|No, sugar may not be extra-healthy, but there's accumulating evidence that it's alleged "no-sugar" replacement maltodextrin may be even worse.|
Scientists have long believed that the ever-increasing number of people suffering from IBD is a consequence of environmental priming or triggering of a genetically susceptible individual to initiate uncontrolled inflammation against commensal bacteria.
In fact, researchers have meanwhile been able to link many IBD-associated genetic risk loci to interactions between the mucosal immune system and microbes (Jostins. 2012) - in conjunction with a certain disposition to develop IBD, the presence of certain dietary ingredients may thus be critical to the eventual disruption of the host-microbial dynamics in the gut with all its ill health consequences (Spooren. 2013). It is thus only logical that recent studies show that
"IBD patients have alterations in both composition and organization of the commensal microbiome, as well as enhanced mucosal permeability. Overall, the bacterial diversity of the IBD microbiome is reduced, with notable decreases in Bacteroidetes and Firmicutes (especially in specific Clostridium species) and increases in Actinobacteria and Proteobacteria (including Escherichia coli). Additionally, E. coli strains with enhanced virulence have been identified in ileal CD patients.8 These strains, termed adherent-invasive E. coli (AIEC), have enhanced adhesive properties and the ability to invade and replicate within epithelial cells and macrophages" (Nickerson. 2015).According to the latest science, the IBD microbiome also has an altered metabolic activity, with decreases in butyrate-producing bacteria and increases in sulfate-reducing strains noted in multiple studies and leads to a decreases in mucosal barrier function ("leaky gut") that leads to bacterial colonization directly on the surface of the intestinal epithelium, increased bacterial translocation, and stimulation of the immune system.
|Figure 1: MDX enhances AIEC biofilm formation and cellular adhesion and does thus contribute to a decrease in intestinal barrier function and an unwanted increase in bacterial translocation from the gut into cirulation (Nickerson. 2015)|
|Figure 2: Concomitant increases in CD incidence and MDX in the American diet (Nickerson. 2015).|
In their latest review, Nickerson et al. do yet go beyond the effects of MDX as the sole motor of the increase in IBD, citing similar and synergistic effects of other dietary additives, such as emulsifying agents or thickeners, which have also been found to have profound detrimental effects on intestinal homeostasis.
"Examples of dietary emulsifiers include carboxymethyl cellulose (CMC), carrageenan, xanthan gum, and MDX, which are derived from natural products and are classified as GRAS. However, carrageenan can be used to induce bacterially-driven intestinal inflammation in rodents and is now under re-evaluation by the FDA. Likewise, in interleukin-10-deficient mice that are genetically predisposed to colitis, CMC consumption synergizes with genetic risk to result in bacterial overgrowth and aggressive ileitis. Further evidence in humans demonstrates the pathogenic potential for these dietary additives when combined with other risk factors, as supplementation of infant formula with a xanthan gum-based thickener induced late-onset necrotizing enterocolitis in premature infants" (Nickerson. 2015).The purported mechanism by which these emulsifiers act mess with your gut is the way by which they act on the mucosal barrier to decrease viscosity, permitting bacterial translocation and thus potentially driving inflammation.
- Jostins, Luke, et al. "Host-microbe interactions have shaped the genetic architecture of inflammatory bowel disease." Nature 491.7422 (2012): 119-124.
- Nickerson, Kourtney P., Rachael Chanin, and Christine McDonald. "Deregulation of intestinal anti-microbial defense by the dietary additive, maltodextrin." Gut microbes 6.1 (2015): 78-83.
- Spooren, C. E. G. M., et al. "Review article: the association of diet with onset and relapse in patients with inflammatory bowel disease." Alimentary pharmacology & therapeutics 38.10 (2013): 1172-1187.