Low-density lipoprotein carries cholesterol & triglycerides from the liver to peripheral tissues.
Is LDL cholesterol bad?
In the natural human process, there is nothing as bad or good cholesterol.
Instead, all cholesterol is excellent! In few occasions, it may end up as bad, why? Cholesterol by accident enters and stick inside the arterial wall. More specifically the coronary or carotid artery. This stuck cholesterol leads to a cascade of the immune response. This immune response results in the obstruction of the artery.
Low-density lipoproteins are good. But, it becomes bad when oxidized, size shrinks, or increase in number.
The primary function of LDL is to deliver cholesterol from the liver to the peripheral cells. Where cholesterol utilized for cellular membrane stability and other health-giving cellular functions.
LDL receptors are on cellular membranes to receive this cholesterol molecule. In 1973, Nobel prize winner Brown and Goldstein discovered LDL receptors.
Unutilized excess LDL-C is collect by the HDL-C, and return to the liver for recycling and reuse. LDL-C is supplying cholesterol (nutrient) to the cellular membranes. Then, it is nonsense to labeling it as “bad".
Laboratory, epidemiological and clinical evidence suggests that LDL-C has a protective role against infection. Many researchers suggested the blood lipids play an important role in the immune system.
Oxy-Cholesterol (Oxidized LDL-C)
LDL is not causing damage; instead, oxidized LDL causing harmful plaque.
What is oxidized LDL? LDL reacts with oxygen and becomes little damaged, like rancid oil.
LDL cholesterol is harmless, until oxidized.
Oxy-cholesterol is a more important heart health indicator. Free radicals in the blood, oxidized the LDL cholesterol to form oxy-cholesterol. Accumulation of this oxidized LDL cholesterol can seriously affect the arterial health.
Usually, small dense LDL particles are always ready to oxidize into oxy-cholesterol.
Research confirms, oxidized-LDL trigger inflammation. So the important cholesterol number is not the LDL cholesterol level. Instead, the amount of the oxidized cholesterol.
One way to inhibit LDL oxidation is by taking antioxidant supplements.
Many studies confirm the ability of ubiquinol CoQ10 to inhibit LDL oxidation. Even it is better than lycopene, alpha-tocopherol, and other lipid-soluble antioxidants.
Another study demonstrates pomegranate has anti-LDL oxidation effects better than any other nutrients.
LDL cholesterol level once reported as a risk for atherosclerosis, but in reality not.
- Optimal: Less than 130 mg/dL (< 3.36 mmol/l)
- Borderline: 130 to 159 mg/dL (3.36 to 4.11 mmol/l)
- High: More than 159 mg/dL (> 4.11 mmol.l)
LDL-C is a weak predictor of heart disease. Whereas, LDL particles number and size are a better predictor.
Where is from LDL-C comes?
The liver synthesizes VLDL to deliver fat and cholesterol to cells around the body. VLDL after delivering fats to the cells, shrink in size called VLDL remnants. The liver makes LDL using this VLDL remnant. Thus, if you want to know which raises LDL level? You should know which raises the VLDL level? Because; VLDL is the only source of LDL. Thus, dietary lipid does not raise LDL cholesterol level.
Any minor liver problem, inflammation, infection, or slow metabolism (hypothyroidism) may raise LDL level.
Will high LDL cause Atherosclerosis?
High levels of LDL-C will not damage the endothelium; instead, oxidized-LDL might cause damage. For instance, if a high LDL-C-level causes atherosclerosis. Then, how a person with low LDL-C develops atherosclerosis.
In-depth research shows, there is two type of LDL cholesterol. LDL subtype pattern A is big fluffy molecules like a cotton ball. This pattern A molecule will not cause any damage. LDL subtype pattern B is small dense molecule like a bullet. This pattern B molecule would cause damage. This LDL oxidize instantly and is a risk for heart disease.
High level of LDL-C is useless information. Until you know the levels of small dense (bad) LDL and big fluffy (good) LDL.
Research study demonstrates, cholesterol is important for the immune system. LDL (bad cholesterol) deactivates more than 90 % of the most toxic bacterial byproducts. Reference: Infection and Immunity, July 1989 vol. 57 No.7 2237-2245.
What causes coronary heart disease? LDL-C or LDL-P
High LDL cholesterol (LDL-C) is not facilitating plaque formation. Instead, the elevated LDL particle (LDL-P) numbers increase the risk of atherosclerosis.
Only apoB containing lipoprotein penetrates endothelium of arterial wall leads to atherosclerosis. Unless an apoB lipoprotein is piercing into the endothelium, no chance for plaque development.
How could LDL-P do a sinister by puncturing the endothelial cell? Well, it may be due to raising the LDL particle number is the key to this evil act.
Once the LDL-P struck into the endothelium, which is unable to clear by the immune system. Then after few days, these LDL-P’s get rancid by subjecting to oxidation. This oxidized LDL-P elicits an inflammatory immune response. This immune response leads to serious disturbance and breaks out of immunological warfare. Monocyte, macrophages and mast cells of immune system investigate the inflammation. Once it locates the struck LDL-Ps, it sends LDL's to cement the damage it caused. Mostly, this immune response turns successful. In other instance, immune response failed and became chronic due to too much of LDL-P number. This chronic immune failure leads to plaque formation, thrombosis, and heart disease.
LDL-P is a better predictor of cardiovascular risk than LDL-C.
- Optimal: Less than 1000 nmol/L
- Borderline: 1000 to 1299 nmol/L
- High: More than 1299 nmol/L
Apo B level is a better predictor of cardiovascular risk than the LDL-C did. Apo B is a protein of the atherogenic LDL and VLDL particle. One Apo B particle associated with one LDL or VLDL molecule makes it a good indicator of CVD risk.
- Optimal: Less than 60 mg/dL (<0.6 g/l)
- Borderline: 60 to 80 mg/dL (0.6 to 0.8 g/l)
- High: More than 80 mg/dL (>0.8 g/l)