The systematic review and meta-analysis, published in Current Opinion in Lipidology, ​noted that recent studies have identified fructose as uniquely contributing to obesity and its cardiometabolic complications - adding that much of the evidence for this view derives from the unique biochemical, metabolic, and endocrine responses that differentiate fructose from glucose.

"To understand whether these proposed mechanisms result in clinically meaningful modification of cardiovascular risk in humans, we update a series of systematic reviews and meta-analyses of controlled feeding trials to assess the cardiometabolic effects of fructose in isocaloric replacement for glucose," ​explained the researchers, led by Dr John Sievenpiper from St. Michael's Hospital and McMaster University, Canada.

Using data from previous research trials Sievenpiper and his team compared the effects of fructose and glucose against several health risk factors, finding that consuming fructose may increase total cholesterol and postprandial triglycerides, but that fructose did not appear to affect insulin production, other fat levels in the bloodstream or markers of fatty liver disease any more than glucose did.

"Despite concerns about fructose's link to obesity, there is no justification to replace fructose with glucose because there is no evidence of net harm,"​ commented the lead researcher.

In fact, fructose showed potential benefits over glucose in some key risk factor categories, he suggested.

"Some health care analysts have thought fructose to be the cause of obesity because it's metabolized differently than glucose,"​ said Sievenpiper. "In calorie-matched conditions, we found that fructose may actually be better at promoting healthy body weight, blood pressure and glycemic control than glucose."​

"In the absence of clear evidence of net harm, there is no justification to replace fructose with glucose in the diet,"​ concluded the research team.

Study details​

The review pooled data from 20 controlled feeding trials involving 344 participants, all of which investigated the effect of fructose in or on cardiometabolic endpoints.

A pooled analyses of this data showed that although fructose may increase total cholesterol, uric acid, and postprandial triglycerides in isocaloric replacement for glucose, it does not appear to be any worse than glucose in its effects on other aspects of the lipid profile, insulin, or markers of nonalcoholic fatty liver disease.

Indeed, Sievenpiper commented that overconsumption, rather than a type of sugar, was likely to be one of the leading causes of obesity.

"Overall, it's not about swapping fructose with glucose,"​ he said. "Overeating, portion size and calories are what we should be refocusing on – they're our biggest problems."​

Source: Current Opinion in Lipidology​

Volume 25, Issue 1, Pages 8-19, doi: 10.1097/MOL.0000000000000042​

"Fructose vs. glucose and metabolism: do the metabolic differences matter?"​

Authors: Sievenpiper, John L.; de Souza, Russell J; et al​