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


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To read more about heart disease and cholesterol, check out this eBook on the Diet–Heart Myth.

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 heart health and 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.

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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.

Want to learn more? Check out my next article in the series “What Causes Elevated LDL Particle Number?“, followed by “Statins Don’t Save Lives in People Without Heart Disease.”

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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Join the conversation

    • The best option is an NMR LipoProfile. It can be ordered through your doctor.

      • 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!


        • ““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,

  1. “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.

  2. 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?

  3. Chris- In the movie Statin Nation: The Great Cholesterol Cover-Up ( http://www.youtube.com/watch?v=iZctVYxiW2w ) 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?

  4. 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?

  5. 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?

  6. 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

    • No, as indicated above, LDL-P may or may not be discordant with LDL. Also, with low trigs, LDL may be off as it is calculated in your standard analysis and not directly measured.

  7. 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!

  8. Hello,

    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.


  9. 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.

  10. 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.

  11. 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

  12. 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?

  13. 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?

    • 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

      • Ah, I didn’t know VAP is measuring LDL-P. I seem to recall they didn’t in the past. Thanks for sharing this.

  14. 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.

    • 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.

  15. 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?


  16. 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?

    • 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).

      • Chris,
        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?

  17. 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?

    • 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.

      • 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.

        • I ordered my VAP test through directlabs.com. 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.

          • Will the regular VAP numbers and the ratios be enough? Is LDL-P a test that can be ordered directly?

            • 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.

      • 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…

  18. 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.

    • 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.

      • “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?

        • 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.

    • Charles,
      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.

      • Glenn

        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.

        • 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.

          • 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??

            • 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.

        • 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.

        • The fact remains that it is oxidation of particles that causes problems.
          In my opinion inflammatory markers are the ones to watch if there is hi LDL-P