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Corresponding Author

Iman Taher Hussein

Authors ORCID

Iman Taher Hussein: https://orcid.org/0009-0002-1018-7908

Abstract

A thyroid–inflammation–insulin pathway has been proposed in which thyroid dysfunction promotes inflammation and thereby reduces insulin sensitivity, but adiposity-adjusted population evidence is limited. This cross-sectional analysis examined whether subclinical hypothyroidism (SCH) and thyroid autoimmunity are associated with insulin resistance independently of body mass index (BMI), and whether C-reactive protein (CRP), the only inflammatory biomarker available, is associated with either, using National Health and Nutrition Examination Survey (NHANES) 2007–2012 data. Non-pregnant adults aged 18–60 years with fasting glucose < 126 mg/dL and normal free thyroxine were included; SCH was defined as thyroid-stimulating hormone (TSH) 4.5–10 mIU/L, and insulin resistance was quantified by the homeostasis model assessment (HOMA-IR). Linear regression of log HOMA-IR accounted for the complex survey design (strata, clusters, weights) and was adjusted for age, sex, BMI, and survey cycle, with sensitivity and interaction analyses. Among 2,434 adults (89 with SCH), no association with HOMA-IR was detected for TSH (β = 0.009 per mIU/L; 95% CI -0.014 to 0.032), SCH (β = -0.035; 95% CI -0.186 to 0.115), or thyroid peroxidase antibody positivity (β = -0.010; 95% CI -0.097 to 0.077). CRP was associated with HOMA-IR independently of BMI (β = 0.047; 95% CI 0.027 to 0.067) but not with TSH (β = -0.029; 95% CI -0.076 to 0.018). Estimates were similar after extended adjustment and exclusion of thyroid-medication users. We found no detectable association between SCH or thyroid autoimmunity and insulin resistance after adjustment for BMI; given the cross-sectional design and modest SCH group, small effects cannot be excluded.

Digital Object Identifier (DOI)

10.70176/3007-973X.1077

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