EMS/IR
- The Metabolic Horse

Content

1. If there’s one client enquiry I hear more often than probably any other ...
2. The Big EMS How&Why?
3. How we've got it so badly wrong
4. Same old, same old - everything starts with the gut
5. The EMS/IR label - what actually physiologically happens?
6. The real deal: Insulin Resistance
7. Managing the metabolic horse
8. Leptin Resistance - the permanently hungry horse
9. The overweight epidemic – it’s a hormonal perspective
10. Obesity - a hormonal mismatch
11. Research, implications, and strategies
12. The amino acid Acetyl L-Carnitine, nickname Alcar - the leptin game changer
13. Final thoughts
14. So how did I fix my meta crew?
15. Supporting naturally

1. If there’s one client enquiry I hear more often than probably any other ...

EMS/IR - and what a syndrome it is, usually accompanied with hindgut discomfort, bloating/gas, pounding digital pulses, footy if unshod, and never mind the fat pads and a crest the size of a small country. And no question - and a factor that's always forefront in the mind of the diligent owner/carer - their horse is very much at risk of, or in the throes of, laminitis.

These horses are usually already on restricted grass management, hay weighed to the n'th degree (and usually soaked, which carries its own significant concerns - see our blog post Steam it! Don't soak it!), and their carers already going to heroic levels to micro-manage their horse's every waking moment. And yet ... very little's working. Welcome to my world; that of the metabolic equine.

This is very close to my heart as out of our original herd of five horses, three were carb-intolerant natives. We sadly lost our beloved Cookie, our little gypsy cob mare, in Oct'22 when her Cushing's finally got the better of her, but we still manage my retired riding horse, Connemara Murphy (image above), who'll be 30 in May'24, and 23yo dartmoor pony MacAttack, our former semi-feral thug who we adopted back in 2017. I say 'former' as he's a whole lot nicer these days since we got his gut cleaned up and his diet right 😉.

I was first introduced to the equine 'metabolic' world around a year after I got Murf back in 2000. He was then aged 7, had just had his first colic episode with me, had a huge crest, and the vet diagnosed him as IR, whatever the heck that was back then. Seriously, no-one really knew, and no-one, including vets, knew how to manage it other than 'avoid molasses' while recommending beet as a feed. These days we know better - beet as a feed contains residual sugar (up to 25%); even unmolassed  carries a 7% sugar residue. (More on this in our 'The Feedbowl' page).

Then cut to 2017 and we took on MacAttack, who arrived with full-blown IR and the worst sweet itch I'd ever seen (hence why we took him on - the YO didn't take much convincing.) When we first adopted him he was gi-normous - a mound of fat pads and a whopping crest, and as we couldn't exercise him (way too thuggery) it didn't take much for him to stay chunky. His reputation also went before him - the village knew him well. Even a practitioner friend of mine had had first-hand experience of his thuggery a few years before I even met him, and was (quote) "terrified" of him. Hmmm ... No-one told me this before the leadrope was in hand, and sure enough it didn't take long for me feel his full force; he would literally drag me into bushes and allsorts. He got better tho ... 😉

I’m the first to put my hand in the air and say that back in those early days I struggled to understand what was going on with Murf. I was clueless. Well, it was over 20-years ago, and back then there wasn't much internet either to look stuff up on. And, lest we forget, laminitis was also considered solely as a hoof malfunction, whereas 2-decades on we now know that it's very much a systemic disrupted gut/endocrine (hormone)/multi-metabolic detoxification disorder, with the resulting laminitis just one of many presentations thereof.

Thankfully, these days I know a whole lot more about this now-epidemic EMS syndrome. Needless to say, I manage my horses very differently than I did 20-years ago, and touch all the wood in the world, and bar a brief LGL episode for MacAttack in 2020 (which was entirely my fault), they’re in pretty good shape, able to live out 24/7 on grass although with ad-lib hay, which frankly they all prefer anyway (clever pones).

2. The Big EMS How&Why?

"When we feed the soil with artificials, it creates artificial plants, which make artificial animals, which make artificial people, and they're all kept alive by artificial medicine."

Sir Albert Howard, the godfather of Modern Scientific Aerobic Composting, "An Agricultural Testament", 1943

'Metabolic' issues have only been around for the last 30+ years, mainly in developed countries where horses aren’t working animals anymore and kept more as pets for sports and leisure, and here's where we have this high rate of chronic equine metabolic syndrome.

Why? Because (a) the feeding, housing, and management of our modern horse is not like it used to be before bicycles/landrovers/tractors/taxis, and (b) us humans thought we knew better than the equine gut on how/what to feed and digest.

It all started to go wrong in the 1960's, the era of 'intensive farming', where our agri-crop landscapes changed beyond all recognition, and gallons of chemicals were sprayed on them. This was modern-day progress, and it was the direction we were all heading in; every-thing was advancing and changing for the so-called better. The wheat - and resulting gluten-intolerance - that we know today is very much part of this story, and it affects our horses as well, because almost every shiny feedbag in our feed merchants today includes a wheat by-product bulk filler (wheatfeed) as an ingredient.

Thing is, the wheat of today is something entirely different to what it was half a century ago, when our horses could happily - or should I say comfortably (as in gut comfort) - eat a grain feed. Cut to today, and they can't. (see our Wheat - the beginning of today's disease culture page in our Feeding our Horses Healthy/Why what we feed has to be right chapter off the main menu able.) Our wheat went from a nutritious, natural, 4ft-high spelt plant, to a mutant 18" GM frankenwheat, that without doubt - along with GM soya suddenly being thought of as the nutritional silver bullet - were the beginnings of today's disease culture as we know it. Whether human or horse 😐.

This means that for those of us buying manufactured horse feeds with numerous ingredients, and unless stated Organic, you can guarantee that your horses are eating pro-inflammatory, gut-damaging, intensively farmed crops, including weird wheat, which have been chemically treated and more often than not GMO mass-produced.

We also now live in an industrial toxic world. There’s chlorine and fluoride in our water (as well as a whole heap of other unpleasantries), and irradiation, pasteurisation and homogenisation of our foods. There's crop spraying, chemtrails and electro-smog (think cell phones and their towers which emit radiation). Basically our air and water are contaminated and our soil is sick.

Another unpleasant example. Mercury, formaldehyde and aluminium are hardcore heavy-metal toxins included in most vaccines. Individually they wreak havoc, but together they're like a nuclear bomb hitting the nervous system. And so the the list goes on. And why I'm obsessed about our entire product range being natural, as in non-synthetic, and our herbs being grown organically, or without the use of agri-chemicals.

There's more. For those of us living next to crop growing, the breeze carries the chemical sprays into the air which we all breathe, and for our horses it lands on their grazing pasture which they ingest. Then there's the ex-dairy farms which diversified as horse-livery businesses. You'll still find the same improved, chemically fertilised uber-rich rye-grass pasture that many of our horses now graze on. And, just for the record, rye grass can contain up to 36% sugars, and also contain endophytes which are not only toxic to the horse but can trigger both laminitis and foal abortion.

There’s no question. Every-thing has changed. Never in human history have we ingested chemical herbicides, fungicides or pesticides before, yet today we have plants that not only absorb them but can withstand them. They're even designed this way (GMO), so we’re all now consuming large amounts of these toxic 'ides' in our feeds, unless we purposely look to avoid them.

And so began the world as we now know it. And of course, you know me ... I've researched the life out of this and have a whole page dedicated to how it all went so horribly wrong. If you fancy a read here's the link: 'So began the world as we now know it' (in our 'Feeding our Horses Healthy' section). Poor yourself a stiff large one beforehand though ...

Meanwhile, back to our horses

50-million+ years shaped the horse that we see today. Our original wild horses lived in harsh environments on dry, long and stemmy, steppe/tundra/semi-desert grasses, which were low in nutrients yet high in fibre (in those stems), and over millenia the equine gut found ways to derive their energy from this very fibre.

This same principal applies today. Today's horse is no different. The equine gut system is exactly the same as that of its ancestors. To this day a horse’s gut is still designed to consume plants low in nutrients - as in low starch, sugar, fat and protein - but with a high cellulose-fibre content (from the stems), so when our horses meet our 21st century short, neon-green grass blades with no stems on their pasture, it blows their gut system - and metabolism - apart.

Instead of mooching contentedly for 20-30 miles/day to find water and a diverse diet of grasses, herbs, leaves, bark, fruits, roots, nuts and seeds, we plonk them on a small area of short grass blades, filled with super-high levels of sucrose/fructose/glucose. To get their essential fibre they’ve got to eat hay for the fibre-filled stems, so today's horse turned out 24/7 on neon-green grass blades will be both nutrient and fibre-deficient. Nuff said.

What we must never lose sight of is that the horse’s metabolism is remarkable; evolution has created the entire musculoskeletal system of the horse to not need much energy for walking. Their energy consumption is low because there’s not much ‘energy’ from their food; the hindgut biome (those friendly colonies of fibre-fermenting bacteria) produces the horse's energy source via three volatile fatty acids - proprionate, butyrate and acetate - from the fibre fermentation process (along with multiple other vital metabolites) - so they don’t have to walk too much.

And contrary to what we think, our modern-day pampered pet horses are actually designed for harsh living – us humans couldn’t survive it! Yet evolution designed horses to be constantly on the move to feed all day long, eating enough low nutrient/high fibre forage feed to produce enough energy and sufficient nutrients for their metabolism to work.

So where did it all go wrong? Ah ... that was down to us humans again. Along we came and started to domesticate the horse. We got it right to start with, originally continuing to feed feeding them how they’d fed themselves in the wild. But then came the advent of intensive farming practices in the 1950s/60s, and since then, the modern way of feeding our horses has very little to do with how evolution created them to feed over 50-million+ years.

No matter how hard we've tried to shake-up the horse’s already very well established inner-engine, we can’t change 50-million years’ of a finely-tuned biological system that works perfectly, in a few decades. It simply won’t work because our 21st century horse’s inner-engine is still exactly the same as that 50-million year-old wild horse. However, with mankind being a typical predator, determined to stubbornly overrule nature, we gave it a darned good go, and the end-results are now here for all of us to see.

How we've got it so badly wrong

• For starters we house them in a closed stable so if they're unlucky enough to stay in it all day they’ll move no more than around 800m/day. In an open barn they might get up to 2-miles.

• There’s little to no diversity in their diet and nowhere near enough roughage; we basically give our horses green grass and, er, dried grass. Our green pasture grass has no fibre whatsoever as it's short leaf blades only, unless we feed hay or let the grass grow long as stemmy 'standing hay', as it's known.

• Horses no longer have to move to get food, especially in winter because we tend to confine them more, so the energy we supply them is higher than their energy consumption. The average 1-hr trail ride with, say, 15-minutes canter barely burns off 1Kj of energy. It’s not work for the horse, only the rider! But because we think they've worked hard we feed them extra concentrate in the form of a high protein, factory-made, ultra-processed fake feed made from artificial, refined ingredients that should never see the inside of a horses’s gut. Back to our page 'The Feedbowl - what's really in those feedbags?'

• Final insult to injury? There's a trend to feed haylage over hay, usually for convenience, but now known to be totally inappropriate for the equine hindgut (where the fibre-fermentation takes place), because ...
• In order to ferment grass to haylage it needs lactic-acid bacteria, a known very-unfriendly, pathogen bacteria for the equine gut, and they produce (burp) lactic-acid as their waste, which comes out in gas form. When LA bacteria get into the GI tract it triggers:
• (a) acidosis in the hindgut.
• (b) bloat/inflammation in the intestines where inflammation should never be. The intestines are thin tubes so when they fill with gas and blow up it’s very, very painful, as well as a colic risk.
• (c) dysbiosis in the hindgut biome with the ever-multiplying colonies of LA bacteria ending up outnumbering the friendly, and very crucial fibre-fermenting bacteria.
• So, now we have an unfriendly bacterial overload (known as SIBO), as well as lactic-acid bloat/inflammation, which splits open the intestinal wall and creates leaky gut. Now we're in real trouble, as this now means undigested, putrefactive, toxic stomach contents and pathogen bacteria leak into the bloodstream. Boom! Cue a whole cascade of systemic toxic disruption, including laminitis. (All covered in our Gut System/Hindgut Acidosis page).

A quick nip back to our short green grass, and while it's very lovely for cows, full of super-high energy to maximise milk and meat yields, so more rich in nutrients - starch, sugar, fat and protein - and much less in fibre value, it's completely not suitable for horses as it’s very unlike the original horse's steppe/tundra/semi-desert grasses where the sugar content is usually below 4%. This is what the equine gut is adapted to. Our UK grass blade pastures are bad enough for our horse's gut system, but - it's also this grass that much of our hay is usually cut from.

These days we’re unlikely to find a hay with a sugar/starch value of less than 10%, with many nearer 12-14%, but we'll not dwell on that too much for now. Lets be conservative and work with the 10% number as round numbers are easier to work with. This means that 1kg hay = 10% sugar, which equals - wait for it - a whopping 100g of sugar.

Now imagine how much sugar is in 1.5-2% horse's bodyweight of hay, which is the daily recommended forage ration. No prizes for realising the equine gut and biology is simply not adapted to this huge volume of sugar. Then we add in a processed factory-made feed with weird ingredients, maybe a slosh of oil (bad - where's why), a few carrots/apples … So we’re now feeding a high-calorie, high-energy power feed, with waaaay too much starch, sugar, fat and protein, and seriously not enough exercise to burn it off, especially if we’re just a weekend trail-ride kind of rider (yep, hands up - that was me).

Its exactly the same for us humans. These days we tend to eat food that's easily accessible, too high in calories, nutrients and energy, then we don’t move enough so we’re not burning it off. Cue weight gain, diabetes type 2, heart disease and so on. And this is exactly what we see in our horses.

Even with world-renowned healthcare, it's said that up to 90% of western-world humans are walking around with undiagnosed insulin resistance. Why? Because most doctors aren’t testing for it correctly. Instead, they test fasting blood sugar (sound familiar?), which measures the glucose in our blood at least 8-hours after our last meal. Pointless! The problem is, no action is taken until our fasting blood glucose reaches 110 mg/dl, and even then, we’re usually just told to "keep an eye on it". What this really means is that we're becoming (or already are) insulin resistant.

Untreated blood sugar levels will continue to creep higher and higher until we're eventually diagnosed with type 2 diabetes and we're put on Metformin (sound familiar again? It's our vet's go-to drug for IR). At this point, our risk for comorbidities has already gone way up.

Same old same old - Everything starts with the gut

So, instead of testing the final destination (high blood sugar), far better to look at the journey it took to get there. And ... it doesn’t happen overnight. It can take years, even decades, to develop. Most chronic human conditions are rooted in IR - diabetes, cancer, heart disease, kidney disease - even Alzheimers is now being called diabetes type 3. And the primary driver? A diet abundant in quickly absorbed sugars and carbs that continually spike our glucose.

Let's pull this together back to our horses - it all begins with how we feed them, but we can expand this to lifestyle and management as well, i.e. housing and exercise. We need to reset our thinking back to the ways of evolution, which is why in the perfect world, having our horses on a track and shelter system, rather than restricted turnout and a stable, is a whole lot more equine-appropriate.

However, how we allow our horses to feed is key, as we need to go back to how a wild horse feeds itself, in order to reduce the nutrient value and energy consumption, as well as increasing movement. Our UK grasslands are overly high in many nutrients, yet cripplingly low in others - if we lose the balance here the small intestine gets overloaded with starch, sugar, fat and protein, and the hindgut gets disturbed because we don’t feed enough cellulose fibre through it, hence why we get dysbiosis shifts in the hindgut biome.

And there it is. Herein lies the mystery behind why the whole metabolism gets out of balance, just as it does for us 2-leggers. Thankfully, we've seen the last decade showing a ton of study and research into the human microbiome, with the science now knowing that a myriad of human ‘metabolic’ diseases are all down to microbiome disturbance in our large intestinal colons.

For our horses, we’ve historically got it round the wrong way. We've focused for so long on how to get the maximum nutrient value digested in the small intestine, that the large intestine – the hindgut, the mother of all the organs where all the vital stuff happens – has been ignored. Only now is research finally realising how much more important the large intestine is than the small intestine. Quick reminder - a horse is nothing more, and nothing less, than a hindgut fibre-fermenting machine, and as a result of our somewhat skewed feeding practices over the last half-century, we’ve highly neglected and disturbed the large intestine and colon, getting it all so badly wrong.

In a nutshell? We’ve fed our horses sick.

So, we absolutely need to get back to a more natural feeding of meagre low-nutrient fibre, i.e. hay, and meadow hay at that, in order to include numerous different grass species in the mix to feed the hindgut biome lots of prebiotic variety, with roughage diversity as well, i.e. barks, leaves, mosses (see our WildFed blend), and stop overloading the small intestine by feeding inappropriate processed ingredients. And there's another reason that this is so vital, because not only will the metabolism shift to a disease-state, but feeding all those extras completely overloads the liver as well, and that’s a whole other subject … see our KPU page.

So, let's get back to it. Our horse has just been labelled EMS so let's fix it.

3. The EMS/IR label - what actually physiologically happens

It's only really since the mid-2000s that vets have recognised the Equine Metabolic Syndrome (EMS), usually accompanied by obesity/fat pads and a high risk of laminitis.

What is an absolute given is that the metabolic horse is uncompromisingly carb-intolerant, which means a lifestyle on our green UK grass is the metabolic horse’s enemy, because grass is carb-rich in what's commonly known as simple sugars, namely fructose, sucrose, glucose, and a relatively new one - pectins, part of the grass leaf cell wall. Which - you've guessed it - are also full of their own sugar nutrients, because pectins are the grass plant's fuel to make the blade grow to a stem and seedhead.

Collectively these create the single biggest hormonal disorder a horse faces - insulin resistance, aka IR, and a body that's resistant/unable to perform the insulin hormone instruction (to move glucose from the blood into the cells). This then creates a damaging domino cascade in the body, driving those excess sugar calories into fat cells that produce other hormone messages that increase hunger (sugar cravings), slow down metabolism, prevent fat burning, and spike inflammation. ⁣

⁣In our human world it's called pre-diabetes or diabetes type 2. Current stats (2021) show that 1 in 2.5 of us here in the UK have pre-diabetes or type 2 diabetes, with 75% of us overweight, all suffering from too much insulin, the result of consuming too much of the 'white menace' - mountains of sugar and flour.

In women too much insulin turns estrogen into testosterone. The result is something misleadingly called polycystic ovarian syndrome, so now we think we have a problem with our ovaries. But It's not an ovarian problem; it's a dietary problem. The extra testosterone in women causes hair loss, facial hair, acne, and infertility. In other words, they become more like men. Worse, it's now being seen as causing ovulation issues where their whole reproductive hormones get screwed up and affects fertility. Seriously - infertility from eating sugar.

Men suffer too but the other way round. In men too much insulin converts their testosterone to estrogen, which is why affected men have man-boobs along with a bloated belly, with low testosterone, impotence, and loss of hair on their bodies. In other words, they become more like women. Long and short, it's major hormone disruption all round ...

That same high sugar and starch diet also spikes the cortisol (stress) hormone. When we eat a sugar-laden diet, the body literally perceives it as a stress, just like when that tiger's on our tail. Adrenaline and cortisol increase, worsening insulin resistance and increasing cravings for sugar and starch. ⁣⁣

Whether human or horse, our hormones are highly influenced by what we eat - it's all part of the body's biology whether we like it or not. The biggest factor impacting our internal communication system is IR, and whether human or horse, the key to it all is reversing it. Easy enough for us humans because we can take control over it with our next forkful. We can dump all that processed, plastic carton junk from the supermarket and go back to eating like our grandparents did - real food, with plants, veg, fibre, and natural protein.

However, not so easy for our horses because they rely entirely on us to get it right for them, and ironically, being grass/carb-intolerant is also the worst prognosis a horse can have, because a horse has evolved over millenia to live their life on, er ... grasses. Just not our ridiculously over-rich, over-carb'd, neon-green no-fibre leaf-blade UK grass that we happily turn our horses out on to eat.

Meanwhile, along with pectins, grass in the the growth phase is also full of fructans which also aren't digested in the small intestine, passing straight to the hindgut where the unfriendly LA-bacteria go manic, blissfully gorging on them. So, these bad bacteria multiply in their millions, killing off the friendly fibre-fermenting microbes (which, remember, are what produce the horse's energy as well as other vital metabolites), and worse, they then burp out their lactic-acid gas, aka inflammation, as their waste, which isn't friendly at all, as we mentioned earlier.

Here's how it all happens in real-time. process in full.

• Lactic acid gas lowers the hindgut pH value to acidic, when it should always remain at neutral.
• Cue 'metabolic acidosis' or 'hindgut acidosis'. Not to be confused with foregut ulcers - hindgut acidosis comes from the accumulation of lactic acidosis (there are no acid-secreting cells in the hindgut).
• Hindgut acidosis creates inflammation in the intestines, which when blown up enough actually tear the intestinal wall membrane, aka leaky gut.
• Meanwhile, when a friendly microbe dies, they release an endotoxin, which, along with undigested putrefactive toxic matter in the intestines, now leaks through that permeable gut wall into the bloodstream, creating an inflammatory reaction and sending the immune cells into manic overdrive. Cue autoimmune syndrome.
• Cue inflamed laminae which can occur literally within hours.
• Also cue a high colic risk which risks a blockage in the large intestine due to critical changes in the gut environment.

4. The real deal - Insulin Resistance

Meet the human equivalent of Type 2 diabetes, which is a cycle of craving the next sweet treat. It could be termed an addiction, because the metabolism - a set of biochemical reactions involved in the body's cells to sustain life - is demanding its sugar top-up. All due to hormone changes resulting in adverse hormone messages sent out by those fat pads (more on these further on), and specifically the leptin hormone, the appetite-control hormone, whose job it is to tell the body to stop eating because it's full.

However, due to disrupted hormone signalling, the leptin message starts to be ignored - now cue leptin resistance (covered further on).

Conventional human medical practice still has type 2 diabetes pegged as a blood sugar problem, yet in reality it's more about resistance to insulin and faulty leptin signalling, caused by chronically elevated insulin in the bloodstream, which blocks the leptin levels, and hence the leptin message. All diet-derived.

Insulin resistance doesn’t happen overnight. When most of the diet includes empty calories (as in, calories that don’t have one iota of regenerative health benefits) and an abundance of quickly absorbed sugars, the body's cells slowly become resistant to the effects of insulin.⁣⁣ So, the body responds by increasingly demanding more insulin to keep the blood sugar levels even, which, because of the insulin overload, eventually means the cells will become resistant to insulin’s message, resulting in insulin resistance.⁣⁣ ⁣

The higher the insulin levels are, the worse the IR. In human health the body starts to age and deteriorate, and it's now well known that insulin resistance is the single most important phenomenon that leads to rapid, premature aging and all its resultant diseases, including obesity (often referred to as diabesity), heart disease, stroke, dementia, cancer et al.⁣⁣

Appetite is now increased because of insulin’s effect on the brain chemistry. The insulin blocks the leptin hormone, so the body becomes more leptin resistant, so the brain is now no longer getting the “We're full now so stop eating” signal. So, the brain thinks the body's still starving, driving the brain to demand more sugar and fuel the sugar addiction.

Fructose makes matters worse. It's sent straight to the liver which starts converting it to fat, triggering more IR and causing chronically elevated blood insulin levels, driving the body to store everything eaten as even more fat; we see it in humans as belly fat. Another problem with fructose is that it doesn’t send informational feedback to the brain to let it know that a load of calories just hit the body, so the brain still think's we're starving. And so the cycle continues.

You simply can't balance a metabolic syndrome with a pill (Metformin), because metabolic diseases such as diabetes are dictated by the dietary lifestyle. However, there's good news coming out for human-driven type 2 diabetes in that it's now showing to be reversible via intermittent fasting and water-only fasting. I know, I know - horses can't intermittently fast or do a water-only fast, but stay with me for a second ...

A recent case series paper (published in BMJ Case Reports by Dr. Jason Fung), details how fasting can be used as a therapeutic alternative for type 2 diabetes. As noted by the authors:

"… demonstrates the effectiveness of therapeutic fasting to reverse insulin resistance, resulting in cessation of insulin therapy while maintaining control of blood sugars. In addition, these patients were able to lose significant amounts of body weight, reduce their waist circumference and also reduce their glycated hemoglobin levels."

Which is great news for humans. Not so great for our horses though without risking significant damage to the gut system as a whole, which then affects the body as a whole, so we have to manage the metabolic equine very differently.

I'll just stay with Dr Fung though, because he also explains IR in an easy-to-understand way, and gives us the simple solution to it all:

"Remember, the glucose goes into the cell, and insulin resistance is when the glucose doesn't get into the cell, so for years we've used this paradigm of lock and key. That is, the cell is sort of gated off. Outside the cell there's blood, and when insulin comes around (in the blood) it turns the cell's key, opens the gate and glucose goes in. So why is the glucose not going in? We look at the insulin receptor, the gate is completely normal. We measure the insulin and the insulin level is high, so there's plenty of it to do its job.

So, conventional medicine said something like, "Well, maybe there's something gumming up the mechanism. Maybe the lock's stuck so it doesn't open properly, therefore the glucose can't get into the cell."

Thing is, if that's happening it should mean the cell has no glucose and should therefore be starving for it. You should be losing lots of weight; you'd have a very thin liver. All your fat should just melt away, because if you think about untreated Type1 diabetes, where you don't have enough insulin, that's exactly what happens. The cell literally starves and everything just wastes away. But that's not what's happening here.

What's happening instead is that it's actually an overflow syndrome. The cell can't accept any more glucose because it's jammed full of glucose already. That's the reason you have insulin resistance. Insulin is trying to move glucose into the cell but the cell is already full of glucose, so it's really an overflow mechanism.

That's also why your liver is full - it's now a big fat liver because the liver is busy trying to get rid of all this glucose by turning it into fat. The bottom line is therefore, if Type 2 diabetes and insulin resistance are the same sort of thing, it's really about TOO MUCH SUGAR IN THE DIET.

And if you understand that the whole problem is too much sugar, then the solution is not to use more insulin to jam more glucose into an already full cell. The key is to get rid of it all. So, what you want to do is:

1) Don't put more sugar into your system, because you have too much sugar in already, and

2) Burn it off."

Simples.

Back to our metabolic horses and a recap

So, we know that:

1. A horse termed 'metabolic' is insulin resistant (IR), with insulin being the hormone that acts as the gateway responsible for transporting the glucose in the bloodstream into the cells, to then be used as a source of energy for that cell.
   
   
2. If this doesn’t happen, the glucose levels in the blood increase, which triggers excessive insulin release (from the pancreas) which leads to elevated levels of insulin. This can all be seen in a blood sample.
   
   
3. Insulin is also a major control hormone for many processes, one of those being storage – fat storage, that is.

So ...

• Elevated glucose leads to elevated insulin.
• Elevated insulin leads to excess body fat.
• Excess body fat leads to more insulin being released into the blood, and the body becomes insulin resistant.
• And ... elevated glucose and insulin is considered toxic and can trigger laminitis.

IR affects many horses but it's not always the same in every horse, although the ultimate consequences can be similar. Most afflicted have extra fat around the middle, but it doesn't always mean there'll be a crest. A horse may be tall or short, thin or porky, or any combination of these - and still have insulin resistance. The only sure way to know is with an insulin response test, but frustratingly we won't know the real numbers because vets insist on a fasting test, i.e. several hours after eating.

Horses affected with IR have signs similar to Cushing's, such as abnormal deposits of fat and being prone to laminitis. And that ‘cresty’ neck? It's basically a hormone factory that manufactures many signalling chemicals that have a major impact on health, and here’s where laminitis becomes a real risk, because elevated insulin and abnormal glucose metabolism causes changes in the vascular and cellular level of the hoof, which leads to inflammation of the laminae.

5. Managing the metabolic horse

Typically, our native horses are predisposed to this 'metabolic' disease because they have such a good survival mechanism; their systems are evolved to survive on what us humans call ‘fresh air’. However, give them a few acres of growing, neon-green leafy grass blades and they simply can't utilise the high glucose they're consuming from the grass as an energy fuel to stay healthy.

Again, let's remind ourselves again that a horse is nothing more, and nothing less, than a hindgut grass forage fibre-fermenting machine, emphasis on the word fibre, so we need to focus on feeding equine-appropriate, fibre-rich forage, i.e. hay, while managing/restricting green grass intake.

If you feed haylage, forget it. If you let a horse run out of hay, especially stabled overnight, forget it. Above all we also need to avoid high starch, high sugar, molassed, ultra-processed foods, stripping back the processed bulk-filler feeds full of pro-inflammatory gut-damaging ingredients.

Which links us nicely back to the aforementioned beet. Non-molassed sugar beet can contain up to 7% residual sugar in the pulp, molassed can contain up to 25% or more, but you'll never see this on the analysis, despite many feedbags advertising 'Safe for Laminitis'. It also tricks the metabolism into thinking sugar is on its way, which causes the body to pump out insulin - reminder, also the fat storage hormone - which lays down more belly fat, leaving the body hungrier and craving even more sugar and starchy carbs.

Something that tastes sweet but says it's 'low sugar' may sound like the perfect cure for sugar addiction, but it’s not, and here’s why. Normally, when something sweet is eaten, it’s accompanied by lots of calories but when it’s ‘low sugar’ yet still tastes sweet, this confuses the brain. It senses that the taste of sugar without the accompanying calories from glucose and fructose is Wrong with a Capital W, and it tries to correct the imbalance by making the body hungrier. Cue the beginnings of leptin resistance.

Not only that, but it also confuses the metabolism so slows it down, so less calories are burned each day.

Bottom line - there is no free ride with beet-related ‘low sugar’ or hidden molasses. They increases cravings, weight gain, IR and EMS. And they're addictive. And worse … they’re sold as safe for laminitics …

No question, the best prevention for IR/EMS horses is simply by not allowing our horses to become obese. Monitor weight, focus on a low sugar, low carb and high fibre hay diet, with the deficient nutrients supplemented back into the diet via forage-balanced minerals, alongside uber-restricted access to green grass. However, it’s very important not to starve the weight off your horse – they need all the nourishment they can get and must have a balanced, nutrient-rich, species-appropriate diet.

I’ll quote here from Dr Eleanor Kellon, Head Vet, ECIR Group, who dedicate their lives to supporting the IR/Cushings horses:

“The primary treatment for equines with IR only, and for equines with both Cushing's and IR, is a low carb and mineral balanced diet. Any grain products and pasture turnout should be eliminated until all signs of IR are totally absent, and reintroduced only with extreme caution. Low carbohydrate hay should be fed.

The ECIR Group has found that ESC + Starch at 10% or less by testing, can be fed safely to all but the most severe IR horses. Attempting to achieve weight loss by reducing feed intake below 1.5% of body weight can worsen IR and precipitate Hyperlipidemia. Hyperlipidemia is an alteration in fat metabolism resulting in elevated triglycerides and cholesterol and is potentially life threatening, especially in ponies, so DON'T STARVE the weight off your horse or pony.”

The IR horse, well, any horse for that matter, must have continuous adlib hay to eat, otherwise, apart from the acid-related foregut ulcer risk, they’ll go into manic overdrive, literally panicking about where their next food is coming from. This brings on hormone-reactive stresses of their own which we need to avoid in order to prevent the negative stress hormone (cortisol, which for the record also induces elevated insulin) being released. A wild horse can simply wander off and find more food, but the domesticated horse is entirely dependent on when we're going to feed them next.

Top Tip - Also, don't, whatever you do, feed straw to your horse, full stop, especially if you think it'll help them lose weight. See our 'Straw - don't feed it' page.

6. Leptin Resistance - the permanently hungry horse

(Leptin resistance - a condition that complicates weight management by disrupting the horse's natural appetite control mechanisms, leading to overeating and weight gain)

In the complex world of bodily functions, hormones play a pivotal role, orchestrating everything from metabolism to circadian rhythms to mood. These chemical messengers, very often underestimated, have a profound impact on one of our most basic functions: appetite.

We’re going to take a look at two of the lesser-known hormones, leptin and ghrelin, and how their critical roles regulate both hunger and fullness, and not just in our horses, but us humans too.

To put some perspective on this, have you ever wondered why, when you break out the box of chocolates, you literally can't stop eating them until the box has gone? Have you ever wondered why you can devour an entire packet of choc-chip cookies, yet you wouldn't do the same for a whole side of wild salmon?

It's not because we're weak-willed or lack self-discipline. It's not that we have no willpower. It's a biological reaction to sugar and carbs, and willpower won't work here.

Personally? I consider myself lucky - I have a savoury palate. Give me Marmite anyday, and no I don't touch sugar - we don't even keep it in the house. If we have visitors and I put the kettle on, suddenly I'm having to apologise profusely for the lack of sugar for their tea or coffee. But if husband brings home a box of Maltesers or Quality Street on a Saturday night, they're gone in one sitting. Shared, of course, but they're gone, and I'm both deliciously happy, courtesy of the massive dopamine reward hormone hit, yet horribly guilty (never mind feeling a bit ick) as it's always completely beyond my control. Sound familiar?

The overweight epidemic – it’s a hormonal perspective

Our modern world presents a paradox where, despite an abundance of food, the majority struggle with being overweight. So what’s driving our eating habits? The answer lies partly with leptin and ghrelin, two hormones that dictate when we feel hungry and when we've had enough. If their respective messages aren’t getting through, or if one is overriding the other, this will affect how appetite is regulated, triggering widespread weight issues.

This has only really been studied since the mid/late 1990s, but is very much an integal part of the IR/EMS horse and Diabetes type II human syndrome. And when it comes to our EMS horses, it's really important for us human carers to understand how and where it fits in.

First up, meet ghrelin, the ‘hunger hormone’, which is produced in the stomach, signalling the need to eat. Its levels fluctuate, peaking before meals and lessening after. On the flip side, leptin, the ‘satiety hormone’, signals fullness, which in the perfect world helps to regulate long-term body weight. However, if these signals are compromised, this leads to a perpetual state of hunger or overeating, despite the body's actual needs.

Ghrelin - the drive to eat

Ghrelin's role extends beyond simply signaling hunger; it also stimulates the release of the growth hormone from the pituitary gland, which has wide-ranging effects on energy metabolism and physical growth, i.e. height, bones and muscles. Interestingly, ghrelin levels increase not just before meals but also during periods of calorie restriction, affecting its role in long-term energy balance. Ghrelin's activity is modulated by factors such as sleep, stress, and exercise, making it a target for interventions such as dieting and promoting a healthy weight.

Leptin – the satiety instruction

Leptin, produced by adipose (fat) tissue, acts on receptors in the hypothalamus of the brain, where (sorry – science-y bit coming up …) it inhibits hunger by counteracting the effects of neuropeptide Y (a potent feeding stimulant secreted by the hypothalamus) and by stimulating the synthesis of α-MSH, an appetite suppressant. However, leptin's effectiveness can be weakened by inflammation and a diet’s fatty acid composition. Cue leptin resistance, which is what we see so often in our EMS horses.

It means that less leptin crosses the blood-brain barrier to signal satiety, so the brain thinks the body is still hungry, making our horses think they're still starving, so they continually eat despite adequate or even excessive fat stores.

Obesity - a hormonal mismatch

The discovery of leptin and ghrelin in the 1990s was a breakthrough for science in understanding obesity. It's not simply a matter of willpower; it's a complex interplay of hormones gone wonky. Leptin resistance, for instance, shows how the body ignores the signals of fullness, leading to continuous eating and weight gain. Similarly, elevated ghrelin levels, especially if stressed or sleep-deprived, makes the brain increase cravings for carbohydrates and sugars, i.e. the bad stuff.

Correcting the imbalance of leptin and ghrelin requires more than just dieting or exercising; it needs a functional approach to lifestyle changes. Dump the junk for real food, get adequate sleep, reduce stressors to lower cortisol levels (which when higher trigger more insulin release), and implement a regular exercise routine, even if it’s just walking – all foundational elements. 

Equine insights

Back to our horses, and here’s breaking news – those crests and fat pads aren’t officially made of ‘fat’. Those crests are adipose tissue, formed as a result of the excess insulin/blood glucose, and are almost a separate organ in themselves, created by the endocrine (hormone) system, because the body has now become leptin resistant, a condition that complicates weight management by disrupting the horse's natural appetite control mechanisms, leading to overeating and weight gain.

So, knowing that it’s the adipose (fat) tissue cells which produce the leptin hormone, you’d be forgiven in thinking that our IR cresty equines would produce even more of the leptin’s 'stop eating' instruction to signal the body to eat less food and normalise weight. Well, you'd be right. But because our cresty metabolic/IR/Cushings horses have become leptin resistant, overridden by the brain's demand for carbs, the vital message that they’re no longer hungry isn't being heard. They're only hearing the ghrehlin hormone telling them that they're still hungry and to eat more and more.

As with all hormone issues, leptin resistance is a complex issue and as I type, probably still not fully understood in the horse-world, but there are many factors that can negatively impact leptin levels including (and I quote from esteemed sources) :

• High fructose, simple carbs and grain consumption.
• High insulin levels.
• High stress levels.
• Overeating.

Kind of obvious I know …

Thing is, we’re up against powerful biochemical mechanisms created by food addiction - willpower becomes useless when sugar is in charge of the brain chemistry. It hijacks the brain, hormones, and metabolism, and the only way to fix this is to rewire the brain.  A researcher at the National Institutes of Health (NIH) actually theorises that the real regulator of a body's weight and metabolism isn’t so much the stomach but the brain chemistry - the brain can only hear the carb cravings, so we need to rewire the brain to send the opposite message and shut down that hunger, while working on reducing that crest where the adipose tissue sits. Don't panic - we go into how to do this a little further on ...

Now here's a thing. For those of us who've already been there, we already know how difficult it is to shift that crest! We know our horses are overweight and we need to do something, so thinking we're doing the right thing we restrict their feed/calories, but this doesn’t work and our cresty equines stay cresty. As Juliet Getty (Equine Nutritionist) says:

“The reason is simple . Dieting restricts calories, which lowers the metabolic rate. Weight loss may occur at first, but the body then goes into 'survival mode' and starts to hold on to fat and becomes sluggish in burning calories, making it extremely easy to put all the weight back on.”

Restricting forage is also detrimental, especially for our metabolic equines, because, as we know, the stress involved increases the stress hormone cortisol, which then induces elevated insulin, which as we know promotes the very thing we're trying to reduce - fat storage. And so we’re back where we started.

For the record, Dr Kellon says that all IR horses have leptin resistance, so there we go. Whether we like it or not, we should be factoring leptin resistance into the whole IR/EMS scenario.

Research, implications, and strategies

Recent human studies have shed light on how high-fat diets can lead to alterations in gut microbiota, which in turn impact the production and function of ghrelin and leptin. No surprise, the conclusions suggested a (very obvious) link between diet, gut, and hormonal regulation of appetite.

Furthermore, research into intermittent fasting and time-restricted feeding has revealed significant impacts on the regulation of these two hormones, offering promising avenues for managing appetite and metabolic health. Which of course, we can’t ever do with our horses. But here’s what we can do, and yes, I know it’s all obvious stuff:

1. Nutritional interventions - research and anecdotal evidence shows that Acetyl L-Carnitine (Alcar) plays a significant role in managing leptin resistance, supporting more effective metabolic regulation.
2. A species-appropriate fibre-rich diet will improve leptin sensitivity and reduce ghrelin levels, promoting satiety and reducing hunger, so I can’t emphasis enough how important it is to dump those feeds with bulk fillers that trigger gut sensitivities (see our ‘The Feedbowl’ page for the main offenders).
3. Incorporating anti-inflammatory foods such as omega-3 fatty acids (linseed) can combat inflammation and improve hormonal signalling. 
   
   
4. Lifestyle – I know, I know, but you can’t dispute the science. Regular physical activity, even if it's just walking, is shown to enhance leptin sensitivity and reduce ghrelin levels. Additionally, prioritising rest/sleep and managing stress can help normalise ghrelin and leptin levels.

So let's talk a bit more about Alcar ...

The amino acid Acetyl L-Carnitine (Alcar) - the leptin resistance game changer

When I was swatting all things leptin for Murf (around 2013/14), I came across an interesting article on a forum, written by another horse owner who was also struggling. Quote:

“I read one piece of equine research (a 2004 study by Woolworth et al) ... on the specific subject of l-carnitine and leptin … which indicates that l-carnitine boosts blood concentration of leptin.”

So, more leptin hormone in the bloodstream courtesy of L-Carnitine (Alcar)? So surely a greater chance of the leptin message being heard? The author also wrote that coincidentally she saw Alcar being advertised as a potential human weight loss drug:

“The last time I spoke to a physician about this, albeit not an endocrinologist, I was given to understand that the advertisement isn't entirely spurious, so I assume there is something I'm missing about how leptin resistance works and/or about how l-carnitine works with leptin.”

Very generously, she edited her post 6-months later to say:

“Update … after 6 months of l-carnitine supplementation, leptin blood levels decreased from abnormally high to within normal range. Not a controlled experiment though.”

So to the good news - research and anecdotal evidence shows that Acetyl L-Carnitine (Alcar) plays a significant role in managing leptin resistance. By addressing leptin resistance, we can support more effective metabolic regulation.

Final thoughts - a multifaceted approach to appetite control

The Equine Metabolic Syndrome (EMS) and Insulin Resistance (IR) both highlight how modern management practices have drifted from their natural evolutionary needs, promoting leptin resistance. It’s a given that addressing these issues through diet and lifestyle adjustments is crucial for their well-being.

By understanding the science and addressing the dysregulation of leptin and ghrelin’s place in appetite control, we can look towards improved wellness for our EMS horses. It's perfectly possible to reset their biology rather than fighting against it, by adopting a functional approach that combines dietary changes, lifestyle adjustments, and, where appropriate, targeted interventions to restore hormonal balance.

Personally? I can honestly say, no word of a lie, that getting diet right and feeding Alcar to my metabolics - Murf, Cookie and MacAttack - was a game-changer. It made a profound difference to their original fat-pad, cresty state. Pro-Found. I started feeding it in 2014 and still do to this day. Our TB mare, HRH Queen Carmen, also gets it to help with her musculoskeletal issues (all explained on our Acetyl L Carnitine product page). I swear by it - even take it myself. Product link as per previous sentence, and also in the Shop link below.

7. So how did I fix my meta crew?

A quick recap. As per the first line in the ECIR para above, IR horses need a low carb, high fibre, nutrient-balanced diet by way of hay and specific minerals that our UK forage is deficient in. Micronutrients are the key to getting the body's chemistry rebalanced, and for me and Murf, other than his herbal support, I noticed hugely positive changes in his hoof integrity with mineral balancing, as in what became our EquiVita forage-balanced mineral solution back in 2013, and thereafter all my horses.

Naturally I restricted his grass intake (skid row grass track system with hay stations), and also put together a blend of blood-glucose-busting herbs which, with a few tweaks to give Murf's filtration organs a gentle daily detox alongside blood cleansers and the all-important gut support, eventually became our MetaTonic, which these days is hands-down our best selling herbal blend next to our DuoBute pain/anti-inflammatory support, which he also got, and still does as a preventative.

And ... here's a bit of trivia for your day - our MetaTonic also contains Galega officinalis (Goat’s Rue) which is known to help regulate blood glucose levels. Remember the pharma drug Metformin? Well, this is the herb that was originally synthesised by scientists back in the day to create Metformin, which is the first drug of choice for human Diabetes Type II and also prescribed by vets to horses. TaDah indeed. 😉

Summer of 2014 I starting giving Murf Alcar, and it seemed like the final part of the puzzle. This got him to a point where his gut and brain no longer seemed to crave food any more - his crest literally vanished in a matter of weeks and it's never come back. These days he’s now a really mellow, balanced, sweet old man, who hasn't mugged me for his feedbowl for, crikey, years now - in fact, I can't remember the last time he did. And as an extra advantage of the Alcar, he also has a much looser, freer, peripheral movement as well, swinging his hips like Elvis. 😉

Murf and MacAttack are permanently on MetaTonic and I continue to pre-empt high pulses and the risk of any laminae inflammation by keeping them both on our DuoBute pain/anti-inflammatory blend during the spring/summer/autumn grass growth. These days they’re all doing great, and - Newsflash - they all live out 24/7 - on grass! Even better, from where I used to put up a track system in March-ish (hay stations all round) which then came down late Oct/Nov allowing them access to winter foggage from the middle, since 2020 they've had permanent access to their field, albeit ancient sheep moorland so it's ideal low-nutrient pasture. They also get adlib access to unsprayed meadow hay all year round, and, clever ponios, they seem to prefer it to the grass - what's not to love about that?!

That's not to say I'm suggesting newly diagnosed EMS owners do the same. To get my horses to this stage has taken years with lots of trial and error, but we finally got there, to where I'm now completely comfortable with their 'metabolic' state. That said ...

Update Sept'21 - Since studying with Dr Christina Fritz, I learned all about the multi-detoxification disorder known as Cryptopyrroluria, nicknamed KPU. I was quite certain that Mac was a KPU candidate, and started managing him as such. A year on and he was a changed man, and remains so to this day (2024).

So let's get to it. Here's the fix-kit ...

8. Supporting naturally

• Detox - start with resetting your horse with our OptimaCARE, a full-body detox/gut restoration programme to clear out the toxins, and reset the gut:liver:kidneys pathway. While there are still toxins flooding the system there's no open pathway to resetting their inner engine. 
• Important - if your horse is in the throes of laminitis, don't detox until your horse has been walking comfortably for at least 2-weeks.

• Alongside this, relook at what you're putting into the feedbowl as the carrier for the supplements - you absolutely need to get rid of those empty calorie, bulk filler feeds. Aim for as low starch as possible - Agrobs (my preferred feed brand) do a fantastically low-starch chaff, namely their Leitchgenus - it's even been nicknamed 'fatties chaff'.
• For help in putting together the ideal feedplan, have a look at My Feed Recommendations page.

• Minerals - For the metabolic horse where hay plays a vital part in the diet due to grass restriction, it's all the more important to supplement back the missing nuts and bolts into the feedbowl to balance their forage and hay.
• If your horse is off grass completely - and many are - remember that hay alone will not a nourished, healthy horse make, being not only deficient in minerals but also the vital omega-3 EFA, so we recommend our VitaComplete balancer.
• If your horse is on restricted grass or with hay in the diet (say, if stabled overnight), you'll need to add pro-rata micronised Linseed for the omega-3. NB - it's already included in our VitaComplete.
  
  
• Salt - Also, don't forget Salt, a critical nutrient, 4g per 100kg bodyweight/day or double this if in hard work/sweating. Again, included in our VitaComplete.
  
  
• Support the EMS with our organic herbal MetaTonic blend - look to be feeding this from at least a month before the spring grass is expected, until the grass stops growing. For the record, some of our clients (including me) feed it year-round.
  
  
• Alcar - Add the amino acid Acetyl L-Carnitine to reverse the leptin resistance.

Also useful

• Feed our BiomeTonic to keep the gut environment friendly (and unfriendly for pathogen microbes and parasites). I found with MacAttack that he did well with it fed for a couple of weeks every couple of months.
  
  
• Have a look at our WildFed blend to add valuable roughage diversity back into the diet, especially useful for those livery horses on postage-stamp individual fenced-off turnout with no natural hedges or trees to browse on. Chuck a handful over hay or in the feedbowl every couple of days or so.

Update - June'21

A recent 'Dr K's Horse Sense' post shows that onset pain may affect IR/ACTH testing, as it's known that both ACTH and cortisol levels are more likely to be higher than normal ranges during acute illness.

A 2020 German study looked at hospitalised horses in pain from various issues including colic, laminitis, orthopedic, and with no clinical signs of PPID. The study found "acute pain resulted in markedly elevated cortisol and insulin resistance." Since acute stress, wounds etc. can cause the adrenal glands to release cortisol without ACTH increase, it’s unclear from that study if acute pain will influence ACTH – although it certainly increases insulin.

The thinking is that testing for both ACTH and insulin levels should be avoided in the first 24-hrs after onset of pain.

And lest we forget, for some horses just seeing the vet's car pull up can also induce stress! So again there's a risk of elevated readings. See the full article here: https://drkhorsesense.wordpress.com/2021/06/08/insulin-acth-and-pain/

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