11b-OH-Etiocholanolone (aka: OHET, 11β-hydroxy-etiocholanolone) is a metabolite of Testosterone. (WRONG, apparantly its a5beta-Reductase reduced metabolite of Cortisol; This thread did turn into a discussion about 5alpha and 5beta reduced metabolites anyway )
Almost veryone that has permanent side effects, and has so far posted their test results, has shown low or out of range low for this steroid. Prehaps it is an important marker in the same way 3-Adiol-G seems to be. It would therefore be useful to accumulate results in one place.
Ive posted some existing test results from the site below. If you have results of this blood test please post with ranges here. Thanks.
I think it would also be beneficial to post any other hormones that were tested at the same time, so as to look at whether there is a common link between this metabolite and other hormones.
“Analysis of 5R activity was performed by comparing the ratio of each 5/5ß product (i.e. androsterone/etiocholanolone, 11ß-hydroxy androsterone/11ß-hydroxy etiocholanolone, 5-tetrahydrocorticosterone (THB)/THB, and 5-THF/THF) as well as the ratio of total 5/total 5ß metabolites. Analysis of 11ßHSD activity was performed by comparing the ratio of each 11-oxo/11ß-hydroxy product [i.e. 11-oxo/11ß-hydroxy (etiocholanolone + androsterone), cortisone/cortisol, THE/(THF + 5-THF), cortolones/cortols, and tetrahydro-11-dehydrocorticosterone/(THB + 5-THB)] as well as the ratio of total 11-oxo/total 11ß-hydroxy metabolites.”
The sticky provided by Mew also goes into some detail about how these metabolites relate to 5aR2, viewtopic.php?f=4&t=1453 “…Blood testing: how to check for 5AR2 deficiency”
The characteristic endocrine features of 5a-reductase 2 deficiency are elevated ratios of urinary 5-beta to 5-alpha metabolites. Here are some of the detailed results of some of those members blood test results;
These results do not show a low ratio of 5-alpha metabolites and do not point towards a 5aR deficiency as a result. In fact for the most part the 5-alpha metabolites are very high compared to the 5-beta metabolites.
Just to be clear, it seems you are posting/discussing both serum and 24 hour urinary metabolites of Etiocholanolone here. These are not the same thing, you can not use the levels and ratios from the Chinese paper on urine testing and apply them to serum results.
Which is it that you want? One andrologist I recently consulted with finds the 24 hour urinary steroid metabolites to be far more accurate than serum testing.
I have looked at two or three other members 24 hour urinary steroid ratios and they all have at least 2 of the 3 relevant ratios at the bottom, or below the range, in fact directly indicating 5 alpha reductase Type 2 deficiency.
Using the format I posted just above, and assuming all the data assembled were from urine, and not serum, testing, I get the following ratios (red below range, orange-yellow means bottom 20% of range from the paper):
Ratio 5a THB/THB : 5a THF/THF
Norm. Range 0.8-3.5 : 0.5-2.5
Finsucks: 2.3 : 0.4
thissucks: 2.7 : 1.3
mystory: 1.3 : 0.4
kazman (T=700) 1.1 : 0.7
This all indicates that we have very low 5 alpha reductase type 2 activity. If I recall correctly, mystory, and Finsucks both have significant adrenal issues, and THF is related to cortisol activity.
Kazman, From the chinese paper. (ps All of those results quoted are RhineLabs 24hr urine tests.)
In the pairs listed above the 5alpha metabolite is first and the second is the 5beta, same as the chinese paper.(see quote above and pic)
I dont see the paper mention lower 20%. It does mention unambigious and extremely low levels of 5alpha reduced metabolites in 5ar2 deficiency. (Although the THB and THF ratios are low.)
The (corrected) results I have posted above therefore reveal a strong ratio in favour of 5alpha metabolites. This cannot be a 5aR deficiency. The only exeption seems to be Tetrahydrocortisol. Might be wrong, it is late
(1) normal to elevated levels of plasma testosterone;
(2) decreased levels of plasma DHT;
(3) an increased testosterone to DHT ratio (or following hCG stimulation);
(4) decreased conversion of testosterone to DHT;
(5) reduced 5α-reductase activity in genital tissue and cultured fibroblasts;
(6) normal metabolic clearance rates of testosterone and DHT;
(7) decreased production of urinary 5α-reduced androgen metabolites with increased 5β/5α urinary metabolite ratios; hkmj.org/article_pdfs/hkm0904p130.pdf
(9) a global defect in steroid 5α-reduction as demonstrated by decreased urinary 5α-reduced metabolites of both C21 steroids and C19 steroids other than testosterone (e.g. cortisol, corticosterone, 11β-hydroxy-androstenedione, and androstenedione). ncbi.nlm.nih.gov/pubmed/4028464
The strongest marker for 5aR Type 2 in the liver is low 5a-THF/THF ratio (see jcem.endojournals.org/cgi/content/abstract/54/5/931) this is what the blood levels reveal here . Results will show low 3α-androstanediol glucuronide as well, a peripheral marker of 5aR type 2 activity. This is point (8) and partially points (7) and (9) above. This cannot be a 5aR Type 2 deficiency but could it be a ‘damaged’ Type 2 enzyme due its repression?
Feed-forward control of prostate growth: dihydrotestosterone induces expression of its own biosynthetic enzyme, steroid 5 alpha-reductase.pnas.org/content/88/18/8044.full.pdf+html
Conclusion…
5a-Reductase mRNA has been reduced and has not recovered after stopping fin. OR. As the paper above suggests, 5a-Reductase may be invoked by DHT interacting with the androgen receptor, if this does not happen, there will be continually reduced 5aR. OR. The 5a-Tetrahydrocortisol ratio is low for some other reason. (Like something interfering with 5aR, see here for one theory viewtopic.php?f=27&t=4260&start=20)
Oscar, the 5a THF/5b THF ratio (or in inverted form with appropriate range) is the one Crisler and many other doctors cite as being the most sensitive and reliable from a diagnostic standpoint. The Chinese paper clearly indicates that one of the other ratios is not sensitive to the condition (don’t feel like looking up that portion of the paper at the moment).
Look, if half our urinary metabolite ratios are low it must mean something, e.g. gene expression at a minimum, possible damage to one or more of the 19 genes that encode SRD5AR2 at the maximum. The men being studied were born with ambiguous genitilia via mutation of the genes at birth/due to inbreeding etc. Therefore they are worse, as exemplified by very low DHT levels (mine and many others are normal or at least mid range). I can not agree with your conclusion just because some of us have 5a metabolites that are not “unambiguously low” via serum testing doesn’t mean the urine ratios aren’t a marker of something wrong. I have further information here I can PM you if you would like.
Mariobros, ever try to get an academic research lab to actually run the genital skin fibroblast testing? I mean one that knows how - they aren’t interested outside of doing it within a research grant setting due to “human subject” regulations/red tape etc. This has been my experience thus far, if anyone has found a lab willing to do this for a reasonable amount of money please let me know.
On a side note, i think that a lab study is something that we should all be focused on at the moment, particularly with Dr. Irwig’s study about to be published. I sent a message to Mew today to see if admin could setup a way for people to donate through the site with Paypal or bank deposit, into a third party managed account. i know this has all been suggested before and it would be no small project but it would be a pro-active step forward.
Comparing the ratio of the below two hormones is suppose to give a good indication of 5-AR-2. Since there has been some debate as to if 3adiolg is the best marker or if its a marker for androgen receptor activity.
24hr Rheins urine analysis provides measurements of THF (tetrahydrocortisol) and 5a-THF (allo-tetrahydrocortisol), and the ratio of 5a-THF to THF ( ie: 5a-THF / THF ) follows the 5alpha reductase activity, ie:
high ( 5a-THF / THF > 1.3 ) shows high 5 alpha reductase activity (above 90 percentile)
