"I have never seen regression"

At a presentation at the American College of Cardiology meetings in New Orleans yesterday (March 27, 2007), Dr. Arthur Agatston declared "I have been doing CT for many years, and I have never seen regression."

Whooooaaaa. Wait a minute here. I have great respect for the work Dr. Agatston has done over the years. He is, after the originator of the scoring algorithm that allows us to score CT heart scans (though a more accurate measure, the volumetric score, is the one we often use behind closed doors because of modestly increased accuracy and reproducibility). His diet program, the South Beach Diet, has achieved enormous success and is indeed an effective approach for both weight loss and correction of many weight-related causes of heart disease.

But he has never seen regression? Why would this be when we see it all the time? When we see heart scan scores drop 30%, it's hard to believe that with some savvy he has never seen regression (drop in score).

I can only attribute the difference to the more intensive endpoints we advocate (e.g., 60-60-60 for lipid values); the incorporation of adjuncts like fish oil, vitamin D, l-arginine; attention to non-cholesterol issues and intensified treatments for each. I doubt that the populations we see differ substantially.

As much as I admire Dr. Agatston's accomplishments, I believe that he is behind the times on this issue. No regression is so starkly different from the Track Your Plaque experience. I believe that relying only on statin drugs and diet will slow but will not stop plaque growth. It will also rarely, if ever, drop your score.

Attention to detail and a little insight into better preventive strategies really pays off. While not everyone in the Track Your Plaque experience will drop their score, a substantial number do. Many more slow plaque growth dramatically. And, as time goes on, our track record gets stronger and stronger.

COURAGE to do better

The results of the long-awaited COURAGE Trial were announced today at the American College of Cardiology meetings in New Orleans.

In this trial, 2200 participants with stable coronary disease (i.e., not unstable, in which heart attack or death is imminent) were randomly assigned ("randomized") to either angioplassty/stent or "maximal medical therapy." Medical therapy means such things as aspirin, beta blocker drugs, and statin cholesterol drugs. There was virtually no difference between the groups in rate of heart attack and death from heart disease over a period of up to 7 years.

These results have caused a stir in the media and my colleagues, trying to sort out of the implications. However, I think there's one observation in particular worth making for those of us who tend to scoff at the conventional approach to coronary disease. That is, 1 of 5 people had a heart attack or died from heart disease in both groups. That's a lot. Even more ended up with a procedure (angioplasty, stent, or bypass). In other words, the "maximal medical therapy" instituted in participants was hardly a success. Though angioplasty and stenting failed to prove superiority, both really stunk. Both permitted a lot of catastrophes to occur.

"Maximal medical therapy," in other words, is a laughable concept. It doesn't include raising HDL, suppressing small LDL, reducing Lipoprotein(a), addressing inflammatory issues. It does not include omega-3 fatty acids from fish oil, nor does it address the severe degrees of vitamin D deficiency that are proving, in the Track Your Plaque experience, to be among the most potent causes of atherosclerotic plaque known. It includes a sad attempt at diet, as advocated by the American Heart Association, a diet that, in my view, causes heart disease and is distorted by the powerful political and financial influence of food manufacturers.

If the trial were to be done again, I'd like to see the "maximal medical therapy" arm be represented by a more effective program like the Track Your Plaque approach.

Value of a zero heart scan score

Margaret is 73. She's a very good 73. She loves children and works full-time in a daycare. She manages her own household, goes to dinner at least once each week with one or more of her adult children. She is slender and has never been in the hospital--until she developed an abnormal heart rhythm called atrial fibrillation.

Most people who develop atrial fibrillation do so with no immediate identifiable cause. However, Margaret has been a widow since her husband died 15 years ago of a heart attack. She was therefore especially frightened of any heart issues in her own health. Her doctor also raised the question of whether atrial fibrillation might represent the first hint of future heart attack.

So we advised a CT heart scan. Score: zero, or no detectable plaque whatsoever. This put Margaret's risk for heart attack as close to zero as humanly possible. (Nobody is truly at zero risk for heart attack for a number of reasons. One reason is that people do irrational things like take cocaine or amphetamines, or they take too much decongestant medication, all of which can trigger heart attack.)

The heart scan settled it. Margaret has the sort of atrial fibrillation which likely simply develops as a result of "wear and tear" on the heart's electrical impulse conducting system and it has nothing to do with coronary heart disease or heart attack.

As that MasterCard commercial goes: Cost of a heart scan: About $200. Peace of mind: priceless.

You're at the cutting edge

If you're a participant in the Track Your Plaque program for atherosclerotic plaque regression, you are at the cutting edge of health.

Few physicians give this issue any thought. Chances are, for instance, that if you were to bring up the subject of reversal of heart disease to your primary care physician, you'd get a dismissive "it's not possible," or " Yeah, it's possible but it's rare."

Ask a cardiologist and you might make a little more progress. He/she might tell you that Lipitor 80 mg per day or Crestor 40 mg per day might achieve a halt in plaque growth or a modest reduction of up to 5-6%. If they've tried this strategy, they would likely also tell you that hardly anybody can tolerate these doses for long due to muscle aches. I'd estimate that 1 of 10 of my colleagues would even be aware of these studies.

Both groups are, however, reasonably adept at diagnosing chest pain, an everyday occurrence in hospitals and offices. Chest pain, for them, is a whole lot more interesting. It holds the promise of acute catastrophe and all its excitement. It also holds the key to lots of hospital revenues. Did you know that 80% of all internal medicine physicians are now employees of hospitals? They're also commonly paid on an incentive basis. More revenues, more money.

Ask Drs. Dean Ornish or Caldwell Esselstyn about reversal of heart disease and they will tell you that a very low-fat diet (<10% of calories)can do it. That's true if you use a flawed test of coronary disease like heart catheterization (angiograms) or nuclear stress tests (Ornish calls them "SPECT"). It would be like judging the health of the plumbing in your house by the volume of water flowing out the spigot. It flows even when the pipes are loaded with rust.

In the Track Your Plaque experience, extreme low-fat diets (i.e., high wheat, corn, and rice diets) grotesquely exagerrate the small LDL particle size pattern, among the most potent triggers for coronary plaque growth. This approach also makes your abdomen get fatter and fatter and inches you closer to diabetes. Triglycerides go up, inflammation increases.

If you were able to measure the rust in the pipes, that would be a superior test. You can measure the "rust" in your "pipes," the atherosclerotic plaque in your coronary arteries, using two methods: CT heart scans or intracoronary ultrasound. Take your pick. I'd choose a heart scan. It's safe, accurate, inexpensive. I've performed many intracoronary ultrasounds for people in the midst of heart attacks or some other reason to go to the catheterization laboratory. But for well people, without symptoms, who are interested in identifying and tracking plaque? That's the place for heart scans.

In our program, 18-30% reductions in heart scan scores are common.

A stent--just in case

Burt came to me last week. He'd received a stent a few months earlier. He'd been feeling fine except for some fatigue. A nuclear stress test proved equivocal, with the question of an abnormal area of blood flow in the bottom (inferior wall) of the heart.

"The doctor said I had a 50% blockage. Even though it wasn't really severe, he said I'd be better off with a stent, just in case."

Just in case what? What justification could there be for implanting a stent "just in case"? (The artery that was stented did not correspond to the area of questionable poor blood flow on the nuclear stress test.)

Just in case of heart attack? If that's the case, what about the several 20 and 30% blockages Burt showed in other arteries? The cardiologist was apparently trying to prevent the plaque "rupture" that results in heart attack by covering it with a stent. Why stent just one when there were at least 7 other plaques with potential for rupture?

That's the problem. And that's why stents do not prevent heart attack (unless the stent is implanted in the midst of heart attack, when the rupturing plaque declares itself.) Of course, when no plaque is in the midst of rupturing, as with Burt, there's no way to predict which plaque will do so in future. Since only one plaque was stented, there is a 7 out of 8 chance (87.5%) that the wrong plaque was chosen. And that's assuming that there aren't plaques not detected by catheterization angiogram; there commonly are. The odds that the right plaque was chosen would be even lower.

In other words, stenting one blockage that is slightly more "severely blocked" in the hopes of preventing heart attack is folly. If it's not resulting in symptoms and blood flow is not clearly reduced, a stent can not be used to prevent plaque rupture. A stent is not a device to be used prophylactically. It is especially silly when an approach like ours is followed, since plague progession is a stoppable process.

Note: This issue is distinct from the one in which symptoms and/or an abnormal stress test show clearly reduced blood flow and flow is restored by implantation of a stent. While some controversies exist here, as well, a stent implanted under these circumstances may indeed provide some benefit.

How will you know your score dropped?

This issue came up twice this week.

Bill is a busy accountant. Two years ago, just after the tumult of the 2005 tax season was over, he got a CT heart scan. His score: 398. At age 53, this was a significant score. His internist did the usual: prescribed a statin (Zocor), told him to cut the fat in his diet, and be sure to exercise. (Yawn.)

Since then, Bill quit preparing tax returns and migrated to a less harried job in corporate accounting. It took two years since his heart scan for Bill to start thinking that perhaps his doctor's advice wasn't enough. If it was, he realized, everyone on a statin drug who made these minimal lifestyle changes would be cured of heart attack risk. Clearly not the case.

So Bill enrolled in the Track Your Plaque program. Our first step: Get another heart scan.

Bill was surprised. "Why another scan? I already had one!"

I explained to Bill that atherosclerotic plaque is like money: it grows in percentages, just like money in a bank account or in a mutual fund. If, for instance, you deposit $500 in a mutual fund and it yields 5% return, then after one year you will have $550. One year later, you will have 5% x $550, or $605. Another year: $665. In other words, growth is not 10% of the original amount you deposited. Growth is compounded, year over year. That's why money, when compounded, can grow so quickly.

Atherosclerotic plaque and your CT heart scan score do the same thing: they grow by a percentage of the current plaque quantity. In fact, we use the compound interest equation to calculate the annualized rate of plaque growth. But plaque grows at the extraordinary rate of 30% per year, on average. Imagine that was the rate of return on your money. You'd be the richest man or woman on earth.

Back to Bill. Now Bill, in his defense, was on a statin drug and did make modest efforts towards a (mis-guided) low-fat diet and walking four days per week. If, on a second CT heart scan, his score was:

398--No change. That's a success, since the expected rate of increase of 30% has been stopped. However, on his current program, this is highly unlikely. (I've seen it happen just once ever out of about 2000 people.)

250--Pop the cork on your champagne, because Bill needs to celebrate. He has substantially reversed his plaque. Highly unlikely on the current effort.

525 --The score is higher by 30%, so it has slowed, but it surely hasn't stopped. This is the most typical result on the sort of program Bill is following.

The message: Don't delay after your first heart scan score. It plaque grows like money with a huge return, there's no time like the present to take the steps to regain control.

Firefighters Face Added Risk of Fatal Heart Attack

Firefighters are twice as likely to die from a heart attack in the line of duty than are policemen, and three times more likely than EMTs.

That's among the headlines run today because of a report in the New England Journal of Medicine documenting a dramatically higher risk for heart attack for fire fighters putting out fires. The above headline is from an excellent report run on NPR radio. You can listen to the webcast at http://www.npr.org/templates/story/story.php?storyId=9047656.

The story sparked comments from experts insisting that all fire fighters should have physicals, should be in better physical condition, should be covered by health insurance (the NPR report said that 1 out of 4 fire fighters lack health insurance). Judging from the indisputable risk firefighters encounter, these are all good ideas.

But if you've been following my blog or the Track Your Plaque program, you know that physicals alone are hopeless exercises for identifying hidden heart disease. Among the solutions: identify whether or not heart disease is present in the first place--do a CT heart scan.

In fact, several local fire companies in my area have done just that: insisting that all firefighters undergo a heart scan. When groups of people like firefighters arrange for heart scans, they gain the advantage of doing so en masse, thereby allowing many scan centers to offer a dramatically reduced price to the city, town, or village that is paying for them. I've even seen many firefighters scanned at no cost.

It would also help to have health insurance, be physically fit, and have a stress test (an exception to my view that stress tests are also useless to screen asymptomatic people for heart disease). But a CT heart scan would settle the question quickly, easily, undeniably, and inexpensively.

Prophylactic bypass surgery?

This question comes up around once a week:

My CT heart scan score is ____. Wouldn't I be better off just getting a bypass (or stent, etc.) and getting it over with? If I know that heart attack is in my future, why not just get it over with?

The most recent source of this question was the wife of a patient. Jack had a heart scan score of 92 in 2005. He made very little effort to correct his causes, permitting pre-diabetic patterns to persist, failed to correct vitamin D, etc. and a repeat heart scan score showed a dramatic rise to 264.

Jack's wife asked whether he should just have a bypass.

There are several problems with this line of reasoning:

1) Bypass surgery does not reduce the long term risk for heart attack.

2) The risk of bypass surgery often outweighs the risk of an asymptomatic heart scan score.

3) Bypass surgery is a temporary "fix," a fancy Band Aid for a disease that progresses after the procedure. One bypass typically prompts another, and another...

4) Bypassing arteries that have vigorous blood flow often causes the bypass graft to not "take" and close within the first few days.


Thankfully, nobody in his right mind has proposed that we perform prophylactic bypass operations.

Of course, hospitals and surgeons would jump at the chance to perform procedures in anybody with some threshhold heart scan score. It would double or triple their business overnight. At $70,000 or more per procedure, they would dance in glee. Of course, you and I would pay for their new burst of wealth by a sharp increase in our health insurance premiums. Not only that, the people who underwent the procedure would not benefit.

Lipitor 80 mg

I'm seeing more and more people taking 80 mg of Lipitor per day. For the most part, these are people who come in for another opinion after a stent or heart attack and are prescribed the drug during their hospitalization.

This practice is based on the results of the PROVE IT-TIMI 22 (PRavastatin Or atorVastatin Evaluation and Infection Therapy-Thrombolysis In Myocardial Infarction) trial, and the Reversal of Atherosclerosis with Aggressive Lipid Lowering (REVERSAL) trial, both reported in 2005. In the PROVE IT Trial, 4,000 people experiencing heart attacks were treated with Lipitor (atorvastatin), 80 mg, or Pravachol (pravastatin), 40 mg. There was a reduction in events like recurrent heart attack from 13.1% in the Pravachol group to 9.6% in the Lipitor group. In the REVERSAL Trial, the Lipitor group also showed no plaque growth compared to the Pravachol group, which did progress, with disease tracked by intracoronary ultrasound.

I believe that many of my colleagues took the bait. In a half-hearted effort to reduce events and trend towards better coronary plaque control, writing a prescription for 80 mg rather than a lower dose has become increasingly popular.

Some problems: Despite the favorable tolerance to high dose Lipitor in these trials, I don't know anybody who can tolerate 80 mg per day for more than a few months in real life. In my experience, people inevitably end up with intolerable muscle aches.

Also, I believe it is folly to believe that we can regress coronary plaque on a broad scale by just using one drug that addresses only a single cause (i.e., LDL cholesterol). Yes, drug companies would argue that the statin drugs are so wonderful because of their so-called "pleiotropic", or non-lipid, effects like reducing inflammation. I have seen regression of plaque once using Lipitor alone. We struggle to reduce coronary plaque using a multi-faceted approach. It is highly unlikely that Lipitor alone at a 80 mg dose will be sufficient in most people to regress plaque. How about lipoprotein(a)? Or vitamin D deficiency? Lipitor has no effect on these patterns and people do not regress just by taking statin agents.

Orlistat for weight loss

In early February, the FDA approved orlistat, formerly known as prescription Xenical, for over-the-counter sale. Orlistat is a blocker of fat absorption.

The new OTC version will be called "Alli" (pronounced like "ally") and will come at a dose of 60 mg to be taken three times a day with meals. Prescription Xenical came as a 120 mg tablet. However, the company claims that the reduced dose sacrifices only 5% in reduced fat absorption, dropping from 30% with Xenical to 25% with Alli. It will cost in the neighborhood of $1 to $2 per day, or $30-60 per month, far less expensive than the $110-150 for the prescription form.

Does it work? Is it worth the money? Clinical trials document around 5-10 lbs lost over a 3 to 6 month period, 50% greater than using diet and exercise alone.

Our experience is that it works, though inconsistently. Results depend heavily on how reliant you are on fat calories. If you were to follow a low-fat diet while on the drug, you likely will lose little or no weight, since there's little fat absorption to block. However, I have witnessed more substantial weight loss of 10-20 lbs. in people who follow a higher fat intake in their diet, e.g., a traditional American diet. However, these people gain the weight back immediately because they've made no effort to modify food choices.

It is messy. Even though the clinical trials claims modest inconvenient effects like gas and greasy stools, I have found that it is, without fail, a very annoying product that results in crampiness and frequent messy stools in nearly everybody.

The company has created a glitzy website that you can view at www.myalli.com and promises to provide a personalized program and support for registrants when it is up and running by summer 2007.
I think that's a good idea, since the drug itself is no more than a temporary fix unless it's combined with long-term diet changes. However, the website, I believe, oversells the value of the drug with a drug company's usual over-the-top hints and innuendoes without actually coming out with straight pitches of the truth.

Beware of the vitamin D-blocking effect of Orlistat. The period of time you take it may be a time to resort to some modest sun exposure (10-15 minutes; be careful not to burn), rather than than oil-based vitamin D capsules, in order to avoid the inevitable vitamin D plunge in blood level.

I am not a fan of orlistat, having seen it tried many times with minimal success. However, it is another option for those who are really struggling. Personally, I would try fasting or some of the other strategies we've detailed on the www.cureality.com website before I resorted to orlistat.
Why small LDL particles are the #1 cause of heart disease in the US

Why small LDL particles are the #1 cause of heart disease in the US

Ask your doctor: What is the #1 cause of heart disease in the US?

Let's put aside smoking, since it is an eminently modifiable risk and none of those crazies read this blog anyway. What will your doctor say? Most like he or she will respond:

High cholesterol or high LDL cholesterol

Too much saturated fat

Obesity

Pfizer, Merck, AstraZeneca and their kind would be overjoyed to know that they can add your doctor to their eager following.

I'd tell you something different. I would tell you that small LDL particles are, by far and away, the #1 cause for heart disease. I base this claim on several observations:

--Having run over 10,000 lipoprotein panels (mostly NMR) over the past 15 years, it is a rare person who does not have a moderate, if not severe, excess of small LDL particles. 50%, 70%, even 90% or more small LDL particles are not rare. Over the course of a year, the only people who show no small LDL particles are slender, athletic, pre-menopausal females.

--In studies in which lipoproteins have been quantified in people with coronary disease, small LDL particles dominate, just as they do in my office. Here's a 2006 review.

--Small LDL is largely the province of people who consume carbohydrates, such as the American population instructed to "cut fat and eat more healthy whole grains." Conventional diet advice has therefore triggered an expllosion in small LDL particles.

--When fasting triglycerides exceed 60 mg/dl, small LDL particles increase as a proportion of total LDL particles. This includes the majority of the US population. (This ignores postprandial, or after-eating, triglycerides, which also contribute to small LDL formation.)

If you were to read the data, however, you might conclude that small LDL affects a minority of people. This is because in most studies small LDL categorize it as either "pattern B," meaning exceeding some arbitrary threshold of percentage of small LDL particles, versus "pattern A," meaning falling below that same arbitrary threshold.

Problem: There is no consensus on what percentage of small LDL particles should mark the cutoff between pattern A vs. pattern B. In many studies, for instance, people with 50% small LDL particles are called "pattern A."

If, instead, we were to set the bar lower to identify this highly atherogenic (atherosclerotic plaque-causing) particle at, say, 20-30% of total, then the number or percentage of people with "pattern B" small LDL particles would go much higher.

I see this play out in my office and in the online program, Track Your Plaque, every day: At the start eating a low-fat, grain-filled diet with lots of visceral fat ("wheat belly") to start, they add back fat and cut out all wheat and limit carbohydrates. Small LDL particles plummet

Comments (77) -

  • Bill

    9/15/2011 1:13:26 PM |

    But is there any real evidence that small LDL is a *cause* of heart disease? Correlation alone isn't sufficient, of course, and Chris Masterjohn has said that even the correlation largely disappears when traditional "risk factors" such as HDL, LDL, and triglycerides are added to the model.

    I ask in part because I am about to arm wrestle with my primary care doctor about my recent cholesterol panel:

    Total: 382
    HDL: 157
    LDL: 217 (calculated)
    Triglycerides: 39

    He's upset about the LDL, of course, especially since it's progressively risen over time (coinciding with dietary changes pretty compatible with TYP and including quite a bit of sat fat after years as a low-fat vegetarian). Naturally, he wants me to reduce my fat consumption and retest in four months, and I'm sure a statin drug recommendation will follow just as the sunset inevitably follows the sunrise.

    I am thinking of asking for a full lipoprotein panel, with the expectation that it will calm him down by showing 1) much lower real, measured LDL with my rock bottom triglycerides and 2) strong Pattern A LDL with my sky high HDL and low triglycerides.

    But I'm not certain if I can really make a convincing empirical case to him that Pattern A is benign with a high LDL. (I'm also hesitating after hearing Chris Masterjohn say that LDL particle size measurements are hugely dependent on the type of assay used and that as a result it's not clear what, biologically, any given result means until these methodological discrepancies are sorted out.)

  • Peter Silverman

    9/15/2011 2:41:59 PM |

    The article you cite says the number of LDL particles may be more important than the size.  Is that your experience?

  • Howard

    9/15/2011 3:02:31 PM |

    @Bill : Chris Masterjohn also mentioned in a recent podcast that the current measurement technology for LDL particle size is just not sufficiently accurate to be useful.

  • chuck

    9/15/2011 3:48:18 PM |

    what is your feeling on oxidized ldl?

  • chuck

    9/15/2011 3:52:16 PM |

    @howard
    yes, based on the hour to hour, day to day, week to week, and month to month natural fluctuations of lipids in the blood it is difficult to make any real judgements about cholesterol readings without doing multiple panels over a period of time.  the whole medical community seems to be screwed up in this respect.

  • Kathy

    9/15/2011 4:13:20 PM |

    I have no idea what Dr. Davis' response will be, but if you're interested in getting an NMR profile done on your own dime (and if there is a convenient location near you), check out directlabs.com for their September special.  An NMR profile will only set you back $79 (reg $127).  I've been waiting for this "sale" and am getting it done to show my own doctor.  Your health is ultimately in your hands - keep up the good fight!
    Best,
    Kathy

  • edward white

    9/15/2011 5:02:18 PM |

    Dr D,
    I totally agree small LDL is driven by excess carbohydrate intake and postprandial
    triglycerides. However there is a substantial subset of people whose small LDL
    is genetically driven. I believe you are aware of this phenomena.
    Please let these folks know what their options are to address this important issue!
    There can be a good deal of frustration when carbs and triglycerides are addressed but
    with little lowering of small LDL.
    Please help this substantial number of people out by outlining their options...
    Gib

  • Unix-Jedi

    9/15/2011 5:22:13 PM |

    Thanks for that information, Kathy.

  • cancerclasses

    9/15/2011 5:57:26 PM |

    It ain't good,  just ask Wikipedia.   From the Wiki page re 'Chronic endothelial injury hypothesis':
    "Once LDL accumulates in the subendothelial space, it tends to become modified or oxidized.[5] This oxidized LDL plays several key roles in furthering the course of the inflammatory process. It is chemotactic to monocytes; oxidized LDL causes endothelial cells to secrete molecules that cause monocytes to penetrate between the endothelial cells and accumulate in the intima.[6]

    Oxidized LDL promotes death of endothelial cells by augmenting apoptosis. Also, through the activation of collagenases, ox-LDL contributes to a process which may lead to the rupture of the fibrous plaque[7] Oxidized LDL decreases the availability of endothelial nitric oxide (NO), which, in turn, increases the adhesion of monocytes to the endothelium.[8] Moreover, NO is involved in paracrine signalling between the endothelium and the smooth muscle that maintains vascular tone; without it, the muscle will not relax, and the blood vessel remains constricted. Thus, oxidized LDL also contributes to the hypertension often seen with atherosclerosis."

  • Bob

    9/15/2011 6:12:21 PM |

    Test reply

  • cancerclasses

    9/15/2011 6:13:54 PM |

    Yes, French cardiologist Guy-Andre Pelouze MD. at the recent Ancestral Health Symposium said in his presentation "Paleodiet and atheroma: A Cardiovascular Surgeon’s Perspective" that:

    1. Native (the reduced form of) LDL cholesterol is NOT atherogenic, only the oxidized form leads to atheroma, atherogenesis & arterial plaque formation.

    2. Without oxidized cholesterol it's very difficult to have arterial plaque formation

    3. Anti-oxidants are ineffective in preventing atheroma.

    4. SDLDL easily enter the subendothelial space because SDLDL are less than 25 nm in diameter and the subendothelial space is 26 nm.

    5. Subendothelial space in humans is very different in humans than other mammals due to the large amount of smooth muscle in the arterial media below the the intima layer.

    And there's much more.  To see a video of Dr. Pelouze's presentation hosted on the Ancestral Health page at Vimeo just google 'vimeo, paleodiet and atheroma', then scroll to video number 33 in the right side box.

  • cancerclasses

    9/15/2011 6:42:38 PM |

    Do you REALLY believe that? We have the ability to measure the distance between the earth and the moon almost down to the millimeter, and certainly down to the centimeter. We have the ability to measure individual atoms with electron and other types of microscopy used in materials engineering and computer chip manufacturing.  Medical, biochemical & physiological textbooks are full of descriptions of the sizes of white and red blood cells, bacteria and viruses, etc. ad infinitum.  Do you REALLY think we lack the ability to measure SDLDL?  Don't be so ready to believe something just because somebody says something about it.  Use your own brain, put together everything you know and can learn on your own and connect ALL the dots before drawing a conclusion.  

    Furthermore, what's the point of a statement like that?  Should we just give up measuring and trying to understand how SDLDL causes atheroma just because ONE guy says we can't measure them to his degree of satisfaction?  Should we just give up worrying about what we eat, and what we are being sold as foods that are arbitrarily declared to be safe to eat by some anonymous bureaucrat at the FDA?  Should we just ignore the ever increasing incidence rates of cancer, heart disease and atherosclerosis that by all applications of observation and simple logic are known to be entirely due to the modern industrial foods diet in every society and the peoples that subsist on them?  

    I don't think so.  Homey don't play that anymore, at least this one doesn't.

  • cancerclasses

    9/15/2011 6:55:16 PM |

    @Bill,  Google and see this study: 'Detection of low density lipoprotein particle fusion by proton nuclear magnetic resonance spectroscopy'.    
    "Abstract: Recent evidence suggests that fusion of low density lipoprotein (LDL) particles is a key process in the initial accumulation of lipid in the arterial intima. In order to gain a better understanding of this early event in the development of atherosclerosis, it would thus be necessary to characterize the process of LDL fusion in detail. Such studies, however, pose severe methodological difficulties, such as differentiation of particle fusion from aggregation. In this paper we describe the use of novel methodology, based on 1H NMR spectroscopy, to study lipoprotein particle fusion."

  • Don

    9/15/2011 7:24:04 PM |

    Bill,
    You have no worry since your triglycerides are quite low and therefore your LDL particles are of healthy size.  Your correctly calculated LDL is only 161 using the Iranian formula (used if triglycerides low).  See LDL calculator here:
    http://homepages.slingshot.co.nz/~geoff36/LDL_mg.htm

    And never use statins, just cut carbs.
    Don

  • cancerclasses

    9/15/2011 7:34:54 PM |

    "About 80% of cholesterol is composed of fats and oils (Current Atherosclerosis Reports 2004). The
    majority of an arterial clog, 55%, comes from defective cooking oils, containing mainly damaged omega 6. Most of us unknowingly purchase these oils in the cooking oil section of the supermarket. These are the oils we fry with and the oils added to most packaged foods; both fresh and frozen.

    Here’s another shocker. It’s not the saturated fat —it’s the adulterated omega-6 from food processing that clogs arteries! Contrary to what we have heard for decades, it is not the saturated fat you eat that clogs your arteries! How do we know this? A 1994 Lancet article reported investigating the components of arterial plaques. In an aortic artery clog, they found that there are over ten different compounds in arterial plaque, but NO saturated fat. This means the bacon, eggs, cheese, steak, whipped cream, etc. isn’t the reason for a clogged artery. These natural saturated fats are actually good for you. You need them for body structure.

    With the consumption and transport of defective processed oils, LDL cholesterol acts like a “poison delivery system,” bringing deadly transfats and other ruined oils  into the cells. It is primarily the oxidized (adulterated) omega-6 that clogs the arteries, NOT saturated fat!"  

    For more just google 'Brian Peskin saturated fat' and read the day away to your heart's content.

  • Jack Kronk

    9/15/2011 8:37:50 PM |

    "just because somebody says something about it. Use your own brain, put together everything you know and can learn on your own and connect ALL the dots before drawing a conclusion. "

    lol. you must not know who CMast is.

  • cancerclasses

    9/15/2011 10:27:09 PM |

    Yeah, I do, and that's why I said that.

  • Dr. William Davis

    9/16/2011 2:40:13 AM |

    Hi, Gib--

    The strategies that reduce small LDL are the same whether it's genetically-driven or acquired. However, when (presumptively) genetically-driven, it's just harder and requires a more meticulous effort.

    We are now seeing more and more people achieve zero or near-zero small LDL with strict carb reduction. The big exception is apo E4 people, who can still struggle because of the peculiar physiologic effects of this pattern.

  • Dr. William Davis

    9/16/2011 2:42:32 AM |

    Big issue. Note that the real culprit in causing plaque may be glycated oxidized LDL.

  • Dr. William Davis

    9/16/2011 2:43:51 AM |

    Hi, Peter--

    No, I think that is wrong. It might be correct if small LDL is regarded in a dichotomous way, i.e., pattern A vs. pattern B. But, when viewed quantitatively, I believe the real culprit is quantity of small LDL.

  • Dr. William Davis

    9/16/2011 2:46:58 AM |

    No question: The various lipoprotein testing companies need to talk and standardize their definitions. But this does not invalidate the concepts.

    Chris Masterjohn is a very bright guy. But on this I disagree. I believe it is wrong to assume that triglycerides and HDL behave in perfect tandem with small LDL. While they do indeed correlate, they do not correlate perfectly and demonstrate independent behavior depending on postprandial phenomena and genetic factors like apo E and apo C.

  • Joyce

    9/16/2011 5:17:54 PM |

    This has nothing to do with LDL, but I don't know where else to ask this, so I'll dive right in.

    I am reading and enjoying your book Wheat Belly, but don't understand why you lump chia seed in with other non-gluten grains to avoid or minimize. .  In my mind it is closer to flax.  Chia is truly an oil-seed and not a grain according to Dr. Coates, the "father" of chia seed research.  I have used it generously, and feel it aids in weight loss.  Chia seed is high in protein and fiber and low in carbs.  Why are you telling us to avoid or limit it?  I feel it is healthier than flax even.

    Please, can you clarify your stance on chia?  I was very disappointed to read that in your book.  Other than that, I really enjoyed Wheat Belly, having avoided gluten for a few years now.

  • Joyce

    9/16/2011 5:33:17 PM |

    P.S.  According to calorieking.com website, 1 oz. raw chia contains 0 carbs and 1 oz. dried chia contains only 1 gram of useable carb.

  • Adriana

    9/17/2011 10:16:37 AM |

    Not everybody who has good HDL, good TG and eats a low carb paleo diet will have low small particle LDL numbers which is why an NMR LipoProfile is important.  People with gut issues, yeast issues,  H. Pylori or an otherwise compromised liver can have unhealthy LDL despite doing everything right on the diet front.  Getting to the root of these issues is critical to resolving it.

  • Dr. William Davis

    9/17/2011 1:23:49 PM |

    Thanks, Joyce. But I don't remember lumping chia with the bad stuff.

    In fact, as you point out, chia belongs with flaxseed as one of the few truly healthy, low-carb foods.

  • Joyce

    9/17/2011 1:45:31 PM |

    Dr. Davies, on p. 212 of your book, chia is lumped in with other non gluten grains.  Maybe in future editions, the publisher can remove that?

    Although I have been gluten free for years, my husband is finally going gluten free..ALL BECAUSE OF YOUR BOOK!  He has some health issues, so for that I humbly thank you.

    Also, his next Toastmasters speech will be on "Wheat Belly"...how about that!

    Thank you so much for a wonderful book.  Your recipes are awesome.  I look forward to a Wheat Belly cookbook!!!!

  • Linda

    9/17/2011 2:57:40 PM |

    There are so many well read and brilliant posters here that I am going to jump in and ask a question totally off topic. This is not Dr. Davis' area of expertise, so I hope others may help.
    I do believe I am dealing with a bone/heel spur. Too much treadmilling, trying to increase speed, etc. I have done research on the condition and I read that turmeric, taken 2-3 times a day, is helpful. I just recently began taking D3 as well, 5000 IU a day. Will the Vit D3 help as well?
    Any thoughts? No, I am choosing not to visit a doctor for a cortisone shot. I am using NSAIDS for the pain and that works very well.

  • nina

    9/17/2011 4:48:56 PM |

    I've just spotted this post.  Never tried chia and wonder what you thought.  Have your patients reported similar effects?

    Nina

  • steve

    9/17/2011 7:26:34 PM |

    We are now seeing more and more people achieve zero or near-zero small LDL with strict carb reduction. The big exception is apo E4 people, who can still struggle because of the peculiar physiologic effects of this pattern

    Could you go in to more depth as to what strict carb reduction menas?  Is it no more than 50grams of starchy carbs such as rice or potatoes, or 100Grams?  I am guessing it is individualized, but some range of restricitons with those who have been successful would be helpful.  
    I have always had a low level of Trigs- never higher tnah 75 even on a hi carb diet, and was surprised to find the NMR showing all small particles!  So Dr. Davis is right to say low Trgs not always indicative of having large LDL.  Switched to elimination of most carbs and totally changed the profile.  Only issue that is while i produced lots of particles with carb diet, i also produce lots of LDL particles with carb restriction.  Genetics i guess!  I am an ApoE 3/3, which was a surprise.  
    Thanks for the good work Dr. D.  Have gotten several to buy Wheat Belly.  It will have an impact!

  • Joyce

    9/17/2011 7:30:40 PM |

    Nina, I am not Dr. Davis (wish I had his knowlege!), and I hope he doesn't mind me jumping in here, but I leaned about chia a few years ago when I read a book by Dr. Wayne Coates on the subject.  Chia has definitely helped me lose weight.  It is very filling.  When mixed with fluids, the chia seeds expand, and they really help to fill you up.  I've found all sorts of wonderful chia recipes on the web - from Chia "Tapioca" to beverages, etc.  I mix  it into many foods.  I think it enhances their taste.  I feel the chia seeds help with weight loss because of their appetite suppressant potential.  I hope this helped, and my apology to the good doctor for hogging the thread.

  • PeteKl

    9/17/2011 10:24:07 PM |

    Your post doesn't provide a lot of info, but if I were to guess I would say your problem is more likely related to walking/running incorrectly than nutritional (assuming you are in reasonable physical condition).  The human foot wasn't designed to be encased in the heavily cushioned shoes we typically wear today.   As a result many of us don't know how to walk or run correctly.

    Some of the better shoe stores will video tape you on a treadmill.  Just seeing the tape may be enough for you to realize what you are doing wrong.  If that doesn't help, there are professionals who should be able to figure out what might be happening.  

    Also consider reading "Born to Run" if you haven't already (it's a good read even for non-runners).  It probably won't give you a direct solution, but it may give you some ideas on where to look.  Good luck.

  • Louise

    9/18/2011 2:10:34 AM |

    Dr. Davis,
       I am 56 and have a strong history of heart disease in my family. I have been eating low carb for a couple of years... ( around 60 gms carb per day average..no pasta, no potato, almost no grain)  My most recent lipid panel showed LDL of 140. HDL 81, Triglycerides 43, CRP 0.2. .  I requested a test to show size of LDL. My doctor declined to order this, saying all LDL is bad.  Instead I was sent for a heart scan  ( paid out of pocket) and my calcium score was 0.  
      So now I'm trying to lower my LDL by lowering saturated fat.  Hard to do when you eat low carb. I wonder if I might be one of those Apo E 4 types that you mention, so thought I should try,.
      Here are my questions:
         Can I test my LDL size myself, through a home test? Or should I try to find out if I have Apo E 4?
          Do I really need to lower LDL if my calcium score is 0?
    Louise

  • Bob Goldstein

    9/18/2011 4:02:36 AM |

    For the last year I have eaten zero fruit, zero grains, zero sugar. Have mostly eaten beef, occasionally eggs cooked in butter. Have done two VAP tests the last year. When I started a year ago, trigs were 115, now 142. HDL was 50, now 46. My LDL did show a change of going from pattern A/B to pattern A.
    Any ideas why a diet for a year devoid of fruit, sugar, grains, would show an increase in trigs, and a slight decrease in HDL. If I have Apo E4 would my ldl go from A/B to A.
    I have lost 25 lbs. in the past year. Could this be a reason my numbers seem to be off?
    Thanks,
    Bob

  • Dr. William Davis

    9/18/2011 3:44:29 PM |

    Hi, Bob--

    Yes, blood drawn in the midst of weight loss can be very misleading.

    Transient effects include increased triglycerides, reduced HDL, even much higher blood sugar. Thankfully, it all gets much better once weight plateaus for a couple of months.

  • Dr. William Davis

    9/18/2011 3:47:39 PM |

    Hi, Louise--

    Sad that you have to educate your doctor.

    I find it unacceptable that a nice person engaged in health is refused a simple, helpful test. Tell your doctor goodbye and find one willing to act as your partner and advocate in health, not an obstruction.

    Yes, you can test it yourself through services like PrivateMDLabs.com. My view is to 1) identify how much, if any small LDL there is, then 2) reduce small LDL with diet. If you have only large LDL, you will absolutely need an LDL particle number by NMR or an apoprotein B to know what the REAL value is.

  • Dr. William Davis

    9/18/2011 3:49:52 PM |

    Thanks, Steve.

    There are a number of posts on this blog that detail how to gauge individual carbohydrate sensitivity. The best way is to check 1-hour after-eating blood sugars. Second best: count carb with the cutoff being determined individually. Just go back over the past 6 months and you will find several discussions.

  • Dr. William Davis

    9/18/2011 3:51:17 PM |

    Hi, Joyce--

    Thank you!

    If chia is listed as among undesirable non-gluten grains, that was my error. Remember what Mark Twain said: "Don't read about health, else you might die of a typo."

  • nina

    9/18/2011 5:13:58 PM |

    Thanks for your response Joyce.  

    The part that fascinated me was the idea that chia triggers a drop in blood sugars without a pre-spike.  I can't find anything on the net about that and wondered if other people had similar experiences.

    Nina

  • Bob Goldstein

    9/18/2011 7:08:22 PM |

    Thanks for the reply Dr. Davis. I have a blood test scheduled six months from now, and hopefully I will see better numbers. My LDL shows pattern A so at least I did see one positive change.
    Love your blog. Have learned a lot and it was the reason I gave up grains and sugar. 1 full year, no cheats.

  • Annlee

    9/18/2011 10:41:56 PM |

    Consider also going barefoot as much as possible - around the house, etc. You don't necessarily have to run barefoot (unless you work into it *gradually* and choose to continue it). I've recovered from heel spurs with stretching my achilles, with emphasis on stretching the soleus, and letting my feet bear my weight without any props underneath. For stretches, Anderson & Anderson have a very good book - Stretching - available on amazon.com. You didn't develop the spurs overnight, and they won't clear that quickly, either. Be patient and work with your body.

    You may also wish to consider vitamin K2, very good for ensuring calcium deposition occurs in the correct locations.

  • Kira

    9/19/2011 6:52:43 AM |

    Hi Doctor Davis, I talked to your about a year ago and you were kind enough then to comment on my blood results saying there was nothing to worry about - according to the Iranian formula.  I would greatly appreciate if you looked at my new results, they scared my whole family, I certainly am not going to show to the family physician, and I don't even want to think about changing from paleo style of eating to some kind of low fat cholesterol lowering diet, and taking any drugs/supplements. But may be I have to? I am 36 y.o., 5'4 and weigh 104lb.
    Glucose 85
    VAP TEST:
    Lipids
    LDL Cholesterol 149!
    HDL 130
    VLDL 14
    CHOLESTEROL, Total 293!
    Triglycerides 48
    Non HDL Col (LDL+VLDL) 163!
    apoB100-calc 96
    IDL Cholest 4
    Remnant Lipo. (IDL+VLDL3) 12
    Sub-Class Information:
    HDL-2  35
    HDL-3  95
    VLDL-3  8
    LDL1 Pattern A 3.1
    LDL2 Pattern A 26.0
    LDL3 Pattern B  71.0
    LDL 4 Pattern B  31.4

    The ordinary, non-VAP Lipid panel shows:
    Cholest TOTAL 279 !
    Triglycerides 48
    HDL Cholest 144
    VLDL Cholest Cal 10
    LDL Cholest Calc 125 !

    Also, I can't understand how my vit. D can be so low - 29.0, when I have been sun tanning all summer here in Orange County, California, at peak hours. Is there anything that you know of that may inhibit the vit. D conversion from the sun?
    Again, I greatly appreciate any insight that you can give me on this situation...

  • Louise

    9/19/2011 4:52:38 PM |

    Dr Davis,
      Thank you for your reply.  For now, I found a lab I can go to and get myself tested. Two hours away.. (Oddly, I must leave NY state to get this done due to billing law.). I'm going to do this! Do you agree that my best choice is the NMR?

  • otterotter

    9/19/2011 5:43:51 PM |

    Hi Gib,

    Option 1 will be cutting the saturated fat and cholesterol from the diet in addition to cutting the carbs. I tried eliminating eggs and cheese and my total cholesterol down from 400 to 260. By adding back "one egg a day", it went back to 320 (that's the impact of the dietary cholesterol on me, confirmed twice). I am currrently trying to replacing all saturated fat with mono unsaturated fat (olive+canola), just want to see how big the impact is. I am also going to test coconut oil separately, it is a cholesterol-free plant based medium-chain saturated fat, there is a chance I might respond to it differently.

    Option 2 will be taking Statin drugs. I know it has side effects, but that's better than small dense LDL. Based on Dr Davis's previous response, for apoE, sometimes we have to go to Statin for the rescue. (My doc was pushing statin really hard on me, and I have been resisting that for the last year)

    otter

  • Joyce

    9/19/2011 5:50:45 PM |

    Dr. Davis, you are so funny.  We'll take your book....typos and all!  Now...how about a cookbook to compliment Wheat Belly/  PLEASE????

  • nina

    9/19/2011 7:41:34 PM |

    Sorry I missed the link:

    http://suzanneloomscreativity.blogspot.com/2011/09/lowering-blood-sugar.html

    Nina

  • PeteKl

    9/19/2011 9:24:31 PM |

    Hi Kira,

    Just out of curiosity, could you summarize your "paleo style of eating".  I have a good friend of mine who has similar numbers (low trigs, high HDL, high LDL).  I would describe her diet as "low-carb (no sugar, no grains), low-veggie (under 15%), high meat, high sat-fat (particularly cheese, eggs and coconut)".  Is your diet somewhat similar?  I would be interested to know how the two of you compare.

  • Dr. William Davis

    9/20/2011 12:36:46 PM |

    NMR is my preferred method, since it yields the LDL particle number, what I believe should be the gold standard.

  • Dr. William Davis

    9/20/2011 12:38:12 PM |

    Thanks for asking, Joyce! I've had very preliminary conversations with my editor, but nothing firm yet.

    In the meantime, in addition to the discussion on this blog, see the Wheat Belly Blog, where I will publish recipes one by one.

  • Dr. William Davis

    9/20/2011 12:41:39 PM |

    Hi, Kira--

    You have a surprising dominance of small LDL particles, despite your slender build and lifestyle (LDL 3+4 divided by "real" LDL). This is likely genetically-determined. The means of correcting this is beyond the scope of this blog, unfortunately. You might consider joining the discussion in the Track Your Plaque website.

    The vitamin D issue is common, an impaired or lost ability to activate vit D in the skin. It means doing it orally.

  • Adam

    9/20/2011 6:40:19 PM |

    Dr. Davis. I'm a type 1 diabetic who is on a low carb diet (mostly primal-esque) with only meat and veg. No fruit, no grains, no legumes. I lost 14 kgs in the first three months, then stabalized at around 89 kgs. Granted my fat is going down a wee bit as muscle mass increases (doing the slow burn exercises, plus HIIT training and martial arts). That is the background.

    The reason I'm posting here is confusion about cholesterol. I just got my latest results back from the lab, and they are the same. While my HbA1C is 5.3 (not bad), my cholesterol numbers don't look hot. Tryglicerides are fine (as I've stopped losing weight quickly), but HDL is low at 39, and LDL (doctor forgot to put in particle size check, but it cna't be that good as I'm a diabetic) was 150 on the spot. This was measured, not calculated.

    I take ~7k miligrams (or whatever the measurement is) of fish oil a day. Well, 7k of EHA/DHA, more in total quanity including inert substances. With my exercise, low carb diet, and fish oil supplements, how is it that my HDL are still so low? Any advice?

    Thanks!

  • Dr. William Davis

    9/20/2011 11:08:46 PM |

    Hi, Adam--

    How timely! See the next post after the one you responded to in which I discuss the transient effects of weight loss, including drops in HDL that rebound over time.

    Also, have you address vitamin D normalization? I aim for 60-70 ng/ml, which usually requires around 6000 units per day (gelcaps or drops only); the HDL-raising effect develops over a year or longer.

  • Adam

    9/21/2011 1:01:18 PM |

    Dr Davis,

    A pleasure to make your (virtual) acquaintance! My vitamin D, according to my last test (results came in yesterday, as I mentioned) levels are 59. A wee bit low, but not too bad, I think.

    I've been consistently 88/89kg for three months (I've been low carb/primal for 6 months total), so haven't lost any weight in the past three months, but still my HDL levels are very low. Do you have any suggestions?

    Cheers,

    Adam

  • Adam

    9/21/2011 1:03:52 PM |

    P.S. I'm pretty sure I've stabalized, as my triglycerides were at 29 or 39 (can't remember off hand, but pretty low). But still I had the low HDL and high LDL?

  • Dr. William Davis

    9/21/2011 9:37:43 PM |

    Hi, Adam--

    Of course, you are wheat-free, low-carb in addition to your vitamin D? Omega-3 fatty acids?

    Note that doing the diet and taking the vitamin D yield rises over 1-2 years. Patience is required.

    Consider a little red wine and dark chocolate, as well.

  • Adam

    9/22/2011 5:10:38 AM |

    Thanks for the response! Yes, I am completely wheat free (and was before I read your book, which was excellent). I am very low carb due to the diabetes. My HDL did go from 29 to 39 this last test (after 6 months), so I suppose, as long as maintaining this diet will continue to increase my HDL, I am ok. My concern isn't immediate gratification but more continuous improvement.

    I'll come bug you again in 3 months if my HDL doesn't continue to increase Smile

    Many thanks!
    ---Adam

    P.S. I've never been accused of not drinking enough red wine Smile While I've been beer free for 6 or 7 months now, I do go through ~2 bottles of red a week.

  • Adam

    9/23/2011 1:35:08 PM |

    Hah! Me too, because if my HDL doesn't start going up I'm gonna freak as I don't know what else to about my numbers. Diet is about as stripped down as it can be, and I'm exercising as much as is reasonable.

    --Adam

  • Kira

    9/24/2011 6:23:22 AM |

    HI Peter. I would say  that my diet could pretty similar, with the exception that I am still eating some low-glycmic fruit everyday (some cantaloup, grapefruits, berries) and eat lots of veggies.

  • Kira

    9/24/2011 6:29:11 AM |

    Dr. Davis, thnx for your reply. I understand this is a blog and it is hard to go into details here, but would you say that it is worth for me to try change this situation by changing the die to using less saturated fat? and would NMR test clarify anything?

    PS How do I further discuss this issue "by joining the discussion in the Track Your Plaque website"?

    Thnx AGAINSmile

  • ShottleBop

    9/25/2011 3:47:09 PM |

    My numbers are like Bill's.  I was diagnosed as pre-diabetic in February, 2008 (today, I'd have been diagnosed as Type 2; my A1c was 6.5, and my FBGs were 127 and 123).  Started low-carbing shortly after that:  cut out grains, starchy veggies, almost all fruit, all milk (still use heavy cream and eat cheese).   My most recent blood lipids (accounting for some variation, but roughly consistent in pattern over the past three years):

    TC:  381
    LDL (direct):  279 (291 calculated)
    HDL:  80 (was 40 at diagnosis)
    Trigs:  52

    (At diagnosis, my numbers were:
    TC: 281
    LDL (direct) 215
    HDL: 40
    Trig: 142)

    I lost 65 pounds in the first 9 months after diagnosis, and, since then, have regained approximately 25 pounds (mostly muscle).  Weight has been stable for months.  My doctor is talking statins, again--which I plan to continue resisting.  I have ordered an NMR test, and will see what it has to say about my particle size.

  • Dr. William Davis

    9/26/2011 12:39:56 PM |

    Hi, Shottle--

    Good plan. I wouldn't be surprised if NMR sheds an entirely different light on your values.

  • ShottleBop

    9/29/2011 4:23:57 PM |

    They drew the blood this morning.

  • Bob

    9/30/2011 11:14:10 PM |

    Dr. Davis, I had my NMR test and the doctor who looked at it suggests that I have familial hypercholesterolemia. My LDL-P 3158
    LDL-C 280 HDL-C 58, TGL 105, HDL-P 28.0 small LDL-P 1122,
    LDL 21.7, LP-IR-33. I have been on no carb, no sugar, no wheat, or fruit for the last 14 months. Have been eating fatty meat twice a day and also eggs. Before I started eating beef, I was eating low carb, very little sat. fat. I was eating a lot of skinless chicken breast, and canned salmon, veggies, nuts, fruit but almost no beef. My LDL according to the basic lipid test was a little high but not crazy high. My HDL was in mid 30's. and trigs were high. I changed to a high saturated fat diet to raise HDL and lower trigs. I have been taking 1 gram of fish oil 2X daily. Is it possible that the fish oil is having an effect on my LDL? Not sure what to do about my diet. Obviously I won't go back to sugar and wheat but what about all the meat I have been eating. Would it be better to go back to skinless chicken and egg beaters even if it means my HDL going down? Just not sure what to do. Doctor believes I am at high risk since my father died at age 62 of sudden death.
    Thanks,
    Bob

  • Dr. William Davis

    10/1/2011 1:48:14 PM |

    Hi, Bob--

    This is a tough situation that, unfortunately, cannot be remedied diet alone. I hate saying that.

    Like people with apo E4, familial heterozygous hypercholesterolemia people are fat sensitive. First order of nutritional business remains carb-restriction to minimize small LDL particles, but you can still show large increases in large LDL with fat intake. If apo E4 is present, too, then even something as great as fish oil can increase LDL measures. However, the dose of fish oil you are using is very small and not a likely factor.

  • Bob

    10/1/2011 2:57:34 PM |

    Thanks for the reply Dr. Davis. I know I won't go back to carbs and sugar, but what about beef. I have eaten almost nothing but beef the last 14 months. Would I be better off going back to skinless chicken breast? Egg Beaters, instead of eggs? Olive oil instead of butter? I know in the past when I limited saturated fat my HDL dropped to mid 30's.
    Bob

  • Dr. William Davis

    10/2/2011 2:46:17 PM |

    Hi, Bob--

    I think we could make a strong argument in favor of variety in diet and that includes meat sources. Yes, I think a broader range of meats (if you eat them; I don't want to sound like a bloodthirsty carnivore; I don't even like meat, personally) is better--fish, shellfish, fowl, pork, as well as eggs.

  • ShottleBop

    10/3/2011 10:02:47 PM |

    Results came back today:
    TC:  373 mg/dL (ref <200)
    LDL-C:  282 mg/dL (ref = 40)
    Trigs:  47 mg/dL (ref < 150)
    Large VLDL:  <0.7 (ref <=2.7)
    LDL-P:  1793 nmol/L (ref = 30.5)
    Large HDL-P:  14.2 umol/L (ref >=4.8)
    Small LDL-P:  146 nmol/L (ref  20.5)
    HDL size:  10.0 nm (ref >=9.2)
    VLDL concentration was too low to determine a size
    According to the interpretive information:
    My HDL-P (total) of 39.1 places me in the lowest category of risk (it is beyone "high")
    My small LDL-P places me well below the 25th percentile (while slightly higher than the "low" level of 117), and is indicative of lower risk for CVD
    My LDL size places me well above the 75th percentile, and well into Pattern A territory (75th percentile level is 20.6), and is indicative of lower risk for CVD

  • ShottleBop

    10/3/2011 10:04:16 PM |

    Correction:  My LDL-C was 282, vs. a reference of " 40"

  • ShottleBop

    10/3/2011 10:06:37 PM |

    I give up.  I am typing things in correctly, and the comment system is dropping words (maybe it's interpreting my use of "greater than" and "less than" symbols as markup code?).  My HDL-C was 82.  The reference level is greater than 40.  My LDL-C was 282; the reference level is less than 100.

  • ShottleBop

    10/3/2011 10:09:37 PM |

    I see it dropped more information than I thought at first.  No matter, the conclusion stays the same: except for my LDL particle number and concentration, all of my lipid values indicate that I am at lower (or much lower) than average risk of CVD.  Now if only my body takes that to heart . . ..

  • ShottleBop

    10/3/2011 10:16:32 PM |

    LDL particle size was 22.1
    HDL-P was 39.1 umol/L

  • Dr. William Davis

    10/4/2011 2:41:25 AM |

    Hi, Shottle--

    Your values highlight this tremendous void we have in knowing just what to do about nearly "pure" large LDL particles.

    In other words, you have lots of LDL particles, but they are nearly all the more benign large variety. What level of large LDL particles are "allowable" before they contribute to atherosclerotic plaque formation? Not known. My preference would be, given the extreme abundance of large LDL, to reduce with statin drug. I hate to say this, but this is the occasional exception in which I believe that statins might indeed be beneficial. This is not to be confused with the general and absurd overuse of the drugs, but an application for a very specific genetic variant.

  • Louise

    12/5/2011 10:58:49 PM |

    At last I have had an NMR.  Thank you for the suggestion of PrivateMDlabs.com.  I can recommend this
    to others who find their doctor unwilling to order tests.
    I am pondering my results, trying to figure out if they are okay, or if I need to cut back on fat now, or go lower with carb reduction. What are your thoughts, Dr Davis?
       LDL Particle Number  1091  ( IS this too high??)
        Small LDL - P    129
          LDL size     21
        Large VLDL - P   < 0.7
           Large HDL - P        12.1
            HDL size           9.7
          LP - IR score    11
    Triglycerides are 32  ( lower since I"ve gone completely
    grain free since my last lipid panel)

  • Dr. William Davis

    12/6/2011 5:26:54 PM |

    These values are excellent, Louise! The only less than perfect value is the large HDL, but this tends to drift higher very slowly.

  • GoodStew

    5/11/2013 1:56:57 AM |

    Seems particle size doesn't matter as much as particle number. According to Dr. Peter Attia, a particle is a particle.  More than 1000 is a risk factor whether they're small, medium or large and fluffy.

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