Emmer, einkorn, and agribusiness 21. May 2010 William Davis (32) 10,000 years ago, Neolithic humans did not obtain wheat products from the bagel shop, grocery store, or Krispy Kreme. They obtained wheat by locating a nearby wild-growing field of wild emmer or einkorn wheat grass, then harvesting it with their stone sickles. Neolithic humans, such as the Natufians of the Fertile Crescent, carried their freshly-cut wheat home, then ground it by hand using homemade mortar and pestle. As yeast-raised bread was still some 5000 years in the future, emmer and einkorn wheat was not used to bake bread, but was consumed as a porridge in bowls. Einkorn has the simplest genetic code of 14 chromosomes, while emmer has 28 chromosomes.A third variety of wheat appeared on the scene around 9000 years ago, a natural hybridization between emmer and goat grass, yielding the 42-chromosome Triticum aestivum species. Egyptians learned how to cause wheat to rise around 3000 BC, yielding bread, rather than the unleavened flatbreads of their predecessors. From the original three basic varieties of wheat available to Neolithic man, over the past 30 years wheat has exploded to over 25,000 varieties. Where did the other 24,997+ strains come from?In the 1980s, thousands of new wheat strains arose from hybridization experiments, many of them conducted in Mexico. Then, in the late 1980s, genetic engineering quietly got underway in which geneticists inserted or deleted single genes, mostly designed to generate specific characteristics, such as height, yield per acre, drought resistance, but especially resistance to various pesticides and weed killers. The fruits of these efforts were introduced into the market in 1994. Most of the genetically modified foods were thought to be only minor modifications of the unmodified original and thus no safety testing in animals or humans was conducted. We now have many thousands of wheat strains that are different in important ways from original emmer, einkorn, and Triticum aestivum wheat. Interestingly, it has been suggested that einkorn wheat fails to provoke the same immune response characteristic of celiac disease provoked by modern wheat gluten, suggesting a different amino acid structure in gluten proteins. Another difference: Emmer wheat is up to 40% protein, compared to around 12% protein for modern wheat. In other words, the wheat of earlier agricultural humans, including the wheat of Biblical times, is NOT the wheat of 2010. Modern wheat is quite a different thing with differing numbers of chromosomes, different genes due to human manipulation, varying gluten protein composition, perhaps other differences.Somewhere in the shuffle and genetic sleight-of-hand that has occurred over the last 30 years, wheat changed. What might have been the "staff of life" has now become the cause of an incredible array of diseases of "wheat" intolerance.
Near-death experience with nattokinase 16. May 2010 William Davis (22) This is a true story that I personally witnessed. A 60-some year old man heard that nattokinase "thinned the blood." So he had been taking it for the past 6 months. One week before he came to see me, he abruptly became quite breathless. He was unable to walk more than 20 feet or bend over to tie his shoes due to the breathlessness. He came to see me in the office. I was alarmed by how breathless he was without signs of heart failure or other obvious explanation. I sent him for an immediate CT pulmonary angiogram. Within 30 minutes, we had the diagnosis: a large "saddle" pulmonary embolus, meaning a large blood clot that straddled the right and left main pulmonary arteries. One wrong move and . . . bang! He would have been dead within a couple of minutes, since a large clot can completely occlude the large arteries feeding the lung, essentially corking any blood circuiting through the lungs and back to the left side of the heart. (Causing, incidentally, electromechanical dissociation, in which the heart keeps beating for a few minutes but no blood is being pumped. CPR can keep you alive for a few minutes, then it's over.) When I advised the patient of the diagnosis (after initiating the REAL anticoagulants), he said, "But I was taking nattokinase!" Exactly. Blood clots are no laughing matter. They are potentially fatal events. Betting your life on some company's advertisement is nothing short of foolish. Anyone who reads The Heart Scan Blog knows that I am an avid supporter of nutritional supplements. I even write articles and consult for the supplement industry. But I truly despise hearing unfounded marketing claims that some supplement companies will make in the pursuit of a fast buck. There is no doubt that we need better, safer methods to deal with dangerous blood clots, whether in the lung, pelvis, or other areas. But, before anyone takes a leap based on the extravagant marketing claims made by a supplement manufacturer, you want to be damn sure there are real data--not marketing claims, REAL data--before you use something like nattokinase in place of a proven therapy. Don't confuse the very interesting, though unpalatable, natto with nattokinase. Natto contains vitamin K2 and some other interesting compounds, including nattokinase.
Blame the gluten? 14. May 2010 William Davis (17) Wheat is among the most destructive components of the human diet, a food that is responsible for inflammatory disease, diabetes, heart disease, several forms of intestinal diseases, schizophrenia, bipolar illness, ADHD, behavioral outbursts in autistic children . . . just to name a few. But why? Wheat is mostly carbohydrate. That explains its capacity to cause blood sugar to increase after eating, say, a turkey sandwich on whole wheat bread. The rapid release of sugars likely underlies its capacity to create visceral fat, what I call "wheat belly." But neither the carbohydrate nor the other components, like bran and B vitamins, can explain all the other adverse health phenomena of wheat. So what is it in wheat that, for instance, worsens auditory hallucinations in paranoid schizophrenics? Is it the gluten?First of all, what is gluten?Gluten protein is the focus of most wheat research conducted by food manufacturers and food scientists, since it is the component of wheat that confers the unique properties of dough, allowing a pizza maker to roll and toss pizza crust in the air and mold it into shape. The distinctive “doughy” quality of the simple mix of wheat flour and water, unlike cornstarch or rice starch, for instance, properties that food scientists call “viscoelasticity” and “cohesiveness,” are due to the gluten. Wheat is mostly carbohydrate, but the 10-15% protein content is approximately 80% gluten. Wheat without gluten would lose its unique qualities that make it desirable to bakers and pizza makers. Gluten is also the component of wheat most confidently linked to immune diseases like celiac. The structure of gluten proteins has proven frustratingly elusive to characterize, as it changes over time and varies from strain to strain. But an understanding of gluten structure may be part, perhaps most, of the answer to the question of why wheat provokes negative effects in humans. The term “gluten” encompasses two primary families of proteins, the gliadins and the glutenens. The gliadins, one of the protein groups that trigger the immune response in celiac disease, has three subtypes: a/ß-gliadins, ?-gliadins, and ?-gliadins. The glutenins are repeating structures, or polymers, of more basic protein structures. Beyond gluten, the other 20% or so of non-gluten proteins in wheat include albumins, prolamins, and globulins, each of which can also vary from strain to strain. In total, there are over 1000 other proteins that serve functions from protection of the grain from pathogens, to water resistance, to reproductive functions. There are agglutinins, peroxidases, a-amylases, serpins, and acyl CoA oxidases, not to mention five forms of glycerinaldehyde-3-phosphate dehydrogenases. I shouldn’t neglect to mention the globulins, ß-purothionin, puroindolines a and b, tritin, and starch synthases. As if this protein/enzyme smorgasbord weren’t enough, food processors have also turned to fungal enzymes, such as cellulases, glucoamylases, xylanases, and ß-xylosidases to enhance leavening and texture. Many bakers also add soy flour to enhance mixing and whiteness, which introduces yet another collection of proteins and enzymes.In short, wheat is not just a simple gluten protein with some starch and bran. It is a complex collection of biological material that varies according to its genetic code. While wheat is primarily carbohydrate, it is also a mix of gluten protein which can vary in structure from strain to strain, as well as a highly variable mix of non-gluten proteins. Wheat has evolved naturally to only a modest degree, but it has changed dramatically under the influence of agricultural scientists. With human intervention, wheat strains are bred and genetically manipulated to obtain desirable characteristics, such as height (ranging from 18 inches to over 4 feet tall), “clinginess” of the seeds, yield per acre, and baking or viscoelastic properties of the dough. Various chemicals are also administered to fight off potential pathogens, such as fungi, and to activate the expression of protective enzymes within the wheat itself to “inoculate” itself against invading organisms. From the original two strains of wheat consumed by Neolithic humans in the Fertile Crescent 9000 years ago (Emmer and Einkorn), we now have over 200,000 strains of wheat virtually all of which are the product of genetic manipulations that have modified the protein structure of wheat. The extraordinary complexity of wheat proteins have therefore created a huge black box of uncertainty in pinpointing which protein causes what. But there's an easy cure for the uncertainty: Don't eat it.
Glycemic gobbledygook 13. May 2010 William Davis (14) The concept of glycemic index is meant to help determine what foods raise blood sugar a lot vs. what foods raise blood sugar a little. Dr. Jennie Brand-Miller's searchable database can be found here.I have to admit that glycemic index provided me with a sense of false assurance for some years. It screwed up my health until I came to understand the issues a lot better. For those of you just starting out in nutritional conversations, glycemic index (GI) represents a comparison of the blood glucose area-under-the-curve (AUC) over 2 hours after consuming 50 grams of the food in question compared to the AUC of glucose or white bread. Volunteers involved in developing these values are healthy people who are generally of normal weight. Glucose, by definition, has a GI of 100. An equal quantity of sucrose (50% glucose, 50% fructose) has a GI of 60, lower than glucose. An equal quantity of whole wheat bread has a GI of 68-77 (Yes: The GI of whole wheat is higher than sucrose). Non-carbohydrate foods, such as eggs or avocado, have no GI since they do not impact on blood glucose. Because the GI is also sensitive to how much carbohydrate is contained, the concept of Glycemic Load (GL) was introduced:GL = (GI x amount of carbohydrate) / 100GL is therefore the GI that incorporates the glycemic potential of the food of interest. GI does not vary with portion size; GL varies with portion size. Let's take whole wheat pasta, a food regarded by most people as a healthy choice. Whole wheat pasta has a GI of 55--fairly low--and a GL of 29. A serving of 180 g (approximately 6 oz cooked) provides 50 g carbohydrates. People who advocate that low-glycemic index foods would say that this is a desirable profile and should therefore replace high-glycemic index foods. I say WRONG. First of all, most of us are not slender 20-somethings. We will therefore not show the same response as a young, slender person (like the GI volunteers), but will show exagerrated blood sugar responses. So this much low-glyemic index whole wheat pasta will typically yield a blood sugar of 120-200 mg/dl in non-diabetic people, high enough to trigger glycation. Sure, a high-glycemic index food, such as white flour birthday cake with plenty of sugary icing, might trigger a blood sugar of 140-250 mg/dl, much worse. But that doesn't make the lower blood sugar following pasta any less bad--it's still terrible. Another issue: GI is assessed over a 2-hour timeline. What if blood sugar remains high in a sustained way, say, over 6 hours? That's precisely what whole wheat pasta will do: Keep blood sugar high for an extended period. So not only does a low-glycemic index food like pasta increase blood sugar in most of us extravagantly, it does so in a sustained way. Lastly, low-glycemic index pasta still triggers small LDL particles to an extreme degree, as I discussed in the previous Heart Scan Blog post, Small LDL: Complex vs. simple carbohydrates. Don't be false reassured by the notion of low GI or GL. In fact, I'd go so far as to say that NO glycemic index is a GOOD glycemic index (or load). The foods we want to dominate our diet are the foods that aren't even listed in the GI database.
Man walks after removing wheat 9. May 2010 William Davis (27) No, this isn't some National Enquirer headline like "Woman delivers alien baby."Tom is a 26-year old man with a complex medical condition, a malformation he was born with and has had reconstructed. Aside from this, he leads a normal life: works, is married, and is, in fact, quite intelligent. He came to me for an opinion regarding his overall health. Tom was worried that his congenital condition would impair his long-term health and longevity prospects, so he wanted to optimize all other aspects of his health.But, when I examined Tom, he could barely get himself up on the exam table without wincing in pain. When I asked him to walk, he hobbled a few steps, again clearly in pain. When I asked him what hurt, he said "everything." He said that all his joints hurt just to move. He told me that his several doctors over the years didn't know why he was in such pain: It wasn't rheumatoid arthritis, gout, pseudogout, or any of the other inflammatory joint diseases that might account for virtually incapacitating this 26-year old man. Even the rheumatologists were stumped. It was also unrelated to hi All posts by william-davis Toggle navigation Home Blog Home Archive Join Now Log in When MIGHT statins be helpful? 7. April 2011 William Davis (17) I spend a lot of my day bashing statin drugs and helping people get rid of them. But are there instances in which statin drugs do indeed provide real advantage? If someone follows the diet I've articulated in these posts and in the Track Your Plaque program, supplements omega-3 fatty acids and vitamin D, normalizes thyroid measures, and identifies and corrects hidden genetic sources of cardiovascular risk (e.g., Lp(a)), then are there any people who obtain incremental benefit from use of a statin drug?I believe there are some groups of people who do indeed do better with statin drugs. These include:Apoprotein E4 homozygotesApoprotein E2 homozygotesFamilial combined hyperlipidemia (apoprotein B overproduction and/or defective degradation)Cholesteryl ester transfer protein homozygotes (though occasionally manageable strictly with diet)Familial heterozygous hypercholesterolemia, familial homozygous hypercholesterolemiaOther rare variants, e.g., apo B and C variantsThe vast majority of people now taking statin drugs do NOT have the above genetic diagnoses. The majority either have increased LDL from the absurd "cut your fat, eat more healthy whole grains" diet that introduces grotesque distortions into metabolism (like skyrocketing apo B/VLDL and small LDL particles) or have misleading calculated LDL cholesterol values (since conventional LDL is calculated, not measured).As time passes, we are witnessing more and more people slow, stop, or reverse coronary plaque using no statin drugs. Like antibiotics and other drugs, there may be an appropriate time and situation in which they are helpful, but not for every sneeze, runny nose, or chill. Same with statin drugs: There may be an occasional person who, for genetically-determined reasons, is unable to, for example, clear postprandial (after-eating) lipoproteins from the bloodstream and thereby develops coronary atherosclerotic plaque and heart attack at age 40. But these people are the exception. Advanced topics in nutrition 5. April 2011 William Davis (0) Nutrition in the modern world has become an increasingly problematic topic. From genetic modification to commercialized methods of mass production, we are having to navigate all manner of complex issues in food choices, particularly if ideal health, including maximal control over coronary plaque, is among our goals. We will therefore be releasing a series of discussions on the Track Your Plaque website in the coming months, a series I call "Track Your Plaque Advanced Topics in Nutrition." These will be, as the series title suggests, discussions for anyone interested in more than the "eat a balanced diet" nonsense that issues from "official" sources. Among the topics to be covered:1)Advanced Glycation End-products--both endogenous and exogenous, including peripheral issues like lipoxidation and acrylamides. 2)Dietary influences on LDL oxidation--including the concept of "glycoxidation." Protection from oxidative phenomena is not just about taking antioxidants. 3) Foods you MUST eat--We've talked a lot about foods that you shouldn't eat. How about foods you should eat? The New Track Your Plaque Guide now available 4. April 2011 William Davis (5) The New Track Your Plaque Guide is now available!The Track Your Plaque program has evolved over its 8 year history. While the original Track Your Plaque book reflected the program details that got the program started back in 2003-2004, plenty has changed. This new version of the book, what I call the program Guide, represents version 2.0 of Track Your Plaque and includes:--Updated lipoprotein treatment strategies--including new and expanded treatment choices for small LDL and lipoprotein(a).--An entire chapter on vitamin D and its crucial role in cardiovascular health and plaque control.--A new and expanded diet--All the reasons why the New Track Your Plaque Diet can achieve spectacular improvement in lipids/lipoproteins, reversal of insulin resistance/pre-diabetes/diabetes, weight loss, reduction in blood pressure, etc. are discussed in considerable detail. The diet is crafted to achieve maximum control over both metabolic responses and coronary plaque. --An entire chapter on the role of omega-3 fatty acids is included. --A detailed discussion on the role of iodine and thyroid health--One of the newest additions to the Track Your Plaque menu of strategies is to achieve and maintain ideal thyroid health. This tips the scales in your favor for improved control over lipids/lipoproteins, weight, blood sugar, and coronary plaque. The new guide, as well as our new Member kits that include the new Track Your Plaque Recipe Book, At-Home Lab Test kits, and nutritional supplements, are all available in the Track Your Plaque Marketplace. Don't wet yourself 3. April 2011 William Davis (13) While there is more to wheat's adverse effects on human health than celiac disease, studying celiac disease provides important insights into why and how wheat--the gluten component of wheat, in this case--is so destructive to human health. Modern wheat, in particular, is capable of causing "celiac disease" without intestinal symptoms---no cramping or diarrhea--but instead shows itself as brain injury (ataxia, dementia), peripheral nervous system damage (peripheral neuropathy), joint and muscle inflammation (rheumatoid arthritis, polymyalgia rheumatica and others), and gastrointestinal cancers. One neurological manifestation of wheat's effect on the human brain is a condition called cerebellar ataxia. This is a condition that can affect adults (average age 48 years) and children and consists of incoordination, falls, and incontinence. Because brain tissue has limited capacity for healing and regeneration, symptoms of cerebellar ataxia usually improve slowly and modestly with meticulous elimination of wheat and other gluten sources. Such observations are relevant even to people without celiac disease. Celiac disease sufferers are more susceptible to such extra-intestinal phenomena, but it can also happen in people without positive celiac antibodies. Some references:Neurological symptoms in patients with biopsy proven celiac diseaseA total of 72 patients with biopsy proven celiac disease (CD) (mean age 51 +/- 15 years, mean disease duration 8 +/- 11 years) were recruited through advertisements. All participants adhered to a gluten-free diet. Patients were interviewed following a standard questionnaire and examined clinically for neurological symptoms. Medical history revealed neurological disorders such as migraine (28%), carpal tunnel syndrome (20%), vestibular dysfunction (8%), seizures (6%), and myelitis (3%). Interestingly, 35% of patients with CD reported of a history of psychiatric disease including depression, personality changes, or even psychosis. Physical examination yielded stance and gait problems in about one third of patients that could be attributed to afferent ataxia in 26%, vestibular dysfunction in 6%, and cerebellar ataxia in 6%. Other motor features such as basal ganglia symptoms, pyramidal tract signs, tics, and myoclonus were infrequent. 35% of patients with CD showed deep sensory loss and reduced ankle reflexes in 14%. Gait disturbances in CD do not only result from cerebellar ataxia but also from proprioceptive or vestibular impairment.Gluten ataxia in perspective: epidemiology, genetic susceptibility and clinical characteristicsTwo hundred and twenty-four patients with various causes of ataxia from North Trent (59 familial and/or positive testing for spinocerebellar ataxias 1, 2, 3, 6 and 7, and Friedreich's ataxia, 132 sporadic idiopathic and 33 clinically probable cerebellar variant of multiple system atrophy MSA-C) and 44 patients with sporadic idiopathic ataxia from The Institute of Neurology, London, were screened for the presence of antigliadin antibodies. A total of 1200 volunteers were screened as normal controls. The prevalence of antigliadin antibodies in the familial group was eight out of 59 (14%), 54 out of 132 (41%) in the sporadic idiopathic group, five out of 33 (15%) in the MSA-C group and 149 out of 1200 (12%) in the normal controls. The prevalence in the sporadic idiopathic group from London was 14 out of 44 (32%). The difference in prevalence between the idiopathic sporadic groups and the other groups was highly significant (P < 0.0001 and P < 0.003, respectively). The clinical characteristics of 68 patients with gluten ataxia were as follows: the mean age at onset of the ataxia was 48 years (range 14-81 years) with a mean duration of the ataxia of 9.7 years (range 1-40 years). Ocular signs were observed in 84% and dysarthria in 66%. Upper limb ataxia was evident in 75%, lower limb ataxia in 90% and gait ataxia in 100% of patients. Gastrointestinal symptoms were present in only 13%. MRI revealed atrophy of the cerebellum in 79% and white matter hyperintensities in 19%. Forty-five percent of patients had neurophysiological evidence of a sensorimotor axonal neuropathy. Gluten-sensitive enteropathy was found in 24%. HLA DQ2 was present in 72% of patients. Gluten ataxia is therefore the single most common cause of sporadic idiopathic ataxia. Wheat brain 30. March 2011 William Davis (52) Among the most common effects of wheat are those on the brain. Consume wheat and susceptible individuals will experience a subtle euphoria. Others experience mental cloudiness or sleepiness. (This is what I personally get.) It gets worse. Children with ADHD and autism have difficulty concentrating on a task and have behavioral outbursts after a cookie. Schizophrenics experience paranoid delusions, auditory hallucinations, and worsening of social detachment. People with bipolar disorder can have the manic phase triggered by a breadcrumb. All these effects are blocked by administering drugs that block the brain's opiate receptors. (This is why, by the way, a drug company is planning to release an oral agent, naltrexone, formerly administered to heroin addicts to help control addiction, for weight loss: block the euphoric effect, take away the temptation, lose weight.) Here is Heart Scan Blog reader, Nicole's, mental fog story:I have been grain-free (no gluten free grains either) for quite a long time (about a year and a half). Earlier this week, I decided to try white bread and pasta. The experiment only lasted two days. I had horrible terminal insomnia both nights, causing me on the second night to wake up at 2:30 am unable to get back to sleep at all. I felt drugged and in a mind-fog all the next day and even dozed off a few times! Luckily I had the day off work.I had very bad forgetfulness also. I forgot that I left my bag and groceries at work, so I had to go back for them. Then I had to use my husband's keys to get in because I thought my keys were in my bag, but it turns out they were in my pocket. Then I got my bag, set the alarm, locked the door and then realized I forgot my groceries. So I had to re-open the door, unset the alarm, and go back for the groceries. Then I locked the door, forgetting to set the alarm, so I had to unlock it, open up and set the alarm. It was just ridiculous, I am NEVER like that!In addition to the insomnia and forgetfulness, I also had horrible anxiety and paranoia, almost to the point of panic. Which I NEVER have, I am usually very easy-going, even-tempered, and worry-free. But this was horrible, I really was quite paranoid and anxious about everything. Weird!And the worst, was that in just two days of eating wheat, I gained 4 lbs and 2% bodyfat!! It's two days wheat-free now, and it's finally going back down, but wow. Just two days of wheat-eating caused that much weight and fat gain!Anyway, I've learned my lesson and will continue to avoid grains (including gluten free grains) entirely.Eat more "healthy whole grains"? Modern dwarf Triticum aestivum, perverted even further by agricultural geneticists and modern agribusiness, subsidized by the U.S. government to permit $5 pizza, is better than any terrorist plot to discombobulate the health and performance of the American people. The Westman Diet 27. March 2011 William Davis (71) Dr. Eric Westman has been a vocal proponent of carbohydrate restriction to gain control over diabetes, as have Drs. Richard Bernstein, Mary Vernon, Richard Feinman, and Jeff Volek. Several studies over the years have demonstrated that reductions in carbohydrate content of the diet yield reductions in weight and HbA1c (glycated hemoglobin, a reflection of average blood glucose over the preceding 60-90 days). Among the more important recent clinical studies is a small experience from Duke University's Dr. Eric Westman. In this study, obese type 2 diabetics reduced carbohydrate intake to 20 grams per day or less: no wheat, oats, cornstarch, or sugars. Participants ate nuts, cheese, meats, eggs, and non-starchy vegetables. After 6 months, average weight loss was 24.4 lbs, BMI was reduced from 37.8 to 34.4. At the end of the study, 95% of participants on this severe carbohydrate restriction reduced or eliminated their diabetes medications. That was only after 6 months. Note that the ending BMI was still quite well into the obese range. Imagine what another 6-12 months would do, or achieving BMI somewhere closer to ideal. Curiously, this idea of severe low-carbohydrate restriction to cure or minimize diabetes is not new. Sir William Osler, one of the founders of Johns Hopkins Hospital and author of the longstanding authoritative text, Principles and Practice of Medicine, advocated an diet identical to Dr. Westman's diet. So did Dr. Frederick Banting, discoverer of the pancreatic extract, insulin, to treat childhood diabetics. Before insulin, Banting and his colleagues at the University of Toronto used carbohydrate elimination (less than 10 g per day) to prolong the lives of children with diabetes. This lesson was also learned many times during war time, when staples like bread were unavailable. The Siege of Paris in 1870 yielded cures for diabetes in many (or at least they stopped passing urine that tasted--yes, tasted--sweet and attracted flies), only to have it recur after the siege was over.These are lessons we will have to relearn. As long as the American Diabetes Association and most physicians continue to advocate a diet of reduced fat, increased carbohydrate that includes plenty of "healthy whole grains," diabetics will continue to be diabetics, taking their insulin and multiple medications while developing neuropathy (nervous system degeneration), nephropathy (kidney disease and failure), atherosclerosis and heart attack, cataracts, and die 8 to 10 years earlier than non-diabetics. All the while, we've had the combined wisdom from antiquity onwards: Carbohydrates cause diabetes; elimination of carbohydrates cures diabetes. (This applies, of course, only to adult overweight type 2 diabetics, not type 1 or some of the other variants.) Handy dandy carb index 25. March 2011 William Davis (21) There are a number of ways to gauge your dietary carbohydrate exposure and its physiologic consequences. One of my favorite ways is to do fingerstick blood sugars for a one-hour postprandial glucose. I like this because it provides real-time feedback on the glucose consequences of your last meal. This can pinpoint problem areas in your diet. Another way is to measure small LDL particles. Because small LDL particles are created through a cascade that begins with carbohydrate consumption, measuring them provides an index of both carbohydrate exposure and sensitivity. Drawback: Getting access to the test. For many people, the most practical and widely available gauge of carbohydrate intake and sensitivity is your hemoglobin A1c, or HbA1c. HbA1c reflects the previous 60 to 90 days blood sugar fluctuations, since hemoglobin is irreversibly glycated by blood glucose. (Glycation is also the phenomenon responsible for formation of cataracts from glycation of lens proteins, kidney disease, arthritis from glycation of cartilage proteins, atherosclerosis from LDL glycation and components of the arterial wall, and many other conditions.) HbA1c of a primitive hunter-gatherer foraging for leaves, roots, berries, and hunting for elk, ibex, wild boar, reptiles, and fish: 4.5% or less. HbA1c of an average American: 5.2% (In the population I see, however, it is typically 5.6%, with many 6.0% and higher.)HbA1c of diabetics: 6.5% or greater. Don't be falsely reassured by not having a HbA1c that meets "official" criteria for diabetes. A HbA1c of 5.8%, for example, means that many of the complications suffered by diabetics--kidney disease, heightened risk for atherosclerosis, osteoarthritis, cataracts--are experienced at nearly the same rate as diabetics. With our wheat-free, cornstarch-free, sugar-free diet, we have been aiming to reduce HbA1c to 4.8% or less, much as if you spent your days tracking wild boar. Battery acid and oatmeal 23. March 2011 William Davis (38) Ever notice the warnings on your car's battery? "Danger: Sulfuric acid. Protective eyewear advised. Serious injury possible."Sulfuric acid is among the most powerful and potentially harmful acids known. Get even a dilute quantity in your eyes and you will suffer serious burns and possibly loss of eyesight. Ingest it and you can sustain fatal injury to the mouth and esophagus. Sulfuric acid's potent tendency to react with other compounds is one of the reasons that it is used in industrial processes like petroleum refining. Sulfuric acid is also a component of the harsh atmosphere of Venus. Know what food is the most potent source of sulfuric acid in the body? Oats. Yes: Oatmeal, oat bran, and foods made from oats (you know what breakfast cereal I'm talking about) are the most potent sources of sulfuric acid in the human diet.Why is this important? In the transition made by humans from net-alkaline hunter-gatherer diet to net-acid modern overloaded-with-grains diet, oats tip the scales heavily towards a drop in pH, i.e., more acidic. The more acidic your diet, the more likely it is you develop osteoporosis and other bone diseases, oxalate kidney stones, and possibly other diseases. Here's one reference for this effect. What'll it be: Olive oil or bread? 21. March 2011 William Davis (0) We frequently discuss the advisability of consuming fats, carbohydrates, and various types within each category. But what's the worst of all? Combining fats with carbohydrates.Putting aside the wheat-is-worst form of carbohydrate issue and treating bread as a prototypical carbohydrate, let's play out a typical scenario, a make-believe feeding study in which a theoretical person is fed specific foods. John is our test person, a 40-year old, 5 ft 10 inch, 210 lb, BMI 27.7 (roughly the mean for the U.S.) He starts with an average American diet of approximately 55% carbohydrates and 30% fat. Starting lipoproteins (NMR):LDL particle number 1800 nmol/LSmall LDL 923 nmol/L (The LDL particle number of 1800 nmol/L translates to measured LDL cholesterol of 180 mg/dl, i.e., drop last digit or divide by 10.)Also, calculated LDL cholesterol is 167 mg/dl (yes, underestimating "true" measured LDL), HDL 42 mg/dl, triglycerides 170 mg/dl.We feed him a diet increased in carbohydrates and reduced in fat, especially saturated fat, with more breakfast cereals, breads and other wheat products, pasta, fruit juices and fruit, and potatoes. After four weeks:LDL particle number 2200 nmol/LSmall LDL 1378 nmol/LNote that LDL particle number has increased by 400 nmol/L due entirely to the increase in small LDL particles triggered by carbohydrate consumption. Lipids show calculated LDL cholesterol 159 mg/dl--yes, a decrease, HDL 40 mg/dl, triglycerides 189 mg/dl. (At this point, if John's primary care doctor saw these numbers, he would congratulate John on reducing his LDL cholesterol and/or suggest a fibrate drug to reduce triglycerides.)John takes a rest for four weeks during which his lipoproteins revert back to their starting values. We then repeat the process, this time replacing most carbohydrate calories with fats, weighed heavily in favor of saturated fats like fatty red meats, butter and other full-fat dairy products. After four weeks:LDL particle number 2400 nmol/LLet's Chocolate peanut butter cup smoothie 19. March 2011 William Davis (18) Here's a simple recipe for chocolate peanut butter cup smoothie. The coconut milk, nut butter, and flaxseed make this smoothie exceptionally filling. If you are a fan of cocoa flavonoids for reducing blood pressure, then this provides a wallop. Approximately 10% of cocoa by weight consists of the various cocoa flavonoids, like procyanidins (polymers of catechin and epicatechin) and quercetin, the components like responsible for many of the health benefits of cocoa. Ingredients:1/2 cup coconut milk1 cup unsweetened almond milk2 tablespoons cocoa powder (without alkali)2 tablespoons shredded coconut (unsweetened)1 tablespoon ground flaxseed1 teaspoon almond extract 1 1/2 tablespoons natural peanut, almond, or sunflower seed butterNon-nutritive sweetener to taste (stevia, Truvia, sucralose, xylitol, erythritol)4 ice cubesCombine ingredients in blender. Blend and serve. If you plan to set any of the smoothie aside, then leave out the flaxseed, as it absorbs water and will expand and solidify if left to stand. For an easy variation, try adding vanilla extract or 1/4 cup of sugar-free (sucralose) vanilla or coconut syrup from Torani or DaVinci and leave out the added sweetener. The compromise I draw here is the use of non-nutritive sweeteners. Beware that they can increase appetite, since they likely trigger insulin release. However, this smoothie is so filling that I don't believe you will experience this effect with this recipe. << Older posts Newer posts >> Newer posts12...8910111213141516...121122Older posts
When MIGHT statins be helpful? 7. April 2011 William Davis (17) I spend a lot of my day bashing statin drugs and helping people get rid of them. But are there instances in which statin drugs do indeed provide real advantage? If someone follows the diet I've articulated in these posts and in the Track Your Plaque program, supplements omega-3 fatty acids and vitamin D, normalizes thyroid measures, and identifies and corrects hidden genetic sources of cardiovascular risk (e.g., Lp(a)), then are there any people who obtain incremental benefit from use of a statin drug?I believe there are some groups of people who do indeed do better with statin drugs. These include:Apoprotein E4 homozygotesApoprotein E2 homozygotesFamilial combined hyperlipidemia (apoprotein B overproduction and/or defective degradation)Cholesteryl ester transfer protein homozygotes (though occasionally manageable strictly with diet)Familial heterozygous hypercholesterolemia, familial homozygous hypercholesterolemiaOther rare variants, e.g., apo B and C variantsThe vast majority of people now taking statin drugs do NOT have the above genetic diagnoses. The majority either have increased LDL from the absurd "cut your fat, eat more healthy whole grains" diet that introduces grotesque distortions into metabolism (like skyrocketing apo B/VLDL and small LDL particles) or have misleading calculated LDL cholesterol values (since conventional LDL is calculated, not measured).As time passes, we are witnessing more and more people slow, stop, or reverse coronary plaque using no statin drugs. Like antibiotics and other drugs, there may be an appropriate time and situation in which they are helpful, but not for every sneeze, runny nose, or chill. Same with statin drugs: There may be an occasional person who, for genetically-determined reasons, is unable to, for example, clear postprandial (after-eating) lipoproteins from the bloodstream and thereby develops coronary atherosclerotic plaque and heart attack at age 40. But these people are the exception.
Advanced topics in nutrition 5. April 2011 William Davis (0) Nutrition in the modern world has become an increasingly problematic topic. From genetic modification to commercialized methods of mass production, we are having to navigate all manner of complex issues in food choices, particularly if ideal health, including maximal control over coronary plaque, is among our goals. We will therefore be releasing a series of discussions on the Track Your Plaque website in the coming months, a series I call "Track Your Plaque Advanced Topics in Nutrition." These will be, as the series title suggests, discussions for anyone interested in more than the "eat a balanced diet" nonsense that issues from "official" sources. Among the topics to be covered:1)Advanced Glycation End-products--both endogenous and exogenous, including peripheral issues like lipoxidation and acrylamides. 2)Dietary influences on LDL oxidation--including the concept of "glycoxidation." Protection from oxidative phenomena is not just about taking antioxidants. 3) Foods you MUST eat--We've talked a lot about foods that you shouldn't eat. How about foods you should eat?
The New Track Your Plaque Guide now available 4. April 2011 William Davis (5) The New Track Your Plaque Guide is now available!The Track Your Plaque program has evolved over its 8 year history. While the original Track Your Plaque book reflected the program details that got the program started back in 2003-2004, plenty has changed. This new version of the book, what I call the program Guide, represents version 2.0 of Track Your Plaque and includes:--Updated lipoprotein treatment strategies--including new and expanded treatment choices for small LDL and lipoprotein(a).--An entire chapter on vitamin D and its crucial role in cardiovascular health and plaque control.--A new and expanded diet--All the reasons why the New Track Your Plaque Diet can achieve spectacular improvement in lipids/lipoproteins, reversal of insulin resistance/pre-diabetes/diabetes, weight loss, reduction in blood pressure, etc. are discussed in considerable detail. The diet is crafted to achieve maximum control over both metabolic responses and coronary plaque. --An entire chapter on the role of omega-3 fatty acids is included. --A detailed discussion on the role of iodine and thyroid health--One of the newest additions to the Track Your Plaque menu of strategies is to achieve and maintain ideal thyroid health. This tips the scales in your favor for improved control over lipids/lipoproteins, weight, blood sugar, and coronary plaque. The new guide, as well as our new Member kits that include the new Track Your Plaque Recipe Book, At-Home Lab Test kits, and nutritional supplements, are all available in the Track Your Plaque Marketplace.
Don't wet yourself 3. April 2011 William Davis (13) While there is more to wheat's adverse effects on human health than celiac disease, studying celiac disease provides important insights into why and how wheat--the gluten component of wheat, in this case--is so destructive to human health. Modern wheat, in particular, is capable of causing "celiac disease" without intestinal symptoms---no cramping or diarrhea--but instead shows itself as brain injury (ataxia, dementia), peripheral nervous system damage (peripheral neuropathy), joint and muscle inflammation (rheumatoid arthritis, polymyalgia rheumatica and others), and gastrointestinal cancers. One neurological manifestation of wheat's effect on the human brain is a condition called cerebellar ataxia. This is a condition that can affect adults (average age 48 years) and children and consists of incoordination, falls, and incontinence. Because brain tissue has limited capacity for healing and regeneration, symptoms of cerebellar ataxia usually improve slowly and modestly with meticulous elimination of wheat and other gluten sources. Such observations are relevant even to people without celiac disease. Celiac disease sufferers are more susceptible to such extra-intestinal phenomena, but it can also happen in people without positive celiac antibodies. Some references:Neurological symptoms in patients with biopsy proven celiac diseaseA total of 72 patients with biopsy proven celiac disease (CD) (mean age 51 +/- 15 years, mean disease duration 8 +/- 11 years) were recruited through advertisements. All participants adhered to a gluten-free diet. Patients were interviewed following a standard questionnaire and examined clinically for neurological symptoms. Medical history revealed neurological disorders such as migraine (28%), carpal tunnel syndrome (20%), vestibular dysfunction (8%), seizures (6%), and myelitis (3%). Interestingly, 35% of patients with CD reported of a history of psychiatric disease including depression, personality changes, or even psychosis. Physical examination yielded stance and gait problems in about one third of patients that could be attributed to afferent ataxia in 26%, vestibular dysfunction in 6%, and cerebellar ataxia in 6%. Other motor features such as basal ganglia symptoms, pyramidal tract signs, tics, and myoclonus were infrequent. 35% of patients with CD showed deep sensory loss and reduced ankle reflexes in 14%. Gait disturbances in CD do not only result from cerebellar ataxia but also from proprioceptive or vestibular impairment.Gluten ataxia in perspective: epidemiology, genetic susceptibility and clinical characteristicsTwo hundred and twenty-four patients with various causes of ataxia from North Trent (59 familial and/or positive testing for spinocerebellar ataxias 1, 2, 3, 6 and 7, and Friedreich's ataxia, 132 sporadic idiopathic and 33 clinically probable cerebellar variant of multiple system atrophy MSA-C) and 44 patients with sporadic idiopathic ataxia from The Institute of Neurology, London, were screened for the presence of antigliadin antibodies. A total of 1200 volunteers were screened as normal controls. The prevalence of antigliadin antibodies in the familial group was eight out of 59 (14%), 54 out of 132 (41%) in the sporadic idiopathic group, five out of 33 (15%) in the MSA-C group and 149 out of 1200 (12%) in the normal controls. The prevalence in the sporadic idiopathic group from London was 14 out of 44 (32%). The difference in prevalence between the idiopathic sporadic groups and the other groups was highly significant (P < 0.0001 and P < 0.003, respectively). The clinical characteristics of 68 patients with gluten ataxia were as follows: the mean age at onset of the ataxia was 48 years (range 14-81 years) with a mean duration of the ataxia of 9.7 years (range 1-40 years). Ocular signs were observed in 84% and dysarthria in 66%. Upper limb ataxia was evident in 75%, lower limb ataxia in 90% and gait ataxia in 100% of patients. Gastrointestinal symptoms were present in only 13%. MRI revealed atrophy of the cerebellum in 79% and white matter hyperintensities in 19%. Forty-five percent of patients had neurophysiological evidence of a sensorimotor axonal neuropathy. Gluten-sensitive enteropathy was found in 24%. HLA DQ2 was present in 72% of patients. Gluten ataxia is therefore the single most common cause of sporadic idiopathic ataxia.
Wheat brain 30. March 2011 William Davis (52) Among the most common effects of wheat are those on the brain. Consume wheat and susceptible individuals will experience a subtle euphoria. Others experience mental cloudiness or sleepiness. (This is what I personally get.) It gets worse. Children with ADHD and autism have difficulty concentrating on a task and have behavioral outbursts after a cookie. Schizophrenics experience paranoid delusions, auditory hallucinations, and worsening of social detachment. People with bipolar disorder can have the manic phase triggered by a breadcrumb. All these effects are blocked by administering drugs that block the brain's opiate receptors. (This is why, by the way, a drug company is planning to release an oral agent, naltrexone, formerly administered to heroin addicts to help control addiction, for weight loss: block the euphoric effect, take away the temptation, lose weight.) Here is Heart Scan Blog reader, Nicole's, mental fog story:I have been grain-free (no gluten free grains either) for quite a long time (about a year and a half). Earlier this week, I decided to try white bread and pasta. The experiment only lasted two days. I had horrible terminal insomnia both nights, causing me on the second night to wake up at 2:30 am unable to get back to sleep at all. I felt drugged and in a mind-fog all the next day and even dozed off a few times! Luckily I had the day off work.I had very bad forgetfulness also. I forgot that I left my bag and groceries at work, so I had to go back for them. Then I had to use my husband's keys to get in because I thought my keys were in my bag, but it turns out they were in my pocket. Then I got my bag, set the alarm, locked the door and then realized I forgot my groceries. So I had to re-open the door, unset the alarm, and go back for the groceries. Then I locked the door, forgetting to set the alarm, so I had to unlock it, open up and set the alarm. It was just ridiculous, I am NEVER like that!In addition to the insomnia and forgetfulness, I also had horrible anxiety and paranoia, almost to the point of panic. Which I NEVER have, I am usually very easy-going, even-tempered, and worry-free. But this was horrible, I really was quite paranoid and anxious about everything. Weird!And the worst, was that in just two days of eating wheat, I gained 4 lbs and 2% bodyfat!! It's two days wheat-free now, and it's finally going back down, but wow. Just two days of wheat-eating caused that much weight and fat gain!Anyway, I've learned my lesson and will continue to avoid grains (including gluten free grains) entirely.Eat more "healthy whole grains"? Modern dwarf Triticum aestivum, perverted even further by agricultural geneticists and modern agribusiness, subsidized by the U.S. government to permit $5 pizza, is better than any terrorist plot to discombobulate the health and performance of the American people.
The Westman Diet 27. March 2011 William Davis (71) Dr. Eric Westman has been a vocal proponent of carbohydrate restriction to gain control over diabetes, as have Drs. Richard Bernstein, Mary Vernon, Richard Feinman, and Jeff Volek. Several studies over the years have demonstrated that reductions in carbohydrate content of the diet yield reductions in weight and HbA1c (glycated hemoglobin, a reflection of average blood glucose over the preceding 60-90 days). Among the more important recent clinical studies is a small experience from Duke University's Dr. Eric Westman. In this study, obese type 2 diabetics reduced carbohydrate intake to 20 grams per day or less: no wheat, oats, cornstarch, or sugars. Participants ate nuts, cheese, meats, eggs, and non-starchy vegetables. After 6 months, average weight loss was 24.4 lbs, BMI was reduced from 37.8 to 34.4. At the end of the study, 95% of participants on this severe carbohydrate restriction reduced or eliminated their diabetes medications. That was only after 6 months. Note that the ending BMI was still quite well into the obese range. Imagine what another 6-12 months would do, or achieving BMI somewhere closer to ideal. Curiously, this idea of severe low-carbohydrate restriction to cure or minimize diabetes is not new. Sir William Osler, one of the founders of Johns Hopkins Hospital and author of the longstanding authoritative text, Principles and Practice of Medicine, advocated an diet identical to Dr. Westman's diet. So did Dr. Frederick Banting, discoverer of the pancreatic extract, insulin, to treat childhood diabetics. Before insulin, Banting and his colleagues at the University of Toronto used carbohydrate elimination (less than 10 g per day) to prolong the lives of children with diabetes. This lesson was also learned many times during war time, when staples like bread were unavailable. The Siege of Paris in 1870 yielded cures for diabetes in many (or at least they stopped passing urine that tasted--yes, tasted--sweet and attracted flies), only to have it recur after the siege was over.These are lessons we will have to relearn. As long as the American Diabetes Association and most physicians continue to advocate a diet of reduced fat, increased carbohydrate that includes plenty of "healthy whole grains," diabetics will continue to be diabetics, taking their insulin and multiple medications while developing neuropathy (nervous system degeneration), nephropathy (kidney disease and failure), atherosclerosis and heart attack, cataracts, and die 8 to 10 years earlier than non-diabetics. All the while, we've had the combined wisdom from antiquity onwards: Carbohydrates cause diabetes; elimination of carbohydrates cures diabetes. (This applies, of course, only to adult overweight type 2 diabetics, not type 1 or some of the other variants.)
Handy dandy carb index 25. March 2011 William Davis (21) There are a number of ways to gauge your dietary carbohydrate exposure and its physiologic consequences. One of my favorite ways is to do fingerstick blood sugars for a one-hour postprandial glucose. I like this because it provides real-time feedback on the glucose consequences of your last meal. This can pinpoint problem areas in your diet. Another way is to measure small LDL particles. Because small LDL particles are created through a cascade that begins with carbohydrate consumption, measuring them provides an index of both carbohydrate exposure and sensitivity. Drawback: Getting access to the test. For many people, the most practical and widely available gauge of carbohydrate intake and sensitivity is your hemoglobin A1c, or HbA1c. HbA1c reflects the previous 60 to 90 days blood sugar fluctuations, since hemoglobin is irreversibly glycated by blood glucose. (Glycation is also the phenomenon responsible for formation of cataracts from glycation of lens proteins, kidney disease, arthritis from glycation of cartilage proteins, atherosclerosis from LDL glycation and components of the arterial wall, and many other conditions.) HbA1c of a primitive hunter-gatherer foraging for leaves, roots, berries, and hunting for elk, ibex, wild boar, reptiles, and fish: 4.5% or less. HbA1c of an average American: 5.2% (In the population I see, however, it is typically 5.6%, with many 6.0% and higher.)HbA1c of diabetics: 6.5% or greater. Don't be falsely reassured by not having a HbA1c that meets "official" criteria for diabetes. A HbA1c of 5.8%, for example, means that many of the complications suffered by diabetics--kidney disease, heightened risk for atherosclerosis, osteoarthritis, cataracts--are experienced at nearly the same rate as diabetics. With our wheat-free, cornstarch-free, sugar-free diet, we have been aiming to reduce HbA1c to 4.8% or less, much as if you spent your days tracking wild boar.
Battery acid and oatmeal 23. March 2011 William Davis (38) Ever notice the warnings on your car's battery? "Danger: Sulfuric acid. Protective eyewear advised. Serious injury possible."Sulfuric acid is among the most powerful and potentially harmful acids known. Get even a dilute quantity in your eyes and you will suffer serious burns and possibly loss of eyesight. Ingest it and you can sustain fatal injury to the mouth and esophagus. Sulfuric acid's potent tendency to react with other compounds is one of the reasons that it is used in industrial processes like petroleum refining. Sulfuric acid is also a component of the harsh atmosphere of Venus. Know what food is the most potent source of sulfuric acid in the body? Oats. Yes: Oatmeal, oat bran, and foods made from oats (you know what breakfast cereal I'm talking about) are the most potent sources of sulfuric acid in the human diet.Why is this important? In the transition made by humans from net-alkaline hunter-gatherer diet to net-acid modern overloaded-with-grains diet, oats tip the scales heavily towards a drop in pH, i.e., more acidic. The more acidic your diet, the more likely it is you develop osteoporosis and other bone diseases, oxalate kidney stones, and possibly other diseases. Here's one reference for this effect.
What'll it be: Olive oil or bread? 21. March 2011 William Davis (0) We frequently discuss the advisability of consuming fats, carbohydrates, and various types within each category. But what's the worst of all? Combining fats with carbohydrates.Putting aside the wheat-is-worst form of carbohydrate issue and treating bread as a prototypical carbohydrate, let's play out a typical scenario, a make-believe feeding study in which a theoretical person is fed specific foods. John is our test person, a 40-year old, 5 ft 10 inch, 210 lb, BMI 27.7 (roughly the mean for the U.S.) He starts with an average American diet of approximately 55% carbohydrates and 30% fat. Starting lipoproteins (NMR):LDL particle number 1800 nmol/LSmall LDL 923 nmol/L (The LDL particle number of 1800 nmol/L translates to measured LDL cholesterol of 180 mg/dl, i.e., drop last digit or divide by 10.)Also, calculated LDL cholesterol is 167 mg/dl (yes, underestimating "true" measured LDL), HDL 42 mg/dl, triglycerides 170 mg/dl.We feed him a diet increased in carbohydrates and reduced in fat, especially saturated fat, with more breakfast cereals, breads and other wheat products, pasta, fruit juices and fruit, and potatoes. After four weeks:LDL particle number 2200 nmol/LSmall LDL 1378 nmol/LNote that LDL particle number has increased by 400 nmol/L due entirely to the increase in small LDL particles triggered by carbohydrate consumption. Lipids show calculated LDL cholesterol 159 mg/dl--yes, a decrease, HDL 40 mg/dl, triglycerides 189 mg/dl. (At this point, if John's primary care doctor saw these numbers, he would congratulate John on reducing his LDL cholesterol and/or suggest a fibrate drug to reduce triglycerides.)John takes a rest for four weeks during which his lipoproteins revert back to their starting values. We then repeat the process, this time replacing most carbohydrate calories with fats, weighed heavily in favor of saturated fats like fatty red meats, butter and other full-fat dairy products. After four weeks:LDL particle number 2400 nmol/LLet's
Chocolate peanut butter cup smoothie 19. March 2011 William Davis (18) Here's a simple recipe for chocolate peanut butter cup smoothie. The coconut milk, nut butter, and flaxseed make this smoothie exceptionally filling. If you are a fan of cocoa flavonoids for reducing blood pressure, then this provides a wallop. Approximately 10% of cocoa by weight consists of the various cocoa flavonoids, like procyanidins (polymers of catechin and epicatechin) and quercetin, the components like responsible for many of the health benefits of cocoa. Ingredients:1/2 cup coconut milk1 cup unsweetened almond milk2 tablespoons cocoa powder (without alkali)2 tablespoons shredded coconut (unsweetened)1 tablespoon ground flaxseed1 teaspoon almond extract 1 1/2 tablespoons natural peanut, almond, or sunflower seed butterNon-nutritive sweetener to taste (stevia, Truvia, sucralose, xylitol, erythritol)4 ice cubesCombine ingredients in blender. Blend and serve. If you plan to set any of the smoothie aside, then leave out the flaxseed, as it absorbs water and will expand and solidify if left to stand. For an easy variation, try adding vanilla extract or 1/4 cup of sugar-free (sucralose) vanilla or coconut syrup from Torani or DaVinci and leave out the added sweetener. The compromise I draw here is the use of non-nutritive sweeteners. Beware that they can increase appetite, since they likely trigger insulin release. However, this smoothie is so filling that I don't believe you will experience this effect with this recipe.