Ok I am going to re cap one more time for you
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...
So here your trying to prove your point. You point is proven only if someone has less than than 200 TT and elevated E. Now as you have re iterated time and time again it is "very common" for someone to have this.
Not trying to teach you anything, just interested in preventing you from misinforming readers. Someone with obesity induced hypogonadism might come to the forum looking for answers and might mistakenly think that they don't have obesity induced hypogonadism because "...when you score under 200 its hard to have enough T to even make E." As I mentioned before, this is incorrect.
As far as your statements regarding obesity and idmd's condition goes: you're a bit late to the party. Maybe you haven't read the whole thread? I'll give you a quick summary:
- obesity induced hypogonadism was an initial guess since idmd was overweight by more than 100 lbs. However, he didn't have a good set of baseline tests, so no one knew for sure.
- once additional tests were done, it was apparent that his E2 wasn't that high, although it was still a bit high compared to his SHBG. His doctor aggressively pushed the obesity hypothesis for this reason, although not all agreed with him. However, all did agree that the root cause for his hypogonadism was unclear at this point.
- idmd opted to eliminate variables to increase the chances of obtaining a definitive diagnosis. Specifically, he opted to correct the thyroid imbalance, and lose the weight to see if the hypogonadism remained after both of these problems were corrected.
- if he is still hypogonadal after the weight loss, some additional tests can be done to determine if his testes or pituitary is the cause. TRT (or any other treatment that suppresses his HPT) will only make this testing more difficult and ambiguous.
Here you proclaim that a value of 31 isn't that high
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...
Here you go on to say how common it is to have a TT lower than 200 and
significantly elevated E.
So let me get this straight.
1. Someone must have a TT of lower than 200.
2. It is not uncommon to have lower than 200 TT and
significantly elevated E
3. you do not consider a value like the OP's (31) to be significantly elevated.
So your argument is based on these 3 things. The argument that proved me wrong that you had to step in and correct me, so that others that come to the site would not think they do not have secondary induced hypo.
Now you say you have proven my point but you have not been able to provide 1 single blood test that backs it up.
On top of that when you scoured the net and THOUGHT you found a single blood test to prove your point you quickly posted it, not realizing the numbers you were proudly displaying were right in line with the ops, because you failed to realize the units were not the same we had been discussing all alone.
Here's an article with numbers:
de Boer H, Verschoor L, Ruinemans-Koerts J, Jansen M.
Letrozole normalizes serum testosterone in severely obese men with hypogonadotropic hypogonadism. Diabetes Obes Metab. 2005 May;7(3):211-5. (See:
Letrozole normalizes serum testosterone ... [Diabetes Obes Metab. 2005] - PubMed - NCBI)
Abstract:
BACKGROUND:
Morbid obesity is associated with increased estradiol production as a result of aromatase-dependent conversion of testosterone to estradiol. The elevated serum estradiol levels may inhibit pituitary LH secretion to such extent that hypogonadotropic hypogonadism can result. Normalization of the disturbed estradiol-testosterone balance may be beneficial to reverse the adverse effects of hypogonadism.
AIM:
To examine whether aromatase inhibition with Letrozole can normalize serum testosterone levels in severely obese men with hypogonadotropic hypogonadism.
PATIENTS AND METHODS:
Ten severely obese men, mean age 48.2 +/- 2.3 (s.e.) years and body mass index 42.1 +/- 2.6 kg/m(2), were treated with Letrozole for 6 weeks in doses ranging from 7.5 to 17.5 mg per week.
RESULTS:
Six weeks of treatment decreased serum estradiol from 120 +/- 20 to 70 +/- 9 pmol/l (p = 0.006). None of the subjects developed an estradiol level of less than 40 pmol/l. LH increased from 4.5 +/- 0.8 to 14.8 +/- 2.3 U/l (p < 0.001). Total testosterone rose from 7.5 +/- 1.0 to 23.8 +/- 3.0 nmol/l (p < 0.001) without a concomitant change in sex hormone-binding globulin level. Those treated with Letrozole 17.5 mg per week had an excessive LH response.
CONCLUSION:
Short-term Letrozole treatment normalized serum testosterone levels in all obese men. The clinical significance of this intervention remains to be established in controlled, long-term studies.
SI Unit Conversion Calculator
So now that I have compiled your entire argument into 3 simple bullet points we can see that you actually haven't proven a thing.
So PUT UP OR SHUT UP.
you will not be able to find it though, as I have said previously high E is merely one tiny piece of obesity induced hypo, which should actually be called insulin induced hypo. "it is a culmination of factors" as I pointed out in my second post in this thread. So i wouldn't be so quick to dismiss hypo induced obesity just cause he doesn't have "elevated E" and this is because he doesn't have enough T to sustain "elevated E"
So as I said in my post directed to you, I wouldn't be so sure high E is the cause but that does not mean he does not have obesity induced hypo, which is really caused by elevated insulin.
thank you for your time and thank you for correcting me, even though every single thing I have said has been spot on............................
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