The authors of these articles [Bliss, 2004: (http://www.ncbi.nlm.nih.gov/pubmed/15293038); Al-Mosawi, 2002: (http://www.ncbi.nlm.nih.gov/pubmed/12042902)] and similar articles have discussed the therapeutic effects that some soluble fibers, such as gum acacia or guar gum, have produced in people with chronic kidney disease that hasn't been life-threatening or in people with liver disease. Those types of very-high-molecular-weight polysaccharides can't be hydrolyzed by human enzymes but can be by the enzymes of bacteria in the colon, primarily, that use the breakdown products as substrates for the energy production that drives the cell division of the bacteria, etc. The oral administration of guar gum or gum acacia, among other soluble fibers, have reduced serum urea, serum phosphate/phosphorus, and serum creatinine in people with kidney disease, and the explanation has been that the bacteria use nitrogen-containing compounds for their cellular functions and proliferation. The effects on some of these parameters are not small or minor, really, in many of the articles, and, in my view, the research has validity. The idea has been that the soluble fibers provide the "fuel source" and cause, as a consequence, the bacteria to incorporate more of the nitrogen-containing compounds in the intestinal luminal fluid into their cellular processes.
Before I write the rest of this, I should mention that I think inulin, as a "probiotic," has the potential to be very problematic, and one of the reasons is that inulin can cross the intestinal barrier in the jejunum of the rat, apparently by passive diffusion in between the epithelial cells [Ma et al., 1991: (http://www.ncbi.nlm.nih.gov/pubmed/2035637)]. That "paracellular" ("alongside" the cells) mode of absorption is not uncommon, and inulin has a very low molecular weight (it's ~5000 or so (Ma et al., 1995)). The colon is also permeable to inulin [Ma et al., 1995: (http://www.ncbi.nlm.nih.gov/pubmed/7806033)], and Ma et al. (1995) discussed the fact that the colon had generally been thought to be impermeable to compounds more than 6 angstroms in diameter. The "cross-sectional diameter" of inulin is 15 angstroms, and so inulin "broke the rule," so to speak. Yeah, this is a really, really serious issue, in part because of the way inulin behaves in vivo. I discussed some of my concerns in past postings [(http://hardcorephysiologyfun.blogspot.com/2009/01/disturbing-articles-on-inulin.html); (http://hardcorephysiologyfun.blogspot.com/2009/01/note-on-inulin.html)]. Another reason the inclusion of inulin in more and more products, all over the place, is worrisome is that gamma-inulin, apparently a conformational isomer of inulin, is an immune adjuvant that's been researched for use in potentiating anticancer treatments (http://scholar.google.com/scholar?hl=en&q=cancer+gamma+inulin&as_sdt=2000&as_ylo=&as_vis=0). [Cooper, 1995: (http://www.ncbi.nlm.nih.gov/pubmed/7551236)], and oral inulin or pectin or oligofructose reduced the growths of tumors at sites outside of the intestinal tract [Taper and Roberfroid, 1999: (http://www.ncbi.nlm.nih.gov/pubmed/10395627); (http://jn.nutrition.org/cgi/reprint/129/7/1488S)]. One could make the argument that the inulin served as an adjuvant and activated dendritic cells, which are antigen-presenting cells in the intestinal tract that are in contact with the luminal fluid, exclusively in the intestinal tract, leading to some kind of 'totally safe,' indiscriminate activation of the immune system or to antigen-specific, pathological T-cell responses to epithelial antigens in the colon (thereby leading to some sort of cross-reactive anti-tumor immune response), etc. Even if inulin were confined to the luminal fluid, that effect would be pathological, in my opinion. But it seems possible, to me at least, that inulin was simply absorbed into the extracellular fluid or portal venous blood or reached the mesenteric lymph nodes, etc. It's interesting that the molecular weights of some components of pectin are as low as 300-400 Daltons [Fishman et al., 1991: (http://cat.inist.fr/?aModele=afficheN&cpsidt=5472774)], and others are less than 7,000 Daltons, etc. I'd be very wary, personally, of any soluble fiber that is of those types of low molecular weights and that could conceivably cross the intestinal barrier. It sounds really bad to me.
In any case, my point is that the effects of guar gum, for example, and perhaps some of the other high-MW polysaccharides (the MW of guar gum is between 2 and 20 million Daltons or something like that) have these effects, such as on bile acid reabsorption and probably on the enterohepatic circulation of unconjugated bilirubin, on liver function that could explain their beneficial effects on renal function. Researchers have found that guar gum, for example, increased the reabsorption of bile acids in the small intestine, after their entry, in the bile from the liver, into the duodenum via the common bile duct, also increased the amounts of bile acids entering the large intestine, and nonetheless led to a net loss of sterols via the large intestine [Moundras et al., 1997: (http://www.ncbi.nlm.nih.gov/pubmed/9187619)(http://jn.nutrition.org/cgi/reprint/127/6/1068.pdf); Favier et al., 1997: (http://www.ncbi.nlm.nih.gov/pubmed/9307936)]. Those articles show similar effects. One way of looking at their effects might be to say that they act as cosurfactants/surfactants in the small intestine (gums, such as guar gum and gum arabic, have been used as surfactants in emulsions), thereby enhancing the reabsorption of bile acids in the ileum by reducing the interfacial energy and promoting their binding to the ileal transporters (or something like that), and probiotic "fuel sources" in the large intestine. I don't have time to go through more articles, but increases in the reabsorption of bile acids in the ileum can tend to reduce the enterohepatic circulation of unconjugated bilirubin. If some of the different bile acids remain in the large intestine "too long," they can solubilize unconjugated bilirubin, a hydrophobic or fat-soluble molecule, usually (in the absence of visible or UVA light, for example), and allow for its reabsorption, with potentially damaging consequences for the liver, given the cytotoxic and respiratory-inhibitory effects that very high concentrations of bilirubin can have. Also, the loss of bacteria in the colon was shown to produce major increases in the serum bilirubin concentrations of rats (from mean values of 186 to 289 uM) [Vitek et al., 2005: (http://www.ncbi.nlm.nih.gov/pubmed/15664250)], and the idea with that is that there's a decrease in the rate of consumption of unconjugated bilirubin by the bacteria (because the bacterial counts are very low). So more bilirubin is available for reabsorption in the ileum or along all parts of the intestinal tract, as it turns out, and for ongoing enterohepatic recycling. Excess concentrations of bilirubin can promote portal endotoxemia by interfering with the sequestration of endotoxin by bile acids or something like that (http://scholar.google.com/scholar?hl=en&q=bilirubin+portal+endotoxemia&as_sdt=2000&as_ylo=&as_vis=0). I forget, but another element is that bile acids can be cytotoxic to bacteria in the colon. So there can be this vicious cycle of deteriorating liver function, increases in the enterohepatic recycling of bilirubin, loss of bacteria in the colon due to pathologically-increased levels of cytotoxic bile acids in the luminal fluid of the intestine, due in part to impairments in the ileal reabsorption of bile acids, and so on. It's obviously much more complex than this, and increases in the availabilities of some bile acids to the liver can be cytotoxic to hepatocytes and cholangiocytes and other liver cells, etc. There's also the impact that the activities of glucuronidase enzymes in bacteria and enterocytes might have on bilirubin recycling. One might say that the "extra" bacteria would deconjugate conjugated bilirubin and increase the amounts of unconjugated bilirubin that would be available for ileal reabsorption. The glucuronide conjugates of bilirubin are hydrophilic (water-soluble), and I'm forgetting why this is normally not an issue, if I'm remembering correctly that it isn't an issue. I'll have to read some stuff on that.
Another issues is the fact that some guar gum preparations can be of low quality. Guar gum shouldn't form a "rubber cement" type of "epoxy-resin-like" material as soon as it comes in contact with water, in my opinion. It should be somewhat dispersible and shouldn't just form these pieces of hard @#$&#@# plastic in a glass of water. But hey, that's just my opinion. I'm joking, but that's "not the way it was meant to be." Additionally, xanthan gum has the potential to be problematic, in my view, and can form "rubber cement" types of aggregations almost instantly in water. Some animal research (a lot, I guess) has shown that xanthan gum is more or less the same as guar gum or the like, but it doesn't seem like they're very similar. Most of these are available as individual supplements. Hydrolyzed or modified gums could contain polysaccharides of relatively low molecular weights and might, conceivably, have more potential to be problematic. It's possible that the low-molecular weight components of something like pectin are not problematic or are present at very low concentrations. I don't know. At least pectin is present in foods, but I'd wonder about that type of issue with very low molecular weights. I'd personally be wary of it. Also, there are cases of esophageal obstructions (blockages in the esophagus) from guar gum, and there's one report of anaphylaxis from guar gum. There are many more reports of allergy from psyllium, incidentally, and there's only one report for guar gum, from what I can tell. If it's non-"rubber cement" guar gum, this esophageal obstruction business seems rather unlikely, in my view, but one is supposed to drink it with adequate water and discuss the issues with one's doctor.
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