It was about time for an artificial sweetener update, wasn't it? |
Whether and to which extent these beneficial effects on gut health are mediated by changes in the gut microbiome is yet still uncertain; and since "uncertain" is a word scientists don't like, Kristian Daily and his colleagues from the University of Liverpool conducted a study to find out, whether the non-negligible health benefits would be brought about by AI <> gut interactions.
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But that's obviously not all that's news-worthy!
I did after all promise you news on products you may be using, as well - aspartame and acesulfame-k, to be precise. Now, while the former is a constant target of public (mostly broscientific) criticism, the latter has been a thorn in my side ever since I have started investigating artificial sweeteners.
Lean more about the "Gut Type Diet" - No Fad, Guaranteed! |
Ok, the results have been derived in a Caenorhabditis elegans, a "worm", but one that has long and actually surprisingly successfully been used as a "model for studying the basic biology of obesity" (Jones. 2009) - I know, I am not convinced either, but if the results do actually translate to humans, this would be major (bad) news for the food industry.
In view of the fact that most companies have been pulling acesulfame-k from their products over the past years, anyway, I would not discard the findings Jolene Zheng et al. present in their latest paper in Chemico-Biological Interactions as meaningless, not despite, but rather because a scientists from PepsiCo was part of the research team which observed these significant increases in intestinal fat (=visceral fat of the worm) when the critters were fed with acesulfam-k sweetened coke.
Cheating? Why would be using artificial sweeteners cheating? In spite of the fact that there is no credible evidence for a causal relationship between the consumption of artificially sweetened foods and obesity (there is a correlation that could well be the result of reverse causation), there is some concerning evidence that the extreme sweet taste and the way people appear to escalate the dosages reduce your bodies ability to control its energy balance by thwarting with its mostly sugar-based first-line energy intake sensor.
What I would not recommend either, though, is to (ab-)use aspartame-containing diet coke as a "weight loss beverage": It's certainly ok to sooth your sweet tooth, when you're dieting and I am not saying that you must not drink one or another Diet Coke or Pepsi on the weekend. What I am saying, though, that I don't believe that the consumption of copious amounts of this stuff will result in a similar body fat reduction (see Figure 2) in you, where compensatory mechanisms, your sweet tongue and a whole host of other things complicate weight and even more so fat loss compared to C. elegans.
That being said, I would be inclined to know, when and if SUCRAM is going to be available as a food additive for humans. It does after all sound quite nice to do your tummy a favor while you're "cheating", right? Although,... when I come to think about it, we actually don't need a "new" sweetener to mess up our gut microbiome. As I already hinted at in a related SuppVersity Classic Article Series with the telling title "Sucralose, Hazardous or Innocent?"(Part I, Part II, Part III), Payne et al. (2012) have already identified fructose, mannitol and d-tagatose as promoters of lactobacillus growth and sucrose as their primary enemy (learn more about the interaction in Part II of the series).
That being said, I would be inclined to know, when and if SUCRAM is going to be available as a food additive for humans. It does after all sound quite nice to do your tummy a favor while you're "cheating", right? Although,... when I come to think about it, we actually don't need a "new" sweetener to mess up our gut microbiome. As I already hinted at in a related SuppVersity Classic Article Series with the telling title "Sucralose, Hazardous or Innocent?"(Part I, Part II, Part III), Payne et al. (2012) have already identified fructose, mannitol and d-tagatose as promoters of lactobacillus growth and sucrose as their primary enemy (learn more about the interaction in Part II of the series).
- Payne, A. N., C. Chassard, and C. Lacroix. "Gut microbial adaptation to dietary consumption of fructose, artificial sweeteners and sugar alcohols: implications for host–microbe interactions contributing to obesity." Obesity Reviews 13.9 (2012): 799-809.
- Pierce, K. M., et al. "The effect of lactose and inulin on intestinal morphology, selected microbial populations and volatile fatty acid concentrations in the gastro-intestinal tract of the weanling pig." ANIMAL SCIENCE-GLASGOW THEN PENICUIK- 82.3 (2006): 311.
- Jones, Kevin T., and Kaveh Ashrafi. "Caenorhabditis elegans as an emerging model for studying the basic biology of obesity." Disease models & mechanisms 2.5-6 (2009): 224-229.
- Vente-Spreeuwenberg, M. A. M., et al. "Effect of dietary protein source on feed intake and small intestinal morphology in newly weaned piglets." Livestock Production Science 86.1 (2004): 169-177.