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Hi,

I was diagnosed with celiac disease eleven months ago. With a change of
diet, my symptoms improved, except that eating any amount of fat still made
me very ill. By last month, I was down to less than 5 grams of fat a day and
still completely miserable. I did not have gall stones or any obvious
physical defect with my gall bladder.

Thanks to Ron Hogan's articles on the gall bladder (
http://www.panix.com/~donwiss/hoggan), some direct correspondence with him,
and some research in a local medical library, I discovered that this problem
could be due to celiac damage. My family doctor and I decided to try to
treat the symptoms without proving the cause. We will leave that to the GI
specialist next month.

I started taking bile salts (what the gall bladder contains) and pancreatic
enzymes to break down the fat. What a difference. As long as I match the
amount of bile salts to the amount of fat I eat, I can tolerate fat again.
My energy levels have picked up and it has been a big psychological boost to
be able to eat in a normal gluten-free way (that sounds kind of odd, but I'm
sure you know what I mean.)

The rest of this post is an explanation of how celiac and fat digestion are
related and a list of references with a summary for anyone who is interested.

*** NOTE ***
This is my own interpretation of what I have read. Check with your doctor
before trying any treatment on your own. Problems with fat digestion and
pain after eating can indicate many different problems and you need to make
sure you are not masking a bigger problem by treating yourself.

-------------------------------------
When you consume fat, cells that line the duodenum, the first part of the
small intestine, produce a hormone called cholecystokinin (CCK). This
hormone causes the gall bladder to release the bile it has stored up. Bile
is produced in the liver and stored in the gall bladder until it is needed.

Bile breaks down the fat into smaller chunks that can be digested by enzymes
that the pancreas produces.  The enzymes from the pancreas break down the
fat into components that can be absorbed into the bloodstream and used or
stored in fat cells.

The research literature shows that untreated celiac patients do not produce
the normal amount of CCK. Many patients, in fact, show no CCK production at
all. As a result, bile is not released and the pancreatic enzymes are not
able to break down the fat efficiently. The result can be pain, diarrhea,
gas, and stools that float or are foamy.

The studies that tested treated celiacs all concluded that this is a
reversible defect, in other words, the ability to produce CCK returns with
healing and fat digestion returns to normal. In those studies, the results
for treated celiacs matched the results for non-celiac patients. Some
studies tested the same patients before they started a gluten-free diet and
again after a period of time on the diet. They confirmed the reversal in
each case.

Note that this effect is happening without any gallstones or other disease
of the gall bladder. There is some discussion in the literature about
whether the gall bladder in celiac patients is less responsive to CCK than
the gall bladder of non-celiacs, but the latest study listed (1991) showed
equivalent response when CCK was administered directly.
-------------------------------------

Curious events, but interesting to me. I hope it is useful to some of you as
well. If you have anything to add, please let me know.


Sue Newell
Waterloo, Ontario
[log in to unmask]



Celiac Disease and Gallbladder Function - Summary

1. Colombato L, Parodi H, Cantor D, "Biliary function studies in patients
with celiac sprue" American Journal of Digestive Diseases 1977; 22(2): 96-98

Summary: Despite normal gallbladder and bile ducts, untreated celiac
patients showed reduced secretion of bile bilirubin. In 4 of 11 cases, bile
in the duodenum was totally absent. Bile flow induced with magnesium sulfate
was also reduced in the celiac patients, with 7 of 11 patients showing no
bile flow to the intestine.


2. Di Magno E, Go W, Summerskill W, "Impaired cholecystokinin-pancreozymin
secretion, intraluminal dilution, and maldigestion of fat in sprue"
Gastroenterology 1972; 63(1): 25-32

Summary: Demonstrated a decrease in pancreatic enzymes and gallbladder
contents after intraduodenal perfusion of essential amino acids in untreated
celiac patients. Gallbladder and pancreatic function were normal after
intravenous cholecystokinin-pancreozymin. Impairment of fat digestion was
greater after the feeding of a second meal.


3. Maton P, Selden A, Fitzpatric M, Chadwick V, "Defective gallbladder
emptying and cholecystokinin release in celiac disease. Reversal by
gluten-free diet" Gastroenterology 1985; 88(2): 391-396

Summary:  Demonstrated little or no gallbladder emptying in response to
drinking arachis oil in untreated celiac patients. In those that showed some
response, onset of contractions was substantially delayed and volume
decreased. Two patients with non-responsive celiac disease showed
intermediate results. Six patients with treated celiac disease (observed
healing) showed rates similar to normal.

Concluded there is a reversible defect of gallbladder emptying and CCK
release in celiac disease.


4. Harvey RF, "Gallbladder emptying in celiac disease" (letter)
Gastroenterology 1986; 90(3): 801-802

Summary: Opposed Maton's conclusion that impaired CCK production entirely
explains reduced response. [He is concerned that reduced gall bladder
response may also play a roll.]


5. Hopman W, Rosenbusch G, Hectors M, Jansen J, "Effect of predigested fat
on intestinal stimulation of plasma cholecystokinin and gall bladder
motility in coeliac disease" Gut 1995; 36(1): 17-21

Summary:  "Cholecystokinin (CCK) release and gallbladder emptying in
response to a fatty meal are completely abolished in coeliac disease." When
the corn oil stimulus was pre-digested with bile and pancreatic juice, CCK
release and gall bladder contractions increased.


6. Masclee A, Jansen J, Driessen W, Geuskens L, Lamers C, "Gallbladder
sensitivity to cholecystokinin in coeliac disease." Scandinavian Journal of
Gastroenterology 1991; 26(12): 1279-1284

Summary:  Gallbladder sensitivity to CCK-analog in treated and untreated
celiac patients did not differ from normals. Concluded reduced gallbladder
contraction is due to reduced CCK secretion, not gallbladder responsiveness
to CCK.


7. Brown AM, Bradshaw MJ, Richardson R, Wheeler JG, Harvey RF, Pathogenesis
of the impaired gall bladder contraction of coeliac disease. Gut 1987; 28:
1426-1432

Summary: Initiated gallbladder emptying with a CCK-analog [a substance that
is biochemically similar to CCK]. Untreated celiac patients required larger
doses to initiate contractions and demonstrated decreased gall bladder
emptying. Did not distinguish between effect of increased gallbladder size
in celiac patients and gallbladder resistance to CCK.