Hormone blocker switches on hair growth.

Though best known as the primary female hormone, estrogen plays a variety of roles in both sexes. One such role, at least in mice, now appears to be the ability to keep hair growth in a dormant state, a new study finds. A compound that blocks estrogen's effect can jump-start arrested hair growth.

If the same estrogenic control of hair growth occurs in humans, says Robert C. Smart, a toxicologist at North Carolina State University in Raleigh who led the study, these findings may suggest new therapies for a range of conditions, from hair loss due to chemotherapy or male pattern baldness to the excessive growth of unwanted hair on women.

Many studies have linked excessive hair growth to an overabundance of male sex hormones and have attributed hair loss to, ironically, increased production of an especially active androgen. Several antibalding drugs now under development seek to block a man's production of that androgen. The idea that a female sex hormone might play a pivotal role emerged while Smart's team was investigating estrogen's role in the carcinogenicity of a pesticide.

In their study, Smart and his colleagues shaved the backs of 6-week-old mice, then applied either estrogen or an estrogen blocker twice a week for 10 weeks. The blocker latches onto, but fails to activate, the same cellular receptors to which estrogen binds. Estrogen cannot attach to the blocked receptors and therefore cannot activate them.

The mice treated with estrogen remained nearly hairless throughout the trial, while those given the blocker grew a full coat within 4 weeks, the researchers report in the Oct. 29 Proceedings of the National Academy of Sciences. In contrast, only 20 percent of the shorn mice given neither drug had regained a full coat of hair by 4 weeks; most took at least 50 percent longer.

To learn more about estrogen's role in hair growth, the researchers looked for receptors on skin cells. Each strand of hair emerges from a follicle that undergoes periodic cycles of production and rest. After each rest period, the follicle degenerates and is remodeled. Dermal papillae orchestrate the cycling. Smart's group found that estrogen receptors appear in these dermal papillae throughout the follicle's resting phase, making them sensitive to estrogen. The receptors gradually disappear during the growth phase.

Ulrike Lichti of the National Cancer Institute in Bethesda, Md., finds these results "very interesting, because at the moment we know very little about endogenous signals that could control the hair cycle."

Because the body can convert androgens to estrogens, observes endocrinologist John J. Wysolmerski of Yale University, this study raises the question of whether hair growth effects formerly attributed to androgens "might actually trace to estrogens converted locally from those androgens."