KPU

Content

1. Everything begins with the microbiome
2. The How&Why behind KPU
3. How to diagnose
4. The critical liver connection
5. Phase 1
6. Phase 2
7. Now to P5P itself
8. What happens if it doesn't work?
9. Trace element deficiency
10. Zinc, Selenium, Sulphur, Manganese & Iron
11. The symptoms
12. What to do meanwhile
13. What NOT to feed!
14. Supporting naturally ...

KPU is known as 'the disease with a thousand faces' as there’s such a wide range of symptoms. We're looking at everything from continuous gut disturbance, skin issues, hoof issues, susceptible to, unexplained tendon/ligament/muscle swelling/injury or swollen sheath/teats, chronic ongoing cough, musculoskeletal issues that can’t be explained, mineral disorders, i.e. bone/tooth demineralization (EOTRH) or brittle bones, various lamenesses, a whole range of continuous illnesses/condition, aka multi-morbid, even headshaking is now being listed. And so the list goes on.

But don't panic ... KPU isn't a disease, but it's certainly a disorder - a growing, and very complex multi-metabolic detoxification disorder in horses which we're only just starting to learn about, and is now starting the look like the missing piece of the metabolic jigsaw that so many owners have battled against.

And the cause? A disrupted hindgut intestinal microbiome, which can literally start from birth if the foal was poorly started.

It's that same-old saying - everything starts with the gut, but ...

1. Everything begins with the microbiome

... And when it comes to the hindgut biome, those awesome hindgut fibre-fermenting microbes not only do the essential job of digesting the cellulose fibre from hay and stemmy grass, but also produce a host of vital byproduct nutrients (metabolites, aka postbiotics) for the horse. These include volatile fatty acids which produce the horse's energy, certain essential amino acids and ... two  crucial B-vitamins, B6 and B12.

Thing is, there's equine-appropriate B6 and B12, and then there's questionable (synthetic) B6 and B12, the difference being that the equine-appropriate versions are produced in the hindgut in a specific activated form, and not the inactive synthetic form. And this is where the difference lies, because ... for the horse's liver to effectively biotransform every nutrient the horse ingests, in order to then send what's useful out into the bloodstream to be utilised, and toxins off to be excreted, it needs this very vital activated B6 to be able to do so.

Let's repeat that again - "the horse's liver needs this activated B6 to be able to effectively biotransform toxins." In other words, if the liver doesn't get it's activated B6 from the hindgut biome's byproduct production, it simply can't detox the body's waste properly, including converting them into an excretable state for elimination. Which means ...

Toxic waste ends up circulating and being stored in the body long-term, causing all kinds of metabolic syndromes.

So what does this have to do with KPU?

KPU is the name given to a multi-metabolic disorder, i.e. several syndromes all happening at the same time which seem impossible to fix. And it all starts from a significant disruption in the hindgut biome, more often than not starting from birth.

If a foal had a poor start in life and wasn't able to create a healthy hindgut biome (see The Foal's Microbiome page), or if further along the line you're feeding bulk-filler feeds produced from refined, artificial, processed carbs, or if you feed haylage which introduces acidic lactic-acid bacteria into the hindgut (which kill off the beneficial fibre-fermenting microbes), or if your horse is stressed ... and so the list goes on ...

This results in a rapid pH drop in the caecum and first part of the colon, in some cases as low as 1.3, when the hindgut should always remain around a neutral 7. Ultimately this leads to a mass dying off of the beneficial fibre-fermenting microbes, which upon death convert to an endotoxin (NB. this can lead to endotoxin laminitis - more on this to come on our Laminitis page which is waiting to be updated).

We now have a state of hindgut dybsiosis - more of the bad, acidic, bacteria microbes than the essential friendly fibre-fermenters, resulting in significant fibre fermentation disruption, which means those vital byproducts are no longer being produced. And one of those vital byproducts is vitamin B6 in its naturally produced, activated form, which is a critical player in the liver being able to convert toxins into an excretable state.

And here lies the crux of it all. Once we have dysbiosis in the hindgut biome, the liver, as in it being the master detoxification organ, is no longer able to detoxify. Which means those toxins remain circulating in the body, so the metabolism now has no choice but to use emergency detours to store those toxins and other waste around the body, instead of them being shifted out via the regular elimination routes.

Result? A horse with a multi-metabolic detoxification disorder, named Cryptopyrroluria, or KPU for short.

Put simply ...

Cryptopyrrolura, nicknamed KPU, means the liver’s natural detoxification talents have gone seriously wonky, meaning dangerous circulating toxins escape into the body, triggering a whole range of metabolic disorders, manifesting in a multitude of unspecific symptoms - often several at a time concurrently, with our horse never seeming to get better from one issue to the next, despite heroic efforts from the owner.

In short, a horse is nothing more, and nothing less, than a hindgut grass-forage fibre-fermenter. A horse is evolved to eat nothing by stemmy grass forage and little else, so a happy healthy hindgut biome will beaver away, day in and day out, digesting (fermenting) the grass-forage fibre from long, stemmy grass and/or hay, creating those byproducts including the horse's main energy source, as well as many other vital metabolites. If there's no fibre in the diet, we end up with dysbiosis - the multiplication of pathogen bacteria which disrupts the production of the activated form of vit.B6 – Pyridoxal-5-Phosphate, aka P5P.

🤓Science Alert! The number ‘5’ relates to the 5th position of the molecule where it needs phosphate attached, which the liver needs in order to deactivate those harmful toxins. So, P5P acts as the catalyst for the equine liver’s biotransformation process to function correctly.

It's thought that KPU underlies many of the well-known metabolic diseases we're now seeing, i.e. IR/EMS, laminitis, recurrent colic, a constant chronic cough, sweet itch, mallenders/sallenders, persistent faecal water/diarrhea, loss of performance – even headshaking's being mentioned; it’s said that all horses with these issues have underlying KPU, hence why it’s known as ‘the disease of a thousand faces’.

The good news is that it’s not genetic, but it can be inherited by a foal from its mother. That said, it can also be reversed but be prepared for an almighty marathon with no sprint in sight. Basically, we have to completely regenerate and stabilise the hindgut to get the liver to start working properly again.

2. The How&Why behind KPU

KPU can literally be triggered from birth. That first year of a foal is crucial, and very much depends on how its mother was fed, because a foal eats its mother’s faeces to build its own microbiome, a process known as coprophagia.

We now know that if the dam has a disturbed microbiome, the foal will end up with same poor-quality microbiome; thankfully new breeding practices are now mixing mares known to have a disturbed hindgut function, in with other mares known to have a healthy microbiome, so the foal will eat mixed faeces in order to give their hindgut a better chance for good biome colonisation. Otherwise, if the foal is unable to establish a healthy microbiome, you have a metabolic-risk patient for life because if a healthy microbiome isn’t there to start with, the immune system is already compromised before they're barely a yearling. We've got this all covered separately in our Creating the Foal's Microbiome page.

In a far-away perfect parallel world that none of us live in, this would be so much easier if we could simply feed healthy, species-appropriate probiotic microbes to our horse, but such a thing sadly doesn’t exist. As I type, there are no approved equine gut-appropriate beneficial bacterial probiotics for use in horses. Imagine if there was - in a perfect world we could install equine species-appropriate, cellulose-digesting microbes into the hindgut whenever there’s a biome disturbance, so they can colonise and outgrow the pro-inflammatory unfriendly bacteria, and recreate the natural microbiome that the equine gut system was evolved for. Just like we can for us humans.

There is a kind-of way to investigate. If it's remotely possible to check the history of our horse back to birth, we’d have more of a clue as to how they were raised and fed as a foal, and that hopefully no antibiotics or haylage were fed in the first 6-months of their life, or identify whether the dam unknowingly already had hindgut dysbiosis.

3. How to diagnose

So, we know that KPU is caused by long-term dysbiosis in the gut microbiome, which disrupts the vit.B6 P5P production, so by regenerating the hindgut biome we’ll restore liver function and we’ll have a healthy horse again. Simples! Until then, it’s the usual rule – fix the gut, fix everything - which means following a nutrient-supportive programme.

There’s also good and kind-of-bad news - KPU can now be diagnosed via a urine test. It’s not an in-depth test yet as it’s still early days, but it will show you whether the fermentation process in the hindgut is right or wrong. The downside? This test is currently only available in Germany and a further issue is that the urine test needs to be tested within 3-days, which is problematic from the UK with the current courier timescales. Rest assured avenues are being explored to get the test more readily available in the UK, but meanwhile it's all about doing what we can to regenerate the gut function.

The other important factor to be aware of is that this is no sprint fix – KPU takes an almighty marathon to repair, as we're potentially dealing with a well-established disruption from birth. Back to the KPU test, and the results will show a numbered gradient:

1. A result of 1 - not perfect but not bad either - change feeding and focus on gut restoration; you're looking at a 1-2 year fix.
2. Between 2-4 - there’s plenty gone wrong; major dysbiosis with major therapeutic help needed to restore the hindgut biome; you're looking at 2-3 years of therapy to get back to normal.
3. A reading over 5+? 5-years at least, because not only do we need to restore the hindgut, but the body needs time to excrete what’s been collected and stored over the years.

KPU is also seasonal-dependent, perfectly matching the well-known metabolic symptoms we’re well aware of – during spring-autumn grass, KPU symptoms go up; during winter they go down.

4. The critical liver connection

Reminder – probably the liver’s most important task is the biotransformation of waste products/toxins, converting them to a state where the kidneys can then excrete them. Agreed? WIth KPU, it’s this vital biotransformation process that’s affected, so, if you want to understand the science behind how detoxification actually happens when it all works as it should, here it is. Warning - it can be a bit brain-freeze-y but give it a go as it's incredibly clever, and just a bit fascinating. Well, to me anyway ...

Lets recap first. We now know that KPU starts with hindgut dysbiosis and causes liver function dysruption, so here's the How&Why behind  what happens in the liver. The process breaks down to 2 phases, and here's where it gets science-y so here goes.

🤓Science Alert!

Phase 1 – the attachment of a Functional Group (FG) molecule.

Imagine a 4x4 jeep, and a separate trailer you’ve filled with hay for your horse. Without a towbar to attach the trailer to the jeep, you’re not going to get your hay to the yard.

The towbar is the grouping-mechanism, aka the ‘functional group’ (FG). And this is what toxins need when they arrive in the liver – the liver cells attach a ‘functional group’ molecule to the waste toxin molecule, in order to prepare it into a form that the kidneys need for excretion. Now go bang head on wall, rinse, repeat, and read again.

Phase 2 - now it needs a catalyst. Meet P5P

So, the liver’s now added the FG - the ‘towbar’ - to the waste molecule. Now it needs a catalyst - a trigger, or as Wiki puts it, "a substance that changes the rate of a chemical reaction ... that speeds up a reaction or enables it to proceed" - in order to actually attach your hay trailer to the towbar, or in this case a 2nd molecule attachment which just happens to be highly water-soluble (the kidneys only excrete water-solubles). And the catalyst? Our new friend, Vit B6 in its activated form - P5P 😉.

This Phase-2 2nd-molecule attachment then makes the whole waste molecule water-soluble. This now signals to the kidneys that the whole complex it's just created with a FG and a P5P catalyst, is now ready to be excreted via the urine.

So, Phase-1 - the attachment of a FG; Phase-2 - the conjugation of a water-soluble molecule courtesy of the activated form of vit.B6 – Pyridoxal-5-Phosphate, aka P5P.

Still with me?

Now to P5P itself

Normally in a healthy horse the P5P creation process runs smoothly 24hrs/day, so we don’t need to even think about it, because a healthy horse has a healthy gut microbiome which produces all the numerous trace elements the metabolism needs, including the activated form of vit B6, aka P5P, so the detoxification process runs as it should as well.

We know that horses don’t usually get deficient in vitamins as the small intestinal biome produces most of them (other than vit.C which the liver produces, and vit.E which comes from grass forage). This also includes most of the very diverse B-family, but B6 and B12 are produced in the hindgut, and because of this, these are the only two B-vits that can go into deficiency.

B12, which builds haemoglobin and red blood cells, isn’t found in plants so can only come from the microbiome. As for B6, you’ll usually see the synthetic inactive version (‘Pyridoxine')  included in many processed feeds and mineral balancers. However, emphasis on both synthetic and inactive - which means the liver won't recognise as beneficial for the body to utilise, so it's therefore automatically ignored and sent on out for excretion. In other words, pointless.

The active B6 form - P5P - is essential to start Phase 2 of the liver transformation process. P5P is the catalyst, and without it, Phase 2 simply cannot start. So … back to our jeep and trailer example – you’ve attached the towbar but without someone to attach the trailer to the towbar (P5P), the hay isn't going anywhere.

What happens if it doesn’t work?

Long and short? If there’s a disturbed gut biome, there’s no activated B6/P5P for the liver biotransformation to work properly.

The liver still attempts to filter toxins from the bloodstream, and still attaches the FG, but if there’s no P5P, the liver literally says, “OhOh, what the f*** do I do now?!” Without P5P the detoxification/biotransformation reaction stops after Phase 1, leaving highly toxic agents circulating in the body.

From hereon it all goes wonky. The good news is that the body has emergency pathways to keep functioning until the environment changes for the better, then the metabolism can return back to its normal functioning in the metabolic pathways. The not so good news is that until this gut:liver:kidneys pathway is fixed, the liver can't transform the toxins into an excretable state, and doesn't know what to do with them, so they're sent out into bloodstream and the water-soluble toxins get stored in the soft-tissue.

Yes, you guessed right - we’re talking tendons/ligaments/muscle/sheath ... This is a completely natural emergency process to store dangerous toxins, but it means one thing … water retention! This is why some horses swell up. Now cue Serious Misunderstanding No.1 because – we get confused because we think it’s fat, so ...

We put our horses on a diet! Except it’s not fat – it’s lymph fluid sent to dilute the waste products because when waste product concentration gets too high, the connective tissue starts to die off so the body needs to dilute the waste products, hence why there’s water retention.

And where does this happen? The typical neck crest and what we think are fat pads on the flanks, as in all signs of EMS/IR, yet it’s actually the lymphatic system trying to dilute the stored water-soluble waste products. That's not to say it's not EMS/IR, but it can easily be mistaken. Sorry, I did say it was complex ... 🥴.

NB. There's a way that might help you tell the difference, and that's knowing what genetic type of horse you have. See our Blog Post Genetic Ancestry - what horse 'type' have you got? The blog explains that some horses are prone to laying down fat, others lymph, so you can usually get a pretty good idea of whether your horse is EMS-prone, or lymph-prone.

Meanwhile, what about fat-soluble waste? Simple – they go to fat tissue, which also creates is big problem! Cue Serious Misunderstanding No.2.

Again, we think our horse has overindulged so we skinny down their rations to make them drop some weight. Wrong. What we’re actually doing is releasing fat-soluble toxins into the body, which now triggers a vicious cycle – if there’s less fat in the body, there’s less storage room for the fat-soluble toxin storage, so they simply circulate back into the body. And this leads us back to the How&Why of the liver biotransformation process.

When liver biotransformation works properly, the waste molecules are made water-soluble courtesy of the two FG phases, so they can be excreted via the kidneys, but without P5P this won't happen. So, by endeavouring to skinny our horse down means an overload of circulating toxins in the body, which as we all know induces laminitis due to re-toxification. So, the body has a really good reason to try and hold onto those fat or lymph pads while the toxins are stored there.

Which means … when we’re faced with a fat-pad/lymph-pad horse, it’s all the more vital that we fix the liver biotransformation process before starting a s-l-o-w weight reduction process, so circulating toxins can then be biotransformed without a queue backing up.

Meanwhile, there is another emergency pathway, but it comes at a price.

5. Trace element deficiency

There’s another emergency pathway for some Phase-1 toxins to still be excreted by the kidneys, because if P5P is missing, the liver can couple certain minerals to certain toxins, depending on the toxin molecule, to excrete at least some of it.

We’re talking certain Phase 1 toxins being coupled to zinc, selenium and sulphur, but manganese and iron can also be used. There is a price though – with the liver utilising these minerals from the stores, the stores themselves can go into false deficiency.

Zinc

Zinc deficiency is historically rare; copper, yes, certainly in European soils, but not zinc. However, zinc deficiency is now being seen in bloodworks. This is interesting as both zinc and copper counteract each other – when zinc goes up copper goes down; when copper’s up zinc is down. If you look at hay analyses you’ll often see high zinc/low copper - this is normal as our soils/forage don’t have much copper, hence why we have to supplement to the NRC RDAs (hence how we formulated our EquiVita/VitaComplete brand of mineral solutions), but despite this it’s still rare to see a zinc deficiency.

However. Over the last 3-5 years we’re seeing many horses with zinc deficiency but not copper, now thought to be due to metabolism changes due to this faulty liver biotransformation process using zinc to bind to toxin molecules for excretion.

There’s a suggestion that we can check this by feeding extra zinc, and if bloods show better levels, we can then stop feeding extra zinc to see if the problems reoccur. However, this is the sticky-plaster approach - it shouldn’t be about compensating with extra zinc; it should absolutely be about repairing the liver biotransformation process first so the horse's system can regulate back to its normal zinc levels. Which kind of makes sense.

NB. A side effect of this is that because the labs aren’t aware of KPU (it's still being denied by many vets and therapists without having an alternative explanation for the clearly visible health problems ) the labs are now reducing what’s thought of as ‘normal’ zinc parameters. So, we should always question this if we get unusual numbers back from bloods, and request that previous ‘normal’ reference values from the literature be used and not necessarily go with what the labs are now saying.

Selenium

And this is interesting because until the mid-1980s, everyone thought selenium was toxic to horses so it was never fed. This was apparently based on American thinking because their soil selenium levels were so high that horses were literally dying of selenium toxicity, so therefore the general thinking became ‘selenium is toxic for horses’.

Cut to the mid-80s and the first research into selenium began with dairy cows – there was a condition known as 'white muscle disease' and calves were dying. A connection was found between selenium and feed for white muscle disease, so the thinking was that cows with low selenium levels meant there wasn’t enough selenium in their forage, so therefore – and here’s where it got ridiculous – there had to be the same problem for horses too! Er ... I thought we all knew that a horse is not a cow?

Thus, reference blood work values for horses were established and selenium began to be measured in every horse. Thing is, the blood parameters were set too high, and many horses were found to have alleged ‘selenium deficiency’ because of where the labs chose to set their reference parameters.

The fact is that horses aren’t normally selenium-deficient. Over the years, the parameters were gradually reduced towards more 'normal' (should be around 40-micrograms per litre), so these days we simply don’t see selenium deficiency.

There’s a connection with zinc though. When either zinc or selenium levels are low, the other is as well. Stop feeding zinc, both levels lower; supplement zinc and selenium levels rise. And … it’s now thought to be connected with KPU.

When horses have KPU, not only are large amounts of zinc used to couple to the waste toxins, but selenium is also used. As soon as you top up zinc, the body uses less selenium to excrete waste and this is why higher selenium levels can be seen.

So, pulling this all together, we always need to be careful when feeding selenium as it may be a cause behind the typically recognised 'metabolic' issues, i.e. trigger IR, EMS, Cushings. There's a very fine line between safe selenium and toxic selenium; selenium in high doses is toxic to horses so we should never feed more than in a mineral feed if there’s selenium-deficiency, but always look at zinc levels first. Long and short, address the KPU, and the selenium levels will rise by themselves.

Sulphur

Again, good and not-so-good news here. In a healthy horse, sulphur is usually sufficiently available through forage/roughage as there are plentiful levels of sulphur-containing amino acids in grass/hay.

However, a KPU horse will use up too much of its sulphur reserves by attaching to waste molecules, which can lead to sulphur deficiency. This is apparently not identifiable in bloods, but we can visibly see the symptoms of sulphur deficiency in poor quality skin, hair and hooves – all kidney markers.

Typically we’ll see poor skin regeneration and/or poor coat change/shedding, which could be related to sulphur deficiency. Over time they’ll lose long hair so develop a thinner mane/tail. As for hooves, they’re built from keratin which has a very high content of sulphur amino acids. Typical signs are noticeably slow hoof growth, i.e. not needing your hoof pro for ages. Weak/soft soles, footy response, poor hoof horn quality – all likely a sulphur deficiency/likely KPU as this doesn’t happen in healthy horses.

If your horse has had these symptoms which then mysteriously improve, perhaps we should be asking Why?, and consider if they have KPU. The good news is that sulphur is easily, and safely, supplemented with MSM (true sulphur).

Manganese

Manganese is rarely deficient as our UK forage is already way too high in it, so a horse should never become deficient. Unless ... they have KPU. Like sulphur, a manganese deficiency is also not traceable in blood tests. Be aware though – there's a new ‘myth’ hitting the headlines is horse feed producers saying there’s an epidemic of manganese-deficiency – they’re always on the lookout for some new spin for us to buy their products, so bear this in mind. Plus, any manganese added into feeds is synthetic, so pointless anyway.

Pulling this section together, we have zinc, selenium, sulphur and manganese involved in this KPU/liver emergency pathway. We should never feed supplementary manganese, but if we see our horses improve with added sulphur (via MSM) and/or zinc, and if there are other typical symptoms presenting (next para), they could have KPU.

6. The symptoms

KPU is known as 'the disease with a thousand faces', as there’s such a wide range of symptoms. This section also goes hand-in-hand with liver/kidney issues, so it may be worth checking our Liver&Kidneys page as well.

• Always check for continuous gut disturbance, i.e. if you’ve got faecal water, continual diarrhea, excess gas, it follows logically that there’s hindgut dysbiosis so P5P deficiency is a given. If you put a healthy horse on fresh grass and they get the squits for a few days, no worries, but continuous? Time to worry.

• Skin problems – sweet itch, eczema, mud fever, cellulitis, continual itching.

• Hooves – poor hoof quality, thrush, WLD, frequent abscessing, permanently footy.

• Susceptible to, or unexplained - tendon/ligament/muscle swelling/injury or swollen sheath/teats.

• Chronic ongoing cough, resistant to meds yet not considered 'allergic'. Always ask Why? is your horse coughing? The wild horse is naturally used to dry, dusty environments – a horse can manage this perfectly well as normally, the cellular epithelium level in the airways is covered with a thick mucous layer which binds to the dust and shifts it out again naturally – no cough required.
• To build this mucus layer the horse needs enough cysteine – an amino acid that contains sulphur – so to build up enough cysteine the body needs enough sulphur. When there’s KPU the horse goes into sulphur-deficiency (see above) so the airways can’t build up enough cysteine; thus they can’t build up the mucous layer so the airway is dry. Dust is inhaled and the horse coughs.
• Cue Serious MisUnderstanding No.3. One method us carers do is turn to haylage instead of hay – well, it’s dust-free innit? Well, yes, but … while this is our well-meaning attempt at alleviating the symptoms, haylage significantly damages the gut microbiome (because it's acidic, courtesy of the presence of LA bacteria, an unfriendly bacteria for the equine gut), which completely runs the immune system, so triggering an autoimmune response which increases allergic reactions – moulds, pollens, insect bites, you name it. This is always a secondary reaction; as always it should be about tracking track back to the root cause; is it hindgut dysbiosis causing B6 disruption, causing liver biotransformation disfunction, causing KPU?

• Musculoskeletal issues that can’t be explained – there’s intermittent lameness so you call the vet, yet the horse is fine when the vet arrives yet a few days later they go lame again; you just can’t explain it. Or constant back tension that the physio can’t explain, where the horse needs 30-40 minutes to warm up the muscles to work comfortably again. This could be KPU because remember, the connective joint tissue around the muscles stores the waste toxins as well as its own waste toxins.

• Mineral disorders – exostosis (a benign growth of new bone on top of existing bone), bone/tooth demineralization (EOTRH), brittle bones, various lamenesses.

• A whole range of continuous illnesses/condition, aka Multi-Morbid. Here at EquiNatural we see this repeatedly, where ‘everything’s wrong’. Usually starting several years previously with, say, a tendon rupture, then soon after the permanent coughing starts, followed by repeat tendon issues, then laminitis, then faecal water, and so on and so on … The symptoms seem to have simply shifted around the body, and as soon as one gets under control, something else pops up. Finally we have a horse with several different issues, and nothing’s helping. Again in the perfect world we need that KPU test, but meanwhile we can make a positive start with a gut/liver/kidney regeneration programme (see below).

• Non-responsive to any therapy – doesn’t respond or responds unexpectedly, say, too weak a response, i.e. pain meds don't work. Many pharma meds have to be activated in the body by design – they absolutely have to run through the biotransformation process but without P5P they won't be! Hence, those pharma components are either automatically excreted without working, or they remain in the body as a toxin. Typical examples are a horse suddenly developing laminitis following chemical worming, or going into toxic shock from a vax – both typical of the 'final straw' scenario, and all due to the disturbed biotransformation process.

• Even headshaking is now being listed; as yet though, we don't have any concrete info but watch this space.

• Finally, the Big One. Our old friend EMS – Equine Metabolic Syndrome. Lami, IR, pseudo Cushings - yes you read that right, psuedo Cushings. Yet no matter what we do, how we supplement, and how we change the feed/forage, nothing works.

7. What to do meanwhile

Yes, we know the test is still only currently available in Germany, so meanwhile what to do now? The key is to restore the natural microbiome in the colon, to start producing P5P again, in order to restore a normal liver biotransformation function.

And the only way to fix the hindgut biome? Simple. Hay, 24/7, 365-days/year, for the cellulose fibre content in the grass stems to restore the beneficial microbe population. If you feed a horse haylage, forget it. If you soak your hay for a long time, forget it. If you let your horse run out of hay, especially if stabled overnight, forget it.

So, feed hay, hay, and more hay, and for the feedbowl feed a basic grass-fibre cob as the base carrier - not alfalfa - to add in a mineral balancer with extra zinc, salt, and micronized linseed for the omega-3 EFA.

If haylage was fed, the gut also needs to deacidify, so feed Spirulina for a couple of weeks which is an excellent toxin-binder and is mainly excreted via the liver-bile-intestine route, thus relieving the kidneys.

Meanwhile, what not to feed! 

No beet, no alfalfa, no sugars, no pectins, no muslis, no pellets, no treats, and definitely no feedbags with pro-inflammatory gut-damaging wheatfeed, oatfeed, soya, NIS ... basically anything listed in our ‘The Feedbowl – what’s really in those feedbags’ page. The more basic the feeding program – in other words, the more species-appropriate, as in grass forage, as in what a horse is meant to eat and what a horse’s gut is meant to digest, the faster the hindgut environment will be restored to normal.

For the full story on how to feed our horses healthy, see our ‘Feeding our Horses Healthy’ section off the main menu. Or, if you’re stuck, feel free to email me your current feed regime in case there are triggers we can identify here – everything that goes in your feedbowl, so all brands/supplements etc., and forage - grass turnout, how long etc., and dried forage, so hay/haylage and how much.

8. Supporting naturally ...

Let's get to it and clean up the hindgut biome:liver:kidneys pathway while re-establishing the P5P production. Don't panic though! If the thought of trying to figure out which your horse needs suddenly seems like a minefield, we do the whole kit as one of our one-stop Wellness Programmes in our KPU shop page, as follows:

1. First up, we alleviate the gut discomfort and inflammation with DuoBute.
2. Then we feed a 1-month course of KPUCARE to stabilise the hindgut, improve the pH value due to the acidosis and dysbiosis/SIBO, address the leaky gut intestinal membrane, and rebuild the hindgut biome:liver pathway.
3. When the gut regeneration is finished, we then tonify the detoxification orders - the liver/kidneys - with a 1-month course of LKLCARE.

Recommended:

• Feed WildFed to add valuable, natural prebiotic roughage into your horse's diet to support the hindgut biome colonies.

The link to our KPU Shop page is at the bottom of this page.

Meanwhile, come back to us for advice on long-term support if needed, as KPU horses may benefit from constant metabolic support until the body is back in balance. For our sweet itch affected horses, feed our LKLCARE blend during the typical sweet itch season.

Sept'21 - Edited to add:

It might also be worth getting bloods done - the following is courtesy of Dr Christina Fritz (please bear in mind this is translated from german):

"You can read a lot from the bloodworks. In KPU horses you usually find:

Erythrocytes = low (within normal, but low)

Hemoglobin = low (within normal, but low)

The horses also don’t build up stamina, you can work them to a certain level but then you kind of get stuck = not enough oxygen for more. Don’t confuse this with a normal anemia where horses lack iron. In KPU horses usually iron values are within normal, since horses have more than enough iron in their roughage.

Zinc = low (sometimes still within normal, but low)

Selenium = low (depending on the reference values, Selenium is usually way below normal, but values down to 40µg/l are normal)

Creatinine Kinase (CK) = high (normal value should be below 130U/L)

Lactate Dehydrogenase (LDH) = high (normal value should be below 400U/L)

Potassium = a little elevated when CK and LDH are high

Horses with high CK / LDH often need a very long time to warm up, riders will tell you that it takes 30-45 min for the horse to loose up and get flexible before you can even think about real training, they might tell you that the horse seems stiff every day like having muscle soreness. In sport horses that „stiffness“ is often the only symptom pointing into the direction of waste products being stored in the connective tissue system. In ponies and other „non-sport“ horses you might also see the lymph pads in the „saddlebag“ area and have a thick neck, full of lymph.

When you take bloodworks, you should also do Glucose from Sodium-fluoride-stabilised blood (beware not to fast the horse! 12h before taking the blood, let the horse consume hay nonstop, but no concentrates, no green pasture, no work) to get reliable results. Glucose should be below 4,9 mmol/l or 83 mg/dl. In sporthorses it is ok when the values are around the upper numbers, in non-sport horses and ponys you want them well below that.

So if everything in the bloodworks points into the KPU direction and also the feeding / health history of the horse (e.g. having been fed haylage in the past or anything like that) you can go ahead and treat for KPU. After all you can't do much harm with this. You supplement with Zinc (you need to feed about 1g/day to achieve over-dosage, you never reach this with normal supplements), organic Sulphur (MSM, you can give up to 15g / day / horse) which is hard to overdose as well.

Also you supplement with P5P (active Vitamin B6) and Vitamin B12, both being watersoluble Vitamins. So if the horse already has plenty, they will be excreted via the kidneys. And a gut restoration in my experience is a good idea for almost every horse, anyways :-)"

NB. Our KPU therapy plan is independently developed and distinct from Dr. Christina Fritz's approach. While I have studied with Dr. Christina Fritz and continue to do so, our method may differ.

Meanwhile, Click on the SHOP link below to see our KPU programme.