Smoking, alpha 1-antitrypsin and decreased fertility in women
Ashley, M.J.
Medical Hypotheses 22(3): 277-285
1987
ISSN/ISBN: 0306-9877 PMID: 3495719 DOI: 10.1016/0306-9877(87)90192-7Document Number: 364604
Despite epidemiological evidence that smoking in women is associated with decreased fertility, the biological mechanisms that underlie this association have not been fully explored. For the 1st time, this paper raises the hypothesis that smoking-induced increases in serum alpha-1-antitrypsin (A1AT) result in higher levels of A1AT in genital secretions, including those at midcycle, thereby compromising fertility. Low midcycle levels of A1AT appear to favor fertility by facilitating sperm migration and/or penetration. Numerous studies of A1AT deficient women have provided supportive evidence for a role for A1AT in fertility, specifically evidence of enhanced fertility. A deficiency of MM x MM genotype combinations in families selected for large size has been documented. Also documented has been an increased prevalence of A1AT deficiency in twins and their parents. An excess of PiMZ and PiMZ phenotypes has been recorded among mothers of twins, particularly those of the opposite sex. Needed is an investigation of the effect of smoking on cervical, uterine, and oviductal secretions in order to confirm or refute the hypothesis suggested. Since the adverse effect of A1AT elevation on fertility in smokers is reversible, confirmation of this hypothesis would have preventive and therapeutic implications.