Estrogen and Osteoporosis
by Raymond Peat, PhD
Excerpts from Ray Peat’s Newsletter: Estrogen and Osteoporosis
The government declared victory in the war on cancer, though the age-specific death rate from caner keeps increasing. In the equally well publicized effort to prevent disability and death from osteoporosis, no one is declaring victory, because the only trend in its incidence that has been reported is an increase. The estrogen-promoting culture tells us that this is because of the aging of the population, but the age corrected numbers still show a great increase—for example, in Finland between 1970 and 1995, the number of women (for a given population of women older than 60) breaking their forearm because of osteoporosis more than doubled (Palvannen, et al., 1998). That this happened during a time when the use of estrogen had become much more common doesn’t present a good argument for the protective effects of estrogen treatment. (And during this period there was a large increase in the consumption of estrogenic soy products.)
Recently our local newspaper had a story at the bottom of the front page reporting that lean women who used estrogen and synthetic progestins had a 80% higher rate of breast cancer. Several days later, across the top of the front page, there was a rebuttal article, quoting some doctors including a “world class expert on hormone replacement therapy” and as woman who has taken Premarin for forty years and urges everyone to take it. The “protection against osteoporosis” and against heart disease, they said, must be weighed against a trifle such as the 80% increase in cancer. It appeared that the newspaper was apologizing for reporting a fact that could make millions of women nervous. (Jan 26, Register-Guard).
Medical magazines, like the mass media, don’t like to miss any opportunity to inform the public about the importance of using estrogen to prevent osteoporosis. Their attention to the bone-protective effect of progesterone has been noticeably less than their mad campaign to sell estrogen, despite the evidence that progesterone can promote bone rebuilding, rather than just slow its loss...
A former editor of Yearbook of Endocrinology had reviewed a series of studies showing that excess prolactin can cause osteoporosis. Then, he presented a group of studies showing how estrogen promotes the secretion of prolactin, and can cause hyperprolactinemia. In that review, he wryly wondered how something that increases something that causes osteoporosis could prevent osteoporosis.
Women have a higher incidence of osteoporosis than men do. Young women have thinner more delicate bones than young men. The women who break bones in old age are generally the women who had the thinnest bones in youth. Menstrual irregularities, and luteal defects, that involve relatively high estrogen and low progesterone, increase bone loss.
Fatter women are less likely to break bones than thinner women. Insulin, which causes the formation of fat, also stimulates bone growth. Estrogen however, increases the level of free fatty acids in the blood, indicating that it antagonizes insulin (insulin decreases the level of free fatty acids), and the fatty acids themselves strongly oppose the effects of insulin. Estrogen dominance is widely thought to predispose women to diabetes.
Between the ages of 20 and 40, there is a very considerable increase in the blood level of estrogen in women. However, bone loss begins around the age of 23, and progresses through the years when estrogen levels are rising.
Osteoarthritis, which involves degeneration of the bones around joints, is strongly associated with high levels of estrogen, and can be produced in animals with estrogen treatment.
Thirty years ago, when people were already claiming that estrogen would prevent or cure osteoporosis, endocrinologists pointed out that there was no x-ray evidence to support the claim. Estrogen can cause a positive calcium balance, the retention of more calcium than is excreted, and the estrogen promoters argued that this showed it was being stored in the bones, but the endocrine physiologists showed that estrogen causes the retention of calcium by soft tissues. There are many reasons for not wanting calcium to accumulate in the soft tissues; this occurs normally in aging and stress.
...The toxic effects of excessive intracellular calcium (decreased respiration and increased excitation) are opposed by magnesium. Both thyroid and progesterone improve magnesium retention. Estrogen dominance is often associated with magnesium deficiency, which can be an important factor in osteoporosis (Abraham and Grewal, 1990; Muneyyirci-Delale, et all., 1999).
As part of the campaign to get women to use estrogen, an x-ray (bone density) test was devised which can supposedly measure changes in the mineral content of bone. However, it happens that fat and water interfere with the measurements. Estrogen changes the fat and water content of tissues. By chance, the distortion produce by fat and water happen to be such that estrogen could appear to be increasing the density of a bone, when it is really just altering the soft tissues. Ultrasound measurements can provide very accurate measurements of bone density, without the fat and water artifacts that can produce misleading results in the x-ray procedure, and don’t expose the patient to radiation, but the ultrasound method is seldom used.
...Recent studies have found that both men and women lose minerals from their bones at the rate of about 1% a year. Although men have lower estrogen in youth than women do, their bones are much heavier. During aging, as their bones get thinner, men’s estrogen levels keep rising.
Besides having weaker bones, old people have weaker muscle, and are more likely to injure themselves in a fall because their muscles don’t react as well. Muscle loss occurs at about the rate of 1% per year.
Women’s muscles, like their bones, are normally smaller than men’s, and estrogen contributes significantly to these differences.
In the case of osteoporosis (A. Murrillo-Uribe, 1999) as in Alzheimer’s disease, the incidence is two to three times as high in women as in men. In both Alzheimer’s disease and osteoporosis, the estrogen industry is arguing that the problems are caused by a suddenly developing estrogen deficiency, rather than by prolonged exposure to estrogen.
Similar arguments were made fifty years ago regarding the nature of the menopause itself—that it was caused by a sudden decrease in estrogen production. The evidence that has accumulated in the last forty years has decisively settled that argument: Menopause is the result of prolonged exposure to estrogen. (Even one large dose destroys certain areas in the brain, and chronic, natural levels damage the nerves that regulate the pituitary. Overactivity of the pituitary leads to many other features of aging.)
...Unsaturated fats, iron, and lactic acid are closely related to the actions and regulation of TNF (Tumor Necrosis Factor), and therefore they strongly influence the nature of stress and the rate of aging.
The fact that cancer depends on the presence of polyunsaturated fats probably relates to the constructive and destructive effects such as multiple organ failure/congestive heart failure/shock-lung, etc. metabolites, which are based on the so-called essential fatty acids. When oxygen and the correct nutrients are available, the hypermetabolism produced by TNF could be reparative (K. Fukushima, et al., 1999) rather than destructive. Stimulation in the presence of oxygen produces carbon dioxide, allowing cells to excrete calcium and to deposit it in bones, but stimulation in the absence of oxygen produces lactic aid and causes cellular calcium uptake.
It is in this context that the therapeutic effects of saturated fats, carbon dioxide, progesterone, and thyroid can be understood. They restore stability to a system that has been stimulated beyond its capacity to adapt without injury.
Ray Peat’s Newsletter(s) can be purchased by writing to: Ray Peat, PhD, PO Box 5764, Eugene, Oregon 97405