Milk fever, one of the most historically relevant diseases of dairy cows, is caused by tremendous calcium expenditure at lactation initiation, so severe that cows can no longer stand and, if left untreated, die. Fortunately, through improvements in nutrition and management, this severe hypocalcemia is now rare. Nonetheless, subclinical hypocalcemia remains pervasive, affecting nearly 50% of cows. Experts know that cows experiencing transient hypocalcemia are high milk producers, whereas cows with prolonged hypocalcemia have suboptimal milk production; however, why these different types of hypocalcemia occur is unknown. Our understanding of how some cows successfully navigate early lactation calcium demands while others do not must improve to support high-producing cows and eliminate development of prolonged hypocalcemia.

We hypothesize that appropriate physiological regulation by the mammary gland and high dry matter intake in high-producing dairy cows support rapid recovery from transient hypocalcemia, whereas chronic inflammation and immune activation contribute to prolonged hypocalcemia and reduced milk-producing potential. Improved knowledge of calcium homeostasis has profound implications on strategies needed to support milk production, therefore we propose to: 1) determine the contribution of the mammary gland to postpartum calcium dynamics and interaction with the inflammatory response, and 2) determine the temporal association of periparturient dry matter intake and inflammation and immune activation with postpartum calcium status and milk production.

Our approach will provide physiologic and epidemiologic foundations for design of effective management strategies that optimize cow well-being through the periparturient period. Therefore, presenting a promising strategy to improve animal health and enhance milk production efficiency.