Put lipstick on a dwarf

Today, virtually all wheat products are produced from the Triticum aestivum dwarf mutant.

You might call it "multi-grain bread,""oat bread," or "flaxseed bread." You could call it "organic," "pesticide-free," "non-GMO," or "no preservatives." It might be shaped into a ciabatta, bruschetta, focaccia, or panini. It might be sourdough, unleavened, or sprouted. It could be brown, black, Pumpernickel, or white. It could be shaped into a roll, bun, bagel, pizza, loaf, pretzel, cracker, pancake, brioche, baguette, or pita. It could be matzah, challah, naan, or Communion wafers.

No matter what you call it, it's all the same. It's all from the dwarf mutant Triticum aestivum plant, the 18-inch tall product of hybridizations, backcrossings, and introgressions that emerged from genetics research during the 1960s and 70s.

According to Dr. Allan Fritz, Professor of Wheat Breeding at Kansas State University, and Dr. Gary Vocke at the USDA, over 99% of all wheat grown today is the dwarf variant of Triticum aestivum. (For you genetics types, Triticum aestivum is the hexaploid, i.e., 3 combined genomes, product of extensive hybridizations, while ancestral einkorn is a diploid, i.e., a single genome, grass. Hexaploid Triticum aestivum contains the especially hazardous "D" genome, the set of genes most commonly the recipient of genetic manipulations to modify the characteristics of flour, such as gluten content. Einkorn contains only the original "A" genome.)

No matter what you call it, add to it, how you shape it, etc., it's all the same. It's all the dwarf mutant product of tens of thousands of hybridizations.

You can put lipstick on a pig, but it's still a pig. By the way, lipstick may contain wheat.

What the Institute of Medicine SHOULD have said

The news is full of comments, along with many attention-grabbing headlines, about the announcement from the Institute of Medicine that the new Recommended Daily Allowance (RDA) for vitamin D should be 600 units per day for adults.

What surprised me was the certainty with which some of the more outspoken committee members expressed with their view that 1) the desirable serum 25-hydroxy vitamin D level was only 20 ng/ml, and 2) that most Americans already obtain a sufficient quantity of vitamin D.

Here's what I believe the Institute of Medicine SHOULD have said:

Multiple lines of evidence suggest that there is a plausible biological basis for vitamin D's effects on cancer, inflammatory responses, bone health, and metabolic responses including insulin responsiveness and blood glucose. However, the full extent and magnitude of these responses has not yet been fully characterized.

Given the substantial observations reported in several large epidemiologic studies that show an inverse correlation between 25-hydroxy vitamin D levels and mortality, there is without question an association between vitamin D and mortality from cancer, cardiovascular disease, and all cause mortality. However, it has not been established that there are cause-effect relationships, as this cannot be established by epidemiologic study.

While the adverse health effects of 25-hydroxy vitamin D levels of less than 30 ng/ml have been established, the evidence supporting achieving higher 25-hydroxy vitamin D levels remains insufficient, limited to epidemiologic observations on cancer incidence. However, should 25-hydroxy vitamin D levels of greater than 30 ng/ml be shown to be desirable for ideal health, then vitamin D deficiency has potential to be the most widespread deficiency of the modern age.

Given the potential for vitamin D's impact on multiple facets of health, as suggested by preliminary epidemiologic and basic science data, we suggest that future research efforts be focused on establishing 1) the ideal level of 25-hydroxy vitamin D levels to achieve cancer-preventing, bone health-preserving or reversing, and cardiovascular health preventive benefits, 2) the racial and genetic (vitamin D receptor, VDR) variants that may account for varying effects in different populations, 3) whether vitamin D restoration has potential to exert not just health-preserving effects, but also treatment effects, specifically as adjunct to conventional cancer and osteoporosis therapies, and 4) how such vitamin D restoration is best achieved.

Until the above crucial issues are clarified, we advise Americans that vitamin D is a necessary and important nutrient for multiple facets of health but, given current evidence, are unable to specify a level of vitamin D intake that is likely to be safe, effective, and fully beneficial for all Americans.


Instead of a careful, science-minded conclusion that meets the painfully conservative demands of crafting broad public policy, the committee instead chose to dogmatically pull the discussion back to the 1990s, ignoring the flood of compelling evidence that suggests that vitamin D is among the most important public health issues of the age.

Believe it or not, this new, though anemic, RDA represents progress: It's a (small) step farther down the road towards broader recognition and acceptance that higher intakes (or skin exposures) to achieve higher vitamin D levels are good for health.

My view: Vitamin D remains among the most substantial, life-changing health issues of our age. Having restored 25-hydroxy vitamin D levels in over 1000 people, I have no doubt whatsoever that vitamin D achieves substantial benefits in health with virtually no downside, provided 25-hydroxy vitamin D levels are monitored.

Coronary calcium: Cause or effect?

Here's an interesting observation made by a British research group.

We all know that coronary calcium, as measured by CT heart scans, are a surrogate measure of atherosclerotic plaque "burden," i.e., an indirect yardstick for coronary plaque. The greater the quantity of coronary calcium, the higher the heart scan "score," the greater the risk for heart attack and other unstable coronary syndromes that lead to stents, bypass, etc.

But can calcium also cause plaque to form or trigger processes that lead to plaque formation and/or instability?

Nadra et al show, in an in vitro preparation, that calcium phosphate crystals are actively incorporated into inflammatory macrophages, which then trigger a constellation of inflammatory cytokine release (tumor necrosis factor-alpha, interleukins), fundamental processes underlying atherosclerotic plaque formation and inflammation.

Here's the abstract of the study:
Proinflammatory Activation of Macrophages by Basic Calcium Phosphate Crystals via Protein Kinase C and MAP Kinase Pathways:

A Vicious Cycle of Inflammation and Arterial Calcification?


Basic calcium phosphate (BCP) crystal deposition underlies the development of arterial calcification. Inflammatory macrophagescolocalize with BCP deposits in developing atherosclerotic lesionsand in vitro can promote calcification through the release of TNF alpha. Here we have investigated whether BCP crystals can elicit a proinflammatory response from monocyte-macrophages.BCP microcrystals were internalized into vacuoles of human monocyte-derived macrophages in vitro. This was associated with secretion of proinflammatory cytokines (TNF{alpha}, IL-1ß and IL-8) capable of activating cultured endothelial cells and promoting capture of flowing leukocytes under shear flow. Critical roles for PKC, ERK1/2, JNK, but not p38 intracellular signaling pathways were identified in the secretion of TNF alpha, with activation of ERK1/2 but not JNK being dependent on upstream activation of PKC. Using confocal microscopy and adenoviral transfection approaches, we determined a specific role for the PKC-alpha isozyme.

The response of macrophages to BCP crystals suggests that pathological calcification is not merely a passive consequence of chronic inflammatory disease but may lead to a positive feed-back loop of calcification and inflammation driving disease progression.



This observation adds support to the notion that increasing coronary calcium scores, i.e., increasing accumulation of calcium within plaque, suggests active plaque. As I say in Track Your Plaque, "growing plaque is active plaque." Active plaque means plaque that is actively growing, inflamed and infiltrated by inflammatory cells like macrophages, eroding its structural components, and prone to "rupture," i.e., cause heart attack. Someone whose first heart scan score is, say, 100, followed by another heart scan score two years later of 200 is exposed to sharply increasing risk for cardiovascular events which may, in part, be due to the plaque-stimulating effects of calcium.

Conversely, reducing coronary calcium scores removes a component of plaque that would otherwise fuel its growth. So, people like our Freddie, who reduced his heart scan score by 75%, can be expected to enjoy a dramatic reduction of risk for cardiovascular events.

Less calcium, less plaque to rupture, less risk.

Wheat one-liners

If you're having difficulty convincing a loved one or someone else that wheat should be eliminated from the human diet, here are some useful one-liners to use:

Wheat makes your boobs big.
(This is true. Priceless for women to use on their husbands.)

Wheat causes dementia.
(And confirmed on examination of brain tissue at autopsy. Yes, autopsy.)

Wheat makes you look pregnant.
(The visceral fat of a wheat belly does a darn good imitation of a near-term infant.)

The first sign of wheat intolerance can be wetting your pants.
(Cerebellar ataxia, i.e., destruction and atrophy of the cerebellum, caused by wheat leads to loss of coordination and bladder control. Average age of onset: 53 years old.)

White flour bad, whole grain better; just as Marlboros are bad, Salems are better.
(The flawed syllogism that led to the "eat more healthy whole grain" colossal blunder.)

Wheat is the only food with its very own mortality rate.
(Celiac disease, osteoporotic hip fractures, and the neurologic diseases triggered by wheat can be fatal.)

"Wheat" is no longer wheat; it's the dwarf mutant that came from genetics research in the 1960s.
(Over 99% of all wheat today comes from the 18-inch tall dwarf mutant.)

Wheat increases blood sugar higher than nearly all other foods.
(Higher than Milky Way bars, higher than Snickers bars, higher than table sugar.)


There you have it: A full arsenal of one-liners to shoot at your husband, wife, or friend when they roll their eyes at your refusal to consume this thing called "wheat."

The happy homeotherm

If you were a "cold blooded" poikilotherm unable to regulate internal body temperature, you would have to sun yourself on rocks to raise your body temperature, just like turtles and snakes. When it got cold, your metabolic rate would slow and you might burrow into the mud to hide.

You and I, however, are homeotherms, terrestrial animals able to regulate our own internal body temperature. Principal responsibility for keeping your body temperature regulated falls with the thyroid gland, your very own thermoregulatory "thermostat."

But internal body temperature, even in a homeotherm, varies with circadian rhythm: Highest temperature occurs in the early evening around 8 p.m.; the low temperature nadir occurs at around 4 a.m.

The notion that normal human temperature is 98.6 degrees Fahrenheit is a widely-held fiction, a legacy of the extraordinary experience of 19th century German physician, Carl Reinhold August Wunderlich, who claims to have measured temperatures of one million people using his crude, uncalibrated thermometer to obtain axillary (armpit) body temperatures.

Dr. Broda Barnes was a 20th century American proponent of using the nadir body temperature to gauge thyroid function. Like Wunderlich, Barnes also used axillary temperatures.

Modern temperature assessments have employed radiotransmitting thermistors that are swallowed, with temperatures tracked as the thermistor travels through the stomach, duodenum, small intestine, large intestine, rectum, then peek-a-boos back out. Such internal "core temperature" assessments have shown that:

--Axillary temperatures do not track with internal core temperatures very well, often veering off course due to external factors.
--Axillary temperatures are subject to ambient temperatures, such as room temperature, and are affected by clothing.
--Axillary temperatures are more susceptible to physical activity, e.g., increased with exercise or physical work.

Even right vs. left axillary temperatures have been shown to vary up to 2 degrees Fahrenheit.

Studies such as this demonstrate that normal oral temperature upon arising is around 97.2-97.3 degrees Fahrenheit. While we lack data correlating thyroid function with circadian temperature variation, the a.m. nadir does indeed, as Dr. Barnes originally suggested, seem to track thyroid status quite well: lower with hypothyroidism, higher with normal or hyperthyroidism.

I have been using 97.3 degrees F orally as the cutoff for confirming or uncovering thyroid dysfunction, particularly when symptoms or blood tests (TSH, free T3, free T4) are equivocal, a value that has held up well in the majority of cases. I find it helpful when, for instance, someone complains of cold hands and feet and has normal TSH (1.5 mIU/L or less in my view) but low free T3. An a.m. oral temperature of, say, 95.7 degrees F, suggests that there will be a favorable response to T3 supplementation. And it nearly always plays out that way.

Wouldn't it be interesting to know if there was insight into thyroid status provided by also examining the circadian behavior of temperature (e.g., height or timing of the peak)?

Statin buster?

Merck recently reported preliminary results with its drug-in-development, anacetrapib.

After six months of treatment, participants showed:

LDL cholesterol was reduced from 81 mg/dl to 45 mg/dl in those taking anacetrapib, and from 82 mg/dl to 77 mg/dl in the placebo group.

HDL increased from 41 mg/dl to 101 mg/dl in the drug group, from 40 mg/dl to 46 mg/dl in those on placebo.

As you'd expect, the usual line-up of my colleagues gushed over the prospects of the drug, salivating over new speaking opportunities, handsomely-paid clinical "research" trials, and plenty of nice trips to exotic locales.

Anacetrapib is a cholesteryl-ester transfer protein inhibitor, or CETP inhibitor, much like its scrapped predecessor, torcetrapib . . . you know, the one that went down in flames in 2006 after 60% excess mortality occurred in people taking the drug compared to placebo. The hopes of many investors and Pfizer executives were dashed with torcetrapib's demise. The data on torcetrapib's lipid effects were as impressive as Merck's anacetrapib.

These drugs block the effects of the CETP enzyme, an enzyme with complex effects. Among CETP's effects: mediating the "heteroexchange" of triglycerides from triglyceride-rich VLDL particles that first emerge from the liver for cholesterol from LDL particles. This CETP-mediated process enriches LDL particles with triglycerides, which then make LDL a target for action by another enzyme, hepatic lipase, that removes triglycerides. This yields a several nanometer smaller LDL particle, now the number one most common cause of heart disease in the U.S., thanks to conventional advice to cut fat intake and increase consumption of "healthy whole grains."

With effects like this, anacetrapib, should it hold up under the scrutiny of FDA-required trials and not show the same mortality-increasing effects of torcetrapib, will be a huge blockbuster for Merck if release goes as scheduled in 2015. It will likely match or exceed sales of any statin drug. Statin drugs have achieved $27 billion annual sales, some of it deserved. Anacetrapib will likely handily match or exceed Lipitor's $12 billion annual revenue.

More than increasing HDL, CETP inhibition is really a strategy to reduce small LDL particles.

As with many drugs, there are natural means to achieve similar effects with none of the side-effects. In this case, similar effects to CETP inhibition, though with no risk of heightened mortality, is . . . elimination of wheat, in addition to an overall limitation of carbohydrate consumption. Not just low-carb, mind you, but wheat elimination on the background of low-carb. For instance, eliminate wheat products and limit daily carbohydrate intake to 50-100 grams per day, depending on your individual carbohydrate sensitivity, and small LDL drops 50-75%. HDL, too, will increase over time, not as vigorously as with a CETP inhibitor, but a healthy 20-30% increase, more with restoration of vitamin D.

Eliminating wheat and adjusting diet to ratchet down carbs is, of course, cheap, non-prescription, and can be self-administerd, criteria that leave the medical world indifferent. But it's a form of "CETP inhibition" that you can employ today with none of the worries of a new drug, especially one that might share effects with an agent with a dangerous track record.

Why does wheat cause arthritis?

Wheat causes arthritis.

Before you say "What the hell is he saying now?", let me connect the dots on how this ubiquitous dietary ingredient accelerates the path to arthritis in its many forms.

1) Wheat causes glycation--Glycation is glucose-modification of proteins in the body that occurs when blood glucose exceeds 100 mg/dl. Cartilage cells are especially susceptible to glycation. The cartilage cells you had at age 18 are the very same cartilage cells you have at age 60, since they lack the ability to reproduce and repair themselves. Proteins in cartilage are highly susceptible to glycation, which makes them stiff and brittle. Stiff, brittle cartilage loses its soft, elastic, lubricating function. Damaged cartilage cells don't regenerate nor produce more protective proteins. This allows destruction of cartilage tissue, inflammation, and, eventually, bone-on-bone arthritis.

Because wheat, even whole wheat, sends blood sugar higher than almost all other foods, from table sugar to Snickers bars, glycation occurs after each and every slice of toast, every whole wheat bagel, every pita wrap.

2) Wheat is acidifying--Humans are meant to consume a diet that is net alkaline. While hunter-gatherers who consume meat along with plentiful vegetables and fruits live a net alkaline diet (urine pH 7 to 9), modern humans who consume insufficient vegetables and too much grain (of which more than 90% is usually wheat) shift the body towards net acid (urine pH 5 to 7). Wheat is The Great Disrupter, upsetting the normal pH balance that causes loss of calcium from bones, resulting in decalcification, weakness, arthritis and osteoporotic fractures.

3) Wheat causes visceral fat--The extravagant glucose-insulin surges triggered by wheat leads to accumulation of visceral fat: wheat belly.

Visceral fat not only releases inflammatory mediators like tumor necrosis factor and various interleukins, but is also itself inflamed. The inflammatory hotbed of the wheat belly leads to inflammation of joint tissues. This is why overweight and obese wheat-consuming people have more arthritis than would be explained by the burden of excess weight: inflammation makes it worse. Conversely, weight loss leads to greater relief from arthritis pain and inflammation than would be explained by just lightening the physical load.

We need a name for this wheat effect. How about "bagel bones"?

Why do morphine-blocking drugs make you lose weight?

Naloxone (IV) and naltrexone (oral) are drugs that block the action of morphine.

If you were an inner city heroine addict and got knifed during a drug deal, you'd be dragged into the local emergency room. You're high, irrational, and combative. The ER staff restrain you, inject you with naloxone and you are instantly not high. Or, if you overdosed on morphine and stopped breathing, an injection of naloxone would reverse the effect immediately, making you sit bolt upright and wondering what the heck was going on.

So what do morphine-blocking drugs have to do with weight loss?

An odd series of clinical studies conducted over the past 40 years has demonstrated that foods can have opiate-like properties. Opiate blockers, like naloxone, can thereby block appetite. One such study demonstrated 28% reduction in caloric intake after naloxone administration. But opiate blocking drugs don't block desire for all foods, just some.

What food is known to be broken down into opiate-like polypeptides?

Wheat. On digestion in the gastrointestinal tract, wheat gluten is broken down into a collection of polypeptides that are released into the bloodstream. These gluten-derived polypeptides are able to cross the blood-brain barrier and enter the brain. Their binding to brain cells can be blocked by naloxone or naltrexone administration. These polypeptides have been named exorphins, since they exert morphine-like activity on the brain. While you may not be "high," many people experience a subtle reward, a low-grade pleasure or euphoria.

For the same reasons, 30% of people who stop consuming wheat experience withdrawal, i.e., sadness, mental fog, and fatigue.

Wouldn't you know that the pharmaceutical industry would eventually catch on? Drug company startup, Orexigen, will be making FDA application for its drug, Contrave, a combination of naltrexone and the antidepressant, buproprion. It is billed as a blocker of the "mesolimbic reward system" that enhances weight loss.

Step back a moment and think about this: We are urged by the USDA and other "official" sources of nutritional advice to eat more "healthy whole grains." Such advice creates a nation of obese Americans, many the unwitting victims of the new generation of exorphin-generating, high-yield dwarf mutant wheat. A desperate, obese public now turns to the drug industry to provide drugs that can turn off the addictive behavior of the USDA-endorsed food.

There is no question that wheat has addictive properties. You will soon be able to take a drug to block its effects. That way, the food industry profits, the drug industry profits, and you pay for it all.

Heart scan tomfoolery 2

In the last Heart Scan Blog post, I discussed the significance of the apparent discrepancy between Steve's heart scan score and volume score. This post addresses his second question, also a FAQ about heart scan scores.

Steve noted that his second scan compared to his first showed:

- Left Main volume went up from 22.4 to 35.6
- LAD went down from 95.2 to 91.3
- LCX volume went down from 23.2 to 0
- RCA volume went up from 0 to 9.3

So there are apparent divergences in behavior in the left main that increased and both LAD (left anterior descending) and LCX (left circumflex) that decreased.

The explanation is simple: When heart scans are "scored," they are viewed in horizontal "slices." When the heart is viewed as horizontal slices, the LAD and LCX originate from the common left main stem. In other words, it's like a tree with the left mainsteam representing the trunk, the LAD and LCX representing two main branches.

Plaque can form, obviously, in all three arteries, but it can do so by starting in the left main, for instance, and extending into either the LAD or LCX, or both. The left main plaque can therefore bridge any 2 or all 3 arteries.

When the plaque is "scored" by taking the computer mouse and circling the calcified plaque in question (to allow the computer program to generate the calcium score and volume score of that particular plaque), the plaque that may extend from left main into the LAD and/or LCX might be labeled "left main," or it might be labeled "LAD" or "LCX." There is no reliable way to "dissect" apart the plaque into the three arteries, since the plaque is coalescent and continuous. So the scoring technologist or physician simply arbitrarily declares the artery "LAD," for instance.

The problem comes when two different interpretation methods are used: Perhaps it's a new technologist or physician, or there was no attention paid to how the previous scan was read. One reader calls it "left main" and the next calls it "LCX."

So the apparent discrepancy has to do with flaws in the methods of segregating plaque location, as well as inattention to scoring techniques. The total score, however, remains unaffected.

Nonetheless, Steve has enjoyed a modest reduction in the score of the left main/LAD/LCX from his original 140.8 down to a second left main/LAD/LCX score of 126.9.

The right coronary artery (RCA), however, is not subject to this difficulty and Steve score shows a modest increase in score. (Why the divergent behavior between left main/LAD/LCX and RCA? There is no clear explanation for this, unfortunately.)

All in all, the news for Steve is good: He achieved these results on his own using nutritional techniques. Because he, in all practicality, stopped the progression of his heart scan score and avoided the "natural" rate of increase of 30% per year, all he needs to do is "tweak" his program a bit to achieve reversal, i.e., reduction of score.


Here's an image from another previous Heart Scan Blog post (about the relationship of osteoporosis and coronary disease) that shows such a plaque that starts in the left mainstem yet extends into both the LAD and LCX:

Heart scan tomfoolery

Heart Scan Blog reader, Steve, sent these interesting questions about his heart scan experience. (I sometimes forget that this blog is called "The Heart Scan Blog" and was originally--several years ago--meant to discuss heart scans. It has evolved to become a much broader conversation.)

The answers are a bit lengthy, so I'll tackle Steve's questions in two parts, the second in another blog post.

Dr. Davis,

I had a heart scan last year. The score was 96. While not a horrible score, it
was a wake up call, and I changed my lifestyle.

I had another scan this year and the heart scan score went up to 105, but the
volume score went down from 141 to 136.

The report I received said this:

'The calcium volume score is less in the current study as compared with the
original or reference study. This is an excellent coronary result and indicates
that there has been a net decrease in coronary plaque burden. The current
prevention program is very effective and should be continued.'

This is all well and good, but I have two questions:

1. Am I really going in the right direction even though the heart scan score
went up 9%?

2. Here are results that make no sense to me:
- Left Main volume went up from 22.4 to 35.6
- LAD went down from 95.2 to 91.3
- LCX volume went down from 23.2 to 0
- RCA volume went up from 0 to 9.3

Why would there be so much variation from year to year, and why would the plaque
move from site to site?

Steve


Questions like Steve's come up with some frequency, so I thought it would be worthwhile to discuss in a blog post.

First of all, the conventional heart scan score, or "calcium score" or "Agatston score" (after Dr. Arthur Agatston, developer of the simple algorithm for calcium scoring, as well as South Beach Diet fame), is the product of the area of the plaque in a single CT "slice" image
multiplied by a density coefficient, i.e., a number ranging from 1 to 4 that grades the x-ray density of the plaque. (1 is least dense; 4 is most dense.) A density coefficient of 1 therefore signifies some calcium within plaque, with higher density coefficients signifying increasing calcium content and density. Incidentally, "soft" plaque, i.e., non-calcified, would fall in the less than 1 range, even the negative range (fatty tissue within plaque).

The volume, or "volumetric," score is the brainchild of Drs. Paulo Raggi and Traci Callister, who expressed concern that, if we cause plaque to shrink in volume, the density coefficient used to calculate the calcium score would increase (since they believed that calcium could not be reduced, contrary to our Track Your Plaque experience, thereby leading to misleading results. They therefore developed an algorithm that did not rely on density coefficients, but used the same two-dimensional area obtained in the standard heart scan score, but replaced the density coefficient with a (mathematically interpolated) vertical axis (z-axis) measure of plaque "height." This 3-dimensional volumetric value therefore provided a method to generate a measure of calcium volume. In their original publication, the volume score proved more reproducible than the standard calcium score. This way, any reduction in plaque volume would not be influenced by the misleading effects of calcium density, but reflect a real reduction in volume.

Callister and Raggi's study also highlighted that calcium scoring in any form is subject to variability. Back in 1998 (when their study was published), there was a bit more variation than today due to the image acquisition methods used. But, even today, there is about 9% variation in scoring even if performed repeatedly (with less percentage variation the higher the score).

Unfortunately, volume scoring never caught on and the calcium score has been the most commonly used value by most heart scan centers and in most clinical studies. And, in all practicality, the two values nearly always track together: When calcium score increases, volume score increases in tandem; when calcium score decreases, volume score decreases in tandem.

Steve is therefore an exception to the general observation that calcium score and volume score travel together. Steve's calcium score increased, while his volume score decreased. From the above discussion, you can surmise a few things about Steve's experience:"

1) In all likelihood, the changes in both calcium score and volume score could simply be due to variability, i.e., variation in the placement of his body on the scan table, variation in position of the heart, variation in data acquisition, etc. There is a high likelihood that neither value changed; both are essentially unchanged.

2) If the changes are not due to scan variability, but are real, then it could be that the calcified plaque is reduced in volume but increased in density. If true, this is probably still a favorable phenomenon, since plaque volume is a powerful predictor of coronary "events" and an increase in plaque density is likely a benign phenomenon. It would also raise questions about the adequacy of vitamin D and vitamin K2 status, both major control factors over calcium deposition and metabolism.

So, in all likelihood, Steve's apparent discrepant results are modest good news, especially since calcium scores can ordinarily be expected to increase at the rate of 30% per year if no action is taken. Experiencing no change in score, calcium or volumetric, carries a very excellent prognosis, with risk for heart attack approaching zero. (I'm impressed that Steve accomplished this on his own, something the majority of my colleagues haven't the least bit of interest doing.)

Part 2 of Steve's question will be tackled in a separate post.
Cureality | Real People Seeking Real Cures

Why haven't you heard about lipoprotein(a)?

Lipoprotein(a), or Lp(a), is the combined product of a low-density lipoprotein (LDL) particle joined with the liver-produced protein, apoprotein(a).

Apoprotein(a)'s characteristics are genetically-determined: If your Mom gave the gene to you, you will have the same type of apoprotein(a) as she did. You will also share her risk for heart disease and stroke.

When apoprotein(a) joins with LDL, the combined Lp(a) particle is among the most aggressive known causes for coronary and carotid plaque. If apoprotein(a) joins with a small LDL, the Lp(a) particle that results is especially aggressive. This is the pattern I see, for instance, in people who have heart attacks or have high heart scan scores in their 40s or 50s.

Lp(a) is not rare. Estimates of incidence vary from population to population. In the population I see, who often come to me because they have positive heart scan scores or existing coronary disease (in other words, a "skewed" or "selected" population), approximately 30% express substantial blood levels of Lp(a).

Then why haven't you heard about Lp(a)? If it is an aggressive, perhaps the MOST aggressive known cause for heart disease and stroke, why isn't Lp(a)featured in news reports, Oprah, or The Health Channel?

Easy: Because the treatments are nutritional and inexpensive.

The expression of Lp(a), despite being a genetically-programmed characteristic, can be modified; it can be reduced. In fact, of the five people who have reduced their coronary calcium (heart scan) score the most in the Track Your Plaque program, four have Lp(a). While sometimes difficult to gain control over, people with Lp(a) represent some of the biggest success stories in the Track Your Plaque program.

Treatments for Lp(a) include (in order of my current preference):

1) High-dose fish oil--We currently use 6000 mg EPA + DHA per day
2) Niacin
3) DHEA
4) Thyroid normalization--especially T3

Hormonal strategies beyond DHEA can exert a small Lp(a)-reducing effect: testosterone for men, estrogens (human, no horse!) for women.

In other words, there is no high-ticket pharmaceutical treatment for Lp(a). All the treatments are either nutritional, like high-dose fish oil, or low-cost generic drugs, like liothyronine (T3) or Armour thyroid.

That is the sad state of affairs in healthcare today: If there is no money to be made by the pharmaceutical industry, then there are no sexy sales representatives to promote a new drug to the gullible practicing physician. Because most education for physicians is provided by the drug industry today, no drug marketing means no awareness of this aggressive cause for heart disease and stroke called Lp(a). (When a drug manufacturer finally releases a prescription agent effective for reducing Lp(a), such as eprotirome, then you'll see TV ads, magazine stories, and TV talk show discussions about the importance of Lp(a). That's how the world works.)

Now you know better.

How to have a heart attack in 10 easy steps

If you would like to plan a heart attack in your future, here are some easy-to-follow steps to get you there in just a few short months or years:


1) Follow a low-fat diet.

2) Replace fat calories with "healthy whole grains" like whole wheat bread.

3) Eat "heart healthy" foods like heart healthy yogurt and breakfast cereals from the grocery store.

4) Use cholesterol-reducing plant sterols.

5) Take a multivitamin to obtain all the "necessary" nutrients.

6) Take the advice of your doctor who declares your heart "in great shape" based on your cholesterol values.

7) Take the advice of your cardiologist who declares your heart "like that of a 30-year old" based on a stress test.

8) Take a statin drug to reduce LDL and c-reactive protein while maintaining your low-fat diet.

9) Neglect sun exposure and vitamin D restoration.

10) Limit your salt intake while not supplementing iodine.



There you have it: An easy, 10-step process to do your part to help your local hospital add on its next $40 million heart care center.

If you would instead like to prevent a heart attack in your future, then you should consider not doing any of the above.

Kick inflammation in the butt

C-reactive protein, or CRP, is a protein produced by the liver in response to inflammatory signals its receives. Thus, CRP has emerged as a popular measure to gauge the underlying inflammatory status of your body. Higher CRP levels (e.g., 3.0 mg/L or greater) are associated with increased risk of heart attack and other cardiovascular events.

The drug cartel have jumped on this with the assistance of Harvard cardiologist, Dr. Paul Ridker. Most physicians now regard increased CRP as a mandate to institute statin therapy, preferably at high doses based on such studies as The JUPITER Trial, in which rosuvastatin (Crestor), 20 mg per day, reduced CRP 37%.

I see this differently. Two strategies drop CRP dramatically, nearly to zero with rare exception: Vitamin D restoration and wheat elimination. Not 37%, but something close to 100%.

Yes, I know it sounds wacky. But it works almost without fail, provided the rest of your life is conducted in reasonably healthy fashion, i.e., you don't live on Coca Cola, weigh 80 lbs over ideal weight, and smoke.

How can something so easily reduced like CRP mean you "need" medication? Easy: Increased CRP means there are fundamental deficiencies and/or inflammation provoking foods in your diet. Correct neither and there is an apparent benefit to taking a statin drug.

Why not just correct the underlying causes?

Life without Lipitor

One of the most common reasons people come to my office is to correct high cholesterol values without Lipitor. (Substitute "Lipitor" with Crestor, simvastatin, Vytorin, or any of the other cholesterol drugs; it's much the same.)

In the world of conventional healthcare, in which you are instructed to follow a diet that increases risk for heart disease and not advised to correct nutrient deficiencies like vitamin D and omega-3 fatty acids, then a drug like Lipitor may indeed provide benefit.

But when you are provided genuinely effective information on diet, along with correction of nutrient deficiencies, then the "need" and apparent benefits of Lipitor largely dissolve. While there are occasional genetic anomalies that can improve with use of Lipitor and other statins, many, perhaps most, people taking these drugs really would not have to if they were just provided the right information.

Anyone following the discussions on these pages knows that wheat elimination is probably one of the most powerful overall health strategies available. Wheat elimination reduces real measured LDL quite dramatically. Provided you limit other carbohydrates, such as those from fruits, as well, LDL can drop like a stone. That's not what your doctor tells you. This approach works because elimination of wheat and limiting other carbohydrates reduces small LDL. Small LDL particles are triggered by carbohydrates, especially wheat; reducing carbohydrates reduces small LDL. Conventional LDL of the sort obtained in your doctor's office will not show this, since it is a calculated value that appears to increase with reduced carbohydrates, a misleading result.

Throw vitamin D normalization and iodine + thyroid normalization into the mix (both are exceptionally common), and you have two additional potent means to reduce (measured) LDL. Not restricting fat but increasing healthy fat intake, such as the fats in lots of raw nuts, olive oil, and flaxseed oil reduce LDL.

While I still prescribe statins now and then, a growing number of people are succeeding without them.

(Note that by "measured" LDL I am referring to the "gold standard," LDL particle number by NMR provided by Liposcience. A second best is measured Apoprotein B available through most conventional labs.)

In search of wheat: Emmer

While einkorn is a 14-chromosome ancient wheat (containing the so-called "A" genome), emmer is a 28-chromosome wheat (containing the "A" and "B" genomes, the "B" likely contributed by goat grass 9000 years ago).

Both einkorn and emmer originally grew wild in the Fertile Crescent, allowing Neolithic Natufians to harvest the wild grasses with stone sickles and grind the seeds into porridge.

Having tested einkorn with only a modest rise in blood sugar but without the gastrointestinal or neurological effects I experienced with conventional whole wheat bread, I next tested bread made with emmer grain.

The emmer grain was ground just like the other two grains, cardiac dietitian Margaret Pfeiffer doing all the work of grinding and baking. Margaret added nothing but water, yeast, and a little salt. The emmer rose a little more than einkorn, but not to the degree of conventional whole wheat.

I tested my blood sugar beforehand: 89 mg/dl. I then ate 4 oz of the emmer bread. It tasted very similar to conventional whole wheat, but not as nutty as einkorn. Also not as heavy as einkorn, only slightly heavier than conventional whole wheat.

One hour later, blood sugar: 147 mg/dl. I felt slightly queasy for about 2-3 hours, but that was the end of it. No abdominal cramps, no sleep disturbance or crazy dreams, no nausea, no change in ability to concentrate.

I asked four other wheat-sensitive people to try the emmer bread. Likewise, nobody reacted negatively (though nobody tested blood sugar).

So it seems to me, based on this small, unscientific experience, that ancient einkorn (A) and emmer (AB) wheat seem to act like carbohydrates, similar to, say, rice or quinoa, but lack many of the other adverse effects induced by conventional wheat.

Modern wheat , Triticum aestivum, contains variations on the "A," "B," and "D" genomes, the "D" contributed by hybridization with Triticum tauschii at about the same time that emmer wheat hybridization occurred. It is likely that proteins coded by the "D" genome are the source of most of the problems with wheat products: immune, neurologic, gastrointestinal destruction, airway inflammation (asthma), increase in appetite, etc. This is consistent with observations made in studies that attempt to pinpoint the gliadin proteins that trigger celiac, the area in which much of this research originates.

If I ever would like an indulgence of cookies or cupcakes, I think that I will order some more einkorn grain from Eli Rogosa.

In search of wheat: Another einkorn experience

Lisa is a trained dietitian. Unlike many of her colleagues, she has "seen the light" and realized that the conventional advice that most dietitians are forced to dispense through hospitals, clinics, and other facilities is just plain wrong. 

I know Lisa personally and we've had some great conversations on diet and nutritional supplements. I told Lisa about my einkorn experience and how I witnessed a dramatic difference between bread made from einkorn wheat and that made from conventional whole wheat. So she decided to give it a try herself. 

Here's Lisa's experience:


This past Friday, June 18th, I conducted my "Einkorn Wheat Experiment".

7 am 
FBG [fasting blood glucose] 97 mg/dl

8 am-9 am 
1 hour high-intensity aerobic workout

10:05 am 
BG 99

10:05 am 
I embarked upon the journey of choking down, I mean enjoying, the hefty piece of Einkorn bread. Wow, was that bread dense!  It was a lot of work chewing. 

10:50 am 
(45 minutes after consumption, wanted to see what BG did a bit before the 1 hr mark)  BG 153

11:05 am 
1hr PP 120

11:35 am 
90 mins PP [postprandial] 113

12:05 pm 
2 hours PP  114 ... at this time I ate an egg & veggie omelet for lunch.

12:50 pm 
BG 100

Before dinner 5:10 pm 
BG 88

I was surprised with the BG of 153. However, it was good to see my insulin response is reactive and decreased BG 33 points in 15 minutes to end up with a BG of 120 1 hr after the bread.  

So, it appears my response is similar. A slight elevation of BG at the 1 hour mark, but not to the degree of conventional whole grain wheat bread.  

Of note, also, was the fact that I cannot remember the last time I ate a piece of wheat bread of this magnitude that did not make me bloated... not at all: No cramps, no brain fog, no headache and, did I mention not bloated?  

I believe you are on to something with tolerance of Einkorn wheat for those of us with wheat sensitivities, in addition to its apparent lower glycemic response.

Along with Lisa, I asked four other people with various acute intolerances (all gastrointestinal) to conventional wheat, i.e., people who experience undesirable effects from wheat within minutes to several hours, to eat the einkorn bread. None experienced their usual reactions.

Obviously, this does not constitute a clinical trial. Nonetheless, I find this a compelling observation: People like myself who generally experience distinct undesirable reactions to wheat did not experience these reactions with einkorn.

Note, however, that einkorn behaves like a carbohydrate. No different, say, from brown rice or quinoa. However, unlike modern whole wheat flour from Triticum aestivum,  in this little experience there were no immune reactions, no neurologic phenomena, no gastrointestinal distress--just the blood sugar consequences.

While this may not be true for all people consuming einkorn, it suggests that primordial einkorn wheat is quite different from modern conventional wheat for most people.

Increased blood calcium and vitamin D

Conventional advice tells us to supplement calcium, 1200 mg per day, to preserve bone health and reduce blood pressure.

Here's a curious observation I've now witnessed a number of times: Some people who supplement this dose of calcium while also supplementing vitamin D sufficient to increase 25-hydroxy vitamin D blood levels to 60-70 ng/ml develop abnormally high levels of blood calcium, hypercalcemia.

This makes sense when you realize that intestinal absorption of calcium doubles or quadruples when vitamin D approaches desirable levels. Full restoration of vitamin D therefore causes a large quantity of calcium to be absorbed, more than you may need. In addition, two studies from New Zealand suggest that 1200-1300 mg calcium with vitamin D per day doubles heart attack risk.

We have 20 years of clinical studies demonstrating the very small benefits of supplementing calcium to stop or slow the deterioration of bone density (osteopenia, osteoporosis). These studies were performed with no vitamin D or with trivial doses, too small to make a difference. I believe those data have been made irrelevant in the modern age in which we "normalize" vitamin D.

Should hypercalcemia develop, it is not good for you. Over long periods of time, abnormal calcium deposition can occur, leading to kidney stones, atherosclerosis, and arthritis.

Until we have clarification on this issue, I have been advising patients to take no more than 600 mg calcium supplements per day. I suspect, however, that the vast majority of us require no calcium at all, provided an overall healthy diet is followed, especially one that does not leach out bone calcium. This means no foods like those made with wheat or containing powerful acids, such as those in carbonated drinks.

Heart health consultation with Dr. Joe D. Goldstrich

Cardiologist, nutritionist, and lipidologist, Dr. Joe D. Goldstrich, is a frequent contributor to the Track Your Plaque Forum, where we discuss the full range of issues relevant to coronary health and coronary plaque reversal.

I have come to value Dr. Goldstrich's unique insights, especially in nutrition. Formerly National Director of Education and Community Programs for the American Heart Association and a physician at the Pritikin Center, his dietary philosophy has evolved away from low-fat and towards a low-carbohydrate focus, much as we use in Track Your Plaque. Like TYP, Dr. Goldstrich is always searching for better answers to gain control over coronary health. His unique blend of ideas and background has helped us craft new ideas and strategies. Dr. Goldstrich has proven especially adept at understanding how to incorporate new findings from clinical studies in our framework of coronary atherosclerotic plaque management strategies.

Dr. Goldstrich is offering to share his expertise with our online community. If you would like a one-on-one phone consultation with Dr. Goldstrich, you can arrange to speak with him at his HealthyHeartConsultant.com website.

Wheat aftermath

Following my 4 oz whole wheat misadventure that yielded the sky-high blood sugar of 167 mg/dl, compared to einkorn wheat's 110 mg/dl, I suffered through a 36-hour period of misery.

After I obtained the blood sugar of 167 mg/dl, I biked hard for one hour. This yielded a blood sugar back down in the 80s. I felt spacey in the ensuing few hours, as well as a little queasy. However, about 12 hours later, I awoke with overwhelming nausea along with that hypersalivating thing that happens just prior to vomiting. It did not come to that, but persisted all through the following day.

The next morning, I could barely concentrate. Trying to read a study (admittedly on the complex topic of agricultural genetics), I had to read each paragraph 4 or 5 times. Abdominal cramps and a bloated feeling also developed, though I was able to eat.

The 2nd night was filled with incredibly vivid dreams and intermittent sleeplessless. I awoke about 5 times through the night, but periods of sleep were filled with detailed, colorful dreams. I dreamt that a large corporation was secretly trying to gain control over the world's water supply, and I snuck onto a complex underwater vessel that was exploring and mapping the coastline of the Great Lakes in preparation. Weird.

I recognized these odd feelings as various facets of wheat intolerance, since they were all reminiscent of feelings I used to experience before I removed wheat from my diet. They were amplified and compressed, likely because I had been wheat-free for so long.

The odd thing is that, despite the modest blood sugar effect of my einkorn experience, none of the gastrointestinal or neurologic effects of wheat developed. So far, two other people with acute gastrointestinal wheat sensitivities have consumed our einkorn bread, also without reproduction of their usual symptoms.

Einkorn contains gluten, though the structure of the many gluten proteins of einkorn differs from that of the wheat bread I consumed, an example of modern Triticum aestivum. 14-chromosome einkorn carries what biologists call the "A" genome, while Triticum aestivum has the combines genomes of 3 plants, the combination of the A, B, and D genomes. It is the D genome that contains the genes coding for the most obnoxious, immunogenic forms of gluten.

So einkorn may not be entirely benign, but it is a good deal less obnoxious than modern Triticum aestivum.

I am awaiting the reports from a few other people on their experiences.

In search of wheat: Einkorn and blood sugar

There are three basic aspects of wheat's adverse health effects: immune activation (e.g., celiac disease), neurologic implications (e.g., schizophrenia and ADHD), and blood sugar effects.

Among the questions I'd like answered is whether ancient wheat, such as the einkorn grain I obtained from Eli Rogosa, triggers blood sugar like modern wheat.

So I conducted a simple experiment on myself. On an empty stomach, I ate 4 oz of einkorn bread. On another occasion I ate 4 oz of bread that dietitian, Margaret Pfeiffer, made with whole wheat flour bought at the grocery store. Both flours were finely ground and nothing was added beyond water, yeast, olive oil, and a touch of salt.

Here's what happened:

Einkorn wheat bread:

Blood sugar pre: 84 mg/dl
Blood sugar 1-hour post: 110 mg/dl

Conventional wheat bread
Blood sugar pre: 84 mg/dl
Blood sugar 1-hour post: 167 mg/dl

The difference shocked me. I expected a difference between the two, but not that much.

After the conventional wheat, I also felt weird: a little queasy, some acid in the back of my throat, a little spacey. I biked for an hour solid to reduce my blood sugar back to its starting level.

I'm awaiting the experiences of others, but I'm tantalized by the possibility that, while einkorn is still a source of carbohydrates, perhaps it is one of an entirely different variety than modern Triticum aestivum wheat. The striking difference in blood sugar effects make me wonder if einkorn eaten in small quantities can keep us below the Advanced Glycation End-Product threshold.
 
All posts by william-davis

Wheat-free and weight loss

With a heart scan score of 1222, Leslie could be in deep trouble in short order.

At 64 years old, Leslie had gained nearly 40 lbs since she'd given up a lot of her activities caring for a husband who'd developed psychological difficulties and stopped contributing to the household duties. A tall woman at 5 ft 9 inches, she held her 202 lbs well, but her lipoprotein patterns were a disaster:

--LDL particle number 2482 nmol/l--an equivalent LDL cholesterol of 248 mg/dl (drop the last digit)
--HDL 38 mg/dl
--Triglycerides 241 mg/dl
--90% of LDL particles were small
--Lipoprotein(a) 240 nmol/l

Blood sugar was in the pre-diabetic range at 112 mg/dl, C-reactive protein was high at 3.0 mg/l, blood pressure was somewhat high at 140/84.

Now, with the exception of lipoprotein(a), these patterns are exquisitely weight-sensitive. A reduction in weight would yield effects superior to any medication I could give her.

Processed wheat products were a big problem for Leslie: whole wheat bread, pretzels for snacks, whole wheat pasta. Yes, they sound healthy, even endorsed by the American Heart Association, often bearing "heart healthy" labels on the packages. Don't you believe it.

In particular, Leslie had the number one cause for heart disease in America: small LDL particles, a pattern that is magnified 30-70% by wheat products. Endorsed by the Heart Association? (As I often tell people, if you want heart disease, follow the diet advocated by the American Heart Association.)

Leslie was skeptical, worried that she would be hungry all the time and would have virtually nothing left to eat. Instead, when she returned to the office three months later, she reported that eating was easy, finding healthy foods not containing wheat was easier than she thought, she felt great, finding more energy than she'd had in years.

She'd also shed 30 lbs.

Leslie's lipoprotein patterns also reflected the weight loss. She achieved her 60:60:60 Track Your Plaque lipid targets, small LDL shrunk dramatically, blood sugar and blood pressure were back in normal ranges.

I see results like Leslie's several times every week. For those of us with patterns like Leslie's, or just obesity that accumulates in the abdomen, going wheat-free is among the most powerful single strategies I know of.

If you need convincing, try an experiment. Eliminate--not reduce, but eliminate wheat products from your diet, whether or not the fancy label on the package says it's healthy, high in fiber, a "healthy low-fat snack", etc. This means no bread, pasta, crackers, cookies, breads, chips, pancakes, waffles, breading on chicken, rolls, bagels, cakes, breakfast cereal. I find elimination of wheat easier than just cutting back. I believe this is because wheat is powerfully addictive. It's very similar to telling an alcoholic that a drink now and then is okay--it just doesn't work. They need to be alcohol-free. Most of us need to be wheat-free, not just cut back.

You won't be hungry if you replace the lost calories with plenty of raw almonds, walnuts, pecans, sunflower and pumpkin seeds; more liberal use of healthy olive oil, canola oil and flaxseed oil; adding ground flaxseed and oat bran to yogurt, cottage cheese, etc.; and more lean proteins like lean beef, chicken, turkey, fish, and eggs.

The majority of people who go wheat-free lose weight, sometimes dramatically. Most people also feel better: more energy, more alert, better sleep, less mood swings. Time and again, people who try this will tell me that the daytime grogginess they've suffered and lived with for years, and would treat with loads of caffeine, is suddenly gone. They cruise through their day with extra energy.

Even without weight loss, going wheat-free usually raises HDL, reduces the dreaded small LDL dramtically. It also reduces triglycerides, blood sugar, C-reactive protein, blood pressure. Blood sugar control in diabetics is far easier, with less fluctuations and sharp rises in blood sugar.

Success at this also yields great advantage for your heart scan score control and reversal efforts.

Collective wisdom


As public consciousness and knowledge about health issues grows, thanks to the internet and other media, I predict that:

1) Hospitals will recede into a role of acute and catastrophic care ONLY, dropping the charade of providing health, which they do NOT.

2) Doctors and other health professionals will begin to see themselves as providers of acute and catastrophic care, also. They will stop providing day to day care, such as treating high blood pressure, cholesterol, breast exams, and other preventive maintenance.

3) Instead, preventive care will be self-provided. The public will have acquired sufficient savvy and know-how to manage issues like blood pressure themselves. They will need the assistance of helpful information resources, web-based for the most part. Much preventive care can, in fact, be algorithm-driven, just like following a simple recipe.

All the worries about runaway health care costs will be much reduced, since excessive testing driven by liability worries will disappear, repeated office visits for day-to-day issues will go away. Yes, you will need a doctor and hospital for a broken leg, car accident, unexpected cancer, or non-compliance or neglect of prevention.

But osteoporosis, high blood pressure, nutrition, weight loss, hormone management, cholesterol issues, minor complaints will all be managed by people themselves with the assistance of web-based knowledge systems.

I already sense this sort of phenomeonon developing, though in its infancy, in venues like the Track Your Plaque Forum and other health portals, places where the information being discussed exceeds the quality of information you can obtain from your doctor. Over and over again, for instance, the sophistication and knowledge demonstrated by our Track Your Plaque Forum discussions shows that the public is capable of far more understanding of health issues than many previously believed. Most of our members could carry on a credible conversation with trained lipid experts. The knowledge base of our members exceeds that of 98% of most of my colleagues when it comes to heart scans, lipoproteins, and nutrition.

I am in awe of Wikipedia, the popular online encyclopedia. Five 20- and 30-somethings have created a knowledge base that has now eclipsed Encyclopedia Britannica in size and scope, with equivalent accuracy, and relatively little cost. I'd like to see the same phenomenon occur in health care information, helping to usurp the current paternalistic "I'll tell you what to do" model.

Success--Slow but sure

John is a gentleman.

At age 76, he continues to teach at a local college. He's a delight to talk to, having written several scholarly books on religious topics. He's a fountain of knowledge on religious history and the roots of faith.

John is one of those incurably optimistic people, always greeting me with a smile and a warm handshake. I can't help but linger for a hour or so to talk with John, unfortunately disrupting my office schedule miserably.

John is another Track Your Plaque success story. Though he didn't set any records in reduction of his heart scan score, he did it simply by adhering to the program over a period of two years, succeeding slowly but surely.

John's first heart scan score: 1190, a score that carries as much as a 25% annual risk for heart attack. Among the list of causes was an LDL cholesterol in the 170 mg/dl range, along with an LDL particle number that verified the accuracy of LDL.

Among John's suggested treatments was a statin drug, since I was not confident he could reduce LDL with diet and nutritional modifications sufficiently to safely reduce both LDL and his risk for heart attack. But he proved terribly intolerant to any dose of any statin, with incapacitating and strange side-effects, like head-to-toe itching, abdominal cramps and diarrhea. It was clear: John needed to do the program without benefit of a statin drug.

I therefore asked John to maximize all efforts that reduce LDL, 70% of which were small LDL paricles despite his very slender build. He used oat bran and ground flaxseed daily, raw nuts, a soy protein smoothie every morning, and eliminated wheat and other high-glycemic index foods (including the Oreos he loved to snack on). Because the mis-adventures with statin drugs wasted nearly a year, I asked John to undergo another heart scan. Score 2: 1383, a 16% increase.

I asked John to keep on going. Thankfully, he did manage to tolerate fish oil, niacin (though it required over a year just to get to a 1000 mg per day dose), and vitamin D. With all these efforts, he did reduce LDL to the 80-90 mg/dl range. Of course, John's unflagging optimism was crucial. He did express his occasional anxiety over his heart scan score, but dealt with it in a logical, philosophical way. He understood that there was no role for prophylactic stents or bypass, and he accepted that much of his program rested on his ability to adhere to the strategies we advised.

Another year later, a 3rd heart scan: 1210, a 12% reduction.

I'm very proud of John and his success. When you think about it, he succeeded in conquering heart disease with some very simple tools, minus statin drugs. It can be done, but requires consistency and patience--and an optimistic outlook.

Vitamin D and octagenarians

Roger practically bounced in his chair vibrating with energy.

"It must be the vitamin D! I haven't felt like this in years. I can work around the yard all day and still have energy left over."

At age 84, Roger started out with pretty good health, despite a prosthetic valve and bypass surgery 5 years earlier. He looked 74, perhaps younger.

I've seen this effect now in about 20 octagenarians. A Track Your Plaque Member mentioned this same effect in his father-in-law in a discussion in our Forum. Most are taking around 6000-8000 units per day (gelcap, of course). The average dose of vitamin D tends to be higher in this age group, since by age 80, you've essentially lost the capacity to convert 7-hydrocholesterol to active vitamin D3 in the skin. Most octagenarians start with 25-OH-vitamin D3 levels of 10 ng/ml or less--profound deficiency.

I believe the effect is real, having now witnessed it multiple times. Unfortunately, my observations are too informal to qualify as a study. (I wouldn't even know how to quantify this. I suppose some sort of muscle and coordination testing might yield quantifiable measures.) However, there are some data emerging that show less fractures, falls, improved coordination, and perhaps improved memory and mentation with vitamin D supplementation, though doses often used in studies tend to be lower than what we are using in practice.

I haven't been so excited about the effects of a nutritional supplement in a long time. Vitamin D continues to yield surprises every day in its array of positive and powerful effects.

Could we say that vitamin D restores youthfulness?

NY Times Jane Brody misses the mark



NY Times' health columnist, Jane Brody, recently wrote a bit of fluff for her paper:

"CT Scans of the Heart Come With Trade-Offs


In her report, she says:

Coronary CT scans are being sold directly to the public, and they have found a market in health-conscious people who can afford them. But screening exams can have downsides. They can cause needless worry, and they sometimes reveal other potential conditions that require invasive procedures like biopsies to diagnose.

I soon learned that among the strongest proponents of CT scans of coronary arteries were physicians with financial ties to drug companies that make statins and others connected to imaging centers that would profit directly from widespread CT screenings.



She then goes on to discuss how the Framingham scoring calculation can tell you whether or not you are at low-, intermediate-, or high-risk for heart disease. She therefore concludes that heart scans are therefore irrelevant for the majority of people. She then proceeds to take a statin agent.

This sort of nonsense continues to get published, despite the clear lack of real "digging" for the truth. She clearly fell for the conventional arguments that continue to mis-guide the majority of people, myths like:

--the Framingham scoring system is reliable--Reliable it is NOT; it is susceptible to substantial "misclassification" bias, meaning people who appear low risk can actually be high risk, and people at high risk can actually be low risk. Among the latest studies that question the scoring system is Family history of premature coronary heart disease and coronary artery calcification: Multi-Ethnic Study of Atherosclerosis (MESA). This study pointed out how the Framingham scoring system, which leaves out family history, can cause people classified as low risk to actually have substantial heart scan scores. This is crucial. A heart scan gets beyond the uncertainties and shows with >95% certainty whether or not hidden coronary atherosclerotic plaque is present.

--"Coronary risk" is a dynammic phenomenon, subject to changes in a person's life. What if, for instance, a person smoked for 20 years, quit 10 years ago, lost 30 lbs, dropped their blood pressure as a result of the weight loss, then relied on the Framingham Risk Calculator to determine risk. They would likely be classified as low- risk, since risk factors now appear favorable. This person could easily have a heart scan score of 500, or 700, or 1000, levels that carry a cardiovascular event risk of 5-25% per year, hardly low-risk, because much of their risk accumulated earlier in life and is no longer revealed by an assessment of risk factors.

--There are sources of risk that have nothing to do with Framingham, such as lipoprotein(a), which is often revealed by family history; the presence of small LDL, which co-varies with HDL and triglycerides, but can behave independently also; and, my favorite, deficiency of vitamin D. This would explain part of the 60-70% of people who are typically mis-classified by Framingham.


Where did Ms. Brody get the idea that proponents of heart scans had ties to drug companies? I think she's barking up the wrong tree on that one. Of course, she ends up on a statin drug. For my part, I am a critic of statin drugs. Yes, they play a role, but they are miserably misused and abused by practicing physicians, based on the endless onslaught of drug company-sponsored trials that have served to distort their usefulness.

If I were Ms. Brody, I would be quaking in my shoes, not knowing what my true risk for heart disease was, relying on the--at best--30% reduction in heart attack risk of Lipitor or other statin drug. Ms. Brody: You are not cured, you're simply wearing a superficial Band-Aid. If you want to know your true risk for heart attack, and you want a precise value that you can track over time, the answer is simple: Reject the conventional notion and get a heart scan.

"There must be a mistake"

Neal is our current male record holder for greatest reduction in heart scan score. (Yes, the ladies have the lead!)

You may remember that this 40-year old man reduced his heart scan score from 339 to 161--a 51% drop. If you haven't yet read his story, go to

http://www.cureality.com/library/fl_07-001nealt51.asp


Neal reminded me of the experience he had when he underwent his second heart scan. Both scans had been performed at the same scanning center. At this center, the radiologists provide the added service of sitting down with people and actually going over the images and results.

After the scan, the radiologist pulled up the result from Neal's first scan for comparison. "There must be a mistake! This score is lower. Scores never drop."

The radiologist was apparently stumped, unable to provide an explanation. However, Neal then proceeded to tell the radiologist that we had warned Neal that this could happen and that he might even be told that it was due to error of some sort. This yielded a puzzled look on the radiologist but no further comment.

Of course it's not a mistake. It's something we achieve on purpose. Curiously, I still get comments that this is impossible, heart scan scores never drop, etc. Of course, those of you following this conversation know this is completely untrue. Heart scan scores DO drop, and sometimes drop enormous amounts, as it did for Neal.

I would have liked the radiologist to have had the lightbulb of understanding go off in his head when he realized that a reduction in heart scan score is a cause for celebration. Unfortunately, this radiologist's reaction is all too common: disbelief, confusion, dismissal.

Heart disease reversal is simply not in the realm of understanding of most doctors, radiologists and cardiologists alike. By conventional thought, if you have it, it just gets worse. "Maybe some high-dose Lipitor might help."

Ironically, when they see it right in front of their eyes, plain as day on the computer screen, they don't understand what has happened. It's Greek to them.

Should this happen to you, don't be surprised. Just bite your tongue, because you know better.

Jimmy Moore Interview: Is saturated fat the villain we thought?

Enter "weight loss" or "low carb" in your web search and you can't help but stumble across the prolific and widely-connected Jimmy Moore.

On his Blog, Livin' la Vida Lo Carb , Jimmy conducts a wide-ranging and informative discussion of the benefits of a low carbohydrate diet, a la Atkins. Though his initial claim to fame was the 180 lbs he lost in his first year of dieting on this approach, Jimmy has extended the conversation and built a considerable community of like-minded individuals, all of whom are participating in this grand "experiment."

Anybody who looks at lipoproteins and associated factors in health will quickly come to the conclusion that processed carbohydrates are the culprits in much of heart disease, diabetes, and heart disease. But I have had a hard time dismissing the ill-effects of saturated fat. After all, we've all been taught--drilled--with the idea that saturated fats cause LDL cholesterol to go higher, cause arterial constriction, growth of atherosclerotic plaque, inflammation, even cancer.

But there does indeed seem to be a growing sentinment that this long-held dogma may not be true. So I went to the ever-entertaining and informative Jimmy Moore, an able spokesman for these concepts.




TYP: It's certainly impossible to argue with the success you had in weight loss and the health you've regained on your program.

I think that the approach we use in diet in the Track Your Plaque program and the nutrition approach you advocate overlap to a great extent. We both emphasize plenty of vegetables, fruits, healthy oils, nuts, etc. The major point of difference seems to lie in saturated fat: We say restrict it, you say don't restrict it. Could you elaborate?





JM: Thank you for inviting me to your blog today, Dr. Davis. I have nothing but deep respect and admiration for the work you are doing to help educate others about how to keep their heart health in tip-top shape. Keep fighting the good fight, my friend.

While we do agree on probably 99% of the basic tenets of what I describe as
"livin' la vida low-carb," the issue of saturated fat to me is one where we
indeed do not. It's not a deal breaker regarding my support for what you do
just as I'm sure you would say the same regarding your backing of what I do. If
we all agreed on everything, then what a boring world this would be!

My thinking on saturated fat has evolved since I started eating this way nearly
four years ago. Like most people, I was terrified to eat ANY fat at all because
of the abject fear that people like Dr. Dean Ornish and other so-called health
"experts" instilled in me about how dangerously unhealthy it is to consume it.
This fat phobia is arguably the single biggest contributor to the ongoing
obesity crisis our world faces today.

With that said, you and I both know fat consumption is a part of a healthy
lifestyle. There are just too many benefits to the body that come from the
consumption of fats and even saturated fats such as coconut oil, butter, lard,
nuts, seeds, and animal fat when it is combined with a restricted carbohydrate
intake.

An intriguing study was presented at a scientific conference in November 2006 by two highly-respected researchers--Dr. Stephen Phinney from the University of California at Davis and Dr. Jeff Volek from the University of Connecticut--who conducted a side-by-side comparison of the amount of saturated fat in the blood of people on a low-carb diet with those following those highly-touted low-fat diets. What they found was the low-carb study participants had "significantly less" saturated fat in their blood than the low-fatties did.

Here are the actual numbers from the study:

- LOW-FAT/HIGH-CARB DIETERS: lowered saturated fat by 24%
- LOW-CARB/HIGH-FAT DIETERS: lowered saturated fat by 57%
- Eating 3X the saturated fat cut the amount in the blood in half

In an interview I conducted at my blog with Dr. Volek last year (here's the
link: http://livinlavidalocarb.blogspot.com/2006/09/volek-high-carb-low-fat-diet-useless-to.html),
he said the conventional wisdom regarding fat, especially saturate fat, is dead
wrong while the significance of carbs is all but ignored by those who claim to
understand the metabolic response mechanism.

Here's what Dr. Volek said in my interview:

"Eating fat does not make you fat, storing fat makes you fat. And carbohydrates play a major role in storing fat. So the level of dietary carbohydrate is really the most important factor to control because it dictates what happens to fat. Carbs are dominant and fat is passive. When carbohydrates are low, fat tends to be burned, and when carbohydrates are high dietary fat tends to be stored. The same holds true for the atherogenic effects of saturated fat. The body handles saturated fat better when carbohydrates are low."

Long-time low-carb practitioner and current President of the American Society of Bariatric Physicians (ASBP) Dr. Mary C. Vernon from Lawrence, Kansas confirms the findings of Dr. Volek and Dr. Phinney in a succinct recap of what their research showed.

Here's what she said:

"Eating fat (whatever kind) does not make you fat. It does not increase blood
stream saturated fat. Eating carbs does make you fat. Eating carbs does put
saturated fat in your blood stream."

To me, as a simple layperson with no medical background, it's all a matter of who you believe. Do we continue to buy into the low-fat propaganda machine and assume that what they are telling us about saturated fat is true? Or do we instead start paying closer attention to the latest research that is coming out about saturated fat that doesn't exactly line up with the edicts of the last three decades? The choice for me is a simple one.

And if you haven't read the brand new Gary Taubes book entitled GOOD CALORIES, BAD CALORIES yet, then it is REQUIRED reading to arm yourself with the research studies about fat. After you read that book, it will be almost impossible for ANYONE to believe fat, including saturated fat, is unhealthy.



TYP: In our program, we advocate a wheat-free approach for many people, because of the addictive potential of wheat products, as well as the flagrant creation of the small LDL pattern that wheat products create, thereby adding to atherosclerotic plaque growth. However, many people express a concern over a lack of fiber in their diets if they eliminate whole wheat bread, pasta, Fiber One, Raisin Bran cereal, etc.

Have you encountered any phenomena of low-fiber on your approach?

JM: What an excellent question and I even wrote a humorous blog post about the importance of fiber intake called "Allow Your Bowel To Shake, Rattle, And Roll" (http://livinlavidalocarb.blogspot.com/2006/06/allow-your-bowel-to-shake-rattle-and.html).

Fiber consumption is another one of those issues that not everyone who advocates
a controlled-carb approach agrees is necessary. I'm on the side that it IS a healthy part of your diet and should be consumed in high enough quantities to keep you regular...something many people think is impossible on a low-carb diet.
Not true! I take a fiber supplement like FiberCon, eat plenty of high-fiber vegetables, drink lots of water, and even consume high-fiber, low-carb products that help me maintain high levels of fiber in my diet (see my favorite ones in this post: http://livinlavidalocarb.blogspot.com/2007/04/there-are-plenty-of-low-carb-fiber.html).

As for consuming the highly-touted "healthy whole grain" cereals that you
mentioned, what a travesty that would be for people trying to manage their
weight and health. While the cereal manufacturers have had a heyday in their
marketing efforts promoting their whole grain content, it's all just a big fat
ruse on the public trying to convince them that these cereals are somehow healthy for their bodies. Sure, they're better than the sugary cereals, but all those grains are metabolized as sugar inside the body, so you might as well be eating Lucky Charms and Fruit Loops!

Many of these "healthy" cereals contain as many carbohydrates in a single bowl
without the milk as I would eat in an entire day. Raisin Bran, for example, which used to be my favorite cereal before my low-carb lifestye, has a whopping 47 grams of carbohydrates. Needless to say, I don't touch that with a ten-foot pole nowadays because I would surely gain weight and get back on the blood sugar rollercoaster ride that I was on prior to beginning the Atkins diet on January 1, 2004. Plus, all those carbs just make you hungrier sooner, so it's better just to eat some delicious eggs cooked in butter, a couple of slices of sausage, and tomato slices to start your day off right. You'll get enough fiber in your body the rest of your day.



TYP: 180 lbs of weight loss in your first year is absolutely astounding.

I take it that you've continued this trend and have lost more weight since your early success. What role did exercise play during your first year and subsequently?
How are your food choices today different from that first year?

JM: Yes, that weight loss was indeed one of the greatest accomplishments I have ever experienced in my life. It was a hard-fought battle that even included a 10-week period where I was stalled with no weight loss. But I knew my chosen diet was the right one for me because I felt better than I ever had on a diet, was never hungry because I ate every 2-3 hours, and could see myself doing this for the rest of my life. So far, so good!

It has been close to four years since I began this journey and I am indeed continuing this pathway to better health. My low weight in 2004 was 230 pounds and I currently weigh 225 pounds. As long as I keep my carbs reduced, I am able to maintain my weight right where it is. I've had minor fluctuations in both directions where I got down to as low as 215 pounds at one point (but didn't feel good at that weight) and as high as 252 pounds (when I was allowing myself one too many high-carb foods here and there).

There's a balance that people need to find for themselves and it's different for
all of us. I am one of the unlucky people who has to keep his carbohydrate
intake below 50g daily or I gain. It's just a fact of life that I've come to
grips with and realize is a necessity in order to manage my weight for the rest
of my life. But I wouldn't have it any other way!

Exercise was indeed a part of my low-carb weight loss success in 2004 as I
forced myself to do cardio every single day as a commitment to this journey. In
hindsight, that was probably not the best thing for me to do since the body has
a rather peculiar way of telling you it needs to wiggle and move spontaneously
on its own rather than forcing the issue. But I consider the exercise I did to
be such an integral part of my success that I dedicated an entire chapter of my
book to the subject.

Today, my daily cardio routine is out the window and I choose instead to engage
in activities outside the gym that let me burn calories and have some fun in the
process. I regularly play volleyball, basketball, and referee flag football at
my church which all give me quite a workout. I'm very physically active and fit
on my 6'3" body and just enjoy burning off all this excess energy that I have
been given since losing nearly have my weight! I do want to get into a little
more organized resistance training routine soon to try to shape and tone some
areas of my body that still show signs of that 410-pound man I used to be
(although the loose, hanging skin in my abdomen and inner thighs isn't going to
get any better with exercise since the elasticity has been ruined from being
stretched out so far). Here is a link to some posts and pictures I have written
about this subject:
http://lowcarblinks.blogspot.com/2007/04/theme-based-low-carb-links-loose-skin.html

As for my food choices today compared to my weight loss year in 2004, they
haven't really changed a whole lot. This was a lifestyle change in every sense
of the phrase and I've learned to implement this way of eating into a permanent
and healthy diet that I can and will gladly live with forever and ever amen. I
probably eat more berries, melons, and nuts today than I did then, but otherwise
it's the identical diet.



TYP: I'm sure that you are as impressed as I am that much of the wisdom in healthy eating doesn't always come from doctors or clinical studies, but from the collective wisdom that emerges from this national experiment (inadvertent, for the most part) in eating. Your Livin' La Vida Low-Carb is, in my view, a perfect example of the sort of wisdom that is helping all of us understand what happened to our health over the last 20 years.

Does the approach you advocate today differ in any substantial way from the diet as originally articulated by Dr. Atkins?

JM: Actually, my personal diet is precisely based on the teaching of the late great Dr. Robert C. Atkins in his classic bestseller DR. ATKINS' NEW DIET REVOLUTION (DANDR) book. But most people are surprised when they learn I do not necessarily advocate the Atkins diet as the nutritional approach for everyone.

Nope, I sure don't!

Instead, my philosophy is simple: Find the diet plan that will work for YOU, read and research everything you can about that chosen plan, follow that plan exactly as prescribed by the author of that book, and then KEEP doing that plan for the rest of your life. If you do that, then there's no reason why you can't succeed just like I did.

Anyone interested in doing the low-carb lifestyle and needs help finding which
plan is right for them, let me HIGHLY encourage you to pick up a copy of Dr. Jonny Bowden's LIVING THE LOW-CARB LIFE (read my review: http://livinlavidalocarb.blogspot.com/2005/05/must-have-book-for-everybody-doing-low.html).
It's the perfect overview of low-carb living with a comparison and recap of the
major plans.

THANK YOU again for allowing me to share my story with you and your readers, Dr.
Davis!

TYP: And thanks to you, Jimmy!



For more on Jimmy Moore's lively and informative discussion of these issues, go to

Livin' la Vida Lo Carb

Also, watch "Livin' La Vida Low-Carb on YouTube"

Join the conversation at Jimmy's new low-carb forum called "Livin' La Vida
Low-Carb Discussion
" at LowCarbDiscussion.com


Also, Jimmy's 2005 book on his weight loss experience:
"Livin' La Vida Low-Carb: My Journey From Flabby Fat To
Sensationally Skinny In One Year"

Mammogram of the heart

Some people have called CT heart scans the "mammogram of the heart." The analogy contains a lot of wisdom.

First of all, both--mammograms and CT heart scans--are screening tests, one for cancer, of course, the other for coronary atherosclerotic plaque. Both are performed in specific age groups, mammograms in women 40 years and over (generally), heart scans in women 50 years and over (generally).


















Mammograms: Left, normal; right, a small mass. (Courtesy Nat'l Institutes of Health and Wikipedia.)



Both are also meant to be repeated periodically when normal as a surveillance process.

Both use low quantities of radiation of about 0.3-0.4 mSv (the most real-life measure of total body exposure), a modest quantity of radiation.

Both are good for their purposes, though not perfect. Can a mammogram performed properly miss a small cancerous mass? Sure it can, but it's still unusual. Can a CT heart scan miss the non-calcified plaque prone to rupture? Sure it can, but this is also unlikely (<5% probability).

Given the exorbitant costs of medical tests, both are quite inexpensive. On the flip side, they are both also quite unprofitable for the centers providing the tests. Unfortunately, this means that mammography centers and heart scan centers come and go because of the difficulties of the profit-side of these services.

Both tests initially struggled to gain acceptance among the medical community. In 1960, for instance, mammograms were performed on standard x-ray devices, the same as that used to perform chest x-rays--low precision, high radiation back then. In 1969, dedicated mammography devices made the scene. However, it took over 10 years for even these new dedicated devices to become widely used. Use of mammograms has gradually increased over the ensuing 20 years. In other words, 47 years have passed since the introduction of mammography.

CT heart scans, of course, have had a shorter history of approximately 20 years, since engineer, Dr. Douglas Boyd, first invented the "ultra-fast" EBT devices, the first devices with sufficient scanning speed to scan the heart and coronary arteries.

One interesting difference between the two: In a woman between the age of 50 and 60, the likelihood of detecting cancer is 1 in 237. The likelihood of detecting coronary atherosclerotic plaque? About 1 in 4. Coronary disease eventually kills 1 in 3 females, hugely overshadowing breast cancer in frequency.


Progress on both fronts, one in cancer detection, the other in atherosclerotic coronary plaque detection. But still lots more progress to go.

Dr. Susie Rockway on conjugated linoleic acid (CLA)

I’m fascinated by the perspectives that nutritionists (free-thinking ones, at least), food scientists, and biochemists bring on nutrition and nutritional supplements.

A few months ago, I met a fascinating nutritionist/biochemist named Susie Rockway, PhD. Dr. Rockway brings a world of experience in the world of nutritional supplements, clinical trials with supplements, and their development. She has special expertise in conjugated linoleic acid (CLA), having been among the scientists who initially developed CLA as a supplement. We are also exploring CLA as a possible addition to the Track Your Plaque program and wanted to get Dr. Rockway’s perspectives.

So I asked Dr. Rockway if she’d answer a few questions for us.






TYP: Dr. Rockway, we understand that you are particularly excited about the prospects of CLA for FAT loss and perhaps for regression of atherosclerosis. Can you tell us about the origins of your interest in CLA and why you're so enthusiastic?

Dr. Rockway: I have been fascinated with this unique fatty acid since the early 1990’s when CLA was first being discussed as nature’s most potent anti-carcinogen. I was then working in the granting/funding section of the National Dairy Council and saw this molecule as truly one of the future functional fats that would likely benefit people (next to omega-3’s!)

I think the benefits of CLA have just begun to be investigated—animal studies are extraordinary for showing fat reduction, lean mass (muscle) increases, immune enhancements, blood glucose normalization, anti-inflammatory properties and plaque reduction!

Human data to date is very encouraging for fat reduction. As a nutritionist seeing the massive increase in abdominal fat (stomach fat) in the world population and the direct relationship to cardiovascular disease, I see CLA as a great supplement to take to help this. Of course eating lots of vegetables, fruit, lean protein and whole grain products is also a must for maximizing good health.

I am studying the impact of CLA in reducing muscle loss in aging women—a condition known as sarcopenia. As we lose muscle with age, we lose strength, falls increase, we become frailer, and eventually many of us lose our independence. Along with the muscle atrophy, most people gain fat—never a good thing! So, if CLA can reduce fat and increase muscle, our bodies are more likely to withstand the hurdles that life throws at us much more efficiently.

So, how can you not be excited about this very bioactive molecule?




TYP: What are your specific areas of interest in nutrition and health?

Dr. Rockway: I strive to understand the role of bioactive molecules that can be taken to improve the aging process and enhance health.

As a trained nutritional biochemist, we tend to look at cell metabolism in a very ideal sense: what we learned in our biochemistry texts years ago where all substrates, proteins, enzymes, etc. are made exactly when we need them, where all cells behave as they should.

Unfortunately, little research has been devoted to understanding the changes in metabolism as we age. Do we still produce everything as efficiently as when we were 20? I suspect not. So, I think we need a little help, and supplements are a key to getting there.

Two nutrients that I think are emerging as “super nutrients” are the fatty acids found in fish oil (EPA and DHA) and vitamin D. Where we know these two nutrients are essential for life, we are seeing that they play a huge role in the QUALITY of life. Mood, depression, PMS, wound healing, bone growth, atherosclerosis, and arthritis are clinical areas where we see a direct benefit with doses of omega-3 and Vitamin D that are probably much greater than the RDA. Our current requirements for nutrients are really based on fixing deficiencies and not maximizing health, and maximizing health is where I’m at.

Thus, I am very interested molecules like CLA as mentioned above, and other bioactive ingredients such as plant derived ingredients (phytochemicals) called flavonoids that may well help explain why people who have diets high in fruits and vegetables are less likely to have certain cancers and heart disease. Reducing oxidative stress through foods that provide these active molecules (think colored fruits and veggies) is a new and exciting area of research.



TYP:The big "diet experiment" in America has clearly steered people in the wrong direction, usually by 50 or more pounds. As a scientist in nutrition, what are your thoughts?

Dr. Rockway: The American Heart Association was keen 20 years ago to promote the low-fat diet for all Americans as the key way to reduce cholesterol levels and decrease chance of heart disease, the number one killer of men and women. However, I must admit the nutritional community bought into this one, too. Unfortunately, the general public took this message to reduce percent fat in their diet (and they did a bit), but increased overall calories instead—and a large portion of the increased calories was from simple carbohydrates. I’m convinced that this in itself has been part of the huge rise in obesity…we simply eat more food and it’s not the healthy kind of food either.

When you increase sugar intake beyond what you burn off, you will store some of it as glycogen in the liver and muscles, but you will convert most of the excess into fat—and that we can store very efficiently! The fat that is made in the liver is sent to the blood as VLDL’s which are the precursor to the class of lipids called low density lipoproteins (LDL) that are the “lethal” type of cholesterol circulating in our blood.

So, Americans now have to listen to a new message that they need to eat more fruits and vegetables in hopes they will cut down on fast foods—tending to be high in fat (saturated particularly), low in fiber and low in nutrients and other high calorie dense foods. We nutritionists have our work cut out for us, that’s for sure.



TYP: We are especially excited that nutritionists are assuming a leading role in shining light on the confusion in diet and nutrition that has characterized the last 40 years. Do you have a sense for the emerging important issues for the next 10 years?

Dr. Rockway: Certainly, the scientists in the nutritional field are well aware of the problems facing this nation—it’s in fixing them that we fall short!

We aren’t very well coordinated to get a single message out, nor do we all agree on what that message should be. I feel that people need to eat healthy MOST OF THE TIME, exercise all of the time, and take supplements that have clear evidence of benefit. Lots of my colleagues would not concur with supplement use. Our bodies were designed to move a lot and eat a lot…we just do the latter now and are paying the price!

One emerging and very exciting area that we have to teach Americans is that all fat is not bad. The different types of fat—omega-6 vs. omega-3, are where we need to focus our education.

Decreasing the corn oil we pour on everything needs to go out the window! Consume olive oil and eat fish or take fish oil supplements—we simply have tons and tons of research showing the benefits of reducing the ratio of omega-6 to omega-3. Did you know that cattle that are grass fed actually have less omega-6 in their tissues and more CLA? But most cattle are fed corn-based diets, so we have perturbed their natural selection of food and their fat composition.

See, it all comes back to CLA!


TYP: Thanks, Susie!




Susie Rockway, Ph.D., C.N.S.

Dr. Susie Rockway is an experienced scientist with accomplishments in both the academic and food and supplement industry business directing science/technology research. Her background includes faculty appointments at the graduate level in teaching and research at Rush University Medical Center and industrial experience managing basic and applied research studies.

Dr. Rockway received her Ph.D. in Nutritional Sciences, Biochemistry from the University of Arizona. Dr. Rockway has authored several publications in journals such as the Physiological Genomics, Journal of Nutrition, the Journal of Food Science, International Archives of Occupational and Environmental Health and has published chapters on nutrition on inflammatory bowel diseases. She is a member of the American Society for Nutrition, American Oil Chemists Society, the Institute of Food Technology, American College of Nutrition and is a Certified Nutrition Specialist.

We're also proud to add Dr. Rockway to our panel of Track Your Plaque Experts.

Which is better?

If you have the common pattern of high LDL particle number (NMR) with small LDL--a pattern highly related to coronary plaque--which is better:




Lipitor or a combination of fish oil, vitamin D, and elimination of wheat?


Lipitor quite effectively reduces LDL particle number, usually on the order of 40% or so. Effect on LDL particle size: None. Side-effects: plenty, including muscle aches (inevitable in my experience, not the ridiculous 2% they claim) and occasionally mental effects such as impaired short-term memory.

Lipitor does seem to exert a modest effect on reduction of C-reactive protein, around 30%. It also reduces cardiovascular events by 30%.



A combination of fish oil, vitamin D, and elimination of wheat:

Reduces LDL particle number commonly by a similar 40% (though variable, depending on body weight). There is substantial improvement in LDL particle size, a large drop in C-reactive protein, often >50%, a 30% or more reduction in cardiovacular events.



On this combination, however, you also:

--Lose weight, often substantially.

--Improve bone health, esp. osteoporosis and arthritis.

--Reduce cancer risk from the vit D supplementation.

--Reduce risk of stroke.

--Reduce postprandial (after-eating) abnormalities like intermediate-density lipoprotein.

--Reduce winter blues.

--Experience more energy.

--Obtain increased clarity of thought (from elimination of wheat).

--Reduce blood pressure.


Oh, and there's no muscle aches.