Sugar-sweetened beverages (SSBs) have been linked to weight gain. It is unclear if other food sources of fructose-containing sugars behave similarly. We conducted a systematic review and meta-analysis of controlled feeding trials to assess the effect of different food sources of fructose-containing sugars on body weight and markers of adiposity. MEDLINE, Embase, and the Cochrane Library were searched through January 2020 for controlled feeding trials ≥2 weeks on the effect of fructose-containing sugars. Trial designs were prespecified by energy control: substitution (energy matched replacement of sugars in diets); addition (excess energy from sugars added to diets); subtraction (energy from sugars subtracted from diets); and ad libitum (energy from sugars freely replaced in diets). The primary outcome was body weight. Secondary outcomes were body mass index, body fat and waist circumference. Independent reviewers extracted data and assessed risk of bias. Certainty of evidence was assessed using GRADE. (NCT02558920) We identified 119 controlled trials (368 trial comparisons, N = 5263) assessing the effect of 10 food sources (SSBs, sweetened dairy alternative (soy), fruit juice, fruit drink, fruit, dried fruit, sweetened cereal grains/bars, sweets, added sweeteners and mixed sources). Total fructose-containing sugars increased body weight (mean difference, 0.29 kg [95% confidence interval, 0.05 to 0.53 kg], P = 0.017) and body fat in addition trials with no effect in other analyses or outcomes. There was evidence of interaction by food source in substitution trials with fruit reducing and mixed sources increasing some outcomes and in addition trials with 100% fruit juice reducing and SSBs and mixed sources increasing some outcomes. The overall certainty of evidence was moderate for the decreasing effect of fruit and fruit juice and the increasing effect of SSBs and mixed sources and high-to-very low for other comparisons. Energy control and food source may mediate the effect of fructose-containing sugars on adiposity. The evidence provides good indication that fruit and 100% fruit juice decrease and SSBs and mixed sources increase markers of adiposity. More high-quality randomized trials of different foods are needed to improve our estimates. American Society for Nutrition, Diabetes Canada, CIHR, Mitacs.
Background: Chronic disease guidelines support tree nut consumption alone or as part of dietary patterns to reduce cardiovascular risk, based on their favorable LDL‐C lowering effect. The effects of nuts on metabolic risk factors other than LDL‐C, however, remain uncertain. Aim: To assess the effect of tree nuts on criteria of the metabolic syndrome, we conducted a systematic review and meta‐analysis of randomized controlled dietary trials. Methods: We searched MEDLINE, EMBASE, CINAHL, and the Cochrane Library (through March 19, 2013). We included relevant randomized controlled trials (RCTs) of 蠅 3 weeks reporting at least 1 criterion of metabolic syndrome. Two independent reviewers extracted all relevant data. Data were pooled using the generic inverse variance method using random effects models and expressed as mean differences (MD) with 95% confidence intervals (CI). Heterogeneity was assessed by Chi² and quantified by I². Study quality was assessed. Results: Eligibility criteria were met by 39 RCTs including 1,676 participants who were otherwise healthy or had dyslipidemia, metabolic syndrome or diabetes mellitus. Tree nut interventions lowered triglycerides compared with control diet interventions (MD=‐0.07 mmol/L [95%CI, ‐0.11, ‐0.04 mmol/L]), but had no effects on waist circumference, HDL‐C, blood pressure, or fasting blood glucose with the direction of effect favoring tree nuts for all except HDL‐C. Limitations: Most of the trials were of short duration (<12 weeks) and of poor quality (MQS<8). Substantial unexplained heterogeneity remained in most analyses. Conclusions: Pooled analyses show a net benefit of tree nuts for metabolic syndrome with decreases in triglycerides across nut types and no adverse effects on other criteria. Longer and higher quality trials are needed. Protocol registration: Clinicaltrials.gov identifier NCT01630980 Grant Funding Source : Supported by the International Tree Nut Council Nutrition Research & Education Foundation
Background and Aims: Elevated postprandial glucose (PPG) levels have been associated with higher incidence of cardiovascular disease and all‐cause mortality. Dietary pulses including beans, lentils and chickpeas have resulted in low and medium PPG responses, however most studies have included few subjects and their overall PPG responses, when taken in equicarbohydrate amounts either alone or in mixed meals, have not been systematically summarized and quantitated. Objective: to synthesize the evidence of the effect of dietary pulses on PPG responses in individuals with diabetes. Methods: MEDLINE, EMBASE, CINAHL and Cochrane were searched through Oct 31, 2013 for all acute human trials in individuals with type 1 and type 2 diabetes reporting data for areas under the PPG curve or glycemic indices. Data were pooled by the generic inverse variance method using random effect models and expressed as ratio of means (RoM) with 95% confidence intervals (CI). Heterogeneity was assessed by Chi2 and quantified by I2. Results: Thirty‐six trials (n=259) from 12 published papers met the inclusion criteria. Pulses significantly reduced the relative PPG by 49% compared to an equicarbohydrate white bread control (RoM: 0.51, CI 0.45‐0.57). Heterogeneity was moderate and statistically significant (I2=30%; p<0.0001), however this effect was consistent across all types of pulses and in mixed meals. Canned pulses showed a weaker effect. Conclusion: Pooled analyses suggest that dietary pulses in diabetic patients result in 50% significantly lower PPG rise compared to an equicarbohydrate white bread control. Grant Funding Source : Pulse Canada and CIHR
To the Editor: The conclusion made by O'Sullivan et al (1) may be unjustified. Proper adjustment for energy is imperative. Although the residuals method (2,3) is valid for the energy-adjustment of nutrient intake, it does not completely adjust for total energy intake. To isolate the effect of a nutrient, the convention is to add total energy to the nutrient residual model (2,3). Important confounding from energy has been observed in the effects of fructose. In a series of systematic reviews and meta-analyses of controlled feeding trials, we found that fructose did not have an adverse effect on markers of nonalcoholic fatty liver disease (NAFLD) (4) or related risk factors (5–10) in comparisons matched for energy. A consistent signal for harm, however, was seen in imbalanced comparisons, in which excess energy from fructose is added to diets compared with diets without the excess energy (4–8). Thus, the effects of fructose appear attributable more to excess energy than fructose. Other confounders associated with NAFLD, absent in the models, include saturated fat, dietary fiber, and physical activity. Although not significantly associated with NAFLD in their univariate models, this does not rule out important residual confounding (2,3), especially because the authors themselves have already shown that a Western dietary pattern is associated with a greater risk of NAFLD in this same cohort (11). Contradictory findings further complicate the matter. Across the total cohort (n = 592), a significant negative association was shown with fructose and NAFLD by liver enzymes (alanine aminotransferase [ALT]), an established marker in the diagnosis and management of NAFLD (12). The positive association with fructose and NAFLD by liver ultrasound was only seen in the obese subset (n = 28). Given the small sample size, there is a real chance this association represents a noncausal false-positive association. To understand whether fructose is independently associated with NAFLD, these results need to be tested in other prospective cohort studies with appropriate adjustments on biopsy-proven NAFLD. To move beyond associations, high-quality randomized trials on biopsy-proven NAFLD are needed.
Background: Tree nut consumption is associated with reduced diabetes risk, however, results from randomized trials on glycemic control have been inconsistent. Aim: We conducted a systematic review and meta‐analysis of randomized controlled trials to assess the effect of tree nuts on glycemic control in individuals with diabetes. Methods: We searched MEDLINE, EMBASE, CINAHL, and Cochrane databases through 14 May 2013 for relevant randomized trials 蠅3‐weeks reporting HbA1c, fasting glucose, fasting insulin, and/or HOMA‐IR. Two independent reviewers extracted relevant data. Data were pooled using the generic inverse variance method and expressed as mean differences (MD) with 95% confidence intervals (CI). Heterogeneity was assessed by Cochran’s Q and quantified by I2. Results: 10 trials (n=374) met the eligibility criteria. Diets emphasizing tree nuts significantly lowered HbA1c (MD=‐0.11 %, 95% CI:‐0.18, ‐0.04 %; P=0.001) and fasting glucose (MD=‐0.20 mmol/L, 95% CI:‐0.38, ‐0.03 mmol/L; P=0.02) compared with isocaloric control diets. No significant treatment effects were observed for fasting insulin and HOMA‐IR. Limitations: Majority of trials were of poor quality and short duration. Conclusion: Pooled analyses show diets high in tree nuts improve glycemic control in individuals with type 2 diabetes. Longer, higher quality trials are needed. Clinicaltrials.gov identifier: NCT01630980 Grant Funding Source : International Tree Nut Council Nutrition Research & Education Foundation
Many clinical practice guidelines recommend dietary pulses for the prevention and management of cardiovascular disease and diabetes. The impact of extracted pulse proteins remains unclear. We therefore conducted a systematic review and meta-analysis of randomized controlled trials of the effect of extracted pulse proteins on therapeutic lipid targets.
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