Heart Scan Curiosities #8: Fat heart 8. July 2007 William Davis (2) Here's a curious incidental finding on a heart scan: an unusual fat accumulation around the heart. The arrows point to an unusually large accumulation of fat tissue on either side of the heart. This man was mildly but not excessively overweight at 5 ft 10 inches and 201 lbs. I know of no specific implications of this curiosity. It makes me wonder if he was very obese at one time and has since lost the weight.
Chocolate and blood pressure 7. July 2007 William Davis (1) A recent very detailed and clean study on the effects of a small serving of dark chocolate on blood pressure was just published in the Journal of the American Medical Association. I was going to do a little Blogging on this interesting study but I read the Fanatic Cook's wonderfully insightful comments. I'd direct you to her discussion, instead: A small daily dose of dark chocalate lowers blood pressure at http://fanaticcook.blogspot.com/. I couldn't have said it any better. By the way, the authors of the study had no financial ties to the chocolate or cocoa industry. Refreshing.
Does prevention save money? 7. July 2007 William Davis (2) Prevention and reversal of heart disease are undoubtedly preferable to the current crash and repair model currently followed by doctors and hospital, the model that has created an enormous medical device industry to support it. But does it save money? This debate often boils down to a metric of "lives saved per $100,000". Thus, the statin drugs (of course) have been subjected to such analyses and have been shown to be "cost-effective." But how does a powerful heart disease prevention and reversal program like Track Your Plaque compare to the current crash and repair procedural approach to heart disease? This is a very difficult analysis, one that is subject to enormous variation, depending on the population studied and the prevalence of disease, the local practice habits (e.g., in the northwest Cleveland suburb of Lorain, virtually everybody going to the hospital for any heart problem gets one or several heart catheterizations), and other factors. There's also the difficulty of what should constitute a prevention program. Is it like that used in the COURAGE Trial of "optimal medical therapy" that included nitroglycerin, aspirin, a beta blocker, and statin drug (which we regard as a laughably silly approach), or one like Track Your Plaque in which we try to correct the causes of heart disease, not just palliate (BandAid) them? Costs vary. The "optimal medical therapy" is very costly due to its reliance on medications to treat symptoms. Our program is somewhat costly because of the reliance on a CT heart scan and lipoprotein analysis (though, in the long perspective, our costs are modest). We asked this question and came up with a lengthy analysis. Bottom line: Following the Track Your Plaque program saves enormous sums of money. Because of the complexity of the analysis, which is theoretical and not a real-world test, we confined our analysis to men in the 40-59 year old age group. If this group alone were to subscribe to a intensive but rational program of prevention like Track Your Plaque, over $20 billion dollars per year would be saved. If the analysis were extended to women of all ages and men older than 59, the numbers would balloon to many more tens of billions of dollars. Such a savings wouldn't cure the healthcare system's growing financial crisis, but it sure would be a big help. Sort of like converting to a hydrid car--you don't eliminate the need for gas, but you'll save a lot in fuel costs. The Track Your Plaque approach makes sense because it is, bar none, the most powerful approach to gaining hold of heart disease risk available. But it also makes sense from a financial standpoint. Now, if we can only convince the hospitals, the $30 million annual salary device manufacturer CEO, and my procedure-crazy colleagues that this way makes more sense. Watch for our analysis on an upcoming Track Your Plaque Special Report.
Where should fiber come from? 7. July 2007 William Davis (1) Ray had the usual protuberant belly overhanging his beltline of someone who was over-reliant on processed starches, particularly wheat. After all, he ran a sandwich bakery. He sheepishly admitted that he ate the products of his own production line every day while at work, even bringing a few sandwiches home.At 5 ft 10 inches, 201 lbs, he wasn't terribly overweight, but all the excess was in his beltline. He had the lipoproteins to match: HDL 38 mg/dl, triglycerides 180 mg/dl, 83% of all LDL particles were small, excess VLDL and IDL. Blood pressure: 140/88. Blood sugar: 112 mg/dl. With a CT heart scan score of 698, Ray had some work to do. Among the strategies we discussed was a need to dramatically reduce, perhaps eliminate, wheat products and other high-glycemic index foods. "You've got to be kidding me!" Besides the inconsistency with his business, he was puzzled on what foods were edible for his pattern. We discussed how he could easily replace his reliance on wheat and breads with more vegetables, more fruits, more lean proteins, and more healthy oils. "But I won't get any fiber!" he declared. That was why he tried to choose whole wheat bread for his sandwiches. This is a common concern when we discuss how grains, particuarly wheat, need to be sharply reduced. In the most recent edition of his Paleo Diet Newsletter, Dr. Loren Cordain has laid out a wonderful graph that beautifully illustrates the issue: (From The Paleo Diet Newsletter at http://www.thepaleodiet.com/newsletter/back_issues.shtml)In other words, reducing or eliminating "fiber-rich" grains and replacing their calories dramatically increases fiber content of your diet.For Ray, whose livelihood depends on promoting and perpetuating the use of wheat breads, it will be tough to keep him on the right track. My prediction: the results he will see will be substantial and it will become difficult to return to eating his own products. There's no doubt that this concept can be economically disruptive for many people, including Ray. It's a tough situation we've created: a huge industrial complex based on growing grains and wheat, processing it into breakfast cereals, bagels, pretzels, crackers, and sandwiches. But it has also contributed to the epidemic of obesity and the patterns that people like Ray have. But the startling fact remains: If replaced with vegetables and fruits, reducing grains increases the fiber content of your diet, and not jsut a little bit, but enormously. If green peppers and spinach had brand names like "Fiber One" and "Smart Start" along with flashy boxes, then maybe it would be an easier concept to grasp. To sign up for Dr. Cordain's wonderfully informative newsletter, go to http://www.thepaleodiet.com/newsletter/back_issues.shtml.
The Detection Gap 5. July 2007 William Davis (3) You've heard of the Generation Gap, the Income Gap, the Technology Gap, the Gender Gap, and the Achievement Gap.How about the Detection Gap? Haven't heard of it? That's the gap between coronary heart disease detected by conventional methods widely practiced in the community and the real prevalence of the disease.The standard approach to coronary heart disease detection is a relatively simple formula. One of three things are sought:1) Symptoms of heart disease like chest pain or breathlessness. 2) An abnormal EKG or abnormal stress test.3) A catastrophe like heart attack or sudden cardiac death. By this equation, the American Heart Association (AHA) estimates that 36% of American men and women have coronary disease. However, we say the number is more like 48%. That's the number we arrive at when we ask: How many men and women have CT heart scan scores above zero?The difference is the Detection Gap. Though only around 12%, it amounts to millions of people. The problem is that, by the conventional approach to detection of heart disease, you often don't know you have it until you're lying on a hospital gurney being wheeled off to a major procedure. Or your friends, family or neighbors find your body.If heart disease is detected by a CT heart scan, it tends to be early, before catastrophe strikes. You can use tools like niacin, vitamin D, flaxseed, etc., all the components of the Track Your Plaque approach. If heart disease is detected by waiting for the appearance of symptoms, then a stress test (usually nuclear) is followed by a heart catheterization, stents, bypass, etc. So there's more than a Detection Gap. There's also a difference in the sorts of therapies chosen. There's certainly a difference in cost. In my view, there is no rational reason not to close the Detection Gap. While CT heart scan scores aren't perfect, they're damn close. The Detection Gap could be closed to around 2%. We'd also save billions of dollars.
Apoprotein B on VAP 3. July 2007 William Davis (3) We've just received an announcement that, if your Vertical Auto Profile lipoprotein test (Atherotech) is provided through the national Quest laboratories (a large national laboratory company), they will include an apoprotein B. This represents an improvement over the previous "direct LDL," a measured LDL cholesterol. Recall that standard lipid panels obtained in hospitals and doctors' offices is a calculated LDL, based on the 40-some year old Friedewald calculation. In my view, the Friedewald calculated LDL is a dinosaur that is virtually useless and needs to be retired. Direct, or measured, LDL is a slight improvement. It removes some of the inaccuracy introduced by the assumptions built into the calculated value. Apoprotein B (also called apoprotein B100) is yet another improvement. Apo B's have been available for years, but was not provided on the VAP. The Atherotech people have done a good job of making VAP more broadly available through "drawing stations" and proponents like Life Extension. Adding an ApoB is a favorable development, since it incorporates the risk of other ApoB-containing particles, like VLDL, IDL, and Lp(a). Several studies like the Quebec Cardiovascular Study have shown that ApoB is a superior predictor of heart disease compared to calculated LDL. I still believe that the gold standard for assessing risk from an LDL standpoint is the LDL particle number along with the other measures provided by the NMR assay (Liposcience). However, the addition of the ApoB to VAP adds greater confidence to the measures provided by this technique. Those of you who rely on the VAP assay provided by Quest for your Track Your Plaque program for control of CT heart scan scores therefore have access to this improved panel.
Estrogens and CT heart scan scores 2. July 2007 William Davis (1) A recent study from the Women's Health Initiative (WHI), the large study that originally showed no reduction in heart attack with use of estrogens in postmenopausal females, has just published a new study.In this new effort, women who took Premarin (horse estogens) had up to 61% lower CT heart scan scores. This new study was confined to the women from the original WHI study who had entered the study between the ages of 50-59 years (average 55 years old), since this was the significant subgroup of women who actually showed a reduction in heart attack risk, whereas other groups showed no benefit or a slightly increased risk. For a full discussion of this fascinating result, see the Track Your Plaque report, Can estrogen reduce CT heart scan scores? at http://cureality.com/library/fl_06-017estrogen.asp. ( Toggle navigation Home Blog Home Archive Join Now Log in You just THINK you're low-carb 27. February 2010 William Davis (72) Systematically checking postprandial (after-eating) blood sugars is providing some great insights into crafting a better diet for many people. I last discussed the concept of postprandial glucose checks in To get low-carb right, you need to check blood sugars.Here are some important lessons that many people--NON-diabetic people, most with normal blood glucoses or just mildly increased--are learning:Oatmeal yields high blood sugars. Even if your fasting blood sugar is 90 mg/dl, a bowl of oatmeal with skim milk, walnuts, and some berries will yield blood sugars of 150-200 mg/dl in many people. Cheerios yields shocking blood sugars. 200+ mg/dl is not uncommon in non-diabetics. (Diabetics have 250-350 mg/dl.) Fruits like apples and bananas increase blood sugar to 130 mg/dl or higher. Odd symptoms, such as mental "fog," fatigue, and a fullness in the head, are often attributable to high blood sugars. A subset of people with lipoprotein(a) can have wildly increased blood sugars despite their slender build and high aerobic exercise habits. Once you identify the high blood sugar problem, you can do something about it. The best place to start is to reduce or eliminate the sugar-provoking food. The LDL-Fructose Disconnect 26. February 2010 William Davis (8) I believe that we can all agree that the commonly obtained Friedewald LDL cholesterol (what I call "fictitious" LDL cholesterol) is wildly inaccurate. 100%--yes, 100% inaccuracy--is not at all uncommon.This flagrant inaccuracy, unacceptable in virtually every other discipline (imagine your airplane flight to New York lands in Pittsburgh--close enough, isn't it?), is highlighted in the University of California study by Stanhope et al I discussed previously.32 participants consumed either a diet enriched with either fructose or glucose. Compared to the effect of glucose, after 10 weeks fructose:Increased LDL cholesterol (calculated) by 7.6%Increased Apoprotein B (a measure of the number of LDL particles) by 24%Increased small dense LDL by 41%Increased oxidized LDL by 12.6% In other words, conventional calculated LDL substantially underestimates the undesirable effects of fructose. The divergence between calculated LDL and small LDL is especially dramatic. (By the way, this same divergence applies to the studies suggesting that calculated LDL cholesterol is reduced by low fat diets--While calculated LDL may indeed be reduced, small LDL goes way up, a striking divergence.) This is yet another reason to not rely on this "fictitious" LDL cholesterol value that, inaccuracies notwithstanding, serves as the foundation for a $27 billion per year industry. I told you bread was bad 26. February 2010 William Davis (10) "I dream about bread" 25. February 2010 William Davis (14) Marion sat in my office, sobbing. It had been 4 weeks since the last piece of bread, bagel, or bun had passed her lips. "I can't do it! I just can't do it! I've tried to eliminate wheat, but it's making me crazy. I'm having dreams about bread!"Yes, Timmy, such dark corners of human behavior are truly unveiled by removing wheat from the diet. (See the previous Heart Scan Blog post, Wheat withdrawal.)This is a real phenomenon: Wheat is the crack cocaine of the masses. Maybe you don't exchange $100 bills in dark corners of an inner city crack house, but I'll bet you paid $3.99 for your latest fix of French bread. Just in the last 2 weeks, people in my office who have eliminated wheat have experienced:14 lbs weight loss in 14 daysIncreased mental clarity, reduced moodiness, deeper sleep70% reductions in small LDL More than 300 mg/dl reductions in triglyceridesRelief from chronic scalp rashI could go on. All the while, the USDA, the American Heart Association, the American Diabetes Association, the American Dietetic Association, the Surgeon General's Office all advise you to eat more "healthy whole grains." 70% of people (NOT 100%, but the majority) will experience unexpected health benefits by eliminating this corrupt, unphysiologic product called wheat from their diet. You won't know until you try. Prototypical Lipoprotein(a) 25. February 2010 William Davis (23) Here's the prototypical male with lipoprotein(a):Several features stand out in the majority of men with lipoprotein(a), Lp(a):Slender--Sometimes absurdly so: BMIs of 21-23 are not uncommon. These are the people who claim they can't gain weight. Intelligent--Above average to way above average intelligence is the rule. Gravitate to technical work--Plenty of engineers, scientists, accountants, and other people who work with numbers and/or technical details are more likely to have Lp(a). Enjoy high levels of aerobic performance--I tell my Lp(a) patients that, if they want to see a bunch of other people with Lp(a), go to a marathon or triathlon. They'll see plenty of people with the pattern among the aerobically-elite. Are rabid fans of Star Trek. Okay, I made the last one up. But the rest are uncannilly true, shared by the majority (though not all) men with Lp(a). Why? I can only speculate that the gene(s) for Lp(a) are closely linked to gene(s) for intelligence of a quantitative kind and some factor that enhances aerobic performance or yields a desirable emotional state with exercise. Oddly, the same patterns tend not to occur in women in Lp(a). I have yet to discern a personality or body configuration phenotype among the ladies. Gastric emptying: When slower is better 20. February 2010 William Davis (18) When it comes to the Internet and Nascar, speed is good: The faster the better. But when it comes to gastric emptying (the rate at which food passes from the stomach and into the duodenum and small intestine), slower can be better. Slower transit time for foods passing through the stomach leads to lower blood sugar, lower blood glucose area under-the-curve (AUC), i.e., reduced blood glucose levels over time. Lower postprandial (after-eating) blood sugars can reduce cardiovascular risk. It can lead to a reduction in net calorie intake and weight loss. Strategies that can slow gastric emptying include:--Minimizing fluids during a meal--Drinking a lot of fluids, e.g., water, accelerates gastric emptying by approximately 20%. --Cinnamon--While the full reason to explain Cassia cinnamon's blood glucose-reducing effect has not been completely worked out, part of the effect is likely to due slowed gastric emptying. Thus, a 1/4-2 teaspoons of cinnamon per day can reduce postprandial blood sugar peaks by 10-25 mg/dl. --Vinegar--Two teaspoons of vinegar in its various forms slows gastric emptying. The effect is likely due to acetic acid, the compound shared by apple cider vinegar, white vinegar, red wine vinegar, Balsamic vinegar, and other varieties. --Increased fat content--Fat is digested more slowly and slows gastric emptying time, compared to the rapid transit of carbohydrates. Not everybody should slow gastric emptying. Diabetics with a condition called diabetic gastroparesis should not use these methods, as they can further slow the abnormal gastric emptying that develops as part of their disease, making a bad situation worse. However, in the rest of us with normal gastric emptying time, a delay in gastric emptying can reduce blood sugar and induce satiety, effects that can work in your favor in reducing cardiovascular risk. Genetic vs. lifestyle small LDL 19. February 2010 William Davis (59) Let me explain what I mean by "genetic small LDL." I think it helps to illustrate with two common examples. Ollie is 50 years old, 5 ft 10 inches tall, and weighs 253 lbs. BMI = 36.4 (obese). Starting lipoproteins (NMR):LDL particle number 2310 nmol/LSmall LDL: 1893 nmol/L (1893/2310 = 81.9% of total, a severe small LDL pattern)Stan is 50 years old, also, 5 ft 10 inches tall, and weighs 148 lbs. BMI = 21.3. Starting lipoproteins:LDL particle number 1424 nmol/LSmall LDL 1288 nmol/L (1288/1424 = 90.4% of total, also severe)Both Ollie and Stan go on the New Track Your Plaque diet and eliminate wheat, cornstarch, and sugars, while increasing oils, meats and fish, unlimited raw nuts, and vegetables. They add fish oil and vitamin D and achieve perfect levels of both. Six months later, Ollie has lost 55 lbs, Stan has lost 4 lbs. A second round of lipoproteins:Ollie:LDL particle number 1810 nmol/LSmall LDL: 193 nmol/L (193/1810 = 10.6% of total)Stan:LDL particle number 1113 nmol/LSmall LDL 729 nmool/L (729/1113 = 65.4% of total)Ollie has reduced, nearly eliminated, small LDL through elimination of wheat, cornstarch, and sugars, along with weight loss, fish oil, and vitamin D. Stan, beginning at a much more favorable weight, reduced both total and small LDL with the same efforts, but retains a substantial proportion (65.4%) of small LDL. Stan's pattern is what I call "genetic small LDL." Of course, this is a presumptive designation, since we've not identified the specific gene(s) that allow this (e.g., gene for variants of cholesteryl ester transfer protein, hepatic lipase, lipoprotein lipase, and others). But it is such a sharp distinction that I am convinced that people like Stan have this persistent pattern as a genetically-determined trait. Carbohydrate sins of the past 17. February 2010 William Davis (15) Fifty years ago, diabetes was a relatively uncommon disease. Today, the latest estimates are that 50% of Americans are now diabetic or pre-diabetic. There are some obvious explanations: excess weight, inactivity, the proliferation of fructose in our diets. It is also my firm belief that the diets advocated by official agencies, like the USDA, the American Heart Association, the American Dietetic Association, and the American Diabetes Association, have also contributed with their advice to eat more “healthy whole grains.” When I was a kid, I ate Lucky Charms® or Cocoa Puffs® for breakfast, carried Hoho’s® and Scooter Pies® in my lunchbox, along with a peanut butter sandwich on white bread. We ate TV dinners, biscuits, instant mashed potatoes for dinner. Back then, it was a matter of novelty, convenience, and, yes, taste. What did we do to our pancreases eating such insulin-stimulating foods through childhood, teenage years, and into early adulthood? Did our eating habits as children and young adults create diabetes many years later? Could sugary breakfast cereals, snacks, and candy in virtually unlimited quantities have impaired our pancreas’ ability to produce insulin, leading to pre-diabetes and diabetes many years later? A phenomenon called glucose toxicity underlies the development of diabetes and pre-diabetes. Glucose toxicity refers to the damaging effect that high blood sugars (glucose) have on the delicate beta cells of the pancreas, the cells that produce insulin. This damage isirreversible: once it occurs, it cannot be undone, and the beta cells stop producing insulin and die. The destructive effect of high glucose levels on pancreatic beta cells likely occurs through oxidative damage, with injury from toxic oxidative compounds like superoxide anion and peroxide. The pancreas is uniquely ill-equipped to resist oxidative injury, lacking little more than rudimentary anti-oxidative protection mechanisms. Glucose toxicity that occurs over many years eventually leaves you with a pancreas that retains only 50% or less of its original insulin producing capacity. That’s when diabetes develops, when impaired pancreatic insulin production can no longer keep up with the demands put on it. (Interesting but unanswered question: If oxidative injury leads to beta cell dysfunction and destruction, can antioxidants prevent such injury? Studies in cell preparations and animals suggest that anti-oxidative agents, such as astaxanthin and acetylcysteine, may block beta cell oxidative injury. However, no human studies have yet been performed. This may prove to be a fascinating area for future.)Now that 50% of American have diabetes or pre-diabetes, how much should we blame on eating habits when we were younger? I would wager that eating habits of youth play a large part in determining potential for diabetes or pre-diabetes as an adult. The lesson: Don’t allow children to repeat our mistakes. Letting them indulge in a lifestyle of soft drinks, candy, pretzels, and other processed junk carbohydrates has the potential to cause diabetes 20 or 30 years later, shortening their life by 10 years. Kids are not impervious to the effects of high sugar, including the cumulative damaging effects of glucose toxicity. Saturated fat and large LDL 16. February 2010 William Davis (44) Here's a half-truth I often encounter in low-carb discussions:Saturated fat increases large LDL particlesFor those of you unfamiliar with the argument, I advocate a low-carbohydrate approach, specifically elimination of all wheat, cornstarch, and sugars, to reduce expression of the small LDL pattern (not to mention reduction of triglycerides, relief from acid reflux and irritable bowel, weight loss, various rashes, diabetes, etc). Small LDL particles have become the most common cause for heart disease in the U.S., exploding on the scene ever since agencies like the USDA and American Heart Association have been advising the public to increase consumption of "healthy whole grains." This has led some to make the pronouncement that saturated fat increases large LDL, thereby representing a benign effect. Is this true? It is true, but only partly. Let me explain. There are two general categories of factors causing small LDL particles: lifestyle (overweight, excess carbohydrates) and genetics (e.g., variants of the gene coding for cholesteryl-ester transfer protein, or CETP). If small LDL is purely driven by excess carbohydrates, then adding saturated fat will reduce small LDL and increase large LDL. If, on the other hand, your small LDL is genetically programmed, then saturated fat will increase small LDL. In other words, saturated fat tends to increase the dominant or genetically-determined form of LDL. If your dominant genetically-determined form is small, then saturated fat increases small LDL particles. So to say that saturated fat increases large LDL is an oversimplification, one that can have dire consequences in the wrong situation. Is glycemic index irrelevant? 14. February 2010 William Davis (20) University of Toronto nutrition scientist, Dr. David Jenkins, was the first to quantify the phenomenon of "glycemic index," describing how much blood sugar increased over 90 minutes compared to glucose. The graph is from their 1981 study, The glycemic index of foods: a physiologic basis for carbohydrate exchange. The research originated with an effort to characterize carbohydrates for diabetics to gain better control over blood sugar.Since Dr. Jenkins’ original work, thousands of clinical studies have been performed by others exploring this concept. The food industry has also devoted plenty of effort exploiting it (e.g., low-glycemic index noodles, low-glycemic index cereals, etc.). Most Americans are now familiar with the concept of glycemic index. You likely know that table sugar has a high glycemic index (60), increasing blood sugar to a similar degree as white bread (glycemic index 71). Oatmeal (slow-cooked) has a lower glycemic index (48), since it increases blood sugar less than white bread. A number of studies have shown that when low glycemic index foods replace high glycemic index foods (e.g., whole wheat bread in place of cupcakes), people are healthier: less diabetes, less heart attack, less high blood pressure. Books have been written about glycemic index, touting its benefits for health and weight control. Health-conscious people will try to substitute low-glycemic index foods for high-glycemic index foods. So what’s not to like here? There are several fundamental flaws with the notion that low-glycemic index foods are good for you:1) Check your blood sugar after a low-glycemic index food like oatmeal. Most non-diabetic adults will show blood sugars in the 140 to 200 mg/dl range. The more central (visceral) fat you have, the higher the value will be. In other words, an apparently “healthy” whole grain food like oatmeal can generate extravagantly high blood sugars. Repeated high blood sugars of 125 mg/dl or greater after eating increase heart disease risk by 50%. 2) Foods like whole wheat pasta have a low glycemic index because the blood sugar effect over the usual 90 minutes is increased to a lesser degree. The problem is that it remains increased for an extended period of up to several hours. In other words, the blood sugar-increasing effect of pasta, even whole grain, is long and sustained. 3) Low-glycemic index foods trigger other abnormalities, such as small LDL particles, triglycerides, and c-reactive protein (a measure of inflammation). While they are not as bad as high-glycemic index foods, they are still quite potent triggers. Low-glycemic index foods trigger the very same responses as high-glycemic index foods—they’re just less bad. But less bad does not equate to good. Low-glycemic index foods cause weight gain, trigger appetite, increase blood pressure, and lead to the patterns that cause heart disease. High-glycemic index foods are bad for you. This includes foods made with white flour (bagels, white bread, pretzels). Low-glycemic foods (whole grain bread, whole wheat crackers, whole wheat pasta) are less bad for you—but they are not necessarily good. Don’t be falsely reassured by foods because they are billed as “low-glycemic index.” View low-glycemic index foods as indulgences, something you might have once in a while, since a slice of whole grain bread is really not that different from a icing-covered cupcake. << Older posts Newer posts >> Newer posts12...282930313233343536...123124Older posts
You just THINK you're low-carb 27. February 2010 William Davis (72) Systematically checking postprandial (after-eating) blood sugars is providing some great insights into crafting a better diet for many people. I last discussed the concept of postprandial glucose checks in To get low-carb right, you need to check blood sugars.Here are some important lessons that many people--NON-diabetic people, most with normal blood glucoses or just mildly increased--are learning:Oatmeal yields high blood sugars. Even if your fasting blood sugar is 90 mg/dl, a bowl of oatmeal with skim milk, walnuts, and some berries will yield blood sugars of 150-200 mg/dl in many people. Cheerios yields shocking blood sugars. 200+ mg/dl is not uncommon in non-diabetics. (Diabetics have 250-350 mg/dl.) Fruits like apples and bananas increase blood sugar to 130 mg/dl or higher. Odd symptoms, such as mental "fog," fatigue, and a fullness in the head, are often attributable to high blood sugars. A subset of people with lipoprotein(a) can have wildly increased blood sugars despite their slender build and high aerobic exercise habits. Once you identify the high blood sugar problem, you can do something about it. The best place to start is to reduce or eliminate the sugar-provoking food.
The LDL-Fructose Disconnect 26. February 2010 William Davis (8) I believe that we can all agree that the commonly obtained Friedewald LDL cholesterol (what I call "fictitious" LDL cholesterol) is wildly inaccurate. 100%--yes, 100% inaccuracy--is not at all uncommon.This flagrant inaccuracy, unacceptable in virtually every other discipline (imagine your airplane flight to New York lands in Pittsburgh--close enough, isn't it?), is highlighted in the University of California study by Stanhope et al I discussed previously.32 participants consumed either a diet enriched with either fructose or glucose. Compared to the effect of glucose, after 10 weeks fructose:Increased LDL cholesterol (calculated) by 7.6%Increased Apoprotein B (a measure of the number of LDL particles) by 24%Increased small dense LDL by 41%Increased oxidized LDL by 12.6% In other words, conventional calculated LDL substantially underestimates the undesirable effects of fructose. The divergence between calculated LDL and small LDL is especially dramatic. (By the way, this same divergence applies to the studies suggesting that calculated LDL cholesterol is reduced by low fat diets--While calculated LDL may indeed be reduced, small LDL goes way up, a striking divergence.) This is yet another reason to not rely on this "fictitious" LDL cholesterol value that, inaccuracies notwithstanding, serves as the foundation for a $27 billion per year industry.
"I dream about bread" 25. February 2010 William Davis (14) Marion sat in my office, sobbing. It had been 4 weeks since the last piece of bread, bagel, or bun had passed her lips. "I can't do it! I just can't do it! I've tried to eliminate wheat, but it's making me crazy. I'm having dreams about bread!"Yes, Timmy, such dark corners of human behavior are truly unveiled by removing wheat from the diet. (See the previous Heart Scan Blog post, Wheat withdrawal.)This is a real phenomenon: Wheat is the crack cocaine of the masses. Maybe you don't exchange $100 bills in dark corners of an inner city crack house, but I'll bet you paid $3.99 for your latest fix of French bread. Just in the last 2 weeks, people in my office who have eliminated wheat have experienced:14 lbs weight loss in 14 daysIncreased mental clarity, reduced moodiness, deeper sleep70% reductions in small LDL More than 300 mg/dl reductions in triglyceridesRelief from chronic scalp rashI could go on. All the while, the USDA, the American Heart Association, the American Diabetes Association, the American Dietetic Association, the Surgeon General's Office all advise you to eat more "healthy whole grains." 70% of people (NOT 100%, but the majority) will experience unexpected health benefits by eliminating this corrupt, unphysiologic product called wheat from their diet. You won't know until you try.
Prototypical Lipoprotein(a) 25. February 2010 William Davis (23) Here's the prototypical male with lipoprotein(a):Several features stand out in the majority of men with lipoprotein(a), Lp(a):Slender--Sometimes absurdly so: BMIs of 21-23 are not uncommon. These are the people who claim they can't gain weight. Intelligent--Above average to way above average intelligence is the rule. Gravitate to technical work--Plenty of engineers, scientists, accountants, and other people who work with numbers and/or technical details are more likely to have Lp(a). Enjoy high levels of aerobic performance--I tell my Lp(a) patients that, if they want to see a bunch of other people with Lp(a), go to a marathon or triathlon. They'll see plenty of people with the pattern among the aerobically-elite. Are rabid fans of Star Trek. Okay, I made the last one up. But the rest are uncannilly true, shared by the majority (though not all) men with Lp(a). Why? I can only speculate that the gene(s) for Lp(a) are closely linked to gene(s) for intelligence of a quantitative kind and some factor that enhances aerobic performance or yields a desirable emotional state with exercise. Oddly, the same patterns tend not to occur in women in Lp(a). I have yet to discern a personality or body configuration phenotype among the ladies.
Gastric emptying: When slower is better 20. February 2010 William Davis (18) When it comes to the Internet and Nascar, speed is good: The faster the better. But when it comes to gastric emptying (the rate at which food passes from the stomach and into the duodenum and small intestine), slower can be better. Slower transit time for foods passing through the stomach leads to lower blood sugar, lower blood glucose area under-the-curve (AUC), i.e., reduced blood glucose levels over time. Lower postprandial (after-eating) blood sugars can reduce cardiovascular risk. It can lead to a reduction in net calorie intake and weight loss. Strategies that can slow gastric emptying include:--Minimizing fluids during a meal--Drinking a lot of fluids, e.g., water, accelerates gastric emptying by approximately 20%. --Cinnamon--While the full reason to explain Cassia cinnamon's blood glucose-reducing effect has not been completely worked out, part of the effect is likely to due slowed gastric emptying. Thus, a 1/4-2 teaspoons of cinnamon per day can reduce postprandial blood sugar peaks by 10-25 mg/dl. --Vinegar--Two teaspoons of vinegar in its various forms slows gastric emptying. The effect is likely due to acetic acid, the compound shared by apple cider vinegar, white vinegar, red wine vinegar, Balsamic vinegar, and other varieties. --Increased fat content--Fat is digested more slowly and slows gastric emptying time, compared to the rapid transit of carbohydrates. Not everybody should slow gastric emptying. Diabetics with a condition called diabetic gastroparesis should not use these methods, as they can further slow the abnormal gastric emptying that develops as part of their disease, making a bad situation worse. However, in the rest of us with normal gastric emptying time, a delay in gastric emptying can reduce blood sugar and induce satiety, effects that can work in your favor in reducing cardiovascular risk.
Genetic vs. lifestyle small LDL 19. February 2010 William Davis (59) Let me explain what I mean by "genetic small LDL." I think it helps to illustrate with two common examples. Ollie is 50 years old, 5 ft 10 inches tall, and weighs 253 lbs. BMI = 36.4 (obese). Starting lipoproteins (NMR):LDL particle number 2310 nmol/LSmall LDL: 1893 nmol/L (1893/2310 = 81.9% of total, a severe small LDL pattern)Stan is 50 years old, also, 5 ft 10 inches tall, and weighs 148 lbs. BMI = 21.3. Starting lipoproteins:LDL particle number 1424 nmol/LSmall LDL 1288 nmol/L (1288/1424 = 90.4% of total, also severe)Both Ollie and Stan go on the New Track Your Plaque diet and eliminate wheat, cornstarch, and sugars, while increasing oils, meats and fish, unlimited raw nuts, and vegetables. They add fish oil and vitamin D and achieve perfect levels of both. Six months later, Ollie has lost 55 lbs, Stan has lost 4 lbs. A second round of lipoproteins:Ollie:LDL particle number 1810 nmol/LSmall LDL: 193 nmol/L (193/1810 = 10.6% of total)Stan:LDL particle number 1113 nmol/LSmall LDL 729 nmool/L (729/1113 = 65.4% of total)Ollie has reduced, nearly eliminated, small LDL through elimination of wheat, cornstarch, and sugars, along with weight loss, fish oil, and vitamin D. Stan, beginning at a much more favorable weight, reduced both total and small LDL with the same efforts, but retains a substantial proportion (65.4%) of small LDL. Stan's pattern is what I call "genetic small LDL." Of course, this is a presumptive designation, since we've not identified the specific gene(s) that allow this (e.g., gene for variants of cholesteryl ester transfer protein, hepatic lipase, lipoprotein lipase, and others). But it is such a sharp distinction that I am convinced that people like Stan have this persistent pattern as a genetically-determined trait.
Carbohydrate sins of the past 17. February 2010 William Davis (15) Fifty years ago, diabetes was a relatively uncommon disease. Today, the latest estimates are that 50% of Americans are now diabetic or pre-diabetic. There are some obvious explanations: excess weight, inactivity, the proliferation of fructose in our diets. It is also my firm belief that the diets advocated by official agencies, like the USDA, the American Heart Association, the American Dietetic Association, and the American Diabetes Association, have also contributed with their advice to eat more “healthy whole grains.” When I was a kid, I ate Lucky Charms® or Cocoa Puffs® for breakfast, carried Hoho’s® and Scooter Pies® in my lunchbox, along with a peanut butter sandwich on white bread. We ate TV dinners, biscuits, instant mashed potatoes for dinner. Back then, it was a matter of novelty, convenience, and, yes, taste. What did we do to our pancreases eating such insulin-stimulating foods through childhood, teenage years, and into early adulthood? Did our eating habits as children and young adults create diabetes many years later? Could sugary breakfast cereals, snacks, and candy in virtually unlimited quantities have impaired our pancreas’ ability to produce insulin, leading to pre-diabetes and diabetes many years later? A phenomenon called glucose toxicity underlies the development of diabetes and pre-diabetes. Glucose toxicity refers to the damaging effect that high blood sugars (glucose) have on the delicate beta cells of the pancreas, the cells that produce insulin. This damage isirreversible: once it occurs, it cannot be undone, and the beta cells stop producing insulin and die. The destructive effect of high glucose levels on pancreatic beta cells likely occurs through oxidative damage, with injury from toxic oxidative compounds like superoxide anion and peroxide. The pancreas is uniquely ill-equipped to resist oxidative injury, lacking little more than rudimentary anti-oxidative protection mechanisms. Glucose toxicity that occurs over many years eventually leaves you with a pancreas that retains only 50% or less of its original insulin producing capacity. That’s when diabetes develops, when impaired pancreatic insulin production can no longer keep up with the demands put on it. (Interesting but unanswered question: If oxidative injury leads to beta cell dysfunction and destruction, can antioxidants prevent such injury? Studies in cell preparations and animals suggest that anti-oxidative agents, such as astaxanthin and acetylcysteine, may block beta cell oxidative injury. However, no human studies have yet been performed. This may prove to be a fascinating area for future.)Now that 50% of American have diabetes or pre-diabetes, how much should we blame on eating habits when we were younger? I would wager that eating habits of youth play a large part in determining potential for diabetes or pre-diabetes as an adult. The lesson: Don’t allow children to repeat our mistakes. Letting them indulge in a lifestyle of soft drinks, candy, pretzels, and other processed junk carbohydrates has the potential to cause diabetes 20 or 30 years later, shortening their life by 10 years. Kids are not impervious to the effects of high sugar, including the cumulative damaging effects of glucose toxicity.
Saturated fat and large LDL 16. February 2010 William Davis (44) Here's a half-truth I often encounter in low-carb discussions:Saturated fat increases large LDL particlesFor those of you unfamiliar with the argument, I advocate a low-carbohydrate approach, specifically elimination of all wheat, cornstarch, and sugars, to reduce expression of the small LDL pattern (not to mention reduction of triglycerides, relief from acid reflux and irritable bowel, weight loss, various rashes, diabetes, etc). Small LDL particles have become the most common cause for heart disease in the U.S., exploding on the scene ever since agencies like the USDA and American Heart Association have been advising the public to increase consumption of "healthy whole grains." This has led some to make the pronouncement that saturated fat increases large LDL, thereby representing a benign effect. Is this true? It is true, but only partly. Let me explain. There are two general categories of factors causing small LDL particles: lifestyle (overweight, excess carbohydrates) and genetics (e.g., variants of the gene coding for cholesteryl-ester transfer protein, or CETP). If small LDL is purely driven by excess carbohydrates, then adding saturated fat will reduce small LDL and increase large LDL. If, on the other hand, your small LDL is genetically programmed, then saturated fat will increase small LDL. In other words, saturated fat tends to increase the dominant or genetically-determined form of LDL. If your dominant genetically-determined form is small, then saturated fat increases small LDL particles. So to say that saturated fat increases large LDL is an oversimplification, one that can have dire consequences in the wrong situation.
Is glycemic index irrelevant? 14. February 2010 William Davis (20) University of Toronto nutrition scientist, Dr. David Jenkins, was the first to quantify the phenomenon of "glycemic index," describing how much blood sugar increased over 90 minutes compared to glucose. The graph is from their 1981 study, The glycemic index of foods: a physiologic basis for carbohydrate exchange. The research originated with an effort to characterize carbohydrates for diabetics to gain better control over blood sugar.Since Dr. Jenkins’ original work, thousands of clinical studies have been performed by others exploring this concept. The food industry has also devoted plenty of effort exploiting it (e.g., low-glycemic index noodles, low-glycemic index cereals, etc.). Most Americans are now familiar with the concept of glycemic index. You likely know that table sugar has a high glycemic index (60), increasing blood sugar to a similar degree as white bread (glycemic index 71). Oatmeal (slow-cooked) has a lower glycemic index (48), since it increases blood sugar less than white bread. A number of studies have shown that when low glycemic index foods replace high glycemic index foods (e.g., whole wheat bread in place of cupcakes), people are healthier: less diabetes, less heart attack, less high blood pressure. Books have been written about glycemic index, touting its benefits for health and weight control. Health-conscious people will try to substitute low-glycemic index foods for high-glycemic index foods. So what’s not to like here? There are several fundamental flaws with the notion that low-glycemic index foods are good for you:1) Check your blood sugar after a low-glycemic index food like oatmeal. Most non-diabetic adults will show blood sugars in the 140 to 200 mg/dl range. The more central (visceral) fat you have, the higher the value will be. In other words, an apparently “healthy” whole grain food like oatmeal can generate extravagantly high blood sugars. Repeated high blood sugars of 125 mg/dl or greater after eating increase heart disease risk by 50%. 2) Foods like whole wheat pasta have a low glycemic index because the blood sugar effect over the usual 90 minutes is increased to a lesser degree. The problem is that it remains increased for an extended period of up to several hours. In other words, the blood sugar-increasing effect of pasta, even whole grain, is long and sustained. 3) Low-glycemic index foods trigger other abnormalities, such as small LDL particles, triglycerides, and c-reactive protein (a measure of inflammation). While they are not as bad as high-glycemic index foods, they are still quite potent triggers. Low-glycemic index foods trigger the very same responses as high-glycemic index foods—they’re just less bad. But less bad does not equate to good. Low-glycemic index foods cause weight gain, trigger appetite, increase blood pressure, and lead to the patterns that cause heart disease. High-glycemic index foods are bad for you. This includes foods made with white flour (bagels, white bread, pretzels). Low-glycemic foods (whole grain bread, whole wheat crackers, whole wheat pasta) are less bad for you—but they are not necessarily good. Don’t be falsely reassured by foods because they are billed as “low-glycemic index.” View low-glycemic index foods as indulgences, something you might have once in a while, since a slice of whole grain bread is really not that different from a icing-covered cupcake.