Gut microbial adaptation to dietary consumption of fructose, artificial sweeteners and sugar alcohols: implications for host-microbe interactions contributing to obesity

Calorie Control Council Comments

Payne AN, Chassard C, Lacroix C. Gut microbial adaptation to dietary consumption of fructose, artificial sweeteners and sugar alcohols: implications for host-microbe interactions contributing to obesity. Obes Rev. 2012 Sep.

A recent review by Payne et al. (1) proposes the hypothesis that sugar compounds—particularly free fructose—contribute to obesity by conditioning gut microbes and altering metabolic capacity. The validity of this hypothesis is compromised, however, by disregard of free fructose generated in sucrosesweetened foods, reliance on outdated notions about fructose consumption and failure to substantiate a cause-and-effect relationship between fructose consumption and obesity.

First, the use of high fructose corn syrup (HFCS) beginning in the early 1970s represented less of a marked change in the delivery of free fructose than the authors imagine. Invert sugar—a syrup product of the sugar industry in which half (medium invert sugar) or nearly all (total invert sugar) of the sucrose is intentionally hydrolyzed (“inverted”) to liberate free fructose and free glucose—was widely used in sugar sweetened beverages prior to the advent of HFCS. And acid-catalyzed hydrolysis (“inversion”) of sucrose in sugar sweetened beverages (SSB) liberating free fructose and glucose is a well-known phenomenon; the amount liberated is dependent on beverage acidity (cola pH is about 3.5), time between bottling and consumption (often months), and storage temperature (increasing temperature accelerates inversion). Sucrose inversion also takes place in acidic fruit (citrus) and vegetable (tomato) preparations. To be sure, the substitution of HFCS (free fructose and free glucose) for sucrose added additional unbound fructose to the diet, but disregard for the significant amounts of free fructose liberated from inversion of sucrose—either through use of invert sugar or through acid hydrolysis in foods and beverages— undermines the authors’ premise that the advent of HFCS resulted in “free fructose overloads.”

Second, the authors’ contention that increased use of HFCS led to a “substantial increase in fructose consumption” relies on outdated fructose exposure data. Initial increases in HFCS use were balanced nearly one-for-one by simultaneous decreases in sucrose use (2), such that available fructose from added sugars has remained remarkably consistent since 1922 at 39 ± 4 grams/day/person (3). And it is not widely appreciated that consumption of added sugars, HFCS and fructose have all been in decline since 1999, while obesity rates have continued to climb. So the authors’ notion that “this substantial increase in fructose consumption has paralleled the increased incidence of obesity in the United States, suggesting its contribution to the development of obesity” is simply untrue and invalid.

And third, the fructose-induced metabolic upsets referenced by the authors are mostly observed in animals and humans using exaggerated protocols (hyperfeeding of individual sugars). In animal models, high fructose diets clearly stimulate hepatic de novo lipogenesis and can cause hepatic steatosis. However, such effects are observed only with high daily fructose intakes; there is no solid evidence that fructose, when consumed in moderate amounts, has undesirable effects in humans (4). It is not surprising, then, that recent meta-analyses (5-12) and reviews (4, 13-16) concluded that within the normal fructose intake range, undesirable effects were not observed (body weight and obesity, blood lipids and hyperlipidemia, blood pressure and uric acid) and that fructose actually improves long-term glycemic control in diabetic subjects. There is no cause-and-effect relationship with obesity over the range of human fructose consumption.

Finally, the authors noted that excessive fructose loads could affect the evolution of the gut microbiome, resulting in increased short-chain fatty acid (SCFA) production, which they guessed could have unfavorable consequences for the host. However, other authors have suggested just the opposite, that increased SCFA production in the colon could have beneficial effects (17). It might best be concluded that effects in humans are inconclusive.

In conclusion, the authors’ hypothesis that sugars affect rising rates of obesity through conditioning of gut microflora, while thought provoking, remains speculative and unproven because it ignores the realities of dietary sugars. Their attempt to implicate free fructose is invalidated by disregard of the substantial free fructose generated in sucrose-sweetened foods, outdated notions about fructose consumption and metabolism, and absence of cause-and-effect data linking fructose intakes with rising rates of obesity.

References
1. Payne AN, Chassard C, Lacroix C. Gut microbial adaptation to dietary consumption of fructose, artificial sweeteners and sugar alcohols: implications for host-microbe interactions contributing to obesity. Obes Rev. 2012 Sep;13:799-809.
2. USDA/Economic Research Service. Food Availability (Per capita) Data System: Loss-adjusted food availability. //www.ers.usda.gov/data-products/foodavailability-%28per-capita%29-data-system.aspx Sugar.xls, updated 13 July 2011.
3. White JS. Challenging the fructose hypothesis: New perspectives on fructose consumption and metabolism. Advances in Nutrition. 2013, January; in press.
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