Vitamin D increased my cholesterol 2. October 2009 William Davis (38) A friend told me this story. Her friend, Linda, had added vitamin D to her daily supplements. Because she'd had a vitamin D blood level of 22 ng/ml, she was taking 6000 units per day. However, Linda also had a high cholesterol value with a total cholesterol of 231 mg/dl. After several months on the vitamin D, she had another cholesterol panel. Total cholesterol: 256 mg/dl. "It must have been the vitamin D! So I stopped it right away." Is this true? Does vitamin D raise the level of blood cholesterol? Yes, it does. But it's a good thing. Let me explain. Followers of The Heart Scan Blog know that total cholesterol is really a mix of 3 other factors:Total cholesterol = LDL cholesterol + HDL cholesterol + triglycerides/5This is the Friedewald equation, still used today in over 95% of cholesterol panels. So, by the Friedewald equation, anything that increases LDL, HDL, or triglycerides will increase total cholesterol. One of the spectacular changes that develops over a year of taking vitamin D is that HDL cholesterol skyrockets. While sensitivity to this effect varies (probably on a genetic basis), HDL increases of 10, 20, even 30 mg/dl are common. A starting HDL, for instance, of 45 mg/dl can jump up to 65 or 70 mg/dl, though the effect requires up to a year, sometimes longer. Vitamin D can also reduce triglycerides, though the effect is relatively small, usually no more than 20 mg/dl or so. Likewise, the effect on LDL is minor, with a modest reduction in the small type of LDL. So the dominant effect of vitamin D from a cholesterol standpoint is a substantial increase in HDL. Looking at the equation, you can see that an increase in HDL is accompanied by a commensurate increase in total cholesterol. If HDL goes up 25 mg/dl, total cholesterol goes up 25 mg/dl. So Linda is absolutely correct: Vitamin D increases cholesterol--but it's a good thing that reduces risk for heart disease and is an important part of a coronary plaque-reversal program. This is yet another reason why I advocate elimination of total cholesterol on lipid panels. There is no useful information in the total cholersterol value, only the potential for misi Toggle navigation Home Blog Home Archive Join Now Log in The Paleo approach to meal frequency 24. November 2009 William Davis (12) Furthering our discussion of postprandial (after-eating) phenomenona, including chylomicron and triglyceride "stacking" (Grazing is for cattle and Triglyceride and chylomicron stacking), here's a comment from the recent Palet Diet Newsletter on the closely related issue, meal timing and frequency:We are currently in the process of compiling meal times and patterns in the worlds historically studied hunter-gatherers. If any single picture is beginning to emerge, it clearly is not three meals per day plus snacking ala the typical U.S. grazing pattern. Here are a few examples:--The Ingalik Hunter Gatherers of Interior Alaska: 'As has been made clear, the principal meal and sometimes the only one of the day is eaten in the evening.' --The Guayaki (Ache) Hunter Gatherers of Paraguay: 'It seems, however, that the evening meal is the most consistent of the day. This is understandable, since the day is generally spent hunting for food that will be eaten in the evening." --The Kung Hunter Gatherers of Botswana. "Members move out of camp each day individually or in small groups to work through the surrounding range and return in the evening to pool the collected resources for the evening meal." --Hawaiians, Tahitians, Fijians and other Oceanic peoples (pre-westernization). 'Typically, meals, as defined by Westerners, were consumed once or twice a day. . . Oliver (1989) described the main meal, usually freshly cooked, as generally eaten in the late afternoon after the day’s work was over." The most consistent daily eating pattern that is beginning to emerge from the ethnographic literature in hunter-gatherers is that of a large single meal which was consumed in the late afternoon or evening. A midday meal or lunch was rarely or never consumed and a small breakfast (consisting of the remainders of the previous evening meal) was sometimes eaten. Some snacking may have occurred during daily gathering, however the bulk of the daily calories were taken in the late afternoon or evening. This pattern of eating could be described as intermittent fasting relative to the typical Western pattern, particularly when daily gathering or hunting were unsuccessful or marginal. There is wisdom in the ways of our hunter gatherer ancestors, and perhaps it is time to re-think three squares a day.In other words, the notion of "grazing," or eating small meals or snacks throughout the day, is an unnatural situation. It is directly contrary to the evolutionarily more appropriate large meal followed by periods of no eating or small occasional meals. I stress this point because I see that the notion of grazing has seized hold of many people's thinking. In my view, grazing is a destructive practice that is self-indulgent, unnecessary, and simply fulfills the perverse non-stop hunger impulse fueled by modern carbohydrate foods. Eliminate wheat, cornstarch, and sugars and you will find that grazing is a repulsive impulse that equates with gorging. The full-text of the Paleo Diet Newsletter can be obtained through www.ThePaleoDiet.com. You can also read and/or subscribe to the new Paleo Diet Blog, just launched in November, 2009. Angioplasty Special: Get it while it's hot! 21. November 2009 William Davis (6) Graphic courtesy Parsemus Foundation Even mummies do it 20. November 2009 William Davis (16) Lady Rai, nursemaid to Queen Nefertari of Egypt, died in 1530 BC, somewhere between the age of 30 and 40 years. Her mummy is preserved in the Egyptian National museum of Antiquities in Cairo. A CT scan of her thoracic aorta revealed calcium, representing aortic atherosclerosis, reported by Allam et al (including my friend from The Wisconsin Heart Hospital, Dr. Sam Wann, who provided me a blow-by-blow tale of this really fascinating project). Ladi Rai and 14 other Egyptian mummies were found to have vascular calcification of a total of 22 mummies scanned. (The hearts of the mummies were too degenerated to make out any coronary calcium.)But why would people of that age have developed atherosclerosis? The authors of the study comment that "Our findings that atherosclerosis was not infrequent among middle-aged and older ancient Egyptians of high social status challenges the view that it is a disease of modern humans. . . Although ancient Egyptians did not smoke tobacco or eat processed food or presumably lead sedentary lives, they were not hunter-gatherers. [Emphasis mine.] Agriculture was well established in ancient Egypt and meat consumption appers to have been common among those of high social status."Fascinating. But I don't think that I'd blame meat consumption. Egyptians were also known to have cultivated grains, including wheat, and frequently consumed such sweet delicacies as dates and figs. Egyptians were also apparently beer drinkers. Unfortunately, no beer steins were seen in any of the scans. Life Extension article on iodine 17. November 2009 William Davis (25) Here's a link to my recent article in Life Extension Magazine on iodine: Halt on Salt Sparks Iodine Deficiency Iodized salt, a concept introduced into the U.S. by the FDA in 1924, slowly eliminated goiter (enlarged thyroid glands), along with an enormous amount of thyroid disease, heart attack, mental impairment, and death. The simple addition of iodine to salt ensured that salt-using Americans obtained enough iodine sufficient to not have a goiter. Now that the FDA, goiters long forgotten from their memories, urges Americans to reduce salt, what has happened to our iodine? I talk at length about this issue in the Life Extension article. The healthiest people are the most iodine deficient 16. November 2009 William Davis (19) Here's an informal observation. The healthiest people are the most iodine deficient. The healthier you are, the more likely you are to:--Avoid junk foods--30% of which have some iodine from salt--Avoid overuse of iodized salt--Exercise--Sweating causes large losses of iodine.So the healthy-eating, exercising person is the one most likely to show iodine deficiency: gradually enlarged thyroid gland (in the neck), declining thyroid function. Over time, if iodine deficiency persists, excessive sensitivity to iodine develops, as well as abnormal thyroid conditions like overactive nodules. Even subtle levels of thyroid dysfunction act as a potent coronary risk factor. It's the score, stupid 14. November 2009 William Davis (4) Sal has had 3 heart scans. (He was not on the Track Your Plaque program.) His scores:March, 2006: 439April, 2007: 573October, 2009: 799Presented with the 39% increase from April, 2007 to October, 2009, Sal's doctor responded, "I don't understand. Your LDL cholesterol is fine." This is the sort of drug-driven, cholesterol-minded thinking that characterizes 90% of primary care and cardiologists' practices: "Cholesterol is fine; therefore, you must be fine, too." No. Absolutely not. The data are clear: Heart scan scores that continue to increase at this rate predict high risk for cardiovascular events. Unfortunately, when my colleagues hear this, they respond by scheduling a heart catheterization to prevent heart attack--a practice that has never been shown to be effective and, in my view, constitutes malpractice (i.e., performing heart procedures in people with no symptoms and with either no stress test or a normal stress test). It's the score, stupid! It's not the LDL cholesterol. Pay attention to the increasing heart scan score and you will know that the disease is progressing at an alarming rate. Accepting this fact will set you and your doctor on the track to ask "Why?"That's when you start to uncover all the dozens of other reasons that plaque can grow that have nothing to do with LDL cholesterol or statin drugs. Heart Scan Blog Redux: Cheers to flavonoids 13. November 2009 William Davis (32) Because in Track Your Plaque we've been thinking a lot about anthocyanins, here's a rerun of a previous Heart Scan Blog post about red wine. (Anthocyanins are among the interesting flavonoids in red wine, along with resveratrol and quercetin.) The case in favor of healthful flavonoids seems to grow bit by bit. Flavonoids such as procyanadins in wine and chocolate, catechins in tea, and those in walnuts, pomegranates, and pycnogenol (pine bark extract) are suspected to block oxidation of LDL (preventing its entry into plaque), normalize abnormal endothelial constriction, and yield platelet-blocking effects (preventing blood clots). Dr. Roger Corder is a prolific author of many scientific papers detailing his research into the flavonoids of foods, but wine in particular. He summarizes his findings in a recent book, The Red Wine Diet. Contrary to the obvious vying-for-prime-time title, Dr. Corder's compilation is probably the best mainstream discussion of flavonoids in foods and wines that I've come across. Although it would have been more entertaining if peppered with more wit and humans interest, given the topic, its straightfoward, semi-academic telling of the story makes his points effectively. Among the important observations Corder makes is that regions of the world with the greatest longevity also correspond to regions with the highest procyanidin flavonoids in their wines. Regarding the variable flavonoid content of wines, he states:Although differences in the amount of procyanidins in red wine clearly occur because of the grape variety and the vineyard environment, the winemaker holds the key to what ends up in the bottle. The most important aspect of the winemaking process for ensuring high procyanidins in red wines is the contact time between the liquid and the grape seeds during fermentation when the alcohol concentration reaches about 6 percent. Depending on the fermentation temperature, it may be two to three days or more before this extraction process starts. Grape skins float and seeds sink, so the number of times they are pushed down and stirred into the fermenting wine also increases extraction of procyanidins. Even so, extraction is a slow process and, after fermentation is complete, many red wines are left to macerate with their seeds and skins for days or even weeks in order to extract all the color, flavor, and tannins. Wines that have a contact time of less than seven days will have a relatively low level of procyanidins. Wines with a contact time of ten to fourteen days have decent levels, and those with contact times of three weeks or more have the highest. He points out that deeply-colored reds are more likely to be richer in procyanidins; mass-produced wines that are usually "house-grade" served at bars and restaurants tend to be low. Some are close to zero. Wines rich in procyanidins provide several-fold more, such that a single glass can provide the same purported health benefit as several glasses of a procyanidin-poor wine. So how do various wines stack up in procyanidin content? Here's an abbreviated list from his book:Australianyphicon-folder-close"> (59) Wheat elimination continues to yield explosive and unexpected health benefits. I initially asked patients in the office to eliminate wheat because I wanted to help them reduce blood sugar and pre-diabetic tendencies. A patient would come to the office, for example, with a blood sugar of 118 mg/dl (in the pre-diabetic range) and the other phenomena of pre-diabetes or metabolic syndrome (high blood pressure, high inflammation/c-reactive protein, low HDL, high triglycerides, small LDL), and the characteristic wheat belly. Eliminate wheat and, within three months, they lose 30 lbs, blood sugar drops to normal, blood pressure drops, triglycerides drop by several hundred milligrams, HDL goes up, small LDL plummets, c-reactive protein drops. People also felt better, with flat tummies and more energy. But they also developed benefits I did not anticipate:--Improved rheumatoid arthritis--I have seen this time and time again. Eliminate wheat and the painful thumbs, fingers, and other joints clear up dramatically. Many former rheumatoid sufferers people tell me that one cracker or pretzel will trigger a painful throbbing reminder that lasts a couple of hours. --Improved ulcerative colitis--People incapacitated with pain, cramping, and diarrhea of ulcerative colitis (who are negative for the antibodies for celiac disease) can experience marked improvement. I've seen people be able to stop all their nasty colitis medications just by eliminating wheat. --Reduction or elimination of irritable bowel syndrome--Reduction or elimination of gastroesophageal reflux--Better mood--Eliminating wheat makes you happier and experience more stable moods. Just as wheat is responsible for a subset of schizophrenia and bipolar illness (this is fact), and wheat elimination generates dramatic improvement, when you or I eliminate wheat, we also experience a "smoothing" of mood swings. --Better libido--I'm not sure whether this is a consequence of losing a belly the size of a watermelon or improvement in sex hormones (esp. testosterone) or endothelial responses, but more interest in sex typically develops. --Better complexion--I'm not entirely sure why, but various rashes will often dissipate, bags under the eyes are reduced, itching in funny places stops.It's also peculiar how, after someone eliminates wheat for several months, re-exposure of an errant cracker or sandwich results in cramping and diarrhea in about 30% of people. Obviously, people with celiac disease, who can even die of exposure to wheat, are even worse. What other common food do you know of that makes us sick so often, even occasionally with fatal outcome? Is Lp(a) part of your legacy to your children? 15. September 2009 William Davis (21) If you have lipoprotein(a), Lp(a)--the most aggressive known cause of heart disease that no one has heard of--then you need to tell your children. Lp(a) is a "cleanly" inherited genetic pattern: If either parent has it, there's a 50% chance that you have it. If you have it, then there's a 50% likelihood that each of your children has it. (Note that each child experiences a likelihood of 50%, not 50% of your children. This is because each child is conceived as an independent statistical event. So much for romance!)The atherogenicity (plaque-causing potential) of Lp(a) also tends to get transmitted. In other words, if your Dad had a heart attack at age 50 due to Lp(a) and you share Lp(a), then you likely share a similar magnitude of risk as your Dad. If your Mom had Lp(a), though passed quietly at age 89 without any overt evidence of heart disease, then you are likely to share the relatively benign form of Lp(a). For most of us with Lp(a), however, it is best to assume that it has at least some potential for causing heart disease, being the most aggressive cause known. (That is, until we have the ability in everyday clinical practice to characterize Lp(a) by assessing such factors as the size of the apoprotein(a) molecule, the number of kringle "repeats" on the tail, etc. Until then, we need to rely on the crude, though helpful, observation of family history.) At what age should you inform your children? There's no hard-and-fast rule. However, I generally suggest to patients that they talk about Lp(a) with their children when they reach their 20s or 30s, old enough to begin to understand the implications and begin to think about adopting healthier lifestyles. Is treatment required at, say, age 35? That depends on the pattern of Lp(a)-related heart disease in the family: With exceptionally aggressive forms, it might be reasonable to begin treatment at this relatively early age. Do "Heart Healthy" sterols cause heart disease? 9. September 2009 William Davis (19) The sterol question continues to pop up.Sterols are an ingredient widely added by food manufacturers that allows a "heart healthy" claim, since sterols have been shown to reduce LDL cholesterol (at least transiently). HOWEVER, sterols have also been implicated in possibly increasing risk for heart disease. After all, people with the genetic condition called sitosterolemia absorb sterols into the blood and develop coronary heart disease in their teens and twenties. Those of us without sitosterolemia who increase sterol intake with sterol-enriched foods increase blood levels of sterols several-fold. Is this healthy, or does it contribute to coronary plaque as it does in people with sitosterolemia? Below, I've reprinted a previous Heart Scan Blog post on sterols. Sterols should be outlawedWhile sterols occur naturally in small quantities in food (nuts, vegetables, oils), food manufacturers are adding them to processed foods in order to earn a "heart healthy" claim.The FDA approved a cholesterol-reducing indication for sterols , the American Heart Association recommends 200 mg per day as part of its Therapeutic Lifestyle Change diet, and WebMD gushes about the LDL-reducing benefits of sterols added to foods.Sterols--the same substance that, when absorbed to high levels into the blood in a genetic disorder called "sitosterolemia"--causes extravagant atherosclerosis in young people.The case against sterols, studies documenting its coronary disease- and valve disease-promoting effects, is building:Higher blood levels of sterols increase cardiovascular events:Plasma sitosterol elevations are associated with an increased incidence of coronary events in men: results of a nested case-control analysis of the Prospective Cardiovascular Münster (PROCAM) study.Sterols can be recovered from diseased aortic valves:Accumulation of cholesterol precursors and plant sterols in human stenotic aortic valves.Sterols are incorporated into carotid atherosclerotic plaque:Plant sterols in serum and in atherosclerotic plaques of patients undergoing carotid endarterectomy.Though the data are mixed:Moderately elevated plant sterol levels are associated with reduced cardiovascular risk--the LASA study.No association between plasma levels of plant sterols and atherosclerosis in mice and men.The food industry has vigorously pursued the sterol-as-heart-healthy strategy, based on studies conclusively demonstrating LDL-reducing effects. But do sterols that gain entry into the blood increase atherosclerosis regardless of LDL reduction? That's the huge unanswered question.Despite the uncertainties, the list of sterol-supplemented foods is expanding rapidly:Each Nature Valley Healthy Heart Bar contains 400 mg sterols.HeartWise orange juice contains 1000 mg sterols per 8 oz serving.Promise SuperShots contains 400 mg sterols per container.Corozonas has an entire line of chips that contain added sterols, 400 mg per 1 oz serving.MonaVie Acai juice, "Pulse," contains 400 mg sterols per 2 oz serving.Kardea olive oil has 500 mg sterols per 14 gram serving.WebMD has a table that they say can help you choose "foods" that are sterol-rich.In my view, sterols should not have been approved without more extensive safety data. Just as Vioxx's potential for increasing heart attack did not become apparent until after FDA approval and widespread use, I fear the same may be ahead for sterols: dissemination throughout the processed food supply, people using large, unnatural quantities from multiple products, eventually . . . increased heart attacks, strokes, aortic valve disease.Until there is clarification on this issue, I would urge everyone to avoid sterol-added "heart healthy" products. Some more info on sterols in a previous Heart Scan Blog post: Are sterols the new trans fat? . Why obese people can't fast 9. September 2009 William Davis (21) Why do obese people claim it is impossible to fast?Most overweight people are terrified at the prospect of facing any period of time without ready access to food. Persuading them to begin a program of intermittent fasting is a hopeless cause. They just refuse. Contrary to popular opinion, this is not just glutonny at work. It is the effect of what I call "the cycle of hunger," the 2-hour up and down cycle of rising sugar and insulin, followed by their inevitable fall. The precipitous fall of sugar and insulin triggers mental fogginess, fatigue, and insatiable hunger. (By the way, this is the same phenomenon underlying the silly notion of "grazing.") According to an LA Times article, fasting may be difficult to impossible for some people: "Ruth Frechman, a registered dietitian in Burbank and spokeswoman for the American Dietetic Assn., says she frequently sees such extreme strategies backfire. 'You're hungry, fatigued, irritable. Fasting is not very comfortable. People try to cut back one day and the next day they're starving and they overeat.'" (Not surprising, coming from the American Diatetic Assn. They, along with such agencies as the American Diabetes Association, are vocal proponents of low-fat, high-carbohydrate, "healthy whole grain" diets--you know, the diets that make us fat and diabetic.)Ms. Frechman is correct: Having someone engage in a period of fasting, no matter how brief, when the diet leading up to the fast is filled with "healthy whole grains" and other carbohydrates will result in painful hunger that eventually overcomes any effort. A period of overeating typically follows the aborted attempt. Fasting cannot work as long as the 2-hour cycle of hunger continues. The first step: Eliminate the 2-hour cycle of hunger by dramatically reducing or eliminating carbohydrates. Our preferred method is to eliminate wheat, cornstarch, and sugars. (Just be aware of wheat withdrawal, the fatigue that develops in the first 5 days after wheat elimination that affects up to 30% of people.)Once wheat, cornstarch, and sugars are eliminated, hunger reverts to that of physiologic need--appetite will be smaller and less intense, since it is driven by your body's needs, not by abnormal stimulation from wheat, cornstarch, and sugar. The fear of not having food dissolves, the 2-hour cycle of mental fogginess, fatigue, and hunger will be gone. Intermittent fasting is a wonderful strategy for reducing weight; gaining control over lipids, lipoproteins, and coronary plaque; regaining appreciation for food; reducing appetite. But it's not even worth trying unless you've already eliminated the unnatural appetite triggers that will booby-trap any fasting effort. Test your own thyroid 7. September 2009 William Davis (15) 134 people responded to the latest Heart Scan Blog poll:When I ask my doctor to test my thyroid, he/she: Accommodates me without question 45 (33%)Questions why, but orders the tests 49 (36%)Refuses because you seem "healthy" 20 (14%)Refuses without explanation 4 (2%)Ridicules your request 16 (11%)That's better than I anticipated: 69% of physicians complied with this small request. After all, you're not asking for major surgery. You're just asking for a very basic test, as basic as a blood count or electrolytes. 36% of respondents said that their doctor asked why, but still complied; this is simply practicing good medicine--If there is a problem, your doctor would like to know about it.However, the remainder--31%--were refused in one way or another. Incredibly, 11% were ridiculed.Although this was not asked in the poll, I believe that it is a safe assumption that you asked with good reason: you're abnormally fatigued, you have been gaining weight for no apparent reason or can't lose weight despite substantial effort, or you feel cold at inappropriate times.Let's say you're tired. Ever since last summer, you've suffered a gradual decline in energy.So you ask your doctor to assess your thyroid. He refuses. "You're just fine! There's nothing wrong with you."You disagree. In fact, you are quite convinced that there is something physically wrong. What do you do?You could:--Drink more coffee--Exercise more in the hopes that it will snap you out of your lethargy--Sleep more--Take stimulants of various sortsOr, you could get your thyroid assessed and settle the issue. But how can you get this done when your doctor won't accommodate you, even though you have perfectly fine health insurance and are simply interested in feeling better and preserving your health?You could test your thyroid yourself. This is why we're making self-testing kits available. Test kits are available here. This is yet another facet of the powerful revolution that is emerging: Self-directed health. Trains, planes, and heart scans 4. September 2009 William Davis (10) A Heart Scan Blog reader posted the following question:It is not clear to me why getting a cardiac scan is the necessary first step, if in fact the next step would be to bring down small LDL particles which is revealed on a NMR lipoprofile or VAP test. Why isn't the NMR or VAP test the first thing?Good question. Think of it this way:Lipoproteins, as measured via VAP (Vertical Auto Profile) or NMR (Nuclear Magnetic Resonance), provide a snapshot of risk from a metabolic viewpoint at that moment. Lipoproteins shift with the tides of age, menopause, weight changes, even what you ate last evening for dinner (especially small LDL). There are also other factors that cause coronary plaque, as well, not revealed through lipoprotein testing, such as vitamin D deficiency, smoking, high blood pressure, phosopholipase A2, lipoprotein(a), inflammatory factors, thyroid dysfunction, omega-3 fatty acid deficiency, etc. A heart scan, providing a coronary calcium score, provides an indirect measure of coronary plaque that is the sum total of lipoprotein and other plaque-causing factors that have accumulated up to the time of your scan--regardless of the cause.It means that two females, each 60 years old, with 70% small LDL, HDL 42 mg/dl, triglycerides 150 mg/dl, and mild hypertension, have identical markers for potential coronary risk, but can have widely different heart scan scores. One might have a score of zero, while the other might have a score of 300. Why would the same panel of causes measured at one moment yield wildly different quantities of plaque? Several reasons:1) The lifestyles, eating habits, and weight of each woman differed during their earlier years, not currently reflected in this moment's lipid or lipoprotein patterns. Perhpaps one experienced several years of extraordinary stress from a failed marriage, or suffered through two years of depression that caused her to smoke and overeat. 2) There are hidden factors that affect coronary plaque growth that we are presently not able to detect, e.g., vitamin D receptor genotype, cholesteryl-ester transfer protein variants, variation in inflammatory factors. If we can't measure it, we won't know whether it might influence coronary plaque risk. With all the changes that occur over a person's life, with the uncertainties of yet-to-be-identified causes for coronary plaque, how can you possible know what your risk for heart disease truly is? Yup--a heart scan. Do it and you will know. << Older posts Newer posts >> Newer posts12...333435363738394041...121122Older posts
The Paleo approach to meal frequency 24. November 2009 William Davis (12) Furthering our discussion of postprandial (after-eating) phenomenona, including chylomicron and triglyceride "stacking" (Grazing is for cattle and Triglyceride and chylomicron stacking), here's a comment from the recent Palet Diet Newsletter on the closely related issue, meal timing and frequency:We are currently in the process of compiling meal times and patterns in the worlds historically studied hunter-gatherers. If any single picture is beginning to emerge, it clearly is not three meals per day plus snacking ala the typical U.S. grazing pattern. Here are a few examples:--The Ingalik Hunter Gatherers of Interior Alaska: 'As has been made clear, the principal meal and sometimes the only one of the day is eaten in the evening.' --The Guayaki (Ache) Hunter Gatherers of Paraguay: 'It seems, however, that the evening meal is the most consistent of the day. This is understandable, since the day is generally spent hunting for food that will be eaten in the evening." --The Kung Hunter Gatherers of Botswana. "Members move out of camp each day individually or in small groups to work through the surrounding range and return in the evening to pool the collected resources for the evening meal." --Hawaiians, Tahitians, Fijians and other Oceanic peoples (pre-westernization). 'Typically, meals, as defined by Westerners, were consumed once or twice a day. . . Oliver (1989) described the main meal, usually freshly cooked, as generally eaten in the late afternoon after the day’s work was over." The most consistent daily eating pattern that is beginning to emerge from the ethnographic literature in hunter-gatherers is that of a large single meal which was consumed in the late afternoon or evening. A midday meal or lunch was rarely or never consumed and a small breakfast (consisting of the remainders of the previous evening meal) was sometimes eaten. Some snacking may have occurred during daily gathering, however the bulk of the daily calories were taken in the late afternoon or evening. This pattern of eating could be described as intermittent fasting relative to the typical Western pattern, particularly when daily gathering or hunting were unsuccessful or marginal. There is wisdom in the ways of our hunter gatherer ancestors, and perhaps it is time to re-think three squares a day.In other words, the notion of "grazing," or eating small meals or snacks throughout the day, is an unnatural situation. It is directly contrary to the evolutionarily more appropriate large meal followed by periods of no eating or small occasional meals. I stress this point because I see that the notion of grazing has seized hold of many people's thinking. In my view, grazing is a destructive practice that is self-indulgent, unnecessary, and simply fulfills the perverse non-stop hunger impulse fueled by modern carbohydrate foods. Eliminate wheat, cornstarch, and sugars and you will find that grazing is a repulsive impulse that equates with gorging. The full-text of the Paleo Diet Newsletter can be obtained through www.ThePaleoDiet.com. You can also read and/or subscribe to the new Paleo Diet Blog, just launched in November, 2009.
Angioplasty Special: Get it while it's hot! 21. November 2009 William Davis (6) Graphic courtesy Parsemus Foundation
Even mummies do it 20. November 2009 William Davis (16) Lady Rai, nursemaid to Queen Nefertari of Egypt, died in 1530 BC, somewhere between the age of 30 and 40 years. Her mummy is preserved in the Egyptian National museum of Antiquities in Cairo. A CT scan of her thoracic aorta revealed calcium, representing aortic atherosclerosis, reported by Allam et al (including my friend from The Wisconsin Heart Hospital, Dr. Sam Wann, who provided me a blow-by-blow tale of this really fascinating project). Ladi Rai and 14 other Egyptian mummies were found to have vascular calcification of a total of 22 mummies scanned. (The hearts of the mummies were too degenerated to make out any coronary calcium.)But why would people of that age have developed atherosclerosis? The authors of the study comment that "Our findings that atherosclerosis was not infrequent among middle-aged and older ancient Egyptians of high social status challenges the view that it is a disease of modern humans. . . Although ancient Egyptians did not smoke tobacco or eat processed food or presumably lead sedentary lives, they were not hunter-gatherers. [Emphasis mine.] Agriculture was well established in ancient Egypt and meat consumption appers to have been common among those of high social status."Fascinating. But I don't think that I'd blame meat consumption. Egyptians were also known to have cultivated grains, including wheat, and frequently consumed such sweet delicacies as dates and figs. Egyptians were also apparently beer drinkers. Unfortunately, no beer steins were seen in any of the scans.
Life Extension article on iodine 17. November 2009 William Davis (25) Here's a link to my recent article in Life Extension Magazine on iodine: Halt on Salt Sparks Iodine Deficiency Iodized salt, a concept introduced into the U.S. by the FDA in 1924, slowly eliminated goiter (enlarged thyroid glands), along with an enormous amount of thyroid disease, heart attack, mental impairment, and death. The simple addition of iodine to salt ensured that salt-using Americans obtained enough iodine sufficient to not have a goiter. Now that the FDA, goiters long forgotten from their memories, urges Americans to reduce salt, what has happened to our iodine? I talk at length about this issue in the Life Extension article.
The healthiest people are the most iodine deficient 16. November 2009 William Davis (19) Here's an informal observation. The healthiest people are the most iodine deficient. The healthier you are, the more likely you are to:--Avoid junk foods--30% of which have some iodine from salt--Avoid overuse of iodized salt--Exercise--Sweating causes large losses of iodine.So the healthy-eating, exercising person is the one most likely to show iodine deficiency: gradually enlarged thyroid gland (in the neck), declining thyroid function. Over time, if iodine deficiency persists, excessive sensitivity to iodine develops, as well as abnormal thyroid conditions like overactive nodules. Even subtle levels of thyroid dysfunction act as a potent coronary risk factor.
It's the score, stupid 14. November 2009 William Davis (4) Sal has had 3 heart scans. (He was not on the Track Your Plaque program.) His scores:March, 2006: 439April, 2007: 573October, 2009: 799Presented with the 39% increase from April, 2007 to October, 2009, Sal's doctor responded, "I don't understand. Your LDL cholesterol is fine." This is the sort of drug-driven, cholesterol-minded thinking that characterizes 90% of primary care and cardiologists' practices: "Cholesterol is fine; therefore, you must be fine, too." No. Absolutely not. The data are clear: Heart scan scores that continue to increase at this rate predict high risk for cardiovascular events. Unfortunately, when my colleagues hear this, they respond by scheduling a heart catheterization to prevent heart attack--a practice that has never been shown to be effective and, in my view, constitutes malpractice (i.e., performing heart procedures in people with no symptoms and with either no stress test or a normal stress test). It's the score, stupid! It's not the LDL cholesterol. Pay attention to the increasing heart scan score and you will know that the disease is progressing at an alarming rate. Accepting this fact will set you and your doctor on the track to ask "Why?"That's when you start to uncover all the dozens of other reasons that plaque can grow that have nothing to do with LDL cholesterol or statin drugs.
Heart Scan Blog Redux: Cheers to flavonoids 13. November 2009 William Davis (32) Because in Track Your Plaque we've been thinking a lot about anthocyanins, here's a rerun of a previous Heart Scan Blog post about red wine. (Anthocyanins are among the interesting flavonoids in red wine, along with resveratrol and quercetin.) The case in favor of healthful flavonoids seems to grow bit by bit. Flavonoids such as procyanadins in wine and chocolate, catechins in tea, and those in walnuts, pomegranates, and pycnogenol (pine bark extract) are suspected to block oxidation of LDL (preventing its entry into plaque), normalize abnormal endothelial constriction, and yield platelet-blocking effects (preventing blood clots). Dr. Roger Corder is a prolific author of many scientific papers detailing his research into the flavonoids of foods, but wine in particular. He summarizes his findings in a recent book, The Red Wine Diet. Contrary to the obvious vying-for-prime-time title, Dr. Corder's compilation is probably the best mainstream discussion of flavonoids in foods and wines that I've come across. Although it would have been more entertaining if peppered with more wit and humans interest, given the topic, its straightfoward, semi-academic telling of the story makes his points effectively. Among the important observations Corder makes is that regions of the world with the greatest longevity also correspond to regions with the highest procyanidin flavonoids in their wines. Regarding the variable flavonoid content of wines, he states:Although differences in the amount of procyanidins in red wine clearly occur because of the grape variety and the vineyard environment, the winemaker holds the key to what ends up in the bottle. The most important aspect of the winemaking process for ensuring high procyanidins in red wines is the contact time between the liquid and the grape seeds during fermentation when the alcohol concentration reaches about 6 percent. Depending on the fermentation temperature, it may be two to three days or more before this extraction process starts. Grape skins float and seeds sink, so the number of times they are pushed down and stirred into the fermenting wine also increases extraction of procyanidins. Even so, extraction is a slow process and, after fermentation is complete, many red wines are left to macerate with their seeds and skins for days or even weeks in order to extract all the color, flavor, and tannins. Wines that have a contact time of less than seven days will have a relatively low level of procyanidins. Wines with a contact time of ten to fourteen days have decent levels, and those with contact times of three weeks or more have the highest. He points out that deeply-colored reds are more likely to be richer in procyanidins; mass-produced wines that are usually "house-grade" served at bars and restaurants tend to be low. Some are close to zero. Wines rich in procyanidins provide several-fold more, such that a single glass can provide the same purported health benefit as several glasses of a procyanidin-poor wine. So how do various wines stack up in procyanidin content? Here's an abbreviated list from his book:Australianyphicon-folder-close"> (59)
Is Lp(a) part of your legacy to your children? 15. September 2009 William Davis (21) If you have lipoprotein(a), Lp(a)--the most aggressive known cause of heart disease that no one has heard of--then you need to tell your children. Lp(a) is a "cleanly" inherited genetic pattern: If either parent has it, there's a 50% chance that you have it. If you have it, then there's a 50% likelihood that each of your children has it. (Note that each child experiences a likelihood of 50%, not 50% of your children. This is because each child is conceived as an independent statistical event. So much for romance!)The atherogenicity (plaque-causing potential) of Lp(a) also tends to get transmitted. In other words, if your Dad had a heart attack at age 50 due to Lp(a) and you share Lp(a), then you likely share a similar magnitude of risk as your Dad. If your Mom had Lp(a), though passed quietly at age 89 without any overt evidence of heart disease, then you are likely to share the relatively benign form of Lp(a). For most of us with Lp(a), however, it is best to assume that it has at least some potential for causing heart disease, being the most aggressive cause known. (That is, until we have the ability in everyday clinical practice to characterize Lp(a) by assessing such factors as the size of the apoprotein(a) molecule, the number of kringle "repeats" on the tail, etc. Until then, we need to rely on the crude, though helpful, observation of family history.) At what age should you inform your children? There's no hard-and-fast rule. However, I generally suggest to patients that they talk about Lp(a) with their children when they reach their 20s or 30s, old enough to begin to understand the implications and begin to think about adopting healthier lifestyles. Is treatment required at, say, age 35? That depends on the pattern of Lp(a)-related heart disease in the family: With exceptionally aggressive forms, it might be reasonable to begin treatment at this relatively early age.
Do "Heart Healthy" sterols cause heart disease? 9. September 2009 William Davis (19) The sterol question continues to pop up.Sterols are an ingredient widely added by food manufacturers that allows a "heart healthy" claim, since sterols have been shown to reduce LDL cholesterol (at least transiently). HOWEVER, sterols have also been implicated in possibly increasing risk for heart disease. After all, people with the genetic condition called sitosterolemia absorb sterols into the blood and develop coronary heart disease in their teens and twenties. Those of us without sitosterolemia who increase sterol intake with sterol-enriched foods increase blood levels of sterols several-fold. Is this healthy, or does it contribute to coronary plaque as it does in people with sitosterolemia? Below, I've reprinted a previous Heart Scan Blog post on sterols. Sterols should be outlawedWhile sterols occur naturally in small quantities in food (nuts, vegetables, oils), food manufacturers are adding them to processed foods in order to earn a "heart healthy" claim.The FDA approved a cholesterol-reducing indication for sterols , the American Heart Association recommends 200 mg per day as part of its Therapeutic Lifestyle Change diet, and WebMD gushes about the LDL-reducing benefits of sterols added to foods.Sterols--the same substance that, when absorbed to high levels into the blood in a genetic disorder called "sitosterolemia"--causes extravagant atherosclerosis in young people.The case against sterols, studies documenting its coronary disease- and valve disease-promoting effects, is building:Higher blood levels of sterols increase cardiovascular events:Plasma sitosterol elevations are associated with an increased incidence of coronary events in men: results of a nested case-control analysis of the Prospective Cardiovascular Münster (PROCAM) study.Sterols can be recovered from diseased aortic valves:Accumulation of cholesterol precursors and plant sterols in human stenotic aortic valves.Sterols are incorporated into carotid atherosclerotic plaque:Plant sterols in serum and in atherosclerotic plaques of patients undergoing carotid endarterectomy.Though the data are mixed:Moderately elevated plant sterol levels are associated with reduced cardiovascular risk--the LASA study.No association between plasma levels of plant sterols and atherosclerosis in mice and men.The food industry has vigorously pursued the sterol-as-heart-healthy strategy, based on studies conclusively demonstrating LDL-reducing effects. But do sterols that gain entry into the blood increase atherosclerosis regardless of LDL reduction? That's the huge unanswered question.Despite the uncertainties, the list of sterol-supplemented foods is expanding rapidly:Each Nature Valley Healthy Heart Bar contains 400 mg sterols.HeartWise orange juice contains 1000 mg sterols per 8 oz serving.Promise SuperShots contains 400 mg sterols per container.Corozonas has an entire line of chips that contain added sterols, 400 mg per 1 oz serving.MonaVie Acai juice, "Pulse," contains 400 mg sterols per 2 oz serving.Kardea olive oil has 500 mg sterols per 14 gram serving.WebMD has a table that they say can help you choose "foods" that are sterol-rich.In my view, sterols should not have been approved without more extensive safety data. Just as Vioxx's potential for increasing heart attack did not become apparent until after FDA approval and widespread use, I fear the same may be ahead for sterols: dissemination throughout the processed food supply, people using large, unnatural quantities from multiple products, eventually . . . increased heart attacks, strokes, aortic valve disease.Until there is clarification on this issue, I would urge everyone to avoid sterol-added "heart healthy" products. Some more info on sterols in a previous Heart Scan Blog post: Are sterols the new trans fat? .
Why obese people can't fast 9. September 2009 William Davis (21) Why do obese people claim it is impossible to fast?Most overweight people are terrified at the prospect of facing any period of time without ready access to food. Persuading them to begin a program of intermittent fasting is a hopeless cause. They just refuse. Contrary to popular opinion, this is not just glutonny at work. It is the effect of what I call "the cycle of hunger," the 2-hour up and down cycle of rising sugar and insulin, followed by their inevitable fall. The precipitous fall of sugar and insulin triggers mental fogginess, fatigue, and insatiable hunger. (By the way, this is the same phenomenon underlying the silly notion of "grazing.") According to an LA Times article, fasting may be difficult to impossible for some people: "Ruth Frechman, a registered dietitian in Burbank and spokeswoman for the American Dietetic Assn., says she frequently sees such extreme strategies backfire. 'You're hungry, fatigued, irritable. Fasting is not very comfortable. People try to cut back one day and the next day they're starving and they overeat.'" (Not surprising, coming from the American Diatetic Assn. They, along with such agencies as the American Diabetes Association, are vocal proponents of low-fat, high-carbohydrate, "healthy whole grain" diets--you know, the diets that make us fat and diabetic.)Ms. Frechman is correct: Having someone engage in a period of fasting, no matter how brief, when the diet leading up to the fast is filled with "healthy whole grains" and other carbohydrates will result in painful hunger that eventually overcomes any effort. A period of overeating typically follows the aborted attempt. Fasting cannot work as long as the 2-hour cycle of hunger continues. The first step: Eliminate the 2-hour cycle of hunger by dramatically reducing or eliminating carbohydrates. Our preferred method is to eliminate wheat, cornstarch, and sugars. (Just be aware of wheat withdrawal, the fatigue that develops in the first 5 days after wheat elimination that affects up to 30% of people.)Once wheat, cornstarch, and sugars are eliminated, hunger reverts to that of physiologic need--appetite will be smaller and less intense, since it is driven by your body's needs, not by abnormal stimulation from wheat, cornstarch, and sugar. The fear of not having food dissolves, the 2-hour cycle of mental fogginess, fatigue, and hunger will be gone. Intermittent fasting is a wonderful strategy for reducing weight; gaining control over lipids, lipoproteins, and coronary plaque; regaining appreciation for food; reducing appetite. But it's not even worth trying unless you've already eliminated the unnatural appetite triggers that will booby-trap any fasting effort.
Test your own thyroid 7. September 2009 William Davis (15) 134 people responded to the latest Heart Scan Blog poll:When I ask my doctor to test my thyroid, he/she: Accommodates me without question 45 (33%)Questions why, but orders the tests 49 (36%)Refuses because you seem "healthy" 20 (14%)Refuses without explanation 4 (2%)Ridicules your request 16 (11%)That's better than I anticipated: 69% of physicians complied with this small request. After all, you're not asking for major surgery. You're just asking for a very basic test, as basic as a blood count or electrolytes. 36% of respondents said that their doctor asked why, but still complied; this is simply practicing good medicine--If there is a problem, your doctor would like to know about it.However, the remainder--31%--were refused in one way or another. Incredibly, 11% were ridiculed.Although this was not asked in the poll, I believe that it is a safe assumption that you asked with good reason: you're abnormally fatigued, you have been gaining weight for no apparent reason or can't lose weight despite substantial effort, or you feel cold at inappropriate times.Let's say you're tired. Ever since last summer, you've suffered a gradual decline in energy.So you ask your doctor to assess your thyroid. He refuses. "You're just fine! There's nothing wrong with you."You disagree. In fact, you are quite convinced that there is something physically wrong. What do you do?You could:--Drink more coffee--Exercise more in the hopes that it will snap you out of your lethargy--Sleep more--Take stimulants of various sortsOr, you could get your thyroid assessed and settle the issue. But how can you get this done when your doctor won't accommodate you, even though you have perfectly fine health insurance and are simply interested in feeling better and preserving your health?You could test your thyroid yourself. This is why we're making self-testing kits available. Test kits are available here. This is yet another facet of the powerful revolution that is emerging: Self-directed health.
Trains, planes, and heart scans 4. September 2009 William Davis (10) A Heart Scan Blog reader posted the following question:It is not clear to me why getting a cardiac scan is the necessary first step, if in fact the next step would be to bring down small LDL particles which is revealed on a NMR lipoprofile or VAP test. Why isn't the NMR or VAP test the first thing?Good question. Think of it this way:Lipoproteins, as measured via VAP (Vertical Auto Profile) or NMR (Nuclear Magnetic Resonance), provide a snapshot of risk from a metabolic viewpoint at that moment. Lipoproteins shift with the tides of age, menopause, weight changes, even what you ate last evening for dinner (especially small LDL). There are also other factors that cause coronary plaque, as well, not revealed through lipoprotein testing, such as vitamin D deficiency, smoking, high blood pressure, phosopholipase A2, lipoprotein(a), inflammatory factors, thyroid dysfunction, omega-3 fatty acid deficiency, etc. A heart scan, providing a coronary calcium score, provides an indirect measure of coronary plaque that is the sum total of lipoprotein and other plaque-causing factors that have accumulated up to the time of your scan--regardless of the cause.It means that two females, each 60 years old, with 70% small LDL, HDL 42 mg/dl, triglycerides 150 mg/dl, and mild hypertension, have identical markers for potential coronary risk, but can have widely different heart scan scores. One might have a score of zero, while the other might have a score of 300. Why would the same panel of causes measured at one moment yield wildly different quantities of plaque? Several reasons:1) The lifestyles, eating habits, and weight of each woman differed during their earlier years, not currently reflected in this moment's lipid or lipoprotein patterns. Perhpaps one experienced several years of extraordinary stress from a failed marriage, or suffered through two years of depression that caused her to smoke and overeat. 2) There are hidden factors that affect coronary plaque growth that we are presently not able to detect, e.g., vitamin D receptor genotype, cholesteryl-ester transfer protein variants, variation in inflammatory factors. If we can't measure it, we won't know whether it might influence coronary plaque risk. With all the changes that occur over a person's life, with the uncertainties of yet-to-be-identified causes for coronary plaque, how can you possible know what your risk for heart disease truly is? Yup--a heart scan. Do it and you will know.