DHT is great, very great. There’s a whole new world beyond dihydrotestosterone though and the pathways to dihydrotestosterone are very many.
Science is even hinting that some of the “effects” from dihydrotestosterone could actually be attributed to downstream metabolites of dihydrotestosterone.
There are multiple endogenous variations of the great dihydrotestosterone, some of which just might be more potent than regular dihydrotestosterone itself.
P.S. The neurochemistry can be complex. Start here.
Conversion Pathways to DHT
Well it all starts with cholesterol. From cholesterol DHEA and pregnenolone are made and convert to all steroid hormones. DHEA and pregnenolone are the most-upstream steroid hormones converting to testosterone and progesterone and their downstream hormones.
Testosterone > DHT via 5 alpha reductase (5ar).
Androstenedione > 5a-androstanedione > DHT via HSD17B3/AKR1C3.
Testosterone > 11OH-T > 11OH DHT > 11k DHT via CYP11B1,2, 5ar, then HSD11B2.
Testosterone > 11OH-T > 11K-T > 11k DHT via CYP11B1,2, HSD11B2, then 5ar.
Androstenedione (A4, AED) > 11OH-AED > 11OH-T > 11OH DHT > 11k DHT via adrenal CYP11B1, HSD17B3/AKR1C3, 5ar, then HSD11B2.
A4, AED > 11OH-AED > 11OH 5a-dione > 11k 5a-dione > 11K DHT via adrenal CYP11B1, 5ar, HSD11B2, then HSD17B3/AKR1C3.
Allopregnanolone > Allopregnanolone-diol > Androsterone > Androstanediol OR 5a-androstanedione > DHT via CYP17A1, then HSD17B3.
17a-OH Progesterone > Androstenedione > 5a-androstenedione > DHT via CYP17A1, 5-ar, then HSD17B3.
17a-OH Progesterone > Androstenedione > Testosterone > DHT via CYP17A1, HSD17B3/AKR1C3, then 5ar.
3a-diol > DHT via reversible enzymes: HSD17B6/HSD17B10/RODH4,RDH5/3A-HSD.
3a-diol > androsterone > 5a-androstenedione > DHT.
Androsterone > 3a-diol > DHT.
Androsterone > 5a-androstenedione > DHT.
Metabolites of DHT
There’s more to dihydrotestosterone than just dihydrotestosterone itself. Dihydrotestosterone can convert into 5a-androstenedione, androsterone, 3a-diol, 3b-diol, and a-triols. All the metabolites of dihydrotestosterone have effects of their own, independent of dihydrotestosterone.
One well-studied property that most if not all dihydrotestosterone metabolites have is strong aromatase inhibiting properties as well as estrogen receptor antagonism properties (study). This is a big factor behind dihydrotestosterone’s strong anti-estrogen effect.
Metabolites of dihydrotestosterone are all pro-GABA, increasing GABA receptor activity (study), producing an unswayed calm and peaceful self-assured mentality.
Another very nice property dihydrotestosterone and it’s metabolites share is 5 alpha reductase stimulation (study). 5 alpha reductase stimulation stimulates production of other 5-alpha reduced steroid hormones such as 5a-dihydroprogesterone, putting the organism in a positive feedback loop that favors androgens and opposes estrogens and stress hormones.
One metabolite of dihydrotestosterone and a neurosteroid, androsterone, has been extensively studied with phenomenal findings – androgenic, anti-estrogenic, potent aromatase inhibitor, GABA agonist, and thyroid mimetic (source).
Other metabolites of dihydrotestosterone weren’t studied much. I have no doubt they have very similar properties though.
Androsterone and other dihydrotestosterone metabolites can even convert back into dihydrotestosterone.
There’s a four-way loop where dihydrotestosterone, androsterone, 5a-androstanedione, and androstanediol inner circle. These 4 androgens can each convert into each other because of they’re reversible conversion mechanisms.
Androstanediol can convert back to androsterone or directly back into dihydrotestosterone and androsterone can either convert to 5a-androstenedione or back to androstanediol and by either path it will convert into dihydrotestosterone.
The downstream conversion of dihydrotestosterone (as far as has been studied) ends at 3b-diol > a-triols and androstanediol (3a-diol) > glucuronides and then gets excreted from the body.
Looking through Haidut’s work I found a very interesting variation of dihydrotestosterone called 11K-DHT. 11K-DHT is produced by the adrenals and is downstream from androstenedione and testosterone.
11K-DHT has the same high androgen receptor affinity as dihydrotestosterone, but 11K-DHT has a significantly longer half-life than dihydrotestosterone itself, possibly making it even more potent than regular dihydrotestosterone via the longer half-life.
“While DHT was completely metabolized after 48 hours, 21% of the 11K-DHT remained detectable after 72 hours.” – study.
11OH-DHT is another weaker variation of dihydrotestosterone, it has about half the androgen receptor affinity of dihydrotestosterone. However 11OH-DHT is a direct precursor to 11K-DHT and can convert into 11K-DHT via HSD11B2.
Manipulating DHT Conversion and Metabolites
Nicotine and cotinine have been found to dose-dependently inhibit the downstream conversion of dihydrotestosterone, keeping dihydrotestosterone in the blood for longer (study), while ethanol has been found to do the opposite – increase downstream conversion of dihydrotestosterone and increase the excretion of dihydrotestosterone (study).
A higher fasting insulin might increase the HSD17B6 enzyme that converts the a-diols back into dihydrotestosterone (study).
LH stimulation increases the HSD11B2 enzyme that converts 11OH-DHT to 11K-DHT and also 11OH-T to 11K-T and 11K-DHT (study).
Linolenic acid is a potent inhibitor of the AKR1C enzyme that converts the a-diols back into dihydrotestosterone and also androsterone to 5a-androstenedione (study).
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