flax and estrogen/gyno

[gerby]

I've always been a big fan of flax. I mix some flax meal in with my night time yogurt and my middle of the night protein shake. Last week at the store I noticed something on a package of flax meal. It said, "helps maintain healthy estrogen levels." It got me curious as to exactly how flax might affect estrogen. So, I did a google search and came away more confused. Some sources say that the lignans in flax can help "flush out" excess estrogen. This would be great for us bodybuilders, as it would help prevent gyno. Many doctors recommend that their cancer patients take a flax supplement, as the lignans have actually been shown to reduce the size of tumors in some cases where the cells are hormone sensitive. Could flax meal possibly be used as part of a treatment for existing gyno? However, other articles mention flax meal in the same vein as soy, which we all know to be the evil protein that can cause ***** tits and sissy fits. That is, the lignans mimic estrogen, and consuming flax is actually like dosing with exogenous estrogen. A bad thing if we're trying to remain ***** titless. So, I thought I'd throw this little query to the minds here at AM and see what happens.

 

[yeahright]

I've always been a big fan of flax. I mix some flax meal in with my night time yogurt and my middle of the night protein shake. Last week at the store I noticed something on a package of flax meal. It said, "helps maintain healthy estrogen levels." It got me curious as to exactly how flax might affect estrogen. So, I did a google search and came away more confused. Some sources say that the lignans in flax can help "flush out" excess estrogen. This would be great for us bodybuilders, as it would help prevent gyno. Many doctors recommend that their cancer patients take a flax supplement, as the lignans have actually been shown to reduce the size of tumors in some cases where the cells are hormone sensitive. Could flax meal possibly be used as part of a treatment for existing gyno? However, other articles mention flax meal in the same vein as soy, which we all know to be the evil protein that can cause ***** tits and sissy fits. That is, the lignans mimic estrogen, and consuming flax is actually like dosing with exogenous estrogen. A bad thing if we're trying to remain ***** titless. So, I thought I'd throw this little query to the minds here at AM and see what happens.

I don't have an answer but I do believe that I can quickly sum-up what the issue is:

The phytoestrogens in flax bind to estrogen receptors to some degree. The question is whether they bind to estrogen receptors (without activating them) thus blocking estrogen from activating them (like a SERM) or whether they bind to the estrogen receptors and activate them. If the former, then good. If the latter, then bad. Another variation is that they might bind and activate but activate in a less potent way than estrogen (there are actually different "estrogens" which have different potencies and functions in the body). If the flax acts like one of the less potent estrogens and displaces regular body estrogens, then good. If it simply increases the total "estrogen" load in the body, then bad. You might try searching pubmed.com and telling us what you dig up.

 

[porkhide]

Search flax lignands.
Will brink had a nice write up about it.

 

[yeahright]

J Toxicol Environ Health A. 1999 Apr 23;56(8):555-70.Links
Dose, timing, and duration of flaxseed exposure affect reproductive indices and sex hormone levels in rats.
Tou JC, Chen J, Thompson LU.

Department of Nutritional Sciences, University of Toronto, Ontario, Canada.

Flaxseed ingestion produces large amounts of mammalian lignans. Since lignans have weak estrogenic/antiestrogenic properties, the objective of this study was to determine in rats whether exposure to 5% or 10% flaxseed affects sex hormone levels and reproductive indices when given at different developmental stages. Rats were exposed to either a basal diet (control), 5%, or 10% flaxseed diet starting at weaning on postnatal day (PND) 21 or continuously from gestation to PND 132 for lifetime exposure. Compared to the control, exposure to 5% or 10% flaxseed after weaning produced no marked reproductive effects, whereas lifetime flaxseed exposure caused significant changes that differed depending on the dose. In female rats, lifetime exposure to 5% flaxseed affected the reproductive tract as indicated by delayed puberty onset. In contrast, lifetime exposure to 10% flaxseed caused earlier puberty onset, higher relative ovarian weight, higher serum estradiol levels, and lengthened estrous cycles. In male rats, lifetime 10% flaxseed exposure raised serum testosterone and estradiol levels and produced higher relative sex organ weights and prostate cell proliferation. In contrast, lifetime exposure to 5% flaxseed reduced adult relative prostate weight and cell proliferation, suggesting potential protection against prostatic disease, although sex hormone levels were unaffected. In conclusion, flaxseed can potentially alter reproduction, depending on the dose and timing of exposure.

PMID: 10321385 [PubMed - indexed for MEDLINE]

 

[yeahright]

Food Chem Toxicol. 2000 Apr;38(4):325-34.Click here to read Links
The effect of maternal exposure to flaxseed on spermatogenesis in F(1) generation rats.
Sprando RL, Collins TF, Black TN, Olejnik N, Rorie JI, Scott M, Wiesenfeld P, Babu US, O'Donnell M.

Division of Toxicological Research, Center for Food Safety and Applied Nutrition, Food and Drug Administration, 8301 Muirkirk Road, Laurel, MD 20708, USA. [email protected]

Pregnant Sprague-Dawley rats were exposed to a flaxseed (20 or 40%), flaxmeal (13 or 26%) or standard NIH AIN-93 (0% flaxseed control) diet throughout gestation and until their offspring were weaned. After weaning, F(1) generation males were placed in the same diet treatment groups as their mothers for 70 days. Statistically significant differences were not observed between either low-dose or high-dose flaxseed and flaxmeal-treated animals and the 0% flaxseed control animals for testis weights, homogenization resistant spermatid counts, daily sperm production rates, epididymal weights, seminal vesicle weights, seminiferous tubule fluid testosterone concentrations and the percentage of sperm abnormalities. The following statistically significant differences were observed when treated groups and the 0% flaxseed control groups were compared: (1) increases in serum LH in the 20% and 40% flaxseed treatment groups and in serum LH and testosterone in the 26% flaxmeal treatment group; (2) increases in the cauda epididymal weight from the 20% and 40% flaxseed groups; (3) increases in cauda epididymal sperm numbers/g epididymis from the 20% and 40% flaxseed and the 13% and 26% flaxmeal treatment groups; (4) a decrease in prostatic weight from the 20% flaxseed and 13% and 26% flaxmeal treatment groups. Prostate weight in the 40% flaxseed treatment group was lower but not statistically significantly different than the 0% flaxseed control group. Histological effects on spermatogenesis were not observed in either the control group, flaxmeal or the flaxseed treated groups.

PMID: 10722886 [PubMed - indexed for MEDLINE]

 

[yeahright]

Food Chem Toxicol. 2000 Oct;38(10):887-92.Click here to read Links
Testing the potential of flaxseed to affect spermatogenesis: morphometry.
Sprando RL, Collins TF, Wiesenfeld P, Babu US, Rees C, Black T, Olejnik N, Rorie J.

Division of Toxicological Research, Center for Food Safety Applied Nutrition, Food and Drug Administration, Beltsville, MD 20708, USA. [email protected]

Quantitative information was collected on male reproductive effects of maternal and postnatal dietary exposure to flaxseed (20 or 40%), flaxmeal (13 or 26%) or standard NIH AIN-93 feed (0% flaxseed control). Measurements were made on the testes of F1 generation males rats (1) whose mothers were exposed to the diets designated above, and (2) who, after weaning, were placed on the same diet as their mothers for an additional 70 days. The seminiferous tubules comprised 86%, 84%, 84%, 84% and 85% of the total testis volume while the interstitial space comprised 12%, 14%, 14%, 14%, 13% of the total testis volume for the 0% flaxseed/flaxmeal, 20% flaxseed, 13% flaxmeal, 40% flaxseed and 26% flaxmeal groups, respectively. Statistically significant decreases in the absolute volume of the seminiferous tubules were observed in the 20% and 40% flaxseed-treated groups when these groups were compared to controls. Borderline statistically significant differences were also observed when Sertoli cell nucleolar number per tubular cross-section were compared in the 13% flaxmeal and 20% flaxseed treatment groups. These effects were not considered biologically significant because other parameters of male reproductive function appeared normal. Overall, the quantitative information obtained suggests that exposure to flaxseed/flaxmeal at the doses used in the present study does not adversely affect testis structure or spermatogenesis in the rat.

PMID: 11039322 [PubMed - indexed for MEDLINE]

 

[yeahright]

Endocrinology. 2000 Oct;141(10):3898-907.Click here to read Links
Comparative effects of neonatal exposure of male rats to potent and weak (environmental) estrogens on spermatogenesis at puberty and the relationship to adult testis size and fertility: evidence for stimulatory effects of low estrogen levels.
Atanassova N, McKinnell C, Turner KJ, Walker M, Fisher JS, Morley M, Millar MR, Groome NP, Sharpe RM.

Medical Research Council Human Reproductive Sciences Unit, Center for Reproductive Biology, Edinburgh, Scotland, United Kingdom.

This study investigated whether neonatal exposure of male rats to estrogenic compounds altered pubertal spermatogenesis (days 18 and 25) and whether the changes observed resulted in long-term changes in testis size, mating, or fertility (days 90-100). Rats were treated neonatally with a range of doses (0.01-10 microg) of diethylstilbestrol (DES; administered on alternate days from days 2-12), a high dose of octylphenol (OP; 2 mg administered daily from days 2-12) or bisphenol A (Bis-A; 0.5 mg administered daily from days 2-12), or vehicle, while maintained on a standard soy-containing diet. The effect on the same parameters of rearing control animals on a soy-free diet was also assessed as was the effect of administering such animals genistein (4 mg/kg/day daily from days 2-18). Testis weight, seminiferous tubule lumen formation, the germ cell apoptotic index (apoptotic/viable germ cell nuclear volume), and spermatocyte nuclear volume per unit Sertoli cell nuclear volume were used to characterize pubertal spermatogenesis. Compared with (soy-fed) controls, DES administration caused dose-dependent retardation of pubertal spermatogenesis on day 18, as evidenced by decreases in testis weight, lumen formation, and spermatocyte nuclear volume per unit Sertoli cell and elevation of the germ cell apoptotic index. However, the two lowest doses of DES (0.1 and 0.01 microg) significantly increased spermatocyte nuclear volume per unit Sertoli cell. Similarly, treatment with either OP or Bis-A significantly advanced this and some of the other aspects of pubertal spermatogenesis. Maintenance of control animals on a soy-free diet also significantly advanced lumen formation and spermatocyte nuclear volume per unit Sertoli cell compared with controls fed a soy-containing diet. Administration of genistein reversed the stimulatory effects of a soy-free diet and significantly retarded most measures of pubertal spermatogenesis. In general, plasma FSH levels in the treatment groups changed in parallel to the spermatogenic changes (reduced when pubertal spermatogenesis retarded, increased when pubertal spermatogenesis advanced). By day 25, although the changes in FSH levels largely persisted, all of the stimulatory effects on spermatogenesis seen on day 18 in the various treatment groups were no longer evident. In adulthood, testis weight was decreased dose dependently in rats treated neonatally with DES, but only the lowest dose group (0.01 microg) showed evidence of mating (3 of 6) and normal fertility (3 litters). Animals treated neonatally with OP or Bis-A had normal or increased (Bis-A) testis weights and exhibited reasonably normal mating/fertility. Animals fed a soy-free diet had significantly larger testes than controls fed a soy-containing diet, and this difference was confirmed in a much larger study of more than 24 litters, which also showed a significant decrease in plasma FSH levels and a significant increase in body weight in the males kept on a soy-free diet. Neonatal treatment with genistein did not alter adult testis weight, and although most males exhibited normal mating and fertility, a minority did not mate or were infertile. It is concluded that 1) neonatal exposure of rats to low levels of estrogens can advance the first wave of spermatogenesis at puberty, although it is unclear whether this is due to direct effects of the estrogen or to associated elevation of FSH levels; 2) the effect of high doses of OP and Bis-A on these processes is essentially benign; and 3) the presence or absence of soy or genistein in the diet has significant short-term (pubertal spermatogenesis) and long-term (body weight, testis size, FSH levels, and possibly mating) effects on males.

PMID: 11014247 [PubMed - indexed for MEDLINE]

 

[Will Brink]

Search flax lignands.
Will brink had a nice write up about it.

Of interest perhaps:

Flaxseed for hot flashes
Medical Studies/Trials
Published: Thursday, 30-Aug-2007

Data from a new Mayo Clinic study suggest that dietary therapy using flaxseed can decrease hot flashes in postmenopausal women who do not take estrogen.

The findings from the pilot study are published in the summer 2007 issue of the Journal of the Society for Integrative Oncology.

A hot flash is often described as a flush of intense warmth across much of the body that may be accompanied by sweating, reddening of the skin, or, occasionally, cold shivers. Hot flashes occur in varying frequency and duration, even during sleep, and often cause or accompany sleep deprivation, anxiety and irritability.

"Hot flashes are a bothersome issue for women experiencing menopause," says Sandhya Pruthi, M.D., Mayo Clinic breast health specialist and the study's primary investigator. "We hope to find more effective nonhormonal options to assist women, and flaxseed looks promising."

Although until recently hormone replacement therapy was the most commonly prescribed treatment for hot flashes, unwanted side effects have led to the search for nonhormonal solutions. Several effective nonhormonal drug therapies have been identified, but they are not always effective, and not all women can use them because of side effects. These limitations have led researchers to explore non-drug agents. They have studied a variety of herbal and dietary supplements in randomized, placebo-controlled trials, including vitamin E, black cohosh and soy, but none has shown to produce any significant reduction in frequency or severity of hot flashes.

The 29 participants in Mayo's clinical trial were women with bothersome hot flashes who did not want to take estrogen because of a perceived increased risk of breast cancer. They also had not received (in the preceding four weeks) antineoplastic chemotherapy, androgens, hormonal agents, or other herbal supplements, including soy. Some patients did not complete the trial, but full data for six weeks of flaxseed therapy, consisting of 40 grams of crushed flaxseed ingested daily, was obtained from 21 of them.

Participants were asked questions that the researchers translated into a hot flash score -- a combined measure of frequency and severity. The frequency of hot flashes decreased 50 percent over six weeks, and the overall hot flash score decreased an average 57 percent for the women who completed the trial. Participants also reported improvements in mood, joint or muscle pain, chills and sweating; which significantly improved their health-related quality of life.

"We are quite pleased with the improvements noted by these women in their quality of life," says Dr. Pruthi. "Not only does flaxseed seem to alleviate hot flashes, but it appears to have overall health and psychological benefits as well."

Dr. Pruthi's team chose to research flaxseed because it is a phytoestrogen (plant-based estrogen source). Flaxseed contains lignans and omega-3 fatty acids. Lignans are antioxidants with weak estrogen-emulating characteristics, and have some anti-cancer effects. Flaxseed also appears to have anti-estrogen properties and has been shown in some recent research trials to decrease breast cancer risk. The researchers hypothesized that patients taking flaxseed might gain some relief for hot flashes.

This pilot trial was designed to determine the effectiveness of flaxseed in alleviating hot flashes and identify possible side effects. Dr. Pruthi cautions that the results are preliminary and taking flaxseed may not give relief to every woman suffering hot flashes.

"While results were promising, we have more research to conduct," she says. "Oftentimes, pilot studies show promising results that upon further study in a large, randomized placebo-controlled study turn out to be much less remarkable."

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