April 25, 2012


The straight dope on cholesterol – Part I

Welcome to a topic near and dear.

Read Time 9 minutes

I’ve been planning to write at length about this topic for a few months, but I’ve been hesitant to do so for several reasons:

  1. To discuss it properly requires great care and attention (mine and yours, respectively).
  2. My own education on this topic only really began about 9 months ago, and I’m still learning from my mentors at a geometric pace.
  3. This topic can’t be covered in one post, even a Peter-Attia-who-can’t-seem-to-say-anything-under-2,000-word post.
  4. I feel a bit like an imposter writing about lipidology because my mentors on this topic (below) have already addressed this topic so well, I’m not sure I have anything to add.

But here’s the thing.  I am absolutely – perhaps pathologically – obsessed with lipidology, the science and study of lipids.  Furthermore, I’m getting countless questions from you on this topic.  Hence, despite my reservations above, I’m going to give this a shot.


A few thoughts before we begin.

  1. I’m not even going to attempt to cover this topic entirely in this post, so please hold off on asking questions beyond the scope of this post.
  2. Please resist the urge to send me your cholesterol numbers.  I get about 30 such requests per day, and I cannot practice medicine over the internet.  By all means, share your story with me and others, but understand that I can’t really comment other than to say what I pretty much say to everyone: standard cholesterol testing (including VAP) is largely irrelevant and you should have a lipoprotein analysis using NMR spectroscopy (if you don’t know what I mean by this, that’s ok… you will soon).
  3. This topic bears an upsettingly parallel reality to that of nutrition “science” in that virtually all health care providers have no understanding of it and seem to only reiterate conventional wisdom (e.g., “LDL is bad,” “HDL is good”).  We’ll be blowing the doors off this fallacious logic.

By the end of this series, should you choose to internalize this content (and pick up a few homework assignments along the way), you will understand the field of lipidology and advanced lipid testing better than 95% of physicians in the United States.  I am not being hyperbolic.

One last thing before jumping in:  Everything I have learned and continue to learn on this topic has been patiently taught to me by the words and writings of my mentors on this subject: Dr. Tom Dayspring, Dr. Tara Dall, Dr. Bill Cromwell, and Dr. James Otvos. I am eternally in their debt and see it as my duty to pass this information on to everyone interested.

Are you ready to start an exciting journey?


Concept #1 – What is cholesterol?

Cholesterol is a 27-carbon molecule shown in the figure below. Each line in this figure represents a bond between two carbon atoms.  Sorry, I’ve got to get it out there.  That’s it.  Mystery over.

All this talk about “cholesterol” and most people don’t actually know what it is.  So there you have it.  Cholesterol is “just” another organic molecule in our body.


Cholesterol molecule

I need to make one important distinction that will be very important later.  Cholesterol, a steroid alcohol, can be “free” or “unesterified” (“UC” as we say, which stands for unesterified cholesterol) which is its active form, or it can exist in its “esterified” or storage form which we call a cholesterol ester (“CE”).  The diagram above shows a free (i.e., UC) molecule of cholesterol.  An esterified variant (i.e., CE) would have an “attachment” where the arrow is pointing to the hydroxyl group on carbon #3, aptly named the “esterification site.”

Since cholesterol can only be produced by organisms in the Animal Kingdom it is termed a zoosterol. In a subsequent post I will write about a cousin of cholesterol called phytosterol, but at this time I think the introduction would only confuse matters.  So, if you have a question about phytosterols, please hang on.


Concept #2 – What is the relationship between the cholesterol we eat and the cholesterol in our body?

We ingest (i.e., take in) cholesterol in many of the foods we eat and our body produces (“synthesizes”) cholesterol de novo from various precursors.   About 25% of our daily “intake” of cholesterol – roughly 300 to 500 mg — comes from what we eat (called exogenous cholesterol), and the remaining 75% of our “intake” of cholesterol — roughly 800 to 1,200 mg – is made by our body (called endogenous production).  To put these amounts in context, consider that total body stores of cholesterol are about 30 to 40 gm (i.e., 30,000 to 40,000 mg) and most of this resides within our cell membranes.  Every cell in the body can produce cholesterol and thus very few cells actually require a delivery of cholesterol. Cholesterol is required by all cell membranes and to produce steroid hormones and bile acids.

Of this “made” or “synthesized” cholesterol, our liver synthesizes about 20% of it and the remaining 80% is synthesized by other cells in our bodies.  The synthesis of cholesterol is a complex four-step process (with 37 individual steps) that I will not cover here (though I will revisit), but I want to point out how tightly regulated this process is, with multiple feedback loops.  In other words, the body works very hard (and very “smart”) to ensure cellular cholesterol levels are within a pretty narrow band (the overall process is called cholesterol homeostasis).  Excess cellular cholesterol will crystalize and cause cellular apoptosis (programmed cell death). Plasma cholesterol levels (which is what clinicians measure with standard cholesterol tests) often have little to do with cellular cholesterol, especially artery cholesterol, which is what we really care about. For example, when cholesterol intake is decreased, the body will synthesize more cholesterol and/or absorb (i.e., recycle) more cholesterol from our gut. The way our body absorbs cholesterol is so amazing, so I want to spend a bit of time discussing it.

In medical school, whenever we had to study physiology or pathology I always had a tendency to want to anthropomorphize everything. It’s just how my brain works, I guess, and understanding cholesterol absorption is a great example of this sort of thinking.  The figure below, from the Gastroenterology Journal, shows a cross-section of a cell in our small intestine (i.e., our “gut”) called an enterocyte that governs how stuff in our gut actually gets absorbed.  The left side with the fuzzy border is the side facing the “lumen” (the inside of the “tube” that makes up our gut).  You’ll notice two circles on that side of the cell, a blue one and a pink one.

[What follows is a bit more technical than I would have liked, but I think it’s very important to understand how this process of cholesterol absorption works.  It’s certainly worth reading this a few times to make sure it sinks in.]

Enterocyte cell


  • The blue circle represents something called a Niemann-Pick C1-like 1 protein (NPC1L1).  It sits at the apical surface of enterocytes and it promotes active influx (i.e., bringing in) of gut luminal unesterified cholesterol (UC) as well as unesterified phytosterols into the enterocyte.  Think of this NPC1L1 as the ticket-taker at the door of the bar (where the enterocyte is the “bar”); he lets most cholesterol (“people”) in.  However, NPC1L1 cannot distinguish between cholesterol (“good people”) and phytosterol (“bad people” – I will discuss these guys later, so no need to worry about it now) or even too much cholesterol (“too many people”). [I can’t take any credit for this anthropomorphization – this is how Tom Dayspring explained it to me!]
  • The pink circle represents an adenosine triphosphate (ATP)-binding cassette (ABC) transporters ABCG5 and ABCG8.  This complex promotes active efflux (i.e., kicking out) of unesterified sterols (cholesterol and plant sterols – of which over 40 exist) from enterocytes back into the intestinal lumen for excretion.  Think of ABCG5,G8 as the bouncer at the bar; he gets rid of the really bad people (e.g., phytosterols as they serve no purpose in humans) you don’t want in the bar who snuck past the ticket-taker (NPC1L1).  Of course in cases of hyperabsorption (i.e., in cases where the gut absorbs too much of a good thing) they can also efflux out un-needed cholesterol.  Along this analogy, once too many “good people” get in the bar, fire laws are violated and some have to go. The enterocyte has “sterol-excess sensors” (a nuclear transcription factor called LXR) that do the monitoring and these sensors activate the genes that regulate NPC1L1 and ABCG5,G8).

There is another nuance to this, which is where the CE versus UC distinction comes in:

  • Only free or unesterified cholesterol (UC) can be absorbed through gut enterocytes.  In other words, cholesterol esters (CE) cannot be absorbed because of the bulky side chains they carry.
  • Much (> 50%) of the cholesterol we ingest from food is esterified (CE), hence we don’t actually absorb much, if any, exogenous cholesterol (i.e., cholesterol in food).  CE can be de-esterified by pancreatic lipases and esterolases – enzymes that break off the side branches and render CE back to UC — so some ingested CE can be converted to UC.
  • Furthermore, most of the unesterified cholesterol (UC) in our gut (on the order of about 85%) is actually of endogenous origin (meaning it was synthesized in bodily cells and returned to the liver), which ends up in the gut via biliary secretion and ultimately gets re-absorbed by the gut enterocyte.  The liver is only able to efflux (send out via bile into the gut) UC, but not CE, from hepatocytes (liver cells) to the biliary system.  Liver CE cannot be excreted into bile. So, if the liver is going to excrete CE into bile and ultimately the gut, it needs to de-esterify it using enzymes called cholesterol esterolases which can convert liver CE to UC.
  • Also realize that the number one way for the liver to rid itself of cholesterol is to convert the cholesterol into a bile acid, efflux that to the bile (via a transporter called ABCB11) and excrete the bile acids in the stool (typically most bile acids are reabsorbed at the ileum).


Concept #3 – Is cholesterol bad?

One of the biggest misconceptions out there (maybe second only to the idea that eating fat makes you fat) is that cholesterol is “bad.”  This could not be further from the truth.  Cholesterol is very good!  In fact, there are (fortunately rare) genetic disorders in which people cannot properly synthesize cholesterol.  Once such disease is Smith-Lemli-Opitz syndrome (also called “SLOS,” or 7-dehydrocholesterol reductase deficiency) which is a metabolic and congenital disorder leading to a number of problems including autism, mental retardation, lack of muscle, and many others.

Cholesterol is absolutely vital for our existence.  Let me repeat: Cholesterol is absolutely vital for our existence. Every cell in our body is surrounded by a membrane.  These membranes are largely responsible for fluidity and permeability, which essentially control how a cell moves, how it interacts with other cells, and how it transports “important” things in and out. Cholesterol is one of the main building blocks used to make cell membranes (in particular, the ever-important “lipid bilayer” of the cell membrane).

Beyond cholesterol’s role in allowing cells to even exist, it also serves an important role in the synthesis of vitamins and steroid hormones, including sex hormones and bile acids.  Make sure you take a look at the picture of steroid hormones synthesis and compare it to that of cholesterol (above). If this comparison doesn’t convince you of the vital importance of cholesterol, nothing I say will.

One of the unfortunate results of the eternal need to simplify everything is that we (i.e., the medical establishment) have done the public a disservice by failing to communicate that there is no such thing as “bad” cholesterol or “good” cholesterol.  All cholesterol is good!

The only “bad” outcome is when cholesterol ends up inside of the wall of an artery, most famously the inside of a coronary artery or a carotid artery, AND leads to an inflammatory cascade which results in the obstruction of that artery (make sure you check out the pictures in the links, above). When one measures cholesterol in the blood – we really do not know the final destination of those cholesterol molecules!

And that’s where we’ll pick it up next time – how does “good” cholesterol end up in places it doesn’t belong and cause “bad” problems?  If anyone is looking for a little extra understanding on this topic, please, please, please check out my absolute favorite reference for all of my cholesterol needs, LecturePad. It’s designed primarily for physicians, but I suspect many of you out there will find it helpful, if not now, certainly once we’re done with this series.


To summarize this somewhat complex issue

  1. Cholesterol is “just” another fancy organic molecule in our body, but with an interesting distinction: we eat it, we make it, we store it, and we excrete it – all in different amounts.
  2. The pool of cholesterol in our body is essential for life.  No cholesterol = no life.
  3. Cholesterol exists in 2 formsUC and CE – and the form determines if we can absorb it or not, or store it or not (among other things).
  4. Most of the cholesterol we eat is not absorbed and is excreted by our gut (i.e., leaves our body in stool). The reason is it not only has to be de-esterified, but it competes for absorption with the vastly larger amounts of UC supplied by the biliary route.
  5. Re-absorption of the cholesterol we synthesize in our body is the dominant source of the cholesterol in our body. That is, most of the cholesterol in our body was made by our body.
  6. The process of regulating cholesterol is very complex and multifaceted with multiple layers of control.  I’ve only touched on the absorption side, but the synthesis side is also complex and highly regulated. You will discover that synthesis and absorption are very interrelated.
  7. Eating cholesterol has very little impact on the cholesterol levels in your body. This is a fact, not my opinion.  Anyone who tells you different is, at best, ignorant of this topic.  At worst, they are a deliberate charlatan. Years ago the Canadian Guidelines removed the limitation of dietary cholesterol. The rest of the world, especially the United States, needs to catch up.
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  1. Absolutely fantastic post, Prof. I especially liked the comparison of steroid hormones synthesis and cholesterol images. So here’s a stupid question: You’re able to get through to lay people like us, we want to learn this stuff, you’re making it possible for us to understand – so why the hell don’t they teach this in med school?!

    • Great question. I suspect there are several reasons:
      1. Most people teaching in med school don’t actually know this.
      2. Once you start having this discussion (e.g., in a classroom), you find yourself realizing that a lot what is being taught is incorrect. I’ll get to it in a few weeks, but the “cholesterol is evil” story and that “fat is the devil” story crossed paths in the early 80’s and have reinforced each other greatly.
      Very slippery slope…

    • Sorry, but that’s letting them off the hook too easily. It’s their job to know this.You yourself said you should have questioned what you were taught. You can’t be alone. There is no excuse for what is going on. How dare they continue to teach what is incorrect. It’s time they were challenged with some facts and real research.
      NuSI can’t come soon enough.

      • I think they’re shutting him down because he’s advocating something in stark contrast to what most doctors say. If he were telling people to eat less fat and/or less red meat I GUARANTEE this would not be happening.

    • He’s doing what he thinks is best to beat his risk factors, just like the rest of us.

      We need to get to the tipping point where that is no longer considered “radical”.

      NuSI – faster, please.

    • I think he should counter-sue the board. They’re the ones not “practicing nutrition!”

      • I agree, though we need a bit more evidence of the harm of “5-6 servings per day of whole grains” before IJ can launch a counter class action lawsuit.

    • Teaching it in med school would involve flying in the face of big pharma. These are companies (I won’t mention any names) that formulate and test statin medications for lowering LDL (erroneously called cholesterol – it’s actually the transport mechanism for cholesterol). Statins also come with a host of side effects one of which is erectile dysfunction (ED for the PC crowd). The same company then come up with a pill for ED. So they have a cash flow from the cause and one from the treatment of a side effect. Studies have been done which show there is a small number of patients who benefit (don’t die of a heart attack) from statin treatment. I don’t want to go off on a rant against the doctors, but this is why it’s not taught in med school. Also doctors tend to forget their chemistry classes after going into practice. Thankfully there are physicians like Dr. Attia and Dr. Graveline (www.spacedoc.com) who are slowly getting the word out.

  2. Peter, iirc, Chris Masterjohn says that cholestrol dietary has ZERO affect on your measured cholestrol levels… for about 80% of us. But something like 20% are affected by it. Does that sound right?

  3. Boy I botched that. I meant to write “dietary cholesterol intake”. Changing words around without reading what you wrote is not a smart thing to do.

  4. Excellent work! I really appreciate what you are doing here.

    Will you possibly talk more about low cholesterol levels? I’ve always been around 160-170 total serum, and a few months ago, I came in at 125 (after a year of low carb/high fat).

    My GP dew a little heart with a smiley face in it, and said “Keep doing what you’re doing!”. But based on some reading I have done since then, I’m not so sure she is right.

    • Oh, how cute! A smiley face! My doc ALWAYS draws a line to his comment: “recommend statin. Is at high risk for CVD” (still to this freakin’ day!) when my LDL reports 175 or so. I have been refusing “statins” for a decade from all CW docs.

  5. Peter, I’m almost speechless with gratitude for all of your work and generosity in sharing this vital information. Thank you.

  6. This is cool. The suspense is killing me though, I can’t wait to see if the villian Insulin has a role in this diabolical plot too!

  7. Hi Peter,
    I agree that VAP or NMR derived LDL-P are far superior to a simple measured LDL cholesterol or even total:HDL ratio. However, change in even the standard lipid profile (SLP) from before to after a low carb/high fat diet can be really illustrative – i.e. the trend over time. For example, my LDL and total cholesterol more than doubled on the low carb, high fat diet. Cardiologists who looked at my SLP thought I had familial hypercholesterolemia, until I told them my baseline. There is a certain proportion of individuals (we guess, what, 10%?) who for some reason may develop dangerous levels of serum hypercholesterolemia (akin to FH levels) from a diet rich in saturated fat and dietary cholesterol. They likely have genetic mutations in intestinal transporters that are unmasked by this diet.

    Bottom line – get your lipids checked when undertaking any diet (both before AND after). The good news is that my CRP, trigs and HDL dramatically improved. The bad news is that I’ve had to take out much of the fat and start on a statin, in order to lower my risk (a meta-analysis of more than a million individuals published in the lancet a few years back suggested that at the present values, my risk of a coronary event was 8.5-fold higher than it was at my pre-diet values).

    • I dunno, Dan. Now that I’m doing standard cholesterol testing and NMR side-by-side on everyone I bump into (including the UPS guy, if he’s not quick getting off the porch), the amount of discordance between LDL-C and LDL-P is staggering. I would not trust a standard panel or VAP alone ever again, if my life depended it. Wait… it does?!

    • On the subject of very high serum lipoproteins:

      When I started doing VLC, my TC & LDL went through the roof (e.g. over 400 from about 200 for TC). FWIW, my TG are about 50 & my HDL is about 100 and pretty much all the LDL is the “good” kind (per NMR or whatever fancy test it is).

      Here is my question: What controls the serum lipoprotein level? The body controls the levels of many chemicals via a negative feedback loop. What is the feedback loop that controls the LDL serum levels — or is there one at all?

      Does the body perhaps control the rate of production and removal and the serum level just follow from the relative rates of change of production and removal?

      I can understand that if the feedback loop keeps production and removal in balance, then if one of those things changes suddenly and it takes a while for the other to catch up, then the serum level could change, possibly dramatically.

      I’ve seen discussions of how LDL receptors (and the numbers thereof) control the rate of removal and how statins control the rate of production but never any discussion of how the serum level itself is controlled — hence my wondering if there is actually any direct mechanism at all.

      FWIW, unless I see any good evidence to the contrary, I no longer give a rip if my LDL levels are way over the “recommended” levels. I plan to handle this by not getting it tested anymore. 😉

      BTW — not FH, unless it is a special kind that only appears on VLC.

      Thanks, Beth

    • DHackman-

      Have you checked thyroid levels? I am going to get mine tested after seeing my LDL unexpectedly soar. I just found this post on Paul Jaminet’s website…. Clearly, low T3 levels can dramatically influence LDL clearance by LDL receptors.


    • Hi. Was looking for a site like this all over! Help please! I bought Gary Taubes’ GCBC and have been on low carb diet for more than 4 months solidly. Thing is my GP will not be happy about this. I am a caucasian South African (Afrikaner) and like some Jews (think Ashkenazi? Jews) and our Indian population I have a thing called Frederickson Type IIA hypercholesterolaemia. Sorry about the metric number but it means that without meds my family’s numbers go into double digits like 12 and 13. None of us can tolerate statins due to rhabdomyolisis? so we’re on fibrates and ezetimibes.
      What now with this diet? I was hoping that at least my trigliserides would come down (sorry bout all the bad science spelling). My lovely mother has it and only learned about this in her 60’s. Only took the pills irregularly. Last year we celebrated her 80th birthday. Her staple is lamb – no really. She grew up on a sheep farm. So what now? I do know that a double gene of this stuff is very precarious for bearers.

    • Hi there, so I did have the lipogram done and my doctor was ecstatic. My Lipogram has almost normalised, for the first time in my life. No statins or fibrates (with or without ezetimibe) could get my numbers below 8.8 ever. Now it’s 5.0. I’m in my fifties and my family are opting into a ketogenic diet. Most of my family have the faulty gene. I now know for sure that I can never go off this diet again. I’m going to trash the ezetimibe and have another lipogram done in a month’s time. Must say I cannot find a single person with FH on the internet who has been on a ketogenic diet. I had to do this of my own accord. No doctor would have wanted to touch me with a barge pole. Have done the same experiment once when I went on zero cholesterol diet for 1 month (all I could stand) and my cholesterol numbers soared then – to the chagrin of my doctors. My doctor says “what a pleasure”. He says the numbers don’t lie so there’s no argument. Thanx for placing this. Would love to know if anyone else with FH ever went onto this diet. My family is still afraid for my sake.

  8. This is shaping up as a great series. Really appreciate your work.

    You mentioned Dr. Dayspring as one of your mentors and that reminded me of a series of youtube videos he appears in with Gary Taubes for Specialty Health. The entire series is good but this video about a case study of a Reno police officer was fascinating.

  9. Thanks for tackling this issue for us! Do you plan on addressing FH? With my levels reaching almost 300 on low fat and 500 on high fat diet, those statins are getting harder to resist.

  10. I agree there is alot of discordance between LDL-C and LDL-P. But that discordance should be subtracted out by measuring {follow-up minus baseline}. After all, the ratio of LDL-C to LDL-P should not radically change in a given individual from baseline to follow-up – am I right? So while a baseline may be of limited value, if there is a great increase from that baseline (trend over time), you have to wonder what is going on in that individual (if nothing else has changed – e.g. medication, exercise, OTC substances like plant sterols, etc). Put another way, why would the divergence increase so much (LDL-P remain same, while LDL-C increase).

    • This can, and does, happen all the time, Dan. A drug can easily reduce LDL-C with no change on LDL-P. Think of this way, if we reduce the amount of cholesterol being carried by each particle, but don’t change the number of particles, LDL-C goes down and LDL-P stays the same. Let’s hold off on this thread until everyone else can catch up on these concepts in subsequent posts.

  11. Please clarify your recommendation for NMR instead of the standard lipid panel(SLP). We read often that an ideal TG/HDL ratio from SLP correlates with mostly ‘large and fluffy’ pattern A in LDL.

    Are you saying that this is not so and that the actual LDL results from NMR may contradict such correlation, as high as 10%?

    You may have an ideal TG/HDL ratio but still have mostly pattern B particles in LDL? If so, what can one do to alter one’s LDL’s composition, within LCHF?

    • If I had a dollar for every instance in which I saw someone with a great TG/HDL-C ratio who had 90th percentile risk from LDL-P, I’d have a LOT of dollars. Stay tuned for this discussion in coming posts. We need to start with the basics, first, though.

    • Peter,

      Chris Kresser (the researcher/”practitioner”) suggests the TG/HDL-C ratio is one’s guiding light. Just FYI how info can spread around. . . I know you will get to all this. Still don’t get what can be done to alter the LDL-P bad stuff. . . As some of us grow and are older, the inevitable sets in.

      • I would suggest this is the “poor man’s” quick test for insulin resistance, but little else. If I had a dollar for every patient I’ve seen with a “great” ratio of TG to HDL-C (i.e., 1.0 or better), who also had “great” LDL-C, but had “horrible” LDL-P, I’d have a lot of dollars. Furthermore, every one of these “dollars” I’d collect represents someone who is almost certain to die sooner than they ought to because a simple test was not ordered.

  12. Phytosterols, is that something like the Benecol butter?

    And I do hope you will talk about super high cholesterol. I’m afraid to get mine tested since changing to low carb. Normal for me was around 265. My mother’s is 400+ when not on a statin. My grandmother’s was similar.

    • Re: Diane’s: Numbers like which? The 256 (hers) or the mother’s (400+)?

      It’s become obvious that we should all know our NMR (LDL-p). A rhetorical question, again: At what point is it . . . the point of no return in terms of age and “damage done”? I am watching the current guiding evidence of Dayspring and Taubes (and you, as I know you were involved with the Specialty Health study) series.

      Thanks for all you do — truly.

  13. Man, fantastic post. Probably a bit sciencey for most but I as a science and medical geek massively appreciate it.

    I seem to constantly get the “watch your cholesterol” thing thrown at me (ketogenic steak fancier) and I ask if they actually know what cholesterol is or does. Almost nobody does, and 100% of people who tell you to be wary of it don’t.

  14. Just wondering. . .At the Mendeley site to which you linked is a statement: “The absorption efficiency of cholesterol is most likely determined by the net effect between influx and efflux of intraluminal cholesterol molecules across the brush border of the enterocyte.” Since, as I understand it, the brush border can be damaged by gluten, and is really damaged by something like Crohn’s, what effects to these conditions have on cholesterol tests, and on cells that depend on cholesterol?

    • That’s a great question. To be honest with you, I don’t know the answer to this question. We do know that folks with intestinal disorders, which can impact ABCG5,G8, have problems with bile reabsorption, which can lead to gallstones…so it seems plausible that this, too, can impact sterol absorption/secretion. The real question, of course, is whether or not this is clinically relevant given the body’s ability to up- or down-regulate synthesis, if necessary, to compensate for changes in gut absorption. If anyone knows the answer, please do share.

  15. I was going to put this where I asked about Pattern A and Pattern B, but maybe it’s more appropriate here:

    Have you told Gary and Tom Naughton? Because they’ve been exhibiting their “pattern A” LDL as a diploma from the low carb school. Though I must say that saying that LDL doesn’t matter and then saying that it does if it’s large and fluffy doesn’t make sense to me.

    But, this particle size thing does seem to matter: What if somebody goes low carb, their TGs go down, their HDL goes up, but their LDL(-C) remains the same? Doesn’t that mean they’ve improved their lipid profile? Because high HDL and low TGs strongly correlate* with large LDL, which would suggest that even though the quantity of cholesterol has remained the same, the number of particles must have gone down?

    *I found a paper – from the Netherlands, I think, though I haven’t been able to find it again – that said NMR was an unnecessary waste of money because of this strong correlation.

    So, now I have to go tell the troll who said low carb was bad because of elevated LDL, that what I told him about different types of LDL was wrong? (Not that it will really matter, because I buried him so deep that he never came back.)

    • I’ll get to this in detail. 30-40% discordance is far to large to rely on a correlation. Furthermore, the cost of NMR is not nearly as great as people make it out to be. Is it really worth pinching pennies if you’re in the 30-40% of the population where LDL-P is higher than predicted by LDL-C?

  16. I love this.. every time the truth about cholesterol is shared, we take the Diet Heart Hypothesis down another peg. I think the “cholesterol is bad” lie is at the root of much of the medical and pharmaceutical deviance in our healthcare system, and yet it continues to thrive, like some kind of mythical zombie.

    I devoted a whole page on the importance of cholesterol and all the stuff it does in the body here. I’m going to link to this series just to drive home that message with the weight of your medical credentials. Thanks for writing this!

  17. This post reminded me of an article in our local paper last week. (I know, a bad source for comments on science) The article referenced media release which suggested that cholesterol may inhibit cancer growth. The researchers at SFU comment on this research, and the published paper, at https://www.sfu.ca/pamr/media-releases/2012/study-finds-cancer-fighting-goodness-in-cholesterol.html
    Clearly not the final word on this subject, but adds to the ‘good’ cholesterol comments made here.
    Thanks for the education.

  18. Thanks Peter, great stuff. I keep hoping that with bloggers like you, my father and brother (both doctors) may one day awake from their dis-interest in this topic and get healthy. I still can’t find the right words to make them think they can learn about health from me (just a Naval officer and aviator and CrossFitter, what do I know about health, eh?).

  19. Thank you, Peter! Another question has been rattling around in my head: Through the years, I’ve read a lot of discussion about the various cholesterol measurements being “associated with” or a “risk factor for” or “predictive of” heart attack, stroke, whatever. I hope you’re planning to discuss whether cholesterol has ever been proven to cause any of the things it’s accused of, and if so, how it does so.

  20. I have my standard colesterol test scheduled for tomorrow… I wonder if I shouldI even bother…

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