LDL cholesterol, statins, and plaque regression

13. April 2008 William Davis (12)
The ASTEROID Trial reported in 2006 examined the effects of LDL cholesterol reduction using the statin drug, rosuvastatin (Crestor), with coronary atherosclerosis quantified and tracked with intracoronary ultrasound. The Track Your Plaque report, New study confirms: LDL of 60 mg reverses plaque, on the ASTEROID Trial provides commentary on the results.


Though I remain skeptical that a statin-only treatment strategy can reverse coronary plaque in the majority of people, I do believe that the AstraZeneca-sponsored ASTEROID Trial does add to the wisdom on heart disease management. More importantly, it has served to raise awareness among both the public and my physician colleagues that atherosclerosis is indeed a potentially reversible condition.


Specifically, the ASTEROID results confirm that, either directly or indirectly, LDL cholesterol reduction achieved with statin agents does correspond to increasing degrees of plaque reversal. The mean (calculated) LDL cholesterol achieved in ASTEROID was 60 mg/dl, the same as the Track Your Plaque suggested LDL target.

Though the ASTEROID Trial is not news, I stumbled on a chart posted on the ASTEROID Trial website that clearly highlights how a number of other studies beyond ASTEROID have fallen into this pattern:





The graph reveals a linear relationship: The greater the reduction in LDL cholesterol with statin drugs, the greater the plaque regression ("change in percent atheroma volume"). (Several other studies not included in the graph also cluster into the same linear relationship.)

I am no supporter of drug companies, nor a defender of their policies and practices. But I do believe that their data can serve to teach us a few lessons. For instance, here is an (cherry-picked, to be sure) example of intracoronary ultrasound cross-sectional images before and after two years of rosuvastatin, 40 mg daily:





The color-coded/outlined atherosclerotic coronary plaque is shown shrinking, while the "lumen," or the path for blood to flow, enlarges. The reduction in coronary plaque is irrefutable. (The small circle within the lumen with the white halo surrounding it is the ultrasound catheter.)

If you and I were to choose a single treatment approach to coronary disease reversal, then 40 mg of rosuvastatin is probably at the top of the list. However, in the Track Your Plaque program, we do not advocate a single treatment strategy. While the Crestor-only approach is relatively straightforward--one pill a day--few people, in my experience, can tolerate this dose for any length of time. Patients invariably have to stop the drug or reduce the dose severely due to muscle aches when I've had patients try it. Contrary to the ASTEROID results, in my experience the majority of people, perhaps all, eventually give up with this improbable "one-size-fits-all" scheme.

The Track Your Plaque approach, while more complicated and involves several nutritional supplements and strategies, in my view addresses more causes of coronary plaque, is better tolerated, and provides health benefits outside of just LDL cholesterol reduction. It also minimizes or eliminates the need for prescription medication.



Studies cited in graph:

1.Nissen S et al. N Engl J Med 2006;354:1253-1263.
2 Tardif J et al. Circulation 2004;110:3372-3377.
3 Nissen S et al. JAMA 2006;295 (13):1556-1565
4 Nissen S et al. JAMA 2004;292: 2217–2225.
5 Nissen S et al. JAMA 2004; 291:1071–1080
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Comments (12) -

  • J Michael Nicholls

    4/13/2008 6:49:00 AM |

    Dear Dr. Davis,
    I have read your blog for some time now, and I consider it to be the no 1 in the nutrition-health-cardiology field. A couple of years ago I became interested in the “cholesterol theory” and I have studied the development of the statins in detail. Having a background in the “hard sciences” I am appalled at the lack of sound science in this field in particular, as well as in some other areas of medical research.

    To my knowledge there is zero evidence that the lowering of any of the cholesterol levels has anything to do with preventing heart disease or reversing plack. On the contrary, an anti-inflammatory mechanism is probably the reason for the little protective effect there is, while the lowering of the cholesterol levels probably causes more harm then good (as can be suspected from the extensive list of side effects).

    Reading this post and the statement, “LDL cholesterol reduction achieved with statin agents does correspond to increasing degrees of plaque reversal”, I couldn’t help feeling that some readers would get it all wrong, especially since “cholesterol lowering” is the healing mantra that is being communicated to the market (and even most doctors seem to advocate).

  • Anonymous

    4/13/2008 11:50:00 PM |

    "Having a background in the hard sciences"? In the "hard siences" they call plaque "plak" ? That was a dead give away that you have no idea what your talking about even before you made the ridiculus statement"to my knowledge there is zero eveidence that the lowering of any of the cholesterol has anything to do with preveting heart disease or lowering plak(sic)" You should read some of the studies, they're easily found on the internet or in journals. By the way did you look at the pictures Dr. davis put up in the article? As Dr. davis always says I don't work for the drug companies and statins certainly aren't miracle drugs but they do have a place. Ever hear of the Framingham Study, just a small study thats been going on for over 60 years now and has studied over 10,000 people( now in its third generation) and they have NEVER had a recorded heart attack in ANYBODY with a cholesterol level under 150. So much for "your knowledge"

  • Anonymous

    4/14/2008 4:40:00 AM |

    Dear Dr. Davis,

    In reading this and about vitamin D, if you have a plaque problem, but your HDL is high and your Vitamin D level in normal, would it still be helpful to take the suppliment?

  • J Michael Nicholls

    4/14/2008 1:56:00 PM |

    Dear Anonymous, there is no need to be so sarcastic, and I apologize for spelling plaque plack. Do you mean to say that all of medical science is of high quality, and that it shouldn’t be questioned? Most of the serious critique against the cholesterol hypothesis comes from medical researchers by the way. I am waiting to be enlightened, please show me the evidence that the LOWERING of cholesterol by it self (per se) is the protective mechanism of statins.

    From your writing it appears that you still believe in the old dogma of high cholesterol CAUSING atherosclerosis. Only a few of the fiercest statinators in the research community still maintain that, and probably so for financial reasons (most statin-advertising is doing its best to communicate just that). Most GPs seem to believe that cholesterol causes atherosclerosis too. It is trivial that in any academic context “correspond to”, “linear relationship” or “associated with” do not mean “direct effect of” or “directly caused by”. With this simple understanding we would have better doctors and better scientist in the medical field, and consequently less treatment of SYMPTOMS such as high cholesterol, high blood pressure and high blood sugar. By the way, is there any proof that atherosclerosis is not causing the higher cholesterol levels instead of the other way around?

    The problem with many defenders of the cholesterol dogma is that they don’t read the scientific literature in a scientific way. I personally don’t know of anyone still believing in the cholesterol hypothesis after having studied it in depth from strictly scientific principles. There is simply no evidence to motivate all the “lowering” of “levels”. It is nothing more than a highly profitable market concept ($30 billion in 2007).

  • Anonymous

    4/14/2008 2:25:00 PM |

    Great write up.

    As  a diabetic, with all of my numbers under very good control, I have been on statins for 8 years and my last two heart scans (5 years apart) had a score of 0 plague.  My question is the following:

    Are you saying that statins are good and should be part of a comprehensive approach?

    Many websites that push your blog are against the use of statins in any approach.  How do you respond to that type of thinking?

    Should you continue taking drugs to reduce your plague if your score is zero?


    Thanks for your time

  • Anonymous

    4/14/2008 6:23:00 PM |

    Playing devil's advocate, I'm not sure if science has proved cholesterol to be a cause of heart disease. What if it's a marker and not a cause?

    Those in the Framingham study with low cholesterol values might not get heart attacks due to lifestyle/genetics, and their low cholesterol is a reflection of their overall good health?

    Those who take high dose statins obtain benefit from less inflammation, but not because of cholesterol reduction?

    I'm not saying the above two statements are true, but it could be possible. It could also explain why statins, as a single treatment, usually don't work for most people, and why the Vytorin/Zetia/Torcetrapib trials failed so miserably.

    Or it could be that the reduction in LDL wasn't enough to matter, or that particle sizes for LDL/HDL wasn't taken into account, or some other factor? It appears that  right now, there isn't hard data that proves what causes heart disease exactly, but simply a lot of risk factors and disease markers instead.

  • Anonymous

    4/15/2008 1:52:00 AM |

    I never suggested that Cholesterol by itself caused heart disease. Clearly many things do, inflamation, CRP, Lp(a)... On the other hand to suppose that cholesterol has NOTHING to do with heart disease is foolish. Show me a cardiologist that believes cholesterol has nothing to do with heart disease and I'll show you a quack. It may not even be the main cause of heart disease in most people but the fact of the matter is reducing LDL lowers the the chance for heart attack in a good number of people. Have you ever heard of Dr. Agagston ? He of the South Beach Diet fame, a cardiologist in South Florida, who by the way the way of scoring calcium scans is named after. See what he thinks of statins and reducing cholesterol levels. and as Im sure you know it gets much more complicated than that when you get into particle size. Take a person who's scans keep going up because he has small LDL and nothing in Dr. Davis program has worked for him 9I am such a patient of the good Dr.s) The best you can do for such a person is lower his LDL as far as you can since its all going to be small particle anyway. I would also refer you to Dr. Greg Browns HATS Study for examples of lowering cholesterol and lowering heart disease or Dr. Davis' example that started this discussion. I apologise if I came off a bit sarcastic in my earlier comments I think this is an important issue to get all points of view on.

  • Anonymous

    4/16/2008 3:32:00 AM |

    Great thead.

    So what are you really saying about statins?  Is there value taking statins in combination with other treatments for men and women?

    How do you address the comments that states statins don't work?

    Thanks for your time.  Your comments are really appreciated.

  • Anonymous

    4/16/2008 6:14:00 PM |

    There is NO DOUBT that statins reduce the chances of a person having a heart attack, NONE. There is question as to what about the statins does that, is it lowering LDL, is it stablising plaque, is it reducing inflamation . . .? Or is it all of these ? And there is no doubt statins have side effects, some serious, but the fact that they reduce heart attacks, that argument has been settled.

  • J Michael Nicholls

    4/16/2008 7:26:00 PM |

    I will not go deeper into the science of atherosclerosis except to say that it has been known for several years now that cholesterol per se does not initiate atheroma, or plaque. You find cholesterol in the lesions but you also find calcium. We find cholesterol and calcium because it is available in the bloodstream. Cholesterol does not have a mind of its own, and it doesn’t one day decide to develop plaque by raising “the level”. Neither does calcium.

    We need cholesterol for many important processes in the body, and it is a part of almost all of our cell membranes. Mother’s milk is packed with it because the baby needs it. Eggs are full of the stuff “because it takes a hell of a lot of cholesterol to make a chicken”. The body has the level it needs at all times, and a higher level could indicate that something is wrong, i e, it is a marker, like someone said. Lowering of levels makes no sense at all.

    It is just dumb luck that the cholesterol lowering statins happen to be anti-inflammatory and therefore have some preventive effect, and may reverse plaque in some cases. The higher the dose the more anti-inflammatory effect, and reversal of atheroma. The higher the dose the bigger the lowering of the cholesterol level, because that is exactly how statins are designed to work. However, there is NO evidence in the scientific literature that the lowering of the cholesterol level has a protective effect, and I am very sorry if this upsets anyone’s religious beliefs. Dumb luck, as I said, the rest is coincidence and correspondence. Big Pharma will do its best to uphold the “religion” though, since it is so profitable. Levels will always be too high, and everybody should be statinated. Statins should be distributed in the drinking water, no less.

    So, why bother, the statins seems to work in a few cases? Well, statins are really poisonous substances, and there are many indications that they cause harm to the human body, particularly by the lowering of cholesterol levels. Side effects are plentiful and it is probable that we will witness statin induced cancers in large numbers in the near future.

    The point to be made here is that there are other and better methods to avoid atherosclerosis and to reverse plaque. Dr Davis is one of the leading proponents of such methods. I personally think it is interesting to se the results of the statin study presented here; I just wanted to stress the point of what statins really do. By all means, we should keep an eye our cholesterol levels. But many people having a hearth attack do not have high cholesterol. But did you know that 90% of them have diabetes or in some other way a pathological sugar metabolism? So what level is the more important?

    About the quacks, who don’t buy the cholesterol dogma, there are thousands of them. Some of them can be found at www.thincs.org. If you are interested in how the cholesterol religion was developed and how science was corrupted to that end, I can recommend Gary Taubes latest book Good Calories – Bad Calories.

    By the way, CRP is just another marker for hearth disease, but I wouldn’t be surprised if there will soon be talk about lowering the level Smile

  • Anonymous

    4/18/2008 1:13:00 AM |

    Well by your klogic there is no scientific proof the lowering inflamation is what cause stsatins to lower your risk of a herat attack, the only thing we do know is that ststins DO infact lower your risk, we just all keep guessing as to why. Well heres another piece to the puzzle: double blind study releasesed this week follow groups of people on statins or placebos and by a slight BUT significant margin the statin takers blood oressure was lowered ! So besides all the other things we think statins do we now KNOW they lower blood pressure. 2 ver5y interesting points for all of our paranoid readers 1. Not one of the study members recieving the statins in the 2 year period had to leave bececause of side effects and 2. this study was NOT paid for by the big bad scarry Drug companies, so there goes your default response.

  • buy jeans

    11/3/2010 4:55:07 PM |

    I am no supporter of drug companies, nor a defender of their policies and practices. But I do believe that their data can serve to teach us a few lessons. For instance, here is an (cherry-picked, to be sure) example of intracoronary ultrasound cross-sectional images before and after two years of rosuvastatin, 40 mg daily:

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The battle for natural hormones

18. April 2007 William Davis (0)
The battle for preservation of availability of compounded natural hormones goes on.

It started with pharmaceutical manufacturer, Wyeth, who petitioned the FDA to disallow the mixing of pharmaceuticals, especially natural human hormones, by specially trained pharmacists at what are called "compounding pharmacies." These are pharmacies that have special equipment and where trained pharmacists can mix up specific preparations for dispensing. These are available by prescription.

For instance, I have been prescribing natural human testosterone and progesterone for nearly 10 years. I have found service to be excellent, with lots of learning materials provided to patients by the pharmacy. The pharmacists I've spoken to have been courteous and knowledgeable. Compounded hormones are also shockingly less expensive. While a testosterone patch from a pharmaceutical company costs around $4.00 per day, the same quantity of testosterone cream formulated by a compouding pharmacy costs around $0.50 per day--87.5% less.

Wyeth hides behind a smoke screen of concern over quality. But the price differences tells the entire story: they want to eliminate the inexpensive competition and hold us all hostage to the far more expensive, often inferior products that they produce. They'd sooner force a woman to use horse-derived Premarin than to allow her access to human estrogens and progesterone.

To me, this is an outrageous affront to our freedom of choice, both as consumers as well as a physician. If you feel as strongly as I do about opposing the unfair and bullying ways of Wyeth Pharmaceuticals and the FDA, the P2C2 association of compounding pharmacists makes writing a letter to your Senator easy by going to

http://iacprx.convio.net/site/PageServer?pagename=P2C2

Just enter your info and personalize the comments, and the e-mails will be generated for you.

Lipitor and memory

17. April 2007 William Davis (2)
At first, I was skeptical. A book from a nutty author and physician named Duane Graveline kept on coming up in conversations with patients. His book, Lipitor: Thief of Memory , details his personal experience with dramatic changes in memory and thought while taking Lipitor.



Now this is a drug that I've seen used thousands of times. But I've now seen about a dozen people who have had distinct struggles with memory and clarity of thinking while taking Lipitor. Most took doses of 40 mg per day or more, though an occasional person takes as little as 10 mg. The association seems to be undeniable, since it improves after two weeks off the drug, recurs when resumed. Just today, I saw two people where this effect may be an issue.

Curiously, I've not seen it with any other statin agent. Unfortunately, uncovering any scientific data on the issue is a hopeless quest. Either it's very uncommon or, worse, the data has been suppressed.

Any way, I believe that Dr. Graveline was right: Lipitor, in a small number of people, does indeed seem to exert real detrimental effects on the mind.

If you take Lipitor, should you stop it in fear of long-term effects on your mental capacity? I think it's premature to toss the drug out based on this relatively uncommon relationship. This particular effect is likely to be idiosyncratic, i.e., peculiar to an occasional person but does not seem to apply to the majority, probably by some quirk of metabolism or penetrability of the barrier between the blood and nervous system tissue.

If, however, you feel that your thinking and memory have deteriorated on the drug, please speak to your doctor.

EKG's and heart disease

16. April 2007 William Davis (6)

How helpful are EKG's for detecting hidden heart disease?

I pose this question because several patients asked this question just this week. It's also a frequent point of confusion and misperception.

Your EKG is nothing more than an expression of the surface electrical activity emitted by heart muscle activity. Multiple (12) leads are attached to the body simply to provide various "views" of this electical activity. EKG, or sometimes "ECG", is short for "electrocardiogram".

What modifies this surface electrical activity? Anything that modifies the electrical activity within the heart itself, or interferes with the detection of the activity. An old heart attack modifies the patterns of electrical conduction in the heart and that can change your EKG. An ongoing heart heart attack likewise. High blood pressure commonly creates changes in the EKG, as does lung disease. A bellyache can change your EKG, as can a stroke. (These non-heart-related phenomena probably are often due to changes in autonomic, or "automatic," nervous system activity.) The heart generates electrical activity in a predictable sequence that generates the heart beat, or "rhythm". EKG's are useful for monitoring heart rhythm, also.

Does having plaque in your coronary arteries have any effect on the EKG? None whatsoever, unless plaque rupture caused heart attack or is about to cause heart attack. So, you can have a horrendous CT heart scan score of, say, 3000, yet maintain a perfectly normal EKG, as long as the heart muscle is normal.

Then why bother with these iffy tests? They are indeed useful to diagnose the cause of active symptoms. For instance, go to the ER with chest pain and an EKG could show changes suggesting that the chest pain is a heart attack. EKG's are also useful for future comparison. Any change in EKG can suggest certain things, like new heart rhythm disturbances unrelated to coronary plaque.

Think of your EKG as just like buying a used car. Say I'm trying to sell you my 1999 Buick Century. It looks pretty good from the outside and I tell you that it has 70,000 miles and runs well. You ask to open the hood, look in the interior and take it out for a drive. I tell you no, you can't do that.

Would you buy the car? Of course you wouldn't. You were permitted only a very superficial examination of the car. You have no idea what's going on inside. Just because the paint job looks brand new doesn't mean the engine and transmission are good.

The same with your EKG: It's a superficial look at one aspect of this used car called your heart. If the EKG is normal, that's good, just like a good exterior on the Buick. But you cannot assume that the heart is otherwise normal.

View the EKG as a simple, superficial test that can only provide minimal reassurance, no matter how often you have it done.

A new Track Your Plaque record

14. April 2007 William Davis (0)
Neal, a 40-year old school principal, and his young wife were terrified on learning of his CT heart scan score of 339, a concerningly high score for any age, particularly age 40.

To make matters worse, all of Neal's plaque was located in the critical left mainstem coronary artery, the shared stem of two of the three coronary arteries. A heart attack in this location is instantly fatal.

So, it was especially gratifying that Neal has set the Track Your Plaque record for largest magnitude of plaque reversal: 51% in his first year.

Studies that show a reduction in heart attack make the news. They talk about 1, 2, up to 6% regression, all achieved with high doses of statin drugs. Yet we are seeing huge, extraordinary quantities of heart disease reversal that haven't yet made headlines, amounts that far exceed those featured in the news. We should be encouraged by experiences like Neal's.

Watch for the upcoming Track Your Plaque newsletter for more details on Neal's story--how he came to the program, how he accomplished this huge effect, and why his experience was such a success. If you haven't yet subscribed, go to the www.cureality.com homepage and click on the upper right hand corner.

The Plavix Scam

12. April 2007 William Davis (3)
Periodically, I'll see a flurry of TV ads for Plavix. It comes with a polished computer-animated cartoon that shows how platelets clump and form a blood clot, causing heart attack.

Imagine there's a pile of oil-soaked rags in a corner of your garage. I come by and tell you to get a good fire extinguisher to keep next to the rag pile in case they spontaneously ignite.

Does that make sense to you?

Wouldn't it be better to get rid of the oily rags and forget about the fire extinguisher?

Plavix is the fire extinguisher. The oil rags are your coronary plaque. The solution is to gain control over plaque behavior. Unfortunately, the TV ads (intentionally, I suspect) give the impression that blood clots just form out of the blue for no reason. Of course that's not true. It requires active, growing, inflamed atheroslcerotic plaque that ruptures, uncovering the "angry" and platelet-adhering material underneath the thin covering or endothelial lining.

Urging everybody to take Plavix is absurd. The TV ads urge many people who have no business taking the drug to take it. There are, without a doubt, groups of people who are better off taking Plavix and aspirin: people who are in the midst of heart attack, people who have unstable plaque, people with recent stents or bypass. Perhaps people at high risk for plaque rupture, e.g., extensive coronary plaque that has continued to grow.

These tactics are consistent with the experiences I've had with the sales representatives from the company (when I used to actually talk to sales reps; my office is now barred from them). The reps very aggressively would urge me to consider having everyone take Plavix. No kidding.


For us, i.e., for people who just have a heart scan score but interested in engaging in a powerful program of prevention and reversal, Plavix rarely provides any advantage. The answer is, just like our oily rag analogy, control the plaque, not put out the fire.

Lipoprotein(a) and small LDL

11. April 2007 William Davis (0)
You won't find a lot of scientific validation for this, but it is my firm impression that small LDL, by some crazy means, has the capacity to "turn on" or "turn off" lipoprotein(a), Lp(a).

Recall that Lp(a) is a specific genetic trait, passed to us (if you have it) by mother or father. It falsely elevates LDL cholesterol and escalates heart disease risk more than just about any other known abnormality.

A frequent hint that Lp(a) might be present is a comment I hear often from patients: "My doctor said statin cholesterol drugs don't work for me. I tried them all and my cholesterol won't go down." Or, the result was substantially less than expected. That's because, when Lp(a) is lurking in your cholesterol value, it is unaffected by the statins.

It's been my in-the-trenches observation that, the more fully expressed the small LDL pattern becomes, the worse the Lp(a) behaves. In other words, if small LDL is suppressed effectively, Lp(a) doesn't seem to carry the same dangers as in someone who has plenty of small LDL. I don't know why this is. (I expect that the answer will come from someone like Dr. Marcovina at Stanford, who is at the forefront of Lp(a) structural research. Lp(a) is a complex molecule with several components. How and why it interacts with other particles remains a mystery.)

There are a little bit of data to confirm this. The Quebec Cardiovascular Study has presented some data to this effect, that the combination of small LDL particles and Lp(a) are a particularly lethal combination. We are trying to correlate our data from a CT heart score perspective to discern any statistical relationships.

This raises a very important therapeutic issue if you have Lp(a): the worst thing you can do if you have Lp(a) is become overweight. Excess abdominal fat is a huge trigger to create small LDL particles. Even though being overweight itself has no effect on the measured level of Lp(a), it activates small LDL which, in turn, throws gasoline on the Lp(a) fire.

If you have Lp(a), stay skinny.

Optimal medical therapy

9. April 2007 William Davis (6)
I was re-reading some of the details behind the recently announced COURAGE Trial comparing angioplasty/stent in 1100 people compared to "optimal" medical therapy in another 1100. You'll recall that no difference was found.

In particular, over approximately 5 years, 20% of participants in each group died, experienced heart attacks, or strokes. Of those treated with "timal" medical therapy, 32% ended up getting a procedure like stents or bypass anyway due to deteriorating symptoms.

What is "optimal" medical therapy? I bring this up again because the study investigators in COURAGE, as well as in similar trials, say this with a straight face. Optimal medical therapy means aspirin and/or Plavix (the anti-platelet, aspirin-like blood thinner); "aggressive" statin drug therapy to reduce LDL cholesterol to 60-85 mg/dl; and "anti-ischemic" therapy (that reduces angina and the phenomena of poor coronary blood flow) using nitroglycerin preparations, beta blockers, and other drugs.

I do give credit to the investigators for having the courage to perform this trial in a world hell bent on doing procedures and still reporting the neutral outcome. But the notion of "optimal" medical therapy begs for comment.

Indeed, this is regarded as optimal by most practitioners. Some would even argue excessive, based on the low LDL target achieved. Would you be satisfied with a 20% likelihood of heart attack, stroke, or death or 5 years, a 1 in 5 roll of the dice? I would not. Recall that we aim for near-total elimination of risk.

What could have been further "optimized"? Plenty. For instance:

--What is the real LDL, not the fabricated, calculated LDL? The two can be commonly 100 mg/dl different.

--How about raising HDL to 60 mgd/?

--What about reducing the proportion of small LDL particles? After all, small LDL is the number one cause of heart disease in the U.S., not high LDL.

--What is Lp(a)? If you treat LDL with a statin drug, Lp(a) is unaffected and continues to trigger huge plaque growth. You will fail if this is not identified and corrected.

--What is vitamin D3? One of the most powerful facilitators of plaque reversal I know of.

--What are triglycerides? Triglycerides create hidden particles in the blood like intermediate-density lipoprotein, potent triggers for coronary plaque growth. Speaking of intermediate-density lipoprotein, that's another very important pattern to identify, the after-eating persistence of dietary fats.

--Why aren't they taking fish oil? With a 28% reduction in heart attack and 45% reduction in sudden death from heart attack, this alone would have halved the number of "events" in the "optimal" medical treatment group.

Of course, there's more. But the idea that aspirin, statins, and anti-ischemic therapy is somehow optimal is silly and sad at the same time. But that's the bias. The COURAGE Trial does represent a step forward, a step away from the "stent everyone and everything" mentality that motivates my colleagues, aided and abetted by their co-conspirators, the hospitals. But you and I know better. "Optimal" medical therapy, in truth, can mean a far better approach that can dramatically reduce, perhaps eliminate, risks for events like heart attack. The conventional "optimal" medical therapy will suffice only if you're content with a 20% likelihood of heart attack, death or stroke, or a 32% likelihood of an urgent procedure in your future.

Niacin, postprandial patterns

9. April 2007 William Davis (0)
For a detailed report on the very important postprandial (after eating) patterns that contribute hugely to heart disease risk, read my recent article in Life Extension Magazine, available (no cost) at:

Uncovering a Hidden Source of Cardiovascular Disease Risk
at http://www.lef.org/magazine/mag2007/mar2007_report_heart_01.htm


For a report on using niacin to reduce risk of heart disease, see another report in the same issue of Life Extension:

Ask the Doctor: Using Niacin to Improve Cardiovascular Health
at
http://www.lef.org/magazine/mag2007/mar2007_atd_01.htm.

Also, keep your eyes open for a lengthy report focused exclusively on the Track Your Plaque program in an upcoming issue of Life Extension. I'll provide links in this Blog when it comes out.

What's better than fish oil?

9. April 2007 William Davis (1)
One of the recent questions on our Track Your Plaque Forum related to what to do about a triglyceride level of 101 mg/dl while on fish oil.

Recall that, contary to conventional thinking like that articulated in the ATP-III cholesterol treatment guidelines, we aim to reduce triglycerides to 60 mg/dl or less. This is important to suppress the formation of abnormal triglyceride-containing lipoprotein particles, especially small LDL, reduced HDL, lack of healthy large HDL, VLDL. ATP-III advises a level of 150 mg/dl or less. Unfortunately, triglyceride levels this high guarantee appearance of all these undesirable particles and an increasing heart scan score.

What's better than 4000 mg of fish oil for its 1200 mg of EPA and DHA (omega-3 fatty acids)? More fish oil. In other words, the 4000 mg fish oil providing 1200 mg EPA + DHA is our minimum. A simple increase to 6000 mg to provide 1800 mg EPA + DHA is usually all that is necessary to reduce triglycerides and put a halt to the cascade of abnormal lipoprotein particles that trigger plaque growth. Occasionally, a somewhat higher dose may be required. Doses are best divided into two, with meals (e.g., three capsules twice a day).

Another important issue: An over-reliance on wheat products can also increase triglycerides. This includes any flour product like breads (regardless of whether it's white, whole wheat, or whole grain--they all raise triglycerides), pretzels, bagels, breakfast cereals, and pasta. A dramatic reduction in wheat-containing products will reduce triglycerides substantially, help you reduce your abdominal fat, reduce blood pressure, raise HDL and reduce small LDL, clear your mind, provide more energy, avoid afternoon "fogginess" . . . Huge benefits.

Valve disease and vitamin D

8. April 2007 William Davis (1)
There are two common forms of heart valve disease: aortic valve stenosis (stiffness) and insufficiency (leakiness), and mitral anular calcification.

Both valve issues are regarded as evidence of senescence, or aging--the older you are, the more likely you will have one or both. Both conditions involve progressive calcium deposition and, to some degree, cholesterol deposition. They might be regarded as phenomena of "wear and tear" just like hip arthritis.

There are no known therapies to stall or stop the development of mitral anular calcification. However, several attempts have been made over the years to identify treatments that can slow or stop the progression of aortic valve disease, which is becoming increasingly common and is addressed by surgical valve replacement when severe. The most recent trials have examined whether high-dose Lipitor (80 mg) has any effect (it did not) and high dose Crestor (40 mg), which slowed but did not stop the deterioration of stiff valves.

It's been my suspicion that vitamins D and K2 may play a crucial factor in valve health. After all, vitamin D is the master controller of calcium deposition. Preliminary data also suggest that people who are intentionally made vitamin K deficient with the drug, Coumadin, develop twice the calcium deposition on aortic valves that non-Coumadin takers develop.

I saw a patient Friday, Marianne. In addition to a moderate heart scan score of 379 at age 71, Marianne had a leaky (insufficient) aortic valve. By an echocardiogram 18 months ago, the valve was moderately leaky. I put Marianne on vitamin D, 4000 units, to raise her blood level to 50 ng/ml.

Last week, I asked Marianne to have another echocardiogram. This time, no leakiness whatsoever--none. I have never seen this happen before. Although Marianne is only one example and we don't want to extrapolate too far from the experience of one person, it's hard not to attribute this phenomenal response to vitamin D supplementation.

I wonder what would have happened if we had added vitamin K2, as well?

Anyway, just another potential wonderful effect of vitamin D restoration.