Studies of the genomic architecture of complex phenotypes, which include common somatic and mental diseases, have shown them to be characterized by high levels of polygenicity, i.e., there are large numbers of genes associated with the risk of developing these diseases. There is interest in establishing the genetic similarity of these two groups of diseases. The purpose of the present review is to analyze genetic studies of the comorbidity of somatic and mental diseases from the point of view of the universality and specificity of mental disorders in somatic diseases, the reciprocal relationships of these types of pathologies, and the modulating influence of external environmental factors on comorbidity. The analysis results point to the existence of a common genetic predisposition to mental and somatic diseases. The existence of genes common to both does not exclude specificity of the development of mental disorders in relation to specific somatic pathologies. We can suggest the existence of genes unique to a particular somatic and comorbid mental illness, as well as genes common to these diseases. Common genes may have varying degrees of specificity, i.e., they are universal in nature, this being apparent, for example, in the development of major depressive disorder in a variety of somatic diseases; common genes can also be specific for only a couple of individual diseases (schizophrenia and breast cancer). Moreover, common genes can have multidirectional effects, which also contributes to the specificity of comorbidity. In addition, the search for common genes for somatic and mental diseases needs account to be taken of the modulating influences of confounding factors (treatment, unhealthy lifestyle, behavioral characteristics), which may also differ in specificity depending on the diseases in question.
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Translated from Zhurnal Nevrologii i Psikhiatrii imeni S. S. Korsakova, Vol. 123, No. 4, Iss. 2, pp. 60–64, April, 2023.
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Golimbet, V.E., Klyushnik, T.P. Genome-Wide Studies of the Comorbidity of Somatic and Mental Diseases. Neurosci Behav Physi 53, 1386–1390 (2023). https://doi.org/10.1007/s11055-023-01531-4
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DOI: https://doi.org/10.1007/s11055-023-01531-4