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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: Sitting time questionnaires have largely been validated in small convenience samples. The validity of this multi-context sitting questionnaire against an accurate measure of sitting time is reported in a large demographically diverse sample allowing assessment of validity in varied demographic subgroups. Methods: A subgroup of participants of the third wave of the Australian Diabetes, Obesity, and Lifestyle (AusDiab3) study wore activPAL3™ monitors (7 days, 24 hours/day protocol) and reported their sitting time for work, travel, television viewing, leisure computer use and "other" purposes, on weekdays and weekend days (n = 700, age 36-89 years, 45 % men). Correlations (Pearson's r; Spearman's p) of the self-report measures (the composite total, contextual measures and items) with monitor-assessed sitting time were assessed in the whole sample and separately in socio-demographic subgroups. Agreement was assessed using Bland-Altman plots. Results: The composite total had a correlation with monitor-assessed sitting time of r = 0.46 (95 % confidence interval [CI]: 0.40, 0.52); this correlation did not vary significantly between demographic subgroups (all >0.4). The contextual measure most strongly correlated with monitor-assessed sitting time was work (p = 0.25, 95 % CI: 0.17, 0.31), followed by television viewing (p = 0.16, 95 % CI: 0.09, 0.24). Agreement of the composite total with monitored sitting time was poor, with a positive bias (B = 0.53, SE 0.04, p < 0.001) and wide limits of agreement (±4.32 h). Conclusions: This multi-context questionnaire provides a total sitting time measure that ranks participants well for the purposes of assessing health associations but has limited accuracy relative to activPAL-assessed sitting time. Findings did not differ in demographic subgroups. [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: 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: 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: 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]