They're actually missing several points, and have been missing it for ages. Maybe even intentionally.
1. As pointed out, cholesterol is not the problem, but is just a symptom. Many cases of heart attacks or strokes occur in people with normal cholesterol values. And even the normal level is being disputed. From 200, drug manufacturers want that lower (so more of their drugs will be used), while other health authorities would even say that 300 is still normal.
2. LDL is simply HDL plus cholesterol. Any biochemistry or physiology reference shows that the liver makes cholesterol and fats out of excess blood glucose. These have to be transported away from the liver, and so they are attached to HDL, thus converting it to LDL and VLDL, to be sent off to the blood. The obvious proof is the way statins act -- by inhibiting the enzyme that converts glucose to cholesterol. So blood cholesterol does not come from dietary fat or cholesterol, but rather, from dietary carbohydrates that increase blood glucose levels (high glycemic load carbs).
If we want to decrease our LDL levels, we simply control our blood glucose and insulin levels. We then deprive the mechanism of raw materials with which to produce LDL.
HDL means high density lipoprotein. So if all we want is to increase our HDL levels, we simply take in more protein. (We don't have to worry about the "lipo" part because our body can easily make fat.)
3. Many statin users suffer heart attacks BECAUSE of statins themselves. These drugs inhibit the liver and cellular enzyme that makes coenzyme Q10. Coenzyme Q10 is an essential co-factor in the energy producing mechanisms of cells (in the electron transport chain). The heart is particularly susceptible to lack of CoQ10 because it's continually pumping. Other muscles are similarly dependent on CoQ10 and thus, statin users usually suffer muscle pain as well, possibly irreversible rhabdomyolysis (lysis/death of muscle cells). So statins may lower one's cholesterol levels, but they also make the user more susceptible to heart attacks. (I strongly suspect that the enzyme inhibited by statins is the same one used to make cholesterol as well as CoQ10.)
4. High blood cholesterol/LDL does not automatically mean attachment to arteries. Many are now realizing that there must first be an initial damage to the arteries before cholesterol attaches to them. And LDL itself has to be oxidized for it to attach to arteries. Initial damage has been attributed to various causes including subclinical scurvy (Dr. Rath), Chlamydia
infection, homocysteine damage, free radical damage (also caused by glucose), and the mentioned LDL oxidation (among others).
Of course, all these fail in comparison to the profits to be made by pushing statins for the smallest possible reason.