A Classification System for Defining and Estimating Dietary Intake of Live Microbes in US Adults and Children.

BACKGROUND: Consuming live microbes in foods may benefit human health. Live microbe estimates have not previously been associated with individual foods in dietary databases. OBJECTIVES: We aimed to estimate intake of live microbes in US children (aged 2-18 y) and adults (≥19 y) (n = 74,466; 51.2% female). METHODS: Using cross-sectional data from the NHANES (2001-2018), experts assigned foods an estimated level of live microbes per gram [low (Lo), <104 CFU/g; medium (Med), 104-107 CFU/g; or high (Hi), >107 CFU/g]. Probiotic dietary supplements were also assessed. The mean intake of each live microbe category and the percentages of subjects who ate from each live microbe category were determined. Nutrients from foods with live microbes were also determined using the population ratio method. Because the Hi category comprised primarily fermented dairy foods, we also looked at aggregated data for Med or Hi (MedHi), which included an expanded range of live microbe-containing foods, including fruits and vegetables. RESULTS: Our analysis showed that 52%, 20%, and 59% of children/adolescents, and 61%, 26%, and 67% of adults, consumed Med, Hi, or MedHi foods, respectively. Per capita intake of Med, Hi, and MedHi foods was 69, 16, and 85 g/d for children/adolescents, and 106, 21, and 127 g/d for adults, respectively. The proportion of subjects who consumed live microbes and overall per capita intake increased significantly over the 9 cycles/18-y study period (0.9-3.1 g/d per cycle in children across categories and 1.4 g/d per cycle in adults for the Med category). CONCLUSIONS: This study indicated that children, adolescents, and adults in the United States steadily increased their consumption of foods with live microbes between the earliest (2001-2002) and latest (2017-2018) survey cycles. Additional research is needed to determine the relations between exposure to live microbes in foods and specific health outcomes or biomarkers.

Association of Milk Consumption and Vitamin D Status in the US Population by Ethnicity: NHANES 2001-2010 Analysis.

Vitamin D has been identified as a nutrient of public health concern, and higher intake of natural or fortified food sources of vitamin D, such as milk, are encouraged by the 2015-2020 Dietary Guidelines for Americans. We, therefore, examined the association of milk consumption and vitamin D status in the United States (US) population. Twenty-four-hour dietary recall data and serum 25(OH)D concentrations were obtained from the National Health and Nutrition Examination Survey 2001-2010 and were analyzed by linear and logistic regression after adjusting for anthropometric and demographic variables. Significance was set at p < 0.05. Approximately 57-80% children and 42-60% adults were milk consumers. Milk intake (especially reduced-fat, low fat and no-fat milk) was positively associated (plinear trend < 0.05) with serum vitamin D status and with a 31-42% higher probability of meeting recommended serum vitamin D (>50 nmol/L) levels among all age groups. Serum vitamin D status was also associated with both type and amount of milk intake depending upon the age and ethnicity. In conclusion, the results indicate that milk consumers consistently have higher serum vitamin D levels and higher probability of meeting recommended levels. Therefore, increasing milk intake may be an effective strategy to improve the vitamin D status of the US population.

The Pattern of Complementary Foods in American Infants and Children Aged 0⁻5 Years Old-A Cross-Sectional Analysis of Data from the NHANES 2011⁻2014.

Proper nutrition early in life can influence children’s present and future health. While several authoritative sources provide eating/food recommendations, only a few studies have assessed whether these recommendations are followed. The goal of this paper was to examine food and nutrient intakes on any given day during infancy and early childhood among various ethnicities. Twenty-four-hour dietary recall data of 0⁻5 years-old children (n = 2431) from the National Health and Nutrition Examination Survey (NHANES) 2011⁻2014 was used to estimate intakes of nutrients and food groups and prevalence of inadequate intake. Data was analyzed separately for various age groups and ethnicities, and differences in means by age and or race/ethnicity were determined by t-tests with p < 0.05 as significant. The results indicate that intakes of all food groups were expectedly low at 0⁻11 months, increased with age, and were influenced by race/ethnicity. Mixed dish consumption, which also increased with age, made substantial contributions to children’s food group intakes. However, there was a substantial percentage of the population among all age and race/ethnic groups who did not consume the recommended amounts for each food group and had inadequate intakes of key nutrients, such as calcium, vitamin D, and vitamin E. Non-Hispanic black children consumed less dairy and more protein foods, and a significantly greater proportion of these children had inadequate intakes of calcium and vitamin D compared to their peers. In conclusion, the results from this study suggest that a substantial population of American infants and children from 0 to five years of age did not meet food group recommendations and had inadequate intakes of key nutrients such as calcium, vitamin D, and vitamin E from foods.

Multiple cytochrome P-450 genes are concomitantly regulated by vitamin A under steady-state conditions and by retinoic acid during hepatic first-pass metabolism.

Vitamin A (retinol) is an essential precursor for the production of retinoic acid (RA), which in turn is a major regulator of gene expression, affecting cell differentiation throughout the body. Understanding how vitamin A nutritional status, as well as therapeutic retinoid treatment, regulates the expression of retinoid homeostatic genes is important for improvement of dietary recommendations and therapeutic strategies using retinoids. This study investigated genes central to processes of retinoid uptake and storage, release to plasma, and oxidation in the liver of rats under steady-state conditions after different exposures to dietary vitamin A (deficient, marginal, adequate, and supplemented) and acutely after administration of a therapeutic dose of all-trans-RA. Over a very wide range of dietary vitamin A, lecithin:retinol acyltransferase (LRAT) as well as multiple cytochrome P-450s (CYP26A1, CYP26B1, and CYP2C22) differed by diet and were highly correlated with one another and with vitamin A status assessed by liver retinol concentration (all correlations, P < 0.05). After acute treatment with RA, the same genes were rapidly and concomitantly induced, preceding retinoic acid receptor (RAR)ß, a classical direct target of RA. CYP26A1 mRNA exhibited the greatest dynamic range (change of log 2(6) in 3 h). Moreover, CYP26A1 increased more rapidly in the liver of RA-primed rats than naive rats, evidenced by increased CYP26A1 gene expression and increased conversion of [(3)H]RA to polar metabolites. By in situ hybridization, CYP26A1 mRNA was strongly regulated within hepatocytes, closely resembling retinol-binding protein (RBP)4 in location. Overall, whether RA is produced endogenously from retinol or administered exogenously, changes in retinoid homeostatic gene expression simultaneously favor both retinol esterification and RA oxidation, with CYP26A1 exhibiting the greatest dynamic change.

Chronic vitamin A status and acute repletion with retinyl palmitate are determinants of the distribution and catabolism of all-trans-retinoic acid in rats.

The relation between vitamin A (VA) nutritional status and the metabolism of all-trans-retinoic acid (RA) is not well understood. In this study, we determined the tissue distribution and metabolism of a test dose of [(3)H]-RA in rats with graded, diet-dependent, differences in VA status. The design included 3 groups, designated VA-deficient, VA-marginal, and VA-adequate, with liver total retinol concentrations of 9.7, 35.7 and 359 nmol/g, respectively, (P < 0.05), and an additional group of VA-deficient rats treated with a single oral dose of retinyl palmitate (RP) 20 h before the injection of [(3)H]-RA. Plasma, liver, lung, and small intestines, collected 30 min after [(3)H]-RA, were analyzed for total (3)H, unmetabolized [(3)H]-RA, polar organic-phase metabolites of [(3)H]-RA, and aqueous phase [(3)H]-labeled metabolites. In all groups, [(3)H]-RA was rapidly removed from plasma and concentrated in the liver. VA deficiency did not prevent the oxidative metabolism of RA. Nevertheless, the quantity of [(3)H]-RA metabolites in plasma and the ratio of total [(3)H]-polar metabolites to unmetabolized [(3)H]-RA in liver varied directly with VA status (VA-adequate > VA-marginal > VA-deficient, P < 0.05). Moreover, supplementation of VA-deficient rats with RP reduced the metabolism of [(3)H]-RA, similar to that in VA-adequate or VA-marginal rats. Liver retinol concentration, considered a proxy for VA status, was correlated (P < 0.05) with [(3)H]-RA metabolites in liver (R(2) = 0.54), plasma (R(2) = 0.44), lung (R(2) = 0.40), intestine (R(2) = 0.62), and all combined (R(2) = 0.655). Overall, the results demonstrate close linkage between dietary VA intake, hepatic storage of VA, and the degradation of RA and suggest that measuring plasma retinoid metabolites after a dose of RA may provide insight into the metabolism of this bioactive retinoid by visceral organs.

Dietary retinoic acid alters vitamin A kinetics in both the whole body and in specific organs of rats with low vitamin A status.

To study the effects of exogenous retinoic acid on vitamin A (VA) metabolism, we analyzed previously collected tracer kinetic data on VA dynamics in rats with low vitamin A (LA) status either with (LA+RA) or without (LA) retinoic acid supplementation. In spite of low VA intake ( approximately 7 nmol/d), the LA+RA rats were in a slight positive VA balance (0.325 nmol/d vs. -0.168 for LA) for 35 d after administration of [(3)H]retinol-labeled plasma. Using the Windows version of the Simulation, Analysis and Modeling software, we determined that the VA disposal rate was lower in LA+RA than in LA rats (3.98 vs. 5.00 nmol/d) as was the system fractional catabolic rate (0.0548 vs. 0.110 d(-1)). Model-predicted traced mass and residence times (the average time that a molecule of retinol spends in an organ before irreversible loss) were higher for liver (19.4 vs. 1.8 nmol; 5.0 vs. 0.36 d), kidneys (7.0 vs. 2.1 nmol; 1.4 vs. 0.42 d), small intestine (2.1 vs. 0.42 nmol; 0.43 vs. 0.084 d), and lungs (3.2 vs. 0.10 nmol; 1.6 vs. 0.021 d) in the LA+RA compared with the LA rats; there were no major differences for eyes, testes, adrenal glands, or remaining carcass. We conclude that RA supplementation of rats with low VA status affects VA metabolism at both the whole-body level and in specific organs. These organs (liver, kidneys, small intestine, and lungs) have the enzymatic capability and an appropriate cell type to store retinyl esters.