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• Innovative phenotype-genotype association analysis for categorical genomic data having non-ignorable missing values. • Statistical learning method of random forest is used for variable selection in the analysis. • Weighted logistic ridge regression with EM algorithm is used for missing data imputation in the analysis. • Linear statistical hypothesis testing is used for determining the missingness mechanism in the analysis. • An application to analyzing real data from Australia breast cancer genome-wide association study (GWAS). Genomic data arising from a genome-wide association study (GWAS) are often not only of large-scale, but also incomplete. A specific form of their incompleteness is missing values with non-ignorable missingness mechanism. The intrinsic complications of genomic data present significant challenges in developing an effective and efficient procedure of phenotype-genotype association analysis by a statistical variable selection approach. In this paper we develop a coherent procedure of categorical phenotype-genotype association analysis, in the presence of missing values with non-ignorable missingness mechanism in genomic data. It is developed by integrating the statistical learning methods of random forest for variable selection, joint weighted logistic ridge regression with EM algorithm for missing data imputation, and linear statistical hypothesis testing for determining the missingness mechanism. Two simulated genomic datasets are used to undertake the phenotype-genotype association analysis by the proposed procedure, with the performance validated. The proposed procedure is then applied to analyze a real data set from breast cancer GWAS. [ABSTRACT FROM AUTHOR]

Background: Individuals with impaired fat taste (FT) sensitivity have reduced satiety responses after consuming fatty foods, leading to increased dietary fat intake. Habitual consumption of dietary fat may modulate sensitivity to FT, with high consumption decreasing sensitivity [increasing fatty acid taste threshold (FATT)] and low consumption increasing sensitivity (decreasing FATT). However, some individuals may be less susceptible to diet-mediated changes in FATT due to variations in gene expression. Objective: The objective of this study was to determine the effect of an 8-wk low-fat or high-fat diet on FATT while maintaining baseline weight (<2.0 kg variation) to assess heritability and to explore the effect of genetics on diet-mediated changes in FATT. Design: A co-twin randomized controlled trial including 44 pairs (mean ± SD age: 43.7 ± 15.4 y; 34 monozygotic, 10 dizygotic; 33 women, 10 men, 1 gender-discordant) was conducted. Twins within a pair were randomly allocated to an 8-wk low-fat (<20% of energy from fat) or high-fat (>35% of energy from fat) diet. FATT was assessed by a 3-alternate forced choice methodology and transformed to an ordinal scale (FT rank) at baseline and at 4 and 8 wk. Linear mixed models were fit to assess diet effect on FT rank and diet effect modification due to zygosity. A variance components model was fit to calculate baseline heritability. Results: There was a significant time x diet interaction for FT rank after the 8-wk trial (P < 0.001), with the same conclusions for the subset of participants maintaining baseline weight (low-fat; n = 32; high-fat: n = 35). There was no evidence of zygosity effect modification (interaction of time x diet x zygosity: P = 0.892). Heritability of baseline FT rank was 8%. Conclusions: There appears to be little to no genetic contribution on heritability of FATT or diet-mediated changes to FATT. Rather, environment, specifically dietary fat intake, is the main influencer of FT sensitivity, regardless of body weight. [ABSTRACT FROM AUTHOR]

Background: It has been widely recognized that parental dietary intake is an important and consistent factor influencing children's food intake. However, there are conflicting results with regard to the strength of the parental-child resemblance in dietary intake. Moreover, this association has rarely been investigated in young adult offspring. Objectives: The aims of this study were to describe the dietary intake and food consumption of middle-aged women and their female and male adult offspring (aged 18-23 y) and to examine the association in dietary intake between sex-specific mother-child dyads. Design: We used cross-sectional dietary data for 2017 mother-child pairs from the 21-y follow-up of the Mater-University of Queensland Study of Pregnancy, a birth cohort study. Dietary information was obtained with the use of a 74-item food-frequency questionnaire. We assessed multivariate-adjusted mother-offspring correlations in selected nutrients and food groups and performed correlational analysis while stratifying by living arrangements. Results: Both sons and daughters had a significantly lower percentage of energy from protein than did their mothers. Sons had a significantly higher percentage of energy from fat and a lower percentage of energy from carbohydrates than did their mothers, whereas there was no difference between daughters and mothers. The mother-offspring correlations were weak (r = 0.12-0.29) for most dietary factors and tended to be slightly higher in motherdaughter dyads than in mother-son dyads. Overall, correlations appeared to be stronger in offspring still living with their parents than with their counterparts not living at home, specifically the correlations for consumption of vegetables and rice. Conclusions: Mother-adult offspring dietary resemblance in this Australian cohort was only weak and varied by nutrients, food groups, and the offspring's sex and living arrangements. Factors other than parental dietary habits and home environment seem to have a stronger influence on the diets of young adults. [ABSTRACT FROM AUTHOR]

Background: Reported associations between protein intake from different sources and type 2 diabetes (T2D) have been inconsistent. Objective: We prospectively examined the relations of total, animal, and plant protein intakes with incident T2D. Design: We followed 21,523 participants (women: 61.7%) between 1990 and 2007 from the Melbourne Collaborative Cohort Study who were free of diabetes, cardiovascular disease, cancer, and kidney stones at baseline. We also conducted a meta-analysis that included the results from our cohort and from 10 previous prospective studies. Results: A total of 929 new cases (4.3%) of T2D were documented during a mean of 11.7 y of follow-up. Multivariate-adjusted ORs for incident T2D in the highest compared with lowest quintiles of total and animal protein intakes as percentages of energy were 1.23 (95% CI: 0.96, 1.56; P-trend = 0.029) and 1.29 (95% CI: 0.99, 1.67; P-trend = 0.014), respectively. These associations appeared to be greater in men and in participants with normal baseline plasma glucose, body mass index, or blood pressure. Plant protein intake was inversely associated with incident T2D in women only (OR; 0.60; 95% CI: 0.37, 0.99). In the meta-analysis of 11 prospective cohort studies with 505,624 participants and 37,918 T2D cases (follow-up range: 5-24 y), pooled RRs for the comparison of the highest with lowest categories of total, animal, and plant protein intakes were 1.09 (95% CI: 1.06, 1.13), 1.19 (95% CI: 1.11, 1.28), and 0.95 (95% CI: 0.89, 1.02), respectively. Associations between animal protein intake and T2D were similar across sex, geographic region, length of follow-up, study quality, and method of expressing protein intake. An inverse association between plant protein intake and T2D was observed in women (RR: 0.93; 95% CI: 0.85, 1.00) and in US populations (RR: 0.91; 95% CI: 0.84, 0.97). Conclusion: Higher intakes of total and animal protein were both associated with increased risks of T2D, whereas higher plant protein intake tended to be associated with lower risk of T2D. [ABSTRACT FROM AUTHOR]

Background: These trials are the first randomised controlled trials of telephone-based weight management and healthy lifestyle interventions for low back pain and knee osteoarthritis. This article describes the protocol and statistical analysis plan. Method: These trials are parallel randomised controlled trials that investigate and compare the effect of a telephone-based weight management and healthy lifestyle intervention for improving pain intensity in overweight or obese patients with low back pain or knee osteoarthritis. The analysis plan was finalised prior to initiation of analyses. All data collected as part of the trial were reviewed, without stratification by group, and classified by baseline characteristics, process of care and trial outcomes. Trial outcomes were classified as primary and secondary outcomes. Appropriate descriptive statistics and statistical testing of between-group differences, where relevant, have been planned and described. Conclusions: A protocol for standard analyses was developed for the results of two randomised controlled trials. This protocol describes the data, and the pre-determined statistical tests of relevant outcome measures. The plan demonstrates transparent and verifiable use of the data collected. This a priori protocol will be followed to ensure rigorous standards of data analysis are strictly adhered to. [ABSTRACT FROM AUTHOR]

Background: The omega-3 (n-3) long-chain polyunsaturated fatty acid (LCPUFA) docosahexaenoic acid (DHA) has proven effective at reducing fat storage in animal studies. However, a systematic review of human trials showed a lack of quality data to support or refute this hypothesis. Objective: We sought to determine whether maternal DHA supplementation during the second half of pregnancy results in a lower body mass index (BMI) and percentage of body fat in children. Design: We conducted a follow-up at 3 and 5 y of age of children who were born to mothers enrolled in the DOMInO (DHA to Optimize Mother Infant Outcome) double-blind, randomized controlled trial, in which women with a singleton pregnancy were provided with DHA-rich fish-oil capsules (800 mg DHA/d) or vegetable-oil capsules (control group) in the second half of pregnancy. Primary outcomes were the BMI z score and percentage of body fat at 3 and 5 y of age. Potential interactions between prenatal DHA and the peroxisome proliferator-activated receptor-γ (PPARγ) genotype as a measure of the genetic predisposition to obesity were investigated. Results: A total of 1614 children were eligible for the follow-up. Parent or caregiver consent was obtained for 1531 children (95%), and these children were included in the analysis. BMI z scores and percentages of body fat of children in the DHA group did not differ from those of children in the control group at either 3 y of age [BMI z score adjusted mean difference: 0.03 (95% CI: 20.07, 0.13; P = 0.61); percentage of body fat adjusted mean difference: 20.26 (95% CI: -0.99, 0.46; P = 0.47)] or 5 y of age [BMI z score adjusted mean difference: 0.02 (95% CI: -0.08, 0.12; P = 0.66); percentage of body fat adjusted mean difference: 0.11 (95% CI: 20.60, 0.82; P = 0.75)]. No treatment effects were modified by the PPARγ genotype of the child. Conclusion: Independent of a genetic predisposition to obesity, maternal intake of DHA-rich fish oil during the second half of pregnancy does not affect the growth or body composition of children at 3 or 5 y of age. This trial was registered at www.anzctr.org. au as ACTRN1260500056906 and ACTRN12611001127998. [ABSTRACT FROM AUTHOR]

Background: The consumption of advanced glycation end products (AGEs) has increased because of modern food processing and has been linked to the development of type 2 diabetes in rodents. Objective: We determined whether changing dietary AGE intake could modulate insulin sensitivity and secretion in healthy, overweight individuals. Design: We performed a double-blind, randomized, crossover trial of diets in 20 participants [6 women and 14 men; mean ± SD body mass index (in kg/m²): 29.8 ± 3.7]. Isoenergetic- and macronutrient-matched diets that were high or low in AGE content were alternately consumed for 2 wk and separated by a 4-wk washout period. At the beginning and end of each dietary period, a hyperinsulinemiceuglycemic clamp and an intravenous glucose tolerance test were performed. Dietary, plasma and urinary AGEs N∈-(carboxymethyl) lysine (CML), N∈-(carboxyethyl)lysin (CEL), and methylglyoxal-derived hydroimadazolidine (MG-H1) were measured with the use of mass spectrometry. Results: Participants consumed less CML, CEL, and MG-H1 during the low-AGE dietary period than during the high-AGE period (all P < 0.05), which was confirmed by changes in urinary AGE excretion. There was an overall difference in insulin sensitivity of -22.1 mg ⋅ kg-1 ⋅ min-1 between diets (P = 0.001). Insulin sensitivity increased by 1.3 mg ⋅ kg-1 ⋅ min-1 after the low-AGE diet (P = 0.004), whereas it showed a tendency to decrease by 0.8 mg ⋅ kg-1 ⋅ min-1 after the high-AGE diet (P = 0.086). There was no difference in body weight or insulin secretion between diets (P = NS). Conclusions: A diet that is low in AGEs may reduce the risk of type 2 diabetes by increasing insulin sensitivity. Hence, a restriction in dietary AGE content may be an effective strategy to decrease diabetes and cardiovascular disease risks in overweight individuals. This trial was registered at clinicaltrials.gov as NCT00422253. [ABSTRACT FROM AUTHOR]

Background: Branched-chain amino acids (BCAAs), particularly leucine, act as nutrient signals regulating protein synthesis and degradation as well as glucose metabolism. In addition, leucine has been demonstrated in animal experiments to modulate eating and energy homeostasis. Objective: We aimed to characterize the effects of physiologic and supraphysiologic loads of intraduodenal leucine on eating, gut hormone and motor functions, and blood glucose in humans. Design: Twelve lean men were studied on 3 occasions in a randomized, double-blind order. Antropyloroduodenal motility, plasma ghrelin, cholecystokinin, glucagon-like peptide 1, peptide YY, insulin, glucagon, blood glucose, appetite perceptions, and gastrointestinal symptoms were measured during 90-min intraduodenal infusions of leucine at 0.15 kcal/min (total 3.3 g, 13.5 kcal), 0.45 kcal/min (total 9.9 g, 40.5 kcal), or saline (control). Ad libitum eating from a buffet lunch was quantified immediately after the infusions. Results: Leucine at 0.45 kcal/min inhibited eating (energy intake by w13%, P , 0.05), increased plasma cholecystokinin, slightly reduced blood glucose and increased plasma insulin, and decreased antral pressures (all P , 0.05). Leucine at 0.15 kcal/min had no effect on food intake, blood glucose, or antral pressures but also slightly increased plasma cholecystokinin (P , 0.05). Neither dose affected plasma ghrelin, glucagon, glucagon-like peptide 1 and peptide YY, or pyloric and duodenal pressures. Plasma leucine concentrations were related to the dose of intraduodenal leucine, with substantial increases during both 0.15 and 0.45 kcal/min. Conclusions: The effects of intraduodenal infusions of free leucine on eating are probably not primarily mediated by changes in gut motor and hormone functions, with perhaps the exception of cholecystokinin. Instead, increased plasma leucine concentrations may be a potential signal mediating the eating-inhibitory effect of leucine. The study was registered as a clinical trial with the Australia and New Zealand Clinical Trial Registry (www.anzctr.org.au) as ACTRN12613000899741. [ABSTRACT FROM AUTHOR]

Background: Few well-controlled studies have comprehensively examined the effects of very-low-carbohydrate diets on type 2 diabetes (T2D). Objective: We compared the effects of a very-low-carbohydrate, high-unsaturated fat, low-saturated fat (LC) diet with a highcarbohydrate, low-fat (HC) diet on glycemic control and cardiovascular disease risk factors in T2D after 52 wk. Design: In this randomized controlled trial that was conducted in an outpatient research clinic, 115 obese adults with T2D [mean 6 SD age: 58 6 7 y; body mass index (in kg/m2): 34.6 6 4.3; glycated hemoglobin (HbA1c): 7.3 6 1.1%; duration of diabetes: 8 6 6 y] were randomly assigned to consume either a hypocaloric LC diet [14% of energy as carbohydrate (carbohydrate ,50 g/d), 28% of energy as protein, and 58% of energy as fat (,10% saturated fat)] or an energymatched HC diet [53% of energy as carbohydrate, 17% of energy as protein, and 30% of energy as fat (,10% saturated fat)] combined with supervised aerobic and resistance exercise (60 min; 3 d/wk). Outcomes were glycemic control assessed with use of measurements of HbA1c, fasting blood glucose, glycemic variability assessed with use of 48-h continuous glucose monitoring, diabetes medication, weight, blood pressure, and lipids assessed at baseline, 24, and 52 wk. Results: Both groups achieved similar completion rates (LC diet: 71%; HC diet: 65%) and mean (95% CI) reductions in weight [LC diet: 29.8 kg (211.7, 27.9 kg); HC diet: 210.1 kg (212.0, 28.2 kg)], blood pressure [LC diet: 27.1 (210.6, 23.7)/26.2 (28.2, 24.1) mm Hg; HC diet:25.8 (29.4,22.2)/26.4 (28.4,24.3) mm Hg], HbA1c [LC diet: 21.0% (21.2%, 20.7%); HC diet: 21.0% (21.3%, 20.8%)], fasting glucose [LC diet: 20.7 mmol/L (21.3, 20.1 mmol/L); HC diet: 21.5 mmol/L (22.1, 20.8 mmol/L)], and LDL cholesterol [LC diet: 20.1 mmol/L (20.3, 0.1 mmol/L); HC diet: 20.2 mmol/L (20.4, 0.03 mmol/L)] (P-diet effect $ 0.10). Compared with the HC-diet group, the LC-diet group achieved greater mean (95% CI) reductions in the diabetes medication score [LC diet: 20.5 arbitrary units (20.7, 20.4 arbitrary units); HC diet: 20.2 arbitrary units (20.4, 20.06 arbitrary units); P = 0.02], glycemic variability assessed by measuring the continuous overall net glycemic action-1 [LC diet: 20.5 mmol/L (20.6, 20.3 mmol/L); HC diet: 20.05 mmol/L (20.2, 20.1 mmol/L); P = 0.003], and triglycerides [LC diet: 20.4 mmol/L (20.5, 20.2 mmol/L); HC diet: 20.01 mmol/L (20.2, 0.2 mmol/L); P = 0.001] and greater mean (95% CI) increases in HDL cholesterol [LC diet: 0.1 mmol/L (0.1, 0.2 mmol/L); HC diet: 0.06 mmol/L (20.01, 0.1 mmol/L); P = 0.002]. Conclusions: Both diets achieved substantial weight loss and reduced HbA1c and fasting glucose. The LC diet, which was high in unsaturated fat and low in saturated fat, achieved greater improvements in the lipid profile, blood glucose stability, and reductions in diabetes medication requirements, suggesting an effective strategy for the optimization of T2D management. This trial was registered at www.anzctr.org.au as ACTRN12612000369820. [ABSTRACT FROM AUTHOR]

Background: The Food Insulin Index (FII) is a novel classification of single foods based on insulin responses in healthy subjects relative to an isoenergetic reference food. Objective: Our aim was to compare day-long responses to 2 nutrientmatched diets predicted to have either high or low insulin demand in healthy controls and individuals with type 2 diabetes (T2DM). Design: Twenty adults (10 healthy adults and 10 adults with T2DM) were recruited. On separate mornings, subjects consumed either a high- or low-FII diet in random order. Diets consisted of 3 consecutive meals (breakfast, morning tea, and lunch), matched for macronutrients, fiber, and glycemic index (GI), but with 2-fold difference in insulin demand as predicted by the FII of the component foods. Postprandial glycemia and insulinemia were measured in capillary plasma at regular intervals over 8 h. Results: As predicted by their GI, there were no differences in glycemic responses between the 2 diets in either group (mean 6 SEM; healthy: 6.2 6 0.2 compared with 6.1 6 0.1 mmol/L $ min, P = 0.429; T2DM: 9.96 1.3 compared with 10.36 1.6 mmol/L $ min, P = 0.485). Compared with the high-FII diet, mean postprandial insulin response over 8 h was 53% lower with the low-FII diet in healthy subjects (mean 6 SEM; incremental AUCinsulin 31,900 6 4100 pmol/L $min compared with 68,100 6 11,400 pmol/L $ min, P = 0.003) and 41% lower in subjects with T2DM (mean 6 SEM; incremental AUCinsulin 11,000 6 1800 pmol/L $ min compared with 18,700 6 3100 pmol/L $ min, P = 0.018). Incremental AUCinsulin was statistically significantly different between diets when groups were combined (P = 0.001). Conclusions: The FII algorithm may be a useful tool for reducing postprandial hyperinsulinemia in T2DM, thereby potentially improving insulin resistance and b-cell function. This trial was registered at the Australian New Zealand Clinical Trials Registry as ACTRN12611000654954. [ABSTRACT FROM AUTHOR]

Background: Krill is an increasingly popular source of marine n-3 (ω-3) PUFA that is seen as a premium product. However, to our knowledge, the effect of krill-oil supplementation on insulin sensitivity in humans has not been reported. Objective: We assessed whether supplementation with a blend of krill and salmon (KS) oil [which is rich in eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)] affects insulin sensitivity in overweight men. Design: The design was a randomized, double-blind, controlled crossover trial. A total of 47 men with a mean ± SD age of 46.5 ± 5.1 y, who were overweight [body mass index (in kg/m²) from 25 to 30] but otherwise healthy, received 5 1-g capsules of KS oil or a control (canola oil) for 8 wk and crossed over to another treatment after an 8-wk washout period. The primary outcome was insulin sensitivity assessed by using the Matsuda method from an oral-glucose-tolerance test. Secondary outcomes included lipid profiles, inflammatory markers, 24-h ambulatory blood pressure, and carotid artery intimamedia thickness. Results: Unexpectedly, insulin sensitivity (per the Matsuda index) was 14% lower with the KS oil than with the control oil (P = 0.049). A mediation analysis showed that, after controlling for the likely positive effects of blood EPA and DHA (i.e., the omega-3 index), the reduction in insulin sensitivity after KS-oil supplementation was more marked [27% lower than with the control oil (P = 0.009)]. Conclusions: Supplementation with a blend of KS oil is associated with decreased insulin sensitivity. Thus, krill-oil supplementation in overweight adults could exacerbate risk of diabetes and cardiovascular disease. This trial was prospectively registered at the Australian New Zealand Clinical Trials Registry as ACTRN12611000602921. [ABSTRACT FROM AUTHOR]

BACKGROUND: Fiscal strategies are increasingly considered upstream nutrition promotion measures. However, few trials have investigated the effectiveness or cost effectiveness of pricing manipulations on diet in real-world settings. OBJECTIVE: We assessed the effects on fruit, vegetable, and beverage purchasing and consumption of a 20% price-reduction intervention, a tailored skills-based behavior-change intervention, and a combined intervention compared with a control condition. DESIGN: The Supermarket Healthy Eating for Life trial was a randomized controlled trial conducted over 3 mo [baseline (time 1) to postintervention (time 2) with a 6-mo follow-up (time 3)]. Female primary household shoppers in Melbourne, Australia, were randomly assigned to a 1) skill-building (n = 160), 2) price-reduction (n = 161), 3) combined skill-building and price-reduction (n = 160), or 4) control (n = 161) group. Supermarket transaction data and surveys were used to measure the following study outcomes: fruit, vegetable, and beverage purchases and self-reported fruit and vegetable consumption at each time point. RESULTS: At 3 mo (time 2), price reduction-alone participants purchased more total vegetables and frozen vegetables than did controls. Price reduction-alone and price reduction-plus-skill-building participants purchased more fruit than did controls. Relative to controls, in the price-reduction group, total vegetable consumption increased by 233 g/wk (3.1 servings or 15% more than at baseline), and fruit purchases increased by 364 g/wk (2.4 servings; 35% more than at baseline). Increases were not maintained 6 mo postintervention (time 3). Price reduction-alone participants showed a tendency for a slight increase in fruit consumption at time 2 (P = 0.09) that was maintained at time 3 (P = 0.014). No intervention improved purchases of bottled water or low-calorie beverages. CONCLUSIONS: A 20% price reduction in fruit and vegetables resulted in increased purchasing per household of 35% for fruit and 15% for vegetables over the price-reduction period. These findings show that price modifications can directly increase produce purchases. The Supermarket Healthy Eating for Life trial was registered at Current Controlled Trials Registration as ISRCTN39432901. [ABSTRACT FROM AUTHOR]

Background: Previously published research that examined the effects of high egg consumption in people with type 2 diabetes (T2D) produced conflicting results leading to recommendations to limit egg intake. However, people with T2D may benefit from egg consumption because eggs are a nutritious and convenient way of improving protein and micronutrient contents of the diet, which have importance for satiety and weight management. Objective: In this randomized controlled study, we aimed to determine whether a high-egg diet (2 eggs/d for 6 d/wk) compared with a low-egg diet ( < 2 eggs/wk) affected circulating lipid profiles, in particular high-density lipoprotein (HDL) cholesterol, in overweight or obese people with prediabetes or T2D. Design: A total of 140 participants were randomly assigned to one of the 2 diets as part of a 3-mo weight maintenance study. Participants attended the clinic monthly and were instructed on the specific types of foods and quantities to be consumed. Results: There was no significant difference in the change in HDL cholesterol from screening to 3 mo between groups; the mean difference (95% CI) between high- and low-egg groups was +0.02 mmol/L (—0.03, 0.08 mmol/L; P = 0.38). No between-group differences were shown for total cholesterol, low-density lipoprotein cholesterol, triglycerides, or glycemic control. Both groups were matched for protein intake, but the high-egg group reported less hunger and greater satiety postbreakfast. Polyunsaturated fatty acid (PUFA) and monounsaturated fatty acid (MUFA) intakes significantly increased from baseline in both groups. Conclusions: High egg consumption did not have an adverse effect on the lipid profile of people with T2D in the context of increased MUFA and PUFA consumption. This study suggests that a high-egg diet can be included safely as part of the dietary management of T2D, and it may provide greater satiety. This trial was registered at the Australia New Zealand Clinical Trials Registry (http://www. anzctr.org.au/) as ACTRN12612001266853. Am J Clin Nutr 2015;101:705-13. [ABSTRACT FROM AUTHOR]

Background: Physical inactivity, inadequate dietary protein, and low-grade systemic inflammation contribute to age-related muscle loss, impaired function, and disability. Objective: We assessed the effects of progressive resistance training (PRT) combined with a protein-enriched diet facilitated through lean red meat on lean tissue mass (LTM), muscle size, strength and function, circulating inflammatory markers, blood pressure, and lipids in elderly women. Design: In a 4-mo cluster randomized controlled trial, 100 women aged 60-90 y who were residing in 15 retirement villages were allocated to receive PRT with lean red meat (~160 g cooked) to be consumed 6 d/wk [resistance training plus lean red meat (RT+Meat) group; n = 53] or control PRT [1 serving pasta or rice/d; control resistance training (CRT) group; n = 47)]. All women undertook PRT 2 times/wk and received 1000 IU vitamin D3/d. Results: The mean (± SD) protein intake was greater in the RT+Meat group than in the CRT group throughout the study (1.3 ± 0.3 compared with 1.1 ± 0.3 g ⋅ kg-1 ⋅ d-1, respectively; P < 0.05). The RT+Meat group experienced greater gains in total body LTM (0.45 kg; 95% CI: 0.07, 0.84 kg), leg LTM (0.22 kg; 95% CI: 0.02, 0.42 kg), and muscle strength (18%; 95% CI: 0.03, 0.34) than did the CRT group (all P < 0.05). The RT+Meat group also experienced a 10% greater increase in serum insulin-like growth factor I (P < 0.05) and a 16% greater reduction in the proinflammatory marker interleukin-6 (IL-6) (P < 0.05) after 4 mo. There were no between-group differences for the change in blood lipids or blood pressure. Conclusion: A protein-enriched diet equivalent to ~1.3 g ⋅ kg-1 ⋅ d-1 achieved through lean red meat is safe and effective for enhancing the effects of PRT on LTM and muscle strength and reducing circulating IL- 6 concentrations in elderly women. This trial was registered at the Australian Clinical Trials Registry as ACTRN12609000223235. [ABSTRACT FROM AUTHOR]

Background: Reports have suggested that the consumption of dairy foods may reduce risk of type 2 diabetes on the basis of evidence of raised circulating ruminant fatty acids. Objective: We determined whether certain phospholipid species and fatty acids that are associated with full-fat dairy consumption may also be linked to diminished insulin resistance. Design: Four variables of insulin resistance and sensitivity were defined from oral-glucose-tolerance tests in 86 overweight and obese subjects with metabolic syndrome. Plasma phospholipids, sphingolipids, and fatty acids were determined by using a lipidomic analysis and gas chromatography-mass spectrometry to provide objective markers of dairy consumption. Food records provided information on dairy products. Associations were determined by using linear regression analyses adjusted for potential confounders age, sex, systolic blood pressure, waist:hip ratio, or body mass index (BMI) and corrected for multiple comparisons. Results: Lysophosphatidylcholine, lyso-platelet-activating factor, and several phospholipid fatty acids correlated directly with the number of servings of full-fat dairy foods. Lysophosphatidylcholine and lyso-platelet-activating factor were also associated directly with insulin sensitivity when accounting for the waist:hip ratio (Matsuda index unadjusted, P < 0.001 for both; adjusted for multiple comparisons, P < 0.02 for both) and inversely with insulin resistance (fasting insulin unadjusted, P < 0.001 for both; adjusted, P = 0.04 and P < 0.05, respectively; homeostasis model assessment of insulin resistance adjusted, P = 0.04 for both; post-glucose insulin area under the plasma insulin curve during the 120 min of the test adjusted, P < 0.01 for both). The substitution of BMI for the waist: hip ratio attenuated associations modestly. Phospholipid fatty acid 17:0 also tended to be associated directly with insulin sensitivity and inversely with resistance. Conclusion: Variables of insulin resistance were lower at higher concentrations of specific plasma phospholipids that were also indicators of full-fat dairy consumption [ABSTRACT FROM AUTHOR]

Background: The gastrokinetic drug erythromycin is commonly administered to critically ill patients during intragastric feeding to augment small intestinal nutrient delivery. However, erythromycin has been reported to increase the prevalence of diarrhea, which may reflect reduced absorption and/or accelerated small intestinal transit. Objective: The objective was to evaluate the effects of intravenous erythromycin on small intestinal nutrient absorption and transit in the critically ill. Design: On consecutive days, erythromycin (200 mg in 20 mL 0.9% saline) or placebo (20 mL 0.9% saline) were infused intravenously between -20 and 0 min in a randomized, blinded, crossover fashion. Between 0 and 30 min, a liquid nutrient containing 3-O-methylglucose (3-OMG), [13C]triolein, and [99mTc]sulfur colloid was administered directly into the small intestine at 2 kcal/min. Serum 3-OMG concentrations and exhaled 13CO2 (indices of glucose and lipid absorption, respectively) were measured. Cecal arrival of the infused nutrient was determined by scintigraphy. Data are medians (ranges) and were analyzed by using Wilcoxon's signed-rank test. Results: Thirty-two mechanically ventilated patients were studied. Erythromycin increased small intestinal glucose absorption [3- OMG AUC360: 105.2 (28.9-157.0) for erythromycin compared with 91.8 (51.4-147.9) mmol/L• min for placebo; P = 0.029] but tended to reduce lipid absorption [cumulative percentage dose 13CO2 recovered: 10.4 (0-90.6) compared with 22.6 (0-100) %; P = 0.06]. A trend to slower transit was observed after erythromycin [300 (39- 360) compared with 228 (33-360) min; P = 0.07]. Conclusions: Acute administration of erythromycin increases small intestinal glucose absorption in the critically ill, but there was a tendency for the drug to reduce small intestinal lipid absorption and slow transit. These observations have implications for the use of erythromycin as a gastrokinetic drug in the critically ill. This trial was Registered in the Australian New Zealand Clinical Trials Registry as ACTRN 12610000615088. [ABSTRACT FROM AUTHOR]

Background: Preterm human milk-fed infants often experience suboptimal growth despite the use of human milk fortifier (HMF). The extra protein supplied in fortifiers may be inadequate to meet dietary protein requirements for preterm infants. Objective: We assessed the effect of human milk fortified with a higher-protein HMF on growth in preterm infants. Design: This is a randomized controlled trial in 92 preterm infants born at <31 wk gestation who received maternal breast milk that was fortified with HMF containing 1.4 g protein/100 mL (higher- protein group) or 1.0 g protein/100 mL (current practice) until discharge or estimated due date, whichever came first. The HMFs used were isocaloric and differed only in the amount of protein or carbohydrate. Length, weight, and head-circumference gains were assessed over the study duration. Results: Length gains did not differ between the higher- and standard- protein groups (mean difference: 0.06 cm/wk; 95% CI: -0.01, 0.12 cm/wk; P = 0.08). Infants in the higher-protein group achieved a greater weight at study end (mean difference: 220 g; 95% CI: 23, 419 g; P = 0.03). Secondary analyses showed a significant reduction in the proportion of infants who were less than the 10th percentile for length at the study end in the higher-protein group (risk difference: 0.186; 95% CI: 0.370, 0.003; P = 0.047). Conclusions: A higher protein intake results in less growth faltering in human milk-fed preterm infants. It is possible that a higher-protein fortifier than used in this study is needed. This trial was registered with the Australian New Zealand Clinical Trials Registry (http://www.anzctr.org.au/) as ACTRN12606000525583. [ABSTRACT FROM AUTHOR]