Study: Gut Bacteria on Artificial Sweeteners

Artificial Sweeteners

Artificial Sweeteners

Since nearly everyone consumes artificial sweeteners in something (toothpaste, protein shakes, diet sodas), there’s impressive coverage of any new study on the topic. This of course is an incentive for the study authors to take their conclusions a bit further than they really should, and the headline writers then compete to jump to even more unwarranted conclusions.

So this Israeli study is everywhere: this writeup, “Saccharin solution? Sugar substitutes may mess with gut bacteria—causing obesity in the process,” from The Economist, is among the responsible ones that carefully mention the context of other studies showing no such effects.

In short, researchers gave mice water with sugar substitutes, sugar, or nothing. These researchers were especially interested in the microbiome and investigated the effects on gut bacteria of the different diets; after a week they dosed them with glucose and noted that the mice on sugar substitutes had higher blood sugar, meaning they had not processed the glucose as effectively (which normally occurs by release of insulin.)

They then killed off the gut bacteria in the mice, and the processing of glucose returned to normal, which supports the theory that the gut bacteria themselves had changed in the presence of artificial sweeteners to increase insulin resistance.

This is very interesting and suggests lots more research possibilities on the influence of our biomes on body processes; it tells us something about mice and artificial sweeteners. But it also reminds us that the response of mice to saccharin was the reason cited to attempt to ban it in the US, but further research in primates showed no significant health concerns at reasonable levels of consumption (though it still tastes bad!)

Reaching for significance (and headlines), the researchers then did something very interesting before publication: they tried to tie their results to human obesity. Noting that some correlation studies show consumption of artificial sweeteners is correlated with weight gain, they suggest the possibility (without claiming it) that human obesity is caused by artificial sweeteners interacting with the gut biome. They recruited 7 (7!) nonusers of artificial sweeteners, gave them maximum allowed doses of saccharin, and observed changes in the gut biomes of 4 of the 7 which looked much like the changes seen in the mice. This result, even if accurate, barely reaches statistical significance.

What can we conclude here? That 90% of human nutrition studies can’t be replicated, meaning no single study means much; that there may well be some very interesting research to be done on the gut flora and fauna, since there are many clues showing the microbiome significantly affects digestive and metabolic processes; that researchers are tempted to direct their results toward headlines which get them notoriety and funding; and that since most studies show reasonable use of artificial sweeteners to substitute for sugar is an aid to weight loss and critical for real diabetics, no one should change their habits because of this study.

Let’s look at the headlines generated by the study:

NYTimes: “Artificial Sweeteners May Disrupt Body’s Blood Sugar Controls”
FT: “Israeli researchers link artificial sweeteners with obesity”
Israel Hayom: “Artificial sweeteners may drive diabetes, Israeli study finds”
ABC: “Study: Artificial Sweeteners May Promote Diabetes”
CBC: “Artificial sweeteners linked to obesity epidemic, scientists say”
WSJ: “Research Shows Zero-Calorie Sweeteners Can Raise Blood Sugar”

Note the better-quality publications (NYTimes, WSJ) avoid sensationalizing the results–it’s especially reprehensible to suggest diabetics should be terrorized and stop using artificial sweeteners, which allow them some semblance of sweetness and have been used for decades without causing problems. The weasel word “linked” in “Artificial sweeteners linked to obesity epidemic, scientists say,” should be a clue to the lack of scientific backing for that headline’s claim.

For further reading, I can recommend the WSJ’s relatively cautious coverage: “Research Shows Zero-Calorie Sweeteners Can Raise Blood Sugar,” by Gautam Naik:

“The scope of our discovery is cause for a public reassessment of the massive and unsupervised use of artificial sweeteners,” said Eran Elinav, a physician and immunologist at Israel’s Weizmann Institute of Science and lead author of the study, which appeared Wednesday in the journal Nature….

They transplanted bacteria from artificial-sweetener-fed mice or sugar-fed mice into other mice that were bred to have no gut bacteria of their own and that had never consumed a sweetener product. They found that the bacterial transfer from the sweetener-fed mice raised the blood sugar levels in the transplant recipients—suggesting that the gut microbes had triggered the higher sugar levels in mice fed fake sweeteners.

Was the same link true for people? Dr. Elinav and his colleagues examined the relationship between long-term consumption of artificial sweeteners and various metabolic measurements in some 380 nondiabetic people.

They found that the bacteria in the gut of those who regularly ate fake sweeteners were notably different from those who didn’t. In addition, there was a correlation between the sweetener consumption and a susceptibility to glucose intolerance, which is a disturbance in the blood glucose level.

Correlation, however, doesn’t necessarily mean causation. In the next experiment, seven volunteers who normally didn’t consume fake sugar were asked to consume products high in the sweeteners. After four days, four of them had significantly higher blood-sugar levels as well as altered populations of bacteria in their gut—an outcome similar to what was seen in mice.

“This susceptibility to sweeteners [can now] be predicted ahead of time by profiling the microbes in the people,” said Eran Segal, a co-author of the study and computational biologist at the Weizmann Institute.

The results need to be corroborated through a study with many more participants.

Our lead author certainly wants to take artificial sweeteners away from people, or at least require prescriptions! Can’t have anything go unsupervised. Such attitudes tend to indicate a less-than-objective scientist.

Here’s a blog post from Suppversity which goes into detail–they have actually read the paper, while I have only seen pieces. Not all the mice suffered ill effects, and the paper’s authors also managed to not publicize the fact that the effects were seen most strongly with saccharin, less with sucralose, and hardly at all with aspartame. So the news trumpeted around the world was (to be charitable) incomplete.

More on Diet:

Getting to Less Than 10% Body Fat Like the Models – Ask Me How!
Starbucks, Jamba Juice Make You Fat
Fat Doesn’t Make You Fat. Government Guidelines Did!
‘Fed Up’ Asks, Are All Calories Equal?
Fructose: The True Villain?
More on “Fed Up”, Sugar Subsidies, and Obesity
Another Study on Diet Drinks
LeBron James Cut Carbs for Lean Look
Why We’re Fat: In-Depth Studies Under Way
Almonds: Superfood, Eat Them Daily for Heart Health
Fish Oil Supplements Ward Off Dementia
More on Diet Drinks: Best Studies Show They Aid Weight Loss
Vani Hari: “Food Babe” and Quack
Cleanses and Detox Diets: Quackery
Sugared Soft Drinks: Health Risk? (and What About Diet Soda?)
Gluten-Free Diets: The Nocebo Effect
Acidic Soft Drinks and Sodas: Demineralization Damages Teeth
Fish and Fish Oil for Better Brain Health
Salt: New Research Says Too Little May Be Unhealthy
Bulletproof Coffee: Coffee, Oil, and Butter for Breakfast?

2 comments

  1. I’m not going to comment on the general topic, but I do want to point out something regarding this line: “Less insulin release in the presence of glucose is a condition called insulin resistance.”

    Insulin resistance generally refers to insufficient cellular response to insulin rather than a reduction of total insulin secreted by the pancreatic cells. For example, cells can become desensitized to insulin (especially when insulin levels remain very high), causing those cells to downregulate production of insulin receptors. Fewer insulin receptors along cell membranes leads to a decrease in cellular glucose uptake, which is often described as insulin resistance.

    Like

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