"Good" and "bad cholesterol" are dumb terms. Instead go for apoB. #11

It’s time to retire the phrases “good cholesterol” and “bad cholesterol.” Clinical science has outpaced these once useful but inferior ways of thinking.

The substance cholesterol is essential for life. You’d die without it. But it is connected to cardiovascular disease and cerebrovascular disease (heart attacks and strokes). How does something vital link to something catastrophic? I explain in the video.

Doctors are used to ordering bloodwork that looks at “good cholesterol” and “bad cholesterol.” But I think there’s a better way, a newer way. It’s called apoB. By “better,” I mean further reducing risk of heart attack.

It’s not my original idea. There is clinical evidence supporting this. But it’s not mainstream practice, either. And I think that’s because new understandings have outpaced clinical guidelines. Hence a new opportunity to help people.

If you believe this is for you but you need to bring it up with your doctor, then get the first linked medical paper below by Allan Sniderman. And get it to your doctor. That should get the ball rolling.

video content timeline

  • “Everything I’m going to teach you is either wrong or incomplete.” [0:00]

  • This presentation is intentionally simple with science so everyone can understand. Links are below for those who want the gory details. [1:02]

  • Some basic clarity about cholesterol and corrections to common but unhelpful ideas:

    • Cholesterol has a bad rap. And yes, there’s a heart attack connection. But cholesterol is essential for life. [2:38]

    • Three examples of how cholesterol is essential: cell membrane integrity, making hormones, and digestion. [2:50 – 3:50]

    • You make your own cholesterol. [3:59]

    • The old terms “bad cholesterol” and “good cholesterol” should be retired. There is only one kind of cholesterol. [4:23]

  • There is a relatively new clinical way to think about cholesterol compared to the old “good” and “bad” framework. [7:17]

  • It seems doctors have not adopted this new framework widely. It’s a missed opportunity to lower risk of heart attack and stroke. [8:05]

  • How does something we require for life and make with our own bodies lead to the catastrophe of a heart attack? Explanation begins here. [9:00]

    • Cholesterol travels through the bloodstream in little bags called lipoproteins. [9:19]

    • I cut toilet paper in half. [10:14]

    • A cholesterol-carrying particle can go into the artery wall. Not good. [11:37]

    • Cholesterol-carrying particles should not be moving in great numbers from the bloodstream into artery walls. This is not healthy organization of tissue. [12:36]

    • The immune system’s macrophage cells move in to clean up the mess. [13:21]

    • An inflammatory response is activated. [15:14]

    • A plaque forms. [16:30]

    • The plaque ruptures. [17:45]

    • Blood by design is at the ready to make clots. But it must be triggered first. [18:12]

    • A clot is triggered and causes a heart attack; in medical terms, a myocardial infarction. [19:48]

  • What’s the most common first sign of a heart attack? (It’s not what you think.) [20:58]

  • The key causal difference between a healthy artery and a diseased artery is whether those cholesterol-carrying particles moved inside the artery wall in the first place. [22:06]

  • Here I explain the difference between counting the number of particles, what I’m calling the “new way,” and the old way of monitoring cholesterol with “good” (HDL-C) and “bad” (LDL-C) measurements. [24:26]

  • Counting the number of cholesterol-carrying particles in the blood gives a better estimate of heart attack risk than standard bloodwork showing “good” and “bad” cholesterol levels. This is the apoB test vs LDL-C and HDL-C tests. [25:47]

  • Without measuring the number of cholesterol-carrying particles, about 10% to 30% of patients are likely to get a false alarm or a false sense of security from a conventional lipid panel. [26:48]

  • The blood test measuring the number of cholesterol-carrying particles is called apolipoprotein B, or apoB. The lab’s cash price in my town is only $16.00. [28:58]

  • Your doctor might not know about this test or think of ordering it. The guidelines don’t advise it.  But I think the guidelines should. [30:03]

  • Scientific knowledge changes. And that’s what’s going on with our understanding of how heart disease starts. [30:52]

  • If you want to act on this but your doctor isn’t on board, I recommend you show your doctor the first paper cited below by Allan Sniderman. Then ask what your doctor thinks. It’s a quick and easy read for your busy doctor and is a good starting point. [32:06]

  • I don’t like the phrase, “prevent death.” “Delayed death” is better. [33:11]

  • A guideline is not fact. A guideline is merely expert agreement. [33:33]

  • I don’t like the phrase, “the science.” And I don’t like the phrase, “settled science.” [34:16]

  • “Here’s THE science” often means “here are the cherry-picked sources supporting my cherished opinion that I’m reluctant to change.” [34:40]

  • The scientific method. [34:54]

  • Bring up apoB with your doctor to start the conversation. [35:54]

resources

  1. Here’s the paper I suggest you take to your doctor to start the conversation. The full citation is below. Click here.

  2. Here is an evidence-based calculator to help with diagnosis. It’s something you can show your doctor.

  3. Want all the details in quasi-lecture format? Peter Attia, M.D. goes into this topic much more deeply than I have here. He has two segments in particular that are especially relevant. The first is a series with Tom Dayspring, M.D. and starts here. The second is with Allan Sniderman, M.D. and is here. Note that the audio is freely available, but you need to pay to view associated graphics, show notes, and links.

  4. Here’s a PDF file of all my presentation drawings.

  5. Correlation and causation are not the same, and this makes that clear (some examples are quite amusing).

citations

  1. Sniderman A. D. (2019). Did the ACC/AHA/AACVPR/AAPA/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA cholesterol guidelines get apoB right?. Journal of clinical lipidology, 13(3), 360–366. https://doi.org/10.1016/j.jacl.2019.05.010

  2. Hopkins, P. N., Brinton, E. A., & Nanjee, M. N. (2014). Hyperlipoproteinemia type 3: the forgotten phenotype. Current atherosclerosis reports, 16(9), 440. https://doi.org/10.1007/s11883-014-0440-2

  3. Johannesen, C., Mortensen, M. B., Langsted, A., & Nordestgaard, B. G. (2021). Apolipoprotein B and Non-HDL Cholesterol Better Reflect Residual Risk Than LDL Cholesterol in Statin-Treated Patients. Journal of the American College of Cardiology, 77(11), 1439–1450. https://doi.org/10.1016/j.jacc.2021.01.027

  4. Sniderman, A. D., Thanassoulis, G., Glavinovic, T., Navar, A. M., Pencina, M., Catapano, A., & Ference, B. A. (2019). Apolipoprotein B Particles and Cardiovascular Disease: A Narrative Review. JAMA cardiology, 4(12), 1287–1295. https://doi.org/10.1001/jamacardio.2019.3780

  5. Sniderman, A., Shapiro, S., Marpole, D., Skinner, B., Teng, B., & Kwiterovich, P. O., Jr (1980). Association of coronary atherosclerosis with hyperapobetalipoproteinemia [increased protein but normal cholesterol levels in human plasma low density (beta) lipoproteins]. Proceedings of the National Academy of Sciences of the United States of America, 77(1), 604–608. https://doi.org/10.1073/pnas.77.1.604

  6. Ference, B. A., Kastelein, J., Ginsberg, H. N., Chapman, M. J., Nicholls, S. J., Ray, K. K., Packard, C. J., Laufs, U., Brook, R. D., Oliver-Williams, C., Butterworth, A. S., Danesh, J., Smith, G. D., Catapano, A. L., & Sabatine, M. S. (2017). Association of Genetic Variants Related to CETP Inhibitors and Statins With Lipoprotein Levels and Cardiovascular Risk. JAMA, 318(10), 947–956. https://doi.org/10.1001/jama.2017.11467

  7. Teng, B., Thompson, G. R., Sniderman, A. D., Forte, T. M., Krauss, R. M., & Kwiterovich, P. O., Jr (1983). Composition and distribution of low density lipoprotein fractions in hyperapobetalipoproteinemia, normolipidemia, and familial hypercholesterolemia. Proceedings of the National Academy of Sciences of the United States of America, 80(21), 6662–6666. https://doi.org/10.1073/pnas.80.21.6662

  8. Sniderman, A. D., Lamarche, B., Contois, J. H., & de Graaf, J. (2014). Discordance analysis and the Gordian Knot of LDL and non-HDL cholesterol versus apoB. Current opinion in lipidology, 25(6), 461–467. https://doi.org/10.1097/MOL.0000000000000127

  9. Ketelhuth, D. F., Rios, F. J., Wang, Y., Liu, H., Johansson, M. E., Fredrikson, G. N., Hedin, U., Gidlund, M., Nilsson, J., Hansson, G. K., & Yan, Z. Q. (2011). Identification of a danger-associated peptide from apolipoprotein B100 (ApoBDS-1) that triggers innate proatherogenic responses. Circulation, 124(22), 2433–7. https://doi.org/10.1161/CIRCULATIONAHA.111.051599

John Fuhrman