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.

Why do the Japanese have less heart disease?

24. April 2011 William Davis (49)
We should look to the Japanese to teach us a few lessons about preventing heart disease. A Japanese male has only 65% of the risk of an American male (despite 40% of Japanese men being smokers), while a Japanese woman has 80% less risk than an American woman. While the U.S. is near the top of the list of nations with highest cardiovascular risk, Japan is the lowest.

What are they doing right?

There is no one explanation, but several. Genetics probably does not play a substantial role, by the way, as demonstrated by observations of Japanese people who emigrate to Western cultures. People of Japanese heritage living in Hawaii, for instance, develop the same cardiovascular risk as non-Japanese living in Hawaii. They also develop obesity and diabetes.

Among the factors that likely contribute to reduced risk in Japanese people:

--A style of eating that does not include a lot of sweet foods. No breakfast cereal or donuts for breakfast, for instance, but miso soup with tofu, fish, green onions, and daikon (as takuan, or pickled radish).
--Seaweed--It's probably a combination of the green phytonutrients and iodine. Typical daily iodine intake is in the neighborhood of 5000 mcg per day from nori, kombu, wakame, and other seaweed forms. (The average American obtains 125 mcg per day of iodine from diet.)
--Seafood--Fish in many forms not seen in the U.S. are popular.
--Green tea--Consumption of green tea has been confidently linked to reduced cardiovascular risk, probably via visceral fat-reducing, anti-oxidative, and anti-inflammatory effects. Although tea in Japan is often the less flavonoid-rich oolong tea, softer benefits from this form are likely.
--Soy--Tofu, miso, and soy sauce are staples. It's not clear to me whether soy is intrinsically beneficial or whether it is beneficial because it serves to replace unhealthy alternatives. (Genetic modification may change this effect.)
--Reduced exposure to cooked animal products (except seafood). This is not a saturated fat issue, but probably an advanced glycation end-product/lipoxidation issue that result from cooking.
--The lack of a "eat more healthy whole grain" mentality, the advice that has plunged the entire U.S. into the depths of a diabetes and obesity crisis (along with high-fructose corn syrup and sugar). Noodles like udon and ramen do have a place in their diet, as do some dessert foods. But the overall wheat exposure is less--no bagels, sandwiches, and breakfast cereals.
--Less overweight and obesity--The above eating style leads to less weight gain.

Japanese foods have a unique taste, consistency, and mouth-feel that go well with saltiness, thus the downside of their diet: salt consumption. On a broad scale, high salt consumption has been associated with hypertension and gastric cancer. But the tradeoff has, on the whole, been a favorable one.


One study trying to find some answers:

Dietary patterns and cardiovascular disease mortality in Japan: a prospective cohort study.

Shimazu T, Kuriyama S, Hozawa A et al.
Division of Epidemiology, Department of Public Health and Forensic Medicine, Tohoku University Graduate School of Medicine, Japan.


We prospectively assessed the association between dietary patterns among the Japanese and CVD mortality. Dietary information was collected from 40 547 Japanese men and women aged 40-79 years without a history of diabetes, stroke, myocardial infarction or cancer at the baseline in 1994.
During 7 years of follow-up, 801 participants died of CVD.

Factor analysis (principal component) based on a validated food frequency questionnaire identified three dietary patterns: (i) a Japanese dietary pattern highly correlated with soybean products, fish, seaweeds, vegetables, fruits and green tea, (ii) an 'animal food' dietary pattern and (iii) a high-dairy, high-fruit-and-vegetable, low-alcohol (DFA) dietary pattern. The Japanese dietary pattern was related to high sodium intake and high prevalence of hypertension. After adjustment for potential confounders, the Japanese dietary pattern score was associated with a lower risk of CVD mortality (hazard ratio of the highest quartile vs the lowest, 0.73; 95% confidence interval: 0.59-0.90; P for trend = 0.003). The 'animal food' dietary pattern was associated with an increased risk of CVD, but the DFA dietary pattern was not.

The Japanese dietary pattern was associated with a decreased risk of CVD mortality, despite its relation to sodium intake and hypertension.

Niacin: What forms are safe?

20. April 2011 William Davis (52)
Niacin, or vitamin B3, remains a confusing issue for many people. It shouldn't be.

It doesn't help that most physicians and many pharmacists also do not understand the basic issues surrounding niacin. The only reason why there is any level of prevailing knowledge about niacin is that Kos Pharmaceuticals managed to "pharmaceuticalize" a niacin preparation, prescription Niaspan, that provided the revenue to fund professional "education."

Niacin can be helpful to increase HDL, reduce small LDL particles and shift them towards the more benign large particles, reduce triglycerides, and reduce lipoprotein(a).

So here's a brief description of the various forms that you will find niacin:

Immediate-release niacin--Also called crystalline niacin or just niacin. This is the original niacin that releases within minutes of ingestion. Because it releases rapidly, it triggers the most intense "hot flush." While this form of niacin works wonderfully well, is the safest, and is dirt cheap, the majority of people are simply unable to tolerate the intense flush. It also works best taken twice a day, generating two intolerable flushes per day.

Slow-release niacin--These preparations were popular in the 1980s, since the slow 12 to 24 hour pattern of release minimized the annoying hot flush. But, with prolonged use, it also became apparent that an unnaceptable frequency of liver toxicity developed. Unfortunately, this means that any niacin preparation that trickles niacin out over an extended period, including many of the slow-release preparations now sold in health food stores and pharmacies, have potential for liver toxicity. These preparations should be avoided.

6-hour release niacin--Releasing niacin more slowly than immediate-release niacin but more rapidly than slow-release niacin, 6-hour release (or what the Niaspan people call "extended-release" niacin) is nearly as effective as immediate-release niacin with approximately the same low potential for liver toxicity. It is far less liver toxic than slow-release niacin. 6-hour release niacin therefore offers the best balance between effectiveness and safety. Preparations that show this pattern of release include Niaspan ($180 per month), the poorly-named Sloniacin (about $8 per month), and Enduracin (about $7 per month) for 1000 mg per day. (Some Track Your Plaque Members have also determined that several other over-the-counter preparations have been demonstrated to share a similar pattern of release.)

Then there are the scam products that have no useful effect at all:

Flush-free or no-flush niacin--Inositol hexaniacinate, or 6 niacin molecules bound to the sugar, inositol, has no effect in humans, at least not with the dozen or so preparations that I've seen used. Nor are there any data to document the effectiveness of flush-free niacin. It's also more expensive.

Nicotinamide--This niacin derivative likewise has no effect on the usual targets for niacin treatment.

While I used to prescribe Niaspan, the ridiculous pricing and aggressive marketing really turned me off. I now advise my patients and our online followers to use only Sloniacin or Enduracin, unless you can tolerate immediate-release niacin.

Introduction to the New Track Your Plaque book, version 2.0

18. April 2011 William Davis (0)

Out with the old,
in with the new  



“I believe that you are suffering from what is called a fatty degeneration of the heart.”

Dr. Tertius Lydgate to Mr. Casaubon on making a diagnosis with the new medical device, the stethoscope.

George Elliot
Middlemarch, 1871





Old notions in medicine have a peculiar way of lingering.

In 1882, Dr. Robert Koch discovered the tubercle bacillus in tissues of people with “consumption.” By connecting a bacterium with the disease, he usurped the long held notion that tuberculosis was a degenerative disease caused by lack of fresh air. But, for decades after Dr. Koch’s revelation, the “bad air” belief persisted. Surgical collapse of the lung, a painful and barbaric treatment for tuberculosis, persisted well into the 1960s, years after effective antibiotics were discovered in 1947.

The medical community of the 19th century viewed mental illness as the hereditary end-product of ancestral nervousness, alcoholism, prostitution and criminal behavior, a bias that remained widespread well into the mid-20th century. Nazi physicians invoked the theory of heritable “mental degeneration” to justify wholesale extermination of schizophrenics. Electro-convulsive therapy (ECT, or “electroshock therapy”) was widely applied to treat schizophrenia, depression, homosexuality, and criminal behavior for over 30 years, gradually abandoned (at least in its original form) after years of abusive application to subdue patients, demonized in the 1975 movie, “One Flew Over the Cuckoo’s Nest,” depicting the author’s real-life experience with ECT.

Long after a theory or practice has been discredited, it can persist, refusing to die. The new and improved may not be adopted into mainstream practice for years, even decades.

Back to the 21st century: What if you realized that, by quirks of human nature and the uneven adoption of health information, your doctor practiced medicine appropriate for 1985? 1975?

While digital information nowadays is transmitted at the speed of light, disseminating as fast as it takes the next juicy tidbit to be “virally” reproduced via social networking websites, it’s the human factor that still operates with the inertia of human behavior. Habits and attitudes slow the adoption of new information in time measured not in seconds, but in years or decades.

A century ago, 20 years were required for the new technology of blood pressure measurement to be adopted after its introduction in the U.S. in 1910, since physicians were long comfortable with the practice of “pulse palpation” (feeling the pulse). (The arcane language of pulse palpation persists to this day, terms like “pulsus parvus et tardus,” the slow rising pulse of a stiff aortic valve; and the "water-hammer" pulse of a leaking aortic valve.)

The discovery of new, health-changing information today in the 21st century disseminates through the ranks of modern healthcare providers at much the same pace as measuring blood pressure did in the early 20th century.

It’s also tempting to paint American medicine as a fiefdom intent on maintaining exclusive rein over health information. Look back over the hierarchical relationship of medicine over nursing in the past century: When blood pressure measurement was adopted on a broad scale in the 1930s, it was practiced only by physicians, since nurses were deemed incapable. (Modern-day nurses should surely have a hearty laugh over this.) Stethoscopes, around even longer than blood pressure cuffs, weren’t permitted to fall into the hands of nurses until the 1960s, since the medical community feared that nurses might command too much control over patient care. Even after nurses were permitted to have their own stethoscopes, great pains were taken to be certain the nurses’ version was readily distinguishable from the “real” tool wielded by physicians; nurses’ stethoscopes were therefore labeled “nurse-o-scopes,” or “assistoscopes,” and were required to be smaller and flimsier.

Old and ineffective doesn’t always give way to new and better at once; it is slowed by habit as well as an unwillingness to relinquish control.

Somehow technology marches on. But it does so unevenly, sweeping some along in its first wave, others in its wake, some never at all.

Just as effective antibiotics to cure tuberculosis were available for 20 years while surgeons continued to remove patients’ lungs, so better solutions to heart disease are already available but not yet employed by your neighborhood physician. The primary care physician may have heard about some of the newest means to prevent heart disease, but is too overwhelmed with the day-to-day of sore throats, diarrhea, and rashes. Cardiologists, intent on inserting the next best stent or defibrillator, have little but passing interest in strategies that might halt or reverse the heart disease that can be “managed,” no matter how imperfectly, with procedural solutions like angioplasty and bypass surgery. We should bear these flawed human tendencies in mind as we explore the world of heart disease prevention.

We need look no farther than the front page of the newspaper to find evidence of the failure of present-day heart disease detection and management. Over the past several years, headlines have carried the likes of Tim Russert, Bill Clinton, Larry King, Dick Cheney, David Letterman, Tommy Lasorda, Ed Bradley, Mike Ditka, Walter Cronkite, Alberto Salazar, all heart disease sufferers. Some, like talk show host David Letterman, survived their brush with heart catastrophe and underwent successful bypass surgery. Others, like marathoners Fixx and Salazar, raised none of the conventional red flags for heart disease. All received standard, “modern” medical care . . . all the way up to their heart attack, bypass surgery, or untimely death.

Like the sphygnomanometer (blood pressure) cuffs of 1910, Track Your Plaque represents an example of the new. But, unlike the simple practice of taking blood pressure in the early 20th century, Track Your Plaque represents an entirely new way to look at coronary heart disease: a new way to measure it, a new way to identify its causes, and a new way to seize control over it, often to the point of achieving reversal of the process. It also puts control over much of this process into your hands and away from hospitals, cardiologists, and heart procedures. 

I could speak of revealing “secrets,” but that’s not true. In Track Your Plaque, I simply convey information about heart disease that you were likely unaware existed, strategies that doctors fail to discuss. I assemble them into a “package” that, together, create an enormously empowering unique approach to prevent heart disease and heart attack.

Track Your Plaque also challenges the high-tech status quo, practices that occupy exalted places in the enormous cardiovascular healthcare machine that has dominated American healthcare for the past 40 years. I propose that high-tech hospital procedures should join the practice of ECT for homosexuality and insanity¾and become yet another relic of the past.

What are "normal" triglycerides?

12. April 2011 William Davis (67)
Among the most neglected yet enormously helpful values on any standard cholesterol panel is the triglyceride value.

Triglycerides traverse the bloodstream by hitching a ride on water (serum)-soluble lipoproteins, or lipid-carrying proteins. We measure triglycerides as an indirect index of triglyceride-containing lipoproteins.

Triglycerides are a basic currency of energy. While the average American ingests around 300 mg of cholesterol per day, he or she also ingests 60,000-120,000 mg (60-120 grams) of triglycerides, i.e., 200 to 400 times greater amounts, from fat intake. Zero triglycerides in the diet or in the bloodstream is not an option.

But what represents too much triglycerides in the bloodstream? There are several observations to help us make this determination:

1) When fasting triglycerides are 133 mg/dl or greater, 80% of people will show show at least some degree of small LDL particles.

2) When fasting triglycerides are 60 mg/dl or less, most (though not all, since genetic factors enter into the picture) people will show little to no small LDL particles.

3) When fasting triglycerides are 200 mg/dl or greater, small LDL particles will dominate and large LDL particles will be in the minority or be gone entirely.

4) When triglycerides are 88 mg/dl or greater after eating, then risk for heart attack is doubled. Non-fasting triglycerides in the 400+ mg/dl range are associated with 17-fold greater risk for heart attack.



From Austin et al 1990. "Phenotype A" means that large LDL particles dominate; "phenotype B" means that small LDL particles dominate.

Note that conventional "wisdom" (i.e., NCEP ATP-3 guidelines) is that triglycerides of up to 150 mg/dl are okay, a level that virtually guarantees expression of small LDL particles and increased cardiovascular risk.

Based on observations like these, in the Track Your Plaque program we aim for fasting triglycerides of no higher than 60 mg/dl and postprandial (after-meal) triglycerides of no more than 90 mg/dl.

Curiously, while fat intake (i.e., triglyceride intake) plays a role in determining postprandial triglyceride blood levels, it's carbohydrate intake that plays a much larger role. That will be an issue for another day.

1985: The Year of Whole Grains

9. April 2011 William Davis (30)
In 1985, the National Cholesterol Education Panel delivered its Adult Treatment Panel guidelines to Americans, advice to cut cholesterol intake, reduce saturated fat, and increase "healthy whole grains" to reduce the incidence of heart attack and other cardiovascular events.

Per capita wheat consumption increased accordingly. Wheat consumption today is 26 lbs per year greater than in 1970 and now totals 133 lbs per person per year. (Because infants and children are lumped together with adults, average adult consumption is likely greater than 200 lbs per year, or the equivalent of approximately 300 loaves of bread per year.) Another twist: The mid- and late-1980s also marks the widespread adoption of the genetically-altered dwarf variants of wheat to replace standard-height wheat.

In 1985, the Centers for Disease Control also began to track multiple health conditions, including diabetes. Here is the curve for diabetes:


Note that, from 1958 until 1985, the curve was climbing slowly. After 1985, the curve shifted sharply upward. (Not shown is the data point for 2010, an even steeper upward ascent.) Now diabetes is skyrocketing, projected to afflict 1 in 3 adults in the coming decades.

You think there's a relationship?

Have some more

7. April 2011 William Davis (37)
Wheat, via exorphin effects, is an appetite stimulant. Eat a whole wheat bagel or bran muffin, you want another. You also want more of other foods. You also want something to eat every two hours due to widely-swinging insulin-glucose responses: blood sugar high followed by a sharp downturn that triggers a powerful impulse to eat (thus the cravings for a snack at 9 and 11 a.m. after a 7 a.m. breakfast).

If wheat is a stimulant of appetite, then removing it should yield reduced appetite and reduced calorie intake. That is precisely what happens.

When wheat products are removed from the diet--without calorie restriction, without counting fat or carbohydrate grams, no exercise program, no cleansing regimen, no skipping meals . . . nothing--calorie intake drops 350 to 400 calories per day. This calorie figure remains curiously consistent across multiple studies in which wheat was eliminated.

400 calories per day results in 21 lbs lost over 6 months, based just on calories. (3500 calories per pound lost.) That is what happens in wheat elimination diets: 21-26 lbs lost over 6 months.

Wheat is the processed food industry's nicotine, a means of ensuring repeat food purchases. It's also low-cost (subsidized by the U.S. government), high-yield, an ingredient that even has its very own withdrawal syndrome should you miss a "hit."
Gretchen's postprandial diet experiment II

Gretchen's postprandial diet experiment II

3. January 2010 William Davis (37)
I previously posted Gretchen's postprandial diet experiment, in which she consumed a low-fat diet for a day, followed by a low-carbohydrate diet for a day. Grethen monitored blood glucose and triglycerides with fingerstick checks. (Blood glucose can be checked on any widely available glucose monitor; triglycerides can be monitored with the Cardiochek device.)

Let's now discuss what happened.

On the low-carb, high-fat day, there was an initial surge in triglycerides to 250 mg/dl late morning, followed by a secondary peak several hours following dinner. Because fat is mostly triglycerides, Gretchen's high-fat (sausage, bacon, butter, whole-fat yogurt) breakfast provided a large quantity of triglycerides that needed to be absorbed. This generally occurs over approximately 6 hours, varying depending on body weight, how accustomed you are to fat, activity level during the day, the kind of fat in the meal. The high content of saturated fat in Gretchen's high-fat breakfast likely caused the somewhat slower drop in triglycerides over approximately 7 1/2 hours.

As Gretchen herself had noted, triglycerides the following day were lower, a typical low-carb response. Blood sugar throughout showed only minor variation, with only small postprandial increases.

Thus, Gretchen experienced what we'd expect with a low-carb, high-fat diet: an initial high surge in triglycerides, followed by a decline in fasting levels, while blood sugar shows a normal contour.







Now, the more confusing low-fat experience:



Blood glucose makes a striking peak at 200 mg/dl after the low-fat breakfast of pasta and rice, in contrast to the low-carb breakfast. Triglycerides behaved very differently from the low-carb experiment: While there was no initial postprandial surge, there was a late surge developing 6-24 hours later. The late surge continued into the next day, with fasting levels the following morning (210 mg/dl) exceeding the starting triglyceride level (60 mg/dl).

The one potentially confusing aspect of all this is Gretchen's late rise in triglycerides on the low-fat diet. This phenomenon is due to something called de novo lipogenesis, or the liver's conversion of carbohydrates to triglycerides that occurs when an excessive carbohydrate load comes through diet. Because the human body cannot store anything beyond a minor quantity of carbohydrates (as glucose and glycogen), carbohydrates are converted to fats.

Another factor causing the late triglyceride increase is insulin resistance, given the high blood sugar response. When insulin resistance is present, the activity of the enzyme, lipoprotein lipase, is reduced. Less lipoprotein lipase activity allows slower VLDL degradation, allowing VLDL (and thereby triglycerides contained in VLDL) to "stack up" in the blood. Thus, the higher triglycerides late after eating and into the next morning.

One issue to be aware of: Acute responses can differ from chronic responses. In other words, had Gretchen had the luxury (and time and money) to conduct the experiment over, say, 4 weeks, rather than a single day, there would be somewhat different responses. The best data on this come from Dr. Jeff Volek of the University of Connecticut, in which 4 weeks of low-carbohydrate eating modify fasting and postprandial responses over time.

Several conclusions can be made from Gretchen's experience:

1) Low-carb, high-fat acutely generates extravagant postprandial triglyceride responses.
2) Low-fat causes a late triglyceride surge and higher fasting triglycerides.
3) Low-fat leads to high blood sugars and, by implication, diabetes.


Both the low-carb and the low-fat responses are undesirable, both leading to increased risk for heart disease. Which is worse? I believe that low-fat is more destructive, since it leads over time to both high triglycerides and diabetes, while low-carb/high-fat only leads to postprandial triglyceride surges, at least acutely.

How to best balance the responses to reduce risk for heart disease? That's a discussion for future.


Again, my thanks to Gretchen and the substantial amount of effort that went into generating these numbers. More of Gretchens' own writing can be found on her blogs:
http://wildlyfluctuating.blogspot.com
http://www.healthcentral.com/diabetes/c/5068
Tags :

Comments (37) -

  • Pythonic Avocado

    1/3/2010 3:53:05 PM |

    Why do you say the low-carb response  is leading to increased risk for heart disease?

  • Stan (Heretic)

    1/3/2010 5:34:56 PM |

    Re: Both the low-carb and the low-fat responses are undesirable, both leading to increased risk for heart disease.

    With due respect, I would disagree that BOTH are undesirable, but I agree that the one caused by the low fat high carb diet (only) is indeed dangerous!  

    It was never proven that high triglycerides alone cause heart disease.  The available trials such as Framingham (1)  may have shown some correlation with the total cholesterol but correlation is not causuation, especially that the statistics do not distinguish between various diets. Furthermore, Framingham's correlation is restricted to men only (not women) and only for the age group 30-55.  For older men and for women of all ages the correlation becomes insignificant or reversed.

    Given the above data, I think the most plausible interpretation leads me to a conclusion that the most likely direct cause of atherosclerotic cardiovascular disease is excessive blood glucose with hyperinsulinemia  (see the following papers, and Stout's papers(2) ).

    Hyperglycemia and hyperinsulinemia also happen to coincide with elevated TG and LDL but those are coincidental markers of metabolic syndrome induced by the common high carb (high sugar) diets rather than causing heart disease.  That I believe has nothing to do with dietary fat.

    Regards,
    Stan (Heretic)

    -----------
    Refs:

    1) JAMA. 2004 May 12;291(18):2243-52. Drug treatment of hyperlipidemia in women. Walsh JM, Pignone M.

    2) INSULIN-STIMULATED LIPOGENESIS  IN ARTERIAL  TISSUE  IN RELATION  TO DIABETES AND ATHEROMA,
    R.W. STOUT, Lancet Sept 28, 1968, p702.

    and

    INSULIN STIMULATION OF CHOLESTEROL
    SYNTHESIS  BY ARTERIAL TISSUE,
    R.W. STOUT, Lancet Aug 30, 1969, p467.

  • Nigel Kinbrum BSc(Hons)Eng

    1/3/2010 5:41:31 PM |

    As serum TG's with the HF meal are lower at the end of the day than at the beginning, does this suggest that successive days of HF meals produce progressively lower & lower TG's?

  • Anonymous

    1/3/2010 6:02:56 PM |

    I would love to hear about how to balance the risk between these extremes!  Wow, nice post.

  • Dr. William Davis

    1/3/2010 10:11:35 PM |

    Pythonic and Stan--

    It's not that triglycerides per se are atherogenic, but the POSTPRANDIAL PARTICLES that triglycerides represent are atherogenic.

    In other words, high triglycerides signals extravagant chylomicron remnants and VLDL, both of which are atherogenic.

    In the ongoing debate over what constitutes a healthy or unhealthy diet, the entire issue of postprandial patterns has been ignored. Yet much of heart disease develops IN THE POSTPRANDIAL PERIOD.

  • shel

    1/3/2010 10:55:38 PM |

    i eat copious amounts of fat with positive effects. i'm a layman, but "postprandial" or not, i'm having a hard time accepting this, as the evidence i've read seems to contradict what you're saying regarding overall benefits.

    why did no one pick up on the "postprandial particle" issue until now?

    will this be a new controversy sweeping through the paleo/low carb blogging community now? ;)

  • Dr. William Davis

    1/4/2010 2:15:45 AM |

    Anyone desiring a full accounting of the hundreds of studies documenting this effect will need to refer to the Track Your Plaque Special Report, Postprandial Lipoproteins: The Storm After the Quiet.

    This literature is, unfortunately, relatively difficult to understand. But just because nobody else has incorporated these findings into diet advice doesn't mean it isn't important.

    Keep in mind that most dietary advice is NOT based on observation of postprandial phenomena.

  • Eric

    1/4/2010 5:53:50 AM |

    I had a stroke last month. (Very minor, I went immediately back to work.)  As a 35 year old non-smoker/non-drinker who generally ate low carb and avoided sweets before the stroke (and had been exercising regularly for 6 weeks), I'm baffled as to why my triglycerides are between 600 and 900.  I'm now on Lovaza.  Against my doctor's advice, I decide to do a paleo type diet.  We'll see how the lipid panel does at the end of this month, but so far avoiding wheat and grains has generally made me feel better.  I've lost some weight as a bonus.

    The doctor is blaming my triglycerides for the stroke, and just calling it hereditary.  It'd be nice to know just what gene I have that causes strokes!  No blood clotting disorders, no diabetes, no pancreaitis, and no hole in my heart either.

  • Alen Kcatic

    1/4/2010 10:58:09 AM |

    First let's take a brief overall look at heart disease because you need to combine two other major lifestyle habits with diet to truly make a difference in reversing or preventing heart disease.


    But here's the good news. You can prevent or reverse heart disease by following care

    Avoid tobacco
    Be more active and walk 30 minutes
    Choose healthier food, including more fiber, less saturated fat, and less salt.

  • Peter

    1/4/2010 12:38:21 PM |

    If it were as simple as low fat leads to diabetes, the Japanese who ate the traditional low fat high rice diet would have had extremely high levels of diabetes, but they hardly had any. I would be more inclined to wonder if our diabetes epidemic is due specifically to flour and sugar rather than low fat in general.

  • shel

    1/4/2010 4:27:36 PM |

    ~Dr Davis, i wonder if this finding is going to point toward advocation of "grazing", rather than two or three meals per day (in a low carb context).

  • kris

    1/4/2010 6:04:12 PM |

    Dr. Davis,
    Happy new year.
    here is the link to videos about FDA and drug giants. An eye opener. just in case you have not looked at it. total of 8 videos.
    http://www.veoh.com/search/videos/q/generation+rx#watch%3Dv18919526gZ4fkAAk

  • StephenB

    1/4/2010 7:16:32 PM |

    Dr. Davis, the abstract of the study you linked read: "Ten men consumed a low-carbohydrate diet rich in monounsaturated fat (MUFA) and supplemented with n-3 fatty acids for eight weeks."

    As you know, there are multiple low carbohydrate diets. This particular study did not examine a high saturated fat diet. I would love to see the result of chronic dieting featuring quality saturated fats like tallow, lard, butter, and coconut milk and avoiding hydrolyzed fats.

  • mark

    1/4/2010 7:19:28 PM |

    Dr. Davis wrote:
    "The one potentially confusing aspect of all this is Gretchen's late rise in triglycerides on the low-fat diet. This phenomenon is due to something called de novo lipogenesis, or the liver's conversion of carbohydrates to triglycerides that occurs when an excessive carbohydrate load comes through diet. Because the human body cannot store anything beyond a minor quantity of carbohydrates (as glucose and glycogen), carbohydrates are converted to fats."

    We don't see triglycerides being converted to glucose. It's a one way street.

    Would having increased carbohydrayte storage space in the body be preferable to storing triglyceride? We have an example of that in hyperglycemia. That's storage in the bloodstream. But the body works quickly to CORRECT that.

    So it's not that the body lacks glucose storage and triglyceride is the bad alternative. Not that at all. The body works hard to push glucose out of blood storage and into triglyceride in fat cells. That's a good thing.

    Postprandial high triglycerides from a high fat diet is a marker of fat intake. Postprandial low triglyceride on a high carb diet is a marker of carbohydrate metabolism. The later increase in triglyceride is the corrective process.

    It's hard to make the case that triglyceride is itself bad when it's one of the body's innate responses to the bad hyperglycemia. If triglyceride is bad, then the body is stuck between a rock and a hard place. It's win-lose, so the low fat diet is worse than the low carb one.

    Given my experience with dieting, I would favour low carb over anything balanced in the way of fat/carb. From dietary intervention trials, I'm unconvinced that high fat is worse (or much better) than a mixed blend of carb and fat from a mortality perspective. But from experience, I favour low carb for general sense of well-being.


    Stan wrote:
    "Hyperglycemia and hyperinsulinemia also happen to coincide with elevated TG and LDL but those are coincidental markers of metabolic syndrome induced by the common high carb (high sugar) diets rather than causing heart disease. That I believe has nothing to do with dietary fat."

    It's tough to isolate lipids as causal as opposed to effects of diet. Smoking and fructose lead to increased LDL. So in this case, high LDL is really a symptom smoking and fructose intake. The latter two likely being causal for anything related to your health. 8 egg yolks a day on a high fat diet and your LDL is a symptom of that. And some people have normal LDL on that even.

    Mark.

  • Dr. William Davis

    1/4/2010 11:33:43 PM |

    Hi, Shel--

    No, absolutely not.

    Quite the opposite: Given what happens after eating, grazing is a destructive practice that likely increases risk for heart disease.

    See the previous Heart Scan Blog post: http://heartscanblog.blogspot.com/2009/11/triglyceride-and-chylomicron-stacking.html

  • shel

    1/4/2010 11:52:20 PM |

    ~hi Dr Davis.

    i agree. and i do much better when i eat two meals within an eight hour window.

    my focus has always been on keeping blood glucose low (i'm not diabetic, but use a glucose meter for my own curiosity), so was a bit floored by the thought that i have to watch every postprandial spike!

    ...so, what's left? huge salads and skinless chicken breasts? ;)

  • vin

    1/5/2010 9:33:36 AM |

    It is pure and simple observation of two parameters after eating a low carb and low fat meal. Nothing more that that.

    After all most of us eat more than just carbs and fat: there are vitamins, enzymes, minerals, fiber and hundreds of other nutrients. I am certain that they more than compensate any damage that glucose or triglycerides can cause to your arteries.

  • Dr. William Davis

    1/5/2010 4:39:02 PM |

    Sorry, Vin.

    You're kidding yourself if you belief that.

    It reminds me of the people I meet who take a list of supplements 30 items long (though lacking the most crucial like vitamin D) prior to their bypass or heart attack. That's called magical thinking.

  • Kurt

    1/5/2010 9:27:14 PM |

    Both diets seem to be extremes, whereas many of us are trying to eat a balanced diet of vegetables, lean meats, nuts, and some legumes and whole grains - call it moderate fat and moderate carbohydrate - but focusing on heart-healthy foods. I'd like to see postprandial data on that.

  • O

    1/5/2010 10:39:05 PM |

    I have been eating a primal low-carb diet for almost 2 years and feel great.  My fasting blood work is : trig = 40, HDL=88, LDL=114 (calculated), total chol=214, testosterone=606.  My heart scan score is 0.  I am physically active muscular male with 4 intense weights + some cardio workouts 2 hours each.  My bodyfat % is about 8-10% (I can see a clear 6-pack), age=43, height=5'7", weight=160 lbs.

    I have made an analysis of my daily intake in a spreadsheet.  My diet on workout days is 3000 kcal, of which 50% fat (167g, out of which 60g saturated), 20% carbs (150g), and 30% protein (200g).  Half the carbs are timed post-workout (workout shake, followed by dinner of meat + sweet potato).  On a non-workout days, I do not have a shake nor sweet potatoes, so the carbs drop to 10% (70g).

    Given the amount of fats I take every day, I am rather alarmed by the postprandial triglycerides.  My breakfast, in particular, has 57g of fat which will cause probably a substantial postprandial triglycerides.  Breaking up my food intake into many smaller meals doesn't seem to be a good thing.   We don't want increasing carbs or protein at expense of fats either.  Therefore, what is the solution here?

  • Dr. William Davis

    1/5/2010 11:21:32 PM |

    O--

    I am afraid there's no quick answer. That question is answered in an exhaustive report on the Track Your Plaque website.

    Alternatively, you could conduct your own do-it-yourself postprandial triglyceride test.

  • Anonymous

    1/6/2010 3:17:23 PM |

    This doesn't detract from any of the points you're making about postprandial triglycerides--but it looks like you're reading the chart from the wrong side here for triglycerides, from the left instead of from the right.

  • Catherine

    1/6/2010 4:16:40 PM |

    YIKES!
    I have been experimenting with a gluten-free, low carb, low sugar diet for 5 months and my LDL just shot UP from 220 to 230 and my HDL went DOWN a little from 66 to 61. (tryglicerides and CRP are excellent). This is opposite what's supposed to happen. Serum D level is good at 54.

    Can someone please tell me the name of the test to request from my doctor to tell if I have the small evil-type LDL or the big fluffy okay-type LDL?

    Thanks for your help,
    Warmly, Catherine

  • Lucy

    1/6/2010 4:33:54 PM |

    These results seem completely contradictory to the way Dr. Eades described the breakdown of saturated fat in his blog "The blood samples were taken two hours after the meal.  Dietary carbohydrate is absorbed directly into the blood and makes a pass through the liver where it stimulates the production of triglycerides, the fat you see in the blood.  Fat, especially long-chain saturated fat digests very slowly, and doesn’t reach the blood until much later than the two hour mark.  While carbs go directly into the blood, fats take a different route."

    Why was there a triglyceride spike after a high fat meal, but not a high carb one?  Were the fats Gretchen consumed not saturated?  It can't be both ways, which metabolic pathway is correct?

  • Catherine

    1/6/2010 9:08:44 PM |

    Oops, sorry i made a mistake.---My LDL went up from 120 to 130 (not 220 to 230)

  • vin

    1/7/2010 11:16:29 AM |

    Thanks for your comment Dr. Davis but for the first time you sound just like my cardiologist. He does not believe in reversal and thinks it is all down to one's genes and there is nothing one can do to change that. Well I think differently having postponed bypass surgery seven years ago. I will continue with 'magical thinking'. Its nice, you should try it sometime.

  • Anonymous

    1/7/2010 4:29:08 PM |

    To eat one extreme one day (low fat) and then eat another extreme (low carb, high fat) the next is a sure-fire way to get whacky blood/lipid results. Also, lipid levels can fluctuate more than 10% within a given day under normal circumstances. Alternating eating radically different extremes in terms of diet is anything but normal in my view.  Stress, exercise, or even one's sex can cause also shifts.  Trying to prevent every potential/alleged problem with postprandial lipids seems like a sure-fire way to increase stress which is also damaging to the heart and body.  I doubt paleo manwoman worried about the spike in his/her triglycerides from gorging on the fat from fatty meat meals.  I think one can micromanage one's self or rather labs, lipids etc to death...

    PS: Forgot to mention lab error.  Before drawing any conclusions from any lab results, have them repeated multiple times and at different labs.  My husband has to communicate with lab techs for his job and was horrified when one kept referring to "esterified" as "stir-fried"! And this was the one of the largest labs in the US...

  • Jim Purdy

    1/18/2010 4:38:41 AM |

    Doctor Davis, have you seen the new PR campaign from manufactured "food" giant Unilever to "Ban butter to save thousands of lives."

    Unilever is the company behind many fake foods, including fake butters Country Crock and  I Can't Believe It's Not Butter!

    I've posted a little about this ban-butter campaign on my blog at blogsthatmakemethink.blogspot.com

  • shoby

    1/28/2010 3:25:55 PM |

    I also have a blog about the diet we can share experiences and exchange links.
    This blog http://just-slim.blogspot.com
    thanks

  • Fran

    2/1/2010 5:51:52 AM |

    "How to best balance the responses to reduce risk for heart disease? That's a discussion for future."

    Please tackle this discussion soon.

  • ET

    2/26/2010 6:52:28 PM |

    I also keep a spreadsheet that details all the different fatty acids and such for every meal.  I've also had three lipid tests this year which were not fasting.  Two were in the afternoon, eight hours after a five-egg omelet with coconut oil, cheese and bacon; 2 hours later I had eight oz of full-fat greek strained yogurt which adds up to over 120 g of fat 6 to 8 hours before the test.  Add another 40 g of fat 2-hours pre-test and according to your theory, my triglycerides should be high.  On each occasion they were 91.  This is on a low-carb (<70g/day) diet.

    There's more to postprandial triglyceride metabolism than is covered here.  My next test will be a non-fasting NMR lipoprotein analysis.  Should be interesting how that stacks up against a fasting NMR test.

  • A. Lanine Pro

    6/21/2010 8:55:09 AM |

    Well I think differently having postponed bypass surgery seven years ago. I will continue with 'magical thinking'. Its nice, you should try it sometime.

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Non-profit hospitals

Non-profit hospitals

30. May 2007 William Davis (0)
Take a look at your local hospital and you're likely to notice several curious things:

1) It is likely non-profit, meaning it enjoys a non-profit status with the Internal Revenue Service and enjoys the tax benefits of not paying taxes on profits. This provides an advantage to tax-protected hospitals. 70% or more of hospitals in the U.S. are "non-profit."

2) Non-profit or no, many hospitals operate under the guise of a religious affiliation, e.g., St. Mary's Hospital, Trinity Hospital, All Saints', Jewish Hospital, etc.

3) Executives in non-profit hospitals can make capitalistic salaries. One CEO of a Milwaukee hospital took home $3.7 million dollars in salary last year. That's not including the very substantial perks and business interests in the spin-off businesses the hospital owns, including pharmacies, drug and medical device disitributors, even a venture capital division. "Non-profit" does not have to mean that executives within the operation can't benefit handsomely.

That same hospital system spends over $10 million dollars in a year in local marketing for TV ads, print advertising, etc. Ads are slick and professionally produced.

Make no bones about it: These are "non-profit" for tax purposes only . They are for-profit in every other sense of the phrase, including rich rewards for the insiders.

Guess how those fat executive salaries and large marketing budgets are paid for? That's right: the 12-inch incision in your chest; the four stents, defibrillator, and repeated nuclear stress tests; the revolving door of hospitalization after hospitalization that typifies the "heart patient" experience.

See the hospital for what it is: In the 21st century, it is no longer a charitable operation worthy of your volunteer time and donations. It is a business no different than Home Depot, IBM, or--Enron. Yes, they do perform needed services, as well. But the perverse equation that often determines who needs hospitalization and who doesn't, who needs a heart procedure and who doesn't, is not always based on necessity but on financial return. Just ask the CEO.
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