Report from Washington II

Today's discussions at the Society for Cardiovascular Computed Tomography (SCCT) focused on atherosclerotic "plaque characterization".

As CT scanners get better and better at imaging the various components of plaque, some fascinating issues emerge:

--CT heart scans provide insights into what exactly is contained in an individual's atherosclerotic plaque that are not often provided even during heart catheterization. In other words, CT heart scanning is, in many instances, superior to heart catheterization, since it provides images of the artery wall, not just the internal contents.

--Progression (i.e., increase) in heart scan score is a powerful predicter of heart attack risk. Dr. Matthew Budoff of UCLA argued persuasively that the annual rate of increase in score is probably the most accurate measure of risk available, superior to cholesterol and calculated measures like the Framingham risk score.

--Coronary calcium scoring remains the best method to gauge total plaque throughout the entire coronary tree. In a person free of symptoms, the risk of a cardiac "event" (heart attack, death, procedures) is low and additional imaging (like CT angiography) is generally unnecessary.


Dr. Budoff, among the true thought leaders in CT heart scanning, also recounted his perspective on the history of heart scans. He noted that the questions asked through the years have evolved:




1995-2000 Should we do coronary calcium scans?

2000-2002 Do high or low risk patients benefit from coronary calcium scoring?

2003-2004 What is the better scanner, EBT or MDCT?

2006 How often should we perform coronary calcium imaging?


I believe that Dr. Budoff summarizes wonderfully where the Track Your Plaque programs fits into the overall scheme of things: Serial (repeated)CT heart scans to gauge progression or reversal is the wave of the future. We shouldn't just be interested in identifying persons at risk for heart attack. We should also be interested in showing the person at risk exactly how to reduce or eliminate that risk.

Report from Washington





I'm presently attending the Society for Cardiovascular Computed Tomography meetings in Washington, DC, along with 500 of my colleagues. It's exciting to see how interest in CT scanning for heart disease has balloonned in the past couple of years.

Several trends are noticeable today, based on the content and tone of the discussions:

--CT scanning of the heart, and imaging in general, is just getting started. In other words, the capabilities for CT scanners and other devices to detect heart disease (coronary and otherwise) are where the gasoline engine was in the 19th century. Scanning is getting faster, easier, safer, and more precise. Just as few people in 1905 could have predicted that automobiles would be computer-enhanced, high-speed, ubiquitous devices with several per household, the potential for CT imaging for heart disease is truly in its infancy.

--CT coronary angiography (so-called "64-slice CT scans") are not screening tests for hidden coronary disease in people without symptoms. I was grateful that this point has been made and reiterated by several speakers, as this is consistent with our views. Simple CT heart scans for coronary calcium scoring, in contrast, are screening tests. When the radiation exposure of CT angiograms are reduced to tolerable levels, then they may be used as screening tests. We are probably 3-4 years away from this point.

--Both stress testing and heart catheterizations will be partially replaced by CT scanning. In particular, over the next decade, you will see a dramatic drop in unnecessary catheterizations, i.e,, far less people saying "I had a heart cath but they told me that it was normal."


There has been heavy focus on applications of CT scanning for acute settings, particularly the emergency room and hospitals.

What has surprised me is that there is virtually no conversation whatsoever about the preventive uses of CT heart scanning. So far, only Dr. Daniel Berman of UCLA has shown that he has "seen the light": CT scans are a crucial tool for identification of early coronary plaque, and this tells us whether prevention is necessary and with what intensity.

There has been, however, no discussion at all about quantification of plaque in a program of reversal. Perhaps that should come as no surprise, given the imaging-technology focus of this convention. For most of my colleagues, prevention is also not terribly interesting. Identification and treatment of acute disease like impending heart attack is.

Of course, applying the information from your CT heart scan to empower you in a program and reversal is what the Track Your Plaque program is all about. I hope you see the light. I admit that it's not always easy to follow what we are advocating here. Perhaps not too different than telling someone in his horse-drawn buggy that one day he'll be driving a sleek car with onboard computerized mapping, air-conditioning, and micro-chips to modulate engine performance. He's probably tell us we're nuts.

I'll continue to update if any news relevant to our interests crops up in these meetings.

What about the Track Your Plaque failures?

I’d love to tell you that the Track Your Plaque program track record is of 100% success. It’s not.

It is very successful. But we’ve had some people who have failed and failed BIG. These are the people who've undergone bypass surgery, received one or more stents, or had heart attacks. Lesser failures are the people who’ve had large, undesirable increases in heart scan scores of >30% in one year. (The expected rate of increase in your heart scan score without preventive efforts is 30% per year, on average.)

What can we learn from those failures? There were several characteristics that stand out among this small group:

· Non-compliance--meaning they just didn’t stick with it. They started out right but then rapidly lost interest in maintaining all the pieces of the program and neglected their fish oil, niacin, gain weight, etc. Matthew did this and ended up with three stents to his left anterior descending. His slow start was due to skepticism that the program worked and just plain forgetfulness.

· Extreme stress--One of our earliest failures was a 38-year old man whose heart scan score doubled in one year, despite doing everything right. But three family members, all close to him, died within the space of six months, including his mother and a brother. I regard this as one of those instances in which we were powerless, unfortunately, though it is a graphic example of the power of unresolved stress and grief.

· Having a “better way”--These are the couple of people who were convinced that they had a better way to control their heart scan score. David firmly believed that his two dozen supplements and exercise program would drop his score. Instead, they permitted a 42% increase. Lee relied exclusively on chelation, along with several supplements of his own design. Lee had three-vessel bypass surgery.

· Starting too late--Gerome started with a score of 1179, but also was having chest pressure with emotional stress. His stress test was abnormal, with the entire upper half of his heart not receiving blood with exercise on a stress nuclear study (“anterior ischemia”). Gerome received four bypass grafts. Unfortunately, Gerome never really had a chance to engage in the Track Your Plaque program, since his health and safety were in jeopardy as soon as he started.

Have we had any big failures of people who did everything right, were compliant, were not subject to extreme stress (more than just job stress, or financial worries), didn’t neglect the basic requirements of the Track Your Plaque program, and had sufficient time (at least 6 months to 1 year)? No, thankfully, we have not.

No one who has stuck to the program has had a big failure.

Be smarter than your cardiologist

“Do you need a stent?”

Sad to say, but that sentence condenses the wisdom of over 90% of practicing cardiologists.

Prevention of heart disease means take Lipitor or some other statin and cutting the saturated fat in your diet. That’s it. Maybe throw in exercise.

Regression of coronary plaque? That phrase has only entered the conversation since the AstraZeneca-supported trial of Crestor succeeded in achieving 8% regression of plaque (Track Your Plaque Members: See News) as demonstrated by intracoronary ultrasound.



In other words, in the minds of my colleagues, it can’t be true until a drug company tells them it’s true. It’s beyond me why this brainwashing of otherwise intelligent people has occurred, but it is blatantly evident in practice.

Fish oil is another example. The spectacular benefits of fish oil have been known for 20 years. But only recently has it become a “mainstream” practice to recommend fish oil, largely because a drug manufacturer has put a preparation through the rigors of FDA approval (Omacor) and is now marketing directly to physicians. All of a sudden, fish oil is a good thing? No, it’s just achieved legitimacy in the eyes of practitioners because it graces marketing literature.

If you’re reading this, you’re likely interested in coronary plaque regression using the only tool available for you to measure, track, and regress coronary plaque: CT heart scans. Intracoronary ultrasound will achieve the same goal, but it is an invasive procedure performed at heart catheterization, involves threading a wire and imaging probe all the way down the artery, involves real risk of tearing the inner lining of the artery, and is costly (around $14,000-$20,000 for the entire package). Do it every year? That’d be nuts.

If you’re thinking about coronary plaque regression, using fish oil, concerned about patterns like low HDL and small LDL, aware of the vitamin D deficiency issue as a coronary risk factor, etc., you are far more aware than the vast majority of practicing cardiologists. They are interested in what new brand of anti-coagulant to use during their heart catheterization (because the product representative gushes about the new agent—only $1200 a dose!). Or, they are interested in gaining the procedural skills to put in a new device like a biventricular pacemaker. Regress/reverse coronary plaque? What for?

You already know that a conversation about coronary plaque reversal will not be obtained in your cardiologist’s office. Your family practice doctor or internist? Fat chance! Knee arthritis, pap smears, pneumovax inoculations, sore throats, gout, back pain—they’re spread far too thin to know anything more than the most superficial amount about coronary plaque control. Most know nothing.

That’s where we come in. That’s our mission: Educate people about the extraordinary tools that you have available to you, all in the cause of control or reversal of coronary plaque.

Why am I here?

Frank came to the office for an opinion, sent by his (proactive) family physician.

"I really don't know why I'm here, to be honest."

Two years earlier, Frank had a heart attack, survived and received two stents to his circumflex coronary artery. He now took Zocor and his LDL cholesterol was a reasonably favorable 89 mg, total cholesterol 183 mg.

"I walk with my wife every other day. I've been avoiding fish fries. You'll never see me eat fast food."

Frank was correct: If we were going to engage in the conventional approach to coronary disease, Frank was on the right track. We would have postponed his next heart attack or procedure by a couple of years. Stroke, aneurysm, and other atherosclerotic manifestations would be set back, likewise, a few years.

Would Frank have profound control over his disease? Absolutely not. In fact, his disease had probably advanced a huge amount just in the two years since his stents were placed and he was on his "prevention" program. Without his current effort, his coronary plaque would be expected to grow 30% per year. On Zocor and his modest lifestyle efforts, plaque growth was probably in the 14-28% per year range.

So I explained the unique Track Your Plaque approach to Frank. First, we start with a CT heart scan to establish where he was starting. Although he had two stents in his circumflex artery, we still had two other arteries (LAD, right coronary) to score and track.

We then attempt to identify all hidden causes of his heart disease and then correct them.

Of course, Frank had multiple hidden causes:

--HDL too low at 38 mg/dl
--Small LDL-severe, in fact, with 95% of all LDL particles in the small category
--Triglycerides too high
--Excesses of several triglyceride-containing particles (VLDL, IDL)
--Pre-diabetes--Frank had both a borderline high blood sugar and a high insulin level. This is a sure-fire stimulus to coronary plaque growth.
--A severe deficiency of vitamin D (<20 ng/ml)
--An excessivelyhigh blood pressure during exercise--With a blood pressure of 190/102 on the treadmill.

There were others(!), but that was the bulk of the causes behind Frank's coronary disease.

Once Frank recognized that there was indeed a huge panel of hidden causes for heart disease, not just too much fat in his diet and LDL cholesterol, he jumped into the program head first.

The message: The conventional approach is absurdly oversimplified, a certain path to failure for the majority of people. Even if you don't have known coronary disease like Frank, but just have a heart scan score >zero, the same principles apply to you.

Catheterization to “define coronary anatomy”

Gary is an avid jogger. On an average day, he runs 5-6 miles at a good clip. On two occasions recently, however, Gary experienced an ache in his left shoulder at mile 4. It was a toothache-like feeling, but he kept on going without difficulty.

Gary also had a heart scan score of 370.

Upon hearing of Gary’s score and his shoulder sensation, the cardiologist who saw him advised a heart catheterization “to define coronary anatomy”. (This is a real incident.)


What exactly does that mean? Why would Gary’s cardiologist need to define it?

In my view, this is an absurd notion. No one needs to “define coronary anatomy”. This catch-all phrase is commonly used to justify heart procedures. I believe what the cardiologist is saying is that it’s the easiest (for the cardiologist) and perhaps most generously reimbursed method to determine whether Gary’s symptoms are warning of an impending heart attack or not.

The problem is that the question can also be answered quite well by doing a stress test. Though not perfect diagnostic tests, stress tests are useful when symptoms are present that are doubtful in nature. Gary’s left shoulder ache could have been related to his heart, but the likelihood was that it was not. A stress test would have answered the diagnostic question quite adequately.

Instead, this man was subjected to an invasive test that was likely unnecessary. This happens dozens, if not hundreds, of times per day just around here. Nationwide, it is an epidemic of malpractice.

There are, indeed, times when a person should proceed directly to a heart catheterization. This is commonly and appropriately performed when a person develops unstable heart symptoms, such as chest discomfort or breathlessness at rest while not doing anything physical, or if the frequency is increasing, or if a stress test shows an important abnormality. There is no question that heart procedures can be lifesaving at times.

The problem is that thousands of people every year are scared into these procedures inappropriately. Beware!

It doesn't matter what I eat!

"How are your food choices?" I asked.

"What does it matter, doc? I take Lipitor. Doesn't that take care of it? I eat what I want!"

So declared Matthew. What he "wanted" was pretty much the diet of a teenager: pizza, cheeseburgers, soft drinks, snacks. His "beer belly" (visceral fat) gave it away. So did his blood work that showed flagrant lipoprotein abnormalities--small LDL, an HDL of 37 mg, and a severe after-eating flood of fat represented by increased "intermediate-density lipoprotein" (IDL).

Like many people, Matthew had been persuaded (or chose to believe) that LDL cholesterol was the sole cause for heart disease. Lipitor was therefore was all he needed. It must be great--how else could they afford all those slick TV commercials?

Well, it is definitely not true. In fact, with the persistence of Matthew's abnormal lipoprotein patterns, we should expect his heart scan score to continue to grow by 30%--the very same rate of increase as if he were taking nothing.

Specifically, Lipitor and drugs like it do not:

--Raise HDL.

--Correct or reduce the proportion of small LDL.

--Block after-eating flood of fat, nor do they accelerate clearance of unhealthy fats persisting in the bloodstream after eating.


Yes, what you eat does have real consequences, even if you take a statin drugs. In fact, the foods you ingest have a remarkably rapid and dramatic effect on what your blood contains. Any diabetic who checks his/her blood sugar knows this. They eat a slice of whole wheat toast and watch their blood sugar skyrocket.

Mind what you eat. Make it enjoyable, of course. But drugs do not provide impunity.

People with higher scores need to try harder

Sam is a 69-year retired physician. He was thoroughly enjoying retirement: golf, travelling, going out to dinner two or three times a week, spending weekends with his grandchildren. His lifestyle tended towards overindulgence, but he managed to stay fit and trim. At 6 ft 1 inch, he weighed 194 lbs and could still run 3 miles without too much difficulty. Not as good as his marathon-running days, but still not too bad for 69.

Sam's heart scan score in 2003 was a concerning 1983--extensive plaque. His doctor wasn't much help in interpreting the scan and so Sam simply chose to ignore it.

A chance conversation with a physician friend 18 months later made Sam think that perhaps this shouldn't be ignored. That's when he came to my office.




I find that sometimes the best way to motivate someone to take action is to demonstrate just how fast plaque grows if action isn't taken. So I advised Sam to get another scan first, since 18 months had passed. His score: 2441, or a 23% increase.




Sam was now starting to catch on. We made several changes in his prevention program (starting from virtually nothing). He did undergo a stress nuclear (thallium type) of test, which he passed without difficulty--normal blood flow in all heart territories despite the extensive plaque.

But, for some reason, Sam simply allowed himself to drift back to old habits: poor choices in food, overindulging in hard liquor, missing his fish oil and other supplements, and his medication, sometimes up to several days a week.

Sam started having unusual feelings in his chest. He described a sort of nervousness along with skipped heart beats. So we repeated a stress test. This time, a large area of reduced blood flow in the front of his heart ("anterior left ventricle") was detected. Sam ended up receiving three stents in a difficult procedure.

The moral: If you're starting out with a lower heart scan score of, say, 100 or 200, maybe you'll get by without trying too hard--maybe. But if your score is higher, say, several hundred or in the thousands, you got to try harder.

You're starting later in the process. Your disease will allow you very little slack. Let your guard down and it will get you. Control over your plaque is, indeed, very possible--we do it all the time. Score reduction is also possible. But your effort must be more serious and consistent.

Money can't buy health

Fallen Enron CEO, Kenneth Lay, was pronounced dead early this a.m. after suffering a heart attack.

Mr. Lay apparently had no history of heart disease and there's been no indication that symptoms provided any warning. His death was therefore classified as "sudden cardiac death".


Yet here's a man previously worth hundreds of millions of dollars with access to any test or medical system he desired--many times over. Even more recently, with his wealth reduced following his legal troubles, he and his wife managed to put away $4 million dollars to ensure an income from the interest through annuities, untouchable by the courts.

Detecting Mr. Lay's heart disease would have cost him around a few hundred dollars or whatever it costs for a CT heart scan in his city. This would have alerted his (hopefully knowledgeable) doctor that he was a time-bomb. Pile on all the stress he'd been suffering, whether deserved or no, and the diagnosis would have required little thought.

Instead, Mr. Lay has joined the thousands of Americans who will die this year because of failing to get a simple, 30-second test that costs one-tenth the cost of a stress test. Mr. Lay wasn't as lucky as former President Bill Clinton, whose doctors likewise blundered their way through and missed obvious levels of heart disease.

All Mr. Lay needed was better information: get a heart scan, then follow a program of prevention like the Track Your Plaque program. You may not have hundreds of millions of dollars, but you have the information on how to not follow in Ken Lay's footsteps. Track Your Plaque--and stay alive.

What's important, what's not in your plaque-control program

Sometimes it's hard to know what is really important in your plaque-control or plaque-reducing efforts.

There are, indeed, crucial make-it-or-break-it factors that are necessary to gain control over plaque. If you hope to stack the odds of reducing your heart scan score as much as possible in your favor, then fish oil, vitamin D, 60-60-60 in the way of standard lipids, elimination of small LDL, etc. -- all the elements of the Track Your Plaque program--are necessary.

But there's lots of things that sidetrack people. I spend much of my day fielding questions from patients about all the things that either provide very little benefit for plaque control, or provide none at all.

Among the things that we have found to be too weak or useless for plaque control, or are "non-issues", include:

--Caffeine--Go ahead and enjoy a couple cups a day (though not a pot). The effect is too trivial to make much difference.

--Hawthorne--Yes, it may dilate coronary arteries modestly, but not enough to make any difference.

--Garlic--with the possible exception of a specific preparation called Aged Garlic Extract (an acqueous, non-oil-based, extract from Kyolic), garlic's effects are too tiny to help, e.g., drop in blood pressure 1-2 points. Use it, but don't expect much. Aged Garlic Extract may be an exception, in that a single study from UCLA suggested specific effects on slowing coronary plaque growth. We await more info on this.

--Anti-oxidants--There is no shortage of extravagant claims about the benefits of anti-oxidants. Unfortunately, there's very little human exerience with pine bark extract, pycnogenol, grapeseed extract, and so on. Is the purported benefit from anti-oxidation or through some other means, e.g., enhancement of nitric oxide synthase? No data.

--Policosanol--If you've followed the Track Your Plaque Special Reports, you already know what a disappointment this agent has been, despite the too-good-to-be-true clinical data. It doesn't work.

--"No-flush niacin"--Unfortunately, no flush, no effect. This high-priced supplement is still sold widely in the U.S. despite its complete lack of efficacy. It does not work in humans. (It works great in rats!)

Track Your Plaque continues to try to be the arbiter of truth in what works, what doesn't in truly stopping or reversing your coronary plaque. The proof positive? Stopping or dropping your heart scan score.
All posts by william-davis

Medicine ain't what it used to be

The practice of medicine ain't what it used to be.

For instance:

White coats are out-of-date--Not only do they serve as filthy reservoirs of microorganisms (since they hang unwashed after repeated use week after week), they only serve to distance the practitioner from the patient, an outdated notion that should join electroshock therapy to treat homosexuality and other "disorders" in the museum of outdated medical practices.

Normal cholesterol panel . . . no heart disease?

I often hear this comment: "I have a normal cholesterol panel. So I have low risk for heart disease, right?"

While there's a germ of truth in the statement, there are many exceptions. Having "normal" cholesterol values is far from a guarantee that you won't drop over at your daughter's wedding or find yourself lying on a gurney at your nearest profit-center-for-health, aka hospital, heading for the cath lab.

Statistically, large populations do indeed show fewer heart attacks at the lower end of the curve for low total and  LDL cholesterol and the higher end of HDL. But that's on a population basis. When applied to a specific individual, population observations can fall apart. Heart attack can occur at the low risk end of the curve; no heart attack can occur at the high risk end of the curve.

First of all, to me a "normal" lipid panel is not adhering to the lax notion of "normal" specified in the lab's "reference range" drawn from population observations. Most labs, for instance, specify that an HDL cholesterol of 40 mg/dl or more and triglycerides of 150 mg/dl or less are in the normal ranges. However, heart disease can readily occur with normal values of, say, an HDL of 48 mg/dl and triglycerides of 125 mg/dl, both of which allow substantial small oxidation-prone LDL particles to develop. So "normal" may not be ideal or desirable. Look at any study comparing people with heart disease vs. those without, for instance: Typical HDLs in people with heart attacks are around 46 mg/dl, while HDLs in people without heart attacks typically average 48 mg/dl--there is nearly perfect overlap in the distribution curves.

There are also causes for heart disease that are not revealed by the lipid values. Lipoprotein(a), or Lp(a), is among the most important exceptions: You can have a heart attack, stroke, three stents or bypass surgery at age 40 even with spectacular lipid values if you have this genetically-determined condition. And it's not rare, since 11% of the population express it. How about people with the apo E2 genetic variation? These people tend to have normal fasting cholesterol values (if they have only one copy of E2, not two) but have extravagant abnormalities after they eat that contribute to risk. You won't know this from a standard cholesterol panel.

Vitamin D deficiency can be suggested by low HDL and omega-3 fatty acid deficiency suggested by higher triglycerides, but deficiencies of both can exist in severe degrees even with reasonably favorable ranges for both lipid values. Despite the recent inane comments by the Institute of Medicine committee, from what I've witnessed from replacing vitamin D to achieve serum 25-hydroxy vitamin D levels of 60-70 ng/ml, vitamin D deficiency is among the most powerful and correctable causes of heart disease I've ever seen. And, while greater quantities of omega-3 fatty acids from fish oil are associated with lower triglycerides, they are even better at reducing postprandial phenomena, i.e., the after-eating flood of lipoproteins like VLDL and chylomicron remnants, that underlie formation of much atherosclerotic plaque--but not revealed by fasting lipids.

I view standard cholesterol panels as the 1963 version of heart disease prediction. We've come a long way since then and we now have far better tools for prediction of heart attack. Yet the majority of physicians and the public still follow the outdated notion that a cholesterol panel is sufficient to predict your heart's future. Nostalgic, quaint perhaps, but as outdated as transistor radios and prime time acts on the Ed Sullivan show.

 

Idiot farm

The notion of genetic modification of foods and livestock is a contentious issue. The purposeful insertion or deletion of a gene into a plant or animal's genome to yield specific traits, such as herbicide resistance, nutritional composition, or size, prompted the Codex Alimentarius Commission, an international effort to regulate the safety of foods, to issue guidelines concerning genetically-modified foods.

The committee is aware of the concept of unintended effects, i.e., effects that were not part of the original gene insertion or deletion design. In their report, last updated in 2009, they state that:

Unintended effects can result from the random insertion of DNA sequences into the plant genome, which may cause disruption or silencing of existing genes, activation of silent genes, or modifications in the expression of existing genes. Unintended effects may also result in the formation of new or changed patterns of metabolites. For example, the expression of enzymes at high levels may give rise to secondary biochemical effects or changes in the regulation of metabolic pathways and/or altered levels of metabolites.

They make the point that food crops generated using techniques without genetic modification are released into the food supply without safety testing:

New varieties of corn, soybean, potatoes and other common food plants are evaluated by breeders for agronomic and phenotypic characteristics, but generally, foods derived from such new plant varieties are not subjected to the rigorous and extensive food safety testing procedures, including studies in animals, that are typical of chemicals, such as food additives or pesticide residues, that may be present in food.

In other words, conventional plant breeding techniques, such as hybridization, backcrossing, and introgression, practices that include crossing parental plants with their progeny over and over again or crossing a plant with an unrelated plant, yield unique plants that are not subject to any regulation. This means that unintended effects that arise are often not identified or tested. Plant geneticists know that, when one plant is crossed with another, approximately 5% of the genes in the offspring are unique to that plant and not present in either parent. It means that offspring may express new characteristics, such as unique gliadin or gluten proteins in wheat, not expressed in either parent and with new immunological potential in consuming humans.

Dr. James Maryanski, the FDA's Biotechnology Coordinator, stated during Congressional testimony in 1999 that:

The new gene splicing techniques are being used to achieve many of the same goals and improvements that plant breeders have sought through conventional methods. Today's techniques are different from their predecessors in two significant ways. First, they can be used with greater precision and allow for more complete characterization and, therefore, greater predictability about the qualities of the new variety. These techniques give scientists the ability to isolate genes and to introduce new traits into foods without simultaneously introducing many other undesirable traits, as may occur with traditional breeding. [Emphasis mine.]

Efforts by the Codex Alimentarius and FDA are meant to control the introduction and specify safety testing procedures for genetically modified foods. But both organizations have publicly stated that there is another larger problem that has not been addressed that predates genetic modification. In other words, conventional methods like hybridization techniques, the crossing of different strains of a crop or crossing two dissimilar plants (e.g., wheat with a wild grass) have been practiced for decades before genetic modification became possible. And it is still going on.

In other words, the potential hazards of hybridization, often taken to extremes, have essentially been ignored. Hybridized plants are introduced into the food supply with no question of human safety. While hybridization can yield what appear to be benign foods, such as the tangelo, a hybrid of tangerines and grapefruit, it can also yield plants containing extensive unintended effects. It means that unique immunological sequences can be generated. It might be a unique gliadin sequence in wheat or a unique lectin sequence in beans. None are tested prior to selling to humans. So the world frets over the potential dangers of genetic modification while, all along, the much larger hazard of hybridization techniques have been--and still are--going on.

Imagine we applied the hybridization techniques applied by plant geneticists to humans, mating an uncle with his niece, then having the uncle mate again with the offspring, repeating it over and over until some trait was fully expressed. Such extensive inbreeding was practiced in the 19th century German village of Dilsberg, what Mark Twain described as "a thriving and diligent idiot factory."

Eat triglycerides

Dietary fats, from olive oil to cocoa butter to beef tallow, are made of triglycerides.

Triglycerides are simply three ("tri-") fatty acids attached to a glycerol backbone. Glycerol is a simple 3-carbon molecule that readily binds fatty acids. Fatty acids, of course, can be saturated, polyunsaturated, and monounsaturated.

Once ingested, the action of the pancreatic enzyme, pancreatic lipase, along with bile acids secreted by the gallbladder, remove triglycerides from glycerol. Triglycerides pass through the intestinal wall and are "repackaged" into large complex triglyceride-rich (about 90% triglycerides) molecules called chylomicrons, which then pass into the lymphatic system, then to the bloodstream. The liver takes up chylomicrons, removes triglycerides which are then repackaged into triglyceride-rich very low-density lipoproteins (VLDL).

So eating triglycerides increases blood levels of triglycerides, repackaged as chylomicrons and VLDL.

Many physicians are frightened of dietary triglycerides, i.e, fats, for fear it will increase blood levels of triglycerides. It's true: Consuming triglycerides does indeed increase blood levels of triglycerides--but only a little bit. Following a fat-rich meal of, say, a 3-egg omelet with 2 tablespoons of olive oil and 2 oz whole milk mozzarella cheese (total 55 grams triglycerides), blood triglycerides will increase modestly. A typical response would be an increase from 60 mg/dl to 80 mg/dl--an increase, but quite small.

Counterintuitively, it's the foods that convert to triglycerides in the liver that send triglycerides up, not 20 mg/dl, but 200, 400, or 1000 mg/dl or more. What foods convert to triglycerides in the liver? Carbohydrates.

After swallowing a piece of multigrain bread, for instance, carbohydrates are released by salivary and gastric amylase, yielding glucose molecules. Glucose is rapidly absorbed through the intestinal tract and into the liver. The liver is magnificently efficient at storing carbohydrate calories by converting them to the body's principal currency of energy, triglycerides, via the process of de novo lipogenesis, the alchemy of converting glucose into triglycerides for storage. The effect is not immediate; it may require many hours for the liver to do its thing, increasing blood triglycerides many hours after the carbohydrate meal.

This explains why people who follow low-fat diets typically have high triglyceride levels--despite limited ingestion of triglycerides. When I cut my calories from fat to 10% or less--a very strict low-fat diet--my triglycerides are 350 mg/dl. When I slash my carbohydrates to 40-50 grams per day but ingest unlimited triglycerides like olive oil, raw nuts, whole milk cheese, fish oil and fish, etc., my triglycerides are 50 mg/dl.

Don't be afraid of triglycerides. But be very careful with the foods that convert to triglycerides: carbohydrates.

 

 

 

 

 

 

 

You've come a long way, baby

In 1945, the room-sized ENIAC vacuum tube computer was first turned on, women began to smoke openly in public, and a US postal stamp cost three cents. And this was the US government's advice on healthy eating:



 

 

 

 

 

 

 

 

 

 

 

 

 

Green and yellow vegetables; oranges, tomatoes, grapefruit; potatoes and other vegetables and fruits; followed by milk and milk products; meat, poultry, fish, or eggs; bread, flour, and cereals, butter and fortified margarine.

In 2011, the computing power of the ENIAC can be performed by a microchip a few millimeters in width, smoking is now banned in public places, and a first class postage stamp has increased in price by 1466%. And this is the new USDA Food Plate for Americans:



 

 

 

 

 

Have we made any progress over the past 65 years? We certainly have in computing power and awareness of the adverse effects of smoking. But have US government agencies like the USDA kept up with nutritional advice? Compare the 2011 Food Plate with the dietary advice of 1945.

It looks to me like the USDA has not only failed to keep up with the evolution of nutritional thought, but has regressed to something close to advising Americans to go out and buy stocks on the eve of the 1929 depression. Most of us discuss issues like the genetic distortions introduced into wheat, corn, and soy; the dangers of fructose; exogenous glycoxidation and lipoxidation products yielded via high-temperature cooking; organic, free-range meats and the dangers of factory farming, etc. None of this, of course, fits the agenda of the USDA.

My advice: The USDA should stay out of the business of offering nutritional advice. They are very bad at it. They also have too many hidden motives to be a reliable source of unbiased information.

 

 

Fasting with green tea

I've been playing around with brief (18-24 hour) fasts with the use of green tea. Of the several variations on fasting, such as juice "fasts,"  I've been most impressed with the green tea experience.

While the weight loss effects of daily green tea consumption are modest, there seems to be a specific satiety effect that has now been demonstrated in multiple studies, such as this and this. In other words, green tea, through an uncertain mechanism, reduces hunger. The effect is not just due to volume, since the effect cannot be reproduced with hot water alone.

I therefore wondered whether green tea might be a useful beverage to consume during a fast, as it might take the "edge" off of hunger. While hunger during a fast in the wheat-free is far less than wheat-consuming humans, there is indeed an occasional twinge of hunger felt.

So I tried it, brewing a fresh 6-8 oz cup evert two hours or so. I brewed a pot in the morning while at home, followed by brewing single cups using my tea infuser at the office. Whenever I began to experience a hunger pang, I brewed another cup and sipped it. I was pleasantly surprised that hunger was considerably reduced. I sailed through my last 18 hours, for instance, effortlessly. The process was actually quite pleasant.

I brew loose Chinese bancha, sencha, and chunmee teas and Japanese gyokuro tea. Gyokuro is my favorite, but also the most expensive. Bancha is more affordable and I've used that most frequently.

If anyone else gives this a try, please report back your experience.

Dreamfields pasta is wheat

An active question on the blogosphere and elsewhere is whether Dreamfields pasta is truly low-carb. Dr. Andreas Eenfeldt of Diet Doctor detailed his high blood glucose experience with it. Jimmy Moore of Livin' La Vida Low Carb had a similar experience, observing virtually no difference when compared to conventional pasta.

The Dreamfields people make the claim that "Dreamfields' patent-pending recipe and manufacturing process protects all but 5 grams of the carbohydrates per serving from being digested and therefore lessens post-meal blood glucose rise as compared to traditional pasta." They call the modified carbohydrates "protected" carbs.



In other words, they are making the claim that they've somehow modified the amylopectin A and amylose molecules in durum wheat flour to inhibit conversion to glucose.

I'd like to add something to the conversation: Dreamfields pasta is wheat. It is a graphic demonstration that, no matter how you cut it, press it, sauce it up, "protect" it, it's all the same thing: wheat. (It reminds me of a bad girlfriend I had in my 20s: She'd put on makeup, a pretty dress, I'd take her out someplace nice . . . She was still an annoying person who whined about everything.)

Wheat is more than a carbohydrate. It is also a collection of over 1000 proteins, including gliadins, glutens, and glutenins. Gliadins, for instance, are degraded to polypeptide exorphins that underlie the addictive potential of wheat, as well as its withdrawal phenomenon on halting consumption. Gliadin-derived exorphins are also the triggers of auditory hallucinations and paranoid delusions in schizophrenia, as well as behavioral outbursts in children with ADHD and autism.

Wheat is a source of lectins that have the curious effect of "unlocking" the proteins of the intestinal lining, the oddly-named "zonulin" proteins, that protect you from ingested foreign molecules. Ingest wheat lectins and all manner of foreign molecules gain entry into your bloodstream. Cholera works by a similar mechanism. (How about a love story: Bread in the time of cholera?)

Glutens, of course, are responsible for triggering celiac disease, the devastating small intestinal disease that now afflicts 3 million Americans, although 2.7 million don't even know it. Glutens are also responsible for neurologic conditions like cerebellar ataxia, peripheral neuropathy, and dementia ("gluten encephalopathy") and the skin condition, dermatitis herpetiformis.

Then there are the conditions for which the active wheat components have not been identified, including acid reflux, irritable bowel syndrome, asthma (excepting "bakers' asthma), rheumatoid arthritis, edema and fluid retention, and a long list of skin conditions from alopecia to gangrene.

My point: Yeah, Dreamfields pastas, from these instructive experiences, acts a lot like conventional durum wheat pasta. But, even if Dreamfields or somebody else perfects the low-carb aspect of it, it's still wheat. Modern wheat is the genetically tarted-up version of Triticum aestivum, the product of genetic shenanigans from the 1960s and 1970s.

Bet you can't fast

People who continue to consume the world's most destructive grain, i.e., wheat, can rarely endure fasting--not eating for an extended period--except by mustering up monumental willpower. That's because wheat is a powerful appetite stimulant through its 2-hour cycle of exaggerated glycemia followed by a glucose low, along with its addictive exorphin effect. Wheat elimination is therefore an important first step towards allowing you to consider fasting.

Why fast? I regard fasting as among the most underappreciated and underutilized strategies for health.

In its purest form, fasting means eating nothing while maintaining hydration with water alone. (Inadequate hydration is the most common reason for failing, often experienced as nausea or lightheadedness.) You can fast for as briefly as 15 hours or as long as several weeks (though I tell people that any more than 5 days and supervision is required, as electrolyte distortions like dangerously low magnesium levels can develop).

Among its many physiological benefits, fasting can:

  • Reduce blood pressure. The blood pressure reducing effect can be so substantial that I usually have people hold some blood pressure medications, especially ACE inhibitors and ARB agents, during the fast since blood pressure will drop to normal even without the drugs. (A fascinating phenomenon all by itself.)

  • Reduce visceral fat, i.e., the fat that releases inflammatory mediators and generates resistance to insulin.

  • Reduce inflammatory measures

  • Reduce liver output of VLDL that cascades into reduced small LDL, improved HDL "architecture," and improved insulin responsiveness. (The opposite of fasting is "grazing," the ridiculous strategy advocated by many dietitians to control weight. Grazing, or eating small meals every two hours, is incredibly destructive for the opposite reason: flagrant provocation of VLDL production.)

  • Accelerate weight loss. One pound per day is typical.


Beyond this, fasting also achieves unique subjective benefits, including reduced appetite upon resumption of eating. You will find that as single boiled egg or a few slices of cucumber, for example, rapidly generate a feeling of fullness and satisfaction. Most people also experience greater appreciation of food--the sensory experience of eating is heightened and your sense of texture, flavors, sweetness, sourness, etc. are magnified.

After decades of the sense-deadening effects of processed foods--over-sugared, over-salted, reheated, dehydrated then just-add-water foods--fasting reawakens your appreciation for simple, real food. On breaking one of my fasts, I had a slice of green pepper. Despite its simplicity, it was a veritable feast of flavors and textures. Just a few more bites and I was full and satisfied.

Once you've fasted, I believe that you will see why it is often practiced as part of religious ritual. It has an almost spiritual effect.

More on fasting to come . . .

Total cholesterol 220

Talking about total cholesterol is like wearing a tie-dyed t-shirt with the peace sign emblazoned on the front: So totally 60s and out of date.

But talk of total cholesterol somehow keeps on coming back. After I spend 45 minutes discussing a patient's lipoprotein patterns, for instance, they'll asking something like, "But what's my total cholesterol?"

To help put this ridiculous notion of total cholesterol to rest, let me paint several pictures of what total cholesterol can tell you. Let's start with a theoretical, but very common, total cholesterol value of 220 mg/dl. Recall that:

LDL cholesterol = total cholesterol - HDL cholesterol - triglycerides/5

Note that LDL cholesterol is nearly always a calculated value. (Yes, your doctor has been treating a calculated, what I call "fictitious," value.)

Rearranging the equation:

Total cholesterol = LDL cholesterol + HDL cholesterol + Triglycerides/5

This relationship means that a great many variations are possible, all under total cholesterol = 220 mg/dl. For example:

LDL 95 mg/dl + HDL 105 mg/dl + Triglycerides 100 mg/dl

(a relatively low-risk pattern for heart disease)

LDL 160 mg/dl + HDL 50 mg/dl + Triglycerides 50 mg/dl

(an indeterminate risk pattern, potentially moderate risk)

LDL 120 mg/dl + HDL 30 mg/dl + Triglycerides 350 mg/dl

(a potentially high-risk pattern)

LDL 60 mg/dl + HDL 25 mg/dl + Triglycerides 675 mg/dl

(an indeterminate risk pattern)

 

That's just a sample of the incredible variation of patterns that can all fall under this simple observation, total cholesterol 220 mg/dl.

Total cholesterol is an outdated concept, one ready long ago for the junk heap of outdated ideas. It's time to throw total cholesterol out in the trash along with beliefs like high-fat intake causes diabetes, whole grains are healthy, and the tooth fairy will leave you money when you leave your molars under the pillow.

Scientists are freakin' liars

So says Tom Naughton, referring to the frequent misinterpretations or misrepresentations of data that characterize much medical research. Dr. Andreas Eenfeldt posted Tom Naughton's recent wonderfully engaging and hilarious talk from Jimmy Moore's Low-Carb Cruise on his Diet Doctor blog.

Comedian and blogger Tom Naughton, also the filmmaker of the movie Fat Head, has brought humor and personality into the low-carb movement. I told my wife to watch it and I could hear her laughing from 30 feet away while watching her laptop.

Dr. Eenfeldt is a sensation of sorts himself, making a big low-carb splash in Sweden. While I missed the cruise this year (due to time pressures), it's clear that Eenfeldt and Naughton have contributed substantially to helping people understand the nonsense that passes as dietary advice in the U.S. and the world.

I watched Naughton's talk while eating my three eggs scrambled with ricotta cheese. I almost spit my eggs out at the computer screen I was laughing so hard.