Vitamin D is a fat-soluble secosteroids. There are two main forms of vitamin D: vitamin D2, also called ergocalciferol, and vitamin D3, also called cholecalciferol. Scientific studies suggest that cholecalciferol is the more effective form of the vitamin. Vitamin D2 is obtained exclusively from the diet and comes mostly from fortified foods and plants like mushrooms grown in UV lights. Vitamin D3 is found in animal foods like oily fish and fish oil, liver, egg yolks and butter. Our skin also manufactures vitamin D3 upon exposure to light.
The Primary Types of Vitamin D and How They Interact With The Body
Specifically, vitamin D3 originates from a compound found in the skin called 7-dihydroxycholesterol when exposed to sunlight, particularly UV-B light. Vitamin D production is complex and involves metabolic processes that take place in the liver and the kidneys. In the liver, vitamin D2 and D3 undergo hydroxylation in the presence of mitochondrial and microsomal hydroxylase producing 25-hydroxyvitamin D (25(OH)D), also referred to as calcidiol. This is further metabolized in the kidneys to produce calcitriol (1,25(OH)2D). To determine the amount of serum vitamin D, one measures 25(OH)D biomarker with a half-life of around 2 to 3 weeks.
Vitamin D plays an important role in bone health, calcium homeostasis and the immune system as well as the cardiovascular and endocrine systems. Vitamin D deficiency is also associated with type-2 diabetes, Alzheimer’s disease, osteoporosis, Parkinson’s disease, and cancer. Recent studies have shown that at least 20 types of cancers are associated with low serum vitamin D.
Vitamin D and The Mammary Glands
A recent review aimed at studying the connection between vitamin D deficiency and breast cancer revealed a correlation between increased breast cancer risk and vitamin D receptor genetic polymorphism (VDR). VDR genes regulate hormone differentiation, milk production, and calcium transport during lactation in the mammary glands. Data from two randomized clinical trials show that women with higher concentrations of vitamin D (>60 ng/ml) had 82% lower incidence rate of breast cancer than women with lower concentrations of vitamin D (<20 ng/ml). A comparison with the healthy controls indicated a significant risk of breast cancer to women with vitamin D levels less than 20ng/ml developed metastases, and 73% died due to the advanced illness.
Reference
Atoum M, Alzoughool F. Vitamin d and breast cancer: latest evidence and future steps. Breast Cancer (Auckl). 2017 Jan;11:117822341774981.
Folate, Vitamin B12, Vitamin B6, Choline
What is the significance of each of your four vitamins? What roles do they play in the body? What bodily systems are affected?
What is the RDA level for each of the vitamins? What is the upper limit for each of the vitamins? What are the signs or symptoms of deficiency and toxicity for each of the vitamins?
Where are these vitamins found in the diet and what may impede availability and absorption? How does the concept of food poverty impact a client’s ability to obtain these vitamins? (For more information on food poverty, click this link Sustain.
Hashimoto thyroiditis is a chronic autoimmune disorder caused by an interaction between genetic factors and environmental triggers. The integrative approach to autoimmune thyroiditis is a multifaceted approach that focuses on diet, lifestyle, and individualized supplementation. The practitioner should also aim at discovering and dealing with the environmental triggers that started the autoantibody attack against the thyroid (Liontiris et al., 2017).
A clinical trial on 34 women showed that a strict gluten-free diet followed for 6 months lowered thyroid antibodies, improved vitamin D levels, and improved the quality of thyroid tissue (Krysiak et al., 2019).
A review published in 2020 in the Annals of Agriculture and Environmental Medicine (AAEM) shows that scientists agree that there are numerous environmental, dietary, and lifestyle factors that exacerbate Hashimoto thyroiditis: including stress, environmental toxins, poor detoxification, gut dysbiosis, leaky gut (Cayres et al., 2021), undernutrition and malnutrition (Ihnatowicz et al., 2020).
Can Inflammation Reduction Help Ease the Symptom’s of Hashimoto’s Disease?
The dietary intervention aims at reducing inflammation and modulating the immune response, and it focuses on a nutrient-dense diet that is gluten and dairy-free. Research shows that consumption of dairy foods negatively interacts with the thyroid medication levothyroxine (Ihnatowicz et al., 2020). Regarding gluten, research shows the negative effects that gliadin has on thyroid antibodies as well as the high prevalence of undiagnosed celiac disease in patients suffering from autoimmune thyroiditis. A study published in 2017 concluded that in patients with Hashimoto’s high levels of anti-tissue transglutaminase and IgA anti-gliadin antibodies are related to antithyroid antibodies. These findings show that dietary intervention in Hashimoto’s patients is crucial in reducing the autoimmune load and preventing the occurrence of celiac disease (Riseh et al., 2017).
Research shows that Hashimoto’s patients share frequent nutrition deficiencies: zinc, selenium, magnesium, potassium, iodine, copper, vitamin A, vitamin C, vitamin D, and B vitamins. Patients suffering from Hashimoto’s also benefit from adequate levels of high-quality protein and omega-3 fatty acids (Ihnatowicz et al., 2020).
Diet and Infflamation Reduction
In my practice, I recommend the paleo autoimmune diet (AIP) to my clients suffering from Hashimoto’s thyroiditis (Abbott et al., 2019). This dietary intervention focuses on nutrient-dense foods; it removes foods that cause inflammation (for example, grains, soy, and peanuts), but it also removes otherwise healthy foods, like tomatoes, that contain compounds known to stimulate the immune system.
Paleo Autoimmune Diet Food List
Grass-fed meals, organic poultry, wild-caught fish, pastured pork, and wild game
Vegetables: all except nightshades
Sweet potatoes
Fruit (limit to 1-2 servings a day to keep fructose consumption to no more than 25gr daily)
Honey and maple syrup in small quantity
Fermented foods: sauerkraut, kombucha, coconut water kefir
Fresh non-seed herbs
Green tea and non-seed herbal teas
Vinegar
Olive, coconut, and avocado oil (plus fats naturally occurring on meat and fish)
Bone broths
Foods not allowed on AIP
Grains
Dairy
Eggs
Nuts
Nightshades
All sugars and non-nutritive sweeteners, except for honey and maple syrup
Processed oils
Alcohol
Coffee
Chocolate
Processed foods
Foods the patient is sensitive or allergic to
Lifestyle Intervention For Hashimoto’s
Smoking is a common risk factor in the development of autoimmune thyroiditis, therefore, smoking cessation is recommended (Köhling et al., 2017). Stress is another common risk factor (Köhling et al., 2017). Stress-management techniques like guided meditation, breathing exercises, yoga, massage, and cognitive-behavioral strategies can help lower stress response (Carlson et al., 2019).
While there are no studies regarding the impact of sleep quality on autoimmune thyroiditis, we know that poor sleep quality negatively influences stress response (Blaxton et al., 2017). For this reason, sleep hygiene is part of my autoimmune thyroiditis recovery program.
In recent years, research has investigated the role of the microbiota in autoimmune disease. H. Pylori and gut dysbiosis have been linked to autoimmune thyroiditis (Köhling et al., 2017). Therefore, a holistic approach to Hashimoto’s must include diagnosis and treatment of gut ecology imbalance.
References
Abbott, R. D., Sadowski, A., & Alt, A. G. (2019). Efficacy of the Autoimmune Protocol Diet as Part of a Multi-disciplinary, Supported Lifestyle Intervention for Hashimoto’s Thyroiditis. Cureus, 11(4), e4556. https://doi.org/10.7759/cureus.4556
Blaxton, J. M., Bergeman, C. S., Whitehead, B. R., Braun, M. E., & Payne, J. D. (2017). Relationships Among Nightly Sleep Quality, Daily Stress, and Daily Affect. The journals of gerontology. Series B, Psychological sciences and social sciences, 72(3), 363–372. https://doi.org/10.1093/geronb/gbv060
Carlson, L. E., Toivonen, K., & Subnis, U. (2019). Integrative Approaches to Stress Management. Cancer journal (Sudbury, Mass.), 25(5), 329–336. https://doi.org/10.1097/PPO.0000000000000395
Cayres, L., de Salis, L., Rodrigues, G., Lengert, A., Biondi, A., Sargentini, L., Brisotti, J. L., Gomes, E., & de Oliveira, G. (2021). Detection of Alterations in the Gut Microbiota and Intestinal Permeability in Patients With Hashimoto Thyroiditis. Frontiers in immunology, 12, 579140. https://doi.org/10.3389/fimmu.2021.579140
Hadizadeh Riseh, S., Abbasalizad Farhang, M., Mobasseri, M., & Asghari Jafarabadi, M. (2017). THE RELATIONSHIP BETWEEN THYROID HORMONES, ANTITHYROID ANTIBODIES, ANTI-TISSUE TRANSGLUTAMINASE AND ANTI-GLIADIN ANTIBODIES IN PATIENTS WITH HASHIMOTO’S THYROIDITIS. Acta endocrinologica (Bucharest, Romania : 2005), 13(2), 174–179. https://doi.org/10.4183/aeb.2017.174
Ihnatowicz, P., Drywień, M., Wątor, P., & Wojsiat, J. (2020). The importance of nutritional factors and dietary management of Hashimoto’s thyroiditis. Annals of agricultural and environmental medicine : AAEM, 27(2), 184–193. https://doi.org/10.26444/aaem/112331
Köhling, H. L., Plummer, S. F., Marchesi, J. R., Davidge, K. S., & Ludgate, M. (2017). The microbiota and autoimmunity: Their role in thyroid autoimmune diseases. Clinical immunology (Orlando, Fla.), 183, 63–74. https://doi.org/10.1016/j.clim.2017.07.001
Krysiak, R., Szkróbka, W., & Okopień, B. (2019). The Effect of Gluten-Free Diet on Thyroid Autoimmunity in Drug-Naïve Women with Hashimoto’s Thyroiditis: A Pilot Study. Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association, 127(7), 417–422. https://doi.org/10.1055/a-0653-7108
Liontiris, M. I., & Mazokopakis, E. E. (2017). A concise review of Hashimoto thyroiditis (HT) and the importance of iodine, selenium, vitamin D and gluten on the autoimmunity and dietary management of HT patients.Points that need more investigation. Hellenic journal of nuclear medicine, 20(1), 51–56. https://doi.org/10.1967/s002449910507
The Integrative Treatment of Thyroid Conditions. (2021). Natural Medicine Journal. https://www.naturalmedicinejournal.com/journal/2017-06/integrative-treatment-thyroid-conditions
The scientific community is still in disagreement as to whether or not obesity is a disease. While some still consider obesity a self-inflicted disease caused by poor eating habits and lack of exercise, there is growing evidence to support the claim that obesity is a disease.
According to Pi-Sunyer (2002), not only is obesity a disease but within the United States it is considered to be a condition of epidemic proportions. Statistics show that, in our country, over 20% of adults are diagnosed as clinically obese (Pi-Sunyer, 2002). The rationale that obesity is a disease is due to the fact that it causes many different comorbidities such as high blood pressure, diabetes, heart disease, etc.
Has Obseity Reached Epidemic Proportions In Western Countries?
I agree with Conway and Rene (2004) who believe that obesity is not only a condition that has reached epidemic proportions, but it is a disabling, multifaceted disease that causes changes in organ function and can come with a host of comorbidities. The excess body weight puts a strain on the heart, leading to changes in anatomical structure and the function of the organ. Obesity has also repercussions on the immune system (de Heredia et al., 2012), endocrine system (Poddar et al., 2017), and pulmonary system (Dixon & Peters, 2018). These repercussions are caused by both mechanical and functional alteration of tissues and organs.
Data Suggests That Obseity Is Associated With Several Very Serious Health Concerns
Research studies show that obesity is associated with an increased risk of developing cancer in at least 13 different organs (Avgerinos et al., 2019). Obesity is also linked to type-2 diabetes (Maggio & Pi-Sunyer, 2003), arthritis (Moroni et al., 2020). At the same time, a systematic review of scientific data that was published in 2017 shows that weight-loss interventions in the obese adult population decrease all-cause mortality (Ma et al., 2017). The same review shows that weight loss has a positive impact on cardiovascular mortality and cancer mortality (Ma et al., 2017).
Lastly, obesity’s status and acceptance as a disease are pivotal in determining its treatment, reimbursement for treatment, and the development of widespread interventions. For these reasons, I believe that obesity should be recognized as a disease.
References
Avgerinos, K. I., Spyrou, N., Mantzoros, C. S., & Dalamaga, M. (2019). Obesity and cancer risk: Emerging biological mechanisms and perspectives. Metabolism: clinical and experimental, 92, 121–135. https://doi.org/10.1016/j.metabol.2018.11.001
de Heredia, F. P., Gómez-Martínez, S., & Marcos, A. (2012). Obesity, inflammation and the immune system. The Proceedings of the Nutrition Society, 71(2), 332–338. https://doi.org/10.1017/S0029665112000092
Ma, C., Avenell, A., Bolland, M., Hudson, J., Stewart, F., Robertson, C., Sharma, P., Fraser, C., & MacLennan, G. (2017). Effects of weight loss interventions for adults who are obese on mortality, cardiovascular disease, and cancer: systematic review and meta-analysis. BMJ (Clinical research ed.), 359, j4849. https://doi.org/10.1136/bmj.j4849
Maggio, C. A., & Pi-Sunyer, F. X. (2003). Obesity and type 2 diabetes. Endocrinology and metabolism clinics of North America, 32(4), 805–viii. https://doi.org/10.1016/s0889-8529(03)00071-9
Moroni, L., Farina, N., & Dagna, L. (2020). Obesity and its role in the management of rheumatoid and psoriatic arthritis. Clinical rheumatology, 39(4), 1039–1047. https://doi.org/10.1007/s10067-020-04963-2
Pi-Sunyer, F. X. (2002). The obesity epidemic: Pathophysiology and consequences of obesity. Obesity Research, 10(S12), 97S-104S. https://doi.org/10.1038/oby.2002.202
Poddar, M., Chetty, Y., & Chetty, V. T. (2017). How does obesity affect the endocrine system? A narrative review. Clinical obesity, 7(3), 136–144. https://doi.org/10.1111/cob.12184
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
Over 2,000 years ago Hippocrates, the father of medicine said: “All disease begins in the gut”. Healthy digestion and a healthy microbiome are fundamental to health. The digestive tract is a long tube that goes from the mouth to the anus. It is composed of several organs and accessory organs that work together to intake, break down and absorb food as well as excrete waste material. Each organ of the digestive tract can be affected by dysfunction from gastroesophageal reflux to H. Pylori infections, leaky gut, malabsorption syndrome, maldigestion, food allergies, celiac disease, irritable bowel syndrome, inflammatory bowel disease, etc. It is important to know that digestive issues are not confined to the affected organ, but that they have repercussions for the entire system. Moreover, digestive dysfunction causes maladies that are not exclusively relegated to the organs of digestion. Research shows that several conditions are caused by or correlated with unhealthy microbiome and digestive dysfunction: obesity, type-2 diabetes (Fan & Pedersen, 2021), connective tissue disease (CTD) (Bizzaro et al., 2003), systemic lupus erythematosus (SLE), Grave’s disease (Shor et al., 2012), just to name a few.
What Laboratory Tests Are Available Today?
There are several laboratory tests available to test gastrointestinal function. Stomach acid can be measured with a Heidelberg capsule (Lord & Bralley, 2012). Pepsin can be tested via a saliva test (Strugala et al., 2015). Fecal and plasma tests can be used to measure pancreatic output of protease and lipase. A fecal fat test can reveal impaired liver or gallbladder function. Stool cultures, DNA stool test, comprehensive stool digestive analysis (CSDA), fecal butyrate testing are tools used to assess colon function (Lord & Bralley, 2012). Colonoscopy, barium enema, magnetic resonance imaging (MRI), computed cosmography scan (CT scan), defecography, ultrasounds and other imaging tests are also available to assess colon health (Digestive Diagnostic Procedures). A hydrogen-methane breath test is used to diagnose small intestinal bacterial overgrowth (SIBO).
Several tests are available to test for food allergies and intolerances: increased levels of IgA can be measured through feces, urine and serum analysis and can reveal the presence of gut inflammation, celiac disease, mucosal infection, food allergies, and other inflammatory conditions (Breedveld & van Egmond, 2019). Serum IgE and IgG levels can be checked to test for food allergies, infections and inflammatory diseases (Mayo Clinic Labs). According to the Genova Diagnostics website, high levels of IgG antibodies can also indicate the presence of leaky gut syndrome.
What Is The Helicobacter Test?
The test I chose for this essay is the Helicobacter Pylori Stool Antigen EIA. The American Gastroenterological Association (AGA) (Talley et al., 2005) and the American College of Gastroenterologists (ACG) (Chey et al., 2007) consider the H. Pylori stool antigen to be superior to the serum testing.
H. Pylori is a bacterium that inhabits the stomach, usually without causing any disease. According to Iisashi et al. (2015) H. Pylori can suppress inflammatory bowel disease (IBD), and it is linked to a reduced incidence of asthma. A study from Talebi Bezmin Abadi (2014) even suggested that an eradication of H. Pylori contributes to an increase of GERD. It is still unknown why, in certain people, H. Pylori colonies wreaks havoc in the stomach, causing stomach ulcers, gastric inflammation, stomach cancer and gastric mucosa-associated lymphoid-tissue lymphoma (Yang it al., 2014). Symptoms associated with H. Pylori infections are burping, bloating, nausea, gastritis presenting with pain and a burning sensation, loss of appetite and weight loss (Mayo clinic, 2017). A patient that presents with these symptoms should be tested for H. Pylori infection. The stool antigen EIA test looks for the present of antigens that reveal the presence of H. Pylori. Certain medications like antibiotics and acid blockers can interfere with the test results; therefore, patients are asked to discontinue the use to these medications for one to two weeks prior to testing.
References
Bizzaro, N., Villalta, D., Tonutti, E., Tampoia, M., Bassetti, D., & Tozzoli, R. (2003). Association of celiac disease with connective tissue diseases and autoimmune diseases of the digestive tract. Autoimmunity reviews, 2(6), 358–363. https://doi.org/10.1016/s1568-9972(03)00055-7
Bravo, D., Hoare, A., Soto, C., Valenzuela, M. A., & Quest, A. F. (2018). Helicobacter pylori in human health and disease: Mechanisms for local gastric and systemic effects. World journal of gastroenterology, 24(28), 3071–3089. https://doi.org/10.3748/wjg.v24.i28.3071
Breedveld, A., & van Egmond, M. (2019). IgA and FcαRI: Pathological Roles and Therapeutic Opportunities. Frontiers in Immunology, 10. https://doi.org/10.3389/fimmu.2019.00553
Chey WD, Wong BC; Practice Parameters Committee of the American College of Gastroenterology. American College of Gastroenterology guideline on the management of Helicobacter pylori infection. Am J Gastroenterol. 2007;102:1808-1825.
Fan, Y., & Pedersen, O. (2021). Gut microbiota in human metabolic health and disease. Nature reviews. Microbiology, 19(1), 55–71. https://doi.org/10.1038/s41579-020-0433-9
Gastrointestinal Test | helicobacter pylori Stool Antigen EIA. (n.d.). Www.gdx.net. Retrieved July 16, 2021, from https://www.gdx.net/product/helicobacter-pylori-stool-antigen-eia-test
IGE – Clinical: Immunoglobulin E (IgE), Serum. (n.d.). Www.mayocliniclabs.com. https://www.mayocliniclabs.com/test-catalog/Clinical+and+Interpretive/8159
Iizasa, H., Ishihara, S., Richardo, T., Kanehiro, Y., & Yoshiyama, H. (2015). Dysbiotic infection in the stomach. World journal of gastroenterology, 21(40), 11450–11457. https://doi.org/10.3748/wjg.v21.i40.11450
Lord, R. and Bralley, J., n.d. Laboratory evaluations for integrative and functional medicine. 2nd ed. (2012), Metametrix institute.
Lu, P. J., Hsu, P. I., Chen, C. H., Hsiao, M., Chang, W. C., Tseng, H. H., Lin, K. H., Chuah, S. K., & Chen, H. C. (2010). Gastric juice acidity in upper gastrointestinal diseases. World journal of gastroenterology, 16(43), 5496–5501. https://doi.org/10.3748/wjg.v16.i43.5496
Mayo Clinic. (2017). Helicobacter pylori (H. pylori) infection – Symptoms and causes. Mayo Clinic; https://www.mayoclinic.org/diseases-conditions/h-pylori/symptoms-causes/syc-20356171
Shor, D. B., Orbach, H., Boaz, M., Altman, A., Anaya, J. M., Bizzaro, N., Tincani, A., Cervera, R., Espinosa, G., Stojanovich, L., Rozman, B., Bombardieri, S., Vita, S. D., Damoiseaux, J., Villalta, D., Tonutti, E., Tozzoli, R., Barzilai, O., Ram, M., Blank, M., … Shoenfeld, Y. (2012). Gastrointestinal-associated autoantibodies in different autoimmune diseases. American journal of clinical and experimental immunology, 1(1), 49–55.
Strugala, V., Woodcock, A. D., Dettmar, P. W., Faruqi, S., & Morice, A. H. (2015). Detection of pepsin in sputum: a rapid and objective measure of airways reflux. European Respiratory Journal, 47(1), 339–341. https://doi.org/10.1183/13993003.00827-2015
Talebi Bezmin Abadi A. (2014). Helicobacter pylori: A Beneficial Gastric Pathogen?. Frontiers in medicine, 1, 26. https://doi.org/10.3389/fmed.2014.00026
Talley NJ; American Gastroenterological Association. American Gastroenterological Association medical position statement: evaluation of dyspepsia. Gastroenterology. 2005;129:1753-1755.
Yang, J. C., Lu, C. W., & Lin, C. J. (2014). Treatment of Helicobacter pylori infection: current status and future concepts. World journal of gastroenterology, 20(18), 5283–5293. https://doi.org/10.3748/wjg.v20.i18.5283
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