"I gained 30 lbs from one cracker"


Let me tell you a story, a tale of a woman who gained 30 lbs by eating one cracker.

At age 50, Claire's health was a disaster. Her initial lipoprotein patterns were a mess, including HDL 36 mg/dl, triglycerides 297 mg/dl, blood sugar 122 mg/dl (pre-diabetic range), blood pressure 155/99. Small LDL comprised over 90% of all LDL particles.

At 5 feet 3 inches, she weighed 210 lbs--90 lbs over her ideal weight. Her face was flushed and red, her eyes swollen and weighted down with bags, her eyes dull. While interested in hearing about how to improve her health, I would hardly call her enthusiastic.

We talked about how removing wheat products entirely from her diet could result in weight loss--enormous weight loss--yet with reduced appetite, increased energy, less daytime sleepiness and fogginess, improved sleep quality. Removing wheat would also allow substantial correction of her lipoprotein patterns with minimal medication.

At first, she seemed confused by this advice. After all, it ran directly opposite to what she'd been told by her family doctor, not to mention the advice from TV, food ads, and food packages.

To my surprise, Claire did it. She didn't return to the office for another 5 months. But she came in, a big beaming smile on her face.

Even at 167 lbs--still overweight--Claire looked great. She glowed. She'd already dropped nearly 2 1/2 inches from her waist. She felt lighter on her feet, discovered energy she thought she'd lost 10 years earlier. Her blood results matched, with dramatic shifts in each and every pattern.

I quizzed Claire on her diet, and she had indeed made substantial changes. In addition to eliminating all foods made of wheat flour, she also eliminated foods made with cornstarch, rice flour, snacks, and other sweets. She ate her fill of vegetables, fruits, raw nuts, lean meats, and healthy oils. She was less hungry while eating less. Even her husband, skeptical at first, joined Claire after the first two months and her initial 20 lbs of weight loss. He, too, was well on his way to dropping to ideal weight.

But a dinner party invitation came. In the few that Claire and her husband had gone to over the few months, she had religiously stuck to her program, choosing cheese, pickles, olives, vegetables that she dipped, but avoided the pretzels, breads, Doritos, potato chips, and others.

This time, a tray of whole wheat crackers was laid on the buffet table, covered with some sort of sweetened cheese. She had just one. She savored the taste that she'd missed. "Maybe one more. I'll be extra good this weekend,'" she told herself.

Now Claire was hungry. The bruschetta covered with tomatoes and mozzarella looked awfully good. "It's got some good things on it, too!" she thought. She had three.

The floodgates opened. I saw Claire three months later, weighing just shy of 200 lbs. "I almost cancelled this appointment," she whispered quietly, tears at the corner of her eyes. "I don't know what happened. I just lost control. After losing all that weight and feeling so good, I blew it!"

I've seen it before: Fabulous success eliminating the foods that created the situation--the insatiable appetite, the endless cycle of hunger, brief satiety, the rolling, rumbling hunger--followed by temptation, then disaster. The weight lost comes right back.

It's experiences like Claire's that have absolutely, positively convinced me: Wheat products are addictive. It's not true for everybody, but it's true for many people, certainly most people who have weight struggles. It triggers some sort of appetite button, a signal to eat more . . . and more, and more. Keep it up long enough, and you have drops in HDL, increases in triglycerides, upward jumps in blood sugar and blood pressure, diabetes, etc. It doesn't matter if it's whole grain, 7-grain, or 12-grain. Yes, the whole grains contain more fiber and more B vitamins. But they all share one characteristic: They trigger a desire for more.

So that's the story of how one whole wheat cracker caused one woman to gain 30 lbs.


Next week's story:

California woman claims: My children are aliens!


Just kidding.


Copyright 2008 William Davis, MD

Wheat-free is not gluten-free

Eliminate wheat from your diet and wonderful things happen:

--Lose 15-20 lbs, sometimes in the first 1-3 months. (More or less, depending on your prior dietary habits, weight, age, etc.)
--HDL cholesterol goes up, triglycerides go down
--Blood sugar drops
--Small LDL is reduced
--C-reactive protein is reduced
--Pre-diabetics often convert to non-diabetics
--Diabetics gain far better control over blood glucose. Some even become non-diabetic (as long as they maintain the wheat-free, low-glycemic index diet and weight control).
--You feel better: Less mental fogginess, more energy, better sleep.
--Appetite shrinks dramatically.


(Many diet programs makes lots of money promising similar results. Prescription medications like the pre-diabetes drugs, Actos and Avandia, and the fibrates, Tricor and Lopid, nearly--nearly--reproduce the effects of eliminating wheat. Of course, these medications do not lead to weight loss or make you feel better. In fact, Actos and Avandia usually trigger a weight gain of 8 lbs in the first year of use.)


All of these wonderful effects develop with elimination of wheat. . . unless you confuse wheat-free with gluten-free. There's a difference.

Remove wheat from your diet, but discover the world of gluten-free products made for people with celiac disease, or gluten enteropathy, and you can regain the weight and recreate many of the phenomena associated with wheat. I've talked about this in past, but it trips up so many people that it's worth talking about again.

The concept that I am advocating is really low-glycemic index (or low glycemic load, actually). Foods that trigger a substantial rise in blood sugar, whether immediate (like whole wheat crackers) or delayed (like whole wheat pasta) are the culprits. The same effects develop with candy, cookies, fruit drinks, pizza, chips, table sugar, and other junk foods.

However, I pick on wheat specifically because it so dominates the American diet. It has grown to fill so many processed food products. It is also a food ingredient that is falsely advertised as healthy. In reality, pretzels, whole wheat crackers, whole grain bread, high-fiber cereals, etc. exert the same effect on blood sugar as candy or white table sugar. They also generate all the "downstream" phenomena listed above.

But wheat is hardly the only food that makes us fat, diabetic, and unhealthy. This is true for foods made with cornstarch (taco shells, cornbread, tortillas, chips, breakfast cereals); rice flour, puffed rice, and polished rice; and potatoes, particularly pulverized potato starch (potato chips). There are others.

These are the gluten-free products that are marketed to the gluten enteropathy (celiac disease) market. Yes, you can make muffins with cornstarch and no wheat gluten, but is it good for you?

No. It is nearly as bad as wheat. It can still skyrocket blood sugar, drop HDL, raise triglycerides, create small LDL, heighten inflammation, etc.

Ground flaxseed, oat bran, barley, quinoa, are some of the alternatives that do not create these effects. But not the majority of gluten-free products on the market.




Ingredients: Potato starch, rice flour, modified corn starch, olive oil, yeast, vegetable protein(lupine), corn syrup, sugar, salt, hydroxypropyl methylcellulose, sodium bicarbonate, ammonium bicarbonate, diacetyltataric acid esters of mono- and diglycerides of edible fats, natural flavor.

". . . only naturally gluten-free and wheat-free ingredients and adhere to the strictest quality processes, testing every batch for gluten using the ELISA assay."

NUTRITION FACTS
Serving Size 7 bread sticks (31g)
Servings per container 5

Calories 120 Calories from fat 25
Amount per serving
Total Fat 2.5g
Saturated Fat 0.5g
Trans Fat 0g
Cholesterol 0mg
Sodium 310mg
Total Carb 24g
Dietary Fiber 1g
Sugars less than 1g
Protein less than 1g

Death to chelation?


Does chelation work?

It's a question I get asked fairly frequently. Although I have never performed chelation, IV or oral, and therefore have no direct experience, my concerns for this purported therapy have included:

1) The concept of extracting calcium from atherosclerotic plaque by removing it first from the blood is absurd. Early chelationists believed that this was the means by which EDTA might reverse coronary atherosclerosis. However, removing calcium from blood would more likely lead to osteoporosis or calcium extraction from bone, since bone is a more ready repository for calcium. Blood calcium levels are also tightly and narrowly controlled; any significant reduction in calcium ("hypocalcemia") can be life-threatening. And, indeed, there have been deaths from hypocalcemia in people receiving chelation.

More recently, chelationists have argued that removal of heavy metals like lead and mercury are responsible for the purported benefits of chelation. And, indeed, blood levels of these heavy metals can be reduced by chelation. That alone may be a benefit. But to then make the leap to say that it also regresses atherosclerotic plaque by the same mechanism has no basis in science.

2) Practitioners associated with chelation tend to be shady. I have seen homeopathic therapies (among THE most ridiculous of concepts), "energy balance" therapies, desiccated organ extracts ("applied kinesiology"), and a variety of other fringe treatments offered by practitioners offering chelation. This doesn't necessarily mean, of course, that chelation is also fringe or suspect, but it tends to be offered by practitioners who engage in generally unscientific, unfounded practices.


The few people I've seen go through multiple courses of chelation (usually 30 or so infusions) have shown no impact on heart scan scores or any other measure of heart disease.

In response to the many questions I receive on chelation, I had been answering that, if we would simply wait for the publication of the NIH-sponsored trial of IV chelation therapy, perhaps we'd know once and for all.

However, in a lengthy criticism, four expert authors argue that the TACT trial to assess chelation study is doomed to failure for an entire list of reasons and should therefore be abandoned. The discussion is available on Medscape Cardiology. (Free sign-in required.)



Why the NIH Trial to Assess Chelation Therapy (TACT) Should Be Abandoned
We investigated the social and the scientific histories of chelation therapy beginning in the 1950s. We examined TACT protocols and consent forms, which, in response to Freedom of Information Act (FOIA) requests, the NIH provided to us with curious redactions. We examined the existing RCTs and the numerous case series cited by the TACT protocols. We examined evidence for risks, including information that is not in the standard medical literature. We examined various hypotheses that advocates have offered to explain how chelation "works."

We present our findings in 4 parts. First, we provide a brief history of the use of disodium EDTA as a treatment for CAD. Next, we describe the origin and nature of the TACT. Next, we discuss the evidence for chelation as a treatment for CAD and for atherosclerosis in general, and place it in the context of other proposed treatments that have been ineffective after an initial period of enthusiasm. Finally, we discuss the risks. For each topic, we contrast our findings with relevant statements in the TACT literature, to the extent that such statements exist.



Among the highlights:

--Since the mid-1970s, court documents and newspapers have reported at least 30 deaths associated with IV disodium EDTA, most of it administered by ACAM members.

--Early chelation investigators had chosen the disodium salt of EDTA, reasoning that if it could remove calcium from atherosclerotic plaques, it might shrink them. That notion was soon demonstrated to be invalid. It has largely been replaced by a "toxic heavy metals" antioxidant hypothesis, which is based on the potential for metal ions to produce free radical damage. Chelationists now cite "removing heavy metals" as the basis for their claim that chelation is effective for approximately 70 conditions, ranging from schizophrenia and autism to cancer. This provides them with numerous reasons to ignore any trial that finds chelation ineffective for CAD.

--Biochemical literature, either not cited or misrepresented in the TACT protocols, has demonstrated that the heavy metals hypothesis is implausible. Antithetically, it also demonstrates that the chelation mixture used in the TACT has pro-oxidant effects in vitro.

--In our opinion, TACT literature -- including 2 versions of the protocol, the consent form, information posted on the NCCAM Web site, and 2 editorials co-authored by the PI -- has misrepresented chelation, its risks, and the facts of the study. It has exaggerated the value of supportive case series, not only by ignoring evidence of bias and incompetence, but by misrepresenting citations and reporting erroneous data. It has minimized the dangers, both by understatements and by omissions of specific, published complications. It has not acknowledged the deaths mentioned above. It has repeatedly conflated disodium EDTA and a different drug, calcium-sodium EDTA.

--The TACT includes nearly 100 "chelation site" co-investigators who, in our opinion, are unsuitable to care for human subjects or to report trial data. Most espouse implausible health claims while denigrating proven methods; several have been disciplined, for substandard practices, by state medical boards; several have been involved in insurance fraud; at least 3 are convicted felons. Several were members of the ACAM or GLACM IRBs mentioned above. Few appear to have real expertise, required by TACT literature, in treating patients with CAD or in conducting clinical trials. Most continue to promote chelation while the TACT is in progress, contrary to good science, to human studies ethics, and to US Federal Code.


While the criticism itself does not prove the point one way or another, as a clinical trial should, anyone contemplating chelation therapy would be well-advised to read the document first. Another reference: EDTA chelation therapy for cardiovascular disease: a systematic review.


The authors of the exhaustive discussion are:
Kimball C. Atwood IV, MD, Anesthesiologist, Newton-Wellesley Hospital, Newton, Massachusetts; Assistant Clinical Professor, Tufts University School of Medicine, Boston, Massachusetts; Associate Editor, Scientific Review of Alternative Medicine
Author's email: katwood@partners.org

Elizabeth Woeckner, AB, MA, President, CIRCARE (Citizens for Responsible Care and Research), Columbia, Maryland

Robert S. Baratz, MD, DDS, PhD, Medical Director, South Shore Health Center, Inc., Braintree, Massachusetts; Assistant Clinical Professor of Medicine, Boston University School of Medicine, Boston, Massachusetts; President, National Council Against Health Fraud, Inc.

Wallace I. Sampson, MD, Clinical Professor of Medicine (Emeritus), Stanford University, Stanford, California; Senior Attending Physician and formerly Chief of Medical Oncology, Santa Clara Valley Medical Center, San Jose, California; Editor-in-Chief, Scientific Review of Alternative Medicine



The authors provided the following disclosures:


Disclosure: Kimball C. Atwood IV, MD, has disclosed no relevant financial relationships in addition to his employment.

Disclosure: Elizabeth Woeckner, AB, MA, has disclosed that she has received compensation for consulting in civil litigation and professional disciplinary actions.

Disclosure: Robert S. Baratz, MD, DDS, PhD, has disclosed that he has been retained by state licensing boards, the Office of the US Attorney, and plaintiff counsel as an expert in disciplinary proceedings and litigation with regard to chelation therapy and associated matters. He is compensated only for his time and has no commercial interest in the outcome of the proceedings or litigation.

Disclosure: Wallace I. Sampson, MD, has disclosed no relevant financial relationships in addition to his employment.

American Diabetes Association


These are actual quotes from the American Diabetes Association website:


Myth #2 (from list of Diabetes Myths): People with diabetes can't eat sweets or chocolate.
If eaten as part of a healthy meal plan, or combined with exercise, sweets and desserts can be eaten by people with diabetes. They are no more “off limits” to people with diabetes, than they are to people without diabetes.



Myth #5: If you have diabetes, you should only eat small amounts of starchy foods, such as bread, potatoes and pasta.
Starchy foods are part of a healthy meal plan. What is important is the portion size. Whole grain breads, cereals, pasta, rice and starchy vegetables like potatoes, yams, peas and corn can be included in your meals and snacks. The key is portions. For most people with diabetes, having 3-4 servings of carbohydrate-containing foods is about right. Whole grain starchy foods are also a good source of fiber, which helps keep your gut healthy.





How can I have sweets and still keep my blood glucose on target?
The key to keeping your blood glucose on target is to substitute small portions of sweets for other carb-containing foods in your meals and snacks. Carb-containing foods include bread, tortillas, rice, crackers, cereal, fruit, juice, milk, yogurt, potatoes, corn, and peas. For many people, having about 45 to 60 grams at meals is about right. Serving sizes make a difference. To include sweets in your meal, you can cut back on the other carb foods at the same meal.

For example, you’d like to have cookies with your lunch. Your lunch is a turkey sandwich with two slices of bread. Your first step is to identify the carb foods in your meal. Bread is a carb. You decide to swap two slices of bread for two slices of low-calorie bread and have the cookies -- it’s an even trade. Your total amount of carbohydrate remains the same for the meal.



Can I eat foods with sugar in them?
For almost every person with diabetes, the answer is yes! Eating a piece of cake made with sugar will raise your blood glucose level. So will eating corn on the cob, a tomato sandwich, or lima beans. The truth is that sugar has gotten a bad reputation. People with diabetes can and do eat sugar. In your body, it becomes glucose, but so do the other foods mentioned above. With sugary foods, the rule is moderation. Eat too much, and 1) you'll send your blood glucose level up higher than you expected; 2) you'll fill up but without the nutrients that come with vegetables and grains; and 3) you'll gain weight. So, don't pass up a slice of birthday cake. Instead, eat a little less bread or potato, and replace it with the cake. Taking a brisk walk to burn some calories is also always helpful.


Or take a look at the recipes for breads, muffins, cakes, pies, cookies, and pizza.


My point? As I often say, while the "official" organizations like the American Diabetes Association, the American heart Association, and the USDA dominate the message provided to mainstream Americans, to those of us who know better, they have become irrelevant. You can see how obviously boneheaded their advice is. I'd go so far as to say that, if you want diabetes, follow the American Diabetes Association diet. If you have diabetes, and you'd like to accelerate complications like kidney disease, heart disease, and neuropathy, then follow the American Diabetes Association diet.

I'm going to bet that American Diabetes Association sponsors like Lilly, Novo Nordisk, Merck, Pfizer, Abbott ($1 million or more annual contributions) and Cadbury Schweppes (3-year, multi-million dollar support for Weight Loss Matters program) will continue to charge full-speed ahead to maintain the status quo. Cadbury Schweppes are the proud makers of Dr. Pepper, Hawaiian Punch, Snapple, Motts' Apple Juice, and Hires Root Beer--you know, the foods and drinks that you can have as long as you adjust your insulin dose or talk to your doctor about adjusting your diabetes medications. And if you gain, say, 30 or 40 lbs eating these foods. . . well, we've got a treatment for that. Merck's Januvia , for instance, can help you out for only about $200 a month!

Looking at the facts this way, and it seems like some cheap conspiracy theory: They're all out to get us. Dispense information that virtually guarantees propagation of the disease, and all your friends and cronies profit. I don't know if it is or it isn't, but it sure smells like it sometimes.

A tan does not equal vitamin D

The sun is getting stronger and the days are getting longer, even here in Wisconsin.

Some people are coming to the office with nice tans obtained by sunning themselves for several hours. Others have come back from winter getaways to Florida, Arizona, or the tropics, also sporting nice, dark tans.

Several people, in fact, were so confident that sunning themselves provided sufficient vitamin D that they reduced their usual dose. Some even stopped their vitamin D altogether.

But, when blood levels of 25(OH) vitamin D were checked, they were virtually all low, sometimes as low as <20 ng/ml. Yet all had nice tans.

Why does this happen? Why would people with dark tans remain deficient in vitamin D?

One big factor is age: Anyone over 40 years old is fooling themselves if they think that a tan ensures raising vitamin D levels to a desirable range. Also, the more you tan, the more melanin skin pigment accumulates, and the more vitamin D activation in the skin is blocked.

Weight is another factor: Heavier people need more vitamin D, sometimes three- or four-fold more than slender people.

Why does aging result in inefficient skin activation of vitamin D? It seems that, once we are beyond our reproductively useful years, this ticking clock of aging gets triggered. The older we get, the less activation of vitamin D occurs in our skin, the less of the youth-maintaining, disease-preventing benefits of vitamin D we obtain with sun exposure.

The message: Don't rely on a tan to gauge the adequacy of vitamin D. Maybe that works when you're 16 years old, but not at age 50 or 60. There's only one way to know your vitamin D status: a blood level of 25(OH) vitamin D.


Copyright 2008 William Davis, MD

Planned obsolence

In the 1960s, you’d purchase a new car. If you changed the oil, adhered to the maintenance schedule—and were lucky—you might expect to get 100,000 miles out of your automobile. Only an occasional car made it beyond that odometer hurdle. Even if the engine made it past the 100,000 mile milestone, the automobile body would inevitably start to develop rusting decay at the edges of the fenders, signaling body rot that threatened to open gaping holes of metal.



Then along came Toyota and Honda, whose cars easily reached 100,000 miles and well beyond, reliably and with bodies intact. As this realization sunk into the American consciousness, many asked, “Why can’t American automakers accomplish the same sort of trouble-free longevity?” “Buy American” emerged as a mantra to preserve American jobs and prop up an economy vulnerable to the superior automotive products from Detroit’s competitors.

Of course, American automakers have since responded to the challenge posed by the Japanese auto industry and produced automobiles that essentially matched the reliability and longevity of Japanese cars. But, the great unanswered question remains: For years before the onslaught of Japanese competition, did Detroit quietly plot to maintain a policy of planned obsolescence that ensured Americans would have to scrap the old and buy a new car every few years whenever the odometer tipped over 100,000 miles?

We will never know. At worst, it may represent the behind-closed-doors, back-slapping sort of plotting that, for many years, maximized revenues, ensured shareholder returns, and secured executive paychecks. Or, perhaps it wasn’t some evil conspiracy but just complacency, a profitable position of comfort at that. There’s little incentive for industry insiders to reveal such self-incriminating information.

But the example set by the American auto industry presents an unusual learning opportunity for us, a chance to make some useful comparisons to the heart healthcare industry.

Is the American healthcare industry also guilty of practicing a policy of “planned obsolescence,” just like Detroit? The product that helplessly crumbles is, of course, not your rust-riddled automobile, but you.

When someone sees a primary care physician year after year, yet appears one morning in the emergency room, clutching his or her chest in agony from the closed coronary artery responsible for a life-threatening heart attack—prompting the flurry of activity that results in $100,000 in hospital procedures . . .

Perhaps “planned obsolescence” is not the perfect phrase to describe the situation, but the principle still applies: A failure to inform the patient that such an outcome was possible—no, probable—makes you wonder whether such an outcome was predictable and thereby preventable in the first place.

What should we do when planned obsolescence leads us down a path engineered by someone who has something, often substantial, to gain? Even if it's just complacency, or adhering to a beaten, ineffective status quo (can you say "low-fat diet?), it all points in the same direction.

You have a choice: Refuse to buy a 1962 Impala of health care, otherwise known as conventional heart disease management.

Melatonin for high blood pressure?

Melatonin is fascinating stuff.

In addition to its use as a sleep aid, melatonin exerts possible effects on cardiovascular parameters, including anti-oxidative action on LDL, reduction in sympathetic (adrenaline-driven) tone, and reduction in blood pressure.

Several studies document the blood pressure-reducing effect of melatonin:

Daily nighttime melatonin reduces blood pressure in male patients with essential hypertension.

Melatonin reduces night blood pressure in patients with nocturnal hypertension.

Prolonged melatonin administration decreases nocturnal blood pressure in women.

Blood pressure-lowering effect of melatonin in type 1 diabetes.


But blood pressure may be increased when melatonin is added to nifedipine, a calcium channel blocker:

Cardiovascular effects of melatonin in hypertensive patients well controlled by nifedipine: a 24-hour study.


Effects on BP tend to be modest, on the order of 5-8 mmHg reduction in systolic, half that in diastolic.

But don't pooh-pooh such small reductions, however, as small reductions exert mani-fold larger reductions in cardiovascular events like heart attack and stroke. NIH-sponsored NHANES data (see JNC VII), for example, document a doubling of risk for each increment of BP of 20/10. The Camelot Study demonstrated a reduction in cardiovascular events from 23% in placebo subjects to 16.7% in subjects taking amlodipine (Norvasc) with a 5 mm reduction in systolic pressure, 2 mmHg drop in diastolic pressure. Small changes, big benefits.

Many people take melatonin at bedtime and are disappointed with the effects. However, a much better way is to take melatonin several hours before bedtime, e.g., take at 7 pm to fall asleep at 10 pm. Don't think of melatonin as a sleeping pill; think of it as a sleep hormone, something that simply prepares your body for sleep by slowing heart rate, reducing body temperature, and reducing blood pressure. (You may need to modify the interval between taking melatonin and sleep, since individual responsiveness varies quite a bit.)

I also favor the sustained-release preparations, e.g., 5 mg sustained-release. Immediate-release, while it exerts a more rapid onset of sleep, allows you to wake up prematurely, The sustained-release preparations last longer and allow longer sleep.

The dose varies with age, with 1 mg effective in people younger than 40 years, higher doses of 3, 5, even 10 or 12 mg in older people. Sustained-release preparations also should be taken in slightly higher doses.

The only side-effect I've seen with melatonin is vivid, colorful dreams. Perhaps that's a plus!

The forces that shape heatlh care

Thinking about the programs for health care reform proposed by the three Presidential candidates highlights a distinct peculiarity of American style health care.

American health care is shaped to an unprecedented degree by five forces:

1) The drug industry

2) The health insurance industry

3) Hospitals

4) Fear of litigation

5) The uniquely American attitude of refusing compromise in access to health care services or products, regardless of the cost (for those who can afford health insurance)


All five of these unique forces have created this thing (monster?) we call health care. Remove or modify any one of these forces, and the health care landscape would look dramatically different.

The drug industry has recently been on the receiving end of plenty of negative press. This warms my bones. Decades of heavy-handed lobbying, sleazy marketing to physicians (all too willing to be wined and dined), and behind-the-scenes manipulation of clinical data are coming back to bite them. Sadly, the drug industry is so powerful that this bit of fuss is not likely to substantially change their ways.

I am thrilled that all three Presidential candidates agree that reimportation of drugs from outside the U.S. is a good idea. While the shrug of the shoulders federal and state attitude towards importation of drugs from Canada has not resulted in cost savings sufficient to impact on overall costs, it surely will lead to savings when practiced on a broad basis by pharmacies, distributors, and other bulk buyers of pharmaceuticals.

Senator Obama, in particular, has used strong language in his criticism of the health insurance industry, tough talk that is needed in an age in which insurance executives bring home salaries in the hundreds of millions of dollars and stock prices are climbing due to substantial profit gains within the industry, going against the grain of increasingly costly premiums. However, the Clinton experiment of federalizing health care during Bill Clinton's term that caused all the big boys to band together (most notably health insurance companies and drug industry) has tempered enthusiasm for attacking the insurance industry head-on. In both Democrats' health care reform proposals, the option of private insurance is preserved, as it is in the McCain proposal.

How about hospitals? Hospitals, though on a smaller scale than the nationwide reach of the drug and insurance industries, aim to maintain health service delivery in hospitals. For instance, the high-tech bypass service in the hospital gets plenty of local media coverage, as does the newest DaVinci robotic surgery, bariatric surgery, and other revenue-rich services. Many hospitals have forgotten that their mission is delivery of health, of which revenue creation and profiting from disease should only be part.

How big is fear of litigation? Estimates vary, but several have quoted numbers in the neighborhood of 20 to 30% of overall health care costs. At the street level from what I see, I'd say at least that much. Fear of litigation is rampant, often unrestrained, and sometimes leads to the craziest, illogical sequence of testing. Chest pain, for instance, no matter how trivial, will typically trigger around $5000 worth of testing (nuclear stress test, echocardiogram, laboratory work, etc.) Emergency room visit for a minor injury? CT scan of head, chest, abdomen. A formula to minimize this aspect of fear in health care delivery would generate enormous savings.

The last issue, the uncompromising nature of Americans in health--always wanting the latest new drug, new procedure, "best" surgeon--often simply causes the health care consumer to fall victim to marketing. If a hospital advertises the newest procedure, people want it regardless of whether it represents genuine improvement over the older procedure. The newest sleeping pill, antidepressant, antihypertensive, etc. replaces the old yet equivalent product, but at considerably greater cost.

I am optimistic that, regardless of which candidate gains the White House, that some reform is on the way. I do fear, however, that progress will be small and incremental, since major change of the sort that would slash hundreds of billions of dollars in costs would rouse the powers-that-be (drug industry, health insurers, etc.) to once again combine forces and combat the disruption of their franchise.

Until you and I see real change and cost savings coming through either legislation or free market advances, we need to continue to make full use of the self-empowering health information that we gain through venues like the web.



Copyright 2008 William Davis, MD

Lipoprotein(a): Surprising Poll Results

No doubt, our little informal poll asking readers whether they have lipoprotein(a), is skewed towards people inclined to respond because they have this genetic trait.

Nonetheless, the response is telling. Of 82 respondents:

--40 (48%) said they did have Lp(a)

--16 (19%) said that they did not have Lp(a)

--26 (31%) said that they did not know whether or not they had Lp(a)


Though admittedly an informal analysis, I'd draw several conclusions from this simple "experiment".

One, while the proportion of people responding that they have Lp(a) may not be accurate, it is a prevalent genetic risk factor that, according to formal studies, is present in 17% of people with coronary or vascular disease, 11% of the broader population. This number may be even higher if the newer particle number assays (measurements) are used (with results expressed in nmol/L), since an occasional person with a "normal" Lp(a) in mg/dl (weight-based) will prove to have increased Lp(a) by nmol/L (particle number-based). (The reason for this phenomenon is not clear. It may be consequent to variation in apo(a) size, with larger apo(a) varieties of Lp(a) occasionally escaping detection .) As our little poll shows, plenty of people have Lp(a).

Two, readers of this blog tend to be highly motivated, sophisticated, and knowledgeable about health and heart disease. Yet a substantial portion--31%--did not know whether they have this crucial risk factor. That shouldn't be. The unnecessary difficulty of getting this simple blood test performed has been driven home to me repeatedly when I identify this factor in someone and then suggest that their grown children and parents, each of whom have a 50% chance of having Lp(a), be tested. It's not uncommon for a 35-year old son, for instance, to say that his doctor refused, claiming it is an unproven risk marker, or to simply say that he/she doesn't know what it is.

No doubt, just knowing whether you have Lp(a) or not is not the end of the story. Reducing Lp(a) and its associated co-factors is no easy matter. With several hundred patients in my practice with Lp(a), it occupies much of my time and energy. Sometimes it leads to enormous successes , but it can also pose a real challenge.

There should no longer be any doubt that Lp(a) is associated with significantly increased risk of cardiovascular disease. This has been demonstrated conclusively across dozens of studies. Risk from Lp(a) is over and above that posed by other risk factors; it also amplifies the risk posed by other factors, e.g., small LDL, inflammatory phenemena, homocysteine, total LDL, low HDL.

In the world of Lp(a), our two most desperate needs for the future are:

1) Better education of physicians and the public, and

2) More effective treatment options.

Thus, our reasons to form The Lipoprotein(a) Research Foundation. Steps to gain tax-exempt status are being pursued as we speak.

I can't help but wonder whether, like vitamin D, a solution is right beneath our noses. An investment in research to fund the trials to better explore both basic science as well as practical treatment options might yield an answer more readily than we think. Wouldn't that be great?
All posts by william-davis

What's for breakfast?

Breakfast, for some reason, seems to be the toughest meal of the day for many people.

I think it's because the quest for sweet has dominated the American breakfast for so long, with its half-century legacy of cartoon character-festooned breakfast cereals; baked flour products like pancakes, waffles, and English muffins; more recently, "healthy" alternatives like bran muffins and oat waffles.

This breakfast lifestyle has also contributed to the obesity and diabetes ("diabesity") epidemic. Breakfasts of wheat- or corn-based cereals, even those labeled "heart healthy," fruit, and whole grain breads are guaranteed paths to low HDL cholesterol, high triglycerides, flagrant small LDL, increased inflammatory responses, high blood pressure, and higher blood sugar. Such foods also make you tired, make your abdominal fat grow (wheat belly), and increase appetite so that you want more.

So what can you eat for breakfast that doesn't provoke these patterns?

I will never pretend to be terribly clever in creating meal menus, but I can tell you what has worked for me and many of my patients. Be warned: It may require you to suspend your previous notions of what "should" be included in a list of breakfast foods.

Here are some examples that you may find helpful:

--Raw nuts--one or several handfuls of raw almonds, walnuts, pecans, pistachios
--Cheeses--the real, traditional sorts like gouda, goat, Swiss, edam, etc. (not Velveeta, Cheez Whiz, etc.)
--Eggs, Egg Beaters--and "spice" them up with sun-dried tomatoes, salsa, olives, tapenades, olive oil, onions, green peppers, etc.
--Yogurt (real, of course), cottage cheese
--Ground flaxseed, oat bran--as hot cereals or added to yogurt, cottage, or other foods. Esp. helpful for reducing both total LDL and the proportion of small LDL.
--Oatmeal--slow-cooked, not the instant nonsense.
--Soups--great for winter.
--Dinner foods--chicken, beef, fish, green beans, asparagus, tomatoes, etc., most easily added by saving left-overs from dinner. You'll be surprised how filling dinner foods eaten at breakfast can be.

It's really not that tough. It just means selecting from an entirely different list of foods than you might be accustomed to.


Copyright 2008 William Davis, MD

The first lawsuit?


The closing arguments in actor John Ritter's wrongful death lawsuit are over and the two doctors charged with negligence cleared, five years after his death from a dissection (tear of the inner lining) of the thoracic aorta. The family sought $67 million in damages, claiming that the aortic dissection was misdiagnosed as a heart attack and that the enlarged aorta should have been reported to Mr. Ritter two years earlier during a full body scan.

The AP story can be viewed at http://ap.google.com/article/ALeqM5gmv6HnJJPBee2gWgEYResT5m6YkAD8VDF9CO0


Well, perhaps this is the start of a trend. Up until now, it has been commonplace for doctors to ignore many of the important findings on heart scans, full body scans, and similar direct-to-the-public imaging services. For instance, similar to John Ritter's case, enlarged thoracic aortas are commonly ignored. I'd even say that as a rule they are ignored. I have seen many patients in consultation who have had large aortas identified on heart scans, yet nothing--not a thing--was done about it. While the doctors escaped a lawsuit this time, it might not happen a second time.

I truly hope that Mr. Ritter's unfortunate experience and the consequent lawsuit do not trigger the usual defensive medicine response of resorting to major procedural "solutions."

A better response would be to 1) identify the problem--enlarged aorta in this case, 2) identify the causes, then 3) correct the causes. It does not necessarily mean that a major procedure like replacing the aorta (a horrendous surgery, by the way) needs to be pursued each and every time.

It is possible that Mr. Ritter's lawsuit is just the first. Over the next several years, it could trigger an avalanche of lawsuits for all the neglected findings on tests like heart scans, body scans, and other imaging methods that are gaining expanded direct-to-consumer access.


Images courtesy Wikipedia.

The origins of heart catheterization: Part II

On the afternoon of October 30th, 1958, nearly 30 years after Werner Forssmann’s fumbling attempts, Dr. Mason Sones, a 5 foot 5 inch, plain-talking, cuss-every-few-words, cigarette-wielding radiologist at the Cleveland Clinic, was performing a routine angiogram of a patient’s aorta (the large vessel emerging from the heart) in a dark basement laboratory. (In Sones’ day, imaging methods remained primitive, disease diagnosis relying more than anything else on the physician’s powers of observation and crude diagnostic procedures. Abdominal pain was assessed with exploratory laparotomy, headaches with air injected into the brain and nervous system (“pneumoencephalography”), an excruciatingly painful ordeal. Being able to track the course of x-ray dye injected into specific internal organs, whether liver, biliary tree, aorta, lungs, or coronary arteries, represented a huge advance in diagnostic tools for human disease.)

In 1958, no one had yet injected dye directly into the coronary artery of a living human.


Just as the dye injector was triggered, Dr. Sones’ eyes widened in horror when the black and white monitor showed that the catheter had inadvertently jumped into the right coronary artery. The injection pump, already triggered to release its load, proceeded to pump 30 cc of X-ray dye straight into the artery. (Modern techniques usually require only 5–10 cc of dye.) Dr. Sones recounts the incident:

“It was late in the day and we were tired. I hit the switch to rev up the x-ray generator so I could see. As the picture came on, I could see that the damn catheter was in the guy’s right coronary artery. And there I was, down in the hole [a recess to shield him from radiation]. I yelled, “Pull it out! Pull it out!”*? By that time, about 30 cc of the dye had gone into the coronary artery. I climbed out of the hole and I grabbed a knife. I thought that his heart would fibrillate and I would have to open his chest and shock his heart. [In Sones’ day, modern CPR hadn’t yet been developed as a method of resuscitation.] But he didn’t fibrillate—his heart stopped. I demanded he cough. He coughed three times and his heart began to beat again. I knew at once that if the heart could tolerate 30 cc of dye, we would be able to safely inject small amounts directly into the coronary artery. I knew that night that we would have a tool to define the anatomic nature of coronary disease.”


*An observer, Dr. Julio Sosa, reported that Dr. Sones, in his shock, also blurted, “We’ve killed him!” After all, conventional wisdom of that era, based on observations from dye injections into the coronary arteries of dogs, was that injecting x-ray dye into human coronary arteries would result in immediate death from the electrical imbalance provoked in heart muscle momentarily deprived of oxygen-carrying blood.

Thus it was established that it was indeed possible to directly inject x-ray dye into human coronary arteries and reveal its internal contours. That’s not to say that the x-ray dyes of 1958 were innocuous. Far from it. In addition to briefly interrupting heart rhythm, as happened with Sones’ first accidental attempt, the dyes used then typically caused dizziness and the sudden urge to vomit. During the first 30 years of direct coronary catheterizations, it was common for hospital staff to run to the patient’s side, bucket in hand to catch the inevitable vomit, once the heart was jump-started by coughing.

Not surprisingly, Dr. Sones’ discovery set off both an avalanche of criticism and bold predictions of how the new technique might change the course of diagnosis in heart disease.

Over the subsequent weeks and months, Dr. Sones proceeded to purposefully insert catheters into coronary arteries and create angiograms that revealed the extent of coronary atherosclerosis. He learned how to fashion new catheter shapes to facilitate access to the arteries. Sones developed an impressive experience in the new technique. For the first time, clear images of the coronary arteries were routinely obtainable for the confident diagnosis of coronary atherosclerosis before death. Dr. Sones became an unlikely celebrity in Cleveland, entertaining physicians from around the world eager to learn about his methods, politicians and celebrities, even Middle Eastern nobility complete with bodyguards and food testers.

Dr. Sones continued to work in Cleveland, furthering the techniques of heart catheterization after his fortuitous error. He died of lung cancer in 1985, 17 years after his discovery.

Thus was born the modern age of heart catheterization.

Today, over 10,000 heart procedures are performed in the U.S. every day, 365 days a year, the vast majority of which involve heart catheterization or begin with a heart catheterization. Dr. Sones' fortuitous blunder was followed by 30 years of productive refinement and development before the blatant excesses of this technique really began to be exploited.


Copyright 2008 William Davis, MD

The origins of heart catheterization: Part I

The modern era of heart disease care was born from an accident, quirky personalities, and even a little daring.

The notion of heart catheterization to visualize the human heart began rather ignominiously in 1929 at the Auguste-Viktoria Hospital in Eberswalde, Germany, a technological backwater of the day. Inspired by descriptions of a French physician who inserted a tube into the jugular vein of a horse and felt transmitted heart impulses outside the body, Dr. Werner Forssmann, an eager 25-year old physician-in-training, was intent on proving that access to the human heart could be safely gained through a surface blood vessel. No one knew if passing a catheter into the human heart would be safe, or whether it would become tangled in the heart’s chambers and cause it to stop beating. On voicing his intentions, Forssmann was ordered by superiors not to proceed. But he was determined to settle the question, especially since his ambitions captured the interest of nurse Gerda Ditzen, who willingly even offered to become the first human subject of his little experiment.

Secretly gathering the necessary supplies, he made his first attempt in private. After applying a local anesthetic, he used a scalpel to make an incision in his left elbow. He then inserted a hollow tube, a catheter intended for the bladder, into the vein exposed under the skin. After passing the catheter 14 inches into his arm, however, he experienced cold feet and pulled it out.

One week later, Forssman regained his resolve and repeated the process. Nurse Ditzen begged to be the subject, but Forssmann, in order to allow himself to be the first subject, tricked her into being strapped down and proceeded to work on himself while she helplessly watched. After stanching the oozing blood from the wound, he threaded the catheter slowly and painfully into the cephalic vein, up through the bicep, past the shoulder and subclavian vein, then down towards the heart. He knew that simply nudging the rubber catheter forward would be sufficient to direct it to the heart, since all veins of the body lead there. With the catheter buried 25 inches into his body, Forssmann untied the fuming Ditzen. Both then ran to the hospital’s basement x-ray department and injected x-ray dye into the catheter, yielding an image of the right side of his heart, the first made in a living human.



Thus, the very first catheterization of the heart was performed.



An x-ray image was made to document the accomplishment. Upon hearing of the experiment, Forssmann was promptly fired by superiors for his brazen act of self-experimentation. Deflated, Forssmann abandoned his experimentation and went on to practice urology. He became a member of the Nazi party in World War II Germany and served in the German army. Though condemned as crazy by some, physicians in Europe and the U.S., after hearing of his experience, furthered the effort and continued to explore the potential of the technique. Forssmann himself was never invited to speak of his experiences outside of Germany, as he had been labeled a Nazi.

Many years after his furtive experiments, the once intrepid Dr. Forssmann was living a quiet life practicing small town medicine. He received an unexpected phone call informing him that he was one of three physicians chosen to receive the 1956 Nobel Prize for Medicine for his pioneering work performing the world’s first heart catheterization, along with Drs. André Cournand and Dickinson W. Richards, both of whom had furthered Forssmann’s early work. Forssmann remarked to a reporter that he felt like a village pastor who was made a cardinal.

Strange, but true.


Copyright 2008 William Davis, MD

Conventional therapy vs. alternative therapy

Rose is a 75-year old woman, mother of four, grandmother of many more.

Rose's story started after a heart attack 18 months ago that resulted in two stents. She was advised to follow an American Heart Association diet and take Lipitor. However, some months later, after her fourth stent, she became disilluioned in the conventional approach to heart disease and sought alternative therapies to help reduce or reverse her heart disease.

She found an alternative health practitioner who advised chelation, antioxidant vitamins for "excessive oxidation," and several homeopathic preparations.

Nothing was said about diet or exercise. Nothing was said about the baked flour products and pastries that occupied at least two meals every day. Nothing was said about the candies she indulged in several times per day, nor the soft drinks. Nothing was said about the wildly fluctuating blood sugars, poorly controlled by an oral diabetes agent. Thirty pounds of weight gain over the past 5 years with no exercise or physical activity? No comment here, too.

In short, Rose was the "graduate" of the conventional approach, as typically offered nationwide thousands of times a week. She was also the recipient of the insight of at least one alternative health practitioner, eager to reject conventional notions of how to achieve heart health.

So I then met her. She was experiencing chest pains every day, several times per day. Blood pressure over 200. At 5 ft, 3 inches, weight: 186 lbs.

Initial laboratory results:

HDL cholesterol 42 mg/dl
LDL 132 mg/dl
Triglycerides 263 mg/dl
Blood sugar 173 mg/dl


You can fill in the rest. In short, Rose was a disaster. Despite the attentions of several professionals from both the conventional as well as alternative camps, she was careening rapidly towards failure. She'd been given various crutches, Band-Aids, and salves, none of which resulted in any possibility of long-term relief from her aggressive disease.

My point: As I've said previously, all we want is truth. We want effective, rational approaches that yield real benefit. A stent? All that provides is temporary restoration of blood flow. Statin agents? They do indeed reduce LDL cholesterol. But what if Rose has 8, 9, or 10 other causes of heart disease unaffected by the statin drug? It will do little or nothing.

Nobody had addressed many of the root causes of Rose's disease: insulin resistance, high triglycerides, inactivity, obesity, hypertension (and identifying the reasons why her blood pressure was so high), vitamin D deficiency (virtually guarantted to be severe), junk foods including the ones known as "whole grains."

My message: Success in heart disease, as well as all aspects of health for that matter, doesn't necessarily have to come from an "alternative" approach, nor a "conventional" approach. It comes from applying what is truly effective, regardless of what label someone applied to it.

I would no sooner trust my health and life to an alternative health practitioner hawking unusual herbs and remedies than I would submit to a heart catheterization, three stents, followed by a statin drug. There's small benefit in both approaches, but none are the best. You've got to look elsewhere for that.


Copyright 2008 William Davis, MD

The JELIS Trial

The Japan eicosapentaenoic acid (EPA) Lipid Intervention Study (JELIS) is a clinical trial that all Track Your Plaquers should know about.

This enormous trial followed a simple design:

Japanese men, between 40-75 years, and Japanese postmenopausal women aged <75 years with total cholesterol 250 mg/dl or greater were enrolled. A total of 18,645 subjects (mean age, 61 years; 31% male) participated: 36% had hypertension, 15% had diabetes, and 20% had coronary disease (history of heart attack or heart procedure). Average starting total cholesterol 275 mg/dl; LDL 180 mg/dl. All participants were treated with pravastatin 10 mg/day or simvastatin 5 mg/day; approximately half also received the omega-3, EPA, 1800 mg/day, in addition to one of the statin drugs.

Treatment resulted in an average LDL reduction of 26% in all participants; the group taking EPA experienced an additional 10% reduction in triglycerides. All major cardiovascular events were tracked and tabulated, including sudden cardiac death, fatal or nonfatal myocardial infarction (MI), unstable angina pectoris, coronary artery bypass surgery, and coronary angioplasty.

After nearly five years, 3.5% of statin-only participants experienced an event; 2.8% of statin + EPA experienced an event. The (often misleading and frequently abused value) "relative reduction" was therefore 19%.

There are several features that make the JELIS trial interesting:

--There were an unusually low number of cardiovascular events in the entire group, lower than nearly all American and European trials of similar design. This likely points to the greater burden of atherosclerotic heart disease in the U.S. compared to Japan. Rates in comparable U.S.-based trials usually range from 6-14%, sometimes more.

--Both the participants without identified heart disease at enrollment and those with heart disease at enrollment obtained a similar magnitude of beneficial reduction in cardiovascular events.

--There was an unusual preponderance of women--69%--unlike most other trials of cardiovascular events. We might therefore argue that JELIS most conclusively showed that benefits of EPA are most confidently demonstrated for females.

--A fish oil preparation containing only EPA was used, rather than the usual EPA + DHA. There are discussions from some corners that argue that DHA is more important than EPA, e.g., algae sources. However, JELIS would argue that EPA does play a role. Is EPA with DHA better, worse, or no different? Unfortunately, there are insufficient data--large, randomized data like JELIS--to help us. Recall that GISSI Prevenzione used a combination of EPA and DHA, as have virtually all other trials examining the effects of fish oil. Also, keep in mind that the epidemiologic observations of the cardiovascular benefits of eating fish suggest that the naturally-sourced omega-3s--a combination of EPA and DHA--are associated with benefit.

--It's surprising that any difference at all was demonstrated, given the high intake of fish in the Japanese. In fact, blood levels of EPA in participants before taking EPA was five-fold higher than in western populations.


One potential difficulty: The study was funded by the manufacturer of the EPA preparation used, Mochida Pharmaceutical Company. We all know what that can do to results.

Nonetheless, the JELIS trial is a study that adds to the emerging wisdom in fish oil.


Copyright 2008 William Davis, MD

Omega-3 MUST be from fish oil

Despite my rants in this blog and elsewhere, at least once a day I'll have a patient say, "I cut back (or eliminated) my fish oil because I get my omega-3s from _______ (insert your choice of flaxseed oil, walnuts, yogurt, mayonnaise, bread, etc.)."

(See prior Heart Scan Blog post: Everything has omega-3.)

When I point out to them that the "omega-3s" in these products are not the same as the EPA and DHA from fish oil, they invariably declare, "But it says so here on the label: 'Contains 200 mg of omega-3 fatty acids'!"

Apparently, some of my colleagues have even endorsed this concept of replacing the omega-3s from fish oil with these "alternatives."

It's simply not true. The linolenic acid that is being labeled as omega-3, while it may indeed provide health benefits of its own, cannot replace the EPA and DHA that fish oil provides.

The most graphic example of the differences between the two classes of oils is in people with a condition called familial hypertriglyceridemia. People with this condition have triglyceride levels of 400, 600, even thousands of mg/dl--very high. Fish oil, usually providing EPA and DHA doses of 1800 mg per day and higher, reduce triglycerides dramatically. A person with a starting triglyceride level of, say, 900 mg/dl, may take 2400 mg of EPA and DHA from fish oil and triglycerides plummet to 150 mg/dl. This person then decides to replace fish oil with a linolenic acid source like flaxseed oil. Triglycerides? 900 mg/dl--no effect whatsoever.

Familial hypertriglyceridemia represents an exagerrated example of the differences between the two oils. Even if you don't have this genetic condition, the differences between the oils still apply.

EPA and DHA are activators of the enzyme, lipoprotein lipase, that accelerates clearance of triglycerides from the blood. Linolenic acid from flaxseed oil, walnuts, and other food sources does not. EPA and DHA block after-eating (post-prandial) accumulation of food by-products that can contribute to coronary and carotid plaque. Linolenic acid does not. EPA and DHA block platelets, reduce fibrinogen, and exert other healthy blood clot-inhibiting effects. Linolenic does not.

The 11,000-participant GISSI-Prevenzione Trial that showed 28% reduction in heart attack, 45% reduction in cardiovascular death with omega-3s used . . . fish oil.

The 18,000 participant JELIS trial that showed 19% reduction in cardiovascular events when omega-3s were added to statin therapy used . . . fish oil. (Actually, in JELIS, they used only EPA wtihout DHA.)

Linolenic acid is not a waste, however. It may exert anti-inflammatory benefits of its own, for instance. But it exerts none of the triglyceride-modifying effects of EPA or DHA.

EPA and DHA from fish oil and linolenic acid from foods each provide benefits in their own way. Ideally, you include both forms of oils--fish oil and linolenic acid sources--in your daily diet and obtain full benefit from each separate class. But they are not interchangeable.


Copyright 2008 William Davis, MD

Osteoporosis and coronary calcium

Several studies over the years have demonstrated a curious paradox:

People with more osteoporosis (thin bones) tend to be more likely to have coronary disease (heart attacks). They also tend to have higher heart scan scores (more coronary calcification as an index of atherosclerotic plaque).

People with more coronary disease and higher heart scan scores tend to have more osteoporosis.



In other words, regardless of which way you tackle the question--osteoporosis first or heart disease first--it leads to the same conclusion: Both conditions are somehow related.

I realize I harp an awful lot on this whole vitamin D issue. But, even after correcting the vitamin D blood levels of many hundreds of people, I remain enthusiastic as ever about the untapped potential of this fascinating factor.

So I couldn't resist showing this amazing comparison of how the long-term effect can be quite graphic.

The first scan is from a 46-year old man and shows normal coronary arteries without calcium and normal density of the vertebra (a common and reliable place to measure bone density).

























The second image is from a 79-year old man with both severe coronary calcification (and therefore severe coronary disease) and severe osteoporosis.
























It makes you wonder if the disordered metabolism of calcium through vitamin D deficiency allows transport of calcium away from bone and into coronaries. This has, however, been shown to not be the case. Instead, they are separate processes, each under local control, but sharing a common pathophysiology (causative factors).

An intriguing question: Would the 79-year old still look like the 46-year old had he begun increasing his vitamin D intake at, say, age 30?

About comment responses and moderation

Just a brief word about my responses to reader comments:

I appreciate the many often insightful and interesting reader comments I receive to the Heart Scan Blog. However, managing them and responding to them has simply become impossible, due to time demands.

I'm afraid that I am unable to answer questions seeking medical advice; this is for your doctor, who knows you and can diagnose and prescribe. I cannot.

I'm also unable to engage in lengthy debates; I've had commenters become very angry when I was unable to engage in lengthy conversations on some topic. Nor am I able to do Google or literature searches for commenters, or review studies, papers, or other materials.

I would urge any readers who wish to engage in in-depth discussions about these issues, talk about lipoproteins, heart disease reversal, etc. to do so on the Track Your Plaque Forums. Yes, it is a fee-for-membership website, a model that has become necessary to pay for the services we provide (not pay me).

I wish that I could answer all the concerns and questions that come my way, but it's simply physically impossible doing so while maintaining a full-time very busy cardiology practice, developing the Track Your Plaque website (which is becoming an enormous responsibility), publishing scientific data, maintaining hospital responsibilities, and spending time with my wife and family. We're all busy and I'm no different. I'm afraid that it's my responses to blog comments that I will have to sacrifice.

I invite commenters to continue to comment on these posts, as I've learned many new things by reading them and find them helpful feedback. And I do read them. Should an especially helpful comment be made, I will feature it in a new blog post, rather than respond directly.

"Flying in the fog"

I received this wonderful response to The Heart Scan Blog post Hammers and Nails:

I am 65 years old. I had a stent inserted in the "widow-maker" artery (80% blockage) a year ago. I had passed out a couple of times (heart rate dangerously low - 30s). I rode to the hospital in an ambulance. Tests revealed short LBBB episodes; mild mitral regurgitation, mild tricuspid regurgitation. Catherization showed 3 vessel CAD. I was told that a medicated stent was absolutely necessary given the situation; regardless, I have to accept that. A pacemaker was installed to prevent bradycardia and keeps heart rate from dropping below 60. I have 20% L distal main blockage and 90% lesion of the high first obtuse marginal at the takeoff. The right coronary had 60% posterior lateral branch stenosis.

Since then I have reduced TG from 360 to 60, LDL from 89 to 82 (although a few months ago it was in the mid-70s), and increased HDL from 30 to 46. I went from 265lbs to 190lbs and hope to eventually get to 180lb this Spring. I did it by progressing from walking to trotting (slow run) and dietstyle changes (low-GI veggies, fruits, etc.) .













On a recent visit the cardiologist said the the LDL needs to be 70 or below to "freeze" the 90% blockage and gave me a prescription for Lipitor. I asked if there were alternatives, like diet, supplements, etc. He admitted that he did not know about those alternative but did know Lipitor. When the only tool you have is a hammer then everything is a nail. I understand that the 90% blockage is important but will not take the Lipitor to achieve the 12 points reduction. Seems like an overkill.

I asked him if there was a way to evaluate my current condition. I was told there was no way. Basically, if I have no symptoms, good. If I have symptoms then it will have to be evaluated. Death could be the only symptom. I swear he was about to say bypass surgery ($$$$$$!) was inevitable. Something is wrong with this "fly-in-the-fog-and-hope-you-don't- hit-a-mountain" approach. Hope is not a strategy!

I am confident that I can reduce LDL to below 70 based on eliminating wheat-products in my diet plus increasing oat bran in my diet. I also take fish oil daily (EPA/DHA-2g). I am looking for a new cardiologist. I just recently purchased your book and find it very instructive. In the meantime I have an appointment with my primary care physician to discuss implementing the Track Your Plaque program. I realize that the one stent will skew the scan numbers but can be used as a baseline number.



Phenomenal weight loss! That alone has likely cut this man's risk in half. But is that it? Is the cardiologist correct--take Lipitor and hope for the best?

Of course not. There are many additional strategies to employ. Eliminating wheat from the diet is an excellent idea: HDL will skyrocket, triglycerides drop even further, small LDL will drop like a stone, blood sugar and blood pressure will drop. He will have more energy, get rid of afternoon energy slumps, sleep better.

He has already added fish oil. If his cardiologist did not mention this, I would say he was guilty of malpractice. The data supporting the addition of fish oil to the treatment program of anyone with heart disease is overhwelming. GISSI Prevenzione: 11,000 participants--28% reduction in heart attack, 45% reduction in death from heart attack. The Japanese JELIS trial of 18,645 participants--19% reduction in dangerous heart events. It's also clear that omega-3 fatty acids from fish oil also compound the benefits of statin agents, should this man choose to begin Lipitor.

Vitamin D brought to normal blood levels is his next "secret weapon" that will further boost his lipids and lipoproteins further into not just "normal" territory, but beyond belief. Even though we aim for 60-60-60 for LDL-HDL-triglycerides in the Track Your Plaque program, adding vitamin D can yield numbers you've never seen before. It's not uncommon, for instance, to see a 10 or 20 mg/dl jump in HDL.

Identify all other hidden causes of coronary plaque. If all the causes have not been fully identified, how can anyone hope to gain full control over coronary plaque growth?

Re: LDL cholesterol of 89 mg/dl at the start. Of course, this is a calculated value, not measured. Because HDL was low and triglycerides high at the start of his program, this means that true LDL--if actually measured--was probably more like 180 to 250 mg/dl, and it was probably nearly all small. So his cardiologist might have advised a helpful treatment, though for the wrong reasons.

Our reader has gone a long way on his own in creating his own prevention program. But there's yet more to do, particularly if the goal is reversal. It is shocking to me that a man like our reader, clearly articulate and motivated, gets virtually no advice beyond "take Lipitor" after all the procedural benefits have been reaped.

Even though one artery can no longer be "scored" due to the presence of the metallic stent, a heart scan would still be invaluable for long-term tracking purposes, just as we advocate in the Track Your Plaque program.



Copyright 2008 William Davis, MD
All posts by william-davis

Thyroid: Be a perfectionist

If you'd like to reduce LDL cholesterol with nearly as much power as a statin drug, think thyroid.

When thyroid is corrected to ideal levels, LDL cholesterol drops 20, 30, 40 mg/dl or more, depending on how poor thyroid function and how high LDL are at the start. The poorer the thyroid function (the higher the TSH or the lower the T3 and T4) and the higher the LDL cholesterol, the more LDL drops with thyroid correction.

(For those of you minding LDL particle size, such as Track Your Plaque Members, the "dominant" LDL species will drop: If you are genetic small LDL, small LDL will drop. If you have mostly large LDL because of being wheat-free and sugar-free, then large LDL will drop.)

One of the problems is that many healthcare providers blindly follow what the laboratory says is "normal" or the "reference range," which is usually nothing more than a population average (actually the mean +/- 2 standard deviations, a common method of developing references ranges). In other words, a substantial degree of low thyroid function, or hypothyroidism, can be present when your doctor adheres to the reference range provided by the laboratory.

What does it mean to achieve ideal thyroid status? My list includes:

--Normal oral temperature of 97.3 F first upon arising. (The thyroid is the body's thermoregulatory organ.)
--TSH 1.0 mIU/L or less
--Free T3 upper half "normal" range
--Free T4 upper half "normal" range
--You feel good: mental clarity, energy, upbeat mood. You lose weight when you try.

Iodine replacement should be part of any thyroid health effort. Iodine is not an optional trace mineral, no more than vitamin C is optional (else your teeth fall out). The only dangers to iodine replacement are to those who have been starved of iodine for many years; increase iodine and the thyroid can over-respond. I've seen this happen in 2 of the last 300 people who have supplemented iodine.

In my view, neglecting T3 replacement is absurd. While it is not clear to me why many otherwise healthy people have low T3 at the low range of "normal" or even in the below-normal range, people feel better and have better health--faster weight loss, reduced LDL, reduced triglycerides, they are happier and enjoy more energy--when T3 is increased to the upper half of the reference range. (Crucial question: Why is the 5'-deiodinase enzyme that converts T4 to T3 inhibited, resulting in reduced free T3? What is in our diets or environment that is exerting this effect? I don't have answer, but we sorely need one.)

It pays to be a perfectionist when it comes to thyroid. Not only do you feel better, but LDL cholesterol can drop with a statin-like magnitude, but with none of the adverse effects.

If interested, Track Your Plaque offers fingerstick blood spot testing that you can perform in your own home. Each test kit will test for: TSH, free T3, free T4, along with a thyroid peroxidase antibody (a marker for Hashimoto's thyroiditis, an autoimmune inflammatory condition of the thyroid).

Nutrition Syllogism

What do you think of these chains of logic?

Cyanide is a potent lethal poison; carbon monoxide is a less lethal poison.
Therefore: plenty of carbon monoxide is good.




Having uterine cancer is a bad thing. Having uterine fibroids is a less bad thing.
Therefore: plenty of uterine fibroids are good.



These are obvious examples of seriously flawed logic. Students of logic and philosophy will recognize the above erroneous sequences as examples of the twisted arguments often used to persuade an argumentative opponent of the logic of a premise. As long ago as 335 B.C., Greek philosopher, Aristotle, recognized the pitfalls of thinking in such arguments. You think we’d know better by now.

Try this one:

White enriched flour is a bad for health; whole grains are less bad for health.
Therefore: plenty of whole grains are good for health.



Ouch!

In the 1960s, we all ate hot dogs on white buns, white flour Wonder Bread® sandwiches, Mom made cookies and cupcakes with white flour. Then, during the 1970s and 1980s, clinical studies were performed demonstrating that whole wheat and whole grains reduced colon cancer, high blood pressure, diabetes, and heart disease compared to white flour. In other words, add back fiber and B vitamins and health benefits develop: No argument here.

Therefore: whole grains must be good for health. Further, lots of whole grains?unlimited quantities of whole grains many times per day, every day?must be even better. Even the USDA says so on their nutrition pyramid, with 8-11 servings of grains per day, 4 of which should be whole grains, at the widest portion of the pyramid.

But what happens when you follow this logic through and fill your diet with whole grains?

Look around you and it’s easy to see: Appetite increases, people become obese, blood sugar increases, diabetes develops, HDL cholesterol plummets, triglycerides skyrocket, inflammatory patterns (e.g., c-reactive protein, or CRP) increase, small LDL (the number one cause for heart disease in the obese U.S.!) shoots through the roof.

I would no more fill my diet with “healthy whole grains” than I would close my garage door with the car running.

Is pomegranate juice healthy?


Pomegranate juice, 8 oz:

Sugars, total 31.50 g

Sucrose 0.00 g

Glucose (dextrose) 15.64 g

Fructose 15.86 g




In your quest to increase the flavonoids in your diet, do you overexpose yourself to fructose?

Remember: Fructose increases LDL cholesterol, apoprotein B, small LDL, triglycerides, and substantially increases deposition of visceral fat (fructose belly?). How about a slice of whole grain bread with that glass of pomegranate juice? The Heart Association says it's all low-fat!


(Coming on the Track Your Plaque website: A full in-depth Special Report on fructose in all its glorious forms and whether this is truly an issue for your health. Fructose tables and the scientific data to establish a safe "threshold" value will be included.)

Image courtesy Wikipedia

Honeydew melon


Honeydew melon:

Sugars, total 51.97 g

Sucrose 15.87 g

Glucose 17.15 g

Fructose 18.94 g

Because sucrose is half fructose (the other half is glucose), there are approximately 26 grams of fructose per one-half honeydew melon.



Image courtesy Wikipedia

Where do you find fructose?

Apple, 1 medium: Fructose 10.74 g




Honey: Fructose 17.19 grams per 2 tablespoons



Barbecue Sauce: HFCS number 1 ingredient
Ingredients: High Fructose Corn Syrup, Vinegar, Concentrated Tomato Juice (Water, Tomato Paste), Water, Modified Food Starch, Salt, Honey, Contains Less Than 2% of Molasses, Natural Flavor, Paprika, Spice, Mustard Flour, Guar Gum, Red 40.



A1 Steak Sauce: HFCS number 2 ingredient
Ingredients: Tomato puree (water, tomato paste), high fructose corn syrup, vinegar, salt, water dried onions, contains less than 2% of black pepper, modified food starch, citric acid, dried parsley, dried garlic, xanthan gum, caramel color, potassium sorbate and calcium disodium EDTA as preservatives, molasses, corn syrup, sugar, spices, tamarind, natural flavor

Do heart scans cause cancer?

Another in a series of data extrapolations that attempt to predict long-term cancer risk from medical radiation exposure was published in the July 13, 2009 Archives of Internal Medicine, viewable here.

Over the years, I've fussed about the radiation dose used by some centers for CT heart scans. (Note: I'm talking about CT heart scans, not CT coronary angiograms, an entirely different test with different radiation exposure.) In the "old" days, when electron-beam devices (EBT) were the best on the block, the old single-slice CT scanners (the predecessor of the current 64-slice MDCT scanners) exposed patients to ungodly quantities of radiation, while the EBT devices required very small quantities (0.5 mSv or about the equivalent of 4 standard chest x-rays or one mammogram).

But CT technology has advanced considerably. While EBT has been phased out (although it was an exceptional technology, GE acquired the small California manufacturer, then promptly scrapped the operation; you can guess why), multi-detector CT (MDCT) technology has improved in speed, image quality, and radiation exposure.

While it has improved, radiation exposure still remains an issue. The authors of the study applied the scanning protocols used at three hospitals and those in several CT heart scan studies, then calculated radiation exposure. They found a more than ten-fold range of exposure, from 0.8 mSv to 10.5 mSv. (All scanners were MDCT, none EBT.)

That's precisely what I've been worrying about: In the rapid rush to develop new devices, radiation exposure has often been a neglected issue. While some scan centers do an excellent job and take steps to minimize exposure, others barely lift a finger and consequently expose their patients to unnecessary radiation.

However, it's not as bad as it sounds. For one, the study included 16-slice MDCT scanners, a scanner type that I warned people to not use because of radiation. On the current most popular 64-slice devices, much lower radiation exposure is possible, on the order of 0.8-1.2 mSv routinely--if the center takes the effort.

This study, while eye-opening, will achieve some good: CT heart scans are here to stay. But the day-to-day practice of heart scanning should be:

1) standardized
2) conducted with radiation exposure as low as possible, preferably <0.8 mSv


To read more about this issue, below I've reprinted a 2007 full Track Your Plaque Special Report, CT Heart Scans and Radiation: The Real Story.




CT heart scans and radiation: The real story

“My personal opinion is that many patients today who are receiving multiple CT scans may well be getting at least comparable doses to subjects that have now developed malignancies from x-ray radiation received in the 1930s and '40s. And, similar to those days when the doses were unknown, the dose that patients receive today over a course of years of multiple CT scans is also completely unknown . . .

“I recommend that all healthcare providers become familiar with the concept that 1 in 1000 CT studies of the chest, abdomen, or pelvis may result in cancer.”


Richard C. Semelka, MD
Professor and Vice Chairman, Department of Radiology
University of North Carolina–Chapel Hill



Is this just hype to generate headlines? Or is the truth buried in the enormous marketing clout of the medical device industry, among which the imaging device manufacturers reign supreme?

It’s been over 110 years since radiation was first used for medical imaging. Over those years, it has had its share of misadventures.

In the 1930s and 1940s, before the dangers of radiation were recognized, shoe shoppers had shoes fitted using an x-ray device of the foot to assess fit. High doses of radiation were used to shrink enlarged tonsils and extinguish overactive thyroid glands. Attitudes towards radiation were so lax that doctors commonly permitted themselves to be exposed without protection day after day, year after year, until an unexpected rise in blood cancers like leukemia was observed. As recently as the 1970s and 1980s, cancers like Hodgkins’ disease were treated with high doses of radiation, also leading to radiation-induced diseases decades later.

Not all radiation is bad. Radiation can also be used as a therapeutic tool and even today remains a useful and reasonably effective method to reduce the size, sometimes eliminate, certain types of cancer. Forty percent of people with cancer now receive some form of radiation as part of their treatment (Ron E 2003).


Just how much does medical radiation add to our exposure?

Estimates vary, but most experts estimate that medical imaging provides approximately 15% of total lifetime exposure. In other words, radiation exposure from medical imaging is simply a small portion of total exposure that develops over the years of life. Exposure can be much higher, however, in a specific individual who undergoes repeated radiation imaging or treatment of one sort or another.

For all of us, exposure to medical radiation is part of lifetime exposure from multiple sources, added to the radiation we receive from the world around us. Just by living on earth, we are exposed to radiation from space and naturally-occurring radioactive compounds, and receive somewhere around 3.0 mSv per year (U.S. Nuclear Regulatory Commission). (Doses for radiation exposure are commonly expressed in milliSieverts, mSv, a measure that reflects whole-body radiation exposure.) People living in high-altitude locales like Colorado get exposed to an additional 30–50% ambient radiation (1.0–1.5 mSv more per year).

Much of the information on radiation exposure comes from studies like the Life Span Study that, since 1961, has tracked 120,000 Japanese exposed to radiation from the atomic bombs dropped in 1945 (Preston DL et al 2003). Although regarded as a high-dose exposure study for obvious reasons, there are actually thousands of people in this study who were exposed to lesser quantities of radiation (because of distance from the bomb sites) who still display a “dose-response” increased risk for cancer many years later in life. Radiation exposures of as little as 5–20 mSv showed a slight increase in lifetime risk.

Occupational and excessive medical exposure to radiation also provides a “laboratory” to examine radiation risk. Miners exposed to radon gas; patients exposed to the imaging agent, Thorotrast, containing radioactive isotope thorium dioxide and used as an x-ray contrast agent in the 1930s and 1940s and possesses the curious property of lingering in the body for over 30 years after administration; radium injections administered between 1945 and 1955 to treat diseases like ankylosing spondylitis and tuberculosis, all provide researchers an opportunity to study the long-term effects of various types of radiation exposure over many years (Harrison JD et al 2003).

The excess exposure of workers and several hundred thousand nearby residents to the Mayak nuclear plant in Russia has also revealed a “dose-response” relationship, with increasing exposure leading to more cancers, including leukemia and solid cancers of the bone, liver, and lung (Shilnikova NS et al 2003). Nuclear waste released into the Techa river between 1948 and 1956 contaminated drinking water used by over 100,000 Russians. A plant explosion in 1957 also released an excess of radiation into the atmosphere, yielding exposure via inhalation. Some sources estimate that at least 272,000 people have been affected by radiation from the Mayak plant. This unfortunate situation has, however, yielded plenty of data on radiation exposure and its long-term effects.

It’s also been known for several decades that people who receive therapeutic radiation for treatment of cancer, even with the reduced doses now employed, are subject to increased risk of a second cancer consequent to the radiation treatment.

From experiences like this, radiation experts estimate that an exposure of 10 mSv increases a population’s risk for cancer by 1 in 1000 (Semelka RC et al 2007).

This question was recently thrust into the spotlight with publication of a study from Columbia University in New York suggesting that a 20-year old woman would be exposed to a lifetime risk of cancer as high as 1 in 143 consequent to the radiation received during a CT coronary angiogram. (Important note: This was estimated risk from a CT coronary angiogram, not a simple heart scan that we advocate for the Track Your Plaque program.) The risk at the low end of the spectrum would be in an 80-year old man (because of the shorter period of time to develop cancer), with a risk of 1 in 5017. If “gating” to the EKG is added (which many scan centers do indeed perform nowadays), risk for a 60-year old woman is estimated at 1 in 715; risk for a 60-year old male, 1 in 1911 (Einstein AJ et al 2007). This study generated some criticism, since it did not directly involve human subjects, but used “phantoms” or x-ray dummies to simulate x-ray exposure. Nonetheless, the point was made: CT coronary angiograms in current practice do indeed expose the patient to substantial quantities of radiation, sufficient to pose a lifetime risk of cancer.


The media frenzy

The NY Times ran an article called With Rise in Radiation Exposure, Experts Urge Caution on Tests in which they stated:

"According to a new study, the per-capita dose of ionizing radiation from clinical imaging exams in the United States increased almost 600 percent from 1980 to 2006. In the past, natural background radiation was the leading source of human exposure; that has been displaced by diagnostic imaging procedures, the authors said."

“This is an absolutely sentinel event, a wake-up call,” said Dr. Fred A. Mettler Jr., principal investigator for the study, by the National Council on Radiation Protection. “Medical exposure now dwarfs that of all other sources.”

Radiation is a widely used imaging tool in medicine. Although CT scans of the brain, bones, chest, abdomen, and pelvis account for only 5% of all medical radiation procedures, they are responsible for nearly 50% of medical radiation used. It’s been known for years that increasing radiation exposure increases cancer risk over many years, but the boom of newer, faster devices that provide more detailed images has opened the floodgates to expanded use of CT scanners.

But before we join in the hysteria, let's first take a look at exposure measured for different sorts of tests:


Typical effective radiation dose values for common tests

Computed Tomography

Head CT 1 – 2 mSv
Pelvis CT 3 – 4 mSv
Chest CT 5 – 7 mSv
Abdomen CT 5 – 7 mSv
Abdomen/pelvis CT 8 – 11 mSv
Coronary CT angiography 5 – 12 mSv


Non-CT

Hand radiograph Less than 0.1 mSv
Chest radiograph Less than 0.1 mSv
Mammogram 0.3 – 0.6 mSv
Barium enema exam 3 – 6 mSv
Coronary angiogram 5 – 10 mSv
Sestamibi myocardial perfusion (per injection) 6 – 9 mSv
Thallium myocardial perfusion (per injection) 26 – 35 mSv

Source: Cynthia H. McCullough, Ph.D., Mayo Clinic, Rochester, MN


A plain, everyday chest x-ray, providing less than 0.1 mSv exposure, provides about the same quantity of radiation exposure as flying in an airplane for four hours, or the same amount of radiation from exposure to our surroundings for 11–12 days. Similar exposure arises from dental x-rays.

If you have a heart scan on an EBT device, then your exposure is 0.5-0.6 mSv, roughly the same as a mammogram or several standard chest x-rays.

With a heart scan on a 16- or 64-slice multidetector device, exposure is ideally around 1.0-2.0 mSv, about the same as 2-3 mammograms, though dose can vary with this technology depending on how it is performed (gated to the EKG, device settings, etc.)

CT coronary angiography presents a different story. This is where radiation really escalates and puts the radiation exposure issue in the spotlight. As Dr. Cynthia McCullough's chart shows above, the radiation exposure with CT coronary angiograms is 5-12 mSv, the equivalent of 100 or more chest x-rays or 20 mammograms. Now, that's a problem.

The exposure is about the same for a pelvic or abdominal CT. The problem is that some centers are using CT coronary angiograms as screening procedures and even advocating their use annually. This is where the alarm needs to be sounded. These tests, as wonderful as the information and image quality can be, are not screening tests. Just like a pelvic CT, they are diagnostic tests done for legitimate medical questions. They are not screening tests to be applied broadly and used year after year.

It’s also worth giving second thought to any full body scan you might be considering. These screening studies include scans of the chest, abdomen, and pelvis. These scans, performed for screening, expose the recipient to approximately 10 mSv of radiation (Radiological Society of North American, 2007). Debate continues on whether the radiation exposure is justified, given the generally asymptomatic people who generally undergo these tests.

Always be mindful of your radiation exposure, as the NY Times article rightly advises. However, don't be so frightened that you are kept from obtaining truly useful information from, for instance, a CT heart scan (not angiography) at a modest radiation cost.


Heart scans, CT coronary angiograms and the future

Unfortunately, practicing physicians and those involved in providing CT scans are generally unconcerned with radiation exposure. The majority, in fact, are entirely unaware of the dose of radiation required for most CT scan studies and unaware of the cancer risk involved. It is therefore up to the individual to insist on a discussion of the type of scanner being used, the radiation dose delivered (at least in general terms), the necessity of the test, alternative methods to obtain the same diagnostic information, all in the context of lifetime radiation exposure.

Our concerns about radiation exposure all boil down to concern over lifetime risk for cancer, a disease that strikes approximately 20% of all Americans. Many factors contribute to cancer risk, including obesity, excessive saturated fat intake, low fiber intake, lack of vitamin D, repeated sunburns, excessive alcohol use, smoking, exposure to pesticides and other organochemicals, asbestos and other industrial exposures, electromagnetic wave exposure, and genetics. Radiation is just one source of risk, though to some degree a controllable one.

Some people, on hearing this somewhat disturbing discussion, refuse to ever have another medical test requiring radiation. That’s the wrong attitude. It makes no more sense than wearing lead shielding on your body 24 hours a day to reduce exposure from the atmosphere. Taken in the larger context of life, radiation exposure is just one item on a list of potentially harmful factors.

It is, however, worth some effort to minimize radiation exposure over your lifetime, particularly before age 60, and by submitting to high-dose testing only when truly necessary, or when the potential benefits outweigh the risks. Thus, with heart scans and CT coronary angiography, some thought to the potential benefits of knowing your score or the information gained from the CT angiogram need to be considered before undergoing the test. Often the practical difficulty, of course, is that your risk for heart disease simply cannot be known until after the test.

In our view, in the vast majority of instances a simple CT heart scan can serve the simple but crucial role of quantifying risk for heart attack and atherosclerotic plaque. CT heart scans yield this information with less than a tenth of the radiation exposure of a CT coronary angiogram. In people without symptoms and a normal stress test, there is rarely a need for CT coronary angiography with present day levels of radiation exposure. Perhaps as technology advances and the radiation required to generate images is reduced, then we should reconsider.

Early experiences are suggesting that the newest 256-slice scanners, now being developed but not yet available, will cut the dose exposure of 64-slice CT angiograms in half (from 27.8 mSv to 14.1 mSv in a recent Japanese study). The 256-slice scanners will allow scanning that is faster over a larger area in a given period of time.

Thankfully, the scanner manufacturers are increasingly sensitive to the radiation issue and have been working on methods to reduce radiation exposure. However, it still remains substantial.


References:
Einstein AJ, Henzlova MJ, Rajagopalan S. Estimating risk of cancer associated with radiation exposure from 64-slice computed tomography coronary angiography. JAMA 2007 Jul 18;298(3):317–323.

Harrison JD, Muirhead CR. Quantitative comparisons of cancer induction in humans by internally deposited radionuclides and external radiation. Int J Radiat Biol 2003 Jan;79(1):1–13.

Hausleiter J, Meyer T, Hadamitzyky M et al. Radiation Dose Estimates From Cardiac Multislice Computed Tomography in Daily Practice: Impact of Different Scanning Protocols on Effective Dose Estimates. Circulation 2006;113:1305–1310.

Kalra MK, Maher MM, Toth TL, Hamberg LM, Blake MA, Shepard J, Saini S. Strategies for CT radiation dose optimization. Radiology 2004;230:619–628.

Mayo JR, Aldrich J, Müller NL. Radiation exposure at chest CT: A statement of the Fleischner Society. Radiology 2003; 228:15–21.

Mori S, Nishizawa K, Kondo C, Ohno M, Akahane K, Endo M. Effective doses in subjects undergoing computed tomography cardiac imaging with the 256-multislice CT scanner. Eur J Radiol 2007 Jul 10; [Epub ahead of print].

Preston DL, Pierce DA, Shimizu Y, Ron E, Mabuchi K. Dose response and temporal patterns of radiation-associated solid cancer risks. Health Phys 2003 Jul;85(1):43–46.

Ron E. Cancer risks from medical radiation. Health Phys 2003 Jul;85(1):47–59.

Shilnikova NS, Preston DL, Ron E et al. Cancer mortality risk among workers at the Mayak nuclear complex. Radiation Res 2003 Jun;159(6):787–798.

Semelka RC, Armao DM, Elias J Jr, Huda W. Imaging strategies to reduce the risk of radiation in CT studies, including selective substitution with MRI. J Magn Reson Imaging 2007 May;25(5):900–9090.


Copyright 2007, Track Your Plaque.

Goodbye, fructose

A carefully-conducted study by a collaborative research group at University of California-Berkeley has finally closed the lid on the fuss over fructose vs. glucose and its purported adverse effects.

The study is published in its entirety here.

Compared to glucose, fructose induced:

1) Four-fold greater intra-abdominal fat accumulation--3% increased intra-abdominal fat with glucose; 14.4% with fructose. (Intraabdominal fat is the variety that blocks insulin responses and causes diabetes and inflammation.)

2) 13.9% increase in LDL cholesterol but double the increase for Apoprotein B (an index of the number of LDL particles, similar to NMR LDL particle number).

3) 44.9% increase in small LDL, compared to 13.3% with glucose.

4) While glucose (curiously) reduced the net postprandial (after-eating) triglyceride response (area under the curve, AUC), fructose increased postprandial triglycerides 99.2%.


The authors propose that fructose specifically increases liver VLDL production, the lipoprotein particle that yields abnormal after-eating particles, increased LDL, and provides building blocks to manufacture small LDL particles. The authors also persuasively propose that fructose metabolism, unlike glucose, is not inhibited (via feedback loop) by energy intake, i.e., it's as if you are always starving.

Add to this the data that show that fructose increases uric acid (that causes gout and may act as a coronary risk factor), induces leptin resistance, causes metabolic syndrome (pre-diabetes), and increases appetite, and it is clear that fructose is yet another common food additive that, along with wheat, is likely a big part of the reason Americans are fat and diabetic.

Fructose is concentrated, of course, in high-fructose corn syrup, comprising anywhere from 42-90% of total weight. Fructose also composes 50% of sucrose (table sugar). Fructose also figures prominently in many fruits; among the worst culprits are raisins (30% fructose) and honey (41% fructose).

Also, beware of low-fat or non-fat salad dressings (rich with high-fructose corn syrup), ketchup, beer, fruit drinks, fruit juices, all of which are rich sources of this exceptionally fattening, metabolism-bypassing, LDL cholesterol/small LDL/ApoB increasing compound. Ironically, this means that many low-fat foods meant to reduce cholesterol actually increase it when they contain fructose in any form.

When you hear or say "fructose," run the other way, regardless of what the Corn Refiners Association says.

The statin-free life

Matt came to me because his doctor couldn't reduce his LDL cholesterol.

His doctor had prescribed Zocor (simvastatin), Lipitor, Crestor, even pravastatin, all of which resulted in incapacitating muscle aches and weakness within a week of starting. No surprise, Matt had a jaundiced view of statin drugs.

We started out by characterizing his lipoprotein patterns:

--LDL 155 mg/dl

--72% of LDL was small LDL, a moderately severe pattern. (This means that small LDL comprised 112 mg/dl of the total 155 mg/dl LDL; large LDL comprised 43 mg/dl--small LDL was the problem.)

--HDL 42 mg/dl --Triglycerides 133 mg/dl

--No lipoprotein(a)

Beyond lipoproteins, Matt proved severely deficient in vitamin D with a starting level of 18 ng/ml.

Matt's doctor had advised that he avoid salt, as his blood pressure had been borderline high. His thyroid assessment disclosed a TSH of 3.89 mIU/ml with thyroid hormones free T3 and free T4 in the lower half of the normal range.

I therefore asked Matt to:

--Eliminate wheat, cornstarch, and sugars to reduce small LDL
--Add iodine
--Supplement 6000 units of an oil-based vitamin D preparation
--Take fish oil to provide at least 1800 mg EPA + DHA per day
--Take Armour Thyroid 1 grain per day


Several months later on this program, Matt had a repeat basic lipid panel:

--LDL 82 mg/dl--a 47% reduction

--HDL 52 mg/dl a 24% increase

--Triglycerides 60 mg/dl--a 55% decrease

In addition, vitamin D was 66 ng/ml, TSH was <1.0 mIU/ml with free T3 and free T4 in the upper half of the "reference range." Matt also felt great.

While the numbers could be slightly better, Matt had made tremendous progress towards achieving perfect values.

There you have it: Marked correction of cholesterol values, no statin drugs involved.

Creatine: Not just for muscle heads

Even if you’re not interested in building big muscles like a bodybuilder, there are health benefits to increasing muscle mass: increased bone density, better balance, and fewer injuries. Greater muscle mass means higher metabolic rate, improved insulin responsiveness, lower blood sugar. The inevitable loss of muscle mass of aging can lead to frailty, an increasingly common situation for the elderly. Muscle loss be reversed, health improved as a result.

Since its introduction in 1994, creatine has exploded in popularity, particularly among bodybuilders and athletes interested in gaining muscle mass and strength. But creatine is not just for young weight lifters. If you are just interested in increasing muscle mass for its health benefits, then creatine is something to consider.

A study of creatine supplementation in men, average age 70 years, demonstrated that, when creatine was combined with strength training, it increased muscle mass 250% better than placebo (7.26 lb muscle vs 2.86 lb muscle), along with improved leg strength and endurance. The same group also demonstrated 3.2% increased bone density (measured using dual energy X-ray absorptiometry) after 12 weeks in participants taking creatine with strength training, while the control (no strength training, no creatine) group decreased by 1.0%.

Benefits are not confined to men. Similar results were observed in another study that included women (age 65 and older), with outcomes in females comparable to males. This is especially important for females, given the common development of osteopenia and osteoporosis in postmenopausal females.

Other studies have shown that benefits are maintained after stopping creatine supplementation.

The most popular form of creatine is the monohydrate, generally taken as a “loading” phase of 15-20 grams per day (generally split into 3-4 doses of 5 grams) for 5-7 days, followed by weeks to months of 2-5 grams per day.

An alternative form, polyethylene glycosylated creatine (PEG-creatine) provides similar effects at one-fourth to one-half the dose of creatine, i.e., 1.25-2.5 grams per day.

Despite previous concerns about kidney toxicity with prolonged use, another study showed that athletes taking creatine for up to 21 months have shown no adverse effects on kidney function, lipid (cholesterol) values, or other basic health measures.

Having healthy muscle mass doesn't make you bulge like a bodybuilder. With modest efforts at strength training, augmented with creatine supplementation, you have a wonderful tool to feel better, reduce injury, increase bone density, and combat abnormal insulin resistance, not to mention accelerate weight loss, since lean muscle mass consumes energy.

The ultimate “bioidentical” hormone

There has been a lot of debate over whether or not “bio-identical” hormones, i.e., hormones identical to the human form, are superior to non-human forms dispensed by the drug industry.

The FDA is currently taking steps to clamp down on availability of bioidentical hormones and their claims of superiority, despite a groundswell of grassroot support for them. The argument has pitted anti-aging practitioners and the public, as well as the likes of Oprah and Suzanne Somers, against Big Pharma and the FDA, the two forces trying to squash the bioidentical hormone movement.

Regardless of what heavy-handed approach the FDA takes, we already have access to hormones identical to the original human form. It requires no prescription and yields downstream hormones that the human body recognizes as human.

That "bioidentical" hormone is pregnenolone.

Pregnenolone is the first biochemical step in the conversion of dietary cholesterol (yes-cholesterol!) to numerous other hormones. Pregnenolone is the source of the hormones that lie at the center of the bioidentical hormone controversy: estrogens, progesterone, and testosterone. We therefore already have our own over-the-counter, non-prescription form of bioidentical hormones.

Supplemental pregnenolone increases estrogens (mildly), progesterone, and testosterone. Prenenonlone supplementation simply provide more of the basic substrate for hormone production. The increase in hormones is usually modest, not as vigorous as direct hormone replacement like, say, testosterone or progesterone topical creams. But pregnenolone can be useful when small to moderate increases are desired, such as for reduction of Lp(a). A theoretical downside is that pregnenonlone can also convert to cortisol, the adrenal gland hormone that regulates fluid and blood pressure. However, I've not seen any measurable increase in cortisol with low doses of pregnenonlone and limited data suggest that it does not. Pregnenolone also converts to the other adrenal gland hormone, DHEA; I call DHEA "the hormone of assertiveness," since some people who take too much pregnenolone (or direct DHEA) acquire excessive assertiveness.

The key to pregnenolone supplementation is to proceed gradually and begin with a small dose, e.g., 5 mg every morning. Hormonal assessment is best conducted periodically to assess the effects and to determine whether a dose adjustment is in order.

Triglyceride and chylomicron "stacking"

Continuing the comments started in Grazing is for cattle, here's an interesting study from the Oxford Center for Diabetes, Endocrinology and Metabolism.

Volunteers were fed a test meal breakfast of Rice Krispies, a banana, and a chocolate milkshake (76.4 grams carbohydrates, 51.9 grams fat, 12.2 grams protein). Lunch was served 5 hours later and consisted of a cheese sandwich and a second chocolate milkshake 43.4 grams carbohydrates, 49.6 grams fat, 24.0 grams protein). Frequent blood samples were then assessed over the day. (Don't try this at home: These are obviously very dangerous foods!)

Here's the pattern of triglycerides that was observed (1st dotted vertical line = breakfast, 2nd dotted vertical line = lunch):



Note that triglycerides only begin to decline 3-4 hours after breakfast, only to peak higher after lunch.


Here's the pattern observed for chylomicrons, the "granddaddy" of lipoproteins that derives from intestinal absorption of fatty acids:



Both graphs from Heath RB et al Am J Phyiol Endocrinol Metab 2006.


With chylomicrons, note a similar pattern to triglycerides: Chylomicrons begin to decline at 3-4 hours, only to peak higher after lunch.

This is the first study to examine the effect of sequential meals on such postprandial (after-eating) patterns. But it makes the graphic point that, if insufficient time is permitted between meals, both triglycerides and chylomicrons will "stack" themselves higher and higher. (Chylomicrons are subjected to processing by the enzyme, lipoprotein lipase, to form highly atherogenic, or plaque-causing, chylomicron remnants.)

While not examined in this study, my bet is that "grazing," i.e., eating small meals or snacks frequently, is an extreme instance of triglyceride, chylomicron, and chylomicron remnant stacking. That can only lead to one thing: accelerated heart and vascular plaque.

What is a healthy vitamin D blood level?

When measuring blood levels of vitamin D (as 25-hydroxy vitamin D), what constitutes a desirable level?

There's no study that directly examines this question, no study that enrolled thousands of people and assigned a placebo group and groups receiving escalating doses of vitamin D and/or achieved higher levels of vitamin D, then observed for development of cancer, diabetes, depression, heart disease, multiple sclerosis, osteoporosis, osteoarthritis, etc. Such a study would requires many thousands of participants (particularly to observe cancer and multiple sclerosis incidence), many years of observation, and many tens of millions of dollars. Nope, only a drug company could afford such costs.

So we have to piece together various observations and extrapolate what we believe to be the ideal level of vitamin D. Epidemiologic observations in several cancers (breast, colon, prostate, and bladder) suggest that a 25-hydroxy vitamin D level of 30 ng/ml or higher is desirable (with less cancer incidence above this level). Other data suggest a level of 52 ng/ml or greater is desirable. Unfortunately, much cancer research looked at intake of vitamin D from food and supplement sources, rather than actual blood levels. We also have to factor in the great individual variation in vitamin D metabolism, with a single dose yielding variable blood levels (as much as a 10-fold difference). There's also the variation introduced by vitamin D-receptor variation (genetic polymorphisms).

A new study using vitamin D administration helps chart the desirable levels of vitamin D.

Vitamin D supplementation reduces insulin resistance in South Asian women living in New Zealand who are insulin resistant and vitamin D deficient - a randomised, placebo-controlled trial.

In this New Zealand study, 42 women (23 to 68 years old) were given 4000 units vitamin D, 39 women given placebo. Median 25-hydroxy vitamin D levels increased from 21 nmol/L (8.4 ng/ml) to 75 nmol/L (30 ng/ml). Both HOMA (a measure of insulin sensitivity) and fasting insulin levels improved, with greatest improvement seen at 25-hydroxy vitamin D levels of 80-119 nmol/L (32-47.6 ng/ml) or greater.

We also know that a vacation on a Caribbean beach in a bathing suit will increase vitamin D blood levels to the 80-110 ng/ml range without ill-effect (at least in young people who maintain the capacity to activate vitamin D in the skin, a phenomenon that declines as we age).

So do we really know the truly ideal level of vitamin D to achieve? I believe that, given the above observations, it is reasonable to extrapolate that the ideal vitamin D blood level likely lies somewhere above 50 ng/ml. We also know that vitamin D toxicity (i.e., hypercalcemia) is virtually unheard of until vitamin D blood levels approach 150 ng/ml, and even then is inconsistent. The health benefits of vitamin D supplementation are so tremendous, that I am not willing to wait for the prospective data to explore this question fully. For now, I aim for a blood level of vitamin D of 60-70 ng/ml (150-175 nmol/L).

Grazing is for cattle

Many dietitians and nutritionists advise many people today to "graze," i.e., to eat small snacks every couple of hours. They argue that it blocks the drop in insulin and blood sugar that can trigger greater appetite and claim it can facilitate weight loss.



This is an absurd notion. Humans are not meant to graze. Humans are meant to find a wild boar or other animal, kill it, gorge on the meat, organs, and fat, then revert to berries, roots, leaves, and other foraged foods until the next kill. A human living in the wild does not have a cupboard or refrigerator full of ready-to-eat snacks to graze on.

The several hours after a meal is the most dangerous for creating coronary atherosclerotic plaque, i.e., the post-prandial period. In other words, eat dinner and, for the next 6-12 hours, your intestinal tract degrades the food; food byproducts are absorbed into the blood or lymph system. The blood is literally flooded with the byproducts of your meal.

Postprandial abnormalities are emerging to be a potent, and much underappreciated, means of causing heart disease and atherosclerosis in other vascular territories (especially carotid arteries and thoracic aorta).

Not eating--i.e., the fasting state--for extended periods is good for you. Encouraging people to graze amplifies atherosclerotic risk, since it creates an abnormal prolonged postprandial state.

The disastrous results of a low-fat diet

Rob was never that committed to following the program in the first place.

I met Rob because of a modest heart scan score and consultation for a cholesterol abnormality. Rob had been cycled through all the statin agents by his primary care physician, all of which resulted in terrible muscle aches that he found intolerable.

I started out, as usual, characterizing his cholesterol abnormality with lipoprotein testing (NMR):

LDL particle number 1489 nmol/L
LDL cholesterol (Friedewald calculation) 143 mg/dl
Small LDL 52% of total LDL
HDL 50 mg/dl
Triglycerides 82 mg/dl

(LDL particle number is the emerging gold standard for LDL quantification, superior to calculated or Friedewald LDL cholesterol for prediction of cardiovascular events.)

Rob is a busy guy. After only a couple of brief visits, life and work got in the way and Rob let his attentions drift away from heart health. Since the information I provided made little impact on his thinking, he reverted to the low-fat diet his primary care doctor had originally prescribed and that he read about in magazines and food packages. He also ran out of the basic supplements I had advised, including fish oil and vitamin D, and just never restarted them.

A couple of years passed and Rob decided that just poking around on his own might not cut it. So he came back to the office. We repeated his NMR lipoprotein analysis:

LDL particle number 2699 nmol/L
LDL cholesterol (Friedewald calculation) 229 mg/dl
Small LDL 81% of total LDL
HDL 53 mg/dl
Triglycerides 78 mg/dl


Two years of a low-fat diet had caused Rob's LDL particle number to skyrocket by 81%, nearly all due to an explosion of small LDL. Recall that small LDL is more susceptible to oxidation, more inflammation-provoking, more adhesive--the form of LDL particles most likely to cause heart disease.

Also, note that, despite the enormous increase in small LDL, HDL and triglycerides remained favorable. This counters the popular rule-of-thumb offered by some that small LDL is not present when HDL is "normal."

Low-fat diets as commonly practiced are enormously destructive. In Rob's case, a low-fat diet caused both calculated Friedewald LDL as well as LDL particle number to increase dramatically. In many other people, low-fat diets increase calculated Friedewald LDL modestly or not at all, but cause the more accurate LDL particle number to increase significantly, all due to small LDL.

I'm happy to say that, once Rob witnessed how far wrong he could go on the wrong program, he's back on Track. (Sorry, pun intended.) He has resumed his supplements and eliminated the food triggers of small LDL--wheat, cornstarch, and sugars.

Dr. David Grimes reminds us of vitamin D

In response to the Heart Scan Blog post, Fish oil makes you happy: Psychological distress and omega-3 index, Dr. David Grimes offered the following argument.

Dr. Grimes is a physician in northwest England at the Blackburn Royal Infirmary, Lancashire. He is author of the wonderfully cheeky 2006 Lancet editorial, Are statins analogues of vitamin D?, questioning whether the benefits of statin drugs simply work by way of increased vitamin D blood levels.


There is a fashionable interest in Omega-3 fatty acids, and these become equated with fish oil.

But fish oil is much more. Plankton synthesise the related squalene (shark oil) which, in turn, is converted into 7-dehydrocholesterol (7-DHC). The sun now comes into play and it converts 7-DHC into vitamin D (a physico-chemical process).

Small fish eat plankton, large fish eat small fish, and we eat large fish. So vitamin D passes through the food chain.

This has been a vital source of vitamin D for the the Inuits and also for the Scots and other dwellers of northwest Europe. (Edinburgh is on the same latitude as Hudson Bay and Alaska, further north than anywhere in China). In these locations there is not adequate sunlight energy to guarantee synthesis of adequate amounts of vitamin D, again by the action of sunlight on 7-DHC in the skin.

When the Scots moved from coastal fishing villages to industrial cities such as Glasgow, they became seriously deficient in vitamin D, and so the emergence of rickets. This was followed by a variety of other diseases resulting from vitamin D deficiency: tuberculosis, dental decay, coronary heart disease, and even multiple sclerosis and depression (the Glasgow syndrome).

And so it was with the Inuits. When their diet changed from fish for breakfast, fish for lunch, fish for dinner, they became deficient of vitamin D and they developed diseases characteristic of industrial cities, where there is indoor work for long hours, indoor activities, and atmospheric pollution.

It is the vitamin D component of fish and fish oils that is important.

I recently saw an elderly lady from Bangladesh living in northwest England. I would have expected her to have a very low blood level of vitamin D, as her exposure to the sun was minimal. However the blood level was 47ng/ml, not 4 as expected. She eats oily fish from Bangladesh every day, showing its value as a source of vitamin D with subsequent good health. I expect her blood levels of omega-3 fatty acids would also be high.

But it is unfashionable vitamin D that is important, not fashionable omega-3.

David Grimes
www.vitamindandcholesterol.com


Excellent point. The health effects of omega-3 and vitamin D are intimately intertwined when examining populations that consume fish.

In this study of Inuits, it is indeed impossible to dissect out how much psychological distress was due to reduced vitamin D, how much due to reduced omega-3s. My bet is that it's both. Thankfully, we also have data examining the use of pure omega-3 fatty acids in capsule (not intact fish) form, including studies like GISSI Prevenzione.

Nonetheless, Dr. Grimes reminds us that both vitamin D and omega-3 fatty acids from fish oil play crucial roles in mental health and other aspects of health, and that it's the combination that may account for the extravagant health effects previously ascribed only to omega-3s.

Why does fish oil reduce triglycerides?

Beyond its ability to slash risk for cardiovascular events, omega-3 fatty acids from fish oil also reduce triglycerides.

There's no remaining question that omega-3s do this quite effectively. After all, the FDA approved prescription fish oil, Lovaza, to treat a condition called familial hypertriglyceridemia, an inherited condition in which very high triglycerides in the 100s or 1000s of milligrams typically develop.

The omega-3 fraction of fatty acids are unique for their triglyceride-reducing property. No other fraction of fatty acids, such as omega-6 or saturated, can match the triglyceride-reducing effect of omega-3s.

But why does fish oil reduce triglycerides?

First of all, what are triglycerides? As their name suggests, triglycerides consist of three ("tri-") fatty acids lined up along a glycerol (sugar) "backbone." Triglycerides are the form in which most fatty acids occur in the bloodstream, liver, and other organs. (Fatty acids, like omega-3, omega-6, mono- or polyunsaturated, or saturated, rarely occur as free fatty acids unbound to glycerol.) In various lipoproteins in the blood, like LDL, VLDL, and HDL, fatty acids occur as triglycerides.

Of all lipoproteins, chylomicrons (the large particle formed through intestinal absorption of fatty acids and transported to the liver via the lymph system) and VLDL (very low-density lipoprotein, very low-density because they are mostly fat and little protein) particles are richest in triglycerides. Thus, we would expect that omega-3s exert their triglyceride-reducing effect via reductions in either chylomicrons or VLDL.

Indeed, that seems to be the case. The emerging evidence suggests that omega-3 fatty acids from fish oil reduce triglycerides through:

--Reduced VLDL production by the liver (Harris 1989)
--Accelerating chylomicron and VLDL elimination from the blood
--Activation of peroxisome proliferator-activated receptor gamma (PPAR-gamma)--Omega-3s ramp up the cellular equipment used to convert fatty acids to energy (oxidation) (Gani 2008)

Combine omega-3 fatty acids from fish oil with wheat elimination and you have an extremely potent means of reducing triglycerides. Read a previous Heart Scan Blog post here to read how a patient reduced triglycerides 93.5% from 3100 mg/dl to 210 mg/dl in just a few weeks using fish oil and wheat elimination.

Fish oil makes you happy: Psychological distress and omega-3 index

For another perspective on omega-3 blood levels, here's an interesting study in northern Quebec Inuits.

Traditionally, Inuits consumed large quantities of omega-3-rich seal, fish, caribou, and whale, even eating the fat. However, like the rest of the world, modern Inuits have increased consumption of store-bought foods, largely processed carbohydrates. Along with this trend has emerged more heart disease, diabetes, and depression.

A group from Laval University and University of Guelph, both in Canada, examined the relationship of plasma EPA + DHA levels and measures of psychological distress. This group had previously shown that Inuits older than 50 years had twice the plasma omega-3 levels (11.5%) compared to those younger than 50 years (6.5%), reflecting the shift away from the traditional diet.

Psychological distress was measured with The Psychological Distress Index Santé-Québec Survey (PDISQS-14): the higher the score, the greater the psychological distress. (In the graphs, tertile 1 is least distressed; tertile 5 is most distressed. Sorry about the small chart graphic--click on the graphic to make it bigger.)


From Lucas M et al 2009 (http://www.nutrasource.ca/NDI/Assets/Articles/Plasma%20omega-3%20and%20psychological%20distress%20among%20Nunavik%20Inuit.pdf)

"Our main finding was that women in the second and third tertiles of EPA+DHA concentrations in plasma PLs [phospholipids] had a 3 times lower risk of having a high-level PD [psychological distress] score than women in the lowest tertile."

While the relationship is stronger for women, you can see that, the higher the EPA + DHA plasma level, the lower the likelihood of psychological distress. Interestingly, the tertile with the greatest distress and lowest EPA + DHA levels had a plasma level of 7.0-7.5%--far higher than average Americans.

(Plasma levels of EPA + DHA were used in this study, which tend to reflect more recent omega-3 intake than the more stable and slower-to-change RBC Omega-3 Index that we use. Plasma levels also tend to run about 10-20% lower than RBC levels.)

Of course, there's more to psychological distress than omega-3 blood levels. After all, eating fish or taking fish oil capsules won't make money worries go away or heal an unhappy marriage. But it is one variable that can be easily and safely remedied.

Hospitals are a hell of a place to get sick

I answered a page from a hospital nurse recently one evening while having dinner with the family.

RN: "This is Lonnie. I'm a nurse at _____ Hospital. I've got one of your patients here, Mrs. Carole Simpson. She's here for a knee replacement with Dr. Johnson. She says she's taking 12,000 units of vitamin D every day. That can't be right! So I'm calling to verify."

WD: "That's right. We gauge patients' vitamin D needs by blood levels of vitamin D. Carole has had perfect levels of vitamin D on that dose."

RN: "The pharmacist says he can replace it with a 50,000 unit tablet."

WD: "Well, go ahead while Carole's in the hospital. I'll just put her back on the real stuff when she leaves."

RN: "But the pharmacist says this is better and she won't have to take so many capsules. She takes six 2,000 unit capsules a day."

WD: "The 50,000 units you and the pharmacist are talking about is vitamin D2, or ergocalciferol, a non-human form. Carole is taking vitamin D3, or cholecalciferol, the human form. The last time I checked, Carole was human."

RN: (Long pause.) Can we just give her the 50,000 unit tablet?

WD: "Yes, you can. But you actually don't need to. In fact, it probably won't hurt anything to just hold the vitamin D altogether for the 3 days she's in the hospital, since the half-life of vitamin D is about 8 weeks. Her blood level will barely change by just holding it for 3 days, then resuming when she's discharged."

RN: (Another long pause.) Uh, okay. Can we just give her the 50,000 units?"

WD: "Yes, you can. No harm will be done. It's simply a less effective form. To be honest, once Carole leaves the hospital, I will just put her back on the vitamin D that she was taking."

RN: "Dr. Johnson was worried that it might make her bleed during surgery. Shouldn't we just stop it?"

WD: "No. Vitamin D has no effect on blood coagulation. So there's no concern about perioperative bleeding."

RN: "The pharmacist said the 50,000 unit tablet was better, also, because it's the prescription form, not an over-the-counter form."

WD: "I can only tell you that Carole has had perfect blood levels on the over-the-counter preparation she was taking. It works just fine."

RN: "Okay. I guess we''ll just give her the 50,000 unit tablet."


From the alarm it raises trying to administer nutritional supplements in a hospital, you'd think that Osama Bin Laden had been spotted on the premises.

I laugh about this every time it happens: A patient gets hospitalized for whatever reason and the hospital staff see the supplement list with vitamin D, fish oil at high doses, iodine, etc. and they panic. They tell the patient about bleeding, cancer, and death, issue stern warnings about how unreliable and dangerous nutritional supplements can be.

My view is the exact opposite: Nutritional supplements are a wonderful, incredibly varied, and effective array of substances that, when used properly, can provide all manner of benefits. While there are selected instances in which nutritional supplements do, indeed, have interactions with treatments provided in hospitals (e.g., Valerian root and general anesthesia), the vast majority of supplements have none.

Does fish oil cause blood thinning?

Omega-3 fatty acids from fish oil have the capacity to "thin the blood." In reality, omega-3s exert a mild platelet-blocking effect (platelet activation and "clumping" are part of clot formation), while also inhibiting arachidonic acid formation and thromboxane.

But can fish oil cause excessive bleeding?

This question comes up frequently in the office, particularly when my colleagues see the doses of fish oil we use for cardiovascular protection. "Why so much fish oil? That's too much blood thinning!"

The most recent addition to the conversation comes from a Philadelphia experience reported in the American Journal of Cardiology:

Comparison of bleeding complications with omega-3 fatty acids + aspirin + clopidogrel--versus--aspirin + clopidogrel in patients with cardiovascular disease.(Watson et al; Am J Cardiol 2009 Oct 15;104(8):1052-4).

All 364 subjects in the study took aspirin and Plavix (a platelet-inhibiting drug), mostly for coronary disease. Mean dose aspirin = 161 mg/day; mean dose Plavix = 75 mg/day. 182 of the subjects were also taking fish oil, mean dose 3000 mg with unspecified omega-3 content.

During nearly 3 years of observation, there was no excess of bleeding events in the group taking fish oil. (In fact, the group not taking fish oil had more bleeding events, though the difference fell short of achieving statistical significance.) Thus, 3000 mg per day of fish oil appeared to exert no observable increase in risk for bleeding. This is consistent with several other studies, including that including Coumadin (warfarin), with no increased bleeding risk when fish oil is added.

Rather than causing blood thinning, I prefer to think that omega-3 fatty acids from fish oil restore protection from abnormal clotting. Taking omega-3 fatty acids from fish oil simply restores a normal level of omega-3 fatty acids in the blood sufficient to strike a healthy balance between blood "thinning" and healthy blood clotting.

Heart Scan Blog readers take impressive doses of omega-3s

Here are the results from the latest Heart Scan Blog poll:

What is your dose of omega-3 fatty acids, EPA + DHA, from fish oil? (Add up the total content of EPA + DHA per capsules; multiply times number of capsules.)

The 479 respondents answered:

Less than 1000 mg per day
65 (13%)

1000-1999 mg per day
145 (30%)

2000-2999 mg per day
98 (20%)

3000-3999 mg per day
79 (16%)

4000-4999 mg per day
33 (6%)

5000-5999 mg per day
14 (2%)

6000 mg per day or more
45 (9%)


The poll did not discriminate between who has heart disease, who does not; who is taking omega-3 fatty acids for high triglycerides or for reduction of lipoprotein(a) (which requires high doses), or other indications. So variation is to be expected.

We can say that nearly all respondents are likely receiving sufficient omega-3s to impact cardiovascular risk, since the benefits begin just by consuming fish twice per month. I am especially impressed at the proportion of respondents (53%) who take at least 2000 mg per day of EPA + DHA. It's clear that people are really embracing the notion that omega-3 fatty acids pack a real wallop of health benefits.

Because different people in different situations and lipid/lipoprotein patterns have different omega-3 needs, there is really no "right" or "wrong" dose of omega-3 fatty acids.

However, there are several factors that enter into knowing your ideal omega-3 intake:

--Higher triglycerides require higher doses
--Lipoprotein(a) can respond to higher doses
--Having coronary or carotid plaque means you desire a "therapeutic" dose of omega-3s, not just a "preventive" dose

Time is a factor, also: The longer you take omega-3s, the higher your blood levels go. You can accelerate the replacement of non-omega-3s with higher doses of omega-3s.

But too much is not good either. Some participants in Track Your Plaque, for instance, have experimented with very high doses of EPA + DHA in the 9000-10,000 per day range and witnessed dramatic increases in LDL.

Much of the uncertainty about dosing will also be cleared up as we get more experience with the Omega-3 RBC Index, i.e, the proportion of fatty acids in red blood cells that are omega-3s. We are currently aiming for an Omega-3 Index of 10%, given the heart attack reductions observed at this level.