Excessive Heart Procedures Makes New York Times Headline


One example of flagrant cardiac procedure excess has made New York Times headlines:


Heart Procedure Is Off the Charts in an Ohio City
The number of angioplasties performed in Elyria is so high that Medicare is starting to ask questions.

(The full article can be accessed through the New York Times website at http://www.nytimes.com/2006/08/18/business/18stent.html?pagewanted=2&ei=5094&en=b81be5f43f98a99b&hp&ex=1155960000&partner=homepage)



Cardiologists in little Elyria, Ohio, about a 30-minute drive west of Cleveland, do more coronary angioplasties and insert more stents than any other location in the U.S.--four times more than the national average, three times more than the Cleveland average. They perform even more than the recently-indicted cardiologist in Louisiana, who performed twice the national average of procedures.


The Times article, part of a series about financial incentives in medical care, provides a responsible and incredibly balanced report on the situation in Elyria. I have to give them credit, because from the eyes of a colleague (myself), this looks like blatant and extreme profiteering: "cathing for dollars".

I find it outrageous that this group of cardiologists claims that they have some special insight into heart care that justifies this extraordinary reliance on heart procedures. There's bound to be variation in practice patterns, but this is so outside the norm that I believe criminal behavior will be exposed. In fact, I believe that even the "norm", or average, rate of procedures is also excessive.

This is symptomatic of the perverse equation in heart disease care. If there's money to be made in major heart procedures, who wants to bother with prevention? Programs like the Track Your Plaque program present real potential to stop coronary heart disease in its tracks for many, if not most, participants--but don't expect to hear about it from your cardiologist. Don't expect to hear about it from the increasingly hospital-employed primary care physician.

Hopefully, media exposure like that in the New York Times is just the beginning of a public re-analysis of not only what's wrong with medicine today, but recognition of the tremendous power in preventive strategies when everyone stops being so enamored with hospital-based procedures. CT-based heart scanning that ignites your heart disease prevention program is your way to dodge the mainstream obsession with procedures.

More on "Bio-identical hormones" and Wyeth Pharmaceuticals

In October 2005, Wyeth petitioned the FDA, requesting that it completely ban the bioidentical alternatives that women have been using in ever-increasing numbers to achieve optimal hormone balance. With bioidentical replacement therapy clearly reducing its market share, Wyeth asked the FDA to outlaw all compounded bioidentical hormone formulations that compete with its own discredited drugs. If Wyeth is successful, then menopausal women will have no choice other than to take potentially life-threatening hormone drugs or to forgo hormone replacement therapy altogether, thus enduring the physically and emotionally debilitating effects of menopause-induced hormone depletion.

Dave Tuttle
Life Extension Magazine
August, 2006



For more commentary on Wyeth Pharmaceutical's outrageous and brazen petition to the FDA to bar prescription "bio-identical" hormones, i.e., hormones that are identical to natural human forms, read Life Extension's article, Health Freedom Under Attack!
Drugmaker Seeks to Deny Access to Bioidentical Hormones





This well-researched article is in the August, 2006 issue of Life Extension Magazine. The article can also be accessed online at http://www.lef.org/magazine/mag2006/aug2006_cover_attack_01.htm

or go to www.lef.org and click on the August, 2006 issue.

The author, Dave Tuttle, details the baseless arguments raised by Wyeth, a pathetic and amazingly selfish act in the name of protecting profits for Premarin, their prescription agent. It's bad enough to be selling this worthless drug. It's even worse--criminal, in my mind--to try to stamp out our right to have a physician write a prescription for a pharmacy to mix up hormones identical to that humans produce, individualized to our needs.

If you are as angry about this as I am, please go to the Life Extension online reprint that provides access to the International Academy of Compounding Pharmacists website to send the FDA an e-mail describing your opinion, or go to www.iacprx.org.

How accurate is LDL cholesterol?

Watch TV and you'd get the impression that the world revolves around LDL cholesterol: Commercials for Lipitor, Zetia, Vytorin, etc., all drugs to reduce cholesterol (total and LDL). Your doctor looks first and often only at LDL cholesterol.

If there's so much attention paid to LDL, how accurate is it? 100%? 90%? 80%?

Well, it varies widely. Occasionally, it's truly accurate, but most of the time it's miserably inaccurate . Every single day, I see people with LDL cholesterols that underestimates true (measured) LDL by 40%, 50%, and even over 100%. In other words, LDL cholesterol might be 120 mg/dl by the conventional method, but the genuine measured value might be 160 mg/dl, or even 240 mg/dl. It can be that far off--and it's not rare.

The converse can occasionally be true, though rarely in my experience: that conventional LDL overestimates true LDL. I saw someone in the office today like this, with a conventional LDL of 142 mg/dl but a true measured LDL of 115 mg/dl. I may see one or two more people like this the rest of this year.




Why is LDL so inaccurate? Several reasons:

--LDL in most labs is calculated, not measured. The "Friedewald calculation" derives LDL by substracting HDL and triglycerides (divided by 5) from total cholesterol. The higher triglycerides are, especially above 150 mg/dl, the more inaccurate the calculation becomes. As HDL drops below 50 mg/dl, this also introduces greater and greater inaccuracy.

--LDL particles vary in size. A more accurate representation and measure of LDL's dangers are therefore found in measures of LDL particle number , rather than a weight-based measure or calculation. LDL particle number can be measure as just that, LDL particle number (NMR), or as apoprotein B, the protein in LDL that occurs one apoB per LDL.

I liken conventionally calculated LDL cholesterol to a broken speedometer. You simply won't have an accurate measure of how fast you're going, though you may have a ballpark sense. But try telling that to the state patrol.

Or, as a cardiologist colleague said to me in a similar conversation about LDL: "Well, it's better than nothing!"

The lesson: If you're interested in plaque control, and control or reduction of heart scan score, you need a measured LDL, preferably LDL particle number by NMR or an apoprotein B. Another option is "direct" LDL.

Green tea: friend or faux?

The www.HealthCastle.com website is a helpful website on healthy eating that sends out a free newsletter. The content is all produced by licensed dietitions and nutritionists. Although I don't agree with everything said on the site, there's still some good information.

I'm a fan of green tea. Although I believe the effects are relatively modest (weight reduction, cholesterol reduction, anti-oxidation, etc., with theaflavin and/or green tea as a beverage,) they alerted me to the fact that the Lipton Green Tea product is one you should steer clear of. Here are their comments:



"More like Soft drink than Green Tea!With 200 calories, 13 teaspoons of added sugar and a long list of artificial ingredients, Lipton Iced Green Tea is more like a bottle of soft drink than tea, in our opinion."


The Lipton website lists the ingredients:

Water, high fructose corn syrup, citric acid, green tea, sodium hexametaphosphate, ascorbic acid (to protect flavor), honey, natural flavors, phosphoric acid, sodium benzoate (preserves freshness), potassium sorbate (preserves freshness), calcium disodium edta (to protect flavor), caramel color, tallow 5, blue1.

An 8 oz serving yields 21 grams of sugar. If you drink the full 20 oz. bottle (not hard to do!), that yields 52.5 grams of sugar! You will also notice that the second ingredient listed after water is high fructose corn syrup. This ingredient, you may recall, causes triglycerides to skyrocket, causes an insatiable sweet tooth, and is a probable contributor to obesity and diabetes.

In their defense, the Lipton people do also offer a sugar-free alternative without the excessive sweeteners and empty calories.

Do the Lipton products offer the same kind of benefits from green tea catechins (flavonoids) offered by freshly brewed teas? This product has not been formally tested by an independent lab to my knowledge, though, in general, commercially prepared and bottled teas tend to have dramatically less catechin/flavonoid content compared to brewed. (The USDA website provides access to an extraordinary collection of flavonoid food content at their USDA Database for the Flavonoid Content of Selected Foods - 2003. You'll find it at http://www.ars.usda.gov/Services/docs.htm?docid=6231.)

I think the HealthCastle people got it right: Brew your own, making sure to steep for at least 3 minutes. Alternatively, a green tea or theaflavin supplement provides many of the benefits. (Theaflavin has been used in trials at doses of 375 to 900 mg per day.) An in-depth report on green tea will be coming in a future Special Report on the www.cureality.com Membership website.

The Track Your Plaque guide to getting grotesquely overweight

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

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

2) Cut your morning calorie intake by skipping breakfast.

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

4) Call walking your dog "exercise".

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

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

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

8) Eat to provide comfort when stressed.

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

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

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

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

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

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

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

Your heart scan is just a "false positive"

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

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

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

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

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

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

What's better than a heart scan?


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

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

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

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

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

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

Lipids are snapshots in time; heart scans are cumulative

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

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

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

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

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

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

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

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

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

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

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

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

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





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

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

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

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

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


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

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

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

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

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

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

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

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

What role DHEA?




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

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

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



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

For instance, DHEA can:

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

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

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



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

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

Diet by LDL

Conventional notions of heart healthy diets, such as that advocated by the American Heart Association, are largely based on observations of total and LDL cholesterol.

So, cut the saturated fat in the diet, cut the overall fat content, and replace them with polyunsaturated oils like safflower, corn, and vegetable oils and increase consumption of whole grains and total and LDL cholesterol show a modest downturn. Thus, diets like the American Heart Association Total Lifestyle Change approach advocate limiting total fat to no more 25 to 35% of calories and saturated fat to no more than 7% of calories.

Orange Cream Cookies

If you loved Creamsicles as a kid, you'll love these Orange Cream Cookies. (Sorry, no photo: We ate them up before I realized we hadn't taken the photo. And, worse, we did it twice!)

Ingredients:
2 cups almond meal
2 tablespoons coconut flour
1 teaspoon baking soda
½ teaspoon sea salt
¼ cup golden raisins
½ cup chopped pecans
Sweetener equivalent to 1 cup sugar
2 tablespoons finely-grated orange rind
1 large egg
2 tablespoons coconut oil, melted
½ cup whipping cream (or coconut milk)
1 tablespoon vanilla extract

Preheat oven to 350º F.

Combine almond meal, coconut flour, baking soda, salt, raisins, pecans, sweetener and orange zest in bowl and mix.

In separate bowl, whisk egg, then add coconut oil, whipping cream, vanilla extract and mix together. Pour wet mix into dry and blend by hand thoroughly.

Spoon onto parchment paper-lined baking pan (or oiled pan) and flatten with spoon to ½-¾ inch thickness. Bake for 20-25 minutes or until toothpick withdraws dry.

Why are heart attacks still happening?

I'm a cardiologist. I see patients with heart disease in the form of coronary artery disease every day.

These are people who have undergone bypass surgery, received one or more stents or undergone other forms of angioplasty, have survived heart attacks or sudden cardiac death, or have high heart scan scores. In short, I see patients every day who are at high-risk for heart attack and death from heart disease.

But I see virtually no heart attacks. And nobody is dying from heart disease. (I'm referring to the people who follow the strategies I advocate, not the guy who thinks that smoking a pack of cigarettes a day is still okay, or the woman who thinks the diet is unnecessary because she's slender.)

Two high-profile deaths from heart attacks occurred this week:

Davy Jones--The iconic singer from the 1960s pop group, the Monkees, suffered sudden cardiac death after a large heart attack, just hours after experiencing chest pain.

Andrew Breitbart--The conservative blogger and controversy-generating media personality suffered what was believed to be sudden cardiac death while walking.

It's a darn shame and it shouldn't happen. The tools to identify the potential for heart attack are available, inexpensive, and simple. The strategies to reduce, even eliminate, risk are likewise available, inexpensive, and cultivate overall health.

The followers of the Track Your Plaque program who

1) get a heart scan that yields a coronary calcium score (for long-term tracking purposes)
2) identify the causes such as small LDL particles, lipoprotein(a), vitamin D deficiency, and thyroid dysfunction
3) correct the causes

enjoy virtual elimination of risk.

My letter to the Wall Street Journal: It's NOT just about gluten

The Wall Street Journal carried this report of a new proposed classification of the various forms of gluten sensitivity: New Guide to Who Really Shouldn't Eat Gluten

This represents progress. Progress in understanding of wheat-related illnesses, as well as progress in spreading the word that there is a lot more to wheat-intolerance than celiac disease. But, as I mention in the letter, it falls desperately short on several crucial issues.

Ms. Beck--

Thank you for writing the wonderful article on gluten sensitivity.

I'd like to bring several issues to your attention, as they are often neglected
in discussions of "gluten sensitivity":

1) The gliadin protein of wheat has been modified by geneticists through their
work to increase yield. This work, performed mostly in the 1970s, yielded a form
of gliadin that is several amino acids different, but increased the
appetite-stimulating properties of wheat. Modern wheat, a high-yield, semi-dwarf
strain (not the 4 1/2-foot tall "amber waves of grain" everyone thinks of) is
now, in effect, an appetite-stimulant that increases calorie intake 400 calories
per day. This form of gliadin is also the likely explanation for the surge in
behavioral struggles in children with autism and ADHD.
2) The amylopectin A of wheat is the underlying explanation for why two slices
of whole wheat bread raise blood sugar higher than 6 teaspoons of table sugar or
many candy bars. It is unique and highly digestible by the enzyme amylase.
Incredibly, the high glycemic index of whole wheat is simply ignored, despite
being listed at the top of all tables of glycemic index.
3) The lectins of wheat may underlie the increase in multiple autoimmune and
inflammatory diseases in Americans, especially rheumatoid arthritis and
inflammatory bowel diseases (ulcerative colitis, Crohn's).

In other words, if someone is not gluten-sensitive, they may still remain
sensitive to the many non-gluten aspects of modern high-yield semi-dwarf wheat,
such as appetite-stimulation and mental "fog," joint pains in the hands, leg
edema, or the many rashes and skin disorders. This represents one of the most
important examples of the widespread unintended effects of modern agricultural
genetics and agribusiness.

William Davis, MD
Author: Wheat Belly: Lose the wheat, lose the weight and find your path back to health

60-year old man dies of high cholesterol

Never saw a headline like this? Neither have I. That's because it doesn't happen.

Cholesterol doesn't harm, maim, or kill. It is simply used as a crude--very crude--marker. It is, in reality, a component of the body, of the cell wall, of lipoproteins (lipid-carrying proteins) in the bloodstream. It is used a an indirect gauge, a "dipstick," for lipoproteins in the blood to those who don't understand how to identify, characterize, and quantify actual lipoproteins in the blood.

Cholesterol itself never killed anybody, any more than a bad paint job on your car could cause a fatal car accident.

What kills people is rupture of atherosclerotic plaque in the coronary arteries. For all practical purposes, you must have atherosclerotic plaque in order for it to rupture (much like a volcano erupts and spews lava). It's not about cholesterol; it's about atherosclerotic plaque. Plaque might contain cholesterol, but cholesterol is not the thing itself that causes heart attack and death.

So why do most people obsess about cholesterol? Good question. It is, at best, a statistical marker for the possibility of having atherosclerotic plaque that ruptures. High cholesterol = higher risk for heart attack, low cholesterol = lower risk for heart attack. But the association is weak and flawed, such that people with high cholesterol can live a lifetime without heart attack, people with low cholesterol can die at age 43.The same holds true for LDL cholesterol, you know, the calculated value based on flawed assumptions about LDL's relationship to total cholesterol, HDL cholesterol, and VLDL cholesterol.

A crucial oversight in the world of cholesterol: There are many other factors that cause atherosclerotic plaque and its rupture, such as inflammatory phenomena, calcium deposition, artery spasm, hemorrhage within the plaque itself, degradative enzymes, etc., none of which are suggested by cholesterol measures.

But one observation has held up, time and again, over the past 40 years of observations on coronary disease: The greater the quantity of coronary atherosclerotic plaque, the greater the risk of atherosclerotic plaque rupture. An increasing burden of atherosclerotic plaque along the limited confines of coronary arteries, just a few millimeters in diameter and a few centimeters in length, is like a house of cards: It's bound to topple sooner or later, and the bigger it gets, the less stable it becomes.

If you are concerned about future potential for heart disease and heart attack, don't get a cholesterol panel. Get a measure of coronary atherosclerotic plaque.

Back to basics: Coronary calcium

After having my attentions pulled a thousand different directions these past 6 months, with the release of Wheat Belly and all the wonderful media attention it has attracted, I've decided to pick up here with a series of discussions about the fundamental issues important to the Track Your Plaque program and prevention and reversal of coronary atherosclerotic plaque.

I fear the discussions at times have drifted off into the exotic. This is great because this is how we learn new lessons, but we can never lose sight of the basics, else we risk losing control over this disease.

Imagine you've got a beautiful new car. You wax it, gap the spark plugs, rotate the tires, etc. and it looks brand-new, just like it came off the dealer's lot. 50,000 miles pass, however, and you realize you've forgotten to change the oil. Ooops! In other words, no matter how meticulous the attention to transmission, tires, and paint job, neglect of the most basic responsibility can ruin the whole thing. We can't let that happen with heart health.

If we propose to reverse coronary atherosclerotic plaque, we've got to have something to measure. First, it tells us whether we have atherosclerotic plaque in the first place, the stuff that accumulates and blocks flow and causes anginal chest pains, and ruptures like a little volcano and causes heart attacks. Second, it gives us something to track over the years to know whether plaque has grown, stopped growing, or been reduced. Without such a measure, you will be driving without a speedometer or odometer, just guessing whether or not you've gotten to your destination.

Of course, the conventional approach to heart disease and heart attack is not to track atherosclerotic plaque in your coronary arteries, but to track some distant "risk factor" for atherosclerotic plaque, especially LDL cholesterol. But LDL cholesterol is flawed at several levels. First, it is calculated, not measured. The nearly 50-year old Friedewald equation used to calculate LDL cholesterol is based on several flawed assumptions, yielding a value that can be 20, 30, or 50% inaccurate as a rule, only occasionally generating a value close to the real value. (No point in publicizing this problem, of course: Why compromise a $27 billion annual cash cow?) It also ignores the effect of diet. (No, cutting fat does not reduce LDL for real, only the calculated value. Cutting carbohydrates, especially wheat--"healthy whole grains"--slashes measured LDL values like NMR LDL particle number and apoprotein B.)

But all risk factors are, at best, snapshots of the situation at that moment in time. They change from day to day, week to week, month to month, year to year. If you do something dramatic in health, like lose 50 pounds, you can substantially change your risk factors values, like LDL cholesterol and HDL cholesterol. But you may not modify the amount of atherosclerotic plaque in your heart's arteries.

Measuring the amount of atherosclerotic plaque in your heart's arteries is, in effect, a cumulative expression of the effects of risk factors up until the moment of measurement.

There are several stumbling blocks, however, in the concept of measuring coronary atherosclerotic plaque. We cannot measure all the unique components of plaque, such as fibrous tissue like collagen, or degradative enzymes like collagenases, or inflammatory proteins like matrix metalloproteinase, or the debris of hemorrhage and inflammation. We struggle to contemporaneously mix in measures of bloodborne inflammation, coagulation and viscosity, and physiological phenomena of the artery itself, like endothelial dysfunction, medial (muscle) tone, and adventitial fat.

So we are left with semi-static measures of total coronary atherosclerotic plaque like coronary calcium, obtainable via CT heart scans as a calcium "score." No, it is not perfect. It does not reflect that moment's blood viscosity, it does not reflect the inflammatory status of the one nasty plaque in the mid-left anterior descending, nor does it reflect the irritating sheer effects of a blood pressure of 150/95.

But it's the best we've got.

If anyone has something better, I invite you to speak up. Carotid ultrasound, c-reactive protein, ankle-brachial index, stress nuclear studies, myoglobin, skin cholesterol, KIF6 genotype . . . none of them approach the value, the insight, the trackability of actually measuring coronary atherosclerotic plaque. And the only method we've got to gauge coronary atherosclerotic plaque that is non-invasive and available in 2012? Yup, a good old CT heart scan calcium score.

Myocardial infraction

I've seen a few heart attacks this past year . . . but none in the people who follow this program.

I saw a heart attack in a priest, a wonderful man who was unable to say "no" to his parishioners who insisted on bringing pies, cakes, and cookies every day.

I saw an impending heart attack in a 74-year old man, a football coach who thought the whole wheat-free, low-carb thing was some wacko trend. Four stents later, he's changed his mind.

A 69-year old woman had to be hospitalized for heart failure due to partial closure of an artery. She repeatedly told me that she simply could not follow the diet because it was "too restrictive."

There were a few others. Interestingly, all felt they were eating healthy, minimizing junk foods and avoiding fatty foods. None were wheat-free nor restricted carbohydrates.

In other words, in the people who follow the basic advice of the Track Your Plaque program to do such simple things as eliminate wheat, don't indulge in junk carbohydrates, normalize vitamin D status, supplement omega-3 fatty acids, supplement iodine and correct any thyroid dysfunction . . . well, they have no heart attacks.

Diet is superior to drugs

Might-o’chondri-AL left this wonderful record of his lipoprotein experience in the comments to the last Heart Scan Blog post. It is a great example of what is achievable with diet and a few supplements . . . without drugs.


(A) Jan. 2011 1st ever NMR lipo-protein analysis was done after 4 months of consistent home food prep of pretty low fat (only olive oil and 1 tablespoon coconut oil daily) but plenty of whole wheat and half potatoes:
* LDL # of particles (P) = 1,676 in nmol/L————being a LDL cholesterol (C) reading of 139 mg/dL
* small LDL # P = 1,021 nmol/L —————yikes! you advise smLDL be less than 117 nmol/L
* HDL # of particles = 28.8 umol/L ————–being a HDL C reading of 45 mg/dL
* Triglycerides = 90 mg/dL ————– true, I never struggled with my weight

(B) May 2011 2nd NMR after another 4 months but added in more fat (1 teaspoon highly concentrated fish oil daily, 90% chocolate, handfulls of nuts, more olive oil and kept coconut oil at 1 tablespoon daily for a controlled experiment), added 500 mg Niacin 3 times a day (in stages up to1,500 mg. total daily), 6000 IU daily vitamin D, deliberately cut out all grains except for social politeness and substituted in daily Koji fermented brown rice (rustic Amazake):
** LDL # P……………= 976 nmol/L ——————————– being LDL C of 100 mg/dL
** small LDL # P …. = 96 nmol/L ——————————– nice surprise
** HDL # P ………… = 27.3 umol/L ——————————being an increase to HDL C of 64 mg/dL
** Triglycerides …… = 42 mg/dL ——————————– despite daily carbs over 150 gr. daily

(C) Dec. 2011 3rd NMR after another 7 more months thinking Doc’s advice is worthwhile I added in yet more fat (mainly daily 2 tablespoons of coconut oil, more 90% chocolate), bumped Niacin up to 1,000 mg twice a day (2,000 mg. total daily), cut out the Amazake, kept up the vitamin D adding daily vitamin K & daily ate main mid-day meal out as lunch on spicy Thai & Chinese fish/shrimp/soup/rice meals (my next control):
*** LDL # P ………. = 764 nmol/L ————— being LDL C of 107 mg/dL ( 2x coconut’s saturated fat)
***small LDL # P… = less than 90 nmol/L ——–surprised me NMR can’t count lower
***HDL # P ……… = 41.4 umol/L ——————– being an increase to HDL C of 88 mg/dL
*** Triglycerides ….= 43 mg/dL ——————- daily carbs below ~ 120 gr. & lost too much weight

Isn't that great? Spectacular job, Might!

MIght achieved values that are superior to that achievable with, say, a high-dose statin strategy. Statins only reduce total LDL particles, reducing small LDL in a non-selective way. And, of course, this diet does not cause muscle aches, memory loss, nor liver problems.

Something to consider: As the diet has become so effective, we can reduce our reliance on niacin. In fact, the benefits of niacin diminish substantially, as small LDL is reduced, HDL increased, triglycerides decreased, and postprandial lipoproteins subdued with the diet only.

Low-carb is heart healthy

Anybody following the discussions in these pages know that: Limiting carbohydrate intake reduces risk for coronary heart disease and heart attack.

First of all, why do conventional diets advocate restricting saturated and total fat? From the standpoint of surrogate markers of cardiovascular risk, cutting saturated and total fat reduces total cholesterol; reduces calculated LDL cholesterol; and may reduce c-reactive protein modestly (an index of inflammation). It also increases blood sugar and HbA1c (reflecting the prior 60 days blood sugars), increases glycation of the proteins of the body leading to cataracts, arthritis, and hypertension.

Problem: Total cholesterol is a combination of HDL cholesterol, an estimate of VLDL cholesterol (triglycerides), and LDL cholesterol. It is a composite of both "good" things (HDL) and "bad" things (LDL and VLDL). Cutting saturated and total fat results in reduced HDL, increased VLDL/triglycerides, and a reduction in calculated LDL. Pretty weak stuff. The last item, i.e., reduction in calculated LDL, is not even a real phenomenon. In fact, the net effect in most genotypes (genetic types) may be negative: increased heart disease risk.

In contrast, what is the effect of reducing carbohydrate without restricting fat? (In the approach I use, we start with elimination of the most destructive of carbohydrates, wheat, followed by reducing exposure to other carbohydrates, especially cornstarch and corn products, sugar, and oats.) If, say, we cut carbohydrate intake into the range of a truly low-carbohydrate diet of 10-15 grams per meal ("net" carbs, or total carbohydrates minus fiber), then we witness a number of metabolic transformations:

Reduced fasting triglycerides and VLDL
Reduced postprandial (after-eating) triglycerides, chylomicrons, and chylomicron remnants
Increased HDL and shift towards large HDL particles (presumably more protective)
Reduced small LDL particles
Reduced glycation and oxidation of small LDL particles
Reduced hemoglobin A1c
Reduced c-reactive protein and other inflammatory markers
Reduced blood pressure

By slashing carbohydrates, we also witness weight loss from visceral fat, reversal of pre-diabetes and diabetes, and reduced phenomena of glycation. And, if the wheat-free part of low-carb is maintained, you can also see marked improvement in gastrointestinal health, relief from joint pains, relief from leg edema, relief from migraine headaches, improved behavior and ability to concentrate in children with impaired learning, ADHD, and autism, better mood, deeper sleep. You will see multiple inflammatory and autoimmune diseases improve or completely relieved, such as rheumatoid arthritis and ulcerative colitis.

Having personally gone down the diabetic path and back by cutting the fat in my diet, now maintaining a HbA1c of 4.8% with fasting glucose 84 mg/d; (without medications), there should be no remaining doubt: Low-carb diets, especially if wheat-free, dramatically reduce the factors leading to heart disease; low-fat diets worsen the factors leading to heart disease.

Mocha Walnut Brownies

Richer than a cookie, heavier than a muffin, brownies are ordinarily an indulgence that leaves you ashamed of your lack of restraint. Have one . .  . or two or three, and you will surely pack on a pound of belly fat.

But these mocha walnut brownies, as with other recipes I provide, will not pack on the pounds. With no wheat to trigger appetite, nor any readily-digestible carbohydrate to generate blood sugar highs and lows, you can have a nice brownie or two or three and nothing bad happens: You don’t send blood sugar sky-high, don’t trigger formation of small LDL particles and triglycerides, you don’t trigger appetite, you don’t gain a pound of belly fat. You simply have your brownie(s) and enjoy them.

Serve these brownies plain or topped with cream cheese, natural peanut or almond butter, or dipped in coffee.


Ingredients:
8 ounces unsweetened baking chocolate (100% chocolate)
4 tablespoons coconut oil or butter, melted
2 large eggs, separated
½ cup coconut milk (or sour cream)
2 teaspoons vanilla extract
2 cups ground almonds
2 tablespoons coconut flour
1 cup chopped walnuts
¼ cup unsweetened cocoa powder
2 teaspoons instant espresso
Sweetener equivalent to 1 cup sugar or to taste (e.g., liquid stevia, Truvía, erythritol)


Preheat oven to 350º F.

Melt chocolate using double boiler method or in 15-second increments in microwave. Stir in melted coconut oil or butter.

In small bowl, beat egg whites until frothy. Add egg whites, egg yolks, coconut milk, and vanilla extract to chocolate mixture and mix thoroughly by hand.

In separate bowl, combine ground almonds, coconut flour, walnuts, cocoa powder, espresso, and sweetener. Mix thoroughly.

Add dry mix to chocolate mix and mix together thoroughly. If dough is too stiff, add additional coconut milk, one tablespoon at a time.

Place mixture in 9-inch baking pan and bake for 25 -30 minutes or until toothpick withdraws dry.

Diabetes: Better than hedge funds

Diabetes is where the action is.

While, for virtually all of history, type 2 diabetes was an uncommon condition of adults, the disease has spread so much to all levels of American society that even kids are now developing the adult form. Researchers from the Center for Disease Control and Prevention predict that, by 2050, one in three adults will be diabetic.

The diabetes market is booming, handily surpassing growth of the oil industry, the housing market, even technology. It makes Bernie Madoff’s billions look like small potatoes. In health, few markets are growing as fast as diabetes—-not osteoporosis, not heart disease, not cancer.

Americans are getting fat from carbohydrate consumption, becoming diabetic along with it. While kids hanging around the convenience store gulp down 26 teaspoons of sugar in 32-ounce sodas and 56-grams-of-sugar in 16-ounce frozen ices, health-minded adults are more likely eating two slices of 6-teaspoons sugar-equivalent “healthy whole grain” bread, wondering why last year’s jeans are too tight.

The U.S. is not the only nation affected. Globally, 2.8% of the world’s population are diabetic, a number expected to double over the next 20 years.

Pharmaceutical companies boast double-digit growth for diabetes drugs, growth rates that keep profit-hungry investors happy. Merck’s Januvia, for instance, introduced in 2006, recently catalogued 30% growth in sales, with annual sales approaching $1 billion. Recently FDA-approved Victoza, requiring once-a-day injection, is expected to reap $4 billion in sales per year for manufacturer Novo Nordisk. Such numbers can only warm a drug company CEO’s heart.

Most diabetics don’t just take one medication, but several. A typical regimen for an adult diabetic after a couple of years of treatment and following the dietary advice of the American Diabetes Association includes metformin, Januvia, and Actos, a triple-drug treatment that costs around $420 per month. Two forms of insulin (slow- and fast-acting), along with two or three oral medications, is not at all uncommon.

“Collateral” revenues from the other health conditions that develop from a diet rich in “healthy whole grains,” such as drugs for hypertension, drugs to slow the progression of kidney disease in diabetes, drugs for “high cholesterol,” and drugs for high triglycerides, and you have a pharmaceutical drug bonanza. You, too, would throw all-expenses-paid, fly-the-entire-sales-force-to-the-Caribbean sales meetings.

The global diabetes market has already topped $25 billion and is growing at double-digit rates. Forget the Internet, gold stocks, or solar energy—-diabetes is where the money is. This fact has not been lost on the very market-savvy pharmaceutical industry. As with any successful business, they have devoted substantial resources to develop and grow this booming business.

270 lb man in diapers

Alex is a big guy: 6 ft 4 inches, 273 lbs.

On 10,000 units per day of vitamin D in gelcap form, his 25-hydroxy vitamin D level was 38.4 ng/ml. One year earlier, his 25-hydroxy vitamin D level, prior to any vitamin D supplementation was 9.8 ng/ml.

According to the latest assessment offered by the Institute of Medicine (IOM):

Vitamin D need for a 13-month old infant: 600 units per day

Vitamin D need for a 6 ft 4 in, 273 lb male: 600 units per day

I paint this picture to highlight some of the absurdity built into the smug assumptions of the IOM's report. It would be like trying to fit a large, full-grown man into the diapers of a 13-month old. Few nutrients or hormones (in fact, I can't think of a single one) are required in similar quantity by an infant or toddler and a full grown adult. However, according to the IOM's logic, their vitamin D needs are identical, regardless of age, body size, skin color, genetics, etc. One size fits all.

Just as the original RDA assessment by the Institute of Medicine kept thinking about vitamin D somewhere in the Stone Age, so does this most recent assessment.

90% small LDL: Good news, bad news

Chris has 90% small LDL particles.

On his (NMR) lipoprotein panel, of the total 2432 nmol/L LDL particles ("LDL particle number"), 2157 nmol/L are small, approximately 90% (2157/2432).

Bad news: Having this severe excess of small LDL particles virtually guarantees heart attack and stroke in Chris' future.

Good news: It means that Chris potentially has spectacular control over his lipoprotein and lipid values, achieving statin-like values without statin drugs.

Typically, extravagant quantities of small LDL particles are accompanied by low HDL, high triglycerides, and pre-diabetes or diabetes. Chris' HDL is 26 mg/dl, triglycerides 204 mg/dl; HbA1c 5.9% (a reflection of prior 60-90 days average blood glucose; desirable 4.8% or less), fitting neatly into the expected pattern.

Chris' pattern tells me several things:

1) He overconsumes carbohydrates, since carbohydrates trigger this pattern.
2) He likely has a genetic susceptibility to this effect (e.g., a variant of the gene for cholesteryl ester transfer protein, perhaps hepatic lipase). Only the most gluttonous and overweight carbohydrate consumers can generate this high a percentage small LDL without an underlying genetic susceptibility.
3) Provided he follows the diet advised, i.e., elimination of all wheat, cornstarch, oats, and sugars, he is likely to have an extavagant drop in LDL particle number. Should he achieve the goal I set of small LDL of 300 nmol/L or less, his LDL particle number will likely be around 500 nmol/L. This translates to an LDL cholesterol of 50 mg/dl . . . 50 mg/dl.

In many people, this notion of taking statin drugs for "high cholesterol" is an absurd oversimplification. But it is a situation that, for many, is wonderfully controllable with the right diet.

The American Heart Association has a PR problem

The results of the latest Heart Scan Blog poll are in. The poll was prompted by yet another observation that the American Heart Association diet is a destructive diet that, in this case, made a monkey fat.

Because I am skeptical of "official" organizations that purport to provide health advice, particularly nutritional advice, I thought this poll might provide some interesting feedback.

I asked:

The American Heart Association is an organization that:

The responses:
Tries to maintain the procedural and medication status quo to benefit the medical system and pharmaceutical industry for money
240 (64%)

Doesn't know its ass from a hole in the ground
121 (32%)

Is generally helpful but is misguided in some of its advice
79 (21%)

Accomplishes tremendous good and you people are nuts
6 (1%)


Worrisome. Now, perhaps the people reading this blog are a skeptical bunch. Or perhaps they are better informed.

Nonetheless, one thing is clear: The American Heart Association (and possibly other organizations like the American Diabetes Association and USDA) have a serious PR problem. They are facing an increasingly critical and skeptical public.

Just telling people to "cut the fat and cholesterol" is beginning to fall on deaf ears. After all, the advice to cut fat, cut saturated fat, cut cholesterol and increase consumption of "healthy whole grains" in 1985 began the upward ascent of body weight and diabetes in the American public.

Believe it or not, my vote would be for something between choices 1 and 3. I believe that the American Heart Association achieves a lot of good. But I also believe that there are forces within organizations that are there to serve their own agendas. In this case, I believe there is a substantial push to maintain the procedural and medication status quo, the "treatments" that generate the most generous revenues.

I believe that I will forward these poll results to the marketing people at the American Heart Association. That'll be interesting!

The formula for aortic valve disease?

I've discussed this question before:

Can aortic valve stenosis be stopped or reversed using a regimen of nutritional supplements?

I had a striking experience this past week. Don has coronary plaque and began the Track Your Plaque program. However, discovery of a murmur led to an echocardiogram that measured his effective aortic valve area at 1.5 cm2. (Normal is between 2.5-3.0 cm2.)

Because of his aortic valve issue, I suggested that, in addition to the 10,000 units of vitamin D required to increase his 25-hydroxy vitamin D level to 70 ng/ml, he also add vitamin K2, 1000 mcg per day, along with elimination of all calcium supplements. (I asked Don to use a K2 supplement that contained both forms, short-acting MK-4 and long-acting MK-7.)

One year later, another echocardiogram: aortic valve area 2.6 cm2--an incredible increase.

This is not supposed to happen. By conventional thinking, aortic valve stenosis can only get worse, never get better. But I've now witnessed this in approximately 10% of the people with aortic valve stenosis. The majority just stop getting worse, an occasional person gets worse, while a few, like Don, get better.

Aortic valve stenosis is to the aortic valve as degenerative arthritis is to your knees: A form of wear-and-tear that leads to progressive dysfunction. When the aortic valve becomes stiff enough (i.e., "stenotic"), then it leads to chest pains, lightheadedness or losing consciousness, heart failure, and, eventually, death. Bad problem.

Aortic stenosis typically starts in your 50s with calcification of the valve, getting worse and worse until the calcium makes the valve "leaflets" unable to move. The treatment: a new valve, a major undertaking involving an open heart procedure.

What if taking vitamins D and K2 and avoiding calcium do not just reverse or stop aortic valve stenosis once established, but prevents it in the first place? Tantalizing possibility.

Pressures on my time being what they are, I've not had the freedom to put together a prospective study to further examine this fascinating question. But it is definitely worth pursuing.

Blood glucose 160

What happens when blood glucose hits 160 mg/dl?

A blood glucose at this level is typical after, say, a bowl of slow-cooked oatmeal with no added sugar, a small serving of Cheerios, or even an apple in the ultra carb-sensitive. Normal blood sugar with an empty stomach, i.e., fasting; high blood sugars after eating.

Conventional wisdom is that a blood sugar of 160 mg/dl is okay, since your friendly primary care doctor says that any postprandial glucose of 200 mg/dl or less is fine because you don't "need" medication.

But what sort of phenomena occur when blood sugars are in this range? Here's a list:

--Glycation (i.e., glucose modification of proteins) of various tissues, including the lens of your eyes (cataracts), kidney tissue leading to kidney disease, skin leading to wrinkles, cartilage leading to stiffness, degeneration, and arthritis.
--Glycation of LDL particles. Glycated LDL particles are more prone to oxidation.
--VLDL and triglyceride production by the liver, i.e., de novo lipogenesis.
--Small LDL particle formation--The increased VLDL/triglyceride production leads to the CETP-mediated reaction that creates small LDL particles which are, in turn, more glycation- and oxidation-prone.
--Glucotoxicity--i.e., a direct toxic effect of high blood glucose. This is especially an issue for the vulnerable beta cells of the pancreas that produce insulin. Repeated glucotoxic poundings by high glucose levels lead to fewer functional beta cells.

A blood glucose of 160 mg/dl is definitely not okay. While it is not an immediate threat to your health, repeated exposures will lead you down the same path that diabetics tread with all of its health problems.

Indian buffet

I took my family to a local all-you-can-eat Indian buffet. It was delicious.

I confined my food choices mostly to vegetables and soups. Within about 30 minutes, I started to get that odd buzz in my head that usually signals a high blood sugar.

When I got home, my fingerstick blood glucose: 173 mg/dl. Darn it! Must have been cornstarch or other sugars in the sauces.

I got on my supine stationary bike and pedaled for 40 minutes at a moderate pace while I played Modern Warfare on XBox. (A great way, by the way, to fit in some low- to moderate-intensity exercise while occupying your brain. My wife often has to yell at me to get off, it's so much fun.)

Blood glucose at the conclusion of exercise: 93 mg/dl-- a nice 80 mg/dl drop.

This is a useful strategy to use in a pinch when you've either been inadvertently exposed to more carbohydrate than you can tolerate, or if you'd like to blunt the adverse glucose effects of a bowl of ice cream or other carbohydrate indulgence.

Should we explore the idea of a "morning-after" pill, or actually a "meal-after" pill, a supplement pill or liquid that blunts or eliminates the blood glucose rise after a meal? I've considered such an idea, but have been fearful that people would start to use it habitually. Thoughts?

American Heart Association diet makes a monkey out of you

Heart Scan Blog reader, Roger, brought this New York Times article to my attention.

In an effort to develop a better experimental model for obesity than mice, scientists have turned to monkeys and other primates. The emerging observations are eerily reminiscent of what you and I witness just by going to the local grocery store or fast food outlet:

"'It wasn’t until we added those carbs that we got all those other changes, including those changes in body fat,' said Anthony G. Comuzzie, who helped create an obese baboon colony at the Southwest National Primate Research Center in San Antonio."

"Fat Albert, one of her monkeys who she said was at one time the world’s heaviest rhesus, at 70 pounds, ate “nothing but American Heart Association-recommended diet,” she said."

Yes, indeed: The American Heart Association diet makes monkeys fat. Extrapolate this a little higher on the evolutionary ladder and guess what?

This is one of the many reasons why, when I have a patient who is counseled by the hospital dietitian on the American Heart Association diet, I advise them to 1) ignore everything the dietitian told them, and then 2) follow the wheat-free, cornstarch-free, sugar-free, whole food diet I advocate.

Not unexpectedly, much of this primate research is not being devoted to just manipulating diet to achieve weight loss and health, but to develop new drugs to "treat" obesity.

Would you like a banana?

Construct your glucose curve

In a previous Heart Scan Blog post, I discussed how to make use of postprandial (after-meal) blood sugars to reduce triglycerides, reduce small LDL, increase HDL, reduce blood pressure and inflammatory measures, and accelerate weight loss.

In that post, I suggested checking blood glucose one hour after finishing a meal. However, this is a bit of an oversimplification. Let me explain.

A number of factors influence the magnitude of blood glucose rise after a meal:

--Quantity of carbohydrates
--Digestibility of carbohydrates--The amylopectin A of wheat, for example, is among the most digestible of all, increasing blood sugar higher and faster.
--Fat and protein, both of which blunt the glucose rise (though only modestly).
--Inclusion of foods that slow gastric emptying, such as vinegar and fibers.
--Body weight, age, recent exercise

Just to name a few. Even if 10 people are fed identical meals, each person will have a somewhat different blood glucose pattern.

So it can be helpful to not just assume that 60 minutes will be your peak, but to establish your individual peak. It will vary from meal-to-meal, day-to-day, but you can get a pretty good sense of blood glucose behavior by constructing your own postprandial glucose curve.

Say I have a breakfast of oatmeal: slow-cooked, stoneground oatmeal with skim milk, a few walnuts, blueberries. Blood glucose prior: 95 mg/dl. Blood glucose one-hour postprandial: 160 mg/dl.

Rather than taking a one-hour blood glucose, let's instead take it every 15 minutes after you finish eating your oatmeal:


In this instance, the glucose peak occurred at 90-minutes after eating. 90-minute postprandial checks may therefore better reflect postprandial glucose peaks for this theoretical individual.

I previously picked 60-minutes postprandial to approximate the peak. You have the option of going a step better by, at least one time, performing your own every-15-minute glucose check to establish your own curve.

Why is type 1 diabetes on the rise?

Type 1 diabetes, also called "childhood" or "insulin-dependent" diabetes, is on the rise.

Type 2 diabetes, or "adult," diabetes, is also sharply escalating. But the causes for this are easy-to-identify: overconsumption of carbohydrates and resultant weight gain/obesity, inactivity, as well as genetic predisposition. A formerly rare disease is rapidly becoming the scourge of the century, expected to affect 1 in 3 adults within the next several decades.

Type 1 diabetes, on the other hand, generally occurs in young children, not uncommonly age 3 or 4. Type 1 diabetes also shares a genetic basis to some degree. But the genetic predisposition should be a constant. Obviously, lifestyle issues cannot be blamed in young children.
Then why would type 1 diabetes be on the rise?

For instance, this study by Vehik et al from the University of Colorado documents the approximate 3% per year increase in incidence in children with type 1 diabetes between 1978 and 2004:


(From Vehik 2007)

(For an excellent discussion of the increase in type 1 diabetes in the 20th century, see this review.)

This is no small matter. Just ask any parent of a child diagnosed with type 1 diabetes who, after recovering from hearing the devastating diagnosis, then has to stick her child's fingers to check glucose several times per day, mind carefully what he or she eats or doesn't eat, watch carefully for signs of life-threatening hypoglycemic episodes, not to mention worry about her child's long-term health. Type 1 diabetes is a life-changing diagnosis for both child and parents.

Various explanations have been offered to account for this disturbing trend. Some attribute it to the increase in breast feeding since 1980 (highly unlikely), exposure to some unidentified virus, or other exposures.

I'd like to offer another explanation: wheat.

Lest you accuse me of becoming obsessed with this issue, let me point out the four observations that lead me to even consider such an association:

1) Children diagnosed with celiac disease, i.e., the immune disease of wheat gluten exposure, have 10-fold greater likelihood of developing type 1 diabetes.

2) Children diagnosed with type 1 diabetes are 10-fold more likely to have abnormal levels of antibodies (e.g., transglutaminase antibodies) to wheat gluten.

3) Experimental models, such as in these mice genetically susceptible to type 1 diabetes, showed a reduction of type 1 diabetes from 64% to 15% with avoidance of wheat.

4) The increase in type 1 diabetes corresponds to the introduction of new strains of wheat that resulted from the extensive genetics research and hybridizations carried out on this plant in the 1960s. In particular, unique protein antigens (immune-provoking sequences) were introduced with the dwarf variant attributable to alterations in the "D" genome of modern Triticum aestivum.

Proving the point is tough: Would you enroll your newborn in a study of wheat-containing diet versus no wheat, then watch for 10 years to see which group develops more type 1 diabetes? It is a doable study, just a logistical nightmare. Perhaps the point will be settled as more and more people catch onto the fact that modern wheat--or this thing we are being sold called "wheat"--is a corrupt and destructive "foodstuff" and eliminate it from their lives and the lives of their young children from birth onwards. Then a comparison of wheat-consuming versus non-wheat-consuming populations could be made. But it will be many years before this crucial question is settled.

Yet again, however, the footprints in the sand seem to lead back to wheat as potentially underlying an incredible amount of human illness and suffering. Yes, the stuff our USDA puts at the bottom, widest part of the food pyramid.