ncbi.nlm.nih.gov/pubmed/17026771
Mew, I haven’t seen this study from Iran (2008) given enough credence. It shows that finasteride causes anxiety and depression. It’s a good study with statistically significant findings.
The study was posted by John (who highlighted the Swedish Prescription Information), but it has not been added to ‘Finasteride Studies’ I think it should be added.
JN
Can anyone in the medical profession explain why these studies conclude things like this…
CONCLUSION: This preliminary study suggests that finasteride might induce depressive symptoms; therefore this medication should be prescribed cautiously for patients with high risk of depression. It seems that further studies would be necessary to determine behavioral effects of this medication in higher doses and in more susceptible patients
To me it would seem that the appropriate conclusion is that finasteride significantly alters brain chemistry and caution should be taken in prescribing for cosmetic purposes until we understand that more fully. They make this neurosteroid issue sound like something that only concerns a handful of depression-susceptible patients.
Finasteride disturbs Neurosteroid Synthesis (Allopregnolnone(THP)).
This is the reason finasteride causes depression because I believe our 5 AR II enzyme isn’t working properly, thus low allopregnolnone levels. There are many studies that I have posted that were done on rats in regards to social isolation and social activity with rats that have high allopregnolone levels and low allopregnolone levels.
I believe when JN takes DHT supplement his body find homeostasis and restores neurosteroid synthesis. The body is able to do it’s job and make proper conversions. This is only my assumption however.
Thinking further however, would it be possible with a drug like ganoloxone which is in phase II studies, which indeed upregulates allopregnlolone levels mean that we wouldn’t need DHT replacement if the drug is effective? Is it DHT levels that is necessary for proper functioning or upregulated allopregnolone levels?
Another idea would to experiment with a very low dose of Prozac. Prozac is an SSRI so I would caution on it’s usage. There are studies that show it prevents downregulation.
To me, ganoloxone would be the drug to really experiment with and see if my theory is correct. For now, go with what works, and that’s DHT replacement if you can sustain a TRT regimen. I’m just throwing out my thought process.
These are both assumptions and until tested cannot be proven. Unfortunately no commercial test exists to measure Allopregnanolone, however I do not believe it has been permanently “downregulated” because as noted in the literature, depression typically clears up within 2 weeks of stopping drug, meaning 5AR is working again. This is precisely what I experienced as well, after I quit.
Mew, I remember you mentioning in a previous post that a genital skin fibroblast would be able to test for 5 alpha reductase activity. If someone was able to get this test then perhaps it would help with this debate over whether or not the problem lies with decreased levels of 5 alpha reductase.
It’s just that it doesn’t look like this issue is going to be resolved anytime soon as most of the theorizing is based on anecdotal evidence. I don’t know how easy this test is to get done commercially but i think it would be an important step forward.
I imagine the ideal situation would be to do a genital skin fibroblast along with 3 Adiol G and a full hormone profile.