Vegans, Vegetarians, and Omnivores: How Does Dietary Choice Influence Iodine Intake? A Systematic Review

Vegan and vegetarian diets are becoming increasingly popular. Dietary restrictions may increase the risk of iodine deficiency. This systematic review aims to assess iodine intake and status in adults following a vegan or vegetarian diet in industrialised countries. A systematic review and quality assessment were conducted in the period May 2019-April 2020 according to Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. Studies were identified in Ovid MEDLINE, Embase, Web of Science, PubMed, Scopus, and secondary sources. Fifteen articles met inclusion criteria. Participants included 127,094 adults (aged ≥ 18 years). Vegan groups presented the lowest median urinary iodine concentrations, followed by vegetarians, and did not achieve optimal status. The highest iodine intakes were recorded in female vegans (1448.0 ± 3879.0 µg day-1) and the lowest in vegetarians (15.6 ± 21.0 µg day-1). Omnivores recorded the greatest intake in 83% of studies. Seaweed contributed largely to diets of vegans with excessive iodine intake. Vegans appear to have increased risk of low iodine status, deficiency and inadequate intake compared with adults following less restrictive diets. Adults following vegan and vegetarian diets living in countries with a high prevalence of deficiency may be more vulnerable. Therefore, further monitoring of iodine status in industrialised countries and research into improving the iodine intake and status of adults following vegan and vegetarian diets is required

Acetylsalicylic acid interferes with embryonic kidney growth and development by a prostaglandin-independent mechanism

AIM: To evaluate the effects of the non-selective, non-steroidal anti-inflammatory drug (NSAID) acetylsalicylic acid (ASA), on ex vivo embryonic kidney growth and development. METHODS: Pairs of fetal mouse kidneys at embryonic day 12.5 were cultured ex vivo in increasing concentrations of ASA (0.04-0.4 mg/mL) for up to 7 d. One organ from each pair was grown in control media and was used as the internal control for the experimental contralateral organ. In some experiments, organs were treated with ASA for 48 h and then transferred either to control media alone or control media containing 10 μmol/L prostaglandin E2 (PGE2) for a further 5 d. Fetal kidneys were additionally obtained from prostaglandin synthase 2 homozygous null or heterozygous (PTGS2-/- and PTGS2-/+) embryos and grown in culture. Kidney cross-sectional area was used to determine treatment effects on kidney growth. Whole-mount labelling to fluorescently detect laminin enabled crude determination of epithelial branching using confocal microscopy. RESULTS: Increasing ASA concentration (0.1, 0.2 and 0.4 mg/mL) significantly inhibited metanephric growth (P < 0.05). After 7 d of culture, exposure to 0.2 mg/mL and 0.4 mg/mL reduced organ size to 53% and 23% of control organ size respectively (P < 0.01). Addition of 10 μmol/L PGE2 to culture media after exposure to 0.2 mg/mL ASA for 48 h resulted in a return of growth area to control levels. Application of control media alone after cessation of ASA exposure showed no benefit on kidney growth. Despite the apparent recovery of growth area with 10 μmol/L PGE2, no obvious renal tubular structures were formed. The number of epithelial tips generated after 48 h exposure to ASA was reduced by 40% (0.2 mg/mL; P < 0.05) and 47% (0.4 mg/mL; P < 0.01). Finally, growth of PTGS2-/- and PTGS2+/- kidneys in organ culture showed no differences, indicating that PTGS2 derived PGE2 may at best have a minor role. CONCLUSION: ASA reduces early renal growth and development but the role of prostaglandins in this may be minor

Trace Mineral Intake and Deficiencies in Older Adults Living in the Community and Institutions: A Systematic Review

© 2020 by the authors. Licensee MDPI, Basel, Switzerland. The global population is ageing with many older adults suffering from age-related malnutrition, including micronutrient deficiencies. Adequate nutrient intake is vital to enable older adults to continue living independently and delay their institutionalisation, as well as to prevent deterioration of health status in those living in institutions. This systematic review investigated the insufficiency of trace minerals in older adults living independently and in institutions. We examined 28 studies following a cross-sectional or cohort design, including 7203 older adults (≥60) living independently in 13 Western countries and 2036 living in institutions in seven Western countries. The estimated average requirement (EAR) cut-off point method was used to calculate percentage insufficiency for eight trace minerals using extracted mean and standard deviation values. Zinc deficiency was observed in 31% of community-based women and 49% of men. This was higher for those in institutional care (50% and 66%, respectively). Selenium intakes were similarly compromised with deficiency in 49% women and 37% men in the community and 44% women and 27% men in institutions. We additionally found significant proportions of both populations showing insufficiency for iron, iodine and copper. This paper identifies consistent nutritional insufficiency for selenium, zinc, iodine and copper in older adults

Remote conditioning or erythropoietin before surgery primes kidneys to clear ischemia-reperfusion-damaged cells: a renoprotective mechanism?

Acute kidney injury is common, serious with no specific treatment. Ischemia-reperfusion is a common cause of acute kidney injury (AKI). Clinical trials suggest that preoperative erythropoietin (EPO) or remote ischemic preconditioning may have a renoprotective effect. Using a porcine model of warm ischemia-reperfusion-induced AKI (40-min bilateral cross-clamping of renal arteries, 48-h reperfusion), we examined the renoprotective efficacy of EPO (1,000 iu/kg iv.) or remote ischemic preconditioning (3 cycles, 5-min inflation/deflation to 200 mmHg of a hindlimb sphygmomanometer cuff). Ischemia-reperfusion induced significant kidney injury at 24 and 48 h (χ(2), 1 degree of freedom, >10 for 6/7 histopathological features). At 2 h, a panel of biomarkers including plasma creatinine, neutrophil gelatinase-associated lipocalin, and IL-1β, and urinary albumin:creatinine could be used to predict histopathological injury. Ischemia-reperfusion increased cell proliferation and apoptosis in the renal cortex but, for pretreated groups, the apoptotic cells were predominantly intratubular rather than interstitial. At 48-h reperfusion, plasma IL-1β and the number of subcapsular cells in G2-M arrest were reduced after preoperative EPO, but not after remote ischemic preconditioning. These data suggest an intrarenal mechanism acting within cortical cells that may underpin a renoprotective function for preoperative EPO and, to a limited extent, remote ischemic preconditioning. Despite equivocal longer-term outcomes in clinical studies investigating EPO as a renoprotective agent in AKI, optimal clinical dosing and administration have not been established. Our data suggest further clinical studies on the potential renoprotective effect of EPO and remote ischemic preconditioning are justified

LIM kinase function and renal growth: potential role for LIM kinases in fetal programming of kidney development

Aims Maternal dietary restriction during pregnancy impairs nephron development and results in offspring with fewer nephrons. Cell turnover in the early developing kidney is altered by exposure to maternal dietary restriction and may be regulated by the LIM-kinase family of enzymes. We set out to establish whether disturbance of LIM-kinase activity might play a role in the impairment of nephron formation. Main methods E12.5 metanephric kidneys and HK2 cells were grown in culture with the pharmacological LIM-kinase inhibitor BMS5. Organs were injected with DiI, imaged and cell numbers measured over 48 h to assess growth. Cells undergoing mitosis were visualised by pH 3 labelling. Key findings Growth of cultured kidneys reduced to 83% of controls after exposure to BMS5 and final cell number to 25% of control levels after 48 h. Whilst control and BMS5 treated organs showed cells undergoing mitosis (100 ± 11 cells/field vs 113 ± 18 cells/field respectively) the proportion in anaphase was considerably diminished with BMS5 treatment (7.8 ± 0.8% vs 0.8 ± 0.6% respectively; P < 0.01). This was consistent with effects on HK2 cells highlighting a severe impact of BMS5 on formation of the mitotic spindle and centriole positioning. DiI labelled cells migrated in 100% of control cultures vs 0% BMS5 treated organs. The number of nephrogenic precursor cells appeared depleted in whole organs and formation of new nephrons was blocked by exposure to BMS5. Significance Pharmacological blockade of LIM-kinase function in the early developing kidney results in failure of renal development. This is likely due to prevention of dividing cells from completion of mitosis with their resultant loss

Remote effects of acute kidney injury in a porcine model

Background: Acute Kidney Injury (AKI) is a common and serious disease with no specific treatment. An episode of AKI may affect organs distant to the kidney, further increasing the morbidity associated with AKI. The mechanism of organ cross-talk after AKI is unclear. The renal and immune systems of pigs and humans are alike. Using a preclinical animal (porcine) model, we test the hypothesis that early effects of AKI on distant organs is by immune cell infiltration leading to inflammatory cytokine production, extravasation and edema. Study Design: In 29 pigs exposed to either sham-surgery or renal ischemia-reperfusion (control, n=12; AKI, n=17) we assessed remote organ (liver, lung, brain) effects in the short-(from 2 to 48h reperfusion) and longer-term (5 weeks later) using immunofluorescence (for leucocyte infiltration, apoptosis), a cytokine array, tissue elemental analysis (electrolytes), blood hematology and chemistry (e.g. liver enzymes) and PCR (for inflammatory markers). Results: AKI elicited significant, short-term (~24h) increments in enzymes indicative of acute liver damage (e.g. AST:ALT ratio; P=0.02) and influenced tissue biochemistry in some remote organs (e.g. lung tissue [Ca++] increased; P=0.04). These effects largely resolved after 48h and no further histopathology, edema, apoptosis or immune cell infiltration was noted in liver, lung or hippocampus in the short- and longer-term. Conclusions: AKI has subtle biochemical effects on remote organs in the short-term including a transient increment in markers of acute liver damage. These effects resolved by 48h and no further remote organ histopathology, apoptosis, edema or immune cell infiltration was noted

Geographical and seasonal variation in Iodine content of cow’s milk in the UK and consequences for the consumer´s supply

Background. Dairy products provide a crucial source of dietary iodine for the majority of the UK population, contributing approximately 30-40 % of daily intake. Fluctuations in the iodine content of purchased milk both seasonally and annually implies potential fragility of iodine supply likely through fluctuating supplementation practices in cow herds. We set out to establish the level of national variation in herds and identify factors which might impact milk iodine content. Methods. Milk samples were obtained from 98 herds across the UK via the National Milk Laboratories in August and December 2016. Iodine concentration of samples was measured using ICP-MS. Milk samples and feed intake data were additionally taken from 22 cows from the University of Nottingham (UON) dairy herd. Results. There was considerable variation in milk iodine content from < 0.012 (Limit of Detection) to 1558 µg L-1, with a summer median of 197 µg L-1 and winter median 297 µg L-1. Overall, winter values were higher than summer counterparts (

Excess maternal salt intake produces sex-specific hypertension in offspring: putative roles for kidney and gastrointestinal sodium handling.

Hypertension is common and contributes, via cardiovascular disease, towards a large proportion of adult deaths in the Western World. High salt intake leads to high blood pressure, even when occurring prior to birth - a mechanism purported to reside in altered kidney development and later function. Using a combination of in vitro and in vivo approaches we tested whether increased maternal salt intake influences fetal kidney development to render the adult individual more susceptible to salt retention and hypertension. We found that salt-loaded pregnant rat dams were hypernatraemic at day 20 gestation (147±5 vs. 128±5 mmoles/L). Increased extracellular salt impeded murine kidney development in vitro, but had little effect in vivo. Kidneys of the adult offspring had few structural or functional abnormalities, but male and female offspring were hypernatraemic (166±4 vs. 149±2 mmoles/L), with a marked increase in plasma corticosterone (e.g. male offspring; 11.9 [9.3-14.8] vs. 2.8 [2.0-8.3] nmol/L median [IQR]). Furthermore, adult male, but not female, offspring had higher mean arterial blood pressure (effect size, +16 [9-21] mm Hg; mean [95% C.I.]. With no clear indication that the kidneys of salt-exposed offspring retained more sodium per se, we conducted a preliminary investigation of their gastrointestinal electrolyte handling and found increased expression of proximal colon solute carrier family 9 (sodium/hydrogen exchanger), member 3 (SLC9A3) together with altered faecal characteristics and electrolyte handling, relative to control offspring. On the basis of these data we suggest that excess salt exposure, via maternal diet, at a vulnerable period of brain and gut development in the rat neonate lays the foundation for sustained increases in blood pressure later in life. Hence, our evidence further supports the argument that excess dietary salt should be avoided per se, particularly in the range of foods consumed by physiologically immature young

Peptic digestion of beef myofibrils is modified by prior marination

Background: Preparatory steps such as seasoning, marination, and cooking may induce changes in meat which affects the ability of the stomach to adequately digest it. This may result in peptide chains reaching the colon intact where resident bacteria ferment them resulting in the formation of putative carcinogenic phenolic by-products. Objective: In this study, we set out to determine whether peptic digestion of beef myofibrils was influenced by prior marination. Design: Cubes of sirloin stewing steak were marinated in balsamic vinegar or left untreated at 48C overnight. Samples were oven cooked and myofibrils were extracted. Myofibrils were subject to proteolytic digestion with pepsin and digestion products analysed spectrophotometrically and with gel electrophoresis. Results: Both marination in balsamic vinegar and cooking significantly reduced the yield of myofibrils from shop-purchased beef (PB0.05). Digestion progressed in all samples as a function of time (PB0.01), varying depending on prior treatment. Marination induced resistance to the digestive effect of pepsin during the early to mid-phase of digestion, and we identified a protein band of 150 kDa which was protected from peptic digestion in samples which had been marinated and cooked, but not in any other groups. Conclusions: Pre-treatment of meat prior to cooking may influence specific peptides such that they become more resistant to the digestive actions of pepsin. Keywords: marination; digestibility; acetic acid; colon cancer; myofibril; cooking; stea