Poor cholesterol—so misunderstood. All animal cells require cholesterol for proper structure and function. The vast majority of cholesterol in the body does not come directly from foods like eggs and meat, but from the liver, which can make cholesterol out of anything we eat. So, if cholesterol-rich foods don’t cause high cholesterol, what does?


Most people have no idea what cholesterol actually is.

Life without cholesterol would be impossible. Cell membranes, which wrap around and protect the inner contents of all cells, must contain cholesterol in order to function properly. Cholesterol contributes firmness to membranes and keeps them from falling apart. But wait, there’s more!

All of the following critical body components are made from cholesterol:

  • Estrogen
  • Testosterone
  • Progesterone
  • Cortisol (anti-inflammatory stress hormone)
  • Aldosterone (regulates salt balance)
  • Vitamin D
  • Bile (required for fat and vitamin absorption)
  • Brain synapses (neurotransmitter exchange)
  • Myelin sheath (insulates nerve cells)


Cholesterol is made of carbon, hydrogen, and oxygen, just like fat is, but it is not fatty; it is a hard, waxy substance that contains no fat. A molecule of fat looks like this:

whereas a molecule of cholesterol looks like this:

As you may be able to appreciate just by looking at them, they are very different from each other.

Fat is a simple long chain, whereas cholesterol is mainly a complicated combination of rings—3 hexagons plus a pentagon; in medical school we affectionately called it “three rooms and a bath.” Fat is relatively easy to build (11 chemical steps from acetyl-coA to triacylglycerol), whereas cholesterol is hard to construct—more than 30 chemical steps are required to build one molecule of cholesterol (from acetyl-coA to cholesterol). The body would not go to the trouble of making it for no reason. Especially since, as it turns out, once it’s built, it’s impossible for the body to break it down—we do not have any way to take apart its complex ringed structure.


How much cholesterol do we need to eat?


Cholesterol is so important that the body can make cholesterol out of ANYTHING—fats, carbohydrates, or proteins. You don’t have to eat cholesterol to make cholesterol. Even if you eat a completely cholesterol-free diet, as vegans do, your body will still make cholesterol. Type “vegans with high cholesterol” into your search engine and you will find plenty of accounts of vegans whose cholesterol is too high—despite the fact that they eat ZERO grams of cholesterol.

Which foods contain cholesterol?

Since every single animal cell contains cholesterol, all animal foods contain cholesterol.

Many people don’t realize that all muscle meats (chicken, fish, beef, pork, etc.) contain about the same amount of cholesterol per serving.

Certain animal foods—liver, egg yolk, dairy fats, glandular organ meats, and brain— are especially high in cholesterol.  Why is that?  Liver is where the body manufactures cholesterol. Egg yolks contain concentrated cholesterol because the growing baby chick needs it to build new cells. Milk fat contains lots of cholesterol because the growing baby calf needs it to build new cells. Glandular organ meats (pancreas, kidney, etc.) contain more cholesterol because glands make hormones, and hormones are made from cholesterol. Brain contains very high amounts of cholesterol in its myelin sheaths, which insulate its electrical circuits.

All plant foods are considered “cholesterol-free.” Well, it would be more accurate to say that plant foods do not contain any animal cholesterol. Plants contain their own special forms of cholesterol called “phytosterols”, but phytosterols are toxic to human cells, so our intestines wisely refuse to absorb them.

So, in most cases, animal foods contain some cholesterol that the body can absorb and use, and all plant foods contain cholesterol that our body cannot absorb. The only exceptions I know of to these rules are shellfish.

There are two types of shellfish: crustaceans (lobsters, shrimp, crabs, etc.) and mollusks (clams, oysters, mussels, etc.). Crustaceans—giant sea insects who hunt for their food—contain animal cholesterols that can be absorbed by the body, but mollusks—who gather nutrients by filtering seawater—contain a different type of cholesterol that we can’t absorb.

In fact, plant cholesterols and mollusk cholesterols are not only rejected by our intestinal cells, they actually interfere with the absorption of animal cholesterols. This is how margarines such as Benecol® work. The manufacturer has added a chemically altered form of plant cholesterol to the spread, which interferes with the absorption of animal cholesterol.


Yes, but only if your body needs more cholesterol.

The cells lining the small intestine each contain transporter molecules (NPC1L1) that absorb cholesterol. [The cholesterol-lowering drug Zetia® works by blocking NPC1L1 yet does not reduce risk of heart disease]. However, if the body doesn’t need any more cholesterol, there are other molecules (ABCG5/8 transporters) that pump the cholesterol right back out into the intestines to be eliminated from the body. This is one reason why it is virtually impossible for cholesterol from food to cause “high cholesterol.” The intestinal cells know exactly how much is needed and will not allow extra to be absorbed.

This is brilliant when you think about it (the body is so smart)—it is impossible for the body to break down the complex structure of the cholesterol molecule, so it would make no sense to absorb too much—once it’s inside the body there’s only one way to get rid of it, and that is to excrete it in the bile. Why take in more than necessary, if it’s just going to have to be eliminated?

However, if your body cholesterol levels are low, the intestinal cells will not kick it out, and it will make it into your bloodstream—because you need it.

What’s more, cholesterol is recycled very efficiently by our bodies, because it is so hard to make. Why make more from scratch if you don’t have to? Remember that it’s also impossible for the body to break down cholesterol, so the only way to get rid of it is to excrete it. The liver gets rid of any excess by excreting free cholesterol into the intestines along with bile. This free form of cholesterol is the only form that intestinal cells are able to absorb. Most of the cholesterol molecules in food (85 to 90% of them) are not free; they are in the form of “cholesterol esters.” [Cholesterol esters are just cholesterol molecules with a fatty acid attached]. Intestinal cells are incapable of absorbing cholesterol ester, which is the major form of cholesterol in food. Therefore, if the intestinal cells sense that the body needs more cholesterol, it will typically reabsorb most of what the body needs from the bile, not from food.

To summarize the relationship between food cholesterol and blood cholesterol:

  1. Most cholesterol from foods does not get absorbed unless body levels are low.
  2. The amount of cholesterol you eat has almost no effect on your cholesterol levels.
  3. The vast majority of cholesterol in your body is made by your body’s own cells. Remember that creepy line from the movie When a Stranger Calls? “The call is coming from inside the house.” The excess cholesterol is coming from inside your body, not from the food you eat.

How does the body make cholesterol?

All cells can make their own cholesterol, but liver cells are especially good at it. Only liver cells are capable of making more than they need for themselves—and shipping it out to other parts of the body.

Remember how it takes more than 30 chemical reactions to build one molecule of cholesterol? The most important of all of these steps is step #3. In this step, a critical enzyme called “HMG-CoA reductase” converts a molecule called HMG-CoA into another molecule called mevalonate. Once this step occurs, there’s no turning back, so it’s a big commitment. This reaction is the one that determines whether or not cholesterol gets made. Therefore, the enzyme that runs this reaction, HMG-CoA reductase, is very important—it’s like the foreman in charge of the cholesterol assembly line. This enzyme needs to be carefully controlled, because we don’t want cells wasting their time and energy building expensive cholesterol molecules willy-nilly.

The activity of this critical enzyme HMG-CoA reductase is controlled primarily by two things:

1) cholesterol levels inside the cell

2) insulin levels in the blood.

This is where things get really interesting. It makes sense that HMG-CoA reductase would respond to the cell’s cholesterol levels—if the cell’s levels are low, you want to turn that enzyme on, so you can make more cholesterol, and if the cell has enough cholesterol, you want to turn that enzyme off and stop making cholesterol. But what is insulin doing in the mix?

We think of insulin as a blood sugar regulator, but its real job is to be a GROWTH HORMONE. Insulin is supposed to turn on when we need to grow. What do we need to make in order to grow? More cells. What do we need to form new cells? Cholesterol. So, at times when we need to grow (babies, teenagers, pregnant women), insulin turns the enzyme HMG-CoA reductase ON, which tells cells to make more cholesterol, so we can build new cells.

What causes high cholesterol?

Why would the body make more cholesterol than it needs?

Now here’s the problem: when people eat too many sugars and starches, especially refined and high glycemic index foods, blood insulin levels can spike. When insulin spikes, it turns on HMG –CoA reductase, which tells all of the body’s cells to make more cholesterol, even if they don’t need any more. This is probably the most important reason why some people have too much cholesterol in their bloodstream. Sugars and starches can raise insulin levels, which fools the body into thinking it should grow when it doesn’t need to. This is how low glycemic index diets and low-carbohydrate diets normalize cholesterol patterns—these diets reduce insulin levels, which in turn lower HMG-CoA reductase activity.

“Statin” drugs, such as Lipitor®, which are prescribed to lower cholesterol levels, work partly by interfering with the activity of HMG-CoA reductase. If your cells happen to need more cholesterol under certain circumstances, but the statin drug is blocking this critical enzyme, your cells may not be able to make cholesterol when needed. And what’s worse is that the cholesterol synthesis pathway doesn’t just make cholesterol; branches of this same pathway are responsible for synthesizing a wide variety of other important molecules, including: Vitamin A, Vitamin E, Vitamin K, and Coenzyme Q. So, you may want to think twice before you artificially interfere with this pathway by taking a statin drug.

When you eat less carbohydrate, you are not artificially blocking the pathway; you are simply allowing HMG-CoA reductase to listen to other more important signals (such as cholesterol levels and growth requirements) and decide naturally when it should turn on and when it should turn off.

So, to recap: refined carbohydrates speed up the cholesterol assembly line and statins slow it down. Which approach would you rather take to manage your “cholesterol problem”—taking a drug that artificially slows down this assembly line, or changing your diet so that the assembly line only runs when it’s supposed to? [Hint: Dietary changes require no monthly co-pays, and have no potentially dangerous side effects.]

Chances are: if you have “high cholesterol” you do not have a cholesterol problem—you have a carbohydrate problem.

Good Cholesterol and Bad Cholesterol

This gets into the very complicated relationship between cholesterol blood tests and heart disease risk. This is an enormous topic that will be covered in future articles on this site, but I’ll summarize some basic points here now.

When you get your cholesterol levels checked, you will see numbers for HDL and LDL, as well as triglycerides.  Triglycerides are fats, so we’ll set them aside and just focus on HDL and LDL.

HDL particles collect extra cholesterol from around the body and carry it back to the liver to be eliminated from the body if we don’t need it. It is typically thought of as “good cholesterol” so higher HDL levels are considered a good sign.

LDL particles carry extra cholesterol made in the liver out to the rest of the cells in the body. We used to think of LDL as “bad cholesterol” so lower levels of LDL were considered a good sign.

The cholesterol inside of HDL and LDL particles is exactly the same, it’s just that, for the most part, HDL is carrying it in one direction and LDL is carrying it in the opposite direction. The reason why LDL had been dubbed “bad” and HDL has been dubbed “good” is that numerous epidemiological studies (most famously, the Framingham Heart Study) told us that high LDL levels were associated with a higher risk of heart attack, and that high HDL levels were associated with a lower risk of heart attack.

We used to think that HDL was good because it acted like a garbage truck, clearing evil cholesterol out of our bodies, and we used to think that LDL was bad because it burrowed its way into our coronary arteries, depositing evil cholesterol there—forming plaques and causing heart attacks.

Cholesterol, Carbohydrates and Heart Disease

However, this simplistic way of thinking about cholesterol and heart disease is changing before our very eyes. It turns out that it is more complicated than this. LDL, for example, exists in a variety of forms. It can be big and buoyant and “fluffy” or small and dense and oxidized (damaged). The new thinking is that small, dense, oxidized LDL may be the only type of LDL that is associated with heart disease. Therefore, instead of thinking of all LDL as “bad”, it would be more accurate to say that all LDL is not created equal—big fluffy LDL is “good” and small, dense, oxidized LDL is “bad.”

Unfortunately, standard blood tests can’t tell you which type of LDL you have because it lumps all types of LDL particles together.  Standard tests can only estimate how much of your cholesterol is travelling inside of LDL particles.  They can’t tell you how many LDL particles you have, how big they are, how dense they are, or how oxidized they are.  [For a detailed explanation of the complexities involved in interpreting cholesterol blood test results, I recommend Dr. Peter Attia’s blog at]

What we do know from research studies is that people who eat a diet high in refined carbohydrates tend to have a higher number of “bad” (smaller, denser, oxidized) LDL particles. This makes sense, because we know that carbohydrates are “pro-oxidants” —meaning they can cause oxidation.

There is also lots of evidence telling us that refined carbohydrates can cause inflammation.  Just because doctors find cholesterol inside artery-clogging plaques does not mean that cholesterol causes plaques. It is now well established that heart disease is a disease of inflammation. It is not simply that an innocent, smooth, buoyant sphere of fat and cholesterol traveling through the bloodstream decides to somehow randomly dig its way into a healthy coronary artery. The first step in the development of a vessel-clogging plaque is inflammation within the lining of the artery itself. When doctors cut into plaques they don’t just find cholesterol—they find many signs of inflammation (such as macrophages, calcium, and T cells). Wherever there is inflammation in the body, cholesterol is rushed to the scene to repair the damage—because we need cholesterol to build healthy new cells. Jumping to the conclusion that coronary artery plaques are caused by the cholesterol found inside of them is like assuming that all car accidents are caused by the ambulances that are found on the scene.

The latest research suggests that diets high in refined and high glycemic index carbohydrates increase the risk of inflammation throughout the body, especially in blood vessels. Diabetes, a disease which is intimately associated with high blood sugar levels, is infamous for causing damage to blood vessels in the retina, kidneys, and tiny vessels that feed nerve endings in the feet. It is well established that people with diabetes are also at higher risk for heart disease. It should therefore not be a stretch for us to imagine that all people with high blood sugar and/or insulin levels due to diets rich in refined carbohydrates may also be at increased risk for cardiovascular disease.

Cardiology researchers are now turning away from the notion that saturated fat and cholesterol cause heart disease. After all, how could saturated fat and cholesterol, which we have been eating for hundreds of thousands of years, be at the root of heart disease, which is a relatively new phenomenon? Cardiologists are finding instead that refined carbohydrate (such as sugar and flour), which we have only been eating in significant quantities for about a hundred years, is the single most important dietary risk factor for heart attacks:

“Strong evidence supports …associations of harmful factors, including intake of trans-fatty acids and foods with a high glycemic index or load.”

“Insufficient evidence of association is present for intake of…saturated and polyunsaturated fatty acids; total fat,… meat; eggs; and milk.” [Mente et al 2009].


There are several plausible mechanisms for how refined carbohydrate could increase risk for heart disease and change cholesterol profiles:

  • Diets high in refined carbohydrate lower HDL levels and set the stage for high insulin levels, oxidation, and inflammation throughout the body, including in the coronary arteries.
  • High blood sugar and insulin levels turn big, fluffy, innocent LDL particles into small, dense, oxidized LDL particles, which are associated with increased risk for heart disease.
  • High insulin levels turn on the cholesterol building enzyme HMG-CoA reductase, forcing the body to make more cholesterol than it needs.

It is becoming increasingly obvious that cholesterol is innocent until corrupted by refined carbohydrate.

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Barclay AW et al. Glycemic index, glycemic load, and chronic disease risk—a meta-analysis of observational studies. Am J Clin Nutr 2008; 87: 627–37.
Boden G et al. Effect of a low-carbohydrate diet on appetite, blood glucose levels, and insulin resistance in obese patients with type 2 diabetes. Annals of Internal Medicine 2005; 142: 4030441.
Brownlee M. The pathology of diabetic complications: a unifying mechanism. Diabetes 2005; : 1615-1625.
Djoussé L, Gaziano JM.. Dietary cholesterol and coronary artery disease: a systematic review. Atheroscler Rep 2009; 11(6): 418-22.
Eaton SB et al. Stone agers in the fast lane: chronic degenerative diseases in evolutionary perspective. Am J Med 1988; 84: 739-749.
Esposito K et al. Inflammatory cytokine concentrations are acutely increased by hyperglycemia in humans: role of oxidative stress. Circulation 2002; 106: 2067-2072.
Greco TP et al. xidized-LDL/beta(2)-glycoprotein I complexes are associated with disease severity and increased risk for adverse outcomes in patients with acute coronary syndromes. Am J Clin Path; 133: 737-743.
Halton TL et al. Low carbohydrate diet score and risk of cardiovascular disease in women. New England Journal of Medicine 2006; 355: 1991-2002.
Jakobsen MU et al. Intake of carbohydrates compared with intake of saturated fatty acids and risk of myocardial infarction: importance of the glycemic index. Am J Clin Nutr 2010; 91: 1764-8.
Mente A et al. A systematic review of the evidence supporting a causal link between dietary factors and coronary heart disease. Archives of Internal Medicine 2009; 169(7): 659-69.
Siri-Tarino PW et al. Saturated fat, carbohydrate, and cardiovascular disease. Am J Clin Nutr 2010.
Welsh JA et al. Caloric sweetener consumption and dyslipidemia among US adults. JAMA 2010; 303(15): 1490-1497.
Westman EC et al. Low-carbohydrate nutrition and metabolism. Am J Clin Nutr 2007; 86: 276-84.
Willett, W. The Great Fat Debate: Total Fat and Health. J Am Diet Assoc 2011; 111(5): 660-662.

Last Modified: Dec 15, 2015