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?



Part 1





Part 2




Part 3




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.

What's that in your mouth?




Fat = triglycerides

In other words, eat fat, whether it's saturated, hydrogenated, polyunsaturated, or monounsaturated, and blood levels of triglycerides will go up over the next 6 hours. This remains true if there are carbohydrates in the meal, or if there are NO carbohydrates in the meal. It also remains true if you chronically consume fats.

While fats are the primary determinant of postprandial (after-eating) triglycerides, carbohydrates are the primary determinant of fasting triglycerides.

So, if your triglycerides are high on a fasting cholesterol (lipid) panel, it's most likely because you overconsume carbohydrates.


Thanks to cartoonist Eli Stein, who has generously allowed me to reprint his artwork on these pages. Mr. Stein has published his work in dozens of magazines and newspapers, including the Wall Street Journal, Barron's, and Good Housekeeping. More of his work can be found at Eli Stein Cartoons.

De Novo Lipo-what?

Humans have limited capacity to store carbohydrates. Beyond the glucose and glycogen in our blood and tissues, we have relatively little carbohydrate to draw from in time of energy need. That's why long-distance runners and triathletes have to carry sugar sources to keep blood sugar from plummeting.

Fat, of course, is different. We have virtually unlimited capacity to store energy as fat.

Because we have limited carbohydrate storage capacity, what can the body do with the excessive quantities of carbohydrates that Americans ingest? What becomes of a bagel for breakfast, wheat crackers for snacks, a whole wheat sandwich for lunch, pretzels, and whole wheat pasta that many people eat every day, not to mention the chips, soft drinks, and juices?

Excess carbohydrates are diverted to an interesting metabolic pathway called de novo lipogenesis (DNL). This refers to the liver's ability to make triglycerides from excessive carbohydrates in the diet. Triglycerides are packaged for release into the blood as VLDL. VLDL, in turn, interacts with other lipoproteins, creating small LDL particles, reduced HDL and smaller, less protective HDL. High VLDL will be measured on a standard cholesterol panel as higher triglycerides.

A University of California (Berkeley, San Francisco) group has done much of the work describing DNL.

A diet weighed towards carbohydrates, especially if 50% or greater calories are carbohydrate, is sufficient to provoke plenty of DNL, even in slender people. DNL is a big part of the reason why low-fat (and, thereby, high-carbohydrate) diets result in higher triglycerides. DNL really gets turned on many-fold if the carbohydrates are "simple," rather than "complex."

Overweight people, however, can demonstrate five-fold greater DNL even with lesser quantities of carbohydrate intake (e.g., 40% fat, 46% carbohydrate, 14% protein):





From Schwarz et al 2003. Mean (± SEM) fractional de novo lipogenesis in lean normoinsulinemic (NI), obese NI, and obese hyperinsulinemic (HI) subjects after 5 d of consuming a high-fat, low-carbohydrate diet and in different lean NI and obese HI subjects after 5 d of consuming a low-fat, high-carbohydrate diet. Values with different superscript letters are significantly different.


Excessive carbohydrates, a la standard low-fat diets, are good for nobody. The concept of de novo lipogenesis fills in a theoretical hole that now explains why people who eat carbohydrates have higher triglycerides, VLDL, and, eventually, insulin resistance and diabetes.

Gretchen's postprandial diet experiment II

I previously posted Gretchen's postprandial diet experiment, in which she consumed a low-fat diet for a day, followed by a low-carbohydrate diet for a day. Grethen monitored blood glucose and triglycerides with fingerstick checks. (Blood glucose can be checked on any widely available glucose monitor; triglycerides can be monitored with the Cardiochek device.)

Let's now discuss what happened.

On the low-carb, high-fat day, there was an initial surge in triglycerides to 250 mg/dl late morning, followed by a secondary peak several hours following dinner. Because fat is mostly triglycerides, Gretchen's high-fat (sausage, bacon, butter, whole-fat yogurt) breakfast provided a large quantity of triglycerides that needed to be absorbed. This generally occurs over approximately 6 hours, varying depending on body weight, how accustomed you are to fat, activity level during the day, the kind of fat in the meal. The high content of saturated fat in Gretchen's high-fat breakfast likely caused the somewhat slower drop in triglycerides over approximately 7 1/2 hours.

As Gretchen herself had noted, triglycerides the following day were lower, a typical low-carb response. Blood sugar throughout showed only minor variation, with only small postprandial increases.

Thus, Gretchen experienced what we'd expect with a low-carb, high-fat diet: an initial high surge in triglycerides, followed by a decline in fasting levels, while blood sugar shows a normal contour.







Now, the more confusing low-fat experience:



Blood glucose makes a striking peak at 200 mg/dl after the low-fat breakfast of pasta and rice, in contrast to the low-carb breakfast. Triglycerides behaved very differently from the low-carb experiment: While there was no initial postprandial surge, there was a late surge developing 6-24 hours later. The late surge continued into the next day, with fasting levels the following morning (210 mg/dl) exceeding the starting triglyceride level (60 mg/dl).

The one potentially confusing aspect of all this is Gretchen's late rise in triglycerides on the low-fat diet. This phenomenon is due to something called de novo lipogenesis, or the liver's conversion of carbohydrates to triglycerides that occurs when an excessive carbohydrate load comes through diet. Because the human body cannot store anything beyond a minor quantity of carbohydrates (as glucose and glycogen), carbohydrates are converted to fats.

Another factor causing the late triglyceride increase is insulin resistance, given the high blood sugar response. When insulin resistance is present, the activity of the enzyme, lipoprotein lipase, is reduced. Less lipoprotein lipase activity allows slower VLDL degradation, allowing VLDL (and thereby triglycerides contained in VLDL) to "stack up" in the blood. Thus, the higher triglycerides late after eating and into the next morning.

One issue to be aware of: Acute responses can differ from chronic responses. In other words, had Gretchen had the luxury (and time and money) to conduct the experiment over, say, 4 weeks, rather than a single day, there would be somewhat different responses. The best data on this come from Dr. Jeff Volek of the University of Connecticut, in which 4 weeks of low-carbohydrate eating modify fasting and postprandial responses over time.

Several conclusions can be made from Gretchen's experience:

1) Low-carb, high-fat acutely generates extravagant postprandial triglyceride responses.
2) Low-fat causes a late triglyceride surge and higher fasting triglycerides.
3) Low-fat leads to high blood sugars and, by implication, diabetes.


Both the low-carb and the low-fat responses are undesirable, both leading to increased risk for heart disease. Which is worse? I believe that low-fat is more destructive, since it leads over time to both high triglycerides and diabetes, while low-carb/high-fat only leads to postprandial triglyceride surges, at least acutely.

How to best balance the responses to reduce risk for heart disease? That's a discussion for future.


Again, my thanks to Gretchen and the substantial amount of effort that went into generating these numbers. More of Gretchens' own writing can be found on her blogs:
http://wildlyfluctuating.blogspot.com
http://www.healthcentral.com/diabetes/c/5068

A wheat-free 2010

A Heart Scan Blog reader sent this fascinating description of his wheat-free adventure.

Whenever I discuss this notion of going wheat-free and the incredible health effects that develop, I invariably receive comments or emails saying something like "I eat wheat and feel fine. That can't be true." The problem is that not everybody needs to go wheat-free. 20-30% of people can include wheat in their diet and suffer little more than weight gain, some not at all.

But stories like Michael's (below) are commonplace in my experience. I've had many patients who, at first, refused to believe that wheat exposure might be the underlying cause for health struggles. But they finally give it a try and find that rashes, arthritis, acid reflux, irritable bowel symptoms, mood swings, anger, etc. are miraculously improved or gone.

Anyway, hear what Michael has to tell us:


Dr. Davis,

I want to thank you. I was browsing the web a while back and happened to stumble upon your blog post about wheat belly. The first thing that caught my attention was that I thought you had somehow gotten a photograph of me. The young man you posted an image of looked exactly like me. So I read what you had to say. After reading, I thought "Four weeks isn’t so bad. I think I can handle this."

It has now been nine weeks and all I can say is that I am completely amazed. Let me say first that twice in the past twenty years I have been tested for allergies. The first time I was tested I showed a slight reaction to Timothy Grass, but not enough to cause me any problems. The second testing I did not show a reaction to anything. So, I have always assumed that my chronic sinus problem were due to sensitivities to environmental pollutions. Now I am not so sure. I would like to list for you everything that has happened to me since I eliminated wheat from my diet.

1. I have lost a total of 12 pounds in the last 9 weeks.
2. I have lost 1 ¼ inches of belly fat
3. I have lost a tremendous amount of fat from my neck.
4. My entire life I have had problems with oily hair. I could wash my hair and three hours later I looked as if I hadn’t washed in a week. Now my hair stays clean and soft for two to three days without shampoo.
5. My hair was always flat and stringy. Now it has lots of body.
6. I used to have thick layers of dry skin on my scalp. It would come loose in chunks as large as a fingernail. That dry scalp is gone.
7. I used to have dry flaky skin that seemed to secrete oil. That no longer happens. My skin is now soft and smooth.
8. I have lived with bad acne for at least 35 years. Now it is hard to find a pimple on my body.
9. I have always had to fight dehydration. That is no longer a problem.
10. I used to drink two large cups of coffee every morning just to be able to function. I now have enough energy that I have eliminated caffeine from my diet.
11. I sleep more soundly than ever before and my dreams are clear and vivid.
12. My thought processes are more active and clear than they have ever been.
13. My chronic sinus issue is now a thing of the past.
14. I used to have problems with getting the “shakes” if I had gone more than a couple of hours without eating. It was as if I was suffering from low blood sugar. I would even be afraid that I would pass out. Now all I feel is hunger. I can go all day without eating and never feel in danger of losing consciousness.


Today is Thursday. This past Monday my wife and I were eating out and I ordered a burger without a bun. What I didn’t realize was that the burger would arrive covered in onion rings. I knocked the mountain of onion rings onto the plate but there were still a couple that were embedded in the cheese. I decided, what the hell, a couple of onion rings shouldn’t make that much of a difference. I will not make that mistake again anytime soon. Within 30 minutes I felt like there was a steel spike going through my left eye socket. I don’t remember ever being in that much pain. My sinuses were exploding. This morning, as I write this, I still feel the vestiges of that pain. Just enough that I know it is there. But after two and a half days, I am at least able to function again.

I owe you a debt of gratitude. You may have just saved my life. In the very least you have given me the means to improve my life in ways that I never thought possible.

Thank you so much,
Michael B.



Now, if wheat exposure can do that in Michael, what damage can it do in other people?

Personally, I previously experienced many of the same symptoms that Michael suffered, all gone with wheat elimination.

My advice: If you have any inkling that you might have a wheat sensitivity, make a New Year's resolution to stay wheat-free for 4 weeks and see whether you can feel any difference. Not everybody will, but many will be telling us about the dramatic health turnarounds they experienced.

Lipoprotein lipase and you

Lipoprotein lipase can make the difference between having heart disease and not having it. Having sky-high triglycerides or normal triglycerides. It can mean dinner hanging around for over 12 hours in the bloodstream, rather than the usual 4-6 hours.

If you take niacin, you must exercise

We use a lot of niacin in the Track Your Plaque program.

Niacin:

--Increases HDL and shifts HDL towards the large, protective fraction

--Reduces small LDL--In fact, niacin is the best treatment we have to reduce small LDL after wheat elimination and carbohydrate reduction.

--Reduces fasting and postprandial (after-eating) triglycerides

--Reduces heart attack risk by 20-28%--even as a sole agent.


But . . . niacin also triggers higher blood sugar because it partially blocks the effects of insulin (insulin "resistance").

While the net effect of niacin remains positive, the provocation of insulin resistance is not such a good thing. Can it be minimized or eliminated?

Yes, through exercise. Here's one interesting observation in obese (BMI 34.0), sedentary men given placebo, exercise, niacin (1500 mg Niaspan, once per day), or niacin + exercise:





From Plaisance et al 2008.

Blood was drawn following a high-fat meal challenge. (Yes, a high-fat challenge, not a carbohydrate challenge. In this study, there were only 17 grams carbohydrates in the test meal, but 100 grams fat. More on this in future.) Exercise consisted of walking for 50 minutes at a moderate pace one hour prior to the meal challenge.

You can see from the graph that exercise partially corrected the increased insulin level provoked by niacin.

Judging from this and other studies, exercise can help minimize the insulin-blocking effects of niacin. It doesn't take much, just moderate exercise for at least 30 minutes.

Adequate sleep can also help, since sleep deprivation is a potent trigger for insulin resistance, only worsened in the presence of niacin. Vitamin D supplementation to achieve desirable blood levels (which I define as 60-70 ng/ml) is also an effective means to minimize this effect.

To track small LDL, track blood sugar

Here's a trick I learned after years of fussing over people's small LDL.

To gain better control over small LDL, follow blood sugars (blood glucose).

When you think about it, all the foods that trigger increases in blood sugar also trigger small LDL. Carbohydrates, in general, are the most potent triggers of small LDL. The most offensive among the carbohydrates: foods made with wheat. After wheat, there's foods made with cornstarch, sucrose (table sugar), and the broad categories of "other" carbohydrates, such as oats, barley, quinoa, sorghum, bulghur, etc.

Assessing small LDL requires a full lipoprotein assessment in which small LDL particles are measured (NMR, VAP, GGE). Not the easiest thing to do in the comfort of your kitchen.

However, you can easily and now cheaply check your blood sugar. Because blood sugar parallels small LDL, checking blood sugar can provide insight into how you respond to various foods and know whether glucose/small LDL have been triggered.

Here's how I suggest patients to do it:

1) Purchase an inexpensive blood glucose monitor at a discounter like Walmart or Walgreen's. You can buy them now for about $10. They're even sometimes free with promotional offers. You will also need to purchase lancets and test strips.

2) With a meal in question, check a blood sugar just prior to the meal, then again 60 minutes after finishing the meal. Say, for example, your pre-meal blood sugar is 102 mg/dl. You eat your meal, check it 60 minutes after finishing. Ideally, the postprandial (after-meal) blood sugar is no more than 102 mg/dl, i.e., no higher than pre-meal.

Perhaps you're skeptical that oatmeal in skim milk with walnuts and raisins will do any damage. So you perform this routine with your breakfast. Blood sugar beforehand: 100 mg/dl. Blood sugar 1 hour post: 163 mg/dl--Uh oh, not good for you. And small LDL will be triggered.

This approach is not perfect. It will not, for example, identify "stealth" triggers of blood sugar and small LDL like pasta, for the same reasons that pasta has a misleadingly low glycemic index: sugars are released slowly and not fully evident with the one-hour blood sugar.

Nonetheless, for most foods and meals, tracking your one-hour postprandial blood sugar can provide important insight into your individual susceptibility to sugar and small LDL-triggering effects.

C-reactive protein: Fiction from the drug industry?

C-reactive protein (CRP) is the liver product of inflammatory responses anywhere in the body. If there's an inflamed left knee, CRP will be increased. If viral bronchitis is making you cough, then CRP will be increased.

The argument put forward by the drug industry is that, because CRP indicates underlying inflammation, very low-grade levels that can be measured in the absence of overt inflammation like the sore knee or bronchitis is associated with increased risk for cardiovascular events. There are now many studies that conclusively demonstrate that, the higher the CRP, the greater the cardiovascular risk.

Naturally, any marker of risk is followed by the inevitable study: Do statin drugs reduce the excess cardiovascular risk of excessive CRP?

And, yes, indeed they do. My statin-crazed colleagues rave about the so-called "pleiotropic," or non-lipid, effects of statins. CRP reduction and the reduction of risk associated with CRP result with statin treatment.

But is life really statin vs. placebo, as most statin trials are constructed? Are there strategies that can outdo statins like Crestor for reduction of CRP?

Watch your fish oil labels

A quick quiz:

How much omega-3 fatty acids, EPA + DHA, are in each capsule of fish oil with the composition shown on the label below:





If you said 1340 mg (894 mg + 446 mg), sorry, but you're wrong. There are 670 mg EPA + DHA per capsule.

Did you notice that the composition, or "Supplement Facts," lists the contents of two capsules? Rather than the usual one capsule contents, this product label lists two capsules.

I don't know why some manufacturers or distributors do this. However, I have seen many people tripped up by this kind of labeling, taking half the omega-3 fatty acids they thought they were taking. This can be important when you are trying to obtain a specific dose of EPA + DHA to reduce triglycerides, reduce Lp(a), control abnormal heart rhythms, reduce bipolar mood swings, or other important effects.

I liken this to pulling up to a gas station where the sign says gasoline for $1.25. Wow! Can't beat that! You then find out that it's really $1.25 for a half-gallon, or $2.50 a gallon.

In truth, the labeling is accurate; it's just very easy to not notice the two capsule composition.

Why do I need a prescription for Olava?

Imagine this:





What is OLAVA?

Olava is prescription olive oil. It is the purest, highest concentration of olive oil available.




Why Do I Need a Prescription for OLAVA?

Studies show that olive oil contains essential fatty acids, "good" fats that:



--Contain natural compounds your body needs for good health but can't produce on its own.

--Has antioxidants that may provide protection from heart disease.



So, it is common for people to ask why they need a prescription for OLAVA if it is made from a natural ingredient--olive oil. It's time to get the facts about OLAVA. Learn why OLAVA is different from olive oil you can buy at a store.



OLAVA Is an FDA-Approved Medication

OLAVA is the only FDA-approved medicine made from olive oil that's proven, along with diet, to reduce risk for heart disease


The FDA enforces standards to make sure that prescription medications like OLAVA are safe, effective, and quality controlled.


The way OLAVA is manufactured is reviewed and approved by the FDA.


OLAVA uses a 10-step purification process that helps remove lead and other environmental toxins that can be present in olive oil.


Each 1-gram capsule of OLAVA contains 1000 mg of pure olive oil.


The FDA-approved dose of OLAVA is 4 capsules per day. It could take up to 2 tablespoons per day of regular olive oil to provide the same amount of active ingredients proven to lower heart disease risk.




What Else You Should Know About Olive Oil

Regular olive oil has not been approved by the FDA to treat any specific disease like heart disease.



Olive oil doesn't have specific dosing information; it has a food label.



Olive oil does not go through an FDA-approved manufacturing process.





Talk to Your Doctor About OLAVA

If you have very heart disease, you may need a prescription medicine, along with diet, to treat your condition. Talk to your doctor about OLAVA. Print a trial offer to use on your first prescription of OLAVA.

Do stents prevent reversal?

I've seen this phenomenon several times now: A highly-motivated Track Your Plaque participant with a stent in one artery will do all the right things--lose weight, achieve 60:60:60 in basic lipids, identify and correct hidden lipoprotein disorders, take fish oil, correct vitamin D, etc.

Follow-up heart scan shows dramatic reduction in scoring in the two arteries without stents--30% per artery. But the artery with the stent will show marked increase in scoring above and/or below the stent. (It's impossible to tell what happens in or around the stent itself from a calcium scoring standpoint, since steel looks just like calcium on a CT heart scan.) In other words, there is marked plaque growth in the vicinity of the stent, despite the fact that dramatic reversal of atherosclerosis has occurred in other arteries without stents.

Should we take this to mean that a stent destroys the opportunity for atherosclerotic plaque reversal in the stented artery? I don't know, but I fear this may be true. What dangers does this different sort of plaque pose? Is it the result of the injury imposed at time of stent implantation, some modification of flow or biologic responses as a result of the presence of the stent?

These are all unanswered questions. But I believe that it is yet another suggestive piece of evidence that the best stent is no stent at all.

At what score should I have a heart cath?

This question comes up frequently: At what specific heart scan score should a heart catheterization be performed? In other words, is there a specific cut-off that automatically triggers a need for catheterization?

In my view, there is no such score. We can't say, for instance, that everybody with a score above 1000 should have a catheterization. It is true that the higher your score, the greater the likelihood of a plaque blocking flow. A score of 1000 carries an approximately 25-30% likelihood of reduced blood flow sufficient to consider a stent or bypass. This can nearly always be settled with a stress test. Recall that, despite their pitfalls for uncovering hidden heart disease in the first place, stress tests are useful as gauges of coronary blood flow.

But even a score of 1000 carries a 70-75% likelihood that a procedure will not be necesary. This is too high to justify doing heart catheterizations willy-nilly.

Unfortunately, some my colleagues will say that any heart scan score justifies a heart cath. I believe this is absolutely, unquestionably, and inexcusably wrong. More often than not, this attitude is borne out of ignorance, laziness, or a desire for profit.

Does every lump or bump justify surgery, radiation, and chemotherapy on the chance it could represent cancer? Of course not. There is indeed a time and place for these things, but judgment is involved.

In my view, no heart scan score should autmatically prompt a major heart procedure like heart catheterization in a person without symptoms.

Niacin makes NY Times

In the wake of the crash and burn of Pfizer's torcetrapib, media attention has turned up the miracles of . . .good old niacin. The NY Times carried a well-written report on niacin in its recent report, An Old Cholesterol Remedy Is New Again.


(Read the entire report at http://www.nytimes.com/2007/01/23/health/23consume.html?em&ex=1169701200&en=670fa84ae2ea648c&ei=5087%0A)

Among their comments:

...torcetrapib worked primarily by increasing HDL, or good cholesterol. Among other functions, HDL carries dangerous forms of cholesterol from artery walls to the liver for excretion. The process, called reverse cholesterol transport, is thought to be crucial to preventing clogged arteries.

Many scientists still believe that a statin combined with a drug that raises HDL would mark a significant advance in the treatment of heart disease. But for patients now at high risk of heart attack or stroke, the news is better than it sounds. An effective HDL booster already exists.

It is niacin, the ordinary B vitamin.

In its therapeutic form, nicotinic acid, niacin can increase HDL as much as 35 percent when taken in high doses, usually about 2,000 milligrams per day. It also lowers LDL, though not as sharply as statins do, and it has been shown to reduce serum levels of artery-clogging triglycerides as much as 50 percent. Its principal side effect is an irritating flush caused by the vitamin’s dilation of blood vessels.

Despite its effectiveness, niacin has been the ugly duckling of heart medications, an old remedy that few scientists cared to examine. But that seems likely to change.

“There’s a great unfilled need for something that raises HDL,” said Dr. Steven E. Nissen, a cardiologist at the Cleveland Clinic and president of the American College of Cardiology. “Right now, in the wake of the failure of torcetrapib, niacin is really it. Nothing else available is that effective.”

In 1975, long before statins, a landmark study of 8,341 men who had suffered heart attacks found that niacin was the only treatment among five tested that prevented second heart attacks. Compared with men on placebos, those on niacin had a 26 percent reduction in heart attacks and a 27 percent reduction in strokes. Fifteen years later, the mortality rate among the men on niacin was 11 percent lower than among those who had received placebos.

'Here you have a drug that was about as effective as the early statins, and it just never caught on,' said Dr. B. Greg Brown, professor of medicine at the University of Washington in Seattle. 'It’s a mystery to me. But if you’re a drug company, I guess you can’t make money on a vitamin.'



Of course, you and I don't have to wait for the media to endorse something. I'm nonetheless thrilled that this hugely helpful vitamin is gaining greater recognition. My preferred form nowadays is over-the-counter SloNiacin (Upsher Smith). Weve seen no liver side-effects and a minimal quantity of flushing. It's also reasonably priced, $13.99 for 100 tablets of 500 mg at Walgreen's. That's a lot cheaper than prescription Niaspan at $130 for 60 tablets.

Perhaps the notoriety will cut back on the silly responses from some physicians that I still hear about from patients: "My doctor said to stop the niacin because it's going to destroy my liver."

Wheat: the nicotine of food

Yes, we know that wheat contributes to creating small LDL, drops HDL, raises triglycerides, and VLDL. We also know it indirectly slows the clearance of after-eating fats from the blood (curious, I know). Wheat products also increase inflammation (C-reactive protein), raise blood sugar, and contribute tremendously to diabetes.

What many people don't know is that wheat products also have an addictive quality: have one donut and you want another. It's true for bread, breakfast cereals, pretzels, cookies, etc. How many times have you had just one Oreo cookie?

Curiously, elimination of wheat products, unlike elimination of nicotine, usually causes the cravings to disappear. In other words, if you stop smoking cigarettes, the desire to smoke doesn't go away. With wheat products, the often overwhelming desire for more wheat products often just goes away.

But most people are simply unable to dramatically reduce or eliminate wheat products from their daily diet and therefore struggle each and every day with excessive cravings for bagels, donuts, cookies, breads, etc.

Try this useful experiment: Eliminate wheat products for a month and see what happens. Most people drop blood pressure, lose the tummy excess, feel more alert, see a drop in blood sugar, experience improvements in lipoproteins, and regain control over appetite.

Good time for a heart attack?

Man Has Heart Attack At Right Place, Right Time

If Robert Ricard had picked the wrong restaurant for lunch, he might have died.

The 71-year-old Michigan man suffered a heart attack shortly after ordering a glass of wine with friends at Bentley's Roadhouse on Saturday.

Luckily, a disaster medical team was sitting nearby.



A TV station in Michigan reported the above story. You've heard these "if it wasn't for ___, so and so would have died" stories. They're reported in all cities at one time or another.

What amazes me about these common local stories is that they're accepted at all. The question that comes to my mind is "Why couldn't the heart attack have been averted in the first place?" Early identification then, as close as humanly possible, elimination of risk would have been a preferable path.

Of course, it may not be the role of the media to cast judgement on why and how the entire episode could have been completely prevented from occurring. But you shouldn't fall into the same trap of complacency. We cannot expect others to save us when the "big one" hits. Your best assurance is to never have one in the first place.

How good is the South Beach Diet?

I'm a fan of the South Beach Diet.

Though it is billed as a program for weight loss (for which it is very effective), it is really a program for health. The basic approach of South Beach involves:

Eat good fats — Choose good fats from olive oil, canola oil, peanut oil, flaxseed oil, walnut oil, avocados, nuts, and fish. Omega-3 (fish oil) supplements are also fine.


Eat good carbs — Good carbs include high-fiber, nutrient-dense fruits, vegetables, legumes, and whole grains.

Eat lean protein — Good sources include eggs, low-fat dairy, nuts, seeds, legumes, skinless white-meat poultry, fish, shellfish, lean cuts of meat, and vegetarian options such as tofu.

(From The South Beach Diet, Dr. Arthur Agatston)


There's no doubt that South Beach can yield dramatic weight loss. In my experience, the success in weight loss depends on 1) how unhealthy your diet was in the first place, and 2) how long you can stick to Phase I, the inital phase during which weight loss is most dramatic. Some people have to periodically cycle back to Phase I to break a "plateau" or to lose faster.

But South Beach is also healthy. It has all the ingredients of a healthy eating program: Low saturated and hydrogenated fats, rich in monounsaturated fats, high fiber, low- to moderate- glycemic index, vegetables and fruits, lean proteins.

The Atkins' diet, in contrast, while very effective for weiglht loss, is an unhealthy process. I've seen lots of bladder infections, constipation, skin rashes, and kidney stones. That's just in the short term. If you stick to the "induction phase" (the no carbohydrate, low fiber, indiscriminate fat initial phase) for an extended period, I suspect that other adverse internal phenemena also develop that might not show for years, like cancer. But--it does work for weight loss!

South Beach's Phase I is also carbohydrate restricted, but steers you towards healthier foods, such as healthy oils from olive and canola, raw or dry roasted nuts, and lean proteins and vegetables.

What really makes South Beach special, however, are its clever recipes. Dr. Arthur Agatston (the author) involved chefs from the restaurants in the South Beach area of Miami to help create healthy yet delicious recipes. We've tried many of them and, while they are different from traditional fare, are delicious and satisfying for the most part.

Criticisms? None, really. But, when my patients choose South Beach (which I often encourage), I often have to impress on them that the Track Your Plaque program is not about weight loss. It is about seizing control of a potentially life-threatening disease. It is a far more important goal with greater implications. Weight loss is just one aspect of a coronary plaque control effort. For this reason, we sometimes have to make changes in the South Beach program to allow for correction of specific lipoprotein patterns.

The most common modification is in people with small LDL particles. This pattern often does indeed respond to weight loss and/or niacin. However, it occasionally persists despite these efforts. We then will ask the patient to continue to restrict the re-introduction of wheat products, though it is allowed after Phase I in South Beach. In other words, for this specific and sometimes difficult to control lipoprotein pattern, a spedific modification of the off-the-shelf South Beach program is sometimes necessary. Of course, the diet is created to suit everybody. Lipoprotein analysis permits detailed insight into your patterns and it's only to be expected that specific modifications might be needed.

But, as written, you can do quite well in your plaque control program by sticking to South Beach.

Be patient with niacin

Mel's HDL started at 37 mg/dl one year ago. Mel had several other abnormal lipoprotein patterns along with his HDL (inc. small LDL and Lp(a)), but HDL was clearly a crucial factor in his panel.

With a heart scan score of 1166, we needed to raise Mel's HDL to the Track Your Plaque target of 60 mg/dl. So Mel started niacin, our number one method to raise HDL, in addition to reducing his exposure to wheat products and other high glycemic index foods; increasing his physical activity; trying to reduce his excess tummy fat; fish oil; dark chocolate (2 oz per day) and red wine (1-2 glasses per day, preferably dark French reds). The form of niacin we often choose is SloNiacin (Upsher Smith), available over-the-counter for about $12-14 per 100 tablets.

Mel started out with niacin 500 mg per day at dinner, increased to 1000 mg at dinner after four weeks. Although this is usually too soon to reassess HDL, Mel insisted. His HDL 41 mg/dl. Mel's disappointment was palpable. He was the usual type A personality: he wanted his HDL higher--now! So Mel insisted that we increase niacin to 1500 mg per day. (We never go higher than this if low HDL or small LDL is the indication for niacin; only when Lp(a) is present do we go higher.)

Six months into this process, HDL: 45 mg/dl. Still a sluggish response.

One year later, HDL: 68 mg/dl. Finally!

That is typical for niacin, as well as combination of lifestyle changes Mel made. None of them result in an immediate rise in HDL; all take months to 1-2 years to exert full HDL-raising effect.

Think of HDL as the 82-year old grandma who takes a long time to cross the street-she does get there!

Note: Doses of niacin >500 mg per day should be taken with medical supervision.

Can vitamin D be a SOLE risk factor?

Here's a crazy question. It occurred to me as I was talking to Drew, a slender, active 54-year old dentist with no bad habits including no smoking.

Drew's heart scan score was 222. His lipoprotein analysis mostly revealed a lot of nothing, which is unusual. The only pattern that showed up was a modestly high LDL of 122 mg/dl with a very slight excess of small LDL. That's it. I would not be satisfied that these were sufficient cause for Drew's level of coronary plaque.

Drew's 25-OH-vitamin D3 level: 15 ng/ml--severe deficiency--despite the fact that his doctor had suggested that he take a vitamin D2 preparation. In other words, Drew had been profoundly deficient, probably for years.

Given the unimpressive cholesterol and lipoprotein values, could vitamin D serve as a trigger for coronary plaque all by itself?

I don't have an answer and know of nobody else who does. However, my opinion is that vitamin D is indeed a potent risk that can cause heart disease as a sole risk factor.

Perhaps it's another piece of circumstantial evidence suggesting that vitamin D has an enormous influence on health, including coronary plaque. Interestingly, the only other health problem Drew has had is prostate cancer, treated a few years ago with prostate removal and radiation. Good evidence suggests that vitamin D deficiency escalates risk of prostate cancer substantially.

By the way, I've seen people taking vitamin D2 preparations, called "ergocalciferol," who are every bit as deficient as those who take no vitamin D at all. Avoid D2 or ergocalciferol preparations: they're worthless.

Does fish oil raise LDL cholesterol?

Katie had an LDL (conventionally calculated) of 87 mg/dl, HDL of 48 mg/dl.

She added fish oil, 6000 mg per day. Three months later her LDL was 118 mg/dl, HDL 54 mg/dl. In other words, LDL increased by 31 mg. What gives?

Several studies have, indeed, shown that fish oil raises LDL cholesterol, usually by 5-10 mg/dl. Occasionally, it may be as much as 20-30.

Unfortunately, many physicians often assume that it's the (minor) cholesterol content of fish oil capsules, or some vague, undesirable effect of fish oil. It's nothing of the kind.

Since we based Katie's program on (NMR) lipoprotein analysis, not conventional lipids (HDL, calculated LDL, triglycerides, total cholesterol), I knew that Katie also had a severe excess of intermediate-density lipoprotein, or IDL, and very-low density lipoproteins, VLDL. This signifies that after a meal, dietary fats persist for 12, 24,or more hours. Fish oil is a very effective method to clear IDL and VLDL, though sometimes it also causes a shift of some IDL and VLDL into the LDL class. Thus, the apparent increase in LDL.

Another contributor: Conventional LDL is a calculated value, not measured. The calculation for LDL is thrown off by any reduction in HDL or rise in triglycerides. In Katie's case, the rise in HDL from 48 to 54 means that calculated LDL is becoming more accurate and rising towards the true measured value. At the start, Katie's true measured LDL was 122 mg/dl, 35 mg higher than the calculated value. Calculated LDL is therefore approximating measured LDL more accurately as HDL rises.

The most important lesson to learn is that, if LDL rises significantly on fish oil and you haven't had lipoproteins formally measured, there may have been a substantial postprandial abnormality like IDL that was unrecognized.

Heart disease is everywhere

If you ever need convincing that heart disease is everywhere, you should do what I do: subscribe to Google Alerts and have them forward news anytime the search phrase "heart attack" crosses the web. (Just go to Google, click on "more" to the right of the search bar, and follow the links.)


Some recent samples:


Workmates resuscitate driver after heart attack

A woman coal mine truck driver had a heart attack and required resuscitation with a defibrillator 3 times on the way to the hospital.





Heart attack kills groom at reception
A 34-year old man died during his wedding reception, leaving behind his 26-year old new wife.






Heart attack ruled as cause of crash

An Alabama man drove his pick-up truck into oncoming traffic while suffering a heart attack.






Heart-attack victim to return to Hamburg stage


Country music artist, Michael Harding, suffered a heart attack and cardiac arrest during a performance. He is apparently recovered and returning to the stage.



That's just a sample from the last two days. While you and I are carry on a conversation on reversal of heart disease, our neighbors and friends drop over every day. Even though I witness successful heart disease reversal routinely, the rest of the world is not participating.

Pass it on: Coronary disease is identifiable, preventable, controllable, and reversible.