ReviewDepression and anxiety2026
Comorbidity Between Mood Disorders and Chronic Somatic Diseases, With a Focus on Cardiometabolic Disease, and Its Mechanistic Crosstalk.
Review in Depression and anxiety, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
1 citing paper in PubMed.
- Comorbidity Between Mood Disorders and Chronic Somatic Diseases, With a Focus on Cardiometabolic Disease, and Its Mechanistic Crosstalk.Depression and anxiety · 2026Review
Corrections and comments
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The comorbidity of mood disorders (MDs), represented by depression and anxiety, with chronic somatic diseases (CDs), particularly cardiometabolic conditions, poses a significant global public health challenge, markedly increasing the risk of adverse prognoses and all-cause mortality. Epidemiological studies indicate that ~36% of patients with multimorbidity exhibit psychosomatic comorbidity, with higher risk populations concentrated among females, older adults, and socioeconomically disadvantaged individuals. This review systematically analyzes the epidemiological distribution patterns of MD-CD comorbidity, with the strongest emphasis on cardiometabolic diseases-diabetes, metabolic syndrome (MetS), obesity, hypertension (HTA), and cardiovascular disease (CVD)-for which the mechanistic data are most developed, while also addressing osteoarthritis, psoriasis, inflammatory bowel disease (IBD), cancer, and neurological disorders. By integrating molecular mechanisms with clinical evidence, we highlight core pathological pathways and critically evaluate the strength of evidence supporting each: hypothalamic-pituitary-adrenal (HPA) axis dysfunction and insulin resistance (IR), substantiated by clinical data and Mendelian randomization; NLRP3 inflammasome-mediated neuroinflammation as a transdiagnostic inflammatory node; gut-brain axis dysregulation involving bile acid-GLP-1 signaling and gut-derived metabolites such as trimethylamine N-oxide (TMAO); and the kynurenine pathway (KP) as a branched metabolite axis with organ-specific consequences. Sex-specific mechanisms, particularly estrogen-regulated neuroendocrine and metabolic pathways, are identified as consistent biological modifiers of this comorbidity. A bidirectional vicious cycle underpins MD-CD comorbidity: metabolic abnormalities exacerbate limbic system dysfunction via HPA-axis hyperactivity, neuroinflammatory cascades, and disrupted gut-brain signaling, while MDs aggravate metabolic dysregulation through neuroendocrine disturbances and reduced treatment adherence.
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Registered trials
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