On The Origin of Pattern Hair Loss: Wrong From The Beginning …

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Castrates are “protected” from balding as long as testosterone therapy isn’t administered. It’s easy to accuse testosterone of inducing baldness, but it’s fucking lazy because new estrogen can be synthesized from testosterone via the aromatase enzyme.

Aromatase activity is increase by aging, fat accumulation (Vermeulen A. et al. 1978; Jensen J. et al. 1985), and general stress (Simpson E. et al. 1981). Castrates have raging pituitary glands (Martin C. 1976), which is analogous to someone under severe stress. I don’t think it’s unreasonable to speculate that injecting testosterone into castrates would result in elevated levels of estrogen.

In addition to never balding, a second feature of male castration is “feminization.” Because women are obviously less prone to pattern hair loss than males, investigating this association seems worthwhile. Finding the hormone(s) responsible for “feminization” may provide insight on castration’s “protective” mechanism against pattern baldness.

When reviewing the hormonal profile of male castrates we find that they produce virtually no testosterone and low levels of estrogen (Selye H. 1947) and prolactin (Bronson F. 1991). While this may seem paradoxical, as we discussed earlier, some estrogen is synthesized from testosterone, and estrogen usually increases prolactin.

While estrogen is often referred to as “the female hormone,” I think there is good evidence that it has masculinizing properties:

  • In the ’80s physiologist Constance R. Martin found that estrogens were “defeminizing” and that they “mimic testosterone” (Martin C. 1976).
  • Even earlier, in the ’40s, Hans Selye found that administering estrogens to female rats interrupted estrus, and was actually “anti-estrogenic” (Selye H. 1947). 
  • By stimulating the adrenal glands, estrogen can increase the production of “male” hormones responsible for masculine characteristics, such as chest hair and whisker growth (Ditkoff E. et al. 1995).
  • Polycystic ovarian syndrome (PCOS), which is the largest endocrine disorder woman face in their reproductive years, is characterized by an unwanted increase in masculine features. Excessive estrogen and androgens are typical in PCOS (Benjamin F. et al. 1993). In regards to pattern hair loss, “…it can be concluded that men with premature alopecia and hormonal changes partially resembling those typical for female PCOS, might probably represent the male equivalent of PCOS” (Dusková M. et al. 2007).

In addition to the lack of estrogen and prolactin, castration increases the activity of the pituitary gonadotropins, “LH” (luteinizing hormone) and “FSH” (follicle stimulating hormone). In males, LH can signal the adrenal glands to produce progesterone, which I believe to be the one of the ‘protective’ elements of castration.

Progesterone promotes feminine characteristics by opposing both androgens and estrogens. Most importantly, progesterone supports thyroid function, which increases carbon dioxide, increasing mitochondrial efficiency, blood flow and further stimulates the production of pregnenolone, progesterone and DHEA.

While castration isn’t a viable therapy for pattern baldness, I think emulating the “hair-protective” features of a castrate’s physiology is possible. For example, keeping estrogen, cortisol, and prolactin low by supporting thyroid function and avoiding indigestible foods while obtaining full nutrition. 

More Articles:

Benjamin F, Toles AW, Seltzer VL, Deutsch S. Excessive estradiol secretion in polycystic ovarian disease. Am J Obstet Gynecol. 1993 Nov;169(5):1223-6

Bronson F. Mammalian Reproductive Biology. 1991;63 “As expected then, castration is followed by a dramatic increase in the frequency of LH pulses and thus a much higher level of LH in the blood. In contrast, blood levels of prolactin fall after castration.”

Ditkoff EC, Fruzzetti F, Chang L, Stancyzk FZ, Lobo RA. The impact of estrogen on adrenal androgen sensitivity and secretion in polycystic ovary syndrome. J Clin Endocrinol Metab. 1995 Feb;80(2):603-7. “Adrenal hyperandrogenism is a common feature of patients with polycystic ovary syndrome (PCO). This may be due to enhanced adrenal sensitivity to ACTH. Because enhanced ovarian androgen secretion does not appear to explain this phenomenon, we explored the role of estrogen in inducing enhanced adrenal sensitivity, in that a state of relative hyperestrogenism exists in PCO.” “In conclusion, these data provide evidence that estrogen is at least one factor that influences adrenal androgen sensitivity in PCO and may help explain the frequent finding of adrenal hyperandrogenism in this syndrome.”

Dusková M, Hill M, Stráka L. The polycystic ovary syndrome and its male equivalent. Cas Lek Cesk. 2007;146(3):251-5.

Hamilton J. Male hormone stimulation is prerequisite and an incitant in common baldness. Am J Anat 71:451-480, 1942

Hamilton. J. Effect of castration in adolescent and young adult males upon further changes in the proportions of bare and hairy scalp. J Clin Endocrinol Metab. 1960 Oct;20:1309-18.

Jensen J, Riis BJ, Hummer L, Christiansen C. The effects of age and body composition on circulating serum oestrogens and androstenedione after the menopause. Br J Obstet Gynaecol. 1985 Mar;92(3):260-5. “Serum concentrations of both oestrogens correlated significantly with the fat mass…” “…conversion rate of androstenedione to oestrone, and of oestrone to oestradiol, increases with age…”

Martin C. Endocrine Physiology. 1976:533 “Plasma FSH and luteinizing hormone (LH) levels rise after castration.”

Martin C. Endocrine Physiology. 1976;556 “When the effects of perinatal gonadectomy and hormone injection were first observed, it seemed reasonable to conclude that testosterone interacts with androgen receptors in the brain to bring about defeminization. However, the concept had to be revised when it was found that estrogens mimic testosterone, whereas DHT does not. It was soon revealed that estrogen receptors begin to appear in the hypothalamus around the time of birth, and that they increase in numbers during the first few postnatal days. Moreover, neurons involved in defeminization contain aromatase enzymes that convert testosterone (but not DHT) to estrogen. The conclusion that estrogens are the defeminizing agents is supported by several findings.”

Selye H. The Textbook of Endocrinology. 1976;661 “Eunuchism decreases urinary testoid. 17-KS and folliculoid elimination, since it removes one of the most important sources of these compounds. The continued excretion, in small amounts, of such steroids in castrates, is probably attributable to adrenal-cortical secretion”

Selye H. The Textbook of Endocrinology. 1976;59 “…Similarly, in many animal species, the so-called “estrogens” do not in themselves cause estrus or heat without simultaneous progesterone treatment, hence the later hormone could be called “estrogenic” with almost equal justification. Furthermore, folliculoids interrupt the estrous cycle in the intact rodent so that they are actually “anti-estrogenic” under ordinary circumstances of bioassay.”

Simpson ER, Ackerman GE, Smith ME, Mendelson CR. Estrogen formation in stromal cells of adipose tissue of women: induction by glucocorticosteroids. Proc Natl Acad Sci U S A. 1981 Sep;78(9):5690-4.

Vermeulen A, Verdonck L. Sex hormone concentrations in post-menopausal women. Clin Endocrinol (Oxf). 1978 Jul;9(1):59-66. “E1 and to a lesser extent E2 as well as the E1/A ratio were significantly corelated with degree of obesity or fat mass, suggesting a possible role of fat tissue in the aromatization of androgens.”

Fat Tissue and Aging – Increased Estrogen – Rob Turner