POST TIME: 5 February, 2018 00:00 00 AM
Iodine deficiency disorders
Prof. Dr. Md. Shahidullah

Iodine deficiency disorders

Iodine is an essential component of thyroxine and triiodothyronine, the hormones synthesized by the thyroid gland. Iodine must be provided in the diet. Inadequate iodine intake leads to inadequate thyroid hormone production, and all the consequences of iodine deficiency stem from the associated hypothyroidism.

The term "iodine deficiency disorders" refers to all of the consequences of iodine deficiency. When severe iodine deficiency occurs during pregnancy, it is associated with fetal hypothyroidism, mental impairment, and increased neonatal and infant mortality. In adults, the most common manifestation is goiter that progresses to nodular goiter and eventually to hyperthyroidism.

In developing countries, iodine deficiency has been identified as one of the modifiable factors that have an adverse effect on child development. In our country, it is more common in the northern districts. It is also a global public health problem and, in combating it, emphasis should be placed on diagnosis and correction at the level of the community rather than the individual.

Iodine Requirements:

Iodide is essential for thyroid hormone synthesis. In order for the thyroid gland to synthesize adequate amounts of thyroxine, approximately 52 mcg of iodide must be taken up daily by the thyroid gland. Severe iodine deficiency develops when iodide intake is chronically less than 20 mcg/day.

Iodine can be obtained by consumption of foods that naturally contain it or to which it is added. Dietary sources include sea fish, sea foods, cod liver oil, vegetables, milk and milk products, meat, cereals, etc. Iodine content in the food depends on the iodine content in the soil where the crops are grown. Dietary iodine is absorbed as iodide and rapidly distributed in the extracellular fluid, which also contains iodide released from the thyroid and by extrathyroidal deiodination of the iodothyronines. Iodide leaves this pool by transport into the thyroid and excretion into the urine.

The World Health Organization (WHO) recommends 90 mcg of iodine daily for infants and children up to 5 years; 120 mcg for children 6 to 12 years, 150 mcg daily for children ≥12 years and adults and 250 mcg daily during pregnancy and lactation

Pregnant women require special attention because their renal threshold for iodine is lower, dietary salt (including iodized salt) is often restricted, and the needs of the fetus and the consequences of iodine deficiency to the fetus are greater.

Consequences of Iodine deficiency:

Diffuse and nodular goiter:

Goiter is the most obvious manifestation of iodine deficiency. Low iodine intake leads to reduced thyroxine and tri-iodothyronine production, which results in increased thyroid-stimulating hormone secretion.

The goiter is initially diffuse but eventually becomes nodular and over time, nodules can enlarge and undergo cystic degeneration, hemorrhage, and calcification. Therefore, in regions of iodine deficiency, children and adolescents generally have diffuse goiters, while adults who lived in conditions of longstanding iodine deficiency have nodular goiter. There is also an increased risk of follicular thyroid cancer in endemic goiter regions.


Hypothyroidism due to very low iodine intake is now extremely rare. Adults have the typical clinical manifestations of hypothyroidism and it is usually a goiter.

Iodine deficiency during pregnancy:

Iodine in the pregnant woman is required for full development of the fetus. For the first 12 weeks of gestation, the fetus is completely dependent upon maternal thyroxine. However, little hormone synthesis occurs until the 18th to 20th week. Thereafter, fetal thyroid secretion increases gradually.

Hypothyroidism during these critical periods of development and that which continues after the fetal thyroid develops in the setting of ongoing maternal iodine deficiency leads to permanent intellectual disability, which, in its most severe form, is known as cretinism.

There may be intrauterine death, spontaneous abortion as well.


 In addition to intellectual disability, cretinism is accompanied by other neurologic and somatic defects. Cretinism is characterized by intellectual disability, deaf mutism, gait disturbances, short stature, and hypothyroidism.


Subnormal intelligence, delayed motor milestones, mental deficiency, deafness, speech defects, strabismus, nystagmus- these can also be results of iodine


Prevention of Iodine


Action at community level:

Iodine deficiency is a global public health problem and, in combating it, emphasis should be placed on diagnosis and correction at the level of the community rather than the individual. Achieving sufficient iodine nutrition in the population would eliminate the need for specific supplementation during pregnancy and lactation.

Iodization of salt:

Iodization of salt is the preferred method of increasing iodine intake in a community. Salt iodination is legally mandated in many countries including Bangladesh. Iodization of salt in low cost is helped in Bangladesh by the UNICEF. Salt is a dietary necessity and often the only one that communities cannot provide for themselves. Adding iodine during the packaging or processing of salt is an efficient means for distributing iodine on a mass basis. It is technically easy and the cost is low.

Iodine can also be obtained by consumption of foods that naturally contain it. Sea fish, seafood, milk, dairy products and vegetables grown in iodine-sufficient soil are some examples of sources of iodine as mentioned earlier.n