How much protein is good for bone? Although it may seem simplistic, the answer appears to be "just the right amount, not too much and not too little."

Protein is important to the integrity of bone, organs, and body systems at all life stages, and protein restriction has been shown to reduce growth hormone. Low protein and low albumin are strongly and independently associated with functional outcome after hip fracture. In addition, short-term studies have suggested that acute intakes of low protein can cause a reduction of intestinal calcium absorption resulting in secondary hyperparathyroidism. Further, higher protein status has been associated with shorter hospital stays, reduced mortality, reduced rate of complications after a hip fracture, and with general attenuation of femoral bone loss in the elderly. Several studies have documented the benefits of using supplemental protein (20 grams/day) for hip fracture patients (Kakar and Einhorn;  Rizzoli et al.). All in all, adequate protein is essential for bone growth, maintenance, and renewal.

On the other hand, it is often argued that excessive protein, particularly animal protein, is deleterious to bone. Some studies suggest that protein intake influences urinary calcium excretion to such an extent that for each 50-gram increment of protein consumed an extra 60 mg of urinary calcium is excreted (Hannan). Thus it follows that, if uncompensated, a high protein intake would lead to bone loss. Cross-cultural studies, in fact, suggest that animal protein intake is positively associated with increased hip fracture incidence. Several worldwide surveys document that the countries with highest animal protein intakes are those with highest hip fracture rates (Abelow et al., Frassetto et al. 2000). The proposed explanation of this relationship between animal protein and hip fracture incidence relates to the fact that animal protein is rich in acid-forming sulfur-containing amino acids and low in base-forming precursors (such as vegetable sources of potassium citrate). Further, the contemporary cultures consuming a high animal protein diet also tend to underconsume vegetables, fruits, nuts, and seeds—foods high in base-forming precursors. This combination contributes to chronic low-grade metabolic acidosis and subsequent bone weakening. The growing body of literature documenting the association between chronic low-grade metabolic acidosis and bone loss bolsters the argument that high dietary protein, if not balanced with high base-forming precursor intake, can have a detrimental impact on bone.

The clinical trials on protein intake and bone health report contradictory results and remind us that there are many variables which need to be considered when discussing the bone/protein relationship. Dietary protein is best considered in the context of the entire diet of each individual, particularly in terms of the balance between acid-forming and base-forming foodstuffs and overall mineral intake. In simple terms this can be seen as the relationship between protein and potassium intakes, as documented by Dr. Lynda Frassetto at the University of California, San Francisco (Frassetto et al. 1998).

In this regard, insights from our evolutionary past might be helpful. Anthropologists speculate that our human ancestral diet during the Paleolithic Period 100,000 years ago was more nutrient dense than contemporary diets not only in protein, but also in calcium, potassium, magnesium, and zinc, while low in sodium chloride, sugars, and void of refined carbohydrates (Eaton and Konner). For example, calcium, potassium, and protein intakes were two to three times higher than current intake levels, while sodium intake was seven times lower. These diets were balanced high protein, high mineral, high phyto-nutrient, alkalizing diets. Overall, in fact, researchers report that 87% of likely prehistoric diets provided an excess of base while contemporary Westernized diets provide an excess of acid (Sebastian et al.). Our diet-induced low grade metabolic acidity could well be the most significant, and least well recognized, of all modern bone-depleting risk factors.

GUIDELINES FOR PROTEIN INTAKE

• In this country as a whole, a low protein and low nutrient diet increases fracture risk and does not favor bone at any life stage.
  
• The elderly and underweight frequently exhibit protein intakes below the RDA (the adult RDA is currently 0.8 grams/kilo/day, roughly 54-70 grams for males and 40-60 grams for females).
  
• A high protein diet (well above or doubled the RDA) in association with low intakes of calcium, magnesium, potassium, and other nutrients increases urinary mineral loss and worsens chronic low grade metabolic acidosis, and is detrimental to bone at all ages.
  
• The average American labors under chronic low-grade metabolic acidosis, which will be worsened by increased protein intake unless compensated for in one way or another. Compensation could involve increasing the intake of base-forming foodstuffs, or supplementing with alkalizing mineral compounds, or reducing intake of non-protein acid-forming foods such as grain products.
  
• Higher proteins diets in the context of a nutrient dense overall diet, which includes high calcium, potassium, and magnesium intakes need not necessarily be detrimental to bone. Such a diet could likely benefit bone if one consumed enough base-forming foodstuffs and nutrients to neutralize net endogenous acid excretion.
  
• In the U.S., diets containing moderate protein intakes are probably optimal for bone health when this protein intake is associated with adequate base-forming precursors and sufficient mineral intake (Ilich and Kerstetter). Such a moderate level of protein would have as its low end the RDA for protein of 0.8 grams per kilo of body weight per day. At the high end it would range from 1.0 to 1.5 grams/kilo/day. (A kilo equals approximately 2.2 pounds. At 1.0 grams of protein per kilo, a 150-pound person would need 68 grams of protein and at 0.8 grams per kilo, they would need 55 grams of protein a day.)

References

Kakar, S. and T.A. Einhorn. 2004. Importance of nutrition in fracture healing. In  Nutrition and Bone Health, ed. M.F. Holick and B. Dawson-Hughes, Totowa, NJ: Humana Press, pp. 85-103.
Rizzoli, R.,  P. Ammann, S. Bourrin, T. Chevalley, and J.P. Bonjour. 2001. Protein intake and bone homeostasis. In Nutritional Aspects of Osteoporosis, ed. P. Burckhardt, B. Dawson-Hughes, and R.P. Heaney. San Diego: Academic Press, pp. 219-35.
Hannan,  M.T. 2001. Dietary protein and effects upon bone health in elderly men and women. In Nutritional Aspects of Osteoporosis, ed. P. Burckhardt, B. Dawson-Hughes, and R.P. Heaney. San Diego: Academic Press, pp. 237-49.
Abelow,  B.J., T. R. Holford, and K. L. Insogna. 1992. Cross-cultural association between dietary animal protein and hip fracture: A hypothesis. Calcif Tissue Int 50(1) pp. 14-8.
Frassetto,  L.A., K. M. Todd, R. C. Morris Jr., and A. Sebastian. 2000. Worldwide incidence of hip fracture in elderly women: Relation to consumption of animal and vegetable foods. J Gerontol A Biol Sci Med Sci 55(10) pp. M585-92.
———. 1998. Estimation of net endogenous noncarbonic acid production in humans from diet potassium and protein contents. Am J Clin Nutr 68(3) pp. 576-83.
Eaton,  S.B. and M. Konner.  1985. Paleolithic nutrition. A consideration of its nature and current implications. New England Journal of Medicine 312(5) pp. 283-9.
Sebastian A., L. A. Frassetto, D. E. Sellmeyer, R. L. Merriam, and R.C. Morris, Jr. 2002. Estimation of the net acid load of the diet of ancestral preagricultural homo sapiens and their hominid ancestors. Am J Clin Nutr 76(6) pp. 1308-16.
 Ilich, J.Z. and  J. E. Kerstetter. 2000. Nutrition in bone health revisited: A story beyond calcium. J Am Coll Nutr 19(6) pp. 715-37.