Masterjohn Right? Treating Fatty Liver

[Amazoniac]

For those trying to get enough choline from Whole Foods first, keep in mind that Chris Masterjohn shows that you can get up to half of your choline needs met by the closely related betaine. Now, betaine doesn’t really seem to be anywhere near effected for fatty liver as choline does, however, it appears that betaine is choline sparing in the sense that it is used for methylation by the body, from a choline to betaine conversion pathway. So, if one wants to get enough egg yolk choline equivalents of betaine, they could consume half of their choline intake in that form so that less or very little choline is converted by the body to betaine for its methylation needs. This will leave the choline that you eat from animal products to utilized for things like fatty liver or whatever, providing there is enough have a caloric deficit in conjunction to it for increased mobilization of stored liver fat.

So, for example, if one finds it hard to get 500 or 800mg of choline per day from foods alone because it may push PUFA intake up higher or for whatever reason, you could theoretically consume half of that in betaine and thus need less total choline. So if I am trying to shoot for 700mg of choline or choline equivalents from my diet and 105g of cooked spinach and 57g of canned beets would give me two egg yolk equivalents of betaine. Double that up and I have half of that for methylation and the other have I can get in the form of choline which then will likely be used for liver health and other things, etc. This comes in handy if you want to get most of your choline form the few low PUFA sources of it that are available, such as milk, liver, low PUFA white fish such as cod, kidney, etc., and do not want to smash down 8, or 12 egg yolks a day as that would really add a lot of PUFA on top of your natural PUFA intake from the rest of diet alone. As I handle milk very well and have a high milk consumption, I’m already easily getting around 5 or so egg yolk equivalents of choline from milk alone. An egg and maybe the occasional low PUFA fish like cod or some liver or kidney really increases it more without increasing the PUFA content to a level I personally don’t want. I could add just 3 oz of liver which has about the same PUFA content or one egg and that would be almost 1000 mg of egg yolk choline equivalents from low PUFA food sources alone. And then maybe throw in canned/cooked beets (which are also low PUFA) for my methylation needs so that most of that choline goes towards liver tissue and other needs and I easily can get enough choline without having to jack up the PUFA. But that would be harder for someone who doesn’t handle dairy or organ meets well to do.

Your posts are always so helpful that I don't think you'll ever need to be worried about being ostrichized.

Here's what you've just described:

- Grant Genereux's Theory Of Vitamin A Toxicity

Since it's down the stream, it indeed has that sparing effect on choline by diverting it from methylation.
Creatine should be useful in this regard, it was discussed on the 'Choline notes' thread. I think this is particularly interesting for those that get most of their proteid from dairy instead of meats. I'm not sure how calcium and phosphate relate to it, but it's something that's also worth investigating.

 

[TeaRex14]

At first I was confused for having missed your post, but after reading, it does give such impression. But I always avoid ambiguous messages, so if it wased towards you, you would know it without doubt.

You look different. Did you cut your hair?

I guess that supplementing is preferable to remaining on insufficient intakes for long. Have you read more about choline chloride? I haven't, but it seems safer than the bitartrate if you can't get the fat-soluble phosphatidylcholine forms. Terma is experienced on choline supplementation, it's worth digging his posts. He uses those other water-soluble forms (that are intermediate metabolites), but (as far as I know) these tend to be more effective at reaching the cerebra than the simpler ones, which isn't the purpose here.

- Not Enough Potassium

One thing that I can comment in advance is that it won't provide colossal amounts of chloride; the whole molecule is mostly choline (75%), so for every 100 mg of choline you're only adding about 35 mg of chloride.

- Scientific Opinion on safety and efficacy of choline chloride as a feed additive for all animal species | EFSA

No haven't looked up choline chloride, I never knew they made it. I'll look into this.

 

[Nicole W.]

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:

Hi there,
I can only share what I have learned from our ND while treating my husband for metabolic syndrome and fatty liver. As she explained to us, fatty liver is essentially a sugar handling problem. They body isn’t utilizing the sugars consumed, just storing them in the liver in the form of triglycerides. My husband’s triglyceride count was around 500 at that time. In order to resolve this problem (she said) she recommended my husband adopt a diet low in sugars and starches in order to encourage his body to start utilizing the stored triglycerides in his liver. When my husband started this program, his allopathic doctor told him he was at great risk for a heart attack or stroke, and wanted to put him on several drugs to manage symptoms and lower risk. To his doctor’s dismay, my husband refused and we promptly called our ND. The Naturopath prescribed the Whole 30 diet but allowed dairy in the form of cheese (which is not Whole 30 compliant under normal circumstances). No alcohol was allowed. He was limited to one serving of fruit daily. His only starch was baby potatoes with skin on. In addition she prescribed Bergamot BPF, Vit. D & K, and another supplement by designs for health called Detox Antiox. In 3 months, all his labs were back within a normal, healthy range which is nothing short of a miracle, trust me. This is a man who enjoyed a huge bowl of ice cream often with a scoop of peanut butter on top EVERY evening for decades! Generally a terrible eater: loved fast food, ordered fries ALL the time, loved to drink socially. So the initial diagnosis came as no surprise, just the quick, fairly easy resolution of it. Just as a foot note, he also lost 40 lbs.

 

[Jib]

Do you eat red meat? Roasts and steaks are a very good source as well. It is where I get most of my choline. Still only half the amount CM says I need though. So I am going to start taking lypo-C again, it has lecithin.

I do. Grass fed ground beef is my go-to. I love paprika, cumin, chilis, and all that, so I usually cook it up in the pan with a bunch of spices like that, and salt, then when it's done I'll throw some shredded cheddar over it and let it melt. A good sized portion of that, with some mandarin oranges on the side, and/or air fried corn tortillas, or corn tortillas fried in coconut oil. Very good.

A lot of times after I work out I'll have that ground beef chili, and many times pretty easily eat the whole pound. So my red meat intake on average is quite high, and 95% of my dairy intake is from cheese, which I have a fair amount of.

I used to make liposomal vitamin C in an ultrasonic cleaner years ago. I might get back into that. It actually tasted quite nice. I just had the idea to do it using orange juice as the liquid instead of water, but I'm not sure if it would work the same. Perhaps the bioflavanoids in the OJ could make it even more effective.

I don't doubt MitoLipin is a great supplement, I've always been impressed with every Idealabs product I've tried thus far. I just find choline l-bitartrate more cost effective for the amount received. I try and save money on supplements wherever I can, without cutting corners on quality wherever possible. Maybe I'm making a mistake, I can't say for sure 100% that choline l-bit isn't harmful. What I can say though is the research on TMAO isn't conclusive, and in fact very controversial, with no established causation. Also any blood platelet aggregation can be effectively blunted by a daily aspirin tablet. Supermarket eggs also provide enough choline if you eat say, 2 or 3 a day. That would give you the minimum requirement, especially if you're eating meat and milk too. I think the lecithin alarmists are probably referring to the fact lecithin is typically an unsaturated molecule.

I am the same way. Any time I can get a bulk form of a supplement, I go for that. Purebulk is great. Lots of times I'll crunch numbers to find out the price per volume and go with the highest quality but cheapest supplement I can find.

I do wonder about the lecithin alarmists, as isn't the lecithin in egg yolks unsaturated as well?

 

[Jib]

You can make your own choline chloride, if you're so inclined:



Alternatively, a much simpler solution that doesn't require any lab equipment:

Choline chloride, Ethanaminium, Reagent 99%,500g | eBay

I'd be curious to give that a try.

 

[Cirion]

Hi there,
I can only share what I have learned from our ND while treating my husband for metabolic syndrome and fatty liver. As she explained to us, fatty liver is essentially a sugar handling problem. They body isn’t utilizing the sugars consumed, just storing them in the liver in the form of triglycerides. My husband’s triglyceride count was around 500 at that time. In order to resolve this problem (she said) she recommended my husband adopt a diet low in sugars and starches in order to encourage his body to start utilizing the stored triglycerides in his liver. When my husband started this program, his allopathic doctor told him he was at great risk for a heart attack or stroke, and wanted to put him on several drugs to manage symptoms and lower risk. To his doctor’s dismay, my husband refused and we promptly called our ND. The Naturopath prescribed the Whole 30 diet but allowed dairy in the form of cheese (which is not Whole 30 compliant under normal circumstances). No alcohol was allowed. He was limited to one serving of fruit daily. His only starch was baby potatoes with skin on. In addition she prescribed Bergamot BPF, Vit. D & K, and another supplement by designs for health called Detox Antiox. In 3 months, all his labs were back within a normal, healthy range which is nothing short of a miracle, trust me. This is a man who enjoyed a huge bowl of ice cream often with a scoop of peanut butter on top EVERY evening for decades! Generally a terrible eater: loved fast food, ordered fries ALL the time, loved to drink socially. So the initial diagnosis came as no surprise, just the quick, fairly easy resolution of it. Just as a foot note, he also lost 40 lbs.

I was just posting in another thread earlier. I agree it's likely a sugar handling problem. But I don't know that limiting carbs is necessarily the answer, or at least not the only answer (since limiting carbs seemed to work also). It seems to me that the "Randle Cycle" is the source of a lot of problems, including diabetes, insulin resistance, obesity, etc etc. FFA's do indeed become a problem when the randle cycle has been activated one too many times, but its not because carbs are the problem, its that your body can't utilize the carbs due to the effects of the RC.

IE, mixing fats and carbs in the same meal causes issues with handling the carbs (sugars). What you said your husband used to eat seems to verify this suspicion. Ice cream with peanut butter for example is a massive randle cycle disaster waiting to happen, not to mention the fact that PB is rich in PUFA. That's like shooting someone then pouring salt into the wound.

It seems you can avoid the effects of the randle cycle without giving up either fat or sugar, you just can't eat them both in the same meal. Eliminating the intake of most sugars/starches would naturally also alleviate the effects of the randle cycle because now all you're eating is fat and there is no interference with carbs. Conversely, eating carbs without fats would have the same effect theoretically. But you could say have a breakfast rich in fats & poor in carbs, and a dinner rich in carbs & poor in fats.

I think people are too quick to blame either fat OR carbs but the truth is that it's a little more complicated than that. I think people are too quick to go to one extreme or the ot her (Keto or low/zero fat). I used to be a keto fan, and then I became a low fat fan, and now I realize the answer is actually in the middle, but that you should not mix fats and carbs in a meal.

Nice job though in such a short time frame. I do absolutely think either going low fat or low carb is probably a lot better than mixing the two. I did use to feel pretty good when I was on keto myself.

 

[Amazoniac]

In case any of you missed..

"Vitamin" D and calcium, both have a direct suppressive effect on fat formation. The fatty liver for example, in animal studies it is corrected by both, venom D and calcium.

--
Transdermal route is not ideal because the goal is to concentrate the dose to the liver, not distribute it throughout the body. However! Issues with choline indigestion can burden the liver further, so this alternative can end up being positive for avoiding contact with yerms.

- First pass effect - Wikipedia​

Worth checking out:

- Recent Trends in Dermal and Transdermal Drug Delivery Systems: Current and Future Prospects "d bos"
- Transdermal drug delivery system: An overview​

Ironically, choline has the lowest molecular weight of all B-vitamins, and chloride doesn't add much.


People requiring Total Paternal Nutrition are under stress, I was wondering if their needs for choline changed compared to normal eating (for skipping digestion); thinking in terms of undesirable utilization by less important organs such as the brain. One of the problems is that when nutrients are injected, the way that they is metabolized is changed. Below they comment'd how methionine metabolism is affected, which in turn can compromise choline synthesis.

The doses suggested for maintenance is similar to those recommended for consumption of wealthy people, which makes us think that transdermal is a relatively efficient (yet inferior) route for this purpose, especially because those people aren't obtaining choline from foods and due to the issues mentioned above.

The highest dose reported on the review below was 20 g (not quoted), so it's alright and it has to be preferable to bitartrate. I think that the tartaric acid is used to mask the nasty smell (I can't remember if this is related to impurities or not) and to utilize an industrial waste. Maybe there are more reasons why choline chloride became unpopular.

- Essential Nature of Choline with Implications for Total Parenteral Nutrition

"As discussed previously (19), these results indicate that the conversion of methionine to choline is affected in cirrhosis and that choline is synthesized from methionine most efficiently when it enters the liver via the portal vein ("first-pass effect"). Parenteral infusion of methionine causes its metabolism to proceed via extrahepatic transamination rather than by intrahepatic transsulfuration, thereby making the methyl group of methionine unavailable for choline synthesis (22,36,37) (Figure 3)."

"[..]intravenous choline [chloride] infusion [in doses ranging from 1-4 g] was an effective and safe tratment for choline deficiency and hepatic steatosis in patients who receive TPN and have minimal oral intake."

"Diets high in choline are likely consumed by many normal wealthy persons every day. Based on food choices and preferences, a person could easily consume a diet with greater than 2,000 mg choline per day (Table 5). This is probably the case for people whose diets routinely include foods such as liverwurst (or pâté), egg custard, and other foods containing high amounts of choline/lecithin."

Spoiler

- The Addition of Choline to Parenteral Nutrition

"[..]when nutrients are infused intravenously, they are not delivered to the liver via the portal vein initially, but via the hepatic artery after passing through the heart. The variation in nutrient assimilation may affect nutrient metabolism and downstream metabolic products. When methionine, a precursor for choline that normally issupplied in PN, is infused systemically, cysteine, similar to choline, a downstream metabolic product of the hepatic transsulfuration pathway, was virtually undetectable even in normal volunteers.[13] When methionine was infused enterally in those same volunteers, plasma cysteine concentrations were slightly lower than when consumed with a meal, but substantially greater than that which resulted from systemic methionine infusion. This landmark investigation showed that the hepatic transsulfuration pathway is impaired when substrate is provided via the systemic rather than the portal circulation. Theobservation of Stegnik and Besten[13] was later observed inpatients who required parenteral feeding.[14]"

"Buchman et al[25,27,28] have shown that paren-teral choline supplementation reverses hepatic steatosis and hepatic amino transaminase abnormalities associated with short-bowel syndrome/PN-associated liver disease (Figure 4)."

"Given that choline is the rate-limiting step in acetylcholine synthesis,[41] and acetylcholine is the most significant neurotransmitter in cholinergic cells,[42] it comes as no surprise that choline might play an important role inmemory. Choline is transported across the blood-brainbarrier in proportion to its plasma concentration.[43] Administration of intravenous choline leads to a rapid increase in brain acetylcholine in rats.[44]"

"Studies in rodents and canine models have indicated that mortality from endotoxin-induced shock is significantly greater,[58] and hepatic injury is more significant,[59] in rats fed a choline-deficient diet."

"Some studies have found female rats are less sensitive to choline deficiency than their male counterparts,[67] perhaps because, as shown in mice, the females synthesize a greater degree of their choline requirement via the phosphatidylethanolamine N-methyltransferase pathway.[68] This represents the only source of choline other than from dietary intake. Other studies in rodents have found that choline-deficient males are more susceptible to development of early hepatic steatosis than females.[69] Clinically in human beings, however, plasma-free choline concentration appears to be lower in females than in males,[35] and females appear to be at greater risk for PN-associated hepatic abnormalities.[35]"

"Choline deficiency may be a required step in the development of more severe liver disease, but not sufficient in and of itself. For example, a second “hit” such as hyperhomocysteinemia, the presence of tumor necrosis factor (TNF), or lipid peroxidation may be necessary to induce progression to more severe liver disease."

"If we go back to Stephen Zeisel's study, in 1992, some normal volunteers developed liver abnormalities when placed on a choline-deficient diet; these resolved when a choline-sufficient diet was provided. Similarly in our studies, one subject had hepatic steatosis, which resolved with choline supplementation only to recur 4-10 weeks after choline-supplemented PN was discontinued. We did use a dose that is 200% of the AI, although certainly one that can be easily attained from a normal diet according to data published by Eva Shronts."

"We don’t know the minimal dose of choline required, but it may indeed be closer to the AI. The AI, however, is for choline, not a choline salt. As such, 2 g choline chloride, for example, is roughly equivalent to 1.1 g of choline. Perhaps a 2-g dose is necessary for treatment over a 2- to 4-week period, and a 1-g dose for a routine daily intake; we don’t have that data."

"Quaternary ammonium compounds are often quite unstable, I wonder if you have any data that would enable the product to be mixed with complete PN mixtures or would it have to be infused separately?

We have found the choline concentration in choline chloride vials remains stable after atleast 5 years. We have also found that recovery of choline from choline chloride ranged between 98% and 102% at 30 days in 3:1 solutions. We have similar data for stabilityat 7 days in 2:1 solutions; we did not evaluate longer periods."​

For some reason they claim that there's 1.1 g of choline in 2 g of choline chloride. I have no idea what is the exact salt they're using, but I don't think that it will add extra chloride.

Here none other than Steven Zeisel and friends used '(d9 methyl)-choline chloride':

- Accelerated uptake of an intravenously administered dose of choline chloride in choline-deficient humans​

More on chloride form supplementation:

- Choline Deficiency During Parenteral Nutrition in Humans​

I couldn't find much information on absorption rate.

- Office of Dietary Supplements - Choline

"Precise estimates of the percentage absorption of the different forms of dietary choline in humans are not available [2,3]."​

- The Vitamins: Fundamental Aspects in Nutrition and Health (978-0-12-802965-7)

"Free choline is absorbed in the [duodenum and jenunum] by a saturable, carrier-mediated process localized in the brush border, and efficient at low lumenal concentrations (<4 mM) [~400 mg]. It is also absorbed less efficiently by passive diffusion; at high intakes, the nonabsorbed major portion passes to the hindgut where it is catabolized by the intestinal microbiome to the end product trimethylamine[15] much of which is absorbed and excreted in the urine. Because PC, being better absorbed, is not subject to such extensive microbial metabolism, it produces less urinary trimethylamine."

[15] "The characteristic fishy odor of this product is identifiable after consumption of a choline supplement."​

- Modern Nutrition in Wealth and Disease (978-1-60547-461-8)

"The extent to which dietary choline is bioavailable depends on the efficiency of its absorption from the intestine. In adults, some ingested choline is metabolized before it can be absorbed from the gut. Gut bacteria degrade choline to form betaine and to make methylamines (26) and may destroy enough diet-derived choline to influence the human dietary requirement (27, 28). Some of the variation in human requirements may be caused by differences in the intestinal microbiome."​

 

[TeaRex14]

I do. Grass fed ground beef is my go-to. I love paprika, cumin, chilis, and all that, so I usually cook it up in the pan with a bunch of spices like that, and salt, then when it's done I'll throw some shredded cheddar over it and let it melt. A good sized portion of that, with some mandarin oranges on the side, and/or air fried corn tortillas, or corn tortillas fried in coconut oil. Very good.

A lot of times after I work out I'll have that ground beef chili, and many times pretty easily eat the whole pound. So my red meat intake on average is quite high, and 95% of my dairy intake is from cheese, which I have a fair amount of.

I used to make liposomal vitamin C in an ultrasonic cleaner years ago. I might get back into that. It actually tasted quite nice. I just had the idea to do it using orange juice as the liquid instead of water, but I'm not sure if it would work the same. Perhaps the bioflavanoids in the OJ could make it even more effective.



I am the same way. Any time I can get a bulk form of a supplement, I go for that. Purebulk is great. Lots of times I'll crunch numbers to find out the price per volume and go with the highest quality but cheapest supplement I can find.

I do wonder about the lecithin alarmists, as isn't the lecithin in egg yolks unsaturated as well?

I believe so, but because of eggs nutrient profile the benefits seem to outweigh the risks. The amount you're getting in say 1 or 2 eggs isn't a lot, you would need to eat like 5-6 eggs a day before you started seeing noticeable accumulation, I would think.

 

[sunraiser]

I'm glad some people could relate to the last post - lots of us probably share similar experiences and states of physiology.

I want to reiterate the fat soluble values I stated are not something to consistently consume as it's possible they'll still cause mineral depletion or imbalance, it was just various self tests I have done on occasion.

I still do not know if vitamin D status is merely a reflection of calcium uptake ability (like masterjohn talks about) or whether it actually needs to be actively taken. When supplementing it might just force magnesium/calcium metabolism when they're not available.

I basically agree with everything you say, but what I was getting at is the direction of causation. I was a bit suprised that you state that intestinal permeability is the cause of bacterial overgrowth. I think it makes more sense to think of this process the other way around. In connection with the liver, everything is a cycle in some way, and it's sometimes hard to conceptualize the degenerative process in successive steps, but I think we can with some certainty think of bacterial overgrowth as the starting point. It's hard for me to imagine how the intestine would become leaky before there is any dysbiosis.

With regards to protein. I think the persorption of undigested peptides (I think for whole proteins to be absorbed you must be really ****88 up) is a significant problem for the liver. Nevertheless, I think the more severe and immediate problem for the liver occurs, again, directly in the intestine. I think too much protein can be just as bad as eating too much fermentable fiber and starch. If your digestion is poor, excess protein will release toxic amounts of hydrogen sulfide, methane, and varius other potential toxins. I'm pretty certain that this is the reason protein consumption is associated with colon cancer, and certain liver diseases. The toxic environment that can be created by either eating too much fermentable fiber/starch or proteins will cause the intestine to become leaky, and become a constant source of toxins for the liver, which in turn will become less effective at regulating the gut-liver axis. The perfect vicious cycle.


Free Radic Biol Med. 2016 Apr;93:155-64.
Detrimental effects for colonocytes of an increased exposure to luminal hydrogen sulfide: The adaptive response.
Beaumont M(1), Andriamihaja M(1), Lan A(1), Khodorova N(1), Audebert M(2), Blouin
JM(1), Grauso M(1), Lancha L(3), Benetti PH(1), Benamouzig R(4), Tomé D(1),
Bouillaud F(5), Davila AM(1), Blachier F(6).

Protein fermentation by the gut microbiota releases in the large intestine lumen
various amino-acid derived metabolites. Among them, hydrogen sulfide (H2S) in
excess has been suspected to be detrimental for colonic epithelium energy
metabolism and DNA integrity. The first objective of this study was to evaluate
in rats the epithelial response to an increased exposure to H2S. Experiments from
colonocyte incubation and intra-colonic instillation indicate that low millimolar
concentrations of the sulfide donor NaHS reversibly inhibited colonocyte
mitochondrial oxygen consumption and increased gene expression of hypoxia
inducible factor 1α (Hif-1α) together with inflammation-related genes namely
inducible nitric oxide synthase (iNos) and interleukin-6 (Il-6). Additionally,
rat colonocyte H2S detoxification capacity was severely impaired in the presence
of nitric oxide. Based on the γH2AX ICW technique, NaHS did not induce DNA damage
in colonocytes. Since H2S is notably produced by the gut microbiota from sulfur
containing amino acids, the second objective of the study was to investigate the
effects of a high protein diet (HPD) on large intestine luminal sulfide content
and on the expression of genes involved in H2S detoxification in colonocytes. We
found that HPD markedly increased H2S content in the large intestine but the
concomitant increase of the content mass maintained the luminal sulfide
concentration. HPD also provoked an increase of sulfide quinone reductase (Sqr)
gene expression in colonocytes, indicating an adaptive response to increased H2S
bacterial production. In conclusion, low millimolar NaHS concentration severely
affects colonocyte respiration in association with increased expression of genes
associated with intestinal inflammation. Although HPD increases the sulfide
content of the large intestine, the colonic adaptive responses to this
modification limit the epithelial exposure to this deleterious bacterial
metabolite.

The directional assumption is based on the idea that chronic stress will deplete vitamin A and zinc, and there will be a weaker mucosal barrier in such a state.

This is going to tax but not destroy your liver; however the longer term the more taxing it will be. Many people turn to paleo or iron and copper rich diets in this state (ie mega heme iron and copper intake in general) and if it continues the liver can't cope and the iron burden grows, then giving way to proliferation of candida and other bacteria to cope with poor digestion and heavy metal presence.

Ray Peat talks about vitamin A being destroyed in the presence of iron toxicity and, if the liver is constantly burdened by leaky gut then how can k2 production meet the levels of vitamin A needed to recover mucosal integrity? It's possible that vitamin D is actually the worst possible thing to take in this state, but I'm still unsure.

I THINK this is why the "low VA" diet works for some - they're simply only eating easily digestible foods (especially avoiding casein) which allows better liver function and prompts iron detox and allows energy production to become more efficient, but it'll eventually plateau imo, as vitamin A needs will become more realistic and the liver will hopefully cope with more k2 conversion.

It's possible various viral or bacterial burdens complicate matters by further heightening VA needs via immune response, but I definite think the relationship can work both ways.

@Douglas Ek posted about iron toxicity creating an innate magnesium deficiency (I'm worried he might be banned, though?) too. So a little supplementation with b6 might help in recovery too.

Meat protein digestion is going to be poor with low stomach acid regardless, so I really think slow cooking and acidic mediums to predigest meat can help in this state, and also mince can be good due to exposed surface area.

 

[TheBeard]

´
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 would tend to disagree.

Tetracyclines did my liver in, and are the main reason why I have gut and liver issues today.

Stay away from antibiotics. It litterally means anti life, how is that not a first clue?

 

[jet9]

Following

 

[tankasnowgod]

Tetracyclines did my liver in, and are the main reason why I have gut and liver issues today.

What was the context? Most specifically, what were you talking Tetracyclines for, and what was dosage, and how long did you take them for?

 

[Rafael Lao Wai]

- 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."​

Most skinny people that I have seen in real life don't shy away from PUFA-laden foods( especially chips, which they sell everywhere, so it makes sense that it is a very popular snack). Quite the opposite. They think weight is all that matters, so they think eating a lot of things fried in PUFA won't affect them. I find it unfair to compare fruitarians, which generally eat high carb and low fat, to skinny people, most of which aren't health-conscious. And Peat even mentioned a study in which, even if you overfeed sucrose to the point of causing fat accumulation in the liver, you won't cause oxidative stress or inflammation( so no steatohepatitis), since the fat produced by cells from excessive carbohydrate intake is palmitic acid, which is great for the liver.

 

[TheBeard]

What was the context? Most specifically, what were you talking Tetracyclines for, and what was dosage, and how long did you take them for?

After eye laser surgery, my meibomian gland ducts were obstructed from the cornea dryness resulting from the surgery.

I took 3 courses of 10 days doxycycline and 3 courses of 5 days azythromycin.

All these courses were at least 3 months apart each.

These antibiotics did exactly what they were supposed to do: unclog my meibomian gland ducts, very satisfied with this.

They also did exactly what they were supposed to do: destroy my gut flora.

I lost 15 pounds of muscle mass, I have an inflammed liver and constantly bloated gut, I became intolerant to alcohol and quite a few foods.

I need 10h of sleep to just be barely functional when I used to feel refreshed after 7.

 

[Amazoniac]

Most skinny people that I have seen in real life don't shy away from PUFA-laden foods( especially chips, which they sell everywhere, so it makes sense that it is a very popular snack). Quite the opposite. They think weight is all that matters, so they think eating a lot of things fried in PUFA won't affect them. I find it unfair to compare fruitarians, which generally eat high carb and low fat, to skinny people, most of which aren't health-conscious. And Peat even mentioned a study in which, even if you overfeed sucrose to the point of causing fat accumulation in the liver, you won't cause oxidative stress or inflammation( so no steatohepatitis), since the fat produced by cells from excessive carbohydrate intake is palmitic acid, which is great for the liver.

It wasn't a comparison between them, it was in response to sugarbaby's wonderment: is it possible to be skinny and still have a fatty liver?
If I'm not wrong, it's common for those dealing with anorexia to avoid fats, and they're also afflicted by this condition, so we can exclude fat as confounder.

Getting more sugar than the person can handle in an inadequate diet might not lead to that sort of stress, but it's compromising nevertheless.

- Polyunsaturated fat in the methionine-choline-deficient diet influences hepatic inflammation but not hepatocellular injury

"Removal of unsaturated fat from the MCD formula results in significant suppression of MCD-mediated hepatic inflammation; it does not, however, have any impact on MCD-mediated injury to hepatocytes."​

--
- Non-Alcoholic Fatty Liver Disease and Nutritional Implications: Special Focus on Copper

"Many anti-oxidant natural compounds are described to counteract NAFLD, its progression towards NASH and related complications [35,49,50,51]." "Interestingly, many of those compounds are able to bind copper, highlighting a direct action on copper-related dysfunction."​

- The absorption and retention of magnesium,... | Ray Peat Forum

 

[bistecca]

https://chrismasterjohnphd.com/blog/2010/11/23/sweet-truth-about-liver-and-egg-yolks/

"the loss of cholesterol-rich foods like egg yolks and organ meats as a result of cholesterol paranoia seems to be at the bottom NAFLD thus far."

Eat nose to tail animals(broth, organs). Avoid modern pufa rich oils. Not too much alcohol.

 

[tankasnowgod]

After eye laser surgery, my meibomian gland ducts were obstructed from the cornea dryness resulting from the surgery.

I took 3 courses of 10 days doxycycline and 3 courses of 5 days azythromycin.

All these courses were at least 3 months apart each.

These antibiotics did exactly what they were supposed to do: unclog my meibomian gland ducts, very satisfied with this.

They also did exactly what they were supposed to do: destroy my gut flora.

I lost 15 pounds of muscle mass, I have an inflammed liver and constantly bloated gut, I became intolerant to alcohol and quite a few foods.

I need 10h of sleep to just be barely functional when I used to feel refreshed after 7.

So why did you only blame the tetracycline class, and not the azythromycin?

 

[Tarmander]

I remember I tried doing 12 egg yolks a day for a month or two in an effort to clear out my gut fat and assumed fatty liver. Didn't do ***t.

Careful supplementing Choline like PC long term. It will mess with you acetylcholine levels in your brain. Check out some nootropic forums to see what that can do.

I have fatty liver and elevated liver enzymes for the last 7 to 8 years and alpha tocopherol succinate 800 iu a day normalized my enzymes and reduced fat and size Of my liver by ultrasound. Enzymes went into normal range within 4 weeks

Nice. Everyone ignored you basically but this is a good testimonial. Did you just do the 4 weeks or continue on?

 

[Kelj]

The Centrality of The Liver in Pattern Baldness: Estrogen, Aspirin, and IGF-1
In this article, Danny Roddy quotes this study:
Another feature of an impaired liver is a decreased level of insulin-like growth factor 1, ...IGF-1 decreases with age and during malnutrition.[54,55] Mezey E. Insulin growth factor I and hypogonadism in cirrhosis. Hepatology. 2000 Mar;31(3):783-4. “Decreased serum IGF-1 concentrations are well documented in children with kwashiorkor, in malnourished adults, and after long-term fasting in obese male subjects."
And regarding fructose and glycogen storage: "While it is true that the liver rapidly uses fructose, it does so primarily to refill hepatic glycogen. In one study, an infusion of fructose resulted in about 360 percent more glycogen than a glucose infusion.[71] And the liver's capacity for glycogen is very large. One study suggested that "de novo lipogenesis [DNL] is not an important pathway in humans" and that chronic overfeeding on carbohydrates increased glycogen stores of about 500 grams before DNL became significant.[72] The liver uses glycogen locally for its various tasks, so keeping it "energized" is a simple and effective way to support its function..." Also, ...".Numerous studies already cited have establish that cirrhosis of the liver can be produced by nutritional deficiency or nutritional imbalance and that B vitamins (especially choline) and the protein content of the diet play a major role in this phenomenon."Biskind, M.S. Nutritional Aspects of Endocrine Disease. Am J Clin Pathol. 1946 Dec;16(12):737-45. This article shows how widely available in the diet choline is:
Choline.
This article
Relationships Between Nutrition, Alcohol Use, and Liver Disease has this to say: "Malnutrition, regardless of its causes, can lead to liver damage and impaired liver function. For example, children in underdeveloped countries whose diets do not contain enough protein can develop a disease called kwashiorkor. One symptom of this disorder is the accumulation of fat in the liver, a condition known as fatty liver. Studies performed during and after World War II indicated that severe malnutrition also could lead to liver injury in adults......Chronic drinkers, particularly those who consume a substantial portion of their daily calories in the form of alcohol, often show evidence of malnutrition such as deficits in amino acids, proteins, and certain vitamins. These deficits can derive from an inadequate diet as well as from alcohol’s effects on these nutrients and their metabolism. Particularly common is a deficit in vitamin A, which is required for proper eye function and bone growth. Moreover, both vitamin A deficits and excessive vitamin A levels can lead to liver damage, including fibrosis. Therefore, administering vitamin A to correct a deficiency is difficult and should be controlled carefully, particularly in the presence of alcohol abuse, which exacerbates vitamin A’s toxicity." So, any talk of vitamin A supplementation for Fatty Liver must take into account that too much vitamin A can cause the condition. How to prevent and treat Fatty Liver, alcoholic and non-alcoholic? Plenty of calories and the nutrients that come from following your body's desire for certain foods. This will lead to the right amount of choline, vitamin A and protein required to have a healthy liver, not to mention a healthy thyroid and everything else. Plenty of calories means whatever your body is asking for daily without saying no. That is not 2000 calories. The liver needs fructose to recover from impairment.

 

[TheBeard]

So why did you only blame the tetracycline class, and not the azythromycin?

They both pertain to the macrolide-antibiotic class.

But regardless of their classification, I’m blaming all antibiotics for deteriorated gut health, as they all destroy gut flora.