Buď máte žltačku (to by ste nebol schopný napísať komentár mimo wc) alebo vám lecitín zvyšuje bilirubín - skúste sa objednať na vyšetrenie krvi. Neviem, koľko užívate lecitínu, ale väčšina suplementov/vitamínov/minerálov má krivku U (resp. J) - to znamená, že turbo dávky sú viac škodlivé ako deficit. Človek je evolučne lepšie adaptovaný na mierny deficit (stravy, vitamínov, minerálov) ako mierny prebytok, čo neplatí pri chorobných stavoch, samozrejme. Znížil by som dávku na polovicu a pozoroval zmenu. Sóji, pokiaľ nie je fermentovaná (tempeh, natto, kórejské meju), by som sa vyhol oblúkom.
Harmful or Harmless: Soy Lecithinhttps://chriskresser.com/harmful-or-har ... -lecithin/Intestinal Microbial Metabolism of Phosphatidylcholine and Cardiovascular Risk
W.H. Wilson Tang, Et al. N Engl J Med. Apr 25, 2013; 368(17): 1575–1584.
Studies in germ-free mice and cross-sectional clinical studies in humans have suggested a role for the intestinal microbiota in the pathogenesis of atherosclerosis in patients with a diet rich in phosphatidylcholine (with major sources including EGGS, LIVER, BEEF, and PORK) through the formation of the metabolite trimethylamine and conversion to TMAO.7,15 In our study, we describe the generation of the proatherogenic metabolite TMAO from dietary phosphatidylcholine through the use of stable-isotope-tracer feeding studies.
We further found a role for the intestinal microbiota in the production of TMAO through its suppression by means of oral broad-spectrum antibiotics and then reacquisition of trimethylamine and the production of TMAO from dietary phosphatidylcholine after the withdrawal of antibiotics and subsequent intestinal recolonization. Finally, we describe the potential clinical significance of this intestinal microbiota-dependent metabolite by showing that fasting plasma TMAO levels predict the risk of incident major adverse cardiovascular events independently of traditional cardiovascular risk factors and the presence or extent of coronary artery disease and within multiple low-risk subgroups, including both participants without angiographic evidence of substantial coronary artery disease (i.e., stenosis of <50% in major coronary vessels) and those with low-risk lipid and apolipoprotein levels.
In conclusion, we have shown that intestinal microbes participate in phosphatidylcholine metabolism to form circulating and urinary TMAO. We also established a correlation between high plasma levels of TMAO and an increased risk of incident major adverse cardiovascular events that is independent of traditional risk factors, even in low-risk cohorts. Our findings suggest that pathways that are dependent on the intestinal microbiota may contribute to the pathophysiology of atherosclerotic coronary artery disease and suggest potential therapeutic targets.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3701945/