Low density lipoprotein cholesterol (LDL-C) is an important factor when assessing the risk for developing heart disease. LDL -particles, in particular those who are small and dense, are atherogenic and increase the risk of cardiovascular disease (CVD). There is a strong and graded correlation between LDL-C and the risk of CVD, both in women and men, although this has been debated by some investigators. The evidence that reducing plasma LDL cholesterol reduces CVD risk is unequivocal. According to the European Society of Cardiology, the results of epidemiological studies as well as trials with angiographic or clinical endpoints conﬁrm that the reduction of LDL cholesterol must be of prime concern in the prevention of CVD.
Cholesterol is an organic molecule included in the sterol family. Sterols are chemical substances, generally classified as lipids, although they are chemically different from other types of dietary fat, such as triglycerides and phospholipids. Unlike triglycerides, sterols contain no fatty acids. Because of the publicity generated by its proposed role in atherosclerosis and cardiovascular disease, Cholesterol is the best known sterol, mainly because of its proposed role in atherosclerosis and cardiovascular disease.
Most people are aware that there are two types of cholesterol, depending on the types of proteins that carry the cholesterol molecules. High density lipoprotein cholesterol (HDL-C) is often termed the “good” cholesterol while low density lipoprotein cholesterol (LDL-C) is usually termed the “bad” cholesterol. These are two of five major lipoproteins that enable transport of different fat molecules in the body, including cholesterol. The other lipoproteins are chylomicrons, IDL (intermediate density lipoprotein) and VLDL (very low density lipoprotein, mainly triglycerides).
Cholesterol travels throughout the body in little packages called lipoproteins which are made up of lipids and proteins. LDL is called low-density lipoprotein because LDL particles tend to be less dense than other kinds of cholesterol particles. It has been known for decades that LDL-cholesterol is somehow involved in the atherosclerotic process. Although its exact role on the pathogenesis of heart disease is complex, and still somewhat debated, cardiovascular disease as we know it today, would not exist without LDL-cholesterol.
Cholesterol is a major structural component of cell membranes and is especially abundant in nerve and brain tissue. It is also a precursor molecule. For example, vitamin D is synthesized from cholesterol. Cholesterol is also a precursor of important hormones such as progesterones, glucocorticoids (cortisol), mineralcorticoids (aldosterone), androgens (testosterone) and estrogens.
Cholesterol occurs only in foods of animal origin. Because the body can synthesize cholesterol, it is not needed in the diet. Most of our cholesterol is synthesized by the liver. Studies have shown that increasing dietary cholesterol may reduce synthesis, although probably not by an equivalent amount.
LDL-C (the bad cholesterol)
Elevated levels of LDL-C in the blood are associated with increased risk of atherosclerosis and heart disease. This has earned LDL-C the nickname “bad cholesterol”. There are special receptors on cell surfaces that bind LDL-C, these are called LDL-receptors. A lack of LDL-receptors may reduce the uptake of cholesterol by the cells, forcing it to remain in the circulation which may be disadvantageous. In familial hypercholesterolemia, which is a genetic disorder, the body is unable to remove LDL from the blood. This leads to high levels of LDL-C in the blood, which may severely increase the risk of cardiovascular disease, even at young age.
Blood tests typically report LDL-C. These numbers are usually based on calculation, using the Friedewald formula which includes total cholesterol, HDL-C and triglycerides. This formula relies on the assumption that the ratio of triglyceride to cholesterol is constant, which is not always the case. Thus, LDL-C calculations may have limitations when blood triglyceride levels are either high or low. Direct LDL -C measurements are also available, but are less often done due to higher costs. Cholesterol levels are measured in milligrams (mg) of cholesterol per deciliter (dL) of blood in the US and some other countries. Canada and most European countries measure cholesterol in millimoles (mmol) per liter (L) of blood. Some studies show that the number of LDL particles (LDL-P) may be a better predictor of risk than LDL-C. LDL particle size may also be important when assessing risk.
How is LDL-C interpreted?
It is considered important to keep cholesterol levels, especially LDL-C within certain limits. If you have other risk factors for heart disease, such as high blood pressure, diabetes, or if you smoke, keeping LDL-C low becomes even more important.
Here you can see how LDL-levels are generally looked at in terms of risk:
- above 190 mg/dL (4.9 mmol/L) is considered very high
- 160 – 189 mg/dL (4.1 – 4.9 mmol/L) is considered high
- 130 – 159 mg/dL (3.4 – 4.1 mmol/L) is considered borderline high
- 100 – 129 mg/dL (2.6 – 3.3 mmol/L) is considered near ideal
- below 100 mg/dL (below 2.6 mmol/L) is considered ideal for people at risk of heart disease
- below 70 mg/dL (below 1.8 mmol/L) is considered ideal for people at very high risk of heart disease
How can you influence your LDL-C?
If your LDL-C is high, your doctor will probably suggest lifestyle changes. Quitting smoking will be helpful and so may eating whole corn, oatmeal, olive oil, beans, fruit and vegetables. Most doctors will recommend eating less fat and cholesterol from meat and dairy products. Some studies show that low carbohydrate diets may positively affect LDL particle size. Regular exercise is desirable. Losing weight may be helpful. If lifestyle changes don´t help, your doctor may suggest medications that lower cholesterol. So-called statins are the most commonly used drugs for lowering cholesterol. Studies have shown that statins improve prognosis among patients with coronary artery disease. Their role for treatment of raised LDL-C in healthy people (primary prevention) is less clear. The decision to give statins in primary prevention should usually depends on total risk, rather than LDL-C itself.