My introduction.....

[newbie23]

I would also like to add to my post for Toolman:

I understand that you want the best care available and you have the money and or insurance to pay for it, so that is fine but there are many guys out there that do not have insurance or much money to pay for there proper care and they have lousy testosterone levels. This is common because most people with low income have carb enriched diets, mac and cheese is cheap but salmon is not.

So what I see with these guys is they just want to feel better and do not have the money to get a 60 panel test every 6 weeks, does this mean we should deprive them of testosterone that will improve there quality of life? Does this mean we should deprive them of supplementation because they do not have the money to closely monitor everything going on in there body?

Think of all the pills they hand out to everyone, viagra, lipitor, anti depressants + many more

Don't think for a second those aren't jacking up there lipids and clogging up there liver while simultaneously suppressing there testosterone most of the time.. Someone will scream "there is no study that proves that", these are the same people that do not realize that the pharm company that produces said medication are the ones responsible for the studies, who is to say they give you the positive results and not the negative? and yes it has happened before multiple times, I can't remember the most recent but it was something like the medication proved to be 70% effective on the initial release, then later they were taken to court when the full data came out and it was only 30% effective and was giving people heart attacks. medication that has only been around for 5 years, not 70 like testosterone.

Should we not allow them an affordable way to get FDA approved testosterone? I don't think so, simply because its not dangerous, and it the effects of low testosterone and insulin resistance are probably much worse for them than a 2x per year 4 panel blood test that they can afford and be happy on.

JustMy2Cents

 

[Structure]

You know what, Im gonna go get my E2 checked, sensitive of course, thats gotta be the problem

Actually, that's not a bad idea. High E2 would help to explain why you're so easily hurt by an opposing viewpoints; I haven't followed your postings on other threads, but at least on this thread, you're kind of like a delicate little flower.

Is there anyone on this thread that hasn't offended you yet?

 

[newbie23]

Actually, that's not a bad idea. High E2 would help to explain why you're so easily hurt by an opposing viewpoints; I haven't followed your postings on other threads, but at least on this thread, you're kind of like a delicate little flower.

Is there anyone on this thread that hasn't offended you yet?

I only get offended by those that give answers and claim they are correct when they couldn't be further from the truth Like the one implying that the only place E is made is in the leydigs [)]

Im not gonna let that go

You can try to follow my posts here but its been years since i posted here heavily, I left when all the vets left.

I know you are green, but one day you will not need an E test to know that it is high grasshopper

 

[Structure]

I only get offended by those that give answers and claim they are correct when they couldn't be further from the truth Like the one implying that the only place E is made is in the leydigs [)]

Im not gonna let that go

You can try to follow my posts here but its been years since i posted here heavily, I left when all the vets left.

I know you are green, but one day you will not need an E test to know that it is high grasshopper

Wow, you're a very interesting guy newbie23. Apparently, on top of your inability to carry on a discussion without having a meltdown, you're delusional as well. (You didn't correct me, I'm the one who corrected you. And honestly, I meant no offense by it. You were just mistaken about the endocrinology of obesity induced hypogonadism. Take another look at the posts I made that sent you into a tailspin: https://thinksteroids.com/community/posts/823615 and https://thinksteroids.com/community/posts/823733).

It's none of my business, really, but you've probably noticed that the meltdown approach doesn't get you very far (nor does denial); you're still wrong. And probably it's not serving you well in other areas of life either. Are you married? It's hard to imagine a woman signing up for what you've got to offer. I guess there's plenty of messed up women out there though. I would guess that the kind of woman that would stay with you would either be like a deer in headlights 24/7, always waiting for the next temper tantrum... Or maybe she's just given up altogether, and just walks around like a zombie, always letting you "be right", always letting you have your way. That can't feel good to see that day in and day out...

Life is full of setbacks. Sometimes you're going to be wrong. Sometimes, you're going to be corrected. It's not the end of the world. Learn to cope. (You'll thank me later.)

 

[newbie23]

Ok buddy lets start over cause obviously this is going to take a while to get through to you.

are your IGF-1 levels decent to high? I mean I don't have time to go through this whole thread but your T is in the tank, basically castrate. your TSH is obviously high and I'm wondering if your cortisol is through the roof. your PRL is in range but its up there, that always makes me sleepy.

My initial guess, and it is a guess, with your BMI being high and T super low, non alcoholic fatly liver disease, or at least developing.

I dont understand the testing so soon after injection, and do not see why your changing your dose and then waiting 8 days.

To me its pretty cut and dry that your T has been low for a while, with the lack of energy and libido in recent years and scoring pretty much nil on the T chart.

I see no reason why you wouldn't supplement, at least temporarily until you get your BMI and diet in check.

On the surface it simply looks diet got you here.

nothing you can't change though.

D3 is more for muscle health, glucosamine is a better supp for joint pain, or Zyflamend to reduce inflammation.


Getting some probiotics would also be beneficial to you.

also as others have pointed out it will be important to know if your primary or secondary.

Hope this helps.

also saw a comment that high E2 may be the cause of your lowT and I don't think so, although it is suppressive, when you score under 200 its hard to have enough T to even make E.

although it is possible.

This is a culmination of multiple factors..... not a singular.

This is what I said.............

Hmmm. There seems to be a problem with your logic here: "...when you score under 200 its hard to have enough T to even make E."

Total T is the amount of testosterone that remains after a portion of it has been converted into E2. Had idmd's problem been due to overconversion of T to E2 (obesity induced hypogonadism), then he could very easily had even less T than this, despite elevated E2; numbers like his are not particularly difficult to achieve from obesity induced hypogonadism.

As far as just throwing T at the problem goes: I think you're off in the weeds here. I also think you're incorrect to blame the patient for being difficult simply because he doesn't see good deductive reasoning in your argument! Seems a bit out of place in this discussion...

This is what you said.

Now I may be mistaken but it looks as if in my post I clearly said it was obesity induced hypo? ok moving on.........then I said I saw a comment, directed at you, that E2 was the cause of all this. Then I said that I highly doubt high E2 was the cause of all this cause the guy doesn't even have enough T to convert to E.

Now here you coming, ready to pounce on me, after I clearly said I did not have time to read the whole thread but I will give a guess cause IBMD wanted me to come over, he was challenging my knowledge on TRT.

So you come in and somehow manipulate the wording to my post to say that I am somehow saying it was not obesity induced hypo, even though I clearly said it was.

You must believe somehow that obesity induced hypo causes your E to go up and that is what smashes your T, when in reality, thats probably the last part of the chain reaction that lead IBMD to his current position.

What really happened was a carb enriched diet kept his inulin abnormally high for long periods of the day, and that is actually what started the chain reaction. Now a side effect of having high insulin and low GH is your body shuttling food to fat stores. In these fat stores, or dense lipids cells, is where the aroma enzyme lies. so because of his high insulin and low GH fat tissue began to flourish and now there were many more dens lipid cells for aroma enzymes to hang out. Now the more of these enzymes the more E. Then E, because it was high, started suppressing his T at the hypothalamus. Was E the only thing that suppressed his T? I highly doubt it, insulin played a big role and also the lack of GH.

 

[newbie23]

then you said " total t is a measurement AFTER estrogen has been made"............now that is what I would like YOU to explain...................

 

[newbie23]

and just so you know, my fiancé is a 10, gorgeous. Blonde, big boobs, little waist and would most likey laugh at you when your started creeping on her at the bar...................[)]

 

[newbie23]

then you said " total t is a measurement AFTER estrogen has been made"............now that is what I would like YOU to explain...................

this will be epic...........................bustin down the structure........[)]

 

[newbie23]

Total T is the amount of testosterone that remains after a portion of it has been converted into E2. Had idmd's problem been due to overconversion of T to E2 (obesity induced hypogonadism), then he could very easily had even less T than this, despite elevated E2; numbers like his are not particularly difficult to achieve from obesity induced hypogonadism.
.

Ok I'm going to bed, i can't wait anymore for you to come up with an excuse for this one. As I said before, this would ONLY be true if E was ONLY made in the leydig cells..................

and just to add to that, what in world were you talking about when you said "despite elevated E2 numbers like his are not difficult to achieve from obesity"

what exactly did that mean? [)] I wanted to say " no shit sherlock but that still doesn't mean it was all caused by estrogen"

You have been misinformed when someone told you that obesity induced hip only has to do with E.

 

[Structure]

Ok buddy lets start over cause obviously this is going to take a while to get through to you.






This is what I said.............





This is what you said.

Now I may be mistaken but it looks as if in my post I clearly said it was obesity induced hypo? ok moving on.........then I said I saw a comment, directed at you, that E2 was the cause of all this. Then I said that I highly doubt high E2 was the cause of all this cause the guy doesn't even have enough T to convert to E.

Now here you coming, ready to pounce on me, after I clearly said I did not have time to read the whole thread but I will give a guess cause IBMD wanted me to come over, he was challenging my knowledge on TRT.

So you come in and somehow manipulate the wording to my post to say that I am somehow saying it was not obesity induced hypo, even though I clearly said it was.

You must believe somehow that obesity induced hypo causes your E to go up and that is what smashes your T, when in reality, thats probably the last part of the chain reaction that lead IBMD to his current position.

What really happened was a carb enriched diet kept his inulin abnormally high for long periods of the day, and that is actually what started the chain reaction. Now a side effect of having high insulin and low GH is your body shuttling food to fat stores. In these fat stores, or dense lipids cells, is where the aroma enzyme lies. so because of his high insulin and low GH fat tissue began to flourish and now there were many more dens lipid cells for aroma enzymes to hang out. Now the more of these enzymes the more E. Then E, because it was high, started suppressing his T at the hypothalamus. Was E the only thing that suppressed his T? I highly doubt it, insulin played a big role and also the lack of GH.

It wasn't relevant to my argument that you do / do not think idmd had obesity induced hypogonadism. I was simply pointing out that you were mistaken when you said "when you score under 200 its hard to have enough T to even make E." That statement is incorrect, and could easily misinform a reader that is new to the subject.

That's actually the only reason I bothered to correct this statement; I didn't want other readers to be mislead. I went on to describe a counterexample showing how your assertion was false: overconversion of T to E2 as seen in obesity induced hypogonadism results in a state where T is very low, and E2 is high. In other words, one first makes T, then a large fraction of it is converted to E2, leaving little remaining T. This example is a direct contradiction to your statement that "when you score under 200 its hard to have enough T to even make E" since a person in this state will show a T of under 200 and yet is producing more than enough T to convert to E2 (that's the problem; it's being converted into E2).

Lastly, I gave you a quick summary of what you had missed by not reading through the thread in its entirety.

That's all that happened, bro. No need for the theatrics.

 

[newbie23]

It wasn't relevant to my argument that you do / do not think idmd had obesity induced hypogonadism. I was simply pointing out that you were mistaken when you said "when you score under 200 its hard to have enough T to even make E." That statement is incorrect, and could easily misinform a reader that is new to the subject.

That's actually the only reason I bothered to correct this statement; I didn't want other readers to be mislead. I went on to describe a counterexample showing how your assertion was false: overconversion of T to E2 as seen in obesity induced hypogonadism results in a state where T is very low, and E2 is high. In other words, one first makes T, then a large fraction of it is converted to E2, leaving little remaining T. This example is a direct contradiction to your statement that "when you score under 200 its hard to have enough T to even make E" since a person in this state will show a T of under 200 and yet is producing more than enough T to convert to E2 (that's the problem; it's being converted into E2).

Lastly, I gave you a quick summary of what you had missed by not reading through the thread in its entirety.

That's all that happened, bro. No need for the theatrics.

Your wrong though, and your not seeing it. E is made after that too...........hence obesity induced hypo....... if the fat cells were not a danger to the floating TT and FT then there would be no obesity induced hypo, so there is the contradiction to your statement. Just in case someone else is looking I don't think there is enough room in his nuts to pack enough fat cells holding aroma enzymes to do much at all. So like I said, your statement only works if E is ONLY made in the leydig cells.

On top of that his E is not high...........soooooo

 

[Structure]

Ok I'm going to bed, i can't wait anymore for you to come up with an excuse for this one. As I said before, this would ONLY be true if E was ONLY made in the leydig cells..................

and just to add to that, what in world were you talking about when you said "despite elevated E2 numbers like his are not difficult to achieve from obesity"

what exactly did that mean? [)] I wanted to say " no shit sherlock but that still doesn't mean it was all caused by estrogen"

You have been misinformed when someone told you that obesity induced hip only has to do with E.

No, you're mistaken here as well. T is made by the leydig cells, but it circulates to adipose tissue. In obesity induced hypogonadism, the overabundance of adipose tissue (and hence aromatase) converts a large fraction of this circulating testosterone into estrogen.

When you draw blood, you only see the steady state values of the system. You don't measure the amount of testosterone being created in the leydig cells, you measure the amount that has not been converted to E2.

Thus, an individual with obesity induced hypogonadism can show a T of under 200 and yet is producing more than enough T to convert to E2. This argument does not imply that this conversion must occur in the leydig cells, as you have stated. Thus stating "this would ONLY be true if E was ONLY made in the leydig cells" is false. Not really sure how you arrived at that conclusion to begin with...

You asked what I meant by "he could very easily had even less T than this, despite elevated E2; numbers like his are not particularly difficult to achieve from obesity induced hypogonadism." What this states is that it is not uncommon for someone with obesity induced hypogonadism to go in for blood tests, and get results showing that they have even less than your prescribed threshold of 200 ng / dL T, and still have significantly elevated E2.

So again, sorry to ruffle your feathers. But I don't think you would be so easily ruffled if you didn't take offense to being disagreed with, or, worse yet, being corrected. That can't be making your life any easier...

 

[Structure]

Your wrong though, and your not seeing it. E is made after that too...........hence obesity induced hypo....... if the fat cells were not a danger to the floating TT and FT then there would be no obesity induced hypo, so there is the contradiction to your statement. Just in case someone else is looking I don't think there is enough room in his nuts to pack enough fat cells holding aroma enzymes to much at all. So like I said, your statement only works if E is ONLY made in the leydig cells.

On top of that his E is not high...........soooooo

This might help you understand how this works: Steady state (chemistry) - Wikipedia, the free encyclopedia

 

[newbie23]

You asked what I meant by "he could very easily had even less T than this, despite elevated E2; numbers like his are not particularly difficult to achieve from obesity induced hypogonadism." What this states is that it is not uncommon for someone with obesity induced hypogonadism to go in for blood tests, and get results showing that they have even less than your prescribed threshold of 200 ng / dL T, and still have significantly elevated E2.
.

first of all his E is not significantly high, second of all it is not common for someone to score that low with high e, at least not in the 300 blood tests I have seen.

Secondly I understand that the measurement is what you got after the T was converted but that is not to say if he was producing more testosterone that his E would have came in higher, cause it would have. The only reason his E is as low as it is, is because he is shut down. If he was not shut down then he would have a much higher E reading...........................because IF HAS ENOUGH AROMA ENZYMES TO CONVERT A BUCKET OF TESTOSTERONE. SINCE HE ONLY HAS A DROP HE ONLY HAS A DROP OF E!!!!!!!!!!!!!!!!!!

this is why men with low T get osteoporosis!!!!! because they have no T to convert to EEEEEEEEEEE

 

[newbie23]

Seriously though you have insulted my woman and now you are pushing something that I rarely see, bout to bust out the white out, and some bloods tomorrow..................lets see just how common it really is................

I even said it was possible but Im not letting you get away with common, cause its not.

 

[Structure]

first of all his E is not significantly high, second of all it is not common for someone to score that low with high e, at least not in the 300 blood tests I have seen.

Then you have not seen many blood tests from people with obesity induced hypogonadism. This chemical state (blood tests showing high E2 and low T concomitantly) is quite common among men with obesity induced hypogonadism. Whether or not idmd himself has obesity induced hypogonadism is immaterial to this fact.

Secondly I understand that the measurement is what you got after the T was converted but that is not to say if he was producing more testosterone that his E would have came in higher, cause it would have. The only reason his E is as low as it is, is because he is shut down. If he was not shut down then he would have a much higher E reading...........................because HE HAS ENOUGH AROMA ENZYMES TO CONVERT A BUCKET OF TESTOSTERONE. SINCE HE ONLY HAS A DROP HE ONLY HAS A DROP OF E!!!!!!!!!!!!!!!!!!

this is why men with low T get osteoporosis!!!!! because they have no T to convert to EEEEEEEEEEE

Again, the reason why your statement that "when you score under 200 its hard to have enough T to even make E" is wrong is because it is not uncommon for someone with obesity induced hypogonadism to go in for blood tests, and get results showing that they have even less than your prescribed threshold of 200 ng / dL T, and still have significantly elevated E2. And no, this statement does not imply that the conversion of T to E2 must take place in the leydig cells.

 

[newbie23]

your wrong man, I just tried to copy paste some numbers but it won't let me. as I just perused the first 10 obese guys with really low t i could find, not one of them had an E reading over 26.

The only time I see high E with men with LowT is when the are marginally suppressed, like 3-400.

then and only then will you see it get into the 35-50's

Now if you wanna say they have a unfavorable ratio I will go with that, but it is VERY UNCOMMON for someone to score higher than 25 on E when their E is under even 300.

If you look at ops blood test, you will see the 31 E reading is AFTER he injected T and his TT was 399- he didn't even get it measured when he was under 200. If he did I can assure you it would be a hell of a lot lower than the 31 it was after injecting a total of 300mg of test.

Im done arguing with this because the only thread your dangling from is " it is common for obese men to score higher E than 31 with a T less than 200" I can assure you it is VERY rare. wether your chemistry set wants you to believe or not.

The 300 blood test i reffered to were only those I have still have access too, over the last 3 years I have seen many many many more than that. I can assure you there is 1 common theme, E goes down with T.

 

[Structure]

Seriously though you have insulted my woman and now you are pushing something that I rarely see, bout to bust out the white out, and some bloods tomorrow..................lets see just how common it really is................

I even said it was possible but Im not letting you get away with common, cause its not.

If you want to see journal articles, search for "obesity", "estrogen", and "hypogonadism" in pubmed or google scholar. Here's one paper on the subject:

Hammoud AO, Gibson M, Peterson CM, Hamilton BD, Carrell DT. Obesity and male reproductive potential. J Androl. 2006 Sep-Oct;27(5):619-26. Epub 2006 Jun 2. (see Obesity and Male Reproductive Potential -- Hammoud et al. 27 (5): 619 -- Journal of Andrology)

Here's an excerpt:

The origin of hypoandrogenism in obese males is multifactorial (Table). It is primarily attributable to an increase in circulating estrogens that appear to result in relative hypogonadotropism, although the diminished levels of sex hormone-binding globulin (SHBG) in obese individuals will by itself result in reduced total testosterone levels, even in the face of unchanged production. In fact, weight correlates negatively with blood testosterone levels and testosterone/estradiol ratio (Fejes et al, 2006). Both estrone and estradiol are increased in obese males compared to controls (Schneider et al, 1979). The aromatization of C19 androgens like testosterone and androstenedione is a key step in estrogen biosynthesis and is catalyzed by the aromatase enzyme, a product of the CYP19 gene. It is believed that the increase in estrogens in obese males is due to increased conversion of adrenal and testicular androgens owing to the increase in available aromatase enzyme in the fatty tissue (de Boer et al, 2005). Estrogen production by adipose tissue is dependent on the availability of androgenic precursors in the circulation (Simpson et al, 1999). Estrogens are biologically active at much lower concentrations and production rates than androgens (testosterone production in adult males is several mg per day, whereas estradiol production in women averages 100 µg per day); thus small increases in aromatization of androgens can result in changes in estrogen levels that are substantial in relation to the range of normal circulating levels. Increased circulating estrogen levels resulting from increased peripheral conversion among the obese may therefore inappropriately enhance negative feedback on gonadotropin secretion. Estradiol has significant biologic activity in the hypothalamus and the pituitary. Estrogen receptors (ER{alpha} and ERß) are present in several hypothalamic nuclei and in pituitary gonadotropes, indicating that estrogen modulates the activity of hypothalamus-pituitary axis. Estrogen acts on the hypothalamus to affect gonadotropin-releasing hormone (GnRH) pulses and at the pituitary level to regulate gonadotropin (follicle-stimulating hormone [FSH] and luteinizing hormone [LH]) secretion (Akingbemi, 2005). In severe obesity, pituitary gonadotropin secretion appears suppressed with normal or decreased levels of LH in the presence of decreased levels of testosterone (Giagulli et al, 1994). Because aromatization also occurs in the hypothalamus itself, precise dissection of the contribution of increases in circulating estradiol associated with obesity to overall negative steroidal feedback on pituitary gonadotropin secretion is problematic.
...
Obese males usually express a characteristic hormonal profile described as "hyperestrogenic hypogonadotropic hypogonadism."
​

My apologies for insulting your woman. I went over the line there in an attempt to show you that I think you might have an issue with being disagreed with...

 

[Structure]

your wrong man, I just tried to copy paste some numbers but it won't let me. as I just perused the first 10 obese guys with really low t i could find, not one of them had an E reading over 26.

The only time I see high E with men with LowT is when the are marginally suppressed, like 3-400.

then and only then will you see it get into the 35-50's

Now if you wanna say they have a unfavorable ratio I will go with that, but it is VERY UNCOMMON for someone to score higher than 25 on E when their E is under even 300.

If you look at ops blood test, you will see the 31 E reading is AFTER he injected T and his TT was 399- he didn't even get it measured when he was under 200. If he did I can assure you it would be a hell of a lot lower than the 31 it was after injecting a total of 300mg of test.

Im done arguing with this because the only thread your dangling from is " it is common for obese men to score higher E than 31 with a T less than 200" I can assure you it is VERY rare. wether your chemistry set wants you to believe or not.

The 300 blood test i reffered to were only those I have still have access too, over the last 3 years I have seen many many many more than that. I can assure you there is 1 common theme, E goes down with T.

This chemical state is common among men with obesity induced hypogonadism. (See journal article above; it explicitly states that men with obesity induced hypogonadism "usually express a characteristic hormonal profile described as 'hyperestrogenic hypogonadotropic hypogonadism.'") Note that being an obese male with hypogonadism does not mean that you have obesity induced hypogonadism.

 

[newbie23]

If you want to see journal articles, search for "obesity", "estrogen", and "hypogonadism" in pubmed or google scholar. Here's one paper on the subject:

Hammoud AO, Gibson M, Peterson CM, Hamilton BD, Carrell DT. Obesity and male reproductive potential. J Androl. 2006 Sep-Oct;27(5):619-26. Epub 2006 Jun 2. (see Obesity and Male Reproductive Potential -- Hammoud et al. 27 (5): 619 -- Journal of Andrology)

Here's an excerpt:

The origin of hypoandrogenism in obese males is multifactorial (Table). It is primarily attributable to an increase in circulating estrogens that appear to result in relative hypogonadotropism, although the diminished levels of sex hormone-binding globulin (SHBG) in obese individuals will by itself result in reduced total testosterone levels, even in the face of unchanged production. In fact, weight correlates negatively with blood testosterone levels and testosterone/estradiol ratio (Fejes et al, 2006). Both estrone and estradiol are increased in obese males compared to controls (Schneider et al, 1979). The aromatization of C19 androgens like testosterone and androstenedione is a key step in estrogen biosynthesis and is catalyzed by the aromatase enzyme, a product of the CYP19 gene. It is believed that the increase in estrogens in obese males is due to increased conversion of adrenal and testicular androgens owing to the increase in available aromatase enzyme in the fatty tissue (de Boer et al, 2005). Estrogen production by adipose tissue is dependent on the availability of androgenic precursors in the circulation (Simpson et al, 1999). Estrogens are biologically active at much lower concentrations and production rates than androgens (testosterone production in adult males is several mg per day, whereas estradiol production in women averages 100 µg per day); thus small increases in aromatization of androgens can result in changes in estrogen levels that are substantial in relation to the range of normal circulating levels. Increased circulating estrogen levels resulting from increased peripheral conversion among the obese may therefore inappropriately enhance negative feedback on gonadotropin secretion. Estradiol has significant biologic activity in the hypothalamus and the pituitary. Estrogen receptors (ER{alpha} and ERß) are present in several hypothalamic nuclei and in pituitary gonadotropes, indicating that estrogen modulates the activity of hypothalamus-pituitary axis. Estrogen acts on the hypothalamus to affect gonadotropin-releasing hormone (GnRH) pulses and at the pituitary level to regulate gonadotropin (follicle-stimulating hormone [FSH] and luteinizing hormone [LH]) secretion (Akingbemi, 2005). In severe obesity, pituitary gonadotropin secretion appears suppressed with normal or decreased levels of LH in the presence of decreased levels of testosterone (Giagulli et al, 1994). Because aromatization also occurs in the hypothalamus itself, precise dissection of the contribution of increases in circulating estradiol associated with obesity to overall negative steroidal feedback on pituitary gonadotropin secretion is problematic.
...
Obese males usually express a characteristic hormonal profile described as "hyperestrogenic hypogonadotropic hypogonadism."
​

My apologies for insulting your woman. I went over the line there in an attempt to show you that I think you might have an issue with being disagreed with...

apology accepted

I have seen many articles on these, some even have the patients blood test numbers in it. This does not prove anything to me though. cause there are no numbers in there, I think you are confusing an unfavorable ratio with elevated E. It just never happens man, I'm speaking from experience, not articles