Excellent advice from Liphook Equine Hospital on their results sheet for a horse with high insulin levels:

"Worth placing on a strict grass-free, non-glycaemic, low calorie, balanced diet to achieve weight loss and improve insulin sensitivity. 

Typically an effective diet must be relatively severe and be strictly implemented for a few weeks to a few months depending on starting body condition. Recommended rates of weight loss are generally between 0.5 to 1% loss of body weight weekly. Total dietary intake should generally be restricted to be in the range of 1.2 to 1.7% of body weight daily (feed weighed as fed rather than dry matter). The staple of the diet should be hay which is weighed dry and then soaked for an hour pre-feeding. It is also important that a feed balancer is included to ensure adequate protein and mins/vits on the restricted dietary plan."

TLS agrees that weight loss should be no more than 0.5 - 1% of bodyweight per week - so 2.5 - 5 kg/wk for a 500 kg horse. Restricting calories excessively can lead to other health problems such as gastric ulcers and hyperlipaemia, and can increase insulin resistance - the opposite of what we want.

For weight loss, energy in (feed) needs to be less than energy out (metabolism/exercise). Equine Applied and Clinical Nutrition (2013) suggests that reducing energy intake to around 70% of maintenance requirements can produce weight loss of 0.5-0.7% of bodyweight/wk.

Interestingly, Gordon et al (2009) found that a decrease in energy of less than 3% led to an average of 32.5 kg weight loss over 12 weeks (a total loss of ~5.6% bw, being ~0.47% per wk) in horses that weren't exercised (diet was calculated according to % bw - horses were fed 1% bw hay and 0.5% bw feed but when the energy was calculated, the diet was estimated to provide 16.64 Mcal/day and maintenance requirements were estimated at 17.09 Mcal/day - so the diet was only just below NRC recommended energy requirements). 

Horses on a slightly stricter diet (as above but the feed was reduced to 0.3% bw halfway) that had moderate exercise lost 52 kg over 12 weeks (a total loss of ~9% bw, being ~0.75% per wk) - their diet was estimated to provide 15.27 Mcal/day (which would be around 89% of their maintenance requirements) but the exercise increased their estimated energy requirements to 25.87 Mcal, therefore their diet was only providing around 59% of the NRC recommended energy requirements.

If actual energy fed cannot be calculated, then basing a diet on % bodyweight is reasonable. The ECIR group suggests feeding 1.5% of the horse's actual weight, or 2% of the horse's target weight. So a 500 kg horse needing to lose weight, if fed at 1.5% bw would need 7.5 kg DM feed (mostly hay) per day, this would be ~8.3 kg as fed (hay is usually around 10% water). Liphook suggest feeding 1.2% (so 6 kg for a 500 kg horse) to 1.7% (8.5 kg for a 500 kg horse) actual bodyweight as fed - so taking their top end recommendation, that works out much the same - around 8.3-8.5 kg of hay/feed as fed per day for an overweight 500 kg horse.

Research has shown that individual horses lose weight at different rates. It is usually recommended to start at the upper end of the suggested diet, and if weight loss isn't seen after a reasonable period, the diet may have to be restricted further. Significant dietary restriction should only be carried out under veterinary supervision.

Interestingly Liphook are suggesting soaking hay for an hour before feeding, (not the 12 hours that is so often suggested in the UK and which often causes hay to become slimy and unappetising) - this is in line with the ECIR group's recommendations. TLS tends to suggest soaking for around 1 - 6 hours, depending on the environmental temperature (sugar will be lost more slowly in colder temperatures) - what is important is the quantity of water used, as hay loses sugar by diffusion down a concentration gradient, so the more water used, the greater the gradient and the more sugar can be lost. If the sugar in the water equals the sugar in the hay, no more sugar can be lost from the hay, no matter how long it is soaked. Changing the water midway increases the concentration gradient and should lead to more sugar being soaked out.

Great that Liphook emphasise that a balancer must be fed to provide adequate mineral, vitamin and protein levels. TLS suggests using a balancer that will provide (close to) the NRC minimum amounts of copper (100 mg/500 kg horse), zinc (400 mg/500 kg horse) and selenium (1 mg/500 kg horse), as these minerals are usually low in UK forage. Good levels of vitamin E (~1000 IU/day) may also be beneficial for horses on a hay diet and/or with PPID. TLS would also recommend feeding micronised linseed to provide essential fatty acids, which are in grass but usually low in hay - linseed is one of the few sources of EFAs with higher omega 3 (anti-inflammatory) than omega 6 (inflammatory) levels. Most balancers/mineral supplements do not provide enough salt, so TLS would also recommend adding salt to the feed (use the NRC program to calculate how much sodium is needed - salt is ~40% sodium). A 500 kg horse at maintenance needs 10 g sodium, so 25 g salt - this is just over a tablespoon (allow for sodium/salt already present in the diet). Allow horses access to a pure salt block too.

More information:
TLS' recommended diet   
Weight loss   
Obesity  

Boehringer Ingelheim, the drug company that makes Prascend, would like owners to report any suspected adverse reactions to Prascend, either to your vet (and ensure that he/she reports it), or direct to Boehringer Ingelheim.

If you message BI yourself, please give the name and contact details of your vet, your full name and contact details, the name, age, breed and approximate weight of your horse, the date the treatment started, the dose of Prascend given, the date you noticed the reaction, for how long you noticed the reaction, the outcome and a description of what happened. BI will ensure these reports are followed up and reported to the Veterinary Medicines Directive.

We know that these adverse effects can be quite common and usually pass quickly, thanks mostly to the ECIR group who have been recording these effects for many years and coined the phrase "pergolide veil". However, it is very important that the drug companies and licencing authorities are also informed, so that any problems can be fully investigated and hopefully advice given to lessen the chances of any adverse effects being seen.

Pergolide appears to be an extremely effective and safe drug, there are horses on the ECIR group who have been on pergolide for 10 years and more, quite a few at high doses (over 5 mg/day), with no problems whatsoever. However, the pathology of PPID, the pharmacokinetics of pergolide and the interactions of neurochemicals and hormones make this an incredibly complicated area of medicine, so it's no wonder there can be a few "teething problems" when first starting treatment. Accurately reporting any problems experienced will almost certainly lead to more knowledge and improvements in the future - so please do it!


NB many owners in the USA have avoided pergolide veil symptoms when using APF at the same time as introducing pergolide - see Pergolide - ECIR Group.  APF can now be bought in the UK from ForagePlus.

The following suggestions for administering 0.25 mg Prascend (as seen on the internet) are not recommended:

Dissolving 0.5 mg tablet in a small quantity of water and giving half one day and the remaining half the next day - the datasheet states that if dissolving the tablet in liquid, the whole amount should be administered immediately.

Giving 0.5 mg every other day - the datasheet states that Prascend should be given once daily. As the average half life of pergolide has been found to be around 6 hours in horses, extending the time between doses seems counter-intuitive.
Wright, Abra M
Pharmacokinetics of Pergolide in normal mares 
MSc Thesis 2009 Kansas State University

Cutting 0.5 mg half tablets into two with a knife - cutting the pills with a knife risks crushing/wasting some of the tablet (the datasheet states that tablets should not be crushed), as well as operator injury (and many horses seem to hate the taste of blood)!

Keep your fingers safe and your horse's medication effective - if you have to divide tablets, use a pill splitter.

How deep should the collateral grooves be?

Pete Ramey suggests that collateral groove depth should normally be: 
10 - 20 mm at the apex of the frog 
15 - 30 mm at the deepest part towards the rear of the frog/beside the bars.

How collateral groove depths can be used to guide the trim

What if the collateral groove depths do not fall into the "ideal" 10-20 mm at the apex, 15-30 mm at the bars, the depth at the apex is less than the depth at the bars, or the measurements are not the same on both sides of the frog?

In some feet the collateral grooves cannot be easily identified at the front of the foot, because the frog has migrated forward into the sole.  Reassess trim.  See Live Sole and Then Some by Christoph Schork - EasyCare Inc.

The science

Researchers at Auburn University looked at the relationship between the external characteristics of the collateral grooves of the hoof capsule and the internal hoof structure on dissected feet.  They noted that the collateral grooves appear to run parallel to and a fixed distance from the solar surface of P3 in the front (dorsal) half of the foot, and the same distance from the base of the lateral cartilages in the back (palmar) half of the foot, and that the orientation of the collateral groove in the front half of the foot parallels the palmar angle of P3.  Based on Pete Ramey's findings, they suggested that in a healthy foot with adequate sole depth, the collateral groove depth at the frog apex should be around 10-20 mm from the ground.  

They measured 96 feet and compared the measurements to lateral x-rays, and found that the depth of the collateral groove at the frog apex was highly associated with sole depth, distance of P3 from the ground, and palmar angle, as measured on the x-rays.
​
​Rouben CM, Taylor DR, Degraves FJ, Schumacher J, Guidry LN
Evaluation of the shape and depth of the collateral groove of the foot as a method to predict the position of the distal phalanx within the hoof capsule
Phi Zeta Research Day Forum 2012 p 34

References and more information

Important - please read Pete Ramey's article Understanding the Horse's Sole thoroughly before you start using collateral groove depths to guide trimming, and/or chapter 16 Evaluating and Trimming the Sole in Care and Rehabilitation of the Equine Foot.
And ideally also One Foot For All Seasons? by Pete Ramey

See also:
Measuring Uniform, Adequate Sole Depth Using the Collateral Grooves - The Thoughtful Horseman

Collateral Groove Depth and Sole Concavity - Precision Hoof Pick

Here are the answers for TLS' first quiz - the General Laminitis Quiz - correct answers in bold:

Q1.  Which is the most common "type" of laminitis
Endocrine laminitis - 61% got this correct
Supporting limb laminitis
Systemic Inflammatory Response Syndrome (SIRS) laminitis

Explanation:
www.thelaminitissite.org/laminitis
"It is currently thought that around 90% of cases of laminitis have an endocrine cause (Karikoski et al. 2011) , either Equine Metabolic Syndrome or Pituitary Pars Intermedia Dysfunction/Cushing’s, 
and that pasture associated laminitis is an endocrine disorder in which horses (particularly ponies) have an abnormal insulin response to the sugars in grass."  

Q2.  A good daily check that can help early identification of laminitis?
Walking on hard ground/turning a tight circle - 72% got this correct
Checking body temperature/respiration rate
Walking a 20 m circle each way
Asking the horse to back up

Explanation:
www.thelaminitissite.org/laminitis
"Symptoms of laminitis include:
Feeling “footy” - preference for soft ground 
Reluctance to turn"

"Daily checks that can help early identification of laminitis:

• Walk on hard ground e.g. concrete - does the stride shorten, does he/she seem at all "pottery"?
  
• Turn in a tight circle - normal or reluctant to turn/stiff behind?
  
• Digital pulses - normal?
  
• Regional fat pads - cresty neck, bulges in hollows above eyes, enlarged sheath, fat above tail?  Hardening of neck crest or increase in any of these fat deposits can indicate imminent laminitis."

Q3.  Which blood tests are recommended if a horse has a history of laminitis?
Insulin, ACTH, glucose - 65% got this correct
Glucose, cortisol, ACTH
Insulin, cortisol, TRH
Glucose, TRH, ACTH

Explanation:
www.thelaminitissite.org/laminitis
Management of laminitis:
"Diagnose the cause – test blood for insulin & glucose EMS plus ACTH for PPID"

Insulin provides information about hyperinsulinaemia/insulin resistance, which diagnoses EMS and indicates laminitis risk.
ACTH diagnoses PPID.
Glucose, although not essential, can add information - glucose can be raised in horses with PPID and in diabetes, which is very rare in horses.
Cortisol used to be considered diagnostic for PPID, but that has since been disproven.
TRH itself isn't tested, but the TRH stimulation of ACTH may be used to diagnose PPID - in which case it is ACTH that is tested.

Q4.  Correct emergency treatment for laminitis?
Call vet, remove from grass, support feet if necessary, confine on deep supportive bedding - 93% got this correct
Call vet, allow access to grass, remove water, encourage to walk
Call vet, remove from grass, remove water, confine on bare concrete floor
Leave in field, give antibiotics and pain killers, encourage to walk

Explanation:
www.thelaminitissite.org/laminitis
"Emergency treatment for laminitis

• call vet (and farrier/trimmer)
• remove horse from grass (but move as little as possible/support feet before moving)
• confine on deep supportive bedding e.g. sand, sawdust, pea gravel
• support the feet if the bedding isn’t sufficient to do this, e.g. with styrofoam, impression material, boots and pads
• give NSAIDs e.g. Bute, Danilon, Equioxx for the inflammation & pain (for as short a time as possible)
• apply cold therapy to the feet to reduce inflammation and pain (but not if cold-induced laminitis/feet cold)"

Never encourage a horse with active laminitis to walk.  There is no reason to remove water - laminitic horses should always have access to water.   Antibiotics have no place in laminitis treatment, unless a bacterial infection is causing the primary illness leading to SIRS laminitis.

Q5.  The Laminitis Site's philosophy for treating laminitis?
Identify and remove/treat the cause, support and realign the feet - 93% got this correct
Give the pills, raise the heels
Find the cause, shoe the horse
Support and realign the feet and the cause of the laminitis will disappear

No explanation needed here - TLS believes that if you identify and remove/treat the cause and support and realign the feet, you'll sort out most cases of laminitis - great that so many people got this one right!
www.thelaminitissite.org/

Q6.  What is the maximum NSC % generally recommended when feeding a laminitic?
10% - 66% got this correct
5%
20%
25%

Explanation:
www.thelaminitissite.org/laminitis
Management of laminitis
"Feed low NSC (<10%) diet based on grass hay (+ protein, minerals, vitamins, linseed?) -do not starve"  
The idea of 10% seems to have come from the ACVIM consensus statement on EMS - see under Dietary Management.

Q7.  Which statement is true?
All/any feet can be affected by laminitis - 95% got this correct
Only the front feet are affected by laminitis
A single foot can't be affected by laminitis
Laminitis in all 4 feet is very rare

Explanation:
Nearly everyone knew that laminitis can affect all/any feet.  Endocrine and SIRS laminitis are systemic, they affect the whole body, therefore all 4 feet have a chance of developing laminitis - more details here:
Can a horse get laminitis in any foot? - TLS forum

Q8.  Signs of previous laminitis episodes in the feet include:
Hoof rings wider at the heel, stretched or deep white line - 83% got this correct
Hoof rings wider at the toe, tight white line

Explanation:
www.thelaminitissite.org/laminitis
"Symptoms of chronic laminitis:
Hoof rings wider at the heel 
Stretched white line - deep black groove between wall and sole - laminar wedge"

Q9.  What are the 3 components of EMS?
Obesity/regional adiposity, hyperinsulinaemia/IR, predisposition to laminitis - 56% got this correct
Diabetes, hyperglycaemia, predisposition to laminitis
Obesity/regional adiposity, hyperglycaemia, hirsutism
Diabetes, hyperinsulinaemia/IR, hirsutism

Explanation:
EMS was defined by the ACVIM consensus statement on EMS as including obesity/regional adiposity, IR or hyperinsulinaemia and a predisposition towards laminitis.
Diabetes is very rare in horses, and horses with EMS very rarely have above normal glucose (hyperglycaemia). 
Hirsutism is diagnostic of PPID, not EMS.

Q10. PPID is initially thought to be caused by
The degeneration of dopamine-producing neurons that control hormone production in the pituitary gland - 54% got this correct
Excess cortisol production from the adrenal glands
A tumour in the pituitary gland
A tumour in the adrenal glands

Explanation:
www.thelaminitissite.org/ppid
"In a healthy horse, dopamine producing neurons from the hypothalamus release dopamine into the pars intermedia.  The dopamine acts as a brake and stops hormone production.
With PPID the neurons are slowly lost (PPID is a neurodegenerative disease - it gets progressively worse) and the reduction in dopamine (there can be up to 9 times less dopamine in the pars intermedia of a horse with PPID than a healthy horse of the same age) causes:
the production of POMC peptide hormones (alpha-MSH, beta-endorphin, CLIP and ACTH) to increase - hormone levels may be more than 100 times greater than in a normal horse;"

It is now known that most horses with PPID don't have above normal cortisol production, and adrenal hyperplasia (increase in cells) and adrenal tumour formation is not commonly seen.  Excess cortisol production is associated with Cushing's disease in humans and dogs - not horses, that's why the disease in horses is now called PPID.
Although a tumour or adenomas can develop in the pituitary gland, this is thought to be as a result of the loss of dopamine-producing neurons and the consequent increase in hormone production, so is not the initial cause.  A difficult question that over half got right - well done!

Q11. Laminitis in the ................... is particularly suggestive of PPID
Autumn - 52% got this correct
Spring
Summer 
Winter

Explanation:
www.thelaminitissite.org/s - see Seasonal Rise:
"Horses that are developing PPID often first present with unexplained autumn laminitis long before coat changes are seen, and any horse having unexplained laminitis for the first time in the autumn should be tested for PPID by testing ACTH".  Sorry, should have said "Autumn/fall" to be international!

Q12. Cortisosteroids increase insulin levels - true or false?
True - 83% got this correct
False

Explanation: 
Am J Vet Res. 2007 Jul;68(7):753-9. (PubMed)
Effects of dexamethasone on glucose dynamics and insulin sensitivity in healthy horses 
Tiley HA, Geor RJ, McCutcheon LJ
"The study revealed marked insulin resistance in healthy horses after 21 days of dexamethasone administration. Because insulin resistance has been associated with a predisposition to laminitis, a glucocorticoid-induced decrease in insulin sensitivity may increase risk for development of laminitis in some horses and ponies." 

And many more examples of corticosteroid causing increases in insulin levels and laminitis here:
http://www.thelaminitissite.org/d.html - under Dexamethasone Suppression Test
http://www.thelaminitissite.org/c.html - under Corticosteroids

A practical guide to body condition scoring horses - Dr Teresa Hollands 

This video 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.

Clinical symptoms of PPID v signs of normal ageing - Dr Jo Ireland

Dr Jo Ireland demonstrates some of the symptoms of PPID and explains how to differentiate between normal ageing changes and changes that should make you suspicious of PPID. This video was shown in the October 2013 The Laminitis Revolution 2 webinar.

It's not uncommon for horses to have a deepening of the hollows above their eyes, more grey hairs around their head and some loss of muscle tone as they get older.

However, pronounced muscle loss along the neck, back and over the hind quarters is suggestive of PPID, as is the development of a pot belly.

The long curly hair coat that doesn't shed is a classic sign of PPID, but this is usually only seen in advanced cases. Warning signs for PPID include more subtle hair coat abnormalities, such as the summer coat being longer or thicker than normal, or long dull coarse hairs in the coat.

Patchy sweating can also suggest PPID, this may be due to an excessively long and thick coat, but can be seen in horses with PPID that have normal coats as well.

Horses with PPID may show signs of chronic laminitis, such as divergent hoof rings.

A common indication of PPID is accumulation of fat under the lower eyelid, giving a puffy appearance to the lower eyelid, and fat may also sometimes be seen in the hollows above the eyes.

Horses with PPID often show few symptoms in the early stages and symptoms vary between horses. If you are at all worried, talk to your vet.

For more information about the clinical signs of PPID, diagnosis and treatment, see Pituitary Pars Intermedia Dysfunction.

Pre-sale has begun on a newly edited paperback version of the book Care and Rehabilitation of the Equine Foot for $90. The high-quality paper and stitched binding has been kept, but with the new soft cover it weighs less than four pounds, meaning that international customers will enjoy much cheaper shipping rates. Pre-sale books should be mailed next week. 

TLS recommends that everyone involved in the trimming and rehab of a horse with laminitis has - and reads - this book! See TLS's review of the book. 

Articles about coffin/pedal bone rotation/sinking by Pete Ramey that recently appeared in Horseback Magazine.

Recognizing Coffin Bone Rotation

Sinking Coffin Bones

How to Reverse Coffin Bone Sinking

The full list of Pete's articles to date for Horseback Magazine

Information about neurological symptoms relating to PPID has been added to the website. Ataxia (weakness/inconsistent gait), blindness, seizures and narcolepsy have been associated with advanced PPID. Blindness has been suggested as being caused by adenomas (tumours) in the pituitary gland compressing the optic nerves, but there doesn't appear to be a known connection between other neurological symptoms and PPID. TLS queries whether direct trauma to the head/brain could play a part in both PPID and these rare neurological symptoms.

The majority of Dianne McFarlane's excellent review of PPID from 2011 can be read on Google books, covering the anatomy and physiology of the equine pituitary gland, epidemiology, pathophysiology and clinical signs, and the start of the section on diagnostic tests for PPID. Not much has changed since 2011, although it's worth bearing in mind that autumn (Aug-Oct) is now considered by many to be the best time to test ACTH to diagnose PPID, as long as a seasonally adjusted reference range is used. Also, no doubt due to increased testing and awareness, horses aged 10 and under are being diagnosed with PPID, and there is thought to be no breed or gender predilection.

McFarlane goes on to say that measuring ACTH and alpha-MSH are useful in the diagnosis of PPID (measuring ACTH is now the most widely used test for PPID in the UK), and that the TRH stimulation of ACTH may be useful (compared to measuring cortisol - further research has been done since McFarlane's paper was published and the TRH stimulation of ACTH is now recommended as a second-tier test when resting ACTH results are equivocal). Insulin is suggested as being increased in around 60% of PPID horses, and monitoring fasting insulin is recommended for all PPID horses to predict laminitis risk. It is suggested that cortisol circadian rhythm loss, urinary cortisol/creatinine ratio and ACTH stimulation test are poor tests for diagnosing PPID. Treatment suggestions include aggressive preventative health care (tooth and hoof care, nutrition, parasite control, clipping, rugging, shelter), and treatment with pergolide. Cyproheptadine is mentioned for possible use in combination with pergolide when pergolide alone doesn't control clinical symptoms, and Trilostane for possible use in horses with hypercortisolemia. Natural remedies, specifically Vitex agnus castus, are warned against due to the lack of evidence of efficacy and safety.

Points we found of particular interest:
Alpha-MSH (increased in horses with PPID) is a potent anti-inflammatory - some owners report increased signs of arthritis and similar problems when horses start treatment with pergolide - is this because "natural" anti-inflammatory levels are reduced?
Similarly beta-endorphin (also increased in horses with PPID) has pain relieving and anti-inflammatory effects.
CLIP (another hormone increased in horses with PPID) stimulates the release of insulin in rodents - this hasn't been studied in horses. Could this be causing laminitis in horses with PPID?
20% of horses testing positive for PPID using ACTH and/or alpha-MSH had no clinical signs of disease - did they really have PPID or were these false positives? We are often asked whether horses with above normal ACTH results but no clinical symptoms should be treated.
McFarlane suggests it would be interesting to study the geographical incidence of PPID cases, and that finding a pattern might suggest that environmental exposures may predispose to PPID, as exposure to agricultural chemicals has been shown to predispose to Parkinson's disease in humans. We know of several owners/yards with what appears to be a greater than normal number of PPID horses - are environmental/management factors involved?
It's now well accepted that PPID is a dopaminergic neurodegenerative disease, and that oxidative stress may contribute to neuronal damage and death.
The mechanisms causing the symptoms of PPID are mostly not understood.
"It is conceivable that PPID is a collection of syndromes each with a unique set of clinical signs and hormone profiles" - this may explain why horses with PPID can have such different symptoms and blood test results, and emphasises that each horse must be treated as an individual. It is also unlikely that one testing method will be ideal for every case of PPID.
Obesity and insulin resistance cause oxidative stress, which may cause PPID. 
Alpha-MSH, beta-endorphin and ACTH all suppress the immune system, possibly causing the increase in infections and parasite burdens often seen in horses with PPID.
Horses with PPID are often lethargic - this could be because of insulin resistance, other diseases due to PPID, or increased beta-endorphin levels.
PPID horses with laminitis often appear to have low-grade laminitis, but this may be because their pain threshold is higher due to increased beta-endorphin levels. They could still be at risk of significant damage.
The diagnosis of PPID is not straightforward!
False negative test results are common in the early stages of PPID, and it is likely that significant effects of the disease have already occurred by the time tests diagnose PPID.
If a horse shows symptoms of PPID but blood tests are negative, repeated testing is recommended.
At post mortem, the pituitary gland of a horse with PPID can be 2 to 5 times the normal size, and compression of other parts of the pituitary gland and rarely the optic chiasm (through which the optic nerves pass) and the hypothalamus can be seen. Evidence of damage may be seen in other organs such as the heart, liver, kidneys and lungs.
And finally, to end on a positive note: "when well cared for, horses with PPID can live into their 30s and even 40s".

For notes of Dianne McFarlane's presentation at the Equine Endocrinology Summit 2011 and a link to view the presentation, see: http://thelaminitissite.myfastforum.org/about126.html

New research by David Rendle et al. into the pharmacokinetics of pergolide was published in the Equine Veterinary Journal supplement Clinical Research Abstracts of BEVA September 2013. 

Rendle DI, Hughes KJ, Doran G, Edwards S
Pharmacokinetics of Pergolide Mesylate in Horses
Equine Veterinary Journal Volume 45, Issue Supplement S44, page 19, September 2013

8 healthy horses were given 0.02 mg/kg bodyweight pergolide intravenously - this is the equivalent of 10 mg for a 500 kg horse - ten times the recommended starting dose of 0.002 mg/kg bw, or 1 mg/500 kg horse. The abstract doesn't say whether it was a one off dose - presumably it was. Blood was analysed for pergolide concentrations for 48 hours following administration. 

The mean half life was 5.8 +/- 2.26 hours - shorter than previously reported, but in line with the mean half life of 5.86 +/- 3.42 hours found by Abra Wright when healthy mares were given 0.01 mg/kg pergolide by mouth after fasting (5 mg/500 kg horse). In Wright's research there was a large variation of half life between horses - from 3.10 to 12.39 hours. There was also a difference in maximum concentration between horses, ranging from 2.11 to 6.20 ng/ml. However in all the horses the pergolide was absorbed quickly, with time to maximum concentration ranging from 0.33 to 1 hour. These results suggest that, as in humans, the metabolism/elimination profile of pergolide varies considerably between treated horses. 

Wright, Abra M
Pharmacokinetics of Pergolide in normal mares 
MSc Thesis 2009 Kansas State University

Rendle concluded that pergolide does not require a loading dose. However giving pergolide twice daily may be more appropriate than once daily.

If this is the case, and the dose currently given once daily would be more effective if split into two doses, surely Prascend tablets need to be capable of being divided into quarters rather than just halves? Or is the suggestion that the daily amount of pergolide split into two doses would be larger than the dose currently given once daily? Good news for Boehringer Ingelheim (by whom David Rendle acts as a paid speaker and consultant) if this research supports giving a larger overall dose!

Both researchers used much larger doses of pergolide than are normally used, the research was carried out on healthy horses, not horses with PPID, only a single dose of pergolide was given in each case, and in both cases the pergolide was not administered in the same way as owners give pergolide - in Rendle's research the dose of pergolide was given intravenously, in Wright's research although the pergolide was given by mouth, it followed an 8 hour fast. So just how relevant is this research in terms of recommending oral dosing of pergolide for horses with PPID?

If you are claiming on your horse insurance for laminitis treatment, it's worth asking whether your policy covers the purchase of hoof boots - we've been told that one insurance company (Petplan Equine) has paid almost the full price of a set of 4 hoof boots. And so they should - if they cover remedial shoeing, they should also cover hoof boots and pads for remedial use.

The Laminitis Site recommends following Pete Ramey's advice on p 351 of Care and Rehabilitation of the Equine Foot: “at the first signs of laminitis, restore P3 to a more natural ground plane” (so 3-5 degree palmar angle), “relieve pressure on the walls and pad the sole with foam rubber – vertical sinking and destructive pressure to the solar corium can be prevented”.

If laminitis is suspected or diagnosed, the feet should be supported/protected, x-rayed and realigned (if necessary) as soon as possible.  For more information, see Laminitis and the Feet.

Just a reminder that if a horse is showing signs of footiness/laminitis between Aug and Oct (in the northern hemisphere), particularly if for the first time or if older than 10 (although plenty of horses are diagnosed younger than this), and there hasn't been an obvious diet/management change that might bring on laminitis, PPID should be seriously considered and eliminated as the cause. ACTH testing is currently free in the UK (Sept - Nov 2013) - http://www.talkaboutlaminitis.co.uk/. Tests for PPID are often negative in the early stages of the disease, so be aware of the symptoms of PPID (see http://www.thelaminitissite.org/ppid.html and http://www.prascend.com/Content/PDF/BIVM-12015%20Prascend%20Diagnosis%20Booklet_WEB.pdf) and don't be afraid to ask for a trial of Pergolide - see Question 3 under Therapy - http://www.prascend.com/Veterinarian/VetFAQs:

"Question: When should horses be treated with PRASCEND?
Answer: A horse exhibiting clinical signs of PPID, including unexplained laminitic episodes, should undergo evaluation for PPID. A horse exhibiting clinical signs or that has positive results on ACTH or DST testing should be treated with PRASCEND. Currently available diagnostic tests are not sensitive in detection of early disease. Therefore, if test results are negative, but a high index of clinical suspicion exists that the horse suffers from PPID, a 6-month trial of PRASCEND may be instituted and response to treatment observed."

NB TLS does NOT advise the use of the dexamethasone suppression test - ever - because of the high risk of causing/exacerbating laminitis in horses that are insulin resistant, and it can't be used between Aug and Oct anyway. The basal ACTH test is the best test for PPID, possibly followed by the TRH stimulation of ACTH if a basal ACTH test is equivocal - although a trial of pergolide (Prascend) and clinical symptom response to treatment may be assumed to be diagnostic.

Despite what some vets are still saying, testing ACTH between Aug and Oct is the best time of year to test, when the difference between normal and PPID horses is more pronounced, as long as seasonally adjusted reference ranges are used. See: http://liphookequinehospital.co.uk/wp-content/uploads/Lab-Book-PPID.pdf. Interpretation of ACTH results is far from an exact science - as already mentioned, horses often test negative in the early stages of PPID, and clinical symptoms must be taken into account too. It is now thought that between Nov and July, although a cut-off of 29 pg/ml is often suggested, results below 20 pg/ml are likely to be negative for PPID, results over 40 pg/ml are likely to be positive for PPID, and horses with a result in the "grey area" between 20 and 40 pg/ml should have further testing (figures based on CIA testing using Immulite as used at Liphook Equine Hospital, other assays may require different interpretation) - see http://onlinelibrary.wiley.com/doi/10.1111/evj.12114/abstract. Between Aug and Oct the cut-off is 47 pg/ml, with the "grey area" likely to extend 10 pg/ml or so either side - so perhaps less than 37 pg/ml is likely to be negative for PPID, and more than 57 pg/ml likely to be positive, although we haven't seen these figures confirmed.

I've just started reading British vet John Stewart's recently published book Understanding the Horse's Feet (now available from many book sellers including Amazon in both the UK and USA: http://www.amazon.co.uk/Understanding-Horses-Feet-John-Stewart/dp/1847974767 and also as an E-book: http://www.crowood.com/details.asp?isbn=9781847974761&t=Understanding-the-Horse%27s-Feet) and so far I'm impressed - more about the book later.

This interview on The Naturally Healthy Horse website talks about how John's training at vet school (Cambridge) focused on the use of shoes, and he voices the interesting opinion that farriers consider foot form, but those involved with the barefoot movement are more likely to consider foot form AND function.

When talking about trimming, the environment and individual horse will greatly influence the trim, but in principle he leaves the sole and frog alone, trims the walls to just above the sole and applies a bevel.

For acute laminitis he advocates confining the horse, providing support under the sole as well as the back of the foot, reducing mechanical forces on the foot and easing breakover, and importantly, reducing heel height as soon as possible to enable the horse to load the back of the foot and reduce the force on the tip of the pedal bone. He doesn't agree with wedging the heels up - hurray! Interestingly he suggests the use of EVA pads - TLS is currently experimenting with the use of EVA foam pads inside boots and finding significantly increased comfort for the horse. 

He goes on to say that in his opinion the biggest mistakes people make when dealing with laminitis are to underestimate the seriousness of laminitis, to over-use Bute, and to not deal with insulin resistance (by controlling sugar and starch in the diet).

I'd add not realigning the feet quickly enough, the over-use of box rest (usually because the feet haven't been realigned quickly enough), and not recognising PPID.

Great news to have a British vet understand feet, the importance of a correct barefoot trim and the role of insulin resistance in laminitis! From only £20 for a full colour hardback version of Understanding the Horse's Feet, this book deserves a place in every vet, farrier/trimmer and horse owner's library.

Slowing Feed Intake Reduces Glycemic Response in Horses - Kentucky Equine Research - August 2013

Nothing new here, but a reminder that feeds should be as spread out as possible through the day to avoid glucose and therefore insulin peaks. Horses with laminitis/EMS/PPID shouldn't (generally) be fed any form of cereal/grain - recommendations are to keep NSC (non-structural carbohydrates, that's sugar, starch and fructan) below 10% for insulin resistant horses. Average NSC for cereals: bran 29%, oats 48%, barley 59% and maize/corn 73% (figures averages from Equi-Analytical common feed profiles http://www.equi-analytical.com/CommonFeedProfiles/). Many horse are now working at higher levels on a high fibre diet based on hay, haylage, grass, sugar beet, alfalfa, with minerals, vitamins, protein and essential fatty acids supplemented according to forage analysis. Insulin resistant horses generally do well on diets based on hay, either analysed <10% or soaked to reduce sugar, plus sugar beet (ideally rinsed/soaked/rinsed to remove excess iron and sugar) to carry minerals and for weight gain/additional energy if required. 

More ideas for slowing eating and general management strategies for insulin resistant horses:
http://www.thelaminitissite.org/management-strategies-for-emsir.html

At TLS we advise owners to ask vets for a copy of all test results.

Here's a good example of why we do this.

A pony with long term chronic laminitis had blood taken for ACTH and insulin tests in mid-August. 2 weeks later the owner spoke to the vet and was told that the pony didn't have PPID, the insulin result wasn't given. TLS advised that the owner should obtain the actual results, not an interpretation of the results. 

Several days later the vet advised of the insulin result, which was well over 100 uIU/ml - a large increase on an insulin test carried out at much the same time last year. The pony's diet, management and foot care were improved on the previous year (when the pony tested negative for PPID) - something had to have worsened.

The following day the lab's results arrived in the post - the pony had an ACTH of 107 pg/ml, the lab was using Liphook's reference range of <47 for Aug to Oct - we know the blood wasn't frozen without being centrifuged, and the pony wasn't ill, wasn't in pain or stressed, hadn't been exercised - there seemed no reason for the high ACTH other than a pretty definitive diagnosis of PPID (plus mild clinical signs - increased hairs on jaw, neck, back of legs, muscle loss, weight loss, fat pads, worsening laminitis in the autumn...).

The pony will soon start on Prascend, and hopefully treatment for his PPID along with a low sugar/starch diet and good management will help to lower his insulin levels. But what would have happened if the owner hadn't asked to see the results - would the pony have been assumed by all to not have PPID? Would another year or more have gone by with worsening symptoms, uncontrolled laminitis, a suffering pony and owners tearing their hair out in frustration at not being able to help their pony?

Looking after a horse with laminitis needs to be a team effort - owner, vet and farrier/trimmer all have an important role to play - for that to be effective, there must be good communication between all parties. We know of at least one owner who changed vets because they wouldn't provide copies of test results....

Some excellent points are made in this hour long webinar by Dr Scott Morrison:

He says rehabilitation of the laminitic foot involves simple mechanics and is easy, the foot is trimmed to realign the hoof to P3 - just as TLS has been saying for some time!

The foot must be set up to relieve pressure on the sole under the tip of P3 and to decrease tension on the laminae.

The foundered foot typically grows a lot of heel, the toe becomes jammed up, there's a lot of pressure on the sole corium and coronary band at the toe - the foot needs to be set up for normal growth to take place.

The sole is designed to be a supporting structure as well as the laminae. The main goal is to thicken the sole depth and use the sole to support P3 while the laminae are compromised. Barefoot horses naturally bear weight on the sole and develop a tough and strong sole callus.

He says domestic (but perhaps this should be shod) horses often have a dysfunctional thin sole that will bend with thumb pressure, which provides no secondary support structure for P3, and which can quickly lead to a "train wreck" when the horse develops laminitis.

Laminitis isn't necessarily failure of laminae at the toe, laminae can fail at any point around the hoof.

The centre of pressure needs to be behind the apex of the frog - TLS recommends trimming the laminitic foot to maximise weight bearing in the back half of the foot.

I struggle to agree with Dr Morrison about the pull of the DDFT and the use of wedges and tenotomy - Pete Ramey's explanation that the DDFT cannot exert a rotational force and oppose the laminae if the sole is in ground contact (active) and the wall at the toe is out of ground contact (passive) seems to make perfect sense. On p 350 of Care and Rehabilitation of the Equine Foot Pete says that although elevating the heels may temporarily reduce tension in the DDFT in a standing horse (although the muscle will quickly adjust), it may increase tension when the horse moves. He believes that concerns about DDFT tension have held back vets and farriers, "preventing rotation reversal by leading people to stand P3 up on its tip and ultimately destroying the foot". Dr Eleanor Kellon and the ECIR group have similar views: http://www.ecirhorse.org/index.php/ddt-overview/ddt-trim

However Dr Morrison goes on to say that wedges and shoes "trash the heels" and he only uses them short-term to shift the centre of pressure back (which others would claim can be done with a good realigning trim) while he tries to fix the toe and develop sole depth, then he likes to rehabilitate laminitics barefoot to allow the heels to recover.

He made me smile when he said that the trim is really important, he never touches the sole, just cleans the frog slightly, trims the heels back to the widest part of the frog (or as far back as possible), rockers the toe and applies a good bevel to the wall all the way round - exactly as we have advised for all our successful rehabs!

He also says that the bars are very important and shouldn't be aggressively trimmed - they have a purpose in stabilising the heels and wall.

He points out that horses often can't stand with one foot up for long - seconds only. I would take this further and say that they should always be allowed to put their foot down (so nail on shoes are not appropriate), and trimmed when standing on a soft supportive surface. 

There are some interesting x-rays of bone remodelling - Dr Morrison says that horses can usually handle a bit of remodelling of the tip of P3, but in his experience when there is a lot of erosion and demineralisation of P3, horses never become completely comfortable, and that once the surface of P3 is damaged, completely healthy laminae will never grow back. However, as long as P3 is healthy, he says feet can be amazingly rehabilitated following laminitis and rotation. This emphasises how important it is to get rotation realigned as soon as possible after a laminitis attack, to prevent changes to the bone from ever happening.

In conclusion, a very positive lecture stressing the importance of a mechanically correct barefoot trim, and whether you agree with everything he says or not, well worth spending an hour watching.

A bit about red blood cells - haemoglogin contains iron – iron binds oxygen. RBCs are broken down all the time by the body, new ones made. Iron is so toxic (for a start, bacteria can use iron to multiply) that the body keeps it under lock and key, so as soon as a red blood cell is broken down, the iron is locked away until it is used to make a new RBC. Many illnesses, e.g. piroplasmosis, involve the breakdown of RBCs - this is haemolysis. Other reasons for haemolysis include feeding garlic, which causes Heinz bodies (damage to the RBCs), causing the spleen to destroy the damaged RBCs prematurely. But in all these cases the iron never leaves the body, it is recycled. The only time iron may need to be given to a horse for anaemia is when blood has actually left the body - through haemorrhage, whether acute (bleeding from a wound) or chronic, e.g. worm damage - although in most cases there would probably be enough iron in the normal diet so supplementation wouldn't be necessary. Anaemia of Chronic Disease is another important cause of anaemia in horses, in this it is thought that the inflammation causes iron to be kept locked up - see: Anaemia of Chronic Disease (Wikipedia) - but the answer is to treat the chronic disease, not to increase iron - the body is already worried about having too much iron! 

When you read about anaemia in humans, iron supplementation is often mentioned - humans have a very different diet to horses, human diets are often low in iron. But soil is full of iron. Hay and grass contain lots of iron. Feeds like alfalfa and sugar beet contain high levels of iron. There is plenty of iron in a horse's diet, as long as it is fed forage and/or has access to soil. So unless haemorrhage had been diagnosed, iron supplementation should generally not be recommended. 

The NRC Nutrient Requirements of Horses 2007 suggests that possible adverse effects of excessive iron might outweigh any supposed advantages, and warns that supplemental iron can be toxic to foals and that iron injections often result in severe reactions and death in horses. Iron is toxic to the liver (hepatotoxic), and vets have reported that excessive iron deposition in the liver is a common finding in liver biopsies from older horses.

When anaemia is suspected, blood should be looked at under the microscope and a CBC (red and white blood cell count) done and correctly interpreted to verify whether the horse really is anaemic, and if so, to indicate the type of anaemia. The cause of the anaemia must be identified and correctly treated - it's treating the primary disease, not feeding an iron supplement, that eliminates anaemia in most cases.

The seasonal rise in POMC hormones, the hormones affected by PPID (Cushing's disease) tends to start around late July/early August and last until late October or into November - this affects all horses, but particularly horses with PPID, and the seasonal rise can be a good time to diagnose horses in the early stages of PPID.

In the first of a series of articles that we'll be running on PPID over the next few weeks, here's a short video in which Dr Hal Schott describes some of the early signs of PPID. These include:
- change in behaviour/attitude/performance - the horse may become more lethargic or dull, less enthusiastic about work;
- muscle loss along top line or rump, you may notice the saddle doesn't fit quite so well;
- you may notice long guard hairs on the back of the legs, under the jaw or along the jugular groove. The long shaggy coat associated with PPID is usually late to develop and indicates advanced PPID;
- the horse may drink and urinate more - horses can become diabetic in the early stages;
- you may notice that the horse is sore footed, or it may develop obvious laminitis - laminitis could be due to PPID or EMS, but any laminitis, and particularly first time laminitis between August and October, could be a symptom of PPID.

More information about the early and advanced symptoms of PPID here.

Besides, surely tendons don't contract - wouldn't it be the muscle, if anything, that was affected - and wouldn't artificially raising the heel actually be likely to cause the muscle fibres to shorten - the very last thing we want - as recent research found in women who wear high heels a lot (High heels "shrink calf muscle fibres").

Dr Debra Taylor and Pete and Ivy Ramey address the role of the DDFT in their Hoof Rehabilitation Protocol article: "our therapy of laminitic horses is based on the concept that tension of the deep digital flexor tendon cannot result in stress to the laminae if the toe wall is not allowed to bear weight at impact, stance or during breakover. While tension of the deep digital flexor does exert a rotational force on P3, this force cannot oppose the laminae if the hoof wall remains out of contact with the ground." 

The ECIR group has this to say about raising the heel (www.ecirhorse.org - ddt-trim):
"There is really no proof anywhere that raising the heel does anything to prevent rotation. The theory of DDFT pull also fails to explain why horses with the most extensive damage sink or how sinkers can have a perfectly aligned bone column with no rotation at all. In fact, some sinkers are more ground parallel than before the laminitis. Raising the heel has negative effects long term by increasing the pressure on the tip of the coffin bone and accelerating bone loss." 

We now know thanks to research by Melody de Laat  (Insulin-Induced Laminitis - An investigation of the disease mechanism in horses 2011) and others that during endocrine laminitis (~90% of all laminitis cases), the laminar cells stretch, and it is likely that this weakening of the connection between the hoof wall and the coffin/pedal bone leads to laminar failure and rotation and/or sinking, exacerbated by the the horse's weight and perhaps poor foot balance. 

We have recently heard of a horse with laminitis, no rotation seen on initial x-rays, heel wedges fitted, then further x-rays revealed rotation - hopefully a correct realigning trim and barefoot rehab will restore this horse to full health - and hopefully this article will prevent this happening to other horses.

See more under DDFT. 

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