how can you dodge a heart attack? today we'll look at atherosclerosis, one of
the most common causes of disease and death in our society. what causes it and the best
lab tests to prevent it. why is this topic so confusing? well, for starters scientists
are horrible at coming up with names. there's ldl and ldl cholesterol and they're different things
but a lot of people call them both ldl and then there's hdl and vldl and there's idl
so let's touch on the basics real quick, the bottom line is cholesterol is carried in our
bloodstream by lipoproteins, so lipoproteins are the buses and cholesterol is the passenger
these buses travel inside our arteries and some of them get stuck in the artery wall
if there's a lot of buses, a lot of lipoproteins in the blood, more of them get stuck and over the
years this forms plaque, aka atherosclerosis. too many buses cause a traffic jam
plaque can block blood flow and cause angina which is chest pain when the heart muscle
doesn't get enough blood. plaque can also break and clot causing a heart attack. and nobody wants that
now these buses, these lipoproteins, they come in different types, there's ldl or low density
lipoprotein, you've heard of that one. there's also vldl or very low density lipoprotein
i told you scientists suck at this name thing. ldl and vldl belong to the same family, they're related
we're simplifying this a bit, in reality there's a couple more members of that family and there's
another family of lipoproteins but these are the two main ones that cause atherosclerosis. so just
like greyhound is a large company that includes several bus lines, one that goes to new york, one
that goes to chicago, etc, this large family of lipoproteins includes several bus lines
we got our ldls, our vldls, etc. now, the good news is they all carry a little tag called
apob. just like the greyhound buses have the symbol on the side, these guys are labeled too. this comes
in really handy because we can measure the number of lipoproteins in this family by measuring the
apob tags. as we'll see this becomes a crucial measure. okay so far so good here's where it
gets a little tricky. it's the buses that cause traffic jams, it's the lipoproteins that cause
atherosclerosis but when we go to the doctor and get our blood work done, for historical reasons
they don't measure the buses, they measure the passengers. you get your ldl-cholesterol which
is the cholesterol carried by the ldl buses and you also get your triglycerides which is another
type of passenger. those passengers serve as an estimate of the number of buses and consequently
of the risk of atherosclerosis. now, generally this works okay because the more passengers are being
carried around the more buses are on the road and the more buses are on the road the higher
the risk of a traffic jam. in the words of the european atherosclerosis society, ldl-cholesterol
is a satisfactory surrogate for ldl particle number under most circumstances. so having high
ldl-cholesterol is usually a red flag and the same for triglycerides. online you'll see this game of
'my marker is better than yours', with some people focusing exclusively on ldl-cholesterol and saying
triglycerides are irrelevant and some other people saying 'no, focus on the triglycerides and forget
the ldl-cholesterol'. but of course these are both markers of lipoproteins that cause atherosclerosis
neither one is supposed to be sky-high. picking one of these markers and ignoring the other
is like pulling up the blanket and uncovering our feet. they're both useful and neither one is
perfect. these researchers spell it out: "the risk of atherosclerosis is determined by the concentration
of apob particles regardless of lipid content. so the benefit of lipid-lowering, meaning
lowering cholesterol or triglycerides, should be proportional to the reduction in apob,
regardless of the change in ldl-cholesterol or triglycerides". for most people the number
of passengers reflects the number of lipoproteins so they're a decent
indicator of risk, but in the exceptions where they don't, where there's a mismatch,
it's the number of lipoproteins that determines risk, not ldl-cholesterol or triglycerides, so the
excessive focus on the passengers, on these markers, misses the point. this mismatch between number of
passengers and number of buses happens in about 25% of people. some of us have normal number
of lipoproteins, so normal apob, but they're packed with passengers, they're over capacity
these people are not at higher risk. risk goes with bus number, not passengers. other people have a
lot of lipoproteins, so apob is high, but they're pretty empty so the total number of passengers
is normal. and those people are at higher risk of atherosclerosis because the number of buses is
high. so ldl-cholesterol and triglycerides are kind of like the check engine light in your car. they're
useful indicators and just ignoring them and driving around like that for years can make things
worse but occasionally the light can be broken or malfunctioning and there's nothing wrong with the
actual engine. if we have reason to think the light isn't working properly we can check the engine
directly by measuring apob. most GPs, most general practitioners don't order that test routinely but
your cardiologists should be all over this. okay, what about hdl-cholesterol, the "good cholesterol"?
endless confusion around that. people with high hdl-cholesterol tend to have less heart disease
but that doesn't mean one factor causes the other. people with six-pack abs tend to own
more gym clothes but just owning more sweatpants is not going to get me ripped. damn it! we need to
actually test if there's a causal relationship by raising hdl-cholesterol specifically and seeing
if the risk comes down. this has been done many times. this analysis looked at 39 clinical trials
raising hdl-cholesterol did not lower atherosclerosis risk. this is one of the most
consistent observations in this field. raising hdl-cholesterol offers no cardiovascular protection
as harvard cardiovascular researcher frank sachs explains, the effects on cardiovascular disease of
foods or nutrients cannot be judged from changes in hdl-cholesterol. so hdl-cholesterol is kind of
like the sweatpants, it correlates with benefit, it tends to be there at the same time but it doesn't
actually cause the benefit. if we can't distinguish between correlation and causation we end up
incredibly confused. the same goes for ratios that include hdl-cholesterol. if i take a number that's
not informative and i throw it in a ratio i just end up with a ratio that's not informative. raising
my hdl-cholesterol makes the ratios appear better but it does nothing for risk. we know
that from the causal evidence. so telling myself that i'm safe because my hdl-cholesterol went up
is like drawing a six-pack with a sharpie and thinking i just got in shape. i know this topic
is a nerd fest with all the acronyms but it's absolutely essential to protect ourselves and
dispel all the confusion that's on the internet, that's why we keep making videos on this, and
it all makes sense when we understand the fundamentals and how these things all fit together
so here are the key concepts to dodge atherosclerosis and dodge that heart attack: number
one, if the apob buses, the apob lipoproteins are high that raises our risk of atherosclerosis
number two, we can measure the apob lipoproteins directly by measuring the apob tag, that's what the
lab test is called, apob. number three, passengers like ldl-cholesterol and triglycerides are useful
estimates of risk, either one being high is a red flag but neither one is perfect. and number four,
be careful with other markers that just correlate but have no causal relationship
like hdl-cholesterol. the most powerful way to improve your lipids including apob is to
optimize your diet, we've covered the key steps before so check that out and here's more detail
on the lipids in your blood work and what they mean