(16-03-2016, 07:40 PM)ellacraig Wrote: Lotus.. You took the boobies away..(avatar)..
Anyway is this correct please?....
3. Introduce estrogen-metabolizing foods
One easy way to do so is by adding two tablespoons of ground flaxseed per day.
Flaxseed has special powers not only to suppress estradiol production, but it also nudges estradiol metabolism into a positive direction by generating a higher ratio of the protective metabolite 2-hydroxy-estrone versus the more harmful 16-hydroxy-estrone.
Ella,
Much debate in the science world about 2-OH & 16a-OH whether there's truth to the theory, my opinion is both have a high affinity for estrogen receptor (alpha), 2-OH is less significant and 16a-OH is the harmful metabolite. I would go with DIM, instead of flaxseed, and for a couple of reasons, flaxseed (though healthy) inhibits aromatase, DIM blocks androgen receptors,( by how much?, not sure yet), and DIM shifts 16a-OH out of the system. So, as the debate goes on, one must judge for themselves based on the different science studies..........aka, be objective.
......
From the Townsend letter:
Flaxseed consumption would not reduce risk of breast cancer according to this theory as it increases 16a levels, Sturgeon et al. reported in 2010. They fed 43 postmenopausal women 7.5 g/day of ground flaxseed for 6 weeks, and then increased the dose to 15 g/day for an additional 6 weeks. There was no significant change in 2-hydroxyestrone excretion in the urine. The urinary 2:16 ratio was lower at the end of 12 weeks compared with baseline. The authors write, "Based on the current paradigm of the effects of estrogen metabolism on breast cancer risk, the regimen of dietary flaxseed intake used in this study did not appear to favorably alter breast cancer risk through shifts in estrogen metabolism pathways in postmenopausal women."23 In other words, flaxseed meal shouldn't be good for breast cancer risk.
http://www.townsendletter.com/Jan2013/estrogen0113.html
Circulating 2-hydroxy and 16-α hydroxy estrone levels and risk of breast cancer among postmenopausal women
data do not support the hypothesized inverse associations with 2-OH estrone and the 2:16α-OH estrone ratio nor the hypothesized positive association with 16α-OH estrone. The significant positive associations with 2-OH estrone and the 2:16 OH estrone ratio among women with ER-/PR- tumors needs to be replicated in future studies.
http://www.ncbi.nlm.nih.gov/pmc/articles...s52956.pdf
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On another note, DHEA is the main androgen produced in women, interesting is what alcohol does to DHEA in postmenopausal women: (smoking too).
The Association of Plasma Androgen Levels with Breast, Ovarian, and Endometrial Cancer Risk Factors Among Postmenopausal Women
Abstract
Although androgens may play an etiologic role in breast, ovarian, and endometrial cancers, little is known about factors that influence circulating androgen levels. We conducted a cross-sectional analysis among 646 postmenopausal women in the Nurses' Health Study to examine associations between adult risk factors for cancer, including the Rosner/Colditz breast cancer risk score, and plasma levels of testosterone, free testosterone, androstenedione, dehydroepiandrosterone (DHEA), and DHEA sulfate (DHEAS). All analyses were adjusted for age, laboratory batch, and other cancer risk factors. Free testosterone levels were 79% higher among women with a BMI of ≥30 vs. <22 kg/m2 (p-trend<0.01) and 25% higher among women with a waist circumference of >89 vs. ≤ 74 cm (p-trend=0.02).
Consuming >30 grams of alcohol a day vs. none was associated with a 31% increase in DHEA and 59% increase in DHEAS levels (p-trend=0.01 and <0.01, respectively). Smokers of ≥25 cigarettes per day had 35% higher androstenedione and 44% higher testosterone levels than never smokers (p-value, F-test=0.03 and 0.01, respectively). No significant associations were observed for height or time since menopause with any androgen. Testosterone and free testosterone levels were approximately 30% lower among women with a hysterectomy vs. without (both p-values<0.01). Overall breast cancer risk was not associated with any of the androgens. Thus, several risk factors, including body size, alcohol intake, smoking, and hysterectomy, were related to androgen levels among postmenopausal women, while others, including height and time since menopause, were not. Future studies are needed to clarify further which lifestyle factors modulate androgen levels.