October 28, 2015

Chiavaroli L,  de Souza RJ,  Ha V,  Cozma AI,  Mirrahimi A,  Wang DD,  Yu M,  Carleton AJ,  Di Buono M,  Jenkins AL,  Leiter LA,  Wolever TM,  Beyene J,  Kendall CW,  Jenkins DJ,  Sievenpiper JL. 

J Am Heart Assoc. 2015 Sep 10;4(9). 

In this paper, Chiavaroli L et al. provide an updated meta-analysis on the effect of fructose on cardiovascular lipid risk factors based on a total of 51 isocaloric trials and 8 hypercaloric trials. When isocalorically exchanged for other non-fiber carbohydrates, fructose had no negative effect on major CVD lipid targets. The observed increase in triglycerides (TG) and apolipoprotein B (apoB) in hypercaloric trials were based on a dose range of 163.4 to 213.0 g/day, representing a 24-35% caloric increase compared to the habitual diet. In isocaloric trials where fructose showed no effect on major lipid targets, the doses ranged from 60.8 to 151.0 g/day.

The US NHANES (1977-2004) reported an average of fructose intake around 49 g/day. Canadians consume one-third less added sugars (fructose being one type) compared to the US population, based on Statistic Canada availability data.

Future randomized controlled trials assessing the effect of fructose on body weight or lipid targets using a more realistic daily intake of fructose would help to answer the question as to whether there is a threshold above which, fructose provided as additional Calories starts to impact TG and apoB.

 

Abstract: 

BACKGROUND: Debate over the role of fructose in mediating cardiovascular risk remains active. To update the evidence on the effect of fructose on established therapeutic lipid targets for cardiovascular disease (low-density lipoprotein cholesterol [LDL]-C, apolipoprotein B, non-high-density lipoprotein cholesterol [HDL-C]), and metabolic syndrome (triglycerides and HDL-C), we conducted a systematic review and meta-analysis of controlled feeding trials.

METHODS AND RESULTS: MEDLINE, EMBASE, CINHAL, and the Cochrane Library were searched through July 7, 2015 for controlled feeding trials with follow-up ≥7 days, which investigated the effect of oral fructose compared to a control carbohydrate on lipids (LDL-C, apolipoprotein B, non-HDL-C, triglycerides, and HDL-C) in participants of all health backgrounds. Two independent reviewers extracted relevant data. Data were pooled using random effects models and expressed as mean difference with 95% CI. Interstudy heterogeneity was assessed (Cochran Q statistic) and quantified (I(2) statistic). Eligibility criteria were met by 51 isocaloric trials (n=943), in which fructose was provided in isocaloric exchange for other carbohydrates, and 8 hypercaloric trials (n=125), in which fructose supplemented control diets with excess calories compared to the control diets alone without the excess calories. Fructose had no effect on LDL-C, non-HDL-C, apolipoprotein B, triglycerides, or HDL-C in isocaloric trials. However, in hypercaloric trials, fructose increased apolipoprotein B (n=2 trials; mean difference = 0.18 mmol/L; 95% CI: 0.05, 0.30; P=0.005) and triglycerides (n=8 trials; mean difference = 0.26 mmol/L; 95% CI: 0.11, 0.41; P<0.001). The study is limited by small sample sizes, limited follow-up, and low quality scores of the included trials.

CONCLUSIONS: Pooled analyses showed that fructose only had an adverse effect on established lipid targets when added to existing diets so as to provide excess calories (+21% to 35% energy). When isocalorically exchanged for other carbohydrates, fructose had no adverse effects on blood lipids. More trials that are larger, longer, and higher quality are required.

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