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15. October 2006 William Davis (0)

Many people, upon first learning of their CT heart scan score, feel like they're on the edge of a sharp drop. It can feel like you're facing a vast, unknown abyss. At the bottom, all those dreaded things that can happen to you: heart attack, heart failure, hospitals, even dying.

I've encountered this "deer in the headlights" look many times. It truly can be frightening to hear that your heart scan score is 300, or 500, or whatever.

What I find truly frightening, however, is when your score prompts the usual array of misinformation commonly dispensed by physicians: "That's so bad you need a heart catheterization", "Nobody knows why people get calcified plaque", or "Reversal is impossible". All absolute bunk.

Let your fear motivate you to do something about your risk for heart disease. Aim for reversal of your coronary plaque and seek out the tools to achieve this. It is possible and, in fact, we do it all the time. I can't claim 100% success, but the majority of people who engage in an effort like the Track Your Plaque program to reverse coronary plaque succeed. Even a substantial slowing of plaque growth from the expected 30% per year is better than submitting to the conventional approach.

At the very least, get both LDL and HDL cholesterol around 60 mg/dl. This alone is a major plus in reducing the risks associated with your heart scan score. It doesn't guaranteee reversal, but it sure tips the odds in your favor.

Organic Rice Krispies?



Breakfast cereal manufacturing giant, Kelloggs, is launching a line of three cereals that will carry the "organic" designation: Organic Rice Krispies, Organic Raisin Bran, and Organic Frosted Mini-Wheats.

This reminds me of the advertisements I've seen for "fresh fried chicken", or "fresh from the can", or "contains only pure cane sugar". How about organic tobacco? Would that make cigarettes healthier?

The TV ad ends with the slogan "Childood is calling!" Oh, those marketers are a shrewd, clever bunch. I worry that they're so clever that most people will fall for these ludicrous tricks.

Don't fall for these thinly-shrouded marketing shenanigans. Organic? Who cares. These foods remain unhealthy whether or not they contain pesticide residues. Take a look at the nutritional composition: Rice Krispies, organic or not, is sugar to your body. It is the sort of food that creates pre-diabetes, diabetes, makes us fat, and fans the flames of lipoprotein patterns like small LDL, VLDL, and postprandial particles, all of which is like throwing cow manure on the weed patch of your coronary plaque.

Nuts as functional foods

Food manufacturers gave nuts a bad name when they started adding evil ingredients to them. "Party mix", "honey-roasted", mixed nuts, etc., are made with added hydrogenated oils, salt, sugar, excessive quantities of raisins, or other added ingredients that turned a healthy food--nuts--into something that made us fat and hypertensive, raised LDL, dropped HDL, and raised blood pressure.

But nuts themselves are, for the most part, very healthy foods. The very best are nuts with a brown fiber coating like almonds, walnuts, and pecans. Nearly all nuts also come rich in monounsaturated oils similar to that in olive oil. Although calorie-dense, nuts tend to be very filling and slash your appetite for other foods. I have never seen anyone gain weight by adding raw nuts to their diet. In fact, I find adding raw nuts cuts craving for sweets.

Nuts are also among the most concentrated sources of magnesium, containing around 150 mg per 1/2 cup serving. As most Americans are at least marginally if not severely deficient in magnesium, this really helps. Magnesium deficiency is a prominent aspect of "metabolic syndrome" and resistance to insulin.




Some nuts have added benefits like the l-arginine content of almonds or the linolenic acid content of walnuts. However, I think the real health "punch" comes from the fiber and monounsaturate content.

Add 1/4-1/2 cup of raw almonds, walnuts, or pecans per day to your diet and what can you expect? The effects that I see every day that are relevant to plaque control/heart scan score-reducing efforts include:

--Reduction in LDL--usually a 20 mg/dl drop, sometimes more.

--Reduction in triglycerides, especially if nuts replace processed carbohydrate calories. This may be because the fiber and monounsaturate content of nuts reduces blood sugar and the effective glycemic index of any accompanying foods.

--Modest blood pressure reduction.

--Though somewhat inconsistent, partial suppression of the dreaded small LDL particle pattern. We struggle with turning off the small LDL pattern in some people, and raw nuts can provide a real advantage.

If that isn't enough, the fiber content also makes your bowels regular.

Unless there's some reason to avoid nuts (e.g., allergy), nuts should be a part of your heart scan score reducing program. Shop around, as prices can vary wildly. I've been paying $12.99 for a 3 lb bag of raw almonds from Sam's Club, though I've seen almonds elsewhere for up to $12.99 per pound.

For additional commentary, go to one of my favorite Blogs, http://fanaticcook.blogspot.com. The Fanatic Cook's recent post, The Season for Walnuts , provides additional discussion on walnuts and the recent study showing how they improve "endothelial function". The nutritionist behind this Blog has fabulous insights into food, including the concept of "functional foods", i.e., using foods as a treatment tool. She is also unfailingly entertaining.

Can you tell the difference?

Stan is 55 years old. He feels fine, is in moderately good physical condition. His LDL cholesterol is 135 mg/dl, HDL 43 mg/dl, triglycerides 167 mg/dl, total cholesterol 211 mg/dl.

Can you tell me whether Stan has heart disease or not?

How about Charles? Charles has an LDL cholesterol of 127 mg/dl, HDL of 44 mg/dl, triglycerides of 98 mg/dl, and total cholesterol of 191 mg/dl. He is also reasonably fit and feels fine. Can you tell whether Charles has heart disease?

If you can't, don't feel bad. Neither can your doctor. But this is the folly of using cholesterol for risk prediction.

Stan's heart scan score: 0

Charles' heart scan score: 978

Look even more closely at Stan's and Charles' cholesterol numbers. Is there some fine distinction we overlooked? What if we calculated total cholesterol to HDL ratio? Or LDL/HDL ratio?

No matter how you squeeze it, shake it, beat it with a stick, you simply cannot use cholesterol numbers to predict heart disease in specific individuals. Yes, the higher your LDL cholesterol and lower your HDL, the higehr your total cholesterol to HDL ratio, the greater the likelihood of heart disease. But you can simply cannot tell in a specific individual at a specific point in time. If you've seen your doctor puzzle over the numbers, understand that he/she is trying to make sense out of something that doesn't make sense, no matter how hard he/she tries.

You simply need to measure the disease itself: get a CT heart scan, the only measure of atherosclerotic coronary plaque that you have access to.

By the way, if you haven't seen it yet, go to the Track Your Plaque website (www.cureality.com) to see the news piece reporting the American Heart Association's much overdue position statement on CT heart scanning. The AHA has finally released a statement which, in effect, provides their "official" endorsement. Blocked by political shenanigans behind the scenes for several years, the guidelines finally made it to press. The only real difference it makes to me is that my patients may finally get their heart scans paid for by insurance, once the insurance companies realize that it's getting tougher and tougher to dodge their responsibility.

Statin agents and muscle aches

How common are muscle aches with the statin drugs?

It depends on who you ask. If you ask the drug manufacturers, they will tell you no more than 2% of people who take them. They back this up with the experience in tens of thousands of people in published clinical trials.

What if we ask people who take them outside of clinical trials. How many then? I estimate, from my large experience, over 80%! In other words, muscle aches are inevitable in nearly everyone who takes them. The longer you take them, the higher your dose, the more likely muscle aches are going to be.

Why the disconnect between published data and real-world experience? I really don't know. In some instances, the differences are dramatic. The ASTEROID trial, for instance, in which Crestor, 40 mg, was given for two years, only resulted in 8% of people dropping out because of side-effects. My experience: everybody--nobody can tolerate this dose for any length of time.

Let me qualify what "muscle aches" mean. It means achiness and/or weakness, usually mild, occasionally moderate to severe, worse upon awakening and less with use. It can affect many muscles or it can involve only one. Rarely is it incapacitating but it is commonly annoying and frightening. It commonly shows up as gradually diminishing strength with exercise. Strength usually returns promptly upon stopping the offending drug.

"Rhabdomyolysis", or true muscle destruction is, fortunately, very unusual in otherwise well people. People with abnormal kidney function, diabetes, and other concurrent illnesses are somewhat more prone. But in reality, rhabdomyolysis is unusual. I've personally seen it twice, both in people sick for other reasons.

Coenzyme Q10 (CoQ10) supplementation has been a godsend for us. At least 4 out of 5 people who require statins and develop muscle aches respond favorably, but it requires 100 mg per day. The preparation must be oil-based to work, not powder in a capsule which exerts no effect. Some people get by with less; some require as much as 300 mg per day. I've had favorable experiences with the CoQ10 from Sam's Club, GNC, Vitamin Shoppe, and Life Extension (www.LEF.org).

The Track Your Plaque target for LDL cholesterol is 60 mg/dl. Many people do indeed use statins to achieve this level, the level of LDL that amplifies your chances of heart disease reversal, i.e., reduction of heart scan score. The only drawback that I'm aware of with CoQ10 replacement is cost. Beyond this, it's a benign supplement that even supplies higher energy for some people who take it.

More catheterizations would make me happy!

I received this fax today from a cardiologist seeking a position:

"I would prefer to perform as many interventions [stents, angioplasties, etc.] as possible..."

That about sums it up, doesn't it? The goal of this young man, trained in major universities including Columbia University, Harvard, and Emory, is not to pursue an avenue of investigation or healthcare that yields real answers. His goal is to perform as many procedures as possible.

This attitude is deeply ingrained in cardiologists. It's also shared by all procedural medical specialties: the drive to do more and more procedures. It's not because it does more good for the public, but it fulfills a primitive impulse to spread your influence, enlarge your territory, and--of course--make more money.

Personally, I find this impulse repulsive. The fact that this young cardiologist looking for a position is willing to make this statement out in the open demonstrates how widely accepted this attitude is. Imagine your cancer surgeon, looking for a new job, said, "I'm looking to remove as many tumors as I can."

My colleagues have lost sight of the fact that we're trying to reduce or eliminate disease, not enrich our pockets or service some primitive impulse to beat others at our game.

"I hate fish oil!"

I get this comment occasionally, usually from the fishy belching that can occur, rarely because of other crazy effects like rash, fishy body odor, etc.

In the vast majority, fish oil is a benign but wonderfully effective agent. Track Your Plaque followers know that fish oil, starting at 4000 mg per day of a standard 1000 mg capsule preparation, dramatically reduces triglycerides and thereby raises HDL, partially suppresses small LDL, and is the best agent available for reducing postprandial (after eating) abnormalities like IDL and certain VLDL fractions.

However, an occasional person (about 1 in 20) just doesn't like the effects. Are there alternatives? Fish oil packs such a wallop of beneficial effects that can not be replaced by any other single agent or lifestyle practice. For this reason, we have a number of easy strategies to enhance your tolerance for fish oil. (Of course, if your and/or you doctor determine that you're allergic to fish oil, then you should indeed avoid it; thankfully, this is rare.)

Helpful strategies include:

--Refrigerate fish oil capsules--this cuts back on fish belching.
--Take only with meals. This also may increase fish oil's benefits on suppressing after-eating lipoprotein abnormalities.
--Take an enteric-coated preparation--this delays breakdown of the tablet/capsule, making fishy belching less of an issue. Sam's Club has an inexpensive preparation.
--Take liquid fish oil. Usually orange or lemon flavored, liquid fish oil may be a faint fishy taste and odor, but usually not as prominent as the capsules. There's also less stomach upset.
--Coromega--a paste form of fish oil available at health food stores or through http://www.coromega.com. Coromega tastes fruity and comes in little squeeze envelopes.
--Frutol--Pharmax, a British company, makes another fruity fish oil that is non-oily and tastes like apricot. It's actually fairly reasonably priced, too. However, it is hard to find. The only way I know to get is to go online at www.pharmaxllc.com. You may have to actually order through a health care provider.

When using any preparation of fish oil, the best way to determine your dose is to add up the EPA and DHA content. For instance, if you use a fish oil liquid that contains 320 mg EPA and 240 mg DHA per teaspoon, you will need two teaspoons a day to achieve the equivalent of our starting dose of 1200 mg of EPA+DHA, usually provided by 4000 mg total in 4 capsules. Note that some lipid and lipoprotein disorders will require higher doses, e.g., 1800 mg EPA+DHA for high triglycerides (>200 mg/dl) or high IDL.

Sudden death in athletes

A recent report in the Journal of the American Medical Association details how a group in the Veneto region of Italy cut back on the incidence of sudden cardiac death in athletes by a simple screening program.



You can read the abstract of the article at http://jama.ama-assn.org/cgi/content/full/296/13/1593.

Although sudden death in athletes is still a rare event, it is especially tragic when it happens. In this population, the incidence was 3.6 deaths per 100,000 athletes aged 12 to 35 years. By implementing a simple screening program that involved only a physical examination and an EKG, an astounding 89% reduction in sudden death was documented.

What lessons does this hold for those of us interested in coronary plaque reversal? Beyond the obvious lesson of pointing out the great benefit of simple screening of athletes, I believe that it tells us the value of simple screening tools for heart disease in general. It is my strong belief that, if we were to implement CT heart scans among the broad population of men 40 years and over, women 50 years and over--without regard to cholesterol or other relatively lame risk identifiers--we could slash the risk for heart attack and death 90% or more. Putting CT heart scans into the hands of the public makes your coronary risk obvious. It takes the guesswork out of risk predictors like cholesterol and high blood pressure.

But heart scans are already available, you say! Yes, of course they are. But the lack of insurance reimbursement continues to be a restricting factor for many people, despite the number of lives that could be potentially saved and the money that would be saved in the long run by reducing need for major heart procedures. The continuing resistance to prevention by my cardiology colleagues and the persistent ignorance of primary care physicians also remain major impediments.

But it's getting better. You don't have to be chained by ignorance. Put your CT heart scan to good use.

My heart scan was wrong!



Tom came into the office ready for a confrontation.

Tom's wife insisted that he see me to discuss the implications of his CT heart scan score of 459. At age 50, this was clearly bad news that placed Tom in the 99th percentile (worst 1% of men in his age group).

But Tom had already undergone a stress test. There had apparently been a small abnormality, and a heart catheterization had been performed by another cardiologist. "They told me they didn't need to do anything. No stent, no ballon, no bypass, nothing!"

I asked, "Did they tell you that there was any plaque or blockages seen?"

"Yeah, but he said it was nothing. So the heart scan was wrong!"

I've been here many times before. I explained to Tom that, no, his heart scan was not wrong. All the tests he'd undergone siimply provided a different perspective on the same disease. You could say:

--The stress test, being a test of blood flow, may have been abnormal because of the abnormal constrictive behavior of arteries containing plaque, known as "endothelial dysfunction", because the inner lining of arteries (the endothelium) control the tone of the artery. Abnormal constriction in arteries with plaque is quite common.

--The catheterization simply showed that no plaque had collected in a configuration to block flow, thus no stent, etc., since flow was normal. But there was indeed plaque.

All three tests were right; none were wrong. They all provided a little different perspective on the same process. Of course, I favor the heart scan as the means to identify, precisely measure, and track the atherosclerotic plaque in your arteries. The stress test is too crude and only measures flow, the catheterization is not something you'd want to undergo year after year. Catheterization also is too crude a measure to precisely track plaque growth or reversal.

So I explained to Tom that, even though a stent or similar procedure was unnecessary, he remained at substantial risk for heart attack due to plaque "rupture". In fact, Tom's heart attack risk was 5% per year, or approximately 50% over the next decade. That is, indeed, substantial. In fact, you might say that, of the three tests Tom underwent, only the heart scan revealed his true risk.
All posts by william-davis

Heart Scans: An Interview with Jimmy Moore

My friend, Jimmy Moore, of The Livin' La Vida Low Carb Show, posted this video of an interview I did with him.

I provide some background on how heart scanning came about and how it led to the creation of the Track Your Plaque program.

It reminds me how far we've come over the 8 years since the program got started. From its modest start as just an information resource to help people understand their heart scan score, to a comprehensive program that helps followers gain incredible control over coronary plaque and coronary risk that has now expanded to over 30 countries. High-tech heart procedures still dominate public consciousness, but the tremendous power of real heart disease prevention efforts are gaining more and more attention as each day passes.

Wheat Belly #5 on New York Times Bestseller list!

The New York Times just released its bestseller list due for release September 18th, 2011 . . . .

Wheat Belly is #5!! (That darned Jane Fonda woman elbowed me out for the #4 spot!

[caption id="attachment_4452" align="alignright" width="574" caption="Wheat Belly hits #5 on New York Times Bestseller List--in 1st week!"][/caption]

Interview with Jimmy Moore of Livin' La Vida Low-Carb

Here's my podcast interview with Jimmy Moore, host of the Livin' La Vida Low-Carb Show. (If you want to fast forward to the interview, go to time marker 41:20 on the slidebar.)



In the podcast, I talk about how the Track Your Plaque program and its focus on lipoprotein testing, along with the need to reverse the incredible epidemic of diabetes and pre-diabetes, led to elimination of all wheat from the diet and the book, Wheat Belly.

An open letter to the Grain Foods Foundation

Readers: Please feel free to reproduce and disseminate this letter any way you see fit.


To:

Ms. Ashley Reynolds
490 Bear Cub Drive
Ridgway, CO 81432
Phone: 617.226.9927
ashley.reynolds@mullen.com


Ms. Reynolds:

I am writing in response to the press release from the Grain Foods Foundation that describes your effort to "discredit" the assertions made in my book, Wheat Belly: Lose the wheat, lose the weight and find your path back to health. I'd like to address several of the criticisms of the book made in the release:

" . . . the author relies on anecdotal observations rather than scientific studies."
While I do indeed have a large anecdotal experience removing wheat in thousands of people, witnessing incredible and unprecedented weight loss and health benefits, I also draw from the experiences already documented in clinical studies. Several hundred of these studies are cited in the book (of the thousands available) and listed in the Reference section over 16 pages. These are studies that document the neurologic impairment unique to wheat, including cerebellar ataxia and dementia; heart disease via provocation of the small LDL pattern; visceral fat accumulation and all its attendant health consequences; the process of glycation via amylopectin A of wheat that leads to cataracts, diabetes, and arthritis; among others. There are, in fact, a wealth of studies documenting the adverse, often crippling, effects of wheat consumption in humans and I draw from these published studies.


"Wheat elimination 'means missing out on a wealth of essential nutrients.'"
This is true--if the calories of wheat are replaced with candy, soft drinks, and fast food. But if lost wheat calories are replaced by healthy foods like vegetables, nuts, healthy oils, meats, eggs, cheese, avocados, and olives, then there is no nutrient deficiency that develops with elimination of wheat. There is no deficiency of any vitamin, including thiamine, folate, B12, iron, and B6; no mineral, including selenium, magnesium, and zinc; no polyphenol, flavonoid, or antioxidant; no lack of fiber. With regards to fiber, please note that the original studies documenting the health benefits of high fiber intake were fibers from vegetables, fruits, and nuts, not wheat or grains.

People with celiac disease do indeed experience deficiencies of multiple vitamins and minerals after they eliminate all wheat and gluten from the diet. But this is not due to a diet lacking valuable nutrients, but from the incomplete healing of the gastrointestinal tract (such as the lining of the duodenum and proximal jejunum). In these people, the destructive effects of wheat are so overpowering that, unfortunately, some people never heal completely. These people do indeed require vitamin and mineral supplementation, as well as probiotics and pancreatic enzyme supplementation.


I pose several questions to you and your organization:

Why is the high-glycemic index of wheat products ignored?
Due to the unique properties of amylopectin A, two slices of whole wheat bread increase blood sugar higher than many candy bars. High blood glucose leads to the process of glycation that, in turn, causes arthritis (cartilage glycation), cataracts (lens protein glycation), diabetes (glycotoxicity of pancreatic beta cells), hepatic de novo lipogenesis that increases triglycerides and, thereby, increases expression of atherogenic (heart disease-causing) small LDL particles, leading to heart attacks. Repetitive high blood sugars that develop from a grain-rich diet are, in my view, very destructive and lead to weight gain (specifically visceral fat), insulin resistance, leptin resistance (leading to obesity), and many of the health struggles Americans now experience.

How do you account for the psychologic and neurologic effects of the wheat protein, gliadin?
Wheat gliadin has been associated with cerebellar ataxia, peripheral neuropathy, gluten encephalopathy (dementia), behavioral outbursts in children with ADHD and autism, and paranoid delusions and auditory hallucinations in people with schizophrenia, severe and incapacitating effects for people suffering from these conditions.

How do you explain the quadrupling of celiac disease over the last 50 years and its doubling over the last 20 years?
I submit to you that, while this is indeed my speculation, it is the changes in genetic code and, thereby, antigenic profile, of the high-yield semi-dwarf wheat cultivars now on the market that account for the marked increase in celiac potential nationwide. As you know, "hybridization" techniques, including chemical mutagenesis to induce selective mutations, leads to development of unique strains that are not subject to animal or human safety testing--they are just brought to market and sold.

Why does the wheat industry continue to call chemical mutagenesis, gamma irradiation, and x-ray irradiation "traditional breeding techniques" that you distinguish from genetic engineering? Chemical mutagenesis using the toxic mutagen, sodium azide, of course, is the method used to generate BASF's Clearfield herbicide-resistant wheat strain. These methods are being used on a wide scale to generate unique genetic strains that are, without question from the FDA or USDA, assumed to be safe for human consumption.

In short, my view on the situation is that the U.S. government, with its repeated advice to "eat more healthy whole grains," transmitted via vehicles like the USDA Food Pyramid and Food Plate, coupled with the extensive genetic transformations of the wheat plant introduced by agricultural geneticists, underlie an incredible deterioration in American health. I propose that you and your organization, as well as the wheat industry and its supporters, are at risk for legal liability on a scale not seen since the tobacco industry was brought to task to pay for the countless millions who died at their product's hands.

I would be happy and willing to talk to you personally. I would also welcome the opportunity to debate you or any of your experts in a public forum.

Wiliam Davis, MD
Author, Wheat Belly: Lose the wheat, lose the weight and find your path back to health (Rodale, 2011)

Do you eat wheat? I thought so.

I'm itching to say that face-to-face to anyone from the wheat industry--agribusiness, baking, retail distribution . . . anybody. Because it's obvious; it's written on the face . . . and belly, and brain, and knees, and hips. And I believe I will soon have the opportunity.

Taking such a controversial stand in my new book, Wheat Belly, i.e., that wheat products, whole or refined, have NO ROLE IN THE HUMAN DIET whatsoever, was bound to provoke criticism and counterattacks. The wheat world has already taken a blow to the chin with the growing popularity of the (misguided) gluten-free movement and they're going to have to get into the business of media damage control.

Take a look at this press release from the Grain Foods Foundation:

RIDGWAY, COLO. — The Grain Foods Foundation has unveiled plans to counter media publicity attracted by “Wheat Belly.”

“Mullen, working with key members of the Grain Foods Foundation’s scientific advisory board, is addressing ‘Wheat Belly’ through proactive media outreach and its ongoing rapid response program,” said Ashley Reynolds, a Mullen account executive. “In particular, the public relations team will be contacting health and nutrition reporters at print and on-line media outlets, as well as editors at major women’s magazines to influence any diet-related stories that may be published in the coming months.”

. . . Ms. Reynolds, a registered dietitian, noted the author relies on anecdotal observations rather than scientific studies; wheat elimination “means missing out on a wealth of essential nutrients;” six servings of grain-based foods are recommended daily in the Dietary Guidelines for Americans; healthy weight loss depends on energy balance rather than elimination of specific foods; and elimination of wheat products makes sense only for those with medical diagnoses such as celiac disease or gluten sensitivity.

She said the group will lean on its scientific advisory board members to “discredit the book and ensure our messages are backed by sound science. “


Here's some of their starting salvos on their Six Servings Blog.

This reminds me of the fight with Big Tobacco in the '70s: "No, sir, we in the tobacco industry know of no research demonstrating that smoking is bad for health," complete with shots of tobacco executives puffing away on cigarettes.

So brace yourself for a fight. These people are protecting a multi-billion dollar franchise, not to mention their livelihoods and incomes. It could get ugly.

Wheat Belly explodes on the scene!



Wheat Belly is finally available in Barnes and Noble and all major bookstores nationwide! Also available at Amazon. Electronic versions for Nook and Kindle, as well as an audio CD, will also be available.

The notion of Wheat Belly got its start right here on The Heart Scan Blog and the diet developed for the Track Your Plaque program to conquer heart disease and plaque.



Chapters in the book include:

Not Your Grandma's Muffins: The Creation of Modern Wheat
Whence and where did this familiar grain, 4 1/2-foot tall "amber waves of grain," become transformed into a 2-foot tall, high-yield genetically unique plant unfamiliar to humans? And why is this such a bad thing?

Cataracts, Wrinkles, and Dowager's Humps: Wheat and the Aging Process
If you thought that bagels and crackers are just about carbs, think again. Wheat consumption makes you age faster: cataracts, crow's feet, arthritis . . . you name it, wheat's been there, done that and brings you one step closer to the big nursing home in the sky with every bite.

My Particles are Bigger than Your Particles
Why consuming plenty of "healthy whole grains" is the path to heart disease and heart attack and why saying goodbye to them is among the most powerful strategies around for reduction or elimination of risk.

Hello, Intestine: It's Me, Wheat
No discussion of wheat is complete without talking about how celiac disease and other common intestinal ailments, like acid reflux and irritable bowel syndrome, fit into the broader concept of wheat elimination.

Here's a YouTube video introduction to the book and concept posted on the YouTube Wheat Belly Channel. Also, join the discussions on The Wheat Belly Blog and Facebook. Have that last bite of blueberry muffin, because I predict you won't be turning back!

Good fat, bad fat

No, this is not a discussion of monounsaturated versus hydroxgenated fat. This is about the relatively benign fat that accumulates on your hips, rear end, or arms--the "good"--versus the deep visceral fat that encircles your intestines, kidneys, liver, pancreas, and heart--the "bad."

And I'm not talking about what looks good or bad. We've all seen the unsightly flabby upper arms of an overweight woman or the cellulite on her bulging thighs. It might look awful but, metabolically speaking, it is benign.

It's that muffin top, love handle, or wheat belly that encircles the waist, a marker for underlying deep visceral fat, that:

--Increases release of inflammatory mediators/markers like tumor necrosis factor, leptin, interleukins, and c-reactive protein
--Is itself inflamed. When examined under a microscope, visceral fat is riddled with inflammatory white blood cells.
--Stops producing the protective hormone, adiponectin.
--Traffics in fatty acids that enter the bloodstream, resulting in greater resistance to insulin, fat deposition in the liver (fatty liver), and increases blood levels of triglycerides
--Predicts greater cardiovascular risk. A flood of recent studies (here's one) has demonstrated that larger quantities of pericardial fat (i.e., visceral fat encircling the heart, visible on a CT scan or echocardiogram) are associated with increased likelihood of coronary disease and cardiovascular risk.

You can even have excessive quantities of bad visceral fat without much in the way of fat elsewhere. You know the body shape: skinny face, skinny arms, skinny legs . . . protuberant, flaccid belly, the so-called "skinny obese" person.

Nobody knows why fat in visceral stores is so much more evil and disease-related than, say, wheat on your backside. While you may struggle to pull your spreading backside into your jeans, it's waist girth that is the problem. You need to lose it.

You could take vitamin D or . . .

You could take vitamin D and achieve a desirable blood level of 25-hydroxy vitamin D (I aim for 60-70 ng/ml), or you could:

--Take Actos to mimic the enhanced insulin sensitivity generated by vitamin D
--Take lisinopril to mimic the angiotensin-converting enzyme blocking, antihypertensive effect of vitamin D
--Take Fosamax or Boniva to mimic the bone density-increasing effect of vitamin D
--Take Celexa or other SSRI antidepressants to mimic the mood-elevating and winter "blues"-relieving effect of vitamin D
---Take Niaspan to mimic the HDL-increasing, small LDL-reducing effect of vitamin D
--Take naproxen to mimic the pain-relieving effect of vitamin D

So, given a choice, what do most doctors choose? Of course, they choose from the menu as presented by the sexy sales representative sitting in the office waiting room. These medications, of course, are among the top sellers in the drug world, taken by millions of Americans and not just one at a time, but several per person.

The Food and Nutrition Board of the Institute of Medicine, the panel of volunteers charged with drafting a Recommended Daily Allowance for vitamin D, says that you are already getting enough vitamin D, so don't bother taking any supplements and continue to wear your sunscreen. Wonder whose side they're on?

I continue to be impressed that many of the conditions that plague modern people are little more than deficiencies peculiar to modern life, such as vitamin D deficiency, or the result of the excesses of modern life, such as consumption of sucrose, fructose, corn, and "healthy whole grains."

I take 8000 units of gelcap vitamin D and haven't felt better.

More lipoproteins zero!

A few posts back, I talked about how more people are showing us zero lipoprotein(a) and zero small LDL. That was about 4 weeks ago. By then, I had seen 3 people with zero values on both.

Well, it's now up to 9 people: 9 people who have achieved zero lipoprotein(a) and zero small LDL. These are people who started with typical lipoprotein(a) values of 150-300 nmol/L and small LDL values of 1000-2000 nmol/L, both substantial.

I still don't know how many people or what percentage can expect to show such extravagant results. But the sharp increase over a relatively brief period of time is extremely encouraging!


Diet: One size does NOT fit all

Heart Scan Blog reader, Frustrated, posted this comment:

Dr. Davis,
I have spent the last 5 months eating a diet that completely eliminated all wheat products. It was very low carb, and consisted of relatively high protein (eggs, grass fed beef, grass fed raw cheese, oily fish, chicken), good level of olive oil, walnuts, fish oil (3 mg per day), raw vegetables, little bit of fruit. So I had good amount of monounsaturated fat as well as saturated fat from eggs and grass fed products.

My recent NMR showed:
LDL-p. 2,800
Small LDL particle 1700
Small HDL particle 20
HDL-C 40
LDL-C 114
Trigs. 224
Total chol 208

So I was disappointed. Where have I gone wrong? No wheat and sky-high LDL-p and 1700 small LDL particles.


This is indeed unusual. I see this perhaps 5 or 6 times over a year's time, while thousands of other people show the usual expected respone. I don't have Frustrated's lipoprotein panel prior to starting the diet, but I'll bet the starting panel was similar to this "after" panel.

The overwhelming majority of people who follow a diet like the one described--no wheat, limited carbohydrate, grass fed beef, fish, chicken, vegetables, limited fruit--obtain extravagant reductions in small LDL, increased HDL, and reduced triglycerides. So why did Frustrated end up with such disappointing results, values that potentially provide for high risk for heart disease?

There are several possibilities:

1) He/she is in the midst of substantial weight loss. When labs are drawn in the midst of weight loss, stored energy is being mobilized into the blood stream. This energy is mobilized as fatty acids and triglycerides which, upon entering the blood stream, cause increased triglycerides, reduced HDL, chaotic or unpredictable small LDL patterns, and increased blood sugar sufficient to be in the diabetic or pre-diabetic range. This all subsides and settles down to better values around 2 months after weight loss has plateaued.

2) Apo E4--If Frustrated has one or two apo E4 genes, then increased dietary fat will serve to exaggerate measures like small LDL despite the reduction in carbohydrates, LDL particle number, and triglycerides. This is a tough situation, since small LDL particles and high triglycerides signal carbohydrate sensitivity, while apo E4 makes this person, in effect, unable to deal with fats and dietary cholesterol. It gives me the creeps to talk about reducing fat intake, but this becomes necessary along with carbohydrate restriction, else statin drugs will come to the "rescue."

3) Apo E2 + Apo E4--It's possible that an apo E2 is present along with apo E4. Apo E2 makes this person extremely carbohydrate-sensitive and diabetes-prone with awful postprandial (after-meal) persistence of dietary byproducts, alongside the hyperabsorption of fats and dietary cholesterol from apo E4. This is a genuine nutritional rock and a hard place.

4) Other variants--There are probably a dozen or more other genetic variants, thankfully rare, such as apo B and apo C2 variants, that are not generally available for us to measure that could influence Frustrated's response.

5) The low-carb diet is not truly low-carb--Frustrated sounds like a pretty sharp cookie. But it's not uncommon for someone to overlook a substantial source of carbohydrate exposure that triggers these patterns. Fruit is a very common tripping point, since people generally regard unlimited fruit as a healthy thing. This does not seem to be Frustrated's problem. Others indulge in quinoa, sweet potatoes, millet or other carbohydrate sources that look and sound healthy but, in sufficient quantities, can still trigger this pattern.

6) Other--Hypothyroidism, kidney disease, nephrotic syndrome, hypercortisolism and some other relatively rare conditions are worth considering if none of the above apply.

Anyway, that's the list I use when this peculiar situation arises. If obvious weight loss is not the culprit, the next step is apo E testing. However, the wrong response is to reject the low-carbohydrate notion altogether and just limit fat, since this typically leads to uncontrolled small LDL, high triglycerides, and diabetes. It can often mean limiting carbohydrates while also limiting fats. Just as with the combination of apo E4 with Lipoprotein(a), I lump many of these patterns into the emerging world of genetic incompatibilities, genetic traits that code for incompatible metabolic phenomena.


Rerun: To let low-carb right, you must check POSTPRANDIAL blood sugars

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

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



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

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

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

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

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

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

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

LDL glycation

The proteins of the body are subject to the process of glycation, modification of protein structures by glucose (blood sugar). In the last Heart Scan Blog post, I discussed how glycated hemoglobin, available as a common test called HbA1c, can serve as a reflection of protein glycation (though it does not indicate actual Advanced Glycation End-products, or AGEs, just a surrogate indicator).

There is one very important protein that is subject to glycation: Apoprotein B.

Apoprotein B, or Apo B, is the principal protein of VLDL and LDL particles. Because there is one Apo B molecule per VLDL or LDL particle, Apo B can serve as a virtual VLDL/LDL particle count. The higher the Apo B, the greater the number of VLDL and LDL particles.

Because Apo B is a protein, it too is subject to the process of glycation. The interesting thing about the glycation of Apo B is that its "glycatability" depends on LDL particle size: The smaller the LDL particle, the more glycation-prone the Apo B contained within.

Younis et al have documented an extraordinary variation in glycatability between large and small LDL, with small LDL showing an 8-fold increased potential.

Think about it: Carbohydrates in the diet, such as wheat products and sugars, trigger formation of small LDL particles. Small LDL particles are then more glycation-prone by up to a factor of 8. Interestingly, HbA1c is tightly correlated with glycation of Apo B. Diabetics with high HbA1c, in particular, have the greatest quantity of glycated Apo B. They are also the group most likely to develop coronary atherosclerosis, as well as other consequences of excessive AGEs.

No matter how you spin it, the story of carbohydrates is getting uglier and uglier. Carbohydrates, such as those in your whole grain bagel, drive small LDL up, while making them prone to a glycating process that makes them more likely to contribute to formation of coronary atherosclerotic plaque.

High HbA1c: You're getting older . . . faster

Over the years, we all accumulate Advanced Glycation End-products, or AGEs.

AGEs are part of aging; they are part of human disease. AGEs are the result of modification of proteins by glucose. AGEs form the basis for many disease conditions.

Accumulated AGEs have been associated with aging, dementia, cataracts, osteoporosis, deafness, cancer, and atherosclerosis. Most of the complications of diabetes have been attributable to AGEs.

There's one readily available method to assess your recent AGE status: HbA1c.

Hemoglobin is the oxygen-carrying protein of red blood cells. Like other proteins, hemoglobin becomes glycated in the presence of glucose. Hemoglobin glycation increases linearly with glucose: The higher the serum or tissue glucose level, the more glycation of hemoglobin develops. Glycated hemoglobin is available as the common test, HbA1c.

Ideal HbA1c is 4.5% or less, i.e., 4.5% of hemoglobin molecules are glycated. Diabetics typically have HbA1c 7.0% or greater, not uncommonly greater than 10%.

In other words, repetitive and sustained high blood glucose leads to greater hemoglobin glycation, higher HbA1c, and indicates greater glycation of proteins in nerve cells, the lens of your eye, proteins lining arteries, and apoprotein B in LDL cholesterol particles.

If AGEs accumulate as a sign of aging, and high blood sugars lead to greater degrees of glycation, it only follows that higher HbA1c marks a tendency for accelerated aging and disease.

Indeed, that is what plays out in real life. People with diabetes, for instance, have kidney failure, heart disease, stroke, cataracts, etc. at a much higher rate than people without diabetes. People with pre-diabetes likewise.

The higher your HbA1c, the greater the degree of glycation of other proteins beyond hemoglobin, the faster you are aging and subject to all the phenomena that accompany aging. So that blood glucose of 175 mg/dl you experience after oatmeal is not a good idea. 

The lesson: Keep HbA1c really low. First, slash carbohydrates, the only foods that substantially increase blood glucose. Second, maintain ideal weight, since normal insulin responsiveness requires normal body weight. Third, stay physically active, since exercise and physical activity exerts a powerful glucose-reducing effect. Fourth, consider use of glucose-reducing supplements, an issue for another day.

While HbA1c cannot indicate cumulative AGE status, it can reflect your recent (preceding 60 to 90 days) exposure to this age-accelerating thing called glucose.

If your doctor refuses to accommodate your request for a HbA1c test, you can perform your own fingerstick test.

Slash carbs . . . What happens?

Cut the carbohydrates in your diet and what sorts of results can you expect?

Carbohydrate reduction results in:

Reduced small LDL--This effect is profound. Carbohydrates increase small LDL; reduction of carbohydrates reduce small LDL. People are often confused by this because the effect will not be evident in the crude, calculated (Friedewald) LDL that your doctor provides.

Increased HDL--The HDL-increasing effect of carbohydrate reduction may require 1-2 years. In fact, in the first 2 months, HDL will drop, only to be followed by a slow, gradual increase. This is the reason why, in a number of low-carb diet studies, HDL was shown to be reduced.--Had the timeline been longer, HDL would show a significant increase.

Decreased triglycerides--Like reduction of small LDL, the effect is substantial. Triglyceride reductions of several hundred milligrams are not at all uncommon. In people with familial hypertriglyceridemia with triglyceride levels in the thousands of milligrams per deciliter, triglyceride levels will plummet with carbohydrate restriction. (Ironically, conventional treatment for familial hypertriglyceridemia is fat restriction, a practice that can reduce triglycerides modestly in these people, but not anywhere near as effectively as carbohydrate restriction.) Triglyceride reduction is crucial, because triglycerides are required by the process to make small LDL--less triglycerides, less small LDL.

Decreased inflammation--This will be reflected in the crude surface marker, c-reactive protein--Yes, the test that the drug industry has tried to convince you to take statins drugs to reduce. In my view, it is an absurd notion that you need to take a drug like Crestor to reduce risk associated with increased CRP. If you want to reduce CRP to the floor, eliminate wheat and other junk carbohydrates. (You should also add vitamin D, another potent CRP-reducing strategy.)

Reduced blood pressure--Like HDL, blood pressure will respond over an extended period of months to years, not days or weeks. The blood pressure reduction will be proportion to the amount of reduction in your "wheat belly."

Reduced blood sugar--Whether you watch fasting blood sugar, postprandial (after-meal) blood sugars, or HbA1c, you will witness dramatic reductions by eliminating or reducing the foods that generate the high blood sugar responses in the first place. Diabetics, in particular, will see the biggest reductions, despite the fact that the American Diabetes Association persists in advising diabetics to eat all the carbohydrates they want. Reductions in postprandial (after-eating) blood sugars, in particular, will reduce the process of LDL glycation, the modification of LDL particles by glucose that makes them more plaque-causing.


You may notice that the above list corresponds to the list of common plagues targeted by the pharmaceutical industry: blood pressure, diabetes (diabetes being the growth industry of the 21st century), high cholesterol. In other words, high-carbohydrate, low-fat foods from the food industry create the list of problems; the pharmaceutical industry steps in to treat the consequences.

In the Track Your Plaque approach, we focus specifically on elimination of wheat, cornstarch, and sugars, the most offensive among the carbohydrates. The need to avoid other carbohydrates, e.g., barley, oats, quinoa, spelt, etc., depends on individual carbohydrate sensitivty, though I tend to suggest minimal exposure.

Normal fasting glucose with high HbA1c

Jonathan's fasting glucose: 85 mg/dl
His HbA1c: 6.7%

Jonathan's high HbA1c reflects blood glucose fluctuations over the preceding 60-90 days and can be used to calculate an estimated average glucose (eAG) with the following equation:

eAG = 28.7 X A1c – 46.7

(For glucose in mmol/L, the equation is eAG = 1.59 × A1C - 2.59)

Jonathan's HbA1c therefore equates to an eAG of 145.59 mg/dl--yet his fasting glucose value is 85 mg/dl. 

This is a common situation: Normal fasting glucose, high HbA1c. It comes from high postprandial glucose values, high values after meals. 

It suggests that, despite having normal glucose while fasting, Jonathan experiences high postprandial glucose values after many or most of his meals. After a breakfast of oatmeal, for instance, he likely has a blood glucose of 150 mg/dl or greater. After breakfast cereal, blood glucose likely exceeds 180 mg/dl. With two slices of whole wheat bread, glucose likewise likely runs 150-180 mg/dl. 

The best measure of all is a postprandial glucose one hour after the completion of a meal, a measure you can easily obtain yourself with a home glucose meter. Second best: fasting glucose with HbA1c.

Gain control over this phenomenon and you 1) reduce fasting blood sugar, 2) reduce expression of small LDL particles, and 3) lose weight.  

Can you handle fat?

No question: Low-carbohydrate diets generate improved postprandial lipoprotein responses.

Here's a graph from one of Jeff Volek's great studies:



Participants followed a low-carb diet of less than 50 g per day carbohydrate ("ketogenic") with 61% fat.   The curves were generated by administering a 123 g fat challenge with triglyceride levels assessed postprandially. The solid line represents the postprandial response at the start; dotted line after the 6-week low-carb effort.

Note that:

1) The postprandial triglyceride (area-under-the-curve) response was reduced by 29% in the low-carb diet.  That's a good thing.

2) The large fat challenge generated high triglycerides of greater than 160 mg/dl even in the low-carb group. That's a bad thing. 

In other words, low-carb improves postprandial responses substantially--but postprandial phenomena still occur. Postprandial triglycerides of 88 mg/dl or greater are associated with greater heart attack risk because they signify the presence of greater quantities of atherogenic (plaque-causing) postprandial lipoproteins.

A full discussion of these phenomena can be found in the Track Your Plaque Special Report, Postprandial Responses: The Storm After the Quiet!, part of a 3-part series on postprandial phenomena.

Statin stupid

If we followed the lead of the pharmaceutical industry and my cardiology colleagues, we would all subscribe to the "statins for all" philosophy. There is now $2 billion of clinical "research" to back up this "evidence-based" practice.

I do not endorse this "statins for all" philosophy. I believe it is a product of the raw profiteering of the pharmaceutical industry, who are adept at recruiting physicians to their cause.

But lost in the confusion of tainted studies and over-the-top media saturation is the fact that there are small groups of people who likely do obtain benefit from statin drugs. They would certainly benefit from better informed scrutiny of their lipoprotein and metabolic abnormalities. But treatment may involve statins.

This is entirely distinct from the "statins for all" argument, the simpleminded rule that primary care physicians and cardiologist are told to follow.

Groups who may indeed benefit from statin therapy include:

Homozygous or heterozygous familial hypercholesterolemia--Lacking a receptor for LDL particles, LDL piles up to very high levels in these people. LDLs of 300+ are common and lead to heart disease and stroke at relatively young ages.

Combined mixed hyperlipidemia--Among the one or more genetic defects underlying this condition involves excessive production of apoprotein B and VLDL particles. This leads to high risk for heart disease.

People unable to follow a diet to correct their lipid disorder--I have 80+-year old patients, for instance, who say, "I've eaten this way for 82 years. I'm not going to change now!" In the absence of diet and other efforts (e.g., omega-3 fatty acids from fish oil), drugs may be the answer.

In other words, of the $27 billion annual bill for statin drugs, perhaps a tiny fraction is truly necessary. The majority of people taking statin drugs would not really need them if they had the real answers. But don't let that confuse us: There are some people who do indeed benefit.

Butter and insulin

In a previous post, Atkins Diet: Common Errors, I commented on butter's unusual ability to provoke insulin responses. I offer this as a possible reason why, after a period of effective weight loss on a low-carbohydrate program, inclusion of some foods, such as butter, will trigger weight gain or stall weight loss efforts.

This develops because of butter's insulin-triggering effect, doubling or tripling insulin responses (postprandial area-under-the-curve). If insulin is triggered, fat gain follows.

Here's one such study documenting this effect: Distinctive postprandial modulation of ß cell function and insulin sensitivity by dietary fats: monounsaturated compared with saturated fatty acids

López et al 2008


From Lopez et al 2008. Mean (± SD) plasma glucose, insulin, triglyceride, and free fatty acid (FFA) concentrations during glucose and triglyceride tolerance test meal (GTTTM) with no fat (control), enriched in monounsaturated fatty acids (MUFAs) from refined olive oil (ROO meal), with added butter, with a mixture of vegetable and fish oils (VEFO) or with high-palmitic sunflower oil (HPSO). N = 14.

The postprandial (after-eating) area-under-the-curve is substantially greater when butter is included in the mixed composition meal. This effect is not unique to butter, but is shared by most other dairy products.

Fat, in general, does not make you fat. But butter makes you fat.

Vitamin D as a cardiovascular risk factor gains ground

If you were reading The Heart Scan Blog back in 2007, or read my Life Extension article on vitamin D deficiency as a cardiovascular risk factor, you already knew that vitamin D deficiency is rampant and adds to cardiovascular risk.

Results of a study from the Intermountain Medical Center Heart Institute in Utah bolster the concept that vitamin D deficiency is a cardiovascular risk factor, vitamin D normalization/supplementation reduces cardiovascular risk.

Science Daily reported:

For the first study, researchers followed two groups of patients for an average of one year each. In the first study group, over 9,400 patients, mostly female, reported low initial vitamin D levels, and had at least one follow up exam during that time period. Researchers found that 47 percent of the patients who increased their levels of vitamin D between the two visits showed a reduced risk for cardiovascular disease.


In the second study, researchers placed over 31,000 patients into three categories based on their levels of vitamin D. The patients in each category who increased their vitamin D levels to 43 nanograms per milliliter of blood or higher had lower rates of death, diabetes, cardiovascular disease, myocardial infarction, heart failure, high blood pressure, depression, and kidney failure. Currently, a level of 30 nanograms per milliliter is considered "normal."


Over the past 4 years, people in our program have been enjoying the extravagant benefits of vitamin D restoration. Cardiovascular benefits are becoming better documented and the bone health, cancer-preventing, insulin-normalizing, mood-adjusting, and anti-inflammatory effects likewise.

Atkins Diet: Common errors

No doubt: The diet approach advocated by the late Dr. Robert Atkins was a heck of a lot closer to an ideal diet than the knuckleheaded advice emitting from the USDA, American Heart Association, American Diabetes Association, and the Surgeon General's office.

But having just spent a week with Atkins low-carbers, here are some common errors that I see many make, errors that I believe have long-term health consequences, including impairment of weight loss.

Excessive consumption of animal products--Non-restriction of fat often leads to over-reliance on animal products. Higher intakes of red meats (heme proteins?) have been strongly associated with increased risk for colon and other gastrointestinal tract cancers. It is not a fat issue; it is an animal product issue. We should consume less meat, more vegetables and other plant-sourced foods.

Consumption of cured meats--Cured, processed meats, such as sausage, hot dogs, salami, bologna, and bacon, have a color fixative called sodium nitrite, an additive that has been confidently linked to gastrointestinal cancers. Risk is likely dose-dependent: The more you ingest, the greater the long-term risk.

Overconsumption of dairy products--Dairy products, especially milk, yogurt, cottage cheese, and butter, are potent insulinotropic foods, i.e., foods that trigger insulin release. There can be up to a tripling of insulin (area-under-the-curve) levels. This is not good in a world populated with tired, overworked pancreases, exhausted from a lifetime of high-carbohydrate eating.

Too many calories--While I agree that "a calorie is a calorie" and "calories in, calories out" are faulty concepts, I have anecdotally observed that long-time low-carbers often trend towards unlimited consumption of food, a phenomenon that seems to result in weight gain, especially in the sedentary. I wonder if this is a reflection of the insulinotropic action of dairy products and other proteins, compounded by the poor insulin responsiveness that develops with lack of physical activity. Factor into this conversation that lower calorie intake extends life, probably substantially (Sirt-2 activation and related phenomena, a la resveratrol). If lower calorie intake extends life, unlimited calorie intake likely shortens life.

Please don't hear this as low-carb bashing--it is not. It is a call to improve diets and not stumble into common traps that can impair heart health, weight loss, and longevity.