the assault continues

the assault continues. Another problem with anti-gliadin antibodies is that they can directly combine with specific proteins found in the brain that look like the gliadin protein found in gluten-containing foods, but the anti-gliadin antibodies just can’t tell the difference. This has been described for decades and again leads to the formation of more inflammatory cytokines. 5 Given this, it’s no wonder that elevated cytokines are seen in Alzheimer’s disease, Parkinson’s disease, multiple sclerosis, and even autism. 6 (Research has even shown that some people who are wrongly diagnosed with ALS, or Lou Gehrig’s disease, simply have a sensitivity to gluten, and eliminating it from the diet resolves the symptoms. 7 ) As England’s Professor Marios Hadjivassiliou, one of the most well-respected researchers in the area of gluten sensitivity and the brain at the Royal Hallamshire Hospital in Sheffield, reported in a 1996 article in the Lancet, “Our data suggest that gluten sensitivity is common in patients with neurological disease of unknown cause and may have etiological significance.” 8 For someone like me who deals with challenging brain disorders of “unknown cause” on a daily basis, Dr. Hadjivassiliou’s statement is sobering when you consider that an estimated 99 percent of people whose immune systems react negatively to gluten don’t even know it. Dr. Hadjivassiliou goes on to state that “gluten sensitivity can be primarily, and at times, exclusively, a neurological disease.” In other words, people with gluten sensitivity can have issues with brain function without having any gastrointestinal problems whatsoever. For this reason, he tests all of his patients who have unexplained neurological disorders for gluten sensitivity. I love how Dr. Hadjivassiliou and his colleagues stated the facts in a 2002 editorial in the Journal of Neurology, Neurosurgery, and Psychiatry titled “Gluten Sensitivity as a Neurological Illness”: It has taken nearly 2,000 years to appreciate that a common dietary protein introduced to the human diet relatively late in evolutionary terms (some 10,000 years ago), can produce human disease not only of the gut but also the skin and the nervous system. The protean neurological manifestations of gluten sensitivity can occur without gut involvement and neurologists must therefore become familiar with the common neurological presentations and means of diagnosis of this disease. 9 In addition, the editorial summed up the findings brilliantly in the conclusion, which reiterated statements made in earlier papers: “Gluten sensitivity is best defined as a state of heightened immunological responsiveness in genetically susceptible people. This definition does not imply bowel involvement. That gluten sensitivity is regarded as principally a disease of the small bowel is a historical misconception.” CELIAC THROUGH THE CENTURIES Although the relationship between gluten sensitivity and neurological disease has received precious little attention in the medical literature, we can trace a prominent thread of accumulating knowledge back thousands of years to a time when gluten wasn’t even part of our vocabulary. The evidence, it turns out, was already mounting. We just weren’t able to document it until the current century. The fact that we can finally identify a link between celiac disease, which again is the strongest reaction to gluten, and neurological problems has implications for all of us, including those who don’t have celiac. The study of celiac patients has enabled us to zoom in on the real dangers of gluten that have largely remained hidden and silent for so long. Celiac may seem like a “new disease,” but the first descriptions of the disorder date back to the first century AD, when Aretaeus of Cappadocia, one of the most distinguished ancient Greek doctors, wrote about it in a medical textbook covering various conditions, including neurological abnormalities such as epilepsy, headache, vertigo, and paralysis. Aretaeus was also the first to use the word celiac, which is Greek for “abdominal.” In describing this malady, he said: “The stomach being the digestive organ, labours in digestion, when diarrhea seizes the patient… and if in addition, the patient’s general system be debilitated by atrophy of the body, the coeliac disease of a chronic nature is formed.” 10 In the seventeenth century, the term sprue was introduced into the English language from the Dutch word sprouw, which means chronic diarrhea—one of the classic symptoms of celiac disease. The English pediatrician Dr. Samuel J. Gee was among the first to recognize the importance of diet in managing patients with celiac; he gave the first modern-day description of the condition in children in a lecture at a London hospital in 1887, noting, “If the patient can be cured at all, it must be by means of diet.” At the time, however, no one could pinpoint which ingredient was the culprit, so recommendations in dietary changes in search of a cure were far from accurate. Dr. Gee, for example, banned fruits and vegetables, which wouldn’t have posed a problem, but allowed thin slices of toasted bread. He was particularly moved by the curing of a child “who was fed upon a quart of the best Dutch mussels daily,” but who relapsed when the season of mussels was over (perhaps the child went back to eating toast). In the United States, the first discussion of the disorder was published in 1908 when Dr. Christian Herter wrote a book about children with celiac disease, which he called “intestinal infantilism.” As others had noted previously, he wrote that these children failed to thrive and added that they tolerated fat better than carbohydrate. Then, in 1924, Dr. Sidney V. Haas, an American pediatrician, reported positive effects of a diet of bananas. (Obviously, bananas weren’t the cause of the improvement, but rather, the banana diet happened to exclude gluten.) While it’s hard to imagine such a diet enduring the test of time, it remained popular until the actual cause of celiac could be determined and confirmed. And this would take another couple of decades, until the 1940s when the Dutch pediatrician Dr. Willem Karel Dicke made the connection to wheat flour. By then, carbohydrates in general had long been suspected, but not until a cause-and-effect observation could be made with wheat in particular did we see the direct connection. And how was this discovery actually made? During the Dutch famine of 1944, bread and flour were scarce, and Dr. Dicke noticed that there was a dramatic decrease in the death rate among children affected by celiac— from greater than 35 percent to virtually zero. Dr. Dicke also reported that once wheat was again available, the mortality rate rose to previous levels. Finally, in 1952, a team of doctors from Birmingham, England, including Dr. Dicke, made the link between the ingestion of wheat proteins and celiac disease when they examined samples of intestinal mucosa taken from surgical patients. The introduction of the small bowel biopsy in the 1950s and ’60s confirmed the gut as a target organ. (To be fair, I should note that historical experts have debated whether or not Dicke’s earlier anecdotal observations in the Netherlands were completely correct, arguing that it would have been difficult if not impossible for him to record such a relapse when flour became available again. But these debaters are not dismissing the importance of identifying wheat as a culprit—they merely aim to highlight the fact that wheat isn’t the only culprit.) So when did we begin to see a connection between celiac and neurological issues? Again, the trail goes back much further than most people realize. More than a century ago the first anecdotal reports began to emerge, and throughout the twentieth century various doctors documented neurological conditions in patients with celiac. Early on, though, when neurological problems were found to correlate to celiac disease, by and large they were thought to represent a manifestation of nutritional deficiencies because of the gut issue. In other words, doctors didn’t think a certain ingredient was necessarily wreaking havoc on the nervous system; they just thought the celiac condition itself, which prevented the absorption of nutrients and vitamins in the gut, led to deficiencies that triggered neurological problems like nerve damage and even cognitive impairments. And they were far from being able to grasp the role of inflammation in the story, which had yet to enter our medical library of knowledge. In 1937, the Archives of Internal Medicine published the Mayo Clinic’s first review of neurological involvement in patients with celiac, but even then the research could not accurately describe the real cascade of events. They attributed the brain involvement to “electrolyte depletion” due principally to the gut’s failure to digest and absorb nutrients properly. 11 To reach the point where we could understand and fully explain the link between sensitivity to gluten and the brain, we needed a great deal of advancements in our technology, not to mention our understanding of the role of inflammatory pathways. But the turnaround in our perspective has indeed been sensational, and relatively recent. In 2006, the Mayo Clinic again came out with a report, published in the Archives of Neurology, about celiac disease and cognitive impairment, but this time the conclusion was a game-changer: 12 “A possible association exists between progressive cognitive impairment and celiac disease, given the temporal relationship and the relatively high frequency of ataxia and peripheral neuropathy, more commonly associated with celiac disease.” Ataxia is the inability to control voluntary muscle movement and maintain balance, most frequently resulting from disorders in the brain; peripheral neuropathy is a fancy way of saying nerve damage. It encompasses a wide range of disorders in which the damaged nerves outside of the brain and spinal cord—peripheral nerves—cause numbness, weakness, or pain. In this particular study, the researchers looked at thirteen patients who showed signs of progressive cognitive decline within two years of the onset of celiac disease symptoms or a worsening of the disorder. (The most common reasons why these patients sought medical help for their brain impairments were amnesia, confusion, and personality changes. Doctors confirmed all cases of celiac disease by small-bowel biopsy; anyone whose cognitive decline could potentially be pinned on an alternate cause were excluded.) One thing became clear during the analysis that instantly invalidated previous thinking: The cognitive decline could not be attributed to nutritional deficiencies. What’s more, doctors noted that the patients were relatively young to have dementia (the median age when signs of cognitive impairment began was sixty-four years with a range from forty-five to seventy-nine years). As reported in the media, according to Dr. Joseph Murray, a Mayo Clinic gastroenterologist and the study investigator, “There has been a fair amount written before about celiac disease and neurological issues like peripheral neuropathy… or balance problems, but this degree of brain problem—the cognitive decline we’ve found here—has not been recognized before. I was not expecting there would be so many celiac disease patients with cognitive decline.” Murray rightfully went on to add that it’s unlikely these patients’ conditions reflected a “chance connection.” Given the association between the celiac symptoms starting or worsening and the cognitive decline within just two years, the likelihood of this being a random event was very small. Perhaps the most stunning finding of all in this study was that several of the patients who were put on a gluten-free diet experienced “significant improvement” in their cognitive decline. When they completely withdrew from gluten consumption, three patients’ mental faculties either improved or stabilized, leading the researchers to highlight that they may have discovered a reversible form of cognitive impairment. This is a huge finding. Why? We really don’t have many forms of dementia that are readily treatable, so if we can stop and in some cases reverse the path to dementia, identifying celiac disease in the presence of cognitive decline should become customary. What’s more, such a finding further argues against chance as an explanation of the link between celiac disease and cognitive decline. When asked about the scientific reasoning behind the link, Dr. Murray mentioned the potential impact of inflammatory cytokines—those chemical messengers of inflammation that contribute to problems in the brain. One more item I’d like to point out from this study: When the researchers performed brain scans on these patients, they found noticeable changes in the white matter that could easily be confused with multiple sclerosis or even small strokes. This is the reason I always check for gluten sensitivity in patients referred to me with a diagnosis of multiple sclerosis; on many occasions I’ve found patients whose brain changes were in fact not related to multiple sclerosis at all and were likely due to gluten sensitivity. And lucky for them, a gluten-free diet reversed their condition. THE BIGGER PICTURE Recall the young man I discussed at the beginning of the chapter who was originally diagnosed with a movement disorder called dystonia. He couldn’t control his muscle tone, resulting in wild and intense spasms throughout his body that prevented him from leading a normal life. Although neurological disease or side effects to drugs are often to blame in cases like this, my belief is that a lot of dystonia and other movement disorders can be attributed simply to gluten sensitivity. In my patient’s situation, once we removed gluten from his diet, his tremors and convulsive twitches came to a screeching halt. Other movement disorders, such as ataxia, which I described earlier, myoclonus, another affliction characterized by spasmodic jerky contractions of muscles, and certain forms of epilepsy are often misdiagnosed—they are attributed to an unexplained neurological problem rather than to something as simple as gluten sensitivity. I’ve had several epileptic patients who’ve gone from considering risky surgery and relying on daily medication regimes to manage their seizures to becoming completely seizure-free through simple dietary shifts. Dr. Hadjivassiliou has similarly examined brain scans from headache patients and documented dramatic abnormalities caused by gluten sensitivity. Even a lay reader without a trained eye can easily see the impact. Take a look at one example: Brain MRI images showing severe changes in the white matter (arrows) related to gluten sensitivity and headaches (left) compared to a normal study (right). Gluten sensitive Normal For more than a decade Dr. Hadjivassiliou has repeatedly shown that a gluten-free diet can result in complete resolution of headaches in patients with gluten sensitivity. In a 2010 review for the Lancet Neurology, he makes a clarion call for change in how we view gluten sensitivity. 13 For him and his colleagues, nothing could be more critical than getting the word out about the connection between seemingly invisible gluten sensitivity and brain dysfunction. And I agree. Dr. Hadjivassiliou’s chronicle of patients with evident signs of cognitive deficits and documented gluten sensitivity, as well as their recovery, is impossible to deny. As we’ve discussed, one of the most important takeaways from all the new information we’ve gained about celiac disease is that it’s not confined to the gut. I would go so far as to say that gluten sensitivity always affects the brain. Neurobiologist Dr. Aristo Vojdani, a colleague who has published extensively on the topic of gluten sensitivity, has stated that the incidence of gluten sensitivity in Western populations may be as high as 30 percent. 14 And because most cases of celiac are clinically silent, the prevalence of the disease itself is now recognized to be twenty times higher than it was thought to be two decades ago. Let me share what Dr. Rodney Ford of the Children’s Gastroenterology and Allergy Clinic in New Zealand proposed in his 2009 article aptly titled “The Gluten Syndrome: A Neurological Disease”: 15 The fundamental problem with gluten is its “interference with the body’s neural networks… gluten is linked to neurological harm in patients, both with and without evidence of celiac disease.” He added, “Evidence points to the nervous system as the prime site of gluten damage,” and he boldly concluded that “the implication of gluten causing neurologic network damage is immense. With estimates that at least one in ten people are affected by gluten, the health impact is enormous. Understanding the gluten syndrome is important for the health of the global community.” Although you may not be sensitive to gluten in the same way an individual with celiac is, I’ve inundated you with data for good reason: It goes to show that we may all be sensitive to gluten from a neurological standpoint. We just don’t know it yet because there are no outward signs or clues to a problem happening deep within the quiet confines of our nervous system and brain. Remember, at the heart of virtually every disorder and disease is inflammation. When we introduce anything to the body that triggers an inflammatory response, we set ourselves up for taking on much greater risk for a medley of health challenges, from chronic daily nuisances like headaches and brain fog to serious ailments such as depression and Alzheimer’s. We can even make a case for linking gluten sensitivity with some of the most mysterious brain disorders that have eluded doctors for millennia, such as schizophrenia, epilepsy, depression, bipolar disorder, and, more recently, autism and ADHD. I’ll be covering these connections later in the book. For now, I want you to get a scope of the problem, with a firm understanding that gluten can exert effects not only on the normal brain but also