Time to stop bashing primary care docs, doc. Online sites are full of B.S.
Show me the evidence that testing with CAC improves outcomes (Sure it predicts risks, not the same as actually preventing disease, especially in those at lower risk of CAD.)

Hi Jan,
Since you accept plaque showing up as being a cardio-vascular risk factor then if Doc reports he has treated some patients whose measurement of plaque has diminished using his protocol would you also accept the proposition that those patients have reduced one of their cardio-vascular risk factors?
If Doc has patient records showing diminished plaque and therefore one less risk might that not be considered preventative due to his patient following his protocol ?
As for those individuals with hypothetically lower risk of CAD (ex: the 63 year old low cholesterol example Doc gave) are they not going to undergo changes as they age ?  
A primary care physician is valuable and yet older westerners are increasingly engaging specialists for good reasons.  Doc has a self-professed specialty tracking plaque  that he wants to impart; sure, his blogging tone may not always be mellow.

Dear Might,
Your comment is akin to those who report the association of statin use with lowered risk of MI. A correlation does not prove causation until valid  scientific research confirms.
How do we know treating CAC lowers risk of MI until a study proves this? Docs have been wild to accept the association of statin use lowering cholesterol components as the mechanism of effectiveness for prevention of MI, ignoring studies in which dietary measures that did the same were ineffective. Just pointing out the need for caution in going so far as to treat a test without evidence that the intervention is working on the test findings (rather than something else).
Perhaps there are studies that are underway or perhaps the evidence, er association, is just considered too strong, (Bradford-Hill criteria) to ethically justify a trial. My concern is for individuals who score in the lower range of abnormal. At what cost do we label and treat those?

just remembret the lyon heart study, by  Renaud & de Lorgeril demonstrating the efficacy  of mediterranean diet in lowering the risk of recurrent MI in French patients. although cholesterol levels were higher with diet than with statins. Dietary measures seem there to demonstrate  efficacy

Not only is it NOT time to stop bashing primary care docs, but it's time to begin accepting that their role is outdated. In fact, an average nurse practitioner or physician's assistant can do an equal, if not better, job than most primary care physicians. How health care is dispensed is going to undergo dramatic transformation, just as the business of travel agents and real estate have been transformed by rapid information exchange.

In our program, we see virtually NO heart attacks. Not a randomized clinical trial, but watching heart attacks drop from a weekly event to almost never is good enough for me to not accept the status quo and continue to work along a path that, from every indication, works exceptionally well.

If high crab diets are considered unhealthy then why do some cultures like the rural Chinese live long healthy lives on nearly 100% crabs,mostly rice and vegetables?

Isn't the best thing for calcium on wrong places vitamin K2 ?
In my country doctors even prescribe it for calcification issues.
Dose is around 100mcg/day for 6-12 mo.

Read Gary Taubes' "Good Calories, Bad Calories" to find several instances of other cultures eating the typicial high carb food yet seemingly stay within the healthy range.

Trust my care (or a family members care) to a NP or PA who does not have the capability of complex medical decision making - no thanks. NP's actually are complimentary to physicians with different skill sets. So glad to know your level of knowledge about them. PA's are nothing but junior medical students with enormous salaries. Working 9 to 5 - oh, yeah!

I'm certain your referral network of primary care docs would be interested in your belief system.

Dr. Davis:
I don't know if you've seen this new video yet, but I think you'll want to.
http://www.youtube.com/watch?v=3vr-c8GeT34&feature=player_embedded
If you do watch it, I have a question. This doctor thinks sugar (by itself) plays a huge role in causing plaque to rupture and cause heart attacks, etc. If after watching the video you agree with him, would you please tell me how (biologically) it does this?
Thanks!

Joe

Hi Jan,
True correlation does not necessarily equate to causation. As for statins, it seems that statins act to lessen inflammatory processes; and it is this dynamic, rather than numerically lowering cholesterol, that is a crucial way that statins correlate with reduced risk. Which, to me,  seems to further support Doc's contention here in this posting that  low cholesterol levels doesn't  tell one if they have abnormal plaque (ex: patient above with "exceedingly high" score) .

I will accept Doc's data, as given ,that very high plaque is a 15-20% risk factor since many other published sources cite even carotid plaque as a risk factor . As far as who to test for what, and when, I am not qualified to make recommendations. I do know that time can remodel some cellular dynamics and the aging cardio-vascular system is vulnerable to alterations.  Doc's got my attention because no one at all in my paternal male ancestral line lived past their late 50's due to heart problems and I am 60; while my 61 year old brother already was hospitalized from transient ischemic attack  .

Mediterranean diet's efficacy for heart health is probably due to the % of poly-amines per calorie consumed and of course isn't in keeping with Doc Davis' detestation of modern wheat (among other protocols). As we age our poly-amine levels decrease and Mediterranean diet supplies lots of poly-amines.

Poly-amines ( molecules inelegantly named spermine, spermadine and putrescine) are all anti-inflammatory, especially spermine; in our body we synthesize poly-amines from arginine. Mediterranean diet's high poly-amine levels spares the amount of arginine our body uses in synthesizing poly-amines; and thus we can more readily produce the vaso-dilator signalling molecule NO (nitric oxide) from body's arginine. NO is valuable to keep oxygenated blood reaching the heart muscle cells; NO keeps vessels from constricting dangerously.

Poly-amines lower inflammation and in the context of age associated problems the less low grade inflammation the better.  Inflammation leads to defectively functioning cells and molecular processes; with time the  over stimulation of immunological responses (both innate and adaptive immunity) leaves the body burdened with unknown clones of T cells (both memory and effector types). Eventually the build up of  T cell clones limits new variants and what occurs is more macrophages circulating; once an over abundant macrophage stage reins the body is essentially always in low grade inflammation , and prone to various age associated pathology (including cardio-vascular).

@jan....
A vast majority of primary care doctors are extremely limited in their abilities to treat/advise patients for CVD risks. They don't understand nutrition, effects of supplements upon serum biomarkers, nor effective diagnostic testing for heart disease.
CAC is a much better biomarker for who is at greater risk of CVD than serum markers:
http://www.eurekalert.org/pub_releases/2011-08/jhmi-sfc081611.php

I seriously doubt even 1:100 primary care docs see studies like the aforementioned one.
And I seriously doubt the one doc would understand it....
Dr. John

An interpretation of the same study for a broader audience just appeared at http://www.webmd.com/heart-disease/news/20110818/is-calcium-test-the-best-way-to-check-for-heart-risk.

I'd accept a bashing of physicians in general.   But to single out primary care physicians - overwhelmed with paperwork and patients with multiple problems, and vastly underpaid and underappreciated, and continually put down by "Partialists" - Really ? Cardiologists are superior? Really ?

Forget my support and admiration henceforth.

CRP (C-reactive protein), an inflammation marker surrogate, does not directly correlate with whether there is coronary artery calcium (CAC), or the degree of CAC severity. CRP is also subject to variables of race and age, so it loses some potential as a predictive marker. Yet looking at CAC along with CRP is considered useful for complex insight into a patients pathology.

Analysis of the Multi-Ethnic Study  of Atherosclerosis (MESA) involving 6,800 men & women seems to indicate that inflammatory markers (ex: CRP) relate to the physiology of pathological processes other than CAC laid down; possibly because plaque undergoes morphological changes over time. The CRP level is proposed, by some, to relate more to the stability of plaque from rupturing and the incidence of blood clotting in a thrombosis.

The inflammatory marker of Interleukin-6 (IL-6) anti-bodies seems to be better than CRP and fibrinogen for correlating an individual's trend toward CAC. Thus the cytokine IL-6 is a better indicator of sub-clinical atherosclerosis; Doc likes to cut to the chase, eyeball the plaque and track it with current technology ( that is not available worldwide).

Is it typical for someone with such low ldl and high hdl to have such a high CAC score? Had he previously had a higher LDL and then been placed on a statin?

The energy expenditure of the rural Chinese is very high.  They don't drive, they walk, or ride bicycles.  They don't sit in office from 9am to 5pm, they work hard in the rice field from 5am to 9pm.  They can eat anything without gaining weight.
For the urban Chinese, it is a different story.  They have the same life sytle as ours, and they are getting heavier every year.  More and more people become diabetic, even young kids.

K2 is indeed a fascinating nutrient. There are extensive discussions about it on the Track Your Plaque website.

Thanks, Joe. I watched the entire thing and was impressed with Dr. Diamond's grasp of the issues.

I'm going to post this on the main page because I think his overview was extremely effective.

Sorry you see it that way. This was a comment directed at the system of primary care in general.

I reread the post and I didn't see the name "Dr. Thomas White" mentioned anywhere. If you choose to feel slighted in some way, that's your choice.

Jan, I would certainly trust my care (or a family members care) to a NP or PA who looks outside just the pharma driven medical journals which primarily support a diagnose & drug philosophy.  And I'll take an NP or PA who actually uses some common sence rather than being a puppet given to the pushy drug rep.

I live in a family of MD's, and they have made it clear as to their terribly limited training and knowledge they gain from med school on the level of building and supporting the body from within.  Example, I have an Aunt that is currently suffering from stage 4 cancer. Due to the chemo treatment that she's instructed to not spend time in the Sun. Her Dr. has not even checked her for vitamin D levels. This is not the exception, but the norm when it comes to common sence treatment, pathetic.

Okay, Dr. Davis.  I'll be looking for it. When you do, please take a moment and explain how you think that sugar might be responsible for plaque rupture.
Thanks again!

Joe

Sugar is just one part of the equation.  As Dr. Davis has covered on this website, small LDL is also a villian and needs to be minimized as much as possible.

Hi Joe,
Thanx for the video ... maybe the following answers you.

Regarding sugar: see 59:33 into presentation, where diagram shows "sugar" blurb  - lecturer is using compact word sugar to represent how glucose's glycation end products alter the artery and make the artery vulnerable. It is not a molecule of sugar acting all by itself; lecturer explains slide when talks of how glycation is a problem (another of  Doc Davis'  peeves).

Follow up at 1:01 into presentation: see diagram's top left  where the various adverse influences on artery  are specified as "modified lipoprotein", "hemodynamic insult" (includes, but is not limited to blood sugar's  glycation end products affect on artery), "reactive oxygen species" (ROS) and "infectious agents".

Thank you for all your hard work and dedication to your web site and education.

I apologize for cluttering up the discussion with a personal statement.

TRW

Thank you, Might. I guess I'm going to have to do some research on glycation before I can fully understand what you're saying above.

I didn't even notice the PowerPoint Presentation that was included with Dr. Diamond's video presentation.  Sigh.

Thanks again!

Joe

AMEN! Right on target.

I don't know if you're aware of the differences between calculated test that most doctors use and NMR that Dr. Davis uses. When your diet consists of mostly carbohydrates leading to chronic high blood sugar level, it tends to raise your SMALL DENSE LDL level but calculated cannot measure it accurately. It often greatly underestimate it.  Dr. Davis has covered it many times. Dig through his website for it.

Optimal vitamin D level helps lower IL-6. It can be a big problem with black people as they tend to have the lowest vitamin D level of any races. Dr. Cannell mentioned that in his new book called Athlete's Edge Faster Quicker Stronger with vitamin D with the hope that the word about vitamin D would spread out faster if more and more professional athletes started using it to gain some advantage over opponents much like what East Germany and formerly USSR used to do in 1960 and 1970s at the Olympic games and other world events.

Yes Joe i have seen the video you linked. That's right i also think the same.

[...] http://blog.trackyourplaque.com/2011/08/how-far-wrong-can-cholesterol-be.html [...]

"If it's any consolation, the plaque that seems to grow because of a previously inserted stent seems to lack the plaque "rupture" capacity of "naturally-occuring" plaque. It is, indeed, somehow different. It is more benign, less likely to cause heart attack."

Dr. Davis:

You'll pardon my obvious question:  Has anybody actually looked at this phenomenon both in structure and composition at (pardon the word) autopsy?  I would wonder if it's a hyper-reaction to a foreign object, a kind of 'normal' scarring, as you mentioned, or something else.  Obviously there is calcium in this plaque, else it wouldn't be visible on scan. Very curious...

madcook

Madcook--
The phenomenon is known as "edge restenosis". When examined at autopsy, or in years past when plaque was actually extracted by procedures like directional atherectomy, the material is the same as that occuring within the stent, known as "neointimal hyperplasia."

The million dollar question is: Can anything modify neointimal hyperplasia? This is the whole dilemma of stent restenosis, the growth of tissue into stents. Of course, the procedural answer tends to involve drug coated stents. However, I know of no specific preventive strategy that has demonstrated substantial impact on the edge restenosis phemenonon. I've tried several agents, including cilostazol, which holds modest promise.

Thank you for that information... I look forward to hearing more about the use of these agents as time goes by.

"Of course, the procedural answer tends to involve drug coated stents."

I just wonder how many people, who 'flunk' a treadmill test, or having an 'equivocal' result, end up in the cath lab and emerge with stent(s)... Are they _really_ aware beforehand that a lot of stent use is "off label" and they just might end up with a year or two (or a lifetime) on Plavix and aspirin?

I lasted a week on Plavix before I refused anymore... after nearly bleeding to death in the kitchen from a cut (where else would a madcook hang out?).  But then I was very lucky, too as I escaped the cath lab without needing stenting.  A rare event I understand... and aspirin will always be my daily friend (along with most of the other TYP recommendations).

Regards and thank you for the Heart Scan Blog.  It is a tremendous resource and very informative.

madcook

RE: "A year later, there will be a "new" plaque at the mouth of the stent or just beyond the far end."

I'm curious whether or not this is a regular or typical occurrence and if there are symptoms one should be sensitive to that indicate such a development. Also does the size of the stent have a baring on the condition? Does vigorous exercise exasperate the condition?

I appreciate your blog. It's very informative and helpful.

John--
It is, unfortunately, a very common occurrence, though the majority of times it does not result in any specific symptom or clinical consequence. Among the 30% or so of people who do re-develop chest pain, breathlessness, or have a new abnormality on a stress test, most of the time another stent is implanted at the area of tissue growth.

Though this is really outside the realm of the Track Your Plaque program, it is yielding confusing results for people who engage in the program yet have a stent or two. It's my believe that the stent modifies the process of scoring in the stented artery. That's why we can see score reduction in arteries without stents, while the artery with a stent shows substantial increase in score.

The larger the artery, the less likely this occurs. Large means 3.5 mm or greater in diameter.

Amen to everything you said Dr. and one other point I heard a nimber of times yesterday, everybody was in shock because Mr. Russert had just had a stress test done in April and passed with no problems ! As all your readers know what a stupid thing to say.

Dr Davis,
I appreciate your posting on Tim Russerts passing.  I was a big fan of his. I believe if he had worked half as hard on his heart health as he did on his career we would be enjoying him on TV for many years to come.  Of all the commentators discussions since his passing, the most important things aren't being discussed.  His diet (low fat I'd guess), his meds (statins I'm sure)...He did have a good stress test April 29.  Lot of good that did.

Russert had both CAD & diabetes.

Newsweek health article about Russert and sudden cardiac arrest:

http://www.newsweek.com/id/141450?from=rss

Usual blather about not being able to prevent/predict sudden cardiac death, risk factors, and usefulness of defibrillators, etc.

Thank you for this commentary.
His passing is very sad.
My uncle had the same thing happen at a relatively young age as well.

By the way, can you suggest a fish oil for those of us whom are allergic to shellfish?
I've heard we can use any type of fish oil; just not krill oil.
Does Sam's Club Maker's Mark fall under that category?

Thank you!

Regarding the death Of Tim Russert:

In the new issue of Newsweek, Dr. Steven Nissen, chair of cardiovascular medicine at the Cleveland Clinic told the magazine when asked about the role of STRESS and heart attacks:

"Most of us do not think it is terribly relevant," and explained this with a shocking lack of logical thinking: Newsweek writes, "After all, he notes, "many people in this world have stressful jobs," and they don't all die of of heart attacks.

Time Magazine named Dr. Nissen one of the 100 Most Influential People In The World in their "Scientists and Thinkers" section.

Think about that.

Now, consider the completely illogical statement from Dr. Nissen bolded above. One thing should be made perfectly clear in light of this statement: He believes cholesterol as very relevant to heart attack risk. Yet, to turn his Newsweek comments around, "many people in this world have **high cholesterol**" and they don't all die of heart attacks.

In fact, study after study shows countries with the highest rates of fat intake and the highest average cholesterol rates have the lowest incidence of heart disease. Imagine that!

Dr. Nissen's irresponsible and illogical comments in Newsweek shows - again - the complete bamboozlement the cholesterol hypothesis has on western medicine just because, "everyone knows," high cholesterol causes Coronary Heart Disease. How do they know this? "Because everyone knows." Ad nauseum. With a little research, the facts show this is simply not true.

What Dr. Nissen said about stress can be said about high cholesterol. Plenty of people live with both without having heart attacks.

Maybe Mr. Russert's death can help in bringing us back to real science as opposed to what Big Pharma dictates as what is science - and what is not. Follow the money.

How ironic that it was Dr. Nissen who made such a horrible misstep in logic with his comments to millions of readers in Newsweek.

I have a couple of questions that were put to me about Heart Scans that I can't answer. Perhaps you will indulge me.

First, from a Doctor friend of mine:  Most of the widely used diagnostic tests have been studied with respect to their Specificity, Sensitivity, positive and negative predictive value, etc. We know how to use them, and we know how to interpret the information they provide. Last I read, there is not enough correlation between the amount of calcium present in the walls of the coronary arteries, and the degree of coronary sclerosis. Maybe in time there will be enough convincing data - but for now, it is wrong to blame the slowness of the acceptance of the test by the medical community solely on financial interest.

Second, from another friend:

I had the EBT test and showed a calcium score of 950. An angiogram showed no blockage. Go figure. The Doc thinks the calcium is in between the artery walls with the lumen free.

Russert traditionally appeared on Charlie Rose right before Father's Day.  They were good friends -- Rose sold his house in Washington DC to him and aired a moving tribute the night after his sudden MI.

Russert loved his father and wrote a famous book about him 'Big Russ'. It is ironic his own death was right before Father's Day today. And so much much more awful for his surviving son whom he loved so much and was very vocal about.

I hope a new movement for cardiovascular and diabetes prevention may be sparked over this needless, rescue-able, tragic event.

He touched so many lives... fathers, Buffalo fans, media, political enthusiasts...

(I'm glad my Dad is aware of Track Your Plaque -- Thank you Dr. Davis... and Happy Father's Day!)

-G

Mike--

Thank you for your thoughtful and insightful comments. I coudn't agree more.

Henry--

I'm sorry, but if friend told you that, you need new friends.

The literature exists and there's quite a bit of it. Just because your friend is completely ignorant of a body of scientific literature several thousand studies long does not mean that it doesn't exist.

All of your questions can be answered on the www.trackyourplaque.com website.

I buy my Fish Oil from Costco. It happens to be Nature Made 1200mg softgels. Don't let anybody worry you about mercury content on this kind of product. None of these brands have any in them.

If it causes any problems, take it with food.

--Far more could have been done to have prevented Mr. Russert's needless death. And I don't mean the idiocy of making AED's available in office buildings. I'm talking about preventing the rupture of atherosclerotic plaque in the first place.

"But small LDL is so ubiquitous, not addressed by conventional strategies like statin drugs or fat restriction (it is made worse, in fact, but reducing fat in the diet)"

Just to be clear about the above quote. You say "it is made worse, in fact, but reducing fat." Did you mean "by" reducing fat?

Also, if that is the case, is that because of the fat itself or because less fat means replacing it with carbs?

In addition to CETP inhibition, some other benefits of red/blue/purple foods (that also include polyphenols other than the anthocyanins - elligitanins, etc) include:

1) inhibition of amylase - less of a blood sugar spike after eating starchy foods, less aberrant glycation and AGEs.
http://www.ncbi.nlm.nih.gov/pubmed/15796622

2) Estrogenic activity - anthocyanin stimulates the beta-estrogen receptors in blood vessels and bone, not much activity in the alpha receptors in breast, uterus.
http://www.ncbi.nlm.nih.gov/pubmed/20049322

3) Phosphodiesterase inhibition!
http://www.ncbi.nlm.nih.gov/pubmed/15769121

I was surprised that Ron Krauss, who did a lot of research on small particle LDL and recently published a mega-study supposedly showing saturated fat is unrelated to heart disease, made these comments in a recent interview:

People should limit saturated fat to 10% of their diet, though some can get away with more.

Optimal carbs intake: 35 to 40%.

People used to get heart disease from high cholesterol, but now its mainly high carbs.

The interview is here, and those ideas are toward the end:

http://www.meandmydiabetes.com/2010/03/26/ldl-cholesterol-ron-krauss-md/

I would love to know if you have any comment.

This is worth knowing about! Low cost (relatively) lab tests without needing a doc visit/prescription

https://summitcountymedicalsociety.prepaidlab.com/

All tests performed by LabCorp

sometimes it comes down to our health being all about our genetics. As a result of the recomendations of this blog with regard to wheat and sugar elimination, normalizing vitamin D i have taken down my LDL from 1810, all small to 609 of which 346 are small; i can only lower my particles with statins- diet alone will not do it.  My understanding of the research is that at low levels, size does not matter. I will note that when my particles were sky high i thought i was follwoing a very healthy low fat, grain oriented diet.  Now, i eat now grains and have a fair amount of mono fats from avocado and olive oil, some sat fat from lean meats, poultry and eggs, and hope i have minimized the progression of artery plaque that shocked me when i found out i had it when i followed healthy heart diet, exercise and maintained a very lean body weight.  Gentics are tough to overcome, but the risks can be minimzed via diet and meds.

Different segments of the same carotid artery can apparently be affected by a different gene. Each segment is itself susceptable to different pathological processes, like shear rate of the near inner arterial wall. Artherosclerosis at different arterial segments seem to predict if pathological event will be ischemic stroke or myocardial infarction.

The North Manhattan Study tried to tweak 145 genes modulated by 702 single nucleotide polymorphisms. That study and the San Antonio, Erasmo Rucphen and Framingham have led to opinions that 30% to 60% of the thickness of the carotid artery's intima-media is geneticly inherited. Then for carotid plaque +/- 28% is passed on geneticly.

Sex of the individual and racial ethnicity are other genetic variables. Doc Davis' clinical observation is telling us something equally important about small LDL's genetic variation.

Is small LDL the "VLDL" on blood results?

Hi, Tommy--

Yes, indeed. Just a typo.

Probably both.

Hi, Jonathan--

Excellent! Yes, the conversation surrounding anthocyanins is becoming increasingly interesting.



Hi, Peter--

I don't personally know Ron Krauss, but I too have been puzzled by the fact that his public comments don't seem to reflect his research findings. If he were to echo the important findings of his research, he would indeed be a low-carb, high-fat advocate.

Steve--

Wonderful results! The diet approach works, no doubt about it.


Hi, Ryan--

No, two different things.

Hello Dr.Davis,
Your comments sound very similar to Dr Ray Strand...do you read his work? If not, I think you would enjoy his thoughts. His website is www.drraystrand.com
Cheers,
Sue in BC Canada

Question for all you Small Particle techies out there.  Always had "Good" lipid panels, even though overweight and borderline type 2 under control with a low carb diet.

Numbers usually average:
Total Cholesterol 125
LDL  65
HDL  45
Tri  90  

Just got first particle size test done, results in VAP format:  

LDL-1 3
LDL-2 0
LDL-3(B) 36
LDL-4(B) 34

I know particle size goes down as the LDL- number goes up, but how do these numbers translate to the NMR numbers Dr. Davis listed as a target for those of us genetically pre-disposed to pattern B LDL?

^I'm interested in the same thing

Brent,

Your small LDL makes up 96% of your total LDL particles. This is a severe pattern.

Also, your HDL is too low and your triglycerides are a tad too high. Dr. Davis' Track Your Plaque goal of 60-60-60 is a good rule of thumb. LDL down to 60, HDL up to 60, trigs down to 60.

If you're currently following a low-carb diet and still have all of this small LDL, your small LDL pattern is probably the genetic type that Dr. Davis talks about here.

David

ThatÂ’s not just logic. ThatÂ’s ralley sensible.

IJWTS wow! Why can't I think of thnigs like that?

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