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Many newly diagnosed celiacs seem to experience an increase in the number
of food allergies and intolerances after starting and maintaining a gluten-
free diet, myself included.  Leaky gut (intestinal permeability) and low
stomach acid (hypochlorhydria) as well as an altered and undesirable mix of
microflora are all likely culprits in the acquisition of the multiple food
allergies.  These conditions can be treated with betaine HCL (acid
supplementation), digestive enzymes and probiotics which seem to reduce or
eliminate the food allergies and intolerances in most cases.  I was puzzled
by one question.  Why do these food allergies begin to flare up only AFTER
starting a gluten-free diet?  One would think one would be more susceptible
to such problems while celiac disease is active and untreated, not while
the intestine is healing on a GF diet.

I could find no research offering a direct explanation for this paradox.
However, based on the following abstracts below, a couple of theories are
possible:

1) One study of young Gambian children being treated for and recovering
from malnutrition and persistant diarrhea showed, at least during the first
months of recovery, an INCREASE in leaky gut instead of a decrease.  It was
noted that the mucosal crypts increased in size while the villi volumes did
not during this initial recovery period.  (The crypts are the valleys
between the finger-like villi.)  Hence, in celiac disease, especially
characterized by symptoms of chronic diarrhea, there may be at least a
temporary increase in leaky gut as the intestine begins to heal on a gluten-
free diet contributing to an increase in food allergies.

2) Studies of both malnourished children and mice have shown a decrease in
the levels of serum IgE compared to normally nourished controls.
Malnutrition diminishes immune system response which leads to more frequent
and increased danger of infection, but at the same time the diminished
immune response seems to decrease IgE mediated reactions (the cause of
allergic reaction) as well as enhancing tolerance to antigens.  Hence,
malnourishment resulting from malabsorption due to active celiac disease,
may result in reducing IgE reactions and increasing tolerance to food
antigens which leak from the gut.  Treating celiac disease with a GF-diet
likely restores or increases IgE levels and causes the immune system to
become less tolerant to food antigens which leak from the gut, thus
resulting in the occurance of multiple food allergies and intolerances
after treatment begins.

These are only theories, but they seem to make sense.

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J Pediatr Gastroenterol Nutr. 1992 Feb;14(2):208-15

Persistent diarrhea and malnutrition--the impact of treatment on small
bowel structure and permeability.

Sullivan PB, Lunn PG, Northrop-Clewes C, Crowe PT, Marsh MN, Neale G.

Dunn Nutrition Centre, University of Cambridge, England.

Previous studies using dual sugar permeability tests suggested that damage
to the small intestinal mucosa plays an important part in the development
of persistent diarrhea in The Gambia. The present study has extended these
findings by examining the effect of nutritional rehabilitation on
intestinal permeability and mucosal morphology. Intestinal permeability,
measured by lactulose:mannitol (L:M) absorption, and mucosal structure,
measured by a quantitative, computerised morphologic technique, were
evaluated in 20 children before and after such treatment. L:M ratios were
high on admission, (0.66 +/- 0.36) and, despite some temporary improvement,
did not significantly improve (0.49 +/- 0.30) following rehabilitation for
one month. The changes in L:M ratio were largely due to an increase in
lactulose absorption, showing that the small intestinal mucosa becomes
more "leaky" as a result of nutritional rehabilitation. Although no
correlation was found between measures of intestinal permeability and
mucosal morphology, nutritional restitution was associated with a
significant increase in size of the mucosal crypt cell compartment, but not
in villous epithelial volumes during the same period. It is necessary to
establish, by further prospective studies, the interval required for full
restitution of small intestinal structure and function during treatment for
persistent diarrhea.

PMID: 1593377 [PubMed - indexed for MEDLINE]

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Allergol Immunopathol (Madr). 2003 Mar-Apr;31(2):83-6

Serum IgE level in malnutrition.

Forte WC, Santos de Menezes MC, Horta C, Carneiro Leao Bach R.

Immunology Section of Santa Casa Medical School and Hospital, Sao Paulo,
Brazil. [log in to unmask]

Infections and malnutrition remain the main causes of infant mortality in
developing countries. In protein-calorie malnutrition, immunologic
responses are affected, which often facilitates infections. However, the
presence of asthma and allergic rhinitis are not commonly recognized in
malnourished individuals. The aim of this study was to evaluate serum IgE
values in children with primary moderate protein-calorie malnutrition.
METHODS: The level of IgE in peripheral blood of 18 children between 2 and
4 old with moderate protein-calorie malnutrition and without associated
parasitic infestation was compared with that of 15 well nourished children
of similar age. IgE serum levels were measured by an immunoenzymatic
method. RESULTS: The median level of serum IgE in malnourished children was
69.30 ng/ml while the control group showed a mean level of 95.97 ng/ml.
This difference was significant (p < 0.01). CONCLUSION: Malnourished
children show decreased serum IgE levels. This might be one of the adaptive
mechanisms of malnutrition employed in an attempt to use energy and protein
reserves for growth and other functions. Our results are coherent with the
decrease in IgE mediated reactions in malnourished patients.

PMID: 12646123 [PubMed - indexed for MEDLINE]

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Clin Immunol Immunopathol. 1983 Sep;28(3):371-82.

IgE responses of malnourished mice: immunogenic and tolerogenic effects of
low-grade antigenic stimulation.

Rose AH, Holt PG, Turner KJ.

Mice maintained on protein-restricted diets after weaning manifested normal
IgE (and IgG) responses following intraperitoneal immunization under
conditions of maximal antigenic stimulation, i.e., antigen adsorbed to
adjuvant. However, antigenic challenge at levels closer to the stimulation
threshold, employing soluble antigen alone, revealed marked differences
between the immune competence of normal and malnourished animals.
Diminished IgE responsiveness to soluble antigen in the malnourished mice
was accompanied by enhanced susceptibility to the induction of antigen-
specific tolerance associated with the appearance of suppressor T cells in
the spleen. It is argued that enhanced susceptibility to suppressor T-cell
induction under conditions of minimal antigenic stimulation may underlie
the diminished IgE responsiveness of the malnourished animals.

PMID: 6224615 [PubMed - indexed for MEDLINE]

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