How to Read a Cholesterol Test | Mark's Daily Apple
Before we get into the big job of interpreting cholesterol numbers, let’s review what cholesterol actually is.
Cholesterol is cholesterol: a waxy steroid of fat that serves as an
essential structural component of cellular membranes and in the
production of steroid hormones, vitamin D,
and bile acids. Contrary to what the terminology indicates, there’s
actually only one “type” of cholesterol in the human body, and it’s
called, quite simply, cholesterol. What we think of when we use the word
“cholesterol” is actually a lipoprotein – a fatty conglomerate of protein and lipids that delivers cholesterol and fat
and fat-soluble nutrients to different parts of the body. It’s not just
free cholesterol floating around in your blood; it’s cholesterol bound
up by lipoproteins.
So LDL, HDL, VLDL, all those (in)famous measurements we get at the
doctor’s office are just different types of lipoproteins. They’re not
actually cholesterol. I discussed this briefly a couple years back, and there’s always Griff’s big primer in the forum, so take the time to go check out both. And also take a peak at The Definitive Guide to Cholesterol for review.
Okay, let’s talk about the most commonly bandied-about cholesterol
numbers: LDL-C and HDL-C. What do they really mean? What are they
actually measuring?
To understand what these numbers mean, let’s play the freeway analogy
game. Both LDL-C and HDL-C, the standard, basic readings you get from
the lab, do not reflect the number of LDL or HDL particles – the number
of lipoproteins – in your serum. Instead, they reflect the total amount
of cholesterol contained in your LDL and HDL particles. Hence, the “C”
in LDL/HDL-C, which stands for “cholesterol.” Measuring the LDL/HDL-C
and then making potentially life-changing health decisions based on the
number is like counting the number of people riding in vehicles on a
freeway to determine the severity of traffic. It’s data, and it might
give you a rough approximation of the situation, but it’s not as useful
as actually counting the number of vehicles. A reading of 100 could mean
you’re dealing with a hundred compact cars, each carrying a single
driver, or it could mean you’ve got four buses carrying 25 passengers
each. Or it could be a couple buses and the rest cars. You simply don’t
know how bad (or good) traffic is until you get a direct measurement of
LDL and HDL particle number.
Say you go ahead and get those particle numbers directly measured.
You’re still limited, because that is just a single datapoint from a
specific time in your life/day/week. Analogies are fun and helpful, I
think, so let’s take this traffic and freeway stuff further. To get an
accurate idea of traffic, you need constant updates, right? Imagine you
counted the number of cars on the freeway at 12:05 on a Saturday
afternoon four weeks ago. That’s great, but what does it tell you about
traffic at 5 PM on a Thursday? Even though it’s the same stretch of
asphalt/artery, we can’t divine much at all from that single
measurement. You need more data points. That traffic fluctuates wildly
is entirely uncontroversial. Any southern Californian could tell you
that. But did you know that LDL, HDL, and total cholesterol readings in
the same person can fluctuate just as wildly,
oftentimes enough to move that person from “desirable” to “high risk”
and back to “desirable” lipid status without any nutritional or
lifestyle changes in the span of a few mere weeks?
In biology, a single snapshot rarely, if ever, tells the whole story.
Who woulda known?
But just because the standard cholesterol test is but a snapshot of a
dynamic system in flux doesn’t negate the potential usefulness of
getting your cholesterol checked. As much as Conventional Wisdom
has gotten things wrong when it comes to cholesterol and heart disease,
the two do have a relationship together. There is a connection;
contrary to what the AHA might think, we just don’t have it ironed out
yet. In my opinion, the most persuasive hypothesis about the real causes
of atherosclerosis and heart disease comes from Chris Masterjohn and is
highlighted in his recent AHS talk, “Heart Disease and Molecular Degeneration,” and on his blog. It’s a synthesis of the two prevailing notions regarding cholesterol and heart disease – the one which says elevated blood cholesterol
plays no causal role in heart disease and the one which says elevated
blood cholesterol is the primary cause of heart disease – and it goes
something like this:
LDL receptors normally “receive” LDL particles and remove them from
circulation so that they can deliver nutrients and cholesterol to cells,
and fulfill their normal roles in the body.
If LDL receptor activity is downregulated, LDL particles clear more
slowly from and spend more time in the blood. Particles accumulate.
When LDL particles hang out in the blood for longer stretches of time, their fragile polyunsaturated fatty membranes are exposed to more oxidative forces, like inflammation, and
their limited store of protective antioxidants can deplete.
When this happens, the LDL particles oxidize.
Once oxidized, LDL particles are taken up by the endothelium – a
layer of cells that lines the inside of blood vessels – to form
atherosclerotic plaque so they don’t damage the blood vessel. This
sounds bad (and is), but it’s preferable to acutely damaging the blood
vessels right away.
So it’s the oxidized LDL that gets taken up into the endothelium and
precipitates the formation of atherosclerotic plaque, rather than
regular LDL. OxLDL, poor receptor activity, and inflammation are the
problems. But since measuring oxidized LDL in serum is difficult
(oxidized LDL gets taken up out of serum and into the endothelium rather
quickly) and expensive, we need other, more realistic, more obtainable
methods. We need to work with what we’ve got. It would be great if a
doctor could quickly order up an “LDL receptor activity” test, but I
don’t see that happening anytime soon.
Enter the various lipid panels.
First up is your basic lipid panel, the standard test the average
doctor is going to order for a patient. If you go this route, you’ll
typically get four measurements: total cholesterol (TC); high density
lipoprotein cholesterol (HDL-C); low density lipoprotein cholesterol
(LDL-C); and triglycerides.
(you’ll have a heart attack or you’ll have to pay a higher health
insurance premium, if we take you on at all).
My take: Mostly meaningless. Even though the epidemiological evidence
suggests a TC between 200 and 240 mg/dl is best for all-cause
mortality, we can’t hang our hats on it. First off, total cholesterol is
limited because it’s only telling us the amount of cholesterol
contained in all our lipoproteins without saying anything about what
kind of lipoproteins we have or how many there are. Second, total
cholesterol is limited because it’s determined by a bizarre formula –
HDL-C+LDL-C+(Triglycerides/5) – that reduces various types of blood
lipids, each with a different role in the body and a unique impact on
our risk for illness, to mere numbers. Someone with low HDL and high
triglycerides could easily have the same TC as someone with high HDL and
low triglycerides, so long as the numbers work out. Whether it’s being
used to predict wellness or disease, total cholesterol by itself is
mostly meaningless.
that cleans up “excessive” cholesterol and fat from tissues, so the
higher the better! Though men and women should strive for levels
exceeding 60 mg/dl, above 40 is acceptable for the former and above 50
is acceptable for the latter.
My take: Higher HDL-Cs correlate strongly with
better cardiovascular health. No real argument here. Higher HDLs are
desirable. Just remember, it’s only a snapshot of a glimpse into the
cholesterol content of your HDL particles. Among most groups tested, the
TC:HDL ratio is actually a strong indicator of heart disease risk, with
higher ratios corresponding to higher risks. Note, though, that no
Primal Blueprint adherents were among the groups analyzed, ever.
want that low density lipoprotein so low as to be nearly nonexistent.
Your body obviously hates you; otherwise, it wouldn’t be producing a
potently toxic substance and sending it directly into your endothelial
cells to form atherosclerotic plaque! Of course, we’re not actually
measuring the number of low density lipoproteins, just the amount of
cholesterol contained in them, but still!
My take: While a high LDL-C may indicate a problem,
remember that LDL-C only indicates the total amount of cholesterol in
your LDL particles. You could easily have a few large particles (good)
or a bunch of smaller, denser ones (bad, might indicate poor LDL
receptor activity and an LDL that likes to hang out in the blood), but
LDL-C alone isn’t enough to know. It’s also just a moment in time,
whereas what you’re interested in is the trend. If the trend indicates a
steady rise in LDL-C, however, that could hint at poorer LDL clearance
and lower LDL receptor activity (and greater susceptibility to
oxidation).
My take: High triglycerides correlate strongly with
low HDL and smaller, denser LDL. High triglycerides, then, could
indicate more oxidized (or oxidizable) LDL. The triglycerides of most Primal
eaters, especially those on the lower carb side of things, usually
hover well below 100 mg/dl. Triglycerides come packaged in VLDL, or very
low density lipoproteins (which are calculated by dividing your
triglyceride count by 5).
So, what can we learn from a standard lipid test? Not much, actually. We can learn from standard lipid tests, however.
If we take a series of regular ol’ lipid measurements, preferably one
pre- and several peri-Primal, we can get an idea of our metabolic
health. Look for:
just aren’t cutting it, you might as well go for one of the premium lab
tests: the NMR LipoProfile or maybe the VAP. Rather than rely on
indirect estimates and formulas, NMR and VAP directly measure the size
of your lipoproteins. I find NMR to be far more useful, because in
addition to measuring particle size, it measures particle count (whereas
VAP only estimates the count).
But you probably have holiday shopping to do, and I don’t want to
drone on for too long, so I’ll leave it at that for now. Next week, I’ll
pick up where I left off and get into what you can expect from NMR and
VAP testing, including the downsides and the advantages. After that,
I’ll go into some strategies for improving your numbers – or, rather,
improving your health which in turn should improve your numbers.
Before we get into the big job of interpreting cholesterol numbers, let’s review what cholesterol actually is.
Cholesterol is cholesterol: a waxy steroid of fat that serves as an
essential structural component of cellular membranes and in the
production of steroid hormones, vitamin D,
and bile acids. Contrary to what the terminology indicates, there’s
actually only one “type” of cholesterol in the human body, and it’s
called, quite simply, cholesterol. What we think of when we use the word
“cholesterol” is actually a lipoprotein – a fatty conglomerate of protein and lipids that delivers cholesterol and fat
and fat-soluble nutrients to different parts of the body. It’s not just
free cholesterol floating around in your blood; it’s cholesterol bound
up by lipoproteins.
So LDL, HDL, VLDL, all those (in)famous measurements we get at the
doctor’s office are just different types of lipoproteins. They’re not
actually cholesterol. I discussed this briefly a couple years back, and there’s always Griff’s big primer in the forum, so take the time to go check out both. And also take a peak at The Definitive Guide to Cholesterol for review.
Okay, let’s talk about the most commonly bandied-about cholesterol
numbers: LDL-C and HDL-C. What do they really mean? What are they
actually measuring?
To understand what these numbers mean, let’s play the freeway analogy
game. Both LDL-C and HDL-C, the standard, basic readings you get from
the lab, do not reflect the number of LDL or HDL particles – the number
of lipoproteins – in your serum. Instead, they reflect the total amount
of cholesterol contained in your LDL and HDL particles. Hence, the “C”
in LDL/HDL-C, which stands for “cholesterol.” Measuring the LDL/HDL-C
and then making potentially life-changing health decisions based on the
number is like counting the number of people riding in vehicles on a
freeway to determine the severity of traffic. It’s data, and it might
give you a rough approximation of the situation, but it’s not as useful
as actually counting the number of vehicles. A reading of 100 could mean
you’re dealing with a hundred compact cars, each carrying a single
driver, or it could mean you’ve got four buses carrying 25 passengers
each. Or it could be a couple buses and the rest cars. You simply don’t
know how bad (or good) traffic is until you get a direct measurement of
LDL and HDL particle number.
Say you go ahead and get those particle numbers directly measured.
You’re still limited, because that is just a single datapoint from a
specific time in your life/day/week. Analogies are fun and helpful, I
think, so let’s take this traffic and freeway stuff further. To get an
accurate idea of traffic, you need constant updates, right? Imagine you
counted the number of cars on the freeway at 12:05 on a Saturday
afternoon four weeks ago. That’s great, but what does it tell you about
traffic at 5 PM on a Thursday? Even though it’s the same stretch of
asphalt/artery, we can’t divine much at all from that single
measurement. You need more data points. That traffic fluctuates wildly
is entirely uncontroversial. Any southern Californian could tell you
that. But did you know that LDL, HDL, and total cholesterol readings in
the same person can fluctuate just as wildly,
oftentimes enough to move that person from “desirable” to “high risk”
and back to “desirable” lipid status without any nutritional or
lifestyle changes in the span of a few mere weeks?
In biology, a single snapshot rarely, if ever, tells the whole story.
Who woulda known?
But just because the standard cholesterol test is but a snapshot of a
dynamic system in flux doesn’t negate the potential usefulness of
getting your cholesterol checked. As much as Conventional Wisdom
has gotten things wrong when it comes to cholesterol and heart disease,
the two do have a relationship together. There is a connection;
contrary to what the AHA might think, we just don’t have it ironed out
yet. In my opinion, the most persuasive hypothesis about the real causes
of atherosclerosis and heart disease comes from Chris Masterjohn and is
highlighted in his recent AHS talk, “Heart Disease and Molecular Degeneration,” and on his blog. It’s a synthesis of the two prevailing notions regarding cholesterol and heart disease – the one which says elevated blood cholesterol
plays no causal role in heart disease and the one which says elevated
blood cholesterol is the primary cause of heart disease – and it goes
something like this:
LDL receptors normally “receive” LDL particles and remove them from
circulation so that they can deliver nutrients and cholesterol to cells,
and fulfill their normal roles in the body.
If LDL receptor activity is downregulated, LDL particles clear more
slowly from and spend more time in the blood. Particles accumulate.
When LDL particles hang out in the blood for longer stretches of time, their fragile polyunsaturated fatty membranes are exposed to more oxidative forces, like inflammation, and
their limited store of protective antioxidants can deplete.
When this happens, the LDL particles oxidize.
Once oxidized, LDL particles are taken up by the endothelium – a
layer of cells that lines the inside of blood vessels – to form
atherosclerotic plaque so they don’t damage the blood vessel. This
sounds bad (and is), but it’s preferable to acutely damaging the blood
vessels right away.
So it’s the oxidized LDL that gets taken up into the endothelium and
precipitates the formation of atherosclerotic plaque, rather than
regular LDL. OxLDL, poor receptor activity, and inflammation are the
problems. But since measuring oxidized LDL in serum is difficult
(oxidized LDL gets taken up out of serum and into the endothelium rather
quickly) and expensive, we need other, more realistic, more obtainable
methods. We need to work with what we’ve got. It would be great if a
doctor could quickly order up an “LDL receptor activity” test, but I
don’t see that happening anytime soon.
Enter the various lipid panels.
First up is your basic lipid panel, the standard test the average
doctor is going to order for a patient. If you go this route, you’ll
typically get four measurements: total cholesterol (TC); high density
lipoprotein cholesterol (HDL-C); low density lipoprotein cholesterol
(LDL-C); and triglycerides.
Total cholesterol
What they say: Get that TC below 200, or else(you’ll have a heart attack or you’ll have to pay a higher health
insurance premium, if we take you on at all).
My take: Mostly meaningless. Even though the epidemiological evidence
suggests a TC between 200 and 240 mg/dl is best for all-cause
mortality, we can’t hang our hats on it. First off, total cholesterol is
limited because it’s only telling us the amount of cholesterol
contained in all our lipoproteins without saying anything about what
kind of lipoproteins we have or how many there are. Second, total
cholesterol is limited because it’s determined by a bizarre formula –
HDL-C+LDL-C+(Triglycerides/5) – that reduces various types of blood
lipids, each with a different role in the body and a unique impact on
our risk for illness, to mere numbers. Someone with low HDL and high
triglycerides could easily have the same TC as someone with high HDL and
low triglycerides, so long as the numbers work out. Whether it’s being
used to predict wellness or disease, total cholesterol by itself is
mostly meaningless.
HDL-C
What they say: “Good” cholesterol. It’s the “garbage truck”that cleans up “excessive” cholesterol and fat from tissues, so the
higher the better! Though men and women should strive for levels
exceeding 60 mg/dl, above 40 is acceptable for the former and above 50
is acceptable for the latter.
My take: Higher HDL-Cs correlate strongly with
better cardiovascular health. No real argument here. Higher HDLs are
desirable. Just remember, it’s only a snapshot of a glimpse into the
cholesterol content of your HDL particles. Among most groups tested, the
TC:HDL ratio is actually a strong indicator of heart disease risk, with
higher ratios corresponding to higher risks. Note, though, that no
Primal Blueprint adherents were among the groups analyzed, ever.
LDL-C
What they say: Get it as low as humanly possible! Iwant that low density lipoprotein so low as to be nearly nonexistent.
Your body obviously hates you; otherwise, it wouldn’t be producing a
potently toxic substance and sending it directly into your endothelial
cells to form atherosclerotic plaque! Of course, we’re not actually
measuring the number of low density lipoproteins, just the amount of
cholesterol contained in them, but still!
My take: While a high LDL-C may indicate a problem,
remember that LDL-C only indicates the total amount of cholesterol in
your LDL particles. You could easily have a few large particles (good)
or a bunch of smaller, denser ones (bad, might indicate poor LDL
receptor activity and an LDL that likes to hang out in the blood), but
LDL-C alone isn’t enough to know. It’s also just a moment in time,
whereas what you’re interested in is the trend. If the trend indicates a
steady rise in LDL-C, however, that could hint at poorer LDL clearance
and lower LDL receptor activity (and greater susceptibility to
oxidation).
Triglycerides
What they say: Lower would be better, sure, but you really gotta do something about that LDL! Anything less than 150 mg/dl is fine.My take: High triglycerides correlate strongly with
low HDL and smaller, denser LDL. High triglycerides, then, could
indicate more oxidized (or oxidizable) LDL. The triglycerides of most Primal
eaters, especially those on the lower carb side of things, usually
hover well below 100 mg/dl. Triglycerides come packaged in VLDL, or very
low density lipoproteins (which are calculated by dividing your
triglyceride count by 5).
So, what can we learn from a standard lipid test? Not much, actually. We can learn from standard lipid tests, however.
If we take a series of regular ol’ lipid measurements, preferably one
pre- and several peri-Primal, we can get an idea of our metabolic
health. Look for:
- Trends – Are your triglycerides going down over time? That’s great. Is your HDL trending up? Also good.
- Normal fluctuations – Your numbers can jump around 20-30 points in either direction between readings without it necessarily meaning anything.
- TC:HDL-C ratio – Lower is better and indicates fewer LDL particles.
- Triglyceride:HDL-C ratio – Lower is better and indicates larger LDL (and, usually, fewer) particles. Ideally, this will be close to 1 or lower; one study (PDF) found that 1.33 was the cut off.
just aren’t cutting it, you might as well go for one of the premium lab
tests: the NMR LipoProfile or maybe the VAP. Rather than rely on
indirect estimates and formulas, NMR and VAP directly measure the size
of your lipoproteins. I find NMR to be far more useful, because in
addition to measuring particle size, it measures particle count (whereas
VAP only estimates the count).
But you probably have holiday shopping to do, and I don’t want to
drone on for too long, so I’ll leave it at that for now. Next week, I’ll
pick up where I left off and get into what you can expect from NMR and
VAP testing, including the downsides and the advantages. After that,
I’ll go into some strategies for improving your numbers – or, rather,
improving your health which in turn should improve your numbers.
