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Part 1 - Dietary Fructose Intolerance
Celiac disease sufferers often continue to experience gastrointestinal
discomfort long after going on a gluten-free diet. [Ref. #1 & #2] Fructose
intolerance has been listed as one cause of these continued problems.
There are 2 forms of fructose intolerance: Hereditary (HFI) and Dietary
(DFI). DFI is also referred to as Fructose Malabsorption. HFI is rare,
incureable and caused by a genetic disorder where the enzyme Aldolase B is
missing and fructose cannot be broken down. (See
http://www.hfi.ch/index.thtml/en/info/index.html ) Only DFI will be
considered here. DFI has only been recently recognized as a significant
medical problem and may affect a substantial portion of the general
population.
(What is fructose? See http://www.ific.org/publications/qa/fructoseqa.cfm )
DFI or fructose malabsorption is characterized by the inability to absorb
fructose efficiently. As a consequence fructose reaches the colon where it
is broken down by bacteria to short fatty acids, CO2 and H2. Bloating,
cramps, osmotic diarrhea and other symptoms of irritable bowel syndrome are
the consequences and can be seen in about 50% of fructose malabsorbers. Up
to 36% of the European population present with fructose malabsorption in a
more or less severe form, and about half of them are symptomatic. Fructose
malabsorption is associated with early signs of mental depression and low
serum tryptophan concentrations. [Ref. #3]
The intestinal absorption of fructose is carried out by the facilitative
hexose transporter, which has been designated as GLUT5. GLUT5 is a high
affinity fructose transporter located on the luminal surface of absorptive
epithelial cells in the small intestine of humans and rodents. [Ref. #4]
Hence, damage to the small intestine by celiac disease could easily
interfere with the GLUT5 transport system and impair fructose absorption.
Celiac disease may therefore be a transitional cause of DFI.
The University Of Iowa Health Care department has set up an informative
website on DFI:
http://www.uihc.uiowa.edu/FRUCTOSE/index.htm
The only treatment for DFI is to avoid foods containing fructose and
sorbital. That means avoiding almost all fruit and many vegetables and
products containing fructose additives like corn syrup and other forms of
sugar. A breath test can be given to determine if one has DFI. A fructose
enzyme supplement, if developed, might offer a future treatment for the
condition.
The dietary basics are outlined here:
http://www.uihc.uiowa.edu/FRUCTOSE/LivingwithDFI.htm
Since the symptoms of DFI are due in large part to bacterial breakdown of
unabsorbed fructose, the use and choice of a probiotic may alleviate some
of the symptoms.
The University of Iowa website considers the following question:
"Does dietary fructose intolerance ever go away?
People with fructose intolerance associated with celiac disease, a chronic
intestinal disorder caused by intolerance to gluten, have returned to a
more normal pattern of eating once the inflammation from celiac disease
resolves. Antidotal evidence suggests a reversal of fructose intolerance
may occur when, after following a gluten free diet, the intestines heal. A
PubMed search did not reveal studies where this reversal is documented."
Reducing dietary fructose and sorbital has been demonstrated to improve
mood and gastrointestinal disturbances. DFI causes low serum tryptophan
levels and is associated with mental depression. [Ref. #3] One might think
that tryptophan supplementation would be a natural course of action for
people with mental depression from DFI. However, the possible association
between 5 hydroxytryptophan (5-HTP) and tryptophan and the potentially
fatal Eosinophilia-Myalgia Syndrome (EMS) has caused these products to be
tightly regulated and restricted as supplements in the United States and in
other countries. (See http://vm.cfsan.fda.gov/~dms/ds-tryp1.html ) In
addition, 5-HTP and tryptophan supplementation have not been shown to be
clearly effective in alleviating depression and other mental states. [Ref.
#5 & #6]
For more information on tryptophan see: http://www.whfoods.com/genpage.php?
tname=nutrient&dbid=103
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[Ref. #1]
Am J Gastroenterol. 2002 Aug;97(8):2016-21
Etiology of nonresponsive celiac disease: results of a systematic approach.
Abdulkarim AS, Burgart LJ, See J, Murray JA.
Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester,
Minnesota, USA.
OBJECTIVES: Nonresponse or relapse of symptoms is common in patients with
celiac disease treated with gluten free diet. Refractory sprue (RS) is
defined as initial or subsequent failure of a strict gluten-free diet to
restore normal intestinal architecture and function in patients who have
celiac-like enteropathy. The aims of this study were: 1) to identify causes
of persistent symptoms in patients referred with presumed diagnosis of
nonresponsive celiac disease (NCD); and 2) to characterize patients with
true RS. METHODS: Patients were identified who had been systematically
evaluated for NCD between January 1997, and May 2001. Patient records and
small bowel biopsy results were reviewed. RESULTS: A total of 55 patients
were referred with a presumed diagnosis of NCD. Six did not have celiac
disease and had other diseases responsible for their symptoms. Diarrhea,
abdominal pain, and weight loss were the most common reasons for evaluation
in cases of NCD, whereas weight loss, steatorrhea, and diarrhea were the
most common presenting features of RS (nine patients). Of the 49 patients
with celiac disease, 25 were identified as having gluten contamination.
Additional diagnoses accounting for persistent symptoms included:
pancreatic insufficiency, irritable bowel syndrome, bacterial overgrowth,
lymphocytic colitis, collagenous colitis, ulcerative jejunitis, T-cell
lymphoma, pancreatic cancer, fructose intolerance, protein losing
enteropathy, cavitating lymphadenopathy syndrome, and tropical sprue.
CONCLUSIONS: Based on this study, we conclude the following: 1) gluten
contamination is the leading reason for NCD; 2) of NCD cases, 18% are due
to RS; and 3) alternative diseases or those coexistent with celiac disease
and gluten contamination should be ruled out before a diagnosis of RS is
made.
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[Ref. #2]
Gastroenterology. 1997 Jun;112(6):1830-8
The prevalence and causes of chronic diarrhea in patients with celiac sprue
treated with a gluten-free diet.
Fine KD, Meyer RL, Lee EL.
Division of Gastrointestinal Research, Baylor University Medical Center,
Dallas, Texas 75246, USA.
BACKGROUND & AIMS: The majority of patients with celiac sprue experience
diarrhea before diagnosis. There have been no studies of the prevalence or
causes of chronic diarrhea in these patients after treatment with a gluten-
free diet. METHODS: Seventy-eight patients with celiac sprue (59 women and
19 men) treated with a gluten-free diet for at least 12 months were
surveyed about their bowel habits. Those with chronic diarrhea, defined as
passage of loose stools three or more times per week for 6 months,
underwent an extensive diagnostic evaluation to determine its cause.
RESULTS: Sixty-two of the 78 patients (79%) experienced diarrhea before
treatment, and 13 (17%) had chronic diarrhea (of lesser severity) after
treatment. The causes of diarrhea in 11 patients consenting to this study
were microscopic colitis, steatorrhea secondary to exocrine pancreatic
insufficiency, dietary lactose or fructose malabsorption, anal sphincter
dysfunction causing fecal incontinence, and the irritable bowel syndrome.
Only 1 patient had antigliadin antibodies detected in serum or small
intestinal villous atrophy. CONCLUSIONS: After treatment of celiac sprue
with a gluten-free diet, chronic diarrhea persists in a substantial
percentage of patients. Although ongoing gluten ingestion is one possible
cause, other causes may be more frequent. Therefore, diagnostic
investigation of diarrhea in celiac sprue after treatment seems warranted.
* * *
Continued in Part 2
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