16 Ways to Fight Gynecomastia

Gynecomastia = Gyno

Most people think the only way to combat gyno is to use Nolvadex or Clomid. Considering the undesirable side-effects of these drugs, I generally don’t prefer these as the first line of defense. I have expressed my concerns about SERM’s in my article – Clomid & Nolvadex – The Dark Side.

In this article I summarize alternative methods for combating the occurrence of gyno. The advice given in this article is the result of over 10 years experience in counseling individuals with AAS induced gyno.

If you have gyno as a result of an endocrine disorder, I advise consulting your doctor before making changes to your prescribed medical regimen.

You Do Not Have Gyno!

During mammary tissue growth (the onset of gyno), you may notice the following symptoms –

  • Puffy or swollen nipples
  • Overly sensitive nipples
  • Itchiness around the nipples

Editorial note: I promise — that is the last time I will ever say nipples.

Now, just because you may have these symptoms does not mean you HAVE GYNO. It simply means that you HAVE GYNO SYMPTOMS. Remember, it is normal to have a small flat pea sized lump under the nipple. This is NOT gyno.

Now, if you allow these above symptoms to progress for several weeks then you may develop gyno. So if you are experiencing any of the above symptoms then you are smart to take action before it’s too late – But please stop emailing me saying you “have gyno” after 3 days on a cycle – this is physiologically impossible.

The good news is that even if you do have a slight case of gyno that you developed from a cycle, it’s probably 100% reversible. Read on…

Nipples.

Gyno Hysteria

No level of gyno is “permanent”. Any level of gyno can be reversed by dietary, supplemental and/or hormonal intervention. Mammary tissue (gyno) can be catabolized like any other tissue in the body. It’s just a matter of creating the right physiological environment within your body. Therefore, as far as I’m concerned, all gyno is temporary or semi-permanent at worse.

Here are the basic levels of gyno –

Level 1 – A dime sized glandular lump – which can emerge as soon as 2-3 weeks after “gyno symptoms” appear. This type of gyno can transform into a more serious level 2 gyno if left untreated for more than 4-6 weeks. In most cases, this initial level 1 gyno disappears once the hormonal environment improves, which is generally 2-3 weeks after the inflicting steroids clear the system.

Level 2 – A quarter sized glandular lump. This type of gyno does not completely disappear on its own, but may gradually shrink to “Level 1” size after discontinuing the inflicting steroids. Completely reversing level 2 gyno requires aggressive dietary and supplemental intervention in conjunction with prescription grade drugs.

Generally, the levels of gyno can be referred to in the following way –

level 1 = temporary

level 2 = semi-permanent

Be warned, if gyno is allowed to grow large enough, the cost of surgery may be more cost efficient than trying to battle the gyno through drug and lifestyle changes – which could otherwise take months or years of intervention.

Following the 16 points below will help you prevent and reverse level 1 & 2 gyno –

The 16 Points

Consider all the following points. Remember, there are many factors that can contribute to gyno and performing just a handful of the points below may be the key to avoiding gyno all together.

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 –

  • 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-shitload-of-everything) will increase most of the growth factors listed above. Cutting calories (especially carbohydrates) 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 SHBG levels, thus allowing more estrogen to freely circulate (by offsetting it from SHBG). Higher levels of freely circulating estrogen can amplify breast tissue growth (20). SHBG also appears to have anti-estrogenic effects at the cell receptor level. (21, 22) Avoiding over suppression of SHBG 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.

discuss this article in the forum

References –

1. Dihydrotestosterone may inhibit hypothalamo-pituitary-adrenal 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 AD, 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-adrenal 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 adrenocortical carcinoma cell line H295R.
Watanabe M, Nakajin S.
J Endocrinol. 2004 Jan;180(1):125-33.

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HCG – Unraveled

Post-Cycle-Therapy is a must upon cessation of steroid use. Many great Post Cycle Therapy protocols have been outlined over the years, and many individuals have had success with following such protocols. Nevertheless, what works can always work better, and I intend to show you the most effective way to recover from AAS. This is especially the case for those that have had a lack of success following popular advice. In this article I will address the misunderstanding and misuse of Human Chorionic Gonadotropin (hCG) and show you the most efficient way to use hCG for the fastest and most complete recovery.

HCG unraveled –

Human Chorionic Gonadotropin (hCG) is a peptide hormone that mimics the action of luteinizing hormone (LH). LH is the hormone that stimulates the testes to increase testosterone levels. (1) More specifically LH is the primary signal sent from the pituitary to the testes, which stimulates the leydig cells within the testes to produce testosterone.

When steroids are administered, LH levels rapidly decline. The absence of an LH signal from the pituitary causes the testes to stop producing testosterone, which causes rapid onset of testicular degeneration. The testicular degeneration begins with a reduction of leydig cell volume, and is then followed by rapid reductions in intra-testicular testosterone (ITT), peroxisomes, and Insulin-like factor 3 (INSL3) – All important bio-markers and factors for proper testicular function and testosterone production. (2-6,19) However, this degeneration can be prevented by a small maintenance dose of hCG ran throughout the cycle. Unfortunately, most steroid users have been engrained to believe that hCG should be used after a cycle, during Post-Cycle-Therapy. Upon reviewing the science and basic endocrinology you will see that a faster and more complete recovery is possible if hCG is ran during a cycle.

Firstly, we must understand the clinical history of hCG to understand its purpose and its most efficient application. Many popular “steroid profiles” advocate using hCG at a dose of 2500-5000iu once or twice a week. These were the kind of dosages used in the historical (1960’s) hCG studies for hypogonadal men who had reduced testicular sensitivity due to prolonged LH deficiency. (21,22) A prolonged LH deficiency causes the testes to desensitize, requiring a higher hCG dose for ample stimulation. In men with normal LH levels and normal testicular sensitivity, the maximum increase of testosterone is seen from a dose of only 250iu, with minimal increases obtained from 500iu or even 5000iu. (2,11) (It appears the testes maximum secretion of testosterone is about 140% above their normal capacity.) (12-18) If you have allowed your testes to desensitize over the length of a typical steroid cycle, (8-16 weeks) then you would require a higher dose to elicit a response in an attempt to restore normal testicular size and function – but there is cost to this, and a high probability that you won’t regain full testicular function.

One term that is critical to understand is testosterone secretion capacity which is synonymous to testicular sensitivity. This is the amount of testosterone your testes can produce from any given level of LH or hCG stimulation. Therefore, if you have reduced testosterone secretion capacity (reduced testicular sensitivity), it will take more LH or hCG stimulation to produce the same result as if you had normal testosterone secretion capacity. If you reduce your testosterone secretion capacity too much, then no amount of LH or hCG stimulation will trigger natural testosterone production – and this leads to permanently reduced testosterone production. (recovering full testosterone production is a topic for another article)

To get an idea of how quickly you can reduce your testosterone secretion capacity from your average steroid cycle, consider this: LH levels are rapidly decreased by the 2nd day of steroid administration. (2,9,10) By shutting down the LH signal and allowing the testis to be non-functional over a 12-16 week period, leydig cell volume decreases 90%, ITT decreases 94%, INSL3 decreases 95%, while the capacity to secrete testosterone decreases as much as 98%. (2-6)

Note: visually analyzing testes size is a poor method of judging your actual testicular function, since testicular size is not directly related to the ability to secrete testosterone. (4) This is because the leydig cells, which are the primary sites of testosterone secretion, only make up about 10% of the total testicular volume. Therefore, when the testes may only appear 5-10% smaller, the testes ability to secrete testosterone upon LH or hCG stimulation can actually be significantly reduced to 98% of their normal production. (3-5) So do not judge how “shutdown” you are by testicular size!

The decreased testosterone secretion capacity caused by steroid use was well demonstrated in a study on power athletes who used steroids for 16 weeks, and were then administered 4500iu hCG post cycle. It was found that the steroid users were about 20 times less responsive to hCG, when compared to normal men who did not use steroids. (8) In other words, their testosterone secretion capacity was dramatically reduced because they did not receive an LH signal for 16 weeks. The testes essentially became desensitized and crippled. Case studies with steroid using patients show that aggressive long-term treatment with hCG at dosages as high as 10,000iu E3D for 12 weeks were unable to return full testicular size. (7) Another study with men using low dose steroids for 6 weeks showed unsuccessful return of Insulin-like factor-3 (INSL3) concentration in the testes upon 5000iu/wk of HCG treatment for 12 weeks (6) (INSL3 is an important biomarker for testosterone production potential and sperm production) 20

In light of the above evidence, it becomes obvious that we must take preventative measures to avoid this testicular degeneration. We must protect our testicular sensitivity. Besides, with hCG being so readily available, and such a painless shot, it makes you wonder why anyone wouldn’t use it on cycle.

Based on studies with normal men using steroids, 100iu HCG administered everyday was enough to preserve full testicular function and ITT levels, without causing desensitization typically associated with higher doses of hCG. (2) It is important that low-dose hCG is started before testicular sensitivity is reduced, which appears to rapidly manifest within the first 2-3 weeks of steroid use. Also, it’s important to discontinue the hCG before you start Post-Cycle-Therapy so your leydig cells are given a chance to re-sensitize to your body’s own LH production. (To help further enhance testicular sensitivity, the dietary supplement Toco-8 may be used)

Based off the above information, an optimal dose of hCG during the cycle would be 250iu every 4 days, or as a less desirable alternative, once a week shot of 500iu. Keep in mind, that the half-life of hCG is 3-4 days, while the half-life of LH is only 1-2 hours. Considering this difference in excretion time, it is best to space each dose of hCG at least 4 days apart for the optimal “peak and valley” replication. However, going more than 7 days between each hCG shot may promote increase the rate of desensitization from lack of LH or hCG stimulation.

If you are starting hCG late in the cycle, one could calculate a rough estimate for their required hCG “kick starting” dosage by multiplying 40iu x days of LH absence. (ie. 40iu x 60 days = 2400iu HCG dose) Remember, since the testes will be desensitized later in a cycle, you will require a higher dose. Also, the maximum daily dose of hCG should not exceed 5000iu, and 4-7 days must be taken off between each shot. Generally, a higher dose will require a longer off period between each shot. (eg., 2500iu = 7 days between each shot)

Note: If following the on cycle hCG protocol, hCG should NOT be used for PCT.

Recap

For preservation of testicular sensitivity, use 250iu every 4 days starting 14 days after your first AAS dose. At the end of the cycle, drop the hCG two weeks before the AAS clear the system. For example, you would drop hCG about the same time as your last Testosterone Enanthate shot. Or, if you are ending the cycle with orals, you would drop the hCG about 10 days before your last oral dose. This will allow for a sudden and even clearance in hormone levels. This will initiate a strong LH and FSH surge from the pituitary, to begin stimulating your testes to produce testosterone. Remember, recovery doesn’t begin until you are off hCG since your body will not release its own LH until the hCG has cleared the system.

In conclusion, we have learned that utilizing hCG during a steroid cycle will significantly prevent testicular degeneration. This helps create a seamless transition from “on cycle” to “off cycle” thus avoiding the post cycle crash.

References –

1. Glycoprotein hormones: structure and function.
Pierce JG, Parsons TF 1981
Annu Rev Biochem 50:466-495

2. Low-Dose Human Chorionic Gonadotropin Maintains Intratesticular Testosterone in Normal Men with Testosterone-Induced Gonadotropin Suppression
Andrea D. Coviello, et al
J. Clin. Endocrinol. Metab., May 2005; 90: 2595 – 2602.

3. Luteinizing hormone on Leydig cell structure and function.
Mendis-Handagama SM
Histol Histopathol 12:869-882 (1997)

4. Leydig cell peroxisomes and sterol carrier protein-2 in luteinizing hormone-deprived rats
SM Mendis-Handagama, et al.
Endocrinology, Dec 1992; 131: 2839.

5. Effect of long term deprivation of luteinizing hormone on Leydig cell volume, Leydig cell number, and steroidogenic capacity of the rat testis.
Keeney DS, et al.
Endocrinology 1988; 123:2906-2915.

6.The Effects of Gonadotropin Suppression and Selective Replacement on Insulin-Like Factor 3 Secretion in Normal Adult Men
Katrine Bay, et al
J. Clin. Endocrinol. Metab., Mar 2006; 91: 1108 – 1111.

7. Successful treatment of anabolic steroid-induced azoospermia with human
chorionic gonadotropin and human menopausal gonadotropin
Dev Kumar Menon, et al.
FERTILITY AND STERILITY VOL. 79, SUPPL. 3, JUNE 2003

8. Testicular responsiveness to human chorionic godadotrophin during transient hypogonadotrophic hypogonadism induced by androgenic/anabolic steroids in power athletes
Hannu et al.
J. Steroid Biochem. Vol. 25, No. 1 pp. 109-112 (1986)

9. Comparison of testosterone, dihydrotestosterone, luteinizing hormone, and follicle-stimulating hormone in serum after injection of testosterone enanthate of testosterone cypionate.
Schulte-Beerbuhl M, et al 1980
Fertil Steril 33:201-203

10. Effects of chronic testosterone administration in normal men: safety and efficacy of high dosage testosterone and parallel dose-dependent suppression of luteinizing hormone, follicle-stimulating hormone, and sperm production.
Matsumoto AM, et al 1990
J Clin Endocrinol Metab 70:282-287

11. Effect of human chorionic gonadotropin on plasma steroid levels in young and old men.
Longcope C et al
Steroids 21:583-590 (1973)

12. Regulation of peptide hormone receptors and gonadal steroidogenesis.
Catt KJ, et al
Rec Prog Horm Res 1980; 36:557-622

13. Effect of human chorionic gonadotropin on the endocrine function of Papio testes
GV Katsiia, et al
Probl Endokrinol (Mosk), Sep 1984; 30(5): 68-71.

14. Reproductive function in young fathers and grandfathers.
Nieschlag E, et al.
J Clin Endocrinol Metab 55:676-681 (1982)

15. The aging Leydig cell III Gonadotropin stimulation in men.
Nankin HR, et al. 1981
J Androl 2:181-189

16. Reproductive hormones in aging men. I. Measurement of sex steroids, basal luteinizing hormone, and Leydig cell response to human chorionic gonadotropin.
Harman SM, et al. 1980
J Clin Endocrinol Metab 51:35-40

17. Prolonged biphasic response of plasma testosterone to single intramuscular injections of human chorionic gonadotropin.
Padron RS, et al. 1980
J Clin Endocrinol Metab 50:1100-1104

18. Gonadotrophins and plasma testosterone in senescence. In: James VHT, Serio M, Martini L, eds. The endocrine function of the human testis.
Mazzi C, et al. 1974
New York: Academic Press, Inc.; 51-66

19. Androgen biosynthesis in Leydig cells after testicular desensitization by luteinizing hormone-releasing hormone and human chorionic gonadotropin.
Dufau ML, et al.
Endocrinology 105 1314-1321 (1979)

20. Insulin-Like Factor 3 Serum Levels in 135 Normal Men and 85 Men with Testicular Disorders: Relationship to the Luteinizing Hormone-Testosterone Axis
K. Bay, S. et al
J. Clin. Endocrinol. Metab., Jun 2005; 90: 3410 – 3418.

21. Stimulation of sperm production by human chorionic gonadotropin after prolonged gonadotropin suppression in normal men.
Matsumoto AM, et al 1985
J Androl 6:137-143

22. Human chorionic gonadotropin and testicular function: stimulation of testosterone, testosterone precursors, and sperm production despite high estradiol levels.
Matsumoto AM, et al. 1983
J Clin Endocrinol Metab 56:720-728

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