Hey, I got some more extensive blood work back recently… does anybody here have high DHT and low 3 adiol G? That’s what I have for some reason:
29 year old…
Total Test…564, range 241-827 ng/dL
DHT…84, range 25-75 ng/dL
3adiolG…173, range 260-1500 ng/dL
What gives? Am I not metabolizing DHT properly?
Does this mean I have low 3aHSD?
To get a window on 3a hydroxysteroid dehydrongenase it would be useful to see your serum androstandione level.
Also, total serum T is much more useful if you get SHBG as well, this way you can use the ISSM calculator to see what your free T level is.
I think high DHT combined with low Adiol-G implies your 5AR1 enzymes are working overtime to make up for the permanently surpressed 5AR2 (and possibly 5AR3) enzymes. Of course this fits more for former propecia sufferers than dutasteride users.
That’s an interesting idea. Does it have any basis?
I’m more of the opinion that the 5ARII is working okay when one exhibits high DHT levels like this. This seems much more logical. Otherwise this would happen even when using fin, which doesn’t seem to have been documented in anybody bloods i’ve ever seen.
The more realistic proposition, in my mind, is that the metabolism of this DHT (and probably testosterone) is completely screwed. This is evidenced by many people’s incongruent urinary and serum levels.
Yeah, my SHBG is high too. I think my free T was around 1.5% if not slightly lower, which is lower than where it should be.
I personally think that the 3aHSD is low because DHT is not metabolizing into 3-adiol-G. I mean if it can’t metabolize, its just going to sit there and pool higher and higher in the blood I would assume.
I don’t have my androstendione levels tested unfortunately. Why would this matter to my question anyway? This helps create testosterone and estrogens. My Test is low, but my DHT is high and being made just fine apparently.
3a-HSD is an enzyme which, amongst other things, is responsible for maintaining correct androgen levels at the cellular level. It’s like the waste gate of a turbo motor, if you can relate to this analogy. One thing that many people seem to miss is that enzymes are themselves regulated, often by the substrate which they process or proteins which are expressed from genes which react to that substrate.
The fact is, that 3a-HSD is regulated by AR gene expression. If, for whatever reason, AR gene expression is not happening at sufficient levels or in the correct (protein) form, 3a-HSD will become downregulated. Low 3a-diol-G, is currently one of the most compelling bits of evidence that we have a problem at the AR signaling level, leading to a specific form of androgen insensitivity. Hence, you can have as much DHT as you want, even supplement it directly, and you won’t get any benefit. Actually, you might well see that increasing DHT levels will actually lead to a reduction of 3a-diol-G- and an increase of your symptoms.
It may be useful to look at the thread about the other 5a/5b Reductase reduced metabolites; viewtopic.php?f=4&t=4674. These metabolites are in fact 5a/5b reductase and 3aHSD reduced metabolites, in the same way 3aDiolG is. The metabolites are of cortisol, corticosterone and androstenedione.
THF - the cortisol metabolite shows a consistently low level both in total and in comparison to its 5beta reduced conterpart. It is also thought to be the most sensitive marker of 5alpha reductase activity - along with 3aDiolG.
Cortisol is not an androgen - the production of its 5a/5b and 3aHSD reduced metabolites are therefore not controlled by the androgen receptor. (Funnily enough the metabolites of androstenedione - another androgen - are normal).
This is more similar to a deficiency of 5alpha Reductase activity - or possibly of 3aHSD (which i favour at the moment see; viewtopic.php?f=27&t=5111). Importantly, there is no way to know if these results where like this pre-fin.
I think you are right. That is what I am thinking for people with high Total T and high DHT, No being used and just floating. I used A gel and got fat on my chest. My total T remained high for 40 days after stopping Agel.
This is WRONG. A study with AIS patients has clearly shown that 3a-diol-G is largely dependent on functional AR gene expression. This strictly implies that 3a-HSD is induced by AR gene expression. I have written a paper which also goes into this, and additionally looks at short chain version of 3a-HSD in bacteria (also androgen regulated). You can PM me and I can give you access to the document.
This 5AR deficiency stuff is absolute BS and it’s high time that we stop cooking up this old crap over and over again.
I was talking about the metabolite of cortisol, 5a-Tetrahydrocortisol, which is used as a marker of 5alpha reductase activity. This liver metabolite is preserved in AIS - exactly because it is not controlled by the androgen receptor. Most people that have had these metabolites tested show a ratio usually seen in a 5alpha reductase deficiency. Therefore maybe the same reason for this is also what is causing 3aDiolG to come back low. I dont know, but it shouldnt be ignored.
Well, thats what the blood and urine tests show. I dont think its whats causing problems: I only developed problems AFTER quitting. However - its certainly important.