New leads, enzyme promoters. Royal jelly (it was only mentioned as an anecdote so far, I went thru all 7 pages), garlic, broccoli. Royal Jelly was studied and concluded to induce, "... acceleration of conversion from DHEA to T by six-month ingestion of RJ, resulting in improvement of erythropoiesis, glucose tolerance and mental health... acceleration of conversion from DHEA-S to T by activation of 3β-HSD2 and/or 17β-HSD3"
Garlic supplementation increases testicular testosterone and decreases plasma corticosterone in rats fed a high protein diet.
Oi Y1, Imafuku M, Shishido C, Kominato Y, Nishimura S, Iwai K. (2001)
The effects of garlic supplementation on protein metabolism were investigated by measuring testis testosterone and plasma corticosterone in rats fed diets with different protein levels. In Experiment 1, rats were fed experimental diets with different protein levels (40, 25 or 10 g/100 g casein) with or without 0.8 g/100 g garlic powder. After 28 d of feeding, testosterone contents in the testis were significantly higher and plasma corticosterone concentrations were significantly lower in rats fed 40 and 25% casein diets with garlic powder than in those fed the same diets without garlic powder. Urinary excretion of 17-ketosteroid (an index of testosterone), nitrogen balance and hepatic arginase activity were significantly higher in rats fed the 40% casein diet with garlic powder than in the 40% casein controls. In Experiment 2, the effect of diallyldisulfide (a major volatile sulfur-containing compound in garlic) on the secretion of luteinizing hormone (LH) from the pituitary gland, which regulates testosterone production in the testis, was investigated in anesthetized rats. Plasma LH concentration increased dose dependently after administration of diallyldisulfide (P < 0.01, r = 0.558). These results suggest that dietary supplementation with 0.8 g/100 g garlic alters hormones associated with protein anabolism by increasing testicular testosterone and decreasing plasma corticosterone in rats fed a high protein diet.
Additional new leads, flavonoids.
Fisetin: A Dietary Antioxidant for Health Promotion
Naghma Khan, Deeba N. Syed, Nihal Ahmad, and Hasan Mukhta (2013)
Interestingly, fisetin possesses higher affinity for the AR than dihydrotestosterone (30). We showed that fisetin interacts with the ligand-binding domain of the AR and interferes with its amino-/carboxyl-terminal interactions with subsequent reduction in receptor stability.
Effects of Apigenin on Steroidogenesis and Steroidogenic Acute Regulatory Gene Expression in Mouse Leydig Cells
Wei Li, Akhilesh K. Pandey, Xiangling Yin, Jau-Jiin Chen (2012)
Previous studies reported that the age-related decline in testosterone biosynthesis is associated with a decrease in the steroidogenic acute regulatory (StAR) protein which regulates the rate-limiting step of testosterone biosynthesis. To explore the possibility of delaying this decline using a dietary approach, we have examined the effect of a natural flavonoid, apigenin, on StAR gene expression in mouse Leydig cells. Incubation of these cells with the flavonoid enhanced cyclic AMP (cAMP)-induced steroidogenesis and StAR protein expression. The results from the analyses of StAR mRNA by reverse transcription-polymerase chain reaction and the luciferase assays of StAR promoter activity indicated that this flavonoid enhanced StAR gene expression at the level of transcription. Further studies showed that apigenin blocked the thromboxane A2 receptor and interrupted the signaling through the cyclooxygenase-2-thromboxane A synthase-thromboxane A2-receptor pathway, resulting in a reduction of DAX-1 (dosage sensitive sex reversal-adrenal hypoplasia congenita critical region on the X chromosome, gene-1) protein, a transcriptional repressor of StAR gene expression. When DAX-1 protein was reduced, the sensitivity of the Leydig cells was dramatically enhanced, with sub-threshold level of cAMP being able to induce maximal levels of StAR protein expression and steroid hormone production. The present study suggests a potential application of apigenin to improve StAR protein expression and steroidogenic sensitivity of aging Leydig cells.
As for DHT, I really think its metabolite 3α-Androstanediol is more important for the whole confidence and relaxed attitude thing. If I'm correct, DHT is just a step in the ladder. Potent GABA agnoist? Best combine with ginseng and ginkgo, antagonists.
... an endogenous inhibitory androstane neurosteroid and weak androgen, and a major metabolite of dihydrotestosterone (DHT).[1][2][3] As a neurosteroid, it acts as a potent positive allosteric modulator of the GABAA receptor,[4] and has been found to have rewarding,[5][6]anxiolytic,[7]pro-sexual,[8] and anticonvulsant effects.[9][10] As androgens such as testosterone and DHT are known to have many of the same effects as 3α-diol and are converted into it in vivo, it is thought that this compound may in part be responsible for said effects.[5][6][7][10] Relative to its isomer 3β-androstanediol, which is a potent estrogen, 3α-androstanediol has substantially lower, though still significant affinity for the estrogen receptors, with a several-fold preference for ERβ over ERα.
And this is what I found out about broccoli and sulfurophane. A word on 3α-HSD: "It is known to be necessary for the synthesis of the endogenous neurosteroids allopregnanolone, THDOC, and 3α-androstanediol. It is also known to catalyze the reversible conversion of 3α-androstanediol (5α-androstane-3α,17β-diol) to dihydrotestosterone (DHT) (5α-androstan-17β-ol-3-one) and vice versa."
Sulforaphane promotes murine hair growth by accelerating the degradation of dihydrotestosterone.
Sasaki M1, Shinozaki S2, Shimokado K1. (2016)
Dihydrotestosterone (DHT) causes the regression of human hair follicles in the parietal scalp, leading to androgenic alopecia (AGA). Sulforaphane (SFN) increases the expression of DHT degrading enzymes, such as 3α-hydroxysteroid dehydrogenases (3α-HSDs), and, therefore, SFN treatment may improve AGA. To determine the effects of SFN on hair growth, we administered SFN (10 mg/kg BW, IP) or vehicle (DMSO) to ob/ob mice for six weeks and examined hair regeneration and the plasma levels of testosterone and DHT. We also tested the effects of SFN on the expression of two forms of 3α-HSD, aldo-keto reductase 1c21 and dehydrogenase/reductase (SDR family) member 9, both in vitro and in vivo. SNF significantly enhanced hair regeneration in ob/ob mice. The mice treated with SFN showed lower plasma levels of testosterone and DHT than those treated with vehicle. SFN increased the mRNA and protein levels of the two forms of 3α-HSD in the liver of the mice and in cultured murine hepatocyte Hepa1c1c7 cells. These results suggest that SFN treatment increases the amount of 3α-HSDs in the liver, accelerates the degradation of blood DHT, and subsequently blocks the suppression of hair growth by DHT.