Could A Gluten Intolerance And Other Immune Reactions To Foods Cause Crohn’s Disease?

I have a close relative with Crohn’s disease. This is another autoimmune disease that causes inflammation and damage in the bowel. Upon diagnosis, he was offered a drug to suppress his immune system and help decrease the inflammation. When he asked about diet, the gastroenterologist told him that diet modification would not help him because Crohn’s disease didn’t appear to be related to diet. I was quite surprised by this guidance because, for me, it seemed logical to suspect that Crohn’s disease could be associated with something in the diet. After all, what is the bowel most exposed to? Food!


Luckily, my relative, a professional engineer, was used to questioning new information and agreed that a change in diet may be needed. He went on the specific carbohydrate diet and was off his medication within 5 months. Further investigation revealed that he reacts to corn and corn derivatives (high fructose corn syrup, dextrose, glucose/fructose, citric acid, etc). Corn is in most grocery store products so this was quite a challenge to remove from his diet. As well, he was surprised to learn that corn can be in milk (1%, 2%, and skim, it carries the vitamin D), table salt (to stabilize the iodine) and it can coat fruit such as apples.

He also has an allergy to almonds, broccoli, cauliflower, chocolate, and legumes. Diet modification has helped him to heal himself. If he accidentally consumes corn or the other foods he reacts to, then the symptoms promptly return. Although he tested negative for celiac disease, he has removed gluten from his diet as well. He hasn’t had the other tests for gluten intolerance, but feels better without these grains in his diet. Currently, he is very healthy with no symptoms. With his last follow-up scope, the gastroenterologist was amazed at the healthy appearance of his bowel.

This story highlights the fact that autoimmune reactions in Crohn’s disease may be triggered by something in the diet. I also met another individual with Crohn’s disease who had the same results. As well, I have met many others who have a underlying gluten intolerance. This strengthens the possibility that diet modification may relieve symptoms in individuals with Crohn’s disease.

Theoretically, I suspect that the ingestion of gluten could be the underlying cause. Some studies have shown that gluten is difficult to digest. This is a problem because undigested gluten can increase the permeability of the bowel (leaky gut effect). Researchers suspect that if the conditions are right and the bowel is is a state of dysbiosis, with some inflammation and low levels of beneficial microbiota, then this along with undigested gluten can trigger the the tight intracellular junctions between the intestinal cells (like gates) to open. This increases the risk for a gluten intolerance because the undigested gluten can gain access to the immune system by entering through the gates. The ever patrolling immune system has a high chance of identifying the undigested gluten as an invader since it appears foreign (it should be digested). The result, an immune reaction can occur leading to a gluten intolerance. Gluten intolerance can present as celiac disease, dermatitis herpetiformis and non-celiac gluten intolerance. It is very elusive and can cause a variety of different types of damage in the body. With Crohn’s disease, it could cause enough inflammation in the bowel to increase the risk for an infection (such as H.pylori and other Helicobacteraceae) and this could potentially contribute to the skip lesions found throughout the bowel.

In developed countries, the risk for dybiosis may be higher due to our increased intake of sugar, highly refined carbohydrate processed diets, and increased use of antibiotics in our food supply (with animals) and for curing infections. This could lead to an imbalance between the health promoting intestinal flora and negative intestinal bacteria further promoting a leaky gut effect.

Once a leaky gut occurs, other undigested food molecules can gain access to the immune system as well. This can increase the risk for other food allergies. Like gluten intolerance, food allergies can cause a variety of symptoms throughout the body and this could further impact the negative effects on health.
If this theory proves true, it may explain why different Crohn’s patients who have used diet modification seem to need their own unique diet to feel well. Gluten intolerance may be the underlying cause, but the associated allergies may be different with each patient. The allergies could be IgE, IgA or IgG mediated. The related allergies may be different for each person and this means that each person would need their own individualized therapeutic diet.

As well, nutrients deficiencies may vary and this can affect the type of supplements needed. Underlying infections could contribute to symptoms as well. Testing for parasites, bacterial infections and fungal infections can help rule this out.

I have met many patients with coexisting celiac disease and Crohn’s disease. Some studies have also identified an association as well. Therefore, I believe it is worthwhile to rule out a gluten intolerance by testing for celiac disease, dermatitis herpetiformis and non-celiac gluten intolerance. Further testing for food allergies (IgE, IgA, and IgG mediated) can help to identify other food reactions. An allergist often only tests for IgE mediated allergies and offers an elimination diet. Naturopathic doctors will generally do blood tests for the other types of allergic reactions. Your physician, allergist or naturopathic doctor may recommend a food log along with an elimination diet if needed.

I wonder, if this approach helps people with Crohn’s disease, why couldn’t it help people with other types of inflammatory bowel diseases?

Lectins

Lectin intolerance may be an underlying cause. Some studies have suggested that immune reactions to lectins can cause bowel changes as well. Antibodies to lectins have been found in people with celiac disease further suggesting that the immune system can react to lectins. A paleolithic diet may provide relief to people with this type of reaction.

Problem With Past Studies

Often, past studies looking at the relationship between food allergies and Crohn’s disease only tested for IgE mediated reactions, totally missing the potential for IgG and IgA mediated reactions to foods.

Future Studies

For a future study, I would like to see a large group of Crohn’s patients tested for the presence of a gluten intolerance (IgA and IgG antibody mediated), lectin intolerance, and food allergies (IgA, IgE, and IgG antibody mediated). This may help to further confirm an association between Crohn’s disease and immune reactions to foods.

Extra Note: Aspergillus, a type of fungus often used to process corn could potentially cause skip lesions as well. Perhaps, this is why my relative feels better without corn and corn derivatives in his diet. He may just have an allergy to corn as well.
Please share this information with your medical doctor, allergist and naturopathic doctor and get advise before making any changes. 

I am dedicating this post to my grandmother, Alma, who died from complications associated with Crohn’s disease when I was in my early teens. Her daughter (my mother), my daughter and I all have celiac disease.

References

1. Curtis WD, Schuman BM, Griffin JW Jr. Association of gluten-sensitive enteropathy and Crohn’s colitis. Am J Gastroenterol. 1992 Nov;87(11):1634-7.
2. Karoui S, Boubaker J, Hamzaoui S, Ben Yaghlene L, Filali A. Association of asymptomatic celiac disease and Crohn’s disease. Ann Med Interne (Paris). 2000 Sep;151(5):411-2.
3. Cheikh I, Maamouri N, Chouaib S, Chaabouni H, Ouerghi H, Ben Ammar A. Association of celiac disease and Crohn’s disease. A case report. Tunis Med. 2003 Dec;81(12):969-71.
4. Malmusi M, Manca V, Girolomoni G. J Am Acad Dermatol. Coexistence of dermatitis herpetiformis, gluten-sensitive enteropathy, and ulcerative colitis. 1994 Dec;31(6):1050-1.
5. Schedel J, Rockmann F, Bongartz T, Woenckhaus M, Schölmerich J, Kullmann F. Association of Crohn’s disease and latent celiac disease: a case report and review of the literature. Int J Colorectal Dis. 2005 Jul;20(4):376-80.
6. Koninckx CR, Giliams JP, Polanco I, Peña AS. IgA antigliadin antibodies in celiac and inflammatory bowel disease. J Pediatr Gastroenterol Nutr. 1984 Nov;3(5):676-82.
7. Rajendran N, Kumar D. Role of diet in the management of inflammatory bowel disease. World J Gastroenterol. 2010 Mar 28;16(12):1442-8.
8. Rijnierse A, Redegeld FA, Blokhuis BR, Van der Heijden MW, Te Velde AA, Pronk I, Hommes DW, Nijkamp FP, Koster AS, Kraneveld AD. Ig-free light chains play a crucial role in murine mast cell-dependent colitis and are associated with human inflammatory bowel diseases. J Immunol. 2010 Jul 1;185(1):653-9. Epub 2010 May 26.
9. Brown AC, Roy M. Does evidence exist to include dietary therapy in the treatment of Crohn’s disease? Expert Rev Gastroenterol Hepatol. 2010 Apr;4(2):191-215.
10. Freeman HJ. Celiac disease (gluten-sensitive enteropathy). Minerva Gastroenterol Dietol. 2010 Jun;56(2):245-9.
11. Triggs CM, Munday K, Hu R, Fraser AG, Gearry RB, Barclay ML, Ferguson LR. Dietary factors in chronic inflammation: food tolerances and intolerances of a New Zealand Caucasian Crohn’s disease population. Mutat Res. 2010 Aug 7;690(1-2):123-38. Epub 2010 Feb 6.
12. LM Solid, J Kolberg, H Scott, J Ek, O Fausa, P Brandtzaeg. Antibodies to wheat germ agglutinin in coeliac disease. Clin Exp Immunol. 1986 January; 63(1): 95–100.
13. K. Fälth-Magnusson, K.-E. Magnusson . Elevated levels of serum antibodies to the lectin wheat germ agglutinin in celiac children lend support to the gluten-lectin theory of celiac disease. Pediatric Allergy and Immunology. Volume 6, Issue 2, pages 98–102, May 1995.
14. Ceri H, Falkenberg-Anderson K, Fang R, Costerton JW, howard R and Barnwell JG. Bacteria-lectin interactions in phytohemagglutinin-induced bacterial overgrowth of the small intestine. Canadian Journal Of Microbiology 34, 1003-8, 1988.
15. JH Ovelgonne, JFJG Koninkxa, A Pusztaib, S bardoczb, W Koka, SWB Ewenc, HGCJM Hendriksa, JE van Dijka. Decreased levels of heat shock proteins in gut epithelial cells after exposure to plant lectins. Gut. 2000 May;46(5):679-87.
16. Lammers KM, Lu R, Brownley J, et al (July 2008). "Gliadin induces an increase in intestinal permeability and zonulin release by binding to the chemokine receptor CXCR3". Gastroenterology 135 (1): 194–204
17. Hausch F, Shan L, Santiago NA, Gray GM, Khosla C. Intestinal digestive resistance of immunodominant gliadin peptides. Am J Physiol Gastrointest Liver Physiol. 2002;283(4):G996–G1003.
18. Shan L, Qiao SW, Arentz-Hansen H, et al (2005). Identification and Analysis of Multivalent Proteolytically Resistant Peptides from Gluten: Implications for Celiac Sprue. J. Proteome Res. 4 (5): 1732–41.
19. Bodinier M, Legoux MA, Pineau F, et al. (May 2007). "Intestinal translocation capabilities of wheat allergens using the Caco-2 cell line". J. Agric. Food Chem. 55 (11): 4576–83.
20. Kaakoush NO, Holmes J, Octavia S, Man SM, Zhang L, Castaño-Rodríguez N, Day AS, Leach ST, Lemberg DA, Dutt S, Stormon M, O’Loughlin EV, Magoffin A, Mitchell H. Detection of Helicobacteraceae in intestinal biopsies of children with Crohn’s disease. Helicobacter. 2010 Dec;15(6):549-57. doi: 10.1111/j.1523-5378.2010.00792.x.
21. Man SM, Zhang L, Day AS, Leach S, Mitchell H. Detection of enterohepatic and gastric helicobacter species in fecal specimens of children with Crohn’s disease. Helicobacter. 2008 Aug;13(4):234-8.

Thank You, Erin Smith, For Reviewing My Book, “Gluten Toxicity”

January 13, 2011 · Filed Under Uncategorized 

Erin Smith, from New York City (USA), increases awareness and provides support to people with celiac disease at her informative blog,  “Gluten-Free Fun”.  On her blog, she discusses gluten-free food, restaurants, gluten-free recipes and many other celiac disease and gluten-free topics.  Today, Erin posted a book review about my new book, “Gluten Toxicity: The Mysterious Symptoms Of Celiac Disease, Dermatitis Herpetiformis And Non-Celiac Gluten Intolerance". It was a wonderful review and includes her opinion about “Gluten Toxicity”. Thank you very much Erin for your interest in my book and for posting a review on your blog. I appreciate your support!

The review can be found at http://glutenfreefun.blogspot.com/2011/01/new-e-book-gluten-toxicity.html

Erin also runs the “NYC Celiac Meet-Up Group”.

Part 5 Of 5 Part Series: Some Final Thoughts About Gluten And Scoliosis

January 11, 2011 · Filed Under Scoliosis 

This is the fifth part in a 5 part series that discusses how gluten could be one of the underlying triggers for scoliosis. In the first post, I discussed whether an association between gluten and scoliosis could exist, described scoliosis, and I provided an outline for the series. In the second post, I discussed how gluten may trigger antibodies against transglutaminases (involved in bone health), antibodies against bone cells, nutrient deficiencies, low melatonin levels, arthritis and how this may lead to scoliosis. In the third post, I discussed how a gluten intolerance may cause scoliosis in various age groups and the fourth post described how lectins may contribute to scoliosis. Today, I would like to share some final thoughts about the link between gluten and scoliosis.


Scoliosis can be disabling and can lead to many complications. Some have to undergo corrective surgery which may have associated risks as well. This can negatively impact self esteem (especially with older children and teenagers), mobility, choice of sports, daily activities, and can affect their overall quality of life, especially in severe cases. If the underlying culprit is gluten or lectins, then a gluten-free or paleolithic diet may be the perfect primary prevention. Many years of suffering could be avoided.

Hopefully, future tests will offer blood tests for IgA and IgG antibodies against tissue transglutaminase 2 and factor XIIIA for all patients with scoliosis. As well, antibodies against various forms of lectins may become widely available at some point and can help to clarify whether a lectin intolerance is present. For now, people who have scoliosis may want to consider testing for celiac disease, dermatitis herpetiformis (with skin symptoms) and non-celiac gluten intolerance. As well, a paleolithic diet could be considered.

I hope this series helps to increase awareness about this association. Over the last six years, many people have asked me whether I think there could be a connection. I believe that a gluten and lectin intolerance could lead to the development of scoliosis. Increased awareness, early diagnosis, and the implementation of a nutrient rich gluten-free or paleolithic diet could be the perfect primary prevention. Unfortunately, it may not correct the damage that has already occurred, but it may offer a drug-free and surgery-free approach to prevent further damage or as a primary prevention technique.

Part 4 of 5 Part Series: How Could A Lectin Intolerance Cause Scoliosis

This is the third part in a 5 part series that discusses how gluten could be one of the underlying triggers for scoliosis. In the first post, I discussed whether an association between gluten and scoliosis could exist, described scoliosis, and I provided an outline for the series. In the second post, I discussed how gluten may trigger antibodies against transglutaminases (involved in bone health), antibodies against bone cells, nutrient deficiencies, low melatonin levels, arthritis and how this may lead to scoliosis. In the third post, I discussed how a gluten intolerance may cause scoliosis in various age groups. Today, I would like to discuss how a lectin intolerance may contribute to scoliosis.

What Are Lectins?

Lectins are glycoproteins that are present in grains (even gluten-free grains) and some other foods such as legumes, seeds, nightshades (i.e. potatoes, tomatoes, etc) and dairy. Lectins can be a problem if increased bowel permeability (leaky gut) occurs and the lectins encounter the immune system or the circulation. Due to gluten and lectin’s combined effect on bowel permeability, this seems likely. Like gluten, lectins are difficult to digest and undigested lectins may cause inflammation, increase bowel permeability, and may stimulate immune responses. If immune-related reactions to lectins occur, this could lead to impaired bone health. The bone damage along with the anti-nutritive effects could contribute to scoliosis symptoms.
IgA and IgG antibodies against wheat germ agglutinin (WGA), a type of lectin, have been found in patients with celiac disease demonstrating that our immune system can react to these glycoproteins. The fact that these antibodies don’t react to gluten, only WGA, further demonstrates that they are specifically reacting to lectins. This suggests that immune reactions to lectins can occur with a gluten intolerance. After reviewing many studies, I’m suspecting that reactions to lectins can occur in isolation without the presence of a gluten intolerance as well.

How Could Lectins Cause Scoliosis?

Lectins Increase The Risk For Gluten Intolerance

Lectins may increase the risk for a gluten intolerance due to the effects on bowel permeability. Research (animal and human) suggests that lectins may increase inflammation, can increase bowel permeability, and may stimulate immune responses, possibly leading to a lectin intolerance. Unfortunately, the leaky gut effect could also increase the risk for an immune reaction to gluten since the gluten would be able to enter the body’s circulatory system through he permeable bowel and freely interact with the immune system. This could increase the risk for a gluten intolerance.
As discussed in the previous posts, a gluten intolerance can significantly increase the risk for scoliosis. A gluten intolerance combined with a lectin intolerance could potentiate the effect.

Lectins May Affect Bone Health

According to studies, lectins may negatively affect the nervous system, the joints, hormonal levels, the cell cycle, and many other parts of the body. As discussed in the previous posts, many of these systems, tissues, and cells support bone health. If damage occurs in any of these areas, then bone health could be hindered and this could, potentially, contribute to scoliosis symptoms.
Lectins  have also been found to have anti-nutritive effects which can affect the availability of nutrients for bone health. Phytates, found in grains and legumes, can also bind with nutrients and this along with the anti-nutritive effects of lectins can hinder absorption of vitamins and minerals that are essential for bone integrity. If the intestinal villi are damaged by immune reactions to lectins or gluten, then the malabsorption of nutrients can be increased. This could lead to the soft bendable bones found in rickets or osteomalacia and the result could be scoliosis.

Could A Paleolithic Diet Help?

A lectin-free/paleolithic diet is recommended for individuals with a lectin intolerance. A paleolithic diet is often referred to as a cave man/woman diet, close to what our ancestors ate when they lived a nomadic lifestyle. The diet eliminates dairy, grains, sugar (except honey), foods from the nightshade family, legumes, mined table salt, and processed refined oils (cold pressed olive oil is okay).
Unfortunately, testing for lectins doesn’t seem to be widely available. Hopefully, testing for IgA and IgG antibodies against wheat germ agglutinin (WGA) and antibodies against other forms of lectins will be widely available in the future. Identifying a lectin intolerance early could prevent complications and could potentially decrease bone related changes.

Books About Lectins And The Paleolithic Diet

1. Loren Cordain. The Paleo Diet: Lose Weight and Get Healthy by Eating the Food You Were Designed to Eat. Wiley (December 20, 2002).
2. Robb Wolf. The Paleo Solution: The Original Human Diet. Victory Belt Publishing, September 14, 2010.
3. Mark Sisson. The Primal Blueprint: Reprogram Your Genes For Effortless Weightloss, Vibrant Health, And Boundless Energy. Primal Nutrition, Inc.; 1ST edition, June 1, 2009.
4. A. Pusztai. Plant Lectins. Cambridge University Press, 1991.

References

1. N. R. Reddy and M. D. Pierson. Reduction in antinutritional and toxic components in plant foods by fermentation. Food Research International, Volume 27, Issue 3, 1994, Pages 281-290.
2. A. Pusztai, S. W. B. Ewen, G. Grant, D. S. Brown, J. C. Stewart, W. J. Peumans, E. J. M. Van Damme and S. Bardocz Antinutritive effects of wheat-germ agglutinin and other N-acetylglucosamine-specific lectins. The British Journal of Nutrition 1993 Jul;70(1):313-21.
3. Borges LF, Sidman RL.Axonal transport of lectins in the peripheral nervous system. Journal Of Neuroscience, 2, pg. 647-53, 1982.
4. A. Pusztai. Plant Lectins. Cambridge University Press, 1991.
5. Tchernychev B, Wilchek M.. Natural human antibodies to dietary lectins. FEBS Lett.1996 Nov 18;397(2-3):139-42.
6. Boldt DH, Banwell JG. Binding of isolectins from red kidney bean (phaseolus vulgaris) to purified rat brush border membranes, Biochimia et Biophysica Acta 843, 230-7, 1985.
7. Hashimoto S, Hagino A. Wheat germ agglutinin, concanavalin A, and lens culinalis agglutinin block the inhibitory effect of nerve growth factor on cell-free phosphorylation of Nsp100 in PC12h cells. Cell Struct and Function 1989 Feb;14(1):87-93.
8. Liu WK, Sze SC, Ho JC, Liu BP, Yu MC. Wheat germ lectin induces G2/M arrest in mouse L929 fibroblasts. J Cell Biochem. 2004 Apr 15;91(6):1159-73
9. JH Ovelgonne, JFJG Koninkxa, A Pusztaib, S bardoczb, W Koka, SWB Ewenc, HGCJM Hendriksa, JE van Dijka. Decreased levels of heat shock proteins in gut epithelial cells after exposure to plant lectins. Gut. 2000 May;46(5):679-87.
10. Gloria V. Guzyeyeva. Lectin Glycosylation As A Marker of Thin Gut inflammation. The FASEB Journal. 2008;22:898.3
11. David L J Freed, Allergist. Do dietary lectins cause disease? The evidence is suggestive—and raises interesting possibilities for treatment. BMJ. 1999 April 17; 318(7190): 1023–1024.
12. LM Solid, J Kolberg, H Scott, J Ek, O Fausa, P Brandtzaeg. Antibodies to wheat germ agglutinin in coeliac disease. Clin Exp Immunol. 1986 January; 63(1): 95–100.
13. K. Fälth-Magnusson, K.-E. Magnusson . Elevated levels of serum antibodies to the lectin wheat germ agglutinin in celiac children lend support to the gluten-lectin theory of celiac disease. Pediatric Allergy and Immunology. Volume 6, Issue 2, pages 98–102, May 1995.
14. Borges LF, Sidman RL.Axonal transport of lectins in the peripheral nervous system. Journal Of Neuroscience, 2, pg. 647-53, 1982.

Part 3 Of 5 part Series: How Could A Gluten Intolerance Cause Scoliosis In Various Age Groups?

This is the third part in a 5 part series that discusses how gluten could be one of the underlying triggers for scoliosis. In the first post, I discussed whether an association between gluten and scoliosis could exist, described scoliosis, and I provided an outline for the series. In the second post, I discussed how gluten may trigger antibodies against transglutaminases (involved in bone health), antibodies against bone cells, nutrient deficiencies, low melatonin levels, arthritis and how this may lead to scoliosis. Today, I would like to discuss how a gluten intolerance may cause scoliosis in various age groups.

I believe that all three forms of gluten intolerance could cause scoliosis and this could affect an individual at any age throughout their lifespan. Theoretically, scoliosis could be caused by celiac disease (CD), dermatitis herpetiformis (DH), and non-celiac gluten intolerance. With all three forms, antibodies against transglutaminases involved in bone health, antibodies against bone cells, and possibly the presence of arthritis might contribute to scoliosis. An additional factor, malabsorption may be a contributing influence with CD and DH as well.

Scoliosis At Birth

With cogenital scoliosis (birth defects to the spine), it reasonable to suspect that autoimmune factors and poor nutritional status in the mother, due to malabsorption issues (associated with undiagnosed CD and DH), could possibly lead to spinal abnormalities during fetal development. A mother with undiagnosed CD may have low levels of calcium, vitamin D, magnesium, phosphorus, and other nutrients necessary for healthy bone development due to malabsorption issues. Many mothers with CD have very little or no symptoms (silent CD), but still experience nutrient deficiencies. Therefore, this could be a hidden cause.

Autoimmune reactions against transglutaminases involved in bone health or against bone cells could also contribute. The antibodies circulating in the mother’s blood may make their way through to the fetus and affect the health of it’s bones.

Scoliosis In Infants And Toddlers

In infantile idiopathic scoliosis, the abnormal spine curvature is diagnosed at age 0-3 years. Apparently, if the curve is below 30 degrees (on the first doctor’s visit), these children have a good chance of it resolving. Why does the curve resolve in some minor cases of scoliosis? Perhaps, this group has less skeletal symptoms, just as some with gluten intolerance have very little symptoms, and the symptoms can come and go. As well, these patients are likely using nutrient supplements once diagnosed. This may help to compensate for malabsorption issues and resolve the minor form of scoliosis. If there was only minor intestinal villi damage with a silent form of CD, then the supplements might be able to compensate for the current malabsorption and mask the underlying problem (damaged villi).

For others, autoimmune activity and malabsorption associated with a gluten intolerance may affect bone integrity and lead to a more severe form of scoliosis. The gluten intolerance symptoms could be vague or atypical and may not be recognized by medical staff. Even when the symptoms are obvious  (I had obvious symptoms for 5 years), the underlying gluten intolerance may not be recognized or diagnosed.

Scoliosis In Children

With juvenile scoliosis, the onset of symptoms is between ages 3-10. The symptoms and damage associated with a gluten intolerance can occur at any age so it is reasonable to suspect that the bone changes could occur later in life. The skeletal effects from malabsorption or autoimmune reactions may not occur until childhood. 

Scoliosis In Adolescence

Adolescent scoliosis occurs between ages 10-18 years. Flexibility is at it’s peak in the teen years so this may increase the risk for scoliosis in this age group. Bone changes associated with a gluten intolerance combined with increased flexibility could significantly increase the risk for scoliosis. A nutrient poor diet (common to eat more processed foods in teenage years) along with malabsorption issues (if CD and DH is involved) may be why the scoliosis symptoms are more prevalent in this age group. The negative effects on bone associated with malabsorption issues might be more prevalent in the adolescent years due to the demand for increased bone growth and nutrients. A poor diet may potentiate the effect.

In this age group, scoliosis tends to be more common in girls. As well, generalized low bone mass, and osteopenia has been found in girls with adolescent idiopathic scoliosis (this is a common finding with CD). There are many hormonal changes occurring at this age and this may be the reason why females have a higher prevalence of scoliosis. Perhaps the difference in hormonal shifts between adolescent boys and girls (i.e. estrogens) helps to account for the gender difference. Estrogens have been suspected of playing a role in the development of scoliosis since estrogen can affect bone remodelling and growth. Theoretically, a gluten intolerance could lead to autoimmune activity and this along with nutrient deficiencies could contribute to hormonal changes, bone changes and scoliosis. This seems likely since many reproductive symptoms have been linked to gluten intolerance and reproductive functions are dependent on nutrients and balanced hormonal levels. A gluten intolerance could affect both of these factors. Females also have a loss of minerals in menses so this could contribute to a higher prevalence as well. A vitamin K deficiency can also occur in CD and may add to the blood loss.

Scoliosis In Adulthood

With a latent or silent gluten intolerance, the symptoms may not be noticeable until adulthood. As well, the symptoms may be atypical and not recognized. This is likely since even the obvious typical symptoms are often missed by physicians and nurses.

Summary

You can see how an underlying gluten intolerance could cause scoliosis and how the symptoms may surface at any age. Gluten intolerance can be quite elusive and this combined with lack of awareness could lead to the bone changes evident with various forms of scoliosis. Since scoliosis can be debilitating, I think it is important to be aware of this possible underlying cause.

Next In The 5 part Series

Part 4 Of 5 Part Series: How Could A Lectin Intolerance Contribute To Scoliosis.
Part 5 Of 5 Part Series: My Thoughts About An Association Between Gluten And Scoliosis

References

1. Scoliosis Research Society http://www.srs.org/
2. Scoliosis Association Inc. http://www.scoliosis-assoc.org/
3. N.A Sims, S Dupont, A Krust, P Clement-Lacroix, D Minet, M Resche-Rigon, M Gaillard-Kelly, R Baron. Deletion of estrogen receptors reveals a regulatory role for estrogen receptors-? in bone remodeling in females but not in males. Bone, Volume 30, Issue 1, Pages 18-25 (January 2002)

Part 2 Of 5 Part Series: How Could A Gluten Intolerance Cause Scoliosis?

This is the second part in a 5 part series that discusses how gluten could be one of the underlying triggers for scoliosis. In the first post, I discussed whether an association between gluten and scoliosis could exist, described scoliosis, and I provided an outline for the series. In this post, I will discuss how antibodies against transglutaminases (involved in bone health), antibodies against bone cells, nutrient deficiencies, low melatonin levels, and arthritis might be underlying contributing factors.
Gluten intolerance can present as celiac disease, dermatitis herpetiformis, and non-celiac gluten intolerance. Since autoimmune activity can exist with all 3 forms, I’m suspecting that bone health could be compromised with all forms of gluten intolerance, not just celiac disease. Autoimmune reactions and cross reactions could lead to inflammation and damage in bone tissue and in other areas of the body that support bone health.

Antibodies Against Transglutaminases

It seems reasonable to suspect that antibodies against specific types of tissue transglutaminases  (enzymes) involved in bone health could be involved in scoliosis. If the tissue transglutaminase involved in bone health became damaged, then the integrity of the bones could be threatened. I’m suspecting that this type of reaction in scoliosis is very likely to occur. With celiac disease, dermatitis herpetiformis, and gluten ataxia (3 forms of gluten intolerance), immune reactions to ingested gluten can lead to cross reactions against our own tissue (i.e. tissue transglutaminase). For example, antibodies cross react against tissue transglutaminase 2 in celiac disease, tissue transglutaminase 3 in dermatitis herpetiformis and tissue transglutaminase 6 in gluten ataxia. With this in mind, why couldn’t a reaction to gluten cause a cross reaction with transglutaminases involved in bone health.
Tissue transglutaminase 2 and FXIIIA (two types of transglutaminases) are found in chondrocytes and osteoblasts which are types of cells involved in bone development and formation. These transglutaminases contribute to osteoblast and chondrocyte differentiation and mineralization of the bone matrix. If antibodies cross reacted with these two enzymes, then the health of the osteoblasts and chondrocytes could be hindered and bone health could suffer. To summarize, these two types of transglutaminases or enzymes (tissue transglutaminase 2 and FXIIIA) are necessary for the development and maintenance of healthy bones. If anything such as antibodies interfered with these two transglutaminases, the integrity of the bones could be compromised. Theoretically, the antibodies involved in gluten intolerance could cross react and damage the transglutaminases involved in bone health.
If this theory proved true, the demineralizing effects associated with this type of immune reaction could eventually lead to soft bendable bones and scoliosis. If transglutaminase isn’t involved, then perhaps autoantibodies are reacting against bone tissue or something else that supports bone health. The autoimmune factors, associated inflammation and malabsorption of nutrients (if celiac disease is present) could start demineralizing sketetal bones in infancy or childhood (rickets) and this can continue into adulthood (osteomalacia). In some, the pathological demineralising effects of gluten intolerance may not be triggered until adulthood.
If affected, the bone structure could become soft, weak, and bendable loosing it’s rigidity. Hypothetically, this could lead to curvature of the spine, as evident in scoliosis. Since muscles support the spine, anything that affects muscle tissue could contribute as well. Gluten intolerance can also affect muscle tone and this weakness could contribute since the spine may not be supported if the muscles are weak. Muscle symptoms (myopathies and muscle hypotonia) may result from immunological reactions affecting the nerves or muscle tissue, a compromised blood supply to the muscles, intramuscular bleeding, and/or nutrient deficiencies.

Malabsorption With Celiac Disease

Celiac disease can lead to poor bone density resulting in rickets, osteomalacia, osteopenia, and osteoporosis. This is a well known and proven association. Autoimmune activity, inflammation and nutrient deficiencies can lead to this undesirable outcome.
With celiac disease, a variety of nutrient deficiencies could result from damaged intestinal villi. In many with undiagnosed CD, the intestinal villi responsible for absorbing nutrients becomes damaged, creating a flattened mucosal surface (villous flattening). Autoimmune reactions to ingested gluten and related prolamines cross-react with intestinal villi and create this damage. Nutrient deficiencies (common in CD) that may contribute to skeletal symptoms include vitamins A, D, E, K, and calcium, magnesium, phosphorus, protein, fatty acids, manganese, molybdenum, copper, boron, flouride, and zinc.

Low Melatonin Levels

In chickens and rats, removal of the pineal gland, led to low melatonin levels and this was associated with scoliosis. Other studies have found that low melatonin might contribute to scoliosis in humans.
With celiac disease, malabsorption of tryptophan (an amino acid) could lead to low serotonin levels (tryptophan can synthesize serotonin) and this could possibly affect melatonin (a neurohormone) since serotonin can convert to melatonin. As well, autoantibodies might affect the pineal gland since antibodies have affected many other organs in the body in undiagnosed gluten intolerance. A damaged pineal gland might lead to low melatonin levels.

Arthritis

Various types of arthritis, such as rheumatoid arthritis, osteoarthritis, polyarthritis, monoarthritis, sarcoilitis, ankylosing spondylitis and psoriatric arthritis, have been associated with gluten intolerance and with food allergies. In arthritis, joint inflammation can lead to destructive tissue damage within and around the joints. Arthritis symptoms can include swelling, pain, stiffness, redness, tenderness, and warmth in the affected areas, loss of function in affected area, and disfigured joint areas. Could a arthritic type reaction in a gluten intolerance contribute to the twisted vertebra that is seen in scoliosis? If this is true, then underlying food allergies (IgA, IgG and IgE mediated) and/or a gluten intolerance could lead to immune reactions that compromise bone and joint health.

Summary

There are likely many factors that contribute to the development of scoliosis. I think it is important to consider gluten intolerance and reactions to other foods as possible contributing factors. If a gluten-free/allergy-free diet provided relief or prevented scoliosis, then much pain, suffering and surgeries could be avoided.

Over the next 2 weeks, I’ll also be posting:
Part 3 Of 5 Part Series: Could Gluten Intolerance Be Involved In All The Various Types Of Scoliosis?
Part 4 Of 5 Part Series: How Could A Lectin Intolerance Contribute To Scoliosis.
Part 5 Of 5 Part Series: My Thoughts About An Association Between Gluten And Scoliosis

References

1. Maria Nurminskaya and Mari T Kaartinen. Transglutaminases in Mineralized Tissues. Frontiers in bioscience. 11, 1591-1606, May 1st 2006.
2. Costantine Albany, MD, Zhanna Servetnyk, MD, PhD. Disabling osteomalacia and myopathy as the only presenting features of celiac disease. A Case report. Department Of Medicine, St. luke’s Roosevelt Hospital Centre, Columbia university, College Of Physicians And Surgeons.
3. Basu RA, et el. Coeliac disease can still present with osteomalacia! Rheumatology (Oxford), 2000. 39(3): pg 335-336.
4. Meyer D, Stavropoulos S, Diamond B, Shane E, Green PHR. Osteoporosis in a north american adult population with celiac disease. Am J Gastroenterol 2001, 96:112-119.
5. Ferretti J, Mazure R, Tanoue P, Marino A, Cointry G, Vasquez H, Niveloni S, Pedreira S, Maurino E, Zanchetta J, Bai JC. Analysis of the structure and strength of bones in celiac disease patients. Am J Gastroenterol 2003;98(2): 382-90.
6. Panush RS. Possible role of food sensitivity in arthritis. Ann Allergy. 1988 Dec; 61(6 Pt 2): 31-5.
7. Carinini C, Brostroff J. Gut and joint disease. Annals of Allergy. 1985;55:624-625.
8. Sadat-Ali M, al-Habdan I, al-Othman A. Adolescent idiopathic scoliosis. Is low melatonin a cause? Joint Bone Spine. 2000 Jan;67(1):62-4.
9. Machida M, Dubousset J, Yamada T, Kimura J. Serum melatonin levels in adolescent idiopathic scoliosis prediction and prevention for curve progression–a prospective study. J Pineal Res. 2009 Apr;46(3):344-8.
8. M Hadjivassiliou, RA Grünwald, GAB Davies-Jones. Gluten Sensitivity As A Neurological Illness. J Neurol Neurosurg Psychiatry 2002:72: 560-563.
9. Sardy M, Karpati S, Merkl B, Paulsson M, Smyth N.Epidermal transglutaminase (TGase 3) is the autoantigen of dermatitis herpetiformis. J Exp Med.Mar 18 2002;195(6):747-57.
10. Hadjivassiliou M, Aeschlimann P, Strigun A, Sanders DS, Woodroofe N, Aeschlimann D. Autoantibodies in gluten ataxia recognize a novel neuronal transglutaminase. Ann Neurol 2008 Sep;64(3):332-43.

Part 1 Of 5 Part Series: Is There An Association Between Scoliosis And A Gluten Intolerance?

Over the past six years, I have talked to many people with celiac disease and scoliosis. This peaked my curiosity. Could the ingestion of gluten trigger a cascade of immune reactions, eventually leading to the development of scoliosis? This is an intriguing question and I believe the connection is likely. With all forms of gluten intolerance, it seems very plausible that autoimmune factors (anti-bone antibodies), inflammation, and malabsorption of nutrients could lead to a soft, bendable bone structure and the development of scoliosis.

Why haven’t doctors  investigated this possible connection? The answer is a sad reality. Many people with a gluten intolerance, including celiac disease (CD), dermatitis herpetiformis (DH) and non-celiac gluten intolerance remain undiagnosed. For example, with CD, over 90% of individuals remain undiagnosed. Likely, it is even higher in non-celiac gluten intolerance since it is more under-recognized by doctors than celiac disease. Unfortunately, many doctors are not very aware of the many elusive symptoms associated with gluten intolerance and as a result, only the symptoms (ie. possibly scoliosis) are diagnosed, not the disease. Typically, it isn’t on the doctor’s radar so it often isn’t investigated as a cause.

What is Scoliosis?

When a spine is viewed from the front or back, it is normally straight. With scoliosis, the spine curves to the right or left in the lumbar or the thoracic area. The vertebra become twisted and the ribs, attached to the vertebra, abnormally protrude. This can lead to thoracic problems and in severe cases breathing problems can occur.


It seems to be more common in adolescence, but it can occur in infancy, childhood, or adulthood. The prevalence of mild scoliosis appears to be fairly equal between boys and girls. However, the more severe forms of scoliosis seem to be more common in girls.
Approx 80-85% of individuals with scoliosis have idiopathic scoliosis which means the cause of the scoliosis is unknown. This type of scoliosis can be hereditary (like CD). Just like gluten intolerance, there doesn’t appear to be a racial or ethnic difference in prevalence.

The Series

Over the next week, I’ll be exploring the possible connection between scoliosis and gluten. Please join in, make comments on the posts and share your stories if you have have experienced this connection or if you have any suggestions that may help others who are wondering whether their scoliosis may be caused by the ingestion of gluten.

The Series Includes:
Part 2 Of 5 Part Series: How Could A Gluten Intolerance Cause Scoliosis 

Part 3 Of 5 Part Series: Could Gluten Intolerance Be Involved In All The Various Types Of Scoliosis? 

Part 4 Of 5 Part Series: How Could A Lectin Intolerance Contribute To Scoliosis.

Part 5 Of 5 Part Series: My Thoughts About An Association Between Gluten And Scoliosis