How important is high blood pressure?


Control of blood pressure is crucial for coronary plaque control and stopping your heart scan score from increasing.

Dr. Mehmet Oz (of Oprah fame and a cardiac transplant surgeon at Columbia University) made graphic point of this on the ABC TV news show, 20/20, last evening on an episode called "Our Bodies: Myths, Lies, and Straight Talk". (See a summary on the ABC News 20/20 website at http://abcnews.go.com/2020/story?id=2109291&page=1)

Although I believe he somewhat overstated the case for hypertension (proclaiming "If you're going to remember one number, if you're going to focus and fixate on one number in your entire health profile, it better be your blood pressure"), he made the point that a blood pressure of 115/75 is what you should have for optimal health.

I couldn't agree more. Unfortunately, the old advice that desirable blood is 140/90 or less is absolutely wrong. At this level, we see flagrant increases in heart scan scores. We also progressive enlargement of the thoracic aorta, the large vessel that leaves the heart and branches to provide the major arteries of the body. Growth of the aorta to an aneurysm is also common at these formerly acceptable blood pressure. (The diameter of your aorta in the chest is an easily obtainable measure on your CT heart scan.)

The blood pressure you need for halting and reversing plaque growth on your heart scan is indeed 115/75 or less. (Not so low, however, that you're lightheaded.) This is the blood pressure that you were meant to have evolutionarily. It's also the blood pressure that helps tremendously in keeping your aorta from enlarging.

Watch for an upcoming exhaustive report on blood pressure and its plaque-raising effects and how to reduce it using nutritional strategies on the www.cureality.com membership website.

Is your doctor in cahoots with the hospital?

I got a call from a doctor about a patient we've seen in past.

"I've got Tricia in the office. She's been having some kind of chest and abdominal pain. I think it's esophageal reflux, but just to be safe I'm sending her to the hospital."

I advised this physician that, given Tricia's low heart scan score, she was unlikely to be having a coronary "event" like heart attack or unstable symptoms. It wasn't impossible, but just highly unlikely.

As the patient was without symptoms at the moment and had driven herself to his office, I offered to perform a stress test immediately. (Though stress tests are of limited usefulness in people without symptoms, they can be useful provocative maneuvers in people with symptoms of uncertain significance.)

The doctor declined. Tricia was, after all, in his office and he was responsible for any decisions despite any objections I voiced. Well, Tricia was directed by her doctor to go to a local hospital, though one with an especially notorious reputation for putting virtually anyone they can get their hands on through as many procedures as possible.

As you might guess, this doctor was closely associated with this hospital. He and his colleagues obtain incentives (or are penalized) if they do not generate revenue-producing procedures for the hospital.

So, guess what? Tricia ended up with several procedures, all of which yielded nothing--except $30,000 in revenues from Tricia's insurance company.

I harp on this deplorable state of affairs because it is utterly, painfully, and shamefully TRUE. Just look at the hospital and you'd better brace yourself for a series of tests that could cost you the equivalent of a nice 3 bedroom home. If they were truly necessary after the failure of preventive and other simple efforts, fine. But, all too often, they are driven by profit motives.

Could I have stopped this somehow from occurring? After all, Tricia was reasonably aware of the way we do things around here. I fear that even this failed to serve Tricia well. But I remain hopeful that, as we build broader awareness of these issues, that more and more people and physicians will stand up and refuse to tolerate the status quo.

Where is the Track Your Plaque program going?

I spend a lot of time worrying about how people can be helped to navigate through this program.

Take, for instance, the man in rural Texas who, while traveling in Dallas, got a heart scan on a whim. His score was 990. When he took the report back to his doctor, he got a smirk--and that's all. When he came to the Track Your Plaque program, he lacked a physician advocate to help him.

Or the woman from Florida who sought opinions from two reputable cardiologists for her heart scan score of 377. Both advised her that she needed a heart catheterization--despite her lack of symptoms, her 5-day-a-week exercise program, and normal stress test. She also lacks a physician advocate who acts on her behalf, helping her achieve success, rather than just churning her for money from hospital procedures.

For people like this and for others, I see the Track Your Plaque program evolving in several directions:

1) An online clinic--You enter and we take your "hand" and lead you step by step through the process, not only at the beginning, but over the months and years. This would help clear up some of the confusion and zigzags that some people experience trying to navigate through the program.

2) Develop physician and non-physician partners--The woman in Florida, for instance, could be referred to a doctor nearby who understands the program and is able to assist her. At present, this is virtually impossible because of the bias towards heart procedures, drugs as the sole treatment for heart disease risk, and the superficial physician-patient relationship. The majority of practicing physicians just don't understand the program despite the fact that it is based on sound clinical and experimental data. But it will in time.

Looking back, we've come a long way. I remember first having patients undergo heart scans 10 years ago. My colleagues laughed or called it "silly". The general public didn't know what they meant.

Now we're talking about how to broadcast the most powerful heart disease prevention program available in the world to a larger audience, but making it easier and more accessible. Mass media like Oprah's two hour-long spots helped, but we need to make the next leap. Not just identifying hidden heart disease to feed the hungry cardiovascular hospital procedure monster, but to educate/inform/empower the public on what to do with the scan once they've had it.

Who cares about triglycerides?

Walter's triglycerides were 231 mg. His LDL cholesterol was "favorable" at 111 mg, HDL likewise at 49 mg.

"Everything looks good," his doctor declared.

"Do you think the triglycerides are okay, too?" Walter asked.

"Well, the guidelines do say that triglycerides should be less than 150, but I believe you're close enough. Anyway, triglycerides don't really cause heart disease."


When I met Walter, I made several comments. First of all, in light of his heart scan score of 713, none of his numbers--HDL, LDL, or triglycerides-- were acceptable. But the triglycerides were glaringly and terribly too high.

Why? What exactly are triglycerides?

Triglycerides are a basic fat particle that, though they do not cause heart disease directly, trigger the formation of an array of abnormal lipoprotein particles in the blood that are among the most potent causes of heart disease known.

These abnormal lipoprotein particles include small LDL, VLDL, and IDL (intermediate-density lipoprotein--a really bad pattern). Excess triglycerides also cause HDL to drop. They also cause a distortion of HDL structure, causing the particles to become abnormally small. Small HDL is also useless HDL, unable to provide the protection that HDL is designed to do.

So Walter's elevated triglycerides are, in reality, a substantial red flag for an entire panel of abnormal particles that contribute to the growth of his coronary plaque.

So, if you get this kind of commentary on your triglycerides, ask for another opinion. (Track Your Plaque Members: Also see Triglycerides: Mother of meddlesome particles at http://www.cureality.com/library/fl_dp002triglycerides.asp.)

Total cholesterol and heart scans

Andy was fearful of heart disease in his life. At age 52, he'd already had four CT heart scans--one each year on or near his birthday.

Yet, when I looked at Andy's scans, his scores had been increasing 20-24% per year. Each and every score was greater by 20% or more over the previous.

So I asked Andy what steps he had taken to stop this relentless progression. "Well, I've always been real health conscious. But ever since my first scan, I really started sticking to a healthy diet, exercising nearly every day, and I take a bunch of supplements."

"What did your doctor advise?" I asked.

"Well, Dr. ---- said that nothing needed to be done, since my total cholesterol was always below 200."



Men's Health magazine's fabulous story about the folly of using total cholesterol to gauge heart disease risk.




Aaaauuuggghhh!! Wrong!

This man was, in fact, at rapidly escalating risk for heart attack. This rate of growth simply can't continue forever without igniting this bomb.

A total cholesterol below 200 is meaningless, as Andy's increasing coronary plaque proved. For instance, you can have a total cholesterol of 165 mg but with an HDL cholesterol of 27 mg. This would constitute very high risk for heart disease despite the low total cholesterol. The low HDL pattern is among the most common reasons for a misleading total cholesterol. Small LDL, high triglycerides, and lipoprotein (a) are other frequent reasons.

Andy, run the other way! Do not heed this doctor's advice! You need a solid answer to the question: Why exactly do I have coronary plaque in the first place?

Then, agree on a treatment program that corrects your specific causes.

Cardiologists out of touch

This weekend, I'm fulfilling some responsiblities I have every so often to some of the local hospitals. It gives me a chance to interact with many of my colleagues who are likewise "on call" for the weekend.

I tried to strike up several conversations with colleagues about how they were managing heart disease prevention. I received blank stares, puzzled looks, indifference. One colleague declared that 80 mg of Lipitor is all you need to know.

These same colleagues are the ones scrambling for the heart attack patients in the emergency room, climbing over one another for consultation in the hospital for patients with chest pain and heart failure. They're consumed with expanding the range of procedures they can perform.

Carotid stenting is hot. So is stenting of the leg arteries. Defibrillators have been a financial bonanza. Opportunities abound on how to add these procedures to a cardiologist's abilities.

But heart disease prevention? How about heart disease reversal?

Frankly, I'm embarassed by my colleagues' lack of interest. Imagine we had a cure for breast cancer--not a palliative therapy that just slows the disease down or prolongs life, but actually cures it once and for all. I would hope that all physicians and oncologists would learn how to accomplish this. What if instead they focused on learning new ways to remove breasts, administer new toxic chemotherapies, etc. but ignored the whole idea of cure?

This is what is happening with coronary plaque reversal. The answer is right in front of them, but the vast majority (99%) of cardiologists choose to ignore it. After all, prevention and reversal simply don't pay the bills.

That means that, in 2006, you simply cannot rely on your cardiologist to counsel you on how to achieve regression or reversal of coronary plaque. How about your internist, family physician, or primary care doctor? Well, they're busy doing pneumovax injections, Pap smears, managing knee and hip arthritis, low back pain, diarrhea, headaches, sinus infections and . . yes, dabbling in heart disease prevention.

And, for the most part, doing a miserable job of it. What you generally get echoes the drug manufacturers pitch: Take a statin drug, cut the fat in your diet.

Until the majority of doctors catch on, you're going to have to rely on sources like the Track Your Plaque program for better information.

What if your lipoproteins are perfect?



Sandy is a 56-year old woman--fit, slender, physically active, with no bad habits. A retired teacher, she has time to devote to her health. She bikes several days per week, mountain bikes, walks, and takes fitness classes. In short, she's the picture of perfect health.

Her heart scan score was not terribly impressive: 41. However, at her age, this modest score placed her in the 77th percentile. This suggested a heart attack risk of around 2-3% per year.

So we measured Sandy's lipoproteins. They were shockingly normal. In fact, Sandy is among the very rare person with absolutely no small LDL particles. All other patterns were just as favorable, including an HDL in the 80s.

This may seem like good news, but I find it disturbing. People are often initially upset by seeing multiple abnormal lipoprotein patterns. But lipoprotein abnormalities are the tools that we use to gain control over coronary plaque.

So what do we do when there are no abnormalities?

There are several issues to consider:

1) Your heart scan score reflects the sum total of your life up until that point. What if you were 20 lbs heavier 10 years earlier and your lipoproteins were abnormal during that period? Or you smoked until age 45 and quit? As helpful as they are, lipoproteins and related patterns are only a snapshot in time, unlike the heart scan score.

2) You have a vitamin D deficiency. This is unusual as a sole cause of coronary plaque. Much more commonly, it is a co-conspirator.

3) The heart scan is wrong--highly unlikely. Heart scans are actually quite easy, straightforward tests. (The only time this tends to happen is when scoring that appears in the circumflex coronary artery is actually in the nearby mitral valve. This really occurs only when there's very minimal calcium in the valve.)

4) There's a yet unidentified source of risk. Probably very rare but conceivable. For instance, there's an emerging sense that phopholipid patterns may prove to be coronary risks. One clinically available measure that we've not found very useful is phospholipase A2, known by the proprietary name "PLAC" test. (See http://www.plactest.com for more information from the manufacturer/distributor of the test.) But there's probably lots of others that may prove useful in future.

How often does it happen that someone fails to show any identifiable source for their coronary plaque? I can count the number of instances on two fingers--very unusual. (Thank goodness!)

Sandy's case is therefore quite unique. How should we approach her coronary plaque? In this unusual circumstance, lacking a cause, we tend to introduce therapies that may regress plaque independent of any measurable lipoprotein parameters. But that's a whole new conversation.

Fly to India for a bypass operation?


In the June 19, 2006 issue of People Magazine, there's an article called "The Doctor is in . . .INDIA". The report talks about how, with health care costs in the U.S. spiralling out of control, more and more Americans are leaving the country to have their procedure performed.

They tell the story of Mr. Carlo Gislimberti of New Mexico and cite these numbers:

Heart Surgery
Cost in U.S.: $200,000

Cost in India: $10,000


Mr. Gislimberti opted to have his coronary bypass operation in India for cost reasons.

But the People magazine report left out one other option: The Track Your Plaque program: $39.00

Do your part to save ballooning health care costs: Engage in a truly powerful program of heart disease prevention like the Track Your Plaque program. The cost difference is laughably huge. And you won't require a 12-inch chest incision.

Follow conventional guidelines and guess what? You're going to have a heart attack. Follow the American Heart Association diet and you'll have heart disease.

Cut to the chase. The only program that is able to detect, track, and control coronary plaque better than any other process I know of is this program.

Note: I am not proposing that a heart disease prevention program like Track Your Plaque can replace a procedure like coronary bypass when a dangerous situation has developed. The Track Your Plaque program is designed to be implemented in the years before heart surgery is required. That's when you have the greatest control over your fate.

Surprise: Heart scan score reversal

Gene is a jovial, fun-loving railroad worker who didn't take anything too seriously--including his heart scan score of 767.

This score placed Gene solidly in the 99th percentile (in the worst 1%). It came as no surprise to Gene. After all, his father died at age 36 of a heart attack and Gene's brother died at 60 of a heart attack. So Gene took life as it came and long ago decided not to fret about his fate.

But Gene's wife prodded him and prodded him to get the heart scan. That's when I met him.

Of course, Gene had been prescribed Lipitor by his doctor for a somewhat high LDL cholesterol. Our assessment uncovered several additional patterns including lipoprotein (a), small LDL, a pre-diabetic tendency, and a severe deficiency of vitamin D.

At 224 lb and 5 ft 6 inches in height, I felt that Gene was at least 40 lbs overweight.

One year later and with reasonable correction of all his patterns except weight loss and Gene's heart scan score was 590--a reduction of 23%!

Gene was thrilled, as was I. But, frankly, I was also surprised. Dramatic regression of coronary plaque tends to not occur so readily as long as pre-diabetic patterns persist and weight is not controlled.

The lesson: Often the only way to tell if you've achieved control or regression of coronary plaque is to have another heart scan. The tremendous variation in human responses never ceases to amaze me.

Call me when you're having chest pain


I met a patient, Anna, yesterday. She was quite frustrated and frightened.

At age 50, Anna suffered a heart attack and received a stent to her left anterior descending coronary artery. What she found upsetting is that, because several members of her family had suffered heart attacks in their 40s (Dad--heart attack at age 45, paternal uncle--heart attack age 40, and even another uncle with heart attack in his late 20s), she had repeatedly asked her doctor whether she was okay.

She received the usual array of false assurances: "You're feeling fine, right? Then don't worry about it." "Look. Your cholesterol is in the normal range. Even your cholesterol/HDL ratio is fine." "Women don't get heart disease until later in life."

All proved absolutely false. As we talked, Anna exclaimed, "I think what I've been told all along is that we'll take you seriously when you finally have a heart attack!"

She's exactly right. The vast majority of times, heart disease is discovered by accident, usually because of an "event" like heart attack. This is like changing the oil in your car when it finally breaks down--it's too late.

CT heart scan, followed by lipoprotein testing and associated values, then correction of your specific causes. It's that simple.
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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