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White coats are out-of-date--Not only do they serve as filthy reservoirs of microorganisms (since they hang unwashed after repeated use week after week), they only serve to distance the practitioner from the patient, an outdated notion that should join electroshock therapy to treat homosexuality and other "disorders" in the museum of outdated medical practices.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

Krill oil: Do the math

The manufacturers of krill oil claim that the phospholipid form of omega-3 fatty acids, EPA and DHA, enhance their absorption. There are indeed some data to that effect:


Here are some representative krill oil preparations available on the market:


MegaRed Krill Oil:
EPA 50 mg
DHA 24 mg
Total omega-3s (EPA + DHA + other forms) 90 mg
Price: $28.99 for 60 softgels

Source Naturals (a fine company otherwise, by the way):

EPA 150 mg
DHA 90 mg
Total omega-3 fatty acids 300 mg
Price: $24.99 for 60 softgels

Alright, let's do some simple math:

Average volume of blood in the human body (all components): 5000 cc
Percentage of red blood cells (RBCs) by volume: 45%
Total volume RBCs: 2250 cc
Percentage of total volume RBCs occupied by fatty acids:

What tests are MORE important than cholesterol?

In the conventional practice of early heart disease prevention, cholesterol testing takes center stage. Rarely does it go any further, aside from questions about family history and obvious sources of modifiable risk such as smoking and sedentary lifestyle.

So standard practice is to usually look at your LDL cholesterol, the value that is calculated, not measured, then--almost without fail--prescribe a statin drug. While there are indeed useful values in the standard cholesterol panel--HDL cholesterol and triglycerides--they are typically ignored or prompt no specific action.

But a genuine effort at heart disease prevention should go farther than an assessment of calculated LDL cholesterol, as there are many ways that humans develop coronary atherosclerosis. Among the tests to consider in order to craft a truly effect heart disease prevention program are:

--Lipoprotein testing--Rather than using the amount of cholesterol in the various fractions of blood as a crude surrogate for lipoproteins in the bloodstream, why not measure lipoproteins themselves? These techniques have been around for over 20 years, but are simply not part of standard practice.

Lipoprotein testing especially allows you to understand what proportion of LDL particles are the truly unhealthy small LDL particles (that are oxidation- and glycation-prone). It also identifies whether or not you have lipoprotein(a), the heritable factor that confers superior survival capacity in a wild environment ("The Perfect Carnivore"), but makes the holder of this genetic pattern the least tolerant to the modern diet dominated by grains and sugars, devoid of fat and organ meats.

--25-hydroxy vitamin D--The data documenting the health power of vitamin D restoration continue to grow, with benefits on blood sugar and insulin, blood pressure, bone density, protection from winter "blues" (seasonal affective disorder), decrease in falls and fractures, decrease in cancer, decrease in cardiovascular events. I aim to keep 25-hydroxy vitamin D at a level of 60 to 70 ng/ml. This generally requires 4000-8000 units per day in gelcap form, at least for the first 3 or so years, after which there is a decrease in need. Daily supplementation is better than weekly, monthly, or other less-frequent regimens. The D3 (cholecalciferol) form is superior to the non-human D2 (ergocalciferol) form.

--Hemoglobin A1c (HbA1c)--HbA1c represents glycated hemoglobin, i.e., hemoglobin molecules within red blood cells that are irreversibly modified by glucose, or blood sugar. It therefore provides an index of endogenous glycation of all proteins of the body: proteins in the lenses of the eyes that lead to cataracts; proteins in the cartilage of the knees and hips that lead to brittle cartilage and arthritis; proteins in kidney tissue leading to kidney dysfunction.

HbA1c provides an incredibly clear snapshot of health: It reflects the amount of glycation you have been exposed to over the past 90 or so days. We therefore aim for an ideal level: 5.0% or less, the amount of "ambient" glycation that occurs just with living life. We reject the notion that a HbA1c level of 6.0% is acceptable just because you don't "need" diabetes medication, the thinking that drives conventional medical practice.

--RBC Omega-3 Index--The average American consumes very little omega-3 fatty acids, EPA and DHA, such that a typical omega-3 RBC Index, i.e., the proportion of fatty acids in the red blood cell occupied by omega-3 fatty acids, is around 2-3%, a level associated with increased potential for sudden cardiac death (death!). Levels of 6% or greater are associated with reduced potential for sudden cardiac death; 10% or greater are associated with reduced other cardiovascular events.

Evidence therefore suggests that an RBC Omega-3 Index of 10% or greater is desirable, a level generally achieved by obtaining 3000-3600 mg EPA + DHA per day (more or less, depending on the form consumed, an issue for future discussion).

--Thyroid testing (TSH, free T3, free T4)--Even subtle degrees of thyroid dysfunction can double, triple, even quadruple cardiovascular risk. TSH values, for instance, within the previously presumed "normal" range, pose increased risk for cardiovascular death; a TSH level of 4.0 mIU, for instance, is associated with more than double the relative risk of a level of 1.0.

Sad fact: the endocrinology community, not keeping abreast of the concerning issues coming from the toxicological community regarding perchlorates, polyfluorooctanoic acid and other fluorinated hydrocarbons, polybrominated diphenyl ethers (PDBEs), and other thyroid-toxic compounds, tend to ignore these issues, while the public is increasingly exposed to the increased cardiovascular risk of even modest degrees of thyroid dysfunction. Don't commit the same crime of ignorance: Thyroid dysfunction in this age of endocrine disruption can be crucial to cardiovascular and overall health.


All in all, there are a number of common blood tests that are relevant--no, crucial--for achieving heart health. Last on the list: standard cholesterol testing.

Cranberry Sauce

Happy Thanksgiving 2012, everyone, from all the staff at Track Your Plaque!

Here’s a zesty version of traditional cranberry sauce, minus the sugar. The orange, cinnamon, and other spices, along with the crunch of walnuts, make this one of my favorite holiday side dishes.

There are 31.5 grams total “net” carbohydrates in this entire recipe, or 5.25 grams per serving (serves 6). To further reduce carbs, you can leave out the orange juice and, optionally, use more zest.

1 cup water
12 ounces fresh whole cranberries
Sweetener equivalent to 1 cup sugar (I used 6 tablespoons Truvía)
1 tablespoon orange zest + juice of half an orange
½ cup chopped walnuts
1 teaspoon ground cinnamon
½ teaspoon ground nutmeg
¼ teaspoon ground cloves

In small to medium saucepan, bring water to boil. Turn heat down and add cranberries. Cover and cook at low-heat for 10 minutes or until all cranberries have popped. Stir in sweetener. Remove from heat.

Stir in orange zest and juice, walnuts, cinnamon, nutmeg, and cloves.

Transfer mixture to bowl, cool, and serve.


Apple Cranberry Crumble

Apple, cranberry, and cinnamon: the perfect combination of tastes and scents for winter holidays!

I took a bit of carbohydrate liberties with this recipe. The entire recipe yields a delicious cheesecake-like crumble with 59 “net” grams carbohydrates (total carbs – fiber); divided among 10 slices, that’s 5.9 grams net carbs per serving, a quantity most tolerate just fine. (To reduce carbohydrates, the molasses in the crumble is optional, reducing total carbohydrate by 11 grams.)

Other good choices for sweeteners include liquid stevia, stevia glycerite, powdered stevia (pure or inulin-based, not maltodextrin-based), Truvía, Swerve, and erythritol. And always taste your batter to test sweetness, since sweeteners vary in sweetness from brand to brand and your individual sensitivity to sweetness depends on how long you’ve been wheat-free. (The longer you’ve been wheat-free, the less sweetness you desire.)


Crust and crumble topping
3 cups almond meal
1 stick (8 tablespoons) butter, softened
1 cup xylitol (or other sweetener equivalent to 1 cup sugar)
1½ teaspoons ground cinnamon
1 tablespoon molasses
1½ teaspoons vanilla extract
Dash sea salt

Filling
16 ounces cream cheese, softened
2 large eggs
½ cup xylitol (or other sweetener equivalent to ½ cup sugar)
1 Granny Smith apple (or other variety)
1 teaspoon ground cinnamon
1 cup fresh cranberries

Preheat oven to 350° F.

In large bowl, combine almond meal, butter, sweetener, cinnamon, molasses, vanilla, and salt and mix.

Grease a 9½-inch tart or pie pan. Using approximately 1 cup of the almond meal mixture, form a thin bottom crust with your hands or spoon.

In another bowl, combine cream cheese, eggs, and sweetener and mix with spoon or mixer at low-speed. Pour into tart or pie pan.

Core apple and slice into very thin sections. Arrange in circles around the edge of the cream cheese mixture, working inwards. Distribute cranberries over top, then sprinkle cinnamon over entire mixture.

Gently layer remaining almond meal crumble evenly over top. Bake for 30 minutes or until topping lightly browned.

Biscuits and Gravy



Biscuits and gravy: the ultimate comfort food . . . one you thought you’d never have again!

The familiar dish of breakfast and holiday meals is recreated here with a delicious gravy that you can pour over piping hot biscuits. Because it contains no wheat or other unhealthy thickeners like cornstarch made with “junk” carbohydrates, there should be no blood sugar or insulin problems with this dish, nor joint pain, edema, acid reflux, mind “fog,” or dandruff—life is good without wheat!

While the gravy is also dairy-free for those with dairy intolerances, the biscuits are not, as there are cheese and butter in the biscuits, both of which are optional, e.g., leave out the cheese and replace butter with coconut or other oil.

Makes 10 biscuits

Gravy:
2 tablespoons extra-virgin olive oil
1 pound loose sausage meat
2½ cups beef broth
¼ cup coconut flour
½ cup coconut milk (canned variety)
1 tablespoon onion powder
1 teaspoon garlic powder
½ teaspoon sea salt
Dash ground black pepper

Biscuits:
1 cup shredded cheddar (or other) cheese
2 cups almond meal/flour
¼ cup coconut flour
¾ teaspoon baking soda
½ teaspoon sea salt
2 large eggs
4 ounces butter, melted (or other oil, e.g., extra-light olive, coconut, walnut)

To make gravy:
In large skillet, heat oil over medium heat. Sauté sausage, breaking up as it browns. Cook until thoroughly cooked and no longer pink.

Turn heat up to medium to high and pour in beef broth. Heat just short of boiling, then turn down to low heat. Stir in coconut flour, little by little, over 3-5 minutes; stop adding when gravy obtains desired thickness. Pour in coconut milk and stir in well. Add onion powder, garlic powder, salt, and pepper and simmer over low heat for 5 minutes. Add additional salt and pepper to taste. Remove from heat and set aside.

To make biscuits:
Preheat oven to 325° F.

In food chopper or processor, pulse shredded cheese to finer, granular consistency.

Pour cheese into large bowl, then add almond meal, coconut flour, baking soda, and salt and mix thoroughly. Add the eggs and butter or oil and mix thoroughly to yield thick dough.

Spoon out dough into 10 or so ¾-inch thick mounds onto a parchment paper-lined baking pan. Bake for 20 minutes or until lightly browned and toothpick withdraws dry.

Ladle gravy onto biscuits just before serving.

The Perfect Carnivore

People who carry the gene for lipoprotein(a), Lp(a), tend to be:

--Intelligent--The bell curve of IQ is shifted rightward by a substantial margin.
--Athletic--With unusual capacity for long-endurance effort, thus the many marathoners, triathletes, and long-distance bikers with Lp(a).
--Tolerant to dehydration
--Tolerant to starvation
--Resistant to tropical infections

In other words, people with Lp(a) have an evolutionary survival advantage. More than other people, they make clever, capable hunters who can run for hours to chase down prey, not requiring food or water, and less likely to succumb to the infections of the wild. In a primitive setting, people with Lp(a) are survivors. Evolution has likely served to select Lp(a) people for their superior survival characteristics.

But wait a minute: Isn't Lp(a) a risk for heart attack and stroke? Don't we call Lp(a) "the most aggressive known cause for heart disease and stroke that nobody gives a damn about"?

Yes. So what allows this evolutionary advantage for survival to become a survival disadvantage?

Carbohydrates, especially those from grains and sugars. Let me explain.

More so than other people, Lp(a) people express the small LDL pattern readily when they consume carbohydrates such as those from "healthy whole grains." Recall that the gene for Lp(a) is really the gene for apoprotein(a), the protein that, once produced by the liver and released into the bloodstream, binds to an available LDL particle to create the combination Lp(a) molecule. If the LDL particle component of Lp(a) is small, it confers greater atherogenicity (greater plaque-causing potential). Thus, carbohydrate consumption makes Lp(a) a more aggressive cause for atherosclerotic plaque. The situation can be made worse by exposure to vegetable oils, such as those from sunflower or corn, which increases production of apo(a).

Also, more than other people, Lp(a) people tend to show diabetic tendencies with consumption of carbohydrates. Eat "healthy whole grains," for instance, or if a marathoner carb-loads, he/she will show diabetic-range blood sugars. I have seen long-distance runners or triathletes, for instance, have a 6 ounce container of sugary yogurt and have blood sugars of 200 mg/dl or higher. The extreme exercise provides no protection from the diabetic potential.

Because carbohydrates are so destructive to the Lp(a) type, it means that people with this pattern do best by 1) absolutely minimizing exposure to carbohydrates and vegetable oils, ideally grain-free and sugar-free, and 2) rely on a diet rich in fats and proteins.

The perfect diet for the Lp(a) type? It would be a diet of feasting on the spoils of the hunt, devouring the wild boar captured and slaughtered and eating the snout, hindquarters, spleen, kidneys, heart, and bone marrow, then eating mushrooms, leaves, nuts, coconut, berries, small rodents, reptiles, fish, birds, and insects when the hunt is unproductive.

Capable hunter, survivor, consumer of muscle and organ meats: I call people with Lp(a) "The Perfect Carnivores."

Track Your Plaque in the news

The NPR Health Blog contacted me, as they were interested in learning more about health strategies and tools that are being used by individuals without their doctors. The Track Your Plaque website and program came up in their quest, as it is the only program available for self-empowerment in heart disease.

Several Track Your Plaque Members spoke up to add their insights. The full text of the article can be viewed here.

How's Your Cholesterol? The Crowd Wants To Know
Mainstream medicine isn't in favor of self-analysis, or seeking advice from non-professionals, of course. And anyone who does so is running a risk.

But there are folks who want to change the course of their heart health with a combination of professional and peer support. Some are bent on tackling the plaque that forms in arteries that can lead to heart disease. They gather online at Track Your Plaque, or "TYP" to the initiates.

"We test, test, test ... and basically experiment on ourselves and have through trial and error came up with the TYP program, which is tailored to the individual," Patrick Theut, a veteran of the site who tells Shots he has watched his plaque slow, stop and regress.

The site was created in 2004 by Bill Davis, a preventive cardiologist in Milwaukee, Wisc. Davis is also the author of Wheat Belly: Lose the Wheat, Lose the Weight and Find Your Path Back to Health, which argues that wheat is addictive and bad for most people's health. Davis recommends eliminating wheat from the diet to most new members of Track Your Plaque.

"The heart is one of the hardest things to self-manage but when you let people take the reins of control, you get far better results and far fewer catastrophes like heart attacks," Davis tells Shots.

Doctors typically give patients diagnosed with heart disease two options: take cholesterol-lowering statin drugs, or make lifestyle changes, like diet. It's usually far easier for both parties — the doctor and the patient — to go with the drugs than manage the much more difficult lifestyle changes, Davis says.

"Doctors say take the Lipitor, cut the fat and call me if you have chest pain," he explains. "But that's an awful way to manage care."

TYP has members submit their scores from heart CT scans, cholesterol values, lipoproteins and other heart health factors to a panel of doctors, nutritionists and exercise specialists. Then they receive advice in the form of an individualized plaque-control program. But the online forum, where users share their results with other members and exchange tips, is where most of the TYP action happens.

The community currently has about 2,400 members who pay $39.95 for a quarterly membership, or $89.75 for a yearly membership. Davis says all proceeds go towards maintaining the website.

Ilaine Upton is a 60-year-old bankruptcy lawyer from Fairfax, Va., and a TYP member. At a friend's suggestion, Upton decided to get a heart CT scan in July. Her score was higher than it should have been (22 instead of 0), so she decided to get her blood lipids and cholesterol tested, too, and sent a sample off to MyMedLabs.com.

She learned that her LDL particle count was over 2,000 ("crazy high," she says), and she posted her results on TYP. Davis advised her that a low-carb diet would reduce it, so she decided to try it.

Since July, she says she has had "excellent results" with the program, and her LDL counts are coming down.

"It would be nice to have a [personal] physician involved in this, but [my insurer] Blue Cross won't pay if you are not symptomatic, and I am trying to prevent becoming symptomatic," says Upton. "I feel very empowered by this knowledge and the ability to take better control of my health by getting feedback on the decisions I make."

Pecan Streusel Coffee Cake


This is about as decadent as it gets around here!

Here’s a recreation of an old-fashioned coffee cake, a version with a delicious chewy-crunchy streusel topping.

I’ve specified xylitol as the sweetener in the topping, as it is the most compatible sweetener for the streusel “crumb” effect and browning.

Variations are easy. For example, for an apple pecan coffee cake, add a layer of finely-chopped or sliced apples to the cake batter and topping.

Additional potential carbohydrate exposure comes from the garbanzo bean flour and molasses. However, distributed into 10 slices, each slice provides 7.2 grams “net” carbs (total carbs minus fiber), a perfectly tolerable amount. Be careful not to exceed two slices!

Yield 10 slices

Cake:
2½ cups almond flour
½ cup garbanzo bean flour
1 tablespoon ground cinnamon
1 teaspoon baking soda
Sweetener equivalent to ¾ cup sugar
Dash sea salt

3 eggs separated
3/8 teaspoon cream of tartar
1 tablespoon vanilla extract
4 ounces butter, melted
Juice of ½ lemon

Topping:
½ cup almond flour
¼ cup pecans, finely chopped
1 tablespoon ground cinnamon
½ cup xylitol
1 tablespoon molasses
6 ounces butter, cut into ½-inch widths, at room temperature

Preheat oven to 325º F. Grease bread pan.

In bowl, combine almond flour, garbanzo flour, cinnamon, baking soda, sweetener, salt, and mix.

In small bowl, whip egg whites and cream of tartar until stiff peaks form. At low speed, blend in egg yolks, vanilla, melted butter, and lemon juice.

Pour liquid mixture into almond mixture and mix thoroughly. Pour into microwave-safe bread pan and microwave on high for 3 minutes. Remove and set aside.

To make topping, combine almond flour, pecans, cinnamon, xylitol, and molasses in small bowl and mix. Mix in butter

Spread topping on cake. Bake for 20 minutes or until toothpick withdraws dry.

Recipe: Peanut Butter and Jelly Macaroons



If you miss peanut butter and jelly sandwiches, you’re going to absolutely love these peanut butter and jelly macaroons!

Not everybody loves the taste or texture of coconut. This issue is solved by the first step: toasting shredded coconut, then reducing them down to a granular consistency. This yields a macaroon consistency without the dominant coconut taste, replaced instead with the flavors of PB & J.

I’ve specified liquid stevia as the sweetener, but this is easily replaced by your choice of sweetener. Note that, regardless of which sweetener used, they vary in sweetness from brand to brand and the quantity required to equal the ½ cup of sugar equivalent can vary. It always helps to taste your batter and adjust sweetness.

Also, I used Swerve in this recipe, the erythritol-inulin mix that enhances texture, but its use is optional.

As written, each macaroon contains just over 3 grams “net” carbohydrates (total carbs minus fiber), meaning you can have several before doing any damage!

Makes 24 macaroons

3 cups shredded unsweetened coconut
2 tablespoons vanilla extract
1 teaspoon almond extract
¼ cup coconut flour
¼ cup dried unsweetened cherries (or other unsweetened berries)
2 tablespoons coconut oil
¼ cup natural peanut butter, room temperature
2 egg whites
½ teaspoon liquid stevia or sweetener equivalent to ½ cup sugar
2 tablespoons Swerve


Preheat oven to 300° F.

In large bowl, combine coconut, vanilla and almond extracts, and mix.

Spread mixture on baking sheet and bake for 10 minutes, stirring occasionally, until very lightly browned. Be careful not to burn. Remove and cool. (Leave oven at 300° F.)

When cooled, using food chopper, food processor, or coffee grinder, pulse coconut mixture until coconut reduced to consistency of coffee grounds. Pour back into bowl. Stir in coconut flour.

Place cherries or other berries in food chopper, food processor, or coffee grinder and pulse until reduced to small granules or paste. Remove with spatula and add to coconut mixture. Set aside.

Place egg whites in bowl and whip until frothy and stiff peaks form.

In small microwave-safe bowl, combine coconut oil and peanut butter and microwave in 10-second increments until warm (not hot) liquid. Stir in egg whites, followed by stevia and Swerve, and blend thoroughly.

Dispense dough onto a parchment paper-lined baking sheet using a 1 ½-inch cookie scooper or spoons.

Bake for 15 minutes or until lightly browned.

I Wish I Had Lipoprotein(a)!

Why would I say such a thing? Well, a number of reasons. People with lipoprotein(a), or Lp(a), are, with only occasional exceptions:

--Very intelligent. I know many people with this genetic pattern with IQs of 130, 140, even 160+.
--Good at math--This is true more for the male expression of the pattern, only occasionally female. It means that men with Lp(a) gravitate towards careers in math, accounting, financial analysis, physics, and engineering.
--Athletic--Many are marathon runners, triathletes, long-distance bicyclists, and other endurance athletes. I tell my patients that, if they want to meet other people with Lp(a), go to a triathlon.
--Poor at hydrating. People with Lp(a) have a defective thirst mechanism and often go for many hours without drinking water. This is why many Lp(a) people experience the pain of kidney stones: Prolonged and repeated dehydration causes crystals to form in the kidneys, leading to stone formation over time.
--Tolerant to dehydration--Related to the previous item, people with Lp(a) can go for extended periods without even thinking about water.
--Tolerant to periods of food deprivation or starvation--More so than other people, those with Lp(a) are uncommonly tolerant to days without food, as would occur in a wild setting.


In short, people with Lp(a) are intelligent, athletic, with many other favorable characteristics that provide a survival advantage . . . in a primitive world.

So when did Lp(a) become a problem? When an individual with Lp(a) is exposed to carbohydrates, especially those from grains. When an evolutionarily-advantaged Lp(a) individual is exposed to carbohydrates, more than other people they develop:

--Excess quantities of small LDL particles--Recall that Lp(a) is a two-part molecule. One part: an apo(a) made by the liver. 2nd part: an LDL particle. When the LDL particle within the Lp(a) molecule is small, its overall behavior is worse or more atherogenic (plaque-causing).
--Hyperglycemia/hyperinsulinemia--which then leads to diabetes. Unlike non-Lp(a) people, these phenomena can develop with far less visceral fat. A Lp(a) male, for instance, standing 5 ft 10 inches tall and weighing 150 pounds, can have as much insulin resistance/hyperglycemia as a non-Lp(a) male of similar height weighing 50+ pounds more.

Key to gaining control over Lp(a) is strict carbohydrate limitation. Another way to look at this is to say that Lp(a) people do best with unlimited fat and protein intake.