A tan does not equal vitamin D 14. May 2008 William Davis (8) The sun is getting stronger and the days are getting longer, even here in Wisconsin. Some people are coming to the office with nice tans obtained by sunning themselves for several hours. Others have come back from winter getaways to Florida, Arizona, or the tropics, also sporting nice, dark tans. Several people, in fact, were so confident that sunning themselves provided sufficient vitamin D that they reduced their usual dose. Some even stopped their vitamin D altogether. But, when blood levels of 25(OH) vitamin D were checked, they were virtually all low, sometimes as low as <20 ng/ml. Yet all had nice tans. Why does this happen? Why would people with dark tans remain deficient in vitamin D? One big factor is age: Anyone over 40 years old is fooling themselves if they think that a tan ensures raising vitamin D levels to a desirable range. Also, the more you tan, the more melanin skin pigment accumulates, and the more vitamin D activation in the skin is blocked. Weight is another factor: Heavier people need more vitamin D, sometimes three- or four-fold more than slender people. Why does aging result in inefficient skin activation of vitamin D? It seems that, once we are beyond our reproductively useful years, this ticking clock of aging gets triggered. The older we get, the less activation of vitamin D occurs in our skin, the less of the youth-maintaining, disease-preventing benefits of vitamin D we obtain with sun exposure. The message: Don't rely on a tan to gauge the adequacy of vitamin D. Maybe that works when you're 16 years old, but not at age 50 or 60. There's only one way to know your vitamin D status: a blood level of 25(OH) vitamin D. Copyright 2008 William Davis, MD
Confessions of a former drug company patsy 12. May 2008 William Davis (0) I admit it: In years past, I spoke for the drug industry.In retrospect, I now regret it. In fact, I'm downright embarassed by it.
Planned obsolence 12. May 2008 William Davis (1) In the 1960s, you’d purchase a new car. If you changed the oil, adhered to the maintenance schedule—and were lucky—you might expect to get 100,000 miles out of your automobile. Only an occasional car made it beyond that odometer hurdle. Even if the engine made it past the 100,000 mile milestone, the automobile body would inevitably start to develop rusting decay at the edges of the fenders, signaling body rot that threatened to open gaping holes of metal. Then along came Toyota and Honda, whose cars easily reached 100,000 miles and well beyond, reliably and with bodies intact. As this realization sunk into the American consciousness, many asked, “Why can’t American automakers accomplish the same sort of trouble-free longevity?” “Buy American” emerged as a mantra to preserve American jobs and prop up an economy vulnerable to the superior automotive products from Detroit’s competitors. Of course, American automakers have since responded to the challenge posed by the Japanese auto industry and produced automobiles that essentially matched the reliability and longevity of Japanese cars. But, the great unanswered question remains: For years before the onslaught of Japanese competition, did Detroit quietly plot to maintain a policy of planned obsolescence that ensured Americans would have to scrap the old and buy a new car every few years whenever the odometer tipped over 100,000 miles? We will never know. At worst, it may represent the behind-closed-doors, back-slapping sort of plotting that, for many years, maximized revenues, ensured shareholder returns, and secured executive paychecks. Or, perhaps it wasn’t some evil conspiracy but just complacency, a profitable position of comfort at that. There’s little incentive for industry insiders to reveal such self-incriminating information. But the example set by the American auto industry presents an unusual learning opportunity for us, a chance to make some useful comparisons to the heart healthcare industry.Is the American healthcare industry also guilty of practicing a policy of “planned obsolescence,” just like Detroit? The product that helplessly crumbles is, of course, not your rust-riddled automobile, but you. When someone sees a primary care physician year after year, yet appears one morning in the emergency room, clutching his or her chest in agony from the closed coronary artery responsible for a life-threatening heart attack—prompting the flurry of activity that results in $100,000 in hospital procedures . . . Perhaps “planned obsolescence” is not the perfect phrase to describe the situation, but the principle still applies: A failure to inform the patient that such an outcome was possible—no, probable—makes you wonder whether such an outcome was predictable and thereby preventable in the first place. What should we do when planned obsolescence leads us down a path engineered by someone who has something, often substantial, to gain? Even if it's just complacency, or adhering to a beaten, ineffective status quo (can you say "low-fat diet?), it all points in the same direction. You have a choice: Refuse to buy a 1962 Impala of health care, otherwise known as conventional heart disease management.
Melatonin for high blood pressure? 10. May 2008 William Davis (15) Melatonin is fascinating stuff. In addition to its use as a sleep aid, melatonin exerts possible effects on cardiovascular parameters, including anti-oxidative action on LDL, reduction in sympathetic (adrenaline-driven) tone, and reduction in blood pressure. Several studies document the blood pressure-reducing effect of melatonin:Daily nighttime melatonin reduces blood pressure in male patients with essential hypertension.Melatonin reduces night blood pressure in patients with nocturnal hypertension.Prolonged melatonin administration decreases nocturnal blood pressure in women.Blood pressure-lowering effect of melatonin in type 1 diabetes.But blood pressure may be increased when melatonin is added to nifedipine, a calcium channel blocker:Cardiovascular effects of melatonin in hypertensive patients well controlled by nifedipine: a 24-hour study. Effects on BP tend to be modest, on the order of 5-8 mmHg reduction in systolic, half that in diastolic. But don't pooh-pooh such small reductions, however, as small reductions exert mani-fold larger reductions in cardiovascular events like heart attack and stroke. NIH-sponsored NHANES data (see JNC VII), for example, document a doubling of risk for each increment of BP of 20/10. The Camelot Study demonstrated a reduction in cardiovascular events from 23% in placebo subjects to 16.7% in subjects taking amlodipine (Norvasc) with a 5 mm reduction in systolic pressure, 2 mmHg drop in diastolic pressure. Small changes, big benefits. Many people take melatonin at bedtime and are disappointed with the effects. However, a much better way is to take melatonin several hours before bedtime, e.g., take at 7 pm to fall asleep at 10 pm. Don't think of melatonin as a sleeping pill; think of it as a sleep hormone, something that simply prepares your body for sleep by slowing heart rate, reducing body temperature, and reducing blood pressure. (You may need to modify the interval between taking melatonin and sleep, since individual responsiveness varies quite a bit.)I also favor the sustained-release preparations, e.g., 5 mg sustained-release. Immediate-release, while it exerts a more rapid onset of sleep, allows you to wake up prematurely, The sustained-release preparations last longer and allow longer sleep. The dose varies with age, with 1 mg effective in people younger than 40 years, higher doses of 3, 5, even 10 or 12 mg in older people. Sustained-release preparations also should be taken in slightly higher doses. The only side-effect I've seen with melatonin is vivid, colorful dreams. Perhaps that's a plus!
The forces that shape heatlh care 8. May 2008 William Davis (5) Thinking about the programs for health care reform proposed by the three Presidential candidates highlights a distinct peculiarity of American style health care. American health care is shaped to an unprecedented degree by five forces:1) The drug industry2) The health insurance industry3) Hospitals4) Fear of litigation5) The uniquely American attitude of refusing compromise in access to health care services or products, regardless of the cost (for those who can afford health insurance)All five of these unique forces have created this thing (monster?) we call health care. Remove or modify any one of these forces, and the health care landscape would look dramatically different. The drug industry has recently been on the receiving end of plenty of negative press. This warms my bones. Decades of heavy-handed lobbying, sleazy marketing to physicians (all too willing to be wined and dined), and behind-the-scenes manipulation of clinical data are coming back to bite them. Sadly, the drug industry is so powerful that this bit of fuss is not likely to substantially change their ways. I am thrilled that all three Presidential candidates agree that reimportation of drugs from outside the U.S. is a good idea. While the shrug of the shoulders federal and state attitude towards importation of drugs from Canada has not resulted in cost savings sufficient to impact on overall costs, it surely will lead to savings when practiced on a broad basis by pharmacies, distributors, and other bulk buyers of pharmaceuticals. Senator Obama, in particular, has used strong language in his criticism of the health insurance industry, tough talk that is needed in an age in which insurance executives bring home salaries in the hundreds of millions of dollars and stock prices are climbing due to substantial profit gains within the industry, going against the grain of increasingly costly premiums. However, the Clinton experiment of federalizing health care during Bill Clinton's term that caused all the big boys to band together (most notably health insurance companies and drug industry) has tempered enthusiasm for attacking the insurance industry head-on. In both Democrats' health care reform proposals, the option of private insurance is preserved, as it is in the McCain proposal. How about hospitals? Hospitals, though on a smaller scale than the nationwide reach of the drug and insurance industries, aim to maintain health service delivery in hospitals. For instance, the high-tech bypass service in the hospital gets plenty of local media coverage, as does the newest DaVinci robotic surgery, bariatric surgery, and other revenue-rich services. Many hospitals have forgotten that their mission is delivery of health, of which revenue creation and profiting from disease should only be part. How big is fear of litigation? Estimates vary, but several have quoted numbers in the neighborhood of 20 to 30% of overall health care costs. At the street level from what I see, I'd say at least that much. Fear of litigation is rampant, often unrestrained, and sometimes leads to the craziest, illogical sequence of testing. Chest pain, for instance, no matter how trivial, will typically trigger around $5000 worth of testing (nuclear stress test, echocardiogram, laboratory work, etc.) Emergency room visit for a minor injury? CT scan of head, chest, abdomen. A formula to minimize this aspect of fear in health care delivery would generate enormous savings. The last issue, the uncompromising nature of Americans in health--always wanting the latest new drug, new procedure, "best" surgeon--often simply causes the health care consumer to fall victim to marketing. If a hospital advertises the newest procedure, people want it regardless of whether it represents genuine improvement over the older procedure. The newest sleeping pill, antidepressant, antihypertensive, etc. replaces the old yet equivalent product, but at considerably greater cost. I am optimistic that, regardless of which candidate gains the White House, that some reform is on the way. I do fear, however, that progress will be small and incremental, since major change of the sort that would slash hundreds of billions of dollars in costs would rouse the powers-that-be (drug industry, health insurers, etc.) to once again combine forces and combat the disruption of their franchise.Until you and I see real change and cost savings coming through either legislation or free market advances, we need to continue to make full use of the self-empowering health information that we gain through venues like the web. Copyright 2008 William Davis, MD
Lipoprotein(a): Surprising Poll Results 6. May 2008 William Davis (5) No doubt, our little informal poll asking readers whether they have lipoprotein(a), is skewed towards people inclined to respond because they have this genetic trait. Nonetheless, the response is telling. Of 82 respondents:--40 (48%) said they did have Lp(a)--16 (19%) said that they did not have Lp(a)--26 (31%) said that they did not know whether or not they had Lp(a) Though admittedly an informal analysis, I'd draw several conclusions from this simple "experiment".One, while the proportion of people responding that they have Lp(a) may not be accurate, it is a prevalent genetic risk factor that, according to formal studies, is present in 17% of people with coronary or vascular disease, 11% of the broader population. This number may be even higher if the newer particle number assays (measurements) are used (with results expressed in nmol/L), since an occasional person with a "normal" Lp(a) in mg/dl (weight-based) will prove to have increased Lp(a) by nmol/L (particle number-based). (The reason for this phenomenon is not clear. It may be consequent to variation in apo(a) size, with larger apo(a) varieties of Lp(a) occasionally escaping detection .) As our little poll shows, plenty of people have Lp(a). Two, readers of this blog tend to be highly motivated, sophisticated, and knowledgeable about health and heart disease. Yet a substantial portion--31%--did not know whether they have this crucial risk factor. That shouldn't be. The unnecessary difficulty of getting this simple blood test performed has been driven home to me repeatedly when I identify this factor in someone and then suggest that their grown children and parents, each of whom have a 50% chance of having Lp(a), be tested. It's not uncommon for a 35-year old son, for instance, to say that his doctor refused, claiming it is an unproven risk marker, or to simply say that he/she doesn't know what it is. No doubt, just knowing whether you have Lp(a) or not is not the end of the story. Reducing Lp(a) and its associated co-factors is no easy matter. With several hundred patients in my practice with Lp(a), it occupies much of my time and energy. Sometimes it leads to enormous successes , but it can also pose a real challenge. There should no longer be any doubt that Lp(a) is associated with significantly increased risk of cardiovascular disease. This has been demonstrated conclusively across dozens of studies. Risk from Lp(a) is over and above that posed by other risk factors; it also amplifies the risk posed by other factors, e.g., small LDL, inflammatory phenemena, homocysteine, total LDL, low HDL. In the world of Lp(a), our two most desperate needs for the future are:1) Better education of physicians and the public, and 2) More effective treatment options. Thus, our reasons to form The Lipoprotein(a) Research Foundation. Steps to gain tax-exempt status are being pursued as we speak. I can't help but wonder whether, like vitamin D, a solution is right beneath our noses. An investment in research to fund the trials to better explore both basic science as well as practical treatment options might yield an answer more readily than we think. Wouldn't that be great?
Are endogenous nutritional supplements better? 4. May 2008 William Davis (6) Just a muse. Endogenous substances are those that are already contained within our bodies. They are part of basic human equipment. Exogenous substances are those that come from outside of our bodies. This includes various substances in foods, drugs (most, though not all), and pesticides. I often mull over all of the tools we use in the Track Your Plaque program to achieve control over this thing called coronary plaque. It struck me that just about all the supplements we use that seem to provide outsized benefits are all endogenous substances themselves:--Omega-3 fatty acids from fish oil--Vitamin D--l-arginine--Niacin (vitamin B3)Many of the other substances, though not directly relevant to our plaque-control efforts, but are among the most effective nutritional supplements, also supplement endogenous levels: calcium pyruvate, creatine, acetylcarnitine, DHEA, testosterone, progesterone, growth hormone, pregnenolone, phenylalanine, tyrosine, melatonin, etc. Curiously, most drugs are not meant to directly supplement endogenous levels, but are designed either to enhance or block an enzyme (e.g., acetylcholinesterase inhibitors that block breakdown of acetylcholine; HMG CoA reductase inhibitors to block cholesterol synthesis; angiotensin converting enzyme inhibitors to reduce blood pressure), to exert toxic effects on an organism (antibiotics, antivirals), or to exert an entirely unique effect that does not ordinarily occur in the human body (some anti-cancer drugs, for instance). (This is an admitted, vast over-simplification.)That's not to say that any endogenous substance is desirable or safe when supplemented. Cortisol, thyroid hormone, and estrogens are three examples of endogenous substances that have downsides when administered at slightly more than physiologic concentrations. Nonetheless, it makes me wonder if the world of endogenous substance supplementation has not been fully explored. Are there other endogenous substances that are as potent and wonderful, for instance, as vitamin D but not yet fully appreciated? I'm sure there are.
Vitamin D Newsletter reprinted 1. May 2008 William Davis (2) Reprinted here is the unfailingly informative Vitamin D Newsletter from Dr. John Cannell. Although there's little here specifically about heart disease, there's so much great information about vitamin D that I thought most would still appreciate it. The Vitamin D NewsletterMay, 2008Yesterday's Washington Post article, Too-Good-To-Be-True Nutrient?, sums up the April 9th vitamin D symposium at UCSD in San Diego, which was nothing short of spectacular. Carole Baggerly outdid herself organizing it and explaining how she got involved. Make no mistake; Carole is both serious and energetic. She told about her efforts to introduce resolutions at upcoming meetings of various professional groups. Then she introduced the volunteers from the San Diego Black Nurses Association who made sure the conference went off without a hitch. Then Carole introduced the four speakers. The slides of each speaker are available at Grassroots Health. Before I tell you the highlights of the conference, I'd like to tell you about another conference, this one in Germany, this May 17th and 18th. It is the Third International Symposium on Vitamin D Analogs in Cancer Prevention and Therapy. Readers know how I feel about giving analogs to vitamin D deficient patients instead of vitamin D but speakers include Michael Holick, Reinhold Veith, Bill Grant, Tai Chen, Heidi Cross, David Feldman, and Roger Bouillon, all of whom know the importance of the nutrient. Most of this conference is for scientists, not lay people. However, Michael Holick is the first speaker and if you have not heard his latest talk about vitamin D, it might be worth a trip to Germany.The first San Diego speaker was Dr. William Grant. Since leaving NASA to begin a full-time career as a vitamin D researcher, Bill has published dozens of studies and has another dozen in the works. Using ecological studies (from Greek oikos, house + German -logie, study or studying your own house) of UVB irradiance and cancer, Bill reported that 15 cancers (colon, esophageal, gallbladder, gastric, pancreatic, rectal, small intestinal, bladder, kidney, prostate, breast, endometrial, ovarian, Hodgkin's lymphoma, and non-Hodgkin's lymphoma) are associated with lower UVB light. He concluded that 257,000 cancer deaths in 2007 in the USA were accounted for by inadequate vitamin D levels. Of course the problem with ecological studies is that it easy to be vitamin D deficient in Miami, all you have to do is listen to your doctor's advice and stay out of the sun. Recently, a group from the Arizona Cancer Center found almost 80% of Arizonians had levels below 30 ng/ml. So much for sunny spots.Jacobs ET, et al. Vitamin D insufficiency in southern Arizona. Am J Clin Nutr. 2008 Mar;87(3):608-13.The next speaker was Professor Cedric Garland. I found myself wondering how he did it. I became convinced that vitamin D prevents cancer five years ago. Cedric and his brother Frank and his colleague Ed Gorham knew it 30 years ago! I know what it is like to tell someone that vitamin D prevents cancer and see them think, "Here we go again, another miracle vitamin." I know what it is like to try and explain and watch people die unnecessarily. But I've only had that experience for five years. Cedric has dealt with that frustration for thirty years. Almost thirty years ago, Cedric and Frank Garland published evidence that vitamin D prevents cancer. In fact, it was Cedric's first publication. Thankfully, the paper was recently recognized as being so important that it was republished in 2006 by the International Journal of Epidemiology. You can read the entire paper for free by clicking on the second link below and then clicking on "free final text", courtesy of Oxford Journals.Garland CF, Garland FC. Do sunlight and vitamin D reduce the likelihood of colon cancer? Int J Epidemiol. 1980 Sep;9(3):227-31.Garland CF, Garland FC. Do sunlight and vitamin D reduce the likelihood of colon cancer? Int J Epidemiol. 2006 Apr;35(2):217-20. Cedric began by showing the incidence of type-1 diabetes and multiple sclerosis by latitude. I had no idea that the latitudinal data was so strong for type 1 diabetes in children. This disease is almost nonexistent around the equator. Type-1 diabetes is but one of the three modern childhood epidemics caused by the sunlight-hating dermatologists, the other two, I think, are autism and asthma. Next he showed latitude and 25(OH)D levels, which reminded me to be suspicious of high levels, unless they use accurate methods of detecting 25(OH)D. Some methods used, even in this country, are over detecting vitamin D and telling patients their levels are above 50 ng/ml when they are, in reality, much lower. Cedric's data showed Thailand had mean levels of 70 ng/ml, which I doubt and suspect were due to inaccurate 25(OH)D tests. He then reviewed evidence of the 25(OH)D levels needed to prevent numerous cancers. The safest levels are somewhere above 50 ng/ml. Cedric spent most of his time presenting an entirely new theory of carcinogenesis, one dependent on vitamin D maintaining cellular junctions. I suspect this paper will also be reprinted in 20 years. The only disagreement I have is with his recommendation for cancer patients to start at fairly low doses. For reasons I recently explained, the risk benefit analysis indicates cancer patients should take 5,000 to 10,000 IU per day and they may have no time to lose. Why worry about the phantom of vitamin D toxicity if you may be dying of cancer? Just have your calcium checked along with frequent 25(OH)D levels. Get your levels up to 70-90 ng/ml if you have cancer.Does vitamin D treat cancer?The next speaker was Professor Bruce Hollis. He reviewed basic physiology of vitamin D and emphasized that the entire system is designed to deal with an excess not with an insufficiency of vitamin D. Numerous mechanisms are available in your body to prevent vitamin D toxicity but few are available to deal with insufficiency. Then he briefly mentioned one of the most important discoveries about vitamin D in the last few years, one where Professor Neil Binkley of the University of Wisconsin was senior author. (In the last four years, Professor Binkley has become a prolific vitamin D expert and I hope Carol Baggerly is able to get him to speak at some of the upcoming conferences she hopes to sponsor.) As I have pointed out before, Hollis and Binkley's crucial discovery was that the body doesn't start storing the parent compound, cholecalciferol, until 25(OH)D levels reach about 50 ng/ml. They showed, using basic steroid pharmacology, that 50 ng/ml should be considered the lower limit of adequate 25(OH)D levels.Hollis BW, Wagner CL, Drezner MK, Binkley NC. Circulating vitamin D3 and 25-hydroxyvitamin D in humans: An important tool to define adequate nutritional vitamin D status. J Steroid Biochem Mol Biol. 2007 Mar;103(3-5):631-4. Bruce kept the audience enthralled with a review of all the disease states that indicate 25(OH)D levels need to be much higher than they are now, that is, the multiple biomarkers that suggest the lower limit of 25(OH)D levels should be above 40 ng/ml and closer to 50 ng/ml. Then Professor Hollis spoke of his ongoing study in pregnant women and how he g>
"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.