Low-calorie Sweeteners and Health—New Developments and Reality Checks-Panelist #2


The following presentation was given at Global Food Forums’ 2017 Sweetener Systems Conference. 

Prof. Richard Mattes, Purdue University, launched his data- rich presentation with a plea: Given the many terms in use for our topic today, “We need consensus!”

Mattes proposed using “low calorie” as the preferred terminology, as it is “easily translatable to consumers.”

Low-calorie sweeteners (LCS) have been recurring subjects of controversy ever since saccharine’s initial discovery in the late 19th century, said Mattes. More recently, in the “sweetener heyday” of the 1980s, controversy swirled around top-line study claims that suggested LCS were associated with weight gain or long-term weight management. Such were the claims that made news headlines.

Closer critical review of the data indicated that aspartame did indeed benefit consumer weight management, when it was substituted for other energy sources—but this did not lead to resolution of the matter. Many subsequent trials continued to raise concerns but without clear supporting data. In study after study cited in Mattes’ presentation, initial top-line conclusions and media headlines ended up being contradicted by either closer examination of the studies’ own data or by subsequent studies.

Today, the use of low-calorie sweeteners in the food supply has increased dramatically, coincident with increases in body mass indices (BMI) and claims that the two trends are causally linked. This has not been substantiated, but three new scientific developments have further contributed to debates on LCSs and health in recent years:

1. Elucidation of the gastrointestinal biome’s roll in energy management
2. Documentation of sweeteners’ effects on dopamine-mediated “reward” mechanisms in the brain
3. The discovery of sweet-taste receptors in the gastrointestinal tract and other organs, such as the pancreas and the brain.

The discovery that sweeteners affect reward centers in the brain led to hypotheses that sweeteners render foods “hyperpalatable,” triggering reward systems in the brain similar to addictive drugs. Mattes, after pointing out that overall per-capita sweetener consumption is down in the U.S., decried the use of terms (such as hyperpalatable). When people are hungry, all foods trigger reward signals in the brain, said Mattes.

In order for any material to be addictive, “There has to be an active component,” Mattes continued. No such components have been identified in foods. Also, even if one applies criteria for “food addictions” to the population at large, it hardly accounts for the growing prevalence of obesity in the population. Even the term addiction is misused in reference to food: “Dopamine responses to addictive drugs are at least an order of magnitude larger than anything observed with any food-related response,” said Mattes.

Mattes cited research purporting to document links between dietary sweeteners, gastrointestinal microflora, obesity and diabetes. Citing two foundational rodent studies for this theory, he once again noted that closer examination of the data refuted the authors’ conclusions.

Sweeteners such as Equal (aspartame), Sweet'N Low (Saccharine) and Splenda (sucralose) are popular among consumers seeking low-calorie options..

Epidemiological studies reveal a link between low-calorie sweeteners and body mass – but in a beneficial way.

Many of the rodent studies cited involved low-calorie sweetener doses (e.g., aspartame) far in excess of an equivalent human Acceptable Daily Intake (ADI). These studies yield contradictory or insignificant results. In order for any material to be addictive, “There has to be an active component,” Mattes continued. No such components have been identified in foods. Also, even if one applies criteria for “food.”

Whether data like this can translate into anything of practical importance is highly suspect,” concluded Mattes. He forensically dispensed with studies postulating that low-calorie sweeteners somehow corrupt brain and appetite “signaling” via alteration of entero-endocrine peptides and receptors. After citing the “intrinsic problems” in using rat models to evaluate human sweet taste perception and energy metabolism (e.g., rats metabolize carbohydrates into fat far more efficiently that humans), Mattes added that “there is no compelling evidence from human studies of any effect of low-calorie sweeteners on entero-endocrine cells.”

Where do we stand now?” asked Mattes. “We know low-calorie sweeteners do affect brain reward mechanisms, but it is not possible to link them to body mass increases. Meanwhile, meta-analyses of epidemiological studies do appear to link low-calorie sweetener consumption to body mass but in a beneficial—rather than problematic—way.”

To those involved in selling low-calorie sweeteners, Mattes offered: “The science supports a beneficial role when used properly. LCS can provide a function tool to manage energy intake and body weight.”

“Low-calorie Sweeteners and Health: New Developments and Reality Checks,” Richard Mattes, MPH, Ph.D., RD, Distinguished Professor of Nutritional Science at Purdue University, Affiliated Scientist at Monell Chemical Senses Center, mattes@purdue.edu

Posted on:January 1, 2017

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