Transcription
The following podcast is taken from a webinar presented by Dr. Mike Van Amberg from Cornell University, titled "Successfully Developing a High Performing Heifer" and "How Colostrum Impacts Heifers." To view the full webinar and access the slides referenced during this podcast, visit balm.com/realscience and use the search bar to jump down to this webinar presented on April 21st, 2020.
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Hi everyone, from my home office in King Ferry, New York, in a 225-year-old house. Here we go. Thank you for the opportunity to do this, Balchem. They asked me to reprise a talk that I've given a few times about the role of colostrum in establishing the metabolism and the anabolic characteristics of a calf. So we're going to jump ahead with that.
A little bit of an introduction: when do we start making a quality heifer? I'm going to define a little bit of quality heifer in a few minutes. I'm going to discuss the effects of colostrum on growth and nutrient use, and we'll talk a little bit about the role of colostrum in gastrointestinal tract development, how it affects the immune system.
When I talk about the immune system today, it's not necessarily going to be about the IGS. I know that sounds kind of funny, but what we now know, although we don't talk about it, is that there are cells in colostrum that actually enhance the immune system of the calf. We'll talk a little bit about that, and then colostrum components and changes in metabolism, and then I'll summarize.
I always like to start with something like this: what are our goals? This is always an interesting discussion with people, sometimes with producers, because we don't always know what we want. We want good heifers, right? We want high-quality heifers. In discussion groups in New York, I'll have people like Jason Cary pull me in, and we'll get dairy producers saying, "We want the best quality heifer we can get." We'll say, "Okay, what does that mean?"
Most of the time, when we reflect that question back to producers, they don't really have good answers. We want them to make good milk; we want them to be cheap. I always hear "inexpensive" as part of that. So Jason has worked on this for many years, and I've kind of partnered with him on a few of these things. This is some of the wording we've put behind those objectives.
The primary goal is to raise the highest quality heifer that can maximize profits when the animal enters the lactating herd. That's going to be herd-specific, and it's going to be a function of your environment. Genetics—there's a lot of discussion around the world about genetics, and I think where we're at today is there's not a lot of genetic differences among most of these animals anymore.
The majority of the difference that we see in performance is really environment, which is why we're going to talk about the topic today. About 70% of what they do on a farm every day is going to be due to their environment; 30% is going to be related to genetics. We could stretch those numbers a little bit either way, but that's about how it works out.
So if you get to the idea of a quality heifer, now we're talking about an animal that carries no limitations. Nothing's going to detract from her ability to produce milk under the farm's management system. That concept of a detractor is really interesting, and we could spend several hours just on that topic.
An example of a detractor would be if the calf was treated three, four, or five times prior to weaning for some sort of respiratory distress or some disease, and a fever—whatever poor respiratory behavior, coughing a lot, snotty nose, whatever it happens to be.
Well, every time we treat that animal, if it's truly sick, we're losing growth; we're losing opportunities for later milk production, probably growth, because maybe the lungs are getting damaged, or maybe they just don't feel good and they don't eat. We now know that the more they grow in that pre-weaning stage, the more milk they're going to produce as a mature animal.
So there's just one example of a detractor, and there are lots of them. It's always fun to make a list like that because then it helps you focus your management structure about how to minimize those kinds of things. Finally, we want to optimize the profits by obtaining the highest quality heifer at the lowest possible cost—not the cheapest, but the lowest cost, usually in the least amount of time.
There's a lot of data out now that says, again, we don't really talk about it, that pretty much says that the younger the calving, the more productive she is, the longer her productive life. This is actually built into our genetic evaluations now. The folks down in Beltsville have incorporated some of that thinking, and they have interesting data out.
We want to get them in fast; we want to get them in healthy. We want to produce heifers that have the greatest capacity to make milk. When we don't know anything about a dairy, one of the things we came up with many years ago now—and you can debate the numbers a little bit, but not too much; they're still pretty good—is this snapshot evaluation of the potential quality of a replacement.
Basically, what this does is it gives you the ability to walk on a farm, or even your own farm, and say, "Okay, how are we doing?" Part of the problem with some of these metrics is we don't keep good records, and that's a real problem.
I lead the Dairy Fellows program at Cornell, at least I try to, and we're in the middle of a case study right now, and they don't take the time to record anything related to heifers. So we have no data. We know they have some problems, but we have no data. That does make it difficult; that's also a problem because you can't manage it if you can't measure it, right?
And then that's the old adage. As far as this data, first calf heifers treated as a CER heifer, we're looking at 24 hours to three months of age. We're doing that because we want to know where's if there's something going on there versus those that are four months to fresh.
We want this to be less than 30%. If the majority of those treatments are in that 24 hours to three months of age, it says, "Hey, we've got to look at management conditions around calving. We've got to look at our calving pens; we've got to look at our housing; we've got to look at our nutrition; we've got to look at our air quality, bedding, and things like that—maybe some of our SOPs around management."
If it's four months to freshening, then we've got an entirely different possible issue. It could be housing; it could be some management techniques, but it allows us to at least focus on where we've got to fix the problem.
DOAs are really on there, male versus female. That stuff is on there simply to call attention to protocols. If you see bias towards males or females, then you've got to talk about what that means. If you see a lot of female DOAs, now you've got to ask about where are they calving in, how are they calving in, who are they coming out of, where's the majority of the DOAs coming from?
Are they coming from heifers that are undergrown? Are they coming from fat cows? Whatever the case might be, but it allows you to kind of decide what the problem is.
I need to modify this one: this next line, first calf average peak—in other words, what happens once they calve. I don't really need to do that one as 80% of mature, because sometimes that's really hard because heifers are so persistent.
The next one, though, is vitally important: are your heifers making at least 80% of the mature cows in the herd? This is really the benchmark that I work from, and if they're not doing that, the question is why.
Ninety percent of the time, if they don't do that, it's because they calved in too light, and they're growing at the expense of milk. If they're not producing at least 80% of the mature cows, then it's a lost opportunity.
It's just lost milk as they have the opportunity to do that if you calve them in early and they calve in light, right? Because we're not meeting the growth benchmarks, then you know they're always going to put growth at the expense of milk. That's always going to be the higher priority of use for nutrients.
Therefore, we're going to take a hit on milk. In some of our herds right now, I see this. In the U.S., there's a lot of herds that are probably losing somewhere between eight and 14 pounds of milk per day on some heifers that are coming in light at 72 to 75% of the mature cows, right?
Because we want them to be 82% of the mature cows so they can achieve that 80% of mature body weight, so they can achieve that 80% of mature milk.
And of course, you've got this calf CS. So I got a question: what is the term DOA? Dead on Arrival.
A DOA has many different definitions. Most dairies will call it the first 24 hours; some dairies extend that out to 48 hours. I like to use 24 as my metric. Some are very strict; it's the calf that comes out and is just not viable.
I just saw that question come in. For the rest of these metrics, first calf calls less than 60 days in milk, we want to be less than 5%. If you spent all that time and money getting them to calving, you don't want to lose them prior to peak milk.
I don't like MEs, but the MEs better be larger and greater than the mature cows. You don't want to treat a lot of those heifers in the first lactation. If you're treating a lot of heifers in the first lactation, you want to understand why.
You want that to at least be less than 15; you'd like it to be less than 10, really. And then 85% retention, right? We just don't want to lose heifers. If you're losing more than 85%, or if you're losing more than 15% of your heifers, you've got to figure out why.
What is it about them that does that? Hey, we'll keep going here, and I'll come back to one of those questions in a little bit.
Real practical stuff, right? Whenever I give a colostrum talk, I always get this question at the end: bottle or tube? I want to show this slide just because it puts the question to rest.
Here's a study that was done, published in the Journal of Dairy Science. They looked at serum IG levels, and they fed three liters, and they either fed it by a bottle or they fed it by tube feeder. You can see that they were identical.
So I think the key to the whole thing is we just have to get colostrum into those calves as soon as possible, at least if we're talking that first six hours, right? Because that's where we want to get the maximum uptake of immunoglobulin.
Once you get past that, we're going to talk about feeding colostrum later than or past that six hours here in a little bit, but for the most part, it doesn't matter how we do it. If you're going to do it by tube, make sure everybody's trained, right?
We don't want people to drown calves, and we don't want people—you don't want to cause bruising down on the esophagus either. I've opened up some calves and done some necropsies on calves where there's been significant bruising down there from somebody being too aggressive on trying to get that tube in there.
So you've got to be a little bit careful, and obviously all the other things related to tubing and tube management, right? So one's out of the way.
So when is the process of creating a quality heifer start? I think, you know, in today's science, what we know about epigenetics and maternal programming and all these things, some people would say, "Well, it probably starts before conception," and that's probably true.
It's really hard for us to know a lot about that in calves and cows, but what we do know is that it definitely is affected during development. Once we have a pregnancy, and this was a paper published several years ago, there have been various permutations on this.
Once these guys published this, several other groups went looking for it; some found it, some didn't. In pasture systems, they don't see this; in more intensive management conditions, they see this outcome.
This was Katie Hind, who's actually an evolutionary biologist that works in primates and humans. We were at a big meeting one day, and she asked me and a couple of other guys, "Hey, if a cow is pregnant to a heifer or a bull, do they change their milk production?"
We thought that was a silly question—not really, because we thought the geneticists might have figured that out already. She had data from primates that said yes, it was true that if they were carrying a female, the mom would produce more milk in different milk than if she was carrying a bull.
So she went and pulled some records; she partnered up with a couple of people at DHI and Barry Bradford, I believe, if I remember right. They did this really fun study where they looked at the effect of fetal sex, either during the first pregnancy or the second pregnancy, on first lactation or second lactation milk.
What they found, they had 2.4 lactations from 1.5 million cattle, basically, and they found that first lactation cattle giving birth to heifers produced about 1,000 pounds more milk over the first two lactations, or about 500 pounds per lactation.
Some of the guys that work on the economics of decision-making quickly put out a paper on the heels of this that said, "You know, there's a $6 per lactation marginal return for average sexed semen and a $12 lactation return for sexed semen."
It's probably not true anymore, given how many heifers we've produced, but anyhow, the idea here is that the moms, the dams, recognize the sex and can modify their behavior based on that. They made a little bit more milk for the females.
Again, there's been others who have backed this data up; there are other groups that have said no, that's not true. When I separate those out, I usually find confinement versus pasture as the difference there.
What else do we know? There was that movie right up front there talking about choline in pregnancy, and this is some data to kind of follow along that path. This is some data from Florida where they fed partum, they fed R-protected choline, and looked at this effect of yes to choline or no to choline and what happened.
You can see here in this data from Zenobi, birth weights were kind of different. There was a trend there at two months—not a big deal; they were pretty much right on top of each other. But at 12 months, you saw significant differences in body weight, and post-calving, we saw significant differences in body weight.
So when you looked at average daily gain of those animals from birth to yearlings, you saw about a tenth of a pound difference in average daily gain per day for those calves that came from dams who were fed choline.
That's really intriguing, right? It says again that there are things going on in utero that will impact the productivity of these animals. If you look at those animals again that hit lactation that came from dams that were given choline, they were a little bit heavier at calving.
You can see that change in body weight and early lactation, and then they recovered that quite well, but you can see that they always maintained a higher weight in those first few weeks post-calving, which should translate into more milk, right?
That's exactly what they saw. So feed choline in the pre-fresh period; those calves respond differently; they grow better, they achieve a higher calving weight, and they make more milk in that first lactation.
Remember, this was all programmed in utero. There's lots more data to this. I'm going to refer you to the folks at the University of Florida to look at that, but this is just another example of when do we start making quality heifers, right?
This comes back to the idea of, well, what are the nutrient requirements of a pre-fresh animal? What are the true nutrient requirements of a cow?
Right here, we're looking at about 2.2 kilos of milk difference over the lactation, which is economically significant. If you look at those same animals, incidences of fever, you have a larger percent of the animals that have fevers from the cows that didn't get choline than the heifers that did receive choline.
Again, this is all in utero. The implication is you've got a more functional immune system. If you look at the leukocyte counts in those calves, again, this is all coming from the in utero effect. The dam received choline or didn't, and those animals that received choline, the calves had higher leukocyte counts, better, stronger immune systems, more white blood cells.
Then if you look at the effect of transition feeding and how that works, and again back to the in utero effect, back to 56 days of age—not a big deal, unlike the previous study—but you look at 300 days of age, and again, you're starting to see those body weights open up.
Over time, there's this long-term effect, and it's back to that tenth of a pound a day difference in average daily gain. So again, this is all being set up in utero.
Then one more time here, if you look at colostrum from cows that were fed choline versus colostrum from cows that weren't fed choline, the NN and the CN—those calves didn't receive colostrum from choline cows, but the C, the NC, and the CC did.
You can see that there's a fairly significant difference in the apparent efficiency of IG absorption. So again, there are some other factors going on here where the choline aided and embedded the quality of the colostrum, which is important in my mind because this is going to enhance the calf over time.
It's not just about the IGS. I'd be interested, from my perspective, what other things were affected during this treatment period, and you'll understand why I asked that here in a little bit.
Greater concentration of white cells, less incidence of fever, greater intake, and greater average daily gain—all because of some in utero effects of the dam being fed choline.
Okay, so what does that mean? If we come back here and you say, "All right, what is the implication?" Well, the implication is that during the dry period, the mammary gland goes through involution, and then it has to rebuild itself.
While it's doing that, there are all sorts of growth factors and hormones in this process. You see this mammary gland here; you've got the pre-partum period, and you've got this dotted line L, and those are some of those bioactive factors.
We hit lactation, and those bioactive factors can be transferred into the calf through colostrum, and then they kind of, in mature milk, become kind of low levels, and the calf is normal lactation.
So we have a normal lactation curve, and then we get to the dry-off period, we go through involution, and the mammary gland begins to rebuild itself one more time. Now we have more of those growth factors and bioactive factors and hormones becoming concentrated in the mammary gland.
This early lactation period is to provide these kinds of things to the calf, and that's what you saw in that previous study. There's a name for this now. Some reproductive physiologists who study many things, but they were looking at the efficiency of reproduction in pigs.
They were looking at how many piglets a sow can have, and they came up with this term, the LRIC hypothesis. Everybody's heard of endocrine, but they came up with this term, the LRIC hypothesis.
Basically, it's the maternal programming extended beyond the uterine environment by consuming milk—by ingesting milk-born factors. Milk, in this case, can include colostrum. I added that last part because they don't actually talk about colostrum in their definition, but it really is about colostrum the way we think about it.
These guys, for years, tried to figure out why certain pigs or certain sows with the same genetic line would have greater numbers of piglets. It took them many years to do this, a little over 30 years, and the advent of molecular biology helped a lot.
It's a great story; I'd encourage you to go read about this if you're interested in this kind of thing. But in neonatal pigs, what they realized is that relaxin, a hormone produced by the uterus, is transferred into the colostrum.
If those baby piglets get a little bit more colostrum, they get more of that relaxin, and that relaxin actually stimulates the expression of estrogen receptors on the stromal epithelial cells of the juvenile uterus, which then allows for greater proliferation.
Basically, the first meal that these baby pigs receive can have this relaxin in it, and the greater the concentration of relaxin or the greater the amount of relaxin they consume in the first couple of hours, the greater expression of estrogen receptors on those cells in the uterus, and the larger the uterus is going to be, hence greater reproductive efficiency.
The larger the uterus, the greater capacity to grow more piglets. They've got a great cartoon about it. Again, they've got the relaxin binding and that being transferred up into the tissue, the epithelial cells, enhancing estrogen receptor and then getting more proliferation.
They looked at how many days this occurs, and it happens for about three days after that first meal. Then other estrogen-mediated events take hold, like normal growth.
So there's this interesting story about what's happening right up front. It's the first meal that sets those calves or those piglets up, right?
So what does this mean? Probably not what you expected to see. When you look at those two pictures, the first question I have is: what does Mom want for her calf? What do all moms want for their offspring?
You've got two bodybuilders there. What are some terms that come to mind immediately? Because we don't have feedback here, I'm just going to talk you guys through it.
Well, I was a wrestler; I lifted a lot of weights. I was never going to look like that. I'm assuming those guys had to do that with a little bit of help. But the first term that comes to my mind—and there's a cheat on the slide if you look in the bottom left corner—you see the word anabolic.
These guys are really anabolic. Mom wants them to grow; she wants them to be healthy; she wants anabolism. The question is, how does she do that?
Well, it's obvious she does that by providing nutrients to the calf because if the calf was under normal conditions, they would suckle mom and eat grass and suckle mom and eat grass, and that would make them anabolic.
But in this early stage of life, the question is, is Mom doing something else to help that calf develop? So that begs the question: with or without the steroids?
It's hard to look like that without a little bit of help, and most people would say, "No, Mom is not going to feed her calf steroids." Well, maybe so.
Let's look at milk here and colostrum. This slide is pulled together from a bunch of different sources. We've got energy. This is colostrum in the middle and then mature milk on the right.
Obviously, there's a lot of IGS in colostrum, not so much in milk. There's a lot of leptin in colostrum, undetectable in milk. I want to highlight a couple of these.
Insulin: 80, 65 micrograms per liter, about one in mature milk. Prolactin: 280 micrograms per deciliter versus about 15 in mature milk. I'd love to know what that prolactin is doing in there, where it's binding.
Growth hormone is actually fairly high for a hormone that isn't really transferred in the milk. That's pretty high for this stage. The one that's really more telling, though, is the IGF-1 at 310 micrograms per deciliter—an incredibly high level.
So you've got these hormones, you've got two hormones like insulin and IGF-1 that stimulate protein synthesis. Yes, they're involved in a bunch of other things, but one of their major roles is to stimulate protein synthesis if they're not working on, you know, up-taking glucose and things like that.
You've got TGF-alpha, a lot of cortisol, of course, that is expected, and then the estradiol. There's a big dose of estradiol there.
So if you look at that, the first thing I would say is, "Hey, Mom wants to make those calves anabolic." The question is, how long does that last?
I pulled some data together here. Again, we got the first three milkings characterized, and we'll go right down to the bottom. You look at IGF-1: 341 micrograms per liter, 242 micrograms per liter, 144 micrograms per liter.
Remember, mature milk is going to be about one. Insulin is still high at the third milking. Vitamin A actually has hormone-like activities early in life, especially at those levels at 200, 95 micrograms per deciliter.
Vitamin E is quite high. So, you know, those first few meals, there's a lot of signaling going on that will tell the calf, "Hey, you can grow; you can develop; you can do things."
It might be not systemically; it might be locally, and that's what we're going to talk about here.
What we know is that colostrum provides IGS, but it contains a high amount of nutrients and has a lot of non-nutrient factors that support things like gut maturation. We talked about IGF-1 and insulin might act through receptors in the gut to stimulate cell proliferation, cell differentiation, and protein synthesis.
So in effect, colostrum is one way the dam communicates to the calf after the calf is born, right? Because they can't have that direct relationship as they had, but now maybe they can do it through milk.
Is there any evidence that there may be something going on there? The answer is yes. This was a paper published, you know, 15 years ago. Brown Swiss calves received two or four liters of colostrum at birth, and then some of them received some more colostrum over another 68 feedings.
Those calves that received four liters a day—that daily gain is actually pre-weaning daily gain. I need to change my slide there, but it's pre-weaning average daily gain.
So we're talking up to about, you know, 600 to 700, 800 pounds, 1.76 versus 2.2. So you're talking not quite just over 3/10 of a pound difference in average daily gain. They were all fed the same thing, all managed the same way, all in pens, right?
So we don't have any intakes. That begs the question: why are they growing faster? The age of conception was pretty well controlled. Survival through the second lactation was greater, actually, for the calves of the four liters, and then milk yield—those that survived made more milk, right?
So you see some indication that more colostrum is better. If we look at early life, we see some efficiencies here where this was a study done with colostrum versus colostrum replacer.
This is over the first 29 days of life, and in the interest of time, I'll just cut to the bottom. There was no real difference in intake, but notice the difference in feed efficiency. The calves that received mom's colostrum had much higher feed efficiency than those that received the colostrum replacer.
There were no differences in IGS, and that's really important. There were no differences in IGS. This is all the extra things in colostrum other than the IGS.
You see the same kind of data again. There's some work from Illinois, and I'm going to go over to this intensified side here, this column on the right. They looked at—they didn't have core data, but they could do it by level of IGS, poor level of IG or good level of IG.
You can see that in the serum concentration: 609 versus 2000. You look at the average daily gain when they were given enough calories and nutrients to allow them to grow, and you can see not quite a 3/10 of a pound difference in average daily gain.
So as we get—it's not just more colostrum; it's better colostrum, or it might be more colostrum. In this case, we don't really know, but if you use IGS as a proxy, you know there's this effect.
We did a similar thing and repeated it: four liters versus two liters. In the four-liter calves, they got an extra two liters at 12 hours. We fed them on auto feeders in an ad libitum system, took lots of samples, and you can see the two liters versus four liters is here.
IG concentrations—this was all pooled colostrum, highly managed. I was going to repeat this study with Fernando; I would probably just add some IGS to make sure that they were equal, but I don't believe that's the effect.
Anyhow, even the two liters were very good IG status; four liters were tremendous at 2700 milligrams per deciliter. But you could see the weaning weights were significantly different, and the average daily gain was significantly different.
We used birth weight as a covariant when we do all these calculations, and each calf is their own control, right? We've taken that into account. If you go to 80 days, you still see that difference.
Now we're post-weaning; we see that difference in average daily gain. We see differences in hip height measurements in terms of hip height gain. The calves that received more colostrum had better bone growth, right?
That's really unusual, and it implies that you're getting some sort of somatotropic axis effect because bone is the slowest growing tissue in the body, and it's really hard to stimulate that kind of growth.
Somatotropin will do that, right? A little bit of difference in feed intake in those animals, but overall, pretty good. Look at the average daily gain post-weaning: 2.4 versus 1.8, basically.
So it looks more like that Brown Swiss study. We're starting to see better intakes in those animals post-weaning. So, you know, it implies that the more colostrum we get in these calves, the better they're going to perform.
We're pretty convinced now that it's not the immunoglobulin; it's all these other factors that are in there, and I'm going to show you why we think that.
So, you know, if you think about what we just talked about, you know, general response is enhanced protein synthesis, enhanced enzyme expression, and greater gastrointestinal development.
The gastrointestinal tract is your barrier, right? The gut is the largest barrier immune system that we have. So, you know, if we make it stronger, we're going to improve health. More surface area is going to get us better digestion and absorption.
We have more capacity to digest nutrients because maybe we're going to get better enzyme secretion, right? So Mom maybe is helping in this process.
Yur BL and Harold Hammond and all of their grad students over the years did a remarkable series of studies—dozens of studies—where they looked at the really short-term effect of colostrum and colostrum extracts on growth.
I'm going to show you just a couple of slides here of where they made a colostrum extract through centrifugation. This was published quite a while ago, but you can see the IG concentrations down here at 23 versus 1.1.
Insulin at 365 versus 67, and leptin actually went down in the extract. It must have gone out with the fat. If you look at what they then fed, it was a milk replacer or colostrum replacers, but basically a milk replacer to these calves, and then it added the extract, right?
Then they harvested the calves and looked at villus heights. They were looking at the length of the villi in the small intestine, which would be an indication of their ability to absorb nutrients.
You can see that adding the extract significantly enhanced the length of the villi and the height of the villi in there, which means they have more surface area to absorb nutrients, right?
So Mom is helping set that up. They looked at the crypt cells at the base of those villi. They used BrdU as a marker for proliferation. You see a trend for that occurring, where you've got greater proliferation in those crypt cells to drive that villus height and that length, right?
Again, creating more surface area. Notice in this data that they're talking about day five of life, right? So it's not just a one-day occurrence; that gut's responsive over the first four to five days of life based on everything that we know.
Again, those studies were repeated where they gave them just colostrum versus a nutrient-identical or nutrient-similar formula. You can see that colostrum always enhanced, or in this case again enhanced crypt cell proliferation in these calves, right?
So something in the colostrum stimulated the development of the gastrointestinal tract. Again, back to an extract, they fed them a formula that gave some of the calves the formula plus the extract.
Again, day eight of life, they see this trend for greater BrdU incorporation or cell proliferation in those crypt cells. Okay, so Mom is helping develop that gastrointestinal tract.
It's not just the first feeding; it's not just the IG. She's trying to do this over time to improve the performance of that calf, right?
So, you know, to ask the question, how would a calf grow better? Then what does this mean? How does that translate? Well, xylos—in this particular slide, we have xylos, which is a non-metabolizable analog of glucose, and glucose on this slide.
On the left side, you have the xylos absorption, and in the dark lines, the diamonds, you have those calves fed the colostrum, and in the open squares, you have the calves fed the formula.
Again, these are nutrient-similar to nutrient-identical formulas. You can see that the xylos absorption is greatly enhanced, significantly enhanced in those calves fed colostrum versus the formula, right?
Then if you looked at the glucose, a lot of times it's hard to look at the glucose because it's metabolized so fast, but in fact, you can see on the right panel this high increase or much greater increase in glucose concentration in the plasma than in the formula-fed calves, all right?
So they're looking at about five millimoles per liter in the formula-fed and about eight millimoles peak in the colostrum-fed calves. Notice this is on day five, right?
So again, we're not looking at that first day; we're looking five days out, and we're still seeing this effect, right? So these guys did a really fascinating study and published it in 2011.
It's a head-scratcher. I'm going to go through the simplest part of it because they used isotopes to figure out where the glucose went and how it moved around. We're not going to do that.
So they had seven calves fed colostrum and seven calves fed a milk-based formula four hours on average after birth—very comparable macronutrients. They took lots of blood, and again, we're not going to talk about the isotope data.
So you got a pretty good idea of how well they did their study. Here's the lactose concentration. The top is the colostrum, day one to day four. You had 21 grams per kilo, 260, 341.
You look at the formula: 20, 1, 260, 338. You can do the same with the protein, the same with the fat, the same with the crude energy, and you realize that that formula very nicely mimics the nutrient profile of the colostrum.
However, you know you're not going to find the hormones in the formula, or if you do, they're going to be very low concentration, right?
So if you look at the IGF-1 levels, though, in that colostrum: 373, 192 days three and four, we're still around 86 micrograms per liter. So again, we're not at mature milk yet.
So that means if we were to ask a cow, "Hey, how many days do you make colostrum?" and let her make the decision, she would probably say at least four days, right?
Whereas we tend to focus on that first 24 hours, when in fact, or maybe first six hours, when in fact, that's maybe not true. It looks like it's not true.
All right, so then if you look at, you know, what's going on with glucose, right? Back to the idea that Mom is trying to make this calf anabolic.
So the blue bars are the calves fed colostrum; the green bars are fed the formula. This is postnatal concentrations before feed intake. This is every day before feed intake, and you can see what's going on here.
The colostrum-fed calves had greater circulating glucose concentrations than the formula-fed calves. If we come out here on day four and they looked at time of feeding, which is basically what they're doing, so is on day four at time of feeding, you see that same difference, right?
Significant difference in plasma glucose. Then the two hours after feeding, yep, the formula-fed calves did increase, but not nearly as high, not nearly as great as the calves fed the colostrum, right?
So something about feeding colostrum enhances the anabolism of the calf by increasing the amount of glucose she can absorb, right? Whether that's facilitated or it's just more mature gut and greater enzyme capacity, we're still not quite sure.
So it's always the fun thing. So when glucose goes up, what's supposed to happen to insulin? Well, it's supposed to increase, right?
So here's day four. This is taken right from the study from the Journal of Dairy Science. Here's day four; here's the insulin on day four at time of feeding. Here's the insulin on day four, two hours after feeding.
Okay, so those of you that are paying attention now realize you have a conundrum because when the glucose goes up, the insulin's supposed to go up. When the insulin goes up, the glucose is supposed to go down.
When in fact, what we see here is that the insulin and the glucose are both up, all right? I've got lots of stories about this. Fernando generated the same kind of data, and it took about two hours of his PhD defense to get through some of this because the two physiologists in the room just did not believe that this could be true.
But we've repeated this several times; it is true. So what it means is the insulin has to be transported across the gastrointestinal tract. It also means that while it's being transported across the gastrointestinal tract, it's facilitating the transport of glucose somehow, right?
Again, true anabolism. This is one way that you could get higher growth rates in these calves if you gave them more colostrum because you're now establishing this greater uptake of glucose.
We haven't chased it forever, but we see that it happens; it seems to persist, right? If you look at—sorry, that slide's out of place.
If you look at the idea of lactase activity and villus height and crypt depth, you can see here the first panel on the left is villus height to crypt depth, and you can see that the colostrum-fed calves had greater villus height, the crypt depth.
If you looked at the right panel, that's lactase activity. Calves fed the colostrum had higher lactase activity, so the colostrum is actually stimulating the synthesis of the digestive enzymes so we can digest more lactose, okay?
So not quite significant, but higher. So glucose uptake is increased even with similar nutrient content. Plasma protein levels were higher, which means you'd have more amino acids available for growth and protein synthesis.
It means that you have less protein turned over, oxidized for gluconeogenesis, okay? So you'd have more efficient growth, right?
So feeding colostrum for four days looks like a good thing. We're going to come back to that. When you don't understand something, you kind of repeat it.
So here's just one of our simple studies. We took 12 calves, went out, purchased, went to the local store, purchased some colostrum replacer. This is made by Saskatoon, purchased through Land O'Lakes.
In half the calves, they received—went into Overton's lab, sold a bunch of his expired human insulin from some of his studies, and then Dan Lopez dosed each one of those colostrum replacers for half the calves with about a thousand IUs, which was much more than we wanted him to do, but he didn't do the math on this.
That's okay; nobody died. We sampled calves; we had catheters in the calves we put in at birth so we could sample blood. This is what we found, right?
So exactly what we would think: you put the insulin in the commercially available colostrum, and you can see the normal insulin rise. The green line is the control; that's the colostrum replacer without the insulin, right?
The blue line is a colostrum replacer with the added insulin. You can see that the insulin is actually being transferred into circulation through the colostrum. That's human insulin, and again, it was simply just added and mixed into the colostrum and fed like normal colostrum.
Again, what's fascinating: you take that same set of calves and you look at the glucose. Here are the controls; we're at about 70 milligrams per deciliter glucose in those control calves, and we're about 81 to 82 grams per deciliter in the treated calves.
So just adding insulin to the colostrum replacer increased the circulating glucose concentration of those calves, right? So it just replicates what we've seen, what was observed in those other studies, and just reinforces the idea that these hormones have a lot of activity and anabolic.
What it also says is Mom is really trying to help the calf. She's trying to help direct nutrients and make those calves more anabolic.
So it's not just about that first feeding of colostrum; it's about how Mom is systematically trying to help that calf get better, which means that all those subsequent milkings—at least, you know, four to five more milkings of that colostrum, or what we would not call colostrum but transition milk—is important for that calf to help her be more anabolic, create better growth and health.
This is a study that one of my master's students did, Katie Andrews, Steenberg now. This was a commercially available colostrum extract. We need to redo the study; this is the preliminary study.
We were trying to figure out how much of this we needed to give, all right? So in our preliminary study, we were feeding a amount of colostrum. You can see that four liters of colostrum, and they have no dose.
They gave one dose of this extract, two doses of the extract, or four doses of the extract. All the calves received the same amount of colostrum, and you can see the difference.
This is for the first 21 days; this is pounds per day gain. So we did that at birth, and then we measured them for 21 days to see if we could see an effect: 1.3 pounds a day, 1.45 pounds a day, 1.65 pounds a day, 1.85 pounds a day.
Those calves all received the same amount of milk replacer, right? So we see this increase in the efficiency of growth fed ison nutrient diets.
We did a large study, but because we're feeding a colostrum extract, I elected—we have a problem with rotavirus at the research farm. We usually give the calves an oral vaccine at birth. I elected not to do that because I didn't want to block any of this effect, and sure enough, we had over 50% clinical rotavirus.
So we lost the big study to rotavirus, and we had, as Daryl Niden would say, "You got really healthy calves for being that clinical." So it says there's an effect here, but we've got to redo the study. That's why I'm showing you this preliminary data.
Okay, so there is something to these extracts and something to colostrum.
I'm going to change gears real quick, watching the time here. I'm running out of time. What happens to immune cells in colostrum? One other thing about colostrum, and I'll go fast through this.
There are other cells in there; there's a lot of leukocytes in there, and there's information now that says that those cells are trafficked into circulation. So you can ask the question: does this have any impact on the immune system?
If you look at the data that exists—and I know there are other scientists out there that are looking at this and have been trying to replicate this—they were able to figure out that maternal leukocytes, what we would call somatic cells—most of those somatic cells in colostrum are leukocytes.
You can see them in circulation in the calf; they get sequestered in the tissue, but they have been measured in circulation up to five weeks after colostrum. Based on what they have, the data they have, there appears to be greater cellular immunity in those calves that received whole colostrum compared to cell-free colostrum.
They've looked at markers on the cells. I'm going to skip over this slide in the interest of time, but this is a really cool study.
What they did is they directly tested this concept. They fed whole colostrum, frozen colostrum, or cell-free colostrum within four hours after birth. Then they pulled leukocytes out of those calves, you know, from 1 to 28 days after ingestion.
What they did then is they looked at proliferative responses against bovine viral diarrhea virus and mycobacteria. The interesting thing is the dams received a vaccine containing inactivated BVD, but were not vaccinated against the mycobacteria.
This is interesting because if these cells are transferred to the calf, then when you pull those cells back out of the calf, they should respond to the vaccine, right?
Which means you directly sent memory into the calf from Mom's cells intact that they could make use of. In fact, you know, no IGS at birth, but a lot at day one. Calves that received full colostrum had enhanced responses to the BVD antigen one and two days after ingestion.
Those that received the frozen or cell-free colostrum did not respond; there was no difference in mycobacteria. The take-home here is that cells from colostrum enhanced cellular immunity by providing mature programmed cells from the dam.
All right, so a bunch of takeaways here. I went through that really fast. What does that mean about pasteurizing colostrum? Well, it means you probably shouldn't, but we're never going to tell people to do that.
Yet we still want people to pasteurize colostrum because we don't know how important this is, but it is interesting, right? So maybe five years from now or ten years from now, somebody will have done the research and said, "All right, we got to figure out how to keep those leukocytes intact and alive for that first feeding so we can get them absorbed."
Because this is really how we get enhanced immune function, right? So there is a really interesting area for active research.
I've been asked to review some of this stuff in the past. I'm not an immunologist, but I find some of these things really interesting, and I know there's at least a couple of researchers out there who have repeated this and published it and can get similar findings, find similar outcomes, right?
So the take-home: colostrum feeding for four days, right? Everybody goes, "Oh my God, that's a lot of work." Well, yeah, maybe we're already doing it a little bit, right?
So first milking colostrum, you know, within six hours of birth, four quarts for large breeds, two quarts for smaller breeds. It doesn't matter; just be efficient about it.
First milking colostrum again at 12 hours. It wouldn't have to be four quarts; it could be two quarts. You don't have to tube it; let them suckle it if they want. Maybe they won't want to because they're already full.
For day two, second milking colostrum, right? The key to the whole thing is because we used to use blanket antibiotic treatments, we had a lot of what we call transition milk that was loaded with antibiotics.
So first and second day usually went someplace else, so that part is not new. What it means is we got to keep it isolated and then give it to those calves one to four days of age. That's really what it's saying.
So second milking, and then third and fourth milking colostrum for days three and four. It doesn't have to be just that colostrum; that doesn't have to be their old meal.
It just means that we want to take that and make sure we get it to those calves one way or another. In the herds, Bob James has fed back to me about this.
He's had a few of the herds that he consults with do this, and he says what happened is he reduced all the standard error around the growth. It didn't necessarily make all of them faster, but you got rid of the outliers.
It made much more uniform outcomes in calves.
Okay, so feeding colostrum for at least three to four days for those younger calves.
So in summary, Mom's trying to send information to the calf via mammary secretions. Some of our management approaches have short-circuited this kind of information flow.
There's a lot of things in colostrum that impact the development of the calf, especially intestinal development, independent of anything related to nutrients. We now know that colostrum can positively impact pre- and post-weaning feed efficiency.
Mom makes colostrum for more than one day, and this has additional impacts on calf development. We just have to figure out how to deliver it.
I'll stop and take any questions.
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All right, thank you very much, Dr. Van Amberg. The first question is: will a heifer calf treated four or five times reach her full potential, or are you better off just culling her at an early stage?
Yeah, if you've got to treat a calf that often, she's a good candidate for somebody else's farm. All the information that we have—if they're chronic, if they're that chronic that early in life—unless you've got some very special calf, we would be moving them off the farm.
Great, great. Next question: what can be done during the dry period to improve on colostrum quantity, but more importantly, colostrum quality?
Well, it's a really complex—it's a great question. It's one that I spend a lot of time on. I think with the advent of these high-fiber diets, the thing that I see happening too many places is we don't analyze some of that straw or some of those poor, what we'd call poor-quality forages for digestibility, and we're not balancing at the right MP levels.
I see a lot of mature cows that are probably deficient on metabolizable protein. I used to think this wasn't possible, but I've done enough case studies here, actually in Europe and in the U.S., where I see a lot of these high-fiber diets, and the MP levels are 100 to 250, almost 300 grams short of metabolizable protein.
Those cows tend to have lower quantities of colostrum and definitely lower quality, and that's very true of the heifers. If I get on a farm, and one of the things that they tell me is that the heifers don't produce a lot of colostrum, the first thing I look at is the dry cow pen or the pre-fresh pen.
Most of the time, a growing heifer should probably not be put on a dry cow diet because she still has significant requirements for growth, fetal development, mammary development, and liver hypertrophy and all those things.
You put her on that high-fiber diet with low MP, and she can't eat enough of it, and now she's really in trouble. I've seen a bunch of heifers that have problems there.
So I now look at that MP level and make sure, you know, at least 1250 in the heifers, and I'd like to be 1300 to 1350 in the mature cows. It could be better; it depends on how big your cows are. If you've got 1,800-pound, 2,000-pound mature cows, then you better be higher than that.
All right, great. Next question: does pasteurization of colostrum have any effect on IGS or other maternal cells in colostrum? What about freezing it?
Yeah, so based on everything that we know, freezing and pasteurizing will knock out those leukocytes. So yeah, that won't happen. It doesn't affect the hormones, though, as long as you follow standard guidelines on pasteurization of 60 degrees Celsius for 60 minutes, and you've got a tight tolerance on your pasteurizer variance, right?
It's 60; it's 59 and 61, or 16 and a half. Then the hormone aspect of that remains intact. We've analyzed that for her in some places; it's published now; I just don't remember where.
But the leukocytes, yeah, they won't survive pasteurization or freezing, and it looks like they have to be alive to have that effect.
Great. In the interest of time, Mike, I know you have a class to teach here in a few minutes. I've got one more question for you.
Can you speak to the efficacy of a colostrum replacer in providing necessary things like relaxin?
Yeah, I'm only laughing because I'd love to know the answer to that question. We analyzed some relaxin; right now, it's not a typical hormone to measure. We didn't have the capacity to make an RA for that.
We bought some kits; they're very expensive. We tested a little bit; I can't find any in colostrum replacers. There's definitely some in cows, but I can't speak to all colostrum replacers.
I just—it's—I would love to be able to test that.
All right, great. Well, listen, I want to thank you, Dr. Van Amberg, for spending a few moments with us today. It's been very insightful.
I'd like to thank everybody for attending today's webinar. If you have any questions, please submit them to marketing@balchem.com.
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