Molecular Iodine Has Extrathyroidal Effects as an Antioxidant, Differentiator, and Immunomodulator

Most investigations of iodine metabolism in humans and animals have focused on its role in thyroid function. However, considerable evidence indicates that iodine could also be implicated in the physiopathology of other organs. We review the literature that shows that molecular iodine (I2) exerts multiple and complex actions on the organs that capture it, not including its effects as part of thyroid hormones. This chemical form of iodine is internalized by a facilitated diffusion system that is evolutionary conserved, and its effects appear to be mediated by a variety of mechanisms and pathways. As an oxidized component, it directly neutralizes free radicals, induces the expression of type II antioxidant enzymes, or inactivates proinflammatory pathways. In neoplastic cells, I2 generates iodolipids with nuclear actions that include the activation of apoptotic pathways and the inhibition of markers related to stem cell maintenance, chemoresistance, and survival. Recently, I2 has been postulated as an immune modulator that depending on the cellular context, can function as an inhibitor or activator of immune responses. We propose that the intake of molecular iodine is increased in adults to at least 1 mg/day in specific pathologies to obtain the potential extrathyroid benefits described in this review.

Iodine Status, Thyroid Function, and Birthweight: A Complex Relationship in High-Risk Pregnancies

(1) Background: The consequences of iodine deficiency and/or thyroid dysfunction during pregnancy have been extensively studied, emphasizing on infant neurodevelopment. However, the available information about the relationship between iodine, thyroid hormones, and fetal growth in high-risk pregnancies is limited. We aim to investigate if iodine metabolism and/or thyroid parameters can be affected by adverse antenatal/perinatal conditions. (2) Methods: A cross-sectional study examined differences in iodine status, thyroid function, and birthweight between high-risk (HR group; n = 108)) and low-risk pregnancies (LR group; n = 233) at the time of birth. Urinary iodine concentration (UIC), iodine levels in amniotic fluid, and thyroid parameters [thyroid-stimulating hormone (TSH), free thyroxine (FT4)] were measured in mother–baby pairs. (3) Results: There were significant differences between HR and LR groups, free thyroxine (FT4) concentration in cord blood was significantly higher in the LR group compared with HR pregnancies (17.06 pmol/L vs. 15.30 pmol/L, respectively; p < 0.001), meanwhile iodine concentration in amniotic fluid was significantly lower (13.11 µg/L vs. 19.65 µg/L, respectively; p < 0.001). (4) Conclusions: Our findings support the hypothesis that an adverse intrauterine environment can compromise the availability of FT4 in cord blood as well as the iodine metabolism in the fetus. These differences are more noticeable in preterm and/or small fetuses.

Key aspects of the iodine metabolism in brown algae: a brief critical review

Giant kelp (Macrocystis pyrifera, pictured here: in Port William, East Falkland, Feb. 2013) has a prolific halogen metabolism.

Maintaining euthyroidism: fundamentals of thyroid hormone physiology, iodine metabolism and hypothyroidism

Thyroid-related pathologies, especially subclinical and clinical hypothyroidism, are commonly described in clinical practice. While illnesses related to aberrant thyroid hormone homeostasis are the most prevalent endocrinological conditions diagnosed, important aspects related to thyroid hormone physiology are often overlooked. Further, the only known physiological purpose of iodine is its requirement for the synthesis of thyroxine (T4) and triiodothyronine (T3). However, although it can be applied as curative agent in the management of thyrotoxicosis, the halogen is often prescribed and used inappropriately with significant, but preventable clinical consequences. In an attempt to kindle a better understanding of aspects related to aberrant thyroid hormone regulation, iodine metabolism, and the clinical management of thyroid related pathology, the current paper provides a physiological and clinical overview of said constructs from a hypothyroid perspective.