Despite obsessing for nearly a half century over the role of lipoproteins in heart disease, researchers seem to be more conflicted than ever.
Most folks who came of age during the 1960s and early ’70s probably recall it as a time of great cultural and political upheaval, what with anti-war protests, civil-rights indignities, and hippie exceptionalism dominating the headlines. I remember it mostly for all the heart attacks.
Uncle Ed, Uncle Ronald, Uncle Bill, and Uncle Ken — four of my dad’s five brothers dropped dead in what seemed to my adolescent view to be fairly short order. None of them made it to 60. So, when I got the call in the winter of 1971 notifying me that my 51-year-old father was lying in intensive care after a heart attack, I was more anxious than surprised.
He pulled through thanks to an early form of bypass surgery, but in some ways, our family would never be the same. My brothers and I began to suspect that going through a pack of Marlboros every day might not be optimal, and we all drifted inexorably toward a weird obsession with cholesterol.
We weren’t alone, of course. As Jeanne Garbarino notes in Scientific American, researchers by the early ’70s had become increasingly convinced that cholesterol was the prime culprit behind America’s spreading epidemic of heart disease. As a result, we all became way too preoccupied with saturated fats, lab tests that measured danger in millimoles per liter, and the mysterious behavior of our lipoproteins.
I vaguely recall the slightly suppressed alarm that accompanied my first cholesterol reading back in the early ’80s: A total count of 200 mmol/L, my doctor noted darkly, was cause for concern. Subsequent reports over the years never yielded anything much lower, but I was always buoyed by the knowledge that my triglycerides were in the normal range and the good lipoproteins were outnumbering the bad.
My older brothers, who pay attention to their doctors, long ago took the pharmaceutical route toward a healthier cholesterol count, while I blithely ignored all the danger signs. Recent developments, however, suggest that there’s plenty of upheaval in the world of lipoproteins.
First, researchers at the University of Copenhagen released a study showing that people with high levels of “good” HDL cholesterol were actually more likely to die than those with moderate levels. Then, like a series of myocardial infarctions, three new studies released last week had me wondering whether anyone really knows what’s going on:
- Researchers at Brigham and Women’s Hospital found that there is essentially no “floor effect” in the lowering of LDL cholesterol. The lower it goes, they reported, the lower the risk of heart attack and stroke. This despite well-documented evidence that low cholesterol levels can damage cognitive skills and mess with memory. The results may be partially explained by the fact that Amgen, the maker of a popular cholesterol-lowering drug, funded the study.
- A paper presented at the European Society of Cardiology’s Congress in Barcelona argued that how you lower LDL cholesterol is more important than the simple act of dropping the number. It’s all about the circulating concentration of LDL particles rather than the total amount of bad cholesterol. When you lower the circulating concentration of those particles, as measured by apolipoprotein-B (apo-B) levels, you lower the risk of heart attack — even if the LDL levels don’t come down. This helps to explain why people taking statins still die from heart attacks.
- And, in a classic case of the right hand not knowing what the left hand is doing, some other folks at Brigham and Women’s Hospital released on the same day as the Amgen-funded study a report arguing that reducing inflammation — not lowering cholesterol — is the best way to prevent heart attacks. “Cardiologists will need to learn about inflammation today, the same way we learned about cholesterol 30 years ago,” said Paul Ridker, director of the Center for Cardiovascular Disease Prevention at the hospital.
Other research has reached similar conclusions as Ridker’s study, which offered momentary hope that the Medical-Pharmaceutical Complex will one day admit that lifestyle remedies may be more effective in preventing heart disease than popping more pills. But then I noted that Ridker’s research was funded by Novartis and designed to test a new anti-inflammatory drug.
We always thought it was a bit ironic that, when my dad died, eight years after his heart attack, his ticker was in pretty good shape. He had quit smoking, retired from his truck-driving job, and took up some hobbies. In some ways, he was probably healthier than he’d been in years when colon cancer took him down.
Now all my brothers talk about is their latest colonoscopy.