OBJECTIVEWe aimed to evaluate goiter prevalence and iodine nutritional status in areas with high levels of water iodine; to monitor the prevalence of iodine deficiency disorders (IDD) in areas at high risk of IDD; and to compare the prevalence of goiter and urine iodine (UI) concentrations between children living in the two areas.

METHODSBased on surveillance from 2012-2014, we analyzed the concentration of UI and prevalence of goiter in 8-10-year-old children from 12 high-risk IDD provinces, and from 8 provinces and municipalities with excessive water iodine. We calculated goiter prevalence for each UI level according to World Health Organization (WHO) standards and constructed predictive prevalence curves.

RESULTSThe goiter prevalence and median UI of children from areas with high water iodine were not optimal, being above the WHO standards (5% and 100-199 μg/L, respectively), whereas those in high-risk areas fell within the standard. UI and goiter prevalence exhibited a U-shaped relationship in high-risk endemic areas and a parabolic relationship in areas of iodine excess.

CONCLUSIONIodine surplus in high-iodine areas leads to high goiter prevalence and UI. However, in high-risk areas, UI was optimal and goiter prevalence met the national criteria for IDD elimination.

Child ; China ; epidemiology ; Dose-Response Relationship, Drug ; Female ; Goiter ; epidemiology ; Humans ; Iodine ; administration & dosage ; deficiency ; urine ; Male ; Prevalence ; Risk Factors

OBJECTIVETo assess the effect of different levels of salt iodine content on thyroid volume (ThV) distribution using data from the 1999, 2011, and 2014 Chinese national iodine deficiency disorder (IDD) surveys.

METHODSProbability proportion to size (PPS) sampling method was used to obtain a representative national sample of 34,547, 38,932, and 47,188 Chinese children aged 8-10 years in 1999, 2011, and 2014 Chinese national IDD surveys, respectively. The iodine content in household iodized salt and urinary iodine concentration were measured and thyroid ultrasound examination was performed. The data were analyzed by SAS software using histograms and box plots. The skewness and kurtosis were calculated for testing the normality of ThV.

RESULTSThe median iodine content in household iodized salt dropped from 42.30 mg/kg in 1999 to 25.00 mg/kg in 2014. The median urinary iodine concentration of children aged 8-10 years decreased from 306.0 μg/L in 1999 to 197.9 μg/L in 2014. The median and interquartile range (IQR) of ThV in 1999, 2011, and 2014 surveys were 3.44 mL and 1.50 mL, 2.60 mL and 1.37 mL, 2.63 mL and 1.25 mL, respectively. The skewness and kurtosis of ThV distribution in 1999, 2011, and 2014 surveys were 1.34 and 5.84, 0.98 and 3.54, 1.27 and 5.49, respectively.

CONCLUSIONWith reduced salt iodization levels, the median urinary iodine concentration and median ThV of children decreased significantly, and the symmetry of the ThV distribution improved.

Child ; China ; Female ; Humans ; Iodine ; analysis ; deficiency ; Male ; Nutritional Status ; Sodium Chloride, Dietary ; analysis ; Thyroid Gland ; diagnostic imaging ; Ultrasonography

BACKGROUNDIodine deficiency is a major factor affecting thyroid auto-regulation, the quantity of iodine may greatly influence the synthesis of thyroid hormones (THs). It has long been believed that TH enters the cell through passive diffusion. Recent studies have suggested that several transporters could facilitate transportation of TH. The monocarboxylate transporter 8 (MCT8) was identified as a very active and specific TH transporter. The purpose of this study was to investigate whether iodine insufficient affected the expression of MCT8 in the thyroid gland.

METHODSSixty BALB/c mice were randomly divided into two groups: control group was fed with standard feed (iodine concentration of 300 µg/kg); while low-iodine (LI) group received iodine-insufficient feed (iodine concentration of 20-40 µg/kg). After 3 months, 10 mice of each group were sacrificed. The remaining 20 mice of each group were kept till 6 months. From the LI group, we randomly selected 15 mice and injected triiodothyronine (T3, 100 µg/kg body weight per day) intraperitoneally for 24, 48 or 72 hours (5 mice for each time-point). Then, all the mice were sacrificed. Mouse serum thyroxine (T4), T3, and thyroid-stimulating hormone (TSH) levels were determined by chemiluminescence immunoassay (CIA). The protein content or messenger RNA (mRNA) level of thyroid MCT8 was measured by Western blotting analysis or real time RT-PCR respectively. MCT8 subcellular location in thyroid tissues was probed with immunohistochemistry (IHC) assay.

RESULTSWe found that mouse serum T3 and T4 levels decreased and TSH level increased by the end of the third month. Consistent with these findings, there was significant goiter and hypothyroidism in the LI group. Meanwhile, the MCT8 mRNA increased to 1.36-fold of the level in the control group at the 3(rd) month. At 6(th) month, the serum T4 level in LI mice remained at a lower level, and MCT8 mRNA expression continued rising to nearly 1.60-fold compared with the control group. The protein content was also about 3 times higher than that in the control group. IHC results also revealed MCT8 was of higher expression and localized in the cytoplasm of thyroid follicular cells. After providing exogenous T3 to iodine deficient mice, the serum T3 and T4 gradually increased, whereas MCT8 mRNA and protein both started to decrease and returned to the same level as the control group.

CONCLUSIONThere is a compensatory increase in thyroid MCT8 expression to enhance its capability to transport TH from thyroid to the blood circulation in iodine deficient mice.

Animals ; Iodine ; deficiency ; Mice ; Mice, Inbred BALB C ; Monocarboxylic Acid Transporters ; genetics ; metabolism ; Thyroid Gland ; metabolism ; Thyrotropin ; blood ; Thyroxine ; blood ; Triiodothyronine ; blood

Child ; China ; epidemiology ; Goiter, Endemic ; epidemiology ; Humans ; Iodine ; deficiency ; Students

Iodine, an essential component of the hormones produced by the thyroid gland, is widely but unevenly distributed in the earth's environment. Great difference exists in the iodine nutritional status of populations residing in different region. Both iodine deficiency and iodine excess can injure the thyroid gland. Iodine deficiency tigers endemic goiter, cretinism, and hyperthyroidism, while iodine excess can result in high iodine goiter, chronic lymphocytic thyroiditis, iodine-induced hyperthyroidism, and hypothyroidism; also, iodine deficiency or excess may affect the histological type of thyroid cancer. In 1996, China began to implement the universal salt iodization policy, which has basically eliminated the iodine deficiency disorders nationwide; however, it also caused the changes in the spectra of other thyroid diseases including iodine-induced hyperthyroidism, autoimmune thyroid disease, and papillary thyroid carcinoma. Individualized iodine nutritional status assessment for the populations, particularly those with thyroid diseases, will be beneficial.
China ; epidemiology ; Humans ; Iodine ; administration & dosage ; adverse effects ; deficiency ; Sodium Chloride, Dietary ; adverse effects ; Thyroid Diseases ; epidemiology ; etiology

China ; Goiter, Endemic ; prevention & control ; Humans ; Iodine ; deficiency

OBJECTIVETo evaluate dietary iodine intake and its potential risks among the Chinese population.

METHODSIndividual dietary iodine intake was calculated using food consumption data multiplying by iodine concentration in foods, table salt and drinking water, followed by summing, and then compared with the corresponding age-specific reference values, including Upper Intake Level (UL) and Recommended Nutrient Intake (RNI).

RESULTSIn areas with water iodine concentration (WI) lower than 150 μg/L, 80.8% of residents had iodine intake between the RNI and UL, 5.8% higher than UL, and the remaining (13.4%) lower than RNI if iodized salt was consumed. However, in the uniodized salt consumption scenario, only 1.0% of residents between RNI and UL, 1.4% higher than UL, and a large part of residents (97.6%) lower than RNI. In areas with WI higher than 150 μg/L, all residents had iodine intake between RNI and UL if iodized salt was consumed, except 10.5% and 24.9% of residents higher than UL in areas with WI at 150-300 μg/L and higher than 300 μg/L respectively. However, in the uniodized salt consumption scenario, only 1.5% and 1.7% of residents had higher iodine intake than UL respectively.

CONCLUSIONThe findings suggested that in general, the dietary iodine intake by the Chinese population was appropriate and safe at the present stage. People in areas with WI lower than 150 μg/L were more likely to have iodine deficiency. While people in areas with WI higher than 150 μg/L were more likely to have excessive iodine intake if iodized salt was consumed.

Adolescent ; Child ; Child, Preschool ; China ; epidemiology ; Diet ; Drinking Water ; chemistry ; standards ; Female ; Goiter ; epidemiology ; prevention & control ; Humans ; Iodine ; administration & dosage ; analysis ; deficiency ; Male ; Nutritional Status ; Sodium Chloride, Dietary ; administration & dosage ; analysis

Adult ; Child ; China ; epidemiology ; Female ; Humans ; Iodine ; deficiency ; urine ; Male ; Thyroid Diseases ; epidemiology ; etiology

Adolescent ; Child ; China ; epidemiology ; Goiter, Endemic ; epidemiology ; Humans ; Iodine ; deficiency ; Rural Population ; Surveys and Questionnaires

OBJECTIVETo explore the effects of selenium and/or iodine deficiency on chondrocyte apoptosis in articular cartilage in rats.

METHODSForty-eight Sprague-Dawley rats were randomly divided into selenium deficiency group, iodine deficiency group, combined selenium and iodine deficiency group, and control group. Chondrocyte apoptosis was detected by terminal deoxynucleotidyl transferase biotin-dUTP nick end labeling (TUNEL) method, and Bcl-2 and Bax in articular cartilage were stained by immunohistochemistry in F3 generation of rats.

RESULTSIn articular cartilage, the positive rate of apoptotic chondrocytes stained by TUNEL in the upper and middle zones in selenium deficiency group, iodine deficiency group, and combined selenium and iodine deficiency group (all P < 0.05) were significantly higher than that in control group. The apoptotic chondrocytes were prominent in the middle zone. The positive percentage of chondrocytes apoptosis was not significantly different among these three groups (P > 0.05). Compared with the control group, the expressions of both Bcl-2 and Bax were significantly higher in the upper and middle zone in the selenium deficiency group, iodine deficiency group, and combined selenium and iodine deficiency group (all P < 0.05); however, the expressions of Bcl-2 and Bax were not significantly different among these three groups (P > 0.05).

CONCLUSIONSelenium and/or iodine deficiency may induce chondrocyte apoptosis.

Animals ; Apoptosis ; Cartilage, Articular ; metabolism ; pathology ; Chondrocytes ; metabolism ; pathology ; Female ; Iodine ; deficiency ; Male ; Rats ; Rats, Sprague-Dawley ; Selenium ; deficiency