Masterjohn Right? Treating Fatty Liver

[InChristAlone]

I've been considering taking a choline supplement, since I don't eat eggs or drink milk, and haven't been eating liver lately. I do eat a fair amount of cheese but I'm not sure if that would be providing enough choline on its own. This reminds me of this article:

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

Are there any "best" forms of choline to supplement with?

Good question, and CM has a database now that gives you amounts of choline in food as compared to one large egg yolk.
https://chrismasterjohnphd.com/2019/04/17/the-choline-database/
He recommends TMG and lecithin.

 

[Kartoffel]

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.

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.

 

[shepherdgirl]

FYI:

Liver Disease Is Caused By Low ATP Driven By Fat (PUFA) Oxidation

Inosine Increases ATP And Reverses NAFLD (and Likely Other Liver Disease)

 

[Spondive]

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

 

[TeaRex14]

I've been considering taking a choline supplement, since I don't eat eggs or drink milk, and haven't been eating liver lately. I do eat a fair amount of cheese but I'm not sure if that would be providing enough choline on its own. This reminds me of this article:

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

Are there any "best" forms of choline to supplement with?

Choline l-bitartrate is the most popular choline supplement, I take the one from PureBulk because it's free of any extra additives. Normally I only take a single 700mg dose, but I also eat eggs, dairy, and beef liver twice a week. Someone not eating any of those should probably take at least an 1,400mg dose daily.

 

[InChristAlone]

Choline l-bitartrate is the most popular choline supplement, I take the one from PureBulk because it's free of any extra additives. Normally I only take a single 700mg dose, but I also eat eggs, dairy, and beef liver twice a week. Someone not eating any of those should probably take at least an 1,400mg dose daily.

Chris Masterjohn says this:
"Phosphatidylcholine prevents fatty liver disease (see here for a primer on fatty liver disease), supports gallbladder health, and assists with fat digestion. It is the least likely form of choline to generate TMAO, generating either none at all, or four times less than similar doses of choline bitartrate (see here and here). "

"Gut microbes convert choline that you don’t absorb into trimethylamine (TMA), and your liver converts it into TMAO.

The most compelling evidence to date for the hypothesis that TMAO contributes to heart disease was published more recently in 2017. The researchers fed 500 mg/d choline bitartrate for 2 months. It raised TMAO levels in the subjects. When they drew their blood and mixed it with factors that cause clotting, their blood clotted more after the choline supplementation than before. They didn’t include a control group, and they didn’t show any clinical endpoints (such as actual heart disease), so the study isn’t very compelling, but it does add to the data suggesting TMAO might not be so great for heart disease."

Might not be so great to supp high doses of choline bitartrate. Best to spread it out or use lecithin.

 

[Jib]

@ sugarbabe and TeaRex

Thanks for the responses. Ordering a 1.5kg tub of Choline L-Bitartrate now. Can't hurt to have on hand. I'll also check that list of choline content in foods and figure out how much I should be taking daily but 1,400mg sounds good.

My dad's homocysteine levels came down to a normal range after supplementing with an activated B-complex. I have an MTHFR gene mutation and found that high dose methylfolate greatly helps my depression. As a matter of fact, without fail, within 1 to 2 weeks of not taking methylfolate, my major depression comes back, and often suicidal thoughts. It's like clockwork. I am a believer, and feel that a full spectrum activated B complex can be beneficial for many things. Possibly fatty liver but I have never looked anything up on this.

EDIT: Well, it seems the choline supplementation could be up for some debate. I used to supplement lecithin but it's been a while. Not sure if sunflower is any different from soy.

EDIT (again): I found this thread from haidut:

MitoLipin - Liquid Saturated Phosphatidylcholine (PC) Mix

MitoLipin can be found here:

IdeaLabs Online Store - Cosmetic Raw Ingredients

I'm still not clear as to whether it can be only used externally, or orally as well, and what the minimum effective dose would be. 40 bucks a month is nothing to sneeze at if a single dose is 40 drops, with there being 30 doses per bottle. But very interesting, and I would like to try it.

 

[rei]

Fasting has been shown to primarily burn visceral and ectopic fat, exactly what you want to treat fatty liver and in the process it also lowers insulin resistance thus preventing it from forming again.

here's the first link i found
Fasting induces a subcutaneous-to-visceral fat switch mediated by microRNA-149-3p and suppression of PRDM16

 

[ecstatichamster]

There is a study that is quite negative about choline supplementation. Maybe it’s just one study but it’s something to be considered. Can’t find it just now.

 

[schultz]

If people could just eat according to what their body desires maybe we wouldn't have this constant debate over which is better.

Isn't this what normal people do? Like the standard American diet?

40 bucks a month is nothing to sneeze at if a single dose is 40 drops, with there being 30 doses per bottle. But very interesting, and I would like to try it.

I think sometimes Haidut just puts sort of a random dose on the bottle. You'd have to check with him. You might only need to take 10 drops or something, but I don't know about this particular supplement. With Energin (which also says 40 drops) I take like 5 or 10 drops at a time.

 

[tankasnowgod]

Isn't this what normal people do? Like the standard American diet?

It's pretty much what almost all humans and every animal has done for all of history. We just are lucky to live in a time when some people and forces have figured out how to manipulate those body signals in order to harm or kill us for doing so.

 

[TeaRex14]

Chris Masterjohn says this:
"Phosphatidylcholine prevents fatty liver disease (see here for a primer on fatty liver disease), supports gallbladder health, and assists with fat digestion. It is the least likely form of choline to generate TMAO, generating either none at all, or four times less than similar doses of choline bitartrate (see here and here). "

"Gut microbes convert choline that you don’t absorb into trimethylamine (TMA), and your liver converts it into TMAO.

The most compelling evidence to date for the hypothesis that TMAO contributes to heart disease was published more recently in 2017. The researchers fed 500 mg/d choline bitartrate for 2 months. It raised TMAO levels in the subjects. When they drew their blood and mixed it with factors that cause clotting, their blood clotted more after the choline supplementation than before. They didn’t include a control group, and they didn’t show any clinical endpoints (such as actual heart disease), so the study isn’t very compelling, but it does add to the data suggesting TMAO might not be so great for heart disease."

Might not be so great to supp high doses of choline bitartrate. Best to spread it out or use lecithin.

Yeah I'm aware of that study, Haidut posted it on the forum a while back. Considering I dose aspirin daily and vitamin E semi regularly, I'm not too worried about excess clotting. Estrogen and serotonin are the two biggest risk factors with blood platelet aggregation. I'm not sure where to find Phosphatidylcholine, so I just go with what's available and is pure (i.e no added ingredients).

 

[Jib]

Yeah I'm aware of that study, Haidut posted it on the forum a while back. Considering I dose aspirin daily and vitamin E semi regularly, I'm not too worried about excess clotting. Estrogen and serotonin are the two biggest risk factors with blood platelet aggregation. I'm not sure where to find Phosphatidylcholine, so I just go with what's available and is pure (i.e no added ingredients).

I suppose I'm still debating about whether to go with a choline supplement or not.

I wonder if Phosphatidylcholine, the only source of which seems to be MitoLipin, can carry all the benefits in low doses? MitoLipin seems to intend to be a therapeutic agent as opposed to a way to meet daily requirements, so I'd imagine these are separate things.

I see some people are conflicted about lecithin as well, because of the PUFA. In the MitoLipin thread many people seem opposed to lecithin and think that supplementing it is harmful. I personally stopped eating eggs for the past two months as all I can afford are cheap supermarket eggs, and I was concerned about the soy content, as well as PUFA.

Would choline supplementation really be any different from getting choline via something like normal supermarket eggs? Are the issues with clotting attributed to choline a result of taking it as a supplement? Why would choline bitartrate be harmful but not an equivalent amount of choline from either soy lecithin or regular supermarket eggs?

I'm not plunking down for MitoLipin just yet, but the anecdotal reviews look very promising. But again, MitoLipin seems to be intended as a therapeutic supplement, like pregnenolone, intended to be taken only in small doses, so it's not like it could replace dietary requirements for substances like choline.

As usual, everyone seems split down the middle: lecithin is bad, lecithin is good, choline supplementation is bad, choline supplementation is good.

I suppose co-factors must play some kind of role, and a person's particular hormonal profile as well. I have not been tested but based on my mood and physical state (slightly overweight with a lot of visceral fat, anxiety and depression), I am most certainly estrogen dominant, and perhaps issues with choline supplementation would be more problematic for me than someone with lower estrogen and better metabolism in general.

 

[InChristAlone]

I suppose I'm still debating about whether to go with a choline supplement or not.

I wonder if Phosphatidylcholine, the only source of which seems to be MitoLipin, can carry all the benefits in low doses? MitoLipin seems to intend to be a therapeutic agent as opposed to a way to meet daily requirements, so I'd imagine these are separate things.

I see some people are conflicted about lecithin as well, because of the PUFA. In the MitoLipin thread many people seem opposed to lecithin and think that supplementing it is harmful. I personally stopped eating eggs for the past two months as all I can afford are cheap supermarket eggs, and I was concerned about the soy content, as well as PUFA.

Would choline supplementation really be any different from getting choline via something like normal supermarket eggs? Are the issues with clotting attributed to choline a result of taking it as a supplement? Why would choline bitartrate be harmful but not an equivalent amount of choline from either soy lecithin or regular supermarket eggs?

I'm not plunking down for MitoLipin just yet, but the anecdotal reviews look very promising. But again, MitoLipin seems to be intended as a therapeutic supplement, like pregnenolone, intended to be taken only in small doses, so it's not like it could replace dietary requirements for substances like choline.

As usual, everyone seems split down the middle: lecithin is bad, lecithin is good, choline supplementation is bad, choline supplementation is good.

I suppose co-factors must play some kind of role, and a person's particular hormonal profile as well. I have not been tested but based on my mood and physical state (slightly overweight with a lot of visceral fat, anxiety and depression), I am most certainly estrogen dominant, and perhaps issues with choline supplementation would be more problematic for me than someone with lower estrogen and better metabolism in general.

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.

 

[ecstatichamster]

I'm seeing a lot having to do with gut transit time.

This may be the whole story.

If we can speed up transit time, don't we lower endotoxins and therefore let the liver defat safely (with caffeine, periodic short very low fat diet periods, a little niacinamide, aspirin).

One thing that has been brought to my attention is methane-producing archaea that are not killed with antibiotics.

Higher methane levels correlate with slower transit times, obesity and type 2 diabetes.

Elevated methane levels in small intestinal bacterial overgrowth suggests delayed small bowel and colonic transit

A retrospective review was performed for 89 patients who underwent a LBT and whole gut transit scintigraphy (WGTS) between 2014 and 2016. Seventy-eight patients were included. WGTS evaluated gastric emptying, SBT (normal ≥40% radiotracer bolus accumulated at the ileocecal valve at 6 hours), and CT (normal geometric center of colonic activity = 1.6–7.0 at 24 hours, 4.0–7.0 at 48 hours, 6.2–7.0 at 72 hours; elevated geometric center indicates increased transit). We also had patients complete a pretest symptom survey to evaluate nausea, bloating, constipation, diarrhea, belching, and flatulence.

A total of 78 patients (69 females, 9 males, mean age of 48 years, mean BMI of 25.9) were evaluated. Forty-seven patients had a positive LBT (H-SIBO 66%, M-SIBO 34%). Comparison of SBT among patients with a positive LBT to normal LBT revealed no significant difference (62.1% vs 58.6%, P = .63). The mean accumulated radiotracer was higher for H-SIBO compared to M-SIBO (71.5% vs 44.1%; P < .05). For CT, all SIBO patients had no significant difference in geometric centers of colonic activity at 24, 48, and 72 hours when compared to the normal group. When subtyping, H-SIBO had significantly higher geometric centers compared to the M-SIBO group at 24 hours (4.4 vs 3.1, P < .001), 48 hours (5.2 vs 3.8, P = .002), and at 72 hours (5.6 vs 4.3, P = .006). The symptom severity scores did not differ between the positive and normal LBT groups. A higher level of nausea was present in the H-SIBO group when compared to the M-SIBO group.

Overall, the presence of SIBO does not affect SBT or CT at 24, 48, and 72 hours. However, when analyzing the subtypes, M-SIBO has significantly more delayed SBT and CT when compared to H-SIBO. These results suggest the presence of delayed motility in patients with high methane levels on LBT.

 

[ecstatichamster]

these can be eradicated with low amounts of, believe it or not, lovostatin, found in oyster mushrooms and some others.

Metabolic effects of eradicating breath methane using antibiotics in prediabetic subjects with obesity. - PubMed - NCBI

OBJECTIVE:
Methanogens colonizing the human gut produce methane and influence host metabolism. This study examined metabolic parameters in methane-producing subjects before and after antibiotic treatment.

METHODS:
Eleven prediabetic methane-positive subjects (9F, 2M) with obesity (BMI 35.17 ± 7.71 kg/m(2) ) aged 47 ± 9 years were recruited. Subjects underwent breath testing, symptom questionnaire, oral glucose tolerance test (OGTT), lipid profile, and stool Methanobrevibacter smithii levels, gastric transit, and energy utilization analyses. After a 10-day antibiotic therapy (neomycin 500 mg bid/rifaximin 550 mg tid), all testing was repeated.

RESULTS:
Baseline stool M. smithii levels correlated with breath methane (R = 0.7, P = 0.05). Eight subjects (73%) eradicated breath methane and showed reduced stool M. smithii (P = 0.16). After therapy, methane-eradicated subjects showed significant improvements in low-density lipoprotein (LDL) (P = 0.028), total cholesterol (P = 0.01), and insulin levels on OGTT (P = 0.05 at 120 minutes), lower blood glucose levels on OGTT (P = 0.054 at 90 minutes), significant reductions in bloating (P = 0.018) and straining (P = 0.059), and a trend toward lower stool dry weight. No changes were detected in gastric emptying time or energy harvest.

CONCLUSIONS:
Breath methane eradication and M. smithii reduction are associated with significant improvements in total cholesterol, LDL, and insulin levels and with lower glucose levels in prediabetic subjects with obesity. The underlying mechanisms require further elucidation.

 

[TeaRex14]

I suppose I'm still debating about whether to go with a choline supplement or not.

I wonder if Phosphatidylcholine, the only source of which seems to be MitoLipin, can carry all the benefits in low doses? MitoLipin seems to intend to be a therapeutic agent as opposed to a way to meet daily requirements, so I'd imagine these are separate things.

I see some people are conflicted about lecithin as well, because of the PUFA. In the MitoLipin thread many people seem opposed to lecithin and think that supplementing it is harmful. I personally stopped eating eggs for the past two months as all I can afford are cheap supermarket eggs, and I was concerned about the soy content, as well as PUFA.

Would choline supplementation really be any different from getting choline via something like normal supermarket eggs? Are the issues with clotting attributed to choline a result of taking it as a supplement? Why would choline bitartrate be harmful but not an equivalent amount of choline from either soy lecithin or regular supermarket eggs?

I'm not plunking down for MitoLipin just yet, but the anecdotal reviews look very promising. But again, MitoLipin seems to be intended as a therapeutic supplement, like pregnenolone, intended to be taken only in small doses, so it's not like it could replace dietary requirements for substances like choline.

As usual, everyone seems split down the middle: lecithin is bad, lecithin is good, choline supplementation is bad, choline supplementation is good.

I suppose co-factors must play some kind of role, and a person's particular hormonal profile as well. I have not been tested but based on my mood and physical state (slightly overweight with a lot of visceral fat, anxiety and depression), I am most certainly estrogen dominant, and perhaps issues with choline supplementation would be more problematic for me than someone with lower estrogen and better metabolism in general.

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.

 

[schultz]

It's pretty much what almost all humans and every animal has done for all of history. We just are lucky to live in a time when some people and forces have figured out how to manipulate those body signals in order to harm or kill us for doing so.

Right, so eating "what the body desires" might not be a great strategy in this modern age. People desire all sorts of crap based on primitive cravings.

When the choice is between plant leaves, or some tuber you found in the ground, vs. a mango, you're probably going to choose the mango. When the choice is between a mango or a bag of gummy bears, a lot of people will choose the gummy bears, unless they've been told that candy is not healthy and choose the mango based on their knowledge of nutrition. A bowl of mashed taro or a bag of potato chips?

I guess it's easier to rely on your instincts the less processed a food is. But even that can't be a rule, because a boiled potato is processed and is healthier than a raw potato. Milk and fruit taste pretty darn good without any processing.

 

[Amazoniac]

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.

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.

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.

You look different. Did you cut your hair?

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 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

 

[Waremu]

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 as (if at all) effective for fatty liver as choline is, however, it appears that betaine is choline sparing in the context of methylation (in the sense that it is used for methylation by the body) from a choline to betaine conversion pathway, though it seems it is not choline sparing outside of methylation needs. So, if methylation needs are met with betaine, you will likely need less total choline than you otherwise would have needed. 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 be 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 to do if they do not handle dairy or organ meats too well.

I’ve increased my choline and added in betaine containing low PUFA foods and increased my folate intake as well and I must say that I definitely do notice some benefits with energy, cognition/mental charity, etc.