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.

Restaurant eating: A fructose landmine

There is no remaining question that fructose is among the worst possible things humans can consume.

Followers of the Heart Scan Blog already know this, from conversations like The LDL-Fructose Disconnect, Where do you find fructose?, and Goodbye, fructose.

But fructose, usually as either high-fructose corn syrup (44%, 55%, occasionally higher percentage fructose) or sucrose (50% fructose), is ubiquitous. I've seen it in the most improbable places, including cole slaw, mustard, and dill pickles.

It's reasonably straightforward to avoid or minimize fructose exposure while eating at home, provided you check labels and focus on foods that don't require labels (like green peppers, salmon, and olive oil, i.e., unprocessed foods). But when you choose to eat at a restaurant, then all hell can break loose and fructose exposure can explode.

So what are some common and unsuspected fructose sources when eating at a restaurant?

Salad dressings--Dressings in all stripes and flavors are now made with high-fructose corn syrup and/or sucrose. This is especially true of low-fat, non-fat, or "lite" dressings, meaning oils have been replaced by high-fructose corn syrup. It can also be true of traditional non-low-fat dressings, too, since high-fructose corn syrup is just plain cheap.

Olive oil and vinegar are still your safest bets. I will often use salsa as a dressing, which works well.

Sauces and gravies--Not only can sauces be thickened with cornstarch, many pre-mixed sauces are also made with high-fructose corn syrup or sweetened with sucrose. Barbecue sauce is a particular landmine, since it is now a rare barbecue sauce not made with high-fructose corn syrup as the first or second ingredient. Sauces for dipping are nearly always high-fructose corn syrup-based.

Ketchup--Yup. Good old ketchup even is now made with high-fructose corn syrup. In fact, you should be suspicious of any condiment.

Highball, Bloody Mary, Margarita, Daiquiri, beer--Even the before-dinner or dinner drink can have plenty of fructose, particularly if a mix is used to make it. While Blood Marys seem the most benign of all, adorned with celery, pickle, and olive, just take a look at the ingredient label on the mix used: high-fructose corn syrup.

Fructose is a stealth poison: It doesn't immediately increase blood sugar; it doesn't trigger any perceptible effect like increased energy or sleepiness. But it is responsible for an incredible amount of the health struggles in the U.S., from obesity, to diabetes, to hyperlipidemias and heart disease, to arthritis, to cataracts.

A glycation rock and a hard place

Advanced Glycation End-products, or AGEs, the stuff of aging that mucks up brains, kidneys, and arteries, develop via two different routes: endogenous (from within the body) and exogenous (from outside the body).

Endogenous AGEs develop via glycation. Glycation of proteins in the body occurs when there are glucose excursions above normal. For instance, a blood glucose of 150 mg/dl after your bowl of stone-ground oatmeal causes glycation of proteins left and right, from the proteins in the lens of your eyes (cataracts), to the proteins in your kidneys (proteinuria and kidney dysfunction), to skin cells (wrinkles), to cartilage (brittle cartilage followed by arthritis), to LDL particles, especially small LDL particles (atherosclerosis).

At what blood sugar level does glycation occur? It occurs even at "normal" glucose levels below 100 mg/dl (with measurable long-term cardiovascular effects as low as 83 mg/dl). In other words, some level of glycation proceeds even at blood glucose levels regarded as normal.

There's nothing we can do about the low-level of glycation that occurs at low blood sugar levels of, say, 90 mg/dl or less. However, we can indeed do a lot to not allow glycation to proceed more rapidly, as it inevitably will at blood sugar levels higher than 90 mg/dl.

How do you keep blood sugars below 90 mg/dl to prevent excessive glycation? Avoid or minimize the foods that cause such rises in blood sugar: carbohydrates.

What food increases blood sugar higher than nearly all other known foods? Wheat.

Is einkorn the answer?

People ask: "What if I would like a piece of bread or other baked product just once in a while? What is safe?"

Eli Rogosa, Director of The Heritage Wheat Conservancy, believes that a return to the wheat of our ancestors in the Fertile Crescent, circa 10,000 years ago, is the answer.

Former science teacher, now organic farmer, farm researcher, and advocate of sustainable agriculture, Eli has been reviving "heritage" crops farmed under organic conditions, some of her research USDA-funded.

In particular, Eli has been cultivating original 14-chromosome ("diploid") einkorn wheat. Although einkorn contains gluten (in lesser quantities despite the higher total protein content), the group of proteins that trigger the immune abnormalities of celiac disease and other immune phenomena, Eli tells me that she has witnessed many people with a variety of wheat intolerances, including celiac disease, tolerate foods made with einkorn wheat. (The variety of glutens in einkorn differ from the glutens of the dwarf mutant that now dominate supermarket shelves.)

Eli travels to Israel every year, returning with "heritage" seeds for wheat and other crops. She formerly worked in the Israel GenBank as Director of the Ancient Wheat Program. She has written a brochure that describes her einkorn wheat.

Eli sent me 2 lb of her einkorn grain that nutritionist, Margaret Pfeiffer, and I ground into bread. Our experience is detailed here. My subsequent blood sugar misadventure, comparing einkorn bread to conventional organic whole wheat bread is detailed here, followed by the odd neurologic effects I experienced here.

Anyone else wishing to try this little ancient wheat experiment with einkorn can also obtain either the unground grain or ground flour through Eli's website, www.growseed.org. Most recently, einkorn pasta is being retailed under the Jovial brand at Whole Foods Market.

If anyone else makes bread or any other food with Eli's einkorn wheat, please let me know:

1) Your blood sugar response (before and 1 hour after consumption)
2) Whether you experienced any evidence of wheat intolerance similar to what you experienced with conventional wheat, e.g., rash, acid reflux, gas and cramping, moodiness, asthma, etc.

But remember: Wheat effects or no, einkorn is still a grain. My belief is that humans do best with little or no grain. The einkorn experience is an effort to identify reasonable compromises so that you and I can have a piece of birthday cake once a year without getting sick.

Genetic incompatibility

Peter has lipoprotein(a), or Lp(a), a genetic pattern shared by 11% of Americans.

It means that Peter inherited a gene that codes for a protein, called apoprotein(a), that attaches to LDL particles, forming the combined particle Lp(a). It also means that his overall pattern responds well to a high-fat, high-protein, low-carbohydrate diet: The small LDL particles that accompany Lp(a) over 90% of the time are reduced, Lp(a) itself is modestly reduced, other abnormalities like high triglycerides (that facilitate Lp(a)'s adverse effects) are corrected. Small LDL particles are, by the way, part of the genetic "package" of Lp(a) in most carriers.

Peter also has another gene for Apo E4, another genetically-determined pattern shared by 19% of Americans. (Another 2% of Americans have two "doses" of Apo E4, i.e., they are homozygotes for E4.) This means that the Apo E protein, normally responsible for liver uptake and disposal of lipoproteins (especially VLDL), is defective. In people with Apo E4, the higher the fat intake, the more LDL particles accumulate. (The explanation for this effect is not entirely clear, but it may represent excessive defective Apo E-enriched VLDL that competes with LDL for liver uptake.) People with Apo E4 therefore drop LDL (and LDL particle number and apoprotein B) with reductions in fat intake.

This is a genetic rock-and-a-hard-place, or what I call a genetic incompatibility. If Peter increases fat and reduces carbohydrates to reduce Lp(a)/small LDL, then LDL measures like LDL particle number, apoprotein B, and LDL cholesterol will increase. Paradoxically, sometimes small LDL particles will even increase in some genetically predisposed people.

If Peter decreases fat and increases carbohydrates, LDL particle number, apoprotein B, and LDL cholesterol will decrease, but the proportion of small LDL will increase and Lp(a) may increase.

Thankfully, such "genetic incompatibilities" are uncommon. In my large practice, for instance, I have about 5 such people.

The message: If you witness paradoxic responses that don't make sense or follow the usual pattern, e.g., reductions in LDL particle number, apoprotein B, and small LDL with reductions in their dietary triggers (i.e., carbohydrates, especially wheat), then consider a competing genetic trait such as Apo E4.

The folly of an RDA for vitamin D

Tom is a 50-year old, 198-lb white male. At the start, his 25-hydroxy vitamin D level was 28.8 ng/ml in July. Tom supplements vitamin D, 2000 units per day, in gelcap form. Six months later in January (winter), Tom's 25-hydroxy vitamin D level: 67.4 ng/ml.

Jerry is another 50-year old white male with similar build and weight. Jerry's starting summer 25-hydroxy vitamin D level: 26.4 ng/ml. Jerry takes 12,000 units vitamin D per day, also in gelcap form. In winter, six months later, Jerry's 25-hydroxy vitamin D level: 63.2 ng/ml.

Two men, similar builds, similar body weight, both Caucasian, similar starting levels of 25-hydroxy vitamin D. Yet they have markedly different needs for vitamin D dose to achieve a similar level of 25-hydroxy vitamin D. Why?

It's unlikely to be due to variation in vitamin D supplement preparations, since I monitor vitamin D levels at least every 6 months and, even with changes in preparations, dose needs remain fairly constant.

The differences in this situation are likely genetically-determined. To my knowledge, however, the precise means by which genetic variation accounts for it has not been worked out.

This highlights the folly of specifying a one-size-fits-all Recommended Daily Allowance (RDA) for vitamin D. The variation in need can be incredible. While needs are partly determined by body size and proportion body fat (the bigger you are, the more you need), I've also seen 105 lb women require 14,000 units and 320-lb men require 1000 units to achieve the same level of 25-hydroxy vitamin D.

An RDA for everyone? Ridiculous. Vitamin D is an individual issue that must be addressed on a person-by-person basis.

Heart scan: Standard of care?

If coronary disease is easy to detect by measuring coronary calcium, shouldn't this represent the standard of care?

In other words, if you've been seeing your doctor and he/she has been monitoring cholesterol levels and, inevitably, talks about statin drugs, then you have a heart attack, unstable angina, or die--yet never knew you had heart disease--isn't this negligence?

Coronary calcium, and thereby coronary atherosclerotic plaque, are markers for the disease itself. Unlike cholesterol, high blood pressure, etc., that represent risk factors for coronary atherosclerotic plaque, coronary calcium is a measure of total plaque: "soft" elements like lipid collections, necrotic tissue, fibrous tissue, as well as "hard" elements like calcium. Because calcium occupies 20% of total atherosclerotic plaque volume, it can be used as an indirect "dipstick" for total plaque.

So why isn't an unexpected heart attack, hospitalization for unstable heart symptions, emergency bypass, etc., not regarded as potential malpractice? These are not benign events, but potentially life-threatening.

The costs of doing drug business?

Here's a telling situation.

Liz had been on prescription niacin, Niaspan, 1500 mg per day (3 x 500 mg tablets) for several years to treat her severe small LDL pattern and familial hypertriglyceridemia (triglycerides 500-1000 mg/dl). Because her health insurance had been paying for the "drug," she insisted on taking the prescription form.

A change in insurance, however, meant that the Niaspan was no longer covered. Her pharmacy wanted to charge $227 per month.

Liz came to the office in tears, worried that she was going to have to choke up $227 per month. I reminded her that, as I had told her several years ago, she could easily replace the Niaspan with over-the-counter Sloniacin or Enduracin. Both release niacin over approximately 6 hours, just like Niaspan.

Here are the prices I've seen with Sloniacin, 100 tablets of 500 mg:

Walgreens: $15.99
Walmart: $12.99
Costco: $8.99

So the most expensive source, Walgreens, would cost Liz just under $15.99 per month to take 1500 mg per day.

$15.99 versus $227.00 per month for preparations that are highly similar. Hmmmmmm.

I wonder what the $211.01 extra per month goes towards? Admittedly, Abbott Labs, the current company selling Niaspan (after Abbott acquired Kos), has invested in a few clinical trials, such as ARBITER-HALTS6. But does supporting research justify this much difference, a difference that amounts to $2532 over a year? If just 100,000 patients are prescribed Niaspan at this dose (a typical dose), this generates $253 million.

Is the cost of developing and marketing a supplement-turned-drug that great? Is this justifiable? Is it any wonder that our health insurance premiums continue to balloon?

I use Sloniacin and Enduracin almost exclusively.

Measurement

A crucial component of self-empowerment in healthcare is to be able to measure various health parameters. More and more measurement tools are entering the direct-to-consumer arena.

Quantification of various phenomena is important in managing many aspects of health. Imagine a carpenter trying to build a house without the use of a tape measure, level, or other measuring tools. In health, as in building a house, measurement, adjustment, and correction are critical.

Among the most helpful health measurement tools:

Blood glucose meters--Blood glucose meters aren't just for diabetics. They are among the most powerful weight loss tools available.

Blood pressure cuffs--There's no better way to assess blood pressure than to assess it under all the varied conditions of life: When you're tired, when you're excited, when you're upset, when you're happy, hungry, stomach full, morning, night. This is a lot better than the one isolated measure in the doctor's office.

Digital thermometers--Your first a.m. oral temperature is a great way to assess thyroid status. We aim to maintain first a.m. oral temperature around 97.3 degrees F, the normal human temperature upon arising that reflects normal thyroid function. (No, Dr. Broda Barnes fans, axillary temperatures should NOT be used due to flagrant variation from right armpit to left armpit, modifying effects of clothing and ambient temperature, etc. Oral temperature tracks internal, "core," temperature fluctuations reliably, including circadian variation, far better than axillary temperatures.)

Fingerstick blood tests--An incredible number of blood tests are now available just by performing a simple fingerstick in your kitchen or bathroom. You can get 25-hydroxy vitamin D, lipids, thyroid measures (TSH, free T3, free T4), hormones (DHEA, testosterone, estrogens). And the list is growing rapidly. Salivary tests are also growing in number for many of the same measures.

A variation on fingerstick blood tests are devices like CardioChek that allow you to do a fingerstick, but also run the test on your own device at home. (The CardioChek device tests total cholesterol, triglycerides, and HDL.)

Urine pH--You can dipstick your own urine to assess the relative acidity or alkalinity of your lifestyle. Acid pH (7 or below) suggests that diet is weighed too heavily in favor of animal products and grains. An alkaline pH (above 7) suggests plentiful vegetables and fruits, not counteracted by animal products and grains.

There are many more, including the ZEO device to monitor sleep quality, RESPeRATE for reduction of blood pressure, HeartMath to manage stress and augment the parasympathatic (relaxation) response. We've come a long way compared to the health monitoring devices of just 25-30 years ago.

Anyway, that's a partial list. Given the rapid advances in technology that allow such home tests, I anticipate a much longer list in the coming few years.

For some perspective on how far these devices have come, here's a great graphic of an early sphygmomanometer, or blood pressure gauge.


Courtesy Wellcome Library, London

I lost 37 lbs with a fingerstick

Jack needed to lose weight.

At 5 ft 7 inches, he weighed in at 273 lbs, putting his BMI at a sobering 42.8. (A BMI of 30 or above is classified as "obese.") In addition to lipoprotein(a), Jack had an extravagant quantity of small LDL (the evil "partner" of lipoprotein(a)), high triglycerides, and blood sugars in the diabetic range. With a heart scan score of 1670, Jack had little room for compromises.

Try as he might, Jack could simply not stick to the diet I urged him to follow. Three days, for instance, of avoiding wheat was promptly interrupted by his wife's tempting him with a nice BLT sandwich. This triggered his appetite, with diet spiraling downward in short order.

So I taught Jack how to check his blood sugars using a fingerstick device, what I call the most important weight loss tool available. I asked Jack to check his pre-meal blood glucose and his one-hour after-meal blood glucose and not allow the after-meal blood glucose to rise any higher than the pre-meal. For example, if blood glucose pre-meal was 115 mg/dl, after-meal blood glucose should be no higher than 115 mg/dl.

If any food or combination of foods increase blood glucose more than the pre-meal value, then eliminate the culprit food or reduce the portion size. For example, if dinner consists of baked salmon, asparagus, and mashed potatoes, and pre-meal blood glucose is 115 mg/dl, post-meal 155 mg/dl, reduce or eliminate the mashed potatoes. If slow-cooked, stone ground oatmeal causes blood glucose to increase from 115 mg/dl to 185 mg/dl (a typical response to oatmeal), then eliminate it.

Having immediate feedback on the effects of various foods finally did it for Jack: It identified foods that were triggering excessive blood sugar rises (and thereby insulin) and foods that did not.

What Jack did not do is limit or restrict calories. In fact, I asked him to eat portion sizes that left him comfortable. There was no need to reduce calories, push the plate away, etc. Just don't allow blood sugars to rise.

Six months later, Jack came back 37 lbs lighter. And he got there without calorie-counting, without regulating portion sizes, without hunger.

The two kinds of small LDL

You won't find this in any publication nor description (at least ones that I've come across) about the ubiquitous small LDL particles. It's an observation I've made having obtained thousands of advanced lipoprotein panels of the sort that break lipoproteins down by size. I've discussed this issue previously here. But small LDL is so ubiquitous, not addressed by conventional strategies like statin drugs or fat restriction (it is made worse, in fact, by reducing fat in the diet), that it is worth keeping at the top of everyone's consciousness.

(Because most of the lipoprotein analyses performed in my office are done via NMR, I will discuss in terms relevant to NMR. This does not necessarily mean that similar observations cannot be made with centrifugation, i.e, VAP from Atherotech, or gel electropheresis from Berkeley, Boston Heart Lab, Spectracell, and others).

There are two basic varieties of small LDL particles:

1) Genetically-programmed--e.g., via cholesteryl-ester transfer protein (CETP) activity
2) Acquired--via carbohydrate consumption


It means that people with acquired small LDL from carbohydrate consumption can reduce small LDL to zero with reduction of carbohydrates, especially the most small LDL-provoking foods of all: wheat, cornstarch, and sucrose.

It also means that people who have small LDL for genetically-determined reasons can only minimize, not eliminate, small LDL. By NMR, we struggle to keep small LDL in the 300-600 nmol/L range when genetically-determined. (People typically start with 1400-3000 nmol/L small LDL particles prior to diet changes and other efforts.) We can only presumptively identify genetically-determined small LDL when all the appropriate efforts have been made, including reduction in weight to ideal, yet small LDL persists.

Here is where we need better tools: when you've done everything possible, yet small LDL persists.

While we break LDL particles (NOT LDL cholesterol, the crude and misleading way of viewing atherosclerosis causation) down by size, it's really about all the undesirable characteristics that accompany small size:

--Distortion of Apo B conformation--i.e., the primary protein that directs LDL particle fate is distorted, making it less likely to be cleared by the liver but more likely to be taken up by inflammatory (macrophages) in the artery wall, creating plaque. It means that small LDL particles linger for a longer time than larger particles.

--Small LDLs are more oxidation-prone. Oxidized LDL are more avidly taken up by inflammatory macrophages.

--Small LDLs are more glycation-prone.

--Small LDLs are more adherent to structural tissues, e.g., glycosaminoglycans, that reside in the artery wall.

You and I cannot measure such phenomena, so we resort to distinguishing LDL particles by size.

The drug industry believes it may have a solution to small LDL in the form of CETP-inhibiting drugs, like anacetrapib. In the way of nutritional solutions beyond carbohydrate reduction, weight loss/exercise, niacin, vitamin D normalization, and omega-3 fatty acid supplementation, there are exciting but very preliminary data surrounding the possibility that anthocyanins may inhibit CETP activity. Having toyed with this concept for the past 6 months, I remain uncertain how meaningful the effect truly is, but it is harmless, since we obtain anthocyanins from foods colored purple or purplish, such as blackberries, blueberries, cherries, red leaf lettuce, red cabbage, etc.

I welcome any unique observations on this issue.