Thank you! Sadly, many physicians are becomming a parody when it comes to "procedures". I've heard a neurolgist (family friend) fret, "I went into the wrong field; I end up spending time examining patients instead of doing procedures and can't make any money! I should have gone into orthopedics." Pitiful. In some practices the push for procedures is as bad or worse than the old "publish or perish" dilema of academia.

Who suffers? The patients. And the clinical skills of the physician.

Well said!

Hi Dr. Davis,

Charlie Rose, just last night, hosted a round table of cardiologists to discuss heart disease.  Hopefully it will be available for viewing on the web.

Among the participants was a President emeritus of the American Association of Cardiology (Steven Nissen).

The discussion was all about quick resuscitation(sp?) and providing "2nd chances" in crisis situations, high cholesterol, blood pressure, etc.

The themes you devote yourself to were essentially undiscussed.  No discussion of nuanced lipid analysis, CT scanning, or advances in understanding of the potential positive impacts of food and supplements.

It is precisely that kind of amorphous discuss of heart disease risk which is so depressing.

I'll see if I can find a link to an archived video to get your feedback.

Here's the link to the Charlie Rose show page that should contain yesterday's discussion of heart disease once the video is put up.  Video #8 is already up.  The Heart Disease video is #9.

href="http://www.pfizer.com/think/think_cr_science.jsp"

Hi Dr Davis,
I am an apoe4 carrier. My trig=62, HDL=69; LDL-C=175 after 16 months on a carbohydrate restricted, gluten free diet. Wondering whether I need to also reduce my fat intake. But then what is left to eat? Making up the calorie difference with protein does not sound too healthy.

David

Hi, David--

I would urge you to NOT rely on the calculated LDL value, since on a low-carb diet with potential conversion of small to large LDL particles calculated LDL can substantially overestimate true LDL.

The best: LDL particle number through NMR lipoprotein analysis. The next best: apoprotein B, widely available from nearly all labs.

When you're armed with this information, then you can make an intelligent decision about diet changes.

Regarding Item 6

There was some traffic between Chris Kresser and Jimmy Moore on Twitter yesterday regarding whether low carb caused low T3 in susceptible individuals. Clearly bad news for heart health.

I am a treated hypothyroid and this was my recent experience - I had gone low carb and ended up with an abscess in the roof of my mouth that needed antibiotics.  When tested, my T3 had fallen from 5.5 to 3.8 (RR 4 - 6.8) - however, my TSH was 0.672 (RR 0.35-4.5).  In the UK, this low T3 would normally would have been missed as there is a TSH only testing policy here unless the TSH is found to be outside the reference range - I elected to pay privately for the T3 test.

I remain on low-carb (and wheat free of course) as it is the only approach which allows me to lose weight, and have increased my meds from 75T4+20T3 to 100T4+40T3.

I would query whether you consider hypothyroidism to be rare. I suspect it is very common.

Hi Dr. Davis:
What if the patient  followed the above diet, had a particle count of 2,100, but only 200 were small and HDL 69 and Trgs 66.  Would this be acceptable, and better than a particle count of 640, less than 90 small, HDL 64, Trgs 45, but on statin and Zetia?  Assume thyroid and D all normal, and Apo E3/3
Thanks for all the input

Hi Dr Davis,
This post really hit home with me (and ironically this is my first visit to your site).  I had a heart attack 2 years ago (34 years old, ate well or so I thought, in great physical condition at 5'9" 150 lbs).  My cardiologist advised the usual low fat diet and pravastatin, and while my lipids are better than they were, I'm still very concerned they are not near where they should be.

About 5 weeks ago I found the primal diet and began eating that diet.  Last week I had another lipid test and my numbers actually got worse (not by much).  Would you mind reviewing my numbers and if you have any suggestions I would appreciate it.

8/31/2009 heart attack
total chol 115
LDL 74
HDL 16
Triglycerides 126
VLDL 25

07/19/2010 checkup
total chol 138
LDL 64
HDL 33
Triglycerides 203
VLDL 41

03/21/2011 Healthfair
total chol 122
LDL 69
HDL 31
Triglycerides 111
VLDL 22

8/19/2011 walk in lab:
total chol 159
LDL 98
HDL 34
Triglycerides 135
VLDL 27

Glucose 97
hsCRP 1.2
A1c 5.5

Do you suggest giving the "primal" diet more time or do you suspect I may have another condition causing this?

Also in May of this year I had the following tests done at the cardiologists:
Date of service: May 13, 2011
CAT Scan MRI & NMR
Diagnostic Radiology X-Ray
Cardiovascular Stress Test

I was told everything was fine.

Track Your Plaque once gave a desirable level of ApoB  as under 70 mg.dl as surrogate marker for the desirable LDL particle number (which is less than 700 nm/l) if one only has ApoB testing.  Maybe some one else can recall the conversion ratio of ApoB into LDL particle numbers.

A cholesterol fractions normal transfer from HDL to ApoB is governed by  the cholesterol ester transfer protein (CETP). Genetic variants of CETP can cause differences in the numbers of  small LDL and sparse CETP can cause cholesterol to stay stuck in HDL  ( CETP has little impact on numerical % of HDL). So genetic variants of ApoB can influence the levels of cholesterol shunting around.

In  the liver ApoB normally gets it's lipids when ApoB goes into a cell's endoplasmic reticulum. And if the ApoB doesn't improperly degrade ( ApoB needs "enough" microsomal triglyceride transfer protein SREBP-1c, the sterol regulatory element binding protein, to avoid degrading) then ApoB can pick up triglycerides to form VLDL molecules. So, if there is not enough liver SREBP-1c  then lipids can't be transferred over to make triglyceride rich VLDL; conversely lots of liver SREBP-1c provokes extra VLDL.

Doc says carbohydrate related  post-prandial high glucose not only induces  more VLDL output  from the liver but that this is part of the mechanism whereby carbs can boost body fat. High carbohydrate intake causes extra lipo-genesis in the liver because a significant  reflex of high post -prandial liver insulin is a signal that upregulates SREBP-1c. Then SREBP-1c expression rises and that in turn activates genes for the lipogenic enzymes (ex: fatty acid synthesase & acetyl CoA carboxylase),

Rogue readings of VLDL may be due to viral hepatitis proteins, flavivirus and pestivirus, which can decrease VLDL formation and secretion while dropping levels of ApoB. Viral proteins "smear" onto lipids and this blocks SREBP-1c action and viral proteins can also "stick" on to the HDL protein fraction ApoA1 inside of the  liver cells' Golgi Apparatus. Thus in chronic liver disease and hepatitis circulating VLDL associated triglycerides eventually decreases so there are more non-VLDL  triglycerides in play.

Hi Dr. Davis,

I was just wondering, due to many healthy cultures including the kitava, okinawan's...etc, who indulge in rather high carb intakes and retain rather pristine health, is it possible that high trigs, low hdl..etc may just be a lipid profile reflecting high carb* intake rather than suggesting atherogenic buildup ?

*when based on safe starchy type carbs

Hi, Paul--
In the population I see, hypothyroidism is exceptionally common, both in people on low-carb but also in people prior to initiating their low-carb efforts. So, without a formal analysis, I'm skeptical that low-carb in and of itself causes free T3 to drop.
There are also numerous inhibitors of the 5'-deiodinase enzyme that converts T4 to T3, including perchlorate residues from fertilizers in vegetables and polyfluorooctanoic acid, the residue of non-stick cookware, just to name a couple.

This is the BIG unanswered question. Sadly, there are next to no data that speaks to this question.
My day to day answer has been to 1) eliminate small LDL, then 2) maintain LDL particle number 1500 nmol/L or less. But that is pure speculation on my part.

Hi, Chris--
Something doesn't compute: Every panel you list is the pattern of excessive carbohydrate consumption and/or sensitivity. So something is sneaking through. There is no question that a "primal" or low-carbohydrate approach works for this pattern.  

You might also have an Apo E2 gene that amplifies carbohydrate sensitivity.

Hi, Might--
As always, you are an incredible fountain of unique insights!

Sorry, Jack, I didn't understand your question. Could you rephrase?

Thanks.  I've only been eating primal/paleo for about five weeks, so only the last panel would reflect this (if thats enough time to be reflected in my lipid panel).  I will re-test after another few months.

Dr Davis. Jeez. This sounds similar to my story (Frustrated's #s). I have eaten Paleo for over a year now, I have done exceedingly well with body composition in that time. See my "Share You Paleo Before and After" here ---> http://paleohacks.com/questions/7058/share-your-paleo-before-and-after/28493#28493. But this only adds to the confusion for me (and others).

For some reason, my labs came back on July 8, 2011 with small dense LDL and pathetic HDL at 40, despite a diet rich in GF beef, pastured eggs, bacon, pasture butter, coconut oil, ghee, veggies, starch and fruits only for carb sources, etc etc. I spend mega money to eat well. We don't mess around. I posted my VAP panel results on PaleoHacks last month and it has resulted in a lot of attention on this very subject. Chris Masterjohn weighed in with his thoughts. Dr Kruse wrote a blog all about it.

http://paleohacks.com/questions/50347/hack-jack-kronks-vap-test-results

I will be retesting again in about a month, as I have made some changes, like eliminating bananas, less heavy cream and pasture butter, etc.

My lab said it's $390 just to do the ApoE test. Is this a normal price? If not, where do you recommend people get the testing done?

I'm genuinely confused. It's like my body is saying... "Yes Jack. Good job. I am very happy with what you are eating. I will continue to keep fat off and pack on muscle." But then my heart is saying "Nooooo. Stop!!"

How can this be?

I was questioning if your pathological interpretation of a blood lipid profile that exhibits low hdl and high triglycerides, could instead just be a reflection of a high carb diet rather than suggesting an increased risk for CVD. I was referencing a couple high carb cultures, such as the Okinawa and the kitava, who exhibit a similar lipid profile but have very small incidence of CVD. Compared to other cultures with similar lipid profiles, such as the Swedes and Americans, who have much higher rates of CVD would suggest it's more about quality of blood lipids rather than their certain partitioning. Hopefully that's a better re-phrasal?

This is the BIG unanswered question. Sadly, there are next to no data that speaks to this question.
My day to day answer has been to 1) eliminate small LDL, then 2) maintain LDL particle number 1500 nmol/L or less. But that is pure speculation on my part.

My understanding related to your above comment is that large LDL is nearly as athrogenic as small LDL and that you want the particle number low with mix between largle and small LDL taking secondary importance.  Of course, that is based on a diet that the avg american consumes,  and not on the low carb with wheat sugar and cornstarch elimination you advocate.
Am i under a correct understanding regarding large LDL being dangerous as well and therefore the need to minimize this even with your dietary recommendations?  Also, i thought you advocated a total LDL particle number to approach 600?  Is your 1500 number a revised viewpoint based on newer diet or clinical observations?
Thank you again.

Server error blocking me again ... testing after hour passed.

ApoE is crucial to VLDL & chylomicron formation. Variant ApoE 2 less efficient at transfering lipids to liver and is binding lipids up an extra +/- 2%; result is that lipids take longer to clear from circulation and more can go wrong. From my notes, here is the rate some ancestral populations have at least 1 copy of ApoE2: 2-4% of Mexican-american & American Indian, also  3-4% of Japanese & West African. There is 0% of South American Indians with ApoE2 and one wonders which variation of  ApoE  might be in Kitava melanesians. .
ApoE4 degrades easiest of all ApoE forms, leaving protein fragments in cell's cytosol which then can affect a mitochondria's lipid binding region impairing the performing of  tasks. In addition ApoE4 fragments diminish gene PPAR gamma expression; and this depresses the desirable bio-genesis of mitochondria. The affects on mitochondria may be why high levels of dietary fat is problematic for ApoE4 individuals; there may be too sparse output of viable mitochondria and mitochondria membranes are involved in how efficiently we burn fat or glucose.  .
In light of these ApoE4 nuances it is interesting to know that fasting raises free fatty acid levels (from fats in the body and not loose fats from recent food); and then those free fatty acids upregulate  gene for PPAR gamma in the liver. Fasting makes one put out ketones  because of the extra PPAR gamma programing and this ketogenesis is also one way that activating more PPAR gamma improves insulin sensitivity. This suggests to me that individuals with ApoE4 may (?) find some benefit from modified fasting; possibly something like decidedly fewer meals in a day and also simply not grazing on snacks (ie: in addition to just trying to select what foods to eat) between meals that are regularly spaced apart (ie: very early breakfast to let meal times spread put more evenly) .

Finally again from my notes, here is the rate some ancestral population have at least 1 copy of ApoE4: .14-19% Germans & Finns, also 7-12%  French & Italians. Of course America is one of the world's melting pots so an individual's propensity for ApoE 4 & ApoE 2 is hard to pin point.

This is fascintaing Might. I have been guilty of snacking too much. All healthy snacks, but still the concept of grabbing bites of delicious foods between meals might be messing with my liver. For my VAP test, I did not fast. Chris Masterjohn believes this was the reason (or at least the reason for dismissal) of my increase in triglycerides in the blood. I am most concerned about my low HDL, because if I raise my HDL, I believe my LDL will become more dominantly pattern A.

Thank you for the reply.  I would like to share a speculation.  Strict low carb means gluconeogenesis means an increased cortisol demand? OK in young fit Paleo men, but what about long-term un(der)treated hypothyroid individuals?

In "Safe Uses of Cortisol", Dr William Mck Jefferies (p. 183/4) observes that low dose (20mg/day) of hydrocortisone taken by a patient with hypothyroidism increases T3,  lowers T4 and improves patient energy levels suggesting such low dose cortisol enhances T4 to T3 conversion.

Could VLC, by putting demands on potentially weakened adrenals, have the opposite effect?

HDL molecules hold triglycerides (there are 45 different variations of triglycerides in circulation, which are based on what their esterified fatty acid component is), cholesterol esters (about 13 - 27% of the HDL surface particles), shingomyelins and glycerophospholipids. HDL's principle proteins are +/- 70% ApoA1 and +/- 20% ApoA2;  yet any changes in the ratio of ApoA2 from genetics (Kitavans?, I propose so) or drugs (ex:fibrates) can have effects.  

Usually people with low levels of  HDL have more trigs on their HDL surface (compared to those with high levels of HDL) and low HDL is associated with the passing of more cholesterol esters to VLDL & chylomicrons. Also, when HDL trig levels go up that makes it easier for the liver enzyme hepatic lipase to cleave off more ApoA1 for the kidneys to clear away; and that further tends to keep HDL levels low.  

In comparison people with high levels of HDL have more cholesterol esters on their HDL; which may be due in part to cholesterol esters affinity for ApoA1 in HDL. And statisticly high levels of HDL are usually associated with bigger ("large") HDL molecule size. Both large HDL and ApoA1 are considered to be more protective factors against atherosclerosis.

I suspect that Kitavan melanesians' low HDL fortuitously correlates with a geneticly higher than normal % of ApoA2; and ApoA2 configures more deeply nestled into the HDL complex than ApoA1. It (ApoA2) influences molecular  interactions all the way to the HDL surface and limits certain lipid dynamics.

ApoA2 holds ApoA1 off of mature HDL molecules and this results in a shunting of ApoA1 into forming up the pre-Beta HDL; these lipid poor ApoA1 configurations are great at doing reverse cholesterol transport that brings back cholesterol  to the liver for excreting as bile acids. Those pre-Beta HDL are small, yet notably excellent at taking cholesterol away from nefarious macrophage foam cells (the large HDL  molecule also picks cholesterol nicely from foam cells).

Experiments see that preceeding type of change with fibrate drug doses, which only minimally raise HDL & ApoA1 yet increase the ApoA2 amount in HDL by over 25%. Since fibrates are agonists activating the peroxisome proliferator activiated receptor PPAR alpha it might be instructive to see if anything in the Kitavan diet is a similar agonist, such as heirloom tuber roots derived from wild yam with high diosgenin content (diosgenin is well known to affect PPAR gamma).

Thanks for the excellent post! Bookmarked! Will come back again…

Hi, Steve--
There really is no final word on what the desired endpoint is when small LDl has been eliminated and you have pure large LDL. In a perfect world, I'd wish for a particle number of 600 nmol/L with pure large LDL. But I'm no longer entirely sure this is necessary. But this remains anecdotal. There are no formal data, nor do I have any formal analysis of our own data on this question.

Hi, Jack--
Don't know, since I've never seen any genuine lipoprotein data on these populations. Most of the data I've seen has been total cholesterol, which is far too crude to draw any conclusions from.

Have you seen lipoprotein data on these populations?

Might. Do you suspect that I have low HDL and highish Trigs/VLDL in the blood for this reason? I do take in a fair amount of protein (including a whey isolate daily). Also, plenty of eggs. Does dietary protein consumption have any actual affect on HDL's principle protein and/or surface cholesterol esters?

Yes Jack Kronk, it seems that you have low HDL and highish Trigs, I do also think.

Just wanted to comment. I've been a long time low carb person, gluten-free too. I also had my thyroid ablated with RAI many years ago. I have found, as have many low carbers, that my reverse T3 is very high and Free T3 is scraping the bottom or below the range.

Unfortunately this does seem to be a common side-effect of low carb eating. It's even documented in studies on the topic.

We had a low carb eater recently watching his LDL climb to very high levels after he began eating low carb. He started taking cytomel and his LDL is coming down very nicely.

Did he get a sudden onset of hypothyroidism that just coincided with low carb eating? I suppose that's possible, but I do think there's something more going on.

I'm taking Armour thyroid myself, but I still have the tendency to turn T4 into reverse T3 and I suppose that means the Free T3 can't get to the receptors. I'm going to experiment with raising my carbs a little higher and sticking to things like yams and squash for my carbs.

Dear dr. Davis,
I just attended the annual cardiology congress of the European Society of Cardiology. Amongst others, the new guidelines on dyslipidemia were presented and I had the opportunity to ask the working group the question you mention above in your first of opportunities : What about measuring lipids during an ongoing substantial weight loss? The were not able to give me a proper answer.
Do you have any scientific references saying that weight loss induce a temporary dyslipidemia or is it based on your experience?
I would be most thankful for your comment on this.
Best regards
Espen Rostrup, MD, PhD-fellow
Bergen, Norway

Dr. Rostrup--

Unfortunately, I know of no published data documenting this effect. However, I have seen it hundreds of times. It is, in fact, quite predictable: drop in HDL, rise in triglycerides, variable small LDL effects, increased blood glucose. It all subsides and improves over time.

It would indeed be an interesting study to chronicle the changes serially in a small number of people.

I am also seeing a heck of a lot of omega-6 intake there.  Also, the healthfulness of monounsaturated fats is a bit overstated.  I've heard of studies where they had 3 groups of people.  One got their normal saturated fat, one group replaced the saturated fat with olive oil and the third group replaced the sat-fat with corn oil.  The corn oil eaters did the worst in health outcomes, but the olive oil group wasn't great either--both groups that replaced the sat-fat did more poorly.  I've heard of other studies where lard was compared with olive oil and the lard-eaters turned out better.  Bottom line, the human body seems to like saturated fat best.  (Lard is not as saturated as butter, but it is more saturated than olive oil.)  If I were in a position to make medical recommendations (I'm not), I'd tell someone like this to ixnay on the plant oils for a while and see what happens.

It should be noted that one of the more dubious selling points of grass-finished meat is that it is lower in saturated fat.  To me, this is not a selling point.  If this person were only getting PUFAs from their grass-finished meat it would be one thing--at least then it'd be closer to a 1:1 omega-6/omega-3 ratio.  But that's not what's going on here.  If they were just eating the fish they might still be OK (depends on the fish--cold-water is better).  But they're adding in walnut oil and chicken consumption and those are going to add more omega-6, even if the chicken's pastured.

I'm curious what this person's inflammation markers are.  If they're off the map the LDL may still be high because the body's trying to repair the inflammation.  That would explain the low HDL too; LDL takes cholesterol out to the body from the liver, and HDL returns it to the liver.  If the cholesterol is *needed* elsewhere in the body then of course it won't be returned to the liver.

Even if inflammation markers are normal, this person's diet may not be meeting their needs for saturated fats in the cell membranes, which may mean they need more cholesterol in their cell membranes to try to make up the deficit.  Not an ideal situation.

Get the PUFA reduced, get the inflammation down if any, see what the lipids do and then we can talk about weird genes.  Absent the necessary DNA profile we really don't know, anyway.

"just eating the fish" = in addition to the pastured beef.  I would not drop beef in favor of fish, there's too much good nutrition a person would be giving up, but fish in addition to beef's not bad.  Chicken used to be a luxury food, you had it on Sundays if then.  Best that it's relegated to that role again.  The white meat is too dry and the dark meat's rife with PUFAs.  Other fowl are not much better.  A foray into the USDA's nutritional database is an eye-opener.

[...] Genetics: Dr. Davis has argued that some combinations of ApoE alleles may make a  person “unable to deal with fats and dietary cholesterol.” [...]

Dr Davis,

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

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

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

Thank you for the valuable information you provide.

:CT

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

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

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

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

4) Normalization of blood pressure, including during exericse.

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

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

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

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

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

Hi, Ross--

Excellent questions.

Several thoughts:

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

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

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

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

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

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

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

Hi, Paul--

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

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

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

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

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

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

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

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

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

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

Harry

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

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

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

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

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

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

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


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


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

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

- Philip

Hi, Philip--

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

Hi, Harry--
Thanks for the help!

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

Thanks!
-Neelesh

Hi, Neeleesh--

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

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

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

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

Dr. Davis,

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

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

1   India has high coronary artery disease incidence.

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

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

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

Thanks!

It is interesting, isn't it?

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

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

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

Hi Doc,

Your explanation makes sense.

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

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

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

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

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

Does all that make sense?

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

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

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

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

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

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

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

Hi Dr Davis,

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

July 2007 Blood work showed

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

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

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

I have not has a blood test for Vit D.

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

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

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


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

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

Dr Davis,

Few more data ....

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

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

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

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

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

Dave-

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

Dr Davis,

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

Dave

Neeleesh and DR. D,

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

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

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

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

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

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

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