Dr. Michael Eades on the Paleolithic diet

18. February 2009 William Davis (16)
Dr. Michael Eades has posted an absolutely spectacular commentary on the Paleolithic diet concept:

Rapid health improvements with a Paleolithic diet

The post was prompted by publication of a study that tried to recreate a Paleolithic-like diet experience over a brief study period:

Metabolic and physiologic improvements from consuming a paleolithic, hunter-gatherer type diet.

Dr. Eades discussion is wonderfully insightful and comprehensive and there's little to say to improve on his discussion.

I'd make one small point: From what I see in my experience, the improvements in lipid patterns seen in the brief period of this study are very likely to have been primarily due to the removal of wheat. Followers of this blog know that wheat elimination is among the most powerful cholesterol-reducing strategies available.

What vitamin D form?

15. February 2009 William Davis (36)
In response to questions regarding why don't vitamin D tablets work, here are my observations.

When I first started correcting vitamin D levels around 3 1/2 years ago, people would begin with starting 25-hydroxy vitamin D blood levels of around 20 ng/ml.

Taking, say, 6000 units vitamin D as tablets over 3 months yielded blood levels of 24-30 ng/ml. Taking 6000 units in an oil-based form, and blood levels would commonly be 60-70 ng/ml.

In other words, tablets are very poorly absorbed. I also saw very erratic absorption with tablets, with tremendous variation in blood levels.

I witnessed this effect many times. I finally began telling patients to avoid the tablets altogether. It's simply not worth it. Taking dose X of tablets, you cannot predict what the blood level of vitamin D will be.

Now, you can sometimes make the tablets get absorbed by either taking with a teaspoon of oil (e.g., olive, flaxseed) or taking with an oil-rich meal. However, I am uncertain just how consistent the absorption is under these circumstances, not having done this enough times to know.

Oil-filled gelcaps are no more expensive than tablets (or perhaps a dollar more). Health food store employees and pharmacists don't know this. I have had many patients come to the office claiming they changed to tablets because that's all their health food store or pharmacy carried and the person behind the counter assured them it was the same. Blood level of vitamin D to confirm: right back down to the starting level or near it--little or no absorption.

The only way to know whether a preparation is absorbed is to check a blood level. But, in my experience, having checked vitamin D blood levels thousands of times, gelcaps never fail; tablets fail over 80% of the time.

Vitamin D for the pharmaceutically challenged

14. February 2009 William Davis (20)
Most Heart Scan Blog readers already know:

Your doctor has been brainwashed by the pharmaceutical industry.

Your doctor more than likely has spent the better part of his or her career in the Guantanamo Bay of healthcare, water-boarded by seductive sales representatives, enticed with promises of fame and riches, threatened with ostracism from the clubby internal halls of healthcare if--gasp!--he or she didn't subscribe to the "rule" that only drugs are good, anything else is bad.

The same FDA-approval-is-necessary-to-be-good brand of nonsense is gaining popularity among my colleagues who, having caught some mention (on the Today Show, Oprah, or similar source of medical information), hope to join the vitamin D hoopla.

People will proudly declare that they are taking a high dose of vitamin D: 50,000 units once per week.

No. They are taking a barely useful form: D2, ergocalciferol.

Studies examining the reliability of the D2 form differ:

There's the Heaney study suggesting that D2 is less effective than D3:
Vitamin D2 is much less effective than vitamin D3 in humans

Then there's the Holick study showing they are equivalent:
Vitamin D2 is as effective as vitamin D3 in maintaining circulating concentrations of 25-hydroxyvitamin D.

My experience is more in line with the Heaney study: Little or no real effect with D2.

One particularly illustrative case I witnessed was a woman who was mistakenly prescribed D2 at 50,000 units per day. She told me that she'd been taking it for a year. I fully expected to see clear-cut signs of toxicity (e.g., high blood calcium levels). Curiously, she showed no signs of toxicity. Nor did she show any vitamin D at all in her blood: 25-hydroxy D level of zero--literally zero.

I've witnessed similar phenomena several times: plenty of vitamin D2 . . . very little vitamin D in the blood.

All in all, I suppose that D2 is better than No-D at all. But you are far better off joining the ranks of the pharmaceutically challenged and go with the stuff that really works: D3.

D3, or cholecalciferol, yields confident increases in blood levels. It is inexpensive, safe, and an exact copy of the human form of vitamin D. (Of course, gelcap or drops only, NEVER tablets.)

There is absolute NO reason to take vitamin D2, the form that sometimes works, sometimes doesn't, the facsimile plant form issued by the drug industry.

Why don't stents prevent heart attack?

12. February 2009 William Davis (11)


No study has ever documented that stents prevent future heart attack. But, in day-to-day practice, stents are frequently implanted for just this reason.

A little clarification. Stents do prevent heart attack--if the heart attack is already underway, either as an "acute myocardial infarction" or "unstable angina."

In other words, a plaque in a coronary artery can rupture just like a little volcano. Rather than spewing lava, the underlying plaque contents--fibrous tissue, inflammatory cells, cholesterol crystals, fatty material, debris--are exposed to flowing blood and trigger spasm of the artery and blood clot formation. A ruptured plaque is typically found in people who go to the emergency room with severe chest pain or have difficulty breathing.

A heart catheterization is performed, a severe (e.g., 90-100%--completely closed) is found. A stent in this situation is of clear-cut benefit.

What is not clearly beneficial is someone with no symptoms, symptoms only with physical activity that has been present for at least several months, or someone with a high heart scan score and no symptoms. In these circumstances, stent implantation does not reduce risk for future heart attack.

Why?



Take a look at this angiogram of a right coronary artery. You can seen plaque all along the artery (represented by areas that appear pinched off. There are at least 4 visible.)

Putting one 15 millimeter stent in the artery will only affect the area of artery stented. (Stents vary in length, but typically are 12-18 millimeters in length.) The right coronary artery is about 10 times or more this length. There are also two other arteries of similar length. A stent at one location will do nothing to affect the potential for rupture in any of the other plaque-laden areas.

Say a stent is implanted in the "worst" blockage in this right coronary artery, the plaque located at around 9 o'clock. What about all the other plaques? They can still rupture.

Why not put in many stents, say, 4 or 5, and stent all the visible plaques?

Two reasons: 1) Plaque you can't even see on an angiogram can still rupture, and 2) it is very costly (easily $30,000 at the very least), 3) incurs greater procedural risk, and 4) messes up the artery for future procedures, since a steel-lined artery that develops more disease in future will be more difficult to re-implant stents, bypass, or perform other procedural manipulations.

The point: Putting in stents does not reduce potential for plaque rupture in the entire artery.

What can prevent plaque rupture? That's the whole point of following an effective prevention program: prevent plaque rupture.

(Of course, this discussion cannot encompass the wide variety of potential situations that may cause your doctor to individualize your approach. Nonetheless, when advised to have an elective heart procedure, a healthy dose of skepticism and is clearly a good practice.)

Top image courtesy National Heart, Lung, and Blood Institute.

Low thyroid: What to do?

8. February 2009 William Davis (25)
I've gotten a number of requests for solutions on how to solve the low thyroid issue if either 1) your doctor refuses to discuss the issue or denies it is present, or 2) there are government mandates against thyroid correction unless certain (outdated) targets are met.

Oh, boy.

While I'm not encouraging anyone to break the laws or regulations of their country (and it's impossible to generalize, with readers of this blog originating from over 30 countries), here are some simple steps to consider that might help you in your quest to correct hypothyroidism:

--Measure your body temperature--First thing in the morning either while lying in bed or go to the bathroom and measure your oral temp. Record it and, if it is consistently lower than 97.0 degrees (Fahrenheit), show it to your doctor. This may help persuade him/her.(You can still be hypothyroid with higher temperatures, but if low temperatures are present, it is simply more persuasive evidence in favor of treatment).

--Supplement with iodine 150 mcg per day to be sure you are not iodine deficient. This is becoming more common in the U.S. as people avoid iodized salt. It is quite common outside the U.S. An easy, inexpensive preparation is kelp tablets.

--Show your doctor a recent crucial study: The HUNT Study that suggests that cardiovascular mortality begins to increase at a TSH of only 1.5 or greater, not the 5.5 mIU usually used by laboratories and doctors.

--Ask people around you whether they are aware of a health practitioner who might be willing to work with you, or at least have an open mind (sadly, an uncommon commodity).

Also, see thyroid advocate and prolific author, Mary Shomon's advice on how to find a doctor willing to work with you. Yes, they are out there, but you may have to ask a lot of friends and acquaintances, or meet and fire a lot of docs. It shouldn't be this way, but it is. It will change through public pressure and education, but not by next week.

Another helpful discussion from Mary Shomon: The TSH Normal Range: Why is there still controversy? You will read that even the endocrinologists (a peculiarly contentious group) seethingly debate what constitutes normal vs. low thyroid function.

Also, you might remind a resistant health practitioner that guidelines are guidelines--they are not laws that restrain anyone. They are simply meant to represent broad population guidelines that do not take your personal health situation into consideration.

Which statin drug is best?

8. February 2009 William Davis (7)
I re-post a Heart Scan Blog post from one year ago, answering the question: Which statin drug is best?

I still get this question from patients in the office and online, nearly always prompted by a TV commercial. So let me re-express my thoughts from a year ago, which have not changed on this issue.


The statin drugs can indeed play a role in a program of coronary plaque control and regression.

However, thanks to the overwhelming marketing (and lobbying and legislative) clout of the drug manufacturing industry, they play an undeserved, oversized role. I get reminded of this whenever I'm pressed to answer the question: "Which statin drug is best?"

In trying to answer this question, we encounter several difficulties:

1) The data nearly all use statins drugs by themselves, as so-called monotherapy. Other than the standard diet--you know, the American Heart Association diet, the one that causes heart disease--it is a statin drug alone that has been studied in the dozens of major trials "validating" statin drug use. The repeated failure of statin drugs to eliminate heart disease and associated events like heart attack keeps being answered by the "lower is better" argument, i.e., if 70% of heart attacks destined to occur still take place, then reduce LDL even further. This is an absurd argument that inevitably encounters a wall of limited effects.

2) The great bulk of clinical data examining both the incidence of cardiovascular events as well as plaque progression or regression have all been sponsored by the drug's manufacturer. It has been well-documnted that, when a drug manufacturer sponsors a trial, the outcome is highly likely to be in favor of that drug. Imagine Ford sponsors a $30 million study to prove that their cars are more reliable and safer. What is the likelihood that the outcome will be in favor of the competition? Very unlikely. Such is human nature.

If we were to accept the clinical trial data at face value and ignore the above issues, then I would come to the conclusion that we should be using Crestor at a dose of 40 mg per day, since that was the regimen used in the ASTEROID Trial that achieved modest reversal of coronary atherosclerotic plaque by intravascular ultrasound.

But I do not advocate such an ASTEROID-like approach for several reasons:

1) In my experience, nobody can tolerate 40 mg of Crestor for more than few weeks, a few months at most. Show me someone who can survive and tolerate Crestor 40 mg per day and I'll show you somebody who survived a 40 foot fall off his roof--sure, it happens, but it's a fluke.

2) The notion that only one drug is necessary to regress this disease is, in my view, absurd. It ignores issues like hypertension, metabolic syndrome, inflammatory phenomena, lipoprotein(a), post-prandial (after-eating) phenomena, LDL particle size, triglycerides, etc. You mean that Crestor 40 mg per day, or other high-intensity statin monotherapy should be enough to overcome all of these patterns and provide maximal potential for coronary plaque reversal? No way.

3) Plaque reversal can occur without a statin agent. While statin drugs may provide some advantage in the reduction of LDL, much of the benefit ends there. All of the other dozens of causes of coronary atherosclerotic plaque need to be addressed.

So which statin is best? This question is evidence of the brainwashing that has seized the public and my colleagues. The question is not which statin is best. The question should be: What steps do I take to maximize my chances of reversing coronary atherosclerotic plaque?

The answer may or may not involve a statin drug, regardless of the subtle differences among them.

Dr. Nancy Sniderman, heart scans on Today Show

5. February 2009 William Davis (6)
While shaving this morning, I caught the report by NBC medical expert, Dr. Nancy Sniderman, about her coronary plaque and CT coronary angiogram.

Visit msnbc.com for Breaking News, World News, and News about the Economy




Those of you in the Track Your Plaque program or who follow The Heart Scan Blog know that we should tell Dr. Sniderman and her doctor that:

She has done virtually nothing that will stop an increasing heart scan score! In fact, Dr. Sniderman is now following the "prevention program" that is eerily reminiscent of Tim Russert's program! We all know how that turned out.

It is pure folly to believe that a combination of Lipitor, exercise, and a "healthy diet" (usually meaning a low-fat diet--yes, the diet that promotes heart disease) will stop the otherwise relentless increase in heart scan score.

Dr. Sniderman, please consider:

1) Having the real causes of your coronary plaque identified. (It is highly unlikely to be just LDL cholesterol, though the drug industry is thrilled that you believe this.)

2) Ask yourself (or, if your doctor knew what she was doing, ask her): Why do I have heart disease? LDL cholesterol is insufficient reason--virtually nobody I know has high LDL cholesterol as the sole cause. LDL cholesterol is, at most, one reason among many others, but is insufficient as a sole cause.

3) What is your vitamin D status? Crucial!

4) What is your thyroid status?

5) Fish oil--a must!

6) Do you have lipoprotein(a)? Small LDL?

Just addressing the items on the above checklist would put you on a far more confident path to stop your heart scan score from increasing.

If you were to repeat your heart scan score, my prediction: Your score will be higher by 18-24% per year.

My personal experience with low thyroid

3. February 2009 William Davis (31)
Something happened to me around October-November of last year.

I usually feel great. Ordinarily, my struggles are sleeping and relaxing. As with most people, I have too many projects on my schedule, though I find my activities stimulating and fascinating.

I blasted through a very demanding November, trying to meet the needs of a book publisher. This involved sleeping only a few hours a night for several days on end, all after a full day of office practice and hospital duties.

But it was getting tougher. My concentration was becoming more fragmented. Getting things done was proving an elusive goal. Exercise became a real chore.

Although I usually force myself to go to sleep, I was starting to fall asleep before my usual bedtime, and I was sleeping longer than usual.

It's been a tough winter in Wisconsin. Let's face it: It's Wisconsin. But it's been tough even for this region, with weeks of temperatures consistently below 10 degrees. Even so, I was having a heck of a time keeping warm. Extra shirts, socks, soaking my hands in hot water--none of it worked and I was freezing.

So I had my thyroid values checked:

Free T3: 2.6 pg/ml (Ref 2.3-4.2)
Free T4: 1.20 ng/dl (Ref 0.89-1.76)
TSH: 1.528 uUI/ml (Ref 0.350-5.500)

Normal by virtually all standards. I measured my first morning oral temperature: 96.1, 96.3, 95.9. Hmmmm.

My experience coincided with the Track Your Plaque and Heart Scan Blog conversations about low thyroid being enormously underappreciated, with the newest data on thyroid disease suggesting that a TSH for ideal health is probably 1.5 mIU or less. (More about that: Is normal TSH too high? and Thyroid perspective update .

Could this simply be a case of medical student-oma in which every beginning medical student believes he has every disease he learns about?

Despite the apparently "normal" thyroid blood tests, I took the leap and started taking Armour thyroid, beginning at 1/2 grain (30 mg), increasing to 1 grain (60 mg) after the first week.

Within 10 days, I experienced:

--Dramatic restoration of the ability to concentrate
--A boost in mood. (In fact, the last few blog posts before I replaced thyroid reflect my deepening crabbiness.)
--Large increase in energy, now restored to old levels
--Need for less sleep
--I'm warm again! (It's still <20 degrees, but I get easily stay warm while indoors.)

I am absolutely, positively convinced of the power of thyroid. I am further convinced from the clinical data, patient experiences, and now my own personal experience, that low levels of hypothyroidism are being dramatically underappreciated and underdiagnosed.

I shudder to think of what my life would have been like 6 months or a year from now without correction of thyroid hormone.

Now, the tough question: Why the heck is this happening to so many people?

Speaking availability

3. February 2009 William Davis (5)
Just a quick announcement:

If you would like to hear more about the concepts articulated in The Heart Scan Blog or in the Track Your Plaque program, I am available to speak to your group.

Among the possible topics:

Return to the Wild: Natural Nutritional Supplements That Supercharge Health
Why this apparent "need" for fish oil and other heart-healthy supplements? I discuss why some nutritional supplements make perfect sense when we are viewed in the context of primitive humans living modern lives, while other supplements do little.


Shrink Your Tummy . . .or, Why Your Dietitian is Fat!
Weight loss doesn't have to involve calorie counting, deprivation, or hunger pangs. But the conventional "rules" for weight loss and health have to be broken.

The Politically Incorrect Guide to Extraordinary Heart Health
Heart health is something that you can seize control over, something identifiable, correctable, and . . . reversible. Much of this can be achieved with little or no medication, nor procedures. I detail all the enormously empowering lessons learned through the Track Your Plaque program.


I can also present in-depth yet entertaining discussions on the power of vitamin D, natural cholesterol control, screening for heart disease, and similar topics covered in the blog.

To learn more, just e-mail us at contact@trackyourplaque, or call my office at 414-456-1123.

Learn how to eat from Survivorman

31. January 2009 William Davis (22)

Look no farther than Discovery Channel to learn how humans were meant to eat.

The Survivorman show documents the (self-filmed) 7-day adventures of Les Stroud, who is dropped into various remote corners of the world to survive on little but ingenuity and will to live. Starting without food or water, the Survivorman scrapes and scrambles in the wilderness for essentials to survive in habitats as far ranging as the Ecuadorian rainforest to sub-arctic Labrador.

What does Survivorman have to do with your nutrition habits?

Everything. The lessons we can learn by watching this TV show are plenty.

Survivorman plays out the life we are supposed to be living: slaughtering wild game with simple handmade tools and his bare hands, identifying plants and berries that are safe to eat, trapping fish, scavenging the kill of other predators. He's even resorted to eating bugs and caterpillars, particularly following several days of unsuccessful hunting and scavenging.

What is notable from the Survivorman experience is what is absent: In the steppe, desert, tundra, or jungle, you will not find bread, fruit drinks, or Cheerios. You won't find farm-fattened, corn-fed livestock with meat marbled with fat.

Imagine the result of such an experience for us, drawn out over 6 months. Even an obese, diabetic, gluttonous, XXX dress size 350-lb woman would return a lean 105 lbs, size 0, non-diabetic, fully able to run miles in the wild tracking game.

Survivorman's quiet desperation of living in the wild, preoccupied with worries over where his next meal might be found, is a stark contrast to the bloated, shelves stacked floor-to-ceiling supermarkets, and our modern society's all-you-can-eat several times per day lifestyle.

Am I advocating selling the car and house and chucking modern society for the "safety" of the jungles of Borneo?

No, of course not. I am advocating taking a lesson from the clever experiment conducted by Mr. Stroud, a return-to-the-wild experience that should teach us something about how perverse our modern nutritional lives have become.

You just THINK you're low-carb

27. February 2010 William Davis (72)
Systematically checking postprandial (after-eating) blood sugars is providing some great insights into crafting a better diet for many people.

I last discussed the concept of postprandial glucose checks in To get low-carb right, you need to check blood sugars.

Here are some important lessons that many people--NON-diabetic people, most with normal blood glucoses or just mildly increased--are learning:

Oatmeal yields high blood sugars. Even if your fasting blood sugar is 90 mg/dl, a bowl of oatmeal with skim milk, walnuts, and some berries will yield blood sugars of 150-200 mg/dl in many people.

Cheerios yields shocking blood sugars. 200+ mg/dl is not uncommon in non-diabetics. (Diabetics have 250-350 mg/dl.)

Fruits like apples and bananas increase blood sugar to 130 mg/dl or higher.

Odd symptoms, such as mental "fog," fatigue, and a fullness in the head, are often attributable to high blood sugars.

A subset of people with lipoprotein(a) can have wildly increased blood sugars despite their slender build and high aerobic exercise habits.


Once you identify the high blood sugar problem, you can do something about it. The best place to start is to reduce or eliminate the sugar-provoking food.

The LDL-Fructose Disconnect

26. February 2010 William Davis (8)
I believe that we can all agree that the commonly obtained Friedewald LDL cholesterol (what I call "fictitious" LDL cholesterol) is wildly inaccurate. 100%--yes, 100% inaccuracy--is not at all uncommon.

This flagrant inaccuracy, unacceptable in virtually every other discipline (imagine your airplane flight to New York lands in Pittsburgh--close enough, isn't it?), is highlighted in the University of California study by Stanhope et al I discussed previously.

32 participants consumed either a diet enriched with either fructose or glucose. Compared to the effect of glucose, after 10 weeks fructose:

Increased LDL cholesterol (calculated) by 7.6%

Increased Apoprotein B (a measure of the number of LDL particles) by 24%

Increased small dense LDL by 41%

Increased oxidized LDL by 12.6%


In other words, conventional calculated LDL substantially underestimates the undesirable effects of fructose. The divergence between calculated LDL and small LDL is especially dramatic. (By the way, this same divergence applies to the studies suggesting that calculated LDL cholesterol is reduced by low fat diets--While calculated LDL may indeed be reduced, small LDL goes way up, a striking divergence.)

This is yet another reason to not rely on this "fictitious" LDL cholesterol value that, inaccuracies notwithstanding, serves as the foundation for a $27 billion per year industry.

"I dream about bread"

25. February 2010 William Davis (14)
Marion sat in my office, sobbing.

It had been 4 weeks since the last piece of bread, bagel, or bun had passed her lips.

"I can't do it! I just can't do it! I've tried to eliminate wheat, but it's making me crazy. I'm having dreams about bread!"

Yes, Timmy, such dark corners of human behavior are truly unveiled by removing wheat from the diet. (See the previous Heart Scan Blog post, Wheat withdrawal.)

This is a real phenomenon: Wheat is the crack cocaine of the masses. Maybe you don't exchange $100 bills in dark corners of an inner city crack house, but I'll bet you paid $3.99 for your latest fix of French bread.

Just in the last 2 weeks, people in my office who have eliminated wheat have experienced:

14 lbs weight loss in 14 days

Increased mental clarity, reduced moodiness, deeper sleep

70% reductions in small LDL

More than 300 mg/dl reductions in triglycerides

Relief from chronic scalp rash


I could go on.

All the while, the USDA, the American Heart Association, the American Diabetes Association, the American Dietetic Association, the Surgeon General's Office all advise you to eat more "healthy whole grains."

70% of people (NOT 100%, but the majority) will experience unexpected health benefits by eliminating this corrupt, unphysiologic product called wheat from their diet.

You won't know until you try.

Prototypical Lipoprotein(a)

25. February 2010 William Davis (23)
Here's the prototypical male with lipoprotein(a):



Several features stand out in the majority of men with lipoprotein(a), Lp(a):

Slender--Sometimes absurdly so: BMIs of 21-23 are not uncommon. These are the people who claim they can't gain weight.

Intelligent--Above average to way above average intelligence is the rule.

Gravitate to technical work--Plenty of engineers, scientists, accountants, and other people who work with numbers and/or technical details are more likely to have Lp(a).

Enjoy high levels of aerobic performance--I tell my Lp(a) patients that, if they want to see a bunch of other people with Lp(a), go to a marathon or triathlon. They'll see plenty of people with the pattern among the aerobically-elite.

Are rabid fans of Star Trek.


Okay, I made the last one up. But the rest are uncannilly true, shared by the majority (though not all) men with Lp(a).

Why? I can only speculate that the gene(s) for Lp(a) are closely linked to gene(s) for intelligence of a quantitative kind and some factor that enhances aerobic performance or yields a desirable emotional state with exercise.

Oddly, the same patterns tend not to occur in women in Lp(a). I have yet to discern a personality or body configuration phenotype among the ladies.

Gastric emptying: When slower is better

20. February 2010 William Davis (18)
When it comes to the Internet and Nascar, speed is good: The faster the better.

But when it comes to gastric emptying (the rate at which food passes from the stomach and into the duodenum and small intestine), slower can be better.

Slower transit time for foods passing through the stomach leads to lower blood sugar, lower blood glucose area under-the-curve (AUC), i.e., reduced blood glucose levels over time. Lower postprandial (after-eating) blood sugars can reduce cardiovascular risk. It can lead to a reduction in net calorie intake and weight loss.

Strategies that can slow gastric emptying include:

--Minimizing fluids during a meal--Drinking a lot of fluids, e.g., water, accelerates gastric emptying by approximately 20%.

--Cinnamon--While the full reason to explain Cassia cinnamon's blood glucose-reducing effect has not been completely worked out, part of the effect is likely to due slowed gastric emptying. Thus, a 1/4-2 teaspoons of cinnamon per day can reduce postprandial blood sugar peaks by 10-25 mg/dl.

--Vinegar--Two teaspoons of vinegar in its various forms slows gastric emptying. The effect is likely due to acetic acid, the compound shared by apple cider vinegar, white vinegar, red wine vinegar, Balsamic vinegar, and other varieties.

--Increased fat content--Fat is digested more slowly and slows gastric emptying time, compared to the rapid transit of carbohydrates.

Not everybody should slow gastric emptying. Diabetics with a condition called diabetic gastroparesis should not use these methods, as they can further slow the abnormal gastric emptying that develops as part of their disease, making a bad situation worse.

However, in the rest of us with normal gastric emptying time, a delay in gastric emptying can reduce blood sugar and induce satiety, effects that can work in your favor in reducing cardiovascular risk.

Genetic vs. lifestyle small LDL

19. February 2010 William Davis (59)
Let me explain what I mean by "genetic small LDL." I think it helps to illustrate with two common examples.

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

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


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

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


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

Ollie:

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


Stan:

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


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

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

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

Carbohydrate sins of the past

17. February 2010 William Davis (15)
Fifty years ago, diabetes was a relatively uncommon disease. Today, the latest estimates are that 50% of Americans are now diabetic or pre-diabetic.

There are some obvious explanations: excess weight, inactivity, the proliferation of fructose in our diets. It is also my firm belief that the diets advocated by official agencies, like the USDA, the American Heart Association, the American Dietetic Association, and the American Diabetes Association, have also contributed with their advice to eat more “healthy whole grains.”

When I was a kid, I ate Lucky Charms® or Cocoa Puffs® for breakfast, carried Hoho’s® and Scooter Pies® in my lunchbox, along with a peanut butter sandwich on white bread. We ate TV dinners, biscuits, instant mashed potatoes for dinner. Back then, it was a matter of novelty, convenience, and, yes, taste.

What did we do to our pancreases eating such insulin-stimulating foods through childhood, teenage years, and into early adulthood? Did our eating habits as children and young adults create diabetes many years later? Could sugary breakfast cereals, snacks, and candy in virtually unlimited quantities have impaired our pancreas’ ability to produce insulin, leading to pre-diabetes and diabetes many years later?

A phenomenon called glucose toxicity underlies the development of diabetes and pre-diabetes. Glucose toxicity refers to the damaging effect that high blood sugars (glucose) have on the delicate beta cells of the pancreas, the cells that produce insulin. This damage isirreversible: once it occurs, it cannot be undone, and the beta cells stop producing insulin and die. The destructive effect of high glucose levels on pancreatic beta cells likely occurs through oxidative damage, with injury from toxic oxidative compounds like superoxide anion and peroxide. The pancreas is uniquely ill-equipped to resist oxidative injury, lacking little more than rudimentary anti-oxidative protection mechanisms.

Glucose toxicity that occurs over many years eventually leaves you with a pancreas that retains only 50% or less of its original insulin producing capacity. That’s when diabetes develops, when impaired pancreatic insulin production can no longer keep up with the demands put on it.

(Interesting but unanswered question: If oxidative injury leads to beta cell dysfunction and destruction, can antioxidants prevent such injury? Studies in cell preparations and animals suggest that anti-oxidative agents, such as astaxanthin and acetylcysteine, may block beta cell oxidative injury. However, no human studies have yet been performed. This may prove to be a fascinating area for future.)

Now that 50% of American have diabetes or pre-diabetes, how much should we blame on eating habits when we were younger? I would wager that eating habits of youth play a large part in determining potential for diabetes or pre-diabetes as an adult.

The lesson: Don’t allow children to repeat our mistakes. Letting them indulge in a lifestyle of soft drinks, candy, pretzels, and other processed junk carbohydrates has the potential to cause diabetes 20 or 30 years later, shortening their life by 10 years. Kids are not impervious to the effects of high sugar, including the cumulative damaging effects of glucose toxicity.

Saturated fat and large LDL

16. February 2010 William Davis (44)
Here's a half-truth I often encounter in low-carb discussions:

Saturated fat increases large LDL particles


For those of you unfamiliar with the argument, I advocate a low-carbohydrate approach, specifically elimination of all wheat, cornstarch, and sugars, to reduce expression of the small LDL pattern (not to mention reduction of triglycerides, relief from acid reflux and irritable bowel, weight loss, various rashes, diabetes, etc). Small LDL particles have become the most common cause for heart disease in the U.S., exploding on the scene ever since agencies like the USDA and American Heart Association have been advising the public to increase consumption of "healthy whole grains."

This has led some to make the pronouncement that saturated fat increases large LDL, thereby representing a benign effect.

Is this true?

It is true, but only partly. Let me explain.

There are two general categories of factors causing small LDL particles: lifestyle (overweight, excess carbohydrates) and genetics (e.g., variants of the gene coding for cholesteryl-ester transfer protein, or CETP).

If small LDL is purely driven by excess carbohydrates, then adding saturated fat will reduce small LDL and increase large LDL.

If, on the other hand, your small LDL is genetically programmed, then saturated fat will increase small LDL. In other words, saturated fat tends to increase the dominant or genetically-determined form of LDL. If your dominant genetically-determined form is small, then saturated fat increases small LDL particles.

So to say that saturated fat increases large LDL is an oversimplification, one that can have dire consequences in the wrong situation.

Is glycemic index irrelevant?

14. February 2010 William Davis (20)


University of Toronto nutrition scientist, Dr. David Jenkins, was the first to quantify the phenomenon of "glycemic index," describing how much blood sugar increased over 90 minutes compared to glucose. The graph is from their 1981 study, The glycemic index of foods: a physiologic basis for carbohydrate exchange. The research originated with an effort to characterize carbohydrates for diabetics to gain better control over blood sugar.

Since Dr. Jenkins’ original work, thousands of clinical studies have been performed by others exploring this concept. The food industry has also devoted plenty of effort exploiting it (e.g., low-glycemic index noodles, low-glycemic index cereals, etc.).

Most Americans are now familiar with the concept of glycemic index. You likely know that table sugar has a high glycemic index (60), increasing blood sugar to a similar degree as white bread (glycemic index 71). Oatmeal (slow-cooked) has a lower glycemic index (48), since it increases blood sugar less than white bread.

A number of studies have shown that when low glycemic index foods replace high glycemic index foods (e.g., whole wheat bread in place of cupcakes), people are healthier: less diabetes, less heart attack, less high blood pressure. Books have been written about glycemic index, touting its benefits for health and weight control. Health-conscious people will try to substitute low-glycemic index foods for high-glycemic index foods.

So what’s not to like here?

There are several fundamental flaws with the notion that low-glycemic index foods are good for you:

1) Check your blood sugar after a low-glycemic index food like oatmeal. Most non-diabetic adults will show blood sugars in the 140 to 200 mg/dl range. The more central (visceral) fat you have, the higher the value will be. In other words, an apparently “healthy” whole grain food like oatmeal can generate extravagantly high blood sugars. Repeated high blood sugars of 125 mg/dl or greater after eating increase heart disease risk by 50%.

2) Foods like whole wheat pasta have a low glycemic index because the blood sugar effect over the usual 90 minutes is increased to a lesser degree. The problem is that it remains increased for an extended period of up to several hours. In other words, the blood sugar-increasing effect of pasta, even whole grain, is long and sustained.

3) Low-glycemic index foods trigger other abnormalities, such as small LDL particles, triglycerides, and c-reactive protein (a measure of inflammation). While they are not as bad as high-glycemic index foods, they are still quite potent triggers.

Low-glycemic index foods trigger the very same responses as high-glycemic index foods—they’re just less bad. But less bad does not equate to good. Low-glycemic index foods cause weight gain, trigger appetite, increase blood pressure, and lead to the patterns that cause heart disease.

High-glycemic index foods are bad for you. This includes foods made with white flour (bagels, white bread, pretzels). Low-glycemic foods (whole grain bread, whole wheat crackers, whole wheat pasta) are less bad for you—but they are not necessarily good.

Don’t be falsely reassured by foods because they are billed as “low-glycemic index.” View low-glycemic index foods as indulgences, something you might have once in a while, since a slice of whole grain bread is really not that different from a icing-covered cupcake.