Why Is My Cholesterol So High On This Diet?

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Lots of people find that eating a WAP-friendly traditional diet has no effect on their blood lipids or improves them, by a conventional standard.  But I’ve had a number of people ask me, “why is my cholesterol so high on this diet?”

Or, “why are my triglycerides so high on this diet?”

There are a number of factors that affect blood lipids, and in the future I’ll present a more comprehensive view of this issue.  For now, I’d like to explore the possibility that many people might experience a temporary increase in triglycerides or cholesterol when they switch to a traditional diet because they are actually curing themselves of fatty liver disease.

Recently over at The Daily Lipid, I’ve posted a series of blogs on fatty liver disease.  Fatty liver is a silent epidemic that probably affects 70-100 million Americans, and is most likely caused by the loss of choline-rich foods like organ meats and egg yolks from the American cuisine.  If you haven’t seen them already, you can find these posts here:

I’ll provide references for the new material in this blog post, but the references for any background information can be found in these recent posts from The Daily Lipid.

The reason that choline is so important to fatty liver is because it is required for the synthesis of phosphatidylcholine, a critical component of very low density lipoprotein (VLDL), which exports fat and cholesterol from the liver.  If choline is deficient, fat and cholesterol stay in the liver instead of going into the blood.

As we can see from the following diagram, providing enough choline to allow efficent export of lipids from the liver should increase the concentration of lipids in the blood:

Many different factors can contribute to plasma triglyceride and cholesterol.  Curing fatty liver disease may temporarily increase blood lipids.

We can see from this diagram how ridiculous it is to use blood levels of triglycerides or cholesterol in and of themselves to diagnose a problem.

Increasing the amount of energy available to the cell, which could be achieved by consuming coconut oil, can increase blood cholesterol, but it also provides lots of energy for good things like detoxification and defending against oxidative stress.

While coconut oil might be especially effective at increasing cholesterol synthesis, fructose is especially effective at increasing the synthesis of fat, which can actually contribute to fatty liver if there isn’t enough choline to export that fat.

Ideally, lipids are efficiently cleared from the blood so that cells can use them for energy and can use the fat-soluble vitamins that are transported with them for all kinds of critical processes.  Lipid clearance is especially dependent on insulin and thyroid hormone.  When lipids are not cleared efficiently, the delicate polyunsaturated fatty acids (PUFAs) among them will begin to oxidize, which makes them toxic to blood vessels.  The immune system then mops up this toxic mess by forming an atherosclerotic plaque, which is protective at first but eventually can contribute to a heart attack or stroke.

Poor lipid clearance will usually increase LDL levels, and the LDL particles will then begin to oxidize.  On the other hand, the portion of LDL that oxidizes is cleared from the blood extremely rapidly, so a very high rate of oxidation could actually decrease LDL levels!  On top of this, there are genetic variations among the various receptors that clear oxidized LDL from plasma, leading to further contradicting effects on blood lipids.

Confused yet?  The main point is this: many different factors affect cholesterol and triglyceride levels, and it is simplistic to immediately assume that an increase indicates something bad is going on.  It is also foolish to ignore high cholesterol or triglyceride levels rather than using them as clues and stepping stones to understanding what’s going on in the body.

Now, let me make the case that resolving fatty liver can increase blood lipids.

First of all, a diet deficient in choline and its precursor, methionine, causes fatty liver disease in lab mice and rats while decreasing blood levels of cholesterol and triglycerides.  The effect of a methionine- and choline- deficient (MCD) diet is dependent on dietary sucrose, because the fructose component of sucrose is used by the liver to make lots of fat.  The graphs below (from ref 1) show the effects of choline-deficient (MCD) and choline-sufficient (MCS) diets using either starch or sucrose in mice.

This one shows that choline increases serum cholesterol, and that sugar exacerbates the effect:

Sugar and choline increase serum cholesterol by curing fatty liver.

By comparing the blue bar to the pink bar, we see that choline increases serum cholesterol even when animals are fed starch.  By comparing the green bar to the red bar, we see that this effect is even more dramatic when the animals are fed sugar.  These effects are all statistically significant.

The next graph shows the same thing for serum triglycerides:

Choline may increase serum triglyercides by curing fatty liver.
In this case the comparison between sugar and starch is not statistically significant, meaning that it is too small to distinguish from the effect of chance.  By comparing the green bar to the red bar, however, or by comparing the blue bar to the pink bar, we can see quite clearly that choline increases serum triglycerides.

The next graph shows the amount of fat in the liver, and makes it quite clear that choline increases blood lipids precisely because it is preventing fatty liver disease:

Choline increases serum cholesterol and triglyceride by preventing their accumulation in the liver.
Here we see a very small effect when the mice are fed starch (blue bar versus pink bar).  By comparing the green bar to the red bar, however, we see a huge effect.  This reflects the fact that the liver makes lots of fat from the fructose component of sucrose while choline deficiency prevents the liver from sending that fat out into the blood.

Those of you familiar with the research on fatty liver disease may be skeptical.  Whoa, you say.  Hold your horses, Mr. Masterjohn!  Why do humans with fatty liver have increased blood lipids when these mice have decreased blood lipids?

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.

Several studies suggest that resolving fatty liver with choline or its close cousin betaine may increase blood lipids.  Betaine is found abundantly in wheat, spinach, and beets.  Choline is a precursor to betaine, which is used in the liver and kidney for an important process called methylation.  It substitutes for vitamin B12 and folate in this process, as shown in the following diagram:

Betaine can spare choline through its participation in the methylation pathway.

Dietary betaine can thus spare choline and allow more of it to be used for the export of lipids from the liver.

The effects of betaine, folic acid (a synthetic form of folate), and choline as demonstrated by several randomized, placebo-controlled trials have been neatly compiled into one paper (2).

These studies found that two to six weeks of betaine supplementation increased total cholesterol, LDL-cholesterol, the total-to-HDL cholesterol ratio, and triglycerides.  Two weeks of choline only increased triglycerides, and folic acid had no effect on blood lipids.

These studies were small and used amounts of these nutrients at the upper end of what is possible to consume from food, but they provide proof of principle that choline and betaine increase blood lipids.

Why did choline only increase triglycerides while betaine increased both triglycerides and cholesterol?  I believe this is most likely because the choline was provided as phosphatidylcholine, which is the main form found in food, and which can be used to help clear cholesterol from the blood.

A portion of phosphatidylcholine is cleaved by our pancreatic enzymes during digestion to yield free choline, which will go straight to the liver where it will help our liver export fat and cholesterol.  However, the uncleaved portion will be absorbed with fat, bypass the liver, travel through the lymphatic system, and circulate throughout the body where it will help our tissues clear cholesterol from blood.  Thus, choline is likely to increase triglycerides in most people but its effect on cholesterol levels will depend on a person’s digestive system as well as the activity of the enzymes involved in clearing the cholesterol from blood.

A nourishing, traditional diet may thus increase blood lipids in many people while healing them from fatty liver disease.

Presumably, this effect should be temporary, and over time this fat should be stored properly or burnt off for energy.

However, I believe that patients and health care practitioners who are “in the know” should start monitoring levels of liver fat as people transition to a healthy diet, especially if their blood lipids increase.  This can provide critical anecdotal information while we wait, wait, and wait some more for the randomized, controlled trials to come in.

These will eventually come in, because as the choline proponents rally for a higher choline RDA or for individualizing the choline recommendations according to genetics, paranoia about its effects on blood lipids will ensue.  It could be another decade or two, however, before we fully understand these interactions in humans, so I hope that people will begin compiling anecdotal information now.

Liver fat can be measured by MRI or ultrasound.

In any case, the information in this post demonstrates why it is necessary but very insufficient to pay attention to blood lipids.  Blood lipids can reflect many contradicting processes, and an increase could be good or bad, depending on what we need to heal from, and whether our diet is truly healing.  Let’s stop the war on cholesterol and start the search for truth.

Read more about the author, Chris Masterjohn, PhD, here.

22 Responses to Why Is My Cholesterol So High On This Diet?

  1. Rabbi Hirsch Meisels says:

    How long do you predict it can take to clear all the extra lipids?

  2. Dear Rabbi,

    That’s an excellent question. Unfortunately, I do not know of any data that can shed light on it. That is why I’m hoping some people may be able to share some anecdotal information on this in the near future.


  3. chuck says:

    i wonder if some people may go overboard with the properly prepared grains? have you seen people who have reduced overall carb intake also have their triglycerides plummet?

  4. Chuck,

    Yes I have seen that, and yes it’s entirely possible some people see their blood lipids go up and it’s a bad thing. I will try to address the different possibilities in the future, but I wanted to offer this one as a follow-up to all my recent posts on choline.


  5. Michi Nas says:

    Many of our clients “test” strongly for phosphatidylcholine when we assess them with that supplement…

    They also test very strongly when we asses them with our home-made liver patte or just plain raw chicken or beef liver or raw yolks.. they raise eyebrow too. lol

    They say, liver must be toxic, yolk must be full of cholesterol… lol. in this case they must be right. Cholesterol phobia never seems to cease from people’s mind..

  6. Hi Michi,

    Thanks for writing. I’m not sure I follow. You are muscle testing and finding that many people do not tolerate liver and egg yolks?


  7. Paul Jaminet says:

    Hi Chris,

    Interesting post. In a few places there’s a missing “Deficiency” after “Choline,” e.g. in the “Choline and Sugar Increase Fatty Liver” figure. Choline of course exports fat from the liver.

    Re the time to clear extra lipids, it shouldn’t take long – four weeks at most. Cholesterol is probably much slower to clear than fats, and according to this paper (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC297165/pdf/jcinvest00237-0003.pdf) radioactive-labeled cholesterol introduced into serum reaches equilibrium with all tissues in four weeks.

    Best, Paul

  8. Jack Kronk says:

    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 and making an 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.

    • Dustin Johnson says:

      I know this is old, but just in case someone else is reading this, I believe that the Betaine they are talking about is very different from Betaine HCl. Perhaps someone else can clarify.

  9. Peter Silverman says:

    It seems like if I eat low carb, my LDL shoots up but my HDL, triglycerides, fasting glucose, and HA1c all improve. Is this a good trade or a bad trade? Or how can I tell?

  10. Tim H says:

    Thanks Chris…This is really starting to tie some things together for me. I have been doing some post-meal BG testing and believe that I am somewhat insulin resistant. I also had a blood lipid panel done that showed my LDL was 161 (at least they were big and puffy). And I believe I was getting almost no choline. I have recently replaced my morning oatmeal with 2-3 eggs and bacon, and have been eating pate several times a week. Hopefully this will improve my liver function.

  11. Paul,

    Thanks! I fixed the graphs. They also said MSC instead of MCS. I should have waited to publish till I proofread it this morning! I do not think a study showing tissue equilibration of injected lipids sheds any light on this question. The question is how long it takes to clean the lipids out of the liver by increasing choline/betaine intake.

    Jack, thanks! I wish you well with your health and if you experience anything that sheds light on these questions please share.

    Peter, sounds like a good change. I would get LDL particle size and ApoB tested, for further information. One thing to look out for is that extended low-carbing can decrease thyroid function, which will cause a *bad* increase in LDL-C, and be bad in itself. So be careful not to go to extremes, or if you do, to monitor thyroid function carefully.

    Tim, I’m glad it’s helping and wish you well with your health. I hope choline-rich foods do help your liver.


  12. B.B says:

    Are there any pages /links that give an example of what foods to eat then, without worrying about cholesterol levles? I hope that makes sense.. but basically I’m trying to gain weight (muscle). I’m 128lbs now, 5″6 female. But would like to get to atleast 135lbs. My cholesterol’s already borderline high from carbs and daily snacks -chocolate /cake, so I don’t know what to do. I’m definitely trying to switch over my diet, but chicken and salad just doesn’t keep me full for more than 2 hours, and I end up a bit lightheaded or sick

  13. Gigi Berardi says:

    Good work — thank you for these postings! I am getting questions all the time about dietary fats and available clinical evidence. Please stay posted on current status of S 510 and local food security. See my newest post on a blog I started right after (and inspired by) the WAPF meetings at: http://resilientfarmsnourishingfoods.blogspot.com/2010/12/cultivating-regional-food-security-and.html

  14. Andrew Brown says:

    Before I started a low-carb diet my cholesterol wasn’t too bad but typical of a diabetics – low HDL and high TAGs with high-ish LDL
    After low-carbing for 6 months my TAGs lowered, although not to the reference range, my HDL went down even more (which was the most surprising) and my LDL leaped up very high.
    I study pharmacy, and have been “taught” about cholesterol and am worried about my results. It’s suggested I go on statins, it’s clear I’m in the group that does seem to benefit (young, male) but I don’t want to, but I don’t know how much to worry about these readings?
    As a side question, as cholesterol is used in membrane synthesis, is it likely that an issue for example haemorrhoids could induce increased blood lipids?

  15. bb says:

    So we should avoid fruits, or eat them with cocoa butter?

  16. Kris Johnson says:

    The WAPF Dietary Guidelines should be a guide for you
    You’ve got to eat more than chicken and salad at a meal. Include something starchy – properly prepared grains or potatoes with plenty of butter, use plenty of olive oil on the salad, make some good gravy with the chicken. It’s hard to gain weight on a low carb diet. If you avoid processed foods, sugar, and polyunsaturated vegetable oils your cholesterol shouldn’t be a problem.

  17. Bella Wilson says:

    EDIT: How does this relate to MTHFR mutation (specifically homozygous C677T, which is apparently very common)? Does liver contain copious methylated B12 and folate, or is supplementation the only way to ensure adequate methylcobalamin and L-5-methyltetrahydrofolate availability in affected individuals, as suggested by Ben Lynch, ND on his site?

  18. MTHFREase says:

    The liver contains the storage form of folate — adensylcobalamin, rather than the methylated form.

    The MTHFR enzyme is one way to help homocysteine convert to methionine in the picture above. The other two are through the CBS mutation and Betaine (TMG). TMG is considered the short, but not preferred path because of its effect on neurotransmitters.

    • Thanks for your comments, but I think you have a few mistakes. Adenosylcobalamin is a form of B12, not folate, and it isn’t a storage form; it’s an active form. By “mutation” do you mean enzyme? CBS diverts homocysteine to cysteine, not methionine. I don’t understand your last statement on neurotransmitters.


      • MTHFREase says:

        Yes you are right, I “misspoke” quite a bit didn’t I?

        I meant B12. Adenosylcobalamin is stored in the liver even though it is active.

        And it’s MTR/MTRR path fed from CBS enzyme step that affects homocsysteine.

        I really should not post so quickly!

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