Hypocalcemia—both clinical and subclinical—can easily be prevented. Yet according to Reinhardt et al., 2011, more than half of multiparous cows develop subclinical hypocalcemia (blood Ca <8.0 mg/dl) shortly after calving. We can do better. Prevention of hypocalcemia should be a primary goal for all transition-cow management and feeding programs. But first you must understand it.
Calcium homeostasis is primarily controlled by the parathyroid glands. When blood calcium declines, these glands secrete more parathyroid hormone (PTH) which triggers action in the bone cells and the kidneys. The bone cells release calcium. The kidneys reduce calcium losses through urine and boost production of a hormone made from vitamin D that instructs intestinal cells to enhance their absorption of calcium. Normally a small decline in blood calcium occurs at the onset of lactation and calcium homeostasis kicks into high gear and blood calcium levels return to normal in a few hours. When the system fails, problems can occur.
Research shows that preventing metabolic alkalosis, as triggered by close-up diets high in potassium, is key. In a study we conducted at USDA (Goff et al., 2014), late gestation cows were fed an alkalinizing diet (high DCAD) or an acidifying diet (low DCAD) and treated with synthetic exogenous PTH. Cows fed the alkalinizing diet had a poor response to the supplemental PTH; at 21 hours after PTH administration plasma calcium concentration was not significantly changed. Their kidneys did not produce as much of the hormone to enhance intestinal absorption of calcium and blood calcium did not rise as quickly. In comparison, cows fed an acidifying diet had a strong response to the supplemental PTH; at 6 hours after PTH administration cows showed a significant change in plasma calcium concentration and normal blood calcium levels were quickly restored.
In another study, we discovered that hypomagnesemia can interfere with normal tissue response to PTH and inhibit the secretion of PTH by the parathyroid glands. Research has shown that boosting calcium levels is not the answer (Goff and Horst, 1997; Beede et al., 2001). In fact, when higher levels of dietary calcium were fed, dry matter intake declined. The degree of hypocalcemia experienced at calving and subsequent milk production were unaffected by diet calcium level.
PREVENTION STARTS HERE
When blood pH and electrolyte balance is normal, cellular functions occur freely. When diet alters the blood pH, cellular functions can experience interference. The difference between the number of cation and anion particles absorbed from the diet determines blood pH. That’s why it’s important to balance the dietary cation anion difference (DCAD) of prepartum diets.
For prepartum cows, research shows a negative DCAD that induces a slight metabolic acidosis works best. The slight metabolic acidosis restores tissue sensitivity to PTH and allows calcium homeostasis to proceed normally. Getting the minerals in the right balance can prevent milk fever, minimize subclinical hypocalcemia and help cows successfully transition into lactation. Listed below is my recommended mineral profile for close-up diets:
- Calcium concentration of 1% is optimal. Similar to lactating diet calcium.
- Magnesium concentration of 0.35 to 0.4%.
- Phosphorus level at 35 g/d or less improves calcium homeostasis.
- Sulfur must be kept above 0.22% but below 0.4%.
- Keep potassium as close to 1.0% of diet as possible.
- Feed chloride anions at 0.5% less than the concentration of K. For example, if K is 1.3%, feed 0.8% Cl. However, too much of traditional chloride salts will decrease intake. More palatable commercial anion supplements encourage intake and can counteract higher levels of K.
- Aim for a DCAD (Na + K) – (Cl + SO4) of -50 to -150 mEq/kg.
- Check urine pH to make sure that acidification has occurred.
During the last week of gestation, the average urine pH in Holsteins should be between 6.2-6.8 and in Jerseys it should be between 5.8-6.2.
