Preventing Dairy Cow Ketosis: Nutritional Management during Transition

- So it's 11 o'clock, and we are gonna start our webinar today.

Just a few housekeeping things.

This webinar will be recorded, and the recordings will be available in the Penn State Extension website.

Attendees, please use the Q&A box for questions, and Dr. Van Saun try to answer them as we go, or after the webinar.

And also, when you log out, when the webinar is over, probably you'll see a popup window with a brief questionnaire or survey.

So if you can actually fill it, we would truly appreciate it.

It'll help us to create future programs.

So now, to our speaker, we would like to introduce Dr. Van Saun, who is a professor of an extension veterinarian at the Department of Veterinary and Biomedical Sciences, Penn State University.

He earned his DVM degree at Michigan State and PhD at Cornell University.

His research and extension interest focus on transition cow metabolism, metabolic diseases and prevention.

So he is gonna discuss actually these subjects during next four Penn State webinars.

And one actually starts today.

The next one will be next week, January 30, and then February 13, and February 20 as you can see on the screen.

Today, Dr. Van Saun is gonna focus and discuss the nutritional management, during the transition period.

So I'm gonna unshare screen, and.

- All right, so we'll go ahead and get started here.

Thank you, Michal.

Glad to be involved in this program, and welcome everybody who's joining in.

I see a few familiar names out there, so hopefully, we'll have a nice interaction in what's going on.

I just got done this morning speaking basically on this same topic to a group of producers and extension, well, not extension, but faculty in Ukraine, in Kyiv.

And so, quite a difference here in audiences, but we all have similar problems, and so there's a need.

So for those of you who don't know me yet, I've been here at Penn State since about about 2000.

I was in private veteran practice in Northern New York State in a large dairy practice, and then again in Michigan.

And then I was on faculty at the vet school at Oregon State University and an ambulatory clinician there and an ambulatory clinician at Michigan State.

And as Michal highlighted, you know, when I did my practice experience, enjoyed practice, but recognized that vet schools didn't really teach me the things that my clients needed me to know.

And that is, how do we prevent these cows from getting sick, and not having to treat the animals or do the surgeries or things, which is what they taught us in vet school.

And so that's why I went back, even though I said I was never gonna go back to school, went back to school and focused in on better understanding reproductive performance and reproduction, and obviously, the nutrition side.

And that has put me in a unique situation, which has resulted, of course, in all kinds of opportunities to interact with many other colleagues here within the Northeast or nationally and even internationally.

And the last 20 years or so, I've been doing a fair amount of work over in Eastern Europe, in Michal's home country of the Czech Republic and Slovak Republics, and now working in Poland, and those, so I hope to bring some of that perspective and overall ideas on how to deal with the problems that we all face here.

So today, what I wanna do is focus in down on the disease, ketosis, but I wanna bring you, maybe a little bit different perspective of what ketosis is, and then we'll go through the nutritional factors that are implicated in risk or prevention of ketosis, potential for some nutritional supplements, and then go through some final summary recommendations that you can take home and try and put into practice.

So, you know, the bottom line is what is ketosis?

And this actually has become a new question or a renewed question amongst the veterinary community.

Classically, we define ketosis as just a metabolic state where ketone bodies, these unique compounds that are produced through metabolism, can be detected, right?

So it's just a matter of finding these things in the blood.

But the question has been brought up, does this really suggest that it's a disease state?

You know, is ketosis just associated with the production of ketone bodies?

Now, the argument here is we naturally make ketone bodies as part of our metabolism depending on the nutrients that are provided.

And we now know that in terms of weight reduction, and humans, we can go on a ketone diet, and actually induce ketosis to do body weight loss.

So, what makes ketosis a disease as opposed to just a metabolic response?

And so probably a better definition of ketosis is that it's a metabolic disease state where ketone bodies are detected in high concentrations, and animal performance or health is compromised.

And that's the definition of disease is an altered state of function or structure in a living organism.

Now, unfortunately, this definition suggests that there's a direct negative association of high ketone concentration.

And part of what I'm gonna talk about today is that may not necessarily be the case.

I'm gonna make the argument that high ketones are a consequence of some underlying issue and not necessarily the thing that we have to fight.

And so, you know, I'm trying gonna answer this question, does high ketones cause the disease, all right?

Now, if we go back into the literature, there was a paper published by a preeminent veterinary nutritionist, Dr. Dave Kronfeld, and he published a paper back in 1982, describing what he called spontaneous ketosis.

And his definition there was ketosis is an accumulation of ketone bodies representing, right, so representing incomplete combustion of fatty acids, during periods of lipid mobilization.

So important points there, and then, which may or may not be dependent upon carbohydrate availability.

So now, I think, David had quite the insight here, you know, that's what, 40 years ago now, that it's a metabolic disruption and not just the production of ketones.

Now, we can also see other forms of ketosis different from what Dr. Kronfeld described as spontaneous ketosis.

There is what we call dietary or elementary ketosis.

And this is a consequence of feeding poorly conserved ensiled forages, where these forages contain high concentrations of butyric acid.

This is that really bad rotten eggs smelling kind of stuff, kind of slimy green looking silage.

We typically see this in grass silages and alfalfa silages, not so much in corn silage.

And this is due to clostridial fermentation of the feeds rather than lactic acid bacteria fermentation.

And so we see very high butyric acid production in our fermentation profiles.

And then this butyric acid, as it's being consumed, is converted in the rumen wall to beta-hydroxybutyrate.

So the rumen actually makes ketone bodies, not just the liver.

Another form of ketosis is basically what I'll call underfeeding or starvation ketosis.

And this could be primary in origin where there's limited feed availability that induces a ketotic state.

And then we can easily correct this by identifying that issue and re-feeding the animals or providing the appropriate feed.

More important from a veterinary standpoint, animal health standpoint is, ketosis could be a secondary disease to many other diseases that reduce voluntary intake.

So if intake goes down, obviously, they're not meeting their energy need, they're gonna mobilize body fat if they have it, and then that could lead to a ketotic state.

So the classic example here from a transition cow is our concern with clinical and subclinical hypocalcemia.

The hypocalcemia has a very dramatic negative effect on voluntary intake as well as many of the other diseases.

All right, so if we think about ketosis as truly as a disease, most of our textbooks and information we're gonna talk about is defining what we call clinical ketosis.

Now, clinical ketosis means that you can actually see clinical signs.

Now unfortunately, with the disease ketosis, these signs aren't very specific.

It's not like rickets where we can see very defined changes in bone structure and know that rickets is there.

And then as a consequence, we know it's either a vitamin D or calcium or phosphorus deficiency issue.

Ketosis isn't quite like that.

Classic clinical signs that are described in the internal medicine textbooks or depressed appetite, yeah, that's you know, so many other things do that, marked reduction in milk yield, that's usually how it's picked up.

Rapid body condition loss, weight loss, it's similar to this cow in the picture you see here.

And then decreased rumination.

So if you're monitoring rumination, you'll see a number of chews going down.

If you're looking at rumen fill, that's gonna be decreased.

And then if this disease gets serious enough, we can see neurologic changes.

And I still don't believe we understand why some of these things come about.

One of my older professors suggested that ketone bodies can chelate or bind magnesium in the central nervous system.

And that can cause the aggressive behavior similar to what we see with hypomagnesemia or low magnesium.

More often, we see a process called pica.

Pica is what we define as abnormal feeding behavior where the animals will chew on pipes and drink urine and eat sand or dirt and things like that.

And we can see pica with other deficiencies.

However, we can define, you know, if we see this collection of signs, we can take blood samples, measure the one of the ketone bodies, there's three different ketone bodies that are products of metabolism, but two of them are very unstable in blood, so not easily measured.

So the one that's classically measured and used as our primary parameter is beta-hydroxybutyrate, or what I'll describe as BHB.

And generally, if it's above 29 milligrams per deciliter or some people use 26, again, it shows that there's some variation here that is pretty much considered consistent with a clinical syndrome of ketosis.

Usually, if we look at other things beyond BHBs, we'll see that the non-steroid fatty acids, which are product of fat breakdown, so this is a compound that we use in blood to look at fat mobilization.

Those will be highly elevated in these animals.

We may or may not see hypoglycemia classically, according to the textbooks, hypoglycemia or glucose deficiency is the predecessor to this disease process.

But if we have insulin resistance and there's some talk of some different forms of ketosis where we might actually see normal glucose or even slightly elevated glucose.

What's more intriguing is the new research coming out, especially, out of Dr. Baumgard's lab at Iowa State University, and some of my colleagues and friends in Italy, Dr. Bertoni's group, that are looking at the role of inflammation as the predecessor to all the problems we are seeing with our transition cows.

And so, you know, the big question then is, do these elevated ketone bodies in the blood cause these clinical signs or are they reflecting an underlying issue?

And give you the quick answer now is, we can infuse beta-hydroxybutyrate, and we don't cause decreases in dry matter intake and we don't cause some of these things.

So, my biased perspective here that I'm gonna support is it probably is more of a reflection of something gone wrong.

All right, now- - I think I've a question. - [Robert] Yeah.

I think you probably even answered this question.

What causes a cow to have a blood BHB of 3.0 and 20 days in milk when the cow is milking heavy and on a high cow diet?

- Okay, I will answer that in just one moment.

If I don't get that answered for the person, have them comment to you again, okay?

All right, so let's define the other side of ketosis.

And there's a newer definition out there, called subclinical ketosis.

This started in the late 1990s, and most of it was done through looking at ketone concentrations in the blood, and then reflecting on cow performance.

All right, so subclinical ketosis, there's no obvious signs of health issues, not like what we just described for clinical ketosis, but it's basically defined solely by blood BHB concentrations.

And depending on who you read and when the paper was done, this started out at about 14 milligrams per deciliter.

We've dropped it down to 12 milligrams per deciliter.

And what we see is cows that have these concentrations in early lactation, they seem to have reduced, or we at least, we've seen in some of the epidemiologic studies that have been done by the Cornell group and by the Wisconsin group, and the Guelph group.

So it's not like one study.

We see reduced performance recognized as decreased milk yield, decreased reproductive performance, and increased risk for culling because of disease.

Now, let's start to address the question that was posed.

What do we do about this animal that's got the high BHB and is milking?

All right, so we did a study here where I had a number of producers or veterinarians collect blood samples in the first three weeks of post-calving, and we ran complete metabolic profiles on these animals and then monitored what their health status was, and we also looked at their DHI records and so on.

And so this is a summary of that work, and what you can see here is, even at 10 milligrams per deciliter as a threshold, that's the criteria that I use.

So I took all this data and identified those cows that had 10 milligrams and higher in their blood of BHB, and those that were less and then looked at their performance and we did the statistical calculation called an odds ratio that basically, what it said is, "Those animals with this higher concentration in the first three weeks, were 2.8 times more likely on average." Now, the range was between 1.2 and 6.4 of having some disease process.

Now, I did not do what the other papers have done where they've looked at BHB relative to risk of ketosis, BHB relative to the risk of LDA, BHB is a relative risk to metritis and so on.

I just said, any disease, so these were cows that had retains or they had milk fever or they had lameness issues or metritis or whatever, okay?

And then you can see then as I change the threshold, as I increase the threshold up towards where the current status or the current suggestion, somewhere it's between 12 and 14, you know, I saw, again, an increasing significance, and obviously, the higher the BHB, the greater the risk of disease.

So does this suggest that BHB is the cause?

And the answer is no, because this is just an association, it's just a statistical connection, and it's not a cause and effect, all right?

So one of our challenges is, we're defining a disease solely on the measurement of one parameter without thinking about what else is going in on this.

And that results in this kind of approach where we look at the BHB concentration, let me get my laser pointer here.

And if you're below whatever threshold you choose, now, there are other papers out there that also show that 10 milligrams per deciliter increases the risk of animals for certain diseases.

So below some level, you're healthy, above a certain level is the clinical disease where they show the clinical signs.

And then in between those two is what we're now defining as this subclinical disease, which is hard to find, only measured through determining blood, but does have some impact on our cows.

All right, now this is where I'm gonna start to address that question.

This is that same data set that I just showed you where I just looked at BHB, and I mentioned that I did a complete metabolic profile.

So I was able to look at many different parameters.

These are the parameters that were highly significant relative to me categorizing cows.

Like, in this picture I just showed you, you know, I kind of looked at this and I used 1.4 here and 2.6 here, which was at the time, back 2004, the time that those were the thresholds we thought.

And so what I'm gonna do here is, you can see, what I did is I found all cows that had 1.4 millimoles or 14 milligrams per deciliter of BHB in their blood.

And this is in the first three weeks postpartum or less.

And then I looked at which cows were healthy, I had healthy cows that had no disease and cows that had one or more diseases.

All right, so that's my sick, and then you can see what the mean values were.

So, you know, there was no difference in BHB, which makes sense because I defined it by this.

There was really no difference in albumin.

Slight increase, but not significant in glucose, surprisingly in the sick animals, really no statistically significant difference in the cholesterol, but the sick animals had higher NEFA values.

And remember, NEFA is a metric of negative energy balance.

So this makes sense, you know, cows that really didn't have high BHBs that were sick or had some problem were off feed, and as a consequence, they had higher non-esterified fatty acids.

But now let's move to the subclinical side.

So these are animals that are between 1.4 and 2.6 millimoles, or 14 and 26.

Again, I had healthy animals and I had sick animals.

And now, we start to see some differences.

So in this range, the healthy animals generally trended more, their mean value was slightly lower than in BHB, than the sick animals.

So more of the sick animals were closer to the 2.6 here.

But now, look at this.

The sick animals had lower albumins, than the healthy animals.

They had lower glucose than the healthy animals.

They had much lower cholesterol than the healthy animals, and much higher non-esterified fatty acids.

So it's not just BHB being elevated, but there's other undertones of metabolic changes.

And so, how do I interpret some of this?

Well, obviously, these animals are either off feed more as indicated by the higher non-esterified fatty acids.

Cholesterol is a marker that we can use for export of fat from the liver.

So this might indicate increased risk of fatty liver disease with low cholesterol, or some of the work that I've looked at is, I think, cholesterol very similar to urea and nitrogen, can be a measure or a metric for intake.

And what we see is, if animals have higher intake, they have higher cholesterols.

So this might suggest lower intake, and some loss of glucose homeostasis, right?

We're increasing the fat mobilization.

And now, let's go to what would be considered clinical ketosis.

And just as that person question, there are animals that have very high beta-hydroxybutyrate, but are not sick.

They're defined as being ketotic only because their BHBs are high, but they're not showing the clinical signs.

This is the argument that Dr. Baumgard and his lab makes that ketones are a natural metabolite.

The production of ketones, the mobilization of fat is normal, it's what's going on or what's bringing about some of the challenges here.

And so let's take a look.

Here, you can see, these cows on average had 37 milligrams per deciliter, absolutely considered ketotic.

But yet these cows are making milk and doing well, right?

But here's the sick ones.

What's different?

Look at the albumins.

Is this suggesting that we're mobilizing more protein tissue?

We have similarly low, right, that even high producing cows are glucose challenge, because they got so much glucose going out through that mammary gland, but they're able to counter that through better feed intake, better liver function, and lower fat mobilization.

Look at this, more than double the fat mobilization here.

So I really think that there's other issues that are underscoring, and for us to just blanket identify ketotic cows as being those cows that have very high BHBs is wrong, and we could be interfering and causing problems in those cows that are going along, cranking along and doing fine.

And so that's the thing, it becomes much more challenging for us to do just based on this simplistic approach of measuring one parameter.

So with that kind of start, and Michal, I'll ask if the question was adequately responded to the person who asked that or if we need to clarify that some more.

- Well, we have another question here.

- [Robert] Okay.

- Is subclinical ketosis likely to be from approximately day eight to day 14 post-calving, and will often correct itself quickly?

- There is the potential of self-correction.

We're working on some data right now, looking at different ketones in milk, and looking at how we characterize or classify animals according to ketone levels at first test day and second test day.

And we do see animals that are high on first test day, and then we'll correct themselves and go off and do fine on second test day.

So the work that's come out of Cornell, just (indistinct) and others have highlighted that if they spike BHBs in that first week or so, those are more problematic.

Some of the work that I'm doing now, a couple papers we've published with my colleague in Poland is, actually, when BHB elevates a little bit later, we're seeing more negative problems on reproduction and so on.

And acetone as we can measure in milk, seems to be a player earlier and in younger animals.

So, there's a lot more to this story that's starting to come out.

All right, so let's move into the nutritional factors of ketosis, what things could potentially cause ketosis in a herd.

So went back in the literature and looked at all the studies that tried to make some looking at risk factors.

You know, I showed you the risk factors, the odds ratio measuring BHB.

What we see is increasing parody.

So older cows generally are more prone to ketosis, and it's probably because older cows produce more milk.

The biggest factor is body condition score, higher body condition score, the presence of greater adipose reserve coupled with reduced dry matter intake.

This is the worst case scenario.

This body condition score five cow, this is from Dr. Morrow's original paper on fat cow syndrome, but that's really, these are the quintessential ketotic cows and ultimately they show up with really severe fatty livers, right?

So this is the worst case scenario type thing.

Now, from the literature, they also said season of calving is a risk factor.

Those cows that calve in spring or summer are at greater risk.

Amylin was a perplexing one to me, and I can only think that those cows calving in spring and summer, we know through DHI records that there is seasonal effects on milk production, and those animals that calve in the spring and in the summer generally have higher milk production, over their lactation than those that calve during the winter or in the fall.

So is this another one with milk production issues, dry period length, cows with longer dry periods are at risk, probably because they are at greater risk of getting fat.

And then the previous lactation length, the longer the previous lactation, again, we're probably dealing with the body condition score.

So even though we have these risk factors, they seem to focus on two things, body condition, fat reserve, and milk production.

So let's take a step back and think about this process.

This is a little diagram from Dr. Jesse Goff, trying to, again, put the connection between, we know that postpartum disease, is not kind of a individual simplistic process, but it's really a collection or a syndrome of diseases, and one disease kind of leads to the other.

And that's what these arrows are showing.

And you know, one thing I think we need to really focus on is how important, and this goes back to the 1980s, and some original Cornell work by Dr. Curtis, that hypocalcemia or milk fever was associated with eight different postpartum diseases.

And if you follow the lines that I highlighted in red, most of these lines of these diseases, all come around to decreasing dry matter intake, around the time of calving.

And so, the current interest right now in postpartum is this immune suppression process.

But I think we need to start thinking about the immune suppression, relative to inflammatory condition type situation.

But the bottom line is, if we have decreasing dry matter intake around the time of calving, this is gonna put that girl into a negative energy balance and a negative protein balance.

This results in that increasing NEFA, which is the underlying issue for ketosis as we saw.

And then this leads to our ketosis fatty liver disease.

So similar to the paper that interesting a very, I guess, highly discussed paper from Dr. Baumgard's lab, where they sort of suggested, they were flipping our whole perspective of postpartum disease upside down, where we usually talked about these diseases leading to the problems of BHBs and NEFAs or that.

But now, I think there's another factor that we need to take into account here, and we'll probably go into that in a little more detail in the next lecture webinar.

Let's take a look at this intake in this postpartum period or prepartum period and ketosis specifically.

So this is some work by Goldhawk and colleagues 2009.

This group out of the University of British Columbia, really looked at factors that lead to disease and animal welfare issues.

And they were one of the first to show that dry matter intake is different in cows that go on to have disease.

So the question is, is this drop in dry matter intake?

It's obviously, that's causing the increase in non-esterified fatty acids, and then ultimately leading to the disease.

But what's causing that?

You know, it's not like they're ketotic before calving, causing the drop in dry matter intake, which is what the current thought is that BHBs cause a drop in dry matter intake.

That's not what the research tells us.

And NEFAs drop dry matter intake, that's not necessarily what the data shows.

So it's not those things that are causing the problem, but something else is causing this drop in dry matter intake, initiating these metabolic changes and then the cows can't compensate properly.

So you can see, ketotic cows consume less dry matter intake, than healthy cows one to two weeks before diagnosis.

They also changed their feeding patterns.

They spent less time feeding.

So if we look at these three graphics, the top line in the squares are healthy cows.

The diamonds here are the ketonic cows, and this is average daily dry matter intake.

And you can see it goes from two weeks prior to calving, one week, and then one, two and three weeks post-calving.

You can see there's obvious significant decline here.

And then it continues in the post-calving period.

Number of visits to the feeder, much lower, all right?

Especially, during the early prepartum period, time spent at the feeder, much lower.

So something is impacting intake that's causing the normal metabolic response, but somehow this leads to the ketotic state.

Now, we did the same thing.

These are retrospective data that I collected from two feeding trials, two controlled feeding trials at Penn State University.

We went back into those two studies.

We had intake data, we had milk production data, we had body condition data, we had blood parameters, and so on.

But you can see we found essentially the same thing that the Goldhawk study had, is cows that went on to have ketosis, they had similar dry matter intakes, but then dropped more dramatically prior to calving, just prior to calving the last two weeks.

And then you can see in the postpartum period, those cows that we defined based on BHB as having clinical ketosis, had much lower dry matter intakes compared to healthy cows, and healthy cows were cows that had absolutely no problems at all.

And you can see what I did is, I highlighted the difference in these in terms of dry matter intake.

This yellow shaded area is equivalent to a loss of 228 kilograms or over 500 pounds, or excuse me, 118 pounds.

I'm going the reverse.

118 pounds, a dry matter that ketotic cows did not eat in the first five weeks postpartum compared to healthy cows.

If we account for the energy loss there, and make up for that by just mobilizing body fat, they would've lost nearly one full body condition score in that five weeks.

Or if we lose it all as milk, they lost 470 kilograms of milk, or you know, well over 800 pounds or 1,000 pounds of milk, 4% milk in that five weeks.

So again, the question is what's causing that prepartum intake drop?

Well, one of the factors, of course, is the composition of the diet.

And one of the most important controllers of feed intake in a ruminant animal is the neutral fiber content of the diet.

And so this graphic on the left here is from the most recent NRC, which is now called NASEM, dairy cattle requirements, and they modeled intake potential.

This is looking at dry matter intake as a percent of body weight for dry cows.

So starting eight weeks, all the way down to the week just prior to calving.

And you can see the different colored lines, represent different NDF content of the diet.

So 30% NDF 40, 45 50, this is not the NDF of the forage, this is the NDF of the total diet, okay?

That's an important thing because as soon as I show this, people start getting all excited, well, we're told to feed starch, not straw.

And straw has like 70% NDF, so I we shouldn't be feeding straw.

No, that's not the case.

We use straw to manipulate the NDF content, all right?

This is the equation out of the large dataset that the committee generated.

And basically, you can see they pretty much think that there's a consistent intake over the majority of this, but just prior to calving, there's this drop, and we can see that drop increases with increasing neutral fiber content.

Now, this black line with the markers in here, this is from the 2001 NRC recommendations, and you can see what's happened is, previously, we expected a more earlier drop in dry matter intake, but you can see how much higher if we're feeding higher NDF rations, we're grossly underestimating the feed intake in these animals.

Now, so that's one important thing, that the NDF content, we'll get into some specifics there.

Another thing that's important, is the body condition score, right?

We've highlighted how important body condition score is as a risk factor to ketosis.

Animals that are heavy body condition score, so we're talking body condition score 3.75 and greater.

They will, as you can see in the curve of this line, they're gonna decrease.

This is over this period right here.

They're gonna decrease their intake much more rapidly.

In other words, they're gonna go into negative energy balance, they're gonna have higher NEFAs and more, okay?

So fiber intake, dry matter intake with body condition.

The other thing that has really been investigated to great detail is the energy density of the dry cow diet.

The work out of Jim Drake Lee's Lab, University of Illinois, Heather Dann did probably one of the earlier studies here where they fed different levels of energy relative to the NRC requirement and looked at the performance of the animals.

And ultimately, what they found was cows that were overfed in the far off period, had lower dry matter intake postpartum and greater negative energy balance.

And they had higher non-esterified fatty acids and beta-hydroxybutyrate in the first 10 days postpartum.

And this is in the blood.

But when they fed the high level in the close-up diet, that wasn't a problem, all right?

And this is another study, a more recent study where again, they fed a controlled energy diet throughout the dry period.

This is that Goldilocks higher fiber diet, a high energy diet throughout the entire dry period.

And then they fed a controlled energy in the far off by a high energy in the close-up.

And so what they found was the high energy in the entire dry period gained more body condition, lost more body condition postpartum, controlled energy during the entire dry period, lower postpartum NEFAs, beta-hydroxybutyrate, and liver fat compared to the high energy.

So this is looking at total lipid in the liver and total triglyceride in the liver.

And this line with the circles as the markers is our high energy throughout the dry period, the squares are high, are controlled energy throughout.

And then the dash line is controlled energy followed by high energy.

And basically, the metabolic health of the cows fed the two-group system was very similar to the controlled energy compared to the high energy diet.

So again, reinforcing that it's that far off dry cow, really is the important one from an energy density standpoint.

And there have been many other studies.

Here's just the summary.

Overfeeding prepartum energy compared to restricted intake.

We get increased postpartum, non-esterified fatty acids, increased postpartum BHBs, and there is some interest in, you know, maybe this excess energy in the dry period, inducing insulin resistance.

We know that insulin drops pretty dramatically, during the late pregnancy period, but then it sort of comes up, but maybe it's just slow to come up that is responsible for some of the metabolic arrangements.

Now, it isn't just energy.

I see a question here, Michal.

- Yes, there is a question, actually two of them.

UK evidence that low body condition score cows have as many problems as the moderate, if I read it correctly, moderate high body condition score counts.

What happens to bloods in cows calving in lower body condition score and how does this affect health issues?

- Yeah, so lower body condition, generally, you're not gonna have near as much fat to be able to mobilize.

Now, lower body condition is gotta be addressed relative to the other side of the coin, which is what I'm about to touch on is protein.

We know that amino acids are very preferentially used to supply glucose through a process called gluconeogenesis.

We also know the starch content of the diet, you know, maintaining some level of starch to produce property in glucose.

So I think, it all revolves around, are they able to maintain that glucose and have the resources especially in the lack of maybe fat mobilization.

That is really more of the issue there.

And we also know from some European and some English work (indistinct)

and this is where we're starting to look at maybe having much thinner body condition score, animals storing the dry period, you know, instead of having the 3.5, 3.25, they're starting to talk about three and 2.75.

And one of the reasons there is, those animals have been definitely shown to have much greater dry matter intake in the postpartum period.

So, there's some combination of effect there.

- It's one thing, it's not a question, it's more a comment or experience that the gentleman says, "I found the high energy closeup made it more difficult to suppress hypocalcemia in older cows." - Okay.

So Michal, say that one more time, quick.

- I found- - High energy diet in the close-up- - In the close-up, made it more difficult to suppress hypocalcemia in older.

- Yeah.

Yeah, I don't have hard data on anything like that, but that's an interesting observation, and again, we need to go back and look at what the high energy level is, and maybe what the change in starch level is, between the close-up and the fresh cow diet, and obviously, also the fiber content.

Our fresh cows, we know from Mike Allen's work of what's called the hepatic oxidation theory.

If we have higher starch in those immediate postpartum fresh cow diets, that can suppress dry matter intake.

And obviously, if you suppress dry matter intake, you're also gonna have potential problems with hypocalcemia, excuse me.

All right, I think time-wise, Michal, we're gonna move on and we'll catch up and deal with some of these at the end, I hope.

The next important thing is here that the role that protein may play.

Now, you know, this is a fairly debatable area.

There's been an awful lot of studies that have really not shown any real positive effect on prepartum protein, but a lot of those studies have looked at endpoints of milk production or milk composition, and not really looked at metabolic parameters.

And so this was an interesting study out of the Netherlands.

They used a marker in blood called 3-methylhistidine.

And this is a byproduct of skeletal muscle breakdown, and is not further metabolized.

And so its concentration in blood is a reflection of protein mobilization.

And what they found is, these were cows that were on a high protein, high quality pasture-based feeding system.

And irrespective of that, they still started the measurements in blood of the 3-methylhistidine.

They still started to show evidence of mobilizing body protein.

They even showed mobilization protein, before non-esterified fatty acids started to increase.

So obviously, there's a draw.

The only reason they'd be mobilizing protein is either to synthesize immunoglobulins to go into colostrum or to generate more glucose to support the fetus.

And what they found in this study is cows that were unable to mobilize protein, had higher beta-hydroxybutyrate concentrations.

So this fits in with some work by Chuck Curtis done back in the '60s where they showed, feeding higher protein prepartum, actually had a positive effect in reducing ketosis.

And so the question here is, if they can't mobilize protein, are they becoming glucose-deficient because the amino acids, aren't being used for gluconeogenesis?

The other thing they noticed in this study, there was a few animals that had severe hyperketonemia, and they found that to be associated with severe protein and fat mobilization, so the combination factors.

But it's interesting that there's a very quick reduction in the skeletal muscle mobilization here, which is consistent with some of the work out of Cornell by Alan Bell and Buzz Burhans back in the '90s.

All right, I wanna put my spin on this.

This is the work that I had done at Cornell during my graduate work.

My premise of my study was that we were at the time, and this was in the late '80s, at the time underfeeding protein to our pregnant cows or underestimating the protein needs of the pregnant cows.

So I fed two controlled diets, which is represented by the blue line here.

This was a diet that was formulated to the current NRC standards that's being current in 1989, although I was running on a calculation about 1,100 grams of metabolizable protein, and then I fed a high protein or a high bypass protein diet.

This was on calculation about 1,350 grams of metabolizable protein using the Cornell model.

And that's the dark line.

So you can see, first of all, BHB, which is what I'm monitoring here, again, defining ketosis, stayed very low throughout the entire dry period except for this red line, which is a cow that had twins.

And that's a no-brainer for all of us.

You can see how high herb BHBs went, right?

So, you know, a typical twin (indistinct) type cow, but you notice that the blue line here spikes in this first two to four weeks post-calving, whereas the black line here kind of remains on the lower side, you know, maybe in that, what I'll call subclinical ketosis range.

But these cows were milking well and didn't have much problems.

Then what else I wanna point out is this one cow, 4165, she actually had twins.

She's not included in this blue one here.

This is the dash line.

She had twins, but she was fed the high bypass protein diet.

Notice that her BHBs did not reflect what we typically saw in the twins.

So again, no real direct impact here, but certainly, metabolizable protein might be something we do need to consider a little bit more.

And where that's important is we need to think that when we feed a group of cows, and this is data from my thesis work, this was all mature Holstein cows, daily intakes measured over the last three weeks of the dry period.

And you can see, these cows were consuming 13 and a half kilograms, you know, 28, almost 30 pounds of dry matter.

But you can see the standard deviation was 3.1 kilograms or over six, almost seven pounds of dry matter.

So if we formulate our MP to this average intake of 13, those cows that eat one standard deviation less, that would be 10.4 kilograms.

That's with the statistics of a normal curve, as we can see, that's 34% of that pen were eating less intake, and then another 14% at two standard deviations.

This is gonna result in a fairly significant proportion of the cows in that pen not getting enough protein.

And so does this start to explain some of the variation in responses we see on farms relative to how we manage the cows in these groups, and our feeding practices.

So some recommendations relative to protein content and the dry cow diets.

This is what the current NRC is sort of recommending.

And then based on some work that Pat French and others have done, you know, trying to boost that to account for the variation in intake so that a greater proportion of the cows in that group eat the minimum amount of metabolizable protein.

All right, we can't forget about hypocalcemia as a key player.

In many of our transition cow diseases, we know calcium controls muscle contractility, this is why it's associated with mastitis.

It's also gonna reduce GI motility.

This is gonna cause dry matter loss, maybe displaced abomasum.

The reduced feed intake in the early postpartum period, due to the hypocalcemia, this is gonna increase negative energy balance and then push us closer to the ketosis/fatty liver problem.

We may have less gut fill, which then brings us back to the abomasal displacement.

And then we also know now that calcium plays an important role in immune function and neutrophil function.

And this also may contribute to infectious issues such as mastitis, metritis, and retained fetal membranes in that postpartum period.

We're gonna talk about hypocalcemia control in another webinar in a couple weeks here.

So I'm just gonna quickly show some recommendations.

There's basically two primary approaches that we can think about.

If you don't wanna use anion salts, have that expense, then you gotta pay attention to how low that dietary anion difference is in your diet.

You wanna keep that potassium low, moderate sodium, moderate sulfur, push that chloride as best you can with what you have.

You know, right now, all the recent research has suggest that we don't have to feed high calcium in these diets.

And then the more current research coming outta Germany, suggests maybe we ought to be feeding lower phosphorus diets and then boost that magnesium to counter any of the potassium.

If you do wanna go with the anionic salts, again, there's a range that we can set this DCAD to.

We don't necessarily have to go as negative as we originally thought from the work that came out in the 1980s and 1990s.

Again, we could be a little more flexible with the potassium.

We still wanna maintain some sodium intake.

And then here's where we're gonna bump the sulfur and the chloride with the anionic products, predominantly, the chloride.

We don't have to go very high with our calcium, but you know, in contrast, we wanna keep it low on the other side.

Again, we may wanna think about lower phosphorus and then get that magnesium up.

And then basically some recent work by just Jesse Golf and others suggested we gotta get that urine pH below 7.5 to have any expectations of a response here.

If we can't get that down there, you're not gonna control your hypocalcemia.

All right, a little bit on nutritional supplements.

What products have potential to minimize ketosis?

So this graphic here shows the percentage of use of various compounds based on whether they're used in the close-up dry, the fresh diet or the high peak milk production.

Of course, anion salts would be in the close-up.

Choline, rumen-protected choline, I think, is gonna become a bigger player here.

Choline can help us relative to liver function and fat export.

Obviously, rumensin has been a big player, use of yeast to maintain dry matter intake, animal proteins to supply some of the more important amino acids like methionine, lysine, histidine, or moving to rumen-protected amino acids.

And then in the rumen-protected fat to try and minimize the negative effects on fiber fermentation intake, but also provide energy for that postpartum cow.

So niacin was a compound that was used and studied in the late '70s and early '80s, and it was shown to decrease non-esterified fatty acids and beta-hydroxybutyrate in ketotic cows, right?

So this started in that, you know, maybe niacin as its player in some of the metabolic reactions with lipolysis and adipose tissue mobilization, would be important.

But then later work showed that when they fed niacin not to ketotic cows, they really didn't get the effect that they saw on ketotic cows with non-esterified fatty acids, milk yield and so on.

Pat French gave very large doses of niacin and saw this decrease in non-esterified fatty acid.

But the problem is, with these B vitamins like niacin, we gotta feed them as a rumen-protected compound because otherwise, the rumen bugs, are gonna just destroy them.

So the current recommendation is, based on this theoretical mode of action in preventing adipose tissue mobilization, the recommendation is about 12 grams to over condition or high risk curve.

So this isn't a blanket recommendation, but this would be, if you got yourself in a situation where because of maybe some reproduction problems or others, cows got a little heavy, this would be one opportunity.

The other option is choline.

There's been tremendous amount of work.

Dr. Jose Santos then at the University of Florida as well as many others, have really provided lots of great information on the use of rumen-protected choline.

Again, choline is a compound that will be metabolized and destroyed in the room.

And this was shown back in the '60s and '70s.

The challenge that we have, most of us expected the NRC committee to provide a recommendation of choline feeding in the newest NRC, the NASEM 2021.

However, the committee basically said, "There just wasn't enough data to establish a recommendation because there's so many interactions with choline with other compounds, betaine, methionine, folate, which is one of the B vitamins, and then vitamin B12." And so it made it very challenging.

We do know if we feed choline-free diets, especially, to like pigs and horses and so on, we can develop fatty liver disease.

So there is some a number of publications that have shown feeding rumen-protected choline, greatly reduces the fat content of the liver in the postpartum period, all right?

But again, the response, was dependent upon the methionine content in the diet as a proportion of the metabolizable protein.

In a recent meta-analysis out of Jose Santos' lab, they looked at no choline versus choline supplementation, all the studies that fed 12.9 grams or greater.

And what they found is, there was significant responses to energy corrected milk yield, milk fat yield, milk protein yield, and energy corrected milk efficiency.

In these studies that were evaluated, choline was fed on an average 22 days prepartum.

So the last three weeks prepartum and 57, almost two months into the postpartum period.

But what they found was the effect on blood metabolites was inconsistent.

They sometimes saw decreases in NEFA and or BHB, so that wasn't borne out, even though many studies suggest that that occurs, that wasn't born out in this meta-analysis.

Okay, so how do we start to put this together in looking at nutritional factors to address preventing ketosis?

So I'll start out with transition formulation guidelines.

One, we need to ensure all transition cows, have a sufficient opportunity to consume a properly balanced diet, all right?

We need to provide a consistent, properly balanced diet that addresses the issues of intake and variability amongst individuals in the group.

We wanna minimize the excess energy intake, especially, in the far off dry period, ensure adequate or better metabolizable protein intake, and ensure good calcium homeostasis.

We need to formulate our dietary nutrient density for the observed dry matter intake and compensate for that variation.

We just assume that the standard, it used to be 1,300 pound, 1,350 now.

We've gotten more realistic, 1,600 pound dry cow, and we had a defined amount of intake.

But as we're gonna talk about on Tuesday next week, there's a lot of management factors that go into to this.

And based on the intake, we wanna increase that MP content at the average intake to make sure that a greater percentage of those cows in that pen eat the minimum amount of metabolizable protein to meet their needs.

All right, some formulation guidelines we wanna formulate for dietary carbohydrates to meet but not exceed the energy needs of the animals.

We need to keep it under 120% of the requirement.

The requirement didn't change very much in the new NRC, and we need to focus predominantly on the far off diet.

Now, how do we do that?

NDF controls intake.

Now, we have this guideline of 1.2% of body weight as NDF intake, but that's only for adapted cows.

Cows that are in lactation.

We see, based on the data that there's a lower NDF intake for pregnant animals, it's very similar.

We see this very much in sheep and goats.

What I've seen in my studies, and what I've calculated from published studies, NDF intake as a percent of body weight in our pre-fresh group runs, somewhere it's around 0.6 for your heifers, up to possibly 0.9 depending on the quality of the NDF.

For your far off cows, you're running about 0.8 to 0.95.

And again, heifers are gonna be on the lower side.

This is why we can't formulate diets very well for both heifers and mature cows.

The other thing, based on some work out of Cornell and out of the minor institute, is we really wanna be cautious about increasing that starch level from the pre-fresh diet to the fresh diets.

Tom Overton at Cornell usually recommends, at least based on some of their work, you know, don't jump above 8%.

So if you're at 15% starch in your pre-fresh diet, you're doing a controlled energy type diet, you shouldn't be going above 23% or so in that immediate fresh cow diet.

Now, it certainly can move up after that.

Use dietary strategy to minimize disturbances in the calcium homeostasis.

Predominantly, this could be done through ionic salts or through very attentive approach to the macro-mineral content in the diet.

So lower phosphorus, lower to moderate sodium, lower potassium, higher magnesium, higher chloride levels, and then utilize these nutritional supplements where the potential return can be expected.

Again, niacin, choline, with higher body condition score animals, certainly, rumensin is a great opportunity.

There's a lot more data on that.

So, to kind of finish up, and we'll get to our questions.

I see you got a couple already.

Some of the control points in managing nutrition in this prepartum or in this transition period, we wanna minimize that drop in prepartum intake.

I mean, the older data in the early 1990s, suggest we wanna maximize dry matter intake.

If we can maintain maximum dry matter intake, that's okay, but the data certainly suggests that we do see this natural drop and what we wanna do is try and minimize that drop.

And so NDF content of the diet sufficient bunk space, which we'll talk about next time, and other factors that go into that.

Adequate dietary supply of ME and MP, the metabolized energy and metabolized protein, controlled energy, especially, that far off period, increased MP based on observed intakes, minimize the risk of hypocalcemia, all right?

DCAD or other, you know, if you're using the zeolite or something like that, maintain the immune response and reduce the inflammatory response.

So this is where some of the trace minerals, the antioxidants and vitamins can come in.

Common problems I see in transition diets, overfeeding energy in that far off group, overdoing the controlled energy.

It's either too bulky or too low in energy.

We can go too far in the other direction.

Anytime we allow cows to make decisions on the farm in terms of sorting, so evaluate chop length of your bulky forages, the moisture content of the diet.

Diets that inadequate and metabolizable protein pre-calving or don't supply enough room and degradable protein to facilitate fiber digestibility.

This is the big one, not identifying mineral changes in forages or other feeds, and disrupting calcium homeostasis.

And then of course, our topic for the next time, the non-nutritional factors, can break great diets really easily.

So no matter how well you do your diet, you know, if you don't do the environment right, you're gonna have problems.

So bottom line here, ketosis can be managed through proper dietary formulation to address appropriate energy, protein, calcium and prepartum diets.

Notice I didn't say postpartum diets, and in management factors, addressing issues of intake and body condition during that transition period.

So with that, Michal, let's go ahead and start with the questions.

- Okay, first question.

Would it be recommended to feed rumensin to dry cow rations even as they tend to be low concentrate rations?

- Yes, yes.

We have data actually, beef cows, where on just a forage-based diet to pregnant beef cows feeding rumensin in a trace mineral salt product, which is not what I would recommend for dairy cows, but we did see improved performance and better calving situation and milk production in those girls recognized through better calf growth.

So I think, prepartum rumensin does have a place here.

- Another question is, I have observed farms limit feeding far off dry cows, leaving bunks empty for up to eight hours per day.

Is this supported by current research?

- No, that is not supported by research, nor is it supported by my observations and problem solving in many cases.

Yes, we do need to maintain a good nutrient intake.

If you got bunks that are empty that long, you better darn well make sure that every cow had the opportunity to get up and eat at the same time, and eat as much as they wanted.

And in most cases, that just is not the case.

And you know, the other thing is, is all the modeling, all the sophisticated modeling and predictions and you know, the AMTS and the NDS and the Cornell model, they all are based on an animal that is in a steady state.

And if you have an animal not eating for over eight hours, that is not a steady state condition.

And so that throws all the predictions out the window.

So my recommendation generally has been that bunk, especially, in these transition cows, should not be empty much more than about two hours, three at the absolute most.

And that's only if we have good bunk space and good water availability and all of those other factors.

- And we have one raised hands, and I will- - [Robert] Yep.

- Ask this lady to go ahead and ask her question.

You have to unmute, and you can ask her question.

- I think you have to unmute her, Mike.

Or can she type in the Q&A?

- Go ahead.

Go ahead, ask your question.

- We're not getting- - Don't think we get it through.

- [Female] Hello, hello. - [Robert] Oh, there we go.

- It looks like we have some troubles- - [Robert] Yeah. - On the other side.

- I see there's another question here by Dr. Draymond.

Comment on the Penn State particle profile for both dry cow diets and especially, with straw.

So we've- (indistinct)

- I'm gonna mute this attendee for a while. - Okay.

So back to the Penn State Particle Separator, I think, some recent work out of Cornell, again, looking at colostrum quality is suggested a little bit more on the upper screen than what we generally recommend.

But with these high straw diets, Jim Drake Lee and others, have really recommended we gotta get that particle size down.

I try to look at a higher level than what we recommend, obviously, for fresh cows or peak milk cows on that top screen.

So I'm generally running in the 25% on that top screen sometimes, and then trying to get a lot in that second screen to look at this.

And we might go a little bit, try and take a little bit more off that top screen into the second screen in those close-ups.

However, I'm really intrigued by the recent work, again, outta minor and out of Cornell, looking at high starch versus low fiber or high fiber, you know, so they had high and low starch, high and low fiber diets, and they were fed immediately postpartum.

And the two studies, or the two groups had kind of different outcomes.

But the bottom line was, we can tolerate the starch more if we get that fiber, we get that digestible fiber into those girls.

And so the high starch, high fiber diet was actually outperforming the other diets.

And the worst diets were the high starch, low fiber diet, which we all would expect.

And then the low starch, high fiber, and then low, and I think it was high and high, they were intermediate there.

So if we go back to Mike Allen's work with the hepatic oxidation theory, these immediate fresh cows are not controlled in intake as much by the fiber.

So I'm not too worried about getting more fiber in there.

It's the propionate availability and the glucose production net controls that intake more.

And that's really gonna be a key player in this immediate postpartum diet that heads us down the path of either ketosis or good milk production.

- We have another question here, but I think that's a quite as the participant says, yeah, it's a quite a broad question for our timeframe here.

So I would actually even skip it, and I would conclude today's webinar.

Thank you, Dr. Van Saun.

It was very good information presented, and I'm looking forward to next week for webinar number two about preventing ketosis in dairy cow.

- All right, Michal, thanks a lot.

- [Michal] Thank you, bye.