A small number of in-vitro studies have investigated the cytotoxic effects of enterodiol and enterodiol on cancer cells. In one study, enterolactone inhibited proliferation of human breast cancer cells by about 75 percent at 33 mM.77 In another, enterolactone decreased proliferation of four human colon cancer cells lines at 50 to 100 mM, and it was more than twice as effective as enterodiol.72 One other study reported that enterodiol was not effective against two human leukemia cell lines.66 From these two studies, it would appear that enterolactone might be more potent than enterodiol in some situations. At least one in-vitro study reported that normal cells were not adversely affected by mammalian lignans; only high concentrations (about 330 mM) of enterolactone were cytotoxic to normal human lympho-cytes.91
At lower concentrations, enterolactone stimulated proliferation of estrogen-dependent cancers, as seen in three studies on human breast cancer cells at concentrations below about 10 mM; above 10 to 20 mM, enterolactone inhibited cell proliferation.73,74,76 It is uncertain if this stimulatory effect would appear in vivo, since one study reported that enterolactone, in the presence of estrogen, did not stimulate the proliferation of estrogen-dependent human breast cancer cells.75 This is not unlike the effects of flavonoids discussed in Chapter 19, and it seems likely that the estrogenic effect of enterolactone and en-terodiol is weaker than that of genistein. More research is needed, but it does not appear that flaxseed would be contraindicated in patients with estrogen-dependent cancers, especially if combined with other anticancer compounds.
Animal studies have reported that flaxseed can reduce cancer risk as well as the volume of established tumors. In one study, a 5 percent flaxseed diet given to rats decreased the number of breast tumors induced by a high fat diet and a carcinogen; urinary enterodiol and enter-olactone excretion increased.83 In another study, oral administration of SD at about 8 mg/kg (equivalent to a 5 percent flaxseed diet) inhibited growth of established breast cancer in rats during the late stages of carcino-genesis (greater than 50 percent reduction in tumor volume). This inhibitory effect correlated with the degree of urinary lignan excretion, indicating that flax lignans may have been partly responsible.92,93 A 5 percent flax-seed diet also reduced the lung metastasis of melanoma cells injected into mice, as well as tumor volumes.94 In another study with melanoma cells, oral administration of SD also reduced the number of lung metastases in mice. Again, tumor volumes were decreased.79 The 5 percent flaxseed diet used in these studies (3.8 g/kg in rats and 6 g/kg in mice) is roughly equivalent to a human flaxseed dose of 60 grams per day, which provides about 60 milligrams of SECO.
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