The biotransformation of estradiol-14C to 2-hydroxyestrone in human subjects is sharply altered by the level of thyroid hormone. The formation of 2-hydroxyestrone is increased by high thyroid levels so that it becomes the major estrogen metabolite; in myxedema the amount of 2-hydroxyestrone is diminished. The previously reported changes in estriol synthesis with thyroid have been confirmed. It is concluded that hydroxylation at C-2 and at C-16 of estrone are competitive reactions for the available substrate.