Are happy people more likely to reduce heart scan scores?

I was talking to Darryl, a patient today: 71 years old with a heart scan score of 378, as well as an enlarged aorta (4.5 cm).

We had identified numerous lipoprotein abnormalities 12 months ago and advised him on a program for correction. His patterns included small LDL, high triglycerides, sky-high IDL (VERY important when you have an enlarged aorta), and lipoprotein(a). Blood pressure was also high, another crucial fact to correct when the aorta is enlarged.

Anyway, Darryl corrected lipoproteins to perfection: basic lipids were substantially better than 60-60-60; lipoprotein(a) was reduced well into the desirable range; IDL was eliminated; blood pressure was 108/64. Repeat heart scan score: 354.

There's nothing spectacular about Darryl's story, except that, despite these issues, Darryl was a happy man. He smiled throughout our conversation. He has told me on several occasions how grateful he is for the life he has.

Darryl is not wealthy. He retired around 4 years ago and fills his day with helping his wife, walking outdoors, helping out at his church, and contributing to the care of his grandchildren. Through all this Darryl is incurably, unfailingly, and irrepressibly happy.

It made me think back through all the other people who've also had great succes in their Track Your Plaque program. It struck me that, for the most part, they too were a happy bunch: generally optimistic, happy, not overly stressed nor prone to extremely stressful responses to stressful situations. All seem to also be grateful for the good in their lives, though most had no more money than the average person and had their share of difficulties in life. In fact, I can only recall one person who reversed coronary plaque who was an angry, pessimistic personality. Just one.

Could it be that happy, optimistic people are more likely to reverse coronary plaque? It would, after all, be consistent with all the other observations that type A personalities have more heart attack, etc.

Anyway, this is just an informal observation but one that seems very consistent. Track your plaque--and be happy!

Don't overdo the vitamin D

As time passes and I advise more and more people to supplement vitamin D, I gain increasing respect for this powerful "vitamin". I am convinced that vitamin D replacement is the reason for a recent surge in our success rates in dropping CT heart scan scores. I believe it is also explains the larger drops we've been witnessing lately--20-30%.

But vitamin D can be overdone, too. Too much of a good thing . . .

Despite being labeled a "vitamin", cholecalciferol is actually a hormone. Vitamins are obtained from food and you can thereby develop deficiencies because of poor intake. Deficiency of vitamin C, for instance, arises from a lack of vegetables and fruits.

Vitamin D, on the other hand, is nearly absent from food. The only naturally-occuring source is oily fish like salmon and sardines. Milk usually has a little (100 units per 8 oz) because milk producers have been required by law to put it there to reduce the incidence of childhood rickets.

A woman came to me with a heart scan score of nearly 3800, the highest score I've every seen in a woman. (Record for a male >8,000!) She was taking vitamin D by prescription from her family doctor but at a dose of 150,000 units per week, or approximately 21,000 units per day. This had gone on for about 3-4 years. This may explain her excessive coronary calcium score. Interestingly, she had virtually no lipoprotein abnormalities identified, which by itself is curious, since most people have some degree of abnormality like small LDL. Obviously, I asked her to stop the vitamin D.

Should you be afraid of vitamin D? Of course not. If your neighbor is an alcoholic and has advanced cirrhosis, does that mean you shouldn't have a glass or two of Merlot for health and enjoyment? It's a matter of quantity. Too little vitamin D and you encourage coronary plaque growth. Too much vitamin D and you trigger "pathologic calcification", or the deposition of calcium in inappropriate places and sometimes to extreme degrees, as in this unfortunate woman.

Ideally, you should have your doctor check your 25-OH-vitamin D3 blood levels twice a year in summar and in winter. We aim for a level of 50 ng/ml, the level at which the phenemena of deficiency dissipate.

"It must have been the statin"

After four years of trying, Randy finally reduced her heart scan score. It not only dropped, it plummeted. After four previous scans that showed 25% or more increases, she'd finally dropped her score 23%. (I Blogged about Randy's case a few weeks ago.)

Randy also works for a cardiologist. When she told him that she had reversed her coronary plaque and reduced her heart scan score by 23%, he said, "It must have been the statin agent."

Randy was indeed on a statin drug at a low dose. But she also had taken great efforts in exercise, food choices, fish oil, and vitamin D. In fact, her score had progressed dramatically while she was taking the drug. Put simply, it was not the statin.

But that is the mindset of the conventionally thinking cardiologist. Stent, bypass, or statin drug--what else is there? Even with crystal clear evidence for coronary plaque regression, they refuse to acknowledge that tools that are not in their everyday consciousness could have achieved so spectacular a result.

Given a choice, 9 out of 10 cardiologists would rather put a stent in and walk away $2000 richer for an hour of work. Don't allow them to have this choice. Take control now.

Statin Drugs May Help the Healthy:
Cholesterol-Lowering Statin Drugs May Benefit People Without Heart Disease


That's the headline on WebMD, reporting the findings of a recent study published in the Archives of Internal Medicine. In reality, it wasn't really a study at all, but a re-analysis of previously published data, a so-called meta-analysis.

Nonetheless, the University of Toronto group re-analyzed the results of several studies, pooling data on 28,000 people, none of whom had known coronary disease. The results were similar to the results of the studies that were reported individually: a 29% reduction in heart attack and other "events" in people taking statin drugs.

What's surprising to me is this notion that statins, or any other treatment for that matter, prevent heart attack in people without heart disease. This is idiotic. Of course they had coronary heart disease. You can't have a heart attack in the absence of coronary disease. (There are very rare exceptions, like cocaine users, who experience coronary spasm from the drug).

What the study shows is that people with unrecognized heart disease experienced a reduction in heart attack. What it also means is that many, many people truly without heart disease were unnecessarily treated. As you'd predict, the drug manufacturers love this sort of broad, untargeted use of their drugs. It's an approach that brings in billions of dollars of revenues. The article on WebMD, in fact, was accompanied by three ads for various cholesterol drugs on this single page story.

What if only people with heart disease, as identified by CT heart scan scores, were treated? You would indeed witness an even larger reduction in heart attack risk, because the group receiving treatment both has the disease and is thereby at greater risk. Treatment should yield even greater risk reduction than treating broad groups who superficially appear to not have heart disease.

Ignore this nonsense about statin drugs reducing heart attack risk in people without heart disease. If you don't look for it, you won't know you have it. Once again, you can be lots smarter than the media. Get a heart scan and find out if your risk is worth reducing.

Heart attack guaranteed

What if you knew for a fact that your risk for heart attack was 100% by, say, age 58? This is indeed true for many people, though at age 60, 65, 70--or 45.

In other words, unless something were done about the causes of heart disease, you would inevitably suffer a heart attack at 58.

What sort of action could you take at age 45?

Obviously, not smoking is an absolute requirement. Continue and you may as well start getting your affairs together.

How about exercising and eating a generally healthy diet? Will your risk be reduced to zero? No. It might be reduced 20-30%, depending on genetic factors.

How about a statin drug? Watch TV ads during Oprah, and you might think it's a cure. But in reality, while it is a financial bonanza for the drug manufacturers, it will reduce risk for heart attack by 30%.

(Note that risk reduction by following multiple strategies is not necessarily additive. In other words, if you have a healthy lifestyle and take a statin agent, is risk reduced 60% (30 + 30)? No, because the effects may overlap.)

So, eating healthy, exercising, and taking a statin drug might reduce risk 35-40%, maybe 50% in the best case scenario. Would you be satisfied? Most would not.

Add fish oil at a truly therapeutic dose. Risk reduction by itself: 28%.

Add niacin or other strategies for correction of your individual, specific causes of heart disease: Now we're up to 90% reduction.

Throw in a tracking process to prove whether or not atherosclerotic plaque has progressed or reversed. Now we're approaching 100% if plaque reverses. The only way I know how to track plaque is through CT heart scans. What other test is readily available to you with low radiation exposure, yet is relatively inexpensive and precise? It certainly is not stress testing, heart catheterization, CT angiograms, or other techniques. Cholesterol won't tell you. Besides CT heart scans, there's nothing else I know of.

Let's fact it: For many people, uncorrected risk for heart attack is truly 100% at some age. Take action while you can.

That, in a nutshell, is the Track Your Plaque program.

Heart scan curiosities 3



This is a sample image from the heart scan of a 54-year old, 212 lb, 5 ft 2 inch woman. The heart is the whitish-gray in the center; lungs are the dark (air-filled) areas on either side of the heart. Note the massive amount of surrounding gray tissues that encircles the heart and lungs. This is fat. At this weight, the diameter of total fat exceeds the combined diameter of the heart and lungs. If we were to show the abdomen, there would be even more fat. (The image shows the body not well centered because the technologist centers the heart, since this is, after all, a heart scan.)





This is a 55-year old, 151 lb, 5 ft 4 inch woman. Note the contrast in the quantity of fat tissue surrounding the chest, a much more normal appearance. Note that this woman is still around 25 lb over ideal weight, but not to the extreme degree of the woman above.

Another curious observation: Note the more whitish streaking in the heavier woman's lungs. Heart scans are performed while holding a deep inspiration (a deep breath inwards), mostly to eliminate lung respiratory motion during image acquisition. Nonetheless, the heavier woman's lungs are not as fully expanded as the more slender woman. In other words, the heavier woman cannot inflate her lungs as effectively as the thinner woman. Ever notice how breathless heavy people are? Some of this effect is just being out of shape. But there's also the added effect of the abdominal fat exerting upwards compression on the lung tissues, and the constrictive effect of the encircling fat mass. At the beginning of inspiration, the chest fat exerts the resistance of inertia to inspiration that is absent, or less, in a slender person. With each breath, the heavy woman must move 50 lbs or so of surrounding fat mass just to inhale.

The heavier woman is, in effect, suffocating herself in fat.

The distortions to the human body incurred by extreme weight gain are both fascinating and shocking. I hope you're breathing easily.

The shameful "standard of care"

John's initial heart scan four years ago showed a score of 329. His physician prescribed Zocor for a somewhat high LDL cholesterol.

One year later, John asked for another scan. His score: 385, a 17% increase. John exercised harder and cut his fat intake.

This past fall--3 years after his last scan--John had yet another heart scan. Score: 641, a 66% increase over the last scan, all the while on Zocor.

John sought an opinion from a reputable cardiologist. He concurred with the prescription of Zocor and advised annual stress tests. That's it.

Followers of the Track Your Plaque approach know that the expected uncorrected rate of increase in heart scan score is 30% per year. On Zocor or other cholesterol reducing statin agent, a common rate of growth is between 18-24% per year--better but not great. Plaque growth is certainly not stopped.

But that is the full extent of interest and responsibility of your cardiologist. Prescribe a statin drug, perform a stress test, and the full extent of his obligation has been fulfilled. In legal terms, your physician has met the prevailing
"standard of care". No more, no less.

In other words, the prevailing standard of care falls shamefully short of what is truly possible. For the majority of the motivated and interested, coronary plaque reversal--reduction of your heart scan score--should be the standard aimed for. It's not always achievable, but it is so vastly superior to the prescribe statin, wait for heart attack approach endorsed by most cardiologists.

Heart scan curiosities 2



This is an example of a so-called "hiatal hernia", meaning the stomach has migrated through the diaphragmatic hiatus into the chest--the stomach is literally in the chest. This example is an unusually large one. Hiatal hernias can cause chest pain, indigestion, and a variety of other gastrointestinal complaints. Heart scans are reasonably useful to screen for this disorder, though very small ones could escape detection by this method.

Sometimes, you can actually hear the gurgling of stomach contents (the common "growling" stomach) by listening to the chest. Large ones like this actually crowd your heart (the gray structure above the circled hernia), irritating it and even causing abnormal rhythm disorders. The dense dark material within the hernia represents lunch.

I would not advocate CT heart scans as a principal method to make a diagnosis, but sometimes it just pops up during a heart scan and we pass it on to the person scanned.

Vitamin D: New Miracle Drug

At the meetings of the American Society of Bone and Mineral Research, Dr. Bruce Troen of the University of Miami detailed his views on the extraordinary benefits of vitamin D replacement. He also talked about the enormous problem of unrecognized vitamin deficiency.

“There’s a huge epidemic of hypovitaminosis D, and the real key here is not just that it’ll benefit you from a bone and neuromuscular standpoint, but if you correct hypovitaminosis D and the corresponding secondary hyperparathyroidism, then you’re going to decrease prostate cancer, colon cancer—actually “up to 17 different cancers, breast cancer included.”

Unfortunately, Dr. Troen did not talk much about the heart benefits of vitamin D, likely since the data is scant, nearly non-existent. However, if the Track Your Plaque experience means anything, I predict that vitamin D replacement will become among the most powerful tools you can use to gain control over coronary plaque.

Read the text of a report from the Internal Medicine World Report to read more of Dr. Troen's comments.


http://www.imwr.com/article.php?s=IMWR/2006/11&p=40

Heart disease "reversal" by stress test


Here's an interesting example of a 71-year old man who achieved "reversal" of an abnormality by a nuclear stress test.

This man underwent bypass surgery around 10 years ago, two stents three years ago. A nuclear stress test in April, 2005 showed an area of poor blood flow in the front of the heart. On the images, normal blood flow is shown by the yellow/orange areas. poor or absent blood flow is shown by the blue/purple areas within the white outline.

Now, I can tell you that this man is no paragon of health. He's only accepted limited changes in his otherwise conventional program--in other words, someone who I'd be shocked achieved true reversal of his heart disease. (I didn't have him undergo any CT heart scans because of the difficulties in scoring someone who has undergone bypass surgery and stents, and because of limited motivation. True plaque reversal is for the motivated.)This patient did, however, accept adding fish oil and niacin to his program.

Nonetheless, stress testing can be helpful as a "safety check". Here's the follow-up stress test:
You'll notice that the blue/purple areas of poor blood flow have just about disappeared. This occurred without procedures.

Does this represent "reversal"? No, it does not. It does represent reversal of this phenomenon of poor flow. It does not represent reversal of the plaque lining the artery wall. That's because improvement of flow, as in this man, can be achieved with relatively easy efforts, e.g., improvement in diet, statin drugs, blood pressure control, etc. True reversal or reduction of coronary plaque, however, is tougher.

If blood flow is improved, who cares whether plaque shrinks? Does it still matter? It does. That's because the "event" that gets us in trouble is not progressive reduction in blood flow, but "rupture" of a plaque. A reduction in plaque--genuine reversal--is what slashes risk of plaque rupture.

Calling all super-duper weight losers!






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

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

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

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

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

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

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.