Jefferson Adams is a freelance writer living in San Francisco. His poems, essays and photographs have appeared in Antioch Review, Blue Mesa Review, CALIBAN, Hayden's Ferry Review, Huffington Post, the Mississippi Review, and Slate among others.
He is a member of both the National Writers Union, the International Federation of Journalists, and covers San Francisco Health News for Examiner.com.
For Dr. Ford, the idea that celiac disease is exclusively an auto-immune condition, and that nutritional mal-absorption is the main cause of related problems, is simply not borne out by the body of clinical data.
Dr. Ford accepts that celiac disease may itself be largely an auto-immune disorder. However, he believes that the broad array of problems associated with gluten intolerance are best explained by looking at the neurological aspects of intolerance to gluten, indeed, treating it as a neurological condition.
That's because gluten intolerance can affect up to up to 10% of the population, and that intolerance to gluten has largely neurological manifestations. That is, up to 10% of the population tests positive for elevated antibodies for gluten, even with no bowel damage.
Under Dr. Ford's hypothesis, neurological causes, rather than gut damage and nutritional deficiency, best explain
the myriad symptoms experienced by sufferers of celiac disease and gluten-sensitivity.
Under Dr. Ford hypothesis, if gluten is the assumed cause of harm, then exposure to gluten in sensitive individuals may cause neurological harm through a combination of cross-reacting antibodies, immune complex disease and direct toxicity.
It's certainly true that a number of celiac patients experience neurological symptoms, often associated with autonomic nervous system malfunction.
Such neurological symptoms can even show up in celiac patients who are otherwise well nourished. Moreover, gluten-sensitivity can be associated with neurological symptoms in patients who have no mucosal gut damage--that is, patients who are clinically free of celiac disease.
Dr. Ford argues that gluten exposure can cause neurological harm through a combination of cross-reacting antibodies, immune complex disease and direct toxicity. These nervous system affects include: dis-regulation of the autonomic nervous system, cerebella ataxia, hypotonia, developmental delay, learning disorders, depression, migraine, and headache. He calls such neurologically-driven sensitivity to gluten ‘‘The Gluten Syndrome."
Hypothesis: Gluten causes symptoms, in both celiac disease and non-celiac gluten-sensitivity, by its adverse actions on the nervous system.
Many celiac patients experience neurological symptoms, frequently associated with malfunction of the autonomic nervous system. These neurological symptoms can present in celiac patients who are well nourished. The crucial point, however, is that gluten-sensitivity can also be associated with neurological symptoms in patients who do not have any mucosal gut damage (that is, without celiac disease).
Gluten can cause neurological harm through a combination of cross-reacting antibodies, immune complex disease and direct toxicity. These nervous system affects include: dis-regulation of the autonomic nervous system, cerebella ataxia, hypotonia, developmental delay, learning disorders, depression, migraine, and headache.
If gluten is the putative harmful agent, then there is no requirement to invoke gut damage and nutritional deficiency to explain the myriad symptoms experienced by sufferers of celiac disease and
gluten-sensitivity. This he calls: ‘‘The Gluten Syndrome."
To support his hypothesis, Dr. Ford cites a study of 921 children carried out at his gastroenterology and allergy clinic. All children were screened for celiac disease via IgG-gliadinantibody (InovaDiagnostics) and tissue trans-glutaminase (tTG); and 190 had a small bowel biopsy. Results showed 724 with high IgG-gliadin levels (>14 units): mean age 5.3 years, s.d. 3.8.
In a key part of the, all children, whatever the biopsy results, were offered a gluten-free diet.
Results fell into three distinct categories:
(a) Deﬁnite celiac disease was revealed in 31 patients (4.3%), via histologic diagnosis. 94% of these patients reported improvement on a gluten-free diet.
(b) Possible celiac was revealed in 48 patients (6.6%), who had elevated tTG antibodies, but normal gut histology: 75% of these patients reported improvement on a gluten-free diet.
(c) Not-celiacs, n=644 (89.1%), with normal tTG antibodies and no evidence of gut damage: 53% reported improvement gluten-free.
Note that last category: More than half of people without celiac disease reported improvement on a gluten-free diet. What's up with that? Well, those are the people Dr. Ford suspects suffer from "gluten syndrome."
The parents of apparently ‘‘asymptomatic” children were interviewed as part of a population study to identify those with celiac disease. They found many children who had positive tests for gliadin antibodies also had irritability, lethargy, abdominal distension, gas, and poor weight gains. A high proportion of children with gastro-intestinal, allergy, and neurological conditions have elevated IgG-gliadin antibodies.
The three groups all shared similar clinical features. In the respective groups, 71%, 65%, and 51% of patients reported behavior issues, such as tiredness, lethargy, irritability, sleep disturbance, while 16%, 15%, and 24% reported gastric reﬂux. Dr. Ford believes these symptoms are likely to be neurologically driven by gluten-sensitivity.
Celiac patients completed a questionnaire regarding the presence of neurological symptoms. Those reporting any neurological manifestations were compared with a control group: celiac patients had more neurological disorders (51.4%) in comparison with controls (19.9%). These conditions included: hypotonia, developmental delay, learning disorders, attention deﬁcit hyperactivity disorder, migraine, headache, and cerebella ataxia.
For Dr. Ford, not only is it significant that such high numbers of people with celiac disease report neurological issues, but it is also significant that the majority of 'non-celiac' patients report improvement on a gluten-free diet.
These patients are likely candidates for what he calls 'gluten syndrome.' These children can likely be spotted via screening for high IgG-gliadin levels.
Dr. Ford believes the next step is to test this hypothesis in a double-blind study.
Certainly, the idea that a whole category of non-celiac gluten-sensitivity exists is intriguing, as is the idea that a neurological take on celiac-disease and gluten-sensitivty might might provide a better or improved understanding of those who suffer from these conditions.