Plasma levels of selenium, selenoprotein P and glutathione peroxidase and their correlations to fish intake and serum levels of thyrotropin and thyroid hormones: A study on Latvian fish consumers

Abstract

Objective: To study the relationships between fish intake and different markers of selenium status and thyroid hormone function.

Design: Cross-sectional study.

Setting and subjects: Sixty-eight men (age 24–79 years) were recruited among coastal fishermen and inland subjects from Latvia. None of the subjects was on selenium medication or had any known endocrine disease.

Main outcome measures: Correlations between fish intake, plasma levels of selenium, selenoprotein P, glutathione peroxidase, organic mercury in erythrocytes and TSH in serum.

Results: Selenium in plasma ranged from 0.30 to 1.56 μmol/1, selenoprotein P from 0.54 to 2.21 arbitrary units relative to pooled plasma, and glutathione peroxidase from 1.20 to 5.73 mg/1. The number of fish meals per month was correlated with plasma selenium, selenoprotein P and glutathione peroxidase (r=0.63, r=0.62 and r=0.50, respectively; P<0.001). Plasma selenium was correlated with selenoprotein P and glutathione peroxidase (r=0.88 and r=0.67, respectively; P<0.001), and also selenoprotein P and glutathione peroxidase were correlated (r=0.63, P<0.001). The mean plasma selenium level in those with a high fish intake (21–50 fish meals/month), was 81% higher than in those with lowest fish intake. TSH in serum was inversely correlated with plasma selenium and selenoprotein P. Thyroid hormone levels were not correlated with plasma selenium, selenoproteins or fish intake.

Conclusions: In this study group, selenium from fish intake had a marked impact on all variables studied on selenium status. No impact of selenium status on T3 and T4 levels was observed. The slightly negative correlation of selenium status with TSH levels might indicate a higher TSH secretion at low selenium status.

Sponsorship: The study was supported by grants from the Swedish Environmental Protection Agency, the Medical Faculty, Lund University, and the Påhlsson Foundation. B.Å. was supported by FAIR CT95.0771.