Active B12 Protocol Basics

Freddd

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Thanks, Fred! Please can you clarify the above quote.

My husband has pernicious anaemia, diagnosed after a severe hpylori infection. I gave him1mg MeCbl injection daily for a year and now he only needs it a few times per week or less, self-injected.

The thing is he began to recover miraculously after just a few months on MeCbl (plus once weekly 10mg AdoCbl) a mineral supplement and a vitamin supplement.

But he never took lithium (we weren't aware of it) and I've just checked - it's not in his mineral supplement.

He was withering away in front of my eyes before this (big weight loss, muscle atrophy, lowered kidney function and lymphocytes, yellow looking in the face, frequent infections) and the GP was only offering one hydroxocobalamin injection every 3 months.

He's completely recovered now and he says to pass on big thanks to you! :thumbsup:

He doesn't have any of your (or mine) odd genetics around b12. Just straightforward pernicious anaemia.

His psoriasis hasn't improved much, but it was never severe. He takes 1mg metafolin daily and there's a little copper with zinc in the mineral supplement.

He drinks the same fluoridated tap water as I do. And he puts too much toothpaste (fluoridated) on his brush!

Should he take a small dose of lithium do you think? I worry if anything happens to me (though I'm still in remission) that he won't keep up the injections etc. Maybe with lithium he would be able to inject less frequently.

Isn't it interesting how well he's done without lithium, even with our awful tap water?

Could he be getting lithium from something else? He has a more varied diet than I do - he's not coeliac like me, and doesn't have any trouble with vegetable folic etc.
Hi Athene,

It's hard to tell how much lithium is needed considering fluoride. Both are naturally occurring in all sorts of waters and local minerals.

I have barely over 5 years distinguished some adequacy indicators. When a person has the micro fast with tiny amounts of lithium and the transcobalamin receptor lithium, gets enough cbl, barely, to stay funtional but no storing of B12 to speak of; appears 1st quintile. Also if taking injections or high doses of sublingual if the kidney has enough TCR-Li for storage and the kidney delays excreting cbl up to nearly a day. This seems to happen at the 4th or fifth quintile. There were variable changes as 6 months to 5 years continued.

The lithium taken combined with cob[ii] appears to grown more TCR-Li or cleans out the fluoride damaging some receptors. If the cob[ii] is lacking, MeCbl and AdoCbl can replace cob[ii] in being able to make more TCR. I titrated up to 30 mg and back down to 20 mg/day a few times. There were no differences I could see.

However, when I took a single extra 10 g or 20 mg of lithium orotate after not taking MeCbl after a week or two or 3 , the single extra lithium dose cleaned out the TCR-Li and absorbs more cob[ii] and retains more catalytic B12 (cob[ii] for longer.
 

Athene*

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Interesting, thanks, Fred.
I'm holding on to my injections for a day or more now and it used to be no more than a couple of hours but still the AdoCbl CNS dose will cause me to lose MeCbl - the next day, the first two 10mg injections will be very visible in the urine pretty much immediately. The third one holds.
Is it correct to hold the 50mg AdoCbl dose for 5 hours (10mg x 5) and after last 10mg AdoCbl then leave 6 hours before next MeCbl 10mg injection?
I wonder if I'm leaving it too long without MeCbl?

As for my husband - he says he never sees even a trace of pink, but then he never had any issues with absorbing or recycling b12 once he got the small dose MeCbl injections he was flying. He's going to see how he gets on with less per week & monitor symptoms.
He does need methylfolate, otherwise high histamine symptoms, sneezing, runny nose. All symptoms fixed with 1mg Mefolate daily whereas I need 50mg daily ☹
 
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Athene*

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Freddd said:
"For somebody to have pernicious anemia (IF missing) a person also needs a lithium deficiency"
@Athene - "Thanks, Fred! Please can you clarify the above quote."
Pernicious anemia was simply untreatable anemia,. It is a disease of inadequate B12. Over time "Pernicious anemia" became equal to "insufficient" "the Intrinsic Factor." rather than AN intrinsic factor. As far as macrocytic anemia goes, it doesn't matter whether injected B12, sublingual TCR-li, or a sublingual, passively absorbed B12 intestine they all supply B12 and either there is enough to not have high MCV or insufficient B12 having high. MCV.

Its like calling all folates are the same as "folic acid". That could be fatal for some people.

I was simply trying to draw attention that the specific cause of anemia is different than the very specific one cause.
Understood, thanks, Fred. I too was diagnosed with pernicious anaemia and hypothyroidism decades after 'ME' and 'Fibromyalgia' but was given hydroxocobalamin & folic & levothyroxine, then nothing when I couldn't tolerate those.
The UK sites just said the same and said methylfolate was dangerous. I was clueless and I really thought I would die.
Thankfully I found your postings.
 
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I have a question for Freddd, or anyone else very familiar with how people have experienced the protocol.

I'm loosely following the protocol, and B12 is absolutely making a difference. But my experience is a little different from the norm.

I understand Freddd to say there's usually a felt startup effect quickly after taking the B12 dose -- like, while it's still in the mouth. I do have a very clear startup effect, but it's never been that fast. I've seen it kick in as soon as six hours later, to 3-4 days after beginning a particular daily dose level.

When it does kick in, it's unmistakable. It feels like a light has been turned on. I described it as a "brightness", and later I saw Freddd described his own experience with the same word. Parts of it felt great; others felt "overstimulated". So it seems like everyone else's experience, just delayed.

That's what I experienced up to 4-5mg. Somewhere past that, I stopped feeling the overstimulation, even though I was now ramping faster. I just felt pretty good generally, better than I've felt in a long time. I'm now at 7mg.

The flip side is what happens if I drop even just 250ug/day below a new high threshold. It's pretty bad. There's an exhaustion in my chest... almost like I can't get quite enough air. There's usually an intense negative mood swing, sometimes a tingling/fatigue in my legs, general fatigue, etc. As with ramping, this would be felt in the same time window of 1-3 days. It's felt the same whether I dropped from 1.5mg or from 7mg. When I eventually restore the prior dosage, within a day or so the engine suddenly revs back up again.

I'm trying to decide whether to keep ramping up. Freddd says to keep increasing until you no longer feel startup effects, but that usually this is 15-20mg. At 7mg, I don't feel any startup effects at all now (unless I'm restoring from a drop). So could this be my target dose?

But if I've reached my target dose, why would I feel so terrible from a slight drop? This suggests I do need to keep ramping, even though I don't feel any obvious positive signs when I raise. But maybe my body is somehow adapting to higher and higher doses for some other, purposeless reason? If I'm going to become dependent (for life, potentially) on a higher dose, it would be really nice to know it's because I'm gaining more health from it.

And if I were to do a "CNS challenge" right now... by these dynamics, I'd quickly get "hooked" on some higher dose and experience withdrawal trying to return to 7mg. Freddd has never mentioned this as a risk of the challenge, so... maybe I need to keep going.

Freddd (or anyone) -- can you share any thoughts on what I should do? My guess is that you'll say I should keep ramping -- but since my experience seems different, this seemed like a good time to stop and get some guidance... Thank you.
 
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I'm only 5 days into the b12 protocol. I noticed some improvements within minutes of the first dose of methylb12!

-Less depression / anxiety / racing thoughts
-Less moments of poor mental concentration
-I no longer feel the need to pace around my house all day worrying. I can now sit down and relax.
-Digestion feels different
-Constipation improved
-Indigestion improved
-Ringing in ear sometimes now
-Hungrier
-Sleep not as deep. More restless sleep.
-Body temp feels warmer
-Frothy/foamy urine first thing each morning

I am only taking miniscule amounts of methylb12. Only taking 3-4 drops per day which is probably 50mcg or less. That dose is plenty for me right now. I'm getting lots of effects (good and bad effects) at that dose so I plan to stay there for a while.

My body does not like folate yet, so ill just stick with the methylb12 for now and wait as things heal. I will add some adenosyl b12 also.
 
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Judee

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I am only taking miniscule amounts of methylb12. Only taking 3-4 drops per day which is probably 50mcg or less. That dose is plenty for me right now. I'm getting lots of effects (good and bad effects) at that dose so I plan to stay there for a while.

My body does not like folate yet, so ill just stick with the methylb12 for now and wait as things heal. I will add some adenosyl b12 also.
Our systems seem to be a bit hypersensitive to sudden drastic changes so I think it's better doing it this way. Start low and go slow.

You may have said somewhere in the thread...sorry if I missed it...but what brand of methyl b12 are you using currently?
 
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Our systems seem to be a bit hypersensitive to sudden drastic changes so I think it's better doing it this way. Start low and go slow.

You may have said somewhere in the thread...sorry if I missed it...but what brand of methyl b12 are you using currently?
past 24 hours I've been using earth harmony brand methyl b12. before that the first 4 days I was using a hydroxo / adenosyl combination. I think i feel the same on both so far. So I plan to stick with methyl b12 for now until I get some adenosyl in the mail. Hard to find just adenosyl that doesnt have a bunch of fillers.
 
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anncavan

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Hi Athene,

Well it has been a while. I started the Lithium about 5 years ago, starting at 5 mg and going to 30 mg daily and then centered in on 20 mg/day. I found several stages of lithium effectiveness. The first one was about 6 months in. I was driving from SLC to Denver by way of the continental divide 2 hours n-east from SLC. I started feeling like I was low on potassium, I was. Having hypokalemia pop up hard in 2 hours was a mystery I had rumn into in studies done in the 50s. Now I know. It is a particular step of cell making that occurs when the lithium "demands" red cells made right now. So one mystery demonstrated. I did early on an N=1000 common language symptoms database from people. About half of them had clusters of low b12 symptoms. Of that 75% taking MeCbl 1000 mcg sublingual had the initial response during the interview. those 75% of responders started responding in 5 to 10 minutes from mouth to brain. Later I found the rest needed different "first nutrient" to start cells being made in 10 minutes or less.

At year 3 I was doing 20mg/day of lithium. I went from MeCbl 10 mg each 8 hours and increased the 2 hours down to 1 injection a day over some weeks. From there I decreased to 3 weeks, 1 day increased between each injection for one injection ranging from 5 mg to 10 mg.

So during 2 to 5 years my liver healed, got rid of non-alcoholic fatty liver, and filled up the TransCobalamin Receptor -Lithium in the liver and my kidneys. My eGFR went from 59% for decades to 79%.. The kidneys are another organ with high levels of TCR-Li. I did thousands of injections through the years of MeCbl. For 10mg injections, plenty of red B12 shows up in the urine in 60-120 minutes. After 4 years of lithium, and 2-3 weeks between injections there is no B12 visible at all until after 8 hours and between 8 to 18 hours before the first visible part of B12 becomes visible and then just a dribble at a time came out over up to about 12 more hours of seeing it coming out slowly.. The TCR-Li passes through the kidneys repeatedly each hour and presumably shedding into the urine whatever the B12 picks up and dumps into the urine. TCR-Li is said to take and clean up all forms of cobalamin where as the haptocorrin is very fussy and only absorbs animal found cobalamins. The TCR-Li strips the ligand each time it goes through the kidney and dumps to urine. That needs to be proved in study and just what it dumps each time through and how it "decides" to dispose of cbl as well after a while.

TCR-Li has a LOT to do with homeostasis, I don't know why or how, but I have experienced it. To make TCR-Li requires cob[ii] which TCR-Li also outputs. In place of cob[ii] one has to have MeCbl and AdoCbl in the right proportion. HyCbl, CyCbl, AdoCbl can all cause methyltrap in place of MeCbl or COB[II].


I found that it is more stable with potassium but it goes down slower and eventually you have to keep it up there or you can get in trouble fast after thinking it is stable. I was unable to get a balance of copper and get it higher and prevents low copper cased high MCV.

I'm glad to here that you are doing so much better. All in all there were about 5 stages of TCR-Li, minimal Li was oral absorption of B12 FROM MEAT in 5 minutes. From tablets the oral TCR-Li can absorb 10 mcg of B12 per minute. A 5 mg tablet can absorb 750-1250 mcg from 5 mg tablet in 1 hour. I do one injection a month right now and experiment with tablets at different. I also take the small amount in B-Right daily and I can see some small amount of cbl 4-8 hours after taking my morning B-Right capsule.

Let's of various effects. Different ways of taking, different doses and responses are different in excretion. I started up . with the B-Right again as I would have one pathway close down and need a different form of a nutrient to work. Lots of hypothecizes, lots still to find out and WOW! is what I can say for now.

Be well.
Hi @Freddd I jumped into this conversation thread by doing a search for "non alcoholic fatty liver disease." I see you have healed yourself of it. CONGRATULATIONS! Are you attributing Lithium and MeCbl? How did you make the connection with this and NAFLD? Is there a resource you'd suggest I look to?

Mine fatty liver was found, quite by accident, in a CT of my abdomen. I'm 43, w 2 very young children. I'm at a loss of what to do next w/o the ability to exercise, and I'm being told low carb, low fat, keto, mediterranean, no alcohol, but not told exactly WHAT to eat or supplement. Every answer cancels the other out, or i'm allergic or can't due to MECFS. About 1.5 years ago I gained 20lbs without a change in diet. I had to really watch my food intake after to at least stop the increase, but can't get it off. I've tried significant attempts at low calorie(no change), low carb/keto(caused blood sugar crashes and huge decline w MECFS). I also have an odd thing where when taking a glucose test (the orange drink), I don't get a spike in my blood sugar. But after, say drinking a coke, I feel fantastic health-wise. I feel like this is connected. I have never been diagnosed with diabetes. But I had been on Valcyte for 5+ years, so have always been concerned a liver issue would pop up. Thoughts?
 
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For anyone interested:

Having insufficient levels of methyl donors such as S-adenosyl-methionine (SAM) can, over time, lead to a type of non-alcoholic fatty liver called "Methionine and Choline-deficient steatohepatitis":

Specific Contribution of Methionine and Choline in Nutritional Nonalcoholic Steatohepatitis
IMPACT ON MITOCHONDRIAL S-ADENOSYL-l-METHIONINE AND GLUTATHIONE
https://www.jbc.org/article/S0021-9258(19)57561-5/fulltext

Excerpt:
Caballero et al 2010 said:
The pathogenesis and treatment of nonalcoholic steatohepatitis (NASH) are not well established. Feeding a diet deficient in both methionine and choline (MCD) is one of the most common models of NASH, which is characterized by steatosis, mitochondrial dysfunction, hepatocellular injury, oxidative stress, inflammation, and fibrosis.

However, the individual contribution of the lack of methionine and choline in liver steatosis, advanced pathology and impact on mitochondrial S-adenosyl-l-methionine (SAM) and glutathione (GSH), known regulators of disease progression, has not been specifically addressed.

Here, we examined the regulation of mitochondrial SAM and GSH and signs of disease in mice fed a MCD, methionine-deficient (MD), or choline-deficient (CD) diet. The MD diet reproduced most of the deleterious effects of MCD feeding, including weight loss, hepatocellular injury, oxidative stress, inflammation, and fibrosis, whereas CD feeding was mainly responsible for steatosis, characterized by triglycerides and free fatty acids accumulation.

These findings were preceded by MCD- or MD-mediated SAM and GSH depletion in mitochondria due to decreased mitochondrial membrane fluidity associated with a lower phosphatidylcholine/phosphatidylethanolamine ratio. MCD and MD but not CD feeding resulted in increased ceramide levels by acid sphingomyelinase.

Moreover, GSH ethyl ester or SAM therapy restored mitochondrial GSH and ameliorated hepatocellular injury in mice fed a MCD or MD diet. Thus, the depletion of SAM and GSH in mitochondria is an early event in the MCD model of NASH, which is determined by the lack of methionine. Moreover, therapy using permeable GSH prodrugs may be of relevance in NASH.
(spacing and emphasis added for readability)
 

anncavan

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For anyone interested:

Having insufficient levels of methyl donors such as S-adenosyl-methionine (SAM) can, over time, lead to a type of non-alcoholic fatty liver called "Methionine and Choline-deficient steatohepatitis":

Specific Contribution of Methionine and Choline in Nutritional Nonalcoholic Steatohepatitis
IMPACT ON MITOCHONDRIAL S-ADENOSYL-l-METHIONINE AND GLUTATHIONE
https://www.jbc.org/article/S0021-9258(19)57561-5/fulltext

Excerpt:

(spacing and emphasis added for readability)
@Pyrrhus I can't thank you enough for sharing this and taking the time! Someone tipped me off to the idea of Choline, but I really didn't know where to start with it. It's so reassuring to see actual research on the topic. Do you see this as a process of supplementing Choline and Methionine? or more of following a methylation plan (I followed Rich Van K's many years go). Is there an updated protocol everyone is following these days? This world has always been a bit overwhelming and tougher for me to grasp than other areas of MECFS. I am not as up to date as I should be. Thanks again!
 
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Do you see this as a process of supplementing Choline and Methionine? or more of following a methylation plan (I followed Rich Van K's many years go)
The article I cited (and many others like it) show how a lack of methyl donors such as S-adenosyl-methionine (AKA SAM AKA SAMe AKA AdoMet) can lead to fatty liver, and how boosting the level of methyl donors can resolve the fatty liver.

Some people refer to a lack of methyl donors as "undermethylation", although that's not exactly a scientific term.

The basic way to boost methyl donors is to supplement with B12, methyl-folate, and B6. There are many "methylation protocols" that include many other things, but these three are the basic elements needed.

Sometimes people take choline or creatine as well. This is because most of the methyl donors in the body are used up in the synthesis of choline and creatine. By supplementing with choline or creatine, you free up many methyl donors that otherwise would have been used up in the synthesis of choline or creatine. This is the reason why choline and creatine are sometimes added to methylation protocols.

Most people who get enough protein in their diet will probably already have sufficient methionine.

I hope that answers your question. But you can't assume that your fatty liver is due to a lack of methyl donors. It may also be due to 5 years of Valcyte, or even something else entirely.

Hope this helps.
 

anncavan

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The article I cited (and many others like it) show how a lack of methyl donors such as S-adenosyl-methionine (AKA SAM AKA SAMe AKA AdoMet) can lead to fatty liver, and how boosting the level of methyl donors can resolve the fatty liver.

Some people refer to a lack of methyl donors as "undermethylation", although that's not exactly a scientific term.

The basic way to boost methyl donors is to supplement with B12, methyl-folate, and B6. There are many "methylation protocols" that include many other things, but these three are the basic elements needed.

Sometimes people take choline or creatine as well. This is because most of the methyl donors in the body are used up in the synthesis of choline and creatine. By supplementing with choline or creatine, you free up many methyl donors that otherwise would have been used up in the synthesis of choline or creatine. This is the reason why choline and creatine are sometimes added to methylation protocols.

Most people who get enough protein in their diet will probably already have sufficient methionine.

I hope that answers your question. But you can't assume that your fatty liver is due to a lack of methyl donors. It may also be due to 5 years of Valcyte, or even something else entirely.

Hope this helps.
@Pyrrhus Cant thank you enough!!! This is so helpful. I have gone down the methylation road a while back, but really didn’t see it through (gave up folic acid but never got in the habit of supplementing the Bs) and this is the perfect reason to get back on board.

I’ve talked to my CFS specialist (Bateman) and 2 GPs. All say diet or diet and exercise. Each one said a different diet and of course I can’t exercise. Could I lose 15 lbs, absolutely. But my BMI is in normal. Vast majority of information online credits alcohol, type 2 diabetes and obesity. None of which I fit.

The information you provided and that I’ve found since searching choline makes more sense. I am allergic to eggs, so haven’t eaten them in over a decade. And the last time I ate liver was while pregnant when I forced myself to eat liverwurst.

I will still actively work to lose 10% body weight simply bc that is the universal recommendation ans can’t hurt me. I’ve chosen intermittent fasting as I’ve had issues with most other approaches causing my blood sugar to crash.

I will set up an appointment with my LLMD that’s educated in Methylation. Ans send him this research. THANKS AGAIN!!
 

pamojja

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The basic way to boost methyl donors is to supplement with B12, methyl-folate, and B6. There are many "methylation protocols" that include many other things, but these three are the basic elements needed.

Sometimes people take choline or creatine as well. This is because most of the methyl donors in the body are used up in the synthesis of choline and creatine. By supplementing with choline or creatine, you free up many methyl donors that otherwise would have been used up in the synthesis of choline or creatine.
Had NAFLD probable most likely caused by malarias and their treatment. After years of lifestyle-changes and comprehensive supplementation it reversed, along with scar tissue in the liver. I do believe suffecient choline aided in its reversal: https://chrismasterjohnphd.com/blog/2016/04/24/start-here-for-fatty-liver-disease/

Though I also used plenty of all other B-vitamins, choline was an exception in that it was the only causing a slight side-effect of chaw-tensions above certain doses at times. Initialy above 500 mg/d, then 300mg, now that limit isn't there anymore, even taking up to 700 mg/d supplemental, additional to the throughout 400 mg from my diet daily. Had the impression this limit lifted by also increasing co-factor B-vitamins, like inositol.

See also https://lpi.oregonstate.edu/mic/other-nutrients/choline#deficiency
 
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I've been taking b12 for 15 days now and feeling much better overall, but my bones started hurting the last few days. The bones in my feet, ankle, hips, neck started hurting a few days ago. Any idea why? It feels like my bones are being leeched for minerals but I have no idea what to supplement. I don't want to stop the b12 because it makes me feel so much better overall.
 
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I've been taking b12 for 15 days now and feeling much better overall, but my bones started hurting the last few days. The bones in my feet, ankle, hips, neck started hurting a few days ago. Any idea why? It feels like my bones are being leeched for minerals but I have no idea what to supplement. I don't want to stop the b12 because it makes me feel so much better overall.
Have a look at https://b12oils.com/rnb.htm

This is Greg's site, you'll see him mentioned on this forum quite a bit.

The link I shared there explains some science behind B12. It explains some of the symptoms that one can have when repleting B12. There are links on the page you can follow for more information on how B12 affects neurotransmitters, adrenaline etc. You might see something that clicks.
 
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I had a blood test done and my folic acid levels were low, I started taking Folic Acid and my bones now feel stronger. I know Fredd says don't take folic acid but it seems to be working for me. I am willing to try methyl folate instead, but I just know I tend to over methylate so I figured folic acid would be good for me as it slows down the process and requires some conversion first.
 

anncavan

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Had NAFLD probable most likely caused by malarias and their treatment. After years of lifestyle-changes and comprehensive supplementation it reversed, along with scar tissue in the liver. I do believe suffecient choline aided in its reversal: https://chrismasterjohnphd.com/blog/2016/04/24/start-here-for-fatty-liver-disease/

Though I also used plenty of all other B-vitamins, choline was an exception in that it was the only causing a slight side-effect of chaw-tensions above certain doses at times. Initialy above 500 mg/d, then 300mg, now that limit isn't there anymore, even taking up to 700 mg/d supplemental, additional to the throughout 400 mg from my diet daily. Had the impression this limit lifted by also increasing co-factor B-vitamins, like inositol.

See also https://lpi.oregonstate.edu/mic/other-nutrients/choline#deficiency
Thank you so much @pamojja !!!

For now I am taking milk thistle and intermittent fasting(with the goal of losing 10% body weight). Besides that, I am so unclear how to manage this. 2 GPs and an MECFS specialist have all told me this is a weight thing. But my BMI is in "normal." I'm going ahead and actively losing with the goal of 10%. Im a third of the way there. But when I dig deeper I see this methylation connection, a hashimotos connection and iron deficiency relationship. All are relevant for me, and none mentioned. I don't really trust any of them to manage this.

I'm curious if you used a practitioner to figure out your fatty liver as well as your treatment with B's and choline? What process have you followed to monitor? I'm also interested if you or folks you know have paid Chris Masterjohn to consult. It's pricey, but I'm sure so helpful.

Luckily I have a LLMD that I can see remotely. He is educated in Methylation. So I'll run this by him at my next appointment in 3 weeks. But I can't imagine he wants to be responsible for my liver remotely. Do I get a local Hepatologist?

Thanks for anything you're comfortable sharing! Really appreciate what you shared already.
 

pamojja

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I've a BMI of ~20 too. Could not find a dedicated practitioner where I life, but also gave up soon (either didn't take any patients soon, or weren't that knowledgable). Nor did any of the MDs later finding an enlarged and scarred liver by sonography consider it worthwile to officially diagnose NAFLD. Probably because its so common these days and no protocol to treat by starndard of care anyway. With the exception when it originally was found after malarias by an Indian GP 20 years ago there, who speculated it caused by a amoebic hepatitis. Scar-tissue was found in 2006.

Worse with my main condition of PAD giving me a walking-disability (from a 80% stenosis at my abdominal aorta). Just paliatives or very risky surgery. With nothing to loose, did an life-style and all-out orthomolecular medicine attack - and just let my many out of order lab-markers be monitored by my GP. Whole story retold here: https://www.longecity.org/forum/stacks/stack/111-pad-and-additional-remissions/

Worked very well against my walking-disabilty, until in the 3th year a long chronic bronchitis melted away almost all progress made. Therefore went to a South-Indian beach to let it heal by sea-air and sun, while tabbing into Ayurvedic herbal remedies. Since overcoming that bronchitis (later diagnosed as COPD1, but asymptomatic since) improvements were again gradually made, untill my walking-disability went into complete remission in the 7th year.

Since I used so many natural medicine modalities against my main condition and all the underlying dysfunctional bodily systems (cardiovascular, lung, liver, kidney, spleen, thyroid, mineral-, vitamin and androgen deficiencies, insulin resistance..) in retrospect I of course can't pinpoint which of so much taken finally also let the liver in particular regenerate. But do think if I didn't tackle the many co-morbitieies for my main condition, the liver couldn't have improved as much as a synergistic side-effect.

However, choline-deficiency probably was a main driver in my case, since I've been low-fat vegetarian (for ethical reasons) for 30 years before my health-odysee, without eggs or any other choline sources.
 
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