DHEA: can you decrease its conversion to DHT?

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Alive

Member
Dr Saya first advised me to take it for my insomnia. 25mg every night. It seemed to make my insomnia worse and give me heart palpitations so I stopped after a week. However I noticed a huge increase in libido and also an increase in my facial hair.

This week I started taking it again to address the mysterious problem of my practically nonexistent libido. This time 10mg in the morning. It has been helping...slowly. Not just that, I seem to have become more cordial and confident. I think all of these have to do with its neurosteroid property.

HOWEVER it didn't take long before my hair started to get thin and my facial hair started to increase like crazy. Acne too. I think this is because of DHEA to DHT conversion. Any way to slow this down? DIM maybe?


My last DHEA-S read from the summer was 341 in 102-416. I tried pregnenolone too but it made me angry and depressed. Others stuff: 25mg of Propionate EOD (soon to try ED) and 400IU of HCG twice a week.
 
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Gman86

Member
Very interesting. I remember when I was researching pregnenolone like crazy, I kept finding guys that reported hair loss with pregnenolone as well. I wonder if the cause of the shedding is the same with both. Like you said, possibly DHT.
 

Vince

Super Moderator
I would have to agree with Vince Carter, I've never had an increase or decrease in DHT related to my DHEA.
 

DragonBits

Well-Known Member
Do you all check DHT often? I have only checked it once as it's expensive and takes longer to get results.

And DHT seems to spike similar to T then fall off, so timing when you test it would likely be important.

The only things that have affected my E2 has been clomid and raising TT. (Boron did raise it to a normal % of TT). I wouldnt have an idea if Preg, dhea, hcg raised DHT as I have never tested for that.
 
it would be interesting if you are gonna use topical dhea because i am 100% topical dhea crashed my estradiol so if you are gonna use it pull labs to see what it's doing to your e2.
 

JPB

Member
DHEA per se is probably not an active hormone, but rather a prohormone that is converted into active androgens and oestrogens in target tissues by intracrine mechanisms. The influence of the dose–response relationships of DHEA substitution on this intracrine regulation of hormone production is not known, although DHEAS, androstenedione and testosterone concentrations increase to low normal values in females receiving a daily dose of 50mg DHEA. In addition, commercially available DHEA preparations are notoriously contaminated with other hormones or substances, which in part explains why DHEA is formally not considered
to be a drug.

Source: Intrinsic imperfections of endocrine replacement therapy : European Journal of Endocrinology Eur J Endocrinol

In peripheral tissues such as hair follicles, adipose tissue and prostate, DHEA and DHEAS are converted into active androgens such as androstenedione, testosterone and dihydrotestosterone, and into active oestrogens such as oestrone and oestradiol.
 
DHEA per se is probably not an active hormone, but rather a prohormone that is converted into active androgens and oestrogens in target tissues by intracrine mechanisms. The influence of the dose–response relationships of DHEA substitution on this intracrine regulation of hormone production is not known, although DHEAS, androstenedione and testosterone concentrations increase to low normal values in females receiving a daily dose of 50mg DHEA. In addition, commercially available DHEA preparations are notoriously contaminated with other hormones or substances, which in part explains why DHEA is formally not considered
to be a drug.

Source: Intrinsic imperfections of endocrine replacement therapy : European Journal of Endocrinology Eur J Endocrinol

In peripheral tissues such as hair follicles, adipose tissue and prostate, DHEA and DHEAS are converted into active androgens such as androstenedione, testosterone and dihydrotestosterone, and into active oestrogens such as oestrone and oestradiol.

THIS is a great point and one often overlooked when only viewing the hormonal landscape superficially. The complexity of the hormonal landscape is appreciated by most, but when one takes into consideration that we are monitoring serum levels as just one indicator...then you dig deeper and think of the next two “dimensions”, as it were, being hormone-receptor interaction and ALSO tissue-specific (vs serum) concentrations (for which we can’t measure in a practical way)...the complexity increases exponentially. This is yet another reason why one cannot simply look at a lab value on a piece of paper and shoot from the hip to make recommendations or adjustments. There’s equal parts art, science, and experience involved.
 
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