What's for breakfast? 16. March 2008 William Davis (106) Breakfast, for some reason, seems to be the toughest meal of the day for many people. I think it's because the quest for sweet has dominated the American breakfast for so long, with its half-century legacy of cartoon character-festooned breakfast cereals; baked flour products like pancakes, waffles, and English muffins; more recently, "healthy" alternatives like bran muffins and oat waffles. This breakfast lifestyle has also contributed to the obesity and diabetes ("diabesity") epidemic. Breakfasts of wheat- or corn-based cereals, even those labeled "heart healthy," fruit, and whole grain breads are guaranteed paths to low HDL cholesterol, high triglycerides, flagrant small LDL, increased inflammatory responses, high blood pressure, and higher blood sugar. Such foods also make you tired, make your abdominal fat grow (wheat belly), and increase appetite so that you want more. So what can you eat for breakfast that doesn't provoke these patterns? I will never pretend to be terribly clever in creating meal menus, but I can tell you what has worked for me and many of my patients. Be warned: It may require you to suspend your previous notions of what "should" be included in a list of breakfast foods.Here are some examples that you may find helpful:--Raw nuts--one or several handfuls of raw almonds, walnuts, pecans, pistachios--Cheeses--the real, traditional sorts like gouda, goat, Swiss, edam, etc. (not Velveeta, Cheez Whiz, etc.)--Eggs, Egg Beaters--and "spice" them up with sun-dried tomatoes, salsa, olives, tapenades, olive oil, onions, green peppers, etc.--Yogurt (real, of course), cottage cheese--Ground flaxseed, oat bran--as hot cereals or added to yogurt, cottage, or other foods. Esp. helpful for reducing both total LDL and the proportion of small LDL.--Oatmeal--slow-cooked, not the instant nonsense.--Soups--great for winter.--Dinner foods--chicken, beef, fish, green beans, asparagus, tomatoes, etc., most easily added by saving left-overs from dinner. You'll be surprised how filling dinner foods eaten at breakfast can be. It's really not that tough. It just means selecting from an entirely different list of foods than you might be accustomed to. Copyright 2008 William Davis, MD
The first lawsuit? 16. March 2008 William Davis (1) The closing arguments in actor John Ritter's wrongful death lawsuit are over and the two doctors charged with negligence cleared, five years after his death from a dissection (tear of the inner lining) of the thoracic aorta. The family sought $67 million in damages, claiming that the aortic dissection was misdiagnosed as a heart attack and that the enlarged aorta should have been reported to Mr. Ritter two years earlier during a full body scan. The AP story can be viewed at http://ap.google.com/article/ALeqM5gmv6HnJJPBee2gWgEYResT5m6YkAD8VDF9CO0 Well, perhaps this is the start of a trend. Up until now, it has been commonplace for doctors to ignore many of the important findings on heart scans, full body scans, and similar direct-to-the-public imaging services. For instance, similar to John Ritter's case, enlarged thoracic aortas are commonly ignored. I'd even say that as a rule they are ignored. I have seen many patients in consultation who have had large aortas identified on heart scans, yet nothing--not a thing--was done about it. While the doctors escaped a lawsuit this time, it might not happen a second time. I truly hope that Mr. Ritter's unfortunate experience and the consequent lawsuit do not trigger the usual defensive medicine response of resorting to major procedural "solutions." A better response would be to 1) identify the problem--enlarged aorta in this case, 2) identify the causes, then 3) correct the causes. It does not necessarily mean that a major procedure like replacing the aorta (a horrendous surgery, by the way) needs to be pursued each and every time. It is possible that Mr. Ritter's lawsuit is just the first. Over the next several years, it could trigger an avalanche of lawsuits for all the neglected findings on tests like heart scans, body scans, and other imaging methods that are gaining expanded direct-to-consumer access. Images courtesy Wikipedia.
The origins of heart catheterization: Part II 13. March 2008 William Davis (0) On the afternoon of October 30th, 1958, nearly 30 years after Werner Forssmann’s fumbling attempts, Dr. Mason Sones, a 5 foot 5 inch, plain-talking, cuss-every-few-words, cigarette-wielding radiologist at the Cleveland Clinic, was performing a routine angiogram of a patient’s aorta (the large vessel emerging from the heart) in a dark basement laboratory. (In Sones’ day, imaging methods remained primitive, disease diagnosis relying more than anything else on the physician’s powers of observation and crude diagnostic procedures. Abdominal pain was assessed with exploratory laparotomy, headaches with air injected into the brain and nervous system (“pneumoencephalography”), an excruciatingly painful ordeal. Being able to track the course of x-ray dye injected into specific internal organs, whether liver, biliary tree, aorta, lungs, or coronary arteries, represented a huge advance in diagnostic tools for human disease.) In 1958, no one had yet injected dye directly into the coronary artery of a living human. Just as the dye injector was triggered, Dr. Sones’ eyes widened in horror when the black and white monitor showed that the catheter had inadvertently jumped into the right coronary artery. The injection pump, already triggered to release its load, proceeded to pump 30 cc of X-ray dye straight into the artery. (Modern techniques usually require only 5–10 cc of dye.) Dr. Sones recounts the incident:“It was late in the day and we were tired. I hit the switch to rev up the x-ray generator so I could see. As the picture came on, I could see that the damn catheter was in the guy’s right coronary artery. And there I was, down in the hole [a recess to shield him from radiation]. I yelled, “Pull it out! Pull it out!”*? By that time, about 30 cc of the dye had gone into the coronary artery. I climbed out of the hole and I grabbed a knife. I thought that his heart would fibrillate and I would have to open his chest and shock his heart. [In Sones’ day, modern CPR hadn’t yet been developed as a method of resuscitation.] But he didn’t fibrillate—his heart stopped. I demanded he cough. He coughed three times and his heart began to beat again. I knew at once that if the heart could tolerate 30 cc of dye, we would be able to safely inject small amounts directly into the coronary artery. I knew that night that we would have a tool to define the anatomic nature of coronary disease.”*An observer, Dr. Julio Sosa, reported that Dr. Sones, in his shock, also blurted, “We’ve killed him!” After all, conventional wisdom of that era, based on observations from dye injections into the coronary arteries of dogs, was that injecting x-ray dye into human coronary arteries would result in immediate death from the electrical imbalance provoked in heart muscle momentarily deprived of oxygen-carrying blood.Thus it was established that it was indeed possible to directly inject x-ray dye into human coronary arteries and reveal its internal contours. That’s not to say that the x-ray dyes of 1958 were innocuous. Far from it. In addition to briefly interrupting heart rhythm, as happened with Sones’ first accidental attempt, the dyes used then typically caused dizziness and the sudden urge to vomit. During the first 30 years of direct coronary catheterizations, it was common for hospital staff to run to the patient’s side, bucket in hand to catch the inevitable vomit, once the heart was jump-started by coughing.Not surprisingly, Dr. Sones’ discovery set off both an avalanche of criticism and bold predictions of how the new technique might change the course of diagnosis in heart disease.Over the subsequent weeks and months, Dr. Sones proceeded to purposefully insert catheters into coronary arteries and create angiograms that revealed the extent of coronary atherosclerosis. He learned how to fashion new catheter shapes to facilitate access to the arteries. Sones developed an impressive experience in the new technique. For the first time, clear images of the coronary arteries were routinely obtainable for the confident diagnosis of coronary atherosclerosis before death. Dr. Sones became an unlikely celebrity in Cleveland, entertaining physicians from around the world eager to learn about his methods, politicians and celebrities, even Middle Eastern nobility complete with bodyguards and food testers. Dr. Sones continued to work in Cleveland, furthering the techniques of heart catheterization after his fortuitous error. He died of lung cancer in 1985, 17 years after his discovery. Thus was born the modern age of heart catheterization.Today, over 10,000 heart procedures are performed in the U.S. every day, 365 days a year, the vast majority of which involve heart catheterization or begin with a heart catheterization. Dr. Sones' fortuitous blunder was followed by 30 years of productive refinement and development before the blatant excesses of this technique really began to be exploited. Copyright 2008 William Davis, MD
The origins of heart catheterization: Part I 12. March 2008 William Davis (2) 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. Copyright 2008 William Davis, MD
Conventional therapy vs. alternative therapy 11. March 2008 William Davis (5) Rose is a 75-year old woman, mother of four, grandmother of many more.Rose's story started after a heart attack 18 months ago that resulted in two stents. She was advised to follow an American Heart Association diet and take Lipitor. However, some months later, after her fourth stent, she became disilluioned in the conventional approach to heart disease and sought alternative therapies to help reduce or reverse her heart disease. She found an alternative health practitioner who advised chelation, antioxidant vitamins for "excessive oxidation," and several homeopathic preparations. Nothing was said about diet or exercise. Nothing was said about the baked flour products and pastries that occupied at least two meals every day. Nothing was said about the candies she indulged in several times per day, nor the soft drinks. Nothing was said about the wildly fluctuating blood sugars, poorly controlled by an oral diabetes agent. Thirty pounds of weight gain over the past 5 years with no exercise or physical activity? No comment here, too. In short, Rose was the "graduate" of the conventional approach, as typically offered nationwide thousands of times a week. She was also the recipient of the insight of at least one alternative health practitioner, eager to reject conventional notions of how to achieve heart health.So I then met her. She was experiencing chest pains every day, several times per day. Blood pressure over 200. At 5 ft, 3 inches, weight: 186 lbs. Initial laboratory results:HDL cholesterol 42 mg/dlLDL 132 mg/dlTriglycerides 263 mg/dlBlood sugar 173 mg/dlYou can fill in the rest. In short, Rose was a disaster. Despite the attentions of several professionals from both the conventional as well as alternative camps, she was careening rapidly towards failure. She'd been given various crutches, Band-Aids, and salves, none of which resulted in any possibility of long-term relief from her aggressive disease.My point: As I've said previously, all we want is truth. We want effective, rational approaches that yield real benefit. A stent? All that provides is temporary restoration of blood flow. Statin agents? They do indeed reduce LDL cholesterol. But what if Rose has 8, 9, or 10 other causes of heart disease unaffected by the statin drug? It will do little or nothing. Nobody had addressed many of the root causes of Rose's disease: insulin resistance, high triglycerides, inactivity, obesity, hypertension (and identifying the reasons why her blood pressure was so high), vitamin D deficiency (virtually guarantted to be severe), junk foods including the ones known as "whole grains." My message: Success in heart disease, as well as all aspects of health for that matter, doesn't necessarily have to come from an "alternative" approach, nor a "conventional" approach. It comes from applying what is truly effective, regardless of what label someone applied to it.I would no sooner trust my health and life to an alternative health practitioner hawking unusual herbs and remedies than I would submit to a heart catheterization, three stents, followed by a statin drug. There's small benefit in both approaches, but none are the best. You've got to look elsewhere for that. Copyright 2008 William Davis, MD
The JELIS Trial 9. March 2008 William Davis (5) The Japan eicosapentaenoic acid (EPA) Lipid Intervention Study (JELIS) is a clinical trial that all Track Your Plaquers should know about. This enormous trial followed a simple design: Japanese men, between 40-75 years, and Japanese postmenopausal women aged <75 years with total cholesterol 250 mg/dl or greater were enrolled. A total of 18,645 subjects (mean age, 61 years; 31% male) participated: 36% had hypertension, 15% had diabetes, and 20% had coronary disease (history of heart attack or heart procedure). Average starting total cholesterol 275 mg/dl; LDL 180 mg/dl. All participants were treated with pravastatin 10 mg/day or simvastatin 5 mg/day; approximately half also received the omega-3, EPA, 1800 mg/day, in addition to one of the statin drugs. Treatment resulted in an average LDL reduction of 26% in all participants; the group taking EPA experienced an additional 10% reduction in triglycerides. All major cardiovascular events were tracked and tabulated, including sudden cardiac death, fatal or nonfatal myocardial infarction (MI), unstable angina pectoris, coronary artery bypass surgery, and coronary angioplasty. After nearly five years, 3.5% of statin-only participants experienced an event; 2.8% of statin + EPA experienced an event. The (often misleading and frequently abused value) "relative reduction" was therefore 19%. There are several features that make the JELIS trial interesting:--There were an unusually low number of cardiovascular events in the entire group, lower than nearly all American and European trials of similar design. This likely points to the greater burden of atherosclerotic heart disease in the U.S. compared to Japan. Rates in comparable U.S.-based trials usually range from 6-14%, sometimes more.--Both the participants without identified heart disease at enrollment and those with heart disease at enrollment obtained a similar magnitude of beneficial reduction in cardiovascular events. --There was an unusual preponderance of women--69%--unlike most other trials of cardiovascular events. We might therefore argue that JELIS most conclusively showed that benefits of EPA are most confidently demonstrated for females. --A fish oil preparation containing only EPA was used, rather than the usual EPA + DHA. There are discussions from some corners that argue that DHA is more important than EPA, e.g., algae sources. However, JELIS would argue that EPA does play a role. Is EPA with DHA better, worse, or no different? Unfortunately, there are insufficient data--large, randomized data like JELIS--to help us. Recall that GISSI Prevenzione used a combination of EPA and DHA, as have virtually all other trials examining the effects of fish oil. Also, keep in mind that the epidemiologic observations of the cardiovascular benefits of eating fish suggest that the naturally-sourced omega-3s--a combination of EPA and DHA--are associated with benefit. --It's surprising that any difference at all was demonstrated, given the high intake of fish in the Japanese. In fact, blood levels of EPA in participants before taking EPA was five-fold higher than in western populations. One potential difficulty: The study was funded by the manufacturer of the EPA preparation used, Mochida Pharmaceutical Company. We all know what that can do to results. Nonetheless, the JELIS trial is a study that adds to the emerging wisdom in fish oil. Copyright 2008 William Davis, MD
Omega-3 MUST be from fish oil 7. March 2008 William Davis (14) Despite my rants in this blog and elsewhere, at least once a day I'll have a patient say, "I cut back (or eliminated) my fish oil because I get my omega-3s from _______ (insert your choice of flaxseed oil, walnuts, yogurt, mayonnaise, bread, etc.)."(See prior Heart Scan Blog post: Everything has omega-3.)When I point out to them that the "omega-3s" in these products are not the same as the EPA and DHA from fish oil, they invariably declare, "But it says so here on the label: 'Contains 200 mg of omega-3 fatty acids'!" Apparently, some of my colleagues have even endorsed this concept of replacing the omega-3s from fish oil with these "alternatives."It's simply not true. The linolenic acid that is being labeled as omega-3, while it may indeed provide health benefits of its own, cannot replace the EPA and DHA that fish oil provides. The most graphic example of the differences between the two classes of oils is in people with a condition called familial hypertriglyceridemia. People with this condition have triglyceride levels of 400, 600, even thousands of mg/dl--very high. Fish oil, usually providing EPA and DHA doses of 1800 mg per day and higher, reduce triglycerides dramatically. A person with a starting triglyceride level of, say, 900 mg/dl, may take 2400 mg of EPA and DHA from fish oil and triglycerides plummet to 150 mg/dl. This person then decides to replace fish oil with a linolenic acid source like flaxseed oil. Triglycerides? 900 mg/dl--no effect whatsoever. Familial hypertriglyceridemia represents an exagerrated example of the differences between the two oils. Even if you don't have this genetic condition, the differences between the oils still apply. EPA and DHA are activators of the enzyme, lipoprotein lipase, that accelerates clearance of triglycerides from the blood. Linolenic acid from flaxseed oil, walnuts, and other food sources does not. EPA and DHA block after-eating (post-prandial) accumulation of food by-products that can contribute to coronary and carotid plaque. Linolenic acid does not. EPA and DHA block platelets, reduce fibrinogen, and exert other healthy blood clot-inhibiting effects. Linolenic does not.The 11,000-participant GISSI-Prevenzione Trial that showed 28% reduction in heart attack, 45% reduction in cardiovascular death with omega-3s used . . . fish oil. The 18,000 participant JELIS trial that showed 19% reduction in cardiovascular events when omega-3s were added to statin therapy used . . . fish oil. (Actually, in JELIS, they used only EPA wtihout DHA.) Linolenic acid is not a waste, however. It may exert anti-inflammatory benefits of its own, for instance. But it exerts none of the triglyceride-modifying effects of EPA or DHA. EPA and DHA from fish oil and linolenic acid from foods each provide benefits in their own way. Ideally, you include both forms of oils--fish oil and linolenic acid sources--in your daily diet and obtain full benefit from each separate class. But they are not interchangeable. Copyright 2008 William Davis, MD
Osteoporosis and coronary calcium 4. March 2008 William Davis (9) Several studies over the years have demonstrated a curious paradox: People with more osteoporosis (thin bones) tend to be more likely to have coronary disease (heart attacks). They also tend to have higher heart scan scores (more coronary calcification as an index of atherosclerotic plaque). People with more coronary disease and higher heart scan scores tend to have more osteoporosis. In other words, regardless of which way you tackle the question--osteoporosis first or heart disease first--it leads to the same conclusion: Both conditions are somehow related. I realize I harp an awful lot on this whole vitamin D issue. But, even after correcting the vitamin D blood levels of many hundreds of people, I remain enthusiastic as ever about the untapped potential of this fascinating factor.So I couldn't resist showing this amazing comparison of how the long-term effect can be quite graphic. The first scan is from a 46-year old man and shows normal coronary arteries without calcium and normal density of the vertebra (a common and reliable place to measure bone density). The second image is from a 79-year old man with both severe coronary calcification (and therefore severe coronary disease) and severe osteoporosis. Why are heart attacks still happening? 4. March 2012 William Davis (10) I'm a cardiologist. I see patients with heart disease in the form of coronary artery disease every day. These are people who have undergone bypass surgery, received one or more stents or undergone other forms of angioplasty, have survived heart attacks or sudden cardiac death, or have high heart scan scores. In short, I see patients every day who are at high-risk for heart attack and death from heart disease. But I see virtually no heart attacks. And nobody is dying from heart disease. (I'm referring to the people who follow the strategies I advocate, not the guy who thinks that smoking a pack of cigarettes a day is still okay, or the woman who thinks the diet is unnecessary because she's slender.) Two high-profile deaths from heart attacks occurred this week:Davy Jones--The iconic singer from the 1960s pop group, the Monkees, suffered sudden cardiac death after a large heart attack, just hours after experiencing chest pain. Andrew Breitbart--The conservative blogger and controversy-generating media personality suffered what was believed to be sudden cardiac death while walking. It's a darn shame and it shouldn't happen. The tools to identify the potential for heart attack are available, inexpensive, and simple. The strategies to reduce, even eliminate, risk are likewise available, inexpensive, and cultivate overall health. The followers of the Track Your Plaque program who 1) get a heart scan that yields a coronary calcium score (for long-term tracking purposes) 2) identify the causes such as small LDL particles, lipoprotein(a), vitamin D deficiency, and thyroid dysfunction3) correct the causes enjoy virtual elimination of risk.
My letter to the Wall Street Journal: It's NOT just about gluten 8. February 2012 William Davis (7) The Wall Street Journal carried this report of a new proposed classification of the various forms of gluten sensitivity: New Guide to Who Really Shouldn't Eat GlutenThis represents progress. Progress in understanding of wheat-related illnesses, as well as progress in spreading the word that there is a lot more to wheat-intolerance than celiac disease. But, as I mention in the letter, it falls desperately short on several crucial issues.Ms. Beck--Thank you for writing the wonderful article on gluten sensitivity.I'd like to bring several issues to your attention, as they are often neglectedin discussions of "gluten sensitivity":1) The gliadin protein of wheat has been modified by geneticists through theirwork to increase yield. This work, performed mostly in the 1970s, yielded a formof gliadin that is several amino acids different, but increased theappetite-stimulating properties of wheat. Modern wheat, a high-yield, semi-dwarfstrain (not the 4 1/2-foot tall "amber waves of grain" everyone thinks of) isnow, in effect, an appetite-stimulant that increases calorie intake 400 caloriesper day. This form of gliadin is also the likely explanation for the surge inbehavioral struggles in children with autism and ADHD.2) The amylopectin A of wheat is the underlying explanation for why two slicesof whole wheat bread raise blood sugar higher than 6 teaspoons of table sugar ormany candy bars. It is unique and highly digestible by the enzyme amylase.Incredibly, the high glycemic index of whole wheat is simply ignored, despitebeing listed at the top of all tables of glycemic index.3) The lectins of wheat may underlie the increase in multiple autoimmune andinflammatory diseases in Americans, especially rheumatoid arthritis andinflammatory bowel diseases (ulcerative colitis, Crohn's).In other words, if someone is not gluten-sensitive, they may still remainsensitive to the many non-gluten aspects of modern high-yield semi-dwarf wheat,such as appetite-stimulation and mental "fog," joint pains in the hands, legedema, or the many rashes and skin disorders. This represents one of the mostimportant examples of the widespread unintended effects of modern agriculturalgenetics and agribusiness.William Davis, MDAuthor: Wheat Belly: Lose the wheat, lose the weight and find your path back to health
60-year old man dies of high cholesterol 1. February 2012 William Davis (12) Never saw a headline like this? Neither have I. That's because it doesn't happen.Cholesterol doesn't harm, maim, or kill. It is simply used as a crude--very crude--marker. It is, in reality, a component of the body, of the cell wall, of lipoproteins (lipid-carrying proteins) in the bloodstream. It is used a an indirect gauge, a "dipstick," for lipoproteins in the blood to those who don't understand how to identify, characterize, and quantify actual lipoproteins in the blood.Cholesterol itself never killed anybody, any more than a bad paint job on your car could cause a fatal car accident.What kills people is rupture of atherosclerotic plaque in the coronary arteries. For all practical purposes, you must have atherosclerotic plaque in order for it to rupture (much like a volcano erupts and spews lava). It's not about cholesterol; it's about atherosclerotic plaque. Plaque might contain cholesterol, but cholesterol is not the thing itself that causes heart attack and death.So why do most people obsess about cholesterol? Good question. It is, at best, a statistical marker for the possibility of having atherosclerotic plaque that ruptures. High cholesterol = higher risk for heart attack, low cholesterol = lower risk for heart attack. But the association is weak and flawed, such that people with high cholesterol can live a lifetime without heart attack, people with low cholesterol can die at age 43.The same holds true for LDL cholesterol, you know, the calculated value based on flawed assumptions about LDL's relationship to total cholesterol, HDL cholesterol, and VLDL cholesterol.A crucial oversight in the world of cholesterol: There are many other factors that cause atherosclerotic plaque and its rupture, such as inflammatory phenomena, calcium deposition, artery spasm, hemorrhage within the plaque itself, degradative enzymes, etc., none of which are suggested by cholesterol measures.But one observation has held up, time and again, over the past 40 years of observations on coronary disease: The greater the quantity of coronary atherosclerotic plaque, the greater the risk of atherosclerotic plaque rupture. An increasing burden of atherosclerotic plaque along the limited confines of coronary arteries, just a few millimeters in diameter and a few centimeters in length, is like a house of cards: It's bound to topple sooner or later, and the bigger it gets, the less stable it becomes.If you are concerned about future potential for heart disease and heart attack, don't get a cholesterol panel. Get a measure of coronary atherosclerotic plaque.
Back to basics: Coronary calcium 30. January 2012 William Davis (42) After having my attentions pulled a thousand different directions these past 6 months, with the release of Wheat Belly and all the wonderful media attention it has attracted, I've decided to pick up here with a series of discussions about the fundamental issues important to the Track Your Plaque program and prevention and reversal of coronary atherosclerotic plaque.I fear the discussions at times have drifted off into the exotic. This is great because this is how we learn new lessons, but we can never lose sight of the basics, else we risk losing control over this disease.Imagine you've got a beautiful new car. You wax it, gap the spark plugs, rotate the tires, etc. and it looks brand-new, just like it came off the dealer's lot. 50,000 miles pass, however, and you realize you've forgotten to change the oil. Ooops! In other words, no matter how meticulous the attention to transmission, tires, and paint job, neglect of the most basic responsibility can ruin the whole thing. We can't let that happen with heart health.If we propose to reverse coronary atherosclerotic plaque, we've got to have something to measure. First, it tells us whether we have atherosclerotic plaque in the first place, the stuff that accumulates and blocks flow and causes anginal chest pains, and ruptures like a little volcano and causes heart attacks. Second, it gives us something to track over the years to know whether plaque has grown, stopped growing, or been reduced. Without such a measure, you will be driving without a speedometer or odometer, just guessing whether or not you've gotten to your destination.Of course, the conventional approach to heart disease and heart attack is not to track atherosclerotic plaque in your coronary arteries, but to track some distant "risk factor" for atherosclerotic plaque, especially LDL cholesterol. But LDL cholesterol is flawed at several levels. First, it is calculated, not measured. The nearly 50-year old Friedewald equation used to calculate LDL cholesterol is based on several flawed assumptions, yielding a value that can be 20, 30, or 50% inaccurate as a rule, only occasionally generating a value close to the real value. (No point in publicizing this problem, of course: Why compromise a $27 billion annual cash cow?) It also ignores the effect of diet. (No, cutting fat does not reduce LDL for real, only the calculated value. Cutting carbohydrates, especially wheat--"healthy whole grains"--slashes measured LDL values like NMR LDL particle number and apoprotein B.)But all risk factors are, at best, snapshots of the situation at that moment in time. They change from day to day, week to week, month to month, year to year. If you do something dramatic in health, like lose 50 pounds, you can substantially change your risk factors values, like LDL cholesterol and HDL cholesterol. But you may not modify the amount of atherosclerotic plaque in your heart's arteries.Measuring the amount of atherosclerotic plaque in your heart's arteries is, in effect, a cumulative expression of the effects of risk factors up until the moment of measurement.There are several stumbling blocks, however, in the concept of measuring coronary atherosclerotic plaque. We cannot measure all the unique components of plaque, such as fibrous tissue like collagen, or degradative enzymes like collagenases, or inflammatory proteins like matrix metalloproteinase, or the debris of hemorrhage and inflammation. We struggle to contemporaneously mix in measures of bloodborne inflammation, coagulation and viscosity, and physiological phenomena of the artery itself, like endothelial dysfunction, medial (muscle) tone, and adventitial fat.So we are left with semi-static measures of total coronary atherosclerotic plaque like coronary calcium, obtainable via CT heart scans as a calcium "score." No, it is not perfect. It does not reflect that moment's blood viscosity, it does not reflect the inflammatory status of the one nasty plaque in the mid-left anterior descending, nor does it reflect the irritating sheer effects of a blood pressure of 150/95.But it's the best we've got.If anyone has something better, I invite you to speak up. Carotid ultrasound, c-reactive protein, ankle-brachial index, stress nuclear studies, myoglobin, skin cholesterol, KIF6 genotype . . . none of them approach the value, the insight, the trackability of actually measuring coronary atherosclerotic plaque. And the only method we've got to gauge coronary atherosclerotic plaque that is non-invasive and available in 2012? Yup, a good old CT heart scan calcium score.
Myocardial infraction 15. January 2012 William Davis (45) I've seen a few heart attacks this past year . . . but none in the people who follow this program. I saw a heart attack in a priest, a wonderful man who was unable to say "no" to his parishioners who insisted on bringing pies, cakes, and cookies every day. I saw an impending heart attack in a 74-year old man, a football coach who thought the whole wheat-free, low-carb thing was some wacko trend. Four stents later, he's changed his mind. A 69-year old woman had to be hospitalized for heart failure due to partial closure of an artery. She repeatedly told me that she simply could not follow the diet because it was "too restrictive." There were a few others. Interestingly, all felt they were eating healthy, minimizing junk foods and avoiding fatty foods. None were wheat-free nor restricted carbohydrates. In other words, in the people who follow the basic advice of the Track Your Plaque program to do such simple things as eliminate wheat, don't indulge in junk carbohydrates, normalize vitamin D status, supplement omega-3 fatty acids, supplement iodine and correct any thyroid dysfunction . . . well, they have no heart attacks.
Diet is superior to drugs 7. January 2012 William Davis (27) Might-o’chondri-AL left this wonderful record of his lipoprotein experience in the comments to the last Heart Scan Blog post. It is a great example of what is achievable with diet and a few supplements . . . without drugs. (A) Jan. 2011 1st ever NMR lipo-protein analysis was done after 4 months of consistent home food prep of pretty low fat (only olive oil and 1 tablespoon coconut oil daily) but plenty of whole wheat and half potatoes:* LDL # of particles (P) = 1,676 in nmol/L————being a LDL cholesterol (C) reading of 139 mg/dL* small LDL # P = 1,021 nmol/L —————yikes! you advise smLDL be less than 117 nmol/L* HDL # of particles = 28.8 umol/L ————–being a HDL C reading of 45 mg/dL* Triglycerides = 90 mg/dL ————– true, I never struggled with my weight(B) May 2011 2nd NMR after another 4 months but added in more fat (1 teaspoon highly concentrated fish oil daily, 90% chocolate, handfulls of nuts, more olive oil and kept coconut oil at 1 tablespoon daily for a controlled experiment), added 500 mg Niacin 3 times a day (in stages up to1,500 mg. total daily), 6000 IU daily vitamin D, deliberately cut out all grains except for social politeness and substituted in daily Koji fermented brown rice (rustic Amazake):** LDL # P……………= 976 nmol/L ——————————– being LDL C of 100 mg/dL** small LDL # P …. = 96 nmol/L ——————————– nice surprise** HDL # P ………… = 27.3 umol/L ——————————being an increase to HDL C of 64 mg/dL** Triglycerides …… = 42 mg/dL ——————————– despite daily carbs over 150 gr. daily(C) Dec. 2011 3rd NMR after another 7 more months thinking Doc’s advice is worthwhile I added in yet more fat (mainly daily 2 tablespoons of coconut oil, more 90% chocolate), bumped Niacin up to 1,000 mg twice a day (2,000 mg. total daily), cut out the Amazake, kept up the vitamin D adding daily vitamin K & daily ate main mid-day meal out as lunch on spicy Thai & Chinese fish/shrimp/soup/rice meals (my next control):*** LDL # P ………. = 764 nmol/L ————— being LDL C of 107 mg/dL ( 2x coconut’s saturated fat)***small LDL # P… = less than 90 nmol/L ——–surprised me NMR can’t count lower***HDL # P ……… = 41.4 umol/L ——————– being an increase to HDL C of 88 mg/dL*** Triglycerides ….= 43 mg/dL ——————- daily carbs below ~ 120 gr. & lost too much weightIsn't that great? Spectacular job, Might!MIght achieved values that are superior to that achievable with, say, a high-dose statin strategy. Statins only reduce total LDL particles, reducing small LDL in a non-selective way. And, of course, this diet does not cause muscle aches, memory loss, nor liver problems. Something to consider: As the diet has become so effective, we can reduce our reliance on niacin. In fact, the benefits of niacin diminish substantially, as small LDL is reduced, HDL increased, triglycerides decreased, and postprandial lipoproteins subdued with the diet only.
Low-carb is heart healthy 4. January 2012 William Davis (88) Anybody following the discussions in these pages know that: Limiting carbohydrate intake reduces risk for coronary heart disease and heart attack.First of all, why do conventional diets advocate restricting saturated and total fat? From the standpoint of surrogate markers of cardiovascular risk, cutting saturated and total fat reduces total cholesterol; reduces calculated LDL cholesterol; and may reduce c-reactive protein modestly (an index of inflammation). It also increases blood sugar and HbA1c (reflecting the prior 60 days blood sugars), increases glycation of the proteins of the body leading to cataracts, arthritis, and hypertension. Problem: Total cholesterol is a combination of HDL cholesterol, an estimate of VLDL cholesterol (triglycerides), and LDL cholesterol. It is a composite of both "good" things (HDL) and "bad" things (LDL and VLDL). Cutting saturated and total fat results in reduced HDL, increased VLDL/triglycerides, and a reduction in calculated LDL. Pretty weak stuff. The last item, i.e., reduction in calculated LDL, is not even a real phenomenon. In fact, the net effect in most genotypes (genetic types) may be negative: increased heart disease risk. In contrast, what is the effect of reducing carbohydrate without restricting fat? (In the approach I use, we start with elimination of the most destructive of carbohydrates, wheat, followed by reducing exposure to other carbohydrates, especially cornstarch and corn products, sugar, and oats.) If, say, we cut carbohydrate intake into the range of a truly low-carbohydrate diet of 10-15 grams per meal ("net" carbs, or total carbohydrates minus fiber), then we witness a number of metabolic transformations:Reduced fasting triglycerides and VLDLReduced postprandial (after-eating) triglycerides, chylomicrons, and chylomicron remnantsIncreased HDL and shift towards large HDL particles (presumably more protective)Reduced small LDL particlesReduced glycation and oxidation of small LDL particlesReduced hemoglobin A1cReduced c-reactive protein and other inflammatory markersReduced blood pressureBy slashing carbohydrates, we also witness weight loss from visceral fat, reversal of pre-diabetes and diabetes, and reduced phenomena of glycation. And, if the wheat-free part of low-carb is maintained, you can also see marked improvement in gastrointestinal health, relief from joint pains, relief from leg edema, relief from migraine headaches, improved behavior and ability to concentrate in children with impaired learning, ADHD, and autism, better mood, deeper sleep. You will see multiple inflammatory and autoimmune diseases improve or completely relieved, such as rheumatoid arthritis and ulcerative colitis. Having personally gone down the diabetic path and back by cutting the fat in my diet, now maintaining a HbA1c of 4.8% with fasting glucose 84 mg/d; (without medications), there should be no remaining doubt: Low-carb diets, especially if wheat-free, dramatically reduce the factors leading to heart disease; low-fat diets worsen the factors leading to heart disease.
Mocha Walnut Brownies 1. January 2012 William Davis (11) Richer than a cookie, heavier than a muffin, brownies are ordinarily an indulgence that leaves you ashamed of your lack of restraint. Have one . . . or two or three, and you will surely pack on a pound of belly fat.But these mocha walnut brownies, as with other recipes I provide, will not pack on the pounds. With no wheat to trigger appetite, nor any readily-digestible carbohydrate to generate blood sugar highs and lows, you can have a nice brownie or two or three and nothing bad happens: You don’t send blood sugar sky-high, don’t trigger formation of small LDL particles and triglycerides, you don’t trigger appetite, you don’t gain a pound of belly fat. You simply have your brownie(s) and enjoy them.Serve these brownies plain or topped with cream cheese, natural peanut or almond butter, or dipped in coffee.Ingredients:8 ounces unsweetened baking chocolate (100% chocolate)4 tablespoons coconut oil or butter, melted2 large eggs, separated½ cup coconut milk (or sour cream)2 teaspoons vanilla extract2 cups ground almonds2 tablespoons coconut flour1 cup chopped walnuts¼ cup unsweetened cocoa powder2 teaspoons instant espressoSweetener equivalent to 1 cup sugar or to taste (e.g., liquid stevia, Truvía, erythritol)Preheat oven to 350º F.Melt chocolate using double boiler method or in 15-second increments in microwave. Stir in melted coconut oil or butter.In small bowl, beat egg whites until frothy. Add egg whites, egg yolks, coconut milk, and vanilla extract to chocolate mixture and mix thoroughly by hand.In separate bowl, combine ground almonds, coconut flour, walnuts, cocoa powder, espresso, and sweetener. Mix thoroughly.Add dry mix to chocolate mix and mix together thoroughly. If dough is too stiff, add additional coconut milk, one tablespoon at a time.Place mixture in 9-inch baking pan and bake for 25 -30 minutes or until toothpick withdraws dry.