Diet Soda Changes Gut Bacteria
Review of: "Artificial sweeteners induce glucose intolerance by altering the gut microbiota." Suez, J, et al. Nature 514, 181-186. 9 Oct 2014.
Many people, including, I'm guessing, most weight loss doctors, have an instinct that diet sodas are a bad idea, but it's been hard to find research that would back this up. While it's true that diet soda and obesity are associated, it seems reasonable to suspect that people turn toward diet drinks because they are getting heavier, rather thinking the weight gain is in any way due to the soda. A previous myth was that the brain-gut-pancreas system couldn't distinguish artificial sweeteners from the real thing, so that drinking diet soda would cause insulin spikes, that over time would lead to obesity. That's been disproved. However, a scientifically sound reason to avoid diet soda has been found.
In this thoughtful series of experiments reported in Nature last fall, the researchers show that diet drinks may sabotage weight loss efforts and hasten diabetes onset through encouraging the growth of unwanted species of bacteria. Suez and colleagues studied whether saccharin, sucralose and aspartame would alter the composition of the bacteria that live in 10 week old, lean mice. They compared the artificial sweetener group to controls drinking water, water + sucrose and water + glucose. The mice drinking water, sucrose or glucose had similar glucose tolerance curves falling in the normal range. They continued to handle blood sugar well, so would be low risk for diabetes. All three of the artificial sweetener groups developed glucose intolerance within weeks. When they combined the saccharin feeding with a high fat diet, they produced obese, insulin resistant mice. They went on to examine the composition of microbiota in the feces of the mice and found that the artificial sweetener groups had overgrowth of unnatural bacterial species of many types. They then demonstrated that they were able to transfer the glucose intolerance from the sweetener group to the healthy lean group by fecal transplantation. The researchers then went on to treat the mice with antibiotics (ciprofloxacin and metronidazole) and found that the changes in tolerance to glucose were reversible with antibiotics.
This is a remarkable series of findings which strings together several proposals:
1. Artificial sweeteners cause glucose intolerance
2. The glucose intolerance is mediated by gut bacteria
3. Glucose intolerance is "infectious" through fecal transfer
4. It is reversible by antibiotic treatment.
So which comes first, obesity or diet soda drinking? This study didn't directly address that, but it gives a biologically plausible explanation for ill effects of artificial sweeteners on our metabolism. With regard to obesity specifically, the experiments have been fairly convincing that bacteria play a role (for example: V.K. Ridaura et al., Science 341, 6 September 2013) In mice, there is evidence that fulfills roughly all of Koch's postulates: fecal transplants from lean and obese humans will produce lean and obese mice with differing intestinal flora. If you take a lean mouse and have him live with the obese mice, he will not grow heavy, but if you take an obese mouse and put him to live in the cage with the lean mice, he will lose weight. This bodes well for the pressing problem of mouse obesity.
In humans, the prospect of fecal transplant is being tried experimentally and when it becomes accepted, I will try to be one of the first to open a walk-in Eat S*#T! clinic on a busy urban street. Until that time, we are stuck trying to guess which dietary factors to manipulate in order to change the bacteria from "obesity prone" to "obesity resistant" colonies. This paper lends support to the idea that bacteria affect our weight and glucose handling and that it may be worth actively searching out certain microorganisms to aid our metabolism.
Still, It's a long way from there to an obesity cure. I've always been sort of amazed at people's willingness to ingest yogurt because it has active cultures of bacteria in it. I think a bit of skepticism is warranted by consumer. If it is a good bacteria in the yogurt, good for what? And shouldn't one get a stool sample to see what one's levels are before trying to add an organism to the mix? What would be the right dose? Can we just hope that the bacteria will duke it out and that some magical balance will occur with more "good" bacteria than "bad"? Are you sure that you are in need of more L. delbrueckii subsp. bulgaricus in your diet? Do you trust the yogurt makers to decide that?
Don't get me wrong, I like yogurt, but not for the bacteria included.
If there were to be clinics which specialized in fecal transplant, before and after tests would likely be routine, so maybe over time, we would find the answers to the above questions. For now, we will have to wait for some human trials to reproduce the mouse proof of concept studies.