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  • LDL is NOT the cause of cardiovascular disease according to Dr. Malcolm Kendrick


    Posted by .(JavaScript must be enabled to view this email address)
    Saturday, December 01, 2018 11:40 am Email this article

    Dr. Malcolm Kendrick, author of The Great Cholesterol Con and the book Doctoring Data, wrote a terrific article summarizing his views on what causes cardiovascular disease, and what does not.

    He explains why the LDL hypothesis of cardiovascular disease makes no sense.

    He says, “The LDL hypothesis is nonsense, it is wrong, and it does not remotely fit with any other factors known to cause CVD [cardiovascular disease].

    He also explains why inflammation is not the cause of cardiovascular disease, and instead, it is simply part of the repair process (which is happening all the time).

    Below are highlights from his article, but I encourage you to read the entire article, because it contains a lot more than just the highlights that I am including below.

    The LDL Hypothesis is Nonsense

    Dr. Kendrick writes:

    The LDL hypothesis is nonsense, it is wrong, and it does not remotely fit with any other factors known to cause CVD.

    The Thrombogenic Theory—plaques are made of blood clots used to repair the artery wall—fits with almost everything known about CVD

    Dr. Kendrick writes:

    “The thrombogenic theory, on the other hand, [as opposed to the LDL hypothesis,] fits with almost everything known about CVD.”

    “Anyway, damage the endothelium, and a blood clot will form.

    “This is the main mechanism the body uses to stop itself from bleeding to death.

    The Thrombogenic Theory first suggested in 1852

    Dr. Kendrick continues by saying:

    “... this is, essentially, the thrombogenic theory, first suggested by Karl von Rokitansky in 1852.

    “He proposed this because he noted that atherosclerotic plaques looked very much like blood clots, in various stages of repair.

    “He further observed they contained red blood cells, fibrin and platelets, which are the main constituents of a blood clot.

    Other researchers have noted that plaques look like blood clots

    Dr. Kendrick writes:

    However, from time to time, other researchers also noted that plaques do look awfully like blood clots.

    Finally, for now, Dr Smith [Elspeth Smith, a researcher who taught Dr. Kendrick at Aberdeen University] stated this in another paper:

    ‘After many years of neglect, the role of thrombosis in myocardial infarction is being reassessed. It is increasingly clear that all aspects of the haemostatic system are involved: not only in the acute occlusive event, but also in all stages of atherosclerotic plaque development from the initiation of atherogenesis to the expansion and growth of large plaques.’3

    “What she [Elspeth Smith] is saying here is that every step of CVD is due to various aspects of blood clotting.

    Artery wall damaged, blood clot forms, then it is incorporated into the artery wall, which starts the plaque which grows

    Dr. Kendrick writes:

    “You damage the artery wall, a blood clot forms, it is then incorporated into the artery wall.

    “A plaque starts, then grows.

    “This description of how CVD starts and develops, is the process that I believe to be correct. With a couple of provisos.

    Artery wall damage is happening all the time; it is a natural process, it is NOT a disease state

    Dr. Kendrick writes:

    “The main proviso is that endothelial damage is going on all the time, in everyone’s arteries, to a greater or lesser extent.

    “Therefore, we are not looking at an abnormality, or a disease, or a ‘diseased’ process.

    The formation of blood clots following endothelial damage is also a healthy, normal, process.

    If it did not happen, then we would all bleed to death.

    The blood clot gets incorporated into the artery wall

    Dr. Kendrick writes:

    “The next normal healthy process is that any blood clots that form must be incorporated into the artery wall.

    Inflammation is part of the repair process

    Dr. Kendrick writes:

    This ‘repair’ process leads to, what is referred to as ‘inflammation’ in the artery wall.

    “Once again, however, this is not a disease process, it is all quite healthy and normal.

    Problems occur when the rate of damage exceeds the rate of repair

    Dr. Kendrick writes:

    “Problems only start to occur when the rate of damage, and resultant blood clot formation, outstrips the ability of the repair systems to clear up the mess.

    Raise fibrinogen was found to be the most potent risk factor, even more potent than smoking

    Dr. Kendrick writes:

    “To my surprise, a raised fibrinogen was found to be the most potent risk factor in the Scottish Heart Health Study, ranking above smoking.

    Factors known to increase the risk of CVD also tend to increase blood clotting

    Dr. Kendrick writes:

    “... all the other things in the list above [which are known to increase CVD] both increase the tendency of the blood to clot and increase the risk of CVD.

    Inflammation is NOT the cause of CVD, because cortisone/cortisol, the most potent anti-inflammatory agent known to man, vastly increases the risk of CVD

    Dr. Kendrick writes:

    “My response to the idea that inflammation may cause CVD has always been that, the most potent anti-inflammatory agent known to man is cortisone/cortisol… vastly increases the risk of CVD.

    “However, as of today, the more potent the anti-inflammatory drug, the greater the increase in CVD.

    “Which suggests that if you interfere with the healing response to arterial injury, you are going to make thing worse – not better.
    ...
    ___

    Hobbs: Again, I encourage you to read the entire article, because it contains a lot more than just the highlights that I included above.

    Reference

    Kendrick, Malcolm. What causes heart disease – part 59. 2018.11.27.
    https://drmalcolmkendrick.org/2018/11/27/what-causes-heart-disease-part-59/

    Dr. Malcolm Kendrick’s blog is here:

    http://drmalcolmkendrick.org

    .)

    Articles on the same subject can be found here:


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