Near-fatal brush with nattokinase 14. April 2010 William Davis (0) Here is precisely why I have spoken out against nattokinase: People may put faith in this "supplement" when there are virtually no data to support its use in such dangerous conditions as pulmonary embolism. Pulmonary embolism occurs when a large volume of blood clots in the veins of the pelvis, abdomen, and into the legs. A clot breaks off and lodges in the pulmonary arteries of the lungs. This can be fatal within minutes to hours, the victim struggling to breathe, since oxygen is not transferred to the blood and it causes terrible pain in the chest. The treatments are fairly obnoxious: intravenous anticoagulants (blood thinners), followed by oral blood thinners like warfarin. While they carry risk of bleeding and other long-term risks, it's better than dying. Would you bet that a "nutritional supplement" manufacturer's vague claims and lack of data are sufficient proof to treat a life-threatening condition? You're a fool if you are. Anyone reading these pages knows that I am a vigorous supporter of nutritional supplements. I even consult for the nutritonal supplement industry. But I am also an advocate of TRUTH, not BS. Here is a woman from England who inquired whether she should stop her husband's warfarin in favor of nattokinase. This is precisely the sort of thing that can happen because of the campaign of misinformation behind nattokinase. Dr. Davis,Thank you for your very interesting blogs, which I came across searching for natural alternative treatments to warfarin. My husband has been following the low carb, high fat, real food regime over the past few years. He got off all the blood pressure and cholesterol drugs and never felt better. He even got his blood sugar down from a recorded high that we are aware of 13 nmol/L (234 mg/dol) to 6.1 nmol/L 109.8 mg/dl). We were on holiday in the Caribbean. Just before our return home, we did a trip to a neighbouring island that included non-alcoholic fruit punches. They tasted great, but were very sweet. I broke my normal refusal to drink these things, but only had a couple of glasses. (After all, we were on holiday!) My husband believes he consumed around 1.5 litres of the stuff and now realises he was feeding his body a very toxic product – fructose. That night, he had an incredible toxic response and we only got him onto the plane with a visit to the hospital and a pain killer injection. The symptoms of pulmonary embolism only showed 2 weeks later . . . and warfarin treatment was started. We would both like to use an alternative therapy if we can find someone with experience to provide the support.Do you know of any studies that support alternative options?Do you know of any practitioners in the England who support a non-drug approach with an understanding of nutrition who we may be able to receive advice and support?FBYork, England
Glucophobia: The Novel 13. April 2010 William Davis (25) Just kidding: No novel here. However, there is indeed a story to tell that should scare the pants off you. If you haven't yet gathered that carbohydrates are a macronutrient nightmare, let me recount the list:Carbohydrates increase small LDL particlesOr, in the cholesterol-speak most people understand, "carbohydrates increase cholesterol." It's counterintuitive, but carbohydrates increase LDL substantially, far more than any fat. Carbohydrates increase blood sugarEggs don't increase blood sugar, nor do chicken, raw almonds, onions or green peppers. But a bowl of oatmeal will send your blood sugar skywards. Carbohydrates make you fatCarbohydrates, whether in the form of wheat flour in your whole wheat bread, sucrose in your ice cream, fructose in your "organic Agave nectar," or high-fructose corn syrup in your dill pickles. They all provoke de novo lipogenesis, or fat formation. They also stimulate insulin, the hormone of fat storage. Carbohydrates cause glycationHigh blood sugar, like the kind that develops after a bowl of oatmeal, triggers glycation, or modification of proteins by glucose (blood sugar). This is how cataracts, kidney disease, and atherosclerotic plaque develop. Small LDL is 8-fold more glycation prone than large LDL, providing a carbohydrate double-whammy. Your glucose meter remains the single best tool to gauge the quality of your diet. Many people have horror stories of the shocking experiences they've had when they finally get around to checking their postprandial glucose.
Drama with the Dr. Oz Show 11. April 2010 William Davis (27) A producer from the Dr. Oz show recently contacted my office. They asked whether we could supply them with a volunteer patient from either my practice or the Track Your Plaque program who would be willing to appear on the show and discuss heart disease prevention. They needed someone to commit within 24 hours. Despite the short notice, we identified a volunteer. He flew to New York the following week where he was interviewed along with several other men and women, all of whom had heart disease (heart attacks, stents, etc.). However, as this young man is very slender and follows most of the Track Your Plaque principles (e.g., vitamin D and omega-3 fatty acid supplementation; no wheat, cornstarch, or sugars, no restriction of fat, etc.), he apparently received less attention than the overweight, I-know-nothing-about-diet interviewees. Then there was an odd turn of events: Dr. Dean Ornish, apparently a friend of Dr. Oz, will be providing the dietary counseling. The producer had made no mention of Dr. Ornish. Now that's an odd collision of philosophies: Our Track Your Plaque version of low-carb with the guru of low-fat, Dr. Ornish. The following week, Dr. Ornish called me and graciously asked whether I was okay with this. I'm not sure just how much he knew about the philosophy I advocate, nor how much I have bashed his program as a destructive approach to diet, nor whether he knew that I gained 30 lbs on the Ornish diet, along with a drop in HDL to 27 mg/dl, increased triglycerides to 350 mg/dl, and type II diabetes that I've talked about on this blog and the Track Your Plaque book and website. I suspect he knew little to none of this. Anyway, I tried to diplomatically explain that my patient's cause for coronary plaque was small LDL particles that he expressed despite his very slender build, likely from excessive carbohydrates, controlled with carbohydrate restriction. Dr. Ornish maintained his usual arguments: Grains are good, provided they are whole grains, heart disease is "reversed" with his diet program, etc. (I didn't want to challenge him in a phone call and tell him that he never actually reversed coronary plaque, but just reversed endothelial dysfunction. But, as Dr. Ornish is not a cardiologist, I wasn't sure how far his understanding of these issues went.) We agreed to disagree. This leaves my poor patient in an odd position: Being asked by Dr. Ornish and the Dr. Oz show to follow a low-fat program for the sake of entertainment, or adhering to the advice we follow that has so far served him well, given his small LDL particle size tendencies. We'll see where this little drama leads.
Response from Nature Made 10. April 2010 William Davis (31) Here's the response from Nature Made when I emailed them about my concern that there appears to be no vitamin D in their vitamin D gelcaps. It is the usually CYA corporate-speak that says nothing. The grammatical errors make it clear that this was a "canned" response. Date: April 9, 2010From: Marissa Reyes, Consumer Affairs DepartmentSubject: Reference #346236Dear William Davis, MD:We recently received your e-mail regarding Nature Made products. We regret to hear that the quality standards of our company. [?]Our company is called Pharmavite, and we manufacture Nature Made nutritional supplements. We have been in business since 1971. We are committed to quality control, and have very high quality standards. Our Quality Control personnel sample and test all raw materials as they enter our plant, and again assay the finished product, before final packaging. Dietary Supplements are regulated under the FDA through DSHEA (Dietary Supplement Health & Education Act of 1994). The United States Pharmacopoeia (USP) establishes standards for the composition of drugs and nutritional supplements. This voluntary non governmental organization was set up in 1820 and has officially been recognized by federal law since 1906. Standards established by USP for products are legally enforceable by the FDA. At Pharmavite we participate in the USP Dietary Supplement Verification Program (DSVP). Many of our products have earned the DSVP seal and additional products are currently being evaluated. Our DSVP certified products will have the DSVP seal on the product label.Our Nature Made Vitamin D 400 IU tablets have been reviewed by the USP and bears the DSVP symbol on the label. Although the USP has not reviewed all of the Nature Made Vitamin D supplements, all of our products go through the same rigorous quality testing at Pharmavite. The products which have earned the seal help us to demonstrate the high quality of our products. We would like to look into the product(s) your patients have been using. If you could provide the UPC and lot numbers of the product(s), we will be happy to review our records. In addition, if you would like us to test the product(s) that you currently have, we will be pleased to send a prepaid postage mailer so you may return the product(s) to us so that our Quality Control Department can examine it. Please let us know if you would like us to send you the prepaid postage mailer. We thank you for contacting us and hope that you will continue to use and enjoy Nature Made products with complete confidence.Sincerely,Marissa ReyesConsumer Affairs CoordinatorPharmavite, LLCMR:346236-10Patients who come to the office do not provide me with the bottles nor lot numbers. In past, when I've gone to the trouble of doing this (with other companies, not Nature Made), it has come to nothing helpful. The information gets passed on to the company and we hear nothing and never learn if there was a problem, or receive some more corporate-speak letter saying everything was fine. This is obviously a liability-avoidance tactic: Admitting that something was wrong would open them up to legal risk. So, frankly, I can't be bothered. So we are left with the unsatisfying experience of relying on street-level experiences. For now, my advice: Avoid Nature Made vitamin D. Too many people have had blood tests demonstrating that they are not obtaining any vitamin D. By the way, the Nature Made brand of fish oil is among the very few problem brands of fish oil we've encountered. Fish oil should be only mildly fish in smell and generally should not cause stomach upset and excessive belching if properly purified. Nature Made is excessively fishy when you smell it, suggesting oxidation. We've had repeated (dozens) of patients who have experienced difficulties with this brand. Rather than dealing with the frustrating gobbledy-gook of this company, just avoid their products.
What to Eat: The diet is defined by small LDL 9. April 2010 William Davis (15) I approach diet from the perspective of small LDL particles. Small LDL particles have exploded in frequency and severity in Americans. It is not at all uncommon to see 70% or more small LDL particles (i.e., 70% of total LDL particle number or Apo B) on lipoprotein testing. (I saw two people today who began with over 95% small LDL.)Small LDL particles are:--More likely to persist in the bloodstream longer than large LDL particles. --More likely to adhere to components of atherosclerotic plaque. --More likely to gain entry to plaque.--More likely to be taken up by inflammatory white blood cells which, in turn, become the mast cells that fill coronary plaque. --More likely to be oxidized. --More likely to be glycated (8-fold more likely than large)To add insult to injury, foods that trigger small LDL formation--i.e., carbohydrates--also cause high postprandial blood sugars. High postprandial blood sugars, in turn, glycate small LDL. That combination of events accelerates 1) plaque growth, 2) plaque instability, and 3) aging. So carbohydrates trigger this sequence, carbohydrates of all stripes and colors. Not just "white" carbohydrates, but ALL carbohydrates. It's all a matter of degree and quantity. So, yes, even quinoa, bulghur, and sorghum trigger this process. I've only recently appreciated just how bad oats and oatmeal are in this regard--really bad.Foods that trigger small LDL also trigger higher blood sugars; foods that trigger higher blood sugars also trigger small LDL. Small LDL and blood sugar are two different things, but they track each other very closely. So, in the Track Your Plaque approach to diet, we craft diet based on these simple principles:1) Eliminate wheat, cornstarch, and sugars--These are the most flagrant triggers of small LDL, blood sugar, and, therefore, LDL glycation. 2) The inclusion of other carbohydrates, such as oatmeal, quinoa, rye, etc. depends on individual sensitivity. Individual sensitivity is best gauged by assessing one-hour postprandial glucose. Stay tuned for more in this series. Also, Track Your Plaque Members: We will be having an in-depth webinar detailing more on thees principles in the next couple of weeks.
Is it or isn't it vitamin D? 7. April 2010 William Davis (63) Jackie takes 10,000 units of vitamin D(3) per day as a gelcap.Her starting 25-hydroxy vitamin D blood level was 18.1 ng/ml. Severe deficiency, no surprise. On her 10,000 units per day, Vitamin Shoppe brand, her 25-hydroxy vitamin D level was 76.2 ng/ml--perfect. It stayed in this range for about two years. She then changed to the Nature Made brand gelcaps she picked up at Walgreen's. Repeat 25-hydroxy vitamin D level: 23 ng/ml. This has now happened with five different people, all taking the Nature Made brand. If you are taking this brand of vitamin D, please be on the alert. You might consider a 25-hydroxy vitamin D blood level to be sure it actually has the vitamin D it's supposed to have. Or, change brands.
What to eat: Part I 6. April 2010 William Davis (0) I've spent a good number of Heart Scan Blog posts detailing what foods to limit or avoid. The list of unquestionably bad foods to avoid include foods made of wheat, cornstarch, and sugars. Fructose is proving to be an exceptionally bad form of sugar, worse than any other. I've issued warnings about levels of carbohydrates that can be determined by postprandial testing. In response to several requests to clarify what foods to eat, this post begins a series discussing what foods are good to eat. I believe that a strong case can be made for eating vegetables in nearly all its varied forms, from cucumbers to peppers to leafy vegetables to eggplant to alliums like onions. The only form we avoid are red and white potatoes due to the blood sugar-increasing effects. While this seems obvious, I am impressed how many people who follow low-carb diets find themselves following a high-animal product diet with vegetables as the sideline. It should be the other way around: A high vegetable diet with animal products as the sideline. Vegetables are your principal source of:1) Flavonoids and polyphenols--e.g., anthocyanins and catechins. All the recently appreciated effects of flavonoids and polyphenols highlight the wonderful effects of compounds originating in plant foods. This includes the anthocyanins and resveratrol in red wine; the catechins and epicatechins cocoa and green tea; the hydroxytyrosol, phenolic acid, and flavonoids of olive oil. 2) Fiber--Fiber is essentially a plant phenomenon, since there is virtually none in chicken, fish, and beef. The benefits of fiber are, I believe, undisputed. Neglecting fiber can, at the very least, lead to a nasty case of hemorrhoids. At the worst, it is related to various cancers, especially colon cancer. 3) Vitamin C--While vitamin C may be old and boring in light of new, exciting discoveries like flavonoids, neglect leads to bad things. Vegetables are generally classified as carbohydrate foods, since they are low in protein and fat. But this is the source of carbohydrates you do not want to sacrifice in a low-carbohydrate diet. There's just too much good from vegetables. Notice that I didn't say "fruits and vegetables." This is a fundamental mistake made by many: Oveconsumption of fruits. I've even seen people who follow an otherwise good diet develop diabetes--just from too much fruit. Vegetables should be the cornerstone of the human diet. But I'll bet you knew that already.
Carbohydrates and LDL 4. April 2010 William Davis (16) There's a curious and powerful relationship between carbohydrates and LDL particles. Understanding this relationship is crucial to gaining control over heart disease risk. (Note that I did not say "LDL cholesterol"--This is what confuses people, the notion that cholesterol is used as a surrogate marker to quantify various lipoproteins, including low-density lipoproteins, LDL. I'm NOT interested in the cholesterol; I'm interested in the behavior of the low-density lipoprotein particle. There's a difference.)Carbohydrates:1) Increase triglycerides and very low-density lipoprotein particles (VLDL)2) Triglyceride-rich VLDL interact with LDL particles, making them smaller. (A process mediated by several enzymes, such as cholesteryl-ester transfer protein.)3) Smaller LDL particles are more oxidizable--Oxidized LDL particles are the sort that are taken up by inflammatory white blood cells residing in the artery wall and atherosclerotic plaque. 4) Smaller LDL particles are more glycatable--Glycation of LDL is an important phenomenon that makes the LDL particle more atherogenic (plaque-causing). Glycated LDLs are not recognized by the LDL receptor, causing them to persist in the bloodstream longer than non-glcyated LDL. Glycated LDL is therefore taken up by inflammatory white blood cells in plaque. Of course, carbohydrates also make you fat, further fueling the fire of this sequence. The key is to break this chain: Cut out the carbohydrates. Cut carbohydrates and VLDL and triglycerides drop (dramatically), VLDL are unavailable to transform large LDL into small LDL, small LDL is no longer available to become oxidized and glycated, blood sugar is reduced to allow less glycation. Voila: Less atherosclerotic plaque growth. Yet the USDA, American Heart Association, and the Surgeon General's office all advise you to eat more carbohydrates. The American Diabetes Association tells you to eat 70 grams or so carbohydrates per meal. (Yes: Diabetes, the condition that is MOST susceptible to these carbohydrate effects.) Follow their advice and you gain weight; triglycerides and VLDL go up; calculated (Friedewald) LDL may or may not go up, but true measured LDL (NMR LDL particle number or apoprotein B) goes way up; small LDL is triggered . . . You know the rest. The dance between carbohydrates and LDL particles requires the participation of both. Allow one partner to drop out of the dance and LDL particles will sit this dance out.
Strange but true: Part II 4. April 2010 William Davis (0) Here's the second part of the Heart Scan Blog post I wrote a couple of years back describing the wacky origins of this thing that has so changed the face of heart care in the U.S., the cardiac catheterization.
Heart catheterization: Strange, but true 3. April 2010 William Davis (1) It's a couple of years old, but this post from March, 2008, remains relevant. It details the curious origins of heart catheterization, the procedure that has saved some lives, but also been responsible for the proliferation of unnecessary heart procedures.The modern era of heart disease care was born from an accident, quirky personalities, and even a little daring. The notion of heart catheterization to visualize the human heart began rather ignominiously in 1929 at the Auguste-Viktoria Hospital in Eberswalde, Germany, a technological backwater of the day. Inspired by descriptions of a French physician who inserted a tube into the jugular vein of a horse and felt transmitted heart impulses outside the body, Dr. Werner Forssmann, an eager 25-year old physician-in-training, was intent on proving that access to the human heart could be safely gained through a surface blood vessel. No one knew if passing a catheter into the human heart would be safe, or whether it would become tangled in the heart’s chambers and cause it to stop beating. On voicing his intentions, Forssmann was ordered by superiors not to proceed. But he was determined to settle the question, especially since his ambitions captured the interest of nurse Gerda Ditzen, who willingly even offered to become the first human subject of his little experiment.Secretly gathering the necessary supplies, he made his first attempt in private. After applying a local anesthetic, he used a scalpel to make an incision in his left elbow. He then inserted a hollow tube, a catheter intended for the bladder, into the vein exposed under the skin. After passing the catheter 14 inches into his arm, however, he experienced cold feet and pulled it out. One week later, Forssman regained his resolve and repeated the process. Nurse Ditzen begged to be the subject, but Forssmann, in order to allow himself to be the first subject, tricked her into being strapped down and proceeded to work on himself while she helplessly watched. After stanching the oozing blood from the wound, he threaded the catheter slowly and painfully into the cephalic vein, up through the bicep, past the shoulder and subclavian vein, then down towards the heart. He knew that simply nudging the rubber catheter forward would be sufficient to direct it to the heart, since all veins of the body lead there. With the catheter buried 25 inches into his body, Forssmann untied the fuming Ditzen. Both then ran to the hospital’s basement x-ray department and injected x-ray dye into the catheter, yielding an image of the right side of his heart, the first made in a living human. Thus, the very first catheterization of the heart was performed.An x-ray image was made to document the accomplishment. Upon hearing of the experiment, Forssmann was promptly fired by superiors for his brazen act of self-experimentation. Deflated, Forssmann abandoned his experimentation and went on to practice urology. He became a member of the Nazi party in World War II Germany and served in the German army. Though condemned as crazy by some, physicians in Europe and the U.S., after hearing of his experience, furthered the effort and continued to explore the potential of the technique. Forssmann himself was never invited to speak of his experiences outside of Germany, as he had been labeled a Nazi. Many years after his furtive experiments, the once intrepid Dr. Forssmann was living a quiet life practicing small town medicine. He received an unexpected phone call informing him that he was one of three physicians chosen to receive the 1956 Nobel Prize for Medicine for his pioneering work performing the world’s first heart catheterization, along with Drs. André Cournand and Dickinson W. Richards, both of whom had furthered Forssmann’s early work. Forssmann remarked to a reporter that he felt like a village pastor who was made a cardinal. Strange, but true.
Rerun: To let low-carb right, you must check POSTPRANDIAL blood sugars 2. April 2010 William Davis (12) Checking postprandial (after-eating) blood sugars yields extraordinary advantage in creating better diets for many people. This idea has proven so powerful that I am running a previous Heart Scan Blog post on this practice to bring any newcomers up-to-date on this powerful way to improve diet, lose weight, reduce small LDL, reduce triglycerides, and reduce blood pressure. To get low-carb right, you need to check blood sugarsReducing your carbohydrate exposure, particularly to wheat, cornstarch, and sucrose (table sugar), helps with weight loss; reduction of triglycerides, small LDL, and c-reactive protein; increases HDL; reduces blood pressure. There should be no remaining doubt on these effects. However, I am going to propose that you cannot truly get your low-carb diet right without checking blood sugars. Let me explain. Carbohydrates are the dominant driver of blood sugar (glucose) after eating. But it's clear that we also obtain some wonderfully healthy nutrients from carbohydrate sources: Think anthocyanins from blueberries and pomegranates, vitamin C from citrus, and soluble fiber from beans. There are many good things in carbohydrate foods. How do we weigh the need to reduce carbohydrates with their benefits?Blood sugar after eating ("postprandial") is the best index of carbohydrate metabolism we have (not fasting blood sugar). It also provides an indirect gauge of small LDL. Checking your blood sugar (glucose) has become an easy and relatively inexpensive tool that just about anybody can incorporate into health habits. More often than not, it can also provide you with some unexpected insights about your response to diet. If you’re not a diabetic, why bother checking blood sugar? New studies have documented the increased likelihood of cardiovascular events with increased postprandial blood sugars well below the ranges regarded as diabetic. A blood sugar level of 140 mg/dl after a meal carries 30-60% increased (relative) risk for heart attack and other events. The increase in risk begins at even lower levels, perhaps 110 mg/dl or lower after-eating. We use a one-hour after eating blood sugar to gauge the effects of a meal. If, for instance, your dinner of baked chicken, asparagus brushed with olive oil, sauteed mushrooms, mashed potatoes, and a piece of Italian bread yields a one-hour blood sugar of 155 mg/dl, you know that something is wrong. (This is far more common than most people think.)Doing this myself, I have been shocked at the times I've had an unexpectedly high blood sugar from seemingly "safe' foods, or when a store- or restaurant-bought meal had some concealed source of sugar or carbohydrate. (I recently had a restaurant meal of a turkey burger with cheese, mixed salad with balsamic vinegar dressing, along with a few bites of my wife's veggie omelet. Blood sugar one hour later: 127 mg/dl. I believe sugar added to the salad dressing was the culprit.) You can now purchase your own blood glucose monitor at stores like Walmart and Walgreens for $10-20. You will also need to purchase the fingerstick lancets and test strips; the test strips are the most costly part of the picture, usually running $0.50 to $1.00 per test strip. But since people without diabetes check their blood sugar only occasionally, the cost of the test strips is, over time, modest. I've had several devices over the years, but my current favorite for ease-of-use is the LifeScan OneTouch UltraMini that cost me $18.99 at Walgreens.Checking after-meal blood sugars is, in my view, a powerful means of managing diet when reducing carbohydrate exposure is your goal. It provides immediate feedback on the carbohydrate aspect of your diet, allowing you to adjust and tweak carbohydrate intake to your individual metabolism.
LDL glycation 1. April 2010 William Davis (11) The proteins of the body are subject to the process of glycation, modification of protein structures by glucose (blood sugar). In the last Heart Scan Blog post, I discussed how glycated hemoglobin, available as a common test called HbA1c, can serve as a reflection of protein glycation (though it does not indicate actual Advanced Glycation End-products, or AGEs, just a surrogate indicator). There is one very important protein that is subject to glycation: Apoprotein B.Apoprotein B, or Apo B, is the principal protein of VLDL and LDL particles. Because there is one Apo B molecule per VLDL or LDL particle, Apo B can serve as a virtual VLDL/LDL particle count. The higher the Apo B, the greater the number of VLDL and LDL particles. Because Apo B is a protein, it too is subject to the process of glycation. The interesting thing about the glycation of Apo B is that its "glycatability" depends on LDL particle size: The smaller the LDL particle, the more glycation-prone the Apo B contained within. Younis et al have documented an extraordinary variation in glycatability between large and small LDL, with small LDL showing an 8-fold increased potential. Think about it: Carbohydrates in the diet, such as wheat products and sugars, trigger formation of small LDL particles. Small LDL particles are then more glycation-prone by up to a factor of 8. Interestingly, HbA1c is tightly correlated with glycation of Apo B. Diabetics with high HbA1c, in particular, have the greatest quantity of glycated Apo B. They are also the group most likely to develop coronary atherosclerosis, as well as other consequences of excessive AGEs. No matter how you spin it, the story of carbohydrates is getting uglier and uglier. Carbohydrates, such as those in your whole grain bagel, drive small LDL up, while making them prone to a glycating process that makes them more likely to contribute to formation of coronary atherosclerotic plaque.
High HbA1c: You're getting older . . . faster 28. March 2010 William Davis (16) Over the years, we all accumulate Advanced Glycation End-products, or AGEs.AGEs are part of aging; they are part of human disease. AGEs are the result of modification of proteins by glucose. AGEs form the basis for many disease conditions.Accumulated AGEs have been associated with aging, dementia, cataracts, osteoporosis, deafness, cancer, and atherosclerosis. Most of the complications of diabetes have been attributable to AGEs.There's one readily available method to assess your recent AGE status: HbA1c.Hemoglobin is the oxygen-carrying protein of red blood cells. Like other proteins, hemoglobin becomes glycated in the presence of glucose. Hemoglobin glycation increases linearly with glucose: The higher the serum or tissue glucose level, the more glycation of hemoglobin develops. Glycated hemoglobin is available as the common test, HbA1c.Ideal HbA1c is 4.5% or less, i.e., 4.5% of hemoglobin molecules are glycated. Diabetics typically have HbA1c 7.0% or greater, not uncommonly greater than 10%.In other words, repetitive and sustained high blood glucose leads to greater hemoglobin glycation, higher HbA1c, and indicates greater glycation of proteins in nerve cells, the lens of your eye, proteins lining arteries, and apoprotein B in LDL cholesterol particles.If AGEs accumulate as a sign of aging, and high blood sugars lead to greater degrees of glycation, it only follows that higher HbA1c marks a tendency for accelerated aging and disease.Indeed, that is what plays out in real life. People with diabetes, for instance, have kidney failure, heart disease, stroke, cataracts, etc. at a much higher rate than people without diabetes. People with pre-diabetes likewise.The higher your HbA1c, the greater the degree of glycation of other proteins beyond hemoglobin, the faster you are aging and subject to all the phenomena that accompany aging. So that blood glucose of 175 mg/dl you experience after oatmeal is not a good idea. The lesson: Keep HbA1c really low. First, slash carbohydrates, the only foods that substantially increase blood glucose. Second, maintain ideal weight, since normal insulin responsiveness requires normal body weight. Third, stay physically active, since exercise and physical activity exerts a powerful glucose-reducing effect. Fourth, consider use of glucose-reducing supplements, an issue for another day.While HbA1c cannot indicate cumulative AGE status, it can reflect your recent (preceding 60 to 90 days) exposure to this age-accelerating thing called glucose.If your doctor refuses to accommodate your request for a HbA1c test, you can perform your own fingerstick test.
Slash carbs . . . What happens? 26. March 2010 William Davis (20) Cut the carbohydrates in your diet and what sorts of results can you expect? Carbohydrate reduction results in:Reduced small LDL--This effect is profound. Carbohydrates increase small LDL; reduction of carbohydrates reduce small LDL. People are often confused by this because the effect will not be evident in the crude, calculated (Friedewald) LDL that your doctor provides.Increased HDL--The HDL-increasing effect of carbohydrate reduction may require 1-2 years. In fact, in the first 2 months, HDL will drop, only to be followed by a slow, gradual increase. This is the reason why, in a number of low-carb diet studies, HDL was shown to be reduced.--Had the timeline been longer, HDL would show a significant increase.Decreased triglycerides--Like reduction of small LDL, the effect is substantial. Triglyceride reductions of several hundred milligrams are not at all uncommon. In people with familial hypertriglyceridemia with triglyceride levels in the thousands of milligrams per deciliter, triglyceride levels will plummet with carbohydrate restriction. (Ironically, conventional treatment for familial hypertriglyceridemia is fat restriction, a practice that can reduce triglycerides modestly in these people, but not anywhere near as effectively as carbohydrate restriction.) Triglyceride reduction is crucial, because triglycerides are required by the process to make small LDL--less triglycerides, less small LDL. Decreased inflammation--This will be reflected in the crude surface marker, c-reactive protein--Yes, the test that the drug industry has tried to convince you to take statins drugs to reduce. In my view, it is an absurd notion that you need to take a drug like Crestor to reduce risk associated with increased CRP. If you want to reduce CRP to the floor, eliminate wheat and other junk carbohydrates. (You should also add vitamin D, another potent CRP-reducing strategy.)Reduced blood pressure--Like HDL, blood pressure will respond over an extended period of months to years, not days or weeks. The blood pressure reduction will be proportion to the amount of reduction in your "wheat belly."Reduced blood sugar--Whether you watch fasting blood sugar, postprandial (after-meal) blood sugars, or HbA1c, you will witness dramatic reductions by eliminating or reducing the foods that generate the high blood sugar responses in the first place. Diabetics, in particular, will see the biggest reductions, despite the fact that the American Diabetes Association persists in advising diabetics to eat all the carbohydrates they want. Reductions in postprandial (after-eating) blood sugars, in particular, will reduce the process of LDL glycation, the modification of LDL particles by glucose that makes them more plaque-causing. You may notice that the above list corresponds to the list of common plagues targeted by the pharmaceutical industry: blood pressure, diabetes (diabetes being the growth industry of the 21st century), high cholesterol. In other words, high-carbohydrate, low-fat foods from the food industry create the list of problems; the pharmaceutical industry steps in to treat the consequences.In the Track Your Plaque approach, we focus specifically on elimination of wheat, cornstarch, and sugars, the most offensive among the carbohydrates. The need to avoid other carbohydrates, e.g., barley, oats, quinoa, spelt, etc., depends on individual carbohydrate sensitivty, though I tend to suggest minimal exposure.
Normal fasting glucose with high HbA1c 23. March 2010 William Davis (24) Jonathan's fasting glucose: 85 mg/dlHis HbA1c: 6.7%Jonathan's high HbA1c reflects blood glucose fluctuations over the preceding 60-90 days and can be used to calculate an estimated average glucose (eAG) with the following equation:eAG = 28.7 X A1c – 46.7(For glucose in mmol/L, the equation is eAG = 1.59 × A1C - 2.59)Jonathan's HbA1c therefore equates to an eAG of 145.59 mg/dl--yet his fasting glucose value is 85 mg/dl. This is a common situation: Normal fasting glucose, high HbA1c. It comes from high postprandial glucose values, high values after meals. It suggests that, despite having normal glucose while fasting, Jonathan experiences high postprandial glucose values after many or most of his meals. After a breakfast of oatmeal, for instance, he likely has a blood glucose of 150 mg/dl or greater. After breakfast cereal, blood glucose likely exceeds 180 mg/dl. With two slices of whole wheat bread, glucose likewise likely runs 150-180 mg/dl. The best measure of all is a postprandial glucose one hour after the completion of a meal, a measure you can easily obtain yourself with a home glucose meter. Second best: fasting glucose with HbA1c.Gain control over this phenomenon and you 1) reduce fasting blood sugar, 2) reduce expression of small LDL particles, and 3) lose weight.
Can you handle fat? 21. March 2010 William Davis (19) No question: Low-carbohydrate diets generate improved postprandial lipoprotein responses.Here's a graph from one of Jeff Volek's great studies: Participants followed a low-carb diet of less than 50 g per day carbohydrate ("ketogenic") with 61% fat. The curves were generated by administering a 123 g fat challenge with triglyceride levels assessed postprandially. The solid line represents the postprandial response at the start; dotted line after the 6-week low-carb effort.Note that:1) The postprandial triglyceride (area-under-the-curve) response was reduced by 29% in the low-carb diet. That's a good thing. 2) The large fat challenge generated high triglycerides of greater than 160 mg/dl even in the low-carb group. That's a bad thing. In other words, low-carb improves postprandial responses substantially--but postprandial phenomena still occur. Postprandial triglycerides of 88 mg/dl or greater are associated with greater heart attack risk because they signify the presence of greater quantities of atherogenic (plaque-causing) postprandial lipoproteins. A full discussion of these phenomena can be found in the Track Your Plaque Special Report, Postprandial Responses: The Storm After the Quiet!, part of a 3-part series on postprandial phenomena.
Statin stupid 19. March 2010 William Davis (0) If we followed the lead of the pharmaceutical industry and my cardiology colleagues, we would all subscribe to the "statins for all" philosophy. There is now $2 billion of clinical "research" to back up this "evidence-based" practice.I do not endorse this "statins for all" philosophy. I believe it is a product of the raw profiteering of the pharmaceutical industry, who are adept at recruiting physicians to their cause. But lost in the confusion of tainted studies and over-the-top media saturation is the fact that there are small groups of people who likely do obtain benefit from statin drugs. They would certainly benefit from better informed scrutiny of their lipoprotein and metabolic abnormalities. But treatment may involve statins. This is entirely distinct from the "statins for all" argument, the simpleminded rule that primary care physicians and cardiologist are told to follow. Groups who may indeed benefit from statin therapy include:Homozygous or heterozygous familial hypercholesterolemia--Lacking a receptor for LDL particles, LDL piles up to very high levels in these people. LDLs of 300+ are common and lead to heart disease and stroke at relatively young ages. Combined mixed hyperlipidemia--Among the one or more genetic defects underlying this condition involves excessive production of apoprotein B and VLDL particles. This leads to high risk for heart disease. People unable to follow a diet to correct their lipid disorder--I have 80+-year old patients, for instance, who say, "I've eaten this way for 82 years. I'm not going to change now!" In the absence of diet and other efforts (e.g., omega-3 fatty acids from fish oil), drugs may be the answer. In other words, of the $27 billion annual bill for statin drugs, perhaps a tiny fraction is truly necessary. The majority of people taking statin drugs would not really need them if they had the real answers. But don't let that confuse us: There are some people who do indeed benefit.
Butter and insulin 19. March 2010 William Davis (83) In a previous post, Atkins Diet: Common Errors, I commented on butter's unusual ability to provoke insulin responses. I offer this as a possible reason why, after a period of effective weight loss on a low-carbohydrate program, inclusion of some foods, such as butter, will trigger weight gain or stall weight loss efforts. This develops because of butter's insulin-triggering effect, doubling or tripling insulin responses (postprandial area-under-the-curve). If insulin is triggered, fat gain follows. Here's one such study documenting this effect: Distinctive postprandial modulation of ß cell function and insulin sensitivity by dietary fats: monounsaturated compared with saturated fatty acidsLópez et al 2008From Lopez et al 2008. Mean (± SD) plasma glucose, insulin, triglyceride, and free fatty acid (FFA) concentrations during glucose and triglyceride tolerance test meal (GTTTM) with no fat (control), enriched in monounsaturated fatty acids (MUFAs) from refined olive oil (ROO meal), with added butter, with a mixture of vegetable and fish oils (VEFO) or with high-palmitic sunflower oil (HPSO). N = 14.The postprandial (after-eating) area-under-the-curve is substantially greater when butter is included in the mixed composition meal. This effect is not unique to butter, but is shared by most other dairy products. Fat, in general, does not make you fat. But butter makes you fat.
Vitamin D as a cardiovascular risk factor gains ground 18. March 2010 William Davis (0) If you were reading The Heart Scan Blog back in 2007, or read my Life Extension article on vitamin D deficiency as a cardiovascular risk factor, you already knew that vitamin D deficiency is rampant and adds to cardiovascular risk. Results of a study from the Intermountain Medical Center Heart Institute in Utah bolster the concept that vitamin D deficiency is a cardiovascular risk factor, vitamin D normalization/supplementation reduces cardiovascular risk. Science Daily reported:For the first study, researchers followed two groups of patients for an average of one year each. In the first study group, over 9,400 patients, mostly female, reported low initial vitamin D levels, and had at least one follow up exam during that time period. Researchers found that 47 percent of the patients who increased their levels of vitamin D between the two visits showed a reduced risk for cardiovascular disease.In the second study, researchers placed over 31,000 patients into three categories based on their levels of vitamin D. The patients in each category who increased their vitamin D levels to 43 nanograms per milliliter of blood or higher had lower rates of death, diabetes, cardiovascular disease, myocardial infarction, heart failure, high blood pressure, depression, and kidney failure. Currently, a level of 30 nanograms per milliliter is considered "normal."Over the past 4 years, people in our program have been enjoying the extravagant benefits of vitamin D restoration. Cardiovascular benefits are becoming better documented and the bone health, cancer-preventing, insulin-normalizing, mood-adjusting, and anti-inflammatory effects likewise.
Atkins Diet: Common errors 18. March 2010 William Davis (74) No doubt: The diet approach advocated by the late Dr. Robert Atkins was a heck of a lot closer to an ideal diet than the knuckleheaded advice emitting from the USDA, American Heart Association, American Diabetes Association, and the Surgeon General's office.But having just spent a week with Atkins low-carbers, here are some common errors that I see many make, errors that I believe have long-term health consequences, including impairment of weight loss.Excessive consumption of animal products--Non-restriction of fat often leads to over-reliance on animal products. Higher intakes of red meats (heme proteins?) have been strongly associated with increased risk for colon and other gastrointestinal tract cancers. It is not a fat issue; it is an animal product issue. We should consume less meat, more vegetables and other plant-sourced foods.Consumption of cured meats--Cured, processed meats, such as sausage, hot dogs, salami, bologna, and bacon, have a color fixative called sodium nitrite, an additive that has been confidently linked to gastrointestinal cancers. Risk is likely dose-dependent: The more you ingest, the greater the long-term risk.Overconsumption of dairy products--Dairy products, especially milk, yogurt, cottage cheese, and butter, are potent insulinotropic foods, i.e., foods that trigger insulin release. There can be up to a tripling of insulin (area-under-the-curve) levels. This is not good in a world populated with tired, overworked pancreases, exhausted from a lifetime of high-carbohydrate eating.Too many calories--While I agree that "a calorie is a calorie" and "calories in, calories out" are faulty concepts, I have anecdotally observed that long-time low-carbers often trend towards unlimited consumption of food, a phenomenon that seems to result in weight gain, especially in the sedentary. I wonder if this is a reflection of the insulinotropic action of dairy products and other proteins, compounded by the poor insulin responsiveness that develops with lack of physical activity. Factor into this conversation that lower calorie intake extends life, probably substantially (Sirt-2 activation and related phenomena, a la resveratrol). If lower calorie intake extends life, unlimited calorie intake likely shortens life.Please don't hear this as low-carb bashing--it is not. It is a call to improve diets and not stumble into common traps that can impair heart health, weight loss, and longevity.