5 ALPHA REDUCTASE II And its importance in brain Function.

Perhaps we all share a common genetic predisposition.

Finasteride is a specific inhibitor of steroid Type II 5α-reductase.
Saw Palmetto is assume to have the ability to inhibit both type II and
type I 5α-reductase although the mecanism of how it works is not
really known and fully understood.

From this specific study we know that there are two major metabolic pathway in the brain

Quote
The two major metabolic pathways that transform steroids in the brain are: the 5alpha-reductase-3alpha-hydroxy-steroid dehydrogenase and the aromatase pathways. Both are present in the brain and probably exert specific roles in the mechanism of action of hormonal steroids.End of Quote.

The study also inform that the two type of alpha reductase enzymes
are present in the brain

Quote
In particular, the recent identification of two isoforms of the 5alpha-reductase, the type 1 and type 2, possessing different structural, biochemical, and distribution characteristics has attracted a considerable attention. The few data available on their brain distribution have been carefully considered. End of Quote.

The importance of 5 alpha reductase 5 (both type) in inhibiting progesterone is also mention

Quote
In particular, some unpublished observations on the effects of two 5alpha-reductase inhibitors on progesterone-induced anesthesia, a phenomenon mediated through the GABAA receptor, are presented. End of Quote.

The link to the study is here
sciencedirect.com/science?_o … 3b4a89bec9

I am proposing a theory that perhaps we all have a bigger 5 alpha
reductase II enzymes in our brain than type I. This should explain
why some male develop side effect almost immediately (within days)
of taking finasteride and the most predominant is Brain Fog or difficulty
of concentrating.

While male in general population have a bigger 5 alpha reductase
I enzymes in their brain than type II. Hence why we are a minority
despite million of people worldwide that use proscar and propecia.

I am afraid i don’t have refence to back my theory but i will try to
do more research on this matter.

I found another published research, i don’t know whether this already
in the finasteride studies or other studies.

link: ncbi.nlm.nih.gov/pubmed/1468601

the title is : The 5 alpha-reductase in the brain: molecular aspects and relation to brain function.

QUOTE:
In the brain, this enzymatic system is not regulated by castration or sex steroid administration; furthermore neural inputs seem to be ineffective at the hypothalamic level. A recent interesting finding is the presence of high concentrations of the 5 alpha-reductase in the white matter. This probably is due to the fact that the white matter is particularly rich in myelin membranes, with which the enzymatic activity appears to be associated. An active 5 alpha-reductase activity has also been shown to be present in peripheral myelinated nerves. The localization in myelin membranes may suggest a possible involvement of 5 alpha-reduced metabolites of the different steroids in the process of myelination. The presence of the 5 alpha-reductase was analyzed in neurons, astrocytes, and oligodendrocytes isolated from the brains of male rats, as well as in neurons and glial cells grown in culture. Neurons appear to be more active than glial cells in converting testosterone into DHT. Only neurons possess aromatase activity.(ABSTRACT TRUNCATED AT 400 WORDS)
END OF QUOTE.

What it does not say in the research is whether “the active 5 alpha reductase in peripheral myelinated nerves is largely TYPE I OR II”

The study is done on mice, human could have different result.

Don’t know about common disposition as to how we got here I think it’s more to do with dosage and manner of drug cessation, ie those on more mg of either stuff and in particular those who stopped abruptly are worse affected. Also with fin those who stopped and started again later on.

That’s a very interesting point. I’d love to know what some of the more scientifically-minded members think of this, since that’s exactly what happened to me. I took Propecia for about 11 months with next to no sexual side effects to speak of; I got a really heavy depression after abruptly quittint the drug, but it almost completely went away after about six months. My current sexual problems date entirely from a second extended (7-8 month) bout with (generic) Fin… I was tapering off, they hit me like a ton of bricks and have lingered ever since. What exactly happened here and what are the implications for our theories about the drug? It was shocking to me because, as I mentioned, the first time around I had next to no noticeable sexual side effects, and certainly none that lasted beyond quitting.

hey guys,

since you seem well-informed, i i was just wondering if any of you knows a studie investigating the effects of GABA-modulating neurosteroids and their impact on GABA/GABA receptor/mRNAexpression… ? Sadely i havent the time at the moment to work my way through pubmed. A friend of mine is doing some research at an institute for mental health, investigating anxiety-disorders in mice and he’a always keen on new ideas. And i thought, why not channeling his efforts in the right direction :slight_smile:

bye
matt

Check sticky posts at top of MENTAL SIDE EFFECTS section.

Hello,

            i read the comments.Very helpful information shared by you  all members.The links that you have given ate also very useful.I hope for better information sharing and healthy discussion in future at here.Thank you for sharing the comment..