Does he/she need to lose weight?
Body Condition Scoring Video
Diet for weight loss

If he/she does have PPID, has pergolide treatment been started?
Starting Pergolide/Prascend

Are you wondering whether a supplement could help?
There are no magic potions!

Are you confused about how much your horse should be moving following laminitis?
Movement - good or bad?

Want some suggestions for managing a horse with EMS, particularly if hay/grazing need to be restricted?
Management Strategies for EMS/insulin dysregulation

Need some inspiration? Here are a few of the horses that have recovered from laminitis following TLS's protocol:
Casareño's recovery
Nutmeg's TLS Rehab
​Sorrel

Need support or more information? Become a Friend of The Laminitis Site and access the Friends of The Laminitis Site 1 discussion/support group on Facebook.  If you are in North America, consider joining the ECIR Group.

**If you suspect your horse has laminitis or is ill, always consult your vet and discuss all aspects of management/treatment with him/her.**

So both on an as fed and a dry matter basis, the carrot wins hands down for having less sugar/starch - just 6.1 g in 100 g.  It has the least calories/energy, it has the most fibre of all the above fresh fruits/veg, and it has a huge amount of vitamin A - a 500 kg horse's minimum requirement for vitamin A is 15,000 IU/day, 100 g of fresh raw carrot provides more than this.  Horses grazing will get plenty of vitamin A, but horses on an all hay diet, especially hay that isn't green or is older than 6 months, may be short of vitamin A, so carrots provide an excellent source.  Carrots also score well as being anti-inflammatory.

But how does the sugar/starch in carrots compare to other common feeds, such as hay?

A 500 kg horse eating 2% of its bodyweight would be having 10 kg dry weight, or approx. 11.2 kg as fed weight hay/day.  Sticking to as fed figures, say the hay is 7.15% combined ESC (simple sugar) and starch (or 8% DM), that would be 800 g of sugar/starch eaten in a day.  If eaten over say 16 hours (so 700 g hay as fed/hour), that would be 50 g of sugar/starch in each of those 16 hours.

So if 700 g of 7.15% sugar/starch hay as fed gives 50 g sugar/starch,
100 g hay as fed would give 7.1 g sugar/starch
and 100 g carrot as fed gives 6.1 g sugar/starch
- so a carrot doesn't look quite so evil now!

To be fair, that 100 g of hay has also provided a lot of fibre, some protein, fat, minerals and vitamins, whereas the carrot has mostly provided water, but also that valuable vitamin A.

And compare a carrot to say Spiller's High Fibre Cubes which were approved by the Laminitis Trust (until 2019 when they were removed from the scheme because the Cubes contain live yeast) (NB The Laminitis Trust Feed Approval Mark should not be taken as indicating that a feed is safe for laminitics - their criteria is that the NSC of the feed should not exceed 40%* - the ACVIM Consensus Statement on EMS suggests that NSC should not exceed 10% of the diet for horses with EMS**) - they contain 10% starch and 4.5% sugar***, so 100 g of High Fibre cubes would give 14.5 g sugar/starch - more than twice as much sugar/starch on an as fed basis as the same weight of carrots.

To help human diabetics, glycaemic index (GI) has been calculated for common foods.  The glycaemic index ranks foods from 0 to 100 according to how much and how quickly blood sugar levels are raised after healthy humans have eaten a certain amount of the food (to provide a controlled amount of digestible carbohydrates).  The University of Sydney gives 80 g raw diced carrots a GI of 35 (2017). The glycaemic load may be more helpful - this takes into account the effect on blood glucose from eating a typical portion.  High water content foods like carrots usually have a low GL (less than 10 is considered low - 80 g raw diced carrots have a GL of 2 according to the University of Sydney (2017)).  See Debunking the Carrot Myth - Glycemic Index Foundation.  NB these figures relate to humans, not horses.  

In her book "The Truth About Feeding Your Horse", equine nutritionist Clare Macleod busts the myth that carrots "should not be fed to .. those prone to laminitis" and agrees that although on a dry matter basis carrots are relatively high in sugar, on a fresh weight basis they are low in sugar (she suggests a fresh carrot contains around 7.5% sugar).  She recommends feeding carrots for their betacarotene content (vitamin A precursor), particularly for older horses, to help provide antioxidants. 

As always, common sense should prevail - if a horse's insulin is too high and/or it currently has active laminitis then hold back on the carrots and keep the diet as strict as possible, just analysed & soaked hay with appropriate levels of protein, minerals & vitamins, plus perhaps linseed to provide Omega 3 if a horse doesn't get grass.  But once insulin levels and symptoms are under control, then a carrot or two a day, particularly if sliced and fed throughout the day rather than in one go, is unlikely to do any harm.  

For more information about feeding horses with laminitis, EMS and PPID, see The Laminitis Site's Diet page.

* Laminitis Trust Approval Mark for horse feeds
"B. Criteria
4. NSC (%) must not exceed 40% of the dry matter of the feed (where NSC is used as an estimate for the hydrolysable and rapidly fermentable carbohydrate feed fractions)."

** ACVIM Consensus Statement Equine Metabolic Syndrome (2010)
It is therefore recommended that NSC be calculated by adding starch and WSC percentages together, and this value should ideally fall below 10% of dry matter when feeding horses or ponies with EMS.

​*** Spillers High Fibre Cubes nutritional analysis

Updated 2017 to include swede, turnip and parsnip (click on the image to enlarge it)

(First posted March 2013 above, updated February 2019 below)

A new ECEIM consensus statement on equine metabolic syndrome was published online in February 2019, which stated that "grains or cereal‐based complementary feeds, fruit, or vegetables such as carrots, apples, or treats should be excluded from the diet because of their high NSC content."

When sharing the statement, The Laminitis Site suggested that "whilst there may be little justification to feed more than small amounts of something that is mostly water and sugar (and a source of vitamin A), on an as fed basis, carrots contain around 6% combined sugar and starch - less than some hays and several feeds that carry "safe for laminitics" marks."

The ECEIM responded to this comment, saying: "Regarding carrots, these may contain more than 60% starch and sugar on a dry matter basis and are clearly high-NSC feed items (Brøkner et al 2012), unlike most hays. Whilst accepting that the absolute amount of sugar in one fresh carrot is quite small, it would still contain more sugar than in other items such as sugar lumps for example, yet we would quite rightly avoid those in an insulin-dysregulated horse. We regard the feeding of high-sugar feed items such as carrots (and sugar lumps) as unnecessary and poor discipline for those governing the diet of laminitis-prone horses. Carrots are not a natural feed item for horses and they add no nutritional value to a well-balanced diet as described in the consensus statement."  The ECEIM comment can be read here. 

We thought it would be interesting to compare the total sugar and starch on an as fed basis (as that is what the horse eats) of sugar cubes, raw carrot and The Laminitis Trust approved (until 2019 - see above) Spillers High Fibre Cubes. 

Sugar: 2 cubes of sugar weighed 5.15 g on a gram scale.  Sugar cubes are 100% sucrose on both an as fed and dry matter basis (sucrose is half glucose, half fructose).

Carrot: 83.5 g of raw carrot contains approximately 5.15 g of sugar and starch combined.
Using the USDA Nutrient Database figures for raw carrot: sugar content 4.74% (0.55% fructose, 0.59% glucose, 3.59% sucrose) and starch content of 1.43%  = 6.17% combined, so 6.17 g of sugar and starch in 100 g.  83.5 g of carrot x 6.17% sugar/starch = 5.15 g of sugar/starch.  Our 15+ cm reasonably thick carrot weighed 83 g.

Spillers High Fibre Cubes: 35.5 g of High Fibre Cubes contains approximately 5.15 g of sugar and starch combined.  The feed label and website give the sugar content as 4.5% and the starch content as 10% = 14.5% combined, so 14.5 g of sugar and starch in 100 g.  35.5 g of Cubes x 14.5% sugar/starch = 5.15 g of sugar/starch. 

So looking at the ECEIM's statement:
1.  Carrots are not fed on a dry matter basis, they are fed on an as fed basis, and their combined sugar and starch levels are low - 5.15 g in a pretty average 83 g carrot, 6.17 g in a 100 g carrot.  It doesn't matter for this discussion whether we talk about carrots on an as fed or dry matter basis.  As fed, a 100 g of carrot contains around 6.17 g of sugar and starch.  On a dry matter basis, the same 100 g carrot contains 88.3 g of water, so is 11.7 g dry matter, and its sugar and starch % is (6.17 / 11.7 =) 52.7%.   So whilst on a dry matter basis you are feeding a carrot with a scary sounding sugar/starch amount of 52.7%, you are only feeding 11.7 g of it (because you aren't counting the water), and 11.7 g x 52.7% = 6.17 g of sugar and starch (surprise, surprise!).

Equine nutritionist Clare MacLeod commented (on The Laminitis Site Facebook page 14 February 2019) "Carrots are NOT high in NSC on an as fed basis. Period. It's a classic but fundamental error to assign the characteristics of a feed material DM when it's fed in its fresh state." 

Brokner et al. 2012 analysed freeze-dried carrots - the DM content of the freeze-dried carrots was 89.1%, sugar 58.1% (glucose 12.4%, fructose 12.5% and sucrose 33.2%), fibre 27.8%, protein 7.4%, starch negligible - all figures given on a dry matter basis.  Using the water content for fresh carrot given in the photo above, 11.7 g per 100 g, these freeze-dried carrots rehydrated to fresh weight would have had 6.8 g of sugar (and no starch) per 100 g.  Freeze-dried carrots are full of sugar, fresh carrots are not - it's all about the water content, as well as the sugar %. 

Equi-Analytical has lower figures for carrots than the USDA figures given above (figures as at February 2019).
Average WSC is 31.05% x DM content of 13.18% = 4.09% as fed, average ESC 20.6% = 2.72% as fed, average starch 2.18% = 0.29% as fed, so total sugar and starch (using WSC) = 4.38% as fed.

​2.  As the photo below shows, on a weight for weight basis, you can feed more than twice as much fresh carrot as High Fibre Cubes, and more than 16 x as much carrot as 2 sugar lumps, for the same amount of sugar and starch.  In our example we're talking about 5.15 g of sugar and starch, out of a possible 999 g for a 500 kg horse eating 2% of his bodyweight and keeping the combined sugar and starch in his diet below 10%.

​​3.  As for the feeding of carrots being "unnecessary and poor discipline", slivers of carrot can make useful training aids, which can be invaluable for encouraging a horse that is perhaps in pain or frightened to work with you, for example to pick up feet for examination or to stand quietly on blocks for x-rays to be taken or to have blood collected.  See Hand-Feeding Treats to Horses by Dale Rudin Feb 2019 for benefits of using food rewards for training.

A slice of carrot can make a perfect hiding place for a Prascend tablet.  Consider also, a horse newly diagnosed with EMS or laminitis has probably already had restrictions and less pleasant management imposed on him - he has probably been removed from going out in the field with his mates and eating grass, and may be shut in a stable for hours on his own, eating what he considers to be boring soaked hay from a small holed haynet that is frustrating him.  He hasn't been naughty, he is ill.  If he is used to having the odd slice of carrot for being well behaved, or perhaps last thing at night, why remove yet another pleasure - his quality of life should be maximized, not minimized.  Put yourself in your horse's place.  Of course you want strict management to reduce his risk of laminitis or to hasten his recovery, but not to the extent of giving him nothing to live for!  It's all about looking at the numbers, thinking about what your horse wants and needs, and finding a balance.  
​
4.  "Carrots are not a natural feed item for horses" - so only natural feed items should be fed to horses?  And what is a "natural feed item" - something a feral horse would find?  So no unmolassed sugar beet, no soya mashes, no mineral balancers....  Feral horses may struggle to dig up a carrot growing in the wild, but they'd certainly eat apples - so does that make apples ok, but not carrots?! 
​
5.  Some owners add single minerals and vitamins to their horse's diet to make up for short falls in their forage, and carrots provide a very useful source of vitamin A.  It is certainly not the case that they add "no nutritional value", although the ECEIM may argue that all horses should be fed a balancer that contains vitamin A.  There are also small amounts of protein (7.9% DM) and fibre (24% DM), minerals and oil in a carrot - compared to a sugar lump which has no nutrients other than sugar (energy).

Perhaps the ECEIM authors deal with owners who would feed kilos of carrots if they were told that horses with ID could have carrots, but that certainly isn't our experience.  We know of many owners of horses with EMS and laminitis who give their horses a small amount of carrot (generally less than 100 g/day) with no problems.

​Durham AE, Frank N, McGowan CM, Menzies-Gow NJ, Roelfsema E, Vervuert I, Feige K, Fey K
ECEIM consensus statement on equine metabolic syndrome
Journal of Veterinary Internal Medicine published online 06 February 2019 https://doi.org/10.1111/jvim.15423

Brokner C, Bach Knudsen KE, Karaman I, Eybye KL, Tauson AH
Chemical and phsiochemical characterisation of various horse feed ingredients
Animal Feed Science and Technology 177 (2012) 86-97

​Sometimes ACTH produced normally by the pars distalis (PD) as part of the hypothalamic-pituitary-adrenal (HPA) axis appears to be confused with ACTH produced by the pars intermedia (PI) due to lack of dopaminergic inhibition in horses with PPID.

All horses, whether they have PPID or not, react to a stress stimulus as follows:
CRH and AVP (vasopressin) are released by paraventricular neurons in the hypothalamus.
CRH and AVP stimulate corticotropes in the pars distalis (or anterior pituitary) of the pituitary gland to secrete ACTH.
ACTH travels in the blood to the adrenal glands, on top of the kidneys, where it stimulates the adrenal glands to release cortisol.
Cortisol is carried in the blood back to the hypothalamus and the pars distalis of the pituitary gland, which recognize the high levels of cortisol, and decrease or turn off CRH, AVP and ACTH release - this is called negative feedback, it prevents excessive hormone production.

In a normal horse, the pars intermedia produces a peptide called POMC, which is changed to ACTH by an enzyme, PC1, then nearly all the ACTH is changed into alpha-MSH, beta-endorphin, CLIP and other hormones by another enzyme, PC2. Hormone production in the PI is controlled by dopamine, released by hypothalamic periventricular dopaminergic neurons, interacting with D2 dopamine receptors on the ​PI.

In horses with PPID, dopamine producing neurons are lost, and with less dopamine to inhibit hormone production, the PI releases massively increased amounts of alpha-MSH, beta-endorphin and CLIP, and also ACTH. 

In a normal horse, only around 2% of circulating ACTH is made in the pars intermedia, 98% comes from the pars distalis, and dopamine plays no part in controlling normal ACTH output from the PD.

The excess levels of alpha-MSH, beta-endorphin and CLIP are thought to contribute to causing the clinical signs of PPID. The plasma ACTH in PPID horses is thought to be less biologically active than plasma ACTH in normal horses, which may explain why horses with PPID rarely have above normal cortisol levels. The lack of dopamine and increase in POMC-derived hormones leads to an increase in the number (hyperplasia) and size (hypertrophy) of the cells in the PI, eventually leading to adenoma (tumour) formation - this has nothing to do with cortisol.

The precise cause of PPID is still unknown, but research suggests that localised oxidative stress may contribute to dopaminergic neuron damage and death. However in 2005 Dianne McFarlane found that "there was no evidence of systemic accumulation of oxidative stress markers or deficiencies in antioxidant capacity in horses with PPID, suggesting that these are unlikely to be major predisposing factors in the development of PPID" (Systemic and pituitary pars intermedia antioxidant capacity associated with pars intermedia oxidative stress and dysfunction in horses). 

In her 2011 paper on Equine PPID, Dr McFarlane states that pituitary antioxidant capacity has not been shown to be impaired in horses with PPID, but that the impairment of the activity of pituitary manganese superoxide dismutase found in older horses may contribute to the risk of PPID developing with age.

She goes on to say that excellent nutrition is important for horses with PPID, and that in theory, feeds high in antioxidants could slow the neurodegenerative process associated with PPID, but that there is currently no evidence for this. Early treatment with pergolide to replace the missing dopamine and reduce excess hormone production and the clinical signs of PPID is advised. Interestingly, research by Gille et al. (2002) found that "pergolide protects dopaminergic neurons under conditions of elevated oxidative stress"; similarly research by Uberti et al. in the same year suggested that "pergolide ... may interfere with the early phases of the oxidative stress-induced neurotoxic process". Dr McFarlane theorises that any antioxidant and neuroprotective properties of pergolide could be beneficial in slowing the progression of PPID.

So in conclusion, optimal management and treatment with pergolide is recommended for horses with PPID, but it appears that further research is needed before we can say for sure exactly what might slow the progression of this common equine neurodegenerative disease.

For more information, join Friends of The Laminitis Site and access our Facebook discussion/support group Friends of The Laminitis Site 1.

Notes from a short video by Andy Durham on Boehringer Academy.

Q: Should I seasonally alter the dose of Prascend in my PPID positive patients?

A: There is clear evidence that pituitary activity increases in the autumn. Some horses test normal throughout the year but positive (for PPID) in the autumn, other horses test routinely positive throughout the year with strong positives in the autumn.

Pergolide decreases pituitary activity, therefore it is logical to consider altering the dose of pergolide during the autumn seasonal rise.

Be aware that if a horse (with PPID) has its ACTH tested in August/September and a loss of endocrine control is identified and the dose of pergolide subsequently increased, by the time ACTH is checked again 30 to 60 days later, the seasonal rise is likely to have peaked and be almost over.

However, if it is established that a horse does lose endocrine control in the autumn, then the dose of pergolide could be increased the following July/August in preparation for the seasonal rise.

​It is a logical approach to increase pergolide for the seasonal rise; it needs further research, but many people have adopted this approach already

​Body condition scoring (BCS), or fat scoring, is a method of assessing the amount of fat a horse is carrying, and can help owners recognize whether their horse is over or under weight.  It should be carried out regularly, ideally every 2 weeks, so that weight gain or loss can be acted upon appropriately.

There are two systems in use:

The 9 point system, developed by Dr Henneke.  6 parts of the body - neck, withers, shoulders, ribs, loins and tailhead - are given a score from 1 to 9, with a body condition score of 5 being considered ideal for leisure/riding horses, and a BCS over 7 indicating obesity.

The 5 or 6 point system, which divides the horse into 3 sections - neck/shoulder, back/ribs and bottom, and gives each section a score between 0 and 5, where 0 = emaciated, 1 = poor, 2 = moderate, 3 = good, 4 = fat and 5 = obese.

Both systems are based on visually assessing the horse and feeling for fat deposits/bones.  

9 point system

Test your knowledge of body condition scoring - Coursera Equine Nutrition 

Body Condition Scoring System - Benefits for Horses and Owners - Mississippi State University Extension ​

Equine Body Condition Score poster - www.thehorse.come Aug 2014

Body Condition Scores - The Henneke System - Robin Easley - photo examples of all body conditions scores

​In this video from Spillers/Horse&Rider Essentials two horses are body condition scored - the first has a BCS of 6.5/9, the second a BCS of 6/9.

​6 point system

Body condition scoring and cresty neck scoring - CARE About Laminitis

How to Condition Score - British Horse Society
​
Fat Horse Slim - The Blue Cross

Is your horse the right weight? - World Horse Welfare

​This video (below) by Dr Teresa Hollands - as shown in the October 2013 The Laminitis Revolution 2 webinar - shows how to body condition score your horse, using the modified 0-5 point scoring system. Horses that are too thin, too fat and just right are used to demonstrate how to assess BCS, including a typical underweight PPID horse and a typical overweight EMS/PPID pony.

The body should be divided into 3 sections: neck, middle and bottom, and each section scored separately by feeling for fat over the skeleton. 3 is the perfect score. Body condition scoring should be carried out ideally every 2 weeks on all horses, and the results recorded.

Neck - there shouldn't be any fat or crest above the nuchal ligament - there is no muscle above the nuchal ligament, anything felt here is fat, not top line. A large crest will score 4 or more, bulges and corregation in the crest will probably score 5.
The shoulder blade should be well defined - if you run your hand down the side of the neck, it should come to a stop at the shoulder blade.

Middle - you should be able to feel the ribs, like feeling stair banisters through a velvet curtain, but hardly see them. If you can neither see nor feel the ribs, that scores 4 or more. 
If you place your hand over the backbone, it should form a nice curve - a triangle is too thin, flat is too fat.

Bottom - you should be able to feel just feel the top of the pelvis, the hip bone and the tail bone. If you can't see or feel these bones, that scores 4 or more.

Research has shown that if a horse is overweight, for the all fat that is visible or can be palpated under the skin, there is probably the same amount inside the horse that can't be seen, wrapped around the organs and killing the horse from the inside.

In summary, if you can feel AND see bones, the horse is too thin.
If you can neither feel nor see bones, the horse is too fat.
If you can feel but not see bones, the horse is just right. 

​In this video from World Horse Welfare, a native pony is assessed and found to have a body condition score of 4.5/5, meaning he is on his way from fat to obese.

In this video from The Blue Cross, use of a weight tape is demonstrated, and a pony is body condition scored and given a score of 4.

Help for weight loss
​
Lightening the load - Redwings
​
Fat Horse Slim - The Blue Cross

Is your horse the right weight? - World Horse Welfare

​Did you know that it is illegal in the UK for a company to sell any substance that claims to treat, prevent or control disease (including laminitis and PPID) in horses, or that claims to restore, correct or modify physiological functions by "exerting a pharmacological, immunological or metabolic action", unless that product has a marketing authorisation. This includes nutraceuticals (food supplements) and herbal products.

A product doesn't actually have to treat, prevent or control disease - it must not give an averagely well-informed person the impression that it treats or prevents disease. This includes claims made on product labels, leaflets, adverts, websites, chat rooms/forums or by spoken recommendation, claims made by a third party where a connection exists with the marketing company, or references in marketing material to studies suggesting that a product or ingredient has a medicinal effect.

"If a product refers, expressed or implied, to the treatment or prevention of a disease or adverse condition, or to improving the condition of the animal treated, it is making medicinal claims. For example, medicinal claims include a reference to the treatment or prevention of scours, mastitis, colic, footrot, laminitis, eczema, or to stress related to nervous conditions such as hyperactivity, or any other condition which is not the normal state of a healthy animal."

See Legal controls on veterinary medicines for details.

Marketing authorisation numbers will be shown on all packaging, and can be checked on the NOAH database
- see the MA for Prascend on the NOAH database -
or on the VMD product information database.

Unauthorised products can be reported by email or post using this form:
Report an animal product being marketed as a medicine

False or misleading advertising claims about a product, but not relating to medicinal claims, should be reported to your local Trading Standards Officers under the Trade Descriptions Act 1968, or to the Advertising Standards Authority.
​

Pituitary Pars Intermedia Dysfunction, or PPID, is an endocrine disease that can affect any horse, pony or donkey, regardless of breed, sex or management.  It’s a progressive, degenerative disease, so incidence increases with age and it generally has a slow insidious onset, making it difficult to detect and diagnose in the early stage.  The excess hormones produced affect various body systems, and individual horses can show different symptoms, some of which can be serious, like laminitis. 

PPID used to be called Equine Cushing’s Disease, as there were thought to be similarities with Cushing’s Disease in humans and dogs, which involves a tumour that causes high levels of ACTH to be produced in the pars distalis of the pituitary gland, leading to high levels of cortisol, but no neurodegeneration.  However, PPID in horses is different and is caused by neurodegeneration, affects the pars intermedia of the pituitary gland, and causes high levels of several hormones, but cortisol levels are often normal.

The pituitary gland lies below the hypothalamus at the bottom of the horse’s brain.  It consists of three major hormone-releasing lobes: the pars distalis, the pars nervosa and the pars intermedia.
 
All horses, whether they have PPID or not, react to stress by releasing ACTH from the pars distalis into the blood.  This tells the adrenal glands to release cortisol, which plays a role in the “fight or flight” response.  The high levels of cortisol in the blood “feed back” on the pars distalis, reducing ACTH production. 

In a normal horse, the pars intermedia plays a role in seasonal changes, metabolism and inflammation, producing a peptide called POMC, which is initially changed to ACTH, then around 98% of that ACTH is changed to alpha-MSH, beta-endorphin and CLIP before being released into the blood. This hormone production is slowed or stopped when neurons originating in the hypothalamus release dopamine (a neurotransmitter or chemical messenger) onto receptors on the pars intermedia.  The pars intermedia is stimulated by the hormone TRH – this can be manipulated for diagnostic testing.

With PPID, the dopamine-producing neurons in the hypothalamus slowly degenerate, and with less dopamine to inhibit hormone production, the pars intermedia releases massively increased amounts of alpha-MSH, beta-endorphin, CLIP and also ACTH, which are thought to cause the clinical signs of PPID.  The excess ACTH produced in horses with PPID may be less biologically active than normal, which may explain why horses with PPID often have normal cortisol levels, even when blood tests report high ACTH levels.

As in any factory, increased production leads to expansion - the pars intermedia cells increase in number (hyperplasia) and size (hypertrophy), often leading to adenoma (benign tumour) formation, and causing the pars intermedia to increase in size (a normal pituitary gland weighs around 2 g, in a horse with advanced PPID it can weigh more than 10 g), which may cause compression of the other lobes of the pituitary gland.  

What causes PPID?

The cause of PPID is still unknown, but research suggests that localised oxidative stress may contribute to dopaminergic neuron damage and cell death.  Dr Dianne McFarlane found decreased activity of the antioxidant manganese superoxide dismutase in the pars intermedia in older horses, which could contribute to the risk of PPID developing with age, and she also found evidence of protein misfolding in the pars intermedia of horses with PPID, similar to that found in Parkinson’s disease. 

In her presentation on the Pathophysiology of PPID at the 2011 Equine Endocrinology Summit, Dr McFarlane suggested that there may be several syndomes that lead to PPID, such as metabolic disorders like EMS, toxins in the environment, stress or genetic predisposition.  This might explain why individual horses with PPID can have differing symptoms and hormone levels.

Diagnosis of PPID  

Diagnosis of PPID is based on clinical signs and history, backed up by above normal ACTH blood test results.  Although incidence increases with age, horses as young as 6 or 7 have been diagnosed with PPID.

Clinical signs  

The clinical signs seen vary between horses and with the stage of the disease, and are often mistaken for normal ageing.  Experts often group clinical signs into early or advanced stage, but there is likely to be overlap.  Symptoms are often worse during the autumn “seasonal rise”.

Early signs may include:

• Long hair on legs, neck and face.
  
• Delayed or patchy shedding of haircoat.
  
• Muscle loss along topline.
  
• Lethargy/depression/docility.
  
• Decreased athletic performance.
  
• Laminitis (usually with abnormal fat deposits and insulin dysregulation). 
  

• Abnormal haircoat – from a thicker than normal summer coat, long coarse hairs in the coat or patches of long hair to a long shaggy coat (hypertrichosis) that doesn’t shed at all.
  
• Hyperglycaemia (above normal blood glucose concentrations).
  
• Neurological symptoms such as ataxia, seizures and blindness.
  

It has been considered that hypertrichosis – the long coat that doesn’t shed – is diagnostic of PPID, but whilst it is highly suggestive, there can be other causes, such as severe malnutrition.

Scooby on arrival at Remus Horse Sanctuary showing hypertrichosis and muscle loss, and after being clipped and starting treatment for PPID.

It is currently thought that some but not all horses with PPID will also be at risk of laminitis – they have PPID and Equine Metabolic Syndrome (EMS), and are likely to have insulin dysregulation and abnormal fat deposits, e.g. cresty neck, filled supra-orbital hollows and fat around the tailhead, in addition to other symptoms of PPID.  To identify these horses and assess laminitis risk, insulin dysregulation should be measured in all horses suspected of having PPID.  Horses with PPID that have never had laminitis and that have normal insulin may not be at greater risk of developing laminitis than any other horse. 

Although it isn’t yet known whether having EMS causes PPID, it seems that horses with EMS may be at greater risk of developing PPID as they get older, and therefore horses with EMS should be monitored and tested for PPID, and their diet, weight and exercise addressed with the aim of reversing EMS.  Vets are also noticing that there appears to be a transitional period as horses with EMS develop PPID during which their insulin concentrations and therefore risk of laminitis increase.  

Blood tests

As PPID is a progressive disease, blood tests are often negative in the early stages, but false positives are also seen when ACTH is released as part of the normal stress response.  Hormone levels are affected by seasons and geographical location, are released in pulses so concentrations can change within minutes, and vary considerably between affected horses. 

When resting ACTH results are borderline or negative despite a suspicion of PPID, the TRH stimulation of ACTH may be recommended.  A resting ACTH blood sample is collected, then 1 mg of TRH is injected and a further ACTH blood sample collected 10 minutes later.  Horses with PPID appear to produce more ACTH in response to an injection of TRH than normal horses.  Currently this test cannot be used in the autumn, and more research is required to define normal reference ranges.

All horses suspected of having PPID should be tested for insulin dysregulation using either a resting insulin test, or if no clinical signs of insulin dysregulation are seen and/or if resting insulin test results are normal, an oral sugar test, to assess laminitis risk. 

The dexamethasone suppression test, once considered the gold standard for PPID testing, is no longer recommended as it may cause laminitis, requires two vet visits, cannot be used in the autumn, and may only detect advanced cases.  Tests measuring cortisol are not diagnostic for PPID.

All horses have a “seasonal rise” in pars intermedia hormone production in the autumn, probably to help them prepare for the winter, which starts as days begin to get shorter and is considered significant from August to October.  The increase is greater in horses with PPID, making this the best time to test ACTH, as long as seasonally adjusted reference ranges are used.  

A diagnosis of PPID should only be made if there are clinical signs of PPID.  There is no way of knowing whether the ACTH in a blood sample is from the pars intermedia and suggests PPID if abnormally high, or has been produced by the pars distalis as part of a normal stress response.  “Stress” can be due to pain (e.g. laminitis), illness, excitement, exercise, travelling, use of a twitch, veterinary procedures e.g. dental work or “white coat phobia”.  Some medicines may increase ACTH, e.g. clenbuterol (Ventipulmin) and some sedation durgs, and current advice (from Liphook Equine Hospital) is that ACTH should not be tested following sedation.  Note also that freezing the blood sample before it has been separated by centrifuge can lead to falsely high ACTH results.

In the future, testing of other PPID hormones may be commercially available, which may make blood testing more accurate.

The initial dose of Prascend recommended is 0.002 mg/kg bodyweight once a day, so 1 mg for a 500 kg horse, but the dose may depend on the stage of the PPID, the season and other factors, and it should be titrated to the lowest effective dose for each individual horse based on response to therapy, whether that is improvement in clinical signs and blood results or signs of intolerance.  Many horses require an increased dose during the seasonal rise, with a subsequent reduction in dose around Christmas.  

Some horses go off their food or become depressed when starting treatment with pergolide, but when introduced gradually, ideally starting with 0.25 mg and slowly increasing to the recommended dose, side effects are minimised.  Giving pergolide at different times to bucket feeds has helped some horses overcome inappetence.

Response to treatment is individual, but the EEG suggests that within 30 days of starting treatment an improvement in lethargy and depression, PU/PD and blood glucose concentrations should be seen, with improvements in haircoat abnormalities, improved topline and reduced incidences of laminitis and infections within a year.  In The Laminitis Site’s experience, improvements are often noticed sooner than this, particularly when the PPID has not yet reached the advanced stage.

Currently there is no research that supports the use of herbal, homeopathic or other non-medical treatments for PPID.  Some owners report improvements in depression and coat shedding with Vitex agnus castus, but research by Jill Beech et al. (2002) found no improvement in hormone levels and that clinical signs sometimes worsened when PPID horses were treated with Vitex agnus castus.

Management is also very important and should be optimized.  Excess hair should be clipped and rugs used to help regulate the horse’s body temperature.  The diet should contain above minimum levels of quality protein, minerals, vitamins and essential fatty acids, with energy levels appropriate for the horse’s lifestyle, and sugar and starch amounts kept low if the horse has insulin dysregulation.  In theory feeds high in antioxidants could help to slow the neurodegenerative process that causes PPID, but there is currently no evidence for this.  Attention should be paid to dental care, foot care, worming and vaccinations, and infections should be treated without delay.

Conclusion

Whilst there is still a lot to learn about PPID, recent advances in our knowledge have enabled horses to be diagnosed and start treatment much earlier in the disease process, with the result that many horses with PPID are living quality lives well into old age.

References:
 
Is it PPID or EMS? Diagnosing Equine Endocrine Disease – a presentation by Dr Dianne McFarlane which can be viewed at www.thehorse.com

Equine Endocrinology Group
Recommendations for the Diagnosis and Treatment of Pituitary Pars Intermedia Dysfunction (PPID) 2014
http://sites.tufts.edu/equineendogroup/
 
AAEP proceedings Vol 48 2002
Comparison of Vitex agnus castus Extract and Pergolide in Treatment of Equine Cushing’s Syndrome
Beech J, Donaldson MT, Lindborg S 

J Neural Transm. 2002 May;109(5-6):633-43
Pergolide protects dopaminergic neurons in primary culture under stress conditions
Gille G, Rausch WD, Hung ST, Moldzio R, Janetzky B, Hundemer HP, Kolter T, Reichmann H

2nd European Equine Endocrinology Symposium 14-16 May 2014
The use of ACTH response to TRH stimulation for monitoring horses with PPID and those receiving long-term pergolide
McFarlane D, Banse HE, J Fredrick, Yang F

Equine Endocrinology Summit 2011
Pathophysiology of Pituitary Pars Intermedia Dysfunction in 2011
Dianne McFarlane

Equine Veterinary Journal Vol45, Issue 1, pages 74–79, January 2013 (published online May 2012)
Prevalence, risk factors and clinical signs predictive for equine pituitary pars intermedia dysfunction in aged horses
McGowan TW, Pinchbeck GP, McGowan CM

CAB Reviews 2015 10. No. 002
Equine Endocrinology
Menzies-Gow NJ

Abbreviations:

Alpha-MSH – alpha-melanocyte-stimulating hormone
ACTH – adrenocorticotropic hormone
CLIP – corticotrophin-like intermediate peptide
EEG – Equine Endocrinology Group
EMS – Equine Metabolic Syndrome
PPID – Pituitary Pars Intermedia Dysfunction
POMC – pro-opiomelanocortin
TRH – thyrotropin-releasing hormone

This article was originally published in The Arabian Magazine July 2015 and has been updated since publication.

Recognising and treating Equine Metabolic Syndrome (EMS) is essential to improve insulin sensitivity and reduce the risk of laminitis.  Experts also now suspect that horses with EMS may be at greater risk of developing PPID as they get older.  EMS is not a disease, it is a cluster of factors that indicate that a horse is at greater risk of developing endocrinopathic laminitis.  It is preventable and reversible with correct management.

Often seen in “easy keeper” breeds including native ponies, Arabians, Morgans and Iberians, a horse with EMS will usually have:

1.  General obesity or regional adiposity (a cresty neck, filled supraorbital hollows, fat behind the shoulders and around the tailhead, swelling around the sheath/mammory glands);

2.  Insulin dysregulation - insulin resistance and/or hyperinsulinaemia (indicated by blood tests); and

3.  A predisposition to or history of laminitis - signs of chronic laminitis such as hoof rings wider at the heels, a less-than-tight white line and a change of angle in the hoof wall may be seen in the feet, and x-rays may show rotation and remodelling of the pedal bone.

Obesity  

Obesity develops when horses have too much food and too little exercise.  As the horse becomes obese and fat cells become full, the insulin signaling pathway is disrupted, causing insulin resistance.  Fat cells release pro-inflammatory chemicals that cause systemic inflammation, and hormones including leptin, a “stop eating” hormone released when the horse has excess energy stored.  High levels of leptin cause the target cells to become less receptive, or resistant, to the message to stop eating, so the horse continues to eat and put on weight.  Obesity may also affect liver function resulting in reduced insulin clearance and consequent hyperinsulinaemia.

Research has suggested that weight gain has a greater impact on insulin sensitivity in certain breeds, with Arabians becoming insulin resistant when fed excess energy, but Thoroughbreds showing no decrease in insulin sensitivity with weight gain.

Measurements to help identify obesity should be carried out regularly (e.g. every 2 weeks):

1. Cresty neck score from 0 to 5, with scores of 3 or greater often being seen in horses with EMS.  A cresty neck score of 3 is described as “Crest enlarged and thickened, so fat is deposited more heavily in middle of the neck than towards poll and withers, giving a mounded appearance.  Crest fills cupped hand and begins losing side-to-side flexibility.”  

2. Neck circumference.

3. Bodyweight using scales, a weight tape or calculations from measurements.

4. Body condition scoring – 8 or 9 on the 9 point Henneke scale is considered obese, 6 and 7 overweight.  A 0 to 6 scale is also used, with scores of 4 and 5 being considered overweight and obese - see Body Condition Scoring Video.

Genetics  

Some breeds appear to be more predisposed to EMS than others and there is likely to be a genetic tendency, but developing EMS may depend on certain environmental factors being present, or multiple genes being involved.  For example, scurry ponies in active competition tend to have low insulin concentrations, but insulin levels rise when they are not in work, suggesting that exercise helps to prevent them developing EMS.

Breeds adapted to survival when feed is scarce, e.g. cold winters, summer droughts, may be particularly likely to become obese and develop insulin resistance when they have plentiful food all year round.

Native ponies naturally gain weight during the summer when food is abundant and lose weight during the winter, and without these seasonal changes in body condition and insulin sensitivity, horses may become increasingly obese and insulin resistant.

Insulin

In 2007 it was first discovered that giving healthy horses high levels of insulin caused them to develop laminitis (Asplin et al.).   It is hyperinsulinaemia, i.e. above normal levels of insulin, not insulin resistance, that causes endocrinopathic laminitis, but they are often linked, hence the term “insulin dysregulation” is now used to cover both hyperinsulinaemia and insulin resistance.

When a healthy horse eats sugar or starch, blood glucose levels rise and the pancreas releases insulin, which enables glucose to enter insulin sensitive cells, such as muscle.

When an insulin resistant horse eats sugar or starch, blood glucose levels rise and the pancreas releases insulin, but the insulin sensitive cells don’t respond to normal amounts of insulin and glucose doesn’t enter the cells efficiently.  The pancreas compensates by releasing more insulin, which enables glucose to enter the cells and keeps blood glucose levels reasonably normal, but results in increased blood insulin levels, or hyperinsulinaemia. 

This is illustrated in research by Katie Borer et al. published in 2012.  Ponies with no history of laminitis (normal) and ponies with a history of laminitis (laminitic) were fed ad lib soaked Timothy hay and a daily feed of 14% sugar/starch chaff, to which 1 g/kg bodyweight of glucose, fructose and inulin, a type of fructan, were added.  The previously laminitic (therefore assumed to have EMS) ponies had a much greater insulin response to glucose than the normal ponies, but their blood glucose levels showed less difference.  Note that chaff plus fructan had no greater effect on insulin or glucose than chaff alone.

Diagnosis of insulin dysregulation  

1. Resting insulin - a single blood sample is tested after the horse has been eating his usual eating hay (note that fasting before a baseline insulin test is no longer recommended for diagnosing EMS; however it may be useful for assessing baseline hyperinsulinaemia in horses with PPID).  “Testing horses in the fed state allows for better assessment of insulin dysregulation” (Frank and Tadros 2013), but results may be harder to interpret if sugar/starch levels of the hay are not known.  Results above 20-30 mIU/ml are often considered diagnostic of hyperinsulinaemia, but the reference range is specific to the testing laboratory. 

If a resting insulin test is normal but the horse has a history of laminitis or is suspected to have EMS, a dynamic test should be carried out.

2. Oral sugar test (OST) – the horse is fasted for at least 6 hours then fed 0.15 ml/kg bodyweight Karo Light corn syrup and blood sampled at 60 and 90 minutes and tested for insulin and glucose.  Insulin <45 mIU/ml is considered normal and >60 mIU/ml is considered diagnostic of insulin dysregulation. 
More recently it has been suggested that the Oral Sugar Test may be more reliable using the higher dose of 4.5 ml/kg bodyweight Karo Light corn syrup.  Originally it was suggested that horses did not need to fast before the higher dose test, but fasting may be recommended by the laboratory/vet.  See Karo Light Corn Syrup test for assessment of insulin dysregulation - Liphook Equine Hospital.  This test measures the horse’s response to sugar in the diet at the level of the digestive system, pancreas and insulin sensitive tissue.

Current tests are not perfect and diagnosis of EMS should be based on history and clinical signs as well as blood test results.  

Managing horses with EMS  

Diet, weight loss if necessary and exercise are key to preventing and treating EMS.

Diet/weight loss 

The total combined sugar (ESC) and starch in the diet should be no more than 10% to keep insulin levels low, and if weight loss is required, energy fed will need to be less than energy expended.  The severity of the horse’s insulin dysregulation will dictate how strict the sugar/starch restriction needs to be.

Vitamin E, copper, zinc, selenium and sodium are typically deficient in hay.  Hay can be soaked in water to reduce sugars, although the amount of sugar loss is variable and may depend on the amount of water used, the temperature of the water, how fibrous the hay is and other factors.  A popular myth is that old hay is better for laminitics – according to Katy Watts of www.safergrass.org, the only nutrients correctly made and stored hay will lose over time are vitamins, not sugars.

A typical diet might consist of grass hay plus the recommended amount of a low calorie balancer or mineral supplement, mixed with a low sugar/starch chaff or unmolassed sugar beet, plus salt and linseed (flaxseed).

Low energy feeds should be selected to maximise intake without oversupplying calories.  Looking at the analysis of feeds rather than the description is important, e.g. some "high fibre" cubes contain almost 20% combined sugar and starch and would not be suitable for most EMS horses, and feeds claiming to be approved or suitable for laminitics can contain over 14% combined sugar and starch. 

Grass will often provide too much energy and be too high in sugar/starch for an EMS/overweight horse. 

Horses with insulin dysregulation that need to gain weight can be fed increased amounts of hay and/or higher energy low sugar/starch feeds such as umolassed sugar beet (beet pulp).

Weight loss is induced by restricting calories eaten and by increasing exercise if the feet are stable.  A common suggestion is to feed a horse 1.5% of its ideal, or current, bodyweight (with the diet based on hay with added minerals as described above).  If weight loss isn’t seen, this amount may need to be reduced, or ideally a lower energy forage sourced.  Feed intake should not go below 1.5% of the horse’s bodyweight without veterinary supervision.  Severe calorie restriction can worsen insulin resistance, risk hyperlipaemia and cause stereotypical behaviour.

Grass  

Access to unrestricted grass commonly triggers laminitis in EMS horses, as sugars increase insulin levels and increased energy intake promotes weight gain.  Access to grass should be restricted until insulin sensitivity has returned to normal, with high risk horses perhaps turned out in a dry lot or dirt paddock if the feet are stable to encourage exercise.  Many horses that have had EMS can return to pasture once weight has been lost and insulin sensitivity has returned to normal, but may need to have access to grass restricted during high risk times, such as during rapid spring growth or when grass is stressed and cannot grow due to cold weather or drought. 

Factors that affect sugars in the grass include:

Sunlight - photosynthesis and sugar production increase with sunlight intensity, so sugar levels will be higher on sunny days and lower on cloudy, overcast and rainy days.  Grass growing in direct sunlight will have more sugar than grass growing in the shade.

Time of day – sugar levels peak around late afternoon on a sunny day, then decrease with respiration once the sun sets, so sugars are likely to be lowest in the early morning.

Temperature – night temperatures below 5’C cause sugars to accumulate in the grass, and laminitic horses should avoid grazing during periods of sunny days and cold nights, until warmer nights or overcast weather returns.

Exercise  

Regular physical exercise is likely to improve insulin sensitivity and help promote weight loss, and is recommended for EMS horses as long as the feet are stable.  The ACVIM consensus statement suggests at least 2-3 sessions of 20-30 minutes of riding or lunging per week, gradually increasing in intensity and duration.  Other recommendations for obese horses free of laminitis include riding or lunging 4 to 7 days a week with at least 30 minutes of trot and canter, plus warm up and cool down.
See Exercise
Movement - good or bad?

Medication  

The ACVIM consensus statement states “Most horses and ponies with EMS can be effectively managed by controlling the horse’s diet, instituting an exercise program, and limiting or eliminating access to pasture.”

Levothyroxine sodium is sometimes given, more commonly in the USA than UK, to induce weight loss.

Metformin is sometimes prescribed for horses that cannot exercise due to laminitis, at the dose of 30 mg/kg bodyweight twice a day.  Giving this dose of Metformin before a glucose feed led to reduced glucose and insulin levels compared to controls, but the paper concluded that the potential benefits of giving Metformin to  horses on a low NSC diet may be questionable (Rendle et al. 2013).

Supplements 

Whilst various supplements such as magnesium, chromium and cinnamon have been suggested for the management of horses with EMS, currently there is insufficient scientific evidence to support the use of any of these supplements, and where research has been carried out, no or little benefit has been found.  
See There are no magic potions!

Is EMS reversible?  

In theory, yes, EMS is both preventable and reversible.  EMS is not a disease, but a collection of factors that increase the risk of endocrinopathic laminitis.  Remove these factors (being overweight, having regional fat deposits, having abnormally high insulin levels), and technically the horse no longer has EMS – although some horses with a stronger genetic tendency may always need more careful management than others.  The reversal of obesity is likely to have the greatest influence on insulin sensitivity, so make weight loss a priority in overweight horses.

Further information:

Laminitis, EMS and PPID

Laminitis and the Feet

Testing Insulin

Diet for horses with laminitis/EMS/PPID

Management Strategies for EMS/Insulin Resistance

Case study: Rosie

Equine Endocrinology Group - Recommendations for the Diagnosis and Treatment of Equine Metabolic Syndrome (EMS) 2018

​Durham AE, Frank N, McGowan CM, Menzies-Gow NJ, Roelfsema E, Vervuert I, Feige K, Fey K
ECEIM consensus statement on equine metabolic syndrome
J Vet Intern Med. Published online 6 Feb 2019. doi: 10.1111/jvim.15423
​
Morgan R, Keen J, McGowan C
Equine metabolic syndrome
Veterinary Record Aug 2015;177:173-179 doi:10.1136/vr.103226​

References:

Asplin KE, Sillence MN, Pollitt CC, McGowan CM
Induction of laminitis by prolonged hyperinsulinaemia in clinically normal ponies 
The Veterinary Journal Vol 174, Issue 3, November 2007, Pages 530-535 

Borer KE, Bailey SR, Menzies-Gow NJ, Harris PA, Elliott J
Effect of feeding glucose, fructose, and inulin on blood glucose and insulin concentrations in normal ponies and those predisposed to laminitis.
J Anim Sci. 2012 Sep;90(9):3003-11

Carter RA, Geor RJ, Burton Staniar W, Cubitt TA, Harris PA
Apparent adiposity assessed by standardised scoring systems and morphometric measurements in horses and ponies
Vet J. 2009 Feb;179(2):204-10

Carter RA, McCutcheon LJ, George LA, Smith TL, Frank N, Geor RJ
Effects of diet-induced weight gain on insulin sensitivity and plasma hormone and lipid concentrations in horses
Am J Vet Res. 2009 Oct;70(10):1250-8

Frank N, Geor RJ, Bailey SR, Durham AE, Johnson PJ
Equine Metabolic Syndrome - ACVIM Consensus Statement
J Vet Intern Med 2010;24:467–475

Frank N, Tadros E M
Insulin dysregulation
Equine Veterinary Journal Volume 46, Issue 1, pages 103–112, January 2014 

A Longland, J Ince, P Harris 
Estimation of pasture intake by ponies from liveweight change during six weeks at pasture 
J Equine Veterinary Science May–June 2011 Volume 31, Issues 5-6, Pages 275–276

Quinn RW, Burk AO, Hartsock TG, Petersen ED, Whitley NC, Treiber KH, Boston RC
Insulin Sensitivity in Thoroughbred Geldings: Effect of Weight Gain, Diet, and Exercise on Insulin Sensitivity in Thoroughbred Geldings
Journal of Equine Veterinary Science , Volume 28 , Issue 12 , 728 - 738

Rendle DI, Rutledge F, Hughes KJ, Heller J, Durham AE
Effects of metformin hydrochloride on blood glucose and insulin responses to oral dextrose in horses
Equine Vet J. 2013 Nov;45(6):751-754

Photos: thanks to Kat, Liz and Selina for use of photos.

TTeam practitioner Danielle Dibbens has worked with The Laminitis Site on several laminitis rehabilitations, and has made a video showing how to carry out several TTouches suitable for horses recovering from laminitis.

Danielle emphasises that bodywork is complementary to veterinary care and that the cause of the laminitis should be identified and removed/treated, and the feet supported and realigned.

She begins by running her hands all over the horse and becoming aware of warm/cool, hard or bumpy areas, watching for feedback from the horse, feeling for textures, tone and temperature, and notes that the back, quarters and hamstrings are often tight in horses that have had laminitis.  This is followed by:

Zebra Zigzag TTouch - can be used all over the body, may help to relieve muscular tension and reconnect the body when the horse's posture has changed following laminitis.  

Python Lift TTouch - good for legs, may help increase circulation, improve proprioception and release muscular tension.

Raccoon TTouch - a light circular touch, which may help increase circulation around the coronary band.

These and other TTouches were used during Herbie's rehabilitation - see:
Herbie and TTouch: Using TTouch to help rehabilitate a pony from long term box rest and laminitis 
by Danielle Dibbens

Notes:

The pressures used are very light.  These techniques can be used on any horse or pony and on other animals, and can be practised on friends and family to check and perfect your technique.

Include pauses to allow the horse to process information, and remember to breathe and smile when working with your horse.

Be aware of feedback from the horse, such as eye blinking, eye size, breathing rate, ear and head position, stepping away from or into the handler or lifting a leg.  Be aware of the horse's comfort zones and areas that the horse may be protecting, and use approach and retreat to slowly increase access to protected areas.

Use EVA gym mats to support the feet if necessary - see EVA foam pads.

For more information about laminitis see www.thelaminitissite.org.
You may enjoy these articles: Laminitis, EMS and PPID and Laminitis and the Feet.

For further information about Tellington TTouch or to find a practitioner near you please visit www.ttouch.com.

Danielle Dibbens is a Tellington TTouch Training practitioner for horses based in south west France.
Website: danielledibbens.fr
​
TLS Tellington TTouch for horses and ponies with laminitis - link to video on https://www.youtube.com/watch?v=_Uw3PuDAVEM

Disclaimer: The information, suggestions and links (hereafter referred to as “information”) contained in this video are provided for information purposes only and should not be relied upon nor replace professional veterinary advice. Information is non-veterinary, is based as far as possible on current research, does not constitute advice or diagnosis, and should be discussed with all relevant vets and hoofcare or other professionals. No responsibility is taken for the accuracy or suitability of information contained in this video, and no liability accepted for damages of any kind arising from use, reference to or reliance on any information contained in this video. It is your responsibility to take appropriate care of your own safety when working with horses. If you suspect your horse has laminitis or is ill, please consult your vet.

Rotation and sinking can be corrected

The philosophy of The Laminitis Site is “identify and remove/treat the cause, and support and realign the feet”.  Thanks to recent research we are now much better at establishing and treating the cause to prevent further laminitis, but what about feet damaged by laminitis – can rotation and/or sinking (also called distal descent) be corrected?

Yes, absolutely.  In many cases the hoof capsule can be realigned with the pedal bone, sinking distance may reduce, and the horse can return to its pre-laminitis level of soundness. 

In 2014 Dr Debra Taylor at Auburn University published a paper: 

Taylor D, Sperandeo A, Schumacher J, Passler T, Wooldridge A, Bell R, Cooner A, Guidry L, Matz-Creel H, Ramey I, Ramey P
Clinical Outcome of 14 Obese, Laminitic Horses Managed with the Same Rehabilitation Protocol
Journal of Equine Veterinary Science Volume 34, Issue 4, Pages 556–564, April 2014

describing how a realigning trim that minimized hoof wall loading, sole protection with boots and pads, and movement, returned 14 out of 14 horses with endocrinopathic laminitis and rotation as severe as 29 degrees to their pre-laminitis level of soundness.  

Take correctly marked x-rays  

Rehabilitation from laminitis starts with correctly marked lateromedial x-rays to assess the damage and to guide trimming.  Any horse that has had clinical laminitis should have x-rays taken.  Ponies in particular can have significant damage in their feet without appearing to be lame, and x-rays should be taken if external signs of chronic laminitis such as hoof rings wider at the heels than the toe, a stretched or deep white line or change of angle in the hoof wall are seen, so that rotation can be identified and corrected.

Case study: Sorrel, a Connemara pony with EMS and later diagnosed with PPID, had had laminitis on and off for 7 years and never had x-rays.  Photos of her feet suggested that her heels were too high, the walls were flared with toe cracks, the frogs were not weight bearing and a deep black groove between wall and sole suggested white line separation.

The realigning trim  

If x-rays show rotation, a realigning trim should be carried out as soon as possible – while the foot is not correctly aligned, the horse is likely to be in pain, and the foot at risk of further damage.  Dr Eleanor Kellon, in her online Cushing’s and Insulin Resistance course, states “ I firmly believe if more horses were trimmed correctly and aggressively from the start of their laminitis, we would see far fewer problems with chronic pain and eventual hoof deformity”.

In Care and Rehabilitation of the Equine Foot, Pete Ramey says “at the first signs of laminitis, restore P3 to a more natural ground plane, relieve pressure on the walls and pad the sole with foam rubber – vertical sinking and destructive pressure to the solar corium can be prevented”.

1. trimming the hoof walls level with the sole plane and bevelling the outer wall at the toe and through the quarters to minimise weight bearing by the hoof walls – the hoof wall at the toe was trimmed out of contact with the ground.  Dr Taylor suggests that whilst the deep digital flexor tendon does exert a rotational force on the pedal bone, it does not result in added stress to the laminae if the hoof wall at the toe is trimmed so that it is not weight bearing.

2.  reducing the palmar angle by lowering the heels to just above the live sole plane, but without removing more than 10 mm in any one trim.  The heels were lowered by rasping a heel plane approximately 2 to 3 degrees away from the solar plane of the pedal bone, and by floating the rasp above the front of the foot to preserve and develop sole depth. 

3.  not rasping hoof wall flare until two thirds of the hoof wall was new growth.

Above left: A typical realigning trim might involve:

Reducing the palmar angle by lowering the heels in 3 close-together trims as suggested by the pink lines (and dictated by the live sole plane) to create a heel plane parallel to the 3-4 degree palmar angle indicated by the green line.

Reducing the dorsal angle of rotation by bringing breakover back to or just in front of the black line drawn down the dorsal surface of the pedal bone to the ground, and allowing for adequate sole depth.  With the toe bevelled to remove it from weight bearing, as suggested by the purple line,  new tightly connected wall will grow down from the coronary band parallel to the pedal bone.  Laminar separation doesn’t just occur at the toe – the outer wall should be bevelled to or past both quarters.

Developing sole depth by ensuring that the area marked orange is protected, by  “floating” the rasp 15 mm above the bottom of the collateral grooves. 

The actual areas of hoof that might be trimmed are marked yellow, the areas that would not be trimmed are marked orange.

Above right: After 3 trims the hoof print would be almost normal, and the hoof should look like this once the sole has developed and the new hoof wall grown down from the coronary band.

Case study: Nutmeg’s owner first contacted The Laminitis Site just hours before Nutmeg was due to be put to sleep because of rotation following probably years of chronic laminitis due to EMS and PPID.  X-rays showed > 20 degrees of dorsal and palmar rotation, she was in a lot of pain and vets considered that her feet had been damaged beyond repair.  Information on www.thelaminitissite.org helped Nutmeg’s farrier to carry out a realigning trim, and she started to improve immediately, being comfortable without pain relief for the first time in seven years.  With boots and pads fitted she was soon going for in-hand walks and being turned out in a mud paddock.

Protect the soles  

To protect and minimize pressure on the weight bearing soles, hoof boots with foam rubber pads were the first choice for Dr Taylor’s rehabilitation cases, with an air space under the rim of the pedal bone where soles were very thin (i.e. less than 7 mm), and pea gravel once horses had developed reasonable sole depth and were comfortable.  Barefoot turnout was not allowed until horses had at least 12 mm of sole depth and were comfortable on the terrain without hoof protection.  The sole can support the pedal bone through laminitis rehabilitation as long as it is well protected during weight bearing and as long as solar pressure is eliminated during hoof flight – this may be critical to maintain solar blood flow and prevent solar corium injury.

Introduce movement  

Under Dr Taylor’s rehabilitation protocol, once the hooves had been bevelled to minimize weight bearing by the hoof wall, a palmar angle of less than 10 degrees had been established, the feet were well protected by soft pads inside hoof boots and the horse was comfortably landing heel first, turnout in a grass-free paddock and in-hand exercise were started.  Exercise appeared to increase comfort, and was built gradually as long as the horse continued to land heel first and showed no discomfort.

See Movement - good or bad?

Rehabilitation protocol success

After following Dr Taylor’s rehabilitation protocol, all the horses returned to their pre-laminitis level of soundness, despite all starting with dorsal rotation > 5 degrees and 6 horses having dorsal rotation > 11 degrees.  Significant improvements were seen in dorsal rotation, palmar rotation, H:L zone thickness and sole depth, and there was a slight reduction in sinking.  Increased heel volume was also noted.

“Too many horses fail to recover from laminitis due to incorrect trimming”
– ECIR Group Inc and Dr Eleanor Kellon

Horses can and should recover from rotation and sinking following endocrinopathic laminitis, and the earlier problems are identified and corrected, the better the chance of a successful outcome.  Horses have recovered from solar penetration and full sloughing of their hoof capsules, and can be made comfortable even with considerable pedal bone loss, once a correct realigning trim and foot protection are in place.


See FAQ: Rehabilitating the feet after laminitis

References:

Taylor D, Sperandeo A, Schumacher J, Passler T, Wooldridge A, Bell R, Cooner A, Guidry L, Matz-Creel H, Ramey I, Ramey P
Clinical Outcome of 14 Obese, Laminitic Horses Managed with the Same Rehabilitation Protocol
Journal of Equine Veterinary Science , Volume 34 , Issue 4, Pages 556-564, April 2014

Care and Rehabilitation of the Equine Foot – Pete Ramey – www.hoofrehab.com

Cushing’s and Insulin Resistance course – Dr Eleanor Kellon – www.drkellon.com

All the case studies mentioned and further information about realigning trimming can be found at www.thelaminitissite.org

With thanks to Pat, Fiona, Tanya and Laurie for use of photos and x-rays.

How is laminitis treated?

The cause must be identified and removed/treated, and the feet must be supported and fully realigned.  With correct treatment, even significant damage to the feet can often be repaired and the horse returned to health.

• VET - laminitis should always be considered an emergency – call your vet (and farrier/trimmer).
• SUPPORT - ensure the feet are well supported and protected from hard ground/surfaces with full solar surface conforming padding, e.g. boots with thick soft pads or taped on EVA foam pads cut to size. Bedding may provide sufficient support.  See also: Sole Support.

• ​CONFINE - confine the horse on wall-to-wall reasonably deep conforming bedding, e.g. sawdust, shavings, sand, to limit movement (pad the feet before moving the horse to the area of confinement, and keep movement to a minimum, e.g. by using a low-loading trailer). If a stable isn't available or suitable, a fenced off shelter or even a stable-sized corner of a field can be used.
• ​DIET - remove the horse from grass and feed a low (<10%) sugar/starch diet based on analysed or soaked hay, plus minerals, vitamins, protein and essential fatty acids to meet minimum requirements. Never starve a horse with laminitis because of the risk of inducing hyperlipaemia – feed no less than 1.5% of the horse’s bodyweight per day (unless under veterinary supervision, and never less than 1.2%).  More..​
• PAIN RELIEF - pain relief such as Bute or Danilon may be prescribed to reduce the pain but may not treat the cause of the laminitis – it is now recognised that there is little inflammation involved in endocrine laminitis.  If pain relief is still required after a week, it may be that the cause of the laminitis hasn’t been correctly identified and removed/treated, and/or the feet haven’t been correctly supported and realigned, and the case should be reassessed.  Sub-solar abscesses can increase pain following laminitis.

Pituitary Pars Intermedia Dysfunction  

PPID is a progressive disease that starts when dopamine-producing neurons in the brain die, possibly due to oxidative damage, causing the pars intermedia in the pituitary gland to release excessive amounts of several hormones (alpha-MSH, beta-endorphin, ACTH and CLIP), and eventually leading to enlargement of the gland.

PPID is treated with daily pergolide (now licensed for horses in many countries as Prascend, and also available as a paste from BOVA UK) to replace the missing dopamine, plus optimized management, with attention to providing a diet that provides all essential nutrients, clipping and rugging if necessary, good dental and foot care and targeted parasite control.

Horses with EMS may be at greater risk of developing PPID as they get older, and it has been suggested that they may have a greater risk of laminitis as they transition from EMS to PPID.

Nutmeg displaying signs of PPID, EMS and chronic laminitis - see Nutmeg's TLS rehab

How can laminitis be prevented?  

The good news is that many cases of endocrine laminitis can be prevented with careful management and simple daily checks for at-risk horses:

• Feed a low sugar, low starch high fibre diet supplemented to provide above minimum levels of minerals, vitamins, protein and essential fatty acids.

• Restrict or prevent grazing when grass is growing fast (increased quantity), or during sunny weather and/or if stressed by drought or cold nights (increased sugar).  Consider using a track (fencing off a strip around the outside of a field), grazing muzzle, and/or strip grazing to limit grass consumption and encourage movement.  See When the grass is greener (University of Liverpool 2018) for good ideas for reducing grass intake and encouraging weight loss.

A grazing muzzle combined with track system allows horses with insulin dysregulation to socialise and exercise (thanks to Fiona for photo use) - see Sorrel's case study

• Ensure horses are regularly exercised as long as their feet are correctly aligned and stable.  If exercise is reduced, consider reducing the energy content of feed – many cases of laminitis follow a reduction in exercise due to lameness, rider illness/holiday or bad weather.
•  Keep feet perfectly balanced and supported, and check regularly for any signs of chronic laminitis – if signs are seen, have x-rays taken and ensure feet are fully realigned as soon as possible.
  
•  Be vigilant for clinical signs of EMS and PPID, and arrange blood tests if suspicious – the aim is to diagnose and treat these conditions before laminitis occurs.
  

If there is any suspicion of laminitis, follow the treatment protocol above.

What we know about laminitis has changed significantly in the last few years. For the latest information visit www.thelaminitissite.org and www.facebook.com/TheLaminitisSite.

A version of this article was first published in The Arabian Magazine March 2015 - download pdf file of The Arabian Magazine article.

Resting insulin tests

This is the easiest test to carry out and involves taking a single sample of blood to measure the amount of insulin in the horse's blood at that moment in time.  It can be either:

1.  Fasting resting insulin - the horse is fasted for at least 6 hours before the blood is collected.
This test has a high false negative rate (around 2/3 of horses with insulin dysregulation have a normal fasting insulin result), so a normal test result does not rule out EMS, and a dynamic or non-fasted resting test should follow a normal fasting insulin test if a horse is suspected of having insulin dysregulation.  If a horse gets stressed from having food withheld - this may be a particular problem on a yard where other horses are being fed and the horse being tested isn't - this could falsely increase the result.

Interpretation:
Results above the laboratory cut-off are diagnostic of hyperinsulinaemia.
Whilst a cut off of 20 mIU/l is often used, reference ranges for insulin are laboratory specific - the reference range given by the testing laboratory should be used.  Note that different assays, e.g. RIA v CIA, may produce different results meaning that results cannot be compared.

Liphook Equine Hospital (Immulite CIA) - 20 mIU/l and above is considered above normal and diagnostic of hyperinsulinaemia.

Reference ranges for insulin may be breed specific, therefore a cut-off of 20 µIU/ml may not be appropriate for all breeds.

TLS comment: due to the high number of false negatives, this test is probably only worth doing if a horse obviously has EMS/insulin dysregulation (e.g. history of laminitis, overweight, fat pads), but the test is diagnostic, accepted by vets, and good for monitoring progress when positive.

2.  Non-fasting resting insulin - the horse eats hay or grass but no bucket feed in the 6 hours before the blood is collected.
Allowing the horse access to food before the resting insulin test measures the horse's insulin response to its normal diet. But if the amount of sugar in the diet isn't known, this adds uncertainty to the test and makes a borderline result more difficult to interpret. 
This was the test recommended by vets/researchers until a few years ago, generally using a cut off of 30 uIU/ml (rather than the 20 uIU/ml cut off used for the fasting test).  Presumably because hay can have differing sugar levels, vets/researchers have decided this test isn't as accurate as the fasting test.  However, it's unlikely hay is going to push a "normal" horse over a cut-off of 30 uIU/ml, or even 20 uIU/ml.
The ECIR group recommends that low sugar/soaked hay is in front of the horse at all times before the test - DDT Diagnosis of PPID and IR.
TLS comment: there seem to be less false negatives with this test and it gives an accurate reflection of the horse's actual day to day insulin levels, but there may be a grey area around the cut-off due to unknown sugar levels in the hay/grass.  With no fasting and no abnormally raised insulin levels involved, it is safe and is probably the test a horse would choose!

Dynamic insulin tests

This measures the horse's insulin response after eating glucose/sugar - a high result suggests insulin dysregulation, therefore it should be a good test for determining which horses are at higher risk of getting laminitis.  However dynamic tests can also give false negative results - Dianne McFarlane suggested that half the horses she tested that she pretty much knew had EMS tested negative - Is it PPID or is it EMS?  

If a baseline (resting) sample is taken before the glucose is fed, the increase in insulin as a result of eating the glucose can be measured.
If insulin is only measured after the horse has eaten the glucose, it isn't possible to know how much the insulin increased as a result of eating the glucose - the horse could have had an above normal insulin concentration even after fasting for several hours.

A dynamic insulin test can be either:
 
3.  Oral Sugar Test (OST) - this uses 0.15 ml/kg bodyweight Karo Light corn syrup, which gives around 75 g sugar to a 500 kg horse, which isn't totally unlike a horse eating grass - say a 500 kg horse eats 2.5% of his bodyweight in 12% ESC/starch grass (fructans don't appear to increase insulin, grass doesn't tend to have more than around 12% simple sugars, after that simple sugars are turned into fructans), that would be 1500 g sugar, over 16 hours grazing, so 94 g sugar/hr of grazing. So 75 g in a few minutes is still likely to be far more than a horse can eat naturally, but it's a lot better than the in-feed glucose test. All research done to validate this test (and the in-feed glucose test) has been done with the horse fasting for at least 6 hours beforehand, so for these dynamic tests the horse should be fasted for accurate interpretation. 

​Recently (2017) it has been suggested that a higher dose Oral Sugar Test can be carried out without the horse having to be fasted beforehand, using 4.5 ml/kg bodyweight Karo Light corn syrup.  See Karo Light Corn Syrup test for assessment of insulin dysregulation - Liphook Equine Hospital.

4.  In-feed Glucose Challenge
The in-feed glucose challenge uses a large amount of glucose (either 1 g or 0.5 g per kg bodyweight, so 500 or 250 g for a 500 kg horse), an amount that a horse could not eat in its natural diet. One problem with this is that glucose enters the blood through glucose transporters, which can become saturated. When a horse is used to having a lot of sugar in its diet, it will increase the number of glucose transporters (this has been proven by feeding increasing amounts of starch). But when a horse is usually on a low sugar diet and is suddenly fed a huge amount of glucose, a large amount of this may be unable to be absorbed in the small intestine and will be carried through to the hind gut. So the number of glucose transporters will have an effect on the insulin result. And the test could potentially cause diarrhoea, gas and colic - we have had reports of diarrhoea following the test using 1g/kg bw glucose. 

As can be seen from the paragraph above, this amount of glucose is FAR more than a horse can possibly eat naturally. So although this test has been used in research to distinguish horses with EMS from horses without EMS, all it really tells you is how much insulin your horse will produce if given a massive amount of sugar that it couldn't possibly get hold of. Sadly we now have loads of horses being treated with Metformin following this test, when they would almost certainly test normal on a hay-fed resting insulin test - i.e. their day to day life is controlling their insulin. 

The in-feed glucose challenge measures how much insulin a horse secretes (and then cannot clear) when it eats a large amount of glucose quickly. It doesn't measure how that horse might respond to its normal diet.

Horses with EMS can have very high insulin results with the in-feed glucose test, over 800 uIU/ml. We know that this insulin level causes laminitic changes in the feet when kept at that level for 6 hours. Whilst the insulin level caused by the test will peak and then fall, the damage caused by exposure to these high levels of insulin for less than 6 hours hasn't been looked at.

TLS suggestions for diagnostic testing:

If a horse has had laminitis or has any clinical signs of EMS, such as being overweight, having a cresty neck or fat pads, start with a resting insulin test - fasting or low sugar hay is a decision for the owner. If this test is negative, then an oral sugar test will give an idea of that horse's insulin response to sugar. However, a positive OST is not a reason to start treatment with Metformin, it indicates that diet, weight control and exercise should be improved.

If a horse has never had laminitis and has no obvious signs of EMS, but seems the type of horse that might be susceptible, then going straight to the OST seems justified, as a resting insulin would be quite likely to come back negative, and the OST shouldn't raise insulin significantly if the normal diet isn't doing so.

For PPID horses with no signs of EMS and that have never had laminitis, either start with a resting insulin or go straight for the OST. All horses with PPID should have insulin tested. If there really is no suspicion of EMS then going straight to the OST is probably justified. But if there's the slightest suspicion of EMS, it's probably best to start with a resting insulin. 

Conclusion:
Resting insulin - best place to start for horses that have had laminitis or are pretty likely to have EMS;
Oral sugar test - best place to start for horses that have never had laminitis and have no obvious signs of EMS.
TLS does not recommend the in-feed glucose challenge.

Monitoring

Insulin is tested to diagnose EMS/insulin dysregulation, to assess laminitis risk and potentially to quantify how significant any laminitis risk is likely to be.  Following initial diagnosis, insulin should continue to be tested to monitor improvements in insulin regulation, until the horse's insulin levels remain normal on his usual diet.  

The factors that cause/contribute to insulin dysregulation/hyperinsulinaemia/insulin resistance can and must be managed or treated so that insulin levels return to normal, or as close to normal as possible.  Remember that EMS is not a disease, it is a cluster of risk factors that increase the risk of laminitis, and these risk factors can be reduced, often to the point where the horse is at no greater risk of laminitis than any other horse, as long as it is managed carefully.

This might mean:
Overweight horses lose weight until they reach their correct weight.
Levels of sugar and starch in the diet are kept low - generally total NSC or ESC plus starch in the diet should be below 10%; some horses may require diets with lower levels of sugar and starch.
Exercise is introduced/increased if the horse's feet are stable and correctly aligned and supported.
PPID is assessed as a cause of hyperinsulinaemia and treated if present.
Corticosteroid use is avoided or discontinued (under veterinary supervision).
Some horses appear to have a stronger genetic disposition to insulin dysregulation than others - they are likely to need stricter management of the above factors.

To monitor improvement, it is often suggested that the test that was used for diagnosis be repeated under the same conditions.  However, what we probably most need to know is whether the horse has above normal levels of insulin every day when eating its usual diet.  If an initial fasting resting insulin was positive, continue to test this under the same test conditions until a normal result is seen.  Once fasting resting insulin is normal (or if a non-fasting resting test was the initial test used), next time test resting insulin with the horse eating his normal hay. When that is normal, if you want to return the horse to grazing, test resting insulin with the horse eating a restricted amount of his normal grass. If the grass causes an above normal insulin result, then you know you probably need to restrict grass further or eliminate grazing completely. If you get a normal insulin result after restricted grazing, you can probably continue to allow access to grass, monitoring closely for signs of laminitis/EMS and testing insulin as often as you can.  There's no science behind this, but it seems logical.

Frequently Asked Questions

Q.  What is insulin resistance?

A.  When a normal horse eats, glucose is absorbed into the blood stream and insulin is released to enable that glucose to enter insulin sensitive tissue – blood levels of both glucose and insulin rise after a meal and then drop back down.

When a horse with insulin resistance eats, glucose is absorbed into the blood stream and insulin is released, 
but the insulin sensitive tissue (primarily muscle) does not respond normally to that insulin, which prevents glucose in the blood from entering the tissue normally.  The pancreas "compensates" by producing more insulin to ensure that glucose does enter the tissue - blood levels of insulin increase and take longer to drop back down (compensatory hyperinsulinaemia).  
 
Q.  What mechanisms can cause high levels of insulin?

A.  Insulin can be increased because of:

1.  hyperinsulinaemia without insulin resistance - e.g. hormones produced in excess when a horse has PPID may cause excess insulin to be produced, regardless of diet - it is possible that CLIP could be responsible for this - it has been shown to raise insulin in pigs.  Chronic hyperinsulinaemia (and hyperglycaemia) are likely to lead to tissue insulin resistance.

2.  insulin resistance at the level of the tissue (muscle), leading to compensatory hyperinsulinaemia (see above).

3.  reduced clearance of insulin by the liver.

If a horse has greater than normal absorption of glucose or greater than normal release of insulin from the pancreas, over time the horse can develop insulin resistance at the level of the tissue - a dynamic oral test will pick up dysfunction at every level.  However, if you only use dynamic and not resting tests, you don't know whether the insulin result after feeding sugar/glucose is due purely to the sugar/glucose, or whether it would have been above normal without the sugar/glucose.

Q.  My horse had a positive fasting resting insulin result, and my vet has now suggested carrying out a glucose challenge test - why?

A.  A reliable positive fasting resting insulin result should be sufficient for a diagnosis of EMS/insulin dysregulation, together with clinical signs and history.  There is no need to carry out a glucose challenge test as well, particularly as a horse with an above normal resting insulin may have a very high insulin response to glucose.  Management changes should be made (reduced sugar/starch diet, weight loss, increased exercise if appropriate) and PPID eliminated as a possible cause of the above normal insulin, and resting insulin retested under the same conditions until a normal result is achieved.  At this point you might consider carrying out the oral sugar test, to see whether the horse still has an abnormal insulin response to sugar, or testing resting insulin when the horse is eating his normal diet, as above. 

  

During sunny weather grass makes and stores sugars (photosynthesis), at night when grass is able to grow these sugars are used up (respiration), but when environmental conditions such as low temperatures (below around 6'C), lack of rainfall or poor fertility prevent growth, sugar (ESC) levels can continue to accumulate in the grass, making it unsuitable for horses and ponies with insulin dysregulation and increasing the risk of laminitis. 

"Ideal conditions for high NSC concentrations are clear skies to maximise photosynthesis, and low night temperatures to minimise loss of carbohydrates through respiration (Fulkerson et al. 1998)" - from: Non-structural carbohydrate content of a perennial ryegrass cultivar bred for high sugar levels, compared to "normal" perennial ryegrass and white clover; Francis et al., Anim. Prod. Aust. 2002 Vol.24:73-76

See:
When is dead grass safer to graze? - Kathryn Watts
Factors affecting NSC levels in grass - Kathryn Watts

Grass facts

Green plants create sugar through the process of photosynthesis.
carbon dioxide + water + sunlight = sugar + oxygen

Plants use the sugar for growth and reproduction - this process is called respiration.
glucose + oxygen = carbon dioxide + water + energy for growth/respiration

When sugar production from photosynthesis > sugar required for growth/reproduction, the excess sugar is stored as fructan or starch (carbohydrates) for later use.

Plants respire all the time, in darkness and in light, but only photosynthesize in light.  Increased light leads to increased photosynthesis (up to a point).
No light/darkness: respiration > photosynthesis (there is no photosynthesis without light).
Dim light: photosynthesis = respiration.
Bright light: photosynthesis > respiration.

Grass hardly grows (respires) when temperatures are below 5 degrees C.

Plant carbohydrates are classified as:
Ethanol Soluble Carbohydrates (ESC) - this is the sum of the simple sugars, particularly glucose, fructose, sucrose.  ESC causes glucose and therefore insulin to rise when eaten by horses.
Water Soluble Carbohydrates (WSC) - this is the sum of ESC plus fructans.  Fructans do not affect glucose and insulin when eaten by horses.
Starch - horses digest starch in the stomach and small intestine to glucose, and glucose causes blood glucose and therefore insulin to rise when eaten by horses.
Non-Structural Carbohydrates (NSC) - this is the sum of WSC plus starch.  
Only ESC and starch are important when talking about horses and endocrinopathic laminitis.

​Other reasons for horses to show signs of laminitis/foot discomfort in cold weather may include:
- circulation damage, or ongoing damage in the feet from rotation that hasn't been corrected making feet more sensitive to hard frozen ground, 
- horses with PPID lose their ability to thermoregulate, therefore get more stressed by extreme temperatures, which could increase cortisol,
- hay soaking is not as effective at colder water temperatures, 
- horses tend to get less exercise/turnout in cold/frosty/snowy weather.

What you can do: 
- prevent or limit access to grass during and after sunny frosty weather until the weather changes to milder nights and overcast days, and feed analysed hay with sugar and starch levels below 10% instead.  It is not the frost itself that is the risk, it is the weather conditions that cause the frost, so do not allow horses to graze once the frost has melted with the sun - wait until the grass has been able to respire and use up some of its sugar.
- keep feet warm and protected - use leg wraps/bandages, pads and boots on feet, warm deep bedding. Thick wool hiking socks can be great for keeping pony feet and legs warm.

​- ensure feet are well trimmed/balanced - even the slightest tipping of the pedal bone onto the sole by high heels or pull on the laminae by long toes can exacerbate pain and discomfort when a horse is walking on hard rough ground. 
- rug well, provide good shelter out of the wind/weather - particularly PPID/underweight horses.  For overweight/EMS horses, cold weather can encourage weight loss so consider whether they really need a thick rug.
- soak hay in warm water.
- cut back feed (calories, not fibre) if exercise/turnout is reduced. 
- provide warm water for drinking to reduce the risk of impaction colic (not such a great risk when soaking hay) - particularly for older/PPID horses that might have tooth problems.

See: 
Winter Laminitis - Dr Eleanor Kellon 2018
Cold weather - The Laminitis Site

Teamwork, handling the vet and farrier

In the first few months the hardest challenge that I faced was that I had serious doubts about whether my horse was getting the right treatment. I had already made contact with The Laminitis Site and had read all the information about laminitis rehabilitation that Andrea had sent me. It all made complete sense. I wanted to follow the TLS recommended protocol as a matter of urgency. My vet and farrier said that it could be “disastrous”! More than 2 months had passed and clearly Casareño was getting worse. I was feeling more and more desperate and helpless.

I found that my horse's recovery only started when I had a vet and farrier team in place that would work to the TLS guidelines. Good teamwork was the key to our eventual success. I needed the vet to take good marked-up x-rays so that accurate trimming guidelines could be produced and I needed the farrier to follow the guidelines. My main role was to make sure that Casareño's diet was correct, that I provided protection for his feet, sought help from TLS when in doubt and arranged regular trimming visits and x-rays, where needed, to provide ongoing guidance for the trim.

What do you do if your hoof-care team does not want to follow the guidelines that have been provided by The Laminitis Site? 

It is very difficult to challenge your vet's treatment plan. Your vet's reaction will typically be “I have studied for 7 years and practised for 'n' years and you have just read something on the internet!”. The farrier may have a similar attitude. The farrier may believe that remedial shoeing is the only solution. A barefoot trimmer may have no experience with laminitic feet or may have their own methodology that they want to follow. 

In addition, I had the language barrier. My vet and farrier's first language was Spanish – discussion and debate was difficult!

I only had 3 options:- 1) Get the team to buy-in to the TLS recommended rehab protocol; or 2) as the owner and the person paying the bills just insist  that they follow this protocol; or 3) change the team. In the end, I used a combination of all 3 options to achieve the eventual successful buy-in.

Getting vet/farrier to buy-in (this is so important because once you have this in place the rest is fairly plain sailing!)

First, you have to have confidence in the TLS guidelines. You may have heard or read different approaches to laminitis treatment. You will probably be feeling under a lot of stress but I urge you to take the time to read the material that TLS will have sent you and check out some of the Case Studies. If you are in the situation where you need to get the vet/farrier to change their approach, you will not be successful if you yourself show uncertainty.

It helps if the vet and farrier can be reassured that the TLS recommended protocol is based on evidence-based scientific research and has been produced by veterinarians and farriers that are highly regarded in this field of expertise (not just some latest fad on the internet!). 

Let the vet and farrier know, when you make the appointment with them, that you want to discuss the treatment plan with them and ask them to allow a little extra time for you to have these discussions. Be prepared to pay for a slightly longer visit if necessary. 

Give the vet and farrier printed copies of TLS's trimming diagrams and the scientific paper on which they are based – Clinical Outcome of 14 Obese, Laminitic Horses Managed with the Same Rehabilitation Protocol by Dr Debra Taylor et al 2014.  Make sure that they know that the authors of the protocol are highly regarded - the current leaders in this field.

Be confident and assertive that you want them to follow this protocol – even offer to put it in writing (professionals are very wary of being sued if things go wrong – if they have your clear instructions it takes that risk away for them).

Don't be shy to tell them that you have been in contact with The Laminitis Site. Give them the link so that they can see how much valuable evidence-based information is available there.

Show them that you are prepared for the rehabilitation – have boots/padding materials and supportive/conforming bedding at the ready.

If all else fails, do not be afraid to change elements of the team. I had to change to an English speaking farrier, partly because my Spanish farrier was going on holiday and was not prepared to carry out the trim before he went away and partly because I did not want to risk having language barrier problems when the situation had become so urgent.

Once I had buy-in from the professional team I nurtured it. I made sure that everyone who was interested in Casareño's case knew of the valuable roles played by my vet and farrier. If you use social network sites this can be a great way to give credit to them. I think they appreciated it and became even more committed to Casareño's recovery

For details of his rehabilitation, see Casareño's recovery

9 x-rays taken over 6 months illustrate Casareño's laminitis story:

24 June - reverse shoes and 5 degree heel wedges had been applied.  The palmar angle was around 23 degrees, dorsal rotation of 5.73 degrees was measured, and the hairline marker indicated considerable sinking.

TLS recommended the rehabilitation protocol published by Debra Taylor et al. (2014) - remove shoes, fully realign the feet, support with thick pads - and on 10 July the shoes and wedges were removed, but the feet were only trimmed to tidy up frogs and bars.  The vet declared that carrying out a realigning trim could be "a disaster" and that the long toes and high heels should not be corrected until more sole depth had developed (TLS disagreed!).  The frogs were infected with thrush, which is common when heels are too high.

17 July - x-rays showed slightly increased palmar and dorsal rotation, which would be expected with no recent trimming.  Personal correspondence from Debra Taylor backed the argument for commencing the realigning trim.  The vet admitted that the situation was very bad and that something must be done as soon as possible, and agreed that a barefoot trimmer could be instructed.  The owner feared that Casareño could be heading towards euthanasia.  

13 Aug - after two trims (apparently without reference to the TLS suggested trim), very little progress had been made with realignment, and an abscess was now evident in the sole beneath, and very close to, the tip of P3.  A third hoofcare professional was instructed, and guided by mark ups from TLS, realigning trimming finally got underway.

25 Aug - after just one trim the dorsal and palmar angles were reduced.  Casareño was finally off of NSAIDs and moving better.

15 Sept - after two further realigning trims the toe was looking much better, but the palmar angle was still too high.  Note the gas pocket indicating abscessing beneath the tip of P3, and the change in the hoof wall at the toe.  At this point Casareño had increased but not full comfort, due probably to a combination of the feet still not being fully realigned, the solar abscess on the right fore, and heel rubs from wearing boots in a sandy environment.

9 Oct - two trims guided by the previous x-rays brought the heels down, reducing the palmar angle further, but probably still not quite far enough.  Note how the frog apex, marked by a drawing pin (that should have had the pin shortened much further!), had migrated forwards - the true frog apex will always be behind the tip of P3.  Casareño was now being walked out in-hand.

01 Dec - the feet had remained stable but probably still needed a little more off the heels to bring the palmar angle down to between 3 and 5 degrees.  This should be guided by the live sole - which can be difficult to find on dry compacted feet that have had high heels for a long time.  Note that the black gas pocket indicating the abscess has grown out and healthy tissue appears to be supporting P3.  The true frog apex has been identified and the frog trimmed back, so the true apex can again be used to guide the trim.  Note the clear shape of the collateral grooves on the x-ray.  Note also the first radiographic signs of bone remodelling at the tip of P3 - we suspect this is due to the long-term high palmar angle and pressure on the tip of P3.    Casareño is now in regular in-hand work and being turned out, with his feet protected by boots and pads.

Sole photos of the right fore from July to November show the abscess and stretching forward of the frog.

In November Casareño's vet posted on owner Pat's Facebook page: "I'm super happy to see Casereño recovered. Now you're probably the person who knows most of laminitis in Spain and I must admit that you made me crazy with so many articles you've read ....hahaha!!
Was fortunate to have the help of people The Laminitis Site but especially with the professionalism of an expert as is the blacksmith Bryn Simmo ..... GRACIAS Pat!!!"

Raising the heel has unfortunately been advocated for laminitis cases for some time.  TLS can see no justification whatsoever for doing this - see Don't raise the heel!  Instead, in Care and Rehabilitation of the Equine Foot, p 351, Pete Ramey says "at the first signs of laminitis, restore P3 to a more natural ground plane, relieve pressure on the walls and pad the sole with foam rubber – vertical sinking and destructive pressure to the solar corium can be prevented”.  Pete also says, on p 350, "I believe that DDFT tension concerns have held back the veterinary and farrier world, preventing rotation reversal by leading people to stand P3 up on its tip and ultimately destroying the foot."  

Although Casareño's recovery from laminitis has been challenging and painful at times, he was lucky to have a vet and farrier who were open to different ideas, and owners who were totally committed to his recovery. The full story of Casareño's rehabilitation will follow soon.


The video below shows Casareño's progress from being crippled in July to jumping for joy in December:

References:
Taylor D, Sperandeo A, Schumacher J, Passler T, Wooldridge A, Bell R, Cooner A, Guidry L, Matz-Creel H, Ramey I, Ramey P
Clinical Outcome of 14 Obese, Laminitic Horses Managed with the Same Rehabilitation Protocol
Journal of Equine Veterinary Science Volume 34, Issue 4, Pages 556–564, April 2014

The Prascend website (www.prascend.com) states: "horses with PPID need their vitamins, especially vitamins E and C, for optimal health" (unfortunately the paragraph on diet and exercise makes no mention of feeding adequate levels of protein, minerals or essential fatty acids...).

The reference given for this statement is: Posnikoff J. Advances against Cushing's disease, available on HorseChannel.com.  This article from 2005 suggests: "Antioxidants, such as vitamins E and C, could play a role in helping to support Cushing’s horses."  No references given.

Equine Applied and Clinical Nutrition, p 297 in a chapter entitled Nutritional considerations for aged horses written by Sarah Ralston and Pat Harris, says "low plasma vitamin C concentrations were observed in horses with documented (on post mortem) adenomas of the pars intermedia (Ralston et al 1988).

The abstract (we haven't yet found the full paper online) for Ralston et al 1988 (Differences in diagnostic test results and hematologic data between aged and young horses) found "In group 1, plasma ascorbic acid values were lower (P less than 0.05) in aged (8 mares > 19 years old) horses than in young horses (6 mares < 6 yrs old) maintained under the same conditions and feeding regimens."  Does this suggest there was no difference between old and young horses in group 2? 

In Management of Geriatric Horses, Sarah Ralston writes "vitamin C supplementation (10 gm twice a day) increased antibody response to vaccines in aged horses, especially those with pituitary dysfunction (Ralston and Quackenbush, unpublished data), and in my experience helps old horses with chronic infections".

Redwing's Equine Cushing's Disease: The Facts "suggests  Your vet may advise a supplement containing 
B vitamins and Vitamin C if grazing is especially restricted, as these are helpful in supporting the immune system". 

More about vitamin C and the older horse in Nutrition of the Aged Horse by Kathleen Crandell - Kentucky Equine Research.

A 2011 abstract (Kentucky Academy of Science) by Jeffrey Chalfant and Dianne McFarlane: CSF and plasma ascorbic acid concentrations in horses with PPID compared to age-matched controls
states that exposure to free radicals leads to oxidative stress damage, suggesting that horses with PPID may be deficient in one or more antioxidants.  Ascorbic acid (vitamin C) decreases with age in horses and is an antioxidant.  Age is the major risk factor for PPID.  Therefore Chalfant and McFarlane hypothesizes that horses with PPID might "have decreased plasma and CSF concentrations of ascorbic acid (vitamin C) compared to age-matched controls".  

3 groups of horses had blood (plasma) and cerebrospinal fluid tested for ascorbic acid concentration:  horses diagnosed with PPID, horses of similar ages that didn't have PPID, and young horses without PPID.  Preliminary results showed that mean CSF ascorbic acid concentrations were higher than mean plasma concentrations, perhaps because of vitamin C degradation, or perhaps because plasma samples were subject to increased handling - no further results were reported, just that further experiments are required to produce accurate samples.

The abstract concludes: "If our hypothesis proves true, and horses with PPID have lower plasma and CSF ascorbic acid, this would suggest that an intervention with vitamin C therapy could potentially benefit horses with PPID by reducing oxidative stress."  However, we have been unable to find any follow up to this research.

OK, so a horse with PPID might benefit from supplementation with vitamin C.  But how much vit C is there in the natural diet of a horse?

The OECD SIDS for L-Ascorbic Acid suggests that there is approx. 500 mg vitamin C per kilogram of grass - this would appear to be the amount as fed (AF), not dry matter (DM).  Grass is around 20% dry matter (source NRC Nutrient Requirements of Horses 2007 p 306 "grass pasture, cool season, veg DM % as Fed 20.1").  If a 500 kg horse ate 2% of its bodyweight in grass per day, that would be 10 kg DM, which would be 50 kg AF.  50 kg x 500 mg = 25 g vit C.

This article from KER states that "plants are a natural source of vitamin C and green growing grass has plenty; however, hay is virtually devoid because of the oxidative instability of vitamin C".
Vitamin C in Horse Diets - Kentucky Equine Research Staff - December 2013

Hmm,interesting.  So when a horse gets laminitis, the first thing we do is remove it from its natural source of vitamin C - grass - and feed it hay, often hay that is a year or more old (although it is a myth that old hay is "safer" for laminitics - generally it is simply lower in vitamin content).  Interestingly a few years ago Andy Durham speculated that removing laminitic horses from grass could be contributing to the development of PPID - now researchers are reasonably certain that there may be a causal link between EMS and PPID, although this may well be due to the high levels of insulin, systemic inflammation... food for thought though - literally!

So are there any disadvantages with supplementing vitamin C?  

Well, possibly - vitamin C increases iron absorption.  And iron may be linked to the development of insulin resistance and PPID.....

The Talk About Laminitis Scheme: 
Vetcare Webinars by Andy Durham in 2013

There seems to be a relationship between ACTH concentration and number of clinical signs of PPID seen. 
PPID is diagnosed in horses under 10 years old. 
In 48% of 2045 PPID cases with laminitis, laminitis was the only clinical sign of PPID. 
In 4623 PPID (TAL) cases with laminitis, most were in the autumn, then winter, then summer, then spring. 
In 1154 PPID cases, Liphook found the highest ACTH in autumn, then winter, summer, spring, and the highest insulin in autumn, then winter, summer, spring. 
Horses over 15 years old with PPID have a 4.65 x greater risk of laminitis than horses of the same age without PPID (McGowan et al. 2013). 
67% of PPID cases demonstrate an excessive insulin response to glucose challenge (Durham, unpublished). 
Pergolide may protect against neuronal oxidative damage (Uberti et al. 2002, Gille et al. 2002). 
"A "grey zone" for results is inevitable with a slowly progressive disease. 
Any horse of any age with laminitis deserves testing for PPID regardless of whether other clinical signs are present." 
"Routine screening for PPID as part of "annual health checks" is justifiable beyond 5-7 years of age." 
Important to realise that "we don't have all the answers" yet.  A 3 year old obese, previously laminitic pony had results of: 
fasted insulin 12 uIU/ml (<20) 
Post glucose insulin 793 uIU/ml (<85) 
ACTH 358 pg/ml (<29). 
The question is asked, should this pony be treated for PPID (pain, stress would have to be taken into account, as well as other symptoms of PPID.  TLS might suggest trying pergolide initially whilst trying to control other factors, but reducing and if possible stopping dose if follow up blood tests show ACTH return to normal, and continuing to monitor ACTH regularly). ​

Owners often get very confused about when to allow a horse to return to movement following laminitis, and unfortunately incorrect and often dangerous advice can be found on the internet suggesting that horses with laminitis should be encouraged to move, without explaining when movement may be beneficial or harmful.  

Movement is thought to be beneficial to healing, but only once the foot is mechanically correct, stable, supported, and the cause of the laminitis has been removed.

1.  Active laminitis - no movement

During active endocrine laminitis, the laminae stretch and weaken, and the basement membrane may become damaged causing complete separation of the laminae (this may be more likely with SIRS laminitis).  The connection of the hoof to the skeleton is unstable.  Movement increases pressure on these damaged structures.  

A horse in pain from laminitis should not be forced to walk - pain tells a horse that he has damage and shouldn't move.  NSAID (Bute, Danilon etc) use should be kept to a minimum, and should be discontinued at least 48 hours before a horse is encouraged to return to movement.  Horses taking NSAIDs should be kept confined and discouraged from moving.

2.  Post active laminitis and realignment - return to movement

Once

• the cause of the laminitis has been diagnosed and removed/treated, and no further "active" laminitis is present;
  
• the feet have been realigned and balanced so that the palmar angle and breakover are correct;
  
• the feet are stable (i.e. there is no reason to expect further rotation/sinking, e.g. no gas pockets which might suggest total separation of the laminae);
  
• the feet are supported and protected with boots and thick pads to maximise weight bearing on the non-painful structures at the back of the foot and the horse is comfortably landing heel first; and
  
• the horse has been off NSAIDs/pain relief for at least 48 hours and is comfortable
  

most horses can return to some free choice movement and controlled in-hand exercise.

Turnout should be in a small, safe, enclosed area with good footing, ideally soft and conforming such as sand, pea gravel, mud.

Taylor D, Sperandeo A, Schumacher J, Passler T, Wooldridge A, Bell R, Cooner A, Guidry L, Matz-Creel H, Ramey I, Ramey P
Clinical Outcome of 14 Obese, Laminitic Horses Managed with the Same Rehabilitation Protocol
JEVS published online 05 Feb 2014
gives this advice for returning to exercise:
"2.5. Management Protocol: Exercise 
Turnout in a grass-free paddock or daily in-hand exercise was encouraged after the following (1) hooves had been trimmed to minimize weight bearing by the hoof wall; the desired heel plane and palmar angle (≤ 10* degrees) had been established by trimming; and when the hooves had been protected by soft protective hoof boots with pads (as described in Section 2.3) that provided enough comfort for the horse to have a heel-first hoof landing. In-hand exercise was increased daily by adding 5- to 10-minute increments to each exercise session until horses were walking 30 to 45 minutes 2 or 3 times daily. Owners were instructed to observe for the intended heel-first impact of the hoof boot and to walk the horse only while the hoof boots were securely in place. They were instructed not to walk the horse if the hoof impact appeared to be toe-first and to discontinue daily walking (and call the veterinary/hoof care provider team) if the horse seemed to have increasing pain after walking."

(* NB there is a mistake in the paper, corrected above - the palmar angle should be < or equal to 10 degrees, not 0 degrees - confirmed in personal correspondence with Debra Taylor).

Returning to work after laminitis - www.thelaminitissite.org

Hoof rehabilitation protocol - Debra Taylor, Ivy Ramey, Pete Ramey - www.hoofrehab.com

Taylor D, Sperandeo A, Schumacher J, Passler T, Wooldridge A, Bell R, Cooner A, Guidry L, Matz-Creel H, Ramey I, Ramey P
Clinical Outcome of 14 Obese, Laminitic Horses Managed with the Same Rehabilitation Protocol
JEVS published online 05 Feb 2014

DDT-Trim - www.ecirhorse.org

Anyone interpreting ACTH results should be aware of David Rendle's research:
Equine Veterinary Journal Volume 46, Issue 1, pages 113–117, January 2014
Investigation of rhythms of secretion and repeatability of plasma adrenocorticotropic hormone concentrations in healthy horses and horses with pituitary pars intermedia dysfunction
Rendle DI, Litchfield E, Heller J, Hughes KJ

One horse, presumably with more advanced PPID (it had hypertrichosis) that wasn't being treated, had ACTH levels that ranged from around 200 to over 1000 pg/ml within 3 weeks. Whereas another horse, also with hypertrichosis and high ACTH results, had consistently similar results. The paper concludes that "caution may be required when using ACTH concentrations to assess relative improvements or deteriorations in pituitary dysfunction in response to treatment". It also states that given that PPID affects different hormone producing cells in individual horses, "it is likely that any system of classification based upon one product from melanotrophs will have inherent limitations" - i.e. just measuring ACTH may not give the full story.

There is little question that blood tests are not yet as accurate as we would like them to be, and that there will always be a grey zone for blood results in the early stages of a progressive endocrine disease. It is important to look at the clinical signs and history and not rely on blood test results.  See Is it PPID or is it EMS? 

Q.  My horse has been prescribed 1 mg of Prascend per day, do I give him the full 1 mg on the first day?

A.  No.  The Equine Endocrinology Group, made up of the leading experts on PPID, now recommends introducing Prascend gradually "by giving partial doses for the first four days or by administering half the dose morning and evening".  EEG Recommendations for the Diagnosis and Treatment of PPID Table 6.  

The ECIR group has been recommending introducing the dose of pergolide slowly for years:
"Whether increasing or decreasing dosage or just starting pergolide for the first time taper at a rate of 0.25 mg every three days."  ECIR - Treatment of PPID.

When prescribed for humans with Parkinson's Disease, pergolide is always introduced very gradually - see Pergolide Dosage and Administration - Pergolide - www.drugs.com.  

Generally the initial amount given should be 0.25 mg, slowly built up in 0.25 mg increments to reach the prescribed dose.  The urgency of reaching full dose and the horse's reaction to pergolide will dictate how quickly the prescribed dose is reached - this must be discussed with the prescribing vet.  Splitting this between morning and evening would be next to impossible - good results are usually seen when the dose is given once a day and slowly built up.

Your vet should be able to obtain a pill cutter from Boehringer Ingelheim to help you split pills into 0.25 mg - see Splitting Prascend Tablets.

Q.  What is the "Pergolide Veil"?

A.  The "Pergolide Veil" is a phrase given to the side effects of inappetence and depression commonly seen when a horse starts on pergolide/Prascend.

Research carried out for the FDA New Animal Drug Application for Prascend in 2011 found that of horses with PPID given a starting dose of 1 mg Prascend, 33% had a decreased appetite at one or more meals, that was usually transient, and 10% of horses that had not previously shown signs of lethargy became lethargic - details here.

Q.  Can the "Pergolide Veil" be avoided?

A.  As above, when pergolide is introduced slowly (in 0.25 mg increments building up over several days), the "Pergolide Veil" seems to be experienced less (anecdotal).

It can be concerning when horses go off their feed when starting pergolide, particularly if they are already underweight.  One owner reported success when her horse (who was ill with a suspected bacterial infection and had lost a significant amount of weight) was given Periactin (cyproheptadine) as an appetite stimulant for the first couple of weeks while starting on Prascend (the horse had previously been tried on Prascend and had gone off feed).  No side effects of either Prascend or Periactin were seen.​

Q.  Does it matter what time of day I give Prascend/pergolide?

A.  No.  There is currently no recommendation for giving Prascend/pergolide at any particular time of day - this was confirmed by Dr Marian Little in The Horse.com's Ask the Vet Live Managing Horses with PPID in February 2014.

Q.  Should pergolide/Prascend be given once or twice a day?

A.  Once a day, usually.  The NOAH data sheet for Prascend says "The product should be administered orally, once daily."  

Q.  What is the difference between pergolide and Prascend?

A.  Pergolide is the name of the drug, i.e. the active ingredient (pergolide mesylate).
When this article was written in 2014, Prascend was the only form of pergolide that was licensed for use in horses.  It is made by Boehringer Ingelheim and comes in 1 mg tablets, which can be easily broken in half.  As at 2024 there are several brands of pergolide available - see Pergolide - brand names include: Prascend, Pergoquin, Pergolife, Prasequine, Pergocoat.

Notes of the TheHorse.com Ask the Vet Live webinar
Managing Horses with PPID with Dr Marian Little and Dr Dianne McFarlane
on 27 February 2014
Sponsored by Boehringer Ingelheim. ​

 
Background:
Dr McFarlane (M) – 12 years studying PPID, understanding causes, diagnosis and treatment protocol.  Wanted to know how best to care for older horses.
Dr Little (L) – vet with BI since 2007, lost 2 horses to PPID.
 
L:  PPID – most common endocrine disorder of aging horses, prevalence 15-30 % of horses over 15, this is probably an under-estimate.  Chronic degeneration of dopamine secreting neurons leads to loss of dopamine controlling effect to pituitary, which leads to enlargement of the intermediate lobe and increased secretion of hormones.
Early clinical signs – changes in behaviour, loss of topline, secondary infections, haircoat changes, late shedding.
Later signs: “woolly mammoth”, leaner body condition.  Some get PU/PD, sweating abnormalities, abnormal fat deposits, laminitis related to insulin.
TLS: laminitis, especially in the autumn, is often the first sign of PPID that is noticed.
 
Q.  What’s the difference between IR and PPID?
M: 1/3-1/2 horses with PPID will also have dysregulation of insulin, i.e. insulin resistance.  They will have high insulin concentrations (tests: resting insulin or Oral Sugar Test), and high insulin causes laminitis, so these horses are at high risk of laminitis.  1/2-2/3 of horses with PPID are not at risk of laminitis.  Both conditions can happen together – insulin dysregulation (EMS) and PPID in the same horse, with these horses we need to be very cautious of how they are fed, particularly whether they have grass, as there is a high risk of laminitis.  But if insulin is normal PPID horses can have grass and as these horses are often thinner, they are likely to need feeding to maintain weight rather than lose weight
 
Q.  How effective is Pergolide as a treatment of PPID, can it be used on a seasonal basis?
L:  In the 1980s research suggested horses with PPID have an 8 fold decrease in dopamine in the pituitary gland, since then pergolide has been considered the treatment of choice.  There are over 25 published references from the past 30 years describing pergolide’s usefulness in improving clinical signs and test results.
Most recent being the 2009 study for FDA approval of Prascend - 76% of 113 horses with PPID were deemed treatment successes http://thelaminitissite.myfastforum.org/about14.html.
Most common side effect is inappetence - 30% of horses in Prascend study had loss of appetite, only 2 required dose reduction and both returned to a normal dose within the first month.
Recommended starting dose is 2 mg/kg bodyweight so 1 mg/1000 lbs, horses should be monitored and dose adjusted appropriately to control both clinical signs and test results.
No data on the intermittent use of pergolide, but given knowledge of Prascend and the disease, she would be skeptical we can just treat in the autumn and expect adequate control throughout the rest of the year.
TLS: From the Equine Endocrinology Group’s Recommendations for the Diagnosis and Treatment of PPID: It is therefore recommended that PRASCEND be introduced gradually by giving partial doses for the first four days or by administering half the dose morning and evening. 
http://sites.tufts.edu/equineendogroup/files/2013/11/EEG-recommendations_-downloadable-final.pdf
   
Q.  How does Pergolide work?
M: Pergolide is a dopamine agonist – acts similar to dopamine – PPID is the result of a loss of dopamine in the pituitary, pergolide replaces lost dopamine and reduces hormones being produced, when hormones return to normal concentration, clinical signs resolve.
 
Q.  Pergolide was banned from human market because risk of heart problems, is it ok for horses?
L:  Some humans taking ~ 3 mg pergolide for Parkinson’s disease developed fibrosis of heart valves.  This is not an issue in horses, likely due to differences in dosing with regard to dose in proportion to body weight, also there are differences in heart muscle receptors that are stimulated and some other minor differences between humans and horses.  In pergolide research carried out in horses to date there have been no issues noted with cardiac abnormalities.  The FDA 6 month Prascend target animal safety study evaluated 32 horses at elevated doses of Prascend, no cardiac abnormalities were observed clinically or at necropsy.
 
Q.  Are minis/ponies dosed the same as horses?
L:  2 mcg/kg bodyweight so ~ 0.5 mg for a pony is the recommended starting dose, watch for inappetance.  Ponies can be worse in terms of clinical signs, progression of disease and insulin dysregulation than horses.
 http://www.noahcompendium.co.uk/?id=-447753

Q.  25 year old gelding diagnosed with PPID last year because he was sweating when other horses weren’t, being treated with Prascend.  His winter coat is longer than other horses but not excessively long and it does shed out almost completely.  What signs would indicate that his dose needs to be increased?
M:  Sweating excessively can be an early sign of PPID and may happen before haircoat abnormalities.  Diagnosis of PPID should take into account clinical signs and blood tests, worsening of either can indicate that the dose of Prascend needs to be increased.
 
Q.  What % of ponies have PPID/EMS, and how many are diagnosed at a young age?
M:  By the time they are in their 30s, prevelence of PPID in ponies may be 50% (guess!).  Ponies are more at risk of insulin dysregulation, particularly if fat – they are bred to be thrifty – therefore at risk of having both conditions, need to watch feet because of risk of laminitis.
 
Q.  Horse had elevated cortisol levels, started on Prascend, when should he be retested?
L:  By cortisol presumably this means post-DST cortisol, as resting cortisol is not recommended as a diagnostic test.  Retest 30 days after starting treatment with Prascend, then every 6 months, with one test in autumn seasonal rise.
In the USA the upper end of the dose range is 4 mcg/kg (10 mcg/kg in the UK).  Some members of the Equine Endocrinology Group recommend a higher, more flexible dose before considering dual treatment but this is an extra label recommendation (i.e. not recommended on the Prascend data sheet).
With an advanced case, it may not be possible to get hormones into the normal reference range even though clinical signs are responding well – either try raising the dose to see if test results will come down into the normal range or stick with the dose as long as it is controlling clinical signs.
In earlier/milder cases best to adapt dose to try to get both hormones within normal range and achieve improvement in clinical signs.
Best not to overly focus on reaching a particular target for blood results, but focus on achieving a significant improvement in clinical signs and when possible a significant improvement in test results as well.
TLS strongly advises against using the dexamethasone suppression test.
http://sites.tufts.edu/equineendogroup/files/2013/11/EEG-recommendations_-downloadable-final.pdf
 
Q.  Will a horse with PPID need Prascend for rest of its life?
M:  Yes.  At the moment we tend to diagnose horses once they have fairly significant disease.  Perhaps in future if recognised early and we understand more about dopaminergic neurons we may be able to change this.  But once dopamine neurons have been lost we need to keep replacing dopamine for life.  Dr Schott has found that many horses do not need increased doses but can be maintained on a consistent dose for a long time and do well.
 
Q.  PPID horse got loose manure on and off all winter when on liquid compound of pergolide, this year he is on Prascend, she increased the dose for the seasonal rise and reduced it in December, and he immediately got loose manure again.  What are the possible causes?
M: PPID causes a decreased ability to deal with infection and parasites.  Study looked at horses with PPID and they had higher fecal egg counts (FECs), so check FEC to check for worms and use strategic worming in consultation with vet.  At the higher dose, the immune system was probably working better, therefore parasite burden should be investigated.
Also there may be problems with efficacy using compounded pergolide.
TLS: also consider any diet changes in December, e.g. starting hay – stalky hay has anecodotally been reported as causing diarrhoea.  We sometimes see diarrhoea in horses on too high a dose of pergolide – when the dose is reduced, the diarrhoea disappears, with no increase in PPID clinical signs –
 http://www.noahcompendium.co.uk/?id=-447754

Q.  How important is owner’s relationship with their vet?
M:  Important to have vet involved with PPID horse, lot of complexity in diagnosis and treatment, owner info is critical, keep good records – e.g. when coat sheds, feet, appetite, BCS, weight tape – to notice problems early.  Schedule routine checks with vet.  Have to keep on top of PPID.
 
Q.  16 year old gelding, ACTH normal but muscle loss, long curly coat, reoccuring laminitis despite controlled diet and exercise.  Vet suggested starting on Prascend – is it a good idea to treat without a positive blood test?
M:  There’s a good clinical indication that this horse has PPID.  If you suspect a horse has PPID, it almost always does have it, as test results often only become positive later in disease.  The TRH stimulation of ACTH may be more effective at picking up early PPID.  This horse is likely to benefit from Prascend.
TLS: insulin dysregulation should be tested in all cases of laminitis.
 
Q.  How should you prioritise testing when finances are tight?
L:  Depends what clinical signs the horse has, in more advanced cases where the horse has overt signs e.g. long shaggy haircoat, muscle loss, PU/PD, diagnostic tests may be less important as the clinical signs indicate PPID, treatment with pergolide would be warranted.  Diagnostic testing may be more critical earlier in the disease if clinical signs are subtle, e.g. recurrent infection, change in behaviour which aren’t obviously PPID.  Start with diagnostic test then follow up test to monitor treatment, then ideally follow up rechecks.
TLS: NB be aware that tests in early stages of PPID may give false negative results.
 
Q.  22 year old Morgan mare diagnosed with PPID in 2012, doing fairly well on pergolide.  Concerned mare isn’t drinking enough which seems to cause dry manure and bouts of colic.  Before starting pergolide the mare drank 5 gallons/day, now only 2 gallons/day.  Can pergolide reduce thirst too much? 
M:  PPID horses can have PU/PD, but 5 gallons is not excessive so no reason to think this horse had PU/PD before treatment.  Dr McFarlane has never seen pergolide reduce drinking other than correcting PU/PD.  Pergolide does not reduce thirst.  Is horse eating the same as it was before?
 
Q.  Is there a difference between pergolide products in terms of effectiveness?
M:  Research looked at some of the different compounded drugs compared to manufactured pergolide.  Pergolide is extremely hard to compound, if compounding companies do not have all the right equipment they will end up with a product that is not consistent so you might not be giving your horse the dose you think you are.  Pergolide is very unstable, it can degrade quickly, liquid forms degrade as it is sensitive to light and temp.  When peroglide is correctly manufactured and packaged it is stable.  2 investigators have done 3 studies that have shown that the compounded drug is not stable.  TLS: see under Pergolide http://www.thelaminitissite.org/p-q.html.
L:  Recent unpublished data: 21 additional compounded pergolide forumulations were looked at at North Carolina State University, “out of those 21 common compounded formulations from major pharmacies at day 0 of the 6 month study only 4 of those compounds met the plus or minus 10% of labelled concentration, which is what would be acceptable.  And in fact, 1 of those 4 there was absolutely no pergolide detectable during that 6 month time frame” (*this needs clarification – see end of notes).  Plenty of data demonstrating the potency and stability issues with compounded pergolide.
M: Compounded drugs are not under regulatory control, don’t know that what it says on label is what’s in drug.  Manufactured drug is guaranteed to contain what it says on the label.
L/M: 4 out of 21 that were plus or minus 10% at day 0 before chance to degrade.
Prascend is a 1 mg tablet packed in a nitrogen sealed blister pack.
 
Q.  How should Prascend be given?
L:  Prascend should be given as soon as it is taken out of the blister pack.  Can be fed by hand, or dissolved in a bit of water.  If the horse has insulin issues, use low sugar treats to give Prascend, e.g. sugar free pancake syrup.  If no problem with insulin, put tablet in e.g. apple, carrot, apple sauce, grape.  Find something horse likes to insert tablet in, may have to try something new every few weeks.  Horses may go off feed if given with pergolide, so may need to give tablet at different time.
TLS: carrot on an as fed basis has less than 7% combined sugar/starch and a small amount should be safe to feed to any horse, insulin dysregulation or not: http://www.thelaminitissite.org/2/post/2013/03/who-said-stop-the-carrots.html.
 
Q.  Are there any issues regarding vaccinating and worming for horses with PPID?
M:  Vaccinate as any aged horse, depending on exposures to pathogens.  PPID horses respond less rigourously to flu.  Ongoing studies about how PPID horses respond to vaccines.  FECs are important for PPID horses, as they can be high egg shedders, and worm strategically according to results, in consultation with your vet.
 
Q.  Horse was diagnosed with PPID and had laminitis in spring 2013, can he be exercised as normal now?
M:  The consideration regarding exercise is the laminitis.  Horses with PPID can continue to work, and if one of the majority of horses that doesn’t have insulin problems and risk of laminitis, there shouldn’t be any concerns.  Need to be sure the horse isn’t over-exercised if still any pain or inflammation in the feet.  If the laminitis has been resolved and managed then horse should be able to return to exercise.  Feet are limiting factor, work with vet and farrier to do corrective trimming and/or shoeing, take radiographs and be sure feet are resolved before doing much in the way of exercise.
TLS: a horse with active laminitis or founder should not be exercised at all and kept confined until the active laminitis has resolved and the feet have been realigned.
 
Q.  Can chaste berry be given in addition to Prascend/at all?
M: Chaste berry is a herb with reportedly similar dopaminergic-type properties to pergolide.  In herbal supplements we don’t know the amount of active substance (if any) from year to year, or forumulation to formulation.  Dr Beech used chaste berry extract for horses with PPID and found no improvement, then found improvement when same horses were treated with manufactured pergolide.  Don’t use, use only Prascend.
TLS: See Vitex agnus castus http://www.thelaminitissite.org/u-v-w-x-y-z.html.
 
Q.  Numerous supplements/homeopathic treatments claim to help horses with PPID – do any work?
M:  Very little research has been done, the ones tested have shown no improvement.  Nothing can be recommended that has any science behind it to suggest that it is helpful.
 
Q.  28 mare that’s been on Prascend for 18 months, no recurrence of laminitis and a more normal haircoat.  Started shedding in February but seems thin, can’t eat hay as bad teeth.  On grass and concentrate mix, what else can she feed?
L:  Start with thorough dental exam, every 6 months.  Ensure good deworming programme.  For diet, as she’s had laminitis she probably has insulin dysregulation so have to be careful with feed.  If she can’t eat hay, make sure she is fed at least 2% of her bodyweight/day, recommend vegetable oil for calories ½ cup to 1 cup/day, rinsed and soaked unmolassed beet pulp for nutrients, fibre and water (to help prevent colic in horses with poor teeth), flax seed for EFAs and calories, and commercial supplements for weight gain, in addition to her concentrate mix.
 
Q.  Is flaxseed (linseed in UK) good for PPID?
L:  Excellent for equine diet – rich in protein, good for muscle wasting; omega 3 fatty acids; seed holds water so may help prevent colic; in humans may improve immune response, may be added benefit.
 
Q. Will PPID horses have improved FECs when treated with pergolide?
M:  This is an area that needs to be studied.  In theory it should, as Prascend improves immune function, but haven’t done FECs pre and post Prascend.
 
Q.  Any supplements PPID horses should not have?
M:  Can’t think of anything that would be contra-indicated in a typical supplement.
 
Q.  28 PPID gelding on pergolide and Thyro-L, never fully sheds, clipped in summer and autumn, can coat be made normal?
L: Haircoat should improve with adequate treatment, retest to ensure on proper dose, make sure actually getting dose!  Check correct deworming programme, parasites can affect haircoat.  Focus on diet, ensure balanced and supplying adequate protein, vitamins and minerals.  Use Prascend not compounded pergolide.
 
Q.  What is the life expectency for a horse with PPID with/without medication?   
M: Horses with PPID can live a long time and have a high quality of life if well managed and able to avoid infectious diseases and laminitis if they  have insulin dysregulation.  If PPID well controlled with pergolide and good management, no reason they can’t live a long quality life, possibly into their 40s (Dr McFarlane knew a 45 year old with PPID) – PPID is not necessarily going to shorten life expectency.
Important that owners are proactive at recognising problems (e.g. infections and laminitis) before they become well established.    

 
Q.  Can a horse with PPID feel discomfort because of the increased size of the pituitary gland?
M:  No indication that PPID horses have head pain.  The hormones that are increased with PPID are anti-inflammatory and analgesic so PPID horses tend to feel good!
 
Q.  Can PPID affect eyesight?
M:  There are a few reports, but no direct link proven.  90% of old horses have eye lesions, old horses will have vision problems, not just PPID horses.  Corneal ulcers heal slower with PPID.
 
Q.  Should pergolide be given at the same time each day?
L:  Give when most convenient, no recommendation for either morning or evening.
 
Q.  Is an increase in tendon & ligament injuries seen with PPID?
M:  No indication that PPID causes more problems with tendons and ligaments.  However reports have been received of horses that have been lethargic due to PPID starting treatment and feeling too good,  and injuring themselves when they are turned out!  So rehab horses, warm up well before exercise – they may feel a lot younger than their body is!
 
Final thoughts.
L: Most important thing for owners to do is to be proactive – learn early signs of PPID, help vet with diagnosis, the earlier we recognise and manage PPID, better quality of life our horses will have.
M: PPID horses still have a lot to give, fabulous that owners are learning about PPID and taking care of these older horses.
 
www.thehorse.com/PPID  - 10 articles about PPID
 
 
TLS:
*We’ve listened to this over and over – best sense we can make is that the FDA standard for potency is that there should be no more than a +/- 10% difference between the active ingredient actually in a drug and the active ingredient declared on the label.
So we are guessing that 4 out of the 21 compounded formulations looked at were found to have a difference of more than 10% between the actual amount of pergolide and the quantity on the label when they were first analysed (at day 0), and that 1 of these 4 had no pergolide detectable at all during the 6 months.
 
More about the stability and potency of pergolide in compounded products under pergolide: http://www.thelaminitissite.org/p-q.html
 
 
Interesting that lots of reference was made to horses being diagnosed later, i.e. in their teens, and a 13 year old horse was described as being young for diagnosis.  However in the UK we are seeing horses being diagnosed younger than this – is this a result of the free testing campaigns by Talk About Laminitis picking up early cases of PPID at a younger age?
 
 
Disclaimer: No responsibility is taken for the accuracy of these notes.
The Horse Ask the Vet Live session is available on-line: http://www.thehorse.com/ask-the-vet/33389/managing-horses-with-ppid-equine-cushings

There are two common equine endocrine diseases:
Equine Pituitary Pars Intermedia Dysfunction – PPID
Equine Metabolic Syndrome – EMS

PPID 

Pathophysiology of PPID (i.e. what goes wrong)

The equine pituitary gland is suspended from the hypothalamus (towards the bottom of the brain) by the infundibular stalk.  It has 4 lobes:

Pars tuberalis – a thin band of tissue around the infundibular stalk;
Pars nervosa – secretes oxytocin and ADH (vasopressin);
Pars distalis (anterior lobe) - secretes many hormones including reproductive hormones: FSH, LH, GH, TSH, Prolactin, ACTH;
Pars intermedia.

The pars intermedia is made up of melanotrope endocrine cells.  Hormone production is reduced when dopamine, released by periventricular dopaminergic neurons which originate in the hypothalamus, interacts with D2 dopamine receptors on the melanotropes of the pars intermedia.

The pars intermedia produces a peptide called POMC.  Two enzymes, PC1 and PC2, cut the POMC into smaller hormones including alpha-MSH, CLIP and beta-endorphin. 

In a normal horse, hardly any ACTH is made in the pars intermedia – it comes from the corticotrope cells of the pars distalis where POMC is cleaved into ACTH by PC1.  PPID horses produce ACTH in both the pars distalis and the pars intermedia.

PPID is a dopaminergic neurodegenerative disease – the dopamine producing neurons are lost, and with less dopamine to inhibit hormone production, the pars intermedia releases massively increased amounts of alpha-MSH, beta-endorphin and CLIP, and also ACTH.  This leads to hypertrophy (increase in cell size) and hyperplasia (increase in cell number), causing the pars intermedia and therefore the pituitary gland to increase in size – a normal pituitary gland weighs around 2 grams, in a horse with advanced PPID the pituitary gland can weigh more than 10 grams.

If the missing dopamine is replaced with a dopamine agonist, e.g. pergolide, hormone abnormalities and clinical signs of PPID are reduced.

Clinical signs of PPID 

A collection of clinical signs can be seen in horses with PPID, some early and others later as the disease progresses.

Early:
Muscle loss
Lethargy/docile – horse becomes more mellow, perhaps nicer (due to increased beta-endorphin)
Infertility in breeding horses
Secondary infections e.g. sinusitis, abscesses

Late:
Abnormal haircoat – including regional abnormalities like long hair on the legs, long tufts on chin and belly which may shed, and hypertrichosis (failure to shed).
Profound weight loss – loss of all fat, not just muscle
Pot belly – due to loss of muscle tone
Abnormal sweating/thermoregulation - hyperhydrosis (increased sweating) or anhydrosis (lack of normal sweating in hot conditions).      

Some but not all horses with PPID will also have the potential for laminitis, hyperinsulinaemia, abnormal fat deposits, PU/PD (excessive drinking and urination), exercise intolerance, infertility, abnormal sweating  – they have PPID and EMS.   Some experts believe that not all horses with PPID are at risk from laminitis – only a subset of horses with PPID are at risk from laminitis (therefore insulin dysregulation should be measured in all horses with PPID to assess laminitis risk).

Diagnosis of PPID 

Early stage PPID can be hard to diagnose – blood tests are often negative early in the condition, and clinical signs can overlap with normal aging.  However, it is worth pursuing a positive test result to provide a useful guide for response to treatment.

A diagnosis of PPID should only be made if there are clinical signs of PPID, based on examination and a complete history – owners should regularly record weight, body condition score, dates of shedding/haircoat changes, how often feet need trimming, signs of laminitis and PPID such as hoof rings, to help the vet reach a diagnosis.

A long haircoat is highly suggestive of PPID in an older horse but it is not an absolute diagnosis – e.g. malnutrition can cause haircoat changes and false positive blood results.  Concurrent disease can also affect clinical signs and blood results.

Diagnostic tests for PPID 

Resting plasma ACTH concentration is now the most common test - the vet collects blood into a purple topped tube (EDTA).  Equine ACTH is not particularly unstable and as long as it is kept cool it can be separated up to 12 hours later, and then kept chilled or frozen until it is tested.

There are 2 methods for measuring ACTH:
Chemiluminescent (CIA) - Immulite as used by Cornell and Liphook
Radioimmunoassay (RIA)
Reference ranges are different between CIA and RIA (and potentially between different RIA assays) – seasonally adjusted reference ranges specific to the testing lab must be used, and results may not be comparable between labs.

There is no way of telling whether the ACTH measured came from the pars intermedia or the pars distalis - ACTH may increase with other diseases or stress.

(TLS comment: more than one ACTH sample will increase diagnostic accuracy as ACTH concentrations can fluctuate significantly).

The dexamethasone suppression test (DST) is no longer recommended – there is a risk of causing/exacerbating laminitis, it requires 2 vet visits, it cannot be used in the autumn, and it may only detect advanced PPID cases.

Dr McFarlane compared ACTH, alpha-MSH, dexamethasone suppression test (DST) cortisol and resting cortisol to pituitary gland cell changes and haircoat changes in 120 older horses, using the pituitary grading scale published by Miller:

Miller MA, Pardo ID, Jackson LP, Moore GE, Sojka JE
Correlation of Pituitary Histomorphometry with Adrenocorticotrophic Hormone Response to Domperidone Administration in the Diagnosis of Equine Pituitary Pars Intermedia Dysfunction
Vet Pathol 45:26–38 (2008)

Findings:
                                    Sensitivity (true positives)            Specificity (true negatives)
Alpha-MSH                             63%                                         90%
ACTH                                      71%                                         81%
DST                                         65%                                         98%

All 3 tests identified advanced (grade 5) PPID.
All 3 tests were poor at identifying early PPID.
ACTH had a weaker correlation with pars intermedia enlargement than Alpha-MSH or DST.
Alpha-MSH had 2/48 false positives, ACTH had 13/48 false positives.
ACTH may be from the pars intermedia or the pars distalis, and may increase with other diseases or stress.
Resting cortisol is not predictive of PPID (this has been known for a long time).

A better test was needed.

Since around 2011 the TRH stimulation of ACTH has been used to diagnose PPID, and further research is being carried out on this test. 

The vet collects a blood sample to measure resting ACTH, then injects 1 mg of the hormone TRH intravenously and collects blood to measure ACTH 10 and/or 30 mins after giving the TRH.

Currently suggested reference ranges are:
PPID if ACTH > 36 pg/ml (using Immulite CIA) at 0 or 30 minutes
PPID if ACTH > 110 pg/ml at 10 minutes
However these reference ranges are likely to change as more data is collected (normal horses have tested above these ranges), and reference ranges have not been established for the autumn seasonal rise.

Sensitivity (true positives) 88-95%, specificity (true negatives) 71-91% so the TRH stimulation of ACTH appears more diagnostic than resting ACTH.

TRH stimulates pars intermedia activity – however, increased activity does not necessarily mean dysfunction, increased activity could be appropriate and not due to lack of dopaminergic inhibition.

Autumn natural stimulation of ACTH 

The pars intermedia becomes more active in the autumn in all horses, with increased hormone output and histological changes.  It isn’t known exactly why this happens, but it may help the horse prepare for winter by changing metabolism and stimulating hair coat growth, as is seen in other species.

The difference between PPID and normal horse resting ACTH is greatest in the autumn, making this the best time to test.

Copas VEN, Durham AE
Circannual variation in plasma adrenocorticotropic hormone concentrations in the UK in normal horses and ponies, and those with pituitary pars intermedia dysfunction 
Equine Veterinary Journal Vol 44, Issue 4, pages 440–443, July 2012

EMS 

EMS is not a disease, it is a cluster of risk factors which indicate that a horse is at greater risk of developing endocrinopathic laminitis.

Frank N, Geor RJ, Bailey SR, Durham AE, Johnson PJ
Equine Metabolic Syndrome - ACVIM Consensus Statement
J Vet Intern Med 2010;24:467–475

The 2010 ACVIM Consensus Statement described the EMS phenotype as including:

• General (obesity = body condition score (BCS) of 7 to 9 on the 9 point scale) or regional adiposity (crest of neck, tailhead, shoulder, sheath/mammory glands),
• Hyperinsulinaemia/abnormal insulin response,
• Predisposition to laminitis.

Plus horses may be described as “easy keepers” or “thrifty”, mares may have abnormal reproductive seasons, blood tests for lipids and leptin may show abnormalities.  Some breeds appear to be more predisposed to EMS than others.

Insulin Dysfunction - Insulin Resistance v Hyperinsulinaemia

Insulin resistance is when the body produces insulin, but the insulin sensitive tissue (primarily muscle) does not respond normally to that insulin, which prevents glucose in the blood from entering the tissue normally.
Insulin resistance is at the level of the tissue (muscle).

Over time, insulin resistance causes the horse to “compensate” by making more insulin to ensure that glucose does enter the tissue – this is compensatory hyperinsulinaemia .

However, chronic hyperglycaemia and hyperinsulinaemia may be the primary problem, and can lead to tissue insulin resistance.

Why is this important?

It is hyperinsulinaemia (high concentrations of insulin), not insulin resistance, that is the risk factor for endocrinopathic laminitis, and this has implications for both testing and treatment.

For example, if the primary problem is at the level of the pancreas, not the level of the tissue, and a drug is given that causes improvement at the tissue level, the health of that animal may not be improved.

When a normal horse eats, glucose is absorbed into the blood stream and insulin is released to enable that glucose to enter insulin sensitive tissue – blood levels of both glucose and insulin rise after a meal and then drop back down (dotted lines above).

When an EMS horse eats, glucose is absorbed into the blood stream and insulin is released, but if the horse has a problem at the level of the insulin sensitive tissue, the glucose doesn’t enter the tissue efficiently, so the pancreas compensates by making more insulin – blood levels of both glucose and insulin increase and take longer to drop back down (solid lines above).

If a horse has greater than normal absorption of glucose or greater than normal release of insulin from the pancreas, over time the horse can develop insulin resistance at the level of the tissue - a dynamic oral test will pick up dysfunction at every level.

Diagnosis of insulin dysregulation

The fasting blood insulin concentration is the easiest test to carry out and involves taking a single sample of blood after the horse has been fasted for at least 6 hours.

An above normal result (20 µIU/ml is often used as the cut-off but see below) is diagnostic of hyperinsulinaemia.  The test has a high false negative rate (around 2/3 of horses with insulin dysregulation have normal fasting insulin), so a normal test result does not rule out EMS, and a dynamic test should follow a normal fasting insulin test for any horse suspected of having insulin dysregulation.

Glucose may be normal or above normal.

Reference ranges for insulin may be breed specific, therefore a cut-off of 20 µIU/ml may not be appropriate for all breeds.

Reference ranges for insulin are laboratory specific, therefore a cut-off of 20 µIU/ml may not be appropriate for all labs (different assays, e.g. RIA v CIA, may produce different results meaning that results cannot be compared).

Dr McFarlane suggests that PPID horses with insulin resistance more commonly have abnormal fasting insulin results than horses with EMS only.

The most appropriate dynamic test is the oral sugar test (OST) – this mimics natural conditions, testing at the level of the GI tract, pancreas and tissue, not just at the level of the tissue.

The horse is fasted for at least 6 hours, then given 0.15 ml/kg bodyweight (so 75 ml for a 500 kg horse) Karo Light syrup by mouth (either syringed directly in to the mouth or in a small low sugar feed).  Blood is collected 60 and 90 minutes later and both insulin and glucose are measured.

Insulin > 60 µIU/ml at 60 or 90 minutes is diagnostic of hyperinsulinaemia.
Insulin between 45-60 µIU/ml at 60 or 90 minutes is equivocal and further testing should be considered.
Insulin below 45 µIU/ml at 60 or 90 minutes is considered normal.
Glucose > 125 mg/dl at 60 or 90 minutes is considered an excessive glucose response.

(For more details see the Equine Endocrinology Group Recommendations for the diagnosis and treatment of PPID).

The combined glucose insulin tolerance test (CGITT) and insulin tolerance test (ITT) measure insulin resistance at the level of the tissue only (NB the ITT may risk causing hypoglycaemia).

However, EMS is a very frustrating condition and the current tests are not that good.  Vets are seeing horses they strongly suspect have insulin dysregulation but are having trouble getting the test results to prove it.
Dr McFarlane looked at horses that appeared to be hyperinsulinaemic, all had a BCS of 8 or 9 and two thirds of them had foundered, but she could not get half of these horses to test positive.

She suggests if there is a clinical indication of a “thrifty” horse then it’s best to consider that it has EMS and treat appropriately.

The purpose of trying to diagnose EMS is to prevent laminitis.

Endocrinopathic laminitis

Endocrine disease (obesity/EMS, PPID) is the most common cause of laminitis, and may be triggered by diet, particularly when grasses are highest in NSC.

Endocrinopathic laminitis can be insidious and may be mistaken for other conditions - radiographic and hoof growth changes may precede clinical symptoms.

Endocrinopathic laminitis was once believed to be the result of excessive cortisol, but there is now strong evidence that it is caused by serum insulin concentration (hyperinsulinaemia), as horses receiving a continuous infusion of insulin consistently develop laminitis.

Endocrine laminitis has different histological characteristics to SIRS laminitis (laminitis secondary to endotoxaemia e.g. colitis, retained placenta).  With endocrine laminitis, the secondary epidermal laminae (SEL) become longer and narrower before clinical signs of laminitis are seen, and there is a general absence of inflammation (compared to SIRS laminitis).  It is currently thought that excessive insulin binds to and activates insulin growth factor–1 (IGF-1) receptors on the laminae causing cell division and elongation of the SEL, making them structurally unsound and causing laminitis.

Potential new drugs for the treatment and/or prevention of endocrinopathic laminitis may target this area.

EMS and PPID Summary 

EMS and PPID are not mutually exclusive – a horse can have EMS and PPID.
Clinical signs common to EMS and PPID include laminitis, hyperinsulinaemia, abnormal fat deposits, PU/PD, abnormal sweating, exercise intolerance, infertility.

EMS by definition is hyperinsulinaemia or an excessive insulin response to a meal stimulus (which increases the risk of laminitis).
PPID by definition is an overly active pars intermedia.

Horses with EMS may be at greater risk of developing PPID as they get older – horses with EMS should be monitored and tested for PPID.
There appears to be a transitional period between the diseases during which horses have both EMS and PPID at the same time.  These horses often have higher insulin concentrations and potentially a greater risk of laminitis, therefore treatment should be instigated as early as possible.

It isn’t yet known whether EMS and PPID are causitively linked – i.e. whether having EMS causes PPID.

In Dr McFarlane’s experience, a horse with PPID that has never had laminitis and has normal insulin is not at greater risk of developing laminitis than any other horse.

Equine endocrine diseases are progressive and difficult to diagnose in the early stages – there will always be a grey zone for testing in the early stages of a progressive disease.  Retest horses that are suspected of having EMS/PPID if they have negative results, and/or instigate treatment.

History and clinical signs are essential for early diagnosis – a diagnosis should not be made on the basis of diagnostic test results if there are no clinical signs.

Tests can be carried out in any season as long as results are interpreted correctly, and autumn is the best time to test for PPID using resting ACTH.

Insulin/insulin dynamics should be measured in all equine endocrine cases (PPID as well as EMS) as insulin dysfunction is predictive of laminitis risk.

Use resting ACTH concentration or TRH stimulation of ACTH for PPID diagnosis.
Use fasting insulin or the oral sugar test to assess risk of laminitis (for both EMS and PPID).

Believe clinical impressions, retest or treat cases that are suspicious – people are better at diagnosing PPID (and EMS) than current blood tests are at confirming it.  However, always get blood tests done too to monitor disease progression/efficacy of treatment.

The goal is to recognise these diseases early to avoid clinical signs, especially laminitis – early intervention may keep horses healthy for longer.

(Above) In the 2014 paper, Clinical Outcome of 14 Obese, Laminitic Horses Managed with the Same Rehabilitation Protocol (without doubt one of the most important papers published regarding laminitis rehabilitation), Debra Taylor et al. returned 14 of 14 laminitic horses with rotation ≥5° (6 had >11.5° of rotation) to their pre-laminitis level of soundness by the time of the endpoint radiographic evaluation.
​

Q.  Even rotation of 30 degrees or more?

A.  Yes, depending on the individual circumstances.  Besides, at some point, talking about the size of an angle of rotation may become rather pointless - what would the angle of rotation be on Cedar's left fore before his realigning trim below (possible position of the pedal bone marked in green)?  After 3 months his realigning trim was pretty much complete, and x-rays a month later confirmed this, although there was still distal descent which would hopefully correct with time.  See photos of Cedar's rehab here.

In Clinical Outcome of 14 Obese, Laminitic Horses Managed with the Same Rehabilitation Protocol, the maximum pre-treatment palmar angle was 31 degrees, and the maximum dorsal angle (degrees of rotation) was 29 degrees.  All horses returned to their pre-laminitis level of soundness.  

A.  Whilst the foot is not correctly aligned there is likely to be an increased risk of rotation, sinking, cellular damage and bone loss.

The x-rays above are of the same foot taken two months apart.  The toes have been brought back slightly but the heels have remained excessively high with a palmar angle of around 17 degrees.  After two months there is less sole depth beneath the tip of the pedal bone, and a gas pocket suggesting total separation of the laminae is now evident.  Luckily this horse was kept confined and his feet well supported and made a good recovery, but leaving the heels high could have caused further sinking and rotation, and his recovery could almost certainly have been much quicker if his feet had been realigned as soon as laminitis was diagnosed.

Insulin resistant pony Mary had been regularly trimmed by a farrier who left her heels too high.  When Jenny Edwards of All Natural Horse Care rescued Mary she had dorsal rotation of around 24 degrees, palmar angles of around 19 degrees, considerable sinking, and bone loss and remodelling (ski tip) of the pedal bone.  A realigning trim and boots and pads made Mary much more comfortable and she was soon trotting happily.  Her story here includes an excellent video showing her increase in comfort from wearing boots and pads despite being on soft sand.

Q.  How can the risk of penetration of the sole be reduced?

A.  By carrying out a correct realigning trim at the earliest opportunity and supporting the feet.  
​See Solar penetration. ​http://www.thelaminitissite.org/feet-faq--articles/solar-penetration

Q.  Can a horse recover if the pedal bone penetrates the sole?

A.  Yes.  But it takes dedication.  See Solar penetration.  http://www.thelaminitissite.org/feet-faq--articles/solar-penetration
Read Paige Poss' inspiring story about Druid.
Druid had rotation (around 18 degrees dorsal rotation in one x-ray) which led to penetration of the pedal (coffin) bones in all four feet.  He could hardly stand at first, had bed sores, gastric ulcers and weeks of abscessing.  However, within 5 months he was able to wander around outside, x-rays at 6 months showed realignment of the feet, and within 10 months he was comfortable on gravel, trotting, and starting to be ridden again.

Blossom, a Clydesdale, recovered from rotation and penetration following laminitis seemingly caused by a liver infection, with a barefoot trim, daily soaks and boots and pads, thanks to Andrew Bowe at www.barehoofcare.com.  Andrew also helped Whisky recover from penetration in all four feet.  And Jenny Wren.

Above: This mare's right fore pedal bone penetrated her sole around 3 months after she developed sepsis-related laminitis due to retaining placenta after foaling, and the left fore almost penetrated. 
Top - a SoleMate pad had been fitted with a hole beneath the tip of the pedal bone which the pedal bone sank into.  Realigning trimming had not been carried out, the toes were too long with force being exerted on the toe to the outside of the large area of separation (black gas pocket) that ran the full length of the laminae, and the heels were too high.
Bottom - 3 months later (the x-ray was taken pre-trim and 4 weeks beyond the recommended next trim date) the foot is almost fully realigned (and was fully realigned at the next trim), and the sole depth has increased significantly (and was reduced in the next trim - there is too much sole depth here).  The area of separation (black gas pocket) has almost grown down past P3, and was mostly removed at the next trim.  An old abscess hole is seen beneath the tip of P3, but no exudate was found.  The tip of P3 shows remodeling and damage.  Options for supporting the foot and preventing infection had been limited during the rehabilitation.  

Q.  Can the hoof wall completely detach from the pedal bone?

A.  Most cases of laminitis are endocrine, that is they are caused by EMS/PPID.  Recent research has shown that with insulin-induced laminitis, the secondary epidermal laminae become longer and narrower - they stretch.  Katie Asplin found that there was minimal basement separation in ponies, and Melody de Laat also found less damage to the basement membrane in horses with insulin-induced laminitis than those with SIRS laminitis.  So it would appear that there is stretching and weakening of the laminae, but not necessarily complete separation.

When extensive laminar separation has occurred, a black gas pocket can often be seen on a lateromedial x-ray between the hoof wall and laminar wedge.  When this is seen, the foot should be fully supported to prevent further mechanical failure of the laminae and further movement of P3 - see Care & Rehabilitation of the Equine Foot p 261.

Once a correct realigning trim has been carried out and a new hoof grown down from the coronet, even a horse with significant gas pockets should be able to return to work, as was the case with Homer, above.

Q.  Is it possible to tell whether damage due to laminitis is recent or old?

In Clinical Outcome of 14 Obese, Laminitic Horses Managed with the Same Rehabilitation Protocol, horses were considered to have chronic laminitis (presumably suggesting long-standing damage) if they had hoof rings that were wider at the heel than at the toe, and/or if their pedal bones showed remodelling, e.g. a ski tip, when x-rayed.  Horses that had neither of these were considered to have acute laminitis (presumably suggesting recent damage)

On p 341 of Care and Rehabilitation of the Equine Foot, Pete Ramey suggests that it usually takes months to form a laminar wedge that is 2 cm thick at ground level, so when a thick laminar wedge is seen, the rotation is not new, and the original laminitic episode could have happened years ago.

This pony (above) appears to have a change of angle in the hoof wall just below the coronet, a large laminar wedge and divergent hoof rings almost to ground level, suggesting long-term chronic laminitis.  X-rays showed remodelling of the pedal bone in both fores, confirming this.

Q.  Does a horse being overweight affect the severity of laminitic damage?

A.  This seems quite likely.  Melody de Laat recorded that all 4 feet of the heavier horses had laminar damage, but only 3/4 feet in the lightest horse in her 2011 RIRDC report Insulin-Induced Laminitis.

Q.  Any more successful rehabilitation case studies?

A.  Here are a few:

Sophie - All Natural Horse Care

Missy - All Natural Horse Care

Pip - All Natural Horse Care

Oscar - www.barehoofcare.com

Charlie - www.barehoofcare.com

Glynn - www.naturalhorseworld.com

And already mentioned above:

Blossom - www.barehoofcare.com

Whisky - www.barehoofcare.com

References:

Asplin KE, Patterson-Kane JC, Sillence MN, Pollitt CC, Mc Gowan CM
Histopathology of insulin-induced laminitis in ponies
Equine Vet J. 2010 Nov;42(8):700-6  (PubMed)

de Laat M, Sillence M, McGowan C, Pollitt C 
Insulin-Induced Laminitis - An investigation of the disease mechanism in horses
RIRDC Dec 2011

Taylor D, Sperandeo A, Schumacher J, Passler T, Wooldridge A, Bell R, Cooner A, Guidry L, Matz-Creel H, Ramey I, Ramey P
Clinical Outcome of 14 Obese, Laminitic Horses Managed with the Same Rehabilitation Protocol
JEVS published online 05 Feb 2014

Pete Ramey - Care and Rehabilitation of the Equine Foot

More Information:

Hoof Rehabilitation Protocol - Debra Taylor, Ivy Ramey, Pete Ramey

Taylor D, Sperandeo A, Bell R, Passler T, Ramey I, Ramey P
Hoof Rehabilitation and Restoration of Soundness in Obese Laminitic Horses 
AAEP