I am sorry if I came across as rude, it is just that I have posted responses to these types of posts so many times before and it can get a bit repetitive and tiring after doing it every other week for two years as the answers are quite long and drawnout....but forgive me that is not your fault and I was a bit boorish.
I did not have to look go away and research anything I have hypogonadism and know only too well all the ins and outs of what I am about to go through.
Ok, let me back up for a minute. I am not saying genetics aren't a reason why some people get gyno. I was merely going into the direct cause. Genetics, I am sure, have a huge role in determining the reason people get gyno. But that is a general explaination.
You have radically changed what you are saying, as prior you were saying that genetics were not a factor, something that was wrong. At least what you are saying now, that genetics have a huge role in determining the reason people get gynecomastia is correct.
Bad genetics are not a general explanation for a poor androgen to estrogen ratio, low level of free testosterone or dihydrotestosterone or inability of the body to deal with androgens. They are top of the food chain in terms of cause and effect and the very heart/reason for androgen related problem and gynecomastia in some men.
A poor androgen to estrogen ratio, low level of free testosterone or dihydrotestosterone or inability of the body to deal with androgens is not the root cause of gynecomastia in men with bad genetics but the symptom or expression of poor genetics in action.
e.g
Many men with Klinefelter Syndrome develop gynecomastia as a result of the expression of the genetic chromosomal abnormality behind the syndrome that causes the relative imbalance of sex hormones.
We wouldn’t say that the direct cause of gynecomastia in men with Klinefelters is the low androgen to estrogen ratio; we would say that this is the expression of genetics.
Gynecomastia occurs in many men during puberty, equally it does not occur in many others; Why?
Well, we all have our very own individual levels of sex hormones, our endocrine system and balance involves many hormones, and negative feedback systems that come together to create a hormonal symphony. Why does one man have a lowish level of testosterone and another man a high level? Why does one man have high dihydrotestosterone and another not? Why does one man have low SHBG another high? Why does one man have a lowish TSH another high? Why is one man naturally muscular and another not? Why does one man naturally get gynecomastia during puberty another not? Why does one man develop gynecomastia on a set steroid and dose and another not?
The root cause, the answer?
Genetics.
It is what programs the endocrine system to start with.
To be fair to you I think you meant to say that the end resulting problem stems from a poor testosterone to estrogen ratio, which is partially right, but partially wrong in the way you word it (I’ll come to that later). But I just wanted to clear up the fact that genetics are higher up the hierarchical structure/ and the root cause of gynecomatia in many cases and that is what results in the problem in the first place.
It is the one of the reasons why taking Tamoxifen post AAS cycle or testosterone boosters does not guarantee that an individual will not develop gynecomastia, particularly if they have been shown to be predisposed to it in the past.
It is part of the reason as to why your advise to NDean was Bad.
Better advice would have been for him to not take AAS or testosterone boosters given he hopefully has A) a healthy endocirne system at present and B) is predisposed to gynecomastia. If he doesn't take the above he will remain healthy and gynecomastia free, something that cannot be gaurenteed if he takes your advice.
Ok so I think I have covered the heart of this debate/problem, but I will explain a few things relating to one of your comments.
The only cause of gynecomastia that I am aware of is a poor ratio of testosterone to estrogen level.
You have read a little and you have a take on matters that isn’t too distant from the truth, but you don’t know enough about what you are talking about.
First of all 10% of all gynecomastia sufferers have the condition as a result of hypogonadism according to the latest research and hypogonadism is a lack of testosterone and or its metabolites. One of those metabolites is dihydrotestosterone.
A lack of or low level of dihydrotestosterone can and dose cause gynecomastia and this has nothing to do with the testosterone to estrogen ratio.
This fact is seen in men taking finasteride or other anti-dihydrotestoterone medications for prostate cancer, and men with 5 alpha Reductase Deficiency.
It is also seen in men taking medications for hair loss that contain finasteride such as Propecia and Proscar etc.
I have seen dozens upon dozens of men come through this website over the past two years who developed gynecomastia as a result of taking these medications.
So dihydrotestosterone is also very important.
The bottom line with gynecomastia is that it occurs due to an abnormality in the ratio of testosterone to estrogens in the body. When this ratio is low, the estrogen effect is stronger and stimulates the growth of the tissue around the breast. The testosterone which is most important is that which is not bound to protein in the blood, in other words, the free serum testosterone. This has been found to be lower in boys with gynecomastia compared to those without, while all the other hormone levels were about the same.
Again you have a reasonable level of knowledge but not enough to make the statements that you do. I have already explained the importance of dihydrotestosterone, something that you have not been aware of, I will now explain how your general and for the most part good explanation of the situation is not good enough to make such strong categorical statements.
You spoke about the importance of free testosterone, that which is not bound in the blood (the protein is called Sex hormone binding Globulin or SHBG). This is true, free testosterone is very important as is free estradiol which you haven’t mentioned, but it is not very important if the individual has PAIS (Partial Androgen Insensitivity Syndrome) or any other defect in the coding of the androgen receptors.
In fact every individual has a differing response to AAS based upon their individual androgen receptor coding and their number of CAG androgen receptor repeats.
The coding of the androgen receptors means that some men are very sensitive to androgens whereas some, some less so and then again som men are quite insensitive to their action. This effect is not something that is down to the testosterone to estrogen ratio, or the free testosterone to free estrogen ratio, neither is it related to the levels of other differing hormones.
As well as the issues relating to the androgen receptors and sensitivity to androgens, we also have issues that relate to the sensitivity to the estrogen receptors and the sensitivity that an individual has to estrogens.
Gynecomastia is known to run in some families even where they have a reasonable androgen to estrogen ratio, reasonable levels of free testosterone and no genetic abnormality relating to the androgen receptor. Such families/male members are very sensitive to estrogen, this is very poorly understood but almost certainly relates to a genetic coding abnormality of the estrogen receptors.
Again the above indicates the huge impact that genetics have when it comes to this issue.
The bottom line is, it is not wise to play with a healthy endocrine system and with AAS irrespective of any PCT that can be taken as you cannot guarantee that gynecomastia will not result. Once again I say your advice was and is bad.
With that said, it really is quite possible to prevent gyno in someone with a usually perfect ratio, but in fact has a low ratio caused by steroid use. Blocking estrogen or preventing aromatization with the use of novaldex, arimidex, clomid, or whatever does work. Now, once you develope gyno, these drugs will not get rid of it. For that is not their purpose. There is no drug that can get rid of already existing gyno. None that I am aware of anyhow.
Yes it is possible and this does work for some men, otherwise they wouldn’t take it. But why play Russian roulette when it comes to getting gynecomastia. You say “it is possible”, this is interesting wording as of course we also know that many people end up coming unstuck even with PCT and develop gynecomastia.
A)
When taking AAS or testosterone boosters, you do not know on a cellular level how sensitive you are to androgens or estrogens and this can result in not taking a high enough dose of PCT and result in gynecomastia, in fact some men will develop gynecomastia on a steroid cycle never mind post cycle. Of course some men will take too high a dose of PCT and as a result will feel all the effects of low free estrogen (thyroid dysfunction, lowered libido, fatigue, hot flushes and erectile dysfunction).
B)
If an individual takes too high a dose of an aromatase inhibitor as PCT, instead of boosting the Hypothalamic pituitary testicular axis (HPTA) and endogenous androgen production, something it does in low doses, it will actually suppress the HPTA and endogenous androgen production. This means that the PCT would leave the individual with a lowered androgen to estrogen ratio post than they had prior to AAS and this can result in the development of gynecomastia. I know this affect of aromatase inhibitors first hand from taking it myself as part of my treatment for hypogoandism. I saw this effect from my own pathology when I was mistakenly overdosed and I have seen it when looking at the pathology of other men.
C)
Some men taking AAS develop hypogondism via damage to the HPTA, they end up with impaired function of the pituitary or the testicles that is semi-permanent or permanent. This has happened in some men after one cycle and in others after multiple cycles. I have known quite a few men that this has happened to. Of course no PCT is likely to recover such function and as a result gynecomastia can develop.
D)
If a man taking AAS has an underlying liver condition (most people who do have no knowledge of such- 8% of all gynecomastia sufferers are thought to suffer from liver disease according to the latest research) then the use of anti estrogens such as Tamoxifen can aggravate the liver and reduce function resulting in gynecomastia. I have known men to take AAS and Tamoxifen as a PCT who have had very high levels of estradiol evidenced by pathology. This was not a problem when they were on Tamoxifen, however once the Selective Estrogen Receptor Modulator (SERM) medication wore off they were left with a still high blood level of estradiol that was now able to act in their system and result in gynecomastia- a rebound effect.
I could go on and on and on but I wont.
I took a great deal of time writing this mail and providing a proper response and I did so from my own knowledge base and it is all in my own words.
I hope it makes you think a little before suggesting to people that they should tamper with their own endocrine system, I’m sure you wouldn’t want your advice to result in a guy developing gynecomastia.
Once again please accept my apologies for being a little rude/boorish in prior posts.
P.S
Just to note anti estrogens, aromatase inhibitors, dihydrotestosterone etc can reduce and sometimes resolve gynecomastia in some men contary to what what you have said and they are sometimes used for this very purpose by competent prescribing endocrinologists. That said surgery remains the most statistically successful treatment of the condition.