December 6, 2012 16:17
Losing shoes is a part of having shoes on a horse. When you look at the physics of what is involved in putting and keeping a shoe on a foot, it is a wonder that we don’t lose more shoes than we do. Horses work and live in a variety of terrains and environments, and keeping a piece of metal between them and the ground with a few square nails can be quite a feat.
Since losing shoes is a fact of life for a horse owner, you should be prepared for when it happens. The first thing you want to do is to call your farrier so that they can have as much time as possible to get an additional stop worked into their schedule. Between the time that you contact the farrier and the farrier’s arrival, you should try hard to find that shoe.
Finding the shoe is important for a couple of reasons. First, it may give clues as to how the shoe was lost, and the farrier can then make changes to keep it on. Second, the farrier won’t have as much work or expense in putting the shoe back on if you have the lost shoe available. No one is happy about a lost shoe, but when the shoe has been found, it is likely that at least the farrier will be a bit happier.
Be patient when you get hold of your farrier. Most farriers are booked from can to can’t, so adding another stop is not necessarily an easy thing.
If you have to use the horse, then try very hard to use it in the gentlest way. Stay to the softer terrain, or look for some of the boots that are offered for this purpose. If the horse is in need of a reset and the feet are long, it is often a good idea to pull the opposite shoe so that the feet wear evenly. Check with your farrier first, because they won’t want to nail on 2 shoes if the horse is not getting reshod.
For shoes that are partially still on but hanging by a couple of nails, you should get those off of the foot immediately. There is good chance that the horse will injure itself with the shoe on the foot in the wrong place.
Every farrier practice has different policies to deal with this situation. For us, we try very hard to shoe in a way that the foot will always be improving and the horse is comfortable. There are times when the best shoeing for the horse is not likely to stay on the foot. Making a decision of millimeters to provide the best support and protection, and still keep the shoe on is part of the learning curve that comes with shoeing each and every individual horse. That being said, the prettiest shoe that won’t stay on is not a good outcome.
For me, I shoe each horse as if it were mine. If it loses a shoe, I will make the changes that I feel are needed to keep that from happening again. Some of the options are clips, tighter length and expansion, and in extreme cases, barbed heels. My policy for the owner is that nailing the lost shoe back on is free if they are able to find the shoe. If not, then it is kind of a case-by-case basis. A mean owner is likely to get charged and lose their farrier, and I rarely charge the ones that really appreciate the extra effort that it takes to service a horse with a lost shoe.
When your horse loses a shoe, remember that the farrier is probably more upset about it than you are. It is a fact of life for horses with shoes on, so deal with it and move on. A lost shoe does not mean a bad farrier, it just means a lost shoe.
Chris Gregory, CJF, FWCF
Heartland Horseshoeing School
327 SW 1st Lane
Lamar, MO. 64759
June 25, 2011 08:29
Have you ever been cleaning your horses hooves and be hit with an odour like you’ve never smelled before? Chances are it could be thrush.
Thrush is a very common ailment of the hoof, simple to deal with if you recognize it and treat it early.
"Thrush is an infective condition of the frog and its sulci which results in degeneration of the horn (the protective frog callous) and the production of foul smelling gray/black discharge.
Factors involved in thrush include:
- Poor Past Trimming or Shoeing - Almost every horse that I take out of shoes has some thrush and other signs of a chronic toe-first landing. Barefoot trimmers need to know that they can contribute to thrush, too! Toes that include a lamellar wedge (long toes) prohibit correct movement, and untrimmed frogs and undiagnosed thrush are a component of good hoof maintenance.
-Past Injuries - Horses with injuries that result in favouring a foot often end up with a contracted heel on that foot, and any contraction results in cracks that welcome Thrush's anaerobic bacteria.
- Hoof Hygiene - Does the horse stand in damp footing that contains Urine? Urine contains Ammonia, and Ammonia dissolves the proteins in the frog! Are the feet picked out regularly? Are the frogs trimmed in an appropriate manner? Is footing dry and clean or soupy filth?
-Frog Conformation - Open and calloused, atrophied or over trimmed? Frogs with deep cracks, crevices and flaps are most susceptible to Thrush, as are frogs robbed of their protective Horn.
-Hoof Capsule Conformation - Are heels contracted or open? High heels or low? Is the outer wall worn too short, or is the inner wall too long? Horses will walk on the sides of their feet or favour their toes when they have thrush to avoid "hoof mechanism", the flexion in the hoof that enables shock absorption. Good blood circulation is necessary for a healthy frog, so good heel-first movement is a priority.
- Environmental Deficiencies - What is footing like? Is it clean and dry or damp? Does the organic material provide a refuge for bacteria and ammonia?
-Diet - Does the horse have a rich diet that emphasizes grains rich forage and alfalfa, or is it a grass based low carb diet?
-Exercise - Horses need to move; is there adequate room for the horse to move and stretch, or is he given adequate exercise opportunities
Symptoms of Thrush:
-Nasty, pungent, foul smell coming from the bottom of the hoof
-Black, pus like substance in and around the frog area
- Soft frog with unusually deep clefts or grooves
-Sore and/or tender heels.
Thrush is a very manageable and treatable disease. Products like Koppercare, Thrush-XX, or Pritox are available at your local tack shop.
Treatment may include using over the counter products or depending on the severity a more aggressive approach.
March 10, 2011 18:01
Navicular syndrome (or navicular disease, or caudal heel pain syndrome) is a degenerative condition of structures in the horse's heel. The navicular bone lies at the back of the heel, and the deep digital flexor tendon runs down the leg and wraps under the navicular bone before anchoring to the coffin bone. Pain results from changes in the bones, bursa (fluid-filled joint structures designed to absorb shock and reduce friction), tendons, and ligaments in this area.
No one knows precisely what causes navicular syndrome.
Lameness is the classic sign of navicular syndrome. This can appear suddenly, but a more common pattern is mild lameness that becomes progressively worse over time. A horse with navicular syndrome feels pain in the heels of the front feet, and its movements reflect attempts to keep pressure off this area. At rest, the more painful foot is often "pointed," or held slightly in front of the other forefoot, thus bearing little or no weight. Because the horse tries to impact the ground flat-footed or toe-first instead of the more normal heel-first pattern, the gaits are short-strided and stiff. A horse with navicular syndrome has difficulty turning sharply, going downhill, and moving on rocky or hard ground. Picking up one front foot for trimming or shoeing is painful because weight is concentrated on the other foreleg, and affected animals may become quite uncooperative during farrier visits.
While there's no guarantee that a particular horse will or will not develop navicular trouble, the problem is most common in stock-type horses (Quarter Horses, Paints, Appaloosas). There is a fairly high incidence in Thoroughbreds and some warmblood breeds. Arabians, on the other hand, are rarely affected. Lameness from navicular syndrome is most often diagnosed in horses between the ages of seven and fourteen.
No one knows precisely what causes navicular syndrome. Like some other lamenesses, a combination of factors is probably to blame. Conformation seems to be important, with more cases occurring in horses with heavy bodies, upright pasterns, and small hooves. A large number of affected horses have a history of work involving front-leg impact (jumping, cutting, roping, and reining) or increased concussion (parade work or other use involving hard or rocky surfaces). Suspicion has also been directed at irregular farrier care, unbalanced hooves, and shoeing practices that reduce contact between the frog and the ground. A common thread seems to be the combination of increased stress and limited oxygenation of structures in the heel area, but the exact cause of tissue damage and inflammation has not yet been determined.
Consultations with a veterinarian and a farrier are the first steps in combating navicular syndrome. While there is no cure, a prompt diagnosis allows treatment—farrier, medical, or surgical—to begin early in the course of the disease. Proper trimming and therapeutic shoeing can provide relief for many horses. Farrier care is aimed at correcting broken-back or broken-forward pastern angles and normalizing underrun or contracted heels. Generally a shortened toe, either through trimming or shoe design, is a goal. Heel support afforded by egg bar or wide-web shoes reduces pain in some horses, and a shock-absorbing polyurethane shoe from Switzerland is being tested as a possible therapeutic aid. Overall, proper trimming and shoeing can relieve discomfort in about 30% of horses with navicular syndrome.
Polysulfated glycosaminoglycans and hyaluronic acid sometimes lead to improvement, possibly by inhibiting enzymes involved in tissue breakdown. Anti-inflammatory medications can be injected into the heel area or given orally for pain relief. Medical treatment combined with therapeutic shoeing can help about 60% of affected horses.
Palmar digital neurectomy, a surgical procedure to sever the nerves to the painful area, is a last resort in treating navicular syndrome. This option eliminates sensation in the rear third of the foot, thus ending pain and lameness, but it is not a permanent cure. Degenerative changes continue to occur within the hoof, and about one-third of treated horses are lame again within two years.
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January 5, 2011 15:26
December 20, 2010
Insulin resistance (IR) is defined as reduced sensitivity to insulin that results in increased insulin release and/or decreased activity of insulin, such as glucose entry into cells, inhibition of glucose production in the liver, and mobilization of fat. Laboratory testing for IR in horses reveals elevated blood insulin concentration or abnormal changes in blood insulin and/or glucose concentrations when the horse is challenged with glucose or insulin. Several tests have been developed to investigate IR, but most involve either oral or intravenous glucose administration, and in some tests, insulin is also administered.
Insulin resistance can be caused by several hormones and drugs that affect the actions or release of insulin.
Insulin resistance can be caused by several hormones and drugs that affect the actions or release of insulin. These are listed below.
Gestational diabetes occurs during pregnancy when progesterone inhibits insulin. This is not common in mares but occurs in other species.
Xylazine and detomidine, two commonly administered equine sedatives, inhibit the release of insulin from the pancreas. In adult horses, these drugs quickly lower blood insulin and can raise blood glucose concentrations for over three hours.
Stress or severe illnesses induce the release of hormones that interfere with insulin, such as cortisol and epinephrine. It is not unusual for stressed or ill horses to have elevated blood glucose concentrations, though these usually return to normal as the animal relaxes or its condition improves.
Pituitary pars intermedia dysfunction (equine Cushing’s disease)occurs in older horses due to dysfunction of the pituitary gland that results in the overproduction of cortisol, which antagonizes insulin.
Equine metabolic syndrome(EMS) is similar to type II diabetes mellitus in humans. Type II diabetes usually affects obese adults and is characterized by elevated blood glucose concentration resulting from impaired insulin utilization and an inability to compensate with increased insulin production. Equine metabolic syndrome usually occurs in overweight younger horses that have abnormal fat deposits. Affected horses are often described as easy keepers that maintain or gain weight despite being fed relatively small amounts. Insulin resistance with EMS is theorized to occur because abnormal fat can secrete hormones (cytokines and adipokines) that down-regulate pathways involved with how insulin acts on cells. The accumulation of fat in tissues such as skeletal muscle is also believed to have some toxic effects on cells and their response to insulin (lipotoxicity). Fat can convert inactive cortisone to its active form cortisol, which can further add to IR. It is important to realize that not all overweight or obese horses are affected with EMS or IR.
to continue readingthis article visit http://www.equinews.com/article/insulin-resistance
November 25, 2010 17:25
The Missing Link in Laminitis:
Healthy Horse - Laminitic Horse
By Joseph Thomas, PhD
Printed in: Natural Horse
Volume 8, Issue 5
One of the greatest impediments to understanding and developing effective treatment for laminitis is embedded in the name itself. The word laminitis literally means ‘inflammation’ (itis) of the laminae. So these horses have continued to be considered as having a “disease” of the hoof and treatment strategies have, for the most part, remained stuck with ministering to the hoof problem and the laminae inflammation. Though there are hoof recoveries, the horse invariably continues to have repeated laminitic episodes. That is because laminitis is a metabolic disease that affects the hoof, not a disease of the hoof per se. My research has shown that laminitis and type 2 diabetes are more than similar and that the damage to the hoof is an end product of this disease process. If there is going to be any possibility of recovery for these horses the “whole” horse needs to considered and not just the hoof.
This is a long and involved article, but it gets to the heart of the story of laminitis. Although this material is difficult to follow, it explains for the first time, how laminitis begins, progresses and continues.
All horses need the sugar glucose to survive - it is the essential energy source of all cell life. Horses have glucose circulating in the blood, available for the cells as needed, including the cells of the laminae. Horses are also able to produce more glucose in the liver from non-carbohydrate sources when the demand is extended. In healthy horses this production of excess glucose stops once the demand is met. In laminitic horses it continues past the immediate needs and contributes to the already excess of glucose in the liver and the circulating blood. To begin to understand how to reverse laminitis it is essential to know where and how this production of excess glucose in the liver starts and stops in the healthy horse and in the laminitic horse.
What has become evident through my research is that laminitis is rooted in the dynamic relationship between the enzyme 11beta-Hydroxysteroid Dehydrogenase-1 (11beta-HSD1) and the sustained activation of glucocorticoids in tissue-specific cells at particular target sites. This enzyme is the pivotal switch in the activation process that not only leads to elevated glucose in the blood but also all the parameters of equine metabolic syndrome.
Glucocorticoids are steroids (hormones) found naturally in the body and produced by the adrenal cortex, the outer layer of the adrenal glands which sit on top of the kidneys. Glucocorticoids regulate carbohydrate, fat and protein metabolism. Glucocorticoids also inhibit the release of adrenocorticotropic hormone (ACTH, a hormone secreted from the pituitary gland. ACTH regulates blood cortisol, and cortisol opposes the action of insulin.) The wide-ranging actions of these steroids are directed at intensifying the production of high-energy fuel, i.e. glucose, and reducing all other metabolic activity (such as immune response) that is not directly supportive of this demand. In the evolution of the horse, this action has been essential for survival as it provides the energy needed for quick response, rapid flight, and endurance.
Among these glucocorticoids that provide this burst of energy are two that are also involved in the origin, development and progression of laminitis and diabetes mellitus (DM). These two are cortisol (which opposes the secretion and the action of insulin) and cortisone (which waits to be converted to cortisol when more cortisol is needed).1 Diabetes mellitus is defined as "belonging to a group of diseases exhibiting elevated blood glucose due to deficient insulin concentration and/or aberrant insulin activity".2 Laminitis shares these aspects of the DM disease process, as well as many others. It is well established that excess glucose in the blood goes along with decreased glucose consumption by the hoof’s laminae and that this glucose deprivation is a significant contributor to laminae separation.3 Insulin, secreted from the beta cells of the pancreas, is responsible for pushing glucose into cells, and of course that means laminae cells as well.
In a healthy horse, cortisone and cortisol convert from one to the other (cortisone being the inactive form and cortisol being active) according to the body’s needs. The self-regulatory nature of this conversion process in healthy horses works on over-drive in laminitic horses resulting in a sustained activation of cortisol thereby producing excess blood glucose. Through this sustained activation, the same metabolic process essential for the horse's survival becomes the source of laminitis.
The Missing Link 11beta-Hydroxysteroid Dehydrogenase-1
The progression of laminitis and diabetes described in the previous article of this series (NHM Volume 8, Issue 4, The Easy Keeper: Myth and Dangers) showed that there is an elevation of circulating blood insulin in the early stage of laminitis and DM followed by a decreasing insulin level and a concomitant rise in serum glucose. Furthermore, it was shown that as laminitis progresses insulin levels in the blood decrease and blood glucose elevates which is indicative of beta cell damage.
Recent research shows, in addition, that: 1) there is a striking increase in the activity of the enzyme known as 11beta-Hydroxysteroid Dehydrogenase-1 (11beta-HSD1) in the beta cells when there is sustained activation of cortisol and 2) that the activity of this enzyme has damaging effects on the pancreatic beta cells after the onset of diabetes but not before.4 As beta cell function is identical across species, the clear implication of this research is that this is the same way that beta cells are damaged in laminitis.
What is 11beta-HSD1's activity and purpose?
11beta-HSD1 regulates glucocorticoid activity. It is through this enzyme’s expression at specific target sites throughout the body that cortisone is converted to cortisol. The term expression is used rather than concentration because it is the effects of 11beta-HSD1 rather than its quantity that influence the glucocorticoid activity at these particular places. 11beta-HSD1’s expression in the liver, fat, muscle and brain tissue is pivotal in the development of laminitis.5 It is through this expression in the fat and muscle cells that the fat deposits develop that are so familiar in laminitic horses. Even more fundamental to the development of these fat deposits is the liver. 11beta-HSD1’s expression in the liver promotes the excess triglycerides that form the fat deposits. The Easy Keeper: Myth and Dangers article in the previous issue of NHM explains exactly how the liver creates these fat deposits in laminitic horses.
The effect of the conversion of cortisone to cortisol through the expression of 11beta-HSD1 occurs through the glucocorticoid receptor (GR). This is a molecular structure within the target cells of the liver, fat, muscle and brain that allows for selective binding of cortisol. This means that the glucocorticoid conversion process is actually a very tissue specific activity, e.g. cortisol binds to a liver cell or a fat cell. 11beta-HSD1 expression in the liver cell, for example, converts inactive cortisone into active cortisol amplifying its effect through the glucocorticoid receptor.6 This has the effect of quickly accumulating an excess of cortisol in the liver cells while rarely effecting a surplus of circulating blood cortisol.
In the liver the intensified expression of 11beta-HSD1 stimulates an increase in phosphoenol-pyruvate carboxykinase (PEPCK), the crucial enzyme that elevates glucose production. This happens through a process known as gluconeogenesis in which glucose is “made” from non-carbohydrate sources in the body, e.g. amino acids. Remember in healthy horses, this is useful when extra glucose is needed for situations such as ‘stress related activities’ that might induce a ‘fight or flight’ response, yet in laminitic horses, this is just more glucose on top of already too much. It doesn’t end there - higher levels of blood glucose are also produced through this enzymatic activity as well as all the other parameters of insulin resistance, including obesity. This strongly suggests that increased local glucocorticoid action in the liver contributes to the development of type 2 diabetes in people6 and laminitis in horses. Figure 1 graphically presents this process.
Both the hypothalamus and the hippocampus, centers in the brain, have high levels of glucocorticoid receptors allowing for the rapid conversion of cortisone to cortisol through 11beta-HSD1 expression. As both of these centers are highly sensitive to stress, the high number of glucocorticoid receptors in these areas indicates that stress is also a trigger for sustained activation of cortisol, and indeed the research indicates that glucocorticoid activation occurs within minutes of a stressful situation.7 This means that stress is a very real factor in laminitis.
Negative Feedback Loop of the Pituitary-Adrenal Glands
The negative feedback loop of the pituitary-adrenal glands is a current explanation of the metabolic breakdown in horses with Cushing’s syndrome and laminitis. This explanation describes these horses as having excess blood levels of ACTH and variable levels of cortisol, occasionally stated in excess, indicating a defective feedback loop of this system.8 Given this understanding, the laboratory blood tests that are frequently chosen to determine the presence or absence of these metabolic issues assess the concentrations of cortisol and ACTH circulating in the blood.
The evolution of this understanding of the Equine Metabolic Syndrome has been heavily influenced by the research into the human condition of Cushing’s disease. In humans, Cushing’s disease involves a pituitary gland tumor or, more rarely, an adrenal gland tumor. The tumors indeed disrupt the normal regulation of the feedback loop and certainly do produce excess blood levels of ACTH and variable levels of cortisol. However, although pituitary tumors have been reported in some elderly horses through post mortem examination, these horses had no previous history or recorded reports of any symptoms or signs of Cushing’s.9
In 1999, Johnson and Gamjam of the University of Missouri, both veterinarians and researchers, presented another model for explaining Cushing’s without a tumor based on the enzymatic activity of 11beta-HSD1 in peripheral tissue, the skin of horses. It was labeled as Peripheral Cushing’s where inactive cortisone converts to active cortisol creating cortisol excess in peripheral skin tissue though not in the blood stream.10 This 1999 veterinarians’ research might have just found the important piece, though not the site.
The Hypothalamic-Pituitary-Adrenal Axis
Circulating ‘free cortisol’, secreted from the adrenal cortex into the bloodstream, has the ability to cross cell membranes for interaction with target receptors. It is this ‘free cortisol’ that is needed at the specific target sites previously mentioned so that the horse has the correct amount of glucose to sustain the life of the body’s cells. Healthy glucocorticoid activity is occurring at these receptors ceaselessly throughout the horse’s daily life. The conversion process between cortisone and cortisol by 11beta-HSD1 dictates glucocorticoid access to receptors at the target sites.
The Hypothalamic-Pituitary-Adrenal (HPA) axis is the supplier of the circulating ‘free cortisol’ through an intricate feedback loop described as simply as possible in the following section. (Figure 2 is offered as visual assistance to the HPA axis description.) The secretion rate and concentration of this ‘free cortisol’ is regulated through the release of ACTH, a derivative of a peptide known as POMC (proopiomelanocortin) located in the pituitary gland. The hypothalamus also has a primary influence through the corticotropin-releasing hormone (CRH) that enhances the secretion of ACTH through the stimulation of POMC.
There are two other primary factors influencing the concentration of free cortisol in the bloodstream at any given time. The first of these is the circadian regulation. This refers to the daily rhythm through high and low concentration times of ACTH release and circulating cortisol. In a healthy horse these concentrations remain relatively constant. In laminitic horses the low cortisol levels are higher than in healthy horses, stimulating a continual ‘over-drive’ of the HPA axis. The second primary factor is stress.11 Both the hypothalamus and the hippocampus are acutely responsive to stressful situations as they trigger the release of CRH thereby enhancing the secretion of ACTH. This can happen within minutes of the stressful situation. These areas are activated by emotional and physical stress, including exercise that goes beyond the physical limits of the individual horse, as well as acute and chronic illness. Illness is a trigger in laminitic horses as they have compromised immune systems due to an aspect of the HPA axis known as the ‘immune-adrenal axis’. Further discussion of this issue is beyond the scope of this article, yet it is important to know that the immune involvement within the metabolic syndrome is also a consequence of the relationship of 11beta-HSD1 and glucocorticoid conversion.
As a horse owner, knowing that the root of laminitis involves sustained activation of glucocorticoids through enzymatic regulation at very specific target receptors may seem too abstract to help you help your horse. But in reality this information reinforces the absolute need to follow careful care and management practices. Because laminitic horses already have this sustained activation of glucocorticoids and the nature of the receptors is to amplify their effects, anything that increases this activity can initiate an acute episode. There are three factors in particular that are clear from this information:
1 – The introduction of any amount of glucose to a laminitic or insulin resistant or Cushing's horse through sources such as grain or sweets or sugar-rich grass sets the enzymatic process into over-drive.
2 – An oral administration of cortisone, one of the many corticosteroids given for a wide range of health problems, is rapidly activated to cortisol and so increases the blood glucose load. The effect of this drug is not new information but the mechanism of the effects can now be explained through the enzymatic activity presented in this article. “One of the side effects of corticosteroid use is laminitis which can occur following even a single dose of corticosteroid. Horses on corticosteroids commonly have an abnormally high level of blood glucose, as in diabetes.”12 Likewise, the intake of grains and sugars by non-diabetic, non-IR, non-laminitic horses on corticosteroids should be limited.
3 – Extreme emotional and physical stress activates the glucocorticoid receptors in the hypothalamus and hippocampus to trigger a release of CRH, which in turn enhances the secretion of ACTH. The results of this activity can push the system into a rapid surge of excess glucose in the blood.
The conversion of cortisone to cortisol occurs through the expression of 11beta-HSD1 at specific target sites in a horse’s body. It is through this local activity that all cells in the horse’s body receive life sustaining energy in the form of glucose. When the horse needs additional energy this enzyme ‘switches on’ to supply the increased demand for glucose. In a laminitic horse, due to the existing overload of blood glucose, this very tissue-specific action of 11beta-HSD1 sets in motion a cascading chain of events that causes laminae separation.
Please note: This laminitic model applies only to horses with a metabolic syndrome and does not involve horses that have laminae separation falling under the category of "mechanical founder".
My Treatment Strategy
So the production of excess glucose in the liver starts from the horse’s need for “extra” glucose by exactly this process where the expression of 11beta-HSD1 at individual liver cells activates cortisol production through the conversion process thereby stimulating the crucial enzyme PEPCK that makes glucose from available non-carbohydrate sources. The excess glucose produced at this moment travels to the blood and increases the level of glucose that is already circulating in the blood. All of the endocrinology research related to 11beta-HSD1 expression where excess blood glucose levels are present along with the full range of parameters involved in metabolic syndromes point to the reduction of this expression in the liver as the most promising target for reversing these diseases.
The whole horse must be considered to address metabolic disorders such as laminitis. My clinical work is rooted in Chinese medical theory that views the horse as a whole rather than a group of anatomical pieces working in isolation. In the same sense, herbal formulations, to be effective, must be created as a whole, not a combination of single herbs that perform different functions. Therefore, to arrive at an effective herbal solution to laminitis, every individual herb of the twenty-five in our Laminitis Solution is formulated to work together in concert. This formulation includes a ‘grouping’ of herbs that enable the body to reduce the expression of 11beta-HSD1 and glucocorticoid sustained activation. As is clear from the work presented in this article, this treatment strategy has a great influence on the recovery process of horses with laminitis.
For a more thorough explanation of the therapeutic properties of our Laminitis Solution read the final section of The Easy Keeper: Myth and Dangers, in the previous issue of NHM. The foundation formula is one of six proprietary Chinese herbal formulas in the Laminitis Intervention Program. This program is designed to address all aspects and stages of this relentless disease and is consistently improving the lives of laminitic horses along the entire continuum of the disease process, naturally.
Is the reversal of laminitis possible? By tracking the bloodwork of the horses using our herbs, over an extended period of time, we are observing changes that are highly indicative of recovery. The elevated glucose is lowering and returning to a healthy range and there is a concomitant elevation in serum insulin (prior levels were low normal) indicating a recovery of pancreatic beta cells. This result alone, recorded in many horses, not only implies beta cell function recovery but also demonstrates empirically the important theoretical findings described within this article.
© Copyright Joseph Thomas, PhD
1. Crystal structures of 11beta-hydroxysteroid dehydrogenase 1, an important therapeutic target for diabetes. Jianjong Zhang, Obesity and Diabetes Week, July 25, 2005.
2. Clinical diagnosis and management by laboratory methods. J.B. Henry MD, W. B. Saunders Company.
3. The relationship between natural hoof wall growth and laminitis. Joseph Thomas, PhD, Natural Horse (2005) Vol 7 Issue 5
4. Increased expression and activity of 11beta-HSD-1 in diabetic islets and prevention with troglitazone. Dyplomb, L. et.al. Biochemical and biophysical research communications; 313 (2004)
5. Glucocorticoids and 11beta-hydroxysteroid dehydrogenase in adipose tissue. Seckl, J.P. et.al. (2004) Rec Prog Horm Res 59.
6. Minireview: 11beta-hydroxysteroid dehydrogenase type 1 – a tissue-specific amplifier of glucocorticoid action. Seckl, J.R. & Walker, B.R. Endocrinology (142)4, 2001.
7. Glucocorticoids, ageing and nerve cell damage. Seckl, J.P. British Society for neuroendocrinology, 2006
8. Equine metabolic syndrome: explanations and possibilities. Joseph Thomas, PhD. Holistic Horse, 2004, Vol 10, Issue 37
9. Equine internal medicine, S.M. Reed, et.al. (2004) Saunders Company.
10. Laminitis, hypothyroidism and obesity: a peripheral cushingoid syndrome in horses. Johnson, P.J., Gamjam, V.K. Proceedings of the seventeenth annual forum of the American College of Veterinary Internal Medicine, Chicago, 1999
11. Principles of Internal Medicine, Vol 11, 16th edition, Kasper, D>L> MD, et.al. 2005, McGraw-Hill.
12. Equine Drugs and Vaccines, Eleanor M. Kellon, V.M.D., Breakthrough Publications, 1995.
November 25, 2010 17:10
IR – Insulin Resistance: What is it really?
Joseph Thomas, Ph.D.
Insulin Resistance (IR) is a commonly used and poorly understood term. Mostly, horse people associate it with “hard, cresty necks,” fat deposits on the rump and shoulders, excess weight, Cushing’s syndrome, and the threat of a laminitic episode. Past these external signs and symptoms though, what is it really?
The concept of Insulin Resistance was first introduced in 1939 as a way to explain why cells become increasingly unable to use glucose in “diabetes mellitus” [Type 2 diabetes]. Cells need to consume glucose to survive and insulin provides the “push” for glucose to be “taken up” by cells. But, researchers found that in Type 2 diabetes, cells are less capable of taking up the glucose they need and that this inability is related to a decrease in insulin’s ability to “push” glucose into the cells. So the term “Insulin Resistance”, now commonly called just IR, was coined to describe the notion that in Type 2 diabetes there is a “resistance” to insulin mediated glucose utilization. Insulin resistance has been studied intensively in human research over the last seventy years and it is now understood to be the root of the metabolic syndrome that frequently results in Type 2 diabetes.
Equine research has demonstrated that the IR process is identical in horses except that they have the additional consequence of laminitis. Insulin resistance in both humans and horses starts the metabolic syndrome course and it is considered to be the root of the disease process; in horses this process is generally referred to as the Equine Metabolic syndrome (EMS). It is widely accepted in human research that IR and the metabolic syndrome are genetically determined and this is becoming increasingly more accepted in the equine research world. Understanding that IR is genetically activated explains why it so often cannot be controlled just by diet and exercise.
It is important to understand that Insulin resistance is an interactive process that escalates. Basically, this is how it works. Once insulin resistance starts, the horse’s body attempts to compensate for the cells becoming less “sensitive” to insulin’s action by increasing the amount of insulin produced. Insulin is secreted from the beta-cells of the pancreas. When IR begins these beta-cells are called on to secrete increasingly more insulin to make up for the resistance and get the needed glucose into the cells.
This compensation in the insulin secretion level by the beta-cells occurs so that the glucose level in the blood is maintained within the “normal” range. The assumption is that if the blood glucose level is “normal” then the appropriate quantity of glucose is entering the cells.
The problem is that even though the glucose level is considered normal the horse’s physiology, i.e. the beta-cells of the pancreas, is now at a place where it takes a much higher concentration of insulin in the blood to push the same amount of glucose into a cell. At this point a horse will be diagnosed as having “compensatory hyperinsulinemia” (high blood insulin levels) and the risk of laminitis begins.
Some of these IR horses are going to reach a place where their pancreatic beta-cells become exhausted and can no longer maintain the necessary “drive” to keep glucose within “normal” limits. For these horses glucose becomes elevated in the blood and they can then be diagnosed as having Type 2 diabetes with the classical definition of elevated blood glucose levels. If blood glucose levels are high, i.e. above normal concentration, then the glucose available for cellular use is deficient and inadequate to meet the needs for their health. Every increase in the severity of insulin resistance and compensatory changes in organ function brings a greater risk for laminitis and associated pathologies.
The familiar signs and symptoms of a horse at risk for laminitis; “hard, cresty neck” and fat deposits on the rump and shoulders stem from this internal process. Once Insulin Resistance has begun, the consequences of the metabolic syndrome that is set in place includes not only the increased risk of laminitis but also decreased immune function, vascular issues, a variety of categories of anemia, and gastrointestinal problems.
Obese horses have IR and contrary to popular opinion non-obese horses also have IR; the external signs and symptoms are merely an “outside” expression of the progressing underlying disease process. “Proper” diet and exercise are necessary for these horses, just like it is for people with the metabolic syndrome and diabetes but, diet and exercise will not reverse the course of this disease. Good/healthy care and management practices are an important part of decreasing the “trigger” aspect of an acute laminitic episode but are not always enough to prevent these damaging and painful experiences from occurring.
Laminitis is a consequence of the above described disease process and not the disease itself. You may well be able to recover the damaged hoof, and you should, but if you don’t effectively treat the root issue of insulin resistance leading to the Equine Metabolic Syndrome [EMS] your horse will have another laminitic episode.
November 25, 2010 16:57
The Relationship Between Natural Hoof Wall Growth and Laminitis
by Dr. Joseph Thomas
Printed in: Natural Horse Magazine
Volume 7, Issue 5
Laminitis is a dynamic molecular process superimposed on normal biology. Many of its features are normal processes appearing at the wrong time and place. - Dr. Christopher Pollitt
Laminitis is the second most-common killer of our horses (colic is first). “Fifteen percent of horses in the United States are estimated to be affected with laminitis over the course of their lifetimes, and seventy-five percent of these horses develop severe or chronic lameness and debilitation that necessitates euthanasia." 1
It is imperative we understand that laminitis is not a disease of the hoof. Until that is clear we will just continue to prolong the misery of our horses and misuse potential treatment time with ineffective protocols. By definition, laminitis is the breakdown between the laminae connection of the inner hoof wall and the coffin bone. This definition, though quite accurate, gives us nowhere to go to find help for our horses. The true complication about laminae separation is that, although it occurs in the hoof, it is actually the end result of a number of metabolic processes. Laminitis enters the developmental stage as soon as these processes have been set in motion by a triggering event, and that happens long before any lameness or hoof pain is evident.
In large part, the confusion about the cause of this disease comes from the vast array and apparent disparity of the triggering events. In a recent study, gastrointestinal tract diseases, such as colic, inflammatory bowel disease, enteritis, and colitis were found to be the primary issue in 54% of the horses that developed acute laminitis. Grain overload, grass founder, mechanical overload due to trauma in a contralateral limb, Cushing’s Disease (Equine Metabolic Syndrome), retained placenta, pleuropneumonia and other illnesses accompanied by the release of endotoxins (a toxin produced by certain bacteria and released upon destruction of the bacterial cell) can also result in laminitis. In addition, laminitis can be induced by the use of a number of medications including corticosteroids, such as dexamethasone and prednisone. Finally, it is also clear that a laminitic episode can occur with no apparent cause. What we do know is that once a triggering event has occurred, before there is any indication of foot pain, the process leading to laminae separation has begun. The actual time between the onset of the developmental stage and the acute stage, where pain and lameness are evident, varies by cause. In the case of grass founder, it may be forty to forty-eight hours between the laminitic trigger and the acute stage, whereas a horse that has ingested a toxic plant could be lame in twelve to twenty-four hours, depending on the plant. This means that given a triggering event, we cannot wait for a “clear” diagnosis for our horse’s lameness to prevent or limit laminae damage.
Effective intervention requires knowledge, and several researchers have committed their talents over many years to develop the body of information we now have available to combat laminitis. Dr. Christopher Pollitt, BVSc, PhD, Director of the Australian Equine Laminitis Research Unit at Queensland University is associated with the most advanced research and understanding of laminitis. As he states, the focus of his work has been“primarily on the cause, pathophysiology and developmental stages of laminitis.”The following is a summary of the results of the many years of devoted research, conducted by Dr. Pollitt, into understanding the hoof’s anatomy and growth as well as the molecular processes that eventually result in laminae breakdown.
Hoof Wall Growth and Matrix Metalloproteinase (MMPs)
The direction of hoof wall growth is from the coronary band down to the ground. One of the most amazing features of the laminae that attach the hoof wall to the coffin bone is that they are able to adjust in such a way as to allow this growth and yet keep the coffin bone suspended perfectly in place. This is due to MMPs, which are enzymes that maintain and control the necessary ‘remodeling’ of these laminae by precise quantitative release. MMPs influence the inner hoof wall laminae's ‘timed’ separation from the coffin bone to allow this 'growing down' process, therefore it is essential for healthy hoof wall growth that MMPs are meticulously regulated. The MMP release must stop at the correct moment, shutting off the laminae separation progression, so that the laminae rejoin and the coffin bone remains suspended correctly. This miraculous moment in time occurs by the release of another enzyme called “tissue inhibitor”.
Common Causes of Laminitis
Whatever the triggering event, the unregulated release of MMPs is the central mechanism of any laminitic episode. When this “floodgate” release occurs, it overrides the intervention of the “tissue inhibitor” enzyme. As a result, some laminae permanently detach and other laminae stretch. This loosens their hold on the coffin bone and allows it to rotate.
The development of laminitis through grain overload and grass founder demonstrates this process clearly as they both stem from the ingestion of a high concentration of sugars, and that results in the uncontrolled release of MMPs. It is not the grain per se that is the problem but the overload of grain. In the same sense, it is not the grass but the concentration of fructans (complex sugars) in the grass that overload the horse's system.
Certain environmental conditions increase the concentration of sugars in pasture grass. The most familiar are seasonal, such as spring and fall. This is the reason that “easy keepers” and horses with a propensity or history of laminitis are put in a dirt lot and given hay for the duration of these seasons. This method has been used by generations of horse-people, long before anyone knew of the relationship of founder and fructan ingestion. Other conditions that may not be so familiar are cold nights that approach freezing, followed by sunny mornings. These conditions dramatically increase the manufacture of high concentrations of sugar in the grass stems. Stressed pasture grass rather than lush pastures are much higher in fructan content. These are just a few environmental conditions that generate fructan levels that can achieve a laminae separation trigger episode. And horses do love fructans – they are beasts with an “incredible sweet-tooth".
The MMP problem with fructans is that they are not metabolized in the small intestine due to the lack of necessary digestive enzymes. Rather the fructans become quickly fermented in the hindgut (colon) resulting in a bacterial population change with a considerable increase in the acidity of the contents of the colon. The bacteria are known as Streptococcus bovis and grow in excess at the expense of the healthy colon bacteria (Enterobacter species). This bacterial exchange along with the rise in acidity damages the hindgut lining, releasing toxins into the bloodstream. When these toxins reach the laminae attached to the inner hoof wall, they trigger an uncontrolled release of MMPs, initiating a laminitic episode that separates the laminae suspending the coffin bone.
The Involvement of Circulation in Laminitis
Dr. Pollitt and his colleagues needed to explain how trigger factors reach the laminae and to clearly define the “floodgate” that brings about an uncontrolled release of MMP’s. Vasodilation (blood vessel expansion, which thereby increases circulation) of the hoof is present during the developmental stage of laminitis giving the toxins released from the colon an accelerated entrance to the laminae of the hoof. In the same research study, hoof vasoconstriction (blood vessel contraction, which decreases circulation) was shown not to produce any laminitic triggers. In fact, vasoconstriction was found to be a feasible protective situation in later studies.
Dr. Pollitt used cryotherapy (the use of cold temperatures as medical therapy) to constrict blood vessels, as a procedure to prevent the uncontrolled release of MMPs during a laminitic triggering, such as fructan ingestion and grain overload. Cryotherapy was applied in the developmental stage prior to any display of lameness or pain. The results of this study are exciting for the development of an effective course of treatment. The limbs that were cooled displayed no lameness, while lameness was evident in the uncooled limbs. The MMP concentration was dramatically less in the hoofs that received cryotherapy treatment and were actually close to normal levels. In this study, the temperature of the cold limb was kept at approximately 41˚F. For practical application a solution of half water and half ice will work to get the results.
The use of cold is a recognized method of slowing metabolism and constricting blood vessels, which slows down the flow of blood to the areas of the body that are affected by the decrease in temperature. Slowing down the blood to a hoof during the developmental stage will reduce the trigger factor of the toxic invasion from the damaged lining of the hindgut and reduce the concentration of the trigger factors in general.
The Glucose Connection
Glucose is the principle circulating sugar in the blood and the major energy source of the body. The “uptake of glucose” refers to the cellular utilization of this sugar source by the literal entry of glucose into cells. This is necessary for the function of the body’s cellular existence. Laminae basal cells deprived of glucose are unable to “hold up” under the tremendous weight of the horse, which is likely to bring about laminae separation and coffin bone rotation. Not all horses that experience a laminitic episode have a glucose uptake problem, but horses with a metabolic dysfunction between the pituitary gland and the adrenal glands DO have compromised glucose uptake. The feedback loop between these organs is functioning improperly and as a result there is an overabundance in the bloodstream of the adrenal glands’ hormone, cortisol. This hormonal excess causes many health issues for the horse, but most importantly here it is directly responsible for breaking down insulin’s most important function of “pushing” glucose into cells.
Some of the health issues that have this dysfunction are Cushing’s disease, obesity where there is an inability to satisfy metabolic energy and hormonal balance, issues that directly affect the liver such as high triglycerides or fatty infiltrations of the liver, infections, and toxins in the blood.
Gastrointestinal overload of fructans is a situation where glucose uptake is compromised and the uncontrollable release of MMPs is activated concurrently. Many of the other metabolic disorders mentioned and not presented in this article are also likely to be MMP activators. There is a lot to be learned.
What is clear, however is that treatments designed to assist peripheral (to the extremities) glucose uptake, and also inhibit laminae MMP activation, may both prevent and help with recovery from a laminitic occurrence.
During the developmental stage of laminitis, there is an increased flow of blood to the hoof carrying toxins that have developed from a variety of causes, including gastrointestinal diseases, fructan abundance, retained placenta, and medications, all examples of laminitic triggers. This vasodilator process leads to an uncontrolled release of MMPs that causes laminae separation. The metabolic dysfunction causing glucose deprivation in the hoof produces the same end result. Both in the majority of laminitic cases conditions must be dealt with as early as possible after a laminitic trigger to limit the damage to the horse. For immediate intervention, the application of cold (half ice and half water) to the affected limbs is an effective possibility.
Over the last ten years I have been steadfastly absorbing the laminitis and hoof wall growth information as it became available for purposes of creating effective herbal solutions for the different stages of laminitis. Visit www.forloveofthehorse.com to review the therapeutic intervention possibilities of sophisticated Chinese herbalism and the practical potentials to treat and prevent the metabolic, MMP overload, pain and chronic issues associated with this dreaded disease.
In a follow-up article I will provide strategies for naturally preventing, managing, and possibly reversing some of these conditions. The process of formulating a sophisticated herbal blend based on Chinese medical theory integrated with western pathology will be presented in line with this issue.
About the author:
Joseph Thomas, PhD has been a practitioner, teacher and consultant in Chinese medicine for more than twenty years. Prior to that Dr. Thomas was a researcher at MIT’s Department of Psychology and Brain Science investigating the development of single cells during congenital eye diseases. He put both these skills together with his love and knowledge of horses and developed www.forloveofthehorse.com, along with his wife and their daughter. For Love of the Horse is a Chinese Herbal Solution company where precision and sophistication of proprietary formulations provide you with effective choices, results, and integrity of service.
The Second International Equine Conference on Laminitis and Diseases of the Foot and the 2003 American Association of Equine Practitioner Annual Conference
Equine Vet J; 27: 364-367, 1995 “Descriptive Epidemiological Study of Equine Laminitis” Slater MR, Hood DM, Carter GK
November 23, 2010 16:00
by Dr. Joseph Thomas, PhD.
Printed in: Natural Horse Magazine
Special Features Section
Volume 8, Issue 4, 2006
Easy Keeper has become such a common term in the horse world that when it’s used a majority of horse people quickly visualize a fat horse with a cresty neck and a rump full of fat deposits. Promptly on the tail of this image is the apparently correct interpretation that this is a horse primed for laminitis.
As horse owners, we are advised to get that weight off fast by severely limiting food intake as though just over feeding them is the cause of the weight condition. This is a dangerous misconception because these horses aren’t just fat and prone to laminitis because of their weight. Actually, an Easy Keeper is a horse with a metabolic disease primarily involving the pancreas and liver that interferes with the digestion and absorption of fats and free fatty acids. These horses have distinct blood work profiles that closely resemble people with Type II Diabetes who also have the identical issues with fat absorption. Until the metabolic problem is dealt with at the source of the disease the Easy Keeper is always going to be an Easy Keeper and taking this horse’s food away is not only cruel it is dangerous.
Laminitis and the Type II Diabetes Connection Laminitis is a metabolic disease that has striking similarities to Type II diabetes mellitus. This is the type of diabetes that does not necessarily require insulin shots but rather comes later in life and is usually controlled by diet and glucose lowering medications. By definition, “Diabetes mellitus (DM) is a group of diseases in which blood glucose levels are elevated because of deficient insulin and/or abnormal insulin action.” Laminitis, according to the insulin resistant (IR) model, also has elevated glucose in the bloodstream yet is considered to have elevated insulin as well.
My research has shown that in the very early stages of both laminitis and DM, insulin is elevated with an associated decrease in glucose levels. As the diabetic process progresses, and during the IR phase of laminitis, the pancreas continues its insulin secretion, injuring and killing off the beta cells (the cells in the islets of the pancreas that secrete insulin) by overstimulation, eventually leading to either normal or decreased levels of insulin and increased levels of glucose in the blood. This insulin deficiency and blood glucose excess leads to both DM in people and laminitis in horses.
This diagram shows the progressive pattern of blood test results and the associated symptoms for Laminitic horses and people with Diabetes Mellitus given no regulation of diet and no glucose lowering intervention. The Results presented are relative ranges taken from the author’s patient records and the blood work profiles of horses benefiting from Dr. Thomas’ Chinese herbal Laminitis Intervention Program. These are relative rather than absolute values that represent patterns derived from the blood work panels analyzed. Click on Chart to Enlarge
A primary function of insulin is to impel glucose into all the cells of the body to provide life sustaining energy and nourishment. When there is too much glucose in the blood stream, there is not enough getting into the cells. In horses that means the laminae cells as well. The glucose starvation of these cells results in the separation and stretching of the laminae with likely coffin bone rotation.
The Liver’s Involvement in the Creation of the Easy Keeper In both laminitis and DM the metabolism of fats and carbohydrates, a function of the liver and pancreas, is seriously impaired. The liver is the largest organ in the horse and, though rarely talked about in laminitis, it is the most important site for the formation of glucose and storage of glycogen, which readily converts to glucose as needed by the body to satisfy its energy needs. Under the influence of insulin and a hormone produced by the pancreas, the liver also regulates plasma glucose concentration.
Given that blood glucose is elevated due to carbohydrate metabolic dysfunction, the liver attempts to regulate this excess through the synthesis of carbohydrates into a neutral fat known as triglycerides. Essentially, these fats function as storage units for excess glucose and carbohydrates. As they are filled and more are produced in the liver, triglycerides become elevated (blood test reference range of high normal to above normal). When this happens, the triglycerides transform the liver into a fatty state that then pumps out fat globules to the muscles in the form of fatty cysts. These fat cells then become enlarged and more resistant to insulin’s influence. They eventually end up in the adipose [fat] tissue of the body giving a swollen appearance and the familiar cresty neck, fat deposits in the rump, shoulder area and above the horse’s eyes.
Bile and Intestinal pH Another important function of the liver is the secretion of bile. In people bile is concentrated in the gallbladder before pouring into the small intestine. Given that horses do not have a gall bladder the liver’s bile duct empties directly into the small intestine. The importance of this information is that bile is responsible for making the contents of the small intestine more alkaline, i.e. less acidic.
The most reliable blood test for liver function assesses bilirubin (the orange-yellow pigment in bile) in three aspects: total bilirubin, direct bilirubin and indirect bilirubin. My research has shown a clear pattern in these test results in laminitic horses: Total bilirubin tends to be low and direct bilirubin tends to be high. Given this bilirubin pattern, the bile duct is always affected because direct bilirubin rises from interference with the flow of bile from the liver. This means that the flow of bile is impaired in these horses.
So with less bile, the small intestine becomes more acidic. Given a familiar laminitic trigger, a fructan (sugar) rich pasture, and a horse with a predisposition towards laminitis in this pasture, this information on bile’s pH becomes more than important.
Currently, it is understood that the small intestine does not contain the appropriate bacteria to assimilate fructans. Accordingly, the fructans, unable to be digested in the small intestine, move on their digestive path to the hindgut (colon) where they quickly ferment. During this fermentation process, the lining of the intestine is damaged with an accompanying drop in pH thereby creating an acidic environment. In the course of this process, toxins are released into the bloodstream. When they reach the hoof and meet with expanded blood vessels, the toxins are expedited to the inner hoof wall releasing a floodgate response of MMP’s (matrix metalloproteinases, an enzyme), resulting in separation and stretching of the laminae.
The bilirubin profile apparent in my research shows that there is an acidic environment in the intestines due to a liver bile dysfunction that is an unrecognized component of the pre-existing metabolic syndrome. Depending on the magnitude of the direct bilirubin elevation, which is another way of saying depending on the relative severity of the individual horse’s metabolic syndrome, the intestines are already proportionally acidic relative to the bile problem. With a comparatively low pH already present before the horse ingests that lush grass, the drop in pH from the hindgut must have an even greater impact on the subsequent chain of events.
Metabolic Acidosis: The Danger Behind the Myth The traditional advice from well-meaning horse people is to seriously restrict the food of Easy Keepers. Clearly it is important to limit their intake of carbohydrates, grains and fructans, but to limit their intake of hay is not advisable. These horses are heavy due to their underlying metabolic condition, similar to the obesity often associated with Type II diabetics. If you deprive them of enough food to lose weight rapidly, not only does it not affect the underlying physiological cause of the weight problem, it also may put them at risk.
All horses have a standing pool of hydrochloric acid sitting in the lower stomach. The evolutionary purpose of this pool of stomach acid is to assist in digestion as horses by their nature are foragers and therefore eat most of their waking hours. When they do not eat, this acid is not absorbed. For horses with a metabolic syndrome, whether laminitis or Cushing’s, who already have acidic intestines, this situation can become critical.
There is a pathological condition called acidosis that results from the accumulation of acid or the depletion of the alkaline reserve (measured by a blood test called Total Bicarbonate - low in laminitic horses). By dramatically reducing the horse’s diet to a point nearing starvation, the horse’s body starts metabolizing their own fat stores very rapidly, breaking them down to fatty acids. This creates a highly acidic environment resulting in something referred to as metabolic acidosis. This is very similar to the Acidosis resulting from ‘uncontrolled’ DM. In both instances, large quantities of ‘ketone bodies’ (three acidic substances that are produced by fatty acid and carbohydrate metabolism in the liver) collect in the urine and tissues of the body, depleting the bicarbonate reserves that are to keep the pH alkaline. Metabolic acidosis occurs in horses from both ‘starvation’ and a progressively ‘uncontrolled’ metabolic disease.
A horse or person in metabolic acidosis can become comatose and die, preceded by severe respiratory difficulties. It is unknown how many horses die in this manner as it is often misdiagnosed. It may not be frequent, but metabolic acidosis in horses occurs more often than is known or talked about – one horse is too many.
Management The point of drawing your attention to the similarities between diabetes and laminitis is to underline the importance of understanding laminitis as a metabolic disease. Horses with laminitis or Cushing’s live along a continuum within the disease process. There are horses that seem to always be on the edge of an episode yet never move into full-blown lameness and other horses that end up with coffin bone rotation in the dead of winter without any apparent trigger. Similarly, some people with DM can control their disease merely by diet regulation while others must use diet and hypoglycemic medications (drugs to lower blood glucose) of varying magnitudes. For both, the management of the disease is a way of life. As long as a horse has a propensity towards this disease, excess glucose in the blood is going to go along with glucose deprivation to the laminae. Whether through some external or internal trigger the end result is going to be laminae separation and stretching and no amount of hoof anti-inflammatory treatment is going to cure this disease – the source of this disease is presented in the horse’s blood work and not in the hoof.
Through my research on laminitis and my twenty-five years experience in Chinese Medicine, I have developed a program of herbal formulas (Laminitis Intervention Program) which is designed to change the course of the patterns described. Each herb used in these formulas has been prepared with pharmacological precision and has been chosen for its unique qualities and contribution to the overall effectiveness of the formula.
My work is rooted in Chinese Medical Theory which views the horse as a whole rather than a group of parts working in isolation. In the same sense, my herbal formulas are created as a whole, not just a combination of single herbs that do different things. Therefore, to effectively arrive at an herbal solution to laminitis, every single herb of the twenty-five in the formula must work in concert. Individual herbs were chosen for their intricate functions, the way they relate to one another and their impact on the involved organ system. For example, in the foundation formula there is a group of herbs that work together with the liver and pancreas to improve the digestion of carbohydrates, decrease blood glucose levels, and improve the insulin-glucose connection. Another group of herbs, in this same formula, improves bile secretion from the liver thereby decreasing the acidity of the intestinal contents and raising the pH of the intestines, making them more alkaline. This is only a brief description of the conceptual framework of the formulation process and is in no way representative of the entire picture.
This program of proprietary Chinese herbal formulas is consistently improving the lives of laminitic horses along the entire continuum of the disease process as it has been presented in this article.
About the author:
Joseph Thomas, Ph.D. has been a practitioner, teacher and consultant in Chinese medicine for more than twenty years. Prior to his commitment to Chinese medicine Dr. Thomas was a researcher at the Massachusetts Institute of Technology engaged in medical research. He joined these skills together with his love of horses and developed For Love of the Horse, LLC along with his wife and daughter.
Acknowledgement: I would like the reader to be aware that this article would not have been possible if not for the editorial skill and countless discussions with my wife Crystal Leaman: general manager, editor and chief of For Love for the Horse.
Fatty acids and insulin resistance in muscle and liver. P. Kovacs, M. Stumvoll. Best Pract Res Clin Endocrinol Metab. (2005)Dec;19(4):625-35.
Clinical diagnosis and management by laboratory methods. J.B. Henry, MD, W.B. Saunders Company.
Equine internal medicine; S.M. Reed, W.M. Bayly, D.C. Sellon. (2004) Saunders Company.
Decreased glucose metabolism causes separation of hoof lamellar in vitro: a trigger for laminitis. M.A. Pass, S. Pollitt, and C.C. Pollitt; Equine Vet J Suppl (26)(1998)133-138.
Dysfunctional fat cells, lipotoxicity and type 2 diabetes. R.A. DeFronzo. Int J Clin Pract Suppl (2004)Oct(143):9-21.
The relationship between natural hoof wall growth and laminitis. Joseph Thomas, PhD. Natural Horse Magazine (2005)Vol 7, Issue
November 16, 2010 15:41
Take the Guesswork Out of Predicting Laminitis
by Dr. Joseph Thomas & Crystal Leaman
Printed in: Natural Horse Magazine
Volume 11, Issue 6
Equine Cushing’s Disease (ECD), Equine Metabolic Syndrome (EMS), and Insulin Resistance (IR) are three primary diagnoses associated with the risk of laminitis (defined as laminae separation and/or stretching). If your horse has been diagnosed with any one of these, he is at risk for laminitis. But do you know how much of a risk, and can you tell if or when your horse is actually going to have laminitis? Does one of these diagnoses imply more risk than another?
Careful management of your horse’s diet and exercise are used to limit risk, but when the degree of metabolic dysfunction is unknown, the prediction of laminitis is merely guesswork. Neither the diagnosis nor the external signs and symptoms can give a clear enough assessment of your horse’s particular health problems to predict laminitis.
But, fortunately, there is a simple, minimally invasive procedure that can: a blood chemistry report, or blood work. A good blood work report not only yields a predictive index of your horse’s risk for laminitis but also offers a comprehensive picture of the other health issues that accompany these metabolic dysfunctions. While watching the external signs and symptoms is important for daily safeguarding, only through blood work is it possible to track the progression or recovery of the underlying metabolic process with accuracy.
Predicting Laminitis: Familiar signs and symptoms vs. blood work profile
Familiar signs and symptoms:
Fat deposits in the rump, over the eyes or on the shoulders, a cresty neck, “hay belly,” polyuria, (urinates a lot), polydypsia (drinks a lot), long curly thick coat that doesn’t shed “properly” are the most familiar. Some of these signs and symptoms may be present in a horse regardless of the diagnostic label. All of them can indicate metabolic dysfunction but none of them are directly indicative of an impending laminitic episode. By themselves these “external” signs and symptoms do not have significant predictive value.
Blood work profile:
Blood work profiles offer an effective and affordable laminitis predictor. Since blood chemistry reports have become more common as a diagnostic tool for the field vet., specific blood tests have been chosen as “standards” to determine metabolic dysfunction related to the risk of laminitis. The blood tests that are used as indicators of predictive value are ACTH (adrenocorticotropic hormone of the pituitary gland), T4 (a thyroid gland hormone), cortisol (a glucocorticoid secreted by the adrenal gland), and insulin (a protein hormone secreted by the beta-cells of the pancreas).
A recently published and well designed research study investigated, for the first time, whether these specific blood tests are correlated with laminitis. 1 The results were strikingly clear. Elevated insulin levels were “highly” correlated with laminitis: the more elevated the insulin concentration, the more likely a laminitic event would occur and the greater the damage there would be to the hoof. This was found in the study’s ECD horses as well as the EMS horses since all had elevated insulin levels. Although the study divided horses into ECD and EMS as diagnostic groups, the results demonstrated that IR was the underlying issue common to each group. IR is defined, through blood work, as “normal” serum/ blood glucose (euglycemia) and elevated serum insulin levels (hyperinsulinemia).
All of the horses studied were either currently laminitic or had a history of laminitis. The ECD horses all had elevated ACTH levels; none of the EMS horses did.
The ECD horses were given daily pergolide treatment for twelve months to analyze the results of lowering ACTH levels on laminitis risk and hoof damage. ACTH levels lowered within the first week of pergolide administration and then remained constant for the rest of the twelve months of giving this drug. There was no correlation between the ACTH reduction and laminitis risk nor did lowering ACTH levels influence the magnitude of hoof damage. The risk of laminitis remained highly correlated only with elevated insulin in all horses despite the initial drop in ACTH levels.
T4 levels had a weak inverse relationship with insulin; i.e. higher insulin correlated with lower T4 levels but T4 changes also did not correlate with laminitis, nor did “fluctuations” in cortisol levels.
The Relevance of Insulin Resistance and a Comprehensive Blood Chemistry Report
IR was the primary connection between all ECD and EMS horses in the research investigation since every horse in these two groups had elevated insulin levels. IR is known to be a progressive metabolic dysfunction. 2 As IR progresses, a number of health problems other than laminitis develop, e.g. immune deficiencies, vascular difficulties, anemia, gastrointestinal disorders, and acid-base disorders (involving extremes of pH). The only way to detect these health problems is through a comprehensive blood work profile: a CBC with differential count, a complete liver panel including serum glucose, and serum insulin. The common tests have no predictive value; these have predictive value and much more.
What are the practical applications of this study’s results?
The most essential point to be taken from this investigation is that testing for insulin levels through blood work is the only predictive test, of the ones investigated, for laminitis and the extent of associated hoof damage. It was also found that the severity of laminitis, i.e. hoof damage, decreased with decreasing insulin levels, making it imperative to determine as early as possible the baseline insulin level.
Because all EMS horses and half the ECD horses had a cresty neck and the combined group had elevated insulin levels, a cresty neck may be considered an “associated” indicator of laminitis risk. As horses without a cresty neck also had elevated insulin levels, a cresty neck cannot be considered an accurate predictor in and of itself.
Blood work should be done whenever a horse is considered to have IR and this should be done as early as possible, hopefully before a laminitic episode. Any and all the signs and symptoms are considered worthy of getting blood work for a horse. Follow up blood work should then be done every six months to examine the progress or recovery of the IR course.
If a horse “lives” at the very early aspect of IR, it is quite possible to reverse the IR course through the correct diet and movement program just as it is in humans. When a horse is beyond this early phase, the only method I know that has an effective track record is my herbal solution program appropriate for that horse’s degree of IR.
Laverne’s Recovery: An example of the benefits of a comprehensive profile
Laverne had been unable to stand for weeks following an acute laminitic episode. The sores seen on her right hip area in Photo 1 are a result of Laverne not being able to get up or roll off her right side.
Her owner, Linda, asked her vet to do a complete blood chemistry report including the test panels previously described in the Relevance of Insulin Resistance section and requested an analysis of the findings from the author. The blood work showed that Laverne was suffering from not only IR but also a life threatening acid-base disorder referred to as a high-anion gap metabolic acidosis (a category known as lactic acidosis) brought about through oxidative “stress” (deficiency of oxygen) in the most severely damaged hoof.3
In addition she had a massive bacterial infection stemming from her hip sores and the hoof abscesses that followed the laminae separation. These serious and painful consequences had suddenly progressed Laverne’s IR to a level where her glucose was significantly elevated (hyperglycemia), which is medically defined as type 2 diabetes. Along with her hoof oxidative “stress” was a change in the viscosity (thickness) of her circulating blood, depriving her hoof of necessary blood and nutrients; further complicating her prognosis.
From this information the author was able to recommend an initial program of select Chinese herbal solutions and Linda began administering them immediately. Within three days Laverne got up and remained standing. The author recommended follow up blood work profiles and made adjustments in his herbal solution program for Laverne based on the findings in these subsequent blood panels and ongoing communication with Linda.
Photo 2 was taken five months and one week after Photo 1 and all of Laverne’s blood work abnormalities were now within the healthy normal range and she was up and about with quality of life.4 The blood work no longer displayed Type 2 diabetes or IR.
The information obtained from the series of comprehensive blood work reports was indeed very beneficial.
1. Correlation of Plasma Insulin Concentration with Laminitis Score in a Filed Study of Equine Cushing’s Disease and Equine Metabolic Syndrome. Walsh, D.M., McGowen, C.M., McGowen, T., et.al. Journal of Equine veterinary Science, Vol 29, No 2, p 87-94, (2009).
2. Insulin Resistance and Insulin Secretory Dysfunction are Independent Predictors of Worsening of Glucose Tolerance During Each Stage of Type 2 Diabetes Development. Weyer, C., Tataranni, P.A., Bogardus, C., Diabetes Care, Vol 24, No 1, p 89-94, (2001).
3. Clinical Biochemistry of Domestic Animals. Academic Press, Kaneko, J.J., Harvey, J.W., Bruss, M. L., p 585-516, (1997).
4. Laverne’s blood work information was taken from the author’s data base of approximately three hundred blood chemistry reports for horses labeled ECD, EMS, IR, and/or laminitis.
August 30, 2010 12:54
Arena footing is made of three distinct layers.
- Sub-base and base material characteristics are similar to that of hard packed material used in road construction. Construction of the sub-base consists of removing the topsoil and compaction of the ground until it is near maximum density.
- The base is constructed of a 4"-12" layer of crushed stone screenings that is compacted and leveled. The result is a solid, impenetrable, non-slippery foundation that will support the surface footing material and allow water drainage.
- Footing is the surface that the animal moves over and through.
Characteristics of Desirable Footing:
- To minimize concussion
- Intermediate shear resistance
- Medium level of impact resistance
- Provide traction
- Not slippery
- Dust Free
- Resistant to freezing
- Cost effective
- Low maintenance
- Abrasiveness of material
To achieve the above characteristics footing needs to by subangular [*1}. A desirable material is cleaned [*2], screened [*3] medium to coarse, hard [*4], sharp sand.
Medium grains (0.25-0.5 mm) and coarse grains (0.5-1.0 mm).
[*1] Subangular - Subangular particles have already had the sharpest corners broken off so they do not fit as tightly together and provide the larger void spaces between particles.
[*2] Cleaned - material has been washed of silt and clay.
[*3] Screened - material has had large, undesirable particles removed.
[*4] Hard - quart sand, subangular sand having sharp particles, obtained from a quarry, will last up to 10 years.
[*5] Compaction occurs when the voids between particles fill with smaller particles, thus "bridging" the matrix of particles together.
Footing material particles should be of similar size to reduce compaction.
Sand can have 5-10% of fines (more will cause sand to become dusty, and to become slippery when wet).
Adding topsoil should be limited to 10-30% of the mixture.
Depth of footing material should begin at 2", adding 1/2" at a time to the desired depth.
Addition of a waterholding material (wood product or commercial additive) reduces dust.
The intended use of the arena will determine the amount of stability required within the footing material and the thickness of the footing material.
Optional Footing Material:
1. Rubber material
- adds cushion to surface
- provides stability when added to sand footing.
- does not degrade like a wood product but does break down into smaller pieces because of grinding action
- too bouncy
- high heat retention (outside arena)
- heavy rainfall/flooding causes rubber to separate out of the footing material.
- reduces glare (outside arena)
- readily available
- good traction
- subangular particles
- common material
- good stability
- drains well
- attractive surface
- requires regular watering and harrowing
- can be very dusty if not maintained regularly
- not desirable due to compaction
- dust problems
- can be very slippery
5. Stall Waste
- sanitation issues
- unpleasant odor
4. Wood products
- provides cushioning but eventually compacts
- provides moisture retention
- variable quality even within a load
- must be kept moist
Riding Arena Footing Material Selection and Management
Eileen Fabian Wheeler - Associate Professor of Agricultural and Biological Engineering
Jennifer Zajaczkowski - Owner/manager Restless Winds Farm