Cardiovascular Health 2026

#81

Thank you for sharing this information. A few thoughts in no particular order.

Vitacost makes a nice supplement mix containing vitamin C, Lysine, Proline, and EECG.

If one limits the evidentiary base to research on humans (which is a good ide in general and more so here because the mouse study is so contrived), my read on the Lp(a), vitamin C, Lysine relationship is that that it is theoretically plausible but lacking in human empirical evidence.

A 2025 review that compiled seven human studies reported that vitamin C supplementation did not significantly change plasma Lp(a) across doses ranging from 500 to 4500 mg/day, in both CAD and healthy cohorts.

The Linus Pauling Institute also summarizes multiple controlled trials (e.g., 1-2 g/day for ~1 month; 4.5 g/day for 12 weeks; 1 g/day for 8 months) that found no significant effect on Lp(a), contrasting with one small uncontrolled study reporting a decrease.

The frequently cited vitamin C/Lysine connection by Dalessandri (Atherosclerosis, 2002) is a letter/comment, with no abstract on PubMed, limiting accessibility of design, controls, and outcomes.

At your age, which is close to mine, I would be concerned that the daily consumption of two grams of vitamin C would be placing undue strain on my kidneys. Most mammals produce vitamin C PRN in response to stress. Maintaining a level that might be eight or more times higher than required to saturate tissues could be doing more harm than good to aging kidneys.

If my Lp(a) level was elevated, I would – in addition to following all of the established data for reducing ASCVD, such as aggressively lowering Apo(b) – immediately initiate therapy with a GLP1 agonist with the idea in mind of switching over to one of the three Lp(a) targeting drugs currently in clinical trials when it becomes available (2027, I believe if all goes well). My understanding is that these new drugs will reduce Lp(a) by 50% or more with no negative side effects and possibly at a relatively low cost. In the interim, you might expect to see a 25-30 percent reduction in Lp(a) from GLP1 agonists and also have to initiate extraordinary measures to preserve muscle mass.

#82

I didn’t know that a GLP1 agonist would reduce Lp(a). But I do know that Repatha will reduce it. It lowered mine from 40 to 27. It was a hard sell to get a script for Repatha. I showed my cardiologist my Prometheus report, which shows a 9p21 mutation that raises risk of cardiovascular disease by (in my case) 1.9x.

#83

My bad Deborah. I meant to say PCSK9. GLP1i is a minor contribution. I wasn’t paying attention for a moment.

#84

80% to 95+%

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#85

Yes. I was taking a conservative view but a couple of the phase II trials were astounding. However, it looks like the higher figures are significantly is modulated by the base level and also perhaps by genetic makeup. The SDs I saw were pretty high.

#86

A new Peter Attia newsletter reminds us all that atherosclerosis is not the only cause of heart attacks, though of course it is the most common. However, ~5% can arise from other causes, in people who have no measurable atherosclerosis.

There are also very notable differences between men and women.

Full article here:
The absence of atherosclerosis is not an excuse to ignore heart attack symptoms—especially for women.pdf (678.3 KB)

AI summary, with key points highlighted by me:

While atherosclerosis is the most common cause, a meaningful fraction of heart attacks—especially under age 65—occur through other mechanisms like artery tears (SCAD), spasms, or oxygen supply–demand mismatch.

Women under 65 have a different risk profile than men. In this group, fewer than half are atherothrombotic, and about 1 in 10 are due to spontaneous coronary artery dissection, which is over 5× more common in women than men.

Low cholesterol does not equal zero heart-attack risk. Good lipid numbers, normal blood pressure, and overall metabolic health greatly reduce risk—but they do not eliminate it

Women have very different symptoms to men. Women are more likely to experience shortness of breath, nausea, fatigue, lightheadedness, or back/abdominal discomfort rather than classic chest, shoulder and jaw pain

Bottom line: Good biomarkers/scans should never be a reason to dismiss sudden, persistent cardiac symptoms—especially for younger women, who are disproportionately affected by non-traditional heart attack mechanisms.

Very useful information IMO. And especially useful for younger women who can have non-ASCVD heart attacks with “atypical” symptoms, and not go to hospital because they don’t suspect MI.

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#87
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#88

Already discussed there: Heart Attacks WIthout Plaque, Women More Affected

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