Addictive Foods

Kraft Foods, Inc. is manufacturer of Kool Aid, Oscar Mayer, Kraft Macaroni and Cheese, Velveeta, Honey Maid Grahams, and hundreds of other processed food products. Post cereals also falls under the umbrella of Kraft with products like Raisin Bran, Post Toasties, and Fruity Pebbles. Annual revenues in 2006 for Kraft: $34.4 billion. A big operation with enormous influence over our eating habits.

Nabisco is manufacturer of Oreos, Ritz Crackers, Chips Ahoy and many others. Like Kraft/Post, it is also a big player.

While Nabisco was owned for several years by tobacco giant RJ Reynolds, in 2000 it was acquired by Philip Morris, another big tobacco manufacturer.

More recently in Spring, 2007, Philip Morris (now called Altria--you'd change your name, too, if it was synonymous with dirt) spun off its Kraft subsidiary for a big profit. However, the management structures remain intertwined.

In other words, despite the shuffling of shares, the two industries, big tobacco and big food, are in many respects one and the same.

Is it any surprise that the same industry that made billions of dollars pushing addictive nicotine products responsible for the deaths of hundreds of thousands of people is now intimately involved with addictive products produced and marketed by the processed food industry?

If you believe that food manufacturers are innocently and honestly conducting their businesses, simply think back to the testimony provided in front of Congress during the tobacco industry hearings. Broad deception, concealed truths, and outright lies were commonplace. There was no conscience involved. This was about money--and lots of it.

Why should the processed food industry, intimate with the tobacco industry, be any different?

If you want control over heart disease and your heart scan score, buy produce and buy local. Spend your time in the produce aisle, not the cereal or chip aisle. Unprocessed food, unadorned by bright labels, cartoon animals, American Heart Association endorsements, that's what we should seek.

Heart Scan Curiosities #7




Here's a situation that crops up once in a while, occurring in perhaps 2% of heart scans.

The white within the circled area represents calcium, and thereby atherosclerotic plaque, situated immediately at the "mouth", or opening, of the the right coronary artery. What is somewhat unusual is that this plaque is not principally coronary, but aortic. That is, the plaque is mostly situated in the large vessel called the aorta. The three coronary arteries arise from the aorta.

In this instance, the aortic plaque involves the mouth of the right coronary artery. (In views not shown, the plaque also extends into the artery as well.) I call this a "double whammy" because the same plaque can post risk for heart attack and stroke.

Generally, aortic plaques pose risk for stroke. When aortic plaque fragments, little bits and pieces can travel upward to the brain and block an artery, thus a stroke.

In the coronaries, disrupted ("ruptured") plaques don't generally shower debris, but permit blood clot formation, resulting in heart attack.

This plaque, however, poses the theoretical risk of both heart attack and stroke because of its strategic location.

Should a plaque like this be handled any differently? I don't think so. But it does provide another reason to take atherosclerotic plaque in any artery seriously.

The nutrition counterculture

When we look back over our American nutritional history over the last 50 years, it's hard not to come to the conclusion that much of the innovation in nutrition did not come from official agencies like the Food and Nutrition Board of the Institute of Medicine, the National Academy of Sciences, the FDA, the USDA, or the AMA.

Instead, it came from the popular culture. It came from bold, extravagant claims made by maverick figures like Ancel Keys, Nathan Pritikin, Dean Ornish, and Robert Atkins. Of course, some ideas have now fallen by the wayside, dismissed in a broad American "experiment" as ineffective, impractical, or kooky. But it permitted experimentation on an extraordinary scale with millions of people following a particular strategy at a time.

The advice of the official agencies tended to be reactionary. When nutritional deficiencies (remember those?) of the early 1900s were prevalent, they issued advice on food choices to help alleviate deficiencies. When deficiency transformed into excess after World War II, "smart" food choices from food groups and "sensible eating" became the theme.

Unfortunately, the advice was always adulterated by the enormous influence of various special interests, anxious to protect their national franchise. Powerful groups like the meat industry, wheat producers, and the dairy industry all made sure they had a big hand in crafting and influencing what was told to the American people.

The result: the advice offered by official groups has always represented the compromise of what some agency wished to convey to the people and the very powerful input of industry. What if the government decided to advise us what automobile to buy? Imagine the uproar in the auto industry when Washington tells us to buy Toyota for fuel economy and reliability. How long would that advice last?

That's why almost no knowledgeable adult follows the advice of the USDA, the National Academy of Sciences, or the Food Pyramid. I believe that we all intuitively recognize that the advice is watered-down, sometimes silly, sometimes downright unhealthy.

Nonetheless, the national experiment in diet that has taken place since 1950 has led to a collective wisdom of what is good and what is bad. The most productive conversations on nutrition therefore take place outside of the USDA and Washington. It occurs, instead, in places like bookstores, websites, and the media. Of course, there's lots of misinformation and profiteering in these sectors, as well. But like the enormous force unleashed by the collective wisdom of those contributing to the Wikipedia phemonenon, we've zig-zagged to something closer to the truth than ever uttered by an official agency.

Prescription vitamin D

Niacin:

Over-the-counter: $2-5 per month
Prescription: $120 per month


Fish oil:


Over-the-counter: $3-6 per month
Prescription: $120 per month


Vitamin D:


Over-the-counter: $2 per month
Prescription: $70 per month



With vitamin D in particular, the prescription form is vastly inferior to the over-the-counter preparation. This is because the prescription form is ergocalciferol, or vitamin D2, not the effective human form, vitamin D3 or cholecalciferol.

When you're exposed to sun, what form of vitamin D is activated in the skin? It's all vitamin D3, no vitamin D2 whatsoever. Vitamin D3 is also far more effective than D2. People taking D3 (as long as it's oil-based) easily obtain healthy levels of vitamin D in the blood. People taking 50,000 units per day of D2 (the recommended quantity) remain miserably deficient, with minor increases in vitamin D blood levels. In short, D2 barely works at all. D3 works easily and effectively.

Moreover, D2 is the plant-based form. It is a form not found naturally in humans. D3 is the mammalian form, the same found in humans that exerts all its biologic benefits.

Then why is the prescription form of vitamin D2 (brand names Driscol and Calciferol) more expensive?

It's the same old pharmaceutical industry scam: Look for something patent protectable, regardless of whether it's superior to the non-patent protectable product, then sell it for exagerated profits. Though it is inferior and the science and clinical experience prove that it's inferior, you can still fool lots of people, including prescribing physicians. So what if you only make $50 or $100 million?

Don't fall for it. Prescription doesn't necessarily mean superior. In fact, the prescription form may be significantly inferior, as with vitamin D2. But the pharmaceutical industry carries such power and persuasion, who's going to know?

Nutrition activist Mike Adams













I borrowed the above comic from the website of nutritionist, more properly nutrition activist and author, Mike Adams. His website, www.newstarget.com, was a pleasant surprise.

I was actually looking for some thoughts on pharmaceutical advertising and its pervasive and destructive effects and came across one of Adam's reports, Pharmaceutical television advertising is a grand hoax at http://www.newstarget.com/021526.html. The piece is a rant against the pharmaceutical industry's constant bombardment of the media, who have also been co-opted into their service, enticed by the enormous advertising revenues the drug industry brings.

But I was surprised to find an insightful, informative website on health issues, particularly healthy eating that rejects the manufactured food industry's intensive effort to persuade us to eat their products. While I don't agree with everything Adams has to say, his website provides some great food for thought. He also provides lots of downloadable information.

There's also some great laughs at his poke at the pharmaceutical industry with his Disease Mongering Engine at http://www.newstarget.com/disease-mongering-engine.asp, in which you get to create your own diseases. I got a real kick out of this.

CT scans and radiation exposure



The NY Times ran an article called

With Rise in Radiation Exposure, Experts Urge Caution on Tests at

http://www.nytimes.com/2007/06/19/health/19cons.html?_r=1&adxnnl=1&oref=slogin&adxnnlx=1182254102-vQpytpx6W/Z9gvAaNPDZvA



“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.”


Where do CT heart scans fall?

Let's first take a look at exposure measured for different sorts of tests:



Typical effective radiation dose values

Computed tomography Milliseverts (mSv)

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 Milliseverts (mSv)

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


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.

A heart scan on a 16- or 64-slice multidetector device, your exposure is 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 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 legimate medical questions. They are not screening tests to be applied broadly and used year after year.

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.



Detail on radiation exposure with CT coronary angiograms on multidetector devices can be found at 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, one of several studies on this issue.

Mediterranean diet vs. American Heart Association Diet

In 1994, the Lyon Heart Study demonstrated a 50-70% reduction in coronary events in participants who followed a diet rich in vegetables, olive oil, fish, nuts, red wine, and enjoyed meals as a family activity. Various other studies have documented similar phenomena with less metabolic syndrome, better lipid patterns, less obesity with the Mediterranean lifestyle.

There are two fundamental differences between the Mediterranean diet and the diet advocated by the American Heart Association (AHA) for people with heart disease: the Mediterranean diet uses olive oil more liberally, such that fat calories can reach 40% of total; and, unlike the AHA diet, processed foods are not a part of the Mediterranean diet. Greeks, for instance, are far less likely to eat Count Chocula cereal for breakfast, or snack on Healthy Choice Premium Caramel Swirl Sandwich (ice cream sandwiches) or Malt-O-Meal Honey Nut Scooters. All three of these foods on listed on the AHA Heart-Check Mark heart-healthy program.

In other words, remove all the processed foods, and the AHA diet pretty closely resembles the Mediterranean diet. There are differences but they tend to be relatively small. If the only major difference is the presence of processed foods, wouldn't you therefore expect the AHA to embrace the Mediterranean diet?

Here's what their official stand on the Mediterranean diet states:

Does a Mediterranean-style diet follow American Heart Association dietary recommendations?

Mediterranean-style diets are often close to our dietary recommendations, but they don’t follow them exactly. In general, the diets of Mediterranean peoples contain a relatively high percentage of calories from fat. This is thought to contribute to the increasing obesity in these countries, which is becoming a concern.



The AHA is actually lukewarm towards the diet that was the first to show a dramatic decrease in heart attack and death. Why?

The answer is obvious, once cast in this light. To wholeheartedly endorse the Mediterranean diet might be seen as an indirect rejection of American processed foods. You know, the foods that have caused an extraordinary and unprecedented epidemic of obesity in the U.S., the foods that are manufactured by ConAgra, General Mills, Kelloggs--all also major financial contributors to the AHA, according to the AHA Annual Report.

I tell my patients: If you want heart disease, follow the American Heart Association diet. In my view, it is a diet founded on politics and money, not on health. How else could Cocoa Puffs be regarded as heart healthy?

Track Your Plaque in 50,000 BC

Imagine we could send you back in a time machine to 50,000 BC.

However, our agreement: no modern tools or equipment. Just your brain, hands, and legs. And your landing spot will be tropical or semi-tropical, the same climate that humans spent much of their evolutionary time in.

Not only might you rub elbows with contemporaries like homo erectus and neanderthalensis, you'd also have to fend for your life and survival.

To eat, you will have to chase and kill wild game, all with your bare hands or crude tools crafted from sticks and stones. You will have to learn what wild berries, roots, and plants are edible and distingusih them from those that make you retch, make your bowels run, or kill you. You won't be able to cultivate grain, at least for a good long time, since you don't have a community that makes such an undertaking easier.

Instead, you are constantly on the run, from the moment you awake until you finally settle back as the sun sets, hopefully with a full stomach, but often empty and growling, anticipating the hunt and forage of tomorrow.

You are outdoors all day, except for the period when you hide in your cave or self-made shelter. You wear what little clothing you can make yourself from your kills, a skin or two. Your skin becomes a dark brown, a 5 foot 10 inch male will weigh 140 lbs, a 5 foot 5 inch woman 95 lbs. There are obvious downsides: your teeth will rot, you will be prone to infections, and predators view you as fair game.

But the result will be that many chronic diseases of modern life will no longer be worries for you. Heart disease? Highly unlikely. Do you need vitamin D? No, because you are outdoors virtually all day with most of your body surface area exposed to sun. Omega-3 fatty acids? You get those from the wild game you eat, since they have higher omega-3 content feeding in the wild, not eating corn like modern livestock. Since your body fat is minimal, just enough for survival, you don't need niacin.

In other words, many of the strategies of the Track Your Plaque program are modern necessities, responses to the "deficiencies" of modern life. Of course, I don't really have a time machine. I also doubt that you wish to hunt wild game every day, forage for plants and roots, run nearly-naked in the sun. You probably also have become accustomed to brushing your teeth and not viewing every animal as a potential threat to your life.

Nonetheless, I find this an interesting exercise for understanding the role of all the tools we use in the Track Your Plaque program for plaque control.

When pessimism wins

When I first met Hank, I immediately sensed it: anger, hostility, fear. His heart scan score of 685 just made it worse.


He didn't want to be there talking to me. His wife was giving him a hard time. Work was a constant source of irritation. The receptionist at the front desk screwed up his paperwork. Our office charges were too much.


In short, Hank was a pessimist. A bad one.


All the nutrition information out there is bunk. Only he knew how he should eat right. It's stupid to take a lot of fish oil. "You want me to grow gills?"


Among the parameters we use in the Track Your Plaque program is blood pressure during exercise, which provides a surrogate measure of blood pressure during emotional stress, anxiety, etc. "No, I don't need that. I already exercise." No amount of justification could change his mind. "A guy at work had a stress test. They said everything was fine, then Bang! He drops dead. What good is that?"


Hank did go along with a few pieces of advice.


A repeat heart scan 12 months after the first: 870, a 27% per year rate of increase. That's about what would happen if Hank had done nothing, had taken no action to try and stop or reduce his heart scan score.


I don't know if Hank will ever succeed in dropping his score. In fact, I suspect that he will fail, meaning that plaque will grow and he will eventually, perhaps in a year, two or three, require several stents, heart bypass, or have a heart attack. In other words, Hank's pessimism is a self-fulfilling phenomenon: If he believes he will fail, he will. If he believes the world is a rotten place, it is.


Is it possible to "cure" someone like Hank of his deeply-rooted pessimistic attitudes? I don't know of any easy solutions for someone with attitudes as deeply-ingrained as Hank's. (See my prior post, "Cure for pessimism?" at http://heartscanblog.blogspot.com/2007_05_01_archive.html.)

I believe it does help to make someone aware of their attitudes and that it does indeed exert ill health-effects--if they will believe it. But this is a very tough nut to crack.

Bad news on CoQ10?

A review of the effects of Coenzyme Q10 (CoQ10) on the muscle aches and weakness (myopathy) of statin drug therapy was just published in the Journal of the American College of Cardiology.

(Marcoff L, Thompson PD. The role of coenzyme Q10 in statin-associated myopathy. J Amer Coll Cardiol 2007;49(23):2231-2237.)

This is not a study, but a review of the existing scientific and clinical data available on this topic. The study authors conclude with a lukewarm statement:

". . .there is insufficient evidence to prove the etiologic [causal] role of CoQ10 deficiency in statin-associated myopathy and that large, well-designed clinical trials are required to address this issue. The routine use of CoQ10 cannot be recommended in statin-treated patients. Nevertheless, there are no known risks to this supplement and there is some anecdotal and preliminary trial evidence of its effectiveness. Consequently, CoQ10 can be tested in patients requiring statin treatment, who develop statin myalgia, and who cannot besatisfactorily treated with other agents. Some patients may respond, if only via placebo effect."

Should the media get hold of this report, be prepared for the usual "Nutritional supplement no help for drug toxicity" headlines, or "Yet another nutritional supplement shows no benefit" with parallels drawn to vitamin C or E.

There are several issue that need to be factored into the discussion:

1) This is not a study, just a review. Thus, any biases of the authors are more likely to exert themselves.

2) The understanding of CoQ10 absorption among different preparations may be an issue. I just received a mailing from Life Extension that made extravagant claims about the superior absorption of ubiquinol, to be distinguished from ubiquinone, the more common form. They claim that eight-fold increased absorption and blood levels of CoQ10 are achievable with ubiquinol. Unfortunately, virtually all the supportive data are unpublished, proprietary observations, i.e., generated by companies who make or sell it. This is as reliable as drug manufacturers who publish glowing reports on their own drugs--perhaps it's true, but it requires unbiased corroboration.

3) Despite the lack of a large, well-funded clinical trial (all are small), the issue continues to live and breathe because of the powerful anecdotal experience.

In our experience, CoQ10 does work. It doesn't work all of the time, perhaps just 80-90% of the time. It does generally require higher doses (100 mg per day, occasionally more). It very clearly must be an oil-based gelcap (just like vitamin D) to work; capsules containing powder do not work.

It's difficult to doubt when someone starts a statin drug, develops the muscle aches and weakness, begins CoQ10 and obtains distinct relief, stops CoQ10 and aches and weakness return, then only to go away again with resumption of CoQ10 . I've seen this countless times.

We do need better information on CoQ10. There's no doubt about it. For people who obtain benefit from statin therapy, I think CoQ10 remains a useful solution. A better solution would be to get rid of the offending drug. But that's not always possible--e.g., LDL cholesterol 190 mg/dl despite the best diet and "adjunctive" food effort. Then CoQ10 can be very useful.
All posts by william-davis

Cholesterol follies

Rudy is a 59-year old man. He's had three heart catheterizations, two of which resulted in stent implantations. Obviously, Rudy should be the beneciary of a prevention program.

His basic cholesterol values:

Total cholesterol 164 mg/dl--pretty good, it seems.

LDL cholesterol 111 mg/dl--Wow! Not too bad.

HDL cholesterol 23 mg/dl--Uh oh, that's not too good.

Triglycerides 148 mg/dl--By national (NCEP ATP-III) guidelines, triglycerides of 150 mg/dl and below fall within the desirable range.


So we're left with an apparently isolated low HDL cholesterol, nothing more. On the surface, it doesn't seem all that bad.

Of course, we need to keep in mind that this pattern landed Rudy in the hospital on several occasions and prompted several procedures.

Should we rely on these results? How about Rudy's lipoproteins?

Here they are (NMR; Liposcience):

LDL particle number 2139 nmol/l--Representing an effective LDL of 213--over 100 mg higher than the standard value (above) suggests.

Small LDL particles 2139 nmol/l--In other words, 100% of all Rudy's LDL particles are small. (Thus, weight-based measures of LDL cholesterol fail to tell us that he has too many small particles.)

Large HDL 0 (zero) mg/dl--Rudy has virtually no functional HDL particles.


If we had relied only on Rudy's standard cholesterol values, we would have focused on raising HDL. However, lipoprotein analysis uncovered a smorgasbord of additional severe patterns. The high LDL particle number comprised 100% of small particles is especially concerning.

Truly, conventional cholesterol testing is a fool's game, one that time and again fails to fully uncover or predict risk for heart disease. One look at Rudy's lipoproteins and it becomes immediately obvious: This man is at high risk for heart disease and the causes are clear.

Of course, many physicians and insurance companies argue that the added information provided by this portion of the lipoprotein test added around $70 more to the expense.

When you see results like this, is there even a choice?

Equal calories, different effects

A great study was just published in the Journal of the American College of Cardiology:

Metabolic effects of weight loss on a very-low-carbohydrate diet compared with an isocaloric high-carbohydrate diet in abdominally obese subjects.

88 obese adults with metabolic syndrome were placed on either of two diets:

1) A very low-carbohydrate, high-fat diet (VLCHF): 4% calories from carbohydrates (truly low-carb); 35% protein; 61% fat, of which 20% were saturated. In the first 8 weeks, carbohydrate intake was severely limited to <20 grams per day, then <40 grams per day thereafter.

2) A high-carbohydrate, low-fat diet (HCLF): 46% calories from carbohydrates; 24% protein; 30% total fat, of which <8% were saturated.

Both diets were equal in calories (around 1400 calories per day--rather restrictive) and participants were maintained on the program for six months.

At the end of the six month period, participants on the VLCHF diet lost 26.4 lb, those on the HCLF diet 22.2 lbs (though the difference did not reach statistical significance). Thus, both approaches were spectacularly successful at weight loss.

Surprisingly, blood pressure, blood sugar, insulin and insulin sensitivity (a measure called HOMA) were all improved with both diets equally. Thus, these measures seemed to respond more to weight loss and less to the food composition.

Lipids differed between the two diets, however:


VLCHF:
Total cholesterol: initial 208.4 mg/dl final 207.7 mg/dl

LDL: initial 125 mg/dl final 123 mg/dl

HDL: initial 55 mg/dl final 64.5 mg/dl

Triglycerides: initial 144 mg/dl final 74 mg/dl

Apoprotein B: initial 98 mg/dl final 96 mg/dl


HCLF
Total cholesterol: initial 208.4 mg/dl final 187.5 mg/dl

LDL: initial 126 mg/dl final 108 mg/dl

HDL: initial 51 mg/dl final 54.5 mg/dl

Triglycerides: initial 157.6 mg/dl final 111 mg/dl

Apoprotein B: initial 100 mg/dl final 95 mg/dl


Some interesting differences became apparent:
--The VLCHF diet more effectively reduced triglycerides and raised HDL.
--The HCLF diet more effectively reduced total and LDL.
--There was no difference in Apo B (no statistical difference).

The investigators also made the observation that individual responsiveness to the diets differed substantially. They concluded that both diets appeared to exert no adverse effect on any of the parameters measured, both were approximately equally effective in weight loss with slight advantage with the carbohydrate restricted diet, and that lipid effects were indeed somewhat different.


What lessons can we learn from this study? I would propose/extrapolate several:

When calories are severely restricted, the composition of diet may be less important. However, when calories are not so severely restricted, then composition may assume a larger role. When calories are unrestricted, I would propose that the carbohydrate restriction approach may yield larger effects on weight loss and on lipids when compared to a low-fat diet.

The changes in total cholesterol are virtually meaningless. Part of the reason that it didn't drop with the VLCHF diet is that HDL cholesterol increased. In other words, total cholesterol = LDL + HDL + trig/5. A rise in HDL raises total cholesterol.

Despite no change in Apo B, if NMR lipoprotein analysis had been performed (or other assessment of LDL particle size made), then there would almost certainly have seen a dramatic shift from undesirable small LDL to less harmful large LDL particles on the VLCHF diet, less change on the HCLF diet.

The lack of restriction of saturated fat in the VLCHF that failed to yield adverse effects is interesting. It would be conssistent with the re-analysis of saturated fat as not-the-villain-we thought-it-was put forward by people like Gary Taubes (Good Calories, Bad Calories).

In the Track Your Plaque experience, small LDL is among the most important measures of all for coronary plaque reversal and control. Unfortunately, although this study was well designed and does add to the developing scientific exploration of diet, it doesn't add to our insight into small LDL effects. But if I had to make a choice, I'd choose the low-carbohydrate, high-fat approach for overall benefit.

Is skinny necessary for reversal?

Nothing we do in the Track Your Plaque program guarantees that coronary atherosclerotic plaque or your heart scan score is reduced or reversed.



But everything we do weighs the odds in your favor of successfully achieving reversal: correction of lipoprotein patterns, uncovering hidden patterns like Lp(a), vitamin D, being optimistic--it all tips the scales in your favor.

But how necessary is it to be skinny, meaning somewhere near your ideal weight?

It is important, but not as important as it used to be. Let me explain.

I used to tell people that plaque would not regress unless ideal weight was achieved and all the parameters of abdominal obesity and metabolic syndrome were corrected. This includes blood pressure, blood sugar, low HDL, small LDL, high triglycerides, and high c-reactive protein. Curiously, though, as we've gotten better and better at reducing coronary calcium scores, I've been finding that complete correction of all parameters, including achieving ideal weight, don't seem to be as necessary to achieve plaque reversal.

I almost hate to say this, but I've even witnessed significant drops in heart scan scores in people with body mass indexes (BMI) of 30--obese.

The necessary change doesn't seem to be weight, per se, but the consequences of weight. In other words, if you remain overweight, but blood sugar, HDL, small LDL, etc. have shown substantial improvement, then reversal is still achievable.

Then is it okay to be fat or overweight?

Reducing weight to ideal weight does indeed tip the scales in your favor, since it represents an observable, perceptible measure of all associated patterns. Dropping weight can also minimize the need for efforts to correct the consequences of overweight--you might need less niacin, fish oil, exercise, blood pressure medication, etc. to succeed at plaque reversal. Achieving ideal weight may also provide benefits like reduced risk of cancers and degenerative diseases of the hips and knees. But, to my recent surprise over the last two years, achieving ideal weight is not an absolute requirement to achieve reversal.

This is contrary to what some others say. For instance, in an upcoming interview with Dr. Joel Fuhrman on the Track Your Plaque website, Dr. Fuhrman argues that 10% body fat for males, 22% body fat for females, accelerates plaque and symptom reversal. Dr. Fuhrman is author of Fasting and Eating for Health, Eat to Live, and a new upcoming 2-part book, Eat for Health, and proponent of high-nutrient vegetarian diets and fasting. Dr. Fuhrman has been helpful in teaching us some important lessons on how to apply periodic fasting to accelerate plaque reversal.

So, which is it, fat or skinny?

If given a choice (which everyone has), I'd choose skinny. But, provided all the parameters associated with overweight are corrected, then remaining overweight doesn't necessarily mean that you can't still succeed at plaque reversal.

If you are interested in knowing what your ideal weight is, there are a number of software calculators and tables available, including the HealthCentral.com calculator and the National Heart, Lung, and Blood Institute BMI Calculator.


Image courtesy Wikipedia.

Copyright William Davis, MD 2008

MESA Study: Track Your Plaque-Lite?

The long-awaited data analyses from the Multi-Ethnic Study of Atherosclerosis (MESA) are finally making it to press.

The MESA Study is an enormously ambitious and important study of 6800 people, 45 to 84 years old, that includes white, black, Hispanic, and Chinese participants from six communities around the U.S. (Forsyth County, NC; Northern Manhattan and the Bronx, NY; Baltimore and Baltimore County, Md; St Paul, Minn; Chicago, Ill; and Los Angeles County, California.) Participants had no history of heart disease at enrollment. All underwent a heart scan (either EBT or multi-detector heart scans) at the start. It is therefore the largest prospective study involving heart scans ever performed. It is, not unexpectedly, yielding some fascinating observations relevant to the Track Your Plaque program. The MESA study is, incidentally, funded by the non-commercial, publicly-funded National Heart, Lung, and Blood Institute and is therefore presumably free of commercial bias.

Among the most recent publications is Risk factors for the progression of coronary artery calcification in asymptomatic subjects: Results from the Multi-Ethnic Study of Atherosclerosis (MESA) In this analysis of 5700 of the MESA participants, a repeat heart scan was obtained an average of 2.4 years after the first. Conventional risk factors for heart disease were obtained at the start (see below for details under Measurement of Covariates.)

After analyzing the data and risk factors assessed, such as age, sex, race, blood pressure, body mass index (BMI), presence of diabetes, blood sugar, and family history of heart disease, two questions were asked:

1) What risk factors predict heart scan scores?

2) What risk factors predict progression (i.e., increase) in heart scan scores?

(The second question is particularly relevant to us and the Track Your Plaque experience.)

The MESA analysis showed that essentially all the risk factors assessed correlated with both the initial heart scan score, as well as the rate of progression. No surprises here.

But the most eye-opening finding was that the conventional risk factors assessed explained only 12% of the variation and progression in heart scan scores (coefficient of determination, or R squared, = 0.12.) In other words:

--Conventional risk factors like LDL cholesterol, diabetes, and excess weight explain only a tiny fraction of why someone develops coronary atherosclerotic plaque as represented by a heart scan score.

--The great majority of risk for a high heart scan score remains unexplained by conventional risk factors.

--The great majority of risk for progressive increase in heart scan scores also remains unexplained by conventional risk factors.


In light of the MESA analysis, it's no surprise that strategies like reducing LDL cholesterol with statin drugs fails to prevent most heart attacks. It's no surprise that conventional prevention programs that talk about "knowing your numbers," eating a "balanced" or low-fat diet, etc., fail miserably to prevent the vast majority of heart attacks and heart procedures.

MESA confirms what we've been saying these past few years: If you want control over coronary heart disease, you won't find it in Lipitor, a low-fat diet, and other limited conventional notions of risk. Correction of conventional risk factors like cholesterol and blood pressure are, in a word, a failure. I wouldn't even call the conventional approach Track Your Plaque-Lite. They don't even come close.

If conventional risk factors can explain only 12% of the reason behind heart disease, we've got to look elsewhere to understand why you and I develop this process.



Measurement of Covariates
Information on demographics, smoking, medical conditions, and family history was collected by questionnaire at the initial examination. Height and weight were also measured at the baseline examination, and blood was drawn for measurements, including lipids, inflammation, fasting glucose, fibrinogen, and creatinine. Resting blood pressure was measured 3 times in the seated position, and the average of the last 2 measurements was used in the analysis. Medication use was determined by questionnaire. Additionally, the participant was asked to bring to the clinic containers for all medications used during the 2 weeks before the visit. The interviewer then recorded the name of each medication, the prescribed dose, and frequency of administration from the containers.


Copyright 2008 William Davis,MD

Risks for coronary disease 2008

According to conventional thinking, there are identifiable risks for coronary disease and heart attack. These risk factors are:

* smoking
* high blood pressure
* high blood cholesterol and excessive saturated fat intake
* diabetes
* being overweight or obese
* physical inactivity

I'd agree with all the factors listed (though I would argue about the importance of high blood cholesterol and saturated fat; they are not as important as commonly made to be.)

Is the list complete?

From the unique perspectives gained in the Track Your Plaque program, I'd offer a significantly different list. Trying to stop or reduce coronary atherosclerotic plaque and heart scan scores makes you a whole lot smarter about what works and what doesn't work.

So, in addition to the risk factors listed above, I would add:

* Small LDL particles--Lots of small LDL particles is MORE important than high LDL.
* High blood pressure with exercise
* Excessive wheat intake and other processed carbohydrates--An issue of explosive importance today. Wheat creates large numbers of small LDL particles, among other adverse effects.
* Vitamin D deficiency--Among the most powerful risks I know of. It belongs at the top of the list.
* Vitamin K2 deficiency
* Low HDL cholesterol
* Blood sugar >100 mg/dl
* High triglycerides--While some argue about whether triglycerides are a risk that behaves independently of patterns like low HDL, they are neglecting the potent force of this risk. Sure, it occurs in tandem with low HDL (usually, though not always), but it is a factor that can leave you with risk even when HDL is raised to healthy levels.
* Lipoprotein(a)--It is eminently, positively crystal clear that lipoprotein(a) is a powerful risk for heart disease. The lack of a profitable treatment keeps it hidden in the shadows.
* Pessimism--Be happy, do better. Be a constantly angry, frustrated, complaining sourpuss and you are more likely to succumb to heart disease, cancer, or other undesirable fate.


These are the risk factors that we address through the Track Your Plaque program, a list that yields a far more powerful and comprehensive approach to control over coronary plaque/atherosclerosis, sufficient to achieve reversal in many (though not in all) instances.

I view the list of conventional risk factors as a "no brainer" list. Sure, smoking is a risk factor. But there are virtually no smokers in the Track Your Plaque program. If you smoke, you clearly don't care enough to engage in a high-intensity prevention program like this.

Saturated fat? Perhaps, but the battlefield of heart disease is riddled with the bodies of those who employed this as their sole strategy and failed catastrophically.

Diabetes, hypertension, and overweight all represent a continuum of risk; the solutions offered in the conventional scheme (i.e., low-fat diet, etc.) make these patterns worse, not better.

The conventional response to heart disease risk is trapped somewhere in 1973 and has not changed in over 30 years. Heart disease continues to be a growth industry for hospitals and the pharmaceutical and medical device industries. The "official" organizations continue to deliver an antiquated, outdated message.

If you want heart disease, follow the American Heart Association diet. If you want established heart disease to get worse, follow the American Heart Association diet. If you want diabetes or, if you already have diabetes or pre-diabetes, if you want it to worsen and develop organ damage (eyes, kidneys, nervous system, etc.), then follow the American Diabetes Association diet. USDA food pyramid? Loosen your belt!

The list of conventional risk factors for heart disease is woefully inadequate. If that is as far as your prevention program takes you, heart disease will not be controlled or prevented. At best, it might be slowed; at worst--and more likely--it might be accelerated.

Food sources of vitamin K2



Vitamin K2 is emerging as an exciting player in the control and possible regression of coronary atherosclerotic plaque. Only about 10% of dietary vitamin K intake is in the K2 form, the other 90% being the more common K1.

The ideal source of K2 is natto, the unpalatable, gooey, slimy mass of fermented soybeans that Japanese eat and has been held responsible for substantial decreases in osteoporosis and bone fractures of aging. Natto has an ammonia-like bouquet, in addition to its phlegmy consistency that makes it virtually inedible to anyone but native Japanese.

I say that the conversation on vitamin K2 is emerging because of a number of uncertainties: What form of vitamin K2 is best (so-called MK-4 vs. MK7 vs. MK-9, all of which vary in structure and duration of action in human blood)? What dose is required for bone benefits vs. other benefits outside of bone health? Why would humans have developed a need for a nutrient that is created through fermentation with only small quantities in meats and other non-fermented foods?

Much of the developing research on vit K2 is coming from the laboratories of Drs. Vermeer, Geleijnse, and Schurgers at the University of Maastricht in the Netherlands, along with several laboratories in Japan, the champions of K2.

MK-7 and MK-8,9,10 come from bacterial fermentation, whether in natto, cheese, or in your intestinal tract; MK-4 is naturally synthesized by animals from vitamin K1. While natto is the richest source of the MK-7 form, egg yolks and fermented cheeses are the richest sources of the MK-4 form.

Chicken contains about 8 mcg MK-4 per 3 1/2 oz serving; beef contains about 1 mcg. Egg yolks contain 31 mcg MK-4 per 3 1/2 oz serving (app. 6 raw yolks). Hard cheeses contain about 5 mcg MK-4 per 3 1/2 oz serving, about 70 mcg of MK-8,9; soft cheeses contain about 30% less. Natto contains about 1000 mcg of MK-7, 84 mcg MK-8, and no MK-4 per 3 1/2 oz serving.











Feta cheese

Thanks to the research efforts of the Dutch and Japanese groups, several phenomena surrounding vitamin K2 are clear, even well-established fact:

--Vitamin K2 supplementation (via frequent natto consumption or pharmaceutical doses of K2) substantially improves bone health. While K2 by itself exerts significant bone density/strength increasing properties in dozens of studies, when combined with other bone health-promoting agents (e.g., vitamin D3, prescription drugs like Fosamax and calcitonin), an exaggerated synergy of bone health-promoting effects develop.



--The MK-4 form of vitamin K2 is short-lived, lasting only 3-4 hours in the body. The MK-7 form, in contrast, the form in natto, lasts several days. MK-7 and MK-8-10 are extremely well absorbed, virtually complete.

--Bone health benefits have been shown for both the MK-7 and MK-4 forms.

--Coumadin (warfarin) blocks all forms of vitamin K.





Interestingly, farm-raised meats and eggs do not differ from factory farm-raised foods in K2 content. (But please do not regard this as an endorsement of factory farm foods.)

Another interesting fact: Since mammals synthesize a small quantity of Vit K2 forms from vitamin K1, then eating lots of green vegetables should provide substrate for some quantity of K2 conversion. However, work by Schurgers et al have shown that K1 absorption is poor, no more than 10%, but increases significantly when vegetables are eaten in the presence of oils. (Thus arguing that oils are meant to be part of the human diet. Does your olive oil or oil-based salad dressing represent fulfillment of some subconscious biologic imperative?)

If we believe the data of the Rotterdam Heart Study, then a threshold of 32.7 micrograms of K2 from cheese yields the reduction in cardiovascular events and aortic calcification.

It's all very, very interesting. My prediction is that abnormal (pathologic) calcium deposition will prove to be a basic process that parallels atherosclerotic plaque growth, and that manipulation of phenomena that impact on calcium depostion also impact on atherosclerotic plaque growth. Vitamins D3 and K2 provide potential potent means of at least partially normalizing these processes.

As the data matures, I am going to enjoy my gouda, Emmenthaler, Gruyere, and feta cheeses, along with a few egg yolks. I'm going to be certain to include healthy oils like olive and canola with my vegetables.


All images courtesy Wikipedia.

Copyright 2007 William Davis, MD

Track Your Plaque: Naughty or nice?



Among the many wonderful surprises we've had at Track Your Plaque this holiday season was a letter from Santa Claus himself!

It seems that Santa, like the rest of us, has been busy surfing the web for useful health information the last few months. He was struck with this curious discussion we've been having about "wheat belly" and all the unhealthy consequences of wheat products in our diet.

He writes:

"I wouldn't have believed it myself, except that my waist size has grown four inches in as many years. Sure, I'm known for my healthy girth, but now even Mrs. Claus calls me fat!

"I was open to new ideas when I came across this crazy discussion about eliminating wheat from your diet. So I said, "What have I got to lose?" Well, four weeks later and 12 lbs lighter, I'm convinced. Now comes the tough part: I've got to deliver all the toys and resist all those cookies the children put out for me. I wonder if wheat makes reindeer fat, too?

"Anyway, thanks to your program I'm back to my old weight again. Doc says my blood sugar and blood pressure are also back down to normal. Thanks, Track Your Plaque! (You'll find something extra special under the tree this year.)"

And so it goes. I'm tempted to put Santa's testimonial on our homepage, but I think that may be tooting our own horn a bit too much.

Have a wonderful holiday!

Vitamin D: Treatment for metabolic syndrome?

Metabolic syndrome is that increasingly common collection of low HDL cholesterol, high triglycerides, high blood sugar, and high pressure that now afflicts nearly 1 in 4 adults, rapidly gaining ground to 1 in 3. Beyond these surface factors, metabolic syndrome also creates small LDL particles, VLDL, intermediate-density lipoproteins (IDL), increased imperceptible inflammation measured as higher c-reactive protein, and greater blood clotting tendencies. Metabolic syndrome is usually, though not always, associated with a big tummy ("beer belly," though I call it "wheat belly").

In short, metabolic syndrome creates a metabolic mess that leads to dramatic increases in heart disease, vascular disease and stroke, and cancer. The medical community has been paying increasingly greater attention to this condition because of its booming prevalence and because of the big bucks invested in "education" by the manufacturers of the diabetes and pre-diabetes drugs, particularly makers of Actos and Avandia.

But here's a curious observation:

Replacement of vitamin D to healthy levels (we aim for 50-60 ng/ml, or 125-150 nmol/l) yields:

--Higher HDL
--Lower triglycerides
--Lower blood sugar
--Reduced c-reactive protein
--Reduced blood pressure
--Reduced small LDL
--Enhanced sensitivity to insulin

(Whether blood clotting and effects on IDL should be added to this list is uncertain.)

It's obvious: Vitamin D is proving to be a very important and powerful corrective influence on many of the facets of the metabolic syndrome. In fact, I would go as far as saying that, side by side, vitamin D yields nearly the same effect as prescription drugs Actos and Avandia--without the extravagant cost (nearly $200 per month), leg swelling, congestive heart failure and heightened heart attack risk (with Avandia), and average 8 lb weight gain. Of course, vitamin D also provides benefits beyond metabolic syndrome like facilitation of coronary plaque regression, increased bone density, reduced arthritis, and reduced risk of several cancers.

You'd think that agencies like the American Diabetes Association (ADA) would be all over vitamin D like white on rice. Yet they remain curiously quiet about the entire issue. (That should come as no surprise to anyone familiar with the behavior and politics of this organization, the same outfit that has widely propagated the ADA diet, a program that accelerates diabetes and its complications. In my view, the ADA is an embarassment.)



For a really great story and video on vitamin D that includes a terrific interview with vitamin D guru and Track Your Plaque friend, California psychiatrist Dr. John Cannell, go to What's the Real Story on Vitamin D?. While the video will yield little new to readers of The Heart Scan Blog or Track Your Plaque members, it just feels really good to see a well-made, high-class video production echoing many of the things we've been talking about these past two years.

Appetite stimulants

Ever have days when you just can't seem to get enough to eat, your stomach gnawing just a hour after a meal? We all get them, some more than others. Other days, you can be content with a few simple foods and hunger is subdued, temptation easy to control.

Why such contrasts on different days?

A major part of the reason can be the presence of appetite stimulants, factors that trigger appetite beyond rational control. The list of common appetite stimulants includes:

--Sleep deprivation--A very important factor. Lack of sleep drives tremendous appetite, and often for the wrong foods (processed carbohydrates). I personally have experienced my most shamefully indulgent days when sleep-deprived. The solution is obvious: Sleep. Another factor that is based purely on personal observation is that of waking mid-phase. In other words, waking up while you're still enjoying the deeper phases of sleep (e.g., phase 3,4, or REM). This can oddly disrupt your day and your impulse control. I usually try and time sleep to increments of 90 minutes to coincide with the average duration of the full cycle of sleep. For example, 7 1/2 hours is better than 8 hours, since the extra half hour puts your square into a deeper sleep cycle.

--Excessive caffeine--Caffeine stimulates stomach acid. This triggers the impulse to eat . . . and eat and eat.













Image courtesy Wikipedia

--Aspirin and other anti-inflammatory agents--If you take aspirin (as many of our Track Your Plaquers do), then beware of the gastritis that can develop. Like excessive caffeine, it also triggers the impulse to eat, likely a protective mechanism, since food sops up excess acid. I ask patients to take periodic breaks from aspirin, e.g., a week off every two or three months, to allow the stomach to heal. Alternatively, an occasional dose of acid-suppressing medication is a safe practice, e.g., Pepcid AC 10-20 mg; Prilosec 10-20 mg.

--Wheat-containing foods--Followers of The Heart Scan Blog know my feelings on this. Wheat is a potent appetite stimulant: Eat something containing wheat like a pretzel or whole wheat bagel, and you want more. You may want more immediately, or a little later when your blood sugar plunges after the wheat-driven insulin surge. Solution: Dump the wheat, one of the most unhealthy food groups around.

--Alcohol--Though perhaps not a direct appetite-stimulating effect, the loss of impulse-control with alcoholic drinks can lead to overindulgence, often in the worst foods. Just beware.

--Hanging around with heavy people. Remember peer pressure? It can be subliminal. People with poor eating habits provide the silent message that it's okay to yield to impulse, overeat, overindulge, and choose the wrong foods.

--Stress--Whether through cortisol stimulation or other means, stress triggers appetite in some people. If you experience this and must give in, reach for raw nuts or nuts, rather than wheat snacks or chips. The effect will be minimal, perhaps even beneficial, rather than the bloating, appetite-stimulating, fattening effect of crackers, chips, or pretzels. This may be the same phenomenon as taking prescription steroids like prednisone.

--Short dark days, long nights--In other words, winter. Though just an anecdotal observation, I am convinced that vitamin D supplementation is an effective antidote to this effect. The short, dark days just don't bother you as much, perhaps not at all, and there's no impulse for comfort foods.


How about appetite suppressants? In this list I would include 1) raw nuts--especially almonds, walnuts, pecans, and pistachios, the sort with a fibrous covering and rich in monounsaturates, 2) other sources of plentiful healthy oils, e.g, use more olive oil in your salad or add it to hummus for your veggie dip, 3) space-occupying fibers such as glucomannan, inulin (such as in Fiber Choice), and psyllium seed products. Counteracting the above appetite stimulants like sleep deprivation is, of course, important.

The coming wheat frenzy, otherwise known as the holidays, is an especially important time to be aware of these effects. Eat, drink, and be merry--but with rational impulse control not driven by subconscious appetite stimulants.

"Heart scans are experimental"

Let me warn you: This is a rant.

It is prompted by a 44-year old woman. She has a very serious lipoprotein disorder. Her family experiences heart attacks in their 40s and 50s. I asked for a heart scan. Her insurance companied denied it.

This is nothing new: heart scans, like mammograms, have not enjoyed reimbursement from most insurers despite the wealth of data and growing acceptance of this "mammogram" of the heart.

However, 10 minutes on the phone, and the "physician" (what well-meaning physician can do this kind of work for an insurance company is beyond me) advised me that, while CT heart scans for coronary calcium scoring are not covered, CT coronary angiograms are.

Now, I've been witnessing this trend ever since the big players in CT got involved in the game, namely Philips, Siemens, Toshiba, and GE. These are enormous companies with hundreds of billions of dollars in combined annual revenues. They, along with the lobbying power of cardiology organizations like the American College of Cardiology, have gotten behind CT coronary angiograms. This is most likely the explanation of why CT coronary angiograms have rather handily obtaining insurance reimbursement. Interestingly, the insurance company I was speaking to is known (notorious?) for very poor reimbursement practices.

A CT heart scan, when properly used, generates little revenue, a few hundred dollars to a scan center, barely enough to pay for a device that costs up to $2 million. However, CT coronary angiograms, in contrast, yield around $2000 per test. More importantly, they yield downstream revenues, since CT angiograms are performed as preludes to conventional heart catheterizations, angioplasty, stents, bypass surgery, etc. Now we're talking tens or hundreds of thousands of dollars revenue per test.

What puzzles me is that much of that increased cost comes out of the insurance company. Why would they support such tests if it exposes them to more costs? I'm not certain. It could be the greater pressures exerted by the big CT companies and powerful physician organizations. I seriously doubt that the insurance companies truly believe that heart scans for coronary calcium scoring are "experimental" while CT coronary angiograms are "proven." If all we did was compare the number of clinical studies that validate both tests, we'd find that the number of studies validating heart scans eclipses that of coronary angiograms several fold. Experimental? Hardly.

The smell of money by physicians eager to jump on the bandwagon of a new revenue-producing procedure is probably enough to have them lobby insurers successfully. In contrast, plain old heart scans just never garnered the kind of vigorous and vocal support, since nobody gets rich off of them.

If CT coronary angiograms are sufficiently revenue producing that my colleagues and the CT scanner manufacturers have managed to successfully lobby the health insurers, even one as financially "tight" as the one I spoke to today, well then I take that as testimony that money drives testing, as it does the behavior of hospitals, many of my colleagues, and can even force the hand of insurers.