Guests: Dr. Jesse Goff, Iowa State University This episode of the Real Science Exchange podcast was recorded during a webinar from Balchem’s Real Science Lecture Series.
This episode of the Real Science Exchange podcast was recorded during a webinar from Balchem’s Real Science Lecture Series.
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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Scott Sorrell (00:07):
Hello everyone, my name is Scott Sorrell and I'll be your moderator today. It's my pleasure to welcome you to the next installment of Balchem’s Real Science lecture series. Today's real science webinar is titled “Why Cows Become Hypocalcemic and Steps to Reduce Impact” with Dr. Jesse Goff from the Iowa State University. Dr. Goff, the floor's now yours.
Dr. Jesse Goff (00:29):
Thank you, Scott. So I wanna make sure that everybody understands a little bit about me that I, I am a little bit biased. I invented a product called SoyChlor some years ago that's sold by, was sold by the West Central local Farmers co-op now it's called Landis Farmers co-op. So realized that I invented it. I still think it's the best one out there and everything else I do is kind of secondary to that thought for this talk. Anyway,
Scott Sorrell (01:09):
The economics of feeding ReaShure Precision Release Choline. ReaShure’s fed during the transition period. And because it's fed for such a short period of time, it costs just $15 per cow and yet the benefits will continue to generate income throughout the year. Cows fed ReaShure produce five pounds more colostrum, which pays for your ReaShure investment on the very first day of lactation cows fed ReaShure also produce five pounds more milk per day every day. That means after the first day every day is payday invest in ReaShure during the transition period and recoup your investment on the very first day of lactation. After that, you got it payday.
Dr. Jesse Goff (02:00):
Well, when I look at this transition cow, I think she's got three major problems. She's gotta face negative energy and protein balance. She's immune suppressed and very often cows are hypocalcemic surveys, including one that we did some years ago suggest about half of the older cows are hypocalcemic, how you define that we'll talk about in some detail later. But even heifers, some of them will be hypocalcemic subclinical. About 3% of dairy cows will have such, such a severe hypocalcemia that they develop this disease called milk fever. Regardless, hypocalcemia is one of the major players in immune suppression and other problems of the transition. Cow, why do cows get hypocalcemic? It's pretty simple. The calcium content of their blood is only three to four grams and they're making milk that puts out a lot more calcium than three to four grams per day. And they'll develop hypo calcium if they don't replace that calcium from either their bone or from the dietary calcium that they're trying to absorb.
Dr. Jesse Goff (03:15):
Now let's look at calcium dynamics. Just at around the time of calving, a day before calving, this cow needs about 18 grams of calcium absorbed from her diet each day for maintenance and fetal skeletal development. The day of calving, she starts making colostrum and then you look at that second milk as well. GU stills a maintenance requirement and somewhere between 50 and 55 grams of calcium that have to be absorbed that first day of lactation, that's about 32 grams of extra calcium that has to be brought in. Those of you really wanna read a great paper. Charlie Berg did all this stuff with radioisotope radioactive calcium back in the late seventies and early eighties that really shows the dynamics of this movement of calcium from the blood into the mammary gland. Well, there is a calcium homeostasis mechanism and it revolves around the parathyroid glands and parathyroid hormone.
Dr. Jesse Goff (04:20):
Parathyroid glands are located in the region of the neck just outside the thyroid gland, and it monitors any kind of change in blood calcium concentration. Even a small drop in blood calcium concentration signals a large release of parathyroid hormone from this, these glands. Now let's take a look at this cow's just calved. She's making a lot of milk calcium's leaving the mammary gland and that will cause a small drop in serum calcium concentration. This is picked up by the parathyroid glands, which then secrete parathyroid hormone. Now that parathyroid hormone circulates travels to the kidney and it travels to the bone. Those are the two major targets in the kidney. Parathyroid hormone drops the amount of calcium excreted out in the urine. Unfortunately, in a cow, this is not very much calcium each day. The other main action of parathyroid hormone on the kidney is to allow conversion of this vitamin D compound that we feed cows. Takes one of those metabolites and converts it to 1 25 Dihydroxy vitamin D. This is the act of hormone. This is the hormonal form of vitamin D that's gonna act on the intestine and hopefully cause intestinal calcium absorption. What that does is the 1 25 vitamin D interacts with the receptor in the intestinal epithelial cells, causes production of a few proteins that are involved in calcium absorption, and they will carry calcium across that cell and pump it into the bloodstream.
Dr. Jesse Goff (06:09):
And when that's working well, we get a nice response. Calcium, it's in our diet is absorbed nicely and we get calcium released from the bone in response to parathyroid hormone. And those bone cells activate bone calcium resorption mechanisms and we'll see a nice rise in serum calcium concentration. This is calcium homeostasis. Unfortunately, calcium homeostasis doesn't work as well as we'd like it to in all cows, particularly older cows. And one of the reasons older cows have more problems with calcium homeostasis is that as they get older, they lose the number of vitamin D receptors in those intestinal epithelial cells. This is true in cows, it's true in humans. Most every other species that's been looked at older cows are no longer growing. You look at a heifer, she's still growing her bones, she's still gaining height. That means the heifer has plenty of osteoclasts this bone resorbing cell in her bones, and those cells are already present and capable of responding to PTH very rapidly.
Dr. Jesse Goff (07:25):
As a cow gets older, osteoclast numbers drop, she has to recruit new osteoclasts and then activate them, and that's what takes so much time for her and allows her blood calcium to fall too low. Well, the final actor in this is pH of the blood and it turns out that as animals become alkaline, they become less responsive to parathyroid hormone. Turns out it's the high dec a diets that cause this metabolic alkalosis, which can lead to milk fever and certainly hypocalcemia. I'll I'll some of this is probably old hat for everybody, but I'm gonna go through it rather quickly. The dec ad. The current equation that's most popular for describing the dietary cation anion difference or dec ad is the number of milli equivalents of sodium in the diet. Plus the milli equivalence of potassium in the diet subtract out the milk equivalence of chloride and sulfate c cation versus anions.
Dr. Jesse Goff (08:33):
Unfortunately, the potassium that's in forages fed to cows is very readily available and it causes the blood and urine of the cow to become alkaline. And these high blood pH levels seem to inhibit parathyroid hormone from binding to its receptor. In this little cartoon, we've got a system here where we've got a blood pH of about 7.35, which would be considered slightly acidic for a cow probably typical of a human. Here we've got parathyroid hormone being released in response to hypocalcemia, it binds to its receptor in a nice lock and key fit that stimulates adenal cyclase and enzyme in the cell membrane. And that stimulates cyclic aMP production and that signals the bone cell or the kidney cell to become active. Unfortunately, in the middle panel, oops, in the middle panel here, we've got a blood pH that's a little bit higher indicative of a cow on a high potassium diet.
Dr. Jesse Goff (09:39):
Now the receptor takes on a strange shape, no longer recognizes parathyroid hormone very well. We don't activate this adenyl cyclase enzyme. The cyclic aMP is not made the bone and the kidney cells are incapable of responding to that parathyroid hormone. Later in the presentation we'll talk about this third situation where you can have an animal that's acidotic, or at least not severely alkali, but if there's no magnesium atom sitting at this site, again, the animal fails to produce cyclic aMP. So hypomagnesemia is something we'll talk about as a cause of hypocalcemia a little later in the talk.
Dr. Jesse Goff (10:23):
So alkalosis, we're not going to get activation of those systems, oh boy, we're not gonna get activation of these systems to bring calcium back into the bloodstream. The animal becomes more and more hypocalcemic A little bit about timing of these things and how long it takes to turn on the different systems. If you look at the kidney, parathyroid hormone can reduce urinary calcium loss to just about zero within a few minutes. In a normal cow, this will only bring about one gram of calcium into the blood. It's better than nothing, but it's not very much calcium. If you look at synthesis of 1 25 di hydroxy vitamin D by the kidney, if the animals in an acidic condition has been fed an anani diet, that will occur within about 10 hours. If they've been fed an alkaline diet, a high potassium diet, it may take as long as 20 hours for them to begin to make a significant amount of 1 25. Diet hydroxy vitamin D. Now we look at the intestine, it takes anywhere from 12 to 24 hours for the intestinal epithelial cells to begin to make those proteins that are crucial to calcium absorption. How much calcium can this bring into the blood? And some degree it depends on the dietary calcium. Particularly in early lactation diets, we probably should be bumping the dietary calcium up a little bit higher.
Dr. Jesse Goff (11:59):
If we look at the bone, osteocytes are able to resorb calcium from the bone fluids and that occurs within six to 12 hours. If the animal's been on an alkaline diet, only about nine grams of calcium are available to be absorbed by this process. If she's been fed an anion diet, a low dec ad diet upwards of 15 grams of calcium may be absorbed rapidly by the osteocytes. Next come the osteoclasts. These cells take anywhere from 16 to 96 hours to become active, and that depends partly on the age of the cow and again on her diet. If she's on an anion diet, this appears to be happening faster than if she's on an alkaline diet. This brings in huge amounts of calcium into the blood. Over the course of the first four to five weeks of lactation, upwards of 1.2 kilograms of calcium can be reabsorbed from the bones of the cow.
Dr. Jesse Goff (13:06):
So let's go over something called the dec ad strategy. First step in this is to reduce dietary potassium because you wanna reduce the alkalosis that the cow is experiencing. To do this, you've gotta use forages from fields that have not had any manure applied to them. This means setting aside some fields that are just for use of growing dry cow forages. Another strategy, oh boy. Another strategy is to use warm season grasses versus cool season grasses. Warm season grasses don't accumulate potassium out of the soil the way the cool season grasses do. And of course, corn or maize is a great warm season grass to use in, in transition. Cow diets, closeup cow diets. As plants mature, whether they're cool season or warm season, the amount of potassium that contain decreases. And so these diets that are using a lot of wheat straw in the in them tend to be lower potassium diets because that old straw is low in potassium. Just as an aside corn stove, you would think corn stove would be great. It's gonna be very low potassium. It has a couple problems. Number one, it has to be chopped very fine to get cows to eat it. And even if you do that, you're gonna find that cows will manage to sort and they don't like corn stove very much so, despite the fact sounds great. We haven't had much luck using corn stove.
Dr. Jesse Goff (14:51):
Okay, you've tried to reduce potassium in the diet as much as you can. Now you're gonna come back in and add anions, these acidifying anions to the diet to try to improve parathyroid hormone responsiveness of the tissue. And those anions are primarily chloride and sulfate. So how do we choose the right anion sources? Well, this is a study we did many years ago now, and the gist of it is that the sulfate sources do not acidify as well as the chloride sources really surprised us at the time we did this because mag sulfate had been the backbone of almost all dec ad programs at the time. Yet mag sulfate wasn't very acidifying. It was however, a very good and available source of magnesium, which is why it probably was so successful in the early days. Another thing that came as a surprise was sulfuric acid. Such a strong acid when fed to the cow, didn't acidify them as well as say calcium chloride or ammonium chloride or even hydrochloric acid. And it's because we now know the sulfate moiety isn't absorbed as well as the chloride moty from the intestinal tract.
Dr. Jesse Goff (16:07):
So after looking at this kind of data the sulfate salts acidify about 60% as well as the chloride salts. Maybe a better dec equation would be to take the milk and sodium milks potassium milk and chloride and discount sulfate a little bit. Next story, palatability of anions anionic diets when they first came out had all kinds of issues. The traditional salts, ammonium chloride, ammonium sulfate mag sulfate that were used in those early diets. Cows had trouble eating 'em when they, when you could get a cow to eat them. They worked great, but there were so many farms where we had so much trouble getting animals to eat those diets and enough, enough amount, enough quantity to acidify the cow.
Dr. Jesse Goff (17:07):
So now, now my little commercial here, I guess SoyChlor was invented for that reason. If I could have cured all the cows of milk fever using traditional anon salts, there's no way I would've spent the time and effort to invent SoyChlor. One of the reasons SoyChlor and some of the other commercial products have become so popular is because they are consumed by the cow. And if you look, this is a study done presented at the A DSA meeting in 2016. Here we have cows that were fed traditional anon salts versus cows were fed SoyChlor both cows at exactly the same urine pH levels. And by about 25 days before calving, all the cows are on their diets for at least a week. And so now you can see that the cows fed the traditional antic salts have a much greater decrease in dry matter intake as calving approaches. And the cows fed the SoyChlor diet and it amounts to one and a half kilos or so per day of intake. And that is probably why not just SoyChlor, but many of the other anion products that are on the market of have taken hold over the traditional anion salts. You can get cows to eat them.
Dr. Jesse Goff (18:30):
Now we're gonna come to the idea of under acidification and over acidification of cows being fed anion products. This is a a bunch of urine phs that I'm stealing from Peter Constable's paper. And then we applied some DCA numbers here from the Spanga and ot work. And then some of my own little twist in here as well. Let's start over here. On the far upper right, let's say you've got a diet where it's about a DCA of about plus 400. You'll find that the urine pH is gonna be somewhere around eight and a half. It doesn't get much higher than eight and a half even if you continue to raise the dca. This is the limit to what the kidney can make in terms of an alkaline urine. It just cannot go much higher than eight and a half. As we reduce the DEC ad, we get a little frustrated here maybe because we're not seeing much of a change in urine pH, there's a lot of buffering built into the system.
Dr. Jesse Goff (19:38):
Finally, as we approach about plus 50 milliequivalents per kilogram, the pH starts to drop and you can see that the, I'm sorry, I keep hitting this button. And you can see that as the pH drops as DCA drops, the pH starts to drop until you hit about zero milli equivalents per kilogram when it starts to change very, very rapidly. And then it starts leveling off again here about minus 100 and beyond, this is a typical acid-based titration curve, just like you did in chemistry class. As you approach the point where the pH changes rather rapidly where you've burned up all the buffer that pH drops very quickly between say zero and minus 50 milliequivalents per kilogram of diet. Now, one of the things that you'll note is that pH of urine rarely drops below around 5.4. That's, that appears to be about the limit for how much acid can be excreted in the urine. In fact, in the Peter Constable study, what you see is that as animals be, are fed an even lower DEC ad diet, their urine pH starts rising. They explain that by showing that these animals actually decrease their dry matter intake. They're trying to save themselves from an uncompensated metabolic acidosis, and the only way they can do it is to decrease dry matter intake.
Dr. Jesse Goff (21:20):
Well, now you're gonna get into my opinion here. This is what I think is a proper approach to d ad management. I I know not everybody agrees with me, but we can argue that out later. Let's say you start out here at the top and you've dropped the DC ad and your urine pH remains above about 7.6. I'm gonna tell you, you've got insufficient acidification. You're not gonna see any real benefit to blood calcium concentration. If you can get them between 7.6 and about 6.8, you'll see some benefit. We can measure it. It's not as good as we would hope, but you will see some benefit to the acidification and lowering of the DCA diet. Some people might have referred to this as the partial DCA diet where you're somewhere around zero milli equivalents per kilogram. I think much do better place to be is somewhere between about 5.9 and about 6.8 with an average pH of about 6.3 being optimal. Now what you can see at this point is that a small difference in dry matter and intake can have a big difference in the urine pH. We'll come back to that idea in a in a second.
Dr. Jesse Goff (22:40):
Some nutritionists would like to see urine pH kept somewhere in this area of around five and a half to say 6.1. To me, this is very close to the point of being overly acidified. I also would challenge you to think about whether or not there's data that shows that this cow is better off than this cow in terms of blood calcium concentration at calving. Now we can further acid further acidify this cow and put her on a minus 200 or so dec a diet and realize that that's probably going to impinge on her dry matter intake because she would be overly acidified in uncompensated metabolic acidosis if she were to eat at the same rate that she might eat that diet when she's up here. So realize that you're seeing this rebound of urine pH coming up here because the cow has compensated for the very negative dec a diet by decreasing our dry matter intake, reducing the amount of anion load her body is seen.
Dr. Jesse Goff (24:00):
So run through some scenarios here. Let's say you're feeding nothing but chloride as your anion. And let's say you're feeding SoyChlor my favorite, and you're feeding a diet that's maybe about 0.6% calcium. To hit my sweet spot here of a urine pH of about 6.3, you're gonna be feeding a diet with a dec ad of about minus 75 milli equivalents per kilogram if you choose to feed more traditional anon salts where chloride and sulfate are used to acidify the animal. To hit my sweet spot here of about 6.3 for a urine pH, you're gonna be feeding a diet with a DCA of about minus 125 because you're relying somewhat on sulfate as an acidifying agent. Now again, we'll go through those DCA equations. The traditional equation doesn't take into account the fact that sulfate is not as acidifying as chloride. You can use a better equation where the sulfate is discounted about 60% as active as chloride.
Dr. Jesse Goff (25:14):
But again, these equations leave out the fact that calcium carbonate might be in a diet or magnesium oxide might be in a diet, and these can be alkalinizing. There's an effect effective phosphate that's acidifying, which we'll talk a little bit more about later. I would suggest I propose this. I'm not saying you have to live by it, but there are some pretty good reasons to make an a, a long equation where you give full credit to sodium and potassium calcium. Maybe a quarter of the calcium is absorbed, maybe 15% of magnesium ions are absorbed and a little bit of ammonium cation can be absorbed. Chloride will give be given full credit sulfate about 0.6 and phosphate, about half of it gets absorbed.
Dr. Jesse Goff (26:05):
So if you're a nutritionist and you like to feed a low DCA diet and you like to feed a high calcium diet, chances are you're adding limestone or calcium carbonate to that diet and realize that when you add limestone calcium carbonate, it is slightly alkalinizing. So to hit that sweet spot of a urine pH of about 6.3 with a diet that's maybe bringing in or raising the calcium to about one point a half percent, your dec ad has to be reduced. You have to feed more anions to hit that same sweet spot of about 6.3 because the limestone is alkalinizing. Okay? That also means that sometimes if you're in a state over here, we're in an uncompensated metabolic acidosis. By adding limestone, you can bring those animals back towards a compensated metabolic acidosis. So limestone is a double-edged sword. It's gonna cost you more anine to achieve the same amount of acidification.
Dr. Jesse Goff (27:21):
And adding limestone can sometimes take a diet, a diet that was too heavily ani, loaded in anions and bring it back to a compensated metabolic acidosis. If you're down here, you urine pH down below 5.4, that animal is in a state of uncompensated metabolic acidosis. It's only reaction that it can do to save its life is to quit eating. It's gonna reduce the amount of anions it's taking in urine. Ph is checking urine pH. Everybody's favorite job. You probably should wear gloves because leptospirosis is a real problem. You wanna make sure it's a midstream collection of the urine and there's various ways to do it. Ph meters are great. However, when I walk on farms and ask when was the last time that pH meter was calibrated, I usually get a blank stare. So I've found these little strips. PH ion is a nice one that's fairly convenient.
Dr. Jesse Goff (28:27):
This one by RBO has a little bit different color scheme. Some people like the red green turning to blue scheme better than the PH ion type scheme, but some of these are nice because they're in sealable bottles. As opposed to the old pH strips that you could unroll the the unroll the roll and throw it back in your truck and realize that three days later it was all hydrated from water in the air, we started looking at plasma calcium nadir. So we take blood samples from cows at least three times on that first day of calving and we find the lowest calcium in each cow and we plotted that against the urine pH of that cow during the week before she caved. And what we see is that if urine pH is above seven and a half, you can have some cows that become quite hypocalcemic.
Dr. Jesse Goff (29:29):
Once you start getting below seven and a half, you see a nice increase in calcium as urine pH drops. So this would suggest that the lower the urine pH the better. However, lemme go back to that. You can see in our data set here because I'm, I'm a very conservative guy. I don't have a lot of cows down here around 5.5. Pedro Melendez presented this at this year's A DSA meeting. This shows a little bit of a curve linear response here where the optimal urine pH is somewhere around six and a half. And once you start getting below that, you start seeing a, something of a decrease in blood calcium concentration around the time of calving. In other words, it may not be optimal to keep acidifying these cows beyond pH of 6.0. This is also a conclusion of this paper from acid glue published in 2016 where they looked at the health of these animals, particularly left displaced abam aum and they found that cows that had left displaced abam AUM had much lower urine pH than the cows that were in the healthy group. Their blood calciums were slightly better maybe, but this impact on other health issues with a very low blood pH and a very low urine pH was something to keep in mind.
Dr. Jesse Goff (31:08):
Okay, moving on to other minerals. Let's talk a little bit about phosphorus. And here's my scheme for how I'd like to feed the closeup cow. I'm gonna keep phosphorus at somewhere around 0.25 to 0.31% that is lower than probably I recommended five years ago, and it's because we've learned a few things about phosphorus in the last 10 years. Now, in addition to stimulating intestinal calcium transport 1 25 vitamin D also stimulates phosphorous absorption by the epithelial cells of the intestine. We now know that there's such a thing as phosphorous homeostasis and it revolves around this strange little bone hormone called fibroblast growth factor 23. And this is what I mean if you should have a rise in blood phosphorus concentration that will stimulate the osteocytes of the bone. Those bone cells are very sensitive to a rise in blood phosphorus concentration. They start producing this hormone called fibroblast growth factor 23, which circulates to the kidney and shuts off the enzyme that will stimulate production of 1 25 Dihydroxy vitamin D. If I shut off production of this hormone, I shut off intestinal phosphorus absorption, which will result in a drop in blood phosphorus concentration. On the other hand, if I've got too low of a blood phosphorus concentration, I shut off production of fibroblast growth factor by the bone osteocytes. That allows the kidney to make more 1 25 di hydroxy vitamin D, which stimulates the intestinal cells to absorb phosphorous and it will raise my blood phosphorous concentration.
Dr. Jesse Goff (33:09):
Unfortunately, if we feed high blood phosphorus or feed diets that are higher in phosphorus to cows and raise their blood phosphorus concentration even just a little bit, we stimulate fibroblast growth factor 23. That's great, it reduces blood phosphorus, but look what else it does. It shuts off calcium absorption so it has a negative impact on calcium homeostasis. I was lucky enough to be involved with Dave Beatty and, and his graduate student and we did a little study. We're looking at diet phosphorus concentrations in closeup cows and they fed either 0.2, 1.31 or 0.44% phosphorus diets. Cows were fed. The higher phosphorus diet had lower blood calcium concentration around the time of calving. Even the cows fed the 0.21% phosphorus diet had normal levels of magnesium or of phosphorus in their blood, four to six milligrams per deciliter. There was no effect on milk production. Many people see this number 0.21% and they're gonna think, oh, this is one of those causes of the hypophosphatemia downer cow. No, it is not.
Dr. Jesse Goff (34:30):
This study goes even further. This is a study done in Germany and they fed 0.15% phosphorus versus 0.28% phosphorus. And in this study on day one, the cows fed the lower phosphorus diet had better calcium concentrations than the ones on the higher phosphorus diet. And that was true even on day three as well. Walter Gruberg did this study in Germany. Unfortunately I don't think they measured fibroblast growth factor 23 in these animals would've been, would've been a great addition to the study. The point is you can feed a very low phosphorus diet to a cow prior to calving, not upset her phosphorus homeostasis. She'll have plenty of phosphorus to maintain her blood phosphorus, but it seems to improve calcium homeostasis. This goes back to studies done by Barb Barton and Tom Cura years ago that showed when you got phosphorus in the diet too high, you actually caused milk fever. Now we're gonna take the other tactic. Let's lower blood, our dietary phosphorus and blood phosphorus to improve blood calcium homeostasis.
Dr. Jesse Goff (35:50):
Next we're gonna look at magnesium and I like to keep magnesium about 0.4% and I'm going to do that to utilize passive absorption of magnesium across the rumen wall. Ruminants are strange little animals. They can only absorb diet magnesium across the rumen wall. The small intestine of adult ruminants is actually a net secretor of magnesium. Now they have several transport processes, two transport processes for pushing magnesium across a room and wall. One is the main transport process, especially when diet magnesium is low. But unfortunately this one's rather easily poisoned by diets that are high in potassium or particularly non-protein nitrogen. There's a second passive transport system that exists, but it only works with ionized magnesium concentration. The RU and fluid is relatively high. And to achieve those kinds of room and fluid ionized magnesium levels, we need to feed magnesium at about 0.4% of the diet, both pre calving and in that early postpartum period. And that's to take advantage of this passive transporter. To do this, make sure your magnesium source is available to the animal and it has to be very finely ground.
Dr. Jesse Goff (37:19):
How do you check if your animals have hypomagnesemia as a problem? Pull a blood sample. If their blood magnesium is less than 1.9 milligrams per deciliter within 12 hours of calving, you have a problem with either inadequate dietary ca magnesium or inadequate availability of the magnesium in your diet. Outcomes will be secondary hypocalcemia. And as an aside, I put this little note in here. This is probably the most common cause of what people call the mid lactation milk fever cow. That is usually a cow who is down. She responds to a bottle of calcium given intravenously. She is truly hypocalcemic, but the underlying causes of failure to have enough magnesium in her diet.
Dr. Jesse Goff (38:10):
Hypomagnesemia all depresses also depresses feed intake can mess up room and fermentation. This is tremendous work done by Clarence Ammerman back in the late sixties, early seventies. If you get really low in magnesium, you'll see grass tetanus and lactation tetanus, and that's when your blood magnesium falls below about 1.2 milligrams per deciliter. This is not common in in confined cows, but actually fairly common in areas where grazing is is occurring. If you're from New Zealand, you know all about this one. Let's take a look at magnesium sources prior to calving. If we're using mag sulfate or mag chloride as anions and almost all the commercial supplements that are sold have either mag sulfate or mag chloride in them. Now that's gonna supply a very readily available, very soluble magnesium source. So that takes magnesium off the table. For pre calving if you're using the anion supplements.
Dr. Jesse Goff (39:22):
The problem for many of these cows becomes the problem after calving, after calving, most nutritious, dramatic adding magnesium oxide as the source of magnesium to the diet. They're doing that because it's gonna supply magnesium to the animal, but they're doing it also to alkalinize the pH of the rumen. Most nutritionists use a combination of sodium bicarbonate, potassium carbonate, and magnesium oxide as their rumen buffer additives to the diet. Magnesium oxide can do all these things, but there's problems with magnesium oxide. All magnesium oxides are not created equal and unfortunately we have found a wide variation in the quality of magnesium oxides that are on dairy farms. Unfortunately, there's a lot of cheap stuff coming into the country that just don't provide an available magnesium source to the animal. So how are you gonna tell if you got a good magnesium oxide versus a bad magnesium oxide?
Dr. Jesse Goff (40:38):
You can do this little test. Weigh out three grams of mag oxide, add 40 mils of white vinegar in the United States. It's all 5% acetic acid across the board. You can go in any grocery store and buy it like this, cap the container and shake it. Well shake it again at the 15 minute mark and then let it sit till it's the 30 minute mark at 30 minutes check the pH vinegar normally has pH 2.6 to 2.8. Good mag oxides will bring the pH up over eight. A lot of the ones on the market are somewhere between 3.8 and about 5.5. These are, these are not adequate in my opinion. Remember pH's logarithmic scale. So let's say you had a pH of 4.2 to go from 4.2 to 5.2. That's a tenfold difference in ionizing action. Go from 5.2 to 6.2 times 10. Now we're up to a hundred fold difference. 6.2 to 7.2 times 10 a thousand fold difference, 7.2 to 8.2 times 10. That's a 10,000 fold difference and how much hydrogen ion can be buffered
Speaker 3 (42:04):
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Dr. Jesse Goff (42:59):
The next strategy that can be used is to try to reduce dietary calcium prior to calving to stimulate parathyroid hormone release well before calving. This is an old study now done by Howard Green where he compared feeding 80 grams of calcium per day to cows versus eight grams of calcium per day. This is the total diet calcium eight versus 80 and cows that were fed the higher calcium diet got rather severely hypocalcemic, got some of 'em, got milk fever, and then re recovered. The cows were fed the very low calcium diet for at least two weeks before calving. You can see that they went through calving with only a very minor drop in blood calcium concentration, feeding low calcium diets like this way below the requirement of the cow. Remember, the cow has to absorb 18 grams of calcium per day prior to calving.
Dr. Jesse Goff (44:02):
You feed much less than that. You'll stimulate parathyroid hormone long before she calves. Prolonged exposure of those tissues to parathyroid hormone even under alkaline conditions will stimulate bone resorption and production of 1 25 vitamin D prior to calving and prevent milk fever. This is an old, old notion it does work, but you have to be very severely restricted on dietary calcium. Restricting it to 40 grams of calcium per day is not enough. You have to be well below 40 grams of calcium per day to make this idea work. Generally this has been impractical on dairy farms as way to prevent milk fever. However, recently a product made from zeolite has become available to use and this zeolite product actually binds calcium and prevents it from being absorbed. Now this is a sodium luminal silicate and you add it to the diet and it binds the calcium in a test tube.
Dr. Jesse Goff (45:25):
You can only find one published remark on this, but sodium aluminosilicate in a test tube will bind one gram of calcium for every 10 grams of zeolite. Typically, this is fed at about 500 grams of zeolite per day, which means it should be able to bind about 50 grams of calcium. Keep in mind it binds phosphate and it binds magnesium also. So you'll see a transient reduction in levels of magnesium and phosphorus in the blood. This is a study published at Cornell a year or so ago where they fed that 500 grams of zeolite to the cows each day. That diet was 0.65% calcium, so a, a low calcium diet. This is within practical realms 0.39% phosphorus, 0.42% magnesium. You can see that the cows fed the zeolite product had higher blood calcium concentration through the per partner period.
Dr. Jesse Goff (46:32):
Then the cows were not fed the zeolite. You can see a huge difference in blood phosphorus concentrations. Zeolite seems to bind the phosphorus, preventing it from being absorbed as well. Maybe this is a good thing in terms of lowering blood phosphorus concentration. I don't know that anybody's examined that yet. It also binds magnesium and this is bringing magnesium down to very low levels. But I can tell you from the reports that there seems to be no major issues caused by this. The animals, when this works, the animals will recover nicely. You still have to control dietary calcium quite carefully. You can't just add this to any old diet. You have to keep diet calcium relatively low so it can bind that calcium that's left and bring the animal to a deficient zone.
Dr. Jesse Goff (47:33):
One of the bad things about zeolite is that it seems to depress dry matter intake. There is a lot of rock that's being added to that diet and so you'll see a decrease in rumination rate and a decrease in dry matter intake, particularly last week or so before calving. However, after calving, just as with all other milk fever prevention type schemes, you see a better or perhaps a trend towards a better dry matter intake after Calvin Vitamin D comes next. And let's just say that vitamin D administration right now is too dangerous and the effective dose is too close to the toxic dose.
Dr. Jesse Goff (48:19):
We'll move on to the oral calcium drenches and boluses. Under special circumstances, you don't need 1 25 vitamin D to absorb dietary calcium. This is called passive transfer of calcium across the gut. It only occurs if you get the ionized calcium concentration in the gut above six millimolar. And at that point, calcium starts flowing between cells into the blood. This was, has been known for a long time. If you've give an animal a drench with a very high amount of calcium in the form of calcium chloride, so it's very readily be readily solubilized, it'll be absorbed very rapidly into the blood.
Dr. Jesse Goff (49:06):
Now, when I got outta vet school, I was told that I should treat every third lactation and greater cow with a bottle of calcium IV to prevent her from getting milk fever. And so this study looks at the effect of that IV bottle of calcium versus no treatment versus cows who are getting a an oral calcium bolus. In this case it happened to be BVA calc. You can see that cows that are not treated with anything, they have some hypocalcemia, but eventually they recover if you give them an iv Yeah, for that first eight or 10 hour, eight or 10 hours, they have nice blood calcium concentration. But when you look at them 24 to 36 hours after calving, their blood calcium concentration is actually lower than if you had done nothing at all to those cows. The oral calcium bolus, as is typical for all studies with oral calcium boluses, you get a small rise in blood calcium concentration, not a very big one, but it seems to hold them a little bit better the next day. That rise in blood calcium concentration, I don't believe is why these animals are better off on day two. I think what it is is that the calcium chloride that's in these boluses tends to be acidifying.
Dr. Jesse Goff (50:28):
I'm gonna jump to this study by Katrina Roberts in New New Zealand where they showed that these boluses actually will acidify cows after calving. So here they gave a calcium chloride type bolus at the first milking, and again, 12 hours later. If you looked at the urine phs of these animals, 12 hours after calving, 41% of the treated cows had urine pH below seven, none of the control cows. The second bolus given 12 hours after calving 13 outta 13, a hundred percent of the treated cows had urine pH below seven, none of the untreated cows. I think some of the effect of these oral calcium boluses is to continue the acidification process of these animals into the first day of lactation when you've switched 'em onto a lactating cow diet.
Dr. Jesse Goff (51:23):
I'm gonna probably end with this 'cause I see the time is running low. This is a great study. I love this study that Jessica McCart did it at Cornell. What she showed by taking blood samples from cows during the first four to five days after calving. What she showed is that there's some cows who go through the calving process, have only a very, very small drop in blood calcium concentration and recover quite nicely. These cows we're gonna call normal calcemic, and then Jessica showed that there are another group of cows that on that day of calving, their blood calcium can fall quite low. But by day two, they've recovered and they go on their merry way. The interesting thing about this study was that the, she showed that the cows were normal. Cal Cmic on the day of calving were not making as much milk as the cows were hypocalcemic on day one.
Dr. Jesse Goff (52:26):
Jessica also showed that there's another form that's most dangerous to these cows, the cows that develop hypocalcemia and take a long time to recover. These are cows that are likely to be called then. She had a smaller group of animals that develop hypocalcemia only after day two. And these animals also seem to have a high risk of Calvin or of being called. What I've found most interesting is that hypocalcemia is normal. It's almost to be expected if you expect to have high milk production. The key is whether they recover quickly after calving, and this is where anon salts and perhaps the zeolite and other treatments you might apply. This is what you're hoping to do is bring them back to normal by day two. And with that, I probably better end it because I'm, I'm probably well past my time.
Scott Sorrell (53:28):
Well, thank you for that Dr. Goff and thank you everyone for attending today's webinar. If you have additional questions, please submit them to anh.marketing at balchem.com and we'll forward them to you. Along with all of the unanswered questions from today's session, please answer our short three question survey. As you exit today's webinar, you also receive a follow-up email within 48 hours with a link to a recording of today's webinar that can be shared with others in your organization. Links to past webinars are also available @balchem.com/realscience. The Balchem Real Science Lecture series is offering a special webinar on August 11th. Due to the dramatic rise in milk protein prices, Dr. Mike Van Amberg Cornell University will speak on three strategies to implement today that increase milk, protein and customer profits. We are finalizing details for the webinar, so please visit balchem.com/realscience for more details. Registration will link will be available as soon as possible on behalf of Balchem. And Dr. Goff, thank you for joining us today.
Dr. Goff (54:39):
Thank you.
Speaker 3 (54:41):
We'd love to hear your comments or ideas for topics and guests. So please reach out via email to anh.marketing at balchem.com with any suggestions and we'll work hard to add them to the schedule. Don't forget to leave a five star rating on your way out. You can request your Real Science Exchange t-shirt in just a few easy steps, just like or subscribe to the Real Science Exchange. And send us a screenshot along with your address and t-shirt size to a h.marketing at alchem.com. Balchems real science lecture series of webinars continues with ruminant focused topics on the first Tuesday of every month. Monogastric focused topics on the second Tuesday of each month, and quarterly topics for the companion animal segment. Visit balchem.com/realscience to see the latest schedule and to register for upcoming webinars.