1: Dr. Peter Attia met Anahad O’Connor in 2012. Both had traveled to France to receive an award from the French-American Foundation.
“We immediately bonded,” Peter writes in his book Outlive. “I think it was because we were the only two guys on the trip who skipped the pain au chocolat and spent our spare time in the gym.
“Also, he wrote about health and science for the New York Times, so we had plenty to talk about.”
Back in the States, “because I am a cholesterol nerd, I badgered Anahad into doing a comprehensive lipoprotein panel,” he notes.
Why? Anahad wondered. “He was only in his early thirties, an extremely fit vegetarian with maybe 6 or 7 percent body fat,” Peter remembers. “But you never know; his father had died of an aneurysm, which may have been a sign of circulatory problems.”
When the results came back, Anahad’s standard numbers were strong. “There was only one thing that seemed off, so I suggested that he should probably also get a calcium scan,” he notes, “so we could get a better sense of the state of his arteries.”
Years earlier, when Peter was thirty-six, he had gotten a calcium test that had come back at 6, placing him at higher risk than 75 to 90 percent of people his age at the time. The result would change the trajectory of his entire life.
“Anahad’s calcium score was 125,” Peter writes, “off the charts for someone so young and otherwise healthy.
“Can this be real?” he asked.
2: Indeed, it was.
“It turned out that the culprit was a little-known but very deadly type of particle called Lp(a),” Peter notes.
“This hot mess of a lipoprotein is formed when a garden-variety LDL particle is fused with another, rarer type of protein called apolipoprotein(a), or apo(a) for short,” Peter writes, “with multiple looping amino acid segments called “kringles,” so named because their structure resembles the ring-shaped Danish pastry by that name.
“The kringles are what make the Lp(a) so dangerous: as the LDL particle passes through the bloodstream, they scoop up bits of oxidized lipid molecules and carry them along.”
These cells have the potential to get stuck in the artery wall and speed up the formation of plaques.
“Often, the way Lp(a) announces itself is via a sudden, seemingly premature heart attack,” Peter writes. “This is what happened to Biggest Loser host Bob Harper, who suffered cardiac arrest at a gym in New York in 2017, at age fifty-two.”
A bystander who performed CPR until the paramedics arrived saved Bob’s life.
“He woke up in the hospital two days later, wondering what had hit him,” Peter observes. “Turns out, his very high level of Lp(a) was what had hit him. He had no idea that he was at risk.”
Which is not an unusual occurrence. Peter writes: “When a patient comes to me and says their father or grandfather or aunt, or all three, died of ‘premature’ heart disease, elevated Lp(a) is the first thing I look for. It is the most prevalent hereditary risk factor for heart disease.”
3: Some people can have over a hundred times Lp(a) than others. “The variation is largely genetic, and an estimated 20 to 30 percent of the US population has levels high enough that they are at increased risk,” Peter writes. “Also, people of African descent tend to have higher levels of Lp(a), on average, than Caucasians.”
Which is why if we have a history of premature heart attacks in our family, we should request an Lp(a) test from our doctor.
Peter tests “every single patient for Lp(a) during their first blood draw,” he shares. “Because elevated Lp(a) is largely genetic, the test need only be done once.”
Anahad was fortunate to discover his heightened Lp(a) while he was relatively young. “Luckily,” Peter notes, “we found the trouble before the trouble found him.”
The fact his calcium score was so elevated “meant that he had already suffered significant atherosclerotic damage,” Peter observes. And unfortunately, there is no “quick fix” for this condition. “It does not seem to respond to behavioral interventions such as exercise and dietary changes.”
For now, “the only real treatment for elevated Lp(a) is aggressive management of apoB [hyperlink to Wed RWD] overall. Though we can’t reduce Lp(a) directly,” Peter writes. “We can lower the remaining apoB concentration sufficiently that we can reduce a patient’s overall risks.”
More next week when we explore how to reduce our cardiovascular risk.
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Reflection: How aware am I of the risks of heart disease?
Action: Talk to my Primary Care Physician about Peter’s work.
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