Metal ions are essential cofactors for a wealth of biological processes, including oxidative phosphorylation, gene regulation and free-radical homeostasis. Failure to maintain appropriate levels of metal ions in humans is a feature of hereditary haemochromatosis, disorders of metal-ion deficiency, and certain neurodegenerative diseases. Despite their pivotal physiological roles, however, there is no molecular information on how metal ions are actively absorbed by mammalian cells. We have now identified a new metal-ion transporter in the rat, DCT1, which has an unusually broad substrate range that includes Fe2+, Zn2+, Mn2+, Co2+, Cd2+, Cu2+, Ni2+ and Pb2+. DCT1 mediates active transport that is proton-coupled and depends on the cell membrane potential. It is a 561-amino-acid protein with 12 putative membrane-spanning domains and is ubiquitously expressed, most notably in the proximal duodenum. DCT1 is upregulated by dietary iron deficiency, and may represent a key mediator of intestinal iron absorption. DCT1 is a member of the 'natural-resistance-associated macrophage protein' (Nramp) family and thus its properties provide insight into how these proteins confer resistance to pathogens.

Cloning and characterization of a mammalian proton-coupled metal-ion transporter

Chapter 1: Overview of Zinc Nutrition ............................................................................................................... S99 1.1 Biological functions of zinc ............................................................................................................................. S99 1.2 Tissue zinc distribution and reserves .............................................................................................................. S99 1.3 Zinc metabolism ........................................................................................................................................... S100 1.4 Importance of zinc for human health........................................................................................................... S101 1.5 Human zinc requirements............................................................................................................................. S105 1.5.1 Adult men ............................................................................................................................................. S106 1.5.2 Adult women......................................................................................................................................... S109 1.5.3 Children ................................................................................................................................................ S110 1.5.4 Pregnancy.............................................................................................................................................. S111 1.5.5 Lactation ............................................................................................................................................... S112 1.6 Dietary sources of zinc and suggested revisions of Recommended Daily Intakes .................................... S112 1.6.1 Dietary sources of zinc and factors affecting the proportion of zinc available for absorption ........ S112 1.6.2 Revised estimates of dietary requirements and recommended intakes for zinc ............................... S114 1.7 Zinc toxicity.................................................................................................................................................... S118 1.8 Causes of zinc deficiency and groups at high risk ....................................................................................... S121 1.9 Summary ........................................................................................................................................................ S123

International Zinc Nutrition Consultative Group (IZiNCG) technical document #1. Assessment of the risk of zinc deficiency in populations and options for its control.

Background High levels of dietary sodium (consumed as common salt, sodium chloride) are associated with raised blood pressure and adverse cardiovascular health. Despite this, public health efforts to reduce sodium consumption remain limited to a few countries. Comprehensive, contemporaneous sodium intake data from around the world are needed to inform national/international public health initiatives to reduce sodium consumption. Methods Use of standardized 24-h sodium excretion estimates for adults from the international INTERSALT (1985–87) and INTERMAP (1996–99) studies, and recent dietary and urinary sodium data from observational or interventional studies—identified by a comprehensive search of peer-reviewed and ‘grey’ literature—presented separately for adults and children. Review of methods for the estimation of sodium intake/ excretion. Main food sources of sodium are presented for several Asian, European and Northern American countries, including previously unpublished INTERMAP data.

Salt intakes around the world: implications for public health

While virtually absent in our diet a few hundred years ago, fructose has now become a major constituent of our modern diet. Our main sources of fructose are sucrose from beet or cane, high fructose corn syrup, fruits, and honey. Fructose has the same chemical formula as glucose (C(6)H(12)O(6)), but its metabolism differs markedly from that of glucose due to its almost complete hepatic extraction and rapid hepatic conversion into glucose, glycogen, lactate, and fat. Fructose was initially thought to be advisable for patients with diabetes due to its low glycemic index. However, chronically high consumption of fructose in rodents leads to hepatic and extrahepatic insulin resistance, obesity, type 2 diabetes mellitus, and high blood pressure. The evidence is less compelling in humans, but high fructose intake has indeed been shown to cause dyslipidemia and to impair hepatic insulin sensitivity. Hepatic de novo lipogenesis and lipotoxicity, oxidative stress, and hyperuricemia have all been proposed as mechanisms responsible for these adverse metabolic effects of fructose. Although there is compelling evidence that very high fructose intake can have deleterious metabolic effects in humans as in rodents, the role of fructose in the development of the current epidemic of metabolic disorders remains controversial. Epidemiological studies show growing evidence that consumption of sweetened beverages (containing either sucrose or a mixture of glucose and fructose) is associated with a high energy intake, increased body weight, and the occurrence of metabolic and cardiovascular disorders. There is, however, no unequivocal evidence that fructose intake at moderate doses is directly related with adverse metabolic effects. There has also been much concern that consumption of free fructose, as provided in high fructose corn syrup, may cause more adverse effects than consumption of fructose consumed with sucrose. There is, however, no direct evidence for more serious metabolic consequences of high fructose corn syrup versus sucrose consumption.

http://www.perishablepundit.com/docs/fructose-and-obesity.pdf

Metabolic Effects of Fructose and the Worldwide Increase in Obesity

Objective To assess the effect of decreased sodium intake on blood pressure, related cardiovascular diseases, and potential adverse effects such as changes in blood lipids, catecholamine levels, and renal function. Design Systematic review and meta-analysis. Data sources Cochrane Central Register of Controlled Trials, Medline, Embase, WHO International Clinical Trials Registry Platform, the Latin American and Caribbean health science literature database, and the reference lists of previous reviews. Study selection Randomised controlled trials and prospective cohort studies in non-acutely ill adults and children assessing the relations between sodium intake and blood pressure, renal function, blood lipids, and catecholamine levels, and in non-acutely ill adults all cause mortality, cardiovascular disease, stroke, and coronary heart disease. Study appraisal and synthesis Potential studies were screened independently and in duplicate and study characteristics and outcomes extracted. When possible we conducted a meta-analysis to estimate the effect of lower sodium intake using the inverse variance method and a random effects model. We present results as mean differences or risk ratios, with 95% confidence intervals. Results We included 14 cohort studies and five randomised controlled trials reporting all cause mortality, cardiovascular disease, stroke, or coronary heart disease; and 37 randomised controlled trials measuring blood pressure, renal function, blood lipids, and catecholamine levels in adults. Nine controlled trials and one cohort study in children reporting on blood pressure were also included. In adults a reduction in sodium intake significantly reduced resting systolic blood pressure by 3.39 mm Hg (95% confidence interval 2.46 to 4.31) and resting diastolic blood pressure by 1.54 mm Hg (0.98 to 2.11). When sodium intake was 0.05). There were insufficient randomised controlled trials to assess the effects of reduced sodium intake on mortality and morbidity. The associations in cohort studies between sodium intake and all cause mortality, incident fatal and non-fatal cardiovascular disease, and coronary heart disease were non-significant (P>0.05). Increased sodium intake was associated with an increased risk of stroke (risk ratio 1.24, 95% confidence interval 1.08 to 1.43), stroke mortality (1.63, 1.27 to 2.10), and coronary heart disease mortality (1.32, 1.13 to 1.53). In children, a reduction in sodium intake significantly reduced systolic blood pressure by 0.84 mm Hg (0.25 to 1.43) and diastolic blood pressure by 0.87 mm Hg (0.14 to 1.60). Conclusions High quality evidence in non-acutely ill adults shows that reduced sodium intake reduces blood pressure and has no adverse effect on blood lipids, catecholamine levels, or renal function, and moderate quality evidence in children shows that a reduction in sodium intake reduces blood pressure. Lower sodium intake is also associated with a reduced risk of stroke and fatal coronary heart disease in adults. The totality of evidence suggests that most people will likely benefit from reducing sodium intake.

https://www.bmj.com/content/bmj/346/bmj.f1326.full.pdf

Effect of lower sodium intake on health: systematic review and meta-analyses

Sodium and potassium intake and balance in adults consuming self-selected diets.

Plasma carotenoid response to chronic intake of selected foods and beta-carotene supplements in men.

Prehospital resuscitation and stabilization of major trauma victims is increasingly employed. To evaluate the benefits of one such maneuver, fluid administration, we reviewed 52 consecutive trauma cases in which patients had a blood pressure of less than 100 mm Hg either at the scene or on arrival to hospital. In all cases, transport time to hospital was less than IV establishment time. Fluid volume infused had little influence on final outcomes. A percentage of patients with correctable surgical lesions might have been salvaged had prompt transport been instituted. Field maneuvers in critically injured patients should be minimized to decrease ultimate mortality.

J C Smith

Papers

Sodium and potassium intake and balance in adults consuming self-selected diets.

Plasma carotenoid response to chronic intake of selected foods and beta-carotene supplements in men.

Prehospital stabilization of critically injured patients: a failed concept.

Plasma carotenoids in normal men after a single ingestion of vegetables or purified beta-carotene.

Indices of copper status in humans consuming a typical American diet containing either fructose or starch.