Since tryptophan to 5-HT' is a substrate limited rxn there's no need for a feedback mechanism, thus excess tryptophan ends up driving 5-HT" production. So it would make sense that an SSRI might drive 5-HT" via increased 5-HT' concentrations. But it doesn't appear to do so at all
PubMed. The SSRIs that affected 5-HT" levels did so by inhibiting degradation. Fluoxetine (Prozac) had no such effect. I suspect fluoxetine was prescribed simply on the basis that severe insomnia and depression are associated (i.e. whether insomnia is a symptom or a cause of the depression).
As an aside I don't know why anyone would take tryptophan when 5-HT" can be bought at vitamin stores. It doesn't make sense to drive 5-HT' production to supraphysiological levels just to get a little 5-HT".
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Since tryptophan to 5-HT' is a substrate limited rxn there's no need for a feedback mechanism, thus excess tryptophan ends up driving 5-HT" production. So it would make sense that an SSRI might drive 5-HT" via increased 5-HT' concentrations. But it doesn't appear to do so at all PubMed. The SSRIs that affected 5-HT" levels did so by inhibiting degradation. Fluoxetine (Prozac) had no such effect. I suspect fluoxetine was prescribed simply on the basis that severe insomnia and depression are associated (i.e. whether insomnia is a symptom or a cause of the depression). As an aside I don't know why anyone would take tryptophan when 5-HT" can be bought at vitamin stores. It doesn't make sense to drive 5-HT' production to supraphysiological levels just to get a little 5-HT".