Why is LDL cholesterol "bad" and HDL cholesterol "good?"

Lipoproteins are actually bundles of fat and protein that enable the fat to be carried in the bloodstream without separating out. There are five main kinds of lipoproteins. Chylomicrons (meaning "little fatties") are synthesized by the gut to carry digested fat to the liver. VLDL, very low density lipoproteins, are synthesized by the liver to carry fat to the tissues. IDL, intermediate-density lipoproteins are less dense than LDL but denser than VLDL. They are less stable in the body and are poorly understood. They are formed when VLDL unloads some of its fat. LDL is similar to IDL and formed in the same way. HDL particles are synthesized by the liver to take cholesterol from non-liver tissue and return it to the liver for processing into hormones and other functions. The cholesterol molecules themselves are the same, but the fat to protein ratio is lower in HDL than in LDL, making HDL denser. The different particles can be differentiated by the so-called apolipoproteins, which are part of the protein shell that holds the fat in and suspends the particle in the blood. HDL and LDL have different apolipoproteins. LDL can bind to receptors on cells of blood vessel walls. In primates (including humans), this can allow deposition of cholesterol into the vessel wall (in an area called the tunica intima). These deposits may be attacked by immune cells called macrophages, and the piling on of these macrophages leads to the development of an atheroma. For unknown reasons, primates get atheromas in the intima, while other species like dogs generally do not. Atheromas have been seen in dogs, but they grow on the outer surface of blood vessels, and usually do not cause trouble. Atheromas are responsible for most cases of coronary artery disease. Because of the different roles HDL and LDL play, it was theorized that coronary artery disease would be related to low HDL and high LDL. Clinical and epidemiological evidence (for example http://www.ncbi.nlm.nih.gov/pubmed/19302897) shows a decrease in risk of heart disease and mortality, on the order of a 10% reduction in risk per 25mg/dL reduction in plasma LDL levels. Investigation of HDL as a treatment target is ongoing but I don't know if there are any good recommendations yet for increasing HDL aside from general health and well-being.

All cholesterols are "triglycerides". There are 3 different densities: Very Low Density Lipoproteins (VLDL) Low Density Lipoproteins (LDL) High Density Lipoproteins (HDL) None of them are "Bad". They are all essential. Your body needs lipids to repair cell walls. LDLs and VLDLs deliver the lipids to the cells. HDLs are heavy duty lipoproteins that go through and suck up all the left over LDLs and VLDLs in your blood stream. The problem comes when you have too many LDLs and VLDLs.  They are so small they're able to get between cells in your artery lining.  Your body will then exhibit an immune response to the LDLs out of place. Inflammation in the artery lining will occur, and over time can become cyclical and eventually cause a blockage or rupture. I suppose LDLs and VLDLs can be considered "bad", but it's not that simple since they are absolutely essential to life, it's just that too many is a bad thing. See also:

LDL is considered bad (and HDL good) because underlying systemic inflammation generally results in elevated LDL and depressed HDL numbers. The reality is that while HDL and LDL serve different metabolic functions, they are both extremely important. Low LDL is at least as harmful as if not more harmful than high LDL or low HDL. This whole story about bad/good being associated with LDL/HDL theory is total nonsense though, and is merely an extension of the perverse and WRONG lipid hypothesis. Just as the lipid hypothesis started out implicating fat and went on to implicate saturated fat, which is actually the healthiest and most important form of fat, it also started out implicating cholesterol and now has a focus on trying to separate out "good" cholesterol from "bad" cholesterol to make their theories somewhat plausible in the face of new evidence (like the fact that dietary cholesterol has absolutely no correlation with blood cholesterol), but it's still totally missing the point. High cholesterol correlates with heart disease, but is not a causal agent. Cholesterol is released by the body to patch up vascular inflammation, like Spackle on a wall. It is the inflammation that CAUSES both the heart disease and the high cholesterol, not the cholesterol that causes the heart disease. For more on cholesterol and disease, and how the science got it so f***ing wrong, check out the book Good Calories, Bad Calories by Gary Taubes. For a nice little primer, Dr. Harris wrote a cool little blog post recently on the cholesterol hypothesis: http://www.paleonu.com/panu-weblog/2010/7/21/statins-and-the-cholesterol-hypothesis-part-i.html.

The LDL as ultra-villain hypothesis is dying a slow but deserved death. The writing is on the wall. The main causative force in coronary artery disease is inflammation, not cholesterol. Although cholesterol is an important pathophysiologic mediator, and reducing LDL particle count will reduce the rate of atherosclerosis, the number of serum LDL particles is more or less independent of dietary cholesterol. Unfortunately, there is a great deal of inertia in clinical medicine. The old guard and pharmaceutical industry all have vested interests, and change even in the face of overwhelming evidence, will come slowly.

LDL cholesterol builds up fat around your arteries and it can cause blockages to your heart and brain a.k.a heart attack or stroke. HDL actually prevents fat from building up in your arteries. Healthy amount of cholesterol should be < 200 mg per DL total: LDL < 130 mg per DL HDL > 40 mg per DL If you want to learn more about blood lipid, you can check out my detailed video here: