March 2006 | Vol.2 | Issue 2

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The Hormone Health Connection Newsletter is a newsletter that provides featured articles on Menopause, PMS, and Natural Progesterone, new product reviews, tips for reducing the pain and dealing with related anxiety of pms and menopause symptoms, and information on how to promote a healthy, balanced lifestyle. The Hormone Health Connection Newsletter is brought to you by

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Featured Article

Osteoporosis Reversal: The Role of Progesterone
By John R. Lee, MD
Published in the
International Clinical Nutrition Review


Present osteoporosis management emphasizes prevention rather than cure since true reversal has proven unobtainable by conventional methods.  With the hypothesis that progesterone is the missing ingredient for normal bone-building in women, transdermal progesterone supplementation (with or without estrogen) was tested in an office-based setting over the past six years.

Treatment resulted in progressive increase in bone mineral density (BMD) and, more importantly, definite clinical improvements evidenced by pain relief, height stabilization, increased physical activity, and fracture prevention.  The benefits achieved were found to be independent of age.  It is concluded that osteoporosis reversal is a clinical reality in a program that is safe, uncomplicated, and inexpensive.


Osteoporosis is a multi-factorial skeletal disorder of progressive bone mass loss, demineralization, and fracture proclivity (most commonly of the proximal femur, vertebral body, distal forearm, proximal humerus, and ribs) which accelerates with menopause.  The annual cost of these fractures in the U.S. has been estimated as over $6 billion (1)  and the personal cost in quality and quantity of life is incalculable.  Osteoporosis predominately affects white postmenopausal women in whom the incidence, if one lives long enough, is 100 percent.

Conventional treatment of estrogen, with or without supplemental calcium and Vitamin D, tends to delay bone mass loss but not reverse it.  The addition of fluoride in doses up to 30-40 mg/day can result (after several years) in a modest increase in bone mass but provides no protection against vertebral fracture and even increases the incidence of non-vertebral (i.e. hip) fractures. (3) Furthermore, adverse side effects of fluoride treatment (gastrointestinal and periarticular inflammation) are excessive and unacceptable.  Clearly, a new approach is needed.


In 1982, after studying the work of Ray Peat, Ph.D., and being challenged by the osteoporotic problems of my aging patients, I felt that progesterone deserved a trial in the treatment of osteoporosis.

The known facts about osteoporosis pathogenesis are much the same now as they were when I went through medical school in the early '50's:  Osteoblasts make new bone, osteoclasts resorb bone.  Both processes go on continually; net bone change is the relative balance between these two processes.  Osteoclast dominance leads to osteoporosis.  It begins several years before menopause and then accelerates (usually at the rate of 1.5 percent or more per year) with menopause, a fact that supports the conclusion that the sex hormones are involved.

It is well established that bone loss in oophorectomized women can be slowed but not truly reversed with estrogen supplementation.  In natural menopause, the decline of progesterone precedes that of estrogen and is of greater magnitude.  The timing of these hormonal events coincides with the development of osteoporosis.  Why not add progesterone to the therapeutic program?  There is no reason to assume that only estrogen is involved in bone growth.  Each of these hormones have many physiological functions other than their uterine effects, why not also in bone building?

Progesterone is uniquely strategic in mammalian physiology.  The primary pathway in the synthesis of adrenal-steroids, estrogen, and even testosterone leads from cholesterol through pregnenalone to progesterone and then to these vital hormones.  These molecules appear amazingly similar yet their biophysiological functions differ greatly.  It is well known that minute differences in molecular structure can facilitate vastly different biological actions.  The difference between estrone and testosterone, for instance, is merely the placement of one hydrogen ion.

Progestins, i.e. altered or synthetic progesterone, have shown limited effect on bone density (7,8), but are expensive as well as burdened with unacceptable side effects.  Natural progesterone, on the other hand, is synthesized by over 5000 plants and is inexpensively extracted from yams.  Furthermore, it is efficiently absorbed transdermally, a route of administration that avoids the first-pass liver loss of oral use and accounts for its amazing freedom from undesirable side effects.

The goal of my progesterone hypothesis is simple:  increasing bone density and prevention of osteoporotic fractures.

Pathogenesis of Osteoporosis

The known factors affecting calcium acquisition and normal bone building are multiple and include the following.  Normal calcium absorption requires sufficient gastric acidity 9 and Vitamin D.  Many older women are deficient in Vitamin D due to insufficient sun exposure and many over age 70 lack sufficient gastric acidity.  Dietary factors are important;  disaccharidase deficiency (common after age 50) leads to lactose intolerance and the avoidance of dairy products are resulting a consequent deficiency of calcium.  Diets must include the vegetable sources of calcium.

Phosphorus intake should be reduced by avoiding artificially carbonated beverages ("phospho-sodas") and limiting red meats.  Proper connective tissue (collagen) requires the micronutrients Vitamins C and A.  Cigarette smoking accelerates osteoporosis and must be discontinued.  Alcohol intake, similarly, must be minimized.  The incorporation of calcium into normal bone requires bone stress (exercise) and appropriate hormonal control, in this case.

It is important to rule out excess thyroid hormone (not uncommon in women taking thyroid medication) and hypercortisolism, especially in patients given corticosteroids.  Osteoporosis is not a disease of calcitonin deficiency:  bone density is relatively unaffected by thyroidectomy.  Nor is it a disease of fluoride deficiency; fracture incidence is found to be either unrelated to or moderately increase after fluoride exposure.

Study Population

The 100 patients in this study are postmenopausal white women in a suburban setting.  They ranged in age from 38 to 83 years.  Average age at time of entry into the program was 65.2 years of age.  The average time from menopause was 16 years.  All women have been followed clinically for more than 3 years and 63 of them have had serial dual photon absorptiometry for at least 3 years.  The majority had already experienced height loss, some by as much as 5 inches.  Each with their own idiosyncrasies, they are the typical patients of family practice.

Osteoporosis Treatment Program

Vitamin D 350-400 IU daily.
Vitamin C 2,000 mg per day in divided doses
Beta Carotene 15 mg per day (25,000 IU)
Calcium 800-1 000 mg per day by diet and/or supplements.
Estrogen 0.3-0.625 mg per day 2 weeks per month (conjugated estrogen) unless contraindicated.
Progesterone 3 percent cream, applied to skin twice daily the last 12 days of the monthly cycle;  use 1/2-1/3 of a 1 oz. jar per month.


Emphasize leafy green vegetables in the diet.


Limit red meat and soft drinks to 3 or fewer per week.


Limit alcohol use -- none, or no more than 1 drink every 2 weeks.


Exercise 20 minutes daily, or 1/2 hour 3 times per week.


No cigarettes.


Report any occurrence of vaginal bleeding.

Treatment Results

The addition of progesterone to this conventional treatment program in postmenopausal women was found to be consistently beneficial.  By the third monthly cycle of treatment, the patients generally experienced a sense of well-being, and this perhaps contributed to the absence of any compliance problems.

During the 3-year observation, patient height was stabilized, aches and pains diminished, mobility and energy levels rose, normal libido returned, and no side effects emerged.  Lipid levels did not rise, contrary to the experiences reported with some progestin use.

All patients were instructed on the application of progesterone cream to the softer skin under the arms or of the neck and face, with alternating sites chosen nightly.  Diet was thoroughly discussed with emphasis on the calcium-rich leafy greens and low-fat cheeses;  artificially carbonated sodas were to be avoided.

Patients were taught to think of calcium incorporation as a chain of events requiring proper intake, proper absorption by gastric acidity and Vitamin D, and bone-building with the help of progesterone, exercise, and micronutrients such as Vitamins A and C and the minerals found in unprocessed foods.

Serial vertebral bone density studies (at 6-month or 1-year intervals) showed a progressive rise.  It was common to see a 10 percent increase in the first 6-12 months and an annual increase of 3-5 percent until stabilizing at the levels of healthy 35-year-olds.  Neither age nor time from menopause was an apparent factor.

The faster increases occurred in those with the lowest initial bone densities.  In three cases in which bone densities did not rise in the first 6 months, causative medical complications were found.  One patient required additional gastric HCl supplementation;  one was found to be taking 3 times the recommended level of thyroid supplement;  and the third case involved a depression (related to the agonizing death of her husband due to throat cancer) during which time she had not eaten properly, did no exercise, and smoked cigarettes heavily.  When the depression lifted and she resumed the treatment program, her bone density increased dramatically.  Several patients showed a jump of 20-25 percent increase in bone density during the first year.

"Serial vertebral bone density studies (at 6 month or 1 year intervals) showed a progressive rise.  It was common to see a 10 percent increase in the first 6-12 months and an annual increase of 3-5 percent until stabilizing at the levels of healthy 35-year-olds. "

More importantly, the occurrence of osteoporotic fractures dropped to zero.  Three patients did have traumatic fractures:  one (aged 80) fractured her knee in a automobile collision; another (in her 70's) fell while hiking a mountain trail and suffered a fracture of her proximal humerus;  the third fell down a flight of stairs at home sustaining a transcondylar humerus fracture.  All three fractures healed well and the treating orthopedists commented on the excellent bone structure of these patients.

This clinical success stands in marked contrast to the experience of patients in the fluoride treatment experiments in which vertebral fractures continued apace with the control patients and non-vertebral fracture incidence increased.  Similarly, the consistent rise in bone density (no patient, after correction of confounding factors, failed to improve) contrasts with the experience of patients on estrogen without progesterone in which only a slowing of the bone density loss is observed.

In this study of 100 patients on progesterone supplementation, there was no difference in results relative to concomitant estrogen use.  The role of estrogen appears to be limited to relief of hot flushes and the benefit to vaginal lubrication.  In this regard, patients commonly volunteered the observation that normal libido had returned by using the progesterone.


The results shown in this study suggest that osteoporosis is not an irreversible condition.  Reversal has been demonstrated by the bone density tests and by the clinical results.  This can not be said of any other conventional therapy for osteoporosis.  It would seem clear that transdermal natural progesterone is the missing link in healthy bone building in postmenopausal women.

Provera, a progestin that differs from progesterone by a methyl group at carbon 6, has also been found to provide modest increases in bone density, but lacks the full biological generality of natural progesterone and is not free of worrisome side effects.  Additionally, its monthly costs are approximately 10 times that of transdermal progesterone.

The safety of supplementing natural hormones is an important consideration.  During her fertile years, a woman endogeriously produces monthly surges of estrogen and progesterone.  Cardiovascular risks and skeletal deterioration accelerate only after she loses these hormones.  Postmenopausal supplementation with progesterone or estrogen balanced with progesterone imposes no increased risks regarding cardiovascular disease (10), breast cancer (11), or endometrial cancer (12).  In fact, progesterone is almost certainly protective.


In this study, transdermal progesterone was added to conventional osteoporosis therapy.  The results demonstrate impressive reversal of osteoporosis in all patients in a program that is safe, uncomplicated, and inexpensive.  It these initial results are borne out by further experience, the benefit to womankind in health costs will be beyond measure.

P.S.  As an addendum to my paper entitled "Osteoporosis Reversal," the following information concerning the use of estrogen should be considered:

Estrogen supplementation is not appropriate for all postmenopausal osteoporotic patients;  e.g., those with obesity, varicose veins, hyperlipidemias, fibrocystic breast disease, a history of breast cancer, endometrial cancer, clotting disorders, or thromboembolism.  Because of these potential deleterious estrogenic side effects, well over one-third of the progesterone-treated patients in the study group received no supplemental estrogens.  During the course of the study it was obvious that the bone-building benefits of the progesterone therapy were independent of the presence or absence of supplemental estrogen.  Transdermal progesterone therapy itself produced no discernible side effects.

For women who have had no history of the listed estrogen contraindications, and who do not have vaginal dryness, hyperplasia, or currently are not experiencing vasomotor flushes, there is probably no need for exogenous estrogen.


  1. McKeown T, Butterfield WJH, Cochrane AL, et al.  The Frequency of Occurrence, Impact and Cost of Selected Musculoskeletal Conditions in the United States. Chicago. Am Acad Ortheopedic Surgeons (1984)

  2. Ettinger B, Genant HK, Cann Cl.  Long-term Estrogen Replacement Therapy Prevents Bone Loss and Fractures. Ann Inter Med 102, 319-324 (1985)

  3. Riggs BL, et al.  Effect of Fluoride Treatment on the Fracture Rate in Postmenopausal Women with Osteoporosis. N. Engl J Med 322, 802-809 (1990)

  4. Peat R.  Nutrition for Women, 3rd Edition. Blake College Publisher (1980)

  5. Peat R.  Progesterone in Orthomolecular Med., lecture, 1977 and personal communications.

  6. Cann Cl, Genant HK, Ettinger B, et al.  Spinal Mineral Loss in Oophoretomized Women. JAMA 244, 2056 (1980)

  7. Prior J.  Reported in "Provera Alone Builds Bone Medical Tribune, pg. 4-5, July 22, 1987

  8. Munk-Jensen N, et al.  Reversal of Postmenopausal Vertebral Bone Loss by Estrogen and Progesteron: A double-blind Placebo Controlled Study, BMJ 296, 1150-1152 (1988)

  9. Bain C Willett W, Hennekens CH, et al.  Use of Postmenopausal Hormones and Risk of Myocardial Infraction. Circulation 64, 42-46 (1981)

  10. Gambrell RD, Maler RC, Sanders Sl.  Decreased Incidence of Breast Cancer in Postmenopausal Estrogen-progesteron Users. Obstet Gynecol 62, 435-443 (1983)

  11. Gambrell RD.  The Menopause: Benefits and Risks of Estrogen-progesteron Replacement Therapy. Fertil Steril 37, 457-474 (1982)


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