Fat free, sugar free, reduced fat, reduced sugar, low carb, low calorie. Sound familiar? Well, it should. These nutritional labels have been on the market for decades and likely will continue for decades to come.

Just like in training, nutrition certainly has well established “trends.” Due to the “trendiness” and smart marketing, the infestation of more and more “products” comes to fruition nearly every year. Gluten is certainly no exception, and we as a society have added one more to the list in “gluten free.”

Less than five years ago, the majority of Americans had no clue what gluten was and many still lack true knowledge and awareness about the specifics concerning gluten. However, given the rapid increase of the gluten-free market worldwide, partially sustained by individuals who claim a medical necessity to initiate a gluten-free diet, there is a need of “separating the wheat from the chaff” (25). Therefore, we now enter “the gluten games.”

Inside the Gluten Games

Gluten refers to the proteins found in wheat endosperm (a type of tissue produced in seeds that’s ground to make flour). Gluten serves numerous functions, among them providing nourishment to plant embryos during germination and even ultimately affecting the elasticity of dough, which produces the chewiness of various baked wheat products. Gluten is actually composed of two different proteins: gliadin (a prolamin protein, which is a storage plant protein found in many cereal grains, barely rye, and corn) and glutenin, the major protein within wheat flour. The ability of wheat flour to be processed into different foods is largely determined by the gluten proteins (3). The gluten proteins represent up to 80–85 percent of total flour protein, and the gliadins and glutenins comprise each around 50 percent of the gluten proteins (3). Though “true gluten” is sometimes defined as being specific to wheat, gluten is often said to be part of other cereal grains, including rye, barley, and various mixtures.

ingredients for italian pizza

Many of the medical and anecdotal evidence claims include “we can’t digest gluten,” “eating gluten free equals weight loss,” and the ever so popular “grains are poison.” A shocking revelation to many is that gluten isn't just found in wheat. It’s found in a whole host of other foods including beer, candies, lunch meats, beverages, supplements (some information not conveyed on the label), sauces, dressings, and gravies. Therefore, considering a wide variety of foods do, in fact, contain gluten, it’s a safe bet that those engaging in the gluten-free diet (GFD) never consume these products, right?

The creation of gluten-free diets is founded on celiac disease (CD), an autoimmune mediated reaction to gluten, which occurs in genetically predisposed individuals (23). The various endorsements by high-powered celebrities like Dr. Oz, Lady Gaga, and Gwyneth Paltrow have created scare tactics among society perpetuating the idea that gluten is somehow a “huge crisis” and one will get inflamed simply by “looking at it.” Perhaps these individuals and those who have jumped on the “gluten bandwagon" need to reexamine their critical thinking skills. Let’s evaluate the numbers, shall we?

Setting Up the Game: The Gluten Numbers

Gluten-free foods (and beverages) have become a multibillion dollar industry. They're easily accessible and are more consumer friendly in terms of packaging and convenience. This phenomenon has sent gluten-free food sales skyrocketing. While growth rates will moderate over the next five years in the wake of market expansion, U.S. sales of products carrying the gluten-free label jumped from $11.5 billion to $23 billion within the past four years alone. According to the market research firm Mintel (5), the gluten-free food category is expected to generate more than $15 billion in annual sales by 2016. While the sales of gluten-free foods (GFF) have risen dramatically, this is very perplexing considering the prevalence of celiac disease (CD) is only estimated to be 0.5–1.25 percent of the general population where there is genetic risk (10, 12, 13, 20). Roughly five percent of individuals in westernized nations may have a true food allergy and only about 0.1 percent has a documented wheat allergy (23).

Single Player

The proliferation of “gluten-free’ products on the shelves and in restaurants marketing and selling gluten-free products display the notion that gluten is the only player in this game. It’s touted as the only factor involved with celiac disease and the associated ailments including wheat allergy and gluten sensitivity. The fact is few know what gluten truly is but erroneously claim that it will make you fat and bloated and that eating it is analogous to Satanism. The problem is the anti-gluten movement has developed into an exaggerated food movement that has disregarded the true nature of society’s unhealthiness—gluttony for food and beverages and shortage of exercise. Instead, they have created a “reign of terror” for gluten. However, the general public’s recent embrace of the gluten-free diet (GFD) lifestyle is also associated with the perception by many in the medical and fitness industries that the GFD is a “fad diet ”(23).

muffin gluten games jon mike 082114

Multiple Players

Because gluten itself is certainly not the only player in the games, let’s discuss the multiple-player level. The level of multiple players can be rather complex, so let’s break it down more simply. There are essentially three main players within the Gluten Games. The first player, which I’ve already introduced, is celiac disease. The other players are wheat allergy (WA) and non-celiac gluten sensitivity (NCGS). Here’s a breakdown of each player.

Multiple player 1: Celiac disease
As previously mentioned, celiac disease is an autoimmune mediated reaction to gluten, which occurs in genetically predisposed individuals (23) and damages the small intestines. Individuals with CD react to dietary proteins called prolamins in certain grains. Although all grain products including rice contain prolamins, the specific prolamins found in wheat (gliadin), rye (secalin), and barley (horedein) have been shown to be the ones implicated to cause an immunologic reaction in those who have CD. A genetic predisposition and exposure to gluten are necessary but not sufficient to develop CD (19). This disease is triggered by gluten ingestion in people who have genetic compatibility of the human leukocyte antigens (HLA). Say what? Yes, it’s a real thing. For simplicity, just use HLA. The HLA is carried by 90 percent of patients with CD (4, 14). Although a significant proportion of the population has these genes (about 40 percent), most do not develop CD.

An interesting characteristic is that CD was once considered to develop during childhood, but recent data shows that the loss of tolerance to gluten does not necessarily occur at the time of gluten introduction. It may occur at any point due to unknown environmental triggers (10). In essence, two main conditions must be necessary for the development of CD: the ingestion of gluten and a genetic predisposition to CD. However, the predisposition depends on a multitude of genes, each of them adding only a modest contribution to disease development (16). There are a myriad of risk factors that correspond to CD, including family history (genetic predisposition), specific positive immune markers, and positive genetic testing (19). In children, other risk factors include method of infant feeding (formula versus duration of breastfeeding [2]), method of birth (11), timing of the introduction of gluten into the diet (2), and infections during early childhood (27). The onset of symptoms is typically gradual and described by a time lag of months or years after gluten introduction. Nevertheless, in patients on long-term treatment with a GFD, the ingestion of gluten may occasionally cause immediate symptoms, such as vomiting and abdominal pain (26). Lastly, the diagnostic gold standard for CD is small bowel biopsy (15, 24).

spaghetti gluten games jon mike 082114

Multiple player 2: Wheat allergy

Although similar to celiac disease, wheat allergy (WA) is an immune-mediated reaction to the proteins found in wheat products. It is sometimes referred to as “baker’s asthma.” Compared to CD, it’s an immune-mediated reaction to the water and salt insoluble gliadins (17). Those with WA usually do not need to restrict other prolamin containing grains such as rye, barley, and oats from their diet. A whole host of symptoms arise from WA, which usually occur in the mouth, nose, eyes, and throat (swelling, itching, and irritation); the skin (rash, hives, swelling); respiratory tract (wheezing, difficulty breathing, anaphylaxis); and gastrointestinal tract (cramps, nausea, emesis, gas, bloating, diarrhea, and abdominal pain). A distinguishing aspect of WA compared with CD is that WA often develops throughout early infancy or the toddler years and is less common in adolescents and adults. Most children with WA also have other food allergies (23).

One of the main reasons to distinguish between CD and WA is that WA is usually outgrown between the ages of three and five years while CD is lifelong (23). Improvements in wheat allergy can certainly be made with the elimination of wheat and wheat products from the diet. The effects can be prevented with strict wheat avoidance and treated with antihistamines and corticosteroids. Current available tests include serum wheat specific immune testing, skin prick tests, patch testing, and oral challenge. The oral food challenge may be the most effective diagnostic technique. Risk factors include family history of allergy, male sex, and a low birth weight, which predispose individuals to developing an allergy.

Multiple player 3: Non-celiac gluten sensitivity

Non-celiac gluten sensitivity (NCGS) is a condition currently defined by clinical symptoms triggered by gluten ingestion in the absence of blood tests con­sistent with celiac disease, small intestine villous atrophy, and wheat allergy (8). Meaning, NCGS is now commonly used to describe those who have a reaction to gluten without meeting the criteria for CD or WA. Despite the severe lack of published epidemiological studies on gluten sensitivity, it is estimated that the prevalence of gluten sensitivity is 3–6 percent (7, 21, 22). Although immune-mediated, the pathogenesis of NCGS is unknown. Symptoms occur soon after the consumption of gluten, disappear with the withdrawal of gluten, and reappear when gluten is even blindly consumed. Symptoms usually correspond with abdominal pain, bloating, diarrhea, or constipation (8). At present, a GFD is the only treatment for NCGS at this time. There­fore, current recommendations include maintaining a GFD to prevent symptoms. However, no known safe or unsafe dose of gluten like that for CD has been described (9). Lastly, there are no studies evaluating risk factors or pre­vention of NCGS.

Brownie Tower

Game On

Now that we have discussed the multiple players of the Gluten Games, hopefully you now have a better understanding of the inside rules. So feel free to consume or toss your gluten-free apple pie and let’s get down to business.

The origination of the Gluten Games stemmed from the 2011 landmark study by Biesiekierski (5). Controversial and biased in its own right, it set off a firestorm of media hysteria about gluten. Further, the body of research was taken out of context to support gluten-related issues. In the more recent, well controlled, double blind follow-up study by the same group of authors (6), it was found that gluten sensitivity, or gluten intolerance, does not exist in the absence of celiac disease. It’s important to note that, in the more recent study (6), the same scientist who had originally published the first report showed that some people exhibit NCGS. However, based on the results from the newer, more well controlled and non-biased study, results confirmed that gluten sensitivity does not exist in the absence of celiac disease.

Specifically, patients in the study participated in a blind tasting diet in which they either ate 16, two, or zero milligrams of gluten each. Over the course of five weeks, all meals were provided for the 37 subjects with self-diagnosed NCGS and irritable bowel syndrome (IBS). While maintaining a daily diary and undergoing tests, the subjects were rotated through gluten-free, low-gluten (2g/day), and high-gluten diets (16g/day) for one week followed by a two-week washout period before crossing over to the next diet. A double blind, placebo-controlled, randomized crossover challenge was then conducted in 22 of these patients, where they were randomized to receive gluten (16 g/day), whey (16 g/day), or placebo for three days each with a minimum of a three-day washout. All food was provided, but in addition to the food being gluten-free, dairy products and food chemicals were also controlled to minimize all potential triggers of gut symptoms.

The common factor across all three diets was that they were all low in fermentable oligosaccharides, disaccharides, monosaccharides, and polyols, or FODMAP (say this ten times fast). Regardless of which diet they consumed, they all reported feeling worse, including on the diet that contained no gluten. This phenomenon is sometimes referred to as the “nocebo” effect. Similar to the placebo effect, the nocebo effect occurs even in the absence of any active substance. In other words, people mistakenly believe that they are gluten sensitive and convince themselves that they feel worse. Thus, they begin to experience real symptoms even though it's purely psychological (i.e., all in their heads). In essence, the researchers found no measurable connection to gluten causing valid digestive concerns and that the “nocebo effect” was in full force.

One of the many claims concerning gluten was that those seeking weight loss choose gluten-free foods and diets as the “healthier option.” While weight loss and GFDs are a subtopic within the whole genre of gluten claims, the FDA defined the term “gluten free” for voluntary use in food labels in August 2013 (1).

cereal gluten games jon mike 082114

To meet the criteria to use this term, the food must not contain (9):

  • a gluten-containing grain
  • an ingredient derived from a gluten-containing grain that has not been thoroughly processed to remove gluten
  • a gluten-containing grain that has been processed if it results in greater than 20 parts per million or more of gluten in food
  • a gluten-containing grain that has greater than 20 parts per million of gluten based on previous studies

This guideline made it very difficult for large food companies that produce a variety of gluten and gluten-free products in the same facility to label their products as gluten free. However, it also opened the doors for many small businesses to obtain additional profits. Due to the preponderance of gluten products provided to local and homemade goods, it has resulted in enormous success for smaller businesses that wish to cash in and triumph in the gluten-free market.

Time’s Up

Due to the power of suggestion, marketing hype, reliance on the emotional triggers of zealous testimonials, and celebrity endorsements, people mistake their anecdotal experience and nocebo effect for actual science and almost nothing can convince them that they don’t actually have sensitivity to gluten. Undeniably, there are people who have celiac disease and these individuals certainly have some challenges to face. Nonetheless, in order to be truly gluten free, you almost need to have a separate area just for those gluten products and the rest of the “normal” items, particularly in restaurants where they market gluten-free foods.

Is it really “gluten free” when it’s being prepared next to fried chicken? The food writer Michael Pollen recently stated that “gluten free is a bit of a social contagion.” Based on the science and considering the nocebo effect, who is to say that those who withdraw from gluten feel better because of the gluten? In all likelihood, it’s because they have eliminated refined, processed foods from their diet. The fact is the promulgation of gluten creating serious adverse health effects for the overwhelming majority of individuals is misleading and erroneous.

Game Over: Is There a Winner?

The idea that gluten itself is the number one villain creating metabolic madness isn't only false but is accompanied by an abundance of pseudoscience and exaggeration. A similar approach was used in the 80s and 90s for saturated fats and cholesterol. Now we know that actual science has refuted that notion. However, gluten isn't entirely without blame. Gluten may not, in reality, be the culprit in non-celiac individuals. So who is to blame?

Well, it could be Monsanto (conspiracy theorist, please stand up) but highly unlikely. Rather, other wheat proteins or carbohydrates may be the major players of gastrointestinal distress in otherwise healthy people who eat wheat and even immune-mediated WA (17). Recent studies also raised the possibility that beside gluten and wheat, low fermentable, poorly absorbed, short chain carbohydrates (6) can contribute to symptoms. Further, even earlier studies reported that the nocebo effect of wheat ingestion can certainly explain the occurrence of NCGS, as patients who believe themselves to be food sensitive are preconditioned to avoidance (18). Lastly, the overwhelming rate of change makes environmental factors a likely cause rather than changes in human genetics. Considering that gluten has a deleterious effect on such a small proportion of the population (and even those who ought to be “careful” represent a small percentage), it’s safe to say that the other 90 percent of individuals are just fine.

References

  1. Federal Register. Gluten-Free Labeling of Foods. Available from: https://http://www.federalregister.gov/articles/2013/08/05/2013-18813/food-labeling-gluten-free-labeling-of-foods. Accessed: July 8, 2013.
  2. Agostoni C, Decsi T, Fewtrell M, Goulet O, Kolacek S, Koletzko B, Michaelsen KF, Moreno L, Puntis J, Rigo J, Shamir R, Szajewska H, Turck D, van Goudoever J, Nutrition ECo (2008) Complementary feeding: a commentary by the ESPGHAN Committee on Nutrition. Journal of Pediatric Gastroenterology and Nutrition 46:99–110.
  3. Anjum FM, Khan MR, Din A, Saeed M, Pasha I, Arshad MU (2007) Wheat gluten: High molecular weight glutenin subunits–structure, genetics, and relation to dough elasticity. Journal of Food Science 72:R56–63.
  4. Barada K, Abu Daya H, Rostami K, Catassi C (2012) Celiac disease in the developing world. Gastrointestinal Endoscopy Clinics of North America 22:773–96.
  5. Biesiekierski JR, Newnham ED, Irving PM, Barrett JS, Haines M, Doecke JD, Shepherd SJ, Muir JG, Gibson PR (2011) Gluten causes gastrointestinal symptoms in subjects without celiac disease: a double-blind randomized placebo-controlled trial. Am J Gastroenterol 106:508–14.
  6. Biesiekierski JR, Peters SL, Newnham ED, Rosella O, Muir JG, Gibson PR (2013) No effects of gluten in patients with self-reported non-celiac gluten sensitivity after dietary reduction of fermentable, poorly absorbed, short-chain carbohydrates. Gastroenterology 145:320–28; e321–23.
  7. Cascella NG, Kryszak D, Bhatti B, Gregory P, Kelly DL, Mc Evoy JP, Fasano A, Eaton WW (2011) Prevalence of celiac disease and gluten sensitivity in the United States clinical antipsychotic trials of intervention effectiveness study population. Schizophrenia Bulletin 37:94–100.
  8. Catassi C, Bai JC, Bonaz B, Bouma G, Calabro A, Carroccio A, Castillejo G, Ciacci C, Cristofori F, Dolinsek J, Francavilla R, Elli L, Green P, Holtmeier W, Koehler P, Koletzko S, Meinhold C, Sanders D, Schumann M, Schuppan D, Ullrich R, Vecsei A, Volta U, Zevallos V, Sapone A, Fasano A (2013) Non-Celiac Gluten sensitivity: the new frontier of gluten related disorders. Nutrients 5:3839–853.
  9. Catassi C, Fabiani E, Iacono G, D’Agate C, Francavilla R, Biagi F, Volta U, Accomando S, Picarelli A, De Vitis I, Pianelli G, Gesuita R, Carle F, Mandolesi A, Bearzi I, Fasano A (2007) A prospective, double-blind, placebo-controlled trial to establish a safe gluten threshold for patients with celiac disease. Am J Clin Nutr 85:160–66.
  10. Catassi C, Kryszak D, Bhatti B, Sturgeon C, Helzlsouer K, Clipp SL, Gelfond D, Puppa E, Sferruzza A, Fasano A (2010) Natural history of celiac disease autoimmunity in a USA cohort followed since 1974. Annals of Medicine 42:530–38.
  11. Decker E, Engelmann G, Findeisen A, Gerner P, Laass M, Ney D, Posovszky C, Hoy L, Hornef MW (2010) Cesarean delivery is associated with celiac disease but not inflammatory bowel disease in children. Pediatrics 125:e1433–440.
  12. Dube C, Rostom A, Sy R, Cranney A, Saloojee N, Garritty C, Sampson M, Zhang L, Yazdi F, Mamaladze V, Pan I, Macneil J, Mack D, Patel D, Moher D (2005) The prevalence of celiac disease in average-risk and at-risk Western European populations: A systematic review. Gastroenterology 128:S57–67.
  13. Fasano A, Berti I, Gerarduzzi T, Not T, Colletti RB, Drago S, Elitsur Y, Green PH, Guandalini S, Hill ID, Pietzak M, Ventura A, Thorpe M, Kryszak D, Fornaroli F, Wasserman SS, Murray JA, Horvath K (2003) Prevalence of celiac disease in at-risk and not-at-risk groups in the United States: A large multicenter study. Arch Intern Med 163:286–92.
  14. Gujral N, Freeman HJ, Thomson AB (2012) Celiac disease: prevalence, diagnosis, pathogenesis and treatment. World J Gastroenterol 18:6036–59.
  15. Hill ID, Dirks MH, Liptak GS, Colletti RB, Fasano A, Guandalini S, Hoffenberg EJ, Horvath K, Murray JA, Pivor M, Seidman EG, North American Society for Pediatric Gastroenterology H, Nutrition (2005) Guideline for the diagnosis and treatment of celiac disease in children: Recommendations of the North American Society for Pediatric Gastroenterology, Hepatology and Nutrition. Journal of Pediatric Gastroenterology and Nutrition 40:1–19.
  16. Hunt KA, Zhernakova A, Turner G, Heap GA, Franke L, Bruinenberg M, Romanos J, Dinesen LC, Ryan AW, Panesar D, Gwilliam R, Takeuchi F, McLaren WM, Holmes GK, Howdle PD, Walters JR, Sanders DS, Playford RJ, Trynka G, Mulder CJ, Mearin ML, Verbeek WH, Trimble V, Stevens FM, O’Morain C, Kennedy NP, Kelleher D, Pennington DJ, Strachan DP, McArdle WL, Mein CA, Wapenaar MC, Deloukas P, McGinnis R, McManus R, Wijmenga C, van Heel DA (2008) Newly identified genetic risk variants for celiac disease related to the immune response. Nat Genet 40:395–402.
  17. Inomata N (2009) Wheat allergy. Current opinion in Allergy and Clinical Immunology 9:238-243.
  18. Jewett DL, Fein G, Greenberg MH (1990) A double-blind study of symptom provocation to determine food sensitivity. N Engl J Med 323:429–33.
  19. Leonard MM, Vasagar B (2014) US perspective on gluten-related diseases. Clinical and Experimental Gastroenterology 7:25–37.
  20. Lohi S, Mustalahti K, Kaukinen K, Laurila K, Collin P, Rissanen H, Lohi O, Bravi E, Gasparin M, Reunanen A, Maki M (2006) Increasing prevalence of celiac disease over time. Alimentary Pharmacology & Therapeutics 26:1217–225.
  21. Lundin KE (2014) Non-celiac gluten sensitivity—why worry? BMC Medicine 12:86.
  22. Lundin KE, Alaedini A (2012) Non-celiac gluten sensitivity. Gastrointestinal Endoscopy Clinics of North America 22:723–34.
  23. Pietzak M (2012) Celiac disease, wheat allergy, and gluten sensitivity: When gluten free is not a fad. JPEN J Parenter Enteral Nutr 36:68S–75S.
  24. Rostom A, Murray JA, Kagnoff MF (2006) American Gastroenterological Association (AGA) Institute technical review on the diagnosis and management of celiac disease. Gastroenterology 131:1981–2002.
  25. Sanders DS, Aziz I (2012) Non-celiac wheat sensitivity: Separating the wheat from the chat! Am J Gastroenterol 107:1908–912.
  26. Sapone A, Bai JC, Ciacci C, Dolinsek J, Green PH, Hadjivassiliou M, Kaukinen K, Rostami K, Sanders DS, Schumann M, Ullrich R, Villalta D, Volta U, Catassi C, Fasano A (2012) Spectrum of gluten-related disorders: consensus on new nomenclature and classification. BMC Medicine 10:13.
  27. Stene LC, Honeyman MC, Hoffenberg EJ, Haas JE, Sokol RJ, Emery L, Taki I, Norris JM, Erlich HA, Eisenbarth GS, Rewers M (2006) Rotavirus infection frequency and risk of celiac disease autoimmunity in early childhood: A longitudinal study. Am J Gastroenterol 101:2333–340.