Steroids: Methandriol is a steroid that is very similar to the prohormone 5-androdiol except that it is C-17 alpha alkylated and also esterified at both ends. It is present in combination with several other steroids especially those manufactured in Australia. In Dan Duchaine’s Underground Steroid handbook II, Duchaine postulated that methandriol enhanced the activity of any steroid used in combination with it. He stated that methandriol did this by binding very strongly to SHBG thereby knocking other steroids into the free and active state (similar to what has been described for mesterolone). Although methandriol does bind to SHBG, it does so fairly weakly and is not capable of knocking most steroids off.
Methandriol is very prone to aromatization (like androdiol) and it has been suggested that it can bind directly to the estrogen receptor without the need for aromatization. When used with other aromatizing steroids, methandriol most likely occupies aromatase to the point that the other steroid is unable to be aromatized allowing it to stay free and active. While this sounds like a good idea at first, the excess estrogen that is produced by adding methandriol could lead to gynecomastia quickly. Methandriol has been found to be a potent inhibitor of 11-beta hydroxylase1,2,3,4,5. This results in a buildup of deoxycorticosterone, a potent mineralocorticoid that elicits retention of sodium and water resulting in hypertension6,7,8. A potentially disturbing aspect of the hypertension induced with methandriol was its apparent irreversibility9. The inhibition of 11-beta hydroxylase reduces the production of cortisol and results in a reduction in the size of the adrenals, also known as adrenal atrophy, which can result in a state of acute adrenal insufficiency upon withdrawal of the use of steroids that inhibit 11-beta hydroxylase.
Methandriol is metabolized to methyltestosterone, estrogenic metabolites and 5-alpha reduced androgens that contribute to the side-effect profile of this steroid10. The “increase in efficacy” that this steroid induces when used in combination with other androgens as proposed by Duchaine and others may be related to the inhibition of 11-beta hydroxylase which will result in water weight gain and an anticatabolic effect through the reduction in serum cortisol. As mentioned elsewhere, the inhibition of 11-beta hydroxylase can cause hypertension and other negative cardiovascular effects.
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2. Brownie AC, Bhasker CR, Waterman MR. Levels of adrenodoxin, NADPH-cytochrome P-450 reductase and cytochromes P-45011 beta, P-45021, P-450scc, in adrenal zona fasciculata-reticularis tissue from androgen-treated rats. Mol Cell Endocrinol. 55(1):15-20, 1988
3. Gallant S, Alfano J, Charpin M, Brownie AC. The inhibition of rat adrenal cytochrome P-45011 beta gene expression by androgens. Endocr Res. 18(2):145-61, 1992
4. Hall CE, Hall O. Methylandrostenediol hypertension induced without salt excess: observations on organ changes and serum composition. Am J Pathol. 54(3):489-505, 1969
5. SAFFRAN M, VOGT M. The effect of 17-methylandrostenediol on the secretory capacity of the adrenal cortex of rats. J Physiol. 151:123-30, 1960
6. McCall AL, Stern J, Dale SL, Melby JC. Adrenal steroidogenesis in methylandrostenediol-induced hypertension. Endocrinology. 103(1):1-5, 1978
7. Hyde PM, Daigneault EA. Adrenal plasma levels of corticosterone and deoxycorticosterone in methylandrostenediol-salt induced hypertension. Steroids. 11(6):721-31, 1968
8. Hyde PM, Weil AC, Daigneault EA. Plasma levels of corticosterone in methylandrostenediol-salt-induced hypertension. Am J Physiol. 213(1):267-70, 1967
9. Molteni A, Brownie AC, Nickerson PA, Skelton FR. Irreversibility of methylandrostenediol-induced hypertension in the rat after suspension of the androgen treatment. Am J Pathol. 69(1):179-94, 1972
10. Schanzer W: Metabolism of anabolic androgenic steroids. Clin Chem. Jul;42(7):1001-20, 1996
Adapted with permission from Seth Robert’s Anabolic Pharmacology, all rights reserved.