Lachie Hulme-Moir BVs

Article first published in “The Swingletree”

As ever the inspiration for this article has arisen from a friend asking me what I know about this syndrome. I had to be perfectly honest, when asked, and say that while I had vaguely heard talk about it I actually knew 'b*****-all'. It is one of those disease syndromes which has really only appeared on the horizon since I retired, hence the paucity of my knowledge. However having said this in actual fact EMS has been around for ages, but we have either not recognised it or ascribed its symptoms to some other diseases. What has happened is that as our diagnostic tests have improved while at the same time research marches forward. We now find that what we thought of as an illness in its own right can in actual fact be just a symptom of another underlying disease. Take Laminitis or Founder for example, as our knowledge has improved and tests become more sensitive we now know that the majority, if not all, cases of Laminitis are in actual fact a symptom or manifestation of EMS. Likewise many cases of Cushings, provisionally diagnosed without specialised testing, are also manifestations of EMS. When I was bright eyed and bushy tailed in the days of yore and new diseases were described and named by the great and learned I and everyone else would rush out and start diagnosing it left right and centre. At the same time wondering why we hadn't realised that these symptoms added up to this particular illness before. Of course when we started digging further to confirm our diagnosis we often found that actually it wasn't all this new the illness we were dealing with. As I have got older I tend to be slightly cynical when a new disease complex is announced and wonder if the rage for diagnosing this new disease will not being fractionally overdone. It may well be, but in the case of EMS there are now definitive tests available to ensure correct diagnosis.

 So what is EMS? Well I went into the International Veterinary Library and ended up with pages and pages on the subject and those were just from professional papers, all presented or published within the last 7 years. All I can say is thank God I didn't Google it! Simplified EMS describes a now recognised clinical entity characterised by middle aged obesity accompanied by insidious-onset laminitis confirmed by proof of insulin resistance. It has been noted, in respect of this obesity, that as well as a general podgyness affected animals have fat deposited in particular places on their bodies. These particular areas are the crest of the neck, over the rump ( love handles!) and in geldings in the prepuce or sheath. Our human equivalent of EMS, ignoring the laminitis although the changes to blood vessels that cause laminitis also occur in humans, is Type 2 Diabetes. Don't be confused by the “insidious-onset” business, all it means is that in some cases there can be sub-clinical laminitis, that is, it is there all right but isn't causing observable lameness or pain. In a nutshell EMS is now recognised as a hormonal dysfunction, Insulin Resistance, induced by obesity in susceptible horses and ponies.

 Affected horses, and here I use the term loosely to include ponies rather than get too technical and use the special term Equid, tend to be between 10 and 20 years of age. All pony breeds and their crosses are susceptible as well as Warmbloods and Morgans; Thoroughbreds, Standardbreds and Quarter Horses appear to much less susceptible. This difference in breed susceptibility strongly suggest there is a genetic component in predisposition to EMS. It has been pointed out that as horses have moved from being a working animal to a recreational companion their change in lifestyle has paralleled our current human dilemma, that of overfeeding combined with a more sedentary lifestyle. As a consequence of this obesity has become a significant problem with the attendant health issues, in the case of horses one of these is EMS.

 The cause of obesity is straight forward, too much tucker! When the intake of calories exceeds the number of calories needed you put on weight primarily in the form of fat. Complicating this is the genetic predisposition of our proverbial 'good doer'. Once you have obesity occurring you have a number of attendant metabolic consequences and one of those is Insulin Resistance (IR) and one of the manifestations of this is Laminitis. So what is IR? Without getting down to the technicalities of   it and confusing everyone, including myself, the bodies cells don't respond to normal levels of insulin but require ever more higher levels to respond. Simply put IR is a state where the body produces and has circulating in the blood stream more of the hormone Insulin than is required normally to ensure that the cells of the body can uptake, among other things, the circulating blood sugar they require for normal function. This is easily demonstrated by giving a fasting horse a sugar (glucose) hit and measuring how much insulin is produced in response to this hit. Horses with IR produce a significant greater amount of Insulin than a normal horse.

 There is a word that was beloved by my lecturers in physiology that still is perennially popular in academia today and that is 'homoeostasis'. Simply put it is that within the body there are innumerable checks and balances that keep it on an even keel. Problems however arise when things get out of balance for whatever reason and then there can be a whole avalanche of knock on effects. So it is when too much insulin is circulating, it stimulates all sorts of hormonal messengers to start getting into the act all in the name of trying to regain that nirvana of homoeostasis Of immediate importance to us in the case of increased insulin are the messengers that stimulate the production of fat tissue. There is also the direct effect of insulin on the cells that line blood vessels, especially the smallest ones, the capillaries, and for horses it is no more important than in that large capillary bed that underlies the wall and sole of the foot. Both excessive insulin and glucose present in the circulating blood have a similar effect on the cells lining the capillaries. Suffice it to say the net result is inflammation of the hoof capillaries complicated by an additional constricting effect on the vessels and a localised increase in blood pressure. End result Laminitis!

 From the veterinarians point of view the important thing is to identify the horses that are at risk before anything starts to happen and get the owners into gear to implement management procedures that will hopefully preclude or at least minimise the risk of their horse developing EMS. In the so called good old days when I first started out in practice we as vets used to worm drench most horses and this would have been an ideal time to assess on a regular basis horses and identify those at risk. Unfortunately owners buy worming paste and vets don't regularly visit the horses they care for. Thus it becomes our responsibility as vets to educate owners, like writing articles, of what to look for.

 Horses and ponies that are at risk are the ones tending to be overweight. There is an official scale to assess body condition but I won't get involved in that at this moment. However, suffice it to say that if you can't easily feel a horse's ribs when you rub the side of its chest then it is in the risk zone. If it is at risk then don't feed concentrates, limit grazing and provide regular exercise. If your horse has shown any signs of laminitis then you are already at the point where you can't navel gaze any longer. Currently medical treatment is limited to the use of thyroid hormone and one human Type 2 diabetic treatment. In respect of dietary supplements current research has shown no advantage in the supplementation with magnesium, chromium, vanadium or cinnamon which have been advocated by some folk for assisting in weight loss and recovery from a laminitis attack.

 This is probably as good a place as any to take a little look back to the history of our horses and ponies. Over millennia they evolved very successfully grazing mountain, moorland and prairies. The food was of low calorific value and they had to work their proverbial little butts off to get a belly full. When we domesticated them and put them to work until the latter half of last century the quality of grass they grazed was not much improved on their original fare and when we did start to hard feed them we really only topped them up with chaff and oats while at the same time they were working for a living. Come the end of the 20th. and our present 21st. centuries and our recreational horses are now being fed high quality grass, the KFC of horse tucker, and concentrated hard feed, the MacDonald of the pony world! Guess what, just as with ourselves a significant percentage can't cope with high calorific intake and minimal periodic exercise. Additionally many are genetically, in respect of ability to put on weight, between a rock and a hard place in these circumstances.

 When it comes to feed what can we do? “Sweet Feeds” and other concentrated feeds with high soluble carbs and a high glycemic index are best avoided at all costs. To be honest it is best to avoid hard feeds completely even if they are marketed as 'low starch'. Also to be avoided is lush pasture and the hays made from such pasture. This applies primarily to hays made from spring pasture and to a lesser extent autumn pasture, as they both have a high soluble carbohydrate content sometimes even equivalent to that of concentrates. When you are fine tuning how you are going to handle this problem you must also be aware that during the day grass produces its sugars (fructan) which constitute your soluble carbs and that overnight the grass uses them up so by first thing in the morning these carbs in the grass are at their lowest. Oh that life was so simple! Frosts or low temperatures mean that the grass does not gobble up its sugar store of energy so in frosty weather the morning level of soluble sugars may not be that low. Hay typically has lower sugar levels than pasture but here again there can be great variation. Hay is often made in early evening because there is some dew about that enhances baling, ergo sugar levels up. If possible find out the history of the hay and if it is summer hay that has been drying off for a period in the summer before being cut and baled that may be your best bet. If you are not sure then soak your hay in water for an hour before feeding and this will leach out a significant amount of the soluble carbs present.

 In the case of an affected individual then a strict diet is essential which over a period of 2 to 3 months should lead to an observable weight loss. It is then incumbent on the owner to continue managing the diet. Here is some food for thought. A horse consumes 2% of its body weight in forage daily for maintenance, but good doers like EMS patients seem to be can get by with as little as 1.5%. To put this into perspective a sedentary 450Kg horse can gain its daily digestible energy needs for maintenance from 7Kg of good quality hay. Problem here is that this quantity will lead an unhappy chappy feeling hard done by who may well decide to start consuming stable or yard rails! To combat this you can increase volume with poor quality or soaked hay, even use oat chaff. Let’s face it, showing my age, in respect of the latter I can still remember the milk and ice delivery horses of my childhood in Sydney with their nosebags full of oaten chaff to stave off boredom and hunger! The difficulty of using pasture as your feed source is that while it overcomes a lot of the boredom problem it is difficult to measure actual pasture intake. The answer probably lies in bare paddocks and/or minimal additional strip grazing. In the end you must aim over 1 to 2 months to achieve a weight loss of about 5% with your EMS patient and this needs to be continued until an acceptable body condition is obtained – loss of fat deposits and what-oh we can see those ribs easily – and then maintain it.

 So much for diet, now let’s not forget about exercise, as it can help with weight control, as well as have other beneficial influences on recovery. The problem here is that of the laminitis, it can be exacerbated by exercise during an attack. So as soon as the patient is deemed comfortable enough to walk one can start with regular hand walking for 20 to 30 minutes 5 times a week. This as well as burning up calories also improves the body’s tissues sensitivity to insulin. It is also essential that you do not overlook providing appropriate hoof care. As far as your vet’s contribution is concerned, as noted above, only two therapies have shown any clinical help and they are the use of thyroid hormone and a human Type 2 Diabetes drug metaformin. Finally a point of interest is that there is only one other condition likely to be confused with EMS and that is Equine Cushing, but this disease has slightly different symptoms and is easily identified by a simple blood test much in the same way that EMS can be identified these days by a simple blood test.

 I would also like to note here that amongst the numerous papers I have consulted one by Professor Schott from Michigan State University to the Italian Association of Equine Veterinarians last year has been my main source of information.


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