As much as it scares me, I truly think that the inability to recover from side effects after stopping the drug is due to a change in a gene expression (not sure which) or a change in our dopamine metablism. Our sexual side effects are just like that of ex SSRI users and SSRI users who do not recover after stopping the drug are thought to have a change in gene expression or dopamine metabolism. If you look at the members here who have taken TRT, none of them have had any success (correct me if I’m wrong). Therefore, I really don’t think it’s hormonal. But, that’s just my two cents. Anyone agree or disagree?
If Im not mistaken, there is some research articles that state that fin does change a gene expression. Anyone know where it is?
I also have a study about Finasteride causing changes in gene expression in Prostate cancer patients, it hasn’t been posted yet but I’ll put it up soon.
as to the second article, why was it tested on cancer patients? it would seem that they would have to use the fin on non cancer patients so they can use the non cancer patients as a control variable, right?
And just to clarify my original post, my theory is that every side effect we are experiencing, including all the hormonal sides, is all a result of this gene alteration - that is why TRT isnt helping. TRT isn’t addressing the cause, but rather one of many effects of altered gene expression. A change in gene expression is also consistent with the fact that fin users who used the drug for only months find that there side effects go away after a while. Their genes weren’t altered. I attend a university that also has one of the leading med schools in the country. I’ve emailed a few of the geneticists to schedule an appointment. I hope one of them allows me some time.
The only way that testosterone, dihydrotestosterone etc can work in the body at all is if they able to correctly fill adequately working androgen receptors.
You can have all the testosterone in the world, but unless the androgen receptors work you can forget it. If the androgen receptors do not work correctly then testosterone does little to nothing.
This is something shown in those that have androgen insensitivity syndrome (AIS), or partial androgen insensitivity syndrome (PAIS), it is also something reflected in various genetic conditions that lead to an altered number of androgen receptors or altered ability of androgen receptors to function. Too many androgen CAG repeats can cause ths problem.
I would doubt that there is any permanent alteration in the androgen receptors from propecia use. We would certainly need to see hard evidence before this was remotely considered.
Until such time it would be more productive at looking at the more likley culprets for post propecia problems.
I also believe its improbable that we have altered our genes or our AR.
At least in my case, many of you know that I have found myself recovered for maybe 8 or 9 times since I stopped fin. However those moments of normality lasted a week or two. And most of the times I would say they did not last because since my hair started to fall again, I started taking beta-sitosterol once, another time I took vitamine B, etc…
And of course that didnt help to my condition at all. I should have let the hair fall and just keep recovering instead of freaking out for my hair again.
So really, I dont think we have altered our genes. If that would be so, at least I would have not felt again the same since stopping propecia. And that has not been the case. I really have really lived periods of complete normality (with no help of sexual med like viagra, of course).
And you can all read my previous posts in the yahoo group. My first name was culchicito2, then I changed to Searchfhealth.
Everything alters gene expression including the foods we eat. Just look it up in google. Our DNA is hundreds of thousands of years old and is ingrained in us and despite our RNA being processed differently from prior drug use we can work on changing gene expression reading again back to its intended state with supplements, diet, time. I agree TRT and any drug is unnatural and will not really help at all just cover up a problem that is still there. We should try to work on natural production of hormones through nourishing our bodies again. I think nuerotransmitter processing is of course the key. Adding artificial chemicals to the body is no cure at all. That is why after time people’s levels should improve as long as they are taking proactive measures. Just look at some of the blood tests of people and how they radically change after months of quitting. Of course nothing is ever a sure thing but I believe improvements and recovery should be possible as some people have gotten back to their baseline levels again by naturally boosting levels by being very proactive.
Mew i have thought of that and talked about it in a previous post. i have also posted the study which says that fin changed gene expression in prostate cells_but hypo said this study was applied on rats so it can’t be cited for humans. anyways, i really hope it is not a problem of gene expression.
i have thought of something also; if it is just a hormonal problem then how come a drug like proviron doesn’t work? i mean, proviron is antiaromatase so it would work if it is a problem of high estrogen. also, proviron increases free testosterone as it has higher affinity to bind to SHBG, so if it was a problem of high SHBG then how come proviron can’t work? how come TRT isn’t a solution even if combined with an aromatase inhibitor or proviron? how come clomid and nolva can’t work if it was a fsh and lh problem? how come our bodies can’t recover even after YEARS for god’s sake?
it is either a modulation of gene expression, or a modulation of AR receptors or it is a defective neurosteroid problem; can’t be anything else.
i started progesterone cream together with alot of supplements to support my liver and my adrenals. will keep you updated!
This is exactly why I think our problem is a lot more complex than hormonal issues… I think that hormonal issues are an effect, not a cause. On a positive note, I have good days where I wake up with an erection, although it completely disappears as soon as I wake up (the brain fog issues are always there but never get better). I just ordered the cream and will start it as soon as it arrives. I’ll keep everyone posted.
Progesterone is a pre cursor to testosterone and when it is taken it increases testosterone, but progesterone is also a pre cursor to estradiol and it increase that to.
In fact progesterone is regarded primarily as an estrogen and it indeed does have a greater estrogenic effect than androgenic effect.
Taking progesterone to me would seem to be a most unlikely answer to anything.
It can help increase or start the development of gynecomastia though and it could help increase ed and low libido.
I can only imagine it helping out men with low estradiol who happen to also have low testosterone who for some reason do not want to instead simply be prescribed testosterone.
Until such time that I see any information that seriously suggests that progesterone is anything other than negative for men be that post finasteride use or not- I will continue to question its use.
I believe Dr John Crisler is also against its use in men.
No it isn’t.
Not necessarily.
Proviron is an oral form of dihydrotestosterone (DHT)
It is a non aromatizable androgen- not an aromatase inhibitor. It does not increase free testosterone as far as I am aware. It increases DHT and lowers total testosterone via negative feedback at the HPTA, this I would presume result in a lower level of free testosterone given the fact that DHT cannot itself be converted to free testosterone.
This is as far as I am aware.
Certainly I can tell you that DHT therapy alone irrespective of the method often leaves its patients exhausted/fatigued due to the fact that it does not have many of the required properties of testosterone. Because Proviron or DHT replacement generally results in recognition by the Hypothalamus and a lowered output of GnRH, this in turn results in a lowered production of LH which in turn results in reduced leydig cell action and lower testosterone. Lower testosterone in this instance can mean (can being the operative word) that there is less raw hormonal ingredient to fuel conversion to estradiol. To put it simply DHT can indirectly sometimes cause a reduced level of estradiol.
But like I say it does not replace the required androgenic actions of testosterone- even if it can sometimes improve libido and erectile function. Also it does not treat elevated SHBG. So if an individual has low testosterone and or high SHBG Proviron is not likely to help, certainly not on its own.
Testosterone isn’t always a straight-up answer because testosterone problems are not always straight-up answers anyway. You only have to take one look at a hypogonadal forum/community to see that there are many people who have struggled for years without getting things sorted out or struggling to find the exact right from of replacement, dosage, ancillary meds etc. I have known men on TRT to take 20 years to find the right answer. You can’t just expect to throw TRT at a problem even if the problem is simply testosterone deficiency such is the multitude of issues involved. I have already explained that Proviron is NOT an aromatase inhibitor. I am perfectly aware of the complete twaddle written on this matter in bodybuilding circles. I am not concerning myself with how they irresponsibly stack drugs in ludicrous ways, I am talking about its use in the context of androgen replacement on its own or in combination with physiological replacement. I was prescribed Andractim dihydrotestosterone for androgen deficiency and I can tell you for a fact that DHT does not increase testosterone- the reverse and I can tell you that it is not an aromatase inhibitor.
There are a multitude of reasons.
For some people they are simply not finding the correct form of androgen replacement, and or not finding what is correct for them and or not finding what the correct dose is for them.
Some people have high SHBG and are trying to throw incorrect medications at the problem. Some have high estradiol with or without high SHBG and are again often not getting on the right medication at the right dosage.
Some people may have additional hormonal issues that have as yet not been uncovered.
What you also have to keep in mind is that this group is a bias/selective subject group in that it might not be representative of those with finasteride problems.
There might be a wider populous out there that have recovered well with or without medical intervention.
What we do know is that the one very obvious problem caused by the known anti-0androgen finasteride is the adverse alteration of sex steroids. That is the one thing that we know it often causes and the one thing we can look to help people fix. Until such time as any other problem comes to light we can only speculate. Given that speculation is of limited use we should try to help people where we can definitely help and that is in looking at how finasteride cause problems with the sex steroids.
egy-chams if you get the necessarily pathology I would gladly take a look and see if I could help you with that.
Yes but that is a laughable way of looking at matters. I mean yes eating a balanced diet for instance can improve the DNA of our sperm, and there are many other examples. BUT this is categorically NOT significant change in DNA expression and cellular action that has been alluded to regarding propecia and androgen receptors. What you are saying is therefore misleading.
The medical community/endocrine societies across the world are not as far as I am aware saying that finasteride or rather propecia causes an adverse affect in male androgen receptors. There is no evidence at all to my knowledge that finasteride causes a form of androgen insensitivity.
If you are saying it does cause this problem, that this problem has been found I would ask if you could provide me with the details of the endocrinologists that are saying this and ask for the white papaers studies etc.
This is pseudo science. Pardon me, but I don’t think you know what you are talking about here (no offence intended). I mean first of all you have no way of knowing the intended state of your genes, you have no way of individually measuring your genetic state before or after your experiments. You have no way of knowing what food sources etc would equate to being most correct for you to improve your DNA given the modern world we live in. E.g the human body has developed eating raw food, cooked food is a relatively new invention. How do you know if cooked food leads to statistical increases in mutations in DNA etc….If you could change your DNA, measure the changes and ensure a lack of mutations in DNA then you could prevent cancer and many other diseases in yourself. Also none of that would account for genetic mutations in your DNA based upon blood lines and family history or the environment within which you live.
And of course none of this alters the fact that you cannot change your gene expression in order to improve your endocrine system, not in any meaningful way that is going to overcome hypogonadism or poor androgen action etc.
I think this is just barmy talk and it doesn’t relate to anyone or this subject matter.
Show me a single natural remedy that has been proven to treat hypogonadism. The courts of Kingdoms used to rely on Eunuch diplomats and servants within harems for thousands of years precisely because hypogonadism was permanent prior to the synthesis and production of male hormones.
Also just to add, straight testosterone as found in testogel is 100% natural testosterone as seen in the body albeit synthesized.
Your logic is the kind that seems to imply that drugs are going to fail and that things that are natural are somehow more likely to work. But modern medicine has saved millions of lives since its introduction, if it were gone tomorrow, for all its failings we would be in the dark ages and millions and millions would be dying without it, also the natural testosterone, chemically unaltered as found in testogel isn’t the answer for many- despite being natural.
The point?
The point is it is hard to see where you have a valid point….
Like I said show me a proven natural remedy for hypogonadism.
Why of course?
That position is to decry modern medicine and to say we would be better off without it, something that is absurd.
Adding artificial chemicals to the body literally IS a cure for thousands of conditions.
Treating hypogonadism with Danazol or Clomid or HCG etc sometimes is the cure, but no natural remedy is- not on any proven basis.
What measures?
No some people have simply been fortunate enough to have had some recovery of their HPTA over time. Time is a healer for many illnesses and woes.
When time isn’t the healer though people need more than a hippy vibe, with pseudo science and whole grains to get by lol.
People left with permanent problems need potential solutions and you don’t offer any, neither does the world of natural remedies. The medical and pharmaceutical world for all its problems does.
Could this perhaps be why so many of us are in a hypogonadal state after quitting Finasteride?
That is, when we quit DHT returns rapidly and possibly at a very high level (as happened to a number of us within 2 weeks of quitting, – libido and erections return full force) but then shortly after (within a few weeks) erections/libido crashes and we end up with low T?
In other words – could it be that by coming off Finasteride, our DHT levels rise so rapidly that we in fact inhibit our own endogeneous production of Testosterone… since after coming off there could be far too high of a DHT level in the body and thus the HPTA shuts down the source – LH and correspondingly, Testosterone?
I can see the logic of that thinking and would need to think further but my initial feeling is that this is not happening.
I think there is probably some rebound effect in terms of the fluctuating changes of hormones post finasteride use that accounts for so many people (too many to my mind for it to be a placebo effect) referring to periods of time of feeling well before symptomatically crashing, but I do not know what the mechanism of action is that explains this
I doubt it is elevated DHT reducing free testosterone because A) I have rarely seen very high DHT in the initial pathology of people with these problems and B) it is certainly very rarely high (again from what I have seen) many months down the line, yet the hypothalamus/pituitary is still often producing insufficient levels of gonadotropins at that time and or in combination with other issues like elevated estradiol and SHBG.
If we were seeing people come off finasteride suddenly having surges in DHT, then that certainly would account for a negative feedback and a resultant drop in testosterone. But even if that happened you would have less of the raw hormonal ingredient required in order to fuel consequent maintenance of that DHT level, because DHT is a metabolite of testosterone and requires testosterone in order to remain high (at least generally speaking). If DHT somehow remained high (not sure how it would) then what you are saying could explain matters as it is I don’t think it does because like I say that isn’t happening at least not in what I have seen.
Stopping finasteride use may well cause a cascade of hormonal changes that account for the problems that people talk about when referring to a symptomatic crash, that is entirely possible. I guess if you had poor human guinea pigs willing to undergo finasteride treatment (the lord knows why they would) under medically controlled conditions to ascertain in a detailed manner what happens not only on the drug, but what happenes from a detailed pathology point of view upon discontinuation;
Then perhaps we would or might know what occurs, unfortunately as it is I certainly do not have an answer as to the mechanism of the problem
P.S
Just to add. Looking back I might have seemed harsh or rude to infectedssri.
I want infectedssri. to know that I was only attacking the concepts/position of his thoughts because they are diametrically opposed to what I believe on this subject/on this single issue. I was not attacking him or making a personal attack, I apologise if any offence is caused none is intended. If people do not have too much ownership of these positions then hopefully no offence is caused. In any event I have put my side of the debate and made my feelings clear, if we do disagree with each other as seems likely then that is fair enough.
UGA btw I have the same symptoms that you have, sometimes I have morning erections which completely disappear as soon as I wake up.
Hypo, I respect your thoughts but I have some replies to your points:
Hypo wrote: “Progesterone is a pre cursor to testosterone and when it is taken it increases testosterone, but progesterone is also a pre cursor to estradiol and it increase that to.
In fact progesterone is regarded primarily as an estrogen and it indeed does have a greater estrogenic effect than androgenic effect.
Taking progesterone to me would seem to be a most unlikely answer to anything.
It can help increase or start the development of gynecomastia though and it could help increase ed and low libido.
I can only imagine it helping out men with low estradiol who happen to also have low testosterone who for some reason do not want to instead simply be prescribed testosterone.
Until such time that I see any information that seriously suggests that progesterone is anything other than negative for men be that post finasteride use or not- I will continue to question its use.
I believe Dr John Crisler is also against its use in men. “
You are right. But you are not talking about our own case. You are talking about using progesterone for healthy men , or may be men who have other problems; not those who suffer from fin sides. Yes Dr. J Crisler is against its use in men, but he didn’t mean those men who suffer from fin sides-so his belief is not applicable to us. The neuronal sides of fen are due to lack of neuroactive steroids due to 5 alpha reductase blockade in the glial cells of the brain. Neuroactive steroids are very important for regulation of nervous functions, they modulate the GABAa receptors and that is why some of us have sides like brain fog, rapid fatigability, anxiety, tremors, twitching…etc. those are sides of inefficient GABA functions in the brain or may be a depletion of GABA. In addition, GABA increases the release of human Growth Hormone; so a lack of GABA means deficient GH release. I have also posted a study that shows that allpregnenolone_a neuroactive steroid –increase the release of GnRH from the hypothalamus; so a deficiency of allopregnenolone will result in decreasing GnRH release-something which further contribute to hypogonadism.
There is another point which support our use of progesterone, which is concerning the adrenals. In our case the adrenals may not be able to produce enough allopregnenolone and hence progesterone to compensate for their reduction by finasteride. That will surely result in adrenal fatigue or hypoadrenia. There is a major mark of hypoadrenia namely “pregnenolone steal”; which result from the adrenal gland shifting towards the production of cortisol on the account of pregnenolone. I think we can support our adrenals by progesterone.
Again, progesterone is totally different from estrogen, progesterone lowers SHBG level, while estrogen actually increases SHBG level. This is of particular interest to our case since most of us have elevated SHBG level which resulted from two factors:
1- increased T level due to the inhibition of its conversion to DHT by fin;
2- increased T level will result in more conversion of T to estradiol which will result in elevated estrogen concentration-which will inturn increase SHBG level.
So we have every right to cry “free free testosterone!” lolz
Hypo wrote: “Proviron is an oral form of dihydrotestosterone (DHT)
It is a non aromatizable androgen- not an aromatase inhibitor. It does not increase free testosterone as far as I am aware. It increases DHT and lowers total testosterone via negative feedback at the HPTA, this I would presume result in a lower level of free testosterone given the fact that DHT cannot itself be converted to free testosterone.
This is as far as I am aware.
Certainly I can tell you that DHT therapy alone irrespective of the method often leaves its patients exhausted/fatigued due to the fact that it does not have many of the required properties of testosterone. Because Proviron or DHT replacement generally results in recognition by the Hypothalamus and a lowered output of GnRH, this in turn results in a lowered production of LH which in turn results in reduced leydig cell action and lower testosterone. Lower testosterone in this instance can mean (can being the operative word) that there is less raw hormonal ingredient to fuel conversion to estradiol. To put it simply DHT can indirectly sometimes cause a reduced level of estradiol.
But like I say it does not replace the required androgenic actions of testosterone- even if it can sometimes improve libido and erectile function. Also it does not treat elevated SHBG. So if an individual has low testosterone and or high SHBG Proviron is not likely to help, certainly not on its own.”
Proviron of course is an aromatase inhibitor. Yes it is a DHT analogue with the replacement of a hydrogen in the alpha position with a methyl group. You can take it like that:
DHT have higher affinity for aromatase than T, that’s why DHT keeps estrogen level in check.
Proviron is a DHT analogue, so it has a high affinity for aromatase than T. so proviron supposedly keeps estrogens in check.
You can search it and you will find thousands of sites talking about proviron as an aromatase inhibitor. I can back up my claim from farrellmanual.com/drugs/arimidex.htm , where I can cite this paragraph:
“Competitive aromatase inhibitors, such as Cytadren, Arimidex,
and probably Proviron, bind to the same binding site on the
aromatase enzyme that testosterone does. By doing this, they
allow less testosterone to bind to aromatase. So, less
testosterone is converted to estradiol (estrogen).”
Also, I didn’t say that proviron treat elevated levels of SHBG , it is just making SHBG less effective as proviron has higher affinity to bind it than T’the same attribute of DHT’, so proviron increase the free level of androgens by displacing them on SHBG. The real problem with proviron in our case is that it can displace estrogens as well; something which is really troublesome because we have/had higher estrogen to testosterone ratio. The more troubling thing is that the binding of estrogens to SHBG is weaker than that of androgens, so in our case proviron will expectedly free more estrogens than androgens.”hell, proviron can even result in gynecomastia for us, shit!”
My third note is that proviron doesn’t inhibit the hypothalamus pituitary testicular axis at the right doses. I can back up my claim by this study:
This study shows no effect on normal LH and FSH with 100-150mg/ d mesterolone, and decrease of FSH/LH that were elevated.
Proviron doesn’t substitute Clomid as hpta therapy, but doesn’t get in the way, either.
The effect of mesterolone on sperm count, on serum follicle stimulating hormone, luteinizing hormone, plasma testosterone and outcome in idiopathic oligospermic men.
Varma TR, Patel RH.
Department of Obstetrics & Gynaecology, St. George’s Hospital Medical School London, U.K.
Two hundred fifty subfertile men with idiopathic oligospermia (count less than 20 million/ml) were treated with mesterolone (100-150 mg/day) for 12 months. Seminal analysis were assa 3 times and serum follicle stimulating hormone (FSH) luteinizing hormone (LH) and plasma testosterone were assa once before treatment and repeated at 3, 6, 9 and 12 months after the initiation of treatment. One hundred ten patients (44%) had normal serum FSH, LH and plasma testosterone, 85 patients (34%) had low serum FSH, LH and low plasma testosterone. One hundred seventy-five patients (70%) had moderate oligospermia (count 5 to less than 20 million/ml) and 75 patients (30%) had severe oligospermia (count less than 5 million/ml). Seventy-five moderately oligospermic patients showed significant improvement in the sperm density, total sperm count and motility following mesterolone therapy whereas only 12% showed improvement in the severe oligospermic group. Mesterolone had no depressing effect on low or normal serum FSH and LH levels but had depressing effect on 25% if the levels were elevated. There was no significant adverse effect on testosterone levels or on liver function. One hundred fifteen (46%) pregnancies resulted following the treatment, 9 of 115 (7.8%) aborted and 2 (1.7%) had ectopic pregnancy. Mesterolone was found to be more useful in patients with a sperm count ranging between 5 and 20 million/ml. Those with severe oligospermia (count less than 5 million) do not seem to benefit from this therapy.
PMID: 2892728 [PubMed - indexed for MEDLINE]
Hypo, thanks so much for offering your help, here is my lab. Results, try to solve that puzzle lol
Total testosterone: 7.6 ng/ml, don’t ask me about free T as I live in a distant area in Egypt and all the labs close to me don’t do it.
Prolactine: 2.8 ng/ml
Tsh: 3.8 mUL/L
SHBG: 55
DHT: 62
LH: 6.3
FSH: 9.2
estradiol: 30
a puzzle,isn’t it? all are almost normal range with the exception of DHT.
No that is incorrect. I am stating that no decent andrologist currently suggests use of progesterone in men to my knowledge- just a few whacky questionable endocrinologists and anti anging doctors that are not well thought of. I am also saying that Dr Crisler IS against progesterone use in men he is seeing who are trying to recover from finasteride use- at least the last time I looked he was saying this.
I’ll stop you there.
The side effects of finasteride are NOT proven to be as a result of those you mention (I honestly think the paper is probably detailing something that you are missing entirely) and could easily be the result of lowered DHT and or lowered free testosterone and or increased estrogens via elevations in estradiol and or SHBG.
I am not sure you really know what you are talking about here. I mean you are talking about the causes of finasteride problems being related to 5 alpha reductase blockade in the glial cells of the brain. First of all I think you have copied and pasted that out of a research paper, probably one not on porpecia but on finasteride (dose is crucial in these things) possibly on humans possibly not, but I certainly do not think you have a comprehension of what the paper that you are quoting is about. On a separate note there is a real problem in obtaining information on the internet, a real problem and that is in people ascertaining the relevance and appropriateness of given articles given the scope and detail involved and the importance of obtaining correct source material.
You have this idea that the brain is affected.
Why focus on the brain?
I mean Alpha 5 reductase blockade or DHT blockade to put it in an easier way causes problems throughout the body, so why focus on the brain?
Just as a lack of testosterone or too high a level of estrogens due to estradiol or SHBG etc, just as with those hormones DHT is seen via effects right throughout the body.
These are some of the exact symptoms reported in hypogonadism.
Hormones effect the entire body, not just the brain, they effect the central nervous system, the skin, the muscles, they effect bone, hair growth, libido, mood, calorie burning, fat distribution etc etc.
Maybe you have this idea of hypogonadism that is incorrect, I think maybe you do.
I have known many people with hypogonadism to suddenly suffer extreme anxiety, nervousness, I have know many men with hypogonadism to develop brain fog, memory problems, fatigue etc.
Perhaps the paper you were reading and quoting from was trying to detail why a lack of androgens in the brain causes memory issue etc. But the bottom line is that the brain is affected yes, but it is only one part of the entire body systems that are affected.
And we are talking hypogonadism whether we are dealing in a lack of testosterone and or dihydrotestosterone.
If it turns out there is a lack of Growth Hormone due to propecia and the finasteride doses involved then that would represent an added issue and cause of problems. I think we would all want to see relevant evidence if that is the case as a lack of growth hormone is a separate issue to hypogonadism.
In fact if people wish to test out this theory then I would recommend obtaining/adding the gold standard dynamic test for growth hormone deficiency, the Insulin Tolerance test to their pathology list. Failing that I would suggest that people are tested for IFG-1 which is the best serum marker for likely Growth Hormone levels.
I honestly think you are cutting and pasting.
But hey this is straightforward enough;
A)
Tell me, do the medical profession and do a significant number of decent forward thinking andrologists currently support the use of progesterone?
I do not think they do.
B)
Are there any studies that link/prove that propecia size doses of finasteride cause adrenal problems in human men?
If there are then can you provide these studies, white papers and the details for the doctors that support this position and also provide where they have sated that progesterone is a legitimate treatment for such?
I doubt you will be able to do that.
Does propecia size doses of finasteride cause adrenal issues at all? I am not sure they do, although I am willing to accept anything that proves the contrary. But even then I would need to see evidence where doctors are also saying that progesterone is the legitimate treatment to answer such issues.
Do all that and then you will have a point- but not until then.
A)
Progesterone IS regarded primarily as estrogenic period.
B)
I cannot comment on its effect on SHBG as it is not something I have looked into.
C)
Danazol also reduces SHBG and it is an androgen as opposed to an estrogen.
D)
Your first point is incorrect. When finasteride has been used for a reasonable period of time both testosterone and DHT are lowered.
E)
Your second point is incorrect. To say that increasing testosterone leads to a vicious circle on increasing estrogens is simply untrue. If your point were true then all men who had high testosterone levels would end up with high estrogen and SHBG levels and this in turn would cause the HPTA to go into a negative feedback cycle which would result suppression of testosterone. In other words you wouldn’t have men with high normal or normal testosterone levels. The fact is the mechanisms are far more complex than your level of understand.
If you want higher free testosterone because SHBG is an issue then I would suggest that the androgen Danazol is a better option.
I will maintain this belief until I see the andrologists and top endocrinologists taking a complete about turn and going with progesterone.
If there comes a time when all the specialists jump ship and agree with the use of progesterone, if this happens I will agree with you and agree that you are right.
Until such time I will have to disagree with you.
NO IT CATEGORICALLY IS NOT!!!
Proviron effectively is DHT. Many men have high DHT levels- does that mean that they have no production of estrogens?
NO!!!
I am telling you now that you are mistaken. Proviron is a non aromatisable androgen= NOT an aromatase inhibitor. Anastrozole- brand name arimidex is an aromatase inhibitor.
I guarantee that you are getting inappropriate information on this from bodybuilding sites.
Having a higher affinity for SHBG just means that more DHT is bound in the blood by SHBG than say estradiol. It means that for similar levels a greater proportion of DHT is rendered inactive by SHBG. You are misunderstanding what this means.
Your notions are based on stacking drugs for bodybuilding purposes, your information is from bodybuilding sites.
When looking at DHT in the setting of androgen replacement you are categorically and utterly wrong.
Proviron or in fact any form of DHT replacement reduces estrogens indirectly, not directly.
What happens is that by taking something that boosts DHT that cannot be metabolized into estradiol, you still increase the overall androgen level. The total steroid levels are then acted upon by the hypothalamus which thinks that too much testosterone is being made. GnRH is consequently reduced, this in turn loweres LH which in turn reduces leydig cell action and reduces endogenous testosterone. With a lowered testosterone level the individual has less hormone to fuel estradiol and consequently estradiol decreases.
So DHT does not reduce estradiol itself or directly, rather it is the effects at the hypothalamic/pituitary level and the indirect lowering of testosterone that reduce estradiol.
When this happens the benefits to libido and erectile function remain.
However the benefits of testosterone are not present and in fact the benefits of this hormone are often reduced due to a now lower level of testosterone.
This is why very often people on DHT treatment feel very tired, because they lack testosterone, it is also why maintaining or increasing muscle mass is an issue.
The idea that DHT works as an aromatase inhibitor is completely misplaced when talking about endogenous testosterone production, misunderstands the mechanism involved. The term aromatase inhibitor is completely misplaced also. Whether when stacking/abusing differing hormones to supraphysilogical levels, whether in those circumstances DHT has a differing effect I do not know and frankly have no need to know.
I don’t think you understand the mechanisms involved.
I am not sure I can continue this conversation as you just do not understand enough to make it worthwhile.
Wrong. It is non aromaizable- meaning it cannot be converted to estrogens. In fact DHT therapy is widely prescribed in Belgium to treat gynecomastia.
Frankly I am not interested in the study, because I have seen dozens of studies showing the complete opposite and I would on that basis simply question the validity of the study. I have been on DHT therapy as well remember and I can tell you that it does inhibit the HPTA and testosterone production.
The cases where it wouldn’t do that, would be in older men or in men with generally high estradiol. That is because estradiol has a very powerful effect on the HPTA and reducing estradiol and testosterone can mean that there is a lower total level of steroids being recognized by the HP and in turn a none effect or even increase in LH. But this is the exception.
I am telling you for a fact that this study is flawed some of their findings and flawed in how you are trying to represent it.
DHT could potentially help from a sperm point of view via the indirect lowering effect on estradiol- that is if estradiol was high.
DHT does inhibit the HPTA particularly in young men…
hypo, i’m not cutting and pasting !- you can think so only if there is another identical forum where i send the same questions that are sent here- then i go there to cut the answers and paste them here! sorry, i’m not going to argue with you.
btw hypo, you are someone who is very intolerant and rude, sorry, but who are you to get so nervous with people who may present with some ideas contrary to what you have ever believed ? even a professor of andrology wouldn’t get so nervous and intolerant with a lay man who doesn’t understand things correctly. your readings-though better than mine-can’t justify such a behaviour.
Message forms are notoriously difficult places when it comes to the ability to express mood or sentiment. I assure you I did not intend to sound intolerant, unreasonable etc and I assure you it was certainly not my intention to upset you.
All I can say is, if you feel offended then I apologise.
My intention was to provide a robust counter-argument to many of your statements which I believe to be wrong, nothing more than that.
I did not mean to attack you personally in any way whatsoever.
I hope you can accept that because I think your subsequent posts of a personal nature mistake what I was doing.
You would have a FAR harder time in any medical setting or in any debating chamber in terms of the language used.
You can/it is possible to debate matters without any intent to make someone feel bad, without any intention to defame etc. Some people can even debate fiercely without ever getting into anything personal. Doing that depends on not having personal ownership of the comments and thoughts involved.
Maybe because I have criticized or strongly disagreed with what you have had to say on these issues, maybe you think I have a problem with you, that is regrettable because I don’t.
I would hope that you could appreciate the fact that it can be difficult sometimes to state basic truths and express honesty.
I would also hope that I included enough detail in my post that would challenge your thoughts on these issue and either change your perspective or at least get you think about the issues involved, I did spend a lot of time detailing things that I though would be of interest and be helpful- maybe that has not come across.
I am out of this thread because like all debates I have had on this site it has degenerated, somehow healthy robust debate seems to always get personal irrespective of why that is.
Like I say no offense has been intended and you have my apology for any offence that has been inadvertently been caused.
I tried to put a great deal of time, effort and thought into this posts as with others. From now on in I am staying out of the general discussions and just helping people individually- if requested. Other than that I’m not posting any further.
It is quite hard to have posted so much detail and information in a such a short space of time and to have given up so much to just somehow always end up as the bad guy…maybe the site is better off without me.
I am sorry but I dont beleive our problems are just hormonal. I have read about too many guys who have gone on TRT and failed miserably. The fact that Dr Crisler has so many patients who have been screwed from finasteride from previous doctors, and he cant get all of them back to normal with TRT tells me a lot. Dr Crisler is VERY thorough. I know full well that administering TRT is no walk in the park, but it is never THIS hard. It seems most of us finasteride guys have far more problems with TRT than those who have never taken it fin.
As for what the actual problem is - I have no idea. Hypo, I can see that you know a lot about hormones and that is of great value to us, but by simply ingoring anything else that is not backed up by science is not the way we should be looking at this problem. The reason is because quite frankly TRT usually DOES NOT fix our problems. It happens over and over again and i think you ignore this fact and put it down to the fact that we might not be on the correct form of TRT.
I also dont think that you realize just how bad our libido is. We are talking COMPLETE numbness with no desire whatsoever. When you replace the testosterone in a person and fine tune it the way Dr Crisler does and still get no response, there is somthing bigger going on in my opinion. In my mind, it is safe to say that one of two things has happened. Either the way our bodies use those hormones is now different OR there is somthing else going on to do with receptors or neurotransmitters or somthing that we dont even know about yet.
Please dont fire up at me, I am not having a go at you, I am simply telling it how I honestly see it.
Some people think that the way that we convert T to DHT is forever changed and this is the cause of our problems, but this is only speculation. Others think its a receptor problem…who knows?
I just dont buy it that its just a simple form of hypogonadism. Sure some have recovered from TRT, but I am yet to meet one them who has said that they are 100% again from using TRT. I am sure their are a few, dont get me wrong, but I am just saying that if it were that easy, they would be more abundant than what they are.
