Official websites use. Share sensitive information only on official, secure websites. Estrogens have significant direct and indirect effects on prostate gland development and homeostasis and have been long suspected in playing a role in the etiology of prostatic diseases.
The present review examines the evidence for a role of estrogens and specific estrogen receptors in prostate growth, differentiation and disease states including prostatitis, benign prostatic hyperplasia BPH and cancer and discusses potential therapeutic strategies for growth regulation via these pathways. While low levels of circulating estrogens are present throughout life in males, there are two time periods, during in utero development and aging, when males are exposed to relatively higher levels of circulating estradiol which have been shown to impact the prostate gland.
This relative increase in estradiol has been shown to directly stimulate extensive squamous metaplasia within the developing prostatic epithelium which regresses immediately after birth when estrogen levels rapidly decline[ 3 , 4 ]. Although the natural role for estrogens during prostatic development is unclear, it has been proposed that excessive estrogenization during prostatic development may contribute to the high incidence of BPH and prostatic carcinoma currently observed in the aging male population [ 5 ].
African-American men have a two-fold increased risk of prostatic carcinoma as compared to their Caucasian counterparts and it has been suggested that this is related, in part, to elevated levels of maternal estrogens during early gestation in this population [ 6 , 7 ].
Indicators of pregnancy estrogen levels such as length of gestation, pre-eclampsia and jaundice indicate a significant correlation between higher estrogen levels and prostate cancer risk [ 8 , 9 ]. In addition, maternal exposure to diethylstilbestrol DES , a potent synthetic estrogen agonist, during pregnancy was found to result in more extensive prostatic squamous metaplasia in male offspring than observed with maternal estradiol alone [ 10 ].
