ADD & ADHD
Attention deficit disorders and mild-moderate iodine deficiency The purpose of this observational study was to determine whether mild-moderate iodine deficiency during pregnancy is associated with attention deficit and hyperactivity disorders (ADHD) (4). The study involved a small sample of women who lived in two areas of Sicily, where iodine intakes were either moderately deficient (area A, n=16) or marginally sufficient (area B, n=11). The iodine status of the general population was known to differ in the two areas, based on the prevalence of goiter (24% in area A vs. 7.8% in area B) and urinary iodine excretion. The authors monitored thyroid function of the mothers during pregnancy and of the children at 18-36 months in 1994 and 8-10 years of age from 2001-2002. Two independent examiners, who were unaware of the mother’s thyroid status, conducted behavioral and neurological evaluations of the children at the same time points.
Thyroid failure occurred in early pregnancy among 50% (n=8) of the women in area A but only transiently among 9% (n=1) of the area B women. All children had normal thyroid function at birth and afterward at the two follow-up time points, and none showed any neurological signs typically seen in iodine deficiency disorders. However, 68.7% of the children from area A (11 of 16) were diagnosed with ADHD, compared to none of the children in area B. Total IQ scores were lower in area A than in area B (92.1 vs 110, p < 0.00005).
A high prevalence of ADHD has been reported before in children with genetic traits that interfere with thyroid function. The authors suggest that varying and mild degrees of thyroid failure occurring early in pregnancy as a result of iodine deficiency may affect fetal brain development and result in the ADHD syndrome. However, the study involved a very small, nonrandom sample, and it is doubtful, on ethical grounds, that a clinical trial could be conducted to confirm these results.
Study of the link between iodine deficiency and ADHD link
Over a period of almost 10 yr, we carried out a prospective study of the neuropsychological development of the offspring of 16 women from a moderately iodine-deficient area (area A) and of 11 control women from a marginally iodine-sufficient area (area B) whose thyroid function had been monitored during early gestation. Attention deficit and hyperactivity disorder (ADHD) was diagnosed in 11 of 16 area A children (68.7%) but in none from area B. Total intelligence quotient score was lower in area A than in area B children (92.1 +/- 7.8 vs. 110 +/- 10) and in ADHD children when compared with both non-ADHD children from the same area and control children (88.0 +/- 6.9 vs. 99.0 +/- 2.0 and 110 +/- 10, respectively). Seven of 11 ADHD children (63.6%) were born to the seven of eight area A mothers who became hypothyroxinemic at early gestation, whereas only one of five non-ADHD children was born to a woman who was hypothyroxinemic at 20 wk of gestation. So far, a similar prevalence of ADHD has been reported only in children with generalized resistance to thyroid hormones. This might suggest a common ADHD pathogenetic mechanism consisting either of reduced sensitivity of the nuclear receptors to thyroid hormone (generalized resistance to thyroid hormones) or reduced availability of intracellular T3 for nuclear receptor binding. The latter would be the ultimate consequence of maternal hypothyroxinemia (due to iodine deficiency), resulting in a critical reduction of the source of the intracellular T3 available to the developing fetal brain.
Any and every emotional disorder can be brought on or simulated by thyroid dysfunction. Hypothyroidism slows the thought process, produces depression and sometimes hallucinations, delusions and even paranoia. Slowness of thought and activity is a hallmark of this disease. When present and untreated from early childhood, the final outcome of severe hypothyroidism is idiocy, growth failure and early death in the late teens or early twenties. In adulthood, a change in personality or depression, fatigue, uncharacteristic irritability or a change in sleep pattern should raise a suspicion of thyroid dysfunction.
During childhood, hyperactivity and a short attention span are typical of hypothyroidism. These children often are treated with Ritalin, an amphetamine-like drug, or amphetamines themselves. Apparently, this solves the problem of fatigue for the child and allows for better concentration and less hyperactivity. The more appropriate treatment, of course, would be thyroid replacement. ,Milder hypothyroidism can allow growth to be normal and even produce extreme height due to a delayed closing of the epiphyses where bone elongation takes place during growth. Tall hypothyroid patients are not rare.
Iodine: For the children with ASD, the mean level of iodine was much lower (45%) than for the control children, and the difference was highly statistically significant (p=0.005). When the subgroup of age 3-6 years was considered, the magnitude of the difference was almost identical (47%), although the difference was not statistically significant due to the smaller number of children in the subgroup. This suggests that iodine could be an important factor in the early development of autism, presumably through its effect on thyroid function. Iodine deficiency was extremely common in parts of the US in the early 1900’s, and caused many cases of goiters (enlarged thyroid) and cretinism (a form of mental retardation due to iodine deficiency). This prompted the federal government to mandate that iodine be added to salt (iodinized salt). However, based on our informal phone survey of several major snack food and fast food manufacturers, non-iodinized salt seems to be the form primarily used in french fries, potato chips, and other snack foods commonly eaten by young children. So, it is plausible that a small fraction of children in the US could still be marginally deficient in iodine, and that this could significantly affect their mental status. Also, it should be pointed out that according to the NHANES surveys I and III , average iodine levels in the US (measured in the urine) have declined more than 50% during the 20 year period from 1971-1974 to 1988-1994, so that an increasing fraction of the population has low levels of iodine that are likely to increase the risk for mental retardation. Thus, low iodine levels could be a cause or exacerbating factor for autism. However, it needs to be pointed out that hair measurements have not been validated for iodine as reflective of body status, so future studies of iodine levels in blood are warranted, as well as studies of thyroid function in autism.
Low iodine is the major cause of mental retardation worldwide (over 80 million cases) - becoming more common in US (decreased use of iodinized salt).
Obsessive Compulsive Disorder