Heart attack guaranteed

What if you knew for a fact that your risk for heart attack was 100% by, say, age 58? This is indeed true for many people, though at age 60, 65, 70--or 45.

In other words, unless something were done about the causes of heart disease, you would inevitably suffer a heart attack at 58.

What sort of action could you take at age 45?

Obviously, not smoking is an absolute requirement. Continue and you may as well start getting your affairs together.

How about exercising and eating a generally healthy diet? Will your risk be reduced to zero? No. It might be reduced 20-30%, depending on genetic factors.

How about a statin drug? Watch TV ads during Oprah, and you might think it's a cure. But in reality, while it is a financial bonanza for the drug manufacturers, it will reduce risk for heart attack by 30%.

(Note that risk reduction by following multiple strategies is not necessarily additive. In other words, if you have a healthy lifestyle and take a statin agent, is risk reduced 60% (30 + 30)? No, because the effects may overlap.)

So, eating healthy, exercising, and taking a statin drug might reduce risk 35-40%, maybe 50% in the best case scenario. Would you be satisfied? Most would not.

Add fish oil at a truly therapeutic dose. Risk reduction by itself: 28%.

Add niacin or other strategies for correction of your individual, specific causes of heart disease: Now we're up to 90% reduction.

Throw in a tracking process to prove whether or not atherosclerotic plaque has progressed or reversed. Now we're approaching 100% if plaque reverses. The only way I know how to track plaque is through CT heart scans. What other test is readily available to you with low radiation exposure, yet is relatively inexpensive and precise? It certainly is not stress testing, heart catheterization, CT angiograms, or other techniques. Cholesterol won't tell you. Besides CT heart scans, there's nothing else I know of.

Let's fact it: For many people, uncorrected risk for heart attack is truly 100% at some age. Take action while you can.

That, in a nutshell, is the Track Your Plaque program.

Heart scan curiosities 3



This is a sample image from the heart scan of a 54-year old, 212 lb, 5 ft 2 inch woman. The heart is the whitish-gray in the center; lungs are the dark (air-filled) areas on either side of the heart. Note the massive amount of surrounding gray tissues that encircles the heart and lungs. This is fat. At this weight, the diameter of total fat exceeds the combined diameter of the heart and lungs. If we were to show the abdomen, there would be even more fat. (The image shows the body not well centered because the technologist centers the heart, since this is, after all, a heart scan.)





This is a 55-year old, 151 lb, 5 ft 4 inch woman. Note the contrast in the quantity of fat tissue surrounding the chest, a much more normal appearance. Note that this woman is still around 25 lb over ideal weight, but not to the extreme degree of the woman above.

Another curious observation: Note the more whitish streaking in the heavier woman's lungs. Heart scans are performed while holding a deep inspiration (a deep breath inwards), mostly to eliminate lung respiratory motion during image acquisition. Nonetheless, the heavier woman's lungs are not as fully expanded as the more slender woman. In other words, the heavier woman cannot inflate her lungs as effectively as the thinner woman. Ever notice how breathless heavy people are? Some of this effect is just being out of shape. But there's also the added effect of the abdominal fat exerting upwards compression on the lung tissues, and the constrictive effect of the encircling fat mass. At the beginning of inspiration, the chest fat exerts the resistance of inertia to inspiration that is absent, or less, in a slender person. With each breath, the heavy woman must move 50 lbs or so of surrounding fat mass just to inhale.

The heavier woman is, in effect, suffocating herself in fat.

The distortions to the human body incurred by extreme weight gain are both fascinating and shocking. I hope you're breathing easily.

The shameful "standard of care"

John's initial heart scan four years ago showed a score of 329. His physician prescribed Zocor for a somewhat high LDL cholesterol.

One year later, John asked for another scan. His score: 385, a 17% increase. John exercised harder and cut his fat intake.

This past fall--3 years after his last scan--John had yet another heart scan. Score: 641, a 66% increase over the last scan, all the while on Zocor.

John sought an opinion from a reputable cardiologist. He concurred with the prescription of Zocor and advised annual stress tests. That's it.

Followers of the Track Your Plaque approach know that the expected uncorrected rate of increase in heart scan score is 30% per year. On Zocor or other cholesterol reducing statin agent, a common rate of growth is between 18-24% per year--better but not great. Plaque growth is certainly not stopped.

But that is the full extent of interest and responsibility of your cardiologist. Prescribe a statin drug, perform a stress test, and the full extent of his obligation has been fulfilled. In legal terms, your physician has met the prevailing
"standard of care". No more, no less.

In other words, the prevailing standard of care falls shamefully short of what is truly possible. For the majority of the motivated and interested, coronary plaque reversal--reduction of your heart scan score--should be the standard aimed for. It's not always achievable, but it is so vastly superior to the prescribe statin, wait for heart attack approach endorsed by most cardiologists.

Heart scan curiosities 2



This is an example of a so-called "hiatal hernia", meaning the stomach has migrated through the diaphragmatic hiatus into the chest--the stomach is literally in the chest. This example is an unusually large one. Hiatal hernias can cause chest pain, indigestion, and a variety of other gastrointestinal complaints. Heart scans are reasonably useful to screen for this disorder, though very small ones could escape detection by this method.

Sometimes, you can actually hear the gurgling of stomach contents (the common "growling" stomach) by listening to the chest. Large ones like this actually crowd your heart (the gray structure above the circled hernia), irritating it and even causing abnormal rhythm disorders. The dense dark material within the hernia represents lunch.

I would not advocate CT heart scans as a principal method to make a diagnosis, but sometimes it just pops up during a heart scan and we pass it on to the person scanned.

Vitamin D: New Miracle Drug

At the meetings of the American Society of Bone and Mineral Research, Dr. Bruce Troen of the University of Miami detailed his views on the extraordinary benefits of vitamin D replacement. He also talked about the enormous problem of unrecognized vitamin deficiency.

“There’s a huge epidemic of hypovitaminosis D, and the real key here is not just that it’ll benefit you from a bone and neuromuscular standpoint, but if you correct hypovitaminosis D and the corresponding secondary hyperparathyroidism, then you’re going to decrease prostate cancer, colon cancer—actually “up to 17 different cancers, breast cancer included.”

Unfortunately, Dr. Troen did not talk much about the heart benefits of vitamin D, likely since the data is scant, nearly non-existent. However, if the Track Your Plaque experience means anything, I predict that vitamin D replacement will become among the most powerful tools you can use to gain control over coronary plaque.

Read the text of a report from the Internal Medicine World Report to read more of Dr. Troen's comments.


http://www.imwr.com/article.php?s=IMWR/2006/11&p=40

Heart disease "reversal" by stress test


Here's an interesting example of a 71-year old man who achieved "reversal" of an abnormality by a nuclear stress test.

This man underwent bypass surgery around 10 years ago, two stents three years ago. A nuclear stress test in April, 2005 showed an area of poor blood flow in the front of the heart. On the images, normal blood flow is shown by the yellow/orange areas. poor or absent blood flow is shown by the blue/purple areas within the white outline.

Now, I can tell you that this man is no paragon of health. He's only accepted limited changes in his otherwise conventional program--in other words, someone who I'd be shocked achieved true reversal of his heart disease. (I didn't have him undergo any CT heart scans because of the difficulties in scoring someone who has undergone bypass surgery and stents, and because of limited motivation. True plaque reversal is for the motivated.)This patient did, however, accept adding fish oil and niacin to his program.

Nonetheless, stress testing can be helpful as a "safety check". Here's the follow-up stress test:
You'll notice that the blue/purple areas of poor blood flow have just about disappeared. This occurred without procedures.

Does this represent "reversal"? No, it does not. It does represent reversal of this phenomenon of poor flow. It does not represent reversal of the plaque lining the artery wall. That's because improvement of flow, as in this man, can be achieved with relatively easy efforts, e.g., improvement in diet, statin drugs, blood pressure control, etc. True reversal or reduction of coronary plaque, however, is tougher.

If blood flow is improved, who cares whether plaque shrinks? Does it still matter? It does. That's because the "event" that gets us in trouble is not progressive reduction in blood flow, but "rupture" of a plaque. A reduction in plaque--genuine reversal--is what slashes risk of plaque rupture.

Calcium reflects total plaque





People frequently ask, "Why measure coronary artery calcium? My doctor said that calcium only tells you if there's hard plaque, and that hard plaque is stable. He/she says that calcium doesn't tell you anything about soft plaque."

Is that true? Is calcium only a reflection of "hard" plaque? Is hard plaque also more stable, less prone to rupture and causes heart attack?

Actually, calcium is a means of measuring total plaque, both soft and hard. That's because calcium comprises 20% of total plaque volume. Within plaque, there may be areas that are soft (labeled "lipid pool" in the diagram). There are also areas made of calcium (shown in white arcs within the plaque). Even though this is just a graphic, it's representative of what is seen when we perform intracoronary ultrasound of a live human being's coronary artery. In other words, this cross section contains both "soft" (lipid pool) as well as "hard" (calcium) elements.

Is this artery "soft" or "hard"? It's both, of course. The artery compostion can vary millimeter by millimeter, having more soft or hard elements. The artery can also change over time in either direction. Thus, "soft" plaque may indeed be soft today, only to be "hard" in 6 months, and vice versa.

The essential point is that measuring just "soft" plaque provides limited information. What the CT heart scan does is provide a gauge of total plaque, soft and hard, and it does so easily, safely, precisely. If your score increases, the lengthwise volume of total plaque has also grown. If your score decreases, the total amount of plaque has also decreased.

Don't mistake marketing for truth

We're all so inundated with marketing messages for food. Unfortunately, many people confuse the messages delivered through marketing with the truth.

For instance:

Pork: "The other white meat." Pork is a high-saturated fat food.

"Bananas: A great source of potassium." Bananas are a high glycemic index (rapid sugar release), low fiber food.

"Pretzels: A low-fat snack." A high glycemic index food made from white wheat flour. It makes you fat and skyrockets blood sugar.

Jif peanut butter: "Choosy moms choose Jif." Do they also choose hydrogenated fats?

Hi-C: Upbeat jingles like "Who put the straw in my Hi-C fruit drink, a new cool straw that wriggles and bends? Who put the straw in my Hi-C fruit drink, with Vitamin C for me and my friends? Who was that man, I'd like to shake his hand, he made my Hi-C cooler than before!" What about the 25 grams of sugar per 4 oz serving? And the high fructose corn syrup that creates an insatiable sweet tooth, raises triglycrides 30%, and exagerates pre-diabetes?


Marketing is not reliable, unbiased information. If Ford boasts that their cars are superior to GM, do you say "Well then, I need to buy a Ford?" Of course not. Take marketing for what it is: A method of persuading people to buy. It may or may not contain the truth. It's a big part of the reason Americans are the fattest people on earth and are experiencing an explosion of chronic diseases of excess.

Tattered Red Dress

"Are you taking your health to heart? Perhaps you understand the importance of eating a diet low in cholesterol or getting 30 minutes of exercise a day. But do you know your own risk of developing cardiovascular disease?


It’s time to take your heart health personally. Heart disease is the No. 1 killer of American women — and that means it is not “someone else’s problem.” As a woman, it’s your problem.

That’s where the Go Red Heart Checkup comes in. This comprehensive evaluation of your overall heart health can help you now and in the future. By knowing your numbers and assessing your risks now, you can work with your doctor to significantly reduce your chances of getting heart disease tomorrow, next year, or 30 years from now!"



So reads some of the materials promoted by the American Heart Association Red Dress campaign to increase awareness of heart disease in women. The effort is well-intended. There is no doubt that most women are unaware of just how common coronary disease is in females.

But I've got a problem with the solutions offered. "Know your numbers"? Eat healthy, don't be overweight, be active, don't smoke. That's the gist of the program's message--nothing new. In 2006, why would some sort of screening effort for detectin of heart disease not be part of the message? Why isn't there any message about the real, truly effective means to detect hidden heart disease in women--namely, heart scanning?

Does a 58-year old woman with normal blood pressure, LDL 144, HDL 51, 20 lbs overweight have hidden heart disease? I've said it before and I'll say it again: You can't tell from the numbers. She could die of a heart attack tomorrow without warning, or maybe she'll be dancing on our graves when she's 95 and never have experienced any manifestation of heart disease. The numbers will not tell you this.

I'm glad the American Heart Association has seen fit to invest its sponsors' money in a campaign to promote prevention. I wish they hadn't fallen so far short of a truly helpful message. Perhaps the sponsors (like Pfizer, maker of Lipitor) will benefit, anyway.

Panic in the streets

Several days ago, I wrote about a local prominent judge in my neighborhood who was unexpectedly found dead in bed of a heart attack at age 49.

As expected, I've received multiple calls from patients and physicians who want heart catheterizations. For instance, an internist I know called me in a panic. He asked that I perform a heart catheterization in a patient with a heart scan score of 768. I've been seeing this patient for about a year. He's without symptoms, even with strenuous exercise; stress tests (i.e., tests of coronary bloow flow) have been normal.

I remind patients and colleagues every day, day in day out: Having a heart scan score revealing some measure of coronary plaque is not a sufficient reason by itself to proceed with procedures. Fear of suffering a fate like the unfortunate judge is also not a reason to proceed with procedures.

Increased awareness of the gravity of heart disease is a good thing. Some good can come out of a needless tragedy like this. The lesson from the judge's unfortunate experience: he needed a CT heart scan. I'm told that the judge's doctor advised him that a heart scan was a waste of time. I hope that appropriate legal action for negligence is taken by the judge's family against this physician.

Not doing a heart scan is wrong. That's the lesson to learn. The lesson is not that everybody with coronary plaque needs a procedure. Had the judge undergone a simple heart scan, intensified prevention could have been instituted and he'd still be alive with his wife and children today.

The indications for procedures are unchanged by your heart scan. If a stress test is abnormal and indicates poor flow to a part of the heart, that would be a reason. If symptoms like chest discomfort or breathlessness appear, that's an indication. If there's evidence of poor heart muscle contraction, that's a reason to proceed with a procedure. But just having coronary plaque is not a sufficient reason.
Genetic vs. lifestyle small LDL

Genetic vs. lifestyle small LDL

Let me explain what I mean by "genetic small LDL." I think it helps to illustrate with two common examples.

Ollie is 50 years old, 5 ft 10 inches tall, and weighs 253 lbs. BMI = 36.4 (obese). Starting lipoproteins (NMR):

LDL particle number 2310 nmol/L
Small LDL: 1893 nmol/L
(1893/2310 = 81.9% of total, a severe small LDL pattern)


Stan is 50 years old, also, 5 ft 10 inches tall, and weighs 148 lbs. BMI = 21.3. Starting lipoproteins:

LDL particle number 1424 nmol/L
Small LDL 1288 nmol/L
(1288/1424 = 90.4% of total, also severe)


Both Ollie and Stan go on the New Track Your Plaque diet and eliminate wheat, cornstarch, and sugars, while increasing oils, meats and fish, unlimited raw nuts, and vegetables. They add fish oil and vitamin D and achieve perfect levels of both. Six months later, Ollie has lost 55 lbs, Stan has lost 4 lbs. A second round of lipoproteins:

Ollie:

LDL particle number 1810 nmol/L
Small LDL: 193 nmol/L
(193/1810 = 10.6% of total)


Stan:

LDL particle number 1113 nmol/L
Small LDL 729 nmool/L
(729/1113 = 65.4% of total)


Ollie has reduced, nearly eliminated, small LDL through elimination of wheat, cornstarch, and sugars, along with weight loss, fish oil, and vitamin D.

Stan, beginning at a much more favorable weight, reduced both total and small LDL with the same efforts, but retains a substantial proportion (65.4%) of small LDL.

Stan's pattern is what I call "genetic small LDL." Of course, this is a presumptive designation, since we've not identified the specific gene(s) that allow this (e.g., gene for variants of cholesteryl ester transfer protein, hepatic lipase, lipoprotein lipase, and others). But it is such a sharp distinction that I am convinced that people like Stan have this persistent pattern as a genetically-determined trait.

Comments (59) -

  • Onschedule

    2/18/2010 8:25:54 PM |

    Your blog entry appears to have been truncated.

  • Anonymous

    2/18/2010 8:29:46 PM |

    How are Stan's blood sugars?

  • zach

    2/18/2010 8:59:48 PM |

    Sounds like Stan is screwed. Of course, there may be other factors mitigating his lipid pattern because he avoids the neolithic agents. Stan would be more susceptible to heart disease than ollie on the SAD, but not when they both have good diets?

  • Jeff

    2/18/2010 10:23:31 PM |

    Is it possible that a different diet might work for Stan? I don't know what it would be, I just wonder if it's possible.

  • Kurt G. Harris MD

    2/18/2010 10:29:07 PM |

    So Ollie and Stan BOTH show substantial improvement on their LC diets.

    The difference between them may well be due to genetics, but where is the evidence that Stan needs to avoid saturated fat?

    Did you advise Stan to increase sat fat and then watch his sdLDL get worse?

    If they accomplished this with "oils" at the expense of saturated fats (oils are liquid due to the paucity of saturated fats in them), then it looks like they both have a saturated fat deficiency, and one could speculate that Stan is even more deficient than Ollie.

    Swap out the nasty oils for more butter and beef fat and coconut fat and maybe Ollie will have sdLDL of 0 (like I do on 35% of calories from sat fat) and Stan will improve even further.

  • Peter

    2/18/2010 10:44:33 PM |

    Hi Dr Davis,

    You describe a fascinating scenario.

    Ollie has clearly lost weight. He has lost 55 lb in 6 months. That is nearly 10 pounds of "lard-equivalents" each month. This has not evaporated. It is exactly what he has been running his metabolism on. Whatever nuts and vegetables he has eaten can have been nothing in comparison to the 4 times half pound blocks of lard he has "eaten" from his own adipose tissue, every week. Result: Metabolism runs on lard and sdLDL plummet.

    Stan has lost minimal weight so has run his metabolism on  his food alone. If this is low in lard he may well be running his metabolism on vegetable derived carbohydrate and nut derived omega 6 PUFA. It's possible he has NOT been eating 2lb of lard a week in his diet, because obviously this might raise his LDL. So he has NOT used lard to fuel his metabolism, he has used nuts and vegetables when Ollie has used lard from his adipose stores.

    Before I would blame genetics I would get rid of the nuts and unlimited vegetables from Stan's diet and replace them with exactly the same the adipose tissue derived fuel that Ollie was using. If Stan cannot spare it from his butt (he certainly cannot at BMI 21), it's going to have to go on his plate. Two pounds of lard a week.

    Then compare sdLDL values, when you have similar metabolic situations... Until then Stan just has nut and vegetable poisoning showing as sdLDL.

    There do not have to be any genetics involved. There might be, but let's keep it simple for the time being... Ollie is on lard while he is losing weight. Mimic that.

    Peter

  • Sue

    2/18/2010 11:16:15 PM |

    Stan did improve.  Maybe he will improve further, the longer on diet?

  • Anonymous

    2/18/2010 11:52:16 PM |

    I think it's somewhat telling that you advise your patients to eat "oils."  What kind of "oils" are they eating?  Why are your patients eating unlimited nuts?

    Until you get off the Omega-6-loaded "heatlhy" polyunstaturated fats bandwagon, it's hard to take your clinical observations on "fats" very seriously.

  • stcrim

    2/19/2010 12:15:07 AM |

    Dr. Davis,

    Help me understand the part about not eliminating meats or fats.  First, here is my blood work 15 days apart.

    Total cholesterol 295 - 15 days later 156
    LDL 200 - 15 days later 102
    HDL   46 - 15 days later  32  (have added 1500mg of niacin since then)
    Triglycerides   242 - 15 days later 109
    VLDL  49 - 15 days later 22
    Vitamin D was 28 – 15 days later it’s 56 (using 10,000 of Carlson’s D3)

    FYI my heart scan was 899 (54 year old male)

    I started on all the main nutrients you recommend here plus a few.  I dropped dairy like a hot potato including 6 or more ounces of cheese a day.  During those 15 days I ate only plant based foods (have since added some salmon and egg whites)

    The only oil I use now (sparingly) is olive.  I have a couple of gallons of coconut oil I assumed would have to be tossed sooner or later.

    Guess you could say I became fat paranoid and downright phobic about any saturated fat.

    Am I understanding I could add back Grass-fed beef (omega-3) pastured chicken and Omega-3 whole eggs?  Coconut oil?   If so, is there some safe percentage of a person’s diet to include those proteins/fats?

    By the way, my doctor wouldn’t let me out of his office without a copy of your book.  He’s one in a million as are you!

    Steve

  • Daddy

    2/19/2010 1:05:49 AM |

    Doc, would you say family history could be a clue towards small-particle tendencies?   I have zero family members with heart issues yet I was given pause by your recent post on saturated fats having a disproportionate affect on these genetically challenged folks.  I ask because I eat a ton of rib eyes and bacon.

  • Dr. William Davis

    2/19/2010 3:08:19 AM |

    I have indeed had many people with presumed "genetic small LDL" load their diets with oils and fats with only minor improvement. Loaded with saturated fat, however, and there seems to be deterioration.

    I know this flies in the face of the "saturated fat is great" dogma, but I don't make this stuff up. Just as I don't make up the deterioration of postprandial triglycerides and chylomicron remnant effect when saturated fats are loaded heavily in the diet.

    The persistence of small LDL is also long-term, i.e., it persists for years despite continuing efforts.

  • Dr. William Davis

    2/19/2010 3:09:48 AM |

    Oils = olive oil, flaxseed oil, canola oil (yes, yes, I know), avocado, almond, oils from raw nuts and meats.

    No polyunsaturates here. You've go the wrong guy.

  • Richard A.

    2/19/2010 3:41:23 AM |

    On Doctor's orders, Ollie did indeed lose a massive amount of weight.
    http://www.youtube.com/watch?v=IYAeYj8-G4w

  • LynP

    2/19/2010 3:41:52 AM |

    @Peter, fascinating...eat lard when slim in attempt to reduce sdLDL.  Doc D thanks for 'splaining 'genetic' tendency to sdLDL & why numbers not reduced on sat fat & only reduced mildly on mono sats.  Great info guys!

  • Kurt G. Harris MD

    2/19/2010 3:52:12 AM |

    "Oils = olive oil, flaxseed oil, canola oil (yes, yes, I know), avocado, almond, oils from raw nuts and meats.

    No polyunsaturates here. You've got the wrong guy."

    But Dr. Davis, those all chock full of PUFAs

    Linseed oil (flax oil) is 71% LA and ALA

    Rapeseed oil (Canola oil) is 33%  LA and ALA

    Almond oil is about 25% PUFA

    Even olive oil can be up to 20% PUFA

    And all of these are mostly Linoleic acid.

    All best left as industrial lubricants and paint additives rather than eaten.

  • LeenaS

    2/19/2010 4:10:32 AM |

    So, you have a fat guy, who has been living on (his own) saturated animal fats, and he has improved a lot.

    Then you have a skinny guy, who has been living on "healthy vegetable fats" with surprisingly much LA in them, and he has not improved that much.

    So, it seems to tell that without saturated fats LDL improvement is much harder in LC, to say it kindly.

    And it sounds as if butter and saturated animal fats would be advantageous for the latter guy, too. Have they ever tried this, under your coucelling?

    With regards,
    LeenaS

  • Anonymous

    2/19/2010 4:30:07 AM |

    Dr. Davis,

    While body composition certainly isn't a prerequisite for being part of a classic comedy team, I couldn't help but notice that Stan had the makings of a skinny-fat bean pole checking in at 5' 10" and only 148 pounds. Those stats make him sound like a diehard distance runner or a chain smoker.

    While it was clearly just for illustrative purposes, I couldn't help but think that, if "Stan" exercises at all, he must not be exerting himself very much. I'm not advocating that every older gentleman suddenly attempt to impersonate Mr. Olympia, but I have to wonder seeing such a lightweight. That's not to say that I think sufficiently intense exercise would remove the problem that is genetically-based small LDL, but it is enough to make me raise an eyebrow when I see that type of weight for a male listed as 5'10".

  • Anonymous

    2/19/2010 4:32:12 AM |

    Dr. Davis,

    Would a take-home point simply be to let the numbers from proper testing be the guide versus what we "think" is right based upon generally-sound dietary advice that may apply to many, but not all, situations?

    Bill Lindvall

  • Anonymous

    2/19/2010 7:25:27 AM |

    Olive oil is monounsaturated but flaxseed oil, canola oil, avocado oil, almond oil, and oils from raw nuts are all polyunsaturated oils!  Yes, flax oil is omega 3 and canola has more omega 3 than omega 6, but both omega 3 and omega 6 are polyunsaturated.

  • Sue

    2/19/2010 8:10:06 AM |

    Do you know how much saturated fat was eaten?

  • Sue

    2/19/2010 8:28:08 AM |

    Maybe too much mono-unsaturates?

  • Anonymous

    2/19/2010 11:18:48 AM |

    In another post, you said that blood sugars parallel small LDL.  Do Stan's blood sugars follow the pattern you would predict for someone with a lot of small LDL?

    http://heartscanblog.blogspot.com/2009/12/to-track-small-ldl-track-blood-sugar.html

  • lightcan

    2/19/2010 12:46:27 PM |

    No polyunsaturates?
    Because olive, flax, canola oils, nuts have no polyunsaturated fats?
    I found something different.
    Even avocados have 10 % PUFAs.
    http://curezone.com/foods/fatspercent.asp

  • Anonymous

    2/19/2010 2:01:52 PM |

    So what about epigenetics? Any way to modify this unknown gene or set of genes?  Pomegranate, etc?

  • Adolfo David

    2/19/2010 2:27:14 PM |

    Please guys, find so other monounsaturated (MUFA) fats with less PUFA..

    I eat almonds, walnuts, extra virgin olive oil as fats and my diet is low in Omega 6, 10% or 20% of Omega 6 PUFA is nothing compared with 70 or 85% of MUFA.

    My experience taking a lot of saturated fats with low carbs is bad, I prefer a diet high in MUFA and low carb.

  • Anonymous

    2/19/2010 3:18:19 PM |

    Maybe the mental stress of having to worry about what to eat is a factor.
    I do find my self stressing about that often and wonder if just enjoying the food would give me a longer nicer life quality which is in then end what matters.

    Which reminds me somehting I have never read in this blog is about cortisol.
    Have you ever tracked cortisol levels in your patients?

  • ET

    2/19/2010 5:37:36 PM |

    A yea ago, i went off niacin and zocor due to elevated liver enzymes.  Before I restarted niacin, an NMR lipoprotein analysis showed:
    LDL particle number - 2197
    Small LDL-P - 1614
    LDL Particle size - 20.3
    Saturated fat (% of calories) - 21%

    Six months later, after radically increasing the amount of coconut oil I consumed, the results were:
    LDL particle number - 896
    Small LDL-P - 466
    LDL Particle size - 21.6
    Saturated fat (% of calories) - 45%


    Five months after that:
    LDL particle number - 946
    Small LDL-P - 120
    LDL Particle size - 21.1
    Saturated fat (% of calories) - 52%

    Carbohydrate consumption has held fairly steady at 10% of calories.

  • Vladimir

    2/19/2010 5:41:33 PM |

    I agree 100% with these comments.  Not a drop of dogma in them; pure science.  Yes, omega-6 is evil; avoid foods with any of it. No nuts, no seeds. Soy -- dangerous.  Milk -- cavemen didn't drink it and it's possibly dangerous too.  Vegetables -- no, no, goodness no, they're mostly made of dreaded carbohydrates, have little fat, an fiber isn't important!  Saturated fat?  I don't know about you, but I'm too scared to go hog wild on it.

    I know, I know!  Let's not eat at all.  That would drive small LDL to 0!  That would end heart disease -- and everything else -- in a flash.

    Or, just maybe, we could be moderate and sensible.  Take some fish oil to balance whatever omega-6 you get in the olive & canola oils and in nuts.  Eat some, but not too much, animal protein, and mostly fish and lean meats at that, because saturated fat isn't out of the woods yet. (Just because saturated fat's risks have been over-hyped doesn't mean that we should eat all meat all the time, because the evidence is not in yet that saturated fat is a panacea.) Eat some, but not tons, of fruits, because they have antioxidants.  And for goodness sake, eat your vegatables -- lots of them, and all kinds of them -- because your mother was right to make sit at the table until you finished them.

  • Anonymous

    2/19/2010 5:51:09 PM |

    "I couldn't help but notice that Stan had the makings of a skinny-fat bean pole checking in at 5' 10" and only 148 pounds. Those stats make him sound like a diehard distance runner or a chain smoker."

    I'm 5'10" and under 145 lbs., and I'm neither.

  • Anonymous

    2/19/2010 6:15:07 PM |

    Kurt G & Lightcan,

    I think when Dr. D said no "No polyunsaturates here. You've got the wrong guy."...he probably meant to say "No (high omega 6) polyunsaturates here.".

    Lastly...I have a question for Dr. Davis:

    Dr. D., is this "genetic small LDL" the same as when you talked about people with ApoE4 in your November 17, 2008 post? If so, do you think it would be helpful to test ApoE before experimenting with diet??

    Thanx!

    John M.

  • zach

    2/19/2010 6:20:59 PM |

    Aren't most nuts full of N-6 PUFA?

  • Rainer

    2/19/2010 6:23:53 PM |

    Hi Dr. Davis,

    and what is happend with the triclycerides of Stan. Are they high too?

  • Anonymous

    2/19/2010 7:14:40 PM |

    This is usually when the good doctor stops answering comments.

    Come on, Dr. D, prove me wrong!

  • Anonymous

    2/19/2010 7:24:49 PM |

    You have really great taste on catch article titles, even when you are not interested in this topic you push to read it

  • Donny

    2/19/2010 7:33:02 PM |

    I'm going to steal a page from T. Colin Campbell here (yechh!)

    Dr Davis, you say that

    "I have indeed had many people with presumed "genetic small LDL" load their diets with oils and fats with only minor improvement. Loaded with saturated fat, however, and there seems to be deterioration."

    Campbell makes the contention that studies showing that low saturated fat intake is beneficial (never mind whether they actually exist or not, just for the sake of argument here) might actually have nothing to do with the type of fat in the diet, and everything to do with the protein which accompanies the fat; most animal fat in our culture comes attached to meat (protein.)

    Adding plant fats and oils to the diet, including nuts, would tend to increase total percentage fat in the diet at the expense of both carbohydrate and protein. Adding animal fat, attached to meat might increase total protein percentage even as it increases total saturated fat.

    Understand, I'm not saying "protein bad," I guess I'm just echoing Peter, really, Stan may be trying to live off of a protein/fat mix that's too rich in protein, entirely aside from the whole issue of saturation.

  • Jeanie Campbell

    2/19/2010 7:57:39 PM |

    Don't tell me no one picked up on the Laurel and Hardy reference! Brilliant!

  • Anonymous

    2/19/2010 10:16:49 PM |

    Could all you saturated fat mafia people please stop polluting the comments section?

  • Sue

    2/20/2010 12:48:15 AM |

    Maybe recommend Stan use only sat fats and no poly oils and then see if there is a change.

  • Anonymous

    2/20/2010 2:29:41 AM |

    Drs. Davis and Harris,

    Googlemaps indicate you two practice your medicinal arts about 154 miles away from each other.

    May I respectfully suggest a summit meeting in Manitowoc to resolve these matters?

  • Scott Miller

    2/20/2010 3:31:43 AM |

    Flax oil, canola oil, any nut oil (except macadamia nut oil), and all of those nuts -- these are all rich with polyunsaturated fats. I never eat these oils, and my Lp(a) is 2, as last measured a few months ago.

    I always recommend nuts as a very moderate snack because of their high PUFA content.  Macadamia nuts are the ONE exception, with a fatty acid profile similar to olive oil.  Basically, I never recommend any food with a PUFA content greater that 12 percent.  That means canola oil is right out!

    Dr. Davis, perhaps try putting a few of these presumed "genetic small LDL" people on a real low PUFA diet for a while (with more coconut oil and butter--but no nuts during this period) and see if there's improvement.

    I'd bet there is.  Nothing really to lose by giving this a shot.

    If it works to your satisfaction, I'll donate $1000 to your Track-the-Plaque program, or a charity of your choice.

  • Dr. William Davis

    2/20/2010 1:58:33 PM |

    Some other features of the presumptive "genetic small LDL" pattern:

    1) It occurs in the minority of people with small LDL, likely less than 20% of people who start with substantial small LDL.

    2) It is associated with insulin resistance and a tendency towards diabetes

    3) It can occur independent of ApoE genotype. However, if it occurs with ApoE2, it means a very potent carb-sensitivity/diabetic tendency.

    4) The "floor" of 600 nmol/L can be broken. We've had success achieving really low body weight and inconsistently with several supplements, e.g., phosphatidylcholine.

    This area is fascinating, though very poorly explored. "Genetic small LDL" is truly one of the problem areas in gaining control over heart disease risk.

  • Henry North London

    2/20/2010 2:23:56 PM |

    I currently consume coconut oil and butter  I do not use any lard or pufas  I consume a moderate amount of almonds a day ( nine) and some ground almonds as a meal replacement about 10-20gs as a meal about two or three times a week

    I eat avocados maybe twice a week  about two-three

    I have started to show my abdominal muscles after two months where before I looked as if I were pregnant of about a 5 month pregnancy

    I have dropped half a stone  My BP is controlled by a sartan

    I consume a moderate amount of frozen blueberries and raspberries May be about 1 kg of each a month

    or less

    I am living on saturated fat and loving it

    My body works better on it but then I have blood group B

    You have to eat right for your blood type perhaps?

  • Miki

    2/20/2010 3:17:30 PM |

    I would like to add support to Dr. Harris' hypothesis. LDL (no NMR in our country) and TG both rise on low carb, high sat fat diet. No weight problem ever. No high protein no high PUFA for me. Pre-diabetic fasting glucose (110-120). Only complication is I had my gallbladder removed (but my brother didn't). Will increase coconut oil and olive oil on account of double cream. Feel so good on low carb it can't be wrong. Also wonder if under healthy low carb diet LDL and TG have atherogenic effect (My calcium score is low)
    In summary I think Dr. Davis is onto something but I would love to know if LDL status corresponded to increased calcium score in the said patients.

  • Donny

    2/20/2010 3:41:44 PM |

    Choline deficiency can lessen hyperglycemia in rodents with fatty livers. Maybe the inconsistent effects of phosphatidylcholine have something to do with that?

    To the person who mentioned the saturated-fat mafia; we have limited information going in here. Trying to guess at alternate explanations isn't the same as insisting that saturated fat is good in all situations for everybody, no matter what. Proper skepticism demands that we question even the most respected sources.

  • Anonymous

    2/20/2010 8:12:29 PM |

    Dr. Davis, this recent article seems congruent with some of your observations:

    http://jn.nutrition.org/cgi/content/abstract/jn.109.115964v1

  • Anonymous

    2/20/2010 8:16:01 PM |

    To all these nutty omega-6 fatphobes - I eat lots of nuts of all sorts, probably 40% of calories, including... peanuts, which I am aware are a legume.  I have no small LDL, undetectable CRP, and lp(a) of 4, high hdl and low homocysteine, HbA1C of 5.2.

  • Anonymous

    2/20/2010 9:06:44 PM |

    Dr. Davis,
    You said "Some other features of the presumptive "genetic small LDL" pattern:

    1) It occurs in the minority of people with small LDL, likely less than 20% of people who start with substantial small LDL."


    So, based on a minority of people with small LDL, you are recommending the same diet to everyone?

  • Dr. William Davis

    2/21/2010 2:28:39 AM |

    Please don't misunderstand: I am NOT saying that saturated fat increases small LDL in most people.

    What I am suggesting is that there is a genetic minority in which saturated fat increases small LDL. These people seem to be the unusually slender, high HDL, low triglycerides, yet diabetes-prone who show apparently intractable small LDL.

    I don't know for a fact why this happens, but I speculate that it is a genetically-determined trait.

    This pattern responds best to a high-protein, high-fat, very low-carbohydrate diet. But saturated fat is the exception in this group.

  • Kurt G. Harris MD

    2/21/2010 3:25:37 AM |

    Hello Dr Davis

    I am only persisting in this as the implications might be important.

    I asked, "Did you advise Stan to increase sat fat and then watch his sdLDL get worse?"

    You later said, "Loaded with saturated fat, however, and there seems to be deterioration."  and ..

    "What I am suggesting is that there is a genetic minority in which saturated fat increases small LDL."

    and...

    "This pattern responds best to a high-protein, high-fat, very low-carbohydrate diet. But saturated fat is the exception in this group."

    Can I assume when you say "seems to be deterioration" and "there is a suggestion that saturated fat increases small LDL" and "saturated fat is the exception" that this is based on the observation of  serially increased sdLDL NMR values after increasing only saturated fat intake in these 100 or so patients?

    If this is what you have, serial NMRs that show increased sdLDL with increased saturated fat intake, why not say so explicitly?

    Or is it just a reasoned (perhaps correct, perhaps not) guess of what would happen to sdLDL in those 100 or so who have this presumed genetic pattern of persistent sdLDL?

  • Rick

    2/21/2010 3:24:07 PM |

    Dr. Davis wrote:

    "I know this flies in the face of the 'saturated fat is great' dogma, but I don't make this stuff up."


    The way that Peter described the scenario you presented, it seems to support the health benefits of saturated fat rather than deride them

    Ollie is mainlining saturated fat from his gut.  Stan is not.  Ollie's sdLDL drops like a rock.  Stan's doesn't.  

    It seems like if this phenomenon of high sdLDL specifically affects low BMI people, their lack of saturated fat intake, whether through their mouths or from their love handles, could be the culprit.

  • kilton9

    2/24/2010 10:45:35 PM |

    Dr. Harris,

    I'm a fan of your blog, but I can't help but notice that you have completely ignored Dr. Harris's questions in this entry as well as the other recent entry about saturdated fat and LDL.  I find his questions to be pertinent.

  • bovinedefenestration

    2/27/2010 7:26:50 AM |

    I'm actually a little surprised no one's brought up this blog, that indicates polyunsaturate consumption over 4% of calories can be detrimental:

    http://wholehealthsource.blogspot.com/2009/05/eicosanoids-and-ischemic-heart-diseas.html

    Eh. Took me long enough to find. At any rate, 10-20% polyunsaturates, especially if they come from omega-6, is a huge amount for a human.

    Imma going to go away and let you argue now.

  • Henry North London

    2/27/2010 7:07:21 PM |

    Hear Hear throwing cows out of windows...  It blows the polyunsaturates out  of the window

    I have the printout of the Rose et al Paper..

    Corn oil increased the death rate

  • Janet -Mich

    2/28/2010 11:16:20 PM |

    My family has a history of high colestral and plaque build-up in the blood.  Should I stay on my Lipator and stay on a low-carb diet ?  Your article brings up some red flags for me.  Maybe I should talk to my Doctor, but my low-carb friends tell me the doctor will tell me to get off the diet !  I would like some advice.

  • dining table

    7/9/2010 9:52:12 AM |

    How did that happen? Is it possible? Different diet will work to Stan? I am curious about that. I will visit this blog again. I am hoping for an update.

  • Derek Weiss

    8/4/2010 9:49:11 PM |

    Obviously another great blog about eating and living right, but at some point we have to take a step back and live.  Food avoidance and constant stressing about food seems it could negate any benefits of just eating a sensible, well balanced, moderately low carb diet.  

    To me, all these nutrition blogs are fun to read at work. But have you ever noticed the incredible difference in opinion from one to the next?  I take all that with a large grain of salt, pun intended.

    Oh my god, I ate a walnut, surely I will be in the cath lab tomorrow getting my LAD stented;)

    You might not find yourself in the cath lab from eating the random 1/2 cup of oatmeal, but you might find yourself there from stressing about it too much.

    Read all the blogs, use all the information to help guide you.  But don't get in line with the zombies and wander off the deep end too far.

    Just a thought.

  • Liz Stanley

    9/16/2010 8:32:32 PM |

    Here's a stumper. I just had my VAP done and the results surprised me. Some background: I'm not on any medication and never have been. Never had a weight problem, body fat below 20%. I exercise regularly (CrossFit 4x/week). Never smoked. Rarely drink. I eat mostly a primal diet w/plenty of grass-fed/organic/cage-free/wild-caught meat/fish and lots of fresh veggies. Some dairy, but only hormone and antibiotic free. Hardly any grains or processed foods. Low fasting blood sugar (76 as of two weeks ago.) Here are my VAP results:

    Total cholesterol: 200
    HDL : 79
    LDL: 106
    VLDL: 14
    Lp(a): 7
    Triglycerides: 43

    With all that I'd expect to have Pattern A LDL. Yet the VAP test says I have Pattern B! I'm not aware of any history of heart disease on either side of my family. But if it's true that my LDL is small and dense, all I can figure is that it must be genetic. I'm not really sure what to make of it! Any ideas?

  • Anonymous

    9/24/2010 10:26:37 PM |

    Liz Stanley - while my HDL and LDL aren't as good as yours (63 and 185 respectively), I also just received VAP results that stumped me for a similar reason.  I exercise frequently, am not overweight, don't smoke or drink, eat low carb, etc., yet I have pattern B as well.  To add to the confusion, my cCRP is 0.7, which my doctor said was excellent and basically renders my test results a wash as I have zero other risk factors.  I don't know what to make of any of this when you put it all together, and I stumbled upon this post because I'm hoping to find some answers online.

  • buy jeans

    11/3/2010 6:33:42 PM |

    While body composition certainly isn't a prerequisite for being part of a classic comedy team, I couldn't help but notice that Stan had the makings of a skinny-fat bean pole checking in at 5' 10" and only 148 pounds. Those stats make him sound like a diehard distance runner or a chain smoker.

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Dr. Agatston to the rescue

Dr. Agatston to the rescue


Dr. Arthur Agatston, author of wildly successful South Beach Diet, has just released a new book titled The South Beach Heart Program. Dr. Agatston has started on a media speaking circuit to promote his book and concepts.


A reporter from Time, who interviewed Dr. Agatston, commented:

". . .not enough doctors prescribe niacin for their heart patients, even though the medicine is a proven treatment for raising 'good' cholesterol. Physicians are reluctant, Agatston suggests, because niacin requires diligent follow-up to watch for side effects, taking time that most primary-care practices cannot afford. On the other hand, he says, too many doctors are performing heart operations that represent a financial windfall for hospitals. Bottom line: there isn't as much money to be made in prevention as in treatment."

Amen.

Dr. Agatston echoes many of the concepts that the Track Your Plaque program advocates. His notoriety is going to help disseminate the idea that 1) CT heart scans are the #1 method to identify hidden atherosclerotic coronary plaque, 2) taking control of your heart scan score is the best way to seize hold of your future, and 3) the present-day popularity of heart procedures like stents and bypass is intolerable, inexcusable, and needs to be reined back.

Agatston also brings great credibility and fairness to the conversation and his comments will gain tremendous attention in the press and with the public.
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