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Would depression management relieve pain and improve function.

Mei-Jen Ho·Joseph Biskupiak
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Abstract

Chronic pain represents an important clinical, social, and economic problem that often is confounded by affective disorders. While clinicians do not know if chronic pain induces depression or depression initiates pain, co-morbidity is common and the burden of illness increases when patients suffer from both illnesses. The patient's quality of life dramatically decreases leading to decreased functioning which makes the treatment for pain more complicated. Patients who have chronic pain also may benefits from antidepressant medications for improved function and quality of life. To obtain optimal clinical outcomes, it is imperative to address both conditions when planning therapy for and studies of chronic pain.

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ComorbidityDepressionHumansOutcome and Process Assessment, Health CarePain ManagementQuality of LifeJournal Article

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Mei-Jen Ho, Joseph Biskupiak. 2004. Would depression management relieve pain and improve function.. https://doi.org/10.1300/j354v18n04_10

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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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