Hospitals: Then and Now

It's 1920. The hospital in your city is a facility run by nuns or the church. It's a place for the very ill, often without hope of meaningful treatment, but nonetheless a place where surgeries take place, babies are born, the injured and chronically ill can find care. No one has health insurance and there's no Medicare. Everyone pays what they can. The hospital is accustomed to doling out plenty of care without compensation. For that reason, they welcome donations and sometimes will build new additions or other facilities in honor of a major donor.

Volunteeers are common, since the wards are understaffed and generally suffering from a shortage of trained nurses and personnel associated with the church. Drugs, such as they are, are often prepared from basic ingredients in the hospital pharmacy. Product representatives hawking medicines and devices are virtually unheard of.

Though their therapeutic tools are limited, the physicians are a proud group, dedicating their careers to healing. The majority of the medical staff volunteer large portions of their time to care for the poor who come to the hospital with very advanced stages of disease: metastatic tumors, advanced heart failure, debilitating strokes, overwhelming septicemia, etc.

Hospitals are usually governed by a board of clergy and physicians who make decisions on how to apply their limited resources and continually seek charitable donations.


Fast forward to present day: Hospitals are high-tech, professional facilities with lots of skilled people, complicated equipment,and capable of complex procedures. While they still house people with advanced illnesses, the floors are also filled with people with much earlier phases of disease. In general, they do a good job, with quality issues scrutinized by a number of official agencies to police practices, incidence of hospital-related infections, medication errors, care protocols, etc.

The hospital of 2006 is a more more effective place than the hospital of 1920. But its aims and operations are different, also. Though some churches are still involved in hospitals, more and more are owned by publicly-traded companies that answer to shareholders--shareholders who want share value to increase. Though donations are still sought, much of the revenues are obtained by concentrating on profitable, large-ticket procedures. More procedures are often generated by advertising.

Because they operate to generate profits, several hospitals in a single city or region compete with one another. The 21st century has therefore witnessed the phenomenon of hospital-owned physicians: more and more practicing physicians are employees of their hospital. That way, the physician brings all his patients and procedures to his hospital, not to a competitor. The top of the funnel is the primary care physician, who tends to see all disease when it first occurs. The primary care physician then sends the patient to the specialist, who is obliged (by contract) to perform his/her procedure in the hsopital paying their salary.




Representatives from companies manufacturing and selling expensive hospital equipment and drugs are everywhere, falling over themselves to gain attention of the physicians using their equipment and the hospital buyers who make purchasing decisions. Millions of dollars can be transacted with just one sale.

The number of volunteers has dwindled. The poor and uninsured are commonly diverted elsewhere, often to a government-funded, and often second-rate, institution. Hospitals measure success by comparing annual revenues and numbers of major procedures.

The hospital of 2006 is a vastly different place than 1920. If you're expecting charitable treatment, compassion, and selfless care, you're in the wrong century. In 2006, the hospital is a business. You don't expect charitable treatment at Wal-Mart or from your car dealer. Don't expect it from your hospital. They are businesses and you are a customer. Recognize this fact, lose the nostalgia for the hospitals of yesterday, and a lot more will become clear to you.
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sponsibility), publishing scientific data, maintaining hospital responsibilities, and spending time with my wife and family. We're all busy and I'm no different. I'm afraid that it's my responses to blog comments that I will have to sacrifice.

I invite commenters to continue to comment on these posts, as I've learned many new things by reading them and find them helpful feedback. And I do read them. Should an especially helpful comment be made, I will feature it in a new blog post, rather than respond directly.

"Flying in the fog"

I received this wonderful response to The Heart Scan Blog post Hammers and Nails:

I am 65 years old. I had a stent inserted in the "widow-maker" artery (80% blockage) a year ago. I had passed out a couple of times (heart rate dangerously low - 30s). I rode to the hospital in an ambulance. Tests revealed short LBBB episodes; mild mitral regurgitation, mild tricuspid regurgitation. Catherization showed 3 vessel CAD. I was told that a medicated stent was absolutely necessary given the situation; regardless, I have to accept that. A pacemaker was installed to prevent bradycardia and keeps heart rate from dropping below 60. I have 20% L distal main blockage and 90% lesion of the high first obtuse marginal at the takeoff. The right coronary had 60% posterior lateral branch stenosis.

Since then I have reduced TG from 360 to 60, LDL from 89 to 82 (although a few months ago it was in the mid-70s), and increased HDL from 30 to 46. I went from 265lbs to 190lbs and hope to eventually get to 180lb this Spring. I did it by progressing from walking to trotting (slow run) and dietstyle changes (low-GI veggies, fruits, etc.) .













On a recent visit the cardiologist said the the LDL needs to be 70 or below to "freeze" the 90% blockage and gave me a prescription for Lipitor. I asked if there were alternatives, like diet, supplements, etc. He admitted that he did not know about those alternative but did know Lipitor. When the only tool you have is a hammer then everything is a nail. I understand that the 90% blockage is important but will not take the Lipitor to achieve the 12 points reduction. Seems like an overkill.

I asked him if there was a way to evaluate my current condition. I was told there was no way. Basically, if I have no symptoms, good. If I have symptoms then it will have to be evaluated. Death could be the only symptom. I swear he was about to say bypass surgery ($$$$$$!) was inevitable. Something is wrong with this "fly-in-the-fog-and-hope-you-don't- hit-a-mountain" approach. Hope is not a strategy!

I am confident that I can reduce LDL to below 70 based on eliminating wheat-products in my diet plus increasing oat bran in my diet. I also take fish oil daily (EPA/DHA-2g). I am looking for a new cardiologist. I just recently purchased your book and find it very instructive. In the meantime I have an appointment with my primary care physician to discuss implementing the Track Your Plaque program. I realize that the one stent will skew the scan numbers but can be used as a baseline number.



Phenomenal weight loss! That alone has likely cut this man's risk in half. But is that it? Is the cardiologist correct--take Lipitor and hope for the best?

Of course not. There are many additional strategies to employ. Eliminating wheat from the diet is an excellent idea: HDL will skyrocket, triglycerides drop even further, small LDL will drop like a stone, blood sugar and blood pressure will drop. He will have more energy, get rid of afternoon energy slumps, sleep better.

He has already added fish oil. If his cardiologist did not mention this, I would say he was guilty of malpractice. The data supporting the addition of fish oil to the treatment program of anyone with heart disease is overhwelming. GISSI Prevenzione: 11,000 participants--28% reduction in heart attack, 45% reduction in death from heart attack. The Japanese JELIS trial of 18,645 participants--19% reduction in dangerous heart events. It's also clear that omega-3 fatty acids from fish oil also compound the benefits of statin agents, should this man choose to begin Lipitor.

Vitamin D brought to normal blood levels is his next "secret weapon" that will further boost his lipids and lipoproteins further into not just "normal" territory, but beyond belief. Even though we aim for 60-60-60 for LDL-HDL-triglycerides in the Track Your Plaque program, adding vitamin D can yield numbers you've never seen before. It's not uncommon, for instance, to see a 10 or 20 mg/dl jump in HDL.

Identify all other hidden causes of coronary plaque. If all the causes have not been fully identified, how can anyone hope to gain full control over coronary plaque growth?

Re: LDL cholesterol of 89 mg/dl at the start. Of course, this is a calculated value, not measured. Because HDL was low and triglycerides high at the start of his program, this means that true LDL--if actually measured--was probably more like 180 to 250 mg/dl, and it was probably nearly all small. So his cardiologist might have advised a helpful treatment, though for the wrong reasons.

Our reader has gone a long way on his own in creating his own prevention program. But there's yet more to do, particularly if the goal is reversal. It is shocking to me that a man like our reader, clearly articulate and motivated, gets virtually no advice beyond "take Lipitor" after all the procedural benefits have been reaped.

Even though one artery can no longer be "scored" due to the presence of the metallic stent, a heart scan would still be invaluable for long-term tracking purposes, just as we advocate in the Track Your Plaque program.



Copyright 2008 William Davis, MD

Goodbye, Dr. Jarvik

HeartWire, the news service of www.theheart.org, posted the following report:

Pfizer pulls Lipitor ads featuring Dr Robert Jarvik in HeartWire

New York, NY - After a series of questions and attacks over its choice of Dr Robert Jarvik to endorse Lipitor in a series of TV commercials, Pfizer has announced that it is withdrawing the ads. As previously reported by heartwire, Jarvik invented the first artificial heart, but he is not a cardiologist, nor does he hold a medical license—factors that drew criticism from detractors and made him and Pfizer a target of a US House Committee on Energy and Commerce investigation into celebrity endorsements in direct-to-consumer advertisements.

In a January 2008 statement, committee chair Rep John D Dingell (D-MI) observed: "Dr Jarvik's appearance in the ads could influence consumers into taking the medical advice of someone who may not be licensed to practice medicine in the United States. Americans with heart disease should make medical decisions based on consultations with their doctors, not on paid advertisements during a commercial break."

Complaints about Jarvik went up a notch this month when the latest ad in the series depicted the inventor rowing a racing scull across a lake, despite the fact that Jarvik himself does not row and the commercial used a body double.


This is typical pharmaceutical industry sleight-of-hand, now you see it, now you don't, that has come to define their policies. And this is just the stuff that comes to light because of some obvious blunders. We can only begin to imagine what sorts of other shenanigans have been swept under the rug, especially adverse effects of drugs that never made it to the light of publication.

Is this just another example of how direct-to-consumer advertising has backfired? I now have patient after patient tell me that they have been so overwhelmed and fed up with TV and magazine ads for drugs that they



Other media outlets have reported that Jarvik was guaranteed $1.35 million for the ads and that Pfizer spent $258 million on Lipitor advertisements between January 2006 and September 2007.

Hammers and nails

I'm sure you've heard the old saying that,

To a man with a hammer, everything looks like a nail.


It couldn't be truer than in heart procedures (the man with the hammer) and heart disease (the nail).

What does it take in 2008 to become an interventional cardiologist trained in all the techniques of angioplasty, stenting, intracoronary ultrasound, etc.? Start with your undergraduate degree (4 years), then medical school (another 4 years), then training in internal medicine (3 years), then general cardiology taining (3 years), then an additional year in interventional cardiology. Each step along the way also involves competing for these spaces, a process that requires much time, money, and sweat.

The total time investment is 15 years after high school. Many if not most college students graduate with debt. Pile on the substantial cost of medical school. Training after medical school pays a modest salary, enough for a single person. Many trainees by then have spouses and a family, would like to buy a house, have bills to pay. (I managed to buy my first house for $69,000 in Columbus, Ohio and paid my mortgage by sleeping only every other night and moonlighting on my off nights.)

By the time the interventional cardiologist-in-training finishes his/her 15 years, they are hungry for a hefty increase in income. After such a time and money investment, I do believe that there is at least some justification for generous income for the years of work involved.

Back to our hammer and nail metaphor. Not only do we now have a man or woman with a hammer, but a really expensive hammer that required a substantial amount of effort to obtain. Now, our hapless hammer-bearer is desperate to see everything in sight as a nail.

You're seen in consultation by this fresh interventional cardiologist in practice for only a few years. Guess what he/she advises? Go straight to the catheterization laboratory, of course. Throw in the fact that insurance reimbursement is most generous for heart procedures, far more than for consulting in the office, doing a stress test, or other simpler, non-invasive tests, and the incentives are clear.

The system, you see, is set up to follow such a path. The path to the cath lab is heavily incentivized, paths in the other direction discouraged, disparaged, or just ignored.

My message: Don't get nailed.

What is abnormal?

What is abnormal?

You'd think that the answer would be easy and straightforward.

However, consider these instances of medical findings that I have witnessed fall repeatedly into the "normal" category:

Diameter of the thoracic aorta: 4.5 cm

Mild coronary plaque by heart catheterization

Carotid plaque of 30-50%


Why isn't a thoracic aorta (the big artery in your chest) of 4.5 cm normal? Because it can be expected to increase in diameter by about 2.5 mm (0.25 cm) per year. Even at its current diameter, it means that stroke risk is greater, since enlarged aortas are diseased aortas that commonly accumulate atherosclerotic plaque with potential to fragment and shower debris to the brain. It means that high blood pressure and/or cholesterol/lipoprotein abnormalities have been uncorrected for years that have allowed the aorta to enlarge.

How about "mild coronary plaque"? Followers of the Track Your Plaque program already know the answer to this one. Mild plaque does not mean mild risk. In fact, most plaques that cause heart attack are mild plaques, not severe blockages. While severe blockages can provide symptom warning and are detected by stress tests, it's the mild blockages that rupture without symptom warning and cause heart attack. So "mild coronary plaque" is no less dangerous than severe coronary plaque.

Likewise, carotid plaque of 30-50%, while it doesn't justify surgery, can grow within just a few years to a severity that allows it to fragment and shower debris to the brain, i.e., a stroke. As with the enlarged aorta, it means that multiple causes of carotid plaque are likely active, including high blood pressure and cholesterol or lipoprotein abnormalities.

Then why would any of these findings be labeled "normal"?

Simple. In the minds of many physicians, if a condition doesn't pose immediate risk, or if it doesn't qualify for surgical "correction," then it is labeled "normal" or "mild."

Thus, an aorta of 4.5 cm cannot justify surgical replacement until it achieves a diameter of 5.5 cm. It is therefore labeled "normal."

"Mild coronary plaque" does not justify insertion of stents or performance of bypass surgery. It must therefore be "normal."

Carotid plaque over 70% is surgically removed, but not 30-50%. 30-50% is therefore "normal."

The tragedy is that many "normal" or "mild" findings, if cast in the proper light, could lead to corrective strategies that could prevent danger long-term or keep surgery from becoming necessary.

The enlarged aorta, for instance, could be stopped and an aneurysm (defined as 5.5 cm or greater) could be prevented, along with dramatically reducing risk for stroke. Carotid plaque, more so than coronary plaque, is a controllable and manipulable condition that should trigger a program of prevention and reversal. Instead, it usually generates advice to have another ultrasound in a year to see if it has yet achieved severity sufficient to justify surgery.

Of course, "mild coronary plaque" is the reason for the Track Your Plaque approach, a chance to seize control over this disease years or decades before procedures are necessary and reduce danger now, not years from now.


Copyright 2008 William Davis, MD

Niacin and hydration

Many people know about niacin's curious effect of the "hot flush," a feeling of warmth that covers the chest and neck, occasionally the entire body.

However, many people are unaware of the fact that hydration can block this effect. In fact, many people who were not advised of this will come to the office describing miserable experiences with niacin--hot flushes that last for hours, intolerable itching, etc.--only to experience little or none of these effects with generous hydration.

The vast majority of the time, two 8-12 oz glasses of water when the hot flush occurs will eliminate the flush within a few minutes.

Sometimes, the hot flush will occur many hours after taking niacin. Nine times out of ten, this delayed effect is also due to poor hydration. For instance, you might be engrossed in your work and forget to keep up with fluid demands. Or, it may be warm and you've lost fluids through sweating. That's when you begin to feel the hot flush creep up on you.

The cure: Lots of water. In this situation, in which you have allowed dehydration to develop, it may require more than two big glasses. Relief from the flush may also take more time, but it still works nearly every time.

On those rare occasions when water by itself is insufficient, then an adult (325 mg), uncoated aspirin or 200 mg ibuprofen can also be used to accelerate relief.

Why go to some much bother? Well, niacin remains the best agent we have for reduction of small LDL, raising HDL (although vitamin D is proving to be a powerful competitor in this arena), and reducing lipoprotein(a). How much do statin drugs contribute to these effects? Very little, if at all.

Several drug manufacturers are also working on "antidotes" to the hot flush effect of niacin that will be packaged within the niacin tablet. Naturally, it will also boost the cost up many times higher.

In the meantime, if or when you experience the niacin hot flush, just think: Put out the "fire" with plenty of water.
All posts by william-davis

Why does wheat cause arthritis?

Wheat causes arthritis.

Before you say "What the hell is he saying now?", let me connect the dots on how this ubiquitous dietary ingredient accelerates the path to arthritis in its many forms.

1) Wheat causes glycation--Glycation is glucose-modification of proteins in the body that occurs when blood glucose exceeds 100 mg/dl. Cartilage cells are especially susceptible to glycation. The cartilage cells you had at age 18 are the very same cartilage cells you have at age 60, since they lack the ability to reproduce and repair themselves. Proteins in cartilage are highly susceptible to glycation, which makes them stiff and brittle. Stiff, brittle cartilage loses its soft, elastic, lubricating function. Damaged cartilage cells don't regenerate nor produce more protective proteins. This allows destruction of cartilage tissue, inflammation, and, eventually, bone-on-bone arthritis.

Because wheat, even whole wheat, sends blood sugar higher than almost all other foods, from table sugar to Snickers bars, glycation occurs after each and every slice of toast, every whole wheat bagel, every pita wrap.

2) Wheat is acidifying--Humans are meant to consume a diet that is net alkaline. While hunter-gatherers who consume meat along with plentiful vegetables and fruits live a net alkaline diet (urine pH 7 to 9), modern humans who consume insufficient vegetables and too much grain (of which more than 90% is usually wheat) shift the body towards net acid (urine pH 5 to 7). Wheat is The Great Disrupter, upsetting the normal pH balance that causes loss of calcium from bones, resulting in decalcification, weakness, arthritis and osteoporotic fractures.

3) Wheat causes visceral fat--The extravagant glucose-insulin surges triggered by wheat leads to accumulation of visceral fat: wheat belly.

Visceral fat not only releases inflammatory mediators like tumor necrosis factor and various interleukins, but is also itself inflamed. The inflammatory hotbed of the wheat belly leads to inflammation of joint tissues. This is why overweight and obese wheat-consuming people have more arthritis than would be explained by the burden of excess weight: inflammation makes it worse. Conversely, weight loss leads to greater relief from arthritis pain and inflammation than would be explained by just lightening the physical load.

We need a name for this wheat effect. How about "bagel bones"?

Why do morphine-blocking drugs make you lose weight?

Naloxone (IV) and naltrexone (oral) are drugs that block the action of morphine.

If you were an inner city heroine addict and got knifed during a drug deal, you'd be dragged into the local emergency room. You're high, irrational, and combative. The ER staff restrain you, inject you with naloxone and you are instantly not high. Or, if you overdosed on morphine and stopped breathing, an injection of naloxone would reverse the effect immediately, making you sit bolt upright and wondering what the heck was going on.

So what do morphine-blocking drugs have to do with weight loss?

An odd series of clinical studies conducted over the past 40 years has demonstrated that foods can have opiate-like properties. Opiate blockers, like naloxone, can thereby block appetite. One such study demonstrated 28% reduction in caloric intake after naloxone administration. But opiate blocking drugs don't block desire for all foods, just some.

What food is known to be broken down into opiate-like polypeptides?

Wheat. On digestion in the gastrointestinal tract, wheat gluten is broken down into a collection of polypeptides that are released into the bloodstream. These gluten-derived polypeptides are able to cross the blood-brain barrier and enter the brain. Their binding to brain cells can be blocked by naloxone or naltrexone administration. These polypeptides have been named exorphins, since they exert morphine-like activity on the brain. While you may not be "high," many people experience a subtle reward, a low-grade pleasure or euphoria.

For the same reasons, 30% of people who stop consuming wheat experience withdrawal, i.e., sadness, mental fog, and fatigue.

Wouldn't you know that the pharmaceutical industry would eventually catch on? Drug company startup, Orexigen, will be making FDA application for its drug, Contrave, a combination of naltrexone and the antidepressant, buproprion. It is billed as a blocker of the "mesolimbic reward system" that enhances weight loss.

Step back a moment and think about this: We are urged by the USDA and other "official" sources of nutritional advice to eat more "healthy whole grains." Such advice creates a nation of obese Americans, many the unwitting victims of the new generation of exorphin-generating, high-yield dwarf mutant wheat. A desperate, obese public now turns to the drug industry to provide drugs that can turn off the addictive behavior of the USDA-endorsed food.

There is no question that wheat has addictive properties. You will soon be able to take a drug to block its effects. That way, the food industry profits, the drug industry profits, and you pay for it all.

Heart scan tomfoolery 2

In the last Heart Scan Blog post, I discussed the significance of the apparent discrepancy between Steve's heart scan score and volume score. This post addresses his second question, also a FAQ about heart scan scores.

Steve noted that his second scan compared to his first showed:

- Left Main volume went up from 22.4 to 35.6
- LAD went down from 95.2 to 91.3
- LCX volume went down from 23.2 to 0
- RCA volume went up from 0 to 9.3

So there are apparent divergences in behavior in the left main that increased and both LAD (left anterior descending) and LCX (left circumflex) that decreased.

The explanation is simple: When heart scans are "scored," they are viewed in horizontal "slices." When the heart is viewed as horizontal slices, the LAD and LCX originate from the common left main stem. In other words, it's like a tree with the left mainsteam representing the trunk, the LAD and LCX representing two main branches.

Plaque can form, obviously, in all three arteries, but it can do so by starting in the left main, for instance, and extending into either the LAD or LCX, or both. The left main plaque can therefore bridge any 2 or all 3 arteries.

When the plaque is "scored" by taking the computer mouse and circling the calcified plaque in question (to allow the computer program to generate the calcium score and volume score of that particular plaque), the plaque that may extend from left main into the LAD and/or LCX might be labeled "left main," or it might be labeled "LAD" or "LCX." There is no reliable way to "dissect" apart the plaque into the three arteries, since the plaque is coalescent and continuous. So the scoring technologist or physician simply arbitrarily declares the artery "LAD," for instance.

The problem comes when two different interpretation methods are used: Perhaps it's a new technologist or physician, or there was no attention paid to how the previous scan was read. One reader calls it "left main" and the next calls it "LCX."

So the apparent discrepancy has to do with flaws in the methods of segregating plaque location, as well as inattention to scoring techniques. The total score, however, remains unaffected.

Nonetheless, Steve has enjoyed a modest reduction in the score of the left main/LAD/LCX from his original 140.8 down to a second left main/LAD/LCX score of 126.9.

The right coronary artery (RCA), however, is not subject to this difficulty and Steve score shows a modest increase in score. (Why the divergent behavior between left main/LAD/LCX and RCA? There is no clear explanation for this, unfortunately.)

All in all, the news for Steve is good: He achieved these results on his own using nutritional techniques. Because he, in all practicality, stopped the progression of his heart scan score and avoided the "natural" rate of increase of 30% per year, all he needs to do is "tweak" his program a bit to achieve reversal, i.e., reduction of score.


Here's an image from another previous Heart Scan Blog post (about the relationship of osteoporosis and coronary disease) that shows such a plaque that starts in the left mainstem yet extends into both the LAD and LCX:

Heart scan tomfoolery

Heart Scan Blog reader, Steve, sent these interesting questions about his heart scan experience. (I sometimes forget that this blog is called "The Heart Scan Blog" and was originally--several years ago--meant to discuss heart scans. It has evolved to become a much broader conversation.)

The answers are a bit lengthy, so I'll tackle Steve's questions in two parts, the second in another blog post.

Dr. Davis,

I had a heart scan last year. The score was 96. While not a horrible score, it
was a wake up call, and I changed my lifestyle.

I had another scan this year and the heart scan score went up to 105, but the
volume score went down from 141 to 136.

The report I received said this:

'The calcium volume score is less in the current study as compared with the
original or reference study. This is an excellent coronary result and indicates
that there has been a net decrease in coronary plaque burden. The current
prevention program is very effective and should be continued.'

This is all well and good, but I have two questions:

1. Am I really going in the right direction even though the heart scan score
went up 9%?

2. Here are results that make no sense to me:
- Left Main volume went up from 22.4 to 35.6
- LAD went down from 95.2 to 91.3
- LCX volume went down from 23.2 to 0
- RCA volume went up from 0 to 9.3

Why would there be so much variation from year to year, and why would the plaque
move from site to site?

Steve


Questions like Steve's come up with some frequency, so I thought it would be worthwhile to discuss in a blog post.

First of all, the conventional heart scan score, or "calcium score" or "Agatston score" (after Dr. Arthur Agatston, developer of the simple algorithm for calcium scoring, as well as South Beach Diet fame), is the product of the area of the plaque in a single CT "slice" image
multiplied by a density coefficient, i.e., a number ranging from 1 to 4 that grades the x-ray density of the plaque. (1 is least dense; 4 is most dense.) A density coefficient of 1 therefore signifies some calcium within plaque, with higher density coefficients signifying increasing calcium content and density. Incidentally, "soft" plaque, i.e., non-calcified, would fall in the less than 1 range, even the negative range (fatty tissue within plaque).

The volume, or "volumetric," score is the brainchild of Drs. Paulo Raggi and Traci Callister, who expressed concern that, if we cause plaque to shrink in volume, the density coefficient used to calculate the calcium score would increase (since they believed that calcium could not be reduced, contrary to our Track Your Plaque experience, thereby leading to misleading results. They therefore developed an algorithm that did not rely on density coefficients, but used the same two-dimensional area obtained in the standard heart scan score, but replaced the density coefficient with a (mathematically interpolated) vertical axis (z-axis) measure of plaque "height." This 3-dimensional volumetric value therefore provided a method to generate a measure of calcium volume. In their original publication, the volume score proved more reproducible than the standard calcium score. This way, any reduction in plaque volume would not be influenced by the misleading effects of calcium density, but reflect a real reduction in volume.

Callister and Raggi's study also highlighted that calcium scoring in any form is subject to variability. Back in 1998 (when their study was published), there was a bit more variation than today due to the image acquisition methods used. But, even today, there is about 9% variation in scoring even if performed repeatedly (with less percentage variation the higher the score).

Unfortunately, volume scoring never caught on and the calcium score has been the most commonly used value by most heart scan centers and in most clinical studies. And, in all practicality, the two values nearly always track together: When calcium score increases, volume score increases in tandem; when calcium score decreases, volume score decreases in tandem.

Steve is therefore an exception to the general observation that calcium score and volume score travel together. Steve's calcium score increased, while his volume score decreased. From the above discussion, you can surmise a few things about Steve's experience:"

1) In all likelihood, the changes in both calcium score and volume score could simply be due to variability, i.e., variation in the placement of his body on the scan table, variation in position of the heart, variation in data acquisition, etc. There is a high likelihood that neither value changed; both are essentially unchanged.

2) If the changes are not due to scan variability, but are real, then it could be that the calcified plaque is reduced in volume but increased in density. If true, this is probably still a favorable phenomenon, since plaque volume is a powerful predictor of coronary "events" and an increase in plaque density is likely a benign phenomenon. It would also raise questions about the adequacy of vitamin D and vitamin K2 status, both major control factors over calcium deposition and metabolism.

So, in all likelihood, Steve's apparent discrepant results are modest good news, especially since calcium scores can ordinarily be expected to increase at the rate of 30% per year if no action is taken. Experiencing no change in score, calcium or volumetric, carries a very excellent prognosis, with risk for heart attack approaching zero. (I'm impressed that Steve accomplished this on his own, something the majority of my colleagues haven't the least bit of interest doing.)

Part 2 of Steve's question will be tackled in a separate post.

Can I see your linea alba?

As more and more people are eliminating wheat from their diet and losing their "wheat bellies," i.e., the muffin top around their waists along with the visceral fat beneath, I am frequently seeing something I haven't seen in years: the linea alba.

Linea alba, or "white line," refers to the band of connective tissue running vertically from sternum to pubic area. It underlies the depression that separates the horizontal abdominal rectus muscles of the "six pack" abdomen.

It's like digging in your closet and finding something you thought you'd lost years earlier. Surprise! It's been there all along. Buried deep beneath the abdominal fat from dozens of deep-crust pizzas, whole wheat pasta, and whole grain sandwiches is this pleasing anatomical feature long lost from most peoples' anteriors.


Can you see your linea alba?

Dwarf mutant wheat

Here's my 12-year old standing next to dwarf wheat grown near my house. The wheat is full-grown, harvested about 2 weeks after I took this photo.

Wheat is no longer the 4-foot tall "amber waves of grain" of the 20th century. Over 99% of all wheat grown worldwide is now the 18- to 24-inch tall dwarf. New size, new biochemistry, new effects on humans. I call it dwarf "mutant" wheat despite its lack of extra limbs or eyes because of the dramatic transformation required to breed this unique synthetic plant. 

Short-stature means less stalk, faster growing. The stockier stalk also means that the heavy seed head won't cause the plant to "buckle," as 4-foot tall wheat used to. 





The thousand-plus proteins of wheat that have been transformed to generate this dwarf mutant also changed wheat's relationship to consuming humans.

Medical education in the days of Big Pharma

I received this detailed email from an unexpected source: a 3rd-year medical student.

In her email, Theresa describes her frustrations in what she is witnessing for the first time, proceeding through her training and getting exposed to the realities of medical life.

Medical training, particularly clinical training from the 3rd and 4th years of medical school, onwards through internship, residency, and fellowship training, consists largely of bullying, "pimping" (meaning rapid-fire grilling of questions at trainees), and sleep deprivation. It is an extended hazing period meant to demoralize and inculcate the trainee into following the lead of superiors. Buck the system and you're . . . out. Imagine you've just sunk $190,000 and 8 years of college into getting to your internship. You are not going to chance being thrown out on principle. So you just swallow your pride, go along with the game, and echo all the answers they want you to repeat.

While Theresa laments the sad state of modern American pharmaceutical- and procedure-obsessed medicine, she provides me with hope that some young people training to practice medicine today will carve out their own paths, not the one laid for them by the pharmaceutical industry, nor fall for the temptation of higher-paying procedural specialties like orthopedics and cardiology. I am impressed with her ability to see this so early in her career.


Dr. Davis,

I am a 3rd year medical student at ________ University. I came across
your blog today, and I'm very glad I did. I appreciate the value of your time,
so I want to be as succinct as possible while still getting across what I'm
really thinking and feeling:

From what I gathered exploring your blog for a while this afternoon, the
wellness strategies you incorporate into your practice are some of the exact
things I want to do with my future patients. Personally, I strongly believe in
staying healthy by eating right, staying active, etc. For instance, I don't eat
grains or much in the way of starches and sugars. So I love the fact that you
are helping your patients make these powerful and foundational changes in their
lives.

As I'm sure was your experience, a full appreciation of nutrition and lifestyle
as a first-line health strategy is not something that was taught to me in
medical school. I came to school with this deep conviction already in my heart
and mind, and now, on my 3rd year rotations, I am still conflicted and at a loss
as to how I'm going to be able to practice medicine the way I want to, which is
to incorporate these all-important principles into the care of my patients.

What I've come to understand about the medical field today is that the
information that exists is primarily subsidized by the pharmaceutical industry,
and dictated to medical professionals as "evidence-based" treatment guidelines
and recommendations by organizations with sincere and official sounding names
like American Heart Association and American Cancer Society. Add to that the
pressure of potential malpractice litigation and the complexities of the
insurance reimbursement game, and it seems to me like what you get is a bunch of
diagnostic and medication management algorithms that any half-trained monkey
could follow. In his sleep. Which I guess would be alright if at least they
weren't algorithms based on misguided, self-serving, profit-seeking Big Pharma,
Food Inc, insurance conglomerates, and agri-politics (I think I just made that
word up.)

A lot of well-intentioned physicians are just parroting the party
line, as their patients dutifully and gratefully chomp down their statins and
diabetes drugs and blood pressure pills. And I'm sorry, but "diabetes
education" programs with curriculum put together by drug companies? How is that
even legal? Massive corporations raking in massive profits that are dependent
on uncontrolled blood sugars telling people how to best control their blood
sugars?!

Anyway, forgive my rant. What I'm getting at is this: How can I practice
medicine, with the freedom to educate/coach/treat my patients with diet and
lifestyle changes to mitigate/reverse their chronic health conditions? Without
feeling like I automatically have to first and foremost prescribe the litany of
drugs dictated by "evidence-based" guidelines? Without excessive fear of
litigation or loss of credibility among my peers? Without having to lie through
my teeth to my patients, and tell them that eating low-fat and heart-healthy
whole grains is the best way (implication also being the only scientifically
proven way) to control their diabetes, lower their cholesterol, etc, etc, etc?

I want my patients to have the full benefit of honest nutrition and lifestyle
information, and medications and surgery as necessary. I'm afraid that there
isn't room for this kind of holistic emphasis in the medical profession today.
Are there residencies that include this kind of training or at least respect
these "unconventional" philosophies? Are there clinics or practice groups that
would allow me to practice with this emphasis, or is there a bias against docs
who do not necessarily conform to the party position? Will I have no other
option but to go it alone under the auspices of my own shingle? How do you
handle these kinds of issues in your professional life?

Sincerely,
Theresa M.


A ray of hope! Perhaps Theresa is just the first among many more medical students who refuse to submit to the brainwashing practices of the pharmaceutical industry, the same mind manipulation that has hopelessly turned most of my colleagues into their unwitting puppets.

I'll be interested in watching how Theresa's experience unfolds. I've asked her to keep us informed every so often.

The Great Low-Carb Connector

The effusive Jimmy Moore of Livin' La Vida Low-Carb asked me to help get the word out about his new podcast subscription service, The Livin' La Vida Low-Carb Show Fan Club.

Jimmy has been The Great Connector for the low-carb discussion, from his ubiquitous online and social media presence, to his annual low-carb cruise. He has also broadcast first class interviews of nutritional notables like Gary Taubes, Dr. Robert Lustig, and blogger Stephan Guyenet. His Fan Club expands listener involvement in the podcast process and, potentially, greater access to his guests:

My faithful listeners have long been asking me about how they can become even more engaged in the behind-the-scenes workings of the show to get the inside scoop about what’s coming next. I’ve heard people ask specifically for access to transcripts of the most popular podcasts, a listing of the interviews I’m currently working on with the ability to ask questions of those guests, to have sneak peek of audio from not-yet-released interviews and more. My amazing podcast producer, Kevin Kennedy-Spaein, and I have been discussing how to best do this for a while in an effort to meet the demands of our biggest fans and we think we’ve got just the answer for you. Introducing The Livin’ La Vida Low-Carb Show Fan Club!

This is for all intents and purposes the quintessential destination for people who can’t get enough of this podcast that goes much deeper than discussion about the low-carb lifestyle. Yes, I speak with a lot of people who are supporters of carbohydrate-restricted diets, but I also talk with fitness gurus, people who support alternative eating plans, those who have interesting theories and beliefs regarding health and much more. Wouldn’t you love to have a chance to know who’s coming up in my schedule to be able to ask them questions BEFORE I interview them? Keep in mind that my interviews are pre-recorded and air sometimes as much as 5-6 months afterwards. Members of the “fan club” would know all about who’s coming and likely will have their question asked on the air just for signing up to be a part of this exciting new addition to “The Livin’ La Vida Low-Carb Show.”


Jimmy is the guy who is bringing this disparate and widely-spread community together. He's the guy we all know, he knows "everybody." I'm looking forward to seeing how this new project makes a more involved, personal delivery of interaction possible.

New Track Your Plaque record!

The record for the largest drop in heart scan score (by percentage of starting score) has been held for around three years, with 63% reduction in score.

Well, the longstanding record was broken this week: 75% reduction in score.

At the start, Freddie has disastrous lipid values:

LDL cholesterol 263 mg/dl
HDL 26 mg/dl
Triglycerides 323 mg/dl
Total cholesterol 354 mg/dl

Lipoproteins (NMR) were worse:

LDL particle number 3360 nmol/L
Small LDL 2677 nmol/L

Heart scan score: 732

Interestingly, Freddie had virtually no vitamin D in his body, with a 25-hydroxy vitamin D level that was unmeasurable.

Freddie was miserably intolerant to statin drugs, with even the smallest dose resulting in intolerable muscle aches. That's when his doctor sent him to me.

Because I felt that the dominant abnormality in Freddie's lipids and lipoproteins was small LDL particles, representing 80% of total LDL particle number, we focused his program on correcting this parameter. Freddie's program was therefore focused elimination of wheat, cornstarch, oats, and sugars, along with an eventual vitamin D dose of 20,000 units to finally achieve a 25-hydroxy vitamin D level of 66 ng/ml. No statin drug in sight.

43 lbs of weight loss and 18 months later, a second heart scan score: 183--a 75% reduction.

While the rest of the world continues to insist that coronary calcium (heart scan) scores cannot be reduced, I am seeing records being broken. I add Freddie's experience to the rapidly growing list of people who have not just stopped coronary plaque from growing, but are seizing control and reducing it, sometimes to dramatic degrees.

The Anti-AGEing Diet

Advanced Glycation End-products, AGEs, are a diverse collection of compounds that have been associated with endothelial dysfunction, cataracts, kidney disease, and atherosclerosis in both animal models and human studies. Not all involve glycation nor glucose, but the catch-all name has stuck.

There are a number of actively-held theories of aging, such as the idea that aging is the result of accumulated products of oxidative injury; a genetically pre-programmed script of declining hormones and other phenomena; genetic "mis-reading" that results in disordered gene expression, debris, and uncontrolled cell proliferation (e.g., cancer); among others.

One of the fascinating theories of aging is, cutely, the AGEing theory of aging, i.e., the accumulation of AGE debris in various tissues. Such AGEs have been recovered in lenses from the eyes, atherosclerotic plaque in arteries, kidney and liver tissue, even brain tissue of people with Alzheimer's dementia. AGEs perform no known useful physiologic function: They are relatively inert once formed (especially polymeric AGEs), they do not participate in communication, they make no contribution of significance. They simply gum up the works--debris. (AGEs are to health as the USDA food pyramid is to dietary advice: material for the junkyard.)

There are two general ways to develop AGEs:

1) Endogenous--High blood glucose (any blood sugar above 100 mg/dl) will permit glycation of the various proteins of the body. The higher the blood glucose, the more glycation will proceed. Glycation also occurs at low velocity at blood glucose levels below 100 mg/dl, though this would therefore represent the "normal," expected rate of glycation. Endogenous glycation explains why people with diabetes appear to age and develop all the phenomena of aging faster than non-diabetics (kidney disease, eye diseases, atherosclerosis, dementia, etc.). Hemoglobin A1c, HbA1c, is a readily-obtainable blood test that can show how enthusiastically you have been glycating proteins (hemoglobin, in this case) over the last 2 to 3 months.

A low-carbohydrate diet is the nutritional path that limits endogenous glycation leading to AGE formation. Restricting the most obnoxious carbohydrates, the ones that increase blood sugar the most, such as wheat, cornstarch, rice starch, potato starch, tapioca starch, and sucrose, will limit endogenous AGE formation.

2) Exogenous--AGEs (here especially is where the "AGE" label is misleading, since many other reactions besides glycation lead to such compounds) are formed with cooking at high temperatures, especially meats and animal products. Therefore, a rare steak will have far less than a well-done steak. A thoroughly baked piece of salmon will have greater AGE content than sashimi.

The forms of cooking that increase AGE content the most: roasting,deep-frying, and barbecuing. Temperatures of 350 degrees Fahrenheit and greater increase AGE formation.

Therefore, cooking foods at lower temperature (e.g., baking, sauteeing, or boiling), eating meats rare whenever possible (not chicken or pork, of course), eating raw foods whenever possible (e.g., nuts) are all strategies that limit exogenous AGE exposure. And minimize or avoid butter use, if we are to believe the data that suggest that it contains the highest exogenous AGE content of any known food.

If we connect the dots and limit exposure to both endogenous and exogenous AGEs, we will therefore not trigger this collection of debris that is likely associated with disease and aging. So following a low-AGE diet may also be an anti-aging strategy.

The New Track Your Plaque Diet, soon to be released on the Track Your Plaque website, has incorporated strategies to limit both endogenous as well as exogenous AGEs.