HDL – Types and What You Need To Know

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HDL/High-Density Lipoprotein (HDL) is one of the five major groups of lipoproteins. Lipoproteins are complex particles composed of multiple proteins that transport all fat molecules (lipids) around the body within the water outside cells. They are typically composed of 80–100 proteins per particle (organized by one, two or three ApoA; more as the particles enlarge picking up and carrying more fat molecules) and transporting up to hundreds of fat molecules per particle.

Recommended Ranges of High-Density Lipoprotein/HDL

The American Heart AssociationNIH and NCEP provide a set of guidelines for fasting HDL levels and risk for heart disease.[rx][rx][rx]

Level mg/dL Level mmol/L Interpretation
<40/50 men/women <1.03 Low HDL cholesterol, heightened risk considered correlated for heart disease
40–59 1.03–1.55 Medium HDL level
>59 >1.55 High HDL level, optimal condition considered correlated against heart disease

High LDL with low HDL level is an additional risk factor for cardiovascular disease.[rx]

NMR measurements

Concentration and sizes of lipoprotein particles can be estimated using nuclear magnetic resonance fingerprinting.[rx]

Optimal total and large HDL concentrations

The HDL particle concentrations are typically categorized by event rate percentiles based on the people participating and being tracked in the MESA[rx] trial, a medical research study sponsored by the United States National Heart, Lung, and Blood Institute.

Total HDL particle Table
MESA Percentile Total HDL particles μmol/L Interpretation
>75% >34.9 Those with highest (Optimal) total HDL particle concentrations & lowest rates of cardiovascular disease events
50–75% 30.5–34.5 Those with moderately high total HDL particle concentrations & moderate rates of cardiovascular disease events
25–50% 26.7–30.5 Those with lower total HDL particle concentrations & Borderline-High rates of cardiovascular disease
0–25% <26.7 Those with lowest total HDL particle concentrations & Highest rates of cardiovascular disease events
Large (protective) HDL particle Table
MESA Percentile Large HDL particles μmol/L Interpretation
>75% >7.3 Those with highest (Optimal) Large HDL particle concentrations & lowest rates of cardiovascular disease events
50–75% 4.8–7.3 Those with moderately high Large HDL particle concentrations & moderate rates of cardiovascular disease events
25–50% 3.1–4.8 Those with lower Large HDL particle concentrations & Borderline-High rates of cardiovascular disease
0–25% <3.1 Those with lowest Large HDL particle concentrations & Highest rates of cardiovascular disease events

The lowest incidence of atherosclerotic events over time occurs within those with both the highest concentrations of total HDL particles (the top quarter, >75%) and the highest concentrations of large HDL particles. Multiple additional measures, including LDL particle concentrations, small LDL particle concentrations, VLDL concentrations, estimations of insulin resistance and standard cholesterol lipid measurements (for comparison of the plasma data with the estimation methods discussed above) are routinely provided in clinical testing.

How do I know what my HDL level is?HDL

A blood test can measure your cholesterol levels, including HDL. When and how often you should get this test depends on your age, risk factors, and family history. The general recommendations are:

For people who are age 19 or younger:

  • The first test should be between ages 9 to 11
  • Children should have the test again every 5 years
  • Some children may have this test starting at age 2 if there is a family history of high blood cholesterol, heart attack, or stroke

For people who are age 20 or older:

  • Younger adults should have the test every 5 years
  • Men ages 45 to 65 and women ages 55 to 65 should have it every 1 to 2 years
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What should my HDL level be?

With HDL cholesterol, higher numbers are better, because a high HDL level can lower your risk for coronary artery disease and stroke. How high your HDL should be depends on your age and sex:

Group Healthy HDL Level
Age 19 or younger More than 45mg/dl
Men age 20 or older More than 40mg/dl
Women age 20 or older More than 50mg/dl


HDL is composed of cholesterol, triglycerides, and various apolipoproteins. In particular, the composition of HDL is apolipoproteins Apo-AI, Apo-AII, Apo-AIV, Apo-AV, Apo-C1, Apo-CII, Apo-CIII, and Apo-E.[1]

  • Apo-AI is the primary structural apolipoprotein of HDL and activates Lecithin–Cholesterol AcylTransferase (LCAT).
  • Apo-AII is also a structural protein in HDL and acts as an activator of hepatic lipase.
  • Apo-IV has an unknown function.
  • Apo-AV activates lipoprotein lipase (LPL), which is responsible for triglyceride lipolysis.
  • Apo-CI is responsible for activating LCAT.
  • Apo-CII is responsible for activating LPL
  • Apo-CIII is responsible for inhibiting LPL.
  • Apo-E is a ligand for the LDL receptor.

Causes of HDL Can Be Decrease

HDL gets tested through blood sampling and is commonly determined within a complete lipid profile. Testing in adults requires fasting for 12 hours before sampling, whereas testing is possible without fasting in the youth without risk factors for heart disease. Without fasting, only total cholesterol and HDL are usable. In this scenario, if the total cholesterol is ≥200 mg/dL or HDL is below 40 mg/dL, the NCEP III guidelines indicate a follow-up lipoprotein profile is necessary for management based on LDL.

A lipid profile, and thus HDL-C, may be ordered for those with risk factors for heart disease, which includes:

  • Smoking (cigarettes)
  • Sedentary lifestyle
  • Being overweight or obesity
  • Poor diet
  • Men over 45 years or women older than 55 years
  • Hypertension (higher than 140/90)
  • Positive immediate family history of premature heart disease (under 55 for men and under 65 for women)
  • Pre-existing heart condition
  • Diabetes or prediabetes

For the youth, the American Academy of Pediatrics recommends that children be tested once between ages 9 and 11 and repeated between the ages of 17 and 21. This screening is recommended for children under the age of 9 if the children’s parents test positive for high cholesterol. The NCEP ATP III guidelines also suggest using agents that will correct the HDL abnormality while also lowering LDL cholesterol, lowering LDL cholesterol being paramount.

Increasing HDL levels

While higher HDL levels are correlated with cardiovascular health, no medication used to increase HDL has been proven to improve health.[rx] In other words, while high HDL levels might correlate with better cardiovascular health, specifically increasing one’s HDL might not increase cardiovascular health.[rx] The remaining possibilities are that either good cardiovascular health causes high HDL levels, there is some third factor that causes both, or this is a coincidence with no causal link.

HDL lipoprotein particles that bear apolipoprotein C3 are associated with increased, rather than decreased, the risk for coronary heart disease.[rx]

  • Eat a healthy diet  – To raise your HDL level, you need to eat good fats instead of bad fats. This means limiting saturated fats, which include full-fat milk and cheese, high-fat meats like sausage and bacon, and foods made with butter, lard, and shortening. You should also avoid trans fats, which may be in some margarine, fried foods, and processed foods like baked goods. Instead, eat unsaturated fats, which are found in avocado, vegetable oils like olive oil, and nuts. Limit carbohydrates, especially sugar. Also try to eat more foods naturally high in fiber, such as oatmeal and beans.
  • Stay at a healthy weight – You can boost your HDL level by losing weight, especially if you have lots of fat around your waist.
  • Exercise – Getting regular exercise can raise your HDL level, as well as lower your LDL. You should try to do 30 minutes of moderate to vigorous aerobic exercise on most, if not all, days.
  • Avoid cigarettes – Smoking and exposure to secondhand smoke can lower your HDL level. If you are a smoker, ask your health care provider for help in finding the best way for you to quit. You should also try to avoid secondhand smoke.
  • Limit alcohol – Moderate alcohol may lower your HDL level, although more studies are needed to confirm that. What we do know is that too much alcohol can make you gain weight, and that lowers your HDL level.
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Diet and exercise

Certain changes in diet and exercise may have a positive impact on raising HDL levels

  • Decreased intake of simple carbohydrates.[rx][rx][rx][rx]
  • Aerobic exercise
  • Weight loss
  • Avocado consumption
  • Magnesium supplements raise HDL-C.
  • Addition of soluble fiber to diet
  • Consumption of omega-3 fatty acids such as fish oil[rx] or flax oil
  • Consumption of pistachio nuts
  • Increased intake of unsaturated fats
  • Consumption of medium-chain triglycerides (MCTs).
  • Removal of trans fatty acids from the diet

Most saturated fats increase HDL cholesterol to varying degrees but also raise total and LDL cholesterol.[rx] A high-fat, adequate-protein, low-carbohydrate ketogenic diet may have similar response to taking niacin (vitamin B3) as described below (lowered LDL and increased HDL) through beta-hydroxybutyrate coupling the Niacin receptor 1.[rx]

Some cholesterol medicines, including certain statins, can raise your HDL level, in addition to lowering your LDL level. Health care providers don’t usually prescribe medicines only to raise HDL. But if you have a low HDL and high LDL level, you might need medicine.

Recreational drugs

HDL levels can be increased by smoking cessation,[rx] or mild to moderate alcohol intake.

Cannabis in unadjusted analyses, past and current cannabis use was not associated with higher HDL-C levels.[rx] A study performed in 4635 patients demonstrated no effect on the HDL-C levels (P=0.78) [the mean (standard error) HDL-C values in control subjects (never used), past users and current users were 53.4 (0.4), 53.9 (0.6) and 53.9 (0.7) mg/dL, respectively].[rx]

Pharmaceutical drugs and niacin

Pharmacological therapy to increase the level of HDL cholesterol includes use of fibrates and niacin. Fibrates have not been proven to have an effect on overall deaths from all causes, despite their effects on lipids.[rx]

Niacin (vitamin B3) increases HDL by selectively inhibiting hepatic diacylglycerol acyltransferase 2, reducing triglyceride synthesis and VLDL secretion through a receptor HM74[rx] otherwise known as niacin receptor 2 and HM74A / GPR109A,[rx] niacin receptor 1.

Understanding the amounts of cholesterol and fats found in foods

Here are some examples of foods and approximately how much cholesterol and fats you can find in each:

Food Amount of cholesterol Amount of saturated fat Amount of trans fat Amount of unsaturated fat
1 large egg 186 mg 1.6 g 0 g 2.7 g
1/4 lb. 95% lean ground beef 70 mg 2.5 g 0.3 g 2.5 g
1/4 lb. 70% lean ground beef 88 mg 13.3 g 2.1 g 16.8 g
6 oz. skinless chicken breast 124 mg 1 g 0.01 g 1.9 g
1 tbsp. salted butter 31 mg 7.3 g 0.5 g 3.4 g
1 tbsp. extra virgin olive oil 0 mg 2 g 0 g 11.5 g
1 cup vanilla ice cream 58 mg 9 g N/A 4.5 g
1 cup low-fat yogurt 15 mg 2.5 g N/A 1.1 g
3 oz. uncooked shrimp 137 mg 0.1 g 0 g 0.2 g
1 avocado 0 mg 4.3 g 0 g 23.4 g
1/2 cup plain walnuts 0 mg 3.1 g 0 g 28.1 g

All of the above values come from the USDA’s National Nutrient DatabaseTrusted Source. These are just some examples of the relative amounts of cholesterol and fats found in your food.

Summary of HDL-raising therapies, mode of action, available clinical evidence on atherosclerosis and cardiovascular risk.

Drugs Mode of action Effect on HDL Available clinical evidence on atherosclerosis and cardiovascular risk
Niacin (nicotinic acid) ↑ Hepatic apoA-I production and ABCA1 transcription ↑ HDL-C 15–40% AIM-HIGH and HPS2-THRIVE: lack of benefit on cardiovascular outcomes []
↓ Hepatic clearance of apoA-I and HDL
↓ CETP activity
↓ Lipolysis of triacylglyerol
Fibrates ↑ ApoA-I transcription and ABCA1 production ↑HDL-C 2–20% VA-HIT and HHS: ↓ 22–34% in CHD with gemfibrozil [].
BIP and FIELD: no benefit of bezafibrate and fenofibrate in reducing CHD events [].
ACCORD-lipid: no further reduction in CV events with fenofibrate plus simvastatin compared with simvastatin alone []
Post hoc analyses: subgroup of patients with low HDL and high triglycerides benefited from fibrates in terms of cardiovascular risk reduction
Inhibitors of CETP Inhibit CETP ↑HDL-C 28–138% Torcetrapib: increase in major cardiovascular events and mortality; increase in BP and aldosterone concentration []
Dalcetrapib: lack of benefit on cardiovascular outcomes []
Ongoing trials with anacetrapib and evacetrapib
PPAR-α and -δ agonists ↑ApoA-I, ApoA-II, LPL activity and RCT ↑ HDL-C 5–15% Toxicity of first-generation drugs: tesaglitazar and muriglitazar
AleCardio phase III trial with aleglitazar halted due to safety signals and lack of efficacy
ApoA-I mimetics Cause a shift from α-HDL particles to pre-β1-HDL particles No effect on HDL-C levels Improved inflammatory index in patients with clinical cardiovascular disease []
↑ Other aspects of RCT
Apo-AI synthesis stimulators (RVX-208) Induce de novo hepatic synthesis of apoA-I ↑ HDL-C 3.2-8.3% ASSURE: no incremental benefit on atherosclerotic plaque compared with placebo []
↑HDL particle 11 -21%
Recombinant HDL infusions Mimic native HDL ↑HDL-C 64% EFFECT: significant reduction in coronary atheroma volume compared to baseline but not to placebo []
Favorable impact on endothelial function []
Delipidated HDL ↑ RCT No effect on HDL-C Nonsignificant decrease in mean atheroma volume []
Preβ HDL ↑28×
LXR agonists ↑ Mobilization of intracellular cholesterol ↑ HDL-C up to 48% Reduced atherosclerosis in animal studies
↑ Transcription of ABCA1 and ABCG1
↑ Intestinal HDL generation
LCAT activators Contributes to maturation of HDL particles ↑ HDL-C 40–68% Reduced atherosclerosis in animal studies
MicroRNA-33 Inhibits ABCA1 mRNA degradation ↑ HDL-C 50% Inhibition of microRNA-33 promotes regression of atherosclerosis in LDLr–/– mice []
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The primary function of HDL is the transport of cholesterol from the peripheral tissues to the liver, playing a role in the biodistribution of lipids. HDL is known for is anti-atherogenic and anti-inflammatory properties, thanks to its uptake and return of the cholesterol stored in the foam cells of atherosclerotic plaques to the liver. Thus, reducing the size of the plaque and its associated inflammation.


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