Kristof Y Neven1, Bianca Cox1, Charlotte Cosemans1, Wilfried Gyselaers2, Joris Penders3, Michelle Plusquin1, Harry A Roels1,4, Karen Vrijens1, Ann Ruttens5, Tim S Nawrot6,7. 1. Centre for Environmental Sciences, Hasselt University, Diepenbeek, Belgium. 2. Department of Obstetrics, East-Limburg Hospital, Genk, Belgium. 3. Laboratory of Clinical Biology, East-Limburg Hospital, Genk, Belgium. 4. Louvain Centre for Toxicology and Applied Pharmacology, Université catholique de Louvain, Brussels, Belgium. 5. Sciensano, SD Chemical and Physical Health Risks, Tervuren, Belgium. 6. Centre for Environmental Sciences, Hasselt University, Diepenbeek, Belgium. tim.nawrot@uhasselt.be. 7. Department of Public Health & Primary Care, Leuven University, Leuven, Belgium. tim.nawrot@uhasselt.be.
Abstract
BACKGROUND: The micronutrient iodine is essential for a healthy intrauterine environment and is required for optimal fetal growth and neurodevelopment. Evidence linking urinary iodine concentrations, which mainly reflects short-term iodine intake, to gestational diabetes mellitus (GDM) is inconclusive. Although the placental concentrations would better reflect the long-term gestational iodine status, no studies to date have investigated the association between the placental iodine load and the risk at GDM. Moreover, evidence is lacking whether placental iodine could play a role in biomarkers of insulin resistance and β-cell activity. METHODS: We assessed the incidence of GDM between weeks 24 and 28 of gestation for 471 mother-neonate pairs from the ENVIRONAGE birth cohort. In placentas, we determined the iodine concentrations. In maternal and cord blood, we measured the insulin concentrations, the Homeostasis Model Assessment (HOMA) for insulin resistance (IR) index, and β-cell activity. Logistic regression was used to estimate the odds ratios (OR) of GDM, and the population attributable factor (PAF) was calculated. Generalized linear models estimated the changes in insulin, HOMA-IR, and β-cell activity for a 5 μg/kg increase in placental iodine. RESULTS: Higher placental iodine concentrations decreased the risk at GDM (OR = 0.82; 95%CI 0.72 to 0.93; p = 0.003). According to the PAF, 54.2% (95%CI 11.4 to 82.3%; p = 0.0006) of the GDM cases could be prevented if the mothers of the lowest tertile of placental iodine would have placental iodine levels as those belonging to the highest tertile. In cord blood, the plasma insulin concentration was inversely associated with the placental iodine load (β = - 4.8%; 95%CI - 8.9 to - 0.6%; p = 0.026). CONCLUSIONS: Higher concentrations of placental iodine are linked with a lower incidence of GDM. Moreover, a lower placental iodine load is associated with an altered plasma insulin concentration, HOMA-IR index, and β-cell activity. These findings postulate that a mild-to-moderate iodine deficiency could be linked with subclinical and early-onset alterations in the normal insulin homeostasis in healthy pregnant women. Nevertheless, the functional link between gestational iodine status and GDM warrants further research.
BACKGROUND: The micronutrient iodine is essential for a healthy intrauterine environment and is required for optimal fetal growth and neurodevelopment. Evidence linking urinary iodine concentrations, which mainly reflects short-term iodine intake, to gestational diabetes mellitus (GDM) is inconclusive. Although the placental concentrations would better reflect the long-term gestational iodine status, no studies to date have investigated the association between the placental iodine load and the risk at GDM. Moreover, evidence is lacking whether placental iodine could play a role in biomarkers of insulin resistance and β-cell activity. METHODS: We assessed the incidence of GDM between weeks 24 and 28 of gestation for 471 mother-neonate pairs from the ENVIRONAGE birth cohort. In placentas, we determined the iodine concentrations. In maternal and cord blood, we measured the insulin concentrations, the Homeostasis Model Assessment (HOMA) for insulin resistance (IR) index, and β-cell activity. Logistic regression was used to estimate the odds ratios (OR) of GDM, and the population attributable factor (PAF) was calculated. Generalized linear models estimated the changes in insulin, HOMA-IR, and β-cell activity for a 5 μg/kg increase in placental iodine. RESULTS: Higher placental iodine concentrations decreased the risk at GDM (OR = 0.82; 95%CI 0.72 to 0.93; p = 0.003). According to the PAF, 54.2% (95%CI 11.4 to 82.3%; p = 0.0006) of the GDM cases could be prevented if the mothers of the lowest tertile of placental iodine would have placental iodine levels as those belonging to the highest tertile. In cord blood, the plasma insulin concentration was inversely associated with the placental iodine load (β = - 4.8%; 95%CI - 8.9 to - 0.6%; p = 0.026). CONCLUSIONS: Higher concentrations of placental iodine are linked with a lower incidence of GDM. Moreover, a lower placental iodine load is associated with an altered plasma insulin concentration, HOMA-IR index, and β-cell activity. These findings postulate that a mild-to-moderate iodine deficiency could be linked with subclinical and early-onset alterations in the normal insulin homeostasis in healthy pregnant women. Nevertheless, the functional link between gestational iodine status and GDM warrants further research.
Authors: Kristof Y Neven; Cédric B D Marien; Bram G Janssen; Harry A Roels; Nadia Waegeneers; Tim S Nawrot; Ann Ruttens Journal: Sci Rep Date: 2020-01-13 Impact factor: 4.379
Authors: Helena Filipsson Nyström; Anne Lise Brantsæter; Iris Erlund; Ingibjörg Gunnarsdottir; Lena Hulthén; Peter Laurberg; Irene Mattisson; Lone Banke Rasmussen; Suvi Virtanen; Helle Margrete Meltzer Journal: Food Nutr Res Date: 2016-06-08 Impact factor: 3.894
Authors: Kristof Y Neven; Bianca Cox; Karen Vrijens; Michelle Plusquin; Harry A Roels; Ann Ruttens; Tim S Nawrot Journal: J Transl Med Date: 2020-11-10 Impact factor: 5.531