These results extend previous reports linking shortened leukocyte telomere length and caregiver stress to more remote stressful experiences in childhood. In this study, reported maltreatment was moderate-severe in degree, and a variety of types of abuse and neglect were represented. Analysis of subtypes of maltreatment suggested that neglect may have the most robust effect, but given the modest sample size we cannot rule out effects of other forms of abuse. Both emotional neglect and physical neglect were linked to shorter telomeres, thus it is possible that in addition to the psychological effects of stress, physical stressors such as inadequate nutrition or illness contributed to the findings.
In contrast with previous work, this study did not find an effect of recent perceived stress on leukocyte telomere length; it is of note that childhood maltreatment was not correlated with recent perceived stress in this sample. This study included only individuals with no current or past Axis I psychiatric disorder because some psychiatric disorders have been linked to telomere shortening. Shortened telomeres may represent a risk factor for such disorders or other adverse health outcomes in this sample. On the other hand, in addition to such a risk factor, these participants may have some factors that confer resilience, given the absence of psychiatric disorder even in the maltreatment group.
This study is limited by the modest sample size and the cross-sectional nature of the study. In addition, the CTQ is a brief, retrospective self-report questionnaire that may be subject to recall and other biases. We did not find an association of telomere length with age in this sample which is not surprising given that all but three subjects were younger than age 40. The rate of telomere sequence loss in human leukocytes varies with age, and little change in telomere length occurs in young adults (34
) Given the range of influences on telomere length, it is possible that other variables, including genetic factors (35
), could have influenced telomere length. However, the findings cannot be explained by effects of age, sex, smoking status, BMI, level of education, medical or psychiatric illness, or a measure of childhood socioeconomic adversity.
The pathway from psychological stress to telomere shortening remains to be elucidated, but glucocorticoid-associated oxidative stress damage is a likely mediator of this association (36
). Glucocorticoids are released from the adrenal gland in response to stress and have been shown to increase neuronal oxidative stress damage (36
). Increased levels of oxidative stress have been seen in subjects reporting psychological stress (13
) and depressive symptoms (41
), and oxidative stress reduces telomere length in vitro
The present findings suggest that links of childhood maltreatment with psychopathology and associated medical problems could be due to effects of stress on cellular aging. Further work is needed to replicate these preliminary findings and determine whether potential mediators of this effect, including glucocorticoid activity, oxidative stress, reduced telomerase levels, and immune activation, may be responsible for telomere shortening in response to psychological stress. Moreover, longitudinal studies on the effects of psychosocial stress and trauma on changes in telomere length over time are needed to more fully characterize this relationship.