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

Rachel Nicoll, John McLaren Howard, Michael Henein


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

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Copyright (c) 2015 Rachel Nicoll, John McLaren Howard, Michael Henein

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