Post by admin on Jun 17, 2007 8:49:44 GMT -1
We have combined several posts originally written by Bellajack into one post in order to take up a little less space. If you do a search in the "Very Useful Posts" forum you will be able to find the original threads. This information is extremely valuable and we are grateful to Bellajack for giving us this resource.
The Royal Veterinary College Laminitis Conference 24th May 2007
I attended this conference under false pretenses as it was really intended to inform Veterinary Surgeons of the results of the latest international research on Laminitis with speakers from both here and abroad, principally USA and New Zealand.
I have summarized the main information as I understood it, but some of it was highly technical so I apologise for any inaccuracies. I think that I understood most of it and have copious notes, both my own and conference literature, so if you want anything clarifying I MAY be able to do so.
Starch Sugar and Fructan
The speaker for this section of the conference was:
Annette C Longland BSc PhD DIC. She gained her PhD in plant pathology and after a post-doctoral fellowship has worked on the detailed chemical analysis of forages and their fermentation by equid and ruminant microbiota.
Plant carbohydrates include Structural and Non Structural Carbohydrates.
Structural carbohydrates are trapped in the cell wall of the plant and are easily digested in the fore gut – no problems.
Non structural carbohydrates are the ones in the cell contents and consist of starch, fructan and simple sugars.
Starch is stored mainly in the seeds of plants and so over consumption is easily avoidable by reducing/avoiding feeding cereals.
Fructan accumulates in the leaves and stems of grasses and can reach substantial levels (as high as 400gms fructan per kg dry matter) with some of the highest levels recorded in a cold sunny January.
The simple sugars in pasture grasses are sucrose, fructose and glucose in order of predominance but these occur in much lower amounts than fructan.
Oat starch is fairly digestible in the fore gut unprocessed (85%) but barley is poorly digested (21%) along with other cereals and they should be micronised or extruded to improve fore gut digestibility if they must be fed at all.
Fructan is not digestible in the fore gut and passes into the hind gut where the entry of large quantities can cause colic and laminitis.
The simple sugars can be digested in the fore gut but large quantities may exacerbate insulin resistance and add to the risk of laminitis. More on signs of insulin resistance later but most Dales Ponies would be suspect on appearance.
Amounts of fructan in grass varies greatly from season to season, day to day, and hour to hour. Also fructan levels vary in varieties of grass (and can be high in weeds, esp. Dandelions). Grass seed mixtures suitable for horses at risk from laminitis are being developed and may be available soon, but are not yet on the market.
Fructan levels depend on the amount of production (photosynthesis) compared to the rate of utilization (plant growth) and variations of as much as 46% increase by afternoon as compared with morning have been recorded. Dull warm days are safer than sunny days and laminitis cases have been shown to rise in proportion to hours of sunlight, regardless of temperature and rainfall.
The fructan levels in hay are equally difficult to predict and will vary according to, among other things, whether the hay was cut in the morning or afternoon. Hay made late in the season, after seed dispersal, and cut in the morning, will be safest for at risk horses.
Haylages, Particularly quite wet ones, are lower in fructans generally than hay but are much more palatable so the amount fed needs to be carefully monitored.
TAKE HOME MESSAGE.
There is no way you can guess on the fructan content of grass or hay by looking.
Remember that it is the overall amount of fructan consumed that is important, so even horses eating grass/hay low in fructan may be consuming a lot if they are eating large amounts of grass/hay.
The Royal Veterinary College Laminitis Conference. 24th March 2007.
Advice for managing horses known to be at highest risk of developing laminitis (those who have had it before) and horses of the type likely to be at high risk of developing it (overweight and/or cresty neck and localised fat deposits partic. around sheath or udder - signs of insulin resistance. Advice as given, word for word, by:
Pat A Harris MA PHD Dip ECVCN Vet MB MRCVS. Qualified Cambridge Veterinary School
in 1983.
Adjunct Professor of Equine Studies at Virginia State University and European Specialist in Veterinary Clinical and Comparative Nutrition. President of The British Equine Veterinary Association 1999.
Due to the highly variable and unpredictable nature of Fructan accumulation in pasture, animals predisposed to laminitis should preferably be denied access to grass pastures during the growing season.
If some grazing is unavoidable, turn animals out very late at night or very early in the morning removing them from the pasture by mid morning at the latest as fructan levels are likely to be at their lowest at night to early morning.
Avoid pastures which have not been properly managed by regular grazing or cutting as mature stemmy grasses may contain more fructan as it is stored in the stem.
Avoid turning horses out to pasture during late spring when Water Soluble Carbohydrate/fructan levels are rising.
Do not turn horses out onto pasture that has been exposed to low temperatures in conjunction with bright sunlight, as occurs in the autumn after the autumn flush of growth, or bright, cold winter days as cold temperatures will reduce grass growth resulting in the accumulation of fructan.
Do not allow horses to graze recently cut hay stubble as fructan is stored predominantly in the stem.
Next installment to follow shortly but basic message is to feed hay soaked for 30mins to remove 50% of Water Soluble Carbohydrates, or haylage if you can slow consumption sufficiently (treble haynets) and chaff based feeds with a high quality vit/min supplement. If cereals must be fed they should be processed to enhance digestibility in the fore gut (micronised or extruded). Also weeds can be very high in fructan.
Report on The Royal Veterinary College Laminitis Conference 24th May 2007
Part 2
How Problems In The Gut Trigger Laminitis In The Foot.
The speaker for this section was:
Jonathon Elliott MA VetMB PhD CertSAC DECVPT MRCVS
He completed his PhD in vascular pharmacology in1989 and is now Professor of Clinical Pharmacology at The Royal Veterinary College and is Vice Principal of Research. He has won awards for his contributions to companion animal medicine, particularly in the area of equine laminitis.
The link between events in the gastrointestinal tract and the foot is still a mystery, although the common pathway to the separation that occurs in the foot due to laminitis seems to be brought about by activation of enzymes called Matrix Metalloprotienase (MMP) and represents an extremely exaggerated response to injury. The question is what triggers this and how is it linked to consumption of carbohydrates?
MMP’s are important enzymes in normal tissue growth and the resident cells in the foot produce them to support the continuous growth of the hoof.
Excessive MMP activity occurs in the developmental and acute phases of laminitis and is responsible for destroying the membrane that bonds the laminae in the foot leading to separation of the pedal bone from the hoof wall.
There are 3 theories as to how these MMP’s are activated:
1) Bacteria derived exotoxins activate MMP’s.
2) Gut derived products trigger inflammation in the foot, leading to MMP activation.
3) Gut derived products trigger vascular disturbances leading to vasoconstriction and ischaemia- reprofusion injury (blood supply to the foot gets compromised and then blood rushes back, like putting a tourniquet on your leg and taking it off again, only much worse because of the lack of expansion of the hoof wall) part of which involves MMP activation. The blood vessels in the foot are highly susceptibly to the vasoconstrictory effects of these substances and the effects of the reduced blood, oxygen and glucose supply that results from vasoconstriction. This has been compared to Raynaud’s Disease in man (impaired blood supply to hands and feet that can lead to amputation) and advances in treatment of this condition could help advance laminitis treatment in the future.
These theories are not mutually exclusive, but none explains why some horses are so much more susceptible to laminitis than others. Recent evidence suggests a strong link between the insulin resistant type of horse and increased susceptibility to vasoconstriction and laminitis.
Carbohydrate overload leads to more of the Gram-positive bacteria that ferment carbohydrate in the hind gut. This lowers the pH in the hind gut (acidosis) and increases the permeability of the gut wall. This allows the entry of undesirable substances into the circulatory system (endotoxins and too many amines) which cause vascular (blood vessel) problems in susceptible horses and trigger MMP activation leading to failure of the foot.
Thus both inflammatory and ischaemic (results of reduced blood supply) stimuli could trigger MMP activation and cause the foot to fail and there is evidence that all 3 theories may contribute to the pathophysiology (the disturbance of the processes underlying normal function) of pasture induced laminitis.
I hope that this makes some sort of sense. I am sorry that it is so complex. I know that it has made my brain hurt! Thank god for a veterinary dictionary!
Next exciting episode ‘Metabolic Predisposition to Laminitis – Obesity and Insulin Resistance.’ It is a bit easier to follow – promise!
The Royal Veterinary Laminitis Conference 24th March 2007
Part 3.
Metabolic Predispositions to Laminitis:
Obesity and Insulin Resistance
The speaker on this section was;
Raymond J Geor BVSc MVSc PhD Diplomate ACVIM
Dr Geor is the Distinguished Chair and Director of Research at The MARE Center and Professor of Large Animal Clinical Services, Virginia-Maryland Regional College of Veterinary Medicine. His research focuses on carbohydrate nutrition of horses in health and disease. Currant areas of study include the role of insulin and obesity in laminitis and the links between carbohydrate nutrition, insulin resistance and laminitis risk.
Metabolic abnormalities, notably obesity and insulin resistance (IR), have long been thought to be involved in the predisposition to laminitis.
Obesity and IR have now been proven to be important predisposing factors for laminitis. Identifying these conditions, particularly IR, means that management strategies can be implemented to assist in avoiding laminitis.
Horse with a condition score of more than 7, on a 9 point scale, are classified as obese.
However this does not take into account the distribution of fat.
It is well known that, in man, people who accumulate fat around the waist are at increased risk of heart disease, high blood pressure, diabetes, etc.
In the horse it would seem that some horses which are not clinically obese but have enlarged fat deposits on the crest, tail head, sheath/udder are predisposed to laminitis.
Research is ongoing in developing a 'cresty neck score', measuring the height and width of the crest and using it to assess laminitis risk.
IR is defined as a metabolic state in which normal concentrations of insulin do not result in a normal biological response in target tissues, such as an increase in cellular glucose uptake.
Compensated IR, evidenced by persistently raised levels of insulin but normal levels of glucose, is a common finding in IR horses.
Recent studies have shown that an IR phenotype (appearance) is strongly linked to a predisposition to laminitis. When studying the metabolic differences of 160 ponies on one farm, findings based on insulin sensitivity, compensated IR, and categorizing the ponies considered to be showing pre-laminitic metabolic syndrome (PLMS), enabled researchers to predict 11 of the 13 cases of laminitis that occurred in May of that year, meaning that the IR ponies were at 10 times higher risk of developing laminitis.
Cushings Disease may result from long term IR.
IR could cause laminitis in 3 possible ways:
1) IR might impair glucose delivery to the foot.
2) IR could alter blood flow to the foot.
3) IR could lead to a pro-inflammatory state, increasing MMP activity (the enzymes that destroy cells in the laminae when they are over- activated, causing separation of the pedal bone from the hoof wall).
There is evidence that high starch and sugar diets increase IR.
Horses thought to be of IR phenotype should be managed to increase insulin sensitivity (see next installment).
TAKE HOME MESSAGE:
If your horse is obese and has a cresty neck, or just has a cresty neck, BEWARE. It has the IR phenotype and is predisposed to laminitis.
It is likely that all horses have a laminitis threshold, but IR lowers this threshold.
IR is reversible, in the early stages at least.
The Royal Veterinary College Laminitis Conference. March 24th 2007
Part 4.
Nutritional Countermeasures to Laminitis.
The speaker for this section was:
Pat Harris MA PhD DipECVCN Vet MB MRCVS
Bibliography in Part 1 - 2nd post.
This will concentrate on 2 main areas:
1) How to reduce the intake of rapidly fermentable material.
2) Nutrients and managemental strategies that may reduce insulin resistance
1) Reducing Intake.
We need to be able to identify the that are high in those components that, under certain conditions,tend to be rapidly fermented to produce, in particular, excess lactic acid, which lowers Ph of hind gut, increases gut permeability, kills bacteria and aids the release of undesirable substances.
A number of terminologies have been used which can be confused:
Water soluble carbohydrates (WSc). These include simple sugars and fructan, but not starch.
Nonstructural carbohydrates (NSc)
The material within the feed which can potentially be rapidly fermented to lactic acid and includes simple sugars, fructan and starch.
The amount of starch that is rapidly fermented rather than digested varies on the amount fed and whether it has been processed. If cereals are to be fed to animals which may be prone to laminitis, unprocessed corn or barley should be avoided, even in small amounts. Oat starch is usually efficiently digested, regardless of processing.
One large feed of unprocessed cereal can result in clinical signs of laminitis within 40hrs.
Even horses used to being fed grain should be fed less than 0.5 kgs per 100kg bodyweight, cereal in one meal.
Pasture.
Research has shown that a bolus of fructan at between 7.5 - 12.5 g/kg bodyweight will reliably produce laminitis, even in a breed not believed prone to the condition.
Many people restrict the time horses have access to grass but preliminary data suggests that they can eat up to40% of their daily dry matter intake in 3hrs of turnout, so just restricting time may not be enough.
For current advice on reducing turnout effectively see Part 1, 2nd post.
2) Reducing Insulin Resistance.
EXERCISE.
A survey showed a high proportion of acute laminitis cases in the 'no regular exercise' category.
Exercise and exercise training have been shown to have numerous benefits including enhanced insulin sensitivity.
Maintaining and if possible increasing the level of activity of horses prone to laminitis would be advantageous, especially if they are obese as well.
OBESITY.
It has been well recognized that obese horses are more prone To laminitis.
It is likely that the risk for laminitis in obese horses is due to the development of insulin resistance (IR).
The syndrome of obesity, IR and laminitis is sometimes referred to as 'equine metabolic syndrome' or peripheral Cushings syndrome.
The link between obesity, insulin sensitivity, and vascular dysfunction is currently under investigation.
Horses are usually overweight because they have stored excess calories as fat ie been overfed relative to their activity level.
Horses turned out to pasture at certain times of the year may be getting several times their calorie requirement.
DIET.
Insulin sensitivity has been found to be affected by diet as well as exercise.
Adaptation to high carbohydrate diets is associated with decreased insulin sensitivity as large fluctuations in glucose and insulin following meals high in sugar may supply inappropriate signals of energy availability to the glucose regulatory system, thereby altering insulin sensitivity of the tissue and may result in changes in metabolic signaling both within and between cells.
It is important to note that certain pastures at certain times of the year can result in marked fluctuations of blood glucose and insulin in a similar way to the feeding of large cereal based meals.
It has been suggested that there may be a progression of IR in laminitis prone horses from compensated IR (insulin sensitivity greatly decreased but made up for by increased insulin secretion), being a predisposing factor in healthy but possibly genetically predisposed horses, to a decompensated IR later in the course of the disease.
It would seem advisable to choose diets that result in low glycaemic and insulinaemic responses.
Feeding a fibre based diet, using oil as an energy source if required for the more athletic horse, has the potential to improve glucose tolerance and insulin sensitivity, as well as , perhaps more importantly for exercise performance,improve metabolic flexibility.
DIETARY SUPPLEMENTS.
There have been few, if any, controlled trials that have tested interventions with dietary supplements, feed additives, or drugs, to prevent laminitis.
The streptogramminn antibiotic 'Virginiamycin' (I think this 'Founderguard') has been used and marketed to prevent pasture induced laminitis by preventing the overgrowth of gramm-positive bacteria. However it is not thought to be effective in all cases and is only available under special licence in Europe.
Areas needing exploration include increasd anti-oxidant supplementation, hind gut buffers, and agents that block the over activation of MMPs.
Current important area of interest is around nutrients or nutraceuticals to counter the development of IR or the effects of being IR.
Two discussed:
Cinnamon.
Cinnamon bark has been reported to act in man as a stimulant astringent to the stomach with antimicrobial, antispasmodic, antioxidant, antidiarrhoea, calmative and antiparasitic properties with a potential natural insulin sensitising action. In man 1gm /day could have significant effects on fasting glucose concentrations.
Tests suggest that cinnamon extract may play a role in blood glucose levels by improving insulin sensitivity, or the release of insulin, or by slowing the absorption of carbohydrates.
This may be a fruitful area for evaluation in laminitic horses where IR is involved.
Cinnamon also contains proanthocyanidins which may improve vascular health and have substantial antioxidant activity - potentially of additional benefit to laminitics.
Magnesium.
May have a role in modulating the action of insulin.
No data yet available to confirm that additional supplementation over and above that currently recommended will affect insulin sensitivity but should ensure all horses have an adequate intake particularly those prone to laminitis.
Take Home Message
Base horses diet on forage/fibre, not sugar/starch.
Feed a broad-spectrum vitamin and mineral supplement to horses on a restricted diet, and ensure an adequate and balanced supply of magnesium.
Do not starve or prevent from eating for long periods in an attempt to reduce bodyweight, and make all dietary changes slowly.
Maintain or increase regular exercise.
Plan an active weight management programme for overweight animals; Meadow hay at 2% current bodyweight for 6 weeks.
Meadow hay at 1.5% current b/w for 6 weeks.
Meadow hay at 1.5% target b/w for 6 weeks.
With increased exercise wherever possible.
Maintain a moderate condition score - between 4 and 5 on 9 point scale.
Get forage analysed and try to feed a forage with less than 10% NSc. Soaking hay in clean water for 30mins will significantly reduce sugar content.
The Royal Veterinary Laminitis Conference Part 5
Medical Management of Laminitis
The speaker for this section was:
Celia M Marr BVMS MVM PhD DEIM Dip ECEIM MRCVS
She is based at Rossdales Equine Hospital in Newmarket. Her particular areas of interest include cardiovascular medicine, internal medicine, adult and neonatal intensive care and medical imaging.
GOALS:
The primary goals are to minimise structural changes within the hoof, alleviate discomfort and restore function without compounding structural changes, and halt the processes that are driving the laminitis. Additional goals are to assess the existing degree of damage in order to plan corrective farriery and provide an accurate prognosis, plus identify, remove or treat predisposing factors and prevent more attacks.
PREVENTING ONGOING DAMAGE TO HOOF:
The single most important thing you can do for any horse showing any sign of laminitis is put a plank across stable doorway, put down a bed 18" thick, covering entire floor, put horse in stable and shut the door (as far as the horse is concerned, for an absolute minimum of 30 days, even if the horse appears to have recovered a lot more quickly than that. Literally do not allow it to step off thick bedding for at least 30 days.
Support to the hoof can be provided by supporting the frog alone or the frog and sole. There is no clear evidence to support one over the other at this time.
PAIN RELIEF:
Pain relief should be aimed at minimising pain, not completely eliminating it or the horse may move about too much, and phenylbutazone is still the drug of choice and may also help as an anti-inflammatory.
Ice can be used to slow the rush of blood back to the foot and help with pain relief, but needs to be applied to leg from above the knee down.
In horses with severe pain opiates may be necessary and recent drug protocols offer new drug combinations for treatment of very severe and debilitating pain, but these require hospitalisation and cost from £75 to £500 a day for the drugs alone.
HALTING PROCESSES DRIVING THE LAMINITIS:
By the onset of clinical systems drugs aimed at this may be too late.
ACP may help as a vasodilator - efficiency unproven - but will help with stress and encourage the horse to lie down more, so is a useful addition to bute.
Asprin may be of use, both as a treatment and possibly as a preventative (as in low dose in man to prevent strokes, etc.) but more research has to be done.
Drugs to block MMP's being activated could represent a major step forward in future.
ASSESSING DAMAGE AND PROGNOSIS.
The diagnosis of laminitis is based on lameness, pain on use of hoof testers on one or more feet and increased digital pulses.
The severity may vary from foot to foot and the most severely affected foot is used to determine the laminitis category.
X-rays can determine the degree of rotation of the pedal bone and the founder distance, but markers need to be used on the wall of the hoof. Sinkers and marked pedal bone rotation merit a poor prognosis.
ADDRESSING PREDISPOSING FACTORS:
Has mostly already been discussed but also include:
Treating mares with metritis following foaling.
Supporting opposite leg in cases of severe, nonweightbearing lameness in one leg.
Treating Cushings Disease (PPID).
Treating Equine Metabolic Syndrome.
PART ONE
The Royal Veterinary College Laminitis Conference 24th May 2007
I attended this conference under false pretenses as it was really intended to inform Veterinary Surgeons of the results of the latest international research on Laminitis with speakers from both here and abroad, principally USA and New Zealand.
I have summarized the main information as I understood it, but some of it was highly technical so I apologise for any inaccuracies. I think that I understood most of it and have copious notes, both my own and conference literature, so if you want anything clarifying I MAY be able to do so.
Starch Sugar and Fructan
The speaker for this section of the conference was:
Annette C Longland BSc PhD DIC. She gained her PhD in plant pathology and after a post-doctoral fellowship has worked on the detailed chemical analysis of forages and their fermentation by equid and ruminant microbiota.
Plant carbohydrates include Structural and Non Structural Carbohydrates.
Structural carbohydrates are trapped in the cell wall of the plant and are easily digested in the fore gut – no problems.
Non structural carbohydrates are the ones in the cell contents and consist of starch, fructan and simple sugars.
Starch is stored mainly in the seeds of plants and so over consumption is easily avoidable by reducing/avoiding feeding cereals.
Fructan accumulates in the leaves and stems of grasses and can reach substantial levels (as high as 400gms fructan per kg dry matter) with some of the highest levels recorded in a cold sunny January.
The simple sugars in pasture grasses are sucrose, fructose and glucose in order of predominance but these occur in much lower amounts than fructan.
Oat starch is fairly digestible in the fore gut unprocessed (85%) but barley is poorly digested (21%) along with other cereals and they should be micronised or extruded to improve fore gut digestibility if they must be fed at all.
Fructan is not digestible in the fore gut and passes into the hind gut where the entry of large quantities can cause colic and laminitis.
The simple sugars can be digested in the fore gut but large quantities may exacerbate insulin resistance and add to the risk of laminitis. More on signs of insulin resistance later but most Dales Ponies would be suspect on appearance.
Amounts of fructan in grass varies greatly from season to season, day to day, and hour to hour. Also fructan levels vary in varieties of grass (and can be high in weeds, esp. Dandelions). Grass seed mixtures suitable for horses at risk from laminitis are being developed and may be available soon, but are not yet on the market.
Fructan levels depend on the amount of production (photosynthesis) compared to the rate of utilization (plant growth) and variations of as much as 46% increase by afternoon as compared with morning have been recorded. Dull warm days are safer than sunny days and laminitis cases have been shown to rise in proportion to hours of sunlight, regardless of temperature and rainfall.
The fructan levels in hay are equally difficult to predict and will vary according to, among other things, whether the hay was cut in the morning or afternoon. Hay made late in the season, after seed dispersal, and cut in the morning, will be safest for at risk horses.
Haylages, Particularly quite wet ones, are lower in fructans generally than hay but are much more palatable so the amount fed needs to be carefully monitored.
TAKE HOME MESSAGE.
There is no way you can guess on the fructan content of grass or hay by looking.
Remember that it is the overall amount of fructan consumed that is important, so even horses eating grass/hay low in fructan may be consuming a lot if they are eating large amounts of grass/hay.
The Royal Veterinary College Laminitis Conference. 24th March 2007.
Advice for managing horses known to be at highest risk of developing laminitis (those who have had it before) and horses of the type likely to be at high risk of developing it (overweight and/or cresty neck and localised fat deposits partic. around sheath or udder - signs of insulin resistance. Advice as given, word for word, by:
Pat A Harris MA PHD Dip ECVCN Vet MB MRCVS. Qualified Cambridge Veterinary School
in 1983.
Adjunct Professor of Equine Studies at Virginia State University and European Specialist in Veterinary Clinical and Comparative Nutrition. President of The British Equine Veterinary Association 1999.
Due to the highly variable and unpredictable nature of Fructan accumulation in pasture, animals predisposed to laminitis should preferably be denied access to grass pastures during the growing season.
If some grazing is unavoidable, turn animals out very late at night or very early in the morning removing them from the pasture by mid morning at the latest as fructan levels are likely to be at their lowest at night to early morning.
Avoid pastures which have not been properly managed by regular grazing or cutting as mature stemmy grasses may contain more fructan as it is stored in the stem.
Avoid turning horses out to pasture during late spring when Water Soluble Carbohydrate/fructan levels are rising.
Do not turn horses out onto pasture that has been exposed to low temperatures in conjunction with bright sunlight, as occurs in the autumn after the autumn flush of growth, or bright, cold winter days as cold temperatures will reduce grass growth resulting in the accumulation of fructan.
Do not allow horses to graze recently cut hay stubble as fructan is stored predominantly in the stem.
Next installment to follow shortly but basic message is to feed hay soaked for 30mins to remove 50% of Water Soluble Carbohydrates, or haylage if you can slow consumption sufficiently (treble haynets) and chaff based feeds with a high quality vit/min supplement. If cereals must be fed they should be processed to enhance digestibility in the fore gut (micronised or extruded). Also weeds can be very high in fructan.
PART TWO
Report on The Royal Veterinary College Laminitis Conference 24th May 2007
Part 2
How Problems In The Gut Trigger Laminitis In The Foot.
The speaker for this section was:
Jonathon Elliott MA VetMB PhD CertSAC DECVPT MRCVS
He completed his PhD in vascular pharmacology in1989 and is now Professor of Clinical Pharmacology at The Royal Veterinary College and is Vice Principal of Research. He has won awards for his contributions to companion animal medicine, particularly in the area of equine laminitis.
The link between events in the gastrointestinal tract and the foot is still a mystery, although the common pathway to the separation that occurs in the foot due to laminitis seems to be brought about by activation of enzymes called Matrix Metalloprotienase (MMP) and represents an extremely exaggerated response to injury. The question is what triggers this and how is it linked to consumption of carbohydrates?
MMP’s are important enzymes in normal tissue growth and the resident cells in the foot produce them to support the continuous growth of the hoof.
Excessive MMP activity occurs in the developmental and acute phases of laminitis and is responsible for destroying the membrane that bonds the laminae in the foot leading to separation of the pedal bone from the hoof wall.
There are 3 theories as to how these MMP’s are activated:
1) Bacteria derived exotoxins activate MMP’s.
2) Gut derived products trigger inflammation in the foot, leading to MMP activation.
3) Gut derived products trigger vascular disturbances leading to vasoconstriction and ischaemia- reprofusion injury (blood supply to the foot gets compromised and then blood rushes back, like putting a tourniquet on your leg and taking it off again, only much worse because of the lack of expansion of the hoof wall) part of which involves MMP activation. The blood vessels in the foot are highly susceptibly to the vasoconstrictory effects of these substances and the effects of the reduced blood, oxygen and glucose supply that results from vasoconstriction. This has been compared to Raynaud’s Disease in man (impaired blood supply to hands and feet that can lead to amputation) and advances in treatment of this condition could help advance laminitis treatment in the future.
These theories are not mutually exclusive, but none explains why some horses are so much more susceptible to laminitis than others. Recent evidence suggests a strong link between the insulin resistant type of horse and increased susceptibility to vasoconstriction and laminitis.
Carbohydrate overload leads to more of the Gram-positive bacteria that ferment carbohydrate in the hind gut. This lowers the pH in the hind gut (acidosis) and increases the permeability of the gut wall. This allows the entry of undesirable substances into the circulatory system (endotoxins and too many amines) which cause vascular (blood vessel) problems in susceptible horses and trigger MMP activation leading to failure of the foot.
Thus both inflammatory and ischaemic (results of reduced blood supply) stimuli could trigger MMP activation and cause the foot to fail and there is evidence that all 3 theories may contribute to the pathophysiology (the disturbance of the processes underlying normal function) of pasture induced laminitis.
I hope that this makes some sort of sense. I am sorry that it is so complex. I know that it has made my brain hurt! Thank god for a veterinary dictionary!
Next exciting episode ‘Metabolic Predisposition to Laminitis – Obesity and Insulin Resistance.’ It is a bit easier to follow – promise!
PART THREE
The Royal Veterinary Laminitis Conference 24th March 2007
Part 3.
Metabolic Predispositions to Laminitis:
Obesity and Insulin Resistance
The speaker on this section was;
Raymond J Geor BVSc MVSc PhD Diplomate ACVIM
Dr Geor is the Distinguished Chair and Director of Research at The MARE Center and Professor of Large Animal Clinical Services, Virginia-Maryland Regional College of Veterinary Medicine. His research focuses on carbohydrate nutrition of horses in health and disease. Currant areas of study include the role of insulin and obesity in laminitis and the links between carbohydrate nutrition, insulin resistance and laminitis risk.
Metabolic abnormalities, notably obesity and insulin resistance (IR), have long been thought to be involved in the predisposition to laminitis.
Obesity and IR have now been proven to be important predisposing factors for laminitis. Identifying these conditions, particularly IR, means that management strategies can be implemented to assist in avoiding laminitis.
Horse with a condition score of more than 7, on a 9 point scale, are classified as obese.
However this does not take into account the distribution of fat.
It is well known that, in man, people who accumulate fat around the waist are at increased risk of heart disease, high blood pressure, diabetes, etc.
In the horse it would seem that some horses which are not clinically obese but have enlarged fat deposits on the crest, tail head, sheath/udder are predisposed to laminitis.
Research is ongoing in developing a 'cresty neck score', measuring the height and width of the crest and using it to assess laminitis risk.
IR is defined as a metabolic state in which normal concentrations of insulin do not result in a normal biological response in target tissues, such as an increase in cellular glucose uptake.
Compensated IR, evidenced by persistently raised levels of insulin but normal levels of glucose, is a common finding in IR horses.
Recent studies have shown that an IR phenotype (appearance) is strongly linked to a predisposition to laminitis. When studying the metabolic differences of 160 ponies on one farm, findings based on insulin sensitivity, compensated IR, and categorizing the ponies considered to be showing pre-laminitic metabolic syndrome (PLMS), enabled researchers to predict 11 of the 13 cases of laminitis that occurred in May of that year, meaning that the IR ponies were at 10 times higher risk of developing laminitis.
Cushings Disease may result from long term IR.
IR could cause laminitis in 3 possible ways:
1) IR might impair glucose delivery to the foot.
2) IR could alter blood flow to the foot.
3) IR could lead to a pro-inflammatory state, increasing MMP activity (the enzymes that destroy cells in the laminae when they are over- activated, causing separation of the pedal bone from the hoof wall).
There is evidence that high starch and sugar diets increase IR.
Horses thought to be of IR phenotype should be managed to increase insulin sensitivity (see next installment).
TAKE HOME MESSAGE:
If your horse is obese and has a cresty neck, or just has a cresty neck, BEWARE. It has the IR phenotype and is predisposed to laminitis.
It is likely that all horses have a laminitis threshold, but IR lowers this threshold.
IR is reversible, in the early stages at least.
PART FOUR
The Royal Veterinary College Laminitis Conference. March 24th 2007
Part 4.
Nutritional Countermeasures to Laminitis.
The speaker for this section was:
Pat Harris MA PhD DipECVCN Vet MB MRCVS
Bibliography in Part 1 - 2nd post.
This will concentrate on 2 main areas:
1) How to reduce the intake of rapidly fermentable material.
2) Nutrients and managemental strategies that may reduce insulin resistance
1) Reducing Intake.
We need to be able to identify the that are high in those components that, under certain conditions,tend to be rapidly fermented to produce, in particular, excess lactic acid, which lowers Ph of hind gut, increases gut permeability, kills bacteria and aids the release of undesirable substances.
A number of terminologies have been used which can be confused:
Water soluble carbohydrates (WSc). These include simple sugars and fructan, but not starch.
Nonstructural carbohydrates (NSc)
The material within the feed which can potentially be rapidly fermented to lactic acid and includes simple sugars, fructan and starch.
The amount of starch that is rapidly fermented rather than digested varies on the amount fed and whether it has been processed. If cereals are to be fed to animals which may be prone to laminitis, unprocessed corn or barley should be avoided, even in small amounts. Oat starch is usually efficiently digested, regardless of processing.
One large feed of unprocessed cereal can result in clinical signs of laminitis within 40hrs.
Even horses used to being fed grain should be fed less than 0.5 kgs per 100kg bodyweight, cereal in one meal.
Pasture.
Research has shown that a bolus of fructan at between 7.5 - 12.5 g/kg bodyweight will reliably produce laminitis, even in a breed not believed prone to the condition.
Many people restrict the time horses have access to grass but preliminary data suggests that they can eat up to40% of their daily dry matter intake in 3hrs of turnout, so just restricting time may not be enough.
For current advice on reducing turnout effectively see Part 1, 2nd post.
2) Reducing Insulin Resistance.
EXERCISE.
A survey showed a high proportion of acute laminitis cases in the 'no regular exercise' category.
Exercise and exercise training have been shown to have numerous benefits including enhanced insulin sensitivity.
Maintaining and if possible increasing the level of activity of horses prone to laminitis would be advantageous, especially if they are obese as well.
OBESITY.
It has been well recognized that obese horses are more prone To laminitis.
It is likely that the risk for laminitis in obese horses is due to the development of insulin resistance (IR).
The syndrome of obesity, IR and laminitis is sometimes referred to as 'equine metabolic syndrome' or peripheral Cushings syndrome.
The link between obesity, insulin sensitivity, and vascular dysfunction is currently under investigation.
Horses are usually overweight because they have stored excess calories as fat ie been overfed relative to their activity level.
Horses turned out to pasture at certain times of the year may be getting several times their calorie requirement.
DIET.
Insulin sensitivity has been found to be affected by diet as well as exercise.
Adaptation to high carbohydrate diets is associated with decreased insulin sensitivity as large fluctuations in glucose and insulin following meals high in sugar may supply inappropriate signals of energy availability to the glucose regulatory system, thereby altering insulin sensitivity of the tissue and may result in changes in metabolic signaling both within and between cells.
It is important to note that certain pastures at certain times of the year can result in marked fluctuations of blood glucose and insulin in a similar way to the feeding of large cereal based meals.
It has been suggested that there may be a progression of IR in laminitis prone horses from compensated IR (insulin sensitivity greatly decreased but made up for by increased insulin secretion), being a predisposing factor in healthy but possibly genetically predisposed horses, to a decompensated IR later in the course of the disease.
It would seem advisable to choose diets that result in low glycaemic and insulinaemic responses.
Feeding a fibre based diet, using oil as an energy source if required for the more athletic horse, has the potential to improve glucose tolerance and insulin sensitivity, as well as , perhaps more importantly for exercise performance,improve metabolic flexibility.
DIETARY SUPPLEMENTS.
There have been few, if any, controlled trials that have tested interventions with dietary supplements, feed additives, or drugs, to prevent laminitis.
The streptogramminn antibiotic 'Virginiamycin' (I think this 'Founderguard') has been used and marketed to prevent pasture induced laminitis by preventing the overgrowth of gramm-positive bacteria. However it is not thought to be effective in all cases and is only available under special licence in Europe.
Areas needing exploration include increasd anti-oxidant supplementation, hind gut buffers, and agents that block the over activation of MMPs.
Current important area of interest is around nutrients or nutraceuticals to counter the development of IR or the effects of being IR.
Two discussed:
Cinnamon.
Cinnamon bark has been reported to act in man as a stimulant astringent to the stomach with antimicrobial, antispasmodic, antioxidant, antidiarrhoea, calmative and antiparasitic properties with a potential natural insulin sensitising action. In man 1gm /day could have significant effects on fasting glucose concentrations.
Tests suggest that cinnamon extract may play a role in blood glucose levels by improving insulin sensitivity, or the release of insulin, or by slowing the absorption of carbohydrates.
This may be a fruitful area for evaluation in laminitic horses where IR is involved.
Cinnamon also contains proanthocyanidins which may improve vascular health and have substantial antioxidant activity - potentially of additional benefit to laminitics.
Magnesium.
May have a role in modulating the action of insulin.
No data yet available to confirm that additional supplementation over and above that currently recommended will affect insulin sensitivity but should ensure all horses have an adequate intake particularly those prone to laminitis.
Take Home Message
Base horses diet on forage/fibre, not sugar/starch.
Feed a broad-spectrum vitamin and mineral supplement to horses on a restricted diet, and ensure an adequate and balanced supply of magnesium.
Do not starve or prevent from eating for long periods in an attempt to reduce bodyweight, and make all dietary changes slowly.
Maintain or increase regular exercise.
Plan an active weight management programme for overweight animals; Meadow hay at 2% current bodyweight for 6 weeks.
Meadow hay at 1.5% current b/w for 6 weeks.
Meadow hay at 1.5% target b/w for 6 weeks.
With increased exercise wherever possible.
Maintain a moderate condition score - between 4 and 5 on 9 point scale.
Get forage analysed and try to feed a forage with less than 10% NSc. Soaking hay in clean water for 30mins will significantly reduce sugar content.
PART FIVE
The Royal Veterinary Laminitis Conference Part 5
Medical Management of Laminitis
The speaker for this section was:
Celia M Marr BVMS MVM PhD DEIM Dip ECEIM MRCVS
She is based at Rossdales Equine Hospital in Newmarket. Her particular areas of interest include cardiovascular medicine, internal medicine, adult and neonatal intensive care and medical imaging.
GOALS:
The primary goals are to minimise structural changes within the hoof, alleviate discomfort and restore function without compounding structural changes, and halt the processes that are driving the laminitis. Additional goals are to assess the existing degree of damage in order to plan corrective farriery and provide an accurate prognosis, plus identify, remove or treat predisposing factors and prevent more attacks.
PREVENTING ONGOING DAMAGE TO HOOF:
The single most important thing you can do for any horse showing any sign of laminitis is put a plank across stable doorway, put down a bed 18" thick, covering entire floor, put horse in stable and shut the door (as far as the horse is concerned, for an absolute minimum of 30 days, even if the horse appears to have recovered a lot more quickly than that. Literally do not allow it to step off thick bedding for at least 30 days.
Support to the hoof can be provided by supporting the frog alone or the frog and sole. There is no clear evidence to support one over the other at this time.
PAIN RELIEF:
Pain relief should be aimed at minimising pain, not completely eliminating it or the horse may move about too much, and phenylbutazone is still the drug of choice and may also help as an anti-inflammatory.
Ice can be used to slow the rush of blood back to the foot and help with pain relief, but needs to be applied to leg from above the knee down.
In horses with severe pain opiates may be necessary and recent drug protocols offer new drug combinations for treatment of very severe and debilitating pain, but these require hospitalisation and cost from £75 to £500 a day for the drugs alone.
HALTING PROCESSES DRIVING THE LAMINITIS:
By the onset of clinical systems drugs aimed at this may be too late.
ACP may help as a vasodilator - efficiency unproven - but will help with stress and encourage the horse to lie down more, so is a useful addition to bute.
Asprin may be of use, both as a treatment and possibly as a preventative (as in low dose in man to prevent strokes, etc.) but more research has to be done.
Drugs to block MMP's being activated could represent a major step forward in future.
ASSESSING DAMAGE AND PROGNOSIS.
The diagnosis of laminitis is based on lameness, pain on use of hoof testers on one or more feet and increased digital pulses.
The severity may vary from foot to foot and the most severely affected foot is used to determine the laminitis category.
X-rays can determine the degree of rotation of the pedal bone and the founder distance, but markers need to be used on the wall of the hoof. Sinkers and marked pedal bone rotation merit a poor prognosis.
ADDRESSING PREDISPOSING FACTORS:
Has mostly already been discussed but also include:
Treating mares with metritis following foaling.
Supporting opposite leg in cases of severe, nonweightbearing lameness in one leg.
Treating Cushings Disease (PPID).
Treating Equine Metabolic Syndrome.