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Masterjohn Right? Treating Fatty Liver

Discussion in 'Diet' started by ecstatichamster, Apr 21, 2019.

  1. ecstatichamster

    ecstatichamster Member

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    What really causes fatty liver?

    I think I have a fatty liver but not sure.

    Here is what Masterjohn says in this video.

    Fatty liver is caused by too much fructose/sugar and fat. Mostly fat people have fatty liver.

    (I’m not fat, but I’m 15 pounds overweight probably.)

    Eat nothing but starch (avoid fructose/sugar) and protein
    Eat several eggs a day for choline
    Eat very low fat proteins
    Eat cups of dark colored vegetables raw or semi raw, for “bulk” and folate (or use legumes)

    That is supposed to help get rid of fatty liver.

    What I’m not sure of is this.

    1. What causes it? I have a feeling that PUFAs are involved

    2. Can you get rid of it with a no fat diet high in starch, really?

    3. Must you avoid fructose/sugar during this time?

    Here is the video:

     
  2. TeaRex14

    TeaRex14 Member

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    He's partially right, the issue with fructose is it needs choline to be exported from the liver as cholesterol. Without sufficient choline, the fructose is converted to liver fat. Eating liver, eggs, and dairy will give you plenty of choline, I also add about 700mgs of choline l-bitartrate to a smoothie I drink daily. Choline is essential for deactivating estrogen as well, so it's pretty essential to the organism. I think another big underlying factor to fatty liver is just a caloric intake that exceeds your demand, whether it be fat or sugar.
     
  3. sugarbabe

    sugarbabe Member

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    The fructose angle doesn't explain why nearly all fruitarians are super skinny. Can you be skinny and still have a fatty liver? Surely fruitarians aren't getting much choline unless they are eating a boatload of beets and spinach and drink gallons of orange juice.
     
  4. Amazoniac

    Amazoniac Member

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    - Non-alcoholic fatty liver disease in underweight patients with inflammatory bowel disease: A case-control study

    "This case-control study assessed the frequency of NAFLD in patients with significantly low body weight compared to patients with normal weight. Underweight patients demonstrated significantly higher liver fat percentages compared to the normal weight patients, corresponding to mild to moderate liver steatosis. Also, underweight patients showed slightly increased liver enzymes and liver diameters, hinting at initial metabolic disturbances."

    "Previous studies on NAFLD might have underestimated the prevalence of mild to moderate hepatic steatosis in lean to underweight patients due to most of them being ultrasound-based with poor accuracy for hepatic steatosis < 30% [28]. Especially mild steatosis might constitute an important proportion among underweight patients with IBD."

    "A recent longitudinal study by Hagström et al. found that lean patients with NAFLD, while showing lower stages of fibrosis and not having an increased risk of overall mortality, were at a higher risk of severe liver disease, independent of available confounders [37]. This highlights the fact that NAFLD in lean or underweight patients is not a simple benign condition."

    "Studies focusing on severely malnourished patients with anorexia found elevated liver enzymes as indicating NAFLD to be common, especially in patients with very low body weight (BMI < 12 kg/m2) [6, 38, 39]. Anorexia-induced lipolysis was discovered to promote late triglyceride and free fatty acid accumulation in the liver and kidney [40]. A previous study suggested an increase in intrahepatic lipid content, following 36 hours of fasting, with a direct association to plasma levels of 3-hydroxybutyrate, which might also serve as an explanation for exacerbations of NAFLD with steatohepatitis seen in patients with anorexia nervosa [41]."

    "A previous study by Miele et al. found intestinal permeability to be increased in patients with NAFLD and to correlate with severity of steatosis, suggesting it to be important in the pathogenesis of hepatic fat deposition [48]."

    "As NAFLD is mostly silent, it is often discovered accidentally through clinical examination in form of hepatomegaly, imaging or elevated liver enzymes at a later stage."​
     
  5. Kartoffel

    Kartoffel Member

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    ´
    If he didn't mention endotoxin in his video, he has missed the point entirely. Fructose isn't more fattening than pure glucose. It might be that excess fructose might have a greater tendency to be stored in the liver than in peripheral fat tissues, but it is not the cause of fatty liver. IBD and increased intestinal permeability are caused by bacterial overgrowth, and so the quickest and easiest way to treat fatty liver would be to take a safe antiobiotic and eat according to hunger.
     
  6. sugarbabe

    sugarbabe Member

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    But what about healthy fruitarians? It would seem underweight people have many things going on or they wouldn't have NAFLD. If fructose is a cause then fruitarians should all have extremely fatty livers. Any evidence that they do?
     
  7. lampofred

    lampofred Member

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    Probably related to high fat consumption, excess prolactin/GH.
     
  8. Peater Piper

    Peater Piper Member

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    He's actually stated that saturated fat has a higher propensity to be stored in the liver due to a higher choline requirement. However, PUFA stored in the liver is more dangerous because the inflammatory response can cause a progression from NAFLD to NASH.

    Yes, possible to be thin and still have NAFLD. https://chrismasterjohnphd.com/2016...-lean-people-get-fat-in-all-the-wrong-places/ Doesn't mean all fruitarians have NAFLD though. Sticking to three meals a day and exercising seems a common recommendation in the lifestyle, which should help burn off the excess fat, and large amounts of folate probably help as well. That said, I've seen examples of people who struggled with rising triglycerides and glucose levels when going fruitarian, which struck me as examples of the liver being overburdened.
     
  9. pinacolada

    pinacolada Member

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    What is a safe antibiotic in your opinion
     
  10. Kartoffel

    Kartoffel Member

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    Ray recommends penicillin and tetracycline. I have used penicillin V (pota VK), and think it's very safe. I have used it several times, always 3-4 days in a row. There are several studies on pubmed showing that antibiotics are very effective at treating fatty liver, IBD, colitis, cirrhosis, etc, in rats and humans.
     
  11. Vinny

    Vinny Member

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    How about UDCA/TUDCA (user @olive said recently in another thread, that is the best for liver health), silymarin, coffee enemas, Niacinamide?
    I`m almost sure i`ve got the fatty liver too, mierda...



    Are there healthy fruitarians?
    If yes, how many globally? Do they exceed two digit number?
     
  12. Kartoffel

    Kartoffel Member

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    Okay, I just watched his video...What is this - 1972? Hello Chris, Dr. Atkins wants his dietary advice back. What happened to the cool Chris Masterjohn that was doing interesting, and innovative research that challenged existing dogmas? I guess he was replaced by that new dude that sells "great meals in a bottle", liver capsules, and posts half naked pictures of himself in the gym.
     
  13. Rick_F

    Rick_F Member

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    What dose do you use? I've got some 250mg tabs. I'll use a quarter or half of one a couple times a day if I feel like I'm coming down with a cold or flu or similar symptoms. This is the first winter I've gone the entire stretch without getting sick.
     
  14. Kartoffel

    Kartoffel Member

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    I always use two or three larger doses, and then several smaller ones. I used to take 125mg and then 60mg doses, but I accidentily ordered the 500mg tabs from farmaciasdelnino last time, and tried 250mg and then 125mg. I think the larger doses are more effective for me.
     
  15. sugarbabe

    sugarbabe Member

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    I'm not arguing for fruitarianism, but as a community we see fructose as not the villain so of course a statement that it causes fatty liver is going to be contested. There are probably threads already about it, but I never know off the top of my head why it doesn't. I believe the proof was in a rat study where they fed them huge huge doses of fructose that a human would never do.
     
  16. Aaron

    Aaron Member

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    The anecdotal evidence is ample actually. Pretty much every fruitarian I've seen has a disproportionate amount of visceral fat while looking emaciated in the face and limbs, in addition to their skin having a look I see most often in alcoholics. The woman in this picture is pregnant obviously, but the guy has a gut and they have both been fruitarian for years.
    https://i.ytimg.com/vi/6HZeNuM5hng/maxresdefault.jpg
     
  17. sunraiser

    sunraiser Member

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    Agree but also disagree. Intestinal permeability is partly the cause of bacterial overgrowth but definitely a big proponent in fatty liver.

    If your vit A / D ratio is messed up then you won't have sufficient mucosal barrier and your liver will constantly have to deal with foreign proteins after eating. Long term vitamin D deficiency while eating retinol rich foods can cause such an issue, too.

    Having proper mineral status and uptake via fat soluble balance should cure any bacterial issues, but it would mean getting sunshine and only eating non retinol vitamin A sources and inoffensive proteins for a while.

    It's why fat soluble supplementation after periods of mega stress (mineral depletion) can be incredibly dangerous to health, imo.
     
  18. Kartoffel

    Kartoffel Member

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    Intestinal permeability is the cause of bacterial overgrowth?

    Source?

    I believe retinal is the only non-retinol form of vitamin A that you can get in detectable amounts from food. What are inoffensive proteins in your opinion?
     
  19. Amazoniac

    Amazoniac Member

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    I amn't aware.

    I was wondering if it has anything to do with bactaeria since in extreme cases there can be even duodenal overgrowth (medicated with Pixels Per Inch):


    Normally most of fucose is adsorbed along with glucose, so it shouldn't be escaping in substantial amounts as it happens when they experiment without enough glucose (searching for sucrose instead of fucose will save you time):


    There appears to be an attempt to correct the excess:


    So it's indeed due to liver processing. Even though it's multifactorial, it's definitely a contributor:

    @Mito - Enemy, attack. Call him a couch potato.

    Kartoffel, I just realized that you still have those quotes in your signature, what a comedian. :lol:
     
  20. Kartoffel

    Kartoffel Member

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    That old hat again. I think of it as the prime example of one of those studies Ray mentioned when he said "they are designed to get the results they want". This study has very little to do with the real world, and if you look at their results, this study actually shows that sucrose is superior to starch with regards to liver inflammation, enzymes, etc. The rats in the sucrose group receiving normal amounts of methionine had lower ALT than starch animals, and significantly lower TNF, CD14, and COX-2 - wait! there is no significance asterix, so these values, eventhough they are twice as large, are of course not significant, at all. Was worried there for a second, but our theory seems to be safe.
    Still, the authors of the paper highlight their stupidity when they say absurd things like this:

    "Dietary PUFAs also accumulate in the liver, possibly in an effort to reduce SFA-induced lipotoxicity."​

    They just showed us that liver TG where much higher in the MCS-sucrose group, and that those animals had signif...I meant insignificantly less inflammation than the MCS-starch group, and then they go on and state that it must be the saturated fat causing the inflammation. Every lab rat since the 1970s is aware that corn oil is highly toxic to the liver, but I guess this doesn't neccessarily mean that we should expect Mr. Pickens and his colleagues to be educated so well.
     
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