Heart Scan Blog Redux: Cheers to flavonoids 13. November 2009 William Davis (32) Because in Track Your Plaque we've been thinking a lot about anthocyanins, here's a rerun of a previous Heart Scan Blog post about red wine. (Anthocyanins are among the interesting flavonoids in red wine, along with resveratrol and quercetin.) The case in favor of healthful flavonoids seems to grow bit by bit. Flavonoids such as procyanadins in wine and chocolate, catechins in tea, and those in walnuts, pomegranates, and pycnogenol (pine bark extract) are suspected to block oxidation of LDL (preventing its entry into plaque), normalize abnormal endothelial constriction, and yield platelet-blocking effects (preventing blood clots). Dr. Roger Corder is a prolific author of many scientific papers detailing his research into the flavonoids of foods, but wine in particular. He summarizes his findings in a recent book, The Red Wine Diet. Contrary to the obvious vying-for-prime-time title, Dr. Corder's compilation is probably the best mainstream discussion of flavonoids in foods and wines that I've come across. Although it would have been more entertaining if peppered with more wit and humans interest, given the topic, its straightfoward, semi-academic telling of the story makes his points effectively. Among the important observations Corder makes is that regions of the world with the greatest longevity also correspond to regions with the highest procyanidin flavonoids in their wines. Regarding the variable flavonoid content of wines, he states:Although differences in the amount of procyanidins in red wine clearly occur because of the grape variety and the vineyard environment, the winemaker holds the key to what ends up in the bottle. The most important aspect of the winemaking process for ensuring high procyanidins in red wines is the contact time between the liquid and the grape seeds during fermentation when the alcohol concentration reaches about 6 percent. Depending on the fermentation temperature, it may be two to three days or more before this extraction process starts. Grape skins float and seeds sink, so the number of times they are pushed down and stirred into the fermenting wine also increases extraction of procyanidins. Even so, extraction is a slow process and, after fermentation is complete, many red wines are left to macerate with their seeds and skins for days or even weeks in order to extract all the color, flavor, and tannins. Wines that have a contact time of less than seven days will have a relatively low level of procyanidins. Wines with a contact time of ten to fourteen days have decent levels, and those with contact times of three weeks or more have the highest. He points out that deeply-colored reds are more likely to be richer in procyanidins; mass-produced wines that are usually "house-grade" served at bars and restaurants tend to be low. Some are close to zero. Wines rich in procyanidins provide several-fold more, such that a single glass can provide the same purported health benefit as several glasses of a procyanidin-poor wine. So how do various wines stack up in procyanidin content? Here's an abbreviated list from his book:Australian--tend to be low, except for Australian Cabernet Sauvignon which is moderate. Chile--only Cabernet Sauvignon stands out, then only moderate in content.France--Where to start? The French, of course, are the perennial masters of wine, and prolonged contact with skins and seeds is usually taken for granted in many varieties of wine. Each wine region (French wines are generally designated by region, not by variety of grape) can also vary widely in flavonoid content. Nonetheless, Bordeaux rate moderately; Burgundy low to moderate (except the village of Pommard); Languedoc-Roussillon moderate to high (and many great bargains in my experience, since these producers live in the shadow of its northern Bordeaux neighbors); Rhone (Cote du Rhone) moderate to high, though beware of their powerful "barnyard" character upon opening; decanting is wise. Italy--Much red Italian wine is made from the Sangiovese grape and called variously Chianti, Valpolicella, and "super-Tuscan" when blended with other varietals. Corder rates the southern Italian wines from Sicily, Sardinia, and the mainland as high in procyanidins; most northern varieties are moderate. Spain--Moderate in general. United States--Though his comments are disappointingly scanty on the U.S., he points out that Cabernet Sauvignon is the standout for procyanidin content. He mentions only the Napa/Sonoma regions, unfortunately. (I'd like to know how the San Diego-Temecula and Virginian wines fare, for instance.)The winner in procyanidin content is a variety grown in the Gers region of southwest France, a region with superior longevity of its residents. The wines here are made with the tannat grape within the Madiran appellation; wines labeled "Madiran" must contain 40% or more tannat to be so labeled (such is a quirk of French wine regulation). Among the producers Dr. Corder lists are Chateau de Sabazan, Chateau Saint-Go, Chateau du Bascou, Domaine Labranche Laffont, and Chateau d'Aydie. (A more complete list can be found in his book.)How does this all figure into the Track Your Plaque program? Can you succeed without red wine? Of course you can. I doubt you could do it, however, without some attention to flavonoid-rich food sources, whether they come from spinach, tea, chocolate, beets, pomegranates, or red wine. Though my wife and I love wine, I confess that I've never personally drank or even seen a French Madiran wine. Any wine afficionados with some advice?
Can wheat elimination cure ulcerative colitis? 13. November 2009 William Davis (0) Tammy is a 36-year old mother of three young children. Since age 20, she has suffered with the debilitating symptoms of ulcerative colitis: constant, gnawing abdominal pain; frequent diarrhea, often bloody. Tammy has had to take several medications, some with significant side-effects, all of which provided only partial relief from the pain and diarrhea. Her gastroenterologist and surgeon were planning a colectomy (removal of the colon) with creation of an ileostomy (rerouting of the small intestine to the abdominal surface, which would require Tammy to wear an ileostomy bag under her clothes for the rest of her life).Although Tammy had previously tested negative for celiac disease (an allergic sensitivity to the gluten in wheat products), I urged her to attempt a trial of a wheat-free diet. Having witnessed many people experience relief from irritable bowel syndrome, acid reflux, and other common gastrointestinal complaints, all while trying to reduce blood sugar and small LDL, I'd hoped that Tammy would obtain at least some small improvement in her terrible symptoms. I therefore urged Tammy to try it. After all, what was there to lose? Tammy grudgingly agreed. She returned 6 months later. Her report: She had lost 38 lbs, virtually all of it within the first 6-8 weeks. Her diarrhea and cramping were not better, but gone. She was down to a single medicine from her former list of drugs. I am unsure what proportion of people with ulcerative colitis or other inflammatory bowel diseases like Crohn's will experience a result like Tammy's. Perhaps it's only a minority. But I take this another piece of evidence that this enormously destructive thing called wheat has no place in the human diet. We have no facts or figures on the prevalence of various forms of wheat intolerance in the U.S. When I contacted the Celiac Disease Foundation, they had no figures on the number of fatalities per year in the U.S. from celiac disease. But if there are 2-3 million Americans with celiac disease, there are probably 100 times that many people with various forms of wheat intolerance.
Postprandial pile-up with fructose 12. November 2009 William Davis (20) Heart disease is likely caused in the after-eating, postprandial period. That's why the practice of grazing, eating many small meals throughout the day, can potentially increase heart disease risk. Eating often can lead to the phenomenon I call triglyceride and chylomicron "stacking," or the piling up of postprandial breakdown products in the blood stream.Different fatty acid fractions generate different postprandial patterns. But so do different sugars. Fructose, in particular, is an especially potent agent that magnifies the postprandial patterns. (See Goodbye, fructose.)Take a look at the graphs from the exhaustive University of California study by Stanhope et al, 2009:From Stanhope KL et al, J Clin Invest 2009. Click on image to make larger.The left graphs show the triglyceride effects of adding glucose-sweetened drinks (not sucrose) to the study participants' diets. The right graphs show the triglyceride effects of adding fructose-sweetened drinks. Note that fructose causes enormous "stacking" of triglycerides, meaning that postprandial chylomicrons and VLDL particles are accumulating. (This study also showed a 4-fold greater increase in abdominal fat and 45% increase in small LDL particles with fructose.)It means that low-fat salad dressings, sodas, ketchup, spaghetti sauce, and all the other foods made with high-fructose corn syrup not only make you fat, but also magnifies the severity of postprandial lipoprotein stacking, a phenomenon that leads to more atherosclerotic plaque.
Track Your Plaque: Safer at any score 11. November 2009 William Davis (0) Imagine two people.Tom is a 50-year old man. Tom's initial heart scan score was 500--a concerning score that carries a 5% risk for heart attack per year.Harry is also 50 years old. His heart scan score is 100--also a concerning score, but not to the same degree as Tom's much higher score. Tom follows the Track Your Plaque program. He achieves the 60:60:60 lipid targets; chooses healthy foods, including elimination of wheat; takes fish oil at a therapeutic dose; increase his blood vitamin D level to 60-70 ng/ml, etc. One year later, Tom's heart scan score is 400, representing a 20% reduction from his starting score.Harry, on the other hand, doesn't understand the implications of his score. Neither does his doctor. He's casually provided a prescription for a cholesterol drug by his doctor, a brief admonition to follow a low-fat diet, and little else. One year later, Harry's heart scan score is 200, a doubling (100% increase) of the original score. At this point, we're left with Tom having a score of 400, Harry with a score of 200. That is, Tom has twice Harry's score, 200 points higher. Who's better off?Tom with the score of 400 is better off. Even though he has a significantly higher score, Tom's plaque is regressing. Tom's plaque is therefore quiescent with active components being extracted, inflammation subsiding, the artery in a more relaxed state, etc. Harry's plaque, in contrast, is active and growing: inflammatory cells are abundant and producing enzymes that degrade supportive tissue, constrictive factors are released that cause the artery to pinch partially closed, fatty materials accumulate and trigger a cascade of abnormal responses.So it's not just the score--the quantity of atherosclerotic plaque present--but the state of activity of the plaque: Is it growing, is it being reduced? Is there escalating or subsiding inflammation? Is plaque filled with degradative enzymes or quiescent? Following the Track Your Plaque program therefore leads us to the notion that it's not the score that's most important; the most important thing is what you're doing about it. We sometimes say that Track Your Plaque makes you safer at any score.
Triglyceride and chylomicron "stacking" 10. November 2009 William Davis (24) Continuing the comments started in Grazing is for cattle, here's an interesting study from the Oxford Center for Diabetes, Endocrinology and Metabolism.Volunteers were fed a test meal breakfast of Rice Krispies, a banana, and a chocolate milkshake (76.4 grams carbohydrates, 51.9 grams fat, 12.2 grams protein). Lunch was served 5 hours later and consisted of a cheese sandwich and a second chocolate milkshake 43.4 grams carbohydrates, 49.6 grams fat, 24.0 grams protein). Frequent blood samples were then assessed over the day. (Don't try this at home: These are obviously very dangerous foods!)Here's the pattern of triglycerides that was observed (1st dotted vertical line = breakfast, 2nd dotted vertical line = lunch):Note that triglycerides only begin to decline 3-4 hours after breakfast, only to peak higher after lunch.Here's the pattern observed for chylomicrons, the "granddaddy" of lipoproteins that derives from intestinal absorption of fatty acids:Both graphs from Heath RB et al Am J Phyiol Endocrinol Metab 2006.With chylomicrons, note a similar pattern to triglycerides: Chylomicrons begin to decline at 3-4 hours, only to peak higher after lunch. This is the first study to examine the effect of sequential meals on such postprandial (after-eating) patterns. But it makes the graphic point that, if insufficient time is permitted between meals, both triglycerides and chylomicrons will "stack" themselves higher and higher. (Chylomicrons are subjected to processing by the enzyme, lipoprotein lipase, to form highly atherogenic, or plaque-causing, chylomicron remnants.)While not examined in this study, my bet is that "grazing," i.e., eating small meals or snacks frequently, is an extreme instance of triglyceride, chylomicron, and chylomicron remnant stacking. That can only lead to one thing: accelerated heart and vascular plaque.
What is a healthy vitamin D blood level? 9. November 2009 William Davis (32) When measuring blood levels of vitamin D (as 25-hydroxy vitamin D), what constitutes a desirable level? There's no study that directly examines this question, no study that enrolled thousands of people and assigned a placebo group and groups receiving escalating doses of vitamin D and/or achieved higher levels of vitamin D, then observed for development of cancer, diabetes, depression, heart disease, multiple sclerosis, osteoporosis, osteoarthritis, etc. Such a study would requires many thousands of participants (particularly to observe cancer and multiple sclerosis incidence), many years of observation, and many tens of millions of dollars. Nope, only a drug company could afford such costs. So we have to piece together various observations and extrapolate what we believe to be the ideal level of vitamin D. Epidemiologic observations in several cancers (breast, colon, prostate, and bladder) suggest that a 25-hydroxy vitamin D level of 30 ng/ml or higher is desirable (with less cancer incidence above this level). Other data suggest a level of 52 ng/ml or greater is desirable. Unfortunately, much cancer research looked at intake of vitamin D from food and supplement sources, rather than actual blood levels. We also have to factor in the great individual variation in vitamin D metabolism, with a single dose yielding variable blood levels (as much as a 10-fold difference). There's also the variation introduced by vitamin D-receptor variation (genetic polymorphisms). A new study using vitamin D administration helps chart the desirable levels of vitamin D. Vitamin D supplementation reduces insulin resistance in South Asian women living in New Zealand who are insulin resistant and vitamin D deficient - a randomised, placebo-controlled trial.In this New Zealand study, 42 women (23 to 68 years old) were given 4000 units vitamin D, 39 women given placebo. Median 25-hydroxy vitamin D levels increased from 21 nmol/L (8.4 ng/ml) to 75 nmol/L (30 ng/ml). Both HOMA (a measure of insulin sensitivity) and fasting insulin levels improved, with greatest improvement seen at 25-hydroxy vitamin D levels of 80-119 nmol/L (32-47.6 ng/ml) or greater. We also know that a vacation on a Caribbean beach in a bathing suit will increase vitamin D blood levels to the 80-110 ng/ml range without ill-effect (at least in young people who maintain the capacity to activate vitamin D in the skin, a phenomenon that declines as we age). So do we really know the truly ideal level of vitamin D to achieve? I believe that, given the above observations, it is reasonable to extrapolate that the ideal vitamin D blood level likely lies somewhere above 50 ng/ml. We also know that vitamin D toxicity (i.e., hypercalcemia) is virtually unheard of until vitamin D blood levels approach 150 ng/ml, and even then is inconsistent. The health benefits of vitamin D supplementation are so tremendous, that I am not willing to wait for the prospective data to explore this question fully. For now, I aim for a blood level of vitamin D of 60-70 ng/ml (150-175 nmol/L).
Grazing is for cattle 5. November 2009 William Davis (17) Many dietitians and nutritionists advise many people today to "graze," i.e., to eat small snacks every couple of hours. They argue that it blocks the drop in insulin and blood sugar that can trigger greater appetite and claim it can facilitate weight loss. This is an absurd notion. Humans are not meant to graze. Humans are meant to find a wild boar or other animal, kill it, gorge on the meat, organs, and fat, then revert to berries, roots, leaves, and other foraged foods until the next kill. A human living in the wild does not have a cupboard or refrigerator full of ready-to-eat snacks to graze on. The several hours after a meal is the most dangerous for creating coronary atherosclerotic plaque, i.e., the post-prandial period. In other words, eat dinner and, for the next 6-12 hours, your intestinal tract degrades the food; food byproducts are absorbed into the blood or lymph system. The blood is literally flooded with the byproducts of your meal. Postprandial abnormalities are emerging to be a potent, and much underappreciated, means of causing heart disease and atherosclerosis in other vascular territories (especially carotid arteries and thoracic aorta). Not eating--i.e., the fasting state--for extended periods is good for you. Encouraging people to graze amplifies atherosclerotic risk, since it creates an abnormal prolonged postprandial state.
The disastrous results of a low-fat diet 4. November 2009 William Davis (16) Rob was never that committed to following the program in the first place. I met Rob because of a modest heart scan score and consultation for a cholesterol abnormality. Rob had been cycled through all the statin agents by his primary care physician, all of which resulted in terrible muscle aches that he found intolerable. I started out, as usual, characterizing his cholesterol abnormality with lipoprotein testing (NMR):LDL particle number 1489 nmol/L LDL cholesterol (Friedewald calculation) 143 mg/dlSmall LDL 52% of total LDLHDL 50 mg/dlTriglycerides 82 mg/dl(LDL particle number is the emerging gold standard for LDL quantification, superior to calculated or Friedewald LDL cholesterol for prediction of cardiovascular events.)Rob is a busy guy. After only a couple of brief visits, life and work got in the way and Rob let his attentions drift away from heart health. Since the information I provided made little impact on his thinking, he reverted to the low-fat diet his primary care doctor had originally prescribed and that he read about in magazines and food packages. He also ran out of the basic supplements I had advised, including fish oil and vitamin D, and just never restarted them. A couple of years passed and Rob decided that just poking around on his own might not cut it. So he came back to the office. We repeated his NMR lipoprotein analysis: LDL particle number 2699 nmol/L LDL cholesterol (Friedewald calculation) 229 mg/dlSmall LDL 81% of total LDLHDL 53 mg/dlTriglycerides 78 mg/dlTwo years of a low-fat diet had caused Rob's LDL particle number to skyrocket by 81%, nearly all due to an explosion of small LDL. Recall that small LDL is more susceptible to oxidation, more inflammation-provoking, more adhesive--the form of LDL particles most likely to cause heart disease. Also, note that, despite the enormous increase in small LDL, HDL and triglycerides remained favorable. This counters the popular rule-of-thumb offered by some that small LDL is not present when HDL is "normal." Low-fat diets as commonly practiced are enormously destructive. In Rob's case, a low-fat diet caused both calculated Friedewald LDL as well as LDL particle number to increase dramatically. In many other people, low-fat diets increase calculated Friedewald LDL modestly or not at all, but cause the more accurate LDL particle number to increase significantly, all due to small LDL. I'm happy to say that, once Rob witnessed how far wrong he could go on the wrong program, he's back on Track. (Sorry, pun intended.) He has resumed his supplements and eliminated the food triggers of small LDL--wheat, cornstarch, and sugars.
Dr. David Grimes reminds us of vitamin D 3. November 2009 William Davis (13) In response to the Heart Scan Blog post, Fish oil makes you happy: Psychological distress and omega-3 index, Dr. David Grimes offered the following argument. Dr. Grimes is a physician in northwest England at the Blackburn Royal Infirmary, Lancashire. He is author of the wonderfully cheeky 2006 Lancet editorial, Are statins analogues of vitamin D?, questioning whether the benefits of statin drugs simply work by way of increased vitamin D blood levels. There is a fashionable interest in Omega-3 fatty acids, and these become equated with fish oil.But fish oil is much more. Plankton synthesise the related squalene (shark oil) which, in turn, is converted into 7-dehydrocholesterol (7-DHC). The sun now comes into play and it converts 7-DHC into vitamin D (a physico-chemical process).Small fish eat plankton, large fish eat small fish, and we eat large fish. So vitamin D passes through the food chain. This has been a vital source of vitamin D for the the Inuits and also for the Scots and other dwellers of northwest Europe. (Edinburgh is on the same latitude as Hudson Bay and Alaska, further north than anywhere in China). In these locations there is not adequate sunlight energy to guarantee synthesis of adequate amounts of vitamin D, again by the action of sunlight on 7-DHC in the skin.When the Scots moved from coastal fishing villages to industrial cities such as Glasgow, they became seriously deficient in vitamin D, and so the emergence of rickets. This was followed by a variety of other diseases resulting from vitamin D deficiency: tuberculosis, dental decay, coronary heart disease, and even multiple sclerosis and depression (the Glasgow syndrome).And so it was with the Inuits. When their diet changed ft-date">28. August 2007 William Davis (4)
Boycott LabCorp 27. August 2007 William Davis (13) Track Your Plaque Members have been following this conversation on the Track Your Plaque Forum. A good number of people have had their blood drawn for NMR lipoprotein analysis through laboratories operated by the Laboratory Corporation of American, or LabCorp. When the results were returned, the very important page 2 of the report was withheld. Many of us have communicated with the company, only to be given some corporate-speak about internal policy. I have personally expressed my dissatisfaction, my outrage, at this silly policy. Why would laboratory results that you or your insurance paid for be denied to you? It is my understanding that, on request, you are legally entitled to the information. The page 2 information is provided by the laboratory (Liposcience, Inc.) that actually performs the testing. LabCorp does nothing more than draw the blood, prepare the specimen, then convey and dilute the results that Liposcience reports to them. My personal suspicion is that the LabCorp people do this to 1) make the results appear that they actually performed the tests and not farmed to an outside laboratory (Liposcience), and 2) not further confuse and befuddle the bungling primary care physician who barely understands cholesterol issues to begin with. "LDL, HDL, triglycerides . . . What now--a bunch of new information, bars even!?To me, this LabCorp policy is criminal. In fact, I wonder if this has the substance to justify a class action lawsuit against LabCorp. I believe that we can easily make a case that crucial health information is being systematically denied to people. If this has affected you, or if you share in the frustration of many people who have had watered down lipoprotein results provided, write to: Ken Younts, VP of Sales at LabCorp. Yountsk@labcorp.com Or, write to:Tom MacMahonChairman of the BoardDavid P. KingPresident and Chief Executive OfficerLaboratory Corporation of America Holdings358 South Main StreetBurlington, NC 27215Thanks to the Track Your Plaque Members who have already participated in this campaign and written to the LabCorp people. And thanks to our Members who uncovered the contact information.Until then, please BOYCOTT LABCORP LABORATORIES. Please do not use LabCorp Laboratories if you can avoid it. Simply ask the laboratory staff who operates the lab and they should tell you. It is your right to know.
Useless low-fat diets 24. August 2007 William Davis (1) If you would like to read an ironic testimonial to the futility of conventional low-fat diets, read:Cutting Cholesterol, an Uphill Battle on the New York Times website at http://www.nytimes.com/2007/08/21/health/21brod.html?_r=2&adxnnl=1&oref=slogin&ref=health&adxnnlx=1187928650-f0mfyzGTFdsLmtInHcGPUwIn this story, author and columnist Jane Brody recounts her struggles with her cholesterol levels. She describes how she followed an increasingly strict low-saturated fat diet, hoping to reduce LDL cholesterol. But she saw the opposite occur: LDL climbed from an initial 134 to 171, a level that caused her doctor to prescribe a statin drug. Yet she states that "About 85 percent of the cholesterol in your blood is made in your body. The remaining 15 percent comes from food. But by reducing dietary sources of saturated fats and cholesterol and increasing consumption of cholesterol-fighting foods and drink, you can usually lower the amount of harmful cholesterol in your blood."Had Ms. Brody and her doctor been just a bit better informed and performed lipoprotein analysis instead, they would have seen some obvious phenomena:--All the increase in LDL was in the fraction of small particles, the sort highly likely to cause heart attack. --The conventional LDL that she quotes is a calculated value that miserably misrepresents the real LDL when actually measured. Her calculated LDL of 171 mg/dl, in fact, was probably more like 220 to 250 mg/dl--much higher than they think.Of course, Ms. Brody turns to her conventionally-thinking physician who then predictably prescribes a statin drug. Ms. Brody's well-articulated story achieves the ironic, unintended result of proving the idiocy of the conventional low-fat diet. The low-fat diet, as currently practiced by most people, raises LDL cholesterol and escalates risk for heart disease. In fact, Ms. Brody probably increased her risk far more than suggested by a 30 mg increase in LDL. One of my favorite blogs, the Fanatic Cook, has a tremendously insightful post on Ms. Brody's misadventures. If all she did was eliminate all wheat flour containing products and reduce the overall glycemic index of her diet, she would witness an enormous drop in LDL cholesterol, both calculated and measured. I hope that Ms. Brody survives her diet mistakes and her doctor's ignorance.
Do statin drugs reduce lipoprotein(a)? 24. August 2007 William Davis (17) Alex had lipoprotein(a), Lp(a), at a high level. With a heart scan score of 541 at age 53, treatment of this pattern would be crucial to his success. Part of Alex's treatment program was niacin. However, Alex complained about the niacin "flush" to his primary care physician. So, his doctor told him to stop the niacin and replace it with a statin drug (Vytorin in this case). Is this a satisfactory replacement? Do statin drugs reduce Lp(a)?No, they do not. In fact, that's how I often meet people who have Lp(a): Their doctor will prescribe a statin drug for a high LDL cholesterol that results in a poor response. The patient will be told that statin drugs don't work for them. In reality, they have Lp(a) concealed in the LDL that makes the LDL resistant to treatment. Lp(a) responds to a limited number of treatments, like niacin, testosterone, estrogen, and DHEA. But not to statin drugs. Now, statin drugs may still pose a benefit through LDL reduction. But they do virtually nothing for the Lp(a) itself. Unfortunately, most practicing physicians rarely go any farther than Lipitor, Zocor, Vytorin, and the like. If your doctor tries to shove a statin drug on you as a treatment for Lp(a), put up a fight. Voice your objections that statins do not reduce Lp(a).
Breakfast cereals and toilet paper 23. August 2007 William Davis (4) (Image courtesy of Brandon Blinkenberg and Wikipedia.)What do breakfast cereals and toilet paper have in common? You guessed it: They both belong in the toilet. If you would like some insight into why your friends and neighbors have protruding bellies that conceal any glimpse of their toes, have to conduct that peculiar side-to-side gait that now characterizes many Americans' walking style, and are pre-diabetic or diabetic, look no further than your supermarket cereal aisle. The Fanatic Cook has some particularly biting comments about this strangely American phenomenon at http://fanaticcook.blogspot.com. Breakfast cereals range in quality from awful to bad. I don't know of any that fit into the Track Your Plaque program that aims to eliminate the risk of heart disease.
Another lipoprotein hurdle 23. August 2007 William Davis (0) A number of our Track Your Plaque Members have encountered unexpected difficulty obtaining the 2nd page of their NMR Lipoprofile lipoprotein results when their blood was drawn in a LabCorp laboratory. This is the page that displays the lipoprotein subclasses in graphic format: VLDL, IDL, LDL, and HDL subclasses. If you are unable to view page 2, you're stuck with the averaged values displayed on page 1. In my view, page 1 is is a drastically "watered down" version that sacrifices some crucial information, particularly if you use NMR lipoprotein analysis in a serial fashion, comparing one study to the next over time. Why would LabCorp do this? The response I received from a Mr. Theo McCormick, Director of Marketing at LabCorp, was some corporate-speak about . . . Actually, I'm not sure what he was saying. (Members can read the complete Track Your Plaque conversation in the Forum.) In my view, withholding this information is none of their business. If you or your insurance company paid for the test, then the information is yours to view. This would be like saying that "Sure you paid for the blood test, but we decided that you really won't know what to do with it, so we're keeping it from you."Please send your objections to the contact info below. Several of the Members who have participated in the Track Your Plaque Forum conversation have already done so. It can only help to add to the growing objections to this silly and unfair practice. Alternatively, just boycott any laboratory associated with LabCorp. If they are capable of such ridiculous withholding of information, who knows what else these people do? Contact info:Theo McCormick, Director of MarketingLaboratory Corporation of America1904 Alexander DriveResearch Triangle Park, NC 27709Phone 919-572-7454 (Direct) 919-361-7700 MainFax 919-361-7149 theo_mccormick@labcorp.comUntil we hear about some real action from them, please DO NOT USE ANY LABCORP LABORATORY.
More on aortic valve disease and vitamin D 22. August 2007 William Davis (22) I hope I'm not getting my hopes up prematurely, but I believe that I've seen it once again: Dramatic reversal of aortic valve disease. This 64-year old man came to me because of a heart scan score of 212. Jack proved to have small LDL, lipoprotein(a), and pre-diabetes. But there was a wrench in the works: Because of a new murmur, we obtain an echocardiogram that revealed a mildly stiff ("stenotic") aortic valve, one of the heart valves within the heart that can develop abnormal stiffness with time. You can think of aortic valve disease as something like arthritis--a phenomenon of "wear and tear" that progresses over time, but doesn't just go away. In fact, the usual history is that, once detected, we expect it to get worse over the next few years. The stiff aortic valve eventually causes symptoms like chest pains, breathlessness, lightheadedness, and in very severe cases, passing out. For this reason, when symptoms appear, most cardiologists recommend surgical aortic valve replacement with a mechanical or a bio-prosthetic ("pig") valve. Now, Jack's first aortic valve area (the parameter we follow by echocardiogram representing the effective area of the valve opening when viewed end on) was 1.6 cm2. A year later: 1.4 cm2. One year later again: 1.1 cm2. In other words, progressive deterioration and a shrinking valve area. Most people begin to develop symptoms when they drop below 1.0 cm2. Resigned to a new valve sometime in the next year or two, Jack underwent yet another echocardiogram: Valve area 1.8 cm2. Is this for real? I had Jack come into the office. Lo and behold, to my shock and amazement, the prominent heart murmur he had all along was now barely audible. I'm quite excited. However, it remains too early to get carried away. I've now seen this in a handful of people, all with aortic valve disease. Aortic valve stenosis is generally regarded as a progressive disease that must eventually be corrected with surgery--period. The only other strategy that has proven to be of any benefit is Crestor 40 mg per day, an intolerable dose in my experience. If the vitamin D effect on aortic valve disease proves consistent in future, even in a percentage of people, then hallelujah! We will be tracking this experience in future.
"How often do you call an ambulance?" 17. August 2007 William Davis (1) I asked one of the CT technologists at Milwaukee Heart Scan what quesetions are often asked by people undergoing their first CT heart scan."That's easy," she said. " 'How often do you call an ambulance?' "She went on. "People are very scared when they have their heart scan. In fact, some people don't even want to see their heart scan images and don't want to know their score--even after they paid $200 for the scan!"I think she's right. People often remember the headlines that some heart scan centers have used: "Heart scan saved so and so's life!," when a high score led to a heart catheterization, stents, or bypass surgery. It's the sort of headline that gives people the impression that ambulances pull up to the scan center whenever a score is high.So, how often is an ambulance called to the scan center? Never. Not once. A CT heart scan score is NEVER an emergency.Emergencies occur in other places when people can't breathe, or are having pain in their chest, or pass out, emergencies that should not take anyone to a heart scan center. When heart scans are used properly, it is the person without symptoms who undergoes a scan to look for hidden heart disease. This cannot lead to an emergency.Of course, that doesn't mean that a high score shouldn't prompt quick action in the next few days or weeks, like seeing your doctor to discuss the results, undergoing a stress test, discussing how to stop the score from progressing.But call an ambulance? Forget about it.If you are contemplating a scan but are scared that it could lead to a 911 call, don't let that stop you. But, in the event that you go to an unscrupulous center or get bad information, be sure to be armed with the best information possible. One good start would be to take look at our free downloadable book, What does my heart scan show? available for free on the www.cureality.com website.
Oat vs. wheat 17. August 2007 William Davis (7) Here's a fascinating 2002 study by Dr. Brenda Davy and colleagues at Colorado State University that examined the NMR lipoprotein differences between a diet enriched in oats and one enriched with wheat. (Davy BM, Davy KP, Ho RC et al. High-fiber oat cereal compared with wheat cereal consumption favorably alters LDL-cholesterol subclass and particle numbers in middle-aged and older men. Am J Clin Nutr 2002; 76:351-358.) 36 sedentary, overweight men (average BMI around 30--obese), aged 50-75 years, were given a diet enriched with either oat bran (as oatmeal and oat bran, providing 5.5 grams of beta-glucan) or wheat (as a hot cereal or Frosted Mini-Wheats), with equivalent calories in each group. All underwent baseline NMR lipoprotein analysis.Three months later, there were no differences in "anthropometrics" like weight, waist size, or BMI (though there was a trend towards larger waistlines in the wheat group). The NMR lipoprotein analysis was repeated. Comparison of the lipoprotein changes revealed:--LDL cholesterol: Down 2.5% with oats, up 8.0% with wheat.--LDL particle number: Down 5% with oats, up 14.2% with wheat.--Small LDL: Down 17.3% with oats, up 60.4% with wheat.--Triglycerides: Down 7.6% with oats, up 22.0% with wheat. The across-the-board differences between the wheat and oat effects were astounding. In particular, note the extraordinary effect on small LDL particles: wheat triggered a 60% increase. Similar studies yielding similar results have been conducted elsewhere, including Dr. Ronald Krauss' group at University of California-Berkeley. Now, this was a study conducted under the somewhat artificial circumstances of a study. But imagine this sort of habitual intake continues, not for just three months, but for years. After all, wheat has expanded and metastasized to all three meals, snacks, every day, 7 days a week in most Americans' diet. What a wonderfully graphic representation of the undesirable effects of wheat products. When you see Mini-Wheats, Shredded Wheat, whole grain bread, whole wheat bread, whole wheat crackers, Raisin Bran, and the thousands of other wheat-containing products that promise health, run the other way. Grab some oat bran on the way out.