Perhaps this information has already been published on the forum. It seemed to me very interesting and worthy of attention.
Excess fat in the liver cells can accumulate due to chronic poisoning with some substances - and most often this substance is alcohol. But fatty liver disease is very common in people who don't drink, and in this case, overeating and various metabolic problems are blamed. But it turns out that in some cases, non-alcoholic fatty liver disease still occurs due to alcohol, only alcohol here is of internal origin - it is produced by special varieties of intestinal bacteria. It all started with a few patients with non-alcoholic fatty liver disease who had blood alcohol levels several times higher than the norm, although none of them drank. At first, everything was attributed to yeast, which ferments carbohydrates in the digestive system: indeed, there are times when the yeast of our microflora is too active and produces too much alcohol. But treatment with antifungal drugs did not help - obviously, someone else produced the alcohol. Among the intestinal bacteria of those few patients, two strains of Klebsiella pneumoniae were found that produced a lot of ethanol. The researchers took microflora samples from dozens more patients with non-alcoholic fatty liver disease and compared them with microflora samples from healthy people. In patients in 60% of cases, "high-alcohol" strains of K. pneumoniae lived in the intestines . When these same strains were transplanted into mice, the animals developed symptoms of non-alcoholic fatty liver disease; if the mice were then given antibiotics, the disease disappeared. That is, in some cases, non-alcoholic fatty liver disease is still alcoholic. Both patients and doctors dealing with non-alcoholic fatty disease should be keep in mind such an alcohol-bacterial factor.
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Fibro2021
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It has been discussed before but it's always interesting to hear of new research etc.
Sometimes the liver damage comes as a knock on effect of this gut fermentation syndrome, endogenous ethanol fermentation also known as auto brewery syndrome and can make non-drinkers drunk and cause others to become more easily drunk on less booze.
HiI think I got my NAFLD through exposure to chemicals, specifically methanol. The good news is that as I am no longer exposed to it then the consistent improvement in my liver might continue.
Still feel shame that my own stupidity got me into this state!
Hi What do you mean by methanol exposure? However, it seems to me not entirely correct to replace the diagnosis of liver damage with some toxic factor with the diagnosis of NAFLD.
Himaking biodiesel, I would also drink rum after to offset any contamination in my blood. Just an all round bad way to live brought on by the need to commute to work.
Thankfully now retired
The ratio of Ast/alt should show the source, ARLD or NAFLD. I cannot find my AST in any LFT results, my ALT is 17 so I am guessing my AST is higher.
I don't think that the ratio of AST/ALT fully reflects the causative factor of liver damage. It is believed that with ARLD AST increases to a greater extent. On the other hand, many patients with end-stage liver disease have normal ALT/AST values. The increase in ALT/AST most likely indicates background condition hepatitis and liver inflammation, if present.
Yes, I meant the impact of many factors, like several arrows flying at one target. For example, a patient who is overweight and regularly consumes alcohol even in moderation, is unlikely to be correctly classified as NAFLD. At least in such a patient, all causative factors should be indicated but the diagnosis of NAFLD is more likely to apply to a completely non-drinking patient or who drinks alcohol very infrequently.
That is very interesting information. I read on another forum a few days that h pylori can cause cirrhosis. I suffered with the symptoms of that for several years and after continually going back to the doctor was finally diagnosed with h pylori and given a strong course of antibiotics. I have always been reluctant to take antibiotics owing to other issues they cause, but this time I just went ahead and took them because I had had enough. My symptoms have all gone.
I read information about h pylori producing ammonia. Ammonia is now recognized as one of the main factors in liver fibrogenesis, since it directly stimulates the transformation of liver stellate cells into fibroblasts. Fibroblasts produce the collagen that consists fibrous tissue. It is necessary to pay attention to the normalization of the intestinal microflora in connection with the possibility of secondary damage to the liver by toxins of pathogenic and opportunistic intestinal bacteria. I heard that in addition to antibiotics and lactulose, transplantation of intestinal microflora from a healthy donor is considered promising.
That is very interesting. I am sure I was suffering from it for years, because I have just checked my Amazon orders record of when I ordered the book "the H Pylori Diet" - and it was in 2013! Which funnily enough is about about 10 months after I had a major lifestyle change and moved back to the UK from the Mediterranean. I am not saying that alcohol did not contribute to my fatty liver disease - but it could explain why some people who drink a lot don't get cirrhosis and others do, and possibly imply a bit of a two-way street between NAFLD and AFLD, that is not yet directly understood. I worry that it never will be, because I am not sure if the medical establishment is interested in this avenue of research. I personally have never been asked to go over my medical history with my consultant. Guess we have to rely that they go through all our GP records with a fine toothed comb! (And not just the blood results, ultrasound parts).
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