What Causes Elevated LDL Particle Number? | Chris Kresser
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What Causes Elevated LDL Particle Number?

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

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 heart health 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.

240 Comments

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  1. 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!

  2. 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. 🙂

  3. 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

    • 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.

  4. 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.

  5. 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!

    • 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?

  6. 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?

    • 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?

  7. 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?

  8. 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!

  9. 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. 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?

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

      • 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.

        • 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:

    • 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.

    • 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.

      • 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.

  11. 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?

  12. 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?

  13. 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?

    • 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

  14. 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!!!!

      • 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.

    • 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!

    • 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.

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

  15. 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.

    • 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.

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

          • 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

  16. 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.

    • 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.

      • 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.

      • Tengo el colesterol LDL en 156, el total en 252 y LDL-P en 1685. Es de alto riesgo? el dr me receto estatinas y las tomo desde hace tiempo ademas de mi dieta sana, creo que mi caso es genetico. Que me recomienda?

  17. 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

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