dutasteride and Memory

[Felk]

I think the memory loss is due to people thinking way too much about their hairloss. Don't continuously dwell about your hairloss and well, you'll remember more.

yes much more likely.

For one thing, finasteride doesn't effect the brain at all, so i dont see how it could have given these people problems with their STM. I'd say defiantely a placebo.

We don;t know about dutasteride and the brain because it effects some 5AR1 there, but lets face it - nothing ever came up in their trials, no mental problems at all.

 

[docj077]

I think the memory loss is due to people thinking way too much about their hairloss. Don't continuously dwell about your hairloss and well, you'll remember more.

yes much more likely.

For one thing, finasteride doesn't effect the brain at all, so i dont see how it could have given these people problems with their STM. I'd say defiantely a placebo.

We don;t know about dutasteride and the brain because it effects some 5AR1 there, but lets face it - nothing ever came up in their trials, no mental problems at all.

Just throwing this in. 5AR type II converts both testosterone and progesterone into their 5 alpha reduced forms. Progesterone is converted into dihydroprogesterone which is the precursor for allopregnanolone. Allopregnanolone is a neuroactive steroid. It's neuroprotective as it reduces cell death, gliosis, and functional deficits.

Again, it's FYI, but I think it's important, as well seeing as how people seem to have cognitive problems while on these drugs.

 

[docj077]

I wanted to throw this in, as well, since I mentioned it in regards to 5AR type II.


Therapeutic Potential of Neurogenesis for Prevention and Recovery from Alzheimer’s Disease: Allopregnanolone as a Proof of Concept Neurogenic Agent

"These endeavors have led to the discovery that the neurosteroid alloprognanolone (APα) is a potent and highly efficacious proliferative agent in vitro and in vivo of both rodent and human neural stem cells. Results of our in vitro studies coupled with our more recent analyses in the triple transgenic mouse model of AD suggest that APα is a promising strategy for promoting neurogenesis in the aged brain and potentially for restoration of neuronal populations in brains recovering from neurodegenerative disease or injury"

 

[Felk]

I think the memory loss is due to people thinking way too much about their hairloss. Don't continuously dwell about your hairloss and well, you'll remember more.

yes much more likely.

For one thing, finasteride doesn't effect the brain at all, so i dont see how it could have given these people problems with their STM. I'd say defiantely a placebo.

We don;t know about dutasteride and the brain because it effects some 5AR1 there, but lets face it - nothing ever came up in their trials, no mental problems at all.

Just throwing this in. 5AR type II converts both testosterone and progesterone into their 5 alpha reduced forms. Progesterone is converted into dihydroprogesterone which is the precursor for allopregnanolone. Allopregnanolone is a neuroactive steroid. It's neuroprotective as it reduces cell death, gliosis, and functional deficits.

Again, it's FYI, but I think it's important, as well seeing as how people seem to have cognitive problems while on these drugs.

Thanks a lot for that, it's good to know more about this stuff. I wasn't aware of people having cognitive problems on finasteride and dutasteride, is this just from people complaining about "brain fog" and STM loss, etc?

I'm wondering if people are getting cognitive problems from finasteride, why wasn't it documented as a side effect in the FDA trials? Have you seen any other studies which hint at finasteride. or dutasteride. causing problems with the brain?

Finally (sorry for all the questions, but you've got me thinking and a little concerned) is there any way we could do something to counteract the inhibition of dihydroprogesterone or allopregnanolone, for our brain's sake?

 

[docj077]

I think the memory loss is due to people thinking way too much about their hairloss. Don't continuously dwell about your hairloss and well, you'll remember more.

yes much more likely.

For one thing, finasteride doesn't effect the brain at all, so i dont see how it could have given these people problems with their STM. I'd say defiantely a placebo.

We don;t know about dutasteride and the brain because it effects some 5AR1 there, but lets face it - nothing ever came up in their trials, no mental problems at all.

Just throwing this in. 5AR type II converts both testosterone and progesterone into their 5 alpha reduced forms. Progesterone is converted into dihydroprogesterone which is the precursor for allopregnanolone. Allopregnanolone is a neuroactive steroid. It's neuroprotective as it reduces cell death, gliosis, and functional deficits.

Again, it's FYI, but I think it's important, as well seeing as how people seem to have cognitive problems while on these drugs.

Thanks a lot for that, it's good to know more about this stuff. I wasn't aware of people having cognitive problems on finasteride and dutasteride, is this just from people complaining about "brain fog" and STM loss, etc?

I'm wondering if people are getting cognitive problems from finasteride, why wasn't it documented as a side effect in the FDA trials? Have you seen any other studies which hint at finasteride. or dutasteride. causing problems with the brain?

Finally (sorry for all the questions, but you've got me thinking and a little concerned) is there any way we could do something to counteract the inhibition of dihydroprogesterone or allopregnanolone, for our brain's sake?

I've just been finding bits and pieces of information about different pathways on the net. I'm sort of making an assumption when it comes to the effects finasteride. or dutasteride. might have as I'm assuming that they inhibit the progestone metabolizing effects as well as the testosterone metabolizing effects. Both drugs inhibit the enzyme 5 AR type II, so I'm making a scientific leap by saying that they inhibit DHT formation in the same way they inhibit dihydroprogesterone formation.

Again, I'm sort of jumping to conclusions and I would need to see a study to take my conclusions to the next level.

However, what I've been saying concerns me, as well. The "brain fog" phenomenon makes sense with what I've been saying. I asked my girlfriend (who is on the progesterone only mini-pill) and she has said that ever since she began taking it, her mind has never been clearer and her brain seems to work "quicker". But, that's female brain and who's to say it's the same in the male brain.

For now, assume the drugs are safe until proven otherwise through one of the forum members.

Look at what I'm typing, but don't take it to heart...please.

 

[Felk]

Hehehe don't worry im not going to stop taking finasteride. or dutasteride. on account of one post

I just find it interesting, because progesterone is a moderate DHT inhibitor I believe? It's added to minoxidil solutions for this reason. What is the purpose of the pill your girlfriend is taking?

However I'd like to hear what Bryan has to say about this, have you asked him what he thinks of your theory?

 

[Bryan]

This is by no means the first time this issue has come up. To show that 5a-reductase clearly affects certain other hormones, see the abstract below. The study mentions (like "docj" did) that not only does it convert progesterone into dihydroprogesterone (DHP), it also converts Doctor into DHDOC. Also, they make the following interesting statement in the Discussion section at the end:

In rodents, finasteride blocks the type I 5a-reductase isoenzyme, which is the predominant form in the brain, as well as the type II form of the prostate and gonads (Russel and Wilson, 1994; Mensah-Nyagan et al., 1999; Poletti et al., 1999).

Assuming that human brains contain predominantly the type 1 form of the enzyme (I think that's a fairly safe assumption), finasteride would obviously be less likely to alter possibly important human brain chemistry than dutasteride.


------------------------------------------------
J Neurosci. 2002 May 1;22(9):3795-805.
"Stress-induced deoxycorticosterone-derived neurosteroids modulate GABA(A) receptor function and seizure susceptibility." Reddy DS, Rogawski MA.

Epilepsy Research Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892, USA.

Stress affects seizure susceptibility in animals and humans, but the underlying mechanisms are obscure. Here, we provide evidence that GABA(A) receptor-modulating neurosteroids derived from deoxycorticosterone (Doctor) play a role in stress-related changes in seizure control. Doctor, an adrenal steroid whose synthesis is enhanced during stress, undergoes sequential metabolic reduction by 5alpha-reductase and 3alpha-hydroxysteroid oxidoreductase to form 5alpha-dihydrodeoxycorticosterone (DHDOC) and allotetrahydrodeoxycorticosterone (THDOC), a GABA(A) receptor-modulating neurosteroid with anticonvulsant properties. Acute swim stress in rats significantly elevated plasma THDOC concentrations and raised the pentylenetetrazol (PTZ) seizure threshold. Small systemic doses of Doctor produced comparable increases in THDOC and PTZ seizure threshold. Pretreatment with finasteride, a 5alpha-reductase inhibitor that blocks the conversion of Doctor to DHDOC, reversed the antiseizure effects of stress. Doctor also elevated plasma THDOC levels and protected mice against PTZ, methyl-6,7-dimethoxy-4-ethyl-beta-carboline-3-carboxylate, picrotoxin, and amygdala-kindled seizures in mice (ED50 values, 84-97 mg/kg). Finasteride reversed the antiseizure activity of Doctor (ED50, 7.2 mg/kg); partial antagonism was also obtained with indomethacin (100 mg/kg), an inhibitor of 3alpha-hydroxysteroid oxidoreductase. Finasteride had no effect on seizure protection by DHDOC and THDOC, whereas indomethacin partially reversed DHDOC but not THDOC. DHDOC, like THDOC, potentiated GABA-activated Cl- currents in cultured hippocampal neurons (< or =1 microm) and directly activated GABA(A) receptor currents (> or =1 microm), compatible with a role for DHDOC in the antiseizure activity of Doctor. Doctor is a mediator of the physiological effects of acute stress that could contribute to stress-induced changes in seizure susceptibility through its conversion to neurosteroids with modulatory actions on GABA(A) receptors including THDOC and possibly also DHDOC.