Effect of Flaxseed Consumption on Urinary Levels of Estrogen Metabolites in Postmenopausal Women.

Key Findings:

The purpose of this study was to examine the effects of dietary flaxseed on urinary estrogen metabolites. The metabolism of estrone (E1) and estradiol (E2) occurs through three major competitive pathways: one involves 16α-hydroxylation to 16α-hyroxyestrone (16α-OHE1) and 16α-hydroxyestradiol (16α-OHE2); the second leads to 2-OHE1 and 2-OHE2; and a third leads to 4-OHE1 and 4-OHE2.  A reduction in the excretion ratio of estradiol (E2) / 16α-hydroxyestradiol (16α-OHE2) followed 12-wk flaxseed intervention. However, flaxseed intake was not associated with a decline in the more optimal 2-hydroxestrogen metabolites as has been observed in other flaxseed studies. It is still to be determined what the optimal estrogen metabolism pattern should be to reduce the risk of breast cancer.

ABSTRACT:

Flaxseed is a rich source of dietary lignans. It has been hypothesized that lignans may decrease breast cancer risk through modulation of endogenous hormone levels. The aim of this study was to determine the effect of flaxseed supplementation on urinary levels of estrogen metabolites that may be involved in the development of breast cancer. Forty-three postmenopausal women participated in this 12-wk preintervention–postintervention study. Participants consumed 7.5 g/day of ground flaxseed for 6 wk, followed by 15 g/day for an additional 6 wk. The mean urinary level of 16α–hydroxyestrone (16α-OHE1) was higher at the end of 12 wk compared to baseline (change of 1.32 ug/day, P = 0.02). There was no significant change in 2-OHE1 excretion. The mean urinary level of the 2-OHE1/16α-OHE1 ratio was lower at the end of 12 wk compared to baseline (change of −1.1, P = 0.02).Mean urinary excretion of 2-methoxyestradiol was also lower at 12 wk than at baseline (P = 0.03). 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. (Author’s abstract)