Early Experience Analyzing Dietary Intake Data from the Canadian Community Health Survey—Nutrition Using the National Cancer Institute (NCI) Method

Background: One of the underpinning elements to support evidence-based decision-making in food and nutrition is the usual dietary intake of a population. It represents the long-run average consumption of a particular dietary component (i.e., food or nutrient). Variations in individual eating habits are observed from day-to-day and between individuals. The National Cancer Institute (NCI) method uses statistical modeling to account for these variations in estimation of usual intakes. This method was originally developed for nutrition survey data in the United States. The main objective of this study was to apply the NCI method in the analysis of Canadian nutrition surveys. Methods: Data from two surveys, the 2004 and 2015 Canadian Community Health Survey—Nutrition were used to estimate usual dietary intake distributions from food sources using the NCI method. The effect of different statistical considerations such as choice of the model, covariates, stratification compared to pooling, and exclusion of outliers were assessed, along with the computational time to convergence. Results: A flowchart to aid in model selection was developed. Different covariates (e.g., age/sex groups, cycle, weekday/weekend of the recall) were used to adjust the estimates of usual intakes. Moreover, larger differences in the ratio of within to between variation for a stratified analysis or a pooled analysis resulted in noticeable differences, particularly in the tails of the distribution of usual intake estimates. Outliers were subsequently removed when the ratio was larger than 10. For an individual age/sex group, the NCI method took 1 h–5 h to obtain results depending on the dietary component. Conclusion: Early experience in using the NCI method with Canadian nutrition surveys data led to the development of a flowchart to facilitate the choice of the NCI model to use. The ability of the NCI method to include covariates permits comparisons between both 2004 and 2015. This study shows that the improper application of pooling and stratification as well as the outlier detection can lead to biased results. This early experience can provide guidance to other researchers and ensures consistency in the analysis of usual dietary intake in the Canadian context

Bisphenol A induces DSB-ATM-p53 signaling leading to cell cycle arrest, senescence, autophagy, stress response, and estrogen release in human fetal lung fibroblasts

Experimental and/or epidemiological studies suggest that prenatal exposure to bisphenol A (BPA) may delay fetal lung development and maturation and increase the susceptibility to childhood respiratory disease. However, the underlying mechanisms remain to be elucidated. In our previous study with cultured human fetal lung fibroblasts (HFLF), we demonstrated that 24-h exposure to 1 and 100 µM BPA increased GPR30 protein in the nuclear fraction. Exposure to 100 μM BPA had no effects on cell viability, but increased cytoplasmic expression of ERβ and release of GDF-15, as well as decreased release of IL-6, ET-1, and IP-10 through suppression of NFκB phosphorylation. By performing global gene expression and pathway analysis in this study, we identified molecular pathways, gene networks, and key molecules that were affected by 100, but not 0.01 and 1 µM BPA in HFLF. Using multiple genomic and proteomic tools, we confirmed these changes at both gene and protein levels. Our data suggest that 100 μM BPA increased CYP1B1 and HSD17B14 gene and protein expression and release of endogenous estradiol, which was associated with increased ROS production and DNA double-strand breaks, upregulation of genes and/or proteins in steroid synthesis and metabolism, and activation of Nrf2-regulated stress response pathways. In addition, BPA activated ATM-p53 signaling pathway, resulting in increased cell cycle arrest at G1 phase, senescence and autophagy, and decreased cell proliferation in HFLF. The results suggest that prenatal exposure to BPA at certain concentrations may affect fetal lung development and maturation, and thereby affecting susceptibility to childhood respiratory diseases