Wednesday, October 22, 2014

Artificial Science On…Artificial Sweeteners

By Michael D. Shaw

This originally appeared here and I would like to thank Mike for allowing me to publish his work.  RK

artificial sweetenersThis one has it all: Research from a prestigious institute published in a prestige journal; a provocative and contrarian set of findings; topical subject matter, sure to attract mainstream media; and the use of ultra high-tech genome sequencing in the too-cool-for-school realm of the gut biome. Just published online in Nature, the study is entitled “Artificial sweeteners induce glucose intolerance by altering the gut microbiota.” [Suez et al.]

At last! We now have a scientific answer to the paradox as described in the official press release: “For years researchers have been puzzling over the fact that non-caloric artificial sweeteners (NAS) do not seem to assist in weight loss, and some studies have suggested they may even have an opposite effect.” Not so fast.

The most significant use of NAS is in diet soft drinks. When first introduced, they were consumed principally by people trying to cut down on their sugar intake, and these people were either overweight, diabetic, or both. Nowadays, although they have gone more mainstream, it is still true that the products are consumed by the overweight/diabetic group. So, let’s first consider human nature.

If you are counting calories, and drink a fair amount of soda, merely by switching to a diet beverage, you could be saving hundreds of calories per day. Given this windfall benefit, might you be inclined to cheat on your diet a wee bit? Could such cheating equal or even surpass the benefits of the diet soda?

Related to this is the inherent difficulty in obtaining accurate data on food consumption. Nearly all diet studies are based on self-reporting, which is not only fudged on a frequent basis, but such falsifications can be glaringly obvious. How many diet studies are full of subjects who are on a 1000 calorie per day regimen, or even less—as documented by their self-reported food logs—but cannot seem to lose a pound?

Could human nature help explain our “paradox”? Nonetheless, if we assume that some dieters don’t cheat, we still have to explain how a non-caloric substance can somehow promote or sustain obesity. A good study might concentrate on the chemistry of a particular NAS, and even focus on how that substance interacts with the intestinal microbiota. Alternatively, a good study could track dietary intake of lean and obese individuals, and subject them to continuous lab tests (students, faculty, and employees of research universities would be convenient participants).

Alas, Suez et al is far from a good study. Indeed, it is fatally flawed right out of the gate. As an aid to readers, the paper highlights its findings in bold type. The very first finding is “Chronic NAS consumption exacerbates glucose intolerance.” And the first sentence of that paragraph betrays the flaw:

To determine the effects of NAS on glucose homeostasis, we added commercial formulations of saccharin, sucralose or aspartame to the drinking water of lean 10-week-old C57Bl/6 mice. Since all three commercial NAS comprise approx. 5% sweetener and approx. 95% glucose, we used as controls mice drinking only water or water supplemented with either glucose or sucrose.”

Here’s the problem. Saccharin, sucralose, and aspartame are vastly different chemicals, even if they are all perceived by human taste receptors as sweet. Yet, these sweeteners were fed—interchangeably—to the subject mice. Note that the researchers are positing some sort of chemical/physiological effect of these NAS with the gut biome, but they are mixing—and are not accounting for—the properties of the three different chemicals. There is no meaning whatsoever to a biochemical evaluation of NAS as a “group.” One wonders why they did not also include lead, notoriously sweet-tasting, and quite sadly consumed in household paint chips by young children in the past.

But, give the researchers their due. They did further work on saccharin, incredibly also putting the mice on a high (60%) fat diet. Surprise! Many of them became glucose intolerant. And that’s a good thing, since otherwise they would have gained weight to beat the band. Basic physiology, anyone?

As almost an afterthought, humans were part of the study, even if they could not be subjected to fecal transplantation, outrageous diets, and bizarre gut biome kill-off, as were the hapless rodents. To be kind, the researchers could have done a better job with the humans, as well.

All told, 381 non-diabetic humans were involved, and evidently some of them were overweight. A number of conclusions were drawn based on questionnaires, and sketchy extrapolation. From this group, seven healthy, non-users of NAS (and presumably normal weight) volunteers became part of a 7-day experimental study, which lacked a control group. Yet, the researchers boldly proclaimed that “most” (4 out of the 7) developed significantly poorer glycemic responses, when given a large amount of saccharin. As before, diet details were based only on questionnaires, and the number of potential confounding factors is massive.

Rest assured that a comprehensive analysis of this work would have yielded dozens more flaws. Do we really need another example of how the post World War II promise of Science has fallen short—unless you happen to be a researcher on the receiving end of bounteous grants?

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