Hi Hao,

In the title you mention plasma lipids and in the explanantion you put plasma LDL-C, which I figger is LDL-CHolesterol (Low Density Cholesterol). I suppose you mean LDL Cholesterol?

Well, the American Heart Association recommends all adults age 20 or older have their cholesterol, and other traditional risk factors, checked every four to six years. Your test report will show your cholesterol levels for example in milligrams per deciliter of blood (mg/dL). Your total cholesterol and HDL (High Denity sometimes called good cholesterol) cholesterol are among numerous factors your doctor can use to predict your lifetime or 10-year risk for a heart attack or stroke. Your test report will show your cholesterol levels in milligrams per deciliter of blood (mg/dL). To determine how your cholesterol levels affect your risk of heart disease, your doctor will also take into account other risk factors such as age, family history, smoking and high blood pressure.

The following variables are important:

Your Total Blood (or Serum) Cholesterol

- Total cholesterol score. It is calculated by the following equation: HDL + LDL + 20% of the triglyceride level. A total cholesterol score of less than 180 mg/dL is considered optimal according to the World Health Organisation (WHO).

- HDL (Good) Cholesterol. With HDL (good) cholesterol, higher levels are better. Low HDL cholesterol puts you at higher risk for heart disease. People with high blood triglycerides usually also have lower HDL cholesterol. Genetic factors, type 2 diabetes, and certain drugs, such as beta-blockers and anabolic steroids, also lower HDL cholesterol levels. Smoking, being overweight and being sedentary can all result in lower HDL cholesterol.

- Your LDL (Bad) Cholesterol. A low LDL cholesterol level is considered good for your heart health. However, your LDL number should no longer be the main factor in guiding treatment to prevent heart attack and stroke, according to the latest guidelines from the American Heart Association. For patients taking statins, the guidelines say they no longer need to get LDL cholesterol levels down to a specific target number. A diet high in saturated and trans fats raises LDL cholesterol. 

- Triglycerides. Triglyceride is the most common type of fat in the body. Normal triglyceride levels vary by age and sex. A high triglyceride level combined with low HDL cholesterol or high LDL cholesterol is associated with atherosclerosis, the buildup of fatty deposits in artery walls that increases the risk for heart attack and stroke.

A downloadable spreadsheet can be found at:

is a companion tool to the 2013 ACC/AHA Guideline on the Assessment of Cardiovascular Risk. The spreadsheet enables health care providers and patients to estimate 10-year and lifetime risks for atherosclerotic cardiovascular disease (ASCVD), defined as coronary death or nonfatal myocardial infarction, or fatal or nonfatal stroke, based on the Pooled Cohort Equations and the work of Lloyd-Jones, et al., respectively. The information required to estimate ASCVD risk includes age, sex, race, total cholesterol, HDL cholesterol, systolic blood pressure, blood pressure lowering medication use, diabetes status, and smoking status.

See: http://my.americanheart.org/professional/StatementsGuidelines/Prevention-Guidelines_UCM_457698_SubHomePage.jsp

Cheers,

Frank

That magnitude were LDL levels?. In some apoB gene defects that produce truncated apoB we can find many possibilities. What were the levels of triglycerides?. Genetically defined low levels of LDL, could be due to alterations of the ApoB gene, the MTTP, the PCSK9 gene or even some more. Sometimes, especially in heterozygotes, there is usually no clinical symptoms or metabolic defects (even been talk of a win-win situation for the patient). At other times, there may be defects in fat-soluble vitamins; extremely important if the defect affects apoB48 formation and less important if the truncated form is larger apoB. If the defect is in the MTTP, only know the effects in homozygotes (abetalipoproteinemia); they say that the heterozygotes are asymptomatic, but there is little experience on that. and even less in the defects with loss of function of PCSK9.

In any case, to venture an answer, it would be necessary to know the complete lipid profile, the concentration of vitamins A and E and the status of first-degree relatives.

Usually low lipid profile is observed in subjects after acute myocardial infarction, when the tissues go for repair. In my studies I found that immediate after AMI the patients lipid profile drastically when to the lowered side but after three months of follow up we observed that the lipid profile was again in the normal reference range. If we talk about lower LDL-C in normal subjects, it could be due to alternation in Apo B gene which can cause truncated LDL-C levels.

Low total cholesterol and LDL-and HDL- cholesterol are typical of HIV infection not on therapy or of chronic hepatitis . However risk factors for HIV and viral hepatitis should be investigated before screening patient.