The results of the latest Heart Scan Blog poll are in.

I went wheat-free and I . . .

Gained weight 6 (3%)

Lost no weight 41 (21%)

Lost less than 10 lbs 28 (14%)

Lost more than 10 lbs 34 (17%)

Lost more than 20 lbs 22 (11%)

Lost more than 30 lbs 28 (14%)

I'm still losing weight! 30 (15%)

(189 respondents)

This means that, by eliminating wheat:

24% had no success

31% had moderate success (less than 10 lbs or more than 10 lbs)

25% had extravagant results with 20 lbs or more lost

It would be interesting to know where along the weight-loss spectrum the last category, "I'm still losing weight," group falls. (Anyone with a good story please speak up!)

I believe we can conclude from this casual exercise that, as a simple strategy, wheat elimination is surprisingly effective.

Why would 3% gain weight? Well, without knowing the details, there are several possible explanations:

1) Weight gain developed through other foods. For instance, I've had people eliminate wheat only to replace it with fattening gluten-free alternatives. Remember: wheat-free is not gluten-free. Others load up on the wrong foods, e.g., Craisins and other dried fruit; overdo dairy; or snack on wheat-free but unhealthy foods like ice cream and chips.

2) Too much alcohol

3) Hypothyroidism--A lot more common than you'd think. In fact, this has been the case with a majority of people who have done everything right, yet either failed to lose weight or gained weight.

Those are the biggies.

I'd like to hear your personal stories of wheat elimination--the ups and downs, your success or failure, how you felt during the process, how easy or difficult, your eventual results. Just post them as a response to this blog post.

A reader of Life Extension reminded me of a piece I wrote about niacin a couple of years back.

Anyone desiring a primer on how and why to use niacin to correct lipid and lipoprotein patterns might find this useful.

While some people, no matter what they do, cannot tolerate niacin (about 10% of people), many others enjoy spectacular benefits.

Q: I recently had a cholesterol profile blood test and learned that I may be at risk of heart disease because my levels of beneficial HDL (high-density lipoprotein) are too low. I read that niacin could help increase my HDL, but my doctor said niacin is dangerous. Whom should I believe?

A: Your doctor would be right—if we were still living in 1985. Since then, however, we have learned how to use niacin (vitamin B3) safely and effectively. Unfortunately, many physicians have not yet caught up, or are still trapped by the idea that cholesterol-lowering statin drugs are the only way to decrease cardiovascular disease risk. I have personally prescribed niacin for thousands of patients as part of our program to reverse coronary disease. In fact, niacin is the closest thing we have available to a perfect treatment that corrects most of the causes of coronary heart disease.

Continued here.

What if coronary heart disease could be prevented--no eliminated--applying methods that were accessible, easy, and cheap?

What if coronary heart disease and, thereby, angina, heart attack, sudden cardiac death, ventricular tachycardia, heart failure, and the cerebrovascular equivalent, stroke, could be eliminated using readily available tools available to virtually everyone in the U.S.? And, over a year, it cost less than a once-a-week latte at Starbucks?

How would the healthcare landscape change? What would become of hospitals, manufacturers of the billions of dollars of hospital equipment necessary to supply the cardiovascular hospital industry (e.g., stent manufacturers, catheter manufacturers, defibrillator and pacemaker manufacturers, pharmaceutical manufacturers who no longer have to produce the volume of antiplatelet agents, inotropic drugs, antiarrhythmic agents, etc.)?

How would our lives change? What would the end of life look like if people stopped dying of heart attack, sudden cardiac death, congestive heart failure at age 55, 65, or 75, but lived out their lives to die of something unrelated?

What if the solution had little or nothing to do with drugs but evolved from simple nutritional strategies, supplements meant to correct the deficiencies that accompany modern lifestyles, and a few unique strategies targeted towards the genetic predispositions that lead to heart disease?

What if all this were possible at a cost of a few hundred dollars per year?

It would certainly be a cataclysmic change. Hospitals would shrink to a small remnant of their current gargantuan, dozens-per-city presence. The need for hospital staff would be slashed by over half. The rare cardiologist would tend to congenital heart disease sufferers and other unusual forms of heart disease and he or she might have a colleague or two in all of a major city.

Healthcare costs would plummet, no longer having to sustain the enormous cardiovascular healthcare machine of hospitals, staff, industry, and long-term care. Health insurance, private or public, would drop by 50%.

It would free up nearly a trillion dollars that could be redirected towards other pursuits, like schools and research. Extraordinary leaps forward in quality of life and science would emerge, given that magnitude of funding.

It's not as grand a thought experiment as Alan Weisman's The World Without Us, in which he imagines what the world would be like without humans altogether.

How long would it take to recover lost ground and restore Eden to the way it must have gleamed and smelled the day before Adam, or Homo habilis, appeared? Could nature ever obliterate all our traces? How would it undo our monumental cities and public works, and reduce our myriad plastics and toxic synthetics back to benign, basic elements?

But I believe this thought experiment--what would life be like without heart disease because it was eliminated using inexpensive tools-- is more plausible, more likely to occur. In fact, it has already begun to occur.

See those vines growing up the side of the hospital?

Total Fat

3 g or less

Less than 6.5 g

Saturated Fat

1 g or less

1 g or less

Cholesterol

20 mg or less

20 mg or less

Sodium

480 mg or less per RACC* & labeled serving

480 mg or less per RACC* & labeled serving

Nutrients

Contain 10 percent or more of the daily value of 1 of 6 nutrients; vitamin A, vitamin C, iron, calcium, protein or dietary fiber

Contain 10 percent or more of the daily value of 1of 6 nutrients; vitamin A, vitamin C, iron, calcium, protein or dietary fiber

Trans fat

Less than 0.5 g per RACC* and labeled serving

Less than 0.5 g per RACC* and labeled serving

Whole Grain

N/A

51 percent by weight/RACC*

Minimum Dietary Fiber

N/A

1.7 g/RACC of 30 g

2.5 g/RACC of 45 g

2.8 g/RACC of 50 g

3.0 g/RACC of 55 g

(RACC=Reference Amount Customarily Consumed)

Rich has been taking Synthroid or levothyroxine for many years.

When Rich came to my office for continuing management 10 years after his bypass surgery, I checked his thyroid panel:

TSH 7.44 uIU/L

Free T4 1.88 ng/dl (Ref range 0.80-1.90 ng/dl)

Free T3 2.0 pg/ml (Ref range 2.3-4.2 pg/ml)

Rich's thyroid hormone distortions--high TSH, low T3--are sufficient to account for a tripling of heart attack risk long-term.

As Richs' thyroid was being managed by his primary care physician, I notified this doctor of Rich's panel. He therefore increased Rich's levothyroxine from 75 mcg per day to 100 mcg per day. Another thyroid panel several months later showed:

TSH 0.98 uIU/L

Free T4 2.38 ng/dl

Free T3 2.0 pg/ml

As you would expect, increasing the intake of the T4 hormone (levothyroxine) increased free T4 and suppressed TSH.

But what about T3? It's unchanged.

Indeed, Rich says that he feels no better and, in fact, wakes up in the morning foggy and requires a nap in the afternoon.

In my experience, the majority (approximately 70%, but not 100%) experience subjective improvement when T3 is added in some form and the free T3 level is increased. While the data (summarized here) are conflicted on whether there is objective benefit to T3 management and supplementation, there seems to be a poorly-quantified subjective improvement.

Rich's increased levothyroxine dose decreased (calculated) LDL cholesterol by 10 mg/dl. Based on my experience, I'll bet that his lipid panel would likely be further improved with T3 correction.

What I find incredible is the absolutely rabid resistance waged by primary care physicians and endocrinologists against this notion of T3, mostly due to fears of the remote likelihood of inducing atrial fibrillation and osteoporosis, while they are ready to prescribe lifelong statin drugs without a moment's hesitation.

Track Your Plaque has just launched a new version of our newsletter. We call it Cardiac Confidential.

Cardiac Confidential is meant to be a no-holds-barred, go-for-the-throat exposé of the world of heart disease. We will expose the dishonest, reveal what we view as the underlying truth. We'll even have an occasional "undercover" report of what goes on in hospitals and the go-for-the-money world of heart procedures.

Read the first issue here (open to everyone) in which "Laurie" describes her encounter with a sleazy, profiteering cardiologist. She survives, but not without paying a dear price.

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

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

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

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

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

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

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

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

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

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

What do you think of these chains of logic?

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

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

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

Try this one:

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

Ouch!

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

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

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

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

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

Pomegranate juice, 8 oz:

Sugars, total 31.50 g

Sucrose 0.00 g

Glucose (dextrose) 15.64 g

Fructose 15.86 g

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

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

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

Image courtesy Wikipedia

Honeydew melon:

Sugars, total 51.97 g

Sucrose 15.87 g

Glucose 17.15 g

Fructose 18.94 g

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

Image courtesy Wikipedia

A friend of mine is a Type I, or childhood onset, diabetic. He's had it for nearly 50 years, since age 6. He's also in the health industry and is a good observer of detail.

He made the following interesting comments to me recently when talking about the effects of various foods on blood sugar:

"When I eat normally, like some vegetables or salad and meat, I dose up to 10 units of insulin to control my blood sugar.

"If I eat a turkey sandwich on two slices of whole wheat, I usually dose 15 units. The bread makes my blood sugar go to 300 if I don't.

"If I eat a Cousins's Sub [a local submarine sandwich chain], I dose 15 units. The bread really makes my blood sugar go up.

"I can only eat a Quarter Pound from McDonald's once a year, because it make my blood sugar go nuts. I dose 15-20 units before having it, and I feel like crap for two days afterwards.

"If I eat Mexican food, I have to dose 15-20 units. For some reason, it's gotten worse over the years, and I need to dose higher and higher.

"Chinese food is the absolute worst. I dose 20-25 units before eating Chinese. I'll often have to dose more afterwards, because my blood sugar goes so berserk."

Nothing beats the real-world observations on the impact of various foods on blood sugar than the observations of people with Type I diabetes. All the insulin they get is in a syringe. Dosing needs to match intake.

Personally, though I love the taste of Americanized Chinese food, I've always been suspicious of what exactly goes into these dishes. But I was unaware of the blood sugar implications.

The impact of Mexican I believe can be attributed to the cornstarch used in the tacos and tortillas, though I also wonder if there are other starches being snuck in, as well.

Image courtesy of apc33.

Japan provides a useful "laboratory" for studying the effect of a culture that relies heavily on eating fish.

The JELIS Trial, the topic of a previous Heart Scan Blog post, showed that supplementation with the single omega-3 fatty acid, EPA, 1800 mg per day (the equivalent of 10 capsules of 'standard' fish oil that contains 180 mg per day of EPA, 120 mg of DHA) significantly reduced heart attack in a Japanese population. Interestingly, this benefit was additive to the already substantial intake of omega-3 fatty acids among the general Japanese population, a population with a fraction of the heart attacks found in western populations like the U.S. (approximately 3% over 5 years in Japanese compared to several-fold higher in a comparable American group).

While there may be genetic and other cultural and lifestyle reasons behind the dramatically reduced cardiovascular risk in Japanese, it is undeniably at least partially due to the increased intake of omega-3 fatty acids from fish. Incidentally, the purported benefits of omega-3 fatty acids provide a vigorous counter-argument to the idea that all humans should be vegetarians.

Anyway, if we were to take some lessons from the Japanese and their greater habitual intake of omega-3 fatty acids from fish, they might include:

--Rural and coastal Japanese are the sub-populations with the highest reliance on fish, about a quarter-pound a day. (Gives new meaning to the idea of a "Quarter Pounder," doesn't it?) This is at least five-times greater than the intake of an average American.

--Likewise, the blood level of omega-3s in the blood of Japanese is 5-fold higher than in Americans.

--The average intake of omega-3s (EPA + DHA) among a broadly-selected population of Japanese is 850 mg per day (320 mg EPA; 520 mg DHA). Intake ranges from 300 mg per day all the way up to 3100 mg per day.

--Greater omega-3 intake (EPA + DHA) is associated with lesser carotid intimal-medial thickness, an index of body-wide atherosclerosis.

--Japanese have far less heart attack and stroke despite greater prevalence of smoking (nearly half of Japanese) and drinking.

--Total fat intake (percent of calories) is nearly identical between Americans and Japanese. It's the proportion of fat calories from omega-3 that is greater, the proportion of omega-6 that is less in Japanese.

The Japanese eat their fish in ways that we do not: As sashimi (raw, as with sushi in its various forms like Nigiri and Chirashi); fried in tempura; shaved, dried fish sprinkled on about anything you can imagine (it's not as bad as it sounds); as a snack, as in dried cuttlefish (which you can purchase in packages as a portable, sweetened fish that you eat on-the-run--I know it sounds awful, but don't poke fun at it until you've tried it); in "soups" with soba noodles. Fish is commonly consumed with rice and soy sauce, as well as other soy-based foods, such as tofu, miso (soy bean paste), or natto.

I believe that there are some lessons to take from the Japanese and their fish-consuming habits:

1) An omega-3 fatty acid intake of at least 1000 mg per day yields measurable cardiovascular benefits.

2) Despite the fears over mercury and pesticide residues in fish, this seems to not have played out to be a real-life effect in the Japanese, who consume five-fold greater quantities of fish.

3) My mother was right after all when she encouraged us to eat more fish.

Drs. Iris Shai and colleagues released results of a new Israeli study, the Dietary Intervention Randomized Controlled Trial (DIRECT) Trial, that compared three different diet strategies. Of those tested, a low-carbohydrate diet was most successful at achieving weight loss.

You can find the full-text of the study on the New England Journal of Medicine website.

322 participants followed one of three diets over two year period. Compared head-to-head, the (mean) weight loss in each group was:

• 2.9 kg (6.4 lbs) for the low-fat group
• 4.4 kg (9.7 lbs) for the Mediterranean-diet group
• 4.7 kg (10.3 lbs) for the low-carbohydrate group

(Average age 52 years at start; average body-mass index, or BMI, 31.)

The conclusion was that the low-carb diet performed the best, with 60% greater weight loss, with the Mediterranean diet a close second.

The diets

The low-fat diet was based on the American Heart Association diet, with 30% of calories from fat (10% from saturated fat) and food choices weighted towards low-fat grains, vegetables, fruits, and legumes and limited additional fats, sweets, and high-fat snacks; calorie intake of 1500 kcal per day for women and 1800 kcal per day for men was encouraged.

The Mediterranean diet was a moderate-fat diet rich in vegetables, with reduced red meat, and poultry and fish replacing beef and lamb. Total calories from fat of 35% per day or less was the goal, with most fat calories from olive oil and a handful of nuts. Like the low-fat program, calories were limited to 1500 kcal per day for women, 1800 kcal per day for men.

The low-carbohydrate diet was patterned after the popular Atkins’ program, with 8% participants achieving the ketosis that Dr. Atkins’ advocated as evidence that a fat-burning metabolism was activated, rather than sugar-burning as fuel. For the 2-month “induction phase,” 20 grams of carbohydrates per day was set as the goal, followed by 120 grams per day once the weight goal was achieved. Unlike the other two diets, calories, protein and fat were unlimited.

Weight loss, lipids, inflammation

You can see from the weight loss graph that the low-carb approach exerted the most dramatic initial weight loss. Interestingly, much of the weight-loss benefit was lost as the carbohydrate intake increased, by study design, back to 120 mg per day. However, the other two diet approaches showed similar phenomena of “giving back” some of the initial weight loss.

The low-carbohydrate diet exerted the greatest change in cholesterol, or lipid, panels: increased HDL 8.4 mg/dl vs. 6.3 mg/dl on low-fat; the triglyceride response was the most dramatic, with a reduction of 23.7 mg/dl vs. 3.7 mg/dl on low-fat. Interestingly, the LDL cholesterol-reducing effect of all three diets was modest, with the most reduction achieved by the Mediteranean diet.

The inflammatory measure, C-reactive protein (CRP), was reduced most effectively by the low-carb and Mediterranean diets, least by the low-fat diet. HbA1c, a measure of long-term blood sugar, dropped significantly more on the low-carb diet.

When the final dietary composition was examined, interestingly, there really were only modest differences among the three diets, with 8% less calories from carbs, 8% greater calories from fat, comparing low-carb to low-fat, with Mediterranean intermediate.

Taken at face value, this useful exercise quite clearly shows that, from the perspective of weight loss and correction of metabolic parameters like triglycerides, HDL,CRP, and blood sugar, low-carbohydrate wins hands down, with Mediterranean diet a close second.

It also suggests that a return to a carbohydrate intake of 120 mg/day allows a partial return of initial weight lost, as well as deterioration of metabolic parameters after the initial positive changes.

Although the study has already received some criticism for such potential flaws as the modest number of Atkins’ followers achieving ketosis (8%), suggesting lax adherence, and the reintroduction of the 120 mg/day carbohydrate advice, I can suspect that these may have been compromises drawn to satisfy some Institutional Review Board. (Whenever a study is going to be conducted involving human subjects, a study needs to pass through the review of an Institutional Review Board, or IRB. IRB’s, while charged to protect human subjects from experimental abuses, also tend to be painfully conservative and will block a study or demand changes even if they are not dangerous, but just veer too far off the mainstream.)

However, several unanswered questions remain:

1) How would the diets have compared if the carbohydrate restriction were continued for a longer period, or even indefinitely? (The divergences would likely have been dramatic.)
2) Will low-carb exert the same cardiovascular event reduction that the Mediterranean approach has shown in the Lyon study and others?
3) Are there effects on health outside of the measures followed that differ among the three diets, such as cancer? (I doubt it, especially given the modest real differences over time. But this will be the objection raised by various "official" organizations.)

I would further propose that:

Low-fat diets are dead

The AHA will cling to their version of low-fat diet, based on difficulty in changing course for any large, consensus-driven organization, not to mention the substantial ($100’s of millions) revenues derived from endorsing low-fat manufactured products. The AHA will also point to the lack of difference in LDL cholesterol among the three, since they cannot get beyond the fact that there’s more to coronary risk—a lot more—than LDL.

Off-the-shelf diets achieve off-the-shelf results

If you just need a T-shirt, a medium might fit fine. But if you’d like a nicely fitting suit or dress, then tailoring to your individual proportions is needed. When aiming towards maximizing benefits on lipoproteins and coronary risk, none of these diets achieve the kinds of changes we often need for coronary plaque reversal, as in the Track Your Plaque program. That requires making dietary changes that exert maximal effects on lipoprotein patterns.

I came across a criticism of the Track Your Plaque program recently that suggested that it was nothing more than a program to sell CT heart scans.

Huh?

I suppose if you say that the Track Your Plaque program is nothing more than a way to sell heart disease prevention, omega-3 fatty acids from fish oil, vitamin D, better nutrition, and better identification of causes of heart disease . . . well, I believe that would be true.

But is the program a "front" to sell heart scans?

No, it is not, nor has it ever been.

I've heard about these peculiar suspicions about the program before. Though I've never taken them seriously, let me clear up any lingering uncertainty:

--I have no relationship with any heart scan center, scanning facility, or hospital other than to interpret heart scans.

I do not own a scanner, I have no financial interest in a scanner or scanning center, nor have I ever had any interest. I also have no plans to do so in the future. Let business people in the imaging business do that. I want no part of it. I have seen what these people go through and, frankly, I want no part of it, nor do I want the appearance that I am advocating scans to make money. I'm accused of trying to make money from scans even when I do not have any financial interest!

--I do not sell heart scans or imaging packages, nor have I ever done so.

You can't buy a scan through Track Your Plaque, The Heart Scan Blog, or through me. To me, heart scans are simply a measuring tool to identify the extent of coronary plaque, as well as a tracking tool to follow its course. Without it, there would be no Track Your Plaque. But there is also no alternative. The closest alternative would be carotid intimal-medial thickness, a technique, while useful, is a distant second choice to indirectly gauge coronary plaque by examining the thickness of the carotid lining (not carotid plaque). Perhaps in 10 years, a better measure to gauge and track coronary plaque will emerge that has superior aspects over CT heart scanning. If reasonable, safe, accessible, and quantitative, then Track Your Plaque may adopt that technology as its measuring tool.

Track Your Plaque is not about heart scanning; Track Your Plaque is about measuring and tracking plaque that, in 2008, is still best accomplished with CT heart scans.

--I make loads of money from heart scans and Track Your Plaque.

Yeah, right.

Track Your Plaque is a volunteer venture for my team; none of us get paid a penny for doing all we do, including me. We charge a membership fee on the website (somewhere around $6-7 a month) to pay our expenses, such as code writing for our proprietary software (much of it remains under development), printing costs, modest legal costs, the costs of doing business (e.g., accountant). Despite the fact that Track Your Plaque and the Heart Scan Blog occupies a substantial part of the day of the Track Your Plaque team, none of us are reimbursed for our time. I do believe, however, that this concept is so enormously powerful that it will, someday, pay us all enough to allow us to devote more time and effort to it.

Personally, I can't wait to devote more time and effort to this concept that is simple, logical, and effective. More research is needed, more development is needed, more discussion is needed. Right now, it is all accomplished outside of our busy schedules, including my full-time cardiology practice. I continue to have 7 am procedures, middle-of-the-night calls, weekend hospital rounds and emergencies (though virtually none of these are the patients involved in prevention, but the "other" people: atrial fibrillation, elderly heart failure patients, rhythm disorders, cardiomyopathies, pulmonary hypertension, peripheral vascular disease, the non-compliant).

--The book, Track Your Plaque, is a gimmick to sell you a heart scan.

No, it's a program that relies on this technology. But there's no special deal, no discounts, no steering to heart scan centers that I have a special arrangement with. No such thing exists, nor has there ever been such an arrangement.

I've heard it all. Early on, when I was helping my friend, Steve Burlingame and his wife, Nancy, set up Milwaukee Heart Scan, I helped by providing medical oversite, education of physicians and public, and interpreting heart scans. After all, in the "early days," nobody knew anything about heart scans. It was a long, hard climb against ignorance, habit, entrenched thinking, stubbornness, and stupidity. I've been paid next to nothing for all this. I told Steve long ago that, given the extraordinary expenses of maintaining an independent scanning center, that he should first pay his expenses, pay his technologists, receptionists, and nurse, pay himself, then pay me for reading scans if he had any money left over. Most of the time, Steve had nothing left over and I was paid nothing.

So, while some of my colleagues were assuming that I was rolling in money from "promoting" heart scans, the reality was that I was doing nearly everything for free. (It certainly wasn't the high life I was living; I don't drive a Mercedes, take fancy vacations, none of that. In fact, I work about 51 weeks a year.)

Why do I do this if it doesn't yield a big flow of money? Because I believe in it as a superior path to the conventional. If I were simply interested in making more money--I wouldn't do it. I would simply do what all my cardiology colleagues are doing: more heart catheterizations, more angioplasties and stents, learning how to do carotid stents, iliac stents, peripheral angioplasty, renal stents, acquiring the skills to put in defibrillators, new device insertion like umbrellas in the interatrial septum, etc. There's plenty more money in that. It's also not that hard. I know, because that is my background: high-risk cardiac interventions. That's what I was trained to do, that's what I did from a number years, until I started to see that this was nothing more than "putting out fires" in people who became increasingly ill and reliant on bail-out procedures. It makes lots of money, but it is also fundamentally wrong.

So, no, I do not sell heart scans, nor is the Track Your Plaque program or The Heart Scan Blog meant to promote heart scans except as a tool for tracking this disease.

That's it, pure and simple.

Which is more important: cholesterol or coronary plaque?

Ask what Dr. Michael Eades' calls "statinators," and you will likely receive a befuddled look. Or, you might receive comments like "Measuring plaque has never been shown to reduce mortality."

While risk factors for heart disease are important, no doubt (my office practice is about half lipid consultation and complex hyperlipidemia management), for many they have become an end in themselves. In other words, LDL cholesterol in particular dominates thinking so much that it has caused many to exclude the fact that plaque---coronary atherosclerotic plaque---is the disease itself.

Dozens of studies, from the St. Francis Heart Study to the 25,000-participant UCLA registry, to the recently-released MESA database (ethic differences, women, as well as superiority to carotid measures) have repeatedly shown that heart scan scores (coronary artery calcium scores) are superior to conventional risk factors (usually via the Framingham risk score) for predicting future heart attack and other events. And the differences are not minor incremental differences. The predictive power of plaque measurement via heart scanning is multiples better: 4 times, 10 times, 20 times or more in various subgroups.

Much of what we do in medicine is not based on long-term studies of outcome, pitting some diagnostic measure or treatment against placebo. It is already standard practice to measure plaque via heart catheterization, crudely via stress testing, and increasingly popular CT coronary angiography. None of these methods have been subjected to studies comparing testing vs. not testing in a large population, followed by some program of prevention to assess differences in mortality, heart attack, and other events.

Why should heart scan be held to such a standard?

Dr. Scott Grundy, lipid guru and one of the experts who sat on the Adult Treatment Panel-II for lipid management guidelines, recently stated [emphasis added]:

"Imaging has at least 3 virtues. It individualizes risk assessment beyond use of age, which is a less reliable surrogate for atherosclerosis burden; it provides an integrated assessment of the lifetime exposure to risk factors; and it identifies individuals who are susceptible to developing atherosclerosis beyond established risk factors. Also of importance, in the absence of detectable atherosclerosis, short-term risk appears to be very low."

Well said, and from a vocal statinator, to boot.

Sadly, Dr. Grundy goes on to say how plaque imaging can serve to better determine who will benefit from statin drug use.

Of course, you and I know that there is far more to reduction of cardiovascular risk applied to a framework of serial plaque quantification ("tracking plaque"!) than statin drugs. I doubt that a man as intelligent as Dr. Grundy truly believes this. I suspect that he is simply stating what he knows what will be published without resistance in the standard medical literature, trying to achieve a modest incremental success just by raising consciousness about heart scanning and plaque imaging: first things first.

Maybe next will be a plaque-tracking, or even a plaque-reducing, mainstream conversation, just like the one we've been conducting for the past four years.

Joe was a Track Your Plaque Success Story. With a starting heart scan score of 278, he dropped it 12 months later to 264, a 5% reduction. Though not a huge reduction, Joe's risk for a heart attack or other coronary event was virtually zero. I was very proud of Joe.

Among the culprit lipoprotein patterns that caused Joe's plaque was lipoprotein(a), or Lp(a). Niacin was therefore crucial to his program. It was among the principal reasons he dropped his heart scan score and reduced his risk for heart attack so dramatically.

Since he retired, Joe has been freewheeling around the country, traveling and having a great time. He consequently stopped thinking about his heart disease and Lp(a). He also tired of the occasional hot flushes he'd experienced with niacin. Though the flushes were promptly aborted by drinking two glasses of water, he simply didn't want to be bothered.

So when Joe saw this interesting and tantalizing "flush-free niacin" on the store shelf, he grabbed it.

Joe came back to the office. His blood pressure was 190/94, so high that he was having occasional chest pains from it (which can happen when something called "left ventricular diastolic dysfunction" develops from hypertension). His lipoprotein patterns were terrible, including a big upward jump in Lp(a) and drop in HDL. So I asked him to have another heart scan right away: Score 371, a 40% increase. In other words, his program went down the toilet.

Why?

Simple: Flush-free niacin. I've said it before (No flush = No effect and No flush niacin kills) and I'll say it again:

Flush-free or No-flush niacin is a complete, unadulterated, completely ineffective SCAM.

Flush-free or no-flush niacin is not a substitute for niacin. Joe is yet another example of how dangerous this scam can be. It turned one of our great success stories into a failure.

Please, please, please do not fall for this misleading and potentially dangerous scam product. While the product itself is not intrinsically dangerous, it denies you the benefits of the real thing: niacin.

Thankfully, the mistake in Joe's program was caught before a heart attack or other catastrophe. He did manage to pass a stress test, though with a flagrantly out-of-control blood pressure response. We'll get him back on track--but with niacin, the real thing.

As always, Dr. John Cannell of The Vitamin D Council continues to teach us new lessons about vitamin D.

Apparently, Dr. Cannell is swamped with the attention that vitamin D is drawing, largely due to his efforts to publicize the enormous deficiency of Americans and his great talent for articulating the science. The most current newsletter, while a bit haphazard, makes some excellent new points that I reprint here.

(I did not reprint his conversation about "any form of vitamin D" being acceptable. My experience differs: In nearly 1000 patients who have taken vitamin D supplements, my experience is that most tablet forms are inconsistently absorbed, sometimes not absorbed at all. I therefore advocate only use of gelcaps or liquids. I'm told by members of Track Your Plaque, however, that they are witnessing reliable increases in blood levels of vitamin D by taking the powdered form of Bio Tech Pharmacal's product.)

Does it matter what reference lab my doctor uses?

Yes, it might make a huge difference. A number of methods exist to measure 25(OH)D in commercial labs. The two most common are mass spectrometry and a chemiluminescence method, LIAISON. The first, mass spectrometry, is highly accurate in the hands of experienced technicians given enough time to do the test properly. However, in the hands of a normally trained technician at a commercial reference lab overwhelmed with 25(OH)D tests, it may give falsely elevated readings, that is, it tells you are OK when in fact you are vitamin D deficient. The second method, chemiluminescence, LIAISON, was recently developed and is the most accurate of the screening, high throughput, methods; LabCorp uses it. Quest Diagnostics reference lab uses mass spec. Again, both Quest and LabCorp are overwhelmed by 25(OH)D requests. The problem is that the faster the technicians do the mass spec test, the more inaccurate it is likely to be. If your 25(OH)D blood test says "Quest Diagnostics" on the top, do not believe you have an adequate level (> 50 ng/ml). You may or may not; the test may be falsely elevated. Let me give you an example. A doctor at my hospital had Quest Diagnostics do a 25(OH)D. It came back as 99 ng/ml of ergocalciferol. He is not taking ergocalciferol (D2), he has never taken ergocalciferol, only cholecalciferol, and he is not taking enough to get a level of 99 ng/ml, 50 ng/ml at the most. His email to Dr. Brett Holmquist at Quest about why Quest identified a substance he was not taking went unanswered other than to say "any friend of Dr. Cannell's is a friend of ours."

Long story short: if your lab report says "LabCorp" on the top, it is probably accurate; if it says Quest Diagnostic, it may be falsely elevated. While LabCorp has also been overwhelmed with 25(OH)D requests, the LIAISON method they use is relatively easy to do and does not rely on technician skill as much as the mass spec methods do. I'm not saying this because I'm a consultant for DiaSorin, who makes LIAISON, I'm saying it because it is true. If you don't believe me, get Quest to make me an offer to be their consultant at 10 times what DiaSorin is supposed to be paying me ($10,000 per year) and see how fast I turn Quest down. If Quest fixes their test, I'd love to consult. The ironic thing: I've made both Quest and LabCorp lots of money via this newsletter, the website, and by repeatedly telling the press that people need to know their 25(OH)D level, which has contributed to the skyrocketing sales of 25(OH)D blood tests.

Demand for vitamin D tests soars as nutrient's potential benefits touted.

Here you can help. Find out which labs in your town use Quest Diagnostics and which use LabCorp. Have a 25(OH)D test at both labs the same day (you will have to pay for them yourself). Then send both results to the Vitamin D Council address below. If Quest Diagnostics does not fix their 25(OH)D test, the Vitamin D Council will fix it for them.

My doctor prescribed Drisdol, 50,000 IU per week. What is it?

Drisdol is a prescription of 50,000 IU tablets of ergocalciferol or D2. Ergocalciferol is not vitamin D but it is similar. It is made by irradiating ergosterol, which is found in many living things, such as yeast. D2 is not normally found in humans and most studies show it does not raise 25(OH)D levels as well as human vitamin D (cholecalciferol or D3) does. However, Drisdol is a lot better than nothing. The best thing to do, if you are vitamin D deficient, and a human, is to take human vitamin D, cholecalciferol, A.K.A. vitamin D3.

What is the ideal level of 25(OH)D?

We don't know. However, thanks to Bruce Hollis, Robert Heaney, Neil Binkley, and others, we now know the minimal acceptable level. It is 50 ng/ml. In a recent study, Heaney et al enlarged on Bruce Hollis's seminal work by analyzing five studies in which both the parent compound, cholecalciferol, and 25(OH)D levels were measured. It turn out that the body does not reliably begin storing the parent compound (cholecalciferol) in fat and muscle tissue until 25(OH)D levels get above 50 ng/ml. The average person starts to store cholecalciferol at 40 ng/ml, but at 50 ng/ml, virtually everyone begins to store it for future use. That is, at levels below 50 ng/ml, the body is usually using up the vitamin D as fast as you make it or take it, indicating chronic substrate starvation, not a good thing.

Hollis BW, Wagner CL, Drezner MK, Binkley NC. Circulating vitamin D3 and 25-hydroxyvitamin D in humans: An important tool to define adequate nutritional vitamin D status. J Steroid Biochem Mol Biol. 2007 Mar;103(3-5):631-4.

Heaney RP, Armas LA, Shary JR, Bell NH, Binkley N, Hollis BW. 25-Hydroxylation of vitamin D3: relation to circulating vitamin D3 under various input conditions. Am J Clin Nutr. 2008 Jun;87(6):1738-42.

I have advanced renal failure and I'm on dialysis, how much vitamin D should I take?

The same as everyone else. Since I have told you about commercial labs ripping you off, let's add some drug companies. Patients with advanced renal failure need activated vitamin D or one of it's analogs, available by prescription. This is very important as their kidneys cannot make enough 1,25-dihydroxy-vitamin D (calcitriol) to maintain serum calcium. However, the rest of their tissues activate vitamin D just fine and when those tissues get enough, and when the kidneys get more vitamin D, the calcitriol spills out into the blood, lowering their need for prescription calcitriol or one of its analogs. The companies that make the analogs don't like that, it means reduced sales. So these companies do nothing, the scientists behind these companies say nothing, and renal failure patients die prematurely from one of the vitamin D deficiency diseases.

Vieth R. Vitamin D toxicity, policy, and science. J Bone Miner Res. 2007 Dec;22 Suppl 2:V64-8.

When I asked my doctor for a 25(OH)D blood test, he just laughed and said it was all idiotic. What can I do?

Help me unleash the dogs of war, the plaintiff attorneys. If you read about past nutritional epidemics caused by society, such as beriberi or pellagra, you will realize that education alone will take decades. Physicians successfully fought against the idea that thiamine deficiency caused beriberi for decades. However, things are different now. The agents of change in modern America, as obnoxious as they are, are plaintiff attorneys. Once the first malpractice lawsuits claiming undiagnosed and untreated vitamin D deficiency led to breast cancer, autism, heart disease, etc., get past summary judgment, and they will, and end up in front of a jury, and they will, things will change rapidly. One of the main reason physicians do what they do is fear of lawsuits. In a matter of months, arrogance and ignorance will give way to 25(OH)D tests and vitamin D supplementation.

Goodwin JS, Tangum MR. Battling quackery: attitudes about micronutrient supplements in American academic medicine. Arch Intern Med. 1998 Nov 9;158(20):2187-91.

And, to help support Dr. Cannell's efforts (I sent him a check for $250 a few months back; time for more), here is his contact info:

John Cannell, MD
The Vitamin D Council

Send your tax-deductible contributions to:

The Vitamin D Council
9100 San Gregorio Road
Atascadero, CA 93422

In 1910, taking a person's blood pressure was considered revolutionary, a high-tech practice that was of uncertain benefit.

Dr. Harvey Cushing of Johns Hopkins Hospital in Baltimore had observed a blood pressure device while traveling in Europe, developed by Dr. Sciopione Riva-Rocci. Cushing brought this new technology back with him to the U.S. and promptly promoted its use, convinced that this insight into gauging the forcefulness of blood pressure would yield useful clinical insights.

But, in 1910, practicing physicians rejected this new technology, preferring to use their well-established and widely practiced technique of pulse palpation (feeling the pulse), skeptical that the new tool added value. Medical practice of the day was rich with descriptions of the strength and character of the pulse: pulsus parvus et tardus (the slow rising pulse of aortic valve stenosis), the dicrotic notch of aortic valve closure transmitted to the pulse, the "water-hammer" pulse of aortic valve insufficiency.

Over the next 20 years, however, the medical community finally gave way to the new technique, although only physicians were allowed to use blood pressure devices, as nurses were regarded as incapable of mastering the skills required to perform the procedure properly.

Stethoscopes were also gaining in popularity in the early 20th century, but were also the exclusive province of physicians trained in their use. Nurses were not allowed to use stethoscopes until the 1960s. Even then, nurses were not allowed to call them "stethoscopes," but "nurse-o-scopes" or "assistoscopes," and the nurses' version of the device was manufactured to look different to avoid confusion with the "real" doctor's tool.

And just half a century ago, if you wanted to look at a medical textbook, you would have to go to the library and ask for special permission. The librarian would lower her glasses and look you up and down to determine whether or not you were some kind of pervert. Only then might you be granted permission to peer into the pictures of organs and naked bodies.

Such has been the spirit of medicine for centuries: Medicine and its practices are meant to be secret, the insider knowledge of a privileged few.

Fast forward to 2008: The Information Age has overturned the rules of privileged information. Now you have access to the same information as I do, the same information available to practicing physicians. The playing field has been levelled.

Curiously, while information access has advanced at an instantaneous digital pace, attitudes in medicine continue to evolve at the traditional analog crawl. Many of my colleagues continue to be dismayed at the new public access to health information, belittle patients for excessive curiosity about their health, lament the erosion of their healthcare-directing authority. And while new concepts race ahead as we race towards a wiki-like collective growth in healthcare knowledge, physicians are still mired by their reluctance to abdicate their once-lofty positions as chief holders of secrets.

I believe that this is part of the reason why family doctors and cardiologists have been slow to adopt technologies like heart scans and self-empowering programs like Track Your Plaque: processes that take heart disease prevention away from the hands of physicians and place more control into the hands of the people.

Imagine the horror felt by physicians in 1935 of a young upstart nurse boldly trying to use a stethoscope to take a patient's blood pressure. You can imagine the internal horror now being felt as you and I dare to take control over heart disease and deny them the chance to put in four stents, three bypass grafts, then direct our future health habits.

But technology has a way of marching on. It will encounter resistance, bumps, and blind-alleys, but it will go on.

Dr. Jeffrey Dach posted a great piece on his blog, Bioidentical Hormone Blog , about his perspective on the Track Your Plaque program.

It's worth reading even for those familiar with the program, just to see a slightly different perspective. He also included many great graphics to illustrate his points.

CAT Coronary Calcium Scoring, Reversing Heart Disease

Also, see Dr. Dach's Heart Disease: Part 2, for some novel thoughts.

As we age, we lose the capacity to activate vitamin D in the skin.

Studies suggest that, between ages 20 and 70, there is a 75% reduction in the ability to activate vitamin D. The capacity of conversion from 25 (OH) vitamin D to 1,25 di(OH) vitamin D also diminishes.

Holick M. Sunlight and vitamin D for bone health and prevention of autoimmune diseases, cancers, and cardiovascular disease.

From Holick, M. 2006

This would explain why 70-year olds come to the office, just back from the Caribbean sporting dark brown tans, are still deficient, often severely, in blood levels of vitamin D (25(OH) vitamin D). A tan does not equal vitamin D.

Courtesy Ipanemic

A practical way of looking at it is that anyone 40 years old or older has lost the majority of ability for vitamin D activation.

This often makes me wonder if the loss of vitamin D activating potential is nature's way to get rid of us. After all, after 40, we've pretty much had our opportunity to recreate and make our contribution to the species (at least in a primitive world in which humans evolved): we've exhausted our reproductive usefulness to the species.

Is the programmed decline of vitamin D skin activation a way to ensure that we develop diseases of senescence (aging)? The list of potential consequences of vitamin D deficiency includes: osteoporosis, poor balance and coordination, falls and fractures; cancer of the breast, bladder, colon, prostate, and blood; reductions in HDL, increases in triglycerides; increased inflammation (C-reactive protein, CRP); declining memory and mentation; coronary heart disease.

Isn't that also pretty much a list that describes aging?

A fascinating argument in support of this idea came from study from St Thomas’ Hospital and the London School of Medicine:

Higher serum vitamin D concentrations are associated with longer leukocyte telomere length in women

Telomeres are the "tails" of DNA that were formerly thought to be mistakes, just coding for nonsense. But more recent thinking has proposed that telomeres may provide a counting mechanism that shortens with aging and accelerates with stress and illness. This study suggests that both vitamin D and inflammation (CRP) impact telomere length: the lower the vitamin D, the shorter the telomere length, particularly when inflammation is greater.

Data supporting vitamin D's effects on preventing or treating cancer, osteoporosis, lipid abnormalities, inflammation, cardiovascular disease, etc., is developing rapidly.

Now the big question: If declining vitamin D is nature's way of ensuring our decline and death, does maintaining higher vitamin D also maintain youthfulness?

I don't have an answer, but it's a really intriguing idea.

Checking postprandial (after-eating) blood sugars yields extraordinary advantage in creating better diets for many people.

This idea has proven so powerful that I am running a previous Heart Scan Blog post on this practice to bring any newcomers up-to-date on this powerful way to improve diet, lose weight, reduce small LDL, reduce triglycerides, and reduce blood pressure.

To get low-carb right, you need to check blood sugars

Reducing your carbohydrate exposure, particularly to wheat, cornstarch, and sucrose (table sugar), helps with weight loss; reduction of triglycerides, small LDL, and c-reactive protein; increases HDL; reduces blood pressure. There should be no remaining doubt on these effects.

However, I am going to propose that you cannot truly get your low-carb diet right without checking blood sugars. Let me explain.

Carbohydrates are the dominant driver of blood sugar (glucose) after eating. But it's clear that we also obtain some wonderfully healthy nutrients from carbohydrate sources: Think anthocyanins from blueberries and pomegranates, vitamin C from citrus, and soluble fiber from beans. There are many good things in carbohydrate foods.

How do we weigh the need to reduce carbohydrates with their benefits?

Blood sugar after eating ("postprandial") is the best index of carbohydrate metabolism we have (not fasting blood sugar). It also provides an indirect gauge of small LDL. Checking your blood sugar (glucose) has become an easy and relatively inexpensive tool that just about anybody can incorporate into health habits. More often than not, it can also provide you with some unexpected insights about your response to diet.

If you’re not a diabetic, why bother checking blood sugar? New studies have documented the increased likelihood of cardiovascular events with increased postprandial blood sugars well below the ranges regarded as diabetic. A blood sugar level of 140 mg/dl after a meal carries 30-60% increased (relative) risk for heart attack and All posts by william-davis

Heart Scan Blog Redux: Cheers to flavonoids

13. November 2009 William Davis (32)

Because in Track Your Plaque we've been thinking a lot about anthocyanins, here's a rerun of a previous Heart Scan Blog post about red wine. (Anthocyanins are among the interesting flavonoids in red wine, along with resveratrol and quercetin.)

The case in favor of healthful flavonoids seems to grow bit by bit.

Flavonoids such as procyanadins in wine and chocolate, catechins in tea, and those in walnuts, pomegranates, and pycnogenol (pine bark extract) are suspected to block oxidation of LDL (preventing its entry into plaque), normalize abnormal endothelial constriction, and yield platelet-blocking effects (preventing blood clots).

Dr. Roger Corder is a prolific author of many scientific papers detailing his research into the flavonoids of foods, but wine in particular. He summarizes his findings in a recent book, The Red Wine Diet. Contrary to the obvious vying-for-prime-time title, Dr. Corder's compilation is probably the best mainstream discussion of flavonoids in foods and wines that I've come across. Although it would have been more entertaining if peppered with more wit and humans interest, given the topic, its straightfoward, semi-academic telling of the story makes his points effectively.

Among the important observations Corder makes is that regions of the world with the greatest longevity also correspond to regions with the highest procyanidin flavonoids in their wines.

Regarding the variable flavonoid content of wines, he states:

Although differences in the amount of procyanidins in red wine clearly occur because of the grape variety and the vineyard environment, the winemaker holds the key to what ends up in the bottle. The most important aspect of the winemaking process for ensuring high procyanidins in red wines is the contact time between the liquid and the grape seeds during fermentation when the alcohol concentration reaches about 6 percent. Depending on the fermentation temperature, it may be two to three days or more before this extraction process starts. Grape skins float and seeds sink, so the number of times they are pushed down and stirred into the fermenting wine also increases extraction of procyanidins. Even so, extraction is a slow process and, after fermentation is complete, many red wines are left to macerate with their seeds and skins for days or even weeks in order to extract all the color, flavor, and tannins. Wines that have a contact time of less than seven days will have a relatively low level of procyanidins. Wines with a contact time of ten to fourteen days have decent levels, and those with contact times of three weeks or more have the highest.

He points out that deeply-colored reds are more likely to be richer in procyanidins; mass-produced wines that are usually "house-grade" served at bars and restaurants tend to be low. Some are close to zero.

Wines rich in procyanidins provide several-fold more, such that a single glass can provide the same purported health benefit as several glasses of a procyanidin-poor wine.

So how do various wines stack up in procyanidin content? Here's an abbreviated list from his book:

Australian--tend to be low, except for Australian Cabernet Sauvignon which is moderate.

Chile--only Cabernet Sauvignon stands out, then only moderate in content.

France--Where to start? The French, of course, are the perennial masters of wine, and prolonged contact with skins and seeds is usually taken for granted in many varieties of wine. Each wine region (French wines are generally designated by region, not by variety of grape) can also vary widely in flavonoid content. Nonetheless, Bordeaux rate moderately; Burgundy low to moderate (except the village of Pommard); Languedoc-Roussillon moderate to high (and many great bargains in my experience, since these producers live in the shadow of its northern Bordeaux neighbors); Rhone (Cote du Rhone) moderate to high, though beware of their powerful "barnyard" character upon opening; decanting is wise.

Italy--Much red Italian wine is made from the Sangiovese grape and called variously Chianti, Valpolicella, and "super-Tuscan" when blended with other varietals. Corder rates the southern Italian wines from Sicily, Sardinia, and the mainland as high in procyanidins; most northern varieties are moderate.

Spain--Moderate in general.

United States--Though his comments are disappointingly scanty on the U.S., he points out that Cabernet Sauvignon is the standout for procyanidin content. He mentions only the Napa/Sonoma regions, unfortunately. (I'd like to know how the San Diego-Temecula and Virginian wines fare, for instance.)

The winner in procyanidin content is a variety grown in the Gers region of southwest France, a region with superior longevity of its residents. The wines here are made with the tannat grape within the Madiran appellation; wines labeled "Madiran" must contain 40% or more tannat to be so labeled (such is a quirk of French wine regulation). Among the producers Dr. Corder lists are Chateau de Sabazan, Chateau Saint-Go, Chateau du Bascou, Domaine Labranche Laffont, and Chateau d'Aydie. (A more complete list can be found in his book.)

How does this all figure into the Track Your Plaque program? Can you succeed without red wine? Of course you can. I doubt you could do it, however, without some attention to flavonoid-rich food sources, whether they come from spinach, tea, chocolate, beets, pomegranates, or red wine.

Though my wife and I love wine, I confess that I've never personally drank or even seen a French Madiran wine. Any wine afficionados with some advice?

Can wheat elimination cure ulcerative colitis?

13. November 2009 William Davis (0)

Tammy is a 36-year old mother of three young children. Since age 20, she has suffered with the debilitating symptoms of ulcerative colitis: constant, gnawing abdominal pain; frequent diarrhea, often bloody.

Tammy has had to take several medications, some with significant side-effects, all of which provided only partial relief from the pain and diarrhea. Her gastroenterologist and surgeon were planning a colectomy (removal of the colon) with creation of an ileostomy (rerouting of the small intestine to the abdominal surface, which would require Tammy to wear an ileostomy bag under her clothes for the rest of her life).

Although Tammy had previously tested negative for celiac disease (an allergic sensitivity to the gluten in wheat products), I urged her to attempt a trial of a wheat-free diet. Having witnessed many people experience relief from irritable bowel syndrome, acid reflux, and other common gastrointestinal complaints, all while trying to reduce blood sugar and small LDL, I'd hoped that Tammy would obtain at least some small improvement in her terrible symptoms.

I therefore urged Tammy to try it. After all, what was there to lose? Tammy grudgingly agreed.

She returned 6 months later. Her report: She had lost 38 lbs, virtually all of it within the first 6-8 weeks. Her diarrhea and cramping were not better, but gone. She was down to a single medicine from her former list of drugs.

I am unsure what proportion of people with ulcerative colitis or other inflammatory bowel diseases like Crohn's will experience a result like Tammy's. Perhaps it's only a minority. But I take this another piece of evidence that this enormously destructive thing called wheat has no place in the human diet.

We have no facts or figures on the prevalence of various forms of wheat intolerance in the U.S. When I contacted the Celiac Disease Foundation, they had no figures on the number of fatalities per year in the U.S. from celiac disease. But if there are 2-3 million Americans with celiac disease, there are probably 100 times that many people with various forms of wheat intolerance.

Postprandial pile-up with fructose

12. November 2009 William Davis (20)

Heart disease is likely caused in the after-eating, postprandial period. That's why the practice of grazing, eating many small meals throughout the day, can potentially increase heart disease risk. Eating often can lead to the phenomenon I call triglyceride and chylomicron "stacking," or the piling up of postprandial breakdown products in the blood stream.

Different fatty acid fractions generate different postprandial patterns. But so do different sugars. Fructose, in particular, is an especially potent agent that magnifies the postprandial patterns. (See Goodbye, fructose.)

Take a look at the graphs from the exhaustive University of California study by Stanhope et al, 2009:

From Stanhope KL et al, J Clin Invest 2009. Click on image to make larger.

The left graphs show the triglyceride effects of adding glucose-sweetened drinks (not sucrose) to the study participants' diets. The right graphs show the triglyceride effects of adding fructose-sweetened drinks.

Note that fructose causes enormous "stacking" of triglycerides, meaning that postprandial chylomicrons and VLDL particles are accumulating. (This study also showed a 4-fold greater increase in abdominal fat and 45% increase in small LDL particles with fructose.)

It means that low-fat salad dressings, sodas, ketchup, spaghetti sauce, and all the other foods made with high-fructose corn syrup not only make you fat, but also magnifies the severity of postprandial lipoprotein stacking, a phenomenon that leads to more atherosclerotic plaque.

Track Your Plaque: Safer at any score

11. November 2009 William Davis (0)

Imagine two people.

Tom is a 50-year old man. Tom's initial heart scan score was 500--a concerning score that carries a 5% risk for heart attack per year.

Harry is also 50 years old. His heart scan score is 100--also a concerning score, but not to the same degree as Tom's much higher score.

Tom follows the Track Your Plaque program. He achieves the 60:60:60 lipid targets; chooses healthy foods, including elimination of wheat; takes fish oil at a therapeutic dose; increase his blood vitamin D level to 60-70 ng/ml, etc. One year later, Tom's heart scan score is 400, representing a 20% reduction from his starting score.

Harry, on the other hand, doesn't understand the implications of his score. Neither does his doctor. He's casually provided a prescription for a cholesterol drug by his doctor, a brief admonition to follow a low-fat diet, and little else. One year later, Harry's heart scan score is 200, a doubling (100% increase) of the original score.

At this point, we're left with Tom having a score of 400, Harry with a score of 200. That is, Tom has twice Harry's score, 200 points higher. Who's better off?

Tom with the score of 400 is better off. Even though he has a significantly higher score, Tom's plaque is regressing. Tom's plaque is therefore quiescent with active components being extracted, inflammation subsiding, the artery in a more relaxed state, etc.

Harry's plaque, in contrast, is active and growing: inflammatory cells are abundant and producing enzymes that degrade supportive tissue, constrictive factors are released that cause the artery to pinch partially closed, fatty materials accumulate and trigger a cascade of abnormal responses.

So it's not just the score--the quantity of atherosclerotic plaque present--but the state of activity of the plaque: Is it growing, is it being reduced? Is there escalating or subsiding inflammation? Is plaque filled with degradative enzymes or quiescent?

Following the Track Your Plaque program therefore leads us to the notion that it's not the score that's most important; the most important thing is what you're doing about it. We sometimes say that Track Your Plaque makes you safer at any score.

Triglyceride and chylomicron "stacking"

10. November 2009 William Davis (24)

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

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

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

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

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

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

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

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

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

What is a healthy vitamin D blood level?

9. November 2009 William Davis (32)

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

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

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

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

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

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

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

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

Grazing is for cattle

5. November 2009 William Davis (17)

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

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

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

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

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

The disastrous results of a low-fat diet

4. November 2009 William Davis (16)

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

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

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

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

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

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

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

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

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

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

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

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

Dr. David Grimes reminds us of vitamin D

3. November 2009 William Davis (13)

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

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

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

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

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

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

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

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

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

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

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

David Grimes
www.vitamindandcholesterol.com

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

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

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

Why does fish oil reduce triglycerides?

2. November 2009 William Davis (9)

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

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

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

But why does fish oil reduce triglycerides?

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

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

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

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

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

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