Vitamin D--A coronary risk factor

Look up "coronary risk factors" in any text and you'll find high cholesterol, smoking, diabetes, and high blood pressure listed. You won't find deficiency of vitamin D listed.

Ask 99% of physicians if a deficiency of vitamin D is a coronary risk factor and you'll get rolling eyes and a sigh.

Yet, in the Track Your Plaque experience, vitamin D is emerging as a very important factor in coronary plaque development. We have observed that there are a substantial number of people whose lipids and lipoproteins are not abnormal enough to fully explain their heart scan score. In other words, there seems to be something else necessary to satisfactorily explain the magnitude of coronary plaque.

I believe that severe vitamin D deficiency is at least one of the most important factors. We've seen many people with blood levels of vitamin in the range of severe deficiency (<20 ng/ml of 25-OH-Vitamin D3) yet bland lipids and lipoproteins.

Correcting vitamin D blood levels to 50 ng/ml also seems to be among the required factors in stopping coronary plaque growth, or stopping your heart scan score from increasing.

Keep your eye on this extremely important and exciting issue. Sadly, it won't be propelled into the media like the conversation about cholesterol or high-tech procedures, since no company stands to profit from it. But you and I don't have to play that game.

Cholesterol is dead!

I saw a patient in the office yesterday. He came to me for an opinion regarding his high heart scan score of 525, putting him in the 90th percentile (5% annual risk of heart attack).

His doctor had been puzzled because his LDL cholesterols had ranged from 110 to 131 mg--actually below average. (The average LDL for the U.S. is 132 mg.) Likewise, HDL was a favorable 63 mg.

Lipoprotein analysis told the story loud and clear. His LDL particle number, a far more precise measure of LDL, was 2448 nmol/l. This means that his true LDL was more like 240-250 mg! (You can get a sense for what the true LDL is from LDL particle number by dropping the last digit: 2448 becomes 244.) Conventional LDL was therefore inaccurate by over 100 mg.

He also had a severe small LDL particle pattern. The cause of his coronary plaque was a large excess of small LDL particles. LDL cholesterol (and total cholesterol, likewise) didn't even hint at this pattern. Nor did his favorable HDL.

Think of LDL particle number as an actual count of LDL particles per volume, e.g., number of particles per cc of blood. This makes it easier to conceptualize. LDL particle number is the measure you get when you have an NMR lipoprotein profile, our preferred method of lipoprotein testing. If this is unavailable to you, apoprotein B is a reasonable second choice, though not as accurate in my view. More info on NMR is available at their website, www.lipoprofile.com.

How to make a $1 million in cardiology

Want to make a $1,000,000 as a cardiologist in the next year? It's easy. All you have to do is:

1) Perform heart catheterizations or other procedures on anybody you can, even if it's not necessary. Perform them even if the patient has no symptoms and the stress test is normal.

2) Perform heart catheterizations if the patient is too timid or ill-informed to object.

3) Insert coronary stents in blockages, even when they're minor and it's not necessary.

4) Turn every heart procedure into a revenue-producing stream by looking for other profit opportunties, such as minor kidney artery blockages.

5) Heart disease is frightening. Scare the heck out of patients by exagerrating the dangers so they'll go through testing and procedures gratefully.


Sound absurd? Well, it would be if these weren't all true.

These are real examples, as awful as it sounds. I've witnessed all these behaviors. Not just occasionally, but with regularity.

Just today, I encountered a colleague who performs heart catheterizations routinely (up to several per day) when any symptom is present and the stress test is entirely normal. This is grossly inappropriate.

Your protection is being better-informed and avoid being sucked into the vast and frightening cardiovascular machine of revenue-yielding procedures. Part of your protection is to get a CT heart scan, then engage in a program of heart disease prevention.

Doctor, do I have lipoprotein (a)?

I met Joyce today for a 2nd opinion. She told me about this conversation she'd had with her cardiologist:

"Doctor, do you think I could have lipoprotein (a)? I read about how it can cause heart attacks even when cholesterol is controlled."

"What does it matter? Even if you have it, there's nothing we can do about it. There's no treatment for it."

Joyce was understandably groping for some means to prevent her coronary disease from causing more danger. At 56, she'd already survived a heart attack that resulted in two stents to her left anterior descending. Around 9 months later, she received a 3rd stent to another artery.

Her doctor had put her on Pravachol and said that was enough. "We know that cholesterol causes heart disease and the Pravachol reduces it. Why do we need to know anything more?"

So Joyce came to me for another view. I explained to her that there are, in fact, several ways to deal with lipoprotein(a). It is, without a doubt, among the more difficult patterns to manage--but not impossible. In fact, we have a growing list of participants in the Track Your Plaque program who have stopped or reduced their heart scan scores.

I continue to be horrified at the level of ignorance that prevails among my colleagues, the cardiologists, and the primary care community. If your doctor gives you advice like this, get a new doctor.

Is it mainstream or alternative?

A question I get about once a week: "Is your program a kind of alternative medicine?"

Our program for control and reversal of coronary plaque using CT heart scans applies an eclectic panel of tools to achieve its goals. We use high-tech methods like lipoprotein analysis and CT heart scans; nutritional supplements like fish oil, vitamin D, and l-arginine; diet strategies and "functional foods" (using foods as a therapeutic tool); and conventional medication.

I don't consider this approach "alternative" in the sense that it uses unmeasurable or spiritual strategies. But I don't consider it mainstream, either, since current mainstream practice of heart disease prevention is far less rigorous with far less satisfactory results.

I think I can sum up the Track Your Plaque approach by saying that we use tools that work. Our measure of success is whether or not your heart scan score is stopped or reduced--that's hard to fudge. You can call it what you will, but I call it the best program for heart disease prevention I know of, alternative or mainstream.

Want to see someone turn diabetic?

If you want to witness the transformation of someone into a pre-diabetic or diabetic, put them on a low fat diet.

Dr. Dean Ornish's program, detailed in his books, Dr. Dean Ornish's Program for Reversal of Heart Disease and Eat More, Weigh Less , are woefully outdated in 2006. Yet the low fat notion continues to show up in the consciousness of people I talk to about heart disease reversal.

"I'm already on a low fat diet. Do you think my heart scan score has reversed?"

Highly unlikely. What Dr. Ornish (as a non-cardiologist, by the way) failed to recognize is that what he did manage to reverse in a small number of people is something called "endothelial dysfunction", but he did not reverse or shrink coronary plaque.

Given the limitations of technology when the Ornish concept got its start, it appeared as if reversal was obtained. In reality, all his approach accomplished was a relaxation in tone of abnormally constricted arteries, thus giving the appearance of reversal. Increased artery tone, or endothelial dysfunction, is extremely common when atherosclerotic plaque is present.

Any cardiologist will tell you that there are many ways to reverse endothelial dysfunction: exercise, weight loss, cholesterol drugs, drugs for high blood pressure, fish oil, hormonal therapy, vitamin C, l-arginine, etc. There is nothing special about a low fat diet.

In fact, Track Your Plaque followers will recognize that a low fat diet is, in fact, potentially harmful, particularly when low HDL or small LDL is part of your pattern.

Let's bury the outdated ideas of the Ornish low fat diet once and for all. It doesn't work. All it may do is confuse you and set you back from your real coronary plaque reversal program.

Inulin: A fiber for weight loss

Here's an interesting product that seems to be gaining some popularity for weight loss: Inulin.

Not to be confused with "insulin", with which it is completely unrelated, inulin is a naturally-occurring plant fiber. It's found in broccoli, asparagus, celery, etc. Like beta-glucan from oats or pectin, inulin is a so-called soluble fiber, a fiber that assumes a gel-like consistency when exposed to water.

Inulin has the effect of increasing satiety, or the sensation of fullness. This cuts your craving for foods. I've tried it recently and I prefer it over glucomannan, another soluble fiber for satiety.

The people at Stonyfield Farms have been adding inulin to their yogurts from some time. The nutritionist at the company tells me that there's 2-3 grams of inulin per 6 ounce container of their yogurt.

You can also find inulin as a supplement that you can add to foods, available from some health food stores and online supplement companies. I came across a neat product called Fiber Choice that's now being distributed widely throughout the U.S. I tried their Weight Management version. It was a delicous strawberry taste. The label says take two chewable tablets twice a day, but I found that two tablets three times a day somewhat better. It's best taken around 30-60 minutes prior to each meal and it causes you to be fuller with less food. One caution: It'll cause loads of gas, especially in the beginning. For that reason, you might try starting with a smaller dose, or start on the weekends when you have the option of some privacy!

More info on the Fiber Choice product can be found at their website, http://www.fiberchoice.com.

Disclaimer: I have no relationship with the manufacturer of this product. I'm simply passing on some thoughts on my experience with this interesting possibility for weight loss.

Will you recognize the truth when you see it?

Do you ever wonder that, if the truth were given to you, that you'd recognize it as such? Or would you dismiss it as just another bunch of nonsense?

After all, you and I live in the Information Age. It means that we have access to mountains of information like never before in human history. But it also means that the truth is often drowned out by an avalanche of mis-truths, sales pitches and marketing, and just plain nonsense.

This struck me the other day when I was talking to a patient.

64 years old with a high heart scan score placing her at significant risk, she looked confused. I'd just described the multitude of causes of coronary plaque that we'd uncovered. The heart scan alone had been a shocker.

"I don't understand. My doctor told me that I had nothing to worry about. I've known him for years and he knows me really well. He did a stress test. That was fine. I don't get all this other stuff you're telling me--lipoprotein whatever..."

Despite my efforts to help her gain an understanding of our intensive approach, she just became increasingly more frustrated. "I just don't think I can do this."

That's the last I've heard from her. As far as I know, she's returned to the comfort of her family doctor who has reassured her over the years. And perhaps there's some good in that. But I do fear for the day when, unexpectedly, she suffers some catastrophe that we told her was coming sooner or later unless real preventive efforts were started.

You could say that she failed to recognize the truth when it was given to her-- boldly, unadorned, and with far greater scientific certainty than the casual reassurances she was accustomed to. But, unfortunately, that's all that some people want.

Don't neglect the basics in your heart disease reversal program

Carl loved new ideas and novel approaches. You could tell by the sheer number of nutritional supplements he took. His list had grown to 18 different supplements over the past two years.

Carl came to me for coronary plaque regression. Lipoprotein analysis did uncover several previously unsuspected abnormalties, most notably small LDL particles and lipoprotein(a). In addition, Carl's LDL cholesterol ranged between 111 mg-156 mg and he was clearly hypertensive, with systolic blood pressures consistently around 150-160. (Recall that people with Lp(a) are more prone to hypertension.)

Carl was more than willing to have his lipoprotein(a) reduced. We did so with niacin and testosterone and the level dropped to near zero. Likewise, we corrected his small LDL pattern with niacin, fish oil, and a reduction in processed carbohydrates.

But Carl really resisted doing much about his LDL cholesterol and high blood pressure. I got the sense that these "boring" issues simply didn't interest him. After all, LDL cholesterol and blood pressure were the stuff of TV commercials and the popular conversation propagated by drug companies.

Carl's follow-up heart scan, however, finally persuaded him: a 24% increase in one year, likely due to the neglect of the basic issues.

I liken Carl's case to being like the teenager with a new car who polishes the paint to a bright finish, puts new wheels and tires on it, spruces up the interior with various doodads--but then fails to change the oil. Sometimes it's the most basic issues that can diminish your success.

Issues like LDL cholesterol and high blood pressure aren't the most glamorous, but they do count in your coronary plaque control program.

Is your doctor a hospital employee?

There's a disturbing trend that's growing--silently but rapidly.

In Milwaukee, three hospital systems compete for the local health care dollar. To gain more control over revenues and the routing of patients, the hospitals are aggressively hiring physicians to work for them. I've witnessed many of my cardiology colleagues, primary care doctors, and a substantial number of procedural specialists enticed by the offers made by hospital employers.

This phenomenon is not unique to Milwaukee but is being used in many, perhaps most, major cities in the U.S.

This means that physicians are employees of the hospital. That way, employee-physicians are obliged to use only the hospital system that employs them. In the old days, your doctor could use any hospital he/she desired, depending on the quality, location, facilities, etc. Now, many physician-employees are given no choice but to use the hospital that pays their salary.

That by itself is not necessarily bad. But combine salary with incentives for bringing in patients for hospitalization and procedures--that the rub. In other words, physician-employees are incentivized to generate more revenue for the system, just as employees in many other industries.

If you're a salesman for an insurance company, your job is to bring in more business. If you're a worker on an auto production line, you're expected to meet certain quotas. These same principles are now being applied to many physicians.

How does this affect you? Well, if your physician--especially procedure-driven specialists like cardiologists, general surgeons, orthopedists, etc.--is a hospital employee, BEWARE! Do you really need that procedure, or is your doctor suggesting you have a procedure because it will add to his track record?

Prevention? In this model of health care, why bother? It certainly doesn't pay for a hospital to keep you well. Then why should your physician-employee?

Be careful who you're dealing with. If your physician is a hospital-employee, don't bet on getting preventive care. It's more likely you're that just a future source of revenue when it's time for your bypass operation, hip replacement, carotid endarterectomy, etc.

What more powerful argument is there for increased self-empowerment and information for health care consumers?
Does high cholesterol cause heart disease?

Does high cholesterol cause heart disease?

How often does someone develop coronary heart disease from high cholesterol alone?

Believe drug industry propaganda and you'd think that everyone does. Physicians have bought into this concept also, driving the $27 billion annual sales in statin cholesterol drugs.

In my experience, I can count the number of people who develop coronary disease from high cholesterol alone on one hand. It happens--but rarely.

That's not to say that cholesterol is not an issue. That rant populates many of the kook websites and conversations on the internet that argue that high cholesterol is a surrogate for some other health issue, or that it is part of a medical conspiracy.

The problem with conventional measurement of cholesterol is that it ignores the particle size issue: whether particles are large or small. Small LDL are flagrant causes of coronary atherosclerotic plaque. Large LDL is a rather meager cause. Simple cholesterol measurement also ignores the presence of other factors that lead to heart disease, like lipoprotein(a) and vitamin D deficiency.

Conventional total and LDL cholesterol do not distinguish between large and small particles, nor reveal the presence of other hidden patterns. An LDL cholesterol of 150 mg/dl, for instance, may contain 100% large LDL--a relatively good situation that by itself is unlikely to cause heart disease, or it might contain 100% small LDL--a very bad situation that is likely to cause heart disease. Just knowing that LDL is 150 mg/dl tells you almost nothing. In 2008, most people have some mixture of the two, particularly with the proliferation of "healthy whole grains" in the American diet, foods that trigger formation of small LDL.

The imprecision and uncertainty of conventional total and LDL cholesterol has provided ammunition for some to discount the entire cholesterol concept. And they are right to a degree: cholesterol by itself is indeed a lousy predictor of heart disease. But small LDL is a very reliable predictor of potential for heart disease. Dismissing the entire concept because the standard measurement stinks is not right, either.

It is therefore an unfortunate oversimplification to say that high cholesterol causes heart disease or that it doesn't. It can--but not always, depending on size and other factors. In my view, it is therefore irreponsible to treat total or LDL cholesterol without knowledge of particle size. I've seen this play out many times: Someone with an LDL cholesterol of 150 mg/dl but all large still gets prescribed a statin drug by his/her doctor. Or someone with an LDL of 100 mg/dl--generally "favorable" by most standards--is not treated but it is all small and the person is truly at high risk. (Also, knowledge that all LDL particles are small does not mean that statins are the preferred agent. In my view, they are not.)

Comments (15) -

  • Anonymous

    10/3/2008 4:41:00 AM |

    I've had no success lowering my very high LDL(350), can't tolerate statins..supposedly have combination of large and small LDL, 20-40% blockages per cardiac cath.My HDL (80), Trig.(70)are good, but still concerned since already show athrosclerosis. I'm 55, 100 lbs., and have had high LDL since a teen. Any suggestions? Thanks!

  • Anonymous

    10/3/2008 5:25:00 PM |

    Isn't inflammation the root cause of atherosclerosis ? Isn't cholesterol's role in heart disease only that it happens to be used as the material, with which the body repairs the lesions caused by inflammation ?

  • Steve

    10/3/2008 6:16:00 PM |

    excellent post. 1. if statins not preferred way to go for small LDL, what is- Niacin and elimination of grains? 2. How is it possible that a VAP test showed large Pattern A(by small margin)and two years later NMR shows nearly 100% small dense Pattern B?  Is one test better than the other? 3. Do genetics overwhelmingly determine pattern size?  I have eliminated all grains,sugars, starchy veggies to see if i can get my LDL to be large and fluffy.  Thank you.

  • Anne

    10/4/2008 5:17:00 PM |

    I am an example of someone with "normal" cholesterol and CAD. I was only 54 years old when my LAD blocked. I went on to bypass as I reblocked after each stent.

    In the past few years I have been looking into many of the other factors may have contributed to my  health problems and trying to optimize my health. Yes, coromary heart disease is so much more than elevated cholesterol.

  • Stan (Heretic)

    10/4/2008 5:37:00 PM |

    No it doesn't!

  • Peter

    10/5/2008 2:41:00 PM |

    Hi Dr Davis,

    Excellent post. The value of total cholesterol is irrelevant. While there is a VERY slightly higher cholesterol level in heart attack patients, the overlap with the normal population is such as to make total cholesterol level meaningless. Once it's meaningless and you can then look back to the initial work of Ancel Keys, who appears to have been the primary architect of the lipid hypothesis, and you can see it is based on this now clearly meaningless measurement.

    The very slight increase in TC in cardiac patients is explicable by the fact that glycation of the apoA particle inhibits its attachment to the LDL receptor. I would expect this to produce a slight rise in TC. You then have to pose the question as to which does most damage: persisting apoA containing particles due to glycation of their surface protein, or glycation of all of the body proteins by the same hyperglycaemia that affected the apo A protein. Using HbA1c as a marker of hyperglycaemia there is a reasonable correlation with CVD even within "normal" HbA1c levels in the EPIC study. Whole grains = hyperglycaemia. Hyperglycaemia = apoptosis of vascular endothelium. What more do you need for vascular damage?

    So, as the lipid hypothesis is based on TC and should have been stillborn or drowned at birth, where does particle size come in? We have the situation of good (HDL) cholesterol and bad (LDL) cholesterol to explain why TC is useless. Then we get good LDL (large fluffy) and bad LDL (small dense) to explain why total LDL (by calculation) is utterly useless too. We even now have good and bad HDL. Never mind good (small) VLDL and bad (large) VLDL to explain why some triglycerides are better/worse than others.

    Ultimately small dense LDL, large VLDL and HDL3 are strong markers of the metabolic syndrome. Hyperinsulinaemia and insulin resistance are the cornerstones of metabolic syndrome according to Reaven, who largely popularised the concept. The lipid changes are easily viewed as a consequence, not a cause, of metabolic syndrome. It is undoubtedly believable that sdLDL is stickier/more oxidisable than other lipoproteins, but that becomes unimportant if it's not there in the first place, ie no metabolic syndrome. This would, simply, explain why reducing wheat products works to reduce sdLDL, unless they are replaced by equally insulinogenic "wheat free" comparable junk foods based on non wheat sugar sources. If it turned out that purple spotted LDL, induced by eating blackberries, was stickier than sdLDL we would no doubt have a drive to eliminate blackberries or (more likely) develop a drug to remove the purple spots.

    Following your blog gives me the distinct impression that one day you really could become a cholesterol skeptic. Stranger things have happened.

    Peter

  • JayCee Botha

    10/6/2008 9:37:00 PM |

    Anonymous and Steve - I stronly believe in a propper low carb (note that I say LOW carb, and not NO Carb) way of eating. I would really like to suggest some awesome reading material. It is from dr. James E Carslon who wrote the book "Genocide. How your doctors dietary ignorance will kill you!!!". In the book he explains amongst other things the actual benefits of dietary cholesterol and how a low-carb way of eating will increase the ldl-particle sizes and bring down the triglycerides and dangerous VLDL.

    From a recent personal answer I got from him, he explained to me the benefits of adding dietary cholesterol from a biochemical point of view. I hope this helps in understanding that a correct dietary change can help.

    Here is what he said :

    OK, so what are the benefits of adding cholesterol to the diet? It's not only fascinating, it'll blow your mind. When we eat cholesterol containing foods, the cholesterol in the food we consume actually binds to an enzyme called HMG CoA reductase and inhibits its function. This enzyme is what's known as the rate limiting enzyme in cholesterol biosynthesis. This means that once this enzyme does what it's supposed to do, cholesterol will be made no matter what. By inhibiting the enzyme's function, choilesterol cannot be made. So eating cholesterol actually inhibts its own production.
    But wait, it gets even better.

    The cholesterol in the foods we eat is what's referred to as fat soluble, or lipophilic (or fat loving). Since cholesterol is lipophilic, it diffuses through not only the outer cell membrane, but the cell's=2 0nucleus membrane and attaches the the DNA. Guess where it attaches to on the DNA? It attaches to the sites on DNA WHERE HMG Co A IS MADE!!!!! That's right, so not only does the cholesterol in the food we eat attache and inhibit the function of the enzyme already present to make cholesterol; the cholesterol in the foods we eat also prevents the production of the enzymes needed to make itself. In biochemical speak, this is known as negative biofeedback.

    Eat more cholesterol, make less cholesterol. By the way, the only thing I've seen in eighteen years considerably raise the good cholesterol known as the HDL, is the consumption of more cholesterol. So EAT MORE CHOLESTEROL IT"S GOOD FOR YOU!

  • moblogs

    10/7/2008 12:11:00 PM |

    Inflammation is essentially the cause of heart disease isn't it?
    I'm not medically trained, but I assume small particle LDL is a signifier of crammed, broken up large particles - perhaps a long time accumulation of what was once sent to the skin hoping to be converted to D by UVB but didn't(there is a study that says British gardeners have lower cholesterol in the Summer which seems very interesting).
    The fact that statins work (albeit with alarming side effects), and that according to a Spanish study, that atorvastatin raises vitamin D some degree shows the problem isn't really cholesterol. That is erroneous cholesterol readings are the 'symptom' of either vitamin D deficiency or associated things that domino on to the ability for the heart to succomb to heart disease. As a rule I still think the general cholesterol hypothesis is a farce, not just because of the way the products are marketed but because it's only looking at one station on the tube system. 'High cholesterol causing heart disease' might be better termed as 'low vitamin D causes heart disease' because that's perhaps the root, or at least one root.

  • Steve L.

    11/14/2008 5:43:00 AM |

    Dr. Davis,

    First let me say a big thank you for your blog.  I follow your's, Jimmy Moore's and the Drs. Eades' blogs closely.  As a result of reading your book and blot, I just had my first heart scan at age 50, and was vert happy to hear zero calcium score.

    I do low carb nutrition (~50g/day), so my triglycerides were very low (28).  I've read that all LDL will be large with triglycerides that low (below 70).  Can you confirm that?  Would I be wasting my money on blood work to determine particle size?  HDL is 62, LDL 136.

    Steve L.

  • Wenchypoo

    4/9/2009 1:14:00 PM |

    Simple cholesterol measurement also ignores the presence of other factors that lead to heart disease, like lipoprotein(a) and vitamin D deficiency.

    Conventional total and LDL cholesterol do not distinguish between large and small particles, nor reveal the presence of other hidden patterns. An LDL cholesterol of 150 mg/dl, for instance, may contain 100% large LDL--a relatively good situation that by itself is unlikely to cause heart disease, or it might contain 100% small LDL--a very bad situation that is likely to cause heart disease. Just knowing that LDL is 150 mg/dl tells you almost nothing. In 2008, most people have some mixture of the two, particularly with the proliferation of "healthy whole grains" in the American diet, foods that trigger formation of small LDL.


    I'm looking for heart disease info that isn't related to cholesterol OR grain intake, because my cat has it--cats are obligate carnivores, and therefore do not take in grains unless fed commercially-prepared foods.  Mine do not--I make their food from scratch, using a UC Davis vet-designed diet recipe.  Cholesterol levels aren't a concern either, although I now know to have the SIZE of cells examined, as well as vitamin D levels checked.  As for anti-inflammatories, fish oil is part of the diet recipe.

    I'm going back to the vet for more blood work (now that I have more clues).

  • TedHutchinson

    10/1/2010 8:48:09 AM |

    Statins Do Not Decrease Small, Dense Low-Density Lipoprotein
    Free full text at link.
    In an observational study, we examined the effect of statins on low-density-lipoprotein (LDL) subfractions.
    Using density-gradient ultracentrifugation, we measured small, dense LDL density in 612 patients (mean age, 61.7 ± 12.6 yr), some with and some without coronary artery disease, who were placed in a statin-treated group (n=172) or a control group (n=440) and subdivided on the basis of coronary artery disease status.
    Total cholesterol, LDL cholesterol, apolipoprotein B, and the LDL cholesterol/apolipoprotein B ratio were significantly lower in the statin group. However, the proportion of small, dense LDL was higher in the statin group (42.9% ± 9.5% vs 41.3% ± 8.5%; P=0.046) and the proportion of large, buoyant LDL was lower (23.6% ± 7.5% vs 25.4% ± 7.9%; P=0.011). In the statin group, persons without coronary artery disease had higher proportions of small, dense LDL, and persons with coronary artery disease tended to have higher proportions of small, dense LDL.
    Our study suggests that statin therapy—whether or not recipients have coronary artery disease—does not decrease the proportion of small, dense LDL among total LDL particles, but in fact increases it, while predictably reducing total LDL cholesterol, absolute amounts of small, dense LDL, and absolute amounts of large, buoyant LDL. If and when our observation proves to be reproducible in subsequent large-scale studies, it should provide new insights into small, dense LDL and its actual role in atherogenesis or the progression of atherosclerosis.

  • buy jeans

    11/3/2010 6:19:10 PM |

    The imprecision and uncertainty of conventional total and LDL cholesterol has provided ammunition for some to discount the entire cholesterol concept. And they are right to a degree: cholesterol by itself is indeed a lousy predictor of heart disease. But small LDL is a very reliable predictor of potential for heart disease. Dismissing the entire concept because the standard measurement stinks is not right, either.

  • Mary

    1/25/2011 8:42:22 PM |

    For years I suffered from high cholesterol and was almost permanently on statin medication. I come for a family with a strong history of heart disease and I personally believe that high cholesterol can cause heart disease. Thankfully I now have my cholesterol under control but it has been hard work, and I done it the natural way, as I suffered from the side effects statins cause.

    How To Lower Cholesterol Without Medication

  • Anonymous

    3/12/2011 8:55:30 AM |

    About eighty percent of our cholesterol is produced by the liver and the rest depends on our diet. Foods such as red meat and butter are rich in cholesterol where as those from plant origin have very little or no cholesterol at all. The control of cholesterol in our body is done by the liver. I think,more can be found out from:
    http://www.heart-consult.com/articles/how-cholesterol-affects-heart

  • doug

    5/9/2011 8:52:46 PM |

    exactly!!!!!

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