Sat fats, sad fats?

OK, so yesterday I told you that, for most people, dietary cholesterol isn’t a big evil thing, because our bodies have nifty, complicated little mechanisms in place to adjust the amount of cholesterol we manufacture up or down, depending on how much we’re consuming in our food.
That said, having a lot of cholesterol in your blood is a bad thing. So what gives?
If you’ve had your cholesterol tested, you know that HDL cholesterol is “good” and LDL cholesterol is “bad,” right. Well, technically, HDL (high-density lipoproteins) and LDL (low-density lipoproteins) aren’t cholesterol—they’re transporters of cholesterol. They are little round structures made up of protein and some other stuff, and they carry cholesterol and a bit of fat (in the form of triglycerides) through your blood.
LDL is “bad” because they are able to get lodged underneath the cells that line the inside of your arteries. Your body recognizes them as foreign invaders, because they are going where they don’t belong, and some of your immune system cells (macrophages, if you’re curious) try to deal with them, and that starts a whole chain reaction of chronic inflammation and other bad things. Essentially, it kicks off a process that leads to fatty streaks in your artery walls, then thick fatty plaques in your artery walls (along with a general hardening of the arteries). If one of those plaques ruptures, a clot can form…and that’s when a heart attack or stroke can happen. (HDL particles can go in and remove some of the cholesterol from underneath the arterial lining…that’s why they’re good.)
So what does saturated fat have to do with this? As I’ve been learning over the last few weeks, saturated fat can interfere with the little receptors (think of them as docking stations) we have on the outside of our cells that allow LDL particles to belly up and deposit their cholesterol inside the cell. If we don’t have enough LDL receptors that are doing their job, then the LDL particles in our blood stay in our blood longer. That’s bad…for two reasons.
  1. The longer LDL particles are in the blood, the more opportunity they have to get wedged in our artery walls.
  2. The longer LDL particles are in the blood, the more opportunity they have to get oxidized.

Oxidized? Yes, oxidized. Rust is a form of oxidation…and while oxidation happens all the time in our bodies, to some degree, suffice to say that you don’t want an excessive amount of oxidation to happen. And you would really like your LDL particles to not be excessively oxidized. Oxidation of LDL particles is a serious contributor to that whole road-to-a-heart-attack process I just mentioned.
In case you’re about ready to reach for a bottle of antioxidant supplements…don’t. That was held up as one of the Great Nutritional Hopes for a while, but many clinical trials have found that antioxidant supplements don’t reduce the risk of arterial plaque buildup or the resulting cardiovascular complications. I’ll be learning more about that in today’s lecture.
So what do you do? Limit saturated fat. Don’t cut it out entirely…we do need some. Keeping it to less than 10 percent of our total calories is common advice. The American Heart Association suggests keeping it below 7 percent (that’s about 140 calories from saturated fat out of a 2,000 calorie diet). And you know that saturated fat comes mostly from meat and dairy, right? I knew you did. I don’t micromanage my calories at the moment, but I am personally looking hard at my cheese consumption. I love cheese, and won’t stop eating it altogether, but I’ve been slipping in my role as nutritional gatekeeper, and have allowed more of it into the house. And once it’s in the house…well, you know how that story goes.
Now go eat an apple.