May 30, 2012


The straight dope on cholesterol – Part VI

by Peter Attia

Read Time 14 minutes

In this post we’ll address the following concept: Why is it necessary to measure LDL-P, instead of just LDL-C?

Previously, in Part I, Part II, Part III, Part IV and Part V of this series, we addressed these 7 concepts:

     #1What is cholesterol?

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

     #3Is cholesterol bad?

     #4 How does cholesterol move around our body?

     #5 How do we measure cholesterol?

     #6How does cholesterol actually cause problems?

     #7Does the size of an LDL particle matter?


(Not so) quick refresher on take-away points from previous posts, should you need it:

  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 formsunesterified or “free” (UC) and esterified (CE) – and the form determines if we can absorb it or not, or store it or not (among other things).
  4. Much of the cholesterol we eat is in the form of CE. It is not absorbed and is excreted by our gut (i.e., leaves our body in stool). The reason this occurs is that CE 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 (i.e., endogenous produced cholesterol) 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.  To see an important reference on this topic, please look here.
  8. Cholesterol and triglycerides are not soluble in plasma (i.e., they can’t dissolve in water) and are therefore said to be hydrophobic.
  9. To be carried anywhere in our body, say from your liver to your coronary artery, they need to be carried by a special protein-wrapped transport vessel called a lipoprotein.
  10. As these “ships” called lipoproteins leave the liver they undergo a process of maturation where they shed much of their triglyceride “cargo” in the form of free fatty acid, and doing so makes them smaller and richer in cholesterol.
  11. Special proteins, apoproteins, play an important role in moving lipoproteins around the body and facilitating their interactions with other cells.  The most important of these are the apoB class, residing on VLDL, IDL, and LDL particles, and the apoA-I class, residing for the most part on the HDL particles.
  12. Cholesterol transport in plasma occurs in both directions, from the liver and small intestine towards the periphery and back to the liver and small intestine (the “gut”).
  13. The major function of the apoB-containing particles is to traffic energy (triglycerides) to muscles and phospholipids to all cells. Their cholesterol is trafficked back to the liver. The apoA-I containing particles traffic cholesterol to steroidogenic tissues, adipocytes (a storage organ for cholesterol ester) and ultimately back to the liver, gut, or steroidogenic tissue.
  14. All lipoproteins are part of the human lipid transportation system and work harmoniously together to efficiently traffic lipids. As you are probably starting to appreciate, the trafficking pattern is highly complex and the lipoproteins constantly exchange their core and surface lipids.
  15. The measurement of cholesterol has undergone a dramatic evolution over the past 70 years with technology at the heart of the advance.
  16. Currently, most people in the United States (and the world for that matter) undergo a “standard” lipid panel, which only directly measures TC, TG, and HDL-C.  LDL-C is measured or most often estimated.
  17. More advanced cholesterol measuring tests do exist to directly measure LDL-C (though none are standardized), along with the cholesterol content of other lipoproteins (e.g., VLDL, IDL) or lipoprotein subparticles.
  18. The most frequently used and guideline-recommended test that can count the number of LDL particles is either apolipoprotein B or LDL-P NMR, which is part of the NMR LipoProfile.  NMR can also measure the size of LDL and other lipoprotein particles, which is valuable for predicting insulin resistance in drug naïve patients, before changes are noted in glucose or insulin levels.
  19. The progression from a completely normal artery to a “clogged” or atherosclerotic one follows a very clear path: an apoB containing particle gets past the endothelial layer into the subendothelial space, the particle and its cholesterol content is retained, immune cells arrive, an inflammatory response ensues “fixing” the apoB containing particles in place AND making more space for more of them.
  20. While inflammation plays a key role in this process, it’s the penetration of the endothelium and retention within the endothelium that drive the process.
  21. The most common apoB containing lipoprotein in this process is certainly the LDL particle. However, Lp(a) and apoB containing lipoproteins play a role also, especially in the insulin resistant person.
  22. If you want to stop atherosclerosis, you must lower the LDL particle number.
  23. At first glance it would seem that patients with smaller LDL particles are at greater risk for atherosclerosis than patients with large LDL particles, all things equal.
  24. “A particle is a particle is a particle.”  If you don’t know the number, you don’t know the risk.
  25. To address this question, however, one must look at changes in cardiovascular events or direct markers of atherosclerosis (e.g., IMT) while holding LDL-P constant and then again holding LDL size constant.  Only when you do this can you see that the relationship between size and event vanishes.  The only thing that matters is the number of LDL particles – large, small, or mixed.


Concept #8 – Why is it necessary to measure LDL-P, instead of just LDL-C?

In the growing list of reasons why I used to refer to myself as “chick-repellant” in college, I have a confession to make: I find the topic of statistical concordance and discordance to be so exciting, I sometimes have a hard time containing myself. This may explain the paucity of girlfriends in college. Let me use an example to illustrate the distinction between these terms.  Let’s say you want to predict the change in home prices in the following year (I used to model this for a living).   There are at least a dozen parameters linked to this, including: GDP growth, unemployment, interest rates (both short term and long term, though to different degrees), housing inventory (i.e., how many houses are on the market), housing absorption (i.e., how quickly houses go from being on the market to being sold), major stock indices, and consumer confidence.  Historically, from the mid-1990’s until about the fourth quarter of 2006, this worked like clockwork.  While each of these variables had differing strengths of predicting changes in home prices, they all moved together.  For example, when GDP growth was robust, unemployment was low, interest rates were modest, housing inventories were about 60 to 90 days, etcetera.  All of these variables pointed to a predictable change in home values.

Around Q42006 (i.e., last 3 months of 2006), one of these variables began to deviate from the others.   The details aren’t important, but the point is one variable began to suggest home prices would fall while the others all pointed to a continued rise.   Prior to Q42006 these parameters were said to be concordant – they all predicted the same thing – either up or down.  By 2007, they became discordant – one variable said the sky was falling while others said everything was fine.

This was true on the “micro” level, too. [What I described above is called “macro” level.]  As a lender, it should be very important to know the risk of each and every loan you make (clearly this was part of the root problem in the age of mass securitization).  Will this person pay the loan back or will they default?

Same game here, but now a new set of even greater variables.  As a lender, if I want to know if YOU will default, I will want to know a lot of things about you, such as your agency credit risk scores, your bank account activity, payroll activity, how much you’re borrowing relative to the value of your house, where your house is located, and about 50 other things (literally).

Not surprisingly, the same thing that happened on the macro side happened on the micro side.  It became difficult to predict who would default and would not default because there were so many variables to consider and lenders didn’t know which ones were still predictive.  The models that predict default are very sensitive to the balance of these inputs.  When all of the variables are concordant, their accuracy is prophetic, as was the case from the mid-1990s until late 2006.  When some variables become discordant with each other, especially variables that were historically concordant with each other, really bad stuff happens, as became evident to me, personally, one Thursday afternoon in November 2007.  It became clear the sky was about to fall.  And, of course, it did.


What does real estate have to do with atherosclerosis?

Fortunately, predicting heart disease is a little easier than predicting changes in home prices.  It’s not perfect, of course, but it’s pretty good.  Why is it not perfect? For one thing, we can’t do the “perfect” experiment.  The “perfect” experiment would look something like this:

Take 100,000 people and randomize them into four matched groups, A, B, C, and D.  Wave a magic wand (you can see why this experiment hasn’t been and won’t be done) and give the folks in Group A an LDL particle concentration of, say, 700 nmol/L; those in Group B you give 1,200 nmol/L; those in Group C you give 1,600 nmol/L; and those in Group D get 2,000 nmol/L.

In our dream world, due to the randomization process, these four groups would be statistically identical in every way except one – they would, thanks to our magic wand, have a different number of LDL particles.  We would follow them without further intervention for 10 years and then compare their rates of heart disease, stroke, and death.

There are some areas in medicine where we can do such experiments.  But, we can’t do this experiment for this question.  Even when we do the next best thing — give people a drug that lowers their LDL-P and measure the impact of this intervention — there is always a chance we’ve done something in addition to “just” lowering LDL-P.   If you’ve been reading this series, you no doubt know my thoughts on this: while other factors are likely to be involved the pathogenesis of atherosclerosis (e.g., endothelial “health”, normal versus abnormal inflammatory response) the primary driver of atherosclerosis is the number of apoB trafficking lipoproteins in circulation, of which LDL particles are the vast majority.

The data below should further clarify this association.


What do concordant LDL-C and LDL-P values look like?

Among the two largest studies tracking the association between cholesterol and atherosclerotic mortality are the Framingham study and the MESA trial (the two largest trials were AMORIS and INTERHEART).  The figure below, which I’ve graciously borrowed from Jim Otvos, shows the risk stratification of LDL-C (top) and LDL-P (bottom) from the Framingham study and MESA trial, respectively. As you can see, conveniently, LDL-C values in mg/dL are about 10x off from LDL-P values in nmol/L.   In other words, in the Framingham population, the 20th percentile value of LDL-C was 100 mg/dL, while the MESA trial found the 20th percentile of the population to have an LDL-P concentration of 1,000 nmol/L.  As you will see by the end of this post, this “rule of the thumb” should never be used to infer LDL-P from LDL-C.


Cut-off points for LDL-C and LDL-P
Image credit: Jim Otvos

If this were always the case – that is, if LDL-C and LDL-P were always concordant – we could conclude that LDL-C and LDL-P would be of equal value in predicting heart disease.  Obviously this is not the case, or I wouldn’t be making such a fuss over the distinction.  But how bad is it?


What do discordant LDL-C and LDL-P values look like?

The figure below, from the Journal of Clinical Lipidology, shows the cumulative incidence of cardiovascular events (e.g., myocardial infarction, death) over time in three sub-populations:

  1. Those with concordant LDL-P and LDL-C (black line);
  2. Those with discordant LDL-P and LDL-C (LDL-P>LDL-C, shown by the red line);
  3. Those with discordant LDL-P and LDL-C (LDL-P<LDL-C, shown by the blue line).

This analysis was done using a Cox proportional hazard model and was adjusted for age, sex, and race.  The steeper the line the more people in that sub-population died or experienced adverse cardiac events relative to other sub-populations.  In other words, the folks in the red group had the worst outcomes, followed by the folks in the black group, followed by the folks in the blue group.



What can we infer from these data?

First, we confirm what I alluded to above.  Namely, that a non-zero percent of the population do not have LDL-C and LDL-P values that predict the same level of risk.  However, and perhaps more importantly, we get another look at an important theme of this series: LDL-P is driving atherosclerotic risk, not LDL-C.   If LDL-P and LDL-C were equally “bad” – even when discordant – you would expect the blue line to be as steep as the red line (and both to be steeper than the black line). But this is not the case.

Let’s look at these data parsed out another way.  Below we see the four possible subgroups, from the top:

  1. Not low LDL-P, low LDL-C (red line);
  2. Not low LDL-P, not low LDL-C (yellow line);
  3. Low LDL-P, low LDL-C (black line); and
  4. Low LDL-P, not low LDL-C (blue line).

Note that “low” is defined below the 30th percentile and “not low” is defined as greater than 30th percentile for each variable.   This figure is even more revealing than the one above.  Again, it demonstrates the frequency of discordance (about 20% in this population with these cut-off points), and it shows the importance of LDL-P’s predictive power, relative to that of LDL-C.

In fact, though not statistically significant, the highest risk group has high LDL-P and actually has low LDL-C (I’ll give you a hint of why, below) while the lowest risk group has low LDL-P and not-low LDL-C.  *This is not a typo.


MESA LDLp vs LDLc 4 groups

The highest risk and lowest risk groups are those with discordant LDL-C and LDL-P.  The high risk group has high LDL-P and low LDL-C, while the lowest risk group has high LDL-C with low LDL-P. Only a minority of physicians would know that there is a segment of the population with elevated LDL-C who are at low risk! The same conclusion will be drawn from the next study.

Let’s look at an even longer-term follow up study, below.  This study followed a Framingham offspring cohort of about 2,500 patients over a median time period of almost 15 years in each of the four possible groups (i.e., high-high, high-low, low-high, and low-low) and tracked event-free survival.  In this analysis the cut-off points for LDL-P and LDL-C were the median population values of 1,414 nmol/L and131 mg/dL, respectively. So “high” implies above these values; “low” implies below these values.  Kaplan-Meier survival curves are displayed over a 16 year period – the steeper the slope of the line the worse the outcome (survival).


Survival curve
Image credit: Cromwell et al., 2007

The same patterns are observed:

  1. LDL-P is the best predictor of adverse cardiac events.
  2. LDL-C is only a good predictor of adverse cardiac events when it is concordant with LDL-P; otherwise it is a poor predictor of risk.

Amazingly the persons with the worst survival had low (below median) LDL-C but high LDL-P.  The patients most likely to have high LDL-P with unremarkable or low LDL-C are those with either small LDL particles, or TG-rich / cholesterol poor LDL particles, or both (e.g., insulin resistant patients, metabolic syndrome patients, T2DM patients).   This explains why small LDL particles, while no more atherogenic on a per particle basis than large particles, are a marker for something sinister.


Populations where LDL-P and LDL-C discordance are even more prevalent

As I described above, the discordance between LDL-P and LDL-C is exacerbated in patients with metabolic syndrome. The figure below, MESA data, again borrowed from Jim Otvos, presents this difference in an elegant way.  The horizontal axes show LDL-P concentration in the usual units, nmol/L.


Otvos ADA
Image credit: Jim Otvos

Patients with LDL-C between 100 and 118 mg/dL (i.e., second quartile of risk: 25th to 50th percentile) are shown without metabolic syndrome (top) and with metabolic syndrome (bottom).  In the patients without metabolic syndrome, LDL-C under-predicts cardiac risk 22% of the time, consistent with the population data I have shown you earlier.  However, when you look at the patients with metabolic syndrome, you can see that 63% of the time their risk of cardiac disease is under-predicted.  Again, not a typo.

There are so many subsets and cut-off points that I could devote ten more posts to showing you every one of these analyses.  Let me finish this point with the most recent, hot-off-the-press (actually, still in press in the American Journal of Cardiology, though you can get a preprint here) analysis of which Tom Dayspring is one of the authors.


Evaluation of Low-Density Lipoprotein Particle Number Distribution
Image credit: Malave et al., 2012

These data were collected from nearly 2,000 patients with diabetes who presented with “perfect” standard cholesterol numbers: LDL-C < 70 mg/dL; HDL-C > 40 mg/dL; TG <150 mg/dL.  However, only in 22% of cases were their LDL-P concordant with LDL-C.  That is, in only 22% of cases did these patients have an LDL-P level below 700 nmol/L.

Remember, LDL-C < 70 mg/dL is considered VERY low risk – the 5th percentile.  Yet, by LDL-P, the real marker of risk, 35% of these patients had more than 1,000 nmol/L and 7% were high risk.  When you do this analysis with the same group of patients stratified by less stringent LDL-C criteria (e.g., <100 mg/dL) the number of patients in the high risk group is even higher.

The real world tragedy: 90-95% of physicians, including cardiologists, would bet their own lives that persons with an LDL-C < 70 mg/dL have no atherosclerotic risk. 

Tim Russert, shortly before his death, had his LDL-C level checked.  It was less than 70 mg/dL.  Sadly, his doctors didn’t realize they should also have been checking his LDL-P or apoB.  The figure below, which is from one of Tom Dayspring’s presentations, shows data from this study of nearly 137,000 patients hospitalized for coronary artery disease between 2000 and 2006.  As you can see, LDL-C fails to even reasonably predict cardiovascular disease in a patient population sick enough to show up in the hospital with chest pain or outright myocardial infarction.


Insulin Resistance Lipids & Lipoproteins

Why are LDL-C and LDL-P so often discordant?

Think back to what you learned in a previous post in this series.  LDL particles traffic not only cholesterol ester but also triglycerides.  Each and every LDL particle has a variable number of cholesterol molecules which, because of constant particle remodeling, is constantly changing.  In other words, of the several quadrillion LDL particles floating in your plasma, no two are carrying the exact same number of cholesterol molecules. It takes many more cholesterol-depleted LDL particles than cholesterol-rich LDL particles to traffic a given cholesterol mass (i.e., number of cholesterol molecules) per volume of plasma (i.e., per dL).  Core cholesterol mass is related to both LDL particle size (the volume of a sphere is a third power of the radius — it can take 40-70% more small particles than large LDL particles to traffic a given cholesterol mass) and the number of TG molecules per LDL particle.

TG molecules are larger than cholesterol ester molecules, so as the number of TG molecules per particle increases, the number of cholesterol molecules will be less – in a very non-linear manner. Regardless of size it takes many more TG-rich LDL particles (which are necessarily cholesterol-depleted) to traffic a given cholesterol mass than TG-poor LDL particles.  The persons with the highest LDL particles typically (though not always) have small LDL particles that are TG-rich.  These are incredibly cholesterol-depleted LDL particles.



Take a look at this figure below from the 2011 Otvos et al. paper I referenced above.  It’s a scatterplot of each data point (i.e., patient) in the study. The solid red line shows perfect concordance between LDL-P and LDL-C.  The dashed red lines show a +/- 12% margin on each side.  Look at how many dots (remember: each dot represents a person) lie OUTSIDE of the dashed red lines. Now look again.


MESA LDLp vs LDLc J Clin Lip2011

When people argue with me about why it’s unnecessary to check LDL-P or apoB because it’s much easier and cheaper to check LDL-C, I like to remind them of what Clint Eastwood would probably say in such a situation:  You’ve got to ask yourself one question: Do I feel lucky? Well, do ya, punk?”


  1. With respect to laboratory medicine, two markers that have a high correlation with a given outcome are concordant – they equally predict the same outcome. However, when the two tests do not correlate with each other they are said to be discordant.
  2. LDL-P (or apoB) is the best predictor of adverse cardiac events, which has been documented repeatedly in every major cardiovascular risk study.
  3. LDL-C is only a good predictor of adverse cardiac events when it is concordant with LDL-P; otherwise it is a poor predictor of risk.
  4. There is no way of determining which individual patient may have discordant LDL-C and LDL-P without measuring both markers.
  5. Discordance between LDL-C and LDL-P is even greater in populations with metabolic syndrome, including patients with diabetes.  Given the ubiquity of these conditions in the U.S. population, and the special risk such patients carry for cardiovascular disease, it is difficult to justify use of LDL-C, HDL-C, and TG alone for risk stratification in all but the most select patients.
  6. This raises the question: if indeed LDL-P is always as good and in most cases better than LDL-C at predicting cardiovascular risk, why do we continue to measure (or calculate) LDL-C at all?

Photo by Aldric RIVAT on Unsplash

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  • Catherine

    I got here first, so I better post.
    Beautifully laid out. Thanks for the reminder about the power of concordant/ discordant variables. Grateful to have gutted through this series! Thank you for the time to pound this out.

    • Glad you like them. Yes, it’s been a bit of a slog, but I think it’s been worth it.

  • greensleeves

    So I guess the upshot so far, Peter, is that 1 – everybody should get themselves the advanced lipid test; 2 – if you are discordant, double down on the low-carb diet and start drug therapy ASAP.

    • Almost. Yes, everyone needs an NMR, at least once. If you are discordant, NMR should be the preferred method for following you. We’ll get into treatment subsequently.

    • > Everyone needs an NMR, at least once.
      > If you are discordant, NMR should be
      > the preferred method for following you.

      Really astounded by this series, Dr. Attia, and I look forward to rereading the whole thing and taking notes. I feel like I only absorbed a fraction of the material you presented.

      When it comes to tests, I hear two mentioned quite frequently in the context of, “Get either an NMR or a VAP test. The standard panel is useless…” You do not mention VAP (that I’ve seen). Do you feel it is inferior to the NMR? I’ve not seen a good explanation for one test over the other, so I’m curious to hear your thoughts on the matter.

      • I address this in part II or III. To be clear, VAP is NOT a good test to get, despite the fact that I used to track my progress until last year. It estimates apoB. Your best bet is NMR (many companies can send out to LipoScience, the only company able to do this with FDA approval), or go with one of the companies can can actually measure apoB directly.

    • Russ C

      I look forward to subsequent post on treatment. I hope you can include some thoughts on the larger view as well – i.e. recognizing that the cardiovascular system is part of a larger system. Given the increasing awareness of potential side-effects of statins (Ref Golomb studies and as recently acknowledged by FDA), how does one weave treatment strategies that maximize total health?

  • Good presentation again Dr. Attia. Question: A lot of interesting studies do comparisons of pattern A (big fluffy particles) vs pattern B (small dense particles) LDL-p without looking at total particle #.

    Can a person make assumptions about particle number based off of total cholesterol and pattern shifts? For example, say a study examined one group of people with pattern B (small dense LDL-P) with a total cholesterol of X. They now give a dietary intervention and the people with pattern B now change to pattern A but with the SAME X amount of cholesterol as before. Can we assume their particle # went down since their cholesterol stayed the same but now the cholesterol is being housed by larger LDL-P which means total particle # should have theoretically gone down?

    I ask because a lot of studies investigate particle size but not total particle number.

    • You’re right, most studies are fixated on LDL size, not count. I’d like to say that I can always “guess” correctly which way LDL-P moves with a change in LDL-C, TG, and particle size, but I can’t. There are certainly clues, as I explain in this post. But at best, that’s all they are.

    • If you shift particle size upwards it will have a larger volume and thus will have to be carrying more lipid molecules. Sotypically the larger LDL will carry more cholesterol molecules and it takes less cholestrerol-rich LDLs to traffic a fiven LDL-C value (mass). However if the particles become larger because they are TG-rich, they will be cholesterool-depleted particles and it takes many more chol-poor than chol-rich LDLs to traffoc a given cholesterol mass

  • Kevin Mobley

    Absolutely excellent. Now off to forward to my doctors.

  • Kypros

    It’s all coming together now! Will you talk more about Lp(a)? Any evidence that it might be even more important than LDL-P (both atherogenic and thrombogenic?). Any data on discordance between LDL-P and Lp(a)?

    Thanks again for your work!

    PS: How is the cookbook coming along?

    • I spoke a bit about Lp(a) in an earlier post. It’s a particle like LDL, but with an apoprotein called apo(a). For most folks the number of Lp(a) particles is a fraction of LDL-P, though we can currently (i.e., for about another year) only estimate Lp(a)-P from 2 other features. Cookbook is a work in progress. NuSI is priority #1, 2, and 3 right now.

  • David Nelsen

    We have a Health for Life program at work where everyone is encouraged (bribed) to get their blook work done every year. I asked them a few months ago why we don’t measure LDL-P in this program. I am going to have another go at it and link this post as justification. Lots of great data rich graphs in this one.

    Maybe I missed it but are you saying that Metabolic syndrome is driving the diconcordance between LDL-P and LDL-C? Did you state whey High LDP-P/Low LDL-C was worse than High Hight? Is it because there is something slightly more protective about LDL-C?

    • Discordance exists at a baseline for reasons I don’t entirely understand, probably 20-30% of the population. However, in MS, the discordance goes WAY up, almost certainly related to the TG-CE swap in LDL particles. In my personal experience, with hundreds of patients, I’m seeing about 30-40% discordance.

    • JohnJ

      Well fatty liver is very common eating fructose and high carbohydrates diets. It can’t be cured in a few weeks or months, maybe that why some still have problem with cholesterol.

      The VCU findings may provide researchers with potential new targets for treatment and also allow clinicians to further refine how they assess cardiovascular risk and develop ways to reduce it in individuals with a more aggressive form of nonalcoholic fatty liver disease called nonalcoholic steatohepatitis, or NASH.

      In the study, published in the May issue of Cell Metabolism, the team has shown that there is not only increased production of cholesterol but a decreased expression of the receptor that takes up cholesterol from the blood. This would be expected to both enhance cholesterol output from the liver and reduce its removal, thereby making it more available to enter blood vessels and contribute to cardiovascular disease. The liver not only makes cholesterol, but also takes up cholesterol from the blood.

      “This indicates that there is excessive cholesterol production in the liver when one develops fatty liver disease,” said lead investigator Arun Sanyal, M.D., professor and chair in the Division of Gastroenterology, Hepatology and Nutrition in the VCU School of Medicine.

  • Again – brilliant and much needed comprehensive reporting on the truth of Cholesterol science. Your effort and time put into propagating the real concepts behind “what people believe” is much appreciated.

    Unfortunately, widely dispersed productions like that recent HBO documentary about the “Weight of America” (or whatever it was called), overlooks the most important parts.

    You are an asset to our community, Peter!

    • I appreciate your kind words. Change takes time. I’m focused on making sure our kids grow up in world where people can decide what to eat to based on real data, in a way few of us can do today. Sort of like smoking today. All I ask is that folks get a fair shot at making a choice for themselves — based on real data. Kick-off scientific meeting for NuSI is Friday…

  • Stipetic

    Great stuff.

    “Regardless of size it takes many more TG-rich LDL particles (which are necessarily cholesterol-depleted) to traffic a given cholesterol mass than TG-poor LDL particles.”

    Is this where diet/lifestyle comes in?

  • Nina

    Thank you – it has been SO “worth it” !!!!

  • 10/10 points for style, substance, and clarity. 😉
    Thank you once again for compiling and filtering the information, Peter.
    It takes a lot of time and effort to do so, I’m painfully aware. 🙂

    So, is this the punchline?… or are we getting more on this subject?

    • Thank you, Vasco. Yes, I think we have a few topics left in this series before we can hand out the graduation caps and call ourselves certified lipidologists. I hope folks can hang on for a few more rounds.

    • Russ C

      Ditto’s to Vasco. 10/10/10 on this one!

  • John Pane

    Awesome, as usual.

    One thing you could add for clarity is to explain the figure “MESA data, again borrowed from Jim Otvos” has LDL-P on the horizontal axis. This is not noted on the figure and might make it easier for readers to see why you say LDL-C under-predicts risk.

    For my annual physical, my doctor runs some standard blood work. If, the next time I see him, I say I want my LDL-P checked, would he be likely to comply? How can I convince him, and what other atypical measures should I request while I’m at it?


    • Great. Just updated. I hope you can get him to comply. Everyone deserves at least one NMR. If they are concordant, they can probably get away with subsequent LDL-C, provided no major metabolic changes take place.

  • Bill

    OK, LDL-P is the best current predictor of CVD risk. But how good is it? How much of the total risk for any individual is “explained” by his or her LDL-P number? That gets to how important it is for any individual to worry about.

    Perhaps an even better way to ask this question would be to ask how much life expectancy is sacrificed by having high LDL-P to varying degrees? IIRC, except at severe extremes life expectancy is decreased by at most several months for those with unfavorable conventional lipid panels, which is one reason why people like Dr. Nortin Hadler advise well people not to even get the tests. I’m curious how many lost months of expected lifespan high LDL-P predicts, and how confidently we can know that.

    This sort of information seems important if people are to rationally decide how much to worry about this, and if it’s worth it to them to incur the potential problems and risks of treatment to lower LDL-P. I know you’ll be covering treatment later, and I’ll be curious to see what you say about the NNT (number needed to treat) for LDL-P lowering treatment in various populations, a related question.

    Thanks for the excellent series.

    • Fortunately, we have pretty decent data for these questions, but it’s deserving on an entire post, not a short response. Fret not, though. Reducing a person’s LDL-P from 2,000 to 1,000 does a lot more than buy them a few months. We’re not talking about esoteric (morally suspect) chemotherapy. This is real primary and secondary prevention.

    • Barkeater

      There is so much good here, I feel guilty about the fact that I am struggling with this series. But . . .

      Bill asks an important question. Reading the summary of previously established points, I thought that Dr. A would have submitted significant evidence that LDL-P is the best predictor in Part IV, but the text there is thin on the point. Yes LDL-C is not a great predictor, and yes Dr. A has now overwhelmed us with data showing that LDL-P is better than LDL-C as a predictor and that LDL-P size does not matter. The assertions are mostly only relative. The case will be harder to make that LDL-P is the be-all and end-all predictor. I believe that a ratio of LDL-P to HDL-P would be better than LDL-P alone. I bet APO A-1 / APO B would beat LDL-P alone (a test I got for around $40 not long ago). Or Dr. William Feeman’s CRF (colesterol retention fraction), which is (LDL-C minus HDL-C)/LDL-C plotted on a graph with systolic BP (see Bowling Green study). Or smoking plus most anything. I guess I don’t see why it is significant to know that LDL-P is by itself the best predictor compared to any single other predictor, if in fact it is not that great. It’s like knowing that Green Bay gained the most yards in 2012 but, oh yeah, they did not win the Super Bowl or even get there.

      I am anxious for the grand train wreck that comes when Dr. A tells Jimmy Moore and the low-carb/ paleo crowd that have achieved > 2000 LDL-Ps (yes, I am in that club, thanks to FH) that they have to get to an 1100 LDL-P, and good luck getting there with anything but statins or unproven crap like zetia (or maybe an Ornish diet – me, I choose to eat food). As TO says, get your popcorn.

      • Lots in here…can’t address this in a short response, which seems all I have time for these days. Certainly ratios carry predictive power, and apoB to apoA1 is possible the best (except for possibly LDL-P to HDL-P). It’s pretty rare (read: I have never seen a case) to see someone with a LDL-P of 2,000 (95% percentile), yet ratio of LDL-P to HDL-P of 20 (probably 10th percentile). It’s possible, but boy, it’s an outlier. What would it mean if you were that fellow? Who knows…
        Maybe you’re right. Maybe in such a case you have so many HDL particles that RCT can fix all the problems of too many LDL particles. We just don’t have the kind of data to make anything other than a best guess. So, I see your point about “offense” vs. “defense” but I hope you realize that atherosclerosis is more complex that football. Think about this way, does the team with the greatest ratio of points for/against always win? Of course not. It probably predicts more success, but it’s not a guarantee.
        I’m not sure where the assertion comes that Jimmy Moore et al. all have LDL-P > 2,000 just because you might? My guess is very folks out there even know their LDL-P.

    • Barkeater



      Hence they assessed the relationship of LDL-P and particle size as measured by a relatively new technique—nuclear magnetic resonance spectroscopy—with the risk of future CAD in more than 25 000 subjects with moderately elevated LDL-C in the European Prospective Investigation into Cancer and Nutrition (EPIC)-Norfolk.

      They matched 1003 cases of individuals who developed CAD during a six-year follow-up with 1885 control subjects and calculated the odds ratios (ORs) for future CAD. They also evaluated whether LDL-P could improve upon the Framingham risk score to predict CAD.

      LDL-P (OR 2.00 for top vs bottom quartiles) was more closely associated with the occurrence of future CAD than LDL-C (OR 1.73) and was related to CAD on top of the Framingham risk score even after adjustment for LDL-C.

      But after adjustment for HDL-C and triglycerides, LDL-P was no longer more predictive than LDL-C. Nor was LDL particle size associated with CAD risk, following adjustment for LDL-P.

      end snip.

      Reviewing EPIC data, information from the standard lipid panel, if interpreted in a sophisticated way, yielded better predicitive value thal LDL-P alone. More interesting to me, top quartile LDL-P had a 2 to 1 odds ratio, vs. a 1.73 to 1 odds ratio for top quartile LDL-C vs bottom quartile. OK, LDL-P was a little better, but not really that great — bottom quartile LDL-P still had significant residual risk. My Framingham score would be half of what it is if I did not have high LDL-C. Dr. A, the absence of a clear statement as to the degree to which LDL-P improves on the predicitive value of LDL-C makes these analyses misleading. LDL-C sucks, and LDL-P is a bit better. You are putting LDL-P on a high pedestal it does not deserve.

    • Barkeater

      Thanks for replying and thanks for this series.

      Jimmy Moore has gotten an NMR, and reported LDL-P of 2130. I see a significant number of low-carbers seem to have spikes in their LDL-C and LDL-P that would appear to be driven by diet. They are not necessarily FHers like me (but I have seen wide ranging LDL-P, from 1500 to 2800, and cannot yet tie it out to diet). Commenter MacKillop below refers to a double-digit percentage of folks on low-carb diets who see very high LDL-C. Mr. and Mrs. Jaminet have blogged at some length on the issue.

      I see the view expressed by some that this phenomenon is due to ApoE4, but I don’t buy it (I am a 3/3).

      • The question we don’t know the answer to is if an LDL-P of 2,000 in someone who eats no carbs is the same as an LDL-P of 2,000 in someone who does. I had breakfast with Eric Westman today and we discussed this topic. Eric makes a pretty compelling case that these 2 states are not, in fact, the same thing. I think we can safely say we don’t know the answer. At least I don’t. I’ll keep looking for clues, though.

    • Russ C

      Glad to hear of your conversation w Eric re implications of high scores on high vs low carb. Isn’t this something that a study could be constructed on? Hard to do double blind, but might be able to at least get clues from population studies? Not sure diet itself is the variable to correlate with, maybe hsCRP, maybe something else?

  • lupo

    Great article! So this is begging for a sequel which answers the question: What kind of food makes LDL-P and LDL-C discordant?

    I suppose given that even most researchers don’t know jack about what you revealed to us, they use LDL(-C) as one of their primary markers in studies. The number of nutritional studies that use LDL-P and LDL-C there I assume to be really small.

    • To your last point, exactly. To your first question, the type of foods that lead to metabolic syndrome are exactly the type of foods that increase the proportion of discordance.

    • lupo

      What I would be interested in is where oxidized LDL fits in… I’m doing my homework on pubmed right now 🙂

    • Gabe

      What would be the draw back of treating a no carb person with LDL-P in the higher levels(assuming no adverse physical reactions to statins)and later on finding out that higher levels of LDL-P in no carb dieters is different and not harmful… For every ying there is a yang. I could be off base here but I think the goal should be fixing any accumulated problems caused by SAD diets and trying to reset, then strictly avoid refined, processed and unnatural “food products” and assume that whatever the body does from there is what it is intended to do. Our bodies have come millions of years figuring out what is the right state and in the absence of SAD should be able to figure that state out again

      • Gabe, I can’t argue with you. I really wish I could say I KNEW the answer to this question. If I told you I did, I’d be misleading you.

    • Russ C


      There are other known side effects of at least today’s treatment regimens (see and

      So there is real risk that focusing on helping the heart only might hurt the brain or muscles or…? Feels like room for much more research.

    • Gabe

      There is much room for research. Like Peter says we just don’t know right now. My plan of attack is rid myself of Insulin Resistance and lower LDL-P to under 1000 (with statins if necessary) once both those goals are reached i’ll consider myself “reset” and hopefully stop medications. I’ll continue low carb paleo lifestyle and what my body does from it’s “reset” state i’ll assume is what it’s supposed to. The question is once I reach my goal does the body really get to start over or will there always be some underlining bit of damage that doesn’t get reversed. Will the statins that helped me “reset” cause issues. No way to tell for now..I guess time will tell.

  • Kypros

    Follow up question on Lp(a). Standard tests of Lp(a) measure cholesterol not particle number. What can we say about a high Lp(a) cholesterol? Is it the same principle as LDL-P vs LDL-C?

    • Currently it’s only possible to measure Lp(a) cholesterol content and mass, but not particle number. If both are low, Lp(a)-P is low; if both are high, Lp(a)-P is high; if mixed it’s harder to tell. Folks are working on this right now. Assays expected to be able to count them directly by next year.

    • Lp(a)-C is a surrogate of Lp(a)-P Lp(a) mass is not

  • Whatisaname

    When can we expect the part that says sugar and other “crap” increases LDL-P? Awesome work!

    • Sounds like you’ve already figured it out! Actually, you’ve already got a big hint in that direction based at least one typical cause of discordance: LDL particles carrying too much TG and not enough CE. Guess what causes that?

  • lorraine

    This was my father’s story. Had “perfect” labs and resting ECG two months before having an early spring round of golf followed by a bagel (!!) and then dropping dead on the living room floor at the age of 64.

    • Very sorry to hear this. I can almost assure you his LDL-P, had it been measured, would have been very high, despite normal LDL-C.

  • lorraine

    Okay, I’m all in convinced. A few installments back I bristled a bit that our history of testing for lipids has sent us barking up some seriously wrong trees, but this evidence for particle testing is compelling.

    Sincere gratitude for the series, both to you and to Drs. Dayspring and Otvos for permission to share their slides in it. I can imagine the work to do the series, but the additional time and energy to be so present here in the comments is really above and beyond.

    I’m also grateful to have been turned onto the work of Drs. Dayspring, Otvos and Dall, and through your direction, have become a regular at Lipidaholics and other features at Lecturepad. But your synthesis of their work here has added a level of analysis that’s been so very helpful. I can’t believe I got it all for free as I’d expect to pay many hundreds (or thousands) for something like this to either of the institutions that educated me.

    • I’m glad you can see why I consider my so fortunate to be able to call these folks mentors and teachers. Their generosity with their time humbles me and it’s my pleasure to “pay it forward” as best I can.

  • Alex Carvalho

    Oh boy, great post! I can hardly wait for the next ones. Thanks again for putting this together. Can I infer that insulin resistant individuals should shoot for TG levels even lower than the 150 currently used as the standard for “optimum”? What should be the desired TG levels for this population?

    • Absolutely. In fact, the most strict lipidologists would argue that a “physiologic” TG level is closer to about 50 mg/dL, well below the 150 touted as “normal.” I would absolutely concur with this.

  • Tom A

    First, best post ever. I saw some of the graphs on one of the testing web sites and almost posted it last week. Good thing I didn’t steal your thunder but it makes a ton of sense. Especially pictorially.

    One question – if you get an NMR and find out your relationship between LDL-C and LPL-P is concordant (or discordant) will that relationship continue to exist in the same way over time? i.e. you will always be discordant or concordant as far as the two variables hence need an NMR test or rely on LDL-C respectively?

    • This is a really good question, Tom. I don’t have enough longitudinal data to really comment. Clearly the relationship between LDL-P and LDL-C changes over time. No doubt about this. Constant re-modeling of particles, changing levels of TG, changing levels of CE. The question, of course, is if you are concordant today, under what circumstances can I be confident you are next year? On a personal level, it’s not worth even risking it. I check LDL-P every single time. At the “policy” level, this is a different matter and probably warrants further investigation.

    • If you corrected their IR via lifestyle and/or meds, particle compositon and size would have a chance of normalizing and the discordance would disappear

    • Tom A

      Dr. Lipid, thanks for the insight and I have viewed a couple of your video interviews online. Fascinating and well done.

      One question, IF (capitals on puspose) I have a High LDL-P and a low LDL-C why would I want that discordant relationship corrected? Seems like that is the best place to be. I am assuming you mean the converse of low LDL-P and high LDL-C?

      • On behalf of Dr. Dayspring, I’d say the reverse form of discordance is probably safer (i.e., high LDL-C and low LDL-P).

  • lorraine

    A couple of comments in the last couple of segments spoke of a “damaged” particle as the possible instigator of vessel wall penetration and retention, the implication being that the LDL particle was damaged previous to penetration and retention. Just yesterday I listened to an interview with Chris Masterjohn who seemed to be saying a similar thing. I’ve been wondering about what this “damage” might be and what the evidence is for it.

    Again, the way I heard it, the particle is damaged while out in the circulation, previous to its penetration and retention in the endothelium, and it’s the damage that accounts for its penetration.

    Any input from anybody?

    • The damage (oxidation) occurs after entry into the arterial wall. However the apoB can also be glycated which would also in effect damage it

    • lorraine

      Glycation, of course. Thank you, Dr. Dayspring

  • Larry Green

    I didn’t see a recommendation to eat pancakes with lots of syrup. Where is this? Or is this the punch line to a joke I’m slow to catch? Great series btw. Thanks.

    • No, this was a joke in response a comment about eating pancakes to reduce LDL-P. Sorry for confusion.

    • KevinF

      Ahem, sorry 😉

  • steve

    Great job again! By the time you are finished with this series you will be able to turn it in to a book.
    Aside from metabolic syndrome, can’t genetics affect LDL size?
    There are high carb eating populations with low levels of heart disease and would have to assume LDL-C/LDL-P discordance not different from here.
    It would be nice to see studies of LDL-C/LDL-P in countries such as Japan and France where low O6,sugar,etc are eaten and see what the heart disease issues are there.

    • Absolutely. Genes are a very big part of this. I’ll be discussing one very important set of genes (apoE) in the future.

    • Russ C

      Peter, Very pleased to hear you will be addressing APOE4 in the future. FWIW, this is the source of my previous questions.

      The dimension I am most interested in is resolving an apparent heart/brain dilemma. Although probably a blog series as big as this if ever done, to me, the collective evidence suggests APOE4’s may want to *higher* LDL levels to overcome inferior transport of cholesterol to/within the brain (to avoid neurodegeneration). But of course this would be bad for the heart, unless this could be mitigated by controlling inflammation as discussed in previous posts.

      Can’t wait for the next (and other future?) post(s)!

  • Ryality34

    This isn’t a slog. Its sooo amazing! I was an art major in college and learning all this stuff is sooo cool!! Are you going to get into TG genesis…like how its actually made and from what? I know people say that TG goes down on LC eating but I really want to know why, Peter style.

    • I like how you think…I’ll see what I can do.

    • Dr Lustig and his sugar videos talks about how the body makes dense LDL and TG from processing sugar. I see the connection

  • are ldl p and apo b concordant? (can easily test for apob but not ldl p )

    • Great question. They are much more concordant than LDL-C and LDL-P, but not 100%. In my personal experience about 2-4% of folks have discordant apoB and LDL-P, but this is obviously quite rare. Remember, though, when I talk about apoB, I’m only talking about the direct measurement, not the estimate.

  • Jeremy

    Peter, I’ve always thought the biggest problem is with whoever came up with the supposed standards of ‘normal’ or ‘good’ cholesterol levels. LDL-C of 100, HDL-C of 40 and TG of 150 is abysmal.

    Why do we have such low expectations?

    You have to look at all three components and the target range should by LDL-C 60 and TG < 75. I've got a buddy who had LDL-C at 72, which by itself looks great but is useless by itself. His HDL-C was only 24 and all his uncles died at an early age of a stroke (dad didn't die but was half-paralyzed). His doctor told him he'd be lucky to get his HDL-C up more than a few points, and the most he'd ever seen it go up was 5 points, lol. What a joke. We got his up to 43 in about 6 months and there is not doubt we can get it over 60.

    Thank you for contributions. We need more people like you to challenge the status quo because this problem is very fixable with a good comprehensive health plan.

    • Jeremy

      Weird, something got cut off in one of my sentences and it hapenned again in this comment before I edited it and got rid of the greater than, less than symbols. The target ranges of standard cholesterol in my opinion should be LDL-C less than 75, HDL-C greater than 60 and TG less than 75. Whoever came up with the current standards needs to be put out for pasture 🙂

    • Anyone thinking they can look at lipid concentrations and guess particle numers with any accuracy is deluded. Go check the graph from my latest paper that Peter included:

    • Jeremy

      Dr. Dayspring, the study from where you pulled your graph info seems to support the point I was trying to make (which wasn’t about particle numbers).

      In the study of the 136,000 folks, only 1.4% of them had HDL greater than 60 and LDL less than 70.

      My point is that most people, doctors included, think you are fine with LDL-C less than 100, HDL-C greater than 40 and TG less than 150. That standard really needs to significantly change.

      As you pointed out in your graph, LDL-C is completely useless as a stand-a-lone figure, even when it’s less than 70.

      While you and Peter are educating your profession about LDL-P (which most doctors have never heard of) getting them also to change the standard cholesterol levels of what is acceptable (which they all have heard of) would benefit a lot of people.

      If people, most doctors included, understood that you may be at high risk unless your LDL-C is less than 75, HDL-C greater than 60 and TG less than 75 (and you have to meet all three criteria, not one or two), it would focus them much better on the fact they have a lot of work to do and not settle for the current low expectations we have with the current standards.

      A big thank you to you and Peter for your pioneering work in this field. Best of luck to you guys in your research.

      • Note to everyone: keep this theme in mind when we eventually have our discussion around hypothyroidism….

    • Jeremy

      Hey Peter, since you brought up your modeling days (financial that is) in this piece, it always cracks me up how those fancy models work great for X number of years until they blow up.

      The problem with them is they do great in a 2 dimensional world for awhile (kind of like an academic simulation) but there is usually a 3rd dimension they miss that ultimately bites them in the butt. The same problem is playing itself out now in the markets in other ways.

      It took the housing price model until Q4 2006 to finally have one variable show as discordant? Wow, what a disaster!

      • Don’t even get me started on the pitfalls of regression-based modeling… that could be (and probably is somewhere) an entire blog…

    • Jeremy

      lol 🙂

    • Susan

      “…keep this theme in mind when we eventually have our discussion around hypothyroidism…”

      I’m looking forward to this part, as a long-term low-carber with hypothyroid issues, including a poor T3/rT3 ratio. Any idea when you might get to this?

      • I’m hoping to by the end of the summer….sorry for the large window. SO MUCH to do and write about.

    • Ed

      I’m glad you are going to be discussing T3/rT3 issues because T3 directly influences LDL-Receptor expression which will impact serum levels of LDL-P and LDL-C.

    • KevinF

      Jeremy: “In the study of the 136,000 folks, only 1.4% of them had HDL greater than 60 and LDL less than 70.”

      Just musing, but that by itself tells us nothing about risk. We’d need to know those comparable numbers per person among the general population — do we know that? i.e., if only 1.4% of all adults in general ALSO have those same “ideal lipid levels” of HDL/LDL, then there’s nothing protective that that. Maybe that’s an unusual combination in a person. And even THAT data still wouldn’t tell us much unless it’s age-adjusted.

      Maybe this general population LDL/HDL data can be found in NHANES, haven’t checked, but it’s not explicitly stated in the study, which is odd because it seems to me to be an obvious thing to include if data is available.

  • alacrity

    Peter, could you please speak to ratios? I have very high TC and LDL, but also very high HDL. My apoB from VAP test was 180, but if converted to ratio of B/A-1, I’m sure it would be quite favorable. Like many low carb eaters, I have no other indications of heart disease, insulin resistance or met sym. Until now, I have been placidly ignoring these tests on the basis of “Pattern A” and good ratios; your approach challenges reliance on Pattern A but are you also challenging ratio information? Thanks very much.

    • Ratios provide guidance, but should not be used for treatment. We treat LDL-P, but often the ratio of LDL-P to HDL-P or TG to HDL-C or ApoB to ApoA1 serve as quick checks of where you’d want to be (ideally, below 30, 1.0, and 0.34, respectively).

    • HDL-C is not apoA-I They also can be very discordant We now know thinking high HDL-C is protectove or low HDL-C is necessarily a riskfactor is BS Go with apoB The level you mention is a horrific nightmare The HDL has little meaning

      But the VAP apoB is calculated– do not beleive it Get it via proetin immunoassay

  • Pingback: Cholesterol Primer - Page 4()

  • Larry Sumners

    From a discordant- LDL-C 94, LDL-P 1723, TG 84
    On a low carb diet for 2 years.
    Is there any data that quantifies the incidents of heart disease with high LPL-P? I know that in the Framington study numbers were manipulated with percentages with the actual incidents were quite small. It would be more meaningful to me to see that if you were at a certain level of LPL-P then you had a 1 in 10 chance of heart disease or 2 in 10 at another level. It would just give some quantification to the risk. I assume however that we just do not have the empirical data to have those kind of statistics.
    The series has been very informative but also scary for those of us who are doing what you are supposed to do and still have high LDL-P.

    • Larry, you’re asking a great question, but to do it justice I need to explain a few things in more detail. Could you sit tight for another week or so? I think this issue is important enough to make sure everyone understands.

    • Ken MacKillop

      I have a similarly unusual, but somewhat different, lipid profile. Please see my general comment. I would be curious what your HDL-c is — that would give a more complete picture. In any event, I can identify with your query, and have done a lot of research on my own behalf.
      My practical advice would be to get a coronary calcium score as a starting point, and go from there. Also, make sure you are fully aware of your status with regard to glycemic regulation. Get (and/or review) both an HbA1c and fasting-glucose. If appropriate follow up with an oral-glucose tolerance test and go from there.
      All of these tests are much more reliably indicative of both status and future risk than blood lipids (advanced or not), based upon my reading of the literature.
      Good luck.

  • Alexandra M

    “I’ve been hanging on the edge of my seat — really surprised me at the end where you recommend eating more pancakes.”

    Well, at least now I understand why “Confused” over on The Diet Doctor’s blog is claiming that you’ve abandoned the insulin hypothesis and gone back to the lipid hypothesis. Looks like “Confused” just skipped over the post and only read the first comment!

    • KevinF

      OK I was all ready to apologize again, but reading Mr. Confused’s comment on Dr. Eenfeldt’s blog, I think he’s implying that anyone who attributes anything of importance to anything having to do with cholesterol is preaching the “lipid hypothesis”, plus he doesn’t seem to like the blog name change!

    • Alexandra M

      “…anyone who attributes anything of importance to anything having to do with cholesterol is preaching the “lipid hypothesis”…”

      It took me a while to figure that out. You’re right, of course – sorry if it sounded like I was accusing you of something, Kevin.

  • Part VI is wonderful. I’m eager to learn more.

    In a different part of the site, you mentioned your current diet and maybe said something like 50 grams/day in protein. I’m guessing that’s a bit low by US standards/customs. I’m also guessing you want to avoid having the body convert excess protein to sugar? That left me wondering, what do you eat that has all the fat calories?

    • No, I’m less than 50 gm/day of CARBS. Protein is 125-ish.

  • Ken MacKillop

    LDL-P is a better risk marker than LDL-c; no argument. But it is still not a very strong risk marker, by the numbers. I do not believe that LDL particles are THE CAUSE, but rather just one of many secondary co-factors, for atherosclerosis.
    I recommend the following paper (Ron Krauss et al) as state-of-the-art risk assessment based upon ONLY blood lipids:
    PC2 is the strongest indicator, and it is INDEPENDENT and a function of many sub-fraction values within the lipid profile (including HDL and LDL types).
    Neither Krauss nor Otvos himself seem to think that NMR is justified for most people. Both are on the record — here’s Otvos:
    Aren’t HDL-c and Tg’s adequate to see what’s going on in the vast majority of cases?
    What about endothelial function? Of course, this is presently not measured in clinical practice.
    Believe me, I care a lot about these issues — I am not trying to be glib. My lipids (mg/dL) are: LDL-c=245;Tg=77;HDL=77. I just had a CT scan result w Agatston score = 0. I have maintained a diet that is probably highly ketogenic (very-low carb, limited protein) for 2 1/2 years. I am 53 years old. I find that a substantial (double-digit) percentage of those on such diets long-term have very high LDL-c. Childhood-epilepsy studies and bariatric-physician experience demonstrates this.
    I think that NMR is a great tool — I am rooting for LipoScience to be successful. But I really think that you are overemphasizing the importance of one risk marker much too much. And the primary clinical use of this tool — prescription of cholesterol-lowering drugs — I believe is totally unjustified in the vast majority of cases.
    I suspect that the LDL particles end up in plaques as a result of their role in the INNATE immune system. Avoid overwhelming this system by avoiding the primary cause(s) of injury to the cardiovascular endothelium, and I suspect LDL-P is meaningless.

    • greensleeves

      Hi Ken:

      “I find that a substantial (double-digit) percentage of those on such diets long-term have very high LDL-c”

      Yes reading the most common low-carbs blogs also gives me this impression. But I also think, as Dr. Westman says, that most people are doing low-carb incorrectly – the “Chet Atkins” diet.

      Post-menopausal women stall out on low-carb frequently; and it seems also that middle-aged men on low-carb develop these very high LDL-C numbers. I don’t see any blogs of middle-aged men talking about how low-carb fixed ALL their numbers. But maybe I just don’t know the right blogs?

      Do these guys all need statins immediately or are they doing low-carb wrong? Does everyone need to go back to 30 total carbs and just stay there forever?

      Why do so many middle-aged men and women have inferior outcomes? Is it because they only have 20-30% of their beta cells still functioning?

      Really curious about this. It does seems anecdotally as if most men’s C number rises astronomically after a year or so on low-carb. Maybe Peter will answer this shortly. I hope so!

      • I completely agree with Eric’s assertion (in fact, I’m having breakfast with Eric in an hour). This brings up a much larger question that I’m sure I will detail more closely in this series: It is possible that all of the risk stratification we have for heart disease is predicated on someone consuming a normal Western diet? Furthermore, is it possible that once the body stops relying on glycogen and turns over to metabolic pathways of ketosis that the “numbers” we target as “normal” are irrelevant? I think I know the answer for some physiologic parameters, but I’m still trying to develop my “universal theory” uniting it all.

    • Patrick

      Brilliant, Peter. I wondered the same thing about the validity of data arising from the particular set of humans living at a particular time, while looking at the first (Framingham) chart, above. Even if the study involved a lot of people over a long period of time, the data could still have something or nothing to say about us today.

      In other words, with LDL-P we are still talking about an association, not a cause, right? In the Framingham data selected, how were confounding factors controlled?

      We just don’t know if the predictive power of LDL-P and cardiovascular health, as good as it might be, arises from good diet, bad diet, or some other “lifestyle”, or even another metabolic agent (biochemical activity) . . . do we? For example, what are the chances that any statistically significant group within that Framingham population ate high fat, moderate protein, and low carb?

      (Pedantic aside: to “beg the question” does not really mean “to raise the question”. You like logic, I think, and this phrase is a term of art, a rhetorical flourish, signifying that the question contains its answer, so that the question is redundant.)

      One other unrelated and possibly trivial question: when you refer to the physical structure, the geometry, of the lipoprotein molecule, and the third power of the radius, you imply that the structure is spherical. Your lovely illustration in Part 1 also shows the molecule as spherical. Is it spherical, or is that just a convenience of illustration?

      Forgive the prolixity. Your work is extremely thought-provoking, highly enjoyable, and incredibly valuable. Many thanks indeed!


      • Yes, the particle is a sphere, hence the 3rd power. You are correct about the associate of LDL-P (and every single other disease marker we look at!). Note the “magic wand” experiment I give up front. Absent THAT experiment, we can never know. So we do other things:
        1. We look at populations with seemingly similar enough other traits, yet large enough disparity in 2 factors: the suspect risk maker AND the disease.
        2. We look at experimental interventions that manipulate the suspect risk factor and measure the impact on risk.

        Both of these have problems, though, and I don’t see how we overcome them:
        1. This does not establish true CAUSE and EFFECT.
        2. These interventions do many more things than just impact one risk factor.

    • I’ve been resisting the urge to publish my personal numbers because I didn’t want to have Peter think I was asking for medical advice. 🙂

      However, it looks like I’m not alone here in “statistical outlier land”, and I am very inclined to agree with Ken McKillop: I certainly wouldn’t dismiss the ratios’ predictive power and blindly adopt LDL-P / ApoB absolute numbers.

      First, a few of my personal numbers:
      TC = 297 mg/dL
      LDL = 210 mg/dL
      ApoB = 119 mg/dL
      Now, these three look pretty consistent, right? according to most guidelines and studies, I’m squarely inside the *top* quintile (80%!!!) of arterial disease risk, and any honest doctor following those “lipid hypothesis” guidelines would not let me exit their consultation room without putting me on statins or something of the kind. Which is why I’m currently avoiding “standard” doctors, I simply don’t have the patience to educate them.

      Now let’s take a look at the rest of the profile:
      HDLc = 76 mg/dL
      TG = 51 mg/dL
      ApoA1 = 153 mg/dL
      It’s starting to look a lot better, no?

      Here’s a few ratios taken as “best innovative indicators compared to standard lipid profile” from several studies:
      ApoB / ApoA1 = 0.78
      TG/HDLc = 0.67
      TC/HDLc = 3.9
      LDL/TG = 4.1
      Now, most of these put me in the *bottom* quintile of arterial disease risk. Some even put me in the 10%, 5%, or lower risk category!!

      Add to this a PCR = 0.03 mg/dL, Homocistein = 1.7 mg/L, and Cortisol = 10.9 ug/dL, and what do you get? A very healthy guy!!!

      What is currently protecting me from the maddening effects of cognitive dissonance is my faith in the practical benefits of the lifestyle I lead. I’ve followed a VLC/Paleo diet for almost a year, I exercise moderately but regularly (mostly HIIT), I’ve lost all my extra flab (solidly resting at 12% body fat mass – “looking good naked”) and I’ve got a rock-solid metabolism (much better than the previous 2 decades).

      So, which is it? Am I at a “very high” or at a “very low” risk? We can’t have it both ways, and there doesn’t seem to be much space for grey area with these numbers. My arterial disease risk seems to firmly depend on who I show them to.

      So that was my personal reason for not believing in the “particle concentration gradient” theory.

      Furthermore, I’m an engineer who is used to dealing with complex dynamic systems, filled with feedback loops and hidden state caches. I believe this description applies equally well to both a Human body or a network of computers or an electro-mechanical system. And my experience with complex dynamic systems tells me that you should never just look at a simple number and expect it to tell you all that you need to know. Everything is relative in Nature and Physics, and I expect relative numbers to trump absolute numbers almost in every situation. The devil is in the details: finding the right absolute numbers to build the relative model.

      For each “force” in our bodies there are one or more “forces” that counter it; we are just filled with an enormous amount of feedback loops that up-regulate and down-regulate almost all of the stuff we have in our blood and in our cells, as well as localized reservoirs that will compensate and confound all our efforts to linearise our observations. I can’t just take a simplistic “plumbing” analogy and consider it a realistic one regarding such a complex system.

      In the case of arterial damage, not only is there the concentration of ApoB-containing particles, there are also their oxidation factors, the robustness of the endothelium, and the several reversing mechanisms that remove the toxic cholesterol portion. So an honest scientific approach to the subject cannot and should not look for a single absolute number, taken from a surrogate test, and call it a day. A high-fidelity *independent* model must be built. LDL-P/ApoB looks like a good starting point, but you certainly can’t stop there!!

      Well… that was far longer than I meant to, sorry. 🙂
      And sorry if I came out too harsh, I am merely expressing my frustration with the “state-of-the-art”. 😉

      I’m eagerly awaiting for the instalment where Peter digresses on the contextual difference of Low Carbers and Ketotic people. 😀

      • Vasco, I can’t disagree with anything you’ve laid out. Your logic is sound and the lack of definitive answer only speaks to the gaping holes in our knowledge as I’ve commented on several times (but it’s worth repeating): Everything we have learned in the last few decades about lipidology must be taken a very important caveat — it was learned on a population of carbivores…
        So what should we do about it?

    • Well, for one, we should be a lot more discretionary and integrative in the collection of data.
      Context matters a lot (and it doesn’t take a Denise Minger to find that out) 🙂
      So, maybe we should pool all the data from the Paleo/Primal/LowCarb crowd?… as a physician, you must have a much better idea than I about which data to collect, and when.
      I believe there is already such a web site to collect low carber clinical data, can’t remember the name. Perhaps the “influential leaders” of the paleosphere should launch a campaign on all the blogs to get people to log their data?
      Sure, the credibility of such data would constantly be challenged, but something tells me that this would not be a problem for our community… after all, we wouldn’t have made such life-altering changes if we didn’t trust each other in the first place. 😉

      • Well, I have just the thing… but you’ll have a wait a while before I roll it out.

    • Russ C

      Dittos again to Vasco. Similar background and situation and see fully the merit of further research. Very much like the idea of using the paleo/LC community data as a research dataset.

      Can’t wait to see your ‘just the thing,’ Peter. Count me as a willing guinea pig!

    • Peter, is your “just the thing” perhaps a launching study within the NuSI framework?
      As good as that sounds, I was thinking more in the lines of cheaper and more robust data analysis.

      To illustrate…

      You know how the satellite and astronomy people gather their data, right? it’s noisy as hell, filled with distorting factors, but in the end they come out with these beautifully detailed awe-inspiring pictures that show so much high-resolution goodness about our universe and planet that it almost makes us cry. 🙂

      Well, it’s all done by statistical power over astronomic (pun intended) amounts of data. In the computer world, more data is always better, even if it is incredibly noisy. Given enough (noisy) data, the patterns of truth emerge.

      So, in my view, instead of trying to make sure that the data is free of noise (confounding factors) or unbiased, I believe the most productive strategy would be to make sure we have enough of it.

      That’s why I suggested a paleo community project, because this way we could easily harness a million data points, noisy as they would be, and thus have enough data to filter through. Plugging the blood test results of a few thousand low carbers along 3 or 4 year quarters, as well as punching into the same database the equivalent data taken from all the studies already available, would probably allow us to take a fresh look at the results of those long-standing studies.

      I say “get a few million data points”, and let the data patterns emerge by themselves. Instead of continuously falling into confirmation bias traps and wasting time with trial-and-error approaches, get a statistics team to swim in a pool of data as large as the 7 oceans and let them identify the confounders as well as the independent correlations.

      And most of this could be done with the help of volunteers, costing almost nothing (fan of wikipedia and peer-to-peer communities here). 🙂

      Just my two cents.

    • Meanwhile, here’s a few dots for you to connect. 😉

      1.High glucose concentrations induce TNF-alpha production
      2.TNF-alpha disrupts endothelial function

      I just ran a fast search and diagonally scanned the papers, I’m sure you’ll find lots of objections about applicability and relevance. There are probably many better studies to enforce this thesis, but I’m not a full time researcher who is paid to write reviews. 🙂

      Still, this is the sort of thing I expected to see researched nowadays – what links metabolic syndrome to arterial disease? – not the same old thing of trying to eek out predictive power from lipid panels.

      It also reinforces my growing notion that cholesterol numbers mean little to nothing regarding arterial disease in the case of LCHF practitioners.

      • Vasco, if there’s one thing I like about you (and there are many!), it’s that you’re always willing to admit the limitations of something. This work, as you suggest, is no exception. It’s tempting in science to look at interesting studies, like these, and extrapolate to other states. This is not necessarily a bad thing, but when we do this at the expense of millions of patient-years in data that we have on other more well understood mediators of CVD, it’s a bit like saying the credit crisis we’re still in is due to the fact the real estate agents are paid commission only on the sale price of a house. Sure that fed into the problem, but it wasn’t the first-order term. Besides, agents have always been paid commission in that fashion. What was unique in this case was the confluence of events: exceptionally cheap capital, mass securtization of loans, an after-market for said securitized loans, and horrible lending practices. Which of these events, if not present would have prevented the greatest destruction of wealth we’ve ever seen? I’d argue if interest rates were higher, lending practices were reasonable (e.g., LTV must be less than 80%), and lenders had to keep some amount of risk on their books, none of this would have happened. Did the fact the real estate agents had incentive to sell house to anyone, even if they couldn’t afford it, make it worse? Of course. But to say that caused the problem in the first place is to miss the point.

        Inflammation clearly makes this problem worse, but to negate the effect of the molecules that actually carry the cholesterol into the subendothelial space and start this inflammatory process is also missing the point. I can tell I’m not going to convince you of this, but hopefully I can provide a balanced counterpoint for others to make up their own mind.

    • No, Peter, you’ve already convinced me with this quite analytical and detailed model. 🙂
      According to the available evidence, inflammation is a consequence, not a cause. Fine. 🙂

      But I still think that LDL-P is NOT the first-order causal factor in atherosclerosis.
      You know, I’m re-reading GCBC, and the whole chapter about insulin and cardiovascular disease makes me wonder how you could name your blog (initially) as “The War on Insulin” and then forget about insulin in this series of articles about cholesterol. 😉

      In fact, according to Taubes, the smoking gun of arterial wall disruption is most probably in the hands of insulin.
      To me, it looks like it is the combination of active disruption (by insulin and blood sugars) AND the available by-standing ammunition (Apo-B containing lipoprotein particles) that is responsible for atherosclerosis.

      Which begs the question (which I take it is being observed in people like me), that perhaps a high Apo-B particle count (high LDL-P) is NOT much more atherosclerotic than a low LDL-P, while in the *absence* of high insulin?…

      So the first-order factor in this disease can very well be insulin resistance and corresponding hyperinsulinemia, with LDL-P being just a powder keg to fuel the fire. Taubes pretty much summarized the data for this case; is there any evidence to the contrary?

      We know that these studies are biased toward carb-eating populations, so… the question remains, I think, open.

      • Vasco, here’s my response to your similar question on the other post:

        This is a very good point, Vasco, and it is the heart of the argument/thesis put forth by folks like Gary Taubes, Eric Westman, and several others, as to why the standards of predictive cut-offs may not apply to the population you describe. However, until we do a properly designed clinical trial to test this hypothesis, it remains a hypothesis. It makes sense, I agree, but we only have bits of the story worked out. Remember the words of Thomas Henry Huxley (Darwin’s “bulldog”): “The great tragedy of science is the slaying of a beautiful hypothesis by an ugly fact.”

    • Sorry for the duplicate comment, Peter, I initially put it in the wrong post and then requested its deletion, but I guess it didn’t work out. 🙂
      So, this NUsI trial that is coming forth, will it cover this angle of insulin too? Or is it just designed to eliminate the confounders of carb-loaded nutrition?

      • The first NuSI trial is still early in the design phase.

  • Shane

    I just received my cholesterol numbers from my doctor after experimenting with a diet comparable to yours–almost identical even–for the last five months. My doctor had a panic attack. My total cholesterol was 457, the highest it has ever been. My HDL was 65. My LDL was 377, which constrained the nurse to tell me to lower these levels in the next four months or statins could be in my future. Of course, the size dimension of the LDLs wasno part of the test. Nor did she specify my triglyceride level, which annoyed me.

    Those are high numbers, I will admit. I’m committed to this diet–it has provided nothing but weight loss and energy for me–but I’m unsure how I should address these numbers with my doctor.

    • Ken MacKillop

      Hi Shane,
      Interesting — your numbers are unusual (like mine) but not rare at all on a ketogenic diet. Your doc MUST have the Tg number, by the way, unless your panel was unfasted and LDL-c measurement was direct. It’s possible but I doubt it. I think you might be interested in this interview:
      In it there are two questioners like us, and Dr. Westman indicates that this type of lipid profile is “classic” for long-term low-carb dieters. You are not yet “long-term”, and part (or even all) of your increase in LDL-c could be due to “transient hypercholesterolemia” — a well known effect following change to low-carb. I recommend strongly against statins or other drugs. I know of about a dozen low-carb bloggers with lipids similar to ours. They are all in excellent health. Barry Groves has been doing it longest — four or more decades, I think.
      I would also recommend to you the same as in my reply to Larry Sumners.
      Bon chance, mon ami!

    • greensleeves

      Hi Shane,

      “the highest it has ever been”

      Again, anecdotally from reading the common blogs, it seems as if men really don’t get better numbers for 6-9 months after they’ve changed to low carb. Especially if you are losing a lot of weight. So if the blogs are any guide, you may have tested too early.

      Following NANY’s advice, you should drop your daily carbs by 10g total a day at least, or even go down to 20g total period and stay there for several months. Then go for your retest. You may have more metabolic damage than you think, and as a result, a very low carb tolerance.

      If that doesn’t work, I guess Peter would recommend you think about drug therapy. But you have to find out what works for you, right? N=1 as they say. Good luck and don’t give up!

      • Actually, what I would recommend is asking the same questions I posed to Peter-NZ with respect to vit K supplementation. Which is the bigger risk?

        1. NOT taking drug X to lower your LDL-P, assuming the results of the trials are relevant to YOU (the only person who matters)?, or
        2. Taking drug X, assuming the opposite?

    • Stipetic

      Shane, I’m not an expert in this, but my understanding is that if you are in the process of losing fat mass (weight), then your lipid profile can be skewed by this (after all, you’re dumping pure fat from your fat cells into your general circulation on top of what you are eating). So maybe once you are weight stable, your lipid profile may be more predictive. It would be interesting to see what Peter or Dr. Dayspring’s experience is with this.

      • This is correct, though I can only comment from personal experience and that of others. I actually am not familiar with this body of literature.

    • LynneC

      What were your numbers prior to starting a paleo diet?
      Are you losing weight?
      Do you have access to apoE genotype testing?
      Google ‘ApoE and diet’ and you will get some additional info that may be helpful…

    • Patrick

      I followed Ken’s link above to the podcast interview with Dr. Eric Westman.

      Dr Westman makes a rather interesting observation. If LDL-C plays a beneficial role (he mentions the transportation of vitamins, and like Dr Attia he uses the boat-cargo metaphor), then we should be cautious about intervening to reduce LDL-C, and perhaps not concerned about a supposedly high number. After all, if it’s doing something good, why try to eliminate it? And when we raise it, we are not choosing to raise it per se; rather, it rises as a consequence of following a healthy diet. Gary Taubes observes, in WWGF, that it’s difficult to accept the idea that a diet that is good for you can also be bad for you. Also note, as we understand, thanks to Dr Attia’s seminar here, LDL-C does not equate to LDL-P, and does not correlate with risk for atherosclerosis.

      As Vasco points out, there are multiple moving parts that are linked in this system involving the lipids and cardio-vascular network. You manually tinker with one thing, and you can expect other components automatically to change their functioning too. The law of unintended consequences operates.

      In writing this, I’m passing along my own self-reassurance about the standard lipid panel results (mine show similarly so-called high LDL-C, calculated, and directly measured via VAP). I’m aware of the confirmation bias–I’m surely finding evidence to support what I already want to believe. But that does not mean that it’s wrong, either.

      • It’s a fair point, and Eric Westman and I had breakfast yesterday and discussed this exact issue at length. I think it’s safe to say we both agree the answer is not known. His hypothesis is reasonable, but not really tested rigorously. One could make the same point about my hypothesis, given that everything I’ve extrapolated is based on people eating carbs.

  • Ken MacKillop

    P.S. I should have included one apo-B test resulting in a reading of 165mg/dL. I think that this would convert to an LDL-P = ~2300nmol/L. My LDL-c = 243mg/dL at the same time.
    My fasting insulin is <2mIU/L (below lowest measurable reading w commercial equipment).
    Interesting, eh? What do you think, Peter?

    • apoB suggests a high LDL-P, but the conversions are best-guesses. Might as well find out. Get a sterol panel while you’re at it. You sure don’t “look” IR, but I would not be comfortable with numbers that high.

    • David

      Ken, you may be interested to know that my apo-B and LDL-C numbers are identical to yours. Apo-B is 162 mg/dL and LDL-C is 242 mg/dL, but I also happened to get an NMR test at the same time and my LDL-P measured pretty high at 3198nmol/L. This is after 1 year of eating HFLC, the last 6 months of which I’ve remained at a stable weight.

  • charles grashow

    So what does it mean if you have high LDL-P and LDL-C and high HDL but very low trigs and you’re on a paleo diet?

    NMR test results

    LDL-P 1500nmol/L
    LDL-C 188mg/dL
    HDL-C 59 mg/dL
    Triglycerides 36 mg/dL

    HDL-P 28.5 umol/L
    Small LDL-P 127 nmol/L Ref range <= 527

    • charles grashow

      If the total particle count is high but appx 91.5% of it is large and only appx 8.5% is small and dense is that really bad?

      • Yes. A particle is a particle. Statistically speaking, someone with lots of large particles will have fewer, but once you know the particle number, size doesn’t predict risk.

    • greensleeves

      Hi Charles:

      “very low trigs and you’re on a paleo diet”

      I guess from what Peter has written, your low trigs are because you’ve been good about avoiding wheat and sugar. However, many people on the paleo diet now eat potatoes and rice.

      So my first thought – derived from Dr. Westman – is that you may still be eating too many carbs for your personal tolerance. Your beta cells may be damaged from decades of the SAD. Have you considered dropping your carbs to 30g total a day for 6 months and then re-testing?

      I know quite a few people on the Atkins forum used to be paleo but came back to Atkins because they saw that they needed the very strict framework of the Atkins plan. Have you ever considered that your current paleo plan may be too liberal for you right now?

    • Ken MacKillop

      Lest you think that your LDL-P is HIGH — it is right around mean for healthy males with no CVD, according to this paper/study by Otvos, Cromwell et al (Table 1):
      Note in Table 2 also that your LDL-P is well below mean for your category (low Tg’s/high LDL-c).
      Your numbers look great from my point of view (but then, I am admittedly biased :))

  • Ken MacKillop

    P.S. again: Combining my Framingham risk (6%) and Agatston score, with age and sex, etc. I have a 1.7% risk of a CV event within the next ten years.

  • Roger L. Cauvin

    This study found that the association between mortality rates and familial hypercholesterolemia has varied greatly over time:

    The authors conclude:

    “We found that the excess mortality from familial hypercholesterolaemia varied over time. In the 19th century, mortality seemed lower than in the general population. It rose after 1915, reached a maximum during the 1950s, and decreased thereafter. During the decades with excess mortality, survival in the branches of the pedigree differed significantly, ranging from normal life expectancy to severe excess mortality. This large variation of risk suggests that previous studies, with families based on selected patients, may have overestimated mortality. Moreover, such large variation in mortality in two directions (over time and within generations) in a pedigree indicates that the disorder has strong interactions with environmental factors.”

    I wonder how LDL-P correlated with heart disease risk in the 19th century.

    • I wonder how homogeneous this population was over time, also? Studies with heterogeneous populations will always have trouble correctly identifying relationships between risk and mortality. I’m guessing people were dying of infectious diseases so rampantly in the 1800’s that dying of heart disease at 45 wasn’t a big enough difference to account for their disease.

    • But isn’t it true that your analysis shows the COMBINATION of high LDL-P levels and the other characteristics of the subjects in the studies are associated with higher risk? For example, it’s possible that high LDL-P combined with a standard diet of highly-processed food is where the risk lies.

      Wouldn’t good science control for these concomitant factors? Isn’t it possible that someone with a very different diet from the subjects in the studies could have high LDL-P but low mortality risk?

      • Yes, but the problem is virtually everyone in these studies is consuming a “standard” diet. Additionally, they typically do not even attempt to control for diet. It just hasn’t been a focus, unfortunately.

  • macoda

    Great series, I learned a lot. I have a couple questions though:
    1. If the partial pressure (concentration) of LDL-p causes the particles to migrate behind the endothelium wall, the this action should be observed for all particles in the blood (as long as they fit). What makes the APO-B particles so pathogenic, and not other particles that may be floating in the blood?
    2. If someone’s metabolism is fat-adapted, and they burn triglycerides as their primary fuel,and the triglycerides are carried by LDL, would that cause higher blood trigs, and more LDL particles? It seems to be if we are buring fat, then there would be more of it in our blood stream.

    • Good questions. Question 1 has been answered a few times previously by me and Tom Dayspring (look back at Parts IV and V) in the comments section and the actual post.
      Question 2: it’s actually the reverse. The person whose body is primarily burning fat virtually always has lower circulating TG for 2 reasons:
      1. Their muscles are consuming it (instead of only glycogen), and
      2. The type of diet necessary to induce this metabolic state largely precludes carbohydrate ingestion which, as far back as the 1950’s has been unambiguously associated with more TG exporting from liver and higher circulating TG.

    • John

      Dietary fat is packaged into chylomicrons in the intestines. These are similar particles to VLDLs but different in that they use the apoB-48 protein rather than the apoB-100 which is used in the liver to create VLDL/LDL and HDL. As Doc says, sugars create triglycerides. Exogenous fat never hits these pathways. The 100 version is the measure of LDL-P.

  • Rachel

    Is there an equation to convert apoB to LDL-P? My doctor uses Berkeley Heart Labs, so I already have the apoB value (which I think is measured, not calculated).

    • Such a formula is probably not accurate enough to justify. I would have our doctor assess risk from your direct apoB.

  • Ken MacKillop

    Peter, I would like to suggest a question for the NMR folks. The Krauss study that I cited implies that stronger risk indicators can be designed based upon functions of multiple subfractions of various lipoprotein classes. Using just one number such as LDL-P is, I believe, throwing away info that is in the NMR lipid panel. Krauss may be keeping his PC1/2/3 formulas “proprietary”, but I am sure that the LipoScience people could generate similar risk functions from MESA cohort and so forth. Why don’t they? Wouldn’t this better differentiate them and help market their instrumentation?

    • Hopefully they have a chance to read your question. This weekend is the largest lipid meeting of the year, so I know they are busy, but perhaps next week Tom or Jim may see this and comment. The problem with “proprietary” formulae (same for VAP’s estimate of apoB) is that they are not able to tested by others and peer-reviewed.

  • Bobby

    Dr. Attia: This series, and your whole site has taught me so much. One of the special qualities of your site is that you are constantly replying to comments. I dare say, I might learn more from the excellent questions and your replies. At a minimum, they fill in the gaps in my understanding. Please keep up the great “give and take” with the comments made.

    • Thanks, Bobby. I’m not sure I’ll be able to keep up quite the same pace of response, but fortunately you as readers seem pretty capable of doing so in my absence.

  • Kypros

    “Furthermore, is it possible that once the body stops relying on glycogen and turns over to metabolic pathways of ketosis that the “numbers” we target as “normal” are irrelevant? I think I know the answer for some physiologic parameters, but I’m still trying to develop my “universal theory” uniting it all.”

    Care to elaborate on which numbers could become irrelevant with ketosis?

    • At the risk of nullifying I’m in the process of explaining with respect to cholesterol, it’s possible (i.e., needs to be tested) that EVERY one of these risk predictors is irrelevant in someone who is ketogenic.

    • KevinF

      Well if a guy can win a Nobel Prize for giving himself an ulcer, I’d say proving THIS is worth a trip to Stockholm. And I hear low-carb high-fat is big in Sweden…

  • Larry Sumners

    Off the subject at hand but have you done any research or reading on the use of heart scans for calcium scoring?

    • I have not personally done so, though I’m familiar with them and had one at the age of 36, which was enough to convince me I needed to change what I was doing…I was in the 92nd percentile of risk despite doing everything “right.”

  • David

    I wonder if anyone has had a coronary angiogram after several years to see if there is any change in atherosclerosis.
    Would looking at the calcification levels of the plaques also be a less invasive test?

  • Peter

    Here’s a summation of your work:

    Normal TC or Normal LDL-C
    Normal LDL-P

    Positive discordance:
    High TC or High LDL-C
    Normal LDL-P

    Negative discordance:
    Normal TC or Normal LDL-C
    High LDL-P

    Normal TC or Normal LDL-C
    Unknown LDL-P

    Standard Lipid Panel: $60
    NMR Lipoprofile: $90

    Worth additional $30 to find out your risk level?

    • Concordance would also include high LDL-C and high LDL-P. Obviously, I think the extra $30 is worth knowing my LDL-P, but we haven’t quite got to where I’ve “armed” everyone with enough info to make their own personal decision.

  • J Perry,MD

    wow,could it be true ketosis changes standard risk factors?BTW as an ApoE 2/3 I,too, have the high LDL and LDL-p (ApoB)with low carb and it is not just an ApoE 4 phenomenon.low carb is necessary for blood sugar and triglyceride contro,but the LDL-p is a problem.looking forward to you addressing this issue.

    • Don’t expect a resolution, however. We are now in the world of hypothesis generation, not assertion.

  • Did the Massai or Inuit supplement their lifetime of ketosis with sodium and magnesium? Off topic but I kept forgetting to ask until now.

    • Sodium definitely (either through the blood of their prey and/or salt water). Magnesium, may have come in sufficient quantities from the meat/blood of the meal.

    • greensleeves

      “Did the Massai or Inuit supplement their lifetime of ketosis with sodium and magnesium? ”

      Yes. The Inuit made soup using the clean top edge of the sea ice, which is obviously salty, but not as salty as the water. Incredibly, they hunt mussels under the ice, and make mussel soup with melted sea ice:

      The majority of the magnesium in their diet comes from eating lots of kelp, which they also add to the soup. Kelp is actually quite mineral rich. As for Vit. C, they got theirs from seal brains and caribou liver.

      The Masai actually do eat leafy greens, which are high in minerals, esp. magnesium. Spinach-like foods have lots of magnesium.

  • JohnJ

    There is some change on the traditional lipid hypothesis;

    Eminent doctor says it is time for a full reappraisal of the cholesterol theory

    Also more on a contrarian cholesterol view;

  • steve

    Peter: If you had a calcium scan at age 36, and changed your dietary regimen based upon your risk at 92% level, how would you know your program(if you are taking meds along with your restricted carb diet) that your risk is not worsening, improving or remaining stable. Sounds like you would have had a high calcium score for 92% risk.
    It is one thing to lower our LDL-P, but how do we actually know what we are doing is working which is ultimately staying event free? You may get particle count to under 1000, but maybe for any given person’s risk profile it needs to be closer to 400, if possible.

    Also, how influenced is NMR test by what you have most recently eaten, say in the last few days or weeks?

    • My score was only 6, but at the age of the 36 that was, obviously, high. Basically, at 36 one shouldn’t have ANY calcium in their artery walls. So “clinically” this was of no value, but it was predicative of something. NMR seems largely insensitive to recent meals/fed state.

  • Bruce Blakely

    OK, so LDL-C alone is not a good predictor of risk. But if LDL-P increases because triglycerides increase, wouldn’t looking at LDL-C together with TG be a good predictor of risk? What’s the concordance between LDL-P and TG?

    Not saying that people shouldn’t get their LDL-P number but it seems that a lot of people are reluctant to do this without their doctor’s cooperation which is not always forthcoming.

  • Catherine

    Life Extension you can order this on your own
    for 90 bucks
    “a lot of people are reluctant to do this without their doctor’s cooperation” Not to be flip but
    adios amigo
    (or don’t tell them if you can’t hire your physician)
    I’ll leave the country before I beg for cooperation…who wants all this in the mothership data base anyway? There is a lot to be said for keeping your labs private, imo

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  • Laura

    A couple of questions:
    1. If we’re discussing the possibility that LDL particle number may not be as clear a risk factor in individuals who are in ketosis, isn’t that basically saying that we’re considering the possibility that LDL particle concentration ISN’T the one true 1st order factor influencing CVD?
    2. Peter, I’m wondering if at some point you plan to discuss the issue of post-prandial serum triglycerides, and whether those are a more useful way to assess risk than are fasting triglycerides, and if so, what that might imply for folks eating a high-fat diet.
    3. My impression has been that the correlation of LDL-C with heart disease risk has generally been weaker in women than men- and that in women (of a certain age, at least) all-cause mortality is actually lower when LDL-C is above the range considered officially desirable. Are the results with LDL-P for women still different from those for men, or do findings for men and women converge more with LDL-P than LDL-C? Which studies could I look at that actually include LDL-P and women?

    • 1. I think this hypotheis, that LDL-P may be less important is ketosis, or other LC state is VERY preliminary. That said, if it were shown to be true, it COULD imply that LDL-P is less important that believed in anyone, but for me even suggest that would be irresponsible beyond words.
      2. The gold standard is TG AUC (area under curve). Since that’s not a practical test for most folks, myself included, it’s easier to standardize the test in a fasting state. That does mean this is a “better” test, just easier to compare.
      3. This is a great question for Tom Dayspring, who actually sub- sub- sub-specializes in this. I’ll defer to Tom for a more robust response.

    • HighlySkeptical

      Hi Peter & Laura:

      I think Laura’s 3 is true for women with periods. Google shows quite a few studies suggesting estrogen protects the endothelium somehow. But post menopause risk seems to rise to that of men.

    • Laura

      Hi, thanks Peter and HighlySkeptical,
      I’m still rather uncertain about serum cholesterol values as they relate to mortality in women, elderly or otherwise. I know one can find a study to support almost any hypothesis, but there have been a number of studies coming out of Scandinavia lately that call some of the CW into question for me. Several specifically on the elderly in Finland, and a big one one from Norway, with abstract pasted in below (the article appears to be freely available). Of course, generally LDL-P is not reported in these studies, but I don’t know that that makes them completely useless.

      J Eval Clin Pract. 2012 Feb;18(1):159-68. doi: 10.1111/j.1365-2753.2011.01767.x. Epub 2011 Sep 25.
      Is the use of cholesterol in mortality risk algorithms in clinical guidelines valid? Ten years prospective data from the Norwegian HUNT 2 study.
      Petursson H, Sigurdsson JA, Bengtsson C, Nilsen TI, Getz L.
      Research Unit of General Practice, Department of Public Health and General Practice, Norwegian University of Science and Technology (NTNU), Trondheim, Norway.
      Many clinical guidelines for cardiovascular disease (CVD) prevention contain risk estimation charts/calculators. These have shown a tendency to overestimate risk, which indicates that there might be theoretical flaws in the algorithms. Total cholesterol is a frequently used variable in the risk estimates. Some studies indicate that the predictive properties of cholesterol might not be as straightforward as widely assumed. Our aim was to document the strength and validity of total cholesterol as a risk factor for mortality in a well-defined, general Norwegian population without known CVD at baseline.
      We assessed the association of total serum cholesterol with total mortality, as well as mortality from CVD and ischaemic heart disease (IHD), using Cox proportional hazard models. The study population comprises 52 087 Norwegians, aged 20-74, who participated in the Nord-Trøndelag Health Study (HUNT 2, 1995-1997) and were followed-up on cause-specific mortality for 10 years (510 297 person-years in total).
      Among women, cholesterol had an inverse association with all-cause mortality [hazard ratio (HR): 0.94; 95% confidence interval (CI): 0.89-0.99 per 1.0 mmol L(-1) increase] as well as CVD mortality (HR: 0.97; 95% CI: 0.88-1.07). The association with IHD mortality (HR: 1.07; 95% CI: 0.92-1.24) was not linear but seemed to follow a ‘U-shaped’ curve, with the highest mortality <5.0 and ?7.0 mmol L(-1) . Among men, the association of cholesterol with mortality from CVD (HR: 1.06; 95% CI: 0.98-1.15) and in total (HR: 0.98; 95% CI: 0.93-1.03) followed a 'U-shaped' pattern.
      Our study provides an updated epidemiological indication of possible errors in the CVD risk algorithms of many clinical guidelines. If our findings are generalizable, clinical and public health recommendations regarding the 'dangers' of cholesterol should be revised. This is especially true for women, for whom moderately elevated cholesterol (by current standards) may prove to be not only harmless but even beneficial.

      • Laura, I think your point about these studies not commenting on LDL-P or apoB is the key point. In fact, most studies looking at overall mortality do not show a strong association between cholesterol levels and mortality, or even disease risk. It’s one of the reasons TC and LDL-C are not even in the criteria for metabolic syndrome. I have no doubt that what is true in men or complete both sexes (in aggregate) may not be true in women, or that what is true in pre-menopausal women, may not be true in post-menopausal women, at least to the same extent. However, the best evidence I have seen still suggests to me that there is no demographic in which high apoB or high LDL-P is not suggestive of more risk.

  • zack

    I am beyond fascinated with this topic and can’t thank you enough for this series. You’re testing the limits of my comprehension, but you still got me with you. I appreciate the explanations without dumbing it down to the point where you don’t show the why or how.

    Very much looking forward to reading more

  • Indy M.

    Hello Dr. Attia –

    great work! Looking forward to your discussion of Treatments.

    I started eating low-carb in 2010 after reading Dr. Cynthia Kenyon’s research work on life-extension by reducing insulin production. I am hoping that there will be an ‘Generalized’ solution that ties her research findings and Cardio Vascular health methods.

    Indy M.

  • JohnnyCakes

    Well, Doc, game on!

    Having been obese for quite a while (30 years), and having been diagnosed with a congential cardiac defect (hypertrophic cardiomyophathy) a half dozen years ago, I’ve gone highly LCHF and it has been a great improvement for me. I’ve lost 25 pounds, lost my interest/obsession with food, lost my ADHD, and am operating at an improved mental capacity, and my negative physical symptoms have diminished, so I’m a big “buyer” of the concept.

    Today I “had it out” with my cardiologist, who prescribed statins for my elevated triglicerides, which occurred after I started an LCHF diet. I pointed him, and his second in command, to your website. We’ll see what happens. As I left, the second in command was quite intrigued by what she was reading. I would like to point out that my doctor has “written the book” on my particular condition and in his field is probably the best there is, but I personally don’t think that makes him qualified to be an expert on blood lipids.

    As I pointed out to him, we both have my longevity as a common interest, and I’d be happy to take whatever test he’d prescribe to either convince me that I have incipient CAD, or not, but I wasn’t going to let one blood lipid test determine whether I’d be taking statins or not – he wants me on them, and I don’t generally believe in conventional wisdom. So we agreed I’d get a coronary calcium scan done first.

    I hate to disagree with my doc, who is so well intentioned and for whom I have great respect. But I’d like to avoid medications with their unknown effects. Whats the best way to get these alternative data points? NMR? It would be useful to get a “laundry list” of tests.

    I’m going to push this as far as I can with my doc. I have no desire to go back to the old me. We could take this off-line if you’d like. It could be useful. Thanks.

  • Mugs

    Hi Peter,

    First time ever posting, so bear with me. I love your site – it has changed my life. I hope too that it might actually save my mom’s. I turned her on to it, and she loves you!
    I read all 6 parts of this so far, and I am just floored. Such good info. I have been eating like you for about 6 or 7 weeks (the sautéed ground beef is my absolute fave!). Weight loss is slow, but everything else is great, so I don’t care as much. However, a friend and I were thinking maybe I am really really insulin resistant. About time to check my blood work and see where I am (horrible numbers about 6 months ago). So I asked my doctor about NMR and the HOMA-IR. He SHUT ME DOWN. It was awful. I have a great relationship with this doctor and I was horrified. I fought for the NMR and won, but he wouldn’t even discuss the HOMA-IR. He said he would have to justify it (The ADA goes by sugar level only) and the results don’t matter – the treatment would be the same. So, my question is: Do you think it’s worth it to try to educate your doctor (do you have any advice if so), or just say screw it and go find a new doctor? I apologize if you have covered this previously. I did look, but I am too angry to keep searching.

    Thanks and keep on doing your thing – can’t wait to see more!

    • Your doctor agreed to the NMR, but not the $3 fasting insulin level (HOMA-IR is calculated with fasting insulin and fasting glucose)? Wow! See what the NMR and fasting glucose and TG show. Best way to triangulate in IR is: HOMA-IR, TG/HDL-C, and LP-IR score (which you will get from Liposcience NMR). Just make sure your doctor also requests that with the NMR data.

  • Dorian


    Very much like the scatterplot of LDL-C vs LDL-P in the Summary. Is it possible to add one more variable to the plot, a variable like cardiovascular risk, or cardiovascular death, or total death — showing the variable with a spectrum of colors (e.g. darkest red for worst quintile, lightest red for best quintile)? The image would be really interesting to see, especially if the color gradient was primarily from the bottom of the plot to the top of the plot. Incidentally, what is the plot’s correlation?

    • I don’t recall and would need to go back and look. I like the idea of the adding more info to this.

  • Rock Climber


    I finally got around to ordering an online NMR LipidProfile via Life Extensions, and was loving the series till I just got my results back, so I have a feeling that there is a lot more to talk about in the series. (Posting results for info, not advice)

    LDL-P : 1932
    LDL-C : 157
    HDL-C : 56
    Trig : 78
    TC : 229
    HDL-P : 30.0
    Small LDL-P: 618
    LDL Size : 21.4

    LP-IR Score: 13 (I was very happy about this despite not knowing how it’s calculated)

    I find these results very concerning just looking at my LDL-P, I’m 28 years old, 6′ 2″ I have been fluctuating between 175-185 pounds (by choice) for almost 12 months now, I eat Ketosis diet for about 2/3 a month, and low carb about 2/9 a month and eat crap about 1/9 a month.

    I feel extremely healthy, and would never have expected my LDL-P to be 1932.

    So to my question, if high LDL-P is very bad to have when on the high carb diet, why is it not bad when on a low carb diet…?
    If both situations are bad, do carbs need a sweet spot of ingestion at 50/100/200g etc to prevent LDL-P rising and inducing plague in the artery walls.

    If high LDL-P while in ketosis is still safe, then what about the high carb diet is modifying the artery wall composition to allow LDL-P inside it (or not letting it out), or worse yet what is ketosis generating that may protect against artery wall penetration/extraction? Worse because that means people that occasionally do a 1 day carb binge may in fact be doing the most damage to their arteries than any other person.

    Also keep up the good work, I feel my mind growing every week, and it starts with your blog post in the morning.

    • The best way to find out what your LDL-P would be on a standard diet would be to return to it for a period, say, 3 months, and re-check.
      The biggest problem we fact in interpreting data like this in a dietary state different from the dietary state people were in when the studies were done, which is a significant differences, is that we don’t know what other factors may be at play.

    • Rock Climber

      Thanks Peter,

      My plan of attack after taking some time to think about it is going to be to go even more strict and do ketosis for 3 months straight, get a follow up NMR, that way i know the direction in which my LDL-P is trending, if it trends further up, then i’m going to see what happens when I diet for 3 months on 200g of carbs a day, then get a follow up NMR. And if it is trending down, then I know I was just in a extremely bad place to start with haha. I’ll try to keep coming back to this specific comment with the updates.

      Let me know if there are any more data points I should collect now, before I start the experiment, that maybe of value/interest at the end of the 6 months.

      • Ask you doc to get the “full panel” from Health Diagnostics Labs, Inc. (HDL, Inc.). I’m going to run through some case studies and give folks a sense of what kind of testing is actually out there.

    • Rock Climber

      So 6 months later I got my follow up NMR Lipid Profile test, I couldn’t bring myself to go back to eating carbs again, and I just feel so good eating a ketogenic lifestyle that I decided to simply keep to it. Here are the updated results:

      LDL-P : 2130
      LDL-C : 175
      HDL-C : 54
      Trig : 52
      TC : 239
      HDL-P : 28.5
      Small LDL-P: 672
      LDL Size : 21.4

      LP-IR Score: 21

      Most noticeably for me, LDL-P continued to rise, triglycerides did plummit while keeping HDL-C stable. Weight wise I was stable during the entire 6 month period, 6′ 2″, 180 pounds, no belly, no six pack either lol.

      I have been genotyped by 23 and me a few years ago, so if there are any traits anyone would like to know for understanding high LDL-P then let me know.

      This test has made me pause and think for a while, haven’t come to an answer, more research is in store for me, but I think i’m going to be focusing on what I can do to lower that LDL-P, whilst it may not be an issue if I don’t generate any inflammation, I still feel like that is saying don’t worry if you never eat carbs again you’ll be fine, whilst it may be true, its still not the stable place I was in when I was 16. Until I can normalise to that level, I’ll always want to tweak what I’m doing.

  • Russ W


    I want to thank you for this amazing resource. I have to admit that I haven’t fully internalized all of it yet, on my third read-through. Very dense, but I will keep at it. My question has to do with how statins and ldl-p interact. I have been on omega-3’s and statins for many years for high cholesterol and triglycerides triggered after an organ transplant (on cyclosporin as well), and although my numbers are much better, they are still high. We have NEVER done a NMR lipid profile. I would like to get a profile, but would it make any sense to do it with or without the statin on board for 6-8 weeks? You’ve discussed it some, but it’s unclear to me how meaningful the test would be as is. I had mostly normal cholesterol before transplant and cyclosporin, so I suspect I won the transplant lottery and lost the genetics lottery in regards to how cyclosporin affects my endogenous cholesterol production. I tolerate statins well, so it’s not an issue of needing to drop it.


    • LDL-P concentration is primarily a function of 3 things: how much cholesterol is produced by your body; how much cholesterol is re-absorbed in your guy (from your bile); how many LDL particles are cleared by your liver. Statins primarily work on the first and third of these. Check under your “normal” conditions (i.e., if you’re on a statin, you might as well how it’s doing).

  • I got my NMR LipoProfile results after strict very low carb for about 5 months (less than 25 grams). I also eat high fat and moderate protein. Maybe I skimped on the calories and messed up some hormones but I’ve been fairly weight stable for a month (losing only about 2-3 pounds maybe) and was at 12.2% body fat when I took the test. The numbers were all great, except for LDL-P. Any idea what might be going on? I’ve been doing some reading and people are suggesting thyroid issues. I’ve started supplementing vitamins and minerals and increasing my calories and increasing exercise since then. But I’m afraid with numbers this high (just in LDL) that I may have some other underlying issues. If it was lipids being poured into my blood from weight loss alone, wouldn’t I see higher triglyceride numbers as well? I’m afraid that even with supplementation and changing things up, I won’t get anywhere within a “normal” range. I won’t even hit average until I drop about 1500 particles.

    (Yes, that does say over three thousand LDL-P down there)

    LDL-P 3132 (>2000 is highest risk)
    LCL-C 323 (>189 highest risk but not concerned about this number)
    HDL-C 63 (This is really good >40)
    Trig 62 (Also very good 30.5. Don’t know much about HDL-P though)
    Small LDL 217 (average is 20.5 for large pattern A)

    Insulin Resistance
    Large VLDL-P 0.9 (Very good. 7.3 is highest percentile in favor of sensitivity so this is good)
    VLDL Size Unknown – “VLDL concentration too low to allow determination of VLDL Size. Low VLDL concentration contributes minimally to the LP-IR score.”
    LDL Size 21.7 (>21.2 best percentile)
    HDL Size 9.2 (50th percentile)
    LP-IR Score 15 (best score is less than 27, worst is over 63 – so this is excellent)

    I requested thyroid free t3/t4 and reverse T3 and my doctor refused to do those tests and instead just tested TSH and Free T4. Which he said were within range. So unless I pay for another test out of pocket, I won’t really know if it is perhaps T3. And even if I did, I haven’t found a good way to interpret what healthy/helpful levels are.

    • Derek, I just can’t imagine an abnormal rT3 (or T3) having this impact on your LDL-P. I don’t know what your LDL-P was on a “standard” diet, but obviously this current level deserves a further work-up (e.g., apoE genotyping, sterol analysis). Please follow up with your physician. In the absence of better data to the contrary, I think we should assume you are at risk.

      NOTE TO READERS: I’m commenting specifically to Derek, but this advice holds to EVERYONE who is sending me elevated LDL-P numbers.

    • Bill

      This is one of the things that concerns me about the idea of monitoring and treating LDL-P, with powerful drugs if necessary. We know that a significant percentage of people who adopt LCHF diets spike their LDL-C, sometimes dramatically. And now with more people getting NMR tests we know that at least some, and perhaps many, of them also wind up with high LDL-P (in fact, some of us get LDL-C so high that it’s hard to believe our LDL-P could be optimal no matter how big and cholesterol-dense our LDL particles are). Peter from Hyperlipid has said this of himself, and it applies to me, too.

      So we have a dietary change that seems incredibly healthy, with many people completely recovering from metabolic syndrome and other ills, including obesity. Yet their LDL-C, and apparently also LDL-P, may spike. Does it make sense that this is a sign of ill health or risk in the context of everything else dramatically improving? I believe this is why Dr. Eric Westman has said that he’s begun to think that spiked LDL-C on LCHF may be a sign of vibrant health, rather than risk. I don’t know if Dr. Westman has addressed spiked LDL-P as well.

      If in fact high LDL-P in the LCHF context is healthy that would suggest it is a marker, rather than a major causal factor, in CVD, a marker that only applies in some contexts. Or maybe a minority of people, with specific genetic variations, are really putting themselves at risk with high saturated fat LCHF? (I don’t like that thought, since I’d likely be one of them.) I’m not clear that current research has disambiguated these possibilities.

      I know that Peter, and others, acknowledge that the research implicating LDL-P has been done on people eating SAD and may or may not apply to those eating LCHF. I appreciate that LDL-P seems to be a much better “risk factor” than standard measures, but I can’t help wondering if the science is still too preliminary to justify taking powerful pharmaceuticals (or even reducing saturated fat?), at least for those of us on LCHF. Obviously, this is an individual decision that has to be made with imperfect information, like so many in life. Since my default position is to avoid medical intervention in the absence of pretty convincing evidence of net benefit, I’m not yet sure if I even want to get the NMR test. But maybe by the end of this series I’ll be convinced!

      Perhaps this is an area where NuSi will be able to promote the needed research.

      Thanks again for the excellent and thought-provoking series.

      • Bill, Eric Westman and I had breakfast last week in DC and discussed this exact topic at length. I *wish* I had an answer or *knew* what was right, but I don’t. This is one of those areas that really warrants each of us making a personal choice with the best data available, however applicable it may or may not be. What I’m hoping to do is provide readers with the current state of knowledge so they might be able to make the most informed decisions possible, but I’m am fully aware of the challenges these seemingly conflicting data provide.

    • Bill

      Thanks, Peter.

      It will be interesting to see whether more docs successfully using LCHF, such as Dr. Westman, will start following LDL-P routinely, and if so what they will recommend. I’ll wait until you complete your series before giving my own doc another headache about this.

      • And most importantly, if we can develop some long-term studies to actually determine the predictive power of LDL-P/apoB in LCHF/ketotic persons.

    • lorraine

      It would be interesting to me if Specialty Health (the firefighters in AZ) would be able to do an analysis of their population on the LDL-P to see what percentage of their population who switches to carb restriction gets this increase in LDL-P with all other markers going in the right direction. It seems like they’re serving a large population and it also seems like everybody is getting an NMR. Looking back over existing data like theirs, and seeing if there are trends, could provide an insight that could lead to a testable hypothesis.

      It would also be great if Drs. Westman, Volek and Phinney could start to look at this, by including the NMR in their lipid analyses of their patients/subjects.

      @Derek, ketosis significantly skewed my thyroid labs (which I”ve been doing regularly for a very long time). My TSH, which has been nailed to the floor at 1.85 for years is now .0016 (!!). My free T3/free T4 which always ran a bit on the low end of normal are now above optimal, and I’m converting a lot into rT3, which is now at the highest end of normal. My antibodies are okay. One of at least three things could account for this: 1) I no longer need the same amount (or any) thyroid med. I have backed way down and will retest in a few weeks 2) I have very early Hashi’s 3) ketosis screws up normal test results. There’s some discussion in the literature that, in a nutshell, dietary carbohydrate is thyroid hormone intensive; i.e., requires thyroid hormone to metabolize. This could be another example of lab “normals” being based on western diets. So I’m just sayin’ that I’m not sure that getting your thyroid tested will get you answers. Having said that, if your thyroid is an issue, I have never known or read of a thyroid patient who didn’t have lots of symptoms in addition to an abnormal lipid result. Thyroid imbalance is very heavy on the symptoms, so if you don’t have any, a bad lipid finding by itself wouldn’t be a strong sign to me of an underlying thyroid issue.

  • I appreciate this is new research but I’d be very interested in hearing Peter’s reaction to it and also the response of other contributors here.
    The real culprit behind hardened arteries? Stem cells, says landmark study
    Differentiation of multipotent vascular stem cells contributes to vascular diseases.
    However it’s a sad reflection on modern medicine that the emphasis is on the development of new treatments rather than improving our ability to prevent vascular disease.
    “If your target is wrong, then your treatment can’t be very effective,” said Dr. Shu Chien, “These new findings give us the right target and should speed up the discovery of novel treatments for vascular diseases.”

    • It’s not clear to me how this information changes the problem statement or remedy any time soon. Perhaps, some time in the future, this insight (assuming it’s correct) will offer alternative treatments.

  • Avner Taieb

    This site is a treasure for me; I am on a ketogenic diet for 2 months, after a break of 10 years for main stream diets. If a site like this would have existed then, I guess I was still on this diet. I am also an ultramarathoner, training for my first 100 mile on a ketogenic diet. So this site is perfect for me. Thank you very much Peter.
    Quick question on this post, LDL-C today is still considered as a risk predictor, and medicines are given to reduce the LDL-C level. If we know now that LDL-C is meaningless, what does it say on the medicine?

    • It’s not that LDL-C is meaningless, it’s just that 30-50% of the time it’s not in line with the actual driver of risk, LDL-P. If all patients were treated based on LDL-C some good would (and is) done. The point is, we should sharpen our pencils, so to speak, and be sure patients are being treated correctly.

  • Hasan Hanachi

    Please people, lets try to remember that this is epidemiology and correlation is NEVER cause. Any association between LDL-P and CVD is confounded by insulin resistance which results in elevated triglycerides and therefore increased small LDL-P (essentially the cause of elevated LDL-P as small particles displace larger ones.) As the Framingham data <a href="; clearly shows, "discordance" begins at TG levels greater than 150. That is why a study <a href="; discussed above found both that controlling for TG's and HDL abolished the predictive power of LDL-P. That study also found that when subjects with MetSyn were stratified by small LDL-P levels, there was no association with CVD suggesting that something else was causing arteriosclerosis (inflammation?, glycation?). "Discordance", then, would seem to be a marker for insulin resistance and MetSyn rather than LDL-P being a cause of anything. Many of the people discussed in these comments with higher range LDL-P are unlikely to be suffering from MetSyn, so before we start medicating otherwise healthy people on the basis of LDL-P, please produce the randomly controlled trials showing that treating to that value results in meaningful reductions in general as opposed to relative risk (NNT- numbers needed to treat). The record of statins in that regard is dismal. First it was TC, then HDL/LDL, then small v. large particles. Now we have LDL-P being pushed by "advanced lipodologists." Anybody see a pattern here?

  • William

    Peter, thank you for taking the time to make this information available. I found your blog just last week from one of your reader’s who linked to it and I’m glad I did.

    Based on the amount I’ve been able to read on your cholesterol posts, I’ve scheduled an NMR test for next week.

    I’m a little stressed because last week my internist told me he wanted me on Lipitor based on a standard lipid profile(total 272, LDL 163, HDL 98, trig 53). I told him “no thanks” for now and am trying to get a better understanding of things before I agree to go on a statin. I’m trying to read as much of your posts as I can along with other information I can find.

    I follow a “lowish” carb Primal diet and have for a little over two years. Work out regularly, and have no weight issues (wouldn’t mind putting on a few pounds actually).

    I have a couple questions:
    • Can the exercise a person does the day before having blood drawn impact the lipid profile? I did a hard sprint session the day before as I had forgot about my appointment.
    • What would be a good resource to help me analyze the results of the NMR test? I have not found a “scale” yet to tell me what would be considered a high LDL-P count. My test is kind of worthless until I can learn what the numbers mean.

    Thanks again

    • William, SO FUNNY that you ask about the impact of hard workouts on lipid profile. I’m just getting ready to kick off one of my most outrageous self-experiments looking at this based on some preliminary data. I would say the following, for now have your NMR done in the “usual” way — overnight fast, no workout that morning.
      As far as NMR goes, an LDL-P of 1,000 nmol/L is considered the 20th percentile of risk; 50th percentile is around 1,250-1,300. 2,000 is about 90-95th percentile.

    • Hasan Hanachi


      You don’t need an NMR. You only need to do one simple thing- ask your internist to quantify for you, hopefully based on randomly controlled trials, the “Number Needed to Treat”, for a person in your risk category. In other words, out of every hundred people in that category, how many need to take Lipitor to effect a change in a hard, clinical endpoint (i.e. death, serious event, etc)? Another way to ask the question is to ask for the change in general risk as opposed to relative risk. In other words, if for a person in your risk category the chance of death or a serious event is 5 in 100, how much does it go down with statin treatment? Take these numbers and bearing in mind the side effects, acknowledged and unacknowledged, make up your own mind. If your internist cannot or will not produce these numbers, change doctors. If you do obtain the numbers, I believe you will be shocked how small they are even in terms of the most optimistic studies.

      You may also wish to review my comment above given your lipid profile. Assuming your BP and blood glucose levels are ok, it is highly unlikely that you are insulin resistant. I am certainly not giving medical advice here but it is my opinion that there is no conceivable reason for an otherwise healthy person to take a statin drug full stop.

      • I disagree entirely with this comment, Hasan, but I agree everyone should have their say.
        It’s important for readers to know that I don’t agree with many comments posted on the blog, but I don’t censor them, either. Obviously, I can’t take the time to respond to all of them.
        William, the choice is yours. In the next few weeks I’ll start go over some “real life” examples of the how advanced lipid and metabolic testing can uncover completely treatable conditions that are missed by only looking at the simple stuff. I’ll cover the number needed to treat issues in a future post, as it’s a fair question posed by Hassan.

  • Hasan Hanachi


    Its no surprise that you completely disagree with me since I also disagree with the very premise of this series which appears to be pushing yet another “screening” to the U.S. medical system. It distresses me greatly that in the discussion, persons such as William are not being asked a single question either about their actual health nor about any other standard parameters used to assess risk. In William’s case, I made some assumptions (age 45, BP 120/80, non-smoker, no BP meds) and came up with a 10-year Framingham risk score of 3%. Even a 2011 Expert Panel of Lipid Specialists:

    with whom I would no doubt disagree on statins, does not recommend LDL-P testing for low-risk patients such as this. On what basis does he need an NMR then? I think you hint at the answer when you say that an NMR can “uncover completely treatable conditions that are missed by only looking at the simple stuff.” This is more screening madness pure and simple and haven’t we gone far enough down the road of turning healthy people into patients (PSA tests and mammograms come to mind not to mention “full-body CT scans” and other insanity)? There is simply no evidence that William is ill in any way and from his comment, I suspect that he is rather healthy. No doubt that if submits to enough testing of various kinds, some kind of “treatable condition” will be uncovered with medication or other treatments to follow. As I said…..madness. (As I wrote above, there isn’t even any evidence that LDL-P testing can improve risk assessment over the standard lipid panel when TG and HDL are taken into account.) Although William did not provide his lipid panels prior to his dietary change, there have been enough reports of increases in LDL-C on such diets to wonder how it might be that so many people have suddenly developed “treatable conditions.” Far more likely is that for reasons yet unknown, these diets simply result in an increased level of LDL (as measured by both LDL-C and LDL-P). As already discussed, whether this is good or bad has yet to be determined. If William is not comfortable with his lipid panel, the easiest thing for him to do is go back to his old way of eating and the issue will likely go away. So, it appears he has three choices- an NMR and the path with statins likely at the end, returning to his old way of life, or choosing to live his life based on something other than a lipd panel. I hope he lets us know which he chooses and how well it works out for him.

    As far as “real life” examples from NMR testing, sorry but irrelevant. Every kind of screening can produce testimonials as to how illnesses were discovered and lives were saved (see the recent controversy over the Preventive Services recommendation on PSA testing). What is always missing is the other side of the coin– all those people who were subject to unecessary medication and/or medical procedures as a result of the test. No doubt that if NMR testing became routine, yet another large sub-group of people would find themselves on statins or other medication. The only relevant consideration is Numbers Needed To Treat and I anxiously await your response in this regard. In the meantime, I suggest that medicine return to its traditional role of treating illness.

    • Hasan, I agree with the spirit of what I think you are saying (make an informed decision on a case-by-case basis), but you’re missing a few points. (For the sake of time, not interest, this will be my last comment on this thread. You only need to respond to me. I need to respond to a 100 others…)

      1. Framingham risk scores, which you reference in your last comment, are driven almost entirely by age. This is not a bad thing, as Allan Sniderman the “father” of understanding apoB as a risk factor has recently written, because exposure to apoB increase with age. However, there are other risk factors that are not well captured by Framingham. It’s important to keep this in mind before suggesting to William that he’s probably fine. Keep everything the same in William’s “case” but increase his age to 65, and watch the risk go up. Why? As Sniderman and others far more knowledgeable on this topic than you-and-I-put-together-squared will argue, it’s because of intimal exposure to apoB. It’s all about the AUC of apoB particles and intima.

      2. I don’t know if you’re a doctor or not, or if you’ve seen the healthcare system on the inside or not, but let me share my thoughts. Both in my time in clinical medicine taking care of patients every day and while at McKinsey doing healthcare consulting for the largest hospital systems in the U.S. and beyond, I gained insights I could not have otherwise appreciated from reading about the problem. You suggest “medicine return to its traditional role of treating illness.” Are you being facetious? Hasan, what the heck do you think we’re doing in medicine? We spend 18% of our GDP on healthcare more than any other country in both absolute AND relative terms. This is the essence of medicine and healthcare in the U.S. — we spend huge dollars treating illness! I don’t recall the exact number, and I’m sure it’s changed since I was last walking the halls of Hopkins, but we looked at clinical data and found that we spent over 80% of a person’s entire healthcare dollars in the last 30 days of their life. If there is one thing medicine is good at it’s dumping the most heroic interventions on at the last moment, often for little good. I could write a book chapter on this topic, but haven’t the time. If you think it’s more economical to treat someone with an LVAD or IABP or even “just” a CAB or PTCA once they’ve had an MI, you’re quite mistaken. Medicine talk about prevention, but actually does a lousy job. Don’t assume because that because the Western medical system is lousy at implementing prevention, that prevention is bad. You’re throwing the baby out with the bath water.

      3. While I know you’re not trying to “play doctor” I’d ask you to reconsider “assuming” William is fine. It’s not your role or mine to do this. You’re free to do and say you like, as is William free to regard or disregard what you or I say, but the internet is funny place. Try to show a bit of restraint when giving advice directly to someone you’ve never laid hands on. If I can’t look someone in the eye and answer every question they have, I don’t give medical advice.

      4. For a NNT analysis look at the following study, Circulation 2000;101:477-484. This study, one of the few to look not only at LDL-C, but also apoB, provides the data you want to do the analysis (i.e., NNT = 1/abs_risk_reduction_rate x 100). As you will see, apoB is better than LDL-C at predicting outcomes and reducing apoB saves lives. Figure 3 addresses your question for one particular statin (lovastatin). This is not the same as saying a reduction of apoB from X to Y with a lifestyle change results in Z abs risk reduction, but unfortunately those data do not exist, so we use the best data we have.

      Finally, I’m not telling anyone to take a drug, to stop eating sugar, or to do more jumping jacks. My personal belief is that dietary intervention (i.e., “proper” lifestyle change) should be first line for most lipid abnormalities. We can have a discussion about the role and risks of statins another time, but I worry you’re guilty of the same thing you’ve accused me of. When I talk about examples of where NMR offers insight standard testing does not, I’m not talking about one-off “testimonials,” which I agree are of little value. I’m talking about 30% of the people I look at. Since I can’t post hundreds of lab results, I will (assuming people are interested in seeing it – I realize you’re not) post select cases where a teaching point can me made. I would argue that your concern of over-use of statins is less robust. If you have patient data showing that 30% of patients on statins develop rhabdo, I’d like to see it.

      It’s always possible to find an example of someone who had an adverse reaction on a statin or an antibiotic, for that matter. In fact, on per dose basis there are more adverse reactions to antibiotics than any other class of drug. Should we abandon antibiotics altogether? When your child has Strep throat are you going to treat it with the appropriate antibiotic (knowing there is a non-zero chance of a horrible reaction) or will you take a chance? What about vaccination? You’re on a slippery slope. I won’t pretend to know all of the answers, and I certainly don’t know the answer for anyone else beyond myself. The reason I’m responding at length is because I think there’s a bit too much arm-chair medicine going on out there. It’s great (and important) to do NNT analyses and machinate about every little possible side-effect of drug X or drug Y, but at some point you have a make a personal decision with imperfect and incomplete information. Do you feel lucky? Sounds like you do. Does William? It’s his call. Not mine and not yours.

    • William

      Peter (and Hasan),
      I can’t tell you how much I appreciate the dialogue and well thought out comments.
      I received my results from the NMR Lipoprofile today and have to admit I feel like I had a heart attack (exaggerating a little) when I saw my LDL-P number of 1611 nmol/L. LDL-C was 181, trig 41, HDL-P 40.8
      I’m trying to remain calm. I realize there’s not a lot I can do right this moment, but now my concern turns to what I can do. I believe in the “primal” type diet. To address some of Hasan’s comments: I’m a 41 y/o male, lean, 6’2″ tall, weigh about 190 lbs. Desk jockey, work out 4 or 5 times weekly. I feel like I have good energy levels and sleep fairly well. I have a 3.5 year old daughter who I have no problem keeping up with.
      I thought I was doing things right.
      It is starting to appear I am doing something wrong, however. I’m still not to the point of wanting to take statins, but wonder what I should do from here. Are there other tests that might help me pinpoint a problem area or should I adjust my diet (still Primal) to try to get the LDL-P down?
      I realize Peter, that you can’t give advice here, but any resources you could point me to would be hugely appreciated.
      Thanks again for all the information you provide and for your consideration and time for this blog. Good luck with your Eating Academy Project.

  • Hasan Hanachi

    1. ” However, there are other risk factors that are not well captured by Framingham. ”

    Ok, like what? As I read it, the only risk factor you have advanced here is LDL-P and, according to the study I referenced, LDL-P lost its predictive power when TG’s and HDL were controlled for.

    2. “Keep everything the same in William’s “case” but increase his age to 65, and watch the risk go up”

    Yes, but why is the 64k question and it is far from being settled, Sniderman and others to the contrary but this is not the place to take that up. Whatever the age, I see no evidence that reducing LDL-P though medication has any significant impact in otherwise healthy people.

    3. “You suggest “medicine return to its traditional role of treating illness.” Hasan, what the heck do you think we’re doing in medicine? This is the essence of medicine and healthcare in the U.S.

    I would suggest that the essence of medicine and healthcare in the U.S. is making money…also beyond this discussion.

    4. “Don’t assume because that because the Western medical system is lousy at implementing prevention, that prevention is bad. You’re throwing the baby out with the bath water.

    Au Contraire! Nobody, myself included, would argue against prevention…thats like arguing against motherhood and apple pie. That said, we are talking here about screening and that is a HUGE difference. Screening only becomes prevention when more good is done than harm and that isn’t event remotely established with LDL-P which is I suspect why the Expert Panel does not recommend it for low risk patients. As noted earlier, the track record on screening is not good (PSA, mammograms, etc, etc) and runs the very real risk of turning healthy people into patients. For more on this I recommend the works of David Newman M.D., H. Gilbert Welch M.D., and writer Sharon Brownleee.

    5. ” I’d ask you to reconsider “assuming” William is fine”

    I believe I said in the absence of anything to the contrary, he seemed fine. I was the one who raised the point of actually assessing a person’s health before concluding that testing is required. Nobody else seems considered about anything but cholesterol.

    6 “If I can’t look someone in the eye and answer every question they have, I don’t give medical advice.”

    Don’t you think that suggesting an NMR for everybody who comes here to be “medical advice.”

    7. “For a NNT analysis look at the following study, Circulation 2000;101:477-484. This study, one of the few to look not only at LDL-C, but also apoB, provides the data you want to do the analysis (i.e., NNT = 1/abs_risk_reduction_rate x 100).”

    Ok, I’m game. If you go to this table from that study:

    you will see that the largest risk reduction is in the fourth group (40 events in the treatment group v. 75 in the placebo.) My calculations therefore show a NNT of 99.3 for three years and that is taking the study on face value without any analyis. This is the study you want to cite as advancing your cause? I, the words of Nortin M. Hadler, professor of medicine at the University of North Carolina at Chapel Hill “Anything over an NNT of 50 is worse than a lottery ticket; there may be no winners.”

    8. “I’m not telling anyone to take a drug, to stop eating sugar, or to do more jumping jacks. My personal belief is that dietary intervention (i.e., “proper” lifestyle change) should be first line for most lipid abnormalities”

    Thats pretty ironic since the low carb/high fat diets you appear to be suggesting are the ones that are spiking the LDL numbers in the first place. I am not saying thats good or bad but to recommend such a diet and then tell people whose LDL is elevated as a result that they need testing and treatment is incomprehensible to me. Perhaps you would advise in these cases some further dietary modification (I will wait for the end of the series to see) but people who go to Dr. Dayspring with these kind of numbers are going to leave with a statin prescription in hand and it is to him and other “advanced lipidologists” you are referring people seeking treatment.

    9. “on per dose basis there are more adverse reactions to antibiotics than any other class of drug. Should we abandon antibiotics altogether? ”

    Please see point #4 above. Its always a question of doing good v. harm which is why I asked for the NNT. With appropriate use of antibiotics, the NNT approaches 1 which is so far away from statins that they shouldn’t be mentioned in the same breath. That said, as we all know, antibiotics are routinely used to treat such things as the common cold for which the NNT is infinite.

    9. ” It’s great (and important) to do NNT analyses and machinate about every little possible side-effect of drug X or drug Y, but at some point you have a make a personal decision with imperfect and incomplete information.”

    Indeed which is why I am taking the time here to try and provide more complete information. As I said, almost everybody who walks into the office of an “advanced lipidologist” with LDL numbers typical of those being reported here is going to end up on a statin. They deserve to get a more complete picture than the on being presented here and, BTW, I wouldn’t so cavalierly dismiss the concern about statin side effects as machinations about “every little possible side-effects.” Do I need to elaborate?

    • Hasan, you have disregarded the single most important line in my previous response: “For the sake of time, not interest, this will be my last comment on this thread. You only need to respond to me. I need to respond to a 100 others.”
      You’re really tempting me to respond, though. But I will refrain. I have to. I have more to get done today and tomorrow and the day after that than you can probably imagine. I don’t expect you to understand or appreciate what I’m doing or trying to do, but don’t interpret my lack of a rebuttal for anything other than a lack of time. I do like your passion, though. Perhaps you should also consider a blog of your own. It seems like you’d have something very valuable to contribute, as I think you are doing here.

    • jw


      Thanks for pointing to new data. One of the reasons that I enjoy Peter’s site so much is that Atkins and other LCHF diet proponents never provided enough scientific justification for their diets and the sheer amount of data here is phenomenal. That being said, I think that may be some flaws in your reasoning.

      Given William’s numbers (total 272, LDL 163, HDL 98, trig 53), I could see three scenarios playing out in doctor’s offices, depending (mostly) on their adoption of the LDL-P hypothesis.

      1. Traditional – Total>200, straight to statins. (May also justifiably be the first course of any doctor in this litigious society, but I digress.)
      2. Curious – Total>200, BUT TC/HDL-C= 2.8, TG/HDL-C=0.54, very interesting, let’s find out more.
      3. LDL-P Aware – Discordant data, not enough information without the LDL-P results.

      When you say that LDL-P testing is unnecessary in these cases, one assumption that you make is that doing the test will lead to more statin prescriptions when the data does not show that. True, if discordant low TC/high LDL-P patients are prescribed statins (as one possible outcome), statin use would go up, but that may also significantly reduce their CVD risk, which they would not have known about without LDL-P. On the other hand, if William’s LDL-P comes back <1000, an LDL-P aware doc may not put him on statins based on just his TC level. Per the Elviser chart on this site and on pg.355 in your link:
      The distribution of the discordancy seems fairly even.

      Which is why it doesn’t make sense to me that the expert panel in that paper recognizes that new data shows LDL-P to be important, recommends it for medium and high risk discordant situations, but then does not recommend it in low risk situations. Without the additional data of LDL-P, I don’t know how they can make that judgment, especially since NMR is not that expensive (IMHO). Their reasoning seems, for lack of a better word, discordant.

      Also, in your cited paper:
      You need to be careful as William does not fit into the cohort studied. His HDL-C is twice as high as the range allowed, something that may apply to many LCHF panels.

      And again, since data trumps assumptions, Dayspring’s algorithms are here:

      So, in the interest of time (for all of us), I think that Peter is in agreement with your desire to see more double-blind, placebo controlled LDL-P studies being done, which is one of his stated goals for NuSI.

      In answer to your question: “First it was TC, then HDL/LDL, then small v. large particles. Now we have LDL-P being pushed by "advanced lipodologists." Anybody see a pattern here?” – I would say yes, there is a pattern, it is called progress.

  • Hasan Hanachi

    As you wish…..we can certainly end it here. I would only add that it is a bit presumptive to assume that you have so more to do than I nor that I am incapable of understanding your purpose here. In fact, I almost never have the time to respond to blogs as I did here but I couldn’t sit back in silence any longer as I read through this series precisely because I believe I do understand your purpose.

    I reserve the right to comment on future postings if so moved.

    • Of course you can and should continue to comment on anything you see fit here! I’m sorry if I suggested I have more to do than you. That may or may not be true. I would like to continue this discussion, but let’s do it in person. Much more efficient. If you ever get to San Diego, please let me know.

  • lorraine

    Props to both sides on the above debate

    • This is SUCH an important topic, it’s a shame we can have the discussion in a live forum.

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  • Ford

    The discussion between Hassan and Peter describes the tense and frustrating debate over the past 10 years between my doctor and me following a high calcium score on a Heart CT scan when I turned 50. After two or three years of pressure, I started on 10mg Lipitor (never overweight, non-smoker, low to medium lipid numbers, low BP), then after increases in the CAC on two subsequent scans, was pushed to 20mg. After 18 months Paleo, standard lipid scores are up and my Doctor wants me on more Lipitor. My hope, from the information provided by Peter here, is that an NMR test might show an LDL-P low enough to make the decision to drop statins easier.

    In any case, the insight provided here by Dr. Attia is a godsend and is greatly appreciated. Decisions about what tests to demand and whether NNT analyses justifies a drug therapy or any particular test are still difficult, but at least can be made from a more informed position.

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  • Hasan Hanachi


    It appears that I was not clear enough above which may have resulted in some confusion about what I was actually saying. To whit:

    “When you say that LDL-P testing is unnecessary in these cases, one assumption that you make is that doing the test will lead to more statin prescriptions when the data does not show that.”

    When I referred to “these cases”, I had in the mind the sub-set of people on various diets described usually as either low carb or paleo. It is my impression that most of these are reporting LDL-C levels in excess of 150 with many if not most higher than 200 (somebody called this Paleo Lipid Syndrome, not sure where). Dayspring himself has said:

    “You certainly cannot rely on the LDL-C level as a lipid surrogate of LDL-P unless the LDL-C is very high (> 140 mg/dL).”

    I am not sure exactly what he means by “surrogate” here but it suggests a reference to this scatterplot:

    Visual inspection suggests that at LDL-C levels of 150+, it is unlikely if not impossible to have an LDL-P under the designated high risk level of 1000. Therefore in the cases I am talking about, people with LDL-C mostly in far excess of 150, an NMR is NOT going to get them “off the hook”, so to say. Other hypothetical scenarios aside, real-world evidence suggests that most, if not almost all. of these people are going to end up on statins.

    “True, if discordant low TC/high LDL-P patients are prescribed statins (as one possible outcome), statin use would go up, but that may also significantly reduce their CVD risk, which they would not have known about without LDL-P.

    In the case of “Paleo Lipid Syndrome”, it makes little sense to talk about discordance as per the above. Anybody with an LDL-C of 150+ (and therefore with an LDL-P > 1000) is going to be considered high-risk under the assumptions of this post but this begs the question of whether or not LDL-P, in the absence of other risk markers, is as definitive as is being claimed. I will accept for purposes of this discussion that LDL-P is superior as a risk marker for CVD over LDL-C but what about other markers such as TC/HDL or similarly LDL/HDL? We have already seen in the above reference that when Triglycerides and HDL were controlled for, LDL-P lost its predictive power which likely explains why LDL-P was superior to LDL-C in the first place- it contains information about TG’s and HDL that is not captured by LDL-C but is captured by ratios such as TC/HDL or simply looking at the standard lipid panel. As I have written, I believe all of this comes down to insulin resistance and MetSyn and if LDL-P is capturing additional risk, its because the LDL-P curve is shifted far to the right in people with MetSyn:

    ” if William’s LDL-P comes back <1000, an LDL-P aware doc may not put him on statins based on just his TC level. "

    This brings us to William's specific case. As already noted, with an LDL-P of over 163,
    William's LDL-P is overwhelmingly likely to be over the designated threshold of 1000. Whether or not that means he is destined for statins, and as you know I believe he is, the real question is whether or not he is, in fact, at high-risk for CVD in the absence of a single other risk parameter or health issue. For those who believe he is on the basis that all people should have an NMR, I have labeled this as an example of screening and for advocates of such NMR screening, they need to produce hard evidence that such screening actually does more good than harm. I won't repeat what I have already written above on this topic. Absent this evidence and given that LDL-P has not been demonstrated to have predictive power when TG's and HDL are controlled for, exactly what is the evidence-based criteria for an NMR? His TC/HDL ratio is more than fine, and that has been shown to be a superior risk marker over the single standard lipid parameters, and nobody here seems even remotely interested in his BP or blood glucose levels despite how important those parameters really are. Finally, my impression only, is that he is in good health and able to do strenuous sprinting sessions which denotes an individual who is taking care of himself. I think it is an example of the madness of the U.S. health care system that a seemingly healthy individual is pushed onto a medication solely on the basis of lab values such as these, whether LDL-C or LDL-P, and when the medication itself has such a small impact on an already small risk. (see discussion above)

    "Also, in your cited paper: You need to be careful as William does not fit into the cohort studied. His HDL-C is twice as high as the range allowed, something that may apply to many LCHF panels."

    I am not sure what you mean by "your cited paper" since it was Peter who cited this paper in support of statins. If anything, it speaks against his argument since the NNT was so small even with a cohort with such unfavorable lipid parameters.

    "it doesn’t make sense to me that the expert panel in that paper recognizes that new data shows LDL-P to be important, recommends it for medium and high risk discordant situations, but then does not recommend it in low risk situations. Without the additional data of LDL-P, I don’t know how they can make that judgment,"

    It makes perfect sense to me given everything I have written. Why submit people to further testing (and likely treatment) who are already at low risk when the marker does not appear to suggest higher risk in the absence of any other information to the contrary?

    "In answer to your question: “First it was TC, then HDL/LDL, then small v. large particles. Now we have LDL-P being pushed by "advanced lipodologists." Anybody see a pattern here?” – I would say yes, there is a pattern, it is called progress."

    You are of course entitled to your interpretation, but I clearly that this progression suggests a long-standing and on-going attempt to confine the totality of CVD to lipid parameters. As for why this might be, I suggest we look to the vast profit and/or profit potential in lipid testing. I don't feel like shelling out $4500 for the full report but this site reports:

    "The global market for Cholesterol and Other Cardiovascular Testing is forecast to cross 2.3 billion units by the year 2015."

    Using a rough figure of $100 per test, the math is easy.

    (P.S. Kudos to Peter for allowing this free debate)

  • Hasan Hanachi

    A correction is needed here for the record. When I said above:

    “That study also found that when subjects with MetSyn were stratified by small LDL-P levels, there was no association with CVD suggesting that something else was causing arteriosclerosis (inflammation?, glycation?). ”

    It should have read:

    Another study:

    found that when researchers stratified subjects with MetSyn by small LDL-P (remember that increased small LDL-P is the reason behind increased LDL-P), they found no association with CVD suggesting that other mechanisms part of MetSyn are the culprits (inflammation, glycation, ???).

    Sorry but I am writing these posts too quickly and four minutes is not enough time for proper editing.

  • First the gratitude: Peter I LOVE this blog series…
    Now the Questions:
    Peter wrote: “The question we don’t know the answer to is if an LDL-P of 2,000 in someone who eats no carbs is the same as an LDL-P of 2,000 in someone who does. I had breakfast with Eric Westman today and we discussed this topic. Eric makes a pretty compelling case that these 2 states are not, in fact, the same thing. I think we can safely say we don’t know the answer. At least I don’t. I’ll keep looking for clues, though.” (May 31 2012)

    My Q: In other words, if 2000 LDL-P is too high for person A it does not necessarily follow that 2000 LDL-P is too high for person B? And if this is true then what happens to the previous statement: “Directly measure the number of LDL particles in your plasma using NMR technology. If this number is high, you are at risk of atherosclerosis.” – What number then should we consider to be “high”?

    Statement: It would be nice to get some LDL-P values from aboriginal peoples who have had a lifelong “palio” type diet – to try to get some kind of base line number.

    And Now I just read: “Furthermore, is it possible that once the body stops relying on glycogen and turns over to metabolic pathways of ketosis that the “numbers” we target as “normal” are irrelevant?” And if that’s true, how can we know what the “new” normal numbers are for an individual who is ketogenic? Then if that is true do the “too many” LDLs still mean high risk of atherosclerosis?

    Thank you for sharing your time! You are appreciated!

    • I think this is correct. I’m not sure I can say that in the absence of carbs/glucose we can disregard LDL-P (or apoB or pick your favorite risk marker). We don’t have the data to know this. It’s a good hypothesis, but still untested. There are many areas where this crops up, such as the “need” for certain vitamins and minerals (e.g., less vitamin C needed; more sodium needed when carbs removed).

  • Tim Williamson

    I’m a reasonably intelligent person, but frankly need a translator. I believe, based on what I’ve gleaned from you and Gary Taubes, that conventional wisdom on cholesterol is just wrong. But I simply don’t have the time and intellectual energy to a)fully understand the technicalities of this discussion, or to b)fight my doctor over conventional treatment regimens (statins). I need a new age Cholesterol for Dummies.

    • Brian

      Tim, I love your comment. You’re right about the complexity. I teeter on the edge of understand and having no clue. I also keep thinking that there’s no way my doctor is going to take MY advice on how to treat patients. Has anyone had this luck? I love Peter’s series, love Taubes, Masterjohn, et al. but I can’t imagine bringing Taubes’ Good Calories Bad Calories, a very heavy read btw, to my doctor and giving him the “assignment” to read it and rethink his entire approach to medicine. He’s a nice enough guy, but I think many if not most doctors would take offense to an assertion that I know more than he does.

  • Dan

    Quick sketch: I’m 45 y.o. guy without major medical issues, eating a low carb diet for 6 months (mostly meat, fish, butter, eggs, coconut oil, cream, dark chocolate, etc. no grain, no sugar, some veggies and fruit occasionally, but very little carbs overall< 50 grams/day.

    Here's the good I've seen so far: weight down from 185ish to 165ish, body composition much improved, mental health much better, sleep is better.

    My labs show: TGs 58, HDL 55, HS-CRP 2.2 and my cortisol, magnesium, CBC, CMP, TSH, free t4, t3 are all normal, Vitamin D 39, HBa1c 5.6 (not great but should continue to come down).

    Over a six month period my total LDLp increased from 1587 to 3076, small LDLp increased 534 to 869, total cholesterol went up from 224 to 343, and LDL went from 153 to 276. This change is from 6 months ago.

    I've been very strict on my diet because I really wanted to see what it could do for me, and for the most part I'm totally happy about my progress, but I'm a bit nervous about my LDL, TC and LDL particles now.

    In poking around various forums, there seems to be a handful of folks like me that get crazy lipids changes when going low carb.

    Would you care to speculate on what might cause this? I'm not expecting any medical advice, but just some education or ideas for "general consumption" for people that get wacky high lipids when the go low carb.

    Thank you in advance.

    P.S. Your blog is great!

    • Yes, Dan, you are not alone in this and I wish I knew why! There are many folks who have generated hypotheses that in the metabolic state you describe, an elevated LDL-P is “different” than if you were consuming a standard American diet (i.e., not predictive of disease risk). But this presents a dilemma. Until we know this is true, how should people like you be advised? If I knew this, I would be the first to say so, but I just don’t at this time. As Thomas Henry Huxley once said, “The great tragedy of science is the slaying of a beautiful hypothesis by an ugly fact.” The hypotheses of why an elevated LDL-P in a carb-restricted person is ok are still hypotheses.

  • Ricky

    How do we lower LDL-P through our diet?

    • We’ll get there soon, Ricky. Promise.

    • jw

      Unless I missed something, anxiously awaiting the payoff.

      • There is still one more post in this series…

  • Simply excellent, Peter. I’m really enjoying these posts!
    One small question: Have you got information about hoe many people (percent) could be in each group? (High-Low, High-High, Low-Low and Low-High)

    • Very dependent on the population you’re studying.

  • OK, thanks. Any suggestion about information sources about this subject? I would like to read about it, because I don´t know if we are talking about 95%, 50% or 10% of the population when we talk about discordances.

    • MESA study and references of Otvos et al.

  • Barb ( A discordant fan)

    Back in May/June the thread was inconclusive whether a high LDL-P made a difference on this WOE. Since just a few months ago the thought was large and fluffly LDL was good and now it’s all about the number of particles, I was hoping there was some emerging evidence one way or the other about the meaning of high LDL-P when eating LCHF. (If you are looking for guinea pigs for a study, I volunteer as long as I don’t have to eat carbs or swallow pills.)

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  • Laura

    You said: The persons with the highest LDL particles typically (though not always) have small LDL particles that are TG-rich.

    If your trigs are super low and your LDL-p is high-that would mean that you are still less likely to have atherosclerosis?

    • Most evidence available to day would say, “probably,” but in reality, we don’t have enough data to really answer this question. This poses a dilemma for the patient with low TG, high HDL-C, and high LDL-P. I hope we can resolve this question.

  • Nick

    Hi Peter,

    I’m in the discordant group and I’m curious about how I should interpret, at an initial level, my NMR results. The test results showed my LDL-C at 105 (20ish percentile) and my LDL-P at 1333 (approximately the 50th percentile). Small LDL-P was <90. Last years VAP test showed apoB100 at 95. The LP-IR was zero.

    I don't smoke and my BMI is 25, age 57. My BP is 120-75, so normal. I eat lowish carbs and I'm gluten free. I'm inclined to think my results are mostly unremarkable, but there is heart disease in my family (father, maternal grandfather – both had heart attacks in their 50's). I've read your thoughts on calcium scores, but I'm curious what actions you might take if the above facts were your scores?

    Many thanks for a great series that has helped my understanding immensely.


    • Nick, I can’t comment specifically on medical care, but hopefully a well-informed doctor can help you think through the issues.

  • Nick

    Thanks, Peter for your reply. My doctor didn’t know what the VAP or NMR test was. If you or any of your readers know how one can source a well-informed doctor in SF or the North Bay, I would appreciate referrals.

    Btw, I also appreciated your post on back pain.

    • I had lunch with Robb Wolf and Chris Kresser to discuss this exact issue today… We need a better directory of doctors who understand these tests (which many do — we just need to be able to connect patients with them). Check Chris’ website and Jimmy Moore’s, also.

  • aerobic1


    I am confused. Above you state “To be clear, VAP is NOT a good test to get, despite the fact that I used to track my progress until last year. It estimates apoB. Your best bet is NMR (many companies can send out to LipoScience, the only company able to do this with FDA approval), or go with one of the companies can can actually measure apoB directly.” LipoScience does not direct measure or calculate apoB that I can see on my recent NMR.

    Dr. Michael Cobble, Chief Medical Director of Atherotech, the VAP people, states: “VAP directly measures NHDLc (VLDLc, IDLc, LDLc and finally Lp(a)-c), and as such, directly measures the amount of apoB100 linked to the protein apo(a). ” .

    Can you please clarify your point about direct measuring or calculated apoB as I seem to be missing something? Thanks for sharing your wealth of information.

    • VAP does not actually measure apoB. It uses an algorithm of other measurements to estimate it. It may well be accurate, but it has never been validated externally. Until that time, it’s probably best to use a lab that truly measures apoB.

  • ad ligtvoet

    Hi Peter,
    I did a bloodtest last week and could get my approve for a APO B test.Here are my numbers:
    TC 248 mg/dl
    hdl C 66 mg/dl
    ldl C 168 mg/dl
    trig. 75 mg/dl
    APO B 1.2 g/l
    25 OHD 129 ng/ml
    This is my third test within 30 months or so and there are no great variations in them,so pretty constant over that timespan.
    I eat under 50 gr. of carbs a day and about 100-120 gr. of protein. I actually thought that my apo b count would be lower , but it isn’t. Would you suggest to ,after seeing these numbers,that I should investigate whether I’m a high absorber? Or could just a high traffic of cholesterol within not so big particles(maybe because of genetics) be the cause?Good to know,I feel really healthy ,never be sick and last time my bloodpressure was checked it was 120/80(age 48,no overweight).
    I see very often the apo b count in nmol. How can I convert these numbers?

    • Actually, most folks read apoB in mg/dL, so you’d multiply by 100 (i.e., 120 mg/dL). I do think additional studies could put this paradoxical numbers in context. I hope to write a post on this exact issue in the coming month or so.

  • Ken MacKillop

    Wow, what a long and interesting string of comments has piled up here! Peter, you have been very gracious in offering and participating in this forum, and humoring all of our sometimes strong opinions.
    My thinking aligns with Hasan’s — i.e. I think that the extra prediction power of LDL-p over LDL-c in a broad cohort is likely contributed only by those with IR (probably the vast majority in our modern societies), as suggested by the EPIC-Norfolk data cited by many already, via reasonably well-understood lipoprotein-particle mechanisms (e.g. CE transfer). And I think that insulin resistance is likely a sine qua non for CVD. More specifically, I suspect that IR of the endothelium is a requirement for atherogenesis. The genetic vulnerability of the endothelial tissue (to developing IR) probably is a primary differentiator between individuals, accounting for the significant variability in susceptibility to CVD amongst us. Vulnerability of the pancreatic islets (to IR-like damage to the bio-energetic and related mechanisms in the cells, such as mitochondria and endoplasmic reticulum), in the same way, explains why ~55% of the population appears to be invulnerable to T2DM and the rest can get it. But it has always been a fundamental research limitation that IR of specific tissues is difficult or impossible to measure, especially in large-cohort epidemiological studies.
    I’d like to offer up some more food for thought based upon my own individual case. I have mild isolated fasting hyperglycemia discovered only a few years ago. Before then I ate a SAD and had signs of IR for decades but didn’t know any better — I thought that gaining weight, etc. just came with middle age and felt basically healthy. I know now that my beta cells have lost ~60% of their efficacy, and at ~80% loss onset of frank diabetes typically occurs. So my primary motivation for maintaining a ketogenic diet is related to some evidence that it could be helpful in regaining (slowly, if at all) beta-cell mass, volume and function. Whole-body IR is NOT involved in my form (i.e. i-IFG) of hyperglycemia. The pathogenesis is NOT IR-driven (as in i-IGT and CGI), but rather involves glucokinase degradation, elevated gluconeogensis, etc. But i-IFG is pretty common, accounting typically for ~1/3 of all pre-diabetes in populations such as ours.
    The research pretty consistently has shown that i-IFG does NOT produce any significant increase in risk for CVD, while the IR-driven forms (i-IGT and CGI) do. And there is no IR in i-IFG — IS is normal. This has been extensively studied, and offers an insight into the etiology of CVD — i.e. insulin resistance is a very important factor. And in frank T2DM the metabolism and endocrinology breaks down in such a way that excessive whole-body IR is always a consequence, and hence (presumably) the well-known big jump in CVD risk for type-2 diabetics.
    In addition to this, research indicates that in i-IFG a supra-normal secretion of GLP-1 (from the gut) is one of the adaptive responses. This adaptive response is believed to be the explanation that in i-IFG the postprandial glucose response is roughly normal relative to the elevated baseline (i.e. the fasting blood glucose). By contrast, in the other two forms of pre-diabetes the postprandial response is severely compromised, even though the beta-cell loss is generally somewhat smaller at a similar stage of progression relative to overt T2DM.
    Now, consider that there is no measurable increase in risk of CVD from the i-IFG form of pre-diabetes. I myself, for example, recently had a coronary calcium test result of zero. And consider that there is much interest and research in the cardiovascular-protective effects of the GLP-1 mimetics (e.g. Byetta, Victoza). Consider also that in i-IFG there is an elevated basal secretion of glucagon (from islet alpha cells) that is part of the altered/abnormal regulation of fasting glucose (since it calls on the liver to produce more endogenous glucose but the basal insulin secretion in i-IFG is normal). And glucagon is cardiovasculature-protective , just like the incretin hormone GLP-1 (glucagon-like peptide, a similar hormone) is protective, and opposite to the atherogenic effect of insulin.
    So I hypothesize that the form of damage to my pancreatic islets is actually protective of my cardiovasculature, ironically. My artery endothelium is (and has been) bathed in supra-normal concentrations of cardio-protective hormones in both the postprandial and the fasting states — essentially all the time. Based upon typical rates of progression of isolated fasting hyperglycemia (which is slower and much less variable between individuals than the IR-driven forms) the damage to my beta cells has probably been accumulating for at least two and more likely three decades, while I ate the SAD and had increasing symptoms of at least some insulin resistance. But maybe the extra glucagon and GLP-1 kept my arteries free of disease. I certainly did not live a “clean” life, based on what I now know.
    It’s a hypothesis, and it’s my own — I haven’t seen this idea anywhere in the literature. But I think that there is some substantial evidence it might be correct, and it is food for thought for epidemiological research I think. Maybe even NuSI, although this is probably too far afield from its already ambitious focus.
    Since there seem to be a lot of very smart people in the comment chain, I offer this as food for thought for all of you.

  • Sam

    Is it true that significant (40#) rapid weight loss, say 2 #week, may temporarily increase ldl-p in order to clear text large amount of TG being released from fat stores? If so, how long can it take for ldl-p to normalize?

    • Yes, this has been observed and described on several occasions. What’s not clear is why it happens in some and not others, how long this phenomenon lasts, or what the significance is.

  • Sam

    Peter, Thanks for the confirmation because it appears to have happened to me. Every marker of health improved except ldl-p, which shot up to 1680 from 1000 (small dense ldl-p < 50 so LDL-C also rose significantly).

    I have been weight stable for six months and am in the process of retesting. My fat loss was 20% of my body weight and fat percentage is now 14%. All good,..almost. Thx again. Sam

  • John T


    Thanks for this series it really helped me understand. I’ve been semi primal for a year and went from 210 lbs to 165 lbs. I just had a regular lipid panel which was
    TG: 71
    TC: 251
    HDL: 60
    LDL: 177

    Now I know you say LDL-C doesn’t mean anything. But if you look on the scatter chart that shows LDL-C and LDL-P when you start getting in my range for LDL-C the data does tend to show the odds are my LDL-P will be >1500. I am in the process of trying to find a doctor that will write a Rx for the NMR Lipidprofile. I will report back.

    • Sam

      John, your experience mimics mine. It seems that in some people LDL-C rises with a LCHF diet. I also note that the scatter plot would suggest that for a high percentage of people, high LDL-C is predictive of high LDL-P, especially above, say 170. i am conflicted by this because this takes us back to some degree to focusing on LDL-C, which we know is a poor predictor of CVD. (You don’t say what your blood work looked like pre weight loss. My LDL-C was 120 and increased to 180 post weight loss. LDL-P tested at 1680 post weight loss but I don’t have a base line particle count. All I can say is my TG/Hdl went from 2:1 to 0.9 to 1 which suggests my LDL-p was in pattern a pre and post.

      Phinney writes about a transient rise in LDL-C in some people in his “art and science” book. Maybe this applies to you. I am also retesting now that I have been weight stable for 6 months. I don’t think you need an Rx for NMR, at least not in all states.

    • John T

      OK just got my results back from LabCorp.

      Here are my numbers.
      LDL-P 1743 nmol/L
      LDL-C 177 mg/dL
      HDL-C 55 mg/dL
      TG 67 mg/dL
      TC 245 mg/dL
      HDL-P 29.4 umol/L
      Small LDL-P 383 nmol/L
      LDL Size 21.6 nm
      LP-IR 30 (no idea what this is).

      The only data I have from before is a blood test from donating blood this was about a month or so after I started loosing weight which only reported TC as 180. Previously when I was +40 lbs I remember always having elevated cholesterol 220+.

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  • KevinF

    Dropping back into this thread just to post some recent lab numbers, including LDL-P, showing a radical change, and thought some people might be interested. Not looking for advice, more like bragging. I’m an insulin resistant, overweight, metabolic syndrome poster boy, 46 yrs old, both parents dead of heart attacks (Though I have lost 40 lbs from my peak of about 3 years ago). Currently eating low carb/high fat, though my bod seems rather resistant to getting into ketosis.

    This isn’t as good an n=1 experiment as I’d like, since I did not get my numbers checked immediately prior to going LCHF, last March. However I did get a basic lipid panel done 2 years ago, so I’ll start with that.

    **2010 – on a conventional healthy-whole-grain, lowish fat diet **
    TC: 219
    HDL-C: 32
    LDL-C: 97 (NOT directly measured)
    TG: 487 (Yes!)
    Note: I suspect my LDL may have been considerably higher, considering it was merely calculated, and my sky-high trigs. I was not aware of NMR in 2010, so I don’t know the LDL-P, although I believe the high TG’s suggest it probably would have been very high.

    ** August 2012 – 5 months into a very low carb, high fat, more-or-less paleo diet . Drug naive, aside from fish oil **
    (Numbers from LipoScience NMR)
    TC: 281
    HDL-C: 40
    LDL-C: 205
    TG: 178
    LDL-P: 2868 (World record????)
    Note: was happy with great improvement in TG and HDL, but obviously LDL-P is a problem, and my TC and LDL would make a doctor panic. Doctor puts me on simvastatin and Niaspan niacin.

    ** December 2012 — continuing LCHF diet, and 4 months into statin/niacin regime **
    (Numbers from LipoScience NMR again)

    TC: 126 (Yes, one twenty-six!)
    HDL-C: 45
    LDL-C: 52 (as in, fifty-two)
    TG: 147
    LDL-P: 1284

    How about that. I feel like stopping strangers on the street to tell them all this. LDL-P isn’t the best 20th percentile, but it’s lower than the 50th percentile, which is pretty good for a genetic time-bomb like me. TC and LDL look so low as to be misprints, but if you can’t trust LipoScience who can you trust?

    A lot of low-carbers are very anti-statin, and I’ve heard Dr. Dayspring say that statins don’t do a good-enough job of lowering LDL-P. All I can say is a combination of LCHF and statins/niacin are doing a bang-up job for me. The drugs made a MASSIVE difference, and perhaps some of that was due to another 4 months of paleo LCHF eating. If I can just get the TG’s down some more maybe I could end up with super-low LDL-P.

    Confession: I’ve had hardly a lick of exercise in about a year. So next I’ll phase in working out, and see what 3 months of that will do in my next NMR. (Which, btw, super-easy to set up through

  • JP

    Wonderful site with lots of great information. The purpose of this post is to solicit opinions. Some of the doctors I see are encouraging a statin. I am mid-50s male with high total cholesterol. My latest test results appear below. My instincts are to refuse the statins, but would be interested in opinions from this board. Thanks very much.

    Total Cholesterol = 227
    LDL-C = 123 (calculated)
    HDL-C = 94
    Triglycerides = 51

    LDL-P = 813 nmo/L

    HDL-P (total) = 45.4
    Small LDL-P = <90
    LDL Size = 21.3
    LP-IR score = 5 (on 0-100 range)
    Large VLDL-P = 1.31
    Large HDL-P = 12.5
    VLDL size = nm (too low to measure)
    HDL Size = 9.8

    • Your LDL-P is around the 5th percentile and your ratio of LDL-P to HDL-P is about 18 (lowest quartile is a ratio of 35). A statin in you would be malpractice, in my opinion…

  • JP

    Thanks very much, Dr. A. I will continue to resist the advice that if cholesterol >200, then you should/must be on a statin. Will also resist the logic that “statins may have side effects, but it’s better than a heart attack.” My wife’s doctor doesn’t even do the NMR…

    Your cholesterol series was superb.

  • Ed C

    Health Diagnostics Lab did my blood profile, They gave me a “low risk” number for apo B and a high risk number for ldl-P (by nmr). They say apo B was measured, not calculated. So, I don’t know what to think of this since they are both particle counts. I’ve tried to get a good explaination from the lab but no luck there. This makes me wonder if the test results are accurate at all? Any ideas?

    • Not entirely. LDL-P is exactly as it is billed. ApoB is, even measured, is an indirect measure of particle count because each LDL particle has one apoB. However, other particles have apoB, also, such as VLDL. When both are presented, LDL-P is the better predictor of risk.

    • Ed C

      I understand that every LDL particle has an apo-b and other particles can also have an apo-b. It just seems to me that the apo-b measurement would tend to reflect more risk and not less risk than the ldl-p (by nmr).
      If I had only the apo-b report, I would be wrongly thinking that my risk is very low. So I’m wondering if others should not count on their apo-b results either ?
      I had a follow-up ldl-p done that also showed high risk ldl-p. This second report came from Direct Labs and only cost $57. It was a very basic lipid panel but does include the all important ldl-p by nmr.
      The advanced lipid panel from Health Diagnostics Labs cost nearly $1000.
      Just throwing that out there so others know that they can often just walk into a lab and request the ldl-p report themselves (no doctor required).
      But now what to do with this knowledge of high risk ldl-p? As my personal experiment, I plan to have another ldl-p report after taking niacin and psyllium fiber for a couple of months. Of course, I’ll be looking for any other suggested treatments that may be found on this blog and other sites. Thank’s to Dr Attia and Dayspring for making this information available to us.

      • Ed, are you sure LipoScience is doing the LDL-P for Direct Labs?

    • Ed C

      Well, I just checked my report. It was LabCorp, not Direct Labs. The LabCorp test number was 884247 and the cost was $58. This included the Lipo Science NMR LipoProfile as well as an IR Score. It’s possible the clerk billed for the wrong test since $58 seems very cheap. However, it’s nice to know that an individual can order their own lipo profile.
      I’ve heard Dr Dayspring say that Lipo Science is the only source for the NMR and all labs must send the blood to Raleigh NC until license agreements allow for additional machines to be located elsewhere. If Lipo Science was a public company, I’d be investing in it 🙂

      • Correct. $58 is reasonable for just the LDL-P.

  • dennis

    Hi Peter:

    Thanks for all the info you’ve presented, and for the most part, I don’t think I’m confused. (That means I could be so confused, I think I got it straight.) It appears as though I too am one of those Low Carb – High LDP-P guys; so I’m very interested in all things cholesterol. I’m also interested in alternate testing methods.

    Anyway, I’ve found an article in the Arizona Sun by Dr Patel, and I’m interested in your thoughts on the Carotid Intima Media Thickness ultrasound test (CIMT). As a lay person, I like the “logic” of measuring plague, even if it isn’t directly on the heart. As well, is there any value in heart scans as advocated by Dr. Davis?

    I’m not going back to medium or high carb. So, I’m looking for other ways to track “potential” damage, or make up coming decisions about statin use. Do you believe any of the above tests, or any other tests will help me to better identify risk, and thereby address treatment?

    • I will definitely cover my thoughts on this when I (gulp…eventually) get to Part X of this series.

  • Rhidian

    hi Peter,

    I have to say i really like how you responded to Hussan, you are clearly a gracious character. I also think Hussan poses some excellent thought provoking questions. Anway, my interest in LCHF diets stems from a guy called Dave Asprey (bulletproof diet), i am not sure your awhere of him. However, i wasn’t satisfied with the level of scientific discussion that this blog clearly has. In saying that, one of the things the bullet proof diet incorporates is not “oxidising your fats” (what ever the definition of that is) (via cooking, such as the preference for raw eggs over hard boiled eggs,) as this is “bad for you”. I am just wondering if you have incounted any such findings in you research? and if you have any thoughts on the matter? cheers :).

    • The more unsaturated a fat, the more likely it is to generate ROS when heated.

  • Chuck B.

    Peter, I was just giving this post my umpty umpth read through (well, reading it with/to someone) and my curiosity has finally piqued: Just what was the discordant variable? GDP, interest rates, unemployment??? I’ve always been curious but figured someone else would have asked by now! Off topic, I know, but, eh, what’s a mind without curiosity?

    • Interest rates. Trailing, not leading indicator.

  • James

    Fanstastic series Peter! Really enjoyed reading it and I can now explain to my mother what her cholesterol numbers really mean. She’s on certain drugs and has been avoiding eating eggs and butter for so many years. It does not make much sense after reading your articles.

    What we are all missing now is some reference markers for people on LCHF diets and nutritional ketosis (like me). A field of research I hope you can help explore with your NuSI 🙂


  • Robin

    I’m a little confused..I had an nmr Lipoprofile test and results were: LDL-p is 1933 But,
    HDL-P 43.4
    Small LDL-P 123
    LDL size 21.8
    All of these above markers are listed as in the Lower CVD Risk catagory and the report further shows me as in (Pattern A) which I read is associated with low CVD risk. Also other markers show me with an lp-ir number of 7 which is insulin sensitive which I guess is also good. Am I reading this right? Thanks in advance for any response.

    • Robin, I can’t weigh in on this, but hopefully your doctor is appropriately versed to explain it in great detail.

  • Robin

    Dr. Attia, Thank you for your response. Out of curiosity is there a reason you can’t weigh in in my results? Is it that there isn’t enough information or maybe my results are controversial? I don’t know if my Doc. is versed in reading NMR results. There were 2 labs he told me I could go to and later i learned that one does standard lipid panel and the other NMR. My doc didn’t specify which he only said it doesn’t matter. I picked the NMR by accident because it was closer. When I got the results I was confused since I never saw such results. When I started researching I found some info stating the total ldl-p number was most important then other info stating small ldl number was most important. I got very confused. Got even more confused when my results show hdl-p total, small ldl-p, ldl size all in the low risk range. Other results were:
    Hdl-p total 43.4
    Large VLDL-P less than 0.7
    Small ldl-P 123
    large hdl-p 10.7
    VLDL size 36.0
    ldl size 21.8
    hdl size 9.5
    lp-ir score 7
    Total lpl-p 1933
    All of the above are listed in the Lower cvd risk category and I am show in Large Pattern A.
    If any of this helps I would really appreciate your thoughts. But I apologize if you still can’t comment. Thanks in advance.

    • No, it’s because I can’t practice medicine over the internet.

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  • Mike


    I started on a low-carb, high-fat (LCHF) diet a couple months ago, and just had an NMR Lipoprofile done. My LDL-P is extremely high. Unfortunately I don’t have a baseline from before I started LCHF, so I’m not sure what to make of the results, especially as I am also losing weight.

    Do you have any recommendations for finding a doctor who is knowledgeable about these matters? It seems like there are so many factors, and so much conflicting information (it’s LDL particle size that matters, no, it’s particle count; no, LDL is irrelevant, it’s HDL / triglyceride ratio that’s important, etc etc).

    As a reasonably intelligent person with a strong math/science background, I’m doing the best I can to understand this stuff, but it would be nice to have a doctor who can give sage counsel. I fear that if I go to a doctor at my current medical practice, I would simply be told “your LDL-C is high; eat heart-healthy grains, cut back saturated fat, and here’s a statin.”

    So how do I find a doctor who is up on the latest research about diet, metabolic syndrome, and cholesterol, who can advise me in my journey towards better health?

  • Jane

    Hello Peter,

    Are the data from Jim Otvos that you showed here published now?
    If you have it, would you please give us the citation?

    I am persuaded, but need to prepare for persuading my internist to order an apo B or NMR test for me.


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  • Huugo

    So what is the blood cholesterol measurement?
    Is it the cholesterol in each lipoprotein?
    Is it the whole lipoprotein?

    Isn’t the free cholesterol content quite the same among lipoprotein subclasses.
    Free cholesterol composition of lipoprotein classes:

    • Plasma cholesterol measures the concentration of cholesterol in the specific lipoprotein (e.g., HDL-C, LDL-C, TC-C).

  • Vicente

    Hi Peter,
    one of your links is not working. It is the one in the following text: “The figure below, from the Journal of Clinical Lipidology, shows the cumulative incidence of cardiovascular events (e.g., myocardial infarction, death) over time in three sub-populations:”

    I think this is a working link for that paper:

    Best regards

  • Angela

    I too never thought I’d find a guy who was both normal(ish) and nerdy enough to put up with my nutrition science ramblings. Luckily, at least one such guy existed, but the trade off is I have to listen to his engineering talk. ‘Tis a small price to pay.

    Thanks so much for the EXCELLENT series! I wish all my dietitian friends would read this. We (dietitians) are an embarrassment to the field nutrition science with our outdated advice!

    • Angela, you may have just posted the comment of the month!

  • Vincent Lin

    Peter, why do you believe that high LDL, whether it is LDL-C or LDL-P disregarding their discordances, increases the risk of cardiovascular diseases?

    If your belief, which is also a common belief, is correct, then the data, shown in Part VI of “Straight Drop on Cholesterol”, should indicate that the population having lower LDL should have lower percentile of CAD diseases, and vice versa. However, my interpretation of the data indicates the opposite that lower LDL-C actually has higher CAD risk, and higher LDL-C has lower risk. If you disagree with my interpretations, would you please kindly show your disagreements?

    If we compare the LDL-C data from the patient hospitalized with CAD diseases with the data of other two groups: Framingham offspring and the patients hospitalized with non-CAD diseases, presented in Part VI of “Straight Drop on Cholesterol”, then the patient having lower LDL-C actually had higher CAD risk, and higher LDL-C had lower risk.

    Let’s assume the data from Framingham offspring representing a typical LDL-C profile for general population. The LDL-C of Framingham offspring has only 20 percentile less than the recommended normal level of 100 mg/dl. If the belief is correct, then we should expect that the population having LDL-C better than this normal level and also having CAD diseases should be less than the 20 percentile. In addition, the more is the difference of the percentile, the more significance of the impact of LDL-C on CAD diseases. Instead, the data showed that 50 percentile of patients hospitalized with CAD diseases were in this LDL-C level. Thus, the 5 out 10 hospitalized CAD patients are from the 2 out of 10 general populations having a healthy LDL-C level.

    Furthermore, by comparing the data for patients hospitalized for CAD and non-CAD diseases, it also shows that the patients having LDL-C better than the recommended 100 mg/dl level have higher percentage of CAD diseases, and the patients having higher LDL-C level have lower percentage of CAD diseases. This conclusion is based on the data that
    (1) For patients with LDL-C less than 70 mg/dl, which is considered to be extremely healthy, 17.6% of the patients were hospitalized with CAD diseases and only 12.5% patients were for non-CAD diseases. Thus, in this extremely healthy LDL-C level, 40.8% more patients had CAD diseases;
    (2) For patients with LDL-C less than 100 mg/dl, which is considered to be normal, 50% of the patients were hospitalized with CAD diseases and only 41.5% patients were for non-CAD diseases. Thus, for patient having LDL-C better than the normal healthy level, 20.5% more patients had CAD diseases;
    (3) On the other hand, for patients with LDL-C greater than 130 mg/dl, which is considered to be extremely unhealthy, 20.5% of the patients were hospitalized with CAD diseases and 29.2% patients were for non-CAD diseases. Thus, in this extremely unhealthy LDL-C level, we should expect many more patients to have CAD diseases. Instead, the data shows that 14.4% less patients had CAD diseases.

    Therefore, the data shows that that lower LDL-C has higher CAD risk and higher LDL-C has less CAD risk.

    • Risk follows LDL-P. When LDL-C and LDL-P are concordant, this means LDL-C is high; when discordant, it means LDL-C is low(ish).

    • Vincent Lin


      Thank you for your promptly reply to my question.

      My understanding of the discordance between LDL-C and LDL-P, is that they have similar trend but only with a minor or moderate shift of peak or patterns, such as the LDL-P graph shown under the LDL-C graph of Framingham offspring in which the peaks are 130 mg/dl for LDL-C and 1300 nmol/L for LDL-P and their patterns are similar with no drastic difference.

      In you answer to my question, do you mean that the discordance can be so drastically that there are an inverse relationship between LDL-C and LDL-P? For instance, there exist cases that a person may have very high LDL-C, such as 200 mg/dl, whose LDL-P is very low, such as 800 nmol/L? If this is what you mean, then are they rare or common? Unless, they are common, then I still have difficulty to use the data to prove the common belief of the relationship between LDL and CAD risk.

      Thanks again for your answering to my question.

      Vincent Lin

  • Stephen Johnson

    Well, I don’t have time to read through the whole thing but the bottom line I get is, my high calculated LDL (low HDL) tells me NOTHING! Hold off still on the provastatin (as prescribed but I assume is a misspelling for pravastatin). I am very healthy otherwise, only this one marker is off.

    • Stephen Johnson

      I will add, the doctor did not even recommend any focused and disciplined change in exercise and diet before prescribing the provastatin. So, I am increasing my exercise and will continue to watch my diet as I have and keep reading!
      THANK YOU!

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  • Eva

    Dear Dr. Attia,
    I´m really greatful for your sharing of your insights and medical information with everyone, who is interested. And thank you for doing this with such dedication and generosity. 🙂

    As I´m reading your posts for the last months, I was changing my eating habits drastically and don´t eat any more sugars, white flour, potatoes, white rice and vegetables with lots of carbohydrates.

    Next week I am going to have my blood checked.
    My doctor unfortunately just lets me test for LDL-C, HDL-C, Triglycerides, but not for LDL-P/apoB.

    So I´m going to pay the laboratory privately for the Apolipoprotein B – blood-test.
    As I am from Vienna, Austria/Europe we seem to have different tests or perhaps just different measuring units:

    So I would kindly ask you, to help me check this out:

    1. When the test is called “Apolipoprotein B” – is this the test for LDL-P?

    2. Their measurement of the “Apolipoprotein B” is mg/dl and they tell me the result of the blood test should be somewhere between 58-104 mg/dl. I´ve read your postings, but the measure units in your posting are in nmol/L.

    – Here is the link to the austrian website of the laboratory, unfortunately it´s in German.

    So may I ask you, what you would believe to be “very low risk”/”low risk”/”high risk”/”very high risk” results in this test expressed in mg/dl?
    Or asked differently: How can I convert my results of mg/dl into the units of nmol/L , which you are using in your charts? (And is it possible to convert the datas or are these different tests?)

    If I knew this, I could compare my results with your scales/charts in your postings and see, if my parameters are concordant/discordant and with the help of your charts, I could see, if I´m at high or low risk.
    With my results in mg/dl – units I can´t.

    Thank you very much for your help, dear Dr. Attia!
    Yours Eva from Vienna, Austria

    • james

      Eva, you may try this if it works for you

      input the values both ways and you can covert them.

      4.30 AM London-Time.

      Am reading since 8PM, this guy is a “real nutter” – DR Attia.On serious note, may God Bless him, for time, effort and humanity he has put on writing all of this!! Best feature remains “quick recap” after every chapter on cholesterol one can re-read main points…and EVEN if you a donkey the good Dr will nail them into you!!

      Provided the donkey can read 🙂

      I go back to some more reading/ 2 chapters left.


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  • Evan

    What about high HDL? i understand that the current testing methodologies are inacurate but currious to know. My blood test came with 157 LDL and 175 mg/dL HDL. Should I be concerned?



  • Peter

    Following a keto lifestyle for over a year and while eating the appropriate foods and testing positive for ketones I am a clear headed fat burning machine who once becomes adapted swears never to touch a carb again. Unfortunately my eating habits are mimicking my manic, bi-polar lifestyle when I crash and devour every trashy form of high carb crap I can get my hands on and then the dark days set in until I muster up the sense to get back on keto . I am concerned about toggling back and forth between 0 carbs a and massive amounts crap, am I harming any organs or systems? I’m 54, 6’2″, exercise and have no real health issues other than mild manic/bi-polar symptoms that I am not on medication for. My blood pressure is always stable however my glucose readings have become erratic averaging 5 mmol while on keto but going as high as 9 when coming off keto. I keep hoping the switch stays on and I can maintain keto full time but am concerned about the risks of bouncing…any thoughts?

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  • Freda Mooncotch


    I’ve been a huge fan of yours since I started ketosis in 2013. While I admit I don’t understand everything that you write, I do my best to follow the concepts. I have to tell you this information is incredible (if I understand it correctly). I had my NMR profile done in December of 2013 and based off of Cholesterol Clarity I thought I was super healthy (everyone said I was) but now after reading this series and looking at my test results I’m a little freaked out!

    These are the results of my NMR Lipo Profile done in 12/13 6 mths into deep ketosis. I was low carb since August 2012, then went ketogenic July 2013 to mid March 2014 when I had to change my diet completely.

    You might find this interesting and maybe this was just one of the reasons why I felt like crap and started having severe blood pressure problems? I don’t know. I’ll never know because everyone said I was healthy. LOL

    LDL-P – 2280
    LDL-C – 221
    HDL-C – 71
    Triglcyerides – 55
    Total C – 303
    HDL-P (total) – 29.9
    Small LDL – P – 177
    LDL Size – 21.4

    According to your last 2 posts I was in the 95th percentile with high LDL-P and high LDL-C!!! Glad I followed my gut and changed my diet.

    Now, I’m really curious to see my NMR Lipo Profile and how changing my diet to more Paleo/high protein/low carb for past 9 months impacts my test results.

    I will keep reading and trying to understand! Thank you for taking so much time to write this series.

  • Rick

    Need some help. I’m an endurance athlete and very fit and lean. I just had lab work and my LDL-P and APO B are high. Here’s the numbers: Total Cholesterol-197; LDL-C 112; HDL-C-81; Apo B-86; LEL-P-1482. Plan is to try to clean up my diet and retake in 4 months. If not lower, statins.

    In researching this, there’s conflicting information on diet. Should a low-carb diet or low-fat diet be used? I’m not sure how to proceed???

    • Rick

      I forgot. Triglycerides are 56.

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  • ben

    Can you elaborate on why Apo-B can be used as a surrogate for particle number?

    • Each LDL particle has one apoB molecule on its surface (though VLDL particles do, but they are few in number compared to LDL).

  • TJ

    Dr. Attia –

    I am new to all this and I’m not fully understanding it. So much conflicting information out there. I had high LDL and total but now I am seeing that these numbers don’t necessarily mean anything. My PCP immediately prescribed Lipitor but from various forum posts, it seems that he may have been wrong to do that? I do not see a lot of the numbers that you mention in this post on my lab results. I setup a visit to a cardiologist …What exact test should I get to get all the numbers that you discuss in this post?

    My test results are below:

    LDL – 200
    HDL – 48
    Total – 269
    VLDL – 21
    Trig – 103

    What do you think about these results?

  • Geordie

    An year back, when I was eating the normal high-carb-moderate-fat diet, I weighed 82 kg (height 175 cm, male) and my lipid profile was:
    TC – 279 mg/dL
    HDL – 47.4 mg/dL
    TG – 176 mg/dL
    LDL (Friedewald) – 196.4 mg/dL

    I’ve been on LCHF (strict) for the past 6 months. I truely enjoyed all the goodness of it, I weigh 71 kg, and I felt great until this morning when I got my new test results ????
    TC – 422 mg/dL
    HDL – 76 mg/dL
    TG – 133 mg/dL
    LDL (Friedewald) – 319 mg/dL

    I suppose with this way too high LDL-C (beyond the range your graphs show), can I infer that my LDL-P must also be too high?

    Anyhow, this is not normal. Even if the cholesterol profile is otherwise good – with high HDL and low triglycerides – it may be unhealthy. Yes, I belong to the unlucky 1-2% who has high LDL-P even with in ketogenic diet (about whom you talk about in a video). After a discussion with my doctor, I’ve decided to go out of ketosis right away, by reducing the intake of saturated fat and including good carbs. I’ll try to do intermittent fasting (which may be difficult while eating carbs). Any other suggestions?

  • james Owens

    Hands down one of the best articles I’ve ever read; you deserve a medal for the time and effort this must have taken. To take such a complex subject surrounded by long standing myths and strip it down so even us non-science folk can grasp it is an epic feat, you my sir are a legend.

  • Baya

    I just got back my lab. This is actually almost a 100 points lower then last year, but first time doing the particles count. How bad is this for 54 year female?
    CHOLS. TOTAL 265
    TRIG. 92
    LDL-P 2071
    LDL-C 179
    HDL-P 39.5
    Small LDL-P 621
    LDL size 21.6
    I calculated ratios below. Are those making the picture any better?
    Total Cholesterol/HDL 3.90
    RATIO HDL/LDL 0.38
    triglycerides/HDL 1.35

    Thanks in advance.

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  • jordan

    Thanks for all of the great info. Do you have a new link for the information for #7 about dietary cholesterol and serum cholesterol. The current link just goes to a dead end…

  • patriawan m. c.

    There shall be some sort of “ratio” of normal concordant of LDL-C and LDL-P. If there’s , what is it ? I calculate the number is between 8 to 10 ?


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