Optimize iron for immune resilience
Gluten and Graves’ Disease: Should You Reduce or Avoid?
Gluten and Graves’ disease – key takeaways
- Researchers are interested in how gluten, the gut microbiome, the intestinal lining (“gut barrier”), and the immune system may interact in autoimmune thyroid disease
- Most gluten-free diet studies have focused on Hashimoto’s thyroiditis or mixed autoimmune thyroid disease populations rather than Graves’ disease specifically
- To date, there have been no large Graves’-specific clinical trials testing whether a gluten-free diet can improve outcomes such as TRAb levels, relapse rates, or symptom control
- Much of the current evidence is therefore indirect, emerging, or based on related autoimmune thyroid disease research
- Gluten can trigger immune and inflammatory responses in people with coeliac disease and may also trigger immune reactions in some individuals with NCGS
- Researchers are investigating whether this could contribute to broader immune dysregulation in susceptible individuals.
- Some small studies suggest gluten-free diets may improve certain thyroid markers in autoimmune thyroid disease, although Graves’-specific evidence is limited
- Avoid with coeliac disease, consider reducing with NCGS, and for those without either condition, consider a temporary reduction if persistent gluten-related symptoms occur during active disease.
How can gluten trigger an immune response in Coeliac disease and, in some cases, NCGS?
Gluten contains proteins called gliadins that humans cannot fully digest (Hausch et al., 2002). For this reason, some gluten fragments survive digestion and remain in the gut.
In many people, these leftover fragments do not trigger a harmful immune response. However, in some genetically susceptible people (especially those who carry the HLA-DQ2 or HLA-DQ8 genes), they may stimulate the release of a protein called zonulin, which may temporarily weaken the gut barrier and allow more substances to pass through (Cardoso-Silva et al., 2019). This may allow more gluten fragments to cross the intestinal lining, where they can then interact with the immune system.
This mechanism is best established in coeliac disease, although some researchers believe similar mechanisms may also occur in certain people with non-coeliac gluten sensitivity (NCGS).
In NCGS, some immune and inflammatory reactions may still occur (Sapone et al., 2011), but the severe autoimmune damage to the small intestine seen in coeliac disease is not typically present.
Could eating gluten contribute to the immune dysregulation seen in Graves’ disease?
The evidence suggests a plausible but not yet proven connection. In people with coeliac disease or NCGS, gluten consumption can trigger immune and inflammatory responses that extend beyond the gut (Sapone et al., 2011). Researchers believe these processes could theoretically influence thyroid autoimmunity in susceptible individuals, although direct evidence linking gluten consumption to Graves’ specific immune dysregulation remains limited.
Studies have found higher rates of autoimmune thyroid disease in people with Coeliac disease (Collin et al., 1994), and some researchers believe there may be a “gut-thyroid connection” (Lerner et al., 2017) linking gluten-related inflammation and gut health changes to conditions such as Graves’ disease.
For people with both coeliac disease and Graves’ disease, strict gluten avoidance is essential. Some researchers also believe that reducing or avoiding gluten may help certain individuals with gluten sensitivity and Graves’ disease, although more Graves’-specific research is still needed.
Gluten and Graves’ disease – key research to date
| Name of study | What researchers found |
| Collin et al., 1994 | Coeliac disease more common in people with autoimmune thyroid disease than in those without. Researchers suggest that coeliac disease and autoimmune thyroid diseases (such as Graves’ disease and Hashimoto’s thyroiditis) may sometimes develop together because they share some of the same genes and overlapping immune system pathways. |
| Freeman, 1995 | Higher-than-expected rates of thyroid autoimmune disease in people with coeliac disease (including both Hashimoto’s and Graves’ disease). Suggested possible shared autoimmune pathways. |
| Ch’ng et al., 2005 | Coeliac more common in people with Graves’ than in healthy controls. |
| Hwang et al., 2015 | Symptoms improved for a patient with both Graves’ and coeliac after eating gluten-free. Single case report only. |
| Freeman, 2016 | Thyroid autoimmunity appears more common in people with coeliac disease. Concluded that the evidence for gluten-free diets improving thyroid disease is mixed. |
| Lerner et al., 2017 | Proposed that the gut and thyroid may be connected. Discussed how changes in gut bacteria, gut inflammation, and immune system activation could potentially influence thyroid autoimmunity. Suggested that gluten-related gut inflammation may play a role in autoimmune thyroid disease in susceptible individuals. |
| Kahaly et al., 2018 | Strong evidence of shared genetic susceptibility between coeliac disease and autoimmune endocrine diseases, including Graves’ disease. Gluten-free diets do not consistently reverse thyroid autoimmunity once established. |
| Losurdo et al., 2018 | Autoimmune thyroiditis was relatively common in people with non-coeliac gluten sensitivity (NCGS). Suggests that gluten-related immune activation may occur even outside classic coeliac disease. |
| Sange et al., 2020 | Did not find proof that gluten causes Graves’ disease. Suggested that shared gut and immune system changes may link gluten-related conditions with autoimmune thyroid disease in susceptible individuals. |
| Pobłocki et al., 2021 | Some thyroid markers & thyroid functions improved with a gluten-free diet, but results inconsistent. Study mainly in Hashimoto’s, not Graves’. Evidence not strong enough to recommend a gluten-free diet for all Hashimoto’s patients. |
| Popoviciu et al., 2023 | Highlighted shared immune and genetic pathways across autoimmune diseases. |
| Esfahani et al., 2024 | Reviewed possible ways gluten could influence autoimmune thyroid disease. Discussed microbiome disruption, “leaky gut” (increased intestinal permeability), and immune reactions that may affect thyroid autoimmunity. Concluded evidence is still emerging, and more research is needed, especially in Graves’ disease. |
Research takeaways
There is good evidence that coeliac disease and autoimmune thyroid diseases often occur together. Researchers believe there may be a shared gut–immune–thyroid connection. Proposed mechanisms include:
- gut inflammation
- changes in gut bacteria
- increased intestinal permeability (“leaky gut”)
- shared genetic risk factors
Some studies suggest that NCGS may also be associated with autoimmune thyroid conditions in certain individuals, although this area is still emerging and not fully understood.
Most existing gluten and autoimmune thyroid disease research has focused on Hashimoto’s thyroiditis rather than Graves’ disease.
There is currently no strong proof that gluten directly causes Graves’ disease.
The strongest evidence for gluten removal currently exists in people who have coeliac disease alongside thyroid autoimmunity. There are also no large Graves’-specific clinical trials proving that a gluten-free diet for Graves’ disease improves the condition.
However, researchers view the gut microbiome, the intestinal lining (“gut barrier”), coeliac disease, and possibly NCGS as promising areas for future Graves’ disease research.
Could gut changes in Graves’ disease make some people more sensitive to gluten – even without celiac disease or NCGS?
Researchers believe that the health of the gut may influence how strongly some people react to gluten. Certain gut bacteria may help break down gluten and support gut health(Caminero et al., 2019), while an unhealthy imbalance in gut bacteria (gut dysbiosis) may worsen inflammation and weaken the gut barrier, potentially allowing more inflammatory substances to interact with the immune system.
Researchers have found that Graves’ disease is sometimes associated with lower gut microbiome diversity and altered gut bacterial patterns (dysbiosis)(Yan et al., 2020). Scientists are now investigating whether these gut changes could influence how some individuals respond to gluten.
If a person with Graves’ disease experiences persistent symptoms after eating gluten, a temporary gluten reduction trial may be a reasonable approach while their thyroid levels and gut health stabilise.
Could findings from Hashimoto’s disease suggest a possible gluten link in Graves’ disease?
Yes – biologically, it is plausible. However, it remains hypothetical at this stage.
The key point is that Graves’ disease and Hashimoto’s thyroiditis are both autoimmune thyroid diseases. They share some overlapping immune pathways, genetic risk factors, gut-immune interactions, and inflammatory processes. Because of this, researchers think it is possible that gluten could influence immune activity in some people with Graves’ disease too.
However, there are important differences between the two conditions.
Hashimoto’s mainly involves antibodies such as TPOAb and TgAb that gradually damage the thyroid, while Graves’ disease is driven mainly by TRAb antibodies that overstimulate the thyroid. The immune signalling patterns are therefore not identical.
This means scientists cannot automatically assume that because a gluten-free diet may modestly influence Hashimoto’s-related antibodies in some studies, it would also improve Graves’ disease.
Some studies have also found higher rates of coeliac disease in people with Graves’ disease compared with the general population. This supports the idea that gluten-related immune mechanisms may be relevant in a subset of individuals with Graves’ disease. However, this does not prove that gluten causes Graves’ disease or that a gluten-free diet improves Graves’ disease itself. More large Graves’-specific clinical trials are still needed.
What we know so far
Current evidence does not prove that gluten causes Graves’ disease or that everyone with Graves’ disease should avoid gluten. However, broader dietary and lifestyle strategies in Graves’ disease remain an active area of research. There is evidence that coeliac disease, non-coeliac gluten sensitivity, gut health, and immune activation may play a role in some individuals, although more Graves’-specific research is still needed.
References
Cardoso-Silva, D. et al. (2019) ‘Intestinal Barrier Function in Gluten-Related Disorders’, Nutrients, 11(10), p. 2325. doi:10.3390/nu11102325.
Hausch, F., Shan, L., Santiago, N. A., Gray, G. M., & Khosla, C. (2002). Intestinal digestive resistance of immunodominant gliadin peptides. American Journal of Physiology-Gastrointestinal and Liver Physiology, 283(4), G996–G1003. https://doi.org/10.1152/ajpgi.00136.2002
Sapone, A., Lammers, K.M., Casolaro, V., Cammarota, M., Giuliano, M.T., De Rosa, M., Stefanile, R., Mazzarella, G., Tolone, C., Russo, M.I. and Fasano, A. (2011) ‘Divergence of gut permeability and mucosal immune gene expression in two gluten-associated conditions: celiac disease and gluten sensitivity’, BMC Medicine, 9, p. 23. Available at: https://doi.org/10.1186/1741-7015-9-23.
Collin, P., Reunala, T., Pukkala, E., Laippala, P., Keyriläinen, O. and Pasternack, A. (1994) ‘Coeliac disease-associated disorders and survival’, Gut, 35(9), pp. 1215–1218. Available at: https://doi.org/10.1136/gut.35.9.1215.
Freeman, H.J. (1995) ‘Celiac-associated autoimmune thyroid disease: A study of 16 patients with overt hypothyroidism’, Canadian Journal of Gastroenterology, 9(5), pp. 242–246. Available at: https://doi.org/10.1155/1995/342519.
Ch’ng, C.L., Biswas, M., Benton, A., Jones, M.K. and Kingham, J.G.C. (2005) ‘Prospective screening for coeliac disease in patients with Graves’ hyperthyroidism using anti-gliadin and tissue transglutaminase antibodies’, Clinical Endocrinology, 62(3), pp. 303–306. Available at: https://doi.org/10.1111/j.1365-2265.2005.02214.x
Hwang, I.K., Kim, S.H., Lee, U., Jin, S.W., Rhee, S.Y., Oh, S., Woo, J.T., Kim, S.W., Kim, Y.S. and Chon, S. (2015) ‘Celiac disease in a predisposed subject (HLA-DQ2.5) with coexisting Graves’ disease’, Endocrinology and Metabolism, 30(1), pp. 105–109. Available at: https://doi.org/10.3803/EnM.2015.30.1.105.
Freeman, H.J. (2016) ‘Endocrine manifestations in celiac disease’, World Journal of Gastroenterology, 22(38), pp. 8472–8479. Available at: https://doi.org/10.3748/wjg.v22.i38.8472.
Lerner, A., Jeremias, P. and Matthias, T. (2017) ‘Gut-thyroid axis and celiac disease’, Endocrine Connections, 6(4), pp. R52–R58. Available at: https://doi.org/10.1530/EC-17-0021
Kahaly, G.J., Frommer, L. and Schuppan, D. (2018) ‘Celiac disease and endocrine autoimmunity – the genetic link’, Autoimmunity Reviews, 17(12), pp. 1169–1175. Available at: https://doi.org/10.1016/j.autrev.2018.05.013
Losurdo, G., Principi, M., Iannone, A., Giangaspero, A., Piscitelli, D., Ierardi, E., Di Leo, A. and Barone, M. (2018) ‘Predictivity of autoimmune stigmata for gluten sensitivity in subjects with microscopic enteritis: a retrospective study’, Nutrients, 10(12), p. 2001. Available at: https://doi.org/10.3390/nu10122001
Sange, I., Mohamed, M.F., Aung, S. et al. (2020) ‘Celiac disease and the autoimmune web of endocrinopathies’, Cureus, 12(12), e12383. Available at: https://doi.org/10.7759/cureus.12383
Pobłocki, J., Pańka, T., Szczuko, M., Tęśliński, A. and Syrenicz, A. (2021) ‘Whether a gluten-free diet should be recommended in chronic autoimmune thyroiditis or not?—A 12-month follow-up’, Journal of Clinical Medicine, 10(15), p. 3240. Available at: https://doi.org/10.3390/jcm10153240.
Popoviciu, M.S., Kaka, N., Sethi, Y., Patel, N., Chopra, H. and Cavalu, S. (2023) ‘Type 1 diabetes mellitus and autoimmune diseases: A critical review of the association and the application of personalized medicine’, Journal of Personalized Medicine, 13(3), p. 422. Available at: https://doi.org/10.3390/jpm13030422.
Esfahani, K.S., Asri, N., Rostami-Nejad, M. et al. (2024) ‘The role of gluten in the development of autoimmune thyroid diseases: A narrative review’, Cureus, 16(12), e75691. Available at: https://doi.org/10.7759/cureus.75691.
Yan, H., An, J., Hao, X., Wang, Y., Li, X., Wang, W., Guo, X. and Wang, Z. (2020) ‘Intestinal microbiota changes in Graves’ disease: a prospective clinical study’, Bioscience Reports, 40(9). Available at: https://doi.org/10.1042/BSR20191242.
Caminero, A., Galipeau, H.J., McCarville, J.L., Johnston, C.W., Bernier, S.P., Russell, A.K., Jury, J., Herran, A.R., Casqueiro, J., Tye-Din, J.A., Surette, M.G., Magarvey, N.A. and Verdu, E.F. (2019) ‘Duodenal bacteria from patients with celiac disease and healthy subjects distinctively affect gluten breakdown and immunogenicity’, Gastroenterology, 156(5), pp. 1267–1281. Available at: https://doi.org/10.1053/j.gastro.2018.12.010
FAQ’s
Does gluten cause Graves’ disease?
No strong evidence currently shows that gluten directly causes Graves’ disease. However, researchers are investigating whether gluten-related immune activation, gut inflammation, gut microbiome changes, and intestinal barrier dysfunction (“leaky gut”) could influence autoimmune thyroid disease in some susceptible individuals.
Should everyone with Graves’ disease go gluten-free?
Not necessarily. Large Graves’-specific clinical trials investigating whether a gluten-free diet improves outcomes such as TRAb levels, relapse risk, thyroid function, or symptom control have largely not yet been carried out. A gluten-free diet is essential for people who also have coeliac disease, but routine gluten avoidance for all Graves’ patients is not currently supported by strong clinical evidence.
Is there a link between coeliac disease and Graves’ disease?
Yes. Studies have consistently found that coeliac disease occurs more frequently in people with autoimmune thyroid diseases, including Graves’ disease. Researchers believe this may be due to shared genetic risk factors and overlapping immune system pathways.
What is non-coeliac gluten sensitivity (NCGS)?
NCGS describes a condition where people experience symptoms after eating gluten despite testing negative for coeliac disease. Unlike coeliac disease, NCGS does not usually cause the same autoimmune damage to the small intestine, but some immune and inflammatory reactions may still occur.
Could gluten worsen symptoms in some people with Graves’ disease?
Possibly. Some individuals with Graves’ disease report digestive symptoms, bloating, fatigue, or other reactions after eating gluten. Researchers believe gut inflammation and gut microbiome changes could potentially influence immune activity in susceptible individuals, although this has not yet been conclusively proven in Graves’ disease.
Can a gluten-free diet improve thyroid antibodies in Graves’ disease?
We currently do not have clinical trials specifically investigating whether a gluten-free diet lowers Graves’-specific antibodies such as TRAb. Some small and indirect studies in autoimmune thyroid disease – mainly in Hashimoto’s thyroiditis – have reported improvements in certain thyroid markers or antibodies, but results remain inconsistent and cannot automatically be applied to Graves’ disease.
What is zonulin and why is it discussed in gluten research?
Zonulin is a protein involved in regulating the tight junctions of the intestinal lining. In genetically susceptible people, gluten may stimulate zonulin release, temporarily weakening the gut barrier and allowing more substances to pass through the intestinal lining. This mechanism is well established in coeliac disease and has also been proposed in non-coeliac gluten sensitivity (NCGS), although evidence is less consistent outside coeliac disease.
Could Hashimoto’s research help us understand gluten and Graves’ disease?
Possibly. Graves’ disease and Hashimoto’s thyroiditis are both autoimmune thyroid diseases and share some overlapping immune pathways, genetic risk factors, and gut-immune interactions. However, the immune mechanisms are not identical, so findings from Hashimoto’s disease cannot automatically be applied to Graves’ disease.
Should people with Graves’ disease get tested for coeliac disease?
It may be worth discussing with a healthcare professional, particularly if digestive symptoms, nutrient deficiencies, chronic bloating, diarrhoea, unexplained weight loss, iron deficiency, or persistent gastrointestinal symptoms are present. Coeliac disease appears to occur more commonly in people with autoimmune thyroid disease compared with the general population.
Is gluten reduction worth trying in Graves’ disease?
For people with coeliac disease, strict gluten avoidance is essential. For those with suspected non-coeliac gluten sensitivity (NCGS), reducing or avoiding gluten may help improve digestive or other symptoms. In people without diagnosed coeliac disease or NCGS, some researchers believe a temporary gluten reduction trial may still be reasonable if persistent gluten-related symptoms occur while Graves’ disease and gut health are stabilising. However, gluten reduction should not replace standard Graves’ disease treatment, and current Graves’-specific evidence remains limited.
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