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Gluten Sensitivity vs Celiac Disease
Posted on 19 April 2012.

Two Distinct Clinical Entities
Nate Champion, ND

It seems as if more and more individuals are being seen with clinical symptoms associated with adverse reactions to gluten, the structural protein component of wheat, barley, and rye. Often, these patients have already been to see a gastroenterologist, and many have had serologic testing performed for celiac disease (CD), wheat allergy, or both. When the results of their blood work come back negative for antibodies to gluten, these patients are often told that wheat or gluten is not a problem and are offered little other advice. These patients are many times left confused, discouraged, and frustrated without any answers and wonder where to go from here. As NDs, we have known for years that individuals can have problems arising from gluten without having true CD. More recently, our understanding and knowledge of gluten sensitivity (GS) has grown, and research has begun to reveal evidence that GS is a separate clinical entity from CD.1

Wheat Allergy and CD

The 2 best-known illnesses related to gluten exposure are wheat allergy and CD, both of which are mediated by the adaptive immune system, with the reaction to gluten being mediated by T-cell activation in the mucosa of the gastrointestinal tract. However, in wheat allergy the release of chemical mediators (histamine) from mast cells and basophils is triggered by the cross-linking of IgE.2 In contrast, CD is an autoimmune disorder indicated by specific serologic markers, most notably serum tissue transglutaminase autoantibodies. Besides CD and wheat allergy, there are many individuals who experience gluten reactions in which neither autoimmune nor allergic mechanisms are involved, generally defined as GS.3

GS vs CD

Gluten sensitivity affects approximately 10% of the general population and is considered a diagnosis of exclusion in which patients are considered to be “gluten sensitive” after CD, wheat allergy, and other clinically overlapping diseases (inflammatory bowel disease, type 1 diabetes mellitus, and Helicobacter pylori infection) have been ruled out. In addition, symptoms are triggered by gluten exposure and are alleviated by gluten avoidance. In contrast to CD, which affects approximately 1% of the general population, these adverse symptoms that occur while eating gluten are not followed by the appearance of autoantibodies in the blood or by persistent damage to the small intestine. Table 1 lists characteristics of GS vs CD. A 2011 landmark study3 reported for the first time evidence of different responses in the intestinal mucosa to gluten in GS vs CD. This study showed significantly reduced small intestinal permeability in patients having GS compared with those having CD when tested with a lactulose and mannitol double-sugar probe.
Patients with GS do not seem to present with significant autoimmune or allergic comorbidities, and their serologic test results are negative for common autoantibodies, including transglutaminase IgA. In CD, there is a strong genetic association with the class II major histocompatibility complex proteins. About 95% of patients with CD carry the HLA-DQ2 gene, and the remaining 5% carry the HLA-DQ8 gene. Only about 50% of patients with GS carry either HLA-DQ2 or HLA-DQ8 (a percentage only slightly higher than that in the general population). This suggests that the adaptive immune system has a much more limited involvement in patients with GS and may explain why this condition is not accompanied by significant autoimmune phenomena, as in CD.3 This adaptive immune response in CD has been shown to be triggered by tissue transglutaminase deaminated gluten peptides bound to DQ2 or DQ8. This mucosal recruitment and activation of the helper T cell, subtype 1 (TH1) and TH17 clones and their associated cytokines (interferon γ and interleukin [IL] 17A) contribute to the initiation of tissue damage and disruption of barrier function. In addition to IL-17A, IL-6 and IL-21 (both of which promote differentiation of TH17 cells) are expressed at significantly increased levels in the mucosa of patients with CD but not in those with GS.4 Furthermore, other investigations have demonstrated that IL-17A cytokines are expressed at significantly higher levels in the small intestinal mucosa of patients with CD but not in those with GS. The authors of one study state: “We conclude that GS, albeit gluten-induced, is different from CD not only with respect to the genetic makeup and clinical and functional parameters, but also with respect to the nature of the immune response.”5(p75)

Toll-like receptors (TLRs) have a crucial role in the initiation or maintenance of various immune responses in the innate immune system. One study3 compared the expression of various TLRs using fresh intestinal biopsy specimens from patients with GS or CD. Small intestine expression of TLR2 was significantly increased in patients with GS. TLR1 and TLR4 were generally higher, without reaching clinical significance. Results of this study suggest that the innate immune system has a prevalent role in the pathogenesis of GS, whereas in CD it is the adaptive immune system that has the primary role. More studies are needed to confirm these results, but this finding may help explain the clinical and serologic differences in GS vs CD.

Clinical Implications

So what is the clinical relevance of identifying patients with GS vs those with CD? Is it possible that changes in the innate immune system may precede or accompany the progression of CD and other autoimmune conditions? Based on the current research, it may be too soon to tell. However, investigations have demonstrated that the expression of various TLRs is increased in the small intestinal mucosa of patients with CD, which may lend support to this idea.6 The typical lesions found in the intestines of patients with CD are thought to be mediated by both innate and adaptive immune pathways. Based on the landmark study3 already cited, it seems that GS is associated with prevalent activation of an innate immune response.

When possible, I believe that it is essential to differentiate between GS and CD (tolle causam). It is important for many obvious reasons to understand if you are working with an autoimmune disorder like CD because it can lead to other secondary disorders (thyroid disorders, infertility, etc), not to mention the importance from a genetic and family history standpoint. More and more research has been demonstrating the adverse effects that gluten can have on an increasing percentage of the population. These often include your typical gastrointestinal symptoms, such as gas, bloating, abdominal pain, diarrhea, and constipation. However, many other extraintestinal symptoms involving psychiatric and neurologic manifestations can often present as well. Neurologic manifestations of GS with or without enteropathy are also common. These clinical manifestations can vary, but the most common syndromes involve peripheral neuropathy and cerebellar ataxia. Earlier detection of GS could provide remarkable benefits to patients with neurologic manifestations.7 Finally, Table 2 gives an immunologic overview of the innate immune system vs the adaptive immune system.8

Summary New research has enhanced our understanding of GS and CD and has shown them to be 2 distinct entities. More double-blind placebo-controlled studies are necessary to further our understanding of GS and to search for specific biomarkers for a proper diagnosis because there is still much we do not know in this regard. The objectives of this article were to inform the clinician about this new research, to further our understanding of these conditions, and to better equip us in the care of our patients. I believe that this information is valuable to our patients as well because it gives credence to what they often experience but rarely have acknowledged by other medical professionals, especially those in allopathic medicine. As NDs, we already have diagnostic tools and specialized testing that we use to detect gluten sensitivities and are in an excellent position to help this growing population of individuals.

Table 1. Characteristics of Gluten Sensitivity vs Celiac Disease

Abbreviation: IL, interleukin.

Table 2. Immunologic Overview of the Innate Immune System vs the Adaptive Immune Systema

aFrom Mayer G. Immunology Textbook. 7th ed. http://pathmicro.med.sc.edu/ghaffar/innate.htm.8
Nate Champion, ND is a graduate of Southwest College of Naturopathic Medicine & Health Sciences, Tempe, Arizona. He is founder and co-owner of Champion Naturopathic Health, LLC, Minnetonka, Minnesota. Dr Champion has a private practice in Minneapolis, Minnesota, with a special focus in digestive disorders, particularly inflammatory bowel disease. In addition to his practice, he regularly reviews research and writes reports on natural medicine for a private health advisory company. 

For more information, please visit www.championnh.com and www.pih-mpls.com.
 References
1. Jackson JR, Eaton WW, Cascella NG, Fansano A, Kelly DL. Neurologic and psychiatric manifestations of celiac disease and gluten sensitivity [published online ahead of print August 30, 2011]. Psychiatr Q. doi:10.1007/s11126-011-9186-y. Medline:21877216
2. Tanabe S. Analysis of food allergen structures and development of foods for allergic patients. Biosci Biotechnol Biochem. 2008;72:649-659.
3. Sapone A, Lammers KM, Casolaro V, et al. Divergence of gut permeability and mucosal immune gene expression in two gluten-associated conditions: celiac disease and gluten sensitivity. BMC Med. 2011;9:e23. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3065425/?tool=pubmed. Accessed November 17, 2011.
4. Castellanos-Rubio A, Santin I, Irastorza I, et al. TH17 (and TH1) signatures of intestinal biopsies of CD patients in response to gliadin. Autoimmunity. 2009;42:69-73.
5. Sapone A, Lammers KM, Mazzarella G, et al. Differential mucosal IL-17 expression in two gliadin-induced disorders: gluten sensitivity and the autoimmune enteropathy celiac disease. Int Arch Allergy Immunol. 2009;152:75-80.
6. Szebeni B, Veres G, Dezsofi A, et al. Increased mucosal expression of Toll-like receptor (TLR)2 and TLR4 in coeliac disease. J Pediatr Gastroenterol Nutr. 2007;45(2):187-193.
7. Hernandez-Lahoz C, Mauri-Capdevila G, Vega-Villar J, Rodrigo L. Neurological disorders associated with gluten sensitivity. Rev Neurol. 2011;53(5):287-300.
8. Mayer G. Immunology Textbook. 7th ed. http://pathmicro.med.sc.edu/ghaffar/innate.htm. Accessed November 16, 2011.

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Are Diet Soft Drinks Bad for You?

ScienceDaily (Jan. 31, 2012) — A new study finds a potential link between daily consumption of diet soft drinks and the risk of vascular events.

Individuals who drink diet soft drinks on a daily basis may be at increased risk of suffering vascular events such as stroke, heart attack, and vascular death. This is according to a new study by Hannah Gardener and her colleagues from the University of Miami Miller School of Medicine and at Columbia University Medical Center. However, in contrast, they found that regular soft drink consumption and a more moderate intake of diet soft drinks do not appear to be linked to a higher risk of vascular events. The research appears online in the Journal of General Internal Medicine published by Springer.

In the current climate of escalating obesity rates, artificially sweetened soft drinks are marketed as healthier alternatives to sugar-sweetened beverages, due to their lack of calories. However, the long-term health consequences of drinking diet soft drinks remain unclear.

Gardener and team examined the relationship between both diet and regular soft drink consumption and risk of stroke, myocardial infarction (or heart attack), and vascular death. Data were analyzed from 2,564 participants in the NIH-funded Northern Manhattan Study, which was designed to determine stroke incidence, risk factors and prognosis in a multi-ethnic urban population. The researchers looked at how often individuals drank soft drinks -- diet and regular -- and the number of vascular events that occurred over a ten-year period.

They found that those who drank diet soft drinks daily were 43 percent more likely to have suffered a vascular event than those who drank none, after taking into account pre-existing vascular conditions such as metabolic syndrome, diabetes and high blood pressure. Light diet soft drink users, i.e. those who drank between one a month and six a week, and those who chose regular soft drinks were not more likely to suffer vascular events.

Gardener concludes: "Our results suggest a potential association between daily diet soft drink consumption and vascular outcomes. However, the mechanisms by which soft drinks may affect vascular events are unclear. There is a need for further research before any conclusions can be drawn regarding the potential health consequences of diet soft drink consumption."

There are many nutrients that can help to improve overall mood and depressive symptoms. A recent study published by the American Journal of Clinical Nutrition looked at vitamin D intake from foods and supplements in 81,189 postmenopausal women from the Women’s Health Initiative. It found that women with higher amounts of vitamin D in their diet may lower their risk of having depressive symptoms by as much as 20%.   Vitamin D is thought to affect the function of dopamine and norepinephrine neurotransmitters involved in depression. They conclude that “improvement of vitamin D status holds promise for the prevention of depression, the treatment of depression, or both.”

Taking a deeper look at vitamin D, we know that it is a fat-soluble vitamin known as the “sunshine vitamin.”  Our bodies can produce vitamin D when our skin is exposed to ultraviolet sunlight. Vitamin D can also be obtained from our foods and is primarily found in oily fish such as salmon, mackerel, tuna and sardines and other animal sources such as liver, beef, veal, and eggs. Other food options for vitamin D sources include foods that have been fortified with vitamin D such as cereals, yogurt, milk, and orange juice.

Dietary intake of vitamin D may not be enough to maintain a healthy level of vitamin D in the body and therefore regular   supplementation may be needed to support adequate levels. In addition, it is important to have your serum vitamin D levels monitored as vitamin D can accumulate in the liver and fat cells. Groups of people that are more at risk for vitamin D deficiency include breastfed infants, older adults, people with limited sun exposure (such as Minnesotans in the winter), people with dark skin, obese people, gastric bypass patients, and people with medical conditions that cause fat malabsorption, such as those with liver disease, Crohn’s disease, and cystic fibrosis.

There are a variety of effective natural therapies for the treatment of depression and vitamin D may play an essential role. Call Partners in Healing at 763-546-5797 and make an appointment with your Naturopathic Doctor (Dr. Nate or Dr. Nita   Champion) to have your vitamin D levels checked to ensure healthy levels for disease prevention and to optimize the health of your mind, body, and overall mood!

By Nate Champion, ND & Nita Champion, ND

We now know that key areas of the brain show significant changes when people are in states of depression.  The affected brain areas regulate working memory, decision-making, information processing, mood regulation and energy management (i.e., metabolism) in the body. We also know that those brain circuits and brain chemicals are highly sensitive to social interactions. For example, research shows that the same areas of the brain that are active when someone is experiencing intense physical pain are active when a person has been rejected or cut off from a major social relationship.  In other words, our social experiences change the structure of the brain.  In turn, those structural and chemical changes in the brain enable new perceptions, new thoughts and new behaviors to emerge.  At PIH, we offer a variety of mind-body therapies (e.g., psychological therapies,  alternative therapies, and nutrition-based  therapies) through which your brain-behavior  connections can be changed to help put you back in charge of your life.  We also collaborate with medical professionals outside of PIH who are part of your care team. Our primary goal is to help you make positive change “with your brain in mind.”

By Dr. Nate Champion, ND

With Fall’s cooler weather, we often resume our “normal” schedules, such as children heading back to school. This is also a common time where the body’s immune system is “weakened” from all the junk food and toxins we’ve consumed all summer. The end result is often becoming acutely ill and this is one of the more frequent times throughout the year where folks “catch a cold”. This acute illness is actually an innate cleansing process where the body is trying to eliminate toxins, purging them from our body!

The good news is there is much that can be done to help support and strengthen your immune system and in turn, your overall health! Some simple ways this can be achieved is through reducing stress in our lives and staying physically active. This can include a simple walk around the block or participating in a local yoga class. The goal is to just get moving! Getting adequate sleep is also imperative. Sleep deprivation suppresses immune system function and has been linked to many mental and physical health problems.

Another way to help enhance immune function is eliminating harmful, unhealthy, and high sugar foods. These include refined, processed foods (white carbohydrates, pastries, desserts, junk food, fast food, sugary drinks, etc.) that are often stripped of their nutrients and high in both calories and sugar. Sugar suppresses the immune system, promotes insulin resistance, inflammation, and leads to weight gain. Focus on eating whole foods and a more plant-based diet. Whole foods are simply foods that are closest to their natural state and have not been processed and refined. Focus more on 100% whole grains such as quinoa, millet, oats, etc. and limiting your wheat intake, along with eating brightly colored and green leafy vegetables that are high in antioxidants. Try some healthy snacks like blueberries, goji berries, chia seeds, raw nuts and seeds (walnuts, almonds, sunflower seeds, etc.), and baked kale chips.

So as the seasons change, stay healthy by getting adequate sleep, becoming more physically active, and choosing foods that support and enhance health! There are many other effective ways and strategies to enhance our immune function & improve health.  To learn more about putting these ideas to work for you, call our office today @ 763-546-5797 to schedule a consultation with Dr.’s Nate or Nita Champion, our Naturopathic  Doctors. 

Naturopathic Medicine focuses on whole-patient wellness, where   medicines are tailored to each person’s specific needs and where attention is paid to finding underlying causes, rather than chasing symptoms.  They focus on all aspects of family health, from prenatal care through geriatric care.  Their practice emphasizes prevention and effective self-care strategies. Naturopathic doctors cooperate with all branches of medical science, making referrals as indicated and when appropriate. 

 (Brought to you by Deborah Simmons, PhD, LMFT)

I have long wondered how nutrition affects our fertility.  This study from The Journal of Reproductive Medicine lends credence to the notion that our high-carbohydrate diet may well explain why some women suffer from unexplained infertility.  My colleagues at Partners in Healing, Dr. Nate Champion and Dr. Nita Champion, specialize in naturopathic medicine and nutrition.  Contact us at 763-546-5797 or info@pih-mpls.com for a holistic team approach to fertility treatment.

Increased Celiac Disease Prevalence in Women With Unexplained Infertility

ScienceDaily (Aug. 18, 2011) — A recent study demonstrated increased rates of celiac disease in women who present with unexplained infertility.

Published in the May-June 2011 issue of The Journal of Reproductive Medicine, the study evaluated 191 female patients presenting with infertility. Each participant underwent serologic screening for celiac disease as well as routine infertility testing. The 4 patients who had positive serum test results were advised to seek evaluation with a gastroenterologist. All 4 patients were confirmed to have celiac disease. They then underwent nutritional counseling to change over to a gluten-free diet.

Among the 188 patients who completed testing, the prevalence of undiagnosed celiac disease was 2.1%. While this rate was not significantly higher than the expected 1.3%, the diagnosis of celiac disease in women with unexplained infertility was found to be significantly higher at 5.9% (3 of 51 women). Interestingly, all 4 patients found to have celiac disease conceived within a year of diagnosis.

Though the study numbers are small, the findings suggest that, at least for some women with infertility, dietary measures may help bolster fertility. "Diagnosing celiac disease in an infertile woman would be particularly beneficial if the low-cost (and low-risk) therapy of pursuing a gluten-free diet could improve chances for conception," says lead author Janet Choi, MD, a reproductive endocrinologist at the Center for Women's Reproductive Care at Columbia University. Co-author Dr. Peter Green, director of the Celiac Disease Center at Columbia University Medical Center, said that these results should be added to the increasing body of knowledge concerning the impact of undiagnosed celiac disease on women's reproductive health.