Fish oil: The natural triglyceride form is better

2. February 2011 William Davis (43)
If you have a choice, the triglyceride form of fish oil is preferable. The triglyceride form, i.e., 3 omega-3 fatty acids on a glycerol "backbone," is the form found in the body of fish that protects them from cold temperatures (i.e., they remain liquid at low ambient temperatures).

Most fish oils on the market are the ethyl ester form. This means that the omega-3 fatty acids have been removed from the glycerol backbone; the fatty acids are then reacted with ethanol to form the ethyl ester.

If the form is not specified on your fish oil bottle, it is likely ethyl ester, since the triglyceride form is more costly to process and most manufacturers therefore boast about it. Also, prescription Lovaza--nearly 20 times more costly than the most expensive fish oil triglyceride liquid on a milligram for milligram basis--is the ethyl ester form. That's not even factoring in reduced absorption of ethyl esters compared to triglyceride forms. Remember: FDA approval is not necessarily a stamp of superiority. It just means somebody had the money and ambition to pursue FDA approval. Period.

Taking any kind of fish oil, provided it is not overly oxidized (and thereby yields a smelly fish odor), is better than taking none at all. All fish oil will reduce triglycerides, accelerate clearance of postprandial (after-eating) lipoprotein byproducts of a meal (via activation of lipoprotein lipase), enhance endothelial responsiveness, reduce small LDL particles, and provide a physical stabilizing effect on atherosclerotic plaque.

But if you desire enhanced absorption and potentially lower dose to achieve equivalent RBC omega-3 levels, then triglyceride forms are better.

Here are cut-and-pasted abstracts of two of the studies comparing forms of fish oil.

Bioavailability of marine n-3 fatty acid formulations.

Dyerberg J, Madsen P, Moller JM et al. 
Department of Human Nutrition, Faculty of Life Sciences, University of Copenhagen, Copenhagen, Denmark.

Abstract

The use of marine n-3 polyunsaturated fatty acids (n-3 PUFA) as supplements has prompted the development of concentrated formulations to overcome compliance problems. The present study compares three concentrated preparations - ethyl esters, free fatty acids and re-esterified triglycerides - with placebo oil in a double-blinded design, and with fish body oil and cod liver oil in single-blinded arms. Seventy-two volunteers were given approximately 3.3g of eicosapentaenoic acid (EPA) plus docosahexaenoic acid (DHA) daily for 2 weeks. Increases in absolute amounts of EPA and DHA in fasting serum triglycerides, cholesterol esters and phospholipids were examined. Bioavailability of EPA+DHA from re-esterified triglycerides was superior (124%) compared with natural fish oil, whereas the bioavailability from ethyl esters was inferior (73%). Free fatty acid bioavailability (91%) did not differ significantly from natural triglycerides. The stereochemistry of fatty acid in acylglycerols did not influence the bioavailability of EPA and DHA.
(Full text of the Dyerberg et al study made available at the Nordic Naturals website here.)



Eur J Clin Nutr 2010 Nov 10. 

Enhanced increase of omega-3 index in response to long-term n-3 fatty acid supplementation from triacylglycerides versus ethyl esters.

Neubronner J, Schuchardt JP, Kressel G et al. 
Institute of Food Science and Human Nutrition, Leibniz Universität Hannover, Am Kleinen Felde 30, Hannover, Germany.

Abstract

There is a debate currently about whether different chemical forms of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) are absorbed in an identical way. The objective of this study was to investigate the response of the omega-3 index, the percentage of EPA+DHA in red blood cell membranes, to supplementation with two different omega-3 fatty acid (n-3 FA) formulations in humans. The study was conducted as a double-blinded placebo-controlled trial. A total of 150 volunteers was randomly assigned to one of the three groups: (1) fish oil concentrate with EPA+DHA (1.01?g+0.67?g) given as reesterified triacylglycerides (rTAG group); (2) corn oil (placebo group) or (3) fish oil concentrate with EPA+DHA (1.01?g+0.67?g) given as ethyl ester (EE group). Volunteers consumed four gelatine-coated soft capsules daily over a period of six months. The omega-3 index was determined at baseline (t(0)) after three months (t(3)) and at the end of the intervention period (t(6)). The omega-3 index increased significantly in both groups treated with n-3 FAs from baseline to t(3) and t(6) (P < 0.001). The omega-3 index increased to a greater extent in the rTAG group than in the EE group (t(3): 186 versus 161% (P < 0.001); t(6): 197 versus 171% (P < 0.01)). Conclusion: A six-month supplementation of identical doses of EPA+DHA led to a faster and higher increase in the omega-3 index when consumed as triacylglycerides than when consumed as ethyl esters.

Diarrhea, asthma, arthritis--What is your wheat re-exposure syndrome?

30. January 2011 William Davis (52)
Have you experienced a wheat re-exposure syndrome?

As I recently discussed, gastrointestinal distress--cramps, gas, diarrhea--is the most common "syndrome" that results from re-exposure to wheat after a period of elimination.

Others experience asthma, sinus congestion and infections, mental "fogginess" and difficulty concentrating, or joint pains and/or overt swelling.

Still others say there is no such thing.

Let's take a poll and find out what readers say.

Marathoners, triathletes, and heart disease

30. January 2011 William Davis (0)
Curious thing: People with lipoprotein(a) gravitate towards elite levels of exercise.

I tell my lipoprotein(a) patients that, if they want to see a lot of other people with lipoprotein(a), go to a marathon or triathlon.

This effect applies more to males than to females, just as the fascination with numbers seems to be confined to men, too. That's why I've posted in past about the "prototypical" lipoprotein(a) male.

I believe this is a big part, perhaps the only, reason why there seems to be a modest increased risk for cardiovascular events despite high exercise levels in marathoners. It has nothing to do with the exercise itself; it has to do with the kind of people who choose to exercise at this level.

The best fish oil

29. January 2011 William Davis (30)
The best fish oils available are the liquid forms. Contrary to many people's expectations, the best liquid fish oils have no fishy odor or taste.

I use a lot of liquid fish oils because of the higher doses we use in the Track Your Plaque program, as well as our strategy of high-dose fish oil to reduce lipoprotein(a). Women, in particular, don't like taking the oodles of capsules required to achieve the higher doses we need. So the ladies really like the liquid forms.

The best liquid fish oils are non-fishy, highly-concentrated, and come in the better absorbed triglyceride form. Many capsules, including prescription Lovaza, are the less well-absorbed ethyl ester form. Several studies, such as this one, have now demonstrated that the naturally-occurring triglyceride form yields higher blood (RBC) levels of omega-3 fatty acids, likely due to more efficient digestion via pancreatic lipase.

While there are many good forms of fish oil and only a few bad, these are the best of the best:

Pharmax
The Pharmax Finest Pure Fish Oil with Essential Oil of Orange contains 1800 mg EPA + DHA per teaspoon. This is the preparation I've been taking.

Nordic Naturals
The Nordic Naturals lemon-flavored ProOmega Liquid contains 2752 mg EPA + DHA per teaspoon, the most concentrated of any fish oil I've seen.

(This list is not exclusive. These are just two brands I've used extensively with good results.)

These highly-concentrated, triglyceride forms are more expensive, due to their concentrated nature. 1 teaspoon Pharmax fish oil, for example, provides an equivalent quantity of omega-3 fatty acids as 6 standard fish oil capsules on a milligram for milligram basis, but more like 8 to 9 capsules when absorption efficiency is factored in. The triglyceride form is also more laborious to manufacture. On our Track Your Plaque Marketplace, our Pharmax 500 ml runs $58.95 list. (500 ml provides 100 teaspoons or 600-capsule equivalent.)

Note that, minus the protection of the capsule, liquid fish oils will oxidize if not refrigerated. So be sure to keep your liquid fish oil in the fridge.

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

28. January 2011 William Davis (22)
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

28. January 2011 William Davis (0)
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

25. January 2011 William Davis (27)
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

24. January 2011 William Davis (39)
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

22. January 2011 William Davis (17)
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

21. January 2011 William Davis (16)
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.

The Big Squeeze

20. June 2008 William Davis (5)
Some colleagues of mine brought this scary phenomenon to my attention last evening.

As insurance and Medicare reimbursement to doctors and hospitals fall (Medicare is enacting a series of substantial cuts, which will be followed by the private health insurers), you would expect the use of hospital procedures to drop. Makes sense, right? Less money paid per procedure, less incentive to do them.

Unfortunately, that's not how it's playing out in the real world. Your neighborhood interventional cardiologist or cardiothoracic surgeon is accustomed to a level of income and lifestyle. That lifestyle is now threatened by shrinking reimbursement. True to the Law of Unintended Consequences, rather than reducing use of procedures, diminishing procedural fees are prompting a good number of practitioners to do more.

In other words, if each heart catheterization pays less, why not do more of them, along with more stents, pacemakers, defibrillators, and the like? If four heart catheterizations per day pays less, why not do five to make up the difference?

Voila! Income protected. Of course, it comes at the cost of more work. But I will give one thing to my colleageus: They are a generally hard-working bunch who rarely balk at 12-16 hours days in the hospital.

How do you do more procedures? Easy. Just lower the bar on who to do a procedure on. Use more aggressive criteria for pacemaker implantation. Interpret the always-fuzzy nuclear stress tests weighed more towards abnormal. Use scare tactics: "You never know--that chest pain could be the last warning you're going to have!" Because the criteria for performing procedures is "soft" in the real world, it is easy to bend the criteria any way you want.

It's too early to measure the full impact of this unintended consequence of reduced reimbursement. But don't allow yourself to become a casualty in the reimbursement war. Remain vigilant. Recognize that, despite the fuzziness at the edges, there are still rational reasons for performing heart procedures. Always be armed with information and the right questions. Never submit unquestioningly or without satisfactory answers to your questions.

Tim Russert's heart scan score 210. . .in 1998

18. June 2008 William Davis (10)
Despite the media blathering over how Mr. Russert's tragic death from heart attack could not have been predicted, it turns out that he had undergone a heart scan several years ago.

A New York Times article, A Search for Answers in Russert’s Death, reported:

Given the great strides that have been made in preventing and treating heart disease, what explains Tim Russert’s sudden death last week at 58 from a heart attack?

The answer, at least in part, is that although doctors knew that Mr. Russert, the longtime moderator of “Meet the Press” on NBC, had coronary artery disease and were treating him for it, they did not realize how severe the disease was because he did not have chest pain or other telltale symptoms that would have justified the kind of invasive tests needed to make a definitive diagnosis. In that sense, his case was sadly typical: more than 50 percent of all men who die of coronary heart disease have no previous symptoms, the American Heart Association says.

It is not clear whether Mr. Russert’s death could have been prevented. He was doing nearly all he could to lower his risk. He took blood pressure pills and a statin drug to control his cholesterol, he worked out every day on an exercise bike, and he was trying to lose weight, his doctors said on Monday. And still it was not enough.

“What is surprising,” Dr. Newman said, “is that the severity of the anatomical findings would not be predicted from his clinical situation, the absence of symptoms and his performing at a very high level of exercise.”

Buried deeper in this article, the fact that Mr. Russert had a heart scan score of 210 in 1998 is revealed.

That bit of information is damning. Readers of The Heart Scan Blog know that heart scan scores are expected to grow at a rate of 30% per year. This would put Mr. Russert's heart scan score at 2895 in 2008. But the two doctors providing care for Mr. Russert were advising the conventional treatments: prescribing cholesterol drugs, blood pressure medication, managing blood sugar, and doing periodic stress tests.

Conventional efforts usually slow the progression of heart scan scores to 14-24% per year. Let's assume the rate of increase was only 14% per year. That would put Mr. Russert's 2008 score at 779.

A simple calculation from known information in 1998 clearly, obviously, and inarguably predicted his death. Recall that heart scan scores of 1000 or greater are associated with annual--ANNUAL--risk for heart attack and death of 20-25% if no preventive action is taken. The meager prevention efforts taken by Mr. Russert's doctors did indeed reduce risk modestly, but it did not eliminate risk.

We know that growing plaque is active plaque. Active plaque means rupture-prone plaque. Rupture prone plaque means continuing risk for heart attack and death. Heart attack and death means the approach used in Mr. Russert was a miserable failure.

While the press blathers on about how heart disease is a tragedy, as Mr. Russert's doctors squirm under the fear of criticism, the answers have been right here all alone. It sometimes takes a reminder like Mr. Russert's tragic passing to remind us that tracking plaque is a enormously useful, potentially lifesaving approach to coronary heart disease.

Who needs to go next? Matt Lauer, Oprah, Jay Leno, some other media personality? Someone close to you? Can this all happen right beneath the nose of your doctor, even your cardiologist?

I don't need to remind readers of The Heart Scan Blog that heart disease is 1) measurable, 2) trackable, 3) predictable. Mr. Russert's future was clear as long ago as 1998. Every year that passed, his future became clearer and clearer, yet his doctors fumbled miserably.



Copyright 2008 William Davis, MD

Another failure of conventional cardiac care

15. June 2008 William Davis (5)

Though Tim Russert was widely known and respected for his political commentary, he will likely be better remembered as an example of the gross shortcomings of the conventional approach to heart disease.

Let's face it:

Standard heart disease prevention efforts are a miserable failure.

A Track Your Plaque member brought this interview of Mr. Russert's doctor to my attention.

It appears that his doctor did all the correct conventional things. You know what became of it. In the eyes of the public and of any attorney, or even of my colleagues, no wrong was committed. The blame does not lie with Mr. Russert's hapless doctor. The blame lies on the system that endorses procedures, prescription medications, the blind adherence to dogma dictated by the pharmaceutical industry and FDA, along with a prevailing philosophy of preferring the management of catastrophes to preventing them. Dr. Newman's idea of a solution: Making an automatic defibrillator (AED) more widely available (!!!).

How long does this sort of idiocy have to go on? How many people have to die before the system uses the tools that are already available, tools that could have prevented this tragedy and many more like it?

If you and your doctor subscribe to the program that the unfortunate Mr. Russert was prescribed and the brainwashing, unthinking nonsense that his doctor follows, you are a fool. Shame on you. You therefore likely subscribe to the same variety of marketing BS that issues from food manufacturers about Cheerios, whole grains, and low-fat diets.

Get with the program. Sadly, Mr. Russert is not the first, he's not the last. The tragedies of conventional advice that line the pockets of drug and food manufacturers number in the millions. We're not talking about some obscure, rare disease. We're talking about the number one cause of death in both males and females nationwide.

I deeply wish this message could have reached Mr. Russert before his untimely death. We could all look forward to another Sunday morning with his usual incisive, unforgiving probing of the day's political figures.

Tribute to Tim Russert

14. June 2008 William Davis (11)
The sudden passing of news giant, Tim Russert, yesterday of sudden cardiac death struck a blow to American consciousness.

Perhaps his hard-hitting interviewing style, while making guests squirm, made him seem invincible. But, of course, none of us is invincible. We are all vulnerable to this disease.

We should not allow Mr. Russert's tragic death to occur without taking some lessons. The media have already resorted to interviewing prominent doctors for their opinion.


Douglas Zipes, M.D., former President of the American College of Cardiology,was quoted in the media:

"An automated external defibrillator (AED) could have been a life-saver. AEDs should be as common as fire extinguishers."

This is typical sleight-of-hand, medicine-is-too-complex-for-the-public-to-understand sort of rhetoric that is surely to issue from the conventionally-thinking medical people and the press. Instead, let's cut the BS and learn the real lessons from Mr. Russert's needless death.

It is virtually certain that:

--Mr. Russert ruptured an existing coronary atherosclerotic plaque, prompting rhythm instability, or ventricular fibrillation.

--Making automatic external defibrillators (AED) available might have Band-Aided the ventricular fibrillation, but it would not have stopped the heart attack that triggered it.

--Though full details of Mr. Russert's health program have not been made available, it is quite likely that he was prescribed the usual half-witted and barely effective panoply of "prevention": aspirin, statin drug, anti-hypertensive medication. Readers of The Heart Scan Blog and members of Track Your Plaque know that this conventional approach is as effective as aspirin for a fractured hip.

--It is highly unlikely that all causes of Mr. Russert's heart disease had been identified--did he have small LDL (it's certain he did, given his body habitus of generous tummy), Lp(a), low HDL, pre-diabetic patterns, inflammatory abnormalities, vitamin D deficiency, etc.? You can be sure little or none of this had been addressed. Was he even taking simple fish oil that reduces the likelihood of sudden cardiac death by 45%?

--Far more could have been done to have prevented Mr. Russert's needless death. And I don't mean the idiocy of making AED's available in office buildings. I'm talking about preventing the rupture of atherosclerotic plaque in the first place.

Far more can be done to prevent future similar deaths among all of us.

Our jobs are to use the tragic death of Mr. Russert to help those around us learn that heart disease is identifiable and preventable. Though Mr. Russert did not stand for BS in his political commentary, he sadly probably received it in his health advice. Don't let this happen to you or those around you.

Why do skinny people get heart disease?

13. June 2008 William Davis (9)
There's no doubt about it: The majority of people with heart disease are overweight. They may not be grotesquely overweight, just a few pounds over. But weight plays a crucial role in activating numerous factors that heighten risk for heart disease.

Excess weight reduces HDL cholesterol, raises triglycerides, increases small LDL (enormously), fans the fires of inflammatory responses (CRP, IL-6, TNF-alpha, etc.) raises blood pressure, increases resistance to insulin and raises blood sugar. Overweight people tend to be less physically active, may develop diseases of obesity like sleep apnea, and on and on. You've heard this all before.

But why do slender people develop heart disease? If we can't blame weight, what is to blame? By slender, I mean body mass index (BMI) of <25. (Yes, I know there are other ways, better ways, to gauge healthy weight. But, for simplicity, I'll use BMI.) Let's put aside the two obvious causes of heart disease, cigarette smoking and Type I diabetes. (I'd be shocked if any cigarette smokers read this blog.)

Slender people develop heart disease because:

1) They have lipoprotein(a)--The big, big neglected risk factor. In fact, the Lp(a) genotype is, in my casual observation, associated with a slender phenotype (genotypic expression). The prototypical example that makes headlines is the marathon runner--slender and superbly fit, but develops heart disease anyway. People wax on about the uncertainties of exercise and fitness when they hear about Jim Fixx and Alberto Salazar. But one factor would explain it all: Lp(a).

2) The murky category of the normal weight obesity. These people are generally recognizable by their flaccid tummies despite falling into a favorable BMI <25. Small LDL is the standout red flag in these people.

3) They were previously overweight but lost it.

4) They were former smokers.

5) Vitamin D deficiency--Deficiency of vitamin D is important for everyone's health. But there appears to be some people for whom it is the dominant risk. I believe that one of our great Track Your Plaque success stories, Neal, falls into this group. Some people who are vitamin D deficient develop colon cancer, others develop diabetes, others develop osteoporosis or multiple sclerosis, while others develop coronary heart disease and plaque. The likely reason for the varied expression is variation in vitamin D receptor genotypes (VDR genotypes).

6) The murkiest of all: Hypertension genotypic variants. This is a poorly sorted-out category, and one principally based on my observations along with scattered observations in such things as variations in the angiotensin converting enzyme genotypes. But I am convinced that there is a small percentage of slender people who show variation in some genetic type that predisposes to hypertension and heart disease. They also show a propensity towards enlargement of the thoracic aorta. This group is also among the most difficult to control in the Track Your Plaque approach, i.e., they have difficulty slowing or stopping the growth of heart scan scores. While blood pressure control in this group is important, it does not seem to remove the excess source of risk.

So, yes, being slender does put you into a lower risk for heart disease category. But it does not mean you are immune.

You can also be an overweight person who still harbors some of the features of the slender--you're an overweight slender person. The above list can still therefore apply.

Cardiology Confidential

11. June 2008 William Davis (9)

Okay, so it's a shameless knockoff of chef Anthony Bourdain's titillating Kitchen Confidential.

But the confidences that I've heard whispered in the corridors of health involve something more provocative than how your food was prepared. Any service for humans performed by other humans is subject to the idiosyncrasies and weaknesses of human behavior. That's just life.

In healthcare for your heart, the consequences can be more profound than eating three day old fish on Monday's dinner menu.

Over my 15 years practicing cardiology in a variety of settings in three different cities, I've witnessed just about everything from shocking to sublime. Some of it speaks to the extraordinary commitment of people in healthcare, the unexpected courage people show in the midst of illness, the devotion of family in difficult times. It can also speak of mewling, sobbing carryings-on over the most minor conditions, the meanness that emerges when people are frightened, the vultures circling just waiting for Grandpa to kick the bucket and leave his will declaring the spoils.

For the most part, my cardiology colleagues are a hard-working bunch committed to . . . Uh oh. I was going to say "Saving lives, preserving health." But that's not true. Once upon a time, it was true for many of my colleagues, often revealed over $2-a-pitcher beer-softened, "we're going to save people" conversations in medical school. Ahhh, medical school. I remember walking along the street alongside my medical school in St. Louis, bursting with pride and a sense of purpose.

But, for many of us, something sours our purpose through the years. Maybe it's the smell of money, maybe it's the series of distasteful experiences that show that healthcare providers are, in the midst of health crises, the innocent recipients of anger, frustration, disappointment.

Whatever the genesis, the stage is set for an imperfect scenario that pits healthcare provider against patient in a less-than-perfect system.

This would read as a mindless rant if it wasn't based on such pervasive and pravalent truths, tales of the flawed deliverers of healthcare driven by motives less lofty than "saving people."

Take Dr. S, a doctor who performs a large number of procedures on patients. I'm told he is very capable. He manages an extraordinary amount of heart work--in between jail time for wife beating and Medicare fraud.

Or Dr. C, well-known in the region for his procedural talents, also. Usually acerbic and freely-swearing, he opens up engagingly when drinking--which is most of the time. Paradoxically, as is true for some serious drinkers, he works more effectively while intoxicated.

Or Dr. ST, who proudly admitted to me one evening over dinner that he has accepted 6-figure payments from medical device companies on a number of occasions to use their products.

Or the manic ups and downs of Dr. J, who refers just about every patient he sees for emergency bypass surgery when in his down phase, mangles coronary arteries in daring angioplasties during his up phase.

How about 310-lb Dr. P, who hounds her patients about indulgent lifestyles? That would be excusable as innocent lack of self-insight if it weren't for her propensity to use heart procedures on patients as punishment. "I have no choice but to take you to the hospital."

Dr. M. manages to maintain the appearance of straight-and-narrow during the day, all the way to attending church twice a week with his children. His daytime persona effectively covers up his frequent visits to prostitutes.


We are ALL flawed. My colleagues are no different. But some circumstances cultivate the flaws, fertilize corruptibility, reward it. Such has become the state of affairs in healthcare for heart disease. Why? Is it the excessive potential for money-making that existed until recently? Is there something about the save-the-day mentality of heart disease that attracts imperfect personalities looking for the adrenaline-charged thrill but morphs over time into near-psychopathic lives?

It's not the end of the world. The fact that my colleagues' behavior has reached such extravagant lows signals a bottom: things are about to change.

In the meantime, let me tell you a few more secrets . . .



Copyright 2008 William Davis, MD

Fanatic Cook on the American Heart Association

8. June 2008 William Davis (7)
The Fanatic Cook has posted a stinging criticism of the American Heart Association (AHA):

American Heart Association My Fat Translator

Beyond the nonsensical nutritional recommendations (e.g., substitute small French fries for large French fries), she lists the major financial contributors to the AHA, a Who's Who in the pharmaceutical and processed food industry.


"For an organization that brought in close to a billion dollars last year, you'd think they could come up with something a little more pronounced. If I was more cynical I'd say the AHA had an interest in keeping Americans fat . . . or at least dependent on a highly-processed, fast food diet, requiring drugs to tweak lab values."

To be sure, the AHA does a great deal of good in funding research and educating the public about the prevalence of heart and vascular disease. But their fund raising interests have clearly subverted the honesty of their nutritional advice. Sadly, it is the AHA dietary advice that hospital dietitians use in counseling people with heart disease after their heart attack, stent, or bypass surgery. After my patients are discharged from the hospital for any reason, I tell them to please forget everything the nice hospital dietitian told them. It is not okay to eat the factory farm-raised hamburger on the sugar-equivalent enriched flour bun. Low-fat ice cream is not a healthy substitute for full-fat ice cream.

The AHA is no different than the USDA and the American Diabetes Association, "official" organizations that have, in effect, sold out to industry.

Sleep for heart health

8. June 2008 William Davis (4)
Sleep is a fascinating phenomenon.

Virtually all animals, certainly all mammals, sleep. While the form and shape of sleep can vary, sleeping is a universal phenomenon. Even fish sleep, though their eyes remain open.

Sleep disorders like sleep apnea ("apnea" = without breathing) are growing in prevalence nationwide as the country gets fatter and fatter. Our throats assume a smaller diameter, even our tongues get obese. This results in intermittent obstruction to the airway during sleep, causing snoring. It also results in sleep interruption, particularly during attempts to "descend" down to the deepest phases of sleep. Dire health and cardiac consequences can sometimes emerge, such as high blood pressure, higher blood sugar, abnormal heart rhythms, impaired heart muscle function, even sudden death.

We are all familiar with the perceptible effects of sleep deprivation: edginess, crabbiness, diminished attention span, slowed reaction time. I'm not talking about sleep apnea or sleep disorders, but just simple duration of sleep. Data are emerging that both sleep deprivation and sleep excess may trigger undesirable changes in lipids (cholesterol values):



Associations of usual sleep duration with serum lipid and lipoprotein levels.

Kaneita Y, Uchiyama M et al.

STUDY OBJECTIVES: We examined the individual association between sleep duration and a high serum triglyceride, low HDL cholesterol, or high LDL cholesterol level. DESIGN AND SETTING: The present study analyzed data from the National Health and Nutrition Survey that was conducted in November 2003 by the Japanese Ministry of Health, Labour and Welfare. This survey was conducted on residents in the districts selected randomly from all over Japan. PARTICIPANTS: The subjects included in the statistical analysis were 1,666 men and 2,329 women aged 20 years or older. INTERVENTION: N/A. MEASUREMENTS AND RESULTS: Among women, both short and long sleep durations are associated with a high serum triglyceride level or a low HDL cholesterol level. Compared with women sleeping 6 to 7 h, the relative risk of a high triglyceride level among women sleeping <5 h was 1.51 (95% CI, 0.96-2.35), and among women sleeping > or =8 h was 1.45 (95% CI, 1.00-2.11); the relative risk of a low HDL cholesterol level among women sleeping <5 h was 5.85 (95% CI, 2.29-14.94), and among women sleeping > or =8 h was 4.27 (95% CI, 1.88-9.72). On the other hand, it was observed that the risk of a high LDL cholesterol level was lower among men sleeping > or =8 h. These analyses were adjusted for the following items: age, blood pressure, body mass index, plasma glucose level, smoking habit, alcohol consumption, dietary habits, psychological stress, and taking cholesterol-lowering medications. CONCLUSIONS: Usual sleep duration is closely associated with serum lipid and lipoprotein levels.

Triglycerides go up with too little or too much sleep. Note especially the extraordinary association of low HDL cholesterol with sleeping <5 hours (nearly 6-fold increased risk) or sleeping >8 hours (more than 4-fold increased risk).

Why do these effects develop? Does sleep deprivation, for instance, trigger higher adrenaline levels, encourage carbohydrate cravings or binges, make us less likely to engage in physical activity? Cortisol is elevated; could this be a factor? I know that I am a different person when sleep-deprived: irritable, less clear-thinking, quicker to anger, more critical, and I develop carbohydrate cravings. It's curious that triglycerides increase when sleep excess is present; what might that represent?

Anyway, the data are growing: Sleep is an important facet of health, both for maintaining a bright outlook and to discourage development of low HDL and high triglycerides. Though not specifically examined in this study, we know that low HDL/high triglycerides are, as a rule, associated with the undesirable small LDL particle pattern.

As a practical matter, you may also find sleep and waking from sleep more satisfying and restful if you sleep in increments of 90 minutes, e.g., 7 1/2 hours (rather than 7 or 8 hours). This is because the full cycle of sleep, from phase 1 to REM (rapid-eye movement sleep), requires 90 minutes for completion. That doped feeling that sometimes develops when awaking will disappear if you sleep according to your sleep cycle, which is usually 90 minutes long.

Is normal TSH too high?

4. June 2008 William Davis (30)
There's no doubt that low thyroid function results in fatigue, weight gain, hair loss, along with rises in LDL cholesterol and other fractions of lipids. It can also result in increasing Lp(a), diabetes, and accelerated heart disease, even heart failure.

But how do we distinguish "normal" thryoid function from "low" thyroid function? This has proven a surprisingly knotty question that has generated a great deal of controversy.

Thyroid stimulating hormone, or TSH, is now the most commonly used index of the adequacy of thyroid gland function, having replaced a number of older measures. TSH is a pituitary gland hormone that goes up when the pituitary senses insufficient thyroid hormone, and a compensatory increase of thyroid hormone is triggered; if the pituitary senses adequate or excessive thyroid hormone, it is triggered to decrease release of TSH. Thus, TSH participates in a so-called "negative feedback loop:" If the thyroid is active, pituitary TSH is suppressed; if thyroid activity is low, pituitary TSH increases.

An active source of debate over the past 10 years has been what a normal TSH level is. In clinical practice, a TSH in the range of 0.4-5.0 mIU/L is considered normal. (Lower TSH is hyperthyroidism, or overactive thyroid; high TSH is hypothyroidism, or underactive thyroid.)

The data from a very fascinating and substantial observation called the HUNT Study, however, is likely to change these commonly-held thyroid "rules."

The association between TSH within the reference range and serum lipid concentrations in a population-based study. The HUNT Study

In this study, over 30,000 Norwegians without known thyroid disease were enrolled. TSH levels and lipid (cholesterol) levels were measured.

In this large and extraordinary observation, increasing TSH levels were associated with increasing levels of LDL cholesterol and triglycerides, and decreasing HDL. At what level of TSH did this relationship start? At TSH levels as low as 1.0!

In other words, there were perturbations in standard lipid measures even with TSH levels ordinarily regarded as "normal," even "perfect."

A subsequent observation from the HUNT Study was even more recently published:

Thyrotropin Levels and Risk of Fatal Coronary Heart Disease: The HUNT Study

Abstract:

Background Recent studies suggest that relatively low thyroid function within the clinical reference range is positively associated with risk factors for coronary heart disease (CHD), but the association with CHD mortality is not resolved.

Methods In a Norwegian population-based cohort study, we prospectively studied the association between thyrotropin levels and fatal CHD in 17 311 women and 8002 men without known thyroid or cardiovascular disease or diabetes mellitus at baseline.

Results During median follow-up of 8.3 years, 228 women and 182 men died of CHD. Of these, 192 women and 164 men had thyrotropin levels within the clinical reference range of 0.50 to 3.5 mIU/L. Overall, thyrotropin levels within the reference range were positively associated with CHD mortality (P for trend = .01); the trend was statistically significant in women (P for trend = .005) but not in men. Compared with women in the lower part of the reference range (thyrotropin level, 0.50-1.4 mIU/L), the hazard ratios for coronary death were 1.41 (95% confidence interval [CI], 1.02-1.96) and 1.69 (95% CI, 1.14-2.52) for women in the intermediate (thyrotropin level, 1.5-2.4 mIU/L) and higher (thyrotropin level, 2.5-3.5 mIU/L) categories, respectively.

Conclusions Thyrotropin levels within the reference range were positively and linearly associated with CHD mortality in women. The results indicate that relatively low but clinically normal thyroid function may increase the risk of fatal CHD.


In other words, the findings of this substantial observation suggest that the ranges of TSH usually regarded as normal contribute to coronary events, cardiac death, as well as lipid patterns. While several other studies have likewise shown a relationship of higher TSH/lower thyroid function with lipid abnormalities and overt heart disease, no previous study has plumbed the depth of TSH to this low level and to such a large scale.

I believe that these findings are enough cause to begin thinking seriously about monitoring thyroid function more seriously to uncover "borderline" TSH increases in the "normal" range. While higher TSH levels predict cardiovascular events, does thyroid replacement at these levels reduce it? Critics will say it's a big leap, but I think that it is worth at least considering.

Stay tuned for a lengthy Special Report followed by a full booklet on these issues on the www.cureality.com website.


Copyright 2008 Wiliam Davis, MD

Talking heads

4. June 2008 William Davis (0)
Tne Philadelphia NBC affiliate's website carried this commentary from a colleague of mine:


Mark from the Lehigh Valley is curious about scans that can detect heart disease.

He asked, "I am in my early 50s. My father had a heart attack in his 40s. I am healthy with no symptoms of heart disease, should I consider a heart scan?"

"Well, Mark, occasionally family history needs to be considered more closely. If your father had coronary disease at a relatively young age at the absence of any known risk factor for heart disease for example diabetes, smoking, obesity, high blood pressure, than your level of risk should be considered more closely," Dr. Kevin Shinal, a cardiologist, said.

"There are a number of studies available to access [sic] your level of risk. One such study is a calcium score. A calcium score is a form of a CAT scan that access [sic] the calcium burden or presence of calcium in your coronary arteries. It assigns you a score and score is translated into a level of cardiovascular risk," Shinal said.

But the doctor warned because Mark doesn't have active symptoms, the scan probably wouldn't be covered by insurance.


Was there an understandable answer in there? I certainly couldn't find it.

Why pick on some yokel responding inarticulately to the local media's quest for content? Because this is, all too often, what the public hears: Ill-informed blather from someone who has little or no understanding of the issues. Maybe this doctor wanted his practice group to get some free publicity. "Doctor, could you just answer a few questions from viewers?"

Unfortunately, it's not just local media who are guilty of consulting with know-nothings with only passing knowledge of an issue. National media are guilty of it, too. The need to fill airtime with content is better filled with talking heads who present a compelling story, whether or not it is accurate or insightful, rather than an expert with deep insight into a topic who might not present as pretty a story. I've seen this countless times. A good portion of my day, in fact, is occupied responding to patient questions based on the misinformation presented in some media report.

My message of this brief rant: Be very careful of the messages delivered by the media, even if provided by some supposed "expert." In fact, I regard "experts" in health about as believable as politicians. Sure, sometimes they provide accurate information. But they often do not, or provide information with limited understanding. Or, worse, information intended to serve some hidden agenda.

Were the media to ask me to respond to the question, however, I would say:

"Yes, you should absolutely have a heart scan--yesterday! With your family history, there is no other way to accurately, easily, and inexpensively quantify the amount of coronary atherosclerosis in your heart's arteries. A stress test only uncovers advanced disease. A heart catheterization is overkill and absolutely not indicated in an asymptomatic man. Judging the presence of heart disease from cholesterol values is folly.

"What's left? A CT heart scan. So, yes, you need a CT heart scan ASAP with no doubt whatsoever."

But they didn't ask.

Green coffee bean extract in AGF Factor I

7. June 2012 William Davis (16)
Track Your Plaque's new and proprietary formulation, AGF Factor I, is designed to to support a program to achieve low levels of endogenous glycation.

Endogenous glycation, discussed at length in a recent Track Your Plaque Special Report, makes LDL particles (especially small LDL particles) more prone to oxidation and thereby more atherogenic, i.e., more likely to contribute to atherosclerotic plaque. Endogenous glycation also exerts unhealthy effects on long-lived proteins in the body, such as the proteins in the lenses of your eyes (cataracts), the lining of arteries (hypertension), and the cartilage cells of joints (brittle cartilage and arthritis).

Endogenous glycation is reduced by slashing carbohydrates in the diet, especially the most offensive carbohydrates of all, the amylopectin A of wheat, sucrose, high-fructose corn syrup and other fructose sources. Endogenous glycation can also be blocked by using blockers of the glycation reaction, such as benfotiamine (lipid-soluble thiamine), pyridoxal-5'-phosphate (a form of vitamin B6 with greater glycation blocking effect), and chlorogenic acid from green coffee beans, all components of AGF Factor I, which also contains Portulaca oleracea (Portusana), or purslane, for reduction of glucose.

Green coffee bean extract, and thereby chlorogenic acid, is receiving increased attention, most recently due to a study demonstrating substantial weight loss with 750-1050 mg green coffee bean extract, providing approximately 325-500 mg chlorogenic acid per day. Participants lost 15.4 pounds over 8 weeks at the higher dose (500 mg chlorogenic acid per day), while participants lost 8.8 pounds over 8 weeks at the lower dose (325 mg chlorogenic acid per day).

AGF Factor I was not formulated for weight loss but, taken twice or three times per day, does indeed mimic the dose of chlorogenic acid from green coffee bean extract used in the weight loss study. If you wish to take advantage of this application of chlorogenic acid/green coffee bean extract, while also maximizing protection from endogenous glycation, our AGF Factor I is one excellent choice to do so.

Lessons learned from the 2012 Low-carb Cruise

14. May 2012 William Davis (13)
I just returned from Jimmy Moore's Low-carb Cruise, a 7-day excursion to Jamaica, Grand Cayman Island, and Cozumel aboard the Carnival Magic. During our 7 wonderful days, a number of authors and experts spoke, each offering their unique perspective on the low-carb world. The focus was the science, experience, and practical application of low-carbohydrate diets.

The event kicked off with a roast by Tom Naughton of Fat Head fame, who entertained with his insightful low-carb humor and predictions of my demise at the hands of Monsanto!

Among the most important lessons provided:

Dr. Andreas Eenfeldt of the Diet Doctor blog discussed how Sweden is leading the world as the nation with the most vigorous low-carbohydrate following, witnessing incredible weight loss and reversal of carbohydrate-related diseases way ahead of the U.S. experience. I spent several hours with Dr. Eenfeldt who, besides being an engaging speaker, is a new father and an all-around gentleman. At 6 ft, 7 inches, he also towered high above all of us.

Dr. Eric Westman of Duke University and author of The New Atkins for a New You, debunked low-carbohydrate myths, such as "low-carb diets are high-protein diets that make your kidneys explode."

Dr. John Briffa, creator of the popular blog, Dr. John Briffa: A Good Look at Good Health, and author of the wonderfully straightforward primer to low-carbohydrate eating, Escape the Diet Trap, stressed the importance of never allowing hunger to rule behavior. Dr. Briffa's serious writing tone conceals an incredible charm and wit that took me by surprise, having spent several thoroughly engaging hours over breakfast, lunch, and dinner with him over the week.

Fred Hahn, exercise expert, founder of Serious Strength and author of Slow Burn Fitness Revolution and Strong Kids, Healthy Kids, debunked a number of trendy exercise methods, boiling many of the purported benefits of exercise down to that of increased strength.

Dr. Chris Masterjohn of The Daily Lipid and supporter of the Weston A. Price Foundation program, provided a comprehensive overview of the data that fails to link saturated fat with heart disease. He also helped me understand the analytical techniques used in studies of advanced glycation end-products.

Denise Minger, brilliant young usurper of China Study dogma and blogger at Raw Foods SOS, proved an engaging speaker and a truly real person (since some critics of her analyses have actually questioned whether there was even such a person!). She also proved every bit as likable as she seems in her captivating blog discussions.

Dr. Jeff Volek, prolific researcher from University of Connecticut, author of over 200 studies validating low-carbohydrate diet effects, and author of the recently released book with Dr. Stephen Phinney, The Art and Science of Low Carbohydrate Living, debunked myths behind carbohydrate dependence and "loading" by athletes. He also talked about how assessing blood ketones may be the gold standard method to ensure low-grade ketosis on a long-term low-carb effort.

Over a bottle of wine, Jimmy Moore and I reminisced over how his modest start with no experience in blogging or media has now ballooned to an audience of over 100,000 readers/viewers.

All in all, Jimmy's Low-carb Cruise experience was worth every minute, with many wonderful lessons and memories!

Chili Sesame Crackers

3. May 2012 William Davis (0)
Looking for something hot and crunchy?

These chili sesame crackers are perfect for dipping into hummus or salsa. As written, the recipe yields a moderately spicy cracker that you can modify readily by increasing or decreasing quantities of cayenne pepper and Tabasco sauce.

This recipe uses sesame seeds as the "flour." Either brown sesame seeds or the lighter version work, though the lighter seeds yield a slightly less bitter flavor with the spices.

For ease of baking, a shallow baking pan measuring 11 x 17 inches works best, as it allows the batter to fill the pan and spread to a cracker thickness. With a smaller pan, you may have to bake in two batches.

Makes approximately 30 chips

2 cups raw sesame seeds
1 cup shredded Parmesan cheese
2 tablespoons extra-virgin olive oil
1 tablespoon chili powder
½ teaspoon cayenne pepper
2 teaspoons onion powder
1 teaspoon garlic powder
1 teaspoon dry mustard
1 teaspoon sea salt
1 teaspoon Tabasco sauce
1¼ cups water

Preheat oven to 350º F.

In food chopper or food processor, grind 1¼ cups sesame seeds to fine meal. Remove and place in large bowl.

Place shredded Parmesan cheese in food chopper or food processor and pulse briefly until reduced to granular consistency. Add to sesame seed meal and mix. Stir in olive oil.

Add remaining (unground) sesame seeds, chili powder, cayenne pepper, onion and garlic powder, mustard, sea salt and mix thoroughly. Add Tabasco sauce and water and mix. Add additional water, if necessary, one tablespoon at a time, to obtain a consistency similar to pancake batter.

Pour mixture into baking pan and smooth to fill pan and obtain a thickness of a cracker. If too thick, remove some batter and re-smooth. Optionally, roll a clean cylindrical glass or bottle over top to smooth and yield a consistent thickness.

Bake for 30 minutes or until edges browned and center firm. If a dry, extra crunchy cracker is designed, bake an additional 10-15 minutes at 250 degrees F.

Remove and allow to cool. Cut with pizza cutter to desired size.

Opiate of the masses

18. April 2012 William Davis (22)
Although it is a central premise of the whole Wheat Belly argument and the starting strategy in the New Track Your Plaque Diet, I fear that some people haven't fully gotten the message:

Modern wheat is an opiate.

And, of course, I don't mean that wheat is an opiate in the sense that you like it so much that you feel you are addicted. Wheat is truly addictive.

Wheat is addictive in the sense that it comes to dominate thoughts and behaviors. Wheat is addictive in the sense that, if you don't have any for several hours, you start to get nervous, foggy, tremulous, and start desperately seeking out another "hit" of crackers, bagels, or bread, even if it's the few stale 3-month old crackers at the bottom of the box. Wheat is addictive in the sense that there is a distinct withdrawal syndrome characterized by overwhelming fatigue, mental "fog," inability to exercise, even depression that lasts several days, occasionally several weeks. Wheat is addictive in the sense that the withdrawal process can be provoked by administering an opiate-blocking drug such as naloxone or naltrexone.

But the "high" of wheat is not like the high of heroine, morphine, or Oxycontin. This opiate, while it binds to the opiate receptors of the brain, doesn't make us high. It makes us hungry.

This is the effect exerted by gliadin, the protein in wheat that was inadvertently altered by geneticists in the 1970s during efforts to increase yield. Just a few shifts in amino acids and gliadin in modern high-yield, semi-dwarf wheat became a potent appetite stimulant.

Wheat stimulates appetite. Wheat stimulates calorie consumption: 440 more calories per day, 365 days per year, for every man, woman, and child. (440 calories per person per day is the average.) We experience this, sense the weight gain that is coming and we push our plate away, settle for smaller portions, increase exercise more and more . . . yet continue to gain, and gain, and gain. Ask your friends and neighbors who try to include more "healthy whole grains" in their diet. They exercise, eat a "well-balanced diet" . . . yet gained 10, 20, 30, 70 pounds over the past several years. Accuse your friends of drinking too much Coca Cola by the liter bottle, or being gluttonous at the all-you-can-eat buffet and you will likely receive a black eye. Many of these people are actually trying quite hard to control impulse, appetite, portion control, and weight, but are losing the battle with this appetite-stimulating opiate in wheat.

Ignorance of the gliadin effect of wheat is responsible for the idiocy that emits from the mouths of gastroenterologists like Dr. Peter Green of Columbia University who declares:

"We tell people we don't think a gluten-free diet is a very healthy diet . . . Gluten-free substitutes for food with gluten have added fat and sugar. Celiac patients often gain weight and their cholesterol levels go up. The bulk of the world is eating wheat. The bulk of people who are eating this are doing perfectly well unless they have celiac disease."

In the simple minded thinking of the gastroenterology and celiac world, if you don't have celiac disease, you should eat all the wheat you want . . . and never mind about the appetite-stimulating effects of gliadin, not to mention the intestinal disruption and leakiness generated by wheat lectins, or the high blood sugars and insulin of the amylopectin A of wheat, or the new allergies being generated by the new alpha amylases of modern wheat.

Jelly beans and ice cream

23. March 2012 William Davis (6)
What if I said: "Eliminate all wheat from your diet and replace it with all the jelly beans and ice cream you want."

That would be stupid, wouldn't it? Eliminate one rotten thing in diet--modern high-yield, semi-dwarf wheat products that stimulate appetite (via gliadin), send blood sugar through the roof (via amylopectin A), and disrupt the normal intestinal barriers to foreign substances (via the lectin, wheat germ agglutinin)--and replace it with something else that has its own set of problems, in this case sugary foods. How about a few other stupid replacements: Replace your drunken, foul-mouthed binges with wife beating? Replace cigarette smoking with excessive bourbon?

Sugary carbohydrate-rich foods like jelly beans and ice cream are not good for us because:

1) High blood sugar causes endogenous glycation, i.e, glucose modification of long-lived proteins in the body. Glycate the proteins in the lenses of your eyes, you get cataracts. Glycate cartilage proteins in the cartilage of your hips and knees, you get brittle cartilage that erodes and causes arthritis. Glycate structural proteins in your arteries and you get hypertension (stiff arteries) and atherosclerosis. Small LDL particles--the #1 cause of heart disease in the U.S. today--are both triggered by blood sugar rises and are 8-fold more prone to glycation (and thereby oxidation).

2) High blood sugar is inevitably accompanied by high blood insulin. Repetitive surges in insulin lead to <em>insulin resistance</em>, i.e., muscles, liver, and fat cells unresponsive to insulin. This forces your poor tired pancreas to produce even more insulin, which causes even more insulin resistance, and round and round in a vicious cycle. This leads to visceral fat accumulation (Jelly Bean Belly!), which is highly inflammatory, further worsening insulin resistance via various inflammatory mediators like tumor necrosis factor.

3) Sugary foods, i.e., sucrose- or high-fructose corn syrup-sweetened, are sources of fructose, a truly very, very bad sugar that is metabolized via a completely separate pathway from glucose. Fructose is 10-fold more likely to induce glycation of proteins than glucose. It also provokes a (delayed) rise in insulin resistance, accumulation of triglycerides, marked increase in formation of small LDL particles, and delayed postprandial (after-eating) clearance of the lipoprotein byproducts of meals, all of which leads to diabetes, hypertension, and atherosclerosis.

I think we can all agree that replacing wheat with jelly beans and ice cream is not a good solution. And, no, we shouldn't have drunken binges, wife beating, smoking or bourbon to excess. So why does the "gluten-free" community advocate replacing wheat with products made with:

rice starch, tapioca starch, potato starch, and cornstarch?

These powdered starches are among the few foods that increase blood sugar (and thereby provoke glycation and insulin) higher than even the amylopectin A of wheat! For instance, two slices of whole wheat bread typically increase blood sugar in a slender, non-diabetic person to around 170 mg/dl. Two slices of gluten-free, multigrain bread will increase blood sugar typically to 180-190 mg/dl.

The fatal flaw in thinking surrounding gluten-free junk carbohydrates is this: If a food lacks some undesirable ingredient, then it must be good. This is the same fatally flawed thinking that led people to believe, for instance, that Snack Well low-fat cookies were healthy: because they lacked fat. Or processed foods made with hydrogenated oils were healthy because they lacked saturated fat.

So gluten-free foods made with junk carbohydrates are good because they lack gluten? No. Gluten-free foods made with rice starch, tapioca starch, potato starch, and cornstarch are destructive foods that NOBODY should be eating.

This is why the recipes for muffins, cupcakes, cookies, etc. in this blog, the Track Your Plaque website, and the Track Your Plaque Cookbook are wheat- and gluten-free and free of gluten-free junk carbohydrates. And put that bottle of Jim Beam down!

Diet by LDL

7. March 2012 William Davis (0)
Conventional notions of heart healthy diets, such as that advocated by the American Heart Association, are largely based on observations of total and LDL cholesterol.

So, cut the saturated fat in the diet, cut the overall fat content, and replace them with polyunsaturated oils like safflower, corn, and vegetable oils and increase consumption of whole grains and total and LDL cholesterol show a modest downturn. Thus, diets like the American Heart Association Total Lifestyle Change approach advocate limiting total fat to no more 25 to 35% of calories and saturated fat to no more than 7% of calories.

Orange Cream Cookies

5. March 2012 William Davis (5)
If you loved Creamsicles as a kid, you'll love these Orange Cream Cookies. (Sorry, no photo: We ate them up before I realized we hadn't taken the photo. And, worse, we did it twice!)

Ingredients:
2 cups almond meal
2 tablespoons coconut flour
1 teaspoon baking soda
½ teaspoon sea salt
¼ cup golden raisins
½ cup chopped pecans
Sweetener equivalent to 1 cup sugar
2 tablespoons finely-grated orange rind
1 large egg
2 tablespoons coconut oil, melted
½ cup whipping cream (or coconut milk)
1 tablespoon vanilla extract

Preheat oven to 350º F.

Combine almond meal, coconut flour, baking soda, salt, raisins, pecans, sweetener and orange zest in bowl and mix.

In separate bowl, whisk egg, then add coconut oil, whipping cream, vanilla extract and mix together. Pour wet mix into dry and blend by hand thoroughly.

Spoon onto parchment paper-lined baking pan (or oiled pan) and flatten with spoon to ½-¾ inch thickness. Bake for 20-25 minutes or until toothpick withdraws dry.

Why are heart attacks still happening?

4. March 2012 William Davis (10)
I'm a cardiologist. I see patients with heart disease in the form of coronary artery disease every day.

These are people who have undergone bypass surgery, received one or more stents or undergone other forms of angioplasty, have survived heart attacks or sudden cardiac death, or have high heart scan scores. In short, I see patients every day who are at high-risk for heart attack and death from heart disease.

But I see virtually no heart attacks. And nobody is dying from heart disease. (I'm referring to the people who follow the strategies I advocate, not the guy who thinks that smoking a pack of cigarettes a day is still okay, or the woman who thinks the diet is unnecessary because she's slender.)

Two high-profile deaths from heart attacks occurred this week:

Davy Jones--The iconic singer from the 1960s pop group, the Monkees, suffered sudden cardiac death after a large heart attack, just hours after experiencing chest pain.

Andrew Breitbart--The conservative blogger and controversy-generating media personality suffered what was believed to be sudden cardiac death while walking.

It's a darn shame and it shouldn't happen. The tools to identify the potential for heart attack are available, inexpensive, and simple. The strategies to reduce, even eliminate, risk are likewise available, inexpensive, and cultivate overall health.

The followers of the Track Your Plaque program who

1) get a heart scan that yields a coronary calcium score (for long-term tracking purposes)
2) identify the causes such as small LDL particles, lipoprotein(a), vitamin D deficiency, and thyroid dysfunction
3) correct the causes

enjoy virtual elimination of risk.

My letter to the Wall Street Journal: It's NOT just about gluten

8. February 2012 William Davis (7)
The Wall Street Journal carried this report of a new proposed classification of the various forms of gluten sensitivity: New Guide to Who Really Shouldn't Eat Gluten

This represents progress. Progress in understanding of wheat-related illnesses, as well as progress in spreading the word that there is a lot more to wheat-intolerance than celiac disease. But, as I mention in the letter, it falls desperately short on several crucial issues.

Ms. Beck--

Thank you for writing the wonderful article on gluten sensitivity.

I'd like to bring several issues to your attention, as they are often neglected
in discussions of "gluten sensitivity":

1) The gliadin protein of wheat has been modified by geneticists through their
work to increase yield. This work, performed mostly in the 1970s, yielded a form
of gliadin that is several amino acids different, but increased the
appetite-stimulating properties of wheat. Modern wheat, a high-yield, semi-dwarf
strain (not the 4 1/2-foot tall "amber waves of grain" everyone thinks of) is
now, in effect, an appetite-stimulant that increases calorie intake 400 calories
per day. This form of gliadin is also the likely explanation for the surge in
behavioral struggles in children with autism and ADHD.
2) The amylopectin A of wheat is the underlying explanation for why two slices
of whole wheat bread raise blood sugar higher than 6 teaspoons of table sugar or
many candy bars. It is unique and highly digestible by the enzyme amylase.
Incredibly, the high glycemic index of whole wheat is simply ignored, despite
being listed at the top of all tables of glycemic index.
3) The lectins of wheat may underlie the increase in multiple autoimmune and
inflammatory diseases in Americans, especially rheumatoid arthritis and
inflammatory bowel diseases (ulcerative colitis, Crohn's).

In other words, if someone is not gluten-sensitive, they may still remain
sensitive to the many non-gluten aspects of modern high-yield semi-dwarf wheat,
such as appetite-stimulation and mental "fog," joint pains in the hands, leg
edema, or the many rashes and skin disorders. This represents one of the most
important examples of the widespread unintended effects of modern agricultural
genetics and agribusiness.

William Davis, MD
Author: Wheat Belly: Lose the wheat, lose the weight and find your path back to health