Pao-Yen Lin1, Yu-Chi Huang2, Chi-Fa Hung3. 1. Department of Psychiatry, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung, Taiwan; Center for Translational Research in Biomedical Sciences, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung, Taiwan. Electronic address: paoyenilin@gmail.com. 2. Department of Psychiatry, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung, Taiwan. Electronic address: ychuang01@gmail.com. 3. Department of Psychiatry, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung, Taiwan. Electronic address: chifa.hung@gmail.com.
Abstract
BACKGROUND: Accelerated telomere shortening is associated with stress-related cell damage and aging. Patients with depression have been shown to have shortened life expectancy and to be associated with multiple age-related systemic diseases. Previous studies have examined leukocyte telomere length (LTL) in patients with depression, but have shown inconsistent results. METHODS: We conducted meta-analyses by pooling relevant results strictly from all eligible case-control studies for cross-sectional comparison of LTL between depressive patients and control subjects (16 studies involving 7207 subjects). The effect sizes (shown as Hedges' g) of each individual study were synthesized by using a random effects model. RESULTS: Our analysis revealed telomere length is significantly shorter in subjects with depression in comparison to healthy controls (Hedges' g = -0.42, p = 1 × 10(-5), corresponding to r = -0.21). Significant heterogeneity among studies examining LTL in subjects with depression was found (Q = 116.07, df = 16, I(2) = 86.21%, p < 1 × 10(-8)), which can possibly be explained by methods used in measuring telomere length (Q = 18.42, df = 2, p = 1 × 10(-4)). There was no significant publication bias, nor moderating effect of age, female percentage, or illness duration of depression on synthesized results. CONCLUSIONS: Our results support the hypothesis that depression is associated with accelerated cell aging. Future studies are required to clarify whether the association is mediated through environmental stress, and whether effective treatment can halt cell aging.
BACKGROUND: Accelerated telomere shortening is associated with stress-related cell damage and aging. Patients with depression have been shown to have shortened life expectancy and to be associated with multiple age-related systemic diseases. Previous studies have examined leukocyte telomere length (LTL) in patients with depression, but have shown inconsistent results. METHODS: We conducted meta-analyses by pooling relevant results strictly from all eligible case-control studies for cross-sectional comparison of LTL between depressivepatients and control subjects (16 studies involving 7207 subjects). The effect sizes (shown as Hedges' g) of each individual study were synthesized by using a random effects model. RESULTS: Our analysis revealed telomere length is significantly shorter in subjects with depression in comparison to healthy controls (Hedges' g = -0.42, p = 1 × 10(-5), corresponding to r = -0.21). Significant heterogeneity among studies examining LTL in subjects with depression was found (Q = 116.07, df = 16, I(2) = 86.21%, p < 1 × 10(-8)), which can possibly be explained by methods used in measuring telomere length (Q = 18.42, df = 2, p = 1 × 10(-4)). There was no significant publication bias, nor moderating effect of age, female percentage, or illness duration of depression on synthesized results. CONCLUSIONS: Our results support the hypothesis that depression is associated with accelerated cell aging. Future studies are required to clarify whether the association is mediated through environmental stress, and whether effective treatment can halt cell aging.
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