Lifestyle and Environment Environmental Exposures
RRM Academy Synopsis
Estrogen-mimicking chemicals disrupt hormones through many routes
A 2013 review of lab, animal and cell studies describes several ways that chemicals that mimic estrogen in food and the environment disrupt hormone signaling. The authors also sum up the tests that detect them.
Key Findings
- Estrogen mimics can disrupt hormone-making enzymes, estrogen breakdown and hormone transport, and can bind estrogen receptors directly.
- The plant estrogen genistein binds estrogen receptor beta with a 20-fold superior affinity to its affinity for estrogen receptor alpha.
- Estrogen mimics generally act at 100–1000 folds greater concentrations than estradiol, yet can add to or amplify estradiol's effect, alone or in mixtures.
- Children exposed in the womb to diethylstilbestrol, once prescribed to prevent miscarriage, developed serious reproductive deformities and disorders, both male and female.
- One mouse study reported more uterine adenocarcinoma in F2 female descendants of mice given diethylstilbestrol developmentally. Developmental vinclozolin exposure was reported to lower fertility in male animals through four generations.
Interpretation
This narrative review gathers lab evidence from cell cultures, yeast, fish and rodent studies, plus some human data, on how estrogen-mimicking chemicals disrupt hormone signaling. In one human study, chlordecone blood levels tracked with higher prostate cancer risk. The authors say cadmium's exact mechanism is still unclear. The findings support larger studies of these chemicals across generations and in humans.
RRM Context
Restorative reproductive medicine looks for root causes in both partners. The review offers molecular biology for one candidate cause: estrogen-mimicking chemicals. Estrogen receptors sit in the ovary, uterus and breast. They also sit in the testicle and prostate. The shared biology matters for men and women alike.
Abstract
In all vertebrate species, estrogens play a crucial role in the development, growth, and function of reproductive and nonreproductive tissues. A large number of natural or synthetic chemicals present in the environment and diet can interfere with estrogen signaling; these chemicals are called endocrine disrupting chemicals (EDCs) or xenoestrogens. Some of these compounds have been shown to induce adverse effects on human and animal health, and some compounds are suspected to contribute to diverse disease development. Because xenoestrogens have varying sources and structures and could act in additive or synergistic effects when combined, they have multiple mechanisms of action. Consequently, an important panel of in vivo and in vitro bioassays and chemical analytical tools was used to screen, evaluate, and characterize the potential impacts of these compounds on humans and animals. In this paper, we discuss different molecular actions of some of the major xenoestrogens found in food or the environment, and we summarize the current models used to evaluate environmental estrogens.
