"My horse has just been diagnosed EMS."
If there’s one client enquiry I hear more often than probably any other, it’s metabolic-related. EMS/IR, very often with hindgut discomfort, bloating/gas, high digital pulses, fat pads and a crest the size of a small country. And no question - they're very often a very definite risk of - or in the throes of - laminitis.
These horses are usually on restricted grass grazing, ad-lib hay (very often soaked, which carries it's own significant dangers - see our blog post Steam it! Don't soak it!), and their guardians have to micro-manage their every waking moment. Welcome to my world; that of the metabolic equine.
This is very close to my heart as out of my four horses, three are carb-intolerant natives - my now retired riding horse, connemara Murphy; our daughter's now retired pony, gypsy cob Cookie; finally, 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 I got his diet right 😉. Murf was diagnosed IR aged 7, Cookie's also been a confirmed Cushing's since 2014, and Mac's a given IR - when we first adopted him he was a mound of fat pads and a whopping crest.
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 spasmodic colic episode with me, had a huge crest, and the vet declared him Insulin Resistant.
I’m the first to put my hand in the air and say that in those early days I really struggled to balance his system. I was clueless; there was so little information available and I totally relied on my vet, who could only offer "avoid molasses". There were very few answers coming back to my numerous questions regarding the How & Why of this apparent 'metabolic' state Murf was afflicted with. Back then, laminitis was also thought of purely as a hoof condition, whereas 2-decades on we now know that it's very much a a systemic disrupted gut/endocrine (hormone) condition with the resulting laminitis just one of many symptoms thereof.
Thankfully, these 2-decades on, I know a whole lot more about this now-epidemic syndrome. Needless to say I manage my horses very differently to 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 adlib hay which frankly they all prefer anyway.
The Big Question - 'Why'?
Chronic metabolic issues have only been around for the last 20-40 years, mainly in developed countries where horses aren’t working animals anymore, kept more as pets for sports and leisure, and its in this category that we have this high rate of chronic metabolic syndromes in our horses. Reason? Simply because (a) the feeding and housing of our modern horse is not like it used to be before bicycles/landrovers/tractors/taxis, and (b) us humans got involved, thinking we knew better than the equine gut on how to feed and digest 😉
50-million+ years has shaped the same horse that we see today – those original wild horses lived in harsh environments on dry, stemmy, steppe grasses which were low in nutrients yet high in fibre (all the fibre is in those stems), and over the millenia the equine gut found ways to derive their energy from this very fibre.
This same principal applies today – our modern day’s equine gut system is exactly the same as that of its ancestors. To this day a horses’s gut is still designed to consume plants low in nutrients - as in starch, sugar, fat and protein - but with a high cellulose-fibre content, so when they meet our 21st century neon-green grass blades with no stems, it blows them apart. And instead of walking slowly for 20-30 miles/day to find water and a meagre yet diverse diet – grasses, herbs, leaves, branches, fruits, roots, nuts and seeds – we plonk them in a small area of grass blades with super-high levels of sucrose/fructose/glucose, or if they’re lucky, hay, where they’ll get fibre-filled grass stems.
The horse’s metabolism is remarkable – evolution has created the whole musculoskeletal system of the horse so they don’t need much energy for walking – their energy consumption is really low because there’s not too much ‘energy’ from their food (the hindgut biome produces the energy via three volatile fatty acids - propionate, butyrate and acetate - from the fibre fermentation) so they don’t have to walk too much. They’re designed for harsh living – us humans couldn’t survive it – yet horses can because evolution has made them to be constantly on the move to feed all day long, eating enough low nutrient/high fibre feed to gain enough energy and sufficient nutrients for their metabolism to work.
Then along came us humans. When mankind started to domesticate the horse, originally we continued feeding them how they’d fed themselves in the wild. It’s only in last 20-40 years that with the advent of intensive farming practices, us humans have stepped in thinking we know better, and sadly, today’s modern way of horse feeding has very little to do with what evolution created in 50-million+ years.
No matter how hard us humans have tried to shake-up the horse’s very well established inner-engine, we can’t change 50-million years’ worth of healthy practice in 20-40-years - it simply won’t work because our horse’s inner engine is still the same as the wild horse. We gave it a darned good go tho, and the end-results are there for all of us to see.
So how have we got it all wrong for our horses?
- 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 it 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 grass and, er, dried grass. Our green pasture has no fibre whatsoever as it's grass leaf blades only, unless we feed hay or let the grass grow long as stemmy standing hay.
- Horses no longer have to move to get food, especially in winter, so the energy supply is higher than their energy consumption. The average 1-hr trail ride with 15-minutes canter (I don’t even think I could sit 15-minutes canter anymore!) barely burns off 1kj of energy. It’s not work for the horse, only the rider! But because we think they worked hard we feed them extra concentrate in the form of a high protein, factory-made processed feed made from ingredients that should never get inside a horses’s gut. See our page 'The Feedbowl - what's really in those feedbags?'
- And … the final insult to injury, for the last 20+ years the trend has been haylage over hay, usually for convenience, but so incredibly damaging to the equine hindgut (where the fermentation takes place), because in order to ferment grass to haylage, it needs lactic-acid bacteria, which produce lactic-acid as their waste. This creates (a) 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 – cue colic risk; and (b) dysbiosis in the microbiome where there’s more of the pathogen biome bacteria than the beneficial, friendly fibre-fermenting bacteria, so now we have SIBO (small intestinal bacterial overload) and leaky gut, which leaks undigested toxic stomach contents and pathogen bacteria into the bloodstream. Cue laminitis. All covered in our Gut System chapter.
A quick nip back to our grass, and it's very lovely for cows, full of super-high energy to maximise milk and meat yields, so it’s more rich in nutrients and less in fibre value. Completely not suitable for horses as it’s very unlike steppe grasses where the sugar content is usually below 4%, which is what the equine gut is adapted to. The grass itself is bad enough for our horse's gut system, but - it's also this grass that our hay is usually cut from.
These days we’re unlikely to find a hay with a sugar value of less than 10%, with many nearer 12-14% but we'll not dwell on that. Being conservative and working with the 10% number, this means that 1kg hay = 10% sugar, which equals a whopping 100g of sugar - now imagine how much sugar is in 1.5-2% bodyweight! The horse is simply not adapted to this. Then we add a processed factory-made feed with weird ingredients, maybe a slosh of oil, a few carrots/apples … so altogether we’re feeding a high-calorie, high-energy power feed, with too much nutrition - starch, sugar, fat and protein - and … not enough exercise to burn any of it off, especially if we’re just a weekend trail-ride kind of rider (yep, that was me - I say was as my lot are all retired now).
A quick digress to us humans and it's exactly the same for us – these days we tend to eat food that is 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 we see exactly the same in horses.
So, pulling this altogether, it all begins with how we feed our horses and where we've got it wrong, but we can expand that to lifestyle as well – housing and exercise. We need to go back to the ways of evolution – it’s much better to have a track and shelter system than minimal, and often restricted, turnout and a stable. However, how we allow our horses to feed is key as we need to go back to how a wild horse feeds itself, to reduce the nutrient value and energy consumption, and increase movement; if we lose the balance here the small intestine gets overloaded with starch, sugar, fat and protein, and the hindgut gets disturbed because don’t feed enough cellulose fibre, so we get dysbiosis shifts in the hindgut biome.
TaDah – herein lies the mystery behind why the whole metabolism gets out of balance, and as before, it’s the same for humans; these days there’s a ton of research into the human microbiome, and science now knows that a myriad of human ‘metabolic’ diseases are all down to microbiome disturbance in our colons.
For our horses, 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 – 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. Thanks to our somewhat skewed focused feeding practice over the last few decades, we’ve highly disturbed and neglected the large intestine and colon. In a nutshell? We’ve fed our horses sick.
We absolutely need to get back to a more natural feeding of meagre, low-nutrient fibre (hay) with roughage diversity (barks, trees, leaves - see our WildFed blend), and stop overloading the small intestine by feeding inappropriate junk feedstuffs. And there's another reason that this is so vital, because not only does 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 …
So, meanwhile. Our horse has just been labelled EMS so we need to address it, understand it, and fix it.
The EMS / Insulin Resistance label
It's only really since the mid-2000s that vets have recognised the Equine Metabolic Syndrome (EMS) among horses, usually recognised by obesity/fat pads and an extreme risk of chronic laminitis. I say 'usually', but recent science (2016) is now showing this isn't necessarily always the case. As Dr Eleanor Kellon has recently posted, "Obesity is widely believed to cause insulin resistance in people but that's not necessarily the case in horses. ... Banase et al  found that markers of inflammation in skeletal muscle were actually lower in horses that were obese, and lowest of all in obese horses with elevated insulin – the exact opposite of what would be expected in a human."
What is an absolute given, though, is that the metabolic horse is uncompromisingly carb-intolerant, which means a lifestyle on our neon-green UK grass is the metabolic horse’s enemy, because grass is carb-rich in what's known as simple sugars, namely fructose, sucrose and glucose, and pectins, part of the grass leaf cell wall and full of its own sugar nutrients.
It creates 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 which creates a domino effect. It drives all those excess sugar calories into fat cells that produce other hormone messages that increase hunger, slow 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, and 75% of us are overweight, all suffering from too much insulin, the result of consuming too much of the mountains of the 'white menace' - sugar and flour.
And it's everywhere! Just last week I was looking at the ingredients of an Aloe Juice that a friend had. She's a little bit overweight, has occasional acne breakouts, and is both uncomfortably conscious about it, enough to now affect her mood levels. She loves this drink, which promises gut health and vitality, and proudly showed it to me. For sure there was aloe, but there was also cane sugar and added sweetener! I mean, seriously ... How different is this to beet feeds being advertised as 'safe' for laminitics?
In women too much insulin turns estrogen into testosterone. The result is something misleadingly called polycystic ovarian syndrome. 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. In men the testosterone gets converted to estrogen, which is why affected men often have man boobs along with the bloated belly, with low testosterone, impotence, and loss of hair on their bodies. In other words, they become more like women. Major hormone disruption ...
The same high sugar and starch diet also spikes the hormone cortisol. 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. The biggest factor impacting our internal communication system is reversing that insulin resistance, and for us humans, it's easy because we can take control it with the next forkful - the cure is dumping all that processed junk in plastic cartons from the supermarket and go back to eating like our grandparents did - a real food, plant, fibre and phytonutrient-rich diet.
Not so easy for our horses though, as they rely completely on us to get it right for them, and ironically, being grass/carb-intolerant is also the worst prognosis a horse can have, as a horse has evolved over millenia to live their life on grasslands. Just not this ridiculously over-rich, over-carb'd, neon-green leaf-blade UK grass that we turn our horses out on to eat. It's completely the wrong type of grass, full stop, and I can't emphase this enough. Reminder - a horse is nothing more, and nothing less, than a hindgut fibre-fermenting machine, and the only source of the right fibre their bodies need is in the stems of long, dry grass, not short, growing, green grass leaves/blades.
The short-leaf stage of grass that's growing is also high in pectins, growth components of the leaf cell walls - they're a crucial part of the growth process to make that grass plant grow to a lovely long stem with a seed head on top. And ... pectins have their own sugar nutrients; along with the grass fructans which also aren't digested in the small intestine, they pass straight to the hindgut where the unfriendly resident lactic-acid bacteria go into overdrive, blissfully gorging on them, so they multiply in their millions, killing off the friendly hindgut fibre-fermenting microbes (which produce the horse's energy) and producing lactic-acid as their waste, which isn't friendly at all - the one thing that should never be in the GI tract is lactic-acid because ...
- It lowers the hindgut pH value to acidic, when it should 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.
- Hindgut acidosis creates inflammation, which creates a leaky gut wall membrane.
- Meanwhile, when a microbe dies (those friendlies), they release an 'endotoxin', which, along with undigested toxic matter in the intestines, now leak through that permeable gut wall into the bloodstream, creating an inflammatory reaction and sending the immune cells into manic overdrive.
- Cue inflamed laminae which can occur literally with hours.
- Also cue a high colic risk depending on the severity of the gut damage and risk of large intestine blockage due to critical changes in the gut environment.
So what’s this metabolic syndrome all about?
In essence it's similar to the human equivalent of Type 2 diabetes, which is a vicious 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; it's job is to tell the body to stop eating because it's full, but through disrupted hormone signalling, the leptin message starts to be ignored - now cue leptin resistance.
Conventional medicine still has Type 2 diabetes pegged as a blood sugar problem, yet in reality it's more about insulin resistance and faulty leptin signalling, caused by chronically elevated insulin which blocks the leptin levels, and hence the leptin message. In other words, it's a diet-derived condition.
Insulin resistance doesn’t happen overnight. When most of the diet includes empty calories 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 eventually means the cells will become resistant to insulin’s call, resulting in insulin resistance.
The higher the insulin levels are, the worse the insulin resistance. in human health the body starts to age and deteriorate, and it's well known that insulin resistance is the single most important phenomenon that leads to rapid, premature aging and all its resultant diseases, including obesity - aka diabesity, heart disease, stroke, dementia, cancer et al.
Appetite is increased because of insulin’s effect on the brain chemistry. The insulin blocks leptin, so the body becomes more leptin resistant, so the brain is now no longer getting the “We're full now so stop eating,” signal. Instead, the brain thinks the body's continually starving. The pleasure-based reward center is triggered, driving the brain to demand more sugar and fuel the sugar addiction.
Fructose just makes matters worse. It heads straight to the liver where it starts manufacturing fat, triggering more insulin resistance 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. Over time, the liver develops what's known as ' fatty liver', which generates more inflammation. Chronic inflammation causes more weight gain and what's now being called diabesity. 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. And so the cycle continues.
You can't treat a metabolic syndrome with a pill, 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.
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, because their gut system is simply not evolved to 'fast' for any period of time, short or long, 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.
Staying with Dr Fung, he explains IR in an easy-to-understand way, whether human or horse:
"Remember, the glucose goes into the cell, and insulin resistance is when the glucose doesn't go out of 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 key, opens the gate and glucose goes in. So why is the glucose not going in? You can measure the insulin and the insulin level is high. You can look at the insulin receptor, the gate is completely normal.
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."
There's a huge problem with this sort of paradigm, because if that is happening, it should mean the cell has no glucose and should therefore be starving. 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 Type 1 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.
In Type 2 diabetes you see that people are generally obese, they have large abdomens. What's happening instead is that it's actually an overflow syndrome. The cell can't accept any more glucose because it's jam packed 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.
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."
A bit more about glucose
No surprise, the word glucose comes from the Greek word for 'sweet'. It's a type of sugar we get from carbohydrate foods, and the body uses it for energy. As it travels through the bloodstream to the cells, it's called blood glucose or blood sugar.
Insulin is the hormone that moves glucose from the blood into the cells for energy and storage. People with diabetes have higher-than-normal levels of glucose in their blood. Either they don't have enough insulin to move it through or their cells don't respond to insulin as well as they should.
Glucose mainly comes from foods rich in carbohydrates. When eaten, the food bolus travels down the esophagus to the stomach, where the carbohydrate digestive enzyme (amylase) begins the process of breaking those carbs down and glucose is released. It's absorbed through the small intestine into the bloodstream, and once there, it needs the insulin hormone to help it get into the body's cells.
The body is designed to keep the level of glucose constant in the blood. The pancreas constantly monitors blood sugar levels and when blood glucose levels rise during eating, the pancreas releases insulin into the bloodstream, to act as the key to unlock muscle, fat, and liver cells so glucose can get inside them.
Most of the cells in the body use glucose along with amino acids (protein) and fats for energy; it's also the main source of fuel for the brain, where nerve cells and chemical messengers need it to help them process information; without glucose, the brain simply wouldn't be able to function. After the body's used the energy it needs, the leftover glucose is stored in little bundles called glycogen in the liver and muscles.
It all goes wrong when there's too much blood glucose, so the pancreas makes more and more insulin to move the glucose into the cells, which are already jammed full of glucose, so the whole process falls apart and begins the damaging inflammatory syndrome of Insulin Resistance.
A bit more about insulin
So let's get back to our metabolic horses. A horse termed 'metabolic' is insulin resistant (IR), insulin being the hormone responsible for transporting glucose in the bloodstream into the cells, to be used as a source of energy for that cell.
Insulin’s role is to act as the gateway for the body’s cells to move the blood glucose into the body's cells, where it's then converted/used as energy. If this doesn’t happen, the glucose levels in the blood increase, which triggers excessive insulin release which leads to elevated levels of insulin - this can all be seen in a blood sample.
Insulin is also a major control hormone for many processes, one of those being storage – fat storage, that is.
Insulin resistance 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.
Here’s the rub:
- 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.
Horses affected with IR have signs similar to Cushing's, such as abnormal deposits of fat and being prone to laminitis. The ‘cresty’ neck is basically a hormone factory that manufactures many signalling chemicals that have a major impact on the health of the horse, 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.
Typically, our native horses are predisposed to this disease because they have such a good survival mechanism; their systems are evolved to survive on what us humans call ‘fresh air’. Give them a few acres of growing, neon-green, leafy grass and they simply can't utilise the high glucose they're consuming from the grass as an energy fuel to stay healthy.
On our part, we need to remember that a horse is nothing more, and nothing less, than a hindgut fibre-fermenting machine, so we need to focus on feeding equine-appropriate, fibre-rich forage, i.e. hay, while managing grass intake. Above all we need to avoid high starch, high sugar, molassed, ultra-processed foods, stripping back the junk feeds full of pro-inflammatory gut-damaging ingredients.
Which links us nicely to a quick digress to 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. It also tricks the metabolism into thinking sugar is on its way, which causes the body to pump out insulin, remember - 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 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.
Managing the metabolic horse
The best prevention for IR/EMS horses is by not allowing our horses to become obese. Monitor weight, focus on a low sugar, low carb and high fibre, dried-forage diet, with the deficient nutrients supplemented back into the diet via forage-balanced minerals, alongside restricted, monitored access to 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.
The IR horse, well, any horse for that matter, must have continuous forage/hay to eat, otherwise, apart from the acid-related foregut ulcerogenic risk, they’ll go into manic overdrive, literally panicking about where their next food is coming from. This brings on hormone-reactive stresses of its 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 how we manage them.
Which means, starving the IR pony to slim is absolutely not the way to go. I’ll quote here from the 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 - (not haylage, due to the increased lactic acid bacteria which will get into the gut) should be fed.
The ECIR Group has found that ESC + Starch at 10% or less by testing, or hay to remove soluble sugars, 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 Hyperlipemia. Hyperlipemia is an alteration in fat metabolism resulting in elevated triglycerides and cholesterol and is a potentially life threatening condition, especially in ponies, so DON'T STARVE the weight off your horse or pony.”
Dr Eleanor Kellon, Head Vet, ECIR Group
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. These pads of adipose tissue are almost a separate organ in themselves, created by the endocrine (hormone) system, which continues to release instructions to the body that it’s hungry, because remember, the body has now become leptin resistant. So let's talk a little more about the leptin hormone.
This is a relatively new subject having only really been studied in the last few years, but very much related to the IR/EMS horse (and Type II human). In the case of the EMS horse it's really important for us human carers to attempt to get our heads around it.
So to leptin, and it's actually a friendly master hormone in the body that controls hunger and feelings of satiety. Grehlin is the master hormone that says the body's hungry; leptin is the one that says the body's full so stop eating. Leptin is secreted from adipose (fat) tissue, and works perfectly well for the normal-weight horse or human.
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 “We’re full!” instruction to signal the body to eat less food and normalise weight.
Not so, unfortunately. Our cresty equines, and especially those labelled metabolic/IR/Cushings, have become leptin resistant, which means they're no longer receiving the message that they’re not hungry any more. In other words, they're only hearing the grehlin hormone so the body thinks it’s permanently starving and keeps telling the body 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, 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
All kind of obvious I know …
For those of us who've been here, we all know how difficult it is to shift that crest. We know our horses are overweight and we need to 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 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 the stress involved increases the stress hormone cortisol, which then induces elevated insulin, which promotes fat storage, and so we’re back where we started. Ad lib is the way, but maybe double-netted to slow the eating process down.
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 to the whole IR/EMS scenario. Which links us nicely to ...
The amino acid Acetyl L-Carnitine, aka Alcar
Alcar is thought to help lower leptin resistance which stems from those cresty pads. 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:
“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 so surely a greater chance of the leptin message being heard. The OP also said that coincidentally she saw Alcar being advertised as a potential human weight loss drug. She wrote: “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.”
As per the first line in the ECIR para, 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 really noticed positive changes in his hoof integrity with mineral balancing (and thereafter all my horses).
Naturally I restriced his grass intake (track system with hay stations), and also put together a blend of herbs which became our MetaTonic. This gave Murf's filtration organs a gentle daily detox alongside blood cleansers and the all-important gut support to prevent toxins leaking into the bloodstream.
The blend also contains Galega officinalis (Goat’s Rue), which is known to help regulate blood glucose levels. This is the herb that was originally synthesised by scientists to create Metformin, which is the first drug of choice for human Diabetes Type II and also prescribed by vets to horses.
Around 2014 I also added Alcar into his feedbowl, 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; these days he’s now a really mellow, balanced, sweet old man, who no longer mugs me for food; in fact, I can't remember the last time he did. As an extra advantage of the Alcar, he also has a much looser, freer, peripheral movement as well.
All my horses are permanently on MetaTonic and they’re all doing great, and - Newsflash - they all live out 24/7. Come March, I put up a track system which then comes down late Oct/Nov allowing access to winter foggage from the middle, although I still put hay out all year round to 'dilute' the grass. I pre-empt pulses by keeping them permanently on our DuoBute pain/anti-inflammatory blend. And as for their crests, Murf's completely vanished, you can barely see Cookie's, and while Mac still has a hint of one during the summer, it's nothing like it was.
Pulling it all together
Here’s what I’d suggest to support rebalancing the metabolic syndrome to regulate itself back to manageable - I'll just add in a quick disclaimer here that this is what works for me - it may not work for everyone so naturally seek opinions/advice:
- Obvious I know, but it's imperative to manage grass intake, and meanwhile feed at least 2% of ideal bodyweight in hay/day. Small mesh hay nets are a great way to make the hay rations last longer.
- The FeedPlan - Relook at what goes into the feedbowl, aiming for as low starch as possible. Agrobs (my favourite feed brand) do a fantastically low-starch chaff, namely their Leitchgenus at less than 2% starch. For help in putting together the ideal feedplan, there are two pages in our Feeding our Horses to Health section off the main menu; firstly, Why What We Feed Has to be Right, which also highlights those poor-quality ingredients out there and why we should be avoiding them; second, my own feedplan explained in the What I Feed page.
- Minerals - If your horse is off grass completely - and many are - remember that hay alone will not a nourished, healthy horse make. For the metabolic horse where hay plays a vital part in the diet due to grass restriction, supplementing the deficient minerals to balance our UK forage and hay is essential.
- Support the EMS with our organic herbal MetaTonic blend.
- Alcar - Add the amino acid Acetyl L-Carnitine to reverse the leptin resistance.
- Apple cider vinegar - it's super-nutrient rich, but specifically it’s high volume of acetic acid may be the most significant for metabolic health, including lymphatic drainage and the body’s natural detoxification processes, which for the IR horse is highly beneficial. Even better, according to new research, ACV’s acetic acid is also showing to benefit the number of energy-producing mitochondria in the body’s cells by stimulating an important metabolic pathway known as PGC-1 alpha. This pathway largely controls mitochondrial function within the cells, which is important if we’re doing all we can to reduce our horses’ blood glucose levels. PGC-1 alpha increases the mitochondrial functional capacity when energy needs are high and reduces it when they are low, so, by adding ACV to the feedbowl, you may actually be able to improve your horse’s mitochondrial efficiency and produce more cellular energy. New research is also showing that ACV is what’s known as a thermogenic, which is the process of burning body fat to generate body heat. Researchers have found that ACV can turn on genes to signal the body to accumulate and store less fat, and can make the body feel more full and suppress appetite. (In one 12-week Japanese study, one group of individuals drank a beverage containing one tablespoon of ACV. Another group drank a beverage with two tablespoons ACV. A a third group had a drink with no vinegar. At the end of the study, the people who drank either of the beverages with vinegar showed less signs of metabolic syndrome compared to the no-vinegar group.) Note – when buying ACV, make sure it has ‘The Mother'; in the perfect world you want organic, raw, unfiltered, and unprocessed ACV, which is murky and brown. An apple cider vinegar without the mother and its beneficial enzymes and probiotics isn’t worth buying.
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 in acute illness.
A 2020 German study looked at hospitalised horses in pain from various conditions including colic, laminitis and orthopedic conditions, 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 a painful condition.
See the full article here: https://drkhorsesense.wordpress.com/2021/06/08/insulin-acth-and-pain/