Thinking About Phosphorus in Transition Cows

My colleague Stacy and I were out on the West Coast taking blood samples from some beautiful gals who were nearing calving and were being fed Nutricow® CalBal® in the close-up pen. I must have been lost in thought as a vial filled up when Stacy nudged me back to earth with a laugh: “Hey Rick… that one’s full.”

She raised an eyebrow and then asked where I had gone in my head – and if it was a good trip. I confessed: I had been thinking about the relationship between dietary phosphorus and serum phosphorus in transition cows and wondered out loud about this fascinating but puzzling area of a dairy cow’s nutritional biochemistry.

Stacy reminded me that Professor Grünberg published a paper tackling just that – what we know (and don’t know) about phosphorus balance in transition dairy cows.

Dr. Grünberg hit the reset button on the latest research about phosphorus balance in transition cows, highlighting the urgent knowledge gaps. Turns out, the regulatory mechanisms are still a bit of a mystery.

I used to think that phosphorus regulation was indirectly controlled through calcium homeostasis—that the two minerals worked hand-in-hand. But the Professor points out that beyond their roles in bone mineralization and milk production, calcium and phosphorus don’t really share much common ground metabolically other than some cell signaling processes. So, the idea of shared regulatory pathways? Not so likely.

The concept of joint calcium and phosphorus regulation came from the fact that hormones controlling calcium (like PTH and vitamin D) also affect phosphorus. However, no mechanism has been found that lets the body sense phosphorus imbalance. Hormones like PTH, vitamin D, and FGF23 have all been linked to downregulating phosphorus in states of hyperphosphatemia. But intriguingly, there’s no evidence that FGF23 helps in the opposite direction, i.e. upregulating phosphorus levels when they’re low.

Recent studies showed that cattle and small ruminants handled phosphorus imbalances efficiently, even when calcium levels were stable, debunking the idea of calcium-dependent phosphorus regulation. It remains a million-dollar question as I think about this aspect of dairy nutrition today.

On the plane back to the East coast, I couldn’t sleep thinking about phosphorus and calcium in diets and so, I hopped on the plane’s WiFi and started digging around in Cornell University’s electronic library.  I think it’s common knowledge that about 98% of a cow’s calcium is stored in bones and teeth. This reservoir supports skeletal strength and serves as a source of calcium during periods of high demand, such as lactation.

Calcium in the bloodstream exists in three forms:

1. Ionized calcium or Ca(i), which is the biologically active form, and is crucial for muscle contractions, nerve signaling, and enzyme functions
2. Protein-bound calcium, which is attached to proteins like albumin, where it acts as a reserve
3. Calcium complexes, which are comprised of calcium bound to anions like phosphate and contribute to overall calcium balance. Dr. Jess McArt explains more about this in part 4 of our Connecting the Dots Lecture Series which you can find here.

But what about phosphorus? Like calcium, a significant portion of phosphorus is stored in bones and teeth as hydroxyapatite, contributing to structural integrity. Phosphorus in the bloodstream exists primarily as inorganic phosphate (Pi), which is involved in energy transactions as a component of ATP (adenosine triphosphate), the molecule that powers cellular activities, buffering and endogenous P secretion in saliva.

I thought to myself, okay, those are the forms of calcium and phosphorus inside the cow’s serum, plasma and GI.  As a dairy nutritionist, I know they come from phytate and/or supplementation but get metabolically converted into forms that can be absorbed in the lower part of the GI.

I summarized it in my own mind like this:

• We know where they come from and the forms they take for absorption.
• We also know the forms they take upon elimination through urination, fecal matter and through the mammary.
• We also know that serum and plasma P measurements are ubiquitous, obvious and not novel, with the clinical and subclinical definitions of serum and plasma P and Ca levels being well known now for over 100 years.

So while we understand a great deal, there is still a lot to discover, which makes the Professor’s assertion about the mystery of homeostatic mechanism for P that much more noteworthy.

I leaned back in my chair for a moment and pondered to myself: what about milk fever and phosphorus?  A few keystrokes later at the ole e-library and I discovered that milk fever was first mentioned in agricultural literature in the late 18^th century and the clinical signs have not changed since these early descriptions.  It wasn’t until the mid-20^th century that it was discovered that milk fever invariably coincided with hypoglycemia and hypophosphatemia in dairy cattle.  A veterinarian named Dr. Mullen from the 1970s tracked just under 200 cases of milk fever with 50% of them having hypophosphatemia.

There was no correlation between the severity of the case and Pi levels.  He suggested that “priming” of the parathyroid gland a month or so before freshening could be a way to get ahead of milk fever.  Mullen was connecting the dots.

A couple of other key things I learned that made me think…hard… were that:

1. 1,25 Hydroxy Vitamin D is inhibited by strong cations which reduces the sensitivity of renal tissue to PTH and
2. High plasma concentrations of Pi inhibit the production of the enzyme that upregulates the active form of vitamin D

Given all that we know about calcium homeostasis and 1,25 Hydroxy Vitamin D, I started to wonder about supplementing with Nutrivit® Puri-D® to help with Ca and P mobilization. I wrote a note to myself on my drink napkin to think more about the removal of strong cation effects and that 1,25 Hydroxy Vitamin D seems to be central to the P mystery and milk fever.

As I drifted off just before the wheels touched down (I hate it when that happens), it made even more sense to me that CalBal® is used to exchange calcium ions in the rumen and then bind phosphorus, perhaps reversibly in part, thereby leveraging the Ca homeostatic mechanism that we know about, as well as the P one that we know less about, but still allows the cow to gear up for calving.