Celiac disease does follow the exact same disease pathway as MS. All autoimmune diseases do. This pathway originates in the exocrine pancreas with missing digestive enzymes that digest proteins. These enzymes are called protease and DNase 1. Gluten is a "protein", which would require these enzymes in order to be properly metabolized.
In the study entitled “Pancreatic endocrine and exocrine changes in celiac disease” researchers concluded, “In summary the endocrine and exocrine function of the pancreas may be impaired in celiac disease and their pathogenesis may be closely linked” (Freeman, 2007).
Under the thread "Some Interesting Connections" I showed how these missing enzymes would lead to every symptom found in MS. For instance, a lack of these enzymes leads to the inability to properly metabolize vitamin B12, a lack of essential amino acids, high homocysteine, increased risk of hypothyroidism, activated kynurenine pathway, spinal cord degeneration, an increased risk of lymphoma, elevated tumor necrois factor, autonomic nervous system dysfunction, white matter lesions, elevated prolactin, etc. In addition, I posted research to show that when celiac disease patients were fed bread with gluten that had been properly broken down with "protease" there was no toxic reaction.
Here are some examples from my book of what I am talking about.
ASSOCIATION WITH HYPOTHYROIDISM
The lack of the essential amino acid phenylalanine would lead to the same association with hypothyroidism in CD that we have seen in autoimmune disease and cancer. In the study entitled “Risk of thyroid disease in individuals with celiac disease” the authors stated, “Celiac disease was positively associated with hypothyroidism…Celiac disease is associated with thyroid disease and these associations were seen regardless of temporal sequence. This indicates shared etiology and that these individuals are more susceptible to autoimmune disease” (Elfström, 2008).
LOW VITAMIN B12
Studies show that patients with CD are also deficient in vitamin B12, which is additional evidence they are not breaking down animal proteins in addition to gluten. Vitamin B12 is only found attached to dietary animal proteins. The study entitled “Low serum vitamin B12 is common in celiac disease and is not due to autoimmune gastritis” concluded, “Low B12 is common in celiac disease without concurrent pernicious anemia, and may be a presenting manifestation” (Dickey, 2002).
WHITE MATTER LESIONS
A lack of vitamin B12 would also lead to myelin damage. White matter lesions would be evidence of myelin damage, which are indeed found in CD. In the study entitled “Brain white-matter lesions in celiac disease: a prospective study of 75 diet-treated patients” seventy-five patients with biopsy proven CD were tested for neurologic complications. Ten patients had neurologic findings such as febrile seizures, single generalized seizures, mild ataxia, and muscular hypotonia with retarded motor development. White matter lesions were detected in 15 patients (20%). The study concluded, “Focal white matter lesions in the brain may represent an extraintestinal manifestation of celiac disease” (Kieslich, 2001).
Studies have shown that even when CD patients follow a careful gluten free diet their homocysteine levels remain high. For instance, in the study entitled “Evidence of poor vitamin status in coeliac patients on a gluten-free diet for 10 years” the researchers stated, “Coeliac patients showed a higher total plasma homocysteine level than the general population, indicative of a poor vitamin status.” The researchers also stated the homocysteine level was a metabolic marker of vitamin deficiency, one of which was vitamin B12. The authors concluded, “This may have clinical implications considering the linkage between vitamin deficiency, elevated total plasma homocysteine levels and cardiovascular disease” (Hallert, 2002).
INCREASED RISK OF CANCER
Elevated homocysteine is also implicated in the dysregulation of vascular endothelial growth factor and cancer metastasis. In a study conducted at the National Cancer Institute (NIH) in Bethesda, Maryland, and the Karolinska Institute in Sweden, researchers found a more than 5-fold increased risk of non-Hodgkin’s lymphoma in patients with celiac disease. The increased risk of developing lymphoma persisted despite a gluten-free diet. “At this time, we do not know what the actual cause of the link is,” Dr. Ying Gao of the NIH stated.“Prior studies have suggested that celiac disease leads to inflammation and that inflammation drives development of lymphomas." Taken together, these findings suggest that there might be some underlying mechanisms that lead to both celiac disease and lymphoma” (Gao, 2009). As we have seen, the “underlying mechanism” that both cancer and autoimmune disease share is homocysteine.
ELEVATED TUMOR NECROSIS FACTOR
In the study entitled “The tumor necrosis factor system and leptin in coeliac disease” the researchers stated that tumor necrosis factor levels were “statistically higher in patients with active CD, suggesting that the TNF system is activated in this disease” (Blanco, 2001).
ACTIVATED KYNURENINE PATHWAY
In the study entitled “Tryptophan metabolism and indoleamine 2,3-dioxygenase expression in coeliac disease” the researchers concluded, “We detected an increase of kynurenine…and of the kynurenine/tryptophan ratio in supernatants of coeliac patients…in comparison with healthy controls” (Torres, 2007).
The activation of the kynurenine pathway produces toxic tryptophan metabolites, which are implicated in brain disorders such as schizophrenia, epilepsy, dementia, and depression. Patients with CD have been found to have an increased risk for developing these disorders. In the study entitled “Range of neurologic disorders in patients with celiac disease” researchers stated, “A growing body of distinct neurologic conditions, such as cerebellar ataxia, epilepsy, myoclonic ataxia, chronic neuropathies, and dementia have been reported…”(Zelnik, 2004).
Researchers at the Johns Hopkins Bloomberg School of Public Health found that patients with CD were three times more likely to develop schizophrenia than those without the disease. In addition, in the study entitled “Psychiatric comorbidities in women with celiac disease” researchers stated, “Despite largely adhering to a gluten-free diet, a substantial subset of women with Celiac disease report clinically relevant symptoms of depression…” (Arigo, 2012).
SPINAL CORD DEGENERATION AND AUTONOMIC NERVOUS SYSTEM DYSFUNCTION
Another common manifestation of a vitamin B12 deficiency is subacute combined degeneration of the spinal cord. Subacute combined degeneration of the spinal cord refers to the neurological symptoms of vitamin B12 deficiency. The reason why the disease is “combined” is because both sensory and motor nerves are affected. Burning, tingling, and numbness in the hands and feet are common symptoms of sensory nerve damage. Sensory neuropathy is often found in patients with CD. The study entitled “Celiac neuropathy” states in the conclusion, “CD is commonly associated with sensory neuropathy and should be considered even in the absence of gastrointestinal symptoms” (Chin, 2003).
Motor neuropathy symptoms, such as ataxia, a condition characterized by jerky, uncoordinated movements and gait, are also a common feature of CD. The Wm. K. Warren Medical Research Center for Celiac Disease stated, “Many patients present with non-gastrointestinal symptoms such as aphthous stomatitis, iron deficiency anemia, reduced bone density, infertility, rash, arthralgias, neurological symptoms (ataxia, peripheral neuropathy, autonomic dysfunction, and headache) or general complaints such as fatigue and depression.” Autonomic dysfunction was also listed as a common symptom. A lack of vitamin B12 would lead to autonomic dysfunction, since acetylcholine, one of the neurotransmitters that control the autonomic nervous system, is derived from vitamin B12.
The autonomic nervous system controls the secretion and flow of salvia. Therefore, we would expect celiac patients to have an increased risk of developing Sjögren’s syndrome. In the study entitled “Celiac disease associated disorders and survival” researchers found that Sjögren’s syndrome occurred in 3.3% of celiac patients and 0.3 of controls (Collin, 1994).
This is just a fraction of the research that directly links CD back to protease. Gluten intolerance doesn't cause MS. MS and gluten intolerance are both caused by the same thing-missing enzymes (IMO).