Laminitis Update by James Hart of Equine Herbals
Laminitis has alway been a problem but some recently published work by researchers in Queensland has made us look at it in a new light. As result our understanding of laminitis has increased significantly. This crippling disease affects thousands of horses world wide and until quite recently has been poorly understood. Evidence that owners and vets have been plagued by laminitis goes as far back as you may care to research and although some of the treatments now seem strange others were close to the latest recommendations. In the 19th century bleeding and hot poultices were popular; not so good. Standing in cold water however was better; Pollitt's recommendation for acute treatment is the ice bath.
The anatomy of the hoof is a masterpiece in engineering in the way in which the hoof is attached to the leg. The main bone of the hoof, the coffin or pedal bone fits snugly inside the hoof. The connecting tissue which attaches the hard hoof wall to the coffin bone are the lamellae These are a multi folded structure almost like velcro or hundreds of fingers each fitting into a glove. These lamellae originate from either the bone or the inner wall of the hoof and link up to bond the hoof onto the bone.
The simplest definition of laminitis is inflammation of the lamellae but more usefully it is:
“failure of the attachment between the distal phalanx (coffin or pedal bone) and the inner hoof wall”. A horse has laminitis when the lamellae of the inner hoof wall, which normally suspend the distal phalanx from the inner surface of the hoof capsule, degenerate and fail. Without the distal phalanx properly attached to the inside of the hoof, the weight of the horse and the forces of movement drive the bone down into the hoof capsule. This process causes trauma within the hoof resulting in huge pain and the characteristic lameness. This is acute laminitis and the horse will have foundered. A sinker is a horse that has suffered complete destruction of the inter-laminar bonding, resulting in a totally loose pedal bone. In extreme cases this can then pierce the sole (See bottom of article for more detail on the different stages of laminitis).
Until recently the detailed cause of laminitis was unknown, but a range of situations are known to increase the risk and may precede an attack. Horses in any one or more of these situations should be regarded as high risk.
Overeating or obesity:- this is perhaps the most commonly seen type in temperate climates and is aggravated by our high quality, highly fertilised pasture. Many horses and ponies are not really given sufficient exercise, but are still hard fed and given high quality pasture. Ponies particularly are at risk. They require very little to eat and can not cope with dairy quality pasture. Most of them are only a few generations from the hills of Wales, Dartmoor or the Shetland Isles. The native grasses in these areas are poor by modern plant breeding standards but suit the digestive systems of the ponies. In these ponies especially, a sudden carbohydrate overload caused by excess grain, sudden access to lush cattle pasture or a sudden change in diet can trigger an attack. Grazing lush pasture or grain overload is the cause of about 50% of liminitis cases.
Toxaemia:- a septic shock or some toxic focus from bacterial, viral, chemical or fungal source can be enough.
Management:- overweight animals, unconditioned animals worked on a hard surface, improper foot care and the administration of corticosteroid drugs to susceptible individuals can all trigger laminitis.
Hormonal imbalance:- laminitis will often appear in cases of hypothyroidism and pituitary dysfunction. (Cushings or Insulin Resistance)
Prolonged high fever:- due to severe colic, retained placenta, pneumonia, pleutritis, potomac horse fever, colitis caused by salmonella or black walnut shaving used as bedding can also trigger laminitis.
What Causes the Laminitis
The research done by Chris Pollitt and his team at the Equine Laminitis Research Unit in Queensland has produced a new hypothesis on the cause. The key points are; Unlike most tissue, glucose uptake in the hoof is not dependant on insulin. Rather it's controlled by specialist glucose transporters (GLUT1-type). The link between high insulin levels and laminitis discovered in pasture induced laminitis in ponies.
This is not classic insulin resistance and highlights that hormones do many things. Insulin not only controls blood glucose levels but can also have effects on blood flow and protein turnover. So an individual although insulin resistant in respect to glucose tolerance may still be insulin responsive in respect to other actions of insulin.
Another important point is that, unlike humans, insulin resistant horses seldom develop pancreatic exhaustion and remain capable of producing high levels of insulin in their blood (see box for more detail on insulin).
The theory developed in Queensland is that laminitis is a direct result of insulin toxicity caused by hyperinsulinaemia. The high blood insulin concentrations were in turn a sign of glucose intolerance coupled with a glucose challenge. This explains why glucose intolerant ponies produce an exaggerated insulin response when fed pasture with a high soluble carbohydrate level. Similarly the excess cortisol found in Cushings or in association with corticosteroid drug treatment, leads to glucose mobilisation and a responding insulin response. This means that it is glucose intolerance that predisposes a horse to laminitis but the insulin that precipitates the damage to the hoof.
The experiment to prove this theory required the maintenance of high blood insulin levels and the results showed that these high levels of insulin did indeed induce laminitis without any of the other factors such as high cortisol or glucose being present.
This new knowledge brings with it a new set of questions and sends us back to rethink the laminitis strategy. The established guidelines of feeding a low GI diet , combined with weight control and exercise remain sound, but there is now a need to address insulin sensitivity and blood glucose concentrations. Thinking about the excess insulin hypothesis perhaps the approach should be to look at glucose levels which will in turn affect insulin. This needs a careful approach because many herbs act on glucose levels by simulating insulin production; exactly what we don’t want.
As a result of the huge increase in diabetes in the human population there has been a lot of research into the usefulness of a wide range of herbs. Although it is not always directly relevant the data generated is useful and there have been a few gems that appear helpful in the control of laminitis. (See box for an explanation of diabetes) When you think about it there are two actions which may be useful.
Firstly the control of glucose into the blood. Remember high glucose levels trigger insulin production by the pancreas. So if we slow glucose absorption insulin levels should be kept lower.
Secondly, given that high insulin levels may cause a laminitic incident we should try to make the action of the insulin more efficient. This means that the horse will need lower levels of insulin to remove a given amount of glucose from the blood.
In researching this article we looked at a wide range of herbs. A few came out showing a lot of promise. Some of these conflicted with those that are indicated for insulin resistance. Because of the close links between Cushings, IR and laminitis these should therefore be avoided. See below
The Good Ones.
As you may expect with such a challenge there are not many herbs that measure up. Luckily however the ones that do are easy to find, not expensive and generally easy to grow.
This first group act by slowing glucose absorption. Interestingly they are both high in soluble fibre.
Fenugreek. (Trigonella foenum-graecum)
This herb is also discussed in the article on Insulin Resistance. Fenugreek seeds contain soluble dietary fibre(SDF) which was fed to normal or diabetic rats and significantly improved oral glucose tolerance. It acts by slowing the absorption of the glucose from the gut and enhancement of the action of insulin. Importantly the insulin levels and insulin secretion were not affected by the Fenugreek SDF.
Psyllium (Plantago ovata).
This well known herb is becoming more important in a number of areas. In the area of insulin levels it seems to act in a similar way to Fenugreek. A 2006 study showed that a hot-water extract suppressed post feeding blood glucose and slowed its absorption with no increase in insulin levels.
This second group probably acts by potentiating the action of insulin.
Cinnamon (Cinnamomum cassia) and Clove (Eugenia aromatica)
Two related 2006 studies provided new evidence for the beneficial effects and Biochemical actions of cinnamon and clove. Both improve how insulin functions and so lower glucose levels. This then acts as a negative feedback to slow insulin production.
Oregano. (Origanum vulgare)
One of the most promising seems to be the common culinary Oregano. (10) The effect of an extract of Oregano leaves on blood glucose levels was investigated in normal and diabetic rats. In the normal rats blood glucose levels were slightly decreased by the herb. In the diabetics there was a significant decrease in blood glucose levels. Importantly, neither group showed any change in blood insulin concentrations after treatment. This indicates that the extract acted without changing insulin secretion. The mode of action is not yet clear but it may be potentiating the action of the available insulin.
Tea (Camellia sinensis)
Amongst the other things that have recently been discovered about tea is its insulin potentiating effect; by up to 20 times. (14) It is important to note that this is the regular tea and can be used as black tea or green. Although not important to this discussion it is interesting to note that the addition of milk very much reduced this effect.
Ivy Gourd (Coccinia indica)
There have been a few studies on this common Indian herb but although it seems helpful in controlling blood sugar in humans it has been postulated that it acts in an insulin like manner. This may or may not therefore act in the lamellae in the way that insulin does. Much more work is needed here. (15)
The research on these herbs was mainly as part of the continuing research on diabetes in humans. The subjects were humans or rats so although they are similar in some areas horses also have different biochemical pathways to other animals so further research is needed before any of the herbs noted above can be used with confidence to help with laminitis management.
Herbs to avoid
The research has revealed a lot of herbs that stimulate insulin production. This is fine for human diabetics but most certainly inappropriate in laminitis prone horses. The following list is not complete but highlights ones that you may come across. They generally act by stimulating the pancreas.
Lucerne; (Medicago sativa)
Unfortunately lucerne should be avoided. This may make feeding hard but work in 1997 showed that an aqueous extract stimulated insulin release. Although it is indicated in hyperglycaemia it stimulates the pancreas and so increases insulin production and hence increases the laminitis risk. (16)
Gymnema ;(Gymnema sylvestre)
Although not a common herb there has been quite a lot of press about the use of this herb in human weight control. As well as acting in a similar way to lucerne on the pancreas it also suppresses sugar receptors in the mouth. (17)
this herb is commonly given to horses as a supplement but should be avoided as it too stimulates the pancreas. (18)
Garlic and onion ;(Allium sp.)
Although many people commonly feed garlic for its other significant benefits it should be avoided if the horse is laminitic. (19,20) The evidence suggests that allicin and allyl propyl disulphide compete with insulin for insulin-inactivating sites in the liver. This results in an increase in free insulin.
Burdock; (Arctium lappa), Dandelion Root; (Taraxacum officinale), Jerusalem Artichoke; (Helianthus tuberosa).
These plants all contain quite high levels of inulin which is an oligosaccharide. Inulin is considered a soluble fibre, but it should not be used in the same way as others, because inulin is a class of fructan. As we have seen these should be avoided. (21)
Yucca; (Yucca schidigera),
Although quite popular as an anti-inflammatory, Yucca should be avoided if there is any suspicion that any degree of laminitis may be present. Certain fractions in Yucca significantly increase serum insulin levels. (22)
A possible protocol
ne of the tenets of herbal medicine is that treatment should be of the whole animal rather than the symptom. The treatment and prevention of laminitis is an area that would seem to particularly appropriate to this approach given the broad range of effects suffered by a laminitic horse. The areas to be considered in developing a protocol are:
not considered in detail here but possibly the most important over the long term.
this is linked to diet and in a laminitis prone animal long term use of a quality probiotic would be appropriate.
as already discussed Psyllium would be a good choice here to slow down glucose absorption.
as well as acting at cellular level about 50% of the insulin secreted by the pancreas acts on the liver. Abnormal liver function is thought to play a role in diabetes and by extrapolation may well be involved in the laminitis as well. The herbs to use here are Milk Thistle (Silybum marianum) or Globe Artichoke (Cynara scolymus).
To round off the actions around insulin we should make the most of what is in the blood, so include Oregano or Tea in the protocol.
the anti-inflammatory action of a range of herbs is becoming quite well understood. Devil’s Claw or Boswellia should both be fine to use. But DO NOT USE Yucca (see above). It may be necessary to use bute under veterinary supervision, in the very early acute stage of a laminitic attack but this is not recommended for more than 3 days. After that Devil’s Claw could be used long term if necessary. Remember that high doses may be required to give the necessary level of support.
After a laminitic attack there will significant tissue damage so the inclusion of comfrey or gotu kola to support tissue regeneration would be worthwhile.
Similarly as a adjunct to the anti inflammatory treatment antioxidants will help to reduce the collateral damage.
As part of the healing process circulation to the capillaries is vital and can be supported by ginger, which is also anti-inflammatory, or bilberry, which is also an antioxidant.
The research being done by Dr Pollitt and others is giving us new insights into laminitis. From the work we have done it appears that there are some areas in which herbs could be of real benefit. Clearly more work is needed to develop and test these ideas.
1 Pollitt: Equine Laminitis:A revised pathophysiology.
2 Huntington and Pollitt: Nutrition and the equine foot; Advances in Equine Nutrition Nottingham University Press (2005)
3 Redden;Laminitis:Causes and Cures; Advances in Equine Nutrition
4 Treiber et al (2006)
5 Sillence et al: What Causes Equine Laminitis?; RIRDC Publication 07/158 (2007).
6 Johnson et al; (2004)
7 Pratt et al; (2006)
8 van Eps et al: Distal Limb Cryotherapy for the Prevention of Acute Laminitis; Clinical Techniques in Equine Practice 3:64-70 (2004)
9 Yeh et al: Systemic review of herbs and dietary supplements for glycemic control in diabetes.
10 Lemhadria et al: Anti-hyperglycaemic activity of the aqueous extract of Origanum vulgare growing wild in Tafilalet region: Laboratory of Endocrinian Physiology, F.S.T.E. Boutalamine and Pharmacology, UFR PNPE, BP 21, Errachidia 52000, Morocco.
11 Hannan et al.; Soluble dietary fibre fraction of Trigonella foenum-graecum (fenugreek) seed improves glucose homeostasis in animal models of type 1 and type 2 diabetes by delaying carbohydrate digestion and absorption, and enhancing insulin action.; Br J Nutr. 2007 Mar;97(3):514-21.
12 Hannan et al.;Aqueous extracts of husks of Plantago ovata reduce hyperglycaemia in type 1 and type 2 diabetes by inhibition of intestinal glucose absorption.;Br J Nutr. 2006 Jul;96(1):131-7
13 Anderson et al.; Experimental Biology 2006
14 Anderson and Polansky ; Tea enhances insulin activity; J Agric Food Chem. 2002 Nov 20;50(24):7182-6.
15 Kuriyan R, Rajendran R, Bantwal G, et al. Effect of supplementation of Coccinia Cordifolia extract on newly detected diabetic patients. Diabetes Care. 2007 Nov
16 Gray and Flatt; Pancreatic and extra-pancreatic effects of the traditional antidiabetic plant, Medicago sativa; Br J Nutr 78:325-34, 1997
17 Baskaran et al.; Antidiabetic effect of a leaf extract from Gymnema sylvestre in non-insulin-dependent diabetes mellitus patients.; J Ethnopharmacol 30:295-305, 1999.
18 Ajabnoor; Effect of aloes on blood glucose levels in normal an dalloxan diabetic mice. J Ethnopharmacol 28:215-20,1990
19 Bever and Zahnd; Plants with oral hypoglycemic action. Quart J Crude Drug Res
20 Augusti and Sheela; Antiperoxide effect of S-allyl cysteine sulfoxide, an insulin secretogogue, in diabetic rats. Experientia 52(2):115-20, 1996
21 Rumessen et al; Fructans in Jerusalem Artichokes; Am J Clin Nutr 52:675-81,1990
22 Duffy et al.; Effects of dietary supplementation with Yucca schidigera Roezl ex Ortgies and its saponin and non-saponin fractions on rat metabolism. J Agric Food Chem. 2001 Jul;49(7):3408-13.Click here to read Links
Human diabetes or formally diabetes mellitus, is a syndrome characterized by disordered metabolism and abnormally high blood sugar (hyperglycaemia). It results from insufficient levels of insulin. The characteristic symptoms are excessive urine production, excessive thirst and increased fluid intake attempting to compensate for increased urination, blurred vision, unexplained weight loss, and lethargy.
The phases of Laminitis.
Developmental laminitis. This is the very earliest of phase of laminitis. It is the period between the initiation of factors that result in delamination, e.g excess levels of insulin, and the emergence of clinical lameness. Since pre-existing illness leads to laminitis, the symptoms of early laminitis are also the symptoms of the precipitating illness. Vigilant owners of such horses should be able to monitor digital pulse and limb temperature and with luck identify a laminitic bout before it becomes acute.Occasionally, no development phase will be recognized and the horse is simply found to be in the acute phase with no apparent ill health preceding or accompanying it.
Acute laminitis. This is the period between the clinical onset of lameness and the stabilization of laminar degeneration/breakdown. It may be as short as 8 – 12 hours’ duration if the horse is exposed to black walnut shavings, or as long as 30 – 40 hours in the case of carbohydrate overload. Symptoms of the primary illness will usually be present along with the lameness, which is often confined to the front feet. When just the forelimbs are affected, the horse will shift weight to the back legs, with the front legs extended. This is the typical laminitis stance. This is an extremely painful condition and a horse may refuse to stand or walk. The pain may also cause increased breathing and pulse rate.
At this stage, the digital pulse will be increased and the hoof will have an elevated temperature. There will be pain when the toe is compressed with hoof testers and there may be a depression of the skin proximal to the wall of the hoof, suggesting rotation or sinking of the pedal bone.
Your vet will probably want to X-ray the hoof, for later comparison purposes, and importantly to determine the position of the distal phalanx relative to the hoof capsule.
Chronic laminitis. This is the stage that occurs when some rotation of the pedal bone has taken place but is not so bad that there is laminar tissue death. Horses with this condition are likely to get recurrent episodes of acute laminitis. Abnormal growth of the hoof may be present. Diverging rings may be noted around the hoof wall. These will be wider at the heel than the toe, indicating that growth at the toe is slower than the heel.
The degree of lameness present depends on the use of the horse and quality of care. (1)
At Metabolic level :Controls cellular intake of certain substances, most prominently glucose in muscle and adipose tissue
Increases DNA replication and protein synthesis by control of amino acid uptake.
Modifies the activity of numerous enzymes.
At Cellular level
Increases glycogen synthesis – forces glucose to be stored in liver and muscle cells in the form of glycogen.
Increases fatty acid synthesis – forces fat cells to take in blood lipids which are converted to triglycerides.
Increases esterification of fatty acids – forces adipose tissue to make fats (i.e., triglycerides) from fatty acid esters.
Decreases proteolysis – decreases the breakdown of protein.
Decreases lipolysis – reduces the conversion of fat cell lipid stores into blood fatty acids.
Decreases gluconeogenesis – decreases the production of glucose from non-sugar substrates, primarily in the liver.
Increases amino acid uptake – forces cells to absorb circulating amino acids.
Increases potassium uptake – forces cells to absorb serum potassium thus lowers potassium levels in blood.
Arterial muscle tone – relaxes arterial wall muscle, increasing blood flow, especially in micro arteries.
Action on Carbohydrates
Increase glucose transport
Increase glycogen synthesis
Action on Fats
Increase lipoprotein lipase activity
Increase fat storage in adipocytes
Inhibit lypolysis (hormone-sensitive lipase)
Increase hepatic lipoprotein synthesis
Inhibit fatty acid oxidation
Action on Proteins
Increase protein synthesis
Increase amino acid transport
In mammals, insulin is synthesized in the pancreas within the beta cells of the islets of
Langerhans. It is released mostly in response to increased blood glucose levels.
Additional insulin synthesis and release takes place at food intake, and is somewhat
influenced by the autonomic nervous system.
Other substances known to stimulate insulin release include amino acids from ingested
proteins, acetylcholine, released from vagus nerve endings (parasympathetic nervous
system), cholecystokinin, released by enteroendocrine cells of intestinal mucosa and
glucose-dependent insulinotropic peptide (GIP).
The sympathetic nervous system inhibits the release of insulin.