Childhood Adversities Are Associated with Shorter Telomere Length at Adult Age both in Individuals with an Anxiety Disorder and Controls (original) (raw)
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The Relationship Between Childhood Psychosocial Stressor Level and Telomere Length: A Meta-Analysis
Health psychology research, 2017
This meta-analysis examined the association between the level of childhood psychosocial stressors and telomere length, an important health biomarker. The meta-analysis, including 27 samples and 16,238 participants, found a significant association of -0.08 between a higher level of childhood stressors and shorter telomere length at a mean age of 42 across studies. Moderator analyses showed a trend in the direction of effect sizes being significantly larger with shorter times between the stressors and telomere measurement. Moderator analyses showed significantly higher effect sizes for studies that used a categorical method for assessing child stressor level and for assays completed with qPCR rather than with the Southern blot method. There was no significant moderation of effect size by whether study assayed leukocytes or buccal cells, whether the study assessed child stressor level by memory-based recall versus archival records, and whether the study controlled for age, sex, or addi...
Psychosomatic Medicine, 2011
To address the question of whether childhood abuse and other adversities have lasting, detectable consequences for inflammation and cell aging late in life, and whether the effects are large enough to be discernible beyond that of a major chronic stressor, dementia family caregiving. Previous research on the physical health consequences of childhood abuse and other adversities has been based on data from young or middle-aged adults. Method: In this community sample of 132 healthy older adults (mean age ϭ 69.70 years; standard deviation ϭ 10.14), including 58 dementia family caregivers and 74 noncaregivers, blood samples were analyzed for interleukin (IL)-6, tumor necrosis factor (TNF)-␣, and telomere length, a measure of cell aging. Depressive symptoms were assessed by the Center for Epidemiological Studies Depression Scale. Results: After controlling for age, caregiving status, gender, body mass index, exercise, and sleep, the presence of multiple childhood adversities was related to both heightened IL-6 (0.37 Ϯ 0.03 log10 pg/mL versus 0.44 Ϯ 0.03 log10 pg/mL) and shorter telomeres (6.51 Ϯ 0.17 Kb versus 5.87 Ϯ 0.20 Kb), compared with the absence of adversity; the telomere difference could translate into a 7-to 15-year difference in life span. Abuse was associated with heightened IL-6 and TNF-␣ levels; for TNF-␣, this relationship was magnified in caregivers compared with controls. Moreover, abuse and caregiving status were associated significantly and independently with higher levels of depressive symptoms. Conclusions: Adverse childhood events are related to continued vulnerability among older adults, enhancing the impact of chronic stressors. Childhood adversities cast a very long shadow.
Telomeres and Early-Life Stress: An Overview
Biological Psychiatry, 2013
The long-term sequelae of adverse early-life experiences have long been a focus in psychiatry, with a historic neurobiological emphasis on physiological systems that are demonstrably stressresponsive, such as the hypothalamic-pituitary-adrenal (HPA) axis and neuroimmune function. However, there has been increasing recognition in the general medical literature that such sequelae might encompass more pervasive alterations in health status and physiology. Recent findings in telomere biology have suggested a new avenue for exploring the adverse health effects of childhood maltreatment. Telomere length in proliferative tissues declines with cell replication, and the effect can be accelerated by such factors as inflammation, oxidative stress, radiation, and toxins. Reduced telomere length, as a proxy for cellular aging, has been associated with numerous chronic somatic diseases that are generally considered to be diseases of aging, such as diabetes, cancer, and heart disease. More recently, shorter telomeres have been demonstrated in several psychiatric conditions, particularly depression. Sustained psychosocial stress of a variety of types in adulthood appears to be associated with shorter telomeres. Now, emerging work suggests a robust, and perhaps dose-dependent, relationship with early-life stress. These findings present new opportunities to re-conceptualize the complex relationships between experience, physical and psychiatric disease, and aging.
Adverse childhood experiences and leukocyte telomere maintenance in depressed and healthy adults
Journal of Affective Disorders, 2014
BACKGROUND-Adverse childhood experiences (ACEs) are associated with poor physical and mental health outcomes in adulthood. Adverse childhood experiences are also associated with shortened leukocyte telomere length (LTL) in adults, suggesting accelerated cell aging. No studies have yet assessed the relationship of ACEs to LTL in individuals with major depressive disorder (MDD), despite the high incidence of antecedent ACEs in individuals with MDD. Further, no studies in any population have assessed the relationship of ACEs to the activity of telomerase, the major enzyme responsible for maintaining LTL, or the relationship between telomerase and LTL in individuals with ACEs. METHODS-Twenty healthy, unmedicated adults with MDD and 20 healthy age-, sex-and ethnicity-matched controls had ACEs assessed and had blood drawn for LTL and peripheral blood mononuclear cell (PBMC) resting telomerase activity. RESULTS-In healthy controls, greater ACE exposure was associated with shorter LTL (p< 0.05) but was unassociated with telomerase activity. In MDD, however, the opposite pattern was
Journal of Affective Disorders, 2010
Although several studies have shown that life adversities play an important role in the etiology and maintenance of both depressive and anxiety disorders, little is known about the relative specificity of several types of life adversities to different forms of depressive and anxiety disorder and the concurrent role of neuroticism. Few studies have investigated whether clustering of life adversities or comorbidity of psychiatric disorders critically influence these relationships. Methods: Using data from the Netherlands Study of Depression and Anxiety (NESDA), we analyzed the association of childhood adversities and negative life experiences across the lifespan with lifetime DSM-IV-based diagnoses of depression or anxiety among 2288 participants with at least one affective disorder. Results: Controlling for comorbidity and clustering of adversities the association of childhood adversity with affective disorders was greater than that of negative life events across the life span with affective disorders. Among childhood adversities, emotional neglect was specifically associated with depressive disorder, dysthymia, and social phobia. Persons with a history of emotional neglect and sexual abuse were more likely to develop more than one lifetime affective disorder. Neuroticism and current affective disorder did not affect the adversitydisorder relationships found. Limitations: Using a retrospective study design, causal interpretations of the relationships found are not warranted. Conclusions: Emotional neglect seems to be differentially related to depression, dysthymia and social phobia. This knowledge may help to reduce underestimation of the impact of emotional abuse and lead to better recognition and treatment to prevent long-term disorders.
Psychological Medicine
Background Childhood maltreatment can result in lifelong psychological and physical sequelae, including coronary artery disease (CAD). Mechanisms leading to increased risk of illness may involve emotional dysregulation and shortened leukocyte telomere length (LTL). Methods To evaluate whether (1) childhood maltreatment is associated with shorter LTL among older adults with CAD or other chronic illnesses; (2) sex and/or CAD status influence these results; and (3) symptoms of anxiety, depression, and stress moderate or mediate the association between childhood maltreatment and LTL, men and women (N = 1247; aged 65 ± 7.2 years) with and without CAD completed validated questionnaires on childhood maltreatment, symptoms of depression, anxiety, and perceived stress. LTL was measured using quantitative polymerase chain reaction. Analyses included bivariate correlations, hierarchical regressions, and moderation/mediation analyses, controlling for sociodemographic and lifestyle variables. Re...
Early-life stress, such as maltreatment, institutionalization, and exposure to violence, is associated with accelerated telomere shortening. Telomere shortening may thus represent a biomarker of early adversity. Previous studies have suggested that responsive parenting may protect children from the negative biological and behavioral consequences of early adversity. This study examined the role of parental responsiveness in buffering children from telomere shortening following experiences of early-life stress. We found that high-risk children had significantly shorter telomeres than low-risk children, controlling for household income, birth weight, gender, and minority status. Further, parental responsiveness moderated the association between risk and telomere length, with more responsive parenting associated with longer telomeres only among high-risk children. These findings suggest that responsive parenting may have protective benefits on telomere shortening for young children exposed to early-life stress. Therefore, this study has important implications for early parenting interventions.
Stress-related telomere length in children: A systematic review
Journal of Psychiatric Research, 2017
Telomeres are repetitive DNA sequences at the ends of chromatids that shorten following each cell replication. Once telomeres reach a critical length, DNA defense mechanisms can direct cells to either a state of arrest (senescence) or apoptosis. Stress induced by adversity is a probable cause of accelerated telomere shortening from an early age. However, few studies have examined the association between stress and telomere length in children, and it remains unclear whether young individuals may show signs of cellular aging early in life. Our aim was to examine whether adversity in childhood is associated with shortening of telomere length. We conducted a systematic review of studies that investigated the association between stress and telomere length in children from 3 to 15 years of age. Eleven studies met our selection criteria. We concluded that adversity in childhood (such as violence, low socioeconomic status, maternal depression, family disruption, and institutionalization) have an impact on telomere length. This suggests that exposed individuals show signs of accelerated erosion of telomeric ends from an early age. We discuss whether telomere shortening is related to negative health outcomes later in life or could be a biomarker predicting health outcomes. We believe that further large-scale longitudinal studies that repeatedly monitor telomere length are very important for providing a better assessment of telomere trajectory in psychologically stressed children. This will verify the extent to which adversity impacts upon the biological development of cell aging in childhood.
Stressful Life Events in Early Life and Leukocyte Telomere Length in Adulthood
2018
Background. Exposure to stressful life events (SLEs) in early life is associated with higher rates of morbidity and mortality from age-related chronic disease. In this study, we considered whether these general patterns extend to leukocyte telomere length (TL), an indicator of cellular aging. We also explored potential subgroup variations by race and age. Methods. Using cross-sectional data from the Nashville Stress and Health Study (2011-2014), a probability sample of 1,108 adults (558 blacks and 550 whites) ages 22-69, we tested whether SLEs experienced in early life were associated with shorter telomeres in adulthood. Leukocyte TL was measured using the monochrome multiplex quantitative polymerase chain reaction method with albumin as the single-copy reference sequence. An index of 32 potentially traumatic events experienced before the age of 18 was employed. An abbreviated index of seven events that are frequently used in telomere research was also employed. Results. The complete SLEs index was unrelated to TL in the full sample (β = -0.003; p = 0.058) and for blacks (β = -0.003; p = 0.28), whites (β = -0.004; p = 0.18), and adults aged 45 or older (β = 0.001; p = 0.68). The complete SLEs index was inversely associated with telomere length (β = -0.007; p = 0.002) for those adults under the age of 45. Each additional SLE experienced before the age of 18 was associated with a reduction in TL equivalent to one additional year of age. The association between the complete SLEs index and TL for those under the age of 45 was statistically different from those aged 45 or older (t = 2.02; p = 0.04). In no case, was the abbreviated SLEs index related to TL. Conclusion. This study confirms that the long-term health consequences of SLEs in early life can extend to shorter leukocyte telomeres in adults aged 22 to 44, but not adults aged 45 to 69. Our analyses also showed that the association between SLEs and TL is sensitive to the precise measurement of SLEs. We discuss the substantive and methodological implications of our findings for research on SLEs and cellular aging.
Pediatric Research
Background Although investigations have begun to differentiate biological and neurobiological responses to a variety of adversities, studies considering both endocrine and immune function in the same datasets are limited. Methods Associations between proximal (family functioning, caregiver depression, and anxiety) and distal (SES-D; socioeconomic disadvantage) early-life adversities with salivary inflammatory biomarkers (IL-1β, IL-6, IL-8, and TNF-α) and hair HPA markers (cortisol, cortisone, and dehydroepiandrosterone) were examined in two samples of young U.S. children (N = 142; N = 145). Results Children exposed to higher SES-D had higher levels of TNF-α (B = 0.13, p = 0.011), IL-1β (B = 0.10, p = 0.033), and DHEA (B = 0.16, p = 0.011). Higher family dysfunction was associated with higher cortisol (B = 0.08, p = 0.033) and cortisone (B = 0.05, p = 0.003). An interaction between SES-D and family dysfunction was observed for cortisol levels (p = 0.020) whereby children exposed to l...