Micro-biologists with the help of gene-mappers are starting to systematically catalog microbe strains’ molecule making abilities. The molecules produced can now be linked to human biochemistry models. A pattern of relationships is emerging that enables tracing links from specific gut microflora microbes to heart disease, hypoglycemia and metabolic syndrome.
Too much Lecithin. A Common human gut bacteria (L. rhamnosus) in gut microflora repopulated mice makes fishy smelling gas, TMA, that liver converts to TMAO and cholesterol. Atherosclerotic plaques grow faster.
Nature Abstract. Changing gut flora with antibiotics and the TMA production stops. Lecithin has choline which is a neural nutrient. In normal dietary concentrations, the effect is moderate. High levels of Lecithin as a supplement are to be avoided. Repopulating your gut with the right probiotics may be the answer
In Reference [7, below] Probiotic modulation of symbiotic gut microbial-host metabolic interactions in a humanized microbiome mouse model, The specific bacteria or strain is identified as follows:
“…we could add bacteria in terms of probiotics, in one mouse model with humanized microbiome variations in output and contraction of TMAO was linked to different species of probiotic used. Livers of mice fed with L. paracasei showed relative decreases in dimethylamine (DMA), trimethylamine (TMA), leucine, isoleucine, glutamine, and glycogen and increased levels of succinate and lactate. Mice supplemented with L. rhamnosus showed relative decreases in leucine and isoleucine and relative increases in succinate, TMA and trimethylamine-N-oxide (TMAO) in the liver compared to controls.”
We now have an emerging methodology to pick the beneficial strains of probiotics by the molecules that they can make and to control the mix of probiotics in our gut to meet our nutritional needs. The following reference contains a wealth of citations that can be studied to see the status of this recent research.
· “The transgenomic metabolic effects of exposure to either Lactobacillus paracasei or Lactobacillus rhamnosus probiotics have been measured and mapped in humanized extended genome mice (germ-free mice colonized with human baby flora).
· “By definition, superorganisms contain multiple cell types, and the coevolved interacting genomes can only be effectively studied as an in vivo unit in situ using top-down systems biology approaches (Nicholson, 2006; Martin et al, 2007a). Interest in the impact of gut microbial activity on human health is expanding rapidly and many mammalian–microbial associations, both positive and negative, have been reported (Dunne, 2001; Verdu et al, 2004; Nicholson et al, 2005; Gill et al, 2006; Ley et al, 2006).
· “Mammalian–microbial symbiosis can play a strong role in the metabolism of endogenous and exogenous compounds and can also be influential in the etiology and development of several diseases, for example insulin resistance (Dumas et al, 2006), Crohn's disease (Gupta et al, 2000; Marchesi et al, 2007), irritable bowel syndrome (Sartor, 2004; Martin et al, 2006), food allergies (Bjorksten et al, 2001), gastritis and peptic ulcers (Warren, 2000; Marshall, 2003), obesity (Ley et al, 2006; Turnbaugh et al, 2006), cardiovascular disease (Pereira and Gibson, 2002) and gastrointestinal cancers (Dunne, 2001).
· “Activities of the diverse gut microbiota can be highly specific and it has been reported that the establishment of Bifidobacteria is important for the development of the immune system and for maintaining gut function (Blum and Schiffrin, 2003; Salminen et al, 2005; Ouwehand, 2007). In particular, elevated counts in Bifidobacterium with reduced Escherichia coli, streptococci, Bacteroides and clostridia counts in breast-fed babies compared to formula-fed neonates may result in the lower incidence of infections, morbidity and mortality in breast-fed infants (Dai et al, 2000; Kunz et al, 2000).
· “As the microbiome interacts strongly with the host to determine the metabolic phenotype (Holmes and Nicholson, 2005; Gavaghan McKee et al, 2006) and metabolic phenotype influences outcomes of drug interventions (Nicholson et al, 2004; Clayton et al, 2006), there is clearly an important role of understanding these interactions as part of personalized healthcare solutions (Nicholson, 2006).”
 Tsai F, Coyle WJ. The microbiome and obesity: is obesity linked to our gut flora? Curr Gastroenterol Rep. 2009 Aug;11(4):307-13. Review.
 Dumas ME, Barton RH, Toye A, Cloarec O, Blancher C, Rothwell A, Fearnside J, Tatoud R, Blanc V, Lindon JC, Mitchell SC, Holmes E, McCarthy MI, Scott J, Gauguier D, Nicholson JK. Metabolic profiling reveals a contribution of gut microbiota to fatty liver phenotype in insulin-resistant mice. Proc Natl Acad Sci U S A. 2006 Aug 15;103(33):12511-6. Epub 2006 Aug
 Zeisel SH, Mar MH, Howe JC, Holden JM. Concentrations of choline-containing compounds and betaine in common foods. J Nutr. 2003 May;133(5):1302-7. Erratum in: J Nutr. 2003 Sep;133(9):2918.
 Fava F, Lovegrove JA, Gitau R, Jackson KG, Tuohy KM. The gut microbiota and lipid metabolism: implications for human health and coronary heart disease. Curr Med Chem. 2006;13(25):3005-21. Review.
 Martin FP, Wang Y, Sprenger N, Yap IK, Lundstedt T, Lek P, Rezzi S, Ramadan Z, van Bladeren P, Fay LB, Kochhar S, Lindon JC, Holmes E, Nicholson JK. Probiotic modulation of symbiotic gut microbial-host metabolic interactions in a humanized microbiome mouse model. Mol Syst Biol. 2008;4:157. Epub 2008 Jan 15.