In an elegant review summarizing the evidence that high serum phosphate compromises vascular health, it was suggested that, “if an atherogenic role for phosphate exposure is demon- strated, then phosphate binders could become the new statins” [9]. In patients with CKD, pharmaceutical phosphate binders such as sevelamer or lanthanum carbonate are commonly employed to minimize absorption of dietary phosphate. How- ever, from the standpoint of primary prevention, pharmaceutical phosphate binders developed for use in patients with chronic kidney failure may be too expensive to be ideal. Fortuitously, however, soluble salts of calcium and magnesium, in sufficient amounts, can do a very effective job of precipitating GI phos- phate, impeding its absorption. In one recent study, daily sup- plementation providing 770 mg calcium and 420 mg magnesium (as calcium acetate and magnesium carbonate), administered with meals, was just as effective for lowering elevated serum phosphate in patients with kidney disease as was the prescrip- tion agent sevelamer hydrochloride [95]. Many well-designed “nutritional insurance formulas” provide comparable supple- mental intakes of calcium and magnesium [96]. Hence, nutri- tional insurance supplementation may provide the unexpected benefit of alleviating adverse health effects of excess phosphate. Moreover, ensuring good magnesium status may be beneficial for cardiovascular health while reducing risk for diabetes and colorectal cancer, and supplemental calcium may modestly aid maintenance of bone density [97–107].