3 Matching Annotations
  1. May 2020
    1. Results reveal a significant shift in the gut microbiome and metabolome within one day following morphine treatment compared to that observed after placebo. Morphine-induced gut microbial dysbiosis exhibited distinct characteristic signatures, including significant increase in communities associated with pathogenic function, decrease in communities associated with stress tolerance and significant impairment in bile acids and morphine-3-glucuronide/morphine biotransformation in the gut.

      Unsurprisingly, various substances appear to disrupt the microbiome; artificial sweeteners are not unique. Given that I don't worry about opioids, I probably shouldn't worry about sweeteners.

      However, opioids are known for causing constipation. That is to say, they have a clear effect on digestion. Perhaps I should worry about opioids rather than not worry about sweeteners.

  2. Apr 2020
    1. Although it has been proposed that NNS do not affect glycemia (3), data from several recent studies suggest that NNS are not physiologically inert. First, it has been demonstrated that the gastrointestinal tract (4,5) and the pancreas (6,7) can detect sugars through taste receptors and transduction mechanisms that are similar to those indentified in taste cells in the mouth. Second, NNS-induced activation of gut sweet taste receptors in isolated duodenal L cells and pancreatic β-cells triggers the secretion of glucagon-like peptide 1 (GLP-1) (4,5) and insulin (6–9), respectively. Third, data from studies conducted in animal models demonstrate that NNS interact with sweet taste receptors expressed in enteroendocrine cells to increase both active and passive intestinal glucose absorption by upregulating the expression of sodium-dependent glucose transporter isoform 1 (5,10,11) and increasing the translocation of GLUT2 to the apical membrane of intestinal epithelia (12).

      This supports my previous assertion that the effects of artificial sweeteners on the microbiome are taste-mediated. However, I did not predict the intestinal taste receptors. That means that my previous way to falsify the claim, such as delivery by oral gavage, is no longer adequate. Nonetheless, interesting things could be learned from such tests.

    1. These variations were related to inflammation in the host

      In which direction? This statement makes me wonder if inflammation caused the changes in the microbiome.

      It seems possible that the sweetness itself is the ultimate cause. To test this, a study using oral gavage. It's easily plausible that the flavor alerts dietary patterns (I believe humans eat more calories in response to sweeteners, will need to check on source). Alternatively, direct effects on the brain, and downstream effects on the body, is also not out of the question.

      The reason I suspect taste-mediated effects is that it seems unlikely that so many completely unrelated sweeteners would have such similar effects. However, one might might expect more similar results than those found if it were the case (or the dose is so high that the taste changes for some, e.g. saccharin).