My problem with Volek's study is that it's analogous to putting someone on a LC diet and then doing a GTT.

They kept people on a low-fat high-carb diet and put others on a high-fat, low-carb diet and then did a lipid tolerance test.

In both cases, your response to the nutrient (carbs in GTT and fat in lipid test) will be impaired because you stop producing enzymes you don't need.

The people on the low-fat diet didn't tolerate fat as well as people who had been on a high-fat diet when suddenly challenged with a tremendous amount of fat.

What I'd want to know would be the lipid responses *during* the 6 weeks on the two diets.

What his results show me is that eating a high-fat diet makes your body adapt to burning fats. This is what I would expect.

While these results are interesting, I wonder how relevant they are in a real life setting. The fat load that generated these results was 123 grams, which would be like eating 1.3 sticks of butter in a single meal, or like sitting down and drinking nearly 3 cups of heavy whipping cream all at once. Who does that?

Dr. Davis, I know you are encouraging 3 hour postprandial TG checks in the TYP program via CardioChek. Are you seeing these types of postprandial results (viz. results similar to Volek's) following meals with less exaggerated (i.e. normal) fat intake?

Here is prospective study done in Sweden with a follow up period of 12 years that shows a higher consumption of dairy fat like butter and cream is associated with a 45% reduction in risk for heart disease. "Nothing in biology must make sense except in the light of evolution"
http://www.mdpi.com/1660-4601/6/10/2626/pdf

After eating low-carb for over a year, my post-prandial triglycerides never go above 100.

I do agree with Gretchen on the adaptation process.  I shudder to think what an OGTT test would show.  Maybe some day, I'll drop $70 to find out if I can get someone to take me.  I'll be in no shape to drive after consuming that much sugar.

I agree Gretchen. There can be a long adaptation period. Dr. Davis's patients are blessed to have him as their doctor, but I suspect he can't quite kick the lipid hypothesis!

At least for me, I think Dr Ron Rosedale's diet is best.  Low carb, protein at 50 to 70 gms. No grain, mostly no dairy.  He says if you want to lose weight you need to avoid saturated fat because saturated fat keeps you insulin and leptin resistant.   Unless you drink olive oil, the diet winds up being low calorie.
Hmmmm.  Maybe that is the answer.

I have to wonder what the mechanism is for high triglycerides causing heart disease? High triglycerides in a high carb diet usually means high insulin, high glucose vs fat metabolism,and low hdl. Aren't high triglycerides in a low carb diet a slightly different picture?

Right or wrong, I admire your willingness to go against the tide (any tide) for what you see as right.

Absolutely!  What amazes me is, in spite of their adaptation to a high fat low carb metabolism, the patients still saw their OGTT triglyceride results improve over time!  This is my experience too.

There is no doubts, on a high animal fat diet or on a high fat diet of any kind, our tolerance to glucose is indeed reduced.  50g in one does is OK for me (I weigh ~65kg) but 100g in one go as sugar would still be too much and would make me feel sick (but the same amount of carbs in vegetables spread over a day would be ok).

It took a good few years to improve my tolerance.  Right after (2 weeks after) I went on a high animal fat LC nutrition (in 1999) I could not tolerate even a 50g of sugar in one shot! Even one bottle of beer (~20g of carbs) would make me feel stomach sick + give me a headache.   It took me more than 2 years to reach this tolerance to carbs, and I even noticed some steady improvement from year 2 to year 7 into this.

It is indeed totally illogical, although unsurprising given the present standards of medical science, to use big glucose shots to assert patients response under  predominantly ketogenic metabolism.

It is a curious lack of curiosity on behalf of the mainstream medicine that no nutrition research group seem interested in studying the exact effects (all beneficial for me), vitamin and nutrient requirements (very different!) and adaptation issues on the high fat low carb diets.

Stan

The last few posts have generated quite a few comments!!!


Anonymous said...
"The last sentence made me cry."


Alfred E. said...
"This is becoming more confusing by the minute. First, no carbs, only fats and protein. Now, no butter, no dairy, no, carbs, just a few drops of fat and protein. I am going to cry, like the previous poster."


Dana Law said...
"I've learned a lot but need some direct guidance. I find that making daily decisions on what to eat difficult. I want to eat healthy and have some variety. Here's the question. What do you eat? What did you have for breakfast this morning? What did you eat last night? What do you keep in the fridge and on the counter to make following your dictates easier. I don't want to over-think it but all this information is overwhelming."


Helen said...
"Again, with so many cautions of what not to eat, I'd love to see a Dr. Davis-approved diet plan. If I were just following all the Don'ts, I'd go crazy (and hungry)."


The bottom line is that Jimmy Moore, William Davis, Matt Stone, Kurt Harris, Stephan Guyenet, Don Matesz, Art Ayers, Billy E., B.G., T., Mark Sisson, Richard Nikoley, Michael Eades, Matt Metzger, Peter, Arthur De Vany, Chris, Ryan Koch, Chris Masterjohn, Jenny Ruhl, Richard Bernstein, Fred Hahn, Jonny Bowden, Larry McCleary, Mary Vernon, Dave Dixon, Mike O'Donnell, Scott Kustes, Gary Taubes, Rob Wolf, Seth Roberts, Loren Cordain, Sally Fallon, Mary Egin, Keith Thomas, Tom Naughton, PaleoDoc, Nora Gedgaudes, Barry Groves, John Briffa, Laura Dobson, Dana Carpender, Keith Norris, Rusty Moore, Doug McGuff, Martin Berkhan, Bryce Lane, Erwen Le Corre, Dan, Drew Baye, Uffe Ravnskov, Eric Westman, Lierre Keith, Brian Peskin, Steve Parker, Jeff Volek, Stephen Phinney, Diana Schwarzbien, Barry Sears, Nina Planck, Lyle McDonald, T.S. Wiley, James Carlson, Steven Gundry, Keith Berkowitz, Richard Feinmann, Jan Kwasniewski, Konstantin Monastyrsky, etc., etc., etc. cannot come to a cohesive way of eating that is workable for everyone. My guess is there are not two of these people whose diet is identical!!

Is it any wonder we are confused? Many folks are looking to emulate the diets of others - a method that will never provide personal optimal health.

Take the time to watch/listen to the following lecture by Dr. Bruce German from UC Davis. It will help to explain why we have this conundrum.

http://www.researchchannel.org/prog/displayevent.aspx?rID=29854&fID=567

Then read the writings of a Venetian gentleman who lived to be almost 100 yars of age (Born 1467 - Died 1566).

http://www.soilandhealth.org/02/0201hyglibcat/020105cornaro.html


Both of these together put nutrition and health in perspective for me.

Tom

Dr. Davis, please comment on the study released today by the Harvard medical School.  How does one avoid saturated fats and still get proteins if he is a low carber??   http://news.bbc.co.uk/2/hi/health/8580899.stm  Thanks!

Hi, David--

Studies are meant to make observations. That is the reason for the unnatural intake of fats.

People on the Track Your Plaque Diet approach rarely show such high levels because they've reduced or eliminated the foods that form the basis for high postprandial responses (wheat, cornstarch, and sugars) and do not indulge in high fat intakes that cause near-term surges of postprandial particles.

Hi, Gretchen--

I agree, but I believe that the observations are still relevant. It shows us that postprandial responses are sensitive to carbohydrate intake over time. It also shows us that average people have substantial surges postprandially with fat challenges on an average American diet.

While I advocate carbodrate restriction and weighing diet more heavily in fats and oils, you can see that the emerging conversation is that unlimited quantities of oils, low-carb or no, have the potential to generate extravagant postprandial responses.

I tested my postprandial triglycerides after having been on a LC diet for about 11 years and wheat-free even longer (because I discovered that it was wheat that was giving me acid reflux). With about 50 g of fat, the TGs went very high, over 400.

Someone else said his rarely went over 100 after only a year on a LC diet.

The author of "Life Without Bread" presented a graph showing that younger people reduced cholesterol on a LC diet but older people didn't.

We may all react slightly differently to different diets (as well as interpreting them differently, as someone else has pointed out; you can be on a LC diet that includes mostly LC junk food or a LC diet that includes a lot of greens and lean meat).

I have type 2 diabetes, and some people think that metabolic syndrome/type 2 diabetes is basically a disease of disturbed lipid metabolism.

So what worries me is that people with insulin resistance, who may not respond the same way as people without IR, are taking LC advice to eat a lot of fat that is based on the experiences of people without IR.

Here's an article that addresses this issue:

http://www.lipidworld.com/content/4/1/21

This is why some time ago I felt the "GO Diet" by Jack Goldberg and Karen O'Mara, which is LC but emphasizes monounsaturated fat, yogurt, and fiber, was the best solution and helped them rewrite it as "The Four Corners Diet."

Apparently very few people agreed with me, and the book bombed.

I still think LC with restrained fat intake, meaning restrained calorie intake, and real foods along with reasonable exercise is the best solution on the basis of today's evidence.

@Tom (anonymous)

Although there are many voices and styles of presentation, I can state, through frequent communication with them, that my approach at PaNu is a tent that fully covers the diets of Eades, Dr. Stephan, Peter at Hyperlipid, Sisson, Nikoley, and although I do not correspond with them, Bernstein and Groves. There is also significant overlap with the Weston A Price Foundation and even Matt Stone.

If you look for a common element in all of our approaches, and indeed the crux move in choosing a healthy alternative to the SAD, it is actually nothing to do with paleo so much as the simple and total rejection of Ancel Keys and the multiple versions of the lipid hypothesis he spawned 50 years ago.

This then allows the realization that humans are evolved to eat substantial calories from animal products, including animal fats, and further including (on purpose, and without limitation or fear) SATURATED FAT.

All versions of the lpid hypothesis have in common the belief that somehow, somewhere, there is a molecule that is fat, tastes like fat, is  kind of like fat, is associated with fat, or reminds us of fat, and that molecule is perversely designed to give us atherosclerosis and coronary heart disease.

Start to view all these dietary approaches through the filter of whether they reject the lipid hypothesis instead of "low carb" or "paleo" and the dividing line will start to look much much brighter.

So for someone that works out a lot and is suppost to gte something in the 3000-4000 calories per day... what would be the addecuate kind of food to use as high calories source?
I was taking unlimited almonds, but this post makes that look like way too much fats.

@ Dr. Harris,

You obviously did not read/listen to the two links that I provided in my comment.  I happen to believe every word you wrote in your response.   My contention is that personal optimal health and longevity is beyond the simplicity of following 12 simple steps (though I do think they are a huge step in the right direction).  Health is determined at the molecular level based upon an individuals genetics as affected by many factors, particularly, stress. Please Google nutrigenomics, epigenetics and metabolomics.

My apologies to Dr. Davis.

(I may have inadvertantly sent a another version of this comment previously.)

Tom

Isn't this just normal for a well adjusted human? I mean TGs are how fuel (free fatty acids) is transported through the blood from its sources (liver and fat cells) to the places where it is needed i.e. everywhere else.

@ Pythonic Avocado

Yup, eating fat raises TG levels temporarily.  I consume a high-fat diet with lots of nuts, and, based on results from a TG meter, do not see extraordinarily high TG levels (starting from a fasting level near 70).  I also spread meals out during the day, thereby reducing both BG and TG spikes.

The only time I saw a high TG spike was after consuming 2 raw egg yolks!  This influenced how I approach eggs (always cooked, one at a time, mixed with other foods).

btw, if you consume too much fat in one meal, a lot of the fat will end up in your stools, since there is a limit to the lipase that your pancreas can generate on short notice.  Another complication when trying to compare diets.

In other words, low-carb improves postprandial responses substantially--but postprandial phenomena still occur. Postprandial triglycerides of 88 mg/dl or greater are associated with greater heart attack risk because they signify the presence of greater quantities of atherogenic (plaque-causing) postprandial lipoproteins.

I'm finishing a jar of "dry" (not oil suspended) Vitamin D3 capsules and taking them with enteric coated fish oil. Might the enteric coating prevent the fish oil from helping the "dry" D3 absorption?

Really interesting post. I think I'm sensitive to wheat, but can't seem to stop eating it right now. Once I gave it up for about two months and lost 20 pounds. I should probably try to eliminate it again. Thanks for the insight.

Interesting.  I have just the opposite experience though.  My very rare (maybe once every 6 months or so) consumption of wheat causes no obvious symptoms whatsoever though I have in the past had severe sinus allergy response to wheat/gluten

When I first went gluten-free, I was not as careful as I am now and had several incidences of acute joint pain (with incredible heat) upon exposure to minute amounts of gluten.  The last time I knowingly ate gluten (crumbs from a crouton on a salad) I woke up the next day with the most intense back pain I have ever had.  My usual response to gluten is in the form of migraines. This pain was definitely not muscle pain but neurological with squeezing pains from my spine to the front.  That was the last time I had any gluten - I am extremely careful now and I have been GF 3 years and feel so much better.   I think gluten is a poison, plain and simple, and everyone would be better off not consuming it in any way.

I'm one of the lucky ones.  I caved during the silly season and stole a couple of my sisters' delicious homemade double chocolate cookies.  Alas, no mad dashes to the procelean apparatus.

Wheat breeding sounds to be at fault for the way it's protein folds into an antigen trigger for a lot of people. Granny gave me jam with bread, pie and sugar cookies which didn't provoke malaise, but that was older breed of wheat.  

Now-a-days professional diet advice is to avoid sugar, substitue sweetener. So, many don't get that sugar binding to  the gluten protein fragments. For people with metabolic syndrome adding back in sugar doesn't make sense; they can't use it to "goop-up" the gluten. Cutting out the wheat for them solves the dilema.

Gluten are metabolized into opioids. Both the digestive system and the immune system have lots of neurons AFAIK. Is a nice system to protect the brain, I would guess. Evolution and natures way to say: Don't eat that, it'll mess you up.

Why diarrhea with wheat rechallenge etc.?
Perhaps because your bacterial intestinal flora has changed since wheat/grain elimination.

I have suffered from gastroparesis for 20+ years. Some medication has helped, but nothing has worked better than a carb/wheat free diet. If I avoid them my digestion seems fine. One cookie and within a few hours the rumbling and belching begins . . .

There's this Ethiopian restaurant here in LA. They serve a flat bread called Injera.

I must have it once or twice a year, I tell you, I must! Even though it causes sores in my mouth by the next morning. It never did that when I was eating wheat regularly. Now that I've given up wheat, BAM! Sores!

Otherwise, I'm a sore-free, wheat-free good boy the rest of the year.

Dr. Davis,

Great post.  I believe I have experienced exactly what you described.  I gave up drinking beer (my only grain) last summer and recent grain encounters led to stomach pain and quick trips to the bathroom.  One time I felt really sick for hours.

There are never a shortage of reasons to avoid grains.

@ Anonymous,
I did some work in Ethiopia in 1970 & ate a lot of Injera;
fermented Teff grain with a soaking phase. This increases the % of Arginine amino acids in Injera. People with cold sores are often agravated by arginine foods. Your sensitive mouth tissue is probably reacting to the high level of arginine. (Your individual sensitivity would likely extend to Indian Idli, soaked/fermented rice with dhall bean puff; it's bio-converted a lot of arginine too.)

For those of us that are cutting way back on wheat in our diets, but not eliminating it - what are our best options?  I'm finding heirloom wheat flour available on the internet.  And here's an interesting article I found on Heirloom wheats:
'Are Heirloom Wheat Varieties the Next Big Baking Trend?"
http://www.seriouseats.com/2010/01/is-heirloom-wheat-the-next-big-baking-trend-jim-lahey.html

And what about Kamut?  Any comments?  Here's a write-up on it - it has some very nice features.
http://www.suite101.com/content/kamut-ancient-grain-in-modern-times-a89648

I try to avoid wheat all the time.

However, I found one bread here, that is made without Flour but uses wheat sprouts instead. The recipe is made by Russian academic scientist.
You have some English language info at

http://www.zernohleb.ru/health_eng.html

What do you think about it ?

Thx

My digestion was always lousy (but I didn't know it) until I cut out wheat.

Now if I reintroduce the reaction varies depending on the form of poison. Pasta is worst, sending the gi tract into the red zone for a week, plus migraines and sinus.

other forms (cookies, pizza) the reaction is less volcanic, but still noticeable. The baseline reaction is the sensation that the lining of my stomach has been scrubbed with a brillo pad, and sometimes joint and back pain, with a touch of sinus fun.

All this I used to think of as"normal".

Anyone have any success with enzyme products (like "Gluten Ease“) to help deal with occasional exposure?

"The majority of people who experience a wheat re-exposure syndrome will have diarrhea and cramps..."

This seems to say that of those who DO have symptoms ("experience a ... syndrome"), a majority will have diarrhea and cramps and a minority will have other symptoms.  But what proportion experience any symptoms?  Like Geoffrey above, I don't.

Wow... that just happened to me.  But only after being wheat free for like a week.  I was experimenting with a gluten free paleo diet but went out with some friends to the mall to see a movie.  I drank one beer ate 4 slices of pizza and a big cookie.  I ended up screaming at a friend over a stupid comment, nothing serious, but I felt SO angry .  Something that is not usual for me.  Then that night I woke up in the middle of the night with stomach pain and diarrhea.  
This was after just 1 week with no wheat.

I forgot to add that I had bad headaches just 30 minutes or so after eating the pizza slices too..

Don't you think this could also have something to do with the 1 in 133 statistic for celiac disease? Alot more are gluten intolerant and on down the spectrum to gluten sensitive.  

That adds up to a whole lot of people out there who are on the continuum of mere sensitivity --->celiac

That's me in a nutshell. Re-exposed to wheat and it was two days of unspeakable nastiness... I lapsed into this silliness as an experiment with the 4HB which necessitates a weekly wild day. It was wild alright...

Great post. I would love it if someone could explain the mechanism by which this re-exposure horror happens.

Since cutting out gluten, even tiny exposures have sent my stomach into paroxysms of pain. This is accompanied by nausea and an all over sick feeling, like I have been poisoned.

My bloods tested negative for coeliac though so I don't understand why I have such a bad reaction.

I am one of those people prone to headaches, migraine and colds. Usually, my first recourse is White Flower Embrocation (embrocation.50webs.com), also called White Flower Oil

Hi Dr. Davis,

This post touches on a point I've been wondering about.

You write that a drop in CT heart scan score signifies a "huge reduction in risk for plaque rupture, or heart attack."

As I understand it, strictly speaking, the score indicates a reduction in the volume of calcium/plaque in the arteries.

In your books and articles you provide references to the studies which document the statistical correlation between FIXED scores and rupture/heart attack.

My question is this (and you may have answered this question already elsewhere):  Have there been studies that document a statistically significant relationship between a reduction in plaque volume (as opposed to a fixed value) and risk of a CAD event?

A follow up question:  Is the actual reason for the risk reduction due to score reduction actually known?  I can imagine that one reason might be that because the arteries have plaque reduced, they are actually larger in terms of blood flow supported than they were before the plaque was reduced.

My belief, however, is that there could be additional reasons for a reduced plaque over time = less risk correlation.

Thoughts about this?

Thanks.

Great questions.

We do know that, if plaque is permitted to grow (by several measures including angiographic studies, carotid ultrasound, as well as heart scan scores), the likelihood of events escalates along with it. This is known with absolute confidence.  

We also know that reductions in plaque burden are also correlated with reductions in risk, also by just about any measure, though the magnitude of reduction varies, since each approach provides a different persective on plaque composition, all differ on incorporation of the Glagov phenomenon ("remodeling"). More data on event reductions are needed, however. But until recently, genuine bona fide reversal had been elusive.

Lastly, actual examination of tissue that has regressed is very limited. As you can imagine, if someone asked you, having regressed, to allow a sample of artery tissue to be removed, you'd likely not be interested. Thus, the observations are indirect and come from animal studies and observations like intracoronary ultrasound.

Actually, reductions in heart scan scores are a surrogate for inactivation of plaque, removal of inflammatory cells, removal of fat-laden tissue, etc. The reduction  in calcium is a parallel phenomenon that we can see. I also wonder, given the wonderful effects of vit D and possibly K2, whether the reduction in calcium provides benefits of its own, independent of the inactivating effects.

While everyone agrees that reduction of atherosclerotic plaque is a good thing, there are several clinical studies that suggest that reduction of calcium in the plaque may not be good. For example, this study found that culprit stenoses in arteries of patients with stable angina had more calcium than those of patients with unstable angina, which had more calcium than those with acute myocardial infarction. This suggests that plaque accumulation in a specific location may actually be beneficial if it stabilizes the plaque and makes it less likely to rupture.

There is not much data on calcium score reduction because it is so rarely seen. What is needed are long-term studies showing that calcium score reduction does reduce the number of adverse coronary events.

I disagree.

There is a commonly offered argument that calcium stabilizes plaque. I think this is nonsense. There are studies by Renu Virmani and others that demonstrate that the shear and tension forces at the edges of calcified plaque are, in fact, areas of greater stress and thereby risk for plaque rupture.

While intracoronary ultrasound will sometimes show that a small segment of a recently ruptured plaque will involve a non-calcified segment, we are NOT using calcium in a lesion-specific fashion. We use it as an index of total plaque.

I also believe that emerging concepts, such as the influence of vitamin D3 on gamma-carboxyglutamic acid Gla protein in vascular tissue are pointing towards the fact that vascular calcification is part of a regulated, active process that influences plaque activity and rupture potential. (See Johnson et al, Vascular calcification: pathobiological mechanisms and clinical implications. Circulation Research 2006 Nov 2006;99(10):1044-59.)

Increasing calcium scores have been conclusively associated with dramatic increases in coronary events. Likewise, emerging data, including our own, show reducing calcium scores is associated with virtual elimination of events.

Do you have something better?

No, I don't have anything better - I don't argue that an increasing calcium score is good, only that we have nothing more than anecdotal evidence to show that calcium score reduction is beneficial. And, there are other experts in the field that do not agree that it is. The recent torcetrapib clinical trial shows that not all ways of increasing a generally beneficial lipid such as HDL are theraputic. Have you considered documenting the results of your practice, i.e., what percent of your patients show calcium score change in each of several percentage ranges including reductions, and what their follow-up results are in terms of hard cardiac events? That might stimulate interest in a controlled clinical trial to verify your results.

What experts "agree" that a reduction in calcium score is not beneficial? Can you specify who? I know the literature on calcium scoring quite well, and I don't ever recall such a study.

Dr. Davis,

The wizard, hmmm, I mean, Dr. Oz says on Oprah that "we'd rather focus on the plaque itself—because the calcium actually might help stabilize the plaque and reduce the chance of it rupturing."

http://www2.oprah.com/health/yourbody/youdocs/youdocs_faqs_io_10.jhtml

So, there's the proof you asked for.  It was on the Oprah show.

And by the way, Oprah's doc says that Ornish has the answer here:

http://www2.oprah.com/health/yourbody/youdocs/youdocs_faqs_io_11.jhtml

Seriously, this question of the Calcium Score relationship to risk reduction is a key issue and I appreciate your sharing your knowledge about the question.

It will be interesting to see if Anonymous gets back to you with expert reference list you've asked for.

I don’t think there is a study that shows that because calcium reduction is so infrequently seen. I have discussed it with the Director of Preventive Cardiology at a State University Hospital who is of the opinion that calcium reduction may not be beneficial. I suspect that most experts would say that there isn’t enough data to conclude that reduction of calcium is either beneficial or detrimental because most have never seen it.

My point is that several studies show that plaque rupture tends to happen in arteries that have “spotty,” but not extensive calcium, and that coalescence of small calcium deposits into larger deposits reduces the surface area in contact with softer plaque, thereby reducing the extent of the stress risers that can lead to plaque rupture. Quoting from some of these

“…double helical computerized tomography demonstrates that extensive calcium characterizes the coronary arteries of patients with chronic stable angina, whereas a first AMI [acute myocardial infarction] most often occurs in mildly calcified or noncalcified culprit arteries.” Shemesh et. al., American Journal of Cardiology, 1998 Feb 1;81(3):271-5, Comparison of coronary calcium in stable angina pectoris and in first acute myocardial infarction utilizing double helical computerized tomography.

“Acute coronary syndromes are associated with a relative lack of calcium in the culprit stenoses compared with stenoses of patients with stable angina.” Joshua A. Beckman et. al., Arteriosclerosis, Thrombosis, and Vascular Biology. 2001;21:1618, Relationship of Clinical Presentation and Calcification of Culprit Coronary Artery Stenoses.

“The relationship between calcification and clinical events likely relates to mechanical instability introduced by calcified plaque at its interface with softer, noncalcified plaque. In general, as calcification proceeds, interface surface area increases initially, but eventually decreases as plaques coalesce. This phenomenon may account for reports of less calcification in unstable plaque.” Moeen Abedin et. al.,  Arteriosclerosis, Thrombosis, and Vascular Biology. 2004;24:1161, Vascular Calcification - Mechanisms and Clinical Ramifications.  

“In AMI patients, the typical pattern was spotty calcification, associated with a fibrofatty plaque and positive remodeling. In ACS [acute coronary syndrome] patients showing negative remodeling, no calcification was the most frequent observation. Conversely, SAP [stable angina pectoris] patients had the highest frequency of extensive calcification…To the best of our knowledge, the present IVUS study is the first to demonstrate the relationship between calcification patterns, arterial remodeling, and the morphology of plaques within the culprit lesion segment. The major finding is that there is a significant difference in the pattern of coronary calcifications at the culprit lesion segment, particularly with respect to size, number, and length of the deposits, among patients with AMI, UAP [unstable angina pectoris], and SAP. Small calcium deposits were significantly more frequent in the culprit lesion segments in ACS than in SAP patients.” Shoichi Ehara, et. al., Circulation. 2004;110:3424-3429, Spotty Calcification Typifies the Culprit Plaque in Patients With Acute Myocardial Infarction.

Also, there is an MRI study of  the carotid arteries of CAD patients who had been given niacin, lovastatin, and colestipol for 10 years. In comparison with matched, untreated patients, the carotid plaque of the treated patients showed much less lipid but much more calcium than the untreated patients. Xue-Qiao Zhao, Arteriosclerosis, Thrombosis, and Vascular Biology. 2001;21:1623, Effects of Prolonged Intensive Lipid-Lowering Therapy on the Characteristics of Carotid Atherosclerotic Plaques In Vivo by MRI.

It seems that reduction of the “spotty” calcium may reduce the likelihood of plaque rupture, but reduction of coalesced calcium such as is seen in stable angina patients may  increase the surface area of calcium (if the coalesced calcium reverts to spotty deposits) and therefore be detrimental. From the standpoint of evidence-based medicine, the only way to be sure of the effects of calcium reduction is to conduct a clinical trial of patients undergoing such reduction.

In the meantime, Dr. Davis, since you are one of the few cardiologists whose patients are experiencing calcium score reduction, it would be of great benefit if you would document the results of your practice in a quantitative way.

I believe that you are confusing two phenomena.  

Tissue characterization of specific plaque locations that are prone to rupture (or have ruptured) examined by techniques such as intracoronary ultrasound, is distinct from the concept of using coronary calcium scoring as a surrogate measure of total plaque volume.

I believe that lipid-laden, calcium-poor plaques do tend to identify sites more prone to rupture. I have witnessed this myself in many intracoronary ultrasound procedures personally performed.

This is different from using calcium as an index of plaque. While we are uncertain of the relationship of calcium to total plaque in people who have experienced calcium score reduction, all circumstantial evidence points towards dramatic regression of lipid laden plaque, regression of inflammatory cell composition, replacement by fibrous tissue matrix, reduction of oxidative capacity, reduction of  matrix metalloproteinase content, in other words, all the factors that trigger plaque rupture.  

Though just my suspicion, I believe that the initial relative composition of calcium to plaque of 20% is likely increased, meaning calcium occupies more of total plaque volume. In other words, my suspicion is that, if calcium regresses, total plaque volume has regressed even MORE.

We plan to publish our data this spring. We had planned to publish our experience much sooner, but the addition of vitamin D to the program has boosted success so much that we decided to start over again around 2 years ago.

hm... bookmarked style )

so great, your arteries are cleared up but you'll get cancer and die from all of those ct scans.
lovely.