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Glinoer
Pregnancy and iodine deficiencyGlinoer, Chapter 14
"During pregnancy, two fundamental changes take place. There is a significant increase in the renal iodide clearance (by ~1.3- to ~1.5-fold) and, concomitantly, a sustained increment in TH production requirements (by ~1.5-fold), corresponding to increased iodine requirements, from 80 to 120 μg iodide/day. Since the renal iodide clearance already increases in the first weeks of gestation and persists thereafter, this constitutes an unavoidable urinary iodine ‘leakage’ which tends to lower circulating PII levels and, in turn, induce a compensatory increase in the thyroidal clearance of iodide. These mechanisms underline the increased physiologic thyroidal activity during pregnancy. Panel C in Figure 9 indicates that when the daily iodine intake is only 70 μg during pregnancy, and despite an increase in glandular uptake to 60 %, the equilibrium becomes more or less rapidly unbalanced, since the iodide entry resulting from both uptake and recycling is insufficient to fulfill the increased requirements for TH production.
"Calculations show that, in such conditions, ~20 μg of iodine are missing daily and, in order to sustain TH production, the glandular machinery must draw from already depleted intra-thyroidal iodine stores. Thus in about one trimester after conception, the already low intra-thyroidal iodine stores become even more depleted and, when iodine deprivation prevails during the first half, it tends to become more severe with the progression of gestation to its final stages. A second mechanism of iodine deprivation for the mother occurs later in gestation, from the passage of a part of the available iodine from maternal circulation to the fetal-placental unit. The extent of iodine passage has not yet been precisely established. At mid-gestation, the fetal thyroid gland has already started to produce TH, indispensable for the adequate development of the fetus. In summary, augmentation of iodide trapping is the fundamental mechanism by which the thyroid adapts to changes in the iodine supply, and such mechanism is the key to understanding thyroidal adaptation to iodine deficiency. During pregnancy, increased hormone requirements and iodine losses alter the preconception steady-state. When the iodine supply is restricted (or more severely deficient), pregnancy triggers a vicious circle that leads to excessive glandular stimulation."
Figure 9a. Schematic representation of the kinetics of iodide in healthy non-pregnant and pregnant adults. Panel A: non-pregnant adult with an adequate iodine intake of 150 μg/day. (from Glinoer; Ref 95)
Figure 9b. Panel B: non-pregnant adult with a restricted iodine intake, corresponding to 70 μg/day. (from Glinoer; Ref 95)
Figure 9c. Panel C: The latter condition is compared with an identically restricted level of iodine intake (i.e. 70 μg/day) in a pregnant woman. Daily TH production was set at 80 μg of iodine/day (in non-pregnant) and increased by 1.5-fold to 120 μg/day during pregnancy. (from Glinoer; Ref 95)
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