You've come a long way, baby

3. June 2011 William Davis (16)
In 1945, the room-sized ENIAC vacuum tube computer was first turned on, women began to smoke openly in public, and a US postal stamp cost three cents. And this was the US government's advice on healthy eating:



 

 

 

 

 

 

 

 

 

 

 

 

 

Green and yellow vegetables; oranges, tomatoes, grapefruit; potatoes and other vegetables and fruits; followed by milk and milk products; meat, poultry, fish, or eggs; bread, flour, and cereals, butter and fortified margarine.

In 2011, the computing power of the ENIAC can be performed by a microchip a few millimeters in width, smoking is now banned in public places, and a first class postage stamp has increased in price by 1466%. And this is the new USDA Food Plate for Americans:



 

 

 

 

 

Have we made any progress over the past 65 years? We certainly have in computing power and awareness of the adverse effects of smoking. But have US government agencies like the USDA kept up with nutritional advice? Compare the 2011 Food Plate with the dietary advice of 1945.

It looks to me like the USDA has not only failed to keep up with the evolution of nutritional thought, but has regressed to something close to advising Americans to go out and buy stocks on the eve of the 1929 depression. Most of us discuss issues like the genetic distortions introduced into wheat, corn, and soy; the dangers of fructose; exogenous glycoxidation and lipoxidation products yielded via high-temperature cooking; organic, free-range meats and the dangers of factory farming, etc. None of this, of course, fits the agenda of the USDA.

My advice: The USDA should stay out of the business of offering nutritional advice. They are very bad at it. They also have too many hidden motives to be a reliable source of unbiased information.

 

 

Fasting with green tea

1. June 2011 William Davis (34)
I've been playing around with brief (18-24 hour) fasts with the use of green tea. Of the several variations on fasting, such as juice "fasts,"  I've been most impressed with the green tea experience.

While the weight loss effects of daily green tea consumption are modest, there seems to be a specific satiety effect that has now been demonstrated in multiple studies, such as this and this. In other words, green tea, through an uncertain mechanism, reduces hunger. The effect is not just due to volume, since the effect cannot be reproduced with hot water alone.

I therefore wondered whether green tea might be a useful beverage to consume during a fast, as it might take the "edge" off of hunger. While hunger during a fast in the wheat-free is far less than wheat-consuming humans, there is indeed an occasional twinge of hunger felt.

So I tried it, brewing a fresh 6-8 oz cup evert two hours or so. I brewed a pot in the morning while at home, followed by brewing single cups using my tea infuser at the office. Whenever I began to experience a hunger pang, I brewed another cup and sipped it. I was pleasantly surprised that hunger was considerably reduced. I sailed through my last 18 hours, for instance, effortlessly. The process was actually quite pleasant.

I brew loose Chinese bancha, sencha, and chunmee teas and Japanese gyokuro tea. Gyokuro is my favorite, but also the most expensive. Bancha is more affordable and I've used that most frequently.

If anyone else gives this a try, please report back your experience.

Dreamfields pasta is wheat

28. May 2011 William Davis (11)
An active question on the blogosphere and elsewhere is whether Dreamfields pasta is truly low-carb. Dr. Andreas Eenfeldt of Diet Doctor detailed his high blood glucose experience with it. Jimmy Moore of Livin' La Vida Low Carb had a similar experience, observing virtually no difference when compared to conventional pasta.

The Dreamfields people make the claim that "Dreamfields' patent-pending recipe and manufacturing process protects all but 5 grams of the carbohydrates per serving from being digested and therefore lessens post-meal blood glucose rise as compared to traditional pasta." They call the modified carbohydrates "protected" carbs.



In other words, they are making the claim that they've somehow modified the amylopectin A and amylose molecules in durum wheat flour to inhibit conversion to glucose.

I'd like to add something to the conversation: Dreamfields pasta is wheat. It is a graphic demonstration that, no matter how you cut it, press it, sauce it up, "protect" it, it's all the same thing: wheat. (It reminds me of a bad girlfriend I had in my 20s: She'd put on makeup, a pretty dress, I'd take her out someplace nice . . . She was still an annoying person who whined about everything.)

Wheat is more than a carbohydrate. It is also a collection of over 1000 proteins, including gliadins, glutens, and glutenins. Gliadins, for instance, are degraded to polypeptide exorphins that underlie the addictive potential of wheat, as well as its withdrawal phenomenon on halting consumption. Gliadin-derived exorphins are also the triggers of auditory hallucinations and paranoid delusions in schizophrenia, as well as behavioral outbursts in children with ADHD and autism.

Wheat is a source of lectins that have the curious effect of "unlocking" the proteins of the intestinal lining, the oddly-named "zonulin" proteins, that protect you from ingested foreign molecules. Ingest wheat lectins and all manner of foreign molecules gain entry into your bloodstream. Cholera works by a similar mechanism. (How about a love story: Bread in the time of cholera?)

Glutens, of course, are responsible for triggering celiac disease, the devastating small intestinal disease that now afflicts 3 million Americans, although 2.7 million don't even know it. Glutens are also responsible for neurologic conditions like cerebellar ataxia, peripheral neuropathy, and dementia ("gluten encephalopathy") and the skin condition, dermatitis herpetiformis.

Then there are the conditions for which the active wheat components have not been identified, including acid reflux, irritable bowel syndrome, asthma (excepting "bakers' asthma), rheumatoid arthritis, edema and fluid retention, and a long list of skin conditions from alopecia to gangrene.

My point: Yeah, Dreamfields pastas, from these instructive experiences, acts a lot like conventional durum wheat pasta. But, even if Dreamfields or somebody else perfects the low-carb aspect of it, it's still wheat. Modern wheat is the genetically tarted-up version of Triticum aestivum, the product of genetic shenanigans from the 1960s and 1970s.

Bet you can't fast

26. May 2011 William Davis (28)
People who continue to consume the world's most destructive grain, i.e., wheat, can rarely endure fasting--not eating for an extended period--except by mustering up monumental willpower. That's because wheat is a powerful appetite stimulant through its 2-hour cycle of exaggerated glycemia followed by a glucose low, along with its addictive exorphin effect. Wheat elimination is therefore an important first step towards allowing you to consider fasting.

Why fast? I regard fasting as among the most underappreciated and underutilized strategies for health.

In its purest form, fasting means eating nothing while maintaining hydration with water alone. (Inadequate hydration is the most common reason for failing, often experienced as nausea or lightheadedness.) You can fast for as briefly as 15 hours or as long as several weeks (though I tell people that any more than 5 days and supervision is required, as electrolyte distortions like dangerously low magnesium levels can develop).

Among its many physiological benefits, fasting can:

  • Reduce blood pressure. The blood pressure reducing effect can be so substantial that I usually have people hold some blood pressure medications, especially ACE inhibitors and ARB agents, during the fast since blood pressure will drop to normal even without the drugs. (A fascinating phenomenon all by itself.)

  • Reduce visceral fat, i.e., the fat that releases inflammatory mediators and generates resistance to insulin.

  • Reduce inflammatory measures

  • Reduce liver output of VLDL that cascades into reduced small LDL, improved HDL "architecture," and improved insulin responsiveness. (The opposite of fasting is "grazing," the ridiculous strategy advocated by many dietitians to control weight. Grazing, or eating small meals every two hours, is incredibly destructive for the opposite reason: flagrant provocation of VLDL production.)

  • Accelerate weight loss. One pound per day is typical.


Beyond this, fasting also achieves unique subjective benefits, including reduced appetite upon resumption of eating. You will find that as single boiled egg or a few slices of cucumber, for example, rapidly generate a feeling of fullness and satisfaction. Most people also experience greater appreciation of food--the sensory experience of eating is heightened and your sense of texture, flavors, sweetness, sourness, etc. are magnified.

After decades of the sense-deadening effects of processed foods--over-sugared, over-salted, reheated, dehydrated then just-add-water foods--fasting reawakens your appreciation for simple, real food. On breaking one of my fasts, I had a slice of green pepper. Despite its simplicity, it was a veritable feast of flavors and textures. Just a few more bites and I was full and satisfied.

Once you've fasted, I believe that you will see why it is often practiced as part of religious ritual. It has an almost spiritual effect.

More on fasting to come . . .

Total cholesterol 220

24. May 2011 William Davis (17)
Talking about total cholesterol is like wearing a tie-dyed t-shirt with the peace sign emblazoned on the front: So totally 60s and out of date.

But talk of total cholesterol somehow keeps on coming back. After I spend 45 minutes discussing a patient's lipoprotein patterns, for instance, they'll asking something like, "But what's my total cholesterol?"

To help put this ridiculous notion of total cholesterol to rest, let me paint several pictures of what total cholesterol can tell you. Let's start with a theoretical, but very common, total cholesterol value of 220 mg/dl. Recall that:

LDL cholesterol = total cholesterol - HDL cholesterol - triglycerides/5

Note that LDL cholesterol is nearly always a calculated value. (Yes, your doctor has been treating a calculated, what I call "fictitious," value.)

Rearranging the equation:

Total cholesterol = LDL cholesterol + HDL cholesterol + Triglycerides/5

This relationship means that a great many variations are possible, all under total cholesterol = 220 mg/dl. For example:

LDL 95 mg/dl + HDL 105 mg/dl + Triglycerides 100 mg/dl

(a relatively low-risk pattern for heart disease)

LDL 160 mg/dl + HDL 50 mg/dl + Triglycerides 50 mg/dl

(an indeterminate risk pattern, potentially moderate risk)

LDL 120 mg/dl + HDL 30 mg/dl + Triglycerides 350 mg/dl

(a potentially high-risk pattern)

LDL 60 mg/dl + HDL 25 mg/dl + Triglycerides 675 mg/dl

(an indeterminate risk pattern)

 

That's just a sample of the incredible variation of patterns that can all fall under this simple observation, total cholesterol 220 mg/dl.

Total cholesterol is an outdated concept, one ready long ago for the junk heap of outdated ideas. It's time to throw total cholesterol out in the trash along with beliefs like high-fat intake causes diabetes, whole grains are healthy, and the tooth fairy will leave you money when you leave your molars under the pillow.

Scientists are freakin' liars

14. May 2011 William Davis (3)
So says Tom Naughton, referring to the frequent misinterpretations or misrepresentations of data that characterize much medical research. Dr. Andreas Eenfeldt posted Tom Naughton's recent wonderfully engaging and hilarious talk from Jimmy Moore's Low-Carb Cruise on his Diet Doctor blog.

Comedian and blogger Tom Naughton, also the filmmaker of the movie Fat Head, has brought humor and personality into the low-carb movement. I told my wife to watch it and I could hear her laughing from 30 feet away while watching her laptop.

Dr. Eenfeldt is a sensation of sorts himself, making a big low-carb splash in Sweden. While I missed the cruise this year (due to time pressures), it's clear that Eenfeldt and Naughton have contributed substantially to helping people understand the nonsense that passes as dietary advice in the U.S. and the world.

I watched Naughton's talk while eating my three eggs scrambled with ricotta cheese. I almost spit my eggs out at the computer screen I was laughing so hard.

 

Tell me your wheat elimination story and receive a copy of my new book, Wheat Belly

6. May 2011 William Davis (68)
I'm looking for interesting wheat-free experiences.

For the past year, I have been writing my new book, Wheat Belly . After many, many late nights and soccer games missed, it's now finished. The book will be out in fall, 2011, to be published by Rodale, the Prevention Magazine people.

Wheat Belly will provide, in excruciating detail, the discussion of how wheat was transformed from innocent wild grass to incredible genetically-altered Frankengrain and why it has become such a health nuisance.

I am looking for interesting stories of wheat elimination for the online and special editions of the book. If you have an interesting tale of wheat-elimination successes, woes, or drama, I'd like to hear about it. Even better, if you would agree to be interviewed by phone (not for live use, just for comments and detail), the editors at Rodale will help tell your story.

If we use your story, I will have a free copy of the new Wheat Belly sent to you when it becomes available.

Please post your story in the comments here. I will then need to obtain your contact info, which we will do privately.

 

Real men don't eat carbs

27. April 2011 William Davis (0)
Real men don't eat carbs. At least they don't eat them without eventually paying the price.

How do carbohydrates, especially those contained in "healthy whole grains," impair maleness? Several ways:

--Consume carbohydrates, especially the exceptional glucose-increasing amylopectin A from wheat, and visceral fat grows. Visceral fat increases estrogen levels; estrogen, in effect, opposes the masculinizing effects of testosterone. Overweight males typically have low testosterone and high estrogen, a cause for depression, emotionality, weight gain, and low libido.

--Sugar-provoking carbohydrates like wheat cause visceral fat to accumulate which, in turn, triggers prolactin to be released. Increased prolactin in a male causes growth of breasts: "man boobs,""man cans," "moobs," etc. This is why male breast reduction surgery is booming at double-digit growth rates. In cities like LA, you can see billboards advertising male breast reduction surgery.

--Carbohydrates increase visceral fat that sets the stage for postprandial abnormalities, i.e., markedly increased and persistent lipoproteins, like chylomicron remnants and VLDL particles, that impair endothelial function literally within minutes to hours of ingestion. Impaired endothelial function underlies erectile dysfunction. This is why Internet spammers so enthusiastically send you offers for discounted Viagra.

--Carbohydrates increase blood sugar which provokes the process of glycation, glucose modification of proteins, that also contributes to endothelial dysfunction followed by erectile dysfunction.

Real men therefore avoid carbs.

Real men don't eat carbs

27. April 2011 William Davis (57)
Real men don't eat carbs. At least they don't eat them without eventually paying the price.

How do carbohydrates, especially those contained in "healthy whole grains," impair maleness? Several ways:

--Consume carbohydrates, especially the exceptional glucose-increasing amylopectin A from wheat, and visceral fat grows. Visceral fat increases estrogen; estrogen, in effect, opposes the masculinizing effects of testosterone. Overweight males typically have low testosterone, high estrogen, a cause for depressions, emotionality, and weight gain.

--Consume carbohydrates like wheat and visceral fat causes prolactin to be released. Increased prolactin in a male causes growth of breasts: "man boobs,""man cans," "moobs," etc. This is why male breast reduction surgery is booming at double-digit growth rates. In cities like LA, you can see billboards advertising male breast reduction surgery.

--Carbohydrates increase visceral fat that sets the stage for postprandial abnormalities, i.e., markedly increased and prolonged lipoproteins like chylomicron remnants and VLDL particles that impair endothelial function. Impaired endothelial function underlies erectile dysfunction. Eat a bagel, become impotent.

Fatal underdose

27. April 2008 William Davis (8)
Since vitamin D has been the topic of a fair amount of media coverage, I've received many questions about this fascinating "nutrient." A day doesn't go by without several nurses, friends, even fellow physicians stopping me to ask about vitamin D.

When I inform them that the average dose for females in this region (upper Midwest) is 4000-5000 units per day, 5000-6000 units per day for males, they are all surprised. "Then why did they say just take your multivitamin every day, or just drink your milk on the news?"

Many people are even more surprised, sometimes completely turned off, when they hear that, to be truly confident of adequate vitamin D dosing, a blood level of 25(OH) vitamin D3 needs to be checked. Now we're talking real hassle!

But there is no other way to do it. In order to obtain the full potential benefits of vitamin D, such as reduction in blood sugar and sensitization to insulin, reduction in cancer risk (especially prostate, colon, and breast), reductions in blood pressure, increased bone density, not to mention markedly increasing the likelihood of stopping or reducing your heart scan score, then achieving a desirable blood level of 25(OH) vitamin D is necessary.

Checking a blood level of vitamin D is no more difficult than having a cholesterol test, unless, of course, your doctor balks at the idea. (Time for a new doctor if that occurs.)

All too often, someone will be convinced they are taking a sufficient dose of vitamin D of, say 2000 units per day, only to discover that their blood level of 25(OH) vitamin D is something like 17 ng/ml--severe deficiency, sufficient to leave them exposed to all the undesirable consequences of vitamin D deficiency. Even though 2000 units per day represents 500% of the Institute of Medicine's recommended Adequate Intake for adults, to those familiar with the Track Your Plaque program it likely sounds like a child's dose.

Many variables enter into the equation in your body that determines your need for vitamin D: body size (heavier or larger people need more, with obese people often requiring enormous doses); sex (men need more than women); age (aging results in dramatic loss of ability to activate vitamin D in the skin); race; skin color (darker skinned people require more). Trying to guess your need is a fool's game. It's also a game that can seriously compromise your health and your hopes of ever stopping or reducing your heart scan score.



The message is clear: You cannot guess what your vitamin D need is. You cannot properly judge your vitamin D requirement by your age, body size, sex, or any other characteristic. Having a tan or a lack of a tan is a lousy indicator, as well. A simple blood level of 25(OH) vitamin D is an absolute necessity to gauge your vitamin D status, both before starting and while on your supplement.

Members of Track Your Plaque: Watch for the 30-some page booklet, The Track Your Plaque Complete Handbook on Vitamin D and Heart Health, which will be released in the next day or two.


Copyright 2008 William Davis, MD

Is direct-to-consumer drug marketing a failure?

23. April 2008 William Davis (4)
According to the poll just completed by 80 participants on The Heart Scan Blog, 50% of respondents said they were less likely to take a drug after viewing an advertisement for it. A whopping 3 (4%) said that they would be more likely to take the drug after viewing an advertisement.

I find that interesting. If half the people responding are less likely to become customers of a drug company, then how does the drug industry justify running around-the-clock, every-few-minute ads? Spending by the drug industry for direct-to-consumer (DTC) advertising has ballooned over the past few years, and is now well over $30 billion dollars per year.

Unfortunately, despite the views of the highly-educated, curious, think-for-yourself, health information-seeking sorts of people who read this blog, drug companies still come out on top by DTC advertising. Estimates vary, with a 2006 U.S. Government Accountability Office study reporting that, for every $1 DTC advertising, sales are increased by $2.20. A 2000 Harvard study showed a higher return of $4.40 for every advertising dollar spent.

I'm sure the drug companies themselves have a very tight accounting handle on their own set of figures. We may not be terribly fond of these people and their often suspect tactics, but they're not stupid. They are certainly not stupid when it comes to making money.

Interestingly, 80% of the funds spent on DTC advertising focus on the 20 or so most popular drugs, all of which are used for treatment of chronic conditions like high cholesterol and high blood pressure, markets that are large and long-term. It pays very little to advertise drugs that may serve small markets for a short period. The implicit message is that this is not at all about informing the public. It is about advertising to grow revenues and profits--pure and simple.

It makes me wonder what the results of our poll would have been had we conducted it in 2000 before many people hadn't yet been brought to the brink of vomiting from the endless onslaught of commercial after commercial, complete with smarmy spokespeople (a la Lipitor's Dr. Robert Jarvik). What will it show in two years? Will the broader public join the more informed people who read this blog and become increasingly inured to the hard sell tactics?

For further discussion of this topic, click here for a reprint of an August, 2007 New England Journal of Medicine study, A Decade of Direct-to-Consumer Advertising of Prescription Drugs provides background, along with commentary on the impact of DTC drug marketing since the FDA allowed it 10 years ago. (Because it is a study and not an editorial, the editors fall short of making any recommendations for improvement or calling for a moratorium.)


Copyright 2008 William Davis, MD

Cheerios and heart health

22. April 2008 William Davis (11)


Anna responded to the Heart Scan Blog post, Can you say "sugar"? with the following wonderfully telling comment:

A measured bowl of Cheerios and a bit of milk (whole, because it's what I had), equal to 75 grams of carbohydrate, gave me the highest ever blood glucose reading from a food (not counting glucose solution from a Glucose Tolerance Test). I was attempting a "homemade" version of a 3 hr GTT before going to my doctor with my concerns about my BG.

My BG started to rise very fast within 15 minutes after eating the cereal, peaked at about 250 mg/dL at 45 minutes, then slowly dropped. By about 60-75 minutes, I experienced strong hunger and carb cravings as the BG began to slowly drop, and by about 2.5 hours after eating, my BG had suddenly dropped quite low (in the low 70s) and I had developed a nasty hypoglycemic feeling (shaky, irritable, craving sugary foods, headache, etc.).

It's hard for me to see "heart healthy" Cheerios (or any other highly processed breakfast cereal) as anything other than a bowl of pre-digested sugar that contributes to roller coaster blood glucose and insulin levels, which a great way to start anyone's day. Certainly, I don't do well with Cheerios because I clearly have a damaged glucose regulatory system (probably a diminished or absent first phase insulin response, but I can't imagine that it is doing any good for people with healthy glucose regulation, either.

I banned prepared cold cereals from our house. If my 9 yr old son gets cereal at all at home, it's whole groats (not even rolled or steel cut because those aren't truly "whole grain" anymore), soaked overnight in some water and a tsp of plain yogurt (soaking neutralizes phytates and reduces cooking time), then cooked about 8-10 minutes (water added as necessary). Sometimes I add a bit of quinoa or almond meal prior to soaking to boost the protein content a bit. I garnish with a pat of butter, some heavy cream, and a dusting of cinnamon. If I'm feeling *really* indulgent, I drizzle about 1 tsp of Grade B maple syrup on top (Grade B is stronger in flavor and so less can be used). I don't eat this cereal myself, and truthfully, I'd rather my son not, either, but he sometimes wants cereal. It's the least damaging compromise I can come up with that we can both live with.


I have also seen diabetic effects from Cheerios: rises in blood sugar, exagerration of small LDL, drops in HDL, rises in triglycerides. Yes, it may reduce LDL a small quantity, but so what?

The Cheerios "heart healthy" claim is based on a piece of research apparently performed by Dr. Donald Hunninghake at the University of Minnesota and reported in 1998:

A study conducted at the University of Minnesota Heart Disease Prevention Clinic and published as "Cholesterol-Lowering Benefits of a Whole Grain Oat Ready-to-Eat Cereal" in the May issue of the Nutrition in Clinical Care journal in 1998, showed that people can lower their blood cholesterol by an average of 3.8% over six weeks by enjoying 3 cups of cold cereal made with 100% whole grain oats everyday as part of the meals and snacks in a healthy lower-fat diet.

(Unfortunately, I could not locate the actual publication. It doesn't mean it doesn't exist; I just couldn't locate it. Perhaps it's in a small journal not entered into the online publication database.)

The purported effects of Cheerios should not be confused with that of actual, intact oat bran, as suggested by studies such as those of Brenda Davy et al, High-fiber oat cereal compared with wheat cereal consumption favorably alters LDL-cholesterol subclass and particle numbers in middle-aged and older men, in which significant reductions in LDL particle number and small LDL (NMR) were obtained. (This study was also supported by Quaker Oats.) Several studies have shown that oat bran does indeed reduce LDL cholesterol, sometimes as much as 30-50 mg/dl. Cheerios can not even come close to this.

If Cheerios were nothing more than finely pulverized oats, then perhaps it wouldn't be so bad. But add corn starch and sugar, and you have ingredients that have potential to distort LDL particle size and yield blood sugar-escalating effects like those described by Anna.

The gravity of perpetuating these myths is brought home by a testimonial posted on the website for Cheerios:

“I had unexpected open heart surgery a year ago. As I adopted heart health habits during my recovery, I realized that I should have been eating the Cheerios cereal I carried around in a plastic baggie so many years for my kids!”

Beverly
Scotch Plains, NJ


It makes me shudder.


Copyright 2008 William Davis, MD

The IF Life: Intermittent fasting

21. April 2008 William Davis (4)
There's a wonderful blog called The IF Life: Intermittent Fasting and Instant Freedom. It is written by personal trainer (and apparently former corporate bigshot), Mike O'Donnell.

Mike has a great take on brief, intermittent fasting that I found helpful and I believe you will also.






Intermitent Fasting 101: How to Start, Part I

The biggest question people have is how to effectively use IF (intermittent fasting) to achieve their goals and maximum results. These results and goals can vary by each person with fat loss, muscle gain, better health, improved performance in your sport of choice and more. With that comes the individuality of what is a person’s insulin resistance, current body composition (bodyfat%), daily lifestyle, eating habits, macronutrient ratios (carbs/protein/fat), type of exercise program, frequency and volume of training, recovery demands, and so forth. You are unlikely to find 2 people with the same set of parameters and same exact responses to an IF protocol. What does this mean? Well just that we need to start with a basic IF program, and then learn how to monitor results and adjust as we go. Even down the road things will change as you will improve health, lower insulin resistance and maybe change performance and recovery needs. So nothing is ever just one set way. Life is dynamic (always changing and evolving) and so should be the way we see our own journey for health and fitness.

What is IF?

For those that may not be familiar to the term, intermittent fasting is just taking times of fast (no food) and working them into your lifestyle. This can be either daily or a couple times a week (will get into that more below). Benefits include improving insulin resistance (which you will hear alot about as being the #1 key marker in so many health factors including weight loss, muscle gain, performance, recovery, anti-ageing and disease prevention) and giving the body a chance to do some internal cleaning (or housework), which can lead to improved immune function and overall health. If you want to see studies of all the benefits of IF/CR, please the resources page.


How do I begin to IF?

Is there only one set way in which to do IF? No. I could easily come up with 10 different IF protocols based on 10 people’s individual’s needs, lifestyle, exercise, goal, macronutrient ratios, and so forth. We will keep it simple and give the 2 most frequent and basic options.

Daily Fasting: Typically done every day and only giving the person a smaller eating window in which to get their calories. (for example, a 18hr daily fast would mean someone would only eat every day between the hours of Noon and 6pm). You will see varying times from 15-19 hours for daily fasting.
Fasting 1-3x a week: This could also be called alternate day fasting/calorie restriction (for those doing it every other day). This is just fasting of usually longer periods 18-24 hours but only 1-3x a week. Many variations to play with here.
“But which one is better and how to I do it now if I want…….”. Whoa, slow down. I know many have questions but let’s still try to keep this simple for now and expand into more specifics later. So far many people have experimented with both types of IF and have seen great results. But you also have to take into account all the other variables such as what is the person eating in that window? Is is junk food? Is it low carb? How many times a week are they doing it? Are they overweight and wanting just fat loss? Are they lower bodyfat but looking for improved performance and health? How many times a week are they exercising? What kind are they doing and what intensity? The list can go on and on, but let’s start to analyze the 2 types of IF and let you decide which one best suits your lifestyle.

Daily Fasting (15-19 hours):

The Advantages are:

--simple eating strategies for every day
--even people that may not eat 100% clean foods can see weight loss due to the smaller window and lower calorie total per day


The Disadvantages are:

--Can possibly lower metabolism if calories are too low for too long (not what you want if your #1 goal is weight loss)
--Not getting enough food in the smaller window may also lead to muscle loss for more active people (not good)
Fasting 1-3x a week:


The advantages are:

--Allows a person to make sure they are getting enough calories on the non-fasting days, and then just keeps to a simple small feed window (if any) on the IF days.
--Simple thinking for people who do not have experience in how to eat clean to eat one day, and then eat in a smaller window the following day (alternate day fasting/CR). This can achieve fat loss for people who are mostly overweight and may not be too active. (of course don’t get me wrong, that eating healthy is our main goal but this can be a good step for some people to start their weight loss jounrey and learn how to make better choices as they go)


Disadvantages:

--Doesn’t force a person to make better choices with their food (as one could probably eat junk one day, and then fast the next and still lose weight). Not something we want long term because this is not going to improve your other health markers (diseases prevention, insulin resistance) like a good IF program on healthy foods.


Again I can’t say it enough, as there are so many variables to play with in an IF program. Some people may say “well it didn’t work for me” or “I didn’t gain any muscle”. Well unless I know everything about what you do for exercise daily, your total calories, when you eat and your macronutrient ratios (protein/carbs/fats), I can’t even begin to help. IF is a simple tool to start with, but you have to take full responsibility for your own health and progress and learn when it is not working and when to change things up! Like I said, if it is NOT working then stop IF and rethink your attack plan (or get a professional to coach you on it).

So to sum up, here are some examples of what you can play with:

Daily Fasting of 15-19 hours. I would highly suggest that if you do this make sure you are recovering from your exercise and start only Mon-Fri and give yourself the weekends to eat all day (hopefully with healthy choices of course)


Fast 1-2x a week to start if you have never done any fasting or do not know how to eat healthy and control your macronutrients. Start with 1-2 days a week with fasts of 18-20 hours (I wouldn’t start with 24 hr fasts to begin as most people can not handle the hunger cravings and in turn will just end up eating all the wrong foods when they do eat) and say eat only from say 1pm-6pm for example. Drink lots of water (add lemon, your liver will appreciate it! and it will help with the hunger). For example, fast Wed and Sun (or whatever days fit into your schedule)

Or you can do a mixed approach and fast every other day for a small eating window. For example eat all day Mon, only 12-6pm on Tues, all day Wed, 12-6pm on Thurs, etc. Start with bigger eating windows and make them smaller as you get used to fasting. This approach may work for people who have alot of weight to lose and can not (I should really say “will not” as everything is a choice!) eat 100% healthy for the moment. This approach may not work for more advanced people who have a high activity level unless you are getting a ton of health calories in that fasting window.
“So What Do I Eat on the Fasting Days?”

That’s the best part, you should be able to eat unlimited healthy foods (healthy proteins, fats, veggies, fruit, nuts…see Paleo Diet in the resources page). If you are eating more processed foods, breads and other high calorie intakes then you may have to monitor and control portions. Please know this is NOT about chronic calorie restriction or starving yourself. When I do weeks of eating 1-7pm, I am eating a ton of protein and veggies (complex carbs pwo also). I am hardly starving myself. I am not taking in 4000 cal a day however, so my daily average of say 2200-2500 cal is still low compared to the alternative. If you want to lose weight of course you will need a calorie deficit to pull the “stored energy” out of fat cells. That is the advantage to eating “Paleo”, you can’t over eat on protein, healthy fats, fruits (in moderation) and veggies. If you are making bad choices or starving yourself on IF, you may lose the effectiveness or slow progress. All goes back to the fact that if it is not working, then change something up! (there is always something that can be changed…and food choices is the #1 place to start!) I don’t count calories, and by eating natural foods that have been around for 100s of years….I don’t need to! (eating healthy natural foods will not only help you lose weight but also improve your health and lower your risks of diseases….so eating for health should always be the #1 goal in any program)

Hopefully this will give a good overview while trying to keep it simple. Remember it’s your journey to take, measure progress and adjust things that are not working. Start with one approach, and modify it. Who knows, your approach may change every couple months and that is ok. Life is always changing and so should your approach to health and fitness (as the body always responds better to change than sticking with the same eating/exercise approach for a long period of time).

Can you say "sugar"?

20. April 2008 William Davis (11)
All of these products bear the American Heart Association Check Mark of approval emblem, signifying that they are "heart healthy":


Kellogg's Frosted Mini-Wheats cereal

Ingredients:WHOLE GRAIN WHEAT, SUGAR, STRAWBERRY FLAVORED CRUNCHLETS (SUGAR, CORN CEREAL, CORN SYRUP, MODIFIED CORN STARCH, PARTIALLY HYDROGENATED COTTONSEED AND/OR SOYBEAN OIL, CITRIC ACID, GLYCERIN, NATURAL AND ARTIFICIAL FLAVOR, RED #40, BLUE #2), NATURAL AND ARTIFICIAL STRAWBERRY AND CREME FLAVOR, SORBITOL, GELATIN, REDUCED IRON, NIACINAMIDE, ZINC OXIDE, RED #40, PYRIDOXINE HYDROCHLORIDE (VITAMIN B6), RIBOFLAVIN (VITAMIN B2), THIAMIN HYDROCHLORIDE (VITAMIN B1), FOLIC ACID, BLUE #1, AND VITAMIN B12. TO MAINTAIN QUALITY, BHT HAS BEEN ADDED TO THE PACKAGING.










Orville Redenbacher popcorns









Dora the Explorer Cereal
























Cheerios
























The following requirements must be met to gain approval of the Check Mark program:

1) total fat 3.0 grams or less per serving

2) saturated fat 1.0 gram or less per serving

3) 20 grams or less cholesterol per serving

4) 480 mg or less sodium per serving

5) "Jelly Bean Rule": 10% of the Daily Value of 6 nutrients (e.g., fiber, vitamins A and C, etc.) must also be contained in each serving.


Had the Check Mark program focused on genuine nutrition and rated products by:

1) Healthy oil content

2) Sugar content or sugar-equivalents, i.e., glycemic index or load

3) Impact on HDL, small LDL, triglycerides

none of these products would have made the list, not even close.

Warfarin is scary stuff

19. April 2008 William Davis (16)
Gilbert is a 58-year old high school science teacher.

When I first met Gil, he'd been having bouts of atrial fibrillation and had required various medications to suppress recurrences of the rhythm. However, because his rhythm proved somewhat difficult to control, his electrophysiologist (heart rhythm specialist) prescribed warfarin to reduce the risk of stroke. With atrial fibrillation, because of blood stagnation (in the left atrial appendage) in the heart, there is a stroke risk of approximately 8% per year. Warfarin reduces this risk substantially, to about 2%.

I met Gil because he had a cholesterol disorder. In my practice, the first step in gauging the implications of a lipid or lipoprotein disorder is to obtain a heart scan. If the heart scan score is zero, great. It means that we have plenty of time to treat the disorder since risk for cardiovascular events is near zero also; it means less intensive efforts less intensive efforts are necessary. But if the heart scan score is, say, 1200, then an aggressive approach in short order is required, since the risk for heart attack may as high as 20-25% per year, even in the absence of symptoms.

Gil's heart scan score: 787--high and posing a risk for heart attack of about 5-10% per year without preventive efforts. Gil did indeed prove to have a complex lipoprotein disorder, as well as high blood pressure, vitamin D deficiency, and several other potential contributors to coronary plaque.

Gil did just about everything right: He exercised, followed the recommended diet, achieved better than the Track Your Plaque 60-60-60, lost 18 lbs of abdominal fat.

Gil's rhythm stabilized for several months, only to have atrial fibrillation break through again. So Gil's electrophysiologist re-prescribed warfarin.

18 months later, Gil's 2nd heart scan score: 1410--a near doubling. Unsettling to Gil and to us, to say the least.

How can this happen in the face of perfect lipids/lipoproteins, correction of hidden causes like lipoprotein(a) and inflammation, along with a vigorous lifestyle effort?

I fear that the culprit might be warfarin.

Warfarin, better known by its brand name, Coumadin, may have some effects that intersect with the Track Your Plaque mission of reducing coronary plaque.

It is no secret that, beyond the obvious risk of bleeding from blood thinning, warfarin also may:

--Accelerate aortic valve calcification
--Accelerate calcification of the framework of the mitral valve (the mitral "anulus")
--Accelerate osteoporosis
--Induce an artificial situation of vitamins K1 and K2 deficiency.

The vitamin K1 deficiency is the route by which blood thinning is achieved. However, the K2 deficiency may have undesirable consequences, among which are the above list of various pathologic calcifications.

I therefore wonder if warfarin dramatically accelerated the coronary calcium that we track to gauge the progression of coronary atherosclerosis. One experience is hardly sufficient reason to sound the alarm. It is also difficult to pinpoint the cause of the explosive growth in Gil's coronary calcium specifically on warfarin.

That all said, I am quite certain it was the warfarin.

Unfortunately, some people are unavoidably committed to warfarin, such as those with specific genetic blood clotting disorders, prosthetic valves, prior deep vein thromboses and pulmonary emboli, etc.--serious reasons. Until an alternative emerges, warfarin remains a necessity for some people. (No, nattokinase is NOT an alternative, at least not one that would permit survival.)

My personal policy is that warfarin be used only when absolutely necessary and the gains markedly outweight the risks--including that of possible accelerated calcification of multiple sites.

Whether we will be able to get Gil off warfarin and potentially gain control over his coronary disease/plaque/calcium remains to be seen. I sure hope so.




Caraballo PJ, Heit JA, Atkinson EJ et al. Long-term use of oral anticoagulants and the risk of fracture. Arch Intern Med 1999; 159 (15): 1750–6. PMID 10448778.

Pilon D, Castilloux AM, Dorais M, LeLorier J. Oral anticoagulants and the risk of osteoporotic fractures among elderly. Pharmacoepidemiol Drug Saf 2004;13(5): 289–294.PMID 15133779.

Gage BF, Birman-Deych E, Radford MJ, Nilasena DS, Binder EF. Risk of osteoporotic fracture in elderly patients taking warfarin: results from the National Registry of Atrial Fibrillation 2. Arch Intern Med 2004; 166(2):241–246.PMID 16432096.



Copyright 2008 William Davis, MD

Lipoprotein(a) Research Foundation

16. April 2008 William Davis (18)
There is no longer any doubt that lipoprotein(a) is a major causal factor in heart disease:

Meta-analysis (combined re-analysis) of 27 prospective studies:
Danesh J et al. Lipoprotein(a) and Coronary Heart Disease: Meta-Analysis of Prospective Studies


Lp(a) and "subclinical" atherosclerosis
Brown SA et al. The relation of lipoprotein[a] concentrations and apolipoprotein[a] phenotypes with asymptomatic atherosclerosis in subjects of the Atherosclerosis Risk in Communities (ARIC) Study.

Lp(a) and oxidized LDL
Tsimikas S et al. Oxidized phospholipids, Lp(a) lipoprotein, and coronary artery disease.

Lp(a) predicts peripheral vascular disease
Valentine RJ et al. Lp(a) lipoprotein is an independent, discriminating risk factor for premature peripheral atherosclerosis among white men.

Peltier M et al.Elevated serum lipoprotein(a) level is an independent marker of severity of thoracic aortic atherosclerosis.


Lp(a) across various populations
Gambhir JK et al. Association between lipoprotein(a) levels, apo(a) isoforms and family history of premature CAD in young Asian Indians.

Weber M et al. Metabolic factors clustering, lipoprotein cholesterol, apolipoprotein B, lipoprotein (a) and apolipoprotein E phenotypes in premature coronary artery disease in French Canadians.



Lp(a) and stroke risk
Jurgens G et al. Lipoprotein(a) serum concentration and apolipoprotein(a) phenotype correlate with severity and presence of ischemic cerebrovascular disease.

Willeit J et al. Lipoprotein(a) and asymptomatic carotid artery disease. Evidence of a prominent role in the evolution of advanced carotid plaques: the Bruneck Study.




From just about any direction, Lp(a) has been conclusively associated with atherosclerotic disease. We have more than enough data proving association.

But there are two areas of desperate need:

1) Data on effective treatments.

2) Raising awareness of this widely unknown (among the public) and ignored (among health professionals) genetic condition.

Treatment remains a real struggle. In a recent detailed Track Your Plaque Special Report, Unique Treatment Strategies for Lipoprotein(a) Reduction, we summarized the treatment approaches that have some power to reduce Lp(a) and/or its potential for causing heart disease. But, even armed with an appreciation for the world's scientific literature on this genetic condition, full control remains difficult for many people.

Track Your Plaque's HeartHawk has Lp(a) and he has struggled with this pattern for the last several years. He details some of his thoughts in a recent blog post.

More research and clinical studies are required and we need it soon if we hope to gain better control over this genetic pattern that affects up to 20% of people with coronary or vascular disease. Much of the needed research is sophisticated, background work similar to that being done by Dr. Santico Marcovina at University of Washington, Dr. Angelo Scanu at the University of Chicago, and Dr. Sally McCormick in New Zealand.

However, much of the needed research also consists of brief clinical experiences that detail whether or not there is an effect of various potential agents. Larger experiences, for instance, with potential treatment agents such as various phospholipid fractions, acetylcysteine, antibiotic regimens, some hormonal treatments, etc. could be performed quickly and simply. These studies would not require the $20 or $30 million typically spent by a drug company for a study, nor the several hundred million dollars to gain FDA approval of a new agent. They would simply be examinations of existing agents. These studies still cost money, require expertise, staff, and equipment. But the cost is a tiny fraction of the drug industry's investment in research. But it also means that investment return is nil from a drug manufacturer's perspective. Yet there are literally dozens, perhaps hundreds, of agents that hold some promise but have not been thoroughly studied.

For instance, if a specific modification of the phosphatidylcholine molecule were to generate a substantial Lp(a) reducing effect, Merck, Pfizer, and AstraZeneca would yawn--it is non-patent protectable, cannot be protected from competitors through the costly FDA approval process, and therefore is simply not worth their investment--regardless of whether it works or not.

(This is yet another example of how the drug industry, as well as hospitals and many health professionals, have lost sight of their real mission: to alleviate disease, not to profit from sickness.)

HeartHawk and I have discussed on a number of occasions whether a Lipoprotein(a) Research Foundation should be formed, an organization that seeks to fund the smaller research efforts that may accelerate productive research in Lp(a) and perhaps yield useful strategies faster than hoping for somebody to simply stumble on a treatment, or wait for the drug industry to create a unique, patentable entity that returns billions.

I'd like to propose that our Track Your Plaque program begin to fund such an effort. But a lot more help will be needed, particularly to generate the money to fund genuine, high-quality research from high-quality researchers.

If any readers of the Heart Scan Blog have any thoughts or insights into this process of creating a foundation, we'd appreciate your input.

More on ASTEROID

16. April 2008 William Davis (3)
Since we are on the topic of the ASTEROID trial and rosuvastatin, I'd make one more point before I start to sound like I'm plugging this drug (which I definitely am not).

In an informative Roundtable Discussion (open to subscribers to the American Journal of Cardiology; sorry) amongst Dr. Steve Nissen, principal investigator behind ASTEROID; and Drs. Vincent Friedewald, Christie Ballantyne, P. Shah, and William Roberts, Dr. Nissen made some interesting comments:


Dr. Shah: In ASTEROID, was the magnitude of atheroma volume change seen across different levels of LDL-C and HDL-C?

Dr. Nissen: No. There was no plaque regression seen in the 17 persons with LDL-Cs >/= 100 mg/dl, and there was little change in persons with LDL-Cs of 70 to 100 mg/dl. Only in persons with LDLs less than or equal to 70 mg/dl was there significant regression. The study was not powered to look for an HDL-C(which increased by 14.7%)-raising effect.



Interesting. In other words, ASTEROID, in a fairly internally consistent way, suggests that the lower the LDL is reduced, the more likely plaque regression is obtained. This is consistent with the Track Your Plaque experience, in which we've advocated reducing (calculated) LDL cholesterol to 60 mg/dl for the past several years.

Unfortunately, the message that the ASTEROID Trial sponsors, AstraZeneca, as well as the roundtable discussion panel (later in the discussion) try to make is that there is something magical about Crestor, that it yields benefits superior to other statin agents or other means of reducing LDL.

I disagree with this message. In the Track Your Plaque experience, we do aim for a similar LDL target. But we also employ a number of other strategies. We have also succeeded in regressing plaque without use of any statin drugs (though, admittedly, many people do require statin drugs to obtain LDLs in this range). We also witness magnitudes of reversal that often far exceed that seen in ASTEROID.

The Rountable Discussion is unfortunately tainted, as is the ASTEROID Trial itself, with deep drug industry financial involvement of the Roundtable participants. In fact, the discussion begins with a listing of the financial disclosures of the participants, a listing that occupies a full column of a two-column page. The potential biases of the participants doesn't necessarily invalidate the arguments, but to me suggests that participants are more likely to argue in favor of the sponsor's drug, or that participants were chosen because of these biases.

Why bother to even mention the ASTEROID Trial in a venue (the Heart Scan Blog, that is) that purports to seek unvarnished, unbiased truth in coronary plaque reversal? Because useful information can sometimes be found in unlikely places. Just like the four-year old child who blurts out an unexpected pearl of wisdom, so it can happen with the gobbledy-gook that emerges from the drug industry.

Every once in a while, they are worth paying attention to.

LDL cholesterol, statins, and plaque regression

13. April 2008 William Davis (12)
The ASTEROID Trial reported in 2006 examined the effects of LDL cholesterol reduction using the statin drug, rosuvastatin (Crestor), with coronary atherosclerosis quantified and tracked with intracoronary ultrasound. The Track Your Plaque report, New study confirms: LDL of 60 mg reverses plaque, on the ASTEROID Trial provides commentary on the results.


Though I remain skeptical that a statin-only treatment strategy can reverse coronary plaque in the majority of people, I do believe that the AstraZeneca-sponsored ASTEROID Trial does add to the wisdom on heart disease management. More importantly, it has served to raise awareness among both the public and my physician colleagues that atherosclerosis is indeed a potentially reversible condition.


Specifically, the ASTEROID results confirm that, either directly or indirectly, LDL cholesterol reduction achieved with statin agents does correspond to increasing degrees of plaque reversal. The mean (calculated) LDL cholesterol achieved in ASTEROID was 60 mg/dl, the same as the Track Your Plaque suggested LDL target.

Though the ASTEROID Trial is not news, I stumbled on a chart posted on the ASTEROID Trial website that clearly highlights how a number of other studies beyond ASTEROID have fallen into this pattern:





The graph reveals a linear relationship: The greater the reduction in LDL cholesterol with statin drugs, the greater the plaque regression ("change in percent atheroma volume"). (Several other studies not included in the graph also cluster into the same linear relationship.)

I am no supporter of drug companies, nor a defender of their policies and practices. But I do believe that their data can serve to teach us a few lessons. For instance, here is an (cherry-picked, to be sure) example of intracoronary ultrasound cross-sectional images before and after two years of rosuvastatin, 40 mg daily:





The color-coded/outlined atherosclerotic coronary plaque is shown shrinking, while the "lumen," or the path for blood to flow, enlarges. The reduction in coronary plaque is irrefutable. (The small circle within the lumen with the white halo surrounding it is the ultrasound catheter.)

If you and I were to choose a single treatment approach to coronary disease reversal, then 40 mg of rosuvastatin is probably at the top of the list. However, in the Track Your Plaque program, we do not advocate a single treatment strategy. While the Crestor-only approach is relatively straightforward--one pill a day--few people, in my experience, can tolerate this dose for any length of time. Patients invariably have to stop the drug or reduce the dose severely due to muscle aches when I've had patients try it. Contrary to the ASTEROID results, in my experience the majority of people, perhaps all, eventually give up with this improbable "one-size-fits-all" scheme.

The Track Your Plaque approach, while more complicated and involves several nutritional supplements and strategies, in my view addresses more causes of coronary plaque, is better tolerated, and provides health benefits outside of just LDL cholesterol reduction. It also minimizes or eliminates the need for prescription medication.



Studies cited in graph:

1.Nissen S et al. N Engl J Med 2006;354:1253-1263.
2 Tardif J et al. Circulation 2004;110:3372-3377.
3 Nissen S et al. JAMA 2006;295 (13):1556-1565
4 Nissen S et al. JAMA 2004;292: 2217–2225.
5 Nissen S et al. JAMA 2004; 291:1071–1080

When is a calorie not a calorie?

10. April 2008 William Davis (8)
One ounce of raw almonds (about 23 nuts) contains:


6 grams protein

14 grams fat

6 grams carbohydrate

3.5 grams fiber

For a total of 163 calories per ounce.


(From the USDA Nutrient Database)


Calorie content of foods is determined by summing up the calories from each constituent: 1 gram of fat = 9 calories; 1 gram protein = 4 calories; 1 gram carbohydrate = 4 calories. Calorie content can also be directly measured using a device called a burn calorimeter, in which the amount of energy released from a specific food is measured by literally burning it and gauging precisely how much energy is released.


The problem with both of these methods is that it is assumed that all foods are digested with equal efficiency. That is, it assumes that a potato chip is as readily digested and absorbed as energy from table sugar, a pretzel, oatmeal, a piece of steak, or a handful of nuts. In real life, of course this is not true. Different foods are absorbed with varying efficiency.

For a long time I've suspected that some foods are very inefficiently absorbed. I've particularly suspected that raw nuts are relatively poorly absorbed and thus yield only a fraction of the calories ingested.

Among the studies recently reported at the Federation of the Association of Societies for Experimental Biology (FASEB) meetings I attended in San Diego this past week were several devoted to almonds.

One study, to my surprise, documented this phenomenon. In Manipulation of lipid bioaccessibility of almonds influences postprandial lipemia in healthy human subjects, it was determined that, of 100 calories ingested from the fat fraction of almonds, only about half was actually absorbed. The remaining half passed out in the stool. (They did this by collecting stool samples and comparing the fat composition after eating the different almonds prepartions. This is not discussed in the limited text of the abstract.) In addition, postprandial (after-eating) surges in triglycerides were much less with whole almonds compared to the oil separated from the nut (i.e., broken down into almond oil + defatted almond flour). The researchers attributed the difference to the inhibitory effects of the almond nut's "food matrix," or the structural properties of chewed foods.

Add to this the fact that, of 6 grams of carbohydrate per ounce of whole almonds, 3.5 grams are indigestible fibers. This means that 6 - 3.5 = 2.5 grams of digestible carbohydrates are present per ounce (assuming 100% release).

If we follow the reasoning that only about half the fat fraction of almonds are absorbed, and assume that the protein and carbohydrate (minus the indigestible fibers) are absorbed efficiently (100%), then we would re-calculate the calorie content of almonds to be 97 calories per ounce, or 40% less than calories calculated by composition or measured with a calorimeter.

If we were to assume that protein and carbohydrates were, like fats, inefficiently absorbed because of the effects of the food matrix, then one ounce of almonds yields 88 calories per ounce, or 46% less. This is, in fact, a likely scenario, since the food matrix is largely created by the cell wall and should impede digestive access to fat, protein, and carbohydrate equally.

My point? Almonds and other nuts at first appear to be calorically dense due to fat composition. However, this simplistic view of nuts is misleading because of the confounding effects of the food matrix. Stated differently: Whole foods yield less calories. And, judging by the postprandial triglyceride effects: Whole foods yield less undesirable effects, such as postprandial rises in triglycerides.

Some other observations with almonds included:

The effect of almonds on plasma lipids in persons with prediabetes This study confirmed the LDL-reducing and modest HDL-raising effects of almonds.

Almonds (Amygdalus communis L.) as a possible source of prebiotic functional food This curious observation suggests that almonds modify the bacterial flora of the intestinal tract in a positive way (like the cultures in yogurts).



Copyright 2008 William Davis, MD
To get low-carb right, you need to check blood sugars

To get low-carb right, you need to check blood sugars

19. January 2010 William Davis (60)
Reducing your carbohydrate exposure, particularly to wheat, cornstarch, and sucrose (table sugar), helps with weight loss; reduction of triglycerides, small LDL, and c-reactive protein; increases HDL; reduces blood pressure. There should be no remaining doubt on these effects.

However, I am going to propose that you cannot truly get your low-carb diet right without checking blood sugars. Let me explain.

Carbohydrates are the dominant driver of blood sugar (glucose) after eating. But it's clear that we also obtain some wonderfully healthy nutrients from carbohydrate sources: Think anthocyanins from blueberries and pomegranates, vitamin C from citrus, and soluble fiber from beans. There are many good things in carbohydrate foods.

How do we weigh the need to reduce carbohydrates with their benefits?

Blood sugar after eating ("postprandial") is the best index of carbohydrate metabolism we have (not fasting blood sugar). It also provides an indirect gauge of small LDL. Checking your blood sugar (glucose) has become an easy and relatively inexpensive tool that just about anybody can incorporate into health habits. More often than not, it can also provide you with some unexpected insights about your response to diet.

If you’re not a diabetic, why bother checking blood sugar? New studies have documented the increased likelihood of cardiovascular events with increased postprandial blood sugars well below the ranges regarded as diabetic. A blood sugar level of 140 mg/dl after a meal carries 30-60% increased (relative) risk for heart attack and other events. The increase in risk begins at even lower levels, perhaps 110 mg/dl or lower after-eating.

We use a one-hour after eating blood sugar to gauge the effects of a meal. If, for instance, your dinner of baked chicken, asparagus brushed with olive oil, sauteed mushrooms, mashed potatoes, and a piece of Italian bread yields a one-hour blood sugar of 155 mg/dl, you know that something is wrong. (This is far more common than most people think.)

Doing this myself, I have been shocked at the times I've had an unexpectedly high blood sugar from seemingly "safe' foods, or when a store- or restaurant-bought meal had some concealed source of sugar or carbohydrate. (I recently had a restaurant meal of a turkey burger with cheese, mixed salad with balsamic vinegar dressing, along with a few bites of my wife's veggie omelet. Blood sugar one hour later: 127 mg/dl. I believe sugar added to the salad dressing was the culprit.)

You can now purchase your own blood glucose monitor at stores like Walmart and Walgreens for $10-20. You will also need to purchase the fingerstick lancets and test strips; the test strips are the most costly part of the picture, usually running $0.50 to $1.00 per test strip. But since people without diabetes check their blood sugar only occasionally, the cost of the test strips is, over time, modest. I've had several devices over the years, but my current favorite for ease-of-use is the LifeScan OneTouch UltraMini that cost me $18.99 at Walgreens.

Checking after-meal blood sugars is, in my view, a powerful means of managing diet when reducing carbohydrate exposure is your goal. It provides immediate feedback on the carbohydrate aspect of your diet, allowing you to adjust and tweak carbohydrate intake to your individual metabolism.
Tags :

Comments (60) -

  • Anne

    1/19/2010 3:29:13 PM |

    I can attest to the fact that doctors ignore what happens to blood glucose after eating. My fasting BG has always been normal but my glucose tolerance tests have always been high. My last glucose tolerance test a few yrs ago went to 201. My doctors told me I had some insulin resistance but assured me that I did not have to do anything about it because my fasting was OK.

    About 1 year ago, after reading this blog and others, I bought a glucometer. Yes, my fasting was "normal" but I could easily push it up to 200 by eating. I did just what Dr. Davis recommends. I used the glucometer to figure out what I can eat and how much I can eat. I am able to keep my blood glucose below 120 now. The glucometer is a powerful tool.

    Is it possible my ignored elevated post meal blood sugars did damage? Well, lets see, I have peripheral neuropathy and have had cardiac bypass. Giving up gluten 6 yrs ago greatly improved my PN and relieved my of shortness of breath and pitting edema. Getting my blood glucose down will make a difference too.

    I recommend Blood Sugar 101 http://www.phlaunt.com/diabetes/

  • sdkidsbooks

    1/19/2010 5:09:59 PM |

    Going to get a glucose meter today and start checking.  Is there a desirable number or range for glucose before and after or is it about how much or how little it rises without regard to the number?
    Seems like somewhere around a 100 is what you are advocating.  

    If a person is not diabetic, is it helpful at all to know your A1C when getting routine blood work done?  Just wondering...

    Thanks.

    Jan

  • Anonymous

    1/19/2010 6:38:43 PM |

    You can get Wavesense Keynote test strips from Amazon for about 35 cents per strip -- the best deal I've ever seen.  (The meter is about $35 there.)  

    I am curious about the right time to test.  If blood sugar goes to 160 at 30 minutes, but is down to, say, 100 at one hour, is that ok? Why is one hour (not 30 mins or 2 hours) the key number?

  • Gretchen

    1/19/2010 7:02:35 PM |

    Ground meat is often cut with breadcrumbs. I won't eat ground meat or meatloaf at a restaurant or potluck supper.

    Balsamic vinegar contains up to 3 g of glucose per tablespoon. And most people do add sugar to salad dressings. One restaurant I went to boiled down cider vinegar until it was sweet.

    You can use those urine glucose test strips to test foods for the presence of glucose before you eat them. If it's starch, you have to chew the food a bit first to break down the starch. See Richard Bernstein's "Diabetes Solution."

  • Anonymous

    1/19/2010 7:16:36 PM |

    When exactly do you take the measurement?  One hour after the start of a meal or one hour after the end?  Sometimes when we eat out, a meal can take an hour or more to finish.

  • DrStrange

    1/19/2010 7:48:44 PM |

    One caution is that blood sugar meters are only accurate to plus or minus 20% which is a huge variance.  Also, many (probably worst w/ the Walmart Relion or similar budget meters) are not very consistent so you can't just compare to a lab test and calibrate.  

    What I generally do is take 3 (or even 4) readings within a few seconds of each other, toss any wild outliers, then average what is left.  If you try this a few times, depending on your meter, you may be shocked at how much difference there is between the readings.

  • Calvin

    1/19/2010 7:51:01 PM |

    Dr. Davis--Great post--I totally agree. Even if someone isn't diabetic or prediabetic (myself),  investing in a glucose meter, then self-testing (especially post postprandial) has got to be one of the absolute best investments one can make in personal health.

    I once read that if most diabetics (and I'll add prediabetics too) had invested in a meter years before their diagnosis, mostly likely they could have/would have avoided many of their accompanying negative health conditions today.  

    That said, there is still a lot of "cognitive dissonance" with regards to diet and health--I think the meter really helps to reinforce the cognition portion of that phrase thereby reducing the dissonance half.  

    And using a glucose meter can actually be fun!

  • Future Primitive

    1/19/2010 10:33:28 PM |

    Here's an example of carbo loading on yam and plantain - there was a 7 hour "fast" prior to eating and then taking the measurements.

    http://tinyurl.com/bg-set-001

    mg/dL is marked at a few key points on the right hand side.

    What I don't get is how to interpret the second rise and fall after the two hour mark ... though it is still inside the post-absorptive window (which closes 3-5 hours after eating, IIRC).

    I'm pretty certain a glass of red wine explains the initial drop to 65 mg/dL, btw.

    Also, for those that would like to make their own graph, it's easy to grab the url and fill in your own data (it's a google charts thing).

  • notrace

    1/20/2010 12:04:01 AM |

    Will there still be production of small LDL from excess blood glucose even if there is ample available glycogen storage space? That is, will the liver simultaneously manufacture LDL and glycogen?

  • Anonymous

    1/20/2010 2:37:04 AM |

    When do you start to count your one hour.  From the time of your first bite of food, or when you have  finished your last bite.  Since it takes about 20-30 minutes to finish eating, when to start the one hour count down is important.

  • Dr. William Davis

    1/20/2010 2:58:57 AM |

    Hi, Anne--

    What a perfect example of the power of postprandial testing!

    Yes, Jenny Ruhl at http://diabetesupdate.blogspot.com  provides a wealth of insight into blood sugar issues. We will also be releasing an in-depth Special Report on this issue on the www.trackyourplaque.com website.

  • Dr. William Davis

    1/20/2010 3:00:50 AM |

    In answer to the questions on timing of blood sugar checks:

    I am guilty of oversimplification. The peak timing of blood sugar varies on the foods consumed and the mix of foods consumed. It will also vary from individual to individual. I believe a reasonable way to start out is to check 60 minutes from the completion of a meal. Even better, you might occasionally perform your own time-course study: Check blood sugars every 30 minutes to determine when you tend to peak.

  • Coach Jeff

    1/20/2010 12:58:55 PM |

    Since an LC diet causes insulin resistance, (Actually a GOOD and protective thing within the context of an LC diet)wouldn't a long-term low carber get a sort of "false positive" reading of high blood sugar from ANY high carb meal?

    Also, what do you think of the theory (that seems to really be gathering momentum lately) that fructose is the actual cause of insulin resistance, while on a "high carb" diet, and that glucose/starch is relatively benign?

  • Anonymous

    1/20/2010 1:12:53 PM |

    I got a blood glucose monitor after I starting taking niacin for HDL (had read that niacin could raise blood glucose) and it was an eye opener. Now I know what foods to avoid.

    Jeanne

  • Dr. William Davis

    1/20/2010 1:43:47 PM |

    Gretchen--

    Great thoughts. I forgot about the bread crumbs in ground meat issue.

  • Dr. William Davis

    1/20/2010 1:45:17 PM |

    Coach--

    I think it's a matter of degree: While fructose is clearly a very bad player, glucose/starch are not benign, just less bad. Look at the responses we can generate with glucose tolerance testing using 75 grams of glucose.

  • Peter

    1/20/2010 2:55:25 PM |

    Since a simple way to reduce after-meal glucose readings is to eat smaller meals and eat more often, I don't quite understand why you think it's a bad idea.

  • Anonymous

    1/20/2010 3:27:43 PM |

    Bloodsugar101 suggests timing from the start of the meal. I always set a timer anyway, and it is easier to do before beginning to eat than at the end of the meal. This can feel awkward at first in restaurants, but I look at it as a way to get the word out.

    The occasional checks every 30 minutes is an excellent suggestion. Anytime you go over 140, you're causing damage. Even if it is only for brief periods, you want to be sure this is not one of your staple foods!

  • Anonymous

    1/20/2010 8:07:02 PM |

    What has happended to your trackyourplaque forum? I can't reach it anymore? Server crash without any backups? :-(

  • P

    1/20/2010 9:26:25 PM |

    hmmm. How painful is it to check the blood sugar that often?

  • Anonymous

    1/20/2010 10:13:42 PM |

    I'm curious to know how to interpret blood sugar readings on the background of a healthy weight and a low-carb diet, with no known diabetes.  

    My fasting sugar is the same as it was before going low-carb (mid-70s).  However, it now takes a lot fewer carbs to spike my postprandial sugars.  

    An example: after 25 grams of carb in the form of a small serving of sweet potato with butter, my 45 minute postprandial reading, measured in triplicate, was 135.  I'm guessing the peak was even higher.  In case it matters, I'm a 36yo woman with a BMI of 18.9.  

    Should I be unconcerned by this kind of spike as long as my typical meals don't spike my sugar?  Is this just the normal insulin resistance caused by a low-carb diet, as Coach Jeff mentioned in his comment?

  • Anonymous

    1/20/2010 11:06:20 PM |

    Dr. Davis, you said, "While fructose is clearly a very bad player, glucose/starch are not benign, just less bad. Look at the responses we can generate with glucose tolerance testing using 75 grams of glucose."

    This does not prove anything about what causes insulin resistance in the first place though.  The person having a response to glucose during a tolerance test may have originally gotten their insulin resistance from fructose.  You can't use fructose in the test since it doesn't raise blood sugar, you can only use glucose.  

    To put it another way, people who don't have insulin resistance don't have abnormal responses to glucose during glucose tolerance tests.  Does that exonerate glucose?  Not really.  

    What I'm saying is you can't indict glucose OR fructose based solely on what is seen in a glucose tolerance test.

  • Dr. William Davis

    1/21/2010 11:59:56 AM |

    Anon--

    Blood sugars are too high. Either too much carbohydrate in the diet or something has caused an abnormal insulin response. While the dangers are not acute, there are long-term consequences of blood sugars this high.

  • frogfarm

    1/21/2010 3:02:19 PM |

    Dr. Davis, if you can spare a moment I hope you would comment on this:

    http://fanaticcook.blogspot.com/2010/01/should-you-take-vitamin-d2-or-vitamin.html

    where Dr. Michael Holick (Mr. Vitamin D, from the look of his pedigree) claims D2 is equally as effective as D3 in raising and maintaining 25OHD levels?

  • DrStrange

    1/21/2010 3:43:05 PM |

    There are two main causes of insulin resistance, dietary fat and possibly fructose.  Fructose is not a cause for many as they can eat a mostly fruit diet without issues but for some it is a big factor.  There are "must have" essential fatty acids needed in proper amounts and ratio, perhaps a bit more fat is needed.  Beyond that minimum amount, any additional adds to insulin resistance. The amounts and ratios are all present in an all plant diet without the addition of any add oils or fats and that w/ minimal nuts/seeds (maybe an ounce of flax).

    After being on strict McDougall diet (total dietary fat approx 10% and no refined carbs, no animal products, no junk) for about 18 months, I did a 75 gm glucose tolerance test and had them do an extra point at 30 minutes just in case. My highest peak was 114.  Previously, on low carb diet I would go to 185 or higher. [I am 5'3" and 110 pounds so small body mass; lbs body per gm glucose if that makes any difference]

  • TedHutchinson

    1/21/2010 8:49:40 PM |

    @ frogfarm said...
    I find it very strange people take this particular study seriously.

    At the end of the trial none of the participants had 25(OH)D levels above 30ng/ml, so they all remained vitamin D insufficient.
    IMO it is unacceptable medical practice to knowingly give people an amount of a supplement that leaves them at such a low 25(OH)D level they remain unable to properly absorb calcium and well below the 58.8ng/ml level at which human breast milk flows replete with D3.
    So too little vitamin D of any kind leaves you vitamin D deficient.
    Is that such a remarkable finding?

    BUY DISCOUNT Ostoforte 50,000 IU (also called Drisdol) ONLINE 50,000 IU (100 capsules)  $168.99 USD
    or you can choose
    Vitamin D3 $26.95 for 100 X 50,000iu capsules.
    Who, but a fool, chooses to pay $169 when there's a better, cheaper alternative costing only $27?
    Or choosing an oilbased gelcap still saves loads of money.
    Healthy Origins, Vitamin D3, 10,000 IU, 360 Softgels $23.95

    I'm not sure of the point or the common sense, involved in trying to prove a synthetic drug, humans have to convert to D3 anyway, may, in trivial amounts too low to get anybody out of insufficiency, may be as good as a natural, cheaper, product or that equivalence seen in a few persons at a very low dose level, also applies at the sensible, natural levels, desirable for optimum health outcomes.

    While there are cases like this listed in Pubmed it is clear some people do not absorb nor are able to use Vitamin D2.
    We report a case of a 56-year-old woman who received supratherapeutic doses of ergocalciferol (150,000 IU orally daily) for 28 years without toxicity.

    A small trial of just 68 people is unlikely to pick up cases like the above.

    Grassrootshealth Banner Graph shows the amounts people have been taking and the 25(OH)D levels they have achieved.
    6000~8000iu approx 1000iu/daily for each 25lbs you weigh generally produces a natural level at which the body is able to store a sufficient reserve of D3 to be effective at times of crisis.
    This LEF study is another example showing 5000iu/d is not sufficient to get most people above 50ng/ml.

    As Holick knows perfectly well human skin naturally makes 10,000iu/daily given a few minutes full body UVB exposure. It does that for a purpose. Only when researchers start using equivalent EFFECTIVE amounts of the same NATURAL Vitamin D3 biologically identical to the form human skin NATURALLY makes, will we see an improvement rates of chronic illness.

  • Anonymous

    1/21/2010 9:13:05 PM |

    Dr Strange, if you're eating low carb, you have to prep for a GTT by carb-loading for 3-5 days beforehand.  Your pancreas won't be prepared to handle 75g of carb unless you give it a few days to rev up insulin production first.

    The reason that you had no problem with the GTT while McDougalling was that your body was used to high-carb loads, and so the test posed no challenge to your pancreas.

  • TedHutchinson

    1/21/2010 9:33:39 PM |

    Testing in Pairs
    Although this idea is for diabetics I feel it may also be useful for others wanting to see how particular food/exercise choices affect their numbers.
    There is also a short video, a downloadable record form and an example to consider.

  • Anonymous

    1/22/2010 5:22:55 AM |

    I can support what others are saying: before I went low carb, I could eat carbs and my blood glucose would never go above 120; now I eat pretty low carb and a single sweet potato can take me to 150.  I guess one should either eat extremely low carb or extremely high carb to avoid glucose spikes.

  • Dr. William Davis

    1/22/2010 3:04:13 PM |

    I worry that chronically eating high-carbohydrate, while generating an "accommodation" response that blunts postprandial blood sugars, will generate pancreatic BURNOUT by constantly challenging the pancreas to overproduce insulin.

  • Vladimir

    1/22/2010 3:47:56 PM |

    I too find that my post-meal glucose goes up much more after I do have carbs, if I'm eating low carb than high carb.  It's kind of amazing, and a little worry-some.

    However, if I eat very low carb, my fasting glucose is in the low 80s, while if I have more carbs, it's in the high 90s the next morning.  For example, I have (following the blog's advice) had absolutely no wheat and minimal sugar since Dec 27.  My fasting glucose had fallen into the low to mid 80s.  Two days ago, I had a large cookie after lunch --  My first wheat/sugar in 3 weeks.  The next morning, my fasting glucose was 98.

  • DrStrange

    1/22/2010 3:57:49 PM |

    Insulin resistance is the key here and dietary fat is a major contributor to IR.  I simultaneously took insulin levels w/ the blood sugar readings in the 75 gm glucose tolerance test above, and they were consistently low normal to slightly below normal, starting w/ undetectable level at fasting. Readings were:

    fasting < 2
    30 minutes = 3
    60 minutes = 5
    120 minutes = 14
    180 minutes = 8


    reference ranges given on lab report:
    fasting  < 17
    30 minutes = 6-86
    60 minutes = 8-112
    120 minutes = 5-55
    180 minutes = 3-20


    Doesn't seem like too much risk of burn out there!  And again, the reason for the low insulin output generating a fairly flat and low sugar curve was that without excess dietary fat (7-10% of total calories), there is dramatically reduced insulin resistance.

  • Matt Stone

    1/22/2010 6:47:00 PM |

    Thanks for bringing up the importance of blood sugar levels. I've done the same thing with my followers in my recent eBook on type 2 Diabetes, Metabolic Syndrome, and Prediabetes.

    What I have done is take it a step further. Instead of noting what my blood sugar reaction is to a large meal full of high GI starch and trying to avoid it, my focus has been finding ways to improve my glucose tolerance to such a meal.

    My glucose response to food is now far better than any single person following the advice of this blog. That much I can guarantee. It is not luck. It is not genetics. I watched my numbers fall as I followed insights that I gained from several years of intense investigation on the subject.

    The big thing that low-carb authors are missing is that unrefined carbohydrates can improve glucose response to food, even if they cause a larger rise in blood sugar in the short-term.

    My blood sugar now peaks at levels below 80 mg/dl after meals, something that the medical and nutrition-sphere probably considers to be impossible. But it's not. It's glucose metabolism perfection, but it's not achieved through limiting glucose intake. In fact, that can make your response to glucose worse, not better.

  • I Pull 400 Watts

    1/22/2010 9:58:30 PM |

    When you say low carb, what percentage of your calories are coming from carbs? Talking under 30% here?

  • Ateronon

    1/23/2010 6:43:30 AM |

    Off topic here but wish you would discuss salt and its effect on heart disease. There has just been a well publicized news story on it:

    http://www.cnn.com/2010/HEALTH/01/21/salt.intake/

    Do you recommend cutting salt intake to your patients?

    Great blog!

  • DrStrange

    1/23/2010 9:38:02 PM |

    "...if I eat very low carb, my fasting glucose is in the low 80s...  Two days ago, I had a large cookie after lunch -- My first wheat/sugar in 3 weeks. The next morning, my fasting glucose was 98."

    Yes, the high fat content of low-carb diet causes insulin resistance!  If you ate low fat (around 10% total calories max) for a couple weeks then you would maintain the lower fasting sugar after a carb load. Though if that cookie had a lot of fat in it, that could be enough to kick up the insulin resistance again.  One other possibility is if you are gluten intolerant, the stress to your system of eating wheat cookie could make fasting bg higher.

  • Vladimir

    1/24/2010 3:28:38 AM |

    Dr. Strange, Do you have any evidence that a diet high in healthy fats -- I'm a vegetarian, so I get little saturated fat -- causes insulin resistance?  I've never seen that theory propounded, and the mechanism seems implausible to me.

  • Matt Stone

    1/24/2010 5:57:21 PM |

    Dr. Strange-

    Interesting thoughts and you are right to question low-carb dogma as well as to show that insulin resistance is the core problem - and that a very high-fat, low-carb diet worsens the core problem.

    Anyone questioning this has not researched the issue thoroughly enough.


    However, you are making the same mistake. Eating a high-carb, low-fat diet for an extended period of time, while lowering your fasting glucose and insulin levels, also makes your glucose tolerance worse.

    Let me explain...

    If you have a basline meal, let's say, a slab of baby back ribs with cornbread and baked beans, and your 1-hour pp is 140 mg/dl, fasting the next day is 100, then you have good base numbers to track improvement.

    Eat low-carb, high-fat for 10 weeks, eat that same meal (ribs), and both your fasting and pp glucose levels will be higher than they were before you went low-carb. This means you're in worse shape than before the experiment.

    If you eat low-fat, high-carb for 10 weeks, and you eat a slab of ribs, cornbread, and baked beans...
    You're pp and FG will measure into the stratosphere (my 1-hour pp actually hit 173 mg/dl breaking a low-fat escapade...nutritarian).

    Both diets made your glucose metabolism worse in response to your baseline meal.  In other words, both strategies give you better numbers in the interim while making you fundamentally unhealthier (not to mention eating low-fat will make you crave more fat and low-carb will make you crave more carbs).

    What I've found is how to improve your glucose levels and insulin sensitivity in response to normal mixed food ratios. That's where real healing is achieved. A low-carber or a "low-fatter" will never get to a point where he or she can eat a large mixed meal with lots of fat, carbohdyrates, protein, and calories without having high postprandial spikes and high fasting glucose levels. Only someone who can eat 2 baked potatoes with 2T of butter and an 8-ounce untrimmed ribeye with fasting levels in the 70's and pp's in the 70-90 range is truly healthy and free of insulin resistance. I've found the secret to achieving that, and it is not low-fat, low-carb, or low-calorie.

    If such a meal sends your blood sugar half way to Mars, then you need to fix that!  Not avoid it!

  • Anonymous

    1/24/2010 11:32:13 PM |

    @ Matt Stone:

    Stop spamming! Yes, "everyone is wrong but I have figured it all out but for won't tell you what it is unless you go to my web site and pay me" is a spam, plain and simple. Please stop it.

  • DrStrange

    1/25/2010 12:42:19 AM |

    MattStone said: "Only someone who can eat 2 baked potatoes with 2T of butter and an 8-ounce untrimmed ribeye with fasting levels in the 70's and pp's in the 70-90 range is truly healthy and free of insulin resistance."

    That is somewhat how I used to eat and my fasting sugar level was creeping skyward.  Switched to low carb and felt gradually worse and worse for the 9 months I did it.  Switched to low-fat/starch based diet and have been feeling very well and not craving fat at all.  I do eat a little over an ounce per day of flax and pumpkin seeds for EFA boost.

    On 4 different occasions over the past couple years I have sent my blood sugar way up from one meal of moderate fat intake.  One was from eating all the seeds in a medium sized Delicata squash in one meal, maybe 1/2 cup or a bit more.

    Admittedly my liver is not in the best of shape due to much solvent exposure working in surfboard industry years ago and this my contribute...

    Don't have evidence handy but my understanding is that saturated fat is the biggest contributor to IR, much more so than unsaturated. There is some saturated fat in veg foods, some are very high in fact like coconut.

  • DrStrange

    1/25/2010 1:53:35 AM |

    Matt, Have read some on your blog site and think I get the overall picture of what you are doing but...

    What about the demographic data showing increasing cancer rates w/ increasing consumption of animal protein?  And the at least transient damage from meals high in sat. fat?:

    http://content.onlinejacc.org/cgi/content/short/48/4/715
    Consumption of Saturated Fat Impairs the Anti-Inflammatory Properties of High-Density Lipoproteins and Endothelial Function
    CONCLUSIONS: Consumption of a saturated fat reduces the anti-inflammatory potential of HDL and impairs arterial endothelial function. In contrast, the anti-inflammatory activity of HDL improves after consumption of polyunsaturated fat. These findings highlight novel mechanisms by which different dietary fatty acids may influence key atherogenic processes.

    And this one is a little concerning (its title tells the tale):
    http://www.ncbi.nlm.nih.gov/pubmed/18263705
    Glucose and leptin induce apoptosis in human beta-cells and impair glucose-stimulated insulin secretion through activation of c-Jun N-terminal kinases.

    More on low fat diet and atherosclerosis:

    http://www.heartattackproof.com/resolving_cade.htm

    It is a fascinating concept that increasing leptin dramatically reduces insulin resistance.  Leptin secretion seems to be induced by increasing glucose level, so eating starch (unrefined carbs like potatoes, whole grains, etc)which converts directly to glucose, should raise leptin level.  What I do not understand is the need for high fat and saturated fat in the diet, nor the need for "overfeeding."  We do need a certain amount of fat in our diets, but a plant based diet, with the addition of an ounce or so of selected seeds/nuts does seem to cover the 10-15% calories from fat we need without the increased disease risks of higher fat intake, and the risks from intake of large amounts of animal protein.

  • billye

    1/25/2010 5:03:20 PM |

    All 42 comments are amazing,

    Lots of varied comments here.  How do you suppose we all arrived here in the first place?  Our genes traveled through the ages,  without the benefit of all of this information.  How did they do this you might ask?  Simple, our ancient ancestors ate what their genes required for survival, full fat wild animal product, supplemented by a few wild not very starchy roots pulled from the ground, and seasonal wild not very sweet tree fruit.  This progressed throughout the last 2.5 million years.  That is how we got here.  Where we went wrong is when agriculture and farming started about 10,000 years ago followed by industry.  Our genes did not change much in the last 2.5 million years of eating high saturated fat including all high fat organs and marrow from the bones, with limited seasonal veggies and fruit.  They did not have the benefit of the sage advice of modern traditional medicine, or electronic devices to guide them, relative to the easy to treat by lifestyle change metabolic syndrome diseases.  Weren't they lucky?  Lest you think I am disparaging all doctors, I am not.  G-d forbid you have a broken leg or a disease that is congenital or inherited  that is difficult or near impossible to treat and need a physician, this group of dedicated highly trained professionals are  a life raft, and much appreciated.  I practice what I preach.  I went from a very ill patient to one that has reversed many of the metabolic syndrome illness that I suffered.  I trust the wisdom of my ancient ancestors and my doctors who practice out of the box evolutionary medicine to guide me.

    Billy E

  • Jared

    1/25/2010 5:04:46 PM |

    The information and anecdotes you provide about various heart disease issues is very interesting and useful. There is a registered dietitian in the Kansas City Area that has produced a series of informational videos about weight loss, nutrition and healthy living that you may be interested in. Here is her latest Nutrition 101 Video Series: http://www.youtube.com/watch?v=7KZCjcCTCOE&feature=related

    Thank you and happy heart month!

  • TedHutchinson

    1/25/2010 5:44:47 PM |

    @ Dr Strange
    Nutrition and Metabolism  Dietary fat research
    Perhaps you haven't yet read the Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease Patty W Siri-Tarino, Qi Sun, Frank B Hu, and Ronald M Krauss, Jan. 2010
    showing there is no significant evidence for concluding that dietary saturated fat is associated with an increased risk of CHD or CVD.

    With reference to Consumption of Saturated Fat Impairs the Anti-Inflammatory Properties
    The mitochondria of people new to consuming coconut oil will not be  adjusted to it. It takes time to acquire appropriate gut flora. A single ingestion of an unfamiliar dietary substance will have different effects from long term use of the same substance.

    Any single trial comparing an omega 6 frequently consumed with a type of saturated fat the general public are not generally accustomed to will fail to spot the long term benefits of MCT (coconut oil, saturated fat) consumption.
    MCTs suppress fat deposition through enhanced thermogenesis and fat oxidation. MCT's preserve insulin sensitivity. MCTs regulate production of adipocytokines (e.g., adiponectin.

  • DrStrange

    1/26/2010 12:37:51 AM |

    Billye, you might want to read these.  It is true that ancestors ate full fat wild game, which is very very lean.  Also, 100% of it ate its natural diet and not corn, soy, and synthetic supplements and drugs.  Also, they most likely ate primarily a lot of starchy roots, leaves, flowers, insects, whatever they could collect and some meat when they could get that.  The meaty, beefy, caveman is a romantic fantasy.  They also did not live very long so degenerative diseases of aging were not an issue

    http://diabetesupdate.blogspot.com/2009/09/lets-not-twist-history-to-support-our.html

    http://diabetesupdate.blogspot.com/2009/11/saying-something-over-and-over-doesnt.html

  • billye

    1/26/2010 2:06:40 PM |

    Dr. Strange,

    The reasons that ancient peoples expired at a relatively young age was because diseases that are cured today through the use of antibiotics such as malaria along with the many natural disasters that occurred throughout the ages account for this fact.  However, what they did not die from were the diseases of the metabolic syndrome that you attribute inaccurately to degenerative diseases of old age. They are brought on by the standard American diet.  The degenerative diseases that you mention are first found in ancient egyptians from about 12,000 years ago after the advent of agriculture.  The patients can do their own trials under the watchful eye and monitored by their doctors.  The plain fact is that when switching to an ancient evolutionary lifestyle most of the diseases of the metabolic syndrome  reverse themselves.  This is being accomplished by thousands of people all over the world today, including my self.  You might read the well documented by clinical trials, Good Calories Bad Calories by G. Taubes, and Trick and Treat by B. Groves.  

    Billy E

  • billye

    1/26/2010 3:30:08 PM |

    DR.Strange,

    This is a P.S.  Archaeologists have found many human bones that had cut marks inflicted by other waring clans, along with the fact that the population of those times was very small compared to today's populations.  This is in contrast to the huge carnivore animal populations that walked the earth devouring humans who were in their food chain.  Also of note was the proven fact that ancient populations prized the fattest parts of the animal, brains, organs, and marrow from the bones etc.

    Billy E

  • donny

    1/26/2010 4:33:37 PM |

    Dr Richard Bernstein is in his mid-70s, and has type I diabetes. His diet is around 30 grams of carbohydrate a day, and he has no fear of saturated fat. It beggars the imagination that a man like him, whose pancreas hasn't produced any of it's own insulin in over half a century, should live to a ripe old age (as a male type one diabetic, he's already done this, and he ain't done yet.), but that the same diet should be deadly to the non-diabetic. Maybe he's lucky; but, before he learned to tightly control his own blood sugars, (and with as little insulin as possible), he suffered all kinds of complications, hardening of the arteries, high triglycerides, low hdl, early kidney disease, etc. I think Dr Bernstein and his patients provide proof of concept for what Dr Davis is trying to accomplish here for those suffering insulin resistance, whether they happen to be diabetic or not.
    Matt, you can't test insulin levels with a glucose meter. You also can't test any possibly progressive damage to glucose homeostasis that *might* be caused by a high everything diet over the course of years or even decades in a matter of weeks or months. Nor can you say flat out that your metabolism has been "healed" by such a diet. Has your system healed, or was it just healthy enough in the first place that over time it was capable of making the hormonal adjustments necessary to function well on a mixed diet? Can everybody make that leap?
    The thing about leptin and insulin resistance... one of the effects of leptin is to decrease the appetite for carbohydrate. (Maybe by increasing ketosis? or at least lipolysis.) It's almost like carbohydrate restriction is built right into the system.;)

  • DrStrange

    1/27/2010 12:22:58 AM |

    "...of note was the proven fact that ancient populations prized the fattest parts of the animal, brains, organs, and marrow from the bones..."

    Proven?  How they do that?

  • Anna

    1/27/2010 5:12:13 AM |

    FYI, a few tips I have picked up in the years I have been testing my BG,

    For the least amount of pain sensation when lancing my finger, I take the blood sample from the *side* of my finger tip, *not* on the pad or the tip.    

    If you have chronially cold hands it can be hard to get a good enough sample.  Wash hands with warm water first, dry well.  Swing arm in a big arc few times if necessary, to force more blood to the hands.  Sometimes my house is a bitt chilly but my car is warm from the sun in the driveway.  A few minutes sitting in the sunny car warms up my hands considerably, making a blood drop easy to get.

    It's ok to slightly "milk" the finger from the palm to the tip once, but with warm hands and a few pre-lancing "swings" (described above), that shouldn't be necessary.  It shouldn't take a lot of "milking" to get a good enough sample.

    There's no need to change the lancet tip for each test sample if you are the only one using the lancet (with clean hands, of course).  In fact, the lancet tips become more comfortable with use.  I change the tip only when it becomes dull and uncomfortable.  It goes without saying the lancet tip should always be changed if it is used to get a blood sample for another person.

    Speaking of clean hands, be sure there is no sugar on your hands or it can affect your results.  Wink

  • TedHutchinson

    1/27/2010 1:04:07 PM |

    @ Anna
    Thanks for tips. I've just started testing (following Dr D's suggestion)
    Bit surprised at some of the numbers.
    5.7=102mg/dl premeal
    8.1=146mg/dl 1hr after meal
    Chicken portion in curry sauce + carrots
    Probably tikka sauce (bought ready meal sugar listed 3rd in marinade and in sauce. Won't buy that again.
    Generally between 6.1 and 6.9 110mg/dl~125mg/dl

  • billye

    1/27/2010 2:20:12 PM |

    Dr. Strange,

    There is so much Paleolithic archaeological proof that ancient populations prized brains, organs, and marrow from bones, that it boggles the mind.  Have you not read about the thousands of bones along with tools found in ancient caves? They were smashed to get at the brains and marrow.  I call your attention to the Quarterly Review Of Biology, Vol 79, No1 March 2004, one of the many studies and reports out there.  Meat eating - dietary shift to increased regular consumption of fatty animal tissues in the course of hominid evolution as mediated by selection for "meat adaptive" genes.  This selection conferred resistance to disease risks associated with meat eating also in life expectancy.  The data was produced at the University of southern California, Los Angeles California.  This argument is long over, unless you wish to ignore all of the indisputable archaeological proof available.  Lets get on with out of the box medicine which supports health.  

    Billy E, nephropal.com

  • The Accidental Farmer

    1/29/2010 12:30:13 PM |

    Coach Jeff said: Since an LC diet causes insulin resistance, (Actually a GOOD and protective thing within the context of an LC diet) . . .

    I am new to this blog, got the link from the Taubes Talk yahoogroups board, and I am curious about this statement.  Why is IR good and protective?  I eat a very high fat diet, as well as low carb, as that is what seems to control my hypoglycemia the best, and so this statement seems counter-intuitive.  Or am I mistaken in thinking that hypoglycemia is a sign that one is developing insulin resistance?  If so, then it would seem that if something relieves the symptoms of hypoglycemia, then it is not leading to further insulin resistance.

  • TedHutchinson

    2/9/2010 3:09:04 PM |

    Following Dr Davis's suggestion I bought a Lifescan Onetouch Ultraeasy from Ebay.
    With too many readings higher than I expected, I needed a better way of recording numbers.
    The people at the freephone number at this link
    Lifescan Onetouch will send a cable and software to load and record your readings quickly and easily directly from the meter together with a simple Quick Start Manual.
    As they don't charge for the disk it's quicker and easier than downloading the software, the cable makes the data transfer from meter even quicker.

    People with different makes of meter may like to download the software anyway and enter their figures manually.
    When you have entered a few days readings, the graphs make it easier to see trends.

  • Ron

    2/11/2010 3:09:33 PM |

    I've always been skeptical about the concept that saturated fat increases insulin resistance and here's an article that addresses that fact directly:

    http://wholehealthsource.blogspot.com/2010/02/saturated-fat-and-insulin-sensitivity.html

  • DrStrange

    2/11/2010 8:01:33 PM |

    "I've always been skeptical about the concept that saturated fat increases insulin resistance..."

    Compared to mono fat, not much if any difference.  Try comparing to very low fat diet ie about 10% of total calories and you will clearly see that fat in and of itself, if too much in diet, will indeed greatly increase IR.

  • Andreas

    2/15/2010 12:57:46 PM |

    Dr. Davis, I followed your advice and bought a glucometer. I got severe cravings from time to time. So last time I could not resist I checked my blood sugar. That was after I ate about 300g of nuts, drank a bottle of red wine and ate a big family chocolate bar. The glucometer showed 86 mg/dl which is within normal range. How is that possible?

    Do you have any further recommendations what to look out for in a case like this? I would really like to find the reason and overcome those cravings. I'm not overweight, in fact more the athletic kind of guy. I started eating paleo/EF about a year ok and am doing mostly great except for the cravings.

    Thank you!
    Andreas

Add comment

Loading