You would almost have to be living in a cave at this point if you haven’t at least heard of gluten. When Miley Cyrus went gluten-free, I felt like the gluten-free diet finally hit popular culture. I still meet a lot of people, however, who have no idea what gluten is. It doesn’t matter how many times I try to explain it, the idea doesn’t sink in.
What the hell is gluten? Gluten is a composite protein found in wheat. It is composed of two other proteins–gliadin and glutenin. To help illustrate the role of gluten, it might help to know that the English word ‘gluten’ is derived from the Latin word ‘gluten’ meaning ‘glue’. Gluten gives elasticity to wheat-based doughs because, as the dough is worked, it forms a matrix which provides structure as well as traps air bubbles. Other grains that contain gluten-like proteins are barley, rye, triticale, spelt, kamut, and all varieties of wheat, of course. With this in mind, you can see then why a baker would want to use bread flour (a high-gluten flour) for baking bread since bread requires structure and shape while another baker would choose cake flour for a more delicate crumb since cake flour is a lower-gluten flour blend. Cakes need structure, but one doesn’t want them to be doughy or tough. Hence, the job of gluten is to provide structure and lift to baked goods. Sort of like a good bra.
When a person is tested for an immune response to gluten, the tests are looking for anti-gliadin antibodies as well as IgA (Immunoglobulin A)–the chief antibody in the gastrointestinal and respiratory tract. If a person has celiac disease, then, through blood work, a physician will look for markers of TG2 (transglutaminase 2)–a celiac disease autoantigen–in the small intestine. There are about five different blood tests that can be done, but the gold standard for celiac testing is still the endoscopy in which a biopsy is taken of the small intestine to check for villious atrophy–a condition in which the villi, finger-like structures lining the wall of the bowel, erode and flatten leading to malabsorption and, eventually, leaky gut. What is leaky gut? “We don’t know a lot but we know that it exists,” says Linda A. Lee, MD, a gastroenterologist and director of the Johns Hopkins Integrative Medicine and Digestive Center. “In the absence of evidence, we don’t know what it means or what therapies can directly address it.” Dr. Lee goes on to explain that “a possible cause of leaky gut is increased intestinal permeability or intestinal hyperpermeability. That could happen when tight junctions in the gut, which control what passes through the lining of the small intestine, don’t work properly. That could let substances leak into the bloodstream. People with celiac disease and Crohn’s disease experience this. ‘Molecules can get across in some cases, such as Crohn’s, but we don’t know all the causes,’ Lee says. Whether hyperpermeability is more of a contributing factor or a consequence is unclear. But why or how this would happen in someone without those conditions is not clear. Little is known about other causes of leaky gut that aren’t linked to certain types of drugs, radiation therapy, or food allergies.” (online source)
Celiac disease, however, is not the only health issue associated with gluten. There is something called “gluten ataxia”. I know. What the heck is gluten ataxia? Let’s start with ataxia. What is ataxia? Our favorite workhorse, Wikipedia, defines ataxia as: “a neurological sign consisting of lack of voluntary coordination of muscle movements. Ataxia is a non-specific clinical manifestation implying dysfunction of the parts of the nervous system that coordinate movement, such as the cerebellum.” The problem with ataxia is that it is often not just a presenting neurological state as it were. Other symptoms exist alongside ataxia like memory issues and depression. This can make ataxia a neuropsychiatric condition as well (See Depressive and Memory Symptoms as Presenting Features of Spinocerebellar Ataxia).
Why do we care about ataxia? Well, having a daughter with an autism spectrum disorder, I hear a lot about ataxia because, depending upon where a child falls on the autism spectrum, ataxia may be at play. More than that, if a child has sensory processing disorder to such a degree that occupational therapy is required, then you can be sure you will meet others with ataxia while sitting in the waiting room. One of the first things that we are told when we receive an ASD diagnosis is to look at dietary changes. The gluten-free/casein-free diet is a common suggestion. It is well-known that this dietary change can help some kids on the autism spectrum. Getting rid of food coloring, particularly Red #40, is often a great choice and makes a huge difference in the health and well-being of the child (See Living in Color: The Potential Danger of Artificial Dyes). All this is to say, it is not unusual in the medical community for suggestions toward dietary changes to be made in the context of an ASD diagnosis, but how often do we see this in, say, something like an ataxia diagnosis? I came across an article, What Is Ataxia, and it was fairly detailed in the symptoms, types, and etiology of ataxia. It failed, however, to disclose one type of ataxia called gluten ataxia. What is gluten ataxia? Simply put, it’s a form of ataxia caused by the ingestion of gluten. The body produces TG2, and, instead of attacking the gut, it attacks the brain. People with gluten ataxia, upon autopsy, will be found to have a concentration of gluten antibodies in their cerebellum. (See Autoantibody targeting of brain and intestinal transglutaminase in gluten ataxia).
How many clinicians know about gluten ataxia? It’s hard to find in the literature. Part of the reason for this, I suspect, is because Western medicine does not generally view nutrition or diet as significant or impactful where our overall health is concerned. This is not how modern physicians are trained. So, information is often siloed because modern medicine is siloed into specialties. For example, did you know that Restless Leg Syndrome (RLS) is caused by a dopamine deficiency in the brain? Sleep specialists, a sub-specialty of neurology, treat RLS. Often, the primary cause of RLS is low ferritin stores. It is suspected that iron deficiency disrupts dopamine production in dopamine-specific areas of the brain (See CFS iron, ferritin, and transferrin levels in restless leg syndrome). If iron deficiency disrupts dopamine production in the brain and dopaminergic action is a widely known contributor to depression (See Dopamine and depression), then why don’t obstetricians take anemia into account when treating anemia and postpartum depression? Do obstetricians look at anemia in pregnancy as a marker for potential postpartum depression? Ferritin stores are different than simply a finger prick. How many clinicians are actually checking a woman’s ferritin stores? This is an example of siloed knowledge in the medical community. What sleep specialists know about iron deficiency in the brain itself and dopamine, other specialists do not. On the surface, it doesn’t seem to matter, but the body cannot be so easily divided.
Here’s where it gets very interesting–the microglial cell. The humble microglial cell is a microphage that lives in the brain and spinal cord. It represents the immune system in the central nervous system (CNS):
Among the many jobs performed by microglia is their surveillance of the entire brain for signs of injury, to which they rapidly respond by migrating to the site, tackling pathogens, and gobbling up damaged nerve-cell components to speed repair. Another item on the microglial resume is what the Science review’s authors call the “sculpting of neural circuits”: Microglia help prune away excessive or inappropriate brain-cell connections. But one can readily imagine how that latter process, if it gets out of hand, could cause problems. The authors suggest that the pathological underpinnings of not only neurodegenerative diseases such as Alzheimer’s but even so-called neurodevelopmental conditions including autism-spectrum and obsessive-compulsive disorders – not traditionally thought of as inflammatory – may turn out to harbor a microglial component. “As our tools and technology for studying microglia grow,” they write, “so too will our understanding of their role in the healthy brain.” (See Neuroinflammation, microglia, and brain health in the balance).
Why do we care? Well, imagine, if you will, that you are experiencing the precursor to almost all disease somewhere else in your body: inflammation. Let’s say that it’s in your gut. You were ill with a bacterial infection, used antibiotics, never replenished the healthy microbiota in your intestines afterwards, and are now experiencing an overgrowth of unhealthy bacteria. The stage has been set for inflammation. Cytokines are released by your immune system and enter your blood stream. Since your brain requires blood, the cytokines will cross the blood-brain barrier (BBB). Microglial cells respond to brain injury and disease. If cytokines are present in the BBB or around the brain, then the microglial cells will be activated. What will they do? What will they recognize in the brain as diseased, injured, or in need of scavenging? Will they do their job and simply attack the cytokines and then stand down, or will they go beyond and prune more neuronal connections than necessary? Or, will they commit suicide in the form of apoptosis?
A recent study done in Israel found that after only five weeks of chronic unpredictable stress exposure, microglial cells died by apoptosis (cell suicide) in the hippocampus resulting in depression. By intervention using two medications one of which was an antibiotic, scientists were able to rescue the remaining microglial cells and stimulate neurogenesis as well as put a stop to the depression. This indicates that at least one kind of depression brought on by stress is rooted in an immune response. It also indicates that chronic stress provokes an immune response in the brain!
Think of the enormity of such an idea. How many of us live with chronic stress? How many of us live with symptoms of inflammation? How many of us don’t understand that what we eat, how we cope, how we sleep, and so on affect every part of us? If we have a child with a mental illness or a developmental delay or disability, then it is our responsibility to look beyond just symptoms. Red #40 has been banned by the EU, for example, but it is not in the United States. Our FDA is not always on the cutting edge. Our doctors, due to the siloing within medical specialties, don’t always interpret symptomology correctly. Is our child at all affected by artificial dyes? Why? There is a spectrum of gluten intolerance that is now known to exist. Ingesting it can cause inflammation, and one doesn’t have to have celiac disease to be adversely affected (See Who Has The Guts for Gluten?). If inflammation is a precursor to disease, and inflammation affects brain health, and microglial action can cause depression and even be the pathogenesis to diseases like Parkinson’s and Alzheimer’s (see Neuroinflammation in the Pathogenesis of Parkinson’s Disease), then why wouldn’t we step back and re-asses our entire lifestyle and the lifestyles of our children? The Hurried Child phenomenon is eroding the physical and mental health of the 21st century child. There is little time for play in pre-schools and even in Kindergarten classes compared to twenty years ago (See The Serious Need for Play). Play and down time, however, are when we organize our experiences, encode memories, process what we’ve learned, and “de-stress”. Adults need it just as much as children. Combine the ever-increasing pace of our American culture with the standard American diet (SAD), and it’s no wonder that we are, well, ill.
If that’s not enough to motivate at least a pause, let’s make it a little more personal. Let’s think about Grace and other people with schizophrenia spectrum disorders. Schizophrenia is a neurodegenerative disorder characterized by loss of white/grey matter. The first five years of onset are typically the time frame wherein the most white matter is lost. A study was done to look for microglial activity in the brains of schizophrenic patients at the time of onset. Here is the conclusion:
Activated microglia are present in schizophrenia patients within the first 5 years of disease onset. This suggests that, in this period, neuronal injury is present and that neuronal damage may be involved in the loss of gray matter associated with this disease. Microglia may form a novel target for neuroprotective therapies in schizophrenia (See Microglial activation in recent-onset schizophrenia).
Keep in mind, microglial cells are part of the immune system. Suddenly, it’s not so simple anymore, is it? It’s not just genetics. Stress must be a part of it. Diet has to be. What else? Why is the immune system jumping in here? If microglial cells are playing such a role in this neurodegenerative illness and they play a role in depression, too, then what else are they doing in our brains? And what can we do to optimize their performance while preventing them from going rogue as was suggested by the Stanford research?
In the end, it is clear that we are complex organisms that can make a variety of choices that will affect our bodies for the better or the worse. We can activate genes and deactivate them with our environments, our diets, and even our relationships! But, now I’m stepping into the realm of epigenetics, and that’s another post.