Dr Michael Colgan 2 April 2013
We got such an overwhelming response to my recent article on gut diseases caused by the gliaden group of proteins in gluten, it has given me confidence that the public is ready to hear what medical science has known for 20 years about the damaging effects of gluten on the human brain.
The main offenders are wheat, rye, and barley in our food supply. Unfortunately, the cereal grains industry is mammoth business and an extremely powerful political lobby that will do whatever it can to conceal and belittle the evidence. What I love most about science is that the truth eventually outs.
Three things are now occurring to let the facts shine. First is the light-speed development of the internet which makes it increasingly more difficult every day for vested interests to hide evidence. Second is the unprecedented growth in public demand for gluten-free foods. For example, a recent gluten-free trade show in Vancouver planned for 5,000 visitors. More than 25,000 showed up, and most could not even get in. In the US alone, the gluten-free foods industry has grown from small in 2000, to a massive $3 billion a year in 2012.
The third change working to bring the facts about gluten toxicity to public notice is the explosion of controlled studies on gluten in the last decade. One summary paper for example, published in the open-access medical journal, Bio Med Central, Medicine, in 2012, is a collaborative effort of 14 universities, to expose the evidence.(1) We now know for sure that a much larger proportion of the population suffers from gluten toxicity than previously thought.(2)
Controlled studies show that gluten is not only a main offender in the group of disorders now collected under the umbrella of celiac disease (CD), but is also involved in many cases of autism, Asperger’s, and similar disorders, now collectively called autism spectrum disorders (ASD).(3-5)
Gluten is also involved in many cases of cerebellar ataxia from damage to motor controls in the cerebellum of the brain, causing loss of balance, dizziness, learning difficulties, and what we term, “Uncoordinated Child Syndrome” (UCS).(3,5) It is also involved in many cases of peripheral neuropathy (death of peripheral nerves, leading to one or several of a large group of disorders), and multiple cases of herpetiform dermatitis (herpes-like blistering rash mainly on elbow, forearms, and knees, but can occur on the face, buttocks, and other areas) (3-5)
It has taken 20 years to bring to public notice that a dominant food, wheat, (also rye and barley) can produce human disease not only of the gut but also the skin, the peripheral nerves, and the brain. The most unfortunate aspect of the gluten problem is that a child, or an adult, can suffer several different manifestations of gluten toxicity simultaneously, and can easily be mis-diagnosed as suffering from different disorders. World expert on gluten toxicity, British neurologist Dr M Hadjivassiliou, has called for physicians and neurologists to learn more about gluten-caused disorders, and treat them promptly before irreversible brain damage occurs.
A typical case we received is a very bright and pretty teenager, I will call Karen. She had been on the gluten-free diet we recommended, and had become symptom-free but we had not seen her for two years. She had eaten an “organic whole wheat sandwich” at school, thinking it would do no harm. Next day she had intestinal upset, and progressively over four days developed numbness and weakness in her legs, and could barely walk. The neurological report showed a large loss of nerve conduction and almost absent pain and temperature sensation in the legs.
On interview, I noticed some rough skin and scarring on Karen’s elbows, which could have come from gluten dermatitis, and asked whether she had been eating sandwiches before. After much mumbling she admitted that she had occasionally been going with school friends to the local organic restaurant, and having a sandwich, but they were “pure organic bread”.
I asked about the elbows. “Oh, that’s my rash, it comes and goes. I have cream for it.” I asked about any previous leg weakness. “Some days I have jelly legs and awful brain fog.” I discovered that her school work was not going well, and she also had quite a few sick days.
I concluded that the sandwich habit, a natural thing for a teen to do to fit in socially, was more frequent than she admitted. As gently as possible, I explained how she was causing all her symptoms herself, schoolwork problems, being sick, brain fog, gut upsets, elbow rashes. After a few minutes consideration, she said, “OMG, you’re right.” She got back on the gluten-free diet, and, within three months, jelly legs had disappeared entirely and she was back on track at school again.
The message of this case is that Karen had been correctly diagnosed by her physician years before, and the antibody tests confirmed it, because gluten was pretty poisonous to her. But there are thousands of children with less severe reactions who are never diagnosed, who stumble through life, variously considered slow, or weak, or anti-social, or weird, when every day they are being poisoned by their morning bowl of cereal, and lovingly packed school lunch. The antibody tests are widely available now, and could be worth their weight in gold for any child with unexplained disorder in their life.
1. Sapone A, et al. Spectrum of gluten-related disorders: consensus on new nomenclature and classification. BMC Med. 2012; 10: 13. Published online 2012 February 7. doi: 10.1186/1741-7015-10-13 PMCID: PMC3292448
2. Bernini P, et al. Are Patients with Potential Celiac Disease Really Potential? The Answer of Metabonomics. Journal of Proteome Research, 2010; : 101213161430042 DOI: 10.1021/pr100896s
3. Hadjivassiliou M, et al. Gluten sensitivity as a neurological illness. J Neurol Neurosurg Psychiatry. 2002 May; 72(5): 560–563.
4. Hadjivassiliou M, et al. Dietary treatment of gluten neuropathy. Muscle Nerve. 2006 Dec;34(6):762-6.
5. Hernandez-Lahoz C, et al. Neurological disorders associated with gluten sensitivity. Rev Neurol. 2011 Sep 1;53(5):287-300.
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