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White coats are out-of-date--Not only do they serve as filthy reservoirs of microorganisms (since they hang unwashed after repeated use week after week), they only serve to distance the practitioner from the patient, an outdated notion that should join electroshock therapy to treat homosexuality and other "disorders" in the museum of outdated medical practices.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

CIS: Carbohydrate intolerance syndrome

Carbohydrate intolerance comes in many shades and colors, shapes and sizes.

I call all of its varieties the Carbohydrate Intolerance Syndrome, or CIS. (Not to be confused with CSI, or Crime Scene Investigation . . . though, come to think of it, perhaps there are some interesting parallels!)

At its extreme, it is called type II diabetes, in which any carbohydrate generates an extravant increase in blood sugar, followed by the domino effect of increased triglycerides, reduction in HDL, creation of small LDL, heightened inflammation, etc. and eventually to kidney disease, coronary atherosclerosis, neuropathies, etc.

An intermediate form of carbohydrate intolerance is called metabolic syndrome, or pre-diabetes. These people, for the most part, look and act like diabetics, though their reaction to carbohydrate intake is not as bad. Blood sugar, for instance, might be 125 mg/dl fasting, 160 mg/dl after eating. The semi-arbitrary definition of metabolic syndrome includes at least three of the following: HDL <40 mg/dl in men, <50 mg/dl in women; triglycerides 150 mg/dl or greater; BP 135/80 or greater; waist circumference >40 inches in men, >35 inches in women; fasting glucose >100 mg/dl.

This is where the conventional definitions stop: Either you are diabetic or have metabolic syndrome, or you have nothing at all.

Unfortunately, this means that the millions of people with patterns not severe enough to match the standard definition of metabolic syndrome are often neglected.

How about Kevin?

Kevin, a 56 year old financial planner, is 5 ft 7 inches, 180 lbs (BMI 28.2). His basic measures:

HDL 36 mg/dl
Triglycerides 333 mg/dl

BP 132/78
Waist circumference 34 inches
Blood sugar 98 mg/dl

Kevin meets the criteria for metabolic syndrome on only two of the five criteria and therefore does not "qualify" for the diagnosis.

Kevin's basic lipids showed LDL 170 mg/dl, HDL 36 mg/dl, triglycerides 333 mg/dl.

But take a look at his underlying lipoprotein patterns (NMR):

LDL particle number 2231 nmol/L (equivalent to a "true" LDL of 223 mg/dl)
Small LDL 1811 nmol/l
Large HDL 0.0 mg/dl


In other words, small LDL constitutes 81% of all LDL particles (1811/2231), a severe pattern. Large HDL is the healthy, protective fraction and Kevin has none. These are high-risk patterns for heart disease. These, too, are patterns of carbohydrate intolerance.

Foods that trigger small LDL and reduction in healthy, large HDL include sugars, wheat, and cornstarch. Kevin is carbohydrate-intolerant, although he lacks the (fasting) blood sugar aspect of carbohydrate intolerance. But he shows all the underlying lipoprotein and other metabolic phenomena associated with carbohydrate intolerance.

We could also cast all three conditions under the umbrella of "insulin resistance." But I prefer Carbohydrate Intolerance Syndrome, or CIS, since it immediately suggests the basic underlying cause: eating carbohydrates, especially those that trigger rapid and substantial surges in blood sugar.

CIS is the Disease of the Century, judging by the figures (both numbers and humans) we are seeing. It will dominate healthcare in its various forms for many years to come.

The first treatment for the Carbohydrate Intolerance Syndrome? Some would say the TZD class of drugs like Avandia. Others would say a DASH or TLC (American Heart Association) diet. How about liposuction, twice-daily Byetta injections, or even the emerging class of drugs to manipulate leptin and adiponectin? How do "heart healthy" foods like Cheerios and Cocoa Puffs fit into this? (Don't believe me? The American Heart Association says they're heart healthy!)

The first treatment for the Carbohydrate Intolerance Syndrome is elimination of carbohydrates, except those that come from raw nuts and seeds, vegetables, occasional real fruit (not those green fake grapes), wine, and dark chocolates.

Making sense out of lipid changes

Maggie had been doing well on her program, enjoying favorable lipids near our 60-60-60 targets (HDL 60 mg/dl or greater, LDL 60 mg/dl or less, triglycerides 60 mg/dl or less). Last fall, her last set of values were:

Total cholesterol: 149 mg/dl
LDL cholesterol: 67 mg/dl
HDL cholesterol: 73 mg/dl
Triglycerides: 43 mg/dl

The holidays, as with most people, involved a frenzy of indulgent eating: Christmas cookies, cakes, pies, stuffing, potatoes, candies, etc.

Maggie returned to the office 6 pounds heavier with these values:

Total cholesterol: 210 mg/dl
LDL cholesterol: 124 mg/dl
HDL cholesterol: 57 mg/dl
Triglycerides: 144 mg/dl

In other words, holiday indulgences caused an increase in LDL cholesterol, a reduction in HDL, an increase in triglycerides, an increase in total cholesterol.

What happened?

At first glance, many of my colleagues would interpret this as fat indulgence and/or a "need" for statin drug therapy.

Having done thousands of lipoprotein panels, I can tell you that, beneath the surface, the following has occurred:

--Overindulgence in carbohydrates from the goodies triggered triglyceride (actually VLDL) formation in the liver, released into the blood.
--Increased triglycerides and VLDL triggered a boom in conversion of large LDL to small LDL (since triglycerides are required to form small LDL particles) via cholesteryl-ester transfer protein (CETP) activity.
--Increased triglycerides and VLDL interacted with HDL particles, causing "remodeling" of HDL particles to the less desirable, less protective small particles, which do not persist as long in the blood, resulting in a reduction of HDL.

The critical factor is carbohydrate intake. This triggered a domino effect that is often misintepreted as excessive fat intake or a genetic predisposition. It is nothing of the kind.

I discussed this phenomenon with Maggie. She now knows to not overindulge in the holiday snacks in future and will revert promptly back to her 60-60-60 values.

How to Give Yourself Hashimoto's Thyroiditis: 101

I borrowed this from the enormously clever Dr. BG at The Animal Pharm Blog.


How to Give Yourself Hashimoto's Thyroiditis: 101

--lack of sunlight/vitamin D/indoor habitation
--mental stress
--more mental stress
--sleep deprivation... (excessive mochas/lattes at Berkeley cafes)
--excessive 'social' calendar
--inherent family history of autoimmune disorders (who doesn't??)
--wheat, wheat, and more wheat ingestion ('comfort foods' craved in times of high cortisol/stress, right? how did I know the carbs were killing me?)
--lack of nutritious food containing EPA DHA, vitamin A, sat fats, minerals, iodine, etc
--lack of play, exercise, movement (or ?overtraining perhaps for Oprah's case)
--weight gain -- which begins an endless self-perpetuating vicous cycle of all the above (Is it stressful to balloon out for no apparent reason? YES)



If you haven't done so already, take a look at Animal Pharm you will get a real kick out of Dr. BG's quick-witted take on things.


We are systematically looking for low thyroid (hypothyroidism) in everyone and findings oodles of it, far more than I ever expected.

Much of the low thyroid phenomena is due to active or previous Hashimoto's thyroiditis, the inflammatory process that exerts destructive effects on the delicate thyroid gland. It is presently unclear how much is due to iodine deficiency in this area, though iodine supplementation by itself (i.e., without thyroid hormone replacement) has not been yielding improved thyroid measures.

I find this bothersome: Is low thyroid function the consequence of direct thyroid toxins (flame retardants like polybrominated diphenyl ethers, pesticide residues in vegetables and fruits, bisphenol A from polycarbonate plastics) or indirect toxins such as wheat via an autoimmune process (similar to that seen in celiac disease)?

I don't know, but we've got to deal with the thyroid-destructive aftermath: Look for thyroid dysfunction, even in those without symptoms, and correct it. This has become a basic tenet of the Track Your Plaque approach for intensive reduction of coronary risk.

Framing

Heart health without a 12" incision



Heart health for less than $44,483 (Cost of a coronary stent according to the American Heart Association 2008 Update)



Track Your Plaque: A drug-free zone



Why an RDA for vitamin D?

The Food and Nutrition Board (FNB) of the Institute of Medicine is charged with setting the values for the Recommended Daily Allowances of various essential nutrients. However, when it comes to vitamin D, the FNB decided that "evidence is insufficient to develop an RDA and [an Adequate Intake, AI] is set at a level assumed to ensure nutritional adequacy."

The National Institutes of Health Office of Dietary Supplements lists the AI's for various groups of people:

14-18 years
Male 200 IU
Female 200 IU

19-50 years
Male 200 IU
Female 200 IU

51-70 years
Male 400 IU
Female 400 IU

71+ years
Male 600 IU
Female 600 IU


A reconsideration is apparently being planned in near-future that will (hopefully) incorporate the newest clinical data on vitamin D.

My question: Who cares what the FNB decides? Let me explain.

I monitor blood levels of 25-hydroxy vitamin D to assess the 1) starting level of vitamin D without supplementation, and 2) levels while on supplementation, preferably every 6 months (during sunny weather, during cold weather). I have done for the past 3 years in over 1000 people.

The requirement for vitamin D dose in adults, in my experience, ranges from as low as 1000 units per day to as high as 20,000 units per day, rarely more. The vast majority of women require 5000 units per day, males 6000 units per day to maintain a blood level in the desirable range. (I aim for 60-70 ng/ml.) A graph of the distribution of vitamin D needs in my area (Milwaukee, Wisconsin) is a bell curve, a curve more heavily weighted towards the upper vitamin D dose range.

Need for vitamin D to achieve the same blood level is influenced by age, sex, body size, race, presence or absence of a gallbladder, as well as other factors. But needs vary, even among similar people. For instance, a 50-year old woman weighing 140 lbs might need 4000 units per day to achieve a blood level of 25-hydroxy vitamin D of 65 ng/ml. Another 50-year old woman weighing 140 lbs might need 8000 units to achieve the same level, and 4000 units might increase her level to only 38 ng/ml. Two similar women, very different vitamin D needs. The differences can be striking.

Being a hormone--not a vitamin, as it was incorrectly labeled--vitamin D needs to be tightly regulated. We should have neither too little nor too much. I would liken it to thyroid hormones, which need to be tightly regulated for ideal health.

Now the FNB, in light of new data, wants to set new AI's, or even RDA's, for vitamin D for the U.S. This is an impossible--impossible--task. There is no way a broad policy can be crafted that serves everyone. It is impossible to state that all men or women, categorized by age, require X units vitamin D. This is pure folly and it is misleading.

The only rational answer for the FNB to provide is to declare that:

It is not possible to establish the precise need for vitamin D in a specific individual because of the multiplicity of factors, only some of which are known, that determine vitamin D needs. Individual need can only be determined by assessing the blood level of 25-hydroxy vitamin D prior to initiation of replacement and periodically following replacement to assess the adequacy of replacement dose. Continuing reassessment is recommended (e.g., every 6-12 months), as needs change with weight, lifestyle, and age.

Sure, it adds around $100-150 per year per person for lab testing to assess vitamin D levels. But the health gains made--reduced fractures, reduced incidence of diabetes, reduced colon, breast, and prostate cancer, less depression, reduced heart attack and heart procedures--will more than compensate.

Bargains for Armour Thyroid

We use Armour thyroid almost exclusively. I take it myself.

I am thoroughly convinced that, for at least 70% of people requiring thyroid replacement, the added T3 component makes a world of difference compared to isolated T4: More energy, greater alertness, better mental clarity, better weight loss, larger effects on lipoprotein(a).

However, there are substantial price disparities in different pharmacies.

For instance, in Milwaukee, a one month supply of 1 grain (60 mg) tablets costs:

Walgreen's: $36.00

Walmart: $9.54


That's a considerable price difference of nearly 400%. It therefore always pays to do a little bit of shopping.

Heart scan mis-information on WebMD

If you want information on how prescription drugs fit into your life, then go to WebMD.

But, if you are looking for information that cuts through the bullcrap, is untainted by the heavy-handed tactics of the drug industry, or doesn't support the "a heart catheterization for everyone" mentality, then don't go there.

A Heart Scan Blog reader turned up this gem on the WebMD site:

Should I have a coronary calcium scan to check for heart disease?

In their report, they list some reasons why a heart scan should not be obtained:

Most of the time, a physical exam and other tests can give your doctor enough information about your risk for heart disease.

You've got to be kidding me. What tests are they talking about?

EKG? An EKG is a crude test that tells us virtually nothing about the coronary arteries or risk for heart attack. It is helpful for heart rhythm disorders and other abnormalities, but virtually useless for coronary disease unless a heart attack is underway or has already occurred.

Cholesterol? What level of cholesterol tells you whether you have heart disease? Tim Russert, for instance, had the same cholesterol values 5 years before his death as on the day of his death. How would cholesterol have told his doctor that heart disease was present? Does an LDL cholesterol of 180 mg/dl tell you that someone has heart disease, while a value of 130 mg/dl does not?

Stress test? You mean like the normal stress test Bill Clinton had 3 months before his near-fatal collapse? Stress tests are a gauge of coronary flow, not of coronary atherosclerosis. Huge amounts of coronary plaque can be present while a stress test--flow--remains normal.

No, a physical exam does not uncover hidden heart disease. The annual physical is, in fact, a miserable failure for detection of hidden heart disease.


You already know that your risk for heart disease is low or high. The test works best in people who are at medium risk but have no symptoms.

This bit of fiction comes from a compromise statement in the American College of Cardiology and American Heart Association "consensus" document detailing the role of heart scans in heart disease detection. Because conventional thinkers don't like the idea of very early detection in seemingly "low risk" people, nor do they like the idea of diabetics and smokers getting a heart scan because it's "obvious" that they are already at high risk, the middle ground was taken: Scan only people at "intermediate risk."

What the heck is "intermediate risk"? Are you intermediate risk?

In real life, using standard criteria (e.g., Framingham scoring) to decide who is low-, intermediate-, or high-risk fails to identify over 1/3 of people with heart disease, while subjecting many without heart disease (plaque) to needless treatment (meaning statins, since that's the only real preventive treatment on most doc's armamentarium).

Another fact: Heart scans are quantitative, not just normal or abnormal. Your heart scan score could be 5, it could be 150, it could be 500, or 5000---it makes a world of difference. The risk of someone with a score of 5000 is at very different risk than someone with a score of 5. It also provides much greater precision in determining a specific individual's risk.



The test could give a high score even if your arteries aren't blocked. This might lead to extra tests that you don't need.

This is true--if you doctor has no idea what he's doing.

This is like saying that you should never take your car to the repair shop because all mechanics are crooks. If you have an unscrupulous cardiologist who tells you that your heart scan score of 25 means you are a "walking time bomb" and heart catheterization is necessary to determine whether you "need" a stent . . . well, this is no different than the shady mechanic who advises you that your car's engine needs to be rebuilt for $3000, when all you really needed was a few new spark plugs.

Coronary plaque is coronary plaque, and all coronary plaque has potential for rupture (heart attack)--even if it doesn't block flow. This is true at a score of 10, or 100, or 1000--all plaque is potentially rupture-prone, though the more plaque you have, the greater the likelihood.


Not all blocked arteries have calcium. So you could get a low calcium score and still be at risk.

They're missing the point: ANY calcium score carries risk, so a low score should not be interpreted as having no risk. But, just because a procedure like stenting or bypass surgery is not necessary to restore flow, it does not mean that risk for plaque rupture is not present--it is.

Any heart scan score should be taken seriously, meaning sufficient reason to engage in a program of heart disease prevention.

Although not perfect, coronary calcium scoring remains the easiest, most accessible, and least expensive means for identifying and quantifying coronary atherosclerosis--whether or not WebMD and drug industry money endorse them.

Heart disease prevention for the helpless, ignorant, or non-compliant

The media outlets are gushing with the "research"/marketing spinoff of the JUPITER trial, an analysis conducted by Dr. Erica Spatz of Yale University, that suggests that statin use should be expanded to many millions more Americans.

USA Today: Study: 11M more should get statins

MedPage: JUPITER Findings Could Boost Statin Use by 20%

Health Day: Millions More Americans Might Be Placed on Statins

WebMD: More May Benefit From Cholesterol Drugs: Study Shows More Would Qualify for Statin Treatment if Levels of C-Reactive Protein Are Considered


You may recall that the JUPITER trial (discussed previously in a Heart Scan Blog post) studied the cardiovascular event risk in people with "normal" LDL cholesterols (calculated, of course, not measured) of 130 mg/dl or less, along with increased c-reactive protein, a crude inflammatory measure, of 2.0 mg/dl or greater. A 54% (relative) reduction in cardiovascular events occured in the group taking Crestor 20 mg per day.

What I see is a confluence of events that have brought us to the "statin drugs are necessary for everybody" mentality:

--The low-fat diet advice of the last 40 years has increased non-fat or low-fat foods that increase LDL, since removing fat from the diet provokes small LDL particle production and increases the inflammatory measure, c-reactive protein (CRP).

--The proliferation of "healthy whole grains" in the diet have also caused an enormous boom in small LDL particles, which is interpreted to the uninformed as "high cholesterol." It has also provoked CRP substantially.

--The advice to reduce salt intake has brought a broad re-emergence of iodine deficiency. When thyroid hormone production flags due to lack of iodine, LDL cholesterol (both large and small) increase.

--Our lives, which are increasingly conducted indoors, have worsened the already substantial vitamin D deficiency. While deficiency of vitamin D primarily reduces HDL cholesterol and increases triglycerides, it can also cause an increase in small LDL and a large increase in CRP.


In other words, a collection of events have converged to provide the appearance of high LDL cholesterol and high CRP. This creates the appearance of a "need" for statin drugs. The JUPITER trial now exploits both the LDL-reducing and CRP-decreasing effects of statins.

I view the foisting of Crestor via the JUPITER argument on the public as taking full advantage of the helpless situation many Americans find themselves in: Reduce fat intake, eat more healthy whole grains and . . . cholesterol and CRP skyrocket! "You need Crestor! See, I told you it was genetic," says the doctor after attending the nice AstraZeneca-sponsored drug dinner.

The notion of using a drug like Crestor to suppress inflammatory patterns is absurd. There are far better, easier, cheaper ways to achieve this goal, along with dramatic reduction in cardiovascular risk. But, to the ignorant, the helpless, or non-compliant with real change in diet and lifestyle, then Crestor does serve a purpose.

I can only hope that the excessive pushing of statin drugs on the public will sooner or later trigger a revolt.

Dangerous mis-information on vitamin D


Please be aware of the ignorant propagating information they have no business talking about.

This is one such example, a newsletter from pop exercise guru, Denise Austin.

Although I'm sure she means well, I have a problem with people who have little to no experience acting as experts, often simply repeating something they heard or read somewhere else. This has become particular problem with the internet, in which bad information can get repeated thousands of times, gaining a veil of "truth" through its repetition. I don't mean to pick specifically on Ms. Austin, since she joins a growing rank of pseudo-experts on vitamin D and other topics, but she provides a good example of how far wrong mainstream information can be.



Simple Steps
Do Your D!


Calcium often gets all the glory when it comes to bone health. But calcium wouldn't benefit your bones much without its partner, vitamin D!

Why? Vitamin D helps your body absorb calcium and keeps your bones strong; without enough vitamin D, the bones become weak and brittle, a condition called rickets in children, and osteomalacia in adults. Adults from 19 to 50 need 200 IU (international units) per day, while those from 51 to 70 need 400 IU daily. Those over 70 need 600 IU per day.

Unfortunately, not too many foods contain vitamin D naturally. (Tuna and sardines canned in oil are exceptions.) The good news is that many foods are now regularly fortified with vitamin D, including milk, some yogurts, margarines, and cereals. You can check the Nutrition Facts panel on packages and containers to see which products contain vitamin D. It should be listed after vitamins A and C, along with the percentage of the Daily Value that a serving of the food contains. The Daily Value (a standardized amount) for vitamin D is 400 IU, so if your milk has 25 percent of the Daily Value, it provides 100 IU per serving.

Your skin can also make vitamin D using sunlight — you need about a half hour of exposure to the midday sun twice a week to make enough. However, because of the increasing incidence of skin cancer in recent years, many experts are wary about recommending sun exposure.

So take a closer look at milk, yogurt, cereal, and margarine selections when you're doing your weekly shopping, and stock up on brands that are fortified with vitamin D. Challenge yourself to consume one source of vitamin D at least three days in the coming week! If you cannot eat or do not like any foods that contain vitamin D or are fortified with it, talk with your health care provider ASAP about taking a supplement. Your bones will thank you for it!



Let me list the mistakes in this piece:

Adults from 19 to 50 need 200 IU (international units) per day, while those from 51 to 70 need 400 IU daily. Those over 70 need 600 IU per day.

This is the same non-information that was the advice originally offered by the Food and Nutrition Board based on a best guesstimate due to lack of data. It is clear from newer data that doses required for full restoration of vitamin D are in the thousands of units. (My personal dose for full restoration of vitamin judged by serum levels of 25-hydroxy vitamin D is 8000 units per day.)

The information coming from the Food and Nutrition Board is about as good as the information coming from the USDA (you know, that "government" agency meant to represent the interests of ConAgra, Cargill, and Big Farming) and the American Heart Association (that represents consensus opinion from data 20 years out of date and now arm-in-arm with Big Food like General Mills, Kraft, and Nabisco). These agencies and the advice they offer has, over the past few years, become increasingly irrelevant and outdated. It is the Information Age, in which ulterior motives are becoming more readily exposed, yet they still operate by the rules of the Industrial Age and deliver a message that serves their own purposes.

Ms. Austin fell for it.


The good news is that many foods are now regularly fortified with vitamin D, including milk, some yogurts, margarines, and cereals.

First of all, what is a "diet expert" doing advocating industrial foods? Cereals, in particular, are among the worst foods on the supermarket shelves, whether or not they are fortified. Candy bars can be fortified, too; that doesn't make them any better for you.

The vitamin D added to these foods is, more often than not, the ergocalcferol, or D2, form that is woefully ineffective. And the dose added is trivial, usually in the 100-200 unit range per serving. The same goes for the milk, an inadequate source that we don't even factor into total intakes because of the low quantity.


Your skin can also make vitamin D using sunlight — you need about a half hour of exposure to the midday sun twice a week.


Nope. This might be true for a young person below age 30 in a southern environment. It is NOT true for the majority of people in northern climates and anyone over age 30 or 40, since we lose most of the capacity to activate vitamin D in the skin as we age. A deep, dark Florida tan does not necessarily mean that vitamin D has been activated. See A tan does not equal vitamin D. Here in Wisconsin, where, despite this darn cold winter, does enjoy wonderfully warm and beautiful summers, the average vitamin D dose need ranges from 4000-8000 units per day in summer, slightly more in winter.

By the way, it is not calcium that is instrumental to bone health. It is vitamin D. Calcium is the passive bricks and mortar of bones, while vitamin D is the bricklayer, the determinant of calcium's fate, the master control of bone health. Calcium supplementation becomes almost immaterial when vitamin D is restored.

I praise Ms. Austin for her hard work, trying to help fat Americans lose weight. But please ignore her advice on vitamin D, along with the numbing repetition of this mis-information that will likely propagate from other exercise gurus, dietitians, and pseudoexperts.

A Tale of Two LDL's

Kurt, a 50-year old businessman with a heart scan score of 323, had a :

--Conventional (calculated) LDL of 128 mg/dl
--Real measured LDL 241 mg/dl.


Laurie, a 53-year old woman who underwent a coronary bypass operation last year (before I met her), had a:

--Conventional LDL of 142 mg/dl
--Real measured LDL was 85 mg/dl.


(By "real, measured" LDL, I'm referring to LDL particle number in units of nmol/L obtained through NMR lipoprotein testing and dividing by 10, or just dropping the last digit to convert the value to mg/dl. This technique was arrived at by comparing the population distributions of these two parameters, LDL particle number and calculated LDL. This is the gold standard in my view. Similar numbers can be obtained by measuring apoprotein B, direct LDL, or calculated non-HDL, with diminishing reliability from first to last.)

In other words, Kurt's conventional LDL underestimated real LDL by 88%. Laurie's conventional LDL overestimated real LDL by 40%.

Interestingly, Laurie's doctor had insisted she take Lipitor for a high LDL cholesterol. Her real LDL was, in fact, low to begin with and benefits of a statin drug would be little to none. (Remember, in our Track Your Plaque approach, multiple other treatments are included, such as omega-3 fatty acids from fish oil, vitamin D normalization, and wheat elimination, strategies that yield benefits that others expect to obtain with statins.) Laurie's real cause of her heart disease proved to have nothing to do with LDL cholesterol, but involved lipoprotein(a) and thyroid issues.

Kurt proved to have a severe preponderance of small LDL particles--the worst kind of LDL, while Laurie had none--a benign pattern.

Then how can anyone make sense of the conventional, calculated LDL cholesterol that is generally (95% of the time) provided? If accuracy can stretch to plus or minus 80% . . . you can't. Conventional LDL is a miserably inaccurate number. The problem is that obtaining a superior number requires a step or two more testing and insight, something most busy primary care doc's simply don't have in the midst of a day filled with arthritis, bronchitis, diarrhea, belly aches, and seborrhea.

Yet conventional--I call it "fictitious"--LDL serves as the basis for this $27 billion (annual revenues) industry selling statin drugs.

This is meant to be neither an argument in favor of nor against statin drugs. However, it is plain as day that any study designed to reduce LDL cholesterol will be hopelessly clouded by calculated LDL imprecision. A calculated LDL of, say, 143 mg/dl might really be 187 mg/dl, or it might be 74 mg/dl--you can't tell by looking just at LDL. Yet billions of dollars of research and billions of dollars of healthcare costs are based on the treatment of this number.

This reminds me of the mark-to-market accounting magic that helped topple Wall Street.

I don't think that the statin world is poised for such a huge downfall. But I do see this as a source of enormous dilution of the effects of statin drugs. People who barely stand to benefit get the drugs, while others who might truly benefit are treated inadequately. It provides fuel to the growing idea that reducing LDL cholesterol fails to truly provide benefit.

I am no lover of statin drugs nor drugs in general. But I am a fan of knowing the truth. Despite my bashing of the drug industry (and make no mistake: the drug industry is a cutthroat, profit-seeking, do-anything-to-increase-sales industry), I do believe that there is a role for statin drugs (though far smaller than $27 billion per year). But the usual method of selecting people for treatment is pure fiction. The ATP-III cholesterol treatment guidelines? An anemic attempt to apply structure to meaningless values.

You and I do not need to subscribe to this sort of non-quantitative nonsense.