Heart disease reversal a big "No No"

I dare you: Ask your doctor whether coronary heart disease can be reversed.

My prediction is that the answer will be a flat "NO." Or, something like "rarely, in extraordinary cases," kind of like spontaneous cure of cancer.

There are indeed discussions that have developed over the years in the conventional scientific and medical literature about reversal of heart disease, like Dean Ornish's Lifestyle Heart Trial, the REVERSAL Trial of atorvastatin (Lipitor) and the ASTEROID Trial of rosuvastatin (Crestor). Reversal of atherosclerotic plaque in these trials tends to be small in scale and sporadic.

Of course, the medical literature is swamped with studies that have nothing to do with reversal, like what stent is best, what platelet-inhibiting intravenous drug is best, when should angioplasty or stents be used and when, do implantable defibrillators save lives, improvements in coronary bypass techniques, etc. There are tens of thousands of these studies for every study that focuses on the question of atherosclerotic plaque reversal.

The concept of reversal of heart disease has simply not gained a foothold in the lexicon nor in the thinking of practicing physicians. Heart disease is a relentlessly, unavoidably, and helplessly progressive disease in their way of thinking. Perhaps we can reduce the likelihood of cardiovascular events like heart attack and death with statin drugs and beta blockers. But reverse heart disease ? In your dreams!

We need to change this mentality. Heart disease is a reversible phenomenon. Atherosclerosis in other territories like the carotid arteries is also a reversible pheneomenon. Rather than throwing medicines and (ineffective) diets at you (like the ridiculous American Heart Association program), what if your doctor set out from the start not just to reduce events, but to purposefully reduce your heart's plaque? While it might not succeed in everyone, it would certainly change the focus dramatically.

After all, isn't this the theme followed in cancer treatment? If you had a tumor, isn't cure the goal? Would we accept an oncologist's advice to simply reduce the likelihood of death from cancer but ignore the idea of ridding yourself completely of the disease? I don't think so.

Then why accept "event reduction" as a goal in heart disease? We shouldn't have to. Heart disease reversal--elimination--should be the goal.

Demystification

Once upon a time, remember how medical information was mysterious, hospitals were places where frightening, inscrutable things happened, diseases were strange maladies that struck without reason, and obtaining information about health was like hunting for buried treasure? The full extent of many peoples' understanding of health came through relatively anemic sources like Readers' Digest. (Remember "I am Joe's Colon"?)

Compare this to what we have now. If I wanted to obtain information about ankylosing spondylitis (a rare genetic disease of the spine), a Google search yields 1.46 million citations. Not all the information, of course, is helpful or relevant, but there's certain to be a bounty of information that far exceeds what you could have uncovered 40 years ago.




Suppose you enter the search phrase "antithrombin III" into your Google search. Citations: over 900,000. (The number of search citations, in fact, exceeds the number of Americans with a deficiency of this blood clotting protein!)

The same is true with heart disease. There was a time, not more than 30-40 years ago, when information about the heart and heart disease was hard to come by. The most you would find were superficial discussions about heart attacks, what chest pain means, descriptions of bypass surgery. Ask your doctor, you'd likely receive a brief, cursory response about how you probably shouldn't worry it.

Even during medical school in the 1980s, I remember struggling to get answers to my questions from faculty during medical school and medical training. It was as if providing too much information would eliminate the advantage superiors wielded over trainees.

The same selfish sentiment, the "I know something you don't know" mentality reminiscent of a schoolboy's "naa na na naa naa!" unfortunately persists. But it is rapidly disintegrating. Soon it will join the junk heap of medical mis-information accumulated over the years (a big pile, to be sure). The internet and, I'll admit (grudgingly), the media, have been responsible for demystifying the formerly mysterious and indecipherable world of health.

You now have, at a moment's disposal, access to an extraordinary array and breadth of health information that was inconceivable just a few years ago.

Times are changing. Doctors no longer hold the monopoly over health information. The public--YOU--are rapidly becoming the arbiters of health, the informed consumers of a soon-to-be retail product called health care, and the increasingly savvy judges of what should join the mainstream path of health. It is all part of this wave of change that I've been advocating: the emerging concept of self-empowerment in healthcare.

Added to the junk heap of health-mistakes-of-years-past will be medical protectionism over health information, heart procedures, drug industry excesses, nutritional mis-information, among others. The demystification of health information will open the floodgates of individual insight into health. It delivers control over your own health destiny straight into your own lap.

Everything has omega-3

Walking the supermarket aisles, you may have lately noticed that numerous new products are appearing sporting "omega-3s" on the label.

Some products simply contain alpha-linolenic acid, a tiny amount of which is converted to the biologically active omega-3s, EPA and DHA. Natural Ovens' Brainy Bagel, for instance, carries a claim of "620 omega-3."



I find this confusing and misleading, since people will often interpret such a claim to mean that it contains 620 of EPA and DHA, similar to two capsules of standard fish oil (1000 mg capsules). Of course, it does NOT. I find this especially troublesome when people will actually stop or reduce their fish oil, since they've been misled into thinking that products like this bread contain active omega-3 fatty acids that yield all the benefits of the "real stuff."


Other products actually contain the omega-3, DHA, though usually in small quantities. Breyer's Smart with DHA is an example, with 32 mg DHA per container.


I find products with actual DHA (from algae) a more credible claim. However, the Center for Science in the Public Interest (CSPI) has looked at the actual contents of DHA in some of these products and found some discrepancies, including amounts of DHA less than the labeled amount and claims of omega-3 wihtout specifying DHA vs. linolenic acid. (It's probably linolenic acid, if it's not specified.)

All in all, the addition of DHA to food products is a nice way to boost your intake of this healthy omega-3. However, keep in mind that these are processed, often highly processed, foods and you will likely pay a premium for the little boost. For now, stick to fish oil, the real thing.

For a brief summary of the CSPI report and a link to the Nutrition Action Newsletter, see Omega-3 Madness: Fish Oil or Snake Oil.

Are cardiologists the enemy?

I'm sitting at dinner with two colleagues. One is a cardiology colleague, another an internist who, in addition to practicing general internal medicine, also takes heart disease prevention very seriously. He has, in fact, participated in the Track Your Plaque program and dropped his heart scan score substantially.

"Why don't we see you in the cath lab much?" my cardiology colleague asked me. He was puzzled, since he knew my background in cath lab work from years before, spending day and night doing procedure after procedure. He spends virtually all his days there.

"Well, my patients simply don't have events any more. Heart attacks and angina among people in my program are just about non-existent. They don't have symptoms and they don't have to go to the hospital. I can't remember the last time that I was woken up in the middle of the night for an urgent procedure for one of my patients."

The internist across the table smiled and expressed his agreement. "That's the same thing I'm seeing: No heart attacks, very few if any referrals to cardiologists for procedures. I remember when it was a several times a week thing. Now, almost never. "

Looking at my cardiology colleague, I saw the usual cardiologist reaction: Eyes searching left and right and behind us for something more interesting. Certainly, talking about a virtual cure for coronary heart disease was just too damn dull.

Such is the attitude of 98% of my colleagues: If it doesn't generate a revenue-producing procedure, why bother? Prevention is for general practitioners, the line of thinking goes. "And anyway, I'm too busy doing procedures! I don't ahve time to talk about prevention and health!" Of course, the poor general practitioner is already overloaded with caring for arthritis, flu, diabetes and all the new drugs for diabetes, headaches, vaccinations, diarrhea, and . . .oh, yes, heart disease prevention.

Are cardiologists the enemy? No, of course they are are not. But they often act like they are. Talking to cardiologists is like going to the car dealer with your checkbook out, pen in hand. The salesman gets to write the check himself and you just sign it. Talk to a cardiologist and more often than not you will end up with a heart procedure--whether or not you need it.

Unfortunately--tragically--they often forget what they are supposed to be doing: Taking care of a disease by preventing it. Putting in a defibrillator is not preventing a disease. Putting in three stents, laser angioplasty, and thrombectomy are not ways of preventing a disease.

I'm thankful for my internist friend who sees the light. Coronary heart disease is a an easily measurable, quantifiable, preventable, and REVERSIBLE process for many, if not most, people when provided the right tools. But don't ask your neighborhood cardiologists to give you those tools.

Are CETP inhibitors kaput?

Was torcetrapib’s crash and burn fatal for this class of drug?

At the 2007 American Heart Association meetings in Orlando, Florida, Dr. Philip Barter of Sydney, Australia, presented an update of the ILLUMINATE drug trial for the once-promising drug, torcetrapib, the billion-dollar bet that Pfizer made on its first entry into the new drug class.

You may recall that the crash and burn of Pfizer’s torcetrapib in December 2006 made headlines and prompted enormous disappointment for many patients and doctors who had hoped for a new drug choice to raise HDL cholesterol. Pfizer executives (heads flew!) and investors were also disappointed, anticipating release of a drug that might have become the number one biggest selling drug in the world—ever, surpassing even Lipitor's® $13 billion annual sales.

Torcetrapib is the first among the “cholesteryl-ester transfer protein inhibitors,” or CETP-inhibitors, drugs that block the exchange of cholesterol and triglycerides between HDL and VLDL particles and prevent formation of the unwanted small LDL particles. Preliminary efforts suggested that effects were positively enormous.

However, the 15,000-participant trial was abruptly terminated after 550 days when an excess of deaths were identified among the group taking the experimental drug: 59 deaths in control group; 93 deaths in the torcetrapib group.

In addition, cardiovascular events were 24% greater in the torcetrapib group, numbering 373 compared to 464 in the no-torcetrapib group, including a substantially greater number of heart attacks and hospitalizations. Another surprise came in the way of cause of death among some of the torcetrapib patients, with an excess of deaths due to cancers (twice as many in the torcetrapib group), strokes, and infections.

Why the divergence: enormous improvements in cholesterol values, yet increase in adverse effects including more heart attack? Deeper digging by the principal investigators uncovered unexpected distortions of electrolytes like sodium and potassium. They then re-analyzed blood samples from participants on both sides of the trial and discovered that participants taking torcetrapib experienced significant rise in the blood pressure hormone, aldosterone. This, they surmised, also likely accounted for the 4 mmHg average rise in blood pressure among those taking the experimental drug. (This is the same pathway blocked by blood pressure drugs like ACE inhibitors lisinopril and enalapril, ARBs like losartan.)

Simultaneously (what a coincidence!) with the torcetrapib data, investigators at competing drug manufacturer, Merck, reported encouraging data with their version of CETP inhibitor, anacetrapib. In a phase II FDA trial of 589 patients, anacetrapib reduced LDL-C levels by up to 40% and increased HDL-C up to 139%.


Spokesman Daniel Bloomfield, M.D., of Merck Research Laboratories reported that "The favorable lipid effects seen in this study with multiple doses of anacetrapib were significant, and confirm the continued evaluation of the clinical benefits of CETP inhibitors in the treatment of dyslipidemia." Quick to distinguish this drug from torcetrapib’s track record of dangerous effects on blood pressure, he added that "the decreased LDL-C concentrations, increased HDL-C concentrations and no demonstrable increase in blood pressure seen with anacetrapib are particularly encouraging results of this study."

However, the data reported only an 8 week expereince. Given the experience with torcetrapib, longer term data will obviously be required to assess safety. After Pfizer spent over $1 billion and sacrificed lives to obtain this experience, Merck will need to tread carefully.

It will clearly be many years before we have a confident answer on whether the CETP-inhibitor class of drugs will be a safe choice for correction of cholesterol abnormalities, especially low HDL. Are we helpless until then?

Though CETP inhibitors offer the potential for a one-stop opportunity to raise HDL substantially, there are still many strategies available to raise HDL.

Strategies that raise HDL and are available today include:
• Weight loss—to your ideal weight. A very effective strategy.
• Reduction in processed carbohydrates—like breads, pasta, cookies, pretzels, etc. Note that very low-fat diets reduce HDL. Often a huge effect.
• Fish oil—A small effect, more dramatic when triglycerides are high.
• Niacin—Vitamin B3, the best we have at present. Doses of 500-1500 mg per day raise HDL 20–50%; work with your doctor if you are contemplating niacin. We use this agent everyday and have had great success; good hydration is key to minimize the annoying “hot-flush” effect.
• Dark chocolate—40 grams, or about 2 inches square, a delicious way to squeeze out a little rise in HDL.
• Alcoholic beverages—Red wines are almost certainly the preferred route, rich in flavonoids.
• Exercise—HDL-raising effects vary, but can sometimes be as much as 10–20 mg.
• Other drugs—Though not commonly used for this effect, drugs like pioglitazone (for diabetes and pre-diabetes); fibrates (Tricor® or fenofibrate; Lopid® or gemfibrozil); and Pletal® or cilostazol are occasionally prescribed.
• Vitamin D—You won’t find validation of this effect in any scientific study, but our emerging experience in our heart disease reversal program is suggesting that this neglected nutrient can exert powerful HDL-raising effects. In fact, supplementing vitamin D has made my life much easier.


And, last I checked, none of these HDL-raising strategies are ever fatal.

Roto Rooter for plaque




Joe, a machinist, was frightened and frustrated.

With a heart scan score of 1644 at age 61, his eyes bulged when I advised him that, if preventive efforts weren't instituted right away, his risk for heart attack was a high as 25% per year. Joe had "passed" a stress test, thus suggesting that, while coronary plaque was present--oodles of it, in fact--coronary blood flow was normal. Thus, there would be no benefit to inserting three stents, say, or a bypass operation.


(Illustration courtesy Wikipedia)

"I don't get it, doc. Why can't you just take it out? You know, like Roto-Rooter it out? Or give me something to dissolve it!"

Of course, if there were such a thing, I'd give it to him. But, of course, there is not. It doesn't mean that there haven't been efforts in this direction over the years. Among the various attempts made to "Roto-Rooter" atherosclerotic plaque have included:

Coronary endarterectomy
This is a drastic procedure rarely performed anymore but enjoyed some popularity in the 1980s and 1990s. Coronary endarterectomy was performed during coronary bypass surgery, but few thoracic surgeons performed it. Milwaukee's Dr. Dudley Johnson was the foremost practitioner of this procedure (retired a few years ago after his own bypass operation) with a mortality in excess of 25%. A very dangerous procedure, indeed. The technical hurdle, beyond the tedium and length of time required to remove plaque that had a tendency to fragment, was blood clot formation after tissue was exposed upon plaque removal. I saw many lengthy hospital stays and deaths following this procedure.

Coronary atherectomy
This is an angioplasty-type procedure that has gone through several variations over the years.

In the early 1990s, transluminal extraction atherectomy (TEC) was a technique involving low-rpm drill bits with a suction apparatus that was used to clear soft debris, usually from large coronary arteries or, more commonly, bypass grafts. Then came direction atherectomy, in which a steel housing contained a sharp drill bit that captured atherosclerotic plaque in an aperture along the housing length and stuffed it into a nosecone, retrieved once the device was removed.

Then came high-speed rotational atherectomy in which a diamond-tipped drill bit rotated up to 200,000 rpm and essentially pulverized plaque to flow downstream and, presumably, eventually captured by the liver for disposal. Rotational atherectomy is still in use on occasion. Laser angioplasty, usually using the excimer wavelength, vaporizes plaque. I did plenty of all of these back in the early and mid-1990s.

While all atherectomy procedures sound clever, they are all plagued by the same problem: vigorous return of plaque. Remove plaque, it grows back. There are few instances today in which atherectomy is still performed.

Chelation
This involves a metal-binding, or "chelating," agent like EDTA normally used in conventional practice for lead poisoning. Usually administered IV, some have also advocated oral use. People who use chelation also tend to believe in faith healing and other practices based on faith, not science. There is an international trial that is nearing completion that should provide the final word on whether there is any role to intravenous chelation.

There are numerous other oral treatments that claim a Roto-Rooter-like effect. Nattokinase, for example--an outright, unadulterated, and unqualified scam.

Unfortunately, the helpless, ignorant, and gullible are many. When frightened by the specter of heart disease, there are plenty of people who will willingly pay for the hope provided by clever ads, fast-talking salespeople, and unscrupulous practitioners.

So, Joe, there is no Roto-Rooter for coronary atherosclerotic plaque, at least one that is safe, doesn't involve a life-threatening effort, provides results that endure beyond a few months, and truly works.

The Track Your Plaque program may not be easy. There are obvious common hurdles to adhering to these concepts: obtaining lipoprotein testing, getting intelligent interepretation of the results, persuading your doctor to measure vitamin D blood levels, battling the onslaught of prevailing food propaganda that confuses and misleads. The Track Your Plaque program also requires time, at least a year.

But it's the best program there is. Do you know of anything better?

"Beware nutritional supplements"



In our effort to expand the reach for the nationwide conversation on heart disease reversal, I'd like to welcome the newest contributor to the Track Your Plaque family, a new Member blogger, Heart Cipher.

We first came to appreciate the insights of Heart Cipher on our Member Forum. His curiousity and ability to cut through the bull--- have won over our hearts and minds. I think you will appreciate his unique perspective as someone who has experienced first hand the inadequacies of the present procedure-focused, drug-obsessed standard of medical care that dominates, yet has the intelligence and worldliness to recognize that there are better ways.

Read his post about meeting a new cardiologist for the first time and the reaction he receives when he describes the Track Your Plaque program here.

http://www.heartcipher.com/

The rules of reversal


For the last few years, most practicing physicians have followed a rough blueprint for cholesterol management provided by the Adult Treatment Panel-III “consensus” guidelines, or ATP-III, a lengthy document last released in 2001, updated in 2004.

For instance, ATP-III suggests reducing LDL cholesterol to 100 mg/dl or less for those deemed to be at high risk for future heart disease, arbitrarily defined as a risk of 20% over a 10-year period. It also suggests that a desirable triglyceride level is no more than 150 mg/dl. The ATP-III guidelines have been the topic of discussion in thousands of medical meetings, editorials, and reports. They have served as the basis for many dinners at nice restaurants, weeks in Vegas or Honolulu, many, many lunches catered by pharmaceutical representatives. For most internists, family doctors, cardiologists, and lipid clinics, ATP-III is the Bible for cholesterol management.

AT-III has also become the de facto standard that could conceivably held up as the prevailing "standard of care" in a court of law in cases of presumed negligence to treat cholesterol values. “Doctor, would you agree that the consensus guidelines issued by the National Institutes of Health and endorsed by the American Heart Association state that LDL cholesterol should be reduced to 100? You do? Then why was Mr. Jones’ LDL not addressed according to these guidelines?”

Who was on the ATP-III panel and on what scientific evidence were the guidelines based? Several problems:

1) Of the 9 physician members of the panel, 8 had ties to industry, some of them quite intimate.

2) The studies upon which the guidelines were based and figure prominently, such as the Heart Protection Study, PROVE IT, and 4S, were all funded by the pharmaceutical industry. Of course, it would be unreasonable to expect anyone other than the pharmaceutical industry to fund drug studies. But prominently neglected or understated in the guidelines are all the other insights and treatments for coronary atherosclerotic risk available that were NOT funded by industry.

Of course, there’s money to be made in reducing LDL cholesterol. Lots of it--$23 billion last year alone, in fact. Just keeping that fact in mind makes the ATP-III guidelines make far better sense.

ATP-III is really not a blueprint for heart disease prevention. It is a blueprint--by industry, for industry--on how and when to treat LDL cholesterol.


But what if ATP-III had been a map for navigating coronary plaque reversal instead? What if it were not obsessed with just reducing LDL cholesterol, but was focused on providing the corner internist, family doctor, or cardiologist a roadmap for navigating the highways and byways of reversal?

That would be interesting. Mainstream reversal. Imagine that.

Among the difficulties is that the path to reversal is not lined with deep pockets. Treat LDL and who gains? That's easy. Reverse heart disease and who gains? Beyond LDL reduction, very few (beyond you and me, of course).

That’s why the call for a new Age of Self-Empowerment in healthcare is necessary now more than ever. In my view, in the foreseeable future, we will not have an ATP-III-like blueprint for heart disease control or reversal, nor will we witness a boom of nationwide appreciation that coronary atherosclerosis is a reversible process.

It’s time to take the control back and put it in our own hands. Don't expect the American Heart Association to do it. Don't expect the pharmaceutical industry to do it. If there's anyone who's going to do it, it's YOU.

Incurable wheataholics

Greg slumped back in his chair.

"I'm sorry, doc. I feel like the world's biggest schlump!"

He was referring to the fact that he had gone wheat-free for two months--eliminated all breads, bagels, donuts, pasta, breakfast cereals, crackers, pretzels--and promptly lost 30 lbs. He felt great, discovered new levels of energy he thought he'd lost long ago.

Then some friends convinced him to have some cheeseburgers at a fast food restaurant.

"After that, it was downhill. I couldn't get enough. My wife made chile and I had to have four slices of bread with it. Then I'd have two more. I just couldn't stop."

Now, having regained the 30 lbs in the space of another two months, Greg was expressing his disgust.

And it's not the first time. Greg has struggled with his wheat-alholism for as long as I've known him. I've tried motivating him by showing him the flagrant lipoprotein patterns that his wheat habit and excess weight caused: markedly elevated LDL particle number, severe small LDL, low HDL, high triglycerides, high C-reactive protein, high blood sugar, high blood pressure. Greg has received a total of 7 stents over the past 5 years. His next stop is the operating room for a bypass if he can't bring his patterns and impulses under control.

But for some reason, Greg seems to always return to the wheat trough, gorging on breads, pretzels, cake, often in great quantities.

I'm not entirely sure what to do with someone with Greg's severe degree of wheat-aholism. I view wheat-aholism as similar to alcoholism. For some, it can be as addictive.

The only strategy that I know can work is to make a clean break and drop wheat products altogether. Just as an alcoholic cannot just satisfy him/herself with a drink or two a day, so a wheataholic can't be satified with just a couple of wheat crackers. It inevitably leads to the avalanche of wheat indulgences.

Perhaps we should form a new group: Wheataholics Anonymous. "Hi. My name is Greg and I'm a wheataholic."

The battle for asymptomatic disease

The heart disease revenue pie is shrinking. So is the "serving size" being shared by competing hospitals.

In other words, as more hospitals open heart programs, there is more competition for the same heart patient. Throw into the mix the drop in "acute" presentations of disease, probably due to the now widespread prescribing of statin drugs. When I first started cardiology practice 15 years ago, for instance, days and nights spent taking care of heart attacks coming through the emergency room was a common event. It still happens, but far less frequently. (I don't mean to suggest that the actual prevalence of coronary heart disease has decreased, just the acute, catastrophic version of it.)

Throw into this mix the results of the COURAGE Trial that has put a damper on the value of stents and angioplasty vs. "optimal" medical therapy in people with stable anginal symptoms, since there was little advantage of procedures. Though it has not stopped the practice, it has reduced the enthusiasm for procedures. Though data are hard to come by, I've heard talk of 10% or greater drops in total procedural volume over the past year.

It's not uncommon for hospitals to have overbuilt heart facilities in anticipation of continued growth of this--until recently--growth industry called heart disease. However, factors are converging that may provide a new profit opportunity for hospitals.

One such opportunity is CT coronary angiography. The usual scenario: Man or woman without symptoms is persuaded somehow--an ad, primary care physician, next door neighbor with a scary event, Dr. Mehmet Oz gushing about this sexy new technology on yet another Oprah episode--to undergo a CT coronary angiogram. A "severe" blockage is found, despite the lack of symptoms, and voila! A stent patient or bypass patient is created out of nothing! Do this repeatedly and systematically, and a hospital can regain its former high-procedural volume glory.

Heart scans, though I believe deeply in them and they are the basis for the Track Your Plaque prevention and reversal program, can also be used and abused this way. Asymptomatic person has a score 150. Concerned, they go to their physician who orders a nuclear stress test. An "inferior perfusion defect" is seen, presumably representing poor flow through the right coronary artery (but often just means that the diaphragm overlaps the heart muscle and yields this apparition, a "false positive" or misleading result). "But--wink--we've got to find out if there's a severe blockage, don't we? You don't want to end up in an early grave!"

Thus, the battle for new patients with asymptomatic disease is getting underway in earnest. The scramble for cardiologists to learn how to use CT coronary angiograms is proceeding at breakneck speed, with new training courses being offered nationwide several times and places every month. CT coronary angiography is a useful test, but it is also subject to enormous abuse. It also provides the ticket for the unscrupulous physician and the revenue-hungry hospital eager to expand its patient volume.

Many people believe that this cannot happen commonly in 2007, given scrutiny of practices, litigiousness, and the expectation of a moral sense in medicine. However, I've witnessed such incidents several times this month alone. If you need graphic proof of just how far this can go before action is taken, read Coronary, Stephen Klaidman's chilling tale of a cardiologist and cardiothoracic surgeon in small-town northern California who built an enormous heart center based on fabricated heart disease diagnoses. You'll also find their story in Shannon Brownlee's recently released Overtreated: Why Too Much Medicine Is Making Us Sicker and Poorer.





Of course, the Track Your Plaque program is meant principally for people without symptoms, also. But we are advocating that asymptomatic disease is a reason for prevention, not procedures. There's a difference.

By the way, the two practitioners who engineered the escapade detailed in these books, cardiologist Chae Hyun Moon and cardiac surgeon Fidel Realyvasquez, walked away with a monetary fine and suspension of their California medical licenses. It is likely that many people died because of their abusive practices, but the state struggled to make a sufficiently persuasive case for reasons that I still don't understand.
All posts by william-davis

Human foie gras

If you want to make foie gras, you feed ducks and geese copious quantities of grains, such as corn and wheat.

The carbohydrate-rich diet causes fat deposition in the liver via processes such as de novo lipogenesis, the conversion of carbohydrates to triglycerides. Ducks and geese are particularly good at this, since they store plentiful fats in the liver to draw from during sustained periods of not eating during annual migration.

Modern humans are trying awfully hard to create their own version of foie gras-yielding livers. While nobody is shoving a tube down our gullets, the modern lifestyle of grotesque carbohydrate overconsumption, like soft drinks, chips, pretzels, crackers, and--yes--"healthy whole grains" causes fat accumulation in the human liver.

Over the past few years, there has been an explosion of non-alcoholic fatty liver disease and non-alcoholic steatosis, two forms of liver disease that result from excess fat deposition. The situation gets so bad in some people that it progresses to cirrhosis, i.e., a hard, poorly-functioning liver that paints a very ugly health picture. The end-result is identical to that experienced by longstanding alcoholics.



While Hannibal Lecter might celebrate the proliferation of human fatty livers with a glass of claret, fatty liver disease is an entirely preventable condition. All it requires is not eating the foods that create it in the first place.

Let go of my love handles

When is fat not just fat?

When it's visceral fat. Visceral fat is the fat that infiltrates the intestinal lining, the liver, kidneys, even your heart. It's the stuff of love handles, the flabby fat that hangs over your belt, or what I call "wheat belly."

Unlike visceral fat, the fat in your thighs or bottom is metabolically quiescent. Thigh and bottom fat may prevent you from fitting into your "skinny jeans," but its mainly a passive repository for excess calories.

Visceral fat, on the other hand, is metabolically active. It produces large quantities of inflammatory signals ("cytokines"), such as various interleukins, leptin, and tumor necrosis factor, that can trigger inflammatory responses in other parts of the body. Visceral fat also oddly fails to produce the protective cytokine, adiponectin, that protects us from diabetes, cancer, and heart disease.

Visceral fat also allows free fatty acids to leave and enter fat cells, resulting in a flood of fatty acids and triglycerides (= 3 fatty acids on a glycerol "backbone") in the bloodstream. This worsens insulin responses ("insulin resistance") and contributes to fatty liver. The situation is worsened when the very powerful process of de novo lipogenesis is triggered, the liver's conversion of sugar to triglycerides.

Visceral fat is also itself inflamed. Biopsies of visceral fat show plenty of inflammatory white blood cells (macrophages) infiltrating its structure.

So what causes visceral fat? Anything that triggers abnormal increases in blood glucose, followed by insulin, will cause visceral fat to grow.

It follows logically that foods that increase blood glucose the most will thereby trigger the greatest increase in visceral fat. Eggs don't lead to visceral fat, nor do salmon, olive oil, beef, broccoli, or almonds. But wheat, cornstarch, potato starch, rice starch, tapioca starch, and sugars will all trigger glucose-insulin that leads to visceral fat accumulation.

Fructose is also an extravagant trigger of visceral fat. Fructose is found in sucrose (50% fructose), high-fructose corn syrup, agave syrup, maple syrup, and honey.

Increased visceral fat can be suggested by increased waist circumference. The inflammatory hotbed created by excess visceral fat has therefore been associated with increased likelihood of heart attack, cardiovascular mortality, diabetes, cancer, and total mortality.

So I'm not so worried that you can't squeeze your bottom into your size 8 jeans. I am worried, however, when you need to let your belt out a notch . . . or two or three.

Surviving a widow maker

Gwen came to me 5 years ago. In her late 60s, she'd been having feelings of chest pressure for the past 4 weeks with small physical efforts, such as climbing a flight of stairs or lifting her grandchildren.

She sat in my office, heaving small sobs, accompanied by her daughter.

Gwen had already undergone a heart catheterization at a hospital near home by a cardiologist who I knew to be honest and competent. She'd been told that she had a 90% stenosis ("blockage") of her proximal left anterior descending (LAD) coronary artery. He called it a "widow maker," since closure of the artery at this point can be fatal within minutes. He advised bypass surgery as soon as possible. Though a stent could be placed at this location, he felt that its proximity to the left main stem (i.e., the "trunk" that divides into the LAD and circumflex arteries) might be jeopardized by expanding a stent in this bulky plaque, what I felt was a reasonable concern.

I reviewed the images that she brought with her. Yes, indeed: a widow maker. The portion of the left ventricle (heart muscle) fed by the LAD was also impaired ("hypokinetic"), reflecting reduced flow through the artery.

I advised Gwen that her first cardiologist's advice was sound: This was a potentially dangerous and severe condition. Either a bypass or stent should be performed near-future, the less delay the better.

But Gwen and her daughter would have no talk of any more procedures. She'd come to me because she heard about the (then rudimentary) effort I'd been making at reversing coronary plaque. "I admire your commitment, Gwen, but I am concerned that there may not be sufficient time to implement a program of prevention or reversal. Prevention is very powerful, but very slow. When symptoms like yours are active, also, it can mean that we won't have full control over the plaque causing the symptoms. This risks closure of the vessel, since flow characteristics in the plaque are abnormal. I think that you should go through a stent or bypass. We can then start your prevention/reversal program once we know you're safe."

Gwen would still have none of it. I asked her to return in a few days after thinking it over. In the meantime, we drew her lipoprotein blood samples while she added fish oil, l-arginine (back then I used a lot of l-arginine for its endothelial health effects), and began the Track Your Plaque diet a la 2004. This was in addition to the aspirin, beta blocker, and statin prescribed by the first cardiologist.

Several days later, Gwen and her daughter returned, as committed as ever to not having a procedure and proceeding with our prevention/reversal efforts.

So off we went. I was nervous about Gwen's safety, but she had clearly made her mind made up. Gwen's lipoprotein analysis revealed a severe small LDL pattern along with markers for prediabetes (high insulin, high blood glucose, hypertension, along with the loose tummy of visceral fat). So I counseled her intensively in diet and added niacin.

Within 2 weeks, Gwen no longer had chest pain. Whether this was due to her efforts or to some resolution of an intraplaque phenomenon (e.g., resorption of internal plaque hemorrhage), I don't know. But her symptoms did not return.

As the program evolved, we added the new strategies along the way--vitamin D supplementation; elimination of all wheat along with other changes in diet; iodine and thyroid normalization; as well as discontinuing l-arginine after the initial two years. She also got rid of the statin drug after losing around 20 lbs on the diet.

It's now been six years with her "widow maker" and Gwen has been fine: no recurrence of her symptoms, all stress tests performed have been normal, reflecting normal blood flow in her coronary arteries.

Should ALL people with symptomatic widow makers undergo such an effort and avoid procedures? No, not yet. Prevention and reversal efforts are indeed powerful, but slow. Some people just may not have sufficient time to accomplish what Gwen did. The fact that Gwen showed evidence for reduced flow in the LAD worried me in particular. There is no question that mortality benefits for stenting or bypass of this location are not as large as previously thought (see here, for instance), but each case needs to be viewed individually, factoring in flow characteristics in the artery, appearance of "stability" or "instability" of the plaque itself, not to mention commitment of the person.

But it can be done.

Fred Hahn's Slow Burn

I just had a workout with personal trainer and fitness expert, Fred Hahn. After a workout that quickly taught me that I had a lot to learn about exercise and strength training, Fred and I had a nice low-carbohydrate dinner at a Manhattan restaurant and shared ideas.

Fred is coauthor of Slow Burn Fitness Revolution: The slow motion exercise that will change your body in 30 minutes a week, written in collaboration with the Drs. Eades, Michael and Mary Dan. Fred also blogs here.

I had heard about Fred's "slow-burn" concept in past, but made little of it. I then met Fred on Jimmy Moore's low-carb cruise this past year, where I gave a talk on how carbohydrate-reduced diets reduce small LDL particles. Fred provided a group demonstration on his slow-burn techniques. I watched the demonstration, even tried it a few times back home in the gym, but never really applied them, losing patience most of the time and just going back to my usual routine.

Well, Fred showed me today how to do his slow-burn. In a nutshell, it is the slow, methodical use of weight resistance until the muscle is exhausted. It involves slow movement--e.g., 5 seconds for a lat pulldown from top to bottom--repeated until exhaustion using a weight that allows, perhaps, 6 repetitions over a 60-second effort.

I've been strength training since I was a teenager. I've seen lots of bad training techniques, injuries, and hocum when it comes to how to use resistance training techniques. But I believe that Fred Hahn's slow-burn technique really provides something unique that I hadn't experienced before.

For one, the burn is nothing like I've felt before. Two, there appears to be nearly zero risk for injury, since the usual momentum-driven, herky-jerky motion often employed with weight machines is entirely gone. Three, if what Fred is seeing is true--enhanced visceral (abdominal) fat loss, reduced blood glucose, increased HDL, decreased LDL/total cholesterol--then there's something really interesting going on here.

I also discovered that Fred is no ordinary personal trainer. He has insights into metabolism that I found truly impressive. After all, he's been hanging around with Mike Eades, who's a pretty sharp guy. What Mike Eades is to metabolic insights is what Fred Hahn is to exercise physiology.

I'm going to take Fred's slow burn training insights home with me. I'll let you know how it goes. Some aspects I'd like to explore: Will strength, muscle mass, and blood sugar responses change?



Fred Hahn's latest book, adapting slow burn techniques for kids.

Can I stop my Coumadin?

Here I go again.

While I will try to keep this blog on topic, i.e., coronary heart disease prevention and reversal using nutritional and other natural strategies, I believe that a "critical mass" of frequently asked, though off topic, questions keep cropping up.

One such question revolves around Coumadin, or warfarin.

Somehow, my Nattokinase scam blog post draws traffic about Coumadin. I tried to make the point that a conventional blood thinning agent like Coumadin that undoubtedly has undesirable side-effects cannot be replaced by an agent that has an uncertain track record. In the case of nattokinase, no track record.

To illustrate how far wrong the "nattokinase as replacement for Coumadin" idea can go, here is a question from Anna:


I came across your blog while perusing.

I am a bit bummed because I have been on Coumadin (warfarin) for around 22 years since I was 6 years old. I have a mechanical heart valve (St. Jude's), as I have heart-related issues, including hypertrophic obstructive cardiomyopathy.

Well, it is just that the warfarin seems to interact with nearly everything. I feel like I can not get the nutrients my body requires. I desire to consume more raw foods and vegan foods, though I do not want anything to damage my heart valve or risk a stroke/heart attack or internal bleeding.

I have been underweight the majority of my life, malnourished , currently am still somewhat underweight, though enjoying food again, as I had what mimicked Crohn's Disease for several years (horrendous pain), from which I am in remission now. I was diagnosed with osteoporosis, which may or may not be caused from consuming warfarin.

Is it possible to get off of warfarin and effectively keep my blood thinned ? I currently take 1.5 mg to 2 mg dosage. Does the warfarin destroy Vitamin K and if so does that mean while on warfarin I never get the Vitamin K nutrients even if I did consume foods with it in it?

Thank you
Anna


No, sorry, Anna. Stopping Coumadin with your unique issues, i.e., a prosthetic mechanical heart valve (likely mitral, judging by your history of hypertrophic obstructive cardiomyopathy, in which the patterns of blood flow ejected from the heart disrupt the natural mitral valve function) and cardiomyopathy, can be fatal. Without blood thinning, the mechanical heart valve can trigger blood clot formation, since it is a foreign object implanted into the bloodstream.

There are no natural alternatives available with track records confident enough to bet your life on. Aspirin nor Plavix are blood thinners, but platelet inhibitors. These two agents, while they work for other forms of arterial (but not venous) blood clot inhibition, will not work for your unique situation.

Likewise, a purported oral lytic agent like nattokinase should not be substituted for Coumadin. Even if there was plausible science behind it, you should demand substantial evidence that it provides at least blood thinning equivalent to Coumadin. Should a blood clot, even a small one, form in or around the prosthetic valve, the valve can stop working within seconds. This can lead to death within minutes.

I believe it would be foolhardy to bet your life based on the marketing--let me repeat: MARKETING--of a "nutritional supplement" by supplement manufacturers eager to make a buck.

Nor are there any other nutritional supplements that can safely replace the Coumadin. I wish that were NOT true, as I am no stranger to the long-term dangers of Coumadin and I am a big believer, in general, in nutritional supplements. I am a BIGGER believer, however, in the truth. Weighing the options available to us today, there really is no rational choice but to remain on Coumadin.

By the way, I tell my patients to eat a substantial amount of green vegetables while they take Coumadin. I know that conventional advice is to reduce or eliminate green vegetables due to their content of Coumadin-antagonizing vitamin K. I think this is wrong, also. Green vegetables are the best foods on earth. They reduce risk for cancer, diabetes, bone disease, and coronary heart disease.

To obtain the benefits of green vegetables without mucking up your blood thinning (your "protime" or International Normalized Ratio, INR), I advise my patients who take Coumadin to eat green vegetables--but do so every day in relatively consistent quantities, so that the protime or INR is not disrupted and remains reasonably constant. It may mean that your total dose of Coumadin may be somewhat higher, e.g., 3 or 4 mg instead of 2 mg, but the dose is immaterial outside of blood thinning. That way, you obtain all the wonderful health benefits of green vegetables while maintaining fairly consistent blood thinning/protime/INR. Coumadin does not block all the health benefits of vegetables, only those related to vitamins K1 and K2.

With regards to protecting yourself from the osteoporosis promoting effects of Coumadin, I would be sure to follow a program of natural bone health, such as the one I discussed in Homegrown osteoporosis prevention and reversal. You will have to be extra careful, however, with the vitamin K2. Ideally, you have a doctor knowledgeable about vitamin K2 who can assist you in managing K2 intake while on Coumadin. This is something you can definitely NOT manage on your own. (I am a big believer in self-managed care, but this is way beyond the limit.)

Lastly, it is my belief that anyone with an inflammatory bowel condition, such as Crohn's disease or ulcerative colitis, should absolutely, positively, and meticulously AVOID WHEAT and all other gluten sources (such as rye, barley, and oats). Even if you test negative for celiac markers (e.g., anti-gliadin antibodies, emdomysium and transglutaminase antibodies), the enhanced intestinal permeability will allow wheat proteins, such as gluten, to gain ready entry into the bloodstream. Not to mention that wheat should have no place in the human diet anyway, in my view.

Homegrown osteoporosis prevention and reversal

I don't like to stray too far off course from discussions of heart disease and related issues in this blog. But the question of bone health comes up so often that I thought I'd discuss the strategies available to everybody to stop, even reverse, osteoporosis.

Coronary atherosclerotic plaque and bone health are intimately interwoven. People who have coronary plaque usually have osteoporosis; people who have osteoporosis usually have coronary plaque. (The association is strongest in females.) The worse the osteoporosis, the greater the quantity of coronary plaque, and vice versa. The two seemingly unconnected conditions share common causes and thereby respond to similar treatments.

Incredibly, rarely will your doctor tell you about these strategies. Your doctor orders a bone density test, the value shows osteopenia or osteoporosis, and a drug like Fosamax or Boniva is prescribed. As many people are learning, drugs like this can be associated with severe side-effects, such as jaw necrosis (death of the jaw bone), a dangerous and disfiguring condition that leads to loss of teeth and disfigurement, followed by reconstructive surgery of the jaw and face. These are not trivial effects.

Note that drugs are approved by the FDA based on assessment of efficacy and safety, NOT proven equivalence or superiority to natural treatments.

In order of importance (greatest to least), here are strategies that I believe are important to regain or maintain bone health. Indeed, I have seen many women increase bone density using these strategies . . . without drugs of any sort.

1) Vitamin D restoration--Vitamin D is the most important control factor over bone calcium metabolism, as well as parathyroid function. As readers of this blog already know, gelcap forms of vitamin D work best, aiming for a 25-hydroxy vitamin level of 60-70 ng/ml. This usually requires 6000 units per day, though there is great individual variation in need.

2) Vitamin K2--If you lived in Japan, you would be prescribed vitamin K2. While it's odd that K2 is a "drug" in Japan, it means that it enjoys the validation required for approval through their FDA-equivalent. Prescription K2 (as MK-4 or menatetranone) at doses of 15,000-45,000 mcg per day (15-45 mg), improves bone architecture, even when administered by itself. However, K2 works best when part of a broader program of bone health. I advise 1000 mcg per day, preferably a mixture of the short-acting MK-4 and long-acting MK-7. (Emerging data measuring bone resorption markers suggest that lower doses may work nearly as well as the high-dose prescription.)

3) Magnesium--I generally advise supplementation with the well-absorbed forms, magnesium glycinate (400 mg twice per day) or magnesium malate (1200 mg twice per day). Because they are well-absorbed, they are least likely to lead to diarrhea (as magnesium oxide commonly does).

4) Alkaline potassium salts--Potassium as the bicarbonate or the citrate, i.e., alkalinizing forms, are wonderfully effective for preservation or reversal of bone density. Because potassium in large doses is potentially fatal, over-the-counter supplements contain only 99 mg potassium per capsule. I have patients take two capsules twice per day, provided kidney function is normal and there is no history of high potassium.

5) An alkalinizing diet--Animal products are acidic, vegetables and fruits are alkaline. Put them together and you should obtain a slightly net alkaline body pH that preserves bone health. Throw grains like wheat, carbonated soft drinks, or other acids into the mix and you shift the pH balance towards net acid. This powerfully erodes bone. Therefore, avoid grains and never consume carbonated soft drinks. (Readers of this blog know that "healthy, whole grains" should be included in the list of Scams of the Century, along with Bernie Madoff and mortgage-backed securities.)

6) Strength training--Bone density follows muscle mass. Restoring youthful muscle mass with strength training can increase bone density over time. The time and energy needs are modest, e.g., 20 minutes twice per week.

Note that calcium may or may not be on the list. If on the list at all, it is dead last. When vitamin D has been restored, intestinal absorption of calcium is as much as quadrupled. The era of force-feeding high-doses of calcium are long-gone. In fact, calcium supplementation in the age of vitamin D can lead to abnormal high calcium blood levels and increased heart attack risk.

These are benign and easily incorporated strategies. They are also inexpensive. I challenge any drug to match or exceed the benefits of this combination of strategies. Keep in mind that strategies like vitamin D restoration provide an extensive panel of health benefits that range far beyond bone health, an effect definitely NOT shared by prescription drugs.

Your enlarged aorta

The thoracic aorta lives happily within the chest.

The aorta is the main artery of the body that emerges from the heart, located just under the sternum. It is the "tree trunk" from which all the major arteries branch off to the rest of the body: the arms, brain, abdominal organs, pelvis, and legs. The aorta receives the high-pressure blood ejected directly out of the heart muscle.

However, there are evil forces in the body that work to weaken the aorta. When the aorta is weakened, it enlarges. Enlarged aortas also tend to grow atherosclerotic plaque. Plaque in the aorta poses long-term risk for stroke and and mini-strokes ("transient ischemic attacks," or TIAs), due to fragmentation.

There are many enlarged aortas in this world. I see at least several every week. It is fairly common, particularly in people with high blood pressure and cholesterol abnormalities, as well as those who are overweight. Smokers get it really bad.

Conventional thinking is that, once an aorta enlarges, it will inevitably continue to enlarge at the average rate of 2.0 mm per year (resulting in 1.0 cm enlargement over 5 years). For this reason, conventional discussions on the topic of thoracic aortic aneurysms all say something like "Enlarged aortas should be monitored yearly. Surgical replacement should proceed when the aorta reaches a diameter of 5.5 cm."

This is because an aortic diameter of 5.5 cm is associated with much greater likelihood that the aorta will rupture (fatal within minutes) or the internal lining will tear, a "dissection." The surgery is a major undertaking that involves opening the chest and usually replacing the aortic valve and inserting a synthetic aorta. The procedure is high-risk, especially if any branch arteries are involved.

So putting a stop to any further aortic enlargement is a worthwhile goal. Unfortunately, conventional thought is that there is nothing you can do to stop the inevitable growth of the thoracic aorta.

Nonsense. There are a number of efforts you can make to halt further increase in aortic diameter. (My experience in this is anecdotal and unpublished, but now numbers several hundred patients.)

There are two categories of factors that cause the aorta to increase in diameter:

1) Internal pressure--Think of blood pressure as the internal inflating pressure on this "balloon." Keeping the "inflating pressure," i.e., blood pressure, low exerts substantial effect on slowing growth of aortic diameter. I aim for normal BP or lowish BP (less than 130/80, preferably 100/70).

2) Factors that weaken the aortic wall--Processes like inflammation, glycation, lipoprotein deposition, and nutritional deficiencies will serve to weaken the supportive tissue of the aorta. For that reason, correction of lipoprotein abnormalities (e.g., small LDL and lipoprotein(a)), reductions in carbohydrate intake and thereby blood glucose/glycation, and "normalization" of vitamin D, vitamin C supplementation (for collagen crosslinking), and omega-3 fatty acids all play a role.

To push even farther, there may be additional advantage to following strategies that impair the production and activity of a crucial enzyme that lives within the aortic wall: matrix metalloproteinase, or MMP. MMP degrades the collagen and other supportive tissues within the aorta, weakening it and permitting expansion. Blocking MMP may prove to be among the most powerful new strategies to halt aortic expansion.

Compounds that have potential MMP-inhibiting effects include:
--Vitamin D--A substantial effect
--Resveratrol--One of the polyphenols from red wine
--Doxycycline--This old antibiotic often used for acne treatment has, in preliminary studies, shown important MMP-blocking effects and slowed aortic expansion.

Anyway, there you have it. A bit complicated, but a "recipe" that has failed me only rarely.

Extreme carbohydrate intolerance

Here's an interesting example of what you might call "extreme carbohydrate intolerance."

May is a 44-year woman who has now had her 7th stent placed in her coronary arteries. She lives on a diet dominated by breads, breakfast cereals, muffins, rice, corn products, along with some real foods.

Her conventional lipid panel and other lab values:

Total cholesterol 346 mg/dl
Triglycerides: 877 mg/dl
HDL cholesterol: 22 mg/dl
LDL cholesterol: incalculable
(Recall that LDL cholesterol is usually a calculated, not a measured value. The excessively high triglycerides make the standard calculation invalid--more invalid than usual.)

Fasting blood glucose: 210 mg/dl
HbA1c (a reflection of previous 60-90 days average glucose): 7.2% (desirable 4.5% or less)
ALT (a "liver enzyme"): 438 (about five-fold normal)


At 5 ft even and 138 lbs (BMI 27.0), May appears small. But the modest excess weight is all concentrated in her abdomen, i.e., in visceral fat.

By lipoprotein analysis via NMR (Liposcience), May's LDL particle number was 2912 nmol/L, or what I would call a "true" LDL of 291 mg/dl. (Drop the last digit.) Of the 2912 nmol/L LDL particles, 2678 nmol/L, or 92%, were small.

The bad news: This pattern of extremely high triglycerides, extremely high LDL particle number, low HDL, predominant small LDL, and diabetes poses high-risk for heart disease--no surprise. It earned her 7 stents so far. (Unfortunately, she has made no effort whatsoever to correct these patterns, despite repeated advice to do so.)

The good news: This collection is wonderfully responsive to diet. LDL particle number, small LDL, triglycerides, blood glucose, and HbA1c drop dramatically, while HDL increases. Heart disease will at least slow, if not stop.

It's amazing how far off human metabolism can go while indulging in carbohydrates, particularly a genetically carbohydrate-intolerance person. (Actually, I wouldn't be surprised if May's diet, as bad as it seems to you and me, still fits within the dictates of the USDA food pyramid.) The crucial step in diet to correct this smorgasbord of disaster is elimination of carbohydrates, especially that from wheat, cornstarch, and sugars.

What's for breakfast? Egg bake

Heart Scan Blog reader and dietitian, Lisa Grudzielanek, provided this recipe in response to the post, What's for breakfast?

Lisa, by the way, is one of the rare dietitians who understands that organizations like the American Dietetic Association have made themselves irrelevant. She therefore advocates diet principles that work, not just echoing the idiocy that emanates from such organizations, often driven by economics more than science. Lisa works in the Milwaukee area and has proven a useful resource person for my patients who have required extra coaching in the Track Your Plaque diet principles.

Egg Bake
My favorite breakfast is what I call an "egg bake." Others may refer to it as a "quiche."

Take a variety of fresh vegetables. This time of year is great for farmers' markets.

I typically use fresh chopped organic spinach, bell peppers, red & white onions, scallions, broccoli, mushrooms, cherry tomatoes halved and, if desired, meat (nitrite-free ham or leftover chicken breasts).

1) Chop veggies and place in casserole dish.
2) Add meat and handful of cheese of your choice.
3) Scramble 8 eggs & little bit of milk & pepper.
4) Add to casserole dish and mix/coat veggies with egg mixture.
5) Put in oven at 450 degress for 30 minutes.

Yummy, ready to eat breakfast that is so easy for the work week.

What's for breakfast?

If you eliminate wheat from breakfast and otherwise adhere to a low-carbohydrate dietary approach, what is there to eat for breakfast?

If you take out English muffins, bagels, all breakfast cereals, pancakes, waffles, and toast, what's left to eat?

Actually, there's plenty left to eat. It just may not look like the traditional American notion of "breakfast." (The traditional idea of breakfast was is, in part, due to the legacy of Dr. John Harvey Kellogg, who, in the latter part of the 19th century, ran a sanitarium in Battle Creek Michigan. He and his brother, Will Keith Kellogg, discovered the idea of turning grains into flakes, the birth of the breakfast cereal. Subscribe to the idea of breakfast cereal for breakfast and you subscribe to the ideas of a man who would administer four enemas for you today to cure your cancer or rheumatism.)

Here are a few ideas. By no means is this meant to be a comprehensive list, just a starting point for a few new breakfast food ideas.

--Eggs--Of course, eat the yolk. Eat three yolks. Scrambled, "fried," (not really deep-fried, of course), hard-boiled, poached, as an omelette. Add pesto, olive oil, vegetables, mushrooms, salsa.

--Ground flaxseed--As a hot cereal with your choice of water, milk (not my favorite because of insulin effects; the fat is immaterial), full-fat soy milk (yeah, yeah, I know), unsweetened almond milk. Add walnuts, blueberries, etc. Ground flaxseed is the only grain I know of that contains no digestible carbohydrates.

--Lunch and dinner--Yes, if you cannot have breakfast foods for breakfast, then have lunch and dinner, meaning incorporating foods you ordinarily regard as lunch and dinner foods into your day's first meal. This means salads, leftover chicken from last night, soup, raw vegetables dipped in hummus or guacamole, stir fry, etc.

--Cheese--For something quick, grab a chunk of gouda or emmentaler along with a handful of raw almonds, walnuts, or pecans. Because of the excess acidity of cheese (along with meats, among the most acidifying of foods), I usually try to include something like a raw pepper or avocado, foods that are net alkaline.

--Avocados--Cut in half, scoop out contents. They're quick and delicious, when available.

I hesitate to mention it, but I sometimes will have tofu, cubed and flavored with whatever is available--soy sauce, miso, pickled vegetables. My mother was Japanese, so I'm comfortable with this, though many people are not.

Anyway, that's a partial list that nonetheless can get you started on a wheat-free, low-carb breakfast.

If you are just starting out, you will notice a number of fundamental changes. You may first experience the characteristic "withdrawal" effect: mental fog and fatigue that lasts about a week. Energy then picks up, often substantially. This is followed by gradually reduced appetite: You will be far less hungry. You will require less food, less often, since appetite will be driven by physiologic need, not the appetite-stimulating properties of wheat (and cornstarch, high-fructose cornsyrup and sucrose).

By the way, do not skip breakfast unless it's part of an occasional fasting effort. Skip breakfast, wind down metabolism, get fat. I am impressed at how consistent skipping breakfast backfires in those who think that it helps you control weight.

I also welcome any suggestions on what you eat as part of your wheat-free, low-carb breakfast. (Thanks for the great suggestions on the last blog post, Anna.)