It’s officially March and there are so many things to look forward to – the arrival of spring, St. Paddy’s Day and Lipoprotein(a) Awareness Day. Never heard of it? I hadn’t either until I came across this little bugger in Peter Attia’s book Outlive and have been diving into the research (there's not much) on this deadly particle for the past year. The following article will discuss what it is, how to manage your risk and why everyone (yes, everyone – that includes you) must have their levels tested at least once.
What’s Lipoprotein(a), also known as Lp(a)?
Lp(a) (pronounced el-pee-little-a) is an LDL (bad cholesterol)-like particle but with a few structural upgrades that make it deadly. It’s basically LDL with really bad eyelash extensions. These amino acid extensions allow this hot mess of a particle to do three things the plain-Jane LDL particle can’t: (1) pick up and carry more lipids, (2) make it far more likely to get stuck in the wall of an artery and (3) contain a pro-clotting factor which speeds up the formation of arterial plaques.
Why should I get tested?
The level of Lp(a) is largely genetically predetermined. Your average level at age 5 will be your average level at age 50 with a few exceptions including menopause, chronic disease, inflammatory states like a virus, pregnancy, hypothyroidism and growth hormone therapy. It is currently estimated that 1 in 5 people worldwide have elevated Lp(a). It is the most prevalent hereditary risk factor and a common independent risk factor for heart disease and stroke, and it’s slipping through the cracks of standard health care. Just having a high level of Lp(a) will have a 3- to 4-fold increase in heart attack, 3-fold increase in aortic stenosis and a 1.5-fold increase in mortality. You can have normal LDL cholesterol levels and still have high Lp(a). The signature move of Lp(a) is a shockingly sudden, premature heart attack exactly like the one celebrity trainer, Bob Harper, from the Biggest Loser had at 52-years-old.
How to manage your risk?
Lp(a) doesn’t seem to respond to exercise and dietary changes, and cholesterol-lowering drugs like statins can’t touch it. The efficacy of statins is a huge can of worms we don’t have time for now, but if you want to jump ahead a few months of blog posts, I highly recommend Dr. Mark Hyman’s podcast episode 506 The Truth Behind Statins: Helpful or Harmful? - Dr. Mark Hyman (drhyman.com). Here is what I don’t understand after reading the research and why this doesn’t make sense. I think we can all agree that Darwin’s theory of natural selection still holds, and that everything in nature is well thought out – nothing happens casually or randomly. Our species has been successfully living with and passing Lp(a) along for at least 65 million years. If it wasn’t beneficial to the survival of the species, heart disease would have killed us quicker than a saber-toothed tiger or it would have been phased out of the genetic code. There must be a benefit to Lp(a) and there has to be an environmental component that has turned this Benedict Arnold particle from a good guy to a bad guy.
Heart disease became the leading cause of death only at the beginning of the 20th century mainly contributed to environmental factors like smoking and diet. Having a high Lp(a) level is not a death sentence, but it does require no-nonsense management to eliminate all of the well-known risk factors that lead to heart disease as early as possible. If you smoke, stop. Manage your weight. Eat a healthy, whole foods diet with monounsaturated fats. Exercise regularly. Manage your blood sugar and your blood pressure. Manage your stress effectively. It may be beneficial to look into HRT if you are menopausal. Supplement with CoQ10, Omega-3 fatty acids and niacin (vitamin B3). Currently, the only therapy approved by the FDA for reducing Lp(a) is lipoprotein apheresis - a nonsurgical therapy that uses a machine to filter the blood and remove LDL and Lp(a).
What do I do now?
At your next annual physical, request the addition of Lp(a) to the standard lipid panel for you and all your family members. It’s a non-fasting, one-time serum test. If you or anyone you know has the following risk factors, I recommend getting tested immediately. Risk factors include: a family history of heart disease, familial hypercholesterolemia, high LDL levels on your most recent cholesterol panel, familial or personal medical history of premature coronary artery disease, suffered from a past heart attack or stroke, a family member has elevated Lp(a). The earlier you, your family, and friends know their Lp(a) levels, the sooner you and they can begin necessary lifestyle changes to dramatically lower the risk of heart attack.
For more information on Lp(a) including Lp(a) levels, please visit and support our social and the Family Heart Foundation (Family Heart Organization - Family Heart).
Resources
An Update on Lipoprotein(a): The Latest on Testing, Treatment, and Guideline Recommendations - American College of Cardiology (acc.org)
How Bob Harper Changed His Diet After His Heart Attack: "I Had to Redefine the Way I Ate" (eatingwell.com)
Lipoprotein(a): from ancestral benefit to modern pathogen? | QJM: An International Journal of Medicine | Oxford Academic (oup.com)
The Epidemic of the 20th Century: Coronary Heart Disease - The American Journal of Medicine (amjmed.com)
Supplementation with coenzyme Q10 reduces plasma lipoprotein(a) concentrations but not other lipid indices: A systematic review and meta-analysis - PubMed (nih.gov)
Omega-3 fatty acid supplementation and lipoprotein(a) concentrations in patients with chronic glomerular diseases - PubMed (nih.gov)
Disclaimer
The content on this site is for informational and educational purposes only. It does not substitute professional medical advice from your healthcare professional.
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