July 30, 2018

Cholesterol

#07 – Deep Dive: Lp(a) — what every doctor, and the 10-20% of the population at risk, needs to know

"Elevated Lp(a) may have conferred a survival advantage for most of human history: a better ability to deal with acute trauma, but possibly at the expense of poor handling of chronic damage. In today's environment, for many people, that's not an advantage." —Peter Attia

Read Time 11 minutes

This is our first “deep dive” episode that goes into detail on one topic. Pronounced, el-pee-little-a, this lipoprotein is simply described as a low-density lipoprotein (LDL) that has an apoprotein “a” attached to it…but Lp(a) goes far beyond its description in terms of its structure, function, and the role that it plays in cardiovascular health and disease. Affecting about 1-in-5 people, and not on the radar of many doctors, this is a deep dive into a very important subject for people to understand.

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* If you would like us to do a deep dive on a particular topic, please submit your request to the comments section of this post. Please look at the existing comments before posting, and “upvote” the topic (or topics) you want us to cover. *

Note: this podcast gets technical at times. The figures in the show notes are your friends. They truly speak more than a 1,000 words apiece. I can’t emphasize enough how helpful it is to look at the figures before, during, and/or after I try verbally walk you through things like kringle repeats, molecular weight isoforms, lysine-binding domains, and plasminogen homology, as a few examples. If you stick with it, I think you will be rewarded.

We discuss:

  • A quick primer on lipoproteins [7:30];
  • Intro to Lp(a) [11:00];
  • Lab tests for Lp(a) and reference ranges [20:00];
  • The physiologic functions of Lp(a) [31:00];
  • The problems associated with high Lp(a) [34:15];
  • Lipid-lowering therapies of Lp(a) [44:45];
  • Lp(a) modification through lifestyle intervention [1:00:45];
  • High LDL-P on a ketogenic/low-carb-high-fat diet [1:05:30]; and
  • More

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34 Comments

  1. In the show notes you mention the 2 Lp(a) SNPs but in the podcast, I didn’t hear mention of those. Can you please feature these SNPs?

  2. Please deep dive dietary ketosis especially talking about risks/benefits of short term, intermittent, and life-long adherence.

  3. I’m one of those 1 in 10 who is homozygous for at least one LPA mutation and have elevated LP(a). Big light went off when I learned this…as despite low cholesterol and not many risk factors, all four of my grandparents died of stroke or MI (although in 70s or 80s). I have known about this for about 7 years now and experimented with all sorts of interventions. I can say hands down, I am also one those people who does not do well on keto..I rarely enter ketosis despite getting 90% of fat (mostly monounsaturated as I follow a mediterranean ketogenic diet: olives, avocado, etc.) and I feel horrible. My LDL-P and fasting blood glucose go up. I think one explanation may be falling into one of the categories for Keto diet contraindications:
    Carnitine deficiency (primary)
    • Carnitine palmitoyltransferase (CPT) I or II deficiency and Carnitine translocase deficiency, CAT
    • Fatty Acid Desaturase Deficiency FADS
    • b-oxidation defects
    • Medium-chain acyl dehydrogenase deficiency (MCAD)
    • Long-chain acyl dehydrogenase deficiency (LCAD)
    • Short-chain acyl dehydrogenase deficiency (SCAD)
    • Long-chain 3-hydroxyacyl-CoA deficiency
    • Medium-chain 3-hydroxyacyl-CoA deficiency
    • Pyruvate carboxylase deficiency
    • Porphyria
    While, the autosomal recessive “xCAD” loss of function metabolic diseases are rare, being heterozygous for some of the responsible alleles is not, and I carry several of those. I suspect my ability to switch from carb to fat burning is compromised/less efficient as compared to someone without those alleles.
    Long story short: Over time what I feel best on (and is supported my significantly improved HbA1C, LDL-P, TG, total Chol, c-peptide, hsCRP) is following a whole foods, plant based diet, switching back to oral estradiol (I’m postmenopausal) and plenty of exercise.

    • I am also someone with Super high LPa. 374 nmols is my norm. On statins it went up to low 500’s nmols. I too feel better on a Mainly all plant based diet. I add in some sardines and fish here and there and some nuts and red wine. But trying to mainly stick to the all plant based. There are some promising Trials right now, with an siRNA drug. I have no inflammation issues, at least based on my blood work, and the results so far. I have always be “fit”, had no symptoms, but long story short when I found out about my high LPa I insisted on a CT Calcium score. That was high at 490. Then had a Nuclear Stress test. That is where they saw a potential block. Next I had 2 Angioplasities (so many blocks they couldn’t do it in one) and a Rotoblation (one aretery so blocked they had to drill it out) and 6 stents. I went from thinking I was the Picture of health to omg, I could have died. LAD 95 to 99% blocked, RCA (drilled out one) close to 100% blocked, 4 stent just in the RCA, and CX-80% (not as bad). They believe my body created new pathways and that is why I had no symptoms. Anyway, it has been a journey and I feel good and like you, I think mostly plant based is the way to go, at least for me. And exercise is super important. When those things are “all in check” I feel very good. I am 58 years old, as a side note.

    • “…switching back to oral estradiol” – would love to hear more about that! I am on transdermal estradiol, so far no beneficial impact on my elevated lp(a). Wondering whether switching is worth the added risks…?

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