Psychological factors such as the stress of caregiving are emerging as predictors of telomere length, an index of biological aging. However, although lifetime major depressive disorder is associated with shorter telomeres, less is known about depressive symptoms. Depression and depressive symptoms are associated with a range of morbidities and mortality, but the extent to which they predict biological aging is unclear. The present study examined participants in the West of Scotland Twenty-07 Study across three age cohorts and four waves of data collection from 1992/1993 to 2007/2008.Methods
Participants were 37, 57, and 76 years old at final data collection. Depressive symptoms were measured using the Hospital Anxiety and Depression Scale at each time point. Telomere length was assessed from 1063 blood samples collected at the final wave in 2007/2008 for respondents who also had depression data.ResultsAverage depression symptoms (β= -.12, p = .047) and their change over time (β = -.12, p = .031) were negatively associated with telomere length, but only in the youngest cohort. Depressive symptoms were not cross sectionally associated with telomere length in 2007 to 2008 (β= -.03, p = .45). In the youngest cohort only, depressive symptoms assessed in 1995 to 1997 and 2000 to 2004 were associated with shorter telomere length (β = .14 [p = .046] and β = .18 [p = .012], respectively), but not 1992 to 1993 or 2007 to 2008; associations in the middle- and older-aged cohorts were nonsignificant.Conclusions
Depressive symptoms are longitudinally associated with shorter telomere length, but only in younger adults.
"The authors argue that the physiological hyperarousal and physiological stress associated with anxiety disorders may cause telomere damage, consistent with other studies linking psychological stress with shorter TL (Ahola et al., 2012; Drury et al., 2012; 2014; Entringer et al., 2011; 2013; Epel et al., 2004; Humphreys et al., 2012; Kananen et al., 2010; O'Donovan et al., 2011; Price et al., 2013; Shalev et al., 2013a; Shalev et al., 2013b; Surtees et al., 2011; Tyrka et al., 2010; Uchino et al., 2012). On the other hand, there are also studies that do not support such an association, among them a most recent study assessing life stress in a 30-year birth cohort (Jodczyk et al., 2014; Phillips et al., 2013; Rius-Ottenheim et al., 2012). Our findings thus add further support to the assumption that shorter TL is not per se a risk factor for psychiatric disorders. "
[Show abstract][Hide abstract] ABSTRACT: Shorter telomere length (TL) has found to be associated with lower birth weight and with lower cognitive ability and psychiatric disorders. However, the direction of causation of these associations and the extent to which they are genetically or environmentally mediated are unclear. Within-pair comparisons of monozygotic (MZ) and dizygotic (DZ) twins can throw light on these questions. We investigated correlations of within pair differences in telomere length, IQ, and anxiety/depression in an initial sample from Brisbane (242 MZ pairs, 245 DZ same sex (DZSS) pairs) and in replication samples from Amsterdam (514 MZ pairs, 233 DZSS pairs) and Melbourne (19 pairs selected for extreme high or low birth weight difference). Intra-pair differences of birth weight and telomere length were significantly correlated in MZ twins, but not in DZSS twins. Greater intra-pair differences of telomere length were observed in the 10% of MZ twins with the greatest difference in birth weight compared to the bottom 90% in both samples and also in the Melbourne sample. Intra-pair differences of telomere length and IQ, but not of TL and anxiety/depression, were correlated in MZ twins, and to a smaller extent in DZSS twins. Our findings suggest that the same prenatal effects that reduce birth weight also influence telomere length in MZ twins. The association between telomere length and IQ is partly driven by the same prenatal effects that decrease birth weight.
Twin Research and Human Genetics 03/2015; 18(02):1-12. DOI:10.1017/thg.2015.3 · 2.30 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Accumulating data have led to a re-conceptualization of depression that emphasizes the role of immune-inflammatory processes, coupled to oxidative and nitrosative stress (O&NS). These in turn drive the production of neuroregulatory tryptophan catabolites (TRYCATs), driving tryptophan away from serotonin, melatonin, and N-acetylserotonin production, and contributing to central dysregulation. This revised perspective better encompasses the diverse range of biological changes occurring in depression and in doing so provides novel and readily attainable treatment targets, as well as potential screening investigations prior to treatment initiation. We briefly review the role that immune-inflammatory, O&NS, and TRYCAT pathways play in the etiology, course, and treatment of depression. We then discuss the pharmacological treatment implications arising from this, including the potentiation of currently available antidepressants by the adjunctive use of immune- and O&NS-targeted therapies. The use of such a frame of reference and the treatment benefits attained are likely to have wider implications and utility for depression-associated conditions, including the neuroinflammatory and (neuro)degenerative disorders.
[Show abstract][Hide abstract] ABSTRACT: There is evidence that persistent psychiatric disorders lead to age-related disease and premature mortality. Telomere length has emerged as a promising biomarker in studies that test the hypothesis that internalizing psychiatric disorders are associated with accumulating cellular damage. We tested the association between the persistence of internalizing disorders (depression, generalized anxiety disorder and post-traumatic stress disorder) and leukocyte telomere length (LTL) in the prospective longitudinal Dunedin Study (n=1037). Analyses showed that the persistence of internalizing disorders across repeated assessments from ages 11 to 38 years predicted shorter LTL at age 38 years in a dose-response manner, specifically in men (β=-0.137, 95% confidence interval (CI): -0.232, -0.042, P=0.005). This association was not accounted for by alternative explanatory factors, including childhood maltreatment, tobacco smoking, substance dependence, psychiatric medication use, poor physical health or low socioeconomic status. Additional analyses using DNA from blood collected at two time points (ages 26 and 38 years) showed that LTL erosion was accelerated among men who were diagnosed with internalizing disorder in the interim (β=-0.111, 95% CI: -0.184, -0.037, P=0.003). No significant associations were found among women in any analysis, highlighting potential sex differences in internalizing-related telomere biology. These findings point to a potential mechanism linking internalizing disorders to accelerated biological aging in the first half of the life course, particularly in men. Because internalizing disorders are treatable, the findings suggest the hypothesis that treating psychiatric disorders in the first half of the life course may reduce the population burden of age-related disease and extend health expectancy.Molecular Psychiatry advance online publication, 14 January 2014; doi:10.1038/mp.2013.183.
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