Back to basics: Coronary calcium

30. January 2012 William Davis (42)
After having my attentions pulled a thousand different directions these past 6 months, with the release of Wheat Belly and all the wonderful media attention it has attracted, I've decided to pick up here with a series of discussions about the fundamental issues important to the Track Your Plaque program and prevention and reversal of coronary atherosclerotic plaque.

I fear the discussions at times have drifted off into the exotic. This is great because this is how we learn new lessons, but we can never lose sight of the basics, else we risk losing control over this disease.

Imagine you've got a beautiful new car. You wax it, gap the spark plugs, rotate the tires, etc. and it looks brand-new, just like it came off the dealer's lot. 50,000 miles pass, however, and you realize you've forgotten to change the oil. Ooops! In other words, no matter how meticulous the attention to transmission, tires, and paint job, neglect of the most basic responsibility can ruin the whole thing. We can't let that happen with heart health.

If we propose to reverse coronary atherosclerotic plaque, we've got to have something to measure. First, it tells us whether we have atherosclerotic plaque in the first place, the stuff that accumulates and blocks flow and causes anginal chest pains, and ruptures like a little volcano and causes heart attacks. Second, it gives us something to track over the years to know whether plaque has grown, stopped growing, or been reduced. Without such a measure, you will be driving without a speedometer or odometer, just guessing whether or not you've gotten to your destination.

Of course, the conventional approach to heart disease and heart attack is not to track atherosclerotic plaque in your coronary arteries, but to track some distant "risk factor" for atherosclerotic plaque, especially LDL cholesterol. But LDL cholesterol is flawed at several levels. First, it is calculated, not measured. The nearly 50-year old Friedewald equation used to calculate LDL cholesterol is based on several flawed assumptions, yielding a value that can be 20, 30, or 50% inaccurate as a rule, only occasionally generating a value close to the real value. (No point in publicizing this problem, of course: Why compromise a $27 billion annual cash cow?) It also ignores the effect of diet. (No, cutting fat does not reduce LDL for real, only the calculated value. Cutting carbohydrates, especially wheat--"healthy whole grains"--slashes measured LDL values like NMR LDL particle number and apoprotein B.)

But all risk factors are, at best, snapshots of the situation at that moment in time. They change from day to day, week to week, month to month, year to year. If you do something dramatic in health, like lose 50 pounds, you can substantially change your risk factors values, like LDL cholesterol and HDL cholesterol. But you may not modify the amount of atherosclerotic plaque in your heart's arteries.

Measuring the amount of atherosclerotic plaque in your heart's arteries is, in effect, a cumulative expression of the effects of risk factors up until the moment of measurement.

There are several stumbling blocks, however, in the concept of measuring coronary atherosclerotic plaque. We cannot measure all the unique components of plaque, such as fibrous tissue like collagen, or degradative enzymes like collagenases, or inflammatory proteins like matrix metalloproteinase, or the debris of hemorrhage and inflammation. We struggle to contemporaneously mix in measures of bloodborne inflammation, coagulation and viscosity, and physiological phenomena of the artery itself, like endothelial dysfunction, medial (muscle) tone, and adventitial fat.

So we are left with semi-static measures of total coronary atherosclerotic plaque like coronary calcium, obtainable via CT heart scans as a calcium "score." No, it is not perfect. It does not reflect that moment's blood viscosity, it does not reflect the inflammatory status of the one nasty plaque in the mid-left anterior descending, nor does it reflect the irritating sheer effects of a blood pressure of 150/95.

But it's the best we've got.

If anyone has something better, I invite you to speak up. Carotid ultrasound, c-reactive protein, ankle-brachial index, stress nuclear studies, myoglobin, skin cholesterol, KIF6 genotype . . . none of them approach the value, the insight, the trackability of actually measuring coronary atherosclerotic plaque. And the only method we've got to gauge coronary atherosclerotic plaque that is non-invasive and available in 2012? Yup, a good old CT heart scan calcium score.
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Comments (42) -

  • cancerclasses

    1/30/2012 4:58:24 AM |

    What about Pulse Wave Velocity (PWV) and Digital Pulse Analysis (DPA)?  
    From the Townsend Letter May 2010 article "Breakthrough in Clinical Cardiology: In-Office Assessment with Pulse Wave Velocity (PWV) and  Digital Pulse Analysis (DPA) by Brian Scott Peskin, BSEE, with Robert Jay Rowen, MD":  http://goo.gl/vihZO
    "This article explores an exciting, noninvasive, easy-to-use, and economical method of assessing patients’ cardiovascular physiologic status that is backed by more than 25 years of advanced research in medical physics. A 2007  Clinical Medicine article points the way to better clinical treatment of CVD, stating: “Arterial stiffness measured by pulse wave velocity (PWV) is an accepted strong, independent predictor of cardiovascular events and mortality.” 1   Anesthesiologists are well aware of this technology, used for monitoring purposes. While pulse oximetry became standard in the operating room and in other critical care areas as a detector of hypoxemia – all pulse oximeters are fundamental photoelectric plethysmographs – PWV has been largely ignored. This is unfortunate, as PWV (plethysmographic) information itself may provide important clues regarding the CV condition of the patient.2  With this advanced technology, cardiovascular science has moved forward, but many physicians have yet to appreciate these advances. As stated in the 1993 issue of the Journal of Hypertension, “Wave reflection is not a subject with which most physicians are familiar and only given mention in undergraduate physiology courses.” Little has changed.

    As this article was going to press, however, “Arterial Stiffness
    and Cardiovascular Events: The Framingham Heart Study,” by
    Gary F. Mitchell, MD, et al. (Circulation. 2010;121:505–511)
    was published and featured on Medscape, stating: “In this
    study, we assessed the incremental value of  adding pulse
    wave velocity [PWV] ... to a risk model that includes standard
    risk factors for a first cardiovascular event. … Adding pulse
    wave velocity led to significant reclassification of risk and
    improvement in global risk prediction. … [W]e need to focus
    our efforts on identifying and implementing interventions that
    can prevent or reverse abnormal aortic stiffness in order to
    prevent a marked increase in the burden of disease potentially
    attributable to aortic stiffness.”  The specific intervention/
    solution will be given later in this article."

    Also, "This video is a preview of a lecture given at the 2010 18th international A4M conference in Orlando."  http://goo.gl/S1xth

    Disclosure: I have no known conflicts of interests in conveying this information, I do not own stock or any financial interests in any of the companies making or distributiing this equipment.

  • Anne

    1/30/2012 5:55:03 AM |

    Hi Dr. Davis, I had a CT scan done about 5 years ago and the results were frightening, it was 1050. I was shocked because I ate healthy, low fat, plenty of healthy  wheat, how could this happen. My Dr. sent me for an EKG ultrasound and ever test possible and all  the tests were perfect. As you know I have changed to no wheat, high fat, low carb way of eating and I gained 5 lbs but my triglycerides came down to 61, LDL is 153 . My other numbers are high but I read that can happen when you have hypothyroidism c reactive protein is 0.7 MG/L. My Dr. said that the clinic that tested my CT scan are no longer in business in Michigan so I don't know if the plaque improved or got worse, any suggestions?

  • Donald Kjellberg

    1/30/2012 7:58:51 AM |

    I have been thinking about the subject of getting back to the basics a great deal lately.

    Trying to synthesize everything into one concept made me realize how complex this whole process of prevention is. I too have been peering into windows on the road of better health.  What a complex and wonderful set of the diversity our homeostatic responses convey.

    What are the basics to me now? I'll serve it up in one word, food . . .

    What we eat determines profoundly how our body responds to the many factors contributing to heart disease (and other systems dysfunctions). One thing I learned along the way is over 50 different species of bacteria have been identified in arterial plaque (in addition to other pathogens).

    Going back to the basics tells me to eat foods that not only reduce markers associated with heart disease but also considers dietary factors that may optimize immune responses and pathogen suppression. Cutting out wheat provides great capital in healing the gut. It sets the groundwork for improved cellular communication and neurological feedback mechanisms.

    . . . and that's getting back to the basics. It sure isn't simple, but learning to prepare and serve up the right type of foods sure can sweeten the journey even if it gets us of track every now and then.

  • JC

    1/30/2012 1:06:30 PM |

    I have a friend who had a 16 slice scan and had a 0 calcium score.Several week after the scan he had a heart attack.Can you point out some studies which show the correlation of calcium scores to cardio incidents?What is the data to suggest it's a better marker than the others such as cholesterol,CRP,etc.

  • JC

    1/30/2012 1:17:26 PM |

    I'm on a near vegan diet as recommended by Dr Joel Fuhrman.It did not solve all my medical issues but it did tame my blood glucose(from the 130s to the low 80s)and my blood pressure(from 210/110  to 125/70).When I tried a diet heavy in meat and fat and low in carbs(50G/day)my blood pressure went up to 150/85.I have a type of salt sensitive hypertension(low renin) that may be a factor.Comments?

  • nina

    1/30/2012 7:57:37 PM |

    I have a friend who has had a stent, bypass and several cardiac incidents.  I find it tough to persuade him to follow your regimen and he's terrified that areas of his heart muscle have died and that there is no hope for him.

    Do you have examples of people who have successfully recovered from such a dire state of health in their 60's?  

    Nina

  • Ronnie

    1/31/2012 1:07:20 AM |

    My 54-year old husband also received a score of 0 on his 64-slice CT scan.  He's had no heart issues, however, he is overweight, has hypertension, he's insulin resistant and he has low HDL and elevated ApoB and LDL-P.  Because of his 0 score he feels he's not at risk.  How can I convince him otherwise?

  • Dr. William Davis

    1/31/2012 2:27:23 AM |

    Yes, I have, Nina. But the answers cannot be found in conventional healthcare with yet more procedures and drugs.

  • Dr. William Davis

    1/31/2012 2:29:13 AM |

    There's no comparison. Coronary calcium scores as a measure of coronary atherosclerosis wins, hands down.

    But it is not perfect. While heart attacks at a score of zero are distinctly uncommon, they can happen.

    For a full discussion of the studies documenting this, I would invite you to read the Track Your Plaque book available through the www.trackyourplaque.com website.

  • Dr. William Davis

    1/31/2012 2:29:49 AM |

    Hear, hear, Donald! You are singing my tune.

  • Dr. William Davis

    1/31/2012 2:30:54 AM |

    Hi, Anne--

    Yes, simply find another center that performs heart scans. They are actually done fairly widely now. It's often not advertised since, like mammograms, they don't make any money.

  • Dr. William Davis

    1/31/2012 2:31:49 AM |

    HI, Cancer-

    You are getting in to issues like endothelial dysfunction that are beyond the scope for this discussion.

    Perhaps something to talk about in future.

  • cancerclasses

    1/31/2012 9:22:08 PM |

    Well to me it''s kinda all the same but I''m also not a practicing cardiologist, and I may have been influenced by this: http://goo.gl/lfsQ7
    "Endothelial dysfunction is thought to be a key event in the development of atherosclerosis and **predates** clinically obvious vascular pathology by many years. This is because endothelial dysfunction is associated with reduced anticoagulant properties as well as increased adhesion molecule expression, chemokine and other cytokine release, and reactive oxygen species production from the endothelium, all of which play important roles in the development of atherosclerosis. In fact, endothelial dysfunction has been shown to be of prognostic significance in predicting vascular events including stroke and heart attacks. Because of this, endothelial function testing may have great potential prognostic value for the detection of cardiovascular disease, but currently the available tests are too difficult, expensive, and/or variable for routine clinical use."  

    I know tests have real costs associated with them, but is seem like DPA/PWV  plus the 64 slice MDCT plus coronary calcium would give a fairly complete picture.  I notice two of the three used in this report with the DPA performed at a later date. http://goo.gl/MS6Gp

  • cancerclasses

    1/31/2012 10:32:21 PM |

    The Oxidized LDL Triple Marker test?

  • PeteKl

    2/1/2012 3:02:01 AM |

    Hi Nina,

    It is hard to say what your friend''s future might hold without knowing how much damage has been done by his "cardiac incidents".  However assuming he is not bedridden, I wouldn''t call his situation hopeless.  If he can still walk around and climb a flight of stairs, I would guess there is still a reasonable amount of heart function left to enable him to live a mostly normal life.  He just needs to avoid losing even more.

    I am younger than your friend (48), but I also had a (very unexpected) MI and emergency bypass a little over a year ago.  My MI was rather mild, but it definitely did some damage.  I am well aware of the fear and sense of hopelessness that your friend is feeling.

    I started following the Doctor''s program about 10 months ago.  I can''t say for sure whether it will help or not, but it definitely makes my numbers look good so I am optimistic.  I would like to have a heart scan to track my own situation, but most places won''t do them if you have already had bypass so I am flying a little blind (BTW Doctor, has there been any change in this situation?).  I also started cardiac rehab a few weeks after my surgery and now exercise at least an hour a day 5-6 times a week.

    I''m not sure what to attribute this to (probably a combination of things), but I am pretty much back to normal.  I was never a super athlete, but I feel I can do anything a normal, fit 48 year old man can do and then some.  This was even confirmed by a recent stress test.  

    For example, I am currently on vacation and spent my afternoon swimming in the ocean and walking several miles up and down the boardwalk.  If someone had told me something like this was possible a year ago, I would have told them they were full of it.  Yet here I am.  

    So do I think your friend could recover? Yes I do.  He may not do as well as I have, but I suspect he can likely do much better than he thinks possible.  However it will take time and effort and may require taking  a few chances like trying the Doctor''s program (his own doctors probably won''t be thrilled).  Sitting at home waiting for a miracle likely won''t work.

    One thing I should mention is that resolving your friend''s difficulty may require more than just fixing his heart.  Having a major cardiac event is extremely traumatic.  Depression and anxiety disorders are common afterward.  From what I have heard, as many as 80% experience it.  Unfortunately most doctors won''t tell you this and they definitely don''t want to deal with it.  At best they will prescribe another pill.

    I was fortunate to have a sister who is a professional counselor.  She realized how distraught I was after my surgery and immediately recommend I start seeing someone.  It was great advise.

    The counselor I saw didn''t have any magical advice that suddenly made me feel better.  What she did  was help me work through what had happened and put it in proper perspective.  Once I could  do that, I started finding increasing motivation to get well.  It took a while (I have had at least 30 sessions over that past year), but it works.  BTW, most insurance will usually cover it.

  • Joanna

    2/1/2012 5:12:55 PM |

    I agree with you Pete, my husband, mid-50''s had a very serious MI about four months ago, also completely unexpected as he appeared in great health with no risk factors.  And although we don''t have all the answers yet about how much damage was done, we know it was a lot.  He is exercising at rehab (he was a regular exerciser before) as well as on his own and has been feeling almost like himself - and considering how serious his condition was this is pretty amazing.  He was already doing a number of the things Dr. Davis advocates and has since added more.
    Pete, if I may ask, do you know what your ejection fraction is now and what it was post MI?  We are struggling to get answers at this stage as to whether this will ever improve and how long it may take.  His is still low despite how well he feels.

  • nina

    2/1/2012 8:26:07 PM |

    Many thanks for the responses.  

    I know that conventional treatments aren''t the answer, but convincing my friend of that is another challenge.  I seem to have several friends who think reducing carbs is harmful and unnatural.  (I''m off sugar and grains, substituting almond flour, flax and desiccated coconut without any problem.)

    Nina

  • Ronnie

    2/2/2012 2:29:40 AM |

    Why aren''t most doctors doing calcium scoring tests instead of stress tests that only show late stage blockages?  If heart attacks occur when arteries are slightly blocked, it appears that calcium scoring should be the first test done on high risk patients.  Is it because the medical community is slow to accept change from the usual way of doing things?  Or is it the fault of the insurance companies who are notorious for not paying for new fangled tests?  I''m a total layman, but I''m high risk (APOE4) and the only test I received was a nuclear stress test (which was negative).  If I want to know my calcium score, I would have to pay $500 out of my pocket to Princeton  Longevity Ctr to have them do it as my doctor will not order it.

  • PeteKl

    2/2/2012 6:46:48 AM |

    Hi Joanna,

    As I mentioned, my MI was rather mild and I don''t think my EF ever went down substantially.  During my surgery (which started about 12 hours after my MI) my EF was measured at 55 percent.  A few weeks ago when I had my stress echo I measured 60 percent at rest and 55 percent under stress (to my knowledge these values are considered normal for most people).  I will admit that overall I was luckier than most people in this area.

    However keep in mind EF only gives you part of the picture.  There are many other variables.  A person can have a completely normal EF and still have major problems.  During my surgery my heart rhythm was very unstable.  My surgeon originally wanted to do a triple bypass but he ended up skipping the third one because he decided it was too risky.  On the other hand someone can have a low EF and still live a long and active life.

    Even if I had your husband''s full medical record, I can''t tell you exactly what his EF means.  You really need to discuss this further with his doctor.  However the following statement you made I think gives a good indication of where you probably stand:

    “He is exercising at rehab (he was a regular exerciser before) as well as on his own and has been feeling almost like himself – and considering how serious his condition was this is pretty amazing.”

    You are right.  This is pretty amazing.  Based on my own experience at cardiac rehab this doesn''t always happen.  I know it isn''t very scientific, but if he looks good and feels good he is probably doing just fine.  His EF might be low, but it must be high enough or he would be having all kinds of problems.

    While it might be nice to see a higher EF, from what you have described I''m not sure it would make a big difference.  It sounds like he either can or soon will be able to do everything he was capable of pre-MI.  If this is correct, it is fantastic news.  Personally I would probably stop worrying about his EF and instead concentrate on making sure he continues to retain every bit of heart muscle he has left.  

    However I am by no means an expert on all of this.  Perhaps the Doctor can weigh in with some better advice.

  • Renfrew

    2/2/2012 4:40:55 PM |

    Now, the most important question:
    HOW do we get rid of the calcium in our arteries ???
    Does Magnesium help as a calcium  antagonist? Chelation?
    Renfrew

  • Gene K

    2/2/2012 7:44:52 PM |

    Why $500? I paid $85 to have my calcium score heart scan done at a local hospital in the Chicago area. Check with radiology departments in the area hospitals.

  • Gene K

    2/2/2012 7:46:25 PM |

    Read Dr Davis''s Track Your Plaque book, 2nd edition, to get the answer.

  • Renfrew

    2/2/2012 8:04:53 PM |

    Dr. Davis,
    I am living in Germany and cannot get the book. About 6 months ago you said you will make it available in downloadable pdf format. Any progress on this front?
    Thanks.
    Renfrew

  • Ronnie

    2/2/2012 8:50:03 PM |

    I was thinking that the 64 slice CT scan was  the only test that measured calcium score, and Princeton Longevity charges $500 (give or take) for it.  I could get it there without a prescription; I would think I''d need a prescription to get the test at a hospital.  I''ll look into it, thank you.

  • Joanna

    2/2/2012 8:50:11 PM |

    Thanks so much Pete.  And you are right, we are doing everything we can to retain as much heart muscle as we can - unfortunately we have been told that with such a low EF, even if he feels great, he is at much greater risk of sudden cardiac arrest and may need an ICD (an internal defibrillator) implanted - something that is both very expensive and may interfere with some of the work he does.  So we wait.  We have been told that his EF may come up over time but no one will give us any odds of this happening (for some people it seems it never does) or over how long a period of time it may take to improve.  

    I would also like to tell Nina to urge her friend to do cardiac rehab/exercise as this seems to be one of the differences between people who are successful in their recovery and those who aren''t.

  • Gene K

    2/2/2012 9:34:12 PM |

    No prescription was necessary in my case. They sent the results to me directly, and also to the doctor who they asked me to specify.

  • Gene K

    2/2/2012 10:16:57 PM |

    Yes, the book is available for download for TYP members.

  • PeteKl

    2/3/2012 6:12:17 AM |

    Hi Joanna,

    I''m going to make a guess here (and hopefully someone who knows more about this will correct me if I am wrong), but I suspect the issue isn''t so much a low EF by itself, as much as it is that a higher EF indicates greater recovery of the damaged heart muscle.  My understanding is that when an MI causes damage to heart muscle, it usually isn''t the loss of pumping capacity that causes death.  Instead the loss of muscle causes an electrical disturbance in the heart''s rhythm causing it to lose its ability to pump  blood.  This is why even a mild MI like mine can be fatal and explains why my surgeon was so concerned (See http://en.wikipedia.org/wiki/Myocardial_infarction#Pathophysiology).

    I suspect what your husband''s doctor might be concerned about is that he may be having a certain amount of arrhythmia because of the damage to his heart.  Apparently this is quite common after an MI and it is also something doctors don''t typically explain very well (at least mine didn''t).  

    After my surgery I was put on the drug amiodarone to help control my heart rhythm (which it did).  However this drug has some rather nasty side effects so they try to pull you off of it as soon as possible.  I stopped taking it after about a month and almost immediately developed some arrhythmia.  

    Fortunately the type of arrhythmia I developed (PVC''s) are usually considered benign.  But it was still extremely disconcerting since no one really explained to me what was going on.  The only thing I was ever told (or at least ever heard) was probably the same thing you have heard 50 times – “if you have any chest discomfort or shortness of breath, go to the emergency room” (needless to say this is not comforting advice).

    I am still having some PVC''s, but they have become increasing less frequent.  The bottom line is that the heart can essentially rewire itself, but it takes time.  Part of the point I am trying to make is that this might occur even if his EF doesn''t change.  

    Again this is a guess since I don''t have much information, but I suspect your husband''s doctors may be waiting to see how well your husband''s heart repairs itself (which may take a year or more) and they will then decide if he needs an ICD.  I''m also guessing they are currently controlling his heart rhythm with some type of drug (there are many) and they eventually want to take him off of it.

    Unfortunately it is my understanding that all you can do is wait.  There is currently no way of predicting who will fully recover and who won''t.  There are simply too many variables.

    However I think there are several factors in your husband''s favor.  The first is that he is young and most of his body''s natural repair mechanisms (which are considerable) are still functional.  

    He is also enthusiastic about doing his cardiac rehab.  The gradual stress of exercise essentially helps remodel and strengthen the heart.  Oddly enough many people don''t do this.  I''m sure your husband has already noticed that many patients quit cardiac rehab (and most likely stop exercising)  at the end of Phase II (about 12 weeks).  Just the fact that your husband is willing to continue with an exercise program puts him in a completely different class.

    Finally he is willing to modify his lifestyle.  He is changing the way he eats and, unless you are withholding something, probably doesn''t smoke or have some other equally bad habit.  When I was recovering from my surgery, my younger brother was in one of the waiting rooms when another patient, who had obviously also recently had heart surgery, was wheeled into the room next to him and started a conversation.  At some point during the conversation the man turned to my brother and said “I really hope when I get out of here they will let me smoke again”.  Like I said, your husband is in a completely different class.

    I know there are at least a few supplements out there that may help heal a heart''s electrical system.  Magnesium and CoQ10 are two that I have heard might help (try googling them for more info).  I doubt they will cause a miraculous recovery, but they might give him that little extra kick that helps him avoid the ICD.  I''m sure there are others on this site that know a hundred times more than I do.  Assuming what I have discussed is even roughly correct, perhaps a few of them can make an even better recommendation.

    I know all of this is frustrating, but try not to give up hope yet.  Four months is still early in the recovery process.  I remember being told that recovery would take at least a year and that turned out to be about right.  Also keep in mind (as I''m sure you have already discovered) that the recovery process is typically a series of two steps forward and one step back.

    BTW, no matter what might happen, please remember your husband is extremely fortunate to have you by his side.  There are many people who don''t have a person they can rely on to help figure this all out.  I doubt my recovery would have been as successful as it has been without the help I received from my partner and my family.  I now understand why so many people simply give up.  The recovery process simply becomes too overwhelming.

  • Roger

    2/4/2012 10:01:12 PM |

    I''ve gotten my calcium score for $50 at a DFW hospital with a 50% off coupon.  The result didn''t take 10 minutes to come out: a big zero! I will be back in 5 years.

  • Ronnie

    2/5/2012 2:47:57 PM |

    Gene, how was your score if you care to share?

  • Gene K

    2/5/2012 6:49:23 PM |

    No secret here, but unless zero, the dynamics are more important than the absolute number. At least, if I understand the whole TYP program correctly. My score was 213 in Feb 2010 and 191 this time, in Sep 2011.

  • Ronnie

    2/5/2012 10:05:46 PM |

    You''re going in the right direction, Gene.   That''s great!

  • Dr. William Davis

    2/7/2012 3:59:06 AM |

    Hi, Renfrew--

    We make the Track Your Plaque Guide available to our members without charge (except our membership fees to cover the costs of operating the website).

  • Dr. William Davis

    2/7/2012 3:59:40 AM |

    Hi, Ronnie--

    The laws differ from state to state. You can always call a center and ask.

  • Stan (Heretic)

    2/9/2012 3:25:12 AM |

    @JC,

    I hope Dr. Davis will respond, and I hope you don''t mind if I respond meantime. (Dr. Davis, please  correct me if my post is not accurate enough)

    I am not a doctor but 150/85 that you had on a high meat, fat and low carb, seems still OK!   Its not clear to me why did you have to change that diet?   Have you not quit a LC diet too prematurely  perhaps?  Experiences of other high fat low carb nutrition proponents in Europe (see especially  books by Dr. J.K.)  have shown that it takes about 2 years to see a significant effect upon cardiovascular health for patients with advanced arteriosclerosis.      

    I hope Dr. Davis can step in to, clarify this.  I know you are above retirement and male but it may help to provide your exact age and a history of your hypertention.  Even if you were practicing some sport and have clear coronary arteries, your peripheral arteries may still be partially occluded creating a condition conjusive towards a hypertention.   AFAIK it is possible to have clear coronary (heart) artieries and at the same time have occluded peripheral arteries.   Also your pre-diabetes may have been a factor too on the SAD since high insulin makes arteries less flexible.
    Stan

  • JC

    2/9/2012 1:40:33 PM |

    Thanks Stan,I looked at my old blood pressure readings to refresh my memory and many of the readings were in the low 170s/90 but the median score was around 156-160/85-88.The rapid rise scared me but it was fun while it lasted because I love butter,meat,cheese,and tons of fat.I don''t know how my low renin hypertension fits into this but I am very sensitive to sodium/salt.The only salt/sodium I get is that found naturally in vegetables,beans,nuts,and potatoes.
    Many years ago (around 2006) you posted some data that correlated blood pressure with cornary events and the link was not as strong as you would expect given all the hysteria about blood pressure.I would have to be convinced blood pressure in the 170s and 180s was not that serious before I would go back to the paleo style diet again.My near vegan diet has also tamed my blood glucose which is now consistently below 85.Before that in was in the 97-99 range.A number of years ago before I lost about 80 lbs it was in the mid 130s.

    So going back to a plaeo style diet I would have to accept higher blood pressure and blood glucose levels....170sBP and high 90s FBG.If I am convinced that those levels are safe it would change my perspective.

  • David

    2/12/2012 8:08:15 AM |

    Dr. Davis,

    Can you clarify the issue of measuring soft plaque?  My understanding is that soft plaque is more unstable and therefore more of a concern that hard plaque.  Does a Ca score infer soft plaque so gives us some sense of soft as well as hard plaque, or gives us no indication at all of soft plaque?  Would the PLA2 test be a better marker of soft plaque than the Ca score?

    Thanks for your great work!
    David

  • David

    2/22/2012 5:09:52 AM |

    Followup to my last question:
    wouldn''t a carotid ultrasound give us a better sense of soft plaque?  Combined with results for PLA2?

    David

  • Emidio

    3/12/2012 11:33:53 PM |

    Another form of very dangerous form of LDL...the glycated one:
    http://diabetes.diabetesjournals.org/content/60/7/1973.full

  • Dr. William Davis

    3/16/2012 12:34:28 AM |

    Absolutely. See the several blog posts back some time about this.

    Also a full length Special Report on the Track Your Plaque website will be coming out.

  • Joanie

    2/8/2013 8:46:56 PM |

    Can someone clarify which CT scan is the recommended "coronary calcium score"? I have been told by 2 medical centers here that they perform BOTH 1.) a "coronary calcium score" CT scan which costs (approximately) $150 and uses no contrast material. In that test, they scan the area from the top to the bottom of the heart, and visualize calcium that may exist in that field. This would include part but not all of the lungs, plus all of the heart.

    2.} a coronary calcium scan CT which costs (approx) $1,700 and does use contrast material, injected into a vein. The scan visualizes the heart aided by the contrast in the vessels. This also is a way to measure calcium.

    WHICH test does Dr. Davis recommend? I've been searching the blog and find repeated mentions of "calcium score" but must have missed a way to discriminate which CT test is the right one? Would appreciate any help with this. Thanks!

  • patricia sage

    3/13/2014 10:49:16 PM |

    I take Calcium with Vitamin K2.
    Vitamin K2 helps direct calcium to the bones and teeth(where it belongs), keeping the calcium from attaching itself to the arteries.
    Natural sources are Natto, egg yolk, butter...problem is I don't like the cholesterol in egg yolk and butter and I don't like the taste of Natto.
    I found this online and order it online as well http://tinyurl.com/q8fjc93
    It is made in USA; head office is in California. That's why delivery and shipping is free in USA. Delivery took about 3 to 7 days.  It has Omega 3+ as well as CoQ10 and Vitamin K2 and it is Extended release(long-term effect).

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Cureality | Real People Seeking Real Cures

The myth of mild coronary disease

19. January 2008 William Davis (27)
I hear this comment from patients all the time:

"They told me that I had only mild blockages and so I had nothing to worry about."

That's one big lie.

I guess I shouldn't call it a lie. Is it a lie when it comes from ignorance, arrogance, laziness, or greed?

"Mild coronary disease" is usually a label applied to coronary atherosclerotic plaque that is insufficient to block flow. Thus, having a few 20%, 30%, or 40% blockages would be labeled "mild." No stents are (usually) implanted, no bypass surgery performed, and symptoms should not be attributable to the blockages. Thus, "mild."

The problem is that "mild" blockages are no less likely to rupture, the eruptive process that resembles a little volcano spewing lava. Except it's not lava, but the internal contents of atherosclerotic plaque. When these internal contents of plaque gain contact with blood, the coagulation process is set in motion and the artery both clots and constricts. Chest pains and heart attack result.

So, the essential point is not necessarily the amount of blood flow through the artery, but the presence of coronary atherosclerotic plaque. Just having plaque--any amount of plaque--sets the stage to permit plaque rupture.

One thing is clear: The more plaque you have, the greater the risk for rupture. But the quantity of plaque cannot be measured by the "percent blockage." It is measured by the lengthwise extent of plaque, as well as the depth of plaque within the wall. Neither of these risk features for plaque rupture can be gauged by percent blockage.


Coronary atherosclerosis is a diffuse process that involves much of the length of the artery. It is therefore folly to believe that a 15 mm long stent has addressed the disease. This is no more a solution than to replace the faucet in your kitchen in a house with rotting pipes from the basement up.

The message: ANY amount of coronary plaque is reason to engage in a program of prevention--prevention of plaque rupture, prevention of further plaque growth, perhaps even regression (reversal). It is NOT a reason to be complacent and buy into the myth of "mild" coronary disease, the misguided notion that arises from ill-conceived procedural heart disease solutions.


Image courtesy Wikipedia.

Copyright 2008 William Davis, MD

Red flags for lipoprotein(a)

17. January 2008 William Davis (24)


Lipoprotein(a), Lp(a), is an important cause for heart disease, heart attack, and coronary atherosclerotic plaque.

How do you know you have it?

Of course, it could be as simple as checking a blood level. But there are also a number of red flags for the presence of Lp(a), tell-tale signs that suggest it is present and contributing to the growth of coronary plaque.

I've seen so much of this pattern over the years that it's gotten so that I can pretty much pick out most of the people with Lp(a) just by either looking at them or by hearing their story. I do this simply by knowing what hints to look for.

Some of the red flags for Lp(a) include:

--High blood pressure in a slender person. Overweight is the overwhelmingly common reason for high blood pressure. However, inappropriate high blood pressure in a slender person can serve to tip you off that Lp(a) is present.

--HIgh LDL cholesterol poorly responsive to statin drugs. For instance, someone's LDL cholesterol of 190 mg/dl will be treated with Lipitor 40 mg, but drops to only 165 mg/dl, a very poor response. This can sometimes point towards Lp(a).

--Family clustering of heart disease in people before age 60. For instance, father with heart attack age 53, uncle with heart attack at age 55, aunt with heart attack age 59, etc. This clustering of risk, more often than not, signals Lp(a).

--Coronary disease or high heart scan score in the presence of relatively bland appearing lipids. For instance, LDL cholesterol 130 mg/dl, HDL 55 mg/dl, triglycerides 70 mg/dl on no medications or other efforts--figures ordinarily not associated with high likelihood of heart disease--yet heart disease is indeed present. This can mean that Lp(a) is the concealed culprit behind coronary atherosclerosis.

These red flags are not perfect. If you lack any of them, it doesn't necessarily rule out the possbility of having Lp(a). They simply serve as signs to suggest that Lp(a) may be lurking.

Once Lp(a) is identified, then the battle begins to gain control over this somewhat troublesome genetic pattern. Resourcesfulness and some ingenuity may be required. However, knowing that you have it shows you where to concentrate your efforts.

Vytorin study explodes--But what's the real story?

15. January 2008 William Davis (28)
The makers of Vytorin, Merck/Schering-Plough Pharmaceuticals, issued a press release about the the Enhance Study yesterday. The news has triggered a media frenzy.

The NY Times reporting of the story:

Drug Has No Benefit in Trial, Makers Say

The 700 participants in the trial all had a condition called "heterozygous hypercholesterolemia," a genetic disorder that permits very high LDL cholesterols. The average LDL at the start was 318 mg/dl.

The Times reported that, while Vytorin cut "LDL levels by 58 percent, compared to a 41 percent reduction with simvastatin alone," but "the average thickness of the carotid artery plaque increased by 0.0111 of a millimeter in patients taking Vytorin, compared to an increase of 0.0058 of a millimeter in those taking only simvastatin." There was no difference in heart attacks or other "events" between the two groups.

(Vytorin is the combination of simvastatin and Zetia.)

In other words, the participants taking Vytorin had 53 ten-thousands of a millimeter more plaque growth than the group taking just simvastatin.

I am always uncomfortable when put in the position of defending a drug or drug company. However, it is patently absurd that this study has generated such attention. I suspect the public and media are waiting for another Vioxx-like debacle, with memories of concealed or suppressed data that suggested heightened heart attack risk that was dismisssed by the drug manufacturer. (That's not to say that the company hasn't been trying to delay or modify the outcome of the study, which they apparently have, much to the objections of the FDA.)

However, at this point, there is no reason to believe that this question possesses any parallels to the Vioxx fiasco.

If we accept the data as reported, however, we might say it calls the entire "Lipid Hypothesis" into question: If LDL cholesterol is significantly reduced but is not correlated with reduction in plaque, is LDL the means by which atherosclerotic plaque progresses? This trial does not answer that question, but does serve to raise some doubt.

Another issue: Heterozygous hypercholesterolemia, and thereby LDL cholesterol, may not be the overwhelming driver of plaque growth in this population. It is probably the number of small LDL particles, a factor which is not revealed by LDL cholesterol. For this reason, heterozygous hypercholesterolemia by itself is insufficient to cause heart disease. Some other factor(s) needs to be present. I would propose that it is the size of the LDL particle: When small, heart disease develops; when large, heart disease is less likely to develop. This issue was not addressed by this study. Readers of The Heart Scan Blog know that conventional LDL cholesterol, the number used in this study, is a virtually worthless number for truly gauging plaque behavior because of its flagrant inaccuracy.

So, there are substantial uncertainties, contrary to the absolute certainty expressed by people like Dr. Steve Nissen (who, by the way, has no expertise in lipoprotein disorders). It is premature to reach any firm conclusions from this study. The only conclusions that I personally come to are 1) Is this yet another reason to question the entire Lipid Hypothesis as it stands? and 2) What would the results have been had LDL particle number and LDL particle size been examined, not just LDL?

I would not automatically conclude that Zetia causes carotid plaque. This is absurd. And I am definitely not one to come to the rescue of a drug or drug manufacturer. I am simply after understanding and truth.

As an interesting aside, Dr. Howard Hodis of the University of Southern California and an expert in carotid scanning for heart disease prevention research, made a comment relevant to us in the Track Your Plaque program:

"Clearly, progression of atherosclerosis is the only way you get events,” Dr. Hodis said. “If you don’t treat progression, then you get events."

Dr. Arthur Agatston in the news

15. January 2008 William Davis (7)


The Miami Herald has a new report on Dr. Arthur Agagtston (of South Beach Diet fame) to announce his new book, The South Beach Heart Health Revolution:
The South Beach Diet doctor takes on cardio care

Agatston, the granddaddy of CT heart scanning, is always at least worth listening to. Although his diet may not be perfect, it clearly has jumped light years ahead of conventional diets like the inane American Heart Association diet. The South Beach Diet focuses on healthy oils, nuts, lean meats, vegetables, and fruits, while slashing grains (except in the often disastrous phase III).

The article lists Dr. Agatston's advice to achieve a "heart healthy" lifestyle:


• Maintain a healthy weight through diet.

• Undergo CT heart scans to check for arterial plaque.

• Do aerobic exercise, along with stretching and strengthening workouts.

• Ask your doctor about taking statins and other cholesterol-lowering drugs.


We wouldn't have CT heart scan scoring (at least in its present form) without Dr. Agatston, who developed the algorithm for scoring years ago in the early days of heart scanning. We also need to credit him with putting together a rational diet despite the counter-information emanating from the Heart Association, the USDA (a la Food Pyramid, the one that makes Americans fat and diabetic), and the American Diabetes Association, among others.

But "Ask your doctor about taking statins and other cholesterol-lowering drugs"? This is where Dr. Agatston begins to falter. While he is putting his enormous notoriety to use, his message is bland and ineffective. "Do aerobic exercise"? We don't need Dr. Agatston to tell us this.

As much as Art Agatston has added to the national conversation on heart disease and diet, he has failed to deliver the message of true heart disease prevention. His approach lacks just a few crucial ingredients like lipoprotein testing, diagnosis of hidden causes of heart disease (like Lp(a)), and vitamin D. (Two years ago I had a patient I saw for an opinion after he'd showed Dr. Agatston his lipoprotein panel. The patient said Dr. Agatston looked at the report and didn't know what to do with it and handed it back to him without comment. He then asked if he wanted his autograph.)

Anyway, the rising tide raises all boats. Agatston's repeated public endorsements of heart scans will help deliver the message that heart disease is detectable in its early stages and should trigger action to follow a heart disease prevention program.

That alone is an accomplishment in a world hell-bent on dragging us into the hospital for procedures.

Take this survey: I DOUBLE-DARE YOU

14. January 2008 William Davis (10)
In a previous post I entitled Heart disease reversal a big "No No", I posed a challenge--a dare--to readers to ask their doctors if coronary heart could be reversed.

Here's what I said:

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.

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.

I know of one person who actually followed through on this challenge and asked his cardiologist whether his heart disease could be reduced or reversed. As predicted, the answer was no. No explanation followed.

But allow me to reiterate: Heart disease is 1) detectable, 2) quantifiable, 3) controllable, and, in many cases 4) reversible.

What if there was a big payoff to your doctor if heart disease was reversed, say $100,000? That's enough to dwarf the payoff from procedures. Guess what? You'd have doctors fighting for your business, a chance to reverse your disease, ads to that effect, champions of reversal emerging. No new tools would be necessary. They could use the tools already available. Then why hasn't this happened? Is the technology unavailable? Are the treatments ineffective?

No, heart disease is a controllable and reversible process with tools that are available today. But there is, of course, no big payoff for doing it. So the financial incentive remains to do procedures, not to reverse the disease.

But I'd like to re-pose this challenge. Ask your doctor if heart disease can be reversed, or at least reduced. I've even posted a Survey at the top left for anyone who tries.

Again, my prediction: Nobody will try it and nobody will post survey results. Why? Despite my rantings (and those of a few others) about the concept of heart disease being a reversible process, in the public's consciousness it remains a death sentence and the only solution is hospital procedures. My colleagues continue to cultivate this attitude and it serves them well financially.

I'll be disappointed if I prove to be right. I hope that I am wrong. But I don't think that I am.



Copyright 2008 William Davis, MD

Michael Pollan on Nutritionism

13. January 2008 William Davis (8)


The wonderfully articulate Michael Pollan has written another book. Although he presents little new to anyone who read his previous book, The Omnivore's Dilemma: A natural history of four meals, he is such a wonderful writer, with such clever ways of seeing the world, that I couldn't resist this new, less ambitious book.

The new book is In Defense of Food: An eater's manifesto.

As in Omnivore's Dilemma, Pollan reminds us that we've lost contact with real food, foods that our great grandmother would recognize, not the just-add-water, dried, pulverized, sweetened, high-fructose, hydrogenated, shrink-wrapped, artificially-colored products that pass as foods in the grocery store.

In particular, Pollan attacks what he calls the ideology of Nutritionism. "The widely shared but unexamined assumption is that the key to understanding food is indeed the nutrient. Put another way: Foods are essentially the sum of their nutrient parts." He calls this "Nutritionism."

In the section called "Nutritionism comes to market," he uses margarine as the prototypical product of this philosophy:

"No idea could be more sympathetic to manufacturers of processed foods, which surely explains why they have been so happy to jump on the nutritionism bandwagon. Indeed, nutritionism supplies the ultimate justification for processing food by implying that with a judicious application of food science, fake foods can be made even more nutritious than the real thing. This of course is the story of margarine, the first important synthetic food to slip into our diet. Margarine started out in the nineteenth century as a cheap and inferior sustitute for butter, but with the emergence of the lipid hypothesis in the 1950s, manufacturers quickly figured out that their product, with some tinkering, could be marketed as better--smarter!--than butter: butter with the bad nutrients removed (cholesterol and saturated fats) and replaced with good nutrients (polyunsaturated fats and then vitamins). Every time margarine was found wanting, the wanted nutrient could simply be added (Vitamin D? Got it now. Vitamin A? Sure, no problem. But of course margarine, being the product not of nature but of human ingenuity, could never be any smarter than the nutritionists dictating its recipe, and the nutritionists turned out to be not nearly as smart as they thought. The food scientists' ingenious method for making healthy vegetable oil solid at room temperature--by blasting it with hydrogen--turned out to produce unhealthy trans fats, fats that we now know are more dangerous than the saturated fats they were designed to replace. Yet the beauty of a processed food like margarine is that it can be endlessly reengineererd to overcome even the most embarrassing about-face in nutritional thinking--including the real wincer that its main ingredient might cause heart attacks and cancer. So now the trans fats are gone, and margarine marches on, unfazed and apparently unkillable. Too bad the same cannot be said of an unknown number of margarine eaters."

Anyone who reads and thinks a lot about nutrition will find little new here. But nobody says it better than Pollan. While Gary Taubes (Good Calories, Bad Calories) is the real thinker of our age about nutrition, Michael Pollan is the true writer about it.

With books like these making the bestsellers list, I believe that we are gradually seeing rationality return to eating. It makes people skeptical of the glitzy ads that run on TV around the clock. I hope that Pollan's new book will make more and more people leery of the latest health claim that adorn some product. "More omega-3!" "A low-fat snack." "Heart Healthy!" "High in healthy fiber!"

Cholesterol follies

11. January 2008 William Davis (5)
Rudy is a 59-year old man. He's had three heart catheterizations, two of which resulted in stent implantations. Obviously, Rudy should be the beneciary of a prevention program.

His basic cholesterol values:

Total cholesterol 164 mg/dl--pretty good, it seems.

LDL cholesterol 111 mg/dl--Wow! Not too bad.

HDL cholesterol 23 mg/dl--Uh oh, that's not too good.

Triglycerides 148 mg/dl--By national (NCEP ATP-III) guidelines, triglycerides of 150 mg/dl and below fall within the desirable range.


So we're left with an apparently isolated low HDL cholesterol, nothing more. On the surface, it doesn't seem all that bad.

Of course, we need to keep in mind that this pattern landed Rudy in the hospital on several occasions and prompted several procedures.

Should we rely on these results? How about Rudy's lipoproteins?

Here they are (NMR; Liposcience):

LDL particle number 2139 nmol/l--Representing an effective LDL of 213--over 100 mg higher than the standard value (above) suggests.

Small LDL particles 2139 nmol/l--In other words, 100% of all Rudy's LDL particles are small. (Thus, weight-based measures of LDL cholesterol fail to tell us that he has too many small particles.)

Large HDL 0 (zero) mg/dl--Rudy has virtually no functional HDL particles.


If we had relied only on Rudy's standard cholesterol values, we would have focused on raising HDL. However, lipoprotein analysis uncovered a smorgasbord of additional severe patterns. The high LDL particle number comprised 100% of small particles is especially concerning.

Truly, conventional cholesterol testing is a fool's game, one that time and again fails to fully uncover or predict risk for heart disease. One look at Rudy's lipoproteins and it becomes immediately obvious: This man is at high risk for heart disease and the causes are clear.

Of course, many physicians and insurance companies argue that the added information provided by this portion of the lipoprotein test added around $70 more to the expense.

When you see results like this, is there even a choice?

Equal calories, different effects

9. January 2008 William Davis (15)
A great study was just published in the Journal of the American College of Cardiology:

Metabolic effects of weight loss on a very-low-carbohydrate diet compared with an isocaloric high-carbohydrate diet in abdominally obese subjects.

88 obese adults with metabolic syndrome were placed on either of two diets:

1) A very low-carbohydrate, high-fat diet (VLCHF): 4% calories from carbohydrates (truly low-carb); 35% protein; 61% fat, of which 20% were saturated. In the first 8 weeks, carbohydrate intake was severely limited to <20 grams per day, then <40 grams per day thereafter.

2) A high-carbohydrate, low-fat diet (HCLF): 46% calories from carbohydrates; 24% protein; 30% total fat, of which <8% were saturated.

Both diets were equal in calories (around 1400 calories per day--rather restrictive) and participants were maintained on the program for six months.

At the end of the six month period, participants on the VLCHF diet lost 26.4 lb, those on the HCLF diet 22.2 lbs (though the difference did not reach statistical significance). Thus, both approaches were spectacularly successful at weight loss.

Surprisingly, blood pressure, blood sugar, insulin and insulin sensitivity (a measure called HOMA) were all improved with both diets equally. Thus, these measures seemed to respond more to weight loss and less to the food composition.

Lipids differed between the two diets, however:


VLCHF:
Total cholesterol: initial 208.4 mg/dl final 207.7 mg/dl

LDL: initial 125 mg/dl final 123 mg/dl

HDL: initial 55 mg/dl final 64.5 mg/dl

Triglycerides: initial 144 mg/dl final 74 mg/dl

Apoprotein B: initial 98 mg/dl final 96 mg/dl


HCLF
Total cholesterol: initial 208.4 mg/dl final 187.5 mg/dl

LDL: initial 126 mg/dl final 108 mg/dl

HDL: initial 51 mg/dl final 54.5 mg/dl

Triglycerides: initial 157.6 mg/dl final 111 mg/dl

Apoprotein B: initial 100 mg/dl final 95 mg/dl


Some interesting differences became apparent:
--The VLCHF diet more effectively reduced triglycerides and raised HDL.
--The HCLF diet more effectively reduced total and LDL.
--There was no difference in Apo B (no statistical difference).

The investigators also made the observation that individual responsiveness to the diets differed substantially. They concluded that both diets appeared to exert no adverse effect on any of the parameters measured, both were approximately equally effective in weight loss with slight advantage with the carbohydrate restricted diet, and that lipid effects were indeed somewhat different.


What lessons can we learn from this study? I would propose/extrapolate several:

When calories are severely restricted, the composition of diet may be less important. However, when calories are not so severely restricted, then composition may assume a larger role. When calories are unrestricted, I would propose that the carbohydrate restriction approach may yield larger effects on weight loss and on lipids when compared to a low-fat diet.

The changes in total cholesterol are virtually meaningless. Part of the reason that it didn't drop with the VLCHF diet is that HDL cholesterol increased. In other words, total cholesterol = LDL + HDL + trig/5. A rise in HDL raises total cholesterol.

Despite no change in Apo B, if NMR lipoprotein analysis had been performed (or other assessment of LDL particle size made), then there would almost certainly have seen a dramatic shift from undesirable small LDL to less harmful large LDL particles on the VLCHF diet, less change on the HCLF diet.

The lack of restriction of saturated fat in the VLCHF that failed to yield adverse effects is interesting. It would be conssistent with the re-analysis of saturated fat as not-the-villain-we thought-it-was put forward by people like Gary Taubes (Good Calories, Bad Calories).

In the Track Your Plaque experience, small LDL is among the most important measures of all for coronary plaque reversal and control. Unfortunately, although this study was well designed and does add to the developing scientific exploration of diet, it doesn't add to our insight into small LDL effects. But if I had to make a choice, I'd choose the low-carbohydrate, high-fat approach for overall benefit.

Is skinny necessary for reversal?

6. January 2008 William Davis (19)
Nothing we do in the Track Your Plaque program guarantees that coronary atherosclerotic plaque or your heart scan score is reduced or reversed.



But everything we do weighs the odds in your favor of successfully achieving reversal: correction of lipoprotein patterns, uncovering hidden patterns like Lp(a), vitamin D, being optimistic--it all tips the scales in your favor.

But how necessary is it to be skinny, meaning somewhere near your ideal weight?

It is important, but not as important as it used to be. Let me explain.

I used to tell people that plaque would not regress unless ideal weight was achieved and all the parameters of abdominal obesity and metabolic syndrome were corrected. This includes blood pressure, blood sugar, low HDL, small LDL, high triglycerides, and high c-reactive protein. Curiously, though, as we've gotten better and better at reducing coronary calcium scores, I've been finding that complete correction of all parameters, including achieving ideal weight, don't seem to be as necessary to achieve plaque reversal.

I almost hate to say this, but I've even witnessed significant drops in heart scan scores in people with body mass indexes (BMI) of 30--obese.

The necessary change doesn't seem to be weight, per se, but the consequences of weight. In other words, if you remain overweight, but blood sugar, HDL, small LDL, etc. have shown substantial improvement, then reversal is still achievable.

Then is it okay to be fat or overweight?

Reducing weight to ideal weight does indeed tip the scales in your favor, since it represents an observable, perceptible measure of all associated patterns. Dropping weight can also minimize the need for efforts to correct the consequences of overweight--you might need less niacin, fish oil, exercise, blood pressure medication, etc. to succeed at plaque reversal. Achieving ideal weight may also provide benefits like reduced risk of cancers and degenerative diseases of the hips and knees. But, to my recent surprise over the last two years, achieving ideal weight is not an absolute requirement to achieve reversal.

This is contrary to what some others say. For instance, in an upcoming interview with Dr. Joel Fuhrman on the Track Your Plaque website, Dr. Fuhrman argues that 10% body fat for males, 22% body fat for females, accelerates plaque and symptom reversal. Dr. Fuhrman is author of Fasting and Eating for Health, Eat to Live, and a new upcoming 2-part book, Eat for Health, and proponent of high-nutrient vegetarian diets and fasting. Dr. Fuhrman has been helpful in teaching us some important lessons on how to apply periodic fasting to accelerate plaque reversal.

So, which is it, fat or skinny?

If given a choice (which everyone has), I'd choose skinny. But, provided all the parameters associated with overweight are corrected, then remaining overweight doesn't necessarily mean that you can't still succeed at plaque reversal.

If you are interested in knowing what your ideal weight is, there are a number of software calculators and tables available, including the HealthCentral.com calculator and the National Heart, Lung, and Blood Institute BMI Calculator.


Image courtesy Wikipedia.

Copyright William Davis, MD 2008

MESA Study: Track Your Plaque-Lite?

4. January 2008 William Davis (11)
The long-awaited data analyses from the Multi-Ethnic Study of Atherosclerosis (MESA) are finally making it to press.

The MESA Study is an enormously ambitious and important study of 6800 people, 45 to 84 years old, that includes white, black, Hispanic, and Chinese participants from six communities around the U.S. (Forsyth County, NC; Northern Manhattan and the Bronx, NY; Baltimore and Baltimore County, Md; St Paul, Minn; Chicago, Ill; and Los Angeles County, California.) Participants had no history of heart disease at enrollment. All underwent a heart scan (either EBT or multi-detector heart scans) at the start. It is therefore the largest prospective study involving heart scans ever performed. It is, not unexpectedly, yielding some fascinating observations relevant to the Track Your Plaque program. The MESA study is, incidentally, funded by the non-commercial, publicly-funded National Heart, Lung, and Blood Institute and is therefore presumably free of commercial bias.

Among the most recent publications is Risk factors for the progression of coronary artery calcification in asymptomatic subjects: Results from the Multi-Ethnic Study of Atherosclerosis (MESA) In this analysis of 5700 of the MESA participants, a repeat heart scan was obtained an average of 2.4 years after the first. Conventional risk factors for heart disease were obtained at the start (see below for details under Measurement of Covariates.)

After analyzing the data and risk factors assessed, such as age, sex, race, blood pressure, body mass index (BMI), presence of diabetes, blood sugar, and family history of heart disease, two questions were asked:

1) What risk factors predict heart scan scores?

2) What risk factors predict progression (i.e., increase) in heart scan scores?

(The second question is particularly relevant to us and the Track Your Plaque experience.)

The MESA analysis showed that essentially all the risk factors assessed correlated with both the initial heart scan score, as well as the rate of progression. No surprises here.

But the most eye-opening finding was that the conventional risk factors assessed explained only 12% of the variation and progression in heart scan scores (coefficient of determination, or R squared, = 0.12.) In other words:

--Conventional risk factors like LDL cholesterol, diabetes, and excess weight explain only a tiny fraction of why someone develops coronary atherosclerotic plaque as represented by a heart scan score.

--The great majority of risk for a high heart scan score remains unexplained by conventional risk factors.

--The great majority of risk for progressive increase in heart scan scores also remains unexplained by conventional risk factors.


In light of the MESA analysis, it's no surprise that strategies like reducing LDL cholesterol with statin drugs fails to prevent most heart attacks. It's no surprise that conventional prevention programs that talk about "knowing your numbers," eating a "balanced" or low-fat diet, etc., fail miserably to prevent the vast majority of heart attacks and heart procedures.

MESA confirms what we've been saying these past few years: If you want control over coronary heart disease, you won't find it in Lipitor, a low-fat diet, and other limited conventional notions of risk. Correction of conventional risk factors like cholesterol and blood pressure are, in a word, a failure. I wouldn't even call the conventional approach Track Your Plaque-Lite. They don't even come close.

If conventional risk factors can explain only 12% of the reason behind heart disease, we've got to look elsewhere to understand why you and I develop this process.



Measurement of Covariates
Information on demographics, smoking, medical conditions, and family history was collected by questionnaire at the initial examination. Height and weight were also measured at the baseline examination, and blood was drawn for measurements, including lipids, inflammation, fasting glucose, fibrinogen, and creatinine. Resting blood pressure was measured 3 times in the seated position, and the average of the last 2 measurements was used in the analysis. Medication use was determined by questionnaire. Additionally, the participant was asked to bring to the clinic containers for all medications used during the 2 weeks before the visit. The interviewer then recorded the name of each medication, the prescribed dose, and frequency of administration from the containers.


Copyright 2008 William Davis,MD