Is there something fishy about fish oil?

27. January 2010 William Davis (0)

To be sure, there's plenty of misinformation out there about fish oil. Take a look at the swill that passes for health information on Woman's Day: On Call with Dr. Sandy: Fish Oil and Mercury:

Reader Question: My doctor recommended that I take a fish oil supplement, but I'm concerned about mercury. Is there any way to tell which brands are lowest in mercury content?

On Call Response: When it comes to OTC supplements, the answer is no. Though most fish oil supplements sold by major brands are probably safe, there's really no way to tell what's in the bottle or how much mercury it might contain.

Perhaps Dr. Sandy should read the many independent analyses performed on nutritional supplement fish oil, including those at Consumer Lab and Consumer Report before she offers her blind criticisms.

Lovaza vs fish oil supplements?

27. January 2010 William Davis (55)

Lovaza is the FDA-approved form of fish oil that is available only by prescription. It contains 842 mg of the omega-3 fatty acids, EPA and DHA, per capsule.

The FDA application for Lovaza is viewable here on the FDA website. Interestingly, while there is plenty of the usual regulatory gobbledy-gook about toxicology, dose escalation, and efficacy in the extensive documentation, there is little said about the issue of contamination.

In other words, critics of nutritional supplement fish oil harp on the possibility of contamination with mercury and pesticide residues, like dioxin and PCBs (polychlorinated biphenyls). Yet there is virtually nothing about these same issues in the FDA application for Lovaza.

Let's take a look at a sample over-the-counter fish oil product. Our friends at PharmaNutrients (a new Track Your Plaque partner for nutritional supplements) have a fish oil product called PharmaNutrients" Cardio. Here's an independent analysis of the Cardio product (per 1000 mg fish oil capsule):

EPA content: 566.1 mg
DHA content: 216.6 mg
(Total EPA + DHA 782.7 mg)

Cardio passed all tests for peroxides, PCBs, dioxin, furans, dioxin-like PCBs, and heavy metals (arsenic, cadmium, lead, mercury) using criteria at least 60% more stringent than European Commission (EC) standards (EC standard <2 picograms/gm for dioxins and furans, PharmaNutrients <1 picograms/gm; EC standard <10 picograms/gm for dioxin-like PCBs, PharmaNutrients <3 picograms/gm). PCBs levels in particular are less than 0.009 ppm, 90% below the industry-wide purity standard of 0.09 ppm. Likewise, mercury is >90% lower than European Commission standards.

In other words, this over-the-counter "pharmaceutical grade" fish oil has virtually nothing but omega-3 fatty acids.

Interestingly, the PharmaNutrients fish oil capsule also contains the third omega-3 fatty acid, docosapentaenoic acid (DPA), a neglected form that some authorities have proposed has superior cardiovascular protective properties over eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). If DPA is included in the analysis, PharmaNutrient's Cardio contains a total of 900 mg omega-3 fatty acids per capsule.

At some point, I'd like to see a head-to-head comparison not just on purity grounds, since I am convinced that high-quality products like Cardio can match or exceed the purity of prescription fish oil, but on efficacy in raising omega-3 blood levels, the omega-3 index. (The omega-3 index is a predictor of heart attack and sudden cardiac death--the higher, the better.) My prediction: High-quality fish oil supplements will match or exceed prescription fish oil.

More on blood sugar

25. January 2010 William Davis (36)

Take any of the following foods:

One chicken breast
Quarter-pound ground beef
6 oz salmon steak
½ cup raw almonds
3 eggs scrambled in olive oil

How much is blood sugar increased by any item in the above list?

If you said virtually zero, you’re correct. Eat any of these foods, regardless of portion size, and blood sugar won’t change substantially. If you started with a blood sugar of, say, 90 mg/dl, 1-2 hours later it would be 90 mg/dl. It might go up or even down a few milligrams, but for all practical purposes it remains substantially unchanged.

How much is blood sugar increased by the foods in this list:

2 slices multigrain bread
1 whole wheat bagel
4 oz high-fiber breakfast cereal
2 whole grain pancakes, 2 oz maple syrup

The foods in this list are a different story from the first. Depending on your body weight, exercise habits, and other factors, a typical blood sugar response in an otherwise healthy non-diabetic person would be 120 mg/dl to 160 mg/dl. In someone with diabetes, it could easily exceed 200 mg/dl.

That isn’t good. Large blood sugar excursions to 140 mg/dl have been clearly associated with greater risk for heart attack, progression to diabetes, inflammatory responses, and other adverse health effects. In fact, blood sugars as low as 100 mg/dl after eating have been associated with increased cardiovascular risk.

Then why are the USDA, American Heart Association, the American Dietetic Association, and the American Diabetes Association telling us to eat more of the foods that shoot blood sugar up to such high levels? “Eat more healthy whole grains”?

To see how much the issue of exaggerated blood sugars after eating applies to you, a simple blood sugar check 1-2 hours after eating can show you. Either your doctor can have the test drawn or you can purchase your own inexpensive glucose meter (e.g., Walmart, Wagreens).

My prediction: You will be very surprised at blood sugar responses after common foods, including “healthy whole grains.” And, by the way, keeping blood sugar excursions to a minimum will facilitate weight loss.

Postprandial blood sugar: Almonds vs. whole wheat bread

22. January 2010 William Davis (0)

Here's my postprandial (after-eating) blood glucose demonstration.

I tested raw almonds vs. 100% whole wheat bread, matched for calories. (Full nutritional composition below.)

Blood sugars:

Raw almonds

Start:

One-hour after eating:

2 slices 100% whole wheat bread

Start:

One-hour after eating:

100% whole wheat bread, 2 large slices

Water (g) 24.69

Energy (kcal) 158

Protein (g) 8.29

Fat, total (g) 2.14

Carbohydrate (g) 26.43

Sugars, total (g) 3.56

Fiber, total dietary (g) 4.4

Cholesterol (mg) 0

Saturated fatty acids, total (g) 0.478

Monounsaturated fatty acids, total (g) 1.022

Polyunsaturated fatty acids, total (g) 0.384

23 almonds, raw

Energy (kcal) 159

Protein (g) 5.86

Fat, total (g) 13.64

Carbohydrate (g) 5.98

Sugars, total (g) 1.07

Fiber, total dietary (g) 3.4

Cholesterol (mg) 0

Saturated fatty acids, total (g) 1.03

Monounsaturated fatty acids, total (g) 8.525

Polyunsaturated fatty acids, total (g) 3.331

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

19. January 2010 William Davis (60)

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 other events. The increase in risk begins at even lower levels, perhaps 110 mg/dl or lower after-eating.

We use a one-hour after eating blood sugar to gauge the effects of a meal. If, for instance, your dinner of baked chicken, asparagus brushed with olive oil, sauteed mushrooms, mashed potatoes, and a piece of Italian bread yields a one-hour blood sugar of 155 mg/dl, you know that something is wrong. (This is far more common than most people think.)

Doing this myself, I have been shocked at the times I've had an unexpectedly high blood sugar from seemingly "safe' foods, or when a store- or restaurant-bought meal had some concealed source of sugar or carbohydrate. (I recently had a restaurant meal of a turkey burger with cheese, mixed salad with balsamic vinegar dressing, along with a few bites of my wife's veggie omelet. Blood sugar one hour later: 127 mg/dl. I believe sugar added to the salad dressing was the culprit.)

You can now purchase your own blood glucose monitor at stores like Walmart and Walgreens for $10-20. You will also need to purchase the fingerstick lancets and test strips; the test strips are the most costly part of the picture, usually running $0.50 to $1.00 per test strip. But since people without diabetes check their blood sugar only occasionally, the cost of the test strips is, over time, modest. I've had several devices over the years, but my current favorite for ease-of-use is the LifeScan OneTouch UltraMini that cost me $18.99 at Walgreens.

Checking after-meal blood sugars is, in my view, a powerful means of managing diet when reducing carbohydrate exposure is your goal. It provides immediate feedback on the carbohydrate aspect of your diet, allowing you to adjust and tweak carbohydrate intake to your individual metabolism.

Food sources of vitamin K2: Reprint

19. January 2010 William Davis (59)

For some reason, my December, 2007, Heart Scan Blog post, Food sources of vitamin K2, has been receiving a lot of traffic.

I therefore reprint the vitamin K2 post below.

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

Family lessons

17. January 2010 William Davis (4)

Lou was recovering from his 3rd bypass operation. This third go-round left him weaker, slower, less quick on the rebound. In fact, he was lucky to have survived.

At 71 years old, Lou went a good 15 years since his second bypass, another 10 years prior to his first bypass at age 46.

In the days immediately following Lou's bypass, I had a chance to talk to his son, who stayed at his Dad's bedside while Lou struggled through post-op recovery.

"Did your Dad tell you about why this has happened, what caused his heart disease?" I asked.

"Sort of. He just said I should get checked," Lou's son, Aaron, replied.

"Did he mention the lipoprotein(a) pattern he has?"

"No. He never mentioned anything like that. He just said to get checked."

That's how it gets played out more often than not: Mom or Dad has a heart attack, stents, or (3rd) bypass, the children are told to get checked. Getting "checked" assumes that the doctor knows what to check for.

In Lou's case, the reason why he was in the hospital getting his 3rd (and final) bypass was lipoprotein(a), along with genetically-determined small LDL particles, low HDL, a postprandial (after-eating) disorder, hypertension, and borderline diabetes, not to mention vitamin D deficiency, omega-3 fatty acid deficiency, and marginal thyroid function. (Lou, a retired city employee, had showed only marginal interest in correcting these patterns. While he accepted medications, he proved unwilling to engage in the diet and nutritional supplement strategies required to correct his patterns.)

So Lou's 3rd bypass operation provided a moment of reflection for Aaron to ask: "Could I share the fate of my Dad?" With Lou's combination of genetic patterns, there was at least a 75% likelihood that he did. Sadly, going to his doctor would likely yield little more than a cholesterol panel, a question about smoking, and a prescription for Lipitor.

Just getting "checked" would be, more than likely, a recipe for disaster for Aaron: heart disease in his 40s or 50s. That's why you need to take control over this sad state of affairs and ask--no, insist--that an effort be made to determine whether you might share your parents' fate.

Look like Jimmy Stewart

15. January 2010 William Davis (23)

"This diet works great," Don declared. "But I think I've lost too much weight."

At 67 years old and 5 ft. 11 inches, Don began the program weighing 228 lbs (BMI 31.9). Because of high triglycerides, high blood sugar, high c-reactive protein, and excessive small LDL, I instructed Don to eliminate all wheat products from his diet, along with cornstarch and sweets. His intake of lean meats, eggs, vegetables, oils, raw nuts, etc. was unlimited.

Don now weighed 194 lbs, down 34 lbs over 6 months (BMI 27.1). Triglycerides, blood sugar, blood pressure, and well-being had improved dramatically; small LDL, however, had dropped only 30%--still room for improvement.

"My friends say I'm too skinny. They ask if I have cancer!"

I've heard this many times: Someone loses weight in a relatively short period of time and friends and family tell you you're too skinny. "It must be cancer. Nobody loses weight like that."

Unfortunately, many Americans have forgotten what normal looks like. Normal is certainly not a 190-lb, 5 ft 4 in woman, nor is it a 228 lb, 5 ft 11 inch man. But Americans have put on so much weight that the prevailing view of what constitutes "normal" weight has been revised upward. Normal is closer to what we see in old movies from the 1940s and '50s with people like Jimmy Stewart and Donna Reed. That's what we are supposed to look like.

So Don actually remains mildly overweight but is judged as "too skinny," or even cancer-ridden, by friends and family.

Ignore such comments. As you lose pounds and approach a truly desirable weight, realize that you are returning to the normal state, not the vision of "normal" now held by most Americans.

Getting vitamin D right

11. January 2010 William Davis (90)

Vitamin D is, without a doubt, the most incredible "vitamin"/prohormone/neurosteroid I have ever encountered. Frankly, I don't know how we got anything accomplished in health pre-D.

Unfortunately, people I meet rarely take their vitamin D in a way that accomplishes full restoration of vitamin D blood levels. It really isn't that tough.

Here's a list of common tripping points with vitamin D:

"I take vitamin D: 1000 units a day."
This is probably the most common mistake I see: Taking a dose that is unlikely to yield a desirable blood level. (We use 60-70 ng/ml of 25-hydroxy vitamin D as our target.) Most men and women require 6000 units per day to achieve this level. There is substantial individual variation, however, with an occasional person needing much more, a rare person requiring as little as 1000 units.

"I bought some vitamin D on sale. They were white tablets."
Time and again, patients in my office who initially have had successful vitamin D replacement, despite being reminded that only oil-based forms should be taken, switch to tablets. While they initially showed a 25-hydroxy vitamin D blood level, for instance, of 67 ng/ml on 8000 units per day with an oil-based capsule, they switch to a tablet form and the next blood level is 25 ng/ml. In other words, tablets are very poorly or erratically absorbed.

I have had people use tablets successfully, however, by taking their vitamin D tablets with a teaspoon of oil, e.g., olive oil. Oil is necessary for full absorption.

"I'm going to Florida. I'll stop my vitamin D because I'm going to lay in the sun."
Wrong. 90% of adults over 40 years old have lost the majority of their ability to activate vitamin D in the skin. A typical response might be an increase in blood level from 25 to 35 ng/ml--a 10 ng increase with a dark brown tan.

There is an occasional person who, with sun exposure, increases blood levels substantially. This can occur in both fair-skinned and dark-skinned people, though I've never seen it happen in an African-American person. The occasional person who maintains the ability to convert vitamin D with sun exposure, or young people, should seasonally adjust their vitamin D dose, e.g., 6000 units winter, 3000 units summer, or some other regimen that maintains desirable blood levels. You can see that monitoring blood levels (we check levels every 6 months for the first 2 years) is crucial: You cannot know what your vitamin D needs are unless you assess 25-hydroxy vitamin D levels.

"I drink plenty of milk. I don't think I need to take vitamin D."
Oh, boy. This is so wrong on so many levels.

First of all, no adult should be drinking plenty of cow's milk. (A discussion for another day.) Second of all, cow's milk averages 70 units of vitamin D, often the D2 form (ergocalciferol), per 8 oz. Even if the FDA-mandated 100 units per day were present, an average adult dose of 6000 units would require 60 glasses of milk per day. Can you say "diarrhea"?

Likewise, other food sources of vitamin D, such as fish (300-400 units per serving) and egg yolks (20 units per yolk), are inadequate. This makes sense: Humans are not meant to obtain vitamin D from food, but from sun exposure over a large body surface area. And this is a phenomenon that is meant to occur only in the youthful, ensuring that nature takes its course and us older folks get old and make way for the young (i.e., unless we intervene by taking vitamin D supplements).

"My doctor said that my vitamin D blood level was fine. It was 32 ng/ml."
Let's face it: By necessity, your overworked primary care physician, who manages gout, hip arthritis, migraine headaches, stomach aches, prostate enlargement, H1N1, depression, etc., is an amateur at nearly everything, expert in nothing. Nobody can do it all and get it right. Likewise vitamin D. The uncertain primary care physician will simply follow the dictates of the laboratory form that specifies "30-100 ng/ml" as the "normal" or "reference range." Unfortunately, the laboratory often quotes population distributions of a lab measure, not an ideal or desirable level.

To illustrate the folly of population distributions of a measure, imagine you and I want to know what women weigh. We go to a local mall and weigh several thousand women. We tally up the results and find that women weigh 172 lbs +/- 25 lbs (the mean +/- 2 standard deviations). (That's true, by the way.) Is that desirable? Of course it isn't. Population average or population distribution does not necessarily mean ideal or desirable.

"My husband's doctor said he should take 4000 units per day. So I just take the same dose."
That would be fine if all adults required the same dose. However, individual needs can vary enormously. A dose that is grossly insufficient for one person may be excessive for another. Once again, vitamin D dose needs can be individualized by assessing 25-hydroxy vitamin levels in the blood.

"I don't need to take vitamin D. I already take fish oil."
I suspect this mistaken belief occurs either because people confuse fish oil with cod liver oil, which does contain some vitamin D. (Cod liver oil is not the best source of vitamin D, mostly because of the vitamin A content; also a discussion for another time), or because they've heard that eating fish provides vitamin D. However, fish oil capsules do not contain vitamin D unless it is added, in which case it should be prominently and explicitly stated on the label.

"I don't have to take vitamin D. It's summer."
For most people I know, if it's a bright, sunny July day, where are they likely to be? In an office, store, or home--NOT lying in the sun with a large body surface area exposed. Also, most people expose no more than 5-10% of surface area in public. I doubt you cut the grass in a bathing suit. Because of modern indoor lifestyles and fashion, the majority of adults need vitamin D supplementation year-round.

I advise everyone that gelcap vitamin D is preferable. Some, though not all, liquid drop forms have also worked. Take a dose that yields desirable blood levels. And blood levels of 25-hydroxy vitamin D are ideally checked every 6 months: in summer and in winter to provide feedback on how much sun activation of D you obtain.

If your doctor is unwilling or unable to perform vitamin D testing, fingerstick vitamin D test kits can be obtained from Track Your Plaque.

Jimmy Moore's thyroid adventure

10. January 2010 William Davis (17)

My friend, Jimmy Moore of Living La Vida Low Carb, describes his thyroid experience here.

As Jimmy points out, he was looking for a way to jump-start a 50-lb weight loss. In my experience, low thyroid hormone levels ("hypothyroidism") are an exceptionally common cause for weight gain. Correcting even marginal hypothyroidism can facilitate weight loss, often resulting in 10 or more pounds of weight loss within the first month.

Unfortunately, Jimmy's thyroid hormone panel proved normal: TSH 1.3, thyroid hormones free T3 and free T4 in the mid- to upper-half of the reference range.

I say "unfortunately" because it is really an easy, inexpensive, and benign solution for losing weight. (I don't, of course, wish that Jimmy or anyone else develops a thyroid condition. But it really can provide gratifying weight loss results when thyroid function is low.) Jimmy might consider taking his oral temperature first thing in the morning as another means of assessing the adequacy of thyroid function.

Perhaps you will be luckier than Jimmy and have thyroid dysfunction that can be corrected and jump-start your weight loss program. Fingerstick thyroid test kits like the one Jimmy used are available here from Track Your Plaque.

All posts by william-davis

Dr. Cannell on vitamin D and cancer

2. December 2007 William Davis (0)

Here is Dr. John Cannell's Vitamin D Council Newsletter reprinted in its entirety. It answers some of the questions that came up on The Heart Scan Blog about the recent release of a study of vitamin D and cancer

The Vitamin D Newsletter

December, 2007

Does vitamin D prevent cancer? If it does, will doctors who ignore the research end up with blood on their hands? The press makes it easy for doctors to believe what they want to believe. Below are six stories about the same scientific study; read the six different headlines. According to your a priori beliefs, you can choose the story you want to believe and read that one. Don't feel bad, we all do it. As Walter Lippman once said, "We do not see and then believe, we believe and then we see."

Vitamin D cuts colon cancer death risk

Study Finds No Connection Between Vitamin D And Overall Cancer Deaths

Vitamin D protects against colorectal cancer

Vitamin D May Not Cut Cancer Deaths

Vitamin D protects against colorectal cancer

Scientists advise a vitamin D downgrade as there is no real proof ...

Another option is to read the study yourself.

Freedman DM, et al. Prospective Study of Serum Vitamin D and Cancer Mortality in the United States. J Natl Cancer Inst. 2007 Oct 30; [Epub ahead of print]

What Dr. Freedman actually discovered is that when you take a very large group of people (16,818), some as young as seventeen, measure their vitamin D levels, and then wait about ten years to see who dies from cancer, you find 536 die and that a vitamin D level from ten years earlier is not a good predictor of who will die from cancer. However, even a level drawn ten years earlier predicted that those with the lowest level were four times more likely to die from colon cancer, suggesting, as Ed Giovannucci has, that colon cancer may be exquisitely sensitive to vitamin D. Furthermore, 28 women got breast cancer, 20 in the group with the lowest vitamin D level but only 8 in the highest. The breast cancer findings were not statistically significant - even during a very long breast cancer awareness month - but can you imagine what critics at the American Cancer Society would be telling women if the numbers were reversed, if the 20 women who got breast cancer were in the high vitamin D group?

Another large epidemiological study appeared about breast cancer the very next day. This time, the press passed on the story and the American Cancer Society was mum, no editorials by Dr. Lichtenfeld, their spokesman, in spite of breast cancer awareness month.

Abbas S, et al. Serum 25-hydroxyvitamin D and risk of postmenopausal breast cancer - results of a large case-control study. Carcinogenesis. 2007 Oct 31; [Epub ahead of print]

In the above study, 1,394 women with breast cancer were case-controlled with a similar number of women without breast cancer. The women with breast cancer were three times more likely to have low vitamin D levels. That is a lot of women who may be dying during next year's breast cancer awareness month.

Both of the above studies were epidemiological, not randomized controlled trials. Of course a randomized controlled trial has already shown a 60% reduction in internal cancers in women taking even a modest 1,100 IU per day of vitamin D.

Lappe JM, et al. Vitamin D and calcium supplementation reduces cancer risk: results of a randomized trial. Am J Clin Nutr. 2007 Jun;85(6):1586-91.

What is interesting is the difference in the response of the Canadian Cancer Society and the American Cancer Society. The Canadian Cancer Society has advised all Canadians to take 1,000 IU per day - not enough but a good first step - and for immediate additional large scale clinical trials. The Canadians simply performed a risk/benefit analysis. What is the risk of treating vitamin D deficiency versus what are the potential benefits? They quote the American Food and Nutrition Board, which says 2,000 IU/day is safe for anyone over the age on one to take, on their own, without being under the care of a physician. If there is little or no risk, then the next question is what are the potential benefits of treating vitamin D deficiency? This is not quantum mechanics.

Cancer society calls for major vitamin D trial

The Canadians acted because the Canadian government knows it could save billions of dollars by treating vitamin D deficiency.

Vitamin D Deficiency Drains $9 billion From Canadian Health Care ...

If wide spread treatment of vitamin D deficiency became the rule, ask yourself, "Who would be helped and who would be hurt." First ask yourself that question about Canada and then about the USA. Remember, in Canada, the government directly pays for its citizen's health insurance; in the USA, private insurance is the norm. In Canada, the government is realizing they could save billions if vitamin D deficiencies were treated. In the USA, a large segment of the medical industry would be hurt, some anti-cancer drug manufacturers would have to close their doors, thousands of patents would become worthless, lucrative consulting contracts between industry and cancer researchers would dry up.

Both Canadians and Americans are shocked to think their doctors care about money, are in the illness business. In some ways people think of their doctors like they do their local public schools. They know medicine is a business and know doctors do things for money but they don't think their own doctors do. Likewise they think public schools are in bad shape but think their local schools are above average. They think their doctor is above average, like their "Lake Woebegone" kids.

Lake Woebegone Effect

The fact is that doctors, hospitals, regional cancer centers, and the cancer drug manufacturers are all in business to make money and all of these businesses make money off the sick, not off the well. Just a fact, but, as Aldous Huxley once observed, "Facts do not cease to exist because they are ignored."

Vitamin D will save the Canadian government enormous amounts of money but will cause widespread economic disruption in the USA. Do the physicians leading the American Cancer Society have strong economic ties to the cancer industry in the form of patents, stock options, and consulting fees? If so, what do you expect them to do? What would you do? It's simple. You would believe what you have to believe, what you need to believe, that is, anything with the word "vitamin" in it is simply the latest Laetrile. Look to Canada, not the USA, to lead the way.

Vitamin D may fight cancer

What about American physicians? They are apparently waiting for the American trial lawyers to smell a tort. After all, the case is quite simple. Doctor, did you advise Mrs. Jones to avoid the sun? Doctor, did you tell her the sun is the source of 90% of circulating stores of vitamin D? Doctor, did you prescribe vitamin D to make up for what the sun would not be making? Doctor, did you measure her vitamin D levels? So you had no way of knowing if your sun-avoidance advice resulted in vitamin D deficiency? Doctor, do you know our expert tested her vitamin D level and it was less than 20? Doctor, did you tell her about any of the studies indicating vitamin D deficiency causes cancer? Doctor, did you know Mrs. Jones has terminal breast cancer and will be leaving behind a loving husband and two young children?

And what about the American Cancer Society? Dr. Lichtenfeld, their spokesman, quickly gave his opinion; from what I can tell the first time he ever commented on a vitamin D study. That is, he has ignored the hundreds of positive epidemiological studies, ignored the incredible randomized controlled trial, but he jumped on this one:

Maybe Vitamin D Isn't The Answer After All

Dr. Lichtenfeld, implied the Canadian Cancer Society has acted precipitously in recommending that all Canadians take 1,000 IU of vitamin D daily. He implied that Americans should placidly wait until more randomized controlled trials, such as Lappe JM, et al (above), accumulate before they address their vitamin D deficiency. That is, nothing should be done until more randomized controlled trials prove vitamin D prevents cancer, one randomized controlled trial is not enough; epidemiological studies are not enough, animal studies are not enough, multiple anti-cancer mechanisms of action are not enough? If that is his position, I challenge him to point to one human randomized controlled trial that proves smoking is dangerous?

If he cannot, then he must admit that the American Cancer Society's position on smoking is entirely derived from epidemiological studies, animal studies, and a demonstrable mechanism of action, not on human randomized controlled trials? Vitamin D not only has hundreds of epidemiological studies, thousand of animal studies, and at least four anti-cancer mechanisms of action, vitamin D deficiency has something smoking does not have, it has a high quality randomized controlled trial. If future randomized controlled trials fail to show vitamin D prevents cancer - and Dr. Lichtenfeld better hope they do - he can have the satisfaction of saying "I told you so." If future randomized controlled trials confirm vitamin D prevents cancer, then he needs to look at his hands, the red he sees is the blood of needless cancer deaths.

John Cannell, MD

The Vitamin D Council

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Atascadero, CA 93422

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"Yes, Johnnie, there really is an Easter bunny"

30. November 2007 William Davis (13)

A Heart Scan Blog reader recently posted this comment:

You wouldn't believe the trouble I'm having trying to get someone to give me a CT Heart Scan without trying to talk me into a Coronary CTA [CT angiogram]. Every facility I've talked to keeps harping on the issue that calcium scoring only shows "hard" plaque...and not soft.

I also had a nurse today tell me that 30% of the people that end up needing a coronary catheterization had calcium scores of ZERO. That doesn't sound right to me. What determines whether or not someone needs a coronary catheterization anyway?

There was a time not long ago when I saw heart scan centers as the emerging champions of heart disease detection and prevention. Heart scans, after all, provided the only rational means to directly uncover hidden coronary plaque. They also offered a method of tracking progression--or regression--of coronary plaque. No other tool can do that. Carotid ultrasound (IMT)? Indirectly and imperfectly, since it measures thickening of the carotid artery lining, partially removed from the influences that create coronary atherosclerotic plaque. Cholesterol? A miserable failure for a whole host of reasons.

Then something happened. General Electric bought the developer and manufacturer of the electron-beam tomography CT scanner, Imatron. (Initial press releases were glowing: The Future of Electron Beam Tomography Looks Better than Ever.The new eSpeed C300 electron beam tomographic scanner features the industry’s fastest temporal resolution, and is now backed by the strength of GE Medical Systems. Imatron and GE have joined forces to provide comprehensive solutions for entrepreneurs and innovative medical practitioners.)

Within short order, GE scrapped the entire company and program, despite the development of an extraordinary device, the C-300, introduced in 2001, and the eSpeed, introduced in 2003, both yanked by GE. The C-300 and eSpeed were technological marvels, providing heart scans at incredible speed with minimal radiation.

Why would GE do such a thing, buy Imatron and its patent rights, along with the fabulous new eSpeed device, then dissolve the company that developed the technology and scrap the entire package?

Well, first of all they can afford to, whether or not the device represented a technological advancement. Second (and this is my reading-between-the-lines interpretation of the events), it was in their best financial interest. Not in the interest of the public's health, nor the technology of heart scanning, but they believed that focusing on the multi-detector technology to be more financially rewarding to GE.

GE, along with Toshiba, Siemens, and Philips, saw the dollar signs of big money with the innovations in multi-detector technology (MDCT). They began to envision a broader acceptance of these devices into mainstream practice with the technological improvements in CT angiography, a device (or several) in every hospital and major clinic.

Anyway, this represents a long and winding return to the original issue: How I once believed that heart scan centers would be champions of heart disease detection and reversal. This has, unfortunately, not proven to be true.

Yes, there are heart scan centers where you can obtain a heart scan and also connect with people and physicians who believe in prevention of this disease. I believe that Milwaukee Heart Scan is that way, as is Dr. Bill Blanchet's Front Range Preventive Imaging, Dr. Roger White's Holistica Hawaii, and Dr. John Rumberger's Princeton Longevity Center.

But the truth is that most heart scan centers have evolved into places that offer heart scans, but more as grudging lip service to the concept of early detection earned with sweat and tears by the early efforts of the heart scan centers. But the more financially rewarding offering of CT coronary angiograms, while a useful service when used properly, has corrupted the prevention and reversal equation. "Entry level" CT heart scans have been subverted in the quest for profit.

CT angiograms pay better: $1800-4000, compared to $100-500 for a heart scan (usually about $250). More importantly, who can resist the detection of a "suspicious" 50% blockage that might benefit from the "real" test, a heart catheterization? Can anyone honestly allow a 50% blockage to be without a stent?

CT angiograms not only yield more revenue, they also serve as an effective prelude to "downstream" revenue. By this equation, a CT angiogram easily becomes a $40,000 hospital procedure with a stent or two, or three, or occasionally a $100,000 bypass. Keep in mind that the majority of people who are persuaded that a simple heart scans are not good enough and would be better off with the "superior" test of CT angiography are asymptomatic--without symptoms of chest pain, breathelessness, etc. Thus, the argument is that people without symptoms, usually with normal stress tests, benefit from prophylactic revascularization procedures like stents and bypass.

There are no data whatsoever to support this practice. People who have no symptoms attributable to heart disease and have normal stress tests do NOT benefit from heart procedures like heart catheterization. They do, of course, benefit from asking why they have atherosclerotic plaque in the first place, followed by a preventive program to correct the causes.

So, beware: It is the heart scan I believe in, a technique involving low radiation and low revenue potential. CT angiograms are useful tests, but often offered for the wrong reasons. If we all keep in mind that the economics of testing more often than not determine what is being told to us, then it all makes sense. If you want a simple heart scan, just say so. No--insist on it.

Take trust out of the equation. Don't trust people in health care anymore than you'd trust the used car salesman with "a great deal."

Finally, in answer to the reader's last comment about 30% of people needing heart catheterizations having zero calcium scores, this is absolute unadulterated nonsense. I'm hoping that the nurse who said this was taken out of context. Her comments are, at best, misleading. That's why I conduct this Heart Scan Blog and our website, www.cureality.com. They are your unbiased sources of information on what is true, honest, and not tainted by the smell of lots of procedural revenue.

Diabetes: controlled or . . . cured?

28. November 2007 William Davis (37)

Russ had a beer belly, a big protuberant, hanging-over-the belt-on-top-of-skinny-legs sort of beer belly. Except he didn't get it from beer (only). Yes, he did drink beer, up to 3 or 4 per day on weekends, rarely during the week.

Russ got his "beer belly" from snack foods, processed foods, and yes, wheat products.

He came to my office for consultation for unexplained breathlessness. His primary care physician was stumped and asked for an opinion.

So, part of Russ' evaluation included laboratory work. Russ proved to have a blood sugar (glucose) of 136 mg/dl, well into the diabetic range. His insulin level was 102 microunits/ml, way above the desirable range of <10. I interpreted this to mean that Russ had early diabetes but still maintained vigorous pancreatic function, since the pancreas is the abdominal organ responsible for insulin production. In pre-diabetes and early diabetes, insulin levels can be high, reflecting the revved up output of the pancreas. However, the pancreas eventually "burns out," unable to keep up with the demand to product enormous quantities of insulin. That's when blood sugar skyrockets.

Along with the blood sugar and insulin, Russ showed all the expected markers of this syndrome (the "metabolic syndrome"): low HDL of 34 mg/dl, high triglycerides of 257 mg/dl, severe small LDL (80% of total LDL), high c-reactive protein, and high blood pressure.

A heart scan showed a surprisingly small amount of coronary plaque with a score of only 4. Thus, Russ' symptoms were unlikely to represent a coronary issue ("ischemia"). Breathlessness was far more likely to be from 1) his obesity and protuberant abdomen, large enough to encroach on his chest and lung volume, and 2) high blood pressure (which can, in turn, lead to high heart pressure and breathlessness, often called "left ventricular diastolic dysfunction").

I persuaded Russ to eliminate his previously flagrant and abundant over-reliance on wheat products and snack foods. Two months later, 15 lbs lighter, and a modestly less protuberant beer belly, Russ' laboratory evealuation showed:

--Blood sugar 90 mg/dl--normal.

--Insulin 12 microunit/ml--darn near normal.

Blood pressure was down 20 points. Russ' breathlessness was now entirely gone. He has another 30-40 lbs to go, but he's off to a great start. He is now clearly, solidly, and confidently NON-diabetic.

I see experiences like this every day, as do committed diabetes fighters like Jenny at Diabetes Update.

Why isn't this common practice? If pre-diabetes and diabetes can be cured by such a simple approach, why isn't it more widely embraced? After all, what other devastating diseases can claim to have such a simple, straightforward way to achieve cure?

And why does the American Diabetes Association (ADA) actually condone the inclusion of abundant carbohydrates in diabetics? Their modified food pyramid shows the widest part of the pyramid filled with "breads, grains, and other starches."

How about this question taken from a Q&A on the ADA website:

Can I eat foods with sugar in them?

For almost every person with diabetes, the answer is yes! Eating a piece of cake made with sugar will raise your blood glucose level. So will eating corn on the cob, a tomato sandwich, or lima beans. The truth is that sugar has gotten a bad reputation. People with diabetes can and do eat sugar. In your body, it becomes glucose, but so do the other foods mentioned above. With sugary foods, the rule is moderation. Eat too much, and 1) you'll send your blood glucose level up higher than you expected; 2) you'll fill up but without the nutrients that come with vegetables and grains; and 3) you'll gain weight. So, don't pass up a slice of birthday cake. Instead, eat a little less bread or potato, and replace it with the cake. Taking a brisk walk to burn some calories is also always helpful.

The answer is simple. Just as the American Heart Association focuses on ways to deliver the message of palliation, so does the ADA. So ADA diet advice is designed to help diabetics maintain a stable blood sugar on their medication. It is definitely not intended to reverse or eliminate diabetes. My patient Russ would be deep into diabetes on the ADA diet, enjoying his rolls, whole wheat bread, breakfast cereals, and birthday cake.

Once again, another example of the growing irrelevance of the "official" arbiters of health information for those of us looking for reversal of disease.

Study review: cerivastatin

27. November 2007 William Davis (10)

I'd like to start an occasional series of blog posts on The Heart Scan Blog in which I review studies relevant to the whole heart scan score reversal experience.

In a previous post, Don't be satisfied with "deceleration,"I discussed the BELLES Trial (Beyond Endorsed Lipid Lowering with EBT Scanning (BELLES)), in which either atorvastatin (Lipitor), 80 mg, or pravastatin (Pravachol),40 mg, was given to 615 women. Both groups showed an average of 15% annual plaque growth, regardless of which agent was taken and regardless of the amount of LDL cholesterol reduction.

I cited another study in which 471 participants received either Lipitor, 80 mg, or Lipitor, 10 mg. The rate of annual score increase was 25-27%, regardless of drug dose or LDL lowering.

Here's yet another study, a small German experience in 66 patients, with a curious design and using the now-defunct statin drug, cerivastatin (Bayccol, pulled in 2001, nearly simultaneous with the publication of this study, due to greater risk of muscle damage, particularly when used in combination with gemfibrozil). Achenbach et al in Influence of lipid-lowering therapy on the progression of coronary artery calcification: A prospective evaluation reported on this trial in which all participants underwent heart scanning to obtain a heart scan score; no treatment was initiated based on the score. A second scan was obtained after the no treatment period, followed by treatment with cerivastatin, 0.3 mg per day. A third scan was finally obtained.

In year one without treatment, the average increase in heart scan scores was 25%. In year two with cerivastatin, the average increase in heart scan score was 8.8%. In 32 participants who achieved LDL<100 mg/dl on the drug, there was an average modest reduction in heart scan scores of 3.7% (i.e., -3.7%).

Now, that was eye-opening. Why did this small study achieve such startlingly different results from the other two studies that showed relentless progression despite even high doses of Lipitor? That remains unanswered. Was cerivastatin unique among statins? Did the unique two-phase trial design somehow change the outcome by triggering participants to change lifestyle habits after their first scan (since most exhibited an increase in score; they were not "blinded" to their scores). Those questions will remain unanswered, since the drug has been made unavailable. This smal l study had actually been intended to be larger, but was prematurely terminated because of cerivastatin's withdrawal.

This experience is unique, as you can see, compared to the two other studies. But it was also smaller. The results are also different than what I have seen in day-to-day practice when I've seen people treated with statin drugs alone (not cerivastatin, of course): rarely do heart scan scores stop increasing. While slowing does usually occur (18-24% per year rates of annual score increase are very common in people who do nothing but take a statin drug and make modest lifestyle changes), I have personally seen only two people stop their score with this strategy alone. Nobody has ever dropped their score taking a statin alone, in my experience.

You can also see the nature of clinical studies: single or limited interventions instituted in order to control for unexpected or complex effects. If three different treatments are used, then what desirable or undesirable effects, or lack of an effect, is due to which treatment agent?

My experience is that no single treatment stops or reduces heart scan scores. It requires a more rational effort that includes 1) identification of all causes of coronary plaque (e.g., low HDL, high triglycerides, Lp(a), small LDL, deficiency of vitamin D, etc, none of which are substantially affected by statin drugs), and 2) correction of all causes. That simple concept has served us well.

Dr. William Blanchet: A voice of reason

24. November 2007 William Davis (21)

I don't mean to beat this discussion to a pulp, but looking back over the comments posted on www.theHeart.org forum, I am so deeply impressed with Dr. William Blanchet's grasp of the issues, that I posted his articulate and knowledgeable comments again.

Here is one post in which Dr. Blanchet, in response to accusations of trying to profit from heart scans, provides a wonderful summary of the logic and evidence behind the use of heart scans as the basis for heart disease prevention.

Yes, I have seen a dramatic reduction in coronary events.

Of 6,000 active patients, 48% being Medicare age and over, I have seen 4 heart attacks over the last 3+ years. 2 in 85 year old diabetics undergoing cancer surgery, one in a 90 year old with known disease and one in a 69 year old with no risk factors, who was healthy, and had never benefited from a heart scan.

The problem with coronary disease is that we rely on risk factors. Khot et al in JAMA 2003 showed that of 87,000 men with heart attacks, 62% had 0 or 1 major risk factor prior to their MI. According to ATP-III, almost everyone with 0-1 risk factors is low risk and most do not qualify for preventive treatment. EBT calcium imaging could identify 98% of these individuals as being at risk before their heart attack and treatment could be initiated to prevent their MI.

Treating to NCEP cholesterol goals prevents 30-40% of heart attacks. Treating to a goal of coronary calcium stability prevents 90% of heart attacks. Where I went to school, a 40% was an F. Why are we defending this result instead of striving to improve upon it? I am not making this up, look at Raggi's study in Arteriosclerosis, Thrombosis, and Vascular Biology 2004;24:1272, or Budoff Am J Card.[I believe it's the study Dr. Blanchet was referring to.]

I strongly disagree with the assertion that the stress test is a great risk stratifier. Laukkanen et al JACC 2001 studied 1,769 asymptomatic men with stress tests. Although failing the stress test resulted in an increased risk of future heart attack, 83% of the total heart attacks over the next 10 years occurred in those men who passed the stress test. Falk E, Shah PK, Fuster V Circulation 1995;92:657-671 demonstrated that 86% of heart attacks occur in vessels with less than 70% as the maximum obstruction. A vast majority of
patients with less than 70% vessel obstruction will pass their stress test.

Regarding [the] question of owning or referring for EBT imaging, I would be amused if it were not insulting. The mistake that is often made is that EBT imaging is a wildly profitable technology. It is not nearly as profitable as nuclear stress imaging. Indeed there are few EBT centers in the country that are as profitable as any random cardiologist's stress lab.

How can we justify not screening asymptomatic patients? Most heart attacks occur in patients with no prior symptoms and according to Steve Nissen, 150,000 Americans die each year from their first symptom of heart disease. My daughter is at this moment visiting with a friend who lost her father a few years ago to his first symptom of heart disease when she was 8 years old. That is not OK! We screen asymptomatic women for breast cancer risk. Women are 8 times more likely to die from heart disease than breast cancer. We do mass screening for colon cancer and we are over 10 times more likely to die from heart attacks than colon cancer. An EBT heart scan costs 1/8th the cost of a colonoscopy.

So what say we drop the sarcasm and look at this technology objectively. Read the literature, not just the editorial comments. This really does provide incredibly valuable information that saves lives.

Yes, a 90% reduction in heart attacks in my patients compared to the care I could provide 5 years ago when I was doing a lot of stress testing and referring for revascularization. Much better statistics than expected national or regional norms. I welcome your scrutiny.

That's probably the best, most concise summary of why heart scanning makes sense that I've ever heard. And it comes from a primary care physician in the trenches. With just a few paragraphs, Dr. Blanchet, in my view, handily trumps the arguments of my colleagues arguing to maintain the status quo of cholesterol testing, stress tests, and hospital procedures.

Note:
Dr. Blanchett talks openly about his affiliation with an imaging center in Boulder, Colorado, Front Range Preventive Imaging. I'm no stranger to the accusations Dr. Blanchet receives about trying to profit from the heart scan phenomenon. Ironically, heart scanning loses money. It is a preventive test, not a therapeutic, hospital-based procedure. Free-standing heart scan centers that do little else (perhaps virtual colonoscopies) usually manage to pay their bills but make little profit. Hospitals that offer heart scans usually do so as a "loss-leader," i.e., an inexpensive test that brings you in the door in the hopes that you will require more testing.

Accusations of profiteering off heart scans are, to those in the know, ridiculous and baseless. On the contrary, heart scans are both cost-saving and life-saving.

Vitamin D2 rip-offs

23. November 2007 William Davis (21)

Here's a sampling of prescription vitamin D2/ergocalciferol products available:

Prescription ergocalciferol (vitamin D2) (Drisdol brand), 50 caps for $130.84.

Alfcip brand of erogocalciferol (vitamin D), 30 capsules for $28.20.

Ergocalciferol (vitamin D2) as Drisdol oral solution, 1 bottle $146.26.

How about vitamin D3/cholecalciferol?

Carlson's brand cholecalciferol (vitamin D3), 120 capsules $5.09.

Cholecalciferol, vitamin D3, is far less expensive than ergocalciferol, vitamin D2. Cholecalciferol is available as a supplement without prescription. Ergocalciferol is available only by prescription.

The price difference must mean that the plant-based form, ergocalciferol, must be far superior to the naturally-occurring human form, vitamin D3.

Of course, that's not true. Dr. Robert Heaney's study is just one of several documenting the inferiority of D2/ergocalciferol, Vitamin D2 Is Much Less Effective than Vitamin D3 in Humans. D2 exerted less than a third of the effect of D3.

In my experience, D2/ergocalciferol often exerts no effect whatsoever. One woman I consulted on came into the office having been prescribed Drisdol capsules, 50,000 units every day for the past 18 months (by mistake by her physician). Blood level of active 25-OH-vitamin D3: Zero.

But the pharmacy and drug manufacturer collected $1413 for her 18-month course. Cost for a 4000 unit per day dose of D3/cholecalciferol: $45--and it would have actually worked.

In my view, prescription vitamin D2 is yet another example of drug manufacturer scams, a product that provides no advantages, costs more, but yields bigger profits.

Yet this wonderful supplement called cholecalciferol, among which Carlson's is an excellent choice, is available to you inexpensively, without prescription, and actually provides the benefits you desire.

Stenosis detection vs. plaque detection

22. November 2007 William Davis (5)

One of the most common misunderstandings encountered by both physicians and the public is that, to create an effective heart disease prevention program, we need tools for atherosclerotic plaque detection. What we do not need is a tool for stenosis detection. (Stenosis means percent blockage. A 50% stenosis means 50% of the diameter of an artery is reduced by atherosclerosis.)

This issue came to mind recently with the ongoing conversation at Heart.org forum, in which the conversation predictably degenerated into a "what good are heart scans when there are better tests to detect blockage" sort of mentality.
They are right: There are better tests to detect stenoses or blockages, such as stress tests, heart catheterization, and CT coronary angiography. If someone is having chest pain or breathlessness, these tests are useful to help understand why. These tests are preludes to stents, bypass surgery, and the like. They are the popular tools in hospitals, the ones that provide entry into the revenue-yielding world of heart disease procedures.

Plaque detection, on the other hand, is principally a tool for the person without symptoms. In this regard, it is more like cholesterol testing. I doubt my colleagues would bash cholesterol because it doesn't reveal blockages. Plaque detection identifies the person who has already started developing atherosclerosis.

Dr. William Blanchett of Colorado articulates this idea well:

EBT calcium imaging not only identifies the vast majority of individuals at risk, it also identifies individuals with minimal risk. In other words, it distinguishes those who are likely to benefit from treatment . . .and it identifies those unlikely to benefit from treatment. Furthermore, the greatest value of EBT calcium imaging is that with serial imaging you can determine who is and who is not responding to treatment.

Those patients not responding to the initial treatment are identified by progression of their calcified plaque on a subsequent scan are then placed on additional therapies. The net result is a remarkable reduction in heart attack rates.

Ahh, the voice of reason. Plaque detection empowers you in your prevention program. If you know how much plaque your begin with, you can track that value to know whether you have having a full effect or not. Stenosis detection, on the other hand, empowers your doctor and provides the irresistible impulse to stent.

Another common objection raised to plaque detection is "why bother if you're going to give everybody a statin anyway?" We know the origins of that argument, don't we? If the only strategy known to your doctor is cholesterol reduction with statin drugs, then perhaps that's right. But, with awareness of all the things that go beyond statin drugs, often make them unnecessary, then knowledge of who should engage in an intensive program of prevention or not is enabled by plaque detection.

Is an increase in heart scan score GOOD?

20. November 2007 William Davis (30)

In response to an earlier Heart Scan Blog post, I don't care about hard plaque!, reader Dave responded:

Hello Dr Davis,

Interesting post about hard and soft plaque. I recently had a discussion with my GP regarding my serious increase in scan score (Jan 2006 = 235, Nov 2007 = 419).

After the first scan we started aggressively going after my LDL, HDL and Trig...196,59,221

And have them down to 103, 65, 92 - we still have a way to go to 60/60/60 [The Track Your Plaque target values]-

So the increase is a surprise, but my doctor said that the increase could in part be cause some of the soft plaque had been converted to hard plaque and the scan would show that conversion.

Dave's doctor then responded to him with this comment:

"Remember that although your coronary calcium score has gone up, this does not mean that you are at greater risk than you were a year ago. Remember that the most dangerous plaque is the not-yet calcified soft plaque, which will not show up on an EBT [i.e., calcium score]. It is only the safe, calcified plaque that can be measured with the EBT. [Emphasis mine.] For your score to go up like it did, while your lipids came down so much, what had to happen was that lots of dangerous unstable plaque was converted to stable, calcified plaque. There are no accepted guidelines for interpreting changes in calcium scores over time, because the scores tend to go up as treatment converts dangerous plaque to safer plaque. We do know that aggressively lowering LDL reduces both unstable and stable plaque, and we know that risk can be further lowered by adjuvant therapy such as I listed above."

Huh?

This bit of conventional "wisdom" is something I've heard repeated many times. Is it true?

It is absolutely NOT true. In fact, the opposite is true: Dave's substantial increase in heart scan score from 235 to 419 over 22 months, representing a 78% increase, or an annualized rate of increase of 37%. This suggests a large increase in his risk for heart attack, not a decrease. Big difference!

Dr. Paulo Raggi's 2004 study, Progression of coronary artery calcium and risk of first myocardial infarction in patients receiving cholesterol-lowering therapy in 495 participants addresses this question especially well. Two heart scans were performed three years apart, with a statin drug initiated after the first scan, regardless of score.

During the period of study, heart attacks occurred in 41 participants. When these participants were analyzed, it was found that the average annual increase in score over the three year period was 42%. The average annual rate of increase in those free of heart attack was 17%. The group with the 42% annual rate of increase--all on statin drugs--the risk of heart attack was 17.2-fold greater, or 1720%.

The report made several other important observations:

--20% of the heart attack-free participants showed reduction of heart scan scores, i.e., reversal. None of the participants experiencing heart attack had a score reduction.
--Only 2 of the 41 heart attacks occurred in participants with <15% per year annual growth, while the rest (39) showed larger increases.
--The intensity of LDL reduction made no difference in whether heart attacks occurred or not. Those with LDL<100 mg/dl fared no better than those with LDL>100 mg/dl.

Dr. Raggi et al concluded:

"The risk of hard events [heart attack] was significantly higher in the presence of CVS [calcium volume score] progression despite low LDL serum levels, although the interaction of CVS change and LDL level on treatment was highly significant. The latter observation strongly suggests that a combination of serum markers and vascular markers [emphasis mine] may constitute a better way to gauge therapeutic effectiveness than isolated measurement of lipid levels."

This study demonstrates an important principle: Rising heart scan scores signal potential danger, regardless of LDL cholesterol treatment. Yes, LDL reduction does achieve a modest reduction in heart attack, but it does not eliminate them--not even close.

These are among the reasons that, in the Track Your Plaque program, we aim to correct more than LDL cholesterol. We aim to correct ALL causes of coronary plaque, factors that can be responsible for continuing increase in heart scan score despite favorable LDL cholesterol values.

So, Dave, please forgive your doctor his misunderstanding of the increase in your heart scan score. He is not alone in his ignorance of the data and parroting of the mainstream mis-information popular among the statin-is-the-answer-to-everything set.

Just don't let your doctor's ignorance permit the heart attack that is clearly in the stars. Take preventive action now.

The Heart.org online debate

20. November 2007 William Davis (9)

There's a fascinating and vigorous debate going on at the Heart.org website among Dr. Melissa Shirley-Walton, the recently publicized proponent of "a cath lab on every corner": Dr. William Blanchet, a physician in northern Colorado; and a Track Your Plaque Member who calls himself John Q. Public.

John Q. has been trying to educate the docs about the Track Your Plaque program. Unfortunately, Dr. Shirley-Walton essentially pooh-poohs his comments, preferring to lament her heavy work load. In her last post, when she discovered that John Q. was not a physician, she threatened to block his posts and delete all prior posts.

However, Dr. Blanchet has emerged as a champion of heart scanning, intensive lipid management, and lipoproteins, much similar to our program. In fact, many of Dr. Blanchet's comments were so similar to mine that John Q. asked me if it was really me! (It is definitely not.)

Here's a sampling of some of the discussion going on now:

Dr. Blanchett started out the discussion by saying:

Stent Insanity
I have no trouble agreeing with the argument that we have initiated the widespread use of DES without adequate study regarding outcomes. Shame on us.

That said, we are ingoring the DATA that shows that most heart attacks occur as a result of non-obstructing plaque and all the talk about which stent to use ignors the majority of individuals at risk. In addition, for a decade we have known that stenting does not improve net outcomes anyway.

What ever happened to effective primary prevention? We discarded EBT calcium imaging like moldy cabbage without even looking at the outcomes DATA. With direction provided by EBT calcium imaging and effective primary prevention, I have been able to reduce myocardial infarction by 90% in my very large Internal Medicine practice. Through effectively identifying patients at risk and measuring success or failure of treatment with serial EBT, I have made the argument as to which stent to use moot. No symptomatic angina and rare infracts equals little need for any stent.

Is anybody listening? Certainly not the cardiologists whose wealth and fortunes are based on nuclaer imaging, angiography and stenting.

Dr. Shirley-Walton, skeptical of Dr. Blanchet's claim of >90% reduction of heart attacks using a prevention program starting with a heart scan:

To rely soley upon a calcium score will deprive you of a lot of information that could be otherwise helpful in the management of your patients.

Without seeming sarcastic, I must refute : "of 6,000 patients I've seen 4 heart attacks in 3 years". Although I certainly hope your statistics are accurate, I will suggest the following:

You've not seen all of the heart attacks since up to 30% of all heart attacks are clinically silent. So unless you are echo'ing or nuclear testing all of these patients in close followup, you aren't certain of your stats.

Secondly, in order to attribute this success to your therapy, you would have to have nearly 100% compliance. In the general population, compliance is often less than 50% with any regimen in any given year of treatment. If you can tell us how you've achieved this level of compliance, we could all take a lesson.

Dr. Blanchett, commenting on his use of heart scanning as a primary care physician:

CAC [coronary artery calcium] is an inexpensive and low radiation exam to identify who is at increased risk for heart attacks.

A study of 222 non-diabetic patients admitted with their first MI found 75% of them did not qualify for cholesterol modifying therapy prior to their initial MI (JACC 2003:41 1475-9). In another study of 87,000 men with heart attacks, 62% had 0 or 1 major risk factors (Khot, et al. JAMA. 2003). Almost all individuals with 0 or 1 risk factor are Framingham "Low risk" and therefore will not qualify for cholesterol lowering therapies. (JAMA. 2001;285:2486-2497)

Risk factors alone are not sufficient. In my practice, of the last 4 patients who have died from heart attacks, none qualified for preventive therapies by NCEP guidelines.

Studies have shown that CAC by EBT provides an independent and incremental predictor of heart attack risk. (1. Kondos et al, Circulation 2003;107:2571-2176, 2. Am Heart J 141. 378-382, 2001, 3. St Francis Heart Study Journal of the American College of Cardiology July, 2005) The old saw that CAC simply reflects risk factors and age is just wrong.

Although CT angiography shows great promise to reduce unnecessary conventional angiography and is helpful in emergency room chest pain evaluation, I do not see CT angiography as a screening study in asymptomatic individuals. 10 times more radiation than EBT calcium imaging plus the risk of IV dye exposure makes CT angiography inconsistent with the principles of a screening test. Taken in the context of a primary care physician's evaluation of heart attack risk, EBT calcium imaging has great value.

Coronary calcium changes management by: 1. Identifying those at risk who do not show up with standard risk stratification (St Francis Heart Study: Journal of the American College of Cardiology July, 2005). 2. Motivating patients to be compliant with therapies (Atherosclerosis 2006; 185:394-399). 3. By measuring serial calcium, we can see who is and who is not responding to our initial treatment so that we can further refine our therapeutic goals (Atherosclerosis, 2004;24:1272).

When used in the primary care preventive setting, CAC imaging is indeed of great incremental value. In my practice, in improves my outcomes so greatly that it compels Melissa Walton-Shirley to question my veracity.

Dr. Melissa Walton-Shirley:

Ahhhhhh.......the aroma of profit making, I thought I smelled it. [Accusing Dr. Blanchett of referring patients for heart scans for personal profit.]

I will tell you that I was a little hurt when I was called "a typical cardiologist with a butcher block mentality" after my primary pci piece for med-gen Med was reviewed by the track your placque [sic] folks.

Though, it's clear that they misunderstood and thought I was cathing for dollars, instead my intention was to "push" for primary PCI for AMI, it left me seething until the blessing of a busy schedule and a forgetful post menopausal brain took its toll.
None the less, an honest open discussion is always welcome here but I would appreciate it if everyone would just divulge their affiliations up front so that the context of their opinions could be better understood.

I also insist that the compliance described by you William B. is rather astounding and a bit unbelieveable, however if it's accurate, you are to be congratulated.

Dr. Blanchett, in response to Dr. Shirley-Walton's statement that she relies on stress testing:

I think that the threshold of comfort you get from stress test stratification is different than what I consider acceptable. It is hard for me to tell a bereaved spouse that the departed did everything I suggested and still died from a MI. Coronary calcium imaging provides me the tool that I need.

Are you aware that there are a number of studies that show a dramatic increase in risk of MI in individuals with an annualized increase in calcified plaque burden of >14%? I consider this to be a valuable measure of inadequacy of medical management. A stress test does not become positive until we have catastrophically failed in medical management. Consequently, even in the patient with “high risk” stratification, one can justify a calcium score to establish a baseline to measure adequacy of primary prevention. Calcium scores by EBT cost about 1/5th the cost of a nuclear stress test and subject the patient to 1/10th the radiation of nuclear imaging and provides more precise information.

Regarding John Q, I do not think that non-medical prospective should be excluded from this blog. I think we as physicians benefit from hearing how the non-physician public views medicine. I have become much better at what I do by listening to my patients and learning from them.

Dr. Blanchett continues:

Yes, I have seen a dramatic reduction in coronary events. Of 6,000 active patients, 48% being Medicare age and over, I have seen 4 heart attacks over the last 3+ years. 2 in 85 year old diabetics undergoing cancer surgery, one in a 90 year old with known disease and one in a 69 year old with no risk factors, who was healthy, and had never benefited from a heart scan.

The problem with coronary disease is that we rely on risk factors. Khot et al in JAMA 2003 showed that of 87,000 men with heart attacks, 62% had 0 or 1 major risk factor prior to their MI. According to ATP-III, almost everyone with 0-1 risk facto is low risk and most are do not qualify for preventive treatment. EBT calcium imaging could have identify 98% of these individuals as being at risk before their heart attack and treatment could be initiated to prevent their MI.

Treating to NCEP cholesterol goals prevents 30-40% of heart attacks. Treating to a goal of coronary calcium stability prevents 90% of heart attacks. Where I went to school a 40% was an F. Why are we defending this result instead of striving to improve upon it? I am not making this up, look at Raggi's study in Ateriosclerosis, Thrombosis, and Vascular Biology 2004;24:1272, or Budoff Am J Card

Melissa, I strongly disagree with the assertion that the stress test is a great risk stratifier. Laukkanen et al JACC 2001 studied 1,769 asymptomatic men with stress tests. Although failing the stress test resulted in an increased risk of future heart attack, 83% of the total heart attacks over the next 10 years occurred in those men who passed the stress test.
Falk E, Shah PK, Fuster V Circulation 1995;92:657-671 demonstrated that 86% of heart attacks occur in vessels with less than 70% as the maximum obstruction. A vast majority of patients with less than 70% vessel obstruction will pass thier stress test.

William, regarding your question of owning or referring for EBT imaging, I would be amused if it were not insulting. The mistake that is often made is that EBT imaging is a wildly profitable technology. It is not nearly as profitable as nuclear stress imaging. Indeed there are few EBT centers in the country that are as profitable as any random cardiologists stress lab.

How can we justify not screening asymptomatic patients? Most heart attacks occur in patients with no prior symptoms and according to Steve Nissen, 150,000 Americans die each year from their first symptom of heart disease. My daughter is at this moment visiting with a friend who lost her father a few years ago to his first symptom of heart disease when she was 8 years old. That is not OK! We screen asymptomatic women for breast cancer risk. Women are 8 times more likely to die from heart disease than breast cancer. We do mass screening for colon cancer and we are over 10 times more likely to die from heart attacks than colon cancer. An EBT heart scan costs 1/8th the cost of a colonoscopy.

So what say we drop the sarcasm and look at this technology objectively. Read the literature, not just the editorial comments. This really does provide incredibly valuable information that saves lives.

Yes, a 90% reduction in heart attacks in my patients compared to the care I could provide 5 years ago when I was doing a lot of stress testing and referring for revascularization. Much better statistics than expected national or regional norms. I welcome your scrutiny.

John Q. Public jumps into the fray with:

Fascinating, isn't it, that there appear to be two doctors, William Blanchet in this forum and Dr. William Davis, FACC, of cureality.com that both claim to have dramatically reduced risk of heart attack among their patients and/or actual calcium plaque score regression and BOTH are ardent proponents of CT Calcium Scoring?

Despite Dr. Blanchet's persuasive arguments backed up with numerous scientific citations and John Q.'s support, I sense they had no effect whatsoever on Shirley-Walton's way of thinking.

Such are the deeply-entrenched habits of the cardiology community. It will be many years and impassioned pleas to see things in a different light before the wave of change seizes hold.

To learn how to eat . . . try fasting

18. November 2007 William Davis (13)

Curious thing about fasting: It teaches you how to eat.

In previous posts, I've discussed the potential benefits of fasting: reduction of blood pressure, reduction of inflammatory responses, drop in blood sugar, weight loss, and reduced heart attack risk. In my recent Heart Scan Blog post, Fasting and Heart Disease, I discussed the just-released results of a study in people who fast for religious reasons and experience less heart disease.

Fasting can mean going entirely without food and just making do with (plenty of) water, or it can mean variations on "fasting" such as vegetable juice fasts, soy milk fasts, etc.

How can fasting teach you any lessons about food and eating?

People who fast will tell you that the experience:

--Helps you appreciate food tastes when you resume eating. After a fast, flavors are stronger; sensations like sweet, sweet, or salty are sharper; you become reacquainted with the variety of wonderful food textures.

--Makes you realize how you ate too much before your fast. After a fast, you are satisfied with less. You will eat more for taste and enjoyment, less for satiety and mindless indulgence.

--Makes you more mindful of the act of eating. For many of us, eating is an automatic activity that provides fleeting satisfaction. After a fast, each bite of food brings its own special enjoyment.

--Reveals to you how awful you felt when many foods were eaten. For example, many people are physically slightly ill after eating pancakes, pizza, or other highly processed foods but cease to recognize it. Remove the offensive foods entirely and you might realize just how bad you felt.

--Takes away fear of hunger. Many people have a gut-wrenching fear of hunger. It's probably partly instinctive, that animal-like fear of not knowing when your next meal is coming, partly the abnormal, artificial drive to eat ignited by processed foods like wheat and corn syrup.

--Makes you realize just how much of your day is spent in some activity associated with food. Shopping, eating, cleaning up afterwards, thinking and talking about food all occupy an extraordinary portion of everyone's life. A fast can open your eyes to just how much time is spent in these pursuits. Sometimes, gaining an awareness of a mindless, repetitive behavior can provide the first step towards changing direction.

Most people consider a fast for rapid weight loss. But fasting is far more than that. Perhaps fasting has become an integral part of many religious practices because of its capacity for enlightenment, reawakening, revelation, but not of only the spiritual, but also of how far many of us have strayed in diet.

Fasting is what Omnivore's Dilemma author Michael Pollen might describe as looking the pig you're about to eat in the eye, an opportunity to open your eyes to what it is you 've been doing all these years.

Track Your Plaque makes Consumer Reports!

8. August 2011 William Davis (27)

. . . but not in a good way.

The September, 2011 issue of Consumer Reports showcases their Protect Your Heart discussion. Third paragraph: "The website Track Your Plaque warns, 'The old tests for heart disease were wrong--dead wrong.' It says heart scans are 'the most important health test you can get.'"

They go on to expose the overuse of heart procedures like angioplasty and stent implantation and offer their advice on how to manage heart disease risk: lower BP, reduce LDL cholesterol, lose weight, stop smoking, take aspirin. They quote Dr. Paul Ridker who declares heart scans are not useful because the "deposits cardiologists worry about are the less stable plaques that CT scans routinely miss."

I thought I'd been transported back to 1995. Not only is it clear that the Consumer Report writers never looked beyond the homepage of Track Your Plaque, but somehow saw our heart disease prevention and reversal program as promoting heart procedures. Incredible.

Of course, the Track Your Plaque program does the exact opposite: Advocates an approach that virtually eliminates the need for procedures and returns control over heart disease to the participant. That's a critical difference.

And, as I've had to remind my colleagues time and time again, what we are really after is an index of total coronary atherosclerotic plaque. Even in 2011, that index remains the simple coronary calcium score, a gauge of total plaque, not just of "hard," stable plaque. Perhaps in 10 years we will be using a better tool to gauge progression and regression of all the components of coronary atherosclerotic plaque, but today it remains the simple, accessible, mammogram-like coronary calcium score.

Consumer Reports does for the idea of heart disease prevention what food manufacturers do for health and weight loss: Echo conventional wisdom of the sort that generally makes us fatter, more diabetic, leads us to more heart procedures and needless deaths. I might use Consumer Reports to rate MP-3 devices or toasters, but I certainly would not rely on them for insightful health advice.

Paging Dr. Basedow

6. August 2011 William Davis (8)

A 23-year old man came to my office having experienced weeks of extreme anxiety, palpitations, and 19 pounds of weight loss triggered by an overactive thyroid.

It all happened because of a large dose of iodine received during a CT scan using iodine-containing x-ray dye. (X-ray dyes are made visible on x-ray due to the iodine content.) This is a reaction first described in the 19th century by German physician, Karl Adolph von Basedow. (Jod is German for iodine.)[caption id="attachment_4313" align="alignleft" width="217" caption="Dr. von Basedow. Image courtesy Wikipedia"]

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Now, here's the kicker: Jod-Basedow only occurs when there is pre-existing iodine deficiency. Indeed, this young man had an enlarged thyroid, signaling longstanding iodine deficiency (a goiter).

This example is among the more flagrant examples of something I have been witnessing: the return of iodine deficiency. As Americans cut back on their intake of iodized salt and fail to obtain iodine in sufficient quantities from seafood, seaweed, or supplementation, goiters and iodine deficiency are making a return in all its glory, reminiscent of the early 20th century, pre-iodized salt.

This young man's frightening experience is yet another way iodine deficiency can show itself, by the overenthusiastic thyroid response to a large dose of iodine when iodine deficiency has been present for a prolonged period.

Iodine deficiency and goiters have been lost to memory for most people. Even the FDA, in its advice for Americans to reduce salt and sodium intake, have forgotten to remind everyone to obtain iodine from an alternative source. "Those who cannot remember the past are condemned to repeat it."

Get your iodine.

Carb counting

5. August 2011 William Davis (20)

In the recent Heart Scan Blog post, Can I eat quinoa, I discussed how non-wheat carbohydrate sources like quinoa, amaranth, black beans, brown rice, fruit, etc. do not exert the inflammation-provoking, appetite-increasing effects of wheat (since gliadin and gluten are not present), nor do they increase blood glucose as enthusiastically as the amylopectin A of wheat--but non-wheat grains can still increase blood sugar quite substantially.

Of course, any food that triggers blood sugar also trigger hepatic de novo lipogenesis, thereby increasing triglyceride levels and postprandial particles (e.g., chylomicron remnants), which, in turn, triggers formation of small LDL particles.

So these non-wheat carbohydrates, or what I call "intermediate carbohydrates" (for lack of a better term; low-glycemic index is falsely reassuring) still trigger all the carbohydrate phenomena of table sugar. Is it possible to obtain the fiber, B-vitamin, flavonoid benefits of these intermediate carbohydrates without triggering the undesirable carbohydrate consequences?

Yes, by using small portions. Small portions are tolerated by most people without triggering all these phenomena. Problem: Individual sensitivity varies widely. One person's perfectly safe portion size is another person's deadly dose. For instance, I've witnessed many extreme differences, such as 1-hour blood sugar after 6 oz unsweetened yogurt of 250 mg/dl in one person, 105 mg/dl in another. So checking 1-hour blood sugars is a confident means of assessing individual sensitivity to carbs.

Some people don't like the idea of checking blood sugars, however. Or, there might be times when it's inconvenient or unavailable. A useful alternative: Count carbohydrate grams. (Count "net" carbohydrate grams, of course, i.e., carbohydrates minus indigestible fiber grams to yield "net" carbs.) Most people can tolerate around 40-50 grams carbohydrates per day and deal with them effectively, provided they are spaced out throughout the day and not all at once. Only the most sensitive, e.g., diabetics, apo E2 people, those with familial hypertriglyceridemia, are intolerant to even this amount and do better with less than 30 grams per day. Then there are the genetically gifted from a carbohydrate perspective, people who can tolerate 50-60 grams, occasionally somewhat more.

People will sometimes say things like "You don't know what the hell you're talking about because I eat 200 grams carbohydrate per day and I'm normal weight and have perfect blood sugar and lipids." As in many things, the crude measures made are falsely reassuring. Glycation, for instance, from postprandial blood sugars of "only" 140 mg/dl--typical after, say, unsweetened oatmeal--still works its unhealthy magic and will lead long-term to cataracts, arthritis, and other conditions.

Humans were not meant to consume an endless supply of readily-digestible carbohydrates. Counting carbohydrates is another way to "tighten up" a carbohydrate restriction.

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

2. August 2011 William Davis (27)

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.

Wheat Belly coming to bookstores!

31. July 2011 William Davis (18)

Anyone following the conversations on these pages know that I have some very serious concerns about this thing being sold to us called "wheat"--cause it ain't wheat! It is the result of incredible genetics shenanigans inflicted on this plant, mostly in the name of increased yield per acre.

I now classify wheat as "Public Enemy #1," the prime nutritional culprit underlying obesity, heart disease, "cholesterol" abnormalities, hypertension, arthritis, psychiatric illness, and on and on. Once you read the full story, I believe that you will agree: Modern Triticum aestivum, the plant that now serves as the source for virtually all the wheat flour products now consumed--organic, whole grain, multigrain, sprouted . . . it makes no difference--does not belong in the human diet. So many people, searching for solutions for their fatigue, weight gain, leg edema, incurable rashes, joint pain, etc., will find their answers here.

Wheat Belly: Lose the wheat, lose the weight and find your path back to health will be on bookstore shelves including Barnes and Noble August 30, 2011 or is available for preorder here at Amazon. Wheat Belly will also be available as a downloadable Kindle book and as unabridged audio CDs.

You can also follow the Wheat Belly conversations on my Wheat Belly Blog. One of my recent posts discusses the herbicide-resistant semi-dwarf wheat strain, Clearfield, that is now making its way to more and more supermarket shelves.

You'll also find more conversation on the Wheat Belly Facebook pages.

The exception to low-carb

31. July 2011 William Davis (60)

I witness spectacular results restricting carbohydrates, both in the office as well as in my online experiences, such as those in Track Your Plaque. Of course, the diet I advocate is not just low-carb; it starts with elimination of wheat (for a long list of reasons). So the diet is wheat-free in the setting of low-carbohydrate.

What does this accomplish? Here's a partial list:

--Weight loss-Specifically, loss of visceral fat, the kind hinted at on the surface as "love handles" or what I call "wheat belly."
--Reduced blood sugar and HbA1c (reflecting prior 60-90 days glucose)
--Marked reduction in small LDL and triglycerides, increased HDL
--Reduced inflammatory measures like c-reactive protein
--Reduced leptin and leptin resistance, increased adiponectin
--Reduced estrogen and prolactin in men, accompanied by shrinkage or loss of enlarged breasts ("man boobs"); reduced estrogen in females accompanied by reduced risk for breast cancer

Pretty impressive. But there's one group of people who can experience unexpected effects with this diet: The 25% of people with apoprotein E4.

Everybody has two genes for apo E; the most common type is apo E 3/3. Around 1 in 4 people have 1, less commonly 2, genes for apo E4.

I hate apo E4. I hate apo E4 because it means I've got to dust off the nonsense I used to tell patients about cutting their fat, cutting their saturated fat. But that's what apo E4 people have to do. But it doesn't end there.

Apo E4 people also typically have plenty of small LDL particles triggered by carbohydrates. Put fats and carbohydrates together and you get an explosion of small LDL particles. Remove fats, small LDL goes down a little bit, if at all. Remove carbohydrates, small LDL goes down but total LDL (mostly large) goes up. The large LDL in apo E4 does seem to be atherogenic (plaque-causing), though the data are fairly skimpy.

So apo E4 creates a nutritional rock and a hard place: To extract full advantage from diet, people with apo E4 have to 1) go wheat-free, low-carb, then 2) not overdo fats, especially saturated fat.

It still gives me the creeps to tell an apo E4 person that they've got to watch their fats, worse than watching Starsky and Hutch reruns.

Can I eat quinoa?

29. July 2011 William Davis (15)

. . . or beans, or brown rice, or sweet potatoes? Or how about amaranth, sorghum, oats, and buckwheat? Surely corn on the cob is okay!

These are, of course, non-wheat carbohydrates. They lack several crucial undesirable ingredients found in our old friend, wheat, including no:

Gliadin--The protein that degrades to exorphins, the compound from wheat digestion that exerts mind effects and stimulates appetite to the tune of 400 additional calories (on average) per day.
Gluten--The family of proteins that trigger immune diseases and neurologic impairment.
Amylopectin A--The highly-digestible "complex" carbohydrate that is no better--worse, in fact--than table sugar.

So why not eat these non-wheat grains all you want? If they don't cause appetite stimulation, behavioral outbursts in children with ADHD, addictive consumption of foods, dementia (i.e., gluten encephalopathy), etc., why not just eat them willy nilly?

Because they still increase blood sugar. Conventional wisdom is that these foods trend towards having a lower glycemic index than, say, table sugar, meaning it raises blood glucose less.

That's true . . . but very misleading. Oats, for instance, with a glycemic index of 55 compared to table sugar's 59, still sends blood sugar through the roof. Likewise, quinoa with a glycemic index of 53, will send blood sugar to, say, 150 mg/dl compared to 158 mg/dl for table sugar--yeah, sure, it's better, but it still stinks. And that's in non-diabetics. It's worse in diabetics.

Of course, John Q. Internist will tell you that, provided your blood sugars after eating don't exceed 200 mg/dl, you'll be okay. What he's really saying is "There's no need for diabetes medication, so you're okay. You will still be exposed to the many adverse health consequences of high blood sugar similar to, though less quickly than, a full diabetic, but that's not my problem."

In reality, most people can get away with consuming some of these non-wheat grains . . . provided portion size is limited. Beyond limiting portion size, there are two ways to better manage your carbohydrate sensitivity to ensure that metabolic distortions, such as high blood sugar, glycation, and small LDL particles, are not triggered.

More on that in the future.

Lipoproteins . . . zero!

27. July 2011 William Davis (23)

With the recent refinements in our approach to correction of the lipoprotein abnormalities that lead to coronary plaque and heart disease risk, I have been witnessing more and more people achieve:

Small LDL particles 0 nmol/L
Lipoprotein(a) 0 nmol/L

For instance, Ted, a 58-year old man I saw in the office today started with:

Small LDL 1673 nmol/L
Lipoprotein(a) 219 nmol/L

In other words, both small LDL particles and lipoprotein(a) are being knocked down to zero values.

Incidentally, the combination of lipoprotein(a) with small LDL is among the most atherogenic (atherosclerotic plaque-causing) patterns known. Despite his athletic, slender build and avoidance of unhealthy habits, Ted's heart scan score was 922--very high.

So Ted followed the diet I advocate, i.e., wheat elimination followed by elimination of cornstarch, oats, and sugars; high-dose fish oil (total daily EPA + DHA of 6000 mg/day); vitamin D supplementation sufficient to achieve a 25-hydroxy vitamin D level of 60-70 ng/ml; iodine supplementation; and thyroid normalization which, in Ted's case, required supplementation with the T3 thyroid hormone, liothyronine, at a small dose.

The result:

Small LDL particles 0 nmol/L
Lipoprotein(a) 0 nmol/L

Not everybody, of course, is achieving these incredible--and previously impossible--results. But the numbers are growing. Ted is the third person to achieve zeroes all around, in fact, over the past 10 days.

Heart disease prevention is getting better and more powerful every day. And it ain't all about Lipitor and low-fat.

Chocolate almond biscotti

22. July 2011 William Davis (8)

Biscotti are twice-baked biscuits or cookies that are perfect for dipping into coffee, latté, or espresso. These wheat-free, low-carb biscotti are rich with the taste of chocolate and almonds.

Yield: approximately 15 biscotti

Ingredients:

2 cups almond meal
½ cup chopped walnuts
1/4 cup cocoa powder (undutched)
½ cup dark chocolate chips
Sweetener equivalent to ½ cup sugar (e.g., liquid stevia, Truvia)
½ cup ricotta cheese, room temperature (replace with coconut milk if lactose intolerant)
4 tablespoons butter, melted (replace with coconut oil if lactose intolerant)
2 large eggs
¼ cup milk, unsweetened almond milk, or soy milk
¼ cup almond, peanut, or sunflower seed butter, room temperature

Preheat oven to 350º F.

Mix almond meal, walnuts, sweetener, cocoa powder, and chocolate chips in bowl. Mix in ricotta, butter, eggs, milk, and nut butter and blend by hand thoroughly.

Pour mix onto baking pan lined with parchment paper or greased with coconut oil or other oil. Shape into loaf approximately 1 inch deep and 3½ to 4 inches in width. Place in oven and bake for 40 minutes.

Remove loaf and allow to cool 15 minutes. Slice into approximately ¾-inch widths and lay each biscotto on its side on baking pan. Put back in oven for 10 minutes.

Remove pan and flip biscotti over. Place back in oven and bake an additional 5 minutes. Remove and cool.

Optional: For a little dark chocolate "icing":
Melt 3-4 oz semisweet or dark chocolate in microwave (in 15 second increments until melted) or in metal bowl placed in heated water. Stir in 1-2 teaspoons butter.
Dip each biscotti into melted chocolate mix or drizzle chocolate mixture over top of each biscotto.

Sun green tea

21. July 2011 William Davis (11)

Here's a great way to enjoy the health benefits of green tea during the summer: sun green tea.

I dropped two green tea bags into approximately one-half gallon of cold water in a clear glass jar. I placed the jar in the sun (with top on) for four hours, then brought it into the kitchen. I served it as iced tea with a slice of lemon and mint leaf.

The sun green tea was a smoother than standard green tea brewed with hot water. Ordinarily, if you brew hot green tea for more than 3-5 minutes, it becomes more bitter or tannic. This sun green tea, despite steeping for four hours, was not the least bit bitter or tannic.

The green tea lasted well for about 48 hours, more than enough to enjoy several glasses per day.