The Case for Gluten-Free
“Not into fad diets and I don’t have Celiac Disease,” I replied to everyone who asked me if I was gluten-free several years ago. In fact, I believed restaurants wasted ink printing “GF” next to their menu items and I questioned the ethics of Whole Foods for devoting entire aisles to this novel and questionable cause. But post-meal bloating continued to plague me and after many meals in utter discomfort, I was open to look elsewhere for help.
Soon thereafter, “Grain Brain,” neurologist David Perlmutter’s book, was recommended to me. With a medical education and clinical experience behind him, this author seemed a credible source and I was interested to hear his professional take on the matter. Meanwhile, my belly hurt continued to painfully bloat after meals, so why not? He introduced me to the science behind a gluten-free diet, and since then, here’s what I’ve learned…
Gluten: what, where, and why?
Gluten, Latin for “glue,” is a protein that holds flour together to make bread products and helps bread rise when wheat mixes with yeast. Gluten can be consumed most commonly through wheat, but also in a variety of grains including rye, barley, oat, spelt, kamut, and bulgur. When you feel the stretchiness of pizza dough or appreciate the soft chewiness of muffins and bread rolls, you have gluten to thank!
Molecularly, a potentially toxic groups of proteins make up gluten called gliadins. In gluten sensitivity, a person may be sensitive to gliadin as a whole or to one of its smaller units.
Gluten sensitivity, allergy, and celiac disease: connecting the dots
Gluten sensitivity (or intolerance) is actually an umbrella term integrating three major gluten-related disorders: 1) autoimmune celiac disease (CD), (2) wheat allergy, and (3) non-celiac gluten sensitivity (NCGS). The first two, CD and wheat allergy (WA), are easy to diagnose by testing for certain antibodies in the blood.
CD, a chronic, immune-mediated enteropathy (disease of small intestine) triggered by dietary gluten exposure in genetically predisposed people, is characterized by specific autoantibodies (IgG or IgA). Specifically, these are antibodies antibodies against tissue transglutaminase 2 (anti-TG2), endomysium (EMA), and/or deamidated gliadin peptide (DGP)s: all things you can ask your doctor to test for in your blood. Worldwide, celiac disease has a prevalence of about 1% . It results from an immune response to gluten in predisposed people that causes damage to the small intestines (resulting in diarrhea), as well as extraintestinal manifestations, such as dermatitis herpetiforme (skin problem), iron-deficiency anemia (from poor iron absorption related to inflamed intestines), osteoporosis, neurologic disorders (peripheral neuropathy and ataxia), and possibly arthritis. Treatment is a gluten-free diet, which should help alleviate symptoms in affected people.
WA is another gluten-related disorder, defined as an adverse immunologic reaction to wheat proteins characterized by the production of wheat-specific antibodies (usually IgE) that play a key role in disease pathogenesis.
Finally, the “NCGS” people include everyone else: people with a “non-allergic and non-autoimmune condition, in which the consumption of gluten can lead to symptoms similar to those seen in CD,” (according to the definition decided upon in 2011-2012 by international panel of experts in London). NCGS is further characterized by resolution of symptoms with gluten withdrawal and relapse of symptoms with gluten exposure. Like in Celiac Disease, people with NCGS can find themselves anemic with low iron stores from intestinal inflammation, as well as other CD-related symptoms above, caused by eating foods with wheat and gluten.
NCGS: Why would this happen to me?
Did you know that 70% of your immune system sits in your gut? It makes sense when you think about how you take medications by mouth and their absorption into your body through your digestive tract.
Current knowledge about NCGS pathogenesis leaves very much to be desired. What we do know is that gliadin is the toxic component of gluten . Our gut lymphoid tissue is protected from it by a barrier (intercellular tight junctions or TJ) that limit passage of macromolecules (like gliadin) across the intestinal lining. In susceptible people, gliadin can interact with your intestinal cells and trigger TJ disassembly (through increased release of a protein, zonulin, that increases intestinal permeability) . What this means is that the lining of the gut becomes “leaky” and eventually, gliadin gets through to intestinal lymph-associated tissue and causes inflammation and immune events that lead to CD or NCGS.
While this is one proposed mechanism, there are other proteins in wheat, besides gluten, that can cause gastrointestinal (GI) symptoms. Wheat is a primary source of “FODMAPS” (fermentable oligo-, di- and mono-saccharides, and polyols, which are molecules inducing fermentation and gas production when metabolized by gut microbiota, evoking bloating, discomfort, and abdominal pain.
However, by reviewing studies that analyzed blood and duodenal tissue samples from NCGS patients, it would appear that gluten can activate both the innate and adaptive immune systems. In addition, the gliadin protein has been shown to cause changes in the gut lining via zonulin, and increase intestinal permeability.
To be gluten-free or not gluten-free, that is the question
Whether or not you have a gluten-sensitivity, when you follow a gluten-free diet, you should be replacing processed foods, which are high in sugar, with more whole-foods, like vegetables, proteins, fats, and fruits. This type of modification will help maintain low glucose levels in your blood, which translates to more energy and less spikes and dips in blood sugar levels (think less post-meal sleepiness). Incorporating more minerals and nutrients in your diet through increased intake of whole-foods and less carbohydrates is arguably where the benefit lies of this diet lies.
Just look at results of the DIRECT2 study. The researchers compared low-carb, low-fat, and Mediterranean-style diets and found that after two years, weight loss and maintenance were better for low-carb and Mediterranean-style diets as compared to low-fat diets. In other words: eating fat doesn’t make you fat, eating carbohydrates (high in sugar) does! A low-carb diet will also help to lower cholesterol levels and improve risk for heart disease.
GF Carbohydrate Substitutes
As a rule, I try to avoid processed “gluten-free” carbohydrates, like bread and crackers, as they just replace wheat less holistic ingredients that will still cause your glucose levels to spike and are lacking in nutritive value. For example, xantham gum, a fermented sugar, often replaces gluten in gluten-free baked goods. Instead, see my favorite substitutes below:
What else can I eat on GF diet?
Try organic and local whole-food choices when possible; even flash-frozen foods are good! Any other food category besides carbohydrates is really fine, including:
· Healthy fat: oils like extra virgin olive, sesame, and coconut; avocados, coconuts, olives; nuts and nut butters, cheese, and seeds (flaxseed, sunflower seeds, pumpkin seeds, sesame seeds, chia seeds).
- Protein: whole eggs; wild fish, shellfish and mollusks; grass-fed meat, fowl, poultry, and pork; wild game.
- Herbs, Seasonings, and Condiments: watch labels! No ketchup and chutney but enjoy mustard, horseradish, tapenade, and salsa if they are free of gluten, wheat, and sugar. There are virtually no restrictions on herbs and seasonings; be mindful of packaged products, however, that were made at plants that process wheat and soy.
Bottom line: You don’t need to go gluten-free if you are symptom-free, but a low carbohydrate diet, higher in whole foods, healthy fats, and proteins is a proven healthier alternative.
1 Ludvigsson, J. F. et al. The Oslo definitions for coeliac disease and related terms. Gut 62, 43-52, doi:10.1136/gutjnl-2011-301346 (2013).
2 Shai, I. et al. Weight loss with a low-carbohydrate, Mediterranean, or low-fat diet. N Engl J Med 359, 229-241, doi:10.1056/NEJMoa0708681 (2008).
3 Hernandez, L. & Green, P. H. Extraintestinal manifestations of celiac disease. Curr Gastroenterol Rep 8, 383-389 (2006).
4 Lammers, K. M. et al. Gliadin induces an increase in intestinal permeability and zonulin release by binding to the chemokine receptor CXCR3. Gastroenterology 135, 194-204 e193, doi:10.1053/j.gastro.2008.03.023 (2008).