59 research outputs found
Do the Poor Pay More for Healthy Food? An Empirical Economic Analysis
Food Consumption/Nutrition/Food Safety,
Consumer-Preferred Attributes of a Fresh Ground Beef and Turkey Product: A Conjoint Analysis
A random sample of 3,400 Louisiana households was surveyed by mail to determine their ratings for a number of product profiles involving a combined fresh ground beef and turkey product. The attributes and levels of the new product included form (fresh, frozen), identity of the packager (retailer, processor), percentage of beef in product (50,70,90), and price of the combined product as a percentage of ground beef (80,90,100). Based on 2,781 observations, the order of importance of the attributes were, in order of declining importance, content, form, price, and packager. Consumer utility was highly sensitive to the content of beef, with a higher content being preferred.Consumer/Household Economics,
TASTE PANEL EVALUATIONS OF THE ACCEPTABILITY AND WILLINGNESS TO PAY FOR ALTERNATIVE BLENDS OF GROUND MEATS
An untrained consumer panel evaluated the acceptability, willingness to purchase and pricing of several different combinations of fresh ground beef and ground turkey. Important product attributes were flavor and texture, along with previous at home experience with the combined product. Thirty percent turkey appears to be the maximum for acceptability.Consumer/Household Economics,
Nutrient Contribution of the Dinner Meal Consumed by Low-Income Minority Preschool Children
Objective: To examine the energy and nutrient intake of dinner of low income preschool minority groups, African-Americans and Mexican-Americans, attending Head Start (HS). Design: Cross-sectional study of intake at dinner using digital photography. Pictorial records were converted to energy and nutrient intakes using NDS-R Nutritional software. Means±SE for total grams of food and beverages, energy, and macro- and micro-nutrients were determined and compared with recommendations. Setting: Home assessment dinner of children enrolled in HS in Houston, TX. Subjects: Low-income children (n=214), 3 to 5 years (mean age 4.4 ± 0.7 years; 48% boys; 53% Mexican-American). Results: Energy from food and beverages and food was 350.29±10.36 kcals and 302.35±10.46 kcals, respectively. Mean protein, carbohydrate, and total fat intakes were 14.22±0.52 g (16.32% of total energy), 44.33±1.25 g (52.24%), and 13.18±0.56 g (32.29%), respectively, which provided 95.4±0.52%, 44.5±1.25%, and 10.4±0.11% of the requirements for protein, carbohydrate, and dietary fiber, respectively; these were consistent with recommendations. Intakes of vitamin D, calcium, and potassium were 0.66±0.08 mcg, 102.61±5.03 mg, and 404.42±13.63 mg, respectively; which constituted only 6.6±0.08%, 12.7±5.03%, and 10.7±13.63% of these nutrients of public health concern. Conclusions: Children participating in HS had low intakes of nutrients of public health concern at the dinner meal. The dinner meal is an integral part of the daily intake of preschool children and this study suggests that micronutrient intakes could be improved. It is important to educate mothers and children as to what constitutes a nutrient-dense meal and to confront barriers to consumption of these meals
Association of candy consumption with body weight measures, other health risk factors for cardiovascular disease, and diet quality in US children and adolescents: NHANES 1999–2004
Objective : The purpose of this study was to determine the effects of total, chocolate, or sugar candy consumption on intakes of total energy, fat, and added sugars; diet quality; weight/adiposity parameters; and risk factors for cardiovascular disease in children 2–13 years of age (n=7,049) and adolescents 14–18 years (n=4,132) participating in the 1999–2004 National Health and Nutrition Examination Survey. Methods : Twenty-four hour dietary recalls were used to determine intake. Diet quality was determined using the Healthy Eating Index-2005 (HEI-2005). Covariate-adjusted means, standard errors, and prevalence rates were determined for each candy consumption group. Odds ratios were used to determine the likelihood of associations with weight status and diet quality. Results : In younger children, total, chocolate, and sugar candy consumption was 11.4 g±1.61, 4.8 g±0.35, and 6.6 g±0.46, respectively. In adolescents, total, chocolate, and sugar candy consumption was 13.0 g±0.87, 7.0 g±0.56, and 5.9 g±0.56, respectively. Total candy consumers had higher intakes of total energy (2248.9 kcals±26.8 vs 1993.1 kcals±15.1, p<0.0001) and added sugars (27.7 g±0.44 vs 23.4 g±0.38, p<0.0001) than non-consumers. Mean HEI-2005 score was not different in total candy and sugar candy consumers as compared to non-consumers, but was significantly lower in chocolate candy consumers (46.7±0.8 vs 48.3±0.4, p = 0.0337). Weight, body mass index (BMI), waist circumference, percentiles/z-score for weight-for-age and BMI-for-age were lower for candy consumers as compared to non-consumers. Candy consumers were 22 and 26%, respectively, less likely to be overweight and obese than non-candy consumers. Blood pressure, blood lipid levels, and cardiovascular risk factors were not different between total, chocolate, and sugar candy consumers and non-consumers (except that sugar candy consumers had lower C-reactive protein levels than non-consumers). Conclusion : This study suggests that candy consumption did not adversely affect health risk markers in children and adolescents
Diet quality is positively associated with 100% fruit juice consumption in children and adults in the United States: NHANES 2003-2006
<p>Abstract</p> <p>Background</p> <p>One hundred percent fruit juice (100% FJ) has been viewed by some as a sweetened beverage with concerns about its effect on weight. Little regard has been given to the contribution of 100% FJ to diet quality.</p> <p>Methods</p> <p>In this study data from the 2003-2006 National Health and Nutrition Examination Survey were used to examine the association of 100% FJ consumption with diet quality in participants 2-5 years of age (y) (n = 1665), 6-12 y (n = 2446), 13-18 y (n = 3139), and 19+y (n = 8861). Two 24-hour dietary recalls were used to determine usual intake using the National Cancer Institute method. Usual intake, standard errors, and regression analyses (juice independent variable and Healthy Eating Index-2005 [HEI-2005] components were dependent variables), using appropriate covariates, were determined using sample weights.</p> <p>Results</p> <p>The percentage of participants 2-5 y, 6-12 y, 13-18 y, and 19+y that consumed 100% FJ was 71%, 57%, 45%, and 62%, respectively. Usual intake of 100% FJ (ounce [oz]/day) among the four age groups was: 5.8 ± 0.6, 2.6 ± 0.4, 3.7 ± 0.4, and 2.4 ± 0.2 for those in age groups 2-5 y, 6-12 y, 13-18 y, and 19+y, respectively. Consumption of 100% FJ was associated with higher energy intake in 6-12 y, 13-18 y, and 19+y; and higher total, saturated, and discretionary fats in 13-18 y participants. Consumption of 100% FJ was associated with higher total HEI-2005 scores in all age groups (< 0.0001). In 100% FJ consumers, total and whole fruit consumption was higher and intake of added sugars was lower in all age groups.</p> <p>Conclusions</p> <p>Usual intake of 100% FJ consumption exceeded MyPyramid recommendations for children 2-5 y, but was associated with better diet quality in all age groups and should be encouraged in moderation as part of a healthy diet.</p
Association of Coding Variants in Hydroxysteroid 17-beta Dehydrogenase 14 (HSD17B14) with Reduced Progression to End Stage Kidney Disease in Type 1 Diabetes
Background Rare variants ingenecodingregions likely have agreater impactondisease-relatedphenotypes than common variants through disruption of their encoded protein. We searched for rare variants associated with onset of ESKD in individuals with type 1 diabetes at advanced kidney disease stage. Methods Gene-basedexome array analyses of15,449genes infivelarge incidence cohortsof individualswith type 1diabetes andproteinuriawere analyzedfor survival time toESKD, testing the top gene in a sixth cohort (n52372/1115 events all cohorts) and replicating in two retrospective case-control studies (n51072 cases, 752 controls). Deep resequencing of the top associated gene in five cohorts confirmed the findings. We performed immunohistochemistry and gene expression experiments in human control and diseased cells, and in mouse ischemia reperfusion and aristolochic acid nephropathy models. Results Protein coding variants in the hydroxysteroid 17- b dehydrogenase 14 gene (HSD17B14), predicted to affect protein structure, had a net protective effect against development of ESKD at exome-wide significance (n54196; P value53.331027). The HSD17B14 gene and encoded enzyme were robustly expressed in healthy human kidney, maximally in proximal tubular cells. Paradoxically, gene and protein expression were attenuated in human diabetic proximal tubules and in mouse kidney injury models. Expressed HSD17B14 gene and protein levels remained low without recovery after 21 days in a murine ischemic reperfusion injury model. Decreased gene expression was found in other CKD-associated renal pathologies. Conclusions HSD17B14 gene ismechanistically involved in diabetic kidney disease. The encoded sex steroid enzyme is a druggable target, potentially opening a new avenue for therapeutic development.Peer reviewe
Expansion of CD4+CD25+ and CD25- T-Bet, GATA-3, Foxp3 and RORγt Cells in Allergic Inflammation, Local Lung Distribution and Chemokine Gene Expression
Allergic asthma is associated with airway eosinophilia, which is regulated by
different T-effector cells. T cells express transcription factors T-bet, GATA-3,
RORγt and Foxp3, representing Th1, Th2, Th17 and Treg cells respectively. No
study has directly determined the relative presence of each of these T cell
subsets concomitantly in a model of allergic airway inflammation. In this study
we determined the degree of expansion of these T cell subsets, in the lungs of
allergen challenged mice. Cell proliferation was determined by incorporation of
5-bromo-2′-deoxyuridine (BrdU) together with 7-aminoactnomycin (7-AAD).
The immunohistochemical localisation of T cells in the lung microenvironments
was also quantified. Local expression of cytokines, chemokines and receptor
genes was measured using real-time RT-PCR array analysis in tissue sections
isolated by laser microdissection and pressure catapulting technology. Allergen
exposure increased the numbers of T-bet+,
GATA-3+, RORγt+ and
Foxp3+ cells in CD4+CD25+
and CD4+CD25- T cells, with the greatest expansion of
GATA-3+ cells. The majority of
CD4+CD25+ T-bet+,
GATA-3+, RORγt+ and
Foxp3+ cells had incorporated BrdU and underwent
proliferation during allergen exposure. Allergen exposure led to the
accumulation of T-bet+, GATA-3+ and
Foxp3+ cells in peribronchial and alveolar tissue,
GATA-3+ and Foxp3+ cells in perivascular
tissue, and RORγt+ cells in alveolar tissue. A total of 28
cytokines, chemokines and receptor genes were altered more than 3 fold upon
allergen exposure, with expression of half of the genes claimed in all three
microenvironments. Our study shows that allergen exposure affects all T effector
cells in lung, with a dominant of Th2 cells, but with different local cell
distribution, probably due to a distinguished local inflammatory milieu
Whole-genome sequencing reveals host factors underlying critical COVID-19
Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2–4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease
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