How to Reduce Our Risk of Atherosclerotic Cardiovascular Disease

First, it's vital to understand that cholesterol is not a deadly poison, but a substance that we need to be healthy.

Here are some reasons why we need cholesterol:

• It contributes to cell membrane integrity and function

• Cholesterol is used to make hormones that help us deal with stress, as well to make sex hormones

• It is converted to vitamin D, which is essential for proper growth, healthy bones, a healthy nervous system, muscle tone, and proper immune system function

• Cholesterol is used to make bile, needed for digestion of fat in food

• It acts as an antioxidant, actually protecting us against cellular damage that can lead to heart disease and cancer

• Cholesterol helps maintain a healthy intestinal lining, which helps protect us against autoimmune illnesses

The cholesterol found in our blood comes from two sources: cholesterol in food that we eat and cholesterol made in our liver and other cells throughout our body. But most of the cholesterol that we eat doesn't enter our bloodstream; rather, much of our dietary cholesterol goes straight through our gastrointestinal tract and gets excreted. The vast majority of the cholesterol found in our blood is made by our liver.

In order for cholesterol in our blood to carry out the essential functions noted above, it needs to be transported through our blood by special molecules called lipoproteins, the two primary ones being LDL (low density lipoprotein) and HDL (high density lipoprotein) - it's important to understand that LDL and HDL are not cholesterol; they carry and transport the same cholesterol.

Lipoproteins like LDL and HDL are wrapped by other molecules called apolipoproteins, which serve to stabilize lipoproteins and give them necessary solubility.

HDL is wrapped by a molecule called apolipoprotein A, abbreviated as apoA.

LDL is wrapped by a molecule called apolipoprotein B, abbreviated as apoB.

This is an important distinction because atherosclerotic cardiovascular disease is caused by LDL and other lipoproteins that are wrapped in apoB. The natural question to ask is why?

As HDL and LDL transport cholesterol through our circulatory system to deliver it to our cells to carry out the essential functions noted above, they can enter the inner lining of our blood vessels, called the endothelium. HDL wrapped by apoA can easily enter and leave the endothelium. But LDL and other lipoproteins wrapped by apoB tend to get stuck within the endothelium.

The longer that LDL and other lipoproteins wrapped by apoB remain stuck within the endothelium, the greater the likelihood that they, including the cholesterol they carry, will get damaged by free radicals that float through our circulatory system. Free radicals are also called reactive oxygen species, which is why free radical-induced damage is called oxidation.

Once lipoproteins and cholesterol wrapped by apoB become damaged within the endothelium (inner blood vessel lining), they become a sort of magnet that attracts other apoB-wrapped lipoproteins and the cholesterol they carry to enter the sub-endothelial space where they, too, become trapped and oxidized (damaged).

As oxidized apoB-wrapped lipoproteins and the cholesterol they carry build up within the endothelium, the endothelial lining itself gets damaged, and if enough damage occurs, our immune system will send specialized white blood cells to the area to deal with this damage.

The specialized white blood cells - called macrophages - eat up as much of the oxidized lipoprotein and cholesterol that they can, and in doing so, grow bigger and turn into what we call "foam" cells. When many foam cells build up in one area, they become visible to the eyes as a fatty streak.

Fatty streaks that build up along the endothelium (inner blood vessel lining) become atherosclerotic plaques, which can grow, become calcified, and cause stenosis (narrowing) of our blood vessels, leaving less space for blood to travel through in order to deliver oxygen, nutrients and other needed elements to our cells.

If we develop enough atherosclerosis in a blood vessel that supplies our heart (a coronary artery), some of our cardiac cells can die from lack of oxygen, which we call a heart attack or a myocardial infarction.

When atherosclerosis develops in a blood vessel delivering oxygen to our brain, we can suffer a stroke - a temporary stroke is called a transient ischemic attack.

Plaques can also become damaged, leading to the formation of clots which can contribute to further narrowing of our blood vessels; clots can also break off and cause problems elsewhere.

It should now be clear that cholesterol itself doesn't cause atherosclerotic cardiovascular disease. The atherosclerotic disease process begins when lipoproteins like LDL and the cholesterol they carry get trapped within the inner lining of our blood vessels, and become oxidized by free radicals. What these lipoproteins have in common is that they are wrapped with a molecule called apoB.

More than any other variable at play in the development of atherosclerotic cardiovascular disease, the total amount of apoB that we have in our circulation is arguably the best marker we have to predict our risk of experiencing a heart attack or stroke.

If your physician isn't ordering apoB for you, even if it costs you out of pocket to include it with your annual blood work, it's well worth doing so. In Canada, many family physicians won't order apoB, preferring to leave this valuable biomarker to cardiologists to write a requisition for when deemed necessary.

It's important to understand that the development of atherosclerotic cardiovascular disease occurs over a long period of time, decades in the vast majority of the population. While fatty streaks are found on autopsy of people even in their teens, it takes multiple decades to develop enough stenosis (narrowing) for there to be an imminent risk of experiencing a heart attack or stroke.

Remember HDL molecules that are wrapped in apoA? These molecules are constantly traveling through our circulatory system, and when they enter the sub-endothelial space where LDL and other lipoproteins wrapped in apoB have lodged and led to accumulation of clusters of foam cells and fatty streaks, HDL can actual vacuum some cholesterol out of the area, a process called delipidation. HDL can then travel back through the endothelial lining to re-enter the bloodstream, through which it can deliver cholesterol to the liver, various glands of the endocrine system, and fat cells where it can be used for the useful purposes listed earlier. This is why HDL is referred to as "good" cholesterol - HDL isn't cholesterol, but it helps protect our blood vessels through a few mechanisms, the primary one being vacuuming out cholesterol stuck in our blood vessel walls and delivering it to other cells of our body where cholesterol can be used to sustain our health.

It should also be understood that beyond apoB, there is another lipoprotein that increases risk of atherosclerotic cardiovascular disease - it's called Lp(a), referred to as "L P Little a." This shouldn't be confused with apoA, the lipoprotein that serves as a wrapper for HDL molecules.

Lp(a) forms when LDL molecules join together with an uncommon lipoprotein called apolipoprotein(a), abbreviated as apo(a) - remember, this is different from apoA which wraps around and transports HDL. What makes Lp(a) particularly bad for cardiovascular health is that as it floats through the circulatory system, it traps and accumulates oxidized lipid particles. Board certified Clinical Lipidologist Dr. Thomas Dayspring explains that Lp(a) actually serves to clear our bloodstream of oxidized lipid particles with a goal of delivering them to our liver from which they can be eliminated.

The problem, as longevity expert Dr. Peter Attia explains, is that Lp(a) is a member of the apoB family of particles that can enter the inner blood vessel lining and get stuck there. But because of its design which causes it to carry a bunch of lipid waste which it is supposed to clear out of our bloodstream, once stuck within the inner blood vessel lining, Lp(a) accelerates the formation of fatty streaks and plaques, significantly increasing risk of heart attack and stroke.

Among physicians like Drs. Dayspring and Attia, elevated Lp(a) is largely considered to be a genetic issue, and the consensus among the lipidology experts that I follow is that it's rational for everyone to get tested for it as a once-in-a-lifetime measure.

How to Reduce Our Risk of Heart Disease and Stroke

So now that we understand the pathogenesis of atherosclerotic cardiovascular disease, what can we do to delay its progression and thereby lower our risk of experiencing a cardiovascular or cerebrovascular accident?

I can only share my best suggestions, which are based on everything that I have learned, observed, and experienced over the past 20+ years. I am by no means an expert in this area, but I keep up to date with the findings and publications of leading experts, and I continue to review enough blood work and health histories to have what I believe is an informed view on this topic.

For people who have little to no interest in being mindful of their dietary and lifestyle choices, including the quality and quantity of their exercise and sleep, if apoB, LDL, and/or Lp(a) are high or in the upper range of "normal," I believe it makes sense to work with a physician to determine which statin and at what dosage is best at bringing these markers down and keeping them as low as possible, a process that often requires some trial and error.

It should be noted that there are a number of negative effects that people can experience while on statins, including muscle pain and potential strain on the liver, but not all statins behave equally in every individual, and many people can tolerate enough of a statin to substantially lower their apoB and LDL.

Some people do well taking red yeast rice, a food supplement that is made by fermenting rice with a type of yeast called Monascus purpureus. Red yeast rice has naturally occurring monacolin K, which is identical to the statin drug, lovastatin, so should be treated like a prescription drug.

For those who wish to avoid statins, action steps that lower our risk of developing atherosclerotic cardiovascular disease include the following:

1. Lower triglycerides.

A high triglyceride level contributes to a higher total apoB count. Effective ways of keeping triglycerides within an ideal range include minimizing intake of sugar and other refined carbohydrates, avoiding alcohol, getting regular exercise, especially strength-building movements, and optimizing body composition i.e. reducing unneeded adipose tissue.

2. Follow a minimally processed, nutrient-dense diet.

Such a diet should prioritize high quality protein, undamaged fatty acids, and a wide spectrum of vitamins, minerals, and other antioxidants. Plant foods that are richly pigmented with vibrant colors and low in natural sugars are helpful in neutralizing excess free radicals that show up in our circulation - less circulating free radicals translates to less oxidation of lipids within our circulatory system, and therefore less damage to our blood vessels that triggers atherogenic activity.

3. Support an active and healthy circulatory system.

By keeping our blood flowing healthfully through our blood vessels, logic dictates that we naturally lower the potential for apoB-wrapped lipoproteins and the cholesterol they carry to embed themselves within the endothelial lining. To this end, it's helpful to ensure that we stay hydrated by eating water-rich foods and drinking healthy liquids like pure water. Regular exercise, sweating, and use of saunas and cold showers or baths are also helpful in supporting a healthy circulatory system. And of course, it is always health-enhancing to maintain high sensitivity to insulin by minimizing intake of sugar and other refined carbohydrates - when we lose insulin sensitivity due to a high sugar diet, and live with higher-than-ideal blood sugar, the viscosity of our blood goes up and our blood flow suffers.

Additional Notes:

As it is with all aspects of our health, the quality and quantity of sleep that we regularly get and our emotional well-being are important determinants of our cardiovascular health.

It should also be understood that chronically high blood pressure can create endothelial damage via the cumulative increased mechanical stress that it puts on our blood vessel walls. Smoking can also hurt our endothelial lining via direct chemical damage. So optimal cardiovascular health requires that we prevent high blood pressure and avoid smoking.

Finally, we can reduce our risk of developing cardiovascular disease by getting enough B vitamins to ensure proper breakdown of an amino acid called homocysteine, as explained here: How High Homocysteine Can Precipitate Atherosclerosis

Some foods that I consider to be supportive of cardiovascular health:

• Lettuces and other common leafy greens, including spinach, arugula, and Asian greens like bok choy
• Perilla leaves (sometimes called sesame leaves)
• Basil, parsley, cilantro, and mint
• Cruciferous vegetables including broccoli, cabbage, and Brussels sprouts
• Avocados, olives, walnuts, pecans, and pistachios
• Anchovies, wild salmon, lake trout, seaweed, and organic eggs
• Antioxidant-rich fruits that are not excessively sweet - examples include most berries, acerola cherries, and pomegranates

It's also worth noting that as long as we are following a nutrient-dense diet and getting enough nutrient-rich calories to optimally fuel our daily physical and mental activities, our cardiovascular health is best served by not overeating, and actually being a little hungry for most of our waking hours - Dr. David Sinclair explains this well in his book, Lifespan.

For those who appreciate more granular details on the pathogenesis of atherosclerotic cardiovascular disease from an allopathic perspective, I can suggest studying the work of Dr. Peter Attia, including his book, Outlive.