The Track Your Plaque guide to getting grotesquely overweight

15. August 2006 William Davis (0)

If you'd like to gain huge quantities of weight, here's a number of helpful tips:

1) Follow the advice of food manufacturers and eat the products they label "healthy", or "heart healthy", or "part of a nutritious breakfast" etc., like Shredded Wheat cereal, pretzels ("a low-fat snack"!), low- or non-fat salad dressings.

2) Cut your morning calorie intake by skipping breakfast.

3) Hang around with other heavy people. They will confirm that it's okay to be overweight.

4) Call walking your dog "exercise".

5) Get a sedentary desk job. Use your swivel desk chair to scoot about whenever possible, rather than getting up to do things.

6) Say "I've worked hard all week long. Weekends are for relaxing, not for physical activities. I deserve a rest."

7) Eat foods without thinking about it: Eat chips while watching football, eat while on the phone, daydream over the sink.

8) Eat to provide comfort when stressed.

9) Eat foods that have sentimental value, whether or not they're good for you: Freshly-baked cakes that remind you of Mom, Pop Tarts that you used to carry in your lunchbox when you were a kid, hot dogs just like Dad would buy at the baseball stadium.

10) Cut back on sleep and generate insatiable starch cravings.

11) Stack your shelves at home with great variety. That way, you'll always have something to suit your mood.

12) Say to your spouse: "It's none of your damn business what I eat! I'm a grown man/woman!" Prove it by over-indulging in obviously unhealthy foods.

13) Tell yourself that you're just too busy to pay attention to food choices. Just grab whatever you can out of a convenience store or vending machine.

See, it's easy! And that just a start.

Of course, I don't really want you to do any of these things. But if you see yourself in any of the above, and you're struggling with weight, you should seriously rethink your approach.

Your heart scan is just a "false positive"

15. August 2006 William Davis (0)

I've seen this happen many times. Despite the great media exposure and the growing acceptance of my colleagues, heart scans still trigger wrong advice. I had another example in the office today.

Henry got a CT heart scan in 2004. His score: 574. In his mid-50s, this placed him in the 90th percentile, with a heart attack risk of 4% per year. Henry was advised to see a cardiologist.

The cardiologist advised Henry, "Oh, that's just a 'false positive'. It's not true. You don't have any heart disease. Sometimes calcium just accumulates on the outside of the arteries and gives you these misleading tests. I wish they'd stop doing them." He then proceeded to advise Henry that he needed a nuclear stress test every two years ($4000 each time, by the way). No attempt was made to question why his heart scan score was high, since the entire process was outright dismissed as nonsense.

I'm still shocked when I hear this, despite having heard these inane responses for the past decade. Of course, Henry's heart scan was not a false positive, it was a completely true positive. I'm grateful that nothing bad happened to Henry through two years of negligence, though his heart scan score is likely around 970, given the expected, untreated rate of increase of 30%.

The cardiologist did a grave disservice to Henry: He misled him due to his ignorance and lack of understanding. I wish Henry had asked the cardiologist whether he had read any of the thousands of studies now available validating CT heart scans. I doubt he's bothered to read more than the title. The cardiologist is lucky (as is Henry) that nothing bad happened in those two years.

Do false positives occur as the cardiologist suggested? They do, but they're very rare. There's a rare phenomenon of "medial calcification" that occurs in smokers and others, but it is quite unusual. >99% of the time, coronary calcium means you have coronary plaque--even if the doctor is too poorly informed to recognize it.

What's better than a heart scan?

13. August 2006 William Davis (0)

Do you know what's better than a heart scan?

Two heart scans. No other method can provide better feedback on the results of your program.

Say you've made efforts to correct high LDL; lost weight to raise HDL and reduce small LDL; added soluble fibers, nuts, and dramatically reduced wheat products; take fish oil, vitamin D, and follow a flavonoid-rich diet. Has it worked?

After a year or so of your program, that's when another heart scan can give you invaluable feedback on whether it's been successful. I tell my patients that it's relatively easy to correct lipid and lipoprotein abnormalities. The difficult part is to know when it's good enough. Is your LDL of 67 mg/dl and HDL of 50 mg/dl good enough? Another heart scan score is the best way I know of to find out.

Variation in plaque growth differs hugely from one person to another, even at equivalent lipoprotein values. Why? Lots of reasons. Humans are inconsistent day to day. Lipoproteins, being a snapshot in time and not a cumulative value, change somewhat from day to day. There's also the possibility of unmeasured, unrecognized factors that influence coronary plaque growth. We may not be smart enough to identify these hidden factors yet. But your heart scan score will incorporate the effects of these hidden factors.

Ideally, we aim for zero growth in plaque (no change in score) or a reduction. But, particularly in the first year, 10% or less plaque growth is still a good result that predicts much reduced risk of heart attack. More than 20% per year and your program needs more work--or else you know what's ahead.

Lipids are snapshots in time; heart scans are cumulative

12. August 2006 William Davis (0)

Let me paint a picture. It's fictional, though a very real portrait of how things truly happen in life.

Michael is an unsuspecting 40-year old man. He hasn't undergone any testing: no heart scan, no lipids or lipoproteins. But we have x-ray vision, and we can see what's going on inside of him. (We can't, of course, but we're just pretending.) Average build, average lifestyle habits, nothing extraordinary about him. His lipids/lipoproteins at age 40:

--LDL cholesterol 150 mg/dl
--HDL cholesterol 38 mg/dl
--Triglycerides 160 mg/dl
--Small LDL 70% of all LDL

At age 40, with this panel, his heart scan score is 100. That's high for a 40-year old male.

Fast forward 10 years. Michael is now 50 years old. Michael prides himself on the fact that, over the past 10 years, he's felt fine, hasn't gained a single pound, and remains as active at 50 as he did in 40. In other words, nothing has changed except that he's 10 years older. His lipids and lipoproteins:

--LDL cholesterol 150 mg/dl
--HDL cholesterol 38 mg/dl
--Triglycerides 160 mg/dl
--Small LDL 70% of all LDL

Some of you might correctly point out that just simple aging can cause some deterioration in lipids and lipoproteins, but we're going to ignore these relatively modest issues for now.)

Lipids and lipoproteins are, therefore, unchanged. Michael's heart scan score: 1380, or an approximate 30% annual increase in score. (Since Michael didn't know about his score, he took no corrective/preventive action.)

My point: If we were to make our judgment about Michael's heart disease risk by looking at lipids or lipoproteins, they would'nt tell us where he stood with regards to heart disease risk. His lipids and lipoproteins were, in fact, the same at age 50 as they were at age 40. That's because measures of risk like this are snapshots in time.

In contrast, the heart scan score reflects the cumulative effects of life and lipids/lipoproteins up until the day you got your scan.

Which measure do you think is a better gauge of heart attack risk? I think the answer's obvious.

11. August 2006 William Davis (0)

The recognition of the metabolic syndrome as a distinct collection of factors that raise heart disease risk has been a great step forward in helping us understand many of the causes behind heart disease.

Curiously, there's not complete agreement on precisely how to define metabolic syndrome. The American Heart Association and the National Heart, Lung, and Blood Institute issued a concensus statement in 2005 that "defined" metabolic syndrome as anyone having any 3 of the 5 following signs:

Waist size 40 inches or greater in men; 35 inches or greater in women

Triglycerides 150 mg/dL or greater (or treatment for high triglycerides)

HDL-C <40 mg/dL in men; <50 mg/dL in women (or treatment for reduced HDL-C)

Blood Pressure >130 mmHg systolic; or >85 mmHg diastolic (or drug treatment for hypertension)

Glucose (fasting) >100 mg/dL (or drug treatment for elevated glucose)

Using this definition, it has become clear that meeting these criteria triple your risk of heart attack.

But can you have the risk of metabolic syndrome even without meeting the criteria? What if your waste size (male) is, 36 inches, not the 40 inches required to meet that criterion; and your triglycerides are 160, but you meet none of the other requirements?

In our experience, you certainly can carry the same risk. Why? The crude criteria developed for the primary practitioner tries to employ pedestrian, everyday measures.

We see people every day who do not meet the criteria of the metabolic syndrome yet have hidden factors that still confer the same risk. This includes small LDL; a lack of healthy large HDL despite a normal total HDL; postprandial IDL; exercise-induced high blood pressure; and inflammation. These are all associated with the metabolic syndrome, too, but they are not part of the standard definition.

I take issue in particular with the waist requirement. This one measure has, in fact, gotten lots of press lately. Some people have even claimed that waist size is the only requirement necessary to diagnose metabolic syndrome.

Our experience is that features of the metabolic syndrome can occur at any waist size, though it increases in likelihood and severity the larger the waist size. I have seen hundreds of instances in which waist size was 32-38 inches in a male, far less than 35 inches in a female, yet small LDL is wildly out of control, IDL is sky high, and C-reactive protein is markedly increased. These people obtain substantial risk from these patterns, though they don't meet the standard definition.

To me, having to meet the waist requirement for recogition of metabolic syndrome is like finally accepting that you have breast cancer when you feel the two-inch mass in your breast--it's too late.

Recognize that the standard definition when you seen it is a crude tool meant for broad consumption. You and I can do far better.

What role DHEA?

9. August 2006 William Davis (2)

DHEA, the adrenal gland hormone, has suffered its share of ups and downs over the years.

Initially, DHEA was held up as the fountain of youth with hopes of turning back the clock 20 years. Such extravagant dreams have not held up. But DHEA can still be helpful for your program.

All of us had oodles of DHEA in our bodies when we were in our 20s and 30s. Gradually diminishing levels usually reach nearly blood levels of around zero by age 70.

In our heart disease prevention program, of course, we aim to stop or reduce your CT heart scan score. Does DHEA reduce your score? No, it most certainly does not. But it can be helpful for gaining control over some of the causes behind coronary plaque.

For instance, DHEA can:

--Help reduce abdominal fat and increase muscle mass (slightly)
--Provide more physical stamina.
--Boost mood.
--It may modestly reduce some of the phenomena associated with the metabolic syndrome (high blood pressure, high blood sugar, high insulin, low HDL, small LDL, etc.)

In my experience, people who feel better do better on their overall program. If you're always tired and run down and run out of steam by 3 pm, I won't see you riding your bicycle outdoors or at the aerobics class. But if you're bursting with energy until you put your head on the pillow, you're more inclined to walk, bike, dance, play with the kids, dance, take Tai Chi, etc.

Some downsides to DHEA: Some people experience aggression. Backing off on the dose usually relieves it. Also, sleeplessness. Taking your DHEA in the morning usually fixes it.

The dose is best tailored to your age and blood levels. People less than 40 years old should not take DHEA. The older you are, the higher the dose, though we rarely ever have to exceed 50 mg per day. If you've never had a blood level and your doctor refuses to obtain one, 25 mg per day is a reasonable dose (10-15 mg in women 40-50 years old). It's always best to discuss your supplement use, particularly agents like DHEA, with your doctor.

Track Your Plaque Members: Stay tuned to the www.cureality.com website for a Special Report more completely detailing the hows and whys behind DHEA.

Brainwashed!

9. August 2006 William Davis (0)

At a social gathering this weekend, as we humans like to do, someone asked me what I did for a living. I told him I was a cardiologist.

"What hospital do you work at?" he asked.

This is invariably the response I get whenever I tell people what I do. I wouldn't make much of it except that it happens just about every time.

This indicates to me just how successful hospitals, my colleagues, cardiac device manufacturers, and others supporting the status quo in heart care, have been in persuading us that the place for heart disease is the hospital--period.

Tense families, drama, high-tech...It all takes place in the hospital.

Yet the people destined to be the fodder for hospital heart care are presently well, mostly unaware of what the future holds. Also unaware that heart disease is readily, easily, inexpensively, and accurately identifiable. Ask anyone in the Track Your Plaque program who's had a CT heart scan.

We all need to rid ourselves of the idea that the hospital is the place for heart disease. If the coronary plaque behind heart attack is easy to detect and controllable, there's little or no need for the hospital for the vast majority of us.

In the majority of instances of coronary disease, the hospital should be the place for the non-compliant and the ill-informed, and not for those of us sufficiently motivated to know and do better. The formula is simple: 1) Quantify plaque with a CT heart scan, 2) Identify the causes, then 3) Correct the causes.

The Fanatic Cook: A fabulous Blog about food and nutrition

7. August 2006 William Davis (0)

I came across this Blog authored by a nutritionist when it was highlighted on Blogger as an interesting site:

The Fanatic Cook at http://fanaticcook.blogspot.com/

I was thoroughly impressed with the insightful and entertaining commentary. I'd highly recommend this site to you for reading on nutrition. In particular, her coenzyme Q10 column was exceptionally well written and clear.(http://fanaticcook.blogspot.com/2005/02/statins-and-not-well-publicized-side.html)

Also read her column, Super NonFoods at http://fanaticcook.blogspot.com/2005/07/super-nonfoods.html.

There's also oodles of recipes, all for the taking.

Eggs: Good, bad, or indifferent?

5. August 2006 William Davis (3)

Eggs have been in the center of the cholesterol controversy almost from the very start.

The traditional argument against eggs went that eggs, high in cholesterol (210-275 mg per egg)and with some saturated fat (1.5-2.5 grams per egg), raised blood cholesterol (and LDL). Out went the daily fried, scrambled, poached eggs that many Americans indulged in most mornings. (We replaced it with more breakfast cereals and other carbohydrate conveniences, then got enormously overweight.)

A large Harvard epidemiologic study in 1999 called this observation into question. They tracked the fate of 117,000 thousand people and then compared the rate of heart attack, death, and other cardiovascular events among various people correlated to the "dose" of eggs they ate. Egg intake varied from none to 7 or more per week. Lo and behold, people who ate more eggs appeared to not suffer more events.

This study, large and well-conducted by an internationally respected group of investigators, seem to reopen the gates for more egg consumption, though most Americans still consume eggs cautiously.

Deeper down in this study, however, was another observation: People with diabetes who ate 1 egg per day had double the risk of heart attack. Because this study was observational, no specific conclusion as to why could be drawn.

A new study conducted by a Brazilian group may shed some light. Healthy (non-diabetic) men were fed an emulsion of several eggs. Inclusion of plentiful yolks caused a dramatic slowing of fat clearance from the blood. Specifically, "chylomicron remnants" were abnormally persistent in the blood. Chylomicron remnants are potent causes of coronary plaque. (Chylomicron remnants can be measured fairly well by intermediate-density lipoprotein and VLDL by NMR, or IDL by VAP.)

Diabetics are know to have substantial disorders of after-meal fat clearance, including an excess of chylomicron remnants. Could the Brazilian observation be the explanation for the increased event rate in diabetics in the Harvard study? Interesting to speculate.

We continue to tell our patients that eating eggs in moderation is probably safe. After all, there are good things in eggs: the high protein in the egg white, lecithin in the yolk. It is the yolk's contents that are in question, not the white. Thus, you and I can eat all the egg whites (e.g., Egg Beaters) we want. It's the safety of yolks that are uncertain.

The abnormal after-eating effect suggested by the Brazilians opens up some very interesting questions and confirms that we should still be cautious in our intake of egg yolks. One yolk per day is clearly too much. What is safe? The exisitng information would suggest that, if you have diabetes, pre-diabetes, or a postprandial disorder (IDL, VLDL), you should minimize your egg yolk use, perhaps no more than 3 or so per week, preferably not all at one but spaced out to avoid the after-eating effect.

Others without postprandial disorders may safely eat more, perhaps 5 per week, but also not all at one but spaced out.

Track Your Plaque Members: Be sure to read our upcoming Special Report on Postprandial Disorders. It contains lots of info on what this important pattern is all about. Postprandial disorders are largely unexplored territory that hold great promise for tools to inhibit coronary plaque growth and drop your heart scan score. The Brazilian study is just one of many future studies that are likely to be released in future about this very fascinating area.

Hu FB, Stampfer MJ, Rimm EB, Manson JE, Ascherio A, Colditz GA, Rosner BA, Spiegelman D, Speizer FE, Sacks FM, Hennekens CH, Willett WC.A prospective study of egg consumption and risk of cardiovascular disease in men and women. JAMA 1999 Apr 21;281(15):1387-94.

Cesar TB, Oliveira MR, Mesquita CH, Maranhao RC. High cholesterol intake modifies chylomicron metabolism in normolipidemic young men. J Nutr. 2006 Apr;136(4):971-6.

Diabetes is Track Your Plaque's Kryptonite!

3. August 2006 William Davis (0)

If there's one thing I truly fear from a heart scan score reduction/coronary plaque regression standpoint, it's diabetes.

I saw a graphic illustration of this today. Roy came into the office after his 2nd heart scan. His first scan 14 months ago showed a score of 162. Roy started out weighing well over 300 lbs and with newly-diagnosed adult diabetes.

Roy put extraordinary effort into his program. He lost nearly 70 lbs by walking; cutting processed carbohydrates, greasy foods, and slashing overall calories. His lipoproteins, disastrous in the beginning, were falling into line, though HDL was still lagging in the low 40s, as Roy remains around 60 lbs overweight, even after the initial 70 lb loss.

Unfortunately, despite the huge loss in weight, Roy remains diabetic. On a drug called Actos, which enhances sensitivity to insulin, along with vitamin D to also enhance insulin response, his blood sugars remained in the overtly diabetic range.

Roy's repeat heart scan showed a score of 482--a tripling of his original score.

Obviously, major changes in Roy's program are going to be required to keep this rate of growth from continuing. But I tell Roy's story to illustrate the frightening power of diabetes to trigger coronary plaque growth.

Like Kryptonite to Superman (remember George Reeves crumbling and falling to his knees when the bad guys got a hold of some?), diabetes is the one thing I fear greatly when it comes to reducing your heart scan score. As you see with Roy's case, diabetes can be responsible for explosive plaque growth, more than anything else I know.

The best protection from diabetes is to never get it in the first place. (See my earlier Blog, "Diabetes is a choice you make".)

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 19^th 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-20^th 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 21^st 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 21^st century disseminates through the ranks of modern healthcare providers at much the same pace as measuring blood pressure did in the early 20^th 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 20^th 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."

When MIGHT statins be helpful?

7. April 2011 William Davis (17)

I spend a lot of my day bashing statin drugs and helping people get rid of them.

But are there instances in which statin drugs do indeed provide real advantage? If someone follows the diet I've articulated in these posts and in the Track Your Plaque program, supplements omega-3 fatty acids and vitamin D, normalizes thyroid measures, and identifies and corrects hidden genetic sources of cardiovascular risk (e.g., Lp(a)), then are there any people who obtain incremental benefit from use of a statin drug?

I believe there are some groups of people who do indeed do better with statin drugs. These include:

Apoprotein E4 homozygotes

Apoprotein E2 homozygotes

Familial combined hyperlipidemia (apoprotein B overproduction and/or defective degradation)

Cholesteryl ester transfer protein homozygotes (though occasionally manageable strictly with diet)

Familial heterozygous hypercholesterolemia, familial homozygous hypercholesterolemia

Other rare variants, e.g., apo B and C variants

The vast majority of people now taking statin drugs do NOT have the above genetic diagnoses. The majority either have increased LDL from the absurd "cut your fat, eat more healthy whole grains" diet that introduces grotesque distortions into metabolism (like skyrocketing apo B/VLDL and small LDL particles) or have misleading calculated LDL cholesterol values (since conventional LDL is calculated, not measured).

As time passes, we are witnessing more and more people slow, stop, or reverse coronary plaque using no statin drugs.

Like antibiotics and other drugs, there may be an appropriate time and situation in which they are helpful, but not for every sneeze, runny nose, or chill. Same with statin drugs: There may be an occasional person who, for genetically-determined reasons, is unable to, for example, clear postprandial (after-eating) lipoproteins from the bloodstream and thereby develops coronary atherosclerotic plaque and heart attack at age 40. But these people are the exception.

Advanced topics in nutrition

5. April 2011 William Davis (0)

Nutrition in the modern world has become an increasingly problematic topic. From genetic modification to commercialized methods of mass production, we are having to navigate all manner of complex issues in food choices, particularly if ideal health, including maximal control over coronary plaque, is among our goals.

We will therefore be releasing a series of discussions on the Track Your Plaque website in the coming months, a series I call "Track Your Plaque Advanced Topics in Nutrition." These will be, as the series title suggests, discussions for anyone interested in more than the "eat a balanced diet" nonsense that issues from "official" sources. Among the topics to be covered:

1)Advanced Glycation End-products--both endogenous and exogenous, including peripheral issues like lipoxidation and acrylamides.

2)Dietary influences on LDL oxidation--including the concept of "glycoxidation." Protection from oxidative phenomena is not just about taking antioxidants.

3) Foods you MUST eat--We've talked a lot about foods that you shouldn't eat. How about foods you should eat?

The New Track Your Plaque Guide now available

4. April 2011 William Davis (5)

The New Track Your Plaque Guide is now available!

The Track Your Plaque program has evolved over its 8 year history. While the original Track Your Plaque book reflected the program details that got the program started back in 2003-2004, plenty has changed.

This new version of the book, what I call the program Guide, represents version 2.0 of Track Your Plaque and includes:

--Updated lipoprotein treatment strategies--including new and expanded treatment choices for small LDL and lipoprotein(a).

--An entire chapter on vitamin D and its crucial role in cardiovascular health and plaque control.

--A new and expanded diet--All the reasons why the New Track Your Plaque Diet can achieve spectacular improvement in lipids/lipoproteins, reversal of insulin resistance/pre-diabetes/diabetes, weight loss, reduction in blood pressure, etc. are discussed in considerable detail. The diet is crafted to achieve maximum control over both metabolic responses and coronary plaque.

--An entire chapter on the role of omega-3 fatty acids is included.

--A detailed discussion on the role of iodine and thyroid health--One of the newest additions to the Track Your Plaque menu of strategies is to achieve and maintain ideal thyroid health. This tips the scales in your favor for improved control over lipids/lipoproteins, weight, blood sugar, and coronary plaque.

The new guide, as well as our new Member kits that include the new Track Your Plaque Recipe Book, At-Home Lab Test kits, and nutritional supplements, are all available in the Track Your Plaque Marketplace.

Don't wet yourself

3. April 2011 William Davis (13)

While there is more to wheat's adverse effects on human health than celiac disease, studying celiac disease provides important insights into why and how wheat--the gluten component of wheat, in this case--is so destructive to human health.

Modern wheat, in particular, is capable of causing "celiac disease" without intestinal symptoms---no cramping or diarrhea--but instead shows itself as brain injury (ataxia, dementia), peripheral nervous system damage (peripheral neuropathy), joint and muscle inflammation (rheumatoid arthritis, polymyalgia rheumatica and others), and gastrointestinal cancers.

One neurological manifestation of wheat's effect on the human brain is a condition called cerebellar ataxia. This is a condition that can affect adults (average age 48 years) and children and consists of incoordination, falls, and incontinence.

Because brain tissue has limited capacity for healing and regeneration, symptoms of cerebellar ataxia usually improve slowly and modestly with meticulous elimination of wheat and other gluten sources.

Such observations are relevant even to people without celiac disease. Celiac disease sufferers are more susceptible to such extra-intestinal phenomena, but it can also happen in people without positive celiac antibodies.

Some references:

Neurological symptoms in patients with biopsy proven celiac disease

A total of 72 patients with biopsy proven celiac disease (CD) (mean age 51 +/- 15 years, mean disease duration 8 +/- 11 years) were recruited through advertisements. All participants adhered to a gluten-free diet. Patients were interviewed following a standard questionnaire and examined clinically for neurological symptoms. Medical history revealed neurological disorders such as migraine (28%), carpal tunnel syndrome (20%), vestibular dysfunction (8%), seizures (6%), and myelitis (3%). Interestingly, 35% of patients with CD reported of a history of psychiatric disease including depression, personality changes, or even psychosis. Physical examination yielded stance and gait problems in about one third of patients that could be attributed to afferent ataxia in 26%, vestibular dysfunction in 6%, and cerebellar ataxia in 6%. Other motor features such as basal ganglia symptoms, pyramidal tract signs, tics, and myoclonus were infrequent. 35% of patients with CD showed deep sensory loss and reduced ankle reflexes in 14%. Gait disturbances in CD do not only result from cerebellar ataxia but also from proprioceptive or vestibular impairment.

Gluten ataxia in perspective: epidemiology, genetic susceptibility and clinical characteristics

Two hundred and twenty-four patients with various causes of ataxia from North Trent (59 familial and/or positive testing for spinocerebellar ataxias 1, 2, 3, 6 and 7, and Friedreich's ataxia, 132 sporadic idiopathic and 33 clinically probable cerebellar variant of multiple system atrophy MSA-C) and 44 patients with sporadic idiopathic ataxia from The Institute of Neurology, London, were screened for the presence of antigliadin antibodies. A total of 1200 volunteers were screened as normal controls. The prevalence of antigliadin antibodies in the familial group was eight out of 59 (14%), 54 out of 132 (41%) in the sporadic idiopathic group, five out of 33 (15%) in the MSA-C group and 149 out of 1200 (12%) in the normal controls. The prevalence in the sporadic idiopathic group from London was 14 out of 44 (32%). The difference in prevalence between the idiopathic sporadic groups and the other groups was highly significant (P < 0.0001 and P < 0.003, respectively). The clinical characteristics of 68 patients with gluten ataxia were as follows: the mean age at onset of the ataxia was 48 years (range 14-81 years) with a mean duration of the ataxia of 9.7 years (range 1-40 years). Ocular signs were observed in 84% and dysarthria in 66%. Upper limb ataxia was evident in 75%, lower limb ataxia in 90% and gait ataxia in 100% of patients. Gastrointestinal symptoms were present in only 13%. MRI revealed atrophy of the cerebellum in 79% and white matter hyperintensities in 19%. Forty-five percent of patients had neurophysiological evidence of a sensorimotor axonal neuropathy. Gluten-sensitive enteropathy was found in 24%. HLA DQ2 was present in 72% of patients. Gluten ataxia is therefore the single most common cause of sporadic idiopathic ataxia.