The myth of small LDL 28. June 2006 William Davis (1) Annie's doctor was puzzled.Despite an HDL cholesterol of 76 mg (spectacular!) and LDL of 82 mg, her CT heart scan showed a score of 135. At age 51, this placed her in the 90th percentile. Not as bad, perhaps, as her Dad might have had, since he died at age 54 of a heart attack. So we submitted blood for lipoprotein testing. Surprise! over 90% of all her LDL particles were small. (By NMR, they're called "small". By gel electropheresis, or the Berkeley Lab test, or VAP (Atherotech) technique, they're called "HDL3".)What gives? Traditional teaching in the lipid world is that if HDL equals or exceeds 40 mg/dl, then small LDL will simply not be present. Well, as you can see from Annie's experience, this is plain wrong. Yes, there is a graded, population-based effect--the lower your HDL, the greater the likelihood of small LDL. But small LDL is remarkably persistent and prevalent--regardless of your HDL.We've seen small LDL even with HDLs in the 90's! I call small LDL the "cockroach" of lipids. If you think you have it, you probably do. Getting rid of small LDL requires a specific bug killer. (Track Your Plaque Members: Read Dr. Tara Dall's interview on small LDL.) Don't let anybody blow off your request for lipoprotein testing just because your HDL is high. That's just not acceptable. Loads can be wrong even with a favorable HDL.
My stress test was normal. I don't need a heart scan! 28. June 2006 William Davis (0) Katy had undergone a stress test while being seen in an emergency room, where she'd gone one weekend because of a dull pain on the right side of her chest. After her stress test proved normal, she was diagnosed (I believe correctly) with esophageal reflux, or regurgitation of stomach acid up the esophagus. She was prescrbed an acid-suppressing medication with complete relief. But Katy also had coronary plaque. Three years ago, her CT heart scan score was 157. She'd made efforts to correct the multiple causes, though she still struggled with keeping weight down to gain full control over her small LDL particle pattern. I felt it was time for a reassessment: another heart scan. After three years, without any preventive efforts, Katy's score would be expected to have reached 345! (That's 30% per year plaque growth.) It's a good idea to get feedback on just how much slowing you've accomplished. But Katy declared, "But I didn't think another heart scan was necessary. My stress test was normal!"What Katy was struggling to understand was that even at the time of her first scan, a stress test would have been normal. Plaque can be present with a normal stress test. Plaque can even show explosive growth all while stress tests remain normal. Just ask former President, Bill Clinton, how much he should have relied on stress tests. (Mr. Clinton underwent annual stress nuclear tests. All were normal and he had no symptoms--all the way up 'til the time he needed urgent bypass surgery!)Of course, at some point even a crude stress test will reveal abnormal results. But that's years into your disease and a lot closer to needing procedures and experiencing heart attack. So, yes, Katy would benefit from another heart scan despite her normal stress test. The message: Don't rely on stress tests to gauge whether or not plaque has grown, stabilized, or reversed. Stress tests can be used to gauge the safety of exercise, blood pressure response, and the potential for abnormal heart rhythms. Stress tests can be used as a method to determine whether blood flow in your coronary arteries is normal through an area with plaque. But a stress test cannot be used to gauge whether plaque has grown. It's as simple as that. Gauging plaque growth requires a heart scan.
Patient-napping: Yet another reason to stay clear of hospitals! 26. June 2006 William Davis (1) When I started practicing medicine around 20 years ago, it was common practice to alert a physician when their patient was seen in an emergency room. If John Smith, for example, went to the emergency room with chest pain, the physician who had an established relationship with the patient--knew their history, had managed their health and illnesses, etc.--was notified, even if the hospital ER had no relationship with the physician. It was not uncommon for the patient to then be transferred to the hospital where their own doctor practiced. Though cumbersome at times, it preserved the relationship of the patient with their doctor. Over the past few years, this practice has crumbled. Nowadays, hospitals and their employed physicians (and other unscrupulous physicians acting in the name of profit) "fail" to notify the physician with an established relationship. Guess what happens? The patient all too often ends up being put through the gamut of testing and procedures. Why? For hospital profit, of course. If failure to notify a doctor who's had a 10-year long relationship with the patient is "overlooked" or, even more commonly, it's "unsafe" to transfer the patient because the patient is too "unstable" to be transferred, then this patient becomes ripe for picking--heart catheterization, stents, bypass surgery, etc. Ten's, if not hundreds, of thousands of dollars can be reaped by this deception. I call it "patient-napping".I see this at least several times every month. As hospitals are becoming increasingly competitive, and as they put pressure on their physicians to churn patients for revenues, you're going to see more and more of this. As always, what is your protection from this expanding influence of hospitals and the doctors too meek to stand up to them? Education and information. Arm yourself with an understanding of what is accomplished in hospitals, when you truly need them, and when you don't. Take it one step further. At least from a heart disease standpoint--the #1 profit-maker for hospitals--aim to 1)identify your coronary plaque, then 2) seize control over your coronary plaque and reduce your risk for heart attack and heart procedures as much as humanly possible. That's the goal of the Track Your Plaque program.
Don't believe the negative press on fish oil 25. June 2006 William Davis (0) A British Medical Journal study released in March, 2006 has prompted a media flurry of reports on the worthlessness of fish oil. (Hooper L, Thompson RL, Harrison RA et al. Risks and benefits of omega 3 fats for mortality, cardiovascular disease, and cancer: a systematic review. BMJ March,2006) Don't believe it for a second. First of all, the study was a re-analysis of the existing published scientific literature. It was not a new study. It included a wild conglomeration of different clinical observations, as the studies examining fish oil over the years have been extraordinarily heterogeneous--in populations examined, omega-3 supplement (e.g., fish vs. capsule), period of observation, endpoints measured. The results were skewed by inclusion of a moderate-sized British study by Burr et al in men with angina. In this study, no benefit was demonstrated and, in fact, a negative effect--more heart attack and death--was observed with fish oil. This was not news, since the study was published in 2003. It's results have been a mystery to everyone, since its unexpected negative result for fish oil was so starkly different from virtually every other study that preceded it (suggesting a study flaw or statistical fluke). Nonetheless, the Burr study served to throw off the overall analysis. It diluted the dramatic and persuasive outcome of the GISSI-Prevenzione Study of 11,000 people in which a 28% reduction in heart attack and 45% reduction in cardiovascular death was observed. Note that the substantial numbers of the GISSI make the study's outcome nearly unassailable.Another important fact: fish oil is among the most powerful tools available to correct elevated triglycerides. Drops of 50% are common. Recall that triglycerides are a necessary ingredient to create the nasty LDL, as well as VLDL, Intermediate-density lipoprotein, and an undesirable shift from large to ineffective small HDL. Reducing triglycerides is therefore crucial for your plaque control program. This re-analysis serves to prove nothing. Such analyses can only pose questions for further study in a real study like GISSI: a randomized (random participant assignment), controlled (treatment vs. placebo or other treatment) study. The weight of evidence remains heavily in favor of fish oil, not only as helpful, but fabulously beneficial, particularly for anyone aiming to reduce coronary plaque.
How important is high blood pressure? 24. June 2006 William Davis (0) Control of blood pressure is crucial for coronary plaque control and stopping your heart scan score from increasing. Dr. Mehmet Oz (of Oprah fame and a cardiac transplant surgeon at Columbia University) made graphic point of this on the ABC TV news show, 20/20, last evening on an episode called "Our Bodies: Myths, Lies, and Straight Talk". (See a summary on the ABC News 20/20 website at http://abcnews.go.com/2020/story?id=2109291&page=1) Although I believe he somewhat overstated the case for hypertension (proclaiming "If you're going to remember one number, if you're going to focus and fixate on one number in your entire health profile, it better be your blood pressure"), he made the point that a blood pressure of 115/75 is what you should have for optimal health. I couldn't agree more. Unfortunately, the old advice that desirable blood is 140/90 or less is absolutely wrong. At this level, we see flagrant increases in heart scan scores. We also progressive enlargement of the thoracic aorta, the large vessel that leaves the heart and branches to provide the major arteries of the body. Growth of the aorta to an aneurysm is also common at these formerly acceptable blood pressure. (The diameter of your aorta in the chest is an easily obtainable measure on your CT heart scan.) The blood pressure you need for halting and reversing plaque growth on your heart scan is indeed 115/75 or less. (Not so low, however, that you're lightheaded.) This is the blood pressure that you were meant to have evolutionarily. It's also the blood pressure that helps tremendously in keeping your aorta from enlarging. Watch for an upcoming exhaustive report on blood pressure and its plaque-raising effects and how to reduce it using nutritional strategies on the www.cureality.com membership website.
Is your doctor in cahoots with the hospital? 21. June 2006 William Davis (0) I got a call from a doctor about a patient we've seen in past."I've got Tricia in the office. She's been having some kind of chest and abdominal pain. I think it's esophageal reflux, but just to be safe I'm sending her to the hospital."I advised this physician that, given Tricia's low heart scan score, she was unlikely to be having a coronary "event" like heart attack or unstable symptoms. It wasn't impossible, but just highly unlikely. As the patient was without symptoms at the moment and had driven herself to his office, I offered to perform a stress test immediately. (Though stress tests are of limited usefulness in people without symptoms, they can be useful provocative maneuvers in people with symptoms of uncertain significance.) The doctor declined. Tricia was, after all, in his office and he was responsible for any decisions despite any objections I voiced. Well, Tricia was directed by her doctor to go to a local hospital, though one with an especially notorious reputation for putting virtually anyone they can get their hands on through as many procedures as possible. As you might guess, this doctor was closely associated with this hospital. He and his colleagues obtain incentives (or are penalized) if they do not generate revenue-producing procedures for the hospital. So, guess what? Tricia ended up with several procedures, all of which yielded nothing--except $30,000 in revenues from Tricia's insurance company. I harp on this deplorable state of affairs because it is utterly, painfully, and shamefully TRUE. Just look at the hospital and you'd better brace yourself for a series of tests that could cost you the equivalent of a nice 3 bedroom home. If they were truly necessary after the failure of preventive and other simple efforts, fine. But, all too often, they are driven by profit motives. Could I have stopped this somehow from occurring? After all, Tricia was reasonably aware of the way we do things around here. I fear that even this failed to serve Tricia well. But I remain hopeful that, as we build broader awareness of these issues, that more and more people and physicians will stand up and refuse to tolerate the status quo.
Where is the Track Your Plaque program going? 21. June 2006 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...
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.