60-year old man dies of high cholesterol

Never saw a headline like this? Neither have I. That's because it doesn't happen.

Cholesterol doesn't harm, maim, or kill. It is simply used as a crude--very crude--marker. It is, in reality, a component of the body, of the cell wall, of lipoproteins (lipid-carrying proteins) in the bloodstream. It is used a an indirect gauge, a "dipstick," for lipoproteins in the blood to those who don't understand how to identify, characterize, and quantify actual lipoproteins in the blood.

Cholesterol itself never killed anybody, any more than a bad paint job on your car could cause a fatal car accident.

What kills people is rupture of atherosclerotic plaque in the coronary arteries. For all practical purposes, you must have atherosclerotic plaque in order for it to rupture (much like a volcano erupts and spews lava). It's not about cholesterol; it's about atherosclerotic plaque. Plaque might contain cholesterol, but cholesterol is not the thing itself that causes heart attack and death.

So why do most people obsess about cholesterol? Good question. It is, at best, a statistical marker for the possibility of having atherosclerotic plaque that ruptures. High cholesterol = higher risk for heart attack, low cholesterol = lower risk for heart attack. But the association is weak and flawed, such that people with high cholesterol can live a lifetime without heart attack, people with low cholesterol can die at age 43.The same holds true for LDL cholesterol, you know, the calculated value based on flawed assumptions about LDL's relationship to total cholesterol, HDL cholesterol, and VLDL cholesterol.

A crucial oversight in the world of cholesterol: There are many other factors that cause atherosclerotic plaque and its rupture, such as inflammatory phenomena, calcium deposition, artery spasm, hemorrhage within the plaque itself, degradative enzymes, etc., none of which are suggested by cholesterol measures.

But one observation has held up, time and again, over the past 40 years of observations on coronary disease: The greater the quantity of coronary atherosclerotic plaque, the greater the risk of atherosclerotic plaque rupture. An increasing burden of atherosclerotic plaque along the limited confines of coronary arteries, just a few millimeters in diameter and a few centimeters in length, is like a house of cards: It's bound to topple sooner or later, and the bigger it gets, the less stable it becomes.

If you are concerned about future potential for heart disease and heart attack, don't get a cholesterol panel. Get a measure of coronary atherosclerotic plaque.

Comments (12) -

  • Henk Poley

    2/6/2012 3:58:02 PM |

    A nice diagram to go with this: http://perfecthealthdiet.com/wp/wp-content/uploads/2011/06/O-Primitivo-Cholesterol.jpg

    The excel file underling this diagram can be found with google.

  • nina

    2/6/2012 5:51:15 PM |

    Dear Dr Davis

    What a great post.  Do you have any idea where we can check calcium scores in the UK?


  • Dr. William Davis

    2/7/2012 3:16:55 AM |

    Hi, Nina--

    I recall that somebody from the UK posted that there was a scanner available for this purpose (London?). But it was not easy, nor are they widely available.

    Perhaps you might vacation in the U.S. and just "happen" to visit a center!

  • aerobic1

    2/7/2012 4:06:58 AM |

    The more I read the more confused I become.  Why then is LDL a part of the TYP rule of 60''s (i.e. LDL 60, HDL 60 and TG 60) if it is not the enemy?  By following a TYP wheat-free/low carb diet, supplementation and statin-free protocol for nearly two years my real LDL has jumped to 112 (it was 50 on a statin), HDL 60, TG vary from 70 to 90 and have managed my BG trend down to a HbA1c of 5.1.  With supplementation, my vitamin D is 75 ng/ml, taking 6 grams of EPA/DHA, iodine and thyroid are within TYP recommendations.  Should I not be concerned with this increase in real LDL and just focus on my other issues of keeping small LDL and Lp(a) to a minimum to manage plaque burden?  Or, if LDL has significance to plaque formation would testing for ApoE genotype be advisable.  Thank you for all your insight and advice.

  • Dennis

    2/7/2012 6:18:46 PM |

    Dr. Davis,
    In regards to inflammatory phenomena you mention, - my understanding is that Lp-PLA2 is a marker for vascular inflammation, and it especially stands out for stroke risk.
    With a high Lp-PLA2 reading – what would be the first thing you’ll focus on?
    I do not eat wheat, grains, dairy, 40 years old, very active.
    VAP showed Pattern A  LDL (103). Total Cholesterol 240. ApoB100 - 66, HDL-126,  hsCRP - 0.3,
    triglycerides - 54, homocysteine - 7, vitamin D - 63.6 ng/mL. Fasting blood glucose  - 85 and does not get
    above 110 one hour after meals.
    Thank you very much,


  • Dr. William Davis

    2/8/2012 3:06:01 AM |

    Hi, Aerobic--

    As the Track Your Plaque principles have evolved, the calculated LDL value is truly the "softest" of all. In fact, it is so soft that I believe we should discard it.

    I hate to give up the nice and memorable sound of the TYP "Rule of 60," but it is now outdated. It should now be something like the rule of "calculated LDL doesn''t matter and HDL and triglycerides should both be around 60 mg/dl." Not very catchy, though.

  • Gene K

    2/8/2012 4:08:59 PM |

    Dr Davis, are you willing to set threshold values for small LDL-P and LDL_P numbers instead?

  • Uncle Roscoe

    2/11/2012 4:14:48 AM |

    Hi Dr. Davis,

    Have you seen this?

    Cancer drug may treat Alzheimer''s

    A cancer drug has succeeded in reversing Alzheimer''s disease in its early stages in mice, according to a new study.

    The drug, bexarotene, is designed to reduce levels of amyloid beta, the protein whose presence in the brain has been most closely tied to the development of Alzheimer''s.

    In a new study, mice treated with bexarotene saw their amyloid beta levels drop 25 percent within six hours and, importantly, they showed a corresponding improvement in their cognitive function.......

    Bexarotene is already approved by the Food and Drug Administration for the treatment of cutaneous T-cell lymphoma, a type of skin cancer, and so it may be able to proceed through clinical trials more quickly than drugs not already known to be safe to administer to people.

    The study appears in the Feb.10 issue of the journal Science......

    Bexarotene works by promoting the production of another protein, called Apolipoprotein E, which binds to and clears amyloid beta from the brain.

    "This paper lends a lot to the mechanism of how ApoE may be involved in Alzheimer''s," Cramer said......

  • Dr. William Davis

    2/12/2012 2:55:33 PM |

    Hi, Uncle--

    No, news to me. Gotta be careful here. The last trial for a similar agent that reduced amyloid plaque worsened the disease.

  • Francis Williams

    2/29/2012 5:34:19 AM |

    Dr. Davis, you wrote
    "The greater the quantity of coronary atherosclerotic plaque, the greater the risk of atherosclerotic plaque rupture. An increasing burden of atherosclerotic plaque along the limited confines of coronary arteries, just a few millimeters in diameter and a few centimeters in length, is like a house of cards: It’s bound to topple sooner or later, and the bigger it gets, the less stable it becomes."

    I wonder what ''bigger'' means here. I have a 1.5mm plaque on my right carotid artery. Would that be considered big? If it does get bigger, I do understand the logic of ''the bigger the less stable'', which makes me wonder, will your program stabilize the plaque?

    Thank you.

  • Gene K

    3/1/2012 6:06:20 PM |

    While Dr Davis seems to be focused on his http://www.wheatbellyblog.com/ these days, as a successful follower of this program, I can attest that stopping the growth and even shrinking of the plaque is the TYP goal. If you read Dr Davis''s book, you will clearly see this goal stated there.

  • Dr. William Davis

    3/5/2012 1:02:08 AM |

    You are starting early, Francis, before the plaque has achieved dangerous proportions.

    Yes, these efforts are wonderfully effective for stabilizing plaque, as evidenced by the virtual absence of cardiovascular "events."