Background/Objectives: Migraine and Hashimoto’s thyroiditis (HT) are frequently comorbid, implying shared biological pathways. Selenium and myoinositol are involved in migraine pathophysiology, and their supplementation has been shown to improve thyroid function, particularly in individuals with HT. This study aimed to evaluate the impact of combined myoinositol and selenium (MYSE) supplementation on thyroid function and migraine outcomes in patients with migraine and HT. Methods: We conducted a retrospective study on a cohort of 163 adults with migraine comorbid with HT who received a 6-month MYSE supplementation. Thyroid parameters, namely thyrotropin (TSH), free thyroxine (fT4), and free triiodothyronine (fT3), and migraine features, namely monthly migraine days (MMDs), monthly migraine attacks (MMAs), and monthly symptomatic drug use (MSDs), were assessed at baseline and at follow-up. Because Shapiro–Wilk testing showed that all thyroid and migraine outcomes deviated significantly from normality, pre–post comparisons were evaluated with the Wilcoxon signed-rank test, between-group comparisons with the Mann–Whitney U test, and a three-tier non-parametric strategy (Aligned Rank Transform with ART-C contrasts, the Brunner–Langer non-parametric mixed model, and a trimmed-means between-within ANOVA) to analyze time × migraine × gender, adjusted for age and illness duration. Spearman rank correlations with percentile-bootstrap 95% confidence intervals were computed, and both robust MM-regression and rank-based Jaeckel regression were carried out. Another analysis stratified participants by baseline thyroid status: euthyroid vs. subclinical hypothyroidism (SCH). Results: After six months of MYSE supplementation, significant reductions were observed in TSH (median 3.60 → 2.80 mIU/L, Wilcoxon p < 0.001, rank-biserial r = −0.94), MMDs (14 → 11, p < 0.001, r = −0.99), and MSDs (14 → 11, p < 0.001, r = −0.99), while fT4 increased slightly (1.30 → 1.50 ng/dL, p < 0.001) and fT3 remained stable. For MMAs, a small effect was detected by the paired Wilcoxon test (p = 0.002) but the main effect of time did not survive adjustment in any of the three covariate-adjusted mixed models (ART p = 0.079; nparLD p = 0.55; WRS2 p = 0.084). Chronic migraine patients had higher baseline and follow-up headache burden but experienced greater reductions in MMDs. The percentage reduction in TSH was positively correlated with improvement in MMDs (Spearman ρ = 0.45, bootstrap 95% CI 0.31–0.57, p < 0.001) and was the only significant predictor in both robust MM-regression (β = 0.28, p < 0.001) and rank-based regression (β = 0.25, p < 0.001). The TSH–MMD association held within each thyroid-status stratum separately (ρ = 0.42 in euthyroid, ρ = 0.51 in SCH; p < 0.001 for both), indicating an individual-level signal rather than a between-group artefact. Conclusions: MYSE supplementation was associated with improved thyroid parameters and a meaningful reduction in migraine burden among patients with migraine and HT. The association between TSH reduction and headache improvement supports the hypothesis of an endocrine–metabolic contribution to migraine severity and warrants confirmation in prospective controlled trials. It also supports the clinical value of assessing and addressing thyroid function in this population.
Lorenzo et al. (Thu,) studied this question.