With the initiation of lactation and continued milk production by the dairy cow, tremendous adaptations occur to support the increased need for nutrients to support milk synthesis. Besides the increased need for energy and amino acids for colostrum and afterward for milk synthesis, the requirement for calcium increases two- to three-fold over those required by the dairy cow before calving. The synthesis of colostrum requires 20 to 30 g/day of calcium, whereas metabolism of the cow and the growing fetus requires approximately 30 g/day. Thus, metabolic adaptations must take place to support the increased need for calcium. If they do not, the concentration of calcium in the blood drops below a critical threshold, and clinical and subclinical hypocalcemia, or milk fever, can result.
Role of Calcium
Calcium is vital for smooth muscle and nerve function as it relates to gastrointestinal motility and skeletal muscle strength. The lowest concentration of blood calcium usually occurs within 12 to 24 hours of calving and generally returns to normal in healthy cows within 2 to 3 days post-calving. Clinical hypocalcemia is the most recognized disease in dairy cattle with an incidence rate around 5%. Jersey and Guernsey cattle are more susceptible to the disorder. One reason for this is that Jersey cattle have fewer vitamin D receptors than Holstein cattle. Incidence increases with higher milk production and increases by 9% with each successive lactation. First-calf heifers rarely develop clinical hypocalcemia because they produce less colostrum and milk and can more rapidly mobilize calcium from bone in their growing skeleton.
The concentration of calcium in blood is tightly regulated through control of absorption of dietary calcium and release or uptake of calcium from bones. Two hormones, parathyroid hormone (known as PTH) and 1,25-dihydroxy vitamin D3, control these processes. As the concentration of calcium decreases in the blood, PTH is secreted and acts at the kidney to decrease the excretion of calcium in the urine. This change allows for only small adjustments in the concentration of blood calcium. If greater amounts of calcium are needed, as with the initiation and maintenance of lactation, PTH acts on bone, and calcium is reabsorbed (released). In addition, PTH acts on the kidney and results in conversion of a vitamin D metabolite into 1,25-dihydroxy vitamin D3. Then 1,25-dihydroxy vitamin D3 can regulate the absorption of calcium from the small intestine through active transport. In order for PTH to be secreted and effectively bind to its receptor, adequate magnesium and a slightly acidic blood pH (known as metabolic acidosis) are needed, thus illustrating the need to provide adequate amounts of magnesium in pre-fresh diets and balance these diets to provide a negative cation-to-anion difference (DCAD) in order to prevent hypocalcemia.
Subclinical Hypocalcemia
Dairy cows with subclinical hypocalcemia do not show clinical symptoms but have a low blood concentration of calcium within 24 hours after calving. Thus, the only way to know whether dairy cows are experiencing subclinical hypocalcemia is to analyze blood for calcium concentration within the first 1 to 2 days after calving. Dairy cows with blood calcium concentrations at or below 8.0 mg/dl (2.0 mmol/l) but not showing clinical signs are considered subclinically hypocalcemic. At this cut-off point, Reinhardt and co-workers in a study with 1,462 dairy cows determined that 50% of mature dairy cows and 25% of first-calf heifers experienced subclinical hypocalcemia. Oetzel at the University of Wisconsin has estimated that the economic cost of subclinical hypocalcemia is four times the cost of a clinical case, resulting in a substantial impact on profitability of dairy operations.
Recently, Martinez and co-workers suggested that this cut-off should be raised to 8.5 mg/dl (2.1 mmol/l) because cows below this concentration were more likely to develop metritis and other metabolic diseases. Using this higher criterion, Reinhardt and co-workers’ data indicate that over 65% of mature cows and 51% of first-calf heifers were below this threshold. These data and those from other researchers indicate (1) subclinical hypocalcemia does occur in a large number of dairy cows, but (2) not all fresh cows experience a drop in blood calcium concentration just after calving. Research suggests that subclinical hypocalcemia may be directly associated with other metabolic disorders and may be the primary or secondary cause of decreased performance.
Implications of Hypocalcemia on Performance
Hypocalcemia impacts fresh cow health, future milk production, and reproductive performance. Studies also have shown that immune function is compromised in dairy cows with low blood calcium concentrations. Cows with lower blood calcium concentrations within the first day after calving are more likely to have a displaced abomasum, ketosis, retained placenta and resulting metritis, and mastitis. Some studies have shown a decrease in feed intake postpartum and rumination and corresponding higher non-esterified fatty acid (NEFA) concentrations. Cows with high body condition at calving also are more likely to have hypocalcemia. Other studies have failed to show a negative response on feed intake and milk production, at least in those cows with subclinical hypocalcemia, but these cows received calcium preventative therapy after calving.
Prevention of Hypocalcemia
Prevention of hypocalcemia generally occurs through modifications to the pre-fresh or close-up diet. These changes allow for the physiological system which mobilizes calcium to be primed and ready for the increased demand for calcium associated with the synthesis of colostrum and milk.
Low calcium diets pre-fresh: Although this practice does reduce the incidence of hypocalcemia, it is difficult to implement on the farm. To be effective, diets must provide less than 20 g of available calcium. These diets often contain very low quality forages that may limit intake, yet low intake pre-fresh is not desired. In some grazing situations (e.g., depending on forage species and pasture fertility), low calcium diets may be possible. Low potassium forages/diets pre-fresh: Incorporating low potassium forages into diets for pre-fresh dairy cows may decrease the likelihood of clinical hypocalcemia but not the incidence of subclinical hypocalcemia. Changes in the dietary cation-anion difference (DCAD) may not be large enough to cause metabolic acidosis and prevent a subclinical drop in blood calcium concentration when low potassium forages are fed without additional dietary modifications of chlorine and sulfur. The DCAD influences the pH of the blood and the responsiveness of tissues to PTH.
