Hello, good readers out there!
I have been suffering from a bit of “paralysis by analysis” combined with writer’s block for a while now and could not come up with a topic to cover next. Then, a couple of weeks ago, I came across an article where the authors have listed several common nutrition & fitness myths and debunked them. In this very article, however, one fairly disturbing notion has caught my eye: they mentioned LDL and called it “the bad cholesterol”! I don’t even know where to begin, really. First, LDL is not cholesterol. Nor is it inherently bad! How do people get this idea in the first place, I wondered. Then I ran a quick Google search, and the first item on the menu was this: http://www.webmd.com/cholesterol-management/ldl-cholesterol-the-bad-cholesterol. Yes, poor LDL seems to have a bad rep with the media. Even some scientific (!) articles sometimes refer to it as “bad”. It is, however, very wrong to think of LDL as bad. Actually, it serves quite an important purpose of transporting cholesterol into the cell when it’s needed there. It does play a crucial role in the pathogenesis of atherosclerosis but that does not make it essentially guilty – it’s what makes LDL “go bad” that’s hurting our blood vessels.
Let’s recap: what is LDL, really, and what do we need it for? LDL stands for low-density lipoprotein. There are several groups of different lipoproteins available to our bodies, different in both particle size and density. The density of lipoprotein particles depends on the lipid-to-protein ratio, with low-density lipoproteins having a higher lipid-to-protein ratio than high-density lipoproteins (HDL, also known as “good cholesterol” – which, as you might have guessed, is also technically wrong). LDL is actually not just one type of particle but a whole group of differently sized protein assemblies. So, there are different types of LDL particles within the LDL group – some are quite small, some are bigger. It is the smaller LDL particles that show some association with pathological conditions, and the same is true for the levels of very-low density LDL (vLDL). All LDL particles have a sole purpose of carrying lipids (among them cholesterol) through the bloodstream. VLDLs mostly carry triglycerides and some cholesterol. Once vLDLs deposit their triglycerides into fat cells, for example, they turn into LDL particles – either big, fluffy ones or small dense ones – that mostly carry cholesterol and have the sole purpose of delivering it to the cells. So what is it that makes LDL the bad guy? Well, the particles themselves do not pose any danger until their ratio changes towards production of small, dense LDLs that have a potential to “invade” the arterial walls. This is where the size comes into play: smaller particles are thought to pass through the wall with more ease, which makes sense. Once those tiny LDLs are stuck there, the fats that they are carrying are exposed to high concentrations of oxygen (and eventual reactive oxygen species!) in the blood (“fun” fact: atherosclerotic plaques only occur in arteries – exactly for this reason!). They become oxidized, turning normal LDL into oxLDL*, which is the real culprit in heart disease. Accumulation of oxLDL attracts macrophages, cells of the immune system, which come to clear the arterial wall of oxLDL. However, if too much oxLDL is produced, it starts to accumulate within macrophages, which subsequently turn into foam cells and accumulate at the endothelial wall. OxLDL per se is also capable of inducing endothelial activation and smooth muscle cell proliferation (see “The Dynamics of Oxidized LDL during Atherogenesis” by Itabe et al, 2011). Foam cells are also prone to ruptures, if they ingest too much oxLDL, and they can release a bunch of inflammation-promoting substances, oxidized cholesterol etc., which in turn attracts even more immune cells to the site of damage. If, on top of it, there are not enough HDL particles to counterbalance the accumulation of oxidized lipids, the pathological process becomes exacerbated, leading, ultimately, to arterial inflammation and plaque formation (atherosclerosis).
Take home message: even though LDL (particularly the small, denser kind) is associated with atherosclerosis, it is not “the bad guy”. The real bad guy here is it’s oxidized form, a sort of “Mr.Hyde” to LDL’s “Dr.Jekill”, if you will. Not only is the oxLDL bad for us, but so are oxysterols that are also thought to contribute to heart disease (as suggested by excellent research performed by Dr. Fred Kummerow as early as the 70s). Interestingly, it is the high consumption of sugar and insulin resistance that comes with it promotes an overall pro-oxidative environment and is probably the real underlying causes of heart disease. Oh sugar, our sweet-sweet drug of choice… More on that later – stay tuned!
*NB: This has been an accepted theory in the field for a while, however, some recent research (as cited in the review by Itabe at al mentioned here) also suggests that oxLDL can be transferred between the vessel wall and circulation.
Ich Bin Dann Mal Veg 