A new study published in the Journal of the American College of Cardiology (March 1, 2022) confirms that “…studies provide robust evidence that Lp(a) levels are causally associated with atherosclerotic cardiovascular (ASCVD) risk.” When coronary artery calcium scores (CAC) AND Lp(a) levels are elevated, the risk of heart attack or stroke goes up nearly five fold! Have you been tested for Lp(a) yet?
Is There A Family History of Heart Disease or Stroke?
During your first meeting with any health professional, there will almost always be a question about family health history. In particular, doctors want to know if anyone in the family has had a heart attack or stroke. If so, it puts you at a greater risk for cardiovascular disease (CVD).
Cardiologists have known for decades that high levels of the blood lipid Lipoprotein (a) [aka Lp(a) also called “Lp little a”] increases the likelihood for cardiovascular complications. Your genes largely determine how high this risk factor is.
That is to say if grandpa, cousin Charlie or dad had high Lp(a) levels, there is a pretty good possibility you will too. If cardiovascular disease runs in the family, you should absolutely be tested for Lp(a) levels!
The MESA and Dallas Heart Study and Lp(a) Plus CAC:
The study published in the highly respected JACC (Journal of the American College of Cardiology, March 1, 2022) involved two big cohorts. MESA involves the study of 4,512 individuals in the Multi-Ethnic Study of Atherosclerosis trial. In addition, there were 2,078 people in the DHS (Dallas Heart Study). None of the subjects had signs of atherosclerosis or cardiovascular disease at the start of the study. The investigators followed their progress for more than 10 years.
Both groups were tested for Lp(a) levels and coronary artery calcium (CAC), a marker for atherosclerosis. The investigators wanted to determine the impact of Lp(a) alone, CAC score alone and the combined impact of high Lp(a) plus CAC upon atherosclerotic cardiovascular disease (ASCVD) risk.
And the Envelope Please:
The big take away from this impressive study was that participants who had both high Lp(a) levels and high coronary artery calcium scores:
…“had a nearly 5-fold increased ASCVD risk as compared with those with non-elevated Lp(a) and CAC = 0.”
Please hit the pause button. A 5-fold increased risk is crazy high! That is like a 500% increased risk of clogged arteries and cardiovascular disease. There are few things that increase the risk of serious disease to that extent. Please keep in mind that coronary artery calcium is not a risk factor per se; it is a measure of atherosclerosis. It is done with X-rays during a CT scan.
Comparing Lp(a) to LDL:
So, how does a high Lp(a) + high CAC score compare to elevated LDL cholesterol? Remember, cardiologists have been telling us that LDL is the primary problem in heart disease for a very long time.
A ten-year Danish study of more than 90,000 individuals reviewed the cardiac risk of people over 70 (The Lancet, Nov. 21, 2020). Those between 70 and 79 years old with high LDL scores around 193 mg/dl had an 82% higher risk of atherosclerotic cardiovascular disease and heart attacks. For older individuals over 80 years old, the risk nearly tripled.
We conclude that while LDL is important, Lp(a) poses a higher risk of atherosclerotic cardiovascular disease. And yet it has been virtually ignored for decades.
Why Haven’t You Been Tested for Lp(a)?
The authors of the new study in the JACC (March 1, 2022) conclude that Lp(a) is independently associated with atherosclerotic cardiovascular disease. So is a high coronary artery calcium score. If both are elevated, the risk is scary high.
The authors conclude:
“Our novel findings indicate that elevated Lp(a) drives ASCVD risk independent of the subclinical coronary atherosclerosis burden captured by CAC score. This is perhaps related to the unique pathways of inflammation and thrombosis that are triggered by elevated Lp(a) and oxidized phospholipid levels.”
With such an important risk factor, you would think that your doctor would have tested for LP(a). Judging from comments on this website, though, that is rare. The authors of this important paper note that if levels are greater than 50 mg/dL, Lp(a) is a “risk-enhancing factor.”
What Happens When You Don’t Have a Hammer?
You have no doubt heard the phrase, “if all you have is a hammer, everything looks like a nail.” I suspect that cardiologists have rarely tested for Lp(a) because they don’t think they have a drug that will lower it.
Statins do not lower Lp(a). If anything, they raise it! We know that sounds like heresy, but that was the conclusion of a paper published in the European Heart Journal (June 21, 2020).
We suspect that meta-analysis made a lot of health professionals quite nervous. How could a drug that they have been prescribing for decades raise a serious risk factor for atherosclerotic cardiovascular disease? Read more about this contradiction at this link.
How to Lower Lp(a):
If you don’t have a hammer, it may be convenient to ignore the nails poking up through your floor. But eventually, they will cause damage. That’s why we think it is prudent to try to lower Lp(a).
Although most health professionals learned in medical school that they can’t lower Lp(a), that is not completely true. A study published in the American Journal of Clinical Nutrition (Jan. 2022) reveals that a low-carbohydrate diet can actually reduce levels of Lp(a). You can listen to the lead author, David Ludwig, MD, PhD, describe the results of this research at this link to our podcast.
What About Niacin?
We wrote an article titled “Is Lp(a) the Best Kept Secret in Heart Disease?” almost two years ago.
In response, Fay posted this message in the comment section:
“You probably saved my life with this article. All 4 of my grandparents and both parents had a heart attack or stroke. I had never heard of Lp(a) and now I know to lower it. Robert Kowalski’s book from 2002 has the clue: The New 8-Week Cholesterol Cure. He quotes numerous reputable studies where SR (sustained release) niacin lowers Lp(a) as much as 33% to 50%. pp.137-141.”
That prompted us to dig up a copy of Robert Kowalski’s book, “The New 8-Week Cholesterol Cure.” We knew he was a big proponent of niacin.
We did not know that he was on to the problems with Lp(a) two decades ago:
“Levels of the blood fat triglycerides fall dramatically with niacin, far more so than with prescribed drugs…In an NIH–sponsored study, triglycerides fell an average of 52 percent. Regardless of percentage of improvement, niacin can bring triglycerides down to normal even if beginning levels are very high.
“The independent risk factor Lp(a) also succumbs to niacin, even though it responds to neither diet nor drugs. Lp(a) levels were down 35% when subjects were given niacin at the Oregon Health Sciences University. At the internationally renowned Karolinska Institute in Sweden, Lp(a) came down an average of 33 percent in all patients treated with niacin.”
What Happened to Niacin?
Doctors used to prescribe niacin. Statins pretty much put an end to that, though. All focus was on LDL cholesterol and statins lower it extremely well. Perhaps it’s time for doctors to rediscover niacin.
To learn more about niacin, check out this article we wrote a few years ago. It reveals some details about why doctors gave up on niacin. That may have been premature.
Learn about niacin side effects at this link. There are some things people can do to lower the likelihood of unpleasant symptoms. We do think a doctor should supervise when a patient takes niacin. There are slow-release prescription products that may reduce the risk of the niacin flush. And a doctor can monitor liver enzymes, which we think is important. And don’t forget to ask your doctor to have you tested for Lp(a).
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