by John R. Lee, MD – a Harvard-trained physician and leading medical authority on natural progesterone, Medical News Letter January 1999
Some years back, a handful of men called or wrote to tell me of their experience with progesterone, usually the result of handling progesterone cream while helping a woman apply it. They reported that their symptoms of prostate enlargement or benign prostatic hypertrophy (3PK) such as urinary urgency and frequency decreased considerably, and their sexual performance increased, Needless to say, this gave me much to think about. Since then, several men with prostate cancer have told me their PSA (Prostate Specific Antigen) level – an indication of prostate cancer – decreased when they started using a daily dab of progesterone cream, and that they have had no progression of their prostate lesions since using the cream. One man called to say his bone metastases are now no longer visible by Mayo clinic X-ray tests.
Though I retired from active practice ten years ago, six of my former patients with early prostate cancer have been using progesterone cream (along with diet, some vitamin and mineral supplements, and saw palmetto) for about five years. All report their cancer has shown no progression.
The Wrong Treatment All These Years
Since Huggins showed, in 1941, that castration (removal of the testicles) slowed progression of prostate cancer, physicians have assumed it was the resulting lack of testosterone that slowed the cancer, and ever since have relied on suppression of testosterone in their treatment of the disease. However, the testosterone suppression benefit only lasts two to three years, and then the prostate cancer progresses to an androgen (male hormone) insensitive state and continues to spread. Despite this, metastatic prostate cancer patients are treated with androgen blockade through castration (orchiectomy) and/or hormone-suppressing drugs
I remember reading studies done 30 to 40 years ago showing that testosterone supplementation prevented survival of prostate cancer cells transplanted to test mammals. In more recent (as yet unpublished) studies it has been shown that in a prostate cancer cell culture, testosterone kills the cancer cells. A 1996 study published in the Proceedings of the National Academy of Sciences showed that in mice, testosterone will shrink human prostate tumors. The benefit of castration in prostate cancer stemmed from estradiol reduction, not testosterone reduction
Tracking the Culprit
Why does prostate cancer occur so often in aging men? Consider the changes in testicular hormone production as men age:
1. Testosterone levels fall;
2. More testosterone is changed (by 5-alpha-reductase enzyme) to dihydrotestosterone (DHT), stimulating prostate growth;
3. Progesterone levels fall. Progesterone is vital to good health in men. It is the primary precursor of our adrenal cortical hormones and testosterone. Men synthesize progesterone in smaller amounts than women do but it is still vital. Since progesterone Is a potent inhibitor of 5-alpha-reductase, the decline of progesterone in aging males plays a role in increasing the conversion rate of testosterone to DHT.
4. Estradiol (an estrogen) effect increases. Testosterone Is a direct antagonist of estradiol. Both the fall in testosterone and the shift from testosterone to DHT allows increased effect of estradiol. Male estradiol levels are equivalent to or greater than that of postmenopausal females, but normally estradiol’s effects are suppressed (antagonized) by the male’s greater production of testosterone. Perhaps estradiol Is also the culprit (along with DHT) in prostate growth.
Getting Down to the Gene Level
Embryology teaches us that the prostate Is the male equivalent of the female uterus. The two organs differentiate from the same embryonic cells and they share many of the same genes such as the oncogene, Bcl-2, and the cancer-protector gene, p53. It is not surprising then, that the hormonal relationships in endometrial cancer will be the same in prostate cancer; that is both are very sensitive to the harmful effects of unopposed estrogen and are protected by progesterone. Researchers T.S. Wiley and Bent Formby, Ph.D. have done test tube studies that verify this relationship, but human studies still need to be done.
The course of prostate cancer growth, like breast cancer growth [is] due to the continued presence of an underlying metabolic imbalance. The underlying metabolic imbalance in all hormone-dependent cancers is estrogen dominance. Prevent the estrogen dominance and you will prevent the cancer. If the cancer is already underway, correcting the estrogen dominance will slow the cancer growth and prolong life. The benefit of castration in prostate cancer stemmed from estradiol reduction, not testosterone reduction. Given the choice, I would choose testosterone and progesterone supplementation….”
Dr. Lee’s Healthy Prostate Program
1. Diet should avoid sugars, refined starches, and other glycemic (insulin-raising) foods as well as high. estrogen food such as feedlot-raised meat and milk.
2. Avoid xenoestrogens such as pesticides and some plastics
3. Maintain a good intake of antioxidants.
4. If you are over 50, monitor saliva hormone levels of progesterone and testosterone.
5. Supplement progesterone and testosterone by transdermal cream to maintain saliva levels consistent with that of healthy mature males. When supplemented in this manner: I recommend 8 to 10 mg per day of progesterone and 1~2 mg per day of testosterone.
6. From my clinical experience, It would not surprise me that exercise and an active sex life are also protective factors against prostate cancer.
7. It is known that chronic inflammation may also be potentially carcinogenic. It is wise, therefore, to maintain one’s intake of antioxidants such as vitamin C, selenium, and the fat soluble anti-oxidant vitamins, A, E, D, and K.
John R. Lee, MD – Medical News Letter January 1999