Increased blood calcium and vitamin D 21. June 2010 William Davis (50) Conventional advice tells us to supplement calcium, 1200 mg per day, to preserve bone health and reduce blood pressure.Here's a curious observation I've now witnessed a number of times: Some people who supplement this dose of calcium while also supplementing vitamin D sufficient to increase 25-hydroxy vitamin D blood levels to 60-70 ng/ml develop abnormally high levels of blood calcium, hypercalcemia.This makes sense when you realize that intestinal absorption of calcium doubles or quadruples when vitamin D approaches desirable levels. Full restoration of vitamin D therefore causes a large quantity of calcium to be absorbed, more than you may need. In addition, two studies from New Zealand suggest that 1200-1300 mg calcium with vitamin D per day doubles heart attack risk.We have 20 years of clinical studies demonstrating the very small benefits of supplementing calcium to stop or slow the deterioration of bone density (osteopenia, osteoporosis). These studies were performed with no vitamin D or with trivial doses, too small to make a difference. I believe those data have been made irrelevant in the modern age in which we "normalize" vitamin D.Should hypercalcemia develop, it is not good for you. Over long periods of time, abnormal calcium deposition can occur, leading to kidney stones, atherosclerosis, and arthritis.Until we have clarification on this issue, I have been advising patients to take no more than 600 mg calcium supplements per day. I suspect, however, that the vast majority of us require no calcium at all, provided an overall healthy diet is followed, especially one that does not leach out bone calcium. This means no foods like those made with wheat or containing powerful acids, such as those in carbonated drinks.
Heart health consultation with Dr. Joe D. Goldstrich 20. June 2010 William Davis (3) Cardiologist, nutritionist, and lipidologist, Dr. Joe D. Goldstrich, is a frequent contributor to the Track Your Plaque Forum, where we discuss the full range of issues relevant to coronary health and coronary plaque reversal.I have come to value Dr. Goldstrich's unique insights, especially in nutrition. Formerly National Director of Education and Community Programs for the American Heart Association and a physician at the Pritikin Center, his dietary philosophy has evolved away from low-fat and towards a low-carbohydrate focus, much as we use in Track Your Plaque. Like TYP, Dr. Goldstrich is always searching for better answers to gain control over coronary health. His unique blend of ideas and background has helped us craft new ideas and strategies. Dr. Goldstrich has proven especially adept at understanding how to incorporate new findings from clinical studies in our framework of coronary atherosclerotic plaque management strategies. Dr. Goldstrich is offering to share his expertise with our online community. If you would like a one-on-one phone consultation with Dr. Goldstrich, you can arrange to speak with him at his HealthyHeartConsultant.com website.
Wheat aftermath 16. June 2010 William Davis (18) Following my 4 oz whole wheat misadventure that yielded the sky-high blood sugar of 167 mg/dl, compared to einkorn wheat's 110 mg/dl, I suffered through a 36-hour period of misery. After I obtained the blood sugar of 167 mg/dl, I biked hard for one hour. This yielded a blood sugar back down in the 80s. I felt spacey in the ensuing few hours, as well as a little queasy. However, about 12 hours later, I awoke with overwhelming nausea along with that hypersalivating thing that happens just prior to vomiting. It did not come to that, but persisted all through the following day. The next morning, I could barely concentrate. Trying to read a study (admittedly on the complex topic of agricultural genetics), I had to read each paragraph 4 or 5 times. Abdominal cramps and a bloated feeling also developed, though I was able to eat. The 2nd night was filled with incredibly vivid dreams and intermittent sleeplessless. I awoke about 5 times through the night, but periods of sleep were filled with detailed, colorful dreams. I dreamt that a large corporation was secretly trying to gain control over the world's water supply, and I snuck onto a complex underwater vessel that was exploring and mapping the coastline of the Great Lakes in preparation. Weird.I recognized these odd feelings as various facets of wheat intolerance, since they were all reminiscent of feelings I used to experience before I removed wheat from my diet. They were amplified and compressed, likely because I had been wheat-free for so long. The odd thing is that, despite the modest blood sugar effect of my einkorn experience, none of the gastrointestinal or neurologic effects of wheat developed. So far, two other people with acute gastrointestinal wheat sensitivities have consumed our einkorn bread, also without reproduction of their usual symptoms. Einkorn contains gluten, though the structure of the many gluten proteins of einkorn differs from that of the wheat bread I consumed, an example of modern Triticum aestivum. 14-chromosome einkorn carries what biologists call the "A" genome, while Triticum aestivum has the combines genomes of 3 plants, the combination of the A, B, and D genomes. It is the D genome that contains the genes coding for the most obnoxious, immunogenic forms of gluten.So einkorn may not be entirely benign, but it is a good deal less obnoxious than modern Triticum aestivum.I am awaiting the reports from a few other people on their experiences.
In search of wheat: Einkorn and blood sugar 14. June 2010 William Davis (32) There are three basic aspects of wheat's adverse health effects: immune activation (e.g., celiac disease), neurologic implications (e.g., schizophrenia and ADHD), and blood sugar effects. Among the questions I'd like answered is whether ancient wheat, such as the einkorn grain I obtained from Eli Rogosa, triggers blood sugar like modern wheat.So I conducted a simple experiment on myself. On an empty stomach, I ate 4 oz of einkorn bread. On another occasion I ate 4 oz of bread that dietitian, Margaret Pfeiffer, made with whole wheat flour bought at the grocery store. Both flours were finely ground and nothing was added beyond water, yeast, olive oil, and a touch of salt.Here's what happened:Einkorn wheat bread:Blood sugar pre: 84 mg/dlBlood sugar 1-hour post: 110 mg/dlConventional wheat breadBlood sugar pre: 84 mg/dlBlood sugar 1-hour post: 167 mg/dlThe difference shocked me. I expected a difference between the two, but not that much.After the conventional wheat, I also felt weird: a little queasy, some acid in the back of my throat, a little spacey. I biked for an hour solid to reduce my blood sugar back to its starting level. I'm awaiting the experiences of others, but I'm tantalized by the possibility that, while einkorn is still a source of carbohydrates, perhaps it is one of an entirely different variety than modern Triticum aestivum wheat. The striking difference in blood sugar effects make me wonder if einkorn eaten in small quantities can keep us below the Advanced Glycation End-Product threshold.
In search of wheat: We bake einkorn bread 12. June 2010 William Davis (6) With the assistance of dietitian and health educator, Margaret Pfeiffer,MS RD CD, author of Smart 4 Your Heart and very capable chef and breadmaker (previously, before she gave up wheat), we made a loaf of bread using Eli Rogosa's einkorn wheat. Recall that einkorn wheat is the primordial 14-chromosome wheat similar to the wild wheat harvested by Neolithic humans and eaten as porridge.The essential question: Has wheat always been bad for humans or have the thousands of hybridization experiments of the last 50 years changed the structure of gluten and other proteins in Triticum aestivum and turned the "staff of life" into poison? I turn to einkorn wheat, the "original" wheat unaltered by human manipulations, to figure this out. While einkorn wheat is still a source of carbohydrates, is it something we might indulge in once in a while without triggering the adverse phenomena associated with modern wheat? Here's what we did:This is the einkorn grain as we received it from Eli's farm. This was enough to make one loaf (approximately 3 cups). The einkorn grain is a dark golden color. I tried chewing them. They taste slightly nutty. They soften as they sit in your mouth.Here's Margaret putting the einkorn grain into the electric grinder.We tried to grind the grain by hand with mortar and pestle, but this proved far more laborious than I anticipated. After about 15 minutes of grinding, this is what I got:Barely 2 tablespoons. That's when Margaret fired up the electric grinder. (I can't imagine having to grind up enough flour by hand for an entire family. Perhaps that's why ancient cultures were thin despite eating wheat. They were just exhausted!)We added water, salt, and yeast, then put the mix into an electric breadmaker to knead the dough and keep it warm. We let the dough rise for 90 minutes, much longer than conventional dough. The einkorn dough "rose" very little. Margaret tells me that most dough made with conventional flour rises to double its size. The einkorn dough increased no more than 20-30%.The einkorn dough also distinctly smelled like peanut butter.After rising, we baked the dough at 350 degrees F for 30 minutes. This is the final product.Because I want to gauge health effects, not taste, the bread we made had no added sugar or anything else to modify taste or physiologic effect.On first tasting, the einkorn bread is mildly nutty and heavy. It had an unusual sour or astringent taste at the end, but overall tasted quite good. Next: What happens when we eat it? I'm going to give the einkorn bread (I've got to make some more) to people who experience acute reactions to conventional wheat and see if the einkorn does the same. I will also assess blood sugar effects since, after all, hybridizations or no, it is still a carbohydrate. Margaret Pfeiffer's book is available on Amazon:
Ezekiel said what? 10. June 2010 William Davis All posts by william-davis Toggle navigation Home Blog Home Archive Join Now Log in Fat and fiber composition of nuts 30. November 2008 William Davis (16) From Mukuddem-Petersen J, Oosthuizen1 W, Jerling JC. J Nutr 2005.If you haven't yet done so, adding raw nuts to your health program yields a broad panel of health benefits.Contrary to conventional advice, nuts can be eaten in unlimited quantities. Provided they are raw--unroasted, unsalted (since salting only accompanies roasted nuts), not roasted in unhealthy oils like hydrogenated cottonseed or soybean (very common)--they do not make you fat, regardless of the quantity consumed. Beer nuts, honey-roasted nuts, mixed nuts roasted in unhealthy oils with salt added are either fattening or exert other unhealthy effects (e.g., hypertension, rise in Lp(a), and cancer from the hydrogenated fats). Some notable observations from the chart:--Hazelnuts and macadamians are the richest in monounsaturates--Walnuts are the richest in the omega-6 linoleic acid, while also richest in the "omega-3" linolenic acid. --From a fat composition standpoint, raw cashews and dry roasted peanuts aren't so bad. --Pistachios figure pretty favorably in this analysis, rich in monounsaturates. --Coconuts are unusually rich in saturated fat, though about half is lauric acid--an issue for future conversation. Here's a listing of the fiber composition of nuts per 1 oz serving (about a handful):Almonds (24 nuts) 3.5 gBrazilnuts, dried (6-8 nuts) 2.1 gCashew nuts, dry roasted, with salt added (18 nuts) 0.9 gHazelnuts or filberts 2.7 gMacadamia nuts, dry roasted, with salt added (10-12 nuts) 2.3 gMixed nuts, dry roasted, with peanuts, with salt added 2.6 gPeanuts, all types, dry-roasted, without salt 2.3 gPecans (20 halves) 2.7 gPine nuts, dried 1.0 gPistachio nuts, dry roasted, with salt added (47 nuts) 2.9 gWalnuts, English (14 halves) 1.9 gData courtesy USDA Nutrient DatabaseNote that almonds are the winners with 3.5 grams fiber per ounce, pistachios a close second. Pine nuts and cashews place last on the fiber content chart. Not addressed by the charts is protein content of nuts, as well as the low sugar content, all additional beneficial aspects of nuts. Nuts are also a moderate source of magnesium (though seeds like pumpkin and sunflower shine in the magnesium content area).Rather than micromanage the specific fat and fiber content of your diet, why not get a little of the good of everything on the list and just mix and match the nuts? (Mixed and matched on your own, of course, not a hydrogenated cottonseed oil nut mixture). Flush-free niacin kills 29. November 2008 William Davis (12) Here, I re-post a conversation I've posted before, that of the scam product, "no-flush" niacin, also known as "flush-free" niacin. I find this issue particularly bothersome, since I have a patient or two each and every week who forgets the explicit advice I gave them to avoid these scam products altogether. Despite costing more than conventional niacin, they exert no effect, beneficial or otherwise. Niacin--the real thing--exerts real and substantial beneficial effects. No-flush or flush-free does nothing except drain your wallet. I continue to marvel at the fact that supplement manufacturers persist in selling this product. Ironically, it commands a significant premium over other niacin forms. They are outright scams that should be avoided altogether. My former post, No-flush niacin kills: Gwen was miserable and defeated. No wonder. After a bypass operation failed just 12 months earlier with closure of 3 out of 4 bypass grafts, she has since undergone 9 heart catheterization procedures and received umpteen stents. She presented to me for an opinion on why she had such aggressive coronary disease (despite Lipitor). No surprise, several new causes of heart disease were identified, including a very severe small LDL pattern: 100% of LDL particles were small. Given her stormy procedural history, I urged Gwen to immediately drop all processed carbohydrates from her diet, including any food made from wheat or corn starch. (She and her husband were shocked by this, by the way, since she'd been urged repeatedly to increase her whole grains by the hospital dietitians.) I also urged her to begin to lose the 30 lbs of weight that she'd gained following the hospital dietitians' advice. She also added fish oil at a higher-than-usual dose. I asked her to add niacin, among our most effective agents for reduction of small LDL particles, not to mention reduction of the likelihood of future cardiovascular events. Although I instructed Gwen on where and how to obtain niacin, she went to a health food store and bought "no-flush niacin," or inositol hexaniacinate. She was curious why she experienced none of the hot flush I told her about. When she came back to the office some weeks later to review her treatment program, she told me that chest pains had returned. On questioning her about what she had changed specifically, the problem became clear: She'd been taking no-flush niacin, rather than the Slo-Niacin I had recommended. What is no-flush niacin? It is inositol hexaniacinate, a molecule that indeed carries six niacin molecules attached to an inositol backbone. Unfortunately, it exerts virtually no effect in humans. It is a scam. Though I love nutritional supplements in general, it pains me to know that supplement distributors and health food stores persist in selling this outright scam product that not only fails to exert any of the benefits of real niacin, it also puts people like Gwen in real danger because of its failure to provide the effects she needed. So, if niacin saves lives, no-flush niacin in effect could kill you. Avoid this scam like the plague. No-flush niacin does not work. Period. Disclosure: I have no financial or other relationship with Upsher Smith, the manufacturer of Slo-Niacin. Copyright 2008 William Davis, MD CT coronary angiography is NOT a screening procedure 28. November 2008 William Davis (3) I've recently had several hospital employees tell me that their hospitals offered CT coronary angiograms without charge to their employees. Among these hospital employees were several women in their 30s and 40s. Why would young, asymptomatic, pre-menopausal women be subjected to the equivalent of 100 chest x-rays or 25 mammograms? Is there an imminent, life-threatening, symptomatic problem here?All of these women were without symptoms, some were serious exercisers. There is NO rational justification for performing CT coronary angiography, free or not.What they really want is some low-risk, yet confident means of identifying risk for heart disease. Cholesterol, of course, is a miserable failure in this arena. Framingham risk scoring? Don't make me laugh. Step in CT coronary angiography. But does CT coronary angiography provide the answers they are looking for? Well, it provides some of the answers. It does serve to tell each woman whether she "needs" a heart procedure like heart catheterization, stent, or bypass surgery, since the intent of CT angiography is to identify "severe" blockages, sufficient to justify heart procedures. Pitfalls: Because of the radiation exposure, CT angiography is not a procedure that can be repeated periodically to reassess the status of any abnormal findings. A CT angiogram every year? After just four years, the equivalent of 400 chest x-rays will have been performed, or 100 mammograms. Cancer becomes a very real risk at this point. CT angiography is also not quantitative. Sure, it can provide a crude estimation of the percent blockage--the value your cardiologist seeks to "justify" a stent. But it does NOT provide a longitudinal (lengthwise) quantification of plaque volume, a measure of total plaque volume that can be tracked over time. What's a woman to do? Simple: Get the test that, at least in 2008, provides the only means of gauging total lengthwise coronary plaque volume: a simple CT heart scan, a test performed with an equivalent of 4 - 10 chest x-rays, or 1 - 2.5 mammograms.Perhaps, in future, software and engineering improvements will be made with CT coronary angiography that reduce radiation to tolerable levels and allows the lengthwise volume measurement of plaque. But that's not how it's done today. The Wheat Deficiency Syndrome 26. November 2008 William Davis (21) Beware the dreaded Wheat Deficiency Syndrome. Like any other syndrome, you can recognize this condition by its many tell-tale signs:--Flat abdomen--Rapid weight loss--High energy--Less mood swings--Better sleep--Diminished appetite--Reduced blood sugar--Reduced blood pressure--Reduced small LDL and total LDL--Increased HDL--Reduced triglycerides--Reduced C-reactive protein and other inflammatory measuresOf course, you could choose to cure yourself of this syndrome simply by taking the antidote: foods made with wheat flour, like bread, breakfast cereals, pastas, pretzels, crackers, and muffins. All the signs of the syndrome will then disappear and you can have back your protuberant abdomen, irrational mood swings, exagerrated appetite, higher blood sugar, etc. The Framingham Crap Shoot 22. November 2008 William Davis (2) The Framingham risk score is a risk-assessment tool that has become the basis for heart disease prediction used by practicing physicians. The Framingham system determines that:· 35% of the adult population in the U.S., or 70 million, is deemed “low-risk.” Low-risk is defined as the absence of standard risk factors for heart disease; low-risk persons have no more than a 1-in-20 chance (5%) of dying from heart disease in the next 10 years. Physicians are advised by the American Heart Association (AHA) and its experts that no specific effort at risk reduction is necessary. · 25%, or approximately 50 million, U.S. adults are deemed “high-risk,” based on the presence of 2 or more risk factors. High-risk persons experience a 20%-30% likelihood of heart attack in the next 10 years. People at high-risk are candidates for preventive efforts according to the guidelines set by the Adult Treatment Panel-III (Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults; ATP-III) for cholesterol-reducing statin drug treatment and for “lifestyle-modifying” advice. · The remaining 40% of the adult population, or 80 million people, are judged “intermediate-risk,” with the likelihood of heart attack between 5-20% over the next 10 years. This group should receive preventive advice and might be considered for statin drug treatment. Let’s do some arithmetic. By the above scheme, the low-risk population will experience 3,500,000 heart attacks over the next decade, or 350,000 heart attacks per year. The intermediate-risk population (without preventive treatment) will experience 8,000,000 heart attacks over the 10-year time period, or 800,000 per year. The high-risk population, the group most likely to receive standard advice on diet, exercise, and be prescribed statin cholesterol drugs, will have their risk reduced by 35% by preventive efforts over the 10-year period. This means that heart attacks over 10 years will be reduced from 12,500,000 to 8,125,000 by standard prevention efforts, or reduced to 812,500 heart attacks per year. These numbers are no secret. They are well known facts that have simply come to be accepted by the medical community. In other words, the standard approach to heart attack prediction makes the fact that two million people will succumb to cardiovascular events in the next year no mystery. This exercise in prediction is coldly accurate when applied to a large population.The problem is that this approach cannot reliably distinguish which individuals will have a heart attack from those who will not. From 100 people chosen at random, for instance, the numbers game played above will not confidently identify who among those 100 will have a heart attack, who will not, who will develop anginal chest pains and end up with stents or bypass surgery, or who will die. We just know that some of them will. Some people at high risk will have a heart attack, some people at intermediate risk will have a heart attack, some people at low risk will have a heart attack. For any specific individual (like you or me), it’s a crap shoot.That's why precise individual measurement of cardiovascular risk is required for real risk assessment, not applying broad statistical observations and forcing them to conform to the unique life of a specific individual, particularly risk calculators with as few risk parameters as the Framingham risk score. At what score should a heart catheterization be performed? 21. November 2008 William Davis (2) That's easy: NONE. (Although I've addressed this previously, the question has come up again many times and I thought it'd be worth repeating.)In other words, no heart scan score--100, 500, 1000, 5000--should lead automatically to procedures in someone who underwent a heart scan but has no symptoms. This question is a common point of confusion. In other words, is there a specific cut-off that automatically triggers a need for catheterization? In my view, there is no such score. We can't say, for instance, that everybody with a score above 1000 should have a catheterization. It is true that the higher your score, the greater the likelihood of a plaque blocking flow. A score of 1000 carries an approximately 25-30% likelihood of reduced blood flow sufficient to consider a stent or bypass. This can nearly always be settled with a stress test. Recall that, despite their pitfalls for uncovering hidden heart disease in the first place, stress tests are useful as gauges of coronary blood flow. But even a score of 1000 carries a 70-75% likelihood that a procedure will not be necessary. This is too high to justify doing heart catheterizations willy-nilly. Unfortunately, some of my colleagues will say that any heart scan score justifies a heart cath. I believe this is absolutely, unquestionably, and inexcusably wrong. More often than not, this attitude is borne out of ignorance, laziness, or a desire for profit. Does every lump or bump justify surgery, radiation, and chemotherapy on the chance it could represent cancer? Of course not. There is indeed a time and place for these things, but judgment is involved. In my view, no heart scan score should automatically prompt a major heart procedure like heart catheterization in a person without symptoms. If a stress test is normal, signifying normal coronary flow (and there are no other abnormal phenomena, such as abnormal left ventricular function), then there is no defensible rationale for heart procedures. Heart procedures like stents and bypass cannot prevent heart attacks in future; they can only restore flow when flow is poor, or stop the heart attack that is about to occur. However, EVERY heart scan score above zero is a reason to engage in a program of prevention. "It's genetic" 17. November 2008 William Davis (17) At 53, Sam had been through the wringer with heart disease. After his first heart attack at age 50, he'd undergone four heart catheterizations, 5 stents, and, most recently, a bypass operation. He came to us to see if there was a better solution. After hearing Sam's story, I asked,"Did your doctors suggest to you why you had heart disease?" "Well, they said it was genetic, since my father went through the same thing in his early 50s, though he died after his second heart attack at age 54. They said it was bad luck and nothing could be done about it."Though Sam's case is more dramatic than most, I hear this argument every day: Risk for heart disease is genetic. It's true: There are indeed multiple reasons for inheriting causes for coronary heart disease, genes that heighten inflammatory responses, oxidative responses, modify lipoprotein particles, increase blood pressure, etc. There has even been some excitement over developing chromosomal markers for heightened risk. That's all well and fine, but what can we do about it today?In practical life, many inherited genetic patterns can be expressed in ways that you and I can identify--and correct. They are not chromosomal markers, but end products of genetic patterns. (Although there are indeed identifiable chromosomal markers, they have not yet led to meaningful treatments to my knowledge.) These readily identifiable patterns include:--Lipoprotein(a)--Clearly genetically transmitted, passed from mother or father to each child with a 50% likelihood, then you onto your children if you have it. --Small LDL--Although small LDL is amplified by high-carbohydrate diets and obesity, it can also occur in slender people who do not indulge in carbohydrates --i.e., a genetic tendency. Or, it can be a combination of poor lifestyle magnifying the genetic tendency for small LDL.--Low HDL--Particularly the extremes of low HDL below 30 mg/dl. (Although, interestingly, I am seeing more of these people, though not all, respond to vitamin D replacement. Perhaps an important subgroup of low HDL people are really Vitamin D Receptor (VDR) variants.)--ApoE--Two variants are relevant: ApoE2 and ApoE4. In my experience, it's the E2 that carries far greater significance, though the data are somewhat scanty. ApoE4 people are more sensitive to the fats in their diet (greater rises in LDL with fats; thus, some people advocate a tighter saturated fat restriction with this pattern, though I am not convinced that is the best solution), while ApoE2 people are exceptionally sensitive to carbohydrates, develop extravagant increases in triglycerides, and are very diabetes-prone with even the most minimal weight gain. If two "doses" of the E2 gene are present (homozygotic), then the tendencies are very exagerrated. E4 people are also subject to greater likelihood of Alzheimer's, though it is not a certain risk in a specific individual. --Postprandial disorders--We use the fasting intermediate-density lipoprotein (IDL) as an easy, obtainable index of the ability to clear after-eating byproducts of meals from the blood. Increased IDL has been related to increased coronary, carotid, and aortic aneurysmal disease. --Hypertriglyceridemia-i.e., increases in triglycerides, While not all forms of high triglycerides confer risk for atherosclerosis, many do, particularly if associated with IDL, small LDL, increased LDL particle number and/or apoB. There are more, but you get the point. There are clear-cut genetically-transmitted reasons for greater risk for cardiovascular disease. Some, like lipoprotein(a), yield very high risk. Others, like increased triglycerides, yield mixed levels of risk. Importantly, all of these patterns--ALL--are identifiable and are treatable. Treatment may not always be the easiest thing, but they are treatable nonetheless. While lipoprotein(a), for instance, is the most difficult pattern to correct in the above list, I remind everyone that our current "record holder" for reversal of plaque and heart scan scores--63% reduction--has lipoprotein(a) that we corrected. If you've been told that your risk for cardiovascular disease or coronary plaque is "genetic" and thereby uncorrectable and hopeless, run the other direction as fast as you can. Get another opinion from someone willing to take the modest effort to tell you precisely why. Tim Russert Revisited 16. November 2008 William Davis (7) A Heart Scan Blog reader brought this piece by Dr. MacDougall to my attention. Dr. MacDougall created a fictitious posthumous conversation between himself and the late Tim Russert. MacDougall paints a picture of a hardworking, hard-living man who adhered to an overindulgent lifestyle of excessive eating. He concludes that a vegetarian, low-fat diet would have saved his life. Beyond being disrespectful, I would differ with Dr. MacDougall’s assessment. In fact, I’ve heard an interview with Mr. Russert’s primary care physician in which the doctor claimed that Mr. Russert had been counseled on the need for a low-fat diet and, in fact, adhered to it quite seriously. Far from being an overindulgent, overeating gourmand, he followed the dictates of conventional dietary wisdom according to the American Heart Association. The low-fat diet articulated by Dr. MacDougall is simply a little more strict than that followed by Mr. Russert.What exactly could Mr. Russert have done to prolong his life? Several basic strategies:--Added fish oil. This simple strategy alone would have reduced the likelihood of dying suddenly by almost half. --Eliminated wheat and cornstarch—Mr. Russert developed diabetes in the last few years of his life. By definition, diabetes is an inability to handle sugars and sugar-equivalents. Wheat and cornstarch yield immediate and substantial surges in blood sugar greater than table sugar; elimination causes weight to plummet, blood sugar to drop, and diabetes (at least in its early phases) can be eliminated in many people, particularly those beginning with substantial excess weight.Just those two strategies alone would more than likely have avoided the tragic death that brought Mr. Russert’s wonderful life and career to an abrupt end. Of course, he could have even taken his heart health program even further, as we do in the Track Your Plaque program. While the conversation has focused on how to avoid tragic events like sudden cardiac death, why not take it a step farther and ask, "How can coronary plaque be measured, tracked, and reversed?"In that vein, Mr. Rusert could have restored vitamin D to normal levels; identified all hidden sources of heart disease using lipoprotein testing (though he had small LDL without a doubt, given his generous waist size, HDL of 36 mg/dl and high triglycerides); considered niacin. Simple, yet literally lifesaving efforts, that make reversal much more likely. Those simple steps, in fact, would have tipped the scales heavily in Mr. Russert’s favor, making a heart attack and/or sudden death from heart disease exceptionally unlikely. Water: Bottled vs. tap 16. November 2008 William Davis (4) The Fanatic Cook has a great post discussing the findings of the Environmental Working Group (EWG) on the quality of bottled water. The full text of the study from the EWG can be viewed here. They report that "the bottled water industry promotes an image of purity, but comprehensive testing by the Environmental Working Group (EWG) reveals a surprising array of chemical contaminants in every bottled water brand analyzed" . . . After analyzing 10 brands, they conclude that "tests strongly indicate that the purity of bottled water cannot be trusted. Given the industry's refusal to make available data to support their claims of superiority, consumer confidence in the purity of bottled water is simply not justified.""EWG's study has revealed that bottled water can contain complex mixtures of industrial chemicals never tested for safety, and may be no cleaner than tap water. Given some bottled water company's failure to adhere to the industry's own purity standards, Americans cannot take the quality of bottled water for granted. Indeed, test results like those presented in this study may give many Americans reason enough to reconsider their habit of purchasing bottled water and turn back to the tap."For these reasons, as well as environmental reasons (plastic bottles filling up dumpsites), I think it is becoming clearer and clearer that bottled water is something we should only use in a pinch, not habitually. Can CRP be reduced? 13. November 2008 William Davis (17) The JUPITER study has sparked a lot of discussion about c-reactive protein, or CRP. If we follow the line of reasoning that prompted this study, reducing CRP may correlate with reduction of cardiovascular events. Thus, in the JUPITER study, Crestor 20 mg per day reduced cardiovascular events by nearly half. From a CRP perspective, starting values were 4.2 mg/dl in the Crestor group of the trial, 4.3 mg/dl in the placebo group. After 24 months, CRP in the Crestor group was 2.2 mg/dl, 3.5 mg/dl in the placebo group, representing a 37% reduction.Now, in our Track Your Plaque program--an experience that has yielded the virtual ELIMINATION of cardiovascular events--we aim for a CRP level of 1.0 mg/dl or less, ideally 0.5 mg/dl or less. The majority of people achieve these ambitious levels. In fact, it is a rare person who does not.How do we achieve dramatic reductions in CRP? We use:--Weight loss through elimination of wheat and cornstarch--This yields impressive reductions. --Vitamin D--I have no doubt whatsoever of vitamin D's capacity to exert potent anti-inflammatory effects. I am not entirely sure why this happens (enhanced sensitivity to insulin, reduced expression of tissue inflammatory proteins like matrix metalloproteinase and others, etc.), but the effect is profound. --Elimination of junk foods--like candies, cookies, pretzels, rice cakes, potato chips, etc. --Exercise--Amplifies the benefits of diet on CRP reduction. --Not allowing saturated fats to dominate--Yes, yes, I know. The demonization of saturated fat conversation has been largely replaced by the Taubesian saturated fat has not been confidently linked to heart disease conversation. But controlled feeding studies, in which a single component of diet is manipulated (e.g., saturated vs. monounsaturated vs. polyunsaturated fat) have clearly shown that saturated fats do activate several factors in the inflammatory response. --Fish oil--Though I am a firm believer in the huge benefits of omega-3 fatty acid supplementation/restoration, the anti-inflammatory effect is modest from a CRP perspective. However, there are anti-inflammatory benefits beyond that of simple CRP (via normalization of eicosanoid metabolism and other pathways). --Weight loss--A BIG effect. Weight loss drops CRP like a stone. The CRP-reducing effect is especially large if achieved via carbohydrate reduction. Of course, this is much more complicated than taking a pill. But it is effective to achieve health benefits outside of cardiovascular risk, is enormously useful as part of a weight loss effort, and doesn't cost $1400 per year like Crestor. In short, if CRP reduction is the goal, it certainly does not have to involve Crestor. << Older posts Newer posts >> Newer posts12...484950515253545556...121122Older posts
Fat and fiber composition of nuts 30. November 2008 William Davis (16) From Mukuddem-Petersen J, Oosthuizen1 W, Jerling JC. J Nutr 2005.If you haven't yet done so, adding raw nuts to your health program yields a broad panel of health benefits.Contrary to conventional advice, nuts can be eaten in unlimited quantities. Provided they are raw--unroasted, unsalted (since salting only accompanies roasted nuts), not roasted in unhealthy oils like hydrogenated cottonseed or soybean (very common)--they do not make you fat, regardless of the quantity consumed. Beer nuts, honey-roasted nuts, mixed nuts roasted in unhealthy oils with salt added are either fattening or exert other unhealthy effects (e.g., hypertension, rise in Lp(a), and cancer from the hydrogenated fats). Some notable observations from the chart:--Hazelnuts and macadamians are the richest in monounsaturates--Walnuts are the richest in the omega-6 linoleic acid, while also richest in the "omega-3" linolenic acid. --From a fat composition standpoint, raw cashews and dry roasted peanuts aren't so bad. --Pistachios figure pretty favorably in this analysis, rich in monounsaturates. --Coconuts are unusually rich in saturated fat, though about half is lauric acid--an issue for future conversation. Here's a listing of the fiber composition of nuts per 1 oz serving (about a handful):Almonds (24 nuts) 3.5 gBrazilnuts, dried (6-8 nuts) 2.1 gCashew nuts, dry roasted, with salt added (18 nuts) 0.9 gHazelnuts or filberts 2.7 gMacadamia nuts, dry roasted, with salt added (10-12 nuts) 2.3 gMixed nuts, dry roasted, with peanuts, with salt added 2.6 gPeanuts, all types, dry-roasted, without salt 2.3 gPecans (20 halves) 2.7 gPine nuts, dried 1.0 gPistachio nuts, dry roasted, with salt added (47 nuts) 2.9 gWalnuts, English (14 halves) 1.9 gData courtesy USDA Nutrient DatabaseNote that almonds are the winners with 3.5 grams fiber per ounce, pistachios a close second. Pine nuts and cashews place last on the fiber content chart. Not addressed by the charts is protein content of nuts, as well as the low sugar content, all additional beneficial aspects of nuts. Nuts are also a moderate source of magnesium (though seeds like pumpkin and sunflower shine in the magnesium content area).Rather than micromanage the specific fat and fiber content of your diet, why not get a little of the good of everything on the list and just mix and match the nuts? (Mixed and matched on your own, of course, not a hydrogenated cottonseed oil nut mixture).
Flush-free niacin kills 29. November 2008 William Davis (12) Here, I re-post a conversation I've posted before, that of the scam product, "no-flush" niacin, also known as "flush-free" niacin. I find this issue particularly bothersome, since I have a patient or two each and every week who forgets the explicit advice I gave them to avoid these scam products altogether. Despite costing more than conventional niacin, they exert no effect, beneficial or otherwise. Niacin--the real thing--exerts real and substantial beneficial effects. No-flush or flush-free does nothing except drain your wallet. I continue to marvel at the fact that supplement manufacturers persist in selling this product. Ironically, it commands a significant premium over other niacin forms. They are outright scams that should be avoided altogether. My former post, No-flush niacin kills: Gwen was miserable and defeated. No wonder. After a bypass operation failed just 12 months earlier with closure of 3 out of 4 bypass grafts, she has since undergone 9 heart catheterization procedures and received umpteen stents. She presented to me for an opinion on why she had such aggressive coronary disease (despite Lipitor). No surprise, several new causes of heart disease were identified, including a very severe small LDL pattern: 100% of LDL particles were small. Given her stormy procedural history, I urged Gwen to immediately drop all processed carbohydrates from her diet, including any food made from wheat or corn starch. (She and her husband were shocked by this, by the way, since she'd been urged repeatedly to increase her whole grains by the hospital dietitians.) I also urged her to begin to lose the 30 lbs of weight that she'd gained following the hospital dietitians' advice. She also added fish oil at a higher-than-usual dose. I asked her to add niacin, among our most effective agents for reduction of small LDL particles, not to mention reduction of the likelihood of future cardiovascular events. Although I instructed Gwen on where and how to obtain niacin, she went to a health food store and bought "no-flush niacin," or inositol hexaniacinate. She was curious why she experienced none of the hot flush I told her about. When she came back to the office some weeks later to review her treatment program, she told me that chest pains had returned. On questioning her about what she had changed specifically, the problem became clear: She'd been taking no-flush niacin, rather than the Slo-Niacin I had recommended. What is no-flush niacin? It is inositol hexaniacinate, a molecule that indeed carries six niacin molecules attached to an inositol backbone. Unfortunately, it exerts virtually no effect in humans. It is a scam. Though I love nutritional supplements in general, it pains me to know that supplement distributors and health food stores persist in selling this outright scam product that not only fails to exert any of the benefits of real niacin, it also puts people like Gwen in real danger because of its failure to provide the effects she needed. So, if niacin saves lives, no-flush niacin in effect could kill you. Avoid this scam like the plague. No-flush niacin does not work. Period. Disclosure: I have no financial or other relationship with Upsher Smith, the manufacturer of Slo-Niacin. Copyright 2008 William Davis, MD
CT coronary angiography is NOT a screening procedure 28. November 2008 William Davis (3) I've recently had several hospital employees tell me that their hospitals offered CT coronary angiograms without charge to their employees. Among these hospital employees were several women in their 30s and 40s. Why would young, asymptomatic, pre-menopausal women be subjected to the equivalent of 100 chest x-rays or 25 mammograms? Is there an imminent, life-threatening, symptomatic problem here?All of these women were without symptoms, some were serious exercisers. There is NO rational justification for performing CT coronary angiography, free or not.What they really want is some low-risk, yet confident means of identifying risk for heart disease. Cholesterol, of course, is a miserable failure in this arena. Framingham risk scoring? Don't make me laugh. Step in CT coronary angiography. But does CT coronary angiography provide the answers they are looking for? Well, it provides some of the answers. It does serve to tell each woman whether she "needs" a heart procedure like heart catheterization, stent, or bypass surgery, since the intent of CT angiography is to identify "severe" blockages, sufficient to justify heart procedures. Pitfalls: Because of the radiation exposure, CT angiography is not a procedure that can be repeated periodically to reassess the status of any abnormal findings. A CT angiogram every year? After just four years, the equivalent of 400 chest x-rays will have been performed, or 100 mammograms. Cancer becomes a very real risk at this point. CT angiography is also not quantitative. Sure, it can provide a crude estimation of the percent blockage--the value your cardiologist seeks to "justify" a stent. But it does NOT provide a longitudinal (lengthwise) quantification of plaque volume, a measure of total plaque volume that can be tracked over time. What's a woman to do? Simple: Get the test that, at least in 2008, provides the only means of gauging total lengthwise coronary plaque volume: a simple CT heart scan, a test performed with an equivalent of 4 - 10 chest x-rays, or 1 - 2.5 mammograms.Perhaps, in future, software and engineering improvements will be made with CT coronary angiography that reduce radiation to tolerable levels and allows the lengthwise volume measurement of plaque. But that's not how it's done today.
The Wheat Deficiency Syndrome 26. November 2008 William Davis (21) Beware the dreaded Wheat Deficiency Syndrome. Like any other syndrome, you can recognize this condition by its many tell-tale signs:--Flat abdomen--Rapid weight loss--High energy--Less mood swings--Better sleep--Diminished appetite--Reduced blood sugar--Reduced blood pressure--Reduced small LDL and total LDL--Increased HDL--Reduced triglycerides--Reduced C-reactive protein and other inflammatory measuresOf course, you could choose to cure yourself of this syndrome simply by taking the antidote: foods made with wheat flour, like bread, breakfast cereals, pastas, pretzels, crackers, and muffins. All the signs of the syndrome will then disappear and you can have back your protuberant abdomen, irrational mood swings, exagerrated appetite, higher blood sugar, etc.
The Framingham Crap Shoot 22. November 2008 William Davis (2) The Framingham risk score is a risk-assessment tool that has become the basis for heart disease prediction used by practicing physicians. The Framingham system determines that:· 35% of the adult population in the U.S., or 70 million, is deemed “low-risk.” Low-risk is defined as the absence of standard risk factors for heart disease; low-risk persons have no more than a 1-in-20 chance (5%) of dying from heart disease in the next 10 years. Physicians are advised by the American Heart Association (AHA) and its experts that no specific effort at risk reduction is necessary. · 25%, or approximately 50 million, U.S. adults are deemed “high-risk,” based on the presence of 2 or more risk factors. High-risk persons experience a 20%-30% likelihood of heart attack in the next 10 years. People at high-risk are candidates for preventive efforts according to the guidelines set by the Adult Treatment Panel-III (Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults; ATP-III) for cholesterol-reducing statin drug treatment and for “lifestyle-modifying” advice. · The remaining 40% of the adult population, or 80 million people, are judged “intermediate-risk,” with the likelihood of heart attack between 5-20% over the next 10 years. This group should receive preventive advice and might be considered for statin drug treatment. Let’s do some arithmetic. By the above scheme, the low-risk population will experience 3,500,000 heart attacks over the next decade, or 350,000 heart attacks per year. The intermediate-risk population (without preventive treatment) will experience 8,000,000 heart attacks over the 10-year time period, or 800,000 per year. The high-risk population, the group most likely to receive standard advice on diet, exercise, and be prescribed statin cholesterol drugs, will have their risk reduced by 35% by preventive efforts over the 10-year period. This means that heart attacks over 10 years will be reduced from 12,500,000 to 8,125,000 by standard prevention efforts, or reduced to 812,500 heart attacks per year. These numbers are no secret. They are well known facts that have simply come to be accepted by the medical community. In other words, the standard approach to heart attack prediction makes the fact that two million people will succumb to cardiovascular events in the next year no mystery. This exercise in prediction is coldly accurate when applied to a large population.The problem is that this approach cannot reliably distinguish which individuals will have a heart attack from those who will not. From 100 people chosen at random, for instance, the numbers game played above will not confidently identify who among those 100 will have a heart attack, who will not, who will develop anginal chest pains and end up with stents or bypass surgery, or who will die. We just know that some of them will. Some people at high risk will have a heart attack, some people at intermediate risk will have a heart attack, some people at low risk will have a heart attack. For any specific individual (like you or me), it’s a crap shoot.That's why precise individual measurement of cardiovascular risk is required for real risk assessment, not applying broad statistical observations and forcing them to conform to the unique life of a specific individual, particularly risk calculators with as few risk parameters as the Framingham risk score.
At what score should a heart catheterization be performed? 21. November 2008 William Davis (2) That's easy: NONE. (Although I've addressed this previously, the question has come up again many times and I thought it'd be worth repeating.)In other words, no heart scan score--100, 500, 1000, 5000--should lead automatically to procedures in someone who underwent a heart scan but has no symptoms. This question is a common point of confusion. In other words, is there a specific cut-off that automatically triggers a need for catheterization? In my view, there is no such score. We can't say, for instance, that everybody with a score above 1000 should have a catheterization. It is true that the higher your score, the greater the likelihood of a plaque blocking flow. A score of 1000 carries an approximately 25-30% likelihood of reduced blood flow sufficient to consider a stent or bypass. This can nearly always be settled with a stress test. Recall that, despite their pitfalls for uncovering hidden heart disease in the first place, stress tests are useful as gauges of coronary blood flow. But even a score of 1000 carries a 70-75% likelihood that a procedure will not be necessary. This is too high to justify doing heart catheterizations willy-nilly. Unfortunately, some of my colleagues will say that any heart scan score justifies a heart cath. I believe this is absolutely, unquestionably, and inexcusably wrong. More often than not, this attitude is borne out of ignorance, laziness, or a desire for profit. Does every lump or bump justify surgery, radiation, and chemotherapy on the chance it could represent cancer? Of course not. There is indeed a time and place for these things, but judgment is involved. In my view, no heart scan score should automatically prompt a major heart procedure like heart catheterization in a person without symptoms. If a stress test is normal, signifying normal coronary flow (and there are no other abnormal phenomena, such as abnormal left ventricular function), then there is no defensible rationale for heart procedures. Heart procedures like stents and bypass cannot prevent heart attacks in future; they can only restore flow when flow is poor, or stop the heart attack that is about to occur. However, EVERY heart scan score above zero is a reason to engage in a program of prevention.
"It's genetic" 17. November 2008 William Davis (17) At 53, Sam had been through the wringer with heart disease. After his first heart attack at age 50, he'd undergone four heart catheterizations, 5 stents, and, most recently, a bypass operation. He came to us to see if there was a better solution. After hearing Sam's story, I asked,"Did your doctors suggest to you why you had heart disease?" "Well, they said it was genetic, since my father went through the same thing in his early 50s, though he died after his second heart attack at age 54. They said it was bad luck and nothing could be done about it."Though Sam's case is more dramatic than most, I hear this argument every day: Risk for heart disease is genetic. It's true: There are indeed multiple reasons for inheriting causes for coronary heart disease, genes that heighten inflammatory responses, oxidative responses, modify lipoprotein particles, increase blood pressure, etc. There has even been some excitement over developing chromosomal markers for heightened risk. That's all well and fine, but what can we do about it today?In practical life, many inherited genetic patterns can be expressed in ways that you and I can identify--and correct. They are not chromosomal markers, but end products of genetic patterns. (Although there are indeed identifiable chromosomal markers, they have not yet led to meaningful treatments to my knowledge.) These readily identifiable patterns include:--Lipoprotein(a)--Clearly genetically transmitted, passed from mother or father to each child with a 50% likelihood, then you onto your children if you have it. --Small LDL--Although small LDL is amplified by high-carbohydrate diets and obesity, it can also occur in slender people who do not indulge in carbohydrates --i.e., a genetic tendency. Or, it can be a combination of poor lifestyle magnifying the genetic tendency for small LDL.--Low HDL--Particularly the extremes of low HDL below 30 mg/dl. (Although, interestingly, I am seeing more of these people, though not all, respond to vitamin D replacement. Perhaps an important subgroup of low HDL people are really Vitamin D Receptor (VDR) variants.)--ApoE--Two variants are relevant: ApoE2 and ApoE4. In my experience, it's the E2 that carries far greater significance, though the data are somewhat scanty. ApoE4 people are more sensitive to the fats in their diet (greater rises in LDL with fats; thus, some people advocate a tighter saturated fat restriction with this pattern, though I am not convinced that is the best solution), while ApoE2 people are exceptionally sensitive to carbohydrates, develop extravagant increases in triglycerides, and are very diabetes-prone with even the most minimal weight gain. If two "doses" of the E2 gene are present (homozygotic), then the tendencies are very exagerrated. E4 people are also subject to greater likelihood of Alzheimer's, though it is not a certain risk in a specific individual. --Postprandial disorders--We use the fasting intermediate-density lipoprotein (IDL) as an easy, obtainable index of the ability to clear after-eating byproducts of meals from the blood. Increased IDL has been related to increased coronary, carotid, and aortic aneurysmal disease. --Hypertriglyceridemia-i.e., increases in triglycerides, While not all forms of high triglycerides confer risk for atherosclerosis, many do, particularly if associated with IDL, small LDL, increased LDL particle number and/or apoB. There are more, but you get the point. There are clear-cut genetically-transmitted reasons for greater risk for cardiovascular disease. Some, like lipoprotein(a), yield very high risk. Others, like increased triglycerides, yield mixed levels of risk. Importantly, all of these patterns--ALL--are identifiable and are treatable. Treatment may not always be the easiest thing, but they are treatable nonetheless. While lipoprotein(a), for instance, is the most difficult pattern to correct in the above list, I remind everyone that our current "record holder" for reversal of plaque and heart scan scores--63% reduction--has lipoprotein(a) that we corrected. If you've been told that your risk for cardiovascular disease or coronary plaque is "genetic" and thereby uncorrectable and hopeless, run the other direction as fast as you can. Get another opinion from someone willing to take the modest effort to tell you precisely why.
Tim Russert Revisited 16. November 2008 William Davis (7) A Heart Scan Blog reader brought this piece by Dr. MacDougall to my attention. Dr. MacDougall created a fictitious posthumous conversation between himself and the late Tim Russert. MacDougall paints a picture of a hardworking, hard-living man who adhered to an overindulgent lifestyle of excessive eating. He concludes that a vegetarian, low-fat diet would have saved his life. Beyond being disrespectful, I would differ with Dr. MacDougall’s assessment. In fact, I’ve heard an interview with Mr. Russert’s primary care physician in which the doctor claimed that Mr. Russert had been counseled on the need for a low-fat diet and, in fact, adhered to it quite seriously. Far from being an overindulgent, overeating gourmand, he followed the dictates of conventional dietary wisdom according to the American Heart Association. The low-fat diet articulated by Dr. MacDougall is simply a little more strict than that followed by Mr. Russert.What exactly could Mr. Russert have done to prolong his life? Several basic strategies:--Added fish oil. This simple strategy alone would have reduced the likelihood of dying suddenly by almost half. --Eliminated wheat and cornstarch—Mr. Russert developed diabetes in the last few years of his life. By definition, diabetes is an inability to handle sugars and sugar-equivalents. Wheat and cornstarch yield immediate and substantial surges in blood sugar greater than table sugar; elimination causes weight to plummet, blood sugar to drop, and diabetes (at least in its early phases) can be eliminated in many people, particularly those beginning with substantial excess weight.Just those two strategies alone would more than likely have avoided the tragic death that brought Mr. Russert’s wonderful life and career to an abrupt end. Of course, he could have even taken his heart health program even further, as we do in the Track Your Plaque program. While the conversation has focused on how to avoid tragic events like sudden cardiac death, why not take it a step farther and ask, "How can coronary plaque be measured, tracked, and reversed?"In that vein, Mr. Rusert could have restored vitamin D to normal levels; identified all hidden sources of heart disease using lipoprotein testing (though he had small LDL without a doubt, given his generous waist size, HDL of 36 mg/dl and high triglycerides); considered niacin. Simple, yet literally lifesaving efforts, that make reversal much more likely. Those simple steps, in fact, would have tipped the scales heavily in Mr. Russert’s favor, making a heart attack and/or sudden death from heart disease exceptionally unlikely.
Water: Bottled vs. tap 16. November 2008 William Davis (4) The Fanatic Cook has a great post discussing the findings of the Environmental Working Group (EWG) on the quality of bottled water. The full text of the study from the EWG can be viewed here. They report that "the bottled water industry promotes an image of purity, but comprehensive testing by the Environmental Working Group (EWG) reveals a surprising array of chemical contaminants in every bottled water brand analyzed" . . . After analyzing 10 brands, they conclude that "tests strongly indicate that the purity of bottled water cannot be trusted. Given the industry's refusal to make available data to support their claims of superiority, consumer confidence in the purity of bottled water is simply not justified.""EWG's study has revealed that bottled water can contain complex mixtures of industrial chemicals never tested for safety, and may be no cleaner than tap water. Given some bottled water company's failure to adhere to the industry's own purity standards, Americans cannot take the quality of bottled water for granted. Indeed, test results like those presented in this study may give many Americans reason enough to reconsider their habit of purchasing bottled water and turn back to the tap."For these reasons, as well as environmental reasons (plastic bottles filling up dumpsites), I think it is becoming clearer and clearer that bottled water is something we should only use in a pinch, not habitually.
Can CRP be reduced? 13. November 2008 William Davis (17) The JUPITER study has sparked a lot of discussion about c-reactive protein, or CRP. If we follow the line of reasoning that prompted this study, reducing CRP may correlate with reduction of cardiovascular events. Thus, in the JUPITER study, Crestor 20 mg per day reduced cardiovascular events by nearly half. From a CRP perspective, starting values were 4.2 mg/dl in the Crestor group of the trial, 4.3 mg/dl in the placebo group. After 24 months, CRP in the Crestor group was 2.2 mg/dl, 3.5 mg/dl in the placebo group, representing a 37% reduction.Now, in our Track Your Plaque program--an experience that has yielded the virtual ELIMINATION of cardiovascular events--we aim for a CRP level of 1.0 mg/dl or less, ideally 0.5 mg/dl or less. The majority of people achieve these ambitious levels. In fact, it is a rare person who does not.How do we achieve dramatic reductions in CRP? We use:--Weight loss through elimination of wheat and cornstarch--This yields impressive reductions. --Vitamin D--I have no doubt whatsoever of vitamin D's capacity to exert potent anti-inflammatory effects. I am not entirely sure why this happens (enhanced sensitivity to insulin, reduced expression of tissue inflammatory proteins like matrix metalloproteinase and others, etc.), but the effect is profound. --Elimination of junk foods--like candies, cookies, pretzels, rice cakes, potato chips, etc. --Exercise--Amplifies the benefits of diet on CRP reduction. --Not allowing saturated fats to dominate--Yes, yes, I know. The demonization of saturated fat conversation has been largely replaced by the Taubesian saturated fat has not been confidently linked to heart disease conversation. But controlled feeding studies, in which a single component of diet is manipulated (e.g., saturated vs. monounsaturated vs. polyunsaturated fat) have clearly shown that saturated fats do activate several factors in the inflammatory response. --Fish oil--Though I am a firm believer in the huge benefits of omega-3 fatty acid supplementation/restoration, the anti-inflammatory effect is modest from a CRP perspective. However, there are anti-inflammatory benefits beyond that of simple CRP (via normalization of eicosanoid metabolism and other pathways). --Weight loss--A BIG effect. Weight loss drops CRP like a stone. The CRP-reducing effect is especially large if achieved via carbohydrate reduction. Of course, this is much more complicated than taking a pill. But it is effective to achieve health benefits outside of cardiovascular risk, is enormously useful as part of a weight loss effort, and doesn't cost $1400 per year like Crestor. In short, if CRP reduction is the goal, it certainly does not have to involve Crestor.