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Comorbidity in depression.

D J Kupfer·E Frank
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Abstract

OBJECTIVE: To define the extent of comorbidity in depression. METHOD: The level of medical comorbidity in depression was assessed on the basis of the empirical literature and results from the National Institute of Mental Health (NIMH) conference on Depression's Toll on Other Illnesses. RESULTS: The global incidence of depression underscores the need to develop integrative treatment strategies for these disorders. An NIMH conference entitled 'The Unwanted Cotraveler: Depression's Toll on Other Illnesses' has highlighted the impact of increased depression prevalence in the presence of medical disorders. Economic data from a large health insurance claims database concludes that the presence of a psychiatric condition, particularly depression, considerably increases the medical costs, as well as the cost of caring for the psychiatric condition. CONCLUSION: Federally sponsored research intervention centres need to address these issues and provide opportunities for diverse medical specialties to collaborate on testing novel treatment approaches.

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ComorbidityDatabases, FactualDepressionHealth Care CostsHealth PolicyHumansInsurance, HealthJournal ArticleResearch Support, Non-U.S. Gov'tResearch Support, U.S. Gov't, P.H.S.Review

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BibTeXRIS

D J Kupfer, E Frank. 2003. Comorbidity in depression.. https://doi.org/10.1034/j.1600-0447.108.s418.12.x

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PubMed2026

Assessing the comorbidity between asthma and depression through polygenic risk scoring and time-to-event models.

BACKGROUND: Patients with asthma have an increased risk of developing depression, affecting their quality of life. To date, the processes contributing to this comorbidity remain unclear. METHODS: We integrated two large genome-wide association studies (88,486 patients with asthma and 447,859 controls; 412,024 patients with depression and 1,587,577 controls) with cross-sectional and longitudinal information available from the All of Us Research Program (N = 87,167) through polygenic risk scoring (PRS), Cox proportional-hazards models, one-sample Mendelian randomization (MR), and gene-set and drug-repurposing analyses. RESULTS: We observed that depression PRS was associated with increased asthma risk (hazard ratio, HR = 1.13, 95% CI = 1.09-1.17), also when accounting for comorbidity status (HR = 1.08, 95% CI = 1.04-1.12). Conversely, the effect of asthma PRS was null after accounting for comorbidity status. One-sample MR analysis showed an effect of depression genetic liability on asthma, ranging from beta = 0.36 ± 0.03 when considering a linear relationship to beta = 3.21 ± 0.31 when considering possible nonlinear relationships. Conversely, the effect of asthma genetic risk on depression was null after accounting for potential confounders. The gene-set analyses showed that asthma and depression polygenic risks share biological processes, molecular functions, and cellular components related to the immune system and the lung-brain axis. CONCLUSIONS: Genetic predisposition contributes to asthma-depression comorbidity through direct effects and shared pathogenic processes. These findings highlight the potential to develop targeted interventions to prevent and treat the co-occurrence of respiratory and neuropsychiatric disorders.

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