Risks for coronary disease 2008

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

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

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

Is the list complete?

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

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

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


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

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

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

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

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

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

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

Food sources of vitamin K2



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

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

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

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

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

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











Feta cheese

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

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



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

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

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





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

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

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

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

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


All images courtesy Wikipedia.

Copyright 2007 William Davis, MD

Track Your Plaque: Naughty or nice?



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

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

He writes:

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

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

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

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

Have a wonderful holiday!

Vitamin D: Treatment for metabolic syndrome?

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

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

But here's a curious observation:

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

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

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

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

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



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

Appetite stimulants

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

Why such contrasts on different days?

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

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

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













Image courtesy Wikipedia

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

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

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

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

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

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


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

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

"Heart scans are experimental"

Let me warn you: This is a rant.

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

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

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

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

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

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

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

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

When meat is not just meat


The edgy nutrition advocate, Mike Adams, over at NewsTarget.com came up with this scary photo tour of a processed meat product from Oscar Mayer: Mystery Meat Macrophotography: A NewsTarget PhotoTour by Mike Adams







Along with increasingly close-up photographs of this meat-product, Adams lists the ingredients in Oscar Mayer's Cotto Salami:


Beef hearts
Pork
Water
Corn syrup
Beef

Contains less than 2% of:
Salt
Sodium lactate
Flavor
Sodium phosphates
Sodium diacetate
Sodium erythorbate
Dextrose
Sodium nitrite
Soy lecithin
Potassium phosphate
Potassium chloride
Sugar


As I reconsider the role of saturated fat in diet, given the startlingly insightful discussion by Gary Taubes of Good Calories, Bad Calories, I am reminded that not all meat is meat, not all saturated fat sources are equal.

I am concerned in particular about sodium nitrite content, a color-fixer added to cured meats that caused a stir in the 1970s when data suggesting a carcinogenic effect surfaced. The public's effort to remove sodium nitrite from the food supply was vigorously opposed by the meat council and it remains in cured meats like sausage, hot dogs, and processed meats like Cotto Salami. A 2006 meta-analysis (combined analysis of studies) of 63 studies did indeed suggest that sodium nitrite was related to increased risk of gastric cancer. This argument is plausible from animal models of cancer risk, as 40 animal models have likewise suggested the same carcinogenic association.

Also, fructose? This is most likely added for sweetness. Recall that fructose heightens appetite and raises triglycerides substantially.

I personally have a natural aversion to meat. I don't like the taste, the look, smell, and the thought of what the animal went through to make it to the supermarket. But, considered from the cold, carnivorous viewpoint of the question, "Is meat okay to eat?", among the issues to consider is whether the meat has been cured or processed, and does that process include addition of sodium nitrite.

Cotto Salami and similar products are not, of course, what carnivorous humans in the wild ate. This is a processed, modified product created from factory farm animals raised in cramped conditions and fed corn and other cheap, available foods. It is not created from free-ranging animals wandering their pastures or pens, eating diets nature intended. This results in modified fat composition, not to mention hormones and antibiotics added. These are not listed on the ingredients. Wild meat does not contain fructose or color-fixers, either.

So don't mistake "meat" in your grocery store for meat. It might look and smell the same--until you look a little closer.



Copyright 2007 William Davis, MD

Don't lament no OTC mevacor

After Merck's third go at FDA approval for over-the-counter (OTC) status for its statin cholesterol drug, Mevacor (lovastatin), the FDA advisory board suggested that its request be denied. They expressed concern that too many people would not understand how the drugs would be used and that misuse would be common.

Similar sentiments were echoed by Dr. Sidney Wolfe, director of the Health Research Group at Public Citizen; the American Medical Association (though the AMA always fights anything that threatens to erode physician control over health); and the de facto spokesman for cardiologists, Dr. Steven Nissen of the Cleveland Clinic.

Although I am a supporter for tools and legislation that yield greater self-empowerment in health care to the public, there is no need to lament the failed OTC status for Mevacor. For one, Merck had no plans to reduce the price on its OTC preparation. For many people, this would have meant an increase in cost, since health insurers would surely not cover a non-prescription agent.

Second, OTC status sends the implicit message that cholesterol is the most common cause of heart disease; it is not. (Small LDL particles are the number one cause, a pattern only partially addressed by any statin drug and a pattern largely responsible for the failure of statin drugs to "cure" heart disease despite pharmaceutical manufacturer's attempts to increase doses to take up any slack in effect.)

Thirdly, you can achieve the same effect--no, a superior effect--by incorporating several simple strategies into your life. These strategies are superior to Mevacor because they do more than just reduce LDL cholesterol. You can achieve similar LDL-reducing effect to Mevacor, 20 mg, just by adding:

--2 tablespoons oat bran or ground flaxseed per day (choose flaxseed if you have sugar problems or small LDL; flaxseed contains no digestible sugars, only protein and fiber)
--Raw almonds or walnuts--at least a handful, though more is fine and will not make you fat. (It's nuts like party mixes, mixed nuts roasted in unhealthy oils, and honey-roasted nuts that make us fat, not raw.)
--Soy protein sources--probably the weakest effect of all foods listed, but a contributor that can be obtained in a variety of forms, such as tofu, soy protein powders, and soy milk.
--Other foods that reduce LDL include pectin sources (e.g., citrus rind), flavonoids (e.g., green tea); stanol esters found in butter substitute Benecol (recall that sterol-containing products like Take Control and the flood of new products on the market like HeartWise orange juice might have potential for allowing sterol esters to enter the blood, so I do NOT recommend them); and, of course, niacin.

Many of these strategies also reduce small LDL, raise HDL, reduce triglycerides, and reduce blood sugar, effects that go beyond that achieved with Mevacor. Of course, a combination strategy is not as easy as popping one pill a day, it's better for you.

I will certainly not shed any tears for Merck and its relentless efforts to gain a stronger foothold in the "transform conditions into diseases" marketing strategy, the same strategy that classifies shyness, toe fungus, and sadness into medical conditions necessitating medication. While I do generally support efforts to increase public access to strategies that increase their health care power, this one was not necessarily all good.

Members of Track Your Plaque can read the complete report, Unique nutritional strategies to Reduce cholesterol naturally on the Track Your Plaque website.



Copyright 2007 William Davis, MD

Damage control

Medical device manufacturer, Cordis, is launching a new marketing program to promote its Cypher drug-coated stent. You can view the details at www.CypherUSA.com , including the slick TV commercial that HeartHawk posted a blog about.

The campaign opens with:

When you open up your heart, you open up your life.

Lives hampered by angina. By shortness of breath. By restricted blood flow. These lives are changing. Because of a state-of-the-art advancement. One that can have a huge impact on arteries around your heart. The CYPHER® Stent. It can open up your arteries. Increase flow of blood and oxygen. And change your restricted life. To an active life worth living. Your new life is...

Life Wide Open


Direct-to-consumer drug advertising has been around for a few years. While it has increased awareness of drugs and the "conditions" they are supposed to treat, it has also highlighted the aggressive profit-motive of the drug industry. This is not health care for the needy and sick, but health care for profit.

So now we're beginning to see the emergence of direct-to-consumer (DTC) advertising for medical devices. There was also a brief, though unsuccessful, foray into DTC advertising for implantable defibrillators, of all things, by Medtronic a couple of years ago, also.

What is the purpose of Cordis' marketing effort? Is it to educate and inform the public who might unknowingly receive non-drug coated stents and be deprived of the restenosis-inhibiting advantage of a drug-coated device? Is it meant to right a systematic wrong, a failure of cardiologists to insert the technologically, biologically, and ethically superior coated stents?

I find that doubtful. A more likely motive is damage control. With some of the (both deserved and undeserved) negative press the drug-coated stents have received lately, Cordis, eager to protect their $20 billion (annual revenues, 2006) medical device franchise, came up with this DTC strategy. After viewing the smiling faces of people , elated because of their "wide open" arteries and lives, Cordis hopes to see people going to their doctors insisting on the stent that is "opening millions of lives," since, "when your arteries narrow, so does your life."

Cool, trendy, liberating. That's the message they wish to deliver. Cool music, beautiful people, flashy high-tech images. Who wouldn't want a Cypher stent?

Beyond damage control, it's a familiar marketing theme: You're slender, glamorous, and sexy if you drink Coke, you're a caring mother if you feed your children Jif peanut butter, you're health conscious and smart if you eat Total cereal . . . you're cool and know what you want from life if you insist on a Cypher stent.

I don't object to advertising. It's part of the capitalistic economic system. It drives awareness and grows businesses. I do get concerned when advertising is so slick and effective that the people who are not properly armed with information can be duped into thinking that they need something that they don't really need.

Or, for which there are powerful, viable alternatives. Even hear about "prevent the disease in the first place?"

Low expectations

The Framingham Risk Calculator is a standard method used by many physicians to predict risk for heart attack or death from heart disease over a 10-year period. Low-risk is defined as <10% risk of heart attack or cardiac death over 10 years; high-risk is defined as 20% or more over 10 years; intermediate-risk is in between.

Let's put it to the test:

Amy is a 53-year old businesswoman. She is 5 ft 4 inches, weighs 150 lbs. Her father had a heart attack in his early 50s followed by the usual list of hospital procedures including bypass surgery at age 60.

What is Amy's risk for heart attack or death from heart disease over the next 10 years? If we enter her data into the Framingham risk calculator, the following result is returned:

Information about your risk score:
Age: 53
Gender: female
Total Cholesterol: 198 mg/dL
HDL Cholesterol: 74 mg/dL
Smoker: No
Systolic Blood Pressure: 120 mm/Hg
On medication for HBP: No
Risk Score: 1% Means 1 of 100 people with this level of risk will have a heart attack in the next 10 years.


So, according to the Framingham calculation, Amy has <1% risk for heart attack or death from heart disease over the next 10 years. Most primary care physicians would, at most, prescribe a statin drug and talk about a reduction in saturated fat.

Thankfully, Amy didn't fall for that bit of conventional mis-information. She instead got a CT heart scan, principally because of her father's history. Her score: 117. At age 53, this put her into 90th percentile, in the worst 10% of scores for women in her age group (50-55). By heart scan criteria, her risk for heart attack is probably more like 4-5% per year, or approximately 40-50% over the next 10 years.

Let's do just a bit more math. If Amy hadn't known about her heart scan score and no preventive action was taken, the expected progression of her heart scan scores would likely be:

Start: 117
Year 1: 152
Year 2: 198
Year 3: 257
Year 4: 335
Year 5: 436
Year 6: 567
Year 7: 737
Year 8: 958
Year 9: 1245
Year 10: 1618

In fact, given Amy's starting heart scan score of 117, it is highly unlikely that she survives the next 10 years without heart attack or a fatal heart event. Yet the Framingham risk calculator puts Amy's risk at less than 1%. Could anything be more wrong?

The folly of the Framingham calculator was highlighted by a recent publication from the large Multi-Ethnic Study of Atherosclerosis (MESA), in which 3600 women (45-84 years), all of whom fell into the "low-risk" category by the Framingham calculator--just like Amy--were tracked over approximately 3 3/4 years. This study generated several observations:

1) 30% of the "low-risk" women had positive heart scan scores.
2) 5% of the "low-risk" women had scores of 300 or greater (very significant for a woman). 8.6% of these women experienced a cardiovascular event like heart attack or death over the period. Women with a heart scan score of 300 or greater had a 22-fold greater event risk compared to women with zero heart scan scores.
3) Women with heart scan scores of 1 to 299 had a cardiovascular event risk of approximately 5-fold greater risk over the period.


Across the U.S., 90% of women younger than 70 years old fall into the Framingham "low-risk" category. Yet this fiction is accepted as the prevailing standard, along with LDL and total cholesterol, for determination of risk in women and men.

In my view, using the Framingham risk calculator is a misguided, misleading path, one that will mis-classify a substantial number of women who could otherwise be spared from heart attack and catastrophe.

By the way, Amy is also the Track Your Plaque program record holder (by percentage drop), with a 63% drop in heart scan score over a 15 month period.
One hour blood sugar: Key to carbohydrate control and reversing diabetes

One hour blood sugar: Key to carbohydrate control and reversing diabetes

Diabetics are instructed to monitor blood glucose first thing in the morning and two hours after eating. This helps determine whether blood sugar is controlled with medications like metformin, Januvia, Byetta injections, or insulin.

But that's not how you use blood sugar to use to prevent or reverse diabetes. Two-hour blood sugars are also of no help in deciding whether you have halted glycation, or glucose modification of proteins the process that leads to cataracts, brittle cartilage and arthritis, oxidation of small LDL particles, atherosclerosis, kidney disease, etc.

So the key is to check one-hour after-eating (postprandial) blood sugars, a time when blood glucose peaks after consumption of carbohydrates. (It may peak somewhat sooner or later, depending on factors such as how much fluid was in the meal; protein, fat, and fiber content; presence of foods like vinegar that slow gastric emptying; the form of carbohydrate such as amylopectin A vs. amylopectin B, amylose, fructose, along with other factors. Once in a while, you might consider constructing your own postprandial glucose curve by doing fingersticks every 15 minutes to determine when your peak occurs.)

I reject the insane notion that after-eating blood sugars of less than 200 mg/dl are acceptable, the value accepted widely as the cutoff for health. Blood sugars this high occurring with any regularity ensure cataracts, arthritis, and all the other consequences of cumulative glycation. I therefore aim to keep one-hour after-eating glucoses 100 mg/dl or less. If you start in a pre-diabetic or diabetic range of, say, 120 mg/dl, then I advise people to not allow blood glucose to go any higher. A pre-meal blood glucose of 120 mg/dl would therefore be followed by an after-eating blood glucose of no higher than 120 mg/dl.

No doubt: This is strict. But people who do this:

--Lose weight from visceral fat
--Heighten insulin sensitivity
--Drop blood pressure
--Drop HbA1c and fasting glucose over time
--Reduce small LDL and other carbohydrate-sensitive measures

By the way, if you inadvertently trigger a high blood sugar like I did when I took my kids to the all-you-can-eat Indian buffet, go for a walk, bike, or burn the sugar off with a 30-minute or longer physical effort. Check your blood sugar again and it should be back in desirable range. But then learn from your lesson: Eliminate or reduce portion size of the culprit carbohydrate food.

Comments (27) -

  • Might-o'chonri-AL

    8/2/2011 6:11:40 AM |

    Glyco-sylation occurs inside a cell's endoplasmic reticulum lumen when certain  carbohydrates  (in the form of N-linked oligo-saccharides) meld with a newly folded protein that gets translated into  a glyco-protein.  There are different rates of activation and de-activation  between glyco-sylated and un-glycosylated proteins; this affects how that protein migrates as it tries to perform it's job and how  glycation can induce degenerative states.  Tissue cells with endoplasmic reticulum stress can exasperate certain disease progression because such "stress" there promotes more glycosylation.

  • Annabel

    8/2/2011 12:40:42 PM |

    I couldn't agree more with the advice to test every 15 minutes as a means of discovering your own "sugar curve." When I tried this, I found that my own peak falls pretty consistently at 75 minutes after beginning a meal. Testing at 2 hours completely overlooks my highest blood glucose levels.

    It's a particularly good technique for those folks whose A1c levels are higher than their fingersticks would predict...it's almost surely because they're doing their sticks way past their glucose peak.

    When test strips cost up to a buck apiece, it may feel hard to justify using six or eight of them on a single meal--but what you learn may save tens of thousands in medical bills!

  • Curt

    8/2/2011 1:31:12 PM |

    Another great article - thank you! I'm curious about your thoughts on controlled 1 hour blood sugars (mine are rarely over 110) but baseline levels that aren't much lower. Typically in the 95-105 range. I will get something in the 80s occasionally, but 100 is more common. I never really spike - even a high carb meal will only get me to 130s or so and that never really happens as I don't eat much sugar/starch at all.

    Another quick question: You've mentioned a couple times recently about this way of eating being particularly good for VISCERAL fat. That is exactly what I've found. Tremendous benefits and I feel great. I have leveled out for a while (months) in fat loss, however, with a good amount of subcutaneous fat still present. Is there another protocol for getting after this type of fat? I'm already no wheat, low carb, paleo.

    Thanks again for your excellent articles! Always learning something new.......

  • ShottleBop

    8/2/2011 1:38:20 PM |

    Do you have citations to support your statement that glycation occurs at BGs of 100 or more?  This is one of the more-commonly discussed issues on diabetes discussion boards--but folks are wont to ask for backup.

  • Jeff C

    8/2/2011 1:47:11 PM |

    Regarding glycation specifically...

    1. Do you agree that fructose ("frucation") causes more AGE than glucose?
    2. What to you make of Ray Peat's assertion that poly-fats are much more glycalating than glucose?

    "The so-called "advanced glycation end products," that have been blamed on glucose excess, are mostly derived from the peroxidation of the "essential fatty acids." The name, “glycation,” indicates the addition of sugar groups to proteins, such as occurs in diabetes and old age, but when tested in a controlled experiment, lipid peroxidation of polyunsaturated fatty acids produces the protein damage about 23 times faster than the simple sugars do." (Fu, et al., 1996)." - Ray Peat

  • Richard

    8/2/2011 3:21:55 PM |

    Thanks for the great article!
    I've just begun tracking blood sugars closely, changed my diet to one very low in carbs and no grains, and am determined to find ways to keep at it. I've started a blog just track my progress and keep me honest: http://transformation-transformative.blogspot.com/
    I'll also try the 15 minute testing to see where my personal peak in blood sugar occurs.
    Again, many thanks!

  • steve

    8/2/2011 3:31:08 PM |

    Hi Dr. Davis:  What is the relationship between fasting BG taken at the Dr's office and A!C?  My fasting BG level is 73.5 but my A1C is 5.4.  I would have expected the A1C to more correspond to the fasting measurement; in the case of my wife it does.  Is it related more to the red blood cells lingering around longer or lipoprotein particles which increases the chance of glycation?  Recently had a larger than normal amount of carbs in a meal- rice and blueberries and BG spiked to 119, not to bad, but will experiment with carb portion to keep under 100 as BG may be a contributing factor to my CAD.  I am also a hyperabsorber of fat despite being an ApoE 3/3.

    As an aside, i have sent around a link of one of your interviews regarding Wheat Belly and many eyes have been opened as well as many looking to buy the book.  Might not be a bad idea to have a link to any of your interviews on Wheat Belly posted to this site.
    Thanks for the enlightening good work!

  • Dr. William Davis

    8/3/2011 12:23:09 AM |

    Hi, Shottle--
    This will be the topic of an upcoming discussion. The documentation of this effect is quite extensive. It is no longer a matter of "if" but "how much."

  • Dr. William Davis

    8/3/2011 12:25:11 AM |

    Hi, Jeff--
    This is one of oranges and apples comparisons.
    Fructose does indeed induce flagrant glycation. Glucose induces glycation, though less vigorously.

    However, there is a separate but very poorly named process called exogenous glycation which has less to do with glycation than with oxidation of fats.

    This will be the topic of future discussions.

  • Dr. William Davis

    8/3/2011 12:26:22 AM |

    My first thought is that, if weight loss is ongoing, there is a temporary situation of insulin resistance that generally dissipates with weight stabilization.

    It's also possible that your pancreas has inadequate baseline production of insulin. I'm hoping it's the first possibility.

  • Dr. William Davis

    8/3/2011 12:28:05 AM |

    Hi, Steve-

    You will find that, if you did frequent fingersticks around the clock, the highish A1c reflects the higher blood glucose values that occur after meals.

    Thanks for the feedback on the Wheat Belly project. I will indeed crosslink some of the more relevant discussions.

  • Might-o'chondri-AL

    8/3/2011 2:39:31 AM |

    Advanced glycation end products (AGE) involve some of haemoglobin's hydro-carbon Beta side chain valine residue linking up to non-polar "glucose" aldehyde compounds and certain non-"glucose" aldehydes. Various pathological kinds of AGEs can occur from distinct events; in one situation it is macrophage activity producing enzymatic myelo-peroxidase, which can activate hypochlorite favoring a serine amino acid wing to form up to make the AGE called glyco-aldehyde.

    Probably the AGE called methyl-glyoxal is the one most relevant to diabetes prevention; since Type 1 diabetics blood serum levels of methyl-glyoxal is +/- 6 times higher than normal. This AGE can be formed when the byproduct triose-phosphate (triose = subset of carbs) is generated from the glycolytic pathway called  Embden-Meyerhof; this  byproduct risks being made into methyl-glyoxal.

    Maybe the most well known AGEs are the non-enzymatic Amadori products formed via hydrolysis; one is called glyoxal coming from glucose oxidation. And the other Amadori type AGE is 3-deoxy-glucosone (3DG), which requires fructo-selysine and the fructos-amine 3 kinase cascade to shuffle together 3DG.

  • Might-o'chondri-AL

    8/3/2011 2:40:38 AM |

    Diabetes reveals the problem with AGEs; this is because diabetics risk incurring kidney nephro-pathy, One of the pathological results is oxidative kidney stress, which limits sodium (Na) excretion thereby fostering  hyper-tension . When AGEs like 3DG, glyoxal & methyl-glyoxal  (among others, like pentosidine ) circulate into the kidneys their carbonyl compounds  are hard to clear by the kidneys; the side effect is to engender  uric uremia problems and meanwhile levels of carbonyls build up in what is called "carbonyl stress".
    Japan research of the plant compound chamaemeloside found that in humans it lowered levels of the AGEs 3DG & pentosidne better than any other natural remedy; optimal response was reduction of down to 1/5 th of subject's starting levels.  Chamaemeloside is the active compound in chamomile (Anthemis noblis); the extraction formula was 1 Kg of chamomile flowers steeped covered in 20 Lt. water for 3 hours at 80* celcius ( a lab temperature probably not critical for home remedy preparation).

  • Peter Silverman

    8/3/2011 12:56:13 PM |

    Volek and Phinney in their new book about carbohydrate restriction think that as you increase  fat from 30% to 60% of your diet, insulin resistance increases, then it drops when you go above 60%.  It seems that among the most experienced researchers of carbohydrate restriction, there's little consensus about the optimal amount of fat or carbs.  Ron Krausse, for instance, thinks 35% to 45% is optimal.

  • steve

    8/3/2011 5:23:50 PM |

    Peter:
    When these researchers talk about carb levels are they considering vegetables to be carbs, or just fruits, grains, potatoes?

  • frank weir

    8/3/2011 6:41:32 PM |

    You must mean, "can exacerbate certain disease progression...." meaning: to increase the severity, violence, or bitterness of; aggravate

  • frank weir

    8/3/2011 6:59:22 PM |

    This is wonderful information BUT I wonder if it might be unfortunate if folks who routinely have post-prandials of 120 to 140 take your 100 level as a sign of "failure"...things are seldom so cut and dried, black and white. I don't know if I'm hitting 100 or less  after every meal, but my A1C has dropped from 7.5 to 5.8 since last November restricting carbs. And I've lost 30 pounds. I will begin to be more dogmatic about one-hour glucose checks but my rough sense is that I'm not at 100 or less a majority of the time. But I might be wrong about that. Do you see what I'm getting at? Glucose control is an ongoing process that includes lots of self education since most GP's are not keen AT ALL on restricting carbs, including mine. When I read your post, my initial feeling was, "Cripes, 100 after EVERY meal? Don't think I can do that...."

  • Might-o'chondri-AL

    8/4/2011 1:05:26 AM |

    From another commentator here, in an  earlier thread of Dr. Davis' here is how to use HbA1c to determine your average blood glucose level (note: this is not a morning "fasting" level) .
    1st: multiply your HbA1c by 28.7
    2nd: subtract 46.7 from 1st amount
    3rd: take last number as your average waking hours mg/dL blood glucose over last  few months  
    ex:  HbA1c of 5.4 x 28.7 = 159.98 minus 46.7 = 108.28 mg/dL of average blood glucose level

  • Peter Silverman

    8/4/2011 2:24:31 AM |

    They don't count non-starchy vegetable as carbs.

  • ShottleBop

    8/4/2011 3:15:11 AM |

    Thanks for the heads up!

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  • Stephanie

    8/4/2011 2:13:27 PM |

    Dr. Davis,
    I have found that if I take my carb level too low (below 50g per day) that my fasting blood glucose levels actually go up rather than down.  If my carb intake is closer to 70-80, my fasting glucose is lower.

    Have you had this experience with some of your patients?  Can you shed any light onto what might be happening?

    Thanks!
    Stephanie

  • Anne

    8/4/2011 2:34:11 PM |

    Non-starchy vegetables do have carbs and I do have to count them. A half cup of broccoli can have about 6 carbs and since I limit my carbs to no more than 15g/meal, that broccoli on my plate is significant.

    I found getting a scale that reads carbs too was an important tool for me. I found I was ofter overestimating how much of a low carb veggie I could eat. If my blood sugar starts to rise, I go back to measuring and that seems to get me back on track.

    Anne

  • majkinetor

    8/14/2011 1:25:56 PM |

    I think thats normal, its commonly encountered on paleo forums/blogs. It has something to do with physiological insulin resistance, Petro @ Hyperlipid talked about. Look here:

    http://high-fat-nutrition.blogspot.com/2007/10/physiological-insulin-resistance.html

  • majkinetor

    8/14/2011 1:38:24 PM |

    I wouldn't suggest that everybody blindly follow CHO < 50g / day. As always, its about the context. People usually forget that. We mostly extrapolate from results of people who already have metabolic problems.

    Anyway, I am currently perfectly healthy apart from some minor dermatology problems (eczema).
    When I have prolonged periods of reduced CHO input (around 50g / day), I eventually start having some mucus problems. Dry eyes particularly, but also joint pain. I am not 100% sure if its about low carb diet, but it looks like it. Now I target 75g < CHO < 100g per day by adding small potato and a bit more chocolate to my diet.

    I think overemphasizing carb reduction is not good thing for most people. Carbs should go down by pretty big amount for most people, but not to extreme. In anyway, its better to measure then to guess. My sugar is never above 110 after meal and fasting is always around 95.

  • John F

    8/13/2012 9:48:10 AM |

    I decided to take this advice and have been tracking my 60 mins postprandial blood glucose for the past two days to see if all the years I've been low carbing have been making any difference. Especially working my way through different foods to see how they affect me and I've ranged from 64 mg/dl to 97 mg/dl so I'm pretty hapy.

    However this evening 60 minutes after my dinner of panfried steak with a creamy cajun sauce I got a reading of just 55 mg/dl. A lot of websites say this is too low. I'm 32, healthy male, 5,9", weigh 160 lbs, not diabetic and I don't feel sick so I'm not sure what to make of this low reading. The only thing I did was finish a hard CrossFit workout about 30 mins before I had dinner... so a total of 90 minutes before the blood glucose test.

    Any advice on what this "low" reading means? I'm hoping it's normal and means I'm burning fat!

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