The objective of this work was to quantify the contribution of fortification (defined here as adding nutrients beyond traditional enrichment standards) to dietary nutrient intakes in the United States. A list of fortified foods was developed that was relevant at the time of the analyses, and prefortification (naturally occurring) nutrients in the fortified foods were determined from industry-supplied data. Using dietary data from the 1989-1991 Continuing Survey of Food Intakes by Individuals (CSFII), intakes of nine nutrients were determined both as reported in the CSFII (i.e., postfortification) and also by using prefortification nutrient levels for the identified fortified foods. We report data for the total population age >/= 1 y based on respondents (n = 11,710) with 3 d of dietary data, as well as select age/gender subgroups. All data were weighted. Fortification substantially increased the intakes of all nutrients examined except calcium, in all age/gender groups but especially in children. In numerous cases, fortification was responsible for boosting median or 25th percentile intakes from below to above the RDA. The breakfast cereal category was responsible for nearly all the intake of nutrients from fortified foods, except vitamin C for which juice-type beverages made as great or a greater contribution. These data from 1989 to 1991 serve as a useful baseline with which to compare contributions of fortification as the practice expands. The large contribution of fortification even in 1989-1991 suggests that continued monitoring of fortification practices, using methods such as those presented here, is important.
Resistant starch (RS) has been associated with beneficial health effects. The purpose of this study was to estimate consumption of RS in the U.S. and to identify key dietary sources. A database of RS concentrations in foods was developed from the publicly available literature. These concentrations were linked to foods reported in 24‐h dietary recalls from the 1999–2002 NHANES and estimates of RS intake were generated. The study population included 18,305 individuals. Intakes were estimated by age/sex and race/ethnicity groups. Three estimates of RS intake were calculated for each population group: estimates based on the mean RS concentrations identified in the literature; estimates based on the minimum RS concentration reported for each food, and estimates based on the maximum RS concentration reported for each food. Food sources of RS were ranked based on mean RS concentrations. Americans aged ≥1 y were estimated to consume 4.9 g/d RS based on mean RS concentrations, with a range of 2.8 to 8.0 g/d based on minimum and maximum values. Mean RS intakes by non‐Hispanic whites, non‐Hispanic blacks and Mexican Americans were 4.6, 4.7, and 5.3 g/d, respectively. Breads, grain products (mainly pasta and rice) and vegetables each contributed 19–21% to the total daily intake of RS, while fruit (mainly bananas) contributed 14%, and legumes provided 9% of the total estimated RS intake.
Supported by National Starch Food Innovation.
Weanling male rats were fed a selenium (Se)-deficient 40% Torula yeast diet for 4 weeks and were then continued on depletion for another 4 weeks or were repleted with 0.1, 0.2, or 0.3 ppm Se as sodium selenite or 0.2 ppm Se as tuna, beef kidney, or high-Se wheat. There were no significant differences in young red blood cell Se, unfractionated red blood cell Se, or liver Se levels in groups fed diets containing 0.2 ppm Se. Glutathione peroxidase (GSH-Px) activity in young red blood cells was lower in the three groups fed food Se than in the group fed selenite (0.2 ppm Se). Young red blood cell GSH-Px was significantly lower in rats fed tuna than in rats fed wheat. Unfractionated red blood cell GSH-Px was lower in rats fed tuna than in rats fed selenite, but did not differ significantly among groups fed food Se sources. Liver GSH-Px was significantly lower in rats fed tuna than in rats fed kidney, wheat, or selenite. Availability of Se was only 54-58% as great from tuna as from selenite for induction of GSH-Px in liver and in red blood cell populations. Therefore, low availability of Se from fish may have to be considered when assessing Se status of human beings from dietary intake.
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