The monooxygenase receptor for vitaletheine is a drug-metabolizing enzyme. When busy with drugs, it is unable to fulfill its functions in maintaining control of our biochemical pathways and our defenses against diseases like cancer, heart disease, and diabetes. The monooxygenase is increased by progesterone and perhaps by the natural biorhythm of early morning cortisol peaks which serves to free progesterone from its common binding globulin. As will be presented in the Thyroid lecture on Sunday, methimazole (Tapazole) and propylthiouracil (PTU) are substrates for the monooxygenase, and they poison the monooxygenase activity in the thyroid, but they aren't as toxic as genistein from soy is reported to be to the thyroid and thymus.