The Diet-Heart Myth: Why Everyone Should Know Their LDL Particle Number

cholesterol test

To read more about heart disease and cholesterol, check out the special report page.

Cardiovascular disease is one of the most misdiagnosed and mistreated conditions in medicine. In the first article in this series, I explained the evidence suggesting that eating cholesterol and saturated fat does not increase cholesterol levels in the blood for the majority of the population.

In this article, I will debunk the myth that high cholesterol in the blood is the cause of heart disease.

Myth #2: High cholesterol is the cause of heart disease

Part of the confusion about cholesterol and its role in heart disease is caused by imprecise terminology. So, before I explain why high cholesterol is not the underlying cause of heart disease, we have to cover some basics.

Cholesterol is not technically a fat; rather, it’s classified as a sterol, which is a combination of a steroid and alcohol. It’s crucial to understand that you don’t have a cholesterol level in your blood. Cholesterol is fat-soluble, and blood is mostly water. In order for cholesterol to be transported around the body in the blood, it has to be carried by special proteins called lipoproteins. These lipoproteins are classified according to their density; two of the most important in cardiovascular disease are low-density lipoprotein (LDL) and high-density lipoprotein (HDL).

I know this can get confusing quickly, so let me use an analogy to make this more clear. Imagine your bloodstream is like a highway. The lipoproteins are like cars that carry the cholesterol and fats around your body, and the cholesterol and fats are like passengers in the cars. Scientists used to believe that the number of passengers in the car (i.e. concentration of cholesterol in the LDL particle) is the driving factor in the development of heart disease. More recent studies, however, suggest that it’s the number of cars on the road (i.e. LDL particles) that matters most.

The crucial test for heart disease risk you’ve probably never heard of.Tweet This

Coronary arteries are essentially hollow tubes, and the endothelium (lining) of the artery is very thin—only one cell deep. The blood, which carries lipoproteins like LDL, is in constant contact with the endothelial lining. So why does the LDL particle leave the blood, penetrate the endothelium and enter the artery wall? The answer is that it’s a gradient-driven process. Going back to our analogy, the more cars there are on the road at one time, the more likely it is that some of them will “crash” into the fragile lining of the artery. It’s not the number of passengers (cholesterol) the cars are carrying that is the determining factor, but the number of cars on the highway.

The significance of this in terms of determining your risk of heart disease is profound. When you go to the doctor to get your cholesterol tested, chances are he or she will measure your total, LDL and HDL cholesterol. This tells you the concentration of cholesterol (passengers) inside of the lipoproteins (cars), which is not the driving factor behind plaque formation and heart disease. Instead, what should be measured is the number of LDL particles in your blood.

LDL cholesterol levels and LDL particle number are often concordant (i.e. when one is high, the other is high, and vice versa), and this is probably why there is an association between LDL cholesterol and heart disease in observational studies. The elevated LDL cholesterol was more of a proxy marker for elevated LDL particle number in these cases. But here’s the kicker: they can also be discordant. In layperson’s terms, it’s possible to have normal or even low cholesterol, but a high number of LDL particles. (1) If this person only has their cholesterol measured, and not their particle number, they will be falsely led to believe they’re at low risk for heart disease. Even worse, the patients that are the most likely to present with this pattern are among the highest risk patients: those with metabolic syndrome or full-fledged type 2 diabetes. The more components of the metabolic syndrome that are present—such as abdominal obesity, hypertension, insulin resistance, high triglycerides and low HDL—the more likely it is that LDL particle number will be elevated. (2)

On the other hand, patients with high LDL cholesterol (LDL-C) and low LDL particle number (LDL-P) are not at high risk of heart disease. In fact, studies suggest they’re at even lower risk than patients with low LDL-C and low LDL-P. (3) Yet they will often be treated with statin drugs or other cholesterol lowering medications, because the clinician only looked at LDL-C and failed to measure LDL particle number. This is a concern for two reasons. First, statin drugs aren’t harmless. (I’ll go into more detail on this in the third post of the series.) Second, studies suggest that low cholesterol can increase the risk of death, especially in women and the elderly.

In one study of over 52,000 Norwegians, researchers found that women with total cholesterol levels below 195 mg/dL had a higher risk of death than women with cholesterol levels above that cut-off. (4) And a study published in the American Journal of Medicine found that people over 70 years of age with total cholesterol levels below 160 mg/dL had twice the risk of death than those with cholesterol levels between 160-199 mg/dL. (5) Low cholesterol is also associated with increased risk of disease—especially mental health and brain disorders. For example:

  • A study in the Journal of Psychiatric Research found that men with low total cholesterol levels were 7 times more likely to die prematurely from unnatural causes such as suicide and accidents than other men in the study. (6)
  • A 1993 study published in The Lancet found that depression was 3 times more likely in men over 70 with low cholesterol than in those with normal or high cholesterol. (7)
  • A Swedish study found that women with the lowest cholesterol suffered significantly more depressive symptoms than other women in the study. (8)
  • A study in the journal Neurology showed that low cholesterol is associated with increased risk of dementia. (9)
  • A paper published in the European Journal of Internal Medicine linked low cholesterol levels with Alzheimer’s disease. (10)

It’s important to note that all of these studies were observational, which means that they don’t prove that low cholesterol was the cause of the increased risk of death or disease that was observed. It’s possible, for example, that these patients had another disease that caused both the lower cholesterol and increase in disease or mortality. However, given what we know about the important roles of cholesterol in the body, it’s certainly plausible that low cholesterol is capable of contributing to these problems directly.

Wrapping up: The map is not the territory!

Before concluding, I’d like to point out that although LDL particle number is superior to LDL cholesterol as a marker for heart disease, it’s still just that—a marker. A marker is not a disease. It’s a risk factor for a disease. Having a risk factor for a disease does not guarantee that you will get that disease—it just increases the chance that you will. There are still several gaps in our knowledge about LDL-P and its usefulness in a clinical setting. For example:

  • Imagine two people with an LDL-P above 2,000, which puts them in the highest risk group. Person A follows a Paleo diet and lifestyle, gets plenty of sleep, manages stress and has no other significant risk factors for heart disease. Person B eats a Standard American Diet, doesn’t exercise, doesn’t get enough sleep, is stressed out and has several other risk factors for heart disease. Logic would dictate that Person A would be at much lower risk for heart disease than Person B, but there isn’t any comparative data to quantify the difference in risk and it’s unlikely such a study will ever be done. (Who would pay for it?)
  • Imagine two people following a healthy Paleo-type diet and lifestyle. Person C has no conventional risk factors for heart disease. Person D has no conventional risk factors either, but does have an LDL-P of 2,000. Logic here would dictate that Person D is at higher risk than Person C, but again, we don’t have actual data to quantify the difference in risk.

Heart disease is a complex, multifactorial process. The likelihood that we’ll have a heart attack depends on numerous factors, including genetics, diet, lifestyle and living environment. The purpose of this article is not to suggest that LDL-P is the only risk factor that matters, or that other risk factors shouldn’t be taken into consideration. It is simply to point out that existing evidence suggests that LDL-P is a much better predictor of heart disease risk than LDL or total cholesterol, and that it appears to be one of the better markers available to us now.

I was going to follow this article with one on statin drugs. But I’m almost certain that all of you are going to ask what increases LDL particle levels after reading this, so I think I’ll cover that next and then move on to statins after that.

Note: if you’re interested in a much more thorough discussion of how to determine your risk of heart disease and how to use diet, supplements and lifestyle changes to protect yourself and those you love, check out the High Cholesterol Action Plan.

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Comments Join the Conversation

  1. charles grashow says

    Three questions

    1) Is an LDL-P of 2,000 or higher in someone who eats no carbs the same as an LDL-P of 2,000 in someone who does.

    2) Is it 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?

    3) Is DR Thomas Dayspring right when he says “Well the 50th percentile cutpoint is not normal if one is trying to prevent atherosclerosis. The 20th percentile cutpoint would be considered desirable: that is 80 mg/dL for apoB and < 1000 nmol/L for LDL-P.

    • Chris Kresser says

      1) There’s no data on this, but I wouldn’t phrase it in terms of carbs. I’d say what I said in the article, which is “Is an LDL-P of 2,000 or higher in someone who eats a crappy SAD the same as an LDL-P of 2,000 in someone who eats a nutrient-dense, low-toxin, whole-foods diet?”

      2) Risk stratification is based on the average person in the average study, so yes. Again, as above, I’m not convinced the differences have anything to do with carbs or quantity of macronutrients per se, but instead are more related to the quality of macronutrients consumed.

      3) Perhaps in a typical western population. But we simply don’t know if that’s true in people following a very healthy diet and lifestyle with low oxidative stress.

      • charles grashow says

        “Is an LDL-P of 2,000 or higher in someone who eats a crappy SAD the same as an LDL-P of 2,000 in someone who eats a nutrient-dense, low-toxin, whole-foods diet?”

        SO – Chris – are you saying that we do not yet know the answer to this question?

        • Chris Kresser says

          Yes, that’s what I’m saying. Logic would dictate that it’s not the same, because LDL-P is not the sole risk factor for heart disease. As I said below, it’s a complex, multi-factorial disease that takes years if not decades to develop.

    • Glenn Atkisson says

      To what Chris provided on 2) regarding “quality of macronutrients” which I agree with, I would add: “Also consider the quantity and quantity of micronutrients.”
      Detailed in this article on LDL from the Journal of American Physicians and Surgeons is some advice on how antioxidants and enzymes from fresh foods are possibly more important to avoiding heart attacks and arterial damage than any measurement of LDL:

      Essentially you can work on your LDL numbers until you are blue in the face and you will find out that you haven’t improved your cardiovascular health as much as you would have if you had just raised your level of micronutrients by eating what we all know is healthy. Fresh, organic fruits and veggies, etc. These become more important the more oxidized fats you have in your blood.

      • charles grashow says


        My question is this – if you go on paleo hacks or read the various blogs on the paleo diet/low carb diet you find many people with both very high LDL-P and very high LDL-C and when concern is expressed the answer is usually “well your HDL-C is high and your triglycerides are low so don’t worry”

        SO – I ask again – if you’re eating a typically paleo diet as talked about today – NOT the low saturated paleo diet as espoused by Boyd Eaton in both of his papers – with lots of grass fed beef, pastured eggs, etc. AND your LDL-P AND LDL-C are both very high should you worry?

        His initial paper in 1985

        The best available estimates suggest that those ancestors obtained about 35% of their dietary energy from fats, 35% from carbohydrates and 30% from protein. Saturated fats contributed approximately 7.5% total energy and harmful trans-fatty acids contributed negligible amounts. Polyunsaturated fat intake was high, with n-6:n-3 approaching 2:1 (v. 10:1 today). Cholesterol consumption was substantial, perhaps 480 mg/d. Carbohydrate came from uncultivated fruits and vegetables, approximately 50% energy intake as compared with the present level of 16% energy intake for Americans. High fruit and vegetable intake and minimal grain and dairy consumption made ancestral diets base-yielding, unlike today’s acid-producing pattern. Honey comprised 2-3% energy intake as compared with the 15% added sugars contribute currently. Fibre consumption was high, perhaps 100 g/d, but phytate content was minimal. Vitamin, mineral and (probably) phytochemical intake was typically 1.5 to eight times that of today except for that of Na, generally <1000 mg/d, i.e. much less than that of K. The field of nutrition science suffers from the absence of a unifying hypothesis on which to build a dietary strategy for prevention; there is no Kuhnian paradigm, which some researchers believe to be a prerequisite for progress in any scientific discipline. An understanding of human evolutionary experience and its relevance to contemporary nutritional requirements may address this critical deficiency.

        His follow-up paper in 2010

        Reduction of carbohydrates to extremely low levels is not consistent with the HG model, but neither is a very high CHO, “meat as a condiment”–type diet; furthermore, CHO sources are important. HG CHO came from fruit, vegetables, and nuts, not from grains. Refined, concentrated CHOs such as sucrose played virtually no role, and the consumption of plant CHO necessarily resulted in high fiber intake. If we were to rebuild the food pyramid along HG lines, the base would not be grains but fruits and vegetables, which could be chosen to provide adequate fiber content. The second tier would be meat, fish, and low-fat dairy products, all very lean. Whole grains might come next (although even these were very unusual for HGs), whereas fats, oils, and refined carbohydrates would occupy the same very small place at the top, essentially functioning as condiments in a healthy diet. These guidelines would not exactly replicate the HG diet in terms of food categories, but it would do so roughly in terms of macronutrients.

        • Colleen says

          Should you worry about high LDL-P assuming a paleo diet? I believe the correct answer is we don’t know. I would look at other markers of inflammation, family history, APOE status, and perhaps consult with someone knowledgable (if you can find such a doctor) on whether there is a concern.

          • charles grashow says

            So if we don’t know if high LDL-P on a paleo type whole food diet is a cause for concern then why test ANYTHING??

            • Chris Kresser says

              In a perfect world, we’d have unambiguous answers to all of these questions. In the real world, we don’t. Heart disease (like most other diseases) is a complex, multifactorial process. LDL-P is one of many variables that can be used to determine risk. The uncertainty surrounding it as a marker in certain situations does not suggest that it’s useless, nor does it suggest that all other tests are useless.

        • Glenn Atkisson says

          Eaton’s articles are interesting, Charles. They focus a lot on macronutrients and their percentages, and when they don’t focus on that, they focus on what the breakdown is for the fats that hunter gatherers ate.

          I have to answer that the article I first replied with was stating something off to the side of all this. I think if you study it you will see that the focus is on micronutrients as protectors of the body. Check it to see if you don’t agree that the main point there is that your mix of macronutrients is not so important, and your mix of particular saturated/unsaturated fats is not so important. What is important for cardiovascular health is how much protection you get from vitamins and enzymes (antioxidants). I know this is not the subject at hand, and not the subject that people want to discuss here today. But the article stands on its own, and seems important to me. It may be a case of us all trying really hard to ignore the obvious.
          Now that being said, I’m never going to speak up and say we can all just start eating transfats and the antioxidants will protect us! But I am saying that there are studies that prove that measuring LDL isn’t going to give us a path to health. The one I cited is one of those. We have to be trying to be blind to ignore such a study.
          So now, the short answer is, on a Paleo diet, does the amount and type of fat you eat and the amount of carbs you eat matter when it comes to heart disease? I say not as much as the quality of foods you eat. If we could all be reverted to eating paleo, and I mean food grown on great fertile soil, and then exercising as paleo man did, then we would be quite healthy. There are studies that show that mummies had athersclerosis, btw!

          But some of this data is from Egyptian mummies. Hardly hunter gatherers. Heavy wheat eaters. Still….

          Personally I stay away from junk food and other sources of ruined fats. Eat organic foods. Eat a paleo diet. Ketogenic. Get good exercise. Stay low stress. I can’t imagine myself having my LDL measured. It’s the furthest thing from my to-do list. But health is a top priority for me. I hardly ever take an action that I can consider a compromise to my diet.

  2. McSack says

    Does your triglyceride count play a role in the type of LDL that you carry? I’ve heard that lower triglycerides equate to large “fluffy” LDL which is supposedly better than more dense LDL. Is there any truth to this? Does cell density also affect the number of LDL particles that are in your blood?

    • Chris Kresser says

      Yes, it does. The more triglycerides you have, the less cholesterol your low density lipoproteins (LDLs) can carry. Your liver then has to make more LDLs to carry the same amount of cholesterol, and you end up with a high number of small, dense LDL. Insulin resistance and metabolic syndrome is one of several causes of elevated LDL-P.

      • Heather says

        This is good to know. My TGs are 45. My HDL is 51. My Total is 210 (Of course this number was in BOLD PRINT with the word “HIGH” next to it. Oh no!! I’m going to keel over!!) As far as I’m concerned the LDL numbers means nothing. My TGs completely threw off the LDL calculation (It isn’t measured; it’s calculated – a “leftover” number with the assumption that all leftover IS LDL – but the article was a few years old so maybe there is new evidence). Will be getting my VAP test done soon (along with CRP and homocysteine. Then it’s on to female hormones). And if ratios still mean something – my ratios are great too.

        • Heather says

          I ordered my VAP test through I get my own testing and do my own research (I am my own PCP. I have no need for one of them. I just checked and I don’t see where they do measure LDL-P. Shoot.

            • Heahter says

              Nevermind. I actually went and finished reading your article. Like you said. Markers. My genetic markers for diabetes put me a 3% below the “average” risk for the population yet I suffer from Reactive Hypoglycemia and was becoming diabetic on the healthiest SAD (mildly calorie restricted, high whole grain and almost no sugar at all) all the while losing weight and getting lots of exercise.

      • Matt says

        Wow! A high triglyceride level leads to less room on the apolipoprotein for cholesterol which in turn leads to more LDL production. Is this widely known Chris? Is there a paper to point to on this? Because if true that would be something I would like to point out to my patients but I’ve never read this anywhere else…

    • Chris Kresser says

      Particle size loses its predictive value after adjustment for particle number. In other words, particle number is more important. This is evident from looking at people with Familial Hypercholesterolemia (FH), who have predominantly large, buoyant LDL particles but are still at three-fold greater risk of death from heart disease (because of their high LDL particle number).

      • Khaled says

        You say “Particle size loses its predictive value after adjustment for particle number”. What about someone who has normal particle number, but predominantly small, dense. How is the risk in his case?

  3. j tiura says

    Chris, Good article but this doesn’t seem right: Logic would dictate that Person A would be at much higher risk for heart disease than Person B.
    Is this what you meant to write?

  4. MIke says

    I, too, have heard that particle size is everything now. My doctor said that a lot of money is going into studying that. What have you heard?


  5. Sharon says

    My last NMR Profile showed LDL-P 1628
    My HDL-C was 87
    HDL P 39.7
    Triglyc was 51
    Small LDL P 123
    LDL size 21.4
    My insulin LP-IR score was 5
    So what am I to do? How can I lower the LDL-P? I eat a fairly low carb/paleo type diet, exercise, etc.
    My suspicion is my TSH was 5.08 and perhaps contributing to LDL.
    I have stopped intermittent fasting and I’m eating more seafood, seaweed, etc to build iodine.
    My Thyroid AB test was 7, so I’m not worried about taking in iodine. I also am adding about 1/2 of a small sweet potato after my workouts (4 days a week). I have to be careful because I’m trying to lower an A1C of 5.5.
    I will test in May and see if any improvement comes of this.

    • bill says

      Sharon. Were you able to drop your ldl-p? I have about the same numbers as you (hdl/tri/ldl/ldl-p).

      I need to get my ldl-p down as well.

  6. zack says

    From a blood test at the end of January

    LDL-P Total Count 919 nmol/L
    Small LDL-P 95 nmol/L
    LDL Particle Size 21.3 nm
    HDL Particle Count 37.0 umol/L
    HDL-P Large 41.1 umol/L

    Howd I do?

    • zack says

      Actually… here’s the whole thing

      VAP Cholesteral Test:

      Total LDL-C (Direct) 113 mg/dL
      Total HDL-C (Direct) 75 mg/dL
      Total VLDL-C (Direct) 13 mg/dL
      Total Cholesterol 201 mg/dL

      Triglycerides (Direct) 45 mg/dL

      Total Non-HDL-C 126 mg/dL

      Total apoB100 (Calculated) 78 mg/dL
      Lp(a) Cholesterol 10.0 mg/dL
      IDL Cholesterol 4 mg/dL
      Real LDL Cholesterol 98 mg/dL
      Real-LDL Size Pattern A
      LDL Size Graph [__________][___][___*_________]
      B A/B A
      Remnant Lipoproteins 12 mg/dL
      HDL-2 (Large, Buoyant) 21 mg/dL
      HDL -3 (Small, Dense) 54 mg/dL
      VLDL-3 (Small, Remnant) 8 mg/dL
      Real LDL Subspecies 4 17.9 mg/dL
      Real LDL Subspecies 3 38.9 mg/dL
      Real LDL Subspecies 2 35.5 mg/dL
      Real LDL Subspecies 1 6.1 mg/dL

      LDL-P Total Count 919 nmol/L
      Small LDL-P 95 nmol/L
      LDL Particle Size 21.3 nm
      HDL Particle Count 37.0 umol/L
      HDL-P Large 41.1 umol/L

  7. Rick says

    Hi Chris,

    First off, thank you for the informative post. I’m in my 20′s and have been doing PHD for about a year. A blood panel I just had done had these results:

    TC: 313
    HDL: 76
    LDL 226
    Triglycerides: 55
    TSH: 3.2
    rT3:226 pg/mL
    fT3: 3.3 pg/mL
    fT4: 1.12 ng/dL
    Glucose: 108.3

    My doctor is really pushing statins, but I’m hesitant to do so, even though I realize it’s possible I have FH. What do you recommend I do?

  8. says

    Hi Chris. Don’t you think it more likely that cholesterol and its carriers enter the intimal and medial spaces through the vasa vasorum instead of by penetrating the endothelium? Best wishes… – lc

  9. Glenn Atkisson says

    Chris, thanks for this article. You continue to be on the forefront in exposing myths that we must plow through to find the best path to health!

    You use the “bloodstream as a highway” analogy to explain: “The lipoproteins are like cars that carry the cholesterol and fats around your body, and the cholesterol and fats are like passengers in the cars. Scientists used to believe that the number of passengers in the car (i.e. concentration of cholesterol in the LDL particle) is the driving factor in the development of heart disease. More recent studies, however, suggest that it’s the number of cars on the road (i.e. LDL particles) that matters most.”

    This makes it seem as though it is still the “amount of traffic” and therefore the heightened “likelihood of an accident” that causes damage to the one-cell-thick endothelium that lines the cardiovascular system, resulting in atherosclerosis. A possibly more plausible explanation for the damage is that instead of sheer numbers of vehicles causing it, there is actually a damaging AGENT being carried in certain “cars” that causes the damage. In your analogy it would be: “Suppose some of the car drivers are DRUNK or ON DRUGS.” Now if this could be proven, it would make sense that it is mostly the drunk-driven vehicles that are plowing off the highway. This also allows an explanation of why some people develop atherosclerosis and others don’t a lot more understandable. And what is the agent that we can identify as the Drunk Driver doing all the damage?
    According to Brian Peskin and Dr. David Sim, the agent is the damaged oils (read trans-fats and oxidized polyunsatured fats) that are being carried around by the lipoprotein “cars”. These damaged fats are like passengers with an axe in their hands which they have sticking out of the windows of the cars they are riding in. During transportation to the cells of the body, the damaged oils score and scar the endothelium, over and over. This is the beginning of atherosclerosis, causing countless “patches” to be manufactured to keep the integrity of the endothelium. Without the lipoprotein having to carry these damaged fats, it wouldn’t matter how many vehicles (LDL) or how much cholesterol was in the blood. It’s a matter of the character of the lipids being carried. Shoddy characters do the damage. Eliminating damaged fats from the diet, by avoiding fried foods, trans fats, cheap veggie and nut oils, processed foods — that is the key to avoiding cardiovascular disease. It could also avoid the need for any testing of blood lipids whatsoever! How amazing that could be! (Costly to the medical profession).
    More here on the cholesterol myth (and totally supporting your exposure to both myth #1 and myth #2):

    More on how wrong treatment of cardiovascular problems can cause cancer:

    More on how the endothelium is damaged by adulterated fats and how, as Chris says, you can have low LDL numbers and still have greater risk of heart disease!:

    Health to you all. Keep reading. It seems to be the only way to guard our health these days.

  10. BarbaraA says

    I love your articles and enjoy learning though them. I like to pass them along to friends and family members, hoping that some of your research will sink in. :)

    There are 2 statements that look like they might need to be corrected:
    At the end of paragraph 9, it states: “Second, studies suggest that low cholesterol can be increase the risk of death, especially in women and the elderly.”
    It’s a little confusing. Can you clarify/update? I’m assuming the word “be” needs to be removed from the sentence.

    In your scenarios (under “Wrapping Up”), it seem like Person B would be at higher risk of heart attack than Person A, but you stated it the opposite.

  11. Lindsay says


    Very interesting stuff!! Thanks. Can you suggest guidelines from the literature regarding LDL-P? Is aiming for less than 2000 LDL-P a good guideline? I recently had my LDL-P tested and was surprised that it is “borderline high” (1491) even though I’ve been eating a primal-type diet for 5 years.

    Also, in your scenario above, wouldn’t we expect Person B to be at higher risk, not Person A ?

    I really appreciate being able to learn from your learning. Thanks for sharing all this information.


  12. says

    Thank you for the great article. I am a 61 year old male and 20 lb overweight, mostly abdominal. My cholesterol numbers are OK but I am wondering about my LDL Particle Number. The next time I have my blood checked I will be sure to get it checked!

  13. Massimo says

    There is a way to estimate LDL-p indirectly from standard analysis?
    I have:
    Total Cholesterol 253
    HDL 71
    LDL 161
    Triglycerides 41
    CRP negative
    HbA1c 5.1

  14. Gin says

    Had the LDL-P done a year or so ago…had to go to a cardiologist as my PCP office doesn’t do this test. Cardiologist agreed that I was eating the best way for me (metabolic syndrome, carb-addicted, PCOS – eating VLC), which rather surprised me. LDL was up a bit and my PCP was trying to get me to take a statin (NO!!). Cardio said if I wanted to try and continue to manage/lower this w/diet, OK but don’t ignore it for 20 years. He also said there was no point to getting the LDL-P checked again…what is your opinion on this? Test this regularly or is once enough?

  15. Les Pechenick says

    Hello Chris,

    The NMR Lipoprofile test, to my understanding , after an extensive search, is not available in Canada. In the High Cholesterol Action Plan you mention that the Apo B test is very comparable
    in terms of determining LDL Particle number. I had the Apolipoprotein B test done and had a score of 1.28 G/L. Is this considered high?

  16. Teresa says

    Chris- In the movie Statin Nation: The Great Cholesterol Cover-Up ( ) the doctors talk about damage to the endothelium and our body’s repair process ( endothelium essentially growing over a scab) as the cause for atherosclerosis….so it’s not so much cholesterol as figuring out what is causing damage to the endothelium. Or do we need to worry about cholesterol because of the atherosclerosis caused by damage to the endothelium because it causes a ‘traffic jam’? What are your thoughts on this?

  17. Wooly says

    So are our thyroid and liver sponsors of the cash for clunkers program to remove the oxLDL and can we get more bang for our buck by aiming for antioxidant rich and nutrient rich diets?

  18. Ben says

    “Who would pay for it?”

    Well, how much would a good study cost? Perhaps this would be an interesting experiment in crowd sourcing, the crowd being the paleo community. The technology exists to do this. With enough support, perhaps matching funds would materialize.

      • says

        Chris, Loved the post as always!

        But I would suggest that instead of urging people to get an NMR LipoProfile, they can simply calculate their “Non HDL-C”. This is a good representation of Apo B and LDL-P and can be calculated easily from a basic lipid panel. Non HDL-C is simply Total-C minus HDL-C.

        I think it will provide the same information at less cost and guide people to the more correct analysis of CVD risk as you pointed out quite correctly in your article…is not really a factor of LDL-C.

        As we know a Paleo (low carbohydrate high fat diet) can provide up to a 50% reduction in TG which may be enough to “treat” an elevated Non-HDL-C. For those who do not reach their Non-HDL-C goal which is identified in the newest ATP III guidelines, they may benefit from treatment. Which could be in the form of high dose Omega-3, Niacin or even a Fenofibrate. In people with established CAD this can have real proven benefits.

        Thanks for this article! Absolutely wonderful!


        • says

          ““Non HDL-C”. This is a good representation of Apo B and LDL-P”

          Where did you read that, Stephen?

          My impression is that it can’t be a good representation of number of particles (LDL-P) because Non HDL-C=Total Cholesterol-C – HDL-C

          Using the road analogy, any -C measure counts passengers, not cars.

          Further, I don’t see how it can measure Apo B.

          I ask these questions principally because my G.P. claimed the -C totals were good measures yet everything else I’ve read states you need the small particle count and a measure of oxidation and inflammation,

  19. Erin R says


    Thanks for the great article and research. My question is this- what test should I specifically request from my MD in order to obtain my LDL particle number?


  20. Henry says


    What are your thoughts on phytosterols on atherosclerosis? Peter Attia mentions this as having a stronger connection than even oxLDL does and in the vein that industrial seed oils have been categorized as “Heart healthy” because they reduce cholesterol… And of course is not the idea ( we are hoping for).
    He also mentions corn as having the highest amount of phytosterols. I’m very interested in the biggest contributors to a westernized Mexican diet to CVD and the least problematic/healthy diet options.


  21. Alina says

    I have always thought that it is inflammation that causes heart disease and cholesterol just patches up the inflamed areas in arteries. This is what I have read everywhere so far. I am confused now.

  22. Marla says

    I had a stent put in my LAD after unstable chest pain getting worse and culminating in 3 almost heart attacks. This was followed by coronary artery bypass graft age 54: normal cholesterol numbers, low blood pressure, healthy SAD. All of my docs said it was a ” plumbing problem” and put me on a statin, blood pressure meds and a blood thinner. This was in 2005, and i read everything i could get my hands on, ending up sending my blood on my own for the NMR lipoprofile. LPL particle size almost 2000! None of my docs saw the significance of this. I put myself on plain flushing niacin, starting out at 50 twice a day, and ended up at 1000 mg x2. ( better to not take more than twice due to elevated liver enzymes). My LDL – P went down to 600. I have been paleo since 2011 and went off niacin to see what would happen, and it shot back up to 1800!
    Statins don’t touch ldl- p, but at one point my cholesterol was around 100 total and i felt very wierd. Long story short, off all heart meds, and HDL was 100 last blood test, Tg was 63 and LDL was 122.
    If you decide to take niacin be careful with the sustained release it can cause problems.

  23. Zingiber says

    A paleo-based diet results in low serum triglyceride and high total cholesterol levels. The three most important factors of cholesterol testing:

    1) The ratio of triglycerides to HDL-cholesterol is what shows strongest association with the extent of coronary disease.

    2) Having triglycerides under 100 is correlated with Pattern A LDL particle size (the healthier pattern), which also often lead to high measured LDL.

    3) “In patients with low serum triglyceride and undesirably high total cholesterol levels, Friedewald equation may overestimate LDL”

    Friedewald equation:
    Total – (HDL + [Trigs/5]) = LDL

    There is a newer equation, called the Iranian Equation, that does a better job of calculating LDL when trigs are below 100. That equation is:
    (Total/1.19) + (Trig/1.9) – (HDL/1.1) -38 = LDL

    • Glenn Atkisson says


      Without you explicitly stating it, the articles and equations you mention are saying to me:

      LDL is computed after measurement of Triglycerides, and analysts don’t trust the LDL to be accurate and also it seems to be higher in patients eating a healthier diet. We are all saying “What gives?”

      It’s possible that by looking at LDL the big-Pharma community has everyone looking the wrong way again? Several readers here have already stated: “Why measure LDL?”.

      It seems to be coming out of all these tests of diet on cardiovascular problems that there are 2 things that really should be focused on, and yet big-Pharma has us looking at LDL.

      The two things are:

      1) Triglycerides – you elevate your triglycerides by eating high carb meals. There is no leeway for allowing elevated glucose in the blood. Eat carbs and you body must store them immediately, as soon as the glucose hits the blood. When the liver is full and the muscles are full (most people on poor diets have their gauges at “full” all the time) then the liver changes the glucose to triglycerides to be transported to storage in your fat cells.

      2) Oxidized polyunsatured fats in the diet – This gets measured as “oxidized LDL”. I believe this just means LDL that happens to be transporting an oxidized fat, which in the SAD is most likely going to be over-heated vegetable oil or else a trans-fat. The lipoprotein itself cannot be oxidized. It is the fat that it is carrying that is oxidized.

      So some of the recent tests seem to show that low triglycerides is good, and that just counting LDL doesn’t prove anything because there is proof that LDL can rise (and WILL rise when you lower triglycerides) and the people are actually less likely to have heart attacks. Other tests show it is the oxidized LDL (which isn’t really the number, size or anything to do with LDL [the vehicle, remember?] but just the passenger being carried [read "transfat"] that is causing the scarring of the endothelium, and thus the atherosclerosis that leads to heart attacks.

      Here’s the kicker. What we are seeing is a “correlations” in a lipid panel and the scientific community has us busy trying to fix our systems by lowering just one number (LDL). This probably is bogus. We are thinking the correlations are due to a 1-factor CAUSE-EFFECT relationship and are trying to bring people to health by adjusting diet to change the one measurement.

      The real “correlation” between triglycerides and LDL and a poor cardiovascular system is based on 2 things in the diet (at least), and is characteristic of the typical SAD diet: eating too many carbs, and eating too much ruined fats. Time and time again, when people are tested on healthy diets (as in organic, paleo) vs SAD, the LDL numbers can rise, yet the people are far less likely to have heart disease.

      As I cited before;

      As many have pointed out here, with LDL being a computed number, all it takes is a change in triglycerides to get a change in LDL. The quickest way to drop triglycerides is to go very low on carbs. The change can be measured within a day. The result in a test will show an elevation in LDL. Big deal. So much for those measurements.

      In a test, they can feed any food they want. They could go low-carb and still have the people eating junk-food type fats.

      But in real life, when people are astute enough to be trying a ketogenic or just a relatively low-carb diet, they are usually also eating more green veggies (vitamins, enzymes, anti-oxidants! yum!) and they are eating mostly healthy fats, and have laid off the cheap veggie oils, fried foods, etc. that would result in “oxidized LDL”. So what you get in this situation is what looks like a “correlation” of certain lipid measurements with heart health, but is in reality measuring a correlation of two things (carbs and ruined fats) that were changed in the diet simultaneously, and resulted in a healthier body. As the cited paper points out, heart health depends more on several things, than one thing, and the most important thing may be the amount of anti-oxidants one eats (meager supply in the SAD) and not the type of fats one eats. Read the study.

      Now here is more on how trans fats cause the endothelial scarring and calcium deposits:

      These studies are showing a correlation between trans fats and atherosclerosis. But there are others that have indicated that any kind of ruined polyunsatured fats in the blood stream also do damage.

      My conclusion (not recommending necessarily to others) is to forget about getting my blood checked, and just change my diet to one that is nutrient dense on micronutrients (green leafy veggies), and is essentially low-carb. That means very healthy organic fresh foods, including all meats, and other sources of oils. It means low-heat cooking.

  24. Michael says

    Hi chris

    Thanks for the article. Just curios if lipo protein b or a is a reliable measurement as they don’t test particle size in Australia

    • Scott says

      Michael, in Australia ApoB is the closest you’ll get to an LDL-P reading. Every LDL particle has one ApoB attached so it’s a fairly close proxy.

  25. Shane Close says

    I guess after reading all of this, is there ever a “good” time for someone to go on statins? My dear friend switched to paleo, and while every other marker in his life improved, his cholesterol didn’t at all. In fact, it is really high. He went to two or three different doctors to make sure, but finally submitted to the last doctor (supposedly the best cholesterol doc in Chicago) and took the statin prescription.


  26. Heather says

    I am very fascinated by these cholesterol articles. I have very high genetic cholesterol. I am 38, in very good physical shape and have been a vegetarian ( to lower my cholesterol for 23 years.) after the birth of my 3rd child, I was diagnosed w Hashimoto’s disease. I refuse to take a statin for cholesterol (it’s in low 300′s range) as I am already taking Synthroid and have adopted a completly gluten free diet for the past year. I am wondering if the Paleo diet would be good for me or only serve the auto immune issue, but make the cholesterol issue worse. Thoughts?

    • Kelly says

      What will make the cholesterol worse is the Synthroid. If you switch to NDT (like Armour), your cholesterol will reduce considerably. The thyroid produces more than just T4, and Synthroid is a T4 only med, which gives many people high cholesterol and sometimes even heart failure.

  27. says

    In your podcast with Chris Masterjohn a couple years ago he stated “The epic Norfolk study measured by NMR, they found that particle size was useful but they found that particle number was much more useful. But when they adjusted particle number for HDL cholesterol and triglycerides once again its usefulness was very questionable.”

    I believe Chirs’s thoughts then were that particle size, number and TC/HDL were all markers for LDL receptor activity and that low LDL receptor activity played a big part in heart disease. At that time he felt that TC/HDL was just as good of marker as particle size/number so if you were unable to get a particle size/number test done then TC/HDL would be a good marker.

    Have there been studies published in the last 2 years that show particle number keeps its predictive value when adjusted for HDL, TG or TC/HDL?

    As well have there been any studies of the particle number of people with heart attacks. ie do people with very low particle number ever have heart attacks or are almost all heart attacks in people with high particle number?

  28. GiGi Eats Celebrities says

    The biggest myth that I ABHOR is that eating cholesterol will make you get high cholesterol. OMFG I want to murder people when they say, “oh no, I cannot eat eggs or shrimp because I have high cholesterol” – GAHHHH!! And then, instead, they start noshing on some trans fatty acid laden food… AWESOME. Way to be educated.

  29. William says

    Chris, I would love to read an article by you (you’re able to make things so clear) discussing particle number vs. particle size. There are some who disagree that is it simply a matter of particle number and that the particle size is the real determining factor although I know that the most current theory is what you have presented regarding particle number. I also tend to wonder if it is really just a concentration gradient issue or what other factors make the endothelium more vulnerable to infiltration in some patients and how big a role those factors play in the process. Thanks for the great articles. You take some of the most complex subjects and make them accessible to everyone. That is a real gift..

  30. Jan says

    Hi! I’ve just discovered this site, so haven’t done a lot of research, but wonder if Chris, or anyone, can tell me about VLDL. Mine measured 82, and my doctor is flipping out. My total cholesterol is 370, HDL 95, I eat really healthy, non-carb foods. Thank you! Really, thank you!

  31. charles grashow says

    Are there any studies – that you know of – that measure the effect of dietary cholesterol on blood cholesterol?

    If the body produces cholesterol naturally why do we need to eat any extra?

    Are there any studies which show that saturated fat is a dietary necessity?

    • Glenn Atkisson says

      To answer your 3 questions:

      There are lots of studies, Charles. Just search for that topic on the internet: “effect of dietary cholesterol on serum cholesterol”

      We can’t avoid eating cholesterol. It’s part an animal’s physiology. Thus it is in our diet because the animals we eat needed it in their bodies.

      Also, physiology textbooks will tell you that saturated fat is a necessity. Read online about “lipid bilayer” – the membrane that surrounds all living cells, and most viruses. Saturated fats provide the strength and tension needed for cell integrity. Unsaturated fats provide the permeability needed to exchange waste for new food and oxygen. As far as cell walls are concerned, it’s mostly just fats and cholesterol.

  32. Sean R says

    Chris – Thanks for your great work.

    This series comes at a critical time for me as my dad had heart issues earlier in the week. I haven’t talked to the docs yet, but was told his heart is very weak and he has “cardiomyopathy”. Will be meeting the docs this week hopefully to find out more.

    I already know it will be a battle with him and the docs. 1st things I found upon arriving tonight (I live on the other side of the world) is a tube of fake fat which he was told to have instead of butter. Meanwhile loaves of white bread and sugar are fine! I may fill the tube with quality butter or lard and just not tell him.

    p.s. this is the junk they recommend:
    Promise Spread: Vegetable Oil Blend (Liquid Soybean Oil, Canola Oil, Palm Oil, Palm Kernel Oil), Water, Whey (Milk), Salt, Vegetable Mono and Diglycerides, Soy Lecithin, (Potassium Sorbate, Calcium Disodium EDTA) Used to Protect Quality, Vitamin E Acetate, Citric Acid, Pyridoxine Hydrochloride (Vitamin B6), Artificial Flavor, Maltodextrin (Corn), Vitamin A Palmitate, Beta Carotene (Color), Cholecalciferol (Vitamin 13), Cyanocobalamin (Vitamin B12).

    • Patrick says

      Hi Chris (and previous poster Sean)

      I’m in a similar situation to Sean in that my Dad three years ago had a heart attack and had two stents put in, as one thing was 100% blocked and another 90%. He has ‘high’ blood cholesterol in the family but I’m unsure if that is the Familial Hypercholesterolemia that you talk about. You seem to have different dietary recommendations for the latter and it has left me a little confused. Will you be doing a blog post about how to deal with Familial Hypercholesterolemia?

      I’m afraid of broaching this topic with my parents as they have for many years followed the notion that low-fat anything is good, margarine is good and butter is bad, whole-grain muesli and bread are fantastic, and they both love biscuits and jam, etc as well as a daily coffee.

      I don’t want my Dad to have another heart attack. What on earth do I do.

      • Sean R says

        Patrick – Great to hear from someone else with similar experiences. Though our fathers are in different situations. Still love to hear more on this. Looking forward to the rest of this series!

        Regarding my father:
        - I suspect viral infection causing cardiomyopathy

        Here’s why:
        - He was sick 4 weeks before entering the hospital (suspected extreme flu though never visited the doctor). From then, until entering the hospital, he began to lose sleep to the point of absolutely no sleep for more than a week, often couldn’t breath and had extreme water retention. Drove himself to the ER! They immediately diagnosed congestive heart failure (which can mean many things). They said he came just in time before a heart attack or worse.

        Based on research relating to cardiomyopathy, I’m thinking it could have been a viral infection.

        More background:
        - Age: 53
        - Is not sedentary (active job)
        - No family history of heart issues
        - Smoked his whole life, but his lungs were perfectly clear
        - Left heart cath: no blockages, no stents
        - No cholesterol issues. Blood pressure is fine. Everything is healthy with him except his heart!
        - Currently wearing a LiveVest defib vest until they determine if he needs a permanent one.

  33. Peter-NZ says

    Hi Chris

    Is there a formula for converting ApoB concentration into LDL-P particle number, maybe taking TGs into account? Also, what are the typical ApoB and LDL-P percentiles?

  34. Amanda says

    So, here’s what I’m really interested to see for us non-technical people who are just looking to make sense of our numbers and look at it different than our non-Paleo docs: A straightforward list of the factors and the numbers that are acceptable. I understand the relationship to TSH and T3 T4, and Trigs, and the ratio of HDL:LDL, and the better predictive factor or LDL-P number – but I haven’t seen a list of what ARE healthy ranges of these numbers. Am I missing it somewhere?? Help!

  35. Ret says

    When we take liposomal Vitamin C or other liposomal products, does this also increase the cars in the blood that may lead the LDL cars to more likely drive through the artery wall, or are we talking about two unrelated kinds of traffic? Thank you.

  36. gene says

    just read an article about the Farmingham study that stated folks with overall cholesterol levels less than 150 had virtually no heart attacks . That seems to contradict the above article . Please Explain

  37. Darren Chun says

    Hi Chris, I enjoyed your article. My cholesterol LDL has been around 7 for the last 2 years. My Doctor insists that I start taking medication to reduce it.
    Let me start by saying that I’m 46 years old, very fit for my age, I do Crossfit 4-5 times/week, weigh 80kg, 186cm tall, body fat around 10%, I eat about 80% paleo meaning that I do eat some dairy (milk in coffee, on muesli) and some grains (oats, muesli, legumes) I do not eat any of the foods that are said to cause high cholesterol, cakes, biscuits, fried foods, processed foods etc. yet my LDL cholesterol remains high.
    I have read that the particle size of LDL is the most important factor in deciding whether to start medication and to know whether you are at risk of further health complications. My question is how do you get a test to measure your LDL particle size? Is it part of a regular blood test? Or does it have to be specially requested by your Doctor?
    Thanks, Darren

  38. Wayne says

    What’s a *lower* bound for the optimal LDL-P?

    As an example, my doc shifted me from simvastatin 20mg to atorvatstatin 20mg (plus 2×500 mg immediate-release niacin) and my LDL-P came down to 622 – but, it has kept declining, and now the HealthDiagnosticsLab test shows total cholersterol 117, LDL-C 53, Tri 49 with LDL-P of 400. So, he’s cutting the atorvastatin to 10mg.

    But I’m not clear on what the target is, what counts as “overshoot” in lowering LDL-P. Is it based on having just enough particles to get the correct amount of cholesterol and triglycerides delivered, so it’s some three-way balance between those 3 numbers?

    • Mark Littlewood says

      Consider yourself lucky. Its been a year since my heart attack and my doctor/cardio has not subjected me to a single blood test or even blood pressure test. Its been a case of take these tablets and go away

      • charles grashow says


        Have you asked your doctor to run blood tests? I get blood tested every 6 months or so – if my doctor puts up any resistance I remind him that he works for me!

      • Wayne says

        Since a *heart attack* and not taking BP, watching for damage?? That’s …unusual!

        But even by common good-care standard, yeah, we’re way lucky with our doc – he’s deeply caring, excellent conversationalist/listener, skillfully puts us at the center of our care (matches to our lives), and is a board-cert lipidologist as well as a family GP. Great staff, too.

        So I’ll certainly follow his advice to cut back on the atorvatstatin, but I forgot to ask about actual optimal targets for LDL-P, and now I’m curious …

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