DHT cream and gynecomastia (and how to make it)

Disclaimer: DHT is very powerful with known side effects. It carries many inherent and potentially serious risks, using a transdermal preparation may not ameliorate these risks. Please familiarize yourself with these and recognize that you are doing this AT YOUR OWN RISK.

There are many posts on the web asking about how to make your own DHT cream, especially from people who have tried SERMs like raloxifene and did not eliminate their gynocomastia. Greymarket DHT cream is becoming harder to source, so making your own gel could be a good alternative.

Causes:

Excess estrogen: Estrogens directly induce development of male and female breast tissue. Increased by aromatization, reduced elimination/clearance.

Androgen deficiency: through primary and secondary hypogonadism, which both cause increased E2:DHT ratio1

Hyperprolactinemia: elevated levels of prolactin might stimulate breast tissue growth because of excessive progesterone receptor activation, and reduced availability of androgen receptors2

Unsurprisingly drugs that cause estrogen-like actions, increased aromatization, reduced T secretion, reduced sensitivity of androgens receptors, can cause gyno. Examples are Antipsychotics, corticosteroids, spironolactone, antiretrovirals, statins, proton pump inhibitors, and opioids3


DHT to treat gynecomastia


Serms have been shown to be effective in reducing gyno. Tamoxifen has been shown has been shown to eliminate gynecomastia at 20mg / day in 62% of patients.4 Another study found , the response rate, defined as a 50% or greater reduction in gynecomastia, was higher for raloxifene 86% than for tamoxifen 41%.5 making ralox likely the superior choice in terms of efficacy and tolerability.

There’s is not a lot of good data on ais for treating gyno, but anastrozole has shown to reduce gynecomastia in patients receiving TRT6

There are not many studies on the effect DHT on gynecomastia, but there are a few older studies. One of which looked at a group of forty men referred because of persistent idiopathic gynecomastia (of more than 18 months duration). Twice daily topical administration of 125mg of DHT was followed by the complete disappearance of gynecomastia in 10, partial regression in 19 and no change in 11 of the 40 patients. This regression was generally observed within the first or the second month of treatment. No side effects were observed. Patients who showed no regression of their gynecomastia had plasma DHT levels of less than 6.8 nmol/l by day 15 of treatment (Fig. 2), and their (T+ DHT)/E2 ratio did not increase significantly during therapy. In contrast, in patients who showed improvement in their gynecomastia: DHT plasma levels were above 6.8 nmol/l by day 15 of treatment.7

A follow up study was done on 4 boys, using injectable DHT ester at 400mg/week breast size in all four boys had decreased 67% to 78.8 They concluded “the mechanism by which breast regression occurred in our patients was not defined by this study, but may be the result of both decreased estradiol production and of the antiestrogen effect of DHT.”

This conclusion makes sense since we know that DHT will shut down LH, T, and E2 production as well as decreasing SHBG, possibly increasing estrogen clearance altering DHT:E2 ratio. DHT may also directly antagonize estrogen from the ER (citation needed). DHT also blocks estrogen-induced prolactin release which may contribute to gynecomastia.9

It is likely that the high doses required for efficacy and DHTs known side effects like hair loss and atherosclerosis limited its further research as a treatment for gynecomastia. But given the relatively short length of treatment may be appealing to some users. I don’t believe you can totally isolate the benefits of DHT from its systemic side effects, do to diffusion, but I would be interesting to see the effects of a continuous transdermal DHT patch or multiple daily applications of cream along with raloxifene.

DHT cream recipe

There is not a lot of good solubility data for DHT base online. Steroid bases are notoriously hard to get in solution at high concentration, based on testosterones solubility and the composition of other DHT creams, dmso is a good candidate as a solvent. For around 2 months supply of cream (300mg/day) add 10g of DHT to 35ml of hot DMSO, stir until dissolved, stir in 55mL of your favorite moisturizer (aloe,peg), allow to cool, you should now have ~100mL of 10%w/v DHT cream. If the dht does not dissolve in the DMSO at 10% (likely), increase the volume of DMSO and moisturizer.

References

1 S.A. Bembo, H.E. Carlson, Gynecomastia: its features, and when and how to treat it. Clevel. Clin. J. Med. 71(6), 511–517 (2004)

2 M.L. Bravo, M.P. Pinto, I. Gonzalez, B. Oliva, S. Kato, M.A. Cuello, C.A. Lange, G.I. Owen, Progesterone regulation of tissue factor depends on MEK1/2 activation and requires the proline-rich site on progesterone receptor. Endocrine 48(1), 309–320 (2015). doi: 10.1007/s12020-014-0288-9

3 L. Di Luigi, F. Romanelli, P. Sgro, A. Lenzi, Andrological aspects of physical exercise and sport medicine. Endocrine 42(2), 278–284 (2012). doi: 10.1007/s12020-012-9655-6

4 Devoto, E. C., Madariaga, M. A., Lioi, X. C., & Mardones, N. (2007). Influence of size and duration of gynecomastia on its response to treatment with tamoxifen. Revista medica de Chile, 135(12), 1558-1565.

5 Lawrence, S. E., Faught, K. A., Vethamuthu, J., & Lawson, M. L. (2004). Beneficial effects of raloxifene and tamoxifen in the treatment of pubertal gynecomastia. The Journal of pediatrics, 145(1), 71-76.

6 Rhoden, E. L., and A. Morgentaler. "Treatment of testosterone-induced gynecomastia with the aromatase inhibitor, anastrozole." International journal of impotence research 16.1 (2004)

7 KUHN, J. M., Roca, R., LAUDAT, M. H., Rieu, M., LUTON, J. P., & Bricaire, H. (1983). Studies on the treatment of idiopathic gynaecomastia with percutaneous dihydrotestosterone. Clinical endocrinology, 19(4), 513-520.

8 Treatment of persistent pubertal gynecomastia with dihydrotestosterone heptanoateEberle, Andrea J. et al. The Journal of Pediatrics , Volume 109 , Issue 1 , 144 - 149

9 Brann, D. W., Putnam, C. D., & Mahesh, V. B. (1989). Antagonism of estrogen-induced prolactin release by dihydrotestosterone. Biology of reproduction, 40(6), 1201-1207