Urinary Lignan and Isoflavonoid Excretion in Premenopausal Women Consuming Flaxseed Powder.

January 1, 1994 Human Health and Nutrition Data 0 Comments

Urinary Lignan and Isoflavonoid Excretion in Premenopausal Women Consuming Flaxseed Powder.

Year: 1994
Authors: J W Lampe, M C Martini, M S Kurzer, H Adlercreutz, J L Slavin.
Publication Name: Am. J. Clin. Nutr.
Publication Details: Volume 60; 122.


Lignans and isoflavonoids may alter steroid hormone metabolism but data on these effects in humans is lacking. SDG, the major lignan precursor in flaxseed, is metabolized to enterodiol which is then oxidized to enterolactone (EL). EL can also be formed directly from another flaxseed lignan, matairesinol (MS). Changes in the synthesis of these lignans can be measured in the urine. The objective of the present study was to assess the effects of flaxseed consumption on urinary lignan and isoflavonoid excretion in healthy premenopausal women and to compare urinary lignan and isoflavonoid excretion in the follicular and luteal phases of the menstrual cycle. Eighteen women consumed their usual omnivorous diets for three menstrual cycles and their usual diets supplemented with flaxseed powder (10 g/d) for three cycles in a randomized, crossover design. They were instructed to avoid dietary sources of soy and flaxseed products. Three-day urine samples from follicular and luteal phases were analyzed for lignans and isoflavonoids by isotope-dilution gas chromatography—mass spectrometry. Excretion of the lignans enterodiol and enterolactone significantly increased following FS supplementation from 1.09 +/- 1.08 and 3.16 +/- 1.47, to 19.48 +/- 1.10 and 27.79 +/- 1.50 mmol/d, respectively. Marked variation in enterodiol and enterolactone excretion, ranging from 3 to 285 – fold increases, was noted among subjects in response to flaxseed feeding. This variation may be due to uncontrollable factors including genetics, types and levels of intestinal flora, background diet, health and hormonal status. There were no differences in excretion of isoflavonoids (daidzein, genistein, equol, and O-desmethyl-angolensin) or the lignan MS following the flaxseed supplementation. The lack of change in MS excretion with flaxseed feeding is consistent with evidence indicating that SDG is the major lignan precursor found in flaxseed. The authors speculated that large amounts of dietary lignans may compete with isoflavonoids for intestinal metabolism. Increased lignan intake may have also enhanced microbial enzyme activity. Lignan excretion was not altered by phase of menstrual cycle which may have been due to subject-to-subject variation and/or the use of a 3-day pooled urine sample which may not have been adequate for monitoring menstrual cycle changes in lignan excretion. Lignan excretion was also not affected by the duration of flaxseed consumption. The authors indicate that their results suggest that daily intake of lignans, rather than intermittent consumption, would be necessary to maintain higher circulating plasma lignan concentrations.

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