Abstract
Iodine is an essential trace mineral necessary for the synthesis of thyroid hormones. Thyroid hormones may play a role in brain development and function through the requirement of 3,5,3’-tri-iodothyronine (T3) for myelin synthesis, and a possible role of T3 in neurotransmitter pathways. Observational studies have shown lower intelligence quotients in children from iodine deficient areas compared with iodine sufficient areas. Two randomised controlled trials found iodine supplementation improved cognitive test scores in mildly and moderately iodine deficient school children, compared with placebo. The brain continues to develop beyond childhood, with white matter volume of the frontal lobes increasing until the fifth decade of life.
The think2 project was conducted with the objectives of assessing the iodine status of young adults who consume no more than two serves of bread per day, and to investigate a treatment effect of daily iodine supplementation on cognition in mildly iodine deficient young adults living in Dunedin.
Participants (n=205) were recruited between July 2010 and January 2011, and were randomised to receive either a daily 150 µg iodine supplement or daily placebo supplement for 32 weeks. At baseline, seven cognitive tests from the Wechsler Adult Intelligence Scale, fourth edition (WAIS-IV) were administered, and a urine sample and finger-prick blood sample obtained. Participants completed a questionnaire assessing demographic characteristics and dietary intake of iodine using an iodine specific food frequency questionnaire. All measures were repeated at 32 weeks.
At baseline, the median urinary iodine concentration (MUIC) (inter-quartile range, IQR) was 69 (40-105) µg/L and 60 (31-92) µg/L in the iodine and placebo groups, respectively, indicating mild iodine deficiency in this sample. Serum thyroglobulin (Tg) concentration indicated borderline mild iodine deficiency with a median (IQR) of 10.0 (6.3-19.7) µg/L and 10.2 (6.1-16.4) µg/L in iodine and placebo groups, respectively. After 32 weeks of supplementation, both groups significantly increased their urinary iodine; however, the placebo group remained mildly iodine deficient with a MUIC (IQR) of 79 (35-136) µg/L (p=0.003), while the iodine group was categorised as iodine sufficient (MUIC: 115; IQR: 78-342 µg/L; p<0.001). The iodine group had a significantly lower median (IQR) serum Tg concentration of 8.2 (5.0-15.2) µg/L (p<0.001) at study completion, while the placebo group did not change (p=0.935). Iodine supplementation was a significant predictor of 32 week urinary iodine (p<0.001) and serum Tg (p=0.008) concentrations. Mean serum total thyroxine (TT4) and free thyroxine index (FTI) were within normal ranges at baseline (TT4: 101.7 nmol/L in iodine group, 99.4 nmol/L in placebo group; FTI: 98.4 in iodine group, 96.7 in placebo group). There was no treatment effect of iodine supplementation on serum TT4 (p=0.601) or FTI (p=0.953) at the end of the 32 week intervention.
After adjusting for baseline cognitive test score, examiner, age, sex, income, and ethnicity, iodine supplementation did not significantly predict 32 week cognitive test scores for Block Design (p=0.385), Digit Span Backward (p=0.474), Matrix Reasoning (p=0.885), Symbol Search (p=0.844), Visual Puzzles (p=0.675), Coding (p=0.858), and Letter-Number Sequencing (p=0.408).
In conclusion, young adults aged 18-30 years who consumed no more than two serves of bread per day were mildly iodine deficient despite mandatory fortification of bread with iodised salt. Daily 150 µg iodine supplementation for 32 weeks improved the iodine status of the iodine group, compared with placebo group. At study completion, iodine supplementation had not resulted in improved cognitive test scores in the iodine group compared with placebo group for any of the seven cognitive tests administered. Mild iodine deficiency does not appear to have an effect on cognition in young adults.