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 struct Toggle navigation Home Blog Home Archive Join Now Log in The myth of mild coronary disease 19. January 2008 William Davis (27) I hear this comment from patients all the time:"They told me that I had only mild blockages and so I had nothing to worry about."That's one big lie. I guess I shouldn't call it a lie. Is it a lie when it comes from ignorance, arrogance, laziness, or greed?"Mild coronary disease" is usually a label applied to coronary atherosclerotic plaque that is insufficient to block flow. Thus, having a few 20%, 30%, or 40% blockages would be labeled "mild." No stents are (usually) implanted, no bypass surgery performed, and symptoms should not be attributable to the blockages. Thus, "mild." The problem is that "mild" blockages are no less likely to rupture, the eruptive process that resembles a little volcano spewing lava. Except it's not lava, but the internal contents of atherosclerotic plaque. When these internal contents of plaque gain contact with blood, the coagulation process is set in motion and the artery both clots and constricts. Chest pains and heart attack result. So, the essential point is not necessarily the amount of blood flow through the artery, but the presence of coronary atherosclerotic plaque. Just having plaque--any amount of plaque--sets the stage to permit plaque rupture. One thing is clear: The more plaque you have, the greater the risk for rupture. But the quantity of plaque cannot be measured by the "percent blockage." It is measured by the lengthwise extent of plaque, as well as the depth of plaque within the wall. Neither of these risk features for plaque rupture can be gauged by percent blockage. Coronary atherosclerosis is a diffuse process that involves much of the length of the artery. It is therefore folly to believe that a 15 mm long stent has addressed the disease. This is no more a solution than to replace the faucet in your kitchen in a house with rotting pipes from the basement up. The message: ANY amount of coronary plaque is reason to engage in a program of prevention--prevention of plaque rupture, prevention of further plaque growth, perhaps even regression (reversal). It is NOT a reason to be complacent and buy into the myth of "mild" coronary disease, the misguided notion that arises from ill-conceived procedural heart disease solutions. Image courtesy Wikipedia. Copyright 2008 William Davis, MD Red flags for lipoprotein(a) 17. January 2008 William Davis (24) Lipoprotein(a), Lp(a), is an important cause for heart disease, heart attack, and coronary atherosclerotic plaque. How do you know you have it?Of course, it could be as simple as checking a blood level. But there are also a number of red flags for the presence of Lp(a), tell-tale signs that suggest it is present and contributing to the growth of coronary plaque. I've seen so much of this pattern over the years that it's gotten so that I can pretty much pick out most of the people with Lp(a) just by either looking at them or by hearing their story. I do this simply by knowing what hints to look for.Some of the red flags for Lp(a) include:--High blood pressure in a slender person. Overweight is the overwhelmingly common reason for high blood pressure. However, inappropriate high blood pressure in a slender person can serve to tip you off that Lp(a) is present. --HIgh LDL cholesterol poorly responsive to statin drugs. For instance, someone's LDL cholesterol of 190 mg/dl will be treated with Lipitor 40 mg, but drops to only 165 mg/dl, a very poor response. This can sometimes point towards Lp(a). --Family clustering of heart disease in people before age 60. For instance, father with heart attack age 53, uncle with heart attack at age 55, aunt with heart attack age 59, etc. This clustering of risk, more often than not, signals Lp(a). --Coronary disease or high heart scan score in the presence of relatively bland appearing lipids. For instance, LDL cholesterol 130 mg/dl, HDL 55 mg/dl, triglycerides 70 mg/dl on no medications or other efforts--figures ordinarily not associated with high likelihood of heart disease--yet heart disease is indeed present. This can mean that Lp(a) is the concealed culprit behind coronary atherosclerosis. These red flags are not perfect. If you lack any of them, it doesn't necessarily rule out the possbility of having Lp(a). They simply serve as signs to suggest that Lp(a) may be lurking.Once Lp(a) is identified, then the battle begins to gain control over this somewhat troublesome genetic pattern. Resourcesfulness and some ingenuity may be required. However, knowing that you have it shows you where to concentrate your efforts. Vytorin study explodes--But what's the real story? 15. January 2008 William Davis (28) The makers of Vytorin, Merck/Schering-Plough Pharmaceuticals, issued a press release about the the Enhance Study yesterday. The news has triggered a media frenzy. The NY Times reporting of the story:Drug Has No Benefit in Trial, Makers SayThe 700 participants in the trial all had a condition called "heterozygous hypercholesterolemia," a genetic disorder that permits very high LDL cholesterols. The average LDL at the start was 318 mg/dl.The Times reported that, while Vytorin cut "LDL levels by 58 percent, compared to a 41 percent reduction with simvastatin alone," but "the average thickness of the carotid artery plaque increased by 0.0111 of a millimeter in patients taking Vytorin, compared to an increase of 0.0058 of a millimeter in those taking only simvastatin." There was no difference in heart attacks or other "events" between the two groups. (Vytorin is the combination of simvastatin and Zetia.) In other words, the participants taking Vytorin had 53 ten-thousands of a millimeter more plaque growth than the group taking just simvastatin.I am always uncomfortable when put in the position of defending a drug or drug company. However, it is patently absurd that this study has generated such attention. I suspect the public and media are waiting for another Vioxx-like debacle, with memories of concealed or suppressed data that suggested heightened heart attack risk that was dismisssed by the drug manufacturer. (That's not to say that the company hasn't been trying to delay or modify the outcome of the study, which they apparently have, much to the objections of the FDA.) However, at this point, there is no reason to believe that this question possesses any parallels to the Vioxx fiasco. If we accept the data as reported, however, we might say it calls the entire "Lipid Hypothesis" into question: If LDL cholesterol is significantly reduced but is not correlated with reduction in plaque, is LDL the means by which atherosclerotic plaque progresses? This trial does not answer that question, but does serve to raise some doubt. Another issue: Heterozygous hypercholesterolemia, and thereby LDL cholesterol, may not be the overwhelming driver of plaque growth in this population. It is probably the number of small LDL particles, a factor which is not revealed by LDL cholesterol. For this reason, heterozygous hypercholesterolemia by itself is insufficient to cause heart disease. Some other factor(s) needs to be present. I would propose that it is the size of the LDL particle: When small, heart disease develops; when large, heart disease is less likely to develop. This issue was not addressed by this study. Readers of The Heart Scan Blog know that conventional LDL cholesterol, the number used in this study, is a virtually worthless number for truly gauging plaque behavior because of its flagrant inaccuracy. So, there are substantial uncertainties, contrary to the absolute certainty expressed by people like Dr. Steve Nissen (who, by the way, has no expertise in lipoprotein disorders). It is premature to reach any firm conclusions from this study. The only conclusions that I personally come to are 1) Is this yet another reason to question the entire Lipid Hypothesis as it stands? and 2) What would the results have been had LDL particle number and LDL particle size been examined, not just LDL? I would not automatically conclude that Zetia causes carotid plaque. This is absurd. And I am definitely not one to come to the rescue of a drug or drug manufacturer. I am simply after understanding and truth. As an interesting aside, Dr. Howard Hodis of the University of Southern California and an expert in carotid scanning for heart disease prevention research, made a comment relevant to us in the Track Your Plaque program: "Clearly, progression of atherosclerosis is the only way you get events,” Dr. Hodis said. “If you don’t treat progression, then you get events." Dr. Arthur Agatston in the news 15. January 2008 William Davis (7) The Miami Herald has a new report on Dr. Arthur Agagtston (of South Beach Diet fame) to announce his new book, The South Beach Heart Health Revolution:The South Beach Diet doctor takes on cardio careAgatston, the granddaddy of CT heart scanning, is always at least worth listening to. Although his diet may not be perfect, it clearly has jumped light years ahead of conventional diets like the inane American Heart Association diet. The South Beach Diet focuses on healthy oils, nuts, lean meats, vegetables, and fruits, while slashing grains (except in the often disastrous phase III). The article lists Dr. Agatston's advice to achieve a "heart healthy" lifestyle:• Maintain a healthy weight through diet.• Undergo CT heart scans to check for arterial plaque.• Do aerobic exercise, along with stretching and strengthening workouts.• Ask your doctor about taking statins and other cholesterol-lowering drugs. We wouldn't have CT heart scan scoring (at least in its present form) without Dr. Agatston, who developed the algorithm for scoring years ago in the early days of heart scanning. We also need to credit him with putting together a rational diet despite the counter-information emanating from the Heart Association, the USDA (a la Food Pyramid, the one that makes Americans fat and diabetic), and the American Diabetes Association, among others. But "Ask your doctor about taking statins and other cholesterol-lowering drugs"? This is where Dr. Agatston begins to falter. While he is putting his enormous notoriety to use, his message is bland and ineffective. "Do aerobic exercise"? We don't need Dr. Agatston to tell us this. As much as Art Agatston has added to the national conversation on heart disease and diet, he has failed to deliver the message of true heart disease prevention. His approach lacks just a few crucial ingredients like lipoprotein testing, diagnosis of hidden causes of heart disease (like Lp(a)), and vitamin D. (Two years ago I had a patient I saw for an opinion after he'd showed Dr. Agatston his lipoprotein panel. The patient said Dr. Agatston looked at the report and didn't know what to do with it and handed it back to him without comment. He then asked if he wanted his autograph.)Anyway, the rising tide raises all boats. Agatston's repeated public endorsements of heart scans will help deliver the message that heart disease is detectable in its early stages and should trigger action to follow a heart disease prevention program. That alone is an accomplishment in a world hell-bent on dragging us into the hospital for procedures. Take this survey: I DOUBLE-DARE YOU 14. January 2008 William Davis (10) In a previous post I entitled Heart disease reversal a big "No No", I posed a challenge--a dare--to readers to ask their doctors if coronary heart could be reversed. Here's what I said:I dare you: Ask your doctor whether coronary heart disease can be reversed.My prediction is that the answer will be a flat "NO." Or, something like "rarely, in extraordinary cases," kind of like spontaneous cure of cancer.There are indeed discussions that have developed over the years in the conventional scientific and medical literature about reversal of heart disease, like Dean Ornish's Lifestyle Heart Trial, the REVERSAL Trial of atorvastatin (Lipitor) and the ASTEROID Trial of rosuvastatin (Crestor). Reversal of atherosclerotic plaque in these trials tends to be small in scale and sporadic.The concept of reversal of heart disease has simply not gained a foothold in the lexicon nor in the thinking of practicing physicians. Heart disease is a relentlessly, unavoidably, and helplessly progressive disease in their way of thinking. Perhaps we can reduce the likelihood of cardiovascular events like heart attack and death with statin drugs and beta blockers. But reverse heart disease? In your dreams!We need to change this mentality. Heart disease is a reversible phenomenon. Atherosclerosis in other territories like the carotid arteries is also a reversible pheneomenon. Rather than throwing medicines and (ineffective) diets at you (like the ridiculous American Heart Association program), what if your doctor set out from the start not just to reduce events, but to purposefully reduce your heart's plaque? While it might not succeed in everyone, it would certainly change the focus dramatically.After all, isn't this the theme followed in cancer treatment? If you had a tumor, isn't cure the goal? Would we accept an oncologist's advice to simply reduce the likelihood of death from cancer but ignore the idea of ridding yourself completely of the disease? I don't think so.Then why accept "event reduction" as a goal in heart disease? We shouldn't have to. Heart disease reversal--elimination--should be the goal.I know of one person who actually followed through on this challenge and asked his cardiologist whether his heart disease could be reduced or reversed. As predicted, the answer was no. No explanation followed.But allow me to reiterate: Heart disease is 1) detectable, 2) quantifiable, 3) controllable, and, in many cases 4) reversible. What if there was a big payoff to your doctor if heart disease was reversed, say $100,000? That's enough to dwarf the payoff from procedures. Guess what? You'd have doctors fighting for your business, a chance to reverse your disease, ads to that effect, champions of reversal emerging. No new tools would be necessary. They could use the tools already available. Then why hasn't this happened? Is the technology unavailable? Are the treatments ineffective?No, heart disease is a controllable and reversible process with tools that are available today. But there is, of course, no big payoff for doing it. So the financial incentive remains to do procedures, not to reverse the disease. But I'd like to re-pose this challenge. Ask your doctor if heart disease can be reversed, or at least reduced. I've even posted a Survey at the top left for anyone who tries. Again, my prediction: Nobody will try it and nobody will post survey results. Why? Despite my rantings (and those of a few others) about the concept of heart disease being a reversible process, in the public's consciousness it remains a death sentence and the only solution is hospital procedures. My colleagues continue to cultivate this attitude and it serves them well financially. I'll be disappointed if I prove to be right. I hope that I am wrong. But I don't think that I am. Copyright 2008 William Davis, MD Michael Pollan on Nutritionism 13. January 2008 William Davis (8) The wonderfully articulate Michael Pollan has written another book. Although he presents little new to anyone who read his previous book, The Omnivore's Dilemma: A natural history of four meals, he is such a wonderful writer, with such clever ways of seeing the world, that I couldn't resist this new, less ambitious book. The new book is In Defense of Food: An eater's manifesto. As in Omnivore's Dilemma, Pollan reminds us that we've lost contact with real food, foods that our great grandmother would recognize, not the just-add-water, dried, pulverized, sweetened, high-fructose, hydrogenated, shrink-wrapped, artificially-colored products that pass as foods in the grocery store. In particular, Pollan attacks what he calls the ideology of Nutritionism. "The widely shared but unexamined assumption is that the key to understanding food is indeed the nutrient. Put another way: Foods are essentially the sum of their nutrient parts." He calls this "Nutritionism."In the section called "Nutritionism comes to market," he uses margarine as the prototypical product of this philosophy:"No idea could be more sympathetic to manufacturers of processed foods, which surely explains why they have been so happy to jump on the nutritionism bandwagon. Indeed, nutritionism supplies the ultimate justification for processing food by implying that with a judicious application of food science, fake foods can be made even more nutritious than the real thing. This of course is the story of margarine, the first important synthetic food to slip into our diet. Margarine started out in the nineteenth century as a cheap and inferior sustitute for butter, but with the emergence of the lipid hypothesis in the 1950s, manufacturers quickly figured out that their product, with some tinkering, could be marketed as better--smarter!--than butter: butter with the bad nutrients removed (cholesterol and saturated fats) and replaced with good nutrients (polyunsaturated fats and then vitamins). Every time margarine was found wanting, the wanted nutrient could simply be added (Vitamin D? Got it now. Vitamin A? Sure, no problem. But of course margarine, being the product not of nature but of human ingenuity, could never be any smarter than the nutritionists dictating its recipe, and the nutritionists turned out to be not nearly as smart as they thought. The food scientists' ingenious method for making healthy vegetable oil solid at room temperature--by blasting it with hydrogen--turned out to produce unhealthy trans fats, fats that we now know are more dangerous than the saturated fats they were designed to replace. Yet the beauty of a processed food like margarine is that it can be endlessly reengineererd to overcome even the most embarrassing about-face in nutritional thinking--including the real wincer that its main ingredient might cause heart attacks and cancer. So now the trans fats are gone, and margarine marches on, unfazed and apparently unkillable. Too bad the same cannot be said of an unknown number of margarine eaters." Anyone who reads and thinks a lot about nutrition will find little new here. But nobody says it better than Pollan. While Gary Taubes (Good Calories, Bad Calories) is the real thinker of our age about nutrition, Michael Pollan is the true writer about it.With books like these making the bestsellers list, I believe that we are gradually seeing rationality return to eating. It makes people skeptical of the glitzy ads that run on TV around the clock. I hope that Pollan's new book will make more and more people leery of the latest health claim that adorn some product. "More omega-3!" "A low-fat snack." "Heart Healthy!" "High in healthy fiber!" Cholesterol follies 11. January 2008 William Davis (5) Rudy is a 59-year old man. He's had three heart catheterizations, two of which resulted in stent implantations. Obviously, Rudy should be the beneciary of a prevention program. His basic cholesterol values: Total cholesterol 164 mg/dl--pretty good, it seems. LDL cholesterol 111 mg/dl--Wow! Not too bad. HDL cholesterol 23 mg/dl--Uh oh, that's not too good. Triglycerides 148 mg/dl--By national (NCEP ATP-III) guidelines, triglycerides of 150 mg/dl and below fall within the desirable range. So we're left with an apparently isolated low HDL cholesterol, nothing more. On the surface, it doesn't seem all that bad. Of course, we need to keep in mind that this pattern landed Rudy in the hospital on several occasions and prompted several procedures. Should we rely on these results? How about Rudy's lipoproteins? Here they are (NMR; Liposcience):LDL particle number 2139 nmol/l--Representing an effective LDL of 213--over 100 mg higher than the standard value (above) suggests.Small LDL particles 2139 nmol/l--In other words, 100% of all Rudy's LDL particles are small. (Thus, weight-based measures of LDL cholesterol fail to tell us that he has too many small particles.)Large HDL 0 (zero) mg/dl--Rudy has virtually no functional HDL particles. If we had relied only on Rudy's standard cholesterol values, we would have focused on raising HDL. However, lipoprotein analysis uncovered a smorgasbord of additional severe patterns. The high LDL particle number comprised 100% of small particles is especially concerning. Truly, conventional cholesterol testing is a fool's game, one that time and again fails to fully uncover or predict risk for heart disease. One look at Rudy's lipoproteins and it becomes immediately obvious: This man is at high risk for heart disease and the causes are clear. Of course, many physicians and insurance companies argue that the added information provided by this portion of the lipoprotein test added around $70 more to the expense. When you see results like this, is there even a choice? Equal calories, different effects 9. January 2008 William Davis (15) A great study was just published in the Journal of the American College of Cardiology:Metabolic effects of weight loss on a very-low-carbohydrate diet compared with an isocaloric high-carbohydrate diet in abdominally obese subjects. 88 obese adults with metabolic syndrome were placed on either of two diets:1) A very low-carbohydrate, high-fat diet (VLCHF): 4% calories from carbohydrates (truly low-carb); 35% protein; 61% fat, of which 20% were saturated. In the first 8 weeks, carbohydrate intake was severely limited to <20 grams per day, then <40 grams per day thereafter. 2) A high-carbohydrate, low-fat diet (HCLF): 46% calories from carbohydrates; 24% protein; 30% total fat, of which <8% were saturated. Both diets were equal in calories (around 1400 calories per day--rather restrictive) and participants were maintained on the program for six months. At the end of the six month period, participants on the VLCHF diet lost 26.4 lb, those on the HCLF diet 22.2 lbs (though the difference did not reach statistical significance). Thus, both approaches were spectacularly successful at weight loss. Surprisingly, blood pressure, blood sugar, insulin and insulin sensitivity (a measure called HOMA) were all improved with both diets equally. Thus, these measures seemed to respond more to weight loss and less to the food composition. Lipids differed between the two diets, however:VLCHF:Total cholesterol: initial 208.4 mg/dl final 207.7 mg/dlLDL: initial 125 mg/dl final 123 mg/dlHDL: initial 55 mg/dl final 64.5 mg/dlTriglycerides: initial 144 mg/dl final 74 mg/dlApoprotein B: initial 98 mg/dl final 96 mg/dlHCLF Total cholesterol: initial 208.4 mg/dl final 187.5 mg/dlLDL: initial 126 mg/dl final 108 mg/dlHDL: initial 51 mg/dl final 54.5 mg/dlTriglycerides: initial 157.6 mg/dl final 111 mg/dlApoprotein B: initial 100 mg/dl final 95 mg/dlSome interesting differences became apparent:--The VLCHF diet more effectively reduced triglycerides and raised HDL. --The HCLF diet more effectively reduced total and LDL. --There was no difference in Apo B (no statistical difference).The investigators also made the observation that individual responsiveness to the diets differed substantially. They concluded that both diets appeared to exert no adverse effect on any of the parameters measured, both were approximately equally effective in weight loss with slight advantage with the carbohydrate restricted diet, and that lipid effects were indeed somewhat different. What lessons can we learn from this study? I would propose/extrapolate several:When calories are severely restricted, the composition of diet may be less important. However, when calories are not so severely restricted, then composition may assume a larger role. When calories are unrestricted, I would propose that the carbohydrate restriction approach may yield larger effects on weight loss and on lipids when compared to a low-fat diet. The changes in total cholesterol are virtually meaningless. Part of the reason that it didn't drop with the VLCHF diet is that HDL cholesterol increased. In other words, total cholesterol = LDL + HDL + trig/5. A rise in HDL raises total cholesterol. Despite no change in Apo B, if NMR lipoprotein analysis had been performed (or other assessment of LDL particle
The myth of mild coronary disease 19. January 2008 William Davis (27) I hear this comment from patients all the time:"They told me that I had only mild blockages and so I had nothing to worry about."That's one big lie. I guess I shouldn't call it a lie. Is it a lie when it comes from ignorance, arrogance, laziness, or greed?"Mild coronary disease" is usually a label applied to coronary atherosclerotic plaque that is insufficient to block flow. Thus, having a few 20%, 30%, or 40% blockages would be labeled "mild." No stents are (usually) implanted, no bypass surgery performed, and symptoms should not be attributable to the blockages. Thus, "mild." The problem is that "mild" blockages are no less likely to rupture, the eruptive process that resembles a little volcano spewing lava. Except it's not lava, but the internal contents of atherosclerotic plaque. When these internal contents of plaque gain contact with blood, the coagulation process is set in motion and the artery both clots and constricts. Chest pains and heart attack result. So, the essential point is not necessarily the amount of blood flow through the artery, but the presence of coronary atherosclerotic plaque. Just having plaque--any amount of plaque--sets the stage to permit plaque rupture. One thing is clear: The more plaque you have, the greater the risk for rupture. But the quantity of plaque cannot be measured by the "percent blockage." It is measured by the lengthwise extent of plaque, as well as the depth of plaque within the wall. Neither of these risk features for plaque rupture can be gauged by percent blockage. Coronary atherosclerosis is a diffuse process that involves much of the length of the artery. It is therefore folly to believe that a 15 mm long stent has addressed the disease. This is no more a solution than to replace the faucet in your kitchen in a house with rotting pipes from the basement up. The message: ANY amount of coronary plaque is reason to engage in a program of prevention--prevention of plaque rupture, prevention of further plaque growth, perhaps even regression (reversal). It is NOT a reason to be complacent and buy into the myth of "mild" coronary disease, the misguided notion that arises from ill-conceived procedural heart disease solutions. Image courtesy Wikipedia. Copyright 2008 William Davis, MD
Red flags for lipoprotein(a) 17. January 2008 William Davis (24) Lipoprotein(a), Lp(a), is an important cause for heart disease, heart attack, and coronary atherosclerotic plaque. How do you know you have it?Of course, it could be as simple as checking a blood level. But there are also a number of red flags for the presence of Lp(a), tell-tale signs that suggest it is present and contributing to the growth of coronary plaque. I've seen so much of this pattern over the years that it's gotten so that I can pretty much pick out most of the people with Lp(a) just by either looking at them or by hearing their story. I do this simply by knowing what hints to look for.Some of the red flags for Lp(a) include:--High blood pressure in a slender person. Overweight is the overwhelmingly common reason for high blood pressure. However, inappropriate high blood pressure in a slender person can serve to tip you off that Lp(a) is present. --HIgh LDL cholesterol poorly responsive to statin drugs. For instance, someone's LDL cholesterol of 190 mg/dl will be treated with Lipitor 40 mg, but drops to only 165 mg/dl, a very poor response. This can sometimes point towards Lp(a). --Family clustering of heart disease in people before age 60. For instance, father with heart attack age 53, uncle with heart attack at age 55, aunt with heart attack age 59, etc. This clustering of risk, more often than not, signals Lp(a). --Coronary disease or high heart scan score in the presence of relatively bland appearing lipids. For instance, LDL cholesterol 130 mg/dl, HDL 55 mg/dl, triglycerides 70 mg/dl on no medications or other efforts--figures ordinarily not associated with high likelihood of heart disease--yet heart disease is indeed present. This can mean that Lp(a) is the concealed culprit behind coronary atherosclerosis. These red flags are not perfect. If you lack any of them, it doesn't necessarily rule out the possbility of having Lp(a). They simply serve as signs to suggest that Lp(a) may be lurking.Once Lp(a) is identified, then the battle begins to gain control over this somewhat troublesome genetic pattern. Resourcesfulness and some ingenuity may be required. However, knowing that you have it shows you where to concentrate your efforts.
Vytorin study explodes--But what's the real story? 15. January 2008 William Davis (28) The makers of Vytorin, Merck/Schering-Plough Pharmaceuticals, issued a press release about the the Enhance Study yesterday. The news has triggered a media frenzy. The NY Times reporting of the story:Drug Has No Benefit in Trial, Makers SayThe 700 participants in the trial all had a condition called "heterozygous hypercholesterolemia," a genetic disorder that permits very high LDL cholesterols. The average LDL at the start was 318 mg/dl.The Times reported that, while Vytorin cut "LDL levels by 58 percent, compared to a 41 percent reduction with simvastatin alone," but "the average thickness of the carotid artery plaque increased by 0.0111 of a millimeter in patients taking Vytorin, compared to an increase of 0.0058 of a millimeter in those taking only simvastatin." There was no difference in heart attacks or other "events" between the two groups. (Vytorin is the combination of simvastatin and Zetia.) In other words, the participants taking Vytorin had 53 ten-thousands of a millimeter more plaque growth than the group taking just simvastatin.I am always uncomfortable when put in the position of defending a drug or drug company. However, it is patently absurd that this study has generated such attention. I suspect the public and media are waiting for another Vioxx-like debacle, with memories of concealed or suppressed data that suggested heightened heart attack risk that was dismisssed by the drug manufacturer. (That's not to say that the company hasn't been trying to delay or modify the outcome of the study, which they apparently have, much to the objections of the FDA.) However, at this point, there is no reason to believe that this question possesses any parallels to the Vioxx fiasco. If we accept the data as reported, however, we might say it calls the entire "Lipid Hypothesis" into question: If LDL cholesterol is significantly reduced but is not correlated with reduction in plaque, is LDL the means by which atherosclerotic plaque progresses? This trial does not answer that question, but does serve to raise some doubt. Another issue: Heterozygous hypercholesterolemia, and thereby LDL cholesterol, may not be the overwhelming driver of plaque growth in this population. It is probably the number of small LDL particles, a factor which is not revealed by LDL cholesterol. For this reason, heterozygous hypercholesterolemia by itself is insufficient to cause heart disease. Some other factor(s) needs to be present. I would propose that it is the size of the LDL particle: When small, heart disease develops; when large, heart disease is less likely to develop. This issue was not addressed by this study. Readers of The Heart Scan Blog know that conventional LDL cholesterol, the number used in this study, is a virtually worthless number for truly gauging plaque behavior because of its flagrant inaccuracy. So, there are substantial uncertainties, contrary to the absolute certainty expressed by people like Dr. Steve Nissen (who, by the way, has no expertise in lipoprotein disorders). It is premature to reach any firm conclusions from this study. The only conclusions that I personally come to are 1) Is this yet another reason to question the entire Lipid Hypothesis as it stands? and 2) What would the results have been had LDL particle number and LDL particle size been examined, not just LDL? I would not automatically conclude that Zetia causes carotid plaque. This is absurd. And I am definitely not one to come to the rescue of a drug or drug manufacturer. I am simply after understanding and truth. As an interesting aside, Dr. Howard Hodis of the University of Southern California and an expert in carotid scanning for heart disease prevention research, made a comment relevant to us in the Track Your Plaque program: "Clearly, progression of atherosclerosis is the only way you get events,” Dr. Hodis said. “If you don’t treat progression, then you get events."
Dr. Arthur Agatston in the news 15. January 2008 William Davis (7) The Miami Herald has a new report on Dr. Arthur Agagtston (of South Beach Diet fame) to announce his new book, The South Beach Heart Health Revolution:The South Beach Diet doctor takes on cardio careAgatston, the granddaddy of CT heart scanning, is always at least worth listening to. Although his diet may not be perfect, it clearly has jumped light years ahead of conventional diets like the inane American Heart Association diet. The South Beach Diet focuses on healthy oils, nuts, lean meats, vegetables, and fruits, while slashing grains (except in the often disastrous phase III). The article lists Dr. Agatston's advice to achieve a "heart healthy" lifestyle:• Maintain a healthy weight through diet.• Undergo CT heart scans to check for arterial plaque.• Do aerobic exercise, along with stretching and strengthening workouts.• Ask your doctor about taking statins and other cholesterol-lowering drugs. We wouldn't have CT heart scan scoring (at least in its present form) without Dr. Agatston, who developed the algorithm for scoring years ago in the early days of heart scanning. We also need to credit him with putting together a rational diet despite the counter-information emanating from the Heart Association, the USDA (a la Food Pyramid, the one that makes Americans fat and diabetic), and the American Diabetes Association, among others. But "Ask your doctor about taking statins and other cholesterol-lowering drugs"? This is where Dr. Agatston begins to falter. While he is putting his enormous notoriety to use, his message is bland and ineffective. "Do aerobic exercise"? We don't need Dr. Agatston to tell us this. As much as Art Agatston has added to the national conversation on heart disease and diet, he has failed to deliver the message of true heart disease prevention. His approach lacks just a few crucial ingredients like lipoprotein testing, diagnosis of hidden causes of heart disease (like Lp(a)), and vitamin D. (Two years ago I had a patient I saw for an opinion after he'd showed Dr. Agatston his lipoprotein panel. The patient said Dr. Agatston looked at the report and didn't know what to do with it and handed it back to him without comment. He then asked if he wanted his autograph.)Anyway, the rising tide raises all boats. Agatston's repeated public endorsements of heart scans will help deliver the message that heart disease is detectable in its early stages and should trigger action to follow a heart disease prevention program. That alone is an accomplishment in a world hell-bent on dragging us into the hospital for procedures.
Take this survey: I DOUBLE-DARE YOU 14. January 2008 William Davis (10) In a previous post I entitled Heart disease reversal a big "No No", I posed a challenge--a dare--to readers to ask their doctors if coronary heart could be reversed. Here's what I said:I dare you: Ask your doctor whether coronary heart disease can be reversed.My prediction is that the answer will be a flat "NO." Or, something like "rarely, in extraordinary cases," kind of like spontaneous cure of cancer.There are indeed discussions that have developed over the years in the conventional scientific and medical literature about reversal of heart disease, like Dean Ornish's Lifestyle Heart Trial, the REVERSAL Trial of atorvastatin (Lipitor) and the ASTEROID Trial of rosuvastatin (Crestor). Reversal of atherosclerotic plaque in these trials tends to be small in scale and sporadic.The concept of reversal of heart disease has simply not gained a foothold in the lexicon nor in the thinking of practicing physicians. Heart disease is a relentlessly, unavoidably, and helplessly progressive disease in their way of thinking. Perhaps we can reduce the likelihood of cardiovascular events like heart attack and death with statin drugs and beta blockers. But reverse heart disease? In your dreams!We need to change this mentality. Heart disease is a reversible phenomenon. Atherosclerosis in other territories like the carotid arteries is also a reversible pheneomenon. Rather than throwing medicines and (ineffective) diets at you (like the ridiculous American Heart Association program), what if your doctor set out from the start not just to reduce events, but to purposefully reduce your heart's plaque? While it might not succeed in everyone, it would certainly change the focus dramatically.After all, isn't this the theme followed in cancer treatment? If you had a tumor, isn't cure the goal? Would we accept an oncologist's advice to simply reduce the likelihood of death from cancer but ignore the idea of ridding yourself completely of the disease? I don't think so.Then why accept "event reduction" as a goal in heart disease? We shouldn't have to. Heart disease reversal--elimination--should be the goal.I know of one person who actually followed through on this challenge and asked his cardiologist whether his heart disease could be reduced or reversed. As predicted, the answer was no. No explanation followed.But allow me to reiterate: Heart disease is 1) detectable, 2) quantifiable, 3) controllable, and, in many cases 4) reversible. What if there was a big payoff to your doctor if heart disease was reversed, say $100,000? That's enough to dwarf the payoff from procedures. Guess what? You'd have doctors fighting for your business, a chance to reverse your disease, ads to that effect, champions of reversal emerging. No new tools would be necessary. They could use the tools already available. Then why hasn't this happened? Is the technology unavailable? Are the treatments ineffective?No, heart disease is a controllable and reversible process with tools that are available today. But there is, of course, no big payoff for doing it. So the financial incentive remains to do procedures, not to reverse the disease. But I'd like to re-pose this challenge. Ask your doctor if heart disease can be reversed, or at least reduced. I've even posted a Survey at the top left for anyone who tries. Again, my prediction: Nobody will try it and nobody will post survey results. Why? Despite my rantings (and those of a few others) about the concept of heart disease being a reversible process, in the public's consciousness it remains a death sentence and the only solution is hospital procedures. My colleagues continue to cultivate this attitude and it serves them well financially. I'll be disappointed if I prove to be right. I hope that I am wrong. But I don't think that I am. Copyright 2008 William Davis, MD
Michael Pollan on Nutritionism 13. January 2008 William Davis (8) The wonderfully articulate Michael Pollan has written another book. Although he presents little new to anyone who read his previous book, The Omnivore's Dilemma: A natural history of four meals, he is such a wonderful writer, with such clever ways of seeing the world, that I couldn't resist this new, less ambitious book. The new book is In Defense of Food: An eater's manifesto. As in Omnivore's Dilemma, Pollan reminds us that we've lost contact with real food, foods that our great grandmother would recognize, not the just-add-water, dried, pulverized, sweetened, high-fructose, hydrogenated, shrink-wrapped, artificially-colored products that pass as foods in the grocery store. In particular, Pollan attacks what he calls the ideology of Nutritionism. "The widely shared but unexamined assumption is that the key to understanding food is indeed the nutrient. Put another way: Foods are essentially the sum of their nutrient parts." He calls this "Nutritionism."In the section called "Nutritionism comes to market," he uses margarine as the prototypical product of this philosophy:"No idea could be more sympathetic to manufacturers of processed foods, which surely explains why they have been so happy to jump on the nutritionism bandwagon. Indeed, nutritionism supplies the ultimate justification for processing food by implying that with a judicious application of food science, fake foods can be made even more nutritious than the real thing. This of course is the story of margarine, the first important synthetic food to slip into our diet. Margarine started out in the nineteenth century as a cheap and inferior sustitute for butter, but with the emergence of the lipid hypothesis in the 1950s, manufacturers quickly figured out that their product, with some tinkering, could be marketed as better--smarter!--than butter: butter with the bad nutrients removed (cholesterol and saturated fats) and replaced with good nutrients (polyunsaturated fats and then vitamins). Every time margarine was found wanting, the wanted nutrient could simply be added (Vitamin D? Got it now. Vitamin A? Sure, no problem. But of course margarine, being the product not of nature but of human ingenuity, could never be any smarter than the nutritionists dictating its recipe, and the nutritionists turned out to be not nearly as smart as they thought. The food scientists' ingenious method for making healthy vegetable oil solid at room temperature--by blasting it with hydrogen--turned out to produce unhealthy trans fats, fats that we now know are more dangerous than the saturated fats they were designed to replace. Yet the beauty of a processed food like margarine is that it can be endlessly reengineererd to overcome even the most embarrassing about-face in nutritional thinking--including the real wincer that its main ingredient might cause heart attacks and cancer. So now the trans fats are gone, and margarine marches on, unfazed and apparently unkillable. Too bad the same cannot be said of an unknown number of margarine eaters." Anyone who reads and thinks a lot about nutrition will find little new here. But nobody says it better than Pollan. While Gary Taubes (Good Calories, Bad Calories) is the real thinker of our age about nutrition, Michael Pollan is the true writer about it.With books like these making the bestsellers list, I believe that we are gradually seeing rationality return to eating. It makes people skeptical of the glitzy ads that run on TV around the clock. I hope that Pollan's new book will make more and more people leery of the latest health claim that adorn some product. "More omega-3!" "A low-fat snack." "Heart Healthy!" "High in healthy fiber!"
Cholesterol follies 11. January 2008 William Davis (5) Rudy is a 59-year old man. He's had three heart catheterizations, two of which resulted in stent implantations. Obviously, Rudy should be the beneciary of a prevention program. His basic cholesterol values: Total cholesterol 164 mg/dl--pretty good, it seems. LDL cholesterol 111 mg/dl--Wow! Not too bad. HDL cholesterol 23 mg/dl--Uh oh, that's not too good. Triglycerides 148 mg/dl--By national (NCEP ATP-III) guidelines, triglycerides of 150 mg/dl and below fall within the desirable range. So we're left with an apparently isolated low HDL cholesterol, nothing more. On the surface, it doesn't seem all that bad. Of course, we need to keep in mind that this pattern landed Rudy in the hospital on several occasions and prompted several procedures. Should we rely on these results? How about Rudy's lipoproteins? Here they are (NMR; Liposcience):LDL particle number 2139 nmol/l--Representing an effective LDL of 213--over 100 mg higher than the standard value (above) suggests.Small LDL particles 2139 nmol/l--In other words, 100% of all Rudy's LDL particles are small. (Thus, weight-based measures of LDL cholesterol fail to tell us that he has too many small particles.)Large HDL 0 (zero) mg/dl--Rudy has virtually no functional HDL particles. If we had relied only on Rudy's standard cholesterol values, we would have focused on raising HDL. However, lipoprotein analysis uncovered a smorgasbord of additional severe patterns. The high LDL particle number comprised 100% of small particles is especially concerning. Truly, conventional cholesterol testing is a fool's game, one that time and again fails to fully uncover or predict risk for heart disease. One look at Rudy's lipoproteins and it becomes immediately obvious: This man is at high risk for heart disease and the causes are clear. Of course, many physicians and insurance companies argue that the added information provided by this portion of the lipoprotein test added around $70 more to the expense. When you see results like this, is there even a choice?
Equal calories, different effects 9. January 2008 William Davis (15) A great study was just published in the Journal of the American College of Cardiology:Metabolic effects of weight loss on a very-low-carbohydrate diet compared with an isocaloric high-carbohydrate diet in abdominally obese subjects. 88 obese adults with metabolic syndrome were placed on either of two diets:1) A very low-carbohydrate, high-fat diet (VLCHF): 4% calories from carbohydrates (truly low-carb); 35% protein; 61% fat, of which 20% were saturated. In the first 8 weeks, carbohydrate intake was severely limited to <20 grams per day, then <40 grams per day thereafter. 2) A high-carbohydrate, low-fat diet (HCLF): 46% calories from carbohydrates; 24% protein; 30% total fat, of which <8% were saturated. Both diets were equal in calories (around 1400 calories per day--rather restrictive) and participants were maintained on the program for six months. At the end of the six month period, participants on the VLCHF diet lost 26.4 lb, those on the HCLF diet 22.2 lbs (though the difference did not reach statistical significance). Thus, both approaches were spectacularly successful at weight loss. Surprisingly, blood pressure, blood sugar, insulin and insulin sensitivity (a measure called HOMA) were all improved with both diets equally. Thus, these measures seemed to respond more to weight loss and less to the food composition. Lipids differed between the two diets, however:VLCHF:Total cholesterol: initial 208.4 mg/dl final 207.7 mg/dlLDL: initial 125 mg/dl final 123 mg/dlHDL: initial 55 mg/dl final 64.5 mg/dlTriglycerides: initial 144 mg/dl final 74 mg/dlApoprotein B: initial 98 mg/dl final 96 mg/dlHCLF Total cholesterol: initial 208.4 mg/dl final 187.5 mg/dlLDL: initial 126 mg/dl final 108 mg/dlHDL: initial 51 mg/dl final 54.5 mg/dlTriglycerides: initial 157.6 mg/dl final 111 mg/dlApoprotein B: initial 100 mg/dl final 95 mg/dlSome interesting differences became apparent:--The VLCHF diet more effectively reduced triglycerides and raised HDL. --The HCLF diet more effectively reduced total and LDL. --There was no difference in Apo B (no statistical difference).The investigators also made the observation that individual responsiveness to the diets differed substantially. They concluded that both diets appeared to exert no adverse effect on any of the parameters measured, both were approximately equally effective in weight loss with slight advantage with the carbohydrate restricted diet, and that lipid effects were indeed somewhat different. What lessons can we learn from this study? I would propose/extrapolate several:When calories are severely restricted, the composition of diet may be less important. However, when calories are not so severely restricted, then composition may assume a larger role. When calories are unrestricted, I would propose that the carbohydrate restriction approach may yield larger effects on weight loss and on lipids when compared to a low-fat diet. The changes in total cholesterol are virtually meaningless. Part of the reason that it didn't drop with the VLCHF diet is that HDL cholesterol increased. In other words, total cholesterol = LDL + HDL + trig/5. A rise in HDL raises total cholesterol. Despite no change in Apo B, if NMR lipoprotein analysis had been performed (or other assessment of LDL particle