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 Post subject: diabetes and laminititis
PostPosted: Tue Jun 02, 2015 10:16 am 
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Here is an interesting article seen in the Thoroughbred Times

Posted: Saturday, August 30, 2003

Veterinary Topics: Too much feed, not enough exercise

Quote:
Adult-onset diabetes might underlie problems currently puzzling owners and
veterinarians

THE MODERN HORSE has been referred to as an excellent example of evolution.
Natural selection has equipped the animal to thrive on forage (grass) and to
adapt to seasonal variations in the availability of that grass. In periods
of good weather and plentiful rain, the horse adjusted to intensive grazing
and the production and storage of fat within its body. These fat deposits
were used in cold weather or in times of drought and poor grass
availability.

Horses that stored fats best were healthier; they survived lean times better
and reproduced more regularly. Their genes were selected for, and,
consequently, are represented in, a reasonable section of the genetics of
the modern horse.

Today's horses rarely have to tolerate times of poor forage availability and
drought. In most situations, in present times they receive plenty to eat and
have had less and less work to do.

"Under modern horse management systems," writes Philip Johnson, B.V.Sc.,
M.S., a leading laminitis researcher from the University of Missouri School
of Veterinary Medicine, "the combination of feeding starch-rich rations over
many years and protracted periods of stall confinement tend to lead to the
acquisition and maintenance of substantial body fat in the domesticated
horse."

Simply put, we are making our horses fat by feeding them too much. We keep
them in stalls and work them too little, which probably contributes to a
number of more serious problems, as well.

Problems of obesity

Diabetes is a common health condition in humans. Until recently, the disease
was not thought to exist in horses. A review of medical literature over the
past 50 years shows only a small number of cases of equine diabetes. The
majority of cases were caused either by pancreatitis (an infection of the
pancreas) or by tumors of the pancreas or pituitary gland.

Recently, many equine researchers are taking a closer look at metabolic
conditions in horses that they believe are strikingly similar to type 2 or
adult-onset diabetes in humans. Johnson has a special interest in such
conditions and has noted the increasing problems associated with obesity in
both horses and humans. Obesity can be difficult enough, but the secondary
problems that tend to occur in overweight horses really concern him.

The tendency for horses to develop obesity and the problems and diseases of
the endocrine system that result from obesity-associated insulin
insensitivity, according to Johnson, "closely parallel the development of
noninsulin-dependent or adult-onset diabetes in humans."

Perhaps equine diabetes is only now understood and accurately diagnosed. Or,
it might have existed all along and been misdiagnosed or under-diagnosed.
Or, the increased attention and medical care currently given to equine
senior citizens have caused the veterinary community to become more
sensitive.

Johnson believes we might have helped create this condition by unknowingly
managing our horses too well in the face of their ability to make and store
fat. Regardless, we are currently seeing higher levels of obesity in horses
and are seeing more and more cases that resemble type 2 diabetes.

Equine insulin production

In a normal horse or human, insulin is secreted by special cells in the
pancreas in response to a rise in blood glucose. Eating a meal rich in sugar
and starch will elevate the glucose or sugar in the blood. The body senses
this increase and releases insulin, which stimulates the body's cells to
take up glucose from the blood and, once in the cell, use it for energy or
convert it for storage.

Glucose typically is converted to glycogen or fat. Type 2 diabetes is the
end stage of breakdown of this system. Typically, horses that have trouble
with insulin sensitivity have cells that slowly lose their responsiveness to
insulin. At first, the body simply increases the production of insulin and
the cells respond to this new, higher level. Normal glucose levels are
maintained. Gradually, however, cells become resistant to higher and higher
levels of insulin. Eventually, the insulin-producing cells of the pancreas
become fatigued and are finally exhausted.

This is the normal progression for this disease in humans, but not in
horses. Horses seem to be able to maintain a high level of insulin
production even in the face of extreme insensitivity of the cells of the
body to that insulin. So, even though horses maintain insulin production,
there comes a point where there is no response to that production, and they
are considered to have type 2 or noninsulin-dependent, adult-onset diabetes.

There are names for the various stages along the way to this conclusion. The
term insulin resistance or impaired glucose tolerance has been used, but the
exact demarcation between these conditions is not clear and the progression
of clinical names is somewhat academic. The bottom line is these are stages
of a disease that leads to a horse having difficulty controlling glucose and
metabolizing fat.

Signs of metabolic problem

Insulin inhibits the breakdown of triglycerides (fat molecules) into free
fatty acids and glycerol. In the absence of insulin--and possibly when the
body no longer responds to insulin even if it is there--the process of
lipolysis can occur allowing the horse's body to release fatty acids.

These acids are transported to the liver, where they are repackaged. Then
they are transported to fat tissues and stored. Insulin generally would keep
these fats in other cells where they are more likely to be used for energy.
Some cresty-necked horses and overly fat ponies might be insulin resistant
as they inappropriately continue to store fat in the tissues of the crest,
back, and hips.

This body condition may be the first clue to an underlying metabolic
problem. These horses also tend to stay fat on minimal rations. Owners often
refer to then as "living on air." They have good appetites and always seem
hungry, despite having more than adequate fat stores. They do poorly with
exercise, tire easily, and do not seem to have much energy. When they do
tolerate exercise, they tend not to develop much muscling, compared to
normal horses with the same workload.

As with human diabetics, there is believed to be a genetic predisposition
for insulin resistance and type 2 diabetes. Johnson mentioned the
evolutionary advantages of being a good fat producer, so it is little wonder
that some ponies, Morgan and other gaited breeds, and certain Arab
bloodlines have all been suspected of a genetic predisposition for insulin
resistance.

Conditions are linked

It is not currently known if obesity leads to insulin resistance or if
insulin resistance contributes to obesity, but the two conditions are
linked. Conditions of temporary insulin resistance have been shown to occur
in horses during times of stress and with infection, inflammation, and even
extreme variations of some hormones.

The exact process of this temporary resistance is unknown, but human studies
have shown that sustained levels of elevated blood glucose can lead to
microvasculature changes in many tissues. Damage to these small blood
vessels leads to a lack of cellular oxygen and to potential cell death.

It is well known that human diabetics are at risk of developing all manners
of infections and have higher percentages of liver and kidney disease.
Damage to the nerves and blood vessels of the hands and lower limbs of
diabetics often lead to the loss of fingers and toes. In fact, the most
common diabetic complication requiring hospitalization in humans is foot
disease. This point might be the most important link between diabetes in
humans and horses.

Insulin resistance and laminitis

Christopher C. Pollitt, B.V.Sc., Ph.D., of the School of Veterinary Sciences
at the University of Queensland in Australia, has been looking at insulin
resistance and laminitis, and he feels the two are related. His research
suggests that altered glucose metabolism could be an underlying or
contributing cause to almost all cases of laminitis.

Lack of glucose in the peripheral tissues (fingers and toes) of humans, as
seen in diabetes, leads to damage of the peripheral nerves (peripheral
neuropathy) and to ischemic damage or lack of cellular oxygen. This process
has been well documented. In Pollitt's studies, lack of glucose in hoof
extract tissue led to damage of the basement membrane and to separation of
the dermal laminae from the epidermal laminae. This is the exact cellular
sequence in cases of laminitis or founder.

This process of insulin resistance leading to excess glucose storage and
decreased glucose availability, and finally to cellular death and laminitis,
would explain a few things. Veterinarians and horse owners often have
wondered why one horse out of many grazing the same field and on the same
management program develops laminitis. Why can one crafty pony continually
get into the feed room and overeat without incident while another pony eats
far less and develops founder?

Veterinarians ponder why some horses fail to respond to aggressive laminitis
treatment when far more horses improve and return to nearly normal under the
exact same treatment regimen. Why do some horses seem to develop laminitis
following a dose of dexamethasone or other corticosteroid that is almost
uniformly tolerated by most horses?

The answer could lie in some degree of insulin resistance in those horses
that develop laminitis and do not respond normally to treatment. Cases of
laminitis following infection, stress, or even grain overload possibly might
share more of a temporary insulin resistance state than strict endotoxemia
(an overload of bacterial toxins in the blood), as has been previously
thought.

Because the idea of an underlying metabolic basis to laminitis potentially
explains so many previously confusing cases, some researchers have been
calling the idea of insulin resistance in horses the "unification theory."
This theory points the way to potentially new methods of treating laminitis
that would be directed more at correcting glucose metabolism and new means
of prevention related to treating insulin resistance and diabetes.



--------------------------------------------------------------------------------

Kenneth L. Marcella, D.V.M., is a practicing veterinarian in Canton, Georgia

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PostPosted: Tue Jun 02, 2015 10:17 am 
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Joined: Wed May 27, 2015 10:20 am
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I have been doing quite a bit of research on diabetes. I am currently
reading "Infectious Diabetes" in which the author puts forth the intriguing
theory that diabetes can be fungi instigated. I know my dog had all the
symptoms of diabetes until I gave her a few drops of MMS (sodium chlorite),
an anti-fungal, causing her to come back to normal. I am wondering how MMS
would circumvent equine laminitis! Like my dog, it probably has to be used
during the initial onset and may have limited affect after tissue damage has
already occurred.

DougA

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PostPosted: Tue Jun 02, 2015 10:18 am 
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I just purchased and read a very intriguing text by Doug Kauffman called "Infectious Diabetes" which may also apply to equine laminititis. Could laminititis be a fungal infection? His premise in the book is that diabetes could probably be a fungi infection and given the right "terrain" manifest itself into diabetes. Kauffman was primarily a nutritionist and he found in his early work that prescribing patients with obvious fungi problems like toe nail and vaginal infections, a low carb diet with antifungal medication often proved very beneficial. He also noticed that many of these same patients were diabetic and, accordingly, their diabetes vastly improved at the same time. He found that the low carb diet and antifungal medication could often drop a patients blood sugar down to normal levels and keep them there, but as soon as they went back to their old diet and stopped antifungal medications, the old problems came back! He was excited that he may have found a unique break through for diabetics and told some MDs which he was working with. They immediately discouraged him from further study basing their opinion on the status quo--that diabetes was never treated by low carb diets (well in the 1970s) and antifungal medication (even now).

One of the main causes of diabetes as proposed by the American Diabetes Assoc is that people are over-weight and they eat too much. Kauffman asks, well if 20-30% of the American people are obese, why do not all of the obese people develop diabetes? We are missing 60-110 million diabetic cases in the rest of the obese population. He reasons that not all obese people get diabetes and 10% of type 2 diabetics are NOT over weight. He also finds the genetic angle to not hold water of which I will not go into in this post. His only logical conclusion is that diabetes is a fungi infection with the mycotoxins they produce.

Fungi is every where. We cannot avoid them. Often antibiotic use can open up our immune system to terrible fungi infections. There is also very real world problem of steroid induced diabetes, Streptozotocin (a fungi mycotoxin) induced diabetes, etc, etc. Might I add here that these and others can be linked to fungi infections with the main stream seemingly oblivious to this connection. Could not steroid usage stimulate fungi infections or statins which are derived from fungi mycotoxins also suggest that diabetes may be fungi based? Kauffman points out that there is evidence linking the drinking of cows milk to type 1 diabetes in children and he suggests it is the mycotoxin in the fat cells of milk that may be the link. The USDA does not screen for mycotoxins and they can be found any where in feed stuffs.


History of the Fungi/diabetic link:
1954...........uric acid can cause lab animals to develop diabetes
1963..........it is found that sacchromyces yeast produces uric acid.
1976...........Cryptococcus fungi is found in the islets of langerhans cells of two diabetic dying children. Later studies, Cryptococcus is injected into lab animals resulting in similar results. Cryptococcus also produces uric acid.

1990..........Type 1 diabetes was reportedly cured by using cyclosporin A an antifungal.
---------------
1973.........it was shown that mutton is loaded with mycotoxins
1981.........a study of preg Icelandic women who ate cured mutton close to their pregnancy gave birth to babies with diabetes.
1980...........alloxan (mycotoxin) damages insulin producing beta cells
1981..........Stremtozotocin, a mycotoxin was shown to produce diabetes in lab animals.
1990...........lab rats on a 10% brewers yeast diet developed diabetes
-----------
1973..........common to see cancer patients treated with mycotoxins develop diabetes.
1990.........lab animals were induced into diabetes with L-asparaginase


Kauffman goes on to point out that a corn mycotoxin that is commonly found on corn may be one reason why there seems to be a diabetic epidemic in Latin America. Asperigillus niger is another fungi that is found in many foodstuffs, particularly peanuts and corn. It generates oxalic acid in large amounts which can inhibit our cells that convert carbohydrates into energy leading to high blood sugar.

Sulfa drugs are commonly used to control blood sugar in diabetics by stimulating the pancreas. It is not normally recognized that sulfa drugs are also antifungals. The use of statin drugs have been shown to coincidently lower the risks of producing diabetes. Antifungal means anticholesterol! The anti-cholesterol drugs were discovered accidently because researchers were looking for antifungal medications! They found the statin group work against fungi because they inhibit an enzyme that our bodies need to process cholesterol. Fungi depend on cholesterol for survival Stopping cholesterol production in the fungi is an effective antifungal mechanism. Statin drugs are fungally derived and are mycotoxins. Fungi can produce cholesterol as well., So the ability of statin drugs to inhibit the enzyme and kill fungi at the same time may be the complex mechanism for statins,,,,,,,not simply a lowering of cholesterol. In short, Kauffman suggests that high cholesterol in the human may also be fungi related.

That's enough of the Kauffman theories for now. I just want to suggest that Turmeric does have antifungal properties and its diabetic prevention properties may work on this mechanism! I also seemed to have stopped diabetis from manifesting in my dog last summer by the use of a anti-microbial, sodium chlorite solution known as MMS. Food for thought!

Thus, going back to the original subject of this thread, equine laminitis, it may not be too far fetched to treat laminitis with an anti-microbial. Also, I would be feeding or injecting mega-doses of Vitamin C which is also known for its anti-microbial properties when given in large doses, plus as a superb universal anti-toxin.

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