Well, no shame in TRT…it may just be a matter of weathering the storm until more permanent solutions are in place. That is, until stem cell therapy eventually becomes available. All we need now are some public officials who give a damn about science…
“Since Leydig cells are responsible for testosterone production, stem cell transplantations may replace the need of life-long testosterone supplementation in testicle failure males and aging population.”
Who on this forum has Hypogonadotropic Hypogonadism? That’s a first. Many have altered hormone levels but not one person has LH values along with T values under the minimum range. Until the AMA changes those ranges or includes symptoms with sub-optimal levels than the Hypogonadism diagnosis does not apply.
Also, if such were the case, simple treatment of TRT would greatly assist the patient with such a diagnosis…which until now hasn’t occured for many (if any) on this forum.
At least half the people who have posted their hormone results on this website look to be hypogonadotropic, categorically NOT a first then!
I am always disappointed, yet never surprised by such a comment.
What on earth makes people who make this comment think that TRT in this setting is easy?
In fact what makes people think that TRT and hypogoandism is easy full stop?
I have been in the hypogonadal communities in the UK and the US for years now with my ear close to the ground. Whilst I can tel you that there are many straightforward cases (usually age realted or primary cases), I can also tell you that there are many people who cannot find a treatment that works, many men have been trying to find answers to why they cannot successfully treat their hypogoinadism for years.
I know of a few guys who did not find proper answers in terms of treatments for over twenty years!!!
Hypogonadism can be very complex or very simple, it depends upon the mechanism of action and it would seem as though finasteride results in a complicated mechanism of action. Most cases appear to be hypogoandotropic- which is far more difficutl to treat generally…
Dr Shippen himself described the difficulty in finding answers and treating finasteride induced hypogonadism himself back in 2002.
Rockin, In future I would appreciate it if you could direct questions to me in a reasonable manner as opposed to trying to make off the cuff statements in order to try and make me look stupid. I don’t think I deserve that and I think you could afford me a little respect, if only for the amount of time and effort I put into trying to help people on the site.
P.S
Nothing you said alters the other fact that stem cell and improvement of testicular function will still categorically NOT help anyone here who has hypogonadotropic hypogonadism and I maintain that is a significant number of men, possibly the majority.
However, I am always amused when you go of your way to share your resume of knowledge regarding male hormones.
Is it Hypogonadotopic or Hypogonadotropic? Just curious. Not sure if there’s much difference or simply a typo. I googled both and they seem the same. It seems like it is linked with KS and such and also pre-puberty. Isn’t any HypoG after puberty considered Primary or Secondary? I don’t know so that is why I’m asking.
So really, when you say you’re helping ppl on this site you really are just letting them know they’re screwed unless they can see a fwd thinking Endo or Uro? I’m not sure, but last I checked you have been the only one to diagnose anyone on this forum. I don’t make off the cuff statements. It’s true that no one has been diagnosed with Hypogonadotopic Hypogonadism from a Licensed Medical Professional. So when there is one than it will be a first. I’m sorry, but your diagnosis doesn’t count as an official one. As far as I’m concerned, it’s an opinion. Which I think you would agree.
I have yet to hear that a Fin patient has been successfully treated by the experts you noted other than the one person you have helped by lowering his SHBG. Are there more?
Yes, you are far more versed on this subject than I am…or ever will be.
You are becoming more and more irksome in your comments. You obvious think this is one big mess around, one big irrelevant joke. I am not interested in your amusement, I am interested in helping people and correcting errors on the matter of endocrinology that may mislead people.
I am interested because giving people the correct information on this subject matter is important.
Now I am not messing around with you any further. I will answer this mail and I would be happy after that point if we can leave It there as I really do not want to waste my time with you any further.
The condition is hypogonadotropic, I think you can forgive a typo don’t you?
You can consider that question rhetorical.
I have the condition so I think I know what I am talking about.
You googled it, that is the point, you haven’t got a clue what you are talking about and yet you are trying to take the piss and are yanking my chain, again because you think this is obviously one big joke to you.
Does it not occur to you that you should not talk to me like I am an imbecile on a subject matter that you know that I am very well versed on when you have to google your darn information?
How about a little bit of respect?
Now to the your questions;
Because you are using google as opposed to well educated on this subject you haven’t got a clue. Hypogonadotropic hypogonadism is sometimes referred to as secondary hypogonadism. It is hypogonadism of a hypothalamic/pituitary origin. Kallman syndrome is one form of hypogonadotropic hypogonadism a pre puberty form due to a chromosomal genetic karyotype error. When someone has a normal of low level of gonadotropins post puberty and they have low testosterone then that is also hypogonadotropic hypogonadism. I developed hypogonadotropic hypogonadism post puberty as a result of chemotherapy. Many men have developed the same due to the use of finasteride.
KS is Klinefelters Syndrome not Kallmans and it is hypergonadotropic, meaning that the cause is testicular or primary in origin. That is another condition that is genetic and of a pre pubertal origin. Again hypergonadotropic hypogonadism can occur post puberty from differing causes- trauma, testicular cancer etc.
So hypogonadotropic hypogonadism is NOT linked to KS and is not even a form of this type of hypogoandism.
Unequivocally NOT, again you do not have an idea of even the basics of the issue involved. I would not say this in such a way if it were not for the fact that you have spoken in the way you have.
A simplistic and derogatory statement of what I have been doing. Given I have been putting quite a lot of time and effort into helping people for no advantage or gain for myself I find these comments in keeping with those you have made prior to be insulting.
Categorically untrue. There have been many men diagnosed and placed on TRT. Theer have also been men on the site diagnosed by Dr Shippen and Dr Crisler and diagnosed with the very condition that I have referred to.
You do and you have.
Categorically untrue as previously stated. Men have been diagnosed with hypogonadism and have either been informed that it is hypogonadotropic/secondary by their doctors or have simply been told hypogonadism and their doctors have not bothered them with the details I have spoken of. Certainly a good few men on this site have been told they are hypogonadotropic or secondary- they mean the same thing as I have enlightened you.
An irritating nasty little remark from a man trying to be a smart arse. Like I said though you don’t have clue what you are talking about so you are totally incorrect. I have not had to diagnose anyone, it has been done for me by the professional you have eluded to.
Yes I have know of lots of men that have at least felt better on TRT- in suitable situations, sorry to disapproint your pettiness there then.
As you say though I have helped someone to overcome finasteride, someone who has even posted on this site.
Have you ever heard of anyone else helping someone overcome these problems?
Have you helped anyone overcome these problems?
I’m guessing NOT!!!
Yet of all the people on the site you choose to try to take me down a peg or two and on a subject you freely admit you know little about, on a subject you freely admit that I am far more versed in.
Well done you obviously that is some achievement.
I mean trying to take the piss out of one of the very few people who has made a difference……I’m sure you can feel good about yourself even if you failed in your endeavor.
I do not need to be told that.
You didn’t reply to anything regarding the original post, you just wanted to try and make someone look a fool- more fool you.
The person who originally posted this thread still has my original and relevant answer. That stem cell therapy for the testicles will not help men with hypogonadotropic hypogonadism and that means many men with finasteride based hypogonadism could not benefit as a result because the testicles are not the problem.
P.S
Please do not post anything to me in future, do not PM me again and do not post to me in threads.
Hypo, I think you need to chill out … this is the Internet of course and the written word can be taken in a variety of ways.
I found most of Jack’s second post apologetic in tone but perhaps you view it as insulting due to personal interpretation…
Jack has tried TRT himself various times so his experience with this is important to those who have not.
Anyway guys, stop arguing, already went through this crap with “Jim1234” awhile back and this place is supposed to be a sanctuary of support, not “you don’t know what you’re talking about” bickering.
Yes none of us are medical professionals, but some (ie, Hypo) have read far more medical literature than others and can thus offer a valuable opinion as to what the issues/potential diagnosis may be for members here… these opinions based on the scientific literature can then be discussed WITH MEDICAL PROFESSIONALS WHEN SEEKING TREATMENT TO FURTHER ONE’S CASE.
I think that’s the main point Jack was trying to get across… we cannot diagnosis with 100% certainty over the Internet, only a medical professional can truly do that. Based on bloodwork alone however, we can get a definite idea as to what a person’s condition most likely may be, based on universal medical guidelines adhered to by the world’s top medical professionals.
I use UpToDate as my wife is a licensed physician (MD) and so I have access to that amongst other medical journals and publications. UpToDate is very reputable amongst the Medical Community…not sure if it’s reputable in your community of experts.
Right, it would only help those with primary hypogonadism, I suppose…
Unless, of course, the particular case of secondary involved hypothalamic damage, maybe, and the regulation issue involved insufficient tissue?
Either way, you’re right it wouldn’t be an effective therapy for fin-induced hypogonadism…
But then if the fin-induced problem is purely metabolic, I presume there must be a way to reverse it? And if not, if the fin-effected hypothalamus has undergone some irreversible change…maybe stem cell therapy, that is, replacing defective hypothalamic cells with cells that do regulate testosterone, would be the only way to produce a “cure”?
Correct. It would only help men who have low testosterone as a result of testicular damage and might not even help those where the damage was pre pubertal, as in Klinefelters Syndrome.
I do not recognize this language in medical terms; I’m not sure what you are saying here. Hypothalamic or pituitary damage that results in lowered LH is hypogonadotropic hypogonadism (secondary hypogonadism) and that is the type of hypogonadism that will not respond to anthing that enhances testicular function.
If a man was to end up with very high LH and hypogonadism post finasteride use then that would indicate testicular damage and hypergonadotropic hypogonadism (primary hypogonadism). If that was the case such treatment would presumably have a chance, I mean if the purpose of the treatment was to improve testicular function then it might be applicable.
My comments are centered on one simple fact, that it would not help those men where the issue was hypogonadotropic hypogonadism.
Your article refers to using stem cells in the testicles to form leydig cells doesn’t it?
I don’t think it referred to stem cells in the context of the hypothalamus or pituitary did it?
If not then you can’t just start applying the article to the hypothalamus/pituitary.
It would appear that many men post finasteride use have hypogonadotropic hypogonadism due to metabolic issues such as high SHBG and or E2. But equally a lot of men simply end up with low or normal LH in the setting of low testosterone levels. In the latter case it looks like a hypogonadotropic hypogonadism without any metabolic influence.
But it is irrelevant if the cause is purely hypothalamic/pituitary or has some metabolic aspect. If the cause of problems is not testicular in origin then improvement of testicular function is NOT going to help as that is NOT where the problem lis.
It is quite simple. Something that improves testicular function has the potential to help those who have impaired testicular function, not those who have fully functioning testicles that d not produce adequate testosterone because of a problem related to the release of gonadotropins.
It is my opinion that if most men post finasteride, men at this website say;
It is my opinion that if most men were placed on HCG or were given the Clomiphene challenge that, most of them would produce adequate to good testosterone levels. This is something that does NOT occur in men with hypergonadotropic hypogonadism (primary hypogonadism). It is NOT something that occurs in men where the problem originates in the testicles.
Now someone may decide to throw some comment at this remark, but I know what I am talking about and am very sure of my words.
Right, I was being purely theoretically, on this point. I was arguing that stem cell therapy, as applied to the hypothalamus, may be the only true “cure” for hypogonadotropic hypogonadism.
Also, I did not fully understand the definition of “metabolic hypogonadism,” apparently. You explain this term as applying to an imbalance of biomolecules in the bloodstream (high SHBG, estrogen, prolactin, etc).
I, however, was assuming that the type of hypogonadotropic hypogonadism that only presents itself only as low/normal LH in a setting of low T, could also be classifed as a type of “metabolic” dysfuction. For if the fin-induced alterations to the hypothalamus did not include cell death, and I assume they did not, they must have involved some other alteration of the biochemistry of the hypothalamic neurons (aka a “metabolic” change).
And isn’t this the greatest mystery here? What exactly was it that changed in these cells that desensitized them to low T? Was it that the AR receptor was downregulated? What could this change have been, that led to an altered, irreversible state? It seems to me that this key detail is essential if any real treatment of the “cause” is to be accomplished.
In regard to stem cells, I’m just saying that if we eventually learn that it is indeed not possible to reverse the fin-induced dysfunctional metabolic state in the hypothalamus, the only possible way to produce might be considered a “cure,” might be to culture stem cells to differentiate into hypothalamic cells that possess the proper metabolic mileau - one that responds properly to low levels of T - and then substitute these cells for the dysfunctional ones. This is all purely theoretical though, of course.
There was a program on tv here in Brasil showing that this therapy is already being tested in some hospitals worldwide. (not for hypogonadism though, but the way it is done, opens a possibilty for us).
(sorry for my english)
The techinque consists of taking bone marrow (is this the right translation? in portuguese they say blood) from the patient’s pelvic bone, separating stem cells and injecting these cells in the bloodstream. So it is not embryo stem cells, but the patients own stem cells.
On the show, they spotted two cases. One was from an english man, that had severe bone loss after an accident, and his doctor was appliyng this technique to grow his femur, the only difference is the cells were injected directly in the bone, and the patient was already able to walk.
The second case, in Brazil, to treat a Chagas Disease patient (the heart grows gradualy to the point the patient needs a heart transplant). This is a very severe disease, it scars the heart muscle over the years. This patients heart had only 32% of its pumping capacity, and after the treatment this jumped to 58% capacity. diabetenet.com.br/conteudoco … teudo=3790
This include Multiple sclerosis, anemia falciforme, Heart disease, stroke and diabetes. It is a pity this is all in portuguese and it is such a long text, but in short it was used the same technique, only difference is in SOME cases they had to go under Chemoterapy before receiving the cells, in order to shut down their imune systems, so it would not attack the cells. This was necessary only in diseases related to the imune system, like Multiple Sclerosis. About the patients: The multiple sclerosis patient now walks without cructhes and claims to have now an almost normal life. There is a picture of him, his name is Cassio de Oliveira.
When i saw this, i couldn’t stop thinking on how it could hypothetically regenerate our prostates, 5 ar II cells, and maybe something else we are not aware of, as the cells are injected in the bloodstream. This is not as far of reach as it used to be. I know some of you guys are working with researchers, i think this is worth some discussion. As the cells are taken from the patient, the risk of rejection is minimum. What are your thoughts about this?
very good article…theres a doctor in sp, who is specialized in this type of procedure, im willing to talk to him about it, even though he might laugh at me.