LDL Cholesterol: Sometimes the Simple Questions are the Most Revealing

Recently, after participating in a meeting attended by a few high-powered CVD researchers I returned home plagued by a most simplistic question: What is the purpose of LDL cholesterol? Please refrain from bursting into uncontrollable spasms of laughter; I am well aware that as a clinical lipidologist I never imagined such a question would have the capacity to keep me up at night. And yet it did. And so I called my faithful counsel, upon whom I can always rely to extricate me from any lipid conundrum. Tom Dayspring responded to my query unflustered, promptly sending me articles to help me find my way. I read them and this is what I realized. LDL cholesterol is essentially garbage. The story goes something like this.

Our livers manufacture triglyceride – (TG) and cholesterol – containing lipoprotein particles called VLDLs. This is old news. VLDL contains about 80% TG and 20% cholesterol. Its purpose is to nourish our organs. As these particles pass through the tiny capillaries of our various organs, enzymes called Lipoprotein Lipase (LPL) snip the fatty acids from their TG backbone, Glycerol. This too is old news. These released fatty acids are either used for energy or stored by our organs for future needs. The shrunken down VLDL particles, devoid of most of their TG energy content, are now re-dubbed. They have become LDL particles. They are cholesterol-rich. Their content represents what most people speak about after visiting their doctors – LDL-C or LDL cholesterol. Here’s where it gets intriguing. Although any lipid specialist can tell you that every single cell in our body has the capacity to make cholesterol, most believe that the cholesterol contained in LDL particles has some greater purpose. Our cells however do not need the cholesterol contained in LDL particles; nonetheless, most of us believe they use it. This belief is untrue. LDL-C is actually not utilized to any significant degree by any organ systems in human beings. Other animals may use some of it here and there, but not us. We just don’t need it. In fact, the goal of LDL particles is to get to the liver ASAP for disposal. Otherwise, these particles tend to land in places where we do not want or need them, our blood vessel walls to be more specific. You know how that story goes – plaque forms; plaque ruptures; heart attacks or strokes ensue…

So when people tell you not to worry about your high LDL-C levels, please reconsider abandoning your doctor’s LDL-C-lowering advice. And definitely don’t worry that low LDL-C levels will deprive your cells of their much-needed cholesterol. It won’t. Your cells are quite capable of making their own supply of cholesterol. On a somewhat esoteric note, it is true that the surface of LDL particles transports some vital nutrients around the body (vitamin E for one). This fact however does not imply that more LDL is better than less. We need just a tiny bit for non-cholesterol purposes. Excess does us no good, and in truth it does us a good deal of harm.

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  1. charles grashow March 17, 2014 at 11:26 am #

    If the body produces all cholesterol needed is dietary cholesterol necessary?

    • Seth J. Baum, MD March 23, 2014 at 1:23 pm #

      Dietary cholesterol is not essential for survival as we do have the capacity to produce it. Fats that are essential include Linoleic Acid (LA) the 18 carbon omega-6 FA, and alpha linolenic acid (ALA) the 18 carbon omega-3 FA. DHA and EPA, the long chain omega-3 FA in fish are considered by many to be “essential” too. Essential means we can’t make it.

  2. charles grashow March 17, 2014 at 12:14 pm #

    Can you furnish the link s to the papers Dr Dayspring sent you?

    • Seth J. Baum, MD March 23, 2014 at 1:26 pm #

      John M. Dietschy,’ Stephen D. Turley, and David K. Spady, Journal of Lipid Research Volume 34, 1993.
      Great paper!

  3. charles grashow March 17, 2014 at 12:19 pm #

    One more question. If LDL-C is essentially garbage does that mean that a diet that contains as close to zero cholesterol is best? After all doesn’t the body produce enough cholesterol on it’s own?

    Also – would you agree with Brown & Goldstein


    The LDL receptor studies lend experimental support to the epidemiologists’ suggestion that the levels of plasma cholesterol usually seen’ in Western industrialized societies are inappropriately high (9). This support derives from knowledge of the affinity of the LDL receptor for LDL. The receptor binds LDL optimally when the lipoprotein is present at a cholesterol concentration of 2.5 mg/dl (28). In view of the 10 to 1 gradient between concentrations of LDL in plasma and interstitial fluid, a level of LDL-cholesterol in plasma of 25 mg/dl would be sufficient to nourish body cells with cholesterol (118). This is roughly one-fifth of the level usually seen in Western societies (Fig. 16 and ref.119). Several lines of evidence suggest that plasma levels of LDL-cholesterol in the range of 25-60 mg/dl (total plasma cholesterol of 110 to 150 mg/dl) might indeed be physiologic for human beings. First, in other mammalian species that do not develop atherosclerosis, the plasma LDL-cholesterol level is generally less than 80 mg/dl (Fig. 16 and ref. 120). In these animals the affinity of the LDL receptor for their own LDL is roughly the same as the affinity of the human LDL receptor for human LDL, implying that these species are designed by evolution to have similar plasma LDL levels (9,119). Second, the LDL level in newborn humans is approximately 30 mg/dl (121), well within the range that seems to be appropriate for receptor binding (Fig. 16). Third, when humans are raised on a low fat diet, the plasma LDL-cholesterol tends to stay in the range of 50 to 80 mg/dl. It only reaches levels above 100 mg/dl in individuals who consume a diet rich in saturated animal fats and cholesterol that is customarily ingested in Western societies (116)

  4. Seth J. Baum, MD March 23, 2014 at 1:36 pm #

    Brown and Goldstein certainly changed our world with their discoveries but much more has been learned since their original work. Alan Sniderman recently published a fascinating paper revealing novel ways of viewing hepatic cholesterol handling. (Hepatic Cholesterol Homeostasis: Is the Low-Density Lipoprotein Pathway a Regulatory or a Shunt Pathway? Arterioscler Thromb Vasc Biol. 2013;33:2481-2490; originally published online August 29, 2013;). Regardless, evidence has emerged that LDL-C as low as 2 or 3 mg/dL is compatible with excellent health. So, I would agree that from a cholesterol standpoint we need not worry about consuming it or saturated fats in our diet.

  5. charles grashow March 31, 2014 at 1:00 pm #

    “evidence has emerged that LDL-C as low as 2 or 3 mg/dL is compatible with excellent health”

    Can you supply links to the evidence?

    SO – what then is “optimal” LDL-C, LDL-P?

  6. DoctorSH April 2, 2014 at 11:36 pm #

    Perhaps the LDL goes up to transport more vitamin E and other nutrients due to diet, inflammation or just bodily need.
    Perhaps lowering LDL by pharmaceutical means is disrupting a normal and necessary, but not always healthy, mechanism.

  7. marcus volke May 6, 2014 at 9:08 am #

    What a ridiculous article, our cells have LDL receptors for a reason…so we can absorb the cholesterol into the cell.

  8. marcus volke May 8, 2014 at 5:37 am #

    To reiterate, if LDL-C has no use in the body than why do our cells have LDL-C receptors? Saying that we don’t need cholesterol because our body can manufacture it is like saying we don’t need carbohydrates because our body can manufacture glucose.
    The fact that our body can manufacture only proves that it is indispensible to our survival…

  9. Brian Edwards February 6, 2015 at 8:14 pm #

    Excellent job. Thank you, Seth.

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