All posts by william-davis

Be patient with niacin

19. January 2007 William Davis (0)

Mel's HDL started at 37 mg/dl one year ago. Mel had several other abnormal lipoprotein patterns along with his HDL (inc. small LDL and Lp(a)), but HDL was clearly a crucial factor in his panel.

With a heart scan score of 1166, we needed to raise Mel's HDL to the Track Your Plaque target of 60 mg/dl. So Mel started niacin, our number one method to raise HDL, in addition to reducing his exposure to wheat products and other high glycemic index foods; increasing his physical activity; trying to reduce his excess tummy fat; fish oil; dark chocolate (2 oz per day) and red wine (1-2 glasses per day, preferably dark French reds). The form of niacin we often choose is SloNiacin (Upsher Smith), available over-the-counter for about $12-14 per 100 tablets.

Mel started out with niacin 500 mg per day at dinner, increased to 1000 mg at dinner after four weeks. Although this is usually too soon to reassess HDL, Mel insisted. His HDL 41 mg/dl. Mel's disappointment was palpable. He was the usual type A personality: he wanted his HDL higher--now! So Mel insisted that we increase niacin to 1500 mg per day. (We never go higher than this if low HDL or small LDL is the indication for niacin; only when Lp(a) is present do we go higher.)

Six months into this process, HDL: 45 mg/dl. Still a sluggish response.

One year later, HDL: 68 mg/dl. Finally!

That is typical for niacin, as well as combination of lifestyle changes Mel made. None of them result in an immediate rise in HDL; all take months to 1-2 years to exert full HDL-raising effect.

Think of HDL as the 82-year old grandma who takes a long time to cross the street-she does get there!

Note: Doses of niacin >500 mg per day should be taken with medical supervision.

Can vitamin D be a SOLE risk factor?

18. January 2007 William Davis (6)

Here's a crazy question. It occurred to me as I was talking to Drew, a slender, active 54-year old dentist with no bad habits including no smoking.

Drew's heart scan score was 222. His lipoprotein analysis mostly revealed a lot of nothing, which is unusual. The only pattern that showed up was a modestly high LDL of 122 mg/dl with a very slight excess of small LDL. That's it. I would not be satisfied that these were sufficient cause for Drew's level of coronary plaque.

Drew's 25-OH-vitamin D3 level: 15 ng/ml--severe deficiency--despite the fact that his doctor had suggested that he take a vitamin D2 preparation. In other words, Drew had been profoundly deficient, probably for years.

Given the unimpressive cholesterol and lipoprotein values, could vitamin D serve as a trigger for coronary plaque all by itself?

I don't have an answer and know of nobody else who does. However, my opinion is that vitamin D is indeed a potent risk that can cause heart disease as a sole risk factor.

Perhaps it's another piece of circumstantial evidence suggesting that vitamin D has an enormous influence on health, including coronary plaque. Interestingly, the only other health problem Drew has had is prostate cancer, treated a few years ago with prostate removal and radiation. Good evidence suggests that vitamin D deficiency escalates risk of prostate cancer substantially.

By the way, I've seen people taking vitamin D2 preparations, called "ergocalciferol," who are every bit as deficient as those who take no vitamin D at all. Avoid D2 or ergocalciferol preparations: they're worthless.

Does fish oil raise LDL cholesterol?

17. January 2007 William Davis (1)

Katie had an LDL (conventionally calculated) of 87 mg/dl, HDL of 48 mg/dl.

She added fish oil, 6000 mg per day. Three months later her LDL was 118 mg/dl, HDL 54 mg/dl. In other words, LDL increased by 31 mg. What gives?

Several studies have, indeed, shown that fish oil raises LDL cholesterol, usually by 5-10 mg/dl. Occasionally, it may be as much as 20-30.

Unfortunately, many physicians often assume that it's the (minor) cholesterol content of fish oil capsules, or some vague, undesirable effect of fish oil. It's nothing of the kind.

Since we based Katie's program on (NMR) lipoprotein analysis, not conventional lipids (HDL, calculated LDL, triglycerides, total cholesterol), I knew that Katie also had a severe excess of intermediate-density lipoprotein, or IDL, and very-low density lipoproteins, VLDL. This signifies that after a meal, dietary fats persist for 12, 24,or more hours. Fish oil is a very effective method to clear IDL and VLDL, though sometimes it also causes a shift of some IDL and VLDL into the LDL class. Thus, the apparent increase in LDL.

Another contributor: Conventional LDL is a calculated value, not measured. The calculation for LDL is thrown off by any reduction in HDL or rise in triglycerides. In Katie's case, the rise in HDL from 48 to 54 means that calculated LDL is becoming more accurate and rising towards the true measured value. At the start, Katie's true measured LDL was 122 mg/dl, 35 mg higher than the calculated value. Calculated LDL is therefore approximating measured LDL more accurately as HDL rises.

The most important lesson to learn is that, if LDL rises significantly on fish oil and you haven't had lipoproteins formally measured, there may have been a substantial postprandial abnormality like IDL that was unrecognized.

Heart disease is everywhere

16. January 2007 William Davis (0)

If you ever need convincing that heart disease is everywhere, you should do what I do: subscribe to Google Alerts and have them forward news anytime the search phrase "heart attack" crosses the web. (Just go to Google, click on "more" to the right of the search bar, and follow the links.)

Some recent samples:

Workmates resuscitate driver after heart attack

A woman coal mine truck driver had a heart attack and required resuscitation with a defibrillator 3 times on the way to the hospital.

Heart attack kills groom at reception

A 34-year old man died during his wedding reception, leaving behind his 26-year old new wife.

Heart attack ruled as cause of crash

An Alabama man drove his pick-up truck into oncoming traffic while suffering a heart attack.

Heart-attack victim to return to Hamburg stage

Country music artist, Michael Harding, suffered a heart attack and cardiac arrest during a performance. He is apparently recovered and returning to the stage.

That's just a sample from the last two days. While you and I are carry on a conversation on reversal of heart disease, our neighbors and friends drop over every day. Even though I witness successful heart disease reversal routinely, the rest of the world is not participating.

Pass it on: Coronary disease is identifiable, preventable, controllable, and reversible.

Watch your weight plummet:Be a super vegetarian

14. January 2007 William Davis (0)

Here's a neat trick for losing weight: Become a strict vegetarian for 3 days.

Before you yawn or say "Yecchhhh!", let me elaborate.

Pick some time period. It doesn't have to be 3 days. It could be 2 days, or 5 days, or two weeks. But, for the period you choose, eat only vegetables. No meat, cereals, breads, milk, cookies, etc.

Vegetables alone could get monotonous, so make them interesting. Possibilities include:

--Hummus--add a little bit of olive-oil, chopped garlic, paprika, red pepper.

--Tabouleh--I get mine from Trader Joe's and it's delicious.

--Salsa--Low in calories, rich in lycopene and other flavonoids, with no nutritional downside. Also, pico de gallo--chopped tomatoes, onions, jalapeno chiles, cilantro, cucumbers.

--Mustards--hot, yellow, brown, spicy, gourmet, horseradish, etc.

--Cocktail sauce--i.e., ketchup and horseradish. Use the low-carb ketchup made without high fructose corn syrup.

--Tapenades--e.g., olive tapenade made with chopped olives, capers, and olive oil.
--Pesto-made with basil, garlic, and olive oil.

--Spices and herbs--basil, arugula, peppers, mustard powder, garlic, cilantro, ginger, etc.

--Vinegars--wine, Balsamic, rice, apple cider.

--Infused olive oils--infused with garlic is especially delicious,e.g., added to hummus.

--Bean dips--white bean dip, roasted bean dip, etc.

With the varieties of ways to jazz up your vegetables, you couldn't possibly be bored.

For example, for breakfast on day 1, eat sliced cucumbers and green peppers dipped in garlic-infused olive oil hummus and a handful of almonds. For a snack, some walnuts, sunflower seeds, sliced zucchini dipped in salsa. For lunch, a salad with an olive oil and balsamic vinegar dressing. For dinner, tablouleh, a cucumber and tomato salad, celery sticks dipped in pico de gallo.

All vegetables can be eaten without restricting portion size, since calorie content of vegetables are so low compared to other calorie-dense foods. (See The Heart Scan Blog from a few days back, "One bit or many mouthfuls?" at http://heartscanblog.blogspot.com/2007/01/one-bite-or-many-mouthfuls.html.)

This approach works nearly as well as fasting. A half-pound per day weight loss or more is common and painless. You'll also feel great living on low glycemic index foods.

(Photos courtesy Wikipedia.)

Dr. Agatston to the rescue

12. January 2007 William Davis (0)

Dr. Arthur Agatston, author of wildly successful South Beach Diet, has just released a new book titled The South Beach Heart Program. Dr. Agatston has started on a media speaking circuit to promote his book and concepts.

A reporter from Time, who interviewed Dr. Agatston, commented:

". . .not enough doctors prescribe niacin for their heart patients, even though the medicine is a proven treatment for raising 'good' cholesterol. Physicians are reluctant, Agatston suggests, because niacin requires diligent follow-up to watch for side effects, taking time that most primary-care practices cannot afford. On the other hand, he says, too many doctors are performing heart operations that represent a financial windfall for hospitals. Bottom line: there isn't as much money to be made in prevention as in treatment."

Amen.

Dr. Agatston echoes many of the concepts that the Track Your Plaque program advocates. His notoriety is going to help disseminate the idea that 1) CT heart scans are the #1 method to identify hidden atherosclerotic coronary plaque, 2) taking control of your heart scan score is the best way to seize hold of your future, and 3) the present-day popularity of heart procedures like stents and bypass is intolerable, inexcusable, and needs to be reined back.

Agatston also brings great credibility and fairness to the conversation and his comments will gain tremendous attention in the press and with the public.

When is a vitamin not a vitamin?

12. January 2007 William Davis (0)

When it's a hormone.

That's the stand that several researchers in vitamin D have taken and I think they're right. Dr. John Cannell has made a fuss over this in his www.vitamindcouncil.com website.

Structurally, vitamin D is most closely related to testosterone, estrogen, and cortisol. You wouldn't call testosterone vitamin T, would you?

Vitamins are also meant to be obtained from food. Yes, vitamin D is in milk but only because humans are required to put it there to prevent childhood rickets. Otherwise, the only substantial food source of vitamin D is in oily fish like salmon and then only a modest quantity.

Vitamin D is cholecalciferol, a hormone. Deficiencies of hormones can have catastrophic consequences. Imagine that every winter your thyroid gland shuts down and produced no thyroid hormone. You'd get very ill, gain 30 lbs, lose your hair, feel awful.

That's what happens when you're sun deprived and thereby deficient in cholecalciferol--you're deficient in a hormone. And it happens to most of us every year for many months.

I continue to witness spectacular effects by bringing 25-OH-vitamin D3 blood levels to 50 ng/ml with supplementation, including an apparent surge in success dropping heart scan scores.

An epidemic of heart disease reversal

10. January 2007 William Davis (3)

Heart disease reversal is nothing new in my office. However, I have to admit that it's not something that generally happens each and every day.

As our approach is refined, we are witnessing an unprecedented frequency of plaque reversal. Since Monday (today is Tuesday), I've seen four people who have regressed their coronary plaque and dropped their heart scan score.

Pat was the most recent addition to this list. At age 53, I was honestly surprised at the ease of dropping her heart scan score from 128 to 42 in the space of a year. I was surprised because among her lipoprotein patterns was the dreaded combination of lipoprotein(a) and small LDL, probably the most aggressive risk for heart disease I know of and also among the most difficult to gain control over. She also suffered a deep personal tragedy in her family, an emotional convulsion that can sometimes wipe out any hope of plaque reversal.

I'm hopeful that this virtual epidemic of heart disease reversal continues. And I hope that you participate in it.

Second heart scan and heart attack risk

9. January 2007 William Davis (0)

At first, Joe felt disappointed, defeated, and frightened. After his heart scan, a radiologist at the center told him that his score of 264 was moderately high. He told Joe that he was at moderate risk for heart attack and that a nuclear stress test was going to be required.

This left Joe feeling confused. After all he'd had a heart scan 18 months earlier and his score was 278, 5% higher.

I reassured Joe that the radiologist had not been aware that Joe had a prior heart scan. The radiologist didn't know that Joe's heart scan score had actually been reduced.

In fact, Joe's risk for heart attack was not moderate--it is now very low, since his score was 5% lower. While growing plaque is active plaque, shrinking plaque is inactive plaque and thereby at far less risk for heart attack.

I wrote about this phemonenon in a previous Blog: When is a heart scan score of 400 better than 200? at http://heartscanblog.blogspot.com/2006_09_01_archive.html. When you've had more than one scan, the risk for heart attack suggested by the score takes a back seat to the rate of change of your score. In other words, even though Joe's score of 264 represented a moderate risk (of approximately 3% per year, roughly 30% over 10 years), this no longer held true, since it actually represented a 5% decrease over a previous score.

Joe's risk for heart attack is probably close to zero. ALWAYS view your second (or any subsequent) heart scan score in the context of your previous score, not in isolation.

Track Your Plaque newsletter subscribers: We will detail more of Joe's story in the coming January 2007 newsletter. If you'd like to read or subscribe to the newsletter, go to http://www.cureality.com/f_scanshow.asp.

Heart scan curiosities #5

8. January 2007 William Davis (1)

Despite the controversy over drug-coated stents, I maintain that the best stent is no stent at all.

Yes, there are indeed times when such things are necessary, but not with the frequency that they are implanted nowadays.

Another reason why stents are an undesirable phenemenon is that they muck up your heart scan. Take a look:

The long white object in the center is a stent in the left anterior descending artery of this 60 year old man. Just beyond the stent (at about 1 o'clock from the stent) is a plaque that could be scored. However, you can see that, with the presence of the stent, the bulk of this artery is no longer "scorable". If this man wishes to "track his plaque", he will have to be content with tracking only the circumflex and right coronary arteries, the other two arteries without stents.

The stainless steel or similar metallic materials of current stents simply prevent us from seeing through them for plaque scoring purposes. It's best if you can simply avoid getting one for this and other reasons.

Track Your Plaque Members: Watch for the upcoming editorial by our Heart Hawk on drug-eluting stents.

Cureality | Real People Seeking Real Cures

Calling all super-duper weight losers!

9. July 2011 William Davis (12)

Have you lost at least 1/2 your weight, e.g., 300 lbs down to 150 lbs? If you have, I have a major national magazine editor looking to talk to you.

If you have gone wheat-free and/or followed the dietary advice offered here in The Heart Scan Blog or through the Track Your Plaque program and would be willing to share your story, please let me know by commenting below. While losing half your body weight is not necessarily a requirement for health, it makes an incredibly inspiring story for others.

If we use your story, I will set aside a copy of my soon-to-be-released book, Wheat Belly.

Lp(a): Be patient with fish oil

8. July 2011 William Davis (35)

High-dose omega-3 fatty acids from fish oil has become the number one strategy for reduction of lipoprotein(a), Lp(a), in the Track Your Plaque program for gaining control over coronary plaque and heart disease risk.

The original observations made in Tanzanian Bantus in the Lugalawa Study by Marcovina et al first suggested that higher dietary exposure to fish and perhaps omega-3 fatty acids from fish were associated with 40% lower levels of Lp(a). Interestingly, higher omega-3 exposure was also associated with having the longer apo(a) "tails" on Lp(a) molecules, a characteristic associated with more benign, less aggressive plaque-causing behavior.

Of course, the 600+ fish- consuming Bantus in the study consumed fish over a lifetime, from infancy on up through adulthood. So what is the time course of response if us non-Bantus take higher doses of fish oil to reduce Lp(a)?

We have been applying this approach in the Track Your Plaque program and in my office practice for the past few years. To my surprise, the majority of people taking 6000 mg per day of omega-3 fatty acids, EPA and DHA, will drop Lp(a) after one year. Some have required two years. Therefore checking Lp(a) after, say, 3 or 6 months, is nearly useless. (An early response does, however, appear to predict a very vigorous 1-2 year response.)

I'm sure that there is an insightful lesson to be learned from the incredibly slow response, but I don't currently know what it is. But this strategy has become so powerful, despite its slow nature, that it has allowed many people to back down on niacin.

Baby your pancreas

1. July 2011 William Davis (35)

There it is, sitting quietly tucked under your diaphragm, nestled beneath layers of stomach and intestines, doing its job of monitoring blood sugar, producing insulin, and secreting the digestive enzymes that allow you to convert a fried egg, tomato, or dill pickle into the components that compose you.

But, if you've lived the life of most Americans, your pancreas has had a hard life. Starting as a child, it was forced into the equivalent of hard labor by your eating carbohydrate-rich foods like Lucky Charms, Cocoa Puffs, Hoho's, Ding Dongs, Scooter Pies, and macaroni and cheese. Into adolescent years and college, it was whipped into subservient labor with pizza, beer, pretzels, and ramen noodles. As an adult, the USDA, Surgeon General's office and other assorted purveyors of nutritional advice urged us to cut our fat, cholesterol, and eat more "healthy whole grains"; you complied, exposing your overworked pancreas to keep up its relentless work pace, spewing out insulin to accommodate the endless flow of carbohydrate-rich foods.

So here we are, middle aged or so, with pancreases that are beaten, worn, hobbling around with a walker, heaving and gasping due to having lost 50% or more of its insulin-producing beta cells. If continued to be forced to work overtime, it will fail, breathing its last breath as you and your doctor come to its rescue with metformin, Actos, Januvia, shots of Byetta, and eventually insulin, all aimed at corralling the blood sugar that your failed pancreas was meant to contain.

What if you don't want to rescue your flagging pancreas with drugs? What if you want to salvage your poor, wrinkled, exhausted pancreas, eaking out whatever is left out of the few beta cells you have left?

Well, then, baby your pancreas. If this were a car with 90,000 miles on it, but you want it to last 100,000, then change the oil frequently, keep it tuned, and otherwise baby your car, not subjecting it to extremes and neglect to accelerate its demise. Same with your pancreas: Allow it to rest, not subjecting it to the extremes of insulin production required by carbohydrate consumption. Don't expose it to foods like wheat flour, cornstarch, oats, rice starch, potatoes, and sucrose that demand overtime and hard labor out of your poor pancreas. Go after the foods that allow your pancreas to sleep through a meal like eggs, spinach, cucumbers, olive oil, and walnuts. Give your pancreas a nice back massage and steer clear of "healthy whole grains," the nutritional equivalent of a 26-mile marathon. Pay your pancreas a compliment or two and allow it to have occasional vacations with a brief fast.

Bread equals sugar

22. June 2011 William Davis (36)

Bread, gluten-free or gluten-containing, in terms of carbohydrate content, is equivalent to sugar.

Two slices of store-bought whole grain bread, such as the gluten-free bread I discussed in my last post, equals 5- 6 teaspoons of table sugar:

Some breads can contain up to twice this quantity, i.e., 10-12 teaspoons equivalent readily-digestible carbohydrate.

Gluten-free carbohydrate mania

18. June 2011 William Davis (14)

Here's a typical gluten-free product, a whole grain bread mix. "Whole grain," of course, suggests high-fiber, high nutrient composition, and health.

What's it made of? Here's the ingredient list:
Cornstarch, Tapioca Starch, Whole Grain Sorghum Flour, Whole Grain Teff Flour, Whole Grain Amaranth Flour, Soy Fiber, Xanthan Gum, Soy Protein, Natural Cocoa and Ascorbic Acid

In other words, carbohydrate, carbohydrate, carbohydrate, carbohydrate and some other stuff. It means that a sandwich with two slices of bread provides around 42 grams net carbohydrates, enough to send your blood sugar skyward, not to mention trigger visceral fat formation, glycation, small LDL particles and triglycerides.

Take a look at the ingredients and nutrition facts on the label of any number of gluten-free products and you will see the same thing. Many also have proud low-fat claims.

This is how far wrong the gluten-free world has drifted: Trade the lack of gluten for a host of unhealthy effects.

Gluten-free is going DOWN

16. June 2011 William Davis (18)

The majority of gluten-free foods are junk foods.

People with celiac disease experience intestinal destruction and a multitude of other inflammatory conditions due to an immune response gone haywire. The disease is debilitating and can be fatal unless all gliadin/gluten sources are eliminated, such as wheat, barley, and rye.

A gluten-free food industry to provide foods minus gliadin/gluten has emerged, now large enough to become an important economic force. Even some Big Food companies are getting into the act, like Kraft, that now lists foods they consider gluten-free.

So we have gluten-free breads, cupcakes, scones, pretzels, breakfast cereals, crackers, bagels, muffins, pancake mixes and on and on. All are made with ingredients like brown rice flour, cornstarch, tapioca starch, and potato starch. Occasionally, they are made with amaranth, teff, or quinoa, other less popular, but gluten-free, grains.

Problem: These gluten-free ingredients, while lacking gliadin and gluten, make you fat and diabetic. They increase visceral fat, cause blood sugar to skyrocket higher than nearly all other foods (even higher than wheat, which is already pretty bad), trigger formation of small LDL and triglycerides, and are responsible for exaggerated postprandial (after-eating) lipoprotein distortions. They cause heart disease, cataracts, arthritis, and a wide range of other conditions, all driven by the extreme levels of glycation they generate.

Eliminating all things wheat from the diet is one of the most powerful health strategies I have ever witnessed. But replacing lost wheat with manufactured gluten-free foods is little better than replacing your poppyseed muffin with a bowl of jelly beans.

Whenever we've relied on the food industry to supply a solution, they've managed to bungle it. Saturated fat was replaced with hydrogenated fat and polyunsaturates; sucrose replaced with high-fructose corn syrup. Now, they are replacing wheat gluten-containing foods with junk carbohydrates.

For this reason, I am bringing out a line of recipes and foods that will be wheat gliadin/gluten-free, do NOT contain the junk carbohydrates that gluten-free foods are made of, and are genuinely healthy. They are tasty, to boot.

The gluten-free industry needs to smarten up. Having a following that is free of cramps and diarrhea but are obese, diabetic, and hobbling on arthritic knees and hips is good for nobody.

Medicine ain't what it used to be

15. June 2011 William Davis (0)

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

For instance:

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

Normal cholesterol panel . . . no heart disease?

15. June 2011 William Davis (19)

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

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

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

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

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

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

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

Idiot farm

11. June 2011 William Davis (10)

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

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

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

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

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

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

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

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

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

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

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

Eat triglycerides

8. June 2011 William Davis (31)

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

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

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

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

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

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

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

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

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