Does Cholesterol Really Cause Heart Disease?

by Ann Marie Michaels on October 30, 2013

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Is cholesterol bad for you? Does cholesterol cause heart disease?

Most people answer yes to both questions.

You might be surprised to know, however, that cholesterol is actually good for you and in fact, it’s been shown in numerous studies that cholesterol found in egg yolks or real butter (as well as in numerous other real food sources, along with saturated fats) does not cause heart disease.

In fact, cholesterol is good for you.

Am I just trying to justify eating things that are bad for me because I like eggs and bacon for breakfast and an after-dinner dessert that isn’t “low-fat”?

Not at all. Not only do I enjoy natural foods that are high in cholesterol, but I can eat them without worry because I know that these real foods are actually good for my body.

Does Cholesterol Really Cause Heart Disease?

The conventional story on why cholesterol is bad for you, the “lipid hypothesis”, suggests that there is good and bad cholesterol, and that the bad type clogs arteries, which increases the risk for heart disease. Many doctors test to see how high or low cholesterol is in order to ascertain risk. According to Uffe Ravnskov, MD, PhD on the Weston A Price Foundation website, this is not valid. Ravnskov writes:

“[T]here are now a large number of findings that contradict the lipid hypothesis. To be more specific, most studies of old people have shown that high cholesterol is not a risk factor for coronary heart disease. This was the result of my search in the Medline database for studies addressing that question.2 Eleven studies of old people came up with that result, and a further seven studies found that high cholesterol did not predict all-cause mortality either.

“Now consider that more than 90 % of all cardiovascular disease is seen in people above age 60 also and that almost all studies have found that high cholesterol is not a risk factor for women. This means that high cholesterol is only a risk factor for less than 5 % of those who die from a heart attack.

“But there is more comfort for those who have high cholesterol; six of the studies found that total mortality was inversely associated with either total or LDL-cholesterol, or both. This means that it is actually much better to have high than to have low cholesterol if you want to live to be very old.”

It’s actually the oxidization of fats in processed foods that leads to harmful LDLs and higher levels of insulin that contribute to heart disease. So it isn’t high levels of cholesterol, but what happens when LDLS are oxidized that can lead to health problems no matter how much intake of cholesterol you might have. Other factors, such as stress, lead to inflammation and heart disease as well. (Source).

Is Cholesterol Actually Beneficial?

Chris Masterjohn is the go-to expert on the benefits of cholesterol. (Visit his website:

His extensive research has led him to dismiss the myth that cholesterol causes heart disease, and instead to conclude that cholesterol is actually good for you.

Cholesterol helps to maintain and regulate cell membranes by maintaining their integrity and fluidity as well as by securing important proteins that keep our cells healthy. Cholesterol is also abundant in the brain and is vital for learning and memory. Chris Masterjohn writes:

Myelin, which covers nerve axons to help conduct the electrical impulses that make movement, sensation, thinking, learning, and remembering possible, is over one fifth cholesterol by weight.

Even though the brain only makes up 2% of the body’s weight, it contains 25% of its cholesterol.

One of the groups of genes that the above study found to be upregulated during sleep were genes important for the synthesis and maintenance of myelin, including myelin structural proteins and genes relating to the synthesis and transport of cholesterol.

But the benefits of cholesterol extend beyond both sleep and myelin. In fact, in 2001, cholesterol was found to be the most important factor in the formation of synapses, the basis of our learning and memory. (Source)

Cholesterol also plays a role in the synthesis of bile acids, which is necessary for digestion.

But just as important, cholesterol is synthesized from Vitamin D, which is extremely important, and from which many American suffer a deficiency. (See The 10 Best Sources of Vitamin D)

Cholesterol also is involved in the synthesis of important steroid hormones, such as Glucocorticoids, which assist in the regulation of blood sugar; Mineralcorticoids for mineral balance and the regulation of blood pressure, and sex hormones.

Statins are Dangerous, Not Cholesterol Managers

Statins are drugs that are often prescribed to help lower cholesterol with the presumption that cholesterol is bad for you and can lead to heart disease. Often, statins can be very dangerous, lead to diminished cognitive abilities, and create numerous health problems. Given the importance of cholesterol for kids, the trend to prescribe statins for children is alarming.

Even Dr. Oz  has come out and said that statins are dangerous, and has even come a long way towards agreeing that cholesterol doesn’t cause heart disease.

These books are good starting points for further research:

Good sources of cholesterol and aracadonic acid: Butter, liver and egg yolks

What’s Your Experience With Cholesterol?

Are you surprised to hear someone say cholesterol is not the enemy and doesn’t cause heart disease? What do you think about this important issue? Share your thoughts and experiences below.

Photo credit: Heart Outtake

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{ 18 comments… read them below or add one }

charles grashow October 30, 2013 at 11:56 AM

” consider that more than 90 % of all cardiovascular disease is seen in people above age 60 also and that almost all studies have found that high cholesterol is not a risk factor for women. This means that high cholesterol is only a risk factor for less than 5 % of those who die from a heart attack.”

SO – if it’s not due to high cholesterol what is it due to??


Jen October 30, 2013 at 12:33 PM

From the article:

“It’s actually the oxidization of fats in processed foods that leads to harmful LDLs and higher levels of insulin, combined with the intake of refined sugars. Other factors, such as stress, lead to inflammation and heart disease as well.”

From the link in the article: “thousands of papers have now been published on the role of oxidized LDL in the development of atherosclerosis. Oxidized LDL causes endothelial cells to secrete “adhesion molecules” and “chemoattractants” that allow white blood cells called monocytes to penetrate in between the endothelial cells and stick to them in the subendothelial space where fatty streaks and atherosclerotic plaques develop.6

Oxidized LDL turns on the expression of genes in monocytes which cause them to convert into macrophages and eventually into foam cells, which makes them gobble up more and more oxidized LDL endlessly — but these macrophages use “scavenger receptors” rather than LDL receptors, so they never take up meaningful amounts of non-oxidized LDL; they only take up oxidized LDL, and it is oxidized LDL itself that initates this endless cycle.7

Oxidized LDL initiates the inflammatory process by causing foam cells to secrete molecules that attract T cells and other inflammatory cells.6 Oxidized LDL enhances the process whereby T cells, foam cells, smooth muscle cells and endothelial cells decrease collagen production and increase collagen degradation, which leads to the rupture of the fibrous plaque.5

Endothelial cells produce nitric oxide, a gas that protects LDL from oxidation, increases blood flow, decreases the adhesion of monocytes to the endothelium, and decreases blood clotting. Oxidized LDL impairs the endothelial cell’s ability to produce nitric oxide.8

In short, oxidized LDL contributes to the entire atherosclerotic process from start to finish. Writers who argue that atherosclerosis has nothing to do with lipids but is all about inflammation and response to injury must contend with the fact that oxidized LDL injures endothelial cells and causes inflammation!”


charles grashow October 30, 2013 at 4:46 PM

Let’s get rid of the nonsense seen all over the internet that atherosclerosis is an inflammatory disease, not a cholesterol disease. That is baloney-with the reality being that it is both. One cannot have atherosclerosis without sterols, predominantly cholesterol being in the artery wall: No cholesterol in arteries – no atherosclerosis. Plenty of folks have no systemic vascular inflammation and have atherosclerotic plaque. However clinicians have no test that measures cholesterol within the plaque – it is measured in the plasma. It is assumed, that if total or LDL-C or non-HDL-C levels are elevated the odds are good that some of that cholesterol will find its way into the arteries, and for sure there, are many studies correlating those measurements with CHD risk. Yet, we have lots of patients with very low TC and LDL-C who get horrific atherosclerosis. We now recognize that the cholesterol usually gains arterial entry as a passenger inside of an apoB-containing lipoprotein (the vast majority of which are LDLs) and the primary factor driving LDL entry into the artery is particle number (LDL-P), not particle cholesterol content (LDL-C). Because the core lipid content of each and every LDL differs (how many cholesterol molecules it traffics) it takes different numbers of LDLs to traffic a given number of cholesterol molecules: the more depleted an LDL is of cholesterol, the more particles (LDL-P) it will take to carry a given cholesterol mass (LDL-C). The usual causes of cholesterol depleted particles are that the particles are small or they are TG-rich and thus have less room to carry cholesterol molecules. Who has small LDLs or TG-rich LDL’s? – insulin resistant patients! After particle number endothelial integrity is certainly related to atherogenic particle entry: inflamed endothelia have inter-cellular gaps and express receptors that facilitate apoB-particle entry. So the worse scenario is to have both high apoB and an inflamed dysfunctional endothelium. Is it better to have no inflammation in the endothelium – of course! But make no mistake the driving force of atherogenesis is entry of apoB particles and that force is driven primarily by particle number not arterial wall inflammation: please see Ira Tabas, Kevin Jon Williams, Jan Borén. Subendothelial Lipoprotein Retention as the Initiating Process in Atherosclerosis Update and Therapeutic Implications Circulation. 2007;116:1832-44.


charles grashow October 30, 2013 at 4:53 PM
Nobel lecture, 9 December, 1985
Department of Molecular Genetics,
University of Texas Health Science
Center, Southwestern Medical School, 5323 Harry Hines Blvd. Dallas, Texas,

When LDL-cholesterol levels are below 100 mg/dl (equivalent to a total plasma cholesterol level of 170 mg/dl), heart attacks are rare. When LDL-cholesterol levels are above 200 mg/dl (equivalent to a total plasma cholesterol level of -280 mg/dl),heart attacks are frequent. Controversy arises over the middle ground, i.e.,individuals with plasma LDL-cholesterol levels between 100 and 200 mg/dl (total plasma cholesterol of 170 to 280mg/dl). This is the, range in which the vast bulk of heart attacks occur. Somewhere within this range there is a threshold value of cholesterol at which heart attacks begin to become more frequent. In this middle ground how much of the heart attack burden is attributable to plasma cholesterol? There is no definitive answer. In addition to cholesterol, heart attacks in this group are aggravated by smoking, hypertension, stress, diabetes mellitus, and poorly understood genetic factors. However, it seems reasonable to propose that plasma cholesterol does have something to do with heart attacks in these subjects, and that the incidence of heart attacks would be reduced if plasma cholesterol could be lowered .

The LDL receptor studies lend experimental support to the epidemiologists’ suggestion that the levels of plasma cholesterol usually seen’ in Western industrialized societies are inappropriately high (9). This support derives from knowledge of the affinity of the LDL receptor for LDL. The receptor binds LDL optimally when the lipoprotein is present at a cholesterol concentration of 2.5 mg/dl (28). In view of the 10 to 1 gradient between concentrations of LDL in plasma and interstitial fluid, a level of LDL-cholesterol in plasma of 25 mg/dl would be sufficient to nourish body cells with cholesterol (118). This is roughly one-fifth of the level usually seen in Western societies (Fig. 16 and ref.119). Several lines of evidence suggest that plasma levels of LDL-cholesterol in the range of 25-60 mg/dl (total plasma cholesterol of 110 to 150 mg/dl) might indeed be physiologic for human beings. First, in other mammalian species that do not develop atherosclerosis, the plasma LDL-cholesterol level is generally less than 80 mg/dl (Fig. 16 and ref. 120). In these animals the affinity of the LDL receptor for their own LDL is roughly the same as the affinity of the human LDL receptor for human LDL, implying that these species are designed by evolution to have similar plasma LDL levels (9,119). Second, the LDL level in newborn humans is approximately 30 mg/dl (121), well within the range that seems to be appropriate for receptor binding (Fig. 16). Third, when humans are raised on a low fat diet, the plasma LDL-cholesterol tends to stay in the range of 50 to 80 mg/dl. It only reaches levels above 100 mg/dl in individuals who consume a diet rich in saturated animal fats and cholesterol that is customarily ingested in Western societies (116)

Once LDL receptors become saturated, the removal rate of LDL is proportional to the number of receptors. Whenever the number of receptors is reduced, plasma LDL levels must rise. Experiments in animals indicate that the consumption of a high fat diet decreases the number of LDL receptors in the liver (123, 124). We believe that this mechanism operates through feedback suppression as described above. That is, when excess dietary cholesterol accumulates in the liver, the liver responds by decreasing the production of LDL receptors (Fig. 13C). The entry of dietary cholesterol into the liver is mediated by a receptor, termed the chylomicron remnant receptor, whose activity is genetically distinct from the LDL receptor (125). The chylomicron remnant receptor is unaffected by cholesterol accumulation (126), and it causes cholesterol to accumulate to high levels in liver when the diet contains excess fat. The combination of saturation and suppression of hepatic LDL receptors contributes in a major way to the buildup of LDL in plasma when a diet rich in saturated fats and cholesterol is ingested. Insofar as such a diet also may increase production of LDL in the face of a fixed or declining removal capacity, the LDL level would rise even higher If the LDL receptor does limit the removal of LDL from plasma, then maneuvers that increase LDL receptor activity might be effective in individuals who have high plasma LDL-cholesterol levels, but who do not have defective LDL receptor genes. Such therapy seems feasible with the development of HMG CoA reductase inhibitors. However, it is still too early to tell whether such therapy would decrease the incidence of myocardial infarctions in individuals with moderately elevated plasma LDL-cholesterol levels in the range of 100 to 200 mg/dl. There is much circumstantial evidence to expect such improvement (127), but unequivocal data are simply not there. Hopefully, with the availability of powerful receptor-stimulating drugs, the hypothesis should be susceptible to testing in the near future. In considering the role of diet and drugs in treatment of high cholesterol levels, physicians and public health authorities must bear in mind the genetic variability between individuals. This variability exists at three levels: 1) The degree of increase in plasma cholesterol upon ingestion of a high cholesterol diet is variable. Not all people develop hypercholesterolemia. Some people, such as the Pima Indians, maintain low plasma cholesterol levels despite ingestion of a high fat diet (10). 2) Even when the plasma cholesterol level becomes elevated, the propensity for atherosclerosis varies. For example, a substantial proportion of FH heterozygotes (10 to 20%) escape myocardial infarction until the 8th or 9th decade despite pronounced hypercholesterolemia from birth (14). 3) Genetic susceptibility to contributory risk factors is variable. Some people can withstand hypertension and cigarette smoking for decades without developing atherosclerotic complications; others are highly sensitive.”;jsessionid=76799A30E730E9813B6C59831A6EBAFD.tobacco03
Lipoprotein Receptors
Genetic Defense Against Atherosclerosis
This is interesting. They explain how LDL rises. First, the LDL receptor fills up:

How might a diet rich in animal fats and cholesterol elevate the plasma LDL-cholesterol level? … As the plasma LDL level rises, the receptors become saturated. This saturation of receptors sets an upper limit on the rate at which LDL can be removed efficiently from plasma (123). … Once the receptors become saturated, the rate of removal of LDL can be accelerated only by an increase in clearance by non-receptor pathways that operate at low efficiency. In order to drive these alternate pathways, the LDL level must be quite high (99).

And then, holy moly:

“When excess dietary cholesterol accumulates in the liver, the liver responds by decreasing the production of LDL receptors.”

So, it isn’t just the input of LDL (via consumption and endogenous production) that makes cholesterol go up, but the inability to clear it.

Michael S. Brown and Joseph L. Goldstein were awarded the Nobel Prize in Physiology or Medicine 1985 for their discoveries concerning the regulation of cholesterol metabolism:


Jen October 31, 2013 at 9:02 AM

Maybe you could simplify this for everyone to get your point across.


charles grashow October 31, 2013 at 1:31 PM

If you READ it you will understand it.


Rick October 31, 2013 at 3:10 PM

When the number of polysyllabic words approaches 25% of your text then the average university student will find it difficult to comprehend. To the rest of the world it’s blah, blah, blah . . .
Unfortunately you’ll not likely be able to simplify it.


Vita @ VitaLivesFree October 31, 2013 at 5:32 PM

Rolling on the floor laughing..Well said, Rick!


charles grashow November 1, 2013 at 1:08 PM

Next time I’ll try to look for studies that do not use long words so people like you can fully understand it.


Norma Tumberg October 30, 2013 at 6:59 PM

I have had total chol readings over 200 for years. HDL is high and LDL is higher than “desired”, trigs are low…. 65 or so.

Recently I started eating more saturated fat, bacon, coconut oil and my total chol dropped 20 points.

So, what’s the deal? I think it’s carbs……..


Jack LaBear November 7, 2013 at 5:53 PM

After I switched to low carb, high fat diet, my TC dropped from 180 to 115.
I deliberately eat 2500mg/day cholesterol in the form of pork brains to get it back up to 150.
After starting to eat that, a nasty longstanding overuse arthritis in my shoulder went away completely in 10 days, and my strength increased by 20% in two months.

Unfortunately, my girlfriend thinks I’m pig-headed ;-)
I say she is for refusing to try them.


Norma Tumberg November 9, 2013 at 4:36 AM

Like your play on words. ;-) How do you cook the brains? Euuuuwwww, that kind of grosses me out. I do like my bacon and pork roasts, but brains…. that would take a bit of…. :-) Do you eat a lot of green vegetables? I think they play a huge huge role on health, chol etc.


Jack LaBear January 10, 2014 at 9:53 AM

Hi Norma.
Sorry about the delay in replying.
There is nothing gross about the brains. They are bland and very soft. I whisk them with an egg (using a steak knife) and put it into a rich stock to make a soup.

Yes, I eat a lot of green vegetables. Other colors too!
I’m not ready to give up the idea that there are health benefits to eating vegetable matter even though randomized interventional studies have failed to find benefits over several years of study duration.
For me, it’s more about improving digestion and stool quality. Vegetables make a good vehicle for eating butter.

BTW, I have been eating more than 50% calories as fat, much of it animal, and I have been eating the brains for about two years. Like Charles, I spent a little too much time listening to vegans, so I got a carotid ultrasound to check my arteries. No sign of narrowing or plaque; all flow parameters are normal. Obviously the prescriptive statements of the vegans do not apply to all people and are therefore unethical and driven by ideology, not health science.


Vita @ VitaLivesFree October 31, 2013 at 3:05 AM

Great article! It’s interesting how so many people blame cholesterol for heart disease just because cholesterol levels are elevated in people with blocked arteries. But somehow not many people actually bother to think analytically – the fact that it’s there, doesn’t mean it’s the cause. High cholesterol is just a symptom of something else, just like blocked arteries. And that’s inflammation due to excessive sugar and carbs in general. I also can’t believe how many people still believe in the old-dated false data that eggs are unhealthy! Just my two cents.


Tosha October 31, 2013 at 9:09 AM

I think this article is wonderful! Good fats are good for you! I have cut out many things over the years but I have never cut back on fat. I buy the healthiest fats I can find. Even when I can’t afford totally organic food, I always buy organic butter and coconut oil.


Annie October 31, 2013 at 11:45 AM

Thank you for posting this very important information


kristy January 6, 2014 at 5:25 PM

Even though I totally agree that eggs are good for us, the bacon not so much. Only bacon that does not contain nitrates would be good for you. Nitrates will cause cancer.


MaryAnne January 8, 2014 at 4:39 AM

This is an overly simplified and somewhat incorrect way of looking at this situation. Some more recent studies have shown that mortality in elderly females is proportional to both EXCEEDINGLY HIGH levels of cholesterol and EXCEEDINGLY LOW levels of cholesterol. Therefore, meeting somewhere in the middle is shown to be directly related to LONGER LIFESPAN.

What this means is that you should balance eating high cholesterol foods with visits to the MD to check levels, get moderate exercise, avoid smoking. I would not say these studies conclusively state that cholesterol is good for you, period. Cholesterol is a life-sustaining substance – we can’t live without it and our bodies (through the liver) create it even if we avoid cholesterol containing foods. However, that should not give anyone a license to eat a large amount of animal-based foods (foods containing cholesterol). That is not a healthy diet. Eat in MODERATION everything, including healthy foods like Kale. Even too much Vitamin A can be bad for you!

Cholesterol is a very complex substance and unless you have specific training in science/medicine, it’s a little tricky to understand. I would take with a grain of salt any health advice given by someone without any formal training.

Last thing about studies showing an inverse relation to high mortality and high cholesterol —- most overweight people with a processed/animal food based diet do not live past 70 and therefore would not be included in any study of elderly people.

I am a critical care nurse and have also worked in nursing homes. Obese people with cardiac risk factors usually have their first cardiac event long before age 65. Fact.

Plant-based diet, low alcohol intake, NO SMOKING, and get a bit of exercise (helps clean out bad cholesterol (which is that that sticks to your arteries, clogging them and forming clots that can lodge in your vessels and cause heart attacks) is the way to go.
Advocating for bacon and cheese is just stupid. These are not health foods and just because you lack willpower to avoid them does not mean you should be searching for pseudoscience to justify your poor lifestyle choices.


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