HORSEMAN #2: HEART DISEASE

This week, as promised, I share Dr. Attia’s advice on heart disease, the second of the four horsemen.

As Dr. Attia notes in Outlive, the most common symptom of heart disease is death. He explains:

“When I was in medical school, my first-year pathology professor liked to ask a trick question: What is the most common “presentation” (or symptom) of heart disease? It wasn’t chest pain, left arm pain, or shortness of breath, the most common answers; it was sudden death. You know the patient has heart disease because he or she has just died from it. This is why, he claimed, the only doctors who truly understand cardiovascular disease are pathologists. His point: by the time a pathologist sees your arterial tissue, you are dead.”

He advises that roughly one-third of the time heart attacks are fatal.? And globally, heart disease and stroke, which he categorises under the single heading of atherosclerotic cardiovascular disease, or ASCVD, is the leading cause of death for both men and women.? It kills an estimated 2,300 people every day in the United States alone, many suddenly and without warning: more than any other cause, including cancer, the 3rd horseman.

However, the real problem is that although this disease is the leading killer, it is, as Dr. Attia notes, “more easily prevented than cancer or Alzheimer’s disease because we know a lot about how and why it begins and the way it progresses. ?Therefore, it is relatively easy to delay if you’re smart and you get on the case early.”

As I noted in the introductory article on Dr. Attia’s work, the primary causes of slow death like heart disease, are disease processes.? We need to spend some more time observing and studying these processes and taking action to prevent the start of these processes or delay their progress.? As Attia notes:

“… we need a new way of thinking about chronic diseases, their treatment, and how to maintain long-term health.? The goal of this new medicine—which I call Medicine 3.0—is not to patch people up and get them out the door, removing their tumors and hoping for the best, but rather to prevent the tumors from appearing and spreading in the first place.? Or to avoid that first heart attack.? Or to divert someone from the path to Alzheimer’s disease. Our treatments, and our prevention and detection strategies, need to change to fit the nature of these diseases, with their long, slow prologues.”

He goes on to state that the problem with Medicine 2.0 is that the tools and approaches currently widely available do not allow us to see very far over the horizon.? Our time frames are too short!

?“We need to begin treating it, and preventing heart disease, much earlier.? If we could get it right, the potential payoff would be huge: the high prevalence of male centenarians on the island of Sardinia, for example, has largely been attributed to their ability to avoid or delay circulatory disease. Fewer Sardinian men die from heart disease between the ages of eighty and one hundred than anywhere else in Italy.”

Outlive by Peter Attia, MD & Bill Gifford

THE HEART

WHEN THE HEART STOPS, WE STOP!

Dr. Attia provides clarity and insight into the heart and heart disease.? Here is what he has to say about the heart in Outlive:

“It is a wondrous organ, a tireless muscle that pumps blood around the body every moment of our lives.? It pounds hard when we are exercising, slows down when we sleep, and even micro adjusts its rate between beats, a hugely important phenomenon called heart rate variability.? And when it stops, we stop.

Our vascular network is equally miraculous, a web of veins, arteries, and capillaries that, if stretched out and laid end to end, would wrap around the earth more than twice (about 60,000 miles).? Each individual blood vessel is a marvel of material science and engineering, capable of expanding and contracting dozens of times per minute, allowing vital substances to pass through its membranes, and accommodating huge swings in fluid pressure, with minimal fatigue.? No material created by man can even come close to matching this.? If one vessel is injured, others regrow to take its place, ensuring continuous blood flow throughout the body.

Incredible as it is, however, our circulatory system is far from perfect—in fact, it is almost perfectly designed to generate atherosclerotic disease, just in the course of daily living. This is in large part because of another important function of our vasculature. In addition to transporting oxygen and nutrients to our tissues and carrying away waste, our blood traffics CHOLESTEROL MOLECULES between cells.”

CHOLESTEROL

And there it is.? That dirty word, cholesterol.? But what is this.? Let’s hear from Dr. Attia:

“Your doctor will probably utter it with a frown, because as everyone knows, cholesterol is evil stuff. ?Well, some of it is—you know, the LDL or “bad” cholesterol, which is inevitably counterpoised against the HDL, or “good” cholesterol. …

Cholesterol is essential to life. ?It is required to produce some of the most important structures in the body, including cell membranes; hormones such as testosterone, progesterone, estrogen, and cortisol; and bile acids, which are necessary for digesting food. ?All cells can synthesize their own cholesterol, but some 20% of our body’s (large) supply is found in the liver, which acts as a sort of cholesterol repository, shipping it out to cells that need it and receiving it back via the circulation.

Because cholesterol belongs to the lipid family (that is, fats), it is not water soluble and thus cannot dissolve in our plasma like glucose or sodium and travel freely through our circulation. ?So it must be carted around in tiny spherical particles called lipoproteins—the final “L” in LDL and HDL—which act like little cargo submarines. ?As their name suggests, these lipoproteins are part lipid (inside) and part protein (outside); the protein is essentially the vessel that allows them to travel in our plasma while carrying their water-insoluble cargo of lipids, including cholesterol, triglycerides, and phospholipids, plus vitamins and other proteins that need to be distributed to our distant tissues.

The reason they’re called high- and low-density lipoproteins (HDL and LDL, respectively) has to do with the amount of fat relative to protein that each one carries. LDLs carry more lipids, while HDLs carry more protein in relation to fat, and are therefore more dense. …

“… it’s not the cholesterol per se that causes problems but the nature of the particle in which it’s transported. ?Each lipoprotein particle is enwrapped by one or more large molecules, called apolipoproteins, that provide structure, stability, and, most importantly solubility to the particle. ?HDL particles are wrapped in a type of molecule called apolipoprotein A (or apoA), while LDL is encased in apolipoprotein B (or apoB). ?This distinction may seem trivial, but it goes to the very root cause of atherosclerotic disease: every single lipoprotein that contributes to atherosclerosis carries this apoB protein signature.”

Every single lipoprotein that contributes to atherosclerosis carries the apoB protein signature

As Dr. Attia notes, and I paraphrase:

“Another major misconception about heart disease is that it is somehow caused by the cholesterol that we eat.? However, research has shown that dietary cholesterol may not have much to do with heart disease because most of the cholesterol that we consume ends up being excreted.? Most of the cholesterol in our circulation is produced by our own cells.? But it was only in 2015 that the advisory committee responsible for the US government dietary guidelines to concede that “cholesterol is not a nutrient of concern for overconsumption.”

The final myth is that cardiovascular disease primarily strikes “old” people and that therefore we don’t need to worry much about prevention in patients who are in their twenties and thirties and forties.? Not true.? This is because 50% of all major adverse cardiovascular events in men (and 33% of those in women), such as heart attack, stroke, occur before the age of 65.? In men, 25% of all events occur before age 54.?

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.”

I will not go into the details here, so I strongly recommend that you read Outlive.? But the key takeaway for me here, as advised by Dr. Attia, is exposure to apoB-tagged particles, over time. ?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.

Next week I will share Dr. Attia’s advice on what we can do to reduce cardiovascular risk.? 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