summarize this "Scientists have been exploring the medical mysteries of the human heart for
almost as long as poets have been probing its metaphorical depths. 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 microadjusts 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 sixty thousand miles, if you’re keeping score).
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.
It’s practically a dirty word, cholesterol. 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. I practically need to be
restrained when I hear these terms, because they’re so meaningless. And your
“total cholesterol,” the first number that people offer up when we’re talking
about heart disease, is only slightly more relevant to your cardiovascular risk
than the color of your eyes. So let’s hit rewind and look at what cholesterol
really is, what it does, and how it contributes to heart disease.
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 percent 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. Also, these particles (and other
lipoproteins) frequently exchange cargo with one another, which is part of
what drives me crazy about labeling them “good” and “bad.” When an HDL
transfers its “good cholesterol” to an LDL particle, does that cholesterol
suddenly become “bad”?
The answer is no—because 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—not only LDL but several others
[*1]—carries this apoB
protein signature.
—
Another major misconception about heart disease is that it is somehow
caused by the cholesterol that we eat in our diet. According to this dated and
simplistic view, eating cholesterol-rich foods causes the so-called bad
cholesterol to accumulate in our blood and then build up on our artery walls,
as if you poured bacon grease down the kitchen drain every time you made
breakfast. Sooner or later, your sink will back up.
The humble egg, in particular, was singled out in a 1968 proclamation by
the American Heart Association, accused of causing heart disease because of
its high cholesterol content. It has remained in nutritional purgatory for
decades, even after reams of research papers showing that dietary cholesterol
(and particularly egg consumption) may not have much to do with heart
disease at all. Eating lots of saturated fat can increase levels of
atherosclerosis-causing lipoproteins in blood, but most of the actual
cholesterol that we consume in our food ends up being excreted out our
backsides. The vast majority of the cholesterol in our circulation is actually
produced by our own cells. Nevertheless, US dietary guidelines warned
Americans away from consuming foods high in cholesterol for decades, and
nutrition labels still inform American consumers about how much cholesterol
is contained in each serving of packaged foods.
Even Ancel Keys, the famed nutrition scientist who was one of the
founding fathers of the notion that saturated fat causes heart disease, knew
this was nonsense. The problem he recognized was that much of the basic
research into cholesterol and atherosclerosis had been conducted in rabbits,
which have a unique ability to absorb cholesterol into their blood from their
food and form atherosclerotic plaques from it; the mistake was to assume that
humans also absorb dietary cholesterol as readily. “There’s no connection
whatsoever between cholesterol in food and cholesterol in blood,” Keys said
in a 1997 interview. “None. And we’ve known that all along. Cholesterol in
the diet doesn’t matter at all unless you happen to be a chicken or a rabbit.”
It took nearly two more decades before the advisory committee
responsible for the US government dietary guidelines finally conceded (in
2015) that “cholesterol is not a nutrient of concern for overconsumption.”
Glad we settled that.
The final myth that we need to confront is the notion 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. I’ll never forget the one-question pop quiz that Allan
Sniderman dropped on me over dinner at Dulles Airport, back in 2014:
“What proportion of heart attacks occur in people younger than age sixtyfive?” I guessed high, one in four, but I was way low. Fully half of all major
adverse cardiovascular events in men (and a third of those in women), such as
heart attack, stroke, or any procedure involving a stent or a graft, occur before
the age of sixty-five. In men, one-quarter of all events occur before age fiftyfour.
But while the events themselves may have seemed sudden, the problem
was likely lurking for years. Atherosclerosis is a slow-moving, sneaky disease,
which is why I take such a hard line on it. Our risk of these “events” rises
steeply in the second half of our lifespan, 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.
"