KPU in Horses

A disclaimer… sort of

If you've read previous versions of this page, you may notice that we're talking about KPU a little differently these days.

That's deliberate – because one of the things I've learned over all my years of disappearing down equine-health rabbit holes is that science doesn't stand still. Questions get asked, ideas are tested, sometimes the evidence underneath them becomes stronger, and sometimes the story becomes more complicated.

And no question – five years after studying KPU with Dr Christina Fritz and working with so many KPU-type horses, there's been an awful lot to learn about the "multi-metabolic" horse. But there are also credible challenges now being made about the evidence supporting parts of the KPU model, while KPU itself is still not currently a validated veterinary diagnosis in horses.

So here's a fresh update to our KPU page – covering the theories I still firmly follow, what I can no longer state with the same certainty, what these stoic multi-metabolic horses have taught me, and how I'd approach a "multi-metabolic" horse today.

So KPU cards on table right at the beginning

Certainly when I first encountered Dr Christina Fritz's work several years ago, KPU was largely unknown within mainstream equine veterinary medicine. And no question – the concept was eye-opening for all owners of horses with a multitude of issues, with many horses experiencing a remarkable improvement in health by following a change in management and nutrition.

But here we are, five or so years on, and there are some important points, including that to date:

• There are still no established horse-specific KPU diagnostic criteria.
• The urine testing historically associated with KPU has also not been validated as a diagnostic test for the condition in horses.
• Perhaps even more importantly – especially for those of us who've followed the KPU story over the years – the proposed biological mechanism, particularly the relationship between urinary pyrroles, active vitamin B6/P5P, hindgut dysfunction and nutrient losses, has also not yet been established through validated equine research.

But...

There’s a rather important ‘but’, though… This doesn't mean there’s nothing here worth investigating. Fritz's work, together with the remarkable changes we've seen reported in many horses we've supported through the hindgut/P5P and nutritional approach that grew from it, gives us plenty of reason to remain curious.

That said, observation and mechanism are two different things. Those outcomes can tell us something changed. What science still can't tell us with certainty is that the complete KPU mechanism originally proposed is necessarily the reason behind why many horses were successfully supported.

So, does that mean we simply delete KPU from the website, pretend we never talked about it and quietly wander off whistling?

Absolutely not. Because the horses behind the label haven't disappeared. And that's where I think this story becomes much more interesting, because KPU essentially is about a pattern – agreed a variable one as the symptoms can be many, but a pattern all the same. And it’s the biology behind those patterns that once you start following… well, you know how that goes for me when there’s a rabbit warren nearby!

The pattern

Long before most owners have ever heard the letters K-P-U, they usually know something isn't right - and hasn't been for a while. There’s the horse with the permanently iffy gut, then their feet start struggling, then there's an itchy summer, and some unexplained swellings, often seem in the sheath, teats, orbital eye regions, and limbs.

They might also have become unexpectedly and increasingly sensitive to grass, or their weight and metabolic picture become harder to manage, then throw in a session of repeat abscessing…

You sort one thing... and something else pops up. Nothing necessarily dramatic enough to explain the whole horse, but collectively? That’s a pattern.

Over the years we've spoken to so many owners of these horses – the ones with the list of apparently unrelated niggles as long as your arm. And that's what originally made Christina Fritz's training and the KPU model so interesting to me. Not because I desperately needed another three-letter acronym in my life – it was because someone was answering a question I'd been asking for years… what if these aren't all separate problems?

What if - instead of looking at the itchy skin over here, the dodgy feet over there, the temperamental gut in another box and the metabolic issues in yet another - we looked at the whole horse?

Five years on that question hasn't become invalid simply because the proposed KPU mechanism remains unproven. In fact, I'd argue it's become more useful, because now we can take away the pressure to make every complicated horse fit KPU and instead ask a much better question: what’s going on underneath the pattern?

And this is what I think is important. Not an argument about whether KPU is "real" or "not real" – biology won’t ever be improved by people shouting at one another from opposite ends of the internet. Instead, let's look at what we actually know, what remains theory, what we've learned since the KPU conversation began – and, most importantly, what might genuinely help the horse standing in front of us.

So where does the KPU idea come from?

KPU – Cryptopyrroluria, sometimes discussed alongside HPU or Haemopyrrollactamuria – originated in human health before being applied to horses.

Within the equine world, the original thinking we've encountered came through the work of German biologist Dr Christina Fritz around 2001, whose teaching brought together observations around hindgut disturbance, vitamin B6/P5P, liver metabolism, trace-mineral status, and horses presenting with multiple apparently unrelated health problems.

And that's why I remain enormously grateful for the door Christina opened, while also being willing to look again at what may lie on the other side of it. Good teachers don't teach us what to think forever - they teach us to keep thinking - and her proposed model was compelling because it seemed to connect a lot of dots.

In simplified form, the theory suggests that significant (emphasis on "significant") disruption within the hindgut microbiome can affect the availability of biologically active vitamin B6 – P5P, or pyridoxal-5-phosphate.

P5P is genuinely important biology. It's the metabolically active coenzyme form of vitamin B6 and participates in a huge number of enzymatic reactions throughout the body, particularly amino-acid metabolism and numerous other metabolic pathways.

Christina's KPU model goes further. It proposes that inadequate P5P availability impairs the liver’s processing (detoxification) function, while abnormal pyrrole-related compounds contribute to losses of nutrients including zinc and B6.

In other words, the theory is that the horse becomes deficient in the active B6 the liver needed to do its job efficiently, while at the same time loses other important nutrients such as zinc. The result is thought to be a bit of a vicious circle – fewer of the nutrients needed to keep everything running normally, and an increasing struggle to process what the body needed to clear.
 
(If you remember my old two-phase jeep-and-trailer analogy, this is where it came from. I described P5P as the ‘towbar’ in the KPU “toxin” model - think of a toxin molecule like a trailer of hay you need to haul away. First up, Phase 1 adds the "towbar" to the toxin, and then Phase 2 hitches the trailer so the kidneys can flush it out in the wee. The critical tool that hitches that trailer is P5P (active Vitamin B6). Without it, the jeep can't move, and the toxins stay trapped in the body.

In short? Without enough P5P, the theory suggests that the liver can’t efficiently pull the metabolic “trailer” through the next stage of processing.)

Hence the cascade involving poor liver function, mineral depletion, tissue accumulation of unwanted toxin molecules, and the enormous collection of apparently unrelated symptoms that led to KPU sometimes being described as "the disease of a thousand faces".  If you read our older KPU material, you'll recognise that story.

But five years and a lot of horses later? There are parts of that model I'd now put a tiny pencil mark against – and others I'm still very interested in, because not everything within that biological landscape is wrong. The hindgut microbiome matters enormously, just as P5P, zinc, copper, protein, liver and kidney function, and the all-important nutrition matter. And gut health absolutely does not exist in some little digestive bubble disconnected from the rest of the horse either.

But joining those perfectly real pieces together into one specific disease mechanism requires evidence – and five years on we still don't have it in peer reviewed published form.

The difference between a model and a diagnosis

This distinction is really important.

A biological model can be useful because it gives us questions to investigate. A diagnosis is different. So for us to say confidently that a horse has KPU, we'd need to know what objectively defines the condition in horses. We'd want validated diagnostic criteria - we'd need to know exactly what we're measuring, what a normal result looks like across a healthy equine population, how reliably the test performs, whether different laboratories can reproduce the result, and whether an abnormal result consistently correlates with a defined biological or clinical condition.

At present, those pieces aren't in place for equine KPU – which is why we prefer to talk about a recognisable KPU-like pattern.

What about the KPU urine test?

Historically, we've previously referred to that test as a way of detecting KPU, but while the testing includes urinary markers such as indican and pyrrole-related compounds, again there are currently no validated horse-specific diagnostic criteria or reference intervals that allow us to say that "This result proves this horse has KPU." Nor does that test directly demonstrate that a horse is deficient in P5P.

However, this doesn't mean research can’t uncover something useful here. Science is full of ideas that begin as observations and become clearer as analytical methods improve.

But back in the day, many of you will have heard me say something along the lines of: “Yes, that sounds like it could be a classic presentation of KPU.”

And today, you’d have to forgive me for recognising a horse as showing the kind of KPU-like pattern we've been talking about – several apparently unrelated problems presenting together, usually involving the gut, skin, feet, metabolism or general resilience.

What's changed is what I think we can conclude from recognising that pattern, because those signs give us a useful clue that this is a horse we need to look at more widely – not a conclusion about what's causing it.

So whether I'd say “this sounds like it could be KPU”, or describe it as “a KPU-like pattern”, my next sentence has always been – and will always be: “Tell me about your horse.” Everything from when did this begin, what's their gut, feet, skin like, their diet/forage, what have you already tried, what's happened throughout this horse's life that might matter, etc etc. And perhaps most importantly… what has this horse been adapting to for months or years before the latest symptom appeared?

If you’ve been on the receiving end of an EquiNatural email you’ll know how this goes, because recognising a pattern is always just the beginning of our conversation.

And today, the difference is that we're much less interested in trying to prove a KPU label – because we can get back to doing something much more useful – following the biology.

Let’s start with the horse

I know. Groundbreaking stuff. 😉

But it's surprisingly easy, once we've found a label that seems to explain everything, to start looking for evidence of the label rather than investigating the individual horse – i.e. sweet itch, so let's give something to soothe the itching, instead of looking at why the horse is itching.

Same if someone comes to us with what we see as a fairly classic KPU picture – perhaps ongoing gut trouble, poor feet, itchy skin, metabolic wobbliness and a collection of apparently unrelated problems. Our first thought is always looking at what might be contributing to this pattern - because there may be several factors. And before disappearing down any exotic metabolic rabbit hole, we need to make sure we haven't walked straight past the enormous horse standing beside it.

For example: has insulin dysregulation been investigated, could PPID be involved, is there pain somewhere, or have any recurrent skin problems being properly investigated? And how about the forage, and is the overall diet supplying enough quality protein and essential amino acids, are copper and zinc adequate, and balanced sensibly against the rest of the diet?

What about dental problems, parasites, infection, medication effects, or another underlying condition? Movement, turnout, social stress and the horse's environment?

And there’s more. If there's persistent diarrhoea, faecal water, recurrent colic, weight loss or another ongoing digestive problem, has that been properly investigated rather than simply being christened "dysbiosis"?

This isn't nearly as exciting as discovering one hidden disorder that explains everything, but biology doesn't owe us an exciting answer. And quite often, the boring foundations turn out to be where the useful answers live.

Everything still begins with the gut

The horse evolved as a fibre-fermenting herbivore with an enormous microbial fermentation chamber at the back end of the digestive tract. Those microbial communities help turn otherwise indigestible plant fibre into metabolites the horse can use – most notably volatile fatty acids, which provide a substantial proportion of the horse's energy. And of course, the infamous activated B6 - P5P.

And the microbiome doesn't operate in isolation. Its activity is influenced by what reaches it – forage first and foremost (diversity hopefully from different fibre types), but then there are changes in diet, medication, illness, stress, movement, age, and probably many other things that we're still only beginning to understand.

Likewise, the products of microbial fermentation don't simply sit in the hindgut minding their own business. They interact with the intestinal environment, epithelial barrier, immune system and host metabolism. So yes... the gut matters enormously.

Within Fritz's KPU model, this is also where the story can begin – with significant disruption of the hindgut microbial ecosystem, which can be traced back as far as the horse's earliest life. Later in life, that microbial ecosystem can further be challenged by changes in diet, illness, medication and chronic stress.

Even the forage itself matters – hay and fermented forages such as haylage are not microbiologically identical, with studies showing that forage type can alter the equine microbial community and fermentation environment. In a horse with persistent digestive problems, haylage is one of the dietary variables I'd certainly want to look at.

In short? It starts with “dysbiosis” – which simply describes an altered or disrupted microbial ecosystem, which depends on its microbial neighbours, its food supply, pH and the wider intestinal environment. Which is where, for me, it all lies – instead of trying to micromanage individual microbes, we look at the whole gut environment and how we’re creating it for the microbial community as a whole.

Give the hindgut microbial ecosystem appropriate fermentable substrate, make dietary changes gradually, and avoid unnecessary disruption.

Meanwhile, equine microbiome science is still young. Gut science is getting there – it can now identify which microbes are present and how microbial communities differ between horses, diets and disease states. What we're less clever at is creating one universal perfect equine probiotic product and then feeding it to the horse from a tub.

As I type there are currently no probiotic supplements that directly mimic the healthy flora of equine gut microbiome – at least, not ones that introduce beneficial, fibre-fermenting microbes capable of digesting cellulose like a horse is meant to.

In a perfect world, we’d be able to install those ideal microbes right into the hindgut whenever there’s been disruption – helping the friendly bugs out-compete the bad and recreate the microbiome horses evolved to have. But we’re not there yet. The general thinking is to feed more probiotically - which means adlib hay for the cellulose fibre stored in the stalks.

And this is where fibre comes marching straight back into our story.

Nutrition – the bigger picture

One of the reasons the KPU model appealed to me was that it brought nutrition into the conversation for horses whose problems weren't necessarily being viewed nutritionally.

We're talking zinc, copper, selenium, sulphur-containing amino acids, protein, manganese and the B vitamins.

Suddenly we were asking whether the horse actually had the raw materials required to build skin, hoof, muscle, enzymes, connective tissue and all the other things we'd been expecting the body to repair - and that's still a great question. But before we look at where my thinking sits today, I think it's important to explain properly what I was actually taught, because the nutritional side of KPU wasn't something I invented along the way.

Within Dr Christina Fritz's KPU teaching, the nutritional picture formed part of the KPU mechanism we were learning about. It proposed that when the liver's Phase 2 processing became impaired through insufficient P5P – active vitamin B6 – the body could use an alternative route involving certain nutrients to help bind and eliminate unwanted compounds via the kidneys.

The consequence, within that model, was an increased drain on particular nutritional reserves – especially zinc, selenium, sulphur and manganese.

And this was where some of the apparently odd nutritional patterns we were seeing in these complicated horses began to make sense.

Zinc

Zinc was a particularly important part of Fritz's teaching. Within the model, falling zinc despite apparently adequate dietary supply could be interpreted as a clue that zinc was being increasingly used within this proposed alternative clearance mechanism.

Fritz also described a practical pattern where zinc could be supplemented and blood concentrations restored, only for them to fall again once supplementation was withdrawn. Within the KPU model, simply continuing to add more zinc was therefore viewed as a sticking-plaster approach – the aim was to address the wider biological picture thought to be driving that increased utilisation.

This was also why zinc became one of the nutrients we paid particular attention to in horses showing that wider KPU-like pattern.

Selenium

Fritz's teaching also linked selenium closely with zinc. Within her model, zinc and selenium status could appear to move together, with altered zinc utilisation influencing the selenium picture too. The emphasis wasn't therefore on automatically adding selenium whenever a blood result appeared low, but on looking at the wider nutritional and metabolic context.

And there's an important practical point here regardless of KPU: selenium is one nutrient where more is most definitely not automatically better, so I've never been a fan of adding it casually without good reason.

Sulphur

Sulphur was another important piece of Fritz's nutritional model. Rather than thinking simply in terms of a measurable blood deficiency, the theory proposed increased use of sulphur-containing compounds as part of the body's normal processing and elimination pathways.

That brought our attention back to the horse's overall protein and amino-acid nutrition, as well as to signs we might be seeing in tissues with a high nutritional demand – skin, coat and hoof in particular.

Within the KPU model, poor coat quality, delayed shedding, thinning mane or tail, slow hoof growth, soft soles and weak hoof horn were therefore considered possible clues within the wider pattern – never particularly useful as standalone signs.

Manganese

Manganese also featured within Fritz's model, although again the emphasis wasn't simply “low manganese = feed more manganese”.

The theory was that altered utilisation could occur within the wider multi-metabolic picture, making the nutritional landscape more complicated than simply looking at how much of an individual mineral appeared on a feed label.

And this, really, was one of the most useful lessons I took from the whole nutritional side of KPU: Nutrition isn't just what went in. It's digestion, microbes, absorption, conversion, utilisation and cellular delivery.

So where would I put my pencil today?

This is where we need to separate two things.

The nutrients themselves are very real biology. Zinc, copper, selenium, manganese, protein, amino acids and vitamin B6 all have important roles within the horse, and asking whether a complicated horse has the nutritional foundations to maintain and repair its tissues remains every bit as relevant today.

What hasn't yet been established through validated equine research is the specific KPU mineral-loss mechanism described above – particularly the proposed chain linking impaired P5P-dependent liver processing with increased use and subsequent depletion of these individual nutrients.

So I'm not throwing the nutritional thinking away. Far from it. What I'm doing is separating what Fritz's KPU model proposed from what we can currently demonstrate in horses. And perhaps most importantly, the KPU model taught me to stop looking at a mineral result, a hoof problem, an itchy coat or a poor topline as an isolated nutritional event and start asking a much bigger question: Does this horse actually have the nutritional resources – and the biological capacity – to use what we're feeding them?

That question is staying firmly on the page.

And what about the liver and kidneys?

Five years' ago Carol was quoting that when these two were struggling due to a multitude of issues, we were looking at a broken “detox pathway” caused by KPU.
 
These days even I’m happy to no longer think of them as this, but does that mean we stop supporting liver and kidney health?

No. It means we get clearer about why we're doing it.

The liver is an extraordinary metabolic organ involved in nutrient processing, protein synthesis, energy metabolism and the transformation and clearance of many endogenous compounds and foreign substances.

Meanwhile the kidneys regulate fluid and electrolyte balance, contribute to acid-base regulation and remove many waste products from the blood.
 
For our multi-metabolic horses formerly known as KPU horses, no question – these organs absolutely belong in a whole-horse conversation – although supporting normal physiology is rather different from assuming we're repairing a broken KPU detox pathway.

So what are we left with?

Quite a lot, actually.

Five years on, without a validated veterinary diagnosis, I don't think we can retain the certainty of that original neat chain:

Dysbiosis → P5P deficiency → failed detoxification → mineral loss → KPU → multiple apparently unrelated problems.

But what we absolutely do still have is a horse living within a network of interacting systems so this is what we still stay mindful of.

• Gut ecology affects and responds to diet, health and environment.
• Nutrition supplies the raw materials those systems require.
• Metabolic and endocrine health influence how nutrients and energy are handled.
• Pain changes behaviour, movement, stress physiology and often feeding patterns.
• Immune activity communicates with tissues throughout the body.Liver and kidneys perform enormous amounts of everyday metabolic housekeeping.

And the horse has been adapting to all of this, every minute of every day, for a lifetime – which sometimes works perfectly, but for some horses, that resilience gradually starts to narrow.

And what we see first depends on how those pathways have been affected. It might be the itchy skin, or the footiness, or obvious gut issues - the sloppy droppings or the horse who's suddenly struggling with spring grass.

Which brings us back to where we started five years ago, where armed with our new knowledge we were asking "Does my horse have KPU?"

Today? Maybe it should be more “Why is this horse struggling to stay well?" Which of course opens a much bigger – and much more useful – door.

The "KPU-like" horse – this is where it gets interesting

So far, I've spent quite a lot of time telling you why we should no longer confidently call KPU KPU.

Which is all very well, but if you're reading this because your horse has dodgy feet, an unpredictable gut, itchy skin, strange swellings, metabolic issues and a supplement shelf that's starting to resemble a small branch of Holland & Barrett... you're probably thinking:

"Lovely, Carol. But my horse is still standing here with all of it."

Quite. And this is why I don't want to throw away the pattern simply because we're questioning the label.

Over the years we've spoken to many owners whose horses don't seem to have one clear problem – they have lots of little problems all alongside each other. And usually with faecal water on and off for years, and one issue settling before another appears. And sometimes there are recognised diagnoses in the mix – insulin dysregulation, PPID, sweet itch, osteoarthritis, gastric disease, respiratory problems – but they still don't seem to explain the whole horse.

Sometimes every individual problem has been investigated and nothing dramatic has been found, and equally we hear a lot of owners simply saying they’ve "never really been right."

Does it mean it’s KPU? We don't currently have a validated way of making that diagnosis, so we simply can't know. But we’ll still be looking not only at today's symptom but at the whole journey that brought this horse here.

The final straw is rarely the whole story

The thing we can see today isn't necessarily where the story began.

• A horse becomes footy after spring grass – but was spring grass the entire problem?
• A horse develops faecal water after a course of antibiotics – but were the antibiotics the whole story?
• An itchy horse suddenly has the worst summer they've ever had – but was that summer uniquely terrible, or had their ability to cope been narrowing for some time?

Sometimes there really is one straightforward cause, but equally we might be seeing the point at which the horse's capacity to keep adapting has finally been reached.

Think of it as accumulated biological load – diet, dis-ease, pain, repeated dietary disruption, metabolic pressure, poor reset, social stress, restricted movement, nutritional inadequacy, ageing, seasonal change, medication when medication was genuinely needed…  all asking something of the horse's adaptive capacity, and some undoubtedly influencing the gut ecosystem along the way.

None of these automatically causes the others, and I certainly don't want us inventing another enormous theory in which Everything Causes Everything – we've only just escaped from the last one! But they all ask something of the horse,and we should ask right back what this horse has been having to adapt to – and for how long – so we can connect those dots.

Mac – the horse who sent me down this particular rabbit hole

Those of you who've been around EquiNatural for a while will probably have heard of Mac.

Mac – or MacAttack when he was being particularly Mac-ish – was an unhappy horse I took on back in 2017 who had chronic sweet itch.

And he was one of the horses who made the KPU model feel very real to me, because when I studied with Christina Fritz, suddenly I had a framework that encouraged me to look beyond Mac's itchy skin and understand why he was reacting in the first place.

I was pretty confident that I’d sorted his diet and nutritional status, but to be honest that barely touched the surface – there was clearly much more going on with Mac than an itchy skin problem. So that took me to his gut, his wider metabolic picture, his history – and the things we could change around him rather than simply trying to suppress what was happening on his skin.

And oh boy did Mac change. Not overnight - it took around 15 months before I felt we'd genuinely turned a corner with him. That experience was huge to me, and I'm not going to rewrite it now simply because we’re having to rethink the mechanism behind KPU. In short? Mac's improvement was an observation; KPU was our explaination for that observation. And at the time, I believed Mac's recovery supported the KPU model.

No question we changed several biologically meaningful things at once. We changed how we fed him, we addressed his nutritional foundations, we paid far more attention to his gut environment, and thanks to Christina’s studies we stopped viewing the skin as an isolated organ and started looking at the whole horse.

Which of those mattered most? Were several working together, and would he have improved if we'd changed only one? I can't honestly tell you, which means Mac's story can’t prove that he had a pyrrole disorder, a P5P deficiency, or KPU. But he still taught me so much - that the visible problem isn't always where to begin - and that lesson has stayed with me ever since. Oh how I wish I could go back int ime to Kelso, who presented almost identically to Mac but without the Attack bit - a geniune case of "If only I knew then what I know now," as back then I only followed the sweet itch sticky-plaster approach with Kelso, and it could have been so different.

And then came the other horses...

While Mac was my own personal experience, over the years we've had owners tell us that horses they've supported through what we called our KPU approach changed dramatically – with many telling us "I've got my horse back."

I will never dismiss those experiences. But – and this is an important but – owner-reported improvement doesn't tell us which proposed biological mechanism caused it.

Our programmes rarely change one thing – it can involve forage, the feed bowl, correcting mineral or nutritional gaps, supporting fibre fermentation and gut health, adding specific nutrients, changing management, addressing discomfort and/or stress, encouraging veterinary investigation where appropriate...

Either way, maybe our KPU talk was pointing to a pattern rather than a "disease" - and this is where I've ended up after going back through all of this – not one diagnostic marker, not one particular symptom, not one missing vitamin – but a recognisable tendency towards complexity.

• The gut horse who was also the skin horse.
• The metabolic horse who was also struggling with their feet.
• The itchy horse whose diet turned out to need serious attention.
• The horse with apparently endless minor problems whose nutritional foundations had never really been looked at.
• The older horse whose lessening resilience had changed what they could cope with.
• And the horse whose owner had spent years treating each new symptom as a completely separate event.

None of that creates a new disease called KPU – instead it reminds us that biology works in networks. And that’s something I can still do something about.

Supporting naturally

If you recognise your horse in this page, please don't panic and please don't immediately order seventeen supplements - you know me better than that by now. 😉

I'd start with a piece of paper and write down your horse's story. And not just today's problem - when did things first begin to change? Which problem appeared first, what came next, and is there a seasonal pattern? Have there been periods when the horse was genuinely well, and what changed before they became less well?

So where does our KPU Reset Programme fit now?

This was probably the question sitting quietly at the back of your mind - because if we're now saying  that KPU isn't a validated diagnosis, why would EquiNatural still have something called a KPU Reset Programme?

Fair question. Thing is, the programme grew out of what we learned while supporting the complicated, multi-system horses historically described as "multi-metabolic horses". But the programme itself doesn't need an unvalidated diagnosis to make its individual components meaningful.

Its purpose now is better described as a structured, step-by-step foundation programme for the horse showing a complex gut–nutritional–metabolic pattern.  In other words – the name reflects where the programme came from – supporting the horse with a programme that gives us a targeted sequence, rather than throwing everything into the bucket at once.

• We can support digestive comfort and gut function.
• We can support normal liver, kidney and lymphatic physiology.
• We can look at the nutritional foundation.
• We reassess the horse as we go rather than assuming every symptom belongs to one underlying disorder.
  

Bloodwork clue

For those able to run bloods, here are some markers Dr Christina Fritz has highlighted (translated from German):

• Erythrocytes / haemoglobin: often low (within normal, but at the low end)
• Zinc: usually low
• Selenium: often below normal, though values down to 40µg/L are fine
• CK (Creatinine Kinase): high (normal <130 U/L)
• LDH (Lactate Dehydrogenase): high (normal <400 U/L)
• Potassium: slightly elevated when CK/LDH are high

Horses with raised CK/LDH often feel stiff daily and can take 30–45 minutes to loosen up. In sport horses, this stiffness may be the only clue. In ponies and non-sport horses, you may also see lymph “pads” around the saddlebag area or a thick crest full of lymph.

)For glucose testing, use sodium-fluoride stabilised blood. Do not fast the horse; allow hay ad lib for 12 hours before testing. Glucose should be below 4.9 mmol/L (83 mg/dL), with sport horses at the upper end of this range and non-sport horses comfortably below

Additional support worth considering

If bloods and history point toward KPU, support can begin straight away. Typical additions include:

• Zinc (safe unless fed in massive excess) (included in our VitaComplete balancer
• MSM (organic sulphur) – up to 15g/day is safe and beneficial (Available in our Nutrients shop page)
• P5P (active B6) and Vitamin B12, both water-soluble so any excess is excreted naturally (available in our Nutrients shop page.

Gut restoration, of course, benefits almost every horse – so it’s a good step regardless. For the practical next step, see our KPU Shop page for the full programme.

NB. Our EquiNatural KPU programme is independently developed. While I have studied extensively with Dr Christina Fritz and continue to learn from her, our method may differ from hers.