aka most of the Thing behind the Flynn effect.
Vegans are deficient.
We assessed the association between maternal iodine status and child IQ at age 8 years and reading ability at age 9 years. We included 21 socioeconomic, parental, and child factors as confounders.
Our results show the importance of adequate iodine status during early gestation and emphasise the risk that iodine deficiency can pose to the developing infant, even in a country classified as only mildly iodine deficient. Iodine deficiency in pregnant women in the UK should be treated as an important public health issue that needs attention.
After adjustment for confounders, children of women with an iodine-to-creatinine ratio of less than 150 μg/g were more likely to have scores in the lowest quartile for verbal IQ (odds ratio 1·58, 95% CI 1·09–2·30; p=0·02), reading accuracy (1·69, 1·15–2·49; p=0·007), and reading comprehension (1·54, 1·06–2·23; p=0·02) than were those of mothers with ratios of 150 μg/g or more.
The present comments are restricted to the role of maternal thyroid hormone on early brain development, and are based mostly on information presently available for the human fetal brain. It emphasizes that maternal hypothyroxinemia – defined as thyroxine (T4) concentrations that are low for the stage of pregnancy – is potentially damaging for neurodevelopment of the fetus throughout pregnancy, but especially so before midgestation, as the mother is then the only source of T4 for the developing brain.
Despite a highly efficient uterine-placental ‘barrier’ to their transfer, very small amounts of T4 and triiodothyronine (T3) of maternal origin are present in the fetal compartment by 4 weeks after conception, with T4 increasing steadily thereafter. A major proportion of T4 in fetal fluids is not protein-bound: the ‘free’ T4 (FT4) available to fetal tissues is determined by the maternal serum T4, and reaches concentrations known to be of biological significance in adults. Despite very low T3 and ‘free’ T3 (FT3) in fetal fluids, the T3 generated locally from T4 in the cerebral cortex reaches adult concentrations by midgestation, and is partly bound to its nuclear receptor. Experimental results in the rat strongly support the conclusion that thyroid hormone is already required for normal corticogenesis very early in pregnancy. The first trimester surge of maternal FT4 is proposed as a biologically relevant event controlled by the conceptus to ensure its developing cerebral cortex is provided with the necessary amounts of substrate for the local generation of adequate amounts of T3 for binding to its nuclear receptor.
Don’t worry, the brain damage was genetic anyway.
Women unable to increase their production of T4 early in pregnancy would constitute a population at risk for neurological disabilities in their children. As mild-moderate iodine deficiency is still the most widespread cause of maternal hypothyroxinemia in Western societies, the birth of many children with learning disabilities may already be preventable by advising women to take iodine supplements as soon as pregnancy starts, or earlier if possible.
This editorial reviews the impact of iodine deficiency (1) on thyroid function in pregnant women and neonates and (2) on the neurointellectual development of infants and children.
All degrees of iodine deficiency (mild: iodine intake of 50-99 µg/day, moderate: 20-49 µg/day, and severe: <20 µg/day) affect thyroid function of the mother and the neonate as well as the mental development of the child. The damage increases with the degree of the deficiency, with overt endemic cretinism as the severest consequence. Maternal hypothyroxinaemia during early pregnancy is a key factor in the development of the neurological damage in the cretin. Selenium deficiency combined with iodine deficiency partly prevents the neurological damage but precipitates severe hypothyroidism in cretins.
Iodine deficiency results in a global loss of 10-15 IQ points at a population level and constitutes the world’s greatest single cause of preventable brain damage and mental retardation.
An entire Standard Deviation, no big deal!
Supplements won’t help, you’ll OD.
Iodine is a micronutrient that is essential for the production of thyroid hormones. The primary source of iodine is the diet via consumption of foods that have been fortified with iodine, including salt, dairy products and bread, or that are naturally abundant in the micronutrient, such as seafood. Recommended daily iodine intake is 150 μg in adults who are not pregnant or lactating. Ingestion of iodine or exposure above this threshold is generally well-tolerated. However, in certain susceptible individuals, including those with pre-existing thyroid disease, the elderly, fetuses and neonates, or patients with other risk factors, the risk of developing iodine-induced thyroid dysfunction might be increased. Hypothyroidism or hyperthyroidism as a result of supraphysiologic iodine exposure might be either subclinical or overt, and the source of the excess iodine might not be readily apparent.
Iodine is critical to human health. It forms the basis of thyroid hormones and plays many other roles in human biochemistry. While the thyroid gland contains the body’s highest concentration of iodine, the salivary glands, brain, cerebrospinal fluid, gastric mucosea, breasts, ovaries and a part of the eye also concentrate iodine. In the brain, iodine is found in the choroid plexus, the area on the ventricles of the brain where cerebrospinal fluid (CSF) is produced, and in the substantia nigra, an area associated with Parkinson’s disease.
Iodine is essential to normal growth and development. Iodine deficiency in utero and during growth can result in cretinism, a condition of severely stunted physical and mental growth due to prolonged nutritional deficiency of iodine or from untreated congenital deficiency of thyroid hormones (hypothyroidism). The condition is characterized by short stature, delayed bone maturation and puberty, infertility, neurological impairment and cognitive impairment ranging from mild to severe. Iodine deficiency also causes goiter, the gradual enlargement of the thyroid gland. Both conditions have led to public health campaigns of iodine administration in many countries. The addition of iodine compounds to table salt or water represents the first attempt to provide nutrient supplementation via “fortification” of common foods.
At least they won’t have grandkids.
China paper here:
IQ so unreal it tracks brain damage.
The level of iodine nutrition plays a crucial role in the intellectual development of children. The intelligence damage of children exposed to severe ID was profound, demonstrated by 12.45 IQ points loss and they recovered 8.7 IQ points with iodine supplementation or IS before and during pregnancy. Iodine supplementation before and during pregnancy to women living in severe ID areas could prevent their children from intelligence deficit. This effect becomes evident in children born 3.5 years after the iodine supplementation program was introduced.
And now… we wait.