218 SOMERS H. Sturgis 



theca luteinization of immature follicles occurs presumably in response to 

 the LH elTect of circulating maternal gonadotropins. Another example of 

 theca proliferation of immature follicles associated with fluctuating LH 

 peaks is also found in the polycystic ovary syndrome. The theca activity in 

 these follicles that are destroyed lasts only a few days in the monkey, probably 

 also in the human. It is highly probable as well that this tissue produces 

 steroids during the transient phase of its existence. Since estrogens are of 

 prime importance at this critical time in the cycle to stimulate optimal 

 cervical secretions, tubal peristalsis and so on, it is a likely guess that this 

 theca thickening helps maintain the level of circulating estrogens. The transient 

 proliferation of theca in early atretic follicles may also be the source of 

 progesterone production before ovulation occurs. Preliminary studies of 

 concentrations of ascorbic acid, typically seen in fully formed corpora in 

 rat and human, are noted in the rat in the theca and granulosa of unruptured 

 follicles only when the latter show signs of early dissolution. It is possible 

 that ascorbic acid appears as a precursor in progesterone production. The 

 depletion of ascorbic acid caused by giving doses of LH in the presence of 

 fully formed corpora is not clearly understood. However, this is a wholly 

 unphysiologic experiment, since in the presence of functioning corpora 

 lutea normally the pituitary does not excrete LH. 



It may be theoretically possible to utilize the above reasoning to create a 

 chronic state of anovulation such as exists in the Stein-Leventhal ovaries, by 

 the correct timing and dosage of substances with LH effect. These would 

 have to be given repeatedly to overstimulate each wave of developing follicles 

 while they are still immature, before any one has reached that stage of maturity 

 and developmental autonomy beyond which the further steps in maturation 

 will inevitably lead to ovulation. Anovulatory cycles thus produced need not 

 be considered necessarily damaging to the ovaries. The use of LH substances 

 in this regard would only be an extension of a normal physiologic process 

 causing the waste of one more follicle each month — a minor loss in relation 

 to the tens of thousands degenerating through a lifetime. Whether or not if 

 this scheme is successful it would eventually produce a persistent and 

 relatively irreversible situation as is found in the polycystic ovary, is a matter 

 of pure speculation. 



REFERENCES 



1 . Corner, G. W., The Hormones in Human Reproduction, Princeton University Press, 1946. 



2. Sturgis, S. H., Contributions to Embryology 33, 67, 1949. 



3. McArthur, J., F. Ingersoll and J. Worcester, /. Clin. Endocrinol. 18, 1202, 1958. 



4. Taymor, M. L., Fertil. & Steril. 10, 212, 1959. 



5. Sturgis, S. H. and W. Achilles, Endocrinology 49, 720, 1951. 



6. Velardo, J. T., Science 131, 357, 1960. 



7. Parkes, a. S., in Conference on Mechanism of Ovulation sponsored by the Planned 



Parenthood Federation of America, August 1959. 



8. Sturgis, S. H., /. Fertil. & Steril. 1, 40, 1950. 



9. Parlow, a.. Fed. Proc. 7, 402, 1958. 



