Until a few years ago, I’d never heard of the blood molecule lipoprotein (a), or Lp(a). Then I started listening to The Drive, a podcast hosted by Peter Attia, who trained as a surgeon, then became a McKinsey consultant, and now runs a concierge medical practice focused on “healthspan”—a term he’s helped to popularize. Unlike lifespan, which is how long you live, healthspan refers to how long you’ll enjoy an active, disease-free lifestyle, and on his podcast, Attia interviews experts about the best ways to do that. He talks frequently about Lp(a), which is rarely included in routine bloodwork but can indicate your inherited risk for heart disease. So after bingeing The Drive, I asked my doctor to measure mine: 307 nanomoles per liter, compared to a normal value of under 75. Yikes. I now see a cardiologist regularly.
Harvard Business Review’s Chasing Longevity explores the booming influence of longevity “gurus” shaping mainstream health culture. From Peter Attia’s Medicine 3.0 and “centenarian decathlon” framework, to Andrew Huberman’s neuroscience-driven podcast empire, and Eric Topol’s tech-fueled vision of AI and genetics, these voices are reframing how executives and affluent patients think about healthspan.
Read the full article:
Chasing Longevity , Harvard Business Review
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RapAdmin. As discussed on this forum, I also have a high LPa. I have traveled to San Diego to meet yearly with Dr. Sam Tsimikas. Happy to discuss what I have learned if you are interested in a zoom or call.
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My LPa is 19, so I’m not super interested, but I’m sure many others here are. Perhaps you could post a short summary of what you’ve learned and what you do currently to counter this issue?
I’m sorry. I misread your post. I thought it was saying YOUR Lpa was 307 nmol/L. This is what I have learned in short:
My LPa was high (140 nmol/L). With Dr. Tsimikas’s guidance and care, I started Repatha injections and Zetia. Both have lowered my LPa to 79 nmol/L (normal levels). Dr. Tsimikas’s goal for high LPa patients is to get LDL, APOB, and Triglycerides to 50. He says very few of his patients achieve that goal. Well, I’m close to achieving it. My latest labs were LDL of 46 mg/dl; APOB of 59 mg/dl and Triglycerides of 46 mg/dl. Those numbers were achieved with diet, exercise, and repatha/zetia combination and perhaps other meds I take (Rapamycin is one of those). The question I’m debating is this: When the meds come out in the next year or two that lower LPa to extremely low levels, is that something I want to do? Or should I be happy with a Repatha/zetia combination that gives me an LPa that is in “normal levels” but not extremely low. In other words, is there a “Too low” a level of Lipoprotein A?
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There are not a small number of people whose levels of Lp(a) are if not zero, then undetectable. No negative effects have been observed. My Lp(a) levels are much higher than yours, but if they were at your new low levels I personally would still take advantage of the coming drugs to crush those levels to zero or near zero. I can see no advantages to having Lp(a) at all - from my reading and understanding (probably incomplete), the function of Lp(a) is no longer relevant in the current environment humans occupy (maintaining vascular integrity in conditions of vitamin C deprivation, low nutritional status and so on). Lp(a) is a classic case of antagonistic pleiotropy, just as sickle cell is - sickle cell protects against malaria, but at the cost of longer term health. Today, malaria can be handled by other means, and therefore sickle cell is an unadulterated negative - eliminate with extreme prejudice. That’s my attitude to Lp(a) - crush it out of existence. YMMV.
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Thank you for this comprehensive reply. I’m leaning this way for sure as long as the new meds are affordable. Your insights are truly helpful.
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