More than adequate or excessive iodine intake may lead to hypothyroidism and autoimmune thyroiditis.

Subjects who were TPOAb and TgAb positive at baseline developed thyroid dysfunctions more frequently than seronegative subjects. High iodine intake was a risk factor for developing hypothyroidism in antibody-positive subjects. A constant exposure to excessive iodine intake increased the incidence of positive TgAb.

BackgroundObstructive sleep apnea syndrome (OSAS) has been indicated to contribute to the development of cardiovascular disease; however, the underlying mechanism remains unclear. This study aimed to test the hypothesis that OSAS may be associated with cardiovascular disease by elevating serum levels of inflammatory markers and causing arterial stiffening and endothelial dysfunction.Methods and ResultsRelated scientific reports published from January 1, 2006, to June 30, 2015, were searched in the following electronic literature databases: PubMed, Excerpta Medica Database, ISI Web of Science, Directory of Open Access Journals, and the Cochrane Library. The association of OSAS with serum levels of inflammatory markers, endothelial dysfunction, and arterial stiffening were investigated. Overall, 18 eligible articles containing 736 patients with OSAS and 424 healthy persons were included in this meta‐analysis. Flow‐mediated dilation in patients with moderate–severe OSAS was significantly lower than that in controls (standardized mean difference −1.02, 95% CI −1.31 to −0.73, P<0.0001). Carotid‐femoral pulse wave velocity (standardized mean difference 0.45, 95% CI 0.21–0.69, P<0.0001), augmentation index (standardized mean difference 0.57, 95% CI 0.25–0.90, P<0.0001), and serum levels of high‐sensitivity C‐reactive protein and C‐reactive protein (standardized mean difference 0.58, 95% CI 0.42–0.73, P<0.0001) were significantly higher in patients with OSAS than in controls.Conclusion OSAS, particularly moderate–severe OSAS, appeared to reduce endothelial function, increase arterial stiffness, and cause chronic inflammation, leading to the development of cardiovascular disease.

Iodine nutrition is an important factor associated with TSH concentration even in the rigorously selected reference population. Baseline TSH of 1.0-1.9 mIU/l is an optimal interval with the lowest incidence of abnormal TSH in 5 years.

The relationship between iodine and the risk for the occurrence of diffuse goiter shows a U-shaped curve. Nodular goiters are more prevalent in iodine-deficient areas.

Inhibition of miRNA-124 exerts neuroprotection on spinal cords against ischemia-reperfusion injury, possibly by induction of mitophagy and antiapoptotic effects.

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To explore the association of sleep patterns with bone mineral density (BMD) in pre- and post-menopausal women, we used a questionnaire to evaluate the sleep patterns and performed calcaneal quantitative ultrasound to estimate BMD, in 6,510 women aged 40 years or older, from June to November 2011 in Nanjing City. We found a 1.7-fold risk of osteoporosis in post-menopausalwomen with bedtime of ≥0:00 am (OR = 1.69, 95 % CI 1.39-2.13), compared to those whose bedtime of <0:00 am. post-menopausalwomen with excessive total sleep (>10 h vs. 8-9 h, OR = 1.54, 95 % CI 1.05-2.02) were shown to have a higher risk of osteoporosis, however, this high risk was not detected in those with excessive nocturnal sleep (>10 h vs. 8-9 h, OR = 0.85, 95 % CI 0.62-1.30). By contrast, post-menopausalwomen with inadequate nocturnal sleep (≤7 h vs. 8-9 h, OR = 1.68, 95 % CI 1.32-2.75), excessive daytime sleep (≥180 min vs. 0 min, OR = 1.52, 95 % CI 1.08-2.13), and noontime nap (>60 min vs. 0 min: OR = 1.37, 95 % CI 1.06-1.76) were demonstrated to have higher risk of bone loss. Nevertheless, these associations were not found in premenopausal women. We conclude that delayed bedtime, nocturnal sleep deprivation, excessive daytime sleep, and noontime nap, but not reduced total sleep duration, could promote bone loss in post-menopausalwomen, which might be related to circadian rhythm disturbances. However, they have limited influences to BMD in women who were still in menstruating. Mechanism responsible for the phenomena warrants further investigation.