Laminitis in Autumn: Why the Risk of Laminitis on Pasture at Cool Temperatures is Underestimated

This article was translated using AI.

Key Takeaways

• Laminitis is not purely a spring disease: large-scale studies demonstrate a laminitis risk throughout the entire year, sometimes with even higher risks in summer and winter than in spring.
• Autumn grass can insidiously contain high levels of sugar or fructan – sunny, cool days with cold nights in particular cause plants to store carbohydrates.
• There are two distinct pathways leading to laminitis: sugar via excessive insulin spikes, and fructan via an unbalanced gut microbiome.
• Switching from an overgrazed pasture to a new batch of hay can also be hazardous – “only hay” does not automatically mean “low in sugar”.
• Those primarily affected are horses with insulin dysregulation and a history of laminitis – often lean, unassuming animals that no one has on their radar.
  
  

Laminitis is Not a Spring Disease

When people talk about laminitis, most think of spring: pastures turn green, horses are turned out again after winter, and the risk rises for sensitive animals. This easily creates the impression that the danger period ends with early summer. The data tells a different story.

In a large British study involving 1,070 horses and ponies, laminitis occurred throughout the entire year, with no clear difference between seasons (Pollard et al. 2019). Another large study found the risk in summer and winter to be even higher than in spring (Wylie et al. 2013). Thus, laminitis does not have just one season; it accompanies at-risk horses all year round.

A finding from the same research is particularly revealing: a good three-quarters of the horses that developed laminitis during the study period had already suffered from it previously. This is a common thread that follows affected horses through autumn and winter – many of these laminitis episodes are less a brand-new illness than a recurrence or derailment of an already compromised system.

Two Pathways, One Outcome: How Carbohydrates Lead to Laminitis

To understand the autumn risk, one must realize that “laminitis” is not a uniform disease. Behind the same clinical picture lie various mechanisms – and in diet- or pasture-associated laminitis, there are primarily two that should be clearly distinguished.

The first pathway is hormonal (endocrine). Sugar produced in grass through photosynthesis in sunlight is directly absorbed in the small intestine and enters the bloodstream. In a horse with insulin dysregulation – meaning a horse whose pancreas responds to sugar with an excessive or prolonged release of insulin because cells no longer respond adequately to it – this drives insulin levels sky-high. Today, sustained hyperinsulinemia is recognized as a key trigger of laminitis: it directly damages the digital lamellae, the finely interlocked suspension mechanism anchoring the pedal bone within the hoof capsule. A trial involving 37 ponies clearly demonstrated how closely linked this is: not a single animal with a low insulin response in the sugar test subsequently developed laminitis when fed a high-carbohydrate diet – whereas six out of seven with a very high insulin response did (Meier et al. 2018).

The second pathway leads through the gut. Fructans are short-term storage carbohydrates produced by the plant when it generates sugar during the day but cannot convert it into growth. Fructans cannot be enzymatically digested in the small intestine; instead, they pass with the digesta into the hindgut. There, they disrupt the balance of the gut flora: specific (lactic acid-producing) bacteria multiply rapidly, the pH drops, and long before any lameness becomes visible, the microbial population has already shifted drastically (Milinovich et al. 2006, 2008). This process produces compounds that enter the bloodstream and can even compromise blood circulation in the hoof: following fructan intake, certain biogenic amines increase in the gut, and in experimental trials, such amines significantly reduced blood flow in the hooves of healthy horses (Crawford et al. 2007, Bailey et al. 2004). The end result is, once again, laminitis.

One is therefore an endocrine pathway, the other an inflammatory one – and a sensitive horse can experience both mechanisms simultaneously. This is precisely why the sweeping statement often heard, “fructan is not the issue at all, only sugar and insulin matter,” falls just as short as claiming that fructans are the sole problem in autumn while sugar is not. Both are always intertwined, and if insulin resistance and/or hindgut dysbiosis are also present – both of which are unfortunately very common – then the next laminitis episode is merely a matter of time.

More on this topic: EMS, MIM, Laminitis: Understanding Carbohydrates in Equine Nutrition

Why Autumn Grass of All Things?

The fact that grass can become dangerous especially in autumn comes down to the plant itself. Our pasture grasses store surplus energy not only as simple sugars, but to a significant extent as fructan – serving both as an energy reserve and antifreeze.

How much sugar is in the grass does not simply depend on the calendar, but on the interplay of grass species, growth stage, temperature, sunlight, water availability, and time of day. The decisive factor is the balance between sugar synthesis and consumption: if the sun shines during the day, the plant busily produces sugar. If it is cold at the same time, however, it barely grows – storing the unused sugar as fructan. It is precisely this scenario – sunny, cool days combined with cold nights – that is typical of autumn and can double or triple the levels of water-soluble carbohydrates (WSC). A particularly high concentration of fructan is found in the lower, ground-level parts of the stems – exactly the plant parts that horses graze on overgrazed pastures.

However, deriving the simple rule “short grass is dangerous, long grass is harmless” from this would be incorrect. What matters is not the height above ground, but the grass species, weather patterns, plant part, time of day, and above all, the actual quantity consumed.

Read more in our articles Sugar levels in grass – when do they become a problem? 

Listening Tip: Sanoanimal Podcast #7 – Pasture Management for Laminitis-Prone Horses: What Every Horse Owner Needs to Know

Caution Regarding the Famous Fructan Experiments

The most well-known experiments used to induce laminitis in research involved extreme amounts: horses were administered five to seven and a half grams of fructan per kilogram of body weight all at once via nasogastric intubation. Yes, this reliably triggers laminitis. However, it far exceeds the amounts encountered in reality. Such “forced administration” is fundamentally different from a horse grazing over several hours. Therefore, one cannot deduce from these trials that every elevated fructan level in an autumn pasture causes the same damage with the same severity.

Yet two things remain remarkable. First, no alteration in insulin was required in these experiments to induce laminitis – the hindgut pathway alone was sufficient. This proves that carbohydrate-induced laminitis can occur entirely without insulin resistance – a factor often overlooked in current research since insulin was identified as a primary trigger and attention shifted almost exclusively to it. Second, considerably more moderate amounts were sufficient to measurably alter the gut flora, even if clinical laminitis did not yet occur. Thus, a continuous intake of low levels of fructan can alter the microbiome over time to the point where a minor additional stressor eventually tips the balance. The correct conclusion is neither “fructan always causes laminitis” nor “fructan plays no role”, but rather: fructan can trigger laminitis completely independently of insulin status, depending on the ingested amount and the horse's individual susceptibility – specifically the stability of its hindgut microbiome.

The Underestimated Change in Hay

In autumn, another shift takes place in many barns that sounds completely harmless: pastures are closed, and overnight horses go from nibbling overgrazed grass back to a hay-only diet. However, “hay” by no means automatically implies “low sugar”.

Preserved forage can vary dramatically in sugar content. One study compared forages with 4.2%, 13.6%, and 18.2% non-structural carbohydrates (NSC) – the two higher levels triggered significantly stronger glucose and insulin responses, and the poorer the individual horse's insulin regulation, the more pronounced the response was. Even more striking: in horses with existing dysregulation, even hay containing only about ten percent non-structural carbohydrates (NSC) could trigger an excessively high insulin response. It is not just the percentage that matters, but the actual quantity of sugar ingested per meal. With high-sugar grasses spreading increasingly across hay meadows, we have observed a steady rise in average annual sugar measurements over recent years. If adverse harvesting conditions are added in a given region, sugar levels in hay frequently surge well above 10%, which quickly becomes highly problematic for sensitive horses.

This is precisely why the seemingly safe transition from an (overgrazed) pasture to a new batch of hay can become problematic for a horse with previously undiagnosed insulin resistance – not because hay is fundamentally worse than grass, but because the intake of sugar can change abruptly. For a horse at risk, “it's just hay” is therefore a dangerous misconception.

Listening Tip: Sanoanimal Podcast #3 – Autumn Pasture to Paddock Transition: How to Ensure a Smooth Transition from Grass to Hay with Dr. Christina Fritz.

Why It Keeps Affecting the Same Horses

We see this time and again in practice: two horses share the same pasture, eat the same hay – and only one develops laminitis. This does not mean grass and sugar are ruled out as triggers. It means the underlying predisposition differs between the two horses – one reacts to the trigger, the other does not.

It is exceptionally well documented that insulin dysregulation significantly increases the risk of laminitis – and this is where the most common misconception lies. People associate the image of “insulin resistance” with an overweight pony displaying a massive cresty neck and a chubby appearance. Not without reason, EMS and insulin resistance are frequently lumped together by horse owners and equine professionals alike. However, the ECEIM consensus statement explicitly clarifies that obesity and insulin dysregulation do not inevitably go hand in hand. There are lean, completely unassuming horses with significant insulin dysregulation. In these cases, laminitis appearing seemingly “out of the blue” is sometimes the very first visible sign of an impaired glucose metabolism. Conversely, there are overweight horses that do not exhibit insulin resistance. Yes, dysregulated insulin metabolism and obesity often go hand in hand – but not always. Read more in our Factsheet: EMS, Cushing, Insulin Resistance.

Added to this is medical history. The fact that so many horses that suffer a bout of laminitis during times of high fructan or sugar levels have had laminitis before is no coincidence: once damaged, the lamellar suspension typically remains a point of vulnerability. This can be understood as a threshold model – a healthy horse has substantial reserves, while a previously affected horse operates constantly near its tipping point. In that state, the final trigger does not need to be large to overwhelm the system. 

What This Means in Practice

Two mistakes are made especially often in autumn: first, assuming that the risk of laminitis is automatically eliminated once pasture turnout ends and horses transition to (potentially high-sugar) hay. Second, continuing to keep horses on overgrazed paddocks – because stressed grass accumulates especially high amounts of hazardous fructan. One should always remain vigilant with horses that have a history of laminitis – even if they have appeared sound for years – and with horses showing unexplained foot sensitivity or notable changes to their hooves. A gradual transition from pasture to hay is always essential; just as horses are introduced to grass gradually in spring, they should also be weaned off pasture gradually in autumn.

A lean horse should also be tested for insulin dysregulation in the event of unexplained laminitis. Obesity is a warning signal, but its absence is no free pass. Pastures should be closed by late September at the latest to allow the grass to recover before frost sets in. And when transitioning to winter feeding, having the new batch of hay analyzed for sugar is worthwhile, and not just for high-risk horses. This provides far greater certainty than assuming “it's just hay, there's nothing in it anyway”.

In-depth online seminar (fee-based): Lecture: Laminitis, Speaker Dr. Christina Fritz. 

You might also find interesting: Laminitis Caused by Dietary Protein: Why Switching Horses from Sugar and Starch to Protein Can Cause Issues and in connection with insulin resistance: Recurring Tendon Problems in Horses: The Underestimated Role of Insulin Resistance

References

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