Dihydrotestosterone

Abbreviation DHT
Molecular formula C₁₉H₃₀O₂
Type Steroid hormone (potent androgen; 5α-reduced metabolite of testosterone)
Administration Topical (cream/gel is preferred), oral (less common), transdermal
Bioavailability Topical: good absorption, favors androgenic pathway; Oral: less effective
Synonyms 5α-Dihydrotestosterone, Stanolone, Androstanolone
Source Produced from testosterone via 5α-reductase enzyme (skin, prostate, hair follicles, liver); pharmaceutical: synthetic
Ray's verdict Generally helps
Strongly positive in miniscule doses, the "safe" androgen, can't convert to estrogen.


Dihydrotestosterone, commonly abbreviated as DHT or androstanolone, is the most potent endogenous androgen in the human body. It is a metabolite of testosterone and plays a crucial role in male sexual development, maturation, and overall health. Despite mainstream medicine's portrayal of DHT as a harmful hormone responsible for hair loss and prostate cancer, emerging research suggests it may actually be protective and beneficial across multiple organ systems.

DHT levels decline rapidly with aging, and DHT administration has been shown to restore vitality even in 90+ year old males.[1] The totality of available studies suggests that testosterone is primarily a precursor to DHT, with DHT being responsible for both the male phenotype and optimal male health.[2]

History

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Etymology

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The name describes its structure directly: "dihydro-" (two added hydrogen atoms) plus "testosterone," since DHT is formed by adding hydrogen across testosterone's double bond.

DHT was first synthesized in 1935, but its role as a distinct, more potent hormone in its own right wasn't established until the 1960s, when 5-alpha reductase was identified as the enzyme that converts testosterone to DHT in target tissues.

The name "dihydrotestosterone" reflects its chemical relationship to testosterone: it is the "dihydro" (two additional hydrogen atoms) derivative of testosterone. DHT was first characterized in the mid-20th century as researchers explored androgen metabolism and the 5-alpha reductase pathway.

In the 1950s and 1960s, medicine recognized that DHT and related steroids had great potential for treating estrogen receptor-positive breast cancer. DHT was used clinically with remarkable success, achieving up to 80% cure rates. However, its strong virilizing effects in women led to the development of methylated derivatives like Proviron (1-alpha-methyl DHT) and Masteron (2-alpha-methyl DHT), which retained anti-estrogenic effects with less virilization.[3]

Clinical proof of DHT's role: 5α-reductase deficiency

[edit]

The clearest human evidence that DHT, not testosterone, drives external male genital development comes from a large Dominican kindred with inherited 5α-reductase deficiency: affected males had normal internal male reproductive structures (driven by testosterone itself) but ambiguous or female-appearing external genitalia at birth, then virilized substantially at puberty as testosterone alone became sufficient to override the missing DHT conversion.[4] These individuals also do not develop male-pattern baldness or benign prostatic hyperplasia later in life, consistent with DHT (rather than testosterone or aging alone) being specifically implicated in those processes.[4]

Structure/Chemical properties

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DHT has the molecular formula C19H30O2 and is classified as a fully saturated steroid. This saturation is particularly significant: saturated steroids tend to be androgenic, while unsaturated steroids tend to be estrogenic. The degree of unsaturation largely determines a steroid's respective strength as an androgen or estrogen. DHT, being fully saturated with no double bonds, is potently anti-estrogenic.[5]

Key chemical characteristics:

  • Non-aromatizable: Unlike testosterone, DHT cannot be converted to estrogen via the aromatase enzyme, making it inherently anti-estrogenic
  • Potency: DHT is 2.5 to 10-fold more potent than testosterone at the androgen receptor in bioassays[6]
  • Systemic levels: Circulating levels of total DHT are about 1/10th the concentration of total testosterone, though local tissue concentrations can be up to 10 times higher in specific areas[7]

Function/Mechanism of Action

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DHT exerts its effects primarily through binding to and activating the androgen receptor (AR), where it displays significantly higher affinity than testosterone. It is the primary hormone responsible for:

  1. Sexual differentiation and maturation: Development of male genitalia, deepening of voice, facial hair, body hair[8]
  2. Anti-estrogenic activity: DHT directly antagonizes estrogen at the receptor level and also inhibits aromatase[3]
  3. Anti-inflammatory effects: DHT demonstrates anti-inflammatory potency comparable to cortisol but without the metabolic side effects[9]
  4. Serotonin suppression: DHT inhibits tryptophan hydroxylase (TPH), the rate-limiting enzyme in serotonin synthesis[10]
  5. PI3 kinase/Akt activation: DHT activates PI3 kinase signaling, responsible for anti-apoptotic activities and cell survival[11]

Notably, DHT is inactivated in muscle tissue by the enzyme 3-alpha hydroxysteroid dehydrogenase, converting it to the weak androgen 3-alpha-androstanediol. This explains why DHT drives sexual maturation but has minimal direct effects on muscle growth.[12]

Medical uses/Effects

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Vitamin A increases DHT formation via 5α-reductase upregulation

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Vitamin A (as all-trans-retinoic acid, ATRA; 60 mg/kg daily for 3 days) increased hepatic microsomal 5α-reductase (Δ4-3-oxosteroid 5α-oxidoreductase) mRNA expression in male rats, raising the rate of DHT formation from testosterone in microsomal fractions.[13]

Stops aging of pancreatic beta-cells (anti-diabetic potential)

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DHT dose-dependently inhibits the aging and dysfunction of pancreatic beta-cells (insulin-producing cells), with the highest doses completely stopping the senescence process. DHT demonstrates:

  • Anti-oxidant protective capacity
  • Significant reduction in stress-induced senescence markers
  • Protection from H2O2-induced oxidative stress
  • Increased SIRT1 expression (longevity-associated)
  • Decreased p16 expression (aging marker)[14]

The results suggest DHT may become viable therapy for conditions related to insulin dysfunction, essentially a treatment for various types of diabetes.[15]

Prevents and may treat prostate cancer

[edit]

Physiological DHT concentrations (100 nM) applied topically accelerated rodent hair-follicle growth, whereas suprapharmacological levels only weakly inhibited growth, arguing against DHT as a primary hair-loss toxin at normal tissue concentrations.[16] In men with low testosterone, topical DHT improved fasting insulin, HOMA index, leptin, and blood pressure more than testosterone at roughly fourfold lower dose, without prostate complications seen in the testosterone arm.[17] In eugonadal men, higher serum DHT inversely correlated with hypogonadal symptom scores independent of total testosterone.[18] Baboon leptomeninges and cardiovascular tissues bound DHT but not testosterone at androgen receptors, supporting DHT as the primary cardiovascular androgen ligand.[19] Lower serum androgens and blunted DHT–androgen-receptor signaling through IL-6/STAT3 associated with abnormal cartilage development in adolescent idiopathic scoliosis.[20] In adrenalectomized female mice, DHT matched glucocorticoid anti-inflammatory effects on gastric ILC2 cytokines but uniquely prevented and reversed spasmolytic polypeptide-expressing metaplasia that cortisol could not repair.[21] Recurrent prostate cancer biopsies contained markedly lower tissue DHT than benign hyperplasia, including cases with undetectable androgens, challenging androgen-excess models of prostate malignancy.[22] Dihydrotestosterone combined with estradiol suppressed breast-cancer cell-cycle entry, while antiandrogens and environmental AR antagonists restored estrogen-driven growth.[23] Luminal-cell androgen-receptor deletion in prostate epithelium triggered cytokine leakiness, immune infiltration, and proliferative signaling, arguing against androgen deprivation as a benign prostate strategy.[24] Contrary to the mainstream "androgen hypothesis," multiple in vivo studies demonstrate that DHT does not cause prostate cancer and may actually prevent or treat it:

  • In vivo studies found that higher doses of DHT completely prevented prostate cancer development while lower doses strongly reduced incidence[25]
  • Testosterone treatment actually increased prostate cancer incidence (due to aromatization to estrogen), while DHT-treated animals had healthy prostates [25]
  • Epidemiological data shows high DHT levels were positively correlated with lower risk of prostate cancer death (HR = 0.44)[26]
  • A study with massive DHT doses (70mg daily) found no ill effects and no increase in androgen levels inside the prostate[27]
  • Drostanolone (a DHT isomer) demonstrated therapeutic effects against prostate cancer, proving more potent than cisplatin chemotherapy
  • A theoretical model proposes estradiol initiates prostate cancer growth (via telomerase activation) while DHT protects established cancer cells from testosterone-induced apoptosis, explaining why the same androgen pathway can appear either pro- or anti-cancer depending on the estradiol/DHT ratio.[28]
  • Preliminary, unpublished rodent data from IdeaLabs found DHT combined with the aromatase inhibitor exemestane produced complete tumor growth arrest in some animals; the small pilot used only a handful of animals per group and was cut short by weight loss and deaths at the tested dose, so it should be read as an early lead rather than confirmed treatment evidence.[29]

Ray has written that prostate cancer appears to be estrogen-driven and has suggested using testosterone as treatment to raise the androgen/estrogen ratio. [25]

Estrogen causes prostate fibrosis/cancer; DHT prevents and reverses it

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The myth that DHT causes prostate disease is increasingly discredited in basic research circles. A pivotal study demonstrated:

  • Estradiol causes and promotes prostate fibrosis (a precursor to prostate cancer)
  • DHT prevents estrogen's fibrotic effects on the prostate
  • DHT reverses established fibrosis when estrogen was administered first
  • A human equivalent dose of just 1-2mg DHT daily replicated these protective effects[30]

Hair loss causation debunked

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Evidence against DHT as the cause:

  • Bald men do not have higher testosterone or DHT levels than men with full hair. Studies conclude "bald men are no more masculine than those with good scalp hair growth"[31]
  • Increased serum concentrations of DHT were not correlated with advancing alopecia[31]
    • DHT decreases with age, but balding increases.[32][33]
  • Studies examining balding scalps find elevated estrogen and prolactin alongside elevated DHT. Nobody has proven DHT alone causes hair loss.[34]
  • When examining the actual hormone situation of people with hair loss, "what you see is an excess of prolactin and cortisol in the people losing their hair, both men and women."[35]
  • Studies found DHT at physiological levels (10⁻⁷ mol/L) promotes hair growth. Only at impossibly high concentrations (10⁻⁶ mol/L) does it inhibit (levels not seen naturally).[36][37]

Evidence androgens promote hair growth:

  • Testosterone was anabolic for hair growth in women with androgenic alopecia[31]
  • Topical testosterone administration regrew hair in older men (1965 study)[38]
  • Testosterone therapy (133mg over 28 months) reversed hair loss in women. Not a single woman receiving T therapy reported hair thinning despite blood T reaching 4 times higher than normal.[39]
  • Estrogen, not androgens, may cause baldness. Administration of estrogen antagonists restored hair back to normal levels in bald mice.[40]
  • Chronic stress via cortisol/estrogen/prolactin pathways is the main driver of hair loss. DHT robustly promoted hair growth in studies using cortisol-blocking interventions.[41]

More in Hair loss

Topical DHT has anti-aging effects on skin

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An extensive 1967 study on 200+ individuals aged 57-88 demonstrated that topical testosterone (1%) cream had the most potent anti-aging effects on skin in both men and women, followed closely by 1% progesterone and 1% pregnenolone. Topical testosterone converts mostly into DHT, and the proposed mechanism is increased androgenic tone. Estradiol, by contrast, showed minimal effects.[42]

A more recent study using topical DHEA (1-2% creams) demonstrated robust anti-aging effects via:

  • 3-fold increase in androgen receptor expression
  • Increased synthesis of DHT by the skin using DHEA as precursor
  • No increase in estrogen receptor expression[43]

Additional therapeutic applications

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  • Cardiovascular health: Declining DHT in aging is linked to cardiovascular disease. DHT administration (even only in the brain) reverses systemic atherosclerosis and associated inflammation.[44]
  • Ischemic heart disease mortality: In a prospective cohort of 3,690 community-dwelling men aged 70-89 followed to 2010, higher plasma DHT was associated with markedly lower ischemic heart disease mortality independent of testosterone — 42% lower risk in the third quartile (HR 0.58, P=.002) and 31% lower in the highest quartile (HR 0.69, P=.026) versus the lowest quartile.[45]
  • Multiple sclerosis: DHT completely reversed MS pathology in animal models by activating the neural androgen receptor[46]
  • Thyroid cancer: DHT may treat thyroid cancer at physiological concentrations (10 nM/L) by inducing G1 cell cycle arrest[47]
  • Chronic kidney disease: Combined aromatase inhibition + DHT supplementation attenuated renal injury in diabetic rats, reversing kidney damage markers to near non-diabetic control levels[48]
  • Diabetic kidney disease, dose-dependent: In castrated, streptozotocin-diabetic rats, 0.75 mg/day DHT cut urine albumin excretion by 67% and glomerulosclerosis by 61% compared to no DHT, and reduced tubulointerstitial fibrosis, collagen IV, TGF-beta, IL-6, and macrophage infiltration. A higher 2.0 mg/day dose reversed the benefit and worsened every one of these measures.[49]

Dosing

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  • For prostate protection: Human equivalent dose of 1-2mg daily[30]
  • For optimal androgenic effects: Studies suggest 5-8mg daily achieves optimal results. DHT is about 3-5 times more potent than testosterone, so this achieves similar effects to 25mg testosterone.[50]
  • For kidney disease/diabetes: The study above used a DHT dose with a human-equivalent of 20-30mg daily; haidut.me extrapolates that 5-10mg daily may suffice, based on the lower doses of DHT-derivative steroids shown to help diabetic complications in humans[51]
  • Ray Peat's recommendation: Ray has stated to not use more than 5-10mg testosterone daily; DHT would require proportionally less due to higher potency so miniscule doses about1-5mg[25]
  • Alternative via DHEA: DHEA administration has been shown to raise DHT metabolite levels (3α-androstanediol and its glucuronide) 2-3 fold in humans; haidut.me suggests 10-15mg daily may replenish the DHT pool over time by this route, though this is an extrapolation rather than a direct dose-response trial of DHEA against DHT itself[51]

Ray has described DHT as "by far the best male steroid you can try" for frail people, and has been recommending it to people with kidney disease, prostate problems, and various cancers.[50]

Ray's caution on DHT supplementation

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https://x.com/i/status/2039109698990092473

While the research on DHT's protective effects is compelling, Ray Peat himself expressed significant reservations about supplementing it directly. His concern centered on the principle that downstream steroids carry more risk than upstream precursors.

The "downstream" problem

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"The farther a substance is from its precursor material, the easier it is to cause unwanted effects when supplementing it."[52]

DHT sits at the far end of the steroidogenic pathway, making it a "defining feature creating hormone" that can shift the entire system unpredictably.

Direct statements on DHT

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When asked about DHT supplementation, Ray stated:

"In general, things like that are not to be messed with unless you have a very specific knowledge of a deficiency, because if you take a little too much, any of those defining feature creating hormones can change the whole system in an unpredictable way."[53]

He recommended instead using vitamin D, DHEA, pregnenolone, and thyroid to increase DHT naturally. Only in serious conditions like breast cancer or prostate cancer did he consider DHT supplementation appropriate:

"In something like breast cancer or prostate cancer, it's one of the things that could give a big push to the system if you're wanting to interrupt the process."[54]

DHT Is not "male progesterone"

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Ray said pregnenolone should come first, then DHEA if more androgenic support is needed:

"(Pregnenolone and DHEA) will push your neurosteroids, the crucial regulating things that you don't want to throw out of balance, and with a strong androgen like DHT, that would be one big risk that you could throw off your neurosteroids."

— Ray Peat

[55]

Preferred approach: upstream support

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Ray consistently advocated for upstream precursors over downstream hormones:

"Yes, pure testosterone on the skin is safe if the diet and thyroid function are good, but it's better to try supplements of pregnenolone first, and then DHEA, to normalize the testosterone production."[56]

For raising androgens safely, Ray recommended: pregnenolone, DHEA (5-10mg), good thyroid function, aspirin, and vitamin D as protective factors against aromatization.

Administration routes

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  • Topical is generally preferred for androgens because skin has high 5-AR expression, favoring conversion to DHT over estrogen. Bioavailability is around 33-70% depending on solvent, and effects last longer than oral. Navel application approaches 80% absorption, rivaling intravenous.[57]
  • Sublingual/buccal (lips, tongue, gums) provides rapid absorption directly into circulation, bypassing first-pass liver metabolism. Ray noted that 1mg testosterone "is very well absorbed by the lips or the tongue" with strong effects. This route avoids liver aromatase.[58]
  • Oral has the poorest bioavailability (around 3% for DHEA) and passes through the liver where aromatase expression is high, increasing estrogen conversion. The androgenic:estrogenic ratio drops to 2:1 compared to 10:1 for topical.[59]
  • Injections (subcutaneous pellets or intramuscular) have 100% bioavailability but bypass skin's 5-AR, resulting in more estrogenic conversion (3:1 ratio). Ray considered testosterone injections risky, noting people commonly inject "30 or 50 milligrams per week, which is several times what a teenage boy would be making" and "it's all going to be going towards estrogen." He also warned that injectable esters typically use toxic solvents.[55]

Important note on esters: Bioidentical DHT appears protective, but esterified forms (DHT propionate, DHT benzoate) promoted tumor development in some studies. This may relate to the solvents used (benzyl benzoate) rather than the DHT itself.[30]

Brands and sources

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AlphaGels ([email protected])

Pandalabs

Side/Adverse effects

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DHT is generally well-tolerated, especially at physiological doses, (ideally less, around 1mg).

Potential considerations:

In women:

  • Shouldn't be supplemented unless directly treating a serious condition
  • Virilizing effects at higher doses: facial hair growth, body hair, voice thickening[3]
  • This led to development of methylated derivatives (Proviron, Masteron) for therapeutic use without virilization

General:

  • One study in eugonadal men noted transient feelings of congestion and irritability during first 3-4 weeks of supraphysiological DHT administration, which then resolved[60]
  • No ill effects observed even at massive doses (70mg daily) in prostate studies[61]
  • Even massive doses (human equivalent 500mg+ single dose) showed beneficial effects in beta-cell studies, contradicting claims that DHT harms in any amount[14]

References

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  1. ↑ Dorfman MD et al., "Central androgen action reverses hypothalamic astrogliosis and atherogenic risk factors induced by orchiectomy and high-fat diet feeding in male mice," American journal of physiology. Endocrinology and metabolism, 2023
  2. ↑ "Raising DHT levels even only in the brain reverses systemic atherosclerosis"
  3. ↑ 3.0 3.1 3.2 "#40: Fasting, Cortisol, and Weight Gain | Is Fruit Just Sugar? | DHT, Estrogen, and Baldness | NAFLD", Danny Roddy, YouTube
  4. ↑ 4.0 4.1 Imperato-McGinley J, et al., "Steroid 5α-reductase deficiency in man: an inherited form of male pseudohermaphroditism," Science. 1974;186(4170):1213-5.
  5. ↑ "Another View of Evolution [Generative Energy #14", Danny Roddy, YouTube]
  6. ↑ "Do You Need DHT To Build Muscle?", More Plates More Dates, YouTube
  7. ↑ "Are Men Beating Women At The Olympics? - The Truth (comprehensive dissection)", More Plates More Dates, YouTube
  8. ↑ "Do You Need DHT To Build Muscle?", More Plates More Dates, YouTube
  9. ↑ "DHT as Anti Inflammatory as Cortisol but Without the Side Effects," Low Tox in Forum thread
  10. ↑ "DHT Lowers Serotonin Synthesis may Treat Testicular Cancer," Low Tox in Forum thread
  11. ↑ Kang SM et al., "Testosterone Protects Pancreatic β-cells from Apoptosis and Stress-Induced Accelerated Senescence," The world journal of men's health, 2021
  12. ↑ "Do You Need DHT To Build Muscle?", More Plates More Dates, YouTube
  13. ↑ Murray M, Butler AM. "Pretranslational up-regulation of the hepatic microsomal delta4-3-oxosteroid 5alpha-oxidoreductase in male rat liver by all-trans-retinoic acid," Biochem Pharmacol. 1999;58(2):355-62. doi:10.1016/s0006-2952(99)00076-3.
  14. ↑ 14.0 14.1 Kang SM et al., "Testosterone Protects Pancreatic β-cells from Apoptosis and Stress-Induced Accelerated Senescence," The world journal of men's health, 2021
  15. ↑ "DHT Can Stop Aging of the Pancreatic Beta Cells Insulin Producing," Low Tox in Forum thread
  16. ↑ Zhang C, et al. "DHT concentration and hair follicle growth," Front Cell Dev Biol. 2020. doi:10.3389/fcell.2020.00577.
  17. ↑ Simonini T, et al. "DHT improves insulin sensitivity in men with low testosterone," Diabetes Care. 2001. doi:10.2337/diacare.24.12.2149.
  18. ↑ Sansone A, et al. "Serum DHT and hypogonadism symptoms," J Endocrinol Invest. 2021. doi:10.1007/s40618-021-01561-0.
  19. ↑ Sheridan PJ, et al. "DHT receptors in baboon brain and CVS," Anat Rec. 1988. doi:10.1002/ar.1092200415.
  20. ↑ Wu T, et al. "Androgen levels and scoliosis cartilage development," Clin Genet. 2021. doi:10.1016/j.clgc.2019.03.021.
  21. ↑ Busada JT, et al. "Glucocorticoids and androgens protect from gastric metaplasia," Gastroenterology. 2021. doi:10.1053/j.gastro.2021.04.075.
  22. ↑ Titus MA, et al. "Testosterone and dihydrotestosterone tissue levels in recurrent prostate cancer," Clin Cancer Res. 2005. doi:10.1158/1078-0432.CCR-05-0525.
  23. ↑ Aubé M, et al. "p,p′-DDE disrupts androgen-mediated protection in breast cancer," Breast Cancer Res. 2008. doi:10.1186/bcr1862.
  24. ↑ Zhang B, et al. "Non-cell-autonomous regulation of prostate epithelial homeostasis by androgen receptor," Mol Cell. 2016. doi:10.1016/j.molcel.2016.07.025.
  25. ↑ 25.0 25.1 25.2 25.3 "DHT Prevents Prostate Cancer and may Even Treat It," Low Tox in Forum thread
  26. ↑ "DHT is negatively associated with death from prostate cancer"
  27. ↑ "DHT Does Not Have Negative Effect on Prostate," Low Tox in Forum thread, post #94707
  28. ↑ Friedman AE. "The Estradiol-Dihydrotestosterone model of prostate cancer," Theor Biol Med Model. 2005;2:10. doi:10.1186/1742-4682-2-10.
  29. ↑ "IDEALABS STUDY: Estrogen causes prostate cancer (PC), DHT and/or aromatase inhibitor may stop/treat PC," haidut.me, December 2024
  30. ↑ 30.0 30.1 30.2 "Estrogen causes prostate fibrosis (cancer?), DHT prevents/treats it"
  31. ↑ 31.0 31.1 31.2 "The Misunderstood Role of DHT in Male Pattern Baldness", Danny Roddy, YouTube
  32. ↑ Nawata H et al., "Age-dependent change of serum 5alpha-dihydrotestosterone and its relation to testosterone in man," Endocrinologia japonica, 1977
  33. ↑ "Do DHT Levels Increase As You Get Older?"
  34. ↑ "A Bioenergetic View of Osteoporosis [Generative Energy #25", Danny Roddy, YouTube]
  35. ↑ Ray Peat, "Ask the Herb Doctor: Hair loss, Inflammation, Osteoporosis", Ask the Herb Doctor, 4:12
  36. ↑ Chen X et al., "Dihydrotestosterone Regulates Hair Growth Through the Wnt/β-Catenin Pathway in C57BL/6 Mice and In Vitro Organ Culture," Frontiers in pharmacology, 2019
  37. ↑ Deng W et al., "miRNA microarray profiling in patients with androgenic alopecia and the effects of miR-133b on hair growth," Experimental and molecular pathology, 2021
  38. ↑ Papa & Kligman, "Stimulation of Hair Growth by Topical Application of Androgens," JAMA, 1965
  39. ↑ "Testosterone therapy (TRT) reverses hair loss (in women)"
  40. ↑ "Estrogen, not androgens, may be the cause of baldness"
  41. ↑ "Stress (cortisol) causes hair loss"
  42. ↑ "Topical DHEA has potent anti-aging effects on human skin"
  43. ↑ El-Alfy M et al., "Skin responses to topical dehydroepiandrosterone: implications in antiageing treatment?," The British journal of dermatology, 2010
  44. ↑ "Declining DHT in aging linked to cardiovascular disease (CVD)"
  45. ↑ Yeap BB, et al. "In older men an optimal plasma testosterone is associated with reduced all-cause mortality and higher dihydrotestosterone with reduced ischemic heart disease mortality, while estradiol levels do not predict mortality," J Clin Endocrinol Metab. 2014;99(1):E9-18. PMID: 24257908.
  46. ↑ "Demyelinating Conditions Like MS Can Be Treated by Androgens," Low Tox in Forum thread
  47. ↑ "DHT may treat thyroid cancer"
  48. ↑ Manigrasso MB, Sawyer RT, Hutchens ZM Jr, Flynn ER, Maric-Bilkan C. "Combined inhibition of aromatase activity and dihydrotestosterone supplementation attenuates renal injury in male streptozotocin (STZ)-induced diabetic rats," American Journal of Physiology-Renal Physiology, 2012;302(9):F1156-63. PMID 22301628
  49. ↑ Xu Q, Prabhu A, Xu S, Manigrasso MB, Maric C. "Dose-dependent effects of dihydrotestosterone in the streptozotocin-induced diabetic rat kidney," Am J Physiol Renal Physiol. 2009;297(2):F307-F315.
  50. ↑ 50.0 50.1 "#49: Cortisol Causes High Blood Sugar | DHT and Aging | PUFA, Immunosuppression, and Hibernation", Danny Roddy, YouTube
  51. ↑ 51.0 51.1 "Aromatase inhibitor (AI) + DHT combo may reverse kidney disease (CKD)", dosing discussion section
  52. ↑ "5-Alpha Dihydroprogesterone (5a-DHP)," Ray Peat email exchange
  53. ↑ Ray Peat, "Protein", Ray Peat Email Q&A
  54. ↑ "Bioenergetic Basics #9: Five Ideas That Are Associated with Ray Peat (That He Never Endorsed)", Danny Roddy, YouTube
  55. ↑ 55.0 55.1 "#27: Thyroid Function & Pulse Rate | Weaponized Culture | Finasteride as an "Insane Decision"", Danny Roddy, YouTube
  56. ↑ "Testosterone," Ray Peat email exchange
  57. ↑ "Navel application/absorption rivals intravenous route, other skin routes not far behind"
  58. ↑ "Ray Takes Low Dose Testosterone," Low Tox in Forum thread
  59. ↑ Labrie C et al., "High bioavailability of dehydroepiandrosterone administered percutaneously in the rat," The Journal of endocrinology, 1996
  60. ↑ "Male sexual function does NOT require estrogen"
  61. ↑ Page ST et al., "Dihydrotestosterone administration does not increase intraprostatic androgen concentrations or alter prostate androgen action in healthy men: a randomized-controlled trial," The Journal of clinical endocrinology and metabolism, 2011