Current Posttraumatic Stress Symptoms Mediate the Relationship Between Adverse Childhood Experiences and Executive Functions

Abstract

Adverse childhood experiences (ACEs) and posttraumatic stress disorder (PTSD) are both associated with lower performances on executive function tasks. However, few researchers have evaluated ACEs, posttraumatic stress (PTS) symptoms, and executive function difficulties in conjunction. Using an online micropayment service, the current study assessed whether PTS symptoms mediated the relationship between ACEs and executive functions. In total, 83 participants (54.2% female, age: M = 28.86, SD = 7.71) were administered the ACE questionnaire, PTSD Checklist for DSM-5 (PCL-5), and the Executive Function Index (EFI). A higher number of reported ACEs was related to greater PTS symptom severity (β = .40, p < .001) and worse self-rated executive functions (β = –.32, p = .002). Controlling for the number of reported ACEs, current PTS symptom severity was related to worse executive functions (β = –.45, p < .001). A bootstrapped 95% confidence interval (CI) indicated a significant indirect effect, β = –.18 (95% CI: –.30, –.08), by which current PTS symptoms mediated the relationship between the number of reported ACEs and executive functions. These results suggest that psychological interventions targeting PTS symptoms, in the context of a history of childhood trauma, may concurrently improve executive functions in adult populations.

Keywords

Executive function adverse childhood experiences ACE trauma and stressor related disorders PTSD posttraumatic stress symptoms

Introduction

Adverse Childhood Experiences (ACEs) describe a variety of traumatic events, troubling experiences, and difficult life circumstances, including physical, sexual, or emotional abuse, physical or emotional neglect, witnessing domestic violence, parental divorce or separation, parental mental illness, substance abuse, and the incarceration of a family member (Felitti et al., 1998). Exposure to these experiences has been associated with detrimental effects on physiological health, as well as psychological, social and cognitive development in both children and adults (Felitti et al., 1998; Kalmakis & Chandler, 2015; Lansford et al., 2002; Monnat & Chandler, 2015; Nurius et al., 2015). Research has demonstrated that self-esteem, emotional regulation, attachment, peer relationships, and school preparedness are some of the domains negatively impacted by ACEs (Arata et al., 2005; Cicchetti & Rogosch, 2002; Cicchetti & Valentino, 2006; Kim & Cicchetti, 2004). Furthermore, individuals exposed to ACEs have an increased risk of mental health concerns across the lifespan, including depression, anxiety, aggression, social withdrawal, suicidality, and posttraumatic stress disorder (PTSD; Anderson et al., 2002; De Bellis, 2001; Felitti et al., 1998; Lansford et al., 2002; Moore et al., 2013; Nurius et al., 2015). Among the mental health concerns linked to ACEs, PTSD and posttraumatic stress (PTS) symptoms are most relevant to the current investigation. This is, in part, due to the high frequency and risk of individuals developing PTS or PTSD after exposure to ACEs (Cougle et al., 2010; De Bellis et al., 2009; Koenen & Widom, 2009).

Association between ACEs and PTS symptoms

PTSD is an illness in which exposure to one or more traumatic events leads to the onset of various clusters of psychiatric symptoms. Commonly referred to as PTS symptoms, these clusters capture intrusive thoughts, persistent avoidance of PTS stimuli, negative changes in mood and cognitions, and altered arousal and reactivity (American Psychiatric Association, 2013). A myriad of research has confirmed the association between ACEs and one or more PTS symptom clusters (Cloitre et al., 2009; Dvir et al., 2014; Herman, 1992; Sullivan et al., 2006), but many individuals exposed to ACEs do not meet diagnostic criteria for PTSD. Notably, ACEs are not always classified as Criterion A traumatic events (i.e., exposure to death, threatened death, or serious injury) – a requirement for PTSD diagnosis (American Psychiatric Association, 2013). A discussion of the debate surrounding the utility of Criterion A for PTSD diagnosis is beyond the scope of this paper (see Rosen et al., 2008; Rosen & Lilienfeld, 2008); however, even in the absence of a PTSD diagnosis, individuals with a history of ACEs are at a heightened risk for developing PTS symptoms across the lifespan. Exposure to ACEs also increases the likelihood of a future PTSD diagnosis following a traumatic event (Koenen et al., 2007). Furthermore, the effects of exposure to ACEs may initially present as a broader range of psychological disturbances prior to the manifestation of PTS symptom clusters (Van Vugt et al., 2014). These disturbances include symptoms of anxiety, depression, impulsivity, and anger – all commonly found in children and adults with trauma exposure (Briere, 1996; Briere & Scott, 2015). Consequently, individuals experiencing PTS symptoms and/or a broader range of psychiatric symptoms are likely experiencing difficulties in multiple areas of functioning, although many may not meet diagnostic criteria for PTSD.

Association between ACEs and executive functions

In addition to the link between ACEs and PTS symptoms, several studies evaluating the relationship between ACEs and cognitive abilities have consistently identified an adverse impact on various domains of cognition (DePrince et al., 2009; Gould et al., 2012; Mothes et al., 2015). More specifically, individuals exposed to ACEs often experience reductions in cognitive abilities that fall under the umbrella term of executive functions (Augusti & Melinder, 2013). Executive functions are recognized as pertinent cognitive abilities necessary for adaptive functioning to support goal-oriented, flexible, and autonomous behavior essential for success in school and work (Jurado & Rosselli, 2007; Spinella, 2005). Executive functions can also be described as different cognitive processes that allow for the control of thought, behavior, and affect (Zelazo & Carlson, 2012). These mental processes are said to facilitate the way individuals adapt to their environment and modify responses to variations in the environment (Stelzer et al., 2014). Moreover, some authors have linked executive functions with the development of conscience and certain social and moral skills, as well as skills that can be clustered under “theory of mind”, such as empathy (Carlson et al., 2004; Kochanska et al., 2000). Models of executive functions also postulate that the study of executive functions can be broken down into three different levels: (a) a construct level, (b) an operating level, and (c) a functional level (Burgess et al., 2006). The construct level is mainly based on the analysis of performance during executive function tasks, whereas the operating level are components of cognition that are not directly observable. Lastly, the functional level refers to the behavioral aspects that are observable, which are the result of a series of operations (Burgess et al., 2006). Subsequent to ACEs, research has shown that executive functions, at both the construct level and functional level, are commonly impaired.

Extensive empirical evidence supports the effects of ACEs on a variety of executive functions, including problem solving, planning, mental flexibility, working memory, inhibition, processing speed, and abstract reasoning (Irigaray et al., 2013; Kirke-Smith et al., 2014; Mothes et al., 2015; Nikulina & Widom, 2013; Vasilevski & Tucker, 2016). In a study of college students, individuals with histories of childhood trauma performed poorer on tasks of inhibition and switching than those without prior trauma exposure (Daly et al., 2017). Moreover, of the participants exposed to childhood trauma, those with more severe trauma histories performed worse on these tasks. Furthermore, a study of young adults exposed to ACEs demonstrated poorer inhibitory control and switching ability in comparison to a control group who did not have prior exposure to ACEs (Ji & Wang, 2018).

Theoretical models of the relationship between ACEs and executive functions are supported by findings from neurodevelopmental research. Namely, increased glucocorticoid secretion from the Hypothalamic-Pituitary-Adrenal (HPA) axis, in response to prolonged stress exposure, can lead to neuronal death and reduced functioning in the hippocampus, corpus callosum, and prefrontal cortex (De Bellis, Baum, et al., 1999; De Bellis, Keshavan, et al., 1999; Sapolsky, 1996) – areas strongly implicated in executive functions. Permanent HPA maladaptation and increased glucocorticoid secretion in maltreated children is one theoretical explanation for the association between ACEs and impairment in executive functions in later adulthood (Cicchetti et al., 2010). Although many factors may account for the association between ACEs and impaired executive functions in adulthood, theoretical and empirical evidence suggests that the presence of PTS symptoms are a potential mediator of this relationship.

Association between ACEs, PTS symptoms, and executive functions

Growing research also indicates that individuals with PTSD show deficits in areas of executive functions such as set shifting (switching), planning, and working memory (Beckham et al., 1998; Olff et al., 2014; Stein et al., 2002). Additional research demonstrates that PTSD is associated with reduced inhibitory control (DeGutis, et al., 2015; Falconer et al., 2008; Koso & Hansen, 2006) along with working memory and attention (Samuelson et al., 2006). Overall, research has indicated that individuals with PTSD or PTS symptoms and individuals with histories of childhood maltreatment both perform more poorly on executive function tasks in comparison to healthy control participants without these histories (Irigaray et al., 2013; Scott et al., 2015). From the behavioral perspective, PTSD and PTS symptoms are fundamentally conditioned responses to a feared stimulus (i.e., features of the traumatic event; Foa et al., 1989). As opposed to singular traumatic events (e.g., a car accident, robbery/mugging), the chronicity and pervasiveness of betrayal trauma, as with ACEs, may lead to a mental blockage of the trauma itself, which can manifest into cognitive impairments (Freyd, 1994). This type of trauma leads to an innumerable number of conditioned stimuli. Consequently, even during benign tasks such as paying attention during class, organizing materials, planning a meal, or keeping track of medication intake, individuals with histories of ACEs may experience PTS symptoms of hyperarousal, altered consciousness, and emotion dysregulation in response to any number of external or internal stimuli. Given the cognitive resources required to manage these symptoms (Compas, 2006), and that executive functions rely on the availability of such resources (Banich, 2009; Best & Miller, 2010; Jurado & Rosselli, 2007), cognitive theory suggests that exposure to ACEs and the presence of subsequent PTS symptoms are likely to negatively impact one’s ability to perform basic, but cognitively demanding, operations that rely on executive functions.

Research continues to support a strong link between ACE exposure, PTS symptoms, and lower executive functions (Cougle et al., 2010; De Bellis et al., 2009; Koenen & Widom, 2009), although empirical research exploring the relationship between these three constructs is limited. One study examined whether PTSD moderates or mediates the relationship between childhood maltreatment and executive functions using performance-based cognitive tasks (Nikulina & Widom, 2013). Although the results of this study indicated that PTSD did not mediate or moderate the relationship between early trauma and executive functions, the operationalization of PTSD as a categorical (i.e., PTSD+/PTSD−) rather than a continuous variable (i.e., PTS symptoms), may have contributed to the null results. For example, participants with subthreshold PTS symptoms may have been represented in the PTSD− group; however, without meeting diagnostic criteria, these symptoms may have still adversely impacted executive functions. Participants with subthreshold PTS symptoms may still experience subjective distress and reduced cognitive functioning (Mylle & Maes, 2004).

In addition to conceptualizing posttraumatic reactions as a present/absent phenomenon, relying solely on performance-based tests of executive functions may not provide a well-rounded approach when examining executive functions. Self-report behavioral measures provide an ecologically valid measurement of executive functions, whereas performance-based measures have limited ecological validity (Barkley, 2012; Chaytor et al., 2006). Self-report measures reflect problems related to executive function difficulties in real-life settings, and are sensitive enough to detect mild executive function difficulties that occur in daily life (Jurado & Rosselli, 2007). Moreover, self-report measures may provide different information than performance-based measures, such as subjective experiences of severity and day-to-day impairment. They also provide information at the functional level of executive functions, rather than solely the construct level. Although self-rating scales for executive function assessment come with psychometric limitations due to their subjective nature (e.g., Denckla, 2002), they provide a different level of information about executive behavior (Toplak et al., 2013).

Current study

The assessment of executive functions and PTS symptoms in individuals exposed to ACEs is of particular interest to allied health professionals, and is something that is lacking in current research. Exposure to ACEs can lead to negative physiological, psychological, and cognitive outcomes, resulting in similar long-term consequences as chronic PTS symptoms. Furthermore, ACEs and PTS symptoms share similar adverse relationships with executive functions, and therefore warrant further investigation of this commonality. Notably, research has demonstrated that trauma-focused treatment has improved executive functions in individuals with PTSD (Nijdam et al., 2018; Walter et al., 2010). Similarly, evidence for PTS symptoms mediating the relationship between ACEs and executive functions could support the notion that interventions focused on reducing PTS symptoms may also improve executive functions among individuals with longstanding cognitive weaknesses related to a history of ACEs. Due to the significance of this research, the current study aimed to assess the relationship between ACEs, PTS symptoms, and executive functions in adults using self-report measures, hypothesizing that current PTS symptoms may mediate the relationship between ACEs and executive functions.

Methods

Participants

Participants from the United States and Canada were recruited through CrowdFlower, an online micropayment service that supported internet-based research. Inclusion criteria were (a) being 18 to 55 years-old and having no history of (b) a neurological disorder, (c) a traumatic brain injury (not including a concussion), (d) a neurodevelopmental disorder (such as autism, fetal alcohol spectrum disorder), or (e) an intellectual disability. A total of 91 participants completed the study and 8 additional participants were further excluded from analysis due to completing the study faster than possible to indicate a valid performance (i.e., < 4 minutes). The 83 remaining participants (54.2% female) were within the age range of 19 to 53 years (M = 28.86, SD = 7.71). Additional demographic information is reported in Table 1.

Table 1.

Sample demographics.

Characteristics (N = 83)	n (%)
Age
Years, M (SD)	28.86 (7.71)
Gender
Male	37 (44.6)
Female	45 (54.2)
Unknown	1 (1.2)
Ethnicity
White/Caucasian	59 (71.1)
Latinx-Hispanic	12 (14.5)
Asian American	6 (7.2)
African American	3 (3.6)
Biracial/Multi-racial	2 (2.4)
Other	1 (1.2)
Education
Less than High School Diploma	3 (3.6)
High School Diploma	18 (21.7)
Some Post Secondary	21 (25.3)
College/University Degree	33 (39.8)
Masters Degree or higher	7 (8.4)
Unknown	1 (1.2)
Highest Parental Education
Less than High School Diploma	3 (3.6)
High School Diploma	31 (37.3)
Some Post Secondary	9 (10.8)
College/University Degree	30 (36.1)
Masters Degree or higher	9 (10.8)
Unknown	1 (1.2)

CrowdFlower

All data collection occurred online in 2016 via CrowdFlower, which was an online labor market where researchers post studies and participants choose which studies to complete for payment. Similar to Amazon Mechanical Turk, this recruitment source was selected because it was compliant with data management requirements of the research institution. CrowdFlower parsed users of their website to participate in online research for small amounts of compensation. Since completing data collection, CrowdFlower has been rebranded and discontinued. The reliability of micropayment research has been assessed, finding no meaningful differences between large online samples and samples recruited through a micropayment service, as well as a high test-retest reliability of scores in micropayment-recruited samples (Buhrmester et al., 2011). Research has also been conducted to assess whether micropayment service samples differ from participants in the laboratory, finding no significant differences between groups (Fehr & Gachter, 2000). Additional research has been conducted focusing on the differences between in-person interviews and online data collection surrounding the collection of sensitive information (i.e., alcohol and substance use), and found few differences (Pedersen et al., 2012). Participants frequently reported feeling more comfortable when completing the online version. Further, a study assessing the reliability and validity of an internet traumatic stress survey measuring trauma exposure, depression, and posttraumatic stress symptoms, found similar psychometric properties of internet-based questionnaires in comparison to more traditional formats (Fortson et al., 2006).

Materials

Participants completed four questionnaires online: a demographic history questionnaire, the Adverse Childhood Experiences Questionnaire (ACE) (Felitti et al., 1998), the PTSD Checklist for DSM-5 (PCL-5) (Weathers et al., 2013), and the Executive Functioning Index (EFI) (Spinella, 2005). Participants first completed the demographic history questionnaire, which screened for exclusion criteria and queried age, gender, education, parental education, and ethnicity.

ACE questionnaire

The ACE is a 10-item self-report questionnaire that examines the number of different types of ACEs that a participant has experienced prior to age 18. This questionnaire covers the main domains of physical abuse, sexual abuse, emotional abuse, physical neglect, emotional neglect, household incarceration, household mental illness, household drug/alcohol abuse, domestic violence, and parental divorce/separation. Each category of adverse experience is assessed by one question, with participants providing a yes/no response in regard to whether they experienced the given experience. A yes response results in a score of one for that category, while a no response results in a score of zero. Scores across the ten domains were summed to calculate a total ACE score, with a higher score representing increased exposure to adversity during childhood. The total ACE score was used in analysis, with a higher score indicative of a more extensive history of ACE. Previous research has demonstrated medium to high test-retest reliability of the scores in each category evaluated by the measure, with intraclass correlation coefficients ranging from .62 to .96 (Pinto et al., 2014); and evidence for good content validity (Saini et al., 2019).

PCL-5

The PCL-5 is a self-report questionnaire that indicates how much participants have been bothered by each symptom over the past month. Participants responded to 20 items capturing all four PTS symptom clusters (i.e., intrusion, avoidance, alterations in cognition and mood, and alterations in arousal and reactivity) on a five-point Likert scale ranging from 0 (“Not at all”) to 4 (“Extremely”). The symptom severity score can range from 0 to 80, which can be obtained by summing the scores from each of the 20 items. This score was used in analysis with a higher score indicative of greater severity of PTS symptoms. The PCL-5 served as a measure of PTS symptom severity, and not a diagnostic tool; and as such, the symptom ratings were not directly linked to any of the ACEs or an index trauma. The PCL-5 test scores have exhibited high internal consistency (α = .94) as well as evidence for convergent validity and discriminant validity (Blevins et al., 2015).

EFI

The EFI is a 27-item questionnaire created as a brief, self-rated measure of executive functions among healthy individuals. There are five subscales: Motivational Drive, Strategic Planning, Organization, Impulse Control, and Empathy. Each item is assessed on a five-point Likert-type response scale that ranges from “Not at all” to “Very much.” The scale asks participants to rate how well each statement describes them. Motivational Drive items address behavioral drive, activity level, and interest in novelty; Strategic Planning items address thinking ahead and planning; Organization items address the ability to carry out organized goal-directed behavior; Impulse Control items address self-inhibition, risk taking, and social conduct; and Empathy items reflect concern for others and prosocial behaviors (Spinella, 2005). Higher scores indicate a higher level of reported executive function abilities. The EFI total sum score was used in analysis, with a higher score indicative of better executive function. The EFI total score had acceptable reliability (α = .82), and its respective subscales showed evidence for convergent and discriminant validity (Spinella, 2005).

Procedure

Participants completed the demographic questionnaire, ACE, PCL-5, and EFI online. Due to the sensitive nature of the questions asked over the course of the study, participants were permitted to withdraw at any time without penalty. The consent form, intermittent pages, and a debriefing note all included psycho-educational and mental health resources for participants to access if needed. The participants were given an incentive of CAD$0.30/USD$0.21 for each questionnaire completed, in total receiving CAD$1.20/USD$0.84 for the entire study. This study received ethics approval from our institutional human research ethics review board.

Statistical analysis

Descriptive statistics and inter-test correlations are reported in Table 2 for each score included in the mediation analysis and all EFI subscales. The relationship between demographic characteristics and ACE, PCL-5, and EFI scores were evaluated via a parametric correlation for age and independent samples t-tests for categorical demographic variables, including gender, race/ethnicity (coded binary as White and non-White), and personal and parental education levels (both coded as college degree or less than a college degree). Any demographic characteristic significantly related to the ACE, PCL-5, or EFI scores was included in the mediation model.

Table 2.

Descriptive statistics and correlation matrix.

	ACE	EFI	EFI-MD	EFI-ORG	EFI-SP	EFI-IC	EFI-EMP	PCL-5
M	2.93	94.02	14.22	16.51	23.96	16.61	22.72	24.87
SD	2.43	12.00	3.34	3.66	3.55	3.73	4.55	17.05
Skewness	0.53	0.22	–0.32	0.34	–0.64	0.08	–0.69	0.17
Kurtosis	–0.54	0.20	0.00	–0.29	1.20	–0.91	1.08	–1.01
ACE	1
EFI	–.329**	1
EFI-MD	–.280*	.566**	1
EFI-ORG	–.227*	.726**	.253*	1
EFI-SP	–.263*	.484**	.292**	0.045	1
EFI-IC	–0.191	.632**	0.074	.637**	–0.035	1
EFI-EMP	–0.116	.743**	.267*	.367**	.275*	.308**	1
PCL-5	.405**	–.511**	–.220*	–.626**	0.005	–.532**	–.249*	1

Note. *p < 0.05; **p < 0.01; ACE: Adverse Childhood Experiences Scale; EFI: Executive Function Index; EFI-EMP: Empathy; EFI-IC: Impulse Control; EFI-MD: Motivational Drive; EFI-ORG: Organization; EFI-SP: Strategic Planning; PCL-5: PTSD Checklist for DSM-5.

To evaluate whether PCL-5 scores mediated the relationship between ACE and EFI scores, a series of regression models were run using the PROCESS Macro in SPSS (Hayes, 2017). These models included (a) a bivariate regression where ACE scores (X) predicted PCL-5 scores (M), (b) a multiple regression where both ACE (X) and PCL-5 (M) scores predicted EFI scores (Y), and (c) a bivariate regression model where ACE scores (X) predicted EFI scores (Y). The total effect was calculated as the regression coefficient from the third model (i.e., EFI on ACE), the direct effect was calculated as the partial regression coefficient for ACE in the second model, and the indirect effect was calculated as the product of the regression coefficient from the first model (i.e., PCL-5 on ACE) and the partial regression coefficient for PCL-5 in the second model. A bootstrapped 95% confidence interval (CI) was calculated for the indirect effect. A CI that did not overlap zero would indicate that the PCL-5 mediated the relationship between ACE and EFI scores. Anticipating medium standardized path weights (i.e., β = .39) between the predictor (ACE) and the mediator (PCL-5) and the mediator and the outcome (EFI), the sample required for sufficient power (i.e., .80) was N = 78 using the percentile bootstrap approach, which was exceeded for the current sample (Fritz & MacKinnon, 2007).

Results

Descriptive analyses

Total scores for the ACE questionnaire (α = .750) ranged from 0 to 9 (M = 2.93, SD = 2.43). Two missing data points were imputed as zero for participants that responded negatively to all other items on the ACE, inferring that a non-response indicated the item was not endorsed. On the ACE questionnaire, participants endorsed emotional abuse (54.2%), emotional neglect (47.0%), parental separation/divorce (38.6%), household alcohol/substance abuse (37.3%), physical abuse (32.5%), household mental illness or suicide (24.1%), sexual abuse (16.9%), witnessing domestic violence (16.9%), physical neglect (14.5%), and a household member going to prison (10.8%).

Total scores for the EFI (α = .815) ranged from 64 to 125 (M = 94.02, SD = 12.00). Few missing cells (n = 18; .01%) were imputed with the intra-individual mean of the corresponding EFI subscale for the missing item. Total scores for the PCL-5 (α = .956) ranged from 0 to 60 (M = 24.87, SD = 17.05). Using a provisional cutoff for defining PTSD diagnosis at ≥31 points on the PCL-5 total sum score (Blevins et al., 2015), 36.1% of participants met or exceeded this cutoff. Only 8.4% of participants endorsed no symptoms on the PCL-5. A small number of missing data points (n = 17; .01%) were filled in by separating out the recommended symptom clusters of the PCL-5 (i.e., intrusion, avoidance, negative alterations in cognitions and mood, and arousal and reactivity; Weathers et al., 2013) and imputing the intra-individual mean for the symptom cluster. For both the EFI and PCL-5, imputed values were rounded to the nearest whole number. This imputation method was selected based on its appropriateness with limited missing data (Shrive et al., 2006).

Demographic variable analyses

There were no significant differences observed between men and women on the ACE (t = 1.26, p = .211, d = .28), PCL-5 (t = –0.21, p = .831, d = –.05), or EFI (t = 0.52, p = .605, d = .12). In terms of education, there were no significant differences based on parental level of education for any variable, ACE (t = 0.83, p = .410, d = .18), PCL-5 (t = –0.15, p = .879, d = –.03), or the EFI (t = –0.71, p = .478, d = –.16), or personal level of education for any variable, ACE (t = 1.65, p = .102, d = .36), PCL-5 (t = 1.09, p = .279, d = .24), or the EFI (t = –1.38 p = .171, d = –.30). Group differences were observed between participants who identified as White versus those who identified as another racial/ethnic identity on the PCL-5 (t = 2.49, p = .015, d = .60), but not the ACE (t = 0.07, p = .942, d = .02) or the EFI (t = –1.12, p = .265, d = –.27). Age was correlated with PCL-5 scores as well (r = –.24, p = .03), but was not correlated with ACE (r = .12, p = .284) or EFI (r = .06, p = .598).

Path analysis

For results reported below, the B value corresponds to the unstandardized beta weight, the β value corresponds to the standardized beta weight, and all ranges provided in brackets correspond to 95% confidence intervals. In assessing the mediation model without the inclusion of covariates, the first bivariate regression analysis demonstrated that ACE significantly predicted EFI, B = –1.62 [–2.65, –.59], β = –.33, t(81) = –3.13, p = .002. The second bivariate regression analysis demonstrated that ACE significantly predicted the mediator, PCL-5, B = 2.84 [1.42, 4.25], β = .40, t(81) = 3.98, p < .001. Including both ACE and the PCL-5 in the model, ACE no longer significantly predicted EFI, B = –.72 [–1.74, .30], β = –.15, t(80) = –1.41, p = .16. Furthermore, the mediator, PCL-5, significantly predicted EFI when controlling for ACE, B = –.32 [–.46, –.17], β = .45, t(80) = –4.35, p < .001. PCL-5 fully mediated the relationship between the ACE and EFI, with an indirect effect of B = –.90 [–1.54, –.38], or for a completely standardized indirect effect of β = –.18 [–.30, –.08], with both 95% confidence intervals based on percentiles from 5,000 bootstraps. The path analysis is displayed visually in Figure 1.

Figure 1.

Unstandardized regression coefficients for the relationship between ACE and EFI mediated by PCL-5. ACE = Adverse Childhood Experiences questionnaire; EFI = Executive Function Index; PCL-5 = PTSD Checklist for DSM-5. The 95% confidence intervals are shown in parentheses. The indirect effect is shown in brackets, with the 95% confidence interval based on percentiles from 5,000 bootstraps. **p≤.01, ***p<.001.

When assessing the model with significant covariates included (i.e., age and racial/ethnic identity), the results followed a similar pattern. ACE significantly predicted EFI, B = –1.66 [–2.70, –.62], β = –.34, t(79) = –3.18, p = .002, and PCL-5 scores, B = 3.02 [1.69, 4.36], β = .43, t(79) = 4.50, p < .001. When both the ACE and PCL-5 were included as predictors, ACE no longer significantly independently predicted EFI, B = –.68 [–1.75, .39], β = –.14, t(78) = –1.27, p = .209, but the PCL-5 was an independently significant predictor of EFI, B = –.32 [–.48, –.17], β = .46, t(78) = –4.05, p < .001. PCL-5 fully mediated the relationship between the ACE and EFI, with an indirect effect of B = –.98 [–1.67, –.41], or for a completely standardized indirect effect of β = –.20 [–.32, –.09], with both 95% confidence intervals based on percentiles from 5,000 bootstraps.

Post hoc EFI subscale assessment

Exploratory correlations were computed between EFI subscales and the PCL-5 to examine the relationship between specific executive function domains and overall reported PTS symptoms. Correlations between PCL-5 total score and Motivational Drive (r = –.220, p < .05), Organization (r = –.626, p < .01), Impulse Control (r = –.532, p < .01), and Empathy (r = –.249, p < 05) were all significant and negative, indicating worse functioning in each domain with greater PTS symptoms. The correlation between Strategic Planning (r = .005) and PCL-5 was not significant. Further correlations can be found in the correlation matrix in Table 2.

Discussion

The current study investigated the relationship between ACEs, PTS symptoms, and executive functions, as well as whether current PTS symptoms mediated the relationship between ACEs and executive functions. Not surprisingly, the frequency of ACEs was associated with greater PTS symptom severity; and, consistent with previous research (Irigaray et al., 2013; Olff et al., 2014), the frequency of ACEs and the severity of PTS symptoms were negatively associated with executive functions. Considering all three variables in tandem, a significant mediation model demonstrated that current PTS symptoms fully mediated the relationship between ACEs and executive functions, indicating that self-reported difficulties in executive functions among participants with a history of ACEs is mediated by current PTS symptomatology.

The reduction in executive functions may be explained by altered developmental trajectories following exposure to trauma. Research has demonstrated childhood and adolescence to be a crucial stage for neurodevelopment, largely in fronto-parietal networks (Best & Miller, 2010), and that exposure to stress and abuse or neglect are related to reduced volume in areas of the prefrontal cortex (Andersen et al., 2008; Hart & Rubia, 2012; Lim et al., 2014). Prefrontal areas are a pivotal node for the networks related to executive functions (Ardila et al., 2017; Collette et al., 2005), and exposure to ACEs during this crucial stage may impede brain development and explain executive function deficits within this population (Bridgett et al., 2015; Miller & Cohen, 2001). In addition to ACE, the negative correlation between PTS symptoms and executive functions may also be explained by prefrontal abnormalities. A PTSD neurocircuitry model posits that the amygdala becomes hyperactive, while the prefrontal cortex remains hyporesponsive, failing to regulate the amygdala and inhibit undesired emotions and cognitions (Pitman et al., 2012; Yehuda & LeDoux, 2007; Yehuda et al., 2015). Supporting this model, researchers have observed PTSD-related abnormalities in fronto-limbic regions (Garfinkel & Liberzon, 2009; Hayes et al., 2012; Patel et al., 2012; Rauch et al., 1998) and reduced volumes in the left amygdala, anterior cingulate cortex, and ventral medial prefrontal cortex (Karl et al., 2006; Morey et al., 2016; Thomaes et al., 2010).

Prior research has demonstrated an increased risk of developing PTSD and executive dysfunction in individuals exposed to ACEs (Augusti & Melinder, 2013; Cougle et al., 2010; De Bellis et al., 2009; Koenen & Widom, 2009), indicating that ACEs likely precede both PTS symptoms and executive dysfunction. However, the causal relationship between PTS symptoms and executive function difficulties remains ambiguous in cross-sectional research designs (Aupperle et al., 2012). The statistical model used in the current study considered PTS symptoms as leading to executive function difficulties. This directionality aligns with prior cognitive research showing an effect of PTS symptoms on executive functions (Scott et al., 2015). It also aligns with prior neurobiological research showing HPA axis dysregulation in PTSD contributing to atrophy in the prefrontal cortex (De Bellis, Baum, et al., 1999; De Bellis, Keshavan, et al., 1999; Sapolsky, 1996; Shea e al., 2005; Tarullo & Gunnar, 2006), which is an area critical for executive functions (Ardila et al., 2017; Collette et al., 2005). However, researchers have conceptualized this relationship in a reverse direction, where executive function difficulties increase susceptibility to PTS symptomology (Bomyea & Lang, 2015).

Under a different theory, the current analyses would have replaced the outcome (i.e., EFI) with the mediator (i.e., PCL-5), in that lower executive functions would precede PTS symptomatology in participants exposed to ACEs. Researchers have demonstrated that interventions focused on executive functions, rather than PTS symptomology, can improve symptoms associated with PTSD. For example, studies have demonstrated that improving inhibitory control has reduced frequency of intrusive thoughts (Bomyea & Amir, 2011) and training working memory or engaging in mindfulness meditation has reduced levels of anxiety or worry (Course-Choi et al., 2017; Sari et al., 2016). These studies imply, causally, that interventions for executive functions lead to reduced psychiatric symptoms.

The directionality proposed by the current study posits that treatment focused on reducing PTS symptoms may improve executive functions in individuals exposed to ACEs. In theory, certain PTS symptoms, such as heightened arousal and re-experiencing, may cause distraction when an individual is attempting to complete a cognitive task, pulling for attention, interrupting working memory, and taxing inhibitory functions (Aupperle et al., 2012). As such, symptoms of PTS may contribute to subjective difficulties in executive functions and reducing PTS symptomology may reduce such internal cognitive distractions that inherently lead to executive function difficulties. The successful mediation model identified by the current study indicates the importance of reducing PTS symptoms to potentially improve executive functions among individuals exposed to ACEs. Trauma-focused interventions have led to improve cognitive functions, such as a clinical trial of PTSD treatment that improved executive functions, specifically in the areas of cognitive flexibility and planning/organization (Walter et al., 2010).

Although researchers may conceptualize the relationship between PTS symptoms and executive function difficulties in either direction, a combined approach to treatment involving both a trauma-focused intervention and cognitive rehabilitation may provide needed symptom improvement without taking a hard theoretical orientation on their causal relationship. A recent study examined combined trauma-focused and cognitive rehabilitation treatments for veterans with co-morbid PTSD and mild traumatic brain injury, which reduced PTS symptom severity and enhanced neuropsychological functioning (Jak et al., 2019). Clinicians can approach executive function difficulties as a co-occurring condition among patients with PTSD, and potentially monitor changes in executive functions over the course of treatment. Whereas symptom reduction is a key target of evidence-based trauma-focused treatments, a positive effect on executive functions through cognitive rehabilitation may provide added incentive for individuals with PTS symptoms to participate in treatment. Rather than a focus on solely symptom reduction, an added focus on improved quality of life through greater organization and impulse control would emphasize the strengths that a client could gain from treatment. Clinicians may best serve their patients by focusing on both PTS symptoms and executive function weaknesses simultaneously.

While the findings align with previous research and have applicability to future intervention research, the study does have limitations worth considering. A key limitation is the cross-sectional design. Mediation models are more appropriate for experimental designs; and without an experimental design, it is not appropriate to imply causality between variables. It is more appropriate to interpret the relationship between variables as strictly correlational. Longitudinal studies have demonstrated the presence of a causal relationship between exposure to childhood trauma and executive functions in adulthood (Nikulina & Widom, 2013); however, in the current context, we cannot imply that ACEs cause executive function difficulties in the presence of PTS symptoms. The relationships examined are, as noted, strictly correlational; however, the direction and significance of the relationships implied by the mediation model are theoretically grounded. First, it is far more likely neurodevelopmentally for ACEs to contribute to executive function difficulties, rather than executive function difficulties leading to ACEs. Second, there is abundant research showing an effect of PTS symptoms on executive functions (Scott et al., 2015). However, there are contrasting theories that imply a causal relationship in the opposite direction, through which poor executive functions lead to PTS symptoms (Aupperle et al., 2012; Bomyea & Lang, 2015, 2016). As a limitation, the cross-sectional design cannot clarify the true directionality; and the relationship may even be bidirectional, in that poor executive functions and PTS symptoms are mutually reinforcing. Future longitudinal research is needed to clarify this relationship.

Due to the intrinsic limitations of research on long-term effects of childhood trauma, it was not possible to assess executive functions prior to exposure to adverse experiences, and the EFI does not provide a retrospective report. In turn, there was not an option to control for executive functions prior to exposure to ACEs in the analysis. Without this information, it becomes difficult to infer that observed executive function difficulties was directly related to exposure to ACEs in individuals with PTS symptoms. Similarly, adulthood trauma was not assessed, and participants may have experienced trauma post childhood. In turn, executive function difficulties observed within the sample may not be strictly related to ACEs. Criterion A was not evaluated in the current study, and despite significant PTS symptoms, it remains unknown if the sample qualifies for PTSD diagnosis, or whether trauma exposure unrelated to ACEs could explain the PTS symptoms. In comparison to other samples evaluated using the PCL-5, this sample showed evidence for clinically significant PTS symptoms (i.e., 36.1% of the current sample) somewhere between an undergraduate student sample (i.e., 16.0% with clinically significant PTS symptoms; Blevins et al., 2015) and a treatment-seeking sample of U.S. service members (76.3% with clinically significant PTS symptoms; Wortmann et al., 2016), which indicates that participants may have included some individuals that, if formally evaluated, would qualify for PTSD diagnosis. Despite this limitation, the current study was not seeking to use the PCL-5 as a diagnostic tool, and the collection of Criterion A information was not necessary to explore the nature of PTS symptoms in the presence of ACE and executive functions.

Overall, this study adds to the cumulative evidence demonstrating a strong association between ACEs and PTS symptoms, and between PTS symptoms and reduced executive functions. In looking at these three variables in tandem, a potential mechanism of how these early adverse experiences affect executive systems has been elucidated. Specifically, the results of this study indicate that exposure to adverse or traumatic experiences in early childhood is related to executive function difficulties, and that this relationship is potentially explained by current PTS symptoms. These findings suggest that interventions targeting symptom reduction may result in a dual improvement, likely improving executive functions in addition to reducing PTS symptoms. These findings are best considered as preliminary, as causal claims cannot be drawn from the cross-sectional design; however, despite study limitations, these findings are among few mediation models linking ACEs with executive functions in the presence of PTS symptoms (Nikulina & Widom, 2013), and warrant further investigation into the relationship between these variables in longitudinal studies and clinical trials of trauma-focused interventions.

Footnotes

Declaration of Conflicting Interests

The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Funding

The author(s) received no financial support for the research, authorship, and/or publication of this article.

ORCID iD

Justin E. Karr

Author Biographies

Rachel A. Maja, completed her M.A. degree in School and Applied Child Psychology. Her clinical and research interests include early exposure to trauma, learning disorders, intellectual disabilities, neurodevelopment, and executive functioning.

Robyn E. Kilshaw, Kilshaw is a doctoral student in the clinical psychology program at the University of Utah. Her research is focussed on the long term consequences of adverse childhood experiences and the quantitative methods that best capture these dynamic trajectories.

Mauricio A. Garcia-Barrera, is an Associate Professor in the Department of Psychology at the University of Victoria, where he leads the CORTEX lab [www.cortex.uvic.ca], a research lab specialized in the study of the neural and behavioural foundations of executive functioning, with a particular interest in its definition, assessment, and examination of the clinical events or environmental variables that may modify its development across the lifespan.

Justin E. Karr, is an Assistant Professor in the Department of Psychology at the University of Kentucky, where he coordinates the Clinical Neuropsychology Concentration. His research interests include cognitive aging, the measurement and development of executive functions, and the psychological, cognitive, and symptom-related sequelae of concussion or mild traumatic brain injury.

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