Abstract
Graves's disease and thyroiditis induce hyperthyroidism, the causes of which remain unclear, although they are involved with genetic and environmental factors. We aimed to evaluate polygenetic variants for hyperthyroidism risk and their interaction with metabolic parameters and nutritional intakes in an urban hospital-based cohort. A genome-wide association study (GWAS) of participants with (cases; n = 842) and without (controls, n = 38,799) hyperthyroidism was used to identify and select genetic variants. In clinical and lifestyle interaction with PRS, 312 participants cured of hyperthyroidism were excluded. Single nucleotide polymorphisms (SNPs) associated with gene-gene interactions were selected by hyperthyroidism generalized multifactor dimensionality reduction. Polygenic risk scores (PRSs) were generated by summing the numbers of selected SNP risk alleles. The best gene-gene interaction model included tumor-necrosis factor (TNF)_rs1800610, mucin 22 (MUC22)_rs1304322089, tribbles pseudokinase 2 (TRIB2)_rs1881145, cytotoxic T-lymphocyte-associated antigen 4 (CTLA4)_rs231775, lipoma-preferred partner (LPP)_rs6780858, and human leukocyte antigen (HLA)-J_ rs767861647. The PRS of the best model was positively associated with hyperthyroidism risk by 1.939-fold (1.317–2.854) after adjusting for covariates. PRSs interacted with age, metabolic syndrome, and dietary inflammatory index (DII), while hyperthyroidism risk interacted with energy, calcium, seaweed, milk, and coffee intake (P < 0.05). The PRS impact on hyperthyroidism risk was observed in younger (<55 years) participants and adults without metabolic syndrome. PRSs were positively associated with hyperthyroidism risk in participants with low dietary intakes of energy (OR = 2.74), calcium (OR = 2.84), seaweed (OR = 3.43), milk (OR = 2.91), coffee (OR = 2.44), and DII (OR = 3.45). In conclusion, adults with high PRS involved in inflammation and immunity had a high hyperthyroidism risk exacerbated under low intakes of energy, calcium, seaweed, milk, or coffee. These results can be applied to personalized nutrition in a clinical setting.
Highlights
Hyperthyroidism is a condition that involves excessive productions of tetraiodothyronine (T4) and/or triiodothyronine (T3) by the thyroid gland and low serum levels of thyroid-stimulating hormone (0–0.4 mU/L; TSH) [1]
No significant association was found between metabolic syndrome (MetS) or its components and hyperthyroidism risk. yroid cancer had a much higher prevalence among cases than controls, and hyperthyroidism risk was 2.9-fold higher in participants with thyroid cancer
We hypothesized that polygenetic variants of genes involved in inflammation and immunity are associated with hyperthyroidism risk and interacted with metabolic parameters and nutritional intakes to modulate the risk of hyperthyroidism. is hypothesis was evaluated in 39,641 individuals aged >40 (847 had hyperthyroidism) who participated in the urban hospitalbased cohort (2004–2013). e present study is the first study to demonstrate that polygenetic risk scores (PRS) derived from genes associated with inflammation and immunity interact with MetS parameters and food intake to modulate the risk of hyperthyroidism
Summary
Hyperthyroidism is a condition that involves excessive productions of tetraiodothyronine (T4) and/or triiodothyronine (T3) by the thyroid gland and low serum levels of thyroid-stimulating hormone (0–0.4 mU/L; TSH) [1]. Graves’ disease (an autoimmune disorder), Plummer’s disease, and thyroiditis (thyroid gland inflammation) accompany hyperthyroidism [2]. E prevalence of Graves’s disease and thyroid inflammation is linked to ethnicity [3]. In a Journal of yroid Research cross-sectional Chinese study since 1995, the prevalence of hyperthyroidism among people living in iodine sufficient and insufficient areas were 1.2% and 1.0%, respectively (P < 0.001) [1], indicating that excess iodine and tetraiodothyronine intakes are involved in the induction of hyperthyroidism [1]. Few studies have demonstrated an association between dietary intake and hyperthyroidism
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