Other than the in vitro erythrocyte hemolysis test, no valid biomarkers of vitamin E status currently exist.
We hypothesized that the urinary vitamin E metabolite α-carboxyethyl hydroxychroman (α-CEHC) could serve as a biomarker.
The relations between urinary α-CEHC, plasma α-tocopherol, and vitamin E intakes were assessed by using a previously validated multipass, Web-based, 24-h self-administered dietary recall, and we concurrently collected plasma and 24-h urine samples from 233 participants of both sexes.
Median vitamin E intakes were 9.7 mg α-tocopherol/d. Intakes were correlated with plasma α-tocopherol (R = 0.40, P < 0.001) and urinary α-CEHC (R = 0.42, P < 0.001); these correlations were essentially unchanged after multivariate adjustments. On the basis of multiple regression analysis, urinary α-CEHC excretion increased by ∼0.086 μmol/g creatinine (95% CI: 0.047, 0.125) for every 1-mg (2.3-μmol) increase in dietary α-tocopherol. Urinary α-CEHC excretion remained at a plateau (median: 1.39 μmol/g creatinine) until dietary intakes of α-tocopherol exceeded 9 mg α-tocopherol/d. The inflection point at which vitamin E metabolism increased was estimated to be at an intake of 12.8 mg α-tocopherol/d. Daily excretion of >1.39 μmol α-CEHC/g creatinine is associated with a greater than adequate α-tocopherol status, as evidenced by increased vitamin E metabolism and excretion.
Thus, urinary α-CEHC is a valid biomarker of α-tocopherol status that can be used to set a value for the Estimated Adequate Requirement of vitamin E.
"Third, associations of nutrient exposure and biomarkers are not linear (e.g. vitamin E) (White et al., 2001; Lebold et al., 2012). The association is not apparent unless the full range of intake is assessed; for example, by including supplement sources (Vogel et al., 1997). "
[Show abstract][Hide abstract] ABSTRACT: Background
Total nutrient intake (TNI) is intake from food and supplements. This provides an assessment of nutrient adequacy and the prevalence of excessive intake, as well as the response with respect to biomarkers. Cod liver oil (CLO) is the most frequently consumed supplement in the UK, containing nutrients that might have varying influences on health. We calculated TNI for vitamins A, D and E, as well as eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), and assessed associations with the respective blood concentrations.Methods
Seven-day diet diaries and blood samples were taken from two subsets of the European Prospective Investigation into Cancer (EPIC-Norfolk) cohort (age range 39–79 years; n = 1400 for vitamin D; n = 6656 for remaining nutrients). TNI was calculated for the subgroups: nonsupplement users, those consuming the nutrient in supplement form and those consuming a supplement without this nutrient.ResultsCLO-related nutrients were supplemented by 15%–33%, which approximately doubled median intakes. Almost everyone in the supplement + vitamin A group reached the estimated average requirement; however, guideline levels were likely to be exceeded. Partial correlations between intake of vitamins A and D and biomarkers were low and modestly strengthened by the inclusion of supplement sources (correlation = 0.01–0.13). Correlations between biomarker and TNI of vitamin E and EPA+DHA were in the range 0.40–0.46; however, vitamin E exceeding food intake resulted in attenuated coefficients. Linear associations between food or TNI EPA+DHA and plasma were weak but consistent across subgroups.ConclusionsCLO-related nutrients contribute substantially to nutrient intake, with a risk of over-consumption. Apart from EPA+DHA, biomarker data suggest that CLO-related nutrients in supplements are not linearly associated with vitamin status.
Journal of Human Nutrition and Dietetics 09/2014; DOI:10.1111/jhn.12271 · 1.99 Impact Factor
"Cereals and grains are a major contributor of dietary vitamin E intake in humans not taking any vitamin supplement . We therefore incorporated TAC in a cereal-based test meal (Adisseo , Commentry, France). "
[Show abstract][Hide abstract] ABSTRACT: Scope:
Vitamin E is present in feed and food mainly as d-α-tocopherol (d-α-TOL) but also as all-rac-α-tocopheryl acetate (rac-α-TAC) through supplementation. Its absorption efficiency is low compared to that of triacylglycerols. The aim of this work was thus to study the fate of TAC during digestion.
Methods and results:
Using an in vitro digestion model, we showed that TAC was distributed between mixed micelles (36%), liposomes (9%), and nonsolubilized food debris (52%). A significant fraction of TAC was also found in emulsions when fat hydrolysis was not complete. Among the candidate esterases tested, i.e. cholesteryl ester hydrolase, pancreatic lipase, and pancreatic lipase-related protein 2, only cholesteryl ester hydrolase was able to hydrolyze TAC to all-rac-α-TOL, about five times more efficiently when it was incorporated into mixed micelles or liposomes than into emulsions or in the food matrix. Caco-2 cells were able to hydrolyze TAC and to uptake TOL when TAC was incorporated into mixed micelles but not into emulsions.
During digestion, most TAC is recovered in matrices where its hydrolysis and its uptake by intestinal cells are markedly less efficient than in mixed micelles.
[Show abstract][Hide abstract] ABSTRACT: The liver is at the nexus of the regulation of lipoprotein uptake, synthesis, and secretion; and the site of xenobiotic detoxification by cytochrome P450 oxidation systems (phase I), conjugation systems (phase II) and transporters (phase III). These two major regulatory systems control vitamin E status. The mechanisms for the preference for α-tocopherol relative to the eight naturally occurring vitamin E forms largely depend upon the liver and include both a preferential secretion of α-tocopherol from the liver into the plasma for its transport in circulating lipoproteins for subsequent uptake by tissues, as well as the preferential hepatic metabolism of non-α-tocopherol forms. These mechanisms are the focus of this review.
The Journal of Lipid Research 03/2013; 54(9). DOI:10.1194/jlr.R032946 · 4.42 Impact Factor
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