There is a great comorbidity of autoimmune thyroid disease and Celiac Disease (CD), which is also an autoimmune disease (against gliadin (from gluten) or transglutaminase (a human enzyme). Basically, proposed mechanisms of comorbidity are that CD causes malabsorption of selenium and iodine, causing HT, that gluten (with or without the diagnosis of CD) causes leaky gut and invading bacterial antigens resemble epitopes on the thyroid such that it is attacked in conjunction with the bacteria (mainly Yersinia) through molecular mimicry, or that one class of antibodies is targeted against both the thyroid and gliadin or transglutaminase.

It is recommended that a gluten free (GF) diet imposed early on in the development of HT such as to change the trajectory of the autoimmune disease into one that is less severe and perhaps deteriorates into hypothyroidism later. In the absence of CD in HT patients implicating a GF diet, they may benefit from preventing the aforementioned leaky gut, which inadvertently creates anti-thyroid antibodies but they also may benefit because they have an undiagnosed gluten intolerance, which is much more common than many realize (see blog post 21), causing unnecessary inflammation and immune system activation that contributes to HT. Gluten sensitivity in the absence of CD is referred to as non-celiac wheat sensitivity. Along these lines, some physicians recommend going dairy-free to minimize such effects and alleviate HT severity. Many people also have a slight intolerance to dairy. Gluten not only causes leaky gut but also has been associated with the upregulation of Toll-like Receptor 2, an innate immune mechanism triggered by lipopolysaccharide that has been noted to play a role in HT. Microbiota may also be affected by gluten, furthering the autoimmune response as the imbalanced microbiome of the gut leads to “transcriptomic, proteinomic and the metabolomics” changes which induce auto-immunity by breaking tolerance to self-antigens (and non-pathogenic gut bacteria antigens).

HT patients who indeed suffer from CD certainly will benefit from a GF diet. CD is known to be causative of many glandular endocrinopathies, not just HT, due to the break in the gut wall barrier. Direct correlation to HT, though, is possibly through the shared embryonic origins of the thyroid and gut, with the thyroid developing from the pharyngeal gut on the 17th day of gestation, explaining the (still in investigation) cross-reaction of HT and CD antibodies. Other, more physical relations are the malabsorption of thyroid regulating vitamins selenium, iodine, iron, vitamin D, and B12. More advanced HT, resulting in hypothyroidism, may mask CD symptoms and also increase chances for gluten reactivity by decreasing diarrhea and weight loss due to lowered levels of circulating thyroid hormone (which regulate homeostatic activities, such as bowel movememnts). In addition, the treatment of HT and hypothyroidism may be quite hindered by the malabsorption characterized by CD, with reduced surface area in the small intestine impeding the absorption of thyroid replacement drugs and supplemental vitamins.

The statistics in support of the comorbidity of CD and HT are consistent, yet the results of a GF diet have not yet concurred.

  • Comorbidity
    • Freeman found that 17% of biopsy-confirmed CD adults to be suffering from autoimmune thyroiditis.
      • Of these comorbid patients, HT was diagnosed first in 13 of the 16 (81%)
    • Merhdad et al found that 2.9% of HT patients also suffer from serologically determined CD.
      • Of these comorbid patients, half suffered from HT and half suffered from non-autoimmune hypothyroidism
    • Larizza et al found that 7.7% of HT patients also suffer from biopsy-confirmed CD.
    • Collin et al found that 4.8% of Finnish HT patients also suffer from CD, compared to a 0.4% natural occurrence rate of CD in the Finnish population.
    • Hakanen et al found that 13.9% of CD patients also suffer from HT, compared to a 2.1% rate of HT in the controls group.
    • Ch’ng et al found that 11-30% of CD patients possess HT antibodies.
    • Kalyoncu and Urganci found that 26-41% of CD patients possess HT antibodies.
    • Hadithi et al found that 21% of CD patients also suffer from HT.
    • Lerner et al’s metaanalysis found that, “The prevalence of [HT] in patients with CD was suggested to be four times higher than that in the general population, though the range is very wide, spanning 1.2–30%. The range for HT in CD is narrower: 1.25–19%.”
    • “In the adult populations with CD the rate of hypothyroidism and/or HT is much higher than that in children, ranging between 12.9 and 30.5%.”

Therefore, as far as comorbidity is concerned, figures for HT found in CD patients range from 11%-41% while figures for CD found in HT patients range from 2.9%-7.7% in the cited studies.

  • Treatment of HT with a GF diet results
    • Sategna Guidetti et al found that a 1 year GF diet reversed 71% of sub-clinical hypothyroidism, while of those suffering from euthyroid autoimmune disease (HT patients who still have a normally functioning thyroid), 25% shifted towards subclinical hyper- or hypo- thyroidism (this is a progression of HT, which most likely would have happened naturally and the study does note that there was poor GF diet compliance among these subjects, and 5.5% of subjects whose thyroid function was normal upon induction of the diet developed thyroid issues by the end of the year.
    • “Cooper et al considered that a gluten-free diet did not prevent development of autoimmune disorders and had little ameliorating effect on their course, apart from an occasional improvement in atopy.” (over-reactive allergic responses i.e. asthma)
    • “Sategna-Guidetti et al, however, noted that a gluten-free diet may reverse the abnormality in those with subclinical hypothyroidism although, like Viljamaa et al,found no correlation between duration of gluten exposure in adult CD and risk of autoimmune disorders.”
    • “Ventura et alfound that… thyroid-related antibodies tended to disappear following a gluten-free diet (14.4% [at diagnosis], 11.1% [at 6 months], 6.6% [at 12 months] and 2.2% [at 12 months] [of patients possessed high titers of] thyroid related antibodies)”
    • “Mainardi et al found no correlation between thyroid antibodies and the introduction of a gluten-free diet.”

Therefore, treatment of HT with a GF diet has been reported, in these cited studies, to be 0%-12.2% successful, though the literature is much more limited than studies concerning the comorbidity of CD and HT.

Ultimately, the research done is not consistent on the true prevalence of CD and HT comorbidity nor the treatment of HT with a GF diet. The quantity and expansiveness of clinical trials must be increased and thereafter meta-analyses will be much more conclusive about such topics. As these endeavors are underway, before anything can be stated with confidence, it seems that a proper recommendation would be for physicians to be cognizant of the possible comorbidities of HT and CD, as to test their patients when proper and for a GF diet to be considered in the case of HT not responsive to medicine or in the case of any HT were the patient feels the low possibility of reward is worth the lifestyle impact that adhering to a strict GF diet may make.

 

https://www.ncbi.nlm.nih.gov/pubmed/11280546

https://valleythyroidinstitute.com/gluten-is-the-first-thing-to-go-with-hashimotos-hypothyroidism-diagnosis/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2111403/

https://www.ncbi.nlm.nih.gov/pubmed/28315909

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3321550/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5422478/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5435852/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3921936/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5064028/

https://universityhealthnews.com/daily/energy/a-hashimotos-diet-can-help-manage-your-autoimmune-disease/

http://gut.bmj.com/content/early/2016/07/21/gutjnl-2016-311964

https://link.springer.com/article/10.1023/A:1012754824553

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2111403/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4350874/

https://www.ncbi.nlm.nih.gov/pubmed/11280546

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