When celiac disease Is Only A Reversible Niacin Deficiency
Joseph Arabasz MD
Feb 19, 2008 19:19 PST
I hope this note finds you well. I actually completed these
Comments several years back, but they were buried under another title.
Note that in 1888 when dr. gee reported the "celiac affliction",
Vitamines hadn't been discovered, which means that nobody knew about Niacin,
Vitamine B3. That particular Vitamine was only alluded to in 1916 and its
crystalline structure wasn't elucidated until 1926, and Niacin's chemical
structure wasn't known until the 1930's.
It has been shown that a severe deficiency of Niacin, as might occur
during the starvations of the second world war, leads to sensitization of
the gut to gluten, i.e. the protein component of barley, oats, rye and
I am quite sure, for that reason, many cases of Niacin deficiency were
labeled celiac disease, when they weren't because I get the impression
that sort of thing happens even today. This would lead the uninformed to
think the patient had a genetic disease, when they only had a Vitamine
deficiency. Some types of fascism would probably imply that to ostracize
a group they couldn't compete with, and ruin a person's reputation.
This is the same idea as the freud misadventures, because Vitamines
hadn't been discovered in either case prior to 1910.
It's possible that even in 1950, Physicians didn't know that a Niacin
deficiency caused the gut to be reversibly sensitized to gluten, or wheat
type products. It would be interesting to evaluate the Niacin stores of
Patients who have been diagnosed with celiac disease, and then replace any
Niacin deficiencies, and, after that has been accomplished, retest for
anti-gluten antibodies and see how the patient does clinically.
While searching many dozens of Medical Texts for this material, I only
found the reference to a Niacin Deficiency once, in an Article in a Text
by Dr DA Roe MD published during 1985, H Sidransky as Editor.
The possibility exists that atrophic villi exist as an end stage
condition to anything causing significant damage to the duodenal portion
of the gut, without proper repair, thus contributing to PIM (post
infection (or possibly any insult to the gut) malabsorption.
Best wishes always.
Joseph W. Arabasz MD
Past Division Chairman, Anesthesiology, Cook County Hospital, Chicago,
Past Chairman, Respiratory Therapy, Cook County Hospital, Chicago,
PO Box 6939
Denver, CO 80206
The ingestion of wheat
The "Coeliac Affection" was first reported by Gee in 1888, however it was
not until 1950 that wheat was proposed to be the cause of celiac disease.
The evidence was based on the observation of a dutch physician named dicke
who noted during World War II, a time when wheat grains were scarce in
Holland, that children with celiac disease who had otherwise failed to
thrive improved on a wheat-poor diet. Since then the large water-insoluble
protein, gluten, present in wheat has been identified as the offending
substance. Extraction of gluten with alcohol has further narrowed activity
to smaller proline-rich proteins called gliadins which are capable of
precipitating disease in previously asymptomatic celiacs. Analogous proteins
exist in other grains such as rye, barley and oats and therefore these
grains are also capable of exacerbating celiac disease. The specific peptide
sequence of the gliadins responsible for triggering intestinal inflammation
has not yet been identified.
The genetic background of the individual
Celiac disease runs in families. First degree relatives of individuals with
celiac disease may or may not manifest symptoms of the disease.
Predisposition to gluten sensitivity has been mapped to the major
histocompatibility (MHC) D region on chromosome 6. The most important HLA
haplotype is DQw2 which is often in linkage with DR3. Other important HLA
haplotypes identified are DR7 and DPB 1, 3, 4.1 and 4.2. The sites on these
MHC class 2 expressed proteins responsible for interacting with gliadin and
host T cell receptors thereby sensitizing the intestine to gluten have not
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