Celiac Disease, Gluten Ataxia and Candidiasis
Subject: Celiac disease, triggered by gluten proteins from wheat
in susceptible people, can damage the central nervous system.
The cell walls of Candida, the yeast responsible for oral thrush, vaginal
infections and intestinal Candidiasis, contain the same protein sequence
as wheat gluten and may trigger or stimulate Celiac Disease.
Our understanding of celiac disease has come a long way in the last few
years. Several recent studies have linked celiac disease to central nervous
system damage which may cause sporadic ataxia. Other studies have
identified the particular protein sequence in gluten which causes celiac
disease. Other researchers have identified a similar protein in
candida yeast and suggest that it may also trigger the same disease. These
studies suggest that the typical digestive symptoms we associate with
celiac disease are present less than 20% of the time. Having "normal"
digestion no longer rules out the disease.
This is a complicated business but I think rather than gloss over it many
people deserve and need the details. So please bear with me and skip over
the parts that get to thick.
First a bit of background:
Celiac disease is also called coeliac disease or celiac sprue. The Merck
Manual defines it as a "chronic intestinal malabsorption disorder
caused by intolerance to gluten."  The villi of the
small intestine atrophy and nutrients are poorly absorbed resulting in
steatorrhea (frequent greasy stools) and malnutrition. Sufferers
usually get better when gluten containing cereal grains are removed from
the diet. Although the syndrome was described earlier, 
it wasn't until 1950 that the link between dietary cereals and the disease
was figured out.  During the Second World War when the
Germans occupied Holland , children with celiac sprue improved dramatically
only to get sick again disease again at the end of the war. During
the war, wheat and rye were in short supply in Holland . The researcher
who noticed this was able to show that it was the gluten protein in grains
which triggered the disease. 
Celiac is a genetic disorder and the incidence varies among different
populations. Ireland and people of Irish descent have the highest
incidence, about 1 person in 300. In Europe and the United States the
incidence is much lower, reported at about 1 in 2,500 or less. The
longer a population has eaten wheat the lower the incidence. Europeans
have cultivated wheat for almost 9,000 years while the Irish have grown
it for only about 3,000 years. I suppose we could rename the disease Celtic
Sprue rather than celiac sprue. When tested 90% of people with celiac
disease are positive for the HLA-B8 antigen in their blood.
The classic problems associated with celiac disease are those of malabsorption
and nutritional deficiency. Children with the disease fail to thrive;
they are deficient in all of the fat soluble vitamins (A, E, K, and D)
and many of the minerals, especially calcium and magnesium. While
children are prone to osteomalacia, adults usually develop osteoporosis.
This has been the description of celiac disease that medical text books
have talked about for decades. Now for what's new.
For the last ten years we have known that celiac disease is associated
with hypothyroid disease, specifically Hashimoto's Disease. About
10- 14% of celiac patients are hypothyroid. Celiac patients are about
ten times as likely to have thyroid nodules. [5,6,7] Is it the same
genetic predisposition making people overly prone to develop autoimmune
diseases that causes both conditions? Or is it the chronic bowel
inflammation that stimulates these autoimmune reactions? At this point
it isn't clear.
Celiac is clearly an autoimmune disease. The gliaden portion of the gluten
protein contains a sequence of amino acids that trigger the immune reaction.
When they bind on to the intestinal mucosa they act as an antigen and
summon killer lymphocytes to attack. The immune system also develops an
immune reaction to the muscle lining of the intestine, the endomysium
and the enzyme transglutaminase.  People with celiac disease make antibodies
which attack both the endomysium and the enzyme transglutaminase.
Once this autoimmune process has been triggered, damage occurs in other
parts of the body and not just the intestine.
Neurological damage occurs with celiac disease. Early on this was
thought to be due to nutrient deficiencies caused by malabsorption.
Current research shows that the problem is more complex. Celiac disease
stimulates the production of antibodies which attack areas besides the
intestine including the central nervous system. About 40%
of patients who suffer from idiopathic sporadic ataxia have celiac disease
which damages their central nervous systems. [9,10,11] The neurological
symptoms of celiac disease mimic the symptoms of multiple sclerosis to
the degree that celiac must always be ruled out when diagnosing this disease.
 The neurological conditions caused by celiac disease are now
called gluten ataxia and cause damage to the cerebellum, the posterior
columns of the spinal cord, and the peripheral nerves. 
The studies on gluten ataxia have revealed a significant statistic.
In patients who had clearly measurable antibodies that are diagnostic
of celiac disease and were suffering from gluten ataxia, only 13% had
any gastrointestinal complaints. In other words, the hallmark symptoms
of poor digestion we associate with celiac disease and use to diagnose
the condition may be absent in 87% of patients with gluten related problems!
 This suggests that celiac may be way under diagnosed.
Now we come to what to me is the most interesting of the recent research
regarding celiac. It seems fitting that the research again comes
from Holland , where celiac disease was first linked to diet. Dr.
Nieuwenhuizen, from the research group TNO Nutrition and Food Research,
published a paper in the June, 2003, Lancet. He links celiac disease with
Candida albicans. Dr. Nieuwenhuizen, knowing the actual sequence of proteins
which trigger celiac disease from the published work of other scientists,
had searched the databases available to him through TNO to see if the
same sequence existed in other places. It turns out the identical
sequence of proteins occur in the cell walls of Candida albicans. 
These Candida gluten-like proteins turn out to be the yeast's "hypha-specific
surface protein" nicknamed Hwp1. This is the yeast's version of Velcro
and allows it to attach and hang onto the endomysium in the wall of the
intestine. It is also targeted by transglutaminase, the enzyme
which acts on the gluten protein and serves as a target for immune antibodies.
Candida species which don't have this Hwp1 protein can't attach themselves
to the digestive tract. 
If Candida can trigger the same chemical and immunological reactions as
wheat gluten do we can imagine a number of interesting implications.
First, in people with celiac disease, symptoms usually get better rapidly
when they eliminate gluten from their diet. This isn't always the
case. Even without gluten some people continue to have symptoms.
They may have intestinal Candidiasis. The Candida in their gut may be
acting like gluten and continues triggering symptoms.
Second, an acute Candida infection may trigger the onset of celiac disease.
Even if the Candida is treated and eliminated, the person could be left
with a permanent sensitivity to wheat gluten. Candida infections
occur frequently with antibiotic usage. In people genetically susceptible
to celiac, extra caution should be exercised when using antibiotics to
prevent Candida overgrowth.
Third, if wheat can cause neurological damage as in gluten ataxia, it
is reasonable to assume that Candida could also do so by the same process.
Reports of Candida infections causing neurological symptoms are not uncommon;
now we have a possible explanation.
Fourth, if only a small portion of the people with gluten ataxia have
gastrointestinal symptoms despite their severe damage elsewhere in their
bodies, it is reasonable to assume that Candida could stimulate significant
problems while producing slight or no digestive symptoms.
So what does all this mean? Here's my bottom line:
Celiac disease may be grossly under diagnosed. It should be ruled out
in any chronic digestive condition even if the symptoms don't fit the
classic picture. Celiac disease should also be ruled out in osteoporosis
and in neurological problems, especially MS. Celiac disease should
also be ruled out in Hashimoto's Disease and other thyroid abnormalities.
Whenever Celiac disease is diagnosed, Candida infections should be tested
for and treated aggressively. People of Irish descent are far more
likely to get celiac disease than others and should be extra cautious
to avoid Candida infections and treat them aggressively if they occur.
1. Merck Manual, Seventeenth Edition
2. Thaysen T, Non-Tropical Sprue. Copenhqagen, Levin and Munsgaard.
3. Dicke, W. Coeliac Disease: Investigation of harmful effects
of certain types of cereal on patients with celiac disease. Doctoral
Thesis, University of Utrecht . Netherlands , 1950.
4. Van de Kramer, Weijers, Dicke. Coeliac Disease. IV. An
investigation into the injurious constituents of wheat in connection with
their action on pateinets with celiac disease. Acta Paediat. 42.223,
5. Counsell et al. Coeliac disease and autoimmune thyroid
disease. Gut 1994;35: 844-846
6. Collin et al. Autoimmune thyroid disorders and coeliac disease.
European Journal of Endocrinology 1994;130:137-140
7. Freeman H. Deliac associated autoimmune thyroid disease: A study
of 16 patients with overt hypothyroidism. 1995; July/Aug: 9(5): 242-246
8. Nat Med. 1997 Jul;3(7):797- Identification of tissue transglutaminase
as the autoantigen of celiac disease.
Dieterich W, Ehnis T, Bauer M, Donner P, Volta U, Riecken EO, Schuppan
9. Brain. 2001 May;124(Pt 5):1013-9. Sporadic cerebellar ataxia
associated with gluten sensitivity.
Burk K, Bosch S, Muller CA, Melms A, Zuhlke C, Stern M, Besenthal I, Skalej
M, Ruck P, Ferber S, Klockgether T, Dichgans J
10. Neurology. 2002 Apr 23;58(8):1221-6The humoral response in the
pathogenesis of gluten ataxia. Hadjivassiliou M, Boscolo S, Davies-Jones
GA, Grunewald RA, Not T, Sanders DS, Simpson JE, Tongiorgi E, Williamson
CA, Woodroofe NM.
11. J Neurol Neurosurg Psychiatry. 2003 Sep;74(9):1221-4
Dietary treatment of gluten ataxia. Hadjivassiliou M, Davies-Jones GA,
Sanders DS, Grunewald RA.
12. Neurol Sci. 2001 Nov;22 Suppl 2:S117-22
Neurological manifestations of gastrointestinal disorders, with particular
reference to the differential diagnosis of multiple sclerosis. Ghezzi
A, Zaffaroni M.
13. Lancet. 1998 Nov 14;352(9140):1582-5 Clinical, radiological,
neurophysiological, and neuropathological characteristics of gluten ataxia.
Hadjivassiliou M, Grunewald RA, Chattopadhyay AK, Davies-Jones GA, Gibson
A, Jarratt JA, Kandler RH, Lobo A, Powell T, Smith CM.
14. J Neurol Neurosurg Psychiatry. 2003 Sep;74(9):1221-4 Dietary
treatment of gluten ataxia. Hadjivassiliou M, Davies-Jones GA, Sanders
DS, Grunewald RA.
15. Lancet. 2003 Jun 21;361(9375):2152-4. Is Candida
albicans a trigger in the onset of coeliac disease?
Nieuwenhuizen WF, Pieters RH, Knippels LM, Jansen MC, Koppelman SJ.
16. Science. 1999 Mar 5;283(5407):1535-8. Adhesive
and mammalian transglutaminase substrate properties of Candida albicans
Hwp1. Staab JF, Bradway SD, Fidel PL, Sundstrom P.
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