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Is The Problem With Fructose Calories, Not Fructose?



Crystalline Fructose

Crystalline Fructose

The virtual omnipresence of high-fructose corn syrup in our diet has prompted significant angst regarding the role that fructose may play in both general health and in obesity.

Despite many interesting theories on how fructose may or may not be ‘metabolically’ different from sucrose or glucose, whether fructose in and of itself is a major player in these problems remains unresolved (despite vehement and passionate arguments on both sides of the debate).

It is therefore of interest, that an extensive systematic review and meta-analysis of the impact of fructose on body weight in controlled feeding trials by John Sivenpiper and colleagues from across Canada, published last week in the Annals of Internal Medicine, fails to find any significant impact of fructose on body weight other than what can be attributed to its caloric content.

Thus, the researchers performed an electronic literature search to identify controlled feeding trials lasting 7 or more days that compared the effect on body weight of free fructose and nonfructose carbohydrate in diets providing similar calories (isocaloric trials) or of diets supplemented with free fructose to provide excess energy and usual or control diets (hypercaloric trials).

As the researchers were specifically interested in whether or not fructose is the culprit, they excluded studies evaluating high-fructose corn syrup, which only contains about 42% to 55% of free fructose.

Thirty-one isocaloric trials (637 participants) and 10 hypercaloric trials (119 participants) were included in the analyses and the authors noted that studies tended to be small (<15 participants), short (<12 weeks), and of low quality.

Nevertheless, there was no evidence that fructose had any effect on body weight in isocaloric trials (mean difference, -0.14 kg [95% CI, -0.37 to 0.10 kg] for fructose compared with nonfructose carbohydrate).

Only at high doses of fructose (+104 to 250 g/d, +18% to 97% of total daily energy intake) in the hyper caloric trials was there a significant, albeit modest, increases in weight (about 1 pound), which the authors largely attribute to increased caloric intake.

According to the authors:

“…aggregate data analyses of controlled feeding trials do not support a body weight–increasing effect of fructose in isocaloric exchange for other sources of carbohydrate in the diet. However, evidence indicates that added fructose providing excess energy at extreme levels of intake may have a body weight–increasing effect over the short term, although confounding from excess energy cannot be excluded.”

Thus, despite methodological limitations, there is currently no clear evidence that fructose contributes to weight gain other than by simply providing (extra) calories. In other words, were you to replace the calories from fructose by the same amount of calories from other sugars, your weight would be exactly the same.

Not that this means that increased consumption of excess calories as fructose or otherwise may not be part of the obesity problem – it just does not seem that there is anything particularly ‘bad’ about fructose, as far as weight is concerned.

Others have suggested that fructose may have other detrimental properties that could cause metabolic problems like insulin resistance, fatty liver disease, or elevated triglycerides, but human data on this is likewise sparse (and was not topic of this review).

I believe, based on these findings, that eliminating fructose from your diet only to replace it with another sugar is unlikely to make any difference as far as weight management is concerned. At least, there does not appear to be any hard data suggesting that it would.

AMS
Edmonton, Alberta

ResearchBlogging.orgSievenpiper JL, de Souza RJ, Mirrahimi A, Yu ME, Carleton AJ, Beyene J, Chiavaroli L, Di Buono M, Jenkins AL, Leiter LA, Wolever TM, Kendall CW, & Jenkins DJ (2012). Effect of Fructose on Body Weight in Controlled Feeding Trials: A Systematic Review and Meta-analysis. Annals of internal medicine, 156 (4), 291-304 PMID: 22351714

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1 Comment

  1. Meta analyses are subject to enormous selection bias. There remains abundant evidence that chronically ingested large doses of fructose induce leptin resistance to a greater degree than isocaloric chronic glucose ingestion. Still, Dr. Sharma’s implicit point: that all sugars are obesigenic because of their caloric content is valid. I don’t think even the most rabid anti-fructose crusaders, Lustig for example, argue for substituting glucose. Nevertheless, the question remains open: is fructose a special case; is it essentially a metabolic ‘poison’ that induces derangement of energy homeostasis? I personally remain concerned that it is. Further study will help clarify the matter.

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