My stress test was normal. I don't need a heart scan!

28. June 2006 William Davis (0)
Katy had undergone a stress test while being seen in an emergency room, where she'd gone one weekend because of a dull pain on the right side of her chest. After her stress test proved normal, she was diagnosed (I believe correctly) with esophageal reflux, or regurgitation of stomach acid up the esophagus. She was prescrbed an acid-suppressing medication with complete relief.

But Katy also had coronary plaque. Three years ago, her CT heart scan score was 157. She'd made efforts to correct the multiple causes, though she still struggled with keeping weight down to gain full control over her small LDL particle pattern.

I felt it was time for a reassessment: another heart scan. After three years, without any preventive efforts, Katy's score would be expected to have reached 345! (That's 30% per year plaque growth.) It's a good idea to get feedback on just how much slowing you've accomplished.

But Katy declared, "But I didn't think another heart scan was necessary. My stress test was normal!"

What Katy was struggling to understand was that even at the time of her first scan, a stress test would have been normal. Plaque can be present with a normal stress test.

Plaque can even show explosive growth all while stress tests remain normal. Just ask former President, Bill Clinton, how much he should have relied on stress tests. (Mr. Clinton underwent annual stress nuclear tests. All were normal and he had no symptoms--all the way up 'til the time he needed urgent bypass surgery!)

Of course, at some point even a crude stress test will reveal abnormal results. But that's years into your disease and a lot closer to needing procedures and experiencing heart attack.

So, yes, Katy would benefit from another heart scan despite her normal stress test.

The message: Don't rely on stress tests to gauge whether or not plaque has grown, stabilized, or reversed. Stress tests can be used to gauge the safety of exercise, blood pressure response, and the potential for abnormal heart rhythms. Stress tests can be used as a method to determine whether blood flow in your coronary arteries is normal through an area with plaque.

But a stress test cannot be used to gauge whether plaque has grown. It's as simple as that. Gauging plaque growth requires a heart scan.
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60-year old man dies of high cholesterol

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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Nutritional approaches to homocysteine reduction

Nutritional approaches to homocysteine reduction

3. October 2006 William Davis (0)

For an in-depth discussion of nutritional approaches to homocysteine reduction, see my new article, Nutritional Therapies for Managing Homocysteine , in the most recent issue of Life Extension magazine. You'll find it at:

http://www.lef.org/magazine/mag2006/oct2006_report_homocysteine_01.htm

The report contains a detailed discussion of how to use foods to control homocysteine levels. Though I'm not a homocysteine-crazed fanatic like Life Extension publisher, William Falloon, I still there's some interesting aspects of homocysteine metabolism that need to be explored. I also think there's some genuine benefit to reducing homocystine, preferably with foods, secondarily with supplements.

Also see our recent update on homocysteine on the www.cureality.com website at:
http://www.cureality.com/library/fl_01-006homocysteine.asp

In the update, we tried to make sense of what the new studies on homocysteine treatment, NORVIT and HOPE-2, tell us in light of all the other studies on homocysteine that preceded them.
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Heart disease "reversal" by stress test

Heart disease "reversal" by stress test

5. December 2006 William Davis (3)

Here's an interesting example of a 71-year old man who achieved "reversal" of an abnormality by a nuclear stress test.

This man underwent bypass surgery around 10 years ago, two stents three years ago. A nuclear stress test in April, 2005 showed an area of poor blood flow in the front of the heart. On the images, normal blood flow is shown by the yellow/orange areas. poor or absent blood flow is shown by the blue/purple areas within the white outline.

Now, I can tell you that this man is no paragon of health. He's only accepted limited changes in his otherwise conventional program--in other words, someone who I'd be shocked achieved true reversal of his heart disease. (I didn't have him undergo any CT heart scans because of the difficulties in scoring someone who has undergone bypass surgery and stents, and because of limited motivation. True plaque reversal is for the motivated.)This patient did, however, accept adding fish oil and niacin to his program.

Nonetheless, stress testing can be helpful as a "safety check". Here's the follow-up stress test:
You'll notice that the blue/purple areas of poor blood flow have just about disappeared. This occurred without procedures.

Does this represent "reversal"? No, it does not. It does represent reversal of this phenomenon of poor flow. It does not represent reversal of the plaque lining the artery wall. That's because improvement of flow, as in this man, can be achieved with relatively easy efforts, e.g., improvement in diet, statin drugs, blood pressure control, etc. True reversal or reduction of coronary plaque, however, is tougher.

If blood flow is improved, who cares whether plaque shrinks? Does it still matter? It does. That's because the "event" that gets us in trouble is not progressive reduction in blood flow, but "rupture" of a plaque. A reduction in plaque--genuine reversal--is what slashes risk of plaque rupture.
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Comments (3) -

  • Anonymous

    12/5/2006 5:17:00 PM |

    What are the measures one takes to reduce or reverse coronary plaque?

  • Dr. Davis

    12/5/2006 11:04:00 PM |

    That's what the entire www.trackyourplaque.com website is about.

  • buy jeans

    11/3/2010 10:04:30 PM |

    Nonetheless, stress testing can be helpful as a "safety check". Here's the follow-up stress test:
    You'll notice that the blue/purple areas of poor blood flow have just about disappeared. This occurred without procedures.

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If you have hypertension, think Lp(a)

If you have hypertension, think Lp(a)

2. July 2006 William Davis (0)
Clair has coronary disease.

Clair first came to attention at age 57 when she suffered a large heart attack involving the front of her heart (the "anterior wall") two years ago. Her cardiologist implanted a drug-coated stent. Her doctors advised her to "cut the fat" in her diet, exercise, and take Lipitor.

One year later, she required a stent to another artery (circumflex). At this point, Clair was thoroughly demoralized and terrified for her future. Her first heart attack left her heart muscle with only 50% of normal strength.

She came to my office for another opinion. Of course, one of the first things we did was to identify all causes of her heart disease. No surprise, Clair had 7 new causes not previously identified, including low HDL (37 mg/dl), a severe small LDL particle pattern (75% of all particles were small), and Lp(a).

Her blood pressure was also 190/88, despite her relatively slender build and 3 medications that reduced blood pressure. That's a Lp(a) effect: Exagerrated coronary risk along with unexpected hypertension that often seems inappropriate.

In fact, I saw several patients just this week with lipoprotein(a), Lp(a), and exagerrated high blood pressure (hypertension). It's not that uncommon.

Though it has not been described in the medical literature, our experience is that hypertension is a prominent part of the entire Lp(a) "syndrome".

Lp(a) is responsible for much-increased potential for coronary disease (coronary plaque). It increases in importance as estrogen recedes in a woman (pre-menopause and menopause) and testosterone in a man, since both hormones powerful suppress Lp(a) expression (though why and how nobody knows).

I believe that Lp(a) is also responsible for hypertension that most commonly develops in a persons mid-50s and onwards, often with a vengeance. 3 or 4 anti-hypertensive medications and still not controlled.



Role of l-arginine

L-arginine may be more helpful in this situation than others. L-arginine, recall, is the supply for your body's nitric oxide, a powerful dilator of the body's arteries and thereby reduces blood pressure. We use 6000 mg twice a day, a large dose that requires use of powder preparations rather than capsules.

More reading about l-arginine and nitric oxide is available through Nobel laureate, Dr. Louis Ignarro's book, NO More Heart Disease : How Nitric Oxide Can Prevent--Even Reverse--Heart Disease and Stroke, available at Amazon.com ( http://www.amazon.com/gp/product/0312335814/104-1247258-6443909?v=glance&n=283155).




Will l-arginine truly reverse heart disease on its own? No, I don't believe so. Contrary to Dr. Ignarro's extravagant claims, I find l-arginine a facilitator of plaque regression, i.e, it helps other strategies achieve regression, but it does not achieve regression or reversal by itself. (Note that Dr. Ignarro is a lab researcher who studies rats and has never treated a human being.)

But l-arginine may have special application in the person with lp(a), particularly if hypertension is part of the syndrome.


Note: As always, please note that I talk frankly about l-arginine and other supplements and medications but have no hidden agenda: I am not selling anything, nor am I affiliated with any source/website/store etc. that sells these products. If I advocate something, I do so because I truly believe it, not because I'm trying to sell something. I make this point because so much nonsense is propagated in the media because of profit-motive. That's not true here.
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