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Isoflavones

Isoflavones belong to the ‘phyto-estrogens’, plant compounds with a chemical structure similar to the endogenous estrogen, oestradiol (see picture). The importance of this structural similarity and its possible favourable effect on hormone-dependent cancers was first discussed in the 1980s. Phyto-estrogens are very common in plants. Large differences however exist in the concentration and type of phyto-estrogens according to the plant, growing conditions etc.

In food research 3 groups of phyto-estrogens get particular attention: isoflavones, coumestans and lignans.

Lignans occur mainly in cereals, fibre, fruit and vegetables under the form of precursors. These are metabolised by the gut flora to enterolactone and enterodiol. Flaxseed is a rich source of lignans.
Coumestans are found mostly in alfa-alfa and animal feed. The content is however strongly dependent upon growing conditions, such as moisture.

The soya bean is unique as it contains the highest levels of isoflavones. Soya contains three types of isoflavones; genistein, daidzein and to a lesser extent glycetein. They appear mostly in the form of sugar conjugates called b-glucoside conjugates1,2. Bioavailability which is crucial for clinical effectiveness of soya isoflavones is dependent on intestinal metabolism because the intact b-glucosides cannot be absorbed into the bloodstream2. Hydrolysis of these sugar groups is an essential first step for absorption and activation of their biological activity and this occurs along the length of the intestine by the action of specific b-glucosidase enzymes located on the mucosal membrane3. Further, metabolic transformation of soya isoflavones takes place by the action of intestinal bacteria leading to the formation of many isoflavone metabolites4,6. One of these metabolites, equol, has been found to possess even greater biological activity than its precursor in soya, daidzin7.

Isoflavones have a low estrogenic potency; 1/10 000 to 1/140 000 of the activity of oestradiol, the major endogenous estrogen. While isoflavones, can behave as estrogen agonists, they may also antagonize the action of estrogens in certain tissues. The reason for this is complex but partly explained by a unique property of isoflavones. Unlike the body’s steroidal estrogens, isoflavones have selective estrogen receptor modulatory (SERM) action7 and show a higher affinity for the estrogen receptor subtype ERb than for ERa 8. Estrogens on the other hand bind with equal affinity to both ERa and ERb. A further distinction between estrogens and isoflavones relates to their conformational fit into the pocket and binding site of the dimerized estrogen receptor9. Isoflavones such as genistein differ significantly from estradiol in this regard and this from that influences the recruitment of co-activators or co-repressors to the complex, resulting in differences in transcriptional activity. Isoflavones appear to show binding similarities to the SERM, raloxifene10 and not to estradiol. In tissues where there is an abundance of ERb, such as bone, brain, vascular endothelium and bladder, soya isoflavones are likely to exert estrogen agonist action while in tissues rich in ERa it is probable that isoflavones antagonize the action of estrogen. The presence of absence of estrogens and the receptor number and distribution may also influence the overall action. The picture is by no means simple but what is clear is that soya isoflavones should not be viewed as being comparable estrogens.
They appear to be without the negative effects of estrogens used in hormone therapy, which has invoked so much fear in women due to the recent negative findings from the large clinical studies of hormone replacement therapy.

References:

  1. Coward L, Barnes NC, Setchell KDR, Barnes S. Genistein and daidzein, and their b-glycosides conjugates: anti-tumor isoflavones in soyabean foods from American and Asian diets. Journal of Agricultural and Food Chemistry 1993;41:1961-1967.
  2. Setchell KDR, Cole SJ. Variations in isoflavone levels in soya foods and soya protein isolates and issues related to isoflavone databases and food labeling. Journal of Agricultural & Food Chemistry 2003;51:4146-55.
  3. Day AJ, DuPont MS, Ridley S, Rhodes M, Rhodes MJ, Morgan MR, Williamson G. Deglycosylation of flavonoid and isoflavonoid glycosides by human small intestine and liver beta-glucosidase activity. FEBS Letters 1998;436:71-5.
  4. Joannou GE, Kelly GE, Reeder AY, Waring M, Nelson C. A urinary profile study of dietary phytoestrogens. The identification and mode of metabolism of new isoflavonoids. Journal of Steroid Biochemistry & Molecular Biology 1995;54:167-84.
  5. Heinonen S, Wahala K, Adlercreutz H. Identification of isoflavone metabolites dihydrodaidzein, dihydrogenistein, 6'-OH-O-dma, and cis-4-OH-equol in human urine by gas chromatography-mass spectroscopy using authentic reference compounds. Analytical Biochemistry 1999;274:211-9.
  6. Bannwart C, Adlercreutz H, Fotsis T, Wahala K, Hase T, Brunow G. Identification of O-desmethylangolensin, a metabolite of daidzein and of matairesinol, one likely plant presursor of the animal lignan enterolactone in human urine. Finn Chem Lett 1984;4-5:120-125.
  7. Brzezinski A, Debi A. Phytoestrogens: the "natural" selective estrogen receptor modulators? European Journal of Obstetrics, Gynecology, & Reproductive Biology 1999;85:47-51.
  8. Kuiper GG, Lemmen JG, Carlsson B, Corton JC, Safe SH, van der Saag PT, van der Burg B, Gustafsson JA. Interaction of estrogenic chemicals and phytoestrogens with estrogen receptor beta. Endocrinology 1998;139:4252-63.
  9. Pike AC, Brzozowski AM, Hubbard RE, Bonn T, Thorsell AG, Engstrom O, Ljunggren J, Gustafsson JA, Carlquist M. Structure of the ligand-binding domain of oestrogen receptor beta in the presence of a partial agonist and a full antagonist. Embo J 1999;18:4608-18.
  10. Jordan VC, Morrow M. Tamoxifen, raloxifene, and the prevention of breast cancer. Endocr Rev 1999;20:253-78.