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.
No more Lovaza 30. July 2010 William Davis (45) That's it: I will NEVER ever write another prescription for Lovaza. I actually very rarely write a prescription for Lovaza, i.e., prescription fish oil. But this was the last straw.I advised a patient that we've had good success using high-doses of fish oil to reduce lipoprotein(a), Lp(a). 6000 mg per day of the omega-3 component (EPA + DHA) from fish oil reduces Lp(a) in 60% of people after one year. (Recall that Lp(a) is the most aggressive known lipid-related cause of heart disease.) The two preparations I generally suggest are either the very affordable Sam's Club Members Mark Triple-Strength Fish Oil with 900 mg EPA + DHA per capsule: 7 capsules per day. Another great product (my personal favorite because of its extreme purity--it doesn't even smell like fish oil): Pharmax Finest Pure Fish Oil with 1800 mg EPA + DHA per teaspoon: 3 to 3 1/2 teaspoons per day. Both preparations work great and are quite affordable, given the high dose. For the Sam's Club preparation, it will cost around $30 per month, while the Pharmax liquid will run around $49 per month. Well, the woman's husband insisted on a prescription for Lovaza. One Lovaza capsule contains 784 mg EPA + DHA per capsule: 7 to 8 capsules per day. Here are some prices for Lovaza from online pharmacy discounters:Prescription Giant: $78.99 for 30 capsules ($2.63 per capsule)Planet Drugs Direct: $135 for 100 capsules ($1.35 per capsule)These are lower than the prices I obtained in past by calling local pharmacies in my area, quite a bit lower, in fact. Filling the Lovaza prescription at Prescription Giant will therefore cost $552.93 to $631.92 per month; at Planet Drugs Direct it will cost $283.50 to $324.00 per month. At local pharmacies, a similar 7 to 9 capsules Lovaza per day will cost upwards of $800 to $900 per month. The patient's husband insisted on the Lovaza prescription because he knew that his insurance would cover it. When I pointed out that this was a large cost that would have to be borne by others in their healthcare premiums, he said that didn't matter to him. I hesitated, but ended up writing the prescription for 7 Lovaza capsules per day. As soon as I handed to him, I regretted it. In fact, I am embarassed and angry at myself for having given in. So I vowed: I will NEVER EVER write another prescription for Lovaza. I do not believe that we should spread the excessive profiteering of the pharmaceutical industry around on the backs of people who pay their healthcare insurance premiums, just so that a few people, like this selfish couple, can save a few dollars a month.
This is your brain on wheat II 29. July 2010 William Davis (24) In the original Heart Scan Blog post, This is your brain on wheat, I discussed how opioid peptides (i.e., small proteins that act like opiates such as heroine or morphine) that result from digestion of wheat cause unique effects on the human brain, particularly addictive behaviors. I also briefly reviewed how elimination of wheat has been shown to reduce auditory hallucinations and other psychotic behaviors in a subset of people with paranoid schizophrenia. These two phenomena, addictions and schizophrenia, are most likely the result of exorphins that cross the blood-brain barrier. Exorphins--exogenous morphine-like compounds--can be blocked by opiate-blocking drugs like naloxone and naltrexone. Naloxone is used in hospitals to reverse morphine or heroine overdoses; naltrexone is being repackaged into a weight loss drug, since blocking wheat-derived exorphins reduces appetite. (Yes: The USDA tells us to eat more wheat, the drug industry sells us the antidote.) There's another way that wheat can affect the brain and nervous system: immune-activated damage. This is similar to the effect seen in celiac. There's even overlap with some of the antibody markers used to diagnose celiac, like the anti-gliadin antibodies and the anti-endomysium antibodies. The most common immune neurological syndrome consequent to wheat consumption is cerebellar ataxia, a condition in which an immune response causes damage to the Purkinje cells of the cerebellum, the portion of the brain responsible for balance and coordination. This results in stumbling, incoordination, incontinence, and eventually leads to reliance on a cane or walker and wearing a diaper. Average age of onset: 53 years. A shrunken, atrophied cerebellum can be seen on an MRI of the brain.Problem: Most people with central nervous system damage caused by wheat do not have any intestinal symptoms, like diarrhea and abdominal pain, the sort of symptoms usually associated with celiac disease. It means the first sign of wheat-induced brain damage may be bumping into walls and wetting your pants.
There's no such thing as a "no-carb" diet 27. July 2010 William Davis (24) When I tell patients how I advise a wheat-free, cornstarch-free, sugar-free diet on the background of a low-carbohydrate diet, some people ask: "But can I live on a no-carb diet?"Well, there's no such thing as a "no-carb" diet. Low-carb, yes. No-carb, no.Here are the carbohydrate contents of various "low-carb" foods:Gouda cheese--3 oz contains 1.65 grams carbohydratesMozzarella cheese--1 cup contains 2.89 grams carbohydrates Walnuts--4 oz (56 nuts) contains 2.96 grams carbohydratesAlmonds--4 oz contains 1.38 grams carbohydratesSour cream--one-half cup contains 3.31 grams carbohydratesRed wine--3.5 oz glass contains 2.69 grams carbohydratesEggplant--1 cup cooked contains 8.33 grams carbohydratesGreen pepper--1 medium-sized raw contains 5.52 grams carbohydratesCucumber--1 medium contains 4.34 grams carbohydratesTomato--1 medium contains 4.82 grams carbohydrates (Nutrition data from USDA Nutrient Database)In other words, foods thought to be "low-carb" actually contain a modest quantity of carbohydrates. Such modest quantities of carbohydrates may not be enough to trip your blood sugar. But add up all the "low-carb" foods you consume over the course of a day and you can easily achieve 30 grams or more carbohydrates per day even without consuming any higher carbohydrate foods.
Why doesn't your doctor try to CURE diabetes? 21. July 2010 William Davis (88) Imagine you have breast cancer. You go to your doctor and she says, "As your pain worsens, we'll help you with pain medication. We'll fit you with a special bra to accommodate the tumor as it grows. That's all we're going to do.""What?" you ask. "You mean just deal with the disease and its complications, but you're not going to help me get rid of it . . . cure it?" It would be incredibly shocking to receive such advice. Then why is that the sort of advice given when you are diagnosed with diabetes? Say you go to the doctor. Lab values show a fasting blood sugar of 156 mg/dl, HbA1c (a reflection of your previous 60 days average glucose) of 7.1%. Both values show clear-cut diabetes. Your doctor advises you to 1) start the drug metformin, then 2) talk to the diabetic teaching nurse or dietitian about an American Diabetes Association (ADA) diet. The ADA diet prescribed encourages you to increase carbohydrates and cut fats at each meal and maintain a consistent intake so that you don't experience hypoglycemic (low blood sugar) episodes. You follow the diet, which causes you to gain 10-15 lbs per year, increasing your "need" for diabetes medication. You doctor adds Actos, then Januvia, then injections of Byetta. Three years and 34 lbs later, you are not responding well to the drug combination with blood sugars rarely staying below 200 mg/dl. You've developed protein in your urine ("proteinuria"), lost 30% of your kidney function, and you are starting to lose sensation in your feet. So the doctor replaces some of your medication with several insulin injections per day. This formula is followed millions of times per year in the U.S. So where along the way did your doctor mention anything about a "cure"?Adult diabetes is the one chronic disease that nobody cares to cure. Treat it, maintain control over blood sugars, but cure it? Most physicians say it's impossible. The tragedy is that diabetes is a curable condition. I've seen it happen many times. Physicians dedicated to curing diabetes like low-carb expert, Dr. Mary Vernon, have cured it countless times. Dr. Eric Westman and colleagues have been building the case for the carbohydrate-restricted cure for diabetes with studies such as this. In this last study, of the 8 participants on insulin + medications at the start of the study, 5 no longer required medications at the close of the study--they were essentially non-diabetic. I tell patients that diabetes, in fact, is a disease you choose to have or not to have--provided you are provided the right diet and tools. Sadly, rarely are diabetics told about the right diet and tools. That's why Cadbury Schweppes has been a major contributor to the American Diabetes Association, as are other processed food manufacturers and the drug industry, all who stand to profit from maintaining the status quo. The cure? Eliminate or at least dramatically reduce carbohydrates, the foods that increase blood sugar. Note: If you have diabetes and you are taking any prescription agents, such as glyburide, glipizide, insulin, and some others, you will need to discuss how to manage your medications if you reduce carbohydrates. The problem is finding a doctor or other resource to help you do this.
LDL pattern B 18. July 2010 William Davis (17) Here's a Q&A I stumbled on in the Forum of MedHelp, where people obtain answers from presumed health "experts." Question:My VAP test results in July 07 identified an LDL Pattern B. Overall results: Total 150 HDL 75 LDL 61 Trig 60 HDL-2 17 LP(a) 6.0 LDL Pattern B Medications: Lipitor 10mg Zetia 10mg Altace 10mg Atenolol 50mg Plavix 75mg Aspirin 81mg I had several heart attacks which resulted in CABG performed May 2000. I am a 53 year old white male , 6'1", 190 pounds, exercise every day, watch my diet and feel great. Everything looks OK except my LDL Pattern B. Is there any therapy to improve the Patten B? Answer from CCF, MD:Your results indicate an LDL pattern B, which generally indicates small atherogenic LDL particles which may cause increased risk for CAD. However, there are several problems with LDL patterning: 1) its unreliability (of LDL pattern testing ), 2) unclear clinical evidence regarding regarding the usefulness of LDL patterns and particle size. The majority of evidence regarding the progression of atherosclerosis is with LDL lowering and to an smaller extent HDL raising. All available clinical evidence shows that any particles in the VLDL, IDL, or LDL range are atherogenic, and there is no evidence that whether belonging to pattern A or B one is more atherogenic than others. Subclass studies have proliferated over the last few years, but many of these studies were funded or subsidized either by suppliers of the assays as a method to expand their use and move them into mainstream practice, or by pharmaceutical companies in an attempt to claim some advantage over other therapeutic agents. Thus, current data on LDL subclasses are at best incomplete and at worst misleading, suffering from publication bias, and now given the recent results of the Ensign et al. study, unreliable. Your LDL, and HDL are at goal. The Lpa level is still not clearly linked as a modifiable risk factor for CAD, although elevated levels are now know to be linked to stroke. Continue with your present treatments: aspirin, plavix, ateonol and altace are all essential medications. Wow. The extent of ignorance that pervades the ranks of my colleagues is frightening. Contrary to the response, LDL particle size assays are quite reliable and accurate. I've performed many thousands of lipoprotein assays and they yield reproducible and clinically believable results. For example, eliminate wheat, oats, cornstarch, and sugars and small LDL drops from 2400 nmol/L to 893 nmol/L (NMR)--huge drops. If repeated within a short period of time, the second measure will correspond quite closely. The data are also quite clear: Small LDL particles (i.e., "pattern B") are a potent predictor of cardiovascular events. What we lack are the treatment trials that show that reduction of small LDL results in reduced cardiovascular events. The reason for this is that small LDL research is not well-funded, since there is no prescription drug to treat small LDL, only nutritional means. Niacin (as Niaspan) is as close as it comes for a "drug" to reduce small LDL. But diet is far more effective. Given the questioner's fairly favorable BMI of 25.1 and his history of aggressive heart disease, it is virtually certain that he has what I call "genetic small LDL," i.e., small LDL that occur on a genetically-determined basis (likely due to variants of the cholesteryl-ester transfer protein, or CETP, or of hepatic lipase and others). Ignoring this man's small LDL will, without a doubt, consign him to a future of more heart attacks, stents, and bypass. Maybe by that time the data supporting the treatment of small LDL will become available.
What increases blood sugar more than wheat? 15. July 2010 William Davis (38) Take a look at these glycemic indexes (GI):White bread 69Whole wheat bread 72Sucrose 59Mars bar 68White rice 72Brown rice 66I've made issue in past of whole wheat's high GI--higher than white bread. Roughly in the same glycemic league as bread are shredded wheat cereal, brown rice, and a Mars candy bar.With few exceptions, wheat products have among the highest GIs compared to the majority of other foods. For instance:Kidney beans 29Chick peas 36Apple 39Ice cream 36Snickers Bar 40Yes, by the crazy logic of glycemic index, Snickers is a low-glycemic index food. While I do not believe that low GI makes a food good or desirable, since low GI foods still provoke high blood sugars, small LDL particles, trigger glycation, and other abnormal phenomena, they are clearly less obnoxious than the items in the first list. Take a look at this list:Cornflakes 80Rice cakes 80Rice Krispies 82Rice pasta, 92Instant potatoes 83Tapioca 81Starches that are dried and/or pulverized, such as cornstarch, potato starch, rice starch, and tapioca starch (cassava root) will increase blood sugar even more than wheat. Foods with these starches have GI's of 80-100. Cornstarch, potato starch, rice starch, and tapioca starch: Sound familiar? These are the main starches used in "gluten-free" foods. A hint of the high GI behavior of these dried starches is seen in the GI for cornflakes of 80.So remember: Wheat-free is not the same as gluten-free. Gluten-free identifies junk carbohydrates masquerading as healthy because they don't contain one unhealthy ingredient, i.e. wheat.
China fiction? 10. July 2010 William Davis (39) Dr. Colin Campbell caused a stir with publication of his 2005 book, The China Study. Dr. Campbell, after extensive animal and epidemiologic research conducted in China over 20 years, concluded that a diet high in animal protein, especially casein, was associated with increased cancer, osteoporosis, and heart disease risk. Richard Nikoley of Free the Animal and Stephan Guyenet of Whole Health Source have been talking about an analysis of the China Study raw data performed by a young woman named Denise Minger. Denise's analysis is nothing short of brilliant, absolutely "must" reading for anyone interested in nutrition. Her comments on the relationship of wheat to heart disease:Why does Campbell indict animal foods in cardiovascular disease (correlation of +1 for animal protein and -11 for fish protein), yet fail to mention that wheat flour has a correlation of +67 with heart attacks and coronary heart disease, and plant protein correlates at +25 with these conditions?Speaking of wheat, why doesn’t Campbell also note the astronomical correlations wheat flour has with various diseases: +46 with cervix cancer, +54 with hypertensive heart disease, +47 with stroke, +41 with diseases of the blood and blood-forming organs, and the aforementioned +67 with myocardial infarction and coronary heart disease?
Carbohydrate-LDL double whammy 9. July 2010 William Davis (14) Carbohydrates in the diet trigger formation of small LDL particles. Because carbohydrates, such as products made from wheat, increase triglycerides and triglyceride-containing lipoproteins (chylomicrons, chylomicron remnants, VLDL, and IDL), LDL particles (NOT LDL cholesterol) become triglyceride-enriched. Triglyceride-enriched LDL particles are "remodeled" by the enzyme, hepatic lipase, into triglyceride-depleted, small LDL particles. The list of reasons why small LDL particles are more atherogenic, i.e., plaque-causing, is long:--Small LDL particles, being smaller, more readily penetrate the endothelial barrier of the arterial wall. --Small LDL particles are more adherent to glycosaminoglycans in the artery wall. --Small LDL particles are poorly taken up by the liver LDL receptor, but enthusiastically taken up by macrophage receptors of the sort in your artery walls. --Because of their poor liver clearance, small LDL persists in the bloodstream far longer than large LDL. --Small LDL particles are more oxidation-prone. Oxidized LDL are more likely to trigger inflammatory phenomena and be taken up by macrophages in the artery wall. Let me add another reason why small LDL particles are more likely to cause plaque: They are more likely to undergo glycation. (More on glycation here.) Glycation occurs when glucose (sugar) molecules in the blood or tissue modify proteins, usually irreversibly. Small LDL particles are uniquely glycation-prone. (This is likely due to a conformational change of the apoprotein B in the small LDL particle, exposing lysine residues along apo B that become glycated.) Here's a great demonstration of this phenomenon by Younis et al:"LDL3" is the small type. Note that small LDL particles are 4-5 times more glycated than large LDL. That's a big difference. Once glycated, small LDL is especially resistant to being taken up by the liver. Like annoying in-laws, they hang around and hang around and . . . The longer they hang around, they more opportunity they have to contribute to plaque formation. So, carbohydrates trigger formation of small LDL particles. Once formed, small LDL particles are glycated when blood sugar increases. While LDL can be glycated even when blood sugars are in the normal range (90 mg/dl or less), glycation goes berserk when blood sugars go higher, such as a blood sugar of 155 mg/dl after a bowl of steel-cut oatmeal.
To lose weight, prick your finger 8. July 2010 William Davis (45) We know that foods that trigger insulin lead to fat storage. Putting a stop to this process allows you to mobilize fat and lose weight. If you're starting out from scratch, rapid and dramatic weight loss can be experienced, as much as one pound per day. So how can you stop triggering insulin?The easiest way is to eliminate, or at least minimize, carbohydrates. My favorite method to restrict carbohydrates is to eliminate wheat and minimize exposure to other carbohydrates, such as oats, cornstarch, and sugars. All these foods, wheat products worst of all, cause blood sugar and insulin to skyrocket. Another way is to check your blood sugar one hour after completing a meal and keep your after-eating, or "postprandial," blood sugar 100 mg/dl or less. Let's say you are going to eat stone ground oatmeal, for example. Blood sugar prior to eating is, say, 90 mg/dl. One hour after oatmeal it's 168 mg/dl--you know that this is going to trigger insulin and make you fat. Oatmeal should therefore be eliminated. Keeping blood sugar to 100 mg/dl or less after eating teaches you how to avoid provocation of insulin. A shrinking tummy will follow. To do this, you will need:1) A glucose meter--My favorite is the One Touch Ultra Mini ($13.42 at Walmart). It's exceptionally easy to use and requires just a dot of blood. Drawback: Test strips are about $1 each. Accuchek Aviva is another good device. (We've had a lot of problems with Walgreen's brand device.) 2) Test strips--This is the costly part of the proposition. Purchased 25 or 50 at a time, they can cost from $0.50 to $1.00 a piece. 3) Lancets--These are the pins for the fingerstick device that comes with the glucose meter. A box should be just a few dollars. No prescription is necessary, nor will insurance pay for your costs unless you're diabetic. To conserve test strips, use them only when a new, untested food or food combination is going to be consumed. If you had two scrambled eggs with green peppers, sundried tomatoes, and olive oil yesterday and had a one hour postprandial glucose of 97 mg/dl, no need to check blood sugar again if you are having the same meal again today.
Iodine update 2. July 2010 William Davis (30) As the iodine experience grows, I've made several unique observations. Up to several times per day, I see people who are responding in some positive way to iodine supplementation. (See previous Heart Scan Blog posts about iodine: Iodine deficiency is REAL and The healthiest people are the most iodine deficient.) Among the phenomena I've observed:1) A free T4 thyroid hormone at the low end of normal, or even in the below normal range, along with a highish TSH (usually >1.5 mIU/L) are the most frequent patterns that signal iodine deficiency. Occasionally, a low free T3 value will also increase, though this is the least frequent development. 2) At a dose of 500 to 1000 mcg iodine per day, it requires anywhere from 3 to 6 months to obtain normalization of thyroid measures.3) Reversal of small goiters also occurs over about 6 months. 4) Iodine intolerance is uncommon. If it occurs, using a low starting dose, e.g., 100-200 mcg per day, usually works. The dose can be increased gradually over the ensuing months. 5) Perceptible benefits of iodine occur only occasionally. The most common perceptible effects are increased energy and increased warmth, especially of the hands and feet. 6) Some people who have taken thyroid hormones for years will develop reduced need for their medication with iodine supplementation. In other words, their physician was inadvertently treating iodine deficiency with thyroid hormone replacement. Anyone already on any thyroid preparation(s), e.g., Synthroid, levothyroxine, Armour thyroid, Naturethroid, etc., should watch for signs of hyperthyroidism when iodine is added. But having your own thyroid gland make its own thyroid hormones is better and healthier than relying on the prescription agents. Just be sure to monitor your thyroid measures. 7) Iodine toxicity can occur--Two people in my clinic population developed iodine toxicity by taking 6000 mcg iodine per day for 6 or more months. (Both patients did it on their own based on something they read). Iodine toxicity is evidenced by shutting down your thyroid, i.e., marked increase in TSH, e.g., 15 mIU/L. Most of the people in my clinic obtain their iodine from kelp tablets. Some use potassium iodine (KI) drops. A handful have used the high-potency Iodoral (12.5 mg or 12,500 mcg iodine per tablet); this was also the form that generated the toxic effects in the two females. All in all, iodine deficiency is actually far more common than I ever suspected. Not everybody is iodine deficient. But a substantial minority of the Midwest population I see certainly are.