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?

    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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Blame the niacin

Blame the niacin

Despite the fact that niacin is:

1) A vitamin--vitamin B3

2) One of the oldest cholesterol-reducing agents around with a long-standing track record of effectiveness and safety

3) Available as a prescription drug as well as a variety of "nutritional supplements"

most physicians remains shockingly unaware of its benefits, effects, and side-effects. Most, in fact, are either ignorant or frightened of advising their patients on niacin use. As a result, I commonly have to tell my patients to resume the niacin that their primary care physician has (wrongly) stopped because of itchy feet, grumpiness, groin rash, urinary tract infections, nightmares, diarrhea, hair loss, runny nose, etc. All of these are REAL reasons doctors have advised patients to stop niacin (though none were actually due to niacin).

Is niacin really that troublesome? No, it's not. In fact, if used properly, it's among the most effective and safe tools available for correction of low HDL, small LDL and other triglyceride-containing lipoproteins, lipoprotein(a), and dramatic reduction of heart attack risk. If added to a statin agent, the heart attack risk reduction can approach 90%.

Statins are just too easy for doctors to prescribe. Niacin, on the other hand, requires a good 15-20 minutes to describe how to use it. It could generate an occasional phone call from a patient who struggles with the annoying but largely harmless and temporary "hot-flush" feeling, a lot like a hot blush. Given a choice, most doctors would simply choose not to be bothered. For this reason, I'll commonly see many, many people with uncorrected low HDLs and other patterns.

Have a serious discussion and press for confident answers if you find your doctor reflexively telling you that the wart on your thumb should be blamed on niacin.

Here are the steps we advise that really make taking niacin easy and tolerable:

1) Take with dinner.

2) Take with 2 extra glasses of water. If you experience the hot-flush later on, drink an additional 2 8-12 oz glasses of water i.e., a total of 16-24 oz). Extra hydration is extremely effective for blocking the hot-flush.

3) Take a 325 mg, uncoated aspirin. This is only necessary in the beginning or with any increase in dose, rarely chronically for any length of time.


This is not to say that there aren't occasional people who are truly and genuinely intolerant to niacin. It does happen. But those people are a small minority, less than 5% of people in my experience. Niacin is far more effective and safe than most physicians would have you believe.

Comments (7) -

  • madcook

    10/31/2006 6:12:00 AM |

    I've taken prescription Niaspan for over an year and a half.  Several times I've had an unintended "untoward" reaction, more than a blush, more than a flush... more like a niacin storm!  Each time I've learned something new, however.  Yes, hydration is very important.  There are certain foods and drugs which apparently dam up the same metabolic pathway as niacin, and can cause a pretty nasty reaction.  Among these, at least for me, are certain long acting antibiotics (Zithromax), spicy chai tea, pepperoni (not supposed to go there anyway!) and very spicy foods, if taken near the time of Niaspan dosing.  I was advised by my Dr. that Benadryl syrup would help to shorten the duration of the "storm".  Mostly it's a case of dietary management and timing of dosage.  The good done by niacin certainly still outweighs the occasional bad side effects!

  • Jim

    3/14/2008 4:03:00 PM |

    Another comment about niacin from this long-time niacin user, maybe folks will find it useful...
    Dr. Davis's advice to hydrate heavily to prevent/reduce flushing is, alas, not completely effective. One can easily prove this for oneself. The next time you experience a big flush, consume as much water as you are able, and see if the flush quickly resides..does it?  No. Hydration is certainly great advice, I'm not knocking it, but as a flush reduction strategy, it isn't enough. One commentor here mentioned quercetin.  It seems some recent research on certain flavonoids (quercetin, luteolin) have produced good results,better than aspirin, which was mentioned in this thread.  One needs to experiment and see if supplements such as these do help, taken maybe 30-45 minutes before the niacin dose. I have some other comments on niacin strategies I've hardly seen mentioned anywhere, but I'll wait until (1) I see my posts are approved (I'm new here), and (2) that people are interested. Let's see if there is any feedback. Regards, Jim

  • mill

    6/27/2008 5:43:00 PM |

    I've been taking niacin  2 times daily for 6 months and dropped my cholestral from 240 to 162.  Can I go back to once daily?

  • Anonymous

    12/30/2008 10:15:00 PM |

    I have seen some research papers that report that NIACIN, Nicotinamide and/or SAMe ( maybe also other methyl donors such as TMG ) can cause Parkinson's disease. I wonder if niacin can be converted to Nicotinamide in the body. Please see their abstracts and URLs below. Thank you.



    Niacin Metabolism and Parkinson’s Disease

    Tetsuhito FUKUSHIMA1)
    1) Department of Hygiene & Preventive Medicine, Fukushima Medical University School of Medicine
    Abstract
    Epidemiological surveys suggest an important role for niacin in the causes of Parkinson’s disease, in that niacin deficiency, the nutritional condition that causes pellagra, appears to protect against Parkinson’s disease. Absorbed niacin is used in the synthesis of nicotinamide adenine dinucleotide (NAD) in the body, and in the metabolic process NAD releases nicotinamide by poly(ADP-ribosyl)ation, the activation of which has been reported to mediate 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced Parkinson’s disease. Recently nicotinamide N-methyltransferase (EC2.1.1.1) activity has been discovered in the human brain, and the released nicotinamide may be methylated to 1-methylnicotinamide (MNA), via this enzyme, in the brain. A deficiency in mitochondrial NADH:ubiquinone oxidoreductase (complex I) activity is believed to be a critical factor in the development of Parkinson’s disease. MNA has been found to destroy several subunits of cerebral complex I, leading to the suggestion that MNA is concerned in the pathogenesis of Parkinson’s disease. Based on these findings, it is hypothesized that niacin is a causal substance in the development of Parkinson’s disease through the following processes: NAD produced from niacin releases nicotinamide via poly(ADP-ribosyl)ation, activated by the hydroxyl radical. Released excess nicotinamide is methylated to MNA in the cytoplasm, and superoxides formed by MNA via complex I destroy complex I subunits directly, or indirectly via mitochondrial DNA damage. Hereditary or environmental factors may cause acceleration of this cycle, resulting in neuronal death.

    Key words:
    nicotinamide N-methyltransferase, 1-methylnicotinamide, poly(ADP-ribosyl)ation, mitochondria, complex I

    Pasted from http://www.jstage.jst.go.jp/article/ehpm/10/1/10_3/_article


    Parkinson's disease: the first common neurological disease due to auto-intoxication?
    A.C. Williams1, L.S. Cartwright2 and D.B. Ramsden2
    From the Divisions of 1Neurosciences and 2Medical Sciences, University of Birmingham, Birmingham, UK
     
    Parkinson's disease may be a disease of autointoxication. N-methylated pyridines (e.g. MPP+) are well-established dopaminergic toxins, and the xenobiotic enzyme nicotinamide N-methyltransferase (NNMT) can convert pyridines such as 4-phenylpyridine into MPP+, using S-adenosyl methionine (SAM) as the methyl donor. NNMT has recently been shown to be present in the human brain, a necessity for neurotoxicity, because charged compounds cannot cross the blood-brain barrier. Moreover, it is present in increased concentration in parkinsonian brain. This increase may be part genetic predisposition, and part induction, by excessive exposure to its substrates (particularly nicotinamide) or stress. Elevated enzymic activity would increase MPP+-like compounds such as N-methyl nicotinamide at the same time as decreasing intraneuronal nicotinamide, a neuroprotectant at several levels, creating multiple hits, because Complex 1 would be poisoned and be starved of its major substrate NADH. Developing xenobiotic enzyme inhibitors of NNMT for individuals, or dietary modification for the whole population, could be an important change in thinking on primary and secondary prevention.


    Pasted from http://qjmed.oxfordjournals.org/cgi/content/full/98/3/215

    see also
    http://www.springerlink.com/content/d5wurtwylvpcy04q/


    But,on the contrary,the paper below seems to suggest that niacin protects from Parkinson's.

    Title: Does diet protect against Parkinson's disease? Part 4 – vitamins and minerals
    Author(s): Isabella Brown
    Journal: Nutrition & Food Science
    ISSN: 0034-6659
    Year: 2004 Volume: 34 Issue: 5 Page: 198 - 203
    DOI: 10.1108/00346650410560343
    Publisher: Emerald Group Publishing Limited
    Abstract: This paper is the fourth in a series on Parkinson's disease and diet and investigates the role which antioxidant vitamins A and C, niacin and selenium may have on the incidence of the disease. Oxidative stress is believed to be a key factor in the development of PD and all of these have a role in preventing oxidative stress mediated cell damage. Dietary information was obtained via questionnaires. Vitamin C was found to reduce the risk of PD by 40 per cent in one study, although this was not supported by other studies. Niacin was associated with an at least 70 per cent reduced risk of PD incidence in a number of studies. No evidence was found to support a role for vitamin A or selenium. There is a need for further research to support or disprove the roles of these antioxidant vitamins within the aetiology of PD.
    Keywords: Diet, Diseases, Lifestyles, Vitamins
    Article Type: Research paper
    Article URL: http://www.emeraldinsight.com/10.1108/00346650410560343

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    Have a serious discussion and press for confident answers if you find your doctor reflexively telling you that the wart on your thumb should be blamed on niacin.

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