Study: Steroids' users hormone balance irreparably damaged after a couple of years -

[greaser13]

I couldn't paste the graphs and charts that were in the article, but the link is below if you want to check them out.

I'd be interested to hear people's thoughts on the subject.

http://www.ergo-log.com/steroids-us...eparably-damaged-after-a-couple-of-years.html

Steroids' users hormone balance irreparably damaged after a couple of years - despite post cycling therapy.


Average steroids users will have messed up their hormone balance beyond recovery after a few years, endocrinologists at Copenhagen University Hospital discovered. The study raises questions about whether post cycling therapy [PCT] after a course of steroids has any point.

Study
The Danes studied 37 bodybuilders who were taking steroids, 33 bodybuilders who had been clean for 2-3 years, and another 30 bodybuilders who had never taken steroids.

The participants were 18-50 years old and did 6-9 hours of weight training per week.

The active steroids users had been taking anabolics for a total of 142 weeks; the ex-users had taken steroids for 112 weeks. Half of the users and ex-users had taken hCG, a hormone that according to manuals for steroids users helps to restore the hormone balance after a steroid cycle. About a third of the users and ex-users had used anti-oestrogens during the post cycling therapy.


Steroids' users hormone balance irreparably damaged after a couple of years - despite post cycling therapy



Results
The total testosterone concentration was significantly lower in the ex-users than in the control group of bodybuilders that never used steroids. Moreover, the ex-users had significantly smaller testes than the subjects who had never used steroids.


Steroids' users hormone balance irreparably damaged after a couple of years - despite post cycling therapy



The free testosterone concentration was significantly lower in the ex-users than in the control group, as the figure below shows.


Steroids' users hormone balance irreparably damaged after a couple of years - despite post cycling therapy



The concentration of LH and FSH, the hormones that stimulate the testes to produce testosterone, was exactly the same in the ex-users as in the never-users. It is therefore unlikely that the permanent damage caused by steroids use occurs in the glands in the brain that control the testes via FSH and LH.


Steroids' users hormone balance irreparably damaged after a couple of years - despite post cycling therapy



The longer the steroids users and ex-users had cycled, the smaller their testes were, which suggests that steroids use causes permanent damage to the testes.


Steroids' users hormone balance irreparably damaged after a couple of years - despite post cycling therapy



Depression, erectile dysfunction and decreased libido were more common in the ex-users than in the subjects who had never used steroids.


Steroids' users hormone balance irreparably damaged after a couple of years - despite post cycling therapy



Conclusion
"The present study showed that a high proportion of former anabolic steroids abusers exhibited biochemical and functional anabolic androgenic steroid-induced hypogonadism several years after anabolic steroids cessation", the Danes summarised. "Current anabolic steroids abusers exhibited biochemical abnormalities suggestive of impaired spermatogenesis, which were associated with increasing accumulated duration of anabolic steroids abuse."



"Anabolic androgenic steroid-induced hypogonadism may become a public health concern with respect to male infertility and hypogonadism."

Source:
PLoS One. 2016 Aug 17;11(8):e0161208.

 

[greaser13]

I do notice that it says "only a third" used antiestrogens (which would include SERMs) during post cycle therapy. Therefore, 2/3rds didn't run a proper PCT, which in my mind distorts the results somewhat. I wish they had controlled for former users who always used SERMs and those who never did. That would have been interesting and useful.

 

[biglizard225]

Interesting study but it just makes me want to say "go figure" lol

 

[Bio]

I don't think this is news to anybody.

 

[heavyhitter]

No shit? Lol

 

[bieberhole69]

[ame="https://www.youtube.com/watch?v=-f_DPrSEOEo"]Dumb and Dumber - We Landed on the Moon! - YouTube[/ame]

 

[VFW]

That's what you get for coming off hahahaha

Sent from my SM-N910V using Professional Muscle mobile app

 

[emeric delczeg]

I do notice that it says "only a third" used antiestrogens (which would include SERMs) during post cycle therapy. Therefore, 2/3rds didn't run a proper PCT, which in my mind distorts the results somewhat. I wish they had controlled for former users who always used SERMs and those who never did. That would have been interesting and useful.

Just curious , what will be the correct PCT in your opinion?

 

[maldorf]

I don't think this is news to anybody.

I agree. Most guys with any experience know this to be true. I do think though that there are some young inexperienced guys out there that think they can tinker around for a few years and not do permanent damage to your own natural testosterone output. They think with proper PCT and maybe even some time off and they will recover. I used to think that 10 years ago but know better now after my own personal experience. I used for about 10 years, doses not higher than most on here, and my natural test never recovered.

 

[Dezzy]

This doesn't surprise me at all. I think you can go back to normal after a cycle or two especially with PCT drugs. But long term use...naw it's gonna mess your shit up eventually.

Sent from my SAMSUNG-SGH-I337Z using Tapatalk

 

[Itachi]

I don't think this is news to anybody.

Was going to more or less say the same

 

[DrivingForward]

Two things:

1) Very small sample size for a study, may not actually reflect the larger population of steroid using young men.

2) PLOS One is a peer reviewed journal... but they publish shit that other reputable journals wouldn't publish. Some of it borders on pseudoscience.

That being said...

They were probably right.

 

[Love_to_Bodybuild]

im more interested in thyroid studies, if thyroidals using them for competition, ripping up, cause thyroid issues after used over and over

 

[jeffro]

if I am understanding this correctly, the information says ex-users and non users both had similar levels of LH and FSH, suggesting the damage caused by AAS is at the level of the testes? In theory, could one use something such as Clomid or Hcg durring a steroid cycle to maintain testicular function and potentially avoid or minimize perminant damage of the testes and its natural test production following a cycle? i know that high test levels inhibit both gnrh and pituitary gonadotropins but could the 2 aforementioned drugs overcome the negative feedback inhibition of high test while on cycle, send signals to the testes so they continue to make endogenous test even in a high test environment? I think I remember Dante talking about this at some point but I can't for the life of me find the post, nor do I understand all the dynamics involved.

 

[asteelz]

Two things:

1) Very small sample size for a study, may not actually reflect the larger population of steroid using young men.

2) PLOS One is a peer reviewed journal... but they publish shit that other reputable journals wouldn't publish. Some of it borders on pseudoscience.

That being said...

They were probably right.

Plos one is a great resource for out of the box stuff

This study though does not confirm anything we as users weren't aware of. That being said many of the medical community are very uninformed about hormones

 

[bieberhole69]

if I am understanding this correctly, the information says ex-users and non users both had similar levels of LH and FSH, suggesting the damage caused by AAS is at the level of the testes? In theory, could one use something such as Clomid or Hcg durring a steroid cycle to maintain testicular function and potentially avoid or minimize perminant damage of the testes and its natural test production following a cycle? i know that high test levels inhibit both gnrh and pituitary gonadotropins but could the 2 aforementioned drugs overcome the negative feedback inhibition of high test while on cycle, send signals to the testes so they continue to make endogenous test even in a high test environment? I think I remember Dante talking about this at some point but I can't for the life of me find the post, nor do I understand all the dynamics involved.

So from my understanding...there's two types of cells that respond to gonadotropins. Leydig cells, which respond to LH and produce testosterone. And sertoli cells, which respond to FSH and produce sperm cells and are all about sperm (production, motility). There's also evidence that FSH is needed in addition to LH for normal testosterone production.

HCG stimulates the leydig cells, but does little for sertoli. You need HMG for that. In the absence of FSH these cells will remain undifferentiated. I could not find substantial evidence of what happens in long-term FSH suppression or how to treat FSH-deficient males only, as this is extremely rare.

Anyways, HCG mimics LH and causes the testicles to continue to produce testosterone. Testosterone regulates the HPTA/pituitary pathway (GnRH secreted from HPTA acts on pituitary to secrete LH / FSH) and in the presence of exogenous testosterone there will be no GnRH production and thus no LH / FSH production--I've verified this with my own bloodwork even in the presence of HCG. Many users including myself note sustained testicular size with HCG therapy alone during blasts. This does not mean we have good sperm production.

So basically, HCG will stimulate the leydig cells and presumably they will still produce testosterone (although to a diminished effect from the research I found without presence of FSH). HCG is also the first-line therapy for infertile males. The research suggested (for infertility, as well as hypogonadism) that clomid alone often did not work.

So what am I trying to say (yea, I know it's long-winded)?

The best thing you could do is at least keep the leydig cells active with HCG, which is relatively inexpensive. Clomid might help in keeping FSH production up and consequently the sertoli cells stimulated, but I could not find good evidence out there supporting this so if going this route you're just having to hope on it.

The real questions to ask are: if I, a long-term steroid user, ever come off...will my body respond appropriately and produce GnRH? If so, will the pituitary respond to it and subsequently produce LH + FSH? If that also happens, will the leydig cells and sertoli cells respond to it and resume normal function?

The study seems to suggest that HPTA/pituitary function is normal since they have LH + FSH, so it's probably a solid bet that there is reduced function of either leydig cells, sertoli cells, or both. Remember that HCG does little to stimulate FSH, and there is evidence that FSH stimulation of the sertoli cells is required for normal testosterone production (as well as healthy mature sperm). It does however keep testicular size up, so that's a start.

Anyways, just some food for thought. I have no conclusive answer for you, unfortunately. Me personally? I've ran HCG the entire time I've been on in hopes that it will mitigate some of the damage done. If HMG was easy to get / affordable I'd be running that too.

 

[maldorf]

So from my understanding...there's two types of cells that respond to gonadotropins. Leydig cells, which respond to LH and produce testosterone. And sertoli cells, which respond to FSH and produce sperm cells and are all about sperm (production, motility). There's also evidence that FSH is needed in addition to LH for normal testosterone production.

HCG stimulates the leydig cells, but does little for sertoli. You need HMG for that. In the absence of FSH these cells will remain undifferentiated. I could not find substantial evidence of what happens in long-term FSH suppression or how to treat FSH-deficient males only, as this is extremely rare.

Anyways, HCG mimics LH and causes the testicles to continue to produce testosterone. Testosterone regulates the HPTA/pituitary pathway (GnRH secreted from HPTA acts on pituitary to secrete LH / FSH) and in the presence of exogenous testosterone there will be no GnRH production and thus no LH / FSH production--I've verified this with my own bloodwork even in the presence of HCG. Many users including myself note sustained testicular size with HCG therapy alone during blasts. This does not mean we have good sperm production.

So basically, HCG will stimulate the leydig cells and presumably they will still produce testosterone (although to a diminished effect from the research I found without presence of FSH). HCG is also the first-line therapy for infertile males. The research suggested (for infertility, as well as hypogonadism) that clomid alone often did not work.

So what am I trying to say (yea, I know it's long-winded)?

The best thing you could do is at least keep the leydig cells active with HCG, which is relatively inexpensive. Clomid might help in keeping FSH production up and consequently the sertoli cells stimulated, but I could not find good evidence out there supporting this so if going this route you're just having to hope on it.

The real questions to ask are: if I, a long-term steroid user, ever come off...will my body respond appropriately and produce GnRH? If so, will the pituitary respond to it and subsequently produce LH + FSH? If that also happens, will the leydig cells and sertoli cells respond to it and resume normal function?

The study seems to suggest that HPTA/pituitary function is normal since they have LH + FSH, so it's probably a solid bet that there is reduced function of either leydig cells, sertoli cells, or both. Remember that HCG does little to stimulate FSH, and there is evidence that FSH stimulation of the sertoli cells is required for normal testosterone production (as well as healthy mature sperm). It does however keep testicular size up, so that's a start.

Anyways, just some food for thought. I have no conclusive answer for you, unfortunately. Me personally? I've ran HCG the entire time I've been on in hopes that it will mitigate some of the damage done. If HMG was easy to get / affordable I'd be running that too.

I know from my personal experience that when I got off steroids for good, after my heart attack, I was off for about 11 months and my LH levels when tested always came back "below measurable level". My LH production never came back.

 

[kscowboy]

I know from my personal experience that when I got off steroids for good, after my heart attack, I was off for about 11 months and my LH levels when tested always came back "below measurable level". My LH production never came back.

I have said this for a long time (Along with Dante) that i personally don't believe you ever get back to 100% after you take your first shot.

 

[bieberhole69]

I know from my personal experience that when I got off steroids for good, after my heart attack, I was off for about 11 months and my LH levels when tested always came back "below measurable level". My LH production never came back.

So if LH never came back, then we can assume (unless you had further labwork done trying to figure it out) that either a) your HPTA no longer produced GnRH or b) it did, but the pituitary was unresponsive to it.

Curiously for my own personal knowledge, did you try clomid or tamoxifen therapy? If so, did it ever stimulate anything? If not, then we know there was a pituitary failure. If so, then I think it would be safe to assume a HPTA failure. Not that anything could have been done to prevent this, just wanting to know for my own personal knowledge.

And I agree that for users it will likely never return to 100% no matter what is done. And in this day and age of everyone getting prescribed T when they're older and things go south anyways...I guess that's acceptable. Unless you're worried about having kids--I know there's been plenty of guys who've had kids while on / came off after long term use. But there could always be a case like yours (maldorf) and if one of the primary goals in life was to have kids then perhaps it would be best not to use at all or at least not use heavily until then for the best chances.

Unless somehow sans LH production you were still producing FSH or fertility drugs were able to overcome this. In which case...blast on?

 

[jeffro]

There's also evidence that FSH is needed in addition to LH for normal testosterone production.

Didnt know that, I just thought in males, FSH mainly stimulated sertoli cells to make androgen binding protein (SHBG analog) for the production and maturation of sperm cells


Anyways, HCG mimics LH and causes the testicles to continue to produce testosterone. Testosterone regulates the HPTA/pituitary pathway (GnRH secreted from HPTA acts on pituitary to secrete LH / FSH) and in the presence of exogenous testosterone there will be no GnRH production and thus no LH / FSH production--I've verified this with my own bloodwork even in the presence of HCG. Many users including myself note sustained testicular size with HCG therapy alone during blasts. This does not mean we have good sperm production.

So basically, HCG will stimulate the leydig cells and presumably they will still produce testosterone (although to a diminished effect from the research I found without presence of FSH). HCG is also the first-line therapy for infertile males. The research suggested (for infertility, as well as hypogonadism) that clomid alone often did not work


The study seems to suggest that HPTA/pituitary function is normal since they have LH + FSH, so it's probably a solid bet that there is reduced function of either leydig cells, sertoli cells, or both. Remember that HCG does little to stimulate FSH, and there is evidence that FSH stimulation of the sertoli cells is required for normal testosterone production (as well as healthy mature sperm). It does however keep testicular size up, so that's a start.

that's why mechanistically, it would make more sense (to me anyway) that clomid would be a better choice since it works at the level of the hypothalamus resulting in a Gnrh pulse and subsequent release of both FSH and LH from the pituitary. This is assuming clomid indeed will work in a high testosterone environment, one could maintain signals to the leydig and sertoli cells with LH and FSH respectively (vs only signaling leydig cells with Hcg; bypassing the hypothalamus and pituitary which are inhibited by negative feedback) and perhaps preserve normal function throughout the cycle, as opposed trying to restart things after the fact and hope for the best. while this makes sense on paper, obviously things are more complicated than that. I am in no way an expert an I am sure other will have more info to add. I would be interested to know if anyone on the board used clomid while on cycle and if indeed LH/FSH levels were preserved while on

Anyways, just some food for thought. I have no conclusive answer for you, unfortunately. Me personally? I've ran HCG the entire time I've been on in hopes that it will mitigate some of the damage done. If HMG was easy to get / affordable I'd be running that too.

obviously as the old adage goes, don't play with fire and you wont get burned. I feel like there has got to be a way to use low dose for infrequent short periods of time and not ruin your endocrine system for life. perhaps that is being a bit arrogant and naieve