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 fibromyalgia 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 fibromyalgia patients have less dopamine activity in the brain indicating it truly is more a brain disease than celiac.

The posters 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 dont 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 posters contention that it is really more a brain disease than celiac disease, the connections between celiac 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 posters perspective.

Finally, if (the poster) says that her fibromyalgia symptoms go away when gluten-free, and return when she eats gluten, I believe her.

Sources:

  • Chiaravalloti G, et al. Platelet serotonin transporter in celiac disease. Acta Paediatr. 1997 Jul;86(7):696-9.
  • Sjolund K, et al. Enteropathy of celiac disease in adults: Increased number of enterochromaffin cells the duodenal mucosa. Gut. 1982 Jan;23(1):42-8.
  • Sjolund K, et al. Duodenal endocrine cells in adult celiac disease. Gut. 1979 Jul;20(7):547-52.
  • Bloom SR. Hormonal peptides of the gastrointestinal tract. Eur J Clin Invest. 1979 Apr;9(2 Pt 1):111-3.
  • Domschke S, et al. Celiac sprue: abnormalities of the hormone profile of gastroduodenal mucosa. Scand J Gastroenterol Suppl. 1989;167:86-9.
  • Marsh MN, et al. Morphology of the mucosal lesion in gluten sensitivity. Baillieres Clin Gastroenterol. 1995 Jun;9(2): 273-93. Review.
  • Hallert C, et al. Psychic disturbances in adult celiac disease. III. Reduced central monoamine metabolism and signs of depression. Scand J Gastroenterol. 1982 Jan;17(1):25-8.
  • De Santis A, et al. Schizophrenic symptoms and SPECT abnormalities in a celiac patient: regression after a gluten-free diet. J Intern Med. 1997 Nov;242(5):421-3.
  • Cronin CC, et al. Celiac disease and epilepsy. QJM. 1998 Apr;91(4):303-8.
  • Bernasconi A, et al. Celiac disease, bilateral occipital calcifications and intractable epilepsy: mechanisms of seizure origin. Epilepsia. 1998 Mar;39(3):300-6.
  • Hernandez MA, et al. Epilepsy, cerebral calcifications and clinical or subclinical celiac disease. Course and follow up with gluten-free diet. Seizure. 1998 Feb;7(1):49-54.
  • Hadjivassiliou M, et al. Clinical, radiological, neurophysiological, and neuropathological characteristics of gluten ataxia. Lancet. 1998 Nov 14;352(9140):1582-5
  • Hoggan, R. Absolutisms Hidden Message for Medical Scientism. Interchange. 1997; 28(2/3): 183-189.

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