Does estrogen really cause cancer? There have been studies removed from the National Library of Medicine that give answers to estrogen-cancer questions. This was done to keep people, doctors and patients, in the dark about hormones, estrogen and how to properly treat patients’ hormone deficiencies. I was able to hire someone to locate a document in Europe by Robert Wilson, MD about estrogen and cancer. Dr. Wilson is my hero and I aim to pick up where he left off. Below is the article kink and text of his article telling the truth about estrogen.
ROBERT A. WILSON, M.D., F.A.C.S., F.A.C.O.G.
Clinical Medicine, August 1964, Brooklyn, NY
Although estrogens have been accused of causing cancer in women, the facts indicate that its administration actually offers hope of diminishing the incidence of malignant lesions including breast and genital cancer whatever the causative factors. Thus, estrogens should be administered postmenopausally.
Again and again, held in the same cell, the accused has faced the same charge. And with each imprisonment the Grand Jury, for lack of any but the most circumstantial evidence, has refused to indict. Released periodically, the accused has wandered friendless and alone, facing, until the next arrest, the suspicions, dread and hatred of most of the world. This has been going on for more than 20 years.
It is the story of estrogen.
In discussions with doctors and patients regarding the long term administration of estrogen, one question almost invariably arises: “But what about cancer?”
This is especially true in lay circles whenever the word hormone enters into the discussion. The literature regarding this aspect of estrogen is profuse and controversial, the confusion probably greatest in the etiology and treatment of breast cancer. It is not unusual to listen to an authority present the menace of estrogen and then terminate the meeting by showing slides of angry cancerous lesions melting away following estrogen administration. How did this paradoxical situation come about?
More than 20 years ago in the early days of cancer and hormone research (and they were largely contemporaneous) certain chemical substances administered to mice resulted in cancerous growths. These chemicals were therefore labeled “carcinogenic” and included many widely different substances among which were a few that also happened to be estrogenic. On this evidence is based, almost exclusively, the accusation that estrogens produce cancer. Mice are not humans, yet these results were heard around the world. The publicity has continued and has been devastating. A typical example is the blatant newspaper publicity given to more recent experiments with mice.
What is not generally known is that the mice used in the early experiments were a special strain which had been inbred for hundreds of generations. These mice had such a high incidence of spontaneous cancer that if they were allowed to live their natural lifetime under the best of conditions (no chemicals at all administered) more than 50% would develop mammary cancer. Certainly nothing is proven if 80 or 90% of such abnormal, unnaturally sensitive mice develop cancers after the administration of an estrogenic chemical. Injections of aspirin would undoubtedly be carcinogenic. What about dosage? These mice were given as much as 1 Gm. of the estrogenic chemical weekly for six months. However, a mouse weighs about 50 Gm. and lives only two years. Actually the susceptible mouse was given half its body weight for one fourth of its life span; it would be impossible to administer a proportionate amount to a woman even over a 20-year span. Is the attempt to translate these experiments into the human area anything but ludicrous?
Attempts to obtain similar results with other animals have failed utterly. That estrogens are not carcinogenic in other animals was shown by investigators who assaulted monkeys for as long as 10 years with estrogens augmented by local trauma and other carcinogens. No malignant growths were produced. Still others administered massive doses of estrogens to Rhesus monkeys for as long as seven years; some received as much as one million rat units per year. There was not one instance of cancerous change in any organ. These experiments with monkeys are important because of the close relationship of monkey to man and are particularly valid in evaluating estrogens in humans. It has been reported that enormous doses of natural estrogens failed to produce new growths in rats and in a large number of human subjects. In spite of the inability of these and many other investigators to induce cancer by means of estrogen in any laboratory animal except the susceptible mouse, the stigma persists. This is indeed surprising, as there is no convincing proof that estrogen has ever induced cancer in the human being.
Normal Estrogen Levels
It is reassuring to realize that a woman has possessed and benefited from estrogen all her life, even long before birth. Her destiny is closely intertwined with it. There is further reassurance in the fact that she has the greatest amount of estrogenic hormone in her body between the years of 18 and 25 and yet during those years breast and genital cancer is at its lowest incidence. Cancer occurs most commonly when the female hormone level drops. Actually the incidence of cancer of all sites in women shows a constant increase with age, at the same time that the production of estrogen is steadily declining (high estrogen in youth-low incidence of cancer; low estrogen in age–high–incidence of cancer). The “dyed-in-the-wool” believer in the “estrogen menace” cannot explain these irrefutable facts, so he avoids them; he pretends they do not exist.
Estrogen Levels in Pregnancy
During the last few months of pregnancy, the placenta pours estrogen into the mother’s blood stream in astronomical amounts. The total estrogen produced during a normal menstrual cycle is about 5 mg. The amount produced in either of the last two months of pregnancy is almost 3000 mg.-an amount 600 times greater monthly than in her non-pregnant sister. At least 50 % of this tremendous amount passes freely into the fetus. There is increasing evidence that an adequate supply of estrogen is vital to the well being of the fetus. There is further evidence that the fetus, male or female, is itself actively concerned with estrogen synthesis. The full-term placenta contains about 51 mcg. of estrone, 170 mcg. of estradiol, and 315 mcg. of estriol per kilogram wet weight. It has been estimated that if the dose of an estrogen administered to a worn: an were 1.5 mg. weekly by injection (an average dose), it would require at least 125 times this amount weekly to approximate the state of pregnancy. If estrogen were carcinogenic, under these circumstances malignancy should be frequently encountered in pregnancy. Yet this is not so – it is relatively rare, only three per 10,000 pregnancies. Even in the occasional case encountered, the tumor may well have ante-dated the pregnancy.
Incidence of Cancer Unchanged
The incidence and mortality rate of breast cancer is the same today as in 1930 when estrogen was not in use. After Daisy’s discovery of estrogen more and more women have been treated by it so that at the present time in the United States it is safe to assume that more than 7,000,000 women consume estrogen with more or less regularity. The amount of estrogenic substance consumed yearly can thus be measured in tons. In view of the unchanged incidence of breast cancer during these years, how can one logically argue that estrogen causes cancer of the breast?
About 10,000 women die of cancer of the cervix in the United States each year. These deaths are at least 90% preventable. It is purely a question of detecting the cancer when it is localized, principally by cytological screening. The time is past when a patient should have to request that a cancer smear be taken; instead it should become so routine that she would believe she has not had a complete examination if it is omitted. By doing this, cancer of the cervix would, in most instances, be detected in its developing or pre-invasive (and thus curable) stages.
Many theories of the cause of cervical cancer have been explored but its cause is not known. Few physicians would implicate estrogen. The situation is rather to the contrary. It is a reasonable assumption that the maintenance of a healthy vaginal epithelium by local or systemic estrogen usage when needed would be cancer protective. An atrophic cervicitis is constantly trying to heal itself and it is under these circumstances of rapid cell growth that a cancer might develop. With hormonal treatment the atrophic cervicitis could have been prevented or cured and a cancer could conceivably have been prevented.
About 15,000 endometrial cancers occurred in the United States in 1963. Just as the anxieties of some regarding estrogens are concentrated primarily upon mammary tissue, so others are more concerned with the endometrium. They seem to ignore the fact that 92% of the cases of endometrial cancer occur after the age of 40 years when most estrogen levels are already decreased, are declining steadily, and when anywhere from 25 to 40% of the endometria are atrophic due to estrogen deficiency (maximum age of incidence is 57 years). The attempt to indict estrogen in this instance is indirect. Endometrial cancers are sometimes encountered simultaneously with endometrial hyperplasia. As hyperplasia is estrogen induced, therefore estrogen is the “cancer culprit”-guilt by association. A complicating factor is the extremely close microscopical similarity of endometrial adenocarcinoma and some forms of hyperplasia. It has been pointed out that there is no sharp line of demarcation between proliferative forms of hyperplasia and early adenocarcinoma. The growing use of progestogens and other steroids has further increased the risk of a mistake in diagnosis. One can only speculate upon the number of patients erroneously treated by irradiation, or hysterectomy, or both, and indexed in the hospital record room as endometrial carcinoma. The late Emil Novak who was intensely interested in this problem, concluded that the occurrence of the two entities is coincidental.
As endometrial cancer is not a disease of the young except in the presence of ovarian failure to produce sufficient estrogen and progesterone, it is extremely important that the hypogonadal, premenopausal female be adequately treated. A logical inference is that if the menopause and the climacteric are prevented by the properly timed cyclic administration of estrogen and progesterone, this form of cancer will be simultaneously prevented. There is increasing evidence that exogenous progesterone and its analogues can produce a regressive effect on advanced and even disseminated endometrial cancer.
Quite apart from this direct effect there is another phenomenon which makes the continued growth of an endometrial cancer almost an impossibility, i.e. menstruation or withdrawal bleeding. Any in situ nest of atypical cells is inevitably uprooted and washed away in the deluge of debris, blood and fluids. This physical, cancer-controlling aspect of rhythmic uterine bleeding, whether natural or induced, has been almost completely overlooked by the profession. Induced postmenopausal bleeding need not necessarily be monthly; probably five or six times yearly is sufficient. Long needed has been an inexpensive practical method for the determination of a woman’s estrogen status. Recently a proven, simple technique was described in which, using a minor modification of the Papanicolaou smear; the percentages of superficial, intermediate and parabasal cells of the vaginal mucosa can be determined. These percentages in turn indicate the individual’s estrogen status.
Recently it was found in a large series of cases that the incidence of malignant lesions was three times greater in myxedematous patients than in those with highly active thyroid glands. Thus it appears that keeping a woman generally endocrinologically rich throughout her life, with the maintenance of adequate levels of estrogen and progesterone, offers hope of diminishing the incidence of malignant lesions including breast and genital cancer, whatever the causative factors (metabolic, receptive constitutions, heredity, viral, etc.) Such a concept inherently includes the elimination of the climacteric and the demolition of the “estrogen-cancer myth.”
This article has a PMID number of 15446202 for the National Library Medicine but the article has been removed so no one can get access to pro-estrogen studies.
The estrogen cancer debate has been a part of our history for years and it’s about time we put it to rest and give women their lives back. You can read more about Dr. Wilson and his practice in his book Feminine Forever.