Microbiota-induced epigenetic alterations in depressive disorders are targets for nutritional and probiotic therapies

Major depressive disorder (MDD), being a complicated condition in nature, affects 280 million individuals globally and is a primary cause of disability. Numerous environmental variables, including medicines, nutrition, and microorganisms, have a role in the pathophysiology of depression disorders. The host immune system, genetics, and epigenetics are some of the contributors to the intricate underlying causes of depression. Alterations to intestinal microbiota and their metabolites affect how people with depressive disorders respond to stress and behave in social situations by influencing immune cell maturation and brain neurogenesis, which is mediated by epigenetic changes. In this study, Nohesara et al. (2023) address the possible contributions of dysregulated gut permeability to the emergence of depressive illnesses through changes in metabolites generated from the gut microbiota that have epigenetic consequences. In addition, the authors discuss how changes in the makeup of the gut microbiota might lead to epigenetic changes that can cause depressive illnesses. Focus is shed on the potential benefits of microbiota-derived metabolites, such as probiotics, butyrate (which acts as an epigenetic modifier), polyphenols, medications (such as antibiotics, antipsychotics, and antidepressants), maternal diet, and fecal microbiota transplantation, in mitigating depressive-like behaviors through altering the epigenetic landscape. Lastly, the authors review the difficulties and potential solutions connected to current treatment techniques for depressive disorders via microbiome-related epigenetic changes. [NPID: Major depressive disorder, gut microbiome, diet, probiotics, epigenetic modifiers]

Year: 2023

Reference: Nohesara, S., Abdolmaleky, H. M., Zhou, J.-R., & Thiagalingam, S. (2023). Microbiota-induced epigenetic alterations in depressive disorders are targets for nutritional and probiotic therapies. In Genes (Vol. 14, Issue 12). https://doi.org/10.3390/genes14122217

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