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The pathogenesis of milk fever is characterized by a rapid increase of calcium requirement with onset of colostrum secretion and the delayed signal cascade of the regulation of calcium homeostasis. This reaction is influenced by magnesium and phosphorous intake. Insufficient magnesium intake impairs the release of Parathormon (PTH) and effects of PTH at the target organs. High magnesium intakes avoid magnesium deficiency, exhibit a significant antagonism on calcium transport in rumen and kidney and reduced the incidence of milk fever in epidemiological studies. High phosphorous intake impairs the regulation of calcium homeostasis and lowers calcium concentration at parturition. Low calcium intake (< 50g/d) is a good preventive measure, but hardly to realize, because calcium contents of the diet are high. Calcium digestibility can be reduced by zeolite and phytate and both are able to stabilize blood calcium concentration at parturition. However, zeolite is reducing phosphorous digestibility and voluntary feed intake particularly at high doses. A combination of high magnesium (0.4% in the DM) and low phosphorous (≤ 0.25% in the DM) intake in combination with protected phytate is a promising measure of prevention of milk fever.