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166<br />
laura briggs<br />
Since preventing ovulation prevents pregnancy, one could employ <strong>the</strong><br />
same principles in birth control. . . . Thus, for example, if an individual<br />
took 1 mg. diethylstilbestrol [DES, a syn<strong>the</strong>tic estrogen] by mouth daily<br />
from <strong>the</strong> fi rst day of her period for <strong>the</strong> next six weeks, she would not<br />
ovulate. (Albright quoted in Reed, 1983, p. 316)<br />
Indeed, when Gregory Pincus presented <strong>the</strong> earliest results from <strong>the</strong><br />
line of research that became <strong>the</strong> fi rst contraceptive “pill” at a conference<br />
in 1955, <strong>the</strong> session’s chair, Sir Solly Zuckerman, felt that he had shown<br />
nothing that was not already well-known: that progestin inhibits ovulation<br />
(Marks, 1998; Vaughan, 1970, pp. 34–35). The scientifi c obstacles<br />
to producing a birth control pill had been solved by 1940, and <strong>the</strong> point<br />
seemed obvious by 1945, yet it was ano<strong>the</strong>r decade before <strong>the</strong>re were<br />
clinical trials. O<strong>the</strong>r forces than <strong>the</strong> purely scientifi c were at work both<br />
in inhibiting and promoting birth control research.<br />
Risks, <strong>the</strong> Pill, and Overpopulation<br />
The principle reason why this line of research was halted in 1940 was that<br />
it seemed too great a risk for too little gain. The “pill” would represent a<br />
major break with previous conventional wisdom about pharmaceuticals;<br />
it was <strong>the</strong> fi rst such systemically active compound given to a population<br />
that was healthy, that did not even have a disease that might counterbalance<br />
<strong>the</strong> dangers of a steroidal drug of unknown effects. Researchers<br />
had no way to know whe<strong>the</strong>r or not <strong>the</strong> Pill was safe. If many people<br />
were aware in 1940 that making a contraceptive pill was possible yet<br />
still did not, it was because it seemed impossible to predict <strong>the</strong> side<br />
effects. Indeed, this was Zuckerman’s warning to Pincus at <strong>the</strong> 1955<br />
Tokyo conference where his initial results were presented; he said:<br />
We need better evidence about <strong>the</strong> occurrence of side effects in human<br />
beings. It is not enough though . . . that we take presumed negative<br />
evidence about <strong>the</strong> lack of side-effects from animal experiments to<br />
imply that no undesirable side-effects would occur in human beings.<br />
There is an urgent need for prolonged observation before we draw<br />
any fi rm conclusions. (Vaughan, 1970, p. 39)<br />
In fact, three pharmaceutical companies—Searle, Parke-Davis, and<br />
Pfizer—possessed patents and animal studies in 1955 that would have<br />
enabled <strong>the</strong>m to begin clinical trials with <strong>the</strong> hope of turning a considerable<br />
profit, but <strong>the</strong>re was no competition. Those at Parke-Davis and<br />
Pfizer believed that clinical trials would be dangerous and unethical;