Digestibility of Gluten
It is now known that gluten is an indigestible substance in humans. This is mainly due to the structure of the protein itself. Our body requires the appropriate enzymes to be able to digest such food by reducing it to its most basic form, the amino acids that can be absorbed.
One concedes that all living organisms evolve and so does the human body. Evolution may be constant but it does not happen overnight. To date, the human intestinal tract has not evolved to digest gluten, mainly due to the fact that previous generations of humans had a gluten-free diet. It turns out that the ancient Greeks and Romans had less gluten in the various grains they used (for beer, for example), at least compared to modern crop varieties. Higher concentrations of gluten entered the human diet as a result of modern cropping and agricultural techniques.
Analysing the current composition of grain, one realizes that gluten now represents not only a sizeable percentage but the largest among the proteins which compose wheat. A few centuries ago, gluten amounted to only 10-20% of the total protein in wheat. Today, gluten comprises an estimated 30 to 40 % of the total dry weight of wheat.
At What Point Can Children Tolerate Gluten Better?
One of the most important concerns of parents coping with celiac disease or gluten sensitivity in the family or even those concerned with the general well-being of their children is learning the right time frame for introducing gluten to their children’s diet. They may fear that bringing in gluten too early may prove to be detrimental. On the other hand, the overarching concern of well-informed parents is that introducing gluten early might build up a kind of natural adaptation, halt the progression of celiac disease, and possibly allow the child to be gluten-tolerant. On balance, the evidence is mixed.
Research into the matter has branched out in different directions and yielded conflicting recommendations.1 In Sweden, a well-meaning milk company decided to create and introduce a ‘fortified formula’ aiming to help infants progress from a milk-exclusive diet to a diet with solids as its main component. The fortified formula contained wheat as one of its main components.2 Infants were started on pure breast milk, introduced to the ‘fortified formula’ at from two to four months, and weaned on solid food afterwards.
Unhappily, the premature move to a high-gluten formula yielded a seven- to nine-fold increase in the prevalence of celiac disease when that cohort of children was monitored in a longitudinal study. After the fortified formula was withdrawn, the prevalence of celiac disease went right back to the ‘norm’ of 1%. The self-evident conclusion: the introduction of gluten too soon could be detrimental to the health of our children.
A Colorado field epidemiological study monitored children who were at risk of celiac disease. The research team discovered a ‘window of opportunity’ for introducing gluten to infants.3 A case-control study of the effect of infant feeding on celiac disease. Annals Nutrution Metabolism;45:135-142. The research found that this window of opportunity exists between four to seven months of life. According to the study, the introduction of gluten prior to, or after, this period substantially raised the risk of triggering gluten sensitivity.
Yet another prospective birth cohort study concluded that introducing gluten to infants past 6 months of age and permitting mothers to breastfeed longer than 12 months also raised the odds of celiac disease. It was found that infants introduced to gluten during their 7th month of life or beyond were at least 27% more likely to develop celiac disease at an early age of two years.4
The search for that elusive window of opportunity continues. When precisely to introduce gluten and how to balance intake is crucial for minimizing the harm that gluten does, particularly in triggering celiac disease. Prevention instead of treatment is a challenging but viable goal for medical practitioners. This is especially true for celiac disease because there is no known treatment and we can only delay the adverse effects of the disease. Like any allergy, one must avoid the trigger or find a way to desensitize the body to the offending agent, so the patient can live a healthy and normal life.
Autoimmunity, Environment and Genes
In the last 50 years, there has been a massive increase in the number of autoimmune diseases diagnosed such as asthma, MS, rheumatoid arthritis and celiac disease. However, autoimmune diseases do not develop overnight.
Genetic predispositions must come into play. They result from genetic alterations that take centuries to develop. Thus, the massive increase in autoimmune diseases is not so much due to improvements in diagnoses and classification as sheer exposure to an environment which the body is unable to adapt to. As a group, the autoimmune diseases are triggered by our immune system trying to defend against a foreign substance which it deems to be dangerous. Continued exposure to the substance causes the body to overreact to the ‘insult’ and results in destruction of healthy cells and tissues.
How Your Intestinal Environment Makes Gluten Sensitivity Worse
Genetic factors and the food a patient eats play major roles in the development of the autoimmune disease and the progression of gluten sensitivity. However, a third element should be considered, and that is the intestinal environment where intake and genetic predisposition interact. The crucial reason: the inflammatory cells that our bodies produce interacts with the food we ingest the moment the latter reach the small intestines.5
The intestinal tissue can be likened to a physical wall which prevents the interaction between food being digested and the inflammatory cells which lie beneath the intestinal tissue. Physiologically, the intestinal wall should prevent any interaction between the harmful substance (gluten) with the inflammatory cells. This is because these inflammatory cells can be a double-edged sword. Though they help eradicate the offending agent, they can also cause harm to the surrounding cells of the patient’s body.6
Going back to the analogy of physical walls, every wall has a point of entry which is usually heavily guarded. In the human body, these “check points” are called tight junctions which can be found between the cells of the intestinal epithelium. These tight junctions are often closed and do not permit any entry from foreign substances. For as long as these junctions remain intact, there will be no interaction between foreign substances and the inflammatory cells within the wall of the small intestine. However, any damage to the tight junctions, such as noxious chemicals (or the proteins from undigested gluten) leads to a loss in barrier function. There is unrestricted entry of these harmful agents then which instigates a reaction from the inflammatory cells. Though the initial purpose of these inflammatory cells is to halt attackers, they are also prone to destroy our intestinal tissue. The greater the damage, the worse the barrier breach.
Aside from genetics and the food people ingest that affect the integrity of the intestinal epithelium, the normal flora of the intestine should also be considered. Normal flora is the medical term for the “good bacteria” which reside within the gut from birth. These organisms are essential for our body to function optimally. Some of these bacteria which can be found in the stomach are responsible for self-production of vitamin K by the body. Without Vitamin K, the body is prone to bleeding disorder.7
A patient who is genetically predisposed to celiac disease may not necessarily acquire the disease later in life. The development of the disease also depends on certain triggers. One such trigger is microbiome balance, the community of good and bad bacteria residing within the gut. In turn, the microbiome is not only influenced by the existing colonies within the gut since birth, but also those acquired from the environment. One of the major influences on the status of the microbiome is the food that we ingest, because food introduces new microorganisms and influences the diet of bacteria already in the microbiome. Pollution, chemicals and radiation also play a role in maintaining microbiome balance.
Normally, the body’s normal flora do no harmful to our body. In fact, these microorganisms prevent the “bad bacteria” from causing harm in our gut by ensuring that the population of the latter is kept to the minimum. Unfortunately, there is risk when patients fail to follow doctor’s instructions or are administered excessive antibiotics. Excessive or prolonged antibiotic intake leads to a decrease in these “good bacteria”. Consequently, the harmful variety proliferates, overruns the gut and damages the intestinal epithelium. If this happens, a patient with gluten sensitivity will be more prone to severe autoimmune reactions even to the smallest amounts of gluten.
The introduction of antibiotics in the intestinal walls and the microbiome residing within it is similar to throwing a nuclear bomb on a city filled with terrorists and civilians. There is no guarantee that you are targeting only the bad bacteria. In fact, it is possible that the antibiotics eliminate the susceptible colonies of the normal flora. When this happens, the environment is primed for the bad bacteria to increase in number and dominate the intestinal microbiome. The result is damage to the intestine and assorted symptoms.
Difficulties of Diagnosing Celiac Condition
One of the main challenges of diagnosing celiac disease is differentiating the symptoms from related syndromes, including one that physicians term “celiac condition”. The latter cases involves patients who develop similar symptoms as the disease but they do not have the autoimmune factor. This means that the person’s inflammatory cells are not reactive to the proteins found in gluten.8
Patient with this condition present with vague symptoms such as abdominal pain, chronic fatigue, headache or depression. It is difficult to ascertain this condition because it mimics thousands of other diseases. If the patient is suffering from symptoms similar to celiac disease, they should not readily adhere to a gluten-free diet without a thorough medical work-up. Since this condition mimics other diseases, it’s important to rule out other diseases first, such as brain haemorrhage, brain tumour, systemic bacterial infection and many more before treating the condition as celiac disease.
The treatment for celiac disease or gluten sensitivity is the avoidance of gluten, which can alleviate most symptoms readily. However, if the patient is suffering from a brain tumour, a neurosurgeon should check on the patient, excise the tumour, and refer the patient to an oncologist for continuous monitoring and further treatment protocols.
The only way to ascertain the condition is through an MRI and tissue examination by pathologists to confirm that it is a brain tumour. Failure to rule out other diseases can be fatal just as celiac disease is fatal in the long run. Thus, it is important that a complete medical work-up is done, with celiac disease or gluten sensitivity always in mind.
- Hill,I.D., Dirks,M.H., Liptak,G.S. et al.(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 Pediatric Gastroenterology Nutrition;40:1-19. ↩
- Falth-Magnusson, K., Franzen,L., Jansson, G., Laurin,P., Stenhammar,L.(1996). Infant feeding history shows distinct differences between Swedish celiac and reference children. Pediatric Allergy Immunology;7:1-5. ↩
- Peters,U., Schneeweiss,S., Trautwein,E.A., Erbersdobler,H.F. (2001). ↩
- Stordal, K., et al (2013). Early feeding and risk of celiac disease in a prospective birth cohort. Pediatrics; 132:1-8. ↩
- Catassi, C. (2005). Where is celiac disease coming from and why? Journal of Pediatrics Gastroenterology & Nutrition, 40 (3): 279. ↩
- Fauci, A. S., Braunwald, E., Kasper, D. L., Hauser, S. L., Longo, D. L., Jameson, J. L. & Loscalzo, J. (Eds.) (2008). Harrison’s principles of internal medicine (17th ed.). New York: McGraw-Hill Professional. ↩
- Brooks, G. F., Carroll, K. C., Butel, J. S., Morse, S. A. & Mietzner, T. A. (2013). Jawetz, Melnick, & Adelberg’s Medical Microbiology, (26th ed.). New York: McGraw-Hill. ↩
- Fasano, A. (2013). Why creating the healthiest intestinal environment possible can arrest your vulnerability to the #3 cause of getting sick and dying. The Gluten Summit. Podcast retrieved from www.theglutensummit.com. ↩