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PubMed · 10824294

Theoretical and methodological issues in psychiatric comorbidity.

Abstract

The occurrence of multiple diagnoses in one patient is a phenomenon of major clinical and theoretical importance. This paper reviews the various factors involved in real and artifactual comorbidity. Important causes of spurious comorbidity are discussed, including invalidity of the individual diagnoses, use of inappropriate diagnostic paradigms, descriptive overlap of diagnostic criteria, ascertainment bias, and diagnostic bias. To illustrate some of the concepts discussed, two examples are presented: the comorbidity of schizophrenia and substance use disorders, and the comorbidity of posttraumatic stress disorder and major depression. The study of comorbidity can advance psychiatry by helping us to clarify our thinking about categories of illness and the boundaries between them, as well as the relationships among these categories.

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BibTeXRIS

M P Bogenschutz, H G Nurnberg. Theoretical and methodological issues in psychiatric comorbidity.. https://pubmed.ncbi.nlm.nih.gov/10824294/

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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.

Comorbidity↗