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.

Background & Hypothesis Psychotic disorders are inequitably distributed by race in the United States, although it is not known whether this is due to assessment biases or inequitable distributions of risk factors. Psychotic experiences are subclinical hallucinations and delusions used to study the etiology of psychosis, which are based on self-report and therefore not subject to potential clinician biases. In this study, we test whether the prevalence of psychotic experiences (PE) varies by race and if this variance is explained by socioenvironmental risk factors. Study Design Data on demographics, PE, and socioenvironmental risk factors were collected through the National Survey of Poly-victimization and Mental Health, a national probability sample of US young adults. Logistic regression analyses were used to determine whether PE prevalence varied by race/ethnicity and, if so, whether this was attenuated with inclusion of indicators of income, education, urban/rural living, discrimination, and trauma exposure. Study Results Black and Hispanic respondents reported PE at significantly greater rates than White or “other” ethnoracial groups, with hallucinations more commonly reported by Hispanic respondents. PE were significantly associated with police violence exposure, discrimination, adverse childhood experiences, and educational attainment. These factors statistically explained ethnoracial differences in the likelihood of overall PE occurrence and of nearly all PE subtypes. Conclusions Previously observed racial differences in psychosis extend beyond clinical schizophrenia, and therefore, are unlikely to be explained entirely by clinician biases. Instead, racial disparities in PE appear to be driven by features of structural racism, trauma, and discrimination.

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