About S-Equol

S-equol and Menopause

The ability of S-equol to play a role in the treatment of estrogen-mediated conditions was first proposed in 1984.13 Studies of postmenopausal women documented that those women who can produce equol after consuming soy had milder menopause symptoms than those who were unable to produce equol.9,14

Not everyone can produce S-equol after eating soy. Therefore, Pharmavite LLC, a subsidiary of Otsuka Pharmaceutical Co., Ltd., developed a rigorous clinical trials program to study a nutritional supplement containing S-equol to help manage menopausal symptoms. Additionally, researchers are studying S-equol for other potential health benefits.

S-equol Production in Humans

Equol producers vary around the worldS-equol [7-hydroxy-3-(49-hydroxyphenyl)-chroman] is a metabolite of the soy isoflavone daidzein. S-equol is produced by intestinal bacteria in some, but not in all, humans after soy consumption. S-equol is not of plant origin, therefore, as it is exclusively a product of the bacterial transformation of daidzein.

About 50 percent of Asians and 20 to 30 percent of North Americans and Europeans, who in general consume less soy than Asians, have the ability to produce S-equol.2,3,7,8 The ability to produce S-equol after soy consumption depends on the types of bacteria present in the large intestine.

In research, determining if a person is a S-equol producer can be done with a soy challenge, which involves a person drinking two 240 milliliter glasses of soy milk per day for three days in addition to their standard diet. The person can not have had antibiotics for at least three months prior to the challenge. On the fourth day, the person's urine is measured for the presence and concentration of S-equol.7

S-equol Biological Activity

The molecular and physical structure of S-equol is similar to that of 17-estradiol,11 the naturally occurring main sex hormone found in women, also referred to as estrogen. When comparing their relative affinities to bind to the human estrogen receptor alpha (ERα) S-equol has only about 1 percent of the affinity possessed by 17-estradiol. S-equol has a stronger affinity for the human estrogen receptor beta (ERβ), yet this affinity is just 20 percent of estradiol's affinity for ERβ. The preferential binding of S-equol to ERβ, compared to ERα and to estradiol's, indicates that S-equol shares some, but not all, of the characteristics of a selective ER modulator (SERM).12