Osteoporosis

Introductory information

The National Institutes of Health have declared the years 2002-2011 to be the Bone and Joint Decade, and from the website of the National Institute of Arthritis and Musculoskeletal and Skin Diseases, we can click to the Surgeon General’s report on bone health and osteoporosis (1). Two sections of the report provide information regarding lifestyle recommendations, the Executive Summary (2), and the chapter on lifestyle for bone health (3).

In the lifestyle chapter, we are given the brief standard suggestion to eat more fruits, vegetables and whole grains, without much emphasis as to their [fruits/veggies] important relationship to bone health. We are also told to drink three 8-ounce glasses of low-fat milk, which will lead to adequate levels of calcium in the diet. Vitamin D is also recommended (3).

Unless one goes hunting in pubmed for additional information, or happens across some key articles by chance, it is unlikely that a busy doctor or interested patient would come to the conclusion that osteoporosis represents a state of chronic subclinical inflammation. I came across this relationship several years ago, which lead me to write a commentary in JMPT on the topic (4).

At first glance, I realize that it seems unlikely that chronic inflammation would promote osteoporosis, and much more likely that the problem is related to a deficiency in calcium. However, the evidence clearly demonstrates that chronic inflammation is a key culprit and we should appreciate that the focus on calcium is likely because there is an abundance of calcium in bone; however, just because there is calcium in bone, we should not jump to the conclusion that eating more calcium will protect bone.

The key cells involved in bone metabolism are osteoclasts and osteoblasts, and they are active throughout life. Our skeletons go through a lifelong process of bone degradation and deposition, referred to as remodeling. The function of osteoclasts is to degrade bone, while osteoblasts function to deposit or form bone. If this balance becomes skewed toward increased osteoclast and/or reduced osteoblast activity, the outcome would be a loss of bone mass. Scientific knowledge of this relationship is translated into risk factors for doctors and patients to consider. The standard view of osteoporosis provides for a list of both modifiable and non-modifiable risk factors for osteoporosis. As would be suspected, based on what was mentioned earlier, calcium is the only nutritional factor mention.

 

Traditional risk factors for osteoporosis

Traditional modifiable risk factors for osteoporosis (5):
     • Cigarette smoking
     • Low body weight (<127 lb)
     • Estrogen or androgen deficiency
     • Low calcium intake
     • Excessive alcohol intake
     • Inadequate physical activity
     • Medications (e.g., steroids, anti-seizure meds, hormone suppressants,
        vitamin A)
     • Chronic conditions (e.g., diabetes; thyroid, liver, or renal disease)

Traditional non-modifiable risk factors for osteoporosis (5):
     • White race
     • Advanced age
     • Female sex
     • Dementia
     • Poor health/frailty
     • History of fracture of first-degree relative
     • Personal history of fracture as adult

Notice again, please, that nothing about a low-grade chronic inflammatory state is mentioned, and we are offered little lifestyle advice, save or stop smoking, exercise regularly, and take in more calcium, which typically means dairy and supplements. As you will see, these changes do not reflect the substantial lifestyle modifications needed to promote bone health.

Evidence-based risk factors for osteoporosis

Approximately 7.2% of women 50 and older have osteoporosis, and another 40% have reduced bone density (6), and this group is progressing towards developing osteoporosis. Based on the evidence that follows regarding nutrition, it seems appropriate to state that women at risk for osteoporosis, or those already diagnosed, are not typically given the best clinical information available.

 The current dietary habits of the average American represent an effort to pursue chronic inflammation and the expression of diseases such as osteoporosis. For example, research suggests that almost 75% of calories of the average American’s diet come from foods that were not consumed by our recent hunter-gatherer ancestors. Consider that 23.9% of our caloric intake comes from grains (20.4% from refined grains), 18.6% from refined sugars, 17.6% from refined omega-6 seed oils (corn, soybean, sunflower, cottonseed, safflower, peanut, etc.) 10.6% from dairy, and about 1.4% comes from alcohol (6).

The remaining 28% comes from a marginal intake of fruits, vegetables, nuts, and legumes, and a substantial intake of domestic, feedlot, grain-fed meat. We know that wild game is about 2-4% by fat by weight, while modern feedlot meat is 20-24% fat by weight. Essentially, this means that we are eating unhealthy, obese animals (7).

In short, our diet in America today consists grains, sugars, omega-6 fatty acids, trans fats, and obese meat, and is substantially deficient in fruits and vegetables. The outcome of this pattern of eating is the typical inflamed, swollen-looking, overweight American, who is prone to osteoporosis and other chronic diseases. Clearly, when keeping the average American’s diet and state of health in mind, it is truly laughable to seriously consider that taking a calcium supplement, drinking milk, and/or taking medications like Fosamax, will help to prevent or effectively treat osteoporosis. Consider the evidence.

We know that refined grains, refined sugar, and omega-6 rich seed oils promote the development of diabetes (6,8). Not surprisingly, we now know that type 2 diabetes is caused by, and promotes, a systemic pro-inflammatory state (8-11). Coincidentally, it appears that type 2 diabetes is associated with reduced bone density (5).

 

Omega-6 fatty acids and bone loss

Recall from above that 17.6% percent of calories come from omega-6 seed oils. We also know that the oil in grains consists mostly of omega-6 fatty acids (8), and we know that modern domestic meat contains increased amounts of omega-6 (7). We have also known for many years that omega-6 fatty acids are pro-inflammatory, and their excessive consumption leads to the development of heart disease, cancer, and numerous other chronic inflammatory conditions (8), including osteoporosis (12-15).

How do omega-6 fatty acids lead to bone loss? Research suggests that the prostaglandin E2, which is formed from arachidonic acid (an omega-6 fatty acid) leads to the stimulation of bone degrading osteoclasts and the inhibition of bone building osteoblasts (12-14).

Which foods in our diet contain an excessive amount of omega-6 fatty acids? All grains and the seed oils mentioned earlier contain the omega-6 linoleic acid, which our bodies then convert into arachidonic acid. We also get arachidonic acid preformed in the obese meat we eat from animals that are fed excessive amounts of corn.

Foods that contain low levels of omega-6 fatty acids and appropriate levels of anti-inflammatory omega-3 fatty acids include green vegetables and grass fed animal products, as well as wild game (6,7,8). Supplementation with omega-3 fatty acids from fish oil is also recommended.

 

Tissue acidity and bone loss

Regretfully, the pro-inflammatory American diet is also rich in foods that lower body pH into the acidic range, which leads to the resorption of alkaline bone minerals to increase pH back to an acceptable level (6). Consider how prominent researchers in the field of diet and pH balance describe this problem (16): 

“Increasing evidence suggests that such persisting, albeit low-grade acidosis, and the relentless operation of responding homeostatic mechanisms, results in numerous injurious effects on the body, including dissolution of bone, muscle wasting, kidney stone formation, and damage to the kidney.”

Which foods promote tissue acidity? First on the list are animal products (meat, fish, fowl, and eggs), which often leads people to condemn animal products, which is a grave mistake. Humans and other mammals have consumed animal products for thousands of years and maintained normal bone density. This is because other than animal products, humans ate only vegetation (fruits and vegetables), which is highly alkaline and served to counterbalance the acidity from meat.

Instead of eating an abundance of alkaline fruits and vegetables, we now consume acid producing grains, cheese, and soda with our meat. So, instead of buffering acidic meat with vegetables and fruit, we now increase the acid load which leads to both bone and muscle loss as we age; and we have known for many years that, like omega-6 fatty acids, an acidic environment leads to the stimulation of bone degrading osteoclasts and the inhibition of bone building osteoblasts (17).

In summary, foods that promote an acidic pH included meat, grains, cheese, and soda. Low fat cheese is thought to be the most acidic food of all. Foods that promote an alkaline pH include fruits, vegetables, potatoes, and nuts. Milk, cream, and legumes are essentially neutral, when it comes to their contribution to our acid/alkaline balance. The chloride in table salt, i.e., sodium chloride, is also acidic, which means that salt intake should be limited considerably (6). 

 

Animal proteins and fruits/vegetables for optimal bone growth

It is not uncommon to read/hear that protein intake will cause bone loss. This is thought only to occur when animal products are consumed along with the other acid promoting foods mentioned above (grains, cheese, salt, and soda). Consider what a leading researcher says when meat is consumed with alkaline vegetation:

“In the combination of a net base-producing, alkalosis-producing diet (from fruits, vegetables, and potatoes) and a high-protein diet (meat, fish chicken, eggs) might optimize peak bone mass achievement during development and greatly mitigate or eliminate age-related decreases in bone mass. Indeed, from an evolutionary perspective, natural selection may have designed human physiology to best fit a dietary environment of high protein consumption and net base production (18).”

In short, protein supplies the amino acid substrates for building bone matrix. The essential amino acids increase bone trabecular architecture, cortical thickness, and bone strength (18). Two randomized controlled trials showed that increased protein intake dramatically improved outcomes after hip fracture. Subsequent work showed that protein supplements reduce bone loss at the contralateral hip in patients with upper-femoral fracture (19).

Substantial literature now suggests that fruit and vegetable intake is the dietary factor that is most correlated with optimal bone mineral density (16-18,20-24). In fact, one review reported that vegetable and fruit consumption, and NOT dairy, was associated with optimal bone mineral density (22).

 

Supplementation for osteoporosis

The environment for optimal bone deposition can only be created by the appropriate diet, as described above. Supplementation without dietary changes is not likely to exert an appreciable effect on bone health.

The goal then for supplementation is to support the anti-inflammatory state created by diet. Accordingly, in addition to eating an anti-inflammatory diet (see the Deflaming Guides), a good choice would be the Bone Health Promotion program that includes a special form of calcium called microcrystalline hydroxyapatitie.

 

References

1. http://www.niams.nih.gov/bone/index.htm
2. http://www.surgeongeneral.gov/library/bonehealth/
3. http://www.surgeongeneral.gov/library/bonehealth/chapter_7.html (Chapter on lifestyle for bone health)
4. Seaman D. Health care for our bones: A practical nutritional approach to preventing osteoporosis. J Manip Physiol Ther. 2004;27:591-95
5. Chau DL, Edelman SV. Osteoporosis and diabetes. Clinical Diabetes. 2002; 20:153-57.
6. Cordain L, Eaton SB, Sebastian A, Mann N, Lindeberg S, Watkins BA, O’Keefe JH, Brand-Miller J. Origins and evolution of the Western diet: health implications for the 21st century. Am J Clin Nutr. 2005; 81(2):341-54.
7. O’Keefe JH Jr, Cordain L. Cardiovascular disease resulting from a diet and lifestyle at odds with our Paleolithic genome: how to become a 21st-century hunter-gatherer. Mayo Clin Proc. 2004; 79(1):101-8.
8. Simopoulos AP. Essential fatty acids in health and chronic disease.Am J Clin Nutr. 1999; 70(3 Suppl):560S-569S.
9. Grimble RF. Inflammatory status and insulin resistance. Curr Opin Clin Nutr Metab Care. 2002; 5:551-59.
10. van Exel E et al. Low production capacity of interleukin-10 associates with the metabolic syndrome and type 2 diabetes: the Leiden 85-Plus Study. Diabetes. 2002; 51:1088-92.
11. Evans JL, Goldfine ID, Maddux BA, Grodsky GM. Oxidative stress and stress-activated signaling pathways: a unifying hypothesis of type 2 diabetes. Endocr Rev. 2002 ;23:599-622.
12. Watkins BA, Lippman HE, Le Bouteiller L, Li Y, Seifert MF. Bioactive fatty acids: role in bone biology and bone cell function. Prog Lipid Res. 2001; 40:125-48.
13. Watkins BA, Li Y, Lippman HE, Seifert MF. Omega-3 polyunsaturated fatty acids and skeletal health. Exp Biol Med 2001; 226:485-97.
14. Watkins BA, Li Y, Seifert MF. Nutraceutical fatty acids as biochemical and molecular modulators of skeletal biology. J Am Coll Nutr. 2001h;20(5 Suppl):410S-416S; discussion 417S-420S.
15. Högström, M., Nordström, P., Nordström, A. n–3 Fatty acids are positively associated with peak bone mineral density and bone accrual in healthy men: the NO2 Study. Am J Clin Nutr. 2007;3:803-807.
16. Sebastian A, Frassetto LA, Sellmeyer DE, Merriam RL, Morris RC. Estimation of the net acid load of the diet of ancestral preagricultural Homo sapiens and their hominid ancestors. Am J Clin Nutr. 2002;76(6):1308-16.
17. Sebastian A et al. Improved mineral balance and skeletal metabolism in postmenopausal women treated with potassium bicarbonate. New Eng J Med. 1994; 330:1776-81.
18. Sebastian A. Dietary protein content and the diet’s net acid load: opposing effects on bone health. Am J Clin Nutr. 2005;82:921-22.
19. Heaney RP. Protein intake and bone health: the influence of belief systems on the conduct of nutritional science. Am J Clin Nutr. 2001;73:5-6.
20. 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.
21. Hegsted DM. Fractures, calcium, and the modern diet. Am J Clin Nutr. 2001; 74: 571-73.
22. New SA. Dietary influences on bone mass and bone metabolism: further evidence of a positive link between fruit and vegetable consumption and bone health? Am J Clin Nutr. 2000; 71: 142-51.
23. Lanham-New SA. F ruit and vegetables: the unexpected natural answer to the question of osteoporosis prevention? Am J Clin Nutr. 2006;83:1254–55
24. Prynne CJ, Mishra GD, O’Connell MA, et al. Fruit and vegetable intakes and bone mineral status: a cross-sectional study in 5 age and sex cohorts. Am J Clin Nutr. 2006;83:1420–28.