hypogonadism and gyne reply to poster

[hypo]

This is what I was sent via pm.

do you know some bodybuilders take up to 1gram of testosterone and stack it with other steroids? crazy stuff...  

I want to ask you is it possible for someone who has a kind of athletic build, like broad shoulders etc and an athletic past to have hypogonadism?

I feel like a fit the mental and some physical (lethargy, joint stiffness, loss of fitness) aspects of hypogonadism. But i don't look like the type. I can grow a beard fine, i am built but i dont think i am as strong as i should be for my size. When i work out i have no problem puttin on muscle, but have a hard time losing fat.
unquote


And my reply.  It relates to how gynecomastia and hypogonadism can occur via steroid abuse and explains the mechanisms.


To the above questioner,

(He has since provided me with a borderline low testosterone level) A hypogonadal level for his age according to many endocrinologists- see below

http://www.wellmanclinic.org/paper2.htm

I am aware of the amounts they use, it is disconcerting to say the least.

There are different forms of hypogonadism and testosterone deficiency is not always as obvious or as simple as "looking the part".

One form of testosterone deficiency, secondary hypogonadism via pituitary insufficiency occurs post puberty and can happen at any time of life.  Mike Tyson could develop it next week.  That is to say that any man can develop it, so your build does not preclude you from having it.  

Lethargy, joint problems and loss of fitness are all symptoms of testosterone deficiency.  

Although a lack of secondary sexual hair such as a beard growth is associated with hypogonadism, being able to grow a beard does not preclude men who are genetically predisposed to being hairy from having borderline low testosterone levels, having all the symptoms of hypogonadism and neither does it preclude a man from being classified as having hypogonadism.

Increases in fat/inability to lose fat is a metabolic problem typically seen in men suffering from testosterone deficiency.

http://www.thefactsaboutfitness.com/research/testvisc.htm

Another form not so well known is called metabolic hypogonadism can also occur post puberty.  This is a form of hypogonadism that few endocrinologists are even aware of, but is explained by Eugene Shippen M.D in his book The Testosterone Syndrome and relates to a change in the androgen to estrogen balance (via various means).

I believe it is possible to develop both these forms of hypogonadism after superphysiological use of anabolic steroids.  Development of secondary hypogonadism via pituitary insufficiency following such use is well documented.  Metabolic hypogonadism looks to happen in the short term and may persist in the long term.  

It is also possible through long term heavy use of steroids to damage the testes as a result of testicular atrophy, but that is less likely to relate to you given the short use of steroids you mentioned.

A basic explanation of the HPTA system and how problems can occur;

You have something called a Hypothalamus-Pituitary-Testicular-Axis.  HPTA negative feedback system.

When you took the steroids, it will over time have been recognized by your Hypothalamus.  Your Hypothalamus would have instructed your pituitary to reduce the signal to your testicles by down-regulating GnRH.  Your pituitary in turn would have down-regulated the gonadotropins LH and FSH.  With reduced pulsatile LH and FSH messaging, your testicles would have reduced the production of leydig cells and with it testosterone and with reduced FSH your sterloi cells would have produced decreasing volumes of sperm.  You may have noticed a reduced volume in ejaculation?  

This is the process that allows for testicular shrinkage that many men experience through steroid use.

During this time you had an excess of testosterone in your body.  Your endocrine system converted some of this excess into estrogens and dihydrotestosterone.  Incidentally you may have had a little hair loss from the elevated DHT level at this time; some people do if they are genetically disposed to male pattern balding.

Whilst you may have seen increased gynecomastia on the steroids due to high estrogens you still at least had high testosterone and elevated DHT, which meant the important balance/ratios between androgens and estrogens still wouldn't have been too bad.

When you came off the testosterone your own (endogenous) natural production of testosterone and dihydrotestosterone would have been virtually non existent, your elevated DHT level would have fallen away due to a lack of testosterone production, but your estrogen levels however would have remained high.

Your balance/ratio between androgens and estrogens would have been very poor at this time and highly favored estrogens, which is why it is much more likely that your gynecomastia got worse at this point.  You may also have experienced a big drop in libido and erection difficulties, excess sweating, and emotional problems akin to women’s pmt during this time as well.

After a while your hypothalamus would have spotted a lack of testosterone and set in motion the reverse of the process explained above.  GnRH would be up-regulated telling the pituitary to increase the LH and FSH respectively.  With increased LH and FSH pulsation gonadotropins, the testicles would have started producing more leydig cells and more testosterone/dihydrotestosterone and the sterloi cells would have started producing more sperm.

At this point it is often possible to notice that the testicles increase in size.

So, ok it is easy to see how you can be left with gynecomastia.

But how could a hormone problem be more permanent?

Well;

The thing is it is easy to suppose that the testosterone production is just switched back on, like hitting a light switch, unfortunately the endocrine systems/mechanisms do not function in such a simple and reasonable manner.

First of all there is one awful flaw in the endocrine system, a flaw that is with us prior to birth at the earliest stages of life.  When an egg is fertilized by a sperm it is capable of being male or female.  All brothers start off in life exactly the same as their sisters and to an extent it is fair to say that the default form of life is female.  This is why men have nipples, why men’s breast development occurs via the exact same process as a women’s, if subjected to elevated estrogens.  It is the reason why the gonadotropin messenger hormones in men and women are the same and work in a similar way in regulating how the testicles and ovaries work respectively.  This is why elevated estrogen status in the male often increases the size of the prostate, because the prostate contains cells identical to the uterus of a female, something that predates the male identity.  

Very early in life in the womb an egg can be hit by a surge of androgens.  If this happens it sets in motion a chain of events that leads to the development of the male.  Estrogens are the primary hormones in women, just as androgens are the primary hormones in men…..and here is where I come to the flaw.
 
The hypothalamus cannot distinguish between testosterone and estrogen, they are seen as being identical as the development of the hypothalamus predates the point at which a life becomes a male life!!  

So when you came off testosterone and were left with a high estrogen status your hypothalamus didn’t see too much wrong for a while and so delayed telling the pituitary to tell the testicles to start working again.  As your estrogen levels dropped slowly over time, the hypothalamus in turn slowly acted in up-regulating the instructions to the pituitary to tell the testicles to produce more testosterone- a little drip, then a larger drip, until eventually the tap was turned back on and normal function was returned.

The above paragraph is what should happen, unfortunately it is does not always work so well.

With heavy steroid use or even one cycle in the unfortunate individual, it is possible to injure the pituitary.  The pituitary is like the boss of a factory, with the testicles being the factory workers who produce testosterone.  Now in real life if a factory boss doesn’t return from lunch because he’s injured in a car accident, the workers stop working and have a lazy afternoon.  But in the real world a new boss takes the old ones place or covers for him while he is off.  But in the male endocrine system the testicles can go on a permanent holiday and produce far less testosterone than the body requires.  This is known as pituitary insufficiency or secondary hypogonadism.    

Another flaw that can occur is this;

Sometimes due to the complex dynamics of the endocrine system the estrogen levels remain permanently higher than they were prior to steroid use (A form of metabolic hypogonadism).

This means that the testosterone production never returns to pre steroid use levels, because the hypothalamus thinks there is sufficient testosterone being produced by the testicles and so doesn’t ask the pituitary to tell the testicles to start working harder to produce more testosterone.  The elevated estrogen levels are seen alongside the testosterone level being produced, the hypothalamus being blind as to the difference between the two competing hormones, takes the combined molecular weight of both hormones together and decides that there is no need to up-regulate testosterone production, despite a testosterone deficiency.  

The other problem incurred here and generally by elevated estrogen status is that estrogens block testosterone receptor sites and reduce the amount of free testosterone that the body is able to actually use.

All this is very basic and other issues can occur such as liver problems which prevent the healthy metabolisation of estrogens, injury to the hypothalamus that results in a reduction in GnRH, primary testicular problems as a result of testicular atrophy as previously mention etc etc.  

You may have one of the problems explained above, a little of one and the other, another related issue- or none of them.

Endocrine investigations will hopefully elucidate the answer for you and treatment if required will hopefully be forthcoming.

All of the above is only for the purposes of gaining a better idea of the processes involved.  It is layman’s knowledge and has come with the advice of seeing an endocrinologist.

PM me once read.

[Paa_Paw]

You astound me with your grasp of these matters.

I have a very simplistic way of looking at the whole thing.

First, I think of the relationships of the various enzymes and hormones as a personal chemistry set.

Then, I think of anyone who takes hormones without competent Medical supervision and oversight as playing, (like a child) unsupervised, with a set of potentially dangerous chemicals.

Finally, I question the thought processes of anyone who plays with their chemistry set and then gets upset at the outcome.

[hypo]

Your take on this is quite correct.

I particularly like your statement quote, 'I think of the relationships of the various enzymes and hormones as a personal chemistry set'.

Your thinking is actually better than many endocrinologists across the world believe it or not.

Your statement maybe simple, but it is fundamentally true.

Endocrinologists in the UK and many other countries disagree with your statement Paw Paw.  They say that there is a normal range for testosterone and that if you are within that range then your testosterone level is normal and you do not need treatment.  They do not take into account that everyone is different and they do not concern themselves with symptoms of low testosterone either, which they treat as having no part in making a diagnosis.

This is what Eugene Shippen M.D one of the worlds leading experts thinks on the matter (quote is verbatim from his book Testosterone Syndrome);

If we confine ourselves to testosterone for the moment, let me point out what is useless is the standard doctrine according to which a man’s testosterone level is within the normal range if it falls between 300ng/dl and 100ng/dl (my edit this equates to 10.5-35nmol/l).

Such a notion of normality is virtually meaningless, unless all you mean by normal is that 90 percent of men do, in fact have testosterone levels within this range.  But a meaningful medical notion of normal surely contains an implicit approval of the level found, a suggestion that when a man’s testosterone is above the lower number and below the higher number, he can rest assured that he is basically on track.  In other words that, his health and vigor should be supported rather than adversely affected by this level- he’s normal.

If that is what doctors mean when they refer to normal testosterone levels, then they are flat out wrong.  Your own personal, ‘normal’ level of testosterone is somewhere between 300ng/dl and 1000ng/dl (my edit 10.5-35nmol/l), but no one can say where in that range it lies.

You maybe somewhat too low at 600ng/dl, or you may be quite adequate at 450gn/dl.  By nature, you may be a high testosterone male and, without baseline levels taken at youth, which you certainly don’t have, no one can tell for sure.

Let’s consider the case of two very different men.  One is a high testosterone male who normally averaged between 800ng/dl and 1000ng/dl when he was healthy and young.  Now consider he is fifty and, has suffered a serious hormonal fall.  His levels are now between 400ng/dl and 500ng/dl.  This is a catastrophe, a 50 percent drop, and he feels every point of it.  Now there comes along another individual who in the days when he was young and obstrepously averaged 400ng/dl to 500ng/dl.  He, also has declined.  They now average 300ng/dl to 400ng/dl.  The drop is relatively slight, and he notices little change in function.  He still feels like a healthy specimen.  

It’s relatively easy to make such an analysis.  Unfortunately, in the real world, the physicians who are treating each of these men don’t have the earlier numbers, the basline youthful highs.  All the physicians know is that one man has levels between 400ng/dl and 500ng/dl, while the other is between300ng/dl and 400ng/dl.  And surprisingly, the man with the lower levels feels much better and reports far fewer symptoms of the gray zone of testosterone deficiency.

unquote

So you see your old fashion take on this is more in keeping with the pioneers and worlds leading experts on this than many endocrinologists and endocrinology societies across the world.  

Thankfully the US use symptoms in conjunction with biochemical markers when assessing this condition.

Other countries would be wise to follow suit and not be so arrogant as to throw hundreds of years of symptomatology out of the window in favor of just biochemical markers simply because its 'relatively new science'.  

Science has come along way and should be helping us, for it to do that the endocrinologists need to take the example laid down by the US AACE and understand that biochemistry alone however advanced does not give us the whole picture.  

Until science has created something more complicated than the human body or mapped out fully its workings it should not second guess the body and say that the body is wrong and the pathology is right.

Male endocrinology is a good twenty years behind that of the gentler gender given the lack of funding and attention paid to this subject and there are many discoveries yet to be made, some of which will directly affect gynecomastia as well as hypogonadism.  There are plenty of archimedean moments of Eureka still to come in this subject, but the body must continue to be listened to particularly when we do not have all the questions never mind all the answers.