Iodine and the Brain

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The traditional view was that since these hormone levels are still within normal range when a person is mildly iodine deficient, the lack of iodine may have no health effects. Still, it is too soon to start routinely treating children with mild deficiencies, according to Dr. Sheila A.

The role of iodine in brain development.

Skeaff, a senior lecturer at the University of Otago in Dunedin and one of the researchers on the work. Skeaff pointed out that there are no standard tests for mild iodine deficiency. The best solution for people who think they might be deficient is to regularly eat foods high in iodine and use iodized table salt.

Iodine for Optimal Performance & Cognition

In the U. A: Iodine deficiency is the main cause of brain damage in childhood. In adulthood, it affects productivity and the ability to find a job. Iodine-deficient people may forfeit 15 IQ points, and nearly 50 million people suffer from some degree of iodine deficiency-related brain damage. It is particularly important that pregnant women receive enough iodine in their diet, as iodine is a key nutrient in the fetal development process, especially with respect to the brain. Iodine deficiency during pregnancy not only results in brain damage to the fetus, but also in low birth weight, prematurity and increased perinatal and infant mortality.

Young children are also particularly at risk because the brain still needs iodine for its development during the first two years of life.

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In addition, iodine deficiency in children is responsible for disorders in physical and cognitive development, and hypothyroidism. Additionally, Alves et al. Blasi et al. Congenital hypothyroid patients also deactivated the inferior parietal cortex to a greater extent than controls.

Figure 4. Map showing the countries that have mild to moderate iodine deficiency based on median urinary iodine concentration UIC as reported in by Anderssson et al. Six studies on hypothyroidism ID related disorder were excluded as ID was not explicitly stated as the cause of the disease [Exclusion criteria]. This indicates that the spectrum of medical imaging techniques applied to study brain changes associated with ID related disorders is wide. Although thyroid disorders related to ID can produce identifiable structural brain abnormalities, these can be highly inconsistent Table 3.

Cerebellar and hippocampal abnormalities were, however, consistently reported throughout few of the studies included, acknowledged by others [6,7] and found in animals [29,30,40,80]. Nevertheless, the majority of the studies included in this review overlooks basic structural brain changes e.

MRI was used in most of the studies included in this review; which was dominated by research in the context of primary and congenital hypothyroidism, both in terms of the number of studies and the subject sample size.

Growth and development

Despite the recognized impact of ID in human health, the low prevalence of ID disorders in the general population may have incidence in the lack of large-sized studies evaluating structural brain changes in this condition. The median sample size was 5, as many of the included studies are single case reports.

Including studies which encompassed iodine deficiency disorders rather than ID alone would have increased the scope of the review, but could also have meant that other non-iodine related consequences of these diseases may have affected the appearance of the brain changes. Several of the case studies also often presented no methods sections and so MRI acquisition methods and statistical analysis methods may have been inadequate.

However, these studies are inclined to create other assumptions. The differences in blood oxygen level dependant response activation between cases and controls may be due to hypothyroid patients disengaging from the task rather than activating different, resultant brain areas [88] and there is also no guarantee in fMRI that subjects are performing the task as intended rather than thinking of other, irrelevant information, thus activating non-task dependent brain areas.

Wheeler et al. The researchers did not clarify how many scans were deemed inappropriate and they did not provide brain scan exclusion criteria specifically and so again, selection bias is prevalent. It also assumes that the disregarded scans would have been similar to those of the other subjects.

Lack of dietary iodine threatens brain development in children

Many studies were conducted to ascertain the effects of levothyroxine therapy in hypothyroid patients i. Since these are not directly related to the effects of ID, dependability becomes more disputable. Other sources of inconsistency include the use of differing field strengths among several studies ranging from 0. Pituitary hyperplasia is often confused with pituitary adenomas [55,62].

Hence, a consistent field strength which adequately displays these differences on MR images is necessary. In the study by Akinci et al. Several studies also did not detail the time-frame between repeat MRI scans and so differences between studies in terms of time elapsed could increase result discrepancies.

However, no distinction is given as to the degree of hyperor hypo-intensity for which an appropriate grading scale consistent across all studies is required. The research in this paper could also have been improved by the additional utilisation of Computed Tomography CT scans in all subjects; this would enable authors to determine whether the change in intensity was due to calcifications and thus prevent assumptions. To the best of our knowledge, there has not been a systematic review before on the appearance of brain changes on MR caused by iodine deficiency.

Despite the large worldwide availability of MR techniques and the importance of the study of iodine insufficiency, given its strong link with neurodevelopment and impaired cognition, most current literature on ID reports histological and cytoarchitectural brain alterations only, with no MR confirmation. In some countries known as having mild to moderate ID the major causes of the disorders included in this review are immunological or iatrogenic rather than ID e. United Kigdom. Therefore this review, rather than reflecting the spectrum of ID related brain abnormalities provides guidance and constitutes a call for future studies in ID and brain health.

Strengths of this work include searching multiple databases over a large time-frame, the use of comprehendsive search terms, the inclusion of fMRI and MRS studies, the inclusion of ID diseases rather than research discussing ID alone, the inclusion of both human and animal studies and the inclusion of healthy and diseased brains. A weakness, however, is the exclusion of nonEnglish papers.

Interobserver bias also affects some of the included studies; for example, in the study by Hasegawa et al. Additionally, the limited description of the signal changes when mentioned lacks from an adequate i. More studies are required which correlate histological findings with MR image results and the utilisation of more standardised sequences and field strengths are necessary.

What does the body need iodine for?

With the increased focus on the consequence of iodine insufficiency both in utero and in infancy, it is important to understand the brain structural modifications caused by ID, given that neurodevelopmental and cognitive outcomes range in severity according to the level and timing of ID. Future work should include global and regional atrophy changes to identify directions for the research that will improve the understanding of the pathophysiological mechanisms related with the effects of ID in the brain.

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Chan, A. Cheng, P. Cheung, et al. Sethi and U. Becker, L. Braverman, F. Delange, J. Dunn, J. Franklyn, J. Hollowell, et al. Ibrahim, J. Sinn and W. CD J. Schroder-van der Elst, D. Van der Heide, G. Vanderpump, J. Lazarus, P. Smith, P. Laurberg, R.

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