Nutritional Treatment of Equine Cushing's Disease and Laminitis
Joyce C. Harman DVM, MRCVS
Madalyn Ward DVM
Equine Cushing's disease is a relatively
common and complex condition that is difficult to treat with
conventional medicine. Cushing's disease involves a hyperplasia or
adenoma of the anterior pituitary gland. Biochemical alterations
include increased endogenous cortisol, insulin resistance, elevated
adrenocorticotrophic hormone and decreased thyroid hormone levels.
Symptoms include hirsutism with no loss of the winter coat in the
summer, refractory laminitis, weight problems (over-or underweight),
polyuria/polydipsia (Pu/Pd), frequent infections, lowered immunity to
intestinal parasites, decreased intestinal wall integrity and
A common and often fatal complication is
laminitis (an inflammation of the laminae of the foot) that tends to be
refractory to conventional treatment. One of the most common therapies
used is phenylbutazone, an NSAID known to cause significant changes in
the permeability of the intestinal wall. Recent research has shown that
an intestinal bacterial exotoxin is one of the triggering factors in
laminitis. By removing the phenylbutazone, healing the intestinal wall,
many cases of laminitis become responsive to treatment.
Correct hoof-care combined with nutritional
management and the application of other modalities including
acupuncture, Chinese and western herbs complete the healing process.
The successful treatment of equine Cushing's
disease is one of the best examples of treating a disease using the
holistic approach. Each case requires different combinations of
modalities, yet the outcome is usually positive with individually
Cushing's syndrome in horses is being diagnosed
with increased frequency. It has been in the horse population for many
years, but generally went unrecognized. Cushing's actually appears to
be increasing in frequency, in part to a better understanding of the
diagnostic tests involved. Symptoms of Cushing's such as unexplained
laminitis cases occurring in the winter or early spring and older
horses with hursitism have been present for many years. However, it
appears to these authors and others that the incidence is increasing
and that the condition is being seen in younger horses.
Laminitis is one of the more frustrating
complications of Cushing's disease to treat in equine practice. Chronic
cases can take a significant amount of time and energy, and still have
unsatisfactory results. Natural medicine provides another toolbox of
treatments to help practitioners deal with both acute and chronic
cases. One of the major factors in getting laminitic horses to heal is
to support intestinal health and repair the basement membrane of the
intestinal tract. Pollitt's landmark work discussed the effects of a
bacterial exotoxin on the laminae of the foot.1 If, using natural
medicine, the basement membrane of the intestinal tract can be
strengthened, less exotoxin should be absorbed from the intestinal
The goal in natural treatment of Cushing's and
Cushing's-based laminitis is to provide nutritional support to prevent
and reverse damage from circulating free radicals, prevent further
damage to and encourage healthy laminar attachments and return the
horse's metabolism to proper balance. When managed correctly, with
patience and attention to detail, most chronic cases can return to
reasonable work. The poorly responsive cases can often be managed and
kept relatively comfortable without the use of drugs.
It is important to remember when treating laminitis
with natural medicine to approach each case individually. It can be
detrimental to any case to use multiple supplements or treatment
modalities without carefully evaluating the case. Because a product is
natural does not rule out harmful effects or the negative effects of
using too many products and overloading the body. Refractory cases may
require many products, however, they should not be used all at once.
Pathophysiology of Cushing's disease
It has been thought that as an almost normal part of aging horses get pituitary adenomas of the pars intermedia.2, 3
However, there are conflicting reports in the texts as to the
prevalence of the true adenoma. Some sources feel that the actual
adenoma is less common and that there is a hyperplasia of the pars
intermedia instead.4, 5 Both adenomas and hyperplasia cause
similar sets of symptoms, however, the hyperplasia, being a functional
disturbance rather that a tumor may be easier to treat. Many horses
respond well to treatment; these cases are probably more functional
The pars intermedia has melanotropes, cells that
normally use dopamine to process its beta endorphin hormones.3 In
Cushing's horses the dopamine is not present, so the melanotropes
produce a small amount of corticotrophin also which stimulates
glucocorticoid production by the adrenal cortex. The normal negative
feedback to decrease production of corticotropin does not work since
the melanotropes in the pars intermedia do not have glucocorticoid
receptors.6 So the corticotropin release continues
endlessly. The pars distalis, which has glucocorticoid receptors,
decreases its production of corticotropin. Normally the hypothalamus
coordinates the activity of the pituitary gland through the secretion
of peptides and amines.7, 8
Why Cushing's is occurring is not understood. Is it
just a hyperplasia of the pars intermedia, or is it from loss of
dopaminergic control by the hypothalamus? If so, what is causing the
hyperplasia? One theory is that chronic stress could affect dopamine
secretion by the hypothalamus, causing a loss of control of the
intermediate lobe and leading to the development of hyperplasia.7 There
are no clear answers at this point.
The clinical signs most commonly associated with
Cushing's syndrome in horses are hirsutism or long hair that does not
shed out in the summer9, refractory laminitis, weight
problems (over-or underweight), lethargy/poor performance,
polyuria/polydipsia and hyperhydrosis [table 1]. 10 Many other symptoms appear in certain individuals, with some horses exhibiting very few clinical signs, while others have many.
One of the most serious symptoms of Cushing's is laminitis, often with no outward reason for its occurrence. 9, 11
It is not uncommon to have some of the most refractory cases of
Cushing's based laminitis to occur in the winter, an uncommon season
for typical cases. Even the more common summer laminitis that appears
to be caused by overeating of grass can be quite refractory to
treatment, especially when other clinical signs of Cushing's are
Many horses diagnosed with Cushing's are overweight
and are very easy keepers, sometimes unable to eat more than a small
amount of hay each day to try to control their weight. In some cases,
horses who were previously easy keepers suddenly start requiring more
food to maintain their body weight. The overweight horses generally
have fat pads in specific places2, 9 and cresty necks. The
fat pads are generally behind the shoulder blades, on each side of the
tail and along the lumbar area, In addition, the fat on their body is
often visibly lumpy. Some of the horses who are beginning to loose
weight also maintain their fat pads despite the obvious weight loss.
Diabetes along with polyuria/polydipsia (Pu/Pd) 12, 9 are seen occasionally.2,5
Pu/Pd can also be caused by the compression of the pars nervosa by the
enlarging pars intermedia, causing a decrease in antidiuretic hormone
Frequent infections of the skin or other organs occur 2, 6 probably due to the hypercortisolism and hyperglycemia 11, 12, 10 It
is well known that increased levels of cortisol are immunosuppressive
and that diabetics are prone to infections due to the high levels of
sugar in their blood.
Sluggish thyroid glands or thyroid dysfunction are
common in horses yet it has been difficult to associate clinical signs
with laboratory findings.13 Some of the conditions
previously attributed to thyroid problems, such as muscle soreness are
also part of the Cushing's syndrome.14
Colic9 and poor teeth, with multiple dental
abnormalities have been reported as clinical signs associated with
Cushing's disease.5 It is unclear in the western literature
exactly what the connection of Cushing's to colic and poor teeth is,
however they may be part of the general breakdown of the system.
The literature also indicates these horses have lowered immunity to intestinal parasites.5, 7
The author's hypothesis for a cause of Cushing's-based laminitis may
have to do with poor integrity of the gut wall since there is evidence
of colic and poor immune system function in Cushing's horses.
Preliminary intestinal function laboratory tests performed by one of
the authors in horses indicate that Cushing's horses can have decreased
intestinal wall integrity (Harman, unpublished data).
Infertility occurs, possibly due to a disturbance
of gonadotropin secretion in conjunction with the disturbance of the
pars intermedia function.7 Examining the problem from a Chinese
perspective, the Kidney Yang deficiency described below gives rise to
When studying the disease from the Chinese medical
perspective, one of the more common diagnoses for Cushing's disease is
Kidney (KI) Yang deficiency. Many of the symptoms fit the classic signs
of Kidney Yang deficiency such as sore back muscles, weakness,
lassitude, increased clear urine, stocking up in the legs and
infertility. 15, 16 Chronic illness from other sources can
lead to KI Yang deficiency. Retention of Dampness from Spleen
deficiency can affect the kidneys by obstructing the movement of
fluids. Just old age contributes to the deficiency of Kidney Yang.
Kidney Yang deficiency affects the digestive tract and can produce
The most important diagnostic tool for identifying
Cushing's as the primary problem, or as the cause of laminitis, is the
history and clinical signs discussed above. A thorough physical exam
may reveal some of the less obvious signs such as poor teeth and
reproductive problems. The supporting lab work can be inconclusive, but
can be helpful and should be performed if possible.2, 5, 8
Laboratory work can be very unrewarding in the
Cushing's patient. Part of the problem is that in equine practice
single blood samples are taken whenever the practitioner is at the
farm, so there is little standardization of the timing of the samples.
Many parameters used have diurnal variations and may change due to
stress or other factors including the amount of exercise a horse has
had before the blood was drawn.
Elevated blood cortisol can indicate high levels of
stress in the body. Is the high cortisol coming from the Cushing's or
has the Cushing's come from chronic stress affecting the feedback
system in the pituitary gland? Cortisol as a single sample appears to
be an inaccurate test for Cushing's disease.10, 14
Resting insulin levels 17, ACTH 10, 18 and glucose are sometimes used. Most of the time a more useful diagnostic test is the ACTH stimulation test.19 The low dose dexamethasone suppression test (LDDS) is perhaps the most often used4, 10.
However, in holistic practice this author avoids using the LDDS and
stressing the adrenals further. Some of these horses have insulin
resistant hyperglycemia, which can be identified with a single insulin
and glucose sample or an insulin/glucose tolerance test.6, 20, 21 Another possible test is the oral glucose absorption test.22
A thyroid panel can be done, however the single
sample test usually performed in equine practice is little more than a
window into thyroid function and rarely proves valuable, except in
motivating the clients to work hard to improve a low test. 13
Some new laboratory profiles are being offered that
combine certain tests taken at certain times of the day. These may be
more accurate in positively diagnosing Cushing's disease, but research
needs to be performed before these tests can be considered more
accurate than those that are already available.
While doing the other laboratory tests, a complete
blood count (CBC) is advisable to help check the immune system status.
Many horses seen in these authors' practices have low white blood cell
(WBC) counts. The neutrophil and lymphocyte counts vary, with one or
both contributing to the low WBC. A chemistry screen is also advisable
since some of these horses have a variety of metabolic problems
associated with their condition, including liver disease and chronic
Many Cushing's horses have elevated insulin levels in their blood17 without concurrently raised or lowered glucose levels.14, 21, 23
A relatively new condition is being recognized in human medicine,
currently called syndrome X.24 Syndrome X is a group of symptoms
related to insulin resistance or hyperinsulinemia.25 The
cells show an inability to transport glucose into them. Insulin
resistance occurs in as much as 25% of the non-diabetic population.26 Cushing's syndrome in horses has some of the same characteristics as syndrome X 17, 27
has in people. Some of the specific symptoms are obviously different,
however, the general seriousness of the metabolic derangements are very
The reason the insulin is elevated is that it is
not able to get into the cells. Normally when a sugar or carbohydrate
is eaten, the blood sugar levels increase, insulin is secreted by the
pancreas, glucose is carried into the cells by the insulin and the
blood sugar goes back to normal. In insulin resistance, the cell wall
insulin receptors cannot transport glucose correctly.28, 29
People that are susceptible to syndrome X are
frequently from a genetic type considered "thrifty"30 or in horse
terms, "easy keepers."31, 32 In this type of individual,
horse or human, the body is very efficient at storing fat for times of
need, and in fact, if fed less, they often become more efficient at
storing fat. In humans much of the fat stored from impaired glucose
metabolism is distributed centrally, especially around the abdomen.
Many horses store their fat in specific places; fat pads on their body
and cresty necks.
The treatment of people with Syndrome X using
natural medicine incorporates many of the ingredients used when
treating the Cushing's horses. The permeability of the cell walls to
insulin is enhanced and nutrients are provided to help insulin and
glucose pathways function better.26 The details are discussed below in the treatment section.
Conventional medical treatment
The accepted drug therapy for Cushing's disease and its related complications is pergolide mesylate.11, 5
Pergolide is an expensive, type 2 dopaminergic receptor agonist that
works on the melanotrope cells in the pituitary gland. The drug
replaces dopamine, so must be given for life, however, horses have been
removed from the drug successfully in this author's experience. This
drug seems to help for a period of time, but does not seem to be a
Cyproheptadine is an anti-serotonin drug that seems
to be partially effective, less expensive, but has no real scientific
basis for its use, as serotonin does not play a role in Cushing's.
Therefore the reasoning behind its use is anecdotal, and most horses
that do respond only seem to get help for a year or two. It may act in
a secondary way. 5
The standard treatment used with laminitis as well
as in many other of the complications associated with Cushing's disease
is the non-steroidal anti-inflammatories (NSAID's) to relieve pain and
decrease inflammation. In cases of laminitis very high doses may be
used as the horses are in extreme pain.
Other drugs that may be used in the laminitis cases
to alter the circulation or reduce swelling, such as DMSO,
nitroglycerine patches and isoxuprine or heparin. Since many of the
horses have chronic infections, high doses or repeated courses of
antibiotics may be used.
Intestinal permeability and its relationship to laminitis
Research has been done regularly on NSAID's effects and toxicity in the horse as well as in humans.33
One recent equine necropsy study showed inflamed small and large
intestinal walls after 12 days of phenylbutazone administration.34
This study also showed the comparative toxicity of several NSAID's
(phenylbutazone, flunixin, and ketoprofen). Phenylbutazone caused edema
in the small intestine and erosions and ulcers in the large intestine.
Phenylbutazone toxicity studies showed hypoprotenemia and suspected
protein-losing enteropathies in a majority of horses in the studies.35-37 Gastric ulcers in horses are common and may be due in part to the use of phenylbutazone.
Pollitt's recent work indicates involvement of a
leaky basement membrane in the intestinal wall as part of the
pathophysiology of carbohydrate overload laminitis.1 A leaky
basement membrane allows the (Streptococcus bovis) bacterial exotoxin
to cross into the bloodstream. This exotoxin is capable of essentially
melting the basement membrane of the laminae in the foot.38
Much research has been done in human medicine
concerning the involvement of the leaky intestinal tract basement
membrane in the pathophysiology of many diseases.39, 40 In
the leaky bowel the basement membrane allows large molecules to pass
through the portal circulation into the liver and form immune complexes
which are then distributed to the joints and other locations in the
body.39 Bacteria and bacterial products are well known to leak through the basement membrane.40 It has been shown that a single dose of endotoxin increases intestinal permeability in humans.41
Human studies have linked "leaky bowel" to various
diseases including arthritis, which is significant since NSAID's are
commonly used to treat arthritis in both the human and animal
populations.39 Many horses spend much of their lives
receiving phenylbutazone on a daily basis for weeks, months and even
years, leaving the intestinal tract basement membrane in poor shape.
The implications of the research are that high
doses of the NSAID's could be detrimental to the integrity of the
intestinal wall in laminitis cases. Consequently, the use of NSAID's in
treating laminitis should be questioned. Also, a potential cause of
laminitis, especially chronic laminitis, may lie with the integrity of
the gut wall. Preliminary results from a well-established human
functional medicine testing laboratory support the hypothesis of poor
intestinal function in some of the Cushing's and laminitis horses
(Harman, unpublished data).
Clinically, in these authors' experience the
removal of the NSAID's is one of the most important aspects of the
success of the holistic treatment. The horses' symptoms are usually
worse for three to five days after removing the NSAID's, so they lie
down more. That can be alarming to the owners and attending
veterinarians, however, it is best for the horse, since they take the
pressure off the feet and allow the antioxidants to work. When the
horses feel better with natural medicine it is because they are better,
not because the pain was masked.
Repairing the gastro-intestinal tract
The integrity of the gastro-intestinal system is
vital in preventing formation and release of exotoxins into systemic
circulation. The authors have adapted many of the treatments that have
been used successfully in humans.
The gastrointestinal tract is also responsible for
the breakdown and assimilation of nutrients needed to maintain and
restore health. The most important first step is to stabilize the
intestinal wall and restore the beneficial flora.
Antibiotic use leads to unbalanced intestinal flora that contributes to the leaky bowel syndrome.42, 43 Probiotics may restore the pH and gut flora to a healthier environment. Beneficial bacteria such as Enterococcus faecium, Lactobacillus acidophilus, L. casei, Bifidobacterium bifidum, and Streptococcus faecim are indigenous to the horse's digestive system. The bacteria help maintain proper pH levels in the system, 44, 45
manufacture vitamins such as biotin and digest fiber. Supplementation
using a variety of equine probiotics should be considered.
Glutamine is an amino acid that is a primary fuel
for the enterocytes of the small intestine. Glutamine levels are
affected by any decrease in feed intake as well as any stress placed on
the intestine such as sepsis or endotoxemia.46 Glutamine has been shown to reduce bacterial translocation across the gut wall47
and should be considered in any horse that is not eating correctly, as
well as any horse where intestinal wall integrity may be questionable.
Doses range from 10 to 35 gm per day, depending on the size of the
Processed grains and hays may lose key ingredients
during manufacturing since pellets and extruded feeds are made at high
temperatures. In some cases horses have difficulty digesting processed
feed, yet in these author's experience, when many horses are fed plain
grains they gain weight and are healthier. Some horses digest their
food better when digestive enzymes are added.
The aphanizomenon flos-aquae strain of blue-green
algae is high in chlorophyll and anti-oxidant nutrients such as
beta-carotene. It also contains active digestive enzymes so it provides
concentrated nutrition to help support healing without placing any
additional stress on the digestive tract.
Aloe vera is an herb that has shown some clinical
efficacy in treating the side effects of the NSAIDs. Its
anti-inflammatory effects are possibly from its inhibitory action on
the arachidonic acid pathway via cyclooxygenase.48
Slippery elm bark is another nutritional herb,
which protects and aids in healing the intestinal wall. It has a
mucilage effect that appears to sooth the intestinal wall, however,
there is little research to support its use.49
Nutritional support is critical in the laminitic
horse and includes the basics of feed, water and hay as well as
specific nutrients. The nutrients discussed here are ones these authors
have found clinically useful.
Once the digestive system is supported, high
quality nutrients should be provided. The nutritional requirements for
horses with laminitis appear to be higher than normal horses. Horses
with Cushing's-based laminitis need high fiber, low carbohydrate diets.
Wheat bran can be added as a source of fiber taking care to keep the
calcium phosphorus ratio correct in the overall diet. Blue-green algae
can be added to the bran to provide amino acids and trace minerals.
Grass or other lower protein hays can be given free choice. Some horses
can tolerate an alfalfa/grass hay, especially if more protein is
needed. Generally alfalfa should not be used alone and should not be
fed to the very overweight horse.
The feed should be low in sugar if the horse has
signs of Cushing's syndrome with altered insulin levels or diabetes.
Sweet feeds should be avoided. In humans increased insulin levels can
begin in childhood.50 Cushing's in horses may begin during
their younger years. Most of the prepared diets for foals and young
growing horses are extremely high in sugar. The connection between
feeding high sugar diets and Cushing's disease has not been proven in
horses, but there is a strong connection being made in humans with high
sugar diets and insulin resistance.51
When evaluating the feeding program, examine the
treats being given. Many people feed treats high in sugar including
large quantities of apples and carrots. Plain corn (about 25%), barley
(about 35%) and oats (about 45%) make a simple, clean grain mixture
without sugar. Some of these grains may not be available or useable in
certain parts of the country depending on harvest situations. Some
horses react poorly to eating oats; if that seems to be the case,
barley and corn together are enough.
Higher levels of protein (up to 14%) and calories
may be needed in the horses with weight loss problems, but should not
be fed to normal or overweight horses.52, 53 Cushing's
horses that are normal weight or underweight often do well on the
senior diets, which are higher in protein and fat. Many chronic
laminitis horses lose weight due to the stress of walking in pain and
actually need increased amounts of feed. Practitioners often restrict
feed in all laminitic horses, however, some horses need extra calories
to maintain normal physiologic functions. Increased calories can be
given as fats (vegetable oils or rice bran) and are well digested by
most horses. Increasing total calories with oils may be preferable to
using high-protein feeds and hays.
Coenzyme Q10 is useful in reversing free radical
damage secondary to sepsis from an endotoxin overload. This is thought
to occur with the coenzyme Q10 acting as an oxygen free radical
scavenger, thus stabilizing mitochondrial membranes, and by inhibiting
the arachidonic acid metabolic pathway and the formation of various
prostaglandins.54 Coenzyme Q 10 clinically seems to be one
of the best antioxidants for use in laminitis cases. Horses become less
painful rapidly when Co Q 10 is used without concurrent NSAID's. The
therapeutic dose is 300-600mg per day for the first week or two, then
the dose can be decreased slowly to a maintenance of about 100 mg per
Vitamin C is an excellent antioxidant that can
regulate the phagocytic process in endotoxic shock, mainly by
decreasing free radical production.55 Vitamin C is also a
nutrient for collagen manufacture as well as offering some immune
system support. Doses range from 3 to 8 gms per day. Horses tolerate
these doses well with few cases of diarrhea or stomach irritation.
Other antioxidant nutrients that may be useful are
Vitamin E, superoxide dismutase (SOD), and dimethylglycine (DMG). These
antioxidants are generally used by the authors in the more refractory
One of the most important aspects of any
nutritional program for horses is the use of free choice minerals with
the salt fed separately. Many laminitis horses will eat large
quantities of minerals for extended periods of time indicating their
need for minerals.
A commercial salt-mineral block contains about 94%
salt so horses that do not crave salt will not consume the amount of
minerals they need. The authors have observed horses consuming large
quantities of minerals when provided mineral supplementation with salt
There are several key minerals needed for glucose
metabolism that help the Cushing's horses. Magnesium affects insulin
secretion and its action in the cells. Magnesium also helps the cells
be more flexible and permeable to insulin.56 Chromium helps
make muscle more sensitive to insulin so glucose can be taken into the
muscle cells more easily. Chromium is also related to elevated blood
sugar and has been shown to be effective in reducing fasting blood
sugar levels.57, 58 Vanadium or vandyl sulfate has actual
insulin-like effects on glucose metabolism59 which helps transport
glucose into the cells.60
MSM is a natural source of sulfur. Sulfur is
important as it helps make up the disulfide bonds in the laminae. The
disulphide bonds are an important part of the connects the hoof wall to
the healthy lamina.61 Sulfur may be an important nutrient for these horses and can be fed free choice or in a supplement such as MSM.
It is important to supply high quality supplements
to help these horses heal. Prepared foods cannot have all the vitamins
needed by a sick animal. However, formulated supplements which contain
low quality, synthetic vitamins, inorganic minerals, and fillers may
actually cause the horse's system to become more out of balance.
Food-source vitamin mineral supplements include: blue-green algae,
kelp, apple cider vinegar, carrots, and oranges. Several companies
manufacture additive-free supplements.
Essential fatty acids
Essential fatty acids (EFA's) are needed to help make the cell wall more sensitive to insulin.62, 63
Omega 3 fatty acids are especially deficient in human diets and may be
deficient in many equine diets. Most of the high fat equine foods use
animal fat that is high in saturated fats rather than vegetable oils.
Flax and hemp oil provide Omega 3 fatty acids that are palatable to the
equine, though fish oils may have an even better fatty acid profile.63
Other compounds that may be useful
The authors have used several other forms of
complementary medicine when treating Cushing's cases. Chinese medicine,
both acupuncture and Chinese herbs, homeopathy and glandulars are used
in many of the cases treated. The research does not support their use
so the inclusion here is purely anecdotal, yet in these author's cases
these modalities have proven useful.
The use of cold baths to cool the foot has at times
been advocated. In light of Pollitt's research cold should be used
regularly in the first 48 hours, especially in known grain overload or
toxic case situations.1
The damage to the hoof in laminitis cases can be kept to a minimum by following a few guidelines.
1: Do not use drugs to mask the pain. If the pain
is masked, the horse will continue to walk on the damaged lamina and
cause more damage. Natural antioxidants will allow healing without
masking the pain. The best thing a horse with severe laminitis can do
is lie down and take weight off the damaged feet.
2: Provide deep sand bedding if possible, or use
Styrofoam taped to the bottom of the feet-- 2 inch thick blue builder's
Styrofoam. Washed river sand will shift under the horse allowing him to
stand in the most comfortable position. It will also shift under
pressure points to keep pressure sores to a minimum. Horses with tight
tendons will often stand with the toes buried in the sand and the heels
elevated. The way the horse stands in sand is a good way to determine
how to shoe him.
3: Keep the hooves soft and pliable. Horses with
laminitis generally have swelling within the hoof capsule and a soft
hoof will expand to relieve pressure. If the hoof gets too hard, a
poultice should be applied overnight. Using a rasp to thin the hoof at
the toe can also give relief.
4: Shorten the toe to ease breakover. A long toe
will act like a lever and cause more tearing of the hoof lamina. The
natural balance approach to trimming the foot in line with the coffin
bone, then raising the heels and slowly lowering them to relieve the
tendon pull with special shoes can be extremely beneficial. Natural
balance trimming must be done correctly in order to work. If the
farrier does not understand the principles, more damage can result.
5: Encourage abscesses to drain. Avoid treating
abscesses with systemic antibiotics or anti-inflammatory drugs. Drugs
may temporarily suppress the maturation of an abscess allowing it to
spread deeper into the foot. Abscesses are natures way of debriding the
dead tissue from the damaged laminae so it is important they are
allowed to drain. Soaking in Epson salts or poulticing will encourage
the abscess to mature and open to the outside of the hoof. Rasping the
hoof wall thin at the toe will give the abscess a place to drain.
6: Avoid shoeing procedures when the feet are
extremely sore. Horses with acute episodes have very sore feet, pulling
shoes and hammering will cause extreme pain. If the toes are long,
carefully remove the shoes and bed in deep sand. Toes can be rasped
back more easily if the hoof has been softened with a poultice. Several
pads are available which can be taped on to provide frog support or
raise the heels.
Many horses are kept in high stress situations that
contribute to adrenal stimulation and cortisol release. If it is
possible to decrease environmental stress, the horse will benefit
greatly. Many of these horses may be past their high-stress years, and
the current owner may not be showing heavily or keeping the horse in
the high stress environment, yet Cushing's disease is still a factor.
These horses are experiencing the previous lifetime of stress,
excessive drug use and poor nutrition. Cushing's is the result of many
years and many factors.
Pasture turn-out time is very important; however
many horses cannot be on rich pasture without exacerbating their
symptoms. Clients should be encouraged not to fertilize their fields or
mow and manage them too carefully. Natural fertilization with trace
minerals is a good practice, though if grass becomes too rich from good
organic practices an overweight horse will result. A few weeds (herbs)
are a good thing. For many horses a "fat pen" will need to be built,
just a small area outside with minimal grass so they can be out in the
sunshine and near their friends, but not have too much grass.
Prevention is still the best way to manage
laminitis in horses, however, chronic laminitis cases can recover with
a multi-faceted, long-term natural treatment plan. Treat each horse as
an individual and seek quality practitioners to help you. Use as much
whole food nutrition as possible, supplement with specific nutrients as
needed, reduce stresses and vaccinations, and support a healthy
- Pollitt, C. Equine laminitis: A revised pathophysiology. Proceedings Am Assoc Eq Pract, 1999:45: 188-192.
- Boujon CE, Bestetti GE, Meier HP et al. Equine pituitary adenoma, a functional and morphological study. J Comp Path. 1993;109: 163-178.
Millington WR, Dybal NO, Dawson R Jr, et al. Equine Cushing's disease:
differential regulation of _ endorphin processing in tumors of the
intermediate pituitary. Endocrinology. 1988;123: 1598-1604.
- Dybal NO, Hargreaves KH, Madigan JE et al. Diagnostic testing for pituitary pars intermedia dysfunction in horses. J Am Vet Med Assoc. 1999;204: 627-632.
- Dybal, N. Pituitary pars intermedia dysfunction (equine Cushing's-like disease). In: Robinson NE, ed. Current Therapy in Equine Medicine. Philadelphia: WB Saunders; 1997:499-503.
DN, Holscher MA, Wilson MG et al. Equine Cushing's disease, plasma
immunoreactive proopiolipomelanocortin peptide and cortisol levels
basally and in response to diagnostic tests. Endocrinology. 1982;110: 1430-1441.
- Greco, D and Stabenfeldt GH. Endocrinology. In Cunningham JG, ed. Textbook of Veterinary Physiology, Philadelphia: WB Saunders; 1997:385-403.
- van der Kolk H. Diseases of the pituitary gland, including hyperadrenocorticism. In: Watson TDG ed. Metabolic and Endocrine Problems of the Horse, Philadelphia: WB Saunders; 1998: 41-59.
- Kolk JH van der, Kalsbeek HC, Garderen E van et al. Equine pituitary neoplasia: a clinical report of 21 cases (1990-1992). Vet Rec. 1993;133: 594-597.
- Hillyer MH, Taylor FGR, Mair TS, et al. Diagnosis of hyperadrenocorticism in the horse. Equine Vet Edu. 1992;4: 131-134.
- Love S. Equine Cushing's disease. Br Vet J. 1993;149: 139-153.
M, Baumgartner W, and Capen CC. Immunocytochemical demonstration of
propiomelanocortin-derived peptides in pituitary adenomas of the pars
intermedia in horses. Vet Path. 1990;27: 419-425.
- Sojka JE, Johndon MA and Bottoms GD. Serum tri-iodothyronine, total thyroxine, and free thyroxine concentrations in horses. Am J Vet Res. 1993;54: 52-55.
Beech J and Garcia M. Hormonal response to thyrotropin-releasing
hormone in healthy horses and in horses with pituitary adenoma. Am J Vet Res. 1985;46: 1941-1943.
- Xie H. Traditional Chinese Veterinary Medicine. Beijing Agricultural University Press. Beijing, China. 1994:255-287.
- Maciocia, G. The Foundations of Chinese Medicine. Churchill Livingstone, New York, NY. 1989:253-254.
MC, and Beech J. Equine intravenous glucose tolerance test: glucose and
insulin responses of health horses fed grain or hay and of horses with
pituitary adenoma. Am J Vet Res. 1986;47: 570-572.
DE, Wilson RG, Groenendijk S, et al. Glucose metabolism in a pony mare
with a tumour of the pituitary gland pars intermedia. Aust Vet J. 1987;64: 379-382.
- Allen JR, Barbee DD and Crisman MV. Diagnosis of equine pituitary tumors by computed tomography, part 1. Compend Contin Educ Pract Vet. 1988;10: 1103-1106.
- Baker JR and Ritchie HE. Diabetes mellitus in the horse: a case report and review of the literature. Eq Vet J. 1974;6:7-11.
- Loeb WF, Capen CC and Johnson LE. Adenomas of the pars intermedia associated with hyperglycemia and glycosuria in two horses. Cornell Vet. 1966;56: 623-626
- Field JR and Wolf C. Cushing's syndrome in a horse. Eq Vet J. 1988;20: 301-304.
- Reed, SM. Pituitary adenomas: equine Cushing's disease. In: Reed SM and Bayly WM, eds. Equine Internal Medicine, Philadelphia: WB Saunders Company; 1998: 912-915.
- Zavaroni I, Bonini L, Fantuzzi M, et al. Hyperinsulinemia, obesity and syndrome X. J Int Med. 1994;235: 51-56.
- Bogardus C, Lillioja D, Mott M, et al. Relationship between degree of obesity and in vivo insulin action in man. Am J Physiol. 1985;248 (Endocrinol Metab II):E286-E291.
- Reaven, GM. Pathophysiology of insulin resistance in human disease. Phys Rev. 1995;75(3): 473-485.
- Reaven, GM. Role of insulin resistance in human disease. Diabetes. 1988;37: 1495-1507.
- Adamo M, LeRoith D, Simon J. Effect of altered nutritional states on insulin receptors. Ann Rev Nutr. 1988;149-166.
GW, Peterson KF, Krssak M, et al. Impaired glucose transport as a cause
of decreased insulin-stimulated muscle glycogen synthesis in type 2
diabetes. N Engl J Med. 1999;341: 240-246.
- Neel JV. The "thrifty genotype" in 1998. Nutr Rev. 1999;57(5): S2-S9.
- Coffman JR, Colles CM. Insulin tolerance in laminitic ponies. Can J Comp Med. 1983;47:347-351.
- Jeffcott LB, Field JR, McLean JG et al. Glucose tolerance and insulin sensitivity in ponies and standardbred horses. Eq Vet J. 1986;18: 97-101.
I, Williams, et al. Effect of non-steroidal anti-inflammatory drugs and
prostaglandins on the permeability of the human small intestine. Gut. 1986;27(11):1292-1297
- MacAllister CG, Morgan SJ et al. Comparison of adverse effects of phenylbutazone, flunixen meglumine, and ketoprofen in horses. J Am Vet Med Assoc. 1993;1:202 (1):71-77.
- Lees P, Creed RF et al. Biochemical and hematological effects of phenylbutazone in horses. Equine Veterinary Journal. 15 (2):158-167, 1983.
- Snow DH, Bogan JA et al. Phenylbutazone toxicity in ponies. Vet Rec. 1979;14:105(2):26-30.
- Snow DH, Douglas TA, et al. Phenylbutazone toxicosis in equidae: a biochemical and pathological study. Am J Vet Res. 1981;42(10): 1754-1759.
CC, and Daradka M. Equine laminitis basement membrane pathology: loss
of type IV collagen, type VII collagen and laminin immunostaining. Equine Hoof Equ Vet J Suppl. 1998;27: 139-144.
- Inman RD. Antigens, the gastrointestinal tract and arthritis. Rheum Dise Clin N Am. 1991;17(2):309-321.
- Wells CL, Jechoreck RP et al. Relative contributions of host and microbial factors in bacterial translocation. Arch Surg, 1991;126:247-252.
- O'Dwyer ST, Michie HR, et al. A single dose of endotoxin increases intestinal permeability in healthy humans. Arch Surg, 1988;123(12): 1459-1464,.
- Darlington, LG. Dietary therapy for arthritis. Nut Rheum Dis/Rheum Dis Clin N Am, 1991;17(2):273-285.
- Schmidt, MA, Smith, LH, & Sehnert, KW. Beyond antibiotics. North Atlantic Books, Berkley, CA. 1993.
- Clarke LL. Feeding and digestive problems in horses. Vet Clin N Amer Eq Prac. 1990;6(2):433-450.
JN, Garner HE, Berg JN, et al. Intracecal endotoxin and lactate during
the onset of equine laminitis: A preliminary report. Am J Vet Res 1979;40: 722-723.
- 4Souba WW, Herskowitz K, et al. The effects of sepsis and endotoxemia on gut glutamine metabolism. An Surg. 1990;211(5): 543-549.
- Souba WW, Klimberg VS, et al. Oral glutamine reduces bacterial translocation following abdominal radiation. J Surg Res. 1990;48(1): 1-5.
- Vazquez B, Avila G, Segura D, Escalante B. Antiinflammatory activity of extracts from Aloe vera gel. J Ethnopharmacol. 1996;55(1): 69-75.
- Physicians Desk Reference for Herbal Medicines. Montvale, NJ: Medical Economics Company. 1999:1196.
R, Ugianskis E, Martin D, et al. Role of diet and exercise in the
management of hyperinsulinemia and associated atherosclerotic risk
factors. Am J Cardiol. 1992;69: 440-444.
A, Bantle H, Henry R, et al. Effects of varying carbohydrate content of
diet in patients with non-insulin-dependant diabetes mellitus, JAMA. 199;271: 1421-1428.
- Glade MJ, et al. Dietary protein in excess of requirements inhibits renal calcium and phosphorus in young horses. Nut Res Intern. 1985;31: 649-660.
PA, Lawrence LM, Foreman JH, et al. Dietary protein level and energy
metabolism during treadmill exercise in horses. J Nutr 1991;121: 1462.
- Lelli JL, Drongowski RA, Gastman B, et al. Effects of coenzyme Q10 on the mediator cascade of sepsis. Circ Shock. 1993;39(3): 178-87.
VV, Guayerbas N, Puerto M, et al. Ascorbic acid modulates in vitro the
function of macrophages from mice with endotoxic shock. Immunopharm. 2000;46(1): 89-101.
- Paolisso G, Sgambato S, Gambardella A, et al. Daily magnesium supplements improve glucose handling in elderly subjects. Am J Clin Nut. 1992;55: 1161-1167.
- Linday LA. Trivalent chromium and the diabetes prevention program. Med Hyp. 1997;49:47-49.
- Evans GW, Bowman TD. Chromium picolinate increases membrane fluidity and rate of insulin internalization. J Inorg Bio. 1992;46:243-250.
- French RJ, Jones PJ. Role of vanadium in nutrition: metabolism, essentiality and dietary considerations. Life Sci. 1992;52:339-346.
LI, Meyerovitch, et al. Insulin-like actions of vanadate are mediated
in an insulin-receptor-independent manner via non-receptor protein
tyrosine kinases and protein phosphotyrosine phosphates. Mol Cell Biochem. 1995;153(1-2): 39-47.
- Grosenbaugh DA, Hood DM. Keratin and associated proteins of the equine hoof wall. Am J Vet Res. 1992;53(10): 1859-63.
- McCarty MF. Complementary measures for promoting insulin sensitivity in skeletal muscle. Med Hyp. 1998;51:451-464.
A, Maixent JM, Ansalki JL, et al. Fish oil supplementation prevents
diabetes-induced nerve conduction velocity and neuroanatomical changes
in rats. J Nutr. 1999;129: 207-213.
not shed out in the summer
weight problems (over-or underweight).
sluggish thyroid glands
poor hair coat.
frequent infections of the skin or other organs
< multiple dental abnormalities
lowered immunity to intestinal parasites
altered intestinal function laboratory tests
decreased intestinal wall integrity.