Key message

Laminitis always has an underlying cause.

Today, research indicates that around 80 to 90 per cent of laminitis cases are associated with abnormally high insulin levels. This is known as hyperinsulinaemia-associated laminitis. The horses most at risk are usually affected by Equine Metabolic Syndrome, PPID, or both.

Understanding why insulin becomes too high is one of the most important steps in treating laminitis and preventing it from happening again.

There is more than one cause of laminitis

Laminitis is not one single disease with one single cause.

It is the end result of different diseases or events that damage the laminae inside the hoof. These causes can produce similar pain and hoof damage, but they may require very different treatment.

The main causes can be grouped into three broad categories:

• Hyperinsulinaemia-associated laminitis
• Laminitis associated with serious systemic illness or carbohydrate overload
• Supporting limb laminitis

Other possible contributors can include mechanical stress, prolonged concussion, severely overgrown feet and corticosteroid use.

These situations should be considered individually, particularly when the usual metabolic causes do not fit the horse’s history.

Hyperinsulinaemia-associated laminitis

This is by far the most common form of laminitis.

Hyperinsulinaemia means that the amount of insulin circulating in the horse’s blood is abnormally high.

Insulin is a normal and essential hormone. It is released after the horse eats carbohydrates that are digested and absorbed as glucose. Insulin helps move glucose from the bloodstream into cells, where it can be used or stored as energy.

The problem occurs when the horse produces a much larger or more prolonged insulin response than normal.

Research published over the past two decades has shown that maintaining very high insulin levels can induce laminitis. The hoof changes produced experimentally are similar to those seen in naturally occurring pasture-associated laminitis in horses with EMS or PPID.

Scientists are still investigating exactly how high insulin causes the laminae to fail. However, the connection between prolonged hyperinsulinaemia and laminitis is now well established.

For most horse owners, the most useful question is therefore not simply:

What did my horse eat?

The more important question is:

Why did my horse produce such a high insulin response?
Why does insulin become too high?

There is rarely one simple answer.

A horse’s insulin response can be influenced by genetics, diet, body condition, exercise, age and underlying hormonal disease.

Each horse has its own combination of risk factors.

Equine Metabolic Syndrome

Equine Metabolic Syndrome, usually shortened to EMS, is one of the most common reasons horses develop hyperinsulinaemia.

A horse with EMS may produce an excessive insulin response after eating sugars and starch.

Some horses with EMS are generally overweight. Others have regional fat deposits, such as:

• A cresty neck
• Fat around the tail head
• Fat behind the shoulders
• Fat above the eyes

 

 

However, a horse does not need to look obviously fat to have EMS or dangerously high insulin.

The 2025 conference proceedings specifically warn against limiting insulin testing only to horses that appear overweight. Some horses have focal fat deposits and hyperinsulinaemia without being generally obese.

PPID

Pituitary Pars Intermedia Dysfunction, or PPID, was previously called equine Cushing’s disease.

PPID becomes more common as horses age. It is caused by changes within the brain and pituitary gland that affect hormone production.

PPID and EMS are separate conditions, but they can occur together.

Some horses with PPID develop hyperinsulinaemia, and it is this high insulin that greatly increases their laminitis risk.

PPID therefore needs to be investigated particularly in older horses, horses with repeated or seasonal laminitis, and horses showing other possible signs such as delayed shedding, muscle loss, increased drinking or recurrent infections.

PPID generally requires medication. If the horse also has hyperinsulinaemia, diet and exercise management will still be needed.

 

Genetics and breed

Some horses are genetically more likely to develop EMS and hyperinsulinaemia.

Ponies, miniature horses and many native or hardy breeds evolved to survive on sparse forage and limited calories. Their ability to use energy efficiently was an advantage in a harsh environment.

 

 

The same efficiency can become a disadvantage when they are kept on improved pasture, fed more calories than they need and given limited exercise.

Breeds such as Morgans, Arabians, Spanish horses and miniature ponies are often  higher-risk groups. More recent research continues to support the importance of genetics and breed susceptibility.

This does not mean every horse from a higher-risk breed will develop laminitis.

It means their weight, insulin and diet may need to be managed more carefully.

Body condition and regional fat

Obesity is strongly associated with EMS and high insulin, but it is not the whole story.

Not every overweight horse is hyperinsulinaemic.

Not every hyperinsulinaemic horse is overweight.

Even so, excess body fat should not be dismissed as harmless. Many owners have become accustomed to seeing overweight horses and may unintentionally consider an unhealthy body condition normal.

 

 

Its been established that owners commonly underestimate their horses’ body condition and that maintaining an appropriate weight is central to lowering metabolic and laminitis risk.

Regional fat can also be important. A horse may carry excess fat around the neck or tail head even when the rest of the body does not appear severely overweight.

Diet and hydrolysable carbohydrates

The carbohydrates of greatest concern in a horse with hyperinsulinaemia are those digested to glucose in the small intestine.

ECIR refers to these as hydrolysable carbohydrates, or HC.

In practical terms, HC is estimated on a feed or forage analysis by adding ESC plus starch.

ESC includes the simple sugars that dissolve in ethanol during laboratory testing.

When a susceptible horse eats too much HC, glucose is absorbed and insulin rises. Horses with insulin dysregulation may produce a far larger insulin response than a metabolically normal horse eating the same feed.

The control of HC intake as central to managing hyperinsulinaemia.

Sources of HC may include:

• Fresh pasture
• Hay
• Grain
• Sweet feeds
• Some bagged feeds
• Treats such as apples and carrots

This is why simply removing hard feed may not be enough. The horse’s total diet needs to be considered.

 

Does grass cause laminitis?

Grass can trigger laminitis, but the full explanation is more complicated than saying that grass itself is poisonous or dangerous.

Most horses can eat pasture without developing laminitis.

The problem occurs when a susceptible horse eats enough hydrolysable carbohydrate from grass to produce an excessive insulin response.

Pasture HC changes with:

• Weather
• Season
• Plant maturity
• Time of day
• Rate of growth
• Grass species
• Grazing conditions

This makes pasture difficult to predict.

The same paddock may be tolerated by one horse but cause dangerously high insulin in another.

The most useful question is not:
When is grass always safe?

The better question is:
Is this horse’s insulin adequately controlled?

For a horse with uncontrolled hyperinsulinaemia, fresh pasture may not be safe even during times commonly believed to be lower in sugar.

What about fructans?

For many years, fructans were widely blamed for pasture-associated laminitis.

Fructans are storage carbohydrates found in cool-season grasses. Horses do not digest fructans to glucose in the small intestine. They are fermented by bacteria in the hindgut.
Very large experimental doses of a fructan derived from chicory root have been used to create severe hindgut disturbance, endotoxaemia and laminitis. These horses became systemically ill, with signs such as fever and diarrhoea.

This is not the usual picture seen in pasture-associated laminitis.

Naturally occurring pasture or hay fructans have not been shown to cause the insulin rise responsible for metabolic laminitis. Instead, simple sugars and starch, the hydrolysable carbohydrates, are the dietary components most relevant to the insulin response.

This does not mean a horse can safely eat unlimited grass.

It means the focus should be on the carbohydrates that raise glucose and insulin, rather than blaming fructans alone.

Lack of exercise

Exercise improves insulin sensitivity.

A horse that is physically active can generally use glucose more efficiently than a horse that is sedentary.

Domesticated horses may live in small paddocks, have easy access to food and move far less than horses living under more natural conditions. A lack of exercise and excessive access to calorie-rich forage are major contributors to laminitis risk.

 

 

Exercise is therefore one of the most useful tools for managing EMS.

However, an acutely laminitic horse should never be forced to exercise. Exercise is introduced only when the feet are stable and the horse is comfortable enough to move safely.

Pregnancy and other influences

Pregnancy naturally changes insulin sensitivity so that more energy is available to support the growing foal.

This does not mean pregnancy automatically causes laminitis, but a pregnant mare that is already predisposed to EMS may require closer attention to diet and body condition.
Illness, pain, medication and other hormonal changes can also influence glucose and insulin. These factors need to be considered as part of the individual horse’s history.

Why can two horses in the same paddock have different outcomes?

This is one of the most common questions owners ask.

Two horses can live together, eat the same grass and receive the same feed, yet only one develops laminitis.

The difference is usually the horse’s individual response.

One may have:
• A genetic predisposition to EMS
• Higher insulin after eating
• PPID
• Regional fat deposits
• Less exercise
• A history of previous laminitis
• Several risk factors occurring together

The other horse may be able to regulate glucose and insulin normally.

The other causes of laminitis

Although most cases are associated with hyperinsulinaemia, not every case is metabolic.

Serious systemic illness

Laminitis can occur when a horse is seriously ill with widespread inflammation, infection or toxins in the body.

Examples include:
• Retained placenta
• Severe colitis or diarrhoea
• Septicaemia
• Peritonitis
• Serious complications following colic or surgery

These horses usually show clear signs of systemic illness and require urgent veterinary treatment.

Grain or starch overload

If a horse breaks into a feed room and consumes a large quantity of grain, undigested starch can overwhelm the hindgut.

This can cause a rapid change in the bacterial population, acidosis, toxin release and severe systemic illness, followed by laminitis.

This is a different process from the insulin response seen in pasture-associated laminitis, although both ultimately damage the laminae.

Supporting limb laminitis

Supporting limb laminitis may develop when a horse cannot bear weight normally on one leg because of a serious injury.

The opposite limb is then forced to support excessive weight for an extended period.
Heavy horses and horses with fractures, severe joint infections or other prolonged non-weight-bearing injuries may be at particular risk. Your original book included this as a distinct cause requiring different management from metabolic laminitis.

Corticosteroids and laminitis risk

Corticosteroid use has long been associated with concern about laminitis, particularly in horses already predisposed to insulin dysregulation.

The level of risk may depend on the individual horse, the underlying disease, the dose and the type of corticosteroid.

A horse with a history of laminitis, obesity, EMS or suspected PPID should be assessed carefully before corticosteroid treatment.

Risk factors are not the same as the immediate cause

It helps to separate the risk factors from the event that finally triggers laminitis.

For example, a horse may have:
• A genetic predisposition
• EMS
• A cresty neck
• Limited exercise
• Increasing access to spring pasture

These factors may exist for months or years.

The first burst of rapidly growing grass may then provide enough HC to push insulin high enough for laminitis to occur.

The grass was the trigger.

The underlying susceptibility was already present.

This distinction is important because removing the horse from one paddock may help in the short term, but it does not remove the underlying EMS or PPID.

Can laminitis be prevented?

Many cases of hyperinsulinaemia-associated laminitis can be prevented.

The greatest opportunities are:
• Recognising high-risk breeds and individuals early
• Maintaining a healthy body condition
• Monitoring cresty neck and regional fat
• Testing insulin where appropriate
• Investigating PPID in older or suspicious horses
• Controlling HC intake
• Managing pasture access
• Providing regular exercise when the horse is sound
• Acting quickly at the earliest signs of foot soreness

Domestication, rich diets, excess weight and limited movement create conditions in which susceptible horses are more likely to become metabolically unwell.

What has become much clearer is the central role of hyperinsulinaemia.

Recognising that connection gives owners something practical to work with.

Rather than simply fearing grass, we can assess the horse, identify the underlying condition and build a management plan that reduces the insulin response.