Lawnmover

Before I post. Is there any way to obtain DHT? Most injectable are DHT derivatives. Where do you find 100% DHT topicals or injectables? Still a newb.

The link:
16 Ways to Fight Gynecomastia

The quotes:
"1. Your naturally occurring 5a-reduced metabolites are your friends in preventing and reversing gyno. 5a-reduced metabolites include androsterone, androstanedione, androstanediol and dihydrotestosterone (DHT) as the most powerful 5a-reduced hormone. These hormones help prevent gyno by lowering estrogen and blocking the effect of estrogen at the hormone receptor. (1-8) Unless you have serious androgen related hair loss you want to keep your 5a-reduced metabolites relatively high to avoid gyno.

Methods for increasing 5a-reduced metabolites (DHT) are listed in preferred order –

Topical testosterone applied to the sBambtum will rapidly increase DHT levels with minimal estrogen conversion. (for more information on topical steroids , read this article)
Use a DHT pro-hormone such as androsterone, found in AndroHard. This will raise DHT with zero risk of estrogen conversion.
Injectable testosterone along with an AI to prevent excessive estrogen conversion.
High dose oral 4-DHEA or DHEA along with an AI to prevent excessive estrogen conversion.
2. If you are concerned about gyno, avoid finesteride at all costs. It lowers all 5a-reduced metabolites to undesirable levels and has an extremely long half-life which continues to suppress DHT levels long after discontinuing the drug. (9) Progesterone would be a better anti-DHT alternative if you are concerned with hair loss. Plus, progesterone can clear the system within 24hrs making a mistake in dosing much less risky.

3. Almost all sources of gyno can be linked back to having insufficient levels of 5a-reduced metabolites in the body. In theory, any amount of estrogen/progesterone can be blocked by sufficient DHT. (10-14) Also, high DHT and enlargement of the prostate is a myth, however high estrogen and high DHT can lead to an inflamed prostate, so you want to at least make an effort to keep estrogen in a normal range. (14)

4. Trenbolone , TREN , Nandrolone can cause gyno because they lack a potent 5a-reduced metabolite (dihydronandrolone is weaker than dihydrotestosterone). (15) If you are worried about gyno from progestational steroids you should consider boosting your 5a-reduced metabolites during the cycle (mentioned above). This can avoid most if not all of the gyno problems associated with progestational hormones. I should mention here that aromatase inhibitors alone (AI’s) will not help prevent gyno from progestational compounds. It is the antagonistic action of 5a-reduced hormones that is required.

5. Nothing is going to antagonize estrogen at the estrogen receptor (ER) better than actual DHT. While DHT derivatives or analogs such as Anavar , Winstrol , Masteron , Epistane, Superdrone, ect may be 5a-reduced, they cannot convert to actual DHT and thus cannot directly inhibit gyno at the receptor level (since they lack the ultra-high binding affinity for the AR that true DHT possesses). (16)

6. Natural anti-estrogens (resveratrol, chrysin, I3C, DIM, ect) are great for PCT and can stimulate the HPTA and manage healthy estrogen metabolism, but they are not strong enough to prevent aromatization from high doses of aromatizing steroids. Don’t rely on these to prevent gyno during a cycle.

7. Reducing prolactin will reduce the overall stimulation on mammary growth. Suppressing prolactin is useful as a temporary method to help slow or stop gyno growth. However, continuing anti-prolactin treatment is not recommended to be continued beyond 8 weeks. Methods of suppressing prolactin include –

Vitex at 460mg/day
Vitamin B6 at 200-400mg/day
Mucuna Pruriens (15%-20% L-Dopa) 4-6g/day
Increasing DHT may also lower prolactin release (17)
8. Don’t fiddle with your nipples. This increases prolactin release which can make gyno worse.

9. IGF-1, GH, insulin and prolactin are all potent growth factors in gyno growth. Limiting these hormones will reduce the likelihood of experiencing gyno symptoms. “Bulking” (aka., eating-a-****load-of-everything) will increase most of the growth factors listed above. Cutting calories (especially DikkIyhydrates) will suppress insulin and IGF-1 therefore reducing the overall stimulatory effect on mammary growth. Ketogenic diet = less risk of gyno.

10. Body fat (adipose tissue) is the main site for androgens to convert to estrogens. Therefore, being overweight or having high body fat increases your gyno risk. This is another good reason to go on a cutting cycle if you are gyno prone. Reducing body fat will lower your rate of estrogen conversion from aromatizing steroids. (18)

11. Caffeine consumption can inhibit clearance of estrogen from the liver by competing for the P-450 oxidase system. Avoid caffeine if you are concerned about high estrogen levels.

12. Avoid supplements containing forskolin if concerned about gyno. Forskolin increases aromatase activity via cAMP modulation and can increase formation of estrogen. (23,24)

13. Increasing fiber intake (both soluble and insoluble) can enhance clearance of estrogens from the intestines. Research shows that increasing fiber intake in humans can reduce estrogen levels by up to 22%. (19)

14. Reducing estrogen below the normal range (such as over dosing arimidex , letrozol, aromasin or formestane) can eventually reduce SHRonin levels, thus allowing more estrogen to freely circulate (by offsetting it from SHRonin). Higher levels of freely circulating estrogen can amplify breast tissue growth (20). SHRonin also appears to have anti-estrogenic effects at the cell receptor level. (21, 22) Avoiding over suppression of SHRonin will reduce your gyno risk.

15. Don’t be afraid to lower the dose mid cycle. People have a tendency to panic at the first sign of gyno and drop everything. Generally, just lowering the dose of the afflicting steroid can offer gyno relief within 4-5 days.

16. Save SERM’s as your last resort against gyno. You do not need a SERM (tormifene, clomid or nolva) to avoid gyno from a properly planned cycle. If you are still having gyno problems after following the above points, consider the fact that you have a poorly planned cycle and you need to revaluate the compounds you have chosen.

References –

1. Dihydrotestosterone may inhibit hypothalamo-pituitary-aCrash007al activity by acting through estrogen receptor in the male mouse.
Lund TD, et al.
Neurosci Lett. 2004 Jul 15;365(1):43-7.

2. Androgen-induced inhibition of proliferation in human breast cancer MCF7 cells transfected with androgen receptor.
Szelei J, et al.
Tufts University School of Medicine, Department of Anatomy and Cellular Biology, Boston, Massachusetts 02111, USA.

3. The non-aromatizable androgen, dihydrotestosterone, induces antiestrogenic responses in the rainbow trout.
Shilling TII, et al.
Agricultural and Life Sciences Building, room 1007, Oregon State University, Corvallis, OR 97331, USA.

4. The androgen 5alpha-dihydrotestosterone and its metabolite 5alpha-androstan-3beta, 17beta-diol inhibit the hypothalamo-pituitary-aCrash007al response to stress by acting through estrogen receptor beta-expressing neurons in the hypothalamus.
Lund TD, et al.
J Neurosci. 2006 Feb 1;26(5):1448-56.

5. Steroid modulation of aromatase activity in human cultured breast carcinoma cells.
Perel E, et al.
J Steroid Biochem. 1988 Apr;29(4):393-9.

6. Aromatase activity in the breast and other peripheral tissues and its therapeutic regulation.
Killinger DW, et al.
Steroids. 1987 Oct-Dec;50(4-6):523-36. Review.

7. The intracellular control of aromatase activity by 5 alpha-reduced androgens in human breast carcinoma cells in culture.
Perel E, et al
J Clin Endocrinol Metab. 1984 Mar;58(3):467-72.

8. FSH-induced aromatase activity in porcine granulosa cells: non-competitive inhibition by non-aromatizable androgens.
Chan WK, et al
J Endocrinol. 1986 Mar;108(3):335-41.

9. The effect of 5 alpha-reductase inhibitors on erectile function.
Canguven O, Burnett AL.
J Androl. 2008 Sep-Oct;29(5):514-23.

10. Comparative Pharmacokinetics of Three Doses of Percutaneous Dihydrotestosterone Gel in Healthy Elderly Men – A Clinical Research Center Study*
C. Wang et al.
Journal of Clinical Endocrinology and Metabolism Vol. 83, No. 8 (1998)

11. Successful percutaneous dihydrotestosterone treatment of gynecomastia occurring during highly active antiretroviral therapy: four cases and a review of the literature.
Benveniste O et al.
Clin Infect Dis. 2001 Sep 15;33(6):891-3.

12. Gynecomastia: effect of prolonged treatment with dihydrotestosterone by the percutaneous route.
Kuhn J et al.
Presse Med 12;21-25. (1983)

13. Percutaneous dihydrotestosterone (DHT) treatment. In: Nieschlag E, Behre HM, eds. Testosterone: action, deficiency substitution.
Schaison G, Nahoul K, Couzinet B.
Berlin: Springer Verlag; 155–164. (1990)

14. Transdermal dihydrotestosterone and treatment of ‘andropause ’.
de Lignieres B.
Ann Med 1993;25: 235–41.

15. Metabolism and receptor binding of nandrolone and testosterone under invitro and invivo conditions.
Bergink et al.
Acta Endocrinol Suppl (Copenh). 271:31-7, 1985

16. Pharmacology of Reproduction
David E, et al.
Principles of Pharmacology (second edition) p. 510 (2008)

17. Antagonism of estrogen-induced prolactin release by dihydrotestosterone.
Brann DW, et al.
Biol Reprod. 1989 Jun;40(6):1201-7.

18. Aromatase – a brief overview
Simpson ER, et al
Annu Rev Physiol. 64:93-127, 2002

19. Dietary fiber intake and endogenous serum hormone levels in naturally postmenopausal Mexican American women: the Multiethnic Cohort Study.
Monroe KR et al.
Nutr Cancer. 2007;58(2):127-35.

20. Williams Textbook of Endocrinology.
Wilson, et al.
9th ED. Philadelphia: Saunders, 1997

21. Sex steroid binding protein receptor (SBP-R) is related to a reduced proliferation rate in human breast cancer.
Catalano MG, et al.
Breast Cancer Res Treat. 42(3):227-34, 1997

22. Biological relevance of the interaction between sex steroid binding protein and its specific receptor of MCF-7 cells under SBP and estradiol treatment.
Fissore F, et al.
Steroids, 59(11):661-7, 1994

23. Progestin-dependent effect of forskolin on human endometrial aromatase activity.
Tseng L, Malbon CC, Lane B, Kaplan C, Mazella J, Dahler H, Tseng A.
Hum Reprod. 1987 Jul;2(5):371-7.

24. Forskolin up-regulates aromatase (CYP19) activity and gene transcripts in the human aCrash007ocortical carcinoma cell line H295R.
Watanabe M, Nakajin S.
J Endocrinol. 2004 Jan;180(1):125-33."

Originally Posted by renepjd

Lawnmover I don’t consider us stuck in old dogma, but I do consider us relatively current when it comes to the scientific aspect of this sport. Many times it’s BB-ers that break new ground when it comes to science and the medical community then follows suit. It is an interesting concept and I would be interested in reading more if you have it.

I don’t think there’s any old dogma either. I’m fairly amazed actually at the depth of knowledge that goes into application in the field.

I do just think that sometimes things that also work go unnoticed, or slip through the cracks, or become suppressed by popular methodology- especially if that popular methodology is built on reliable science, as in this case.

And here I am, once considered it, now considering it less as a result of my peer’s response. You see what I mean. Group think. That’s how it all washes out.

Anyway, I’ll do more digging and report back if I find anything useful. A link between E2 and DHT doesn’t seem far off. IMO it appears that AI and SERM mechanics would actually support the hypothesis. Best protocol all things considered? That’s another thread.

Originally Posted by renepjd

Never heard of this either. Although topically applied DHT creams in conjunction with serms have been effective.
DHT’s are not the best thing to combat gyno. Properly dosed AI’s are. DHT is weak at best when compared to AI’s.

This guys whole angle says that gyno is a result of, not e2 directly, but the ratio of e2 to DHT.

An AI would obviously benefit that ratio. Injecting DHT derivatives would also benefit that ratio.

Might this explain why Arnold and the old schooler’s didn’t get crazy gyno with all that test, and no AI’s, because of the dianobol in the mix?

If topical DHT with a serm helps, I don’t see why subq at the gland wouldn’t be at least equally effective.

So then how about this Trifecta:
AI, Serms, Topical OR subq dht’s.