HDL Cholesterol

 

14995023_mIf you’ve had a blood sample drawn for assessment of lipid panel you probably already know if your cholesterol level is acceptable or not.

You might also recall something about good and bad cholesterol and the ratio between these two.

Of course there is only one type of cholesterol. The “good” and “bad” has to do with the lipoproteins that carry cholesterol molecules in our blood stream.

A standard lipid panel provides information about total cholesterol, triglycerides, low density lipoprotein cholesterol (LDL cholesterol) and high density lipoprotein cholesterol (HDL cholesterol).

LDL cholesterol is often termed “the bad cholesterol” because high levels are associated with increased risk of heart disease.

On the other hand, HDL cholesterol is usually nicknamed “the good cholesterol” because high blood levels are associated with less risk of heart disease and low levels are associated with increased risk.

In other words; there is an inverse relationship between HDL cholesterol and the risk of heart disease. It is believed that HDL’s act as scavengers, picking up excess cholesterol in the blood and transporting it to the liver where it’s broken down.

Atherosclerosis and Heart Disease

Atherosclerosis is the hallmark of coronary artery disease. It may be described as a chronic inflammation of the arterial wall.

Atherosclerosis leads to formation of lesions or plaques that protrude into the lumen of the artery causing arterial narrowing, which can disturb blood flow. If this occurs in the coronary arteries, it may cause chest pain often termed angina pectoris.

The coronary arteries supply blood to the heart muscle. Acute heart attack (myocardial infarction) occurs when there is a sudden disruption of blood flow in a coronary artery.  A sudden blockage is usually caused by a rupture of an atherosclerotic plaque within the vessel wall, with subsequent formation of a blood clot (thrombosis) at the rupture site. Sudden disruption of blood flow causes death of heart muscle cells (infarction), and may impair the function of the heart muscle.

In 1961 the Framingham Study reported that high blood levels of cholesterol and high blood pressure were associated with increased risk of coronary artery disease and acute heart attack. This lead to the term “coronary risk factors” being defined.

Cigarette smoking, various fractions of cholesterol, insulin resistance, diabetes, obesity, physical activity, mental stress and depression are all examples of modifiable risk factors which, if present increase the risk of heart attack. However, although many risk factors have been identified, coronary heart disease remains a common disorder. Despite extensive research, our understanding of the mechanisms behind this disease is incomplete.

Lipids and Lipoproteins

Lipids, like cholesterol and triglycerides are important substances for the human body. They are used by cells for energy utilization, hormone production, bile acid formation and much more.

Because lipids are insoluble in blood they are carried by lipoproteins that transport them to various tissues and organs. Lipoproteins consist of cholesterol, triglycerides, phospholipids and protein. The lipoproteins act as carriers transporting important fats to the organs of the body.

There are five major types of lipoproteins; chylomicrons, very low density lipoprotein (VLDL), intermediate density lipoprotein (IDL), low density lipoprotein (LDL) and high density lipoprotein (HDL).

HDL and LDL lipoprotein particles have very different roles. Therefore, measuring the amount of cholesterol within these particles tells two different stories.

High levels of LDL cholesterol are associated with increased risk of heart disease, but high levels of HDL cholesterol are associated with low risk. HDL particles seem to be involved in clearing and removing cholesterol from arteries and atherosclerotic plaques, while LDL particles appear directly involved in the atheroslcerotic process.

HDL Cholesterol and HDL Particles

It is important to understand that measurements of HDL cholesterol only provide information about the amount of cholesterol carried by HDL particles. HDL particles differ in size and function, and  there are many types, both small and large.

HDL particle number can be measured by NMR (Nuclear Magnetic Resonance). Studies have shown that such measurements  are more strongly associated with atherosclerosis than measurements of HDL cholesterol.

Recent studies have shown that simple measurements of HDL cholesterol may not always reflect HDL function. Thus, there is growing evidence that in some cases HDL function may be impaired although measurements of HDL cholesterol are normal. Therefore, measuring HDL cholesterol may not be the best method to assess HDL function.

Although incomplete, HDL cholesterol is still the most widely used measurement to assess HDL.

Other metrics that are currently being tested include HDL particle number, average HDL size, specific HDL subclasses, and HDL functional properties.

HDL Cholesterol and Heart Disease

An inverse relationship exists between HDL cholesterol and the development of coronary artery disease. This means that high levels of HDL cholesterol are associated with low risk of heart disease and low levels are linked to high risk.

Based upon data from the Framingham Heart Study the risk of heart attack increases about 25 percent for every 5 mg/dl (0.13 mmol/L) decrement in blood levels of HDL-C. However, whether HDL cholesterol is a causal risk factor or merely a marker of risk is still intensely debated.

The most widely accepted hypothesis regarding the protective properties of HDL when it comes to atherosclerosis is that it promotes the uptake of cholesterol from tissues, including the vascular wall, and returns the cholesterol to the liver from where it is excreted. This process is often termed “reverse cholesterol transport”.

It has also been postulated that HDL’s may promote normal function of the endothelium which is the innermost layer of the arteries. Furthermore, HDL’s may reduce inflammation, protect against oxidation of LDL, and interfere positively with blood clotting (thrombosis).

What Are Optimal Levels of HDL Cholesterol?

The table below shows the reference values that are used when assessing HDL-cholesterol

HDL cholesterol (mg/dL)
(U.S. and some other countries)
HDL cholesterol (mmol/L
(Canada and most of Europe)
Below 40 mg/dL (men)
Below 50 mg/dL (women)
Below 1.0 mmol/L (men)
Below 1.3 mmol/L (women)
Too Low
40-49 mg/dL (men)
50-59 mg/dL (women)
1-1.3 mmol/L (men)
1.3-1.5 mmol/L (women)
Acceptable
60 mg/dL and above 1.6 mmol/L and above Very good

High HDL cholesterol, above 60 mg/dl (1.6 mmol/L) is associated with low risk of coronary heart disease. This pattern is more likely to occur in women than men.

Individuals with high HDL cholesterol often have large LDL particles. They are also likely to have low LDL particle number (LDL-P). LDL-P is a strong marker of risk for coronary artery disease.

Measuring apolipoprotein B or LDL-P may be helpful in order to estimate risk among individuals with high levels of both LDL-and HDL cholesterol. Calculating non-HDL cholesterol may also be useful to assess risk under these circumstances. Assessing the triglyceride/HDL cholesterol ratio may provide further information.

HDL cholesterol below 40 mg/dL (1.0 mmol/L) is considered too low and appears to be an independent risk factor for coronary artery disease. Furthermore, the definition of metabolic syndrome includes low HDL cholesterol as one of the five criteria for classification. Low HDL cholesterol is one of the most common phenotypes seen in persons with premature heart disease.

HDL cholesterol in the range of 20-40 (0.5-1.0 mmol/L) may appear in isolation, but is often associated with high triglyceride concentration. This is often associated with insulin resistance and increased risk of type 2 diabetes. Furthermore, some drugs, such as beta blockers may lower HDL cholesterol. Anabolic steroids can markedly reduce HDL cholesterol and should be suspected particularly in young healthy men with unexpectedly low HDL cholesterol levels.

HDL cholesterol less than 20 mg/dL (0.5 mmol/L) is uncommon. It can sometimes be attributed to very high triglycerides. It may also be due to rare genetic mutations, such as Tangier disease and fish-eye disease.

How Can HDL Cholesterol Be Influenced?

HDL-cholesterol can be influenced by lifestyle modification.

Smoking reduces HDL-cholesterol and smoking cessation is associated with modest increase in HDL-cholesterol.

Regular aerobic exercise can modestly increase HDL cholesterol. This increase is related to the frequency and intensity of physical activity, with greatest increases in HDL cholesterol occurring with frequent, low-intensity exercise, such as five 30-minute sessions per week.

Obesity is associated with low HDL cholesterol levels and high triglyceride levels. A negative correlation exists between HDL cholesterol and body-mass index (BMI), meaning that HDL cholesterol tends to be lower with increasing BMI. Weight loss usually raises HDL cholesterol.

Dietary choices affect HDL cholesterol. If the intake of fat is reduced, levels of LDL- and HDL cholesterol both decline. In one study comparing calorically balanced diets, those who consumed a low-fat diet had lower HDL-cholesterol than those who were fed a high-fat diet.

Intake of saturated fats usually increases both LDL- and HDL cholesterol. Substituting monounsaturated fat for saturated fatty acids may improve the ratio between LDL- and HDL cholesterol.

Limiting intake of simple carbohydrates is usually helpful, in particular if triglycerides are elevated. This is often the case in obese people and those with metabolic syndrome.

A diet rich in n–3 polyunsaturated fatty acids (omega-3) – sources include oils (olive, canola, soy, flaxseed), nuts (almonds, peanuts, walnuts, pecans), cold-water fish (salmon, mackerel), and shellfish — with limited carbohydrates, such as those found in ready-to-eat cereals, potatoes, white bread, and snack foods, can be recommended to increase HDL cholesterol levels.

Moderate alcohol consumption raises HDL-cholesterol but is generally not recommended for that purpose.

Several classes of medications increase HDL cholesterol levels; these include niacin and fibrates, and, to a lesser degree, statins. With the exception of statins, drug therapy that elevates HDL cholesterol has not been shown to improve outcome or reduce the risk of coronary events.

The 2013 American College of Cardiology/American Heart Association guidelines on the treatment of blood cholesterol to reduce cardiovascular risk does not make a recommendation to add therapy to raise low HDL cholesterol in patients who are on maximal statin therapy.

Comments

  1. Mie says

    Axel, you claimed that

    “With the exception of statins, drug therapy that elevates HDL cholesterol has not been shown to improve outcome or reduce the risk of coronary events.”

    This is the case only when statin therapy is the point of comparison. See e.g. this meta-analysis of niacin trials done before the “statin age” – niacin reduces the risk of coronary events:

    http://www.atherosclerosis-journal.com/article/S0021-9150(09)01031-4/abstract

    And fibrates reduce the risk of non-fatal MI

    http://www.amjmed.com/article/S0002-9343(09)00490-2/abstract

  2. michael goroncy says

    As you know Mie
    ‘Thrive” and another trial put the ‘Cross’ on Niacin (nicotinic acid,B3) due to the effectiveness of Statins.
    However if the patient cannot be treated to goal with statins…Niacin is an excellent add-on,
    elevating HDL and lowering ApoB.

  3. RichardLDL says

    Doc,

    what about the people who are born with very low HDL levels which persist throughout the lives of these people? Are these people at higher risk of developing CHD compared to people who have genetically elevated HDL since birth? What about the lean and fit rural Japanese of the 1950s who smoked more than the Americans did at the time and certainly had much lower HDL cholesterol than the Americans and Eastern Finns did, did these Japanese have more CHD compared to Americans? Care to elaborate?

    BTW, the people at UT Southwest Medical Center in Dallas Texas do not believe that atherosclerosis is a disease of inflammation. This is the school that harbors Brown & Goldstein and the people who did the preliminary work on PCSKY9-inhibitors. In animal models inflammation does not persist when LDL is lowered.

    The chief editor of American Journal of Cardiology stated:

    “..In contrast to feeding cholesterol and/or saturated fat, it is not possible to produce atherosclerotic plaques in herbivores by raising the blood pressure chronically, by blowing cigarette smoke in their faces for their entire lifetimes, or by somehow raising the blood glucose levels without simultaneously feeding them an atherogenenic diet. Presently, it is commonly stated that “atherosclerosis is an inflammatory disease.” Inflammatory cells, however, are infrequent in plaques of coronary arteries studied at necropsy or in endarterectomy specimens. When present, the few mononuclear cells—even giant cells—appear to be present due to a reaction to the deposits of lipid (pultaceous debris) present in the plaque.“ Inflammation” appears to be a surrogate for elevation of serum C-reactive protein or various cytokines (interleukins 1 and 6, tumor necrosis factor, etc), not for inflammatory cells in plaques. Thus, it is a definition situation, and the morphologic definition of inflammation is not applicable”.

    http://ncp.sagepub.com/content/23/5/464.full

    Prevention of heart disease: is LDL reduction the outcome of choice? Absolutely yes

    “There is only one well-established relationship between blood cholesterol lipid fractions and coronary artery disease (CAD) that meets all the Heiss and Tyroler criteria of causality. While there are a number of blood lipid fractions, only LDL cholesterol satisfies these criteria”

    http://www.ncbi.nlm.nih.gov/pubmed/16674358

  4. says

    My diet and lipid results are both usual, so I would like your opinion. I am 67 years old, body fat about 10% (5’11” 155 pounds). Last spring I developed peripheral neuropathy with an A1C of 5.7, despite being lean and eating a low carb diet. Since June I have eaten a very low carb, very high fat paleo diet. I feel very good on this diet, work full time and also exercise (running, cycling, kayaking, hiking and weight lifting) about 12 hours per week. I eat a lot of saturated, monunsaturated and omega-3 fatty acids, but try to avoid oils rich in omega 6 fatty acids. I eat a lot of nonstarchy vegetables, but almost no grains or potatoes.

    My total cholesterol, HDL and LDL were all high (268, 94 and 164 mg/dL, respectively and my triclycerides was low 48 on a test two weeks ago. Two months ago, the values were total 250, HDL 106 and LDL 140 with TG 43.

    I take extra Na in my diet to hydrate well befor exercise, getting my BP up to about 130/80 in the morning. By bedtime my BP is typically 110/65.

    I am assuming that my lipids are good, since my ratio of TG/HDL is about 0.50 (mg/dl units). In any case, I would prefer to have high LDL than to have nerve damage in my feet. What do you think? I have been an athelete all my life and can race at a high level in my age group.

    Bill

    P.S. In my view, the idea that saturated fat is a risk is false as long as one doesn’t combine high fat with high carbs.

    • Axel F Sigurdsson says

      Bill.
      I think you’re doing fine. Don’t worry too much about the numbers. As you said TG/HDL ratio is good and Non HDL-C is only borderline high. Although many experts would like to see LDL-C a bit lower, the low TG may indicate a pattern of predominantly large particles.

      In my opinion the important thing is to choose a healthy diet rich in fresh foods and avoid refined carbs and sugar. A food that makes you feel well. I also do believe exercise is a key feature of a healthy lifestyle. So, I guess the only thing I can say is “keep up the good work”.

  5. says

    hello my name rajesh bhardwaj my TRIGLYCERIDES level is 110.0mg AndHDL level is 99.0 mg And LDL level is164.0 VLDL level is 22.0 mg BUT CHOLESTEROL level is 285.o can there is any risk of heart deased. THank

  6. Scot says

    I had a blood test recently;
    My results were:
    Triglycerides 1.2 mmol/L
    Cholesterol 3.1 mmol/L
    HDL Cholesterol 1.1 mmol/L
    LDL Cholesterol 1.5 mmol/L

    Non- HDL Cholesterol 2.0 mmol/L

    I am 55 male, 184 lbs and 5ft 7in
    Is this normal?

  7. James S. says

    Dear Doctor Sigurdsson, Just had a concern about my very high HDL Levels. I am a 47 year old male, of South Asian heritage, no chronic illnesses, no medications for anything, on a paleo/LCHF diet, supplements that I use are fish oil, magnesium, vitamin d, vitamin k2, vitamin c and a probiotic. My Cholesterol profile is-(all mg/dl) TC 248, LDL 123 (measured directly) HDL 120, Trigs 67 and VLDL 5. My BP is about 115 over 70. CT Heart Scan score of 0 (3 years ago) and a fasting glucose of about 80-85 mg/dl. HBA1C 5.1 My HDL keeps rising every year and is worrying me. People keep telling me that there can be too much of a good thing. Please give me your feedback. Thanks.

    • Axel F Sigurdsson says

      Hi James
      I don’t think there’s a reason for you to worry. High HDL cholesterol isassociated with low risk in almost all studies. There’s now evidence suggesting that “too much” HDL-choletserol is a problem. Besides, a calcium score of zero confirms low risk.

  8. James S. says

    Sorry Doctor Sigurdsson, I forgot to mention I’m 5ft 8 inches tall, 134 lbs and I exercise moderately. I don’t drink excessively and do not smoke. Thanks.

Let me know what you think!