Near-fatal brush with nattokinase

Here is precisely why I have spoken out against nattokinase: People may put faith in this "supplement" when there are virtually no data to support its use in such dangerous conditions as pulmonary embolism.

Pulmonary embolism occurs when a large volume of blood clots in the veins of the pelvis, abdomen, and into the legs. A clot breaks off and lodges in the pulmonary arteries of the lungs. This can be fatal within minutes to hours, the victim struggling to breathe, since oxygen is not transferred to the blood and it causes terrible pain in the chest.

The treatments are fairly obnoxious: intravenous anticoagulants (blood thinners), followed by oral blood thinners like warfarin. While they carry risk of bleeding and other long-term risks, it's better than dying.

Would you bet that a "nutritional supplement" manufacturer's vague claims and lack of data are sufficient proof to treat a life-threatening condition? You're a fool if you are.

Anyone reading these pages knows that I am a vigorous supporter of nutritional supplements. I even consult for the nutritonal supplement industry. But I am also an advocate of TRUTH, not BS.

Here is a woman from England who inquired whether she should stop her husband's warfarin in favor of nattokinase. This is precisely the sort of thing that can happen because of the campaign of misinformation behind nattokinase.


Dr. Davis,

Thank you for your very interesting blogs, which I came across searching for natural alternative treatments to warfarin.

My husband has been following the low carb, high fat, real food regime over the past few years. He got off all the blood pressure and cholesterol drugs and never felt better. He even got his blood sugar down from a recorded high that we are aware of 13 nmol/L (234 mg/dol) to 6.1 nmol/L 109.8 mg/dl).

We were on holiday in the Caribbean. Just before our return home, we did a trip to a neighbouring island that included non-alcoholic fruit punches. They tasted great, but were very sweet. I broke my normal refusal to drink these things, but only had a couple of glasses. (After all, we were on holiday!) My husband believes he consumed around 1.5 litres of the stuff and now realises he was feeding his body a very toxic product – fructose. That night, he had an incredible toxic response and we only got him onto the plane with a visit to the hospital and a pain killer injection.

The symptoms of pulmonary embolism only showed 2 weeks later . . . and warfarin treatment was started. We would both like to use an alternative therapy if we can find someone with experience to provide the support.Do you know of any studies that support alternative options?

Do you know of any practitioners in the England who support a non-drug approach with an understanding of nutrition who we may be able to receive advice and support?

FB
York, England

Glucophobia: The Novel

Just kidding: No novel here. However, there is indeed a story to tell that should scare the pants off you.

If you haven't yet gathered that carbohydrates are a macronutrient nightmare, let me recount the list:


Carbohydrates increase small LDL particles
Or, in the cholesterol-speak most people understand, "carbohydrates increase cholesterol." It's counterintuitive, but carbohydrates increase LDL substantially, far more than any fat.


Carbohydrates increase blood sugar
Eggs don't increase blood sugar, nor do chicken, raw almonds, onions or green peppers. But a bowl of oatmeal will send your blood sugar skywards.


Carbohydrates make you fat
Carbohydrates, whether in the form of wheat flour in your whole wheat bread, sucrose in your ice cream, fructose in your "organic Agave nectar," or high-fructose corn syrup in your dill pickles. They all provoke de novo lipogenesis, or fat formation. They also stimulate insulin, the hormone of fat storage.


Carbohydrates cause glycation
High blood sugar, like the kind that develops after a bowl of oatmeal, triggers glycation, or modification of proteins by glucose (blood sugar). This is how cataracts, kidney disease, and atherosclerotic plaque develop. Small LDL is 8-fold more glycation prone than large LDL, providing a carbohydrate double-whammy.


Your glucose meter remains the single best tool to gauge the quality of your diet. Many people have horror stories of the shocking experiences they've had when they finally get around to checking their postprandial glucose.

Drama with the Dr. Oz Show

A producer from the Dr. Oz show recently contacted my office. They asked whether we could supply them with a volunteer patient from either my practice or the Track Your Plaque program who would be willing to appear on the show and discuss heart disease prevention. They needed someone to commit within 24 hours.

Despite the short notice, we identified a volunteer. He flew to New York the following week where he was interviewed along with several other men and women, all of whom had heart disease (heart attacks, stents, etc.). However, as this young man is very slender and follows most of the Track Your Plaque principles (e.g., vitamin D and omega-3 fatty acid supplementation; no wheat, cornstarch, or sugars, no restriction of fat, etc.), he apparently received less attention than the overweight, I-know-nothing-about-diet interviewees.

Then there was an odd turn of events: Dr. Dean Ornish, apparently a friend of Dr. Oz, will be providing the dietary counseling. The producer had made no mention of Dr. Ornish.

Now that's an odd collision of philosophies: Our Track Your Plaque version of low-carb with the guru of low-fat, Dr. Ornish.

The following week, Dr. Ornish called me and graciously asked whether I was okay with this. I'm not sure just how much he knew about the philosophy I advocate, nor how much I have bashed his program as a destructive approach to diet, nor whether he knew that I gained 30 lbs on the Ornish diet, along with a drop in HDL to 27 mg/dl, increased triglycerides to 350 mg/dl, and type II diabetes that I've talked about on this blog and the Track Your Plaque book and website. I suspect he knew little to none of this.

Anyway, I tried to diplomatically explain that my patient's cause for coronary plaque was small LDL particles that he expressed despite his very slender build, likely from excessive carbohydrates, controlled with carbohydrate restriction. Dr. Ornish maintained his usual arguments: Grains are good, provided they are whole grains, heart disease is "reversed" with his diet program, etc. (I didn't want to challenge him in a phone call and tell him that he never actually reversed coronary plaque, but just reversed endothelial dysfunction. But, as Dr. Ornish is not a cardiologist, I wasn't sure how far his understanding of these issues went.)

We agreed to disagree. This leaves my poor patient in an odd position: Being asked by Dr. Ornish and the Dr. Oz show to follow a low-fat program for the sake of entertainment, or adhering to the advice we follow that has so far served him well, given his small LDL particle size tendencies.

We'll see where this little drama leads.

Response from Nature Made

Here's the response from Nature Made when I emailed them about my concern that there appears to be no vitamin D in their vitamin D gelcaps.

It is the usually CYA corporate-speak that says nothing. The grammatical errors make it clear that this was a "canned" response.



Date: April 9, 2010
From: Marissa Reyes, Consumer Affairs Department
Subject: Reference #346236

Dear William Davis, MD:

We recently received your e-mail regarding Nature Made products. We regret to
hear that the quality standards of our company. [?]

Our company is called Pharmavite, and we manufacture Nature Made nutritional
supplements. We have been in business since 1971. We are committed to quality
control, and have very high quality standards. Our Quality Control personnel
sample and test all raw materials as they enter our plant, and again assay the
finished product, before final packaging.

Dietary Supplements are regulated under the FDA through DSHEA (Dietary
Supplement Health & Education Act of 1994). The United States Pharmacopoeia
(USP) establishes standards for the composition of drugs and nutritional
supplements. This voluntary non governmental organization was set up in 1820
and has officially been recognized by federal law since 1906. Standards
established by USP for products are legally enforceable by the FDA. At
Pharmavite we participate in the USP Dietary Supplement Verification Program
(DSVP). Many of our products have earned the DSVP seal and additional products
are currently being evaluated. Our DSVP certified products will have the DSVP
seal on the product label.

Our Nature Made Vitamin D 400 IU tablets have been reviewed by the USP and bears
the DSVP symbol on the label. Although the USP has not reviewed all of the
Nature Made Vitamin D supplements, all of our products go through the same
rigorous quality testing at Pharmavite. The products which have earned the seal
help us to demonstrate the high quality of our products.

We would like to look into the product(s) your patients have been using. If you
could provide the UPC and lot numbers of the product(s), we will be happy to
review our records. In addition, if you would like us to test the product(s)
that you currently have, we will be pleased to send a prepaid postage mailer so
you may return the product(s) to us so that our Quality Control Department can
examine it. Please let us know if you would like us to send you the prepaid
postage mailer.

We thank you for contacting us and hope that you will continue to use and enjoy
Nature Made products with complete confidence.

Sincerely,
Marissa Reyes
Consumer Affairs Coordinator
Pharmavite, LLC
MR:346236-10



Patients who come to the office do not provide me with the bottles nor lot numbers. In past, when I've gone to the trouble of doing this (with other companies, not Nature Made), it has come to nothing helpful. The information gets passed on to the company and we hear nothing and never learn if there was a problem, or receive some more corporate-speak letter saying everything was fine. This is obviously a liability-avoidance tactic: Admitting that something was wrong would open them up to legal risk. So, frankly, I can't be bothered.

So we are left with the unsatisfying experience of relying on street-level experiences.

For now, my advice: Avoid Nature Made vitamin D. Too many people have had blood tests demonstrating that they are not obtaining any vitamin D.

By the way, the Nature Made brand of fish oil is among the very few problem brands of fish oil we've encountered. Fish oil should be only mildly fish in smell and generally should not cause stomach upset and excessive belching if properly purified. Nature Made is excessively fishy when you smell it, suggesting oxidation. We've had repeated (dozens) of patients who have experienced difficulties with this brand. Rather than dealing with the frustrating gobbledy-gook of this company, just avoid their products.

What to Eat: The diet is defined by small LDL

I approach diet from the perspective of small LDL particles.

Small LDL particles have exploded in frequency and severity in Americans. It is not at all uncommon to see 70% or more small LDL particles (i.e., 70% of total LDL particle number or Apo B) on lipoprotein testing. (I saw two people today who began with over 95% small LDL.)

Small LDL particles are:
--More likely to persist in the bloodstream longer than large LDL particles.
--More likely to adhere to components of atherosclerotic plaque.
--More likely to gain entry to plaque.
--More likely to be taken up by inflammatory white blood cells which, in turn, become the mast cells that fill coronary plaque.
--More likely to be oxidized.
--More likely to be glycated (8-fold more likely than large)

To add insult to injury, foods that trigger small LDL formation--i.e., carbohydrates--also cause high postprandial blood sugars. High postprandial blood sugars, in turn, glycate small LDL. That combination of events accelerates 1) plaque growth, 2) plaque instability, and 3) aging.

So carbohydrates trigger this sequence, carbohydrates of all stripes and colors. Not just "white" carbohydrates, but ALL carbohydrates. It's all a matter of degree and quantity. So, yes, even quinoa, bulghur, and sorghum trigger this process. I've only recently appreciated just how bad oats and oatmeal are in this regard--really bad.

Foods that trigger small LDL also trigger higher blood sugars; foods that trigger higher blood sugars also trigger small LDL. Small LDL and blood sugar are two different things, but they track each other very closely.

So, in the Track Your Plaque approach to diet, we craft diet based on these simple principles:

1) Eliminate wheat, cornstarch, and sugars--These are the most flagrant triggers of small LDL, blood sugar, and, therefore, LDL glycation.
2) The inclusion of other carbohydrates, such as oatmeal, quinoa, rye, etc. depends on individual sensitivity. Individual sensitivity is best gauged by assessing one-hour postprandial glucose.

Stay tuned for more in this series. Also, Track Your Plaque Members: We will be having an in-depth webinar detailing more on thees principles in the next couple of weeks.

Is it or isn't it vitamin D?

Jackie takes 10,000 units of vitamin D(3) per day as a gelcap.

Her starting 25-hydroxy vitamin D blood level was 18.1 ng/ml. Severe deficiency, no surprise.

On her 10,000 units per day, Vitamin Shoppe brand, her 25-hydroxy vitamin D level was 76.2 ng/ml--perfect. It stayed in this range for about two years.

She then changed to the Nature Made brand gelcaps she picked up at Walgreen's. Repeat 25-hydroxy vitamin D level: 23 ng/ml.

This has now happened with five different people, all taking the Nature Made brand.

If you are taking this brand of vitamin D, please be on the alert. You might consider a 25-hydroxy vitamin D blood level to be sure it actually has the vitamin D it's supposed to have.

Or, change brands.

What to eat: Part I

I've spent a good number of Heart Scan Blog posts detailing what foods to limit or avoid.

The list of unquestionably bad foods to avoid include foods made of wheat, cornstarch, and sugars. Fructose is proving to be an exceptionally bad form of sugar, worse than any other. I've issued warnings about levels of carbohydrates that can be determined by postprandial testing.

In response to several requests to clarify what foods to eat, this post begins a series discussing what foods are good to eat.

I believe that a strong case can be made for eating vegetables in nearly all its varied forms, from cucumbers to peppers to leafy vegetables to eggplant to alliums like onions. The only form we avoid are red and white potatoes due to the blood sugar-increasing effects.

While this seems obvious, I am impressed how many people who follow low-carb diets find themselves following a high-animal product diet with vegetables as the sideline. It should be the other way around: A high vegetable diet with animal products as the sideline.

Vegetables are your principal source of:

1) Flavonoids and polyphenols--e.g., anthocyanins and catechins. All the recently appreciated effects of flavonoids and polyphenols highlight the wonderful effects of compounds originating in plant foods. This includes the anthocyanins and resveratrol in red wine; the catechins and epicatechins cocoa and green tea; the hydroxytyrosol, phenolic acid, and flavonoids of olive oil.

2) Fiber--Fiber is essentially a plant phenomenon, since there is virtually none in chicken, fish, and beef. The benefits of fiber are, I believe, undisputed. Neglecting fiber can, at the very least, lead to a nasty case of hemorrhoids. At the worst, it is related to various cancers, especially colon cancer.

3) Vitamin C--While vitamin C may be old and boring in light of new, exciting discoveries like flavonoids, neglect leads to bad things.

Vegetables are generally classified as carbohydrate foods, since they are low in protein and fat. But this is the source of carbohydrates you do not want to sacrifice in a low-carbohydrate diet. There's just too much good from vegetables.

Notice that I didn't say "fruits and vegetables." This is a fundamental mistake made by many: Oveconsumption of fruits. I've even seen people who follow an otherwise good diet develop diabetes--just from too much fruit.

Vegetables should be the cornerstone of the human diet. But I'll bet you knew that already.

Carbohydrates and LDL

There's a curious and powerful relationship between carbohydrates and LDL particles. Understanding this relationship is crucial to gaining control over heart disease risk.

(Note that I did not say "LDL cholesterol"--This is what confuses people, the notion that cholesterol is used as a surrogate marker to quantify various lipoproteins, including low-density lipoproteins, LDL. I'm NOT interested in the cholesterol; I'm interested in the behavior of the low-density lipoprotein particle. There's a difference.)

Carbohydrates:

1) Increase triglycerides and very low-density lipoprotein particles (VLDL)
2) Triglyceride-rich VLDL interact with LDL particles, making them smaller. (A process mediated by several enzymes, such as cholesteryl-ester transfer protein.)
3) Smaller LDL particles are more oxidizable--Oxidized LDL particles are the sort that are taken up by inflammatory white blood cells residing in the artery wall and atherosclerotic plaque.
4) Smaller LDL particles are more glycatable--Glycation of LDL is an important phenomenon that makes the LDL particle more atherogenic (plaque-causing). Glycated LDLs are not recognized by the LDL receptor, causing them to persist in the bloodstream longer than non-glcyated LDL. Glycated LDL is therefore taken up by inflammatory white blood cells in plaque.

Of course, carbohydrates also make you fat, further fueling the fire of this sequence.

The key is to break this chain: Cut out the carbohydrates. Cut carbohydrates and VLDL and triglycerides drop (dramatically), VLDL are unavailable to transform large LDL into small LDL, small LDL is no longer available to become oxidized and glycated, blood sugar is reduced to allow less glycation. Voila: Less atherosclerotic plaque growth.

Yet the USDA, American Heart Association, and the Surgeon General's office all advise you to eat more carbohydrates. The American Diabetes Association tells you to eat 70 grams or so carbohydrates per meal. (Yes: Diabetes, the condition that is MOST susceptible to these carbohydrate effects.) Follow their advice and you gain weight; triglycerides and VLDL go up; calculated (Friedewald) LDL may or may not go up, but true measured LDL (NMR LDL particle number or apoprotein B) goes way up; small LDL is triggered . . . You know the rest.

The dance between carbohydrates and LDL particles requires the participation of both. Allow one partner to drop out of the dance and LDL particles will sit this dance out.

Strange but true: Part II

Here's the second part of the Heart Scan Blog post I wrote a couple of years back describing the wacky origins of this thing that has so changed the face of heart care in the U.S., the cardiac catheterization.

Heart catheterization: Strange, but true

It's a couple of years old, but this post from March, 2008, remains relevant.

It details the curious origins of heart catheterization, the procedure that has saved some lives, but also been responsible for the proliferation of unnecessary heart procedures.



The modern era of heart disease care was born from an accident, quirky personalities, and even a little daring.

The notion of heart catheterization to visualize the human heart began rather ignominiously in 1929 at the Auguste-Viktoria Hospital in Eberswalde, Germany, a technological backwater of the day. Inspired by descriptions of a French physician who inserted a tube into the jugular vein of a horse and felt transmitted heart impulses outside the body, Dr. Werner Forssmann, an eager 25-year old physician-in-training, was intent on proving that access to the human heart could be safely gained through a surface blood vessel. No one knew if passing a catheter into the human heart would be safe, or whether it would become tangled in the heart’s chambers and cause it to stop beating. On voicing his intentions, Forssmann was ordered by superiors not to proceed. But he was determined to settle the question, especially since his ambitions captured the interest of nurse Gerda Ditzen, who willingly even offered to become the first human subject of his little experiment.

Secretly gathering the necessary supplies, he made his first attempt in private. After applying a local anesthetic, he used a scalpel to make an incision in his left elbow. He then inserted a hollow tube, a catheter intended for the bladder, into the vein exposed under the skin. After passing the catheter 14 inches into his arm, however, he experienced cold feet and pulled it out.



One week later, Forssman regained his resolve and repeated the process. Nurse Ditzen begged to be the subject, but Forssmann, in order to allow himself to be the first subject, tricked her into being strapped down and proceeded to work on himself while she helplessly watched. After stanching the oozing blood from the wound, he threaded the catheter slowly and painfully into the cephalic vein, up through the bicep, past the shoulder and subclavian vein, then down towards the heart. He knew that simply nudging the rubber catheter forward would be sufficient to direct it to the heart, since all veins of the body lead there. With the catheter buried 25 inches into his body, Forssmann untied the fuming Ditzen. Both then ran to the hospital’s basement x-ray department and injected x-ray dye into the catheter, yielding an image of the right side of his heart, the first made in a living human.

Thus, the very first catheterization of the heart was performed.

An x-ray image was made to document the accomplishment. Upon hearing of the experiment, Forssmann was promptly fired by superiors for his brazen act of self-experimentation. Deflated, Forssmann abandoned his experimentation and went on to practice urology. He became a member of the Nazi party in World War II Germany and served in the German army. Though condemned as crazy by some, physicians in Europe and the U.S., after hearing of his experience, furthered the effort and continued to explore the potential of the technique. Forssmann himself was never invited to speak of his experiences outside of Germany, as he had been labeled a Nazi.

Many years after his furtive experiments, the once intrepid Dr. Forssmann was living a quiet life practicing small town medicine. He received an unexpected phone call informing him that he was one of three physicians chosen to receive the 1956 Nobel Prize for Medicine for his pioneering work performing the world’s first heart catheterization, along with Drs. André Cournand and Dickinson W. Richards, both of whom had furthered Forssmann’s early work. Forssmann remarked to a reporter that he felt like a village pastor who was made a cardinal.

Strange, but true.
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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