Is an increase in heart scan score GOOD?

20. November 2007 William Davis (30)
In response to an earlier Heart Scan Blog post, I don't care about hard plaque!, reader Dave responded:

Hello Dr Davis,

Interesting post about hard and soft plaque. I recently had a discussion with my GP regarding my serious increase in scan score (Jan 2006 = 235, Nov 2007 = 419).

After the first scan we started aggressively going after my LDL, HDL and Trig...196,59,221

And have them down to 103, 65, 92 - we still have a way to go to 60/60/60 [The Track Your Plaque target values]-

So the increase is a surprise, but my doctor said that the increase could in part be cause some of the soft plaque had been converted to hard plaque and the scan would show that conversion.


Dave's doctor then responded to him with this comment:

"Remember that although your coronary calcium score has gone up, this does not mean that you are at greater risk than you were a year ago. Remember that the most dangerous plaque is the not-yet calcified soft plaque, which will not show up on an EBT [i.e., calcium score]. It is only the safe, calcified plaque that can be measured with the EBT. [Emphasis mine.] For your score to go up like it did, while your lipids came down so much, what had to happen was that lots of dangerous unstable plaque was converted to stable, calcified plaque. There are no accepted guidelines for interpreting changes in calcium scores over time, because the scores tend to go up as treatment converts dangerous plaque to safer plaque. We do know that aggressively lowering LDL reduces both unstable and stable plaque, and we know that risk can be further lowered by adjuvant therapy such as I listed above."


Huh?

This bit of conventional "wisdom" is something I've heard repeated many times. Is it true?

It is absolutely NOT true. In fact, the opposite is true: Dave's substantial increase in heart scan score from 235 to 419 over 22 months, representing a 78% increase, or an annualized rate of increase of 37%. This suggests a large increase in his risk for heart attack, not a decrease. Big difference!

Dr. Paulo Raggi's 2004 study, Progression of coronary artery calcium and risk of first myocardial infarction in patients receiving cholesterol-lowering therapy in 495 participants addresses this question especially well. Two heart scans were performed three years apart, with a statin drug initiated after the first scan, regardless of score.

During the period of study, heart attacks occurred in 41 participants. When these participants were analyzed, it was found that the average annual increase in score over the three year period was 42%. The average annual rate of increase in those free of heart attack was 17%. The group with the 42% annual rate of increase--all on statin drugs--the risk of heart attack was 17.2-fold greater, or 1720%.

The report made several other important observations:

--20% of the heart attack-free participants showed reduction of heart scan scores, i.e., reversal. None of the participants experiencing heart attack had a score reduction.
--Only 2 of the 41 heart attacks occurred in participants with <15% per year annual growth, while the rest (39) showed larger increases.
--The intensity of LDL reduction made no difference in whether heart attacks occurred or not. Those with LDL<100 mg/dl fared no better than those with LDL>100 mg/dl.

Dr. Raggi et al concluded:

"The risk of hard events [heart attack] was significantly higher in the presence of CVS [calcium volume score] progression despite low LDL serum levels, although the interaction of CVS change and LDL level on treatment was highly significant. The latter observation strongly suggests that a combination of serum markers and vascular markers [emphasis mine] may constitute a better way to gauge therapeutic effectiveness than isolated measurement of lipid levels."

This study demonstrates an important principle: Rising heart scan scores signal potential danger, regardless of LDL cholesterol treatment. Yes, LDL reduction does achieve a modest reduction in heart attack, but it does not eliminate them--not even close.

These are among the reasons that, in the Track Your Plaque program, we aim to correct more than LDL cholesterol. We aim to correct ALL causes of coronary plaque, factors that can be responsible for continuing increase in heart scan score despite favorable LDL cholesterol values.

So, Dave, please forgive your doctor his misunderstanding of the increase in your heart scan score. He is not alone in his ignorance of the data and parroting of the mainstream mis-information popular among the statin-is-the-answer-to-everything set.

Just don't let your doctor's ignorance permit the heart attack that is clearly in the stars. Take preventive action now.
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Comments (30) -

  • Anonymous

    11/20/2007 5:41:00 PM |

    Dr Davis,

    What should Dave do?  He appears to have improved his LDL:HDL ratio as well as his total C to HDL ratio substantially, but his CAC score jumped significantly.  Maybe look at other risk factors?

    The info here gives no indication of median blood pressure for Dave.  LP(a)?  No indication of particle sizes. But, which of these or others would be most likely to be Dave's downfall in attempting to mitigate a future hard endpoint?

    I don't ask this lightly, I myself am trying to follow the TYP program and keep my high-for-my-age 29 CAC score from growning.  But, I'm frankly not looking forward to my rescan in about a year.  I'm a bit worried about the, "What if my scan shows a dramatic increase?  What then?"

    Thank you for the valuable information you provide.

    :LaughingCT

  • Dr. Davis

    11/20/2007 11:17:00 PM |

    I would urge Dave to follow all the principles of the Track Your Plaque program, including:

    1) Fish oil to provide minimum 1200 mg EPA + DHA per day

    2) Correction of all concealed lipoprotein patterns such as IDL and Lp(a)

    3) Vitamin D raised to 50 ng/ml--crucial!

    4) Normalization of blood pressure, including during exericse.

    5) Normal blood sugar (<100 mg/dl).

    Further efforts might be required, depending on the long-term effects on rate of plaque growth.

  • Ross

    11/21/2007 3:41:00 AM |

    My question is: how repeatable do you think the scores are on the CT scan?  Are they bulletproof (+/- 5% no matter where measured), consistent by analyst (+/- 5% with the same doctor analyzing the scan), or...?  

    I am currently visiting my brother in law, who is an FP doctor with a private practice.  One of his professional friends, a cardiologist who seems a cut above (thinks stenting is a cop-out), recently told him that he only trusted two centers in the mid-Ohio region to score a 16-slice CT scan accurately, and that even then, the variability was still too high for his taste.  Two numbers within 20% were within his expected error bars and weren't different enough to indicate any change to him.  Two different scan centers?  He wouldn't even compare the two scan scores.

    In my own job (software), I've had to manage human-measured numbers over and over again.  One observation keeps coming up: a single value doesn't mean much without an understanding of the accuracy of that value.  I really am curious about how you estimate confidence intervals on CT scan scores.

  • Dr. Davis

    11/21/2007 3:55:00 AM |

    Hi, Ross--

    Excellent questions.

    Several thoughts:

    1) 16-slice scanners are, unfortunately, prone to wider error in heart scan scoring, perhaps as much as 20%. The variation in scoring on an EBT or 64-slice device is far less.

    2) Variation from scan to scan, when expressed as percent, depends to a great degree on the score itself. Lumping all scores together, variation should be no more than 8-9%. However,a low score of, say 2, then repeated at 4 means 100% variation. However, the same absolute difference of 2 but with a score of 1002 and repeated at 1004 is <1% variation. Therefore, higher scores assume much less percent variation, usually <5%.

    3) Variation among different reading physicians tends to be a minor issue, since much of the scoring is done by standard criteria determined by software, not the human eye. The only real source of human variation comes from disputable areas, such as the mitral valve (which can sometimes encroach into the coronary area and appear like plaque) and the mouth of arteries, which can be debated as being in the aorta or in the coronary arteries themselves. However, these disputable areas are issues in <5% of scans.

  • Tom

    11/21/2007 4:30:00 AM |

    It's interesting that a 29 year old is able to track his plaque. I'm in my 60's now and recently found your site AFTER bypass surgery and a calcium score >700 via a 64 slice scan.
    In reading past comments, those of us having had the heart procedure are now unable to follow our progress via the cac score. Until this post I had hoped to use your recommended blood tests for indication of progress, but if LDL reduction achieves a modest risk reduction, we are left without a specific guide.
    Question: Was the progress in blood tests in dave's case a result of statins ?

  • Dr. Davis

    11/21/2007 12:46:00 PM |

    That's why lipoproteins are so important--they provide other indicators. In my experience, people who have LDL cholesterol as the sole cause of heart disease are a very small minority. The vast majority of people have multiple causes beyond LDL.

    Also, about 50% of people can still get a heart scan score after bypass surgery if you find a center willing to do a detailed analysis. You will need to ask.

    Also, I don't know what Dave did, since he is a reader and everything he posted is above. Are you there, Dave?

  • Dr. Davis

    11/21/2007 5:41:00 PM |

    Hi, Paul--

    I think your doctor might be confusing heart scans with CT coronary angiograms. She is right in saying that CT angiograms (using X-ray dye) require a lot of radiation; 100 chest x-rays worth with present technology.

    However, a plain heart scan to generate a heart scan score requires 4 chest x-rays worth on an EBT device, 8-10 on an 64-slice multi-detector device.

    See the Track Your Plaque Special Report, Radiation and Heart Scans: The Real Story at http://trackyourplaque.com/library/fl_06-021radiation.asp.

  • Anonymous

    11/21/2007 6:01:00 PM |

    Regarding repeatability, there is a 2005 study by Serukov, Bland, and Kondos that shows that the repeatability is a function of the square root of the calcium score, and that volume score is more repeatable than Agatston score. The reference is

    “Serial Electron Beam CT Measurements of Coronary Artery Calcium: Has Your Patient's Calcium Score Actually Changed?” Alexander B. Sevrukov, J. Martin Bland and George T. Kondos, American Journal of Roentgenology 2005; 185:1546-1553
    http://www.ajronline.org/cgi/content/full/185/6/1546

    In this report, the standard deviation of the difference between two sequential calcium scored is

    SDAG130 = 2.515 *sqrt(avg score)
    SDVol130 = 1.758 *sqrt(avg score)

    This results in the following values, where SDA is the standard deviation for the Agatston score and SDV is the standard deviation for the volume score.

    Score-SDA--%SDA--SDV--%SDV
    5-----5.62---112%---3.93--79%
    10----7.95---79%----5.55--56%
    20----11.2---56%----7.86--39%
    50----17.7---35%----12.4--25%
    100---25.1---25%----17.5--18%
    200---35.5---17%----24.8--12%
    300---43.5---14%----30.4--10%
    400---50.3---12%----35.1---9%
    500---56.2---11%----39.3---8%
    600---61.6---10%----43.0---7%
    700---66.5----9%----46.5---7%
    1000--79.5----7%----55.5---6%

    These values show why many people use 15% as a breakpoint - only if the score has changed by more than 15% can it be said that the change is real. And this is only true for scores above 200 or so.

    Harry

  • Anonymous

    11/21/2007 7:17:00 PM |

    My cardiologist told me that EBT scanning is not recommended for anyone under the age of 30. Is this true? If so, how do I (29 years) reliably know that I am at risk?

    I discovered your blog recently. Since I have a very bad family history of diabetes, high blood pressure, and cholesterol, I decided to visit a cardiologist last month so that I can request for an EBT scan. He said that I'm too young for that, and has instead asked me to take a Carotid IMT and Stress test - are these tests reliable enough to provide insight on my risk? Could these tests return "false positive" values?

    I had found during a blood test I did this July only to find that my triglycerides were at 600!! The other cholesterol values were bad too - totalC-HDL-LDL-Tri (255-31-Not measurable-600)

    Since then I have found your blog, lost around 25 lbs and did a VAP recently (I asked for NMR and all I got from doctors - what? What the heck is that?) So I settled for a VAP, since they knew about it.

    I did a VAP along with a comprehensive blood test and the measures that came up high were.

    LIPID related:
    Total LDL-C Direct:130 (Normal<130)
    Real LDL-C:110 (N<100)
    Sum Total LDL-C: 130 (<130)
    Remnant LIPO (IDL+VLDL3): 30 (<30)
    HDL-2:9 (>10)
    VLDL3: 14 (<10)

    Non-LIPID related high values:
    Uric Acid: 8.3  (4.0-8.0)
    Fasting Glucose: 104 (65-99)
    Creatine Kinase Total: 631 (<=200)


    LP PLA2 is normal: 164 (115-245)
    HBA1C suggests prediabetic: 5.7 (Normal <6%)


    Due to my very high value of CK Total, I researched online and found that this can increase due to high exercise, and I had it repeated after taking rest, and it returned normal results. My doctor was really surprised about this and initially hesitant to fractionise my CK. I feel empowered that I am able to take charge of my health and preventative care with the
    information that is available online (of course, one needs to tread that carefully and make an informed decision due to various conflicting opinions out there).

    Sorry for the long post, Doc. I have a newfound awareness of my health thanks to your blog, and am very much interested in knowing your inputs. I just hope that more physicians in our country follow your noble path and understand the true value and empowerment of preventive care.

    - Philip

  • Dr. Davis

    11/21/2007 8:09:00 PM |

    Hi, Philip--

    In general, 29 is very young, perhaps too young, unless there is an outstanding family history (e.g., father with heart attack at age 37). Although your lipid/lipoproteins are concerning, it would be highly unusual to have anything but a zero heart scan score at your age.

  • Dr. Davis

    11/21/2007 8:14:00 PM |

    Hi, Harry--
    Thanks for the help!

  • Neelesh

    11/22/2007 4:51:00 AM |

    Hi Dr. Davis,
      I've just bought the Track Your Plaque book, waiting for its arrival. I've had a heart attack a year back.I'm 30 years old with no family history, non-alcoholic, non-smoker and vegetarian.
    The event was attributed to ectatic arteries(Type-III) and a very high level of LP(a)- between 120-130. The standard lipid profile was also marginally higher. If I had not insisted for an LP(a) test after reading Dr Agatston's South Beach Heart Program, I would have never found the LP(a) factor.
       I was stented during the hospitalization and now I'm wondering how effective the heart scan will be, given that the accuracy reduces  with stented arteries (http://circ.ahajournals.org/cgi/content/meeting_abstract/114/18_MeetingAbstracts/II_692-a)

    Thanks!
    -Neelesh

  • Dr. Davis

    11/22/2007 2:35:00 PM |

    Hi, Neeleesh--

    I do advocate heart scanning in people with stents, but I generally suggest that only the unstented arteries be scored. It's imperfect, excluding the most diseased artery, but it's proven a useful compromise, leaving you with two "scorable" arteries.

    The study you cite, however, is not about heart scans, it's about CT coronary angiography, a study that yields "percent blockage" sort of information, not an index of plaque.

    Beyond Lp(a), you should strongly consider vitamin D normalization.  By your first name, I take it you are from India/Pakistan or similar background, an ethnic origin that is associated with severe vitamin D deficiency.

  • Neelesh

    11/22/2007 3:00:00 PM |

    Thanks Dr. Davis. And yes, I'm from India.

  • wccaguy

    11/22/2007 3:13:00 PM |

    Dr. Davis,

    I found your answer to Neeleesh to be interesting in the extreme.  I have a  follow up question to it.

    I don't have specific references for the two facts I have heard but couldn't reconcile:

    1   India has high coronary artery disease incidence.

    2   Your answer to Neeleesh states that vitamin d levels are low in India and Pakistan.  And that would help much to explain the high rate of coronary artery disease in these countries.

    3   And yet India is close to the equator and so vitamin d levels should be relatively high because of sun exposure right?

    The question then is this:  What is the cause of the low vitamin d level in those countries?

    Thanks!

  • Dr. Davis

    11/22/2007 4:00:00 PM |

    It is interesting, isn't it?

    I believe part of the explanation is that, the darker your skin complexion, the more you are "protected" from intense and prolonged sun exposure. But, activation of 7-hydrocholesterol to 25-OH-vitamin D3 may require many hours more exposure. Thus, a fair skinned person might activate D within minutes, while a dark skinned individual might require hours.

    Another factor that has not been thoroughly explored but has potential for yielding enormous insights: Vit D receptor genotypes. That is, vitamin D deficiency may express itself in different ways in different populations. Some might get colon cancer, others multiple sclerosis, others coronary disease.

    I believe that the dark-skinned phenomenon becomes especially an issue when migrating to sun-deprived climates such as the northern U.S.

  • wccaguy

    11/22/2007 6:12:00 PM |

    Hi Doc,

    Your explanation makes sense.

    I did a quick google search and found experts on the problem in India attributing it to the increasing extent to which Indians were staying indoors and not "being active."

    But the vitamin D issue throws the whole question of "activity" into question doesn't it?  It might not be the activity per se but instead the amount of sunlight reduction.

    And if, per your explanation, darker skinned people need more time in the sun than lighter skinned people for Vitamin D3 to be "activated" then than a decrease in sunlight would have more effect on darker skinned people than lighter skinned people.

    Very interesting...  And perhaps INCREDIBLY good news!!!

    Because it means that there might be a cheap effective treatment for the coronary disease epidemic in India.

    Does all that make sense?

  • wccaguy

    11/22/2007 6:19:00 PM |

    Just to follow up one more point on this D3 question...

    I guess what we need to do is find a study which shows a correlation between degree of skin pigmentation and Vitamin D3 activation?

    (I'm not sure if the word "degree" is the right word, but perhaps the question is understood anyway?)

    Answering that question would certainly set up the basis for a scientific study right?

  • Dr. Davis

    11/23/2007 12:56:00 AM |

    Yes, it does. It could serve as the basis for a tremendously interesting study.

  • Dr. Davis

    11/23/2007 1:09:00 AM |

    There are indeed a few studies that document this effect, e.g., Factors that influence the cutaneous synthesis and dietary sources of vitamin D (abstract viewable at Arch Biochem Biophys. 2007 Apr 15;460(2):213-7.)

    However, I am not aware of any study that examines the effect of vitamin D supplementation specifically in this population that tracks coronary atherosclerosis. One British study  in Bangladeshi adults did demonstrate dramatic reduction in inflammatory markers with vit D replacement (Circulating MMP9, vitamin D and variation in the TIMP-1 response with VDR genotype: mechanisms for inflammatory damage in chronic disorders? at http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=12454321&ordinalpos=22&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum  ).

  • Dave K

    11/24/2007 12:21:00 AM |

    Hi Dr Davis,

    Sorry - I have been offline for a couple of days.  Interesting discussion.  I will try and add some detail lipid info.

    July 2007 Blood work showed

    My Lp(a) is 7
    IDL = 10
    VLDL=11
    HDL-2 = 15
    HDL-3 = 50
    VLDL C = 18
    VLDL1+2 = 7

    Currently taking fishoil 1700 mg of DHA+EHA
    Vitamin D 800mg - just incresed to 2000
    Baby Aspirin
    Multivitamin
    Crestor
    Just started Zetia after getting this last scan result
    Eat basic South Beach phase 3
    BMI - 27
    Glucose is 105
    Exercise 4X week...
    Lp-PLA2=120

    Blood pressure high-normal but I don't know about during exercise.  Cardilogist scheduled me for a stress test after this volume increase.

    I have not has a blood test for Vit D.

    Also - I had an angiograham after the first scan because I was having chests pains .... it turned up that I had no blockages whatsoever.  So we judged the chest pains as non cardiac.

    So I am following your list pretty close.  I guess I just have to wait to see how these changes do.  How long would you wait for another scan?

    Not sure what else to add - your website says to consider L-arginie...


    I do have a specific question.  In the scan report it shows where the calcium was found.  Don't know the software, but there was one spot where it showed in the early report that it didn't show in this report (of course there was several new areas) - could that have actually been a reversal at that spot?

  • Dr. Davis

    11/24/2007 1:25:00 AM |

    Small LDL and a deficiency of large HDL, along with modest excess weight, high blood sugar, high blood pressure all suggest you are (or were) likely over-dependent on processed carbohydrates like wheat products. Your pattern would likely respond vigorously to reduction or elimination of these foods and weight loss. Niacin can help this pattern. In our experience, normalization of vitamin D is crucial.

  • Dave K

    11/26/2007 5:51:00 AM |

    Dr Davis,

    Few more data ....

    Some of the treatments have only been for the last 6 months or so.  The Statin was first (of course) and it took almost a year to get something I could tolerate.  The we talked about Vit D (700) and fish oil (800 Omega 3).  After a full Lipid scan around 9 months ago - we decided to add more fish oil.  So the full dosage I listed is only 6 months old or so.

    Also - I love my red wine and I know the number says two glasses and i rarely do two - so its three or four ... which might be my next step....

    From your last response, I assume the VLDL and IDL levels are the ones you would target hardest at this point.

    Don't do a lot of sugar or wheat... Do eat Oatmeal everyday with rasins or blueberries.

    Oh and my other question was with this kind of increase how long would you wait for the next scan?

  • Dr. Davis

    11/26/2007 12:08:00 PM |

    Dave-

    I generally recommend waiting a year after all identifiable causes have been corrected. However, given your minimal doses of vit D, I usually have my patients wait at least six month after vitamin D blood levels are corrected.

  • Dave

    11/26/2007 8:01:00 PM |

    Dr Davis,

    Thank you ... keep up the great work and I'll keep reading... and tracking.

    Dave

  • G

    11/27/2007 12:39:00 AM |

    Neeleesh and DR. D,

    This Canadian physician appears to have a lot of indepth awareness of the diff phenotypes. He suggests (in the author's response) that D2 may not work as well in East Indians (may worsen glycemic control) versus D3 (the more biologically active vitamin D). Very fascinating!!

    http://www.cfp.ca/cgi/reprint/53/9/1435
    Repletion of vitamin D with vitamin D2 is common
    practice, and vitamin D2 can be used safely when monitored
    to achieve normal levels of 25(OH)D. This might
    take 2 to 3 months, as discussed in your letter and in my
    paper, because the half-life is about 2 weeks. Using vitamin
    D3 (1000 to 5000 IU) daily, depending on the level
    of deficiency, will also achieve this goal. I also agree
    that the goal is to achieve levels of 25(OH)D higher than
    100 nmol/L, preferably 100 to 125 nmol/L.
    My concern regarding vitamin D2 is that it is a synthetic
    analogue and might interact with the vitamin D
    receptor differently in various cell systems. It has been
    reported that vitamin D3 might improve glycemic control.
    7 Vitamin D2 has been reported to cause worsening
    of glycemic control in people of East Indian descent.8
    Is this because of vitamin D receptor polymorphism, or
    because of enhanced 24-hydroxylase enzyme activation,
    or is it due to how vitamin D2 interacts with the receptor?
    Until this has been sorted out, I feel safest using
    vitamin D3. There are about 2000 synthetic analogues
    of vitamin D. The search is on for one that can cross the
    blood-brain barrier to treat certain types of brain cancers
    without causing hypercalcemia.9 But then again,
    what other effects would this compound have? There
    are still so many unknowns.
    The first step is to recognize that most Canadians
    do not get enough vitamin D, especially in the winter
    months, because of where we live. This recognition
    might reduce the need for expensive drugs to treat
    various conditions and might improve the well-being of
    many Canadians.
    An ounce of prevention is worth a pound of cure.
    —Gerry Schwalfenberg MD CCFP
    Edmonton, Alta
    by e-mail

    here's the orig article which is one of the most excellent summaries I've seen so far -- great minds think alike -- they advise > 50ng/ml like DR. Davis as well!
    http://www.cfp.ca/cgi/reprint/53/5/841

  • Neelesh

    11/27/2007 4:05:00 AM |

    D,
    Interesting study indeed. Thanks for the information. I guess I have a lot of things to discuss with my cardiologist next week. Smile
    -Neelesh

  • chickadeenorth

    12/2/2007 11:16:00 PM |

    Hi to Gerry Schwalfenberg MD CCFP, do you know any Dr In Edtmn who practices Track your Plague, if so could you suggest names to help me. I live out by Jasper and need a skilled Dr in this treatment program, I would travel to Edtmn.Many thanks.
    chickadeenorth
    (hope its ok for me to ask this here)

  • cadoce66

    4/5/2008 8:37:00 PM |

    hi my aunts 63 yrs and she underwent an angioplasty with a medicated stent .. Shes on PLAVIX and her artery was 90% blocked and she had an evolving AWMI...
    Please advise what she should taketo prevent another blockage or heart attack!
    Thanks!

  • buy jeans

    11/3/2010 10:34:10 PM |

    So, Dave, please forgive your doctor his misunderstanding of the increase in your heart scan score. He is not alone in his ignorance of the data and parroting of the mainstream mis-information popular among the statin-is-the-answer-to-everything set.

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Don't be satisfied with "deceleration"

16. November 2007 William Davis (2)
In the Track Your Plaque program, we aim to stop or reduce your heart scan score.

Recall that, without any preventive efforts, heart scan scores can be expected to increase at the average rate of 30% per year (faster at lower scores, slower at higher scores by a quirk of arithmetic).

I am continually surprised at how often people--that is, people not in the Track Your Plaque program--are often content with what I term "deceleration," or the slowing of plaque growth. In truth, most people are content with deceleration of plaque growth because they simply don't know that plaque continues to grow.

For instance, the BELLES Trial (Beyond Endorsed Lipid Lowering with EBT Scanning (BELLES)), reported in 2005 showed that 650 women participants continued to increase heart scan scores 15% whether they took "high-intensity" statin therapy in the form of Lipitor 80 mg or "low-intensity" statin therapy as pravastatin 40 mg, even though the group taking Lipitor experienced twice the amount of LDL reduction. In other words, heart scan scores continued to increase at the same rate of 15% per year regardless of the intensity of LDL lowering by statin drug.

Another study reported in 2006, Effect of intensive versus standard lipid-lowering treatment with atorvastatin on the progression of calcified coronary atherosclerosis over 12 months: a multicenter, randomized, double-blind trial reported similar results. Of the 471 participants, those taking Lipitor 80 mg per day experienced 27% per year plaque growth (LDL cholesterol 87 mg/dl); those taking 10 mg Lipitor experienced 25% plaque growth (LDL 107 mg/dl). The intensity of statin therapy made no difference on the rate of plaque growth.

In other words, if we are content to sit back and take Lipitor or other statin drug, follow the conventional American Heart Association low-fat, low-cholesterol diet, we will experience somewhere between 15 to 27% annual plaque growth--year after year.

No wonder that conventional advice offered by your friendly neighborhood doctor will avoid (postpone?) only one heart attack in four.

Such is the nature of coronary plaque deceleration: growth is modestly slowed, but is not stopped. Nor is it reversed.

In the Track Your Plaque program, we grade deceleration of plaque growth into three distinct stages out of a total of five. (See Winning Your Personal War with Heart Disease: The Track Your Plaque 5 Stages of Success.)

Why be satisfied with deceleration? Why not aim for a total stop to plaque growth? Why not aim for stage 5 of Track Your Plaque success: reversal?

Whole grains and half truths

14. November 2007 William Davis (13)
(For followers of the Heart Scan Blog, below is a re-posting of a recent post. I've moved it up to make it accessible to a number of patients that I asked to look at this post for some conversation about the concept of wheat-free diets.)


TV ads, media conversations, magazine articles, even advice from the American Heart Association and USDA (a la Food Pyramid) all agree: eat more whole grains, get more fiber.

What happens when you follow this advice to add more and more whole grains to your diet? Look around you: People gain weight, they become pre-diabetic and diabetic. Lipids and lipoprotein patterns emerge: increased triglycerides and VLDL, reduced HDL, small LDL. Blood sugar goes up, inflammatory responses are ignited. You feel crumby, cancer risk is increased.

"Official" agencies have urged us to eat more grains, get more fiber and most Americans have complied. We now have a nationwide health disaster that will eventually lead to more people with coronary plaque, more heart disease, more heart attack, more heart procedures.

This is why I've been urging patients to go wheat-free. It has proven an extraordinarily and surprisingly effective strategy for:

1) rapid and profound weight loss
2) raising HDL and reducing triglycerides, VLDL, and small LDL
3) reducing blood sugars, pre-diabetes and diabetes

So here I (re-) post just a sampling of the comments sent by readers of the Heart Scan Blog who have given this idea a try.






Barbara W said:

It's true! We've done it. My husband and I stopped eating all grains and sugar in February. At this point, we really don't miss them any more. It was a huge change, but it's worth the effort. I've lost over 20 pounds (10 to go)and my husband has lost 45 pounds (20 to go). On top of it, our body shapes have changed drastically. It is really amazing. I've got my waist back (and a whole wardrobe of clothes) - I'm thrilled.

I'm also very happy to be eating foods that I always loved like eggs, avocados, and meats - without feeling guilty that they're not good for me.

With the extremely hot weather this week in our area, we thought we'd "treat" ourselves to small ice cream cones. To our surprise, it wasn't that much of a treat. Didn't even taste as good as we'd anticipated. I know I would have been much more satisfied with a snack of smoked salmon with fresh dill, capers, chopped onion and drizzled with lemon juice.

Aside from weight changes, we both feel so much better in general - feel much more alert and move around with much greater flexibility, sleep well, never have any indigestion. We're really enjoying this. It's like feeling younger.

It's not a diet for us. This will be the way we eat from now on. Actually, we think our food has become more interesting and varied since giving up all the "white stuff". I guess we felt compelled to get a little more creative.

Eating out (or at other peoples' places) has probably been the hardest part of this adjustment. But now we're getting pretty comfortable saying what we won't eat. I'm starting to enjoy the reactions it produces.


Weight loss, increased energy, less abdominal bloating, better sleep--I've seen it many times, as well.


Dotslady said:

I was a victim of the '80s lowfat diet craze - doc told me I was obese, gave me the Standard American Diet and said to watch my fat (I'm not a big meat eater, didn't like mayo ... couldn't figure out where my fat was coming from! maybe the fries - I will admit I liked fries). I looked to the USDA food pyramid and to increase my fiber for the constipation I was experiencing. Bread with 3 grams of fiber wasn't good enough; I turned to Kashi cereals for 11 years. My constipation turned to steattorrhea and a celiac disease diagnosis! *No gut pains!* My PCP sent me to the gastroenterologist for a colonscopy because my ferritin was a 5 (20 is low range). Good thing I googled around and asked him to do an endoscopy or I'd be a zombie by now.

My symptoms were depression & anxiety, eczema, GERD, hypothyroidism, mild dizziness, tripping, Alzheimer's-like memory problems, insomnia, heart palpitations, fibromyalgia, worsening eyesight, mild cardiomyopathy, to name a few.

After six months gluten-free, I asked my gastroenterologist about feeling full early ... he said he didn't know what I was talking about! *shrug*

But *I* knew -- it was the gluten/starches! My satiety level has totally changed, and for the first time in my life I feel NORMAL!


Feeling satisfied with less is a prominent effect in my experience, too. You need to eat less, you're driven to snack less, less likely to give in to those evil little bedtime or middle-of-the-night impulses that make you feel ashamed and guilty.



An anonymous (female) commenter said:

My life changed when I cut not only all wheat, but all grains from my diet.

For the first time in my life, I was no longer hungry -no hunger pangs between meals; no overwhelming desire to snack. Now I eat at mealtimes without even thinking about food in between.

I've dropped 70 pounds, effortlessly, come off high blood pressure meds and control my blood sugar without medication.

I don't know whether it was just the elimination of grain, especially wheat, or whether it was a combination of grain elimnation along with a number of other changes, but I do know that mere reduction of grain consumption still left me hungry. It wasn't until I elimnated it that the overwhelming redution in appetite kicked in.

As a former wheat-addicted vegetarian, who thought she was eating healthily according to all the expert advice out there at the time, I can only shake my head at how mistaken I was.


That may be a record for me: 70 lbs!!


Stan said:

It's worth it and you won't look back!

Many things will improve, not just weight reduction: you will think clearer, your reflexes will improve, your breathing rate will go down, your blood pressure will normalize. You will never or rarely have a fever or viral infections like cold or flu. You will become more resistant to cold temperature and you will rarely feel tired, ever!


Ortcloud said:

Whenever I go out to breakfast I look around and I am in shock at what people eat for breakfast. Big stack of pancakes, fruit, fruit juice syrup, just like you said. This is not breakfast, this is dessert ! It has the same sugar and nutrition as a birthday cake, would anyone think cake is ok for breakfast ? No, but that is exactly the equivalent of what they are eating. Somehow we have been duped to think this is ok. For me, I typically eat an omelette when I go out, low carb and no sugar. I dont eat wheat but invariably it comes with the meal and I try to tell the waitress no thanks, they are stunned. They try to push some other type of wheat or sugar product on me instead, finally I have to tell them I dont eat wheat and they are doubly stunned. They cant comprehend it. We have a long way to go in terms of re-education.

Yes. Don't be surprised at the incomprehension, the rolled eyes, even the anger that can sometimes result. Imagine that told you that the food you've come to rely on and love is killing you!


Anne said:

I was overweight by only about 15lbs and I was having pitting edema in my legs and shortness of breath. My cardiologist and I were discussing the possible need of an angiogram. I was three years out from heart bypass surgery.

Before we could schedule the procedure, I tested positive for gluten sensitivity through www.enterolab.com. I eliminated not only wheat but also barley and rye and oats(very contaminated with wheat) from my diet. Within a few weeks my edema was gone, my energy was up and I was no longer short of breath. I lost about 10 lbs. The main reason I gave up gluten was to see if I could stop the progression of my peripheral neuropathy. Getting off wheat and other gluten grains has given me back my life. I have been gluten free for 4 years and feel younger than I have in many years.

There are many gluten free processed foods, but I have found I feel my best when I stick with whole foods.


Ann has a different reason (gluten enteropathy, or celiac disease) for wanting to be wheat-free. But I've seen similar improvements that go beyond just relief of the symptoms attributable to the inflammatory intestinal effects of gluten elimination.



Wccaguy said:

I have relatively successfully cut carbs and grains from my diet thus far.

Because I've got some weight to lose, I have tried to keep the carb count low and I've lost 15 pounds since then.

I have also been very surprised at the significant reduction in my appetite. I've read about the experience of others with regard to appetite reduction and couldn't really imagine that it could happen for me too. But it has.

A few weeks ago, I attended a party catered by one of my favorite italian restaurants and got myself offtrack for two days. Then it took me a couple of days to get back on track because my appetite returned.

Check out Jimmy Moore's website for lots of ideas about variations of foods to try. The latest thing I picked up from Jimmy is the good old-fashioned hard boiled egg. Two or three eggs with some spicy hot sauce for breakfast and a handful of almonds mid-morning plus a couple glasses of water and I'm good for the morning no problem.

I find myself thinking about lunch not because I'm really hungry but out of habit.

The cool thing too now is that the more I do this, the more I'm just not tempted much to do anything but this diet.


Going wheat-free, along with a reduction in processed sugary foods like Hawaiian Punch, sodas, and candy, is the straightest, most direct path I know of to lose weight, obtain all the health benefits listed by our commenters, as well as achieve the lipoprotein corrections we seek, like reduction of small LDL particles and rise in HDL, in the Track Your Plaque program.

Fasting and heart disease

14. November 2007 William Davis (10)
Followers of the Track Your Plaque program know that we advocate periodic fasts to reduce heart disease risk.

I came across an interesting report form an abstract presented at last week's American Heart Association meetings in Orlando:

(Read the report at HeartWire. You will need to register or sign-in.)

In this study, the investigators tried to determine why members of the Church of Jesus Christ of Latter-Day Saints (LDS) tended to have reduced risk of heart disease compared to others in the area but not in the LDS faith. While the reduced risk of heart disease in LDS members had been traditionally attributed to the no smoking policy advocated by the Mormon church, the investigators suspected that there was more to the reduced risk.

Of 515 people interviewed, periodic fasting, whether for religious or other reasons, was found to distinguish people who were less likely to have coronary disease by conventional catheterization (59% vs. 67%). (Since the study was published in only abstract form, it's not clear why all these people underwent heart catheterization in the first place.)

Nonetheless, it's an interesting observation and one consistent with the benefits we see when someone fasts: reduced blood pressure, reduced inflammatory responses, improved lipids and lipoproteins, weight loss.

Fasting can be an especially effective method to gain control over heart disease and coronary plaque if rapid control is desired. In fact, I wonder if the normally year-long process of plaque control that I advocate can be much abbreviated. Fasting, I believe, is a crucial component of rapid control, what I've talked about in Instant Heart Disease Reversal

There's also additional thoughts on fasting in my Heart Scan Blog post, For rapid success, try the "fast" track.

Fasting is not something to fear. It can be an enlightening process that can serve to abruptly sever bad habits, perhaps even turn the clock back on prior dietary and lifestyle excesses. My favorite variation on fasting is to use soy milk (yes, yes, I know! I can already hear the the soy bashers screaming!) as a meal substitute. It is an easy, less dramatic way that still maintains most of the benefit of a full, water-only fast.

Coronary arteries aren't what they seem

12. November 2007 William Davis (5)
Why do stress tests so often fail to detect coronary atherosclerotic plaque? Why do even heart catheterizations--the "gold standard"--fail to disclose the full extent of plaque within the walls of coronary arteries?

We owe much of the explanation of these phenomena to Dr. Seymour Glagov, retired professor of pathology at the University of Chicago.



When studying the coronary arteries of people who died, he observed that people commonly had plenty of atherosclerotic plaque lining the artery wall, yet it did not necessarily impinge on the artery "lumen," or the internal path for blood to flow.

The only time the lumen became obstructed by plaque was when either 1) plaque grew to overwhelming levels and was severe and extensive, or 2) when a plaque had "ruptured," meaning its thin covering had been penetrated and eroded by the underlying plaque tissue like a volcano emerging from the surface and erupting.

This groundbreaking observation, now dubbed "the Glagov phenomenon," explains why someone can have a normal stress test on Tuesday but erupt a plaque on Wednesday.

The Glagov phenomenon also explains why heart scans can detect plaque when both stress tests and heart catheterizations fail to do so. Many physicians will then interpret this to mean that the heart scan was wrong. With the Glagov phenomenon in mind, you can see that the heart scan is not wrong, it is simply detecting coronary atherosclerotic plaque at a stage that is not yet detectable by the other methods.

In the illustration, you can see that the lumen of the vessel is maintained--despite the artery on the left having minimal plaque, the artery on the right containing moderate plaque. If either artery were examined by a test that relies on blood flow--stress test or heart catheterization--both would appear normal. But a test that examines the artery wall, such as a heart scan, would readily detect the artery on the right and probably even the artery on the left.




I am very grateful to Dr. Glagov and his insight into this important process. Otherwise, we might still be floundering around trying to understand the apparent discrepances between these tests that simply provide different perspectives on the same problem.

Heart disease reversal a big "No No"

11. November 2007 William Davis (7)
I dare you: Ask your doctor whether coronary heart disease can be reversed.

My prediction is that the answer will be a flat "NO." Or, something like "rarely, in extraordinary cases," kind of like spontaneous cure of cancer.

There are indeed discussions that have developed over the years in the conventional scientific and medical literature about reversal of heart disease, like Dean Ornish's Lifestyle Heart Trial, the REVERSAL Trial of atorvastatin (Lipitor) and the ASTEROID Trial of rosuvastatin (Crestor). Reversal of atherosclerotic plaque in these trials tends to be small in scale and sporadic.

Of course, the medical literature is swamped with studies that have nothing to do with reversal, like what stent is best, what platelet-inhibiting intravenous drug is best, when should angioplasty or stents be used and when, do implantable defibrillators save lives, improvements in coronary bypass techniques, etc. There are tens of thousands of these studies for every study that focuses on the question of atherosclerotic plaque reversal.

The concept of reversal of heart disease has simply not gained a foothold in the lexicon nor in the thinking of practicing physicians. Heart disease is a relentlessly, unavoidably, and helplessly progressive disease in their way of thinking. Perhaps we can reduce the likelihood of cardiovascular events like heart attack and death with statin drugs and beta blockers. But reverse heart disease ? In your dreams!

We need to change this mentality. Heart disease is a reversible phenomenon. Atherosclerosis in other territories like the carotid arteries is also a reversible pheneomenon. Rather than throwing medicines and (ineffective) diets at you (like the ridiculous American Heart Association program), what if your doctor set out from the start not just to reduce events, but to purposefully reduce your heart's plaque? While it might not succeed in everyone, it would certainly change the focus dramatically.

After all, isn't this the theme followed in cancer treatment? If you had a tumor, isn't cure the goal? Would we accept an oncologist's advice to simply reduce the likelihood of death from cancer but ignore the idea of ridding yourself completely of the disease? I don't think so.

Then why accept "event reduction" as a goal in heart disease? We shouldn't have to. Heart disease reversal--elimination--should be the goal.

Demystification

11. November 2007 William Davis (2)
Once upon a time, remember how medical information was mysterious, hospitals were places where frightening, inscrutable things happened, diseases were strange maladies that struck without reason, and obtaining information about health was like hunting for buried treasure? The full extent of many peoples' understanding of health came through relatively anemic sources like Readers' Digest. (Remember "I am Joe's Colon"?)

Compare this to what we have now. If I wanted to obtain information about ankylosing spondylitis (a rare genetic disease of the spine), a Google search yields 1.46 million citations. Not all the information, of course, is helpful or relevant, but there's certain to be a bounty of information that far exceeds what you could have uncovered 40 years ago.




Suppose you enter the search phrase "antithrombin III" into your Google search. Citations: over 900,000. (The number of search citations, in fact, exceeds the number of Americans with a deficiency of this blood clotting protein!)

The same is true with heart disease. There was a time, not more than 30-40 years ago, when information about the heart and heart disease was hard to come by. The most you would find were superficial discussions about heart attacks, what chest pain means, descriptions of bypass surgery. Ask your doctor, you'd likely receive a brief, cursory response about how you probably shouldn't worry it.

Even during medical school in the 1980s, I remember struggling to get answers to my questions from faculty during medical school and medical training. It was as if providing too much information would eliminate the advantage superiors wielded over trainees.

The same selfish sentiment, the "I know something you don't know" mentality reminiscent of a schoolboy's "naa na na naa naa!" unfortunately persists. But it is rapidly disintegrating. Soon it will join the junk heap of medical mis-information accumulated over the years (a big pile, to be sure). The internet and, I'll admit (grudgingly), the media, have been responsible for demystifying the formerly mysterious and indecipherable world of health.

You now have, at a moment's disposal, access to an extraordinary array and breadth of health information that was inconceivable just a few years ago.

Times are changing. Doctors no longer hold the monopoly over health information. The public--YOU--are rapidly becoming the arbiters of health, the informed consumers of a soon-to-be retail product called health care, and the increasingly savvy judges of what should join the mainstream path of health. It is all part of this wave of change that I've been advocating: the emerging concept of self-empowerment in healthcare.

Added to the junk heap of health-mistakes-of-years-past will be medical protectionism over health information, heart procedures, drug industry excesses, nutritional mis-information, among others. The demystification of health information will open the floodgates of individual insight into health. It delivers control over your own health destiny straight into your own lap.

Everything has omega-3

8. November 2007 William Davis (5)
Walking the supermarket aisles, you may have lately noticed that numerous new products are appearing sporting "omega-3s" on the label.

Some products simply contain alpha-linolenic acid, a tiny amount of which is converted to the biologically active omega-3s, EPA and DHA. Natural Ovens' Brainy Bagel, for instance, carries a claim of "620 omega-3."



I find this confusing and misleading, since people will often interpret such a claim to mean that it contains 620 of EPA and DHA, similar to two capsules of standard fish oil (1000 mg capsules). Of course, it does NOT. I find this especially troublesome when people will actually stop or reduce their fish oil, since they've been misled into thinking that products like this bread contain active omega-3 fatty acids that yield all the benefits of the "real stuff."


Other products actually contain the omega-3, DHA, though usually in small quantities. Breyer's Smart with DHA is an example, with 32 mg DHA per container.


I find products with actual DHA (from algae) a more credible claim. However, the Center for Science in the Public Interest (CSPI) has looked at the actual contents of DHA in some of these products and found some discrepancies, including amounts of DHA less than the labeled amount and claims of omega-3 wihtout specifying DHA vs. linolenic acid. (It's probably linolenic acid, if it's not specified.)

All in all, the addition of DHA to food products is a nice way to boost your intake of this healthy omega-3. However, keep in mind that these are processed, often highly processed, foods and you will likely pay a premium for the little boost. For now, stick to fish oil, the real thing.

For a brief summary of the CSPI report and a link to the Nutrition Action Newsletter, see Omega-3 Madness: Fish Oil or Snake Oil.

Are cardiologists the enemy?

7. November 2007 William Davis (12)
I'm sitting at dinner with two colleagues. One is a cardiology colleague, another an internist who, in addition to practicing general internal medicine, also takes heart disease prevention very seriously. He has, in fact, participated in the Track Your Plaque program and dropped his heart scan score substantially.

"Why don't we see you in the cath lab much?" my cardiology colleague asked me. He was puzzled, since he knew my background in cath lab work from years before, spending day and night doing procedure after procedure. He spends virtually all his days there.

"Well, my patients simply don't have events any more. Heart attacks and angina among people in my program are just about non-existent. They don't have symptoms and they don't have to go to the hospital. I can't remember the last time that I was woken up in the middle of the night for an urgent procedure for one of my patients."

The internist across the table smiled and expressed his agreement. "That's the same thing I'm seeing: No heart attacks, very few if any referrals to cardiologists for procedures. I remember when it was a several times a week thing. Now, almost never. "

Looking at my cardiology colleague, I saw the usual cardiologist reaction: Eyes searching left and right and behind us for something more interesting. Certainly, talking about a virtual cure for coronary heart disease was just too damn dull.

Such is the attitude of 98% of my colleagues: If it doesn't generate a revenue-producing procedure, why bother? Prevention is for general practitioners, the line of thinking goes. "And anyway, I'm too busy doing procedures! I don't ahve time to talk about prevention and health!" Of course, the poor general practitioner is already overloaded with caring for arthritis, flu, diabetes and all the new drugs for diabetes, headaches, vaccinations, diarrhea, and . . .oh, yes, heart disease prevention.

Are cardiologists the enemy? No, of course they are are not. But they often act like they are. Talking to cardiologists is like going to the car dealer with your checkbook out, pen in hand. The salesman gets to write the check himself and you just sign it. Talk to a cardiologist and more often than not you will end up with a heart procedure--whether or not you need it.

Unfortunately--tragically--they often forget what they are supposed to be doing: Taking care of a disease by preventing it. Putting in a defibrillator is not preventing a disease. Putting in three stents, laser angioplasty, and thrombectomy are not ways of preventing a disease.

I'm thankful for my internist friend who sees the light. Coronary heart disease is a an easily measurable, quantifiable, preventable, and REVERSIBLE process for many, if not most, people when provided the right tools. But don't ask your neighborhood cardiologists to give you those tools.

Are CETP inhibitors kaput?

6. November 2007 William Davis (9)
Was torcetrapib’s crash and burn fatal for this class of drug?

At the 2007 American Heart Association meetings in Orlando, Florida, Dr. Philip Barter of Sydney, Australia, presented an update of the ILLUMINATE drug trial for the once-promising drug, torcetrapib, the billion-dollar bet that Pfizer made on its first entry into the new drug class.

You may recall that the crash and burn of Pfizer’s torcetrapib in December 2006 made headlines and prompted enormous disappointment for many patients and doctors who had hoped for a new drug choice to raise HDL cholesterol. Pfizer executives (heads flew!) and investors were also disappointed, anticipating release of a drug that might have become the number one biggest selling drug in the world—ever, surpassing even Lipitor's® $13 billion annual sales.

Torcetrapib is the first among the “cholesteryl-ester transfer protein inhibitors,” or CETP-inhibitors, drugs that block the exchange of cholesterol and triglycerides between HDL and VLDL particles and prevent formation of the unwanted small LDL particles. Preliminary efforts suggested that effects were positively enormous.

However, the 15,000-participant trial was abruptly terminated after 550 days when an excess of deaths were identified among the group taking the experimental drug: 59 deaths in control group; 93 deaths in the torcetrapib group.

In addition, cardiovascular events were 24% greater in the torcetrapib group, numbering 373 compared to 464 in the no-torcetrapib group, including a substantially greater number of heart attacks and hospitalizations. Another surprise came in the way of cause of death among some of the torcetrapib patients, with an excess of deaths due to cancers (twice as many in the torcetrapib group), strokes, and infections.

Why the divergence: enormous improvements in cholesterol values, yet increase in adverse effects including more heart attack? Deeper digging by the principal investigators uncovered unexpected distortions of electrolytes like sodium and potassium. They then re-analyzed blood samples from participants on both sides of the trial and discovered that participants taking torcetrapib experienced significant rise in the blood pressure hormone, aldosterone. This, they surmised, also likely accounted for the 4 mmHg average rise in blood pressure among those taking the experimental drug. (This is the same pathway blocked by blood pressure drugs like ACE inhibitors lisinopril and enalapril, ARBs like losartan.)

Simultaneously (what a coincidence!) with the torcetrapib data, investigators at competing drug manufacturer, Merck, reported encouraging data with their version of CETP inhibitor, anacetrapib. In a phase II FDA trial of 589 patients, anacetrapib reduced LDL-C levels by up to 40% and increased HDL-C up to 139%.


Spokesman Daniel Bloomfield, M.D., of Merck Research Laboratories reported that "The favorable lipid effects seen in this study with multiple doses of anacetrapib were significant, and confirm the continued evaluation of the clinical benefits of CETP inhibitors in the treatment of dyslipidemia." Quick to distinguish this drug from torcetrapib’s track record of dangerous effects on blood pressure, he added that "the decreased LDL-C concentrations, increased HDL-C concentrations and no demonstrable increase in blood pressure seen with anacetrapib are particularly encouraging results of this study."

However, the data reported only an 8 week expereince. Given the experience with torcetrapib, longer term data will obviously be required to assess safety. After Pfizer spent over $1 billion and sacrificed lives to obtain this experience, Merck will need to tread carefully.

It will clearly be many years before we have a confident answer on whether the CETP-inhibitor class of drugs will be a safe choice for correction of cholesterol abnormalities, especially low HDL. Are we helpless until then?

Though CETP inhibitors offer the potential for a one-stop opportunity to raise HDL substantially, there are still many strategies available to raise HDL.

Strategies that raise HDL and are available today include:
• Weight loss—to your ideal weight. A very effective strategy.
• Reduction in processed carbohydrates—like breads, pasta, cookies, pretzels, etc. Note that very low-fat diets reduce HDL. Often a huge effect.
• Fish oil—A small effect, more dramatic when triglycerides are high.
• Niacin—Vitamin B3, the best we have at present. Doses of 500-1500 mg per day raise HDL 20–50%; work with your doctor if you are contemplating niacin. We use this agent everyday and have had great success; good hydration is key to minimize the annoying “hot-flush” effect.
• Dark chocolate—40 grams, or about 2 inches square, a delicious way to squeeze out a little rise in HDL.
• Alcoholic beverages—Red wines are almost certainly the preferred route, rich in flavonoids.
• Exercise—HDL-raising effects vary, but can sometimes be as much as 10–20 mg.
• Other drugs—Though not commonly used for this effect, drugs like pioglitazone (for diabetes and pre-diabetes); fibrates (Tricor® or fenofibrate; Lopid® or gemfibrozil); and Pletal® or cilostazol are occasionally prescribed.
• Vitamin D—You won’t find validation of this effect in any scientific study, but our emerging experience in our heart disease reversal program is suggesting that this neglected nutrient can exert powerful HDL-raising effects. In fact, supplementing vitamin D has made my life much easier.


And, last I checked, none of these HDL-raising strategies are ever fatal.

Roto Rooter for plaque

4. November 2007 William Davis (4)



Joe, a machinist, was frightened and frustrated.

With a heart scan score of 1644 at age 61, his eyes bulged when I advised him that, if preventive efforts weren't instituted right away, his risk for heart attack was a high as 25% per year. Joe had "passed" a stress test, thus suggesting that, while coronary plaque was present--oodles of it, in fact--coronary blood flow was normal. Thus, there would be no benefit to inserting three stents, say, or a bypass operation.


(Illustration courtesy Wikipedia)

"I don't get it, doc. Why can't you just take it out? You know, like Roto-Rooter it out? Or give me something to dissolve it!"

Of course, if there were such a thing, I'd give it to him. But, of course, there is not. It doesn't mean that there haven't been efforts in this direction over the years. Among the various attempts made to "Roto-Rooter" atherosclerotic plaque have included:

Coronary endarterectomy
This is a drastic procedure rarely performed anymore but enjoyed some popularity in the 1980s and 1990s. Coronary endarterectomy was performed during coronary bypass surgery, but few thoracic surgeons performed it. Milwaukee's Dr. Dudley Johnson was the foremost practitioner of this procedure (retired a few years ago after his own bypass operation) with a mortality in excess of 25%. A very dangerous procedure, indeed. The technical hurdle, beyond the tedium and length of time required to remove plaque that had a tendency to fragment, was blood clot formation after tissue was exposed upon plaque removal. I saw many lengthy hospital stays and deaths following this procedure.

Coronary atherectomy
This is an angioplasty-type procedure that has gone through several variations over the years.

In the early 1990s, transluminal extraction atherectomy (TEC) was a technique involving low-rpm drill bits with a suction apparatus that was used to clear soft debris, usually from large coronary arteries or, more commonly, bypass grafts. Then came direction atherectomy, in which a steel housing contained a sharp drill bit that captured atherosclerotic plaque in an aperture along the housing length and stuffed it into a nosecone, retrieved once the device was removed.

Then came high-speed rotational atherectomy in which a diamond-tipped drill bit rotated up to 200,000 rpm and essentially pulverized plaque to flow downstream and, presumably, eventually captured by the liver for disposal. Rotational atherectomy is still in use on occasion. Laser angioplasty, usually using the excimer wavelength, vaporizes plaque. I did plenty of all of these back in the early and mid-1990s.

While all atherectomy procedures sound clever, they are all plagued by the same problem: vigorous return of plaque. Remove plaque, it grows back. There are few instances today in which atherectomy is still performed.

Chelation
This involves a metal-binding, or "chelating," agent like EDTA normally used in conventional practice for lead poisoning. Usually administered IV, some have also advocated oral use. People who use chelation also tend to believe in faith healing and other practices based on faith, not science. There is an international trial that is nearing completion that should provide the final word on whether there is any role to intravenous chelation.

There are numerous other oral treatments that claim a Roto-Rooter-like effect. Nattokinase, for example--an outright, unadulterated, and unqualified scam.

Unfortunately, the helpless, ignorant, and gullible are many. When frightened by the specter of heart disease, there are plenty of people who will willingly pay for the hope provided by clever ads, fast-talking salespeople, and unscrupulous practitioners.

So, Joe, there is no Roto-Rooter for coronary atherosclerotic plaque, at least one that is safe, doesn't involve a life-threatening effort, provides results that endure beyond a few months, and truly works.

The Track Your Plaque program may not be easy. There are obvious common hurdles to adhering to these concepts: obtaining lipoprotein testing, getting intelligent interepretation of the results, persuading your doctor to measure vitamin D blood levels, battling the onslaught of prevailing food propaganda that confuses and misleads. The Track Your Plaque program also requires time, at least a year.

But it's the best program there is. Do you know of anything better?