Breaking free from the chains of the past Where
truth moves faster than a Holstein calf No law
waiting on some printed page We're charting new
ground in the digital age From genomic codes
to robot facts We cut through the noise, no hold
them back not your daddy's dairy news tonight
we're sparking Welcome back to the Bullvine Podcast,
where we cut through dairy industry noise to
get you the insights that actually matter for
your operation. And today we're diving deep into
a feature piece that's got some serious buzz.
This deep dive focuses on the December 2025 Journal
of Dairy Science. Yeah. And the stack of findings
here, I mean, from calves all the way to culls,
it has layers that will make every farmer rethink
their approach. It really will. We're talking
about these long -held standard protocols. The
ones we just inherited. Exactly. The ones we
just do because that's how it's done. And now
it's being proven that they are, well, significantly
underperforming. And the central theme, when
you look at all this research together, it's
just brutal honesty. It is. It's saying that
if you're sticking to the way you've done things
for the last decade, just because, you know,
that's the standard. You're leaving money on
the table. Quantifiable money. Or, and I think
this is even worse. you might be actively inflicting
some minor harm on your animals without even
realizing it. We're talking about everything.
The maximum volume of colostrum we push into
a calf. The subtle signs of lameness we are missing
for weeks. And even the beef sire choices we're
making right now. Yeah. And look, this is mandatory
listening because the stakes here, they aren't
academic. This is dollars and cents. Quantified
by the best research in the world. We're quoting
specific massive financial gaps. Just think about
lameness for a second. Okay. That 23 -day delay
in detection, the difference between a modern
AI system catching it and, you know, you or your
standard activity caller finally flagging it.
That's a huge one. It's the difference between
a $50 early intervention when you can still fix
the root cause and a $400 plus treatment after
the cows got a severe structurally damaging lesion.
That completely changes the whole conversation
around investing and monitoring tech, doesn't
it? It has to. I mean, if you buy a system and
it only makes you, say, 10 % faster at spotting
a lame cow, the ROI is in still weeks. Right.
But if technology buys you 23 days of preventative
time before there's even a lesion. Yeah. The
investment justifies itself almost immediately.
You prevent just a handful of those chronic cases
and it's paid for. It's a totally different business
decision for you to make. Absolutely. And it's
not just. the big numbers on the cow side. On
the calf side, we've been operating under this
assumption that, you know, more is better with
colostrum volume. We all have. And it was driven
by a necessary push to guarantee minimum IgG
absorption. We get that. But the new data proves
that beyond a certain point, we're just sacrificing
calf comfort. We are sacrificing absorption efficiency.
We are literally causing colic. Yeah. Causing
distress for a negligible, almost meaningless
gain in antibody transfer. Exactly. So we're
going to be myth busting today. And that colostrum
rule is target number one. Yeah. We'll show you
why the idea that more colostrum is better is
just flat out wrong past about 8 % of a calf's
body weight. And we'll get into the most exciting
part for me, for the financially minded farmer.
Okay. How the data you are already collecting
on your DHI reports, specifically the de novo
fatty acids, is a completely free, immediate
resource. Something you can use right now. Right
now! For managing methane production and improving
room and health. Free environmental selection
plus immediate health insight. You really can't
beat that. You can't. So let's unpack this monumental
stack of research. And let's start where every
successful operation starts. With the calves.
Okay, let's do it. First meal of life. The core
issue, and this is validated by the University
of Guelph research, is that we've been overfeeding
colostrum volume. especially in that first critical
meal to the point where we are causing, well.
verifiable physical pain and discomfort. And
for context, we have to acknowledge the history
here. I mean, this goes against two decades of
industry training. It does. The traditional rule
became volume, volume, volume. And for a good
reason. You know, Dr. Godin's foundational work
in the early 2000s was crucial. Absolutely essential.
It moved the entire industry away from tragically
underfeeding colostrum, which was causing massive
failure of passive transfer. FPT was a huge problem.
A huge problem. So that guidance suggesting we
feed 10 % of body weight was a necessary life
-saving advance to make sure we hit those minimum
IgG levels. It was. It was essential for correcting
FPT, but science is always refining the boundaries,
right? And it seems like we've gone too far on
the volume side. We have. The Gulf study, Frederick
and his colleagues, they specifically refined
that upper boundary. They looked at IgG absorption
efficiency across four different volumes. Okay,
what were they? 6%, 8%, 10%, and 12 % of birth
weight. Right. The whole goal was to find that
saturation point. Where the benefit stops. And
the physiological cost begins. And what we found
is that efficiency peaks and then it just plateaus.
really fast. You look at that 8 % mark and the
absorption rate is excellent. It's fantastic.
Cabs fed 8 % of body weight reached a 24 -hour
serum IgG concentration of 37 .4 grams per liter.
That is far, far above the minimum threshold.
Okay, so that's great. That's success. But here's
the brutal ROI calculation. When they push the
volume up by 50 % to 12 % of body weight, the
serum concentration only hit 43 .4 grams per
liter. So wait, you're making the calf drink
50 % more? 50 % more fluid volume. For a tiny
gain of just 6 grams per liter of IgG. It's the
law of diminishing returns hitting a brick wall.
And that minimal gain in IgG, it comes at a cost
you can actually see. A cost in discomfort. And
this is the data point that should make every
farmer listening just stop what they're doing.
This is the one. We're talking about actual recorded
physical distress documented by researchers.
40 colic -like kicking episodes. 40. It's a huge
number. 40 recorded total episodes of abdominal
kicking, arching, visible GI discomfort among
the calves fed at 12%. And the 10 % group, which
is still the standard for many farms. They restored
21 kicks. Still way too many. And the groups
fed the new. Evidence -based maximum, the 6 %
and 8 % volumes. Zero. Zero kicks. Zero observable
distress after feeding. So if you're tube feeding
a calf and it stands up and starts kicking at
its belly or it's just really restless, this
study is telling you it's not the colostrum quality.
It's not. It's the sheer volume overwhelming
its system. We are causing pain because we are
fixated on a volume that the calf just doesn't
need. Let's talk about the mechanics for just
a second because it's important. We have to remember
penocytosis. That's the process where the gut
absorbs those huge IgG molecules. Right. It's
finite. It happens fast in the first few hours.
And then the gut capacity for absorption just
gets saturated. So when you push all that extra
fluid in. And extra antibodies just pass through.
They're wasted. But the massive liquid volume
stretches the abomasum. It stretches the gut.
And that's what causes the pain. So for a standard,
let's say, a 40 -kilogram Holstein calf, a pretty
typical size, 8 % of body weight works out to
3 .2 liters maximum for that first feeding. That's
the number. And if you push that to 4 liters,
which is 10%, you're pretty much guaranteeing
distress for very, very little immunological
return. Now, I can hear a lot of farmers saying,
wait a minute. I spend time mixing that high
quality colostrum and I want to maximize my total
IgG delivery. I need that extra volume. That's
a valid concern, and this is where we have to
talk about the operational reality. We're not
saying you should reduce the total amount of
IgG you deliver. No, absolutely not. We're saying
you have to respect the gut's immediate capacity.
The fix is just split feeding. Exactly. If you've
got a total of, say, 5 liters, you want to get
into that calf to ensure adequate IgG, you cap
the first feeding at 3 .2 liters. At that 8 %
body weight mark. Right. Then you wait 6 to 12
hours, and you give the remainder in the second
feeding. You respect the biology. You let the
calf system process that first load and reset.
And you still get the full benefit of all that
IgG. Without the 40 kicking episodes. But wait,
let's inject a dose of reality here. Splitting
the feed means I'm doubling my labor time. And
this is during the busiest window of the day.
Is reducing a little colic really worth that
increased labor and time? That is the critical
question. And I think the answer is yes. Because
colic and distress. They have hidden costs. It's
not just the immediate discomfort. A colicky
calf is a stressed calf. A stressed calf has
higher cortisol levels. And that can depress
feed intake in the next 24 hours. It can slow
down when they start on starter grain. And ultimately
delay your growth targets. Right. We're talking
about sacrificing days to weaning for a minimal
IgG gain that you could have gotten in the second
feeding anyway. Plus, you reduce stress. You
reduce the chances you need a vet call for a
distressed calf. calf. Which is easily $150 right
there. Minimum. So we're trading, what, 15 minutes
of labor for better feed efficiency, faster growth,
and zero vet calls for simple gut distress. When
you put it that way, yeah, the return on that
labor investment is pretty clear. And before
we move on, we have to just hammer this point
home. Quality still trumps volume. Always. Right.
This whole conversation assumes high -quality
colostrum. Exactly. If you don't have a Bricks
refractometer, you are... Frankly, gambling with
your CAF program. Those tools cost, what, maybe
$150 to $300? Cheap insurance. They pay for themselves
immediately. If one batch of colostrum that you
thought was great only tested 18 bricks instead
of 22, and you catch that mistake? Yeah. You
just prevented a $400 FPT case. It's a no -brainer.
And you mentioned the Wisconsin Extension data.
That colostrum production tends to slump in the
fall months. Yeah, it's a real phenomenon. So
if you're banking colostrum, that refractometer
is absolutely essential for deciding which dam's
colostrum is good enough to freeze and use later.
The long -term strategy here is using that Brix
meter to identify and bank those high -quality
batches. So you're never scrambling, no matter
what time of year it is. So the bottom line on
calves is stop equating your effort with results.
Pouring more in doesn't mean the calf absorbs
more. It just means the calf is uncomfortable.
The new evidence -based cap is 8 % of body weight
for that first meal. Respect the biology. Right.
Speaking of foundations, if we shift from the
calf's gut health to the cow's mobility, we find
a structural problem that's just as serious.
The very foundation she walks on. Exactly. And
this lameness data. This is where that $400 problem
really starts. The industry reality check here
is that we are consistently, consistently missing
the optimal intervention window. We're missing
it by weeks. We often wait until the damage is
already structural. It's already permanent. And
look, it's not about farmer negligence. It's
about human capability versus technology. I agree.
The average busy farmer, you're trying to spot
subtle changes during a crowded feed alley walk.
You're only going to identify about a third of
the lameness cases that a trained researcher
would catch. A researcher who's using slow standardized
scoring protocols. It's just a fundamental difficulty
of catching subtle changes in a really dynamic
environment. And that failure to catch it early.
That's what turns a minor stone bruise or mild
sole hemorrhage into a devastating chronic repeat
offender case. And the new research explains
exactly why that happens. It drills right down
to the cellular level. OK, let's unpack that,
because understanding this is critical for understanding
why lameness becomes chronic. It is. So Wilson
and colleagues at the University of Nottingham.
They examined the collagen composition in the
digital cushions of cull cows. So that's the
fatty cushion above the hoof horn, the main shock
absorber? That's the one. And the finding was
this. Cows with chronic histories of hoof horn
lesions had significantly lower type I collagen
in their digital cushions. Okay, so type I collagen
is the good stuff, right? That's the resilient
structure, the tensile strength, the elasticity.
It's like the dense foam in a good running shoe.
That is the perfect analogy. Okay. Type I is
the healthy shock -absorbing sponge. When that
cushion gets traumatized over and over again,
the body's repair mechanism replaces that type
I collagen with type III collagen. And type III
is basically just disorganized scar tissue. Exactly.
It's stiff. It lacks resilience. It cannot absorb
shock correctly. It's like swapping the rubber
sole of your work boots for a thin piece of rigid,
brittle plastic. Which means the cow is now walking
on a compromised foundation. The weak cushion
leads to more trauma on every step. Which leads
to more scar tissue. And that cow is now structurally
and permanently predisposed to getting lame again
and again. You're fighting a cellular deficiency
every time she steps on the concrete. This explains
those repeat offenders that drive producers crazy.
You trim them, you block them, you foot bath
them, and three months later, they're back. And
you're spending 400 bucks every single time fighting
a structural deficiency that was set in stone
or in scar tissue because you missed that first
crucial preventative window. And we have to talk
about the financial compounding here. The Robsis
study from 2023 JDS, it put the base direct cost
of lameness at around 307 euros. 330, 340 bucks
US. Right. But that's the conservative number.
That often doesn't even account for the secondary
costs. The lost milk, the cost of treating metritis
that follows a painful calving. Delayed breeding,
increased risk of culling. When you factor all
that in, that cost can easily surge towards $800
or even $1 ,000 for a serious case. So if prevention
costs $50 and a serious case costs $800, the
data is clear. Prevention isn't just better,
it's economically mandatory. So how do we get
there? We need detection that operates at the
level of the cow's compensatory behavior, not
her pain threshold. And that brings us right
back to the AI advantage and that critical 23
-day gap. The AI gait analysis systems, the ones
that use cameras and vision processing, they
are detecting mobility changes three weeks before
activity callers or human observation flag the
issue. Wait, I have to push back here for the
average farmer. My callers cost thousands of
dollars and they're supposed to track lameness.
Why is my activity collar failing to catch this
early window? Because the collar measures the
quantity of movement, step count, resting time.
It's designed to catch the moment the cow is
so sore she stops walking or feeding. Which is
when the lesion is already severe. Exactly. But
AI gait analysis, it measures the quality of
movement, the kinetics, the weight distribution.
The cow changes how she walks long before she
drops her total step count. That's it. So walk
me through what that looks like. What's the AI
catching that I'm not? It's subtle. But visually,
it's that uneven tracking of the hind feet. It's
a slightly shorter stride length on one side
when she makes a turn. Okay. It's the slight
increase in the duration of the head bob when
that sore foot hits the ground, even if her total
head motion hasn't dropped yet. Or, and this
is a big one, it's the increased standing time
before she lies down because she's testing that
painful limb. Right. She's compensating for discomfort.
She hasn't dropped her dry matter intake yet.
That compensation is happening 23 days before
the system that only tracks steps even notices
a drop in quantity. So the AI system is identifying
the cow acting like she's walking on glass, while
the activity caller is waiting until she's just
decided to stand still. That is the fundamental
difference. And that's the difference between
the $50 intervention window and the $400 treatment
window. If you catch it in that compensatory
phase, you can make a minor adjustment, maybe
a quick look at the foot, a change in bedding.
And you prevent the type I collagen from turning
into that type 3 scar tissue. You stop the chronic
cycle before it even starts. This raises an absolutely
vital, skeptical challenge for farmers who are
evaluating technology. Yes. If you... are going
to invest heavily in a monitoring system. You
have to pressure the vendors. They need to prove
they are measuring quality of gait, not just
quantity of activity. You need to ask them that
critical question. What specific behavioral change
does your system detect? And at what stage of
disease progression does that change become measurable?
Right. And if they can't point to kinetics, or
weight distribution or the head bob and they
only talk about a general drop in activity you're
probably buying a system that only detects the
problem a week before your herdsman would caught
it anyway you're not buying the 23 days of prevention
if it only catches the quantity drop it is detecting
pain not preventing structural damage the investment
has to be justified by its ability to break that
type 3 collagen cycle okay let's shift gears
completely From the structure of the foot to
the structure of the breeding program. Let's
talk beef on dairy. Yeah, the conversation is
always, almost always fixated on the dollar premium
you get for that calf. Right. But the new data
confirms that chasing the biggest premium can
absolutely wipe out your profitability. And then
some on the cow side. This is a textbook example
of prioritizing a short -term gain over the long
-term health of your herd. We have seen operations
get financially burned by this. Absolutely. The
study in the December JDS was massive on this,
a genetic analysis of 231 ,000 calving ease records.
Across 1 .2 million lactations. Right. They looked
at Holsteins and Jerseys bred to the Big Three,
Angus, Charolais, and Cemental. They had the
data to see the true trade -off. And the core
finding, this should be non -negotiable for every
single producer out there. Profitability hinges
entirely on the calving ease EPDs. The expected
progeny differences. Exactly. It is not the beef
breed itself that determines success or failure.
It is the specific CE score of the sire you choose.
You can't just generalize. And the evidence for
success is there. Which is encouraging. Research
from Penn State and the University of Kentucky
showed that when you select beef sires with favorable
CE indices. And this is a key distinction. Specifically
for mature dairy cows, not first calf heifers.
Right. When you do that, dystocia rates show
no significant increase compared to just using
dairy semen. So the U .S. sire selection parameters,
when you apply them with diligence, they are
not inherently bad for the cow. Which proves
the program can work. But it works conditionally.
It's a management program first and a genetics
program second. And the warning sign is that
anecdote that became a damaging trend for the
early adopters. I heard one producer put it perfectly.
He said they got greedy on the calf side and
forgot about the cow side. This is exactly what
happened. They chased the high -dollar calves
using powerful, high -growth sires that had just
terrible cavanese EPDs. They were focused on
that $300 calf check premium. And they watched
their heifer dystocia rates climb to 25, even
30 percent. You cannot afford that. Let's just
break down the economics of one difficult calving.
You get a $200 premium for that beef calf. That
profit is gone with the first complication. Instantly.
What are the costs? You've got the direct vet
assistance. That's easily $100 to $250 for a
difficult pull, especially if it's after hours.
Then you have the post -calving trauma. A difficult
calving dramatically increases the risk of a
retained placenta. Which requires more treatment,
adds another $75 to $150. And if that leads to
metritis. You're looking at more treatments,
more labor, and potentially a lifetime hit on
fertility. And the biggest cost is the opportunity
cost. The delayed breeding cycle. Right. A cow
that suffers dystocia takes significantly longer
to resolve her uterus and cycle back. If that
extends her voluntary waiting period by just
10 or 15 days, we're sacrificing hundreds of
pounds of milk in her next lactation. That $200
calf premium suddenly looks tiny compared to
a $600 to $1 ,000 cost of a complicated recovery.
So the operational framework for successful beef
on dairy based on this research is really simple.
One, you must select sires with documented favorable
CEEPDs. No exceptions. You can't just pick a
Charolais because the cows look good. Two, you
limit beef breeding primarily to mature proven
cows and you strictly avoid your high -risk heifers.
And three, you actively religiously monitor your
dystocia rates. If your percentage of assisted
calvings goes up even 2%, you immediately tighten
your CE selection threshold. It has to be a non
-negotiable threshold. I mean, if you look at
specific examples, Angus and Hereford, they generally
have lines that work reliably because their CE
scores are often better managed. But breeds like
Charolais or Belgian Blue, they offer that tempting
premium. But they require extreme diligence on
CE selection. Without that, you're just financially
exposing your herd to a totally unnecessary risk.
Don't let the potential premium distract you
from the cost of the event. The cow is the primary
asset. Her recovery and her next lactation must
always come first. Okay, let's look forward now.
The regulatory and environmental pressures on
dairy. They're not going away, especially on
methane. It's hard to chance. But the good news
from the genetic side is that reducing methane
might be way more tractable than we assumed.
And we can do it without trade -offs or cost.
This is the ultimate free win segment. It really
changes the environmental conversation for dairy
producers. The major finding from SumEx, Lectinet,
and Gulf, and this is from analyzing over 700
,000 milk MIR records, is massive. Methane efficiency
traits show heritability of about 23%. 23 % heritability.
To put that in perspective for you, that is comparable
to key production traits like milk yield and
fat percentage. And it is dramatically higher
than health and fertility traits, which usually
land somewhere between, what, 3 % and 8%. So
this means genetic selection for methane reduction
is highly effective. It's fast. We can move the
needle on this quickly. It's an incredibly powerful
lever. But here's the other piece of just seismic
good news. And this removes the biggest barrier
to environmental selection in a production system.
Which is? The genetic correlation between methane
efficiency and milk yield is, statistically speaking,
zero. Zero. No tradeoff required. You can select
for a more efficient, high -producing cow and
reduce her emissions at the same time. The environmental
choice is no longer an economic penalty. So what
does that mean for a long -term strategy? Cimex
is projecting that a 20 to 30 percent reduction
in herd methane output by 2050 is absolutely
achievable. Through genetics alone, depending
on how intensely the industry selects for it.
And the timeline is fast enough to make a real
difference in your lifetime. Generation one,
that's about two years, gets you a three to four
percent herd reduction. By generation three,
so six to eight years, you're looking at a 10
to 12 percent cumulative reduction. That is significant.
verifiable environmental progress. And it's achieved
just by refining your sire selection criteria.
So here's the practical application. You don't
need to overhaul your program. You keep selecting
for what's profitable. Fat, protein, net merit,
health. Right. You then use methane efficiency
as a tiebreaker. Between two otherwise equivalent
bowls, it costs you nothing to add that criterion.
And you're quietly stripping carbon footprint
with every single generation. It's the ultimate
why not. Exactly. If Bull A and Bull B offer
identical projected profitability and health,
but Bull A is a 5 % more efficient methane reducer,
the choice is obvious. And here's the best part
of all. You are already paying for the data that
feeds these efficiency scores. The methane efficiency
scores are derived from the same DHI test you
run every month. Right. Most operations are already
submitting samples for DHI testing, which generates
that mid -infrared spectral data to measure fat
and protein. And the mechanism here is actually
really elegant. It ties directly back to rumen
function. Okay, so explain the biology simply.
Focus on the hydrogen management in the rumen.
The rumen is a constant hydrogen factory. High
methane cows, they tend to have fermentation
pathways that churn out a lot of acetate. That
acetate production releases hydrogen as a byproduct.
That hydrogen is then quickly captured by methanogens
and converted into methane, which the cow belches
out. And that acetate -rich environment leaves
a distinct signature in the milk. A signature
of milk, rich in de novo fatty acids. Conversely,
the low -methane cows, they're channeling that
hydrogen into a more efficient pathway, producing
more propionate. Which is a source of glucose
for the cow. Right. Productive energy. So when
the cow produces more propionate and less acetate,
the fatty acid profile of the milk changes. So
propionate is the productive pathway. Acetate
leads to waste in the form of methane. Precisely.
So if I see high novo fatty acid readings on
my DHI report, that's not just a fat number.
It's a free, actionable warning sign that this
cow is running a high acetate, potentially high
methane, and slightly less energy efficient rumen.
But hold on. I'm looking at my DHI sheet right
now. It says fat, protein, MUN, SCC. It doesn't
say methane profile or... de novo fatty acids.
How do I actually get this data that I'm supposedly
already paying for? That is the practical hurdle.
The data is being generated by the spectrometer,
but often the DHI processing center doesn't automatically
print the full fatty acid profile on the standard
sheet. So I have to ask for it. You have to call
your DHI processor or your extension specialist
and specifically request the detailed fatty acid
breakdown. It might be under a section called
fatty acid breakdown or MER profiles. Once you
get that sheet, you're looking for the percentage
of de novo fatty acids. So if I start tracking
that de novo percentage, I get two wins for the
price of one. You do. First, I get a free early
warning system for acidosis, which we absolutely
need to monitor in transition cows. Yes. Low
de novo can be a primary signal of a compromised
rumen. And second, I get a baseline for selecting
for lower methane genetics over time. You nailed
it. You get rumen health and methane efficiency
information from one piece of paper you already
paid for. It is sitting there waiting for you
to use it as a powerful diagnostic tool and a
free environmental selection criterion. That's
efficiency you just can't ignore. All right,
let's step back into skeptic mode for a minute.
We've talked about free genetic solutions. Now
let's talk about the expensive additive solutions
hitting the market. The methane reduction product
market is flooding with sales pitches. And as
an operator, you need extreme caution and a set
of really rigorous questions before you spend
a single dime. Absolutely. You have to assume
the rooming adapts. It has been optimizing itself
for millions of years. If someone claims they've
fundamentally changed that fermentation vat with
a plant extract. They need robust, sustained,
and verified proof. So we developed four buyer
beware questions, and I want every farmer listening
to print these out and bring them to your next
sales meeting. These questions force the vendor
to prove biological efficacy, not just marketing
claims. Okay, question one, the basic sanity
check. Show me the DMI data alongside the methane
data. Right. If the results show a drop in methane,
but also a proportional drop in dry matter intake,
you might just be buying an expensive appetite
suppressant. If the cow eats 5 % less feed, methane
drops 5%. That's not a change in efficiency.
That's just a reduced feed bill that leads to
less milk. It's a false economy. You are trading
necessary feed intake for a climate claim. Question
two separates true mitigation from just intake
depression. Is this reduction measured in grams
per day or grams per kilogram DMI? This is crucial.
Total daily methane can drop simply because the
cow ate less. That's meaningless. It is. Methane
yield grams per kilogram of DMI. That is what
proves the additive actually altered the fermentation
pathways, diverting hydrogen to propionate. So
if they only show you a reduction in grams per
day, you tell them you need to see the yield
data. A 500 gram per day reduction sounds great,
but if DMI dropped four kilos, the yield is the
same. You need that specificity. Question three
focuses on endurance. How long did the trials
run? If the trials ran under eight weeks, I am
raising a serious skeptical eyebrow. The rumen
microbiome adapts quickly. We see this all the
time with plant extracts or oils. You get a beautiful
15 % or 20 % reduction in methane initially.
And then the methanogens figure out a workaround,
and the reduction is gone by week 10. You need
trials that run for a minimum of 12 weeks, ideally
across multiple lactations, to prove sustained
efficacy. And the final, biological gut check.
Pun intended. Where did the hydrogen go? Yes.
If you are blocking the methanogens from making
methane, you are blocking the cow's primary hydrogen
disposal route. The vendor must explain the new
hydrogen sink. Ideally, the hydrogen is being
channeled into propionate, a useful productive
energy source for the cow. And if they can't
explain that pathway and quantify the corresponding
increase in propionate, the rumen might just
be building up hydrogen pressure. which stresses
the cow and can lead to her going off feed. It
forces vendors to show they understand the complex
biology, not just the simple marketing tagline.
Okay, let's pivot to another health topic where
the science is still emerging, and we need to
counsel significant caution. The bovine leukemia
virus BLV connection to calf health. Right. There's
emerging research suggesting an association between
the BLV status in dams and calf health outcomes,
specifically respiratory disease. But this is
a classic case where we have to emphasize uncertainty.
We need to avoid massive operational changes
based on preliminary findings. So why the uncertainty?
Because the mechanisms are completely unclear
and the potential for confounding factors is
enormous. Right. Is it that BLV -infected dams
produce colostrum with compromised immunity?
Is it a direct immune effect on the calf? Or
is this just a marker for something else? That
third point, the confounding management, is huge.
USDA NHMS data shows 94 % of U .S. dairy herds
have at least one BLV -positive cow. The average
prevalence is 46%. So high prevalence herds might
systematically have lower biosecurity practices
overall, higher calf housing density, poorer
ventilation. Factors that independently drive
respiratory disease. We don't know if the BLV
status is the root cause or just a flag for a
riskier management environment. So let's focus
on what we do know with confidence. Economic
analyses already show that reducing BLV is financially
sound, regardless of any calf link. Right. Every
10 % increase in herd prevalence is associated
with losses in the 430 to 540 pound rolling herd
average range. Due to reduced longevity, increased
culling, subtle production drops. The known reasons.
Therefore, our bullvine position remains consistent.
Don't overhaul your calf respiratory program
solely based on this emerging link yet. Continue
to pursue BLV reduction for the already validated
financial reasons, production, cow longevity,
overall immune health. Any calf health benefit
you see down the line is a bonus, not the primary
driver for a costly intervention today. Manage
what you know and monitor the data on what you
don't. Solid advice. Manage the cost drivers
first. All right, so a farmer just finished milking.
They've internalized this mountain of data and
they're driving to the feed store right now.
What are the three most actionable things they
need to remember from this deep dive? The three
steps that save them money immediately. First
thing, right size your colostrum. Stop causing
colic for no benefit. Okay, take away one. Immediate
action this week. If you don't own a Bricks refractometer,
buy one. Make it standard protocol, non -negotiable.
Second, set a hard cap on that first feeding
at 8 % of the calf's body weight. So 3 .2 liters
maximum for a standard 40 kilo calf. Exactly.
We're cutting out the colic, not the IgG delivery.
And the medium term strategy, three to six months
out. Implement a split feeding protocol for any
total volume needs that exceed that 8 % maximum.
Give the calf 8 % immediately, then the remainder
six to 12 hours later. And make sure your calf
crew is tracking comfort scores to ensure that
visible distress is gone. Long term, one to two
years. Start refining your dam selection for
your colostrum bank based on consistently excellent
Brix readings. You need to be prioritizing cows
with superior IgG quality and aggressively banking
that colostrum during peak seasons to cover those
inevitable fall slumps. Takeaway number two,
enforce genetic non -negotiables, especially
when you're chasing that beef on dairy premium.
The cow always comes first. Immediate action
this week. Pull your current inventory of beef
on dairy semen. Audit the calving ease EPDs.
Right now, if any sires fall below a strict minimum
CE threshold that you've set, pull them from
the stack. I don't care what the calf premium
is, you can't afford the dystocia costs. Medium
term, three to six months. Start using those
methane efficiency scores as a tiebreaker when
selecting your new sires. Capitalize on that
23 % heritability with zero production trade
-off. And enforce the rule, limit beef breeding
primarily to your mature cows. And long term,
one to two years out. Systematically track your
herd's dystocia rate for beef on dairy calves
specifically. If that rate climbs even slightly
above your baseline, you immediately adjust your
CE selection threshold until that rate returns
to normal. Profitability is defined by the health
of the dam, not the size of the calf check. And
takeaway number three, stop paying for data you
don't use. Yes. Leverage your existing DHI investment.
Immediate action this week. Locate your last
few DHI reports. Call your DHI processor and
specifically request the detailed fatty acid
profile, focusing on the de novo fatty acid percentages.
Start using it as a baseline indicator for early
rumen health monitoring. Watch for signs of acidosis
in your transition cows. It's a free window into
your herd's health. Medium term, three to six
months. If you are evaluating new lameness monitoring
tech, use our research evaluation checklist.
Ask vendors specifically about that 23 -day detection
window. Make sure the system measures the quality
of gait, not just the quantity of steps. You've
got to guarantee you're preventing that type
3 collagen damage. And long term, one to two
years. Integrate that de novo fatty acid profile
into your nutritional and genetic strategy. Use
that data to subtly select for lower methane,
more efficient rumens over time. It's an environmental
and efficiency benefit delivered via your existing
DHI infrastructure without spending a single
dollar on questionable feed additives. This has
been another Bullvine podcast from The Bullvine
Podcast. For more straight -talking industry
analysis, including those crucial skeptical questions
for feed vendors, head to www .thebullvinepodcast
.com. vine .com subscribe wherever you get podcasts
we're out with new episodes every day and upcoming
topics we'll be analyzing the true cost of parlor
automation labor dynamics and the shifting consumer
demand for a2 milk proteins we'll see you next
time