SSRIs as COVID treatment

gaze

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i mean, its possible. SSRIs dont necessarily always increase serotonin. Its possible its regulating it somehow, and given we know that covid is serotonin syndrome it could be having some beneficial effect by normalizing it and/or changing how its attached to receptors. granted I know absolutely nothing about fluvoxamine
 
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Peat said:
"One of the many actions of the "SSRI" (such as fluoxetine, Prozac), which aren’t related to their effect on serotonin, is to increase the concentration of allopregnanolone in the brain, imitating the action of increased progesterone. Following this discovery, Lilly got Prozac approved as a treatment for premenstrual syndrome. Since the production of allopregnanolone and progesterone depends on the availability of pregnenolone and cholesterol, a low cholesterol level would be one of the factors making this an inappropriate way to treat PMS."
 

davidgraham

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my friend has healed her severe meniers disease using sertraline. She couldnt work before now she is completely well on it. No idea why
 

aliml

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Fluvoxamine increases nitric oxide


 

haidut

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We live in a clown world


In addition to the allopregnanolone effect mention by Peat, some of the SSRI drugs are antagonists on specific serotonin receptors. So, while they increase serotonergic tone over time, some of them have partial anti-serotonin effects, and that receptor antagonism effect may relieve depression or help mitigate a viral infection.
 

aliml

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Fluoxetine hydrochloride associated with a lower mortality risk among patients with COVID-19

In this multicenter cohort study analyzing electronic health records of 83 584 patients diagnosed with COVID-19, including 3401 patients who were prescribed SSRIs, a reduced relative risk of mortality was found to be associated with the use of SSRIs—specifically fluoxetine—compared with patients who were not prescribed SSRIs.

These findings suggest that SSRI use may reduce mortality among patients with COVID-19, although they may be subject to unaccounted confounding variables; further investigation via large, randomized clinical trials is needed.


Several mechanisms by which SSRIs can reduce the severity of COVID-19 symptoms have been proposed in the literature. The severe respiratory illness of COVID-19 is primarily triggered by an intense proinflammatory host response. Selective serotonin reuptake inhibitors may benefit patients with COVID-19 owing to the link between serotonin and the immune system.

More specifically, severe outcomes of COVID-19 have been associated with several proinflammatory cytokines, including interleukin 6, whose increased levels contribute to the cytokine storm.7 Various studies have indicated that SSRIs and specifically fluoxetine can decrease levels of these cytokines and interleukin 6 signaling activity.

Some SSRIs, such as fluoxetine and fluvoxamine, may modulate the sigma-1 receptor-IRE1 pathway, thereby reducing damaging aspects of the inflammatory response.

Another potential explanation could be related to their inhibiting effect on the acid sphingomyelinase/ceramide system, whose activation may play an important role in SARS-CoV-2 infection because it leads to the formation of ceramide-enriched membrane domains that facilitate viral entry and infection by clustering angiotensin-converting enzyme 2, the cellular receptor of SARS-CoV-2

Metabolic markers of ceramide metabolism have also been associated with respiratory severity and inflammation in patients hospitalized for COVID-19.15 Finally, some evidence suggests that SSRIs and especially fluoxetine could have antiviral effects.
 
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