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Comorbidity Between Mood Disorders and Chronic Somatic Diseases, With a Focus on Cardiometabolic Disease, and Its Mechanistic Crosstalk.

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Title: Comorbidity Between Mood Disorders and Chronic Somatic Diseases, With a Focus on Cardiometabolic Disease, and Its Mechanistic Crosstalk.
Authors: Du, Hongzhen (AUTHOR), Du, Gangqiang (AUTHOR), Zhang, Qian (AUTHOR), Zhao, Yixuan (AUTHOR), Fan, Jilin (AUTHOR), Zhou, Yufeng (AUTHOR), Sun, Zihao (AUTHOR), Li, Chen (AUTHOR), Li, Wei (AUTHOR), Bose, Chandra (AUTHOR)
Source: Depression & Anxiety (1091-4269). 7/24/2026, Vol. 2026, p1-27. 27p.
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. [ABSTRACT FROM AUTHOR]
Copyright of Depression & Anxiety (1091-4269) is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
Database: Psychology and Behavioral Sciences Collection
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  Data: Comorbidity Between Mood Disorders and Chronic Somatic Diseases, With a Focus on Cardiometabolic Disease, and Its Mechanistic Crosstalk.
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  Data: <searchLink fieldCode="AR" term="%22Du%2C+Hongzhen%22">Du, Hongzhen</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Du%2C+Gangqiang%22">Du, Gangqiang</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Zhang%2C+Qian%22">Zhang, Qian</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Zhao%2C+Yixuan%22">Zhao, Yixuan</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Fan%2C+Jilin%22">Fan, Jilin</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Zhou%2C+Yufeng%22">Zhou, Yufeng</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Sun%2C+Zihao%22">Sun, Zihao</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Li%2C+Chen%22">Li, Chen</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Li%2C+Wei%22">Li, Wei</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Bose%2C+Chandra%22">Bose, Chandra</searchLink> (AUTHOR)
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  Data: <searchLink fieldCode="JN" term="%22Depression+%26+Anxiety+%281091-4269%29%22">Depression & Anxiety (1091-4269)</searchLink>. 7/24/2026, Vol. 2026, p1-27. 27p.
– Name: Abstract
  Label: Abstract
  Group: Ab
  Data: 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. [ABSTRACT FROM AUTHOR]
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  Data: <i>Copyright of Depression & Anxiety (1091-4269) is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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