We all owe fitness guru and TV host of The Biggest Loser series Bob Harper much gratitude for educating the public over the last 3 months of his near death experience from closure of his “widowmaker” heart artery while exercising. His efforts to highlight his missed warning signs, recovery in cardiac rehabilitation classes, his ongoing emotional recovery with the support of his dog and fans, and the use of automatic external defibrillators (AEDs) in gyms and other public settings to save lives has received much media attention and undoubtedly has done more to raise awareness of these issues than many prior efforts. Now Harper pushes the envelope again by announcing that testing has revealed that he carries a high level of a form of cholesterol that is neither rare or benign. Harper recently described that his heart attack was due to an elevated level of Lipoprotein (a), something I have written on previously in regards to Harper’s health journey. As most have not heard of Lipoprotein a, a few comments are timely.
1) What is Lipoprotein (a)?
Lipoprotein (a) is also know as Lp(a), LP little a, and “sticky cholesterol”. It is a particle in the blood that carries cholesterol, fats and proteins. Whether it is detectable in your blood depends on whether you inherited the ability to produce it from one or both parents. You can be thin, exercise, and eat a lot of kale and still have a very high level, just like Bob Harper. The level of Lp (a) usually does not change much over time except for women, as levels increase with menopause. Diet, exercise, and statin medications like Lipitor have little impact on lowering the level of Lp (a).
2) What does Lipoprotein (a) do?
Lp (a) is a big molecule that is a combination of fats, proteins and cholesterol that may circulate in your blood. High level increase the risk for atherosclerosis and calcification in arteries to your heart, legs, brain and even on heart valves. A high level increases the risk of heart attack, stroke, and valve blockages. It is the strongest inherited risk factor for heart blockages and aortic stenosis so it is a very important molecule. It may raise the risk of heart disease by 200–400%, just like Bob Harper had.
3) How common is Lp (a)?
Approximately 20–30% of people have high levels of Lp(a). That means over 60 million people in the USA alone have elevated levels. It is elevated more commonly in African-Americans and those of Asian background. All that is needed to check on this is a simple blood test that is widely available and not expensive. However, is not included in most standard cholesterol panels. Levels of Lp(a) are reported in different units, either mg/dL or nmols/L. A normal level is less than 30 mg/dL or less than 75 nmols/L. Some people I treat have Lp(a) levels of over 400 mg/dl! Bob Harper has not mentioned his Lp(a) level.
4) Who needs to be checked?
The European Society of Atherosclerosis recommends widespread measurement of Lp(a) for the public at risk but this has not reached most doctor’s offices. I believe everyone should find out early in life if they carry this silent artery clogger. However, certain groups without question should ask for the test. These include:
• You have a family member with early heart disease or stroke (men younger than 55 years of age and women less than 65 years of age)
• You know of a family member with high Lp(a). If a parent has high Lp(a), their children have a 1 in 2 chance of being high.
• You suffered a heart attack or stroke with no other known risk factors. This might describe the status of Bob Harper and a thorough evaluation of laboratory findings, as I previously described, is recommended.
• Your cholesterol is high despite taking a statin medication. It might be the LDL cholesterol in Lp(a) that is adding to the result and was not previously measured separately.
5. What can be done about a high Lp(a)?
To date, most attention has been to correct lifestyle and all other factors in patients with a high Lp(a). This is wise. This would include:
• Eat a healthy diet. People with high Lp(a) appear to benefit from a whole food, plant based diet or a Mediterranean Diet emphasizing vegetables, whole fruits, whole grains, and legumes while limited dairy, meats, eggs, added sugars, and refined grains.
• Exercise 30–60 minutes a day.
• Stop smoking
• Control your weight to keep your waistline thin.
• Lower stress with 7–8 hours of sleep along with relaxation like yoga or meditation.
There is no direct inhibitor of Lp(a) at this time. A variety of supplements, all of which I use in patients in my specialized heart longevity center, are known to lower Lp(a). Niacin or vitamin B3 lowers Lp(a) effectively while it also lowers LDL-cholesterol and triglycerides and raises HDL-cholesterol. Other than flushing after large doses, this agent has been used for decades with safety. L-carnitine is an amino acid that lowers Lp(a) and has been shown in other studies to improve outcome after heart attacks. Recent data about L-carnitine in meat and supplements and a new marker of heart risk and development called TMAO has thrown some doubt on using L-carnitine. In my clinic, I measure TMAO levels on patients treated with L-carnitine for an elevated Lp(a) and continue it if the level does not shoot up. Ginko biloba is derived from the tree and has been used for brain health. It has been reported to lower Lp(a). In post-menopausal women, a recent review demonstrated a powerful effect of hormone replacement therapy on Lp(a) levels. New injectable drugs used to lower cholesterol are now FDA approved and also lower Lp(a). As of this time, they are not approved for those with only elevated Lp(a) levels but it is hoped this may change in the near future. New injectable drugs are beginning clinical trials to directly lower Lp(a) but it will be several years before results are available. Finally, a therapy called apheresis that is like hemodialysis and cleanses the blood of Lp(a) through a filter. This is available and approved for use. This is an invasive and time intensive approach that will likely be relied on less in the future due to new developments.
I hope the compelling story of Bob Harper continues to be played out in the public eye as it is teaching us much about survival and recovery. The focus now needs to shift to early detection, prevention and reversal. Harper’s excitement on finding out about his inherited Lp(a) was palpable as he said related that he notified Dr. Mehmet Oz by text about his Lp(a) level and immediately got a call back. Dr. Oz told him this was great news and I agree. Harper asked ‘This is great news?’ [He said] ‘Yes, because now you know what’s going on with you and now we know what to do.” I agree and there is much to do to help Harper for the next 51 years. I hope that Mr. Harper will also make sure that his relatives get tested along with all of his followers at risk.