The importance of trace elements as essential dietary constituents is not sufficiently appreciated by the medical profession, although in recent years a significant increase of new finding on their essential character in nutrition occurred as well as of data on changes in the composition of the diet which can cause their deficiency and in some instances a toxic excess. The diagnosis of deficiency or excess of these substances in the organism is very complicated. because their blood level frequently does not provide sufficient information on their reserves in the organism and new laboratory methods suited for this purpose must be developed and tested. The interpretation of the assembled results is very pretentious and it will be therefore necessary to expand teaching of nutrition, where the problem of trace elements no doubt belongs, into undergraduate and postgraduate medical curricula to prevent health damage due to inadequate intake of trace elements as well as uncontrolled intake of freely available preparations sold as supplements.

[Trace elements, human nutrition and health]

Objective: The intent of this review is to evaluate the scientific evidence for the assessment of adequacy of selenium status and of the requirements for selenium. From this evidence, attempts have been made to define levels of plasma selenium and dietary selenium intake, which could be used for the assessment of deficiency or adequacy of selenium status. Method: The first section briefly reviews the methods for assessment of selenium status. The second section outlines the requirements for selenium based on a number of criteria, and how these have been translated into recommended intakes of selenium. In the final section, levels of plasma selenium and dietary intake based on different criteria of adequacy have been proposed. Results and conclusion: The minimum requirement for selenium is that which prevents the deficiency disease, Keshan disease. The recommended intakes of selenium have been calculated from the requirement for optimum plasma glutathione peroxidase (GPx) activity that must, because of the hierarchy of selenoproteins, also take account of the amounts needed for normal levels of other biologically necessary selenium compounds. Whether optimal health depends upon maximization of GPx or other selenoproteins, however, has yet to be resolved, and the consequences of less-than-maximal GPx activities or mRNA levels need investigation. Intakes, higher than recommended intakes, and plasma selenium concentrations that might be protective for cancer or result in other additional health benefits have been proposed. There is an urgent need for more large-scale trials to assess any such beneficial effects and to provide further data on which to base more reliable estimates for intakes and plasma selenium levels that are protective.

Assessment of requirements for selenium and adequacy of selenium status: a review

Although the need for selenium in human and animal nutrition is well recognized, the question concerning the proper form of selenium for supplemental use is still being debated. Ideally, selenium should be supplemented in the form in which it occurs naturally in foods. Because the L-isomer of selenomethionine (Se-met) is a major natural food-form of selenium, synthetic L-Se-met or enriched food sources thereof such as selenium yeast are appropriate supplemental forms of Se for humans; for animals, DL-Se-met is acceptable. Ingested Se-met is either metabolized directly to reactive forms of selenium or stored in place of methionine in body proteins. Se-met metabolism is closely linked to protein turnover. At constant intakes in the nutritional range, tissue Se levels increase until a steady state is established, preventing the build-up to toxic levels.

Selenomethionine: A Review of Its Nutritional Significance, Metabolism and Toxicity

Background
This review is an update of the first Cochrane publication on selenium for preventing cancer (Dennert 2011).

Selenium is a metalloid with both nutritional and toxicological properties. Higher selenium exposure and selenium supplements have been suggested to protect against several types of cancers.

Selenium for preventing cancer

Worldwide, there are more than 10 million new cancer cases each year, and cancer is the cause of approximately 12% of all deaths. Given this, a large number of epidemiologic studies have been undertaken to identify potential risk factors for cancer, amongst which the association with trace elements has received considerable attention. Trace elements, such as selenium, zinc, arsenic, cadmium, and nickel, are found naturally in the environment, and human exposure derives from a variety of sources, including air, drinking water, and food. Trace elements are of particular interest given that the levels of exposure to them are potentially modifiable. In this review, we focus largely on the association between each of the trace elements noted above and risk of cancers of the lung, breast, colorectum, prostate, urinary bladder, and stomach. Overall, the evidence currently available appears to support an inverse association between selenium exposure and prostate cancer risk, and possibly also a reduction in risk with respect to lung cancer, although additional prospective studies are needed. There is also limited evidence for an inverse association between zinc and breast cancer, and again, prospective studies are needed to confirm this. Most studies have reported no association between selenium and risk of breast, colorectal, and stomach cancer, and between zinc and prostate cancer risk. There is compelling evidence in support of positive associations between arsenic and risk of both lung and bladder cancers, and between cadmium and lung cancer risk.

/pdf/trace-elements-and-cancer-risk-a-review-of-the-epidemiologic-e7d5054ufg.pdf

Trace elements and cancer risk: a review of the epidemiologic evidence

We examined the validity of using the selenium level in a single biological specimen as a surrogate measure of usual intake. We used data from 77 free-living adults from South Dakota and Wyoming. Subjects provided multiple 1-day duplicate-plate food composites, repeated specimens of blood and toenails, and 24-hour urine collections. We developed a statistical calibration method that incorporated measurement error correction to analyze the data. The Pearson correlation coefficients between selenium intake and a single selenium status measure, after deattenuation to adjust for the effect of within-person variation in intake, were: 0.78 for whole blood, 0.74 for serum, 0.67 for toenails, and 0.86 for urine. We present formulas to estimate the intake of individuals, based on selenium levels in a single specimen of blood, toenails, or urine. In these data, the concentration of selenium in a single specimen of whole blood, serum, or toenails served reasonably well as a measure for ranking subjects according to long-term selenium intake but provided only a rough estimate of intake for each subject.

Use of selenium concentration in whole blood, serum, toenails, or urine as a surrogate measure of selenium intake.

A model is developed to describe the kinetics of sodium selenite metabolism in humans, based on plasma, urine, and fecal samples obtained from six subjects over a 4-wk period after a single oral 200-micrograms dose of the enriched stable isotope tracer 74Se. The model describes absorption, distributed along the gastrointestinal tract, and enterohepatic recirculation. The model includes four kinetically distinct plasma components, a subsystem consisting of the liver and pancreas, and a slowly turning-over tissue pool. For the six subjects, the ranges of mean residence times for the four plasma components are, respectively, 0.2-1.1 h, 3-8 h, 9-42 h, and 200-285 h; for the hepatopancreatic subsystem 4-41 days; and for the tissue pool 115-285 days. Approximately 84% of the administered dose was absorbed, and after 12 days approximately 65% remained in the body. The model predicts that after 90 days approximately 35% of this Se would be retained, primarily in the tissues. Separating Se metabolism into several distinct kinetic components is a first step in identifying the efficacious, nutritious, and toxic forms of the element.

Human selenite metabolism: a kinetic model

Because Se content of food varies widely, estimates of intake based on Se status are more accurate than those based on food composition tables. 77 free-living subjects from South Dakota and Wyoming, where the range of Se intake was large, provided blood, toenails, and 24-hour urines. Se intake, measured by chemical analysis of 4-8 days of duplicate-plate food composites from each subject, was estimated on the basis of the Se indices. To predict the natural logarithm of Se intake from serum Se the best fit was provided by : {minus}0.465 + 0.568{asterisk}SSe. Addition of lean body mass (LBM (kg)) and energy intake (EI (MJ)) to the model markedly improved the fit. Models based on Se in blood or urine gave slightly better estimates than those based on toenail Se. Consideration of data in addition to indices of Se status resulted in improved estimates of intake.

Estimation of selenium (Se) intake from Se in serum, whole blood, toenails, or urine

Human [74Se]selenomethionine metabolism: a kinetic model.

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Use of selenium concentration in whole blood, serum, toenails, or urine as a surrogate measure of selenium intake.

Human selenite metabolism: a kinetic model

Estimation of selenium (Se) intake from Se in serum, whole blood, toenails, or urine

Human [74Se]selenomethionine metabolism: a kinetic model.