Iodine: Deficiency Signs and Symptoms

PRIMARY DEFICIENCY

Iodine deficiency results when iodide intake is <20 µg/day. In situations of moderate deficiency, TSH induces thyroid hypertrophy in order to concentrate iodide, resulting in a goitre. Most of these cases remain euthyroid, but in cases of severe iodine deficiency, myxoedema may result in adults and cretinism in infants, both of which are serious conditions.

Myxoedema is characterised by swelling of the hands, face, feet and peri-orbital tissues and can lead to coma and death if sufficiently severe and left untreated. Endemic cretinism is divided into two forms, neurologic or myxoedematous, depending on the interplay of genetics and iodine deficiency. Usually children with neurologic cretinism are mentally deficient and often deaf mute but of normal height and strength and may have goitre. Myxoedematous cretinism is characterised by dwarfism, mental deficiency, dry skin, large tongue, umbilical hernia, muscular incoordination and puffy facial features. Concomitant selenium deficiency may be a contributing factor in myxoedematous cretinism. Early treatment with thyroid hormone supplementation can promote normal physical growth; however, intellectual disability may not be prevented and in very severe cases death may ensue.

The term ‘iodine deficiency disorders’ (IDD) has been coined to refer to the collection of health problems that result from iodine deficiency, ranging from the mild and common (e.g. goitre) to severe and life threatening (e.g. cretinism and myxoedema).

Although severe iodine deficiency is rare in Australia and New Zealand, many parts of the world are well known for their low iodine levels. Countries where iodine deficiency is a primary concern include China, Latin America, South-East Asia and the eastern Mediterranean. A report conducted by the World Health Organization in 2005 found that while many countries had succeeded in reaching optimal iodine nutrition through enhanced monitoring and fortification programs over the past decade, an estimated 285 million school-age children and close to 2 million adults worldwide still suffer from iodine deficiency.

Fetal deficiency

The fetus depends solely on maternal thyroid hormones during the first trimester of pregnancy. From week 11 of gestation, thyroid hormone synthesis usually begins but remains dependent on the maternal provision of iodine. Consequently adequate functioning of both the maternal and the fetal thyroid glands plays a critical role in fetal neuropsycho-intellectual development. A range of studies has confirmed that ‘mild but measurable’ psychomotor deficits in early childhood are the potential sequelae of subclinical hypothyroidism and hypothyroxaemia caused by mild to moderate iodine deficiency in pregnancy.

Because of the severe neurological consequences of untreated congenital hypothyroidism, neonatal screening programs have been established in some developed countries.

SECONDARY DEFICIENCY

High consumption of goitrogens can induce a secondary deficiency state. Goitrogens are substances that inhibit iodine metabolism and include thiocyanates found in the cabbage family (e.g. cabbage, kale, cauliflower, broccoli, turnips and Brussels sprouts) and in linseed, cassava, millet, soybean and competing entities, such as other members of the halogen family (e.g. bromine, fluorine and lithium, as well as arsenic). Most researchers agree, however, that moderate intake of goitrogens in the diet is not an issue, except when accompanied by low iodine consumption. A very rare cause of secondary iodine deficiency and hypothyroidism isTSH deficiency.

Low selenium intake Low dietary intake of selenium is a factor that exacerbates the effects of iodine deficiency. Selenium is found in the thyroid gland in high concentrations, and while iodine is required for thyroid hormone synthesis, selenium-dependent enzymes are required for the peripheral conversion of thyroxine (T4) to its biologically active form triiodothyronine (T3), as well as the general recycling of iodine. Selenium deficiency results in decreased T4 catabolism, which leads to increased production of peroxide and thyroid cell destruction, fibrosis and functional failure.

Signs and Symptoms

MILD HYPOTHYROIDISM

This refers to biochemical evidence of thyroid hormone deficiency in patients who have few or no apparent clinical features of hypothyroidism.

CONGENITAL HYPOTHYROIDISM

According to Isselbacher (2005), the majority of infants appear normal at birth and < 10% are diagnosed based on clinical features:

  • prolonged jaundice
  • feeding problems
  • hypotonia
  • enlarged tongue
  • delayed bone maturation
  • umbilical hernia.

Importantly, permanent neurologic damage results if treatment is delayed.

ADULT HYPOTHYROIDISM

According to Beers (2005), the clinical signs of hypothyroidism in adults are:

  • weakness, tiredness and sleepiness
  • dry skin
  • cold intolerance
  • hair loss and diffuse alopecia
  • poor memory and difficulty concentrating
  • constipation
  • reduced appetite and weight gain
  • dyspnoea
  • hoarse voice
  • increased susceptibility to infectious diseases
  • increased susceptibility to cardiovascular diseases
  • paraesthesia
  • puffy hands, feet and face and peripheral oedema
  • impaired hearing
  • menorrhagia (later amenorrhoea)
  • carpal tunnel and other entrapment syndromes are common, as is impairment of muscle function with stiffness, cramps, and pain
  • reduced myocardial contractility and pulse rate, leading to a reduced stroke volume and bradycardia.