The present data demonstrate that young to middle-aged adults with PTSD have shorter LTL than do non-psychiatric control persons, even in the absence of chronic physical illness. This finding extends a small but growing body of literature showing short LTL in individuals experiencing chronic psychological stress (17
) or psychiatric illness (16
). However, our data additionally indicated that only participants with PTSD who had been exposed to multiple types of childhood trauma had significantly shorter LTL than controls, indicating that childhood trauma may have accounted for the observed finding of short LTL in PTSD. Moreover, our data indicated that exposure to multiple categories of childhood trauma may have a cumulative effect on LTL, as number of categories of trauma exposure was linearly associated with shortening LTL across the entire sample and within the group of participants with PTSD. These findings of short LTL in association with childhood trauma add to a growing literature specifically showing short LTL in individuals exposed to traumatic events in childhood (29
). Our results are particularly compelling in light of the relatively young age and good physical health of our sample.
Our primary finding was that individuals with PTSD and multiple categories of childhood trauma had significantly shorter LTL than both controls and participants with PTSD who had none or one category of childhood trauma. Childhood trauma and PTSD could exert separate and combined effects on the rate of telomere shortening through biological and behavioral pathways. First, both childhood trauma and PTSD are associated with exaggerated reactivity to negative stimuli and events, which may lead to repeated and prolonged activation of the biological stress response (43
). Products of the biological stress response, in turn, have been causally linked with leukocyte telomere shortening. High levels of stress hormones including cortisol and catecholamines indexing activation of the HPA axis and SNS respectively have been associated with short LTL (8
). Stress-related elevations in inflammatory activity may also promote leukocyte telomere shortening in individuals with PTSD and childhood trauma (8
). Second, individuals with PTSD or childhood trauma exposure may be less likely to engage in the kinds of behaviors, such as maintaining a healthy weight, exercising regularly and not smoking, that could protect against the negative effects of psychological stress on TL (48
). While smoking and obesity, two major risk factors for short LTL, did not appear to contribute to our findings, other behavioral factors such as exercise and diet remain plausible as mediators of the relationship between PTSD and childhood trauma and LTL.
A particularly striking finding from our study is that childhood trauma was linearly associated with shorter LTL across the full sample and in the subsample with PTSD, indicating an additive effect of childhood trauma on LTL. Previous research has shown that cumulative childhood trauma is associated with increased risk for PTSD and other adverse outcomes (26
). In our sample, groups with and without cumulative childhood trauma were not significantly different on severity of overall or domain-specific symptoms of PTSD. However, exposure to multiple traumatic events in childhood has been associated with greater complexity of trauma-related symptoms in adulthood (53
). Thus, participants in our study with more categories of childhood trauma may have greater complexity of trauma-related symptoms, which could extend to greater physiological dysregulation and more accelerated telomere shortening. Further research will be necessary to test this hypothesis.
Our finding of short LTL in participants with PTSD and multiple categories of childhood trauma contributes to a recent debate concerning observed associations between childhood trauma and short LTL. In particular, one published study indicated that self-reported childhood maltreatment, including neglect, was associated with short LTL in a sample of 31 women and men without current Axis I disorders (29
). In a subsequent study, 20 participants who reported experiences of physical abuse in childhood did not have significantly different LTL than 520 controls, and 34 participants who reported experiences of sexual abuse in childhood did not have significantly different LTL than 516 controls (28
). The authors of the first paper argue that difficulties with accurate measurement of childhood trauma with only 2 questionnaire items in the latter study, as well as disparate controls for concomitant psychiatric and medical illnesses and medications may have contributed to the inconsistent findings between the two studies (55
). Our study has the potential to contribute to this debate. First, our study was focused on PTSD and trauma exposure and as such, childhood trauma was carefully assessed and quantified by expert clinical interviewers using methods validated by our group in previous research (45
). Second, we had strict inclusion criteria for both participants with PTSD and controls, selecting participants who were physically healthy and free of potential confounding medications. Finally, we tested for the contribution of age, sex, smoking, BMI and education to our findings. Thus, we believe that our finding reinforces the conclusion that childhood trauma impacts LTL.
Primary limitations of the present study include the cross-sectional design, the relatively small sample size and the absence of a control sample who experienced multiple categories of childhood trauma. Combined, these limitations reduce the extent to which any statements can be made about causality in relationships among PTSD, childhood trauma and short LTL. In particular, it is not clear whether more chronic experiences of PTSD or childhood trauma per se
contributed to the observed difference in LTL between groups. However, given that cumulative childhood trauma is such a strong risk factor for the development of later PTSD, individuals with PTSD and childhood trauma form a large proportion of the PTSD population (27
). Thus, the present findings may be applicable to a large number of the approximately 8% of people who experience PTSD in their lifetime (57
A further limitation is the use of a mixed sample of leukocytes including both granulocytes and agranulocytes in our measurement of telomere length. Future research focused on elucidating the relationship between psychosocial factors and LTL might productively measure telomere length in specific leukocyte subpopulations. A history of serious illness may lead to T-cell clonal expansion and thus contribute to short leukocyte telomere length in later life. We excluded participants with current chronic illness, but did not systematically assess experiences of chronic illness throughout the life course. We did collect data on lifetime history of hospitalization and found that participants who had experienced either childhood or lifetime hospitalization for illness (n = 10 and n = 20 respectively) or any cause (n = 12 and n = 33 respectively) were not significantly different from other participants in leukocyte telomere length (all p’s > .44). Our data indicates that the relationship of PTSD and childhood trauma with short LTL is independent of several major potential confounds and mediators including age, BMI, gender and years of education. However, behavioral factors including supplement use and physical activity and indicators of socioeconomic status beyond years of education were not assessed in our study and cannot be ruled out as potential confounds or mediators of the observed relationships.
This study represents the first demonstration of short LTL in PTSD, and additionally indicates that only patients with PTSD and a substantial history of childhood trauma have short LTL. Our findings that even physically healthy young to middle-aged adults with PTSD and childhood trauma bear markers of cellular aging suggest the need for further research to understand the biologic affects of trauma and to prevent future adverse health outcomes in this population.