Blood Lipids
Relevant Social Security Medical Listings
No specific listing, but may appear in medical records.
Type
Objective/Chemistry (Blood)
Can SSA Purchase?
Yes, but the SSA would only suspect hyperlipidemia in a child if the treating doctor had already diagnosed such a disorder, and follow-up information were need to determine if the listing were satisfied despite treatment. Test results should always be considered as part of the evidence of record when provided by a treating doctor whether in child or adult claims.
Purpose
Predict the risk of atherosclerotic vascular disease, especially coronary artery disease (CAD) and related complications such as myocardial infarction (heart attack) and death.
General
Cholesterol and triglycerides are the main blood lipids (fats). Elevated blood cholesterol is an important risk factor for development of coronary artery disease (CAD), also known as coronary heart disease (CHD). Elevated blood triglycerides can also constitute a risk factor. Since lipids are insoluble in water, they must transported in the blood by special proteins known as apolipoproteins or apoproteins. The resulting lipid-apolipoprotein complexes are called lipoproteins. Apolipoproteins perform other functions than carrying lipids in the bloodstream. They also solubilize lipids inside cells, so the lipids can be transported out of cells into the blood; they bind to receptors on the surface of cells so that lipoproteins can be transported into cells; and they participate in enzymatic processes involving the degradation of lipoproteins.
A particular type of lipoprotein may contain more than one type of apolipoprotein subunit. Examples of possible apolipoprotein subunits are A-I, A-II, B-100, C-II, C-III, and E. Apolipoprotein A is taken to mean apolipoprotein A-I.
Both cholesterol and triglycerides are necessary for human life, and animal life in general. Triglycerides are used for storage fat. Cholesterol is needed for cell membranes and vitamin D synthesis, as well as sex and adrenal hormones.
Chylomicrons perform the role of carrying away dietary fat from the intestine, and consist of about 95% triglyceride. Chylomicrons are collected in the lymphatic system and then enter the bloodstream through the thoracic duct at the junction of the left subclavian and jugular veins. The thoracic duct is the largest lymphatic channel in the body.
Very low-density lipoprotein (VLDL) is a triglyceride-rich particle synthesized in the liver, and can provide triglycerides for the body’s energy needs even in a fasting state.
Intermediate-density lipoproteins (IDL) are derived from VLDL. Low-density lipoprotein (see below) is derived from IDL.
Low-density lipoprotein (LDL) and high-density lipoprotein (HDL) carry most of the cholesterol. LDL cholesterol (LDL-C, LDLC) is popularly known as “bad cholesterol,” because it is responsible for atherosclerosis. LDLC is mainly transported in the blood by apolipoprotein B. HDL cholesterol (HDL-C, HDLC) is known as “good cholesterol,” because it helps protect arterial walls from the fatty build-up of atherosclerotic plaques by removing cholesterol from tissues and transporting it to the liver. Apolipoprotein A-I is important in the transport of HDLC. Although total HDL is usually measured when studying risk for coronary artery disease, there are actually three HDL fractions: HDL1, HDL2, and HDL3. In individuals with Type 2 diabetes mellitus, HDL2 is a better predictor for heart disease than total HDL. HDL has its origin in various tissues.
Increased blood lipids of any kind is called hyperlipidemia. A diet high in fats (total fat, saturated fat, cholesterol), and lack of regular exercise contribute to the hyperlipidemia of high cholesterol. Obesity, Type II diabetes mellitus, lack of regular exercise, alcohol, and excessive sugar intake contribute to the hyperlipidemia of high triglycerides (hypertriglyceridemia). These rules apply to children as well as adults. However, genetic contributions to hyperlipidemia can be strong and there are several such disorders, such as familial hypercholesterolemia and familial hypertriglyceridemia.
Technique
Chemical laboratory tests are performed on a sample of venous blood. Usually, serum cholesterol is measured. Prolonged application of a tourniquet (over 2 minutes) should be avoided, as this can increase the cholesterol content of the sample by 2 – 5%.
For meaningful results, the patient should have maintained a stable diet and body weight for at least 3 weeks prior to testing. Also, the patient should fast (take water only) for 12 hours before testing.
Posture can affect cholesterol levels, and repeat tests should be taken in the same body position. Cholesterol levels can drop by 10 – 15% after 20 minutes lying down. Also, changing form a standing to a sitting position can lower cholesterol values by as much as 6% after 20 minutes.
The specific nature of blood lipid testing depends on the nature of the information sought. Simple total cholesterol testing can be done in a few minutes in a physician’s office. Accurate testing for multiple lipids and lipoproteins must be done in a laboratory, e.g., lipoprotein electrophoresis. Lipoprotein (a) is measured with enzyme-linked immunosorbent assay (ELISA).
Interpretation
Note: Blood lipids may be expressed in either conventional (mg/dl, which is the same as mg%) or international units (SI units, mmol/L). To convert cholesterol (total, HDLC, or LDLC) from conventional to SI units, multiply by 0.0259. To convert cholesterol from SI units to conventional units, multiply by 38.61. To convert triglycerides from conventional to SI units, multiply by 0.0113. To convert from triglycerides from SI units to conventional units, multiply by 88.5.
Cholesterol
Serum Total Cholesterol
Desirable: less than 200 mg/dl (5.17 mmol/L)
Borderline: 200 – 239 mg/dl (5.17 – 6.18 mmol/L)
High: equal to or greater than 240 mg/dl (6.21 mmol/L)
High-density Lipoprotein Cholesterol
Desirable lower limit: 40 mg/dl (1.04 mmol/L)
Most beneficial: greater than 60 mg/dl (1.55 mmol/L)
Low-density Lipoprotein Cholesterol
Desirable: less than 130 mg/dl (3.36 mmol/L)
Borderline: 130 – 159 mg/dl (3.36 – 4.11 mmol/L)
High: greater than 160 mg/dl (4.14 mmol/L)
Very Low-Density Lipoprotein Cholesterol (VLDL)
Normal: About 30 mg/dl; normal values often cited as 5 – 40 mg/dl
Triglycerides
Desirable: Less than 200 mg/dl (2.26 mmol/L)
Borderline high: 200 – 400 mg/dl (2.26 – 4.52 mmol/L)
High: Over 400 mg/dl (4.52 mmol/L)
Risks
Age influences risk of coronary artery disease; a younger individual with the same elevated cholesterol level as an older individual carries higher long-term risk. Serum also cholesterol tends to steadily increase with age. Overall risk is also influenced by the presence or absence of other diseases (e.g., diabetes mellitus, hypertension) as well as whether there is already established CAD, and other risk factors such as obesity, smoking, and sedentary lifestyle. Any evaluation of a blood lipid level must take into consideration all of the factors influencing a patient’s medical condition. A blood lipid level may be low enough to be considered no significant risk in the absence of other risk factors, but be considered elevated when other risk factors such as obesity and smoking are present.
There are a large number of studies and statistics regarding various kinds of risks in regard to blood lipids, especially cholesterol. In evaluating this data, careful attention should be paid to the exact type of risk specified, and population group studied (e.g., men, women, children).
It is important to recognize that blood lipid levels are not “normal” or “abnormal” in the sense that, for example, an elevated serum creatinine reveals kidney dysfunction. Lipid levels are interpreted in light of their capacity to influence the risk of cardiovascular disease.[1] It is in perspective of this risk that lipids may be considered too high. The distinction is important, because many people in the U.S. have cholesterol levels that put them at high risk and should not be considered “normal” just because they constitute a substantial portion of the population. That population, with its diet high in junk food and saturated fats, pays a high mortality price for its resulting hyperlipidemia. Chinese, on the other hand, may normally have a serum total cholesterol level under 120 mg/dl if not eating American or other Western food; vascular disease such as coronary artery disease (CAD) is virtually non-existent at such levels. Most Americans are not willing to radically alter their diet. However, there is a substantial long term improvement in risk with cholesterol levels of under 200 mg/dl in adults, and fatty vascular lesions may actually regress at levels of less than 150 mg/dl. It is not possible to completely remove the risk of vascular disease, but risk can be markedly lowered in the U.S. population. It should be remembered that blood fat levels are only one determinant of the development of coronary artery disease. Genetic predisposition plays a strong role, and a significant number of people with heart attacks actually have “normal” cholesterol levels.
Hypertriglyceridemia is associated with a higher risk of CAD when a patient also has decreased HDLC.
There is a steady increase in of risk of coronary artery disease (CAD), heart attacks, and death as total cholesterol increases. Total cholesterol in males of about 180 mg/dl is associated with a 6 year death-rate from CAD of about 4 per 1000 men. With a cholesterol of 240 mg/dl the death-rate is doubled, and climbs to about 17 per 1000 men with a total cholesterol of 300 mg/dl.
Increasing levels of HDLC are associated with decreased risk of CAD in both men and women. In men, a low HDLC of 25 mg/dl has twice the average risk of CAD. Average risk is at 45 mg/dl for men. Women, however, have an average risk at 55 mg/dl and 1.6 times average risk with a HDLC of 45. At a HDLC of 65 mg/dl a man has half the average risk, but a woman doesn’t halve her risk until her HDLC reaches 70 mg/dl. There is evidence that levels of the enzyme hepatic lipase that breaks down HDLC are inversely related to the risk of developing coronary artery disease. People with the highest levels of hepatic lipase apparently have half the risk of CAD as those with the lowest levels, but more research needs to be done on this issue.
Sometimes, a total cholesterol/HDLC ratio is used to express risk. In middle- aged men (50 – 70 years) a average risk of CAD is associated with a ratio of about 4.4, while risk drops to half average with a ratio of about 3.0. Risk is doubled with a ratio of about 6 and four times higher than average with a ratio of about 9.5.
It is the LDLC that accounts for much of the increased risk associated with increases in total cholesterol. A 10% reduction in total cholesterol may be associated with as much as a 20% reduction in risk of death from CAD, and an even higher (17%) reduction in the incidence of heart attacks. However, it is a mistake to assume that control of LDLC alone will control risk. Almost 75% of people with the first onset of acute coronary syndrome have LDLC below 130 mg/dl, nearly half have LDLC below 100 mg/dl, and about 17% have LDLC values below 70 mg/ml. This is a wake-up call to the previous conventional wisdom that LDLC is the only lipid that needs control. There is increasing awareness that this is not the case.
All of the cholesterol forms that are not HDLC are sometimes clumped into the term “non-HDL cholesterol.” Non-HDLC consists of two atherogenic components: LDLC and VLDLC, i.e., the cholesterol carried by LDL and VLDL. Very low-density lipoprotein (VLDL) levels have largely been disregarded in the medical literature in regard to coronary risk calculations, possibly because the triglyceride-rich VLDL particles were assumed to only confer risk through their triglyceride content, and triglycerides are already considered in risk management. In other words, the risk of elevated non-HDLC has been assumed to be associated only with elevated LDLC. However, there is now evidence that elevated VLDL levels are an independent risk factor for development of CAD—that is, still present when adjusted for other known risk factors. In fact, a specific VLDL receptor has been identified in tissues that cannot be occupied by LDL. Because of the risk conferred by increased VLDLC, non-HDL cholesterol is a better determinant of risk than the conventionally considered LDL alone. The increased risk of CAD with increased VLDLC exists whether triglyceride levels are low (less than 200 mg/dl) or high (200 mg/dl or more)—clear evidence that triglyceride levels do not account for all the risk in elevated VLDLC. Most physicians and laboratories do not measure VLDL in assessment of risk, but perhaps this should change.
Apolipoprotein A-I (Apo A-I) is the major protein of HDL; therefore, increased apo A-I levels are associated with decreased risk of atherosclerosis such as coronary artery disease. Normal values for Apo A-I in males are 119 – 240 mg/dl. However, normal values vary significantly between laboratories, and some laboratories have different normal ranges for men and women. It should be noted that the long-held belief that HDLC is always a “good cholesterol” and that high values mean decreased cardiovascular risk may be incorrect without further qualification. It is questionable that HDLC taken alone can be used as a marker for cardioprotection; drug trials that increased HDLC surprisingly increased adverse cardiovascular events. Recent evidence shows that when Apo A-I is not also increased, increasing HDLC is not only not cardioprotective—it is an adverse risk factor, particularly at levels of greater than 70 mg/dl. Very large HDLC particles greater than 9.5 nanometers (nm) are also thought to be an additional adverse risk factor. These findings fly in the face of decades of conventional wisdom—the assumption that HDLC per se is beneficial. Most lipid laboratories serving clinical medicine report HDLC, but not Apo A-I. It is important that Apo A-I be measured as a part of a lipid profile, as the amount of risk to attach to HDLC levels otherwise cannot be properly evaluated. However, additional research is going to be required regarding the relationship of Apo A-I, HDLC, and risk to get a clearer understanding of risk.
Apolipoprotein B (Apo B) is the major protein of LDL; therefore, increased Apo B levels are associated with increased risk of atherosclerosis such as coronary artery disease. Normal values for apolipoprotein B are 52 – 163 mg/dl. However, normal values vary significantly between laboratories, and some laboratories have different normal ranges for men and women. It was originally thought that low density lipoproteins and Apo B were surrogates for the same cardiovascular risk—thus, it was unnecessary to measure both. Additional studies have shown that this viewpoint was in error: non-high density lipoproteins (such as LDL) and Apo B levels are independent risk factors for coronary artery disease. Apo B levels below 128 mg/dl are not thought to be associated with increased risk for CAD; for high levels of Apo B the risk can be doubled.
Since elevated levels of apolipoprotein A-I carry decreased atherosclerotic risk and elevated levels of apolipoprotein B carry increased risk, their ratio is sometimes used to evaluate the risk of coronary artery disease. In this regard, the normal apo B/apo A-I ratio is considered to be 0.35-0.98, and this ratio may be more useful for prediction of risk than the measurement of individual apolipoproteins.
Lipoprotein (a) should not be confused with apolipoprotein A. Increased levels of lipoprotein (a) are associated with increased risk of atherosclerosis. Values exceeding 20 mg/dl are generally considered abnormal; however, some laboratories put the upper limit of normal at 30 mg/dl. Like many other tests, “normal” vs. “abnormal” is a question of risk, not any absolute value required by nature. By the time lipoprotein (a) reaches 30 mg/dl, the risk of coronary artery disease may be doubled.
Accuracy of Blood Lipid Measurements
Lipid profiles are performed in hospital or other clinical laboratories and are more complex than a simple total cholesterol screening test. They typically consist of total cholesterol, HDLC, LDLC, and triglycerides. More sophisticated testing (e.g., lipoproteins) may also be done.
LDLC measurement in the past has usually been done using the Friedewald formula, because direct measurement of LDLC required expensive and time-consuming ultracentrifugation.
The Friedewald formula for LDLC in mg/dl is:
LDLC = total cholesterol – (HDLC + 0.20 x triglycerides).
The Friedewald formula for LDLC in mmol/L is:
LDLC = total cholesterol – (HDLC + 0.46 x triglycerides).
The Friedewald equation is too inaccurate when triglyceride levels are over 400 mg/dl. Even when triglyceride levels are under 400 mg/dl, the Friedewald equation can lead to underestimation of the true LDLC level, and is subject to the combined errors of the three separate tests needed for the calculation.
Direct LDLC measurement is now possible using an immunoseparation technique that is much more accurate.
Comments
In men and women of all ages, total cholesterol can be reduced about 5% by eating frequent (6 or more) meals daily, rather than a few large meals.
