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Mildly deficient iodine intake

MAI More than adequate iodine intake MDI Mildly deficient iodine intake... [Pg.1213]

In 1999, three representative rural communities with different levels of iodine intake were chosen for the study Panshan - a community with long-term mildly deficient iodine intake (MDI) level Zhangwu - a community with more than adequate iodine intake (MAI) level whose iodine status shifted from mild deficiency due to USI and Huanghua - a community with El owing to the... [Pg.1213]

In the most simplistic physiological model, inadequate intake of iodine results in a reduction in thyroid hormone production, which stimulates increased TSH production. TSH acts directly on thyroid cells, and without the ability to increase hormone production, the gland becomes hyperplastic. In addition, iodine trapping becomes more efficient, as demonstrated by increased radioactive iodine uptake in deficient individuals. However, this simplistic model is complicated by complex adaptive mechanisms which vary depending on the age of the individual affected. In adults with mild deficiency, reduced intake causes a decrease in extrathyroidal iodine and reduced clearance, demonstrated by decreased urinary iodine excretion, but iodine concentration in the gland may remain within normal limits. With further reduction in intake, this adaptive mechanism is overwhelmed, and the iodine content of the thyroid decreases with alterations in iodination of thyroglobulin, in the ratio of DIT to MIT, and reduction in efficient thyroid hormone production. The ability to adapt appears to decrease with decreasing age, and in children the iodine pool in the thyroid is smaller, and the dynamics of iodine metabolism and peripheral use more rapid. In neonates, the effects of iodine deficiency are more directly reflected in increased TSH. Diminished thyroid iodine content and increased turnover make neonates the most vulnerable to the effects of iodine deficiency and decreased hormone production, even with mild deficiency. [Pg.239]

Urinary Iodine Excretion (UIE) provides the best single measurement of iodine intake of the population and Should be used for initial and follow up assessment. For epidemiological studies, population and not individual levels are is required. To achieve this 40 casual samples from a particular group can be collected (may be collected from schoolchildren at the same time as the goiter is assessed). The values are expressed as a median. Median UIE in the population below 100 pg/1 indicate iodine deficiency. Thus median UIE 10 pg/1 means no deficiency, 50-99 pg/1 indicates mild, 20 9 pg/1 moderate, and <20 pg/1 severe IDD. [Pg.765]

The complexity of the interaction between iodine intake and autoimmune thyroid disease has been highlighted by reports of evidence that iodide (compared with thyroxine) induces thyroid autoimmunity in patients with endemic (iodine deficient) goiter (43), while in those with pre-existing thyroid autoimmunity, evidenced by the presence of antithyroid (thyroid peroxidase) antibodies, administration of iodine in an area of mild iodine deficiency led to subclinical or overt hypothyroidism (44). [Pg.319]

Hyperthyroidism and toxicity Iodine-induced hyperthyroidism A mild increase in the incidence of hyperthyroidism worldwide has been described following iodized salt programs (Connolly et al. 1970, Stewart et al. 1971, Bauch 1985, Koutras etal. 1999, Joseph 1989, Meng etal. 1989, Lobbers etal. 1989, Pickardt 1989). Joseph et al. (1980) reported that iodine intakes of < 100 xg per day pose no risk for patients with autonomous tissue due to iodine deficiency critical amounts are between 100 and 200 jg I per day. The absence of iodine deficiency in the Japanese population accounts for the absence of iodine-induced thyrotoxicosis (Nagataki 1987). Hyperthyroidism is easily controlled with antithyroid drugs. [Pg.1485]

In mild and moderate iodine deficiency, endemic cretinism is not observed. However, in a population there is a certain spread of iodine intake, and women at the lower end of the range of iodine intake may still be at risk of insufficient iodine intake during pregnancy. Deficiency of other nutrients and intake of goitrogens from food or from tobacco smoking may increase the risk. [Pg.449]

Over the years, people living with iodine deficiency tend to develop multifocal thyroid autonomy, and multinodular toxic goiter is a common cause of hyperthyroidism. The difference in relative distribution of the four most common causes of hyperthyroidism in Iceland, with high iodine intake, and Judand, Denmark, with mild-to-moderate iodine deficiency, is shown in Figure 47.3. In Iceland, Graves ... [Pg.450]

Figure 47.3 Nosological types of hyperthyroidism with different iodine intake levels. Relative frequency of the four most common nosological types of hyperthyroidism in Iceland, with relatively high iodine intake from consumption of fish and high iodine content of dairy products, and from East Jutland, Denmark, with mild-to-moderate iodine deficiency. MNTG, multinodular toxic goiter GD, Graves disease STA, solitary toxic thyroid adenoma SAT, subacute thyroiditis. Data from Laurberg et al., (1991). Figure 47.3 Nosological types of hyperthyroidism with different iodine intake levels. Relative frequency of the four most common nosological types of hyperthyroidism in Iceland, with relatively high iodine intake from consumption of fish and high iodine content of dairy products, and from East Jutland, Denmark, with mild-to-moderate iodine deficiency. MNTG, multinodular toxic goiter GD, Graves disease STA, solitary toxic thyroid adenoma SAT, subacute thyroiditis. Data from Laurberg et al., (1991).
A similar finding of more subclinical hypothyroidism with abundant iodine intake compared with mild iodine deficiency was reported in nursing home residents living in Hungary (Szabolcs et al, 1997). In China, people having excessive iodine intake from a combination of high groundwater... [Pg.451]

In Denmark, we studied the incidence of overt hypothyroidism before the Danish iodine program in two areas with a small difference in iodine intake caused by different iodine contents of groundwater. The population hv-ing in the area with only mild iodine deficiency had a considerably higher incidence of overt hypothyroidism than the population with moderate iodine deficiency, whereas the lower iodine intake was associated with more hyperthyroidism (Figure 47.5) (Billow Pedersen et aL, 2002). Subtyping of disease revealed that the difference in hypothyroidism was caused by 50% more cases of spontaneous autoimmune hypothyroidism in the area with the highest iodine intake (Carld et ai, 2006). [Pg.452]

Taken together, these studies may suggest that any increase in iodine intake of a population living with mild-to-moderate iodine deficiency may be associated with an increase in the occurrence of hypothyroidism in the population. The higher the iodine intake, the more cases of hypothyroidism will develop. [Pg.452]

The World Health Organization (WHO), the United Nations International Childrens Emergency Fund (UNICEF), and the International Council for Control of Iodine Deficiency Disorders (ICCIDD) have defined three degrees of severity of iodine deficiency mild (iodine intake of 50—99p,g/day), moderate (20 9 p,g/day), and severe (<20p,g/day) (WHO/UNICEF/ICCIDD, 1994). Severe iodine deficiency was eradicated from many parts of the world, but milder forms stiU exist and may escape detection. Thirty-two European countries were still affected by mild-to-severe iodine deficiency in the late 1990s (Delange, 2002). Turkey is one of these mild-to-moderate iodine-deficient areas (Yordam et ai, 1999). [Pg.626]

In the same group of women, the incidence of hyperthyroidism was 1.3 cases/1000/year and of hypothyroidism 1.0 cases/1000/year. These data can be compared to data from studies from Denmark (Laurberg et ai, 2006), which show that only a small difference in iodine intake is associated with a large difference in incidence of overt hyper- and hypothyroidism. Thus, the incidence rate of hyperthyroidism for women in a region with moderate iodine deficiency (urinary iodine 45 lig/1) was higher than in a region with mild iodine deficiency (urinary iodine 61pg/l) 1.5 cases/1000/year compared to 1.0 cases/1000/year. In... [Pg.767]

Urinary iodine concentration and palpation of goiter among schoolchildren is the most frequent method used by cross-sectional surveys to measure iodine deficiency. Because iodine is excreted by the kidneys, the urinary concentration of iodine is an indicator of iodine intake. Lower production of thyroxine leads to increased production of the thyroid-stimulating hormone, which results in thyroid hyperplasia known as goiter. The World Health Organization (2001) classifies iodine deficiency into mild, moderate and severe when urinary excretion is, respectively, 50—99, 20 9 and <20 p,g/l of urine. [Pg.779]

The two most recent NHANES surveys showed that for women of childbearing age and pregnant women, the median UI excretion levels were adequate (127 and I4lpg/1, respectively, in 1988-1994 132 and 173 pg/1, respectively, in 2001-2002) (Table 115.3) (Caldwell et al., 2005). Thyroid hormone, requiring adequate iodine intake, is critical for neural development in utero and in early life. Although cretinism due to iodine deficiency is not a problem in the United States, subtle developmental delays could result from mild maternal iodine deficiency. [Pg.1132]

Teng et al. (2006) explored the effect of iodine intake on thyroid diseases in China. Baseline characteristics of three populations were estabfished in three communities in 1999 and then again 5 years later. The communities had different levels of iodine nutrition mild deficiency more than adequate and excessive intake. Salt iodization had been implemented in China in 1996. In the general population, median UI increased from 165 pg/1 in 1995 to approximately 300 pg/1 in 1999. The concern was with oversupplementation of iodine to a level that is more than adequate, in a region in which iodine intake was previously mildly deficient, which in turn may accelerate the development of subclinical hypothyroidism to overt hypothyroidism. High levels of iodine intake may increase the incidence and prevalence of autoimmune thyroiditis, making it imperative to tailor supplementation needs to each region. [Pg.1134]

The assessment of iodine intake and status is important in elderly subjects. Mild-to-moderate iodine deficiency is associated with a high incidence and prevalence of goiter and nodular hyperthyroidism in middle-aged and elderly subjects (Laurberg et ai, 1991 Pedersen et ai, 2002). In populations with high iodine intake, there is an increased risk of hypothyroidism, especially among... [Pg.1139]

Notes-. Iodine intake expressed as iodine dietary intake and urinary iodine excretion in elderly males (M) and females (F). The early Danish surveys indicate mild-to-moderate iodine deficiency, even among users of dietary supplements. The 68-year-old Danes were also compared to elderly subjects in Iceland with a long-standing relatively high iodine intake. After the mandatory fortification of salt in 2000-2001, the Danish National Survey 2002 indicates a sufficient iodine intake among elderly subjects. N, numbers 7-D R, 7-days food record FFQ, food frequency questionnaire. [Pg.1141]

There were no statistically significant differences P > 0.05) between urinary iodine concentration when data were adjusted for sex and region, except for the group of children with mild iodine deficiency, between boys with more than adequate iodine intake and between girls with excessive iodine intake P < 0.05) (Figure 120.5). [Pg.1173]

Figure 125.2 The cumulative incidence of supranormai thyrotropin levels among subjects with euthyroidism and high levels of TPO antibody or thyrogiobuiin antibody iodine intake was mildly deficient in Panshan, more than adequate in Zhangwu, and excessive in Huanghua. The cumulative incidence increased with increasing iodine intake. Figure 125.2 The cumulative incidence of supranormai thyrotropin levels among subjects with euthyroidism and high levels of TPO antibody or thyrogiobuiin antibody iodine intake was mildly deficient in Panshan, more than adequate in Zhangwu, and excessive in Huanghua. The cumulative incidence increased with increasing iodine intake.
Figure 125.5 Levels of thyrotropin in euthyroid subjects from three communities with different levels of iodine intake. In the baseline study, we separated out 228 persons (6.1% of 3761 participants) who reported a family history of thyroid diseases, 126 persons (3.4%) who reported a personal history of thyroid disorders, 511 persons (13.6%) with high serum autoantibody values, and 1155 persons (30.7%) who had goiter and/or nodules and/or abnormal echo patterns in thyroid ultrasonography, leaving a sample group of 2237 individuals (636 in Panshan, 855 in Zhangwu, 743 in Huanghua) who composed the reference population. It was clearly shown that there was a urinary iodine-related increment of serum TSH levels (r = 0.21, P = 0.000). The median levels of TSH in the reference populations from Panshan (mild iodine deficiency), Zhangwu (more than iodine adequacy) and Huanghua (iodine excess) were 1.22, 1.41, and 1.99mlU/l, respectively (P = 0.000). Figure 125.5 Levels of thyrotropin in euthyroid subjects from three communities with different levels of iodine intake. In the baseline study, we separated out 228 persons (6.1% of 3761 participants) who reported a family history of thyroid diseases, 126 persons (3.4%) who reported a personal history of thyroid disorders, 511 persons (13.6%) with high serum autoantibody values, and 1155 persons (30.7%) who had goiter and/or nodules and/or abnormal echo patterns in thyroid ultrasonography, leaving a sample group of 2237 individuals (636 in Panshan, 855 in Zhangwu, 743 in Huanghua) who composed the reference population. It was clearly shown that there was a urinary iodine-related increment of serum TSH levels (r = 0.21, P = 0.000). The median levels of TSH in the reference populations from Panshan (mild iodine deficiency), Zhangwu (more than iodine adequacy) and Huanghua (iodine excess) were 1.22, 1.41, and 1.99mlU/l, respectively (P = 0.000).

See other pages where Mildly deficient iodine intake is mentioned: [Pg.317]    [Pg.1896]    [Pg.55]    [Pg.61]    [Pg.66]    [Pg.347]    [Pg.371]    [Pg.419]    [Pg.469]    [Pg.491]    [Pg.559]    [Pg.565]    [Pg.575]    [Pg.682]    [Pg.802]    [Pg.874]    [Pg.1061]    [Pg.1077]    [Pg.1129]    [Pg.1140]    [Pg.1145]    [Pg.1153]    [Pg.1213]    [Pg.1214]    [Pg.1216]   
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