The estrogen-like structure of phytoestrogens enables them to bind to estrogen receptors in humans. They have been shown to bind to both ER alpha as well as ER beta, but have a higher affinity for ER beta. The phytoestrogens are weaker than endogenous estrogens and can exhibit both estrogenic and antiestrogenic effects depending on the individual’s amount of circulating endogenous estrogens and the type and number of estrogen receptors in the target tissue. For example, brain and bone tend to have higher numbers of ER beta. On the other hand, although they are relatively weak estrogens, they are generally present in the body in much greater amounts than are the endogenous estrogens. Another hormonal effect is the stimulation of sex hormone binding globulin synthesis. Higher amounts of SHBG increases the chances that endogenous estrogen will be bound and less bioavailable to target tissues. Hormonal effects are not the only mechanism by which phytoestrogens can act. Other mechanisms by which phytoestrogens could affect carcinogenesis include inhibition of angiogenesis and cell cycle progression, aromatase enzyme inhibition, and antioxidant effects.