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10 Facts About Cholesterol and Why a Personalized Approach is Best

Heart Health Cholesterol Genetics

Cholesterol.

Who would have thought this one organic molecule could inspire so much controversy? Well, if you follow the diet wars, you certainly believe it. In fact dietary cholesterol is one of the nutrition topics that inspires the fiercest debates, with health experts like Dr. Mark Hyman and Dean Ornish completely disagreeing on what is the best approach.

At Gene Food, our passion is empowering readers with a personalized approach to nutrition. To that end, we have compiled 10 science backed facts about cholesterol that will, hopefully, bring some clarity to your approach.

#1. Cholesterol is not a fatty acid

Because of the various health guidelines, most people think of cholesterol as a fat similar to the triglycerides. However, whilst cholesterol is a lipid, it is not a triglyceride fat. Very different in structure, it contains carbon rings rather than long chains of carbon atoms which results in a very different activity in the body.

#2. Cholesterol is essential for life

Indeed, cholesterol is essential for life, forming about 30% of all our cell membranes and providing flexibility in our cells. Additionally, cholesterol is the key component of many hormones including estrogen and testosterone, and is also required for the synthesis of vitamin D.

Cholesterol also forms bile acids which facilitate the digestion of fats and oils in the intestine as well as aiding the absorption of the fat-soluble vitamins A, D and E.

#3. Cholesterol is unique to animals

Cholesterol is associated with meat and dairy products, with plant based foods containing little, if any, cholesterol. Cholesterol is a type of zoosterol, meaning it is a lipid that is only found in animals.

By contrast, fats that are unique to plants are called phytosterols.

#4. Most of the cholesterol in the body is made by the body

Because cholesterol is essential to life, our bodies make the majority of cholesterol in the body.

The liver makes cholesterol, as do red blood cells. Cholesterol made by the body is called “endogenous” cholesterol, whereas the 20% or so we get from cholesterol in the diet is called “exogenous” cholesterol.

#5. Cholesterol is hydrophobic

This means cholesterol can’t move freely in blood, which is essentially water, without assistance.

As with triglycerides, cholesterol is not soluble in water, and so to be transported around the circulatory system it requires assistance. 1

#6. Cholesterol doesn’t cause heart disease, but LDL does 

To transport the insoluble triglycerides and cholesterol around the body in the blood, lipoproteins are required. Lipoproteins are particles made up of thousands of molecules which encase triglycerides and cholesterol allowing these insoluble molecules to be transported around the circulatory system.

There are several different types of lipoproteins, the most commonly known being low-density lipoproteins (LDL) and high-density lipoproteins (HDL).

LDL delivers cholesterol to the tissues within the body. However, where there is an excess of LDL, harmful depositions of cholesterol, particularly in the blood vessels, can occur, contributing to the build-up of fatty plaques on blood vessel walls. This is why LDL is often referred to as ‘bad cholesterol’, even though LDL is not made of cholesterol, it just transports it!

This is a key lesson: it’s not cholesterol that causes heart disease, it’s LDL and other lipid carrying particles. The inflammatory process of heart disease begins when an LDL particle deposits a piece of cholesterol, fatty acid, or plant sterol in the artery wall.

It should also be noted that damaged polyunsaturated fats, and trans fats, are not heart healthy, and the regular addition of these fats to processed foods in the form of vegetable oils has contributed to the rise of heart disease.

In contrast, HDL is responsible for transporting excess cholesterol from the tissues within the body (including removing cholesterol from the arteries) for disposal by the liver, and is referred to as “good cholesterol.” 2

#7. Eating cholesterol doesn’t always mean high cholesterol

Historically, studies proposed that eating high levels of cholesterol in foods like eggs, led to an increase in blood cholesterol levels, which congealed inside the blood vessels eventually resulting in poor heart health. And so, the idea that a high cholesterol diet is bad was born. 3

However, numerous studies have since pointed out several flaws with this hypothesis. 4

First, while a high level of total cholesterol is associated with an increased risk of heart disease, most people who suffer from heart disease have normal blood cholesterol levels. 5

Second, as cholesterol is so fundamental to life, it is directly synthesized in the body, mainly in the liver, but also in red blood cells. Excess dietary cholesterol is excreted in stool, and any dietary cholesterol which is absorbed results in a decrease in cholesterol synthesis in the liver. 6 7

Together this means that even a diet very high in cholesterol has little, if any, impact on the cholesterol levels in the blood which are maintained at a steady state in most people

#8. Not everyone has the same reaction to dietary cholesterol

While much of the advice on dietary cholesterol has ignored the rule of cholesterol homeostasis, in which the body tightly regulates cholesterol levels, not everyone fits neatly under this umbrella.

In fact, there is tremendous variability in cholesterol absorption, with some of us absorbing only 20% of the cholesterol we eat, while others absorb as much as 85%!  We now know that genetic variants in genes like ABCG5 and ABCG8 determine how much cholesterol an individual will absorb. Research by world renowned lipid expert Dr. Tom Dayspring also indicates that APOE4 carriers are far more likely to be hyper-absorbers

In people who hyper-absorb cholesterol, eating high cholesterol foods like eggs will have an impact on their LDL levels, and as a result, their risk for heart disease over time.

It is shocking to me that, despite compelling science from some of our best medical journals, our nutrition experts and commentators still push one size fits all approaches with dietary cholesterol. There is no single rule for cholesterol, advice has to be tailored to each individual based on lifestyle and genetic predisposition.

For many people, eating eggs will have no impact on blood lipid markers, while others will be at increased risk. In a previous podcast, we covered the American Journal of Clinical Nutrition study on egg consumption and the impact on biomarkers like LDL-C. The ACJN study, which found minimal impact on cholesterol levels even when subjects ate 7 eggs per week, is well worth a read. 

However, I also implore anyone interested in this topic to read the excellent 2020 paper from the European Heart Journal titled: Genetic variability in the absorption of dietary sterols affects the risk of coronary artery disease. So much of the cholesterol discussions you find online and via Google search are outdated and based on either old science, or partisan science. 

A side note: you get op-ed style articles like this one, which appeared in the Guardian, discussing “cholesterol deniers.” We agree that cholesterol denial, to the extent that means arguing that LDL is not causal in heart disease, is a major problem in the nutrition community. There are two things to point out here:

  1. Yes, some people, tend to hyper-absorb cholesterol and plant sterol. These people need to keep a closer eye on cholesterol than others.
  2. The article lumps saturated fat in with cholesterol, but as we’ve learned, the two are very different. Especially in some genotypes, saturated fat may indeed increase the risk for heart disease, but let’s not conflate these two separate issues.

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#9. Saturated fat and cholesterol are two different animals

In the majority of people, eating cholesterol doesn’t raise cholesterol levels because the body simply makes less cholesterol when it absorbs more. Conversely, when the body makes more cholesterol, it absorbs less. However, here is where the rubber meets the road. As pointed out in our first cholesterol fact, saturated fat and cholesterol are two different things. 

The general rule for cholesterol is that eating it doesn’t meaningfully increase blood levels. If you’re in doubt, see the ACJN egg study cited above.

However, the same cannot be said for saturated fat.

The body doesn’t make saturated fat and eating it causes an uptick in LDL-C in all people, it’s just a matter of degree as to how much LDL goes up. In some of us with genetic predispositions, eating a high saturated fat diet causes the body to make a lot more cholesterol which results in lab results that make physicians very uncomfortable. To demonstrate this point, have a look at this study from 2019. Study authors measured blood lipid markers for 30 healthy individuals placed on a ketogenic style diet. On average the participants saw a 44% increase in LDL-C levels on the high fat diet, but the results varied by individual from between 5-107%! This means that some of us can incorporate healthy amounts of saturated fat in the diet without the corresponding rise in LDL, while others have to be much more cautious. Part of what we are doing at Gene Food is developing an algorithm that will help classify people into different camps so they have a good idea of how much dietary fat is healthy for them.   

As I discussed in the point above, there are a lot of LDL skeptics, some of whom can rightly be classified as “cholesterol deniers.” For example, paleo advocates will tell you that there is no evidence that eating saturated fat causes heart disease, but this isn’t exactly right.

In order to conclusively “prove” that saturated fat causes heart disease, you would need to control the diets of different groups of people for decades and then report results. It is simply not possible to create the types of nutrition studies we need to settle the matter. Instead, we have biochemistry and cardiovascular trials. Paleo advocates suggest that statin trials which are aimed at lowering LDL-C, fail to show a drop in all-cause mortality, and therefore we needn’t concern ourselves with LDL at all. This is just flat out bad science. If you are eating a high fat diet and you don’t see the corresponding uptick in LDL, it could be a sign that that diet is working for you, perhaps as a way of controlling blood sugar. Conversely, if you go high fat and see severely elevated levels of LDL, you are very likely at an increases risk for heart disease.

There are a few things to note here: 

  1. Some statin trials do show drops in all cause mortality when LDL-C is lowered. For example, this 2018 JAMA meta analyses of over 270,00 participants found that all cause mortality dropped when LDL-C was lowered from 160 mg/DL to 130 mg/DL and again from 130 mg/dL to 100 mg/dL, but that all cause mortality benefits ceased when LDL-C went below 100 mg/dL. In other words, lowering LDL beneath 100 mg/dL didn’t show increased drops in all cause mortality although heart attack and stroke risk continued to go down as LDL levels fell.  
  2. Statin trials are designed to prove the efficacy of a drug as quickly as possible, they aren’t designed to demonstrate the lifetime impact of high cholesterol caused by a fat heavy diet. This issue came up when we interviewed Dr. Tom Dayspring last year
  3. Lowering LDL-C, and especially APOB, is associated with lower incidence of heart disease across the board. 

So, what is the bottom line here? Know your baseline levels of LDL and other heart health biomarkers. Watch how they change when you go on a high fat diet. If your numbers go through the roof, don’t think a healthy TG/HDL ratio will lower your risk. Eating cholesterol won’t contribute to heart disease in most of us, but eating loads of saturated fat will increase LDL and heart attack risk in some populations. 

Know your numbers and listen to your cardiologist, not the blogosphere. If you have some time, listening to this podcast interview with Dr. Peter Attia and low carb diet advocate Dave Feldman is valuable.

Dr. Attia so throughly debunks Dave’s “energy model” of cholesterol metabolism that I have been surprised Dave kept on publicly advocating for it after the interview. 

#10. Dietary cholesterol interacts with the microbiome

We close on cholesterol and the microbiome. It’s not just about how we make and absorb cholesterol, another important factor is what the microbiome does with the cholesterol we eat.

The New England Journal of Medicine has published some excellent studies on how eating eggs and dietary cholesterol changes the microbiome, specifically causing the production of a compound known as TMAO, which is linked to heart disease.

For example, in one trial, the NEJM researchers fed subjects eggs and measured TMAO levels, which went up. When the same subject were placed on antibiotics and then fed eggs, TMAO levels didn’t rise, suggesting that it is the composition of the microbiome which leads to TMAO production and the increased cardiovascular risk that comes with it. I’ve had the privilege of interviewing Integrative Cardiologist, and television personality, Dr. Joel Kahn on the Gene Food Podcast. Dr. Kahn tests his patients for TMAO and reduces eggs and supplements, like L-carnitine, that cause increases in TMAO when levels are high. 

In closing 

In closing, while it’s true that dietary cholesterol has been improperly demonized, there are exceptions to every rule.

In order to determine what the best approach is for your health, learn how much cholesterol you absorb, how your body responds to saturated fats, and last, the state of your microbiome.

As Carl Jung famously said, “the more a law lays claim to universal validity, the less it does justice to the individual facts.” 

Good luck. 

Dr. Dan Deakter, MD

Dr. Dan Deakter, M.D., serves as the Medical Advisor of Gene Food. He trained in General Surgery at The Albert Einstein School of Medicine in NYC, and is an ABEM certified Emergency Physician. His medical practice is currently focused on improving health span and longevity.

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