Iodine And The Brain

This volume contains the proceedings of a conference held at the National Institutes of Health in Bethesda on March 21-23. 1988. jointly sponsored by the International Council for Control of Iodine Deficiency Disorders (ICCIDD) and the Fogarty International Center of the National Institutes of Health. Several themes converged to make this meeting timely. The first is an increasing awareness of iodine deficiency disorders as a world-wide problem of public health and a preventable cause of mental deficiency. and as a subject of scientific effort. Increased interest in these problems owes a great deal to accessibility to remote and under developed areas of the world where iodine deficiency persists. As with any subject. greater scrutiny yields unexpected complexity and interest. It is true that provision of iodine. typically as iodized salt, is the necessary and sufficient preventative for iodine deficiency disorders. without including endemic cretinism. This provision is a governmental, economic and social problem. Apart from this, however, the scientific and medical problem of iodine deficiency and its effect on brain development and function is one of great interest and importance for developmental neurology and psychology. Even though the specific preventative agent is known, we do not totally understand the neurobiological questions raised.

Over two billion people worldwide are at risk for the spectrum of disorders known as "The Iodine Deficiency Disorders." 1-10% will suffer cretinism; 5-30% will have some sort of brain damage or neurological impairment and 30-70% will be hypothyroid. The causes of iodine deficiencies can be considered from both simplistic and more complex perspectives: From the leaching of iodine from soil resulting in crops with low iodine content to malnutrition resulting in impaired iodine absorption. Poor dietary diversification and impoverished socio-economic development can also lead to iodine deficiencies. Although it is possible to diagnose and treat deficiencies, there is still an ongoing dialogue regarding the detailed molecular pathology of iodine homeostatis, how hypothyroidism impacts the body tissues, and efficient diagnosis and treatment of the Iodine Deficiency Disorders. This Handbook provides a resource of information on the various pathways and processes based on different countries or diseases. Because there is a constant flow of new information on iodine and related disorders, the goal of this Handbook is to provide a base of scientific information upon which additional knowledge can be applied. Provides important information on one of the most common micro-nutrient deficiencies in the world, the most important "single nutrient-multiple consequences" paradigm today Includes information on iodine-related diseases, including those that are common, preventable and treatable Provides insight from a broad perspective of viewpoints -- from subcellular transports to economic impact

Responding to a renewed interest in the growing problem of iodine deficiency worldwide, Drs. Charles Oxnard and Peter Obendorf, along with experienced translator and anatomist John Dennison, take a fresh look at the classic text, Der endemische Kretinismus, published in 1936 by Springer. Translated here for the first time into English, this landmark text will be a welcome resource for researchers confronting the problem of iodine deficiency. Oxnard and Obendorf point out that there is very little detailed knowledge or numerical data on cretinism available in the English-speaking world. In addition, highly-renowned Professor Basil S. Hetzel, recently-retired World Health Organization Chairman of the International Council for Control of Iodine Deficiency Disorders, published in 2009 with Dr Chen Zu-pei on the resurgence of iodine deficiency in China. Indeed, throughout the entire developing world there may be as many as two billion people at risk to iodine deficiency; perhaps three quarters of a billion have goiter, and ten million may be cretins. Even in developed countries, iodine deficiency is re-emerging (as in New South Wales in 19% of children) with the result of significantly reduced numbers of gifted children (though this is not cretinism per se). Certain to be of significant interest to a wide range of researchers, health providers and professionals, including government health administrators, this English translation of Endemic Cretinism is a major contribution to the literature.

The disorders induced by iodine deficiency affect at least one billion people. Because ofits effects on brain development, iodinedeficiency is the single most preventable cause of mental retardation in the world. Therefore, the United Nations and the Heads of State of almost all the world's countries represented at the Summit for Children in 1990 adopted resolutions to eradicate the disorders induced by iodine deficiency (IDD) by the year 2000. For geological and socio-economic reasons, most of the populations affected by iodine deficiency disorders live in isolated and usually mountainous areas, in pre industrialized parts ofthe world. The problem of iodine deficiency in Europe has been greatly underestimated in the last decades. After the remarkable studies on the effects of iodine deficiency and their prevention and correction in Switzerland, IDD was generally considered no longer a significant public health problem in Europe. However, surveys carried out in the early 1980's under the auspices of the European Thyroid Association, clearly demonstrated the persistence of moderately or even severely affected areas. These surveys also highlighted the lack ofinformation about large parts ofEurope, especially its eastern part. It is only quite recently, following major changes in international relations and thanks to the support of UNICEF, WHO, the International Council for the Control of Iodine Deficiency Disorders and the European Thyroid Association, that more extensive surveys have been conducted in several parts of Europe hitherto almost unexplored. These surveys showed that most European countries were iodine deficient.