Self-empowerment is coming!

I've discussed this before: The coming wave of self-empowerment in health. Health that is driven by you, not a hospital, not a doctor, not by procedures, but by information and access to tools that are powerful and effective.

The seeds are being planted right now and won't take full root for many years or decades. But it's going to happen.

I previously cited several broad trends that are examples of this emerging wave:

--The nutritional supplement movement. Contrary to the media's ill-informed bashing, nutritional supplements are getting better: improved quality, better substantiation of when/how to use them, new agents that appear rapidly, since introduction is not slowed by the molasses of the FDA.

--Medications moving to over-the-counter status. Health insurers are driving this one. OTC means not paid for by insurance. That also means access to you.

--What I call "retail imaging", i.e. screening ultrasound, heart scans, full body scans, etc. that are available in most states without a doctor's order.

--The Internet. The mind-boggling rapidity and depth of information available on the Internet today is fueling the self-empowerment movement by providing sophisticated information to health care consumers. Information here is uneven at present. But, as consumer sophistication increases and the system of checks and balances evolves, internet-driven information will be often superior to what you get from a doctor or other health professional.

--High-deductible health insurance plans. If health care consumers bear more and more of the costs of health care, they will seize greater responsibility for early identification and prevention and minimize long-term costs.

This trend does not mean treating your own infection, taking out your own gall bladder, repairing your own broken leg. It means that conventional routes of health delivery will recede into providing only catastrophic care.

It means that you and your family will take a larger role in learning how to eat and exercise properly, use foods to maintain and promote health (the "designer food" and "nutraceutical" movement), take supplements that have real benefits, use medications for treatment of many everyday ailments.

It also means seizing control of diseases that previously were only treated in hospitals, like coronary heart disease. This, of course, is where our program, Track Your Plaque, is an example of how you can have a powerful and effective role in your heart health. Track Your Plaque goes so far beyond the "eat low-fat, exercise, and know your numbers" media mantra that it's like comparing a brand-new Mercedes to a rusted, run-down '87 Ford Escort. There truly is no comparison. (Sorry if you're an Escort driver!) But you get the idea.

Another option for lipoprotein testing


For those of you who have been frustrated in trying to get your lipoprotein analysis performed, here's another option.

The Life Extension Foundation at www.lef.org provides access to the VAP test, or Vertical Auto Profiler. This is the lipoprotein test run by the Atherotech company in Birmingham, Alabama. The name refers to the method used, a form of centrifugation, or high-speed spinning of your blood (plasma) to separate the various components by density.

This is a fine technique that works well. Though our preferred method is NMR (www.Lipoprofile.com, Liposcience Inc.), the Atherotech VAP is a reasonable alternative.

If you go through the Life Extension process, they will direct you to blood draw sites in your area. They charge $185 for Life Extension members, $247 for non-members. (Membership in Life Extension costs $75.) Drawback: No billing for health insurance reimbursement.

A full description of the significance of lipoproteins can also be found in my article posted on-line at the www.lef.org website at http://www.lef.org/magazine/mag2006/may2006_report_heart_01.htm

Weight and lipoproteins

Tom, an accountant, came into the office eager to know what his 2nd heart scan score showed.

A year ago, Tom's view of himself as a healthy, middle-aged man was shattered when he found out his heart scan score: 1236. Tom had severe coronary plaque with a heart attack risk of 25% per year (without intensive preventive action).

In the way of lipoprotein abnormalities, he had several: low HDL, deficient large HDL, small LDL, high triglycerides, IDL (the after-eating inability to clear dietary fats), and a high blood sugar in the pre-diabetic range. In addition, Tom was hypertensive, with blood pressure so high it even landed him in the emergency room last winter.

In addition to our approach to correct all these patterns, Tom was urged to lose a significant quantity of weight. Starting at 225 lb., at 5 ft 7 inches, Tom was clearly at least 40 lbs over his ideal weight.

I stressed to Tom that the entire spectrum of causes of coronary plaque were weight-related. I likened his patterns to throwing gasoline on a fire: As weight increased, his lipoprotein and other abnormalties flared dramatically.

But each time Tom came back to the office over the ensuing year, he'd gained another 3 to 6 lbs. And each time he had an explanation. "My daughter just got married. I couldn't turn down wedding cake, now could I?" Or, I just survived another tax season. I was working day and night--no time for exercise!" "It's getting too hot to walk anymore."

Well, despite multiple treatments, Tom's repeat heart scan showed a score of 1677, a 35% increase. That's a dangerous rate of growth that virtually guarantees that plaque is building up momentum to "rupture", which results in heart attack.

I therefore stressed to Tom that weight loss was crucial. Control of coronary plaque was simply not going to occur without weight loss to our target. Alternatively, we could add several new prescription medicines and hope that they could achieve the same effect, though at a price (side-effects, expense).

I tell Tom's story to highlight again just how important weight loss can be for a number of lipoprotein abnormalities.

What measures specifically are sensitive to weight? They are:

--HDL cholesterol
--Triglycerides
--Small LDL
--VLDL
--Blood pressure
--Blood sugar and insulin
--C-reactive protein
--LDL

Weight exerts profound influence on these patterns. In Tom and people like him, weight can be a "make it or break it" issue.

If you, like Tom, have any of the above patterns, consider weight loss as a potent tool you can use to gain control of coronary plaque.

Variation in vitamin D requirements


For Track Your Plaque followers, you know we are very concerned about vitamin D blood levels. My prediction is that, in 10 years, vitamin D will be regarded as an important item on the list of coronary artery disease risk factors.

In our experience of trying to stop or reverse heart scan scores, restoration of vitamin D to a blood level of 50 ng/ml appears to have increased our success rate dramatically.

As we've talked about before, on the bell curve of vitamin D dosing in a northern climate, the majority of women require 2000 units per day, men require 3000 units per day to achieve a level of 50 ng. However, there are "outliers" on this bell curve, i.e., people who require much more or much less.

This week, I saw two people who were very instructive cases of extreme requirements on the high end of vitamin D dosing. Both started with unmeasurable blood levels, i.e., essentially zero ng/ml. On 5000 units of vitamin D per day, both raised their blood levels to around 17-18 ng/ml--in the range of severe deficiency (defined as <20 ng/ml). I advised both to increase their oral dose of vitamin D to 8000 units per day.

Notably, both people avoided sunlight and lived in Wisconsin, a terribly sun-deprived locale 10 months a year. Both were also substantially overweight (around 300 lbs each).

The vitamin D issue continues to be endlessly fascinating in all its nuances and twists.

Heart attacks in your own backyard

Two men from my community just died of heart attacks. Both were in their 40s.

What bothers me most about these all too frequent stories is that it is so preventable. You can bet that both had little or no symptoms prior to their deaths. You can also bet that they've had cholesterol panels taken by their doctors.

Followers of the Track Your Plaque program know that these are sure-fire paths to failure. The absence of heart disease symptoms should provide no reassurance whatsoever. High cholesterol, in-between cholesterol, low cholesterol--none are confident indicators in a specific individual.

Stress test? How about the patient I saw today who, until I met him, had been undergoing stress test after stress test, every year--all while the quantity of coronary plaque tripled. False reassurances provided by his cardiologist led him to believe that all was well--while this stack of oily rags was just waiting for the spark to ignite.

Too little time, too much money, too far away--there's a hundred excuses for not getting a heart scan. Or, you've had a heart scan and no one can tell you what to do about it. If you're reading this, however, you've found the most intensive source of information available on how your heart scan can serve as the start of a program of heart attack prevention for a life free of dangers.

It's not that tough. But it won't just go away on its own. I just have to look around me in my own community, watch the local news, talk to friends, and I'll heart about all the people just in my neighborhood who should be learning these lessons. I rant and rave about this but some people need to hear it from a friend, colleague, neighbor, rather than some crazy doctor bucking the standard line.

You, too, should be telling anyone who will listen about how heart disease can be identified and controlled.

Pilot lands safely after heart attack, then dies

That was the disturbing headline on a report from MSNBC, also reported nationally on all the major news networks.

The story goes on:

"A pilot suffering a heart attack made an emergency landing on a highway, saving his three passengers shortly before he died...He landed the single-engine Cessna 185 on Utah 30 near Park Valley and was taken to Bear River Hospital in Tremonton, where he died."

We track these sorts of stories and it's frightening just how common they are. A school bus driver recently had a heart attack while driving 30 children; the bus crashed but no one was hurt. A 52-year old commercial bus driver suffered a heart attack while transporting 49 conference attendees; the bus plunged 400 feet down a ravine. Remarkably, 17 passengers suffered only minor injuries and there were no deaths.

There have even been incidents where the pilot of a jet liner suffered a heart attack in-flight. In 2000, the 53-year old pilot of a Northwest Airlines DC-10 died while in-flight from a heart attack while landing in Minneapolis. The 290 passengers were landed safely by co-pilot.

Most incidents where the driver or pilot has been incapacitated or died resulted in the deaths of only a handful of people. No major catastrophe has yet occured. But--mark my words--it will. These incidents just happen too frequently.

Virtually all of these and similar incidents could have been prevented. If the FAA, for instance, would insist that all pilots have a simple CT heart scan, it would become immediately obvious which pilots should be grounded and who should fly. Similar requirements could easily be applied to persons in charge of the welfare of many people, most notably school bus drivers.

It's not that tough! The FAA currently requires stress testing and cholesterol testing. Well, guess what? Followers of the Track Your Plaque program know that these tests do not effectively identify the person at risk for heart attack in the majority of individuals. Just ask former President Bill Clinton how helpful his stress tests (five in a row!) were. Or how valuable his cholesterol monitoring was--all prior to his emergency bypass surgery.

Large new clinical study launched to study. . .niacin


Oxford University has issued a press release announcing plans for a new clinical trial to raise HDL cholesterol and reduce heart attack risk. 20,000 participants will be enrolled in this substantial effort. The agent? Niacin.

How is that new? Well, this time niacin comes with a new spin.

Dr. Jane Armitage, formerly with the Heart Protection Study that showed that simvastatin (Zocor) reduced heart attack risk regardless of starting LDL, is lead investigator. She hopes to prove that niacin raises HDL cholesterol and thereby reduces heart attack risk. But, this time, niacin will be combined with an inhibitor of prostaglandins that blocks the notorious "flushing" effect of niacin.

The majority of Track Your Plaque participants hoping to control or reverse coronary plaque take niacin. Recall that niacin (vitamin B3)is an extremely effect agent that raises HDL, dramatically reduces small LDL, shifts HDL particles into the effective large fraction, reduces triglycerides and triglyceride-containing particles like IDL and VLDL. Several studies have shown that niacin dramatically reduces heart attack. The HATS Study showed that niacin combined with Zocor yielded an 85-90% reduction in heart attack risk and achieved regression of coronary plaque in many participants.

In our experience, approximately 1 in 20 people will really struggle using niacin. Flushes for these occasional people will be difficult or even intolerable. Should Dr. Armitage's study demonstrate that this new combination agent does provide advantages in minimizing the hot flush effect, that will be a boon for the occasional Track Your Plaque participant who finds conventional niacin intolerable.

But you already have access to niacin, an agent with an impressive track record even without this new study. And you have a reasonably effective prostaglandin inhibitor, as well: aspirin. Good old aspirin is very useful, particularly in the first few months of your niacin initiation to blunt the flush.

Although this study is likely to further popularize niacin and allow its broader use, it's also a method for the drug companies to profit from an agent they know works but is cheap and available.

You don't have to wait. You already have niacin and aspirin available to you.

The dark side of CT heart scans

"I just got a heart scan!" declared Eric to his doctor. He handed the report to him.

"Oh my. Your score is 154." The doctor paused, then looked at Eric with a serious look on his face. "If we're going to understand whether or not you're in danger, you'll need a heart catheterization."


I've seen this happen countless times. How can I say this diplomatically? THIS IS WRONG!! In my view, it's absolutely criminal for this to happen. Physician ignorance, profiteering, whatever--it is wrong.

There's very few reasons why someone who has no symptoms should go directly to the cath lab for a procedure. (A rare exception might be an exceptional quantity of plaque in the left mainstem artery, e.g., >100. This is highly unusual.)

Even a nuclear stress test (e.g., thallium) at this level of scoring is only 10-15% likely to be abnormal. That means 85-90% likelihood of being normal. There's rare reasons to perform a heart catheterization in a person with no symptoms and an entirely normal stress test. The vast majority of people like Eric do not need a heart catheterization to discern risk.

If Eric's doctor had been up-to-date on the published literature on the prognostic value of heart scans, he could have advised Eric what the risks were--without a catheterization. Many doctors simply don't want to be bothered. Or, they opt for the more profitable method--a hospital procedure.

Always discuss your heart scan with your doctor--but be armed with information in case your doctor is uninformed or unscrupulous. Unfortunately, that's not uncommon. The Track Your Plaque program is your advocate, a source for unbiased information.

The dirty little secret about aneurysms

Jake had an abdominal aneurysm identified--by accident.

While getting a CT scan of his abdomen for unexplained abdominal pain, a 4.4 cm aneurysm was discovered. Jake's abdominal pain eventually passed without explanation, but he was left with this aneurysm.

Jake's primary care doctor referred him to a surgeon. "It's too small to require surgery right now. Wait a few years and it'll probably get bigger. When it gets to around 5.5 cm, that'll be the time to operate. Let's schedule an abdominal ultrasound or CT scan every 6 months."

Jake then got himself a heart scan. His high score of 879 then led him to my office. Lipoprotein testing, a stress test, correction of his lipoprotein patterns, changes in lifestyle followed. One year later, Jake's heart scan score was unchanged.

How about his abdominal aneurysm? 4.2 cm--a modest quantity of regression. When Jake's surgeon learned of the change, he just shrugged. "Okay, we'll just watch it from here."

Shockingly, the conversation surrounding aneurysms is just like the one Jake received: Let's just watch it grow until you need surgery.

If you've every seen anyone have abdominal aneurysm surgery, you know it is an awful, painful, barbaric process with high risk for major complications like kidney failure and loss of the legs. Waiting for an aneurysm to grow is a lousy solution. Surgeons point out that, although surgery is imperfect, it's better than the alternative: rupture, which is catastrophic with a 50% chance of dying.

But what about stopping the growth of the aneurysm? Or even reversing, or shrinking, it?

Surgeons say it can't be done. Yet we've done it--many times. And it's not that difficult.

The steps to take are very similar to that in the Track Your Plaque program for coronary plaque regression, with a few different strategies. Suppression of inflammation, for instance, plays a more important role and blood pressure must be abolutely normal, even during exercise.

More to come on this important topic in the future, including an upcoming Special Report on the www.cureality.com membership website.

Heart scan scores dropping like stones!!

I saw two instances of dramatic coronary plaque regression today.

John, a 53-years old mechanical lift operator, dropped his heart scan score from 479 to 323--a 32% regression of coronary plaque volume!

Eric, a 50-year consulting engineer, dropped his heart scan score from 668 to 580--a 13% reduction.

Both men did nothing special beyond the principles advocated in the Track Your Plaque program. Recall that, without preventive efforts, your heart scan score is expected to increase by 30% per year. Both men are well on their way to freedom from risk of coronary "events".

Two less people to feed the revenue-hungry hospital procedure system! We need many more like them.
e 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.