Oxidants are increased and antioxidants decreased in euthyroid HT patients. As a result, the oxidative/antioxidative balance is shifted toward the oxidative side. Moreover, this study reports on a possible significant involvement of AGEs in HT, thus contributing to a better definition of the redox homoeostasis dysregulation in HT.

Background: There is a growing awareness that nutritional habits may influence risk of several inflammatory and immune-mediated disorders, including autoimmune diseases, through various mechanisms. The aim of the present study was to investigate dietary habits and their relationship with redox homeostasis in the setting of thyroid autoimmunity. Materials and Methods: Two hundred subjects (173 females and 27 males; median age, 37 years) were enrolled. None were under any pharmacological treatment. Exclusion criteria were any infectious/inflammatory/ autoimmune comorbidity, kidney failure, diabetes, and cancer. In each subject, serum thyrotropin (TSH), free thyroxine, antithyroid antibodies, and circulating oxidative stress markers were measured. A questionnaire on dietary habits, evaluating the intake frequencies of food groups and adherence to the Mediterranean diet, was submitted to each participant. Results: Among the 200 recruited subjects, 81 (71 females and 10 males) were diagnosed with euthyroid Hashimoto's thyroiditis (HT); the remaining 119 (102 females and 17 males) served as controls. In questionnaires, HT subjects reported higher intake frequencies of animal foods (meat, p = 0.0001; fish, p = 0.0001; dairy products, p = 0.004) compared with controls, who reported higher intake frequencies of plant foods (legumes, p = 0.001; fruits and vegetables, p = 0.030; nuts, p = 0.0005). The number of subjects who preferentially consumed poultry instead of red/processed meat was lower in HT subjects than in controls ( p = 0.0141). In logistic regression analysis, meat consumption was associated with increased odds ratio of developing thyroid autoimmunity, while the Mediterranean diet traits were protective. In HT subjects, serum advanced glycation end products (markers of oxidative stress) were significantly higher ( p = 0.0001) than in controls, while the activity of glutathione peroxidase and thioredoxin reductase, as well as total plasma antioxidant activity, were lower ( p = 0.020, p = 0.023, and p = 0.002, respectively), indicating a condition of oxidative stress. Stepwise regression models demonstrated a significant dependence of oxidative stress parameters on consumption of animal foods, mainly meat. Conclusions: The present study suggests a protective effect of low intake of animal foods toward thyroid autoimmunity and a positive influence of such nutritional patterns on redox balance and potentially on oxidative stress-related disorders.

Vitamin D deficiency and/or reduced function, as per certain polymorphisms of the vitamin D receptor (VDR) gene, have been related to several autoimmune disorders. The present study was aimed to investigate the association of Hashimoto's thyroiditis with vitamin D status and functional polymorphisms (SNPs) of the VDR gene. In this case-control study, 200 euthyroid subjects were enrolled: 100 newly diagnosed HT patients (87 F, 13 M; mean age ± SD 42 ± 15 year) and 100 healthy individuals, matched for age, sex, BMI, and month of blood sampling. Serum 25(OH)D was measured by HPLC. The VDR SNPs BsmI, ApaI, and TaqI, in strong linkage disequilibrium with each other, were detected by restriction fragment length polymorphism-PCR. The prevalence of vitamin D deficiency in HT patients was significantly higher than that in the control group (70 vs 18.2 %; p < 0.0001), and median serum 25(OH)D level was significantly lower in HT patients than controls (median value: 16.2 vs 37.4 ng/ml; p = 0.026). Moreover, there was a significant inverse correlation between serum 25(OH)D and TPOAb concentration (r = -0.669; p = 0.034). Contrarily, the genotype distribution of the studied SNPs was not different in the two groups (BsmI p = 0.783; ApaI p = 0.512; TaqI p = 0.471), as was the allelic frequency [f(B) p = 0.776, f(b) p = 0.887; f(A) p = 0.999, f(a) p = 0.999; f(T) p = 0.617; f(t) p = 0.617]. The present study first investigates newly diagnosed untreated HT and suggests that vitamin D deficiency may contribute to HT development and/or progression, acting as an environmental trigger, while the VDR locus does not appear to be involved in conditioning the genetic susceptibility to the disease, at least in Caucasians.

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