HORSEMAN #2: REDUCING THE RISK OF HEART DISEASE

While heart attacks may seem sudden, the problem was likely lurking for years.? Atherosclerosis is a slow-moving, sneaky disease and our risk of these “events” rises steeply in the second half of our lives

This week, as promised, I continue to share Dr. Attia’s advice on heart disease, the second of the four horsemen.? This week we will look at what we can do to reduce the risk of heart disease.

As advised in last week’s article, Dr. Attia notes in Outlive :

“The point to note is that while heart attacks may seem sudden, the problem was likely lurking for years.? Atherosclerosis is a slow-moving, sneaky disease and our risk of these “events” rises steeply in the second half of our lives, but some scientists believe the underlying processes are set into motion in late adolescence, even as early as our teens. The risk builds throughout our lives, and the critical factor is time.? Therefore, it is critical that we understand how it develops, and progresses, so we can develop a strategy to try to slow or stop it.”

We also noted that every single lipoprotein that contributes to atherosclerosis carries the apolipoprotein B (or apoB) signature.? Note that apoB particles—LDL, VLDL, Lp(a)—are causally linked to atherosclerotic cardiovascular disease, or ASCVD.? So, to gauge the true extent of your risk, you must know how many of these apoB particles are circulating in your bloodstream.

Therefore, you should test for apoB regularly.? Ask for this apoB test the next time you see your doctor!? Dr. Attia recommends that you do a comprehensive lipoprotein panel and get a calcium scan to get a clear picture of the state of your arteries.?

LIPOPROTEIN Lp(a)

One of these apoB particles, Lp(a) is particularly destructive.

As Dr. Attia notes:

“It is a little-known but very deadly type of particle, formed when an LDL particle is fused with another, rarer type of protein called apolipoprotein(a) (apo(a)).? Since Lp(a) is a member of the apoB particle family, it has the potential to penetrate the endothelium and get lodged in an artery wall; because of its structure, Lp(a) may be even more likely than a normal LDL particle to get stuck, with its extra cargo of lipids gone bad.? Even worse, once in there, it acts partly as a thrombotic or proclotting factor, which helps to speed the formation of arterial plaques."

Often, the way Lp(a) announces itself is via a sudden, seemingly premature heart attack.

Dr. Attia also advises that

“People of African descent tend to have higher levels of Lp(a), on average, than Caucasians.? This is why, if you have a history of premature heart attacks in your family, you should definitely ask for an Lp(a) test.? Because elevated Lp(a) is largely genetic, the test need only be done once (and cardiovascular disease guidelines are beginning to advise a once-a-lifetime test for it anyway).

Beyond the harm it causes to coronary arteries, Lp(a) is particularly destructive to the aortic valve, one of the more important structures in the heart, by promoting the formation of tiny, bony particles in the valve leaflets, which leads to stenosis or narrowing of the aortic outlet.”

So, the first step in risk reduction is identifying the primary causative agent in the disease process: apoB. ?Then treat the causal agent in both cases—lowering the forty-five-year-old’s apoB as much as possible. ?The only way to stop the disease is to remove the cause, and the best time to do that is now.

Here is what Dr. Attia does when he looks at a patient’s blood work:

“When I look at a patient’s blood panel for the first time, my eyes immediately dart to two numbers: apoB and Lp(a) because these two tell me the most when it comes to predicting their risk of ASCVD.? ApoB not only tells me the concentration of LDL particles, but it also captures the concentration of VLDL particles, which as members of the apoB family can also contribute to atherosclerosis.? Furthermore, even someone whose apoB is low can still have a dangerously elevated Lp(a).”

Once you establish apoB’s importance, the next question becomes, how much does one need to lower it (or its proxy LDL-C—the cholesterol content in your LDL particles, i.e., your “bad” cholesterol number)?

TREATMENT

Dr. Attia does not believe that you can lower your “bad” cholesterol number too much.? He suggests an LDL-C target as low as 10 to 20 mg/dL and believes that many doctors would be shocked at this low target.? This is because “most guidelines consider lowering LDL-C to 70 mg/dL to be “aggressive,” even for secondary prevention in high-risk patients, such as those who have already had a heart attack.”

But he notes that atherosclerotic disease shouldn’t even be in the top ten causes of death if we treated it more aggressively. ?Instead, we have over eighteen million cases of fatal atherosclerotic disease per year globally.

The heart disease process unfolds very slowly—not over two or three or even five years, but over many decades.

So, what can we do to lower our apoB levels or its proxy LDL-C?? Here are Dr. Attia’s recommendations:

?

1.??? Stop smoking.

2.??? Bring your blood pressure under control.

3.??? Change your diet to lower your triglycerides and insulin levels.? Consider shifting to monounsaturated fats, found in high quantities in extra virgin olive oil, macadamia nuts, and avocados (among other foods), that promote a better lipid profile.

4.??? Ask your doctor about lipid or “cholesterol-lowering” drugs like Statins

The key takeaway here is that the disease process unfolds very slowly—not over two or three or even five years, but over many decades.

The risk of heart disease is proportional to apoB exposure over time. ?The sooner we lower apoB exposure, thus lowering risk, the more the benefits compound over time—and the greater our overall risk reduction.

As Dr. Attia notes:

“The fact that younger people have been found to have lesions and plaques, without suffering many events, tells us that there is a considerable period when the disease is not harmful.? Dying from cardiovascular disease is certainly not inevitable: the centenarians delay it for decades, and many avoid it altogether, their arteries remaining as clean as those of people a generation younger.? Somehow, they manage to slow the process down.

Nearly all adults are coping with some degree of vascular damage, no matter how young and vital they may seem, or how pristine their arteries appear on scans.? There is always damage, especially in regions of shear stress and elevated local blood pressure, such as curves and splits in the vasculature.? Atherosclerosis is with us, in some form, throughout our life course.? Yet most doctors consider it “overtreatment” to intervene if a patient’s computed ten-year risk of a major adverse cardiac event (e.g., heart attack or stroke) is below 5%, arguing that the benefits are not greater than the risks, or that treatment costs too much. In my opinion, this betrays a broader ignorance about the inexorable, long-term unfolding of heart disease. ?Ten years is far too short a time horizon. ?If we want to reduce deaths from cardiovascular disease, we need to begin thinking about prevention in people in their forties and even thirties.”

The bottom-line is that risk of heart disease is proportional to apoB exposure over time. ?The sooner we lower apoB exposure, thus lowering risk, the more the benefits compound over time—and the greater our overall risk reduction.

Next week I will share Dr. Attia’s research and advice on the 3rd horseman, Cancer.? Again, I strongly urge you to read Outlive and I hope that these excerpts will help convince you to do so.?

Have a disciplined week as you work to build your financial freedom and improve your health span.? If you find this advice helpful, please share with your friends and colleagues.? As usual, I look forward to your questions and comments.? Be safe.? Take good care, and if you can, help someone in need.

Cheers, Nigel

Nigel Romano, Senior Director, Moore Trinidad & Tobago, Chartered Accountants