Gluten is a family of storage proteins found in wheat, rye, triticale, and barley. In predisposed individuals, ingestion of gluten causes disease reactions that are grouped under the term gluten-related disorders (GRD). Only a decade ago, GRD were rare in the United States, but the rate of gluten-related disorders has greatly increased since then. It is now estimated that GRD affect close to 10% of the population (Sapone et al., 2012).
There are five kinds of gluten-related disorders recognized by the medical community. Each disorder presents with unique pathophysiology and etiology. Celiac disease, dermatitis herpetiformis, and gluten ataxia are autoimmune conditions; wheat allergy is an allergic disease (Taraghikhah et al., 2020), and non-celiac gluten sensitivity is a non-autoimmune-allergic disease (Sharma et al, 2020).
Celiac Disease and Gluten
Celiac disease (CD) is a chronic, auto-immune condition that affects genetically predisposed individuals. It is thought that genetically predisposed individuals develop an immune response to unknown environmental factors which is then triggered by the ingestion of gluten (Lebwohl et al., 2018). CD can cause atrophy of the small intestinal villi, which leads to malabsorption, diarrhea, and failure to thrive. But manifestations of CD can also be minimal, like negligible mucosal lesions, or it can have an asymptomatic presentation, which often causes delayed diagnosis. Celiac disease can also present with extraintestinal manifestations ranging from neurologic disorders, psychiatric disorders, infertility, recurrent miscarriages, osteoporosis and osteopenia, arthritis, aphthous stomatitis (a disease my mother suffers from), dental enamel hypoplasia, and elevations in transaminases (Barker & Liu, 2008).
Dermatitis Herpetiformis and Gluten
Dermatitis Herpetiformis (DH), also known as Duhring-Brocq disease, is an auto-immune condition that affects the skin and causes chronic blistering and lesions. The lesions and blisters generally cover the areas of the scalp, knees, elbows, ankles, and buttocks, producing intense burning and itching. The skin of people affected by DH presents with the same protein IgA1 with J chain and secretory component found in the small intestinal mucosa in adult celiac disease, suggesting a strong correlation between the two conditions (Cohen et al., 1997). For this reason, DH is also called the “celiac disease of the skin”, and the European Society for Pediatric Gastroenterology, Hepatology and Nutrition now states that a dermatitis herpetiformis diagnosis confirms the celiac disease diagnosis without the need for intestinal biopsy. People affected by DH can suffer from various degrees of gastrointestinal issues that vary from milk lesions of the mucosal lining of the small intestine to villous atrophy (Mendez et al., 2013).
Gluten Ataxia as an Autoimmune
Gluten ataxia (GA) is an autoimmune disease triggered by the ingestion of gluten that affects primarily the cerebellum, the part of the brain responsible for coordination and movement. The cerebellum is also responsible for balance, eye movement, and the kind of motor learning abilities involved in learning movements that require practice and fine-tuning, for example, riding a bike or playing an instrument (Leopold, 2018). In GA, the immune system creates antibodies that attack and destroy the Purkinje cells, causing problems with vision and fine motor skills, gait abnormalities, and balance issues. It can also cause peripheral neuropathy, also known as gluten neuropathy (Hadjivassiliou et al., 2004). The damage to the Purkinje cells is irreversible, and studies involving brain MRIs show that up to 60% of subjects affected by GA suffer from permanent shrinkage of the cerebellum (Sapone et al., 2012).
Wheat Allergies and Gluten
Wheat allergy (WA) is an allergic reaction to gluten in which the immune system produces immunoglobulin E antibodies in response to wheat proteins. It can present with gastrointestinal symptoms similar to celiac disease, but unlike CD, WA has a fast onset. When inhaled (baker’s asthma), WA can cause asthma and rhinitis. When someone affected by WA touches wheat, skin reactions occur. When ingested, wheat causes gastrointestinal pain, diarrhea, malabsorption, and, if untreated, it can lead to failure to thrive. WA can also cause anaphylactic shock, but it does not cause villi atrophy (Elli et al., 2015).
Gluten Sensitivity
Non-celiac gluten sensitivity (NCGS) is a non-autoimmune-allergic disease that presents with gastrointestinal and/or extraintestinal symptoms similar to the ones seen in CD (altered bowel habits, skin rashes, bone pain, headaches, fatigue, and depression). Laboratory testing shows no serum antibodies, and intestinal biopsies do not show villous atrophy. This lack of biomarkers makes NCGS difficult to diagnose, and it also can lead to misdiagnosis. NCGS can be misdiagnosed as IBS, and oftentimes only a strict elimination diet allows for a conclusive diagnosis (Biesiekierski et al., 2011). Molina-Infante et al. (2014) estimate that the prevalence of NCGS is 6 to 10 times higher than CD and WA and that it is more prevalent in family members of CD sufferers.
References
Barker, J. M., & Liu, E. (2008). Celiac disease: pathophysiology, clinical manifestations, and associated autoimmune conditions. Advances in pediatrics, 55, 349–365. https://doi.org/10.1016/j.yapd.2008.07.001
Biesiekierski, J. R., Newnham, E. D., Irving, P. M., Barrett, J. S., Haines, M., Doecke, J. D., Shepherd, S. J., Muir, J. G., & Gibson, P. R. (2011). Gluten causes gastrointestinal symptoms in subjects without celiac disease: a double-blind randomized placebo-controlled trial. The American journal of gastroenterology, 106(3), 508–515. https://doi.org/10.1038/ajg.2010.487
Cohen LM, Skopicki DK, Harrist TJ, Clark WHJ. Elder D, Elenitsas R, Jarsorsky C, Johnson BJ. Lever’s Histopathology of the Skin. 8. Raven: Lippincott; 1997. Noninfectious Vesiculobullous and Vesiculopustular Diseases; pp. 209–252.
Elli, L., Branchi, F., Tomba, C., Villalta, D., Norsa, L., Ferretti, F., Roncoroni, L., & Bardella, M. T. (2015). Diagnosis of gluten related disorders: Celiac disease, wheat allergy and non-celiac gluten sensitivity. World journal of gastroenterology, 21(23), 7110–7119. https://doi.org/10.3748/wjg.v21.i23.7110
Hadjivassiliou, M., Williamson, C. A., & Woodroofe, N. (2004). The immunology of gluten sensitivity: beyond the gut. Trends in Immunology, 25(11), 578–582. https://doi.org/10.1016/j.it.2004.08.011
Mendes, F. B., Hissa-Elian, A., Abreu, M. A., & Gonçalves, V. S. (2013). Review: dermatitis herpetiformis. Anais brasileiros de dermatologia, 88(4), 594–599. https://doi.org/10.1590/abd1806-4841.20131775
Molina-Infante, J., Santolaria, S., Montoro, M., Esteve, M., & Fernández-Bañares, F. (2014). Sensibilidad al gluten no celiaca: una revisión crítica de la evidencia actual [Non-celiac gluten sensitivity: a critical review of current evidence]. Gastroenterologia y hepatologia, 37(6), 362–371. https://doi.org/10.1016/j.gastrohep.2014.01.005
Sapone, A., Bai, J. C., Ciacci, C., Dolinsek, J., Green, P. H., Hadjivassiliou, M., Kaukinen, K., Rostami, K., Sanders, D. S., 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. https://doi.org/10.1186/1741-7015-10-13
Sharma, N., Bhatia, S., Chunduri, V., Kaur, S., Sharma, S., Kapoor, P., Kumari, A., & Garg, M. (2020). Pathogenesis of Celiac Disease and Other Gluten Related Disorders in Wheat and Strategies for Mitigating Them. Frontiers in Nutrition, 7. https://doi.org/10.3389/fnut.2020.00006
Taraghikhah, N., Ashtari, S., Asri, N., Shahbazkhani, B., Al-Dulaimi, D., Rostami-Nejad, M., Rezaei-Tavirani, M., Razzaghi, M. R., & Zali, M. R. (2020). An updated overview of spectrum of gluten-related disorders: clinical and diagnostic aspects. BMC Gastroenterology, 20(1). https://doi.org/10.1186/s12876-020-01390-0
Carbohydrates are an important macronutrient and a significant source of energy in the diets of multiple populations across the globe.
Carbohydrate intake over the past 75-100 years has varied greatly from region to region, and there is huge disparity in data between developed and developing countries. In the western world carbohydrate processing and consumption has drastically changed during the past 100 years. During this time, there has been an overwhelming increase in chronic disease and diseases of lifestyle.
According to the FAO, in the past century, starch consumption has declined in western countries while it has been steady or increasing in developing countries. In the United States, 42% of energy is provided by low-quality carbohydrates coming from refined grains, sugar (especially high fructose corn syrup), and some starchy vegetables. Unhealthy diet and lack of exercise are the primary causes of obesity, which in our country has gone from 14.5% to 30.9% during 1971-2000.
What Is The History Behind Our Current Cultural Consumption Of Carbohydrates?
But how did we get to this? The answer is in the changes in farming and food processing that have taken place in approximately the past 80 years. We have switched from natural farming, which was based on crop rotation and soil fertilization that depended on the use of crop leftovers and manure to industrial and scientific farming. This change has grossly depleted our land, yielding impoverished crops. The past century has also seen changes in food processing with the advent of the food revolution that followed World War II. And while the food revolution “liberated 1950s housewives”, it has brought about a decrease in quality carbohydrates associated with the rise of many chronic and degenerative disease.
Carbohydrate consumption seems to have increased in the past few years, with bread and breakfast cereals forming a large part of modern western diets. The percentage of carbohydrates consumed is high, but the nutrient content of our diet has gone down due to impoverished soil, modern farming techniques and food processing.
Available data shows that carbohydrate consumption in developing countries contributes to 60-70 percent total energy (Shan et al., 2019). There is increasing evidence that carbohydrate consumption patterns in western countries are also growing, and it is believed that percentages will soon be close to that of developing countries. Despite this trend, many North Americans have an increasingly negative perception of carbohydrates. This is particularly shown by the low carb diets that have been popular in the past few decades, starting with the Atkins Diet. Dr. Atkins published his first book, “Dr. Atkins’ Diet Revolution”, in 1972, and since then, several dietary approached have focused on limiting, or at least controlling, carbohydrate intake: from the Zone diet, to South Beach, to the ketogenic, the primal and the paleo diet.
Childhood Obesity and Consumption Of Carbohydrates
As far as childhood nutrition is concerned, the past 70 years has seen a reduction in caloric intake, but an increase in body weight and childhood obesity. According to the data, there has been a 19% reduction in calorie intake in 50 years for boys, and 29% reduction for girls, but sugar consumption has increased. Fewer overall calories paired with increasing consumption of sugars means that the diet of our children is very low in nutrient-dense food. Food quality in school diets all over the country has also declined over the past 40 years. We should not be surprised to see that iron deficiency is the most common deficiency in our kids. It should not surprise us to learn that nutrient deficiency in our children is rampant and that our country ranks #39 in the world on the “child flourishing index”.
References:
Cassidy, C.M., “Nutrition and Health in Agriculturalists and Hunter-Gatherers,” Nutrtional Anthropology, Jerome, Norge W., Randy F. Kandel and Frettel H. Pelto, editors, Pleasantville, New York, pp. 117-179, (1980).
Food Agricultural Organization (2020). Global trends in production and consumption of carbohydrate foods. Retrieved 27 October 2020, from http://www.fao.org/3/W8079E/w8079e0g.htm.
Shan, Z., Rehm, C. D., Rogers, G., Ruan, M., Wang, D. D., Hu, F. B., … & Bhupathiraju, S. N. (2019). Trends in dietary carbohydrate, protein, and fat intake and diet quality among US adults, 1999-2016. Jama, 322(12), 1178-1187.
Trends in Intake of Energy and Macronutrients — United States, 1971–2000 [Internet]. [cited 2020 Oct 23]. Available from: https://www.cdc.gov/mmwr/preview/mmwrhtml/mm5304a3.htm
30 Interesting Facts About The Green Revolution, A New Age For Agriculture [Internet]. Facts.net. 2020 [cited 2020 Oct 28]. Available from: https://facts.net/science/technology/green-revolution-facts
How Highly Processed Foods Liberated 1950s Housewives [Internet]. National Women’s History Museum. [cited 2020 Oct 28]. Available from: https://www.womenshistory.org/articles/how-highly-processed-foods-liberated-1950s-housewives
Crohn’s disease is genetic chronic inflammatory disorder of the digestive system that affects any part of the digestive tract, with the ileum and proximal colon being affected the most. Crohn’s disease causes gastrointestinal symptoms ranging from diarrhea, blood in the stool, abdominal pain, loss of appetite, weight loss, and malnutrition. Liver disorder can also occur.
In some cases, parts of the digestive tract need removal. This client has had a small bowel resection, and it important to provide nutritional therapy to prevent malnutrition.
The small intestine is the site of absorption of carbohydrates, fats, proteins, calcium, magnesium, trace elements and vitamins. It is also in the small intestine that bile salts are recycled.
Removal of the ileum reduces the absorptive surface area of the small intestine. Bile acids cannot be absorbed. This causes fat maldigestion and malabsorption of fat-soluble vitamins. Bile acids also spill in the colon causing watery diarrhea. The watery diarrhea is usually present in the post-operative period, and oftentimes medications are prescribed to manage the symptoms. The watery diarrhea causes dehydration; therefore, it is important to support electrolyte and fluid balance.
If this patient is not a renal patient, I recommend liberal use of unrefined salt. I cannot stress enough the importance of hydration: this client should drink filtered or spring water, away from meals, as well as nourishing bone broths. He should also reduce caffeine, soda, and alcohol to a minimum, as these beverages are dehydrating as well as irritating to the digestive tract. Should this client also be a renal patient, I would work collaboratively with his renal nurse specialist to find the right sodium and water requirements.
The Importance Of Vitamin B 12 When the Ileum Is Removed
Vitamin B 12 is absorbed in the lower ileum; it is necessary for red blood cell formation, DNA synthesis, and nerve function. Removal of the ileum causes vitamin B12 deficiencies; therefore, it is necessary for this client to start supplementing vitamin B12 immediately. I would recommend vitamin B12 injections, which are more bioavailable as they bypass the digestive tract. It is important to monitor vitamin B 12 levels yearly and adjust supplement dosage accordingly.
Altered anatomy also leads to fat maldigestion and deficiencies of fat-soluble vitamins. Vitamin D is necessary for healthy bones, calcium metabolism and immune system function, and deficiency can cause bone disease and osteoporosis. Supplementation of vitamin D as well as sun therapy are very important. Vitamin K is important for blood clotting and bone structure; deficiency can cause bleeding and bruising. Vitamin K deficiency is rare because the flora of the large intestine manufactures most of the vitamin K our bodies need. Vitamin A deficiency can be present. This fat-soluble vitamin is important for eyesight as well as tissue growth and healing, and deficiencies can cause night blindness and infections. Vitamin A is stored exclusively in the liver, and serum levels may not be a good indicator of body reserves. Ancient Egyptians treated vitamin A deficiency with liver.
What Happens During The Post-Operative Period?
In the immediate post-operative period a low-residue diet is indicated to control diarrhea. In some cases, enteral nutrition is necessary.2
I recommend for this client a nutrient-dense diet, high in protein diet but moderate in fats. Carbohydrates should be easy to digest and void of fibers (no whole grains for now, focus on potatoes without the skin, bananas, white rice). The diet will be low in oxalates and low-residue, as fiber, and especially insoluble fiber, is hard to digest in the post-operative period. Small amounts of well cooked vegetables can be added if tolerated (starting with ½ cup). Raw vegetables need to be avoided at this time. I recommend excluding vegetables that cause intestinal gas and discomfort: onions and garlic, vegetables of the brassica family, and legumes.3
References:
1 Costantini A, Pala MI. Thiamine and fatigue in inflammatory bowel diseases: an open-label pilot study. Journal of Alternative and Complementary Medicine (New York, NY). 2013 Aug;19(8):704–8.
2 Boelens PG, Heesakkers FFBM, Luyer MDP, van Barneveld KWY, de Hingh IHJT, Nieuwenhuijzen GAP, et al. Reduction of Postoperative Ileus by Early Enteral Nutrition in Patients Undergoing Major Rectal Surgery: Prospective, Randomized, Controlled Trial. Annals of Surgery. 2014 Apr;259(4):649–655.
3 Nutrition Guidelines for People With Short Bowel Syndrome | Memorial Sloan Kettering Cancer Center [Internet]. [cited 2020 Oct 10]. Available from: https://www.mskcc.org/cancer-care/patient-education/nutrition-guidelines-patients-short-bowel-syndrome
Celiac disease is an autoimmune gastrointestinal condition that causes a variety of health issues including nutrient malabsorption and deficiencies, changes in bowel habits, anemia, bone diseases, and eczema. It is more prevalent in females, and it usually occurs early in life.
Celiac disease is caused by an immune response to gluten in genetically sensitive individuals. One of the main culprits is gliadin, a protein component of gluten found in wheat, barley, rye, oats, malt, spelt, triticale, semolina, and bulgur.
Celiac disease causes an immune-system mediated damage of the digestive tract. This is carried out mostly by T-cells that become activated when sensitive individuals are exposed to gluten. Ingestion of gluten causes the body to produce antibodies against it; the presence of antibodies causes a mucosal inflammatory response, which triggers the T-cells to come to the site of inflammation and infiltrate the intestinal mucosa. Over time, repetitive exposure to gluten, and consequent autoimmune response, causes intestinal damage. The duodenum is the part of the small intestine that is affected the most. The autoimmune response causes hyperplasia of the crypts of Lieberkuhn, and atrophy of the villi and microvilli. This greatly decreases the absorptive surface area of the lumen, causing the small intestine to lose its ability to absorb nutrients, which leads to a myriad of nutrient deficiencies and symptoms.
How Genetic Make-Up Plays A Role In Determining Who Expresses Celiac Disease
Genetics play a big role in the development of celiac disease. There is a 10-15% chance of suffering from this autoimmune condition if a first degree relative suffers from it; rates are considerably higher in identical twins. People suffering from other autoimmune conditions (Type-1 diabetes, Sjogren’s Syndrome, juvenile chronic arthritis) have increased risk of developing celiac disease. Among other genetic conditions that can increase risk of developing celiac disease are Down’s Syndrome, Turner Syndrome and William Syndrome.
Gastrointestinal symptoms include abdominal pain, diarrhea (chronic or recurrent), weight loss, and malabsorption. Distention, bloating and steatorrhea can also be present. Celiac disease is accompanied in 10-15% of cases by a painful skin condition called dermatitis herpetiformis. Dermatitis herpetiformis, also called celiac rash, causes intense pruritus and painful vesicles and papules, most often on forearms, buttocks, knees, and scalp. Other features of celiac disease include failure to thrive, osteoporosis and metabolic bone disease, anemia, idiopathic peripheral neuropathy, fatigue, headaches, infertility, dental enamel hypoplasia, and stomatitis.
Diagnosis involves testing to serum autoantibodies while the patient is on a gluten-containing diet, and small intestine biopsy that requires 4 to 6 samples. The biopsy looks for increased intraepithelial lymphocytes, villous atrophy, and crypt hyperplasia, all of which must be present to distinguish celiac disease from non-celiac gluten sensitivity.
Treatments For Celiac Disease
Treatment for celiac disease is a strict celiac disease diet: all foods containing gliadin and gluten must be removed and completely avoided. Even traces amounts can be deleterious, and, unfortunately, gluten is hidden in foods, medications, and even non-food stuff, from make-up to stamps, to play dough. People with celiac disease need be careful when eating out, as cross-contamination is unfortunately widespread even in restaurants with gluten free menus.
The good news is that when followed strictly, the diet reduces inflammation to the small intestine and individuals can see improvement of symptoms within 3 months. In the presence of severe nutritional deficiencies and anemia, it is important to supplement with multi vitamins and minerals as well with targeted nutrients. When the digestive system can’t handle vitamin pills, injections may be prescribed. In some cases, steroid medications can be prescribed to keep inflammation under control while the small intestine regenerates. Unfortunately, about 1 in 50 people affected by celiac disease suffer from refractory celiac disease. People affected by refractory disease show no improvement in malabsorption and villi atrophy 6 to 12 months after strict gluten free diet. There is currently no treatment for refractory celiac disease.
References:
Caio G, Volta U, Sapone A, Leffler DA, De Giorgio R, Catassi C, et al. Celiac disease: a comprehensive current review. BMC Medicine. 2019 Jul 23;17(1):142.
Autoimmune Disorders [Internet]. Celiac Disease Foundation. [cited 2020 Oct 7]. Available from: https://celiac.org/about-celiac-disease/related-conditions/autoimmune-disorders/
What Are the Different Types of T Cells? [Internet]. Celiac Kids Connection. 2018 [cited 2020 Oct 7]. Available from: https://www.celiackidsconnection.org/2018/05/06/what-are-the-different-types-of-t-cells/
Reunala T. Dermatitis herpetiformis: coeliac disease of the skin. Annals of Medicine. 1998 Oct;30(5):416–8.
Carbohydrates are an important class of organic molecules found in all organisms. They are synthesized from carbon, oxygen, and hydrogen atoms. They are a source of energy, a form of stored energy, and they can have structural roles.
Monosaccharides, also called sugars, are the simplest form of carbohydrates. They are soluble and sweet tasting. They have between 3 and 6 carbon atoms, and their general formula is (CH2O)n, They are named according to the number of carbon atoms (triose C3H6O3, tetros C4H8O4, pentose C5H10O5, hexose C6H12O6). Glucose, fructose and galactose are all hexoses; while they all have the same chemical formula, they are structurally and chemically different.
Understanding The Importance of Glucose
Glucose is the main source of energy in respiration, and it is the building block for larger carbohydrates. It is a small, soluble monosaccharide that is easily transported in and out of cells through carrier proteins. It is less reactive than other monosaccharides; therefore, its breakdown must be catalyzed by enzymes. There are two forms of glucose: alpha-glucose and ß-glucose, which differ by the position of the hydroxyl group. The presence of either one yields very different polysaccharides.
Monosaccharides are joined together via a condensation reaction to form disaccharides and polysaccharides. During a condensation reaction one oxygen and two hydrogen atoms are removed from monosaccharides forming water. The removal of water bonds the monosaccharides together by a covalent bond known as a glycosidic bond. The names of glycosidic bonds depend on the location of the carbon atoms between which they are formed. For example, a bond formed between carbon 1 and carbon 4 is called a 1,4 glycosidic bond (i.e. maltose). Conversely, disaccharides and polysaccharides can be broken down into monosaccharides through hydrolysis. Being the opposite of condensation, a hydrolysis reaction requires water.
Disaccharides, also called sugars, are sweet-tasting and soluble. Different combinations of monosaccharides will form different disaccharides. For example, two molecules of alpha-glucose form maltose; alpha-glucose and fructose combine to form sucrose; ß-glucose and galactose combine to form lactose. Sucrose is formed by alpha glucose and beta fructose.
The Structure Of Sugar
Polysaccharides are polymers of simple sugars bonded via condensation reactions. Unlike monosaccharides and disaccharides, polysaccharides are not sweet-tasting nor easily soluble; they are not sugars. There is a variety of polysaccharides, depending on which monomers bond together to form the polysaccharide and where the bond takes place. For example: a polymer of alpha-glucose monosaccharides creates amylose. A polymer of ß-glucose gives us cellulose. A 1,4 glycosidic bonding gives us amylose, while a 1,4 and 1,6 glycosidic bonding gives us amylopectin.
Polysaccharides are the main source of stored energy for both plants and animals; they can also have structural roles. They are very compact, allowing storage of a lot of energy in a small space. They are insoluble in water; therefore, they do not affect the osmotic balance of the cell. They are large molecules that do not diffuse in and out of the cells. Finally, they can be easily hydrolyzed in alpha-glucose when energy is needed. Cellulose, chitin, starch, and glycogen are all examples of important polysaccharides.
Cellulose consists in beta glucose units connected via 1,4 glycosidic bonds and is important for the overall structure of plants. Chitin is made of N-acetyl-D-glucosamine polymers and it has a similar structure to cellulose. It is present in some fungi and in the exoskeleton of arthropods providing structure and strength that protect these organisms from the outside world. Starch is made from alpha-glucose, and it is found in photosynthesizing cells in leaves and storage cells in seeds. Glycogen is an important form of energy storage in animals. It is made of alpha-glucose molecules joined together by 1,4 and 1,6 glycosidic bonds. In times of strenuous activities or in between meals enzymes break down some of this glycogen in individual glucose molecules. When in excess, other enzymes add glucose units back to the chain to store them for later use.
This website collects cookies. Please read our Privacy Policy to review the updates about which cookies we use and what information we collect on our site. By continuing to use this site, you are agreeing to our updated privacy policy.
