Lipoprotein(a) Research Foundation 16. April 2008 William Davis (18) There is no longer any doubt that lipoprotein(a) is a major causal factor in heart disease: Meta-analysis (combined re-analysis) of 27 prospective studies:Danesh J et al. Lipoprotein(a) and Coronary Heart Disease: Meta-Analysis of Prospective Studies Lp(a) and "subclinical" atherosclerosisBrown SA et al. The relation of lipoprotein[a] concentrations and apolipoprotein[a] phenotypes with asymptomatic atherosclerosis in subjects of the Atherosclerosis Risk in Communities (ARIC) Study.Lp(a) and oxidized LDL Tsimikas S et al. Oxidized phospholipids, Lp(a) lipoprotein, and coronary artery disease.Lp(a) predicts peripheral vascular diseaseValentine RJ et al. Lp(a) lipoprotein is an independent, discriminating risk factor for premature peripheral atherosclerosis among white men.Peltier M et al.Elevated serum lipoprotein(a) level is an independent marker of severity of thoracic aortic atherosclerosis.Lp(a) across various populationsGambhir JK et al. Association between lipoprotein(a) levels, apo(a) isoforms and family history of premature CAD in young Asian Indians.Weber M et al. Metabolic factors clustering, lipoprotein cholesterol, apolipoprotein B, lipoprotein (a) and apolipoprotein E phenotypes in premature coronary artery disease in French Canadians.Lp(a) and stroke riskJurgens G et al. Lipoprotein(a) serum concentration and apolipoprotein(a) phenotype correlate with severity and presence of ischemic cerebrovascular disease. Willeit J et al. Lipoprotein(a) and asymptomatic carotid artery disease. Evidence of a prominent role in the evolution of advanced carotid plaques: the Bruneck Study.From just about any direction, Lp(a) has been conclusively associated with atherosclerotic disease. We have more than enough data proving association. But there are two areas of desperate need: 1) Data on effective treatments.2) Raising awareness of this widely unknown (among the public) and ignored (among health professionals) genetic condition. Treatment remains a real struggle. In a recent detailed Track Your Plaque Special Report, Unique Treatment Strategies for Lipoprotein(a) Reduction, we summarized the treatment approaches that have some power to reduce Lp(a) and/or its potential for causing heart disease. But, even armed with an appreciation for the world's scientific literature on this genetic condition, full control remains difficult for many people.Track Your Plaque's HeartHawk has Lp(a) and he has struggled with this pattern for the last several years. He details some of his thoughts in a recent blog post. More research and clinical studies are required and we need it soon if we hope to gain better control over this genetic pattern that affects up to 20% of people with coronary or vascular disease. Much of the needed research is sophisticated, background work similar to that being done by Dr. Santico Marcovina at University of Washington, Dr. Angelo Scanu at the University of Chicago, and Dr. Sally McCormick in New Zealand. However, much of the needed research also consists of brief clinical experiences that detail whether or not there is an effect of various potential agents. Larger experiences, for instance, with potential treatment agents such as various phospholipid fractions, acetylcysteine, antibiotic regimens, some hormonal treatments, etc. could be performed quickly and simply. These studies would not require the $20 or $30 million typically spent by a drug company for a study, nor the several hundred million dollars to gain FDA approval of a new agent. They would simply be examinations of existing agents. These studies still cost money, require expertise, staff, and equipment. But the cost is a tiny fraction of the drug industry's investment in research. But it also means that investment return is nil from a drug manufacturer's perspective. Yet there are literally dozens, perhaps hundreds, of agents that hold some promise but have not been thoroughly studied. For instance, if a specific modification of the phosphatidylcholine molecule were to generate a substantial Lp(a) reducing effect, Merck, Pfizer, and AstraZeneca would yawn--it is non-patent protectable, cannot be protected from competitors through the costly FDA approval process, and therefore is simply not worth their investment--regardless of whether it works or not.(This is yet another example of how the drug industry, as well as hospitals and many health professionals, have lost sight of their real mission: to alleviate disease, not to profit from sickness.) HeartHawk and I have discussed on a number of occasions whether a Lipoprotein(a) Research Foundation should be formed, an organization that seeks to fund the smaller research efforts that may accelerate productive research in Lp(a) and perhaps yield useful strategies faster than hoping for somebody to simply stumble on a treatment, or wait for the drug industry to create a unique, patentable entity that returns billions. I'd like to propose that our Track Your Plaque program begin to fund such an effort. But a lot more help will be needed, particularly to generate the money to fund genuine, high-quality research from high-quality researchers. If any readers of the Heart Scan Blog have any thoughts or insights into this process of creating a foundation, we'd appreciate your input.
More on ASTEROID 16. April 2008 William Davis (3) Since we are on the topic of the ASTEROID trial and rosuvastatin, I'd make one more point before I start to sound like I'm plugging this drug (which I definitely am not).In an informative Roundtable Discussion (open to subscribers to the American Journal of Cardiology; sorry) amongst Dr. Steve Nissen, principal investigator behind ASTEROID; and Drs. Vincent Friedewald, Christie Ballantyne, P. Shah, and William Roberts, Dr. Nissen made some interesting comments:Dr. Shah: In ASTEROID, was the magnitude of atheroma volume change seen across different levels of LDL-C and HDL-C?Dr. Nissen: No. There was no plaque regression seen in the 17 persons with LDL-Cs >/= 100 mg/dl, and there was little change in persons with LDL-Cs of 70 to 100 mg/dl. Only in persons with LDLs less than or equal to 70 mg/dl was there significant regression. The study was not powered to look for an HDL-C(which increased by 14.7%)-raising effect. Interesting. In other words, ASTEROID, in a fairly internally consistent way, suggests that the lower the LDL is reduced, the more likely plaque regression is obtained. This is consistent with the Track Your Plaque experience, in which we've advocated reducing (calculated) LDL cholesterol to 60 mg/dl for the past several years. Unfortunately, the message that the ASTEROID Trial sponsors, AstraZeneca, as well as the roundtable discussion panel (later in the discussion) try to make is that there is something magical about Crestor, that it yields benefits superior to other statin agents or other means of reducing LDL. I disagree with this message. In the Track Your Plaque experience, we do aim for a similar LDL target. But we also employ a number of other strategies. We have also succeeded in regressing plaque without use of any statin drugs (though, admittedly, many people do require statin drugs to obtain LDLs in this range). We also witness magnitudes of reversal that often far exceed that seen in ASTEROID. The Rountable Discussion is unfortunately tainted, as is the ASTEROID Trial itself, with deep drug industry financial involvement of the Roundtable participants. In fact, the discussion begins with a listing of the financial disclosures of the participants, a listing that occupies a full column of a two-column page. The potential biases of the participants doesn't necessarily invalidate the arguments, but to me suggests that participants are more likely to argue in favor of the sponsor's drug, or that participants were chosen because of these biases. Why bother to even mention the ASTEROID Trial in a venue (the Heart Scan Blog, that is) that purports to seek unvarnished, unbiased truth in coronary plaque reversal? Because useful information can sometimes be found in unlikely places. Just like the four-year old child who blurts out an unexpected pearl of wisdom, so it can happen with the gobbledy-gook that emerges from the drug industry. Every once in a while, they are worth paying attention to.
LDL cholesterol, statins, and plaque regression 13. April 2008 William Davis (12) The ASTEROID Trial reported in 2006 examined the effects of LDL cholesterol reduction using the statin drug, rosuvastatin (Crestor), with coronary atherosclerosis quantified and tracked with intracoronary ultrasound. The Track Your Plaque report, New study confirms: LDL of 60 mg reverses plaque, on the ASTEROID Trial provides commentary on the results. Though I remain skeptical that a statin-only treatment strategy can reverse coronary plaque in the majority of people, I do believe that the AstraZeneca-sponsored ASTEROID Trial does add to the wisdom on heart disease management. More importantly, it has served to raise awareness among both the public and my physician colleagues that atherosclerosis is indeed a potentially reversible condition.Specifically, the ASTEROID results confirm that, either directly or indirectly, LDL cholesterol reduction achieved with statin agents does correspond to increasing degrees of plaque reversal. The mean (calculated) LDL cholesterol achieved in ASTEROID was 60 mg/dl, the same as the Track Your Plaque suggested LDL target. Though the ASTEROID Trial is not news, I stumbled on a chart posted on the ASTEROID Trial website that clearly highlights how a number of other studies beyond ASTEROID have fallen into this pattern: The graph reveals a linear relationship: The greater the reduction in LDL cholesterol with statin drugs, the greater the plaque regression ("change in percent atheroma volume"). (Several other studies not included in the graph also cluster into the same linear relationship.) I am no supporter of drug companies, nor a defender of their policies and practices. But I do believe that their data can serve to teach us a few lessons. For instance, here is an (cherry-picked, to be sure) example of intracoronary ultrasound cross-sectional images before and after two years of rosuvastatin, 40 mg daily: The color-coded/outlined atherosclerotic coronary plaque is shown shrinking, while the "lumen," or the path for blood to flow, enlarges. The reduction in coronary plaque is irrefutable. (The small circle within the lumen with the white halo surrounding it is the ultrasound catheter.) If you and I were to choose a single treatment approach to coronary disease reversal, then 40 mg of rosuvastatin is probably at the top of the list. However, in the Track Your Plaque program, we do not advocate a single treatment strategy. While the Crestor-only approach is relatively straightforward--one pill a day--few people, in my experience, can tolerate this dose for any length of time. Patients invariably have to stop the drug or reduce the dose severely due to muscle aches when I've had patients try it. Contrary to the ASTEROID results, in my experience the majority of people, perhaps all, eventually give up with this improbable "one-size-fits-all" scheme. The Track Your Plaque approach, while more complicated and involves several nutritional supplements and strategies, in my view addresses more causes of coronary plaque, is better tolerated, and provides health benefits outside of just LDL cholesterol reduction. It also minimizes or eliminates the need for prescription medication. Studies cited in graph:1.Nissen S et al. N Engl J Med 2006;354:1253-1263.2 Tardif J et al. Circulation 2004;110:3372-3377.3 Nissen S et al. JAMA 2006;295 (13):1556-15654 Nissen S et al. JAMA 2004;292: 2217–2225.5 Nissen S et al. JAMA 2004; 291:1071–1080
When is a calorie not a calorie? 10. April 2008 William Davis (8) One ounce of raw almonds (about 23 nuts) contains:6 grams protein14 grams fat6 grams carbohydrate 3.5 grams fiberFor a total of 163 calories per ounce. (From the USDA Nutrient Database)Calorie content of foods is determined by summing up the calories from each constituent: 1 gram of fat = 9 calories; 1 gram protein = 4 calories; 1 gram carbohydrate = 4 calories. Calorie content can also be directly measured using a device called a burn calorimeter, in which the amount of energy released from a specific food is measured by literally burning it and gauging precisely how much energy is released. The problem with both of these methods is that it is assumed that all foods are digested with equal efficiency. That is, it assumes that a potato chip is as readily digested and absorbed as energy from table sugar, a pretzel, oatmeal, a piece of steak, or a handful of nuts. In real life, of course this is not true. Different foods are absorbed with varying efficiency. For a long time I've suspected that some foods are very inefficiently absorbed. I've particularly suspected that raw nuts are relatively poorly absorbed and thus yield only a fraction of the calories ingested. Among the studies recently reported at the Federation of the Association of Societies for Experimental Biology (FASEB) meetings I attended in San Diego this past week were several devoted to almonds. One study, to my surprise, documented this phenomenon. In Manipulation of lipid bioaccessibility of almonds influences postprandial lipemia in healthy human subjects, it was determined that, of 100 calories ingested from the fat fraction of almonds, only about half was actually absorbed. The remaining half passed out in the stool. (They did this by collecting stool samples and comparing the fat composition after eating the different almonds prepartions. This is not discussed in the limited text of the abstract.) In addition, postprandial (after-eating) surges in triglycerides were much less with whole almonds compared to the oil separated from the nut (i.e., broken down into almond oil + defatted almond flour). The researchers attributed the difference to the inhibitory effects of the almond nut's "food matrix," or the structural properties of chewed foods. Add to this the fact that, of 6 grams of carbohydrate per ounce of whole almonds, 3.5 grams are indigestible fibers. This means that 6 - 3.5 = 2.5 grams of digestible carbohydrates are present per ounce (assuming 100% release). If we follow the reasoning that only about half the fat fraction of almonds are absorbed, and assume that the protein and carbohydrate (minus the indigestible fibers) are absorbed efficiently (100%), then we would re-calculate the calorie content of almonds to be 97 calories per ounce, or 40% less than calories calculated by composition or measured with a calorimeter. If we were to assume that protein and carbohydrates were, like fats, inefficiently absorbed because of the effects of the food matrix, then one ounce of almonds yields 88 calories per ounce, or 46% less. This is, in fact, a likely scenario, since the food matrix is largely created by the cell wall and should impede digestive access to fat, protein, and carbohydrate equally. My point? Almonds and other nuts at first appear to be calorically dense due to fat composition. However, this simplistic view of nuts is misleading because of the confounding effects of the food matrix. Stated differently: Whole foods yield less calories. And, judging by the postprandial triglyceride effects: Whole foods yield less undesirable effects, such as postprandial rises in triglycerides. Some other observations with almonds included:The effect of almonds on plasma lipids in persons with prediabetes This study confirmed the LDL-reducing and modest HDL-raising effects of almonds. Almonds (Amygdalus communis L.) as a possible source of prebiotic functional food This curious observation suggests that almonds modify the bacterial flora of the intestinal tract in a positive way (like the cultures in yogurts). Copyright 2008 William Davis, MD
Track Your Plaque data abstract 10. April 2008 William Davis (7) An extraordinary thing happened about 2 1/2 years ago. While we have been following the Track Your Plaque program for coronary plaque regression for nearly 10 years, about 2 1/2 years ago we witnessed an extraordinary surge in success--bigger, faster, and more frequent drops in heart scan scores.Up until then, we did witness significant reversal of coronary plaque by heart scan scores. We were planning to publish the data to validate this approach, but then . . .Heart scan scores starting dropping not just 2%, or 8% . . . but 24%, 30%, 50% and more. Why? I attribute the surge in success to the addition of vitamin D. Unfortunately, it also meant that the preceding 8 or so years of data lacked experience with supplementing vitamin D. The hundreds of participants in the Track Your Plaque program had not, until then, included vitamin D in their program. So I decided to start from scratch (from the standpoint of data collection, not for the participants). That also meant that the preceding years of experience went unreported, though even that data far exceeded the results of what is achieved in conventional heart disease prevention.Thus, the data I presented at the Experimental Biology Proceedings (FASEB 2008) in San Diego this week included only experiences in the group of participants that included vitamin D in their program, with data collected until mid-2007. The number of experiences is therefore modest. However, the Track Your Plaque experience, as reported, far exceeds any prior experience in coronary plaque regression. The full abstract will be published in the Track Your Plaque website. Copyright 2008 William Davis, MD
Small fish oil capsules 3. April 2008 William Davis (12) Many people complain about the size of fish oil capsules. Let's face it: They're usually big and kind of smelly. Women in particular struggle with big capsules. This becomes a real problem when somebody requires high-dose fish oil for treatment of post-prandial (after-eating) abnormalities, high triglycerides, or lipoprotein(a), when 6 or more--occasionally up to the equivalent of 20--standard fish oil capsules are required. I came across a small capsule alternative for people who struggle with the big capsules. It's a product called Learn from PharmaOmega, a source of super purified fish oil. The Learn product is actually made for children, since omega-3 fatty acid supplementation has been linked with improved intellectual performance. But the small capsule size is convenient for women and other people who would like to avoid the big standard-sized capsules. Each capsule is about 60% of the size of a standard fish oil capsule (the smaller capsule in the photo, next to a standard size fish oil capsule), yet contains 375 mg EPA + DHA per capsule, 25% more than standard capsules (which contain 300 mg per capsule). The ratio of of EPA:DHA is a little more heavily weighted towards EPA with a 5:2 ration, compared to 3:1 of standard capsules. The capsules are also faintly orange flavored and non-fishy. Disclosure: I receive no compensation for discussing or promoting this product. Copyright 2008 William Davis, MD
Low-carb eating for diabetes 2. April 2008 William Davis (15) Jenny provided permission to reprint her very excellent introduction to low-carbohydrate eating for people with diabetes. You can also view the original version on her Diabetes 101 website. Jenny is a stickler for monitoring the effects of blood sugar. We might take some lessons from her experiences for improving management of people with metabolic syndrome or borderline blood sugars. In other words, monitoring the blood sugar-raising effects of various foods and food portions can provide great feedback on what foods are preferable, what undesirable, given your physiology. Even if you are not a diabetic, Jenny's discussion is must reading to gain a better understanding of food choices, particularly carbohydrates. Along with seizing control of health, she has also gained deep wisdom in how to best manage this disease and its physiology. Introduction to low-carb nutrition for diabeticsIt's carbohydrates that raise blood sugar. Sugars and starches, not the fats that dietitians have been warning you about for so long. If you've been testing your blood sugar after meals, you've probably noticed that already and you are starting to understand why a healthy diabetes diet will have to be one that limits carbohydrates to an amount that doesn't push your blood sugar up over the level where you are damaging your body.But if your previous experience with restricting carbohydrates involved doing a weight loss diet like Atkins or Protein Power, which worked well for you until you crashed off it entirely and gained back all the weight you'd lost, you may be hesitant to embark on another course of dieting that requires some carb restriction.I've been there myself. I've done the extremely low carb diet Dr. Richard Bernstein recommends for months on end. I did Protein Power for 3 years. And I've gone on the "Eat all the carbs you didn't eat over the past three years all at once" diet, too. The following observations grew out of my 8 years of experience with learning how to make carb restriction work long-term.Unlike much of what you've read before, there are no scholarly references for this section. It's based entirely on my own observations and the experience of many dozens of people who have participated in online discussion groups devoted to low carb dieting and diabetes.Weight Loss Diets Usually Fail but Diabetes Diets Can't Afford To FailPeople who adopt a low carb diet to lose weight tend to start out with great enthons-learned-from-the-2012-low-carb-cruise.html">Lessons learned from the 2012 Low-carb Cruise 14. May 2012 William Davis (13) I just returned from Jimmy Moore's Low-carb Cruise, a 7-day excursion to Jamaica, Grand Cayman Island, and Cozumel aboard the Carnival Magic. During our 7 wonderful days, a number of authors and experts spoke, each offering their unique perspective on the low-carb world. The focus was the science, experience, and practical application of low-carbohydrate diets.The event kicked off with a roast by Tom Naughton of Fat Head fame, who entertained with his insightful low-carb humor and predictions of my demise at the hands of Monsanto!Among the most important lessons provided:Dr. Andreas Eenfeldt of the Diet Doctor blog discussed how Sweden is leading the world as the nation with the most vigorous low-carbohydrate following, witnessing incredible weight loss and reversal of carbohydrate-related diseases way ahead of the U.S. experience. I spent several hours with Dr. Eenfeldt who, besides being an engaging speaker, is a new father and an all-around gentleman. At 6 ft, 7 inches, he also towered high above all of us.Dr. Eric Westman of Duke University and author of The New Atkins for a New You, debunked low-carbohydrate myths, such as "low-carb diets are high-protein diets that make your kidneys explode."Dr. John Briffa, creator of the popular blog, Dr. John Briffa: A Good Look at Good Health, and author of the wonderfully straightforward primer to low-carbohydrate eating, Escape the Diet Trap, stressed the importance of never allowing hunger to rule behavior. Dr. Briffa's serious writing tone conceals an incredible charm and wit that took me by surprise, having spent several thoroughly engaging hours over breakfast, lunch, and dinner with him over the week.Fred Hahn, exercise expert, founder of Serious Strength and author of Slow Burn Fitness Revolution and Strong Kids, Healthy Kids, debunked a number of trendy exercise methods, boiling many of the purported benefits of exercise down to that of increased strength.Dr. Chris Masterjohn of The Daily Lipid and supporter of the Weston A. Price Foundation program, provided a comprehensive overview of the data that fails to link saturated fat with heart disease. He also helped me understand the analytical techniques used in studies of advanced glycation end-products.Denise Minger, brilliant young usurper of China Study dogma and blogger at Raw Foods SOS, proved an engaging speaker and a truly real person (since some critics of her analyses have actually questioned whether there was even such a person!). She also proved every bit as likable as she seems in her captivating blog discussions.Dr. Jeff Volek, prolific researcher from University of Connecticut, author of over 200 studies validating low-carbohydrate diet effects, and author of the recently released book with Dr. Stephen Phinney, The Art and Science of Low Carbohydrate Living, debunked myths behind carbohydrate dependence and "loading" by athletes. He also talked about how assessing blood ketones may be the gold standard method to ensure low-grade ketosis on a long-term low-carb effort.Over a bottle of wine, Jimmy Moore and I reminisced over how his modest start with no experience in blogging or media has now ballooned to an audience of over 100,000 readers/viewers.All in all, Jimmy's Low-carb Cruise experience was worth every minute, with many wonderful lessons and memories!
Chili Sesame Crackers 3. May 2012 William Davis (0) Looking for something hot and crunchy?These chili sesame crackers are perfect for dipping into hummus or salsa. As written, the recipe yields a moderately spicy cracker that you can modify readily by increasing or decreasing quantities of cayenne pepper and Tabasco sauce.This recipe uses sesame seeds as the "flour." Either brown sesame seeds or the lighter version work, though the lighter seeds yield a slightly less bitter flavor with the spices.For ease of baking, a shallow baking pan measuring 11 x 17 inches works best, as it allows the batter to fill the pan and spread to a cracker thickness. With a smaller pan, you may have to bake in two batches.Makes approximately 30 chips2 cups raw sesame seeds1 cup shredded Parmesan cheese2 tablespoons extra-virgin olive oil1 tablespoon chili powder½ teaspoon cayenne pepper2 teaspoons onion powder1 teaspoon garlic powder1 teaspoon dry mustard1 teaspoon sea salt1 teaspoon Tabasco sauce1¼ cups waterPreheat oven to 350º F.In food chopper or food processor, grind 1¼ cups sesame seeds to fine meal. Remove and place in large bowl.Place shredded Parmesan cheese in food chopper or food processor and pulse briefly until reduced to granular consistency. Add to sesame seed meal and mix. Stir in olive oil.Add remaining (unground) sesame seeds, chili powder, cayenne pepper, onion and garlic powder, mustard, sea salt and mix thoroughly. Add Tabasco sauce and water and mix. Add additional water, if necessary, one tablespoon at a time, to obtain a consistency similar to pancake batter.Pour mixture into baking pan and smooth to fill pan and obtain a thickness of a cracker. If too thick, remove some batter and re-smooth. Optionally, roll a clean cylindrical glass or bottle over top to smooth and yield a consistent thickness.Bake for 30 minutes or until edges browned and center firm. If a dry, extra crunchy cracker is designed, bake an additional 10-15 minutes at 250 degrees F.Remove and allow to cool. Cut with pizza cutter to desired size.
The standard cholesterol panel . . . dissected 18. April 2012 William Davis (0) There are four values typically reported on any standard cholesterol panel:
Opiate of the masses 18. April 2012 William Davis (22) Although it is a central premise of the whole Wheat Belly argument and the starting strategy in the New Track Your Plaque Diet, I fear that some people haven't fully gotten the message:Modern wheat is an opiate. And, of course, I don't mean that wheat is an opiate in the sense that you like it so much that you feel you are addicted. Wheat is truly addictive. Wheat is addictive in the sense that it comes to dominate thoughts and behaviors. Wheat is addictive in the sense that, if you don't have any for several hours, you start to get nervous, foggy, tremulous, and start desperately seeking out another "hit" of crackers, bagels, or bread, even if it's the few stale 3-month old crackers at the bottom of the box. Wheat is addictive in the sense that there is a distinct withdrawal syndrome characterized by overwhelming fatigue, mental "fog," inability to exercise, even depression that lasts several days, occasionally several weeks. Wheat is addictive in the sense that the withdrawal process can be provoked by administering an opiate-blocking drug such as naloxone or naltrexone. But the "high" of wheat is not like the high of heroine, morphine, or Oxycontin. This opiate, while it binds to the opiate receptors of the brain, doesn't make us high. It makes us hungry. This is the effect exerted by gliadin, the protein in wheat that was inadvertently altered by geneticists in the 1970s during efforts to increase yield. Just a few shifts in amino acids and gliadin in modern high-yield, semi-dwarf wheat became a potent appetite stimulant. Wheat stimulates appetite. Wheat stimulates calorie consumption: 440 more calories per day, 365 days per year, for every man, woman, and child. (440 calories per person per day is the average.) We experience this, sense the weight gain that is coming and we push our plate away, settle for smaller portions, increase exercise more and more . . . yet continue to gain, and gain, and gain. Ask your friends and neighbors who try to include more "healthy whole grains" in their diet. They exercise, eat a "well-balanced diet" . . . yet gained 10, 20, 30, 70 pounds over the past several years. Accuse your friends of drinking too much Coca Cola by the liter bottle, or being gluttonous at the all-you-can-eat buffet and you will likely receive a black eye. Many of these people are actually trying quite hard to control impulse, appetite, portion control, and weight, but are losing the battle with this appetite-stimulating opiate in wheat. Ignorance of the gliadin effect of wheat is responsible for the idiocy that emits from the mouths of gastroenterologists like Dr. Peter Green of Columbia University who declares:"We tell people we don't think a gluten-free diet is a very healthy diet . . . Gluten-free substitutes for food with gluten have added fat and sugar. Celiac patients often gain weight and their cholesterol levels go up. The bulk of the world is eating wheat. The bulk of people who are eating this are doing perfectly well unless they have celiac disease."In the simple minded thinking of the gastroenterology and celiac world, if you don't have celiac disease, you should eat all the wheat you want . . . and never mind about the appetite-stimulating effects of gliadin, not to mention the intestinal disruption and leakiness generated by wheat lectins, or the high blood sugars and insulin of the amylopectin A of wheat, or the new allergies being generated by the new alpha amylases of modern wheat.
Jelly beans and ice cream 23. March 2012 William Davis (6) What if I said: "Eliminate all wheat from your diet and replace it with all the jelly beans and ice cream you want."That would be stupid, wouldn't it? Eliminate one rotten thing in diet--modern high-yield, semi-dwarf wheat products that stimulate appetite (via gliadin), send blood sugar through the roof (via amylopectin A), and disrupt the normal intestinal barriers to foreign substances (via the lectin, wheat germ agglutinin)--and replace it with something else that has its own set of problems, in this case sugary foods. How about a few other stupid replacements: Replace your drunken, foul-mouthed binges with wife beating? Replace cigarette smoking with excessive bourbon?Sugary carbohydrate-rich foods like jelly beans and ice cream are not good for us because:1) High blood sugar causes endogenous glycation, i.e, glucose modification of long-lived proteins in the body. Glycate the proteins in the lenses of your eyes, you get cataracts. Glycate cartilage proteins in the cartilage of your hips and knees, you get brittle cartilage that erodes and causes arthritis. Glycate structural proteins in your arteries and you get hypertension (stiff arteries) and atherosclerosis. Small LDL particles--the #1 cause of heart disease in the U.S. today--are both triggered by blood sugar rises and are 8-fold more prone to glycation (and thereby oxidation). 2) High blood sugar is inevitably accompanied by high blood insulin. Repetitive surges in insulin lead to <em>insulin resistance</em>, i.e., muscles, liver, and fat cells unresponsive to insulin. This forces your poor tired pancreas to produce even more insulin, which causes even more insulin resistance, and round and round in a vicious cycle. This leads to visceral fat accumulation (Jelly Bean Belly!), which is highly inflammatory, further worsening insulin resistance via various inflammatory mediators like tumor necrosis factor.3) Sugary foods, i.e., sucrose- or high-fructose corn syrup-sweetened, are sources of fructose, a truly very, very bad sugar that is metabolized via a completely separate pathway from glucose. Fructose is 10-fold more likely to induce glycation of proteins than glucose. It also provokes a (delayed) rise in insulin resistance, accumulation of triglycerides, marked increase in formation of small LDL particles, and delayed postprandial (after-eating) clearance of the lipoprotein byproducts of meals, all of which leads to diabetes, hypertension, and atherosclerosis.I think we can all agree that replacing wheat with jelly beans and ice cream is not a good solution. And, no, we shouldn't have drunken binges, wife beating, smoking or bourbon to excess. So why does the "gluten-free" community advocate replacing wheat with products made with:rice starch, tapioca starch, potato starch, and cornstarch?These powdered starches are among the few foods that increase blood sugar (and thereby provoke glycation and insulin) higher than even the amylopectin A of wheat! For instance, two slices of whole wheat bread typically increase blood sugar in a slender, non-diabetic person to around 170 mg/dl. Two slices of gluten-free, multigrain bread will increase blood sugar typically to 180-190 mg/dl.The fatal flaw in thinking surrounding gluten-free junk carbohydrates is this: If a food lacks some undesirable ingredient, then it must be good. This is the same fatally flawed thinking that led people to believe, for instance, that Snack Well low-fat cookies were healthy: because they lacked fat. Or processed foods made with hydrogenated oils were healthy because they lacked saturated fat.So gluten-free foods made with junk carbohydrates are good because they lack gluten? No. Gluten-free foods made with rice starch, tapioca starch, potato starch, and cornstarch are destructive foods that NOBODY should be eating.This is why the recipes for muffins, cupcakes, cookies, etc. in this blog, the Track Your Plaque website, and the Track Your Plaque Cookbook are wheat- and gluten-free and free of gluten-free junk carbohydrates. And put that bottle of Jim Beam down!