Activity dependence of cortical axon branch formation: a morphological and electrophysiological study using organotypic slice cultures.

This paper reviews evidence suggesting that iodine deficiency can have deleterious effects on the cardiovascular system, and correspondingly, that a higher iodine intake may benefit cardiovascular function. In recent years, public health bodies have aggressively promoted sodium restriction as a means of reducing hypertension and the risk of cardiovascular disease. These inducements have led to a general decline in iodine intake in many developed countries. For example, a United States national health survey conducted in the early 1970s observed that 1 in 40 individuals had urinary iodine levels suggestive of moderate or greater iodine deficiency; twenty years later, moderate to severe iodine deficiency was observed in 1 in 9 participants. Regional iodine intake has been shown to be associated with the prevalence of hypothyroidism and hyperthyroidism, where autoimmune hypothyroidism is the more common of the two in regions with moderate to high iodine intake. Both of these thyroid abnormalities have been shown to negatively affect cardiovascular function. Selenium, an important antioxidant in the thyroid and involved in the metabolism of iodine-containing thyroid hormones, may play an interactive role in the development of these thyroid irregularities, and in turn, cardiovascular disease. Iodine and iodine-rich foods have long been used as a treatment for hypertension and cardiovascular disease; yet, modern randomized studies examining the effects of iodine on cardiovascular disease have not been carried out. The time has come for investigations of sodium, hypertension, and cardiovascular disease to also consider the adverse effects that may result from mild or greater iodine deficiency.