Antidepressants Enhance Host-Resistance in the Body
Research Article
DOI:
https://doi.org/10.70829/ijrmcs.v02.i02.013Keywords:
antidepressant, acid sphingomyelinase enzyme, immunity, infection, stressAbstract
A review of scientific literature indicates that the use of antidepressants can be generalized to all forms of stress and inflammation as an adjunctive therapy that enhances host resistance. The effects of antidepressants on mood are well-documented through their emotional, cognitive, and behavioral impacts, but these effects do not fully explain their cellular actions. Antidepressants exert trophic effects on cells, inducing neurogenesis and synaptic connectivity. These trophic effects are highlighted in studies showing that antidepressants increase survival in cells, animals, and humans, as well as promote stem cell proliferation. In both depressed patients and animal models of depression, antidepressants reduce the perception of danger (mood effects). The acid sphingomyelinase (ASM) theory offers a more comprehensive explanation than the monoamine theory for the cellular effects of antidepressants. On a cellular level, antidepressants reduce ceramide production by functionally inhibiting the ASM enzyme. This leads cells toward a state that enhances survival, cyto-protection (cyto-resistance), cell reproduction, and mood improvement. This article reviews studies demonstrating that antidepressants increase host resistance to infections, immunological conflicts, stress, and depression. These findings support the use of antidepressants to enhance host resistance in cases of infections, vaccinations, cell damage, stress, depression, and aging.
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