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close this bookThe Prevention and Control of Iodine Deficiency Disorders - Nutrition policy discussion paper No. 3 (UNSSCN, 1988, 130 p.)
close this folder1. INTRODUCTION
View the document(introduction...)
View the document1.1 WHAT IODINE DEFICIENCY DISORDERS ARE
View the document1.2 THE MECHANISM OF IODINE DEFICIENCY
View the document1.3 NATIONAL AND INTERNATIONAL PROGRAMMES TO CONTROL IODINE DEFICIENCY DISORDERS (IDD)

1.2 THE MECHANISM OF IODINE DEFICIENCY

Iodine deficiency causes depletion of thyroid iodine stores with reduced daily production of thyroid hormone (T-4). A fall in the blood level of T-4 triggers the secretion of increased amounts of pituitary thyroid-stimulating hormone which increases thyroid activity with hyperplasia of the thyroid. Increased efficiency of the thyroid iodine pump occurs, with faster turnover of thyroid iodine. This can be demonstrated by an increased thyroidal uptake of radioactive isotopes 1(131) and 1(125) (Hetzel and Maberly, 1986; Buttfield et al., 1966).

Iodine deficiency is demonstrated by determining urinary iodine excretion using either 24-hour samples or more conveniently, casual samples, to measure iodine per gram of creatinine (see Section 5). In general iodine intake in endemic goitre areas is well below 100 mcg per day, with the appearance of goitre at intake levels below 50 mcg (Stanbury and Hetzel, 1980; Clements et al., 1960; Pretell et al., 1972). The prevalence of goitre increases as iodine excretion falls, so that goitre may be almost universal at iodine intake levels below 10 mcg per day (Karmarkar et al., 1974).