Autoimmune Protocol Diet – the Secret Cure to Hashimoto’s Thyroiditis?

Within the past 5 years the autoimmune protocol diet (AIP, and sometimes referred to as the autoimmune paleo diet) has been hyped as the key to reversing the symptoms of autoimmune disorders, including hypothyroidism from autoimmune thyroiditis (AIT) a.k.a.Hashimoto’s Thyroiditis. The idea behind this diet is that it reduces the role of the intestine and inflammation, making intestinal inflammation a less likely cause of autoimmune symptoms. The AIP diet itself is much like a paleo diet in that it focuses on protein-rich foods. Like a paleo diet, the AIP recommends no grain or milk products and limits the amount of fruits (to limit fructose intake). Where the AIP differs from the paleo diet is that it also eliminates nuts, legumes and seeds.

But you may ask, what is the science? Well, that’s a good question.

The main theory surrounding the AIP diet and reducing HT symptoms is based on the association between celiac disease (CD) and autoimmune thyroiditis (AIT). Both are autoimmune disorders. It seems logical that if someone has auto-antibodies that are attacking one area of the body, they might be prone to have auto-antibodies attacking another area of the body. In fact, one review article cited ten articles that identified populations with AIT that were subsequently screened for CD. The rate of CD in these AIT populations ranged from 2% to 7.8%.1 This is much higher than the estimated general prevalence of CD which is approximately 1 in 133 people (around 0.7%).2

One study may shed light on how a gluten-free diet could help correct a thyroid disorder. An Italian study enrolled 241 adult patients with a new diagnosis of CD, and matched them to 212 control subjects (matched for age, sex, and ethnic origin).3 Investigators then drew thyroid assays (serum TSH, fT3, fT4, thyroid microsome antibodies [TM-Ab] and thyroperoxidase antibodies [TPO-Ab]) to ascertain thyroid function status. In total, 30.3% of the CD patients had a thyroid disorder, compared to 11.3% of controls (p<0.0005). When sex was taken into consideration, this difference was only significant for females (P<0.0005). Of the 73 patients with CD and a thyroid disorder, 31 were found to have hypothyroidism (10 were able to be identified as autoimmune in nature), 3 had hyperthyroidism, and 39 were euthyroid but with AIT detected. In the 24 subjects in the control group with a thyroid disorder, 9 had hypothyroidism (4 were autoimmune in nature), 7 hyperthyroid, and 8 euthyroid but with AIT detected. In a continuation of this study, 128 of the original 241 subjects with CD were instructed to maintain a gluten free diet. The results are highlighted in the table below. The interesting thing about the results is that a gluten-free diet resulted in half of the patients with autoimmune hypothyroidism and about A few things to note about this study as we apply it to all patients with HT. First and foremost, this was a study in patients with celiac disease. This study has not been replicated in a randomized controlled trial in the general population with thyroid disease (although many anecdotal successes exist on the internet). Furthermore, reversion to a euthyroid state was seen in patients with both autoimmune and non-autoimmune thyroiditis. If a gluten-free diet were to decrease autoimmune antibodies, one might expect to see the reversion to a euthyroid state in only the patients with auto-immune hypothyroidism. Finally, it should be noted that the two patients who remained with overt disease were still treated with pharmacotherapy.

 

Thyroid Function Patients Assessed (n) Outcome after Diet Trial (n)
Hypothyroid, autoimmune Overt (1)* Subclinical hypothyroidism (1)
Subclinical (5) Euthyroid (3)
Unchanged (2)
Hypothyroid, non-autoimmune Subclinical (14) Euthyroid (11)

Unchanged (3)

Hyperthyroidism Overt (1)* Subclinical hyperthyroidism (1)
Euthyroid with AIT detected (16) Normalization (3)

Unchanged (9)

Subclinical hypothyroidism (3)

Subclinical hyperthyroidism (1)

Normal (no thyroid disease detected during screen) (91) Non-autoimmune hypothyroidism (2)

Subclinical hyperthyroidism (1)

Euthyroid with AIT detected (2)

Normal (86)

Adapted from Sategna-Guidetti, et al.
*patients with over thyroid disease were also treated with drug therapy

A second study looked at TSH levels in subjects with hypothyroidism (HT) and lactose intolerance.4 The results showed that when these subjects adhered to a strict lactose-free diet, their TSH decreased (from 2.06 ± 1.02 IU/mL to 1.51 ± 1.1 IU/mL in euthyroid subjects and 5.45 ± 0.74 IU/mL to 2.25 ± 1.88 IU/mL in subclinical subjects). It should be noted that this same diet in subjects with HT but without lactose intolerance did not produce a similar decrease in TSH.4 This study was limited in the length of time of the lactose-free intervention was given.

Where should we go from here? We certainly need more randomized controlled trials on how diet can influence thyroid disease. The above mentioned articles were the only ones found with definitive evidence. There is a plethora of information on the internet regarding the AIP for HT, but these are anecdotal, and weak on evidence. Patients interested in an AIP diet for HT should be warned that it is an intense diet and can be difficult and frustrating to keep up with, and those with overt disease should be maintained on pharmacotherapy during their diet trial.

References

  1. Chin CL, Jones K, Kingham JGC. Celiac disease and autoimmune thyroid disease. Clin Med Res. 2007;5:184-92.
  2. Barker JM, Liu E. Celiac disease: pathophysiology, clinical manifestations, and associated autoimmune conditions. Adv Pediatr. 208;55:349-55.
  3. Sategna-Guidetti C, Volta U, Ciacci C, et al. Prevalence of thyroid disorders in untreated adult celiac disease patients and effect of gluten withdrawal: an Italian multicenter study. Am J Castroenterol. 2001;96:751-7.
  4. Asik M, Gunes F, Binnetoglu E, et al. Decrease in TSH levels after lactose restriction in Hashimoto’s thyroiditis patients with lactose intolerance. Endocrine. 2013;46:279-84.
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