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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:
- Does Your Liver Look Like an Eskimo’s Dinner? Fatty Liver Is a Silent Epidemic
- The Sweet Truth About Liver and Egg Yolks — Choline Matters More to Fatty Liver Than Sugar, Alcohol, Or Fat
- Does Choline Deficiency Contribute to Fatty Liver in Humans?
- Meeting the Choline Requirement — Eggs, Organs, and the Wheat Paradox
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:
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:
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:
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:
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:
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.