Masterjohn Right? Treating Fatty Liver

Amazoniac

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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.
Disagree and also disagree.

The confounder is that fructose favors saturated fat synthesis and it can mitigate some of the problems from PUFA. Those inflammatory markers would likely disappear if the fat used wasn't rich in them, whereas the accumulation/ballooning aspect would persist (or made worse), along with higher fasting glucose, cholesterol (seems out of mice normal), triglycerides (blood and liver) and Foreign Agricultural Service.

And these are mice that aren't dealing with dysbiosis, because this could put them under extra stress.

The increase in lean weight is interesting, they should've tracked food intake.
 

Runenight201

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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.


I agree. Even if his protocol is correct in ameliorating fatty liver, a starch and animal protein diet with no fruit/sucrose and no fat is going to cause other health issues. Starch and meat are what inflame me the most and give me terrible cystic acne, and while I do need some in my diet, I can always tell when I overdo it as I’ll begin to see cysts forming. To counteract I strictly consume fruits and dairy/eggs until the inflammation subsides and I’m at homeostasis again.
 

CLASH

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Endotoxin, alcohol and PUFA (possibly iron) seem to be the main determinants of hepatic steatosis and hepatic fibrosis. Non-alcoholic fatty liver seems to be mainly endotoxin and PUFA (possibly iron).

Fructose is an associated factor, as an excess of fructose in ratio of glucose reliably leads to increases in endotoxin. 1:1 proportions, especially in the form of fruit sugars actually lowers endotoxin and prevents/reverses fatty liver.

It is highly doubtful that fruit and saturated/ monounsatureated fatty acids cause fatty liver in humans (Mice are different than humans...) Both should be protective, especially in the context of adequate protein.

If you have fatty liver adequate protein from animal sources, carbs from fruits, yams, potatoes, and adequate fats from saturated sources should be protective and allow for a reversing of the pathology. Blood donations and nutrient suppport (barring excess vit A in this circumstance, atleast initially) would be very helpful (especillay if iron overload is suspected). Specific supplements can include taurine, glycine, bile acids, vit K, b vitamins, maybe caffeine depending on tolerance. If these interventions are falling short I would look into a possible intestinal dysbiosis. A stool test would give some idea of the pathogens present and their sensitivity to specific antibiotics so that guessing in the dark on wether or not a specific antibiotic will work is avoided. Allergies or issues with dairy can also be a concern. I would personally avoid refined sugars and starches in this circumstance as well. If starches from potatoes/ yams are giving digestive issues then a reliance on fruits and juice could be done, I would just choose juices that dont have fodmaps and have 1:1 ratios of glucose to fructose like orange, grape, pineapple, pomegranate, blueberry, guava etc. Apple and pear juice are some of the worst in terms of glucose: fructose ratio and fodmaps and every cheap juice seems to be diluted with them.... In rat/ mice studies juice prevents/ reverses fatty liver. In human correlation studies juice/ fruit is either not related at all, protective or so marginally related the correlation is worthless.
 

InChristAlone

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So how do we all feel about the high fructose corn syrup in coke? I have been drinking 1-2 cans a day for most of my adult life (and drank soda for most of childhood, as a teenager I drank almost exclusively soda). I am still not obese or insulin resistant. Though I know my liver could use some loving. My younger son drinks more than me and he's so strong and lean.
 

Amazoniac

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Disagree and also disagree.

The confounder is that fructose favors saturated fat synthesis and it can mitigate some of the problems from PUFA. Those inflammatory markers would likely disappear if the fat used wasn't rich in them, whereas the accumulation/ballooning aspect would persist (or made worse), along with higher fasting glucose, cholesterol (seems out of mice normal), triglycerides (blood and liver) and Foreign Agricultural Service.

And these are mice that aren't dealing with dysbiosis, because this could put them under extra stress.

The increase in lean weight is interesting, they should've tracked food intake.
I forgotted to comment that even though the MCS-diets protected animals against most issues regardless of diet, if Table 2 didn't specify the diets, we could probably tell just by using the values which is which, so they still retain some of the features.

Outside of labs, people are hopefully not consuming refined sugar as their main source of carb or not making up for it elsewhere, and this is already enough to negate the problems:
- Treatment Of Cirrhosis Of The Liver By A Nutritious Diet And Supplements Rich In Vitamin B Complex

By the way, an issue with feeds is that animals don't have choices, they don't have the flexibility that people have and out of instinct increase protein or choline intake (unless there's something adverse from their consumption), for animals it's either what's imposed to them or starve.

But purified nutrients are useful for the sake of ecuditalion, and fucose is clearly more demanding in this aspect, as evidenced when animals are made vulnerable (which can happen when people are under stress).

So how do we all feel about the high fructose corn syrup in coke? I have been drinking 1-2 cans a day for most of my adult life (and drank soda for most of childhood, as a teenager I drank almost exclusively soda). I am still not obese or insulin resistant. Though I know my liver could use some loving. My younger son drinks more than me and he's so strong and lean.
- HFCS vs Sugar | HFCS Nutritional Information

upload_2019-4-22_6-9-42.png
 

yerrag

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Did I miss something here? Did I scan through and not see any mention of thyroid at all? Doesn't thyroid regulate lysosomal acid lipase, and doesn't lysosomal acid lipase deficiency cause cholesteryl ester to form in the liver? How did Cris Masterjohn fail to mention this?

I mean, doesn't it start with asking about thyroid first? And perhaps right along with thyroid would be PUFA, as PUFA affects thyroid?

I listened to Cris' podcast, and was not too impressed with it. It jumps right into the "take this take that" approach that doesn't go deeply enough. Maybe that's why it's the "schmeetails details, just tell me what works" approach that's showing how most instant advice is wrong and a waste of time and a source of endless frustration. Yet, this is what most people want: the simple foolproof lowdown, which is a oxymoronic.
 
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Kartoffel

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Disagree and also disagree.

The confounder is that fructose favors saturated fat synthesis and it can mitigate some of the problems from PUFA. Those inflammatory markers would likely disappear if the fat used wasn't rich in them, whereas the accumulation/ballooning aspect would persist (or made worse), along with higher fasting glucose, cholesterol (seems out of mice normal), triglycerides (blood and liver) and Foreign Agricultural Service.

And these are mice that aren't dealing with dysbiosis, because this could put them under extra stress.

The increase in lean weight is interesting, they should've tracked food intake.

Triglycerides weren't elevated that much, and triglycerides usually have a broad variety of protective functions. The high fasting glucose levels and the significantly higher leptin levels do suggest that the sucrose mice were taking in much more food than they needed. I guess it's hard to avoid when you aren't offered any alternatives. Besides the amount of food intake, it would also be intersting to know whether all components of the diet were pressed into the same palets, or whether the mice could at least choose between the different components. I guess the former is more likely. Generally, when mice are offered free access to standard chow and sucrose, they will consume extra sucrose and more calories, but have the same weight as controls.

Outside of labs, people are hopefully not consuming refined sugar as their main source of carb or not making up for it elsewhere, and this is already enough to negate the problems:
- Treatment Of Cirrhosis Of The Liver By A Nutritious Diet And Supplements Rich In Vitamin B Complex

By the way, an issue with feeds is that animals don't have choices, they don't have the flexibility that people have and out of instinct increase protein or choline intake (unless there's something adverse from their consumption), for animals it's either what's imposed to them or starve.

But purified nutrients are useful for the sake of ecuditalion, and fucose is clearly more demanding in this aspect, as evidenced when animals are made vulnerable (which can happen when people are under stress).

I guess we can agree that it's unlikely to be good in the long-term to consume most of your calories in the form of refined sucrose. I think Zeus gets quite a bit of refined sugar in his diet since he avoids starch completely and mentions getting a lot of his sucrose from pepsi/coke, some juice, and sweets. Then again, he mentions his protein intake is pretty high, and in addition to that he probably has the most powerful arsenal of liver supportive substances in his secret, underground lab.
I am not convinced that that much sucrose from fruits or honey would have the same negative effects, since things like orange juice, honey, and other fruit juices produce distinctly different metabolic effects in experiments where they are compared to refined glucose or sucrose.
 

sunraiser

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Intestinal permeability is the cause of bacterial overgrowth?

It's at least partly the cause - this is the view that's most compelling to me via overall experience. When digestion isn't adequate then bacteria will always proliferate to deal with partially digested food - this is almost a given when the liver is impaired (that digestion won't be robust). But another angle is that iron (or general heavy metal) overload will produce an internal state that's conducive to bacterial overgrowth or "candida". It's often stated that candida "feeds on" iron, but I believe it's a protective response by the body to deal with iron excess that has unpleasant byproducts. Iron uptake, but also iron removal, is dependant on liver function - the same goes for copper. This state would create paradoxical iron deficiency and toxicity, but high heme iron and copper intake during poor liver/metabolic health would also almost guarantee a degree of heavy metal toxicity as the liver and adrenals are responsible for ceruloplasmin production to deal with both metals. This is why recommendations here for very sick people to eat lots of liver and shellfish can often end badly, imo.

Regarding poor liver function and bacterial overgrowth I have found the most influential and compelling theories to be those of Andreas Moritz, as much as I'm sure he's someone you'd hate! I don't agree with lots of his conclusions, however I HAVE seen people resolve candida issues via lots and lots of liver flushes (gbolduev is an example, right?). I don't believe in avoiding fat as a coping mechanism or lots of the forced dietary requirements Moritz talks about, but I feel pretty strongly that bacterial/fungal issues generally stem from the liver and overall digestive process. I also think liver flushes can be imbalancing and sometimes dangerous - I have just taken his ideas about liver sluggishness and bacterial overgrowth issues.


Regarding the vitamin A and vitamin D balance and mucosal barrier, it's important to note that everything comes down to mineral metabolism and proper transport issues, for me. Zinc plays an important role in proper mucosal function, but it's dependant on vitamin A for proper uptake, and must be in balance with calcium and magnesium (but this is handled by proper fat soluble status).

Here is a useful article, though it exagerrates vitamin A and doesn't establish properly the importance of vitamins K and D, imo - I would say the article notes excessive VA intake. You can easily google "vitamin D mucosal barrier" and the same for vitamin A, if you want further studies to look at.

Vitamin A: The Key to A Tolerant Immune System? | Clinical Education

The struggle that I believe many people are encountering is via having a leaky gut and the liver constantly being overburned by dealing with foreign proteins (causing an "autoimmune" response) in the bloodstream (proteins that should not be breaching then mucosal barrier). Having an overworked liver and a slow digestive process is going to cause innate undereating and, over time, chronically increased cortisol.

Chronic stress in general can contribute to the same response, but the chronic demand for cortisol and adrenaline to meet energy needs in the body means there's a constant demand for pregnenolone to convert to cortisol (sacrificing progesterone at the same time), and vitamin A is required in the creation of these hormones. So in this state you have a cycle of stress via undereating (due to poor digestion) and yet needing the "stress" resources to repair ones state. It's really really hard to get into such a severe state as the body shuts down the metabolism into a resource saving state long before mineral depletion will occur, but via severe forced overtraining or taking isolated or unbalanced fat solubles you can ruin the equilibrium the body is trying to protectively keep.

As you mentioned, eating to appetite is the best approach, and me calling it "under eating" should hopefully not paint an inaccurate picture - it doesn't mean forcing calories, as that would be the worst thing to do for liver respite, it just means undereating in that the calories one is able to metabolise are not enough to support full metabolic health. I don't think this "undereating" is the worst thing in the world as the body tends to give all sorts of signs to slow down (like anhedonia) so resources are saved, however when forced to continue with life stress in such a state it's far from ideal.

As a last important factor, I believe liver function is key for proper K1 > K2 conversion (I don't have a source, sorry), and that iron toxicity in the liver, alongside a constantly overburdened liver via poor digestion can completely limit K2 availability in the body. This would mean that extremely low doses of vitamin D might be necessary for slow building recovery (i.e. working or being outside in spring time sun or like <400iu doses) because the liver simply couldn't support higher vit A D uptake in balance with the available K2 - one could raise the dose as they feel better; however the body does this innately via sunshine and it's much more complex with supplementation. Weston A Price is correct about vitamin K2 being an activator for A and D, in my opinion and experience.

My personal experiences have compounded these ideas in my mind. If I take vitamins A and D together they seem to have some kind of poor effect, or no effect when healthier. If I take A, K2 and D together, they can either create horrendous inflammation and endotoxin type feelings or they can create balance.

Taking big doses of K2 alone can cause awful endotoxin issues for me and I'm concerned about the lightness with which these things are prescribed on the forum. I think many people have turned slightly poor health into chronic health issues via supplemental approaches suggested on here (I have absolutely been guilty of suggesting bad things as well).

Just to highlight further personal example in my case (I messed up my health by eating tons of liver not to craving; but it was already not ideal probably due to accutane and definitely due to severe overtraining).

K2 (mk4) alone = awful sleep, terrible digestion and headachey, restless and general feelings of illness after eating.

K2 1.5mg + 10kiu vitamin A + 1kiu vitamin D = better, but still lack of appetite and symptoms of severe inflammation

K2 1.5mg + 10kiu vitamin A + 4kiu vitamin D (or lower amount amounts of A and D in a similar ratio) = much better appetite, no real inflammatory symptoms, but bigger cravings for magnesium, zinc and calcium rich foods.

Fat solubles consistently influence my food cravings and they're clearly directly responsible for mineral uptake and correct transport.

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?

I phrased poorly - I meant carotenoids or inactive forms. By inoffensive proteins it would mainly be eating to combat low stomach acid that would be common after long term vitamin A and, in turn, zinc deficiency.

This would mean avoiding high liquid based calories that could further dilute stomach acid (i.e. lots of milk, or waterlogged foods like boiled potatoes and rice - in the past I have found night and day difference between cooking potatoes and rice in acidic (tomato) stew or curry dishes so some of the liquid is cooked out (also more acidic that just water). Casein seems to be difficult to digest for some people, too. It would also mean avoiding larger sources of retinol for a while until innate K2 production and actual ability to store fat solubles returns a little (eating liver would be for a much much healthier person, then it can be extremely enhancing).

It's not that the proteins are evil in themselves, it's that some are harder or slower digesting and therefore have a higher likelihood of passing through the mucosal barrier undigested. HOWEVER this is something of a coping mechanism.

There's a big difference between a simple state of supressed metabolism and actual chronic health issues, but it's easy to create something chronic via imbalanced fat soluble supplementation.

I really think it's as "simple" as working outside during spring time and being on your feet for lots of the day (hugely promotes digestion) to recover metabolic health, then proper sunbathing when craved while eating balanced diet to craving. BUT, if a person has screwed themselves up via pushing metabolism with supplements, then a balanced intake of fat solubles might be necessary. Even though they don't appear to be stored, taking A K and D in the balanced I've mentioned can facilitate mineral metabolism and enough semblance of mucosal health to stop severe endotoxin issues. As mineral metabolism restores, liver health can come back and more importantly, appetite fit for the endogenous progesterone conversion needed for health and vibrance.

This is my jumble of theorising and experience - I find it really hard to coordinate all the ideas in my head cohesively as there are so many gaps in my understanding, but also because it's a lot to note down and I don't conceptualise it as such a whole entity in my mind.

nb: I do not necessarily endorse or suggest anyone tries this. I mainly want to put across that fat solubles are unlikely to be inert or "stored" during poor liver health and, when out of balance, they can be causes of chronic health issues and genuine life anguish as well as healing tools.
 
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Cirion

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Well this is n=1 but I know I can't handle all my carbs from sugar, and I also had to drop almost all dietary fat because of chronic weight gain that was getting completely out of control, and I've actually gravitated to almost the diet it seems Chris recommends (starch, very little fruit, very little fat). Also, extreme amounts of sugar was ruining my teeth as well.

I used to beat the "Peat drum" of sugar like a lot of folks in this very thread until I realized too much sugar just wasn't doing my health any favors. Experience trumps research at the end of the day.

To be fair, I'm nearly 100% sure that I have gut dysbiosis as well, but the fact remains that sugar does not seem to do me many favors. I do still eat some but not nearly as much nowadays.
 

Amazoniac

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Triglycerides weren't elevated that much, and triglycerides usually have a broad variety of protective functions. The high fasting glucose levels and the significantly higher leptin levels do suggest that the sucrose mice were taking in much more food than they needed. I guess it's hard to avoid when you aren't offered any alternatives. Besides the amount of food intake, it would also be intersting to know whether all components of the diet were pressed into the same palets, or whether the mice could at least choose between the different components. I guess the former is more likely. Generally, when mice are offered free access to standard chow and sucrose, they will consume extra sucrose and more calories, but have the same weight as controls.



I guess we can agree that it's unlikely to be good in the long-term to consume most of your calories in the form of refined sucrose. I think Zeus gets quite a bit of refined sugar in his diet since he avoids starch completely and mentions getting a lot of his sucrose from pepsi/coke, some juice, and sweets. Then again, he mentions his protein intake is pretty high, and in addition to that he probably has the most powerful arsenal of liver supportive substances in his secret, underground lab.
I am not convinced that that much sucrose from fruits or honey would have the same negative effects, since things like orange juice, honey, and other fruit juices produce distinctly different metabolic effects in experiments where they are compared to refined glucose or sucrose.
Whenever someone appears praising only fruit I assume that the person is being sponsored by the Morse industry; starch, McDougall. For those of us that are somewhere in between, we're sponsored by both.

It's complex outside of a purified diet:
- Moro orange juice prevents fatty liver in mice
 

Cirion

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If the McDougall comment is directed towards me, I don't necessarily advocate 100% starch. I actually still eat 30-40% of my carbs from sugar still, but that's instead of 80-100% "Morse" style that I was doing before. I do indeed believe in a balance. It's just that I strongly advocate against Morse-ism now which could make me seem like a McDougall supporter, lol.
 

InChristAlone

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Oh the great starch vs sugar debate. I get a mixture, but usually more sugar than starch. I didn't do well on a heavy dairy and sugar diet. Although I was healing from chronic stress back then so it's hard to say if I implemented now what would happen. If I do only starch I think I'd crave sugar, if I do only sugar I'd eventually want some starch, the sugar becomes sickeningly sweet. If people could just eat according to what their body desires maybe we wouldn't have this constant debate over which is better. If starch bloats you up like a balloon and you don't desire it, then don't push it! If sugar gives you awful symptoms and you are only pushing it because Peat said sugar is great for the metabolism then listen to your body. Everyone is different.
 

Kartoffel

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Oh the great starch vs sugar debate. I get a mixture, but usually more sugar than starch. I didn't do well on a heavy dairy and sugar diet. Although I was healing from chronic stress back then so it's hard to say if I implemented now what would happen. If I do only starch I think I'd crave sugar, if I do only sugar I'd eventually want some starch, the sugar becomes sickeningly sweet. If people could just eat according to what their body desires maybe we wouldn't have this constant debate over which is better. If starch bloats you up like a balloon and you don't desire it, then don't push it! If sugar gives you awful symptoms and you are only pushing it because Peat said sugar is great for the metabolism then listen to your body. Everyone is different.

Relying on both in varying proportions is what most traditionally-living people in warm climates tend to do. Kitava usually have two starchy main meals and snack a lot of frruit in between. The Hadza, and other hunter gatheres in Africa name honey as their favorite food, and eat tubers only when neccessary. When your body has had enough sugar, it will let you know, so it's hard to get too much sugar unless your force yourself to eat it because your protocol tells you to.
 
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By the way, nobody is saying ONLY fruit is good for you. Masterjohn is saying that you should avoid fructose during this liver defatting period.
 

Mito

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Did I miss something here? Did I scan through and not see any mention of thyroid at all? Doesn't thyroid regulate lysosomal acid lipase, and doesn't lysosomal acid lipase deficiency cause cholesteryl ester to form in the liver? How did Cris Masterjohn fail to mention this?

I mean, doesn't it start with asking about thyroid first? And perhaps right along with thyroid would be PUFA, as PUFA affects thyroid?

I listened to Cris' podcast, and was not too impressed with it. It jumps right into the "take this take that" approach that doesn't go deeply enough. Maybe that's why it's the "schmeetails details, just tell me what works" approach that's showing how most instant advice is wrong and a waste of time and a source of endless frustration. Yet, this is what most people want: the simple foolproof lowdown, which is a oxymoronic.

The first hour of this podcast (https://peterattiamd.com/chrismasterjohn/) with Masterjohn discusses the subject in more detail than his LITE video. @ecstatichamster

We discuss:
  • Chris’s background, falling in love with biochemistry, and decision to pursue research over medicine [7:45];
  • Choline: what it is, why it is important, and how a deficiency can cause non-alcoholic fatty liver disease [11:45];
  • NAFLD: increasing prevalence and potential causes [25:00];
  • TMAO: Should we be worried about the TMAO content in choline and our foods? [39:15];
  • Types of fatty acids: How they may predispose us to different types of illnesses [53:30];
  • Why don’t we see low VLDL in patients with NAFLD? [59:45]
 
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