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White coats are out-of-date--Not only do they serve as filthy reservoirs of microorganisms (since they hang unwashed after repeated use week after week), they only serve to distance the practitioner from the patient, an outdated notion that should join electroshock therapy to treat homosexuality and other "disorders" in the museum of outdated medical practices.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

 
All posts by william-davis

Fish oil: What's the difference?

Ultra-purified, pharmaceutical grade, molecularly distilled. Over-the-counter vs. prescription. Gelcap, liquid, emulsion.

There's a mind-boggling variety of choices in fish oil today. A visit to any health food store, or any "big box" store for that matter, will yield at least several, if not dozens, of choices, all with varying and often extravagant claims of purity and potency.

So what's the real story?

Given the analyses conducted over the years, along with my experience with dozens of different preparations, I believe that several conclusions can be reached about fish oil:

Fish oil is free of contamination with mercury, dioxin, PCBs, or furans. To my knowledge, only one fish oil preparation has been found to have a slight excess of PCBs. (This is different from cod liver oil that has been found by one source to have a slight excess of PCBs.)

Oxidative breakdown products differ among the various brands. Consumer Lab (http://www.consumerlab.org/), for instance, has found that several widely available brands of fish oil contained excessive oxidative breakdown products (TOTOX). You can perform you own simple test of oxidative breakdown products: Sniff it. Your fish oil should pass the "sniff test." High quality fish oil should smell non-fishy to lightly fishy. Rancid fish oil with excessive quantities of oxidative breakdown products will smell nasty fishy.

FDA approval does not necessarily mean greater potency, purity, or effectiveness. It just means that somebody assembled the hundreds of millions of dollars to obtain FDA approval, followed by lots of marketing savvy to squash the competition.

This means that there are a number of excellent fish oil products available. My favorites are the liquid fish oils from Pharmax, Nordic Naturals, and Barleans. Capsules from Carlson, PharmaNutrients, and Fisol have also performed consistently. The "big box" capsules from Sam's Club and Costco have also performed well and are wonderfully affordable.

Wheat-free pie crust

I've been working on wheat-free yet healthy recipes these past two months.

You can buy wheat-free, gluten-free foods at the store, of course. But the majority of these products are unhealthy because cornstarch, rice starch, potato starch, or tapioca starch are commonly used in place of wheat. Recall that these are among the few foods that increase blood glucose higher than even wheat.

Here's a simple recipe for wheat-free pie crust that works best for cheesecake, pumpkin pie, and cream pies, but not for berry or other fruit pies like apple.

You will need:
?
1½ cups ground pecans
6 tablespoons melted butter?or melted coconut oil
1 teaspoon vanilla extract?
2 teaspoons cinnamon
1 medium egg
2 tablespoons Truvia™ or ½ teaspoon stevia extract or ½ cup Splenda®

Mix all ingredients thoroughly in bowl. Pour mixture into pie pan and press onto bottom and sides.

Fill pie crust with desired filling. You can fill it with your favorite cheesecake recipe (e.g., Neufchatel or cream cheese, sour cream, eggs, vanilla, and stevia; add pumpkin for pumpkin cheesecake) and bake, usually at 350 degrees F for one hour. 

Yes, the butter provokes insulin and artificial sweeteners can trigger appetite. But, for the holidays, a slice or two of pie made with this crust will not increase blood sugar nor trigger the uncontrolled impulse eating that wheat crust will trigger.

Have a cookie

Here's a great insight dating all the way back to 1966 from one of the early explorations in lipoproteins from the National Institutes of Health lab of Levy, Lees, and Fredrickson:

The nature of pre-beta (very low density) lipoproteins

The subject is a 19 year old female (among the total of 11 in the this small, diet-controlled study) who was first fed a low-carbohydrate (50 grams per day), low-cholesterol diet; followed by a high-carbohydrate (500 grams per day), low-fat (5 grams per day) diet.






To B or not to B

Apoprotein B (apo B) is the principle protein that resides in LDL particles along with other proteins, phospholipids, triglycerides, and, of course, cholesterol.

There's a curious thing about apo B. Just like one child per family in China or one television per household in 1950s America, there is only one apo B for every LDL particle.

So measuring apo B, in effect, provides a virtual count of LDL particles. (Actually, VLDL particles, the first lipoprotein to emerge from the liver, also have one apo B per particle but LDL particles far outnumber VLDL particles.) While apo B structure can show limited structural variation from individual to individual, the effect on measured apo B is negligible.

One apo B per LDL particle . . . no more, no less. What about the other components of LDL particles?

The other components of LDL particles are a different story. Cholesterol and triglycerides in LDL particles vary substantially. Diet has profound effects on cholesterol and triglyceride content of LDL particles. A diet rich in carbohydrates, for instance, increases triglycerides in LDL particles while reducing cholesterol. This means that measuring cholesterol in the LDL fraction will be misleading, since cholesterol will be falsely low. LDL cholesterol is therefore a flawed means to assess the behavior and composition of LDL particles. In particular, when LDL particles become enriched in triglycerides, they go through a process that transforms them into small LDL particles, the variety most likely to cause atherosclerosis.

In other words, when the worst situation of all--an abnormal abundance of small LDL particles develops--it is usually not signalled by high LDL cholesterol.

Because apo B is not sensitive to the composition of LDL particles--high cholesterol, low cholesterol, high triglycerides, etc.--it is a superior method to characterize LDL particles. While apo B doesn't tell you whether LDL particles are big, small, or in between, it provides a count of particles that is far more helpful than measuring this deeply flawed thing called "LDL cholesterol."

(Even better: Count LDL particles and measure LDL size, since size gives us insight into sensitivity to oxidation, glycation, adhesiveness, ability to trigger inflammatory pathways via monocyte chemoattractant protein, various interleukins, tunor necrosis factor and others. This is why cholesterol panels should go the way of tie dye shirts and 8-track tapes: They are hopelessly, miserably, and irretrievably inaccurate. Cholesterol panels should be replaced by either apoprotein B or lipoprotein measures.)

Put lipstick on a dwarf

Today, virtually all wheat products are produced from the Triticum aestivum dwarf mutant.

You might call it "multi-grain bread,""oat bread," or "flaxseed bread." You could call it "organic," "pesticide-free," "non-GMO," or "no preservatives." It might be shaped into a ciabatta, bruschetta, focaccia, or panini. It might be sourdough, unleavened, or sprouted. It could be brown, black, Pumpernickel, or white. It could be shaped into a roll, bun, bagel, pizza, loaf, pretzel, cracker, pancake, brioche, baguette, or pita. It could be matzah, challah, naan, or Communion wafers.

No matter what you call it, it's all the same. It's all from the dwarf mutant Triticum aestivum plant, the 18-inch tall product of hybridizations, backcrossings, and introgressions that emerged from genetics research during the 1960s and 70s.

According to Dr. Allan Fritz, Professor of Wheat Breeding at Kansas State University, and Dr. Gary Vocke at the USDA, over 99% of all wheat grown today is the dwarf variant of Triticum aestivum. (For you genetics types, Triticum aestivum is the hexaploid, i.e., 3 combined genomes, product of extensive hybridizations, while ancestral einkorn is a diploid, i.e., a single genome, grass. Hexaploid Triticum aestivum contains the especially hazardous "D" genome, the set of genes most commonly the recipient of genetic manipulations to modify the characteristics of flour, such as gluten content. Einkorn contains only the original "A" genome.)

No matter what you call it, add to it, how you shape it, etc., it's all the same. It's all the dwarf mutant product of tens of thousands of hybridizations.

You can put lipstick on a pig, but it's still a pig. By the way, lipstick may contain wheat.

What the Institute of Medicine SHOULD have said

The news is full of comments, along with many attention-grabbing headlines, about the announcement from the Institute of Medicine that the new Recommended Daily Allowance (RDA) for vitamin D should be 600 units per day for adults.

What surprised me was the certainty with which some of the more outspoken committee members expressed with their view that 1) the desirable serum 25-hydroxy vitamin D level was only 20 ng/ml, and 2) that most Americans already obtain a sufficient quantity of vitamin D.

Here's what I believe the Institute of Medicine SHOULD have said:

Multiple lines of evidence suggest that there is a plausible biological basis for vitamin D's effects on cancer, inflammatory responses, bone health, and metabolic responses including insulin responsiveness and blood glucose. However, the full extent and magnitude of these responses has not yet been fully characterized.

Given the substantial observations reported in several large epidemiologic studies that show an inverse correlation between 25-hydroxy vitamin D levels and mortality, there is without question an association between vitamin D and mortality from cancer, cardiovascular disease, and all cause mortality. However, it has not been established that there are cause-effect relationships, as this cannot be established by epidemiologic study.

While the adverse health effects of 25-hydroxy vitamin D levels of less than 30 ng/ml have been established, the evidence supporting achieving higher 25-hydroxy vitamin D levels remains insufficient, limited to epidemiologic observations on cancer incidence. However, should 25-hydroxy vitamin D levels of greater than 30 ng/ml be shown to be desirable for ideal health, then vitamin D deficiency has potential to be the most widespread deficiency of the modern age.

Given the potential for vitamin D's impact on multiple facets of health, as suggested by preliminary epidemiologic and basic science data, we suggest that future research efforts be focused on establishing 1) the ideal level of 25-hydroxy vitamin D levels to achieve cancer-preventing, bone health-preserving or reversing, and cardiovascular health preventive benefits, 2) the racial and genetic (vitamin D receptor, VDR) variants that may account for varying effects in different populations, 3) whether vitamin D restoration has potential to exert not just health-preserving effects, but also treatment effects, specifically as adjunct to conventional cancer and osteoporosis therapies, and 4) how such vitamin D restoration is best achieved.

Until the above crucial issues are clarified, we advise Americans that vitamin D is a necessary and important nutrient for multiple facets of health but, given current evidence, are unable to specify a level of vitamin D intake that is likely to be safe, effective, and fully beneficial for all Americans.


Instead of a careful, science-minded conclusion that meets the painfully conservative demands of crafting broad public policy, the committee instead chose to dogmatically pull the discussion back to the 1990s, ignoring the flood of compelling evidence that suggests that vitamin D is among the most important public health issues of the age.

Believe it or not, this new, though anemic, RDA represents progress: It's a (small) step farther down the road towards broader recognition and acceptance that higher intakes (or skin exposures) to achieve higher vitamin D levels are good for health.

My view: Vitamin D remains among the most substantial, life-changing health issues of our age. Having restored 25-hydroxy vitamin D levels in over 1000 people, I have no doubt whatsoever that vitamin D achieves substantial benefits in health with virtually no downside, provided 25-hydroxy vitamin D levels are monitored.

Coronary calcium: Cause or effect?

Here's an interesting observation made by a British research group.

We all know that coronary calcium, as measured by CT heart scans, are a surrogate measure of atherosclerotic plaque "burden," i.e., an indirect yardstick for coronary plaque. The greater the quantity of coronary calcium, the higher the heart scan "score," the greater the risk for heart attack and other unstable coronary syndromes that lead to stents, bypass, etc.

But can calcium also cause plaque to form or trigger processes that lead to plaque formation and/or instability?

Nadra et al show, in an in vitro preparation, that calcium phosphate crystals are actively incorporated into inflammatory macrophages, which then trigger a constellation of inflammatory cytokine release (tumor necrosis factor-alpha, interleukins), fundamental processes underlying atherosclerotic plaque formation and inflammation.

Here's the abstract of the study:
Proinflammatory Activation of Macrophages by Basic Calcium Phosphate Crystals via Protein Kinase C and MAP Kinase Pathways:

A Vicious Cycle of Inflammation and Arterial Calcification?


Basic calcium phosphate (BCP) crystal deposition underlies the development of arterial calcification. Inflammatory macrophagescolocalize with BCP deposits in developing atherosclerotic lesionsand in vitro can promote calcification through the release of TNF alpha. Here we have investigated whether BCP crystals can elicit a proinflammatory response from monocyte-macrophages.BCP microcrystals were internalized into vacuoles of human monocyte-derived macrophages in vitro. This was associated with secretion of proinflammatory cytokines (TNF{alpha}, IL-1ß and IL-8) capable of activating cultured endothelial cells and promoting capture of flowing leukocytes under shear flow. Critical roles for PKC, ERK1/2, JNK, but not p38 intracellular signaling pathways were identified in the secretion of TNF alpha, with activation of ERK1/2 but not JNK being dependent on upstream activation of PKC. Using confocal microscopy and adenoviral transfection approaches, we determined a specific role for the PKC-alpha isozyme.

The response of macrophages to BCP crystals suggests that pathological calcification is not merely a passive consequence of chronic inflammatory disease but may lead to a positive feed-back loop of calcification and inflammation driving disease progression.



This observation adds support to the notion that increasing coronary calcium scores, i.e., increasing accumulation of calcium within plaque, suggests active plaque. As I say in Track Your Plaque, "growing plaque is active plaque." Active plaque means plaque that is actively growing, inflamed and infiltrated by inflammatory cells like macrophages, eroding its structural components, and prone to "rupture," i.e., cause heart attack. Someone whose first heart scan score is, say, 100, followed by another heart scan score two years later of 200 is exposed to sharply increasing risk for cardiovascular events which may, in part, be due to the plaque-stimulating effects of calcium.

Conversely, reducing coronary calcium scores removes a component of plaque that would otherwise fuel its growth. So, people like our Freddie, who reduced his heart scan score by 75%, can be expected to enjoy a dramatic reduction of risk for cardiovascular events.

Less calcium, less plaque to rupture, less risk.

Wheat one-liners

If you're having difficulty convincing a loved one or someone else that wheat should be eliminated from the human diet, here are some useful one-liners to use:

Wheat makes your boobs big.
(This is true. Priceless for women to use on their husbands.)

Wheat causes dementia.
(And confirmed on examination of brain tissue at autopsy. Yes, autopsy.)

Wheat makes you look pregnant.
(The visceral fat of a wheat belly does a darn good imitation of a near-term infant.)

The first sign of wheat intolerance can be wetting your pants.
(Cerebellar ataxia, i.e., destruction and atrophy of the cerebellum, caused by wheat leads to loss of coordination and bladder control. Average age of onset: 53 years old.)

White flour bad, whole grain better; just as Marlboros are bad, Salems are better.
(The flawed syllogism that led to the "eat more healthy whole grain" colossal blunder.)

Wheat is the only food with its very own mortality rate.
(Celiac disease, osteoporotic hip fractures, and the neurologic diseases triggered by wheat can be fatal.)

"Wheat" is no longer wheat; it's the dwarf mutant that came from genetics research in the 1960s.
(Over 99% of all wheat today comes from the 18-inch tall dwarf mutant.)

Wheat increases blood sugar higher than nearly all other foods.
(Higher than Milky Way bars, higher than Snickers bars, higher than table sugar.)


There you have it: A full arsenal of one-liners to shoot at your husband, wife, or friend when they roll their eyes at your refusal to consume this thing called "wheat."

The happy homeotherm

If you were a "cold blooded" poikilotherm unable to regulate internal body temperature, you would have to sun yourself on rocks to raise your body temperature, just like turtles and snakes. When it got cold, your metabolic rate would slow and you might burrow into the mud to hide.

You and I, however, are homeotherms, terrestrial animals able to regulate our own internal body temperature. Principal responsibility for keeping your body temperature regulated falls with the thyroid gland, your very own thermoregulatory "thermostat."

But internal body temperature, even in a homeotherm, varies with circadian rhythm: Highest temperature occurs in the early evening around 8 p.m.; the low temperature nadir occurs at around 4 a.m.

The notion that normal human temperature is 98.6 degrees Fahrenheit is a widely-held fiction, a legacy of the extraordinary experience of 19th century German physician, Carl Reinhold August Wunderlich, who claims to have measured temperatures of one million people using his crude, uncalibrated thermometer to obtain axillary (armpit) body temperatures.

Dr. Broda Barnes was a 20th century American proponent of using the nadir body temperature to gauge thyroid function. Like Wunderlich, Barnes also used axillary temperatures.

Modern temperature assessments have employed radiotransmitting thermistors that are swallowed, with temperatures tracked as the thermistor travels through the stomach, duodenum, small intestine, large intestine, rectum, then peek-a-boos back out. Such internal "core temperature" assessments have shown that:

--Axillary temperatures do not track with internal core temperatures very well, often veering off course due to external factors.
--Axillary temperatures are subject to ambient temperatures, such as room temperature, and are affected by clothing.
--Axillary temperatures are more susceptible to physical activity, e.g., increased with exercise or physical work.

Even right vs. left axillary temperatures have been shown to vary up to 2 degrees Fahrenheit.

Studies such as this demonstrate that normal oral temperature upon arising is around 97.2-97.3 degrees Fahrenheit. While we lack data correlating thyroid function with circadian temperature variation, the a.m. nadir does indeed, as Dr. Barnes originally suggested, seem to track thyroid status quite well: lower with hypothyroidism, higher with normal or hyperthyroidism.

I have been using 97.3 degrees F orally as the cutoff for confirming or uncovering thyroid dysfunction, particularly when symptoms or blood tests (TSH, free T3, free T4) are equivocal, a value that has held up well in the majority of cases. I find it helpful when, for instance, someone complains of cold hands and feet and has normal TSH (1.5 mIU/L or less in my view) but low free T3. An a.m. oral temperature of, say, 95.7 degrees F, suggests that there will be a favorable response to T3 supplementation. And it nearly always plays out that way.

Wouldn't it be interesting to know if there was insight into thyroid status provided by also examining the circadian behavior of temperature (e.g., height or timing of the peak)?

Statin buster?

Merck recently reported preliminary results with its drug-in-development, anacetrapib.

After six months of treatment, participants showed:

LDL cholesterol was reduced from 81 mg/dl to 45 mg/dl in those taking anacetrapib, and from 82 mg/dl to 77 mg/dl in the placebo group.

HDL increased from 41 mg/dl to 101 mg/dl in the drug group, from 40 mg/dl to 46 mg/dl in those on placebo.

As you'd expect, the usual line-up of my colleagues gushed over the prospects of the drug, salivating over new speaking opportunities, handsomely-paid clinical "research" trials, and plenty of nice trips to exotic locales.

Anacetrapib is a cholesteryl-ester transfer protein inhibitor, or CETP inhibitor, much like its scrapped predecessor, torcetrapib . . . you know, the one that went down in flames in 2006 after 60% excess mortality occurred in people taking the drug compared to placebo. The hopes of many investors and Pfizer executives were dashed with torcetrapib's demise. The data on torcetrapib's lipid effects were as impressive as Merck's anacetrapib.

These drugs block the effects of the CETP enzyme, an enzyme with complex effects. Among CETP's effects: mediating the "heteroexchange" of triglycerides from triglyceride-rich VLDL particles that first emerge from the liver for cholesterol from LDL particles. This CETP-mediated process enriches LDL particles with triglycerides, which then make LDL a target for action by another enzyme, hepatic lipase, that removes triglycerides. This yields a several nanometer smaller LDL particle, now the number one most common cause of heart disease in the U.S., thanks to conventional advice to cut fat intake and increase consumption of "healthy whole grains."

With effects like this, anacetrapib, should it hold up under the scrutiny of FDA-required trials and not show the same mortality-increasing effects of torcetrapib, will be a huge blockbuster for Merck if release goes as scheduled in 2015. It will likely match or exceed sales of any statin drug. Statin drugs have achieved $27 billion annual sales, some of it deserved. Anacetrapib will likely handily match or exceed Lipitor's $12 billion annual revenue.

More than increasing HDL, CETP inhibition is really a strategy to reduce small LDL particles.

As with many drugs, there are natural means to achieve similar effects with none of the side-effects. In this case, similar effects to CETP inhibition, though with no risk of heightened mortality, is . . . elimination of wheat, in addition to an overall limitation of carbohydrate consumption. Not just low-carb, mind you, but wheat elimination on the background of low-carb. For instance, eliminate wheat products and limit daily carbohydrate intake to 50-100 grams per day, depending on your individual carbohydrate sensitivity, and small LDL drops 50-75%. HDL, too, will increase over time, not as vigorously as with a CETP inhibitor, but a healthy 20-30% increase, more with restoration of vitamin D.

Eliminating wheat and adjusting diet to ratchet down carbs is, of course, cheap, non-prescription, and can be self-administerd, criteria that leave the medical world indifferent. But it's a form of "CETP inhibition" that you can employ today with none of the worries of a new drug, especially one that might share effects with an agent with a dangerous track record.