Medicine ain't what it used to be

15. Juni 2011 William Davis (0)
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White coats are out-of-date--Not only do they serve as filthy reservoirs of microorganisms (since they hang unwashed after repeated use week after week), they only serve to distance the practitioner from the patient, an outdated notion that should join electroshock therapy to treat homosexuality and other "disorders" in the museum of outdated medical practices.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?

15. Juni 2011 William Davis (19)
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

11. Juni 2011 William Davis (10)
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

8. Juni 2011 William Davis (31)
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

3. Juni 2011 William Davis (16)
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

1. Juni 2011 William Davis (34)
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

28. Mai 2011 William Davis (11)
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

26. Mai 2011 William Davis (28)
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

24. Mai 2011 William Davis (17)
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

14. Mai 2011 William Davis (3)
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.

 
Cureality | Real People Seeking Real Cures

Overweight, hungry, diabetic, and fat-free

15. December 2009 William Davis (52)
Let me tell you about my low-fat experience from 20 years ago.

At the time, I was living in Cleveland, Ohio, and served on the faculty at a large metropolitan university-affiliated hospital, supervising fellows-in-training and developing high-tech cath lab procedures like directional athererectomy and excimer laser coronary angioplasty. (Yes, another life.)

I was concerned about personal heart disease risk, though I knew next to nothing about lipids and coronary risk prediction outside of the little I learned in training and what the drug industry promoted.

I heard Dr. Dean Ornish talk while attending the American College of Cardiology meetings in Atlanta. Dr. Ornish spoke persuasively about the dangers of fat in the diet and how he "reversed" coronary disease using a low-fat, no added oils, no meat, vegetarian diet that included plenty of whole grains. So I thought I'd give it a try.

I eliminated all oils; I removed all meat, eggs, and fish from my diet. I shunned all nuts. I ate only low-fat products like low-fat yogurt and cottage cheese; and focused on vegetables, fruit, and whole grains. Beans and brown or wild rice were a frequent staple. I loved oatmeal cookies--low-fat, of course!

After one year of this low-fat program, I had gained a total of 31 lbs, going from 155 lbs to 186 lbs. I reassessed some basic labs:

HDL 28 mg/dl
Triglycerides 336 mg/dl
Blood sugar 151 mg/dl (fasting)


I became a diabetic. All through this time, I was also jogging. I ran on the beautiful paths along the Chagrin River in suburban Cleveland for miles north and south. I ran 5 miles per day most days of the week.

It was diabetes that hit me alongside the head: I was eating low-fat meticulously, exercising more than 90% of the population, yet I got fat and diabetic!

I have since changed course in diet. Last time I checked, my lipid values on NO statin agent:

HDL 67 mg/dl
Triglycerides 57 mg/dl
Blood sugar 91 mg/dl

That was my lesson that fat restriction is a destructive, misguided notion. The data since then have confirmed that restricting total fat is unnecessary, even undesirable, when fat calories are replaced by carbohydrate calories.

This is your brain on wheat

10. December 2009 William Davis (32)
Here's just a smattering of the studies performed over the past 30 years on the psychological effects of wheat consumption.

Oddly, this never makes the popular press. But wheat underlies schizophrenia, bipolar illness, behavioral outbursts in autism, Huntington's disease, and attention deficit hyperactivity disorder (ADHD).

The relationship is especially compelling with schizophrenia:

Opioid peptides derived from food proteins: The exorphins.
Zioudrou C et al 1979
"Wheat gluten has been implicated by Dohan and his colleagues in the etiology of schizophrenia and supporting evidence has been provided by others. Our experiments provide a plausible biochemical mechanism for such a role, in the demonstration of the conversion of gluten into peptides with potential central nerovus system actions."


Wheat gluten as a pathogenic factor in schizophrenia
Singh MM et al 1976
"Schizophrenics maintained on a cereal grain-free and milk-free diet and receiving optimal treatment with neuropleptics showed an interruption or reversal of their therapeutic progress during a period of "blind" wheat gluten challenge. The exacerbation of the disease process was not due to variations in neuroleptic doses. After termination of the gluten challenge, the course of improvement was reinstated. The observed effects seemed to be due to a primary schizophrenia-promoting effect of wheat gluten."


Demonstration of high opioid-like activity in isolated peptides from wheat gluten hydrolysates
Huebner FR et al 1984


Is schizophrenia rare if grain is rare?
Dohan FC et al 1984
"Epidemiologic studies demonstrated a strong, dose-dependent relationship between grain intake and the occurrence of schizophrenia."

Small LDL: Perfect index of carbohydrate intake

8. December 2009 William Davis (15)
Measuring the number of small LDL particles is the best index of carbohydrate intake I know of, better than even blood sugar and triglycerides.

In other words, increase carbohydrate intake and small LDL particles increase. Decrease carbohydrates and small LDL particles decrease.

Why?

Carbohydrates increase small LDL via a multistep process:

First step: Increased fatty acid and apoprotein B production in the liver, which leads to increased VLDL production. (Apoprotein B is the principal protein of VLDL and LDL)

Second step: Greater VLDL availability causes triglyceride-rich VLDL to interact with other particles, namely LDL and HDL, enriching them in triglycerides (via the action of cholesteryl-ester transfer protein, or CETP). Much VLDL is converted to LDL.

Third step: Triglyceride-rich LDL is "remodeled" by enzymes like hepatic lipase, which create small LDL.


Carbohydrates, especially if they contain fructose, also prolong the period of time that triglyceride-rich VLDL particles persist in the blood, allowing more time for VLDL to interact with LDL.

Many people are confused by this. "You mean to tell me that reducing carbohydrates reduces LDL cholesterol?" Yes, absolutely. While the world talks about cutting saturated fats and taking statin drugs, cutting carbohydrates, especially wheat (the most offensive of all), cornstarch, and sugars, is the real key to dropping LDL.

However, the effect will not be fully evident if you just look at the crude conventional calculated (Friedewald) LDL cholesterol. This is because restricting carbohydrates not only reduces small LDL, it also increases LDL particle size. This make the calculated Friedewald go up, or it blunts its decrease. Conventional calculated LDL will therefore either underestimate or even conceal the real LDL-reducing effect.

The reduction in LDL is readily apparent if you look at the superior measures, LDL particle number (by NMR) or apoprotein B. Dramatic reductions will be apparent with a reduction in carbohydrates.

Small LDL therefore serves as a sensitive index of carbohydrate intake, one that responds literally within hours of a change in food choices. Anyone following the crude Friedewald calculated LDL will likely not see this. This includes the thousands of clinical studies that rely on this unreliable measure and come to the conclusion that a low-fat diet reduces LDL cholesterol.

Fat "conditioning"

4. December 2009 William Davis (0)
Here's a great study from the prolific laboratory of Dr. Jeff Volek from the University of Connecticut. (Full text here.)


http://jn.nutrition.org/cgi/content/full/134/4/880

Video Teleconference with Dr. William Davis

2. December 2009 William Davis (0)

Dr. Davis is available for personal
one-on-one video teleconferencing

to discuss your heart health issues.


You can obtain Dr. Davis' expertise on issues important to your health, including:

Lipoprotein assessment

Heart scans and coronary calcium scores

Diet and nutrition

Weight loss

Vitamin D supplementation for optimal health

Proper use of omega-3 fatty acids/fish oil


Each personalized session is 30 minutes long and by appointment only. To arrange for a Video Teleconference, go to our Contact Page and specify Video Teleconference in your e-mail. We will contact you as soon as possible on how to arrange the teleconference.


The cost for each 30-minute session is $375, payable in advance. 30-minute follow-up sessions are $275.

(Track Your Plaque Members: Our Member cost is $300 for a 30-minute session; 30-minute follow-up sessions are $200.)

After the completion of your Video Teleconference session, a summary of the important issues discussed will be sent to you.

The Video Teleconference is not meant to replace the opinion of your doctor, nor diagnose or treat any condition. It is simply meant to provide additional discussion about your health issues that should be discussed further with your healthcare provider. Prescriptions cannot be provided.

Note: For an optimal experience, you will need a computer equipped with a microphone and video camera. (Video camera is optional; you will be able to see Dr. Davis, but he will not be able to see you if you lack a camera.)

We use Skype for video teleconferencing. If you do not have Skype or are unfamiliar with this service, our staff will walk you through the few steps required.

Track Your Plaque challenges

1. December 2009 William Davis (31)
Of all the various factors we correct in the Track Your Plaque program in the name of achieving reversal of coronary plaque, there are two factors that are proving to be our greatest challenges:

1) Genetic small LDL

2) Lipoprotein(a)

More and more people are enjoying at least marked slowing, if not zero change or reduction, in heart scan scores following the Track Your Plaque program. We achieve this by correcting a number of factors. Some factors, like vitamin D deficiency, are easily corrected to perfection--supplement sufficient vitamin D to achieve a blood level of 25-hydroxy vitamin D of 60-70 ng/ml. Correcting standard lipid values--LDL cholesterol, HDL cholesterol, and triglycerides--child's play, even to our strict targets of 60-60-60.

However, what I call "genetic small LDL" and a subset of lipoprotein(a) are proving to be the most resistant of all.

Let's first consider genetic small LDL. Small LDL is generally the pattern of the carbohydrate-ingesting, overweight person. It has exploded in severity over the past decade due to overconsumption of carbohydrates due to the ridiculous low-fat notion. Reduce or eliminate carbohydrates, especially wheat, which permits weight loss, and small LDL drops like a stone. But there is a unique subset of people who express the small LDL pattern who start at or near ideal weight. Take Chad, for instance. At 6' 2" and 152 lbs and BMI of 19.6, there's no way excess weight could be triggering his small LDL. Yet he starts with 100% small LDL particles. All efforts to reduce small LDL, such as wheat, cornstarch, and sugar elimination; niacin; vitamin D normalization; thyroid normalization; and several supplements that yield variable effects, such as phosphatidylcholine, all leave Chad with more than 90% small LDL.

Lipoprotein(a) is a bit different. Over the past 5 years, our choices in ways to reduce Lp(a) expression have improved dramatically. Beyond niacin, we now have high-dose EPA + DHA, thyroid normalization that includes use of T3, and hormonal manipulation. In the Track Your Plaque experience, approximately 70% of people with Lp(a) respond with a reduction in Lp(a). (In fact, the 4 out of the 5 record holders for reduction of heart scan scores have Lp(a) that was successfully treated.) But about 30% of people with Lp(a) prove resistant to all these treatments--they begin with a Lp(a) of, say, 260 nmol/L and, despite niacin, high-dose EPA + DHA, and various hormones, stay at 260 nmol/L. It can be frustrating and frightening.

So these are the two true problem areas for the Track Your Plaque program, genetic small LDL and a subset of Lp(a).

We are actively searching for better options for these two problem areas. Given the collective exploration and wisdom that develops from such collaborative efforts as the Track Your Plaque Forum, I am optimistic that we will have better answers for these two stumbling blocks to plaque reversal in the future.

I'll supply the tar if you supply the feathers

30. November 2009 William Davis (13)
The results of the latest Heart Scan Blog poll are in.


DIRECT-TO-CONSUMER PHARMACEUTICAL ADVERTISING HAS:

Increased public awareness of medical conditions and their treatment
19 (11%)

Has had little overall effect on health and healthcare
29 (18%)

Needlessly increased healthcare costs
81 (50%)

Further empowered the revenue-obsessed pharmaceutical industry
130 (81%)


Clearly, there's a lot of negative sentiment against direct-to-consumer (DTC) drug advertising.

It looks as if a small minority believe that good has come from DTC advertising, judging by the meager 11% who voted for increased awareness. In fact, the poll results are heavily weighed towards the negative: 50% voted for "needlessly increased healthcare costs," while an astounding 81% voted for "empowered the revenue-obsessed pharmaceutical industry."

It is, indeed, an odd situation: Pharmaceutical agents available only by prescription being hyped directly to the consumer.

Personally, I would vote for choices 1,3, and 4. While awareness has increased, it has come with a hefty price, not all of it well spent. I believe the pharmaceutical industry still adheres to the rule that, for every $1 spent on advertising, $4 is made in revenue. They are, in effect, printing money.

What goes up can't come down

28. November 2009 William Davis (13)
According to conventional wisdom, heart scan scores cannot be reduced.

In other words, say you begin with a heart scan score of 300. Conventional wisdom says you should take aspirin and a statin drug, eat a low-fat "heart healthy" diet, and take high blood pressure medications, if necessary.

If your heart scan score goes up in a year or two, especially at an annual rate of 20% or more, then you are at very high risk for heart attack. If the heart scan score stays the same, then your risk is much reduced. These observations are well-established.

But more than 99% of physicians will tell you that reducing your heart scan score is impossible. Don't even try: Heart scan scores can go up, but they can't go down.

Baloney. Heart scan scores can indeed go down. And they can go down dramatically.

It is true that, following conventional advice like taking a statin drug, following a low-fat diet, and taking aspirin will fail to reduce your heart scan score. A more rational approach that 1) identifies all causes of coronary plaque, 2) corrects all causes while including crucial strategies like omega-3 fatty acid supplementation, vitamin D supplementation, and thyroid function normalization, is far more likely to yield a halt or reduction in score.

While not everybody who undertakes the Track Your Plaque program will succeed in reducing their heart scan score, a growing number are enjoying success.

A small portion of our experience was documented this past summer. (I collected and analyzed the data with the help of Rush University nutrition scientist, Dr. Susie Rockway, and statistician, Dr. Mary Kwasny.)


Effect of a combined therapeutic approach of intensive lipid management, omega-3 fatty acid supplementation, and increased serum 25 (OH) vitamin D on coronary calcium scores in asymptomatic adults.

Davis W, Rockway S, Kwasny M.

The impact of intensive lipid management, omega-3 fatty acid, and vitamin D3 supplementation on atherosclerotic plaque was assessed through serial computed tomography coronary calcium scoring (CCS). Low-density lipoprotein cholesterol reduction with statin therapy has not been shown to reduce or slow progression of serial CCS in several recent studies, casting doubt on the usefulness of this approach for tracking atherosclerotic progression. In an open-label study, 45 male and female subjects with CCS of > or = 50 without symptoms of heart disease were treated with statin therapy, niacin, and omega-3 fatty acid supplementation to achieve low-density lipoprotein cholesterol and triglycerides < or = 60 mg/dL; high-density lipoprotein > or = 60 mg/dL; and vitamin D3 supplementation to achieve serum levels of > or = 50 ng/mL 25(OH) vitamin D, in addition to diet advice. Lipid profiles of subjects were significantly changed as follows: total cholesterol -24%, low-density lipoprotein -41%; triglycerides -42%, high-density lipoprotein +19%, and mean serum 25(OH) vitamin D levels +83%. After a mean of 18 months, 20 subjects experienced decrease in CCS with mean change of -14.5% (range 0% to -64%); 22 subjects experienced no change or slow annual rate of CCS increase of +12% (range 1%-29%). Only 3 subjects experienced annual CCS progression exceeding 29% (44%-71%). Despite wide variation in response, substantial reduction of CCS was achieved in 44% of subjects and slowed plaque growth in 49% of the subjects applying a broad treatment program.

Gretchen's postprandial diet experiment

27. November 2009 William Davis (11)
Gretchen sent me the results of a little experiment she ran on herself. She measured blood glucose and triglycerides after 1) a low-fat diet and 2) a low-carb diet.









Gretchen describes her experience:

Several years ago I received a windfall of triglyceride strips that would expire in a week or so. I hated to waste them, so I decided to use them to test my triglyceride and BG responses to two different diets: low carb and low fat.

The first day I followed a low-fat diet. For breakfast I ate a lot of carbohydrate, including 1 oz of spaghetti cooked al dente and ¾ cup of white rice. For the rest of the day I ate less carbohydrate but continued to eat low fat.

The second day I followed a low-carb diet. For breakfast I ate a lot of fat, including a sausage, mushrooms fried in butter, 2 slices of bacon, and ¼ cup of the creamy topping of whole-milk yogurt. For the rest of the day I ate less fat, especially less saturated fat, but continued to eat low carb.

Both days I measured both BG and triglyceride levels every hour until I went to bed. On the low-carb day I had 3 meals. On the low-fat day, I was constantly hungry, had 4 meals, and kept snacking.

You can see the results in Figure 1. On the low-fat diet, after a “healthy” low-fat breakfast of low-glycemic pasta with low-fat sauce, my BG levels shot up to over 200 mg/dL and took more than 6 hours to come down. My triglycerides, however, remained low, and at first I thought perhaps the low-fat diet might be better overall. However, after about 6 hours, the triglyceride levels started to increase steadily, and by the next morning, they were higher than they had been the day before.
On the low-carb diet, my BG levels stayed low all day. However, after meals, the triglyceride levels skyrocketed. After meals they came down, and by the next morning they were lower than they had been the day before.

As I interpret these results, the high triglyceride levels after eating the high-fat meals represent chylomicrons, the lipoproteins that transport fat from your meals to the cells of your body. The high triglyceride levels the morning after eating the low-fat meals represent very low density lipoprotein, which takes the cholesterol your liver synthesizes when your intake of dietary cholesterol is low and distributes it to cells that need it, or again, to the fat for storage.

There are several interesting factors to consider here. First, when you have a lipid test done at the lab, it’s usually done fasting, which means first thing in the morning after not eating for 8 to 12 hours. It tells you nothing about what your triglyceride levels were all day.

Second, the low-carb diet resulted in lower fasting triglyceride levels, but much higher postprandial triglyceride levels. Which are more dangerous? I’m afraid I don’t know. You should also note that the high-fat, low-carb breakfast was extremely high in fat, including saturated fat. I don’t normally eat that much fat but wanted to test extremes.

Third, although the low-fat diet didn’t produce the very high postprandial triglyceride levels that the high-fat diet did, it produced extremely high BG levels that persisted for 6 hours. Some people think that it’s oxidized and glycated lipids that are the dangerous ones, so high BG levels and normal triglyceride levels might be more dangerous than very high triglyceride levels and normal BG levels. Note that high BG levels also contribute to oxidation rates.

Fourth, this shows the results of an experiment with a sample size of one. My physiology might not be typical. If you want to know how your own body’s lipids respond to different types of diets, you should get a lipid meter and test yourself. Unfortunately, your insurance is unlikely to want to pay for this, so it will be an expensive experiment.

The main point of this is that the results of different diets are complex. We have to eat. And what we eat can affect many different systems in our bodies. Finding the ideal diet that matches our own physiology and results in the best lipid levels as well as BG levels is a real challenge.



This was a lot of effort for one person. Thanks to Gretchen for sharing her interesting experience.

Gretchen makes a crucial point: Some of the effects of diet changes evolve over time, much as triglyceride levels changed substantially for her on the day following her experiment. Wouldn't it be interesting to see how postprandial patterns develop over time if levels were observed sequentially, day after day?

The stark contrast in blood sugars is impressive--Low-carb clearly has the advantage here. Are there manipulations in diet composition in low-carb meals that we can make to blunt the early (3-6 hour) postprandial lipoprotein (triglyceride) peak? That's a topic we will consider in future.

More of Gretchen's thoughts can be found at:

http://wildlyfluctuating.blogspot.com
http://www.healthcentral.com/diabetes/c/5068

After-eating effects: Carbohydrates vs. fats

25. November 2009 William Davis (17)
In the ongoing debate over whether it's fat or carbohydrate restriction that leads to weight loss and health, here's another study from the Oxford group examining the postprandial (after-eating) effects of a low-fat vs. low-carbohydrate diet. (Roberts R et al, 2008; full-text here.)

High-carbohydrate was defined as 15% protein; 10% fat; 75% carbohydrate (by calories), with starch:sugar 70:30.

High-fat was defined as 15% protein; 40% fat; 45% carbohydrate, with starch:sugar 70:30. (Yes, I know. By our standards, the "high-fat" diet was moderate-fat, moderate-carbohydrate--too high in carbohydrates.)

Blood was drawn over 6 hours following the test meal.




Roberts R et al. Am J Clin Nutr 2008

The upper left graph is the one of interest. Note that, after the high-carbohydrate diet (solid circles), triglyceride levels are twice that occurring after the high-fat diet (open circles). Triglycerides are a surrogate for chylomicron and VLDL postprandial lipoproteins; thus, after the high-carbohydrate diet, postprandial particles are present at much higher levels than after the high-fat diet. (It would have been interesting to have seen a true low-carbohydrate diet for comparison.) Also note that, not only are triglyceride levels higher after high-carbohydrate intake, but they remain sustained at the 6-hour mark, unlike the sharper decline after high-fat.

It's counterintuitive: Postprandial lipoproteins, you'd think, would be plentiful after ingesting a large quantity of fat, since fat must be absorbed via chylomicrons into the bloodstream. But it's carbohydrates (and obesity, a huge effect; more on that in future) that figure most prominently in determining the pattern and magnitude of postprandial triglycerides and lipoproteins. Much of this effect develops by way of de novo lipogenesis, the generation of new lipoproteins like VLDL after carbohydrate ingestion.

We also see this in our Track Your Plaque experience. Rather than formal postprandial meal-testing, we use intermediate-density lipoprotein (IDL) as our surrogate for postprandial measures. A low-carbohydrate diet reduces IDL dramatically, as do omega-3 fatty acids from fish oil.
Cureality | Real People Seeking Real Cures

Boy, was I wrong!

1. August 2006 William Davis (0)
Around 10 years ago, I was talking to a balloon and stent manufacturer's representative, who was raving about some new device that was due for release to the market. Back then, the sky seemed the limit to cardiac device manufacturers, who were falling over themselves scrambling to design and market the next new device.

The angioplasty market then had ballooned (no pun intended) from nothing to a multi-billion dollar industry. Stents were just getting underway but clearly had potential for being at least as large.

But this was a time when preventive therapies were also beginning to get quite powerful. We had just gotten started doing CT heart scans and were excited about the possibilities, statin drugs were gaining evidence through clinical trials, and the power of many nutritional supplements was finally achieving validation. We were even learning the error of our prior low-fat ways.

So I broadly pronounced to the enthusiastic product representative, "In 10 years, balloons, angioplasty, and stents will occupy this little corner of cardiac care because prevention will have become so powerful. We won't talk about heart procedures. We'll talk about coronary plaque regression!"

I even advised the representative that he should consider a career change in anticipation of the coming wave of preventive strategies.

Was I ever wrong. Despite the power of heart disease prevention--which is indeed true--cardiac device and procedure technology has boomed, both in popularity as well as in revenue success. Device manufacturing and sales are hugely successful. Implanting devices into people is a hugely profitable enterprise.

Since my ill-timed comments to the salesman, Boston Scientific, a major manufacturer of stents and other cardiac devices, reported revenues of $6.2 billiondollars in 2005, a 12% increase over the prior year. Medtronic reported 2005 revenues of $11.3 billion, growing at 15% per year. Clearly, cardiac procedures are still quite popular--and profitable.

My timing was off, but not for long. The huge crest of change in preventive therapies is upon us. That's the premise behind the Track Your Plaque concept: heart disease prevention can't be found in a hospital, is not supported by cardiac device manufacturers, and is not being advocated by most cardiologists or primary care physicians. Yet the tools are getting better and better every day.

Those of you who succeed in halting or reducing your heart scan score are extremely unlikely to add to Boston Scientific's or Medtronic's revenues. Help me spread the word.

Don't forget how dangerous heart disease can be

29. July 2006 William Davis (0)
Sometimes it's easy to get smug when coronary plaque is a reversible process.

When you see people day in, day out, week in, week out, drop their heart scan scores, reversing what could be a dangerous disease, you can sometimes lose sight of just how dangerous coronary disease can be.

Whether I like it or not, I maintain a reasonably active role in hospitals out of necessity. I do need their services occasionally for people with advanced heart disease when I meet them (when regression is not the initial conversation for safety reasons), or valve disease is diagnosed, or someone shows up with congenital or heart muscle diseases. In other words, although we focus on coronary issues, there's more to heart disease than just coronary disease.

This unfortunate case just served to remind me how powerful coronary disease can be. Elizabeth, an active 67-year old, finally came to the hospital after suffering 6 months of chest pain and increasing breathlessness. She hated hospitals and hadn't seen a doctor in 30 years since she was successfully treated for cancer.

In those 30 years, she'd been quite active with family and a small business. But she also smoked 2 packs of cigarettes most of those years.

After she was admitted to the hospital, it became clear that Elizabeth had experienced one, if not several, heart attacks along the way. The entire front 2/3 of her heart was non-functional. If that wasn't bad enough, two of her heart valves were severely diseased and dysfunctional: Her aortic valve barely opened (aortic valve "stenosis", or stiffness) and the mitral valve leaked severely (mitral valve "insufficiency", or leakiness). All of this was confirmed with conventional testing in the hospital, including a heart catheterization.

Elizabeth ended up in emergency surgery--very unusual, by the way, for valve surgery of the sort she had--but died in the first few hours after her procedure. Her heart had simply been too damaged from her heart attacks, and the extraordinary stress of surgery that included two valves was too much. She died on the ventilator.

Coronary disease is a very serious matter. When I see cases like Elizabeth, it boosts my commitment to tell everyone that heart disease--when identified early enough--is a controllable, preventable, even reversible process. For poor Elizabeth, she was much too far down the path of severe, irreversible disease that control or reversal was simply not an option. She was in imminent danger of dying even upon arrival.

It's exciting yet sometimes frightening to know what you have in your hands: The means to control this monster called coronary disease. Use it wisely. But don't lose sight of what it can do it you permit it to grow, fester, and explode.

How many ways can you disguise sugar?

28. July 2006 William Davis (0)
I came across this shockingly silly report on AOL, who obtained their info courtesy Health Magazine:

The Best New Healthy Foods for Busy People
from Health

The foods on their list:

Kettle Brand Bakes Hickory Honey BBQ--the healthy claim is based on the lack of trans-fatty acids and low-fat.










Post Healthy Classics Raisin Bran Cereal Bars, Cranberry--Likewise, low-fat, sweet, and addictive means healthy to these people.




Amy’s Mediterranean Pizza With Cornmeal Crust --Please!!



Horizon Organic Colby Cheese Sticks --Because it's made by cattle without use of growth hormone or antibiotics, they declare this healthy. I guess we can ignore the saturated fat content and high total fat content.

100% Whole Grain Chips Ahoy! Cookies --You mean we can add the bran back to wheat products and make it healthy?!


This kind of mass-market marketing trickery leaves me incredulous. Don't believe it for a moment. This is typical of the food industry: Take one aspect of nutrition that is truly healthy, such as high-fiber, or low-fat, or organic. Then add undesirable, unhealthy ingredients. The current fad is to add lots of sugar and or sugar-equivalents (usually flour and other wheat products). Because there's one healthy ingredient, they'll call the end-product healthy, too.

If you want to see what health looks like if you indulge in "healthy" products like this, just look up and down the grocery aisles at your neighborhood grocery store. You're likely to see the results: Gross obesity, diabetes, and arthritis.

You won't, of course, see the huge acceleration of growth in coronary plaque, but it's there, ticking away.

To remind us what ideal body weight is: Watch an old movie!

26. July 2006 William Davis (0)
Jack was skeptical. At 273 lbs, 5 ft 11 inches, he felt that he was "just right".

"I feel fine. I don't see why you think I should lose weight," he declared. "In fact, when I lost 25 lbs a couple of years ago, everyone said I was too skinny!"

I showed Jack why: He had an HDL of 35 mg/dl, small LDL (over 90% of all LDL particles), an elevated blood sugar of 123 mg/dl (diabetes is officially 126 mg/dl or greater), high blood pressure, and increased inflammation (C-reactive protein). These were all manifestations that his body weight was too much for it to handle.




So I told Jack that we've all forgotten what ideal weight should look like. Our perception of "normal" has been so utterly and dramatically distorted by the appearance of our friends, family, co-workers, and other people around us that we've all lost a sense of what a desirable weight for health should be.




So I suggested to Jack that, if he wanted to rememember what ideal weight is and what people are supposed to look like, just watch old movies.

Old movies, like the 1942 production of Casablanca, or the 1952 production of Singin' in the Rain, show the body build that was prevalent in those days. Look at Humphrey Bogart or Gene Kelly--men with average builds, weighing 140-160 lbs--that's how humans were meant to look.

A report this morning on the Today Show showed the "after" photos of several people following bariatric (weight reduction) surgery. The "after" pictures, from the perspective of ideal weight and ideal health, remain hugely overweight.

We need to readjust our perceptions of weight. The average woman in the U.S. now weighs 172 lbs(!!!). Don't confuse average with desirable.

Diabetes is a choice you make

24. July 2006 William Davis (0)
Tim had heart disease identified as a young man. He had his first heart attack followed by a quadruple bypass surgery at age 38. Recurrent anginal chest pain and another small heart attack led to several stents over three procedures in the first four years after bypass.

Tim finally came to us, interested in improving his prevention program. You name it, he had it: small LDL, low HDL (28 mg/dl), lipoprotein(a), etc. The problem was that Tim was also clearly pre-diabetic. At 5 ft 10 inches, he weighed 272 lbs--easily 80 or more pounds overweight.

Tim was willing to make the medication and nutritional supplement changes to gain control over his seeminglly relentless disease. He even turned up his exercise program and lost 28 lbs in the beginning. But as time passed and no symptoms recurred, he became lax.

Tim regained all the weight he'd lost and some more. Now Tim was diabetic.

"I don't get it. I eat good foods that shouldn't raise my insulin. I almost never eat sweets."

I stressed to Tim that diabetes and pre-diabetes, while provoked acutely by sugar-equivalent foods (wheat products, breads, breakfast cereals, crackers, etc.), is caused chronically by excess weight. If Tim wants to regain control over his heart disease, he needed to lost the weight.

Unlike, say, leukemia, an unfortunate disease that has little to do with lifestyle choices, diabetes is a choice you make over 90% of the time. In other words, if you become diabetic (adult variety, not children's variety) as an adult, that's because you've chosen to follow that path. You've neglected physical activity, or indulged in too many calories or poor food choices, or simply allowed weight to balloon out of control.

But diabetes is also a path most people can choose not to take. And it is a painfully common choice: Nearly two-thirds of the adults in my office have patterns of pre-diabetes or diabetes when I first meet them.

Let me stress this: For the vast majority of adults, diabetes is a choice, not an inevitability.

I'll call the doctor when I feel bad!

24. July 2006 William Davis (0)
Max just had his heart scan. He sat down with the x-ray technologist at the work console while she pointed out the white areas in his coronary arteries that represented plaque.

"It looks like you're going to have a fairly high score," the technologist commented. "The final report will be available after one of our cardiologists reviews your images."

Max shrugged. "Well, I don't feel anything. I'm always running around with work, with my kids, stuff like that. That's better than any stress test. I guess I'll worry about it if it starts to bother me."


You'd be surprised how common this view remains: If it's not bothering you, then just forget about it. It's easy to do, since you have no symptoms, nothing to impair your physical activities. But what are the potential consequences of ignoring your heart scan? Here's a few:

--Prevention and plaque reversal efforts are most effective the earlier you start. From a heart scan score viewpoint, the lower your starting score, the easier it is to gain control over it. More people will succeed in reducing their score when the starting score is lower.

--The role of prevention of heart disease instantly crystallizes when you know your score. Your LDL cholesterol of 142 mg/dl or HDL of 41 mg/dl no longer seem like just numbers of borderline signficance. Instead, they become useful tools to gain control over plaque. They cast your numbers in a new and clear light.

--Knowing your heart scan score today gives you a basis for comparison in future. Your score of, say 250, today, can be 220 in one year. Without your preventive efforts, it will be 30% higher: 325. That's a big difference!

--Sudden death or heart attack--can occur in up to 35-40% of people with hidden heart disease--without warning.

Don't even bother getting a heart scan if you're going to ignore it. I've said it before and I'll say it again: A heart scan is the most important health test you can get--but only if you do something about it.

Coenzyme Q10 and statin drugs

23. July 2006 William Davis (0)
Although drug manufacturers claim that muscle side effects from statin drugs occurs in only around 2% or people or less, my experience is very different.

I see muscle weakness and achiness develop in the majority of people taking Lipitor, Crestor, Zocor, Vytorin, etc. I'd estimate that nearly 90% of people get these feelings sooner or later.

Thankfully, the majority of the time these feelings are annoyances and do not lead to any impairment. Full-blown muscle destruction is truly rare--I've seen it once in over 10 years and thousands of patients.

The higher the dose of statin drug and the longer you take it, the more likely you're going to have muscle aches.

I experienced a strange phemomenon myself today. I worked outdoors for about 4 hours, pulling weeds, digging in the dirt, spreading topsoil. (I have an area of overgrowth in the front yard.) Admittedly, I worked pretty hard and it was a warm, humid day.

I was sore, as you'd expect at age 49. But, much more than that, I was exhausted--my muscles ached and I had barely enough strength to get up the stairs.

Hoping for some relief, I took an extra dose of coenzyme Q10. I usually take 50-100 mg per day. Today, when I felt this overwhelming muscle fatigue, I took an additional 200 mg. Within 10 minutes, I felt a surge of energy. It was, in fact, a perceptible, quite dramatic feeling.

I am thoroughly convinced, through my own experiences on Lipitor (I have a high LDL particle number despite a healthy lifestyle, among other abnormalities), and the experiences of many other people, that coenzyme Q10 can be an extremely useful tool to minimize the muscle aches and weakness of the statin drugs.

If you do indeed need to take one of these agents, coenzyme Q10 is worth knowing about. Supplementing coenzyme Q10 has, for me, been a real lifesaver. For many people, LDL reduction is a crucial part of their heart scan score control program. In my experience, many of them would not be able to take the drug without eozyme Q10.

Blast your LDL with oat bran and almonds

21. July 2006 William Davis (1)
Nearly all of us can use an extra boost in reducing LDL cholesterol. We have a large number of people, in fact, who have reduced LDL into the Track Your Plaque range of 60 mg/dl or less without the use of statin cholesterol-reducing drugs.




Oat bran is among my favorite ways to reduce LDL. Three tablespoons per day is a really effective method to drop your LDL around 20 points. There's twice the beta glucan (soluble, or "viscous", fiber)in oat bran, as compared to the more popular oatmeal. Add oat bran to anything you can think of: yogurt, cottage cheese, vegetarian chili, oatmeal, top desserts with it, etc. Some people struggle to find oat bran in the grocery store. Most health food stores that sell bulk products will have oat bran, usually less than a $1 per pound. Many grocery stores will also have an oat bran hot cereal along with the Cream of Wheat and oatmeal. That's okay, provided the only ingredient is oat bran--no added sugars, etc.





Another dynamite method to reduce LDL 10-20 points is adding raw almonds to your daily food choices. One or two handfuls per day works great. We find it at Sam's Club for around $12.99 for a 3 lb. bag. The plentiful fibers and monounsaturates in almonds keep you full and satisified, take the edge off your sweet tooth, and even blunt the blood sugar rise caused by other foods.

Both these foods are also great ways to combat the metabolic syndrome. Since both fiber-rich oat bran and almonds slow the release of sugars into the blood, blood insulin level is also reduced. This results in a happy cascade of less small LDL, increased HDL, and a reduction in inflammation.

All these wonderful effects contribute to inching you closer to success: dropping your heart scan score.

Pre-diabetes with normal blood sugar

20. July 2006 William Davis (0)
We pay special attention to pre-diabetes, in all its varied manifestations, in the Track Your Plaque program. This is because these factors are potent instigators of coronary plaque growth.

Early in the Track Your Plaque program we ignored these measures. After all, this is a program for heart disease risk reduction, not for mangement of diabetes. But we saw explosive rates of plaque growth when pre-diabetic factors were not controlled--even when cholesterol and related factors were under excellent control.

It became increasingly clear that factors associated with pre-diabetes needed to be managed, as well. This includes small LDL, increased blood sugar, high blood pressure, increased inflammation (as CRP).

Many people, however, have normal blood sugars (100 mg/dl or less) with a high blood insulin level (>10 microunits/ml). (This blood test is available in most laboratories.) This means that they have early resistance to insulin. The pancreas, the source of insulin, responds to the body's unresponsiveness to insulin by increasing insulin production.

Increased blood insulin with normal blood sugar will drive production of higher triglycerides, a drop in HDL, creation of small LDL, and inflammation--and coronary plaque growth, as evidenced by increasing CT heart scan score.

Blood insulin levels can be very effectively dropped by weight loss; exercise; reduction of processed carbohydrates like breads, pretzels, and breakfast cereals; and increased raw nuts and oat products; and vitamin D replacement to normal levels. Drug manufacturers are desperately trying to make this a mandate for drug treatment (Actos, Avandia), but are encountering resistance, since most people without overt diabetes don't want to take diabetic medication (rightly so!).

You and your doctor should consider insulin as a factor to track, especially if you have small LDL, low HSL, or high triglycerides, or any of the other manifestations listed above.

Sometimes small LDL is the only abnormality

19. July 2006 William Davis (0)
Janet is a 58-year old schoolteacher. At 5 ft 3 inches and 104 lbs, she had barely an ounce of fat on her size-2 body. For years, Janet's primary care physician complimented her on her cholesterol numbers: LDL cholesterol values ranging from 100 to 130 mg/dl; HDL cholesterol of 50-53 mg/dl.

Yet she had coronary disease. Her heart scan score: 195.

Lipoprotein analysis uncovered a single cause: small LDL. 95% of all of Janet's LDL particles were in the small category. What was surprising was that this pattern occurred despite her slender build. Weight is a powerful influence on the small LDL pattern and the majority of people with it are overweight to some degree. But not Janet.

How did she get small LDL if she was already at or below her ideal weight? Genetics. Among the genetic patterns that can account for this pattern is a defect of an enzyme called cholesteryl-ester transfer protein, or CETP. This is the exact step, by the way, that is blocked by torcetrapib, the new agent slated for release sometime in future (The manufacturer, Pfizer, is apparently going to sell this agent only packaged in the same tablet as Lipitor. This has triggered an enormous amount of criticism against the company and they are, as a result discussing marketing torcetrapib separately.)

Also note that Janet had a severe excess of small LDL despite an HDL in the "favorable" range. (See my earlier conversation on this issue, The Myth of Small LDL at http://drprevention.blogspot.com/2006/06/myth-of-small-ldl.html.)

With Janet, weight loss to reduce small LDL was not an option. So we advised her to take fish oil, 4000 mg per day; niacin, 1000 mg per day; vitamin D, 2000 units per day; use abundant oat bran and raw almonds, both of which suppress small LDL. This regimen has--surprisingly--only partially suppressed her small LDL pattern by a repeat lipoprotein analysis we just performed. We're hoping this may do it, i.e., stop progression or reduce her heart scan score.

The lesson: Small LDL is a very potent pattern that can be responsible for heart disease, even if it occurs in isolation. And, contrary to conventional thinking, small LDL can occur as an independent abnormality, even when HDL is at favorable levels.