Nutritional Therapy For Hashimoto’s

Nutritional Therapy For Hashimoto’s

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. 


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.

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.

Carlson, L. E., Toivonen, K., & Subnis, U. (2019). Integrative Approaches to Stress Management. Cancer journal (Sudbury, Mass.), 25(5), 329–336.

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.

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.

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.

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.

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.

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.

The Integrative Treatment of Thyroid Conditions. (2021). Natural Medicine Journal.

The Four Primary Types Of Gluten Related Disorders

The Four Primary Types Of Gluten Related Disorders

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. 


Barker, J. M., & Liu, E. (2008). Celiac disease: pathophysiology, clinical manifestations, and associated autoimmune conditions. Advances in pediatrics, 55, 349–365.

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.

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.

Hadjivassiliou, M., Williamson, C. A., & Woodroofe, N. (2004). The immunology of gluten sensitivity: beyond the gut. Trends in Immunology, 25(11), 578–582.

Lebwohl, B., Sanders, D. S., & Green, P. (2018). Coeliac disease. Lancet (London, England), 391(10115), 70–81.

Leopold, C. (2018, August 31). Everything you need to know about the cerebellum. Medical News. 

Mendes, F. B., Hissa-Elian, A., Abreu, M. A., & Gonçalves, V. S. (2013). Review: dermatitis herpetiformis. Anais brasileiros de dermatologia, 88(4), 594–599.

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.

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.

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.

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).

This website collects cookies. Please read our Privacy Policy to review the updates about which cookies we use and what information we collect on our site. By continuing to use this site, you are agreeing to our updated privacy policy.