CorePsychBlog: Hard Evidence: Gluten Sensitivity and Neurologic Impairment

Gluten Sensitivity: A neurological problem with gait, peripheral neuropathy
and cognitive disturbances. Comments on testing with IgG Antigliadin Antibodies: Some facts for the medical readers and those interested in more information.

The brain and the bowel really are connected: check out this evidence.

Please do share this with your medical provider if they doubt the celiac material [copied all the refs here, and link below to the article itself]. Directly from this article:

Gluten sensitivity as a neurological illness
M Hadjivassiliou, R A Grünewald and G A B Davies-Jones [Department of Neurology, The Royal Hallamshire Hospital, Glossop Road, Sheffield, S10 2JF, UK]
Journal of Neurology Neurosurgery and Psychiatry
2002;72:560-563

AT: http://jnnp.bmj.com/cgi/content/full/72/5/560
[Italics my own emphasis- these are only portions of the full text]

RECENT ADVANCES: PREVALENCE, SMALL BOWEL
HISTOLOGY, AND GENETIC SUSCEPTIBILITY

Some studies looking at normal populations have
shown that the prevalence of CD [celiac disease]
is much higher than previously thought
(approximating to 1 in 100). Most of such
patients have no gastrointestinal symptoms. In
addition, experimental data in patients with
gluten sensitivity suggest that there is a range
of mucosal abnormalities affecting the small
bowel ranging from preinfiltrative
(histologically normal) to infiltrative, to
hyperplastic to flat destructive (seen in CD),
and finally to the irreversible hypoplastic
atrophic lesions.

Now that I have your attention, let's dig into the details:

Increasing the gluten load may result in progression
of the severity of the lesion. In those patients where
the histology is normal, staining of the T cell subpopulations
of the intraepithelium of the small bowel biopsies
shows alteration of T cell subpopulations of the
intraepithelial lymphocytes (increase of the / T
cells). This finding is said to be a marker of
potential CD. This procedure is only available
in a very few pathology laboratories, rendering
its use limited.

Finally, CD has a very strong association with
the human lymphocyte antigen (HLA) of the major
histocompatibility complex. Ninety per cent of
patients with CD have the HLA DQ2; the rest have
DQ8.
These advances suggest that gastrointestinal
symptoms are absent in most patients with CD,
that the definition of gluten sensitivity can no
longer be solely based on the presence of an
enteropathy and that genetic susceptibility may
be an important additional marker for gluten
sensitivity. Given the knowledge of these
advances and approaching gluten sensitivity from
a neurological perspective we set up to address
the following question: Does cryptic gluten
sensitivity play a part in neurological illness?

THE NEUROLOGY OF GLUTEN SENSITIVITY 

Over the past 8 years we have used antigliadin
antibodies to screen patients with neurological
dysfunction of unknown aetiology. Our original
study concluded that gluten sensitivity played an
important part in neurological illness.

The evidence was statistical: Patients with
neurological disease of unknown aetiology were
found to have a much higher prevalence of
circulating antigliadin antibodies (57%) in their
blood than either healthy control subjects (12%)
or those with neurological disorders of known
aetiology (5%).

Since then, we have identified 131 patients with
gluten sensitivity and neurological disorders of
unknown aetiology. [Table 2 in the full article shows the neurological
diagnoses we have encountered.] Perhaps not
surprisingly the commonest manifestations are
ataxia (also known as gluten ataxia) and
peripheral neuropathy.

CONTENTIOUS ISSUES :
"But antigliadin antibodies lack specificity."

IgG anti-gliadin antibodies have been the
best diagnostic marker in the neurological
population we have studied. IgG anti-gliadin
antibodies have a very high sensitivity for CD
but they are said to lack specificity. In the
context of a range of mucosal abnormalities and
the concept of potential CD, they may be the only
available immunological marker for the whole
range of gluten sensitivity of which CD is only a
part. Further support for our contention comes
from our HLA studies:
Within the group of patients with neurological
disease and gluten sensitivity (defined by the
presence of anti-gliadin antibodies) we have
found a similar HLA association to that seen in
patients with CD: 70% of patients have the HLA
DQ2 (30% in the general population), 9% have the
HLA DQ8, and the remainder have HLA DQ1. The
finding of an additional HLA marker (DQ1) seen in
the remaining 20% of our patients may represent
an important difference between the genetic
susceptibility of patients with neurological
presentation to those with gastrointestinal
presentation within the range of gluten
sensitivity.

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Just take a moment to look at the reference topics, and you will start to think more about the psych/neurologic implications of this overlooked problem.

Next post on Vitamin B12 deficiency those symptoms with the downstream findings from gluten sensitivity... and we're only scratching the surface of the bowel thing.