Gretchen's postprandial diet experiment II

3. January 2010 William Davis (37)
I previously posted Gretchen's postprandial diet experiment, in which she consumed a low-fat diet for a day, followed by a low-carbohydrate diet for a day. Grethen monitored blood glucose and triglycerides with fingerstick checks. (Blood glucose can be checked on any widely available glucose monitor; triglycerides can be monitored with the Cardiochek device.)

Let's now discuss what happened.

On the low-carb, high-fat day, there was an initial surge in triglycerides to 250 mg/dl late morning, followed by a secondary peak several hours following dinner. Because fat is mostly triglycerides, Gretchen's high-fat (sausage, bacon, butter, whole-fat yogurt) breakfast provided a large quantity of triglycerides that needed to be absorbed. This generally occurs over approximately 6 hours, varying depending on body weight, how accustomed you are to fat, activity level during the day, the kind of fat in the meal. The high content of saturated fat in Gretchen's high-fat breakfast likely caused the somewhat slower drop in triglycerides over approximately 7 1/2 hours.

As Gretchen herself had noted, triglycerides the following day were lower, a typical low-carb response. Blood sugar throughout showed only minor variation, with only small postprandial increases.

Thus, Gretchen experienced what we'd expect with a low-carb, high-fat diet: an initial high surge in triglycerides, followed by a decline in fasting levels, while blood sugar shows a normal contour.







Now, the more confusing low-fat experience:



Blood glucose makes a striking peak at 200 mg/dl after the low-fat breakfast of pasta and rice, in contrast to the low-carb breakfast. Triglycerides behaved very differently from the low-carb experiment: While there was no initial postprandial surge, there was a late surge developing 6-24 hours later. The late surge continued into the next day, with fasting levels the following morning (210 mg/dl) exceeding the starting triglyceride level (60 mg/dl).

The one potentially confusing aspect of all this is Gretchen's late rise in triglycerides on the low-fat diet. This phenomenon is due to something called de novo lipogenesis, or the liver's conversion of carbohydrates to triglycerides that occurs when an excessive carbohydrate load comes through diet. Because the human body cannot store anything beyond a minor quantity of carbohydrates (as glucose and glycogen), carbohydrates are converted to fats.

Another factor causing the late triglyceride increase is insulin resistance, given the high blood sugar response. When insulin resistance is present, the activity of the enzyme, lipoprotein lipase, is reduced. Less lipoprotein lipase activity allows slower VLDL degradation, allowing VLDL (and thereby triglycerides contained in VLDL) to "stack up" in the blood. Thus, the higher triglycerides late after eating and into the next morning.

One issue to be aware of: Acute responses can differ from chronic responses. In other words, had Gretchen had the luxury (and time and money) to conduct the experiment over, say, 4 weeks, rather than a single day, there would be somewhat different responses. The best data on this come from Dr. Jeff Volek of the University of Connecticut, in which 4 weeks of low-carbohydrate eating modify fasting and postprandial responses over time.

Several conclusions can be made from Gretchen's experience:

1) Low-carb, high-fat acutely generates extravagant postprandial triglyceride responses.
2) Low-fat causes a late triglyceride surge and higher fasting triglycerides.
3) Low-fat leads to high blood sugars and, by implication, diabetes.


Both the low-carb and the low-fat responses are undesirable, both leading to increased risk for heart disease. Which is worse? I believe that low-fat is more destructive, since it leads over time to both high triglycerides and diabetes, while low-carb/high-fat only leads to postprandial triglyceride surges, at least acutely.

How to best balance the responses to reduce risk for heart disease? That's a discussion for future.


Again, my thanks to Gretchen and the substantial amount of effort that went into generating these numbers. More of Gretchens' own writing can be found on her blogs:
http://wildlyfluctuating.blogspot.com
http://www.healthcentral.com/diabetes/c/5068
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Comments (37) -

  • Pythonic Avocado

    1/3/2010 3:53:05 PM |

    Why do you say the low-carb response  is leading to increased risk for heart disease?

  • Stan (Heretic)

    1/3/2010 5:34:56 PM |

    Re: Both the low-carb and the low-fat responses are undesirable, both leading to increased risk for heart disease.

    With due respect, I would disagree that BOTH are undesirable, but I agree that the one caused by the low fat high carb diet (only) is indeed dangerous!  

    It was never proven that high triglycerides alone cause heart disease.  The available trials such as Framingham (1)  may have shown some correlation with the total cholesterol but correlation is not causuation, especially that the statistics do not distinguish between various diets. Furthermore, Framingham's correlation is restricted to men only (not women) and only for the age group 30-55.  For older men and for women of all ages the correlation becomes insignificant or reversed.

    Given the above data, I think the most plausible interpretation leads me to a conclusion that the most likely direct cause of atherosclerotic cardiovascular disease is excessive blood glucose with hyperinsulinemia  (see the following papers, and Stout's papers(2) ).

    Hyperglycemia and hyperinsulinemia also happen to coincide with elevated TG and LDL but those are coincidental markers of metabolic syndrome induced by the common high carb (high sugar) diets rather than causing heart disease.  That I believe has nothing to do with dietary fat.

    Regards,
    Stan (Heretic)

    -----------
    Refs:

    1) JAMA. 2004 May 12;291(18):2243-52. Drug treatment of hyperlipidemia in women. Walsh JM, Pignone M.

    2) INSULIN-STIMULATED LIPOGENESIS  IN ARTERIAL  TISSUE  IN RELATION  TO DIABETES AND ATHEROMA,
    R.W. STOUT, Lancet Sept 28, 1968, p702.

    and

    INSULIN STIMULATION OF CHOLESTEROL
    SYNTHESIS  BY ARTERIAL TISSUE,
    R.W. STOUT, Lancet Aug 30, 1969, p467.

  • Nigel Kinbrum BSc(Hons)Eng

    1/3/2010 5:41:31 PM |

    As serum TG's with the HF meal are lower at the end of the day than at the beginning, does this suggest that successive days of HF meals produce progressively lower & lower TG's?

  • Anonymous

    1/3/2010 6:02:56 PM |

    I would love to hear about how to balance the risk between these extremes!  Wow, nice post.

  • Dr. William Davis

    1/3/2010 10:11:35 PM |

    Pythonic and Stan--

    It's not that triglycerides per se are atherogenic, but the POSTPRANDIAL PARTICLES that triglycerides represent are atherogenic.

    In other words, high triglycerides signals extravagant chylomicron remnants and VLDL, both of which are atherogenic.

    In the ongoing debate over what constitutes a healthy or unhealthy diet, the entire issue of postprandial patterns has been ignored. Yet much of heart disease develops IN THE POSTPRANDIAL PERIOD.

  • shel

    1/3/2010 10:55:38 PM |

    i eat copious amounts of fat with positive effects. i'm a layman, but "postprandial" or not, i'm having a hard time accepting this, as the evidence i've read seems to contradict what you're saying regarding overall benefits.

    why did no one pick up on the "postprandial particle" issue until now?

    will this be a new controversy sweeping through the paleo/low carb blogging community now? ;)

  • Dr. William Davis

    1/4/2010 2:15:45 AM |

    Anyone desiring a full accounting of the hundreds of studies documenting this effect will need to refer to the Track Your Plaque Special Report, Postprandial Lipoproteins: The Storm After the Quiet.

    This literature is, unfortunately, relatively difficult to understand. But just because nobody else has incorporated these findings into diet advice doesn't mean it isn't important.

    Keep in mind that most dietary advice is NOT based on observation of postprandial phenomena.

  • Eric

    1/4/2010 5:53:50 AM |

    I had a stroke last month. (Very minor, I went immediately back to work.)  As a 35 year old non-smoker/non-drinker who generally ate low carb and avoided sweets before the stroke (and had been exercising regularly for 6 weeks), I'm baffled as to why my triglycerides are between 600 and 900.  I'm now on Lovaza.  Against my doctor's advice, I decide to do a paleo type diet.  We'll see how the lipid panel does at the end of this month, but so far avoiding wheat and grains has generally made me feel better.  I've lost some weight as a bonus.

    The doctor is blaming my triglycerides for the stroke, and just calling it hereditary.  It'd be nice to know just what gene I have that causes strokes!  No blood clotting disorders, no diabetes, no pancreaitis, and no hole in my heart either.

  • Alen Kcatic

    1/4/2010 10:58:09 AM |

    First let's take a brief overall look at heart disease because you need to combine two other major lifestyle habits with diet to truly make a difference in reversing or preventing heart disease.


    But here's the good news. You can prevent or reverse heart disease by following care

    Avoid tobacco
    Be more active and walk 30 minutes
    Choose healthier food, including more fiber, less saturated fat, and less salt.

  • Peter

    1/4/2010 12:38:21 PM |

    If it were as simple as low fat leads to diabetes, the Japanese who ate the traditional low fat high rice diet would have had extremely high levels of diabetes, but they hardly had any. I would be more inclined to wonder if our diabetes epidemic is due specifically to flour and sugar rather than low fat in general.

  • shel

    1/4/2010 4:27:36 PM |

    ~Dr Davis, i wonder if this finding is going to point toward advocation of "grazing", rather than two or three meals per day (in a low carb context).

  • kris

    1/4/2010 6:04:12 PM |

    Dr. Davis,
    Happy new year.
    here is the link to videos about FDA and drug giants. An eye opener. just in case you have not looked at it. total of 8 videos.
    http://www.veoh.com/search/videos/q/generation+rx#watch%3Dv18919526gZ4fkAAk

  • StephenB

    1/4/2010 7:16:32 PM |

    Dr. Davis, the abstract of the study you linked read: "Ten men consumed a low-carbohydrate diet rich in monounsaturated fat (MUFA) and supplemented with n-3 fatty acids for eight weeks."

    As you know, there are multiple low carbohydrate diets. This particular study did not examine a high saturated fat diet. I would love to see the result of chronic dieting featuring quality saturated fats like tallow, lard, butter, and coconut milk and avoiding hydrolyzed fats.

  • mark

    1/4/2010 7:19:28 PM |

    Dr. Davis wrote:
    "The one potentially confusing aspect of all this is Gretchen's late rise in triglycerides on the low-fat diet. This phenomenon is due to something called de novo lipogenesis, or the liver's conversion of carbohydrates to triglycerides that occurs when an excessive carbohydrate load comes through diet. Because the human body cannot store anything beyond a minor quantity of carbohydrates (as glucose and glycogen), carbohydrates are converted to fats."

    We don't see triglycerides being converted to glucose. It's a one way street.

    Would having increased carbohydrayte storage space in the body be preferable to storing triglyceride? We have an example of that in hyperglycemia. That's storage in the bloodstream. But the body works quickly to CORRECT that.

    So it's not that the body lacks glucose storage and triglyceride is the bad alternative. Not that at all. The body works hard to push glucose out of blood storage and into triglyceride in fat cells. That's a good thing.

    Postprandial high triglycerides from a high fat diet is a marker of fat intake. Postprandial low triglyceride on a high carb diet is a marker of carbohydrate metabolism. The later increase in triglyceride is the corrective process.

    It's hard to make the case that triglyceride is itself bad when it's one of the body's innate responses to the bad hyperglycemia. If triglyceride is bad, then the body is stuck between a rock and a hard place. It's win-lose, so the low fat diet is worse than the low carb one.

    Given my experience with dieting, I would favour low carb over anything balanced in the way of fat/carb. From dietary intervention trials, I'm unconvinced that high fat is worse (or much better) than a mixed blend of carb and fat from a mortality perspective. But from experience, I favour low carb for general sense of well-being.


    Stan wrote:
    "Hyperglycemia and hyperinsulinemia also happen to coincide with elevated TG and LDL but those are coincidental markers of metabolic syndrome induced by the common high carb (high sugar) diets rather than causing heart disease. That I believe has nothing to do with dietary fat."

    It's tough to isolate lipids as causal as opposed to effects of diet. Smoking and fructose lead to increased LDL. So in this case, high LDL is really a symptom smoking and fructose intake. The latter two likely being causal for anything related to your health. 8 egg yolks a day on a high fat diet and your LDL is a symptom of that. And some people have normal LDL on that even.

    Mark.

  • Dr. William Davis

    1/4/2010 11:33:43 PM |

    Hi, Shel--

    No, absolutely not.

    Quite the opposite: Given what happens after eating, grazing is a destructive practice that likely increases risk for heart disease.

    See the previous Heart Scan Blog post: http://heartscanblog.blogspot.com/2009/11/triglyceride-and-chylomicron-stacking.html

  • shel

    1/4/2010 11:52:20 PM |

    ~hi Dr Davis.

    i agree. and i do much better when i eat two meals within an eight hour window.

    my focus has always been on keeping blood glucose low (i'm not diabetic, but use a glucose meter for my own curiosity), so was a bit floored by the thought that i have to watch every postprandial spike!

    ...so, what's left? huge salads and skinless chicken breasts? ;)

  • vin

    1/5/2010 9:33:36 AM |

    It is pure and simple observation of two parameters after eating a low carb and low fat meal. Nothing more that that.

    After all most of us eat more than just carbs and fat: there are vitamins, enzymes, minerals, fiber and hundreds of other nutrients. I am certain that they more than compensate any damage that glucose or triglycerides can cause to your arteries.

  • Dr. William Davis

    1/5/2010 4:39:02 PM |

    Sorry, Vin.

    You're kidding yourself if you belief that.

    It reminds me of the people I meet who take a list of supplements 30 items long (though lacking the most crucial like vitamin D) prior to their bypass or heart attack. That's called magical thinking.

  • Kurt

    1/5/2010 9:27:14 PM |

    Both diets seem to be extremes, whereas many of us are trying to eat a balanced diet of vegetables, lean meats, nuts, and some legumes and whole grains - call it moderate fat and moderate carbohydrate - but focusing on heart-healthy foods. I'd like to see postprandial data on that.

  • O

    1/5/2010 10:39:05 PM |

    I have been eating a primal low-carb diet for almost 2 years and feel great.  My fasting blood work is : trig = 40, HDL=88, LDL=114 (calculated), total chol=214, testosterone=606.  My heart scan score is 0.  I am physically active muscular male with 4 intense weights + some cardio workouts 2 hours each.  My bodyfat % is about 8-10% (I can see a clear 6-pack), age=43, height=5'7", weight=160 lbs.

    I have made an analysis of my daily intake in a spreadsheet.  My diet on workout days is 3000 kcal, of which 50% fat (167g, out of which 60g saturated), 20% carbs (150g), and 30% protein (200g).  Half the carbs are timed post-workout (workout shake, followed by dinner of meat + sweet potato).  On a non-workout days, I do not have a shake nor sweet potatoes, so the carbs drop to 10% (70g).

    Given the amount of fats I take every day, I am rather alarmed by the postprandial triglycerides.  My breakfast, in particular, has 57g of fat which will cause probably a substantial postprandial triglycerides.  Breaking up my food intake into many smaller meals doesn't seem to be a good thing.   We don't want increasing carbs or protein at expense of fats either.  Therefore, what is the solution here?

  • Dr. William Davis

    1/5/2010 11:21:32 PM |

    O--

    I am afraid there's no quick answer. That question is answered in an exhaustive report on the Track Your Plaque website.

    Alternatively, you could conduct your own do-it-yourself postprandial triglyceride test.

  • Anonymous

    1/6/2010 3:17:23 PM |

    This doesn't detract from any of the points you're making about postprandial triglycerides--but it looks like you're reading the chart from the wrong side here for triglycerides, from the left instead of from the right.

  • Catherine

    1/6/2010 4:16:40 PM |

    YIKES!
    I have been experimenting with a gluten-free, low carb, low sugar diet for 5 months and my LDL just shot UP from 220 to 230 and my HDL went DOWN a little from 66 to 61. (tryglicerides and CRP are excellent). This is opposite what's supposed to happen. Serum D level is good at 54.

    Can someone please tell me the name of the test to request from my doctor to tell if I have the small evil-type LDL or the big fluffy okay-type LDL?

    Thanks for your help,
    Warmly, Catherine

  • Lucy

    1/6/2010 4:33:54 PM |

    These results seem completely contradictory to the way Dr. Eades described the breakdown of saturated fat in his blog "The blood samples were taken two hours after the meal.  Dietary carbohydrate is absorbed directly into the blood and makes a pass through the liver where it stimulates the production of triglycerides, the fat you see in the blood.  Fat, especially long-chain saturated fat digests very slowly, and doesn’t reach the blood until much later than the two hour mark.  While carbs go directly into the blood, fats take a different route."

    Why was there a triglyceride spike after a high fat meal, but not a high carb one?  Were the fats Gretchen consumed not saturated?  It can't be both ways, which metabolic pathway is correct?

  • Catherine

    1/6/2010 9:08:44 PM |

    Oops, sorry i made a mistake.---My LDL went up from 120 to 130 (not 220 to 230)

  • vin

    1/7/2010 11:16:29 AM |

    Thanks for your comment Dr. Davis but for the first time you sound just like my cardiologist. He does not believe in reversal and thinks it is all down to one's genes and there is nothing one can do to change that. Well I think differently having postponed bypass surgery seven years ago. I will continue with 'magical thinking'. Its nice, you should try it sometime.

  • Anonymous

    1/7/2010 4:29:08 PM |

    To eat one extreme one day (low fat) and then eat another extreme (low carb, high fat) the next is a sure-fire way to get whacky blood/lipid results. Also, lipid levels can fluctuate more than 10% within a given day under normal circumstances. Alternating eating radically different extremes in terms of diet is anything but normal in my view.  Stress, exercise, or even one's sex can cause also shifts.  Trying to prevent every potential/alleged problem with postprandial lipids seems like a sure-fire way to increase stress which is also damaging to the heart and body.  I doubt paleo manwoman worried about the spike in his/her triglycerides from gorging on the fat from fatty meat meals.  I think one can micromanage one's self or rather labs, lipids etc to death...

    PS: Forgot to mention lab error.  Before drawing any conclusions from any lab results, have them repeated multiple times and at different labs.  My husband has to communicate with lab techs for his job and was horrified when one kept referring to "esterified" as "stir-fried"! And this was the one of the largest labs in the US...

  • Jim Purdy

    1/18/2010 4:38:41 AM |

    Doctor Davis, have you seen the new PR campaign from manufactured "food" giant Unilever to "Ban butter to save thousands of lives."

    Unilever is the company behind many fake foods, including fake butters Country Crock and  I Can't Believe It's Not Butter!

    I've posted a little about this ban-butter campaign on my blog at blogsthatmakemethink.blogspot.com

  • shoby

    1/28/2010 3:25:55 PM |

    I also have a blog about the diet we can share experiences and exchange links.
    This blog http://just-slim.blogspot.com
    thanks

  • Fran

    2/1/2010 5:51:52 AM |

    "How to best balance the responses to reduce risk for heart disease? That's a discussion for future."

    Please tackle this discussion soon.

  • ET

    2/26/2010 6:52:28 PM |

    I also keep a spreadsheet that details all the different fatty acids and such for every meal.  I've also had three lipid tests this year which were not fasting.  Two were in the afternoon, eight hours after a five-egg omelet with coconut oil, cheese and bacon; 2 hours later I had eight oz of full-fat greek strained yogurt which adds up to over 120 g of fat 6 to 8 hours before the test.  Add another 40 g of fat 2-hours pre-test and according to your theory, my triglycerides should be high.  On each occasion they were 91.  This is on a low-carb (<70g/day) diet.

    There's more to postprandial triglyceride metabolism than is covered here.  My next test will be a non-fasting NMR lipoprotein analysis.  Should be interesting how that stacks up against a fasting NMR test.

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Alternatives to fish oil capsules

27. October 2006 William Davis (2)
Occasionally, someone will be unable to take fish oil due to the large capsule size, excessive fishy belching, or stomach upset. The easiest solution is usually just to try a different brand, e.g., Sam's Club (Makers' Mark brand) enteric-coated.

However, sometimes liquid fish oil preparations may be preferred. Here'a list of products we've used successfully. All cost more than plain old fish oil capsules, but fish oil is so crucial to your heart scan/coronary plaque control efforts, that it really pays to search out alternatives.



Liquid fish oil alternatives to capsules:

Liquid fish oil--e.g., Carlson's liquid fish oil. Most liquid fish oil comes flavored either lemon or orange.



Frutol--A very clever re-formulation of fish oil that makes it water-soluble and non-oily. The Pharmax company has put their fish oil into a fruit flavored base that tastes pretty good and is not too expensive.
Go to www.pharmaxllx.com for more information. Unfortunately, I do not believe it's available in stores.





Coromega--another non-oily preparation, though available in some health food stores. Coromega comes in little single-serving foil dispensers. It tastes kind of fruity (though I personally like the Frutol better for taste and consistency). It's kind of pricey ($1.40 per day for two packets).



Regardless of what preparation you choose, you can determine the dose needed by adding up the EPA+DHA content. For the basic prevention effect, the starting dose for the Track Your Plaque program, you need a total of 1200 mg per day of EPA+DHA. Higher doses, e.g., 1800-2400 mg per day, may be required for correction of high triglyceres or postprandial (after-eating) abnormalities.

Ignoring your heart scan is medical negligence

26. October 2006 William Davis (0)
I continue to be dumbfounded that many doctors continue to pooh-pooh or ignore CT heart scans when people get them.

I can't count the number of people I've seen or talked to through the Track Your Plaque program who've been told to ignore their heart scan scores. The most extreme example was a man whose physician told him his heart scan score of nearly 4000 was nothing to worry about!


A real-life story of a retired public defense attorney whose heart scan score of 1200 was ignored, followed two years later by sudden unstable heart symptoms and urgent bypass prompted us to write this fictitious lawsuit. Though it's not real, it could easily become real. To our knowledge, no single act of ignorance about heart scans has yet prompted such a lawsuit, but it's bound to happen given the number of scans being performed every year and the continued stubbornness of many physicians to acknowledge their importance.



Major Malpractice Class Action Lawsuit Looms for Doctors Who Ignore Heart Scan Tests

It's been several years since new medical discoveries have debunked old theories regarding heart disease and heart attack and have verified the efficacy of CT heart scans for detecting both early and advanced heart disease. Doctors who fail to keep apprised of these finding or refuse to change their practice for financial reasons put themselves at risk for becoming defendants in a major malpractice class action lawsuit. The plaintiffs will be a growing class of persons who were debilitated by avoidable heart attacks and heart procedures and the heirs and estates of those who have died.
Milwaukee , WI (PRWEB) November 29, 2005 -- This press release outlines a template for a potential class action lawsuit that may be on the horizon for the medical industry. The class of plaintiffs for this theoretical action remains latent but is growing on a daily basis. However, it requires only one such plaintiff to find an attorney who recognizes the scale and magnitude of the potential damages and move forward on a contingency basis. In real terms, this class could include 80% of those who had a heart attack, underwent a heart procedure, or subsequently died. According to the latest American Heart Association statistics, this number is estimated to be a least 865,000 persons and the entire class could easily be 10 times that number. Using a conservative estimate of $500,000 in damages per class member, the total damages could exceed $400 billion.

The plaintiffs, defendants, third parties, and facts surrounding the following moot complaint represent an actual incident. The names, specific health information, and dates have been changed to protect potential litigants.

Plaintiff, through his attorneys, brings this action on behalf of himself and all others similarly situated, and on personal knowledge as to himself and his activities, and on information and belief as to all other matters, based on investigation conducted by counsel, hereby alleges as follows:

NATURE OF THE ACTION

1.Plaintiff brings this class action on behalf of himself and all other persons who suffered physical damages or mental distress as a result of receiving a medical diagnosis indicating they had no identifiable heart disease, elevated risk for heat attack, or who were prescribed medications not suited to treat their heart disease once detected.

2.Substantial and irrefutable medical evidence has established that cardiac stress testing is an ineffective method for detecting heart disease of the type that is the root cause in over 90% of all heart attacks and other complications of heart disease that result in death or debilitating injury. A readily available and well-publicized test known as “CT heart scanning” is capable of detecting virtually all heart disease of this nature. It has also been established that simple cholesterol testing often fails to detect persons like likely to develop serious heart disease and prevents them from receiving common treatments capable of reducing or eliminating the source of their undetected heart disease. Readily available blood testing techniques exist that are capable of detecting non-cholesterol related sources of heart disease.

3.The medical community has made significant investments in outdated methods of detecting and treating heart disease. They rely on the revenue streams generated by providing these treatments to persons whose heart disease has progressed to the stage that intervention is required to prevent death or debilitation. Any change in diagnostic or treatment methods resulting in the prevention of heart disease would require substantial investments in new technologies and would severely reduce the market for current treatments. Plaintiffs believe this is a motivating factor in the neglect and willful suppression of readily available technology capable of detecting and preventing heart disease and represents gross medical malpractice.

SUBSTANTIVE ALLEGATIONS

On January 23, 1999, Plaintiff underwent a CT Heart Scan which was interpreted by a cardiologist at the ABC Scan Center . Plaintiff received a report from the Scan Center cardiologist indicating that his “calcium score” placed him in the top 1% for heart attack risk among men in his age group. The report also included the comment “Patient has a high risk of having at least one major stenosis (50% or greater blockage) in his Left Anterior Descending (LAD) artery and is urged to consult with a physician regarding this finding.”

On March 3, 1999 Plaintiff presented Defendant with the results of the January 23, 1999 CT Heart Scan. Defendant told Plaintiff to disregard the CT Heart Scan Results and ordered a physical including a stress test and cholesterol blood test.

On April 1, 2005, Plaintiff had a heart attack and a subsequent coronary angiography that confirmed multiple obstructive coronary plaques in his LAD. Plaintiff received an emergency balloon angioplasty to relieve his acute condition. Substantial damage to plaintiff's heart was incurred before emergency angioplasty could be instituted.

On April 3, 2005, per Defendant's recommendation, Plaintiff underwent open heart surgery to insert three bypasses in his LAD to resolve substantial obstructive heart disease, the same artery identified as having likely obstructive heart disease over 5 years earlier via CT heart scan.

On July 7, 2005, Plaintiff independently obtained additional blood testing not ordered by Plaintiff and was found to have several additional blood abnormalities not discovered by Defendant that are known to contribute to the development of heart disease and were readily treatable using lifestyle changes, nutritional supplements, and prescription drugs.

As early as September, 1996, the American Heart Association (AHA) issued a “Scientific Statement” to health professionals acknowledging the strong link between heart attacks and high calcium scores in asymptomatic patients. Extensive studies and references have confirmed the ineffectiveness of stress testing to reveal early heart disease in asymptomatic patients.

Plaintiff alleges that Defendant failed to utilize readily available medical tests and protocols to identify, aggressively treat, and potentially delay, halt, or reverse advanced heart disease that later resulted in extensive physical and emotional trauma to the Defendant.

PRAYER FOR RELIEF

WHEREFORE, Plaintiff herein demands judgment:

A. Declaring this action to be a proper class action maintainable pursuant to Rule 23 of the Federal Rules of Civil Procedure and declaring Plaintiff to be a proper Class representative;

B. Awarding damages against each defendant, joint and severally, and in favor of Plaintiff and all other members of the Class, in an amount determined to have been sustained by them, awarding money damages as appropriate, plus pre-judgment interest;

C. Awarding Plaintiff and the Class the costs and other disbursements of this suit, including without limitation, reasonable fees for attorneys, accountants, experts; and

JURY DEMAND

Plaintiff hereby demands a trial by jury.

Light the fuse of heart disease

26. October 2006 William Davis (1)
Father Bob, despite his calling as a priest and counselor, led a stressful life. His average day was packed tightly with commitments: counseling members of his congregation, visiting the hospital, more official priest and church duties.

At age 53, his heart scan score of 799 came as a complete surprise. Even more of a surprise, his stress test was dramatically abnormal showing poor flow in the front of his heart at a level of exercise that wouldn't challenge most 75 year olds. His blood pressure with exericse: 230/100. Bob was shocked.

A few stents to the LDL later, Bob was trying to turn a new leaf on lifestyle. His life prior to the diagnosis of heart disease was driven by convenience. Because his day was so filled with commitments, he simply grabbed what he could from hospital cafeterias, fast foods, etc.

But after his procedure, Bob committed to choosing healthier foods, walk every day, and resist the food temptations presented by convenience.

However, temptation defeated him twice in the first few weeks after his stents. On the first occasion, Bob gave into eating a cheeseburger. On the second, Bob was at a fish fry (this is Wisconsin, after all) and ate a large serving of deep-fried fish.

On both occasions, Bob started feeling awful within minutes after eating: foggy, bloated, gassy, and fatigued. He took his blood pressure after each incident: 210/90, even though his blood pressure had more recently been trending down towards 130/80.

What happened? Grotesquely unhealthy foods like the deep-fried fish and cheeseburger provoke an abnormal constrictive process body wide. Some call this "endothelial dysfunction". Regardless, it is a graphic and frightening demonstration of the power of these sorts of unhealthy foods to wreak immediate and dangerous effects. Father Bob's response was more exagerrated than most, but it happens to all of us.

Eat badly and your body will pay the price. Even that occasional hot chocolate sundae or Egg McMuffin will yield cumulative injury, among which will be a rise in your heart scan score.

"I don't know what I'm doing here"

25. October 2006 William Davis (0)
Jim came to the office at the prompting of his wife.

At age 52, Jim was semi-retired, having to work only a few hours a week to maintain his business. He'd had a high cholesterol identified about 10 years earlier and had been taking one or another statin drug ever since.

However, Jim's wife was a pretty savvy girl and understood the inadequacies of the conventional approach to heart disease prevention. Nonetheless, when Jim came in, he declared, "I feel great. I don't know what I'm doing here!"

I persuaded Jim to undergo a heart scan. His score: 2211, in the 99th percentile (the worst 1% for men in his age group). However, it was worse than that. Any score above 1000 carries a heart attack risk of 25% per year unless prevention issues are fully addressed.

Indeed, Jim proved to have far more than a high LDL cholesterol. Among the patterns uncovered with his lipoprotein analysis were small LDL, the postprandial (after-eating) abnormality of intermediate-density lipoprotein (IDL), and high triglycerides and VLDL. All would require correction if Jim is to hope to gain control of his extensive coronary plaque.

The message: Trying to discern risk for heart disease from cholesterol is complete folly. This man was going to die or have an urgent major heart procedure within the next year or two, all while taking his statin drug.

Discard the silly notion that cholesterol tells you everything you need to know about heart attack risk. It does not. It helps a little but leaves vast voids in risk determination. Fill those gaps with a heart scan, plain and simple.

I had a heart attack--and I don't know why!

25. October 2006 William Davis (0)
Kevin came to my office for another opinion.

A husband and father of two teenagers, Kevin had his first heart attack at age 39. Kevin received two stents to his right coronary artery. The entire process took place in a flurry with little explanation over 48 hours, start to finish.

He smoked a pack of cigarettes a day, but the only history of heart disease in his family was his father, who, also a smoker, had his heart disease uncovered in his late 70s.

His internist subsequently prescribed Zocor even though Kevin's LDL cholesterol was a relatively unimpressive 128 mg/dl.

Kevin subsequently asked his cardiologist, "Where did I get the heart disease from?"

"Cigarettes. And genetics. You can quit the first. There's nothing you can do about the second." End of explanation.

This left Kevin frightened and demoralized. If much of the cause of his heart disease couldn't be identified, why bother quitting smoking? Why not enjoy what time he had left?

Kevin was understandably shocked when I told him that genetic causes were 1)identifiable, 2)quantifiable, and 3) correctable.

Kevin's full lipoprotein analysis subsequently showed the most dire combination that commonly accounts for coronary disease in young people: Lp(a) with small LDL particles. This, along with smoking, fully accounted for this young father of two's heart disease.

Along with starting Kevin on a new program for correction of his patterns, I also persuaded him to get a heart scan. What usefulness is a heart scan after the fact? Plenty. Even though Kevin's right coronary was no longer "scorable" because the steel in the stent obscured our measurements, the two remaining unstented arteries would still yield a score. This provides a baseline for future comparison. Even after a stent, Kevin could "track his plaque".

Butter basics

24. October 2006 William Davis (3)
There’s lot of confusion about butter, margarines, and their substitutes. Butter/margarine substitutes that avoid the negative aspects and provide modest health benefits are available, but I find that people confuse what's what. So here’s a brief primer.


Butter--Avoid it. Plain and simple. Butter is a rich source of saturated fat. Of 11.5 grams total fat per tablespoon, 7.3 grams are saturated. It is not better than margarine, contrary to simple-minded reports from some media sources. Butter raises LDL cholesterol, raises blood pressure, and has been related to various cancers.

Margarine--Not better than butter, arguably worse. Some argue that the trans-fatty acids, or hydrogenated oils, used to solidify vegetable oils to make margarine solid are worse than butter. In addition to the ill-effects of butter, margarine reduces HDL and raises cancer risk, perhaps even more than saturated fats. Hydrogenation yields a very unnatural structure that modifies cellular behavior of the sort that may promote the appearance of cancer cells. More recently, however, some of the major manufacturers, like Blue Bonnet, have produced soft spread products without hydrogenation. These are reasonable substitutes when used sparingly.

Smart Balance--This is a product made with canola oil, a source of monounsaturates (the best oil source after omega-3s), but manufactured without hydrogenation and therefore has no trans-fats. It does have, in my view, a bit too much saturated fat (1.5 gm per tbsp. in the 37% Light Spread; 2.5 gm per tbsp in the 67% regular spread). This is a reasonable product to use in small quantities.

There is also a Smart Balance Omega PLUS product that contains added flaxseed oil and sterol esters. I do not recommend this product because of the sterol content (see below). I also object to the manufacturers who label their products “rich in omega-3s” when they mean linolenic acid (in flaxseed), which is converted to a trivial quantity of omega-3s. Linolenic acid may pose unique benefits of its own, but it should not be listed as an omega-3 source.

Benecol--This is a butter substitute that contains stanol esters, a substance that reduces total and LDL cholesterol. Two tablespoons a day reduces LDL around 20 mg/dl, more or less depending on your starting cholesterol.
There’s a light and regular spread. The light contains 20 calories less per tablespoon but somewhat less monounsaturates, but the same LDL-reducing stanol esters. The manufacturer does hydrogenate the oils, yielding 0.5 mg trans-fats per tablespoon--a small drawback.

Take Control--Similar to Benecol, but made with sterol esters. Take Control also reduces LDL cholesterol. However, data from several high-quality studies from Finland suggest that sterol esters may, in some people, be absorbed into the blood. This is potentially concerning. There is a rare disease called sitosterolemia that results in coronary disease in teenagers and young adults in their 20s from increased absorption of sterol esters. While you can’t acquire this genetic disease, some people have the capacity to absorb sterol esters from their intestines very efficiently. I find it very disturbing and I suggest that you stay away this product and other sterol-containing products like HeartWise orange juice and Smart Balance Omega PLUS until the issue is clarified and safety assured.

Brummel and Brown--A blend of vegetable oils (soybean and partially hydrogenated soybean) with calories and fats reduced by blending in yogurt. This is an okay product. The hydrogenation yields trans-fats below the FDA required declaration limit of 1.0 mg.
There’s also 1.0 mg each of saturated and monounsaturated fats. The calories are relatively low as a consequence of the added yogurt, only 45 calories per tablespoon. This makes the Brummel and Brown a reasonable choice.


Other products are making their way out to supermarkets. Look for the type of oil used. Canola, olive, and flaxseed are the best. Also look for trans-fats and saturated fat content; both should be low, preferably <1.0 mg per tablespoon, ideally none.

The best choice among the above products in my view is Benecol, though it’s also the most expensive. It will yield substantial drops in LDL cholesterol. All the products in our informal tastings taste a lot like butter, or at least as well as we can remember what butter tasted like! The key with all of these products is use in moderation, since they all provide between 45?80 calories per tablespoon.

Let Dr. Friedewald rest in peace

24. October 2006 William Davis (1)
In the 1960s, doctors struggled with the concept of cholesterol and its relationship to heart disease. It was becoming clear that higher levels of cholesterol were predictive of heart disease. It was also becoming clear that the low-density fraction of cholesterol, or LDL, was somewhat better than total cholesterol in predicting heart attack.

Cholesterol was easily measurable in the 1960s. LDL was not. So, Dr. Friedewald, a noted lipid researcher at the National Institutes of Health, proposed an easy method to calculate LDL cholesterol from total choleseterol, HDL, and triglycerides:

LDL cholesterol = Total cholesterol – HDL cholesterol – triglycerides/5

This simple manipulation would put LDL cholesterols into the hands of the practicing physician and the American public. Dr. Friedewald recognized that this calculation only represented an approximation of LDL cholesterol and that it was thrown off, sometimes substantially, by any abnormal rise in triglycerides or reduction in HDL. But it served its purpose at an age when most doctors hadn’t even heard of cholesterol and the public was still sold on whole milk and “farm-fresh” butter, and Chesterfields were the cigarette choice of most doctors.



The world has since changed. Most doctors have heard about cholesterol and, along with the public, have been drowned in drug company marketing for cholesterol-reducing drugs. Most people with some level of common sense and health awareness no longer use butter or whole milk, and no longer believe that the brand of cigarette you choose can be healthy. But we’re still using Dr. Friedewald’s original calculation for LDL cholesterol. When you get an LDL cholesterol from your clinic, doctor, or hospital, >99% of the time it is obtained using Dr. Friedewald’s calculation.

Is it because there’s nothing better available? No, it’s not. There’s two reasons why your neighborhood primary care physician or cardiologist is still using this dinosaur of testing called LDL:

1) The lag in science to practice is 20 years. Accept that most primary care doctors are 20 years behind the times on many issues, LDL cholesterol included.

2) Insurance companies vigorously discourage testing beyond conventional lipids. The array of objections we get from insurance companies is mind-boggling. It would be funny if human life and finances weren’t at stake. These “new” tests are “experimental”, “unproven”, not endorsed by standard guidelines, not approved by some internal committee, or simply “We don’t know what this test is” ?we’ve heard them all.

What are the tests that are superior to Dr. Friendewald’s calculated LDL? There are several, listed here in order of best to worst:

1) LDL particle number--the value generated by NMR lipoprotein testing. This is the gold standard, most reliable test available, and the one I recommend.

2) Apoprotein B--More widely available even from conventional laboratories in hospitals. Not as accurate as NMR LDL particle number, but a pretty good choice. Apo B is the principal protein in LDL, VLDL, and IDL particles, and so it’s a better reflector of risk from all of these lipoprotein fractions, not just LDL.

3) “Direct” LDL--This is LDL that is actually measured. Unfortunately, it ignores the issues of LDL size and has some other pitfalls, but it’s still better than calculated LDL

4) Non-HDL cholesterol--So-called because it incorporates all undesirable cholesterol-containing lipids except good HDL, thus “non-HDL”. This is another calculation, though better than LDL (because it sums up the risk from other apoprotein B-containing lipoproteins). Non-HDL is calculated from Total cholesterol – HDL. It’s therefore available from any standard lipid panel. It’s little used in everyday practice, however, because most people and their physicians find it confusing.

5) Friedewald calculated LDL--You can see that calculated LDL is last on a list of choices. Yet this is the measure that doctors use day in, day out. It’s the measure that drug companies base billions of dollars of revenue and profits on.

It’s an everyday occurrence in my office that calculated LDL is 89 mg/dl, but the real value is somewhere between 160 and 200 mg/dl. That’s a big difference. Imagine your realtor tells you your house’s estimated value is $200,000 and that’s what you sell it for to an eager buyer. After closing, you find out your house was really worth $300,000. You’d be upset. But that’s what you’re often getting with LDL cholesterol?a bum deal.

It’s part of the reason people will say, “My doctor said my cholesterol was fine and that no cause for my heart disease can be found. He said it was genetic.” In reality, they could have sky-high LDL cholesterol revealed by LDL particle number or apoprotein B.

Use LDL cholesterol in a pinch when you’ve got nothing else. It’s also helpful to gauge any treatment effect of diet, functional foods, drugs, etc. But it is a seriously flawed tool to diagnose your initial level of risk.

The key to losing weight

23. October 2006 William Davis (0)
I saw three people this past week, all of whom set off on an effort to lose substantial quantities of weight. And all seriously needed to.

All three started with at least 70 lbs. excess weight; all showed substantial weight-sensitive lipoprotein patterns like low HDL, small LDL, high triglycerides, VLDL, and pre-diabetic levels of blood sugar. They also all shared high blood pressure.

All three also had high heart scan scores. Kate’s score was just over 1200. Tom, a 58-year old real estate developer, had a score of nearly 600. Susan, the youngest of the three at 52, had a heart scan score of 377¾99th percentile at this age. Losing weight was an absolute requirement for their plaque control program. Because their lipoprotein abnormalities and pre-diabetic patterns were triggered by weight, weight loss would provide powerful correction. Each and every one of them would need to lose much of their excess weight¾at least 50 lbs¾if they hoped to halt the relentless progression of their heart scan scores.

All three of them returned after 6-8 weeks, and all had lost between 17-24 lbs: spectacular results.

There’s no secret to weight loss. Each of them achieved their weight loss in slightly different ways. But they also shared several critical ingredients in their weight-loss efforts:

1) All three dramatically slashed their intake of wheat flour-containing foods and other processed carbohydrates and did so consistently. All also avoided the usual high-fat, high caloric-density foods like butter, margarine, fried foods, greasy foods, nuts roasted in oil, etc. They concentrated on vegetables, salads, raw nuts, lean proteins (inc. turkey, chicken, fish, lean red meats, low-fat cottage cheese and yogurt).

2) They stopped using food as a reward or as a consolation tool.

3) Exercise for one hour a day at least 5 days a week. The exercise in 2 of 3 of these people was just walking. It wasn’t strenuous, it wasn’t expensive. The women both liked walking with friends or their spouse. Tom followed a more common male path of more strenuous work on his treadmill, elliptical, and biking at the fitness club. But they all did it religiously and missed rare sessions.

4) They refrained from any and all alcoholic beverages. Yes, there are some advantages to 1-2 glasses of wine per day, but it stalls weight loss efforts.

5) They didn’t allow themselves any major indiscretions. There were no binges, major pig-outs at weddings, barbecues, or all-you-can-eat buffets. They did allow themselves an occasional “treat” but did so in small portions.

That’s it. But for most people, that’s simply too much. Adhering to an effort to lose dramatic weight requires day-after-day consistency. Nobody can lose the equivalent of 70,000 calories (20 lbs.) just by skipping a meal, a 20-minute walk, skipping the mashed potatoes at dinner.

It can be done. You’ve just got to be consistent about it.

How can I get my lipoproteins tested?

20. October 2006 William Davis (0)
This question came up on our recent online chat session and comes up frequently in phone calls and e-mails.

If lipoprotein testing is the best way to uncover hidden causes of coronary heart disease, but your doctor is unable, unknowledgeable, or unwilling to help you, then what can you do?

There are several options:

1) Get the names of physicians who will obtain and interpret the test for you. Go to the websites for the three labs that actually perform the lipoprotein tests: www.liposcience.com (NMR); www.berkeleyheartlab.com (electropheresis or GGE); www.atherotech.com (VAP or centrifugation). None of them will provide you with the names of actual physicians. They will provide you with the name of a local representative who will know who the doctors in your area who are well-acquainted with their technology. I prefer this route to just having a representative identify a laboratory in your area where the blood sample can be drawn, because you will still need a physician to interpret the results¾this is crucial. The test is of no use to you unless someone interprets it intelligently and understands the range of treatment possibilities available. Don’t be persuaded by your doctor if he/she agrees to have the blood drawn but has never seen the test before. This will be a waste of your time. That’s like hoping the kid next door can fix your car just because he says he fixed his Mom’s car once. Interpretation of lipoproteins takes time, education, and experience.
2) Seek out a lipidologist. Lipidologists are the new breed of physician who has sought out additional training and certification in lipid and lipoprotein disorders. Sometimes they’re listed in the yellow pages, or you can search online in your area.
3) Contact us. I frankly don’t like doing this because I feel that I can only provide limited information through this method. I provide a written discussion of the implications and choices for treatment with the caveat to discuss them with your doctor, since I can’t provide medical advice without a formal medical relationship. We also charge $75 for the interpretation. But it’s a lot better than nothing.
4) Make do with basic testing. Basic lipids along with a lipoprotein(a), C-reactive protein, fibrinogen, and homocysteine would provide a reasonable facsimile of lipoprotein testing. You’ll still lack small LDL and postprandial (after-eating) information, but you can still do reasonably well if you try to achieve the Track Your Plaque targets of 60-60-60.

In 20 years, this will be a lot easier. But for now, you can still obtain reasonably good results choosing one of the above alternatives.

What do you think about those heart scans?

20. October 2006 William Davis (1)
52-year old Jerry came in for a stress test. He displayed the usual apprehension: fidgeting while he sat on the bed, examining his surroundings, asking lots of questions.

“Your doctor asked you have have a stress test?” I asked.

“All the males in my family have had heart attacks by age 56, so my doctor suggested I have a stress test,” Jerry explained.

Jerry went on to tell me that he had exercised vigorously this morning for 45 minutes without symptoms. He had, in fact, gone surfing just several weeks earlier and described how aerobically challenging it was keeping up with the 20 year olds. “But I did it!” he proudly declared.

As he neared the end of his brisk walk on the treadmill, Jerry asked, “What do you think about those heart scans?”

Jerry had asked his primary care physician the same question. His doctor had apparently told him that they were just a gimmick. “We’ll get you a real test.”

Of course, Jerry’s stress test proved entirely normal. The likelihood of an abnormal stress test with his history of vigorous exercise was <2%. I explained to Jerry that not getting heart scan would be a mistake. In fact, a heart scan was the only easily obtainable test that would uncover hidden heart disease. In truth, the stress test was a waste of time—and an unneeded exposure to radiation.

If Jerry’s heart scan score turned out to be zero, great! He was probably spared the genes from the other males in his family, and his risk of heart attack in the next decade was nearly zero.

If his heart scan turned out be 1000, then an urgent scramble to uncover the causes and correct them to create a truly effective prevention program would be crucial for his long term health. Or, perhaps his score lies somewhere in between, but Jerry would then know how far along he stood on his way to heart disease.

Don’t be a victim of the ignorance of your doctor. Despite all the attention heart scans have received, the majority of doctors remain miserably, inexcusably in the dark. I say inexcusable because CT heart scans can uncover the number one killer of Americans, the number one cause of all deaths in any primary care physician’s practices, and it’s laughably easy. How can a physician not advise patients on the value of heart scans?

If given a choice and you’re without symptoms, a heart scan is far and away the superior test.