NY Times Jane Brody misses the mark



NY Times' health columnist, Jane Brody, recently wrote a bit of fluff for her paper:

"CT Scans of the Heart Come With Trade-Offs


In her report, she says:

Coronary CT scans are being sold directly to the public, and they have found a market in health-conscious people who can afford them. But screening exams can have downsides. They can cause needless worry, and they sometimes reveal other potential conditions that require invasive procedures like biopsies to diagnose.

I soon learned that among the strongest proponents of CT scans of coronary arteries were physicians with financial ties to drug companies that make statins and others connected to imaging centers that would profit directly from widespread CT screenings.



She then goes on to discuss how the Framingham scoring calculation can tell you whether or not you are at low-, intermediate-, or high-risk for heart disease. She therefore concludes that heart scans are therefore irrelevant for the majority of people. She then proceeds to take a statin agent.

This sort of nonsense continues to get published, despite the clear lack of real "digging" for the truth. She clearly fell for the conventional arguments that continue to mis-guide the majority of people, myths like:

--the Framingham scoring system is reliable--Reliable it is NOT; it is susceptible to substantial "misclassification" bias, meaning people who appear low risk can actually be high risk, and people at high risk can actually be low risk. Among the latest studies that question the scoring system is Family history of premature coronary heart disease and coronary artery calcification: Multi-Ethnic Study of Atherosclerosis (MESA). This study pointed out how the Framingham scoring system, which leaves out family history, can cause people classified as low risk to actually have substantial heart scan scores. This is crucial. A heart scan gets beyond the uncertainties and shows with >95% certainty whether or not hidden coronary atherosclerotic plaque is present.

--"Coronary risk" is a dynammic phenomenon, subject to changes in a person's life. What if, for instance, a person smoked for 20 years, quit 10 years ago, lost 30 lbs, dropped their blood pressure as a result of the weight loss, then relied on the Framingham Risk Calculator to determine risk. They would likely be classified as low- risk, since risk factors now appear favorable. This person could easily have a heart scan score of 500, or 700, or 1000, levels that carry a cardiovascular event risk of 5-25% per year, hardly low-risk, because much of their risk accumulated earlier in life and is no longer revealed by an assessment of risk factors.

--There are sources of risk that have nothing to do with Framingham, such as lipoprotein(a), which is often revealed by family history; the presence of small LDL, which co-varies with HDL and triglycerides, but can behave independently also; and, my favorite, deficiency of vitamin D. This would explain part of the 60-70% of people who are typically mis-classified by Framingham.


Where did Ms. Brody get the idea that proponents of heart scans had ties to drug companies? I think she's barking up the wrong tree on that one. Of course, she ends up on a statin drug. For my part, I am a critic of statin drugs. Yes, they play a role, but they are miserably misused and abused by practicing physicians, based on the endless onslaught of drug company-sponsored trials that have served to distort their usefulness.

If I were Ms. Brody, I would be quaking in my shoes, not knowing what my true risk for heart disease was, relying on the--at best--30% reduction in heart attack risk of Lipitor or other statin drug. Ms. Brody: You are not cured, you're simply wearing a superficial Band-Aid. If you want to know your true risk for heart attack, and you want a precise value that you can track over time, the answer is simple: Reject the conventional notion and get a heart scan.

"There must be a mistake"

Neal is our current male record holder for greatest reduction in heart scan score. (Yes, the ladies have the lead!)

You may remember that this 40-year old man reduced his heart scan score from 339 to 161--a 51% drop. If you haven't yet read his story, go to

http://www.cureality.com/library/fl_07-001nealt51.asp


Neal reminded me of the experience he had when he underwent his second heart scan. Both scans had been performed at the same scanning center. At this center, the radiologists provide the added service of sitting down with people and actually going over the images and results.

After the scan, the radiologist pulled up the result from Neal's first scan for comparison. "There must be a mistake! This score is lower. Scores never drop."

The radiologist was apparently stumped, unable to provide an explanation. However, Neal then proceeded to tell the radiologist that we had warned Neal that this could happen and that he might even be told that it was due to error of some sort. This yielded a puzzled look on the radiologist but no further comment.

Of course it's not a mistake. It's something we achieve on purpose. Curiously, I still get comments that this is impossible, heart scan scores never drop, etc. Of course, those of you following this conversation know this is completely untrue. Heart scan scores DO drop, and sometimes drop enormous amounts, as it did for Neal.

I would have liked the radiologist to have had the lightbulb of understanding go off in his head when he realized that a reduction in heart scan score is a cause for celebration. Unfortunately, this radiologist's reaction is all too common: disbelief, confusion, dismissal.

Heart disease reversal is simply not in the realm of understanding of most doctors, radiologists and cardiologists alike. By conventional thought, if you have it, it just gets worse. "Maybe some high-dose Lipitor might help."

Ironically, when they see it right in front of their eyes, plain as day on the computer screen, they don't understand what has happened. It's Greek to them.

Should this happen to you, don't be surprised. Just bite your tongue, because you know better.

Jimmy Moore Interview: Is saturated fat the villain we thought?

Enter "weight loss" or "low carb" in your web search and you can't help but stumble across the prolific and widely-connected Jimmy Moore.

On his Blog, Livin' la Vida Lo Carb , Jimmy conducts a wide-ranging and informative discussion of the benefits of a low carbohydrate diet, a la Atkins. Though his initial claim to fame was the 180 lbs he lost in his first year of dieting on this approach, Jimmy has extended the conversation and built a considerable community of like-minded individuals, all of whom are participating in this grand "experiment."

Anybody who looks at lipoproteins and associated factors in health will quickly come to the conclusion that processed carbohydrates are the culprits in much of heart disease, diabetes, and heart disease. But I have had a hard time dismissing the ill-effects of saturated fat. After all, we've all been taught--drilled--with the idea that saturated fats cause LDL cholesterol to go higher, cause arterial constriction, growth of atherosclerotic plaque, inflammation, even cancer.

But there does indeed seem to be a growing sentinment that this long-held dogma may not be true. So I went to the ever-entertaining and informative Jimmy Moore, an able spokesman for these concepts.




TYP: It's certainly impossible to argue with the success you had in weight loss and the health you've regained on your program.

I think that the approach we use in diet in the Track Your Plaque program and the nutrition approach you advocate overlap to a great extent. We both emphasize plenty of vegetables, fruits, healthy oils, nuts, etc. The major point of difference seems to lie in saturated fat: We say restrict it, you say don't restrict it. Could you elaborate?





JM: Thank you for inviting me to your blog today, Dr. Davis. I have nothing but deep respect and admiration for the work you are doing to help educate others about how to keep their heart health in tip-top shape. Keep fighting the good fight, my friend.

While we do agree on probably 99% of the basic tenets of what I describe as
"livin' la vida low-carb," the issue of saturated fat to me is one where we
indeed do not. It's not a deal breaker regarding my support for what you do
just as I'm sure you would say the same regarding your backing of what I do. If
we all agreed on everything, then what a boring world this would be!

My thinking on saturated fat has evolved since I started eating this way nearly
four years ago. Like most people, I was terrified to eat ANY fat at all because
of the abject fear that people like Dr. Dean Ornish and other so-called health
"experts" instilled in me about how dangerously unhealthy it is to consume it.
This fat phobia is arguably the single biggest contributor to the ongoing
obesity crisis our world faces today.

With that said, you and I both know fat consumption is a part of a healthy
lifestyle. There are just too many benefits to the body that come from the
consumption of fats and even saturated fats such as coconut oil, butter, lard,
nuts, seeds, and animal fat when it is combined with a restricted carbohydrate
intake.

An intriguing study was presented at a scientific conference in November 2006 by two highly-respected researchers--Dr. Stephen Phinney from the University of California at Davis and Dr. Jeff Volek from the University of Connecticut--who conducted a side-by-side comparison of the amount of saturated fat in the blood of people on a low-carb diet with those following those highly-touted low-fat diets. What they found was the low-carb study participants had "significantly less" saturated fat in their blood than the low-fatties did.

Here are the actual numbers from the study:

- LOW-FAT/HIGH-CARB DIETERS: lowered saturated fat by 24%
- LOW-CARB/HIGH-FAT DIETERS: lowered saturated fat by 57%
- Eating 3X the saturated fat cut the amount in the blood in half

In an interview I conducted at my blog with Dr. Volek last year (here's the
link: http://livinlavidalocarb.blogspot.com/2006/09/volek-high-carb-low-fat-diet-useless-to.html),
he said the conventional wisdom regarding fat, especially saturate fat, is dead
wrong while the significance of carbs is all but ignored by those who claim to
understand the metabolic response mechanism.

Here's what Dr. Volek said in my interview:

"Eating fat does not make you fat, storing fat makes you fat. And carbohydrates play a major role in storing fat. So the level of dietary carbohydrate is really the most important factor to control because it dictates what happens to fat. Carbs are dominant and fat is passive. When carbohydrates are low, fat tends to be burned, and when carbohydrates are high dietary fat tends to be stored. The same holds true for the atherogenic effects of saturated fat. The body handles saturated fat better when carbohydrates are low."

Long-time low-carb practitioner and current President of the American Society of Bariatric Physicians (ASBP) Dr. Mary C. Vernon from Lawrence, Kansas confirms the findings of Dr. Volek and Dr. Phinney in a succinct recap of what their research showed.

Here's what she said:

"Eating fat (whatever kind) does not make you fat. It does not increase blood
stream saturated fat. Eating carbs does make you fat. Eating carbs does put
saturated fat in your blood stream."

To me, as a simple layperson with no medical background, it's all a matter of who you believe. Do we continue to buy into the low-fat propaganda machine and assume that what they are telling us about saturated fat is true? Or do we instead start paying closer attention to the latest research that is coming out about saturated fat that doesn't exactly line up with the edicts of the last three decades? The choice for me is a simple one.

And if you haven't read the brand new Gary Taubes book entitled GOOD CALORIES, BAD CALORIES yet, then it is REQUIRED reading to arm yourself with the research studies about fat. After you read that book, it will be almost impossible for ANYONE to believe fat, including saturated fat, is unhealthy.



TYP: In our program, we advocate a wheat-free approach for many people, because of the addictive potential of wheat products, as well as the flagrant creation of the small LDL pattern that wheat products create, thereby adding to atherosclerotic plaque growth. However, many people express a concern over a lack of fiber in their diets if they eliminate whole wheat bread, pasta, Fiber One, Raisin Bran cereal, etc.

Have you encountered any phenomena of low-fiber on your approach?

JM: What an excellent question and I even wrote a humorous blog post about the importance of fiber intake called "Allow Your Bowel To Shake, Rattle, And Roll" (http://livinlavidalocarb.blogspot.com/2006/06/allow-your-bowel-to-shake-rattle-and.html).

Fiber consumption is another one of those issues that not everyone who advocates
a controlled-carb approach agrees is necessary. I'm on the side that it IS a healthy part of your diet and should be consumed in high enough quantities to keep you regular...something many people think is impossible on a low-carb diet.
Not true! I take a fiber supplement like FiberCon, eat plenty of high-fiber vegetables, drink lots of water, and even consume high-fiber, low-carb products that help me maintain high levels of fiber in my diet (see my favorite ones in this post: http://livinlavidalocarb.blogspot.com/2007/04/there-are-plenty-of-low-carb-fiber.html).

As for consuming the highly-touted "healthy whole grain" cereals that you
mentioned, what a travesty that would be for people trying to manage their
weight and health. While the cereal manufacturers have had a heyday in their
marketing efforts promoting their whole grain content, it's all just a big fat
ruse on the public trying to convince them that these cereals are somehow healthy for their bodies. Sure, they're better than the sugary cereals, but all those grains are metabolized as sugar inside the body, so you might as well be eating Lucky Charms and Fruit Loops!

Many of these "healthy" cereals contain as many carbohydrates in a single bowl
without the milk as I would eat in an entire day. Raisin Bran, for example, which used to be my favorite cereal before my low-carb lifestye, has a whopping 47 grams of carbohydrates. Needless to say, I don't touch that with a ten-foot pole nowadays because I would surely gain weight and get back on the blood sugar rollercoaster ride that I was on prior to beginning the Atkins diet on January 1, 2004. Plus, all those carbs just make you hungrier sooner, so it's better just to eat some delicious eggs cooked in butter, a couple of slices of sausage, and tomato slices to start your day off right. You'll get enough fiber in your body the rest of your day.



TYP: 180 lbs of weight loss in your first year is absolutely astounding.

I take it that you've continued this trend and have lost more weight since your early success. What role did exercise play during your first year and subsequently?
How are your food choices today different from that first year?

JM: Yes, that weight loss was indeed one of the greatest accomplishments I have ever experienced in my life. It was a hard-fought battle that even included a 10-week period where I was stalled with no weight loss. But I knew my chosen diet was the right one for me because I felt better than I ever had on a diet, was never hungry because I ate every 2-3 hours, and could see myself doing this for the rest of my life. So far, so good!

It has been close to four years since I began this journey and I am indeed continuing this pathway to better health. My low weight in 2004 was 230 pounds and I currently weigh 225 pounds. As long as I keep my carbs reduced, I am able to maintain my weight right where it is. I've had minor fluctuations in both directions where I got down to as low as 215 pounds at one point (but didn't feel good at that weight) and as high as 252 pounds (when I was allowing myself one too many high-carb foods here and there).

There's a balance that people need to find for themselves and it's different for
all of us. I am one of the unlucky people who has to keep his carbohydrate
intake below 50g daily or I gain. It's just a fact of life that I've come to
grips with and realize is a necessity in order to manage my weight for the rest
of my life. But I wouldn't have it any other way!

Exercise was indeed a part of my low-carb weight loss success in 2004 as I
forced myself to do cardio every single day as a commitment to this journey. In
hindsight, that was probably not the best thing for me to do since the body has
a rather peculiar way of telling you it needs to wiggle and move spontaneously
on its own rather than forcing the issue. But I consider the exercise I did to
be such an integral part of my success that I dedicated an entire chapter of my
book to the subject.

Today, my daily cardio routine is out the window and I choose instead to engage
in activities outside the gym that let me burn calories and have some fun in the
process. I regularly play volleyball, basketball, and referee flag football at
my church which all give me quite a workout. I'm very physically active and fit
on my 6'3" body and just enjoy burning off all this excess energy that I have
been given since losing nearly have my weight! I do want to get into a little
more organized resistance training routine soon to try to shape and tone some
areas of my body that still show signs of that 410-pound man I used to be
(although the loose, hanging skin in my abdomen and inner thighs isn't going to
get any better with exercise since the elasticity has been ruined from being
stretched out so far). Here is a link to some posts and pictures I have written
about this subject:
http://lowcarblinks.blogspot.com/2007/04/theme-based-low-carb-links-loose-skin.html

As for my food choices today compared to my weight loss year in 2004, they
haven't really changed a whole lot. This was a lifestyle change in every sense
of the phrase and I've learned to implement this way of eating into a permanent
and healthy diet that I can and will gladly live with forever and ever amen. I
probably eat more berries, melons, and nuts today than I did then, but otherwise
it's the identical diet.



TYP: I'm sure that you are as impressed as I am that much of the wisdom in healthy eating doesn't always come from doctors or clinical studies, but from the collective wisdom that emerges from this national experiment (inadvertent, for the most part) in eating. Your Livin' La Vida Low-Carb is, in my view, a perfect example of the sort of wisdom that is helping all of us understand what happened to our health over the last 20 years.

Does the approach you advocate today differ in any substantial way from the diet as originally articulated by Dr. Atkins?

JM: Actually, my personal diet is precisely based on the teaching of the late great Dr. Robert C. Atkins in his classic bestseller DR. ATKINS' NEW DIET REVOLUTION (DANDR) book. But most people are surprised when they learn I do not necessarily advocate the Atkins diet as the nutritional approach for everyone.

Nope, I sure don't!

Instead, my philosophy is simple: Find the diet plan that will work for YOU, read and research everything you can about that chosen plan, follow that plan exactly as prescribed by the author of that book, and then KEEP doing that plan for the rest of your life. If you do that, then there's no reason why you can't succeed just like I did.

Anyone interested in doing the low-carb lifestyle and needs help finding which
plan is right for them, let me HIGHLY encourage you to pick up a copy of Dr. Jonny Bowden's LIVING THE LOW-CARB LIFE (read my review: http://livinlavidalocarb.blogspot.com/2005/05/must-have-book-for-everybody-doing-low.html).
It's the perfect overview of low-carb living with a comparison and recap of the
major plans.

THANK YOU again for allowing me to share my story with you and your readers, Dr.
Davis!

TYP: And thanks to you, Jimmy!



For more on Jimmy Moore's lively and informative discussion of these issues, go to

Livin' la Vida Lo Carb

Also, watch "Livin' La Vida Low-Carb on YouTube"

Join the conversation at Jimmy's new low-carb forum called "Livin' La Vida
Low-Carb Discussion
" at LowCarbDiscussion.com


Also, Jimmy's 2005 book on his weight loss experience:
"Livin' La Vida Low-Carb: My Journey From Flabby Fat To
Sensationally Skinny In One Year"

Mammogram of the heart

Some people have called CT heart scans the "mammogram of the heart." The analogy contains a lot of wisdom.

First of all, both--mammograms and CT heart scans--are screening tests, one for cancer, of course, the other for coronary atherosclerotic plaque. Both are performed in specific age groups, mammograms in women 40 years and over (generally), heart scans in women 50 years and over (generally).


















Mammograms: Left, normal; right, a small mass. (Courtesy Nat'l Institutes of Health and Wikipedia.)



Both are also meant to be repeated periodically when normal as a surveillance process.

Both use low quantities of radiation of about 0.3-0.4 mSv (the most real-life measure of total body exposure), a modest quantity of radiation.

Both are good for their purposes, though not perfect. Can a mammogram performed properly miss a small cancerous mass? Sure it can, but it's still unusual. Can a CT heart scan miss the non-calcified plaque prone to rupture? Sure it can, but this is also unlikely (<5% probability).

Given the exorbitant costs of medical tests, both are quite inexpensive. On the flip side, they are both also quite unprofitable for the centers providing the tests. Unfortunately, this means that mammography centers and heart scan centers come and go because of the difficulties of the profit-side of these services.

Both tests initially struggled to gain acceptance among the medical community. In 1960, for instance, mammograms were performed on standard x-ray devices, the same as that used to perform chest x-rays--low precision, high radiation back then. In 1969, dedicated mammography devices made the scene. However, it took over 10 years for even these new dedicated devices to become widely used. Use of mammograms has gradually increased over the ensuing 20 years. In other words, 47 years have passed since the introduction of mammography.

CT heart scans, of course, have had a shorter history of approximately 20 years, since engineer, Dr. Douglas Boyd, first invented the "ultra-fast" EBT devices, the first devices with sufficient scanning speed to scan the heart and coronary arteries.

One interesting difference between the two: In a woman between the age of 50 and 60, the likelihood of detecting cancer is 1 in 237. The likelihood of detecting coronary atherosclerotic plaque? About 1 in 4. Coronary disease eventually kills 1 in 3 females, hugely overshadowing breast cancer in frequency.


Progress on both fronts, one in cancer detection, the other in atherosclerotic coronary plaque detection. But still lots more progress to go.

Dr. Susie Rockway on conjugated linoleic acid (CLA)

I’m fascinated by the perspectives that nutritionists (free-thinking ones, at least), food scientists, and biochemists bring on nutrition and nutritional supplements.

A few months ago, I met a fascinating nutritionist/biochemist named Susie Rockway, PhD. Dr. Rockway brings a world of experience in the world of nutritional supplements, clinical trials with supplements, and their development. She has special expertise in conjugated linoleic acid (CLA), having been among the scientists who initially developed CLA as a supplement. We are also exploring CLA as a possible addition to the Track Your Plaque program and wanted to get Dr. Rockway’s perspectives.

So I asked Dr. Rockway if she’d answer a few questions for us.






TYP: Dr. Rockway, we understand that you are particularly excited about the prospects of CLA for FAT loss and perhaps for regression of atherosclerosis. Can you tell us about the origins of your interest in CLA and why you're so enthusiastic?

Dr. Rockway: I have been fascinated with this unique fatty acid since the early 1990’s when CLA was first being discussed as nature’s most potent anti-carcinogen. I was then working in the granting/funding section of the National Dairy Council and saw this molecule as truly one of the future functional fats that would likely benefit people (next to omega-3’s!)

I think the benefits of CLA have just begun to be investigated—animal studies are extraordinary for showing fat reduction, lean mass (muscle) increases, immune enhancements, blood glucose normalization, anti-inflammatory properties and plaque reduction!

Human data to date is very encouraging for fat reduction. As a nutritionist seeing the massive increase in abdominal fat (stomach fat) in the world population and the direct relationship to cardiovascular disease, I see CLA as a great supplement to take to help this. Of course eating lots of vegetables, fruit, lean protein and whole grain products is also a must for maximizing good health.

I am studying the impact of CLA in reducing muscle loss in aging women—a condition known as sarcopenia. As we lose muscle with age, we lose strength, falls increase, we become frailer, and eventually many of us lose our independence. Along with the muscle atrophy, most people gain fat—never a good thing! So, if CLA can reduce fat and increase muscle, our bodies are more likely to withstand the hurdles that life throws at us much more efficiently.

So, how can you not be excited about this very bioactive molecule?




TYP: What are your specific areas of interest in nutrition and health?

Dr. Rockway: I strive to understand the role of bioactive molecules that can be taken to improve the aging process and enhance health.

As a trained nutritional biochemist, we tend to look at cell metabolism in a very ideal sense: what we learned in our biochemistry texts years ago where all substrates, proteins, enzymes, etc. are made exactly when we need them, where all cells behave as they should.

Unfortunately, little research has been devoted to understanding the changes in metabolism as we age. Do we still produce everything as efficiently as when we were 20? I suspect not. So, I think we need a little help, and supplements are a key to getting there.

Two nutrients that I think are emerging as “super nutrients” are the fatty acids found in fish oil (EPA and DHA) and vitamin D. Where we know these two nutrients are essential for life, we are seeing that they play a huge role in the QUALITY of life. Mood, depression, PMS, wound healing, bone growth, atherosclerosis, and arthritis are clinical areas where we see a direct benefit with doses of omega-3 and Vitamin D that are probably much greater than the RDA. Our current requirements for nutrients are really based on fixing deficiencies and not maximizing health, and maximizing health is where I’m at.

Thus, I am very interested molecules like CLA as mentioned above, and other bioactive ingredients such as plant derived ingredients (phytochemicals) called flavonoids that may well help explain why people who have diets high in fruits and vegetables are less likely to have certain cancers and heart disease. Reducing oxidative stress through foods that provide these active molecules (think colored fruits and veggies) is a new and exciting area of research.



TYP:The big "diet experiment" in America has clearly steered people in the wrong direction, usually by 50 or more pounds. As a scientist in nutrition, what are your thoughts?

Dr. Rockway: The American Heart Association was keen 20 years ago to promote the low-fat diet for all Americans as the key way to reduce cholesterol levels and decrease chance of heart disease, the number one killer of men and women. However, I must admit the nutritional community bought into this one, too. Unfortunately, the general public took this message to reduce percent fat in their diet (and they did a bit), but increased overall calories instead—and a large portion of the increased calories was from simple carbohydrates. I’m convinced that this in itself has been part of the huge rise in obesity…we simply eat more food and it’s not the healthy kind of food either.

When you increase sugar intake beyond what you burn off, you will store some of it as glycogen in the liver and muscles, but you will convert most of the excess into fat—and that we can store very efficiently! The fat that is made in the liver is sent to the blood as VLDL’s which are the precursor to the class of lipids called low density lipoproteins (LDL) that are the “lethal” type of cholesterol circulating in our blood.

So, Americans now have to listen to a new message that they need to eat more fruits and vegetables in hopes they will cut down on fast foods—tending to be high in fat (saturated particularly), low in fiber and low in nutrients and other high calorie dense foods. We nutritionists have our work cut out for us, that’s for sure.



TYP: We are especially excited that nutritionists are assuming a leading role in shining light on the confusion in diet and nutrition that has characterized the last 40 years. Do you have a sense for the emerging important issues for the next 10 years?

Dr. Rockway: Certainly, the scientists in the nutritional field are well aware of the problems facing this nation—it’s in fixing them that we fall short!

We aren’t very well coordinated to get a single message out, nor do we all agree on what that message should be. I feel that people need to eat healthy MOST OF THE TIME, exercise all of the time, and take supplements that have clear evidence of benefit. Lots of my colleagues would not concur with supplement use. Our bodies were designed to move a lot and eat a lot…we just do the latter now and are paying the price!

One emerging and very exciting area that we have to teach Americans is that all fat is not bad. The different types of fat—omega-6 vs. omega-3, are where we need to focus our education.

Decreasing the corn oil we pour on everything needs to go out the window! Consume olive oil and eat fish or take fish oil supplements—we simply have tons and tons of research showing the benefits of reducing the ratio of omega-6 to omega-3. Did you know that cattle that are grass fed actually have less omega-6 in their tissues and more CLA? But most cattle are fed corn-based diets, so we have perturbed their natural selection of food and their fat composition.

See, it all comes back to CLA!


TYP: Thanks, Susie!




Susie Rockway, Ph.D., C.N.S.

Dr. Susie Rockway is an experienced scientist with accomplishments in both the academic and food and supplement industry business directing science/technology research. Her background includes faculty appointments at the graduate level in teaching and research at Rush University Medical Center and industrial experience managing basic and applied research studies.

Dr. Rockway received her Ph.D. in Nutritional Sciences, Biochemistry from the University of Arizona. Dr. Rockway has authored several publications in journals such as the Physiological Genomics, Journal of Nutrition, the Journal of Food Science, International Archives of Occupational and Environmental Health and has published chapters on nutrition on inflammatory bowel diseases. She is a member of the American Society for Nutrition, American Oil Chemists Society, the Institute of Food Technology, American College of Nutrition and is a Certified Nutrition Specialist.

We're also proud to add Dr. Rockway to our panel of Track Your Plaque Experts.

Which is better?

If you have the common pattern of high LDL particle number (NMR) with small LDL--a pattern highly related to coronary plaque--which is better:




Lipitor or a combination of fish oil, vitamin D, and elimination of wheat?


Lipitor quite effectively reduces LDL particle number, usually on the order of 40% or so. Effect on LDL particle size: None. Side-effects: plenty, including muscle aches (inevitable in my experience, not the ridiculous 2% they claim) and occasionally mental effects such as impaired short-term memory.

Lipitor does seem to exert a modest effect on reduction of C-reactive protein, around 30%. It also reduces cardiovascular events by 30%.



A combination of fish oil, vitamin D, and elimination of wheat:

Reduces LDL particle number commonly by a similar 40% (though variable, depending on body weight). There is substantial improvement in LDL particle size, a large drop in C-reactive protein, often >50%, a 30% or more reduction in cardiovacular events.



On this combination, however, you also:

--Lose weight, often substantially.

--Improve bone health, esp. osteoporosis and arthritis.

--Reduce cancer risk from the vit D supplementation.

--Reduce risk of stroke.

--Reduce postprandial (after-eating) abnormalities like intermediate-density lipoprotein.

--Reduce winter blues.

--Experience more energy.

--Obtain increased clarity of thought (from elimination of wheat).

--Reduce blood pressure.


Oh, and there's no muscle aches.

Heart health for stupid people

I'm kidding.

What I'm referring to is the incredibly lame information I come across that passes as "heart health" on the internet, magazines, and other media. Just to keep abreast of what is being said, I subscribe to multiple newsletters and magazines and I witness the sorts of advice offered to the reading public.

A recent long-winded article on a popular website listed the "exciting" strategies available for a healthy heart:

Eat healthy--by eating a "balanced" diet low in saturated fat

Don't smoke

Exercise

Don't ignore chest pain symptoms or breathlessness

Know your numbers! meaning your cholesterol numbers. "If your cholesterol is high, you may need to speak to your doctor about medication to reduce it."


Surely they must all believe we're stupid. Otherwise, why would they repeat the same obvious information over and over again? Quit smoking? Gee, you think so?

How about some real heart healthy advice:

Get a heart scan--since we have to accept that cholesterol values are a miserable failure in detecting hidden heart disease. So is waiting for symptoms to appear.

If you have any measure of coronary plaque, ask your doctor to assess lipoproteins, not lipids (cholesterol).

Take fish oil for omega-3 fatty acids--At a dose of 1000 mg or more of EPA + DHA, heart attack risk is reduced by at least 28%.

Eliminate wheat and other processed carbohydrates --Small LDL has emerged as the number one cause of coronary plaque, not high cholesterol from saturated fat.

Get vitamin D assessed--The effects are huge--HUGE. There's already a study in a kidney disease population that showed a substantial reduction in mortality with vitamin D supplementation. More data are coming, including our own.


That's a start--truly effective, practical heart healthy strategies that go way beyond the conventional bland advice.


Copyright 2007 William Davis, MD

Money, money, money, money

I've been asked the question numerous times:

Why aren't heart scans more popular?

First, let me qualify by saying that heart scan have indeed grown in popularity over the past decade. I think the real question is:

Given the enormous usefulness of CT heart scanning to detect hidden, asymptomatic coronary atherosclerotic plaque, why haven't they more readily been incorporated into conventional medical practice?

That's easy: There's no money in it.


Say, for instance, your doctor orders a heart scan and somehow receives a $1000 for the test. Scan centers would be scanning 100 people a day, falling over themselves to do scans.

This would be similar to a heart catheterization. Order a catheterization, do 30 minutes of work, and get $1000. Or, order a nuclear stress test. Depending on how its done and where, $1800-4000 is paid by the insurer.

Order a CT heart scan and how much is paid to the doctor? Usually nothing. At most, a nominal fee might be paid if the doctor reads the scan.

With heart scans, there simply is no big payoff.

We learned the implications of this situation 10 years ago when I was trying to help my friend, Steve Burlingame, the owner of Milwaukee Heart Scan. (I am NOT and NEVER WAS an owner.) Steve was trying to let everybody know about this great new $2 million dollar heart scan device in the Milwaukee area.

The first few years were tough for Steve: Carrying the substantial expense of this device while doctors essentially gave the technology the cold shoulder. It simply did not fit into the financial equation. Why change the way things were, particularly when there was virtually no financial reason to do so? To counter this, Milwaukee Heart Scan followed the model many other scan centers have followed and marketed directly to the public.

I see this as yet another example of why people need to take control of health care away from doctors and hospitals, the current controllers of the system who are providing a disservice to the public they are supposed to be serving. These institutions, for the most part, serve their self-serving financial interests, not your health interests. It's the same equation that drives food manufacturers to make more and more processed carbohydrate foods that they sell for substantial markups, not green peppers and cucumbers that make little money.

I regard heart scans as among the greatest self-empowering tools in health ever conceived. It was that way in 1997; it remains that way in 2007.

The many faces of LDL

Ginnie came in for an opinion about her heart scan score of 393. At age 57, this put her in the 99th percentile, a high score.

As usual, we did a lipoprotein analysis by NMR (Liposcience). Some numbers:

LDL cholesterol: 96 mg/dl
This value puts Ginnie's LDL in the most favorable 25% in the country.


LDL particle number: 2140 nmol/l
This value is in the worst 25% of the country and is the equivalent of an LDL cholesterol of 214 mg/dl (take off the zero).

In addition, over 90% of Ginnie's LDL particles fell into the small class.

Had we run some other values, how would they have turned out? These are my estimates (since we didn't actually run them in Ginnie), but having run side-by-side numbers in past, reasonable estimates would have put:

Apoprotein B somewhere in the 120 to 140 mg/dl range

Direct LDL 100-130 mg/dl range.


In other words, conventional calculated LDL is the least reliable of all the ways of examining low-density lipoprotein.

It can also go the other way: High calculated LDL, low LDL particle number or ApoB or direct LDL. And, indeed, these other measures have proven superior in their ability to predict "events" like heart attack over conventional calculated LDL.

Unfortunately, relying on conventional LDL is like a broken speedometer on your car. You really can't gauge accurately how fast you're going; sometimes you could be way off. While insurance companies and many physicians still continue to balk at this argument, the data have already been generated that show that lipoprotein analysis (my bias is NMR) is not just superior, but enormously superior for accuracy and event prediction.

In addition, lipoprotein analysis has proven a crucial tool that accounts for our extraordinary success in reducing and controlling CT heart scan scores in the Track Your Plaque program. I doubt that we could have achieved the same level of success using conventional lipids.

I'm also aware of the logistical difficulties obtaining lipoprotein testing in a world enthusiastically supportive of hospital procedures and smugly ignorant of superior prevention tools like lipoprotein analysis. I've learned just how difficult it can be in our Track Your Plaque Member Forum; I've also learned about some strategies for obtaining these tests that I hadn't been aware of, thanks to the resourcefulness of our Members.

We will be working on some solutions in the coming months.


Copyright 2007 William Davis, MD

What does "Success" mean in the Track Your Plaque program?

Say you begin with a CT heart scan score of 400.

You correct your lipoprotein pattterns, take fish oil, correct 25-OH-vitamin D3 to 50 ng/ml, correct your other hidden patterns, follow a diet suited to your patterns.

One year later, you get another heart scan. What score would constitute "success"?

With all of our recent talk about record-setting reductions in heart scan scores, is it really necessary to drop your score that much to succeed?

For instance, is our latest record-setting 63% drop in score better than "only" a 10% drop in score? Both represent reversal of coronary plaque. Both signify huge reductions in risk for plaque rupture, or heart attack.

You can read about how we view the various forms of success in the program by reading our latest Track Your Plaque Special Report, Winning Your Personal War with Heart Disease: The Track Your Plaque 5 Stages of Success.

We are making the Report available to everyone. Just go to the www.cureality.com homepage.

Unexpected effects of a wheat-free diet

Wheat elimination continues to yield explosive and unexpected health benefits.

I initially asked patients in the office to eliminate wheat because I wanted to help them reduce blood sugar and pre-diabetic tendencies.

A patient would come to the office, for example, with a blood sugar of 118 mg/dl (in the pre-diabetic range) and the other phenomena of pre-diabetes or metabolic syndrome (high blood pressure, high inflammation/c-reactive protein, low HDL, high triglycerides, small LDL), and the characteristic wheat belly. Eliminate wheat and, within three months, they lose 30 lbs, blood sugar drops to normal, blood pressure drops, triglycerides drop by several hundred milligrams, HDL goes up, small LDL plummets, c-reactive protein drops.

People also felt better, with flat tummies and more energy. But they also developed benefits I did not anticipate:

--Improved rheumatoid arthritis--I have seen this time and time again. Eliminate wheat and the painful thumbs, fingers, and other joints clear up dramatically. Many former rheumatoid sufferers people tell me that one cracker or pretzel will trigger a painful throbbing reminder that lasts a couple of hours.

--Improved ulcerative colitis--People incapacitated with pain, cramping, and diarrhea of ulcerative colitis (who are negative for the antibodies for celiac disease) can experience marked improvement. I've seen people be able to stop all their nasty colitis medications just by eliminating wheat.

--Reduction or elimination of irritable bowel syndrome

--Reduction or elimination of gastroesophageal reflux

--Better mood--Eliminating wheat makes you happier and experience more stable moods. Just as wheat is responsible for a subset of schizophrenia and bipolar illness (this is fact), and wheat elimination generates dramatic improvement, when you or I eliminate wheat, we also experience a "smoothing" of mood swings.

--Better libido--I'm not sure whether this is a consequence of losing a belly the size of a watermelon or improvement in sex hormones (esp. testosterone) or endothelial responses, but more interest in sex typically develops.

--Better complexion--I'm not entirely sure why, but various rashes will often dissipate, bags under the eyes are reduced, itching in funny places stops.


It's also peculiar how, after someone eliminates wheat for several months, re-exposure of an errant cracker or sandwich results in cramping and diarrhea in about 30% of people.

Obviously, people with celiac disease, who can even die of exposure to wheat, are even worse. What other common food do you know of that makes us sick so often, even occasionally with fatal outcome?

Is Lp(a) part of your legacy to your children?

If you have lipoprotein(a), Lp(a)--the most aggressive known cause of heart disease that no one has heard of--then you need to tell your children.

Lp(a) is a "cleanly" inherited genetic pattern: If either parent has it, there's a 50% chance that you have it. If you have it, then there's a 50% likelihood that each of your children has it. (Note that each child experiences a likelihood of 50%, not 50% of your children. This is because each child is conceived as an independent statistical event. So much for romance!)

The atherogenicity (plaque-causing potential) of Lp(a) also tends to get transmitted. In other words, if your Dad had a heart attack at age 50 due to Lp(a) and you share Lp(a), then you likely share a similar magnitude of risk as your Dad. If your Mom had Lp(a), though passed quietly at age 89 without any overt evidence of heart disease, then you are likely to share the relatively benign form of Lp(a).

For most of us with Lp(a), however, it is best to assume that it has at least some potential for causing heart disease, being the most aggressive cause known. (That is, until we have the ability in everyday clinical practice to characterize Lp(a) by assessing such factors as the size of the apoprotein(a) molecule, the number of kringle "repeats" on the tail, etc. Until then, we need to rely on the crude, though helpful, observation of family history.)

At what age should you inform your children? There's no hard-and-fast rule. However, I generally suggest to patients that they talk about Lp(a) with their children when they reach their 20s or 30s, old enough to begin to understand the implications and begin to think about adopting healthier lifestyles. Is treatment required at, say, age 35? That depends on the pattern of Lp(a)-related heart disease in the family: With exceptionally aggressive forms, it might be reasonable to begin treatment at this relatively early age.

Do "Heart Healthy" sterols cause heart disease?

The sterol question continues to pop up.

Sterols are an ingredient widely added by food manufacturers that allows a "heart healthy" claim, since sterols have been shown to reduce LDL cholesterol (at least transiently). HOWEVER, sterols have also been implicated in possibly increasing risk for heart disease. After all, people with the genetic condition called sitosterolemia absorb sterols into the blood and develop coronary heart disease in their teens and twenties. Those of us without sitosterolemia who increase sterol intake with sterol-enriched foods increase blood levels of sterols several-fold. Is this healthy, or does it contribute to coronary plaque as it does in people with sitosterolemia?

Below, I've reprinted a previous Heart Scan Blog post on sterols.


Sterols should be outlawed

While sterols occur naturally in small quantities in food (nuts, vegetables, oils), food manufacturers are adding them to processed foods in order to earn a "heart healthy" claim.

The FDA approved a cholesterol-reducing indication for sterols , the American Heart Association recommends 200 mg per day as part of its Therapeutic Lifestyle Change diet, and WebMD gushes about the LDL-reducing benefits of sterols added to foods.


Sterols--the same substance that, when absorbed to high levels into the blood in a genetic disorder called "sitosterolemia"--causes extravagant atherosclerosis in young people.

The case against sterols, studies documenting its coronary disease- and valve disease-promoting effects, is building:

Higher blood levels of sterols increase cardiovascular events:
Plasma sitosterol elevations are associated with an increased incidence of coronary events in men: results of a nested case-control analysis of the Prospective Cardiovascular Münster (PROCAM) study.

Sterols can be recovered from diseased aortic valves:
Accumulation of cholesterol precursors and plant sterols in human stenotic aortic valves.

Sterols are incorporated into carotid atherosclerotic plaque:
Plant sterols in serum and in atherosclerotic plaques of patients undergoing carotid endarterectomy.




Though the data are mixed:

Moderately elevated plant sterol levels are associated with reduced cardiovascular risk--the LASA study.

No association between plasma levels of plant sterols and atherosclerosis in mice and men.




The food industry has vigorously pursued the sterol-as-heart-healthy strategy, based on studies conclusively demonstrating LDL-reducing effects. But do sterols that gain entry into the blood increase atherosclerosis regardless of LDL reduction? That's the huge unanswered question.

Despite the uncertainties, the list of sterol-supplemented foods is expanding rapidly:




Each Nature Valley Healthy Heart Bar contains 400 mg sterols.












HeartWise orange juice contains 1000 mg sterols per 8 oz serving.













Promise SuperShots contains 400 mg sterols per container.














Corozonas has an entire line of chips that contain added sterols, 400 mg per 1 oz serving.














MonaVie Acai juice, "Pulse," contains 400 mg sterols per 2 oz serving.














Kardea olive oil has 500 mg sterols per 14 gram serving.










WebMD has a table that they say can help you choose "foods" that are sterol-rich.

In my view, sterols should not have been approved without more extensive safety data. Just as Vioxx's potential for increasing heart attack did not become apparent until after FDA approval and widespread use, I fear the same may be ahead for sterols: dissemination throughout the processed food supply, people using large, unnatural quantities from multiple products, eventually . . . increased heart attacks, strokes, aortic valve disease.

Until there is clarification on this issue, I would urge everyone to avoid sterol-added "heart healthy" products.


Some more info on sterols in a previous Heart Scan Blog post: Are sterols the new trans fat? .

Why obese people can't fast

Why do obese people claim it is impossible to fast?

Most overweight people are terrified at the prospect of facing any period of time without ready access to food. Persuading them to begin a program of intermittent fasting is a hopeless cause. They just refuse.

Contrary to popular opinion, this is not just glutonny at work. It is the effect of what I call "the cycle of hunger," the 2-hour up and down cycle of rising sugar and insulin, followed by their inevitable fall. The precipitous fall of sugar and insulin triggers mental fogginess, fatigue, and insatiable hunger. (By the way, this is the same phenomenon underlying the silly notion of "grazing.")

According to an LA Times article, fasting may be difficult to impossible for some people:

"Ruth Frechman, a registered dietitian in Burbank and spokeswoman for the American Dietetic Assn., says she frequently sees such extreme strategies backfire. 'You're hungry, fatigued, irritable. Fasting is not very comfortable. People try to cut back one day and the next day they're starving and they overeat.'"
(Not surprising, coming from the American Diatetic Assn. They, along with such agencies as the American Diabetes Association, are vocal proponents of low-fat, high-carbohydrate, "healthy whole grain" diets--you know, the diets that make us fat and diabetic.)

Ms. Frechman is correct: Having someone engage in a period of fasting, no matter how brief, when the diet leading up to the fast is filled with "healthy whole grains" and other carbohydrates will result in painful hunger that eventually overcomes any effort. A period of overeating typically follows the aborted attempt.

Fasting cannot work as long as the 2-hour cycle of hunger continues. The first step: Eliminate the 2-hour cycle of hunger by dramatically reducing or eliminating carbohydrates. Our preferred method is to eliminate wheat, cornstarch, and sugars. (Just be aware of wheat withdrawal, the fatigue that develops in the first 5 days after wheat elimination that affects up to 30% of people.)

Once wheat, cornstarch, and sugars are eliminated, hunger reverts to that of physiologic need--appetite will be smaller and less intense, since it is driven by your body's needs, not by abnormal stimulation from wheat, cornstarch, and sugar. The fear of not having food dissolves, the 2-hour cycle of mental fogginess, fatigue, and hunger will be gone.

Intermittent fasting is a wonderful strategy for reducing weight; gaining control over lipids, lipoproteins, and coronary plaque; regaining appreciation for food; reducing appetite. But it's not even worth trying unless you've already eliminated the unnatural appetite triggers that will booby-trap any fasting effort.

Test your own thyroid

134 people responded to the latest Heart Scan Blog poll:


When I ask my doctor to test my thyroid, he/she:

Accommodates me without question 45 (33%)

Questions why, but orders the tests 49 (36%)

Refuses because you seem "healthy" 20 (14%)

Refuses without explanation 4 (2%)

Ridicules your request 16 (11%)



That's better than I anticipated: 69% of physicians complied with this small request. After all, you're not asking for major surgery. You're just asking for a very basic test, as basic as a blood count or electrolytes. 36% of respondents said that their doctor asked why, but still complied; this is simply practicing good medicine--If there is a problem, your doctor would like to know about it.

However, the remainder--31%--were refused in one way or another. Incredibly, 11% were ridiculed.

Although this was not asked in the poll, I believe that it is a safe assumption that you asked with good reason: you're abnormally fatigued, you have been gaining weight for no apparent reason or can't lose weight despite substantial effort, or you feel cold at inappropriate times.

Let's say you're tired. Ever since last summer, you've suffered a gradual decline in energy.

So you ask your doctor to assess your thyroid. He refuses. "You're just fine! There's nothing wrong with you."

You disagree. In fact, you are quite convinced that there is something physically wrong. What do you do?

You could:

--Drink more coffee
--Exercise more in the hopes that it will snap you out of your lethargy
--Sleep more
--Take stimulants of various sorts

Or, you could get your thyroid assessed and settle the issue. But how can you get this done when your doctor won't accommodate you, even though you have perfectly fine health insurance and are simply interested in feeling better and preserving your health?

You could test your thyroid yourself. This is why we're making self-testing kits available. Test kits are available here.

This is yet another facet of the powerful revolution that is emerging: Self-directed health.

Trains, planes, and heart scans

A Heart Scan Blog reader posted the following question:

It is not clear to me why getting a cardiac scan is the necessary first step, if in fact the next step would be to bring down small LDL particles which is revealed on a NMR lipoprofile or VAP test. Why isn't the NMR or VAP test the first thing?

Good question. Think of it this way:

Lipoproteins, as measured via VAP (Vertical Auto Profile) or NMR (Nuclear Magnetic Resonance), provide a snapshot of risk from a metabolic viewpoint at that moment. Lipoproteins shift with the tides of age, menopause, weight changes, even what you ate last evening for dinner (especially small LDL). There are also other factors that cause coronary plaque, as well, not revealed through lipoprotein testing, such as vitamin D deficiency, smoking, high blood pressure, phosopholipase A2, lipoprotein(a), inflammatory factors, thyroid dysfunction, omega-3 fatty acid deficiency, etc.

A heart scan, providing a coronary calcium score, provides an indirect measure of coronary plaque that is the sum total of lipoprotein and other plaque-causing factors that have accumulated up to the time of your scan--regardless of the cause.

It means that two females, each 60 years old, with 70% small LDL, HDL 42 mg/dl, triglycerides 150 mg/dl, and mild hypertension, have identical markers for potential coronary risk, but can have widely different heart scan scores. One might have a score of zero, while the other might have a score of 300.

Why would the same panel of causes measured at one moment yield wildly different quantities of plaque? Several reasons:

1) The lifestyles, eating habits, and weight of each woman differed during their earlier years, not currently reflected in this moment's lipid or lipoprotein patterns. Perhpaps one experienced several years of extraordinary stress from a failed marriage, or suffered through two years of depression that caused her to smoke and overeat.

2) There are hidden factors that affect coronary plaque growth that we are presently not able to detect, e.g., vitamin D receptor genotype, cholesteryl-ester transfer protein variants, variation in inflammatory factors. If we can't measure it, we won't know whether it might influence coronary plaque risk.


With all the changes that occur over a person's life, with the uncertainties of yet-to-be-identified causes for coronary plaque, how can you possible know what your risk for heart disease truly is? Yup--a heart scan. Do it and you will know.

D2 and D3 are two different things

Helena posted this instructive comment in response to the Heart Scan Blog post, Weight loss and vitamin D. It illustrates the confusion common among physicians and pharmacists on the differences between D2 and D3.

(Edited slightly for clarity.)

Not many weeks ago a colleague of mine (let’s call him Eric) asked me if I knew the difference between D2 and D3 and I told Eric that D2 comes from irradiated mushrooms and D3 comes from wool. In other words, D3 is the same kind of vitamin as humans get from the sun. Humans just don’t get enough and we can’t produce it on our own, like the sheep can. (D3 is natural for humans, D2 is not.)

After telling Eric this, he asked me how he would know what he is taking and I gave him the medical definitions of them both (D2 = Ergocalciferol; D3 = Cholecaliciferol). Since I was aware that he had gotten his Vitamin D by prescription, I told him “I am 99.9% sure that you are taking D2, but I would be thrilled to find out I am wrong.”

Eric called his pharmacy right away and got the answer I was expecting: ergocalciferol. On confronting the person Eric was talking to, the answer he got back was that Ergocalciferol is the only Vitamin D they are giving out.

A week later, Eric had a new appointment with his doctor and decided to ask him about the D2/D3 issue. The doctor said he knew that there was a difference in them both, but could not say what, not even the basic facts I mentioned above. But the doctor stamped a post-it with what he had sent to the pharmacy just to show Eric. “Vitamin D3; 50,000IU tab” is what the stamp said.

Eric, off course, got confused and was starting to believe that the pharmacy had made a mistake by giving him Ergocalciferol (D2) since the doctor had given him D3, or at least that is what was stamped on the little note he had.

Today, after getting a refill of his Vitamin D he also got and kept all his paperwork that came along with it. Still believing that stamp the doctor had given Eric earlier, he asked me to double and triple check that my definition of D2 and D3 was correct. I did, just for my own sanity, and I was still right.

One of the sheets Eric brought me today was the “Patient Education Monograph” sheet stating the drugs and how to use it and so on. The thing that jumped out the most to me was this:

Generic Name: Vitamin D – Oral
Common Brand name(s): Drisdol, Maximum D3
Identification: PA140 Green Oval Capsule

This is the Drug Eric was given: Vitamin D 1.25 MG softgel; Generic name: Ergocalciferol

My researching mind went into high concentration mood and I started to dig. And this is what I found:

The brand name Drisdol is Ergocalciferol (D2), not D3. The Brand name Maximum D3 seems to be hard to find out there in cyber space as a brand name. But the ones I found that were called Maximum D3 seems to be the real stuff, however none of them required a prescription.

When trying to find out through the identification number on the pills (PA140) I now know for sure that Eric is taking Vitamin D2 and not the preferred Vitamin D3. The brand name, Drisdol, had the identification W on one side and D92 on the other, but it is still Ergocalciferol.

The only conclusion I can draw from all this is that the medical industry does not know or care about the difference in D2 and D3 – it is all same to them. And as long as the pharmacies only give out D2 it does not matter what the doctor prescribe anyway.

I know that people are most likely to be prescribed a D2 pill than to be told to buy over-the-counter D3. But it was almost heart breaking to see the letter D and number 3 right next to the drug Drisdol, as we know is a D2 vitamin. It just didn’t make sense to me that they can be labeled as the same type of medication, when we know it is not!



Incredible.

Why prescribe plant form D2 when you can get perfectly reliable, safe, effective D3--the human form, at the health food store for about $6?

Once again, it's the peculiar false bias of physicians and pharmacists: If it's prescription, it must be good; if it comes from a health food store, it must be bogus.

Humans need human vitamin D. Plain and simple.

For more on the D2 vs. D3 issue, see the Heart Scan Post, The case against vitamin D2.

Weight loss: Different causes, different solutions

Heart Scan Blog reader, Kris, related this enlightening story of weight loss (slightly edited for clarity).

Kris learned that excess weight is gained through multiple causes. The solutions are therefore multiple, not just one change in diet or two.


I started studying about my thyroid issue much earlier and did lose some weight. But ever since I started following Dr. Davis’s blog, it has given me confidence that I was on the right track. I did have my thyroid and iodine figured out from other sources, but Dr. Davis helped me to understand the issues with not only the thyroid but vitamin D3, fructose, fish oil, niacin, wheat etc. I have lost 43lb in last 14 months.

It seems to me that there are certain percentages of weight connected with different issues. For example, after I gave up alcohol and sugar, I lost about 14lbs from total weight of 243lbs, weight came down to about 229lb. Then it stopped at 229lb, even though I was in the gym almost 5 to 6 days a week with full workouts.

After I changed my thyroid medication to natural thyroid hormones (took synthetic T4 for over 10 years), the weight dropped down further 13lbs or so in matter of few days, shape of the face changed from moon shape/double chin to ordinary long face. Then it kind of stopped at around 213-216 lbs.

After giving up wheat, reducing carbs, increasing protein intake (whey protein, chicken etc. no soya, no fructose) the weight came down another 14lbs. Now it is around 200-202lbs and I am over 6.2 tall with heavy set of bones.

I feel better than I have ever in my life. More stamina, more clarity/no fog, more confidence and 99% of the time relaxed and being able to see the situation from multiple angles.

I use to be able to drink a liter or more jack denial without a problem in one evening but now can’t stand half a can of beer (I miss JD). Drinking alcohol makes me sick. I sleep well and if I wake up in the middle of the night, I have no problem going back to sleep. No more out of breath stair climbing at all.

One other thing: I used to be the most attractive meal to the mosquitoes, but not anymore. This year I haven’t been bitten once. I take my dog to the park everyday and I do not use any mosquito repellent, what a relief. I don’t know if it is because of thyroid, iodine, wheat or something else. Skin texture has changed dramatically. I do not use full soap or shampoo, 20% borax, 10 percent of my soap or shampoo for scent and rest water, mixed in a 500ml bottle. No more dandruff, dry skin, pimples for me.

Dr. Davis I am thankful to people like you who have the ability to see beyond what you have been taught and have the guts to say the way it is. Most of us work to make living on daily basis but some make their living while spreading their knowledge to save lives. Dr Davis you are one of those few people. Please keep it going.

Calling all losers!

I'd like to invite anyone who has followed the Track Your Plaque Break the Weight Barrier program to consider posting their stories and photos on the Heart Scan Blog.

Because our focus is prevention and reversal of coronary heart disease, we have not made an effort to catalog the weight loss experience that people have while on the program. For many, weight loss has been substantial. (Several people this week alone have reported weight loss of 9 to 46 lbs in the past 6 months.)

It would be helpful to hear and see these results.

For those of you who don't mind having a story and photo on this Blog, please come back in future to post your results. You will find this post by entering "weight loss" into the site-specific search bar at the top of the page.

Weight loss and vitamin D

At the start of her program, Penny's 25-hydroxy vitamin D blood level showed the usual deficiency at 22 ng/ml.

She supplemented with 8000 units of vitamin D. Another 25-hydroxy vitamin D blood level several months later showed a level of 67.8 ng/ml, right on target.

But Penny also began our diet, including the elimination of wheat, cornstarch, and sugars, and, over 6 months, lost 34 lbs.

Now a much trimmer 146 lbs (still more to go!), another vitamin D blood level: 111 ng/ml.

Penny's weight loss means that the vitamin D is distributed in a smaller total volume, particularly a lower volume of fat.

This is a common phenomenon with substantial weight loss: lose weight and the need for vitamin D is reduced. The reduction in dose is roughly proportion to the weight lost. Vitamin D should therefore be reassessed with any substantial change in weight of, say, 10 lbs or more, either up or down, because of the influence of fat on vitamin D blood levels.

Some references on this effect:

Men and women over age 65:
Adiposity in relation to vitamin D status and parathyroid hormone levels: a population-based study in older men and women.

Obese women:
Low 25-hydroxyvitamin D concentrations in obese women: their clinical significance and relationship with anthropometric and body composition variables

Obese children:
Hypovitaminosis D in obese children and adolescents: relationship with adiposity, insulin sensitivity, ethnicity, and season.

African-Americans:
Relationship of vitamin D and parathyroid hormone to obesity and body composition in African Americans.

Although the bulk of the effect is most likely due to sequestration by fatty tissue, perhaps less sun exposure in obese people also contributes:
Body mass index determines sunbathing habits: implications on vitamin D levels.

How old are you?

George walks into my office. I ask him his age.

"I'm 21 years old," he declares.

Yet I look at George. He's got gray thinning hair, his posture is slumped forward rather than erect, the flesh on his upper arms hangs loosely, he's got wrinkles on his hands and face, brown spots on the back of his hands and arms. He looks more like 70 years old to me. "I don't think you're 21 years old. I think you're 70."

"Prove it," he says.

Okay. What now? Minus any formal identification like a driver's license, how do I prove that George is really 70-something and not 20-something? Not an easy thing, when you think about it. If George were a tree, I'd cut him down and count his rings. Is there such a phenomenon in humans?

This is actually a fascinating area of research, looking for reliable biomarkers of aging.

Among the most quantitative markers of aging is telomere length. Telomeres were once dismissed as nonsense sequences in DNA. However, more recent thought among geneticists is that telomeres shorten with aging and provide the body's cells a timeline of aging. This way, George's cells act like they are 70, not 13, and don't start producing gobs of growth hormone and testosterone in preparation for puberty.

What can slow or stall the shortening of telomere length? There are two I'm aware of:

1) Caloric deprivation--i.e., taking in fewer calories. This was among the theories explored by Dr. Roy Walford during his Biosphere2 experience, based on his work in mice that showed that caloric deprivation nearly doubled lifespan.

2) Vitamin D--Richards et al (2007) found that, the higher the vitamin D, the longer the telomere length. The highest vitamin D levels conferred a 5-year effective difference in telomere length.

So, if I could look inside George's cells and count his telomeres, I could judge with confidence whether he was 21 or 70. Or, he could take vitamin D sufficient to increase blood levels to a healthy range and be more like 65.

No high blood pressure

Primitive cultures that were, until recently, unexposed to the modern world, reveal some important insights into blood pressure.

The Yanomamo of South American, the Xingu Indians of Brazil, rural Kenyans, and the natives of Papua, New Guinea have average blood pressures of 103/63 mmHg. Even more incredibly, while 90% of modern Americans will develop high blood pressure as they age, the members of these primitive cultures do not develop age-related hypertension.

What's the secret? Perhaps the full "secret" of their remarkably low blood pressure has not been fully unraveled, but several observations have emerged:

--They are not exposed to modern processed foods like pretzels, crackers, and breakfast cereals.
--Low-carbohydrate foods. Carbohydrates are largely the product of the food industry, convenience foods bought in stores. No such thing in the jungle.
--Living outdoors, having to forage and hunt, walk to your destination, not drive or wait in line for food.
--Outdoor lives, wearing little more than a few strands of clothing, exposes you to plentiful vitamin D activation from sunlight exposure.
--Consuming wild game, rich in omega-3 fatty acids, enhances endothelial health and reduces blood pressure.
--Wild plants, roots, and berries, as well as wild game, along the coast, are richer in iodine.

The studies examining the habits of the Yanomamo and other primitive cultures focused principally on sodium intake. Indeed, the very low sodium intake of primitive cultures was associated with lower blood pressure--up to 6 mmHg reduction. But there's clearly more to learn than "cut your salt."

Name that food

What common food can:

• Cause destructive intestinal damage that, if unrecognized, can lead to disability and death?
• Increase blood sugar higher and faster than table sugar?
• Trigger an autoimmune inflammatory condition in the thyroid (Hashimoto’s thyroiditis)?
• Create intestinal bloating, cramps, and alternating diarrhea and constipation, often labeled irritable bowel syndrome?
• Trigger schizophrenia in susceptible individuals?
• Cause behavioral outbursts in children with autism?
• Cause various inflammatory diseases such as rheumatoid arthritis, ulcerative colitis, dermatitis herpetiformis, systemic lupus, pancreatic destruction, and increase measures of inflammation like c-reactive protein?
• Cause unexplained anemia, mood swings, fatigue, fibromyalgia, eczema, and osteoporosis?


The food is wheat. Yes, the ubiquitous grain we are urged to eat more and more of by the USDA (8-11 servings per day, according to the USDA food pyramid), American Heart Association, American Dietetic Association, and the American Diabetes Association. Wheat is among the most destructive ingredients in the modern diet, worse than sugar, worse than high-fructose corn syrup, worse than any fat.

What other common food can result in such an extensive list of diseases, even death?

Celiac disease alone, a severe intestinal inflammatory condition from wheat gluten, affects an estimated 3 million Americans (Celiac Disease Foundation). The medical literature is filled with case reports of deaths from this disease, often after many years of struggle with incapacitating intestinal dysfunction and the sufferer's last days plagued by encephalopathy (brain inflammation).

What happens when you remove wheat from the diet?

The majority of people quickly shed 20-30 lbs in the first few weeks, selectively lost from the abdomen (what I call “wheat belly”); blood sugar plummets; triglycerides drop up to several hundred milligrams, HDL increases, LDL drops (yes, wheat elimination is a means of achieving marked reduction in LDL cholesterol, especially the small, heart disease-causing variety); c-reactive protein plummets. In addition to this, intestinal complaints improve or disappear, rashes improve, inflammatory conditions like rheumatoid arthritis improve, diabetes can improve or be cured, and behavioral disorders and mood improve.

Along with the ill-fated low-fat dietary advice of the last 40 years, the advice to eat plenty of "healthy whole grains" is responsible for untold disease and suffering. Yes, if you start with a fast food and junk diet and replace some of the calories with whole grains, you will be better off. (That was the logic--the Nutritional Syllogism--of the studies that established the benefits of whole grains over processed, "white" grains.)

But eliminate wheat grains and health takes a huge leap forward. And, no, there is no such thing as wheat deficiency--B vitamins, insoluble fiber, some protein--can easily be replaced by other foods.

Heart Defects Simplified



For as long as I've known him, echocardiography technologist, Ken Heiden, has had a deep fascination with congenital heart disease. Ken has just written a wonderful book on congenital heart disease called Heart Defects Simplified.

While this is a bit off-topic for the Heart Scan Blog, I know that there is a serious lack of helpful information for people with congenital heart disease and parents of children with congenital heart defects. So I asked Ken to tell us something about his book.



WD: I've reviewed your book and have been thoroughly impressed with the clarity and detail with which you handle a complicated topic. You somehow manage to make it easy to grasp, far more than any other resource I've used in past. Do you feel that your book serves a previously unmet need?

KH: This book serves an unmet need in that it presents the complex subject of congenital heart defects in a simplified manner. Most books on this subject are anywhere from 300-1700 pages in length and tend to be written for doctors. Further, most of these books have very few diagrams, and they rely upon their explanations to describe these defects.

Heart Defects Simplified is 104 pages in length, describes the most common defects, including surgical repairs, in a two-page format with full-color diagrams on the left and complete descriptions on the right of each chapter. The book is particularly written for sonographers, nurses and parents, but it is valuable for anyone interested in this subject. It is particularly useful in clinical situations because it is convenient to lay out at your side with a coil-bound format and durable pages. Further, there are appendixes which include "Surgical Procedures in Alphabetical Order," "Prevalence of Congenital Heart Disease," "Scanning Protocols for Echocardiographers," "Imaging Tips," a glossary and a worksheet for echocardiographers.


WD: I know that many people with loved ones who have congenital heart defects, particularly parents of children with such conditions, are often kept in the dark about the details of the condition. Is your book suitable for the non-technical reader, such as parents?

KH: This book is an excellent resource for parents. It is written in language that is understandable by parents as well as technologists and nurses. The full-color diagrams provide invaluable insight into this very complex world. Most importantly, this book attempts to make the subject of congenital heart defects accessible to anyone who wishes to comprehend this subject.


WD: I understand that people with congenital heart defects and parents are active participants in online discussion groups. Will your book serve as a resource for people who participate in these groups?

KH: This book is not only a resource for sonographers and parents, but the book is accompanied by a blog (HeartDefectsforEveryone.blogspot.com) that attempts to address many of the concerns commonly encountered with congenital heart defects. This blog is a work in progress, but I hope to provide a forum for parents, healthcare personnel, and others to share their questions and concerns about congenital heart disease.

My experience with the omega-3 index

I just got back my own results from the Gene Smart laboratory reporting my omega-3 index and omega-6:omega-3 ratio.

My results:

Omega-3 index: 8.2%

Omega-6:omega-3 index: 3.2 to 1

Not too bad, but not as good as I'd expected. Hmmm.

Although the omega-3 index of 8.2% puts me in the lower risk category for sudden cardiac death, I was hoping for a level of 10% or slightly greater, the level that I believe is more likely to be related to plaque inactivation or reversal. I obtained this level of omega-3 averaging an intake of EPA and DHA of about 2500 mg per day.

I was somewhat disappointed by the omega-6:omega-3 index. Although it's clearly better than the American average range of 20:1, it is short of the ideal of 2:1 or even 1:1. Since I purposely avoid omega-6-rich sources like corn oil, vegetable oils, sunflower or safflower oils, I wonder if I've overdone the nuts. The two ways to improve the omega-6:omega-3 ratio are to 1) decrease omega-6, or 2) increase omega-3. I'm going to do both.

So I thought I was doing pretty well. But there's clearly room for improvement.

Remember: If just reduction of cardiovascular risk is your interest, then a lackadaisical attitude towards these issues might work. But if your interest is elimination of risk and reversal of atherosclerotic plaque, then it pays to go the extra mile. In this case, knowing your omega-3 index and omega-6:omega-3 ratio might tighten up your program.

The Omega-3 Index: The higher, the better?

So you take a few fish oil capsules every day and eat fish once or twice a week. What is the blood and tissue level of omega-3 fatty acids generated by your habits?

A number of variables enter into the equation. For instance, if you take fish oil capsules, what is the concentration of omega-3 fatty acids? How well are they absorbed? After absorption, how effectively are omega-3 fatty acids incorporated into cell membranes?

Even if you take fish oil supplements, it is hard to know just how much you’ve increased blood levels. It is now possible to measure the amount of omega-3 fatty acids in your bloodstream, a value called the omega-3 index. Too little and you might still be at high risk for cardiovascular events.


The Omega-3 index and sudden cardiac death

Two large studies have demonstrated that higher omega-3 blood (the level in red blood cells, or RBCs) levels were associated with reduced likelihood of sudden cardiac death. The risk for sudden cardiac death was 10-fold higher for the lowest omega-3 RBC levels compared to the highest.



Harris WS 2008; adapted from Siscovick DS et al 1995 and Albert CM et al 2002
(The omega-3 Index was derived from whole blood omega-3 levels, which correlate with RBC omega-3 levels, and are thus “estimated.”)



What’s the average omega-3 RBC level for Americans? Most Americans have omega-3 RBC levels in the 2.5-4.0% range, consistent with the tallest bars at the left and associated with greatest risk for sudden cardiac death. People with heart disease can have levels less than 1%. Some authorities propose that this new measure be called the omega-3 index.

Subsequent studies have shown that the omega-3 index has greater power to discriminate who will have a heart attack or die from sudden cardiac death better than any other common laboratory measure of coronary risk, including LDL cholesterol, HDL cholesterol, triglycerides, total cholesterol to HDL ratio, homocysteine, and c-reactive protein.

Just as hemoglobin A1c offers a 3-month look into blood glucose levels, the omega-3 index reflects your long-term omega-3 intake. The quantity of RBC omega-3s also closely parallels the quantity of omega-3s in heart tissues.


What is an ideal omega-3 index?


The above studies relating RBC omega-3 levels and sudden cardiac death suggest that a level of 6.3-7.3% is associated with far fewer fatal events?but events are not eliminated at this level. Is there even greater benefit with levels higher than 6.3-7.3%?

A recent analysis of females from the Harvard School of Public Health suggested that RBC omega-3 levels as high as 8.99% were still associated with non-fatal heart attack (myocardial infarction), compared to 9.36% in those without heart attacks. This suggests that even higher levels are necessary to prevent non-fatal events.

Should we target 10%? 12%? Maybe higher? Any higher and we are toeing the level achieved by the Inuits, the “Eskimoes” of Greenland, northern Canada and Alaska who have been observed to have a low rate of heart disease.


What’s your omega-3 index?

The appreciation of the importance of omega-3 fatty acids marks one of the greatest health revelations of the last 50 years. We can now measure it.

The ability to measure the proportion of omega-3 fatty acids in red blood cells may provide yet another means for all of us to further reduce risk for cardiovascular events.

If you are interested in knowing your omega-3 index, we are now making the fingerstick test kits available by going here.

Vitamin D increased my cholesterol

A friend told me this story.

Her friend, Linda, had added vitamin D to her daily supplements. Because she'd had a vitamin D blood level of 22 ng/ml, she was taking 6000 units per day.

However, Linda also had a high cholesterol value with a total cholesterol of 231 mg/dl. After several months on the vitamin D, she had another cholesterol panel. Total cholesterol: 256 mg/dl.

"It must have been the vitamin D! So I stopped it right away."

Is this true? Does vitamin D raise the level of blood cholesterol? Yes, it does. But it's a good thing. Let me explain.

Followers of The Heart Scan Blog know that total cholesterol is really a mix of 3 other factors:

Total cholesterol = LDL cholesterol + HDL cholesterol + triglycerides/5

This is the Friedewald equation, still used today in over 95% of cholesterol panels. So, by the Friedewald equation, anything that increases LDL, HDL, or triglycerides will increase total cholesterol.

One of the spectacular changes that develops over a year of taking vitamin D is that HDL cholesterol skyrockets. While sensitivity to this effect varies (probably on a genetic basis), HDL increases of 10, 20, even 30 mg/dl are common. A starting HDL, for instance, of 45 mg/dl can jump up to 65 or 70 mg/dl, though the effect requires up to a year, sometimes longer.

Vitamin D can also reduce triglycerides, though the effect is relatively small, usually no more than 20 mg/dl or so. Likewise, the effect on LDL is minor, with a modest reduction in the small type of LDL.

So the dominant effect of vitamin D from a cholesterol standpoint is a substantial increase in HDL. Looking at the equation, you can see that an increase in HDL is accompanied by a commensurate increase in total cholesterol. If HDL goes up 25 mg/dl, total cholesterol goes up 25 mg/dl.

So Linda is absolutely correct: Vitamin D increases cholesterol--but it's a good thing that reduces risk for heart disease and is an important part of a coronary plaque-reversal program.

This is yet another reason why I advocate elimination of total cholesterol on lipid panels. There is no useful information in the total cholersterol value, only the potential for misinformation.

Nutrtional ignorance is not unique to the U.S.

Heart Scan Blog reader from Australia, Michaela, also a mother of a son with a complex congenital heart defect, wrote this series of e-mails to me. (Published with Michaela's permission.)


I've been reading the article, Valve disease and Vitamin D from April '07, by Dr William Davis. I'm hoping you may have some information on the topic. I'm hoping someone will have time to help me.

I have been supplementing my 15 year old son with Vit D for 4 months but only 1000 (U) per day. I would like to increase the dosage but am not sure if I would do him more harm than good.

I have been researching vitamins and supplements on the net for a few months and have been amazed at what I have found. I only wish I had done it years ago. My son has been let down by the Australian Medical Profession and it's a race against time now to keep him well and avoid a heart transplant.

My son was born with aortic stenosis and had a valvotomy at 4 weeks of age. This damaged the aortic valve and he had a Ross Repair procedure at aged 3. This left him with a damaged heart muscle and leaking aortic & pulmonary valves. In May '08, his heart grew more enlarged, causing the mitral & tricuspid valves to also leak.

I took him to Bangkok in Feb this year where he had 70 million of his own Adult Stem Cells directly injected into his heart muscle with the hope of strengthening the muscle and eventually valve replacement.

My son has recovered from the surgery and is once again symptom-free, thanks to the wonderful advice followed by the Author & Cardiologist, Stephen T. Sinatra. I have followed his supplement regime and what a difference! Of course, this won't last while my son's valves continue to leak.

My son has also developed secondary hyperparathyroidism, bone thinning and hypothyrodism. Vit D & Calcium have something to do with this I believe.

My Australian Doctors have never made mention of any vitamins or supplements .... EVER! Transplant is all they will consider and we are not having it.

If you have any info or links to any sites which may be useful to me, could you email them to me? I would be grateful for any help I could get.

Sincerely
Michaela



I responded to Michaela's e-mail:

Hi, Michaela--

Vitamin D is extremely important. Sometimes, hyperparathyroidism and calcium derangements are caused by vitamin D deficiency. You might be able to get help with this from an endocrinologist, since they are the ones who deal with hyperparathyroidism. An endocrinologist might even be familiar with several recent studies that document this phenomenon:

Vitamin D therapy in patients with primary hyperparathyroidism and hypovitaminosis D

Vitamin D deficiency and primary hyperparathyroidism

Also, see the discussions at www.vitamindcouncil.org from Dr. John Cannell.

Because of the complexity of your son's health, it might be hazardous to stray too far away from conventional care though you and I know that there are limitations to that perspective. For that reason, I would urge you to press for answers from a knowledgeable endocrinologist.

I hope you find the answers you need.

William Davis, MD



Several months later, Michaela provided this update:

Hi Dr Davis,

I wrote to you back in July regarding my 15 year old son's need for a Heart Transplant through a failed Ross Repair and the possible Vitamin D connection. You sent me some valuable links and I thank you again for that.

I just wanted to let you know, I think you have given me the answers. I increased Lee's Vitamin D supplement to 6000U a day and, along with the recommended nutritional supplements of US Cardiologist Dr Stephen T Sinatra, there have been remarkable improvements! Lee also had 70 million of his own Adult Stem Cells injected into his heart in February. As we know, Stem Cell Therapy takes time and Lee was looking like time was quickly running out.

I have removed him from the transplant list. He is now reading normal Kidney function, the BNP (Brain Natriuretic Peptide, a measure of heart failure] has dropped by 7000 and his liver size has reduced to where it no longer causes him discomfort. The liver tests show it's still affected but it's function is improving each month. His last Echo was in early July and there had been a reduction in the size of his heart, which is so important.

To the Doc's, Lee can't get better, there is only transplant or death so you can imagine the surprise on their faces to see him looking and feeling so well with their tests to back it up. Still, even though it's staring them in the face, they don't want to know about it. They have no interest in what supplements he is on or Stem Cell therapy. God help their other patients. I view them in the waiting room and think of them as lambs to the slaughter.

We are not spoiled for choice with Doc's here in Western Australia. I have to take what I can get and there is not many who would take on Lee's case. He was number 1 on the transplant list and a most urgent case. Not many were willing to even look at him with his cardiac history and all I had to help was the arrogant Doc's at the Advanced Heart Failure Unit. They were not at all interested in his secondary hyperparathyroidism. I suppose it didn't matter what else he had compared to his heart problems.

Anyway, I'm writing to thank you. Lee would be transplanted or dead now if it wasn't for Dr's like you sharing their knowledge online. I wish I had researched things years ago, Lee might not have sunk so low if I had. I don't know if the transplant can be held off indefinitely, but like I tell Lee, "Stay well. There are amazing people out there doing amazing things, if you can just hang on. The miracle is around the corner." He's so well, you'd have to see him to believe it. But I have 7 kids and Lee is as physically active and as well as the other 6! For how long he can stay like this, I don't know but if his ejection fraction [a measure of left ventricular strength] can keep climbing and his body gets stronger, I have hope for another attempt at valve replacement.

I'm still shocked and angry that nutritional supplements have never been mentioned in the 15 years I've been dealing with cardiologists. Surely they know about them. I have read through dozens of reports online of the benefits of them--Why haven't they?! Thank God for the online Doc's such as yourself, the valuable info would never make it out of a Doctor's office in Western Australia! I've had to leave my country for Stem Cell therapy and then implore overseas Doc's for advice and information. What does that say for the Australian Medical Profession? Not a lot! They put him in the position he is in yet don't want to help get him out.

I'm so very grateful to you, thank you and God bless.

Michaela



Note: The above is not meant to be an implicit endorsement of stem cell therapy. This was just part of Michaela's story about her son.

Eat cranberries

Most people already know that cranberries are useful for preventing urinary tract infections. Cranberries can also be useful for preventing other sorts of infections, such as dental cavities and stomach ulcers because of cranberry's ability to block bacterial adhesion.

Cranberries can also be a useful component of a heart healthy program.

Several unique properties of cranberries contribute to various aspects of heart health:

• Cranberries are a rich source of pectin--Pectin is a soluble fiber, the sort that binds bile acids in the intestinal tract and naturally reduces LDL cholesterol.
• Cranberries are a rich source of polyphenols and flavonoids--Including the wonderfully fascinating anthocyanins, the flavonoids that confer the beautiful red color. Surprisingly, cranberries are richer in polyphenols and flavonoids than blueberries, strawberries, and grapes. Cranberry juice is also rich in these compounds. However, beware of cranberry juice "cocktail," which is diluted with other liquids such as high-fructose corn syrup. Like grapes, cranberries are a source of resveratrol, the polyphenol also found in red wines that some believe is responsible for reduced risk for heart disease and extending life.
• Cranberries have high antioxidant activity--Cranberries are among the highest in antioxidant capacity against superoxide radicals, hydrogen peroxide, and hydroxyl radicals, oxidizing factors believed to underlie heart disease, cancer, and aging. Cranberries also reduce the oxidation of LDL cholesterol particles.
• Cranberries block uric acid production--Cranberries have the unique ability to block the activity of an enzyme, xanthine oxidase, that converts xanthine to uric acid. Uric acid is believed to add to heart disease risk and is the factor responsible for gout.
• Cranberries increase HDL cholesterol--Cranberry juice increases HDL by 3-4 mg/dl.

Cranberries are only modest sources of sugars, with 7.19 grams “net” carbohydrates (total carbohydrates minus fiber content) per cup of whole raw cranberries.

The best way to eat cranberries is to consume the real thing: eat the whole berry, as in sugar-free cranberry sauce or added to baked dishes like chicken. Second best are dried cranberries. However, be careful of the overly-sweetened dried cranberries that contain added sugar (for a total of 78 grams sugar per cup--far too much). Unsweetened dried cranberries can be purchased, or you can dry them yourself.

Cranberry juice is another way to obtain the health benefits of cranberries; the unsweetened juice, while quite tart, is the best with 30.5 grams sugar per 8 oz--so don't drink more than 4 oz at a time. The more common cranberry juice “cocktails” are generally too sugary and/or too dilute for full health benefit.

The cranberry harvest season in Wisconsin, Michigan, Oregon, Massachusetts, and New Jersey is just getting underway, so we should be seeing fresh cranberries on store shelves or farmers' markets any day now.

Procedures 'R Us

Kay came to the office for an opinion.

Over the past 8 months, she'd received a stent to the left anterior descending coronary artery and, during a separate procedure, a stent to the left subclavian artery.

"My cardiologist was very capable doing procedures. But when I asked, 'What do I do now?' he barely said a word and handed me a presciption for Crestor."

This kind of incredible neglect is the norm: Write a prescription for statin drug, delegate dietary advice to the hospital dietitian who advocates a heart disease-causing low-fat diet, followed by hospital discharge. You are expected to report any recurrent symptoms (which are inevitable), at which point you might "qualify" for another procedure.

It would be malpractice if it were not the prevailing standard in the community. Yes, the prevailing standard is neglect--neglect to identify, quantify, and correct all the identifiable causes of heart disease; neglect to discuss the nutritional methods that actually correct the abnormal patterns that cause heart disease; neglect to discuss nutritional supplements or medications beyond statins that further reduce heart disease risk and "need" for more procedures. In other words, the prevailing community standard is to stent, bypass, prescribe statin. It is not to understand why the disease occurred in the first place, correct the causes and minimize or eliminate any future danger or need for procedures.

I see consultation after consultation involving stories just like Kay's. People are frightened and they sense intuitively that nobody raised the question of why they have a potentially fatal disease.

Don't allow yourself to fall victim to this incredibly neglectful mode of practice, the one that has enriched hospitals, the drug industry, many cardiologists, but does little to address the actual disease.

Restaurant eating: A fructose landmine

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

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

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

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

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

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

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

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

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

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

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

A glycation rock and a hard place

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

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

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

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

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

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

Is einkorn the answer?

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

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

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

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

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

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

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

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

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

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

Genetic incompatibility

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

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

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

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

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

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

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

The folly of an RDA for vitamin D

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

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

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

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

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

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

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

Heart scan: Standard of care?

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

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

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

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

The costs of doing drug business?

Here's a telling situation.

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

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

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

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

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

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

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

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

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

I use Sloniacin and Enduracin almost exclusively.

Measurement

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

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

Among the most helpful health measurement tools:

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

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

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

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

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

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

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

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

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


Courtesy Wellcome Library, London

I lost 37 lbs with a fingerstick

Jack needed to lose weight.

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

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

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

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

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

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

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

The two kinds of small LDL

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

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

There are two basic varieties of small LDL particles:

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


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

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

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

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

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

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

--Small LDLs are more glycation-prone.

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

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

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

I welcome any unique observations on this issue.