Generally re-generates 30 days after consuming your last pill of finasteride.
Though depending on the dosage you took, pretty sure most guys DHT goes back to normal. There’s things you can take to increase enzyme production. Cooking oils such as canola and vegetable oil, also creatine increases action of 5AR (Really works).
Things like Zinc, Coconut oil, Green Tea etc reduce 5AR2.
It increases energy production via ATP during anaerobic exercise. It’s a non essential nutrient though it’s found in food.
When I used to take it, my drive was massive.
I’m guessing your testosterone is also low which essentially converts to dht. As dht is more potent than testosterone, you may feel worse taking zinc. Try get your hormonal panel done, may be a private company that does it, look online.
Jonson, where did you hear that Toco 8 is a 5ar Inhibitor? I have looked all over the place for this information and I cannot find it. I’m currently taking Toco 8 and am going to stop if this is true. Can someone confirm this?
I’m currently doing an experiment, but it’s too early to talk about it. I’ve been researching growth factors for a while too, but it’s hard to find information. I believe that our bodies aren’t replacing those enzymes like they should. If we figure out which growth factors that are involved with replacing enzymes, we could compare our levels with normal men.
Serotonin can do it. My brain fog cleared on 5htp. There is no doubt a serotonin link to all this. Anxiety, Depression, libido serotonin is known to have effects on all of them.
Serotonergic 5-HT2A receptor stimulation induces steroid 5alpha-reductase gene expression in rat C6 glioma cells via transcription factor Egr-1.
Morita K, Arimochi H, Her S.
Source
Department of Pharmacology, Tokushima University School of Medicine, 3-18-15 Kuramoto, Tokushima 770-8503, Japan. km@basic.med.tokushima-u.ac.jp
Abstract
Selective serotonin reuptake inhibitors (SSRIs) are widely used for the treatment of depressive mood disorders and well known to inhibit the reuptake of neurotransmitter serotonin into nerve terminals. Thus, it seems conceivable that these drugs may induce the outflow of serotonin from the synapse as a consequence of inhibiting the reuptake, resulting in the stimulation of glial cells surrounding nerve terminals. On this hypothesis, the effect of serotonin on steroid 5alpha-reductase type 1 (5alpha-R) gene expression in rat C6 glioma cells was examined as one of the in vitro model experiments for investigating the indirect influence of SSRIs on glial cells. Serotonin elevated 5alpha-R mRNA and protein levels through the stimulation of serotonin 5-HT2A receptors, and also elevated Egr-1 mRNA and protein levels prior to 5alpha-R gene expression in the glioma cells. Furthermore, serotonin failed to significantly increase 5alpha-R mRNA levels in the cells preloaded with the antisense oligodeoxynucleotide targeted on Egr-1 gene. These results indicate that serotonin may stimulate 5alpha-R gene expression via transcription factor Egr-1 in glial cells, thus suggesting that serotonin flowing out of the serotonergic synapse may be implicated in SSRI-induced changes in neurosteroid metabolism in brain