Why healthy can make us fat


Brian Wansink, author of Mindless Eating: Why we eat more than we think (see yesterday's Heart Scan Blog post), also has a Blog. Despite the bland advice offered on much of the Prevention Magazine and website, Wansink's Food Think Blog is a winner.

In a recent post, Wansink quotes a report from Science Daily that described a study he recently published in the Journal of Consumer Research. Wansink's study describes how just applying the label "healthy" to fast food choices increased consumers' calorie intake:


"When we see a fast-food restaurant like Subway advertising its low-calorie sandwiches, we think, 'It's OK: I can eat a sandwich there and then have a high-calorie dessert,' when, in fact, some Subway sandwiches contain more calories than a Big Mac."

In one study, Chandon and Wansink had consumers guess how many calories are in sandwiches from two restaurants. They estimated that sandwiches contain 35% fewer calories when they come from restaurants claiming to be healthy than when they are from restaurants not making this claim.

The result of this calorie underestimation? Consumers then chose beverages, side dishes, and desserts containing up to 131% more calories when the main course was positioned as "healthy" compared to when it was not--even though, in the study, the "healthy" main course already contained 50% more calories than the "unhealthy" one.

"These studies help explain why the success of fast-food restaurants serving lower-calorie foods has not led to the expected reduction in total calorie intake and in obesity rates," the authors write.


Interesting. In fact, I've had many patients say that they eat at Subway or similar chains and choose the "healthy" options. "That's got to be better than a cheeseburger and fries!" Perhaps not. (Of course, you can't leave Subway or other fast food operation feasting on wheat products.)

Wansink can be counted on for some truly fascinating observations into many behaviors that are subconscious but explain at least part of the reason why we're so fat. Though his Blog has a relatively short history of posts, there's lots of great commentary.

Pierre Chandon and Brian Wansink. "The Biasing Health Halos of Fast Food Restaurant Health Claims: Lower Calorie Estimates and Higher Side-Dish Consumption Intentions" Journal of Consumer Research, October 2007.

Outsmarting the enemy


"Everyone--every single one of us--eats how much we eat largely because of what's around us. We overeat not because of hunger but because of family and friends, packages and plates, names and numbers, labels and lights, colors and candles, shapes and smells, distractions and distances, cupboards and containers. This list is almost as endless as it's invisible.

Invisible?

Most of us are blissfully unaware of what influences how much we eat . . . We all think we're too smart to be tricked by packages, lighting, or plates. We might acknowledge that others could be tricked, but not us. That is what makes mindless eating so dangerous. We are almost never aware that it is happening to us."



So opens Brian Wansink's book, Mindless Eating: Why we eat more than we think.

Wansink studies consumer behavior at Cornell University. He's the guy who scrutinizes in excruciating detail why we eat what we do, what factors determine what we eat like food color and smell, the company we keep, product packaging. He works without food industry funding, though there are plenty of researchers who do this sort of research funded by the likes of Kraft, Nabisco, and Kellogg's.

His book is packed full of the conclusions he and his team have come to over the years studying our buying and eating habits. While this information could (and is) be easily used by the food industry to coerce us to eat more and more, understanding many of the concepts Wansink talks about can also open your eyes to their clever tactics.

He especially details how our internal satiety signals fail us when external cues are present that easily trip us up. He talks about one experiment he ran in which soup bowls were rigged with concealed rubber tubes in the bottom that continually replenished the soup as the person consumed it. Thus, with the bowl continually refilled, the eater had no idea how much he or she had consumed. When the quantity of soup eaten from the endless bowl was compared to people eating from standard bowls, there was as much as a three-fold increase in the quantity and calories eaten.

Just be aware that, while Wansink is an expert in consumer eating behavior, he is not necessarily an expert in nutrition. Just as a card shark can show you lots of clever tricks to hoodwink your opponent, he might not be the best person to teach you how to play bridge.

For a great hint at some of the interesting and all-too-human observations Wansink makes, the online Prevention Magazine posted a brief video:

http://link.brightcove.com/services/link/bcpid1155399889/bclid1171884988/bctid1113465050

We might not be able to stop Big Food from selling garbage foods, but we can at least be armed with insight into how we are subconsciously coerced into eating more.

Test Of Scanner Saves A Doctor's Life


















Read the story online at http://www.courant.com/news/health/hc-luckydoc.artsep10,0,7572510.story?coll=hc_features_promo

I personally hate these stories, the ones that turn heart scans into drama by describing how someone had a heart scan, then turned out to have so much coronary plaque that they had to have bypass surgery.

But I point this one out because the story is related in an interesting way. It highlights the utter ignorance that operates in heart disease detection.

The story highlights how a 50-year-old, 5 ft 8, 150 lb slender, exercising neurologist underwent a CT coronary angiogram in a newly installed device in a Hartford, Connecticut hospital (not a heart scan) that detected entirely unsuspected severe and diffuse coronary disease. You know the rest: abnormal stress test, heart catheterization, bypass surgery of the hapless doctor-now-patient, followed by grateful patient saying things like "This machine saved my life."

It probably is true. You've seen these stories before. I've witnessed these sorts of headline-makers for the past decade. I remain surprised that it still happens.

The doctor is not some ignorant, uninformed man who can't even fill out his income tax forms. Yet how does a man like this walk around with life-threatening disease and not know it? Why does it still make headlines?

Anyway, despite all my jawing about heart scans and early heart disease detection, many physicians and the public remain in the stone age of heart disease. Even though this neurologist's story made headlines, the many other people who 1) identified their heart disease earlier with a simple heart scan, then 2) took action to put a stop to it, do not make headlines. But that's the way to go.

Why isn't the rest of the story being told? Why was this man's heart disease uncovered only in its late phases? Hartford, Connecticut is not some backwater. I've been there. It's a major city with large hospitals and a University Medical Center. But a professional with presumed knowledge of health and his doctor(s) allowed this to happen?

In other words, this is not a story of success, but of failure--failure to identify coronary disease years earlier when preventive action would have prevented bypass. But that's not such a compelling headline, is it?

As an aside, I'll bet you that this man has lipoprotein(a), a severe small LDL pattern, and severe deficiency of vitamin D. Correct these and it's unlikely he'll need bypass again. But that's kind of boring, isn't it?

The great food industry deception

I'd forgotten what a powerful report Peter Jennings and ABC News produced about the enormous deception perpetrated by the food industry and its effects on health until Dr. Joe Mercola posted the YouTube clips from the report on Mercola.com.

(This is not meant to be an endorsement of everything Dr. Mercola has to say. He says lots of things; I agree with only a fraction of it. But this is a gem.)

Although made in 2004, the report remains every bit as relevant today as it was then. It concerns me deeply that, despite reports like this being broadcast to Americans, the obesity epidemic continues unabated. In fact, it's worse just in the short three years since then.

Be aware of what the food industry is up to. They intensively market high profit margin foods to us--and especially our children--to increase sales. As Jennings points out, the U.S. government (USDA) is, for a variety of reasons both good and bad, complicit with this massive deception. While many media reports continue to focus on lack of exercise as the root cause for the obesity epidemic, it is really the active and purposeful selling of processed junk foods to Americans that is principally to blame.

By the way, how many of these foods proudly boast the American Heart Association Check Mark of approval?



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Part 4




Part 5

Dr. Joseph Prendergast and l-arginine

In response to a discussion started by Track Your Plaque Member, Rich, on the Member Forum, I tracked down Dr. Joseph Prendergast, who had posted a video on his unique experiences, both personal and professional, with l-arginine.

Dr. Prendergast describes some of this in a brief webcast. Here, I quote Rich:

“This 90-second video by a Palo Alto physician (internal/endocrine, diabetes specialist) will totally blow your mind.

http://enews.endocrinemetabolic.com/2007/08/16-12-years.html

You will see in the link below that he reversed his personal atherosclerotic disease, diagnosed in abdominal aorta at age 37—completely reversed. He's now much older."

http://www.endocrinemetabolic.com/about/press/larginine.pdf



I contacted Dr. Prendergast to find out more.

Dr. Joseph Predergast is founder of the Endocrine Metabolic Medical Center in Palo Alto, California, focused on providing care for people with diabetes. In addition to the website, he provides Blogs and newsletters, though most of his conversation is about diabetes issues. Dr. Predergast’s website is located at http://www.endocrinemetabolic.com.

I asked Dr. Prendergast several questions about his l-arginine experience. His brief answers are below.



1) What dose of l-arginine have you employed in your patients and why this dose?

The dose is 3 - 6 grams as suggested by the Stanford Cardiovascular Research Department Chairman John Cooke. http://med.stanford.edu/profiles/John_Cooke/

2) I gather that you have preference for specific preparations of l-arginine. Can you say why some preparations seem superior to others in your experience?

I started with pharmaceutical l-arginine from the pharmacy. I gradually began to add components that would augment the power of the l-arginine and have gone through 12–15 different products. I have completely reversed my own very severe atherosclerosis discovered at age 37 and there has been less than 0.05% cardiovascular disease in my endocrine practice in almost 17 years. Both my exams were evaluated with CT technology. I am now using ProArgi9 Plus that includes several anti-aging components and will likely never switch. http://www.synergyworldwide.com/synergycorp/home.aspx

3) Are you employing any other unique practices in your patients to reduce cardiovascular events?

Withdrawing as many prescription drugs as possible.




Interesting. Of course, I also advocate l-arginine as a facilitator of atherosclerotic plaque regression, though I am not as ebullient about its use as Dr. Prendergast.

Instead, I see l-arginine as a method that yields forced normalization of “endothelial dysfunction,” the abnormal constriction and other effects that develop when abnormal lipoproteins and unhealthy food by-products are present in the circulation. Endothelial dysfunction is an inevitable accompaniment of plaque.

However, unlike Dr. Predergast’s experience, despite our use of doses higher than he uses, I have never seen plaque regression just using l-arginine alone. Nonetheless, it’s good to hear that others are seeing at least some positive effects.

By the way, we have also had some positive posts on our Forum about the ProArgi9 product he uses.

Dr. Dwight Lundell on omega-3s and CLA



An interview with Dr. Dwight Lundell, cardiac surgeon and author of the new book, "The Cure for Heart Disease."


Dr. Lundell comes to us with a unique pedigree. He is a cardiothoracic surgeon practicing in the Phoenix, Arizona, area. Despite having performed thousands of coronary bypass operations, including numerous "off-pump" procedures earning him a place in the Beating Heart Hall of Fame and a listing in Phoenix Magazine’s Top Doctors for 10 years, more recently Dr. Lundell has turned his attentions away from traditional surgical treatment and towards prevention of heart disease and.

In particular, Dr. Lundell is a vocal advocate for omega-3 fatty acids from fish oil and conjugated linoleic acid, or CLA.

When I heard about Dr. Lundell’s unique perspectives, I asked him if he’d like to tell us a little more about his ideas. Here follows a brief interview with Dr. Lundell.



You’re a vocal advocate of the role of omega-3 fatty acids from fish oil in heart disease prevention. Can you tell us how you use it?

In my book, I recommend 3 g of fish oil daily. This would normally yield about 1000 mg of EPA and DHA depending on the concentration of the supplement. This is approximately the dose that reduced sudden cardiac death by 50%, and all cause death, by 25% in patients with previous heart attack.

In patients with signs of chronic inflammation such as heart disease, obesity, arthritis, metabolic syndrome or depression or in those patients with elevation of CRP, I would recommend higher doses, 2000 to 3000 mg per day of EPA and DHA. The FDA has approved up to 3400 mg for treating patients with severely elevated triglycerides.

I personally take a 2000 mg EPA and DHA per day because I have calcium in my coronary arteries.




Of course, in the Track Your Plaque program we track coronary calcium scores. Do you track any measures of atherosclerosis in your patients to chart progression or regression?

Carotid ultrasound with measurement of IMT [intimal-medial thickness] has been shown to be a good surrogate marker for coronary disease, as has vascular reactivity in the arm. CT scanning with calcium scoring is a direct marker of coronary disease. CT does not differentiate between stable or unstable plaque but there is no good noninvasive way of doing this.

The dramatic value of CT scan calcium scoring is to demonstrate to people that they actually do have coronary disease and to motivate them to make the necessary lifestyle and nutritional changes to reduce it. CT scan with calcium scoring is a direct way to measure the progression or regression of coronary artery disease. If there is a choice between a direct measurement and indirect measurement, always choose the direct method.

Every patient treated with CLA in my clinic, experienced significant reductions in C-reactive protein. These patients were also on a weight-loss program, so I can't prove whether it was the CLA or the weight-loss that improved their inflammatory markers. In the animal model for arteriosclerosis, CLA has a dramatic effect of reducing and preventing plaque. This has not yet been proven in humans.

Normally, when people lose weight 20% or more of the loss is lean body mass (muscle) this lowers the metabolic rate and frustrates further weight-loss. My patient, from teenagers to retirees, lost no lean body mass and continued to have satisfactory weight-loss when CLA was used as part of the plan.



In reading your book, your use of conjugated linoleic acid (CLA) as a principal ingredient struck me. Can you elaborate on why you choose to have your patients take CLA?

My enthusiasm for CLA is based on:

1) Safety?this is of paramount importance. Animal toxicity studies have been done, as well as multiple parameters measured in human studies, both of these are well reviewed recently in the American Journal of Clinical Nutrition (2004:79(suppl)1132s). CLA, a naturally-occurring substance, is not toxic or harmful to animals or humans. The only negative report is by Riserus in Circulation (2002), where he found an elevated c- reactive protein; however, he used a preparation that is not commercially available and not found in nature as a single isomer.

2) Effectiveness?also critically important. A recent meta-analysis [a reanalysis of compiled data] in the American Journal of Clinical Nutrition (2007; 85:1203-1211) demonstrated the effectiveness of CLA in causing loss of body fat in humans. The study also reconfirmed the safety of CLA.

Since we now know that atherosclerosis is an inflammatory disorder, any strategy that reduces low-grade inflammation without significant side effects would seem to be beneficial in the treatment and prevention of atherosclerosis. CLA not only has antioxidant properties, but it modulates inflammatory cascade at multiple points. CLA reduces PGE2 (in much the same way as omega-3) CLA also has been shown to reduce IL-2, tumor necrosis factor-alpha and Cox–2. It reduces platelet deposition and macrophage accumulation in plaques. It also has some beneficial effect in the PPAR [peroxisome proliferator-activated receptors, important for lipid and inflammatory-mediator metabolism] area.

Part of the effect of CLA may be because it reduces fat mass and thus the amount of pro-inflammatory cytokines produced by fat cells.

I reiterate and fully admit that CLA has not been shown to have any effect on atherosclerosis in human beings. However, the results in the standard animal models for atherosclerosis (rabbits, hamsters,APO-E knockout mice) are very dramatic.

From all I know, it appears that the effective dose for weight loss and the animal studies in atherosclerosis would be equal to about 3 g of CLA per day. The anti-inflammatory properties of CLA seem to work better in the presence of adequate blood levels of omega-3.



I’m curious how and why a busy cardiothoracic surgeon would transform his practice so dramatically. Was there a specific event that triggered your change?

The transition from a very busy surgical practice to writing and speaking about the prevention of coronary disease has not been particularly easy, but it has been very interesting. I can't really point to any specific epiphany, it was a general feeling of frustration that we were not making any progress in curing heart disease, which is what I thought I was doing when I began my medical career.

Of course, I enjoyed the technical advances, the dramatic life-saving things that you do and I did on a daily basis. American medicine is spectacularly good at managing crises and spectacularly horrible at preventing those crises.

The lipid hypothesis is old and tired, even the most aggressive statin therapy reduces risk of heart attack by about 30% in a relatively small subset of people. It's interesting that we're now looking at statins as an anti-inflammatory agent.


Thanks, Dr. Lundell. We look forward to future conversations as your experience with CLA and heart disease prevention and reversal develops!


More about Dr. Lundell's book, The Cure for Heart Disease can be found at http://www.thecureforheartdisease.net.


Note: We are planning a full Special Report on CLA for the Track Your Plaque website in future.

High-tech heart attack proofing


I was reminiscing the other day about what I was taught about heart disease in medical school some 20 years ago.

In the 1980s, the world was still (and remains) fascinated with this (then) novel "solution" to heart disease called coronary bypass surgery. As medical students, we all fought for a chance to watch a bypass operation being performed. And there was lots of opportunity. I was a medical student at St. Louis University School of Medicine, a center that boasted of a busy thoracic surgery service, performing up to 10 bypass operations every day.

Back then, coronary angioplasty was just a twinkle in Andreas Gruentzig's eye, still contemplating whether it was possible to put an inflatable device in the blockages of coronary arteries to re-establish blood flow. Risk detection for heart disease consisted of EKGs, screening for symptoms, detection of heart failure, and tests that are long forgotten in the dust bin of medical curiosities, tests like systolic-time intervals, phonocardiography (using amplified sound to detect abnormal heart sounds), and detailed physical examination. Treatment for heart attack involved nitroglycerin and extended bedrest. Bypass surgery would come after you recovered.

In other words, NONE of the tools we now use in the Track Your Plaque program for heart disease control and reversal were available just twenty years ago. There was no lipoprotein testing, no CT heart scans. Nobody recognized the power of omega-3 fatty acids (although epidemiologic observations were just beginning to suggest that eating fish might be the source of reduced risk for heart attack and cardiovascular death). Vitamin D? Why, that's in your milk so your babies don't get rickets.

So much of what we do today was not available then, nor were they even in the crystal ball of forward-looking people. I certainly had no idea whatsoever that I'd be talking and obsessing today about reversal of heart disease based on what I saw and learned back then.

Things have certainly come a long way and all for the better. The problem is that much of the world is stuck in 1985 and haven't yet heard that coronary disease is a manageable and reversible process. They've been sidetracked by the fiction propagated by the likes of Dr. Dean Ornish, the nonsense of low-fat diets aided and abetted by the food manufacturing industry and the USDA, the extravagant claims of some practitioners and the supplement industry. They haven't yet stumbled on the real-life experiences that are chronicled here in this Blog and the accompanying Track Your Plaque website.

Our program has been criticized for being too "high-tech," involving too many sophisticated measures like small LDL, lipoprotein(a) treatment, vitamin D blood levels. But when you see a woman reduce her heart scan score 63%, or a school principal's score plummet 51%, then that's reward in itself.

It's all about plaque

Just to keep my finger on the pulse of what is being said in the world of heart disease by the media, I subscribe to many publications.

Conversations abound about cholesterol, low-fat diets, now low-carb diets, not smoking, inflammation, etc. No doubt, these all have some importance in the conversation.

But the great majority of discussions fail to identify the one truly crucial factor to identify and track: coronary atherosclerotic plaque.

Sugar for breakfast

We were reviewing Stuart's diet because of his persistent small LDL, low HDL, modestly elevated triglycerides, and blood sugar of 107 mg/dl.

"I've changed my diet, doc. No kidding. We never fry our foods. No butter, no goodies. I don't know what else I can possibly do."

"Okay. Let's review your diet. What did you have for breakfast?"

"Orange juice, a big glass. Gotta get my potassium. Then cereal like Cheerios or Shredded Wheat, sometimes Kashi or Raisin Bran, always in skim milk. Gotta have my one slice of toast, no butter. I'll put some fruit preserves on it. You know, real fruit. Only whole wheat bread, never white. On Sundays, we always go out for pancakes, but now we order only whole wheat."

Many of us have gotten into a peculiar habit: Having what amounts to pure sugar for breakfast. Perhaps there's a little fiber thrown in with it, but many people indulge in breakfasts that are sugar and plenty of it. That's precisely what Stuart is doing: A breakfast that, while it doesn't contain a huge amount of sugar outside of the orange juice, is promptly converted to sugar. If we were to check his blood sugar just after his standard breakfast, it would rise substantially.

This pattern has become deeply ingrained into the American psyche. Some people will act like I've suggested we overthrow the government when I suggest that breakfast cereals need to be eliminated from their lives. We all share memories of Tony the Tiger, the leprechaun on Lucky Charms ("They're magically delicious!), reading the brightly colored boxes often including games and prizes. Breakfast cereals seem as American as apple pie. But the wheat and corn content ensures a big rise in blood sugar, the sort that create small LDL, low HDL, etc.--all the patterns Stuart is showing--and make us fat.

Orange juice? Too much sugar all at once. Get your potassium from whole vegetables and fruits, not from orange juice. (Bananas are another problem source of potassium for similar reasons despite being a whole fruit.)

Toast? Any diabetic who monitors their blood sugar after meals will tell you: Even one slice of bread, ANY bread, skyrockets blood sugar. Add the fruit preserves made with sugar syrup and it's doubly worse.

Pancakes? Even if made with plenty of fiber, blood sugars go absolutely berserk after a meal like this, especially if maple syrup is added.

In other words, the seemingly healthy breakfast Stuart eats guarantees that he fails to control all his patterns that contribute to his coronary plaque growth.

After I pointed out Stuart's dietary faux pas, he asked, "Then what the heck can I eat?"

"There's actually lots of good choices: Eggs (preferably free-range, if available, or the 'omega-3' enriched) or Egg Beaters; oat products, but true oat products like slow-cooked oatmeal, or the best of all, oat bran, used as a hot cereal; ground flaxseed as a hot cereal with added fruit, berries, nuts; a handful of raw almonds, walnuts, pecans; some cheese, preferably traditional fermented cheese and not processed; low-fat cottage cheese; low-fat yogurt that you flavor yourself with berries and nuts; raw seeds like sunflower and pumpkin.

"Try and save some of your dinner foods for breakfast. For instance, save some green peppers and onions from your salad and put it in your scrambled eggs along with some olive oil. Save some of the chicken and add it to your breakfast. Save some of the cooked vegetables and have them as they are. You'll be surprised how filling dinner foods can be when eaten for breakfast."

It's not that tough. But Stuart and many other people need to break the hold that the food manufacturers have created. If you're hoping to seize hold of your heart scan score, get rid of the sugar foods in your morning, even the ones cleverly disguised as healthy.

The Low-Carb Man

If ever there was an enthusiastic disciple of deceased Dr. Robert Atkins of Atkins' Diet fame, it's Mr. Jimmy Moore.








Jimmy tells the story of how he was transformed by the Atkins' approach, losing 180 lbs in the course of one year. He continues to develop this conversation, in many ways elaborating on the conversation in more sophisticated ways than even Atkins did in his lifetime.

Though we've agreed to disagree on some points of nutrition, Jimmy and I had a recent discussion about heart disease, the mis-guided ways of conventional cardiac care,and the evils of processed carbohydrates. We do differ on the role of saturated fat in heart disease and health, but beyond that difference I was impressed (reading his Blog and listening to his many webcasts) with his level of understanding of the issues. Jimmy is not some over-enthusiastic dieter. He has a grasp of the issues that exceeds that of 99% of my colleagues.

If you are interested in reading our discussion or just perusing a really fun, informative Blog/website, go to LivinLaVidaLowCarb.com. The interview is posted at:

http://livinlavidalocarb.blogspot.com/2007/08/davis-wanna-cut-plaque-in-your-arteries.html


See Jimmy Moore's before and after pictures at http://livinlavidalocarb.blogspot.com/2005/07/my-before-pictures.html. He's quite an entertaining read.
Cureality | Real People Seeking Real Cures

Beating the Heart Association diet is child's play



In response to the Heart Scan Blog post, Post-Traumatic Grain Disorder, Anne commented:


While on the American Heart Association diet my lipids peaked in 2003. I even tried the Ornish diet for a short time, but found it impossible.

Total Cholesterol: 201
Triglycerides: 263
HDL: 62
LDL: 86

After I stopped eating gluten (I am very sensitive), my lipid panel improved slightly. This past year I started eating to keep my blood sugar under control by eliminating sugars and other grains. Now this is my most recent lab:

Total Cholesterol: 162
Triglycerides: 80
HDL: 71
LDL: 75


Isn't that great? This is precisely what I see in practice: Elimination of wheat and sugars yields dramatic effects on basic lipids, especially reductions in triglycerides of up to several hundred milligrams, increased HDL, reduced LDL.

Beneath the surface, the effects are even more dramatic: reductions or elimination of small LDL particles, reduction or elimination of triglyceride-containing lipoproteins, elimination of the marker for abnormal post-prandial (after-eating) lipoproteins, IDL, reduced c-reactive protein. Add weight loss from abdominal fat stores and reduced blood pressure.

In fact, I would go so far as to speculate that, if the entire nation were to follow Anne's lead and eliminate wheat and sugars, "need" for 30% of all prescription medications would disappear. The incidence of diabetes would be slashed, the U.S. would no longer lead the world in obesity.

Anne and I are not the first to make this observation. It has also been made in several studies, such as:

The Duke University study of low-carbohydrate diets in type II diabetics. In this study, 50% of low-carb participants became non-diabetic: They were cured.

One of the many studies conducted by University of Connecticut's Dr. Jeff Volek, demonstrating dramatic improvement in glucose, insulin (reduced 50%) and insulin responses, and lipids.

Dr. Ron Krauss' early studies that hinted at this effect, even though the "high-fat" diet wasn't really low-carbohydrate.

If wheat and sugar elimination has been shown to achieve all these fabulous benefits, why hasn't the American Heart Association spoken in favor of this dietary approach and other- low-carbohydrate diets ? Why does the American Heart Association maintain its "Check-Mark" stamp of approval on Cocoa Puffs and Count Chocula cereals?

Victim of Post-Traumatic Grain Disorder

Heart Scan Blog reader, Mike, shared his story with me. He was kind enough to allow me to reprint it here (edited slightly for brevity).



Dr. Davis,

I was much intrigued to stumble onto your blog. Heart disease, nutrition, and wellness are critically important to me, because I’m a type 2 diabetic. I’m 53 and was diagnosed as diabetic about 5 years ago, though I suspect I was either diabetic or pre-diabetic 5 years before that. Even in a metropolitan area it's next-to-impossible to find doctors sympathetic to any approach beyond the standard get-the-A1c-below 6.5, get LDL <100, get your weight and blood pressure normal, and take metformin and statins.

I’m about 5’10-and-a-half and when I was young I had to stuff myself to keep weight on; it was an effort to get to 150 pounds, and as a young man, 165 was the holy grail for me. I always felt I’d look better with an extra 10-15 pounds.
I ate whatever I wanted, mostly junk, I guess, in my younger years.

When I hit about age 35, I put on 30 pounds seemingly overnight. As I moved toward middle age I became concerned with the issue of heart health, and around that time Dr. Ornish came out with his stuff. I was impressed that he’d done a
study that supposedly showed measurable decrease in atherosclerotic plaque, and had published the results of his research in peer-reviewed journals. It looked to me as though he had the evidence; who could argue with that? I tried his plan on and off, but as so many people note, an almost-vegan diet is really tough. It was for me, and I could never do it for any length of time. But given that the “evidence” said that I should, I kept trying, and kept beating up on myself when I failed. And I kept gaining weight. I got to almost 200 pounds by the time I was 40 and have a strong suspicion that that’s what caused my blood sugar to go awry, but my doctor at the time never checked my blood sugar, and as a relatively young and healthy man, I never went in very often.

I’ve had bouts of PSVT [paroxysmal supraventricular tachycardia, a rapid heart rhythm] every now and again since I was 12 or so. I used to convert the rhythm with Valsalva, but as I moved into my forties, occasionally my blood pressure would be elevated and it made me nervous to do the procedure because it was my understanding that it spikes your blood pressure when you do it. So I began going to the ER to have the rhythm converted, which they do quite easily with adenosine. On one of my infrequent runs to the ER to get a bout of PSVT converted, they discovered my blood glucose was 500 mg/dL, and I’d never experienced any symptoms! They put me in the hospital and gave me a shot of insulin, got it town to 80 mg/dL easily,
diagnosed me as diabetic, and put me on 500 mg. metformin a day.

I was able to get my A1c down to 7, then down to 6.6, and about that time I read a number of Dr. Agatston’s books, and began following the diet, and pretty quickly got my A1c down to 6.2, and my weight down, easily, to 158. That was fine with my doctor; he acted as though I was in good shape with those numbers. Soon I ran into Dr. Bernstein’s material, and came face to face with a body of research that suggested I needed to get the A1c down to below 5! That was both discouraging and inspiring, and frankly it’s been difficult for me to eat as lo-carb as I appear to need to, so I swing back and forth between 6.2 and 6.6. I know I need to work harder, be more diligent in my carb control, and I see with my meter that if I eat low-carb I have great postprandial and fasting blood sugars, but since I don’t particularly get any support or encouragement from
either my doctor or my wife for being so “radical,” it’s hard to pass the carbs by.

One thing that always confused me was that though I saw on my meter that BG [blood glucose] readings were better with a lo-carb diet, and though I saw the preliminary research suggesting that lo-carb could be beneficial in controlling CVD, I didn’t understand why Ornish had peer-reviewed research demonstrating reversal of atherosclerosis on a very-lowfat diet. How could two opposing approaches both help? I wondered if it were possible that one diet is good for diabetes, and the
other good for heart health. That would mean diabetics are screwed, because they always seem to end up with heart disease.

From time to time I’d look for material that explained this seeming contradiction. I was determined to try to stay lo-carb, simply because I saw how much better my blood sugars are when I eat lo-carb; but it’s hard in the face of this or that website that tells you about all the dangers of a lo-carb diet and that touts the lo-fat approach. That tends to be the conventional wisdom anyway.

Finally in one of those searches I came across your material, and saw you offer what was at last an explanation of what Ornish had discovered--it wasn’t a reversal of atherosclerotic plaques he was seeing; it was that his diet was improving endothelial dysfunction in people who had had high fat intakes.

Odd as it may seem to you, that little factlet has been enough to allow me to discard entirely the lingering ghost of a suspicion that I ought to be eating very-lowfat. In fact, I was very excited to see your claim that your approach can reverse atherosclerotic plaque.

It would be nice to find a doctor who’d be supportive of your approach. My doctor isn’t much interested in diet or
nutrition. He just wants my weight in the acceptable range, my blood pressure good, and my LDL 100 or below (which I know isn’t low enough). He’s not particularly interested in getting a detailed lipid report. I hope I can talk him into ordering one so that it’s more likely I can get it covered by my insurance.

I very much appreciated the links you gave to Jenny’s diabetes websites, and I’ve resolved to get even better control of my BG by being more diligent with my diet. I’m planning on joining your site, reading your book, and following your advice. I just have this sort of deflating feeling that it would have been better if I’d stumbled upon this before I had diabetes. Still, it’s nice to have a site that offers to laypeople the best knowledge available concerning how to take care of their heart.



Mike is yet another "victim" of the "eat healthy whole grains" national insanity, the Post-Traumatic Grain Disorder, or PTGD. The low-fat dietary mistake has left many victims in its wake, having to deal with the aftermath of corrupt high-carbohydrate diets: diabetes, heart disease, and obesity.

We should all hope and pray that "low-fat, eat healthy whole grains" goes the way of Detroit gas guzzlers and sub-prime mortgages.

Drug industry "Deep Throat"

A Heart Scan Blog reader brought the following letter from a former pharmaceutical sales representative to congress to my attention.

Interesting excerpts:

As a former drug representative for Eli Lilly, I spent 20 months increasing the market share of my company’s drugs. I was recruited fresh from college with an eager desire to employ my degree in molecular biology and biochemistry. Shortly after my hiring, it became clearly apparent that a drug sale had much more to do with establishing personal relationships than it did with understanding the latest science. However, any doubts I held regarding the effectiveness of such methods were dispelled by the results of my persuasiveness and the financial rewards I received for my efforts. The latter also helped me rationalize the many ethically dubious situations I routinely encountered in my work. Upon my departure from the industry, I began working for the public’s health. Seven years later, as a result of my experiences and education I am more convinced than ever that the goals of the pharmaceutical industry often stand in direct conflict with the practice of ethical and responsible medicine. Nothing in my recent research causes me to believe that my experiences were anything but typical of the training and practice of the majority of drug reps plying their trade today.


“There’s a big bucket of money sitting in every [doctor’s] office.” – Michael Zubillaga, Astra Zeneca Regional Sales Director, Oncology


The majority of drug reps entering the work force today are young and attractive. The ranks of reps are replete with sexual icons: former cheerleaders, ex-military, models, athletes. Of course, as a sales job, the reps must be eloquent and convincing. Depending on the population, certain ethnicities are preferred either to make the rep distinct among other reps or to provide them with a cultural advantage in connecting with their clients. Noticeably lacking among most new reps is any significant scientific understanding. My personal case illustrates this point rather vividly: In my training class for Eli Lilly's elite neuroscience division, selling two products that constituted over 50% of the company's profits at the time, none of my 21 classmates nor our two trainers had any college level scientific education. In fact, that first day of training, I taught my class and my instructors the very basic but crucial process by which two nerve cells communicate with one another. It is very likely that the majority of my class couldn't explain the difference between a neuron and a neutron prior to sales school. While it's certainly a bonus to have a scientifically educated representative, it is far from a primary recruitment criterion. Youth is a much higher criterion for the sales position.

Sales representative trainers are almost always veteran sales representatives and consequently, much of the training they offer is implicit in the anecdotes they give. This informal training parallels the standard training offered by the industry and in many ways compliments it. It is tacitly accepted by management and perceived as the "real" training by many veteran sale representatives. Among the more dubious "unofficial" lessons a new rep learns are: how to manipulate an expense report to exceed the spending limit for important clients, how to use free samples to leverage sales, how to use friendship to foster an implied "quid pro quo" relationship, the importance of sexual tension, and how to maneuver yourself to becoming a necessity to an office or clinic.

The most troubling aspect of pharmaceutical sales is systematic befriending of our clients. In addition to the psychological profiling mentioned above, drug reps are taught to constantly be on the lookout for personal effects that will help us connect to our doctors. When entering an office for the first time, we nonchalantly survey it for clues to ingratiate ourselves with our client. Similarly, conversations are intentionally steered into the realm of personal details such as religion, family, or hobbies to acquire similar information. As a matter of training, we collect this data subtly. In the course of a conversation with clients, we may glean facts about their prescribing preferences, the dates of their children’s birthdays, where they were born, or what music they enjoy. Training encourages us to commit these details to memory just long enough to return to our cars and instantly type up a “call report” listing the details of our conversation. On a daily basis, we connect our computers to a central database that uploads the information we’ve acquired, allowing us to share it with our partner drug reps and company marketers. Subsequently, drug reps interweave pieces of conversation specifically tailored to appeal to their client drawn from personal information that wasn’t necessarily shared with them. For example, Dr. Jones will be nothing but grateful when I supply him with a cake celebrating his children’s birthday when, in fact, he told my partner (and not me) the birthdates several months prior in a personal conversation.


The writer's comments ring true: The relentless attention-grab of sales representatives, using clever tactics that include access to detailed records of physician prescribing habits, big smiles and eye-winking, are detailed perfectly.

There's nothing wrong with a business doing its job by marketing its products and services. What is so wrong about this picture is that one side is so well-equipped, heavily funded, with access to extraordinary resources that the other side (physicians) don't have. And the physicians aren't the victims--YOU are.

A middle-aged, receding hairline physician, faced with a 28-year old attractive woman asking all manner of ingratiating questions but knowing full well what she is doing, having strategized for weeks on how to manipulate the behavior of her "mark," is helpless.

Like the mortgage-backed security crisis, we've reached another phenomenon of crisis proportions. Direct-to-consumer drug advertising, drugs for non-conditions and well people, pinpoint marketing of drugs to physicians--it's all gone too far.

Personally, drug representatives are not welcome in my office. This generally prompts puzzled, followed by angry, looks from the representatives, often traveling with a district supervisor hoping to help polish their pitch. If patients didn't request free samples, the reps would not step foot in the office.

Triglyceride Buster-Update

In the last Heart Scan Blog post, I described Daniel's experience reducing his triglycerides from 3100 mg/dl to around 1100 mg/dl with use of omega-3 fatty acids from fish oil, along with modifications in his diet. This was accomplished in the space of around two weeks.

An update: Daniel has continued another 10 days on his fish oil, along with elimination of wheat, cornstarch, and sugars.

Repeat triglyceride: 202 mg/dl. That's 93.5% reduction in the space of three weeks--no drugs involved.

Daniel really did nothing extraordinary. He simply followed the simple advice I provided to take a moderate dose of EPA+DHA from over-the-counter fish oil supplements, along with elimination of the foods that are extravagant triggers of triglycerides.

He's got just a little further to go to achieve the biologically ideal level of less than 60 mg/dl. You can see that it is not really that difficult--provided someone didn't load you down with nonsense about "cutting your fat," or statin or fibrate drugs.

Triglyceride buster

Two weeks ago, Daniel started with a triglyceride level of 3100 mg/dl, a dangerous level that had potential to damage his pancreas. The inflammatory injury incurred could leave him with type I diabetes and inability to digest foods, since the insulin-producing capacity and the enzyme producing capacity of the pancreas are lost.

Daniel added 3600 mg of omega-3s per day. Within 10 days, his triglycerides dropped nearly 2000 mg to just over 1100 mg/dl--still too high, but an incredible start.

The power of omega-3 fatty acids from fish oil to reduce triglycerides is illustrated most graphically by people with a condition called "familial hypertriglyceridemia" that is responsible for triglyceride levels of 500, 1000, even several thousand milligrams. That's what Daniel has. Given appropriate doses of omega-3s, triglycerides drop hundreds, even thousands, of milligrams.

No question: Omega-3 fatty acids from fish oil are the best tool available for reduction of triglycerides. The effect is dose-dependent, i.e., the more you take, the greater the triglyceride reduction.

How omega-3s exerts this effect is unclear, though there is evidence to suggest that omega-3s suppress several nuclear receptors involved in triglyceride (VLDL) production and increase the expression or activity of the enzyme lipoprotein lipase, an enzyme that clears triglycerides from the blood.

I am continually surprised at the number of people with high triglycerides who are still treated with a fibrate drug, like Tricor, or a statin drug, when fish oil--widely available, essentially free of side-effects, with a proven cardiovascular risk-reducing track record--should clearly be the first choice by a long stretch.

Among its many benefits, omega-3 fatty acids from fish oil also:

Reduce matrix metalloproteinases (MMP)--Two fractions of MMPs, MMP-2 and MMP-9, are inflammatory enzymes present in atherosclerotic plaque that are suspected to trigger plaque "rupture." Omega-3s have been shown to reduce both forms of MMP.

Block uptake of lipids in the artery wall--Suggested by a study in mice.

Modify postprandial responses--In the first few hours after eating (the "postprandial" period), a flood of digestive byproducts of a meal are present in the bloodstream. While research exploring postprandial effects is still in its infancy, it is clear that omega-3 fatty acids have the capacity to favorably modify postprandial patterns. One common surrogate measure for postprandial abnormalities is intermediate-density lipoprotein, or IDL, that we obtain in fasting blood through lipoprotein panels like NMR and VAP. With sufficient omega-3s alone, IDL is completely eliminated.

Unfortunately, most of my colleagues, if they even think to use omega-3s, choose to use the prescription form, Lovaza. Indeed, several representatives from AstraZeneca, the pharmaceutical outfit now distributing this miserably overpriced product, frequently barge their way into my office poking fun at our use of nutritional supplements instead of the prescription Lovaza. "But insurance covers it in most cases!" they plead. "And your patients will know that they're getting the real product, not some fake. And they'll have to take fewer capsules!"

I never use Lovaza to reduce triglycerides, even in familial hypertriglyceridemia--the FDA-approved indication for Lovaza--and have not yet seen any failures, only successes.

Newsweek, Time, and other fronts for the drug industry

I used to believe that conventional print media--newspapers, magazines--were unbiased, untouchable flames of truth. Perhaps there was a time when this was true, when the young reporter, eager to change the world, uncovered the story that righted some huge wrong.

Those days are drawing to a close.

Today, the once powerful print media are collapsing due to the competition of the cheaper, broader reach of the internet.

Jogging does NOT cause heart disease


Periodically, I'll come across a knuckleheaded report like this one from Minneapolis:

Marathon Man’s Heart Damaged by Running?


Of course, the obligatory story about how a cardiologist came to the rescue and "saved his life" with a stent follows. In other words, a stent purportedly saved the life of this vigorous man with no symptoms and high capacity for exercise.

Does vigorous exercise, whether it's marathon running, long-distance biking, or triathlons, cause coronary disease? Should all vigorous athletes run to their doctor to see if they, too, need their lives to be "saved."

Let me tell you what's really going on here. People with the genetic pattern lipoprotein(a), or Lp(a), tend to be slender, intelligent and athletic. For genetic reasons, these people gravitate towards endurance sports like long-distance running. Lp(a) is a high-risk factor for coronary disease. It is the abnormality present in the majority of slender, healthy people who are shocked when they receive a high heart scan score or have a heart attack or receive a stent. (I call Lp(a) "the most aggressive known coronary risk factor that nobody's heard about.")

The association between endurance exercise and heart disease is just that: an association. It does not mean that exercise is causal. Having seen coronary plaque detected with heart scans in many runners, virtually all of whom demonstrated increased Lp(a), I believe that Lp(a) is causal.

Unfortunately, the man in the Minneapolis story, now that his life is "saved," will likely be advised to take a statin drug and follow a low-fat diet . . . you know, the diet that increases Lp(a).

Warning: Your pharmacist may be hazardous to your health

Pharmacists can be very helpful resources when it comes to questions about prescription drugs.

The operant word here is drugs.

What they are most definitely not expert on are nutritional supplements. In fact, a day doesn't pass by without having to dispell one falsehood or another conveyed to a patient about a nutritional supplement by a pharmacist.

Among the more common falsehoods told to patients by pharmacists:

"You have to take Niaspan. Sloniacin doesn't work."

Patent nonsense. A few years back, I was the largest prescriber of Niaspan in Wisconsin. Although I am embarassed to admit it, I also spoke for the company, educating fellow physicians on the value of niacin for correction of lipid disorders.

Then I shifted to Sloniacin due to cost--it costs 1/20th the cost of prescription Niaspan. I examined the pharmacokinetic data (pattern of release in the body), the published literature (e.g., the famous HATS Trial), and have used Sloniacin over 1000 times in patients. In my experience, there is no difference: no difference in efficacy, no difference in safety, no difference in side-effects. There is a BIG difference in price.

Unfortunately, most pharmacists get their information on niacin from the Niaspan representative.


"You shouldn't be taking vitamin D supplements. I have prescription vitamin D here."

What the pharmacist means is that you should replace your vitamin D3, or cholecalciferol--the form recognized as vitamin D by the human body--with the plant form of vitamin D, vitamin D2 or ergocalciferol.

Since when is a plant form of a hormone (vitamin D is a potent hormone, not a vitamin; it was misnamed) better than the human form?

I've previously talked about this issue in a blog post called Vitamin D for the pharmaceutically challenged.

The notion that D2 is somehow superior to the real thing, D3, is absurd. I use D3 only in my practice and have checked blood levels thousands of times. As long as the D3 comes as a gelcap, drops, or powder in a capsule, it works great, yielding predictable and substantial increases in blood levels of 25-hydroxy vitamin D. If it comes as prescription D2 (or over-the-counter D2), I have seen many failures: no increase in blood levels of vitamin D or meager increases.

Prescription status is no guarantee of effectiveness.


"Why do you need iodine? You already get enough from food."

The NHANES data over the last 25 years argue otherwise: Iodine deficiency is growing, particularly as people are avoiding iodized salt and the iodine content of processed foods is diminishing. The explosion in goiters in my office also suggest this is no longer a settled issue.

On the positive side, it is exceptionally easy to remedy with an inexpensive iodine supplement. That is, until the pharmacist intervenes and injects his bit of nutritional mis-information.


I'm not bashing pharmacists. In fact, Track Your Plaque's own Dr. BG has a pharmacy background, and she is an absolute genius with nutritonal supplements. But she is a rare exception to the rule: Most pharmacists know virtually nothing about nutritional supplements. You might as well ask your hairdresser.

"Healthy" people are the most iodine deficient

Ironically, the healthiest people are the most likely to be deficient in iodine.

Why?

Healthy people tend to:

--Avoid iodized salt because of public health advice to limit sodium
--Use sea salt to obtain minerals like magnesium--but sea salt contains little iodine
--Limit meat--Carnivores obtain more iodine than vegetarians or vegans. In one study, up to 80% of vegans were iodine-deficient (Krajcovicova-Kudlackova M et al 2003).
--Exercise--Substantial amounts of iodine are lost through sweating. In a study of high school soccer players, 38.5% were severely iodine deficient, compared to 2% of sedentary students (Mao IF et al 2001).


That is indeed what I am seeing in my office, as well: The healthiest, most attentive to healthy eating, and most physically active are the ones showing up with small goiters (enlarged thyroid glands) and increased TSH and low free T4 levels.

Why am I checking thyroid and talking about iodine? Because even the smallest degree of thyroid dysfunction can double, triple, or quadruple your risk for cardiovascular events. See the posts Is normal TSH too high? and Thyroid perspective update.

What kind of iodine do you take?

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

204 respondents answered the question:


Do you take an iodine supplement?

The responses:

Yes, I take Iodoral, Lugol's, or SSKI
26 (12%)

Yes, I take potassium or sodium iodide
19 (9%)

Yes, I take kelp tablets or powder
64 (31%)

No, I rely on generous use of iodized salt
23 (11%)

No, I don't supplement iodine at all
66 (32%)

Isn't iodine something you put on cuts and scratches?
6 (2%)


I am heartened by the number of respondents taking iodine in some form. After all, iodine is an essential trace mineral. Without it and health suffers, often dramatically.

However, I am concerned by the percentage of people who don't supplement iodine at all: 32%. Interestingly, this is approximately the proportion of people who come to my office who also do not supplement iodine who are now showing goiters, or enlarged thyroid glands due to iodine deficiency. Goiters lead to hypothyroidism (low thyroid hormone levels), followed by hyperactive nodules, not to mention undesirable effects like weight gain, fatigue, hair loss, constipation, intolerance to cold, higher LDL cholesterol and triglycerides, and heart disease.

11% of respondents report using lots of iodized salt. This may or may not be sufficient to provide enough iodine to prevent goiter and allow normal thyroid function. The success of this strategy depends to a great extent on how often salt is purchased. Salt that sits on the shelf for more than a month is devoid of iodine, given iodine's volatility.

I am also favorably impressed by the number of people who take "serious" iodine supplements like Lugol's solution, Iodoral, or SSKI. Of course, people who read The Heart Scan Blog tend to be an unusually informed, healthy population. The 12% of people in the poll who take these forms of iodine does clearly not mean that 12% of the general population also takes them. But 12% is more than I would have predicted.

On the Track Your Plaque website, we are awaiting an interview with iodine expert, Dr. Lyn Patrick. I'm hoping for some juicy insights.
Cureality | Real People Seeking Real Cures

Is there something fishy about fish oil?

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



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



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




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

Lovaza vs fish oil supplements?

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

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

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

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

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

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

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

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

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

More on blood sugar

Take any of the following foods:

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

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

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

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

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

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

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

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

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

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

Postprandial blood sugar: Almonds vs. whole wheat bread

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



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



Blood sugars:

Raw almonds

Start:

One-hour after eating:





2 slices 100% whole wheat bread

Start:

One-hour after eating:





100% whole wheat bread, 2 large slices

Water (g) 24.69

Energy (kcal) 158

Protein (g) 8.29

Fat, total (g) 2.14

Carbohydrate (g) 26.43

Sugars, total (g) 3.56

Fiber, total dietary (g) 4.4

Cholesterol (mg) 0

Saturated fatty acids, total (g) 0.478

Monounsaturated fatty acids, total (g) 1.022

Polyunsaturated fatty acids, total (g) 0.384





23 almonds, raw



Energy (kcal) 159

Protein (g) 5.86

Fat, total (g) 13.64

Carbohydrate (g) 5.98

Sugars, total (g) 1.07

Fiber, total dietary (g) 3.4

Cholesterol (mg) 0

Saturated fatty acids, total (g) 1.03

Monounsaturated fatty acids, total (g) 8.525

Polyunsaturated fatty acids, total (g) 3.331



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

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

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

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

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

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

If you’re not a diabetic, why bother checking blood sugar? New studies have documented the increased likelihood of cardiovascular events with increased postprandial blood sugars well below the ranges regarded as diabetic. A blood sugar level of 140 mg/dl after a meal carries 30-60% increased (relative) risk for heart attack and other events. The increase in risk begins at even lower levels, perhaps 110 mg/dl or lower after-eating.

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

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

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

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

Food sources of vitamin K2: Reprint

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

I therefore reprint the vitamin K2 post below.





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

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

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

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

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

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















Feta cheese

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

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



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

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

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





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

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

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

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

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


All images courtesy Wikipedia.

Copyright 2007 William Davis, MD

Family lessons

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

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

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

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

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

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

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

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

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

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

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

Look like Jimmy Stewart


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

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

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

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

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

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

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

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

Getting vitamin D right

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

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

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

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


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

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


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

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


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

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

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


"My doctor said that my vitamin D blood level was fine. It was 32 ng/ml."

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

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


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


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


"I don't have to take vitamin D. It's summer."

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


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

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

Jimmy Moore's thyroid adventure

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

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

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

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

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

Are you hungry?

Eliminate modern high-yield semi-dwarf Triticum aestivum . . . and what is the effect on appetite?

A reduction in appetite is among the most common and profound experiences resulting from wheat elimination. I know that I have personally felt it: Wake up in the morning, little interest in breakfast for several hours. Lunch? Maybe I'll have a few bites of something. Dinner . . . well, I'd like to exercise first.

The wheatless report that:

--Appetite diminishes to the point where you can't remember whether you've eaten or not. It is not uncommon to miss a meal, perfectly content. Calorie intake drops by 400 calories per day, on average, calories you otherwise would not have needed but all went to . . . you know where.
--Hunger feels different: It's not the gnawing, rumbling hunger that plagues you every 2 hours. In its place, you will find that hunger feels like a soft reminder that, gee, maybe it's time to have something to eat because you haven't had anything in--what?--4 to 6 hours. And it's a subtle reminder, not a desperate hunt that makes you knock people aside at the food bar, steal coworkers' lunches stored in the refrigerator, salivating at the mere thought of food.
--The simplest foods satisfy--It no longer requires an all-you-can-eat buffet to satisfy, but a few small pieces of healthy food. (Yeah, but what happens to revenues at Kraft, Nabisco, and Kelloggs, not to mention the revenues at agribusiness giants ADM and Monsanto? Slash consumption by, say, 30%, you likewise slash revenues by 30%. What would shareholders say?)
--Even prolonged periods of not eating, i.e., fasting, is endured with ease.

Hunger and the relentless search for something to eat disappear for most people. By eliminating the appetite-stimulating properties of wheat, we return to a natural state of eating for sustenance, to satisfy physiologic need. We are no longer victims of this incredibly powerful appetite-stimulant called gliadin from wheat.

This is why many diets fail: They fail to remove this powerful appetite stimulant. You might eat only lean meats, limit your calories, and exercise 90 minutes per day, but as long as the gliadin protein is pushing your appetite button, you will want to eat more or you will have to mount monumental willpower to resist it. You can lose 20 pounds on phase 1 of the South Beach diet, for instance, only to regain it in phases 2 and 3 when "healthy whole grains" are added back.

So the key is to remove the gliadin protein from your life, i.e., eliminate all things wheat.

 

Chocolate . . . for adults only

If you've got a serious chocolate addiction and you'd like to make it as healthy as possible, give this X-rated dark chocolate a try.
I call it X-rated because it is certain to not satisfy young, sugar-craving palates, but is appropriate for only the most serious chocolate craver. This is a way to obtain the rich flavors and textures of cocoa, the health benefits (e.g., blood pressure reduction, antioxidation) of cocoa flavonoids, while obtaining none of the sugars/carbohydrates . . . and certainly no wheat!

It is easy to make, requiring just a few ingredients, a few steps, and a few minutes. Set aside and save for an indulgence, e.g., dip into natural peanut or almond butter.

Ingredients:
8 ounces 100% unsweetened cocoa
5 tablespoons coconut oil, melted
1/2 cup dry roasted pistachios
1/4 cup whole flaxseeds or chia seeds
Truvia or other non-aqueous sweetener

Using double-boiler method, melt cocoa. Alternatively, melt cocoa in microwave in 15-20 second increments. Stir in coconut oil, pistachios, and flaxseeds or chia seeds. Stir in sweetener, mixing thoroughly. (Note that the sweetener must be non-aqueous, as water-based sweeteners will separate in the oils.)

Lay a sheet of parchment paper out on a large baking pan. Pour chocolate mixture slowly onto paper, tilting pan carefully to spread evenly until thickness of thick cardboard obtained. Place pan in refrigerator or freezer for 20 minutes.

Remove chocolate and break by hand into pieces of desired size.

"Friday is my bad day"

At the start, Ted had a ton of small LDL particles. His starting (NMR) lipoprotien values:

LDL particle number: 2644 nmol/L

Small LDL: 2301 nmol/L

In other words, approximately 85% of all LDL particles were abnormally small. I showed Ted how to use diet to markedly reduce small LDL particles, including elimination of wheat, limiting other carbohydrates, and even counting carbohydrates to keep the quantity no higher than 15 grams per meal ("net" carbs).

Ted comes back 6 months later, having lost 14 pounds in the process (and now with weight stabilized). Another round of lipoproteins show:

LDL particle number: 1532 nmol/L

Small LDL: 799 nmol/L

Better, but not perfect. small LDL persists, representing nearly 50% of total LDL particle number.

So I quiz Ted about his diet. "Gee, I really stick to this diet. I have nothing made of wheat, no sugars. I count my carbs and I almost never go higher . . . except on Fridays."

"What happens on Friday?" I asked.

"That's when I'm bad. Not really bad. Maybe just a couple of slices of pizza. Or I'll go out for a big custard cone or something. That wouldn't do it, would it?"

That's the explanation. Your liver is well-equipped to recognize normal, large LDL particles. Large LDL particles therefore "live" for only a couple of days in the bloodstream. But the human liver does not recognize the peculiar configuration of small LDL particles, so it lets them pass--over and over and over again. The result: Once triggered by, say two slices of pizza, small LDL particles persist for 5 days, sometimes longer.

So Ted's one "bad" day per week is enough to allow a substantial quantity of small LDL particles to persist. While a fat indulgence (if there is such a thing) pushes large LDL up, the effect is relatively short-lived. Have a carbohydrate indulgence, on the other hand, and small LDL particles persist for up to a week. It means that Ted's one "bad" day per week is enough to allow his small LDL particles to persist at this level, preventing him from gaining full control over coronary plaque.

It also means that, if you have blood drawn for lipoprotein analysis but had a carbohydrate goodie within the previous week, small LDL particles may be exaggeratedly high.

HDL 80 mg/dl

More and more people in my clinic are showing HDL cholesterol values of 80 mg/dl or higher, males included.

Think about it: Nationwide, average HDL for males is 42 mg/dl and for females 52 mg/dl. Even though these average values are generally regarded as favorable, HDL cholesterol values at these levels are nearly always associated with higher levels of triglycerides, postprandial (after-eating) lipoprotein abnormalities, and excessive quantities of small LDL particles.

HDL particles are, of course, protective and are powerfully anti-oxidative. Higher levels of HDL have been associated with reduced potential for cancer, as well as reduced risk for heart disease.

Following the simple regimen that we follow to gain control over coronary plaque has therefore increased levels of HDL to heights that are uncommon in the rest of the population, levels that readily top 80, 90, or 100 mg/dl. That regimen includes:

1) Elimination of all wheat--Yes, consumption of "healthy whole grains" sets you up to have lower HDL levels; elimination of wheat increases HDL.
2) Limited carbohydrate consumption--While eliminating wheat is a powerful nutritional strategy to increase HDL, non-wheat carbohydrates like quinoa, millet, beans, rice, and fruit can still cause high triglycerides that lead to reduced levels of HDL. Limited exposure helps keep HDL at higher levels.
3) Omega-3 fatty acid supplementation--Because omega-3 fatty acids reduce both triglycerides and blunt the postprandial rise in lipoproteins that can cause HDL degradation, HDL rises with omega-3s from fish oil.
4) Vitamin D supplementation--The effect is slow, but it is BIG. HDL just goes up and up and up over about 2 years of supplementation. Before vitamin D, HDL levels of 60 mg/dl were the best I could hope for in most people. Now 80 mg/dl is an everyday occurrence.

Other factors can also be used to increase HDL levels, such as weight loss, red wine and alcohol, exercise, cocoa flavonoids, green tea, and niacin. But following the regimen above sends HDL through the roof in the majority.

Lessons from the 20-year statin experience

Readers of the Heart Scan Blog know that, while I recognize that statins are useful in a small segment of the population with genetically-determined disorders, they are wildly overused, misused, and abused. In my view, the majority of people taking statins have no business doing so and could, in fact, obtain superior results by following some of the strategies advocated in these pages.

Nonetheless, the 30-year long statin experience has taught us some important lessons. Statin drugs have enjoyed more "research" than any other class of drugs ever conceived. They have received more media attention and embraced by more physicians than any other class of drugs. Combine these social phenomena and I believe that several lessons can be learned:

Small LDL particles and increased HbA1c--An evil duo

Small LDL particles are triggered by consumption of carbohydrates. Eat more "healthy whole grains," for instance, and small LDL particles skyrocket.

Increased hemoglobin A1c, HbA1c, a reflection of the last 60-90 days' blood sugars, is likewise a reflection of carbohydrate consumption. The greater the carbohydrate consumption and/or carbohydrate intolerance, the greater the HbA1c. Most regard a HbA1c of 6.5% or greater diabetes; values of 5.7-6.4% pre-diabetes. However, note that any value of 5.0% or more signifies that the process of glycation is occurring at a faster than normal rate. Recall that endogenous glycation, i.e., glucose modification of proteins, ensues whenever blood sugars increase over the normal range of 90 mg/dl (equivalent to HbA1c of 4.7-5.0%). Glycation is the fundamental process that leads to cataracts, arthritis, and atherosclerosis.

Put the two together--increased quantity of small LDL particles along with HbA1c of 5.0% or higher--and you have a powerful formula for heart disease and coronary plaque growth. This is because small LDL particles are not just smaller; they also have a unique conformation that exposes a (lysine residue-bearing) portion of the apoprotein B molecule contained within that makes small LDL particles uniquely glycation-prone. Compared to large LDL particles, small LDL particles are 8-fold more prone to glycation.

So glycated small LDL particles are present when HbA1c is increased above 5.0%. Small, glycated LDL particles are poorly recognized by the liver receptor that ordinarily picks up and disposes LDL particles, unlike large LDL particles, meaning small LDL particles "live" much longer in the bloodstream, providing more opportunityt to do its evil handiwork. Curiously, small LDL particles are avidly taken up by inflammatory white blood cells that can live in the walls of arteries, where they are oxidized--"glycoxidized"--and add to coronary atherosclerotic plaque.

The key is therefore to tackle both small LDL particles and HbA1c.

Unforgiving small LDL particles

Small LDL particles are triggered by carbohydrates in the diet: Eat carbohydrates, small LDL particles go up. Cut carbohydrates, small LDL particles go down.

A typical scenario would be someone starts with, say, 2000 nmol/L small LDL (by NMR) because they've been drinking the national Kool Aid of eating more "healthy whole grains" and consuming somewhere around 200 grams carbohydrates per day, including the destructive amylopectin A of wheat. This person slashes wheat followed by limiting other carbohydrates and takes in, say, 40-50 grams per day. Small LDL: 200 nmol/L.

In other words, reducing carbohydrate exposure slashes the expression of small LDL particles, since carbohydrate deprivation disables the liver process of de novo lipogenesis that forms triglycerides. Abnormal or exaggerated postprandial (after-eating) lipoproteins that are packed with triglycerides are also reduced. Because triglycerides provide the first lipoprotein "domino" that cascades into the formation of small LDL particles, carbohydrate reduction results in marked reduction in small LDL particle formation.

So let's say you are doing great and you've slashed carbohydrates. Small LDL particles are now down to zero--no small LDL whatsoever. What LDL particles you have are the more benign large variety, say, 1200 nmol/L (LDL particle number), all large, none small. You are due for some more blood work on Thursday. On Tuesday, however, you have four crackers because, what the heck, you've been doing great, you've lost 43 pounds, and have been enjoying dramatic correction of your lipoprotein abnormalities.

Your next lipoprotein panel: LDL particle number 1800 nmol/L, small LDL 700 nmo/L--substantially worse, with a major uptick in small LDL.

That's how sensitive small LDL particles can be to carbohydrate intake. And the small LDL particles can last for up to several days, since small LDL particles are not just smaller in size, they also differ in conformation, making them unrecognizable by the normal liver receptor. The small LDL particles triggered by the 4 crackers therefore linger, outlasting the normal-conformation large LDL particles that are readily cleared by the liver.

This phenomenon is responsible for great confusion when following lipoprotein panels, since a 98% perfect diet can yield dismaying results just from a minor indulgence. But, buried in this simple observation is the notion that small LDL particles are also extremely unforgiving, being triggered by the smallest carbohydrate indulgence, lasting longer and wreaking their atherosclerotic plaque havoc.

I eliminated wheat . . . and I didn't lose weight!

Elimination of wheat is a wonderfully effective way to lose weight. Because saying goodbye to wheat means removing the gliadin protein of wheat, the protein degraded to brain-active exorphins that stimulate appetite, calorie consumption is reduced, on average, 400 calories per day. It also means eliminating this source of high blood sugar and high blood insulin and the 90-minutes cycles of highs and lows that cause a cyclic need to eat more at the inevitable low. It means that the high blood sugar and insulin phenomena that trigger accumulation of visceral fat are now turned off. It may possibly also mean that wheat lectins no longer block the leptin receptor, undoing leptin resistance and allowing weight loss to proceed. And weight loss usually results effortlessly and rapidly.

But not always. Why? Why are there people who, even after eliminating this appetite-stimulating, insulin-triggering, leptin-blocking food, still cannot lose weight? Or stall after an initial few pounds?

There are a list of reasons, but here are the biggies:

1) Too many carbohydrates--What if I eliminate wheat but replace those calories with gluten-free breads, muffins, and cookies? Then I've switched one glucose-insulin triggering food for another. This is among the reasons I condemn gluten-free foods made with rice starch, cornstarch, tapioca starch, and potato starch. Or perhaps there's too many potatoes, rices, and oats in your diet. While not as harmful as wheat, they still provoke phenomena that cause weight loss to stall. So cutting carbohydrates may become necessary, e.g., no more than 12-14 grams per meal.

2) Fructose--Fructose has become ubiquitous and has even assumed some healthy-appearing forms. "Organic agave nectar" is, by far, the worst, followed by maple syrup, honey, high-fructose corn syrup, sucrose,and fruit--yes, in that order. They are all sources of fructose that causes insulin resistance, visceral fat accumulation or persistency, prolongation of clearing postprandial (after-meal) lipoproteins that antagonize insulin, and glycation. Lose the fructose sources--as much of it as possible. (Fruit should be eaten in very small portions.) Watch for stealth sources like low-fat salad dressings--you shouldn't be limiting your fat anyway!

3) Thyroid dysfunction--A real biggie. Number one cause to consider for thyroid dysfunction: iodine deficiency. Yes, it's coming back in all its glory, just like the early 20th century before iodized salt made it to market shelves. Now, people are cutting back on iodized salt. Guess what's coming back? Iodine deficiency and even goiters. Yes, goiters, the disfiguring growths on the neck that you thought you'd only see in National Geographic pictures of malnourished native Africans. Number two: Exposure to factors that block the thyroid. This may include wheat, but certainly includes perchlorate residues (synthetic fertilizer residues) on produce, pesticides, herbicides, polyfluorooctanoic acid residues from non-stick cookware, polybrominated diphenyl ethers (flame retardants), and on and on. If you are iodine-deficient, it can even include goitrogenic iodine-blocking foods like broccoli, cauliflower, and soy. Thyroid status therefore needs to be assessed.

4) Cortisol--Not so much excess cortisol as disruptions of circadian rhythm. Cortisol should surge in the morning, part of the process to arouse you from sleep, then decline to lower levels in the evening to allow normal recuperative sleep. But this natural circadian cycling is lost in many people represented, for instance, as a flip-flopping of the pattern with low levels in the morning (with morning fatigue) and high levels at bedtime (with insomnia), which can result in stalled weight loss or weight gain. Cortisol status therefore needs to be assessed, best accomplished with salivary cortisol assessment.

5) Leptin resistance--People who are overweight develop an inappropriate resistance to the hormone, leptin, which can present difficulty in losing weight. This can be a substantial issue and is not always easy to overcome. It might mean assessing leptin levels or it might mean taking some steps to overcome leptin resistance.

Okay, that's a lot. Next: More on how to know when thyroid dysfunction is to blame.

Do the math: 41.7 pounds per year

Consumers of wheat take in, on average, 400 calories more per day. Conversely, people who eliminate wheat consume, on average, 400 calories less per day.

400 calories per day multiplied by 365 days per day equals 146,000 additional calories over the course of one year. 146,000 calories over a year equals 41.7 pounds gained per year. Over a decade, that's 417 pounds. Of course, few people actually gain this much weight over 10 years.

But this is the battle most people who follow conventional advice to "cut your fat and eat more healthy whole grains" are fighting, the constant struggle to subdue the appetite-increasing effects of the gliadin protein of wheat, pushing your appetite buttons to consume more . . . and more, and more, fighting to minimize the impact.

So, if you eat "healthy whole grains" and gain "only" 10 pounds this year, that's an incredible success, since it means that you have avoided gaining the additional 31.7 pounds that could have accumulated. It might mean having to skip meals despite your cravings, or exercising longer and harder, or sticking your finger down your throat.

400 additional calories per day times 365 days per year times 300,000,000 people in the U.S. alone . . . that's a lot of dough. Is this entire scenario an accident?

Or, of course, you could avoid the entire situation and kiss wheat goodbye . . . and lose 20, 30, or 130 pounds this year.

We got the drug industry we deserve

A biting commentary on just who is writing treatment guidelines for diabetes and cardiovascular disease was published in the British Medical Journal, summarized in theHeart.org's HeartWire here.

"About half the experts serving on the committees that wrote national clinical guidelines for diabetes and hyperlipidemia over the past decade had potential financial conflicts of interest (COI), and about 4% had conflicts that were not disclosed.

"Five of the guidelines did not include a declaration of the panel members' conflicts of interest, but 138 of the 288 panel members (48%) reported conflicts of interest at the time of the publication of the guideline. Eight reported more than one conflict. Of those who declared conflicts, 93% reported receiving honoraria, speaker's fees, and/or other kinds of payments or stock ownership from drug manufacturers with an interest in diabetes or hyperlipidemia, and 7% reported receiving only research funding. Six panelists who declared conflicts were chairs of their committee.

"Of the 73 panelists who had a chance to declare a conflict of interest but declared none, eight had undeclared COI that the researchers identified by searching other sources. Among the 77 panel members who did not have an opportunity to publicly declare COI in the guidelines documents, four were found to have COI.
"

The closing quote by Dr. Edwin Gale of the UK is priceless:
"Legislation will not change the situation, for the smart money is always one step ahead. What is needed is a change of culture in which serving two masters becomes as socially unacceptable as smoking a cigarette. Until then, the drug industry will continue to model its behavior on that of its consumers, and we will continue to get the drug industry we deserve."

It's like having Kellogg's tell us what to each for breakfast, or Toyota telling us what car to drive. The sway of the drug industry is huge. Even to this day, I observe colleagues kowtow to the sexy sales rep hawking her wares. But that's the least of it. Far worse, even the "experts" who we had trusted to have objectively reviewed the evidence to help the practitioner on Main Street appears to be little more than a hired lackey for Big Pharma, hoping for that extra few hundred thousand dollars.