Evidence of iodine deficiency and use during pregnancy and autism
Basal Body Temperature
Broda Barnes, M.D. popularized the basal body temperature for evaluating thyroid function. It relies on a morning, waking, underarm temperature, which should average 97.8 to 98.2 to indicate normal thyroid function. Temperatures below 97.8 indicate a sign of possible low thyroid function such as can result from iodine deficiency. These are preovulatory temperatures, to be taken on days 2 or 3 of the period in menstruating women, but on any day for other women, children, or men.
Simply because the basal body temperature is normal does not prove that iodine is sufficient. Long before hypothyroid signs and symptoms occur, other less obvious signs and symptoms of iodine deficiency become apparent. The reason for this is because the thyroid is extremely good at trapping any small amounts of iodine that are present in the body, so it suffers last from iodine deficiency, way after other organs.
Recent data on iodine excretion in the urine of adults, adolescents and newborns and on the iodine content of breast milk indicate a high prevalence of iodine deficiency (moderate in many cases and severe in a few) in many European countries. These cases may manifest as subclinical hypothyroidism in neonates and as goitre in adolescents and adults. Lack of iodine causes not only goitre, but also mental deficiency, hearing loss and other neurological impairments, and short stature due to thyroid insufficiency during fetal development and childhood. Although iodinated salt is available theoretically in most countries where it is needed, its quality and share of the market are often unsatisfactory. In many countries where only household salt is iodinated the iodine content has been set too low owing to an overestimation of household salt consumption. Governments are therefore urged to pass legislation and provide means for efficient iodination of salt wherever this is necessary.
Thyroid gland size was ultrasonographically determined in 35 pregnant women who live in an area with moderate iodine deficiency. Iodide salt was administered to group A (n = 17), whereas group B (n = 18) was used as a control. Each group was tested for thyroid-stimulating hormone serum levels, iodine excretion, and thyroid volume. In both groups thyroid-stimulating hormone levels were similar and did not change throughout pregnancy. The iodine excretion at the third trimester in the treated group was significantly (p less than 0.01) higher than that of group B (100.0 +/- 39.0 versus 50.0 +/- 37.0 micrograms iodine per 24 hours, respectively). Initially, thyroid volume did not differ between the two groups. At the end of pregnancy, no difference was found in thyroid size in group A, whereas in the untreated women it increased significantly (p less than 0.0001) with a mean increase of 1.6 +/- 0.6 ml (16.2% +/- 6.0%). These results show that the increased thyroid size in the control group was mainly a result of relative iodine deficiency and that iodoprophylaxis should be warranted even in areas with moderate iodine deficiency to prevent the increase in thyroid size and, probably, to avoid the risk of maternal and fetal hypothyroidism.
Arch Med Res. 2013 Oct;44(7):555-61. doi: 10.1016/j.arcmed.2013.09.012. Epub 2013 Oct 10.
Iodinedeficiency in Egyptian autistic children and their mothers: relation to disease severity.
Because autism may be a disease of early fetal brain development, maternal hypothyroxinemia (HT) in early pregnancy secondary to iodinedeficiency (ID) may be related to etiology of autism. The aim of the study was to assess the iodine nutritional status in Egyptian autistic children and their mothers and its relationship with disease characteristics.
Fifty autistic children and their mothers were studied in comparison to 50 controls. All subjects were subjected to clinical evaluation, measurement of urinary iodine (UI), free triiodothyronine (fT3), free tetraiodothyronine (fT4) and thyroid-stimulating hormone (TSH) along with measurement of thyroid volume (TV). In addition, electroencephalography (EEG) and intelligence quotient (IQ) assessment were done for all autistic children.
Of autistic children and their mothers, 54% and 58%, respectively, were iodine deficient. None of the control children or their mothers was iodine deficient. UI was lower among autistic patients (p <0.001) and their mothers (p <0.001). Childhood Autism Rating Scale (CARS) score correlated negatively with UI (r = -0.94, p <0.001). Positive correlations were detected between autistic patients and their mothers regarding UI (r = 0.88, p <0.001), fT3 (r = 0.79, p = 0.03), fT4 (r = 0.91, p <0.001) and TSH (r = 0.69, p = 0.04). Autism had a significant risk for association with each of low UI (OR: 9.5, 95% CI: 2.15-33.8, p = 0.02) and intake of noniodized salt (OR: 6.82, 95% CI = 1.36-34.27, p = 0.031).
ID is prevalent in Egyptian autistic children and their mothers and was inversely related to disease severity and could be related to its etiology.
Pregnant woman are at increased risk for iodinedeficiency, which may induce thyroid insufficiency and have damaging effects not only on the mother but also the fetus. We hypothesize that iodine supplementation during pregnancy reduces the risk for iodinedeficiency.
Cross-sectional study to assess iodine levels in random urine specimens during pregnancy in New York City. One hundred eighty-two women visited a clinic where free iodine supplementation was offered (150 μg of potassium iodide daily; Group A), and 183 women were seen at a practice at which no supplementation was offered (Group B).
Overall, more than one out of two pregnant women in New York City were at risk for iodinedeficiency with a spot urinary iodine (UI) level less than 150 μg/L and could be defined as at risk for iodinedeficiency. The median urine iodine concentration for the entire group was 152.5 μg/L, but there was considerable variation from 10.9 to 1210 μg/L. The median UI level of the supplemented Group A (169.8 μg/L) was significantly greater than that of Group B (128.4 μg/L; p<0.01). Based on World Health Organization (WHO) guidelines, 38.9% of Group B women were at risk for mild, moderate, or severe iodinedeficiency, compared with 22.8% of Group A women.
New York City pregnant women were significantly less prone to iodinedeficiency when provided with iodine supplementation. Nevertheless, when spot UI levels were used to estimate iodine sufficiency, more than 20% of supplemented women were still at risk for iodinedeficiency according to WHO guidelines, suggesting that current supplementation practices remain insufficient.