{"title":"Could antidepressants increase mood and immunity at the same time?","authors":"Francis Lavergne, Therese M Jay","doi":"10.3389/fpsyt.2025.1340179","DOIUrl":null,"url":null,"abstract":"<p><p>A review of scientific literature suggests that the use of antidepressants can be broadly extended to address various forms of stress and inflammation as an adjunctive therapy that enhances host resistance. While the effects of antidepressants on mood are well-documented in terms of their emotional, cognitive, and behavioral impacts, these aspects do not fully explain their cellular mechanisms of action. At the cellular level, antidepressants exert trophic effects that promote neurogenesis and synaptic connectivity. Studies demonstrate that antidepressants improve cell survival, enhance stem cell proliferation, and reduce danger perception (mood effects) in depressed patients and animal models of depression. These trophic properties highlight a deeper biological mechanism beyond their mood-related benefits. The acid sphingomyelinase (ASM) theory of mood offers a more compelling explanation of the cellular effects of antidepressants compared to the monoamine hypothesis. Antidepressants functionally inhibit the ASM enzyme, thereby reducing the production of ceramide, which directs cells toward increased survival, cytoprotection, and reproduction, as well as improved mood. This review also highlights research demonstrating that antidepressants enhance host resistance to infections, immunological challenges, stress, and depression. These findings support the potential use of antidepressants to bolster host resilience in scenarios involving infections, vaccinations, cellular aggression, stress, depression, and even aging.</p>","PeriodicalId":12605,"journal":{"name":"Frontiers in Psychiatry","volume":"16 ","pages":"1340179"},"PeriodicalIF":3.2000,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11936885/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Frontiers in Psychiatry","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.3389/fpsyt.2025.1340179","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/1/1 0:00:00","PubModel":"eCollection","JCR":"Q2","JCRName":"PSYCHIATRY","Score":null,"Total":0}
引用次数: 0
Abstract
A review of scientific literature suggests that the use of antidepressants can be broadly extended to address various forms of stress and inflammation as an adjunctive therapy that enhances host resistance. While the effects of antidepressants on mood are well-documented in terms of their emotional, cognitive, and behavioral impacts, these aspects do not fully explain their cellular mechanisms of action. At the cellular level, antidepressants exert trophic effects that promote neurogenesis and synaptic connectivity. Studies demonstrate that antidepressants improve cell survival, enhance stem cell proliferation, and reduce danger perception (mood effects) in depressed patients and animal models of depression. These trophic properties highlight a deeper biological mechanism beyond their mood-related benefits. The acid sphingomyelinase (ASM) theory of mood offers a more compelling explanation of the cellular effects of antidepressants compared to the monoamine hypothesis. Antidepressants functionally inhibit the ASM enzyme, thereby reducing the production of ceramide, which directs cells toward increased survival, cytoprotection, and reproduction, as well as improved mood. This review also highlights research demonstrating that antidepressants enhance host resistance to infections, immunological challenges, stress, and depression. These findings support the potential use of antidepressants to bolster host resilience in scenarios involving infections, vaccinations, cellular aggression, stress, depression, and even aging.
期刊介绍:
Frontiers in Psychiatry publishes rigorously peer-reviewed research across a wide spectrum of translational, basic and clinical research. Field Chief Editor Stefan Borgwardt at the University of Basel is supported by an outstanding Editorial Board of international researchers. This multidisciplinary open-access journal is at the forefront of disseminating and communicating scientific knowledge and impactful discoveries to researchers, academics, clinicians and the public worldwide.
The journal''s mission is to use translational approaches to improve therapeutic options for mental illness and consequently to improve patient treatment outcomes.