It would be very interesting to know the allopregnanolone levels (and levels of other neurosteroids) in Type II 5AR pseudohermaphrodites. Are they more predisposed to Alzheimer’s?
Thanks for the above post Alex.
We appreciate your input very much.
JN
The same effect was demonstrated at 1mg in “The influence of low dose finasteride…” by Duskova, Hill, Starka. The abstract is in the studies section - the full PDF was on-line as of yesterday but they seem to have pulled it down now. Mew, perhaps you have the full PDF? If not, I could scan it.
12 men were treated with 1mg finasteride. Allopregnanolone started at .37 nmol/L before treatment. After 4 months: .25. After 8 months: .16. After 12 months: .12. The full drop was 67.5% and got worse throughout the treatment duration.
Etiocholanolne only increased by 30% in this study.
While this is excellent news people are waking up and taking notice, better news would be how to fix the problem. Can it be fixed? Can the damage done from eradicated allepregnanolone levels be repaired?
Given the (unfortunately) impressive reduction of allopregnanolone, I have not heard of any sufferer having a seizure or a fit in my 9 years of suffering.
I have researched whether allopregnanolone can be replaced, and it seems that it can be taken (I came across a website that sold allopregnanolone powder), but I know of no trials. Certainly, this is way beyond my comprehension and the stampede to find a cure or prevention to Alzheimer’s disease has lots of momentum.
I was of the understanding that the neurosteroid are produced ENDOGENOUSLY in the myelin sheath, so replacement may be difficult??
Certainly, allopregnanolone has been given to rats to assess anxiety behaviour, with good effect.
JN
Yes, I have it, and may attach it to the abstract in future.
Here it is as a research chem:
tocris.com/dispprod.php?ItemId=236051
Reading this thread and the paper neurosteroids in sexual behavior really makes me think it may have a huge impact. Its a pity it no one can test for it (commercially)
I believe it would have a huge impact. For me, when my head is “quiet” everything falls into place sexually. Libido starts in the brain and works it’s way down. It’s definitely a huge component.
For what it’s worth, I used to get brutal grand mal seizures. Things used to be so bad I would get one every three weeks, unless I took medication. The finasteride has killed my brain activity to the point where I don’t even need my medications anymore
Hey,
I am really sorry but I need to confess something to you: I am not the real alex.miller 
. Actually I am a finasteride user who experiences severe brain fog and depression as side effect after using it for several years and I have seen the new thread over at hairlosshelp and did more research by using the search function and found alex.miller’s thread. I then found the study I posted before and in order for it to look authentic I was lying and impersonating alex.miller. I was acting out of desperation . I am not even sure whether it is consistent with what the real Alex said. Please forgive me. I got really scared because of the whole demyelination thing and decided to quit using finasteride after reading the whole thread; I hope the brain fog goes away quickly! I am so sorry - I better confess this now because I don’t have the knowledge to imitate the real alex.miller. Feel free to ban me or delete my account - I deserved it. You can delete all my posts if you want. I feel really ashamed of doing this, it was a stupid thing.
Again, I am so sorry I wasn’t thinking. Please forgive me.
sigh…
Regardless of alex being fake… I think the neurological aspect of the condition can’t be ignored. Especially the study regarding the loss of allopregnanolone
I saw that lithium may raise allo.
ncbi.nlm.nih.gov/pubmed/18257969
In addition, lithium “decreas(es) norepinephrine release and increasing serotonin synthesis.” And i have read that too much noripinephrine can cause loss of libido, shaking (some of us have this), anxiety, etc. Another very interesting thing is that it may “reset” the brains master clock, so perhaps this would actually allow us to sleep correctly again.
(From Wikipedia)
Another study about neuroprotection of lithium:
ncbi.nlm.nih.gov/pubmed/12071510
Another:
ajol.info/index.php/ajpsy/articl … 0169/22788
It even forms new synapses:
ncbi.nlm.nih.gov/pubmed/19188338
Thoughts?
There’s nothing here we really didn’t know.
Not very helpful 3pm - and there are really barely any other post on lithium on the site - and zero from you.
Don’t take my previous post personally - I meant the posts of and since imposter alex.miller. And why would I even choose to post about lithium? We aren’t bipolar.
My opinion of your post is that it’s wonderful you found something that elevates that neurosteroid, bravo. What further discussion is necessary? Post it in the Other Studies section and stop pretending it’s a breakthrough in our cause; I highly doubt lithium will cure anyone from long term impotence.
I think we should create a thread on individual allopregnolne levels similiar to 3-adiol g thread.
This is a good site…Mew or 3pm, not sure what thread you want to put this under, but this is definitely worth looking at.
sigmaaldrich.com/life-scienc … e=18433831
Ganaxolone solid Ganaxolone (3alpha-hydroxy-3beta-methyl-5alpha-pregnane-20-one) is a positive allosteric modulator of the GABAA receptor subtype; synthetic analog of the endogenous neurosteroid allopregnanolone; effective against chemically induced seizures in rats and mice. Ganaxolone is an orally active analog of allopregnanolone that is not converted to the hormonally active 3-keto form. The enhanced anticonvulsant potency of ganaxolone after neurosteroid withdrawal supports the use of ganaxolone as a specific treatment for perimenstrual catamenial epilepsy.
I’ve said this before… no one has evidence that allopregnanolone even is to blame for most of these ongoing issues. We acknowledge that it is an important part of mental health which finasteride impairs, but there’s no indications to suggest that it doesn’t revert itself once 5ar comes back. Confusion and even to an extent, anxiety, can also be attributed to lack of androgenic action.
Interesting article regarding the long-term role of allopregnanolone…
alzforum.org/new/detail.asp?id=2399
Some highlights…
“19 March 2010. Contrary to earlier dogma, scientists now know that the human brain does make new neurons throughout life. This raises two fundamental questions about age-related neurodegenerative disorders such as Alzheimer disease (AD): Could failing neurogenesis be part of the problem, and could boosting the process be part of a solution? Judging by recent papers, the answer to both may be yes. In the March 5 Journal of Neuroscience Research online, Orly Lazarov and colleagues at the University of Chicago, Illinois, report that neurogenesis is compromised prior to any overt signs of AD-like pathology in a double-transgenic mouse model of the disease. “The decline in neurogenesis happens so early that it might not be just a side effect, but part of the mechanism of cognitive impairment,” said Lazarov. A second paper, in this week’s PNAS online, goes further, suggesting that the impaired neurogenesis leads to cognitive deficits and that both can be reversed pharmacologically. Roberta Brinton and colleagues at the University of Southern California, Los Angeles, report that allopregnanolone, a neurosteroid, revitalizes weak neurogenesis in young triple-transgenic mice and protects them against deficits in hippocampal-based learning and memory. Whether allopregnanolone will benefit older animals with established pathology is unclear at present, but Brinton told ARF that such studies are underway.”
“What brings neurogenesis down in these animals? Brinton’s lab tested allopregnanolone, a progesterone derivative that stimulates proliferation of neuron precursors (see ARF related news story). Her associates found that its levels were lower in the 3xTg mice compared to wild-type animals. Intriguingly, when the researchers gave the steroid to three-month-old 3xTg mice, it dose-dependently boosted neurogenesis. On top of that, a single sub-cutaneous injection of allopregnanolone restored associative learning by the fifth day of training in the eye-blink test. Mice that received this single dose performed like wild-type animals when tested nine days after training. The data suggest that at least in young transgenic animals, allopregnanolone can restore learning and memory”
Another interesting study regarding allopregnanolone. Of course, we don’t know which way the cause-effect runs. (3α,5α-THP = allopregnanolone)
3α,5α-THP: a potential plasma neurosteroid biomarker
in Alzheimer’s disease and perhaps non-Alzheimer’s dementia
Charles D. Smith . David R. Wekstein .
William R. Markesbery . Cheryl A. Frye
Abstract Rationale: A plasma biomarker for neurodegenerative
disease is desirable because blood is relatively
simple to obtain compared with other biological samples
such as cerebrospinal fluid. Recent literature suggests that
neurosteroid metabolism may be altered in Alzheimer’s
disease (AD). Objectives: We sought to measure the plasma
levels of seven steroids to assess their potential as biomarkers
for dementia and AD. Methods: Steroids were
measured using validated radioimmunoassay methods in
AD (n=15), non-AD dementia (n=4), and control subjects
(n=20). Demented subjects were in the mild-to-moderate
stages of illness. Measurements were done blind to subject
status in an independent laboratory. Results: The notable
finding was the significantly lower 5α-pregnan-3α-ol-20-
one (3α,5α-THP) level in demented subjects compared
with controls (25% decrease; p=0.004); 3α,5α-THP was
the only one of the steroids demonstrating an effect of
dementia. Conclusion: Lowered 3α,5α-THP levels appear
promising as a biomarker in dementia, but further work is
needed to establish the sensitivity and specificity of these
findings in AD.
Okay well then if demyelination is the cause then how is it that large doses of testosterone improves sexual function? Wouldnt you just be F’d regardless of the intake of testosterone