Osteoporosis

Osteoporosis is a multifunctional skeletal disorder of progressive bone mass loss and demineralisation, causing an increased risk of fracture. It is the most common metabolic bone disorder in the U.S., afflicting a great majority of Post-menopausal women, annually, causing over 1.3 million fractures at a cost of over $ 10 billion.

The role of Progesterone in menopausal osteoporosis has been overlooked by conventional medicine. Along with a program of good diet, exercise and attention to other nutritional factors, the addition of bio-identical hormones, Progesterone, DHEA and Oestrogen are an important factor in the prevention and treatment of Osteoporosis.

JC Prior, publishing in Endocrine Reviews, has identified Progesterone as a bone trophic hormone. Dr John Lee used serial bone density measurements on his practice patients and reported a 10% mean increase in bone density in the first 6 to 12 months with annual increases of 3-5%. There are other numerous anecdotal/clinical reports of post-menopausal women using bio-identical hormones increasing bone mineral density.

Risk Factors for Osteoporosis:

Genetic or hereditary factors.
White women of Northern European extraction
Thin physique.
Lack of exercise.
Cigarette smoking (leads to metabolic acidosis and calcium loss in urine).
Lack of Vitamin D (needed for calcium absorption and mineralization of bone).
Calcium and Magnesium deficiency.
Meat based (high protein) diet (leads to metabolic and calcium loss in urine).
Alcoholism.
Excess Thyroid.
Cortisone medication.
Lack of balanced hormones.
Lack of gastric HCI (needed for calcium absorption).
Diuretics.
Lack of Silicon, Boron, Vitamins C and A.
Living in an industrialised country.

Bone Physiology

Bone is living tissue, made of mineralised cartilage, being made, un-made and made anew.

PRE-PUBERTAL bone growth is mediated by the Pituitary growth Hormone. At puberty, Oestrogen fuses growth plates (epiphyses) and stops further bone growth. After puberty, bone restoration and bone renewal are dependent on sex hormones. Bone mass reflects the balance of resorption and new bone formation. 'Osteoclasts' re-absorb old bone and 'Osteoblasts' make new bone.

Remodeling or Bone Turnover time:
Cortical bone 12-14 years
Trabecular bone 3-5 years
(Cortical bone is laminar, like a tight roll of papers, and more dense (for torsion strength). Trabecular bone is made of struts with space between and are less dense (compression strength)

Oestrogen restrains bone resorption and Progesterone stimulates new bone formation.
Osteoporosis accelerates with Menopause, when the decline of Oestrogen allows temporary surge of Osteoclast-mediated bone resorption causing bone loss of 5 -7% a year. 5-6 years after Menopause bone loss continues at 1.5% per year regardless of Oestrogen. Progesterone (and Testosterone) receptors are found in Osteoblasts where Progesterone and/or Testosterone stimulate new bone formation.

Calcium Chain

Soil is the source of all minerals. Plants are the primary food source of digestible, absorbable calcium. Ingestion of plants puts calcium in the stomach. Absorption into the blood stream requires Vitamin D and gastric HCI (Hydrochloric-acid). Incorporation into the bone requires (a)bone stress (exercise), (b) Progesterone or Testosterone which stimulates Osteoblasts, (c) Oestrogen which restrains Osteoclasts, and (d) proper micronutrients (vitamins and minerals). It is important that excess protein intake, long term antibiotics, calcium-loosing diuretics and Fluoride are avoided.

Conventional Treatment

Conventional treatment consists of Oestrogen, Vitamin D and Calcium. Since this does not result in bone improvement, newer treatments include Calcitonin, Di-Phosphonates such as Etidronate (Didronel) and Alendronate(Fosamax) and Fluoride. In some cases, Doctors are recommending Testosterone. Sadly, to date, Natural Hormone therapy has been overlooked.

Progesterone Hypothesis:

Peak bone mass occurs in women at age 35. Progressive loss of bone mass starts 15 years before Menopause. Oestrogen decline does not occur until Menopause. Progesterone decline matches the early occurrence of bone mass loss, an indication of less new bone formation despite Oestrogen. Pre-menopausal female Athletes develop Osteoporosis when Progesterone declines despite their exercise and good levels of Oestrogen. Oestrogen therapy does not increase bone mass, it only slows bone loss. Therefore, other factors being present, Osteoporosis is due largely to Progesterone deficiency.

In Post-menopausal women, bone mass will increase on average 15% over three years when Progesterone is given in normal physiologic doses along with correct diet, exercise and a few important Nutritional Supplements. Usually, the lower the initial bone mass, the greater the beneficial effects of Progesterone in women with adequate bone mass. Progesterone therapy maintains good bones!

Having underlined the fact that treatment needs to start with Progesterone it is also critical to note that multiple therapies will often achieve quicker rises in BMD. This Includes bio-identical DHEA and/or Oestrogen hormones, healthy organic diet, appropriate vitamin and mineral supplementation and regular weight bearing exercise.

Ref: Bennett F. M.D