Tell me what you eat, I’ll tell you who you are.
—ANTHELME BRILLAT-SAVARIN (1755–1826)
MOST EVERYONE HAS EXPERIENCED the throb of a headache and the agony of severe congestion. In many instances, we can point to a probable cause when symptoms descend on us, such as a long day in front of the computer in the case of a tension headache, or a passing cold bug when it hurts to swallow and the nose clogs up. For relief we can usually turn to over-the-counter remedies to manage our symptoms until the body returns to a normal, healthy state. But what do you do when the symptoms don’t go away and the culprit is much harder to pin down? What if, like so many patients I treat, you find yourself in an unending war with nagging pain and misery for years?
For as long as she could remember, Fran struggled to chase the pulsating sensation out of her head. When I first examined her on a warm January day, Fran was as pleasant as could be for a sixty-three-year-old who endured daily migraine headaches. Of course she had tried all the usual headache medications and was taking Imitrex (sumatriptan), a powerful migraine drug, several times a week. In reviewing her medical history, I noted that in her early twenties she’d undergone “intestinal exploratory surgery” because she was suffering from “severe intestinal discomfort.” As part of her evaluation, I tested her for gluten sensitivity and, not to my surprise, found that she was strongly positive in eight of the markers. I prescribed a gluten-free diet.
Four months later, I received a letter from Fran stating: “My almost daily migraine symptoms have abated since removing gluten from my diet…. The two biggest changes in my body are the lack of a very hot head in the night with resulting migraines, and the huge increase in my energy levels. Today my level of daily accomplishment is enormous compared to my life before seeing you.” She went on to conclude: “Thank you, once again, for finding what seems to be the solution to my many years of migraine misery.” I wish she could have gotten the years back, but at least now I could give her a pain-free future.
Another woman who came to me with a totally different set of symptoms but a similarly long history of suffering was Lauren. At just thirty years old, she told me squarely on our first meeting that she was “having some mental problems.” Lauren detailed the previous twelve years, which she described as a consistent downhill ride in terms of health. She told me how her early life was quite stressful once she lost both her mother and grandmother at a young age. When she started college she was hospitalized on several occasions for “mania.” During this time she would experience episodes of becoming highly talkative and overly grandiose about herself. She would then eat excessively, gain a lot of weight, and become severely depressed and suicidal. She had just started taking lithium, a medication used to treat bipolar disorder. Mental illness ran in her family; her sister had schizophrenia and her father was bipolar. Aside from Lauren’s dramatic account of her mental issues, the rest of her medical history was fairly unremarkable. She had no laments of bowel issues, food allergies, or any other of the standard types of complaints associated with gluten sensitivity.
I went ahead and ordered a test for gluten sensitivity. We found profoundly elevated levels of six important markers for the condition. In fact, several of these markers were more than twice the normal range. Two months after starting a gluten-free diet, Lauren wrote a letter to me that echoed what I’d been hearing from so many patients who’d gone gluten-free and experienced striking results. She stated:
Since being off gluten, my life has taken a complete 180. The first change that comes to mind, and the most important one, is my mood. When I was eating gluten, I would struggle with feeling depressed. I would always have to fight a “dark cloud over my head.” Now that I’m off gluten, I don’t feel depressed. The one time I ate some by mistake, I felt depressed again the next day. Other changes I’ve noticed include having more energy and being able to stay focused for longer periods. My thoughts are as sharp as ever. I can make a decision and come to a logical, confident conclusion like never before. I am also free of a lot of obsessive-compulsive behavior.
Let me give you one more example of a case that’s emblematic of another set of symptoms linked to the same culprit. Kurt and his mother came to see me when he was a twenty-three-year-old young man suffering from abnormal movements. His mother stated that six months prior to their visit, he began “looking like he was shivering.” Initially his tremors were subtle, but then they increased with time. He had been to two neurologists and received two different diagnoses: one for what’s called “essential tremor,” and another for “dystonia.” The doctors had offered him a blood pressure medication, propranolol, which is used to treat some types of tremor disorders. The other recommendation was to have the various muscles in his arms and neck injected with Botox, the botulinum toxin that would temporarily paralyze the spastic muscles. Both he and his mother had elected not to use either the pills or the injections.
What was interesting about his history were two things. First, he was diagnosed as having a learning disability in the fourth grade; his mother said that “he could not handle excessive stimulation.” And second, for several years he had complaints of stomach pain with loose bowel movements to the extent that he had to see a gastroenterologist, who took a biopsy of his small intestine to test for celiac disease. It proved negative.
When I examined Kurt, his excessive movement problem was very evident. He could not control the shaking of his arms and neck and appeared to be suffering mightily. I reviewed his laboratory studies, which, for the most part, were unrevealing. He had been checked for Huntington’s disease, an inherited disorder known to cause a similar movement abnormality in young people, as well as Wilson’s disease, a disorder of copper metabolism also associated with a movement abnormality. All of these tests were negative. Blood work for gluten sensitivity did, however, show some elevated levels of certain antibodies indicative of vulnerability. I explained to Kurt and his mother that it was important to make sure gluten sensitivity wasn’t the cause of his movement disorder, and I provided them information on how to pursue a gluten-free diet.
After several weeks I received a phone call from Kurt’s mother indicating that without question his movements had calmed down. Because of his improvement he elected to stay on a gluten-free diet, and after approximately six months, the abnormal movements had all but disappeared completely. The changes that occurred in this young man are breathtaking, especially when you consider that a simple dietary change had such a life-transforming impact.
We are just beginning to see medical literature documenting a connection between movement disorders and gluten sensitivity, and physicians like me have now identified and treated a handful of individuals whose movement disorders have completely abated with a gluten-free program and for whom no other cause was identified. But unfortunately, most mainstream doctors are not on the lookout for the dietary explanation for such movement disorders and they are not aware of the latest reports.
These cases are not outliers. They reflect patterns that I’ve witnessed in so many patients. They all might come to me with vastly different medical complaints, but they share a common thread: gluten sensitivity. It’s my belief that gluten is a modern poison, and that the research is compelling doctors like me to notice and re-examine the bigger picture when it comes to brain disorders and disease. The good news is that knowing this common denominator now means we can treat and, in some cases, cure a wide spectrum of ailments with a single prescription: the eviction of gluten from the diet.
Walk into any health food store, and now even a regular grocery store, and you’re sure to be amazed at the selection of “gluten-free” products. In the past couple of years, the volume of gluten-free products sold has exploded; at last count, the industry clocked in at $6.3 billion in 2011 and continues to grow.1 Spin-offs of everything from breakfast cereals to salad dressing are now positioned to take advantage of the ever-increasing number of individuals who are choosing foods without gluten. Why all the hype?
No doubt media attention may be playing a role. A 2011 Yahoo! Sports article asking “Is Novak Djokovic’s new, gluten-free diet behind his winning streak?” goes on to say, “A simple allergy test could have led to one of the most dominant stretches in tennis history.”2
But beyond this one athlete’s epiphany, what does the scientific community have to say about gluten sensitivity? What does it mean to be “gluten sensitive”? How does it differ from celiac disease? What’s so bad about gluten? Hasn’t it always been around? And just what exactly do I mean by “modern grains”? Let’s take a tour.
THE GLUE OF GLUTEN
Gluten—which is Latin for “glue”—is a protein composite that acts as an adhesive material, holding flour together to make bread products, including crackers, baked goods, and pizza dough. When you bite into a fluffy muffin or roll and stretch pizza dough prior to cooking, you have gluten to thank. In fact, most of the soft, chewy bread products available today owe their gumminess to gluten. Gluten plays a key role in the leavening process, letting bread “rise” when wheat mixes with yeast. To hold a ball of what is essentially gluten in your hands, just mix water and wheat flour, create a dough by kneading the ball with your hands, and then rinse the glob under running water to eliminate the starches and fiber. What you’re left with is a glutinous protein mixture.
Most Americans consume gluten through wheat, but gluten is found in a variety of grains including rye, barley, spelt, kamut, and bulgur. It’s one of the most common food additives on the planet and is used not only in processed foods, but also in personal care products. As a trusty stabilizing agent, it helps cheese spreads and margarines retain their smooth texture, and it prevents sauces and gravies from curdling. Thickening hair conditioners and volumizing mascaras have gluten to thank, too. People can be as allergic to it as they can be to any protein. But let’s get a better look at the scope of the problem.
Gluten is not a single molecule; it’s actually made up of two main groups of proteins, the glutenins and the gliadins. A person may be sensitive to either of these proteins or to one of the twelve different smaller units that make up gliadin. Any of these could cause a sensitivity reaction leading to inflammation.
When I speak with patients about gluten sensitivity, one of the first things they say is something like, “Well, I don’t have celiac disease. I’ve been tested!” I do my best to explain that there’s a huge difference between celiac disease and gluten sensitivity. My aim is to convey the idea that celiac disease, also known as sprue, is an extreme manifestation of gluten sensitivity. Celiac disease is what happens when an allergic reaction to gluten causes damage specifically to the small intestine. It’s one of the most severe reactions one can have to gluten. Although many experts estimate that 1 in every 200 people has celiac disease, this is a conservative calculation; the number is probably closer to 1 in 30, since so many individuals remain undiagnosed. As many as one in four people are vulnerable to the disease due to genetics alone; people of northern European ancestry are particularly susceptible. What’s more, people can carry genes that code for mild versions of gluten intolerance, giving rise to a wide spectrum of gluten sensitivity. Celiac disease doesn’t just harm the gut. Once the genes for this disease are triggered, sensitivity to gluten is a lifelong condition that can affect the skin and mucous membranes, as well as cause blisters in the mouth.3
Extreme reactions that trigger an autoimmune condition such as celiac aside, the key to understanding gluten sensitivity is that it can involve any organ in the body, even if the small intestine is completely spared. So while a person may not have celiac disease by definition, the rest of the body—including the brain—is at great risk if that individual is gluten sensitive.
It helps to understand that food sensitivities in general are usually a response from the immune system. They can also occur if the body lacks the right enzymes to digest ingredients in foods. In the case of gluten, its “sticky” attribute interferes with the breakdown and absorption of nutrients. As you can imagine, poorly digested food leads to a pasty residue in your gut, which alerts the immune system to leap into action, eventually resulting in an assault on the lining of the small intestine. Those who experience symptoms complain of abdominal pain, nausea, diarrhea, constipation, and intestinal distress. Some people, however, don’t experience obvious signs of gastrointestinal trouble, but they could nevertheless be experiencing a silent attack elsewhere in their body, such as in their nervous system. Remember that when a body negatively reacts to food, it attempts to control the damage by sending out inflammatory messenger molecules to label the food particles as enemies. This leads the immune system to keep sending out inflammatory chemicals, killer cells among them, in a bid to wipe out the enemies. The process often damages our tissue, leaving the walls of our intestine compromised, a condition known as “leaky gut.” Once you have a leaky gut, you’re highly susceptible to additional food sensitivities in the future. And the onslaught of inflammation can also put you at risk for developing autoimmune disease.4
Inflammation, which you know by now is the cornerstone of many brain disorders, can be initiated when the immune system reacts to a substance in a person’s body. When antibodies of the immune system come into contact with a protein or antigen to which a person is allergic, the inflammatory cascade is provoked, releasing a whole host of damaging chemicals known as cytokines. Gluten sensitivity in particular is caused by elevated levels of antibodies against the gliadin component of gluten. When the antibody combines with this protein (creating an anti-gliadin antibody), specific genes are turned on in a special type of immune cell in the body. Once these genes are activated, inflammatory cytokine chemicals collect and can attack the brain. Cytokines are highly antagonistic to the brain, damaging tissue and leaving the brain vulnerable to dysfunction and disease—especially if 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).
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 sensitivityalways 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 on the vulnerable abnormal brain. It’s also important to keep in mind that each one of us is unique in terms of our genotype (DNA) and phenotype (how genes express themselves in their environment). Unchecked inflammation in me could result in obesity and heart disease, whereas the same condition in you could translate to an autoimmune disorder.
Once again, it helps to turn to the literature on celiac disease, since celiac reflects an extreme case; it allows us to identify patterns in the course of the disorder that can have implications for anyone who consumes gluten, regardless of celiac. Multiple studies, for example, have shown that people with celiac have significantly increased production of free radicals, and they exhibit free radical damage to their fat, protein, and even DNA.16 In addition, they also lose their ability to produce antioxidant substances in the body as a result of the immune system’s response to gluten. In particular, they have reduced levels of glutathione, an important antioxidant in the brain, as well as vitamin E, retinol, and vitamin C in their blood—all of which are key players in keeping the body’s free radicals in check. It’s as if the presence of gluten disables the immune system to such a degree that it cannot fully support the body’s natural defenses. My question is, if gluten sensitivity can compromise the immune system, what else does it open the door to?
Research has also shown that the immune system’s reaction to gluten leads to activation of signaling molecules that basically turn on inflammation and induce what’s called the COX-2 enzyme, which leads to increased production of inflammatory chemicals.17 If you’re familiar with drugs like Celebrex, ibuprofen, or even aspirin, you’re already familiar with the COX-2 enzyme, which is responsible for inflammation and pain in the body. These drugs effectively block that enzyme’s actions, thus reducing inflammation. High levels of another inflammatory molecule called TNF alpha have also been seen in celiac patients. Elevations of this cytokine are among the hallmarks of Alzheimer’s disease and virtually every other neurodegenerative condition. Bottom line: Gluten sensitivity—with or without the presence of celiac—increases the production of inflammatory cytokines, and these inflammatory cytokines are pivotal players in neurodegenerative conditions. Moreover, no organ is more susceptible to the deleterious effects of inflammation than the brain. It’s one of the most active organs in the body, yet it lacks bulletproof protective factors. Although the blood-brain barrier acts as a gatekeeper of sorts to keep certain molecules from crossing over from the bloodstream into our brain, it’s not a foolproof system. Plenty of substances sneak past this portal and provoke undesirable effects. (Later in the book I’ll go into richer detail about these inflammatory molecules and the ways in which we can use the power of food to combat them.)
It’s time we created new standards for what it means to be “gluten sensitive.” The problem with gluten is far more serious than anyone ever imagined, and its impact on society is far greater than we’ve ever estimated.
A GLUT OF GLUTEN IN MODERN FOOD
If gluten is so bad, how have we managed to survive so long while eating it? The quick answer is that we haven’t been eating the same kind of gluten since our ancestors first figured out how to farm and mill wheat. The grains we eat today bear little resemblance to the grains that entered our diet about ten thousand years ago. Ever since the seventeenth century, when Gregor Mendel described his famous studies of crossing different plants to arrive at new varieties, we’ve gotten good at mixing and matching strains to create some wild progeny in the grain department. And while our genetic makeup and physiology haven’t changed much since the time of our ancestors, our food chain has had a rapid makeover during the past fifty years. Modern food manufacturing, including genetic bioengineering, have allowed us to grow grains that contain up to forty times the gluten of grains cultivated just a few decades ago.18 Whether this has been intentional to increase yield, appeal to people’s palates, or both is anyone’s guess. But one thing we do know: Modern gluten-containing grains are more addictive than ever.
If you’ve ever felt a rush of euphoric pleasure following the consumption of a bagel, scone, doughnut, or croissant, you’re not imagining it and you’re not alone. We’ve known since the late 1970s that gluten breaks down in the stomach to become a mix of polypeptides that can cross the blood-brain barrier. Once they gain entry, they can then bind to the brain’s morphine receptor to produce a sensorial high. This is the same receptor to which opiate drugs bind, creating their pleasurable, albeit addicting, effect. The original scientists who discovered this activity, Dr. Christine Zioudrou and her colleagues at the National Institutes of Health, named these brain-busting polypeptides exorphins, which is short for exogenous morphine-like compounds, distinguishing them from endorphins, the body’s naturally produced painkillers.19 What’s most interesting about these exorphins, and further confirms their impact on the brain, is that we know they can be stopped by opiate-blocking drugs like naloxone and naltrexone—the same drugs used to reverse the action of opiate drugs such as heroine, morphine, and oxycodone. Dr. William Davis describes this phenomenon well in his book Wheat Belly: “So this is your brain on wheat: Digestion yields morphine-like compounds that bind to the brain’s opiate receptors. It induces a form of reward, a mild euphoria. When the effect is blocked or no exorphin-yielding foods are consumed, some people experience a distinctly unpleasant withdrawal.”20
Given what I just explained, is it any wonder that food manufacturers try to pack as much gluten into their products as possible? And is it any surprise to find so many people addicted to gluten-filled foods today—fanning the flames of not just inflammation but the obesity epidemic? I think not. Most of us have known and accepted the fact that sugar and alcohol can have feel-good properties that entice us to come back for more. But gluten-containing foods? Your whole-wheat bread and instant oatmeal? The idea that gluten can change our biochemistry down to our brain’s pleasure and addiction center is remarkable. And scary. It means we need to re-think how we categorize these foods if they are indeed the mind-altering agents that science proves they are.
When I watch people devour gluten-laden carbohydrates, it’s like watching them pour themselves a cocktail of gasoline. Gluten is our generation’s tobacco. Gluten sensitivity is far more prevalent than we realize—potentially harming all of us to some degree without our knowing it—and gluten is hiding where you least suspect it. It’s in our seasonings, condiments, and cocktails, and even in cosmetics, hand cream, and ice cream. It’s disguised in soups, sweeteners, and soy products. It’s tucked into our nutritional supplements and brand-name pharmaceuticals. The term “gluten-free” is becoming just as vague and diluted as “organic” and “all natural” have become. For me, it’s no longer a mystery why going gluten-free can have such a positive impact on the body.
For the greater part of the past 2.6 million years, our ancestors’ diets consisted of wild game, seasonal plants and vegetables, and the occasional berries. As we saw in the previous chapter, today most people’s diets are centered on grains and carbs—many of which contain gluten. But even casting the gluten factor aside, I should point out that one of the main reasons why consuming so many grains and carbs can be so harmful is that they raise blood sugar in ways other foods, such as meat, fish, poultry, and vegetables, do not.
High blood sugar, you’ll recall, produces high insulin, which is released by the pancreas to move sugar into the body’s cells. The higher the blood sugar, the more insulin must be pumped from the pancreas to deal with the sugar. And as the insulin increases, cells become less and less sensitive to the insulin signal. Basically, cells cannot hear insulin’s message. What the pancreas does, as anyone would do if a person couldn’t hear your message, is speak louder—that is, it increases its insulin output, creating a life-threatening feed-forward process. Higher levels of insulin cause the cells to become even less responsive to the insulin signal, and in order to deal with lowering the blood sugar, the pancreas works overtime, increasing its insulin output further, again to maintain a normal blood sugar. Even though the blood sugar is normal, the insulin level is climbing.
Since cells are resistant to the insulin signal, we use the term “insulin resistance” to characterize this condition. As the situation progresses, the pancreas finally maximizes its output of insulin, but it’s still not enough. At that point, cells lose their ability to respond to the insulin signal, and ultimately, blood sugar begins to rise, resulting in type 2 diabetes. The system has essentially broken down and now requires an outside source (i.e., diabetes drugs) to keep the body’s blood sugars balanced. Remember, though, that you don’t have to be diabetic to suffer from chronic high blood sugar.
When I give lectures to members of the medical community, one of my favorite slides is a photo of four common foods: (1) a slice of whole-wheat bread, (2) a Snickers bar, (3) a tablespoon of pure white sugar, and (4) a banana. I then ask the audience to guess which one produces the greatest surge in blood sugar—or which has the highest glycemic index (GI), a numerical rating that reflects a measure of how quickly blood sugar levels rise after eating a particular type of food. The glycemic index encompasses a scale of 0 to 100, with higher values given to foods that cause the most rapid rise in blood sugar. The reference point is pure glucose, which has a GI of 100.
Nine times out of ten, people pick the wrong food. No, it’s not the sugar (GI = 68), it’s not the candy bar (GI = 55), and it’s not the banana (GI = 54). It’s the whole-wheat bread at a whopping GI of 71, putting it on par with white bread (so much for thinking whole wheat is better than white). We’ve known for more than thirty years that wheat increases blood sugar more than table sugar, but we still somehow think that’s not possible. It seems counterintuitive. But it’s a fact that few foods produce as much of a surge in blood glucose as those made with wheat.
It’s important to note that the rise in gluten sensitivity is not only the outcome of hyper-exposure to gluten in today’s engineered foods. It’s also the result of too much sugar and too many pro-inflammatory foods. We can also make a case for the impact of environmental toxins, which can change how our genes express themselves and whether or not autoimmune signals start to fire. Each of these ingredients—gluten, sugar, pro-inflammatory foods, and environmental toxins—combines to create a perfect storm in the body, and especially the brain.
If any food that foments a biological storm—despite the presence of gluten—is hazardous to our health, then we must raise another critically important question in terms of brain health: Are carbs—even “good carbs”—killing us? After all, carbs are often the main source of these antagonizing ingredients. Any conversation about blood sugar balance, gluten sensitivity, and inflammation has to revolve around the impact carbohydrates can have on the body and brain. In the next chapter, we’ll look at how carbs in general raise risk factors for neurological disorders, often at the expense of our brain’s real lover: fat. When we consume too many carbs, we eat less fat—the very ingredient our brain demands for health.
SIGNS OF GLUTEN SENSITIVITY
The best way to know if you’re sensitive to gluten is to get tested. Unfortunately, traditional blood tests and small-intestine biopsies are not nearly as accurate as the newer tests that can identify gluten antibodies just as well as genetic testing. Below is a list of symptoms and illnesses associated with gluten sensitivity. Even if you don’t have any of these conditions, I urge you to employ the latest testing technology (here).
ataxia, loss of balance
autoimmune disorders (diabetes, Hashimoto’s thyroiditis, rheumatoid arthritis, to name a few)
constantly getting sick
digestive disturbances (gas, bloating, diarrhea, constipation, cramping, etc.)
irritable bowel syndrome
malabsorption of food
neurological disorders (dementia, Alzheimer’s, schizophrenia, etc.)
THE GLUTEN POLICE21
The following grains and starches contain gluten:
The following grains and starches are gluten-free:
The following foods often contain gluten:
baked beans (canned)
bouillons/broths (commercially prepared)
chocolate milk (commercially prepared)
flavored coffees and teas
French fries (often dusted with flour before freezing)
fruit fillings and puddings
imitation crabmeat, bacon, etc.
instant hot drinks
oat bran (unless certified gluten-free)
oats (unless certified gluten-free)
processed cheese (e.g., Velveeta)
soy sauce and teriyaki sauces
The following are miscellaneous sources of gluten:
non-self-adhesive stamps and envelopes
vitamins and supplements (check label)
The following ingredients are often code for gluten:
amino peptide complex
brown rice syrup
caramel color (frequently made from barley)
fermented grain extract
hydrolyzed malt extract
hydrolyzed vegetable protein
modified food starch
vegetable protein (HVP)