60-year old man dies of high cholesterol

1. February 2012 William Davis (12)
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.
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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?

    Nina

  • 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,

    Dennis

  • 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?

    http://www.foxnews.com/health/2012/02/10/cancer-drug-may-treat-alzheimers/
    ------------------------------------------
    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."

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Lipitor 80 mg

Lipitor 80 mg

20. March 2007 William Davis (4)
I'm seeing more and more people taking 80 mg of Lipitor per day. For the most part, these are people who come in for another opinion after a stent or heart attack and are prescribed the drug during their hospitalization.

This practice is based on the results of the PROVE IT-TIMI 22 (PRavastatin Or atorVastatin Evaluation and Infection Therapy-Thrombolysis In Myocardial Infarction) trial, and the Reversal of Atherosclerosis with Aggressive Lipid Lowering (REVERSAL) trial, both reported in 2005. In the PROVE IT Trial, 4,000 people experiencing heart attacks were treated with Lipitor (atorvastatin), 80 mg, or Pravachol (pravastatin), 40 mg. There was a reduction in events like recurrent heart attack from 13.1% in the Pravachol group to 9.6% in the Lipitor group. In the REVERSAL Trial, the Lipitor group also showed no plaque growth compared to the Pravachol group, which did progress, with disease tracked by intracoronary ultrasound.

I believe that many of my colleagues took the bait. In a half-hearted effort to reduce events and trend towards better coronary plaque control, writing a prescription for 80 mg rather than a lower dose has become increasingly popular.

Some problems: Despite the favorable tolerance to high dose Lipitor in these trials, I don't know anybody who can tolerate 80 mg per day for more than a few months in real life. In my experience, people inevitably end up with intolerable muscle aches.

Also, I believe it is folly to believe that we can regress coronary plaque on a broad scale by just using one drug that addresses only a single cause (i.e., LDL cholesterol). Yes, drug companies would argue that the statin drugs are so wonderful because of their so-called "pleiotropic", or non-lipid, effects like reducing inflammation. I have seen regression of plaque once using Lipitor alone. We struggle to reduce coronary plaque using a multi-faceted approach. It is highly unlikely that Lipitor alone at a 80 mg dose will be sufficient in most people to regress plaque. How about lipoprotein(a)? Or vitamin D deficiency? Lipitor has no effect on these patterns and people do not regress just by taking statin agents.
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Comments (4) -

  • Craig

    8/26/2009 8:08:35 PM |

    Can Kamagra and lipitor used at the same affects me ? I have heart related problem

  • buy jeans

    11/2/2010 8:49:42 PM |

    Some problems: Despite the favorable tolerance to high dose Lipitor in these trials, I don't know anybody who can tolerate 80 mg per day for more than a few months in real life. In my experience, people inevitably end up with intolerable muscle aches.

  • Anonymous

    1/24/2011 7:44:01 PM |

    As one who has taken Lipitor 80 over several years with no adverse results, including problems with liver function I disagree entirely with your statement.

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