Iodine deficiency prevalence

In Mexico, Villalpando et al. (2003) mentioned that information from the 1999 Mexican National Nutrition Survey showed that iodine deficiency prevalence was negligible in both women and children. They also emphasized that abnormal distribution results were so scattered that no observation could be made regarding geographical distribution. On the contrary, in the same survey, ID in preschoolers between 12 and 24 months was as high as 67%, 50% of which were anemia related, whereas in schoolchildren it was around 35%. 

WHO/UNICEF/ICCIDD (1991) Global prevalence of iodine deficiency disorders. Micronutrient Deficiency Information System Working Paper No. I. Geneva, WHO... 

Countries affected by iodine deficiency require to develop national programmes to assess the extent and severity of the problem. Once an IDD control programme is initiated monitoring and evaluation are required. There are three major components needed to meet this goal, namely determination of thyroid size and goitre prevalence, the determination of urinary iodine excretion, and the measurement of thyroid function, including serum TSH levels. 

Hypothyroidism, a condition in which the circulating concentrations of thyroid hormones are too low, is the most prevalent thyroid disease. Primary hypothyroidism, the commonest form, is an autoimmune disease (Hashimoto s thyroiditis) often associated with goitre. Like other autoimmune diseases, it is more prevalent in women (4 per 1000) than in men (1 per 1000). Other causes include thyroidectomy, radioac tive ablation and, in some countries, iodine deficiency. Hypothyroidism can also be caused by several drugs, including lithium, interleukin-2 and interferon. Secondary hypothyroidism is a disease caused by decreased secretion of TSH by the pituitary. 

Because of reports of severe hyperthyroidism after the introduction of iodized salt in two severely iodine-deficient African counties (Zimbabwe and the Democratic Republic of the Congo), a multicenter study has been conducted in seven countries in the region to evaluate whether the occurrence of iodine-induced hyperthyroidism after the introduction of iodized salt was a generalized phenomenon or corresponded to specific local circumstances in the two affected countries (46). Iodine deficiency had been successfully eliminated in all of the areas investigated and the prevalence of goiter had fallen markedly. However, it was clear that some areas were now exposed to iodine excess as a result of poor monitoring of the quality of iodized salt and of the iodine intake of the population. In these areas, iodine-induced hyperthyroidism occurred only when iodized salt had been recently introduced. 

Some degree of iodine dietary deficiency was estimated to affect 750 million people in the developing world in 1990 with around 10 million were suffering from stunted growth and mental retardation. In 1993 the WHO published a database of iodine deficiency based on the number of goitre victims in 121 countries where the element was in short supply. This shortage was most prevalent where soils have suffered repeated glaciations or heavy rainfall which had removed most of the iodide that may once have been present, because this is a particularly soluble material and so easily washed away. Those most at risk lived in India and China. 

Another example of a maternal condition that contributes to birth defects is low circulating iodine. Cretinism is one of the most profound, but completely preventable, syndromes of malformation known. Characteristic consequences of prenatal iodine deficiency include pervasive mental and physical retardation, deaf-mutism (due to primary malformation of the inner ear), lack of muscle tone with a spastic or rigid walk, and failure to attain a height at maturity of more than 1 m. Today, this condition (known as endemic cretinism) is most prevalent in impoverished areas of African and East Asian countries. Prior to implementation of a national program of iodized salt in the early part of the twentieth century, endemic cretinism was commonplace in Switzerland. After institution of iodized salt, deaf-mutism declined 50% within 8 years and no cretins have been born in that country since 1930. 

Relatively few studies have examined environmental influences on the development of autoantibodies. A complex relation is seen between dietary iodine and prevalence of antithyroid antibodies, with increased prevalence reported in relation to iodine deficiency and to excess intake. This issue is discussed in greater detail in section 8.10 on iodine. 

Iodine in minute quantity is a normal constituent of the human body and the average person requires a daily dose of 0 000,017 gm. Absence of the requisite amount leads to general debility and in more severe cases to goitre or big-neck . In very severe cases mental weakness develops known as cretinism, from Latin creta, chalk, because of its prevalence in Alpine districts. In Switzerland sodium iodide is added to table salt by legal regulation to ensure that everybody receives his necessary ration of iodine. In Britain there are several areas of iodine deficiency in the soil and addition of iodides to the feeding-stuffs of cattle, etc, effects an enormous improvement in the herds. 

In areas of the world in which the soil is deficient in iodide, hypothyroidism is prevalent. The thyroid gland enlarges (forms a goiter) in an attempt to produce more thyroid hormone. In the United States, table salt (NaCI) enriched with iodide (iodized salt) is used to prevent hypothyroidism caused by iodine deficiency. 

The thyroid gland is the only part of the body that absorbs iodine. Thyroid cells use iodine to produce thyroid hormones, which regulate metabolism. Low levels of iodine in the diet can lead to thyroid-hormone deficiencies and goiters, which are enlarged thyroid glands. In serious cases, low levels of thyroid hormones can cause birth defects and brain damage. In the United States, potassium iodide is added to most table salt to protect against dietary iodine deficiency. Even small amounts of added iodine can prevent iodine-deficiency disorders. However, there are parts of the world in which iodine deficiency is still prevalent. 

Gastric cancer, as well as thyroid disease, is more prevalent in areas of iodine deficiency. 

Based on such evidence on iodine-induced disease in individual patients, it would be expected that an increase in population iodine intake would lead to an increase in the incidence and prevalence of certain thyroid disorders. To evaluate this in more detail, and to obtain information on the level of iodine intake where such an increase will take place, epidemiological studies are necessary. As shown in Table 47.1 there is evidence to suggest that a number of abnormalities may be more common when iodine intake becomes high. However, in general the evidence is less strong, compared with the evidence for less disease with eradication of iodine deficiency (Table 47.1), and the sum of burdens is lower (Figure 47.1). 

In a population-based study of 68-year-old people living in Iceland and in Jutland, subclinical hypothyroidism was much more prevalent in Iceland, with sufficient to excessive iodine intake, than in an area of Jutland, with moderate iodine deficiency (Figure 47.4) (Laurberg et al., 1998). Subclinical hyperthyroidism was much more common in Jutland, as discussed above (Figure 47.4). 

Figure 47.4 Serum TSH (mU/l) below and above reference in 68-year-old people from fhe populafion in Iceland and in East Jutland. Prevalence rates of fhyroid hyperfuncfion wifh serum TSH below fhe reference range and fhyroid hypofunction with TSH above the TSH reference range (0.4-4.0mU/l) in 68-year-old people living in Iceland wifh relatively high iodine intake and in Jutland with moderate iodine deficiency. Dafafrom Laurberg etal., (1998).

Iodine deficiency with impairment of thyroid hormone production may have severe consequences. To compensate for the low iodine supply that was previously highly prevalent in the world, complex mechanisms have been developed in the thyroid gland. On the one hand, mechanisms are able to accumulate and utilize even very small supplies of iodine. On the other hand, the thyroid immediately reacts to a sudden load of iodine to avoid overproduction of thyroid hormone. As usual when complex mechanisms are involved, this leads to a risk of malfunction — and disease. To minimize such a risk at the level of the population, iodine intake is best kept within a relatively narrow range around the recommended level. 

Until the 1990s, total goiter prevalence (TGP) in school-age children was the primary indicator for the assessment of functional consequences of iodine deficiency in the population (WHO et al., 2001). Thyroid size was traditionally determined by palpation, but the reliability of this method is limited by high inter-observer and intra-observer variations. The measurement of thyroid size by ultrasound has therefore been an important step in the detection of mild-to-moderate iodine deficiency. International reference values for normal thyroid size are now available from iodine-sufficient children (Zimmermann et al., 2004). Because TGP is not a sensitive indicator of recent changes in iodine status in the... 

The estimate of the current worldwide iodine deficiency situation is based primarily on UI data. However, TGP is also included in order to compare prevalence figures to previous estimates. The most recent estimates for both indicators utilized several types of data in the time frame of 1993—2003, but prioritized recent data (1998—2003). Thus, data were selected as follows recent national surveys (1998—2003) recent subnational data (1998—2003) older national surveys (1993—1997) and older subnational data (1993—1997). When subnational data were utilized, surveys within the time frame were combined and weighted by the sample size of each survey. Data for school-age children were prioritized. In the absence of data for this group, data from the next closest population groups were utilized as follows children closest to school-age adults the general population preschool-age children and other population groups. The estimates utilized 2002 UN population estimates to determine the number of individuals affected (United Nations Population Division, 2003). 

If compared to 1993 estimates, the current TGP data suggest that there is an overall increase of 31.7% in goiter prevalence throughout the world. The prevalence increased in the WHO regions of Africa, the Eastern Mediterranean, Europe and Southeast Asia, but decreased in the Americas and the Western Pacific (Figure 48.1). However, these data must be interpreted with much caution, as TGP does not reflect recent changes in iodine intake. Furthermore, the majority of the available TGP data in the time span of 1993—2003 were collected before 1998 — a time when many programs of iodine deficiency control had not yet been implemented (WHO et ai, 1993). 

---