The Multiple Roles of a Remarkable Hormone
A woman’s bones are strongest in her early 30’s. Afterward, there is a gradual decline in bone mass until menopause when bone loss accelerates for 3 to 5 years, and then continues at about 1 to 1.5% per year. Because of the accelerated bone loss during menopause, most doctors have assumed that the rapid decline in estrogen that occurs during menopause is the cause of this bone loss. In the 1960’s, when estrogen was found to reduce the side effects of menopause, including hot flushes and the loss of bone mass, doctors began giving their patients large doses of estrogen at menopause and thereafter.
However, upon more thorough examination, studies in the United States indicate that estrogen replacement therapy was found to produce a wide variety of side effects, including, most notably, a significantly increased risk of endometrial cancer in women with an intact uterus. Other known side effects of estrogen therapy are:
- increased salt and water retention, resulting in increased risk of hypertension.
- increased blood clotting, resulting in increased risk of heart attack and stroke.
- increased fat synthesis, resulting in unwanted weight gain.
- increased risk of uterine fibroids and breast fibrocysts.
- increased risk of liver dysfunction and gall bladder attacks.
- increased risk of pituitary cancers and possibly breast cancer.
Moreover, it was found that after 3 to 5 years of estrogen treatment, the ability of estrogen to prevent the loss of bone mass associated with menopausal aging declines rapidly, resulting in rapidly accelerated bone loss leading to osteoporosis.
Adding Progesterone to Estrogen
When scientists observed the lethal side of estrogen replacement therapy, they reasoned that giving progesterone (the other sex hormone lost during menopause) in addition to estrogen, might counteract the side effects of estrogen.
It was found that the combination of estrogen and (synthetic) progestins eliminated the risk of endometrial cancer without diminishing the benefits of estrogen therapy. In the mid 1970’s, doctors meeting at the Mayo Clinic concluded that estrogen should never be given to any woman with an intact uterus without also giving her progestin to protect against endometrial cancer. This 20 year old consensus still eludes some doctors.
Dangers of Synthetic Progestins
Because synthetic progestins decrease the side effects of estrogen and because the sale of synthetic hormones has produced huge profits for the pharmaceutical industry, it has been assumed since the 1970’s that only estrogen (either natural or synthetic) can help reduce bone loss in aging women, that the only purpose of giving progestins, is to reduce estrogen’s side effects, and that synthetic progestins are just as effective and no more risky than natural progesterone. Some doctors have held to these assumptions in spite of persuasive scientific evidence that:
- Synthetic progestins produce numerous adverse side effects.
- Natural progesterone does not produce these side effects.
- Natural progesterone (and, to some degree, progestins) are far more effective in preventing and treating osteoporosis than estrogen!
Synthetic progestins produce adverse effects on blood lipids, and can elevate blood pressure, in contrast to favorable effects of natural progesterone, which improves cholesterol/triglyceride profiles.
How Estrogen Temporarily Slows Bone Loss
Bones are living tissues that continually renew themselves throughout life. Bone is primarily composed of a collagen matrix, strengthened by calcium and magnesium.
Bone forming cells are comprised of osteoclasts and osteoblasts. Osteoclasts constantly travel through bone tissue seeking older bone that has hardened (become mineralized) and needs to be replaced. Osteoclasts resorb (dissolve away) older bone tissue, leaving tiny unfilled spaces behind. Osteoblasts then move into these spaces and produce new bone tissue.
This process of dissolving older bone tissue and generating new bone tissue is the mechanism by which our bones are repaired, regenerated, and maintained in strength.
Osteoporosis occurs when osteoclasts dissolve more bone tissue than osteoblasts are able to replace.
How Progesterone Reverses Bone Loss
Progesterone, on the other hand, stimulates the production of osteoblasts, which are required to generate new bone tissue. Natural progesterone has been shown to stimulate osteoblast mediated new bone formation, which is required to prevent osteoporosis. Some synthetic progestins also stimulate new bone formation, but to a lesser degree than progesterone.
In a lengthy review on the effects of progesterone on bone formation (Endocrine Reviews 1990), J.C. Prior of the university of British Columbia in Canada concluded that:
“Experimental epidemiological and clinical data indicate that progesterone is active in bone metabolism Progesterone appears to act directly on bone. Progesterone seems to promote bone formation and or increase bone turnover.”
Clinical Benefits of Transdermal Progesterone
Studies that have been conducted have shown that natural progesterone is better and safer than synthetic progestins. It has also been shown that transdermal progesterone can readily penetrate the skin to stimulate therapeutic bone regeneration.
The foremost exponent of natural transdermal progesterone therapy for osteoporosis is California physician John R. Lee, M.D., who uses a skin cream containing progesterone derived from an extract of wild yam,which penetrates the skin safely and effectively. Dr. Lee has published the results of his extensive clinical experience with progesterone skin cream in Lancet 1990 and others including the book Natural Progesterone: The Multiple Roles of a Remarkable Hormone.*
In a study of 100 postmenopausal women, aged 38 to 83, many of whom had suffered one or more bone fractures and had lost height (common signs of osteoporosis), Dr. Lee reported that “97 of them showed 5% to 40% new bone formation within 6 to 48 months after using a wild yam progesterone cream. Some women attained as much as 105% of the average bone density of a 35 year old. It was common to see a 10% increase in bone density during the first 6 to 12 months of treatment and an annual increase of 3% to 5% until stabilization at the bone strength level of healthy 35 year olds.” Dr. Lee added that “the occurrence of osteoporotic bone fractures dropped to zero.”
This article is reprinted fromClinical Nutrition News. * Dr. Lee’s book is available from FACT See Book List on page 15.