What follows is just about exactly how I educate my patients during appointments, in about 7 minutes. Minus the butcher paper, ballpoint pen diagrams, and waving arms.
Cholesterol is important…
…if dying prematurely from the #1 cause of death in the developed world is something you want to avoid.
True, it’s not all about cholesterol; improving other factors like stress, inflammation, and oxidation can lower your risk. But if you have a ton of cholesterol particles floating around, that’s an awful lot of risk mitigation for your alternative treatments to neutralize.
There are numerous cholesterol types to track, but there are 2 that I watch: the LDL, and Apolipoprotein B (aka Apo B). Apo B is better, but the LDL is way more commonly tested and reported.
Most folks in my corner of the world are walking around with an LDL around 140. The recommendation used to be aiming for an LDL under 130, but the American Heart Association now recommends 100 as the cutoff for the general population. Average LDL numbers are associated with “average” heart attack risk: more than 600,000 Americans dead per year, or two hundred 9/11s each and every year.
If you’re at higher risk, like having diabetes or a previously narrowed artery, the target I recommend to my patients is under 70.
If you’re at super high risk, like you’ve had a heart attack, gotten a stent, then closed off your stent, the target drops to under 35.
So, the lower the LDL, the lower your risk of clogged heart arteries. It can be lowered via diet, exercise, and medications, and how low to go depends on one’s tolerance for risk, how hard it is to push the numbers down, and whether keeping them down is sustainable.
Sidebar: the statistical vs. the individual testing option
The aforementioned is based on lab results, and where the numbers fall on a spectrum of risk. I use the analogy of driving on bald tires while living in Florida or Louisiana. If your tires are 80% bald, you’re more likely to slide off the road during monsoon season than if they were 60% bald, or 20% bald, or brand new. But you might never slide off the road — maybe you’re a super cautious and slow driver — or you might slide off the road tomorrow.
It’s about your odds, based on how your numbers stack up to a population model. It assumes that their numbers are representative of your risk.
There is a way to test YOU as an individual, to see if you actually have plaque narrowing your heart arteries. That’s the CAC score (rhymes with “rack”), aka the coronary artery calcium score. Your coronary arteries slowly build up cholesterol plaques, and over time those plaques calcify, and those calcium sprinkles light up on CT scanning and translate into a numerical score. Anything above zero means hello plaque, and I start talking about considering under-70 as the target.
Where I practice, radiologists prefer this to the CT angiogram to say meaningful things about plaque burden, although Dr. Peter Attia points out that the CTA can see both soft and calcified plaque. But the point is, with one of these CT results, we’re no longer treating a number instead of a person, we’re dealing with an individual’s heart arteries having demonstrable plaque. Some folks with awful cholesterol numbers have CAC scores of zero, and many folks with “slightly high” numbers have CAC scores in the thousand range.
Why not get CACs on everyone? Because a) there’s this little thing called ionizing radiation, and b) some folks don’t need additional convincing. CT scans use x-rays to generate their images, x-rays can cumulatively damage DNA, and every bit contributes to one’s lifetime cancer risk (and for women, a CAC irradiates breast tissue, too). And many folks are already sold on getting their numbers down with a low dose daily statin, no extra testing required.
Then there’s Apo B, and freeway crashes
This was a really cool analogy that I’m stealing with no shame from the aforementioned luminary, Dr. Peter Attia (I can’t find the podcast/blog post, I’d appreciate it if you can send me the link – pbk).
The LDL cholesterol has been around for decades, and we know a thing or two about it by now. In particular, how folks with good LDL numbers can still suffer heart attacks about 30% of the time, what the hell?
Turns out, the LDL is generally not actually measured; it’s calculated based on a formula where other cholesterol numbers are plugged in, like your triglycerides and HDL. The formula gives a decent read on the LDL value, but the model the formula is based on isn’t always correct, so there’s that.
Then there’s the freeway analogy.
Think of your coronary arteries as lengths of freeway, and car crashes being heart attacks.
There’s a correlation between the number of people on the road and the number of car crashes: with 500 people on the road, the chance of a collision is higher than if there were 5 people on the road. The LDL value is analogous to the number of people on a stretch of the freeway at a given moment.
But, some cars actually carry more than 1 person. Vans or buses can carry half a dozen souls.
What’s more accurate is correlating the number of cars on the road to the number of collisions. Even if there are plenty of cars with just a single driver, there’s still a higher risk of collision than if you had a few buses with the same number of people overall.
The Apo B marker tells us the number of cars. The particles that float around in our bloodstream carrying potentially spackling cholesterol only carry ONE Apo B maker per particle.
Translation: lots of Apo B, higher risk of heart attack, even if the LDL is low. I order a lipid to Apo B cascade for this reason: if a patient’s LDL is high, they’re at elevated risk regardless and we’re going to talk; if their LDL is not-high, let’s see what the Apo B says, and if that’s high, then we’re definitely going to talk.
And this was all just a prelude
The finale is the discussion about treatment options, including exercise, the different dietary options, why I usually recommend Paleo but am not dogmatic about it, the various statins, and when PCSK-9 inhibitors come into the discussion.
There’s another sidebar, more of another prelude, when folks have another elevated lab result called the Lipoprotein A, abbreviated Lp(a) (aka “ell-pee little A”). If that genetically determined result is way off (should be 30, a patient’s is 300), we’re jumping straight to the LDL-under-70 talk.
But this was the good parts version. Less than 7 minutes to set the stage for discussion: here’s what’s going on, here’s what the numbers mean, here are additional testing options, and let’s discuss what you want to do next.
Next time, we’ll go over how this all fits in with living in an age of wonders, and the different flavors of Goldilocks.