The Difference Between LDL-C and LDL-P

Estimated reading time: 7 minutes

The lipid hypothesis, suggesting a causative role for cholesterol in atherosclerotic heart disease is by many considered one of the best proven hypotheses in modern medicine.

Measurements of total cholesterol, and the amount of cholesterol bound to different lipoproteins, are commonly used to assess the risk of future cardiovascular events.

However, recent research into the role of lipoproteins in atherosclerosis, the role of oxidation and inflammation, has indicated that cholesterol in itself does not cause atherosclerosis. It is only when cholesterol bound to atherogenic lipoproteins becomes trapped within the arterial wall, that it becomes a part of the atherosclerotic process.

Certainly, atherosclerosis as we know it will not occur in the absence of cholesterol. Thus, cholesterol is definitively involved, and necessary for atherosclerosis to occur, but so are many other important organic molecules that play a role in health and disease.

The presence of cholesterol in the atherosclerotic plaque does not prove its causative role. So, to understand the pathophysiology of atherosclerosis and the role of lipoproteins and inflammation, we may have to loosen our grip on cholesterol, at least for the time being.

Lipoproteins and Atherosclerosis

The insolubility of lipids in water poses a problem because lipids must be transported through aqueous compartments within the cell as well as in the blood and tissue spaces.

Lipoproteins are biochemical structures that enable transport of lipids throughout the body. A lipoprotein includes a core, consisting of a droplet of triglycerides and/or cholesterlyl esters, a surface layer of phospholipid, unesterified cholesterol and specific proteins (apolipoproteins).

Lipoprotein particles are commonly classified according to their density, thus the terms high density lipoprotein (HDL) and low density lipoprotein (LDL). Apolipoprotein B (apoB) is the primary lipoprotein in LDL. ApoB containing lipoproteins play a hugely important role in atherosclerosis. In atherosclerosis aplipoprotein containing lipoproteins become trapped within the arterial wall, even when blood levels of cholesterol are normal.

Atherosclerosis is a complex process. Initially, LDL and other apoB containing lipoproteins enter the arterial wall. Why this happens and why lipoproteins are retained in the wall of the artery is still not completely clear. Chemical substances called proteoglycans play an important role for the retention of apoB containing lipoproteins within the arterial wall. This chemical intrusion then appears to initiate a maladaptive and chronic inflammatory response leading to the formation of an atherosclerotic plaque. Such plaques may cause narrowing of important vessels such as the coronary arteries. A rupture of such a plaque with subsequent thrombosis may lead to an acute occlusion of a coronary artery causing an acute myocardial infarction.

The Difference Between LDL-C and LDL-P

In the clinical world, an important question is how we can use laboratory measurements to assess individual risk. Calculated, or less frequently measured low density lipoprotein cholesterol (LDL-C ) is the most commonly used marker to assess risk. LDL-C is also used to target therapy in primary as well as secondary prevention of cardiovascular disease. This is partly due to the fact that most of the cholesterol in the blood is carried in LDL’s. Moreover, there appears to be a strong and graded association between LDL-C and the risk for cardiovascular disease. However, LDL-levels may not be correctly assessed by the measurements of cholesterol carried within these particles.

Let me explain this a little bit further. LDL-C is a measurement of the cholesterol mass within LDL-particles. Due to the fact that LDL-C has been traditionally used for so many years to reflect the amount of LDL, LDL-C and LDL have become almost synonymous. This may be quite misleading, because the cholesterol content of LDL particles varies greatly.

Thus, LDL-C is a surrogate measure that only provides an estimate of LDL levels. Studies indicate that the risk for atherosclerosis is more related to the number of LDL particles (LDL-P) than the total amount of cholesterol within these particles.

It is also important to remember that LDL particles carry other molecules than cholesterol. For example, triglycerides (TG) are also carried within LDL-particles. Similar to total cholesterol and LDL-C, there is an association between serum TG and the risk of cardiovascular disease. TG molecules are larger than cholesterol ester molecules.

If the number of TG molecules in an LDL-particle is high, there will be less space for cholesterol molecules. Therefore, if triglycerides are high, it may take many more LDL particles to carry a given amount of cholesterol. Therefore high LDL particle count may be associated with small, cholesterol depleted, triglyceride rich particles. Research has shown that high levels of triglycerides are associated with small LDL particle size.

Now, what does all this mean? It means that one person (person A) may have large cholesterol rich LDL particles, while another (person B) may have smaller cholesterol depleted particles. These two persons may have the same LDL-C concentration. However, person B will have higher LDL particle number (LDL-P). Despite similar levels of LDL-C, person B is at higher risk four future cardiovascular events. Furthermore, person B will have more small LDL-particles.

Some studies have suggested that the size of LDL-particles may be of importance. People whose LDL particles are predominantly small and dense, have a threefold greater risk of coronary heart disease. Furthermore, the large and fluffy type of LDL may actually be protective. However, it is possible that the association between small LDL and heart disease reflects an increased number of LDL particles in patients with small LDL. Therefore, the LDL particle count could be more important in terms of risk than particle size in itself.

ApoB and LDL-P both reflect the number of atherogenic lipoprotein particles.  Measurements of ApoB and LDL-P are better predictors of cardiovascular disease risk than LDL-C. Furthermore, ApoB and LDL-P may predict residual risk among individuals who have had their LDL-C levels lowered by statin therapy.


Discordance is when there is a difference between LDL-C and LDL-P. If LDL-C is high and LDL-P is low, there is discordance. If LDL-C is low and LDL-P is high, there is discordance. If both are low or both high, there is no discordance.

Studies have indicated that if there is discordance between LDL-C and LDL-P, cardiovascular disease risk tracks more closely with LDL-P than LDL-C. Specifically, when a patient with low LDL-C has a level of LDL-P that is not equally low, there is higher “residual” risk. This may help explain the high number of cardiovascular events that occur in patients with normal or low levels of LDL-C.

An analysis of “Get With the Guidelines” data published in 2009 studied almost 137 thousand patients with an acute coronary event. Almost half of those had admission LDL levels <100 mg/dL (2.6 mmol/L). Thus, LDL-C does not seem to be predicting risk in these patients. However, low HDL-C and elevated TG was common among these patients. Low HDL-C and high TG is generally associated with higher LDL-P.

Among discordant patients in the Framingham Offspring Study the group with the highest risk for future cardiovascular events had high LDL-P and low LDL-C, while the group with the lowest risk had low LDL-P but higher LDL-C.

Many patients with the metabolic syndrome or type-2 diabetes have the type of discordance where LDL-P is elevated but LDL-C may be close to normal. In these individuals, measurements of LDL-C may underestimate cardiovascular risk. Measurements of ApoB or LDL-P may therefore be helpful in these individuals.

Discordance may be an important clinical phenomenon. Sometimes the question of medical therapy in primary prevention arises when there is intermediate risk, based on LDL-C. In these cases a low LDL-P level might help to confirm that the risk is indeed low, which might justify avoiding statin therapy.

Statins tend to lower LDL-C more than LDL-P. Many individuals who reach the target for LDL-C with statins, may still have raised LDL-P. This may indicate residual risk despite what is generally defined as adequate treatment.

Effect of Therapies

In general, most methods that lower LDL-C have some ability to lower LDL-P. However, there are some differences.

Much has been written about how to lower LDL-C. Most doctors will recommend eating less fat and cholesterol from meat and dairy products. Statin therapy significantly lowers LDL-C. Therapies may affect LDL-P differently. Interventions that will lower LDL-C more than LDL-P include statins, estrogen replacement therapy, some antiretrovirals, and a low-fat, high-carbohydrate diet. Interventions that lower LDL-P more than LDL-C include fibrates, niacin, pioglitazone, omega-3 fatty acids, exercise and Mediterranean and low carbohydrate diets. Although statins lower LDL-P, they may leave a significant number of patients above the LDL-P target.

Patients with high levels of triglycerides and low HDL-C  are likely to have high LDL-P despite normal or low LDL-C. Such a lipid profile is typical for individuals with the metabolic syndrome. Studies indicate that these patients may benefit most from low carbohydrate diets and that carbohydrate restriction reduces LDL-P.

LDL-P is not generally used in Europe to assess cardiovascular risk. So far, these measurements have primarily been performed in the United States. Clinical guidelines in Europe still recommend measurements of LDL-C to assess risk. Furthermore, LDL-C is still recommended to assess the effect of statin therapy. However, due to the fact that LDL-C is only a surrogate marker of the availability of atherogenic lipoproteins, its use may be of limited value. Measurements of LDL-P and ApoB are better predictors of cardiovascular risk and provide a better reflection of the atherogenic potential of lipoproteins.

41 thoughts on “The Difference Between LDL-C and LDL-P”

  1. Very nice post. Thanks clarifying this pretty complicated subject. How convincing is the evidence in your opinion that LDL-P should be the primary parameter to follow? Does it add anything on top of ApoB?

    • Thanks Reijo. The problem with the LDL-P measurements using NMR spectroscopy is that it is still rather expensive. It has been suggested that looking at non-HDL cholesterol (total cholesterol minus HDL cholesterol), HDL-C and triglycerides may be helpful when LDL-P and ApoB are not available. This could be important in patients with the metabolic syndrome, where LDL-C may underestimate risk. Non-HDL cholesterol reflects the cholesterol within all lipoprotein particles currently considered ateherogenic. Many studies have indicated that it is a better predictor of cardiovascular events than is LDL-C. However I still think LDL-P measurements may often give important additive information and I my guess is that it´s use will become more common in the near future. However, the clinical utility of these measurements is still limited because the technique is not widely available and it is relatively expensive.

      In clinical terms, LDL-P does not add much to ApoB. LDL-P measures the number of LDL-particles while ApoB measures the number of all atherogenic particles (chylomicrons, VLDL,IDL,LDL and Lp(a)). Usually 85-90% of ApoB represent LDL-particles.Therefore, in most cases you don´t need ApoB if you have LDL-P available and vice versa.

  2. I like your question Reijo. I hope we can get an answer. In my case I have discordance between APO-B and LDL-P. I’d sure like to know how that can happen. My APO-B is low-normal but LDL-P is “high risk” so nothing has been clarified for me as yet.


  4. “l…HD-CL and triglyserides …important in patients with the metabolic syndrome, where LDL-C may underestimate risk” Have you a solid reference to this statement? Would be very interesting as almost all the fuss is about LDL-C.

    • Reijo. Here is a study on the use of Non-HDL cholesterol to predict risk in patients with type-2 diabetes. It is a stronger predictor of risk than LDL-C. Another study arrived at the following conclusion: Non-HDL is a stronger predictor of CHD death among those with diabetes than LDL and should be given more consideration in the clinical approach to risk reduction among diabetic patients. Here is another study comparing ApoB and Non-CHDL cholesterol with LDL-C.
      In this short video Dr. Richard F Wright explains discordance and the populations most likely to be at increased risk despite normal LDL-C. It turns out that that patients with diabetes often have high LDL-P despite normal LDL-C. Here Dr Thomas Dayspring explains why LDL-C is a much worse predictor of risk in insulin resistant patients than ApoB or LDL-P.

  5. Excellent post. Here is another study: Cui Y, Blumenthal RS, Flaws JA et al.: Non-High-Density-Cholesterol Level as a Predictor of Cardiovascular Disease Mortality. Arch Intern Med. 161, 1413-1419 (2001).

    • @ Richard. Evidence suggests that there is an association between TG/HDL-C ratio and cardiovascular risk. This ratio has also been shown to be associated with insulin resistance. Thus, the higher your TG and the lower your HDL-C, the greater degree of insulin resistance. Therefore it may be particularly helpful in individuals with the metabolic syndrome where the traditional LDL-C often underestimates risk.A TG/HDL-C ratio above 3.5 has often been used as cutoff for identifying insulin resistance. As you say, this ratio is easy to obtain, it is included in the traditional lipid panel, and therefore relatively cheap.

  6. I get asked many times why the arterial wall gets damaged in the first place. I am also asked if this can be reversed – the implication being by non surgical/medicinal means.
    I know smoking, insulin spikes etc. can lead to inflammation, but why does (rhetorical) the wall become weakened before this happens. Age? Yes possibly…… and yet I still seem to need to dig deeper, especially when arterial damage was detected in me at the age of 49 years – not particularly ancient!

    Have you ever considered the Rath – Pauling theory? Explained here by Dr. Dach.

    Curious and also wondering what your treatment regime would be for natural reversal of plaques?

    Clare in Tasmania

  7. As far as I know the only attempt to establish a logical hypothesis of atherosclerosis explaining at least a big chunk of observed data is the one by Drs. Ravnskov and McCully where damage is first inflicted in the vasa vasorum: see for example Infections May Be Causal in the Pathogenesis of Atherosclerosis (available at last International Health News issue). For me confusing correlation with causation (LDL-P hypothesis?) and ignoring how LDL particles jump through supposedly healthy tissue doesn’t cut it.

    This being said I am all in for vitamin D, magnesium, vitamin C, vitamin K2, iodine etc.

  8. This article was hugely helpful albeit upsetting for me. I am a very fit 38 y/o male; I bike race and have always enjoyed a high carbohydrate/low fat diet. After getting the VAP test, it turns out my LDL-P is 1733 nmol/L !! Total Chol is 202, LDL-C Direct = 127, HDL-C = 63, TG’s=104. My father has CAD. I took Lipitor for 40 days and developed severe, debilitating muscle pain in my wrists, forearms and biceps. After 2 weeks off it I can start to pick up my 6 mo. old son again. I’m terrified of the statin drugs but do I have no other choice? Should I restrict CHO’s? Should I get a more specific test like the NMR LipoProfile? Thank you for responding.

    • Lipitor 95% ineffective but it may lower your LDL-c.
      Try a higher fat diet instead of high carb diet. The carbs may be causing inflamation. People are way too antifat. Just keep the calorie levels within needed limits. At least limit the carbs try around 100g a day and get therest from high protein medium fat diet. Get much of the carbs from fruits and veg as possible. Then test in 6 months. Fatty fish nuts etc but also meat fat i truly believe has benefit especially when eaten with veg and tje meat and nutrients it comes with.

      Sometimes bro science works better than medical science. Because they are slow to adopt new natural treatments and focus on only what they can prove over time clinically.

  9. Great article. Very helpful in understanding LDL-P. I have high LDL-C, LDL-P, and apoB. In addition, I was tested and told my LDL are the “large and fluffy” ones. Yet I still have damage. I have about 60% blockage in my carotid- so atherosclerosis is there despite my LDL size. I’m trying to understand the cardiac risk relationship of LDL-P and the size of the particles. I keep reading “large and fluffy” LDL is not suppose to be harmful (or as the link above says “relatively benign”). I don’t see how that is true- looking at my own labs. Can you shed some light on this or provide additional links that don’t just explain what size is but the thinking/facts/studies behind the larger size and lower risk factor? At some point does high LDL-P negate the size and size no long becomes protective or benign? Do we know those tipping point levels or have answers to these types of questions yet? Thanks so much!!

    BTW I’m only 42 and been vegetarian most my life and am active. I’m getting genetic testing to confirm probable FH or FDB.

    @ Dan – I can’t tolerate statins either and need more than lifestyle to lower my Total Cholesterol, LDL-C (my TG are normal). I’m in a clinical trial for a new drug that lowers LDL-C levels (I don’t know if it lowers LDL-P and/or apoB too). It doesn’t appear to have the muscle degrading problems that people experience on statins. It’s still in it’s trial stage but seems promising. You may want to look into it – it’s a PCSK9 inhibitor.

    • Try eating a different diet. Carbs are maybe the culprit elevating insulin levels and affecting hormones. I personally dont agree with the so called science behind vegitarian diets.

      I mean your unhealthy so maybe try a new diet for 6 months. Low carb high protein relatively higher fat and variety of foods.

  10. 60 year old woman. Had the very expensive blood tests. The results of my tests are all over the place.

    total cholesterol: 184 (optimal)
    LDL-C: 116 (intermediate risk)
    HDL-C: 56 (optimal)
    Triglycerides: 82 (optimal) under 150 is optimal, so mine are great
    Non-HDL_C: 128 (optimal)
    sdLDL-C:20 (optimal)

    All looks great. BUT …

    ApoB: 94 (high risk)
    LDL-P: 1596 (high risk)
    Lp(a) Maa: 73 (high risk)
    Lp(a)-P:268 (high risk)

    From what I read, Lp(a) is genetic and nothing I can do about it.

    From your article, looks like I have “discordance” and I’m not the typical patient. Triglycerides are opposite of ApoB and LDL-P.

    sdLDL-C being 20 looks like I have few small, dense LDL particles. That is great. But LDL-P is 1596, which means I have LOTS of LDL particles, and that isn’t good. And APO-B is total of ALL atherogenic particles, and mine are very high.

    Have not had any cardiac incidents and have no idea what my arteries look like.

    What to do …. what to do ….

    • Enjoy your life. Stop stressing about it
      Probably stress will cause more risk for heart disease than your numbers. It especially affects stress related hormones and that is bad.

  11. i had a heart attack 6 years ago , i went through a bypass operation and had to change 4 arteries that were totally blocked .
    My cholesterol levels were normal and my sugar level was good so i never knew the reason for what happened .

    Last week ( six years later ) i made this test showing the LDL-P and was shocked to learn they are above 2000 despite normal LDL-C (91) normal triglycerides levels (116 ) & normal total cholesterol (158)

    So i guess the LDL-P is the most important indicator to assess a risk factor , i am on Crestor 20 but it doesn’t seem to have any affect of it , My Dr has added Zetia 10mg and i will see its effect in my next blood test 3 months from now .

  12. I see in my practice all to common, people hold a false security. Their LDL-p still lives above 1500 and their CRP> 5 and their HbA1c > 6.

    I belive it is like carmolizing an onion. The inflation is the heat, which causes the sugar to damge the endothelial tissue, which allows the LDL-P to infiltrate – thus causing plaque to accumulate.
    Metabolic syndrome seems to be the perfect storm for CAD creation.

    I have also witnessed the lowering of LDL-P by 50% in 4 weeks by eliminating homoginted fats from the diet and adding avicodo and almonds.
    Overall I’m of the opinion that statins are over rated and encourage a false seance of security – the American Dream.

  13. Dear Dr Sigurdsson,
    I have had very discordant lipid profile tests over the past few years. I’m 35 yrs old Male with family h/o MI in my father @ 65 yrs of age (he had poorly treated high LDL-C and HT). My mother has typical metabolic syndrome.
    I have Gilbert’s syndrome (supposedly associated with high HDL and low CAD).
    ~5 yrs ago, I had a HDL of 76 mg/dl, LDL of ~ 55 mg/dl and Total Cholesterol ~ 150 with low TG. I was exercising regularly and was quite fit (nowhere near a college athlete).

    With the VAP test in Nov 2013, My profile was (non- fasting)
    Total cho: 194, LDL-P 2181 !!! TG- 249 HDL only 60!, LDL total- 106, Apo B 95, Apo A1 167,
    IDL- 9, Total VLDL- 27, VLDL3- 12. LDL density pattern buoyant.

    I wasn’t as fit but by no means overweight,etc with good diet. I couldn’t believe and I rechecked with my family doc, who could only do a routine profile and now the values for HDL are off again.. HDL ~ 55 or something.

    I have 3 questions:
    1) HDL usually remains constant and is genetic (as far I know) + Gilbert’s have high HDL. So why my HDL is fluctuating to this extent.
    2) How can the LDL particle count be so high although the TG aren’t that high.
    3) Is a low density LDL (buoyant) associated with a lower or a higher risk for CAD?
    I apologize for a long post but could’nt make it shorter. Thank you very much.

  14. So right and well described. I was trying to explain this to my Japanese doctor but unfortunately hes too old and my Japanese is not good enough. Medical practice is behind clinical research. He saw elevated LDL-C and was wondering why i wouldnt want to take statins. No further testing or diet was suggested. I am also a eeightlifter with 13% body fat and 44years old. Tg and HDL were normal. But of course my BMI says im obese because i have muscle mass- 74kg and 5foot7.

    • “Medical practice is behind clinical research” Wow. What an understatement. Thats the whole reason for this thread.

  15. could be more concise at the outset, just defining each one in first paragraph so we don’t need to wade through it to extract the information.

  16. If both are low or both high, there is no discordance.So does this mean I can use ldl-c as my marker??And if not why?Thanks Doc

      • Thanks Doc…I have been getting the NMR for 3 years now and every time my ldl-c went up or down my ldl-p followed…latest ldl-c was 73 ldl-p is 722.

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  18. Nicely written article – thank you!
    My Question is when there is a discordance between LDL P and ApoB? Would you try therapies to address LDL P?

    Total Cholesterol 172
    Trigs 31,
    LDL C (NMR measured) 97,
    HDL 78
    Non HDL Cholesterol 94
    ApoB 80 and LDL P 1300

    This is lean male, 40s, exercises and on low carb diet, either in ketosis or flirting with it at all times. And is not main lining saturated fat…although it is present in diet

    Thanks again!

  19. What is the VAP test? I do keto – healthy fats only, very low carbs. My A1C is well within normal levels, where it was high before I started keto. Of course my doctor want to put me on statins. I’m not at all convinced that I need them and would like to learn more about what my numbers actually mean.

    My fasting results are:
    Component Your value Standard range
    Cholesterol 292 mg/dL 0 – 199 mg/dL
    Triglyceride 105 mg/dL =40 mg/dL
    LDL, Calculated 212 mg/dL <130 mg/dL
    Non HDL Chol, Calculated 233 mg/dL <=159 mg/dL
    Cholesterol/HDL Ratio 4.9

  20. Hi! I’m a 51 year old female. 5’6″ 132lbs. Fit and exercise. My Dad, an ER physician with about the same build, died at 51 after a jog, was on statins with cholesterol about 210 and the autopsy showed 98% blockage (occlusion?) and possible prior heart attacks he didn’t know about. Mother just had a triple bypass at 70. Bad family history. My Dad and I have been watching my cholesterol since I was 16 yrs old. Generally heart healthy diet..rarely have cheese or creams, never vegetable oil….only olive oil…. No clue what has caused this recent spike except I have been cutting back on red meat eating turkey and chicken. I have not gone through menopause yet. Any ideas? Oh, my calcium score on the X-ray was 0. I’m pretty scared about these latest numbers.

    I just had the following results from NMR lips Profile
    LDL-P: 1695 (in 2018 was 1258)
    LDL-C: 134 (in 2018 was 109)
    HDL-C: 91 ( in 2018 was 77)
    Trig: 119 (in 2018 88)
    Total Cholesterol: 245 (was 204 in 2018
    Small LDL-P <90 (same in 2018)
    HDL-P 38.5 (in 2018 was 35.3)
    LDL size 22.1 ( in 2018 was 22.3)


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