Are Higher Protein
Intakes Responsible for Excessive
Calcium Excretion?

by Loren Cordain, Ph.D.
Copyright © 1999 by Loren Cordain. All rights reserved.

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IMPORTANT WORD DEFINITIONS: Calciuresis: Excretion of calcium in the urine. Dermis: The second layer of skin underneath the epidermis, or surface, layer. Renal: Of, or relating to, the kidneys. Serum: Refers to levels of nutrients as measured in the blood.
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Based on and edited from postings made to the Paleodiet listgroup on 8/14/97, 10/9/97, and 6/11/98.

The paradox of high bone mass in Paleolithic skeletons

The question of high levels of protein in the diet and the issue of calcium excretion is of particular interest in light of Paleolithic diet research for two reasons. First, because estimates of the levels of protein--and specifically animal protein--in the human diet during at least the last 1.7 million years of human evolution (from the time of Homo erectus) are much higher than considered prudent in some sectors of the nutritional research community today. And second because, at the very same time, the fossil evidence shows Paleolithic humans to have had high bone mass that would have been robust and fracture-resistant compared to that of modern Western humans: in exact opposition to some of current nutritional theory about the alleged role of protein in causing osteoporosis. Here we'll take a look at this apparent paradox.
Protein's effect on bone loss. Three recent papers which concern the topic of high dietary protein intake and bone loss are:


Heaney RP (1998) "Excess dietary protein may not adversely affect bone." Journal of Nutrition, vol. 128, pp. 1054-1057.

Massey LK (1998) "Does excess dietary protein adversely affect bone? Symposium overview." Journal of Nutrition, vol. 128, pp. 1048-1050.

Barzel US, Massey LK (1998) "Excess dietary protein can adversely affect bone." Journal of Nutrition, vol. 128, pp. 1051-1053.

Heaney [1998] concluded that if the calcium-to-protein ratio (mg:g) is greater than or equal to 20, then there is probably adequate protection for the skeleton. Using an assumed plant/animal subsistence ratio of 35:65 as representative of estimated intake during Paleolithic times, the calcium/protein ratio for modern diets based upon Stone-Age food categories (fruits, vegetables, and lean meats, including fish, poultry, shellfish, game meat, and organ meats), would be about 2.47. (The plant/animal-food ratio of 35:65 comes from our research group based on an updated reanalysis of recent-day hunter-gatherer diets as recorded in the Ethnographic Atlas; we hope to publish this analysis in an upcoming journal paper.) If one assumes a subsistence ratio exactly opposite (65% plant and 35% animal), as my colleague Boyd Eaton has [Eaton et al. 1985], and uses his wild plant and animal food database, then the calcium/protein ratio would be 6.29 for Stone-Age humans. The median calcium/protein ratio for 50 to 59-year-old women as shown using NHANES III (National Health and Nutrition Examination Survey) data is 9.30 [Heaney 1998].
The paradox of Stone-Age humans. From these data, it appears that it would be virtually impossible for Stone-Age humans, living in their native environment and eating wild plant and animal foods, to have come remotely close to a dietary calcium/protein ratio equaling or exceeding 20. Paradoxically, the fossil record shows Stone-Age humans to have thick bones with large cortical cross-sectional areas [Ruff et al. 1993]. Consequently, it is likely that the skeleton of Stone-Age man and woman would have been more robust and fracture-resistant than that of Western, industrialized men and women [Ruff et al. 1993; Cordain, Gotshall, and Eaton 1997].


Multiple factors aside from protein also affect calcium balance

How could this apparent paradox be possible? There are several notable differences between modern diets and Paleodiets other than protein consumption that can affect calcium balance.

Sodium chloride (salt) consumption. One is that Stone-Age men and women did not consume supplemental dietary sodium chloride (salt), which like protein can also cause increased calciuresis (calcium excretion) [Nordin et al. 1993] and loss of bone mass [Devine et al. 1995]. Because the kidney must obligatorily excrete calcium with sodium [Nordin et al. 1993], high levels of dietary sodium are now generally recognized to be the single greatest dietary risk factor for osteoporosis [Matkovic et al. 1995; Devine et al. 1995; Cappuccio 1996]. It should go without saying that in this context, "high" levels of dietary sodium are simply normal levels in Western societies.

Imbalance in the calcium/magnesium ratio . Further, the calcium/magnesium ratio was about 1:1 in pre-agricultural diets, whereas in modern Western diets it can be as high as 4:1 [Varo 1974]. High dietary calcium can cause magnesium deficiencies, even when normal levels of magnesium are ingested [Evans and Weaver 1990]. Because supplemental magnesium appears to prevent bone fractures and can result in increased bone density [Sojka and Weaver 1995], it is possible that the high consumption of dairy products (which are high in calcium), at the expense of magnesium-rich fruits and vegetables, may unexpectedly result in reduced bone-mineral density.

A few details regarding the specific effects of magnesium on calcium retention are of particular interest here in light of the aforementioned differences between Paleolithic diets compared to the typical modern Western diet. In pre-agricultural diets consisting of meats, fruits, vegetables, nuts, etc., the calcium (Ca) to magnesium (Mg) ratio is approximately 1:1. Because the Ca:Mg ratio of milk and dairy products is 12:1, the inclusion of milk and milk products into post-agricultural diets can raise the overall dietary Ca:Mg ratio to 3 to 4:1 [Varo 1974]. In animal models, it has been shown that rats develop clinical signs of magnesium deficiency after three weeks on high-calcium, normal-magnesium diets [Evans and Weaver 1990; Luft et al. 1988; Sellig et al. 1974].

Ironically, high-calcium diets may have a deleterious effect upon bone mineralization because of their hypomagnesic (magnesium-depleting) effect. Conversely, magnesium deficiency is a known cause of hypocalcemia (low calcium) [Rude et al. 1976]. (In other words, for either calcium or magnesium utilization to be optimum, both must be in balance with each other.) The resultant hypocalcemia stems from parathyroid hormone (PTH) unresponsiveness [Rude et al. 1978], since the effects of PTH are magnesium-dependent [Estep et al. 1969]. Gross, clinical hypocalcemia and hypomagnesia tend not to occur in otherwise healthy post-menopausal, osteoporotic women; however, serum measures (blood levels) of magnesium concentrations are not good indicators of magnesium status, and subjects with magnesium deficiencies (as measured intracellularly) frequently maintain normal serum magnesium levels [Ryzen et al. 1990].

Consequently, over a lifetime, a marginal or reduced intracellular magnesium level may adversely influence PTH responsivity which in turn likely compromises bone-mineral content. A recent review article [Sojka and Weaver 1995] showed that post-menopausal women given magnesium supplements over a two-year period had a significant increase in their bone-mineral density, whereas meta-analyses of calcium supplementation and bone-mineral density have been equivocal.

Acid/alkaline dietary load . Additionally, bone mass is also dependent upon the relative acid/alkaline dietary load [Massey 1998; Barzel and Massey 1998]. Acid generated by the diet is excreted in the urine and can cause calciuresis. Meat and fish have a high potential renal acid load (PRAL) whereas fruits and vegetables have a negative PRAL, meaning they reduce acid excretion. The human kidney cannot excrete urine with a pH lower than 5; consequently the acids (mainly phosphate and sulfate) of acid-producing foods such as meats, fish, and some cereals must be buffered partially by calcium which is ultimately derived from the skeleton [Massey 1998; Barzel and Massey 1998].

Because fruits and vegetables can act as alkaline buffers for the acids derived from meats and fish, they have been recently shown to decrease urinary calcium excretion even when dietary protein and calcium are held constant [Appel et al. 1997]. In other words, without reducing either dietary protein or calcium in the diet, calcium balance is improved when the percentage of fruits and vegetables in the diet is increased. Thus, the high levels of fruits and vegetables that Stone-Age people consumed may have partially counteracted the calciuretic effects of high-protein diets.

Excessive intake of cereals (grains). The effects of cereal phytate in limiting mineral absorption are well-known and thereby unfavorably impact calcium uptake, though this is often not noted when considering the overall picture of calcium balance in relation to the potential for osteoporosis. In addition, the acidifying effects of cereals upon the urine [Barzel and Massey 1998] (via the kidney), cause calcium carbonates from bone mineral reserves to be used to buffer the slight metabolic acidosis caused by cereals.

Exposure to sunlight and vitamin D. An additional factor is that our Stone-Age ancestors would have likely had higher plasma levels of vitamin D than modern man because of their greater exposure to sunlight. Vitamin D, synthesized in the dermis via ultraviolet radiation, enhances calcium absorption and can prevent bone loss.

Physical activity levels . Lastly, because our ancestors were more active than modern humans [Cordain et al. 1997], their increased activity levels may have also improved their bone mass despite a high protein intake.


Conclusion

In summary, calcium retention or excretion is dependent on additional key factors besides protein consumption. To fully assess the net effect requires an analysis of the entire diet and lifestyle in its overall context rather than focusing on any one factor in isolation.

--Loren Cordain, Ph.D.


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REFERENCES

Appel LJ et al. (1997) "A clinical trial of the effects of dietary patterns on blood pressure." New England Journal of Medicine, vol. 336, pp. 1117-1124.
Barzel US, Massey LK (1998) "Excess dietary protein can adversely affect bone." Journal of Nutrition, vol. 128, pp. 1051-1053.

Cappuccio FP (1996) "Dietary prevention of osteoporosis: are we ignoring the evidence?" American Journal of Clinical Nutrition, vol. 63, pp. 787-788.

Cordain L, Gotshall RW, Eaton SB (1997) "Evolutionary aspects of exercise." World Review of Nutrition and Dietetics, vol. 81, pp. 49-60.

Devine A et al. (1995) "A longitudinal study of the effect of sodium and calcium intakes on regional bone density in postmenopausal women." American Journal of Clinical Nutrition, vol. 62, pp. 740-745.

Eaton SB et al. (1985) "Paleolithic nutrition: A consideration of its nature and current implications." New England Journal of Medicine, vol. 312, pp. 283-289.

Estep H et al. (1969) "Hypocalcemia due to hypomagnesia and reversible parathyroid hormone unresponsiveness." J Clin Endocrinol, vol. 29, pp. 842-848.

Evans GH, Weaver CM et al. (1990) "Association of magnesium deficiency with the blood-lowering effects of calcium." J Hypertension, vol. 8, pp. 327-337.

Heaney RP (1998) "Excess dietary protein may not adversely affect bone." Journal of Nutrition, vol. 128, pp. 1054-1057.

Luft FC et al. (1988) "Effect of high calcium diet on magnesium, catecholamine, and blood pressure of stroke-prone spontaneously hypertensive rats." Proc Soc Exp Biol Med, vol. 187, pp. 474-481.

Massey LK (1998) "Does excess dietary protein adversely affect bone?" Symposium overview. Journal of Nutrition, vol. 128, pp. 1048-1050.

Matkovic V et al. (1995) "Urinary calcium, sodium and bone mass of young females." American Journal of Clinical Nutrition, vol. 62, pp. 417-425.

Nordin BEC et al. (1993) "The nature and significance of the relationship between urinary sodium and urinary calcium in women." Journal of Nutrition, vol. 123, pp. 1615-1622.

Rude et al. (1978) "Parathyroid hormone secretion in magnesium deficiency." J Clin Endocrinol Metab, vol. 47, pp. 800-806.

Rude et al. (1976) "Functional hypoparathyroidism and parathyroid hormone end organ resistance in human magnesium deficiency." Clin Endocrinol, vol. 5, pp. 209-224.

Ruff CB et al. (1993) "Post-cranial robusticity in Homo. I: Temporal trends and mechanical interpretation." American Journal of Physical Anthropology, vol. 91, pp. 21-53.

Ryzen E et al. (1990) "Low intracellular magnesium in patients with acute pancreatitis and hypocalcemia." West J Med, vol. 152, pp. 145-148.

Sellig MS et al. (1974) "Magnesium interrelationships in ischemic heart disease: a review." Am J Clin Nutr, vol. 27, pp. 59-79.

Sojka JE, Weaver CM (1995) "Magnesium supplementation and osteoporosis." Nutr Rev, vol. 53, pp. 71-74.

Varo P (1974) "Mineral element balance and coronary heart disease." Int J Vit Nutr Res, vol. 44, pp. 267-273.

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