Childhood trauma and gender: Synergistic and additive effects on sleep in healthy young adults

Abstract

Objectives:

To examine whether gender moderates the effects of childhood trauma on subjective and objective sleep measures.

Design:

Secondary data analysis, exploratory

Settings:

Sleep research lab

Participants:

A total of 213 men and 278 women aged 18–30 completed subjective measures. A subsample of 172 participants without any psychiatric, medical, or sleep disorders completed objective polysomnography for 1 night at baseline, before sleep manipulation.

Measurements:

Subjective measures: Childhood Trauma Questionnaire (CTQ), Pittsburgh Sleep Quality Index, Insomnia Severity Index, and Epworth Sleepiness Scale. Objective measures: Standard polysomnography measures. Multiple regressions determined whether gender moderated CTQ score on any objective or subjective sleep measures. If gender was not a moderator, we examined additive effects of gender and CTQ score. Models were adjusted for race and age.

Results:

Gender and CTQ score interactions were non-significant for both subjective (p > .675) and objective (p > .110) sleep. Women demonstrated better subjective sleep quality (Pittsburgh Sleep Quality Index, B = −0.264, p = .041) and more delta sleep than men (B = 3.032, p =.005). Greater CTQ score was associated with increased sleepiness (Epworth Sleepiness Scale, B = 0.029, p = .042), increased insomnia severity (Insomnia Severity Index, B = 0.027, p = .005), and lower REM density (B = −0.132, p = .045).

Conclusion:

Our finding of greater delta sleep and better subjective overall sleep quality in women suggests that, among people without comorbidities, women may experience better sleep. Childhood trauma is associated with objective and subjective sleep measures, but this association is non-specific to gender. Clear links between childhood trauma and sleep are detectable in a sample of healthy sleepers with no comorbidities.

Introduction

Childhood trauma is pervasive; studies have found that 59.4% of adult individuals reported at least 1 trauma in their lifetime¹ and up to 60.6%² of children and adolescents experience at least 1 trauma per year. Childhood trauma has been associated not only with mental illness^3–5 but with chronic disease, premature mortality⁶, and lifelong effects via long-term neurobiological, biomedical, and epigenetic consequences.⁷

Childhood trauma consists of distressing events, including childhood maltreatment—as well as other traumatic events—that occur during the developmentally vulnerable period of childhood and have lasting effects on mental and physical health⁷. Childhood maltreatment encompasses physical and emotional abuse and neglect as well as sexual abuse. The body of childhood trauma literature not only includes childhood maltreatment, but also includes measures of household dysfunction as well as other traumatic events during childhood. In this study, we use the term childhood trauma to refer to the previous literature of adverse childhood experiences (ACEs) and to be consistent with the measure used in this study.

Childhood trauma exposure has a dose-response relationship to sleep-disturbances that persists into adulthood,⁷ showing increased sleep disturbances with additional trauma exposure. Childhood trauma is a significant risk factor for poor adult sleep health⁸ and sleep quality.⁹ People who report more than one instance of childhood trauma exposure were 3.64 times more likely to have poor compared to adults without exposure are more likely to have sleep disorders¹² and have longer sleep onset latency,¹³ poorer subjective sleep quality,¹³ insufficient sleep,¹³ sleep quality,¹⁰ as well as more nocturnal arousals and more disturbed sleep in later life.¹¹ Adults with childhood trauma exposure compared to adults without exposure are more likely to have sleep disorders¹² and have longer sleep onset latency,13 poorer subjective sleep quality,¹³ insufficient sleep,¹³ daytime sleepiness,¹³ insomnia,¹³ and shorter sleep durations even decades later.¹⁴ A model of early life trauma leading to sleep disturbances has even been demonstrated in animal models, with lifelong spindle decreases and later life nonRapid Eye movement (NREM) sleep fragmentation.¹⁵ However, the impact of childhood trauma on sleep in young men and women, in the absence of concurrent comorbid psychological or physical illnesses, is unknown. Understanding the impact of childhood trauma exposure on sleep in healthy young adults may provide new insights into the factors and mechanisms that contribute to chronic sleep disturbances and/or later-life psychological vulnerability.

Gender may be an important moderator of the impact of childhood trauma exposure on sleep and health. Multiple factors contribute to disparities in sleep between men and women; compared to men, women with childhood trauma are more likely to feel hopelessness¹⁶ and have depression and/or anxiety disorders in adulthood.¹⁷ Compared to men, women are at greater risk for insomnia throughout life and report disrupted and insufficient sleep more frequently.¹⁸ However, few studies have simultaneously considered the interactive and/or additive effects of gender and childhood trauma on subjective and objective sleep measures. Kajipeeta et al¹² highlighted that there is a known lacuna of studies examining ACEs and adult sleep using multivariable analytical techniques to adjust for possible confounding factors.¹²

Thus, the purpose of this study was to examine the association of both gender and childhood trauma on objective and subjective measures of sleep with a large, healthy community sample. The use of a healthy sample, stringently screened for many medical and psychiatric comorbidities allows clearer relationships to be seen, limiting confounding factors. The use of a non-clinical sample allows us to determine the “uncomplicated” strength of the effect of childhood trauma exposure on subjective and objective sleep measures to identify which, if any, sleep parameters are associated with childhood trauma. Understanding the relationships between childhood trauma and sleep in young adults may provide new insights into mechanisms and factors that adversely impact resilience and contribute to vulnerability to sleep disorders. We hypothesized that gender would moderate the relationship between childhood trauma on objective and subjective sleep. Specifically, we hypothesized that gender and childhood trauma would have (1) an interactive effect on both objective and subjective sleep measures and (2) additive effects on both objective and subjective sleep measures. This line of investigation may offer new pathways to prevention of sleep disorders in the future.

Methods and materials

This study is a secondary analysis of data from a parent project (Log #11293006) with protocols and informed consent that was approved by the Institutional Review Board at the University of Pittsburgh and DoD Human Research Protection Office. All participants gave informed consent and the study was performed in accordance with all relevant guidelines and regulations. The current analysis is based on self-reported subjective sleep measures and objective polysomnography (PSG) data over 1 night obtained at baseline, before sleep manipulation. The full sample and a subset, the PSG sample, were used to analyze subjective and objective sleep measures, respectively. The 2 samples are described in further detail with an accompanying sensitivity analysis in the supplement.

All participants in the full sample (n = 491) were screened and included if they were healthy, 18–30 years old, reported regular and sufficient sleep patterns, and did not use any medications that affected sleep (ie, hypnotics, benzodiazepines, antidepressants, anxiolytics, stimulants, antipsychotics, decongestants, beta-blockers, corticosteroids, and sedating anti-histamines). Participants were excluded if they reported a history of seizure, bipolar, psychotic, or neurologic disorder. Participants were also excluded if they had a sleep disorder or reported current treatment for suicide ideation, substance use, or a mood or anxiety disorder in the last year as determined by the Structured Clinical Interview for DSM-IV. Participants who had a positive urine drug screen during screening were also excluded.

Women who were not using hormonal contraception, who were currently pregnant or lactating, or who were having irregular or absent menstrual cycles were excluded.

All participants in the full sample completed the Childhood Trauma Questionnaire (CTQ), the Pittsburgh Sleep Quality Index (PSQI), the Epworth Sleepiness Scale (ESS), and the Insomnia Severity Index (ISI) (see below for descriptions of measures). Those in the PSG sample had PSQI scores of ≤5, ESS scores of ≤10, and ISI scores of ≤7.

Participants in the PSG sample (n = 172) met the above selection criteria and underwent additional sleep and behavioral assessments. Participants first completed a 14-day sleep diary with actigraphy to verify the consistency and regularity of their sleep patterns. They were excluded if they went to sleep, on average, earlier than 9 PM or later than 12 AM and if they awoke, on average, earlier than 5:30 AM or later than 8:30 AM. Participants were also excluded if they got less than 6 hours or more than 9 hours of sleep on average per night. Eligible participants consumed less than 2 caffeinated beverages per day on average and did not nap over the 2-week period. Descriptive statistics of the full and PSG samples are included in Table 1.

Table 1.

Sample characteristics

	Full sample n = 491		PSG sample n = 172
	n	%	n	%
Male	213	43.4	77	44.8
Female	278	56.6	95	55.2
White	319	65	119	69.2
Black or African American	86	17.5	32	18.6
Asian	74	15.1	17	9.9
Other	5	1.02	1	0.6
Undisclosed	7	1.4	3	1.70
	M	SD	M	SD
Age	23.55	3.38	23.86	3.36
CTQ total score	31.01	7.98	29.65	5.37
Subjective sleep measures
PSQI total score	2.07	1.42	1.85	1.12
ISI total score	1.45	1.67	1.28	1.32
ESS total score	3.64	2.55	3.49	2.15
Objective sleep measures
Sleep Latency (min)			15.79	14.63
Total sleep time (min)			438.07	32.023
Wake after sleep onset (min)			28.28	23.34
Sleep efficiency			90.96	5.47
Stage 1%			4.95	2.89
Stage 2%			48.07	7.22
Delta %			22.08	7.58
Delta ratio			1.78	1.10
NREM %			75.11	4.93
REM %			24.89	4.93
REM density*			8.76	4.63
REM fragmentation			4.94	3.34

CTQ, childhood trauma questionnaire; ESS, Epworth Sleepiness Scale; ISI, Insomnia Severity Index; PSQI, Pittsburgh Sleep Quality Index.

^*n = 171 due to incomplete data.

Measures

Gender and trauma measures

Although there is increasing recognition that gender is not binary,¹⁹ for the purposes of data analysis, gender was measured as a dichotomous categorical variable. Participants self-identified gender on a self-report demographic questionnaire.

Childhood trauma was measured using the CTQ,²⁰ a retrospective 28-item self-report questionnaire in which participants rate their adolescent experiences on a 5-point Likert scale (never true to very often true). The CTQ contains 5 trauma subscales (emotional abuse, emotional neglect, physical abuse, physical neglect, and sexual abuse) rated on scales of 5 (less trauma) to 25 (more trauma). The 5 trauma scales are summed to create a total score to broadly indicate childhood trauma. Possible total score ranges from 25 to 125. The CTQ has a high internal consistency (α = 0.79–0.94) and a good test-retest reliability (intra-class correlation = 0.88).²⁰

Subjective and objective sleep measures

The PSQI is an 18-item self-report questionnaire that is considered a global indicator of sleep quality, assessing 7 subjective components (subjective sleep quality, sleep latency, duration, efficiency, disturbances, use of sleep medication, and daytime dysfunction). Each component is rated on a scale of 0–3, referring to the composite score derived from the frequencies of each disturbance, where 0 = not in the past month and 3 = three or more times a week; component scores are summed to create a total score. The total score can range from 0 (better) to 21 (worse). The PSQI is widely used and has demonstrated high internal consistency (Cronbach α = 0.83), test-retest reliability of (0.85–0.87), and convergent validity.²¹

The ESS is an 8-item questionnaire that assesses daytime sleepiness. Each item is rated on a scale of 0–3, where 0 = no change of dozing and 3 = high chance of dozing. Higher scores indicate greater sleepiness and total scores can range from 0 to 24. A score of 10 or greater indicates significant sleepiness and the potential of sleep disordered breathing. The ESS has been shown to have high internal consistency (Cronbach a = 0.88) and high test-retest reliability in healthy and sleep-disordered patients.²²

The ISI is a 7-item self-report questionnaire that assesses subjective severity of insomnia symptoms, degree of satisfaction with sleep, nature and noticeability of daytime impairments, and sleep-related concerns. Each item is rated on a 0- to 4-point scale, with 0 = none and 4 = very severe. The total score can range from 0 to 18. Scores from 0 to 7 reflect clinically insignificant insomnia, whereas scores greater or equal to 8 reflect subthreshold and clinically significant insomnia.²³

Objective sleep measures were obtained with overnight PSG. PSG was conducted using standard procedures to define sleep staging, including electroencephalogram, bilateral electro-oculogram, and bilateral submentalis electromyogram. Electroencephalogram signals were recorded at 30-second epochs, were digitized at 256 Hz, decimated to 128 Hz, and sleep stages were visually scored according to the American Academy of Sleep Medicine criteria. Structural sleep measures were obtained (sleep latency, sleep duration, sleep efficiency, wake after sleep onset (WASO), stage N1 percent, Stage N2 percent, Delta percent, Delta ratio, NREM percent, REM percent, REM density, and REM fragmentation).

Statistical analyses

SPSS Version²⁴ (IBM, Chicago, IL) was used for data analysis; a p < .05 was considered statistically significant for the unadjusted analysis. Corrections for multiple comparisons in the adjusted analysis used the Benjamini-Hochberg procedure. Subjective measures were tested using the full sample (n = 491) and objective measures were tested using the PSG sample (n = 172).

We regressed each of the subjective (PSQI, ISI, ESS) and objective (sleep latency, sleep duration, sleep efficiency, WASO, stage N1 percent, stage N2 percent, Delta percent, Delta ratio, NREM percent, REM percent, REM density, and REM fragmentation) sleep measures on gender, childhood trauma, and gender*childhood trauma interactions, while controlling for age and race. Gender was coded as a dichotomous categorical variable (Female vs. Male). Age was coded as a continuous variable. Race was coded as a dichotomous categorical variable (White and Not White). If no interaction variables were significant, main effects of gender and childhood trauma were tested in the same model, controlling for age and race.

We first computed unstandardized regression coefficients for both unstandardized and standardized outcomes; these coefficients are denoted B and B_z, respectively. The coefficient B has the standard interpretation that a 1-unit increase in CTQ score or being female vs. male is associated with a B-unit increase in the outcome. In contrast, the coefficient B_z allows for a comparison of the associations across outcomes with different scales. Specifically, a 1-unit increase in CTQ score or being female vs. male is associated with a B_z-unit increase in the standardized outcome. Finally, as a one-unit change in CTQ may not be the most clinically meaningful increment, the standardized coefficient of beta (β) was calculated, indicating the extent to which one standard deviation change in the CTQ score relates to a one standard deviation change in the dependent variable.

Results

For subjective sleep measures, none of the gender*childhood trauma interactions were significant (all p ≥ .675); therefore, the interactions were removed from the models.

Gender was significantly associated with subjective global appraisals of sleep with women subjectively reporting better overall sleep quality than men (PSQI, B (SE_B) = −0.264 (0.129), B_z (SE_Bz) = 0.186 (0.091), p = .041). Being female was associated with a decrease in the PSQI score by 0.264 and a decrease in 0.186 standard deviations of the PSQI score, meaning better overall sleep quality. Childhood trauma was also significantly associated with subjective appraisals of sleepiness (ESS, B (SE_B) = 0.029 (0.014), B_z (SE_Bz) = 0.012 (0.006), β = 0.092, p = .042) and insomnia (ISI, B (SE_B) = −0.027, (0.009), B_z (SE_Bz) = 0.016 (0.006), β = 0.128, p = .005) symptoms. For every one-point increase in the CTQ score, there was a 0.029 increase in ESS score and an increase in 0.012 standard deviations of the ESS score. For every one point increase in the CTQ score, there was a 0.027 increase in ISI score and an increase in 0.016 standard deviations of the ISI score. No other associations were considered statistically significant with regard to subjective sleep measures. Regression coefficients, standard errors, and p values can be found in Table 2.

Table 2.

Summary of multiple regression analyses for subjective measures

n = 491		Gender			Childhood trauma
	B (SEB)	Bz (SEBz)	p	B (SEB)	Bz (SEBz)	β	p
PSQI	−0.264 (0.129)	−0.186 (0.091)	.041	0.014 (0.008)	0.010 (0.006)	0.080	.076
ISI	−0.269 (0.152)	−0.161 (0.091)	.78	0.027 (0.009)	0.016 (0.006)	0.128	.005
ESS	0.298 (0.233)	0.117 (0.091)	.201	0.029 (0.014)	0.012 (0.006)	0.092	.042
n = 172		Gender			Childhood Trauma
	B (SEB)	Bz (SEBz)	p	B (SEB)	Bz (SEBz)	β	p
PSQI	−0.475 (0.172)	−0.425 (0.154)	.007	0.018 (0.016)	0.016 (0.014)	0.086	.255
ISI	−0.313 (0.206)	−0.237 (0.156)	.131	0.012 (0.019)	0.009 (0.014)	0.050	.514
ESS	0.102 (0.334)	0.047 (0.155)	.760	0.041 (0.030)	0.019 (0.014)	0.102	.181

ESS, Epworth Sleepiness Scale; ISI, Insomnia Severity Index; PSQI, Pittsburgh Sleep Quality Index; B, unstandardized coefficient of beta; B_z, unstandardized coefficient of beta calculated w/standardized outcome/dependent variable; SE_B, standardized error of the coefficient; β, standardized coefficient of beta indicating the extent to which a one standard deviation change in the independent variable relates to a one standard deviation change in the outcome; p, p value.

Note: bolded p < .05 and survived Benjamini–Hochberg correction for multiple comparisons. SDs in full sample (n = 491) as follows: CTQ_SD = 7.98, PSQI_SD = 1.42, ISI_SD = 1.67, ESS_SD = 2.55. SDs in the PSG sample (n = 172) as follows: CTQ_SD = 5.37, PSQI_SD = 1.12, ISI_SD = 1.32, ESS_SD = 2.15.

For objective sleep measures, none of the gender*childhood trauma interactions were significant (all p ≥ .110); therefore, the interactions were removed from the models.

Gender and childhood trauma, controlling for age and race, were analyzed to predict objective structural sleep measures in the PSG sample. Gender or childhood trauma predicted specific structural sleep measures. Gender was significantly associated with the percentage of Delta sleep (B (SE_B) = 3.032 (1.077), B_z (SE_Bz) = 0.400 (0.142), p = .005) with women having a higher percentage of slow wave sleep. Being female was associated with a 3.032% increase in Delta sleep and 0.400 standard deviations of Delta sleep. Childhood trauma predicted specific structural sleep measures. Increased childhood trauma was significantly associated with decreased REM density (B (SE_B) = −0.132 (0.066), B_z (SE_Bz) = −0.029 (0.014), β = −0.154, p = .045). For every one-point increase in the CTQ score, there was a decrease in REM density by 0.132 and a decrease in 0.029 standard deviations; for every 5.37 point increase in CTQ score, there was a 0.154 decrease in REM density. No other associations were considered statistically significant with regard to objective sleep measures. Regression coefficients, standard errors, and p-values can be found in Table 3.

Table 3.

Summary of multiple regression analyses for objective measures

n = 172		Gender			Childhood trauma
	B (SEB)	Bz (SEBz)	p	B (SEB)	Bz (SEBz)	β	p
Sleep latency (min)	−3.305 (2.283)	−0.226 (0.156)	.150	−0.126 (0.208)	−0.009 (0.014)	−0.046	.544
Total sleep time (min)	8.535 (4.952)	0.267 (0.155)	.087	0.651 (0.450)	0.020 (0.014)	0.109	.150
Wake after sleep onset (min)	0.514 (3.654)	0.022 (0.15	.888	0.145 (0.332)	0.006 (0.014)	0.033	.663
Sleep Efficiency	0.672 (0.863)	0.123 (.0158)	.437	0.012 (0.078)	0.002 (0.014)	0.011	.883
Stage 1%	−0.408 (0.452)	−0.141 (0.156)	.368	0.016 (0.041)	0.005 (0.014)	0.029	.701
Stage 2%	−1.617 (l.085)	−0.224 (0.150)	.138	−0.144 (0.099)	−0.020 (0.014)	−0.107	.146
Delta %	3.032 (1.077)	0.400 (0.142)	.005	0.052 (0.098)	0.007 (0.013)	0.037	.597
Delta ratio	−0.074 (0.172)	−0.067 (0.156)	.669	−0.009 (0.016)	−0.008 (0.014)	−0.046	.550
NREM %	1.007 (0.771)	0.204 (0.156)	.193	−0.076 (0.07)	−0.015 (0.014)	−0.083	.279
REM %	−1.007 (0.771)	−0.204 (0.156)	.193	0.076 (0.07)	0.015 (0.014)	0.083	.279
REM density*	0.416 (0.721)	0.090 (0.156)	.565	−0.132 (0.066)	−0.029 (0.014)	−0.154	.045
REM Fragmentation	−0.585 (0.525)	−0.175 (0.157)	.267	0.055 (0.048)	0.017 (0.014)	0.089	.249

B, unstandardized coefficient of beta; B_z, unstandardized coefficient of beta calculated w/standardized outcome/dependent variable; SE_B, standardized error of the coefficient; β, standardized coefficient of beta indicating the extent to which a one standard deviation change in the independent variable relates to a one standard deviation change in the outcome; p, p value. SDs in the PSG sample (n = 172) as follows: CTQ_SD = 5.37, Delta%_SD = 7.58, REM Density_SD = 4.63.

Note: bolded p < .05 and survived Benjamini-Hochberg correction for multiple comparisons.

Discussion

The purpose of this study was to examine the associations of both gender and childhood trauma with objective and subjective measures of sleep in a large, healthy community sample. Our primary hypothesis was that we would observe an interaction effect of gender and childhood trauma; however, our findings show no such effect. We did, however, observe several findings with regard to the main effects of trauma and gender on objective and subjective measures of sleep. The absence of current comorbid medical and psychiatric conditions allowed for the reduction of potential confounds and clearer evaluation of the long-term impacts of childhood trauma on sleep. While current comorbidities were removed, childhood psychiatric history was not assessed and could be a confounding variable.

On subjective sleep measures, women scored slightly lower on the PSQI than men, indicating a better subjective quality of sleep even among healthy sleepers. The previous literature is inconsistent in regards to gender differences seen in subjective reports of sleep as measured by the PSQI; some studies have found no significant effect of gender²⁴ while others have found that women have a higher prevalence of poor subjective sleep quality and score higher on the PSQI—and therefore report poorer quality of sleep—compared to men.²⁵ Our findings are inconsistent with more recent studies, which find that women tend to self-report worse sleep quality on subjective sleep measures;²⁶ this discrepancy may be due to our use of a healthy and non-clinical sample.

The literature is also inconsistent in regards to gender and excessive sleepiness as measured by the ESS with studies reporting no gender difference,²⁷ higher ESS scores in males,²⁸ or higher ESS scores in females.²⁹ The current study showed no statistical association of gender and ESS scores in healthy sleepers. However, a statistically significant association of childhood adversity and ESS was detected. This finding is consistent with the childhood trauma literature as a dose-response relationship, as a higher CTQ score (more reported trauma) is associated with an increased ESS score (more sleepiness). Trauma-related disorders including PTSD are associated with increased central arousal, which is typically manifested as hyperarousal symptoms. Increased daytime sleepiness may result from hyperarousal during sleep.

The literature typically reports a female preponderance of self-reported insomnia³⁰ with some studies reporting that women are approximately 40% more likely to have insomnia than men.³⁰ However, the current study reports no association of gender and insomnia symptoms based on ISI. There was an association of childhood trauma and ISI, such that higher CTQ scores are associated with increased in ISI scores. This is consistent with the childhood trauma literature as a dose-response relationship. As this is a sample of healthy sleepers, this could be an early indicator of vulnerability to later insomnia.

Though statistically significant, the effect sizes of (a) gender on the subjective global measure of sleep as measured by the PSQI and (b) childhood trauma on daytime sleepiness and insomnia as measured by the ESS and ISI, respectively, were small. Small effect sizes are to be expected in a healthy sample, but nevertheless, may be important indicators of risk for sleep disorders among healthy sleepers. Furthermore, longitudinal studies may reveal different relationships between age, gender, and subjective sleep quality over time.

Taken together, the findings suggest that gender has more global associations with subjective experiences of sleep among healthy sleepers, while childhood trauma seems to have more specific effects on clinical domains such as insomnia or sleepiness. Furthermore, our findings suggest that in samples of healthy participants without comorbidities, women may subjectively report better sleep quality than men. The general assumption that women report poorer sleep may reflect the impact of other factors (psychiatric comorbidities, risk for illnesses, and/or a combination of the preceding factors) beyond gender in clinical samples.

Gender, childhood trauma, and the interaction between these 2 variables did not predict the majority of the objective sleep measures, with one exception. Healthy young women had a higher percentage of Delta sleep, confirming previous findings of gender effects on slow wave activity.³¹ This higher percentage of Delta sleep could account for higher self-reported subjective sleep quality in women as measured by the PSQI.

Mirroring the findings in the subjective measures, exposure to childhood trauma appears to have small but specific effects associated with decreased REM density, and this effect was independent of gender. A decrease in REM density is somewhat unexpected as the literature shows that adults with depression³² and PTSD³³ have increased REM density. While this sample was specifically screened to exclude depression and PTSD, the literature robustly finds childhood trauma exposure to be a significant contributor to the etiology and pathogenesis of both depression³⁴ and PTSD.³⁵ As such, it might be expected that the REM density patterns in people with childhood trauma exposure, but without depression and PTSD, would also be elevated compared to those with no trauma exposure; indeed, research with high-risk populations detected increases in REM density just before psychiatric disorder onset.³⁶ Thus, while increased REM density has been reported in clinical populations; exposure to childhood trauma may show a different relationship in REM density in a non-clinical population. Early exposure to adversity may differentially impact REM sleep and its features across developmental periods. It is possible that trauma exposure attenuates REM density during early developmental periods but later increases it in adulthood, as seen in adults with depression and PTSD.

While the effect size of childhood trauma on REM density is small, this finding highlights the persistent detectable effects of childhood trauma on objective PSG sleep measures. It is important to highlight that the PSG sample is not a clinical sample, but a community sample of young adults selected for healthy sleeping patterns. As such, medical illnesses and psychiatric comorbidities such as disorders of mood, anxiety (including PTSD), and substance use as well as neurological and sleep disorders were excluded, and the clearer effects of childhood trauma can be seen. Moreover, the observed range of CTQ scores in the PSG sample was limited and on the low end (range 25–54 out of a total possible range of 25–125) and the mean level of measured trauma was well within the “none to minimal” category. Thus, it appears that even low levels of trauma could alter very specific objectively-measured sleep characteristics; however, future studies will need a full range of CTQ scores to further explore this relationship.

This was a non-clinical sample consisting of young, healthy adults with no psychiatric or medical comorbidities, healthy sleep patterns, and very little exposure to trauma; furthermore, factors such as age and race were controlled in the statistical analyses. Thus, statistically significant associations emerging in both objective and subjective measures of sleep indicate that even minimal levels of childhood trauma can be associated with sleep changes. While these changes were subtle, they may nonetheless be an important early sign of sleep disorder.

Limitations

In this secondary data analysis, the use of a healthy non-clinical sample allowed us to understand associations without confounders from comorbidities. However, there were also limitations with the sample and study design that should be noted. There was very little variability in sleep or exposure to childhood trauma, resulting in limited ability to detect interactions. Further studies with more variability in both sleep and childhood trauma exposure will be needed to further explore gender and childhood trauma interactions. This data set does not include a measure of SES, as lower SES has been shown to be associated with worse sleep parameters.³⁷ The inclusion of this variable would be an important consideration in future studies.

Since this analysis uses the baseline sleep night from the parent study, these results are vulnerable to “first night effects”³⁸—the possibility that the first night of PSG would produce altered sleep architectural measures due to adaptation to the environment and sleep recording equipment—confounding the results. Additionally, measures of childhood trauma/ACEs in this study are based on retrospective self-report, which is subject to recall bias and possible false-positives. However, false-positives seem to be rare³⁹ and childhood maltreatment measures, specifically, have been found to have concordance in retrospective and prospective measures.⁴⁰

The participants selected for objective measures of sleep have a narrow age range (18–30); as a result, these findings may not be generalizable across the lifespan as some of the gender and childhood trauma/ACE effects may be seen more easily and/or might be seen earlier or later in life. However, to examine optimal sleep circumstances devoid of confounding comorbidities, it was necessary to restrict the age range as physiological dysfunction both accumulates and becomes more likely as people age. Further research in the form of longitudinal studies is needed to more clearly determine the nature of our current findings.

Furthermore, the data were not analyzed in an age-graded fashion. More evidence is accumulating that the age at which trauma occurs is associated with the risks of psychiatric disorder,⁴¹ and the duration and timing of exposure to stress hormones at different periods of life, including prenatal periods and infancy, have specific effects in brain development.⁴¹ Therefore, further research is warranted in more granular detail including age of trauma exposure, preferably in the form of prospective studies.

Finally, the term gender included both biological effects of sex and psychosocial impacts of gender on sleep. Both sex and gender have been historically defined as binary constructs; however, defining and coding both on a continuum will yield more nuanced and inclusive insights.

Conclusion

No interaction of gender and childhood trauma was detected in the sample of healthy sleepers; however, this does not mean that the absence of this evidence should be considered as evidence of the absence of this association. Further research with larger and more heterogeneous samples in trauma exposure and sleep disturbances, including resilient individuals, are needed. Gender had global associations with both subjective and objective measures of sleep. Childhood trauma was specifically associated with both objective and subjective sleep measures even in extremely healthy adults, independent of gender. The detection of statistically significant associations suggests that even low levels of childhood trauma exposure are associated with sleep changes. Given the persistence of the association of childhood trauma and sleep changes in adults coupled with what is known about childhood trauma’s long-lasting and pervasive health outcomes, additional studies exploring the association between REM density and childhood trauma exposure may be a fruitful future line of inquiry.