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 general attenuation of femoral bone loss in the elderly. Several studies have documented the benefits of using supplemental protein (20 g/day) for hip fracture patients. 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-g increment of protein consumed, an extra 60 mg of urinary calcium is excreted. 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. 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 under-consume vegetables, fruits, nuts and seeds, food 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, particularity 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. 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. 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. 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, which are suboptimal (the adult RDA is currently 0.8 g/kg/day, roughly 54-70 g for males and 40-60 g for females).
A high-protein diet (well above or double 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 foods, 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 intake — need not necessarily be of detriment to bone. Such a diet could likely benefit bone if one consumed enough base-forming foods and nutrients to neutralize net endogenous acid excretion.
In the US, 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. Such a moderate level of protein would have as its low end the RDA for protein of 0.8 g per kg of body weight per day. At the high end it would range from 1.0 to 1.5 g/kg/day. (A kilogram equals approximately 2.2 pounds. At 1.0 g of protein per kg, a 150-pound person would need 68 g of protein, and at 0.8 g per kg, he or she would need 55 g of protein a day.)