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Male fertility... a good reason to LOWER your anti-estrogen intake

Phidias

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A good read. Yes men need estrogens. :) At least when they're trying to have kids...


1997


From: University of Illinois at Urbana-Champaign

Estrogen Linked To Sperm Count, Male Fertility CHAMPAIGN, Ill. --

Testosterone may be the hormone that makes the man, but it is estrogen -- the so-called 'female' hormone -- that gives sperm its reproductive punch, a team of researchers report in Thursday's (Dec. 4) issue of the journal Nature.
Estrogen is vital to male fertility -- specifically to sperm count. That discovery, coupled with the debate over declining sperm counts worldwide, means "we must be concerned about the potential for environmental chemicals to influence male reproductive function," said Rex A. Hess, a professor of veterinary biosciences at the University of Illinois and principal author of the Nature report.

"If there is a normal function for estrogen in the male, and that function is required for normal fertility, then it is logical to hypothesize that chemicals that interfere with estrogen receptors may interfere with fertility," Hess said. "Until now, there has been no known function for estrogen in the male. We have had nothing to focus on. Now we can ask the question: Does this chemical or that chemical interfere?"

Potential environmental influence on fertility, such as exposure to pesticides and industrial chemicals, has sparked controversy since 1992, when Copenhagen University researchers concluded that sperm counts were declining around the world. In late November, a team led by Shanna Swan of the California Department of Public Health reached a similar conclusion after reconsidering the data from the 61 studies used in the Copenhagen findings.

The Nature paper focuses on the regulatory role of estrogen-induced fluid reabsorption during the transfer of sperm in fluid from the testis through the efferent ductules -- a series of small tubes that act like kidneys, producing concentrated semen instead of urine -- to the epididymis, where sperm mature and are stored.

"We have found that estrogen regulates fluid reabsorption in the efferent ductules of the male," Hess said. "It is important for the uptake of water, ions and proteins from the fluid that carries the sperm. The efferent ductules are responsible for reabsorbing nearly 90 percent of the water from this fluid. Without the reabsorption, the sperm remain diluted and therefore incapable of normal maturation in the epididymis."

The paper is part of three collaborative studies done over seven years on male estrogen -- funded in part by the U.S. Department of Agriculture and the U. of I.-- by a team that includes Janice Bahr, a professor of physiology, molecular biologist David Bunick and Hess.

In another study, published in the December issue of the Journal of Adrology, the researchers report that the number of genes that express estrogen receptors in the efferent ductules of rats -- when operating normally -- is 3.5 times greater than the estrogen receptor message in the female reproductive tract.

"This means you have a target for estrogen, and there are plenty of targets for the estrogen to bind to," Hess said. "It was surprising to find the protein in such a high concentration. We knew it would be there, but finding so much was unexpected."

The Nature findings resulted from studies of estrogen function in the reproductive tracts of mice, including genetically produced mice whose estrogen receptors are non-functional. As in humans, the mice used in the research had similarities in their estrogen, estrogen receptors and efferent ductules.

Hess, Bahr and Bunick reported in the 1994 Proceedings of the Estrogens in the Environment, that they had found a new source of potential estrogen synthesis in males, in the germ cells of the testis and sperm in the epididymis of mice, rats and chickens. Similar findings have been made in black bears.

When estrogen receptors are knocked out, the fluid "accumulates at the site of production " just as happens when you get a blocked waste pipe and run the tap," writes Richard M. Sharpe of the Medical Research Council Reproductive Biology Unit in Edinburgh, Scotland, in an accompanying "News and Views" article on Hess' findings. "This build-up progressively impairs sperm production because of the increased fluid pressure within the testis."

In 1993, Sharpe theorized that declines in sperm counts might be occurring because of a complex interference with hormones involving the hypothalamus in the brain and the pituitary gland during development of the testis.

Now that the research has provided the first recognized physiological function for estrogen in males, Hess said, the next step in the research is to determine the biochemical action. "We have known that estrogen is present in the male, and in high concentrations in the seminal fluids, but we did not know why it was there," he said. "Now we can focus on the function of fluid reabsorption and on what genes are regulated by the estrogen."

"Estrogen is not only important in the female for fertility, but it also exerts its influence on the male, from birth to death," Hess said. "We can now say that this female hormone is intimately involved in regulating fertility in the male, because if you block the estrogen receptor's function as we've shown here, you will have infertility. It is very likely that this will be a similar finding in humans."

Coauthors of the Nature paper are Hess, Bunick and Bahr, along with Ki-Ho Lee of the U. of I. department of veterinary biosciences; Julia A. Taylor and Dennis B. Lubahn of the departments of biochemistry and child health at the University of Missouri at Columbia; and Kenneth S. Korach of the National Institutes of Health National Institute of Environmental Health Sciences at Research Triangle Park, N.C.

Coauthors of the paper in the Journal of Andrology are Hess, Bunick, Lubahn, Bahr, Daniel H. Gist of the department of biological sciences at the University of Cincinnati, Amy Farrell and Paul S. Cooke of the U. of I. department of veterinary biosciences, and Geoffrey L. Greene of the Ben May Institute for Cancer Research at the University of Chicago.
 
you're slighty wrong

PURPOSE: Testosterone-to-estradiol ratio levels in infertile men improve during treatment with the aromatase inhibitor, testolactone, and resulting changes in semen parameters. We evaluated the effect of anastrozole, a more selective aromatase inhibitor, on the hormonal and semen profiles of infertile men with abnormal baseline testosterone-to-estradiol ratios. MATERIALS AND METHODS: A total of 140 subfertile men with abnormal testosterone-to-estradiol ratios were treated with 100 to 200 mg. testolactone daily or 1 mg. anastrozole daily. Changes in testosterone, estradiol, testosterone-to-estradiol ratios and semen parameters were evaluated during therapy. The effect of obesity, diagnosis of the Klinefelter syndrome, and presence of varicocele and/or history of varicocele repair on treatment results was studied. RESULTS: Men treated with testolactone had an increase in testosterone-to-estradiol ratios during therapy (mean plus or minus standard error of the mean 5.3 +/- 0.2 versus 12.4 +/- 1.1, p <0.001). This change was confirmed in subgroups of men with the Klinefelter syndrome, a history of varicocele repair and those with varicocele. A total of 12 oligospermic men had semen analysis before and during testolactone treatment with an increase in sperm concentration (5.5 versus 11.2 million sperm per ml., p <0.01), motility (14.7% versus 21.0%, p <0.05), morphology (6.5% versus 12.8%, p = 0.05), and motility index (606.3 versus 1685.2 million motile sperm per ejaculate, respectively, p <0.05) appreciated. During anastrozole treatment, similar changes in the testosterone-to-estradiol ratios were seen (7.2 +/- 0.3 versus 18.1 +/- 1.0, respectively, p <0.001). This improvement of hormonal parameters was noted for all subgroups except those patients with the Klinefelter syndrome. A total of 25 oligospermic men with semen analysis before and during anastrozole treatment had an increase in semen volume (2.9 versus 3.5 ml., p <0.05), sperm concentration (5.5 versus 15.6 million sperm per ml., p <0.001) and motility index (832.8 versus 2930.8 million motile sperm per ejaculate, respectively, p <0.005). These changes were similar to those observed in men treated with testolactone. No significant difference in serum testosterone levels during treatment with testolactone and anastrozole was observed. However, the anastrozole treatment group did have a statistically better improvement of serum estradiol concentration and testosterone-to-estradiol ratios (p <0.001). CONCLUSIONS: Men who are infertile with a low serum testosterone-to-estradiol ratio can be treated with an aromatase inhibitor. With treatment, an increase in testosterone-to-estradiol ratio occurred in association with increased semen parameters. Anastrozole and testolactone have similar effects on hormonal profiles and semen analysis. Anastrazole appears to be at least as effective as testolactone for treating men with abnormal testosterone-to-estradiol ratios, except for the subset with the Klinefelter syndrome, who appeared to be more effectively treated with testolactone.

PMID: 11792932 [PubMed - indexed for MEDLINE
 
James Buchanan Brady Urology Foundation and Cornell Institute for Reproductive Medicine, New York Presbyterian Hospital, Weill Medical College of Cornell University, New York, New York, USA.

PURPOSE: We establish whether a subset of infertile men have decreased serum testosterone-to-estradiol ratios and whether this condition can be corrected with an oral aromatase inhibitor. MATERIALS AND METHODS: The serum testosterone-to-estradiol ratios of 63 men with severe male factor infertility or hypergonadotropic hypogonadism (mean follicle-stimulating hormone 21.2 +/- 1.8) were compared with those of an age matched, fertile, control reference group. Of the 63 men 43 were azoospermic with biopsy proved severe male infertility and 20 were oligospermic. The men with the lowest ratios (less than 20th percentile) were treated with 50 to 100 mg of the aromatase inhibitor testolactone orally twice daily. Testosterone-to-estradiol ratios and semen analyses were evaluated during testolactone therapy. RESULTS: Men with severe male infertility had significantly lower testosterone (328 versus 543 ng/dl, p <0.01) and higher estradiol (58.4 versus 43.5 ng/l, p = 0.01) than fertile control reference subjects, resulting in a decreased testosterone-to-estradiol ratio (x10(-1) = 6.9 +/- 0.6 versus 14.5 +/- 1.2, respectively, p <0.01). Of the 45 men treated with testolactone a correction of these abnormalities was seen and ratios (x10(-1)) increased into the normal range (5.0 +/- 0.3 to 12.7 +/- 1.2, p <0.01). Semen analyses were considered evaluable only in men with sperm in the ejaculate before aromatase inhibitor treatment. Semen analyses before and during testolactone treatment revealed significant increases in sperm concentration (16.1 to 28.9 million sperm per ml, p = 0.03) and motility (27.1% to 45.3%, p <0.01) in 12 oligospermic men. CONCLUSIONS: We identified an endocrinopathy in men with severe male factor infertility that is characterized by a decreased serum testosterone-to-estradiol ratio. This ratio can be corrected by aromatase inhibition, resulting in a significant improvement in semen parameters in oligospermic patients.
 
Division of Metabolism, Endocrinology and Nutrition, University of Washington School of Medicine, Seattle, WA 98195-6246, USA.

BACKGROUND: A 29-year-old man presented to a clinic with infertility and hypogonadism in the setting of morbid obesity. On presentation, he had notable gynecomastia and a low testicular volume. The patient's weight was 154 kg and his height was 168 cm (BMI 54.5 kg/m(2)). Before referral to the clinic, the patient had been treated with testosterone therapy for 4 months for hypogonadism. This treatment had caused his initially low sperm concentration to fall to undetectable levels. INVESTIGATIONS: Measurement of reproductive hormone levels, pituitary MRI, and semen analysis. DIAGNOSIS: Infertility secondary to hypogonadotropic hypogonadism and an elevated estrogen:testosterone ratio. MANAGEMENT: Treatment with an aromatase inhibitor, anastrozole, led to normalization of the patient's testosterone, luteinizing hormone and follicle-stimulating hormone levels, suppression of serum estradiol levels, and to normalization of spermatogenesis and fertility.
 
related

Department of Endocrinology, Ghent University Hospital, De Pintelaan 185, 9000 Ghent, Belgium. [email protected]

CONTEXT: Aging in men is associated with a decline in serum testosterone (T) levels. OBJECTIVE: Our objective was to assess whether decreased T in aging might result from increased estradiol (E2) negative feedback on gonadotropin secretion. DESIGN AND SETTING: We conducted a comparative intervention study (2004) in the Outpatient Endocrinology Clinic, Ghent University Hospital. PARTICIPANTS: Participants included healthy young and elderly men (n = 10 vs. 10). INTERVENTIONS: We used placebo and letrozole (2.5 mg/d) for 28 d, separated by 2 wk washout. MAIN OUTCOME MEASURES: We assessed changes in serum levels of free E2, LH, and FSH, free T, SHBG, and gonadotropins response to an i.v. 2.5-microg GnRH bolus. RESULTS: As assessed after 28 d of treatment, letrozole lowered E2 by 46% in the young men (P = 0.002) and 62% in the elderly men (P < 0.001). In both age groups, letrozole, but not placebo, significantly increased LH levels (339 and 323% in the young and the elderly, respectively) and T (146 and 99%, respectively) (P value of young vs. elderly was not significant). Under letrozole, peak LH response to GnRH was 152 and 52% increase from baseline in young and older men, respectively (P = 0.01). CONCLUSIONS: Aromatase inhibition markedly increased basal LH and T levels and the LH response to GnRH in both young and elderly men. The observation of similar to greater LH responses in the young compared with the elderly does not support the hypothesis that increased restraining of LH secretion by endogenous estrogens is instrumental in age-related decline of Leydig cell function.
 
testosterone-estrogen ratio is the key
 
testosterone-estrogen ratio is the key

Yes that is corect.

If the estrogen level in man is lower than 18 picogram per ml, than it can be a problem. I would think that 18 to 20 picograms estrogen per ml would be planti for sperm production.
 
So in otherwords UP My anti-E's so I don't make any munchkins:D
 

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