Cholesterol follies 11. January 2008 William Davis (5) Rudy is a 59-year old man. He's had three heart catheterizations, two of which resulted in stent implantations. Obviously, Rudy should be the beneciary of a prevention program. His basic cholesterol values: Total cholesterol 164 mg/dl--pretty good, it seems. LDL cholesterol 111 mg/dl--Wow! Not too bad. HDL cholesterol 23 mg/dl--Uh oh, that's not too good. Triglycerides 148 mg/dl--By national (NCEP ATP-III) guidelines, triglycerides of 150 mg/dl and below fall within the desirable range. So we're left with an apparently isolated low HDL cholesterol, nothing more. On the surface, it doesn't seem all that bad. Of course, we need to keep in mind that this pattern landed Rudy in the hospital on several occasions and prompted several procedures. Should we rely on these results? How about Rudy's lipoproteins? Here they are (NMR; Liposcience):LDL particle number 2139 nmol/l--Representing an effective LDL of 213--over 100 mg higher than the standard value (above) suggests.Small LDL particles 2139 nmol/l--In other words, 100% of all Rudy's LDL particles are small. (Thus, weight-based measures of LDL cholesterol fail to tell us that he has too many small particles.)Large HDL 0 (zero) mg/dl--Rudy has virtually no functional HDL particles. If we had relied only on Rudy's standard cholesterol values, we would have focused on raising HDL. However, lipoprotein analysis uncovered a smorgasbord of additional severe patterns. The high LDL particle number comprised 100% of small particles is especially concerning. Truly, conventional cholesterol testing is a fool's game, one that time and again fails to fully uncover or predict risk for heart disease. One look at Rudy's lipoproteins and it becomes immediately obvious: This man is at high risk for heart disease and the causes are clear. Of course, many physicians and insurance companies argue that the added information provided by this portion of the lipoprotein test added around $70 more to the expense. When you see results like this, is there even a choice?
Equal calories, different effects 9. January 2008 William Davis (15) A great study was just published in the Journal of the American College of Cardiology:Metabolic effects of weight loss on a very-low-carbohydrate diet compared with an isocaloric high-carbohydrate diet in abdominally obese subjects. 88 obese adults with metabolic syndrome were placed on either of two diets:1) A very low-carbohydrate, high-fat diet (VLCHF): 4% calories from carbohydrates (truly low-carb); 35% protein; 61% fat, of which 20% were saturated. In the first 8 weeks, carbohydrate intake was severely limited to <20 grams per day, then <40 grams per day thereafter. 2) A high-carbohydrate, low-fat diet (HCLF): 46% calories from carbohydrates; 24% protein; 30% total fat, of which <8% were saturated. Both diets were equal in calories (around 1400 calories per day--rather restrictive) and participants were maintained on the program for six months. At the end of the six month period, participants on the VLCHF diet lost 26.4 lb, those on the HCLF diet 22.2 lbs (though the difference did not reach statistical significance). Thus, both approaches were spectacularly successful at weight loss. Surprisingly, blood pressure, blood sugar, insulin and insulin sensitivity (a measure called HOMA) were all improved with both diets equally. Thus, these measures seemed to respond more to weight loss and less to the food composition. Lipids differed between the two diets, however:VLCHF:Total cholesterol: initial 208.4 mg/dl final 207.7 mg/dlLDL: initial 125 mg/dl final 123 mg/dlHDL: initial 55 mg/dl final 64.5 mg/dlTriglycerides: initial 144 mg/dl final 74 mg/dlApoprotein B: initial 98 mg/dl final 96 mg/dlHCLF Total cholesterol: initial 208.4 mg/dl final 187.5 mg/dlLDL: initial 126 mg/dl final 108 mg/dlHDL: initial 51 mg/dl final 54.5 mg/dlTriglycerides: initial 157.6 mg/dl final 111 mg/dlApoprotein B: initial 100 mg/dl final 95 mg/dlSome interesting differences became apparent:--The VLCHF diet more effectively reduced triglycerides and raised HDL. --The HCLF diet more effectively reduced total and LDL. --There was no difference in Apo B (no statistical difference).The investigators also made the observation that individual responsiveness to the diets differed substantially. They concluded that both diets appeared to exert no adverse effect on any of the parameters measured, both were approximately equally effective in weight loss with slight advantage with the carbohydrate restricted diet, and that lipid effects were indeed somewhat different. What lessons can we learn from this study? I would propose/extrapolate several:When calories are severely restricted, the composition of diet may be less important. However, when calories are not so severely restricted, then composition may assume a larger role. When calories are unrestricted, I would propose that the carbohydrate restriction approach may yield larger effects on weight loss and on lipids when compared to a low-fat diet. The changes in total cholesterol are virtually meaningless. Part of the reason that it didn't drop with the VLCHF diet is that HDL cholesterol increased. In other words, total cholesterol = LDL + HDL + trig/5. A rise in HDL raises total cholesterol. Despite no change in Apo B, if NMR lipoprotein analysis had been performed (or other assessment of LDL particle size made), then there would almost certainly have seen a dramatic shift from undesirable small LDL to less harmful large LDL particles on the VLCHF diet, less change on the HCLF diet. The lack of restriction of saturated fat in the VLCHF that failed to yield adverse effects is interesting. It would be conssistent with the re-analysis of saturated fat as not-the-villain-we thought-it-was put forward by people like Gary Taubes (Good Calories, Bad Calories). In the Track Your Plaque experience, small LDL is among the most important measures of all for coronary plaque reversal and control. Unfortunately, although this study was well designed and does add to the developing scientific exploration of diet, it doesn't add to our insight into small LDL effects. But if I had to make a choice, I'd choose the low-carbohydrate, high-fat approach for overall benefit.
Is skinny necessary for reversal? 6. January 2008 William Davis (19) Nothing we do in the Track Your Plaque program guarantees that coronary atherosclerotic plaque or your heart scan score is reduced or reversed. But everything we do weighs the odds in your favor of successfully achieving reversal: correction of lipoprotein patterns, uncovering hidden patterns like Lp(a), vitamin D, being optimistic--it all tips the scales in your favor. But how necessary is it to be skinny, meaning somewhere near your ideal weight? It is important, but not as important as it used to be. Let me explain. I used to tell people that plaque would not regress unless ideal weight was achieved and all the parameters of abdominal obesity and metabolic syndrome were corrected. This includes blood pressure, blood sugar, low HDL, small LDL, high triglycerides, and high c-reactive protein. Curiously, though, as we've gotten better and better at reducing coronary calcium scores, I've been finding that complete correction of all parameters, including achieving ideal weight, don't seem to be as necessary to achieve plaque reversal. I almost hate to say this, but I've even witnessed significant drops in heart scan scores in people with body mass indexes (BMI) of 30--obese. The necessary change doesn't seem to be weight, per se, but the consequences of weight. In other words, if you remain overweight, but blood sugar, HDL, small LDL, etc. have shown substantial improvement, then reversal is still achievable. Then is it okay to be fat or overweight? Reducing weight to ideal weight does indeed tip the scales in your favor, since it represents an observable, perceptible measure of all associated patterns. Dropping weight can also minimize the need for efforts to correct the consequences of overweight--you might need less niacin, fish oil, exercise, blood pressure medication, etc. to succeed at plaque reversal. Achieving ideal weight may also provide benefits like reduced risk of cancers and degenerative diseases of the hips and knees. But, to my recent surprise over the last two years, achieving ideal weight is not an absolute requirement to achieve reversal. This is contrary to what some others say. For instance, in an upcoming interview with Dr. Joel Fuhrman on the Track Your Plaque website, Dr. Fuhrman argues that 10% body fat for males, 22% body fat for females, accelerates plaque and symptom reversal. Dr. Fuhrman is author of Fasting and Eating for Health, Eat to Live, and a new upcoming 2-part book, Eat for Health, and proponent of high-nutrient vegetarian diets and fasting. Dr. Fuhrman has been helpful in teaching us some important lessons on how to apply periodic fasting to accelerate plaque reversal. So, which is it, fat or skinny? If given a choice (which everyone has), I'd choose skinny. But, provided all the parameters associated with overweight are corrected, then remaining overweight doesn't necessarily mean that you can't still succeed at plaque reversal. If you are interested in knowing what your ideal weight is, there are a number of software calculators and tables available, including the HealthCentral.com calculator and the National Heart, Lung, and Blood Institute BMI Calculator. Image courtesy Wikipedia.Copyright William Davis, MD 2008
MESA Study: Track Your Plaque-Lite? 4. January 2008 William Davis (11) The long-awaited data analyses from the Multi-Ethnic Study of Atherosclerosis (MESA) are finally making it to press. The MESA Study is an enormously ambitious and important study of 6800 people, 45 to 84 years old, that includes white, black, Hispanic, and Chinese participants from six communities around the U.S. (Forsyth County, NC; Northern Manhattan and the Bronx, NY; Baltimore and Baltimore County, Md; St Paul, Minn; Chicago, Ill; and Los Angeles County, California.) Participants had no history of heart disease at enrollment. All underwent a heart scan (either EBT or multi-detector heart scans) at the start. It is therefore the largest prospective study involving heart scans ever performed. It is, not unexpectedly, yielding some fascinating observations relevant to the Track Your Plaque program. The MESA study is, incidentally, funded by the non-commercial, publicly-funded National Heart, Lung, and Blood Institute and is therefore presumably free of commercial bias. Among the most recent publications is Risk factors for the progression of coronary artery calcification in asymptomatic subjects: Results from the Multi-Ethnic Study of Atherosclerosis (MESA) In this analysis of 5700 of the MESA participants, a repeat heart scan was obtained an average of 2.4 years after the first. Conventional risk factors for heart disease were obtained at the start (see below for details under Measurement of Covariates.)After analyzing the data and risk factors assessed, such as age, sex, race, blood pressure, body mass index (BMI), presence of diabetes, blood sugar, and family history of heart disease, two questions were asked:1) What risk factors predict heart scan scores?2) What risk factors predict progression (i.e., increase) in heart scan scores?(The second question is particularly relevant to us and the Track Your Plaque experience.) The MESA analysis showed that essentially all the risk factors assessed correlated with both the initial heart scan score, as well as the rate of progression. No surprises here.But the most eye-opening finding was that the conventional risk factors assessed explained only 12% of the variation and progression in heart scan scores (coefficient of determination, or R squared, = 0.12.) In other words:--Conventional risk factors like LDL cholesterol, diabetes, and excess weight explain only a tiny fraction of why someone develops coronary atherosclerotic plaque as represented by a heart scan score. --The great majority of risk for a high heart scan score remains unexplained by conventional risk factors.--The great majority of risk for progressive increase in heart scan scores also remains unexplained by conventional risk factors. In light of the MESA analysis, it's no surprise that strategies like reducing LDL cholesterol with statin drugs fails to prevent most heart attacks. It's no surprise that conventional prevention programs that talk about "knowing your numbers," eating a "balanced" or low-fat diet, etc., fail miserably to prevent the vast majority of heart attacks and heart procedures. MESA confirms what we've been saying these past few years: If you want control over coronary heart disease, you won't find it in Lipitor, a low-fat diet, and other limited conventional notions of risk. Correction of conventional risk factors like cholesterol and blood pressure are, in a word, a failure. I wouldn't even call the conventional approach Track Your Plaque-Lite. They don't even come close.If conventional risk factors can explain only 12% of the reason behind heart disease, we've got to look elsewhere to understand why you and I develop this process. Measurement of CovariatesInformation on demographics, smoking, medical conditions, and family history was collected by questionnaire at the initial examination. Height and weight were also measured at the baseline examination, and blood was drawn for measurements, including lipids, inflammation, fasting glucose, fibrinogen, and creatinine. Resting blood pressure was measured 3 times in the seated position, and the average of the last 2 measurements was used in the analysis. Medication use was determined by questionnaire. Additionally, the participant was asked to bring to the clinic containers for all medications used during the 2 weeks before the visit. The interviewer then recorded the name of each medication, the prescribed dose, and frequency of administration from the containers.Copyright 2008 William Davis,MD
Risks for coronary disease 2008 31. December 2007 William Davis (27) According to conventional thinking, there are identifiable risks for coronary disease and heart attack. These risk factors are: * smoking * high blood pressure * high blood cholesterol and excessive saturated fat intake * diabetes * being overweight or obese * physical inactivityI'd agree with all the factors listed (though I would argue about the importance of high blood cholesterol and saturated fat; they are not as important as commonly made to be.)Is the list complete? From the unique perspectives gained in the Track Your Plaque program, I'd offer a significantly different list. Trying to stop or reduce coronary atherosclerotic plaque and heart scan scores makes you a whole lot smarter about what works and what doesn't work. So, in addition to the risk factors listed above, I would add: * Small LDL particles--Lots of small LDL particles is MORE important than high LDL. * High blood pressure with exercise * Excessive wheat intake and other processed carbohydrates--An issue of explosive importance today. Wheat creates large numbers of small LDL particles, among other adverse effects. * Vitamin D deficiency--Among the most powerful risks I know of. It belongs at the top of the list. * Vitamin K2 deficiency * Low HDL cholesterol * Blood sugar >100 mg/dl * High triglycerides--While some argue about whether triglycerides are a risk that behaves independently of patterns like low HDL, they are neglecting the potent force of this risk. Sure, it occurs in tandem with low HDL (usually, though not always), but it is a factor that can leave you with risk even when HDL is raised to healthy levels. * Lipoprotein(a)--It is eminently, positively crystal clear that lipoprotein(a) is a powerful risk for heart disease. The lack of a profitable treatment keeps it hidden in the shadows. * Pessimism--Be happy, do better. Be a constantly angry, frustrated, complaining sourpuss and you are more likely to succumb to heart disease, cancer, or other undesirable fate. These are the risk factors that we address through the Track Your Plaque program, a list that yields a far more powerful and comprehensive approach to control over coronary plaque/atherosclerosis, sufficient to achieve reversal in many (though not in all) instances. I view the list of conventional risk factors as a "no brainer" list. Sure, smoking is a risk factor. But there are virtually no smokers in the Track Your Plaque program. If you smoke, you clearly don't care enough to engage in a high-intensity prevention program like this. Saturated fat? Perhaps, but the battlefield of heart disease is riddled with the bodies of those who employed this as their sole strategy and failed catastrophically. Diabetes, hypertension, and overweight all represent a continuum of risk; the solutions offered in the conventional scheme (i.e., low-fat diet, etc.) make these patterns worse, not better.The conventional response to heart disease risk is trapped somewhere in 1973 and has not changed in over 30 years. Heart disease continues to be a growth industry for hospitals and the pharmaceutical and medical device industries. The "official" organizations continue to deliver an antiquated, outdated message. If you want heart disease, follow the American Heart Association diet. If you want established heart disease to get worse, follow the American Heart Association diet. If you want diabetes or, if you already have diabetes or pre-diabetes, if you want it to worsen and develop organ damage (eyes, kidneys, nervous system, etc.), then follow the American Diabetes Association diet. USDA food pyramid? Loosen your belt!The list of conventional risk factors for heart disease is woefully inadequate. If that is as far as your prevention program takes you, heart disease will not be controlled or prevented. At best, it might be slowed; at worst--and more likely--it might be accelerated.
Food sources of vitamin K2 27. December 2007 William Davis (46) Vitamin K2 is emerging as an exciting player in the control and possible regression of coronary atherosclerotic plaque. Only about 10% of dietary vitamin K intake is in the K2 form, the other 90% being the more common K1. The ideal source of K2 is natto, the unpalatable, gooey, slimy mass of fermented soybeans that Japanese eat and has been held responsible for substantial decreases in osteoporosis and bone fractures of aging. Natto has an ammonia-like bouquet, in addition to its phlegmy consistency that makes it virtually inedible to anyone but native Japanese. I say that the conversation on vitamin K2 is emerging because of a number of uncertainties: What form of vitamin K2 is best (so-called MK-4 vs. MK7 vs. MK-9, all of which vary in structure and duration of action in human blood)? What dose is required for bone benefits vs. other benefits outside of bone health? Why would humans have developed a need for a nutrient that is created through fermentation with only small quantities in meats and other non-fermented foods? Much of the developing research on vit K2 is coming from the laboratories of Drs. Vermeer, Geleijnse, and Schurgers at the University of Maastricht in the Netherlands, along with several laboratories in Japan, the champions of K2.MK-7 and MK-8,9,10 come from bacterial fermentation, whether in natto, cheese, or in your intestinal tract; MK-4 is naturally synthesized by animals from vitamin K1. While natto is the richest source of the MK-7 form, egg yolks and fermented cheeses are the richest sources of the MK-4 form. Chicken contains about 8 mcg MK-4 per 3 1/2 oz serving; beef contains about 1 mcg. Egg yolks contain 31 mcg MK-4 per 3 1/2 oz serving (app. 6 raw yolks). Hard cheeses contain about 5 mcg MK-4 per 3 1/2 oz serving, about 70 mcg of MK-8,9; soft cheeses contain about 30% less. Natto contains about 1000 mcg of MK-7, 84 mcg MK-8, and no MK-4 per 3 1/2 oz serving. Feta cheese Thanks to the research efforts of the Dutch and Japanese groups, several phenomena surrounding vitamin K2 are clear, even well-established fact: --Vitamin K2 supplementation (via frequent natto consumption or pharmaceutical doses of K2) substantially improves bone health. While K2 by itself exerts significant bone density/strength increasing properties in dozens of studies, when combined with other bone health-promoting agents (e.g., vitamin D3, prescription drugs like Fosamax and calcitonin), an exaggerated synergy of bone health-promoting effects develop. --The MK-4 form of vitamin K2 is short-lived, lasting only 3-4 hours in the body. The MK-7 form, in contrast, the form in natto, lasts several days. MK-7 and MK-8-10 are extremely well absorbed, virtually complete. --Bone health benefits have been shown for both the MK-7 and MK-4 forms. --Coumadin (warfarin) blocks all forms of vitamin K. Interestingly, farm-raised meats and eggs do not differ from factory farm-raised foods in K2 content. (But please do not regard this as an endorsement of factory farm foods.) Another interesting fact: Since mammals synthesize a small quantity of Vit K2 forms from vitamin K1, then eating lots of green vegetables should provide substrate for some quantity of K2 conversion. However, work by Schurgers et al have shown that K1 absorption is poor, no more than 10%, but increases significantly when vegetables are eaten in the presence of oils. (Thus arguing that oils are meant to be part of the human diet. Does your olive oil or oil-based salad dressing represent fulfillment of some subconscious biologic imperative?) If we believe the data of the Rotterdam Heart Study, then a threshold of 32.7 micrograms of K2 from cheese yields the reduction in cardiovascular events and aortic calcification.It's all very, very interesting. My prediction is that abnormal (pathologic) calcium deposition will prove to be a basic process that parallels atherosclerotic plaque growth, and that manipulation of phenomena that impact on calcium depostion also impact on atherosclerotic plaque growth. Vitamins D3 and K2 provide potential potent means of at least partially normalizing these processes. As the data matures, I am going to enjoy my gouda, Emmenthaler, Gruyere, and feta cheeses, along with a few egg yolks. I'm going to be certain to include healthy oils like olive and canola with my vegetables. All images courtesy Wikipedia. Copyright 2007 William Davis, MD
Track Your Plaque: Naughty or nice? 24. December 2007 William Davis (6) Among the many wonderful surprises we've had at Track Your Plaque this holiday season was a letter from Santa Claus himself!It seems that Santa, like the rest of us, has been busy surfing the web for useful health information the last few months. He was struck with this curious discussion we've been having about "wheat belly" and all the unhealthy consequences of wheat products in our diet. He writes:"I wouldn't have believed it myself, except that my waist size has grown four inches in as many years. Sure, I'm known for my healthy girth, but now even Mrs. Claus calls me fat!"I was open to new ideas when I came across this crazy discussion about eliminating wheat from your diet. So I said, "What have I got to lose?" Well, four weeks later and 12 lbs lighter, I'm convinced. Now comes the tough part: I've got to deliver all the toys and resist all those cookies the Cureality | Real People Seeking Real Cures Toggle navigation Home Blog Home Archive Join Now Log in Add Boston Globe to the list of heart scan blunders 17. September 2008 William Davis (15) Yet another piece of mass media misinformation hit the airwaves today. This time it's not from the New York Times or the LA Times, both of which have previously mangled the issues surrounding heart scans. This time it's from the Boston Globe. In an article titled What is a calcium scan for heart disease, and who should undergo the test?, the report states: ". . . calcium scans may not be a good idea, or prove terribly useful, for most people. For one thing, the scans expose a patient to significant radiation - equivalent to roughly 50 chest X-rays" said Dr. Warren Manning, chief of noninvasive cardiac imaging at Beth Israel Deaconess Medical Center."As many before him, Dr. Manning is confusing two tests: CT coronary angiography and CT heart scanning. Perhaps we can't blame him: This technology has had its weakest following in the northeast, for reasons not entirely clear to me. (In fact, Track Your Plaque followers have had the greatest struggle obtaining heart scans in that part of the country.) Nonetheless, you'd think he'd have his simple facts straight before talking to the press. Unfortunately, hospital public relations departments will usually just grab whoever they can willing to talk to the press--regardless of their expertise or lack of. The story goes on to say:. . ." it's not clear what to do with the results from a calcium scan. If you have diabetes, high cholesterol, high blood pressure, or a family history of heart disease, you already know - or should know - that you are at increased risk of heart problems and should lower these risk factors. So, a calcium scan provides little additional information," Manning said. "Moreover, even a high score doesn't necessarily mean that the calcified plaque in your arteries is obstructing blood flow, said Dr. Adolph Hutter, a cardiologist at Massachusetts General Hospital.""The vast majority of people with high calcium tests don't have obstructions and they do fine long-term. So you'd have to test lots and lots of people to prevent one heart attack or sudden death," said Manning.And if you get a low calcium score, a sign of little or no calcification of plaques, that's not very useful, either, because it could be wrong, or it could be right but lull you into believing you do not have to exercise and watch your diet, cholesterol, and blood pressure levels. "You can still be at risk even if your calcium test is negative," Hutter said.It is truly shocking how little many (not all, thank goodness) of my colleagues really know about 1) heart scans, 2) coronary disease prevention, and 3) prevention in general. These same "experts" likely advocate high-dose statin drugs and low-fat diets for people at risk. They likely refer patients to the American Heart Association for diet advice and themselves obtain a lot of information from the pharmaceutical industry. The notion of identification, tracking, and purposeful reversal of coronary plaque is entirely foreign to this bunch. "The vast majority of people with high calcium tests don't have obstructions and they do fine long-term. So you'd have to test lots and lots of people to prevent one heart attack or sudden death." Well, take a look at a graph from a database of 25,000 people undergoing heart scans then observed for several years afterwards:You can see quite clearly from the curves that heart scan scores very clearly predict your future (if no preventive action is taken). The higher the score, the greater the likelihood of heart attack and death. How much clearer can it get? The most recent addition to this literature is the PREDICT study which concluded:Hazard ratios relative to CACS [coronary artery calcium scores] in the range 0-10 Agatston units (AU) were: CACS 11-100 AU, 5.4 (P = 0.02); 101-400 AU 10.5 (P = 0.001); 401-1000 AU, 11.9 (P = 0.001), and >1000 AU, 19.8 (P < 0.001). In other words, a heart scan score of >1000 is associated with a 20-fold increased risk of cardiovascular events (without preventive efforts). That kind of predictive power and quantitative confidence simply cannot be squeezed out of blood pressure and cholesterol values. How about the 2008 University of California-Irvine study from the New England Journal of Medicine (do the northeast docs even pay attention to something that is published in their own neighborhood?) that reported:There were 162 coronary events, of which 89 were major events (myocardial infarction or death from coronary heart disease). In comparison with participants with no coronary calcium, the adjusted risk of a coronary event was increased by a factor of 7.73 among participants with coronary calcium scores between 101 and 300 and by a factor of 9.67 among participants with scores above 300 (P<0.001 for both comparisons). Among the four racial and ethnic groups, a doubling of the calcium score increased the risk of a major coronary event by 15 to 35% and the risk of any coronary event by 18 to 39%. How about the Prospective Army Coronary Calcium (PACC) project (men average age 43 years):"In these men, coronary calcium was associated with an 11.8-fold increased risk for incident coronary heart disease (CHD) (p = 0.002) in a Cox model controlling for the Framingham risk score. Among those with coronary artery calcification, the risk of coronary events increased incrementally across tertiles of coronary calcium severity (hazard ratio 4.3 per tertile)." Calcium score provided additional information even after factoring in the Framingham risk score. That's just a sample of the studies. There are a number more. Add to these conversations the fact that, unlike reducing blood pressure or LDL cholesterol, the heart scan score is a quantification of the disease itself. It can also be tracked over time to gauge the success or failure of prevention efforts. To believe that blood pressure reduction or LDL cholesterol reduction is sufficient to eliminate risk is something only a fool would believe. Contary to the above statements, the data are clear:--The higher the heart scan score, the greater the risk. This has been demonstrated beyond any shadow of a doubt in at least a dozen published studies. In fact, heart scan scores outshine lipid/cholesterol values several-fold. --A person with a zero score has a nearly zero risk for cardiovascular events over a 5-year timeline. --Heart scans are the only quantitative test available of coronary atherosclerotic plaque. This means that they can be repeated to gauge progression or regression. Cholesterol does not do that. Stress tests do not do that. --Heart scans are not the same as CT coronary angiography. --The lack of "need" for a procedure does not equate to the absence of disease. The power of heart scans is that they can uncover evidence for coronary atherosclerotic plaque 10 years before a cardiac disaster strikes. Witness Tim Russert's heart scan score of 210 in 1998 at age 48. 10 years later, you know what happened. Beware the camipaign of misinformation and ignorance that continues that is hell-bent on maintaining the procedural status quo or locking us into a "drugs for all" mentality. What's worse than sugar? 16. September 2008 William Davis (11) There are a number of ways to view the blood sugar-raising or insulin-provoking effect of foods. One way is glycemic index (GI), simply a measure of how high blood sugar is raised by a standard quantity of a food compared to table sugar. Another is glycemic load (GL), a combination (multiplied) of glycemic index and carbohydrate content per serving. Table sugar has a GI of 65, a GL of 65. Obviously, table sugar is not good for you. The content of white table sugar in the American diet has exploded over the last 100 years, totaling over 150 lb per year for the average person. (Humans are not meant to consume any.) What is the GI of Rice Krispies cereal, organic or not? GI = 82-- higher than table sugar. GL is 72, also higher than table sugar.How about Corn Flakes? GI 81, GL 70--also both higher than sugar. How about those rice cakes that many dieters will use to quell hunger? GI 78, GL 64. How about Shredded Wheat cereal? GI 75, GL 62. All of the above foods with GI's and GL's that match or exceed that of table sugar are made of wheat and cornstarch. Some, like Shredded Wheat cereal and rice cakes, don't even have any added sugar.Stay clear of these foods if you have low HDL, high triglycerides, high blood sugar, or small LDL. Or, for that matter, if you are human. Keep the eloquent words of New York University nutritionist, Marion Nestle, author of the book, Food Politics, in mind:“Food companies—just like companies that sell cigarettes, pharmaceuticals, or any other commodity—routinely place the needs of stock holders over considerations of public health. Food companies will make and market any product that sells, regardless of its nutritional value or its effect on health. In this regard, food companies hardly differ from cigarette companies. They lobby Congress to eliminate regulations perceived as unfavorable; they press federal regulatory agencies not to enforce such regulations; and when they don’t like regulatory decisions, they file lawsuits. Like cigarette companies, food companies co-opt food and nutrition experts by supporting professional organizations and research, and they expand sales by marketing directly to children, members of minority groups, and people in develop countries—whether or not the products are likely to improve people’s diets.” ?? Are sterols the new trans fat? 13. September 2008 William Davis (16) By now, I'm sure you're well-acquainted with the hydrogenated, trans fat issue.Hydrogenation of polyunsaturated oils was a popular practice (and still is) since the 1960s, as food manufacturers sought a substitute for saturated fat. Bubbling high-pressure hydrogen through oils like cottonseed, soybean, and corn generates trans fatty acids. These man-made fatty acids, while safe in initial safety testing, proved to be among the biggest nutritional mistakes of the 20th century. Trans fatty acids have been associated with increased LDL cholesterol, reduction in HDL, oxidative reactions, abnormal rigidity when incorporated into cell membranes, and cancer. Trans fats still dominate many processed foods like chips, cookies, non-dairy creamers, food mixes, and thousands of others. They're also found prominently in fast foods. Fast forward to today, and most Americans have become aware of the dangers of trans fats and many try to avoid them. But I worry there is yet another substance that has worked its way into the American processed food cornucopia that has some potential for repeating the trans fat debacle: sterol esters. Sterols are naturally-occurring oils found in vegetables, nuts, and numerous other foods in small quantities. Most of us take in 200-400 milligrams per day just by eating plant-sourced foods. Curiously, the chemical structure of sterols are very similar to human cholesterol (differing at one carbon atom). Sterols, by not fully understood means, block the intestinal absorption of cholesterol. Thus, sterol esters, as well as the similar stanol esters, have been used to reduce blood levels of total and LDL cholesterol. So far, so good. The initial commercial products, released in the late 1990s, were Take Control (sterol) and Benecol (stanol), both of which were marketed to reduce cholesterol when 2-3 tbsp are used daily, providing 3400 – 5100 mg of sterol or stanol esters, about 10- to 20-fold more than we normally obtain from foods. Several clinical trials have conclusively confirmed that these products reduce cholesterol levels. They do indeed perform as advertised. Add either product to your daily diet and LDL cholesterol is reduced by about 10-15%. In fact, in the original Track Your Plaque book, these products were advocated as a supplemental means of reducing LDL when other methods fell short. In 2008, there are now hundreds of products that have additional quantities of sterol esters in them, such as orange juice, mayonnaise, yogurt, breakfast cereals, even nutritional supplements. Most of these products proudly bear claims like "heart healthy." Stanol esters have not enjoyed the same widespread application. (I believe there may be patent issues or other considerations. However, it's the sterols that are the principal topic here, not stanols.) Now, here's where it gets a bit tricky. There is a rare (1 per million) disease called sitosterolemia, a genetic disorder that permits the afflicted to absorb more than the usual quantity of sterols from the intestine. While you and I obtain some amount of sterols from plant-based foods, absorption is poor, and we absorb <10% of sterols ingested. However, people with sitosterolemia absorb sterols far more efficiently, resulting in high blood levels of sterols that result in coronary disease and aortic valve disease, with heart attacks occurring as young as late teens or 20s. Treatment to block sterol absorption are used to treat these people. There are also a larger number, though still uncommon (1/500) of people who have only one of the two genes that young people with sitosterolemia have. These people may have an intermediate capacity for sterol absorption. Okay, so what does this have to do with you? Well, if you and I now take in 10-20 times greater amounts of sterol esters, do our blood levels of sterols increase? Several studies now suggest that, yes, sterol blood levels increase with sterol ingestion. One study from Finland, the STRIP Study, showed that children who had double usual sterol intake increased blood levels by around 50%. Similarly, a Johns Hopkins study in adults with only one of the genes ("heterozygotes") for sitosterolemia increased sterol blood levels by between 54-116% by ingesting 2200 mg of sterols added per day, despite reduction of LDL cholesterol levels. Even people with neither gene for sitosterol hyperabsorption can increase their blood levels of sterols. But the crucial question: Do the blood levels of sterols that occur in unaffected people or in heterozygotes increase the risk of coronary heart disease? The answer is not known. Despite the several clinical trials performed with sterol esters, all of them have examined LDL and total cholesterol reduction as endpoints, not cardiovascular events. It is conceivable that, while sterol esters reduce cholesterol, risk for heart disease is increased due to higher blood levels of sterols.The question is not settled. For now, it is just a suspicion. But that's enough for me to steer clear of processed foods supplemented with these uncertain sterol esters. My previous recommendations for sterol ester products will be removed with the next edition of Track Your Plaque. Until we have solid evidence that there are no adverse cardiovascular effects of sterol esters, in my view they should not be part of anyone's heart-disease prevention program. (The same argument does not seem to apply to stanol esters, such as that contained in butter-substitute Benecol, since stanol esters are not absorbed at all and remain confined to the intestine.) The Diabetes Gold Rush 11. September 2008 William Davis (9) Lou came into the office. Clearly, his program had gone sour.Lou had initially obtained wonderful control over his heart scan score of 1114, having reversed modestly in his first three years of effort through correction of his multiple causes (including low HDL, severe small LDL, Lp(a), and a diabetic tendency). But Lou now came into the office red-faced and sporting a big bulging abdomen. Blood sugar? Now in the overtly diabetic range. Lou said that his primary care doctor had suggested that he start on three new medications (glucophage, injectable Byetta, and Actos) to control his blood sugar. His doctor also told him to increase his intake of fibers by eating more "healthy" breakfast cereals like Cheerios. Lou had apparently done just that (added "healthy" fiber-rich foods) even before his doctor had suggested it. (Lou failed to remember the several conversations we'd had about healthy eating.) Unfortunately, Lou also failed to connect his increased intake of "healthy fiber-rich foods" and his growing abdominal girth (his "wheat belly").Here's the dirty little secret: Much of the world wants you to be diabetic. It is the health gold rush of this century. "Go West, young man!" To find out what I mean, you need only ask: Who profits when people become diabetic? That's easy:The pharmaceutical industry--Diabetes is a booming growth industry, a source of tens of billions of dollars of revenue, poised for enormous growth as the population ages and gets fatter. It is common for a newly-diagnosed diabetic to be given new prescriptions for two or three drugs with a monthly cost of $300. Of course, the chronic nature of the disease make this far more profitable than, say, a two week course of antibiotics. Presently, 70 new drugs are under development. Diabetes drug maker Novo Nordisk reported a 25% increase in revenues in 2007 from diabetic agents in the North American market, along with near $2 billion increase in profit for the year. Merck's recently-released DPP-4 inhibitor, Januvia, has already sold $668 million in 2007 and is growing rapidly. The medical device and supply industry. Take a look at the Medtronic quarterly earnings report, detailing the breakdown of their record-setting quarterly revenue of $3.7 billion:Diabetes revenue of $269 million grew 12 percent driven by salesof consumables, the accessories required by insulin pump users, andcontinuous glucose monitoring products. Revenue from internationalsales grew 31 percent over the same quarter last year.That's what I call a growth industry.The processed food industry. The food industry is as big or bigger than the drug industry. ADM, Kraft, General Mills all have annual revenues in the $12-50 billion range. There are plenty of others. When we're told, for instance, that Cheerios reduces cholesterol, we're not told that it skyrockets blood sugar or triggers small LDL. When we're sold whole wheat crackers, Cocoa Puffs (which the American Heart Asscociation says is heart-healthy), or granola bars, hunger is stimulated, impulse to eat more grows, blood sugar escalates, we get fat, we get diabetic. It's a simple formula.So be aware that there is little incentive among corporate giants in the food, medical device, or drug industries to encourage behaviors that decrease the incidence of diabetes. In fact, there is enormous financial incentive to make sure that diabetes continues to grow at the startling rate it has over the last decade. To be sure, the drug and medical device industry will also develop better tools to deal with diabetes and its complications. But the very best way to deal with diabetes is to not develop it in the first place. What else is there? 7. September 2008 William Davis (11) This question comes up frequently: Aren't there any alternatives to heart scans performed on a CT or EBT device?Yes, there are. First of all, heart scans are performed best on an electron-beam CT device (EBT) or a 64-slice multi-detector CT (MDCT) device. (While they are also obtainable through less-than-64 slice CT devices (e.g., 16 slices and less), I would advise against it because of the excessive radiation exposure and poor accuracy.) CT heart scans are not to be confused with now more popular CT coronary angiograms, which are performed on the same devices but require intravenous x-ray dye and many times more radiation.(See CT scans and radiation exposure and Heart scan frustration.) Heart scans currently form the basis for the Track Your Plaque program, a program of tracking plaque in the hopes of stopping or reversing the otherwise inevitable 30% per year increase. Let's confine our discussion to people without symptoms, meaning people like you and me sitting at home, not in an emergency room having chest pain or other similar acute symptomatic presentation. Among the other ways to uncover hidden coronary plaque:--Heart catheterization--to yield a coronary angiogram. Yes, this does tell us whether coronary plaque is present. However, it is invasive, expensive, and crude. (I've performed 5000 over my career; they are crude, though useful, tools in acute settings like unstable symptoms or heart attack, a different situation.) Coronary angiography is also non-quantitative. While they provide a value like "40% blockage mid-way in right coronary" or "90% blockage in left anterior descending" they do not provide a trackable lengthwise index of total plaque volume. Identifying severe blockages in people with symptoms leads to stents, bypass surgery and the like, but it is not practical nor of long-term usefulness in apparently, healthy people without symptoms. --Carotid ultrasound--Here's is where a lot of confusion comes from. Standard carotid ultrasound (U/S) performed in virtually every hospital and many clinics will yield crude qualitative results, e.g., "16-49% stenosis (blockage) in right internal carotid artery". The crude value range is because much of carotid U/S is based on flow velocities, not just direct visualization of the plaque itself ("2-D imaging). However, if carotid stenosis of any degree is identified, the likelihood of silent coronary plaque is much greater. Limitations: The qualitative, non-quantitative nature of carotid U/S make it difficult to follow long-term in a precise way. Also, this is carotid plaque, not coronary plaque. It makes it very difficult to follow carotid plaque as an indirect means of tracking coronary plaque. The two arterial territories, carotid and coronary, do not track together: there are divergences in many people, with carotid plaque absent in some people with advanced coronary plaque, carotid plaque more susceptible to different risk factors than coronary. So carotid U/S is helpful for its own purposes, but not terribly helpful for coronary tracking. How about carotid intimal-medial thickness (CIMT) obtained also with carotid U/S? CIMT is a useful index of bodywide atherosclerosis. CIMT is simply a measure not of plaque (and is measured in regions of the carotid artery away from plaque), but of the thickness of the lining of the carotid arteries. Everybody has a measurable CIMT, but it thickens as atherosclerosis grows. CIMT is a radiation-free test that takes several minutes. Limitations: Hardly anybody does it outside of research protocols. I know of no hospital or clinic in my area that performs CIMT, though it is slowly being adopted in some centers. It is also difficult to rely on repeated tests, because there is substantial variation when one technologist or another performs it. CIMT is also a flawed index of coronary plaque. When CIMT is compared to heart scan scores, CT coronary angiography, or conventional coronary angiography, CIMT correlates about 60-70% with the degree of coronary atherosclerosis. CIMT is therefore a useful test for research, but a distant 2nd choice--if you can obtain it. --Ankle-brachial index (ABI)--ABI is a crude measure, simply a comparison of the blood pressure (obtained with a blood pressure cuff) in the legs divided by blood pressure in the arms. The ratio is called ABI. Any ABI <1.0, meaning less pressure in the legs compared to the arms, is indirectly indicative of advanced coronary disease. ABI is, in fact, a very powerful predictor of cardiovascular events. If ABI is <1.0, your future risk for heart attack is very high, even in the absence of symptoms. Limitations: The vast majority of people with heart disease, even those having undergone stents or bypass surgery, have normal ABI's. Virtually all people with high heart scan scores have normal ABI's. In other words, ABI is a measure of very advanced atherosclerosis only. --Stress tests--I lump all stress tests together in their various forms, e.g., stress thallium, stress Cardiolite, stress Myoview, persantine/adenosine Cardiolite, dobutamine echocardiography, etc. Stress tests are tests of coronary blood flow, not of plaque. Stress tests are useful in people with symptoms, like chest pain or breathlessness, since stress tests are provocative tests that can help determine whether reduced coronary blood flow is the cause behind a symptom, or whether hiatal hernia, esophagitis, gallstones, pleurisy, musculoskeletal causes, or some other process is behind symptoms. Limitations: Stress test are virtually useless in people without symptoms. This is why people like Tim Russert and Bill Clinton, both without symptoms, underwent several (Russert 3, Clinton 5) nuclear stress tests---all normal. You know what happened to them. Stress tests do not reliably uncover hidden coronary plaque in people without symptoms. Stress tests are, like coronary angiograms, non-quantitative. They are normal or abnormal. Outside of experimental settings, that's it. You can probably see why I advocate CT heart scans for tracking plaque. I do not advocate heart scans because I sell them (I don't), because scan centers pay me to say these things (they don't, and in fact my relationship with my usual heart scan centers has become deeply contentious, though I still endorse the technology). I say that heart scans are superior because they are, in 2008, the only way to 1) identify and 2) track coronary plaque that is easy, safe, low-radiation, and reasonably priced (<$200 in Milwaukee at 5 centers). The need for a technology that allows tracking of plaque, not just initial identification, is also an important distinction. People who've had some measure of atherosclerosis all catch on to this eventually. "Can I reverse it?" is an inevitable question once the disease is identified in some way. So a tool for tracking over time to gauge the success or failure of a program of prevention can be assessed. Perhaps in 10 years, another technology will emerge as the preferred means to do the same, but better. If that proves true, we will convert to that technology. But today heart scans performed on CT heart scans are the only rational way to both detect, then track, coronary atherosclerotic plaque. Let's gamble with your health 5. September 2008 William Davis
Add Boston Globe to the list of heart scan blunders 17. September 2008 William Davis (15) Yet another piece of mass media misinformation hit the airwaves today. This time it's not from the New York Times or the LA Times, both of which have previously mangled the issues surrounding heart scans. This time it's from the Boston Globe. In an article titled What is a calcium scan for heart disease, and who should undergo the test?, the report states: ". . . calcium scans may not be a good idea, or prove terribly useful, for most people. For one thing, the scans expose a patient to significant radiation - equivalent to roughly 50 chest X-rays" said Dr. Warren Manning, chief of noninvasive cardiac imaging at Beth Israel Deaconess Medical Center."As many before him, Dr. Manning is confusing two tests: CT coronary angiography and CT heart scanning. Perhaps we can't blame him: This technology has had its weakest following in the northeast, for reasons not entirely clear to me. (In fact, Track Your Plaque followers have had the greatest struggle obtaining heart scans in that part of the country.) Nonetheless, you'd think he'd have his simple facts straight before talking to the press. Unfortunately, hospital public relations departments will usually just grab whoever they can willing to talk to the press--regardless of their expertise or lack of. The story goes on to say:. . ." it's not clear what to do with the results from a calcium scan. If you have diabetes, high cholesterol, high blood pressure, or a family history of heart disease, you already know - or should know - that you are at increased risk of heart problems and should lower these risk factors. So, a calcium scan provides little additional information," Manning said. "Moreover, even a high score doesn't necessarily mean that the calcified plaque in your arteries is obstructing blood flow, said Dr. Adolph Hutter, a cardiologist at Massachusetts General Hospital.""The vast majority of people with high calcium tests don't have obstructions and they do fine long-term. So you'd have to test lots and lots of people to prevent one heart attack or sudden death," said Manning.And if you get a low calcium score, a sign of little or no calcification of plaques, that's not very useful, either, because it could be wrong, or it could be right but lull you into believing you do not have to exercise and watch your diet, cholesterol, and blood pressure levels. "You can still be at risk even if your calcium test is negative," Hutter said.It is truly shocking how little many (not all, thank goodness) of my colleagues really know about 1) heart scans, 2) coronary disease prevention, and 3) prevention in general. These same "experts" likely advocate high-dose statin drugs and low-fat diets for people at risk. They likely refer patients to the American Heart Association for diet advice and themselves obtain a lot of information from the pharmaceutical industry. The notion of identification, tracking, and purposeful reversal of coronary plaque is entirely foreign to this bunch. "The vast majority of people with high calcium tests don't have obstructions and they do fine long-term. So you'd have to test lots and lots of people to prevent one heart attack or sudden death." Well, take a look at a graph from a database of 25,000 people undergoing heart scans then observed for several years afterwards:You can see quite clearly from the curves that heart scan scores very clearly predict your future (if no preventive action is taken). The higher the score, the greater the likelihood of heart attack and death. How much clearer can it get? The most recent addition to this literature is the PREDICT study which concluded:Hazard ratios relative to CACS [coronary artery calcium scores] in the range 0-10 Agatston units (AU) were: CACS 11-100 AU, 5.4 (P = 0.02); 101-400 AU 10.5 (P = 0.001); 401-1000 AU, 11.9 (P = 0.001), and >1000 AU, 19.8 (P < 0.001). In other words, a heart scan score of >1000 is associated with a 20-fold increased risk of cardiovascular events (without preventive efforts). That kind of predictive power and quantitative confidence simply cannot be squeezed out of blood pressure and cholesterol values. How about the 2008 University of California-Irvine study from the New England Journal of Medicine (do the northeast docs even pay attention to something that is published in their own neighborhood?) that reported:There were 162 coronary events, of which 89 were major events (myocardial infarction or death from coronary heart disease). In comparison with participants with no coronary calcium, the adjusted risk of a coronary event was increased by a factor of 7.73 among participants with coronary calcium scores between 101 and 300 and by a factor of 9.67 among participants with scores above 300 (P<0.001 for both comparisons). Among the four racial and ethnic groups, a doubling of the calcium score increased the risk of a major coronary event by 15 to 35% and the risk of any coronary event by 18 to 39%. How about the Prospective Army Coronary Calcium (PACC) project (men average age 43 years):"In these men, coronary calcium was associated with an 11.8-fold increased risk for incident coronary heart disease (CHD) (p = 0.002) in a Cox model controlling for the Framingham risk score. Among those with coronary artery calcification, the risk of coronary events increased incrementally across tertiles of coronary calcium severity (hazard ratio 4.3 per tertile)." Calcium score provided additional information even after factoring in the Framingham risk score. That's just a sample of the studies. There are a number more. Add to these conversations the fact that, unlike reducing blood pressure or LDL cholesterol, the heart scan score is a quantification of the disease itself. It can also be tracked over time to gauge the success or failure of prevention efforts. To believe that blood pressure reduction or LDL cholesterol reduction is sufficient to eliminate risk is something only a fool would believe. Contary to the above statements, the data are clear:--The higher the heart scan score, the greater the risk. This has been demonstrated beyond any shadow of a doubt in at least a dozen published studies. In fact, heart scan scores outshine lipid/cholesterol values several-fold. --A person with a zero score has a nearly zero risk for cardiovascular events over a 5-year timeline. --Heart scans are the only quantitative test available of coronary atherosclerotic plaque. This means that they can be repeated to gauge progression or regression. Cholesterol does not do that. Stress tests do not do that. --Heart scans are not the same as CT coronary angiography. --The lack of "need" for a procedure does not equate to the absence of disease. The power of heart scans is that they can uncover evidence for coronary atherosclerotic plaque 10 years before a cardiac disaster strikes. Witness Tim Russert's heart scan score of 210 in 1998 at age 48. 10 years later, you know what happened. Beware the camipaign of misinformation and ignorance that continues that is hell-bent on maintaining the procedural status quo or locking us into a "drugs for all" mentality.
What's worse than sugar? 16. September 2008 William Davis (11) There are a number of ways to view the blood sugar-raising or insulin-provoking effect of foods. One way is glycemic index (GI), simply a measure of how high blood sugar is raised by a standard quantity of a food compared to table sugar. Another is glycemic load (GL), a combination (multiplied) of glycemic index and carbohydrate content per serving. Table sugar has a GI of 65, a GL of 65. Obviously, table sugar is not good for you. The content of white table sugar in the American diet has exploded over the last 100 years, totaling over 150 lb per year for the average person. (Humans are not meant to consume any.) What is the GI of Rice Krispies cereal, organic or not? GI = 82-- higher than table sugar. GL is 72, also higher than table sugar.How about Corn Flakes? GI 81, GL 70--also both higher than sugar. How about those rice cakes that many dieters will use to quell hunger? GI 78, GL 64. How about Shredded Wheat cereal? GI 75, GL 62. All of the above foods with GI's and GL's that match or exceed that of table sugar are made of wheat and cornstarch. Some, like Shredded Wheat cereal and rice cakes, don't even have any added sugar.Stay clear of these foods if you have low HDL, high triglycerides, high blood sugar, or small LDL. Or, for that matter, if you are human. Keep the eloquent words of New York University nutritionist, Marion Nestle, author of the book, Food Politics, in mind:“Food companies—just like companies that sell cigarettes, pharmaceuticals, or any other commodity—routinely place the needs of stock holders over considerations of public health. Food companies will make and market any product that sells, regardless of its nutritional value or its effect on health. In this regard, food companies hardly differ from cigarette companies. They lobby Congress to eliminate regulations perceived as unfavorable; they press federal regulatory agencies not to enforce such regulations; and when they don’t like regulatory decisions, they file lawsuits. Like cigarette companies, food companies co-opt food and nutrition experts by supporting professional organizations and research, and they expand sales by marketing directly to children, members of minority groups, and people in develop countries—whether or not the products are likely to improve people’s diets.” ??
Are sterols the new trans fat? 13. September 2008 William Davis (16) By now, I'm sure you're well-acquainted with the hydrogenated, trans fat issue.Hydrogenation of polyunsaturated oils was a popular practice (and still is) since the 1960s, as food manufacturers sought a substitute for saturated fat. Bubbling high-pressure hydrogen through oils like cottonseed, soybean, and corn generates trans fatty acids. These man-made fatty acids, while safe in initial safety testing, proved to be among the biggest nutritional mistakes of the 20th century. Trans fatty acids have been associated with increased LDL cholesterol, reduction in HDL, oxidative reactions, abnormal rigidity when incorporated into cell membranes, and cancer. Trans fats still dominate many processed foods like chips, cookies, non-dairy creamers, food mixes, and thousands of others. They're also found prominently in fast foods. Fast forward to today, and most Americans have become aware of the dangers of trans fats and many try to avoid them. But I worry there is yet another substance that has worked its way into the American processed food cornucopia that has some potential for repeating the trans fat debacle: sterol esters. Sterols are naturally-occurring oils found in vegetables, nuts, and numerous other foods in small quantities. Most of us take in 200-400 milligrams per day just by eating plant-sourced foods. Curiously, the chemical structure of sterols are very similar to human cholesterol (differing at one carbon atom). Sterols, by not fully understood means, block the intestinal absorption of cholesterol. Thus, sterol esters, as well as the similar stanol esters, have been used to reduce blood levels of total and LDL cholesterol. So far, so good. The initial commercial products, released in the late 1990s, were Take Control (sterol) and Benecol (stanol), both of which were marketed to reduce cholesterol when 2-3 tbsp are used daily, providing 3400 – 5100 mg of sterol or stanol esters, about 10- to 20-fold more than we normally obtain from foods. Several clinical trials have conclusively confirmed that these products reduce cholesterol levels. They do indeed perform as advertised. Add either product to your daily diet and LDL cholesterol is reduced by about 10-15%. In fact, in the original Track Your Plaque book, these products were advocated as a supplemental means of reducing LDL when other methods fell short. In 2008, there are now hundreds of products that have additional quantities of sterol esters in them, such as orange juice, mayonnaise, yogurt, breakfast cereals, even nutritional supplements. Most of these products proudly bear claims like "heart healthy." Stanol esters have not enjoyed the same widespread application. (I believe there may be patent issues or other considerations. However, it's the sterols that are the principal topic here, not stanols.) Now, here's where it gets a bit tricky. There is a rare (1 per million) disease called sitosterolemia, a genetic disorder that permits the afflicted to absorb more than the usual quantity of sterols from the intestine. While you and I obtain some amount of sterols from plant-based foods, absorption is poor, and we absorb <10% of sterols ingested. However, people with sitosterolemia absorb sterols far more efficiently, resulting in high blood levels of sterols that result in coronary disease and aortic valve disease, with heart attacks occurring as young as late teens or 20s. Treatment to block sterol absorption are used to treat these people. There are also a larger number, though still uncommon (1/500) of people who have only one of the two genes that young people with sitosterolemia have. These people may have an intermediate capacity for sterol absorption. Okay, so what does this have to do with you? Well, if you and I now take in 10-20 times greater amounts of sterol esters, do our blood levels of sterols increase? Several studies now suggest that, yes, sterol blood levels increase with sterol ingestion. One study from Finland, the STRIP Study, showed that children who had double usual sterol intake increased blood levels by around 50%. Similarly, a Johns Hopkins study in adults with only one of the genes ("heterozygotes") for sitosterolemia increased sterol blood levels by between 54-116% by ingesting 2200 mg of sterols added per day, despite reduction of LDL cholesterol levels. Even people with neither gene for sitosterol hyperabsorption can increase their blood levels of sterols. But the crucial question: Do the blood levels of sterols that occur in unaffected people or in heterozygotes increase the risk of coronary heart disease? The answer is not known. Despite the several clinical trials performed with sterol esters, all of them have examined LDL and total cholesterol reduction as endpoints, not cardiovascular events. It is conceivable that, while sterol esters reduce cholesterol, risk for heart disease is increased due to higher blood levels of sterols.The question is not settled. For now, it is just a suspicion. But that's enough for me to steer clear of processed foods supplemented with these uncertain sterol esters. My previous recommendations for sterol ester products will be removed with the next edition of Track Your Plaque. Until we have solid evidence that there are no adverse cardiovascular effects of sterol esters, in my view they should not be part of anyone's heart-disease prevention program. (The same argument does not seem to apply to stanol esters, such as that contained in butter-substitute Benecol, since stanol esters are not absorbed at all and remain confined to the intestine.)
The Diabetes Gold Rush 11. September 2008 William Davis (9) Lou came into the office. Clearly, his program had gone sour.Lou had initially obtained wonderful control over his heart scan score of 1114, having reversed modestly in his first three years of effort through correction of his multiple causes (including low HDL, severe small LDL, Lp(a), and a diabetic tendency). But Lou now came into the office red-faced and sporting a big bulging abdomen. Blood sugar? Now in the overtly diabetic range. Lou said that his primary care doctor had suggested that he start on three new medications (glucophage, injectable Byetta, and Actos) to control his blood sugar. His doctor also told him to increase his intake of fibers by eating more "healthy" breakfast cereals like Cheerios. Lou had apparently done just that (added "healthy" fiber-rich foods) even before his doctor had suggested it. (Lou failed to remember the several conversations we'd had about healthy eating.) Unfortunately, Lou also failed to connect his increased intake of "healthy fiber-rich foods" and his growing abdominal girth (his "wheat belly").Here's the dirty little secret: Much of the world wants you to be diabetic. It is the health gold rush of this century. "Go West, young man!" To find out what I mean, you need only ask: Who profits when people become diabetic? That's easy:The pharmaceutical industry--Diabetes is a booming growth industry, a source of tens of billions of dollars of revenue, poised for enormous growth as the population ages and gets fatter. It is common for a newly-diagnosed diabetic to be given new prescriptions for two or three drugs with a monthly cost of $300. Of course, the chronic nature of the disease make this far more profitable than, say, a two week course of antibiotics. Presently, 70 new drugs are under development. Diabetes drug maker Novo Nordisk reported a 25% increase in revenues in 2007 from diabetic agents in the North American market, along with near $2 billion increase in profit for the year. Merck's recently-released DPP-4 inhibitor, Januvia, has already sold $668 million in 2007 and is growing rapidly. The medical device and supply industry. Take a look at the Medtronic quarterly earnings report, detailing the breakdown of their record-setting quarterly revenue of $3.7 billion:Diabetes revenue of $269 million grew 12 percent driven by salesof consumables, the accessories required by insulin pump users, andcontinuous glucose monitoring products. Revenue from internationalsales grew 31 percent over the same quarter last year.That's what I call a growth industry.The processed food industry. The food industry is as big or bigger than the drug industry. ADM, Kraft, General Mills all have annual revenues in the $12-50 billion range. There are plenty of others. When we're told, for instance, that Cheerios reduces cholesterol, we're not told that it skyrockets blood sugar or triggers small LDL. When we're sold whole wheat crackers, Cocoa Puffs (which the American Heart Asscociation says is heart-healthy), or granola bars, hunger is stimulated, impulse to eat more grows, blood sugar escalates, we get fat, we get diabetic. It's a simple formula.So be aware that there is little incentive among corporate giants in the food, medical device, or drug industries to encourage behaviors that decrease the incidence of diabetes. In fact, there is enormous financial incentive to make sure that diabetes continues to grow at the startling rate it has over the last decade. To be sure, the drug and medical device industry will also develop better tools to deal with diabetes and its complications. But the very best way to deal with diabetes is to not develop it in the first place.
What else is there? 7. September 2008 William Davis (11) This question comes up frequently: Aren't there any alternatives to heart scans performed on a CT or EBT device?Yes, there are. First of all, heart scans are performed best on an electron-beam CT device (EBT) or a 64-slice multi-detector CT (MDCT) device. (While they are also obtainable through less-than-64 slice CT devices (e.g., 16 slices and less), I would advise against it because of the excessive radiation exposure and poor accuracy.) CT heart scans are not to be confused with now more popular CT coronary angiograms, which are performed on the same devices but require intravenous x-ray dye and many times more radiation.(See CT scans and radiation exposure and Heart scan frustration.) Heart scans currently form the basis for the Track Your Plaque program, a program of tracking plaque in the hopes of stopping or reversing the otherwise inevitable 30% per year increase. Let's confine our discussion to people without symptoms, meaning people like you and me sitting at home, not in an emergency room having chest pain or other similar acute symptomatic presentation. Among the other ways to uncover hidden coronary plaque:--Heart catheterization--to yield a coronary angiogram. Yes, this does tell us whether coronary plaque is present. However, it is invasive, expensive, and crude. (I've performed 5000 over my career; they are crude, though useful, tools in acute settings like unstable symptoms or heart attack, a different situation.) Coronary angiography is also non-quantitative. While they provide a value like "40% blockage mid-way in right coronary" or "90% blockage in left anterior descending" they do not provide a trackable lengthwise index of total plaque volume. Identifying severe blockages in people with symptoms leads to stents, bypass surgery and the like, but it is not practical nor of long-term usefulness in apparently, healthy people without symptoms. --Carotid ultrasound--Here's is where a lot of confusion comes from. Standard carotid ultrasound (U/S) performed in virtually every hospital and many clinics will yield crude qualitative results, e.g., "16-49% stenosis (blockage) in right internal carotid artery". The crude value range is because much of carotid U/S is based on flow velocities, not just direct visualization of the plaque itself ("2-D imaging). However, if carotid stenosis of any degree is identified, the likelihood of silent coronary plaque is much greater. Limitations: The qualitative, non-quantitative nature of carotid U/S make it difficult to follow long-term in a precise way. Also, this is carotid plaque, not coronary plaque. It makes it very difficult to follow carotid plaque as an indirect means of tracking coronary plaque. The two arterial territories, carotid and coronary, do not track together: there are divergences in many people, with carotid plaque absent in some people with advanced coronary plaque, carotid plaque more susceptible to different risk factors than coronary. So carotid U/S is helpful for its own purposes, but not terribly helpful for coronary tracking. How about carotid intimal-medial thickness (CIMT) obtained also with carotid U/S? CIMT is a useful index of bodywide atherosclerosis. CIMT is simply a measure not of plaque (and is measured in regions of the carotid artery away from plaque), but of the thickness of the lining of the carotid arteries. Everybody has a measurable CIMT, but it thickens as atherosclerosis grows. CIMT is a radiation-free test that takes several minutes. Limitations: Hardly anybody does it outside of research protocols. I know of no hospital or clinic in my area that performs CIMT, though it is slowly being adopted in some centers. It is also difficult to rely on repeated tests, because there is substantial variation when one technologist or another performs it. CIMT is also a flawed index of coronary plaque. When CIMT is compared to heart scan scores, CT coronary angiography, or conventional coronary angiography, CIMT correlates about 60-70% with the degree of coronary atherosclerosis. CIMT is therefore a useful test for research, but a distant 2nd choice--if you can obtain it. --Ankle-brachial index (ABI)--ABI is a crude measure, simply a comparison of the blood pressure (obtained with a blood pressure cuff) in the legs divided by blood pressure in the arms. The ratio is called ABI. Any ABI <1.0, meaning less pressure in the legs compared to the arms, is indirectly indicative of advanced coronary disease. ABI is, in fact, a very powerful predictor of cardiovascular events. If ABI is <1.0, your future risk for heart attack is very high, even in the absence of symptoms. Limitations: The vast majority of people with heart disease, even those having undergone stents or bypass surgery, have normal ABI's. Virtually all people with high heart scan scores have normal ABI's. In other words, ABI is a measure of very advanced atherosclerosis only. --Stress tests--I lump all stress tests together in their various forms, e.g., stress thallium, stress Cardiolite, stress Myoview, persantine/adenosine Cardiolite, dobutamine echocardiography, etc. Stress tests are tests of coronary blood flow, not of plaque. Stress tests are useful in people with symptoms, like chest pain or breathlessness, since stress tests are provocative tests that can help determine whether reduced coronary blood flow is the cause behind a symptom, or whether hiatal hernia, esophagitis, gallstones, pleurisy, musculoskeletal causes, or some other process is behind symptoms. Limitations: Stress test are virtually useless in people without symptoms. This is why people like Tim Russert and Bill Clinton, both without symptoms, underwent several (Russert 3, Clinton 5) nuclear stress tests---all normal. You know what happened to them. Stress tests do not reliably uncover hidden coronary plaque in people without symptoms. Stress tests are, like coronary angiograms, non-quantitative. They are normal or abnormal. Outside of experimental settings, that's it. You can probably see why I advocate CT heart scans for tracking plaque. I do not advocate heart scans because I sell them (I don't), because scan centers pay me to say these things (they don't, and in fact my relationship with my usual heart scan centers has become deeply contentious, though I still endorse the technology). I say that heart scans are superior because they are, in 2008, the only way to 1) identify and 2) track coronary plaque that is easy, safe, low-radiation, and reasonably priced (<$200 in Milwaukee at 5 centers). The need for a technology that allows tracking of plaque, not just initial identification, is also an important distinction. People who've had some measure of atherosclerosis all catch on to this eventually. "Can I reverse it?" is an inevitable question once the disease is identified in some way. So a tool for tracking over time to gauge the success or failure of a program of prevention can be assessed. Perhaps in 10 years, another technology will emerge as the preferred means to do the same, but better. If that proves true, we will convert to that technology. But today heart scans performed on CT heart scans are the only rational way to both detect, then track, coronary atherosclerotic plaque.