Preconception vs. postconception iodine supplementation: Effect on thyroglobulin decline in a Québec pregnancy cohort

Meeting the increased iodine needs in pregnancy is vital, as deficiency, especially early on, can cause irreversible cognitive impairment of the infant. The American Thyroid Association advises that women who are planning a pregnancy should begin taking a daily iodine supplement containing 150 µg of iodine at least three months before conception to meet iodine needs in early pregnancy. Recently, it was reported that just 36% of women in a Québec pregnancy cohort initiated iodine supplementation before conception.

Using thyroglobulin (Tg) as a sensitive, functional marker, this study compared the effect of pre- vs. postconception iodine supplement initiation on long-term iodine (thyroid) status in this Québec cohort.

Serum Tg, thyroid stimulating hormone (TSH), and free thyroxine (FT4) were measured in pregnant women at 10.1-14.9 (T1) and 19.7-24.9 (T2) weeks gestation, with pre- vs. postconception iodine groups compared using Generalized Linear Mixed Models.

Of the 474 participants analysed, 64% began iodine-inclusive multivitamin/mineral supplementation after conception. Iodine dose (median 220 µg/day) and daily usage rates (90.5-95.3%) were similar between preconception and postconception groups (p > 0.05). Tg estimated marginal means declined in both groups from T1 to T2 (p < 0.0001), with the postconception group showing a significantly greater reduction (interaction p = 0.049; median change: -1.22 µg/L vs. -2.14 µg/L, p = 0.008). At T1, median Tg levels (10.2 µg/L preconception vs. 12.5 µg/L postconception) failed to meet a recommended iodine sufficiency requirement (median Tg <10 µg/L and <3% of values ≥44 µg/L). Differences between groups were not observed in TSH and FT4 and prevalence of subclinical (0.7-2.6%) or primary (0-0.3%) hypothyroidism was low.

In this observational cohort, the greater T1-to-T2 decline in Tg in women who began iodine supplementation postconception suggests that supplementation may have helped normalize thyroid stimulation caused by prior iodine deficiency.