Laminitis

Laminitis and E.M.S (Equine Metabolic Syndrome)

Laminitis is not so much a disease in itself, because of a cascade of events that ultimately result in lamanitic changes that can be devastating. Vets are quite clear that they have no cure for laminitis, and once your horse has reached the chronic stages management starts to become very difficult. The key is very much prevention and staying vigilant for any slight changes to hoof formation that are likely to appear before visible lameness.

While some horses will be intrinsically predisposed to laminitis, it is environmental factors that tip the scales. Native ponies are especially prone, probably because they have evolved to be very hardy, using poor feed sources incredibly efficiently and storing fat easily to see them through tough winter months. Green pastures and hard feed to such ponies is like feeding your child nothing but lard and sugar! Other types of horses also seem predisposed to laminitis, maybe for the same reason, or it could be because of genetic traits that effect a number of other systems in the body that are also linked to laminitis and this is where it starts to get complicated.

Laminitis is very much linked to changes in certain hormones. Hormones tend to exert a systemic effect, meaning that they make delicate changes all round the body, and those changes will trigger a whole series of other changes in an ever increasing cascade effect, and this inevitably makes it incredibly hard to establish a direct cause.

Laminitis is characterized by reduced blood flow and inflammation of the laminae, the fine interlocking layers that attach the hoof to the coffin bone. It is an extremely painful condition that can lead to irreversible physiological changes to the hoof structure.

Cushing’s Disease

It is important to separate Cushing’s from the start, although certain changes and problems are very much the same, the initial trigger is quite different. Cushing’s is thought to be the result of continual oxidative stress that causes degeneration of neurons that inhibit a part of the pituitary gland called the pars intermedia. As a result this area is allowed to grow. Glands are responsible for making and secreting hormones. The growth of the pars intermedia increases the release of ATCH, a hormone which is used to regulate cortisol. Cortisol is often referred to as ‘the stress hormone’ and is responsible for a predisposition toward laminitis and insulin resistance. It is the effect Cushing’s has on cortisol levels that gives it so much in common with more classic laminitis and E.M.S. cases.

 

 

 

E.M.S (Equine Metabolic Syndrome)

E.M.S. describes a group of metabolic conditions that tend to coincide and is characterized by adiposity (fatty deposits typically on the neck crest, behind the shoulders and at the top of the tail), insulin resistance and laminitis.

Normally horses are obese but not always, it is the irregular forming of fat which is key and probably the equivalent of the buildup of abdominal fat in humans (that occurs in response to stress and insulin resistance).

Its name marks its similarities to the human condition of Metabolic Syndrome which is a collection of factors that predict the occurrence of coronary artery disease and type 2 diabetes mellitus. The reason we do not see the same development of the disease in horses is probably in part due to their low fat diet and simply because they do not live long enough. Certain other factors associated with E.M.S. have also been recognized including the increase of certain inflammatory markers, arterial hypertension (increased blood pressure) and high levels of low-density lipoprotein triglycerides. These are indicators of a series of changes that reduce circulation and increase inflammation, thus probably causing laminitis. 

Obesity

Obesity is a major predisposing factor for Laminitis. The reason for this is still being studied but it is now recognized that fat tissue is not simply an inactive store of energy. Fat cells have many functions and are responsible for the production of certain hormones and abnormalities in this function are likely to cause insulin resistance, systemic inflammation and hypertension.

Among the many chemicals produced in the fat tissue are inflammatory cytokines that increase inflammatory responses. In humans this can be seen as a state of low-grade chronic inflammation in obese patients. This may be a critical fact because inflammation of the hoof laminea is a key component of laminitis.

Another chemical released from adipose tissue is resistin. This is significant because it reduces insulin sensitivity and is also associated with inflammatory responses and energy metabolism.

 

 

 

 

Insulin Resistance

It is not known whether obesity is the trigger for insulin resistance, or whether insulin resistance occurs (as a result of increase cortisol levels for example) thus resulting in obesity. It is likely that both scenarios combine in an ongoing cycle with some variation between individuals.

Insulin is the hormone the body uses to control blood sugar levels and is therefore a critical component in maintaining constant energy metabolism and correct energy storage. Insulin resistance is a scenario in which the body becomes less sensitive to the action of insulin. The equine diet does not contain much fat but the body is able to turn glucose into lipid fat molecules which can be used for energy or storage, but the body’s ability to do this is finite, and overloading will mean that fat has to be stored in other tissues where it can exert negative effects on functionality, including changes in insulin regulation.

Normally horses are obese but not always, it is the irregular forming of fat which is key and probably the equivalent of the buildup of abdominal fat in humans (that occurs in response to stress and insulin resistance).

Insulin resistance affects different tissues in different ways and basically has the same, but exaggerated and speeded effect as obesity in that it causes the accumulation of fat in areas that are simply not designed for the purpose. Insulin resistance means that blood glucose is allowed to increase and some body tissues become hyperglycemic (too much glucose), in humans this leads to the accumulation of fat particularly in the abdominal region with the liver being the major concern. Accumulation of fat in these areas can cause changes to normal cellular activity that may have multiple systemic effects. It is likely that the regional adiposity we see in horse’s results from this same mechanism.

Insulin has many regulating properties including an effect on the blood vessels. Normally insulin acts to increase blood vessel size (vasodilation) through the syntheses of Nitric Oxide, NO. In a state of insulin resistance you would expect to see elevated levels of insulin, however levels of glucose will also be elevated. Some tissues are not dependant on insulin for glucose uptake and abnormally high levels of glucose can be harmful. This particularly effects the endothelial cells which line all of our blood vessels and are therefore critical in maintaining and adapting circulation to meet the body’s needs. Despite the increase in circulating insulin, coexisting hyperglycemia actually reduces the amount of NO produced (that would dilate the blood vessels) and increases the production of another chemical that works to constrict them (endothelin-1), thus potentially compromising circulation and increasing the likelihood of laminitis.

Chronic hyperglycemia is also related to several other changes that happen in the blood that make it thicker, and this is shown clearly by the predisposition humans with diabetes have to thrombosis (the forming of blood clots in the vessels). Insulin resistance leads to hormonal changes that cause the blood to become more coagulant and sticky. It is very likely that the same changes occur in horses and contribute to cases of laminitis.

While scientist are not yet able to prove the direct cause and effect relationship that exists between obesity, insulin resistance and laminitis, we do know from human medicine that insulin resistance brings about systemic changes that increase inflammation, cause vasoconstriction and thicken the blood. It is probable that the same processes exist in the horse and explain the association between laminitis and obesity/insulin resistance.

Stress and Cortisol

Thus far we have made the odd reference to the hormone Cortisol but have tried to avoid it until this section to minimize confusion! Cortisol is dubbed ‘the stress hormone’ because it is released in response to stress, both physical and psychological, and it has a number of direct and indirect consequences.

The stress response is a complex series of actions that equip the body for ‘fight or flight’. This includes the combined effects of cortisol and adrenaline that work to redirect blood flow from the peripheries to the working muscles, increase blood glucose, decrease insulin sensitivity and promote blood clotting (to prevent excessive bleeding when injury is incurred). All of these changes are incredible adaptations for an animal that needs to fight for its survival, but when these factors are permanently elevated it causes problems that can be obviously linked to an increased chance of laminitis.

Cortisol receptors are found in the endothelium and are known to increase the release of vasoconstrictors and suppress synthesis of vasodilators, thus it has the potential to limit blood flow to the hooves and contribute to laminitis.

Stress is also associated with the phenomenon of adiposity because the resulting increase in cortisol levels causes the deposition of abdominal fat and promotes its activity, thus making these areas of fat self perpetuating. It is this type of fat that has already been discussed and is known to contribute to insulin resistance and metabolic syndrome. This is a well documented problem in other species, particularly cats and dogs that can develop fatty livers after illness or trauma. This information could be particularly pertinent when discussing laminitis, because it is an extremely traumatic and painful condition. The resulting stress and increased cortisol levels might help explain why it is so notoriously difficult to overcome a bout of laminitis and avoid rapid reoccurrence.

It is not uncommon for people to discuss stress laminitis. It is this set of responses that alter the body in a way that makes it more susceptible to laminitis. Indeed stresses such as trauma, transport and isolation are all known contributory factors.

 

 

Seasonal Changes and Endotoxemia

Throughout the year the nutritional value of grass changes. In rapidly growing grass when there is plentiful levels of sunshine, grass produces sugars in excess of what it actually requires for growth. These excesses are stored as carbohydrates, and this is the cause of the seasonal changes in laminitis susceptibility. Because the grass is so much richer, the load on the horse’s energy metabolism is much greater and it simply can’t cope. Again this is often enough to tip the balance on a pony that was already predisposed to laminitis.

In addition to this it has been observed that insulin sensitivity naturally cycles through the year, decreasing in the summer. This is probably a natural evolutionary tactic that promotes fat storage ready for the winter, but for the domesticated horse it may exacerbate the underlying problem.

Another cause of laminitis that is very much seasonal is endotoxemia. This also occurs as a result of the high carbohydrate content of lush grass which causes problems when it enters the large intestine. Carbohydrates lower intestinal pH (making it more acidic), alter the existing balance of hind gut bacteria and increase intestinal permeability. An endotoxin is found as a structural part of bacteria (as opposed to a chemical that the bacteria secretes), it is normal for certain bacteria to live in the horses gut but they are prevented from entering the horses blood circulation by the membrane barrier that lines the gut. The increase in carbohydrate consumption upsets the guts healthy balance and these bacteria are allowed to enter the blood stream causing mild endotoxemia which increases inflammatory responses, vasoconstriction and insulin resistance, thus setting up all of the conditions already discussed.

Another factor with spring grass is the high calcium to magnesium ratio. Calcium is the key trigger for the stress response, and it is controlled by magnesium. Spring grass can make a horse magnesium deficient because of the overwhelming amounts of calcium, and this in turn increases the release of stress hormones, including cortisol, and increases insulin resistance.

Conclusion

The pathology of laminitis involves an array of delicate control mechanisms, all of which are interrelated making it very difficult to identify any one specific cause. Obviously some horses are more prone to laminitis, and it is likely that if any of the above scenarios are increased or coincide with one another then the body is no longer able to cope. It can be that subtle changes occur with only very mild responses, but at other times the changes are too great leading to massive and rapidly developing cases of laminitis that can be very hard to get under control. The cascading and ever increasing nature of the inflammatory response and insulin resistance means that a dormant, underlying tendency toward laminitis can very easily spiral into a severe case. Veterinary help is critical and hopefully greater understanding will lead to more effective treatments, but prevention remains the best form of management.