Ectopic calcification and bone: a comparison of the effect of dietary carbohydrates, sugars and protein

Abstract

A number of studies have shown that severe calcification of the arteries, heart and kidneys commonly coexists with<br />osteoporosis, particularly in renal disease. We have already shown that with respect to dietary fats, those that promote<br />ectopic (mainly cardiovascular) calcification are also detrimental to bone, with a similar relationship seen in fats which inhibit<br />ectopic calcification. This review of dietary carbohydrates, sugars and protein has shown a similar correspondence of effect,<br />with protein proving protective against ectopic calcification, at least in animals, and beneficial to bone. There appears to be<br />an interaction with calcium intake, with the beneficial effects of high protein being negated in a calcium deficiency, while a<br />high calcium intake enhances the dangers of a low protein intake; the cut-off for calcium intake may be around 800mg/d<br />for bone health. The results of studies on carbohydrates are unclear. Although there are no human studies on ectopic<br />calcification and intake of sugars, diabetes mellitus, insulin resistance and high blood glucose are known risk factors and are<br />also detrimental to bone. Fructose consistently promotes ectopic calcification in animals and is detrimental to bone in both<br />animals and humans, although the results for sucrose, glucose and lactose are mixed. Protein and prebiotics, both protective<br />against ectopic calcification and beneficial to bone, appear to act by increasing calcium absorption. Mechanisms of action<br />shared between inhibition of ectopic calcification and increased bone mineral density (BMD) include insulin-like growth factor<br />(IGF)-1, which can be directly induced by protein and glucose, and advanced glycation end products (AGEs), which decrease<br />expression of IGF-1 and generate reactive oxygen species, promote ectopic calcification and increased bone resorption.