Report from Washington II

Today's discussions at the Society for Cardiovascular Computed Tomography (SCCT) focused on atherosclerotic "plaque characterization".

As CT scanners get better and better at imaging the various components of plaque, some fascinating issues emerge:

--CT heart scans provide insights into what exactly is contained in an individual's atherosclerotic plaque that are not often provided even during heart catheterization. In other words, CT heart scanning is, in many instances, superior to heart catheterization, since it provides images of the artery wall, not just the internal contents.

--Progression (i.e., increase) in heart scan score is a powerful predicter of heart attack risk. Dr. Matthew Budoff of UCLA argued persuasively that the annual rate of increase in score is probably the most accurate measure of risk available, superior to cholesterol and calculated measures like the Framingham risk score.

--Coronary calcium scoring remains the best method to gauge total plaque throughout the entire coronary tree. In a person free of symptoms, the risk of a cardiac "event" (heart attack, death, procedures) is low and additional imaging (like CT angiography) is generally unnecessary.


Dr. Budoff, among the true thought leaders in CT heart scanning, also recounted his perspective on the history of heart scans. He noted that the questions asked through the years have evolved:




1995-2000 Should we do coronary calcium scans?

2000-2002 Do high or low risk patients benefit from coronary calcium scoring?

2003-2004 What is the better scanner, EBT or MDCT?

2006 How often should we perform coronary calcium imaging?


I believe that Dr. Budoff summarizes wonderfully where the Track Your Plaque programs fits into the overall scheme of things: Serial (repeated)CT heart scans to gauge progression or reversal is the wave of the future. We shouldn't just be interested in identifying persons at risk for heart attack. We should also be interested in showing the person at risk exactly how to reduce or eliminate that risk.

Report from Washington





I'm presently attending the Society for Cardiovascular Computed Tomography meetings in Washington, DC, along with 500 of my colleagues. It's exciting to see how interest in CT scanning for heart disease has balloonned in the past couple of years.

Several trends are noticeable today, based on the content and tone of the discussions:

--CT scanning of the heart, and imaging in general, is just getting started. In other words, the capabilities for CT scanners and other devices to detect heart disease (coronary and otherwise) are where the gasoline engine was in the 19th century. Scanning is getting faster, easier, safer, and more precise. Just as few people in 1905 could have predicted that automobiles would be computer-enhanced, high-speed, ubiquitous devices with several per household, the potential for CT imaging for heart disease is truly in its infancy.

--CT coronary angiography (so-called "64-slice CT scans") are not screening tests for hidden coronary disease in people without symptoms. I was grateful that this point has been made and reiterated by several speakers, as this is consistent with our views. Simple CT heart scans for coronary calcium scoring, in contrast, are screening tests. When the radiation exposure of CT angiograms are reduced to tolerable levels, then they may be used as screening tests. We are probably 3-4 years away from this point.

--Both stress testing and heart catheterizations will be partially replaced by CT scanning. In particular, over the next decade, you will see a dramatic drop in unnecessary catheterizations, i.e,, far less people saying "I had a heart cath but they told me that it was normal."


There has been heavy focus on applications of CT scanning for acute settings, particularly the emergency room and hospitals.

What has surprised me is that there is virtually no conversation whatsoever about the preventive uses of CT heart scanning. So far, only Dr. Daniel Berman of UCLA has shown that he has "seen the light": CT scans are a crucial tool for identification of early coronary plaque, and this tells us whether prevention is necessary and with what intensity.

There has been, however, no discussion at all about quantification of plaque in a program of reversal. Perhaps that should come as no surprise, given the imaging-technology focus of this convention. For most of my colleagues, prevention is also not terribly interesting. Identification and treatment of acute disease like impending heart attack is.

Of course, applying the information from your CT heart scan to empower you in a program and reversal is what the Track Your Plaque program is all about. I hope you see the light. I admit that it's not always easy to follow what we are advocating here. Perhaps not too different than telling someone in his horse-drawn buggy that one day he'll be driving a sleek car with onboard computerized mapping, air-conditioning, and micro-chips to modulate engine performance. He's probably tell us we're nuts.

I'll continue to update if any news relevant to our interests crops up in these meetings.

What about the Track Your Plaque failures?

I’d love to tell you that the Track Your Plaque program track record is of 100% success. It’s not.

It is very successful. But we’ve had some people who have failed and failed BIG. These are the people who've undergone bypass surgery, received one or more stents, or had heart attacks. Lesser failures are the people who’ve had large, undesirable increases in heart scan scores of >30% in one year. (The expected rate of increase in your heart scan score without preventive efforts is 30% per year, on average.)

What can we learn from those failures? There were several characteristics that stand out among this small group:

· Non-compliance--meaning they just didn’t stick with it. They started out right but then rapidly lost interest in maintaining all the pieces of the program and neglected their fish oil, niacin, gain weight, etc. Matthew did this and ended up with three stents to his left anterior descending. His slow start was due to skepticism that the program worked and just plain forgetfulness.

· Extreme stress--One of our earliest failures was a 38-year old man whose heart scan score doubled in one year, despite doing everything right. But three family members, all close to him, died within the space of six months, including his mother and a brother. I regard this as one of those instances in which we were powerless, unfortunately, though it is a graphic example of the power of unresolved stress and grief.

· Having a “better way”--These are the couple of people who were convinced that they had a better way to control their heart scan score. David firmly believed that his two dozen supplements and exercise program would drop his score. Instead, they permitted a 42% increase. Lee relied exclusively on chelation, along with several supplements of his own design. Lee had three-vessel bypass surgery.

· Starting too late--Gerome started with a score of 1179, but also was having chest pressure with emotional stress. His stress test was abnormal, with the entire upper half of his heart not receiving blood with exercise on a stress nuclear study (“anterior ischemia”). Gerome received four bypass grafts. Unfortunately, Gerome never really had a chance to engage in the Track Your Plaque program, since his health and safety were in jeopardy as soon as he started.

Have we had any big failures of people who did everything right, were compliant, were not subject to extreme stress (more than just job stress, or financial worries), didn’t neglect the basic requirements of the Track Your Plaque program, and had sufficient time (at least 6 months to 1 year)? No, thankfully, we have not.

No one who has stuck to the program has had a big failure.

Be smarter than your cardiologist

“Do you need a stent?”

Sad to say, but that sentence condenses the wisdom of over 90% of practicing cardiologists.

Prevention of heart disease means take Lipitor or some other statin and cutting the saturated fat in your diet. That’s it. Maybe throw in exercise.

Regression of coronary plaque? That phrase has only entered the conversation since the AstraZeneca-supported trial of Crestor succeeded in achieving 8% regression of plaque (Track Your Plaque Members: See News) as demonstrated by intracoronary ultrasound.



In other words, in the minds of my colleagues, it can’t be true until a drug company tells them it’s true. It’s beyond me why this brainwashing of otherwise intelligent people has occurred, but it is blatantly evident in practice.

Fish oil is another example. The spectacular benefits of fish oil have been known for 20 years. But only recently has it become a “mainstream” practice to recommend fish oil, largely because a drug manufacturer has put a preparation through the rigors of FDA approval (Omacor) and is now marketing directly to physicians. All of a sudden, fish oil is a good thing? No, it’s just achieved legitimacy in the eyes of practitioners because it graces marketing literature.

If you’re reading this, you’re likely interested in coronary plaque regression using the only tool available for you to measure, track, and regress coronary plaque: CT heart scans. Intracoronary ultrasound will achieve the same goal, but it is an invasive procedure performed at heart catheterization, involves threading a wire and imaging probe all the way down the artery, involves real risk of tearing the inner lining of the artery, and is costly (around $14,000-$20,000 for the entire package). Do it every year? That’d be nuts.

If you’re thinking about coronary plaque regression, using fish oil, concerned about patterns like low HDL and small LDL, aware of the vitamin D deficiency issue as a coronary risk factor, etc., you are far more aware than the vast majority of practicing cardiologists. They are interested in what new brand of anti-coagulant to use during their heart catheterization (because the product representative gushes about the new agent—only $1200 a dose!). Or, they are interested in gaining the procedural skills to put in a new device like a biventricular pacemaker. Regress/reverse coronary plaque? What for?

You already know that a conversation about coronary plaque reversal will not be obtained in your cardiologist’s office. Your family practice doctor or internist? Fat chance! Knee arthritis, pap smears, pneumovax inoculations, sore throats, gout, back pain—they’re spread far too thin to know anything more than the most superficial amount about coronary plaque control. Most know nothing.

That’s where we come in. That’s our mission: Educate people about the extraordinary tools that you have available to you, all in the cause of control or reversal of coronary plaque.

Why am I here?

Frank came to the office for an opinion, sent by his (proactive) family physician.

"I really don't know why I'm here, to be honest."

Two years earlier, Frank had a heart attack, survived and received two stents to his circumflex coronary artery. He now took Zocor and his LDL cholesterol was a reasonably favorable 89 mg, total cholesterol 183 mg.

"I walk with my wife every other day. I've been avoiding fish fries. You'll never see me eat fast food."

Frank was correct: If we were going to engage in the conventional approach to coronary disease, Frank was on the right track. We would have postponed his next heart attack or procedure by a couple of years. Stroke, aneurysm, and other atherosclerotic manifestations would be set back, likewise, a few years.

Would Frank have profound control over his disease? Absolutely not. In fact, his disease had probably advanced a huge amount just in the two years since his stents were placed and he was on his "prevention" program. Without his current effort, his coronary plaque would be expected to grow 30% per year. On Zocor and his modest lifestyle efforts, plaque growth was probably in the 14-28% per year range.

So I explained the unique Track Your Plaque approach to Frank. First, we start with a CT heart scan to establish where he was starting. Although he had two stents in his circumflex artery, we still had two other arteries (LAD, right coronary) to score and track.

We then attempt to identify all hidden causes of his heart disease and then correct them.

Of course, Frank had multiple hidden causes:

--HDL too low at 38 mg/dl
--Small LDL-severe, in fact, with 95% of all LDL particles in the small category
--Triglycerides too high
--Excesses of several triglyceride-containing particles (VLDL, IDL)
--Pre-diabetes--Frank had both a borderline high blood sugar and a high insulin level. This is a sure-fire stimulus to coronary plaque growth.
--A severe deficiency of vitamin D (<20 ng/ml)
--An excessivelyhigh blood pressure during exercise--With a blood pressure of 190/102 on the treadmill.

There were others(!), but that was the bulk of the causes behind Frank's coronary disease.

Once Frank recognized that there was indeed a huge panel of hidden causes for heart disease, not just too much fat in his diet and LDL cholesterol, he jumped into the program head first.

The message: The conventional approach is absurdly oversimplified, a certain path to failure for the majority of people. Even if you don't have known coronary disease like Frank, but just have a heart scan score >zero, the same principles apply to you.

Catheterization to “define coronary anatomy”

Gary is an avid jogger. On an average day, he runs 5-6 miles at a good clip. On two occasions recently, however, Gary experienced an ache in his left shoulder at mile 4. It was a toothache-like feeling, but he kept on going without difficulty.

Gary also had a heart scan score of 370.

Upon hearing of Gary’s score and his shoulder sensation, the cardiologist who saw him advised a heart catheterization “to define coronary anatomy”. (This is a real incident.)


What exactly does that mean? Why would Gary’s cardiologist need to define it?

In my view, this is an absurd notion. No one needs to “define coronary anatomy”. This catch-all phrase is commonly used to justify heart procedures. I believe what the cardiologist is saying is that it’s the easiest (for the cardiologist) and perhaps most generously reimbursed method to determine whether Gary’s symptoms are warning of an impending heart attack or not.

The problem is that the question can also be answered quite well by doing a stress test. Though not perfect diagnostic tests, stress tests are useful when symptoms are present that are doubtful in nature. Gary’s left shoulder ache could have been related to his heart, but the likelihood was that it was not. A stress test would have answered the diagnostic question quite adequately.

Instead, this man was subjected to an invasive test that was likely unnecessary. This happens dozens, if not hundreds, of times per day just around here. Nationwide, it is an epidemic of malpractice.

There are, indeed, times when a person should proceed directly to a heart catheterization. This is commonly and appropriately performed when a person develops unstable heart symptoms, such as chest discomfort or breathlessness at rest while not doing anything physical, or if the frequency is increasing, or if a stress test shows an important abnormality. There is no question that heart procedures can be lifesaving at times.

The problem is that thousands of people every year are scared into these procedures inappropriately. Beware!

It doesn't matter what I eat!

"How are your food choices?" I asked.

"What does it matter, doc? I take Lipitor. Doesn't that take care of it? I eat what I want!"

So declared Matthew. What he "wanted" was pretty much the diet of a teenager: pizza, cheeseburgers, soft drinks, snacks. His "beer belly" (visceral fat) gave it away. So did his blood work that showed flagrant lipoprotein abnormalities--small LDL, an HDL of 37 mg, and a severe after-eating flood of fat represented by increased "intermediate-density lipoprotein" (IDL).

Like many people, Matthew had been persuaded (or chose to believe) that LDL cholesterol was the sole cause for heart disease. Lipitor was therefore was all he needed. It must be great--how else could they afford all those slick TV commercials?

Well, it is definitely not true. In fact, with the persistence of Matthew's abnormal lipoprotein patterns, we should expect his heart scan score to continue to grow by 30%--the very same rate of increase as if he were taking nothing.

Specifically, Lipitor and drugs like it do not:

--Raise HDL.

--Correct or reduce the proportion of small LDL.

--Block after-eating flood of fat, nor do they accelerate clearance of unhealthy fats persisting in the bloodstream after eating.


Yes, what you eat does have real consequences, even if you take a statin drugs. In fact, the foods you ingest have a remarkably rapid and dramatic effect on what your blood contains. Any diabetic who checks his/her blood sugar knows this. They eat a slice of whole wheat toast and watch their blood sugar skyrocket.

Mind what you eat. Make it enjoyable, of course. But drugs do not provide impunity.

People with higher scores need to try harder

Sam is a 69-year retired physician. He was thoroughly enjoying retirement: golf, travelling, going out to dinner two or three times a week, spending weekends with his grandchildren. His lifestyle tended towards overindulgence, but he managed to stay fit and trim. At 6 ft 1 inch, he weighed 194 lbs and could still run 3 miles without too much difficulty. Not as good as his marathon-running days, but still not too bad for 69.

Sam's heart scan score in 2003 was a concerning 1983--extensive plaque. His doctor wasn't much help in interpreting the scan and so Sam simply chose to ignore it.

A chance conversation with a physician friend 18 months later made Sam think that perhaps this shouldn't be ignored. That's when he came to my office.




I find that sometimes the best way to motivate someone to take action is to demonstrate just how fast plaque grows if action isn't taken. So I advised Sam to get another scan first, since 18 months had passed. His score: 2441, or a 23% increase.




Sam was now starting to catch on. We made several changes in his prevention program (starting from virtually nothing). He did undergo a stress nuclear (thallium type) of test, which he passed without difficulty--normal blood flow in all heart territories despite the extensive plaque.

But, for some reason, Sam simply allowed himself to drift back to old habits: poor choices in food, overindulging in hard liquor, missing his fish oil and other supplements, and his medication, sometimes up to several days a week.

Sam started having unusual feelings in his chest. He described a sort of nervousness along with skipped heart beats. So we repeated a stress test. This time, a large area of reduced blood flow in the front of his heart ("anterior left ventricle") was detected. Sam ended up receiving three stents in a difficult procedure.

The moral: If you're starting out with a lower heart scan score of, say, 100 or 200, maybe you'll get by without trying too hard--maybe. But if your score is higher, say, several hundred or in the thousands, you got to try harder.

You're starting later in the process. Your disease will allow you very little slack. Let your guard down and it will get you. Control over your plaque is, indeed, very possible--we do it all the time. Score reduction is also possible. But your effort must be more serious and consistent.

Money can't buy health

Fallen Enron CEO, Kenneth Lay, was pronounced dead early this a.m. after suffering a heart attack.

Mr. Lay apparently had no history of heart disease and there's been no indication that symptoms provided any warning. His death was therefore classified as "sudden cardiac death".


Yet here's a man previously worth hundreds of millions of dollars with access to any test or medical system he desired--many times over. Even more recently, with his wealth reduced following his legal troubles, he and his wife managed to put away $4 million dollars to ensure an income from the interest through annuities, untouchable by the courts.

Detecting Mr. Lay's heart disease would have cost him around a few hundred dollars or whatever it costs for a CT heart scan in his city. This would have alerted his (hopefully knowledgeable) doctor that he was a time-bomb. Pile on all the stress he'd been suffering, whether deserved or no, and the diagnosis would have required little thought.

Instead, Mr. Lay has joined the thousands of Americans who will die this year because of failing to get a simple, 30-second test that costs one-tenth the cost of a stress test. Mr. Lay wasn't as lucky as former President Bill Clinton, whose doctors likewise blundered their way through and missed obvious levels of heart disease.

All Mr. Lay needed was better information: get a heart scan, then follow a program of prevention like the Track Your Plaque program. You may not have hundreds of millions of dollars, but you have the information on how to not follow in Ken Lay's footsteps. Track Your Plaque--and stay alive.

What's important, what's not in your plaque-control program

Sometimes it's hard to know what is really important in your plaque-control or plaque-reducing efforts.

There are, indeed, crucial make-it-or-break-it factors that are necessary to gain control over plaque. If you hope to stack the odds of reducing your heart scan score as much as possible in your favor, then fish oil, vitamin D, 60-60-60 in the way of standard lipids, elimination of small LDL, etc. -- all the elements of the Track Your Plaque program--are necessary.

But there's lots of things that sidetrack people. I spend much of my day fielding questions from patients about all the things that either provide very little benefit for plaque control, or provide none at all.

Among the things that we have found to be too weak or useless for plaque control, or are "non-issues", include:

--Caffeine--Go ahead and enjoy a couple cups a day (though not a pot). The effect is too trivial to make much difference.

--Hawthorne--Yes, it may dilate coronary arteries modestly, but not enough to make any difference.

--Garlic--with the possible exception of a specific preparation called Aged Garlic Extract (an acqueous, non-oil-based, extract from Kyolic), garlic's effects are too tiny to help, e.g., drop in blood pressure 1-2 points. Use it, but don't expect much. Aged Garlic Extract may be an exception, in that a single study from UCLA suggested specific effects on slowing coronary plaque growth. We await more info on this.

--Anti-oxidants--There is no shortage of extravagant claims about the benefits of anti-oxidants. Unfortunately, there's very little human exerience with pine bark extract, pycnogenol, grapeseed extract, and so on. Is the purported benefit from anti-oxidation or through some other means, e.g., enhancement of nitric oxide synthase? No data.

--Policosanol--If you've followed the Track Your Plaque Special Reports, you already know what a disappointment this agent has been, despite the too-good-to-be-true clinical data. It doesn't work.

--"No-flush niacin"--Unfortunately, no flush, no effect. This high-priced supplement is still sold widely in the U.S. despite its complete lack of efficacy. It does not work in humans. (It works great in rats!)

Track Your Plaque continues to try to be the arbiter of truth in what works, what doesn't in truly stopping or reversing your coronary plaque. The proof positive? Stopping or dropping your heart scan score.
Fat is not the demon

Fat is not the demon

So my patient, Dane, generously volunteered to be on the Dr. Oz show, as I discussed previously.

What we didn't know, nor did the producer who contacted us mention, that Dane would be counseled by low-fat guru Dr. Dean Ornish on a strict low-fat diet. The teaser introduction essentially tells the entire story.

Ironically, that is the exact opposite of the dietary program that I advocate. I rejected the 10% fat diet long ago after I became a type II diabetic, gained 30 lbs, and suffered miserable deterioration of my cholesterol values on this diet. I also witnessed similar results in many hundreds of people, all following a strict low-fat diet. In fact, elimination of wheat--whole, white, or otherwise--along with limitation or elimination of all other grains has been among the most powerful health strategies I have ever witnessed.

I now regret having subjected my patient to this theatrical misinformation. Dane is a smart cookie--That's probably why he was not allowed more than a "yes" or "no" during Dr. Oz's monologue, else Dane might have pitched in about some ideas that would have tripped Oz and Ornish up.

In their defense, if we took 100 Americans all following a typical 21st century diet of fast food, white bread buns, Coca Cola and other soft drinks, chips, barbecue sauce, and French fries, converting to a plant-based, high-carbohydrate, grain-rich diet is indeed an improvement. People will, at first, lose weight and enjoy an initial response. (The occasional person with the Apo E4 genetic pattern, heterozygote or homozygote, may even enjoy long-term benefits, a topic for another day.)

But the majority of people, in my experience, after an initial positive response to an Ornish-like low-fat, high-carbohydrate diet will either plateau (stay overweight, have low HDL, high triglycerides, plenty of small LDL, and high blood sugars) or deteriorate, much as I did.

Thankfully, Dane has been a good sport about this, understanding that this is essentially show business. I believe he understands that the information was all well-intended and, after all, we are all working towards the same goal: reduction of heart disease risk.

By the way, regardless of which diet you follow, it is, in my view, absurd to believe that diet alone will do it. What about vitamin D normalization, thyroid normalization (thyroid disease is incredibly common), omega-3 fatty acids from fish oil, identification of hidden sources of risk (something that is unlikely in Ornish, since small LDL particles skyrocket on a low-fat diet), postprandial glucoses, etc., all the pieces we focus on to gain control over coronary plaque? Eating green peppers and barley soup alone is not going to do it.

Comments (36) -

  • Matt Stone

    4/16/2010 1:09:27 PM |

    You might wanna revise the last statement in parenthesis about a low-carb diet causing small LDL to skyrocket Smile  I assume you meant low-fat.

  • Eloise

    4/16/2010 1:23:10 PM |

    I´ve been a low fat healthy anything victim myself for over 12 years and know exactly that it is a difference to SAD - but as you said only at the beginning. But maybe it´s easier to take those first changing steps into the right direction even if it´s the wrong way.
    Low fat, tons of fruits and whole grains are not the solution.
    Now I´m VLC for over one year, keto the last half got rid of eczema, asthma, mood issues and much more. Laboratory always repeat the tests because they can´t believe it: HDL 199, triglyceride 35. That´s high fat.

  • Dr. John Mitchell

    4/16/2010 1:26:29 PM |

    Dr. D
    You are on the mark with the last paragraph...it's more than one "magic pill" to solve the health problem. The solution appears to be a combination of many aspects of human existence...diet exercise and mental state.
    Eat right, exercise right, and think right...making the right choices for a healthier lifestyle.

  • Anonymous

    4/16/2010 2:08:30 PM |

    (something that is unlikely in Ornish, since small LDL particles skyrocket on a low-carb diet)

    Should this not read either

    "Low-Fat" or "High-Carb" diet?

  • John

    4/16/2010 4:07:42 PM |

    I applaud Dane--I don't know how long I'd be able to contain my frustration if I had to not only watch the Dr. Oz show, but actually receive direct advice from Ornish and Oz about low fat...

  • Chuck

    4/16/2010 4:33:16 PM |

    You mean "skyrocket on a *low fat* diet", right?

  • Anna

    4/16/2010 4:37:00 PM |

    "since small LDL particles skyrocket on a low-carb diet"

    I think this is a typo that was meant to say "high-carb diet", right?  Or perhaps it was large LDL particles skyrocket on a LC diet.

  • Nigel Kinbrum

    4/16/2010 5:31:01 PM |

    "since small LDL particles skyrocket on a low-carb diet"
    I think you meant high-carb diet

  • Anonymous

    4/16/2010 5:56:34 PM |

    I think you have a mistype here:

    (something that is unlikely in Ornish, since small LDL particles skyrocket on a low-carb diet)

  • Anonymous

    4/16/2010 7:38:14 PM |

    Dr. Davis,

    I watched Dr. Oz's show on reversing heart disease and it was interesting to read your comments.  

    Regarding the reversal of heart disease, while I admittedly haven't read your publication, do you have Heart Scans/Calcium Scores, angiograms or PET Scans that show the same results Dr. Oz (and other MDs like Dr. Caldwell Esselstein or K. Lance Gould) that show the same results with your program?  

    Thank you again and look forward to your feedback.

  • Anonymous

    4/16/2010 7:46:00 PM |

    maybe I am reading into this wrong but " (something that is unlikely in Ornish, since small LDL particles skyrocket on a low-carb diet)"

  • Anonymous

    4/16/2010 8:27:32 PM |

    ''something that is unlikely in Ornish, since small LDL particles skyrocket on a low-carb diet''   You surely meant low-fat diet.

  • jd

    4/16/2010 8:45:38 PM |

    Thanks as always.  Please fix third line from bottom, after skyrocket,"low-carb," to help the newbies.

  • pjnoir

    4/16/2010 8:53:34 PM |

    See- it was an AMBUSH. They write the rules and that is that. WE, the low carb HIGH fat diet, community must be the grass roots driving force. We are like Galileo committing hiFat heresy among an antiFat, Whole grain Inquisition. Fight on and screw tv talk shows.

  • Drs. Cynthia and David

    4/16/2010 10:51:34 PM |

    I will be curious to see how this goes down on the Oz show, but am afraid we'll be left wanting to bang our heads on the wall.  Does this mean that Dane did not get a chance to respond at all to their advice or that he must agree to follow their advice (maybe with a  follow up to show improvement, or NOT).

    I agree with you that their diet advice is probably better than what most of their featured patients eat.  And you probably can show improvements to a degree that way in many people.  Just cutting the enormous glycemic load in conjunction with omega-6 rich oils should help a lot.  But that doesn't make it optimal for health.

    What's it going to take to shut up the low fat dogmatists?  A class action lawsuit?

    Why don't you have a show of your own?  I think it would be a good thing.

    BTW, I think you meant to say "small LDL particles skyrocket on a low-FAT diet" in your penultimate sentence.

    Cynthia

  • Phil

    4/16/2010 11:32:21 PM |

    Dr. Davis,
    Should the next-to-last sentence read "...small LDL particles skyrocket on a low-fat diet..."?  I thought low-carb diets reduced small LDL.

  • Steve

    4/17/2010 12:42:09 AM |

    Typo should be fat
    "small LDL particles skyrocket on a low-carb diet"

    I've enjoyed reading your blog.

    Other ideas...
    Niacin and phosophorous suppression causal for insulin resistance?

    Fibrates?

  • Dr. William Davis

    4/17/2010 4:41:10 AM |

    Ooops!

    Thanks, all for catching the typo.

    The sentence should have read:

    . . . small LDL particles skyrocket on a low-FAT diet.

    I guess everyone is paying attention!

  • Gys de Jongh

    4/17/2010 8:55:20 AM |

    not every body agrees ....

    Am J Clin Nutr. 2010 Mar;91(3):578-85.

    Lack of suppression of circulating free fatty acids and hypercholesterolemia during weight loss on a high-fat, low-carbohydrate diet.

    Abstract
    BACKGROUND: Little is known about the comparative effect of weight-loss diets on metabolic profiles during dieting. OBJECTIVE: The purpose of this study was to compare the effect of a low-carbohydrate diet (< or =20 g/d) with a high-carbohydrate diet (55% of total energy intake) on fasting and hourly metabolic variables during active weight loss. DESIGN: Healthy, obese adults (n = 32; 22 women, 10 men) were randomly assigned to receive either a carbohydrate-restricted diet [High Fat; mean +/- SD body mass index (BMI; in kg/m(2)): 35.8 +/- 2.9] or a calorie-restricted, low-fat diet (High Carb; BMI: 36.7 +/- 4.6) for 6 wk. A 24-h in-patient feeding study was performed at baseline and after 6 wk. Glucose, insulin, free fatty acids (FFAs), and triglycerides were measured hourly during meals, at regimented times. Remnant lipoprotein cholesterol was measured every 4 h. RESULTS: Patients lost a similar amount of weight in both groups (P = 0.57). There was an absence of any diet treatment effect between groups on fasting triglycerides or on remnant lipoprotein cholesterol, which was the main outcome. Fasting insulin decreased (P = 0.03), and both fasting (P = 0.040) and 24-h FFAs (P < 0.0001) increased within the High Fat group. Twenty-four-hour insulin decreased (P < 0.05 for both groups). Fasting LDL cholesterol decreased in the High Carb group only (P = 0.003). In both groups, the differences in fasting and 24-h FFAs at 6 wk were significantly correlated with the change in LDL cholesterol (fasting FFA: r = 0.41, P = 0.02; 24-h FFA: r = 0.52, P = 0.002). CONCLUSIONS: Weight loss was similar between diets, but only the high-fat diet increased LDL-cholesterol concentrations. This effect was related to the lack of suppression of both fasting and 24-h FFAs.

    PMID: 20107198

  • Fred Hahn

    4/17/2010 2:15:57 PM |

    If I'm correct, the study cited in the comments section fails to reflect LDL particle size. IOW, your total LDL can go up and still result in a superior outcome.

    Also, weight loss isn't the issue - fat loss is. We want to know which group lost the most fat, not weight.

    Additionally, A calorie restricted, low fat diet that places carb intake at only 55% (FAR lower the the USRDA recc's) is still a relatively low carb diet.

  • Lou

    4/17/2010 3:28:45 PM |

    Gys de Jongh,

    I've seen that study before. I can't access to the whole study but did they use NMR lipid test or traditional lipid test? Huge difference! I'd bet the study was flawed.

  • TedHutchinson

    4/17/2010 8:38:20 PM |

    @ Gys de Jongh
    In this study Subjects were told that polyunsaturated fats
    and monounsaturated fats were healthier sources of dietary fatty acids than were saturated fats,

    readers here know Dr Davis makes his recommendations on the basis every effort is made to improve omega 3 status while avoiding omega-6-rich sources like corn oil, vegetable oils, sunflower or safflower oils.

    Similarly New Atkins devotes a lot of time explaining the importance of raising omega 3 while reducing omega 6 sources.

    It is a pity these researchers didn't make similar recommendations.

    I would also like to point out that  in this study, concentrations of LDL cholesterol were estimated by using the Friedewald equation
    You may be interested in Dr Davis's  previous comments on Making Dr. Friedewald an honest man

    The point is that in the context of  high omega3 ~ low omega6 intakes, we would normally expect to see a low carbohydrate diet produce a beneficial effect on triglycerides and free fatty acids without reducing TOTAL cholesterol but this may seriously throw Friedewald off target.

    Without any positive recommendations to address the omega3<>omega6 ratio, the low carb diet used in this research is not a low carb diet that either Atkins proponents or Dr Davis would support.

  • donny

    4/17/2010 11:03:08 PM |

    Gys--

    So how much did the high carb group eat? The abstract only says that calories were restricted, it doesn't say to what extent.

    What was the composition of the weight loss?

    "There was an absence of any diet treatment effect between groups on fasting triglycerides or on remnant lipoprotein cholesterol, which was the main outcome."

    Triglycerides at the same level probably means different things, depending on the overall picture.

    A particular triglyceride level in a high carb diet might be a measure of the continuous production of triglycerides in the liver. In a low carb diet,  triglycerides might be at a similar level, and if this comes alongside a higher level of free fatty acids, those free fatty acids will be in competition for takeup with the triglycerides; so the same level of serum triglycerides could be reached, even though triglyceride production itself might be decidedly lower.

  • marshall

    4/17/2010 11:04:44 PM |

    Gys,

    It would be interesting to see if it was the large, fluffy LDL or the small, dense LDL that increased. Were the high fat diets consisting of a lot of Omega 6 or PUFAs? Or did the high fat come from coconut, grass fed meats, and omega 3 fatty acids?

  • Bobby

    4/18/2010 12:02:18 AM |

    I know lots of folks on a low fat high carb diet who flourish and do not have your experience. I know folks who are on a diet you recommend who also flourish. This whole subject must be more complex than currently understood. Either folks are different or we are missing some variables. The oriental cultures flourish on a high carb diet and they do well (until the SAD influences them).

  • nightrite

    4/18/2010 4:01:27 PM |

    It's not uncommon for LDL to increase with a high-fat diet. This increase however is in the large fluffy LDL subparticles and not in the small, dense type LDL.
    Small LDL is the real "bad guy" in the cholesterol story.

  • Jan-Peter

    4/18/2010 4:26:54 PM |

    I recently had the Berkley Heart panel done and found out I was a 3/4 APO E carrier.  Their recommendation of a 20% low fat diet I found misguided.  Instead I went on a restricted calorie (1,700/day I'm 5' 11") diet consisting of no grains, some limited fruit (mostly berries)and lots of veggies (daily carbs 110g), lean protein (grass fed if red meat) about 125g. And I eat a ratio of fats (80g) mostly from avacado, olive oil, nuts, and yes some saturated (20g).
    The Macro ratio is 46% fat/30 % protein/24% carbs.
    By being high fat I am able to maintain this low calorie diet without feeling depreived.
    After 2 months on this diet I lost 24 pounds my LDL went from 130 to 91, my HDL went from 45 to 54, and my triglycerides from 230 to 94.

    DESPITE THESE #'S MY PHSYCIAN AND THE DIETIAN FROM BERKLEY WARNED ME THAT MY GENOTYPE DOES NOT METABOLIZE FATS WELL!
    I know there are conflicting studies (Krauss). I would love Dr. D to take on this APO E subject.  I can't believe from an evolutionary standpoint that 20 % of the population can't eat high fat diets, something is wrong with this hypothesis.

  • Norm

    4/18/2010 9:41:03 PM |

    Gys de Jongh, maybe you should read this interpretation of the study on Dr. Eades' blog.

  • Gys de Jongh

    4/19/2010 11:11:00 PM |

    @ TedHutchinson :
    The Friedewald equation works fine in this case because the baseline Trig's were 117 mg/dl

    If Trig's < 100 mg/dl, LDL is over estimated by 12.17 mg/dL or if you have a (very) good lipid panel your LDL might be over estimated by 10% . Nothing to worry about I would say Smile

    The article is free :
    Arch Iran Med. 2008 May;11(3):318-21.
    The impact of low serum triglyceride on LDL-cholesterol estimation.

    PMID: 18426324

  • Gys de Jongh

    4/19/2010 11:17:49 PM |

    @Lou
    Total cholesterol and triglycerides were measured enzymatically with a colorimetric endpoint (Roche Diagnostic Systems, Indianapolis, IN), as were HDL-cholesterol concentrations (Diagnostic Chemicals Ltd, Oxford, CT). LDL cholesterol was calculated from plasma total and HDL cholesterol and triglyceride concentrations

  • Gys de Jongh

    4/19/2010 11:23:07 PM |

    @donny
    Suggested caloric intakes for women initially were set at 1200–1500 kcal/d, with the higher intakes recommended for those with a BMI > 36. Men were instructed to eat 1500–1800 kcal/d, again with the higher intakes recommended for those with a BMI > 36. Subjects were encouraged to consume about 30% of calories from fat, 15% from protein, and 55% from carbohydrate.

  • Gys de Jongh

    4/19/2010 11:30:30 PM |

    @Bobby
    The best "diet" for you depends on what your genes do with the food after you eat it  Smile
    Int J Circumpolar Health. 2007 Dec;66(5):390-400.
    Common variants APOC3, APOA5, APOE and PON1 are associated with variation in plasma lipoprotein traits in Greenlanders.
    Abstract
    OBJECTIVES: We undertook studies of the association between common genomic variations in APOC3, APOA5, APOE and PON1 genes and variation in biochemical phenotypes in a sample of Greenlanders. STUDY DESIGN: Genetic association study of quantitative lipoprotein traits. METHODS: In a sample of 1,310 adult Greenlanders, fasting plasma lipid, lipoprotein and apolipoprotein (apo) concentrations were assessed for association with known functional genomic variants of APOC3, APOA5, APOE and PON1. For significantly associated polymorphisms, between-genotype differences were examined in closer detail. RESULTS: We found that (1) the APOE restriction isotype was associated with variation in plasma total and LDL cholesterol and apo B (all p < .0001); (2) the APOC3 promoter genotype was associated with variation in plasma triglycerides, HDL cholesterol and apo A-I (all p < .002); (3) the APOA5 codon 19 genotype was associated with variation in plasma triglycerides (p = .027); and (4) the PON1 codon 192 genotype was associated with variation in total and LDL cholesterol and apo B (all p < .05). CONCLUSIONS: Taken together, our results suggest that common genetic variations in APOC3, APOA5, APOE and PON1 are associated with significant variation in intermediate traits in plasma lipoprotein metabolism in Greenlanders; the associations are similar to those observed for these variants in other populations.

    PMID: 18274205

  • Gys de Jongh

    4/19/2010 11:35:35 PM |

    @marshall
    High-fat/low-carbohydrate-diet treatment
    Participants in the high-fat condition were instructed to consume a diet that was low in carbohydrate and thus higher in percentage fat and/or protein (13). The central feature of this approach is carbohydrate restriction with unlimited consumption of fat and protein. Subjects were told that polyunsaturated fats and monounsaturated fats were healthier sources of dietary fatty acids than were saturated fats, but it was clear that the primary goal was to limit carbohydrate by whatever means were required. Participants were provided a treatment manual, which described the rationale for a low-carbohydrate diet as well as numerous suggestions for meal plans. The treatment manual for the highcarbohydrate diet plan was modified to make it parallel to the high-fat (low-carbohydrate) recommendations. This substudy took place during the first phase (“induction”) of the intervention. During this phase, participants were instructed to consume ’20 g carbohydrate/d. They were told to eat until full while remaining within the carbohydrate limit.

  • Lou

    4/20/2010 10:38:22 PM |

    Gys,

    What about small LDL particle vs large LDL particle? Did they use vegetable oil? What kind of carbohydrates?

    How do you explain this clincal study - http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=PubMed&list_uids=17583796&dopt=AbstractPlus?

    I rapidly lost a lot of viseral fat past month after cutting most of wheat flour based food AND adding more healthy fat like avacado, coconut milk, olive oil, egg yolk and plenty of various meat. I feel better. I tried low fat high carbs diet and it was not sustainable because I go hungry all the time.

    Unless I have full access to that study, I'm going to write it off as flawed misleading study. The author was clearly trying to promote high carbs and low fat diet. I'll have to see where they got grants from to do the study.

  • Catatonic Eyes

    4/22/2010 3:15:12 PM |

    Dr. Davis what brand of fish oil do you recommend? I have been taking Flameout by Biotest but am feeling it may not be the best choice. I am hopeful to find something reasonably priced that works well. When my Vit d tested at nine in December when I was admitted to the hospital, I started taking the NOW brand of Vit d 3 and mid March was at 53.....my new doctor is having me increase my dose as he wants it higher. Any brand recommendations for someone struggling on one income for the family for fish oil? Thanks for all of your articles. I am learning so much and will regain my health in time!

  • wendys

    4/26/2010 9:42:26 PM |

    Did they do a full colesteral work-up and will they show the results if it shows that Dane's numbers got worse instead or better?

Loading