The health effects of an insufficient iodine intake depend on the severity of the deficiency. The severity of iodine deficiency in the population can be classified on the basis of the median concentration of iodine in urine (see table).
WHO classification of iodine supply, based on excretion of iodine in urine
Median urinary iodine excretion
[micrograms/litre]
Iodine intake
Iodine supply
School aged children and adults
< 20
insufficient
severe iodine deficiency
20-49
insufficient
moderate iodine deficiency
50-99
insufficient
mild iodine deficiency
100-199
adequate
adequate iodine supply
200-299
above requirement
likely adequate intake for pregnant women and breastfeeding mothers, but may contain a slight risk of an intake that is more than sufficient for the entire population
≥ 300
excessive
Risk of adverse health effects (iodine-induced hyperthyroidism, autoimmune thyroid disorders)
Pregnant women
< 150
insufficient
150 - 249
adequate
250 - 499
above requirement
≥ 500
excessive
excessive means far above the amount needed to prevent and inhibit iodine deficiency
Breastfeeding mothers*
> 100
adequate
Infants <2 years
> 100
adequate
*Although breastfeeding mothers have the same requirement as pregnant women, the average adequate urine concentration is lower, as iodine is also excreted via breast milk. Modified in accordance with the World Health Organization (WHO, 2007).
Long-term insufficient supply of iodine can lead to an enlargement of the thyroid gland (goitre). This represents a physiological adaptation of the body in order to compensate for the chronic iodine deficiency with more hormone-producing tissue. Uniform enlargement is known as “diffuse goitre”, while growth with nodule formation is known as “nodular goitre”. In the so-called “cold nodules” the cells have given up their function and no longer produce thyroid hormones. The vast majority of cold nodules are benign, but in a very few cases they can also be malignant. Within so-called “hot” nodules, active or overactive cells produce too much hormone regardless of need (functional autonomy). “Hot” nodules are usually benign, but can cause a thyroid hyperfunction. This usually develops slowly and can be recognised by a drop in thyroid-stimulating hormone (TSH). A sudden, very high intake of iodine (well above the tolerable upper intake level of 500 μg/day) can lead to acutely triggered hyperthyroidism in individuals with existing functional autonomy, some of which may be undiagnosed. Functional autonomy particularly affects older people who were exposed to more severe iodine deficiency before the start of iodised salt prophylaxis.
Furthermore, chronic iodine deficiency can lead to an underactive thyroid gland with a reduced production of thyroid hormones in both adults and children (hypothyroidism). Slightly elevated TSH levels can be the first sign of this. Hypothyroidism can be accompanied by symptoms such as fatigue, weakness, reduced mental and physical performance, reduced basal metabolic rate with weight gain, slow heartbeat, dry and pale skin, brittle nails, apathy, concentration disorders, loss of appetite, constipation and depressive moods.
In children and adolescents, an underactive thyroid can result in delayed development in addition to reduced mental and physical performance. Studies have shown that treatment of mild to moderate iodine deficiency in children led to improved cognitive performances. Severe iodine deficiency during pregnancy increases the risk of miscarriages and stillbirths, and deformity. In children, it can result in dwarfism, deaf-muteness and delayed mental development (symptoms of so-called ‘cretinism’).
There is still insufficient research on the consequences of mild to moderate iodine deficiency during pregnancy. However, several studies show an association between mild iodine deficiency during pregnancy and decreased cognitive abilities in children.
The health effects of an insufficient iodine intake depend on the severity of the deficiency. The severity of iodine deficiency in the population can be classified on the basis of the median concentration of iodine in urine (see table).
WHO classification of iodine supply, based on excretion of iodine in urine
Median urinary iodine excretion
[micrograms/litre]
Iodine intake
Iodine supply
School aged children and adults
< 20
insufficient
severe iodine deficiency
20-49
insufficient
moderate iodine deficiency
50-99
insufficient
mild iodine deficiency
100-199
adequate
adequate iodine supply
200-299
above requirement
likely adequate intake for pregnant women and breastfeeding mothers, but may contain a slight risk of an intake that is more than sufficient for the entire population
≥ 300
excessive
Risk of adverse health effects (iodine-induced hyperthyroidism, autoimmune thyroid disorders)
Pregnant women
< 150
insufficient
150 - 249
adequate
250 - 499
above requirement
≥ 500
excessive
excessive means far above the amount needed to prevent and inhibit iodine deficiency
Breastfeeding mothers*
> 100
adequate
Infants <2 years
> 100
adequate
*Although breastfeeding mothers have the same requirement as pregnant women, the average adequate urine concentration is lower, as iodine is also excreted via breast milk. Modified in accordance with the World Health Organization (WHO, 2007).
Long-term insufficient supply of iodine can lead to an enlargement of the thyroid gland (goitre). This represents a physiological adaptation of the body in order to compensate for the chronic iodine deficiency with more hormone-producing tissue. Uniform enlargement is known as “diffuse goitre”, while growth with nodule formation is known as “nodular goitre”. In the so-called “cold nodules” the cells have given up their function and no longer produce thyroid hormones. The vast majority of cold nodules are benign, but in a very few cases they can also be malignant. Within so-called “hot” nodules, active or overactive cells produce too much hormone regardless of need (functional autonomy). “Hot” nodules are usually benign, but can cause a thyroid hyperfunction. This usually develops slowly and can be recognised by a drop in thyroid-stimulating hormone (TSH). A sudden, very high intake of iodine (well above the tolerable upper intake level of 500 μg/day) can lead to acutely triggered hyperthyroidism in individuals with existing functional autonomy, some of which may be undiagnosed. Functional autonomy particularly affects older people who were exposed to more severe iodine deficiency before the start of iodised salt prophylaxis.
Furthermore, chronic iodine deficiency can lead to an underactive thyroid gland with a reduced production of thyroid hormones in both adults and children (hypothyroidism). Slightly elevated TSH levels can be the first sign of this. Hypothyroidism can be accompanied by symptoms such as fatigue, weakness, reduced mental and physical performance, reduced basal metabolic rate with weight gain, slow heartbeat, dry and pale skin, brittle nails, apathy, concentration disorders, loss of appetite, constipation and depressive moods.
In children and adolescents, an underactive thyroid can result in delayed development in addition to reduced mental and physical performance. Studies have shown that treatment of mild to moderate iodine deficiency in children led to improved cognitive performances. Severe iodine deficiency during pregnancy increases the risk of miscarriages and stillbirths, and deformity. In children, it can result in dwarfism, deaf-muteness and delayed mental development (symptoms of so-called ‘cretinism’).
There is still insufficient research on the consequences of mild to moderate iodine deficiency during pregnancy. However, several studies show an association between mild iodine deficiency during pregnancy and decreased cognitive abilities in children.