What Causes Elevated LDL Particle Number?

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

In the last article in this series, I explained that LDL particle number (LDL-P) is a much more accurate predictor of cardiovascular disease risk than either LDL or total cholesterol. In this article, I’m going to briefly outline the five primary causes of elevated LDL-P.

Conventional medicine is primarily focused on suppressing symptoms. If your blood pressure is high, you take a medication to lower it. If your blood sugar is high, you take a medication to lower it. If your cholesterol is high, you take a medication to lower it. In most cases there is rarely any investigation into why these markers are high in the first place, with the possible exception of some basic (but often incorrect) counseling on diet and exercise.

On the other hand, functional medicine—which is what I practice—focuses on treating the underlying cause of health problems instead of just suppressing symptoms. If your blood sugar, blood pressure or cholesterol are high, the first question a functional medicine practitioner will ask is “why?” If we can identify the root cause of the problem, and address it at that level, medication is often unnecessary.

To use a simple analogy, if you have weeds in your garden, what happens if you just cut the weeds from the top? They grow right back—and sometimes faster than before! If you really want to get rid of them once and for all, you have to pull them up by their roots.

With this in mind, let’s look at some of the potential causes of elevated LDL particle number. If your LDL-P is high, it makes sense to test for and treat any of the conditions below (with the exception of the last, which is genetic and thus can’t be treated) before—or at least along with—taking pharmaceutical drugs.

5 common causes of elevated LDL particle number that can increase your risk of heart disease.Tweet This

Insulin resistance and metabolic syndrome

LDL particles don’t just carry cholesterol; they also carry triglycerides, fat-soluble vitamins and antioxidants. You can think of LDL as a taxi service that delivers important nutrients to the cells and tissues of the body.

As you might expect, there’s a limit to how much “stuff” that each LDL particle can carry. Each LDL particle has a certain number of cholesterol molecules and a certain number of triglycerides. As the number of triglycerides increases, the amount of cholesterol it can carry decreases, and the liver will have to make more LDL particles to carry a given amount of cholesterol around the body. This person will end up with a higher number of LDL particles.

Consider two hypothetical people. Both have an LDL cholesterol level of 130 mg/dL, but one has high triglycerides and the other has low triglycerides. The one with the high triglyceride level will need more LDL particles to transport that same amount of cholesterol around the body than the one with a low triglyceride level.

Numerous studies have found an association between increased LDL particle number, and metabolic syndrome. One study measured ApoB, a marker for LDL particle number, in a group of 1,400 young Finns with no established disease. The participants with the highest LDL particle number were 2.8 times more likely to have metabolic syndrome than those with the lowest levels of LDL-P. (1) A much larger study of over 300,000 men also found a strong association between LDL-P and metabolic syndrome and its components (i.e. insulin resistance, abdominal obesity, high blood pressure, etc.). (2)

Poor thyroid function

Poor thyroid function is another potential cause of elevated particle number. Thyroid hormone has multiple effects on the regulation of lipid production, absorption, and metabolism. It stimulates the expression of HMG-CoA reductase, which is an enzyme in the liver involved in the production of cholesterol. (As a side note, one way that statins work is by inhibiting the HMG-CoA reductase enzyme.) Thyroid hormone also increases the expression of LDL receptors on the surface of cells in the liver and in other tissues. In hypothyroidism, the number of receptors for LDL on cells will be decreased. This leads to reduced clearance of LDL from the blood and thus higher LDL levels. Hypothyroidism may also lead to higher cholesterol by acting on Niemann-Pick C1-like 1 protein, which plays a critical role in the intestinal absorption of cholesterol. (3, 4)

Studies show that LDL particle number is higher even in subclinical hypothyroidism (high TSH with normal T4 and T3), and that LDL particle number will decrease after treatment with thyroid hormone. (5)

Infections

Another cause of high cholesterol profile is infection. Multiple studies have shown associations between bacterial infections like Chlamydia pneumoniae and H. pylori, which is the bacterium causes duodenal ulcers, and viral infections like herpes and cytomegalovirus and elevated lipids. (6) For example, H. pylori leads to elevated levels of total cholesterol, LDL cholesterol, lipoprotein (a), ApoB or LDL particle number, and triglyceride concentrations as well as decreased levels of HDL. (7)

Several mechanisms have been proposed to explain the association between infections and elevated blood lipids. Some evidence suggests that viral and bacterial infections directly alter the lipid metabolism of infected cells, and other evidence suggests that lipids increase as a result of the body’s attempt to fight off infection. Other evidence suggests that LDL has antimicrobial properties and is directly involved in inactivating microbial pathogens. This has been confirmed by studies showing that mice with defective LDL receptors—and thus very high levels of LDL—are protected against infection by gram-negative bacteria like H. pylori. (8)

Leaky gut

One of the primary functions of the intestinal barrier is to make sure that stuff that belongs in the gut stays in the gut. When this barrier fails, endotoxins such as lipopolysaccharide (LPS) produced by certain species of gut bacteria can enter the bloodstream and provoke an immune response. Part of that immune response involves LDL particles, which as I mentioned above, have an anti-microbial effect. A protein called LPS-binding protein, which circulates with LDL particles, has been shown to reduce the toxic properties of LPS by directly binding to it and removing it from the circulation. (9) Studies have also shown significant increases in LPS-binding protein (and thus LDL particles) in cases of endotoxemia—a condition caused by large amounts of circulating endotoxins. (10)

Though more research is needed in this area, the studies above suggest that a leaky gut could increase the level of LPS and other endotoxins in the blood, and thus increase LDL particle number as a result. I have seen this in my practice. I recently had a patient with high LDL-P and no other risk factors. I tested his gut and discovered H. pylori and small intestine bacterial overgrowth (SIBO). After treating his gut, his LDL-P came down to normal levels.

Genetics

The final cause of elevated LDL-P is genetics. Familial hypercholesterolemia, or FH, involves a mutation of a gene that codes for the LDL receptor or the gene that codes for apolipoprotein B (ApoB). The LDL receptor sits on the outside of cells; the LDL particle has to attach to the LDL receptor in order to deliver the nutrients it’s carrying and be removed from the circulation. ApoB is the part of the LDL particle that binds to the receptor. If we use a door lock as an analogy, apolipoprotein B would be the key, and the LDL receptor is the lock. They both need to be working properly for LDL to deliver its cargo and to be removed from the bloodstream.

Homozygous carriers of FH have two copies of the mutated gene. This condition is very rare. It affects approximately 1 in a million people. And people that are homozygous for this mutation have extremely high total cholesterol levels, often as high as 1000 mg/dL. And unfortunately they usually die from severe atherosclerosis and heart disease before the age of 25.

Heterozygous carriers, however, only have a single copy of the mutated gene, and the other copy is functioning normally. This is much more common. The prevalence is between 1 in 300 to 1 in 500 people, depending on which study you look at. These heterozygous carriers of FH have total cholesterol levels that often range between 350 and 550 mg/dL, along with very high LDL particle number. They have about three times higher risk of death from heart disease than people without FH if it goes untreated.

It’s important to note that people with FH have primarily large, buoyant LDL particles, and yet are still at much higher risk for cardiovascular disease. While it’s true that small, dense, oxidized LDL particles are more likely to cause atherosclerosis, large, buoyant particles can also be harmful when their concentration is high enough. This is one reason why LDL particle number is a superior marker to LDL particle size.

In the next article in this series, I will debunk the myth that statins extend lifespan in healthy people with no pre-existing heart disease.

Like what you’ve read? Sign up for FREE updates delivered to your inbox.

  • I hate spam too. Your email is safe with me.

Comments Join the Conversation

  1. John says

    Thank you for this, and your whole series. Very informative!

    My question relates to the following, “Thyroid hormone also increases the expression of LDL receptors on the surface of cells in the liver and in other tissues. The decrease in the number of LDL receptors then leads to reduced clearance of LDL from the blood and thus higher LDL levels.”

    The transition between the two sentences confused me. Would it be correct to interpret the second sentence like this? “If thyroid hormone is too low, this can result in an insufficient number of LDL receptors, which leads to reduced clearance of LDL from the blood and thus higher LDL levels.”

    Thanks,
    John

  2. says

    I would like to commend you for focusing on the topic of VLDL particles and metabolic syndrome, esp. heart disease. I became familiar with this topic reading Dr. William Davis’s book _Wheat Belly_. Now that I encountered your blogs on the topic, I found the science on this more reassuring. Davis discusses this topic in his tenth chapter alarmingly stating that 98 percent of physicians do not know much about this. It’s called “My Particles Are Bigger Than Yours: Wheat and Heart Disease,” and in it he implicates wheat consumption as the culprit in inducing the increased production of small LDL particles that cause atherosclerosis plaque.

    • Chris Kresser says

      The research has progressed since Dr. Davis wrote his book. It’s now clear that the number—not the size—of LDL particles is a more significant predictor of risk. People with small, dense LDL are more likely to have a higher LDL particle number, but that’s not always the case.

      • StenBjorsell says

        William Davis says indeed in his book Wheat Belly that the only way to asses LDL particle size is through LDL particle number, or the measure called apolipoprotein B, giving one count per LDL particle. Whatever the exact connection, he says to measure same thing. Another measure is apolipoprotein A which does same for HDL and the quotient (ap-B/ap-A) was found in the huge Inter heart study to be best available.predictor of heart attack or risk for it: Double it and the risk doubles, etc. Normal range 0.7-0.9. Elevated above and reduced below. After a year on low carb my was 0.63. Before I had severe effort angina that disappeared after a month or more on strict low carb eating. Indeed Davis emphasize that it is excess carbs that move blood sugar and triglycerides high after every meal that is the main culprit, which agrees with my case 100% but we are not all exactly the same. The metabolic processes from high VLDL to high triglycerides and many and small LDL particles are however very similar and Davis has used it for years to help his cardiac patients to reverse heart disease. In my opinion too much carbs causing metabolic syndrome is corrected the 4 other causes mentioned can be looked as at dine adjustments. And not limiting the carbs means the others will have small or no effect.
        It may cost a little more to measure apo_B and apo-A but it is even a lot less than statin medications for a year, and doingthe right things they can then usually be removed, so with its side effects in increased risk for depression and hormonal disturbances due to insufficient raw materials to produce the hormones: LDL cholesterol!
        My 5 cents.

  3. syd says

    I appreciate all your hard work and enjoy your posts.

    FYI: My doc is a cutting edge, holistic cardiologist and says even the LDL particle number is part of the obsession with cholesterol, etc. and not a helpful focus as it relates to heart disease.

    • Chris Kresser says

      I’ve presented a lot of research that suggests otherwise in this series. Ultimately everyone has to make their own decision.

      What I would say is that heart disease is multifactorial and complex, and there is no single marker that can accurately predict risk. LDL-P is a useful marker, but it’s only part of a much larger picture.

      • syd says

        Just hope folks can see the forest for the particle-trees, but absolutely agree. Thanks again for your ongoing work.

          • eddie b says

            Cant one with a wound /say surgery have a larger amount of LDL-P or even try’s since the role of cholesterol is to go to the area in need to heal???? and rebuild the area?? was wondering as I have been playing with my health for almost 2 years… I had crohns disease but with a diet of paleo / candida I have removed my disease.. Never any big pharm meds. I ve used many advanced tests not commonly used and can show yeast and low bacteria as my cause…mainly YEAST The more fat I have consumed…. and as my levels raised.. my health has gotten better.. But ive noticed my LDL-P raise but I had a good size wound from surgery 2 1/2 months ago… my diet has stay pretty much the same except for alot of avacado… but wonder if the real reason say in ones case like me the up tick LDL-1230 to 1435 could be from diet or the wound my small LDL was 128 now 135

    • Chris Kresser says

      That would be more like a series, or rather a book! I did create the High Cholesterol Action Plan with that in mind. I originally planned it as a series of blog posts, but it turned into a 9-week course with a massive amount of content because it’s such a detailed subject.

    • Chris Kresser says

      Forgot to mention: the final article in this series will have general recommendations based on everything we’ve covered so far.

  4. Pam Schoenfeld says

    I highly recommend the high cholesterol action plan. My husband has what we think is heterozygous familial hypercholeterolemis (say that fast 3 times!) so we are going through each of the modules. Both his parents had pretty high cholesterol levels, but we have not had genetic testing as of yet due to the expense. We have at this point decided that since his LDL particle number is high, we need to reduce it. Besides a lower carb moderate fat diet with a little less saturated fat, he has started taking with Red Yeast Rice/lipotrienols, which worked to lower his total cholesterol from over 280 to 230 in less than a week – we are doing home testing to monitor his progress. We will follow with another LDL- P test in a couple of months. If it was not for work by Chris Kresser (and others such as Chris Masterjohn and Peter Attia) we would not have the understanding of how to handle this situation. Thanks!!!!

      • Pam Schoenfeld says

        I am assuming this is not Chris Kresser’s question ;-).

        I think from what I have read a quality RYR has less side effects than pharma statin meds. Certainly, liver enzymes and CPK need to be monitored, and CoQ10 is taken with it. But for some people diet won’t do very much, and I think that is where my husband is. He has no signs or symptoms of low thyroid. He may have some mercury toxicity, but his strong family history probably means he is genetically pre-determined to have high LDL P. We need to get the genetic test at some point – it is just that our bare bones med insurance does not cover lab tests. Direct Labs BTW is great.

    • Myhealthtoo says

      I seem to have high cholesterol for at least 20 years and still can’t get it under control I don’t eat red meat just chicken veggies, fruit mostly organic foods always good food. exercise at least one or twice a week I am 5-11 weigh 170 or a little less. My family from both sides of my parents don’t have chesterol problems, statins always give reaction to my liver and muscles so I am trying Red yeast rice two pills a day with food. It’s been second day and my muscles are aching. Total cholesterol is 266 and trycls are normal. Dont smoke never did drink wine red on occasions or social gatherings don’t take any other meds the only thing I could be guilty of is going to bed late and waking up early but that it. Please help with any ideas thank you!

  5. Sean Grady says

    I do Crossfit and am also fully Paleo. I am also recovering from a triple bypass on January 30. I’ve had 2 labs this year. One just before my surgery and the 2nd in the middle of April. They both give me numbers, on LDL, HDL, VDL, etc. My problem is I don’t know what they mean. They have an “Expected” amount next to my measured amount, nut no other guidance. My cardiologist is useless. In fact he’s mad at me for discontinuing the statins and beta blockers he put me on (they were making me miserable). How do I decipher the numbers?

    • Whitefox says

      http://www.mayoclinic.com/health/cholesterol-levels/CL00001

      TC is total cholesterol and is basically the sum of LDL(all types)+HDL.
      LDL is a sum of all LDL types.
      VLDL is a subset of LDL (stands for Very Low Density Lipoprotein) and it is typically good to have this number be as low as possible because VLDLs are precursors to small, dense LDLs (sdLDLs) which are the most dangerous (most likely to cause atherosclerosis) type. So compare your numbers to those ranges of “desirable” numbers and see if you can get them in that range – note: when MayoClinic states that REALLY low LDL isn’t a bad thing, they’re wrong – it’s associated with higher stroke rates.

      Obviously, ignore the diet advice on page 2 of the MayoClinic link, because they don’t know what they’re talking about. Paleo’s fine, and cholesterol in your diet isn’t cholesterol in your bloodstream (ignore your cardiologist if he’s worrying about this).

      Hypertension (and healthyness in general) can be helped by controlling your Na+/K+ ratio, so no added table salt (maybe a little sea salt is okay) and plenty of veggies. But maybe you’re probably on beta blockers just to prevent a future heart attack and aren’t hypertensive? Either way it’d help.

      Lastly, cholesterol numbers can be helped by lots of intense crossfit, as-strict-as-you-can-handle paleo (low sugar), lots of sleep, not overtraining the crossfit (but do workout hard at least 3 days a week), and having fun. Good luck

  6. Jenny says

    This is great information. For those that are genetically handicapped with high levels of LDLs what alternatives do you recommend to lower them? Is there a specific supplementation protocol they should follow besides a clean diet and exercise?

  7. says

    My12 year old adopted daughter’s blood work just came back as having high total cholesterol with normal triglycerides but especially high LDL. She is very thin and eats very little meat but her doctor recommended a vegetarian diet anyway and mentioned she may need medication later. Her TSH was normal but she does have a nodule on her thyroid which we are going to need to follow up on. I have started her on fish oil and am considering asking her doctor about artichoke extract as I have heard it can lower LDL. Are there any other tests that she should have? I have no family history. Should she be tested for FH?

    • gregory barton says

      This is a matter of contention.

      On one hand, there are those who claim that there is no connection and that the claimed connection is a myth to discredit low carb.

      On the other hand, there are those who claim that carbs are necessary to convert T4 to T3 and that dropping carbs too low can inhibit this conversion leading to hypo symptoms and/or promote reverse T3 dominance.

      In the middle is the camp that suggests that dropping carbs too quickly is the culprit and that a gradual reduction of carbs obviates this problem.

      Sorry I don’t have references up my sleeve. But all of these claims can be googled.

      • Whitefox says

        http://high-fat-nutrition.blogspot.com/2012/07/measuring-thyroid-hormone-level-is-very.html

        “Summary: Despite the limited fall in T3 on higher carb diets, the brain is not happy with thyroid status. TSH goes up. Gimme gimme gimme, more more more.

        So will low carbohydrate eating lead to thyroid deficiency? Who knows, in the long term. This was a very short study. But in this paper the brain seems quite happy with 108ng/dl of total T3 as judged by a TSH of 1.11microIU/ml.

        This does not look like hypothyroidism to me.”

        Higher carb was like 200 and 300g/day and the low-carb was 50g = ketosis = VLC.

  8. David says

    In my last bloodwork my LDL was 150 but my HDL was 107 and my triglycerides were 26. Is it safe to say I probably have a low LDL particle number?

    • Pam Schoenfeld says

      Hey David – if your doctor does not want to run the LDL P – go through direct labs if you can.

      • Lian says

        From what I’ve seen I would think it’s safer to assume you have a high ldl particle count. Ldl-p tends to go up with LDL for people without some kind of metabolic syndrome.

        • Zain says

          I tend to disagree.
          His TGs (Triglycerides) are very low and his LDL-C is high according to the conventional standards.
          An LDL particle is a carrier of TGs and LDL-C (along with other things). A healthy LDL particle is large, and it is also “cholesterol-enriched” which means it should have 4 times more cholesterol than TGs.
          His low TGs indicate that his LDL particles are cholesterol-enriched, and this will result in not needing a whole lot of LDL particles to transport the cholesterol. So, there is a good likelihood that his LDL-P is normal and he should get it tested.
          In cases of metaboblic syndrome, the TGs are high and the LDL particles are “cholesterol-depleted” as they have to pack on a lot of TGs on them thereby compromising the cholesterol content. This results in a high LDL-P count even if the LDL-C is normal.
          Dr. Kresser has explained it well in this article and
          Dr. Thomas Dayspring explains it well too:

    • Whitefox says

      Are you otherwise healthy? Eating healthy, working out, not very overweight etc?

      Your LDL is “high” by doctor standards but your HDL is also quite high. Triglycerides are quite low (I assume that’s in mg/dl). VLDL = 5.2 TC = 262.2 calculated from your LDL, HDL, and Trigs.

      Your ratios are: HDL/TC = .41 (should be > .24) check. Trigs/HDL = .24 (should be < 2) check.

      So without knowing how healthy you are… you seem healthy haha.

  9. Tamee says

    What are your thoughts on risks/benefits of red yeast rice and Niavasc? I was told my particle number is “high” and my doctor recommended both of these products, as well as fish oil. From what I have read, the red yeast rice contains the same component as a statin drug (monoclonin K I think) and there are risks of liver and renal failure. I think insulin resistance is more a cause of this in my case. Is it possible to lower the particle number with diet, exercise, and “natural” supplements such as the fish oil, or at what point are these products, and/or statins necessary?

  10. Claudia Santiesteban says

    Thank you Chris.
    I have a question regarding the metabolic syndrome section. You mentioned that “there’s a limit to how much “stuff” that each LDL particle can carry” and that higher levels of triglycerides will result in the creation of more LDL particles. Since the LDL particles also carry cholesterol, wouldn’t the same thing happen if cholesterol levels were higher? If so, then it seems like we once again have to question whether cholesterol is the culprit. And I don’t mean to go against anything you’ve said, I’m just trying to understand the facts. I would, therefore, really love to see your response. Thanks!

  11. Gin says

    Repeating my question of 6/26…

    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?

  12. Sharon says

    Byron Richards, clinical nutritionist who wrote Mastering Leptin, claims that giving thyroid hormone is not an effective or safe way to fix the thyroid.
    He thinks it can cause damage in the long run. His advice is iodine, tyrosine and a few more things that slip my mind right now. I know you will say that iodine feeds Hashimoto’s, but he claims that by getting to the root cause of why the thyroid is showing symptoms, you avoid misdiagnosing and he feels that MDs as well as alternative docs are just going right to the cabinet for thyroid hormones and this is not a good thing.
    Yes, he sells products, but doesn’t everybody these days? Any thoughts on his logic, Chris?

    • Bet says

      The thyroid is showing symptoms because it’s being attacked by antibodies. The root of the problem can be diet, especially gluten. But for most people, once the thyroid has been affected, it’s not likely to become completely functional again, even after changing your diet. I was gluten free for a year, but when I tried not taking synthroid, my TSH levels were through the roof, the highest they’ve ever been. If found early enough, perhaps with diet the thyroid will not be destroyed. But if you don’t have symptoms, then how would you know enough to change your diet?

  13. Glenn Atkisson says

    Chris, thanks. This is a great follow-on to the first article on LDL. It’s always good to get down to the nitty-gritty of the cause. This is all still assuming that LDL particle number is indicative of, and therefore a good marker of a serious condition that we need to correct. You have convinced me that it just may be!

    I like the detail on each of the sections here. Maybe you can also provide another article on some holistic solutions to each of these.

    For instance, that just cutting out consumption of excessive carbohydrates can immediately reduce tryglycerides, which, as you point out will reduce the need for vast numbers of LDL particles. What is of course of great importance to the reader is that the cutting of carb calories will eventually remedy insulin resistance and metabolic syndrome. LDL particles are a marker. Insulin resistance is a symptom. But what people should be most focused on is getting back to health, and eliminating disease (diabetes and cardiovascular disease, most likely, in this case), so it would be nice to end the series wrapping up with what can really be fixed if one improves their “marker” and reduces the “symptoms”. I’m afraid that sometimes people get lost in the details of the markers and forget that they should always demand to see that their footsteps lead them very clearly to better health. I know that you can do this with your method of breaking even difficult subjects into digestible pieces and presenting only one piece at a time. Keep up the good work.

    To continue the request, I would like it if in the future you could go more into the Poor Thyroid section as it pertains not just to energy, but lipid transport and metabolism, and numbers of LDL particles as a possible reaction to something so simple as insufficient iodine available for chemical reactions and disease prevention. According to Jack Kruse, iodine is critical in preventing oxidation of lipids during transport.

    http://www.jackkruse.com/brain-gut-12-dare-to-disagree/

    Iodine is such a powerful protector of our species from Reactive Oxygen Species (ROS), and can protect our giant brains from oxidation of our AA and DHA resident there, which vitamin C has no chance of effecting, that Kruse speculates that this is precisely the reason our species no longer produces vitamin C. There is no way, bodily to produce enough vitamin C to protect our overgrown brains. Iodine can do it though.

    My feeling is that iodine is so important, and yet so deficient in the average population, that what we call “thyroid problems” is probably just a very handy wake-up call to modern science to fix the much larger problem of infections due to inadequate iodine by simply educating the public to it’s importance. Therefore, iodine shortage may be another cause of heightened LDL particle numbers.

    I’m looking forward to more on all this in your atticles in the future. Thanks again for the diligent research!

    • Whitefox says

      Iodine’s clearly important, but isn’t table salt iodinated such that iodine deficiency isn’t so common anymore? Or do you have data showing that the supplementation hasn’t helped?

  14. Jason says

    Chris: could you verify that FH people die before young. I heard that some of FH can live in their eighties.

    Thanks for the article.

  15. Robert Cooney, MD says

    Chris,

    You don’t need an expanded lipid panel to identify or treat the conditions you discussed in your piece. It is an unnecessary expense in this day and age.

    Regards,

    Robert Cooney, MD

    • Heather says

      Unnecessary expense??? To whom? If the patient wants the test then it isn’t an unnecessary expense to him. Unnecessary expense to you? How much does it cost you to let a patient get a more thorough test. So if one of your patients said “I want this test” you would tell him it’s an unnecessary expense and that he doesn’t need it?…I’m glad you’re not my doctor.

  16. Merpig says

    Yeah, 3 years ago I had total cholesterol of 296 and LDL-P of 2018. I have Hashimotos and while i begged to try Armour thyroid my endo insisted it was deadly and dangerous and demanded I use Synthroid, and they wanted to put me on a statin. She flipped when I refused and said treating my numbers with statins was like treating a flood by throwing sponges into the water without wondering where the water was coming from. I finally found a holistic nurse practitioner willing to try Armour, and on Armour my total cholesterol has come down over 100 and my ldl-p has come down about 1000. Sure would love to show those numbers to the first doctor. :-)

  17. says

    It frustrates me that every time I get my blood drawn, I ask for a cholesterol reading as well but they always fail to do it. I know that high cholesterol runs in my family, but HDL not LDL… So hopefully that is the same in my case!

  18. Mark says

    Chris,
    If you had RA and type 1.5 diabetes and had cholesterol of 193, HDL of 60, LDL of 119, and TG of 79, would you consent to taking a statin as my GP and endo doc want me to do? I’ve never had heart issues. 62, 138 lbs, 5’9″, exercise 5 days per week, eat paleo. Have reduced HBA1c from 7.4 to 6.0 and heading south from that based on my daily readings. I plan to get the particle number test. Is red rice yeast a good or bad idea (take methotrexate and Enbrel for RA – read that red yeast rice can be not so good for the liver as a combo with those two).

    Thanks,
    Mark

    • Kathy says

      Mark — Both of your conditions are autoimmune in nature. You sound like a very proactive patient (the kind many docs don’t appreciate). I’m not a medical professional but I’m familiar with dealing with them! Do yourself a favor — make up your mind that you want a partner in your health care, and find a doctor, ARNP, or naturopath who specializes in reversing autoimmune diseases. Remember, your body wants to get well — we just have to get out of the way!

  19. Eric says

    Chris – You mention LDL particles not only carry cholesterol but also trigs, fat soluble vitamins and antioxidants. As the amount of trigs increases this decreases the amount of cholesterol the LDL particle can carry and therefore the production of LDL particles increases. Would high amounts of fat soluble vitamins or antioxidants also reduce the amount of cholesterol an LDL particle could carry and therefore also increase their production?
    Eric

  20. Vir Koul says

    Hi Chris,
    My son suffered arrhythmia when around 15 with unknown cause. It developed to Sick Sinus Syndrome. He was treated with drug Sotalol for a few years and the he was cleared and drug stopped when he was around 20 years. He is now 34 and leads a normal life. However being slightly obese he is on statins off and on under medical advice.
    Should I presume the statins he takes are superfluous? Would appreciate your comments.

  21. Karthik says

    This is great information!

    I do have high LDL particle number -> 2000 and my PCP advised me to start Statins -?? I am not even sure if Statins even address LDL-P.

    However, after reading this, I wonder if its the dormant herpis that is causing this. During winter, pretty every year, I get blisters in my nose, and my PCP said it was herpis and advised acyclovir to treat it.

    Otherwise, I don’t have metabolic syndrome, or any family history of cholesterol. I exercise everyday and on a healthy diet.

    Would to love to see what you think.

    Regards

  22. Raph s says

    “Niemann-Pick C1-like 1 protein, which plays a critical role in the intestinal absorption of cholesterol. (3,”

    Your reference “3″ links directly to the Apple Home Page. Should I be scared or reassured Apple may have something to say about nutrition? :p

  23. Bill says

    I had an ApoB of 1.2 and I’m on a paleo type diet, so started taking 1500 mg of niacin daily.
    ApoB now 0.8 and I’m happy with that.

  24. zahir says

    Hi
    can you recommend any books on diet and fitness as i want to lose some weight. I think your website is very informative and cuts through the cr*p.
    i wish you all the best and keep up the good work

  25. says

    I come from a genetic predisposition of diabetes and heart disease on the paternal side. My husbands parents both died of heart attacks at 63 and 62. I found out that my son had high cholesterol at the age of 9 and took the necessary steps with regard to diet. However, both the LDL and HDL lowered with in the same ratio…..the LDL being higer. That did not change. Am I to understand that the particle number is the only thing he should test for to determine his risk of atherosclerosis? Anyone may answer. Thanks!
    BTW my son is now early thirties, healthy on the outside, however, underweight. Tall, very small boned, 71 inches at about 135. Paleo/organic diet for the most part and not much interested in food….same as his Dad.

    • Glenn Atkisson says

      Caette, Chris explains that “…particle number (LDL-P) is a much more accurate predictor of cardiovascular disease risk than either LDL or total cholesterol.” What he is saying is that when LDL-P is measured, studies have correlated the reading with the occurrence of some manifestation of cardiovascular disease. We would have to see the studies to know exactly what the correlation is based on. What matters, I think, is that LDL-P might be measured today and then a problem may show up tomorrow, but it might show up years from now. LDL-P is being used as a leading indicator, to give some warning ahead of time, before the atherosclerosis or other problem shows up, just as you used the “cholesterol” measurements when your son was only 9, and when he probably had no symptoms, to change his diet to try to head off a problem.

      One thing I have already suggest on this series of articles by Chris is to use a different measurement: digital pulsewave analysis. Your son is over 30. Actual signs of damage could be showing up in his circulatory system at this age. It is possible to precisely detect these, including inflexibility, plaque, slow responses to rises in blood pressure – all signs of atherosclerosis. I would say it is more important, if one is actually possibly suffering the symptoms of atherosclerosis, to determine the degree of progression of the disease, rather than to just be testing for a “marker” like LDL, The “marker” has relevance when the disease is not present, because it can give an early warning. But it doesn’t at all measure the disease or the progression of the disease! It only measures an assumed tendency toward the disease.

      It is time now to measure if there is any atherosclerosis. And if there isn’t, to get a baseline measurement of cardiovascular health to measure against if the disease should show up down the road.

      This is all done with a digital pulsewave analysis. It’s very simple, is done with inexpensive equipment, and gives several invaluable measurements in just minutes.

      Here is a video on one manufacturer’s equipment that was reviewed by the news media several years ago:

      http://www.youtube.com/watch?v=Jeh1s-820Pk There are other videos on this on the same page.

      Here is a very complete description of the technology:

      http://sterlinghart.com/?page_id=452

      Good luck with helping your son toward better health.

      • says

        Thank you so much for that valuable info! I forgot to mention too that my father had aortic stenosis and was type one diabetic, beginning heart disease at age 47 and died of a heart attack at 56. His father had his first heart attack at age 40 but lived to 72 at which time he had another. I am very concerned about my son so your note was very much appreciated!

  26. Dave says

    1.7% of population (119 millions people) have homozygous APOE mutation (4/4) which seriously affects fat metabolism. It is still not clear what would the optimal Paleo version in regards to overall macronutient ratios, fats, sat. fats, and cholesterol foods for these people in order to get high HDL, low LDL and good particle numbers. It would be sooooooooooooooo enlightening to read a detailed science-based post with practical recommendations on this topic!

    • Heather says

      I’m a 3/4. I’m reading an essay by MIT Sr. Research Scientist Stephanie Seneff. http://people.csail.mit.edu/seneff/alzheimers_statins.html. Only IDL contains ApoE but LDL can bind to ApoE and the cell can access its nutrients. People that carry the defect tend to have higher cholesterol levels at a younger age. Her theory is that since there is a defect in the IDL connection LDL will be higher to ensure enough nutrients (fats, cholesterol, etc) are getting to the brain. Maybe LDL is higher and there are more particles to ensure there is enough in the bloodstream for ApoE to grab onto and use. There’s one thing I can say about going Primal. I never thought I would be reading and thoroughly enjoying biochemistry.

  27. christine says

    I wanted to confirm that LDL-P is not the same thing as Lp(a) which was what was elevated in my cholesterol profile (I don’t see an LDL-P).
    Thanks!

  28. Wenchypoo says

    Interesting that you mention family history as the last one–I bet Bill Clinton would’ve benefited more from this post than the statins, bypasses, and vegetarian diet doctors put him on! Now, he looks like his head is too big for his body because he’s lost so much weight in muscle mass.

    Question concerning thyroid hormones: I told my doctor to test me for thyroid problems because I was freezing to death in a 70 degree room–menopause had come home to roost. She tested me, and said the usual “nothing’s wrong.” What kind of specific test should I have asked her to run besides the usual TSH, T-3 and T-4 tests? Is this something a GP can do, or do I have to see an actual endocrinologist?

  29. Chris says

    Chris–

    Although I have not been tested for a genetic cause for my hyperlipidemia, I am almost certain it is genetic in nature, as I fit most of the characteristics (low triglycerides, large LDL particle size but immeasurably high particle number, dad died of second heart attack at the age of 50.) I eat almost entirely paleo and stay very active. It would appear saturated fat intact actually drives my numbers up even higher. What are the treatment options for someone in my situation? Am I one of the unfortunate individuals who might have to resort to statin use?

  30. Zingiber says

    1) The “elevated LDL” may not even be elevated, just calculated wrong: “In patients with low serum triglyceride and undesirably high total cholesterol levels, Friedewald equation may overestimate LDL” – http://www.ncbi.nlm.nih.gov/pubmed/18426324

    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

    2) Having triglycerides under 100 is correlated with Pattern A LDL particle size (the healthier pattern), which also often lead to high measured LDL. – http://www.ncbi.nlm.nih.gov/pubmed/1420088

    3) A paleo-based diet results in low serum triglyceride and high total cholesterol levels, but what matters is the ratio of triglycerides to HDL-cholesterol is what shows strongest association with the extent of coronary disease. – http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2664115/

    • tammy says

      Your post has been helpful. I have been on a paleolithic diet for 8 months now and my ldl is up to 190. So discouraged till I recalculated. It is only 163. My triglycerides are down from 127 to 81. Lost 30 lbs this year.

  31. Stephen says

    Today I listened to your third podcast on high LDL where you discuss the role of the thryoid in LDL uptake (I think) and the impact of low Iodine and Selenium. I have been on a low carb high fat diet since October last year. As it happens I have concentrated on cruciferous veggies AND at the same time have changed from iodised salt to Himalayan rock salt (OK because it was pink and came in a scrunchy shaker – this was not all science). My LDLs are really high at 239 mg/dl (The lab report marked that as ‘measured’). I also had my apo-A1 and apo-B measured which are also high.(1.56 and 1.66 respectively).

    In his ‘straight dope on cholesterol’ series Peter Attia highlights high LDL as a predictor of atherosclerosis so I need to take this seriously. I have not read your response to this but intend to read more of your site in the future.

    I have lost 6 kgs on this diet and am feeling more energy than I have for decades.

    My strategy is to ramp up my iodine slowly as you suggest in the podcast, as well as selenium. I will measure again in two months (all going well) and will then consider the impact of the low carb jolt to which I have subjected my body. I suspect in the long term I will go for a more balanced paleo menu.

    I appreciate the information you are making available here. Medicine for the 21st century indeed!

  32. Leslie says

    My 21yo daughter who is extremely physically active, within normal weight (135), has very low blood pressure and the diet of an athlete, was just informed that for the second year in a row, her triglycerides and LDL are unusually high. There is no family history of early onset metabolic syndrome. She has had a nodule on her thryoid scanned once (benign) and she currently take Zoloft (150mg) and Birth Control Pills. I had hyperthyroid when I was pregnant with her. Any thoughts ???

  33. K Chase says

    What if the LDL is High, and the non HDL, but overall is not, nor are trglycerides…all Thyroid is normal EXCEPT T3 which is very high…Eosinophls high too. I recently cut all meat, flour and have been raw juicing for at least three months (along with salads, some soups and protein drinks etc)…so I was shocked my bad cholesterol is up. I had EKG, and stress test…heart function looks fine. What do you think of high LDL number in this scenario?

  34. Roberta says

    Great article! After dealing with chronic and intermittent upper abdominal pain for well over six months, my new doctor gave me a battery of blood tests. My SED was 36, my Vitamin D was 16, and my LDL was 127. We are still waiting on the ultrasound results.

    After reading this article, I am intrigued (albeit a smidgen worried) to find out what could be going on. My father had a history of high cholesterol as well.

    Thanks for a great read!

  35. Sam says

    Hi

    Great article. You are right about all doctors treating symptoms and not root cause.
    I have been having rash/hives recurring issues and saw about 8 doctors (PCP and dermatologists) with no results. Irecently identified a high LDL of 196 which I never had. I used to take niacin and i stopped for 6 months as part of the elimination strategy but I do not think that my LDL goes from 140 to 196 just because of niacin.

    I think i have internal bacerial infection that no one has been able to diagnose.

    Are you local in Reston, Virginia area and if not can you recommend any doctor who does the functional medicine.

    many Thanks,

  36. pone says

    What are all of the cardiology tests that one should ask a physician to do? I am inferring from this discussion:

    Triglycerides
    Total-C
    HDL-P
    HDL-C
    LDL-P (the one I know about is LipoScience NMR LipoProfile test)
    LDL-C (does anyone have an opinion on the Berkeley Heartlab test to graph different LDL particle sizes versus something like the VAP test?)

  37. Shazlan says

    Hi, I have subscribed to the Cholesterol Action Plan, and there you mentioned that ApoB:ApoA1 ratio is a good indicator of LDL-P, especially for those without access to NMR. Now that I have my APO results I have difficulty trying to figure out how to interpret whether they are good or not.I couldn’t find it in the course materials.

    I see from some of the previous comments here that they are aware that there levels are high and I am just wondering how I can make the same determination. Most of the information online on the subject were very medically heavy and was really beyond me. Hope to get some clarity. Many thanks.

    • Shazlan says

      I managed to get some information on this from Chris’s team and I thought I would also share it here.

      Range – The ideal range for ApoB is 40–125 with <100 mg/dL considered desirable in low/intermediate risk individuals and <80 mg/dL desirable in higher risk individuals.

      An ApoB:ApoA1 ratio of <0.8 is considered optimal.

      Correlation to LDL-P – In general, you have 1 ApoB for every LDL particle. It's not exact, but it acts as a solid estimate. Chris explains this in a blog series regarding cholesterol. http://chriskresser.com/what-causes-elevated-ldl-particle-number

  38. Domlika says

    hi, my total cholesterol is 5.22 mmol/ l and my ldl is 2,69 mmol/l, my hdl is 2.11 mmol/ l, triglycerides are 0,92 mmol/l , and vldl cholesterol is 0.42 mmol/l. i am 21 years old (woman ) and my BMI is 23, 5 . So should i take some steps to reduce it ? and is there some serious reason to bother about it ?

  39. Glenn Atkisson says

    I just finished reading Fat Chance (pub. Dec. 2012) by Dr. Robert Lustig. It is a great, but somewhat technical look at the effects of fats and sugars on health, and specifically on lipid numbers.
    Yes, Chris, you are right that LDL number of particles can be taken as an important marker of cardiovascular health. But it is a secondary count, based on, as you say, the “needs” of other substances to be carried around in the plasma, and therefore the needs of the other substances for “taxis” to do the transportation.
    Lustig states that if one wants to “fix the numbers”, it is as simple as removing most sugars from the diet, and especially fructose, and definitely commercial fructose, as opposed to the lesser quantities found in natural, raw foods.
    His does a credible job of showing that moving the diet away from sugars improves all 3 commonly accepted measures of cardiovascular health: It raises HDL, and lowers triglycerides and small dense LDL substantially! It can easily be seen, with the numbers of 2 items reduced, and only 1 (HDL) increased, that this will also reduce the number particles that your article emphasizes. But the way the particles numbers are reduced is actually what is important, as there are still strong technical reasons to look at types of LDL present, at HDL, and at triglycerides. I would suggest that people continue to let their doctors focus them on these numbers if they continue to have lipids tested.
    I think most people though could just cut the sugars and rest assured that their “cholesterol” will be fine after reading “Fat Chance”.

  40. Lilu says

    I know this question has been asked, but i am not sure if it was answered. I do eat tons of nutrient rich foods ( like liver at least twice a week, tons of lard, grass-fed butter and full fat meat, gelatinous stocks, pastured fertile eggs, and i additionally supplement with minerals etc.) and my cholesterol sky-rocketed to 350. LDL is the highest at 242. If LDL is a transport for nutrients, could such a high number be connected to the diet and the need for numerous nutrient transportation? When i was eating SAD with a “healthy” angle (low-fat with no saturated fat, lots of plants etc) my cholesterol was still around 250 (considered “high”), but i was always depressed, had more weight, was plagued by candida and literally had no libido. Now my cholesterol is super high, but i feel great, MUCH better than before.

  41. Les says

    I recently had an NMR particle test and my numbers were high (1887). I am currently taking 2 supplements which are recommended in the High Cholesterol Action Plan, Annatto Tocotrienols and Pantethine. Will these supplements reduce my particle number or are they specifically geared to reducing the concentration of cholesterol?

  42. Ramin says

    Hi Doc,
    I am 46 years old male with familial history of high lipid profile. My recent tests show:
    LDL-P 2053
    HDL-P 25.6
    LDL particle size 20.9
    Large VLDL particle number 7.4
    Large HDL particle number 0.9
    VLDL size 50
    HDL size <8.3
    LP-IR 73

    My LDL-C was always high (150-170); fasting glucose always 105-112, A1C 5.4-5.9.
    I have this stupid belly fat that does not want to go away.
    After looking at the numbers, do you have any suggestions? I started taking Niacin 500 mg/day and 500 mg of Artichoke Extract. I don’t want to go on statin drug for as long as I can.
    Thank you.

  43. Janet says

    Was having side effects from Crestor (20MG), and asked to go on another statin and Dr. put me on 40MG of Pravastatin although I had asked for Simvastatin. Well, my total cholesterol is now 299, my LDL is 202, and my HDL is 81. I am reading all these posts with people trying to avoid going on a statin with their high numbers and I am on a statin! Always had a high LDL but NEVER as high as 202. Any advise on what I need to discuss with my Doctor – follow-up in a few days. BTW, have been tested for thyroid and things are normal. I am starting to wonder if I do have some type of bacterial infection going on. What tests do I ask for?

      • Janet says

        Well, today I go see my Dr. Doing some research on my own I realized that there may be a connection between taking 2000 mg of Vit D a day and a connection between high calcium blood levels I have had for years (10.4-10.5). Asked for a Vit D test, came back at 20.3, and was told to take supplement. Vit D can cause cholesterol levels to rise ‘significantly’ and could cause pains in arms and legs. Will discuss this connection with my Dr. and possibility of having hyperparathyroid issues. From what I am reading, calcium is not being absorbed correctly in my body and taking a mega dose of Vit D was the wrong thing to prescribe. Might be time to find another Dr.

  44. ERIC MANLEY says

    I am 55 good health just got my blood work back and total cholestrol was 213 and LDL was 155 which is down 22 points from last blood test a year ago. I use Red Yeast Rice 200mg instead of a statin and have for the last 3 years and the numbers are about the same as far as LDL levels as they were on a statin. I eat mainly fruits and vegs very little red meat some pork and chicken. 2 questions how can I move this LDL number down more and or is it necessary to worry much about it. My doctort wants me on Lipitor but I am not agreeable.

  45. Chris says

    I find it interesting that so many people mimicking starvation with their nutritional ketosis seem to have elevated LDL-P numbers in the setting of low or low-normal thyroid function tests, low hs-CRP, and, almost uniformly, CT coronary calcium scores of zero. Rakesh Patel documents his LDL-P in the three thousands and REVERSAL of coronary plaque on his IMT. So, taking into consideration what we know of the “survival phenotype” associated with caloric restriction–and ketosis, at least in vivo as demonstrated by Hirschey, et. al in 2013, we expect the following:

    (1) Inflammation to be low due to upregulation of cellular and mitochondrial antioxidants through the concerted effects of sirtuin-class proteins and their associates.
    (2) Low or lowered levels of thyroid hormone.
    (3) Absence of atherosclerosis, which can be inferred by the longevity associated with CR.

    In light of these observations, perhaps the assumption that elevated LDL-P in the setting of VLC or KDs is detrimental to health is wrong.

    In fact, one might hypothesize the oppposite, that it is beneficial. Perhaps the increase in LDL-P does actually reflect a “thrifty gene effect,” however not so much as Dr. Davis suggests in terms of improved energy shuttling in times of famine, but in terms of immune function. FH, for example, is thought to confer an immunologic benefit to individuals. Furthermore, it has repeatedly been shown that conserved sequences on apoB protein play an important role in innate immune function. I think it is entirely concievable that the elevated LDL-P’s in so-called “hyperresponders” might reflect and entirely normal range of expression in terms of individual polymorphisms reflective of increased immune “surveillance” in times of famine.

    I think it is an interesting hypothesis that mechanistically makes sense–in times of famine, thyroid function goes down to conserve energy and LDLr expression (regulated by thyroid function) is decreased, leading to an increase LDL-P numbers and aid in the organism’s immunologic defense efforts. What does not make sense is how a diet that mimics at the molecular level the one thing known to extend life span in non-human primates and that also, in humans, improves all markers of health including radiologic studies of atherosclerosis would singularly increase the strongest marker for CAD against all the other benefits.

    I haven’t quite had the time to comb PubMed to find literature to support or refute, other than to quickly find a few studies showing that cholesterol levels in CR’ed rats usually fall. Far more intersting would be to observe the LDL-P response to CR or a ketogenic diet in an animal model of FH…

  46. kris says

    A doctor who had a high ldl-p http://azsunfm.blogspot.com/2012/09/font-definitions-font-face-font-family.html , has an interesting take, did his more advanced scan for fat around the arteries yield better results, I read in a blog it did,

    So is there a more accurate test than ldl particle size or number or apo-b, many low carbs have high ldl-c but ok ldl-p, some don’t but don’t seem to have heart issues.

    So in an effort to defend a lower-carb diet if your ldl-c is high the high ldl-p and apo-b will bring nagging statin advice from the doctor, meanwhile should you be prompted if your ldl-c is low to just not ask for the test that the doctor does not want to do or in some cases does not really know about so you won’t get nagged, and then the doctor will get stressed saying “well you asked for these advanced tests so know what the results are not good”.

    This is important because jumping to a better test that is still imperfect without further explanation can get folks confused and worrisome. So what is the best tests to ask the doctor, assuming of course you do not seem to be at a high risk of heart disease but may have metabolic syndrome or not. Obviously I state that because those with genetic backgrounds or liver filtration issues will have more tests, so there is not one single test for everyone, but what’s the test that should clear up issues for those with a lower risk of heart disease with metabolic syndrome or not and those who are on lower-carb diets.

  47. Donna says

    I’m 65 & have always lived a healthy lifestyle but left the grains & sugars several years ago & changed to grass fed meats,coconut oils, low carb& lots of home grown veggies & our girls give us beautiful eggs. Last few years cholesterol has been heading upwards, it is now , total 412, hdl 95,LDL 306 ( scary) & triglycerides are56 . Doctor says Statin…. She thinks I have the gene for high cholesterol , is she right or this just as things should be naturally ?

  48. Alan says

    Does anyone know why it seems to be totally impossible to print the *comments* on the Chris Kresser website?

    I like to review what I read here at leisure, making notes on the pages. But it looks like the website designer made it impossible to print the comments – just the base text from Chris.

    I realize that often people will want just the blog post – but other times people will want it all. How about a website design that lets us *choose* what we want to print?

  49. Lauren says

    Thanks for these informative articles. After doing a fair share of research on atherosclerosis, I know that LDL buildup in the vessel is usually initiated by damage to the endothelium and that damage leaving an “opening” for oxidized LDL to enter the vessel. Risk factors for this damage are often cited as smoking, hypertension, diabetes and high cholesterol itself. Im having trouble processing that last one. How does high cholesterol itself contribute to endothelial damage? It really seems to me that molecules of LDL need a reason to start piling up and its amazing that its often difficult to find good research that explains that reason. Thanks!

    • Glenn Atkisson says

      Lauren, good question.

      Part of the answer, firstly, lies in the confusion caused by misuse of terms. People often say “LDL cholesterol”, as though that is a kind of cholesterol. It really means cholesterol that is currently being carried around by LDL. LDL is just a vehicle for getting fats to travel through an aqueous medium like plasma. It can carry cholesterol, but it can also carry triglycerides or phospholipids.

      When people say “oxidized LDL” they may mean “an LDL particle carrying oxidized cholesterol”.

      Chris’ whole article is about the dangers of having “high” numbers of LDL particles. One, and just one, of the reasons for “high” numbers is that if there is more cholesterol being carried than is being called for by the tissue (where it is used in cell membranes, etc.) then this means there are less LDL receptors in cells, across the total body, than there are LDL particles in circulation, because cellular receptors get REDUCED when there is less need for more cholesterol.

      This leaves excess LDL particles circulating that are carrying cholesterol. This cholesterol is essentially “aging” as it circulates in the plasma. Aging means oxidation. Once the LDL particle, with oxidized cholesterol as the passenger is identified by the immune system, as Wiki says, the LDL particles “are taken up by macrophages, which become engorged and form foam cells. These cells often become trapped in the walls of blood vessels and contribute to atherosclerotic plaque formation….”

      So going back to Chris’s original claim that a single LDL particle can only carry so much cholesterol because it must also transport triglycerides, but that it will probably always carry SOME cholesterol, and you can see that, if the body already has plenty of cholesterol in place in it’s cell membranes, but has an overload of triglycerides that must be deposited in fat cells because the person is overeating, then there is going to be LDL circulating that is doing it’s job of depositing triglycerides, but just has nowhere to dump the cholesterol. The cholesterol on such LDL particles will age and age until the whole particle is deemed “suspect” by the immune system, and when the macrophages are called out to gobble up that LDL, that starts the cascade of events that bring that particular macrophage into vile contact with the endothelium where it lodges and starts the cycle of atherosclerosis.

      So even though it is true that the cholesterol in such a situation is “high” (relative to what is needed in the cells), the critical issue is really that because excess triglycerides need transportating, the number of LDL particles has reached such a high number (from the point of view of cholesterol again) that small amounts of cholesterol is aging in the LDL (but undeliverable, because there’s no demand) while more and more triglycerides get picked up and delivered to fat cells.

      It’s the carbohydrates, eaten to excess, that cause this oxidation of cholesterol.

  50. Anthony says

    Hello, I was wondering if some expert could help me with an ldl-p question. I just had blood work taken and received the results last week. I was shocked to see that my cholesterol was at 233, while the most shocking (and unknown) number was my ldl-p count. Apparently, people are to be >1000. Mine was at 3375. When I researched that, it does not look good. But then why didnt my PCP call me back and explain that to me to get it remedied? Also, my father in law who is an internist looked at my results and was concerned until he asked me if I had been fasting prior to the blood work. I had not. In fact, I had eaten lunch a couple hours beforehand. But I cannot imagine lunch would have impacted my numbers that much. I am a 37 year old, 6’0 185 pounds who does not drink or smoke. Any thoughts as to what is going on with those numbers?

    Thanks in advance.
    Anthony

      • Anthony says

        LDL-Cholesterol=156
        Total HDL Cholesterol=43
        non-HDL Cholesterol=190
        cholesterol rich LDL=131
        TOTAL VLDL=34
        APO B=124

        Does that help?

        • charles grashow says

          It is NOT possible to have LDL-P of 3375 AND LDL-C of 156

          ApoB is a surrogate for LDL-P. With ApoB of 124 your LDL-P CANNOT be 3375!

          Again – are you sure that you’re not misreading the test results?

          • Anthony says

            Everything I wrote is directly from my bloodwork results sheet.

            Should I be deceased? Do I have leaky gut?

            Did the fact that I ate a couple hours before the bloodwork have any effect on the numbers?

  51. pone says

    What if the patient is prediabetic, insulin resistant, but has low triglycerides? Would low triglycerides alone rule out metabolic syndrome as the cause for high LDL particle counts?

  52. Joe says

    Anthony.

    I am kind of like you same build and age . My LDL- p is 1883 ans as you also I didn’t fast before blood work

  53. david gary says

    Just had NMR… TC 121, LDL 59, TG 100, HDL 42, Particle number 832, APOB/APOA ratio .39, CRP .5, LP(a) was high 161—one doc says excellent another says very mixed….have been on Ornish program for 2 years….mixe doc says it is not a good program…prefers Paleo…Thoughts?

  54. charles grashow says

    @david gary

    IMHO – your lipid profile is excellent with the exception of the high lp(a) which is genetic in nature – did your doctor give you a valid reason for switching to paleo which will probably elevate very lipid marker you have?

    The only suggestion I can make is to investigate the Pauling Protocol

    http://www.drlam.com/opinion/Lp%28a%29.asp

    • david gary says

      Thanks for your comment Charles. The mixed result physician says because I restrict my fats to 10-15 percent per the Ornish theory, I eat too many carbs which raises my LP(a).
      He feels I need more fats and a lot less carbs. He feels these LP(a) particles are a serious problem. BTW… my insulin level was reported as optimal on the NMR, my A1C was 5.4, my fasting blood sugar was 86, and all my inflammation and cardiac stress markers were reported as optimal. I lost 50+ pounds over 2 years using the Ornish model and greatly improved my lipid results and am reluctant to alter my methods.

        • david gary says

          Charles….

          Thanks again for your comment. I will certainly read the links you provided.

          My PCP has told me that the LP(a) is mostly genetic, but did have me start using an 81 mg aspirin a day as one study showed it affected LP(a) to a 20% degree. He believes the best way for me to manage my risk is to keep the LDL_C low and the particle number low and do what we can on the LP(a). He is not a big believer in Niacin use due to side effects especially so in my case because my overall lipid profile was in his words “excellent” and I have modified lifestyle factors considerably over 2 years. My other doc feels more should be attempted to lower the LP(a) such as niacin use and increasing fats which he says may favorably impact the LP(a). It has gotten a little confusing honestly as I am just a layman, trying to be as wise/informed as I can in making choices.

      • pone says

        NMR Lipoprofile does not measure insulin levels?

        Remember you can have a very good A1C level and be very insulin resistant and have persistently high insulin levels. Cardiac disease risk tracks to the high insulin levels, and those are never measured in a time series except during a glucose-insulin challenge test.

        • david gary says

          Thanks for the comment Pone. I am not as well versed as many who post here. Relative to insulin my NMR test reported an insulin test result of 7 with an optimal range being 3-9. Perhaps I do not understand what that means. I have not done a challenge, but will raise that issue with my PCP.

          • pone says

            David, it gets complicated.

            First, it looks like the good people at NMR Lipoprofile created their own proprietary metric, and very inappropriately called it the LP-IR. In fact they never measured insulin at all. It looks like they are simply inferring that the reason for a bad LDL-P reading is because you are insulin resistant. But that’s patently false. There are many other reasons you can have high LDL-P, such as familial hypercholesterolemia or bacteria or viruses. I wish they would not have named their internal metric by insulin resistance, because it isn’t a direct measure of that.

            Regarding your one-time reading of insulin at 7, unfortunately that doesn’t mean anything. When you are in a fasted state, insulin travels up and down in patterns that resemble big sine waves. Taking one static reading doesn’t tell us much.

            What’s more useful is to see how your insulin responds to a glucose challenge. Can you ask your doctor for a “glucose-insulin challenge test” and make sure you tell him “I do NOT want just a glucose challenge. I want them to record both the glucose and the insulin reading together, at each point during the test.”

            The above test would show more clearly if you have a very large insulin response to glucose that your body doesn’t respond to appropriately (insulin resistance).

            • david gary says

              Thanks for the explanation. You have a great point. I will ask my PCP about the glucose-insulin challenge. I am learning day by day.

  55. charles grashow says

    @david gary

    What was your LP-IR score on the NMR test?

    As to niacin – Dr William Davis – Track Your Plaque – is a big believer in SloNiacin at doses of 500-1500mgs/day – you might do some research on that

    Aspirin for LP(a) has some validity

    http://www.clinchem.org/content/48/9/1454.full

    I would combine both of your doctors advice – they both have some good points

    Here’s a post by Dr Davis on Treating Lipoprotein(a)
    http://www.healthcentral.com/heart-disease/c/1435/44295/lipoprotein/

    Have you had a thyroid panel done?
    Have you have your Vit D levels checked?

  56. Renee says

    I am reading my recent labs and have a LDL-P of 2262 and LDL (calculated) 152
    Cholesterol 233
    Small LDL-P 897
    I do have hypo thyroid
    will get tested for h pylori (have had in past) also SIBO will test for
    Heard that it is important to know if you are pattern A or B??
    What are the risks for either or with conjunction to these levels.
    I have never had such high markers in prior labs.
    Thank you!!
    Renee’

    • charles grashow says

      @Renee

      You should read this

      http://www.lecturepad.org/dayspring/lipidaholics/pdf/LipidaholicsCase291.pdf

      ““Let’s get rid of the nonsense seen all over the internet that atherosclerosis is an inflammatory disease, not a cholesterol disease. That is baloney-with the reality being that it is both. One cannot have atherosclerosis without sterols, predominantly cholesterol being in the artery wall: No cholesterol in arteries – no atherosclerosis. Plenty of folks have no systemic vascular inflammation and have atherosclerotic plaque. However clinicians have no test that measures cholesterol within the plaque – it is measured in the plasma. It is assumed, that if total or LDL-C or non-HDL-C levels are elevated the odds are good that some of that cholesterol will find its way into the arteries, and for sure there, are many studies correlating those measurements with CHD risk. Yet, we have lots of patients with very low TC and LDL-C who get horrific atherosclerosis. We now recognize that the cholesterol usually gains arterial entry as a passenger inside of an apoB-containing lipoprotein (the vast majority of which are LDLs) and the primary factor driving LDL entry into the artery is particle number (LDL-P), not particle cholesterol content (LDL-C). Because the core lipid content of each and every LDL differs (how many cholesterol molecules it traffics) it takes different numbers of LDLs to traffic a given number of cholesterol molecules: the more depleted an LDL is of cholesterol, the more particles (LDL-P) it will take to carry a given cholesterol mass (LDL-C). The usual causes of cholesterol depleted particles are that the particles are small or they are TG-rich and thus have less room to carry cholesterol molecules. Who has small LDLs or TG-rich LDL’s? – insulin resistant patients! After particle number endothelial integrity is certainly related to atherogenic particle entry: inflamed endothelia have inter-cellular gaps and express receptors that facilitate apoB-particle entry. So the worse scenario is to have both high apoB andan inflamed dysfunctional endothelium. Is it better to have no inflammation in the endothelium – of course! But make no mistake the driving force of atherogenesis is entry of apoB particles and that force is driven primarily by particle number not arterial wall inflammation.”

  57. ken says

    My wife dealt with many bouts of sinus infections and was given may doses of antibiotics. She then began having serious gut issues. She switched to a pure paleo eating meats, veggies, butter, coconut oil, etc. things got worse and she eventually was diagnosed with ulcerative colitis earlier this year. They wanted to start here on steroids but she decided to go with a GERD diet with bone broth, cooked carrots and broccoli coconut oils and other GERD foods. She has stopped all grains, sugar, hi carb foods. Trying to stick with It’s been 3-4 months and she has improved greatly. Also her achy hands and feet have stopped aching. Her allergies were gone too. She lost weight and overall the colitis symptoms (mucus and runny stools) and began having regular stools and everything seems to be working right. She has always had higher cholesterol thinking it’s due to FH. Like above the 200’s. she is 49 years old 5’2 120 lbs her BP is like 100/60 and pulse is usually in the 60’s. she is in great shape. She recently had here blood work done so we could see if she had the big fluffy partials. We got the results back and we were very shock.
    Here are the results
    Lipids
    Total 398
    LDL-C 290
    HDL-C 104
    TRI 58
    Non-HDL-C 294

    Particle
    Apo B 198
    LDL-p 3150
    sdLDL-C 65
    SDldl-c 23
    Apo A-1 170
    HDL-P 48.4
    HDL2-C 50
    Apo B:Apo A-1 ratio 1:16
    Lp (a) 22

    Inflamation
    Hs-CRP 0.4
    Lp-PLA 303

    Metabolis
    All were optimal except
    Her free fatty acids were 1.40

    Thyroids
    TSH 1.96
    T4 7.1
    T4 free 1.27
    T3 88

    Were kinda super concerned now.
    I read this article and were thinking its FH and leaky gut
    Could it also be SIBO and or H. pylori.???
    I know you cant answer personal questions but we need some help here and be directed to who we can talk to in the Portland Oregon area.
    HELP!

  58. George says

    I had a blood test last week and my triglycerides were 62 mg/DL.
    My particle count was 1802.
    Your article states that a high Trigl. will equate to a high LDL-P. Is that true?
    How do I verify the cause of the High LDL-P? If caused by the thyroid, what test is needed?
    Is my only hope of lowering my LDL-P through medication?

  59. Sherry says

    Great info! I’m struggling and seeking guidance regarding my recent cholesterol #’s. I am a 51 y/o menopausal female who is slim, exercises vigorously @3-4x/wk, vegan with little to no sugar or processed food intake, drinks water and green tea only. My trigylcerides are 58 (excellent), HDL is 67 (good) with LDL of 132 (border high). Past 3 years all #s the same except LDL been rising slowly. MD prescribed Rx. I dont take any prescriptions and question this option. If this is genetics I’m not sure what are my options? Any info or suggestions is greatly welcomed

Join the Conversation