As cows transition from late pregnancy to early lactation, they experience an incredible increase in demand for energy, nutrients, and minerals to support milk production. When feed intake and biological mechanisms fail to adequately meet this challenge, cows can experience metabolic disruption, materializing as diseases such as hyperketonemia or hypocalcemia. Subclinical manifestations of these disorders pose a particular threat to the health and productivity of the cow as they are invisible to the observer; however, put the cow at increased risk for additional disease development, reduced reproductive success, and decreased production. Broadly, the objectives of this thesis were to gain a deeper understanding of energy related metabolites and Ca homeostasis during the early lactation period, how we can identify cows experiencing metabolic disruption through the analysis of milk metabolites, the impacts that reduced blood Ca has on intake, reproduction, and milk production, and finally, treatment strategies to minimize the negative outcomes associated with reduced blood Ca. Through this work, we found that energy related metabolites in blood cycle across the day relative to feed delivery and that cows with hyperketonemia experience a greater magnitude of change in circulating energy related metabolites than cows without hyperketonemia. We also observed decreased concentrations of de novo fatty acids and increased concentrations of preformed fatty acids in the milk of hyperketonemic cows relative to non-hyperketonemic cows, suggesting that milk fatty acid analysis may be a useful tool to identifying cows with hyperketonemia. We also saw differences between mediators of Ca homeostasis in cows that experienced reductions in blood Ca at 4 days in milk (DIM), a timepoint not traditionally associated with subclinical hypocalcemia diagnosis. This suggested potential disruption in Ca homeostasis in cows with reduced blood Ca at 4 DIM, however the root of said disruption has yet to be elucidated. Furthermore, we found that dynamics of blood Ca in early lactation are associated with dry matter intake postpartum. Cows with low blood Ca at 4 DIM consumed less feed for the first 3 wk of lactation than cows with normocalcemia at 4 DIM. Similarly, cows with reduced blood Ca at 4 DIM produced less milk and were less likely to become pregnant at first service or by 150 DIM and had a greater median time to pregnancy than cows who were normocalcemic at 4 DIM. Finally, in an effort to ameliorate the associated negative outcomes of reduced blood Ca at 4 DIM, we delayed the supplementation of oral Ca boluses to 2 and 3 DIM, as opposed to the traditional 0 and 1 DIM supplementation scheme. At the population level, we saw no difference in milk production between cows receiving Ca boluses at 2 and 3 DIM, 0 and 1 DIM, or no supplemental Ca. When stratified by parity, we observed increased milk production in parity 3 cows that received oral Ca at 2 and 3 DIM compared to parity 3 cows who received oral Ca at 0 and 1 and those receiving no supplemental Ca. Interestingly, we found no evidence for a difference in blood Ca between bolus strategy treatments or cows receiving no oral Ca supplementation. The culmination of results presented herein suggest that time relative to feeding is important to consider when diagnosing hyperketonemia and that analysis of milk fatty acids offer a useful tool in identifying hyperketonemia. Furthermore, while the etiology remains unclear, differences exist in mediators of Ca homeostasis between cows with differing blood Ca dynamics after calving and reductions in blood Ca at 4 DIM are negatively associated with intake, reproduction, and production. Delaying oral Ca supplementation to 2 and 3 DIM in parity 3 cows offers a useful strategy to minimize the aforementioned negative outcomes, however more appropriate treatment strategies are still needed for advanced parity cows.