Why Cows Become Hypocalcemic and Steps to Reduce Impact with Dr. Goff – Iowa State University

Podcast Topic

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Guests:

Dr. Jesse Goff, Iowa State University

Episode 110: Why Cows Become Hypocalcemic and Steps to Reduce Impact

Timestamps:

Dr. Goff sees three main challenges for transition cows: negative energy and protein balance, immune suppression, and hypocalcemia. About half of all older cows experience hypocalcemia, and around 3% will experience milk fever. Cows develop hypocalcemia if they are unable to replace the calcium lost in milk from either their bone or diet. Compared to the day before calving, a cow needs around 32 extra grams of protein the day of calving to meet her increased requirements. (2:00)

Dr. Goff reviews the pathways of calcium homeostasis and the actions of parathyroid hormone (PTH). Aged cows may have a harder time maintaining calcium homeostasis due to the loss of vitamin D receptors in the intestine with age and fewer sites of active bone resorption capable of responding quickly to PTH once they have finished growing. Blood pH plays a role in calcium homeostasis: when blood pH becomes alkaline, animals become less responsive to PTH. Dr. Goff reviews the impacts of high vs low DCAD diets and reviews the amount of time it takes for the kidney and bone to respond to PTH. (4:20)

There are several strategies to reduce the risk of hypocalcemia. One is to reduce dietary potassium so the cow is not as alkaline. Using forages from fields that have not had manure applied to them is one way to accomplish this. In addition, warm-season grasses (corn) accumulate less potassium than cool-season grasses, and all grasses contain less potassium as they mature (straw). A second strategy is to add anions such as chloride or sulfate to the diet to acidify the blood to improve bone and kidney response to PTH. Research has shown that sulfate salts acidify about 60% as well as chloride salts. The palatability of anionic diets has led to commercial products such as Soychlor. (13:06)

Dr. Goff then discusses the over- and under-acidification of diets and gives his opinion on the appropriate range of urine pH for proper DCAD diet management, including a new proposed DCAD equation to account for alkalizing and acidifying components of the diet. He also gives some options for pH test strips to use for urine pH data collection. (18:30)

Dr. Goff’s lab has found that as prepartum urine pH increases, the calcium nadir decreases. The inflection point is right around pH 7.5, where above 7.5 indicates a higher risk of hypocalcemia. Data from other researchers suggests that urine pH lower than 6.0 may result in lower blood calcium, indicating an overall curvilinear response. Low urine pH (under 6.0) has also been associated with a higher incidence of left-displaced abomasum. (29:02)

Moving on to other minerals, Dr. Goff discusses phosphate homeostasis and how that interacts with calcium in the close-up cow. Feeding too much phosphorus can decrease calcium absorption and feeding low phosphorus diets before calving can improve blood levels of calcium. He recommends less than 0.35% phosphorus in close-up cow diets. For magnesium, he recommends 0.4% prepartum and immediately postpartum to take advantage of passive absorption across the rumen wall. (31:08)

Another strategy to reduce milk fever risk is to reduce dietary calcium prior to calving to stimulate parathyroid hormone release well before calving. A zeolite product that binds calcium is now available and may make this much easier to achieve. (42:59)

In closing, Dr. Goff reminds the audience that some level of hypocalcemia post-calving is normal and in fact, is associated with higher milk production. The key is making sure that the cow’s blood calcium levels can bounce back to normal by day two after calving. (51:23)

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