An Interview About Heart Disease That May Change Some Of Your Preconceptions

See these numbers?
Total cholesterol: 248 mg/dl
LDL cholesterol: 171 mg/dl

They may, by themselves, have very little to say about your actual coronary plaque buildup.

Dr. Davis from The Heart Scan Blog was recently interviewed by Jimmy Moore on his Livin' La Vida Low-Carb™ Blog.They discussed:

• Typical Cholesterol Panel vs. Lipoprotein Testing
  
• Saturated Fat Intake
  
• The Atkins Diet
  
• Heart Scans

The entire interview is on Jimmy Moore's blog:
Davis: Wanna Cut Plaque In Your Arteries? Slash Your Carbohydrates!

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Here were a few passages that stood out for me:

From Question 3:

Moore: Why is [LDL cholesterol] such a poor way to gauge heart disease risk?


Dr. Davis: It's no secret: LDL cholesterol has proven a miserable failure as a detector of coronary heart disease.

Abundant clinical trial experience has borne this fact out: LDL cholesterol of the average American: 132 mg/dl; average LDL cholesterol of someone suffering a heart attack: 134 mg/dl - they’re virtually indistinguishable.

Cholesterol is a predictor on a statistical basis, but fails miserably when applied to a specific individual.

From Question 4:

Moore: What’s wrong with the low-fat, low-salt, low-cholesterol (DASH) diet recommendation that Dr. Ornish and virtually every other medical professional prescribes to people who are developing or already have heart disease?

Dr. Davis: The misguided advice offered to most people is that a low-fat diet reduces cholesterol and heart disease. This is simply untrue for the majority of people.

In fact, the opposite is true: a low-fat, high-carbohydrate diet filled with wheat products like whole grain bread, wheat crackers, pretzels, fiber breakfast cereals, and wheat pasta raise cholesterol. Corn starch-containing products, white rice, potatoes, and processed carbohydrates are similarly to blame.

They raise small LDL cholesterol particles, the worst form of cholesterol of all. While large cholesterol particles are rather harmless, the small cholesterol particles are the ones behind heart disease in over 70% of cases. And it's small LDL cholesterol that is hugely magnified by high-fiber, high-carbohydrate diets.

From Question 8:

Moore: Just so we're perfectly clear about what you are saying, am I right in assuming you believe people should stop worrying about their cholesterol numbers because they really don’t have a bearing on heart disease? How about those who are taking cholesterol-lowering statin medications like Lipitor, Zocor, and Crestor, among many others to lower their “high” cholesterol? Is there a reason for them to remain on those drugs in light of what we now know about heart disease?

Dr. Davis: The cholesterol reducing drugs do have role - unfortunately, the majority of people are put on these drugs for the wrong reasons.

Let me explain. Someone will come in because of a reportedly high cholesterol. We do more testing and discover that the majority, say, 90%, of the cholesterol particles are small. This pattern is very likely to contribute to formation of plaque in the arteries. It also responds exceedingly well to a reduced carbohydrate diet. Many, many times, a person with this pattern will follow a diet that slashes carbohydrate content and cholesterol levels drop like a stone. In this instance, statin cholesterol drugs may be entirely unnecessary.

Another exception: A person with a high cholesterol that is not truly high. When you are provided an LDL cholesterol from your doctor’s office, it has not been measured, it has been estimated. The crude estimation is based on a calculation called the "Friedwald equation," an equation derived in the 1960s when new technology for testing was not yet available.

It sounds ridiculously simple, but simply measuring cholesterol can provide insights that can often suggest that a statin cholesterol drug is not necessary. The more sophisticated testing is called "lipoprotein testing."

From Question 9:

Moore: Who or what do you believe is driving this heart disease “business”?

Dr. Davis: Performing heart procedures pays big money. Prevention of heart disease does not.

Physicians and hospitals ... operate businesses that are meant to profit from treatment of disease. ... Put in a stent and reap about $2000 to the cardiologist, $25000 or more to the hospital. Perform a heart bypass operation, and the physician gets at least $5000, the hospital $70-100 thousand.

Prevent a heart attack and you get paid . . . maybe a couple of hundred dollars for several hours work.

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A point Dr. Davis drove home here for me was the rising significance of small, dense LDL cholesterol in the formation of arterial plaque ... and the waning significance of LDL alone.

LDL cholesterol is especially nebulous as a indicator for coronary risk:

1. When that LDL-C amount is estimated, not measured. This is a point Dr. Davis makes often on his blog. The estimate, as I understand it, is provided by the Friedewald equation:
   LDL = TC - HDL - TG/5
   That is, LDL cholesterol = Total cholesterol, minus HDL cholesterol, minus one-fifth of Triglycerides. TG/5 is an estimation for VLDL. All concentrations in mg/dl.
   
   
2. When that LDL amount is not considered together (as a ratio) with other cholesterol fractions and fats in the blood.
   This is a reason why total cholesterol (TC), by itself, also doesn't say much. For example, if your TC is in the desirable range (less than 200 mg/dl), but that portion of it that is HDL is relatively low, that would be a worse atherosclerotic scenario than if HDL's contribution was higher.

The development of atherosclerotic plaque involves many players. One player I've been reading about is lipoprotein(a) or Lp(a) for short. LP(a) is a particle of LDL attached to a carbohydrate-rich particle that contains a specific protein: apolipoprotein(a) or apo(a) for short.

Some things about Lp(a):

1. It responds very weakly if at all to statin drugs.
   
2. The attached protein, apo(a), causes the whole Lp(a) complex to behave in a pro-atherosclerotic way. More on that later.
   
3. The Friedewald-equation-estimate of LDL has buried in it the LDL contained in Lp(a). If your statin therapy is not producing desirable outcomes, it may be that statin-resistant Lp(a) makes up a sizable portion of your LDL.

There's a whole lot more about Lp(a) and other lipoproteins on Dr. Davis' blog.
For some basic information about cholesterol, spurred by Melinda's question, "Are the "small LDL" cholesterol particles the same as VLDL?", see my post, Serum Cholesterol Basics.


A question I have after reading the above interview:
How do insurance companies weigh in? Do they make more money in premiums, deductibles, and copays than they put out in invasive heart procedures? (It would seem they do, as they continue to prioritize pay-outs for these procedures over prevention methods.)

One thing I like about Dr. Davis ... He's an optimist. His eyes are always open. And for him, as I see it, the answer to a reduction in heart disease is not static. It's dynamic, a collaborative journey.
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