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Hi All,
Don Wiss forwarded the following post to me:

>I know you have studied celiac disease for a long time.  However, I need to
>disagree with the statement that fibromyalgia indicates celiac disease.   It
>has been proven that persons with fibromyalagia have a decreased amount of
>serotonin  and an increased amount of substance P in their spinal fluid.
>This indicates it is a result of not enough serotonin in the brain.   Many
>of us who suffer from fibromyalgia do not have any problems with the
>digestive system at all.   There are also PET scans that indicate that
>fibroymalgia patients have less dopamine activity in the brain indicating it
>truly is more a brain disease than celiac.

The poster's first point differentiating celiac disease from fibromyalgia on
the basis of reduced serotonin in fibromyalgia may be unaware of the finding
that celiac patients have fewer serotonin receptors on their platelets (1).

Although I don't know about the spinal fluid, elevated levels of substance P
have also been reported in the intestinal mucosa of celiac patients (2,3,4,5).

A lack of digestive problems does not rule out celiac disease, as one of the
foremost researchers in that area has reported that 50% to 60% of untreated
celiacs are asymptomatic (6).

Altered dopamine activity has also been reported in celiac disease (7).

As regards the poster's contention that it is really more a brain disease than
celiac disease, the connections between celaic disease and altered brain
perfusion (8), epilepsy without cerebral calcifications (9), epilepsy with
cerebral calcifications (10, 11), a wide variety of neuropathic symptoms (12),
and a number of psychiatric ailments (13), all counter the poster's perspective.

Finally, if Suzanne Romey says that her fibromyalgia symptoms go away when
gluten-free, and return when she eats gluten, I believe her.


Sources:
1. Chiaravalloti G, et al.
Platelet serotonin transporter in coeliac disease.
Acta Paediatr. 1997 Jul;86(7):696-9.

2. Sjolund K, et al.     Enteropathy of coeliac disease in adults:
increased number of enterochromaffin cells the duodenal mucosa.
Gut. 1982 Jan;23(1):42-8.

3. Sjolund K, et al.  Duodenal endocrine cells in adult coeliac disease.
Gut. 1979 Jul;20(7):547-52.

4. Bloom SR.    Hormonal peptides of the gastrointestinal tract.
Eur J Clin Invest. 1979 Apr;9(2 Pt 1):111-3.

5. Domschke S, et al.  Coeliac sprue: abnormalities of the hormone
profile of gastroduodenal mucosa. Scand J Gastroenterol Suppl.
1989;167:86-9.

6. Marsh MN, et al. Morphology of the mucosal lesion in gluten
sensitivity. Baillieres Clin Gastroenterol. 1995 Jun;9(2):
273-93. Review.

7. Hallert C, et al.    Psychic disturbances in adult coeliac disease.
III. Reduced central monoamine metabolism and signs of depression.
Scand J Gastroenterol. 1982 Jan;17(1):25-8.

8. De Santis A, et al.    Schizophrenic symptoms and SPECT
abnormalities in a coeliac patient: regression after a gluten-free
diet. J Intern Med. 1997 Nov;242(5):421-3.

9. Cronin CC, et al.  Coeliac disease and epilepsy.
QJM. 1998 Apr;91(4):303-8.

10.  Bernasconi A, et al.  Celiac disease, bilateral occipital
calcifications and intractable epilepsy: mechanisms of seizure
origin. Epilepsia. 1998 Mar;39(3):300-6.

11. Hernandez MA, et al.       Epilepsy, cerebral calcifications
and clinical or subclinical coeliac disease. Course and follow
up with gluten-free diet. Seizure. 1998 Feb;7(1):49-54.

12. Hadjivassiliou M, et al. Clinical, radiological,
neurophysiological, and neuropathological characteristics of
gluten ataxia. Lancet. 1998 Nov 14;352(9140):1582-5

13. Hoggan, R.   Absolutism's Hidden Message for
Medical Scientism.  Interchange. 1997; 28(2/3): 183-189.

best wishes,
Ron Hoggan
Calgary, Alberta