Great post, and painfully true for me; my father had to undergo his 2nd coronary bypass operation this past April 2007, and despite the strangely 'status-quo' or 'business as usual' attitude of both the surgeons and assisting doctors and nurses involved in my dad's procedure (yes, the whole thing seemed like such a regular day at the beach to them because Holy Cross in Fort Lauderdale performs so many of these operations on a daily basis, with success, of course) did nothing really to quell my family's fears of the severity of this operation; this is still a monstrous operation that not only takes a heavy toll on the patient, but on the family sitting in that waiting room as well.
I still cry at the memory of having to tell my dad, "hey Pop, you need another CABG" after an invasive angiogram revealed disaster after disaster in his arteries.
And this is why your message is so important, and why it needs to get out every day, and loudly.

I'm rooting for you. And I'm thankful you're here.

A few thoughts about this post:
The first is a question. What do you think about ultrasound screenings for carotid artery plaque, abdominal aortic aneurysm, and peripheral arterial disease? A company called Life Line offers these, saying that they show evidence of plaque build-up in the arteries. Are they useful in conjunction with a heart scan, or can they indicate risk similar to a heart scan? It sounds like they are intended to be early detectors of stroke risk. Are they worth the investment?

The second comment is an observation. Those of us not in the medical field tend to assume that anyone who is knows what he or she is talking about on the subject of the human body and illness. However it is apparent that those with M.D.'s can come to very different conclusions about what causes us to get sick and what we should do to prevent illness. Dr. Dean Ornish is an M.D. You are an M.D. Dr. Atkins was an M.D. Yet the dietary advice differs noticeably, so how do we know who is right and who to listen to? I've learned not to believe something just because a doctor says so, because when I followed the low-fat high-carb advice I got fat and felt horrible, but now that I am following a low-carb plan with plenty of protein and fat, I've lost 25 lbs. and feel great. My bloodwork also supports your claims: low triglycerides, high HDL, and low fasting blood sugar. It's kind of sad in a way that I actually get better medical advice from doctors whose blogs I read on the internet (I'm also a Dr. Eades fan) than from my personal physician. And finally, a thank-you: since reading your advice about Vitamin D, my flower garden is in the best shape it's been in in years, since I have a new knowledge about why it's so important spend some time in the sun and a new motivation, therefore, to be outside pulling the weeds.

And concerning your recent post  about breakfast cereals,congratulations are in order: I've broken my husband's cereal for breakfast habit. (I broke my own years ago.)

I have had good results with the Lifeline service, but only when used in conjunction with a heart scan. It cannot replace a heart scan. This is because, while atherosclerosis is a body-wide process, this disease does not perfectly track in parallel in all arteries of the body. You can, for instance, have lots of plaque in the carotid arteries while having only a modest amount of plaque in the coronary arteries, and vice versa.

I agree with your second comment. In fact, I have posted on this Blog about this.

We are all swimming in a sea of information and mis-information, and blind alleys along the way to the truth. We can only educate ourselves as best as possible and then come to our own judgements about the value of this or that argument.

I have a comment too: I think one reason there is so much confusion is because dietery connection with heart disease hasn't been sufficiently studied. We only saw some partial studies by Drs Ornish, Agatston, Atkins, Hayes but not much independent verification, AFAIK. For example there are some studies done by now on the effects of a high fat low carb nutrition in diabetes and epilepsy but virtually nothing that I know of for cardiac patients.  The only one such study I heard of was halted half way through (after showing very promising results) when the funding was cancelled, 27 years ago.
Stan (Heretic)

A somewhat updated comparison of old care versus new care: I was on American Airlines this week, and looked through their magazine. There was a full page ad from the Cooper Clinic in Texas; a 46 year old woman pictured said "I had no idea I had heart disease, but had a family history...an EBT scan and four stents later, with some lifestyle changes, I'm a new woman".

I understand you can't generalize from one case, and while this seems to represent cutting edge treatment, it also gives me the creeps thinking about the obvious drive for revenue here. Couldn't they have tried your approach for awhile before invading? Thanks.

I think that they tell the stories that have a "WOW!" factor. The Cooper Clinic does indeed engage in a low-level grade of preventive care (AKA Lipitor, etc.)

But I really hate those stories, too.

Saw a lady at shul today, she is convinced of Dr. Esselstein's more carbs- is- better method. Ornish, Esselstein.....hard to refute the drumbeat of eat carbs, cut meat and fat.

Very interesting.

The article also contains this potential nugget:

Dr. Daniel S. Berman M.D., chief of Cardiac Imaging and Nuclear Cardiology at Cedars-Sinai reports that the danger in not testing for non-calcified blockages is great. These plaques, he says, are “more prone to rupture than calcified plaques. The new procedure, which does test for these, provides “better risk assessment.”

Any thought about these "non-calcified blockages"?  This is somewhat related to a question I asked a while back about "reducing plaque as measured by calcium score" and reducing risk by reducing risk of rupture in the artery.  You had a good answer to the question but it seems like there is more to explore here.

Thanks for the info.

Here is a similar study using ct to diagnose degree of stenosis:

Dual-source CT non-invasively detects coronary stenoses

15 October 2007

MedWire News: Dual-source multi-slice computed tomography (DSCT) angiography can accurately detect coronary stenoses in patients with an intermediate likelihood of coronary artery disease (CAD), even in the presence of arrhythmias and raised heart rates (HRs), researchers say.

Alexander Leber (University of Munich, Germany) and team explain in the European Heart Journal that using multi-slice CT to detect coronary stenoses can be limited by the appearance of motion artefacts.

The researchers tested the newly-developed DSCT technique in 90 patients with an intermediate pretest likelihood of CAD referred for invasive coronary angiography. They obtained data sets providing image quality sufficient for analysis in 88 patients.

The image quality was diagnostic in six of seven patients with atrial fibrillation, and in 46 out of 48 patients with HR >65 beats per minute (bpm).

In 1165 of 1174 segments, significant (>50% stenosis) disease was correctly ruled out using DSCT.

All patients (n=9) with at least one stenosis >75% (sensitivity 100%) and 11 of 12 (sensitivity 88%) patients with at least one stenosis ranging from 50-75% were correctly identified by DSCT.

Meanwhile DSCT-angiography correctly excluded a lesion >50% in 60 of 67 patients (specificity 90%, positive predictive value 74%).

The accuracy to detect coronary stenoses >50% was similar in patients with HR >65 bpm and those with HR =65 bpm (sensitivity 92 and 100%, specificity 88 and 91%, respectively).

The researchers conclude: "DSCT is a non-invasive tool that allows to accurately rule out coronary stenoses in patients with an intermediate pretet likelihood for CAD, independent of the HR."

Eur Heart J 2007; 28: 2354-2360

I thought I'd take another shot at stating the question I have about the relationship of a declining calcium score and plaque rupture risk.

If the calcium within plaque is reduced at greater rate than the plaque it had calcified, hence leaving that plaque non-calcified, then, does that recently non-calcified plaque qualify as being a type of plaque that, as Berman puts it, is "more prone to rupture than calcified plaques"?

There are a lot of different ways to state the question I guess.  Here's another try.

Does the process of calcium/plaque reduction per se result a type of instability that is "more prone to rupture"?

Perhaps it does not.  But if it does, then, it seems as if it would be important to understand how to increase stability per se.

In that case, aren't BOTH plaque reduction and plaque stability important?

How is plaque stability promoted?

Hope all this make sense.

Thanks.

Great questions. Not all answers are available.

However, there are several things we do know, mostly from intracoronary ultrasound studies, autopsy studies, and extrapolations from animal studies. (Real, live human data is not generally available, since few people would allow us to remove plaque.)

We know that:

--The lipid components of atherosclerotic plaque are fairly readily regressible, e.g., LDL cholesterol reduction. Lipid resorption precedes calcium extraction.

--Plaque instability is determined less than calcium presence or absence than by the presence of high-rupture risk markers, like collections of lipid near the surface, so called "lipid pools" and think fibrous "caps" at the surface-to-lumen interface, as well as inflammatory cell collections and enzymatic activity, e.g., matrix metalloproteinase.

--Calcium is probably the least resorbable factor in plaque. If you resorb calcium by x percent, you've probably resorbed the lipid and inflammatory elements hugely. However, given the rarity of profound regression in studies, these observations are scant.

--The trend towards substantial reductions in cardiovascular events in people who have not progressed heart scan score (or other measures of coronary atherosclerotic burden) vs. those who progress confirm that progressively increasing scores are accompanied by increasing risk of events, "plaque rupture."

--There are not enough data on event rates in people who drop their score substantially because: 1) Nobody except our program has achieved this, and 2) Events in people who reduce their score are, for all practical purpose, non-existent. We are collecting our data for publication in the coming year, as well as assembling the pieces for subsequent studies for full validation of these concepts.

Dr. Davis,

Thanks for an answer right on point.

You continue to amaze with your knowledge that speaks to an issue and makes common sense while at the same time you acknowledge that sometimes "we just don't know".

I know I've already said thanks for the answer but I thought I'd make one last point here.

There is a clear distinction between plaque reduction and plaque rupture risk reduction.

I think your last comment contained solid evidence, to the extent we now have it, that plaque reduction doesn't increase plaque rupture risk but in fact decreases it.

This has settled my mind on the issue (until there is more evidence to evaluate).

I understand that this is a needling kind of point but it seems to me an important one and I think the answer you gave is a great start on a new TYP Program Special Report.

You probably have a long list of these kinds of reports to write.  I'd recommend adding this topic to that queue.

Thanks again for everything you do.

Eventually, I'd like to see a two armed study comparing the Track Your Plaque appraoch to a control group using statins and an American Heart Association diet. My prediction is that there will be no comparison. However, I doubt a drug company would sponsor such a study that likely would cost several million dollars, given the large numbers of people required for conclusive outcome (i.e., cardiovascular events) data.

A more practical approach would be to do side-by-side serial heart scans with intracoronary ultrasound. I think this may be more achievable in the foreseeable future, but will require a great deal of planning. Believe it or not, I tried such a study nearly 12 years ago but encountered tremendous resistance, since such a study needs to be performed in a hospital setting.

Another thought: With the tremendous experience we are developing on line, this could be construed as a "virtual clinical trial" that allows us to quantify events among a growing number of people. Not as "clean" but still persuasive.

A pdf file with a more detailed description of how they do the mini-dose CCTA is at the cedars-sinai website here.

They reduce the radiation dose by using x-rays produced during only 1/10th of the cardiac cycle.

Thanks for the lead.

I looked at the press release but it leaves me puzzled. Many scan centers "gate" to the EKG. I'm not sure what they are doing differently. I'll do some digging.

No smart drug company will do a drug trial versus the TYP plan. (if they're smart!!) In the PROVE-IT trial, Bristol Myers conclusively demonstrated that their drug (pravastatin) sucked...  maybe you can use your favorite colleague's patients for the control-arm? *wink wink*

You definitely need to publish a 'metabolic' arm, including any T2DM patients. I think by distinguishing the difference, you may demonstrate even more accelerated plaque regression compared with non-metabolic.  Perhaps most pts are 'metabolic?'.  

remember if you have Asians or Indo-Asian patients, the BMI >= 27.5 is considered 'obese' and waist circumference > 35.5 inches for men is 'metabolic'...  hope that helps!

I agree.

Our first release of the data this coming spring will lump together people with metabolic syndrome and diabetes along with everybody else. As the experience grows, I believe that a subset analysis will be possible.

"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.

"hunger-gatherers"?

The original article said hunter-gatherers.

However, I like hunger-gatherers better.

Hunger is certainly quite a motivator to go seek food.

I don't know why they blamed the meat either as Ancient Egyptians  wouldn't have been eating indoor raised grain fed high omega 6 low omega 3 meats.  

It seems Beer, together with bread, oil and vegetables, was an important part of the wages workers received from their employers. The standard daily ration during pharaonic times was two jars containing somewhat more than two litres each.

When you have eaten three loaves of bread and swallowed two jugs of beer, and the body has not yet had enough, fight against it. But if another is satiated, do not stand, take care not to approach the table.

As a person who can't figure it out, the mummy scans are interesting.

It's not clear to me if saturated fat or grains and sugar are largely to blame for heart disease, or something else.

It made an impression on me that Jimmy Moore (low carb blogger who eats mostly meat) and Dean Ornish (who eats mostly grains and vegetables) both scored zero on their heartscans.  They both avoid flour and sugar, that might be a point of agreement and a possible explanation.  I wish I was privy to the nutritional studies that come out a hundred years from now: long-term studies of different diets.

On what ground are they basing their assumption that meat is the culprit?

It is just blatant and annoying!

Dr. Davis, I love the way your mind works.  Which only proves once again, that the advent of agriculture produced diseases of the metabolic syndrome, even in ancient Egypt.  Wheat, Beer, and date consumption indeed.  If the ancient Egyptians avoided all starch, grains, legumes, and sweet fruit in excess, particularly high fructose types, it is quite apparent that they would have been healthier and lived longer, even in those ancient times.  We should all take heed, and throw out the so called and wrong "healthy diet", the diet that advcates eating low fat and high carbohydrates. This is the dogma that for the last 60 years pervades all medical decisions.  For the sake of our good health we must,MUST all switch to the very healthy low carbohydrate and high saturated fat diet that our ancient genes crave.  If this is not true, how did we all get here?

Yep, the always ASSUME it's the meat or fat.  It just couldn't be all those "healthy whole grains."  

It seems to me that the Egyptian diet was a nutritionist's dream.

Thanks for blogging on this fascinating topic, doc.

Unfortunately, the media reports seem to emphasize meat consumption as if that was the conclusion of the researchers.

I'm betting they don't actually go that far in the JAMA article.

Ooops!

Yes, hunter-gatherers, not hunger-gatherers.

I have been reading about the wealthy ancient Egyptian diet. It is interesting that they used many types of vegetable oils. Many were high in omega 6. They often fried foods. The rich ate meat, bread and some dairy products. They used Honey(fructose) as a sweetner. So I ask the qestion. Was their diet much different than the modern diet?

I understand the McTut burger, although quite unhealthy, was all the rage.
This could explain it.

I love how the LA Times summed things up in their article about this study.

"Both groups, however, share some risk factors. The high-status Egyptians ate a diet high in meat from cattle, ducks and geese, all fatty.

And because mechanical refrigeration was not available, salt -- another contributing factor in heart disease -- was widely used for food preservation."

Sigh...

It occurs to me that the atherosclerosis could have been at least partially due to a vitamin D deficiency resulting from eating grain, which depletes the body of vitamin D.  

Dr. Davis, are you familiar with the theory that Europeans lost their skin pigment in part as an adaptation to eating grain?

If this was the dawn of grain-eating, it could also have been the dawn of selecting for lighter (not to say white, necessarily) skin pigments in grain-eating peoples.  (I think the same vitamin D depletion may hold true for eating dairy, so if they ate this, too, even more so.)  

I wonder if this was also the dawn of largely indoor living for some members of the population - like the wealthy and their servants - and if this could have contributed to a vitamin D deficiency.

but here we are again; Peter points out that there was no difference in calcium score between the veggie and meat diets, yet those of the paleo-diet religion will summarily dismiss this and continue to believe a meat diet is the healthy true diet for humans.  What was the life expectancy of Paleolithic man.... under 20 years maybe?  It wasn't until the diversification of diet that life span increased.... but maybe that is irrelevant if your point is to justify one's own choices

Hi, Helen--

No, I wasn't aware of that particular theory. I am aware of the notion that northern Europeans lost dark pigmentation as they settled in sun-poor regions. I was not aware that grain had added to it.

@Anonymous who claims that food diversity was the chief cause of the increase in life expectancy. First, ancient hunter-gatherers had a life expectancy of around 35 years. This dropped to under 20 years AFTER the advent of agriculture. Ask ANY anthropologist who can tell at a glance whether the bones they've found are pre or post agriculture (pre are strong, straight and healthy with no dental decay. Post are small, brittle, and diseased with plenty of dental decay.)

As to food diversity. It is estimated that hunter-gatherers had hundreds of different food choices ranging from animals great to small, insects, and hundreds of indigenous plants/nuts/seeds/fruits. Early agriculturists primarily ate the grains that could be cultivated locally, and their food choices dropped perilously.

As for mummies, only Egyptian royalty were mummified and ancient Egyptian royalty were known for their high-carb food depravity, where meals included plenty of honey, grains, starches, and beer. The feasts were frequent and included ritual bulimia so that the eating could continue indefinitely. That these people had heart disease should be no surprise to anyone.

As a final note, life expectancy is much less about living long, and more about infant mortality. Infant mortality did not go down significantly until the advent of modern medicine and birthing techniques in the 19th and 20th centuries (at least for western societies.)

@Allen - There's no evidence that ancient Egyptian royalty engaged in ritual vomiting during feasts. Perhaps it may have happened right at the end of the last dynasties when Rome's influence was strong, as purging during a Roman feast was not uncommon. BTW, feasting Romans would just vomit right at the table and a slave would clean it up. A vomitorium is not for vomiting, it's a kind of passageway.

Talking about an 'Ancient Egyptian diet' is a little silly anyway. Which kingdom/era? We're talking over thousands of years here with influences from many cultures and changing weather and environmental conditions. Modern analysis of residue in beer jars over various times shows that the ancient Egyptian beer was actually almost opaque and had a relatively high protein content, interestingly.

Interesting that we just need to refine the notion of "good and bad cholesterol," and it seems to be about particle size, not density. Are lp(a) small? Is there a treatment that converts small LDL to benign LDL but doesn't raise HDL?

Keith.

Lp(a) particle size tracks LDL particle size. Small, dense LDL therefore occurs with small, dense Lp(a) (referring to the LDL part of Lp(a), not the apo(a) portion).

Small LDL responds to the same treatments that raise HDL. I do not know of any treatments that diverge on this point with the exception of alcohol, which principally raises HDL.

That's an eye opener. In England all we get is LDL, HDL and trigylceride reports, and even then the decision to put someone on statins varies between doctors and deviates from guidelines. It's all messed up.

Just to deliver some more from Trevor Marshall (against vit D), what's your opinion of this article? It's a lengthy one. http://bacteriality.com/2008/01/26/cad/
I'm guessing the reason this has shown effect is not really the reduction of vitamin D but antibiotics that mimic it's effects. Do note that the author of that author is biased because she follows Marshall.

Every so often, a kooky idea comes along that seizes the attentions of the fringes. Linus Pauling and high-dose vitamin C to cure heart disease, cancer, and most human illnesses was this way. Nanobacteria did this. Chelation is another.

From what I've read of the so-called Marshall Protocol, I would lump this with the above.

The focus of this blog and the www.trackyourplaque.com website is reduction of coronary calcium scores and regression of coronary plaque. I do not think that we need to invoke these sorts of ideas and reinvent the wheel to accommodate the rants of people like this.

By the way, the article states that the causes of heart disease are not often revealed by conventional cholesterol values. I heartily agree with this. The answers will be found in lipoprotein analysis and associated laboratory and lifestyle examination. It is not in antibiotics.

I did find a web site that outlined the risks for someone that follows the Marshall Protocol. I should point too that Dr. Marshall is not a MD.

http://lassesen.com/cfids/MarshallProtocolRisks.htm

    *  Major risk of Addison Syndrome (5%-25% of CFS that complete the protocol)
    * Increased risk (100 300%) of Heart Attack
    * Increased risk (100+%) of Cancer (Breast, Colon and Prostate are well documented)
    * Increased risk (67+%) of Multiple Sclerosis
    * Increased risk (400+%) of Diabetes
    * Increased risk of Depression
    * Increased risk (500+%) of Osteoarthritis and Osteoporosis
    * Increased risk of nephrotic syndrome, schizophrenia and severe bipolar disorder.
    * Increased risk of Hyperparathyroidism
    * Increased risk of Crohn Disease and Sjogren's syndrome
    * Increased risk of Rheumatoid Arthritis
    * Increased risk of Systemic Lupus Erythematosus
    * May cause fetal and neonatal morbidity and death
    * Risk of Angioedema

Another from the UK!  I've often wondered how cholesterol is measured in a standard lab (as described my moblogs)   If cholesterol is contained within or is a part of a lipoprotein, how on earth do they separate out the different contents of the lipoproeins and then measure them with any precision?

Of course, LDL is NOT measured.

The other cholesterol fractions are measured enzymatically and separated by density.

I looked at the article linked by mobloogs.  At first I was surprised it didn't list his background like it did the others it mentioned, until I looked around the site and realized the whole site is just a PR piece for Marshall.  The site states Trevor Marshall, Ph.D., is a biomedical researcher.
His site http://trevormarshall.com/ says "Prof. Marshall is currently a Director of the Autoimmunity Research Foundation, an Adjunct Professor of the School of Biological Sciences and Biotechnology, Murdoch University (Western Australia)"
Wikipedia lists him as "Trevor Marshall received his PhD in Electrical Engineering from the University of Western Australia in 1984 [3]. He also possesses an undergraduate and a masters (1978) degree in Electrical Engineering.[4]"
Murdoch dosn't show him on their research page
http://www.bsb.murdoch.edu.au/research/interests/

Thanks Dr Davis  (anon from the UK)

Dr. Davis - I have been a faithful reader of your blog for about a year and try to follow your protocol for plaque reduction even though I have not been able to afford a CT Heart Scan.   I did have a lipoprotein breakdown and believed that Vitamin D, Fish Oil, and Vitamin K are very important.   My Vit D level was 36 while taking 2,000IU of Carlson's capsules.  I doubled it to 4,000IU and my blood level went to 48.   I then decided to try to get it closer to 60, so I started taking 6,000IU back in Sept.  I have a lot of cancer in my family history, have already been diagnosed with borderline osteopenia (-2.0) and fear heart disease, so Vitamin D seemed the logical thing to supplement up to a blood level of 60-70.   Then...

In December I came down with a c-diff infection out the blue, my immune system now seems to be in really bad shape which is a complete shock to me, a self-proclaimed health nut who strives to eat right, exercise and take multiple supplements.  I am really devastated to think I might have done this to myself.

A few weeks ago I ran across this new study indicating that high Vitamin D doses could harm the immune system.

http://www.sciencedaily.com/releases/2008/01/080125223302.htm

Please comment on this study to ease my mind....I dropped back to 2,000IU a day of the D supplement as I'm scared to death!
Thanks,
Noreen

I've commented on this bit of nonsense several times, both here and in the Track Your Plaque forum. It is patent nonsense based on the rants of a single man. Yes, there is a sliver  of science in his comments, but nothing more. Vit D has nothing to do with catching an infectious bacterial disease in the gastrointestinal tract.

Thank you Dr. Davis -- I felt like you would have an unbiased opinion on this.  Its just scarey to read about immunosuppression, especially when you seem to be suffering from it!   I've also had a flu-like episode and a cold since the first of Dec!  

I feel like I am literally starving myself on (ugh) white bread, white potatoes and white rice, but thats all I can eat at this time.   Things I haven't eaten in over 5 years!

Thanks for clarifying the Vitamin D issue.  I'll go back to my 6,000IU dose.

Noreen (who is healing slowly)

Knowing that Pam has Lp(a) can point us in an entirely different direction than just LDL cholesterol. It might mean high-dose fish oil, a more serious approach to niacin, hormonal treatments like DHEA or testosterone. It might mean more attention to warning your children about the possibility that they, too, might share this genetic trait.