By Ron Hoggan, Ed D
Achievement in school is an important predictor of children’s futures. In a more general sense, children’s achievement in school can also be used to predict the future of a given culture. Amid growing rates of very troubling behavioral disturbances and perplexing learning disorders we must, to secure the future, open ourselves to new ideas. Problems with learning and behavior have caused concern among parents and educators for some time now. However, these concerns have often been accompanied by the optimistic view that such learning and behavior problems have always been with us. The sentiment sounds something like “they are just being reported more frequently and are probably being dealt with more effectively.” While there may be some truth in this perspective, there is persuasive evidence that the incidence of learning disabilities and behavior problems is increasing independent of increasing case finding. Further, gluten grains may be a major factor in causing these scholastic problems. Our per-capita rate of grain consumption is definitely on the rise and the mismatch between human evolutionary diets and our current and growing reliance upon cereal grains as the primary staple in our diets(1) may be at the root of many, perhaps most, learning disabilities and behavior problems.
Although cultivation of cereal grains was begun more than 10,000 years ago it is important to recognize that time span as a mere moment in the human dietary adaptation to our environment (1). Further, by the time the people in the Fertile Crescent were cultivating grains, human populations were widely distributed across Europe, Asia, Australia, the Americas, and, of course, Africa. Thus, the genetic makeup of most of the world’s population was not impacted by either the genes or the food production of those earliest grain farmers. It is also worthy of note that these early farmers experienced dramatic reductions in stature when compared with their hunter-gatherer grandparents (2). Even those among us who have descended from those earliest farmers may or may not be well adapted to cereal grain consumption, especially since human intervention has led to significant changes in these very grains. With each generation only one year apart, genetic changes can be induced much more rapidly in grains than is possible in humans, both because of the time differences in reproductive cycles, and because the impact of grain consumption on reproduction is, although significant, far less than total among susceptible individuals.
It is also important to recognize that the spread of agriculture throughout Europe was necessarily slowed by the need for the grains to evolve increased gluten content, which allowed for maturation during the shorter growing seasons as it was cultivated further from the equator. Thus, our ancestors’ earliest exposure to cereal grains would be quite variable, according to where and when they lived. Further, due to the labor required to grow, harvest, grind, and cook grains, logic suggests that grain-derived foods would comprise a much smaller portion of the diet than is the case today.
Especially during the last century, the machinery for cultivating, milling, and transporting grains has become so efficient that the cost per calorie has become tiny compared to almost any other food group. Even the processing of flour, and manufacturing of the wide range of gluten-derived foods we now enjoy, has given us such economies of scale that the trend of steadily reducing costs can easily be tracked. It is a trend that, along with faulty dietary recommendations from the USDA and the Canada Food Guide, has helped fuel today’s plague of obesity, autoimmunity, and cancer in much of North America. Adding to this trend, a growing body of evidence is now demonstrating that our gluten consumption is also helping to create and/or exacerbate the behavior and learning problems that beset our children.
Gluten grains have been shown to cause neurological damage. They incite an autoimmune attack on neurological tissues through a process called molecular mimicry. Gliadin, a protein sub-group of gluten, has also been shown to be cytotoxic (3) causing the destruction of a range of tissues including neurological cells. Whether directly or indirectly, gluten grains are clearly causing neurological damage, some of which may be connected to learning disabilities and behavior problems.
Neurological damage is only one of several processes by which gluten grain consumption can cause behavior and learning problems in genetically susceptible individuals. The partial digests of gluten have long been known to have psychoactive properties (4). Dubbed “exorphins” by the research team that first discovered them, these peptides have repeatedly been shown to behave like morphine. More recently, researchers have shown that there are five separate exorphin peptides in wheat alone (5, 6).
Long dismissed as interesting but probably irrelevant, it was commonly assumed that the tight epithelial junctions that form the blood-brain barrier would protect us from gluten-derived exorphins. However, the discovery and characterization of zonulin has led to the recognition that gluten can, through inciting increased zonulin production, induce leaks in protective epithelial tight junctions both in the intestinal wall and at the blood-brain barrier (7). Thus, it is now clear that genetic susceptibility, when combined with gluten consumption, can result in compromised learning readiness in a small but significant percentage of the population.
It is important, when discussing learning and behavior problems, in association with exorphins, to recognize the multiple impacts these peptides can impose on the brain. As with morphine, they function as a central nervous system depressant. They slow neurotransmission, cause drowsiness, apathy, and induce mental confusion. They even act as a vasodilator, which might well contribute to the altered blood flow patterns often seen in the context of learning and behavior problems.
Such abnormal blood flow patterns in the brain are also reported as common among celiac patients, observed in 71% of 34 celiac patients tested (8). This is congruent with reported rates of attention deficit hyperactivity disorder (ADHD) among celiac children ranging from 66% to 70% (9, 10). Further, learning disabilities have been reported as overrepresented among celiac disease patients (11). and celiac disease, along with milk protein allergy, has been found more frequently in children with dyslexia (12).
Because learning and behavior problems have long been recognized as overly frequent among celiac disease patients, several other contributing factors have been suggested. For instance, the common finding of reduced plasma concentrations of tryptophan, a precursor of several important neurotransmitters involved in issues of learning and attention, has been suggested as a possible contributor to these problems. The broad range of nutrient deficiencies that is often found in the context of the malabsorption that characterizes celiac disease has also been offered to explain these behavior and learning difficulties.
While these factors may make a small contribution to learning and behavior problems in the context of celiac disease, new evidence now allows us to narrow our focus to the most important factors which include direct and indirect gluten-induced neurological damage along with the many facets of the impact of exorphins on brain function.
Our work (13) (unpublished data) has revealed that gluten sensitivity is associated with signs and symptoms that would interfere with learning and behavior which are very similar to those found in newly diagnosed celiac patients. Gluten sensitivity is not characterized by malabsorption, but shares the increased intestinal permeability (leaky gut) feature of celiac disease. For this reason, it may reasonably be inferred that the shared ground between celiac patients and gluten-sensitive patients with learning and/or behavior problems is the leakage of neurotoxic gliadins and gliadin fractions, along with absorption of exorphins into the blood, ultimately reaching the brain. One or all of these factors, given the current evidence, is the likely culprit(s) causing a significant minority of children to fare poorly at school.
Several reports indicate that the learning and behavior problems associated with celiac disease are abolished after six months to one year of strict compliance with a gluten-free diet (9, 10, 11). Celiac disease afflicts about 1% of most populations studied (13) and more than 5% among the Arab people of the Saharawi (15). In the context of gluten sensitivity, which is found in 11% to 12% of random groups in the U.S. and U.K. (16, 17), we observed similar improvements in learning readiness after at least three months of strict compliance with a gluten-free diet (13).
Others have shown that gluten sensitivity is a common finding in the context of neurological disease of unknown origin, and accounts for twice as many cases as celiac disease (17). Again, gut leakage of exorphins along with cytotoxic gliadins and gliadin fractions offer the most likely line-up of culprits responsible for these neurological ailments. When some of these patients with gliadin-mediated neurological disease were autopsied, the anti-gliadin antibodies found in the central nervous system were shown to cross-react with white matter in the brain (18).
The parallels are clear. Behavior and learning problems in the context of gluten sensitivity should be treated with a gluten-free diet. We have observed almost as dramatic a positive response to the gluten-free diet among gluten-sensitive patients with signs and symptoms suggestive of learning and/or behavior problems as is reported for celiac children.
The new food guides from the USDA and Canadian Government continue to advocate gluten grains and dairy products as healthful. Celiac disease and gluten sensitivity comprise about 12% of the population. Milk protein allergies are common and lactose intolerance afflicts the majority of the world’s adult populations, with African and Mexican Americans impacted most and earliest (19) on this continent. The food guide recommendations are both misleading and dangerous. Following the recommendations of their own government, the parents of a significant minority of children are unwittingly feeding their children foods that will compromise their school performance, their futures, and their health.
I am confident that no nefarious intent underlies the newest, or any other revisions of the healthy eating guides published by the USDA and Canadian governments. Nonetheless, the indoctrination of children, their parents, and teachers through the current healthy eating guides which are published, sanctioned, and promoted by our governments, is a form of institutionalized racism that promises to continue the subjugation of many members of racial minorities while also seriously compromising the futures of a small but significant minority of Caucasian children.
Ron Hoggan, Ed. D., has been teaching special needs secondary students for almost 20 years. Ron is co-author of Dangerous Grains and is editor of Scott-Free Newsletter, a publication that serves the celiac and gluten-sensitive community. He may be contacted at firstname.lastname@example.org
1. Cordain, L. (1999). Cereal grains: humanity’s double edged sword. World Rev Nutr Diet 84: 19-73.
2. Lutz, W. (1995). The Colonization of Europe and Our Western Diseases. Medical Hypotheses. 45: 115-120.
3. Hudson, D., Purdham, D., Cornell, H., Rolles, C. (1976). Non-specific cytotoxicity of wheat gliadin towards cultured human cells. The Lancet, February 14, 339-341.
4. Zioudrou, C., Streaty, R., Klee, W. (1979). Opioid Peptides Derived from Food Proteins. The Journal of Biological Chemistry 254(7), 2446-2449.
5. Fukudome, S., & Yoshikawa, M. (1993). Gluten exorphin C. Febs Letters. 316(1), 17-19.
6. Fukudome, S., & Yoshikawa, M. (1992). Opioid peptides derived from wheat gluten: their isolation and characterization. FEBS Letters. 296(1), 107-111.
7. Fasano, A., (2000). Regulation of intercellular tight junctions by zonula occludens toxin and its eukaryotic analogue zonulin. Ann N Y Acad Sci. 915, 214-22.
8. Usai P, Serra A, Marini B, Mariotti S, Satta L, Boi MF, Spanu A, Loi G, Piga M. (2004). Frontal cortical perfusion abnormalities related to gluten intake and associated autoimmune disease in adult coeliac disease: 99mTc-ECD brain SPECT study.Dig Liver Dis. Aug;36(8):513-8.
9. Paul, K., Todt, J., Eysold, R. (1985). EEG Research Findings in Children with Celiac Disease According to Dietary Variations. Zeitschrift der Klinische Medizin. 40, 707-709.
10. Kozlowska, Z: (1991). Results of investigation on children with coeliakia treated many years with glutethen free diet Psychiatria Polska. 25(2), 130-134.
11. Zelnik et. al. Range of Neurologic Disorders in Patients with Celiac Disease. Pediatrics 2004; 113; 1672-1676
12. Knivsberg AM. (1997). Urine patterns, peptide levels and IgA/IgG antibodies to food proteins in children with dyslexia. Pediatr Rehabil. Jan-Mar;1(1):25-33.
13. Ford, R., Hoggan, R., Fung, T., Marini, A. (unpublished)
14. Tommasini A, Not T, Kiren V, Baldas V, Santon D, Trevisiol C, Berti I, Neri E, Gerarduzzi T, Bruno I, Lenhardt A, Zamuner E, Spano A, Crovella S, Martellossi S, Torre G, Sblattero D, Marzari R, Bradbury A, Tamburlini G, Ventura A. (2004). Mass screening for coeliac disease using antihuman transglutaminase antibody assay. Arch Dis Child. Jun;89(6):512-5.
15. Catassi C, Ratsch IM, Gandolfi L, Pratesi R, Fabiani E, El Asmar R, Frijia M, Bearzi I, Vizzoni L. (1999). Why is coeliac disease endemic in the people of the Sahara? Lancet. Aug 21;354(9179):647-8.
16. Fine, Kenneth (2006). private communication
17. Hadjivassiliou M, Gibson A, Davies-Jones GA, Lobo AJ, Stephenson TJ, Milford-Ward A. (1996). Does cryptic gluten sensitivity play a part in neurological illness? Lancet. Feb 10;347(8998):369-71.
18. Hadjivassiliou M, Boscolo S, Davies-Jones GA, Grunewald RA, Not T, Sanders DS, Simpson JE, Tongiorgi E, Williamson CA, Woodroofe NM. (2002). The humoral response in the pathogenesis of gluten ataxia. Neurology. Apr 23;58(8):1221-6.
19. Simoons FJ. (1980). Age of onset of lactose malabsorption. Pediatrics 66:646–8
20. Niederhofer H, Pittschieler K. (2006). A preliminary investigation of ADHD symptoms in persons with celiac disease.J Atten Disord. Nov;10(2):200-4.