Im not going to email you a pic but trust me i went totally bald.
went totally bald or are totally baldâŚsorry for the semantics but its my job.
The first two years off of Fin I lost little to no hair. Ever since then it started accellerating and now I have very little hair.
Have to agree with SA here. Itâs ridiculous people on this board believe one of us here, even Awor, is going to single handedly drive the direction of the medical research in one area or another particularly now with the launch of the foundation. You believe the research is âhyperfocusedâ on AR theory on what grounds? Because someone here said it who also has no idea whatâs going on? If you believe this you really have no idea how research is conducted on the University level. The proposed studies listed on foundationâs website are comprehensive not to mention the upcoming neurosteroid conference. As he said this is the last thing you should be concerned about.
i agree completely
people put too much stock into the opinions people write on this site
Interesting stuff. Thanks.
I donât know about everyone else, but I think its becoming pretty clear that the root of our problem has to do with neurosteroids. First of all, as Awor said, significant results were found and the study will be published soon. Dr. Traish is speaking about neurosteroids this February. Accutane (also inhibits 5AR) has been been linked with later development of multiple sclerosis. Multiple sclerosis (MS) patients have low allopregnenalone. An allopregnenalone pill is currently being developed as a treatment for MS (which has shown to stop, even reverse MS symptoms). Our sleep, anxiety, and stress issues can be explained by abnormal allopregnenalone levels as allopregnenalone modulates GABA and GABA is important in all of these processes. I even remember reading somewhere that allopregnenalone (I think via GABA) relaxes smooth muscle. I know Awor is very partial to the androgen receptor theory, but I find a much greater abundance of literature on allopregnanolone and finasteride. If the problem was androgen receptor, why isnât Dr. Traish speaking about that in February?
There is so much bickering on this forum about possible causes and bizarre theories (candida, infections, etc.) and there are studies out there that when put together can account for our symptoms. It seems like the source of our problems are staring right at us in the face. Statements such as âwe have no idea what going onâ are simply not true. Imagine how much more constructive this forum would be if we simply spent time reading scientific journal articles and then discussed them on here.
Now I donât know if the problem is that our brains are no longer making allopregnanolone (or THDOC or whatever other neurosteroid), if we are insensitive to a neurosteroid, or we have dys-regulated GABA or whatever. But there are many smart people on this forum that I think can contribute to more constructive discussions.
For example, here is an interesting article:
ncbi.nlm.nih.gov/pubmed/11744076
IMO it most certainly is neurosteroids, and neurosteroids only. To add to your points:
- Finasteride has been extenesively tested and has known effects on gaba receptors
- This theory can actually explain the entire comprehensive list of problems from anxiety/brain fog all the way down to estrogen dominant problems, including premature greying.
- Alcohol as an unmistakable effect on us (sometimes negative)
- I am a genius and I am hardly every wrong
dgreene said ⌠âI know Awor is very partial to the androgen receptor theory, but I find a much greater abundance of literature on allopregnanolone and finasteride. If the problem was androgen receptor, why isnât Dr. Traish speaking about that in February?â
I disagree with the above statement ⌠no one can sit and say awor is partial to any one exact thing because that would be untrue, and this seems to be a common misconception ⌠re read his posts, he fully acknowledges that nuerosteroids are very much involved, and that his first round of nuerosteroid research showed âsignificant resultsâ
i agree nuerosteroids are veyr important in all of this ⌠my mind was the very first thing to start having issues when i was on finasteride, and to this day it is my single biggest issue, though it has improved
Allopregnanolone is made via both 5ar-s, right? Or are you convinced now that itâs ONLY 5ar2 now?
Do you think allopregnanolone is behind the semen changes and penile shrinking too or do you just not have those side effects?
For those who have mental symptoms, this theory works.
I am not sure. For sure the neurosteroids are contributing to the sexual (not just mental) side effects. To what extent I donât know and I donât know how the androgen receptor theory is playing into this. Awor, brainbug, mew and them think that is the root and the neurosteroids follow. I think it could be the other way around, and I am still waiting to see what the AR data says.
However, look at the side effects caused by SSRIs and drugs such as Respirdal. These drugs act on the CNS, yet have great influence on hormones, sexual function etc. This tells me that the CNS problems (neurosteroids) could be driving the sexual problems in our cases.
Here is a good video about Respirdal. Around halfway through, they talk about the side effects of this drug. Its amazing when you see the pictures of menâs chests.
imblance of neurosteroids could lead to depletion or increase in any one hormone creating an imbalance which downregulates thyroid, testosterone etc.
Here is an interesting study. While on fin, our progesterone probably increased (canât become allopregnanolone). I donât know what happens when we come off but probably some extreme fluctuations in neurosteroids which leads to the crash. But also keep in mind some people didnât experience a crash.
ncbi.nlm.nih.gov/pubmed/11744076
Itâd be great if we knew all the tests the people did for the neurosteroid study. That way we could go get the tests as well, and who knows, maybe a doctor here that sees that will think of something. Or are the tests conducted too âtop secretâ of information as well?
Nevertheless, very curious to see if something will show up on a PET scan.
Role of allopregnanolone in regulation of GABA(A) receptor plasticity during long-term exposure to and withdrawal from progesterone.
Follesa P, Concas A, Porcu P, Sanna E, Serra M, Mostallino MC, Purdy RH, Biggio G.
Department of Experimental Biology Bernardo Loddo, CNR Center of Neuropharmacology, University of Cagliari, 09123, Cagliari, Italy.
Abstract
Here we summarize recent data from our laboratory pertaining to the effects of fluctuations in the brain concentrations of the progesterone (PROG) metabolite allopregnanolone (3alpha,5alpha-TH PROG) on the expression and function of gamma-aminobutyric acid type A (GABA(A)) receptors. The effects of long-term exposure to progesterone and of its sudden withdrawal on the activity of GABA(A) receptors and on the abundance of receptor subunit mRNAs were examined in cultured rat cerebellar granule cells and cortical neurons.
Fin increased progesterone in our brains because it couldnât convert to allopregnanolone. The sudden withdrawal could be stopping finasteride, so progesterone becomes allopregnanolone. This affects the GABA receptors.
The effects of a persistent reduction in the brain concentration of 3alpha,5alpha-TH PROG on GABA(A) receptor function and gene expression were examined in vivo in rats subjected to long-term administration of oral contraceptives. Our results demonstrate that long-lasting changes in the exposure of GABA(A) receptors to this PROG metabolite induce marked effects on receptor structure and function.
Persistent reduction of allopregnanolone changes GABA receptors.
These effects of 3alpha,5alpha-TH PROG appear to be mediated through modulation of GABA(A) receptor signaling mechanisms that control the expression of specific receptor subunit genes. Furthermore, the specific outcomes of such signaling appear to differ among neurons derived from different regions of the brain. Neuroactive steroids such as 3alpha,5alpha-TH PROG might thus exert differential actions on GABA(A) receptor plasticity in distinct neuronal cell populations, likely accounting for some of the physiological effects induced by these compounds.
This is an excellent study which I think directly relates to what has happened to us.
In addition, Nandrolone Decanoate, which is known to cause âdeca-dickâ acts as a progestin in the body and thus stimulates the progesterone receptor. I feel as though things are starting to tie in together. Doctors currently try to treat âdeca-dickâ with drugs that increase dopamine (with mixed success). Maybe this explains life at the endâs and corriovip improvements by increasing dopamine.
Fasting increases dopamine receptors which could explain why some people feel better after a fast. I felt a little better after my eight day fast. Nothing big tho.
What we can do, is get our progesterone and allopregnanolone (tetrahydroprogesterone) levels measured. That canât be that hard. In some countries it must be possible.
I have the full study in my hands right now and firstly, everything is based on rats and their cells. This studyâs goal is to tell something about women taking high doses of progesterone and therefore getting too much allopregnanolone in their brains. We can no way have too much allopregnanolone in our brains, if we inhibited its production. Itâs completely different. What we can do, though, to raise our allopregnanolone levels in the brain is to take excessive amounts of progesterone, which will have no other way to channel itself to allopregnanolone. If you think itâs really all about allopregnanolone, this will make the situation a lot better. What we learned in the chemistry class: the more the substrate, the more the product. Somebody must have tried it already, no?
Whatâs good about it is that probably every study with finasteride regarding neurosteroids is mentioned in it. But what itâs ultimately trying to say is that low allopregnanolone in the brain is good not bad. And it may be possible to understand that finasteride is good for women taking contraceptives.
en.wikipedia.org/wiki/Progesterone
Adult males have levels similar to those in women during the follicular phase of the menstrual cycle.
Anyway, Iâm trying to make a human study out of this. Hopefully the smarter and richer ones here are fascinated by it. We canât get results, if we donât have guinea-pigs. Fingers crossed and perhaps weâll see results soon.
yes, I have neen asking everyone to get their progesterone to estrogen ratios and progesterone levels checked. It seems that many people are highish. Everything points to estrogen dominance/low progesteroneâŚhowever I did find recently literature that says too much progesterone can actually downregulate the progesterone receptor.