Exploration of the safe upper level of iodine intake in euthyroid Chinese adults: a randomized double-blind trial.

BACKGROUND: The beneficial health effects associated with Universal Salt Iodization are well known. Yet, little is known about the possible adverse health effects in people with high iodine intake and the safe daily intake upper limit in the Chinese population. OBJECTIVE: The objective of this study was to explore the safe upper level of total daily iodine intake among adults in China. DESIGN: A 4-wk, double-blind, placebo-controlled, randomized controlled trial was conducted in 256 euthyroid adults. Participants were randomly assigned to 12 intervention groups with various iodine supplement doses ranging from 0 to 2000 µg/d. Total iodine intake included iodine from both supplements and diet. Multiple outcome measures were used to evaluate possible adverse effects, including thyroid function, thyroid size, and urinary iodine. RESULTS: The mean iodine intake from the diets and salt intake of the participants were 105 ± 25 and 258 ± 101 µg/d, respectively. In comparison with the placebo group, all iodide-supplemented groups responded with significant increases in median urinary iodine concentrations (P < 0.05) and in thyroid-stimulating hormone concentration (P < 0.05). Thyroid volume decreased after 4 wk in the high-iodine intervention groups (1500-2000 µg). Subclinical hypothyroidism appeared in the groups that received 400 µg I (5%) and 500-2000 µg I (15-47%). CONCLUSIONS: This study showed that subclinical hypothyroidism appeared in the participants who took the 400-µg I supplement, which provided a total iodine intake of ∼800 µg/d. Thus, we caution against a total daily iodine intake that exceeds 800 µg/d in China and recommend further research to determine a safe daily upper limit.

The impact of dietary iodine intake on lipid metabolism in mice.

The present study has been designed to investigate the impact of dietary iodine intake on lipid metabolism in mice, including iodine deficiency and iodine excess. Different amounts of iodine mixed in the drinking water were continuously administered to mice. The body weights and the levels of urinary iodine were measured 8 months after the treatment. Thyroid hormones in the serum were detected by chemiluminescence immunoassay. Serum total cholesterol (TC), triglyceride (TG), high-density lipoprotein cholesterol and low-density lipoprotein cholesterol (LDL-C) were determined enzymatically by automatic analyzer. Results showed that the urine iodine concentrations paralleled the amounts of iodine intakes. No statistical differences of body weights among different groups were found. The levels of thyroid hormones were dramatically decreased in iodine deficiency while no significant differences were found between iodine excess groups and normal iodine group. In iodine deficiency groups, the levels of TG, TC, and LDL were increased at varying degrees. In iodine excess groups, the levels of TG in the male mice and the levels of TC in the female mice were much lower than normal iodine group. In conclusion, dietary iodine intake may affect the metabolism of serum lipids. Hypothyroid function induced by iodine deficiency may be responsible for the changes of lipids. Higher iodine intake might benefit lipid metabolism.

[The effects of iodine/selenium on the function of antigen presentation of peritoneal macrophages in rats].

OBJECTIVE: To observe the effects of iodine/selenium on the function of antigen presentation of peritoneal macrophages in rats and explore the immunological mechanisms of iodine/ selenium's role in pathogenesis of autoimmune thyroid diseases (AITD). METHODS: Female Lewis rats were randomly divided into four groups including (1) low selenium and normal iodine group (L(sE)N(I)) (2) low selenium and high iodine group (L(Se)H(I)) (3) normal selenium and normal iodine group (N(Se)N(I) ) (4) normal selenium and high iodine group (N(Se)H(I)). All rats were fed by a special diet with lower selenium and iodine in it and drunk ion-free water containing different levels of iodine and selenium for 3 months. Peritoneal macrophages of each group and OVA allergized T cells were prepared and cultured together. Then the function of antigen presentation were estimated by detecting the levels of IL-2 in the culture supernatant. The levels of the expression of co-stimulator CD86 in the spleen of each group were determined by RT-PCR. RESULTS: The level of IL-2 in the supernatant in N(Se)H(I) (43.22 +/- 3.27) pg/ml was much stronger than N(Se)N(I) [the level of IL-2 was (25.74 +/- 2.45) pg/ml, P < 0.05]. The level of IL-2 in L(Se)N(I) (15.79 +/- 2.13) pg/ml was significantly lower than N(Se)N(I) (P < 0.05). The expression of CD86 mRNA in N(Se)H(I) (CD86/beta-actin: 0.52 +/- 0.10) were higher than N(Se)N(I) (CD86/beta-actin: 0.35 +/- 0.04), P < 0.05. CONCLUSIONS: High iodine could promote the presentation function of macrophages to a higher state than normal. Therefore, high iodine intake might become an importantly inducing factor in thyroid autoimmunity. Low selenium could weaken the ability of recognizing and presenting OVA antigen of peritoneal macrophages which might destroy immunological homeostasis and thus the low selenium intake might also become an inducer of AITD.

[Overdose of iodine on expression of CCK gene in rat brains].

OBJECTIVE: To observe the effect of overdose iodine on the expression of CCK gene in brains of rats and identify the possible mechanisms. METHODS: One-month weaning Wistar rats were randomly divided into five groups which were fed with normal feedstuff and water supplemented with different concentrations of potassium iodide, named A group (iodine ration was about 6.15 microg per day), B group (iodine ration was about 30.75 microg per day), C group (iodine ration was about 61.5 microg per day), D group (iodine ration was about 307.5 microg per day) and E group (iodine ration was about 615 microg per day). Rats were sacrificed after being fed for three or six months. Then serum thyroid hormones were measured by radioimmunoassay and the mRNA level of CCK gene was studied by using RT-PCR technique. RESULTS: At the end of three months, the values of thyroid hormones in E group [TT4 (45.2 +/- 13.7) nmol/L, TI'3 (0.65 +/- 0.20) nmol/L, FT3 (0.93 +/- 0.45) pmol/L, FT4 (7.07 +/- 2.43) pmol/L, rT3 (0.15 +/- 0.04) nmol/L] were all lower than those in A group [TT4 (76.0 +/- 18.8) nmol/L, TT3 (1.34 +/- 0.41) nmol/L, FT3 (2.45 +/- 0.62) pmol/L, FT4 (15.12 +/- 3.40) pmol/L, rT3 (0.24 +/- 0.04) nmol/L]. There were significant differences between E group and A group on the levels of serum TH (F values are 14.68, 16.03, 21.16, 20.25, 13.52 respectively, P < 0.01); FT3 levels in C and D groups were significantly decreased as compared to A and B groups (F = 21.16, P < 0.05). rT3 level in D group was significantly decreased compared with A,B and C groups (F = 13.52, P < 0.05). At the end of six months, the levels of serum TH in E group (TT4 (51.84 +/- 15.83) nmol/L, TT3 (0.77 +/- 0.22) nmol/L, FT4 (6.88 +/- 2.23) pmol/L, FT3 (0.74 +/- 0.28) pmol/L, rT3 (0.14 +/- 0.03) nmol/L) were lower than those in any other groups (F values were 6.05, 12.22, 11.25, 13.42, 5.89 respectively, P < 0.05). At the end of both three and six months, the mRNA levels of CCK gene in E group were lower than any other groups (F values were 4.04, 3.95 respectively, P < 0.01). The results of correlation analysis showed that serum FT4 had linear correlation with levels of CCK mRNA (r values were 0.990, 0.948 respectively; P < 0.05); However serum FT3 had no linear correlation with the levels of CCK mRNA (r values are 0.970, 0.932 respectively). CONCLUSIONS: Exposure to overdose of iodine (iodine ration was 100-fold higher than that of A group) could decrease the mRNA level of CCK gene. Compared with FT3, FT4 might have more important role on the regulation of CCK mRNA induced by excess of iodine.

[Study on content of iodine in food in Tianjin market and iodine nutrition conditions among college students].

OBJECTIVE: To know about content of iodine in foods sold in Tianjing markets presently, and the iodine nutrition conditions in college students. It was also aimed to probe the functions of the iodized salt complement with the dietary iodine intake, and whether the urine iodine could reflect dietary iodine intake. METHODS: 278 food samples in markets were collected by a randomly stratified sampling method, while the arsenic-cerium catalytic contact method was used to determine the content in food. The dietary information of students for seven days was recorded, and the urine iodine was determined through the arsenic-cerium catalytic spectrophotometry. RESULTS: The determination of 47 kinds and 278 food samples indicated that the content of iodine within animal foods (7.8 microg/100 g - 30.8 microg/100 g) was higher than that within plant foods (1.8 microg/100 g - 16.1 microg/100 g). The investigation also showed that students who regarded vegetarian food as principle accounted for 70. 19%. The amount of dietary iodine intake among those students, based on the dietary survey, was (111.67 +/- 53.18) microg/d, while supplementary iodine from iodized salt was about (230.27 +/- 45.55) microg/d. Therefore, the total iodine provided from diet would be (341.95 +/- 89.58) microg/d. Modified by urine creatinine, the median of urine iodine was 271.28 microg/gCr, and the urine iodine and dietary iodine intake was found positively related (r(s) = 0.463, P < 0.01). CONCLUSIONS: Regarding the vegetarian food as the principle, most of students investigated are not rich. The dietary iodine intake is lower than RDA (150 microg), but it can be obtained the iodized salt by 230. 27 microg, which is the possible supplement to the shortage from foods.

[Meta-analysis on the relationship between children's intelligence and factors as iodine deficiency, supplement iodine and excessive iodine].

OBJECTIVE: To estimate the role and extent of iodine deficiency, iodine supplement and iodine excess on mental development of children. METHODS: Meta-analysis was applied to study 128 independent items from 63 published and non-published papers and reports. The standards of references collected included: age of sample declared by references was 5 - 15; belong to comparison study; children lived in iodine deficiency disorders (IDD) and iodine excess areas; no difference of social economic and culture development level between the study group and the control group. RESULTS: Sixty-seven percent and 79% of the reports mainly involved severe IDD areas respectively. Hunter test of each studies, i.e. iodine deficiency, iodine supplement and excessive iodine group had not discovered statistic difference at the level of alpha = 0.05. The weighted average ES of damage affecting on children's intelligence by iodine deficiency achieved 0.69, which was equivalent to a marked drop in 10.4 IQ points [95% confidence interval (CI): 9.9 - 10.9] when comparing with the children living under non-IDD. The weighted average ES of protective effect on children's intelligence by iodine supplement reached 0.81, which meant that the IQ of children born after correction of iodine deficiency increased 12.2 points (95% CI: 11.5 - 12.9) in comparison with those born at least one year before the correction of iodine deficiency. Most of the references about the relationship between iodine excess and intelligence were gathered from proceedings, while the others were from journals. They location were in some areas of Shandong, Hebei, Shanxi and Inner Mongolia. The mean ES of the role of iodine excess on intelligence was 0.21, which was corresponding to 3.2 IQ points (95% CI: 2.5 - 4.0). CONCLUSION: 1) Iodine deficiency played a role of intermediate strength compared with other causes in delaying brain development making children to be at least 10 IQ points loss in IDD areas. 2) Effective iodine supplement plays a remarkable strengthening role in promoting brain development and can cause 12 IQ points increase for children who were born after the correction of iodine status. 3) Iodine excess has not shown significant important role in children's intelligence.