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I recently received the question from a reader that I have paraphrased below. My answer follows.
Q. In John Barron’s Heart Health Program Newsletter from February 24, 2004 and December 21, 2009, he writes that excess fats in the diet can clog the liver and cause cholesterol to clog up the membranes of liver cells, completely stopping the function of the LDL receptor and preventing the liver from taking up LDL from the blood. From what I have read, this should caused LDL oxidation, which is a bad thing. Is it true that too much fat and cholesterol in the diet clogs liver cells, and if so, how much fat and cholesterol should we eat so that we get the nutrients we need without clogging our livers?
A. There are two issues here. First, the issue of fatty liver (build up of fatty deposits). Second, the role of the LDL receptor in health and of cholesterol in regulating that receptor.
There are a few animal models used to induce fatty liver. One is alcohol, but it has been shown that if animals consume 40% of their diet as cocoa butter instead of corn oil, as much as 30% of calories from alcohol does not cause fatty liver. In the same model, medium-chain triglycerides, derived from coconut oil, and beef fat, have dose-dependent protective effects against the alcoholic damage. Another model is methionine- and choline-deficient diets, which cause fatty liver disease. Methionine is an amino acid especially abundant in meat, and choline is found most abundantly in liver and egg yolks. Saturated fat protects against this model of fatty liver disease, although not completely. The third model usually used is a very high fat diet (about 60% of calories), but highly saturated fats have shown very little ability to cause fatty liver disease in this model and polyunsaturated fats have shown a very high ability to do so.
You can find a more detailed review of these studies with references in my other blog over at The Daily Lipid by using this link:
The second issue is the role of the LDL-receptor and the role of cholesterol in the liver. It is true that liver clearance of LDL-cholesterol plays a huge role in heart disease risk. This is clear from the fact that people with a defective gene for the LDL-receptor get heart disease very early — in infancy in the most extreme case — and people with a defective gene for an enzyme that degrades the LDL-receptor have virtual immunity to heart disease.
However, LDL-receptor is not suppressed by “clogging” per se. When the cholesterol level in the liver goes up, it expresses less LDL-receptor for the simple reason that it does not need any more cholesterol. The principal issue with high LDL-receptor function is thyroid hormone status. This is the main determinant among people who do not have genetic defects. Also, oxidative stress, which is promoted by intake of polyunsaturated fatty acids and is protected against by intake of saturated fatty acids and to some extent by monounsaturated fatty acids (and wihch is also influenced by many other factors, such as toxins and heavy metals), decreases LDL-receptor function.
I have reviewed this subject in greater detail here:
High Cholesterol And Heart Disease — Myth or Truth?
Intake of cholesterol has no effect on cholesterol levels in 70% of people, and in the other third, it raises LDL and HDL similarly and does not affect the ratio. This is more consistent with the concept that the ingested cholesterol is being sent into the blood, rather than that the LDL-cholesterol is not being cleared. When this is the case, the LDL-to-HDL cholesterol ratio will tend to increase because the longer the time LDL spends in the blood, the more cholesterol is transferred from HDL to LDL.
Dr. Maria-Luz Fernandez of the University of Connecticut has reviewed this subject in greater detail here:
Dietary Cholesterol Provided by Eggs and Plasma Lipoproteins in Healthy Populations
Intake of certain fatty acids increases cholesterol levels, but again this is more consistent with greater cholesterol synthesis. For example the most powerful increaser of total cholesterol is probably lauric acid, but lauric acid is also the most powerful reducer of the LDL-to-HDL-cholesterol ratio — this is consistent with lauric acid being burned for quick energy, thus increasing the energy state of the liver cell and allowing for greater cholesterol synthesis. Not “blocking” the LDL receptor.
For more information on this subject, see my blog post over at The Daily Lipid:
In any case, experimental evidence has shown in humans that saturated fats protect against in vivo LDL oxidation. You can see this by looking at the rightward most column in this graph: Dietary Fat and LDL Oxidation.
This shows a graded increase in LDL oxidation occuring within the blood of live humans as the diet goes from 1) butter and palm oil to 2) olive oil to 3) sunflower oil and finally 4) sunflower oil and fatty fish, all diets being about 35% of calories from fat. The first two diets were statistically significant from the second two diets, but the increase between butter/palm and olive oil was not significant, nor was the increase between sunflower and sunflower/fatty fish. So what we can conclude here is that it is primarily dietary polyunsaturated fats from seed oils and excess amounts of fatty fish that contribute to LDL oxidation.
In summary, eating traditional saturated and monounsaturated fats does not clog the liver and does not promote LDL oxidation.
Read more about the author, Chris Masterjohn, PhD, here.