Can I see your linea alba?

2. November 2010 William Davis (19)
As more and more people are eliminating wheat from their diet and losing their "wheat bellies," i.e., the muffin top around their waists along with the visceral fat beneath, I am frequently seeing something I haven't seen in years: the linea alba.

Linea alba, or "white line," refers to the band of connective tissue running vertically from sternum to pubic area. It underlies the depression that separates the horizontal abdominal rectus muscles of the "six pack" abdomen.

It's like digging in your closet and finding something you thought you'd lost years earlier. Surprise! It's been there all along. Buried deep beneath the abdominal fat from dozens of deep-crust pizzas, whole wheat pasta, and whole grain sandwiches is this pleasing anatomical feature long lost from most peoples' anteriors.


Can you see your linea alba?

Dwarf mutant wheat

31. October 2010 William Davis (13)
Here's my 12-year old standing next to dwarf wheat grown near my house. The wheat is full-grown, harvested about 2 weeks after I took this photo.

Wheat is no longer the 4-foot tall "amber waves of grain" of the 20th century. Over 99% of all wheat grown worldwide is now the 18- to 24-inch tall dwarf. New size, new biochemistry, new effects on humans. I call it dwarf "mutant" wheat despite its lack of extra limbs or eyes because of the dramatic transformation required to breed this unique synthetic plant. 

Short-stature means less stalk, faster growing. The stockier stalk also means that the heavy seed head won't cause the plant to "buckle," as 4-foot tall wheat used to. 





The thousand-plus proteins of wheat that have been transformed to generate this dwarf mutant also changed wheat's relationship to consuming humans.

Medical education in the days of Big Pharma

30. October 2010 William Davis (43)
I received this detailed email from an unexpected source: a 3rd-year medical student.

In her email, Theresa describes her frustrations in what she is witnessing for the first time, proceeding through her training and getting exposed to the realities of medical life.

Medical training, particularly clinical training from the 3rd and 4th years of medical school, onwards through internship, residency, and fellowship training, consists largely of bullying, "pimping" (meaning rapid-fire grilling of questions at trainees), and sleep deprivation. It is an extended hazing period meant to demoralize and inculcate the trainee into following the lead of superiors. Buck the system and you're . . . out. Imagine you've just sunk $190,000 and 8 years of college into getting to your internship. You are not going to chance being thrown out on principle. So you just swallow your pride, go along with the game, and echo all the answers they want you to repeat.

While Theresa laments the sad state of modern American pharmaceutical- and procedure-obsessed medicine, she provides me with hope that some young people training to practice medicine today will carve out their own paths, not the one laid for them by the pharmaceutical industry, nor fall for the temptation of higher-paying procedural specialties like orthopedics and cardiology. I am impressed with her ability to see this so early in her career.


Dr. Davis,

I am a 3rd year medical student at ________ University. I came across
your blog today, and I'm very glad I did. I appreciate the value of your time,
so I want to be as succinct as possible while still getting across what I'm
really thinking and feeling:

From what I gathered exploring your blog for a while this afternoon, the
wellness strategies you incorporate into your practice are some of the exact
things I want to do with my future patients. Personally, I strongly believe in
staying healthy by eating right, staying active, etc. For instance, I don't eat
grains or much in the way of starches and sugars. So I love the fact that you
are helping your patients make these powerful and foundational changes in their
lives.

As I'm sure was your experience, a full appreciation of nutrition and lifestyle
as a first-line health strategy is not something that was taught to me in
medical school. I came to school with this deep conviction already in my heart
and mind, and now, on my 3rd year rotations, I am still conflicted and at a loss
as to how I'm going to be able to practice medicine the way I want to, which is
to incorporate these all-important principles into the care of my patients.

What I've come to understand about the medical field today is that the
information that exists is primarily subsidized by the pharmaceutical industry,
and dictated to medical professionals as "evidence-based" treatment guidelines
and recommendations by organizations with sincere and official sounding names
like American Heart Association and American Cancer Society. Add to that the
pressure of potential malpractice litigation and the complexities of the
insurance reimbursement game, and it seems to me like what you get is a bunch of
diagnostic and medication management algorithms that any half-trained monkey
could follow. In his sleep. Which I guess would be alright if at least they
weren't algorithms based on misguided, self-serving, profit-seeking Big Pharma,
Food Inc, insurance conglomerates, and agri-politics (I think I just made that
word up.)

A lot of well-intentioned physicians are just parroting the party
line, as their patients dutifully and gratefully chomp down their statins and
diabetes drugs and blood pressure pills. And I'm sorry, but "diabetes
education" programs with curriculum put together by drug companies? How is that
even legal? Massive corporations raking in massive profits that are dependent
on uncontrolled blood sugars telling people how to best control their blood
sugars?!

Anyway, forgive my rant. What I'm getting at is this: How can I practice
medicine, with the freedom to educate/coach/treat my patients with diet and
lifestyle changes to mitigate/reverse their chronic health conditions? Without
feeling like I automatically have to first and foremost prescribe the litany of
drugs dictated by "evidence-based" guidelines? Without excessive fear of
litigation or loss of credibility among my peers? Without having to lie through
my teeth to my patients, and tell them that eating low-fat and heart-healthy
whole grains is the best way (implication also being the only scientifically
proven way) to control their diabetes, lower their cholesterol, etc, etc, etc?

I want my patients to have the full benefit of honest nutrition and lifestyle
information, and medications and surgery as necessary. I'm afraid that there
isn't room for this kind of holistic emphasis in the medical profession today.
Are there residencies that include this kind of training or at least respect
these "unconventional" philosophies? Are there clinics or practice groups that
would allow me to practice with this emphasis, or is there a bias against docs
who do not necessarily conform to the party position? Will I have no other
option but to go it alone under the auspices of my own shingle? How do you
handle these kinds of issues in your professional life?

Sincerely,
Theresa M.


A ray of hope! Perhaps Theresa is just the first among many more medical students who refuse to submit to the brainwashing practices of the pharmaceutical industry, the same mind manipulation that has hopelessly turned most of my colleagues into their unwitting puppets.

I'll be interested in watching how Theresa's experience unfolds. I've asked her to keep us informed every so often.

The Great Low-Carb Connector

28. October 2010 William Davis (15)
The effusive Jimmy Moore of Livin' La Vida Low-Carb asked me to help get the word out about his new podcast subscription service, The Livin' La Vida Low-Carb Show Fan Club.

Jimmy has been The Great Connector for the low-carb discussion, from his ubiquitous online and social media presence, to his annual low-carb cruise. He has also broadcast first class interviews of nutritional notables like Gary Taubes, Dr. Robert Lustig, and blogger Stephan Guyenet. His Fan Club expands listener involvement in the podcast process and, potentially, greater access to his guests:

My faithful listeners have long been asking me about how they can become even more engaged in the behind-the-scenes workings of the show to get the inside scoop about what’s coming next. I’ve heard people ask specifically for access to transcripts of the most popular podcasts, a listing of the interviews I’m currently working on with the ability to ask questions of those guests, to have sneak peek of audio from not-yet-released interviews and more. My amazing podcast producer, Kevin Kennedy-Spaein, and I have been discussing how to best do this for a while in an effort to meet the demands of our biggest fans and we think we’ve got just the answer for you. Introducing The Livin’ La Vida Low-Carb Show Fan Club!

This is for all intents and purposes the quintessential destination for people who can’t get enough of this podcast that goes much deeper than discussion about the low-carb lifestyle. Yes, I speak with a lot of people who are supporters of carbohydrate-restricted diets, but I also talk with fitness gurus, people who support alternative eating plans, those who have interesting theories and beliefs regarding health and much more. Wouldn’t you love to have a chance to know who’s coming up in my schedule to be able to ask them questions BEFORE I interview them? Keep in mind that my interviews are pre-recorded and air sometimes as much as 5-6 months afterwards. Members of the “fan club” would know all about who’s coming and likely will have their question asked on the air just for signing up to be a part of this exciting new addition to “The Livin’ La Vida Low-Carb Show.”

Jimmy is the guy who is bringing this disparate and widely-spread community together. He's the guy we all know, he knows "everybody." I'm looking forward to seeing how this new project makes a more involved, personal delivery of interaction possible.

New Track Your Plaque record!

27. October 2010 William Davis (19)
The record for the largest drop in heart scan score (by percentage of starting score) has been held for around three years, with 63% reduction in score.

Well, the longstanding record was broken this week: 75% reduction in score.

At the start, Freddie has disastrous lipid values:

LDL cholesterol 263 mg/dl
HDL 26 mg/dl
Triglycerides 323 mg/dl
Total cholesterol 354 mg/dl

Lipoproteins (NMR) were worse:

LDL particle number 3360 nmol/L
Small LDL 2677 nmol/L

Heart scan score: 732

Interestingly, Freddie had virtually no vitamin D in his body, with a 25-hydroxy vitamin D level that was unmeasurable.

Freddie was miserably intolerant to statin drugs, with even the smallest dose resulting in intolerable muscle aches. That's when his doctor sent him to me.

Because I felt that the dominant abnormality in Freddie's lipids and lipoproteins was small LDL particles, representing 80% of total LDL particle number, we focused his program on correcting this parameter. Freddie's program was therefore focused elimination of wheat, cornstarch, oats, and sugars, along with an eventual vitamin D dose of 20,000 units to finally achieve a 25-hydroxy vitamin D level of 66 ng/ml. No statin drug in sight.

43 lbs of weight loss and 18 months later, a second heart scan score: 183--a 75% reduction.

While the rest of the world continues to insist that coronary calcium (heart scan) scores cannot be reduced, I am seeing records being broken. I add Freddie's experience to the rapidly growing list of people who have not just stopped coronary plaque from growing, but are seizing control and reducing it, sometimes to dramatic degrees.

The Anti-AGEing Diet

22. October 2010 William Davis (36)
Advanced Glycation End-products, AGEs, are a diverse collection of compounds that have been associated with endothelial dysfunction, cataracts, kidney disease, and atherosclerosis in both animal models and human studies. Not all involve glycation nor glucose, but the catch-all name has stuck.

There are a number of actively-held theories of aging, such as the idea that aging is the result of accumulated products of oxidative injury; a genetically pre-programmed script of declining hormones and other phenomena; genetic "mis-reading" that results in disordered gene expression, debris, and uncontrolled cell proliferation (e.g., cancer); among others.

One of the fascinating theories of aging is, cutely, the AGEing theory of aging, i.e., the accumulation of AGE debris in various tissues. Such AGEs have been recovered in lenses from the eyes, atherosclerotic plaque in arteries, kidney and liver tissue, even brain tissue of people with Alzheimer's dementia. AGEs perform no known useful physiologic function: They are relatively inert once formed (especially polymeric AGEs), they do not participate in communication, they make no contribution of significance. They simply gum up the works--debris. (AGEs are to health as the USDA food pyramid is to dietary advice: material for the junkyard.)

There are two general ways to develop AGEs:

1) Endogenous--High blood glucose (any blood sugar above 100 mg/dl) will permit glycation of the various proteins of the body. The higher the blood glucose, the more glycation will proceed. Glycation also occurs at low velocity at blood glucose levels below 100 mg/dl, though this would therefore represent the "normal," expected rate of glycation. Endogenous glycation explains why people with diabetes appear to age and develop all the phenomena of aging faster than non-diabetics (kidney disease, eye diseases, atherosclerosis, dementia, etc.). Hemoglobin A1c, HbA1c, is a readily-obtainable blood test that can show how enthusiastically you have been glycating proteins (hemoglobin, in this case) over the last 2 to 3 months.

A low-carbohydrate diet is the nutritional path that limits endogenous glycation leading to AGE formation. Restricting the most obnoxious carbohydrates, the ones that increase blood sugar the most, such as wheat, cornstarch, rice starch, potato starch, tapioca starch, and sucrose, will limit endogenous AGE formation.

2) Exogenous--AGEs (here especially is where the "AGE" label is misleading, since many other reactions besides glycation lead to such compounds) are formed with cooking at high temperatures, especially meats and animal products. Therefore, a rare steak will have far less than a well-done steak. A thoroughly baked piece of salmon will have greater AGE content than sashimi.

The forms of cooking that increase AGE content the most: roasting,deep-frying, and barbecuing. Temperatures of 350 degrees Fahrenheit and greater increase AGE formation.

Therefore, cooking foods at lower temperature (e.g., baking, sauteeing, or boiling), eating meats rare whenever possible (not chicken or pork, of course), eating raw foods whenever possible (e.g., nuts) are all strategies that limit exogenous AGE exposure. And minimize or avoid butter use, if we are to believe the data that suggest that it contains the highest exogenous AGE content of any known food.

If we connect the dots and limit exposure to both endogenous and exogenous AGEs, we will therefore not trigger this collection of debris that is likely associated with disease and aging. So following a low-AGE diet may also be an anti-aging strategy.

The New Track Your Plaque Diet, soon to be released on the Track Your Plaque website, has incorporated strategies to limit both endogenous as well as exogenous AGEs.

Butter: Just because it's low-carb doesn't mean it's good

21. October 2010 William Davis (59)
The diet I advocate in the Track Your Plaque program to gain control over the factors that lead us to coronary plaque and heart attack is a low-carbohydrate diet. We begin with elimination of wheat, cornstarch, oats, and sugars in the context of an overall carbohydrate-reduced diet. We refine the program by monitoring postprandial (after-meal) glucoses.

But not everything low-carb is good for you. Fried sausages, for instance, are exceptionally unhealthy, despite having little to no carbohydrates.

An emerging but potentially very powerful issue is that of Advanced Glycation End-products, or AGEs. There are two general varieties of AGEs: endogenous (formed within the body) and exogenous (formed in food that is consumed).

Endogenous AGEs form in the body as a result of high blood glucose, i.e., glycation. When exposed to any blood glucose level of 100 mg/dl or greater, some measure of glycation will develop due to a reaction between glucose and various proteins, e.g., proteins in the lens of the eye, forming cataracts over time.

Exogenous AGEs form in food, generally as a result of heating to high-temperature. (AGEs is really a catch-all term; there are actually a number of reactions that occur in foods, not all of them involving sugars. However, the "AGE" label is used to signify all the various related compounds. The values quoted here are from Dr. Helen Vlassara's Mt. Sinai Hospital laboratory; reference below.)

Beef cooked to high-temperature yields plentiful AGEs. One gram of roast beef, for instance, contains 306,238 units. This means that an 8-oz serving yields 13.8 million units AGEs. Compare this to a boiled egg with 573 units per gram, raw tomato with 234 units per gram.

Butter contains an impressive 264,873 units AGEs per gram, the highest content per gram in the entire list of 250 foods tested in the Mt. Sinai study. A couple pats of butter (10 g) therefore contains 2.64 million units. A stick of butter that you might add to cake batter to make a cake therefore yields 30 million units of AGEs.

So there's nothing wrong with the fat of butter. It's AGEs that appear to be responsible for the endothelial dysfunction/artery-constricting, insulin-blocking, oxidation and inflammation reactions that are triggered. Among all of our food choices, butter is among the worst from this viewpoint.

Throw in the peculiar "insulinotrophic" effect of butter, and you have potent distortion of metabolic pathways, courtesy of the butter on your lobster.

(AGE data from Goldberg 2004. In this analysis, carboxymethyllysine was the marker used for AGE content.)

Incidentally, the new Track Your Plaque diet will soon be released as chapter 9 of the new Track Your Plaque book on the website.

Einkorn now in Whole Foods

16. October 2010 William Davis (19)
I just saw this at Whole Foods: einkorn pasta.

In my einkorn bread experience (In search of wheat: We bake einkorn bread), I was spared the high blood glucose and neurologic and gastrointestinal effects of conventional whole wheat grain (dwarf Triticum aestivum). I shared the einkorn bread  with four other people with histories of acute wheat sensitivities, only one of whom experienced a mild diffuse joint reaction, the other three not experiencing any symptoms.

Anyone wishing to try einkorn can now obtain commercial pasta from Jovial, an Italy-based manufacturer. It comes in spaghetti, linguine, rigatoni, fusilli, and penne rigate shapes.

Eli Rogosa, founder of The Heritage Wheat Conservancy, tells me that, in her experience, celiac suffers seem to not experience immunologic phenomena triggered by conventional wheat.

However, we've got to be careful here. The so-called ("diploid") "A" genome of einkorn shares many of the same genes as the ("hexaploid") "ABD" genomes of modern wheat, including overlap in the sequences coding for the 50-or so different glutens and glutenins. Most of the genes that code for the glutens that cause celiac and related illnesses reside in the "D" genome that are absent in the einkorn "A" genome. However, the "A" genome still codes for glutens. So there is potential for activating celiac disease in some people. Insufficient research has been devoted to this question. It is a question of extreme importance to people with celiac and other immune-mediated conditions, since re-exposure to the wrong form of gluten can increase risk of intestinal lymphoma 77-fold, as well as risk of other gastrointestinal cancers.

So einkorn should not be viewed as a cure-all for all things wheat, but as something to consider for a carbohydrate indulgence. Yes, indeed: It is a carbohydrate, with 61 grams ("net") carbs per 4 oz (uncooked) serving.
Should anyone give it a try, please be sure to report back your experience, especially if you have a history of wheat intolerance. If you have a glucose meter, pre- and 1-hour post values are the ones to measure to gauge the blood sugar effects of consumption. Because pasta tends to cause long sustained blood sugar rises, another value at 2-4 hours might be interesting.

Noodles without the headaches

14. October 2010 William Davis (26)
If you are looking for a wheat-free noodle or pasta, shirataki noodles are worth a try.

Shirataki noodles are low-carbohydrate (less than 3 g per 8 oz package) and, of course, do not trigger all the unhealthy effects of wheat--no blood sugar/insulin provocation, no addictive brain effects (exorphins), no gluten-mediated inflammatory effects.

(I advise avoiding gluten-free pasta alternatives made with rice flour and other common gluten alternatives, since they trigger blood sugar, small LDL, and growth of visceral fat just like wheat.)

I made a stir-fry using the shirataki-tofu noodles, shown below. (Tofu is added to make the noodles more noodly in consistency, as opposed to the chewier non-tofu variety.) The noodles were a lot like the ramen I used to eat as a kid. They were filling and tasted great in the sesame oil, soy sauce, tofu, and vegetables I used.


The noodles are easy to use. Just drain liquid out of package. (The noodles come in water.) Rinse in collander 30 seconds, then boil for 3 minutes. Add to your stir-fry or other dish. Some manufacturers, such as House Foods, also have angel hair and fettucine style noodles.

You're fried

13. October 2010 William Davis (26)
If I could invent a food that illustrates nearly all of the shortcomings of the American diet, it would be French fries, the familiar fixture of fast food.

What we have come to view as French fries contain just about every one of the unhealthy ingredients that lead us down the path of obesity, diabetes, heart disease, high blood pressure, etc.

Let's take them one by one:

Potato starch--Potato starch exerts an effect on blood sugar similar to that of table sugar, only worse. (Glycemic index french fries 75; glycemic index sucrose 65.)

Advanced Glycation End-products (AGEs)--AGEs form when proteins and fats are subjected to high temperature cooking; the longer the high temperature, the more the food reaction creating AGEs proceeds. AGEs are the likely culprit in roasted and fried foods that made it appear that saturated fats were bad, when it was really AGEs all along. AGEs have been shown to block insulin's effects, increase blood sugar, cause endothelial dysfunction and high blood pressure.

Acrylamides--Acrylamides, like AGEs, are created through high-temperature heating. French fries are unusually rich in AGEs. Brewed coffee also contains a small quantity, while French fries contain 82-fold greater quantities, among the highest of all known sources of acrylamides.

Oxidized oils--The amount of oxidized oils will depend on what sort of oil was used for frying. As more restaurants are trying to get away from hydrogenated oils, many are turning back to polyunsaturates. Others are turning to commercial-grade oils that contain both hydrogenated and polyunsaturates. If oils are permitted to oxidize, then they will trigger oxidative phenomena in your body upon consumptions, e.g., LDL oxidation (Staprans 1994).

In other words, the innocent appearing French fry unavoidably triggers oxidation, all the phenomena triggered by high blood glucose (high insulin, glycation, visceral fat accumulation), along with the cascade of effects arising from AGEs and acrylamides.

Top your French fries with some ketchup made with high-fructose corn syrup that exagerrates AGE formation, visceral fat, and distorts postprandial (after-eating) effects.

Is it any wonder that we've lost control over diet?
Genetic vs. lifestyle small LDL

Genetic vs. lifestyle small LDL

19. February 2010 William Davis (59)
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.
Tags :

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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