174a Steptoe et al 2004 Job stress (over-commitment), malesJS 83 .23 AINC
174b Steptoe et al 2004 Job stress (over-committment), malesJS 83 .12 AUCg
174c Steptoe et al 2004 Job stress (over-committment), femalesJS 81 .12 AINC
174d Steptoe et al 2004 Job stress (over-committment), femalesJS 81 .05 AUCg
175a Steptoe, Owen, et al 2004 LonelinessGL 163 .13 AINC
175b Steptoe, Owen, et al 2004 LonelinessGL 163 .14 AUCg
176a Steptoe et al 2005 Chronic economic stress, malesAX 88 .18 AINC
176b Steptoe et al 2005 Chronic economic stress, malesAX 88 .27 AUCg
176c Steptoe et al 2005 Chronic economic stress, femalesAX 72 .00 AINC
176d Steptoe et al 2005 Chronic economic stress, femalesAX 72 .28 AUCg
177a Steptoe et al 2007 State happinessPO 73 -.20 AUCi
177b Steptoe et al 2007 State happinessPO 73 -.36 AUCg
178 Stetler et al 2005 DepressionDE 69 -.47 AUCg
179a Strahler et al 2010 Somatic trait anxietyAX 17 -.04 AUCg
179b Strahler et al 2010 Trait worryAX 17 -.15 AUCg
180 Tang et al 2014 ShynessGL 24 -.29 ACOR
181a terWolbeek et al 2007 FatigueFA 132 .00 AINC
181b terWolbeek et al 2007 FatigueFA 132 .00 AUCg
182a Therrien et al 2007 Depression, malesDE 50 -.17 AINC
182b Therrien et al 2007 Depression, femalesDE 28 -.22 AINC
182c Therrien et al 2007 Trait anxiety, malesAX 50 -.22 AINC
182d Therrien et al 2007 Trait anxiety, femalesAX 28 -.42 AINC
183 Thomas et al 2012 CaregivingGL 45 -.21 AINC
184 Thorn et al 2011 Seasonal affective disorderDE 52 -.25 ACOR
185a Tomiyama et al 2014 Weight stigma consciousnessGL 42 .23 AINC
185b Tomiyama et al 2014 Weight stigma frequencyGL 41 .30 AINC
186 Tops et al 2008 Depressive moodDE 194 .14 AUCi
187 Tu et al 2013 DepressionDE 121 -.18 Slope
188 Ulrike et al 2013 DepressionDE 131 .08 ACOR
189a Vammen et al 2014 Depressive symptoms (2009 sample)DE 474 -.06 MINC
189b Vammen et al 2014 Depressive symptoms (2007 sample)DE 376 -.06 MINC
189c Vammen et al 2014 Clinical depression (2009 sample)DE 297 -.06 MINC
189d Vammen et al 2014 Clinical depression (2007 sample)DE 214 -.07 MINC
190a van Liempt et al 2013 Trauma with PTSDPT 24 -.15 AUCg
190b van Liempt et al 2013 Trauma without PTSDGL 29 .24 AUCg
191a van Santen et al 2011 AgreeablenessPO 337 .04 AUCi
191b van Santen et al 2011 AgreeablenessPO 337 .00 AUCg
191c van Santen et al 2011 Anxiety sensitivityAX 337 .07 AUCi
191d van Santen et al 2011 Anxiety sensitivityAX 337 .04 AUCg
191e van Santen et al 2011 ConscientiousnessPO 337 -.08 AUCi
191f van Santen et al 2011 ConscientiousnessPO 337 -.02 AUCg
191g van Santen et al 2011 ExtraversionPO 337 -.09 AUCi
191h van Santen et al 2011 ExtraversionPO 337 -.01 AUCg
191i van Santen et al 2011 MasteryPO 337 -.10 AUCi
191j van Santen et al 2011 MasteryPO 337 .01 AUCg
191k van Santen et al 2011 NeuroticismAX 337 .07 AUCi
191l van Santen et al 2011 NeuroticismAX 337 .08 AUCg
191m van Santen et al 2011 Openness to experiencePO 337 -.06 AUCi
191n van Santen et al 2011 Openness to experiencePO 337 -.04 AUCg
192a Vargas et al 2014 Anticipatory stressGL 58 .34 AINC
192b Vargas et al 2014 Previous day stressGL 58 -.17 AINC
193a Veen et al 2011 DepressionDE 118 .27 AINC
193b Veen et al 2011 DepressionDE 118 .09 AUCg
193c Veen et al 2011 AnxietyAX 118 .06 AINC
193d Veen et al 2011 AnxietyAX 118 .03 AUCg
193e Veen et al 2011 Comorbid depression & anxietyDE 118 .04 AINC
193f Veen et al 2011 Comorbid depression & anxietyDE 118 .10 AUCg
194a von Polier et al 2013 Callous unemotionalityGL 75 -.13 AUCg
194b von Polier et al 2013 HyperactivityGL 75 -.26 AUCg
195a Vreeburg et al 2009 Current MDD (vs. control)DE 1009 .04 AUCi
195b Vreeburg et al 2009 Current MDD (vs. control)DE 1009 .11 AUCg
195c Vreeburg et al 2009 Remitted MDD (vs. control)DE 887 .09 AUCi
195d Vreeburg et al 2009 Remitted MDD (vs. control)DE 887 .09 AUCg
196a Vreeburg, Zitman, et al 2010 Current anxiety disorderAX 1116 .05 AUCi
196b Vreeburg, Zitman, et al 2010 Current anxiety disorderAX 1116 .09 AUCg
196c Vreeburg, Zitman, et al 2010 Remitted anxiety disorderAX 653 .03 AUCi
196d Vreeburg, Zitman, et al 2010 Remitted anxiety disorderAX 653 .05 AUCg
197a Vreeburg et al 2010 Diagnosed parental depression historyDE 256 .13 AUCi
197b Vreeburg et al 2010 Diagnosed parental depression historyDE 256 .15 AUCg
197c Vreeburg et al 2010 Self-reported parental depression historyDE 303 .05 AUCi
197d Vreeburg et al 2010 Self-reported parental depression historyDE 303 .01 AUCg
198 Wahbeh et al 2008 Caregiver stressGL 30 .31 AINC
199 Wahbeh et al 2013 PTSD (vs. control)PT 71 -.12 AINC
200 Walker et al 2011 Trait anxietyAX 40 -.35 AUCg
201a Wardenaar et al 2011 Anhedonic depressionDE 1029 .02 AUCi
201b Wardenaar et al 2011 Anhedonic depressionDE 1029 .02 AUCg
201c Wardenaar et al 2011 Anxious arousalAX 1029 .02 AUCi
201d Wardenaar et al 2011 Anxious arousalAX 1029 .02 AUCg
201e Wardenaar et al 2011 General distressGL 1029 .04 AUCi
201f Wardenaar et al 2011 General distressGL 1029 .04 AUCg
202a Weekes et al 2008 Examination stress, malesGL 31 .00 ACOR
202b Weekes et al 2008 Examination stress, femalesGL 35 .51 ACOR
203 Weik et al 2010 Exam stressGL 24 -.19 AINC
204 Wessa et al 2006 PTSD symptomsPT 63 -.38 AUCg
205a Wilcox et al 2014 DepressionDE 460 .00 AUCi
205b Wilcox et al 2014 Quality of lifePO 460 .00 AUCi
206a Williams et al 2013 Family functioning (aff. involvement), momPO 27 .00 Slope
206b Williams et al 2013 Family functioning (aff. involvement), childPO 27 .00 Slope
206c Williams et al 2013 Family functioning (aff. responses), momPO 27 .00 Slope
206d Williams et al 2013 Family functioning (aff. responses), childPO 27 .00 Slope
206e Williams et al 2013 Family functioning (behavior control), momGL 27 .00 Slope
206f Williams et al 2013 Family functioning (behavior control), childGL 27 .00 Slope
206g Williams et al 2013 Family functioning (communication), childPO 27 .00 Slope
206h Williams et al 2013 Family functioning (communication), momPO 27 .49 Slope
206i Williams et al 2013 Family functioning (problem solving), momPO 27 .00 Slope
206j Williams et al 2013 Family functioning (problem solving), childPO 27 .00 Slope
206k Williams et al 2013 Family functioning (roles), momPO 27 .00 Slope
206l Williams et al 2013 Family functioning (roles), childPO 27 .41 Slope
207a Wirth et al 2011 Depressive symptomsDE 123 .09 AUCi
207b Wirth et al 2011 Depressive symptomsDE 123 .01 AUCg
207c Wirth et al 2011 Shift workJS 123 .05 AUCi
207d Wirth et al 2011 Shift workJS 123 -.07 AUCg
208a Wolfram et al 2013 BurnoutFA 21 .31 AUCg
208b Wolfram et al 2013 DepersonalizationJS 21 .40 AUCg
208c Wolfram et al 2013 Effort-reward imbalanceJS 21 .31 AUCg
208d Wolfram et al 2013 Emotional exhaustionFA 21 .22 AUCg
208e Wolfram et al 2013 Lack of accomplishmentJS 21 .15 AUCg
208f Wolfram et al 2013 Over-committmentJS 21 .02 AUCg
209a Wright et al 2005 Financial strainGL 76 .17 AINC
209b Wright et al 2005 Financial strainGL 76 .13 AUCg
210a Wüst et al 2000 Chronic worryAX 102 .17 ACOR
210b Wüst et al 2000 Job stress (overload)JS 102 .00 ACOR
210c Wüst et al 2000 Job stress (discontent)JS 102 .00 ACOR
210d Wüst et al 2000 Lack of social recognitionGL 102 .22 ACOR
210e Wüst et al 2000 Social stressGL 102 .21 ACOR
210f Wüst et al 2000 Self-efficacyPO 104 -.19 MINC
210g Wüst et al 2000 Self-efficacyPO 104 -.06 AUCg
210h Wüst et al 2000 Self-esteemPO 104 -.16 MINC
210i Wüst et al 2000 Self-esteemPO 104 -.01 AUCg
211a Zeiders et al 2012 AcculturationPO 100 .15 AINC
211b Zeiders et al 2012 Daily life stressGL 100 .12 AINC
211c Zeiders et al 2012 MDD symptomsDE 100 .04 AINC
211d Zeiders et al 2012 Family incomePO 100 .07 AINC
211e Zeiders et al 2012 Life stressorsGL 100 .13 AINC
211f Zeiders et al 2012 Perceived discriminationGL 100 .13 AINC
212 Zoccola et al 2011 Trait perseverative cognitionAX 119 .03 AINC

Notes: Italicized findings indicate that they were drawn from the Chida & Steptoe (2009) meta-analysis. Bolded findings indicate that they were included in p-curves for their respective sets.

Abbreviations: N = sample size, r = correlation; ADHD = Attention deficit hyperactivity disorder; CD = conduct disorder; DC = demand/control; ERI = effort/reward imbalance; MDD = major depressive disorder; ODD = oppositional defiant disorder; PTSD = posttraumatic stress disorder

*

Abbreviations for outcome type superscripts JS = job stress, GL = general life stress; DE = depression; AX = anxiety/neuroticism/negative affect, FA = fatigue/burnout/exhaustion, PT = posttraumatic stress, and PO = positive psychosocial traits

±

Abbreviations for measure: CARi was assessed using the following methods: Absolute increase of cortisol during the waking period (AINC), area of cortisol increase under the curve (AUCi), the mean value of cortisol values post-awakening minus wakening value (MINC), absolute value post-awakening evaluated by repeated analysis of variables (ACOR), slope of cortisol increase (slope), and ratio of cortisol at time 1 divided by cortisol at time 0 (T1/T0). AUCw was assessed using the following methods: area under the curve relative to ground (AUCg) and 30-minute absolute cortisol value (30min).

Findings Associating Worse Psychosocial Functioning with Higher CARi

P-curve analysis revealed that the findings associating worse psychosocial functioning with higher CARi had evidential value (k = 37; p = .001; see Figure 2a). The p-curve-derived estimate of effect size for this set of findings was r = .08. When using traditional meta-analytic techniques (n = 273), the overall effect size was r = .09, CI = [0.08, 0.11], p < .001. Approximately 37% of the significant findings in this set involved general life stress, 15% depression, 14% anxiety/neuroticism/negative affect, 12% positive psychosocial traits, 11% job stress, 8% posttraumatic stress, and 3% fatigue/burnout/exhaustion.

Figure 2. P-curves of Findings Relating the CAR to Psychosocial Functioning.

Figure 2

Figure 2

Figure 2

Figure 2

Worse psychosocial functioning with higher CARi

Worse psychosocial functioning with lower CARi

W orse psychosocial functioning with higher AUCw

Worse psychosocial functioning with lower AUCw

Notes: To compute p-curves, directionality for all predictors was changed so that higher values reflected worse psychosocial functioning. To test for evidential value, the p-curve calculator compares observed p-values to p-values that would be obtained if the null were true (i.e., a null hypothesis of zero effect, as shown with the red line). The blue line shows the observed p-curve from significant p-values. If studies contain evidential value, the blue line will be right-skewed. Flat blue lines (neither right nor left skewed) indicate that findings lack evidential value or are underpowered to detect evidential value. These alternatives are differentiated by testing the set of findings against a null of 33%, shown in the green line. For detailed explanation of p-curves, see Simonsohn et al., 2014.

Evidential Value of Findings Associating Worse Psychosocial Functioning to Lower CARi

P-curve analysis revealed that the findings associating worse psychosocial functioning with lower CARi also had evidential value (k = 42; p < .001; see Figure 2b). The p-curve-derived estimate of effect size for this set of findings was r = .09. When using traditional meta-analytic techniques (n = 275), the overall effect size was r =.12, CI = [0.10, 0.15], p < .001. Approximately 33% of the significant findings in this set involved general life stress, 23% positive psychosocial traits, 17% depression, 9% anxiety/neuroticism/negative affect, 7% posttraumatic stress, 6% fatigue/burnout/exhaustion, and 5% job stress.

Findings Associating Worse Psychosocial Functioning with Higher AUCw

Similar to CARi findings, p-curve analysis revealed that the findings associating worse psychosocial functioning with higher AUCw had evidential value (k = 19; p = .008; see Figure 2c). The p-curve-derived estimate of effect size for this set of findings was r = .09. When using traditional meta-analytic techniques (n = 120), the overall effect size was r = .08, CI = [0.07, 0.10], p < .001. Approximately 24% of the significant findings in this set involved depression, 19% general life stress, 17% positive psychosocial traits, 16% anxiety/neuroticism/negative affect, 12% job stress, 7% fatigue/burnout/exhaustion, and 5% posttraumatic stress.

Findings Associating Worse Psychosocial Functioning with Lower AUCw

Finally, p-curve analysis revealed that the findings associating worse psychosocial functioning with lower AUCw had evidential value (k = 19; p = .006; see Figure 2d). The p-curve-derived estimate of effect size for this set of findings was r = .19. When using traditional meta-analytic techniques (n = 87), the overall effect size was r = .10, CI = [0.08, 0.13], p < .001. Approximately 22% of the significant findings in this set involved general life stress, 18% positive psychosocial traits, 16% anxiety/neuroticism/negative affect, 14% posttraumatic stress, 11% job stress, 10% depression, and 9% fatigue/burnout/exhaustion.

Predictor-Specific Effects

P-curves and meta-analyses were conducted to describe the evidential value and directionality of the relationships among specific psychosocial predictors and CARi. Results from p-curve and meta-analysis did not corroborate. Results from p-curve analysis suggest stronger evidential value for findings associating general life stress, depression, and posttraumatic stress with CARi. However, using meta-analytic estimates, the fatigue/burnout/exhaustion predictors were most strongly associated with a lower CARi (r = .09, p = .003; Table 2), although there was a trend-level indication of publication bias (Egger's test: p = .07). Meta-analyses did not find significant results for any other predictor, but p-curve analyses could not conclude that evidential value for these other predictors was lacking; it may be that true effects exist but that the current study was underpowered to detect them. Table 3 and Figure 3 present p-curve and meta-analytic results of the seven predictors and CARi.

Table 3.

P-curve Estimates and Mean Effect Sizes by Predictor Type for CARi.

P-curve Meta-Analysis

Predictor Type k Evidential Value Present? Evidential Value Absent?± k r CI p Heterogeneity p
(1) Job stress 6 No, p=.06 No, p=.73 41 .03 -0.004 to 0.07 .08 <.001
(2) General life stress 35 Yes, p=.005 - 181 .005 -0.01 to 0.02 .57 <.001
(3) Depression or hopelessness 18 Yes, p=.26 No, p=.88 81 -.01 -0.08 to 0.06 .79 <.001
(4) Anxiety, neuroticism, or negative affect 16 No, p=.09 No, p=.63 59 .03 -0.01 to 0.07 .13 <.001
(5) Fatigue, burnout, or exhaustion 6 No, p=.21 No, p=.71 22 -.09 -0.15 to -0.03 .003 <.001
(6) Posttraumatic stress 11 Yes, p=.003 - 39 .01 -0.04 to 0.06 .63 <.001
(7) Positive psychosocial traits 10 No, p=.68 No, p=.84 88 -.004 -0.029 to 0.02 .75 .001

Notes:

±

Test against evidential value is only reported if no evidential value is present

Aggregate effect sizes that are significantly different from zero are highlighted in bold.

P-Curves that indicate evidential value are italicized

Figure 3. Combined Effect Sizes by Predictor Type.

Figure 3

Notes: Forest plot displays predictor-specific associations with both CARi and AUCw. For each association, the aggregate effect size r is shown with its 95% confidence interval. Solid diamonds represent the aggregate effects in relation to zero and the size of the diamonds is proportional to the variance of the combined effect size from the random-effects meta-analysis. Aggregate effects that are significantly different from zero (CIs do not overlap with zero) are highlighted in bold font in the left column.

With regard to AUCw, both p-curve and meta-analysis results revealed that depression predictors had evidential value and were linked to greater AUCw output (r = .07, p < .001, Table 4). Posttraumatic stress predictors also contained evidential value and were associated with lower AUCw output (r = .08, p = .03, Table 4). There was no evidence of publication bias for the meta-analysis regarding depression predictors (Egger' test: p = .56), however, there was a trend suggesting publication bias for studies reporting associations of posttraumatic stress (Egger's test: p = .06). P-curve analyses were not able to establish lack of evidential value for any of the seven predictors, again leaving open the possibility that true effects exist but that the current study was underpowered to detect them. Figure 3 reveals forest plots for the predictor-specific associations with both CARi and AUCw.

Table 4.

P-curve Estimates and Mean effect sizes by predictor type for AUCw.

P-curve Meta-Analysis

Predictor Type k Evidential Value Present? Evidential Value Absent?± k r CI p Heterogeneity p
(1) Job stress 3 No, p=.56 No, p=.32 23 .02 -0.03 to 0.06 .44 .023
(2) General life stress 8 No, p=.64 No, p=.10 40 -.01 -0.04 to 0.02 .51 <.001
(3) Depression or hopelessness 8 Yes, p<.001 - 37 .07 0.04 to 0.10 <.001 <.001
(4) Anxiety, neuroticism, or negative affect 6 Yes, p=.02 - 32 .03 -0.01 to 0.07 .15 <.001
(5) Fatigue, burnout, or exhaustion 4 No, p=.45 No, p=.57 15 -.01 -0.12 to 0.10 .82 .01
(6) Posttraumatic stress 11 Yes, p=.002 - 17 -.08 -0.15 to -0.01 .03 <.001
(7) Positive psychosocial traits 6 Yes, p<.001 - 34 -.05 -0.10 to 0.00 .05 <.001

Notes:

±

Test against evidential value is only reported if no evidential value is present;

Aggregate effect sizes that are significantly different from zero are highlighted in bold.

P-Curves that indicate evidential value are italicized

Quality of the Study as a Potential Source of Variance

Analysis of variance (ANOVA) was conducted to test if different sets of findings differed in study quality. There was no difference in mean study quality among those findings associating worse psychosocial functioning to higher CARi (M = 6.00, SD = 1.70), lower CARi (M = 6.08, SD = 1.73), higher AUCw (M = 6.14, SD = 1.49), or lower AUCw (M = 6.38, SD = 1.20), F (3,203) = 0.25, p = .83. Additionally, neither of the seven predictor types significantly differed from each other in study quality, F (6, 693) = 0.87, p = .52.

Discussion

Psychosocial predictors are thought to influence the CAR, but describing the nature of these associations has proven difficult because of heterogeneity in the literature. This heterogeneity is partially the result of methodological and operationalization inconsistencies across studies and potential measure-dependent and/or predictor-specific associations (Chida & Steptoe, 2009; Stadler et al., 2016). Meta-analysis has attempted to clarify the nature of the relationships between psychosocial predictors and the CAR, but meta-analyses can be biased by Type 1 error. P-curve analysis tests whether a set of findings in the published literature contains evidential value (Simonsohn et al., 2014a, 2014b, 2015), making p-curves an ideal complement to meta-analysis. Together, p-curves and meta-analysis can describe the evidential value of a set of findings and provide an estimate of the effect size of those findings.

The present study aimed to combine p-curve and meta-analytic techniques to answer four questions in the literature of psychosocial predictors and the CAR: first, did findings associating psychosocial functioning to higher or lower CAR differ in evidential value? Second, what was the effect size for these sets of findings? Third, was there any evidence for systematic bias in the literature? Fourth, did some psychosocial predictors demonstrate greater evidential value than others?

Evidential Value of Findings Associating Psychosocial Predictors to the CAR

The co-existence of positive and negative association between psychosocial predictors and the CAR could be explained in one of three potential ways: 1) there is no true relationship, and both the positive and negative associations are spurious; 2) there is either a positive or negative relationship between psychosocial predictors and the CAR, and the other direction is spurious; or 3) there are true positive and negative associations between psychosocial predictors and the CAR, and neither set is spurious. The current study independently examined the evidential value of four sets of findings: those associating worse psychosocial functioning to higher or lower CARi, and those associating worse psychosocial functioning to higher or lower AUCw. Results revealed that all four sets of findings demonstrated significant evidential value (scenario 3 above). Although seemingly contradictory, these results suggest that there are likely important moderators that explain which predictors are associated with what measures, and for whom. In other endocrinological outcomes like diurnal cortisol, stressor-dependent factors like the duration, intensity, and appraisal of the stressor are known to moderate biological responses (e.g., Armario, Marti, Molina, De Pable, & Valdes, 1996; Burke, Dacis, Otte, & Mohrn, 2005; Segerstom & Miller, 2004), and they likely play a role in the CAR as well. Unfortunately, the current study was underpowered to detect such individual difference- or stressor-dependent effects: there are not enough findings in the extant literature, nor is there a theoretical framework for making predictions about moderation. Analysis revealed that study quality among different CAR measures and different predictor types was similar, suggesting that the methodological inconsistencies are not systematically biasing the literature in any predictable way. Future work aimed at identifying moderators of the psychosocial functioning and CAR relationship is essential, as the current lack of empirically-supported theory in this area represents perhaps the greatest shortcoming in the CAR literature.

Effect Sizes of Findings Associating Psychosocial Predictors to the CAR, and Implications for Power Analysis

Despite all four sets of findings demonstrating significant evidential value, the estimate of p-curve-derived effect sizes across the four sets was not equivalent. Effect sizes for each of the four sets of findings were calculated in two ways: using p-curve-derived estimates and using traditional meta-analytic techniques. Corroboration of these two methods was high. The associations between psychosocial predictors and CARi were small, with psychosocial predictors explaining approximately 1% of variance in CARi (r = .08 for higher CARi and .11 for lower CARi using p-curve-derived estimate, r = .09 and .12 for meta-analytic estimates, respectively). These small effects were similar to those reported by Chida and Steptoe (2009), with r's ranging from -.065 to .069 depending on the specific predictor.

For findings examining total cortisol output, those associating worse psychosocial functioning to greater AUCw has a similar effect size (r = .09 from the p-curve-derived estimate and .08 from the meta-analytic estimate). However, findings associating worse psychosocial functioning to lower AUCw had a larger effect, with approximately 3.6% of variance being accounted for (r = .19 from the p-curve-derived estimate and .10 from the meta-analytic estimate). To the extent that the p-curve-derived estimate can be considered a less biased measure for gauging effect size, this finding suggests that total cortisol output during the waking period is more heavily affected by psychosocial predictors than is the dynamic increase that occurs after awakening. It may be that worse psychosocial functioning over time blunts the overall output of the CAR system while keeping the dynamic component intact. If indeed the CARi represents an adaptive response to stressors, this may be the most adaptive pattern for those high in psychosocial stress: it would allow them to maintain dynamic flexibility in the CAR system without having chronically high levels of cortisol output overall. Nevertheless, this explanation remains speculative and remains to be tested with future research.

One implication of these estimates is that regardless of CAR measure, future studies should be powered to detect small effects (r = .10). Using two publicly-available power calculators (GPower and the UCSF Clinical and Translation Science Institute Sample Size Calculator [http://www.sample-size.net/correlation-sample-size/]), a cross-sectional study would need a minimum sample size of 617-783 to detect true effects with 80% power. In the current study, approximately 11% of the studies had at least this sample size; approximately 58% had a sample size less than 100, and 28% had a sample size less than 50. Although obtaining over 600 people for a study may seem unfeasible or prohibitively expensive, there are also substantial costs to running underpowered studies. On one hand, underpowered studies may fail to find significant effects when in reality they exist; in those instances, the resources spent for that study are lost and Type II error appears in the literature or, more likely, contribute to the file drawer problem. On the other hand, correlations obtained with small sample sizes are unstable and can result in Type I error. As a result, running underpowered studies can significantly contribute to the current replicability crisis in psychology; running adequately powered studies presents a costly but feasible and scientifically rigorous solution. Thus, future work with larger samples is needed to help clarify the relationships between psychosocial predictors and the CAR.

The small effect sizes also beg the question of clinical significance: are these effects meaningful in the real world? Prentice and Miller (1992) argue that small effects are impressive when the dependent variable is not expected to be easily influenced by the independent variable. The fact that psychosocial events - even those that are imagined, anticipated, or long-passed - can produce reliable shifts in a physiological system associated with energy mobilization is meaningful. It suggests that the CAR may promote adaptive physiological responses to complex social stimuli, and may have implications for when, how, and why the CAR evolved (for a review of the functions of the CAR, see Fries, Dettenborn, & Kirschbaum, 2009). Moreover, small effects of psychosocial variables on other endocrinological and immunological outcomes are found in the literature, yet these lines of study remain active because psychosocial stressors are common enough that even small effects, if they occur frequently enough and for long enough, can produce a sizeable impact on physiology. For example, diurnal cortisol levels demonstrate small to moderate correlations with depression (r = .18; Burke et al., 2005) and chronic stress (Miller, Chen, and Zhou, 2007), and these relationships depend on a number of measurement, appraisal, and contextual variables (Miller, Chen, and Zhou, 2007). Likewise, some enumerative measures of immune functioning like monocyte counts, T-lymphocyte counts, and granulocyte counts have small to moderate correlations (r's < .10) with acute time-limited stress and chronic stress, although correlations are larger for other measueres of immunity like immunoglobulin and cytokine levels (r's between .10 and .30; Segerstrom & Miller, 2004). Thus, in the greater context of psychoneuroendocrinological research, the CAR may not be the most sensitive biological marker for chronic stress, but still sensitive enough that continuing to study the relationships is a worthwhile endeavor.

Future studies investigating the CAR and psychosocial functioning should sample the CAR over more days. The modal number of sampling days in the studies reviewed was one (range = 1 to 9). As is true for other diurnal cortisol parameters (Segerstrom et al., 2014), the amount of variance in the CAR that generalizes beyond the day on which it was collected is small (36-60% for AUC [baseline, 30, 45, and 60 minutes]; 15-37% for increase; Hellhammer et al., 2007.) As a consequence, reliable measurement of the CAR can require sampling over up to 6 days (Hellhammer et al., 2007). Notably, there were too few studies with a sufficient number of days to compare the p-curves of those with theoretically insufficient and sufficient sampling frames for reliability, and almost none of the studies reported the empirical reliability of their CAR measurement. Future research on the CAR should be evaluated in light of the reliability of cortisol measurement, particularly because unreliable measurement can yield estimates of relationships that are incorrect in both magnitude (e.g., an estimate is either larger or smaller than the true underlying relationship) and sign (e.g., a positive estimate is obtained when the true underlying relationship is negative) (Gelman & Carlin, 2014). When effect sizes are small, reliable measurement is also important to maintain statistical power (Kanyongo, Brook, Kyei-Blankson, & Gocmen, 2007).

Testing for Systematic Bias in the Literature

Systematic bias in the literature occurs when there are publishing practices that make some findings (i.e., significant findings) more likely to make their way into the published literature than others. Because p-curve calculations use only published significant effects, comparing estimates of effect sizes between p-curves and standard meta-analysis can highlight systematic bias. As discussed above, the only discrepancy betweet p-curve-derived estimates and meta-analytic estimates was in the set associating worse psychosocial functioning to lower AUCw. However, the directionality of the discrepancy suggests that the published literature is systematically underestimating the true effects (i.e., the p-curve estimate is larger than the meta-analysis estimate). It should be noted that this set had a relatively small number of independent, statistically significant findings (k = 19). Future work should examine associations of psychosocial predictors and AUCw using large samples so that more precise estimates of these associations can be calculated. Aside from this notable exception, the high corroboration between p-curve and meta-analytic estimates suggests a lack of systematic bias in the literature. This is corroborated by the fact that Egger's test of publication bias in the meta-analytic estimates were nonsignificant for both CARi and AUCw.

A second cause of systematic bias is introduced by researchers who engage in questionable research practices (QRPs; Simmons et al., 2011). One particularly common QRP is p-hacking, where researchers perform unplanned post-hoc analyses to reduce the p-value of a hypothesized relationship to below the .05 cutoff. Examples of p-hacking include adding covariates atheoretically, selectively removing outliers, or performing analyses on a subset of the population, among other strategies. In most cases, researchers will p-hack until the p-value falls to just under .05. If a set of findings contains a substantial number of p-hacked findings, the p-curve for that set of findings will contain more p-values in the .04 - .05 bin than any other bin, and will be right-skewed.

A visual analysis of the four sets of p-curves in the current study reveals that they were all left-skewed (see Firgure 2), suggesting that p-hacking is not biasing the CAR literature. Thus, despite the recent controversies surrounding questionable research practices in psychology and other disciplines, evidence from this study suggests that the associations of psychosocial functioning and the CAR represent true effects with evidential value. This is particularly refreshing news because the potential for researchers to engage in p-hacking and other questionable research practices is high in CAR research, as there are a number of design decisions, analytical techniques, and ambiguities with operational definitions which can be modified post-hoc. Adherence to guidelines (Stadler et al., 2016) will ensure that the field continues moving in the current direction of honest, reliable science.

Predictor-Specific Effects

A secondary aim of the current study was to examine whether specific categories of psychosocial predictors were associated with CARi or AUCw. Of the seven categories previously defined by Chida and Steptoe (2009), it was found that only fatigue/burnout/exhaustion was negatively correlated with CARi. This corroborates meta-analytic results from Chida and Steptoe (2009). It may be that fatigue takes a physiological toll on the body's ability to respond dynamically. Alternatively, under conditions of fatigue, the body may attempt to conserve resources in anticipation of anticipated challenges (Evans, Boggero, & Segerstrom, 2016). The other six categories had nonsignificant effects. However, p-curve analysis testing against evidential value were non-significant in all cases, suggesting that the extant literature is underpowered to detect effects if they exist.

AUCw was positively associated with depression but negatively associated with PTSD. As with CARi, the other associations were not statistically significant, but p-curves could not rule out the possibility that they contain evidential value. Despite not being statistically significant, the direction of the correlations revealed that job stress and anxiety/neuroticism/negative affect were positively correlated with CARi and AUCw, whereas general life stress and positive psychosocial traits were negatively correlated with CARi and AUCw. These trends highlight the possibility that future-oriented predictors like anxiety and job stress, where there is an anticipation of future negative events, may be associated with increased CAR, but this observation is speculative and should be corroborated by future research.

Limitations

The current study is not without limitations. First, the articles and findings reported in the current study were all from the published literature; poster abstracts, conference proceedings, and unpublished data were not included. The p-curves could test for the presence of systematic bias in the literature. A full examination of the true, unbiased estimates of CAR in published and unpublished findings was beyond the scope or aims of the study. Nevertheless, the inclusion of only published studies should be taken into consideration when interpreting the findings; it may be that the true CAR effects are smaller than those reported in the current study. A second limitation is that the study only tested bivariate correlations among psychosocial predictors and levels of CARi and AUCw, but other more dynamic measures of the CAR are possible. For example, some have argued that the flexibility of the CAR rather than its magnitude is more strongly linked to psychosocial predictors (Mikolajczak et al., 2010). A third limitation is that the current study only examined linear effects, despite some studies describing quadratic effects (Gustafsson et al., 2010). A fourth limitation is that alternate conceptualizations of psychosocial predictors besides the seven categories reported are possible. Some of the seven categories are theoretically ambiguous and frequently co-occur in the real world (e.g., depression and anxiety). Nevertheless, solid theoretical scaffolding exists for the seven categories, and in an attempt to build upon the scaffolding, the same categories were retained. A fifth limitation is that the time window of psycholosocial predictors was not assessed. Questionnaires that ask about lifetime history of depressive symptoms, for example, may have different relations to the CAR than those that ask about depressive symptoms in the last two weeks, or even in the last 24 hours. Theoretical advances in predicting the time window that would be most meaningfully related to the CAR remains an important area for future research; it is possible that these associations will be predictor-specific. Finally, a limitation of the current study is that it used strict inclusion criteria of healthy participants and as such, results cannot generalize to medically compromised populations.

Despite these limitations, the study has several significant strengths. First, it provides a concrete example of how p-curves and meta-analysis can complement each other to shed light on situations where there appears to be a “tale of two literatures.” Second, the current study presents the most complete analysis of the literature on psychosocial functioning and CAR to date – a literature that has more than doubled within the last six years and will probably continue to expand. Third, the current study provides specific goals for future research in the area of theory development, and provides concrete recommendations for the power of future studies. It addresses concrete strategies that could help to increase the replicability of CAR findings.

Conclusion

In conclusion, psychosocial functioning is known to influence the CAR. The current study found that the largest evidential value existed for findings associating worse psychosocial functioning with lower AUCw. Findings associating depression, posttraumatic stress, anxiety, and fatigue demonstrated evidential value, and evidential value could not be ruled out for other psychosical predictors. Moving forward, theoretical developments regarding why some predictors but not others are associated with some measures of CAR but not others remains an important question – perhaps the most important question. To answer this question, more adequately powered, methodologically rigorous studies are needed. Recently published guidelines provide concrete and clear recommendations for researchers (Stadler et al., 2016), and results from the current study suggest that large samples are needed to minimize the likelihood that Type I and II error rates make their way into the literature. Nevertheless, the current study finds reliable evidence that psychosocial functioning influence the CAR, and provides the most thorough estimate of effect sizes by predictor and CAR measure to date. Future exploration of these associations may lead to meaningful insights regarding the effects of psychosocial functioning on human stress physiology.

Highlights.

  • Psychosocial predictors explained 1%-3.6% of variance in CAR responses

  • Depression was linked to higher AUCw and posttraumatic stress to lower AUCw

  • Inconclusive results were obtained for predictor-specific effects on CARi

  • Cross-sectional studies of CAR need Ns of 617-783 to detect effects with 80% power

  • There were no indications of questionable research practices biasing the CAR literature

Acknowledgments

The authors would like to thank Tim Bogg, Nienke Bosch, Joaquín Cabrera, Lea Doughterty, Kimberly Dienes, Andrea Dietrich, Nanna Eller, Romano Endrighi, Gloria Garcia-Banda, Meena Kumari, Lindsay Hoyt, Brian Lovell, Andrea Oskis, Michael Sladek, Richard Slatcher, Robert Stawski, and Michael Wirth for providing additional requested data. The authors would also like to thank Uri Simonsohn and Andrew Steptoe for providing requested statistical and methodological help. Finally, the authors would like to thank Greg Miller for his helpful comments throughout the project and on earlier versions of the manuscript.

Research reported in this publication was supported by the National Institute on Aging of the National Institutes of Health (F31-AG048692, K02-AG033629). The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.

Footnotes

NOTE: * = included in the Chida & Steptoe (2009) meta-analysis; ** = added for current meta-analysis

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