Anyone have any experience/knowledge on this little know testosterone metabolite?
I'm very interested in Testosterone therapies these days as I slowly shrivel up from ADT
Supposedly this Testosterone variant is anti-carcinogenic, stimulates estrogen receptor beta, and more. Sounds very interesting but hard to find any info in the clinical realm.Anyone have any experience on this topic?
Short name: 3β-diol.
I have written about this but it is such a pain trying to search for things on this site.
Many hormones are not under the control of the endocrine system. A feature of the endocrine system is that enzymes are secreted for use elsewhere, & there is a feedback loop to stop the secretion.
So, how does a normal prostate cell stop T converting to DHT & causing uncontrolled cell division?
When DHT is created, it has a very narrow window to act in. It's presence stimulates its clearance. A metabolite of DHT is 3β-diol, which is actually an estrogen.
In the normal prostate, the alpha estrogen receptor [ERbalpha] is found in stromal cells, whereas epithelial cells contain ERbeta. It is thought that 3β-diol is the natural ligand for ERbeta. It has a much lower affinity for ERalpha.
The role of ERalpha is essentially to promote eoithelial growth (in a paracrine fashion), while the role of ERbeta is to inhibit growth. So, while DHT acts to stimulate growth, it is quickly followed by ERbeta, which puts the brakes on.
There is a lot more going on, but at the end of the day, in the young adult prostate, the size of the prostate doesn't change. DHT is not an enemy (nor is estradiol, at this stage).
When I began using androstenedione 13 years ago, I didn't know about 3β-diol. But I did know that the androgen receptor was generally normal in men before ADT. I also knew that PCa (which occurs in epithelial cells) tends to down-regulate ERbeta & upregulate ERalpha occurrence.
When I did find out about 3β-diol, I was happy to allow DHT to do its thing, in the hope that there was still some ERbeta in those cells.
In time, my PSA doubling time shortened at a rate where I realized that DHT was no longer my friend. That's when I started using Avodart.
Incidentally, I was concerned when the two 5alpha- reductase PCa prevention trials reported less PCa but more serious Gleason scores, that suppression of DHT, & thereby 3β-diol, was to blame. T & DHT are growth regulators in the normal prostate. Healthy men should have normal levels.
In summary, 3β-diol is invaluable when a PCa cell still has ERbeta. (As is DHT when the AR hasn't undergone mutation during ADT.)
-Patrick
So if you go on ADT then the AR will be mutated so then DHT is not controlled and causes unregulated growth? Is there a way to naturally manage this?
What I have been trying to do is avoid ADT adaptations. I have limited castrate periods to 3 months & immediately followed with 3 months of high testosterone.
When one becomes ADT-resistant [CRPC], DHT is the enemy. In a percentage of cases, cells are making DHT - but not from T. Nonetheless, I understand that Avodart can inhibit.
-Patrick
May I ask how the 3-month cycle is related to your recent post stating:
My BAT: - T cypionate injected on 1st of each month
- 1 mg DES each day 8th to 31st of each month
?
Sorry if I am being dense.
My experimentation with testosterone has been going on for 13+ years. First with androstenedione followed by Androderm patches. That phase lasted for ~5 years. Then I switched to the 3 month cycle (which is a form of BAT IMO). Finally, recently, the protocol you describe.
What I said in the above post was that: "I have limited castrate periods to 3 months".
Meaning, that I was scared of giving the cells any more time to adapt. & that was effective for me. I might have successfully continued on it for some time, I think. But the monthly cycle has its appeal.
In the monthly BAT cycle, I am castrate at the end of the month. However, I know that when I inject on the 1st of the month, my T on the 8th is still >1,000 ng/dL. I don't know how many days I am actually castrate. It could be that a 6 week BAT cycle might be better.
Sam Denmeade (at Hopkins) cycles rapidly, but his castration phases might be too short to cause serious damage.
& perhaps BAT needs to be customized for each BAT man.
-Patrick
Hi Nala,
Apologies for the delay.
With "5α-androstane-3β,17β-diol?" as the title, I doubt that many read any further - you & I were there only responders.
You make a good point. A separate thread, though.
-Patrick
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