Add Boston Globe to the list of heart scan blunders

Yet another piece of mass media misinformation hit the airwaves today. This time it's not from the New York Times or the LA Times, both of which have previously mangled the issues surrounding heart scans. This time it's from the Boston Globe.

In an article titled What is a calcium scan for heart disease, and who should undergo the test?, the report states:

". . . calcium scans may not be a good idea, or prove terribly useful, for most people. For one thing, the scans expose a patient to significant radiation - equivalent to roughly 50 chest X-rays" said Dr. Warren Manning, chief of noninvasive cardiac imaging at Beth Israel Deaconess Medical Center."

As many before him, Dr. Manning is confusing two tests: CT coronary angiography and CT heart scanning. Perhaps we can't blame him: This technology has had its weakest following in the northeast, for reasons not entirely clear to me. (In fact, Track Your Plaque followers have had the greatest struggle obtaining heart scans in that part of the country.) Nonetheless, you'd think he'd have his simple facts straight before talking to the press. Unfortunately, hospital public relations departments will usually just grab whoever they can willing to talk to the press--regardless of their expertise or lack of.


The story goes on to say:

. . ." it's not clear what to do with the results from a calcium scan. If you have diabetes, high cholesterol, high blood pressure, or a family history of heart disease, you already know - or should know - that you are at increased risk of heart problems and should lower these risk factors. So, a calcium scan provides little additional information," Manning said.

"Moreover, even a high score doesn't necessarily mean that the calcified plaque in your arteries is obstructing blood flow, said Dr. Adolph Hutter, a cardiologist at Massachusetts General Hospital."

"The vast majority of people with high calcium tests don't have obstructions and they do fine long-term. So you'd have to test lots and lots of people to prevent one heart attack or sudden death," said Manning.

And if you get a low calcium score, a sign of little or no calcification of plaques, that's not very useful, either, because it could be wrong, or it could be right but lull you into believing you do not have to exercise and watch your diet, cholesterol, and blood pressure levels. "You can still be at risk even if your calcium test is negative," Hutter said.



It is truly shocking how little many (not all, thank goodness) of my colleagues really know about 1) heart scans, 2) coronary disease prevention, and 3) prevention in general. These same "experts" likely advocate high-dose statin drugs and low-fat diets for people at risk. They likely refer patients to the American Heart Association for diet advice and themselves obtain a lot of information from the pharmaceutical industry. The notion of identification, tracking, and purposeful reversal of coronary plaque is entirely foreign to this bunch.

"The vast majority of people with high calcium tests don't have obstructions and they do fine long-term. So you'd have to test lots and lots of people to prevent one heart attack or sudden death." Well, take a look at a graph from a database of 25,000 people undergoing heart scans then observed for several years afterwards:




You can see quite clearly from the curves that heart scan scores very clearly predict your future (if no preventive action is taken). The higher the score, the greater the likelihood of heart attack and death. How much clearer can it get?

The most recent addition to this literature is the PREDICT study which concluded:

Hazard ratios relative to CACS [coronary artery calcium scores] in the range 0-10 Agatston units (AU) were: CACS 11-100 AU, 5.4 (P = 0.02); 101-400 AU 10.5 (P = 0.001); 401-1000 AU, 11.9 (P = 0.001), and >1000 AU, 19.8 (P < 0.001).

In other words, a heart scan score of >1000 is associated with a 20-fold increased risk of cardiovascular events (without preventive efforts). That kind of predictive power and quantitative confidence simply cannot be squeezed out of blood pressure and cholesterol values.

How about the 2008 University of California-Irvine study from the New England Journal of Medicine (do the northeast docs even pay attention to something that is published in their own neighborhood?) that reported:

There were 162 coronary events, of which 89 were major events (myocardial infarction or death from coronary heart disease). In comparison with participants with no coronary calcium, the adjusted risk of a coronary event was increased by a factor of 7.73 among participants with coronary calcium scores between 101 and 300 and by a factor of 9.67 among participants with scores above 300 (P<0.001 for both comparisons). Among the four racial and ethnic groups, a doubling of the calcium score increased the risk of a major coronary event by 15 to 35% and the risk of any coronary event by 18 to 39%.

How about the Prospective Army Coronary Calcium (PACC) project (men average age 43 years):

"In these men, coronary calcium was associated with an 11.8-fold increased risk for incident coronary heart disease (CHD) (p = 0.002) in a Cox model controlling for the Framingham risk score. Among those with coronary artery calcification, the risk of coronary events increased incrementally across tertiles of coronary calcium severity (hazard ratio 4.3 per tertile)."

Calcium score provided additional information even after factoring in the Framingham risk score.

That's just a sample of the studies. There are a number more.

Add to these conversations the fact that, unlike reducing blood pressure or LDL cholesterol, the heart scan score is a quantification of the disease itself. It can also be tracked over time to gauge the success or failure of prevention efforts. To believe that blood pressure reduction or LDL cholesterol reduction is sufficient to eliminate risk is something only a fool would believe.



Contary to the above statements, the data are clear:

--The higher the heart scan score, the greater the risk. This has been demonstrated beyond any shadow of a doubt in at least a dozen published studies. In fact, heart scan scores outshine lipid/cholesterol values several-fold.

--A person with a zero score has a nearly zero risk for cardiovascular events over a 5-year timeline.

--Heart scans are the only quantitative test available of coronary atherosclerotic plaque. This means that they can be repeated to gauge progression or regression. Cholesterol does not do that. Stress tests do not do that.

--Heart scans are not the same as CT coronary angiography.

--The lack of "need" for a procedure does not equate to the absence of disease.

The power of heart scans is that they can uncover evidence for coronary atherosclerotic plaque 10 years before a cardiac disaster strikes. Witness Tim Russert's heart scan score of 210 in 1998 at age 48. 10 years later, you know what happened.

Beware the camipaign of misinformation and ignorance that continues that is hell-bent on maintaining the procedural status quo or locking us into a "drugs for all" mentality.

Comments (15) -

  • Anna

    9/17/2008 7:34:00 PM |

    I hate to dump on Northeasterners (I was one for the first 25 years of my life) but perhaps they have greater cognitive difficulties stemming from lack of Vit D & over-statinating?  Can't see the forest for the Framingham trees?

  • rabagley

    9/18/2008 4:46:00 AM |

    Dr. Davis, I think that you well know exactly why those statements are made the way they are Smile  The issue is that the CT heart scan does not clearly show any indication of a need for medical intervention, and therefore is considered worthless by those who think that the only justifiable reason for a diagnostic procedure is to determine if medical intervention is appropriate.

    Your argument for the utility of the heart scan is based on the ability of the scan to predict the utility of preventive behavior, reversing the accumulation of plaque by changing the composition of blood lipids.  Preventive action isn't even on these guys' radar.  You've also told us why it's not on their radar: prevention isn't profitable and doesn't pay off the student loans that cardiologists incur or the capital costs of the cardiology facilities in big medi-business.

    If I was cynical, I would say that they know the actual value of statins by the argument they use to dismiss the primary indicator of ongoing heart disease.  They know that statins have little or no effect on accumulated calcium in the heart and know that someone paying attention to heart scan scores would quickly realize the significant, painful and common side effects of statins are not worth the limited benefit.

    But anyone reading your blog or on the TYP program already knows why this is the rhetoric because you have repeatedly clearly explained what's going on any why (as usual: follow the money)

  • Anonymous

    9/18/2008 12:56:00 PM |

    50 x-rays? is that true?

  • lizzi

    9/18/2008 3:23:00 PM |

    Dr Davis.  Do you have any data that decreasing coronary calcium scores actually saves lives or decreases cardiac morbidity? As you show in this post, the association of Coronary calcium score and atherosclerotic heart disease is undeniable as well as prolific.  I would just love to believe that decreasing one's score really prevented heart attacks.

  • Anonymous

    9/18/2008 6:38:00 PM |

    It would be nice if you could address what tests us 20 and 30 somethings can have done since CT scans are not recommeneded for our age group.

  • jean

    9/18/2008 6:54:00 PM |

    "If I was cynical, I would say that they know the actual value of statins by the argument they use to dismiss the primary indicator of ongoing heart disease. They know that statins have little or no effect on accumulated calcium in the heart and know that someone paying attention to heart scan scores would quickly realize the significant, painful and common side effects of statins are not worth the limited benefit."
    -rabagley
    And knowing all of the above, why would they espouse knowledge that makes a mockery (!yes!) of their entire professional life? Having worked 10 years in a CCU as a nurse, a little thing called EGO is possibly involved (ah, the turf fights, I remember them well). Just possibly. Oh, and money. Money, money, money!
    Thank you for trying to bring these folks, kicking and screaming, into the 21st century.

  • Peter Silverman

    9/19/2008 2:58:00 PM |

    I wonder if anyone has scanned John McCain's 1000 pages of medical records to see if he's had heart scan?

  • Anonymous

    9/19/2008 10:42:00 PM |

    “The most difficult subjects can be explained to the most slow-witted man if he has not formed any idea of them already; but the simplest thing cannot be made clear to the most intelligent man if he is firmly persuaded that he knows already, without a shadow of doubt, what is laid before him.”
         - Leo Tolstoy

  • Anonymous

    9/20/2008 2:56:00 AM |

    Dr Davis,

    As someone who is "in between" scores - first one 230 at 52 and 410 at 54 - with huge changes in Vit D, fish oil, etc and great results in both Berkley and MNR results.... I do wonder.

    Have there been studies that show the hard to soft ratio of calcium is constant, or in people who have declining heart scan scores, or *slowing* scores, that the soft dangerous plaque for those people is lower than those whose scores are growing.

    It seems (logically) that declining scores would indicate a change in percentages (e.g. flat scores show a significant reduction in the amount of "soft" plaque.

    Dave K

  • Anonymous

    9/20/2008 12:03:00 PM |

    Re:"50 x-rays? is that true?"

    From July 3, 2008

    On present-day CT devices, heart scans expose a patient to 0.4 mSv of radiation on an electron-beam, or EBT, device, and on up to 1.2 mSv on a 64-slice multi-detector, or MDCT, device, compared to 0.1 mSv during a standard chest x-ray. CT heart scans are therefore performed with about the same quantity of radiation as a mammogram done to screen women for breast cancer, or about the equivalent of four chest x-rays on an EBT scanner, up to 12 chest-xrays on a MDCT scanner.

  • Alan S David

    9/24/2008 2:56:00 PM |

    I have cut the wheat to less than 3% of my diet.I do eat a once a wekk lower fat pizza Smile
    My calcium scan score was a 90 last January and I am hoping ( at age 59+) to see the same or better this January. I also added 6-8 fish oil caps a day, take niacin and L-arginine, as well as increased my cardio program.
    Lost 18 pounds from an already somewhat trim weight level. My ldl though went from 170 to 220, while HDL went from 40 up to 55. Not sure why on this, other than the fish oil maybe?

  • Rick

    6/25/2009 6:55:55 AM |

    >My ldl though went from 170 to 220, while HDL went >from 40 up to 55. Not sure why on this, other than >the fish oil maybe?

    My take (based on my reading of Dr Davis's work and that of Dr Michael Eades) is that:
    1. The score is probably inaccurate because they've calculated the LDL for you rather than actually measuring it;
    2. Since your HDL has gone up (and probably triglycerides have gone down), it probably doesn't matter even if your LDL has actually gone up. ( I think Dr Davis might disagree with this second one.)

  • Rick

    6/25/2009 6:58:52 AM |

    BTW, Dr Davis, although you say that Dr Manning has confused CT coronary angiography and CT heart scanning, you don't mention what the difference is or why people would confuse them.

  • Anonymous

    9/21/2009 3:46:44 PM |

    AS A CARDIOLOGIST MYSELF: Unfortunately, this article is overly opinionated and incorrect at times. Much of the info IS correct, such as the fact that calcium DOES predict risk of coronary disease. But using this to track progression/regression is NOT appropriate and this has been shown in a very large published trial (mainly because calcium tends not to regress with treatment on statins).

    I don't mind a blog post like this with an opinion, but it is irresponsible to suggest that another physician (and one of the most respected in the field) is incorrect without confirming your facts. Dr. Manning is correct in his statments about calcium scoring, the radiation exposure, and general lack of usefulness in practice. Please post response if you would like me to further address the specifics on this issue.

  • Dr. William Davis

    12/16/2010 2:29:07 AM |

    Anonymous cardiologist--

    I'd be happy to hear more about your opinions.

    First, credible opinions do not originate from "anonymous." For all I know, you are a plumber or the guy who changes oil at the Quick Change station.

    Second, credible opinions do not start with criticizing a blog for expressing opinion. This is a BLOG, not a JACC or NEJM publication.

    As a start, I would say you've been sucker-punched into believing that serial coronary calcium scores do not work because statins don't have an effect on reducing scores. What if they were the wrong treatment to begin with?

    Are you the same guy who invites the good looking sales rep for Pfizer into your office who tells you that their "data" shows extravagant improvement in endpoints? Do you also believe that heart disease prevention ends with your prescription pad?

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Lethal lipids

Lethal lipids

There's a specific combination of lipids/lipoproteins that confers especially high risk for heart disease. That combination is:

Low HDL--generally less than 50 mg/dl

Small LDL--especially if 50% or more of total LDL

Lipoprotein(a)--an aggressive risk factor by itself



This combination is a virtual guarantee for heart disease, often at a young age. It's not clear whether each risk factor exerts its own brand of undesirable effect, or whether the combined presence of each cause some adverse interaction.

For instance, lipoprotein(a), or Lp(a), by itself is the most aggressive risk factor known (that nobody's heard about--there's no blockbuster revenue-generating drug for it). Each Lp(a) molecule is a combination of an LDL cholesterol molecule with a specific genetically-determined protein, apoprotein(a). If the LDL component of Lp(a) is small, then the combination of Lp(a) with small LDL is somehow much worse, kind of like the two neighborhood kids who are naughty on their own, but really bad when they're together.

Interestingly, the evil trio responds as a whole to many of the same corrective treatments:

Niacin--increases HDL, reduces small LDL, and reduces Lp(a)

Elimination of wheat, cornstarch, and sugars--Best for reducing small LDL; less potent for Lp(a) reduction.

High-fat intake--Like niacin, effective for all three.

High-dose fish oil--Higher doses of EPA + DHA north of 3000 mg per day also can positively affect all three, especially Lp(a).


If you have this combination, it ought to be taken very seriously. Don't let anybody tell you that it is uncorrectable--just because there may be no big revenue-generating drug to treat it on TV does
not mean that there aren't effective treatments for it. In fact, some of our biggest successes in reducing heart scan scores have had this precise combination.




Comments (15) -

  • Jenny

    5/8/2009 12:22:00 PM |

    Isn't it time we stopped talking about "risk factors" which is a flaky idea invented by drug companies and often means "associations" and start talking about causes?

    In this case, a CAUSE of heart problems is probably glycosylation [permanent binding of glucose to the protein] of receptors used in lipid removal. That's why cutting back on carbs which lowers glycosylation helps.  

    The CAUSE explanation for why  wheat is an issue for many people is most likely that they have genes for mild gluten intolerance which leads to systemic inflammation. New genes have been discovered recently which are making many more people test positive for gluten intolerance, usually people with other autoimmune markers.

    Without those genes wheat behaves just like another glucose-source in the diet. I do eat wheat, just not much of it, but I keep all my carbs low and have very low Apo-A and very high HDL.

    I do occasionally hear from people with diabetes who are fat sensitive and whose insulin requirements and blood sugar go up not down on a high fat/low carb diet. That's probably another genetic error at work. It's rarer, but it does exist. For such people the cause profile may be different.

    It would be nice to know what's the cause behind the positive effects of the fish oil on heart disease. Any clue?

    As long as we stick with "risk factors" we can end up thinking that yacht ownership is a "risk factor" for wealth since studies have repeatedly shown that people who own yachts are more wealthy than those who don't.

  • prophets

    5/8/2009 1:23:00 PM |

    i have this pathology.  the causes are pretty clear, imo.  i take nicotinic acid, fish oil, etc.  unfortunately, i had to self-diagnose my condition because every cardiologist i saw was so fixated on low-ldl/lipitor-is-everything analysis.

    thx for the note.

  • Steve

    5/8/2009 2:13:00 PM |

    high fat intake is a surprise! are you saying high saturated fat or unsaturated fat from oily fish for example?  
    Does elimination of sugar mean not eating fruit?

  • Anonymous

    5/8/2009 2:31:00 PM |

    After reading your post about the use if niacin to improve low HDL, I started niacin.
    I just got my test results:In 6 months, I've gone from 42 to 79!
    I'm still waiting for the results from my vitamin d level and CRP, but I bet I'm not disappointed.
    Thanks again for great information.
    Jeanne

  • Anonymous

    5/8/2009 2:33:00 PM |

    Oh, and my total cholesterol went up a little, to 211, but my tryglycerides are still very low (38), so I'm guessing my small dense LDL particles are very few.
    Jeanne

  • Kurt

    5/8/2009 2:51:00 PM |

    I've been reading this blog with interest for the past week. I'm a 44 year old male who had my first coronary artery calcium scan. My doctor wanted to prescribe statins for my cholesterol (LDL 155, HDL 65, Triglycerides 78) so I decided to have a scan first. I was hoping my high HDL had kept my arteries healthy. My score was 42 (LAD 42, the rest were 0). I thought that was pretty good ("mild plaque burden," the test result said), but the doctor told me I was in the 85th percentile - only 15% of men in my age group have a higher score. I'm wondering, do you see any good news in my results? Thanks.

  • waxjob

    5/8/2009 10:29:00 PM |

    I've just read a Norwegian study that was recently cited in a cardiology journal that has found high HDL readings can be dangerous.
    I'm a 57 yr old male and this is my lipid profile:
    185 (TC)
    76 HDL
    103 LDL
    29 Triglycerides (TRG)
    My HDL is nearly as high as my LDL and my triglycerides are almost non-existant. Nobody in my family has ever had heart problems but my profile doesn't look like any of the other ones I see and I'm wondering if I should go back and ask to see a cardiologist for a follow up?

  • billye

    5/9/2009 1:32:00 AM |

    I am already taking 7000mg fish oil providing a little more than 2400mg EPA and DHA on a daily basis. What is your reference of north of 3000mg talking about, total fish oil or just EPA and DHA?.  You say high fat intake like niacin.  Did you also mean to infer that high fat animal protean and cheese could be helpful? My doctor stopped me from taking all Staten's and I already stopped sugar, wheat and high carbohydrates.

    Billy E.

  • Rick

    5/9/2009 3:06:00 AM |

    Dr Davis,
    Could you qualify the high-fat intake treatment a bit? Is any kind of fat effective? And presumably there are conditions for what the fat can be combined with, too?

  • David

    5/9/2009 4:00:00 AM |

    Saturated fat in particular is the most effective for increasing HDL, decreasing Lp(a) (by nearly 12% in one study), and decreasing sdLDL. One should note that saturated fat may cause an increase in calculated LDL, but this is inconsequential, as the LDL particles will be of the larger, fluffier, more benign type. Also, if triglycerides are decreased (as they would be -- oftentimes dramatically -- on a lower carb, higher saturated fat diet), of course calculated LDL will go up. According to the Friedewald calculation: LDL cholesterol = Total cholesterol – HDL cholesterol – Triglycerides/5. Therefore, if all you do is decrease triglycerides (a good thing, to be sure!), your LDL could go up! This is why the NMR is a much better way to track changes. It measures particle number and size instead of making a mere "calculation."

  • Anonymous

    5/9/2009 2:09:00 PM |

    Dr Davis:

    Would you comment or send a link to a comment about when you would do a calcium scan vs a full CTA for stratification of cardiac risk?

    DoctorSH

  • Anonymous

    5/9/2009 11:13:00 PM |

    David -  I would love to read more about this.  Can you point me to any studies where they have gotten these results.

    Thanks,

    Bonnie

  • David

    5/11/2009 4:02:00 AM |

    Bonnie,

    Certainly. Here's a study with all of the things I mentioned: Increased HDL, decrease in small LDL (increase in LDL particle size, which is good), and ~12% reduction in Lp(a) -- and all with a low-carb/high-fat (60%) diet.

    http://www.nutritionandmetabolism.com/content/3/1/19

  • Ricardo

    5/21/2009 3:03:51 PM |

    Dear Dr. Davis, I believe these recent studies tell us that LDL is not as bad as we were thinking. When shall we expect to see small LDL as a standard medical test/marker, and LDL discarded?

    1- http://www.journals.elsevierhealth.com/periodicals/jac/article/PIIS0002870308007175/
    2- http://astute.cardiosource.com/2007/vposters/pdf/275_Fonarow.pdf
    3- http://www.journals.elsevierhealth.com/periodicals/jac/article/PIIS0735109706004797/
    4- http://www.ncbi.nlm.nih.gov/pubmed/17134630

  • mongander

    8/17/2009 9:16:53 PM |

    My HDL just doubled from under 40 to 80.  Have been on niacin and also use 1 oz of 190 proof Everclear to dissolve supplement powders which I then add to hot cocoa.  My doc thinks the increased HDL was due to the alcohol.

    Coincidentally, at the same time my HDL doubled, so did my PSA.  Now I'm scheduled for a prostate biopsy.  I'm 70.

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Exploitation of trust

Exploitation of trust

Once upon a time, the tobacco industry was guilty of conducting a widespread, systematic, highly organized campaign to deliver their product to as much of the unsuspecting public as possible.

As clinical data mounted linking smoking and health problems like cancer and heart disease, tobacco producers labored fiercely to counter these claims despite darkening public sentiment. When individual company executives were questioned on why they continued to perpetuate the industry’s scandalous practices, the invariable justification offered was “Well, I had to pay my mortgage.” That tidy ends-justifies-the-means rationalization has a familiar ring when you examine the behavior of those in the heart "industry."

Things are not what they seem. The hospital, once an institution to serve the sick, a place for clergy, volunteers, and other altruists, has evolved into a business serving a thriving bottom line. You are the “product” they seek. The cardiologist, ostensibly in the service of alleviating heart disease, instead seeks to grow his checkbook by performing procedures that have nothing to do with lessening the burden of heart disease. He dives into the water to save drowning victim after drowning victim, but fails to simply toss in the life preserver that has been close at hand all along.

The woeful family practitioner, who is expected to bear undue responsibility for the broad spectrum of health, ignorantly permits heart disease to grow under his or her nose and, by default, allows heart disease to become the exclusive province of the proceduralist. Worse, the family practitioner or internist in the employ of the hospital (a situation that has quietly grown to encompass 80% of all primary care physicians) labors to fatten hospital business by directing patients into hospital services. The comparative lowly incomes of the primary care physician are substantially supplemented by participating in this huge revenue-generating machine called heart care.

The astounding grasp of the system has caused one of every 10 adults in the U.S. to have undergone a heart procedure. The lemming-like procession to the hospital creates a crowd mentality among some sectors of the frightened public. “My friends and neighbors have all had bypass operations. Sooner or later I guess it’s going to be my turn.”

Tragically, the system has grown through the exploitation of trust. The faith we have in doctors, hospitals, and the institutions and people associated with healthcare has been subverted into the service of profit. Many practitioners and institutions choose to operate under the guise of doing good, but instead capitalize on the public’s willingness to accept as fact the need for major heart procedures and all its associated costly trappings.

Comments (5) -

  • Diabetes Supply

    7/25/2008 5:16:00 AM |

    At first, your blood sugar level may rise so slowly that you may not know that anything is wrong. One-third of all people who have diabetes do not know that they have the disease. If you do have Type 2 Diabetes Symptom, they may include: Feeling thirsty. Having to urinate more than usual, Feeling more hungry than usual, Losing weight without trying to. http://diets-diabetes.blogspot.com/

  • Jenny

    7/25/2008 11:13:00 AM |

    Thanks for drawing attention to this very real problem.

    As you may have read in my blog, I went to my local hospital last December because I'd inhaled a small piece of peanut and the ER doctor and hospitalist did all they could to turn that visit into a cardiac emergency despite a completely normal EKG.

    Had I not been an ornery bitch I'd have ended up paying for the nuclear stress test they ordered for me on top of the several thousand bucks I was charged for staying over night with a monitor on me.

    My heart was 100% fine--all this cardiac nonsense was because I have the word "diabetes" on my chart and because my lung--which is in my chest, hurt--after 24 hours of coughing--which the ER doctor interpreted as "chest pain--Heart attack???.

    If I'd had that stress test with the false positives I might well have ended up with unnecessary surgery.

  • Jenny

    7/25/2008 2:11:00 PM |

    From a different Jenny  (Jennytoo):  You are getting to the essence of the problem, and it's not just cardiology that is rife with what is at bottom malpractice.  There is little incentive for the profession as a whole to know anything about or promote prevention, and many incentives from hospitals, drug and insurance companies to stick with the status quo or to change it in their corporate favor.  The formulaic, conventional statements purporting to be guidelines for prevention that are put out by various interest groups and in such publications as hospital-sponsored newsletters ("eat a 'balanced diet', avoid stress, etc.")  are useless sops to the concept of prevention.  It is, and I fear is going to remain, up to motivated individuals, both physicians and patients, to reshape the system, and it's going to be a long frustrating struggle.  It's my personal conviction that if just 4 things were promoted to the public, and people actually practiced them, we could change the health profiles of the majority of people in this country for the better within two years or less.  They are (1) education on and promotion of a true low-carbohydrate, whole foods, diet, (2) measurement and supplementation of Vitamin D3 (3)supplementation with DHA/EPA (found in Fish Oils) and (4)measurement and supplementation of  intracellular Magnesium.   I am not a health professional, and others may want to add to this list, but I don't think any strong case can be made against any of the items.  The wonderful and hopeful thing is that each of us can implement them ON OUR OWN, and thereby take charge of our own well-being.  (The Life Extension Foundation is one organization which provides access to lab tests you can request on your own.)  If you have a physician who is willing and capable of being your partner, you are richly blessed, and that is the ideal we all should hope for.   But in the more likely event that you do not have such a physician, and if your physician demonstrates little potential for becoming one, think about firing the one you have and finding another.  Sometimes we are forced by circumstances, particularly urgent ones, to deal with physicians who are not ideal, but the main impetus for change will come from us, the patients, and the expectations we communicate to our individual doctors.  In the meantime, we can be self-reliant in our own prevention practices.  Learn from Dr. Davis and Jenny Ruhl and the Dr.'s Eades and the Vitamin D Council (and many others), and put what you learn into practice for your own benefit, and when in health-care settings, be friendly and accommodating when you can and ornery when accommodating doesn't work.  Your health is your own, and shouldn't be at the mercy of any other whose interests are competing.

  • Dr. William Davis

    7/25/2008 4:41:00 PM |

    Eloquently said!

  • Mike Dodge

    7/28/2008 10:38:00 PM |

    I haven't visited the medical community in over 5 years. I think that I am healthier for that.

    In the past, I had lots of expensive tests done that resulted in nothing of significance being done, but lots of money spent. Doctors can easily scare people into having lots of tests done. Who wants to drop dead? If I break a bone, I will, most likely, go to a physician. I see no need to get the recommended no-symptom tests done as they are just looking for the needle in the haystack but finding lots of pitchforks.

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The rules of reversal

The rules of reversal


For the last few years, most practicing physicians have followed a rough blueprint for cholesterol management provided by the Adult Treatment Panel-III “consensus” guidelines, or ATP-III, a lengthy document last released in 2001, updated in 2004.

For instance, ATP-III suggests reducing LDL cholesterol to 100 mg/dl or less for those deemed to be at high risk for future heart disease, arbitrarily defined as a risk of 20% over a 10-year period. It also suggests that a desirable triglyceride level is no more than 150 mg/dl. The ATP-III guidelines have been the topic of discussion in thousands of medical meetings, editorials, and reports. They have served as the basis for many dinners at nice restaurants, weeks in Vegas or Honolulu, many, many lunches catered by pharmaceutical representatives. For most internists, family doctors, cardiologists, and lipid clinics, ATP-III is the Bible for cholesterol management.

AT-III has also become the de facto standard that could conceivably held up as the prevailing "standard of care" in a court of law in cases of presumed negligence to treat cholesterol values. “Doctor, would you agree that the consensus guidelines issued by the National Institutes of Health and endorsed by the American Heart Association state that LDL cholesterol should be reduced to 100? You do? Then why was Mr. Jones’ LDL not addressed according to these guidelines?”

Who was on the ATP-III panel and on what scientific evidence were the guidelines based? Several problems:

1) Of the 9 physician members of the panel, 8 had ties to industry, some of them quite intimate.

2) The studies upon which the guidelines were based and figure prominently, such as the Heart Protection Study, PROVE IT, and 4S, were all funded by the pharmaceutical industry. Of course, it would be unreasonable to expect anyone other than the pharmaceutical industry to fund drug studies. But prominently neglected or understated in the guidelines are all the other insights and treatments for coronary atherosclerotic risk available that were NOT funded by industry.

Of course, there’s money to be made in reducing LDL cholesterol. Lots of it--$23 billion last year alone, in fact. Just keeping that fact in mind makes the ATP-III guidelines make far better sense.

ATP-III is really not a blueprint for heart disease prevention. It is a blueprint--by industry, for industry--on how and when to treat LDL cholesterol.


But what if ATP-III had been a map for navigating coronary plaque reversal instead? What if it were not obsessed with just reducing LDL cholesterol, but was focused on providing the corner internist, family doctor, or cardiologist a roadmap for navigating the highways and byways of reversal?

That would be interesting. Mainstream reversal. Imagine that.

Among the difficulties is that the path to reversal is not lined with deep pockets. Treat LDL and who gains? That's easy. Reverse heart disease and who gains? Beyond LDL reduction, very few (beyond you and me, of course).

That’s why the call for a new Age of Self-Empowerment in healthcare is necessary now more than ever. In my view, in the foreseeable future, we will not have an ATP-III-like blueprint for heart disease control or reversal, nor will we witness a boom of nationwide appreciation that coronary atherosclerosis is a reversible process.

It’s time to take the control back and put it in our own hands. Don't expect the American Heart Association to do it. Don't expect the pharmaceutical industry to do it. If there's anyone who's going to do it, it's YOU.

Comments (12) -

  • gc

    11/3/2007 11:26:00 PM |

    Man oh man I wish I lived closer and you were my doc!!!!

    I try nicely to get docs to think that low carb and being off insulin is ok, that not being on a statin may be ok even though my ldl goes up but my lipoprotein a is low.....I don't know what to do about this new doc I am seeing as don't want to turn her off but want to turn her onto TYP.

  • G

    11/10/2007 4:05:00 PM |

    Unfortunately we all do have to be our own advocates... thanks for giving us the means and tools to do so for our family and friends (and patients)!

    The article you mentioned about MMPs (tissue metalloproteinases), CRP and D3 deficiency was quite frankly phenomenal.
    Q J Med: 2002;95:787-796.
    Cirgulating MMP9, vit D and variation in the TIMP-1 response with VDR genotype: mechanisms for inflammatory damage in chronic disorders?

    Again, I think you are correct, the implications revealed here and elsewhere are blatant omissions from discussion in the ATP guidelines (the 'bible' when I was in pharmacy school).  

    One-yr Post-supplementation with intra-muscular Vitamin D(from pre-8 to post-14 ng/ml) produced statistically reduced MMP9, as well as decreased CRP (another marker for chronic inflammation). These are all increased in acute MIs and unstable angina and in active arterial plaques. (unfortunately they did not raise the 25(OH)D levels sufficiently 50-70 ng/ml otherwise perhaps they might've seen substantial primary CAD prevention at the 5yr followup -- *bummer!*).

    Thank you for the info on Doxy. I remember reading > 10yrs ago how doxy helped in arithritis.  It makes sense now!!!

    With the role of D3 emerging that it's vital and affects all organ systems, do you think your TYP program is also treating and preventing ALL chronic conditions? Are you aware that you may be creating an immortal human subpopulation *ha haaa haa*. But alas, we are human...

    Do you think that perhaps since D3 is a steroid structure, D3 may be depleted in cortisol-driven activities (ie, chronic stress -- physical, mental, genetic)?  Perhaps a cascade of events occurs, triggered by (let's conjecture) a marginal reduction in sunlight (since we obtain naturally about 99% of D3 activation from sunlight) which leads to broad widespread decline in D3-dependent cellular activities. Unfortunately D3-dependent cell functions appear to me (from your blog and the literature) to be literally ALL functions...

    Immune cells--flu, infections, MS, lupus, asthma/copd, T1DM, RA
    Thyroid & parathyroid--TSH and PTH irregularities (then eventually Graves/Hashimotos), osteoporosis
    Bones/GI system--without D, GI incapable of absorbing calcium (absorb more Hg, Pb? ...autism spectrum?)
    Colon--cancer, mortality
    Cerebral arteries--migraines
    Brain--depression, less euphoria
    Nerve endings--peripheral neuropathy
    Kidney/renin--hypertention, pre-eclampsia (during pregnancy when E2 and P hormone production is ramped up)
    Pancreas/beta-islet--Metabolic Syndrome, glucose intolerance, Type 2 diabetes
    Liver--PPAR changes, high TG/low HDLs (less HDL to scavenge out LDL)
    Adipose--insulin resistance, weight gain
    Coronary arterial plaque--CAD, MI
    Nephrotic atherosclerosis--CKD, dialysis
    Cerebral vasculature--stroke
    Ovary, breast--infertility, PMS, cancer
    Prostate--cancer
    Hair follicles--male pattern baldness(?)
    Overused joints--osteoarithritis

    In the literature, D supplementation (sometimes with calcium, but I don't think it's necessarily relevant) improves all these chronic conditions. Is it all more interconnected then we suspect? I see all these conditions in the primary care setting, and I find that recently I'm giving the same 'dog-and-pony show' to all pts (migraines, perimenopause, T2DM, HTN, CKD, etc). 'fish oils, nuts/seeds, oat bran, relax, exercise, get some sunlight midday, low GI foods, Ezekiel bread, and on and on'.
    I wonder now...wouldn't it be just easier to put 'the D' in the water?  There are so many challenges in overcoming the havoc caused by MMP and other inflammatory constituents(ie,'target organ disease').  The TYP plan truly seems to offer vitality... and immortality! Another medical genius said ( Hippocrates) "your food is your medicine, and your medicine your food."  He was so right, after all these centuries. Keep up the strong work and don't stop the rhetoric!

  • G

    11/10/2007 4:13:00 PM |

    BTW, is there any tissue that is devoid of VDRs (vitamin D receptors)? toenails?  THANKS!!

  • G

    11/10/2007 5:41:00 PM |

    Additionally...i forgot several disease states...so embryonic tissue in utero are affected too. does calcium modulation make such a difference at age 'zero'? there appears to be evidence. perhaps even for heart disease?

    Skin--psoriasis (treated w/Dovonex a D analogue)
    Maternal D nadirs--schizophrenia (in summer babies; see Oprah Nov's issue! *HA HAAA HAA*), Type 1 DM
    Brain--Alzheimers (D improved cognition, cheaper than Aricept)
    Muscles--chronic pain syndromes, fibromyalgia

    do you have a cure for addiction to reading about disease reversal?

  • Dr. Davis

    11/10/2007 11:07:00 PM |

    G--

    I've had the very same thoughts.

    Every day, I witness some new aspect of vitamin D replacement that I had not appreciated before. All of this needs to be systematically recorded and reported. Our first report on the effects of vitamin D, along with the Track Your Plaque program in all other aspects, will be reported next spring in the scientific literature.

    I'm seeing so many fabulous effects. We will follow our initial report with more on these issues, though little by little. That's how it works, though I tell you about these things before the official report hits the press.

  • Dr. Davis

    11/10/2007 11:08:00 PM |

    Curious thing, G: You will see accelerated growth of toenails and fingernails with vitamin D supplementation!

  • Dr. Davis

    11/10/2007 11:10:00 PM |

    LOL!

    Well, the enormous abyss of ignorance among physicians on these issues is a sobering thought.

  • G

    11/13/2007 3:24:00 AM |

    That's funny. You are so right again! I've always noticed my nails always grower faster in the summer!

    Did you get a chance to see Planet Earth on the Discovery channel?  AMAZING! Do you now what they focused on?!!!

    The sun and the earth...'Sunlight is the engine of life... whether on land or sea, sunlight shapes life... it triggers birth and death...'  

    I guess it's NO SURPRISE that VDRs are hinged next to other steroid receptors estrogen, progesterone,  and thyroid receptors (and possibly glucocortocoid and retinoic acid).
    (is that why TAN MUSCULAR athletes probably procreate more than cardiologists and pharmacists? *ha haaa haaa*)

    You notice and document here the tremendous disease reversal with testosterone, E2, vitamin D and DHEA...
    It A-L-L makes sense!!!!!

  • G

    11/13/2007 3:45:00 AM |

    can u translate?  I know this must mean something...

    Heterodimers of Retinoic Acid Receptors and Thyroid Hormone Receptors Display Unique Combinatorial Regulatory Properties
    http://mend.endojournals.org/cgi/content/full/19/4/863

    There is an interesting discussion about PPAR and other nuclear steroid receptors. I think that Actos and Fibrates improve HDLs and TG and hence plaque reversal with their PPAR activities (gamma- and alpha- respectively).  Do you think that are other nuclear steroid receptors that can be explored for plaque reveral and ultimately reduction in chronic inflammation?

    my health food store nutritionist recommends cod liver because it includes Vitamin A which is a cofactor for D (he said) compared with D3 alone. I'm hesitant because I've read that A can block (perhaps through competition) D activity. I had a *bad* reaction with Chicken liver pate once... ate a whole chunk then drank ONE sip of beer and had the WORSE etoh-dehydrogenase reaction!  I worry about vitamin A toxicity... it also had worse mortality for lung CA patients.

  • Dr. Davis

    11/13/2007 4:04:00 AM |

    I wasn't aware of the proximity of those genes. Thanks, G.

  • Dr. Davis

    11/13/2007 4:07:00 AM |

    Hi, G-

    I'm afraid you've exceeded my scope of experience with that one.

    However, I know of no such vit A/vit D interaction. I prefer single supplement preparations, in general, because it allows independent adjustment of doses.

  • G

    11/13/2007 7:28:00 PM |

    I think you'll like this.  Bruce Ames discusses keeping mitochrondria happy (and preventing DNA damage and antagonistic pleiotropy). Vitamin D deficiency is mentioned as well.

    http://www.pnas.org/cgi/content/short/0608757103v1?rss=1

    Low micronutrient intake may accelerate the degenerative diseases of aging through allocation of scarce micronutrients by triage

    Bruce N. Ames *
    Nutrition and Metabolism Center, Children's Hospital of Oakland Research Institute, 5700 Martin Luther King Jr. Way, Oakland, CA 94609



    Contributed by Bruce N. Ames, October 6, 2006 (sent for review September 20, 2006)

    Inadequate dietary intakes of vitamins and minerals are widespread, most likely due to excessive consumption of energy-rich, micronutrient-poor, refined food. Inadequate intakes may result in chronic metabolic disruption, including mitochondrial decay. Deficiencies in many micronutrients cause DNA damage, such as chromosome breaks, in cultured human cells or in vivo. Some of these deficiencies also cause mitochondrial decay with oxidant leakage and cellular aging and are associated with late onset diseases such as cancer. I propose DNA damage and late onset disease are consequences of a triage allocation response to micronutrient scarcity. Episodic shortages of micronutrients were common during evolution. Natural selection favors short-term survival at the expense of long-term health. I hypothesize that short-term survival was achieved by allocating scarce micronutrients by triage, in part through an adjustment of the binding affinity of proteins for required micronutrients. If this hypothesis is correct, micronutrient deficiencies that trigger the triage response would accelerate cancer, aging, and neural decay but would leave critical metabolic functions, such as ATP production, intact. Evidence that micronutrient malnutrition increases late onset diseases, such as cancer, is discussed. A multivitamin-mineral supplement is one low-cost way to ensure intake of the Recommended Dietary Allowance of micronutrients throughout life.

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Yet another reason to avoid fructose

Yet another reason to avoid fructose

Have you seen the Corn Refiners Association commercial campaigns to educate the American public on the safety of fructose? If you haven't, you can view these interesting specimens on You Tube:

"Get the facts--You're in for a sweet surprise: Fructose is safe in moderation!"

Two Moms

Two lovers


Beyond the fact that fructose stimulates liver production of glycerol, which thereby increases liver VLDL production and raises blood levels of triglycerides; likely stimulates appetite; increases cholesterol levels; fructose has also been clearly implicated in increasing blood levels of uric acid.

Uric acid is the substance that, in some people, precipitates in joints and causes gout, the painful inflammatory arthritis that has been increasing in prevalence over the last four decades since the introduction of fructose in 1967. While blood levels of uric acid in the early part of the 20th century averaged 3.5 mg/dl, more recent population assessments have averaged 6.0 mg/dl or higher. (Non-human mammals who don't eat processed foods, drink fruit drinks or beer, and don't eat candy have uric acid levels of <2.0 mg/dl.)

Uric acid is looking like it may prove to be an important risk factor for coronary disease and atherosclerotic plaque. It is no news that people with higher blood levels of uric acid are more likely to experience adverse cardiovascular events like heart attack. People with features of the metabolic syndrome also have higher uric acid blood levels; the more characteristics they have, the higher the uric acid level. However, the prevailing view has been that uric acid is simply an accompaniment of these processes, but not causal.

However, more recent observations suggest that increased levels of uric acid may instead be a cause of metabolic syndrome and high blood pressure.

Increased blood levels of uric acid have been shown to:

--Increase blood pressure
--Induce kidney damage (even in the absence of uric acid kidney stones)
--Antagonize insulin responses

A diagnosis of gout is not required to experience all of the adverse phenomena associated with uric acid. (For not entirely clear reasons, some people, perhaps based on pH or other factors, are more prone to trigger crystallization of uric acid in joints, similar to the phenomena of sugar crystallization when making rock candy.)

Which brings us back to fructose, a sweetener that clearly substantially increases uric acid levels. I suppose that the mothers and lovers in the Corn Refiners' commercials are right to a degree: Our kids will survive, as will you and I, despite increases in triglycerides, enhanced diabetic tendencies, amplified appetites, and increased uric acid due to fructose in our diet. We will also likely survive despite being 100 lbs overweight, partly due to the effects of fructose.

But if long-term health is your desire for you and your family, fructose has no role whatsoever to play.

Interestingly, the obviously expensive and slick ad campaigns from the Corn Refiners' videos have triggered some helpful video counterarguments:

High-fructose corn syrup
Conspiracy for Fat America
High-fructose corn syrup truth


A full discussion of uric acid, the scientific data behind uric acid as a coronary risk factor, and the nutritional means to reduce uric acid will be the topic of a thorough discussion in an upcoming Special Report on the Track Your Plaque website.

Comments (5) -

  • Kevin

    12/12/2008 8:02:00 PM |

    There was an article this week in USA Today about new research pertaining to high fructose corn syrup (independent of your uric acid argument). Check it out here: http://www.usatoday.com/news/health/2008-12-08-fructose-corn-syrup_N.htm

    -Kevin on behalf of the Corn Refiners Association

  • BenignaMarko

    12/18/2008 5:28:00 PM |

    This all sounds doable.  It does seem that fructose is causing such health problems that the FDA should make sure it is removed from products.  We all know that we consume too much everything, so, can't they make the stuff without the fructose?  There is so much to worry about in recent years, we might as well not eat.
    Benigna Marko

  • Anonymous

    1/4/2009 10:36:00 PM |

    I don't deny the research posted in this post.  However, things are not as simple as they seem.

    I have done quite a lot of research on Multiple Sclerosis, and high levels of uric acid are actually implicated in LOWER levels of MS.  Uric acid actually can work as an antioxidant in the body; gout and MS are almost mutually exclusive.  You will almost never see someone who has gout having MS, and vice versa.

    In fact, increasing uric acid in MS patients has been shown to DECREASE RELAPSE RATES (see abstract below.)

    So, things are not as simple as they appear.  

    Just thought I'd post this information.

    -gb

    FROM MEDLINE


    5: Vojnosanit Pregl. 2006 Oct;63(10):879-82.Links
        Therapeutic value of serum uric acid levels increasing in the treatment of multiple sclerosis.
        Toncev G.

        Clinical Center Kragujevac, Center of Neurology, Kragujevac, Srbija.

        BACKGROUND/AIM: Uric acid was successfully used in both, prevention and treatment of the animal model of multiple sclerosis (MS). Recently it has been shown that inosine, a ribosylated precursor of uric acid, might be used to elevate serum uric acid levels in MS patients. The aim of this study was to evaluate the safety and efficacy of oral inosine as a single drug treatment in patients with MS. METHOD: We administered inosine orally to 32 MS patients from 2001-2004 year at doses from 1-2 g daily (given twice) depending on the pretreatment serum uric acid levels. The mean follow-up interval was 37.69+/-6.55 months. The other 32 MS patients, without any treatment except for a relapse period (matched by age, sex, duration of disease and functional disability), were used as controls. The follow-up interval of these patients was 36.39 +/- 2.68 months. The neurological disability was evaluated by the Expanded Disability Status Scale score (EDSS). RESULTS: During the observed period the treated MS patients were found to have the lower relapses rate than the non-treated MS patients (Chi-square test, p = 0.001). None of the patients have showed any adverse effect of inosine treatment. The non-treated MS patients were found to have a higher increasing in the mean EDSS score than the treated ones (two-way ANOVA-repeated measures/factor times, p = 0.025). CONCLUSION: Our results suggested that the treatment approaches based on the elevation of serum uric acid levels might prove beneficial for some MS patients


    1: Eur J Neurol. 2008 Apr;15(4):394-7. Epub 2008 Feb 26.Click here to read Links
        Variation of serum uric acid levels in multiple sclerosis during relapses and immunomodulatory treatment.
        Guerrero AL, Martín-Polo J, Laherrán E, Gutiérrez F, Iglesias F, Tejero MA, Rodríguez-Gallego M, Alcázar C.

        Neurology Unit, Hospital Río Carrión, Palencia, Spain. aguerrero@hcuv.sacyl.es

        Uric acid (UA), a product of purine metabolism, may be an antioxidant, perhaps acting as a scavenger of peroxynitrite. Patients with gout have a reduced incidence of multiple sclerosis (MS). A number of studies found that patients with MS have low serum levels of UA, although it has not been established whether this represents a primary deficit or a secondary effect. UA has also been proposed as a marker of disease activity and response to immunosuppressive or immunomodulatory treatment. We retrospectively reviewed 83 relapsing-remitting or secondary progressive MS patients (64 females and 19 males) followed in our Neurology Unit. We collected data concerning demographic variables as age and sex, and clinical variables as age of onset, clinical type, disease duration, EDSS score and total number of relapses. We considered UA levels in three different situations: during a relapse, during remission period and during remission period under immunomodulatory treatment [Interferon Beta 1a i.m. (Avonex; Biogen Idec Inc., Cambridge, MA, USA), Interferon Beta 1a s.c. (Rebif; Serono Europe Limited, London, UK), Interferon Beta 1b (Betaferon; Bayer Schering Pharma AG, Berlin, Germany) or Glatiramer Acetate (Copaxone; TEVA Neuroscience LLC, Kansas City, MO, USA)]. A Wilcoxon matched pairs test was carried out to determine differences between groups. A P-value less than 0.05 was considered statistically significant. In 33 patients, we were able to compare at least one UA value obtained during a relapse with at least one when remission without treatment. Mean serum UA levels were significantly lower when measured during a relapse (r: 0.39, P: 0.024). In 27 cases, we compared at least one remission value without treatment with at least one obtained during remission and immunomodulatory treatment. Mean serum UA levels significantly increased when determined during Interferon Beta or Glatiramer Acetate therapy (r: 0.84, P < 0.001). Although we do not know exactly whether and how UA is involved in MS pathogenesis, our data suggest that UA might reflect disease activity or treatment response in MS.

  • karl

    2/28/2009 3:56:00 AM |

    I read that Fructose is 10 times more reactive than glucose in forming AGE - Advanced Glycogen End-products - the process thought to start CAD.

    I avoid all sugar - but wonder if the extra 5-10% might make a difference.

  • Free Teleconferencing

    2/22/2011 11:49:58 AM |

    Very... Nicee... Blog.. I really appreciate it... Thanks..Smile

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