Osteoporosis is estimated to cause 1.5 million fractures—mainly of the spine and hip— annually in the United States. The morbidity and indirect mortality rates are very high; 50% of hip fractures result in mortality and of the 50% that leave the hospital, 50% go to nursing homes and never leave. Osteoporosis is characterized by a decrease in the amount of bone present to a level below which it is capable of maintaining the structural integrity of the skeleton.1 Sometimes the first symptom of osteoporosis is a spontaneous vertebral fracture. The rate of bone formation in osteoporosis is often normal, whereas the rate of bone resorption is increased. The most common cause of osteoporosis is declining levels of estrogen associated with menopause in women, although other causes such as alcoholism and celiac disease exist as well.

Modifiable osteoporosis risk factors include smoking cessation, moderation in alcohol consumption, and weight-bearing physical activity. The most important factors that increase the risk of osteoporosis are a family history of osteoporosis in a first-degree relative, current cigarette smoking, and low body weight, regardless of height.

Osteoporosis and osteopenia (low bone mineral density) are confirmed by a DXA scan of the femur, lumbar spine, and non-dominant radius. X-rays are only able to identify significant osteoporosis.

What can I do to prevent and/or treat osteoporosis?

Anthropological and epidemiological studies, as well as studies at the molecular level, indicate that human beings evolved on a diet with a ratio of omega-6 to omega-3 essential fatty acids (EFA) of approximately 1/1, whereas in Western diets the ratio is 15/1 to 16.7/1. 2

A high omega-6/omega-3 ratio, as is found in today’s Western diets, promotes the pathogenesis of many diseases, including cardiovascular disease, cancer, osteoporosis, and inflammatory and autoimmune diseases, whereas increased levels of omega-3 polyunsaturated fatty acids (PUFA) (a lower omega-6/omega-3 ratio), exert suppressive effects.

Here is the biochemistry: omega-6 fatty acids are precursors to prostaglandin E2 (PGE2), an inflammatory fatty acid. Bone formation and resorption are regulated by hormones and local environmental factors. The most important local factor is PGE2, a potent stimulator of bone resorption and, to date, the principle prostaglandin affecting bone metabolism. 3 As noted above, since in osteoporosis bone formation is usually normal, and the rate of bone resorption is increased, over the course of a lifetime, decreasing factors that cause increased bone resorption is essential to the management of bone loss.

Why is our diet so high in omega-6 fatty acids? We get most of our omega-6 fatty acids from polyunsaturated fat acids found primarily in vegetable oils such as corn oil (59% PUFA’s), sunflower oil (69% PUFA’s), and safflower oil (79% PUFA’s).

Therefore, my first recommendation is to cook with anti-inflammatory oils; olive oil (10% PUFA’s), coconut oil (3% PUFA’s), and butter (4% PUFA’s).

Many of the foods we eat are prepared in these oils. Even foods that don’t look oily, like bagels and breads, are prepared with omega-6 fatty acid-laden oils. For example, corn chips and potato chips both have a staggering omega-6:omega-3 fatty acid ratio of 60:1.

White bread has a ratio of omega-6:omega-3 fatty acids of a dismal 21:1, whole wheat bread 27:1 and oatmeal 21:1. Clearly, grains in and of themselves are high in omega-6 fatty acids.

In contrast, a white potato has a much more favorable omega-6:omega-3 ratio of 3:1 and a sweet potato 4:1. 4

As a result, my second recommendation is to avoid the grain family!

Further reason to avoid grains is that they are acidic in the body, and alkaline producing dietary components (specifically, potassium, magnesium, and fruits and vegetables) contribute to the maintenance of bone mineral density. 5A 2003 article in the American Journal of Physiology – Renal Physiology reports that neutralizing (or alkalinizing) our western diet inhibits bone resorption, the very element that is increased in osteoporosis.

Magnesium supplementation has been found to increase bone density and stop bone loss, decrease bone pain and deformity of vertebrae in osteoporotic women. 6 In this study, supplementation of magnesium was 250-750 mg/day for 24 months. Calcium is important too, but it is already fortified in many foods. Studies show that 33-43% of our population is Magnesium deficient. The primary reason for this is that our diet is too acidic. Studies show that if we alkalinize our diet, even without taking Magnesium supplements, our intracellular Magnesium levels go up. What this means is that the acidity in our diet (too many grains) prevents Magnesium from being absorbed. When we are acidic, we excrete rather than absorb Magnesium from our foods.

I recommend taking magnesium glycinate and microcrystaline hydroxyapatite calcium in supplements.

Finally, vitamin D3 is now being focused upon as a vital ingredient to maintain bone density. It is more usual than unusual for us to be deficient in the northern hemispheres, especially in the winter. I recommend getting your vitamin D3 level tested and supplementing to ideal levels, which are 50-70 ng/ml. The literature now states that serum vitamin D levels are often low in osteoporotic patients. Vitamin D supplementation reduces the incidence of vertebral fractures by 37%.

Bone mineral density peaks in women around age 25. I find this very interesting because in Traditional Chinese Medicine, kidney qi in women peaks around age 25 as well. Kidney qi is responsible for both fertility and bone mineral density, among other things.

Research suggests that the benefit of exercise is not so much that weight-bearing exercise and resistance exercise increases bone mineral density, but rather that it decreases the risk of falls. It creates more coordination, strength and stability. Since falls and subsequent hip fractures have such a high morbidity rate, anything that decreases the possibility of this occurring is beneficial.

I therefore finally recommend aerobic exercise and muscle maintaining or muscle-building resistance exercise.

Osteoporosis is defined by a DXA T-Score of -2.5 in the absence of risk factors for fracture and -1.5 in the presence of risk factors for fracture. It is essential that pharmacologic medication be taken to restore bone density. Biphosphonates work by significantly increasing bone density and reducing the incidence of both vertebral and nonvertebral fractures. Recent news suggesting that biphosphonate therapy resulted in spontaneous jaw fractures failed to mention that this only occurred in cancer patients who were receiving very high doses intravenously for bone metastases, and not those taking oral medication for osteoporosis. Biphosphonates, in addition to calcium, magnesium and vitamin D supplementation is recommended for the management of osteoporosis.

In Summary

Dietary factors can exert considerable influence on the development and progression of osteoporosis. Limiting the amount of omega-6 fatty acids in our diet will decrease the production of the inflammatory chemical PGE2 and decrease bone resorption. Decreasing the amounts of highly refined vegetable oils and grains will limit the omega-6 fatty acids in our diet. Alkalinizing our diet by consuming lots of vegetables and fruits, which contain a lot of potassium, will help our body absorb magnesium and decrease bone resorption. Supplementing with omega-3 fatty acids, taking magnesium, calcium and vitamin D3 will benefit bone density. Exercise is beneficial to improve balance and coordination. And taking biophosphonates, in addition to the supplements mentioned above, if you are already osteopenic or osteoporotic, will decrease your risk of fracture.

Other Resources

Definition of Osteoporosis: http://en.wikipedia.org/wiki/Osteoporosis

National Institute of Health: http://www.niams.nih.gov/Health_Info/Bone/Osteoporosis/


  1. McPhee J, Papadakis M. 2011 Current Medical Diagnosis & Treatment. McGraw Hill, Lange, 50th Anniversary Edition. p. 1099.
  2. Simopolous AP. Evolutionary aspects of diet, the omega-6/omega-3 ratio and genetic variation: nutritional implications for chronic disease. Biomed Pharmacother. 2006; 60 (9):502-07.
  3. Watkins BA et al. Omega-3 polyunsaturated fatty acids and skeletal health. Exp Biol Med 2001; 226:485-97.
  4. Enig MG. Know your fats. Silver Spring: Bethesda Press; 2000: p. 123, 142, 280-292.
  5. Tucker KL. Potassium, magnesium, and fruit and vegetable intakes are associated with greater bone mineral density in elderly men and women. Am J Clin Nutr 1999; 69:727-36.
  6. Dreosti IE. Magnesium status and health. Nutr Rev 1995; 53(9):S23-S27.


I liked your article, except I don’t agree with your position on bisphosphonates. Bisphosphonates work by killing the osteoclasts which are responsible for breaking down old bone, which is then replaced by new bone by the osteoblast cells. Healthy bone structure depends upon the continuous remodeling of bone by the osteoclasts and osteoblasts. When the osteoclasts are killed, the bone will appear denser on scans, but will become more fragile with time. The spontaneous pathological fractures of the femur in patients on long-term bisphosphonate therapy are much more worrisome than the jaw fractures that you sited.

See: http://www.nejm.org/doi/full/10.1056/NEJMc0707493

Also, the hormone progesterone stimulates new bone synthesis. Your pre and post menopausal patients should be checked for saliva progesterone levels. Those who are low should be supplemented with bioidentical progesterone in physiologic doses.

I wrote an article several years ago on this subject:


Some studies suggest that people who don’ t get enough of some essential fatty acids (particularly EPA and GLA) are more likely to have bone loss than those with normal levels of these fatty acids. In a study of women over 65 with osteoporosis, those who took EPA and GLA supplements had less bone loss over 3 years than those who took placebo. Many of these women also experienced an increase in bone density.

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