What do Salmonella, E coli, and bread have in common?

Say you happen to eat some chicken fingers contaminated with bacteria because the 19-year old kid behind the counter failed to wash his hands after using the toilet, or because the kitchen is poorly managed with unwashed counters and cutting boards, or because the food is undercooked. You get a bout of diarrhea and cramps, along with a desire to banish chicken from your life.

Here's yet another odd wheat phenomenon: About 30% of people who eliminate wheat from their lives experience an acute food poisoning-like effect on re-exposure. You've been wheat-free for, say, 6 months. You've lost 25 lbs from your wheat belly, you've regained energy, joints feel better. You go to an office party where they're serving some really yummy looking bruschetta. Surely a couple won't hurt! Within a hour, you're getting that awful rumbling and unease that precede the explosion.

The majority of people who experience a wheat re-exposure syndrome will have diarrhea and cramps that can last from hours to days, similar to food poisoning. (Why? Why would a common food trigger a food poisoning-like effect? It happens too fast to attribute to inflammation.) Others experience asthma attacks, joint pains that last 48 hours to a week, mental fogginess, emotional distress, even rage (in males).

Wheat re-exposure in the susceptible provides a tidy demonstration of the effects of this peculiar product of genetic research. So if you are wheat-free but entertain an occasional indulgence, don't be surprised if you have to make a beeline to the toilet.

The world of intermediate carbohydrates

There are clear-cut bad carbohydrates: wheat, oats, cornstarch, and sucrose. (Fructose, too, but in a class of bad all its own.)

Wheat: The worst. Not only does wheat flour increase blood sugar higher than nearly all other carbohydrates, it invites celiac disease, neurologic impairment, mental and emotional effects, addictive (i.e., exorphin) effects, asthma, irritable bowel syndrome, acid reflux, sleepiness, sleep disruption, arthritis . . . just to name a few.

Oats: Yeah, yeah, I know: "Lowers cholesterol." But nobody told you that oats, including slow-cooked oatmeal, causes blood sugar to skyrocket.

Cornstarch: Like wheat, cornstarch flagrantly increases blood sugar.It also stimulates appetite. That's why food manufacturers put it in everything from soups to frozen dinners.

Sucrose: Not only does sucrose create a desire for more food, it is also 50% fructose, the peculiar sugar that makes us fat, increases small LDL particles, increases triglycerides, slows the metabolism of other foods, encourages diabetes, and causes more glycation than any other sugar.

But there are a large world of "other" natural carbohydrates that don't fall into the really bad category. This includes starchy beans like black, kidney, and pinto; rices such as white, brown, and wild; potatoes, including white, red, sweet, and yams; and fruits. It includes "alternative" grains like quinoa, spelt, triticale, amaranth, and barley.

For lack of a better term, I call these "intermediate" carbohydrates. They are not as bad as wheat, etc., but nor are they good. They will still increase blood glucose, small LDL, triglycerides, etc., just not as much as the worst carbohydrates.

The difference is relative. Say we compare the one-hour blood glucose effects of 1 cup of wheat flour product vs. one cup of quinoa. Typical blood sugar after wheat product: 180 mg/dl. Typical blood sugar after quinoa: 160 mg/dl--better but still pretty bad.

Some people are so carb-sensitive that they should avoid even these so-called intermediate carbohydrates. Others can have small indulgences, e.g., 1/2 cup, and not generate high blood sugars.

Heroin, Oxycontin, and a whole wheat bagel

For a substantial proportion of people who remove wheat from their diet, there is a distinct and unpleasant withdrawal syndrome. Here are the comments of Heart Scan Blog reader, Scott, from Texas:

Hello Dr. Davis,

I've been experimenting with diet, converging upon a Paleo type diet, but I keep running into problems. I have isolated the problem to cutting out wheat.

Sugar, rice, fruit, corn, potatoes, etc. are relatively ok to add or remove from the diet, but cutting out wheat in particular brings on a moderate headache with heavy fatigue all day long. This resembles the wheat withdrawal symptoms I found on your blog. As I write this, I'm on day 8 of wheat-free. I consume a fair variety of meat and veggies each day with a moderate amount of white rice for carbs. Perhaps a bowl of corn flakes with milk and half a bar of dark chocolate a day. I've learned from experience over the past 5 months or so that none of these foods affect the withdrawal. It's purely wheat.

My question is, what is the range of times for withdrawal symptoms that you've heard from different people? Has there been anyone who never recovered from the wheat withdrawal symptoms even after many months?

It's very tough to get work done like this, and even though my body and head feel much healthier in general, my sinuses have cleared, don't have to take a big nap after I eat, etc., I don't want to go down a path where this is the way things are going to be forever. 



People who have never experienced wheat withdrawal pooh-pooh the effect. But, for about 30% of people, wheat withdrawal is a real, palpable, and sometimes incapacitating experience.

Beyond removing an exceptionally digestible carbohydrate that yields blood sugar rises higher than nearly any other known food (due to the unique amylopectin structure of wheat-derived carbohydrate), wheat withdrawal is a form of opiate withdrawal, somewhat like stopping heroin, Oxycontin, and other opiates. Stop eating whole wheat toast for breakfast, whole grain sandwiches for lunch, or whole grain pasta for dinner, and the flow of exorphins, i.e., exogenous morphine-like compounds, stops. You experience dysphoria (sadness, unhappiness), mental "fog," inability to concentrate, fatigue, and decreased capacity to exercise. It is milder than withdrawal from prescription opiates. Unlike withdrawal from more powerful opiates like heroine, there are, thankfully, no seizures or hallucinations. There are also no deaths.

In my experience, most people get through with wheat withdrawal in about 5 days. An occasional person will struggle for as long as 4 weeks. Thankfully for Scott, I've never seen it last longer than 4 weeks. (Interestingly, people who survive the withdrawal syndrome are often prone to a peculiar re-exposure phenomenon that I will discuss in future, i.e., they get sick upon re-exposure.)

The modern dwarf mutant variant of Triticum aestivum (that our USDA urges us to eat more of) contains greater proportions of gluten proteins compared to wheat pre-1970; glutens are the source of wheat-derived exorphins.

Incidentally, a drug company should be releasing a drug in the next year that will contain naltrexone, an oral opiate blocking drug, for a weight loss indication. They claim it is a blocker of the "mesolimbic reward system." I say it's a blocker of wheat exorphins.

The five most powerful heart disease prevention strategies

You've seen such lists before: 5 steps to prevent heart disease or some such thing. These lists usually say things like "cut your saturated fat," eat a "balanced diet" (whatever the heck that means), exercise, and don't smoke.

I would offer a different list. You already know that smoking is a supremely idiotic habit, so I won't repeat that. Here are the 5 most important strategies I know of that help you prevent heart disease and heart attack:

1) Eliminate wheat from the diet--Provided you don't do something stupid, like allow M&M's, Coca Cola, and corn chips to dominate your diet, elimination of wheat is an enormously effective means to reduce small LDL particles, reduce triglycerides, increase HDL, reduce inflammatory measures like c-reactive protein, lose weight (inflammation-driving visceral fat), reduce blood sugar, and reduce blood pressure. I know of no other single dietary strategy that packs as much punch. This has become even more true over the past 20 years, ever since the dwarf variant of modern wheat has come to dominate.

2) Achieve a desirable 25-hydroxy vitamin D level--Contrary to the inane comments of the Institute of Medicine, vitamin D supplementation increases HDL, reduces small LDL, normalizes insulin and reduces blood sugar, reduces blood pressure, and exerts potent anti-inflammatory effects on c-reactive protein, matrix metalloproteinase, and other inflammmatory mediators. While we also have drugs that mimic some of these effects, vitamin D does so without side-effects.

3) Supplement omega-3 fatty acids from fish oil--Omega-3 fatty acids reduce triglycerides, accelerate postprandial (after-meal) clearance of lipoprotein byproducts like chylomicron remnants, and have a physical stabilizing effect on atherosclerotic plaque.

4) Normalize thyroid function--Start with obtaining sufficient iodine. Iodine is not optional; it is an essential trace mineral to maintain normal thyroid function, protect the thyroid from the hundreds of thyroid disrupters in our environment (e.g., perchlorates from fertilizer residues in produce), as well as other functions such as anti-bacterial effects. Thyroid dysfunction is epidemic; correction of subtle degrees of hypothyroidism reduces LDL, reduces triglycerides, reduces small LDL, facilitates weight loss, reduces blood pressure, normalizes endothelial responses, and reduces oxidized LDL particles.

5) Make exercise fun--Not just exercise for the sake of exercise, but physical activity or exercise for the sake of having a good time. It's the difference between resigning yourself to 30 minutes of torture and boredom on the treadmill versus engaging in an activity you enjoy and look forward to: go dancing, walk with a friend, organize a paintball tournament outdoors, Zumba class, plant a new garden, etc. It's a distinction that spells the difference between finding every excuse not to do it, compared to making time for it because you enjoy it.

Note what is not on the list: cut your fat, eat more "healthy whole grains," take a cholesterol drug, take aspirin. That's the list you'd follow if you feel your hospital needs your $100,000 contribution, otherwise known as coronary bypass surgery.

Topping up your vitamin D tank

Now that my vitamin D replacement experience dates back nearly 5 years, I've been witnessing an unusual phenomenon:

The longer you take vitamin D, the less you need.

Let me explain. You take 10,000 units D3 in gelcap form. 25-hydroxy vitamin D levels, checked every 6 months, have remained consistently between 60 and 70 ng/ml. Three years into your vitamin D experience and 25-hydroxy vitamin D level rises to 98 ng/ml--an apparent need for less vitamin D.

So we cut your intake from 10,000 units per day to 8000 units per day. Another 25-hydroxy vitamin D level 6 months later: 94 ng/ml. We cut dose again to 6000 units, followed by another 25-hydroxy vitamin D level of 66 ng/ml.

This has now happened in approximately 20% of the people who have been taking vitamin D for 3 or more years. I know of no formal analysis of this effect, what I call the "topping up" phenomenon. Reasoned simply, it seems to me that, once your vitamin D "tank" is topped up (i.e., tissue stores have been replenished), it requires less to keep it full.

No one has experienced any adverse consequence of this topping up effect though it has potential for some people to develop toxic levels if 25-hydroxy vitamin D levels are not monitored long-term. In my office, I measure 25-hydroxy vitamin D levels every 6 months.

It means that long-term monitoring of 25-hydroxy vitamin D is crucial to maintain favorable and safe levels.

Thirteen catheterizations later

When I first met her, Janet couldn't stop sobbing. She'd just been through her 10th heart catheterization in two years.

It started with chest pains at age 56, prompting her first heart catheterization that uncovered severe atherosclerotic blockages in all three coronary arteries. Her cardiologist advised a bypass operation.

Six months after the bypass operation, Janet was back with more chest pains, just as bad as before. Another heart catherization showed that two of the three bypass grafts had failed. The third bypass graft contained a severe blockage that required a stent, along with multiple stents in the two now unbypassed arteries.

In the ensuing 18 months, Janet returned for 8 additional catheterizations, each time leaving the hospital with one or more stents.

Janet's doctor was puzzled as to why her disease was progressing so aggressively despite Lipitor and the low-fat diet provided by the hospital dietitian. So he had Janet undergo lipoprotein testing (NMR):

LDL particle number: 3363 nmol/L
Small LDL particle number: 2865 nmol/L
HDL cholesterol: 32 mg/dl
Triglycerides: 344 mg/dl
Fasting blood glucose 118 mg/dl
HbA1c 5.8%

Unfortunately, Janet's doctor didn't understand what these values meant. He pretty much threw his arms up in frustration. That's when I met Janet.

From her lipoprotein panel and other values, it was clear to me that Janet was miserably carbohydrate-sensitive and carbohydrate-indulgent, as demonstrated by the extravagant quantity (2865 nmol/L) and proportion (2865/3363, or 85%) of small LDL, the form of LDL particles created by carbohydrate exposure. Janet struggled with depression over the years and had been using carbohydrate foods as "comfort" foods, often resorting to cookies, pies, cakes, breads, and other wheat-containing foods for emotional solace.

It took a bit of persuasion to convince Janet that it was low-fat, "healthy whole grains," as well as comfort foods, that had led her down this path. I also helped Janet correct her severe vitamin D deficiency, mild thyroid dysfunction, and lack of omega-3 fatty acids.

Since meeting Janet and instituting her new prevention program, she has undergone three additional catheterizations (performed by another cardiologist), all performed for chest pain symptoms that struck during periods of emotional stress. All showed . . . no significant blockage. (Apparently, the repeated "need" for stents triggered a Pavlovian response: chest pain = "need" for yet more stents.)

In short, correction of the causes of coronary atherosclerotic plaque--small LDL, vitamin D deficiency, omega-3 fatty acid deficiency, and thyroid dysfunction--and Janet's disease essentially ground to a halt.

Imagine, instead, that Janet had undergone 1) a heart scan to identify hidden coronary plaque 5-10 years before her first heart procedure, then 2) corrected the causes before they triggered symptoms and posed danger. She might have been spared an extraordinary amount of life crises, hospital procedures, expense (nearly $1 million), and emotional suffering.

High blood pressure vanquished

Heart Scan Blog reader, Eric, related his blood pressure success story to me:

I'm 34 and have been battling chronic hypertension (systolic 150-200, depending on my anxiety levels) even with multiple prescriptions for over a decade now. I've seen four different cardiologists, all stumped as to what is causing my hypertension. First, they suspected coarctation of my aorta [a constriction in the aorta], but an angiogram determined blood pressure readings were the same on both sides of the narrowing.

The second angiogram performed last year to determine if my coarct had worsened determined that it had not, but that my aorta had calcium build up. The cardiologist was stumped because he told me he hasn't seen calcium in a patient so young. Needless to say, this scared me to death, with my wife being pregnant with our first child. I asked if it could be reversed and he didn't know so he sent me to get a Berkeley lab.

The Berkeley came back with LDL 91, HDL 41, Triglycerides 73, CRP 4.1, vit D 26. The doctors weren't very knowledgeable about explaining to me what these meant and how I could correct the low vit D and high CRP. They told me to follow the low-fat diet recommended by Berkeley. Well I've already tried the DASH diet and didn't like how I felt or my energy levels, so I didn't transition.

I was at a loss until I encountered your blog and it was truly a gift. It was a refreshing feeling to meet a knowledgeable Dr. who knew what I was going through and seems to truly care about reversing calcium in the heart (something I never got from my any of my cardiologists). With your blog I have an appointment to get a heart scan here in CO and take that number along with my Berkeley results and join Track Your Plaque.

For the past 2 weeks I've been following your advice by taking a D3+K2 supplement with Omega3 Fish oil and avoiding all grain, wheat, sugar and I'm already down 4lbs to 223.5lbs at 6'5" tall and my blood pressure readings have been 128/54 and 129/60 the past 2 days! With your help I may not have the dark future my father had: dead at 48 with a massive heart attack.

Stay on the look out because I look forward to telling you how I'm one of your top calcium losers!

Eric, Colorado


Conventional medical care fails at so many levels for so many people. While Eric's doctors were busy contemplating the next angiogram, they were neglecting several crucial aspects of his health.

It's really not that tough. But it can mean doing the opposite of what conventional "wisdom" tell us.

DHEA and Lp(a)

DHEA supplementation is among my favorite ways to deal with the often-difficult lipoprotein(a), Lp(a).

DHEA is a testosterone-like adrenal hormone that declines with age, such that a typical 70-year old has blood levels around 10% that of a youthful person. DHEA is responsible for physical vigor, strength, libido, and stamina. It also keeps a lid on Lp(a).

While the effect is modest, DHEA is among the most consistent for obtaining reductions in Lp(a). A typical response would be a drop in Lp(a) from 200 nmol/L to 180 nmol/L, or 50 mg/dl to 42 mg/dl--not big responses, but very consistent responses. While there are plenty of non-responders to, say, testosterone (males), DHEA somehow escapes this inconsistency.

Rarely will DHEA be sufficient as a sole treatment for increased Lp(a), however. It is more helpful as an adjunct, e.g., to high-dose fish oil (now our number one strategy for Lp(a) control in the Track Your Plaque program), or niacin.

Because the "usual" 50 mg dose makes a lot of people bossy and aggressive, I now advise people to start with 10 mg. We then increase gradually over time to higher doses, provided the edginess and bossiness don't creep out.

The data documenting the Lp(a)-reducing effect of DHEA are limited, such as this University of Pennsylvania study, but in my real life experience in over 300 people with Lp(a), I can tell you it works.

And don't be scared by the horror stories of 10+ years ago when DHEA was thought to be a "fountain of youth," prompting some to take megadose DHEA of 1000-3000 mg per day. Like any hormone taken in supraphysiologic doses, weird stuff happens. In the case of DHEA, people become hyperaggressive, women grow mustaches and develop deep voices. DHEA doses used for Lp(a) are physiologic doses within the range ordinarily experienced by youthful humans.

No more cookies

Jeanne enjoyed her Christmas holidays. She especially liked sharing the cookies she made for her grandchildren, sneaking 2 or 3 every day over a couple of weeks. On top of this, she enjoyed the Christmas candy, egg nog, leftover stuffing and cranberry sauce, topped off with a night of nutritional debauchery on New Year's Eve.

Lipid panel in October:

Total cholesterol 146 mg/dl
LDL cholesterol 72 mg/dl
HDL cholesterol 64 mg/dl
Triglycerides 49 mg/dl

Lipid panel in early January:

Total cholesterol 229 mg/dl
LDL cholesterol 141 mg/dl
HDL cholesterol 59 mg/dl
Triglycerides 147 mg/dl


I call the holidays The Annual Wheat and Sugar Frenzy. It's the carbohydrates, especially those from products made of wheat and sucrose, that caused the marked shifts in Jeanne's lipid patterns. Let's take each parameter apart:

--Triglycerides go up due to de novo lipogenesis, liver conversion of carbohydrates into triglycerides. Triglycerides enter the bloodstream as VLDL particles which, in turn, interact with LDL and HDL.

--LDL goes up because carbohydrate exposure increases VLDL, followed by conversion to LDL. The triglyceride-rich LDL created is converted to small LDL particles. Had we measured small LDL changes in Jeanne, we likely would have measured something like an increase (by NMR) from 800 nmol/L to 1600 nmol/L, a carbohydrate effect.

--The increased VLDL also makes HDL triglyceride-rich, cause more rapid degradation of HDL particles. (It also makes them smaller, like LDL.) Given sufficient time (a few more months), HDL would drop into the 40's.

--Total cholesterol changes reflect the composite of the above numbers. (Total cholesterol = LDL cholesterol + HDL cholesterol + Trig/5) (Note that, as HDL drops, so will total cholesterol; that's why this value is worthless and should be ignored.)

So don't be surprised by the above distortions after a period of carbohydrate indulgence. Although your unwitting primary care doc will see such changes as opportunity for Lipitor, it is nothing more than the cascade of effects from a carbohydrate-driven distortion of lipoproteins.

How to become diabetic in 5 easy steps

If you would like to become diabetic in as short a time as possible, or if you have someone you don't like--ex-spouse, nasty neighbor, cranky mother-in-law--whose health you'd like to booby trap, then here's an easy-to-follow 5-step plan to make you or your target diabetic.


1) Cut your fat and eat healthy, whole grains--Yes, reduce satiety-inducing foods and replace the calories with appetite-increasing foods, such as whole grain bread, that skyrocket blood sugar higher than a candy bar.

2) Consume one or more servings of juice or soda per day--The fructose from the sucrose or high-fructose corn syrup will grow visceral fat and cultivate resistance to insulin.

3) Follow the Institute of Medicine's advice on vitamin D--Take no more than 600 units vitamin D per day. This will allow abnormal levels of insulin resistance to persist, driving up blood sugar, grow visceral fat, and allow abnormal inflammatory phenomena to persist.

4) Have a bowl of oatmeal or oat cereal every morning--Because oat products skyrocket blood sugar, the repeated high sugars will damage the pancreatic beta cells ("glucose toxicity"), eventually impairing pancreatic insulin production. (Entice your target even further: "Would you like a little honey with your oatmeal?") To make your diabetes-creating breakfast concoction even more effective, make the oatmeal using bottled water. Many popular bottled waters, like Coca Cola's Dasani or Pepsi's Aquafina, are filtered waters. This means they are devoid of magnesium, a mineral important for regulating insulin responses.

5) Take a diuretic (like hydrochlorothiazide, or HCTZ) or beta blocker (like metoprolol or atenolol) for blood pressure--Likelihood of diabetes increases 30% with these common blood pressure agents.

There you have it! Perhaps we should assemble a convenient do-it-yourself-at-home diabetes kit to help, complete with several servings of whole grain bread, a big bottle of cranberry juice, some 600 unit vitamin D tablets, a container of Irish oatmeal, and some nice bottled water.

Fish oil in the news



Hooray for the New York Times. They ran an article pointing out the miserable and inexcusable failure of American physicians to use fish oil after heart attack.

“It is clearly recommended in international guidelines,” said Dr. Massimo Santini, the hospital’s chief of cardiology, who added that it would be considered tantamount to malpractice in Italy to omit the drug.

...in the United States, heart attack victims are not generally given omega-3 fatty acids, even as they are routinely offered more expensive and invasive treatments, like pills to lower cholesterol or implantable defibrillators. Prescription fish oil, sold under the brand name Omacor, is not even approved by the Food and Drug Administration for use in heart patients."

The article focuses on the use of fish oil only after heart attack and doesn't tackle the larger issue of how fish oil is crucial for coronary disease in general. Of course, the article doesn't address the extraordinary effects of fish oil on lipoproteins, particularly triglyceride-containing varieties like VLDL and the postprandial (after-eating) intermediate-density lipoprotein (IDL).

It also talks about prescription fish oil and just glosses over fish oil as a nutritional supplement. I know of few reasons to use the prescription form. More than 90% of the time, nutritional sources of fish oil do the trick. (That is, fish oil capsule supplements, not just eating fish which doesn't provide enough for coronary plaque reduction or control.)

Occasionally, I'll meet someone who has a severe hypertriglyceridemia (very high triglycerides), or is a Apo E 2/2 homozygote (very rare). These special instances may, indeed, do better using prescription fish oil, since it is more concentrated--one prescription capsule providing the same omega-3 fatty acid content as three conventional capsules (1000 mg fish oil, 300 mg EPA+DHA).


But for most of us, the standard fish oil supplement you buy at the health food store or department store does just fine. If you read about the impurity of fish oil supplements (likely prompted by the manufacturer of Omacor, prescription fish oil), refer to the studies by Consumer Reports and Consumer Labs, both of which found no mercury or pesticide residues in dozens of fish oil preparations tested.

Look on the bright side. The conversation is growing. Fish oil, whether prescription or my favorite, Sam's Club Members' Mark brand, is a fabulously effective supplement with benefits that, in nearly all cases, exceeds the benefits of drugs.

Fish oil is an absolute requirement for your Track Your Plaque program and for you to hope to achieve control or reduction of your heart scan score.

Nutritional approaches to homocysteine reduction


For an in-depth discussion of nutritional approaches to homocysteine reduction, see my new article, Nutritional Therapies for Managing Homocysteine , in the most recent issue of Life Extension magazine. You'll find it at:

http://www.lef.org/magazine/mag2006/oct2006_report_homocysteine_01.htm

The report contains a detailed discussion of how to use foods to control homocysteine levels. Though I'm not a homocysteine-crazed fanatic like Life Extension publisher, William Falloon, I still there's some interesting aspects of homocysteine metabolism that need to be explored. I also think there's some genuine benefit to reducing homocystine, preferably with foods, secondarily with supplements.

Also see our recent update on homocysteine on the www.cureality.com website at:
http://www.cureality.com/library/fl_01-006homocysteine.asp

In the update, we tried to make sense of what the new studies on homocysteine treatment, NORVIT and HOPE-2, tell us in light of all the other studies on homocysteine that preceded them.

The American Heart Association diet guarantees you get heart disease!

Perhaps I stated that too strongly.

But the fact remains: the diet advocated by the American Heart Association is awful. The foods endorsed by their approach have no place on a list of healthy foods. Yes, you will find vegetables and fruits, etc.. But you will also find that the 2006 American Heart Association Diet and Lifestyle Recommendations dance around the issue of what foods to avoid. There's no explicit mention of how, for instance, common foods like Shredded Wheat cereal, ketchup, low-fat salad dressings, etc, among thousands of others, should be avoided.

No matter how you time your meals, mix them, combine proteins, fats, and carbohydrates, etc., you simply cannot squeeze health out of products like breakfast cereals, instant mashed potatoes, dried soup mixes, wheat crackers, etc. Yet these are the sorts of foods that are implicitly allowable in the Heart Association's diet program.

You can obtain a little insight into the motivations behind the diet design by looking at the Heart Association's Annual Report list of major supporters:

--ACH Food Companies--maker of Mazola margarine and corn oil. A contributor of between $500,000 and $999,000 to the Heart Association.

--ConAgra Foods--You know them as Chef BoyArdee, Peter Pan peanut butter, Kid Cuisine (pizza, macaroni and cheese). ConAgra contributed between $500,000 and $999,000 to the Heart Association.

--Archer Daniels Midland--Huge worldwide supplier of wheat flours, high-fructose corn syrup, and basic ingredients for manufacture of soft drinks, candies, and baked foods. ADM contributed between $1-4.9 million dollars to the American Heart Association.

Of course, the Heart Association provides many hugely positive services like funding research. But, on many official statements, you need to read between the lines. The Heart Association is funded by industry: medical device makers, drug makers, food manufacturers. Yes, some is contributed in the interest of health. But you can be sure that lots of money is also contributed in the hope of protecting specific commercial interests. Many of those decisions are made behind closed doors or on the golf course.

Be skeptical. Just because the Heart Association diet is a Casper Milquetoast version of a health program, it does not mean that you have to subscribe to their watered-down, politically correct, and downright useless nutrition recommendations.

I'm just right!

Ben is an energetic 45-year old entrepreneur. He started his own security alarm company and has, with tremendous hard work and long hours, built it into a successful local business. Despite his long hours, he found time to coach his son's football team and help with raising his 3 kids.

Ben's life took a detour when he had urgent bypass surgery at age 39. Just three years later, the chest pains and fatigue he'd experienced before bypass returned. Another heart catheterization revealed that all of his bypass grafts except one had closed. Three stents were implanted to salvage his original coronary arteries.

That's when I met Ben. Shockingly (perhaps I should know by now!), Ben was taking Lipitor and had been advised to follow a low-fat diet. That was the full extent of his heart disease prevention program. The burning question that I wanted answered was "Why did a 39-year old man have heart disease?".

Our analysis uncovered a smorgasbord of hidden patterns. You name it, Ben had it: postprandial (after-eating) patterns like IDL, low HDL, and, most notably, small LDL and lipoprotein(a). That's why Ben had heart disease as a 39-year old man--plain and simple.

We proceeded to correct all of his patterns. But the one aspect of his program that he struggled with: weight. At 5 ft 9 inches, Ben started at 285 lbs before bypass. He did manage to get to 270 after his surgery. I told him that, if he was going to get full control of his small LDL pattern, he needed to get to <210 lbs, perhaps even lower. Without substantial weight loss, he would never seize full control over coronary plaque.

Ben was satisfied that we had identified the hidden causes of his heart disease. But he remained skeptical that that magnitude of weight loss was necessary. Built like a football player, he looked stocky but not outright fat. He got down to 240 lbs but then he decided that he looked too skinny and just went right back up to 250-260 in weight.

At a weight of 250, this puts Ben's BMI (body mass index) at around 37, way over the cut-off of 30 for obesity. Now, the BMI can be misleading in people with larger frames and more muscle. But Ben undeniably had a generous abdomen, encasing the visceral fat that drives small LDL.

Unfortunately, Ben remained skeptical until I put three more stents into his right coronary artery last evening.

Small LDL is a powerful activator of lipoprotein(a). In other words, there's something peculiarly evil about the combination of small LDL and lipoprotein(a) that brings out the worst in both. You can't correct just one or the other. You've got to correct both. Don't learn this lesson the hard way.

I think (hope) that Ben is on track to get to around 200 lbs.

Prevention: Bad news in bits and pieces

Jan clearly did not want to talk about her heart scan. Her score of 502 came as a shock to her. After all, she'd survived breast cancer just a year earlier, having been through dozens of radiation treatments, chemotherapy, not the mention the emotional upheaval.

Now I was telling Jan that she had a very high heart scan score with a heart attack risk of 5% per year. Then we got to her lipoprotein patterns: Jan had several striking abnormalities, including a misleading LDL cholesterol that underestimated her true LDL by nearly 100% (LDL particle number), small LDL, and the dreaded lipoprotein(a).

"I can't handle this! Why did I get the stupid scan in the first place?!"

Giving her a chance to collect her emotions, I discussed how, even though this business can be frightening, it's far--FAR--better than the alternative: heart attack at 3 am, rush to the hospital, stents, bypass surgery, etc. Or, death for the >30% of people who don't make it to the hospital in time.

That's why I often tell people that prevention of disease is bad news in bits and pieces. But it's a lot more manageable this way. Coronary plaque is a controllable process. You don't have much control in the midst of a heart attack.

A second chance

Stewart had a CT heart scan in 2004. Score: 475.

As always in the Track Your Plaque program, Stewart had his lipoproteins assessed. Among his patterns were LDL 157 mg/dl, severe small LDL, and the (post-prandial, or after-eating) IDL. Stewart was also "pre-diabetic" with a blood sugar of 123 mg/dl. Blood pressure was also a major issue. Although initially concerned, life and distractions got in the way, and Stewart's attentions drifted away.

Two years of a lackadaisical effort and Stewart's heart scan score was 600, a 26% increase. Not as bad as it could have been doing nothing (i.e., 30% per year), but still far from great. But, even with the increase in score, we still really didn't get Stewart's attention. He went about his business with a very lax dietary program, overindulging in breads, crackers, goodies, hot dogs, etc., and following a virtually non-existent exercise program except for playing golf once or twice a week.

Unfortunately, Stewart started having pains in his chest with very minimal efforts like climbing a single flight of stairs. His stress test proved abnormal. Stewart then received a stent in his left anterior descending coronary and another in his circumflex. His right coronary artery had a 40-50% blockage, close to requiring a stent.

I stressed to Stewart that this had been preventable. Should motivation remain unchanged, the next step would be bypass surgery.

I think I finally succeeded in getting Stewart's attention. He found the prospect of a bypass operation a lot more concrete than the idea of progression or regression of coronary plaque. So Stewart is being given a second chance. Unfortunately, we will no longer be able to track Stewart's plaque very effectively, since two of three arteries now contain stents, and only the right coronary remains scorable.

I hope Stewart succeeds. But I sure wish he had done this earlier. He had realistic hopes of never requiring stents or bypass surgery.

Learn from Stewart's mistakes. Attention to your program requires vigilance. You can't ignore the causes of your coronary plaque for any length of time without it catching up to you. But seize your first and best chance.

Are you a skinny fat person?

AT 186 lbs. and 5 feet 10 inches, Doug did not regard himself as overweight. Sure, he had a little extra "love handles", a small bulge in the belly and a waist of 34 inches. But he was by no means fat, particularly compared to most of his friends, neighbors, and co-workers, many of whom were 50-100 lbs heavier.

But examine Doug's lipoprotein patterns and, if you didn't know what he looked like, you'd guess that he's at least 50 lbs or more overweight. His prominent patterns included low HDL, small LDL, high triglycerides, the after-eating IDL, and borderline high blood sugar of 116 mg/dl. His blood pressure usually ranged around 138/82.

In other words, Doug is among the 5-10% of people who have most of the features of the so-called "metabolic syndrome", but don't look the part. They usually (though not always) have a modest excess of visceral abdominal fat. While some people have to be 100 lbs overweight before they express these patterns, someone like Doug could do it with minimal excess weight, sometimes as little as 5-10 lbs.

Several specific genetic patterns can account for this exagerrated sensitivity to weight, but the solutions remain much the same. Heightened sensitivity to processed carbohydrates, particularly those containing wheat, is commonly present. A sharp reduction in processed carbohydrates like breads, breakfast cereals, and pretzels yields a huge benefit. Reduction in weight, of course, can also yield marked improvement in these patterns. This means that Doug should consider achieving his truly ideal weight of <175 lbs and become a truly skinny skinny person. Though his patterns might not be fully corrected, he will see substantial improvement across the board.

These patterns are also potent triggers for coronary plaque growth. Correction of low HDL, small LDL, etc. is crucial if you are to seize hold of your heart scan score.

Heart disease "reversal" gives health a bad name

Put the search phrase "reverse heart disease" into your internet search engine, and you'll uncover an astonishing range of sites, all making extravagant promises.

The treatment programs offered range from the bizarre (colonic irrigation, magnetism, etc.), to centers using conventional approaches like statin drugs and low-fat diets, to sites that make lofty predictions with few unique tools (slash the fat and heart disease dissolves).

95% or more of the sites you turn up are clearly pandering to the unknowing, the unsophisticated, the hopeless, or other helpless niche groups. Homeopathic preparations, chelation, magnical combinations of herbals, you name it, you'll find it attached to claims for heart disease reversal.

I've seen people use many of these treatments. Is there any effect on the rate of increase of the heart scan score? Do they impact on the 30% per year expected rate of increase? Absolutely not.

Unfortunately, this gives anyone practicing truly effective methods to reverse coronary plaque a bad name. Just associating with this suspect group of "practitioners" can make us look bad--guilt by association.

Whenever someone claims to have the secret of heart disease reversal, I ask "Can you prove it?" Show me some evidence. It doesn't necessarily have to be $30 million drug company sponsored study, but some evidence of effectiveness should be available. The only thing we should take on faith is our religion, not our health care.

Our growing number of people who have, indeed, reversed their heart scan scores--reversed heart disease--to me is persuasive evidence of the value of the Track Your Plaque approach. Not foolproof, not 100%, but the best damned approach I'm aware of, by a long shot.

Trans fats to be banned

Sometimes good may come from legislation.

The City of New York is contemplating a ban on trans-fat use by restaurants, bakeries, and other food establishments in preparation of their foods. (Trans-fats are also known as hydrogenated fats.)

At this point, I believe it's unclear, should this pass, what the response will be. If food preparers turn to butter, that's not much better. (Don't get fooled by the non-sensical argument of which is better, butter or margarine--they're both terrible.) Subtracting hydrogenated fats will no doubt cause major disruption of food preparation habits. It may even increase the cost of food slightly.



I believe that the true positive effect of this situation, however, will be the tremendously heightened awareness it will raise in the public, both in New York and elsewhere, on just how bad and pervasive trans-fats are. It may increase awareness that foods like donuts and pastries are not just about excessive quantities of sugars, but also trans-fat content.

If you're already a Track Your Plaque follower, you already know that the easiest way to dodge trans-fats in your diet is to minimize your use of processed foods--the cellophane-wrapped, pulverized, dried, just-add-water, microwavable and ready-to-eat foods that line supermarket shelves. Trans-fats are purely man-made. You won't find them--not a stitch--in green peppers, lettuce, olive oil, almonds. . .unprocessed foods. Watch for an in-depth report on trans-fats on the Track Your Plaque website in which we will detail the scientific evidence behind this movement, how to recognize when foods contain trans-fats, etc.

Back to basics!

Harold is energetic and highly motivated. His heart scan score of 997 really threw him for a loop: his view of himself as a healthy, slender, 58-year old clearly needed revision.

So Harold set himself on a quest to find new ways to help him deal with his heart disease risk. He enrolled in the Track Your Plaque program. Unfortunately, he skimmed through the information but didn't really put much of it to use.

Instead, he wanted the "secret" information that other people didn't know about, "insider" information that couldn't be found in magazines, wasn't know by doctors.

He'd read that hawthorne was useful for opening coronary arteries, so he bought hawthorne at the health food store. He read that coenzyme Q10 was a little know way to strengthen the heart, so he added that. A Chinese doctor in town was advertising chelation therapy that "dissolved plaque". He subscribed to a once-a-week intravenous infusion at the doctor's holistic clinic of Eastern medicine. He'd heard that testosterone opened up arteries, so he purchased a preparation of chrysin, horny goat weed, yohimbine, and saw palmetto. He was suspicious of many conventional medicines, but he didn't want to ignore his LDL cholesterol of 172 mg/dl. So he added guggulipid and a combination cholesterol-reducing product that contained about 10 ingredients.

Harold pursued his quest, often adding new agents that came with promising stories. One year later, Harold eagerly got another heart scan, certain that his extraordinary efforts were sure to yield a dramatic drop in his heart scan score. The score: 1372, a 37% increase.

Harold was therefore several thousand dollars poorer and several steps closer to taking the plunge, allowing a potentially fatal disease to cut his life short.

The message: There's no need to re-invent the wheel. There are no top-secret ways to reverse atherosclerotic plaque.


Don't neglect the basics. You can't do calculus until you learn how to add, subtract, and divide. From a heart scan score reducing perspective, achieving 60-60-60 in basic lipids, normalizing blood pressure and blood sugar, identifying any hidden lipoprotein patterns like small LDL and Lp(a), losing weight to your ideal weight, taking fish oil, normalizing vitamin D blood levels to 50-70 ng/ml--these are the necessary prerequisites to achieve control over your coronary plaque and stop the increase in your heart scan score.

You don't need to waste your time with the rants of some supplement-hawker eager to sell you the next cure for heart disease. I'm often amazed at the number of people who do so yet have never even taken care of someone with heart disease. Would you allow someone to try and repair your car if they've never actually laid their hands on an engine before? Then why would you entrust such a person with your health?

The Track Your Plaque approach is not fool-proof, but it's the best there is by a long shot.

The Paleo approach to meal frequency

Furthering our discussion of postprandial (after-eating) phenomenona, including chylomicron and triglyceride "stacking" (Grazing is for cattle and Triglyceride and chylomicron stacking), here's a comment from the recent Palet Diet Newsletter on the closely related issue, meal timing and frequency:


We are currently in the process of compiling meal times and patterns in the worlds historically studied hunter-gatherers. If any single picture is beginning to emerge, it clearly is not three meals per day plus snacking ala the typical U.S. grazing pattern. Here are a few examples:

--The Ingalik Hunter Gatherers of Interior Alaska: 'As has been made clear, the principal meal and sometimes the only one of the day is eaten in the evening.'
--The Guayaki (Ache) Hunter Gatherers of Paraguay: 'It seems, however, that the evening meal is the most consistent of the day. This is understandable, since the day is generally spent hunting for food that will be eaten in the evening."
--The Kung Hunter Gatherers of Botswana. "Members move out of camp each day individually or in small groups to work through the surrounding range and return in the evening to pool the collected resources for the evening meal."
--Hawaiians, Tahitians, Fijians and other Oceanic peoples (pre-westernization). 'Typically, meals, as defined by Westerners, were consumed once or twice a day. . . Oliver (1989) described the main meal, usually freshly cooked, as generally eaten in the late afternoon after the day’s work was over."

The most consistent daily eating pattern that is beginning to emerge from the ethnographic literature in hunter-gatherers is that of a large single meal which was consumed in the late afternoon or evening. A midday meal or lunch was rarely or never consumed and a small breakfast (consisting of the remainders of the previous evening meal) was sometimes eaten. Some snacking may have occurred during daily gathering, however the bulk of the daily calories were taken in the late afternoon or evening. This pattern of eating could be described as intermittent fasting relative to the typical Western pattern, particularly when daily gathering or hunting were unsuccessful or marginal. There is wisdom in the ways of our hunter gatherer ancestors, and perhaps it is time to re-think three squares a day.



In other words, the notion of "grazing," or eating small meals or snacks throughout the day, is an unnatural situation. It is directly contrary to the evolutionarily more appropriate large meal followed by periods of no eating or small occasional meals.

I stress this point because I see that the notion of grazing has seized hold of many people's thinking. In my view, grazing is a destructive practice that is self-indulgent, unnecessary, and simply fulfills the perverse non-stop hunger impulse fueled by modern carbohydrate foods.

Eliminate wheat, cornstarch, and sugars and you will find that grazing is a repulsive impulse that equates with gorging.


The full-text of the Paleo Diet Newsletter can be obtained through www.ThePaleoDiet.com. You can also read and/or subscribe to the new Paleo Diet Blog, just launched in November, 2009.

Even mummies do it


Lady Rai, nursemaid to Queen Nefertari of Egypt, died in 1530 BC, somewhere between the age of 30 and 40 years. Her mummy is preserved in the Egyptian National museum of Antiquities in Cairo.

A CT scan of her thoracic aorta revealed calcium, representing aortic atherosclerosis, reported by Allam et al (including my friend from The Wisconsin Heart Hospital, Dr. Sam Wann, who provided me a blow-by-blow tale of this really fascinating project). Ladi Rai and 14 other Egyptian mummies were found to have vascular calcification of a total of 22 mummies scanned. (The hearts of the mummies were too degenerated to make out any coronary calcium.)

But why would people of that age have developed atherosclerosis?

The authors of the study comment that "Our findings that atherosclerosis was not infrequent among middle-aged and older ancient Egyptians of high social status challenges the view that it is a disease of modern humans. . . Although ancient Egyptians did not smoke tobacco or eat processed food or presumably lead sedentary lives, they were not hunter-gatherers. [Emphasis mine.] Agriculture was well established in ancient Egypt and meat consumption appers to have been common among those of high social status."

Fascinating. But I don't think that I'd blame meat consumption. Egyptians were also known to have cultivated grains, including wheat, and frequently consumed such sweet delicacies as dates and figs. Egyptians were also apparently beer drinkers. Unfortunately, no beer steins were seen in any of the scans.

Life Extension article on iodine

Here's a link to my recent article in Life Extension Magazine on iodine:

Halt on Salt Sparks Iodine Deficiency

Iodized salt, a concept introduced into the U.S. by the FDA in 1924, slowly eliminated goiter (enlarged thyroid glands), along with an enormous amount of thyroid disease, heart attack, mental impairment, and death. The simple addition of iodine to salt ensured that salt-using Americans obtained enough iodine sufficient to not have a goiter.

Now that the FDA, goiters long forgotten from their memories, urges Americans to reduce salt, what has happened to our iodine?

I talk at length about this issue in the Life Extension article.

The healthiest people are the most iodine deficient

Here's an informal observation.

The healthiest people are the most iodine deficient.

The healthier you are, the more likely you are to:

--Avoid junk foods--30% of which have some iodine from salt
--Avoid overuse of iodized salt
--Exercise--Sweating causes large losses of iodine.

So the healthy-eating, exercising person is the one most likely to show iodine deficiency: gradually enlarged thyroid gland (in the neck), declining thyroid function. Over time, if iodine deficiency persists, excessive sensitivity to iodine develops, as well as abnormal thyroid conditions like overactive nodules.

Even subtle levels of thyroid dysfunction act as a potent coronary risk factor.

It's the score, stupid

Sal has had 3 heart scans. (He was not on the Track Your Plaque program.) His scores:

March, 2006: 439

April, 2007: 573

October, 2009: 799

Presented with the 39% increase from April, 2007 to October, 2009, Sal's doctor responded, "I don't understand. Your LDL cholesterol is fine."

This is the sort of drug-driven, cholesterol-minded thinking that characterizes 90% of primary care and cardiologists' practices: "Cholesterol is fine; therefore, you must be fine, too."

No. Absolutely not.

The data are clear: Heart scan scores that continue to increase at this rate predict high risk for cardiovascular events. Unfortunately, when my colleagues hear this, they respond by scheduling a heart catheterization to prevent heart attack--a practice that has never been shown to be effective and, in my view, constitutes malpractice (i.e., performing heart procedures in people with no symptoms and with either no stress test or a normal stress test).

It's the score, stupid! It's not the LDL cholesterol. Pay attention to the increasing heart scan score and you will know that the disease is progressing at an alarming rate. Accepting this fact will set you and your doctor on the track to ask "Why?"

That's when you start to uncover all the dozens of other reasons that plaque can grow that have nothing to do with LDL cholesterol or statin drugs.

Heart Scan Blog Redux: Cheers to flavonoids

Because in Track Your Plaque we've been thinking a lot about anthocyanins, here's a rerun of a previous Heart Scan Blog post about red wine. (Anthocyanins are among the interesting flavonoids in red wine, along with resveratrol and quercetin.)


The case in favor of healthful flavonoids seems to grow bit by bit.

Flavonoids such as procyanadins in wine and chocolate, catechins in tea, and those in walnuts, pomegranates, and pycnogenol (pine bark extract) are suspected to block oxidation of LDL (preventing its entry into plaque), normalize abnormal endothelial constriction, and yield platelet-blocking effects (preventing blood clots).

Dr. Roger Corder is a prolific author of many scientific papers detailing his research into the flavonoids of foods, but wine in particular. He summarizes his findings in a recent book, The Red Wine Diet. Contrary to the obvious vying-for-prime-time title, Dr. Corder's compilation is probably the best mainstream discussion of flavonoids in foods and wines that I've come across. Although it would have been more entertaining if peppered with more wit and humans interest, given the topic, its straightfoward, semi-academic telling of the story makes his points effectively.

Among the important observations Corder makes is that regions of the world with the greatest longevity also correspond to regions with the highest procyanidin flavonoids in their wines.




Regarding the variable flavonoid content of wines, he states:

Although differences in the amount of procyanidins in red wine clearly occur because of the grape variety and the vineyard environment, the winemaker holds the key to what ends up in the bottle. The most important aspect of the winemaking process for ensuring high procyanidins in red wines is the contact time between the liquid and the grape seeds during fermentation when the alcohol concentration reaches about 6 percent. Depending on the fermentation temperature, it may be two to three days or more before this extraction process starts. Grape skins float and seeds sink, so the number of times they are pushed down and stirred into the fermenting wine also increases extraction of procyanidins. Even so, extraction is a slow process and, after fermentation is complete, many red wines are left to macerate with their seeds and skins for days or even weeks in order to extract all the color, flavor, and tannins. Wines that have a contact time of less than seven days will have a relatively low level of procyanidins. Wines with a contact time of ten to fourteen days have decent levels, and those with contact times of three weeks or more have the highest.

He points out that deeply-colored reds are more likely to be richer in procyanidins; mass-produced wines that are usually "house-grade" served at bars and restaurants tend to be low. Some are close to zero.

Wines rich in procyanidins provide several-fold more, such that a single glass can provide the same purported health benefit as several glasses of a procyanidin-poor wine.

So how do various wines stack up in procyanidin content? Here's an abbreviated list from his book:

Australian--tend to be low, except for Australian Cabernet Sauvignon which is moderate.

Chile--only Cabernet Sauvignon stands out, then only moderate in content.

France--Where to start? The French, of course, are the perennial masters of wine, and prolonged contact with skins and seeds is usually taken for granted in many varieties of wine. Each wine region (French wines are generally designated by region, not by variety of grape) can also vary widely in flavonoid content. Nonetheless, Bordeaux rate moderately; Burgundy low to moderate (except the village of Pommard); Languedoc-Roussillon moderate to high (and many great bargains in my experience, since these producers live in the shadow of its northern Bordeaux neighbors); Rhone (Cote du Rhone) moderate to high, though beware of their powerful "barnyard" character upon opening; decanting is wise.

Italy--Much red Italian wine is made from the Sangiovese grape and called variously Chianti, Valpolicella, and "super-Tuscan" when blended with other varietals. Corder rates the southern Italian wines from Sicily, Sardinia, and the mainland as high in procyanidins; most northern varieties are moderate.

Spain--Moderate in general.

United States--Though his comments are disappointingly scanty on the U.S., he points out that Cabernet Sauvignon is the standout for procyanidin content. He mentions only the Napa/Sonoma regions, unfortunately. (I'd like to know how the San Diego-Temecula and Virginian wines fare, for instance.)

The winner in procyanidin content is a variety grown in the Gers region of southwest France, a region with superior longevity of its residents. The wines here are made with the tannat grape within the Madiran appellation; wines labeled "Madiran" must contain 40% or more tannat to be so labeled (such is a quirk of French wine regulation). Among the producers Dr. Corder lists are Chateau de Sabazan, Chateau Saint-Go, Chateau du Bascou, Domaine Labranche Laffont, and Chateau d'Aydie. (A more complete list can be found in his book.)

How does this all figure into the Track Your Plaque program? Can you succeed without red wine? Of course you can. I doubt you could do it, however, without some attention to flavonoid-rich food sources, whether they come from spinach, tea, chocolate, beets, pomegranates, or red wine.

Though my wife and I love wine, I confess that I've never personally drank or even seen a French Madiran wine. Any wine afficionados with some advice?

Can wheat elimination cure ulcerative colitis?

Tammy is a 36-year old mother of three young children. Since age 20, she has suffered with the debilitating symptoms of ulcerative colitis: constant, gnawing abdominal pain; frequent diarrhea, often bloody.



Tammy has had to take several medications, some with significant side-effects, all of which provided only partial relief from the pain and diarrhea. Her gastroenterologist and surgeon were planning a colectomy (removal of the colon) with creation of an ileostomy (rerouting of the small intestine to the abdominal surface, which would require Tammy to wear an ileostomy bag under her clothes for the rest of her life).



Although Tammy had previously tested negative for celiac disease (an allergic sensitivity to the gluten in wheat products), I urged her to attempt a trial of a wheat-free diet. Having witnessed many people experience relief from irritable bowel syndrome, acid reflux, and other common gastrointestinal complaints, all while trying to reduce blood sugar and small LDL, I'd hoped that Tammy would obtain at least some small improvement in her terrible symptoms.



I therefore urged Tammy to try it. After all, what was there to lose? Tammy grudgingly agreed.



She returned 6 months later. Her report: She had lost 38 lbs, virtually all of it within the first 6-8 weeks. Her diarrhea and cramping were not better, but gone. She was down to a single medicine from her former list of drugs.



I am unsure what proportion of people with ulcerative colitis or other inflammatory bowel diseases like Crohn's will experience a result like Tammy's. Perhaps it's only a minority. But I take this another piece of evidence that this enormously destructive thing called wheat has no place in the human diet.



We have no facts or figures on the prevalence of various forms of wheat intolerance in the U.S. When I contacted the Celiac Disease Foundation, they had no figures on the number of fatalities per year in the U.S. from celiac disease. But if there are 2-3 million Americans with celiac disease, there are probably 100 times that many people with various forms of wheat intolerance.



Postprandial pile-up with fructose

Heart disease is likely caused in the after-eating, postprandial period. That's why the practice of grazing, eating many small meals throughout the day, can potentially increase heart disease risk. Eating often can lead to the phenomenon I call triglyceride and chylomicron "stacking," or the piling up of postprandial breakdown products in the blood stream.

Different fatty acid fractions generate different postprandial patterns. But so do different sugars. Fructose, in particular, is an especially potent agent that magnifies the postprandial patterns. (See Goodbye, fructose.)

Take a look at the graphs from the exhaustive University of California study by Stanhope et al, 2009:



From Stanhope KL et al, J Clin Invest 2009. Click on image to make larger.

The left graphs show the triglyceride effects of adding glucose-sweetened drinks (not sucrose) to the study participants' diets. The right graphs show the triglyceride effects of adding fructose-sweetened drinks.

Note that fructose causes enormous "stacking" of triglycerides, meaning that postprandial chylomicrons and VLDL particles are accumulating. (This study also showed a 4-fold greater increase in abdominal fat and 45% increase in small LDL particles with fructose.)

It means that low-fat salad dressings, sodas, ketchup, spaghetti sauce, and all the other foods made with high-fructose corn syrup not only make you fat, but also magnifies the severity of postprandial lipoprotein stacking, a phenomenon that leads to more atherosclerotic plaque.

Track Your Plaque: Safer at any score

Imagine two people.

Tom is a 50-year old man. Tom's initial heart scan score was 500--a concerning score that carries a 5% risk for heart attack per year.

Harry is also 50 years old. His heart scan score is 100--also a concerning score, but not to the same degree as Tom's much higher score.

Tom follows the Track Your Plaque program. He achieves the 60:60:60 lipid targets; chooses healthy foods, including elimination of wheat; takes fish oil at a therapeutic dose; increase his blood vitamin D level to 60-70 ng/ml, etc. One year later, Tom's heart scan score is 400, representing a 20% reduction from his starting score.

Harry, on the other hand, doesn't understand the implications of his score. Neither does his doctor. He's casually provided a prescription for a cholesterol drug by his doctor, a brief admonition to follow a low-fat diet, and little else. One year later, Harry's heart scan score is 200, a doubling (100% increase) of the original score.

At this point, we're left with Tom having a score of 400, Harry with a score of 200. That is, Tom has twice Harry's score, 200 points higher. Who's better off?

Tom with the score of 400 is better off. Even though he has a significantly higher score, Tom's plaque is regressing. Tom's plaque is therefore quiescent with active components being extracted, inflammation subsiding, the artery in a more relaxed state, etc.

Harry's plaque, in contrast, is active and growing: inflammatory cells are abundant and producing enzymes that degrade supportive tissue, constrictive factors are released that cause the artery to pinch partially closed, fatty materials accumulate and trigger a cascade of abnormal responses.

So it's not just the score--the quantity of atherosclerotic plaque present--but the state of activity of the plaque: Is it growing, is it being reduced? Is there escalating or subsiding inflammation? Is plaque filled with degradative enzymes or quiescent?

Following the Track Your Plaque program therefore leads us to the notion that it's not the score that's most important; the most important thing is what you're doing about it. We sometimes say that Track Your Plaque makes you safer at any score.

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.