https://www.thelancet.com/pdfs/journals/landia/PIIS2213-8587(14)70225-6.pdf

Iodine deficiency and thyroid disorders

Nitric oxide (NO) is a key redox-active, small molecule involved in various aspects of plant growth and development. Here, we report the identification of an NO accumulation mutant, nitric oxide excess1 (noe1), in rice (Oryza sativa), the isolation of the corresponding gene, and the analysis of its role in NO-mediated leaf cell death. Map-based cloning revealed that NOE1 encoded a rice catalase, OsCATC. Furthermore, noe1 resulted in an increase of hydrogen peroxide (H2O2) in the leaves, which consequently promoted NO production via the activation of nitrate reductase. The removal of excess NO reduced cell death in both leaves and suspension cultures derived from noe1 plants, implicating NO as an important endogenous mediator of H2O2-induced leaf cell death. Reduction of intracellular S-nitrosothiol (SNO) levels, generated by overexpression of rice S-nitrosoglutathione reductase gene (GSNOR1), which regulates global levels of protein S-nitrosylation, alleviated leaf cell death in noe1 plants. Thus, S-nitrosylation was also involved in light-dependent leaf cell death in noe1. Utilizing the biotin-switch assay, nanoliquid chromatography, and tandem mass spectrometry, S-nitrosylated proteins were identified in both wild-type and noe1 plants. NO targets identified only in noe1 plants included glyceraldehyde 3-phosphate dehydrogenase and thioredoxin, which have been reported to be involved in S-nitrosylation-regulated cell death in animals. Collectively, our data suggest that both NO and SNOs are important mediators in the process of H2O2-induced leaf cell death in rice.

Nitric Oxide and Protein S-Nitrosylation Are Integral to Hydrogen Peroxide-Induced Leaf Cell Death in Rice

Iodine deficiency early in life impairs cognition and growth, but iodine status is also a key determinant of thyroid disorders in adults. Severe iodine deficiency causes goitre and hypothyroidism because, despite an increase in thyroid activity to maximise iodine uptake and recycling in this setting, iodine concentrations are still too low to enable production of thyroid hormone. In mild-to-moderate iodine deficiency, increased thyroid activity can compensate for low iodine intake and maintain euthyroidism in most individuals, but at a price: chronic thyroid stimulation results in an increase in the prevalence of toxic nodular goitre and hyperthyroidism in populations. This high prevalence of nodular autonomy usually results in a further increase in the prevalence of hyperthyroidism if iodine intake is subsequently increased by salt iodisation. However, this increase is transient because iodine sufficiency normalises thyroid activity which, in the long term, reduces nodular autonomy. Increased iodine intake in an iodine-deficient population is associated with a small increase in the prevalence of subclinical hypothyroidism and thyroid autoimmunity; whether these increases are also transient is unclear. Variations in population iodine intake do not affect risk for Graves' disease or thyroid cancer, but correction of iodine deficiency might shift thyroid cancer subtypes toward less malignant forms. Thus, optimisation of population iodine intake is an important component of preventive health care to reduce the prevalence of thyroid disorders.

Iodine defi ciency and thyroid disorders

The iodine intake level in a population is determined in cross-sectional studies. Urinary iodine varies considerably and the reliability of studies of iodine nutrition and the number of samples needed is unsettled. We performed a longitudinal study of sixteen healthy men living in an area of mild to moderate iodine deficiency. Iodine and creatinine concentrations were measured in spot urine samples collected monthly for 13 months. From these data we calculated the number of urine samples needed to determine the iodine excretion level for crude urinary iodine and for 24 h iodine excretion estimated from age- and gender-specific creatinine excretions. We found that mean urinary iodine excretion varied from 30 to 87 microg/l (31 to 91 microg/24 h). Sample iodine varied from 10 to 260 microg/l (20 to 161 microg/24 h). Crude urinary iodine varied more than estimated 24 h iodine excretion (population standard deviation 32 v. 26; individual standard deviation 29 v. 21; Bartlett's test, P < 0.01 for both). The number of spot urine samples needed to estimate the iodine level in a population with 95 % confidence within a precision range of +/- 10 % was about 125 (100 when using estimated 24 h iodine excretions), and within a precision range of +/- 5 % was about 500 (400). A precision range of +/- 20 % in an individual required twelve urine samples or more (seven when using estimated 24 h iodine excretions). In conclusion, estimating population iodine excretion requires 100-500 spot urine samples for each group or subgroup. Less than ten urine samples in an individual may be misleading.

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Reliability of studies of iodine intake and recommendations for number of samples in groups and in individuals.

Following a request from the European Commission, the Panel on Dietetic Products, Nutrition and Allergies (NDA) derived Dietary Reference Values (DRVs) for iodine, which are provided as Adequate Intake (AI). Iodine is essential for the synthesis of thyroid hormones. Through these hormones, iodine has an important role in energy-yielding metabolism and many other physiological processes. Iodine deficiency is associated with an increased frequency of goitre and hypothyroidism in a population. The AI for iodine is based on a large epidemiological study in European school-aged children showing that goitre prevalence is lowest for a urinary iodine concentration above around 100 μg/L. From this study, a urinary iodine concentration of ≥ 100 μg/L has been accepted as the threshold indicating sufficient iodine intake of school-aged children. In the absence of similar suitable data for other age groups it is proposed that this threshold also be applied for adults, infants and young children. Taking into account urinary volume and an absorption efficiency for iodine of 92 %, an AI of 150 μg/day is proposed for adults. For infants aged 7–11 months and for children, AIs range between 70 μg/day and 130 μg/day. For pregnant women, an AI of 200 μg/day is proposed, taking into account additional needs due to increased maternal thyroid hormone production and the iodine uptake by the fetus, placenta and amniotic fluid. The proposed AI for lactating women of 200 μg/day takes into account the existence of large iodine stores in conditions of adequate iodine status before pregnancy and considers that a full compensation for the iodine secreted in breast milk is not justified for the derivation of an AI for iodine for lactating women. © European Food Safety Authority, 2014

Scientific Opinion on Dietary Reference Values for iodine.

Iodine intake is important for thyroid function. Iodine content of natural waters is high in some areas and occurs bound in humic substances. Tap water is a major dietary source but bioavailability of organically bound iodine may be impaired. The objective was to assess if naturally occurring iodine bound in humic substances is bioavailable. Tap water was collected at Randers and Skagen waterworks and spot urine samples were collected from 430 long-term Randers and Skagen dwellers, who filled in a questionnaire. Tap water contained 2mg/l elemental iodine in Randers and 140mg/l iodine bound in humic substances in Skagen. Median (25; 75 percentile) urinary iodine excretion among Randers and Skagen dwellers not using iodine-containing supplements was 50 (37; 83) mg/24h and 177 (137; 219) mg/24h respectively (P,0·001). The fraction of samples with iodine below 100mg/24h was 85·0% in Randers and 6·5% in Skagen (P,0·001). Use of iodine-containing supplements increased urinary iodine by 60mg/24h (P,0·001). This decreased the number of samples with iodine below 100mg/24h to 67·3% and 5·0% respectively, but increased the number of samples with iodine above 300mg/24h to 2·4% and 16·1%. Bioavailability of iodine in humic substances in Skagen tap water was about 85%. Iodine in natural waters may be elemental or found in humic substances. The fraction available suggests an importance of drinking water supply for population iodine intake, although this may not be adequate to estimate population iodine intake. Iodine bioavailability: Humic substances: Drinking water: Population-based study

/pdf/naturally-occurring-iodine-in-humic-substances-in-drinking-5bqew3hpat.pdf

Naturally occurring iodine in humic substances in drinking water in Denmark is bioavailable and determines population iodine intake

More hypothyroidism and less hyperthyroidism with sufficient iodine nutrition compared to mild iodine deficiency--a comparative population-based study of older people.

Steen Terpling

Papers

Naturally occurring iodine in humic substances in drinking water in Denmark is bioavailable and determines population iodine intake

More hypothyroidism and less hyperthyroidism with sufficient iodine nutrition compared to mild iodine deficiency--a comparative population-based study of older people.

Iodine deficiency influences thyroid autoimmunity in old age – A comparative population-based study