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