Thursday, December 9, 2010

Why Is My Cholesterol So High On This Diet? You May Be Curing Yourself of Fatty Liver

by Chris Masterjohn

New blog over at WestonAPrice.Org about how a nourishing diet may sometimes increase blood lipids by curing somone of fatty liver disease:

Why Is My Cholesterol So High On This Diet?

Read more about Chris Masterjohn, PhD, here.


  1. hey chris, i'm a bit confused by something here...

    after the first graph you say "we see that choline deficiency increases serum cholesterol", but that graph looks to me like the deficient mice have *lower* serum cholesterol, as does the table you got it from on pubmed.

    so am i looking at this wrong or did you mean to say choline *sufficiency* increases, or choline deficiency *decreases*?

    this has me confused further on when you say "Why do humans with fatty liver have increased blood lipids when these mice have decreased blood lipids?", since it looks like the mice have increased blood lipids as well.

    you also labeled the green bars MSC instead of MCS.

    anyways, love this series on choline and everything else you write, thanks so much!

  2. Hey Justin,

    Aye! Should have proofread this in the morning before publishing it, thanks. I will fix it soon.

    I meant that choline increases serum cholesterol, not that its deficiency increases cholesterol.

    The mice with fatty liver (MCD, mostly MCD-sugar) have decrease blood lipids, in contrast to humans with fatty liver, who have increased blood lipids.

    The green bars should be MCS, thanks for pointing that out!


  3. Hi Chris,

    Very interesting. But I absolutely love this 'way of thinking'... specifically when compared to the 'mainstream' way of thinking, which would be something more along the lines of "It is clear that choline and betaine increase triglycerides and total cholesterol, contributing to heart disease."

    This is exactly why you predict paranoia will likely ensue, because most people love jumping to assumptions without checking all angles first to arrive instead at well rounded and fully informed conclusions.

    As for me, I've been taking Betaine with pepsin supplements for a few weeks now, mostly because I am having a tough time fighting off an annoying onslaught of heartburn as soon as I switched over to a more whole foods, lower carb diet. It seems that my gut flora did not correctly 'adjust' to the new foods I began eating and therefore 'threw off the grove' of my resident H.pylori. I am still quite confused by it all, but that is my understanding (at this point), hence the supplementation of Betaine HCI to increase stomach acid for better digestion.

    Anyway, as for your research here, it will be interesting to see how this complex puzzle is put together as more information becomes available. I'm glad you're on the trail. Bravo, once again.

    Jack K.

  4. Interesting post! It's been two years now since I gave up gluten grains, sugar and high-PUFA vegetable oils, and my total cholesterol keeps going up and up! From 229 to 270 to 280, to 295 in October. It causes huge fights with my doctor as she wants to put me on statins which I feel is the worst thing I could possibly do! But no worries about my triglycerides, they keep going down and down - from 80 to 70 to 65 to 50 in October, and my HDL keeps going up, from 50-something to 74 in October. Of course LDL keeps going up and up too (though an NMR test showed it to be 90% pattern A as I suspected). But there still has to be some underlying cause for the big zoom. So darn many things to think about and consider.

  5. Japanese perenial vine "Jiao-gu-lan" (Gynostemma pentaphyllum) is easy to grow hydroponicly and trellis across your ceiling.((Viable roots can be shipped from internet suppliers; we can detail technique here with blog's permission.))

    The tri-terpene saponin in it is indicated for fatty liver disease and it's fibrosis. The saponin is alcohol soluble so suitable
    for an old style low tech extraction.

    In fatty liver it's use over 4 months lowered body mass index, aspartate aminotransferase, insulin and insulin resistance more than calorie controlled diet.

    In fibrosis of the liver it decreases
    pro-inflammatory cytokines by inhibiting
    hepatic stellate cells; indicators drops
    for SGOT, SGPT and get 1/3 less collage laid down. The effect from the plant's saponin is due to molecular action that
    upregulates the enzyme protein serine/threonine phosphatase. This enzyme also down regulates transforming growth factor Beta.

  6. Thanks ...AL for the info. Green tea also looks promising for fatty liver.

    I responded to Jack's comment over on the article itself.


  7. Can you address this part in more detail?

    "I believe this likely reflects the fact that humans with fatty liver tend to be insulin resistant and leptin resistant. Insulin is a major hormone that clears triglycerides from plasma. *Leptin causes us to make and activate thyroid hormone, which activates the LDL receptor.* When people are choline deficient, much of the fat and cholesterol their livers make will stay in the liver. When they are insulin resistant and leptin resistant, whatever fat and cholesterol makes it out into the blood will stay there until it eventually oxidizes and gets mopped up by the immune system into an atherosclerotic plaque."

    This is the first time I have ever heard that Leptin causes Thyroid hormone production. I am confused now about the thyroid hormone's role in all this...leptin resistance, insulin resistance, blood fats, specifically LDL oxidation, and fatty liver disease. I have been following these articles, but now there is this new element...thyroid hormone. Considering how many people in this country are on supplemental thyroid hormone, I think this may be a HUGE key to understanding the "diseases of civilization".

    And on a personal note, I have been on thyroid since I was 25 after the birth of my first child. Now I am wondering what role this has played in other struggles I have with health issues.

  8. Hi Shelley,

    Leptin increases production and activation of thyroid hormone, and prevents its deactivation to reverse T3. Most overweight and obese people are probably leptin resistant, which means they effectively have a form of hypothyroidism.

    Thyroid hormone governs the expression of the LDL receptor. More thyroid means more LDL receptor, which means that LDL particles will be efficiently cleared from plasma, thus preventing their oxidation and protecting against heart disease.

    Most people who have thyroid problems probably have no idea, so most of them are not on thyroid medication. Those that are generally are put on T4, which in many people probably does nothing whatsoever to resolve their thyroid problems.


  9. NAFL associates with obesity. For thin folks elevated serum cholinesterase test warns of NASH.

    NAFL involves portal vein and parenchymal lobe inflammation. Obese put more insulin through that vein, yet liver uptake of insulin is reduced. Normally the liver clears up to 70% of insulin with a 1/2 life as short as 5 minutes. (Insulin does not split tri-glycerides into it's components of fatty acids plus glycerol.)

    ((T4 conversion to T3 also occurs in the liver and thyroid. One key enzyme responds to levels of glucose in the liver. Our bodies make "x" mcg of T3 per hour; the liver takes some of it out of circulation.))

    Bile in the gall bladder is a cholesterol "sink" missing from the discussion. It will bulk up with more cholesterol, relative to normal % of bile acid content. NFAL pro-inflammatory prostaglandins often cause the gall bladder to generate glycoproteins for lipogranulomas.

    Choline raises (?) triglycerides and (you may know otherwise) might push up bile cholesterol. Choline data shows the triglycerides are still around. The 1/2 life for circulating triglycerides in normally 1 - 2 hours.

    The liver makes VLDL when there's lots of triglycerides; it moves it to body tissues for storage. The obese have an extra problem because any and all excess carbon will be made into triglycerides.

    As for cholesterol molecules 80% are made in the liver and only 20% cholesterol in the blood is from dietary ingestion (under a balanced diet). Glucagon slows that cholesterol manufacturing and causes receptors to scavenge LDL from the blood. It would be interesting to hear if choline switches on glucagon in the NAFL.

    Betaine data shows it is getting everything out of a NAFL liver that just can't handle the constant loads. Seems OK if obesity not under control.

    The 1/2 life for LDL is 1.5 - 2 days (LDL degrades from glucose and free hydroxyl radicals; also healthy individual's macrophages scavenge it, and having no cholesterol sensors can load up; unfortunately it can also plaque out in arteries). Choline's lower LDL reading in NAFL may come from better 1/2 life efficiency.

  10. Chris,
    Ive read L-Carnitine can help with NAFLD

    How does this fit in with Choline etc

    (Apologies I put this in the Egg Blog by mistake)


  11. Extra % phosphatidyl-choline incorporated into the lipid bi-layer membrane of liver cells makes for more adenylate cyclase enzyme potential. That enzyme lets glucagon (not glycogen) bind to it's receptors and get inside target liver cells.

    Obese have the same total number of glucagon receptors as person normally would. The phosphatidyl-choline incorporated into hepatocyte membranes re-boots the dynamics and then get improved glucogon coupling to it's receptors.

    Since the insulin in NAFL is just breezing on through the liver the patient's hyper-insulinism doesn't function the same in relation to glucagon. It doesn't block the catabolic action of glucagon in the liver. Glucagon slows the manufacture of cholesterol causing LDL to be scavenged from the blood.

    Elevated blood lipid fractions are not neccessarily the molecules recently purged out from fatty liver tissues. Dietary choline in (say) eggs comes in with it's own lipid components; ingest more & that load shows up in the cholesterol blood tests.

  12. Firmicutes prausnitzii "aberrant" species of bacteria in the human gut predispose many for aberrant choline metabolism. The micro-biome % of them can be different in men and women.

    With this strain the ingested choline gets catabolized by tri-methyl-amines into di-methyl-amines. Di-methyl-amine is a compound implicated in fatty liver and, of course, insulin resistance.

    The are two keys to that predisposition. First the di-methyl-amine link is for high fat intake diets. The second is what the individuals consumes sets the gut environment where Firmicutes prausnitzii can proliferate.

    Firmicutes prausnitzii impeeds the taurine rich bile acids being excreted, or at least them being temporarily held-up at the ilium. The extra % of re-cycled taurine compounds in the liver disrupts the way ingested fats are handled.

    The results are seen in elevated lipid fractions in the blood. As part of the dynamic the % of glutathione used up is greater and thus more triglycerides go out into the blood.

    Firmicutes prausnitzii has a systemic influence on human host's energy availability (the obese can't just "burn"
    away the weight). It produces n-butyrate as a byproduct of it's own metabolism in the gut to "contaminate" us. Their metabolites get excessive access to our insides due to havoc these strains wreck on mucosa of our gut.

    The test indicators to hunt down an "aberrant" strain would be urinary taurine, glycine, di-methyl-amine, amino-iso-butyrate, hydroxy-iso-butyrate, glycolate and hydroxl-benzoate.

  13. Hi Chris, quick question for ya on an unrelated topic. I loved your choline series, but wonder if MCTs like those present in coconuts need choline for utilization like the longer chain fats. If they do not, it may explain some of their extra benefits.

  14. Hi Chris,

    Is there a way to increase T3 without taking Cytomel?
    It seems I am one of those with 'bad' LDL increase, after an extended low-carb diet. What should I do? If I increase carbs I put weight on.

  15. Very interesting reading!
    When you have low readings of HDL and high readings of both LDL and triglycerides, could that be an indicator of low thyroid?

  16. Interesting reading Chris. This could explain why gallstones prevalence increases in rapid weight loss as well as obesity.
    If bile stasis (most likely caused by allergenic reactions to food) is present, the bile would be far more lithogenic while 'curing' itself than in normal functioning.
    It's an important distinction, as I've seen people mistakenly blaming saturated fats newly introduced into diets as the cause of gallstones.

  17. Switched from vegan diet to full bore, strict Robb Wolf-approved eating 5 months ago.

    Then: Total Cholesterol was 178, with ldl of 113, hdl of 38 and triglycerides of 135.

    Now: TC is 299, hdl is 73 and triglycerides is 57. Not so sure of ldl, as it's calculated.

    I guess I'm happy. I guess. Sure is tough to be blown away, stuck in my old mindset that I am.

  18. Reviving an old thread...I have had TC of around 250 for about 5 years. I have been low carb/ primal for 18 months and the TC number has not budged, but I have seen improvement in triglycerides (67) and HDL(63). I tried a kinds of intervention - fish oil, krill oil, vitamin D, exercise, copper, grapefruit pectin, etc, etc. Nothing brought the TC down.

    I just got diagnosed with severe candida overgrowth and I am finding out that high LDL is a typical side effect.

  19. I tried to read the blog post and it appears it has been deleted since you initially posted, can it be reposted and/or the link fixed?

  20. Hi Adriana,

    It is worth noting that Kitavan women experience total cholesterol levels this high during their 40s and 50s, so depending on your age this might not be very far from "normal," although the Kitavans do not eat anything resembling low-carb diets.

    Dealing with infections is important and may have effects on blood lipids levels. Of course, candida is real and very prevalent but sometimes poorly diagnosed.


  21. all of this great research that you have analyzed. I have a thought that I wanted to throw out for debate. When we choose to eat the liver and egg yolks, would it be a good idea to also supplement with Lugol's Iodine? There are some great studies from the 50s that show it can lower cholesterol.

  22. FACTS:
    Male, white, 52
    approx. 130lbs fat-free mass
    Bodyfat: approx. 19%

    GOAL: <10% bf using a LC PaIeo diet combined with Intermittent Fasting which means I must lose at least 17lbs of bf, both subcutaneous and visceral.

    Resistance train 4xs/week
    Cardio interval train 2-3xs/week

    I was dx'd via ultrasound with non-alcoholic fatty liver disease (NAFLD) two years ago. It is indeterminate how long I've had it. Liver enzymes continue to remain within normal range and I notice no symptoms

    I am hypothyroid and have been taking 75mcg of sustained-release T3. My latest thyroid numbers are posted in the link below [p2, 3, 10].

    TSH has improvement over last labs. Both T4 and T3 show depressed, however, I was fasting for nearly 20 hours on the first day. rT3 is less this time, which is a good thing.

    Have been on LC Paleo diet for last three months and doing between a Lean Gains [ ] 16/8 IF protocol to as much as 20/4 IF protocol. I do mini-carb refeeds (about 50-60g) on my workout days only. If I increase carbs more than this, my post-prandial BG will exceed 125.

    What's freaking me out are my latest lipid tests. I had the top three done in a matter of two consecutive days [p2, 5, 11-14].


    If we’re clearing lipids from the liver, then this is a good thing, but HOW CAN I DETERMINE THAT IT'S THIS AND NOT FROM THE DIET ITSELF?

    In other words, is the increase due to CREATION or CLEARANCE (resolution of NAFLD)?

    I have not changed any macros in my diet, maybe slightly more lean grass-fed animal protein, but saturated fat intake has remained constant throughout. And most of the saturated fat is drained because I steam all my meats, so how can it be CREATION?

    The only other fats I eat with frequency are O3s (2-4g), coconut, flax, macadamia and olive oil.

    What evidence supports this unconventional theory?

    I understand that one of the key problems with fatty liver disease is that the lipids get stuck in the liver and they’re not being released into the bloodstream.

    How could this be the case when taking liver support supplements like milk thistle, dessicated liver, choline, lecithin, etc.? Why wouldn't such intervention spur on the purge also?

    Why wouldn't free fatty acids (FFAs) from stored subcutaneous fat be released into the bloodstream as well?

    Could this explanation be the mechanism behind the clearance of FFAs: During fasting or starvation, free-fatty-acids are released during lipolysis into the liver and muscles to be burned as energy, this is called fat-oxidation. During the fed-state and especially while eating a starch-based-diet, fat-oxidation is inhibited and replaced with carbohydrate-oxidation, insulin is what mediates this shift. When carbohydrate-oxidation is taking place, fatty-acids are shuttled back and "locked away" in adipose-tissue... where they belong.

    In addition to LC Paleo/IF, I also began taking 1g of choline nearly a month before the labs + 3mg methylfolate/day to help with a genetic methylation defect.

    Could the above combination have created a mega-purge?

    Could the answer be that the best predictor of fatty liver is obesity and insulin resistance?

    Anomalies to purge theory:

    Why the decreased HDL when I was making nice progress before?

    Lastly, I had been fasting for 18-20 hrs prior to my blood being drawn. My fasting insulin was only 5.2. Then why an elevation in HbA1c (5.8) and FBG (95)? Should've been in the low 80s, especially when fasting for LONGER periods AND on LC Paleo.

    So, why is my insulin sensitivity is taking a nosedive during this so-called healing crisis as well [see Insulin Resistance Score - p12, 14]?

    Can someone please interpret my lipid profiles, especially the NMR LipoProfile and tell me what is going on?

  23. Chris -

    Since choline promotes purging of lipids from the liver, the question then would be why other tissues, like adipose tissue, don’t take them up.

    Please advise.

  24. the link to this article says it's been deleted. Can you put it up again? I'm very interested in reading it.

  25. Link to the article,
    Apparently they changed their folder structure a bit.


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