These are some of the articles [Salminen et al., 2002: (http://toxicology.usu.edu/endnote/Lactobacillus-safety-humans-Fin.pdf)(http://www.ncbi.nlm.nih.gov/pubmed/12410474); Land et al., 2005: (http://www.ncbi.nlm.nih.gov/pubmed/15629999); Kunz et al., 2004: (http://www.ncbi.nlm.nih.gov/pubmed/15085028); De Groote et al., 2005: (http://www.ncbi.nlm.nih.gov/pubmed/15750472); (http://scholar.google.com/scholar?hl=en&q=bacteremia+probiotic+OR+prebiotic+OR+yogurt&as_sdt=2000&as_ylo=&as_vis=0)] whose authors have discussed evidence that the use of the preformed, live strains of Lactobacillus bacteria or other bacteria can cause bacterial endocarditis or sepsis, etc. So-called Lactobacillus bacteremia can occur in a person who isn't taking any "probiotic" supplement, but the point is that disease states in which intestinal permeability has been increased could increase a person's susceptibility to this kind of dramatic, potentially devastating event. It's important to realize that portal endotoxemia, in which there's an abnormally-elevated concentration of endotoxin(s) in the portal venous blood but not in the systemic circulation, in many cases, is not something that only occurs in severe disease states, in which a person is falling on the floor and so forth. There's evidence that portal endotoxemia occurs in some obese people and may contribute to nonalcoholic fatty liver disease in people who may or may not be obese [see Brun et al. (2007) and others: (http://scholar.google.com/scholar?hl=en&q=portal+endotoxemia+%22fatty+liver%22&as_sdt=2000)], and some researchers have estimated that 20-30 percent of people in the US have fatty liver disease [Cave et al., 2007: (http://www.ncbi.nlm.nih.gov/pubmed/17296492); (http://hardcorephysiologyfun.blogspot.com/2009/03/nonalcoholic-fatty-liver-disease-nafld.html)]. It's important to note that bacteremia or sepsis or bacterial endocarditis are not minor events but could permanently devastate a person's intellectual capacity, leaving the person mentally disabled, lead to kidney or liver failure leading to death or transplantation, etc.
The other side of the issue is that there are lots and lots of articles showing that Lactobacillus bacteria can reduce endotoxemia in the context of liver diseases or a variety of traumas (http://scholar.google.com/scholar?q=lactobacillus+endotoxin&hl=en&as_sdt=2001&as_sdtp=on). Even though the use of any old oligosaccharide doesn't sound good to me, Wang et al. (1998) [Wang et al., 1998: (http://www.ncbi.nlm.nih.gov/pubmed/9757556)] found that the administration of a "soluble fiber" polysaccharide reduced the liver damage in D-galactosamine-induced liver failure in rats. The polysaccharide doesn't have to leave the GI tract to exert these effects, and Wang et al. (1998) found evidence that the increases in numbers of Bifidobacteria can reduce the numbers of gram-negative bacteria that endotoxin can be derived from. Cherbut et al. (2003) [Cherbut et al., 2003: (http://cat.inist.fr/?aModele=afficheN&cpsidt=15118468)] found that people were able to tolerate gum acacia (from a commercial standpoint, this is the same thing as "acacia fiber," "gum arabic," or "acacia gum," etc.) easily, and gum acacia promoted the proliferation of Bifidobacteria, etc. There are many reasons that acacia gum and, for example, guar gum would be superior to something like inulin, in my view, in many contexts, but that's just my opinion. I've probably been too inclined toward caution with something like "apple pectin" or "grapefruit pectin" (I'm not sure how that differs from apple pectin), but the low-molecular weight fraction might just be glycoproteins or something. I can't imagine how apples would be innocuous and apple pectin would be "poisonous" or "horrendous." There's a ton of research on pectin, incidentally, and some other mechanisms basically have to do with the overlapping of these effects of soluble fibers with the effects of cholestyramine, a resin that sequesters bile acids. Pectin and some of these other polysaccharides can sequester bile acids but can also promote the reabsorption of the bile acids and act as generalized emulsifiers/surfactants/cosurfactants. Cholestyramine is not really a surfacant (http://scholar.google.com/scholar?hl=en&q=cholestyramine+surfactant&as_sdt=2000&as_ylo=&as_vis=0) and has been associated with various side effects, such as steatorrhea (http://scholar.google.com/scholar?hl=en&q=cholestyramine+steatorrhea&as_sdt=2000&as_ylo=&as_vis=0), in which there's malabsorption of dietary fats (potentially as a consequence of the sequestration of bile acids), and hyperchloremic, normal-anion-gap, metabolic acidosis (http://scholar.google.com/scholar?hl=en&q=cholestyramine+%22metabolic+acidosis%22&as_sdt=2000&as_ylo=&as_vis=0). Arginine hydrochloride can also cause that type of hyperchloremic metabolic acidosis (http://hardcorephysiologyfun.blogspot.com/2009/03/arginine-hydrochloride-and.html). Either pectin or cholestyramine can increase cholesterol 7alpha-hydroxylase activity in hepatocytes and increase the overall pool of bile acids [(http://scholar.google.com/scholar?hl=en&q=pectin+hydroxylase+cholesterol+bile&as_sdt=2000&as_ylo=&as_vis=0); (http://scholar.google.com/scholar?hl=en&q=pectin+hydroxylase+cholesterol+bile+cholestyramine&as_sdt=2000&as_ylo=&as_vis=0)]. Pectins can also decrease the activities of bacterial beta-glucuronidase enzymes and thereby lead to a decrease in the rate at which unconjugated bilirubin is formed in the large intestine [(http://scholar.google.com/scholar?hl=en&q=pectin+glucuronidase&as_sdt=2000&as_ylo=&as_vis=0); Kim et al., 1996: (http://kmbase.medric.or.kr/Main.aspx?d=KMBASE&m=VIEW&i=1007519960050020124)], and that effect could reduce the enterohepatic recycling of bilirubin, potentially (http://scholar.google.com/scholar?q=glucuronidase+bacteria+enterohepatic+recycling+bilirubin&hl=en&as_sdt=2001&as_sdtp=on). Only about half of the articles on pectin and glucuronidase activity have shown a decrease. Some of those have shown increases. But increases in the enterohepatic recycling of bilirubin are thought to contribute to the development of some types of gallstones in adults [Brink et al. (1999) and Vitek et al. (2003), shown here: (http://scholar.google.com/scholar?hl=en&q=enterohepatic+bilirubin&as_sdt=2000&as_ylo=&as_vis=0)]. It's important to note that the complex effects of these polysaccharides on bile acid reabsorption could account for those effects, but the research showing that pectin or guar gum, etc., can inhibit gallstone formation or the like, such as in animals or in association studies in humans, could be explained in terms of the polysaccharides' effects on bile acids or on the enterohepatic recycling of bilirubin [(http://scholar.google.com/scholar?hl=en&q=pectin+gallstone&as_sdt=2000&as_ylo=&as_vis=0); (http://scholar.google.com/scholar?hl=en&q=gallstone+pectin+OR+%22guar+gum%22&as_sdt=2000&as_ylo=&as_vis=0)]. There's also the whole pancreatic cancer risk-reduction-association stuff (http://scholar.google.com/scholar?hl=en&q=%22soluble+fiber%22+pancreatic+cancer&as_sdt=2000&as_ylo=&as_vis=0), and some of these soluble, indigestible, high-molecular weight polysaccharides can increase pancreatic exocrine function (http://scholar.google.com/scholar?hl=en&q=pancreatic+exocrine+acacia+OR+pectin+OR+%22guar+gum%22&as_sdt=2000&as_ylo=&as_vis=0). I discussed some of the risks of some of these things in a previous posting (http://hardcorephysiologyfun.blogspot.com/2009/12/potential-effects-of-soluble-fibers-as.html), and those things are worth keeping in mind, in my opinion. But hey, it's no skin off my nose. Have a nice trip, as they say. In any case, the research is a bit chaotic, but there's a large amount of it. The main point is that I think the use of specific indigestible polysaccharides would potentially pose a less extreme range of possible outcomes than the use of the actual bacteria would, particularly since the supplements, as opposed to the foods sold in groceries or whatever, contain larger amounts of bacteria and need to be shipped with ice. I dunno. That doesn't sound so good to me. I used to think the main problem would be the destruction of the bacteria by stomach acid, but apparently it's not even the most important issue, necessarily. Then I thought that the products might be contaminated. That's not even the issue. It's the "good" bacteria themselves that are thought to have entered the bloodstream in some of these cases. The quality control in the realm of the actual baterial supplements seems to be lacking, as discussed in this article [Hamilton-Miller et al., 2002: (http://www.ncbi.nlm.nih.gov/pubmed/11852901)]. It seems really chaotic to me, in the context of the actual bacterial supplements (as opposed to the soluble fibers that are fuel sources for the existing bacteria). But even some of these lowly foods may pose risks to vulnerable individuals [Presterl et al., 2001: (http://scholar.google.com/scholar?hl=en&q=lactobacillus+bacteremia+yogurt&as_sdt=2000&as_ylo=&as_vis=0)]. A person should discuss this type of thing with one's doctor, however, and I obviously can't make any statements about the safety or lack of safety of any product or supplement.
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