Testosterone

Abbreviation T
Molecular formula C₁₉H₂₈O₂
Type Steroid hormone (androgen)
Administration Topical (oil/cream, preferred), oral (in oil), injection (caution with esters)
Bioavailability Topical: good; oral in oil: workable; injections: high but solvent/ester concerns
Synonyms 17β-Hydroxyandrost-4-en-3-one
Source Testes (men), ovaries/adrenals (women); from cholesterol → Pregnenolone → DHEA pathway
Ray's verdict Depends on context
Supportive at physiological doses; skeptical of TRT megadosing; aromatizes to Estrogen.


Testosterone is the primary androgen in men and has important anabolic roles in women. Normal endogenous production in men is on the order of a few milligrams per day.

Physiological androgen levels are supportive; megadose TRT protocols that ignore upstream metabolism are approached skeptically. Low testosterone often tracks low Thyroid, high Estrogen, excess PUFA, and chronic Stress rather than isolated testicular failure.[1]


History

[edit]

Etymology

[edit]

The name combines "testis" (the gland that produces it) with "sterol" and the ketone suffix "-one."

Ernst Laqueur's group isolated testosterone from bull testicles in 1935. That same year, Adolf Butenandt and Leopold Ruzicka independently synthesized it from cholesterol, work for which they shared the 1939 Nobel Prize in Chemistry.

Aromatization and estrogen

[edit]

Testosterone aromatizes to Estrogen (estradiol). Free PUFA in circulation can increase estrogen activity by displacing estradiol from sex-hormone-binding globulin, making more estrogen biologically available.[1]

Deficiency of testosterone causes vascular leakage into the prostate.

— Ray Peat[2]

Stress and male fertility

[edit]

In prospective military cohort data, testosterone buffered cortisol-linked PTSD risk: cortisol predicted worse outcomes when testosterone was low, consistent with reciprocal hormonal regulation of stress reactivity.[3] Two weeks of added sugar (~450 g/day on top of a healthy baseline diet) normalized poor sperm motility in all young men who started below reference range, with rapid shifts in sperm small-RNA profiles.[4] Retinoic acid receptor-α antagonism or dietary vitamin A deficiency produces male sterility by the same pathway used clinically to reversibly suppress spermatogenesis at low milligram-per-kilogram doses.[5] Hindlimb unloading (disuse stress) in rats raises corticosterone, estradiol, and prolactin, suppresses intratesticular DHT and gonadotropins, and produces oligospermia and prostate enlargement within 30 days.[6]

Fasting and testicular steroids

[edit]

Four days of fasting in rats raises testicular corticosterone, suppresses side-chain cleavage and 3β-HSD, and reduces intratesticular testosterone roughly 98% despite only modest changes in serum testosterone.[7]

DHT and pancreatic beta cells

[edit]

DHT protects insulin-secreting INS-1 cells from oxidative senescence and may represent a senolytic strategy for type 2 diabetes prevention.[8]

DHT and morphogenesis

[edit]

In rats, ETU-induced severe hypothyroidism aligned with reduced DHT despite higher testosterone, supporting that 5α-reductase blockade can mimic hypothyroid androgen profiles seen in post-finasteride syndrome.[9] Pharmaceutical 5α-reductase inhibitors (finasteride, dutasteride) dose-dependently disrupt gastropod shell coiling during embryogenesis, indicating a conserved morphogenetic role for DHT-pathway steroids beyond androgen-receptor signaling.[10]

Prostate inflammation and androgen deprivation

[edit]

Androgen receptor activation decreased proliferation in thyroid cancer cell lines and downregulated PD-L1 (an immune-evasion checkpoint protein) in thyroid cancer, two independent mechanisms by which androgen/DHT signaling may suppress rather than promote thyroid cancer growth.[11][12]

Drostanolone (a DHT isomer) and several microbial metabolites showed moderate-to-potent cytotoxicity against prostate (PC-3), cervical, lung, and colon cancer lines, with some compounds outperforming cisplatin in vitro.[13] Deleting the androgen receptor in prostate luminal cells disrupted tight junctions, leaked inflammatory cytokines, recruited immune cells, and promoted epithelial proliferation in a self-amplifying inflammatory cycle.[14]

Intermittent (not continuous) DHT administration enhanced the cytotoxic effect of docetaxel chemotherapy in a prostate-cancer xenograft model, via modulation of ERβ, androgen receptor, and NEK2, consistent with the bipolar-androgen-therapy paradox where cycling high-dose androgen can suppress rather than promote prostate tumor growth, while estradiol strongly promotes it.[15]

Central androgen signaling and atherosclerosis

[edit]

Men studied months after myocardial infarction had persistently low urinary androgen metabolites including testosterone-derived 17-ketosteroids alongside elevated glucocorticoid activity.[16] Childhood poverty predicted shallower pubertal testosterone rises, smaller adolescent hippocampal growth, and worse emotion regulation and depression in both sexes.[17] Low-testosterone men randomized to testosterone or DHT gels showed androgen-driven improvements in insulin sensitivity; DHT achieved greater metabolic benefit at about one-quarter the absorbed dose.[18] Among men with normal testosterone, each 10% rise in DHT associated with roughly 4.7% fewer hypogonadism symptoms, emphasizing tissue DHT over circulating testosterone for androgenic function.[19] Six months of DHEA 50 mg daily reduced abdominal visceral fat about 7–10% and improved insulin sensitivity in elderly men and women in a randomized trial.[20] In vitro testing of fluoxetine, sertraline, paroxetine, citalopram, escitalopram, and fluvoxamine showed reduced testosterone, DHT, DHEA, and progesterone production from gonadal and adrenal tissue.[21] Hospitalized men with COVID-19 who died had lower testosterone and higher estradiol-to-testosterone ratios predicting hyperinflammation and in-hospital mortality independent of comorbidities.[22] Adolescent scoliosis patients showed lower serum androgen levels and impaired androgen-receptor control of chondrocyte IL-6, linking androgen deficiency to structural cartilage deformity.[23] Prostate tissue dihydrotestosterone was about 90% lower in recurrent prostate cancer than in benign disease, with one-third of cancer specimens showing undetectable DHT despite preserved testosterone.[24] Prospective data in women over 70 linked low circulating testosterone and DHEA (but not low estrone) to roughly doubled incidence of major cardiovascular events.[25] Androgen-receptor blockade by hydroxyflutamide or p,p′-DDE abolished dihydrotestosterone's protective effects against estrogen-driven breast-cancer cell proliferation in vitro.[26] Serum dihydrotestosterone was 61% lower in older men with higher carotid intima-media thickness, pulse-wave velocity, and inflammatory markers, correlating inversely with arterial stiffness indices.[27] Central dihydrotestosterone infusion in orchiectomized mice prevented mediobasal hypothalamic astrogliosis and reduced liver and leukocyte inflammatory signaling and monocytosis on a high-fat diet.[28]

Soda and androgen signaling

[edit]

Fifteen days of ad-libitum undiluted cola raised mouse testis weight, serum testosterone, and testicular androgen-receptor mRNA versus water controls.[29]

DHT in elderly men

[edit]

Intramuscular stanolone (DHT) 50 mg every other day in men over 70 improved nitrogen, potassium, and phosphorus retention on adequate or low-protein diets, increased 17-ketosteroid excretion, and restored libido and mood in long-stay geriatric patients.[30]

= Androgen loss and Parkinson's disease

[edit]

In Wobbler mice modeling ALS, testosterone falls in testis, plasma, brain, and spinal cord while corticosterone rises; plasma steroid levels correlate with cervical spinal cord concentrations.[31]= Castration in male mice raises nigral iNOS, lowers GDNF, and produces Parkinson-like motor deficits and dopamine neuron loss; DHT pellet replacement preserves tyrosine hydroxylase neurons, striatal dopamine, and motor performance.[32]

Male sexual function without estrogen

[edit]

Transdermal DHT for 24 months in eugonadal men suppressed serum testosterone, LH, FSH, and estradiol to castration-range levels without spontaneous complaints or discontinuations for adverse sexual effects; DHT changed none of 33 sexual-function and mood measures except a mild, reversible decrease in overall sexual desire, while age and BMI were the main predictors of sexual decline.[33] In separate trials, tamoxifen (raising endogenous testosterone without lowering estradiol), testolactone (~50% lower circulating estradiol), and DHT replacement in hypogonadal men did not impair established sexual function, supporting that aromatization to estrogen is not required to maintain male sexual function in adults with an established sex life.[34]

In a controlled feeding study, shifting men from a low-fat, high-fiber diet to a higher-fat, lower-fiber diet raised plasma and urinary androgens (including free testosterone), while the opposite shift lowered them, one of the earliest clean demonstrations that dietary fat/fiber composition, not just genetics, drives circulating androgen levels.[35]

Klotho (anti-aging gene)

[edit]

Androgens, especially DHT acting through the androgen receptor, directly increase expression of the anti-aging gene Klotho in the kidney, with AR shown to bind the klotho gene promoter directly; the effect is blocked by the AR antagonist flutamide.[36] Estrogen has the opposite effect, decreasing klotho expression, with more potent estrogens (e.g. synthetic ethinyl estradiol) suppressing it more than endogenous estradiol.[37] Klotho decline tracks with most major chronic diseases (diabetes, cardiovascular disease, cancer, neurological and mental-health conditions), consistent with androgen/estrogen antagonism as a general axis of aging rather than a reproductive-only effect.

Exercise and stress (human data)

[edit]

Testosterone and DHT accelerate resolution of influenza-induced pulmonary inflammation in male mice; testosterone depletion or castration worsens morbidity and prolongs inflammatory monocyte and eosinophil accumulation in the lungs.[38] Intense interval exercise raised testosterone ~38% post-exercise in trained male athletes (along with prolactin and estradiol).[39] This shows acute stress shifts multiple gonadal steroids together, not testosterone in isolation.

Zinc status

[edit]

Zinc deficiency is directly linked to low testosterone. A controlled study in healthy men found that dietary zinc restriction produced a significant decline in serum testosterone, while zinc supplementation in marginally deficient elderly men raised testosterone levels.[40] Serum testosterone was significantly correlated with cellular zinc concentrations across all age groups. Since zinc is required for steroidogenesis and is antagonized by copper and iron excess, adequate zinc intake from foods like oysters, liver, and eggs is relevant to maintaining healthy androgen levels. See Zinc.

Social behavior

[edit]

A pre-registered placebo-controlled trial found no support for testosterone increasing utilitarian moral reasoning; if anything, testosterone-treated participants showed greater sensitivity to moral prohibitions than placebo.[41] Contrary to the stereotype that testosterone promotes aggression or antisocial behavior, a double-blind placebo-controlled study (91 healthy men) found that transdermal administration of 50 mg of testosterone significantly reduced lying compared to placebo.[42] Participants in a die-roll task where they could increase their payoff by misreporting results did so less under testosterone (p<0.01). This finding contributes to the evidence that testosterone promotes prosocial behavior (status-seeking through honesty rather than deception) and counters the framing of testosterone as purely an "aggression" hormone.

Two large-scale randomized controlled trials found no evidence that exogenous testosterone impairs men's cognitive empathy (accuracy at inferring others' mental states), contradicting the popular assumption that testosterone blunts social/emotional sensitivity.[43]

Belief about testosterone can override its real effect. In a double-blind ultimatum-bargaining game (n=60), women given a single sublingual dose of testosterone offered significantly more (3.90 money units) than those given placebo (3.40 MUs; ANOVA F=4.92, P=0.031); but subjects who merely believed they had received testosterone, regardless of what they actually got, offered 0.92 MU less than those who believed they got placebo (F=8.22, P=0.006), a belief effect larger than the 0.64 MU real testosterone effect. Actual testosterone made offers fairer; the cultural stereotype that testosterone causes selfish, aggressive behavior made people act that way when they thought they had taken it.[44]

A placebo-controlled trial found a single 0.5mg testosterone dose increased women's implicit sense of agency and produced more optimistic affective forecasting versus placebo.[45] This links testosterone to agency in a controlled single-dose context; it doesn't itself establish that men's natural age-related decline drives reduced agency or cognitive decline.

I haven't heard of any bad effects from DHT, but that might be because it's so rarely used... A little DHT should be safe, but I don't think mesterolone is safe in any quantity.

— Ray Peat[46]

Peat put normal daily androgen production for young men at about 4 mg testosterone and 15 mg DHEA, with roughly half that amount effective for middle-aged men absent other problems, suggesting typical TRT dosing often overshoots physiological replacement.[47]

Sperm counts and environmental exposure

[edit]

Active-duty U.S. military women reported infertility rates near 37% versus ~12% nationally, with male service members showing comparably poor reproductive markers despite high fitness standards.[48] A 2017 meta-analysis of 185 studies (~45,000 men) found sperm concentration declined 52.4% and total sperm count declined 59.3% among unselected men in North America, Europe, Australia, and New Zealand between 1973 and 2011, with no sign of the decline leveling off.[49] Environmental estrogens such as BPA are among the suspected contributors, consistent with Ray Peat's view of estrogen as a population-level, multi-generational hazard rather than a purely individual one; see Estrogen: Environmental estrogens.

  • Sperm metabolism and motility: Swim-up–selected bull sperm with higher motility show higher metabolic rates and longer flagella than low-motility sperm, supporting energetic intensity as a direct determinant of fertilization capacity.[50] Progesterone and pregnenolone sulfate activate the sperm CatSper calcium channel via ABHD2; physiological testosterone, cortisol, and estradiol can inhibit progesterone-driven CatSper activation, and plant triterpenoids can block hyperactivation.[51]

Medical uses/Effects

[edit]

In triple-negative breast cancer, androgen-receptor expression correlated with better prognosis and DHT inhibited glucocorticoid-promoted cell migration and SGK1 induction.[52] In older men, dihydrotestosterone, not free testosterone, was most consistently inversely associated with insulin resistance and incident diabetes over roughly ten years of follow-up.[53] Higher serum DHT associated with lower long-term prostate-cancer mortality in a prospective cohort, contradicting androgen-deprivation assumptions.[54] Sebum palmitate-to-stearate ratio rises with androgenic steroids and falls with prolactin, offering a non-invasive skin-lipid index of whole-body androgenic versus estrogenic tone.[55]

Androgen receptor requirement

[edit]

Androgen-receptor knockout chickens produce testosterone yet lack combs, wattles, sexual behavior, and fertility; exogenous testosterone cannot induce male secondary traits without functional AR, underscoring receptor signaling over circulating hormone alone.[56] Topical testosterone in oil is closer to physiological pulsatile delivery than large injection doses. Progesterone and adequate Thyroid are prerequisites for healthy androgen status.[57]

Low-T symptoms (fatigue, low libido, poor recovery) overlap Hypothyroidism; addressing thyroid, estrogen/progesterone, PUFA, and endotoxin takes priority over androgen supplementation.

Dosing

[edit]

See Harm reduction for dosing discussion. Prescription TRT decisions belong with a clinician and laboratory monitoring.

Oral free testosterone vs. esters

[edit]

Percutaneous testosterone through the navel reached roughly 80% of intravenous bioavailability versus about 50% through forearm skin in primates, using acetone as the vehicle.[58] Free (unesterified) testosterone is orally bioavailable on its own, unlike esters such as undecanoate which require dissolving in oil and taking with a fatty meal to absorb at all.[59] In eunuchs and castrates with no endogenous testosterone, oral free testosterone (100mg 4 times daily, or 400mg/day) produced normal male serum testosterone levels and was clinically effective in a double-blind trial, with artificial testosterone derivatives showing no advantage in either effect or cost.[60] A follow-up study of men on continuous oral free testosterone reported liver function remaining normal over long-term use, in contrast to 17α-methyltestosterone and other alkylated androgens, which are established as hepatotoxic.[61] A separate trial found that 400mg/day of oral free testosterone for 21 days accelerated hepatic drug-metabolizing enzyme activity (antipyrine half-life fell from 8.0 to 5.7 hours) without any adverse change in liver markers (albumin, bilirubin, prothrombin, transaminases).[62]

Liver disease (NAFLD, NASH, cirrhosis)

[edit]

Italian clinical series from the 1960s–1970s reported high rates of improvement or remission in hepatic cirrhosis with combined high-dose injectable testosterone and thiamine (vitamin B1).[63] In a high-fat-diet NASH rabbit model, oral LPCN 1144 (lipid-based testosterone undecanoate formulation) improved NASH histology, reduced hepatic fibrosis markers, and corrected HFD-induced low testosterone and insulin resistance; co-formulation with alpha-tocopherol showed additive benefit.[64] In men with type 2 diabetes, higher serum total testosterone is independently associated with lower odds of NAFLD (adjusted OR 0.58 per unit increase in model 4); no similar association was seen for androgens in women in the same cohort, see Testosterone in women below.[65]

Testosterone in women

[edit]

Testosterone has an anabolic role in women alongside estrogen and progesterone, made by the ovaries and adrenals through the same Pregnenolone → DHEA pathway used in men.

Elevated testosterone in women (as in PCOS) is usually read as purely pathological, but part of the rise may be adaptive rather than incidental: prolonged stress promotes sodium loss, and androgens act directly on the kidney to increase sodium reabsorption. Female rats given testosterone developed higher blood pressure and lower urinary sodium excretion than untreated females on the same high-sodium diet.[66] See Polycystic ovary syndrome for the fuller thyroid/estrogen/stress mechanism this fits into.

In women over 70 with no prior cardiovascular disease, low blood testosterone and DHEA, not low estrogen, predicted double the risk of a cardiovascular event compared to women with higher testosterone.[67]

In 284 women on long-term subcutaneous testosterone therapy, self-reported hair thinning reversed and none reported new hair loss despite serum testosterone roughly fourfold above normal; lower pretreatment testosterone correlated with prior hair loss.[68]

Mutual antagonism with glucocorticoids in fat storage

[edit]

The androgen receptor is expressed and functional during early human fat-cell differentiation, and its activation inhibits fat maturation. Glucocorticoids tightly regulate and inhibit androgen-receptor expression, facilitating fat storage, particularly in visceral fat, confirming a bidirectional antagonism between androgens and glucocorticoids in body-fat regulation.[69]

Diet and testosterone

[edit]

A systematic review and meta-analysis of 27 studies (309 men, 12 randomized) found the effect of low-carbohydrate diets on testosterone depends on protein intake, not carbohydrate restriction itself: high-protein (over 3.4 g/kg bodyweight/day) low-carbohydrate diets lowered total testosterone by roughly 5.23 nmol/L, while low-carbohydrate diets with lower protein intake showed no consistent decrease. The same review found low-carbohydrate diets raised resting and post-exercise cortisol short-term (under 3 weeks), with resting cortisol normalizing afterward while the post-exercise rise persisted.[70]

See also

[edit]

References

[edit]
  1. ↑ 1.0 1.1 Ray Peat, "Unsaturated Vegetable Oils: Toxic," raypeat.com.
  2. ↑ Ray Peat, "Leaky Vessels, Leaky Cells, Leaky Minds," raypeat.com.
  3. ↑ Josephs RA, et al. "Testosterone and cortisol predict PTSD risk," Psychoneuroendocrinology. 2017. doi:10.1016/j.psyneuen.2017.03.014.
  4. ↑ Nätt D, et al. "High-sugar diet and human sperm," PLoS Biol. 2019. doi:10.1371/journal.pbio.3000559.
  5. ↑ Chung SSW, et al. "Oral administration of a retinoic acid receptor antagonist reversibly inhibits spermatogenesis," Endocrinology. 2011. doi:10.1210/en.2010-0941.
  6. ↑ Moustafa A, et al. "Hindlimb unloading suppresses male reproduction," Reprod Biol Endocrinol. 2021. PMID 33663539.
  7. ↑ Koga M, et al. "Fasting suppresses gonadal steroidogenesis," J Endocr Soc. 2021. PMID 34843801.
  8. ↑ Kim HJ, et al. "DHT protects pancreatic beta cells," Diabetes Metab J. 2021. PMID 33474846.
  9. ↑ De Angelis S, et al. "ETU, hypothyroidism, and DHT," Genes Nutr. 2017. doi:10.1186/s12263-017-0555-5.
  10. ↑ Baynes A, et al. "5α-reductase inhibitors disrupt snail shell morphogenesis," Sci Rep. 2019. doi:10.1038/s41598-019-52850-x.
  11. ↑ "Androgen receptor activation decreases proliferation in thyroid cancer cells," J Cell Biochem. 2021. PMID 33876852.
  12. ↑ "Androgen activity is associated with PD-L1 downregulation in thyroid cancer," Front Cell Dev Biol. 2021. PMID 34422798.
  13. ↑ Yousuf S, et al. "Drostanolone metabolites and cancer cell lines," Steroids. 2018. PMID 29326586.
  14. ↑ 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.
  15. ↑ Tinzl M, Dizeyi N, Zhang H, et al. "Intermittent DHT administration enhances effect of docetaxel in a xenograft model by modulation of ERβ, AR and NEK2," Eur Urol Suppl. 2008. doi:10.1016/S1569-9056(08)60824-6.
  16. ↑ Mendelson GL, et al. "Hormonal status after myocardial infarction," J Clin Endocrinol Metab. 1974. PMID 4270621.
  17. ↑ Barch DM, et al. "Early poverty, testosterone, and hippocampal development," Proc Natl Acad Sci U S A. 2021. doi:10.1073/pnas.2018303117.
  18. ↑ Simonini T, et al. "DHT improves insulin sensitivity in men with low testosterone," Diabetes Care. 2001. doi:10.2337/diacare.24.12.2149.
  19. ↑ Sansone A, et al. "Serum DHT and hypogonadism symptoms," J Endocrinol Invest. 2021. doi:10.1007/s40618-021-01561-0.
  20. ↑ Villareal DT, et al. "DHEA, abdominal fat, and insulin action," JAMA. 2004. doi:10.1001/jama.292.18.2243.
  21. ↑ Hansen C, et al. "SSRIs decrease androgens and progestogens," Toxicol In Vitro. 2017. doi:10.1016/j.tiv.2017.02.001.
  22. ↑ Infante M, et al. "Testosterone and COVID-19 mortality in men," Eur Rev Med Pharmacol Sci. 2021. doi:10.26355/eurrev_202110_26865.
  23. ↑ Wu T, et al. "Androgen levels and scoliosis cartilage development," Clin Genet. 2021. doi:10.1016/j.clgc.2019.03.021.
  24. ↑ 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.
  25. ↑ Islam RM, et al. "Associations between blood sex steroid concentrations and cardiovascular disease risk in older women," Lancet Healthy Longev. 2022. doi:10.1016/S2666-7568(22)00001-0.
  26. ↑ Aubé M, et al. "p,p′-DDE disrupts androgen-mediated protection in breast cancer," Breast Cancer Res. 2008. doi:10.1186/bcr1862.
  27. ↑ Grandys M, et al. "Age-related DHT decline and arterial stiffness," Exp Gerontol. 2023. PMID 36693531.
  28. ↑ Meek TH, et al. "Central androgen action and cardiometabolic risk," Am J Physiol Endocrinol Metab. 2023. doi:10.1152/ajpendo.00059.2023. PMID 37053049.
  29. ↑ Gong ZF, et al. "Carbonated beverages and androgen receptor expression," Acta Endocrinol (Buchar). 2022. PMID 36699165.
  30. ↑ Kenigsberg S, et al. "Metabolic effects of stanolone in elderly men," J Clin Endocrinol Metab. 1953;13(4):420-427. PMID 13242770.
  31. ↑ Gonzalez Deniselle MC, et al. "Steroid profiling in Wobbler mice," Endocrinology. 2016. doi:10.1210/en.2016-1244.
  32. ↑ Pahan K, et al. "Castration induces Parkinson's disease-like symptoms in male mice via iNOS and nitric oxide," J Neurosci. 2017;37(35):8393-8406. PMID 28770670.
  33. ↑ Idkowiak J, et al. "A randomized, placebo-controlled pilot trial of exogenous testosterone in aging men with low serum testosterone levels," J Clin Endocrinol Metab. 2015;100(6):2386-2393. PMID 24751323.
  34. ↑ Slob AK, et al. "Sexual arousal and orgasm in aging men: effects of testosterone replacement therapy," Arch Sex Behav. 1985;14(6):505-515. PMID 4084053.
  35. ↑ Dorgan JF, Judd JT, Longcope C, et al. "Effects of dietary fat and fiber on plasma and urine androgens and estrogens in men: a controlled feeding study," Am J Clin Nutr. 1996;64(6):850-855. PMID 8942407.
  36. ↑ Hsu SC, Huang SM, Lin SH, et al. "Testosterone increases renal anti-aging klotho gene expression via the androgen receptor-mediated pathway," Biochem J. 2014;464(2):221-229.
  37. ↑ Oz OK, Hajibeigi A, Howard K, et al. "Aromatase deficiency causes altered expression of molecules critical for calcium reabsorption in the kidneys of female mice," J Bone Miner Res. 2007;22(12):1893-1902.
  38. ↑ Robinson DP, Klein SL, et al. "Testosterone protects against influenza," Biol Sex Differ. 2016. PMID 27815260.
  39. ↑ PubMed 8495701.
  40. ↑ Prasad AS, Mantzoros CS, Beck FW, Hess JW, Brewer GJ. "Zinc status and serum testosterone levels of healthy adults," Nutrition. 1996 May;12(5):344-8. PMID 8875519.
  41. ↑ Brannon SM, et al. "Testosterone and moral decision-making," Nat Hum Behav. 2019. doi:10.1038/s41562-019-0641-3.
  42. ↑ Wibral M, Dohmen T, Klingmüller D, Weber B, Falk A. "Testosterone administration reduces lying in men," PLoS One. 2012;7(10):e46774. PMID 23071635.
  43. ↑ Nadler A, Camerer CF, Zava DT, et al. "Does testosterone impair men's cognitive empathy? Evidence from two large-scale randomized controlled trials," Proc R Soc B. 2019. doi:10.1098/rspb.2019.1062.
  44. ↑ Eisenegger C, Naef M, Snozzi R, Heinrichs M, Fehr E. "Prejudice and truth about the effect of testosterone on human bargaining behaviour," Nature. 2010;463:356-359. doi:10.1038/nature08711. PMID 19997098.
  45. ↑ van der Westhuizen D, Moore J, Solms M, van Honk J. "Testosterone facilitates the sense of agency," Conscious Cogn. 2017;56:58-67.
  46. ↑ DHT - Ray Peat Email Exchanges
  47. ↑ "DHT," Ray Peat email exchange
  48. ↑ Britt LD, et al. "Infertility in U.S. military women," Fertil Steril. 2019. PMID 31419810.
  49. ↑ Levine H, Jørgensen N, Martino-Andrade A, et al. "Temporal trends in sperm count: a systematic review and meta-regression analysis." Human Reproduction Update. 2017;23(6):646-659. https://academic.oup.com/humupd/article/23/6/646/4035689
  50. ↑ Magdanz V, et al. "The motility-based swim-up technique separates bull sperm based on differences in metabolic rates and tail length," PLoS One. 2019;14(10):e0223576. PMID 31600297.
  51. ↑ Mannowetz N, et al. "Regulation of the sperm calcium channel CatSper by endogenous steroids and plant triterpenoids," Proc Natl Acad Sci U S A. 2017;114(22):5743-5748. PMID 28507119.
  52. ↑ Murakami M, et al. "GR and AR in triple-negative breast cancer," Breast Cancer. 2020. PMID 31989378.
  53. ↑ Mukamal KJ, et al. "DHT and diabetes risk in older men," J Clin Endocrinol Metab. 2016. PMID 27732332.
  54. ↑ Nordström T, et al. "DHT and prostate cancer death," Prostate. 2020. doi:10.1002/pros.23991.
  55. ↑ Downing DT, Strauss JS, Pochi PE. "Androgens and sebum fatty-acid composition," J Endocrinol. 1973. PMID 4249302. doi:10.1677/joe.0.0480373.
  56. ↑ Lengyel E, et al. "Androgen receptor signaling in avian sexual development," Nat Commun. 2024. doi:10.1038/s41467-024-52989-w.
  57. ↑ Ray Peat, "Cortisone, Aging, and Longevity: Three Hormones," raypeat.com.
  58. ↑ Malkonduoglu B, Patel SK, Chien YW. "Navel versus forearm testosterone absorption," J Pharm Sci. 1984. PMID 6707906.
  59. ↑ Frey H, Aakvaag A, Saanum D, Falch J. "Bioavailability of oral testosterone in males," Eur J Clin Pharmacol. 1979;16(5):345-349.
  60. ↑ Johnsen SG, Bennett EP, Jensen VG. "Therapeutic effectiveness of oral testosterone," Lancet. 1974;2(7895):1473-1475.
  61. ↑ "Long-term oral testosterone and liver function," Lancet. 1978;311(8069):867.
  62. ↑ Johnson SG, Kampmann JP, Bennett EP, Jørgensen FS. "Enzyme induction by oral testosterone," Clin Pharmacol Ther. 1976;20(2):233-237.
  63. ↑ Girolami M, et al. "Possible clinical cure in a high percentage of cases of liver cirrhosis with a treatment based on high doses of testosterone and vitamin B 1," Minerva Med. 1973;64(27):1835-1839. PMID 4577116.
  64. ↑ Comeglio P, et al. "Treatment potential of LPCN 1144 on liver health and metabolic regulation in a non-genomic, high fat diet induced NASH rabbit model," J Endocrinol Invest. 2021;44(10):2187-2199. PMID 33586025.
  65. ↑ Wang Y, et al. "Association between serum testosterone and non-alcoholic fatty liver disease in patients with type 2 diabetes mellitus," Diabetes Metab Syndr Obes. 2022;15:2801-2810. PMID 36065220.
  66. ↑ Liu B, Ely D. "Testosterone increases: sodium reabsorption, blood pressure, and renal pathology in female spontaneously hypertensive rats on a high sodium diet," Adv Pharmacol Sci. 2011;2011:817835. PMID 21603136.
  67. ↑ Davis SR, et al., Monash University, reported in "Low testosterone levels in women associated with double the risk of cardiac events", Monash University, 2022. Published in The Lancet Healthy Longevity.
  68. ↑ Glaser R, et al. "Testosterone therapy and hair growth in women," Int J Impot Res. 2012. doi:10.1038/ijir.2011.47.
  69. ↑ Hartig SM, Mancini MA, et al., reported in "Androgens, glucocorticoids duke it out in the fat cell", ScienceDaily, 2012. Published in Chemistry & Biology.
  70. ↑ Whittaker J, Harris M. "Low-carbohydrate diets and men's cortisol and testosterone: Systematic review and meta-analysis", Nutr Health. 2022. PMID 35254136.