Why are fat ponies at more risk of developing laminitis than fat horses? What is different about their metabolism that commonly results in an increased incidence of laminitis?
It is generally accepted that there is a breed susceptibility in laminitis. There are regular surveys on the incidence of laminitis and risk factors and, although the results vary between surveys at how the observations are analysed and what constitutes laminitis (some surveys, for example, look at lameness per se, some at metabolic causes etc.), the consensus is that some breeds appear more susceptible. There are indications that age may be the most important factor, followed by season, sex, breed, height and weight all gave conflicting results.
However, other research surveys do find a very strong risk factor in ponies, those less than 1.5m. These include native British ponies, Norwegian Fjord and Icelandic breeds. Other surveys also include Morgan breed, Miniature horses, Spanish Mustang, Saddlebred, Warmblood, Haflinger, Peruvian Paso and Paso Fino breeds, Tennessee Walking and non-Quarter horses. Quarter horses and Thoroughbreds gave variable results, and it appears we are looking at a spectrum of breeds where the risk factor varies with some parameter of height; draught horses, for example, seem to have the lowest risk of all.
Beyond these parameters, the major triggers for laminitis and these are common to all breeds, are reported to be seasonal grass changes (spring and autumn) and obesity, both of which are indicative of too great an energy (sugar/starch) intake.
Where this maybe resonates with the question of why some breeds are more susceptible, is the relationship between the metabolism of the horse or pony and sugar rich diets.
Every spring there is an outpouring of articles on the dangers of spring grass and its impact on the laminitic, and it is always worth running through the broad nutritional effects.
The gastro-intestinal tract of the horse is designed to deal with a fibrous diet. Whilst we have bred animals for activities, some of which mean we need to supplement energy and whilst we have changed the nutrient profile of grass, the horse’s gut has not really changed. It means, unless we are very careful, we are supplying our horses with protein and sugars in excess. One result is obesity, but another is the inability of the small intestine to digest and absorb all the protein and sugar we feed. These then flood the hindgut (along with those bacteria that utilise them in the small intestine) where disruption of the normal hindgut environment occurs. Acidity in the hindgut increases as sugar is fermented, and the normal hindgut fibre fermenters die releasing endotoxins. Excess protein is broken down to amines and nitrites and the absorption of all these is enabled by the production of lactic acid, which increases the permeability of the gut wall cells. These products are oxidative, pro-inflammatory agents and vasoconstrictors, which means they pool where blood flow is poorest – in the hooves. Although this mechanism is well understood, it is now becoming apparent that it may not be the sole cause of laminitis, but underlying factors rather exacerbating conditions and tipping the biochemical/physiological processes that govern inflammation.
Inflammation is the body’s first reaction to dysfunction. The trigger can be physical (impact damage), nutritional (as described above), microbial (immune response) or metabolic dysfunction (EMS). Whatever the cause the body releases pro-inflammatory factors, such as cytokines, to ring fence the damage and stop the problem dispersing. The healing cycle happens next (very much dependent on what the problem is, but has many common factors) and then anti-inflammatory factors are released (modified cytokines). However, there are external factors that can affect this process. As described above the nutritional impact of overfeeding adds to the inflammatory load and reduces the ability of the blood to flush away these elements which adds to hoof soft tissue inflammation that is laminitis.
However other factors can interact with this, and it is these factors which may explain why ponies and cold bloods are more likely to succumb to laminitis.
Alongside reviews into the risk factors that cause laminitis, there have been others looking at metabolic cues. It has been proposed that EMS, in particular insulin resistance, may be a powerful driver of laminitis. As such, it distinguishes the condition from Cushing’s which can cause laminitis through a different route.
There does appear to be a hereditary link with the development of EMS, and it seems strongly correlated with ponies, the native British breeds, Norwegian Fjords, miniatures, etc. Those not so affected are Thoroughbreds and Standardbreds. It is known that ponies have a greater tendency to IR and now a direct link to EMS/IR and breed has been theorised.
So ponies are more susceptible to IR and obesity is a component of EMS and IR. The role of insulin is primarily to promote the passage of glucose (the base unit of starch and interconverted to other sugars such as fructose, galactose) into the cells where it is metabolised for energy or converted into glycogen. However, it also has a role in fat deposition in adipose tissue and arterial blood flow. High levels of absorbed sugars can overwhelm the process leading to high circulating levels and insufficient being absorbed into the cells. Additionally, high fat reserves cause the release of the hormone resistin that promotes insulin resistance. The vascular bed of the hooves appears to be sensitive to this mix. Coupled with naturally low blood flow, the situation arrives where there is little glucose actually absorbed into the cells of the soft tissue of the hooves leading the breakdown of other nutrients (protein, fat) for energy and restricting the blood flow then leading to oxygen starvation. All these factors raise the potential for inflammation, reperfusion and the build-up of toxins in the region of the hoof. In addition, the possible overproduction of insulin has an impact on acid release in the stomach. If buffering is insufficient (and this is dependent on feed type), there could be an increase in the acidification of the gut which will have a direct impact on hindgut dynamics and the potential absorption of pro-laminitic cues.
In summary, therefore, it would appear fat ponies are more susceptible than fat horses because they are more prone to IR. We are not sure why, some scientists think it may be related to body mass index (ponies tend to be stockier), or it could simply be that the breeds are more attuned to poor quality feeds. While we have bred horses alongside our development of more sugar rich feeds and selection has helped in their resistance to laminitic cues. Whatever the reason, feeding horses high levels of sugars, too much protein and insufficient fibre all put a stress on the metabolism of the horse.
We should be feeding horses and ponies with a top limit on their sugar and starch intake and keep protein to a sensible level. There are high energy fibre alternatives that should support activity without the negative aspects of too much carbohydrate in the metabolism, and coupled with plenty of exercise – physical activity improves blood flow in the extremities and can help counteract pooling – we needn’t worry too much about susceptibility to laminitis.