Thumb your nose at swine flu 29. April 2009 William Davis (35) Judging from what we know about vitamin D, it is highly probable that it confers substantial protection from viral infections, including swine flu. Dr. John Cannell of the Vitamin D Council (www.vitamindcouncil.com) first connected the dots, identifying the possibility of an influence of vitamin D on incidence of flu.In 2006, Dr. Cannell reports noticing that the patients in his psychiatric ward in northern California were completely spared from the influenza epidemic of that year, while plenty of patients in adjacent wards were coming down with flu. Dr. Cannell proposed that the apparent immunity to flu in his patients may have been due to the modest dose of 2000 units vitamin D per day he had prescribed that the patients in other wards had not been given. (Since the hospital was run by the state of California, Dr. Cannell apparently had only so much leeway with vitamin D dosing.) While it’s not proof, it’s nonetheless a fascinating and compelling observation. A similar conclusion was reached in a recent analysis of the National Health and Nutrition Examination Survey demonstrating that the higher the vitamin D blood level, the less likely respiratory infections were. Personally, I used to suffer through 2 or 3 episodes of a runny nose, sore throat, hacking cough, fevers and feeling crumby every winter. Over the last 3 years since I’ve supplemented vitamin D, I haven’t been sick even once. The past two years I didn’t bother with the flu vaccine, since I suspected that my immunity had been heightened: no flu either winter. And so it has been with the majority of my patients. Since I began having patients supplement vitamin D to achieve normal blood levels (we aim for 60-70 ng/ml), viral and bacterial infections have become rare. New research is uncovering myriad new ways that vitamin D enhances natural immune responses to numerous infections, including tuberculosis, bacteria such as those causing periodontal disease and lung infections, and viruses like the influenza virus. Enhanced immunity against cancer is also an intensive area of research on vitamin D. Will vitamin D supplementation sufficient to achieve desirable blood levels confer sufficient immunity to swine flu should it come to your door? From what we know and what we’ve seen in the few years of vitamin D experience, I think it will in the majority. But I do believe that we should still heed public health warnings to avoid contact with others, minimize exposure to crowds, avoid travel to affected areas, etc.
Will the real LDL please stand up? 26. April 2009 William Davis (13) The results of the latest Heart Scan Blog poll are in.The question: How has your LDL been measured? The 187 responses broke down as:I have only had a conventional calculated value 108 (57%)NMR LDL particle number 35 (18%)Apoprotein B 21 (11%)Direct LDL cholesterol 21 (11%)Non-HDL cholesterol 8 (4%)I don't know what you're talking about 23 (12%)Remember the TV game show, To Tell the Truth? Celebrities would have to guess which of three guests represented the real person, such as the notorious con man, Frank Abagnale, Jr., or Mad Magazine publisher, William M. Gaines (who stumped celebrity Kitty Carlisle, heard to exclaim, "I never figured it was him. I mean look at the way he's dressed. I was looking for someone who ran a very successful magazine, so I thought it couldn't be him!")The celebrities playing the game were permitted to ask the three guests a series of questions, hoping to discern who was the real person vs. the two impostors. At the end, each celebrity had to guess who was truly the person of interest. "Will the real Frank Abagnale, Jr. please stand up!" If we were to act as the celebrities in our LDL game, we quickly discover some telling facts:--Conventional LDL cholesterol (the only value 57% of our poll respondents have had) is calculated, not measured. LDL is calculated using the 40-year old Friedewald calculation. --Directly measured LDL cholesterol (the value 11% of respondents had) is just that: directly measured. It eliminates some of the uncertainties of calculated LDL. --Apoprotein B-Every LDL and VLDL particle produced by the liver contains one apoprotein B molecule. ApoB therefore provides a crude particle count measure of LDL and VLDL particles. Of course, it includes VLDL and is not completely the same as just an LDL measure. Some lipid authorities Like Dr. Peter Kwiterovich have advocated that apoB replace calculated LDL, and that calculated LDL essentially be discarded.--Non-HDL cholesterol--I mention this more for completeness. Hardly anybody uses this crude value in practice--Indeed, only 4% of our poll respondents had this measure/calculation. Non-HDL is simply total cholesterol minus HDL cholesterol = Non-HDL cholesterol. It is thus a combination of cholesterol in LDL and VLDL (triglycerides), similar to apoprotein B. While, like apoB, it is a bit different in that it includes VLDL, it has proven a superior measure of risk.--LDL particle number--In my view, this is the gold standard for LDL and risk measurement, obtained by only 18% of our poll respondents. LDL particle number is proving superior for discriminating who is truly at risk for a cardiovascular event, particularly when metabolic syndrome or diabetes is part of the picture, i.e., when HDL and triglycerides are considerably distorted, leading to substantial corruption of calculated LDL. While 18% is a minority, it still represents growth in recognition that conventional calculated LDL cholesterol is an unreliable, inaccurate, and outdated value. If the real LDL were to stand up, I believe that it is LDL particle number that would spring to its feet.
Vitamin D and inflammation 25. April 2009 William Davis (9) We already know that vitamin D reduces inflammatory processes, since several markers, including c-reactive protein and IL-6 have previously been shown to drop substantially with vitamin D. Inflammation underlies coronary atherosclerotic plaque growth, as well as plaque rupture that triggers heart attack. A German group has now shown that the important inflammatory marker, tumor necrosis factor (TNF), is also reduced by vitamin D supplementation. Many studies have implicated increased TNF levels in promoting cancer.In this study, a modest vitamin D dose of 3320 units (83 micrograms) was given vs. placebo. The 25-hydroxy D level reached in the treated group was 34.2 ng/ml (85.5 nmol/L), which resulted in a 26.5% reduction in TNF compared with 18.7% reduction (?) in the placebo group.Vitamin D supplementation enhances the beneficial effects of weight loss on cardiovascular disease risk markers.Zitterman A, Frisch S et al.BACKGROUND: High blood concentrations of parathyroid hormone and low concentrations of the vitamin D metabolites 25-hydroxyvitamin D [25(OH)D] and calcitriol are considered new cardiovascular disease risk markers. However, there is also evidence that calcitriol increases lipogenesis and decreases lipolysis. OBJECTIVE: We investigated the effect of vitamin D on weight loss and traditional and nontraditional cardiovascular disease risk markers in overweight subjects. DESIGN: Healthy overweight subjects (n = 200) with mean 25(OH)D concentrations of 30 nmol/L (12 ng/mL) received vitamin D (83 microg/d) or placebo in a double-blind manner for 12 mo while participating in a weight-reduction program. RESULTS: Weight loss was not affected significantly by vitamin D supplementation (-5.7 +/- 5.8 kg) or placebo (-6.4 +/- 5.6 kg). However, mean 25(OH)D and calcitriol concentrations increased by 55.5 nmol/L and 40.0 pmol/L, respectively, in the vitamin D group but by only 11.8 nmol/L and 9.3 pmol/L, respectively, in the placebo group. (Calcitriol = 1,25-dihydroxy vitamin D.)Knowing your vitamin D blood level is crucial, as individual need for vitamin D varies widely from one person to the next. You can get your vitamin D tested at home by going to Grassroots Health or the Track Your Plaque Marketplace.
Even monkeys do it 24. April 2009 William Davis (6) It all started back in the 1960s, when ape-watching anthropologists, Drs. Jane Goodall and Richard Wrangham, observed chimps foraging for a specific variety of leaf, which they consumed whole while wrinkling their noses in presumed disgust. Subsequent study showed that the leaves contained a powerful anti-parasitic compound. A similar observation followed in 1987 by Dr. Michael Huffman from the University of Kyoto. During his year of living in the jungles of Tanzania, he observed chimpanzees in their native habitat. On one unexpected morning, he observed a female chimp, Chausiku: “Chausiku goes directly to and sits down in front of a shrub and pulls down several new growth branches about the diameter of my little finger. She places them all on her lap and removes the bark and leaves of the first branch to expose the succulent inner pith. She then bites off small portions and chews on each for several seconds at a time. By doing this, she makes a conspicuous sucking sound as she extracts and swallows the juice, spitting out most of the remaining fiber. This continues for 17 minutes, with short breaks as she consumes the pith of each branch in the same manner.” Dr. Michael Huffman’s description of Chausiku documents a fascinating example of animal self-medication what some call "zoopharmacognosy."In this instance, the chimpanzee, weak, clutching her back in pain, and listless, was ingesting the leaves of the plant, Vernonia amygdalina, to purge an intestinal parasite. She recovered by the next morning. Vernonia leaves have since been found to contain over a dozen potential anti-parasitic compounds. Chimps in this region commonly suffer infestations of parasites like Strongyloides fuelleborni (thread worm), Trichuris trichiura (whip worm), and Oesophagostomum stephanostomum (nodular worm). They have somehow stumbled onto a treatment that they administer themselves. Chimpanzees have inhabited earth for over 6 million years. Who knows how long they and other primates have practiced some form of self-medication. If chimpanzees can do it, I believe that we, as human primates, can also practice a similar form of self-directed health--homopharmacognosy?Image courtesy Wikipedia
Cath lab energy costs 22. April 2009 William Davis (6) In honor of Earth Day, I thought I'd highlight the unexpectedly high carbon costs of activities in hospitals, specifically the cardiac catheterization laboratory. A patient enters the cath lab. The groin is shaved using a plastic disposable razor, the site cleaned with a plastic sponge, then the site draped with an 8 ft by 5 ft composite paper and plastic material (to replace the old-fashioned, reusable cloth drapes). A multitude of plastic supplies are loaded onto the utility table, including plastic sheaths to insert into the femoral artery (which comes equipped with a plastic inner cannula and plastic stopcock), a multi-stopcock manifold that allows selective entry or removal of fluids through the sheath, a plastic syringe to inject x-ray dye, plastic tubing to connect all the devices (total of about 5 feet), and multiple plastic catheters (3 for a standard diagnostic catheterization, more if unusual arterial anatomy is encountered).All these various pieces come packed in elaborate plastic (polyethylene terephthalate or other polymers) containers, which also come encased in cardboard packaging. Should angioplasty, stenting, or similar procedure be undertaken, then more catheters are required, such as the plastic "guide" catheters that contain a larger internal lumen to allow passage of angioplasty equipment. An additional quantity of tubing is added to the manifold and stopcock apparatus, as well as a plastic Tuohy-Borst valve to permit rapid entry and exit of various devices into the sheath. Several new packages of cardboard and plastic are opened which contain the angioplasty balloon, packaging which is usually about 4 feet in length. The stent likewise comes packaged in an 18-inch or so long package with its own elaborate cardboard and plastic housing. At the conclusion of the procedure, another cardboard/plastic package is opened, this one containing the closure device consisting of several pieces of plastic tubes and tabs. If the procedure is complicated, the number of catheters and devices used can quickly multiply several-fold. By the conclusion of the procedure, there are usually two large, industrial-sized trash bins packed full of cardboard, plastic packaging, and discarded tubing and catheters. The trash is so plentiful that it is emptied following each and every procedure. None of it is recycled, given the contamination with human body fluphicon glyphicon-user">William Davis (47)
Coronary calcium: Cause or effect? 28. November 2010 William Davis (25) 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, 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 26. November 2010 William Davis (22) 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 24. November 2010 William Davis (14) 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? 19. November 2010 William Davis (20) 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? 13. November 2010 William Davis (48) 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? 10. November 2010 William Davis (24) 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 9. November 2010 William Davis (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 9.3So 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 4. November 2010 William Davis (12) 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 9.3Why would there be so much variation from year to year, and why would the plaque move from site to site?SteveQuestions 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.