What is cholesterol?

Cholesterol is an essential component of our bodies. Although there are convincing data showing an association between having high blood-cholesterol levels and increased cardiovascular risk, it is not clear that elevated cholesterol always equates with increased cardiovascular risk for everyone.

This guide will explain the basics of cholesterol and the different subtypes. To keep things brief, we’ll present most of the information about the different particles in bulleted lists.

You can learn more in our evidence-based guides about whether elevated LDL cholesterol is harmful, cholesterol and low carb diets, and the specific situation of low-carb LDL hyper-responders.

The basics: What is cholesterol?

• Cholesterol is a waxy substance that is essential for the life of all animals, including humans.¹
• Your body needs cholesterol for cell-membrane integrity, hormone synthesis, creation of bile acids, and myelin formation (myelin is the material that coats specialized nerve cells).²
• Your body makes most of the cholesterol that circulates in your bloodstream. It’s primarily produced in the liver, although many other tissues can make small amounts of cholesterol.
• Dietary cholesterol makes up a smaller portion of your blood-cholesterol pool and has only a minor effect on blood levels.³

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How is cholesterol transported in your body?

Since cholesterol is a wax-like substance, it can’t dissolve in the blood. Think about what happens when you add oil to water — it doesn’t mix. Your body has different carriers, called lipoproteins, which shuttle cholesterol through your bloodstream.

Triglycerides are commonly discussed along with cholesterol, but technically triglycerides aren’t cholesterol. Rather, triglycerides are the body’s form of mobile fat energy, providing energy to tissues when necessary and moving excess energy to fat storage when energy is abundant. In this guide, we’ll start with triglycerides and then move on to discuss the lipoproteins.

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Triglycerides

• Triglycerides are a type of fat that your body can either use for energy or store in fat cells for later use.
• Lipoproteins transport triglycerides in the blood, packaged along with cholesterol. Triglycerides are more prevalent in remnant particles such as VLDL, and less prevalent in LDL and HDL.
• Elevated triglycerides are likely independently associated with increased cardiovascular risk.⁴
• Some medications can lower triglycerides, such as fibrates, fish oil, and niacin.
• Your body can make triglycerides from dietary fat but often makes them to store excess carbohydrate intake.⁵
• One of the best lifestyle interventions for lowering triglycerides is following a low-carb diet.​​⁶
• The standard target for triglycerides is less than 150 mg/dL (1.7 mmol/L), but there is still a lot unknown about ideal triglyceride levels.⁷ Many clinicians familiar with low-carb nutrition believe levels below 100 mg/dL (1.1 mmol/L), or even 70 mg/dL (0.8mmol/L), may be better targets.⁸
• Another helpful target is to have a triglyceride to HDL ratio below 1.5.⁹
• Our guide, How to lower triglycerides, has helpful tips for bringing your levels down.

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Very-low-density lipoprotein (VLDL)

• The liver makes VLDL particles with a high concentration of triglycerides and a much lower concentration of cholesterol.
• VLDL particles transport triglycerides to tissues for fuel or for storage. VLDLs transition to intermediate-density lipoprotein (IDL) and eventually LDL as they drop off their triglyceride cargo.
• VLDL and other triglyceride-rich — sometimes called “remnant” — particles can contribute to cardiovascular disease, and some studies show them to be a more significant risk factor than LDL.¹⁰
• The diseases of insulin resistance, such as metabolic syndrome and type 2 diabetes, often come with elevated VLDL.¹¹
• Low-carb nutrition effectively lowers VLDL levels.¹²
• Target VLDL levels have not been well studied but are frequently listed as less than 30 mg/dl (1.7 mmol/L).

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High-density lipoprotein (HDL)

• HDL has long been considered the “good cholesterol,” but this is an oversimplification.
• The concept of HDL being “good” comes from two main lines of evidence: ¹³
  • There is a strong association between low HDL and the risk of heart disease. In fact, low HDL may be a more significant risk factor for heart disease than elevated LDL.¹⁴
  • HDL transports cholesterol to the liver, effectively removing it from circulation.
• However, attempts to raise HDL with medications have not shown clinical benefit, and genetically-elevated HDL is not always associated with decreased heart risk.¹⁵ These findings call into question whether HDL is “good” or simply a marker of metabolic health. They also highlight the potential importance of HDL function, which is currently difficult to measure clinically.
• Based on the evidence, it’s clear that you want to avoid having low HDL or the metabolic conditions that are associated with low HDL.
• While raising HDL with medications may not improve overall health outcomes, raising it naturally through diet and lifestyle may.¹⁶ The lifestyle habits that raise HDL are usually the same ones that improve insulin resistance and metabolic disease. Medications for HDL, on the other hand, have no metabolic benefits.
• Low-carb nutrition and strenuous exercise are likely the two most beneficial lifestyle habits for raising HDL.¹⁷
• Alcohol consumption may also raise HDL but is less likely to produce metabolic benefits.
• Men should aim for an HDL above 40 mg/dL (1.0 mmol/L), and women should aim for an HDL above 50 mg/dL (1.3 mmol/L).

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Low-density lipoprotein (LDL)

• Observational studies and longitudinal intervention studies show an association between elevated LDL cholesterol and an increased risk of developing cardiovascular disease.¹⁸ This association is true of studies in the general population and those done in people with specific genetic mutations that increase LDL levels.¹⁹
• Medical societies recommend lowering LDL cholesterol to reduce heart-disease risk, and cholesterol-lowering medications are among the most widely-prescribed medications in the industrialized world.²⁰
• Many medical societies agree that LDL is causative of heart disease.²¹
• An alternative idea is that LDL is necessary for the development of atherosclerosis but not causative in the absence of other factors that can cause vascular injury.²²
• Elevated LDL may not have equal risk across all subgroups. For instance, those with high HDL and low triglycerides may have less risk.​​²³
• Not all LDL particles are the same. See below for a more detailed description of the main kinds.
• Goal levels of LDL are usually based on the presence or absence of other cardiac risk factors. However, the American College of Cardiology (ACC) recommends less than 70 mg/dL for people with heart disease or at very-high risk for heart disease.

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ApoB and LDL-P

• LDL-P is a direct count of the number of LDL particles in blood, usually expressed as nmol/L.
• Apolipoprotein B (ApoB) is a protein present on every LDL lipoprotein — as well as VLDL and IDL particles, and LDL variants like Lp(a). An ApoB test is a measure of the amount of ApoB protein in a set amount of blood, reported in mg/dL.
• ApoB and LDL-P are likely better markers than LDL cholesterol level for predicting cardiovascular-disease risk.²⁴
• Also, many experts believe ApoB is likely a better marker than LDL-P since it includes VLDL and IDL in the count.
• ApoB is also a more reliable test with less potential variability and is more widely available than an LDL-P test.
• Goal levels of ApoB: The ACC recommends:²⁵
  • less than 80 mg/dL for those with cardiovascular disease or with diabetes plus an additional risk factor
  • Less than 90 mg/dL for those without cardiovascular disease but with two risk factors
• Less consensus exists for a goal LDL-P, but some labs recommend less than 935 nmol/L.

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Small and large LDL particles

• LDL particles come in different sizes and are generally grouped into large or small particles.
• Small particles contain less cholesterol and are more likely to become oxidized. They are associated with a greater increased risk of cardiovascular and metabolic disease than larger particles.²⁶
• The increased risk is likely due to a combination of the unique characteristics of smaller particles and the added risk from associated metabolic diseases such as insulin resistance and type 2 diabetes.²⁷
• Larger LDL particles contain more cholesterol and are less associated with cardiovascular disease. That doesn’t mean they have no association with heart-disease risk. Some studies show no significant risk, but others show a persistent risk, just significantly lower than the risk associated with small particles.²⁸ This question remains an active topic of debate within the medical community.
• There are no official recommendations for levels of small LDL particles, but some labs set their “safe level” at less than 467 nmol/L. Some clinicians familiar with low-carb lipid abnormalities recommend less than 30% small LDL particles.²⁹

Oxidized LDL

• A more pro-oxidative environment, such as with metabolic syndrome, likely leads to greater LDL oxidation.³⁰
• Oxidized LDL plays an important role in plaque formation and instability.³¹
• It’s not clear that antioxidant medications or supplements help reduce cardiovascular-disease risk. However, avoiding pro-oxidation triggers — such as tobacco, refined carbohydrates and sugars, and visceral adiposity — is likely an effective starting point.
• There are no agreed-upon measurement techniques or targets for oxidized LDL. Boston Heart uses Oxidized Phospholipid on ApoB (OxPl-apoB) and targets less than 5nM/L. Cleveland Heart Lab uses a more basic oxidized LDL and sets the standard at less than 60 U/L.

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Lipoprotein(a) [Lp(a)]

• Lp(a) — pronounced “LP little a” — is an LDL particle modified with a “kringle,” which is an extra tail attached to LDL that changes the particle shape and function.³²
• One potential mechanism for its effect is that LDL receptors can’t clear Lp(a) well, so it stays in circulation longer than regular LDL and is more prone to oxidation and retention in vessel walls.
• Lp(a) is independently associated with cardiovascular disease and may be more predictive than LDL.³³
• Lp(a) also mimics a clotting protein in the blood.
• Genetics mostly determine your Lp(a) level with minimal and inconsistent dietary effects.³⁴ However, case reports suggest a keto diet can modestly reduce Lp(a).³⁵
• There are no approved Lp(a)-lowering drugs, but some are in development.
• Niacin and PCSK9 inhibitors can lower Lp(a) by 15-20% as an “off-label” use. ³⁶ However, data showing that specifically lowering Lp(a) improves cardiovascular events are currently lacking.
• There are no agreed-upon targets. Many labs set a goal of less than 75 nmol/L or less than 25 mg/dL.