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In the 1960s, a new estrogen-based drug for assisted fertility entered the U.S. drug market: clomiphene citrate, branded as Clomid. Born from a failed contraceptive, this synthetic estrogen promoted ovulation and helped women conceive years before in vitro fertilization (IVF) emerged. While there is a rich historiography detailing how the contraceptive pill changed reproduction and motherhood, how its hormonal components became part of the opposite project—promoting conception—has received scant attention. But Clomid did not only make mothers, it also made for scientific disagreement. This analysis examines the disputes between two researchers over how, precisely, Clomid functioned in the body. Olive Smith of the Fearing Laboratory at Harvard and Robert Greenblatt at the Medical College of Georgia disagreed over whether the drug acted primarily on the pituitary or the ovary, a distinction that would influence their perceptions of its safety. Taking a “practices” approach and drawing on scientific publications, professional correspondence, and Merrell’s promotional materials, this paper argues that these differences expose multiple, competing ways of knowing the drug, from the radioactive bioassay to clinical frameworks centered on patient charts, symptoms, and case-by-case dosing. In doing so, this paper shows that Clomid resisted singular explanations: competing lab protocols and opposing interpretive frameworks produced parallel, sometimes incompatible, interpretations of its mechanism. This epistemic instability reflects the hormonal system itself—variable across bodies, responsive to context, and resistant to any singular, definitive account, despite the best efforts of researchers.