Evaluating the role of salt intake in achieving WHO NCD targets in the Eurasian Economic Union: A PRIME modeling study.

The World Health Organization has set clear global targets in reducing non-communicable disease mortality by 2030 in its sustainable development goals. This study models the number of deaths that could be averted if Eurasian Economic Union (EEU) member states met the target of reducing their population's current mean salt intake by 30% to achieve mortality reduction targets. Using the WHO Preventable Risk Integrated ModEl (PRIME), we modelled the mortality impact of reducing salt consumption by 30%, as well as according to WHO recommended levels (5 g/person/day), for the five member states of the EEU. PRIME models the number of averted deaths from reducing salt intake by applying established risk ratios to a given population. The baseline demographic and mortality data that are required to generate these estimates were obtained from the relevant government statistical bodies, and salt intake data were referenced from surveillance studies. Uncertainty intervals were generated using Monte Carlo simulation. If salt consumption was reduced by 30%, we estimate that there would have been 94,150 (95%UI: 47,329 to 137,131) fewer deaths due to cardiovascular disease in the EEU in the baseline year, with males and the elderly being more affected. If the WHO-recommended maximum salt intake of 5 g/day was achieved, a total of 193,155 (95%UI: 98,548 to 272,536) deaths would have been prevented. These findings underline the importance of incorporating effective policy changes to meet targets in reducing NCD mortality by one-third by 2030.

Propylthiouracil, Perchlorate, and Thyroid-Stimulating Hormone Modulate High Concentrations of Iodide Instigated Mitochondrial Superoxide Production in the Thyroids of Metallothionein I/II Knockout Mice.

BACKGROUND: Increased oxidative stress has been suggested as one of the underlying mechanisms in iodide excess-induced thyroid disease. Metallothioneins (MTs) are regarded as scavengers of reactive oxygen species (ROS) in oxidative stress. Our aim is to investigate the effects of propylthiouracil (PTU), a thyroid peroxidase inhibitor, perchlorate (KClO4), a competitive inhibitor of iodide transport, and thyroid stimulating hormone (TSH) on mitochondrial superoxide production instigated by high concentrations of iodide in the thyroids of MT-I/II knockout (MT-I/II KO) mice. METHODS: Eight-week-old 129S7/SvEvBrd-Mt1(tm1Bri) Mt2(tm1Bri)/J (MT-I/II KO) mice and background-matched wild type (WT) mice were used. RESULTS: By using a mitochondrial superoxide indicator (MitoSOX Red), lactate dehydrogenase (LDH) release, and methyl thiazolyl tetrazolium (MTT) assay, we demonstrated that the decreased relative viability and increased LDH release and mitochondrial superoxide production induced by potassium iodide (100 µM) can be relieved by 300 µM PTU, 30 µM KClO4, or 10 U/L TSH in the thyroid cell suspensions of both MT-I/II KO and WT mice (P<0.05). Compared to the WT mice, a significant decrease in the relative viability along with a significant increase in LDH release and mitochondrial superoxide production were detected in MT-I/II KO mice(P<0.05). CONCLUSION: We concluded that PTU, KClO4, or TSH relieved the mitochondrial oxidative stress induced by high concentrations of iodide in the thyroids of both MT-I/II KO and WT mice. MT-I/II showed antioxidant effects against high concentrations of iodide-induced mitochondrial superoxide production in the thyroid.