Green coffee bean extract in AGF Factor I

Track Your Plaque's new and proprietary formulation, AGF Factor I, is designed to to support a program to achieve low levels of endogenous glycation.

Endogenous glycation, discussed at length in a recent Track Your Plaque Special Report, makes LDL particles (especially small LDL particles) more prone to oxidation and thereby more atherogenic, i.e., more likely to contribute to atherosclerotic plaque. Endogenous glycation also exerts unhealthy effects on long-lived proteins in the body, such as the proteins in the lenses of your eyes (cataracts), the lining of arteries (hypertension), and the cartilage cells of joints (brittle cartilage and arthritis).

Endogenous glycation is reduced by slashing carbohydrates in the diet, especially the most offensive carbohydrates of all, the amylopectin A of wheat, sucrose, high-fructose corn syrup and other fructose sources. Endogenous glycation can also be blocked by using blockers of the glycation reaction, such as benfotiamine (lipid-soluble thiamine), pyridoxal-5'-phosphate (a form of vitamin B6 with greater glycation blocking effect), and chlorogenic acid from green coffee beans, all components of AGF Factor I, which also contains Portulaca oleracea (Portusana), or purslane, for reduction of glucose.

Green coffee bean extract, and thereby chlorogenic acid, is receiving increased attention, most recently due to a study demonstrating substantial weight loss with 750-1050 mg green coffee bean extract, providing approximately 325-500 mg chlorogenic acid per day. Participants lost 15.4 pounds over 8 weeks at the higher dose (500 mg chlorogenic acid per day), while participants lost 8.8 pounds over 8 weeks at the lower dose (325 mg chlorogenic acid per day).

AGF Factor I was not formulated for weight loss but, taken twice or three times per day, does indeed mimic the dose of chlorogenic acid from green coffee bean extract used in the weight loss study. If you wish to take advantage of this application of chlorogenic acid/green coffee bean extract, while also maximizing protection from endogenous glycation, our AGF Factor I is one excellent choice to do so.

Lessons learned from the 2012 Low-carb Cruise

I just returned from Jimmy Moore's Low-carb Cruise, a 7-day excursion to Jamaica, Grand Cayman Island, and Cozumel aboard the Carnival Magic. During our 7 wonderful days, a number of authors and experts spoke, each offering their unique perspective on the low-carb world. The focus was the science, experience, and practical application of low-carbohydrate diets.

The event kicked off with a roast by Tom Naughton of Fat Head fame, who entertained with his insightful low-carb humor and predictions of my demise at the hands of Monsanto!

Among the most important lessons provided:

Dr. Andreas Eenfeldt of the Diet Doctor blog discussed how Sweden is leading the world as the nation with the most vigorous low-carbohydrate following, witnessing incredible weight loss and reversal of carbohydrate-related diseases way ahead of the U.S. experience. I spent several hours with Dr. Eenfeldt who, besides being an engaging speaker, is a new father and an all-around gentleman. At 6 ft, 7 inches, he also towered high above all of us.

Dr. Eric Westman of Duke University and author of The New Atkins for a New You, debunked low-carbohydrate myths, such as "low-carb diets are high-protein diets that make your kidneys explode."

Dr. John Briffa, creator of the popular blog, Dr. John Briffa: A Good Look at Good Health, and author of the wonderfully straightforward primer to low-carbohydrate eating, Escape the Diet Trap, stressed the importance of never allowing hunger to rule behavior. Dr. Briffa's serious writing tone conceals an incredible charm and wit that took me by surprise, having spent several thoroughly engaging hours over breakfast, lunch, and dinner with him over the week.

Fred Hahn, exercise expert, founder of Serious Strength and author of Slow Burn Fitness Revolution and Strong Kids, Healthy Kids, debunked a number of trendy exercise methods, boiling many of the purported benefits of exercise down to that of increased strength.

Dr. Chris Masterjohn of The Daily Lipid and supporter of the Weston A. Price Foundation program, provided a comprehensive overview of the data that fails to link saturated fat with heart disease. He also helped me understand the analytical techniques used in studies of advanced glycation end-products.

Denise Minger, brilliant young usurper of China Study dogma and blogger at Raw Foods SOS, proved an engaging speaker and a truly real person (since some critics of her analyses have actually questioned whether there was even such a person!). She also proved every bit as likable as she seems in her captivating blog discussions.

Dr. Jeff Volek, prolific researcher from University of Connecticut, author of over 200 studies validating low-carbohydrate diet effects, and author of the recently released book with Dr. Stephen Phinney, The Art and Science of Low Carbohydrate Living, debunked myths behind carbohydrate dependence and "loading" by athletes. He also talked about how assessing blood ketones may be the gold standard method to ensure low-grade ketosis on a long-term low-carb effort.

Over a bottle of wine, Jimmy Moore and I reminisced over how his modest start with no experience in blogging or media has now ballooned to an audience of over 100,000 readers/viewers.

All in all, Jimmy's Low-carb Cruise experience was worth every minute, with many wonderful lessons and memories!

Chili Sesame Crackers

Looking for something hot and crunchy?

These chili sesame crackers are perfect for dipping into hummus or salsa. As written, the recipe yields a moderately spicy cracker that you can modify readily by increasing or decreasing quantities of cayenne pepper and Tabasco sauce.

This recipe uses sesame seeds as the "flour." Either brown sesame seeds or the lighter version work, though the lighter seeds yield a slightly less bitter flavor with the spices.

For ease of baking, a shallow baking pan measuring 11 x 17 inches works best, as it allows the batter to fill the pan and spread to a cracker thickness. With a smaller pan, you may have to bake in two batches.

Makes approximately 30 chips

2 cups raw sesame seeds
1 cup shredded Parmesan cheese
2 tablespoons extra-virgin olive oil
1 tablespoon chili powder
½ teaspoon cayenne pepper
2 teaspoons onion powder
1 teaspoon garlic powder
1 teaspoon dry mustard
1 teaspoon sea salt
1 teaspoon Tabasco sauce
1¼ cups water

Preheat oven to 350º F.

In food chopper or food processor, grind 1¼ cups sesame seeds to fine meal. Remove and place in large bowl.

Place shredded Parmesan cheese in food chopper or food processor and pulse briefly until reduced to granular consistency. Add to sesame seed meal and mix. Stir in olive oil.

Add remaining (unground) sesame seeds, chili powder, cayenne pepper, onion and garlic powder, mustard, sea salt and mix thoroughly. Add Tabasco sauce and water and mix. Add additional water, if necessary, one tablespoon at a time, to obtain a consistency similar to pancake batter.

Pour mixture into baking pan and smooth to fill pan and obtain a thickness of a cracker. If too thick, remove some batter and re-smooth. Optionally, roll a clean cylindrical glass or bottle over top to smooth and yield a consistent thickness.

Bake for 30 minutes or until edges browned and center firm. If a dry, extra crunchy cracker is designed, bake an additional 10-15 minutes at 250 degrees F.

Remove and allow to cool. Cut with pizza cutter to desired size.

Opiate of the masses

Although it is a central premise of the whole Wheat Belly argument and the starting strategy in the New Track Your Plaque Diet, I fear that some people haven't fully gotten the message:

Modern wheat is an opiate.

And, of course, I don't mean that wheat is an opiate in the sense that you like it so much that you feel you are addicted. Wheat is truly addictive.

Wheat is addictive in the sense that it comes to dominate thoughts and behaviors. Wheat is addictive in the sense that, if you don't have any for several hours, you start to get nervous, foggy, tremulous, and start desperately seeking out another "hit" of crackers, bagels, or bread, even if it's the few stale 3-month old crackers at the bottom of the box. Wheat is addictive in the sense that there is a distinct withdrawal syndrome characterized by overwhelming fatigue, mental "fog," inability to exercise, even depression that lasts several days, occasionally several weeks. Wheat is addictive in the sense that the withdrawal process can be provoked by administering an opiate-blocking drug such as naloxone or naltrexone.

But the "high" of wheat is not like the high of heroine, morphine, or Oxycontin. This opiate, while it binds to the opiate receptors of the brain, doesn't make us high. It makes us hungry.

This is the effect exerted by gliadin, the protein in wheat that was inadvertently altered by geneticists in the 1970s during efforts to increase yield. Just a few shifts in amino acids and gliadin in modern high-yield, semi-dwarf wheat became a potent appetite stimulant.

Wheat stimulates appetite. Wheat stimulates calorie consumption: 440 more calories per day, 365 days per year, for every man, woman, and child. (440 calories per person per day is the average.) We experience this, sense the weight gain that is coming and we push our plate away, settle for smaller portions, increase exercise more and more . . . yet continue to gain, and gain, and gain. Ask your friends and neighbors who try to include more "healthy whole grains" in their diet. They exercise, eat a "well-balanced diet" . . . yet gained 10, 20, 30, 70 pounds over the past several years. Accuse your friends of drinking too much Coca Cola by the liter bottle, or being gluttonous at the all-you-can-eat buffet and you will likely receive a black eye. Many of these people are actually trying quite hard to control impulse, appetite, portion control, and weight, but are losing the battle with this appetite-stimulating opiate in wheat.

Ignorance of the gliadin effect of wheat is responsible for the idiocy that emits from the mouths of gastroenterologists like Dr. Peter Green of Columbia University who declares:

"We tell people we don't think a gluten-free diet is a very healthy diet . . . Gluten-free substitutes for food with gluten have added fat and sugar. Celiac patients often gain weight and their cholesterol levels go up. The bulk of the world is eating wheat. The bulk of people who are eating this are doing perfectly well unless they have celiac disease."

In the simple minded thinking of the gastroenterology and celiac world, if you don't have celiac disease, you should eat all the wheat you want . . . and never mind about the appetite-stimulating effects of gliadin, not to mention the intestinal disruption and leakiness generated by wheat lectins, or the high blood sugars and insulin of the amylopectin A of wheat, or the new allergies being generated by the new alpha amylases of modern wheat.

Jelly beans and ice cream

What if I said: "Eliminate all wheat from your diet and replace it with all the jelly beans and ice cream you want."

That would be stupid, wouldn't it? Eliminate one rotten thing in diet--modern high-yield, semi-dwarf wheat products that stimulate appetite (via gliadin), send blood sugar through the roof (via amylopectin A), and disrupt the normal intestinal barriers to foreign substances (via the lectin, wheat germ agglutinin)--and replace it with something else that has its own set of problems, in this case sugary foods. How about a few other stupid replacements: Replace your drunken, foul-mouthed binges with wife beating? Replace cigarette smoking with excessive bourbon?

Sugary carbohydrate-rich foods like jelly beans and ice cream are not good for us because:

1) High blood sugar causes endogenous glycation, i.e, glucose modification of long-lived proteins in the body. Glycate the proteins in the lenses of your eyes, you get cataracts. Glycate cartilage proteins in the cartilage of your hips and knees, you get brittle cartilage that erodes and causes arthritis. Glycate structural proteins in your arteries and you get hypertension (stiff arteries) and atherosclerosis. Small LDL particles--the #1 cause of heart disease in the U.S. today--are both triggered by blood sugar rises and are 8-fold more prone to glycation (and thereby oxidation).

2) High blood sugar is inevitably accompanied by high blood insulin. Repetitive surges in insulin lead to <em>insulin resistance</em>, i.e., muscles, liver, and fat cells unresponsive to insulin. This forces your poor tired pancreas to produce even more insulin, which causes even more insulin resistance, and round and round in a vicious cycle. This leads to visceral fat accumulation (Jelly Bean Belly!), which is highly inflammatory, further worsening insulin resistance via various inflammatory mediators like tumor necrosis factor.

3) Sugary foods, i.e., sucrose- or high-fructose corn syrup-sweetened, are sources of fructose, a truly very, very bad sugar that is metabolized via a completely separate pathway from glucose. Fructose is 10-fold more likely to induce glycation of proteins than glucose. It also provokes a (delayed) rise in insulin resistance, accumulation of triglycerides, marked increase in formation of small LDL particles, and delayed postprandial (after-eating) clearance of the lipoprotein byproducts of meals, all of which leads to diabetes, hypertension, and atherosclerosis.

I think we can all agree that replacing wheat with jelly beans and ice cream is not a good solution. And, no, we shouldn't have drunken binges, wife beating, smoking or bourbon to excess. So why does the "gluten-free" community advocate replacing wheat with products made with:

rice starch, tapioca starch, potato starch, and cornstarch?

These powdered starches are among the few foods that increase blood sugar (and thereby provoke glycation and insulin) higher than even the amylopectin A of wheat! For instance, two slices of whole wheat bread typically increase blood sugar in a slender, non-diabetic person to around 170 mg/dl. Two slices of gluten-free, multigrain bread will increase blood sugar typically to 180-190 mg/dl.

The fatal flaw in thinking surrounding gluten-free junk carbohydrates is this: If a food lacks some undesirable ingredient, then it must be good. This is the same fatally flawed thinking that led people to believe, for instance, that Snack Well low-fat cookies were healthy: because they lacked fat. Or processed foods made with hydrogenated oils were healthy because they lacked saturated fat.

So gluten-free foods made with junk carbohydrates are good because they lack gluten? No. Gluten-free foods made with rice starch, tapioca starch, potato starch, and cornstarch are destructive foods that NOBODY should be eating.

This is why the recipes for muffins, cupcakes, cookies, etc. in this blog, the Track Your Plaque website, and the Track Your Plaque Cookbook are wheat- and gluten-free and free of gluten-free junk carbohydrates. And put that bottle of Jim Beam down!

Diet by LDL

Conventional notions of heart healthy diets, such as that advocated by the American Heart Association, are largely based on observations of total and LDL cholesterol.

So, cut the saturated fat in the diet, cut the overall fat content, and replace them with polyunsaturated oils like safflower, corn, and vegetable oils and increase consumption of whole grains and total and LDL cholesterol show a modest downturn. Thus, diets like the American Heart Association Total Lifestyle Change approach advocate limiting total fat to no more 25 to 35% of calories and saturated fat to no more than 7% of calories.

Orange Cream Cookies

If you loved Creamsicles as a kid, you'll love these Orange Cream Cookies. (Sorry, no photo: We ate them up before I realized we hadn't taken the photo. And, worse, we did it twice!)

Ingredients:
2 cups almond meal
2 tablespoons coconut flour
1 teaspoon baking soda
½ teaspoon sea salt
¼ cup golden raisins
½ cup chopped pecans
Sweetener equivalent to 1 cup sugar
2 tablespoons finely-grated orange rind
1 large egg
2 tablespoons coconut oil, melted
½ cup whipping cream (or coconut milk)
1 tablespoon vanilla extract

Preheat oven to 350º F.

Combine almond meal, coconut flour, baking soda, salt, raisins, pecans, sweetener and orange zest in bowl and mix.

In separate bowl, whisk egg, then add coconut oil, whipping cream, vanilla extract and mix together. Pour wet mix into dry and blend by hand thoroughly.

Spoon onto parchment paper-lined baking pan (or oiled pan) and flatten with spoon to ½-¾ inch thickness. Bake for 20-25 minutes or until toothpick withdraws dry.

Why are heart attacks still happening?

I'm a cardiologist. I see patients with heart disease in the form of coronary artery disease every day.

These are people who have undergone bypass surgery, received one or more stents or undergone other forms of angioplasty, have survived heart attacks or sudden cardiac death, or have high heart scan scores. In short, I see patients every day who are at high-risk for heart attack and death from heart disease.

But I see virtually no heart attacks. And nobody is dying from heart disease. (I'm referring to the people who follow the strategies I advocate, not the guy who thinks that smoking a pack of cigarettes a day is still okay, or the woman who thinks the diet is unnecessary because she's slender.)

Two high-profile deaths from heart attacks occurred this week:

Davy Jones--The iconic singer from the 1960s pop group, the Monkees, suffered sudden cardiac death after a large heart attack, just hours after experiencing chest pain.

Andrew Breitbart--The conservative blogger and controversy-generating media personality suffered what was believed to be sudden cardiac death while walking.

It's a darn shame and it shouldn't happen. The tools to identify the potential for heart attack are available, inexpensive, and simple. The strategies to reduce, even eliminate, risk are likewise available, inexpensive, and cultivate overall health.

The followers of the Track Your Plaque program who

1) get a heart scan that yields a coronary calcium score (for long-term tracking purposes)
2) identify the causes such as small LDL particles, lipoprotein(a), vitamin D deficiency, and thyroid dysfunction
3) correct the causes

enjoy virtual elimination of risk.

My letter to the Wall Street Journal: It's NOT just about gluten

The Wall Street Journal carried this report of a new proposed classification of the various forms of gluten sensitivity: New Guide to Who Really Shouldn't Eat Gluten

This represents progress. Progress in understanding of wheat-related illnesses, as well as progress in spreading the word that there is a lot more to wheat-intolerance than celiac disease. But, as I mention in the letter, it falls desperately short on several crucial issues.

Ms. Beck--

Thank you for writing the wonderful article on gluten sensitivity.

I'd like to bring several issues to your attention, as they are often neglected
in discussions of "gluten sensitivity":

1) The gliadin protein of wheat has been modified by geneticists through their
work to increase yield. This work, performed mostly in the 1970s, yielded a form
of gliadin that is several amino acids different, but increased the
appetite-stimulating properties of wheat. Modern wheat, a high-yield, semi-dwarf
strain (not the 4 1/2-foot tall "amber waves of grain" everyone thinks of) is
now, in effect, an appetite-stimulant that increases calorie intake 400 calories
per day. This form of gliadin is also the likely explanation for the surge in
behavioral struggles in children with autism and ADHD.
2) The amylopectin A of wheat is the underlying explanation for why two slices
of whole wheat bread raise blood sugar higher than 6 teaspoons of table sugar or
many candy bars. It is unique and highly digestible by the enzyme amylase.
Incredibly, the high glycemic index of whole wheat is simply ignored, despite
being listed at the top of all tables of glycemic index.
3) The lectins of wheat may underlie the increase in multiple autoimmune and
inflammatory diseases in Americans, especially rheumatoid arthritis and
inflammatory bowel diseases (ulcerative colitis, Crohn's).

In other words, if someone is not gluten-sensitive, they may still remain
sensitive to the many non-gluten aspects of modern high-yield semi-dwarf wheat,
such as appetite-stimulation and mental "fog," joint pains in the hands, leg
edema, or the many rashes and skin disorders. This represents one of the most
important examples of the widespread unintended effects of modern agricultural
genetics and agribusiness.

William Davis, MD
Author: Wheat Belly: Lose the wheat, lose the weight and find your path back to health
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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