Depression, anxiety and telomere length in young adults: evidence from the National Health and Nutrition Examination Survey

Abstract

Telomere length has been hypothesized to be a marker of cumulative exposure to stress, and stress is an established cause of depression and anxiety disorders. The goal of this study was to examine the relationship between depression, anxiety and telomere length, and to assess whether this relationship is moderated by race/ethnicity, gender, and/or antidepressant use. Data were from the National Health and Nutrition Examination Survey, 1999–2002. Telomere length was assessed using the quantitative polymerase chain reaction method of telomere length relative to standard reference DNA. Past year major depression (MD), generalized anxiety disorder (GAD) and panic disorder (PD), as well as depressed affect and anxious affect, were assessed using the Composite International Diagnostic Inventory (N=1,290). Multiple linear regression was used to assess the relationship between depression and anxiety disorders and telomere length. Among women, those with GAD or PD had shorter telomeres than those with no anxious affect (β: −0.07, p<0.01), but there was no relationship among men (β: 0.08, p>0.05). Among respondents currently taking an antidepressant, those with MD had shorter telomeres than those without (β: −.26, p<.05), but there was no association between MD and telomere length among those not using antidepressants (β: −.00, p>.05). Neither depressive nor anxiety disorders were directly associated with telomere length in young adults. There was suggestive evidence that pharmacologically-treated MD is associated with shorter telomere length, likely reflecting the more severe nature of MD that has come to clinical attention.

Telomere length and telomerase in a well-characterized sample of individuals with major depressive disorder compared to controls

“…This may have limited severity and chronicity of the sample; of note, less than half of the sample reported lifetime antidepressant use for over 6 months (40%). Of interest, a recent population based study of young adults with depression also found no difference in telomere length overall or in Caucasians specifically, except in the subsample currently taking antidepressants—a subset interpreted as having severest disease as indicated by prior medical presentation with treatment-warranting symptoms (Needham et al, 2015). Nonetheless, in our study, the cumulative duration of depressive episodes was long (mean of 12.6 (SD=12.8) years) and the mean time from MDD onset was 21.8 years (SD = 14.3, range 4 – 61), representative of chronic MDD.…”

“…Other investigations found no overall association between LTL and MDD but significant association with subpopulations with greater cumulative depression exposure (Wolkowitz et al, 2011) or on antidepressants (Needham et al, 2015). Additionally, Shalev et al (2014) reported significant acceleration of telomere length erosion from age 26 to 38 in males with major depression, but not females.…”

Psychiatric disorders and leukocyte telomere length: Underlying mechanisms linking mental illness with cellular aging

“…Of these, seven found significantly shorter LTL in currently depressed individuals (or in individuals with mixed mood disorders including MDD) compared to controls (Garcia-Rizo et al, 2013; Hartmann et al, 2010; Hoen et al, 2011; Lung et al, 2007; Simon et al, 2006; Verhoeven et al, 2014a; Wikgren et al, 2012b), while four did not (Needham et al, 2014; Schaakxs et al, 2015; Teyssier et al, 2012; Wolkowitz et al, 2011a). Of studies having greater than 40 depressed subjects, all except two (Needham et al, 2014; Schaakxs et al, 2015) found significantly shorter LTL in MDD (Hartmann et al, 2010; Hoen et al, 2011; Lung et al, 2007; Simon et al, 2006; Verhoeven et al, 2014a; Wikgren et al, 2012b). …”

“…Somewhat arguing against this latter explanation, a study in anxiety disorder subjects (reviewed below in section 2.5) found significant LTL shortening only in older subjects (ages 48– 87 years old) (Kananen et al, 2010). The negative study by Needham et al (2014) found that individuals with MDD who were receiving antidepressants did have significantly shorter LTL than controls, but depressed individuals not taking antidepressants did not, and the authors speculated that the former group may have had more serious depressions that required medication treatment. A small-scale negative study (17 MDD and 16 controls) found no significant difference between subjects with MDD and controls, although the MDD sample was largely comprised of recently diagnosed subjects whose current episodes were all less than six months (Teyssier et al, 2012).…”

Stress and telomere shortening among central Indian conservation refugees

“…However, in vivo research linking self-reported levels of experienced psychosocial stress, stress biomarkers (i.e., catecholamines and glucocorticoids), and telomere maintenance are few (60,61), severely limiting our understanding of potential connections and hypothesized mechanisms, such as inflammation and oxidative stress (60,62), in naturally occurring contexts. Furthermore, current population-based stress and telomere studies typically rely on quantitative real-time PCR methodology, which evaluates all of a cell's DNA to assess an average telomere length across many different cell types (19,28,63). Although certainly representing progress in the field, such an approach is still limited by lack of specificity, not only in regard to cell type, but also in evaluation of particular populations of telomeres (e.g., distributions of shortest and/or longest).…”