I had a heart attack--and I don't know why! 25. October 2006 William Davis (0) Kevin came to my office for another opinion. A husband and father of two teenagers, Kevin had his first heart attack at age 39. Kevin received two stents to his right coronary artery. The entire process took place in a flurry with little explanation over 48 hours, start to finish.He smoked a pack of cigarettes a day, but the only history of heart disease in his family was his father, who, also a smoker, had his heart disease uncovered in his late 70s. His internist subsequently prescribed Zocor even though Kevin's LDL cholesterol was a relatively unimpressive 128 mg/dl. Kevin subsequently asked his cardiologist, "Where did I get the heart disease from?""Cigarettes. And genetics. You can quit the first. There's nothing you can do about the second." End of explanation. This left Kevin frightened and demoralized. If much of the cause of his heart disease couldn't be identified, why bother quitting smoking? Why not enjoy what time he had left?Kevin was understandably shocked when I told him that genetic causes were 1)identifiable, 2)quantifiable, and 3) correctable. Kevin's full lipoprotein analysis subsequently showed the most dire combination that commonly accounts for coronary disease in young people: Lp(a) with small LDL particles. This, along with smoking, fully accounted for this young father of two's heart disease. Along with starting Kevin on a new program for correction of his patterns, I also persuaded him to get a heart scan. What usefulness is a heart scan after the fact? Plenty. Even though Kevin's right coronary was no longer "scorable" because the steel in the stent obscured our measurements, the two remaining unstented arteries would still yield a score. This provides a baseline for future comparison. Even after a stent, Kevin could "track his plaque".
Butter basics 24. October 2006 William Davis (3) There’s lot of confusion about butter, margarines, and their substitutes. Butter/margarine substitutes that avoid the negative aspects and provide modest health benefits are available, but I find that people confuse what's what. So here’s a brief primer. Butter--Avoid it. Plain and simple. Butter is a rich source of saturated fat. Of 11.5 grams total fat per tablespoon, 7.3 grams are saturated. It is not better than margarine, contrary to simple-minded reports from some media sources. Butter raises LDL cholesterol, raises blood pressure, and has been related to various cancers. Margarine--Not better than butter, arguably worse. Some argue that the trans-fatty acids, or hydrogenated oils, used to solidify vegetable oils to make margarine solid are worse than butter. In addition to the ill-effects of butter, margarine reduces HDL and raises cancer risk, perhaps even more than saturated fats. Hydrogenation yields a very unnatural structure that modifies cellular behavior of the sort that may promote the appearance of cancer cells. More recently, however, some of the major manufacturers, like Blue Bonnet, have produced soft spread products without hydrogenation. These are reasonable substitutes when used sparingly. Smart Balance--This is a product made with canola oil, a source of monounsaturates (the best oil source after omega-3s), but manufactured without hydrogenation and therefore has no trans-fats. It does have, in my view, a bit too much saturated fat (1.5 gm per tbsp. in the 37% Light Spread; 2.5 gm per tbsp in the 67% regular spread). This is a reasonable product to use in small quantities. There is also a Smart Balance Omega PLUS product that contains added flaxseed oil and sterol esters. I do not recommend this product because of the sterol content (see below). I also object to the manufacturers who label their products “rich in omega-3s” when they mean linolenic acid (in flaxseed), which is converted to a trivial quantity of omega-3s. Linolenic acid may pose unique benefits of its own, but it should not be listed as an omega-3 source. Benecol--This is a butter substitute that contains stanol esters, a substance that reduces total and LDL cholesterol. Two tablespoons a day reduces LDL around 20 mg/dl, more or less depending on your starting cholesterol. There’s a light and regular spread. The light contains 20 calories less per tablespoon but somewhat less monounsaturates, but the same LDL-reducing stanol esters. The manufacturer does hydrogenate the oils, yielding 0.5 mg trans-fats per tablespoon--a small drawback.Take Control--Similar to Benecol, but made with sterol esters. Take Control also reduces LDL cholesterol. However, data from several high-quality studies from Finland suggest that sterol esters may, in some people, be absorbed into the blood. This is potentially concerning. There is a rare disease called sitosterolemia that results in coronary disease in teenagers and young adults in their 20s from increased absorption of sterol esters. While you can’t acquire this genetic disease, some people have the capacity to absorb sterol esters from their intestines very efficiently. I find it very disturbing and I suggest that you stay away this product and other sterol-containing products like HeartWise orange juice and Smart Balance Omega PLUS until the issue is clarified and safety assured. Brummel and Brown--A blend of vegetable oils (soybean and partially hydrogenated soybean) with calories and fats reduced by blending in yogurt. This is an okay product. The hydrogenation yields trans-fats below the FDA required declaration limit of 1.0 mg. There’s also 1.0 mg each of saturated and monounsaturated fats. The calories are relatively low as a consequence of the added yogurt, only 45 calories per tablespoon. This makes the Brummel and Brown a reasonable choice. Other products are making their way out to supermarkets. Look for the type of oil used. Canola, olive, and flaxseed are the best. Also look for trans-fats and saturated fat content; both should be low, preferably <1.0 mg per tablespoon, ideally none. The best choice among the above products in my view is Benecol, though it’s also the most expensive. It will yield substantial drops in LDL cholesterol. All the products in our informal tastings taste a lot like butter, or at least as well as we can remember what butter tasted like! The key with all of these products is use in moderation, since they all provide between 45?80 calories per tablespoon.
Let Dr. Friedewald rest in peace 24. October 2006 William Davis (1) In the 1960s, doctors struggled with the concept of cholesterol and its relationship to heart disease. It was becoming clear that higher levels of cholesterol were predictive of heart disease. It was also becoming clear that the low-density fraction of cholesterol, or LDL, was somewhat better than total cholesterol in predicting heart attack. Cholesterol was easily measurable in the 1960s. LDL was not. So, Dr. Friedewald, a noted lipid researcher at the National Institutes of Health, proposed an easy method to calculate LDL cholesterol from total choleseterol, HDL, and triglycerides:LDL cholesterol = Total cholesterol – HDL cholesterol – triglycerides/5This simple manipulation would put LDL cholesterols into the hands of the practicing physician and the American public. Dr. Friedewald recognized that this calculation only represented an approximation of LDL cholesterol and that it was thrown off, sometimes substantially, by any abnormal rise in triglycerides or reduction in HDL. But it served its purpose at an age when most doctors hadn’t even heard of cholesterol and the public was still sold on whole milk and “farm-fresh” butter, and Chesterfields were the cigarette choice of most doctors.The world has since changed. Most doctors have heard about cholesterol and, along with the public, have been drowned in drug company marketing for cholesterol-reducing drugs. Most people with some level of common sense and health awareness no longer use butter or whole milk, and no longer believe that the brand of cigarette you choose can be healthy. But we’re still using Dr. Friedewald’s original calculation for LDL cholesterol. When you get an LDL cholesterol from your clinic, doctor, or hospital, >99% of the time it is obtained using Dr. Friedewald’s calculation. Is it because there’s nothing better available? No, it’s not. There’s two reasons why your neighborhood primary care physician or cardiologist is still using this dinosaur of testing called LDL:1) The lag in science to practice is 20 years. Accept that most primary care doctors are 20 years behind the times on many issues, LDL cholesterol included.2) Insurance companies vigorously discourage testing beyond conventional lipids. The array of objections we get from insurance companies is mind-boggling. It would be funny if human life and finances weren’t at stake. These “new” tests are “experimental”, “unproven”, not endorsed by standard guidelines, not approved by some internal committee, or simply “We don’t know what this test is” ?we’ve heard them all. What are the tests that are superior to Dr. Friendewald’s calculated LDL? There are several, listed here in order of best to worst:1) LDL particle number--the value generated by NMR lipoprotein testing. This is the gold standard, most reliable test available, and the one I recommend. 2) Apoprotein B--More widely available even from conventional laboratories in hospitals. Not as accurate as NMR LDL particle number, but a pretty good choice. Apo B is the principal protein in LDL, VLDL, and IDL particles, and so it’s a better reflector of risk from all of these lipoprotein fractions, not just LDL. 3) “Direct” LDL--This is LDL that is actually measured. Unfortunately, it ignores the issues of LDL size and has some other pitfalls, but it’s still better than calculated LDL4) Non-HDL cholesterol--So-called because it incorporates all undesirable cholesterol-containing lipids except good HDL, thus “non-HDL”. This is another calculation, though better than LDL (because it sums up the risk from other apoprotein B-containing lipoproteins). Non-HDL is calculated from Total cholesterol – HDL. It’s therefore available from any standard lipid panel. It’s little used in everyday practice, however, because most people and their physicians find it confusing.5) Friedewald calculated LDL--You can see that calculated LDL is last on a list of choices. Yet this is the measure that doctors use day in, day out. It’s the measure that drug companies base billions of dollars of revenue and profits on. It’s an everyday occurrence in my office that calculated LDL is 89 mg/dl, but the real value is somewhere between 160 and 200 mg/dl. That’s a big difference. Imagine your realtor tells you your house’s estimated value is $200,000 and that’s what you sell it for to an eager buyer. After closing, you find out your house was really worth $300,000. You’d be upset. But that’s what you’re often getting with LDL cholesterol?a bum deal. It’s part of the reason people will say, “My doctor said my cholesterol was fine and that no cause for my heart disease can be found. He said it was genetic.” In reality, they could have sky-high LDL cholesterol revealed by LDL particle number or apoprotein B. Use LDL cholesterol in a pinch when you’ve got nothing else. It’s also helpful to gauge any treatment effect of diet, functional foods, drugs, etc. But it is a seriously flawed tool to diagnose your initial level of risk.
The key to losing weight 23. October 2006 William Davis (0) I saw three people this past week, all of whom set off on an effort to lose substantial quantities of weight. And all seriously needed to. All three started with at least 70 lbs. excess weight; all showed substantial weight-sensitive lipoprotein patterns like low HDL, small LDL, high triglycerides, VLDL, and pre-diabetic levels of blood sugar. They also all shared high blood pressure. All three also had high heart scan scores. Kate’s score was just over 1200. Tom, a 58-year old real estate developer, had a score of nearly 600. Susan, the youngest of the three at 52, had a heart scan score of 377¾99th percentile at this age. Losing weight was an absolute requirement for their plaque control program. Because their lipoprotein abnormalities and pre-diabetic patterns were triggered by weight, weight loss would provide powerful correction. Each and every one of them would need to lose much of their excess weight¾at least 50 lbs¾if they hoped to halt the relentless progression of their heart scan scores. All three of them returned after 6-8 weeks, and all had lost between 17-24 lbs: spectacular results. There’s no secret to weight loss. Each of them achieved their weight loss in slightly different ways. But they also shared several critical ingredients in their weight-loss efforts:1) All three dramatically slashed their intake of wheat flour-containing foods and other processed carbohydrates and did so consistently. All also avoided the usual high-fat, high caloric-density foods like butter, margarine, fried foods, greasy foods, nuts roasted in oil, etc. They concentrated on vegetables, salads, raw nuts, lean proteins (inc. turkey, chicken, fish, lean red meats, low-fat cottage cheese and yogurt). 2) They stopped using food as a reward or as a consolation tool. 3) Exercise for one hour a day at least 5 days a week. The exercise in 2 of 3 of these people was just walking. It wasn’t strenuous, it wasn’t expensive. The women both liked walking with friends or their spouse. Tom followed a more common male path of more strenuous work on his treadmill, elliptical, and biking at the fitness club. But they all did it religiously and missed rare sessions.4) They refrained from any and all alcoholic beverages. Yes, there are some advantages to 1-2 glasses of wine per day, but it stalls weight loss efforts. 5) They didn’t allow themselves any major indiscretions. There were no binges, major pig-outs at weddings, barbecues, or all-you-can-eat buffets. They did allow themselves an occasional “treat” but did so in small portions. That’s it. But for most people, that’s simply too much. Adhering to an effort to lose dramatic weight requires day-after-day consistency. Nobody can lose the equivalent of 70,000 calories (20 lbs.) just by skipping a meal, a 20-minute walk, skipping the mashed potatoes at dinner. It can be done. You’ve just got to be consistent about it.
How can I get my lipoproteins tested? 20. October 2006 William Davis (0) This question came up on our recent online chat session and comes up frequently in phone calls and e-mails. If lipoprotein testing is the best way to uncover hidden causes of coronary heart disease, but your doctor is unable, unknowledgeable, or unwilling to help you, then what can you do?There are several options:1) Get the names of physicians who will obtain and interpret the test for you. Go to the websites for the three labs that actually perform the lipoprotein tests: www.liposcience.com (NMR); www.berkeleyheartlab.com (electropheresis or GGE); www.atherotech.com (VAP or centrifugation). None of them will provide you with the names of actual physicians. They will provide you with the name of a local representative who will know who the doctors in your area who are well-acquainted with their technology. I prefer this route to just having a representative identify a laboratory in your area where the blood sample can be drawn, because you will still need a physician to interpret the results¾this is crucial. The test is of no use to you unless someone interprets it intelligently and understands the range of treatment possibilities available. Don’t be persuaded by your doctor if he/she agrees to have the blood drawn but has never seen the test before. This will be a waste of your time. That’s like hoping the kid next door can fix your car just because he says he fixed his Mom’s car once. Interpretation of lipoproteins takes time, education, and experience.2) Seek out a lipidologist. Lipidologists are the new breed of physician who has sought out additional training and certification in lipid and lipoprotein disorders. Sometimes they’re listed in the yellow pages, or you can search online in your area. 3) Contact us. I frankly don’t like doing this because I feel that I can only provide limited information through this method. I provide a written discussion of the implications and choices for treatment with the caveat to discuss them with your doctor, since I can’t provide medical advice without a formal medical relationship. We also charge $75 for the interpretation. But it’s a lot better than nothing. 4) Make do with basic testing. Basic lipids along with a lipoprotein(a), C-reactive protein, fibrinogen, and homocysteine would provide a reasonable facsimile of lipoprotein testing. You’ll still lack small LDL and postprandial (after-eating) information, but you can still do reasonably well if you try to achieve the Track Your Plaque targets of 60-60-60. In 20 years, this will be a lot easier. But for now, you can still obtain reasonably good results choosing one of the above alternatives.
What do you think about those heart scans? 20. October 2006 William Davis (1) 52-year old Jerry came in for a stress test. He displayed the usual apprehension: fidgeting while he sat on the bed, examining his surroundings, asking lots of questions. “Your doctor asked you have have a stress test?” I asked. “All the males in my family have had heart attacks by age 56, so my doctor suggested I have a stress test,” Jerry explained. Jerry went on to tell me that he had exercised vigorously this morning for 45 minutes without symptoms. He had, in fact, gone surfing just several weeks earlier and described how aerobically challenging it was keeping up with the 20 year olds. “But I did it!” he proudly declared. As he neared the end of his brisk walk on the treadmill, Jerry asked, “What do you think about those heart scans?”Jerry had asked his primary care physician the same question. His doctor had apparently told him that they were just a gimmick. “We’ll get you a real test.” Of course, Jerry’s stress test proved entirely normal. The likelihood of an abnormal stress test with his history of vigorous exercise was <2%. I explained to Jerry that not getting heart scan would be a mistake. In fact, a heart scan was the only easily obtainable test that would uncover hidden heart disease. In truth, the stress test was a waste of time—and an unneeded exposure to radiation.If Jerry’s heart scan score turned out to be zero, great! He was probably spared the genes from the other males in his family, and his risk of heart attack in the next decade was nearly zero. If his heart scan turned out be 1000, then an urgent scramble to uncover the causes and correct them to create a truly effective prevention program would be crucial for his long term health. Or, perhaps his score lies somewhere in between, but Jerry would then know how far along he stood on his way to heart disease. Don’t be a victim of the ignorance of your doctor. Despite all the attention heart scans have received, the majority of doctors remain miserably, inexcusably in the dark. I say inexcusable because CT heart scans can uncover the number one killer of Americans, the number one cause of all deaths in any primary care physician’s practices, and it’s laughably easy. How can a physician not advise patients on the value of heart scans? If given a choice and you’re without symptoms, a heart scan is far and away the superior test.
Olive oil for gourmets 19. October 2006 William Davis (0) "The finest extra-virgin olive oils should not be used as a medium for hot cooking, but rather as a condiment or a finisher on top of your favorite savory foods. They are expensive, but if stored properly they will last for up to a year..."You all know that olive oil is among the preferred oils to use: rich in monounsaturates, low in saturates, high in polyphenols. For a fascinating perspective for the olive oil gourmet, go to www.npr.org, the website for National Public Radio. (Scroll down to the article or enter olive oil into their site search.) Their article, "Like fine wines, fine olive oils boast subtle joys" provides an insightful discussion on squeezing maximum enjoyment out of this wonderful "functional food".As we emerge from the mis-directed low-fat craze of the past 20 years, we're re-discovering the joys of healthy oils. You'll find some great thoughts here
Vitamin D must be oil-based 18. October 2006 William Davis (10) As part of the Track Your Plaque coronary plaque reversal program, we advocate vitamin D supplementation. Vitamin D has been shown to reduce blood sugar and reduce pre-diabetic tendencies, reduce blood pressure (it's a renin antagonist, a blood pressure hormone), it's far more important for bone health than calcium, and it may help prevent colon cancer, prostate cancer, and multiple sclerosis. And, oh yes, it may facilitate coronary plaque regression.One lesson I've learned is that vitamin D MUST be taken as a oil-based capsule or gelcap. You'll recognize it as a transparent or translucent, sometimes opaque, capsule. The list of ingredients may say something like "cholecalciferol [vitamin D] in a base of soybean oil", indicating that the active ingredient is oil-based. Oil-based vitamin D3 skyrockets blood levels of 25-OH-vitamin D3 in to the normal range reliably and easily. Tablets are a different story. These are generally white powdery tablets. The rise in blood levels of vitamin D3 are minimal, sometimes none. Women will often say "I get vitamin D with my calcium tablets." People taking this form almost always have blood levels of vitamin D that are low, as if they were taking nothing.If you're going to take vitamin D, the oil-based tablets are the way to go. They're not necessarily any more expensive. We've had good experiences with the Nature's Life 2000 unit capsule, as well as preparations from Life Extension. We have had negative experiences with the preparations from GNC, Sam's Club, and Walgreen's, all tablets and non-oil-based.
When is LDL cholesterol NOT LDL cholesterol? 18. October 2006 William Davis (0) Darlene had a high LDL cholesterol, at times as high as 200 mg/dl. Her primary care doctor first tried Mevacor, then Pravachol, then Zocor, then Lipitor. Every statin drug failed to reduce Darlene's LDL below 160 mg/dl, even when maximum doses were used. The higher doses also resulted in nearly intolerable muscle aches and weakness. When we sent Darlene's blood sample off for lipoprotein analysis, a surprise came back: she had a high lipoprotein(a), or Lp(a). This explained a lot. LDL cholesterol is not always just LDL cholesterol. One of the particles that can masquerade as LDL is Lp(a). Darlene's story is typical of many people who've had high cholesterol levels poorly responsive to the statin drugs. That's because their LDL conceals Lp(a), which does not respond to these agents. LDL cholesterol does drop some because there's also some real LDL mixed in.A poor response to statin agents or to nutritional strategies to reduce LDL is a tip-off that Lp(a) may be hidden. The answer: just measure Lp(a)! If you and your doctor don't measure it, you won't know whether or not you have it. Rather than a statin drug, we put Darlen on niacin. Not only did her Lp(a) drop, but her LDL also plummeted.
What is a desirable triglyceride level? 17. October 2006 William Davis (0) Though well-intended, the National Cholesterol Education Panel's Adult Treatment Panel, or ATP-III, (whew!) guidelines for cholesterol have been responsible for loads of misinformation. The intention was to educate the internist or family doctor who treats sore throats, performs Pap smears, administers pneumovax vaccine, treats arthritic knees---and dabbles in heart disease prevention. The ATP-III guidelines are the "Cholesterol for Dummies" approach. What standard guidelines definitely do not represent are the ideal values to achieve. They do not ensure protection from heart disease. Thi Toggle navigation Home Blog Home Archive Join Now Log in Niacin vs. low-carb weight loss 10. December 2007 William Davis (28) Niacin:--Raises HDL and shifts HDL towards the healthier large (HDL2b) subclass.--Reduces total LDL.--Reduces small LDL particles.--Reduces triglycerides and triglyceride-containing particles like VLDL and IDL (intermediate-density lipoprotein). --Reduces fibrinogen.--Reduces inflammatory responses. Weight loss achieved through a low-carbohydrate (read "wheat-free") diet: --Raises HDL and shifts HDL towards the healthier large (HDL2b) subclass.--Reduces total LDL.--Reduces small LDL particles.--Reduces triglycerides and triglyceride-containing particles like VLDL and IDL (intermediate-density lipoprotein). --Reduces fibrinogen.--Reduces inflammatory responses.Curious, isn't it? Niacin achieves virtually the same effect as weight loss achieved through a low-carbohydrate diet, particularly if free of wheat products. The only major difference is that niacin also reduces lipoprotein(a), though even that distinction shrinks if monounsaturated fat sources like almonds are included in a low-carbohydrate program. So which should you do first if you have any of the above patterns? Well, it's a question of 1) severity, 2) how carbohydrate-rich your starting diet is, 3) how much weight you could stand to lose, and 4) how urgent your program is (determined largely by your heart scan score). Niacin can also be very helpful if you've taken full advantage of weight loss through a carbohydrate-restricted program, yet still retain some of the abnormal lipoprotein patterns that could continue to grow coronary plaque. For instance, if HDL cholesterol rises from 28 to 40 mg/dl by eliminating wheat and reducing carbohydrates and losing weight, niacin could raise HDL to 50 mg/dl or higher. As much as I love and use niacin for its broad array of plaque-controlling effects, a low-carbohydrate, wheat-free diet can achieve many of the same effects. Use this strategy to full advantage. Explosive plaque growth 10. December 2007 William Davis (3) Every once in a while, we will see someone experience more-than-expected rate of coronary plaque growth, a sudden jump in heart scan scores. I'm talking about increases in score of 50%, even 100%, sometimes despite favorable lipid and lipoprotein patterns.It's not always easy to pin this phenomenon down, since we often detect it after a year or more on a repeat heart scan. It would be wonderfully insightful to perform heart scans more frequently and track plaque growth more precisely, but of course, radiation exposure is the most important limiting factor, as is cost.So this list is, admittedly, speculative. It is based on observation, on presumptive associations between events and heart scan scores. But, judging from what we do confidently know about coronary atherosclerotic plaque, I think these observations make physiologic sense.These are the sorts of increases in heart scan score that can scare the heck out of you, silent yet explosive growth of coronary atherosclerotic plaque that can grow with no warning whatsoever.Image courtesy Wikipedia and the United States Geological Survey.Factors which I have observed to possibly be responsible for explosive plaque growth include:--Overwhelming tragedy such as death of a loved one, financial ruin, divorce. One of my early and catastrophic failures was a young man in his early 40s who, in the space of just a few months, suffered the loss of his mother, a brother, and his mother-in-law, while working a high-stress job. His heart scan score doubled from around 100 to 200 in one year, despite perfect lipoproteins. He had a heart attack shortly after the second score, despite a normal stress test just months earlier. (Pessimism is tragedy's weak cousin, but one that still holds power to corrupt our otherwise best efforts at plaque reversal.) --Substantial weight gain. In the early years of the Track Your Plaque program, before it was even called "Track Your Plaque," I witnessed a man more than double his score from 1100 to 2400 in 18 months just by allowing himself to gain 40 lbs. (I don't know what became of him. His life apparently suffered other disasters, as well, and we lost track of him.)--Poorly-controlled diabetes. High blood sugars out of control have yielded explosive growth.--Kidney disease--However, I am uncertain of how much this overlaps with a deficiency of vitamin D's active form, 1,25-OH-vitamin D3, the form that is often deficient in people with dysfunctional kidneys.--An inflammatory disease that is out of control, e.g., rheumatoid arthritis.--This is very speculative, but I've witnessed explosive growth after vaccine administration that yielded strange viral-like symptoms. In this one instance, the man was getting heart scans (on his own) every three to six months and described a severe illness following a vaccine administered in preparation for travel out of the U.S.--Unrecognized low thyroid function--i.e., hypothyroidism. This is easily corrected with thyroid hormone replacement. These factors can also be relative and they can be overcome. Look at our current Track Your Plaque reversal record-holder: a 53-year old woman who dropped her heart scan score an amazing 63% despite the loss of a loved one during the 15 months of her program. Despite an overwhelming tragedy, she overcame the potential adverse effects and set a record, probably a record for the entire world. Dr. Cannell on "How much vitamin D?" 6. December 2007 William Davis (14) In his most recent Vitamin D Council Newsletter (reprinted in its entirety below, minus clickable links, as Dr. Cannell apparently lost his webmaster and this issue of the newsletter is therefore not posted on the Vitamin D Council website; if you would like to either donate money to the Vitamin D Council or pitch in with help with his website, go to www.vitamindcouncil.com), Dr. John Cannell once again enlightens us with some new insights into vitamin D and its enormous role in health. In this issue, he discusses the role of vitamin D in people diagnosed with cancer (treatment, not prevention). While cancer is not our focus on the Heart Scan Blog, Dr. Cannell's always insightful comments provide some helpful thoughts for our management of vitamin D doses and blood levels. Dr. Cannell cites a recent study from vitamin D research expert, Dr. Bruce Hollis:In the first study of its kind, Professor Bruce Hollis of the Medical University of South Carolina gave all of us something to think about. He asked and answered a simple question: How much vitamin D do you have to take to normalize the metabolism of vitamin D? Remember, unlike other steroid hormones, vitamin D has very unusual metabolism in most modern humans, called first-order, mass action, kinetics. All this means is that the more vitamin D you take, the higher the 25(OH)D level in your blood, and the higher the 25(OH)D level in your blood, the higher the levels of activated vitamin D in your tissues. No other steroid hormone in the body behaves like this. Think about it: would you like your estrogen level to be dependent on how much cholesterol you ate? Or your cortisol level? (I'd ask the same about testosterone levels but I know men well enough not to ask.) No, the body must tightly regulate powerful steroid hormones through substrate inhibition, that is, if an enzyme turns A into B, when the body has enough B, B inhibits the enzyme and so limits its own production. Not so with vitamin D, at least at modern human vitamin D levels. Professor Reinhold Vieth was the first to write about this and Vieth's Chapter 61 in Feldman, Pike, and Glorieux's wonderful textbook, Vitamin D (Elsevier, 2005, second edition), is a great reason to buy the textbook or have your library do so. (I'm glad to see Amazon is out of stock of the new ones (someone must be reading about vitamin D) but you can still buy used editions.) Why would the kinetics of vitamin D be different from all other steroids? Maybe they are not, Hollis reasoned, like Vieth before him. Maybe vitamin D levels are so low in modern humans that its metabolic system is on full blast all the time in an attempt to give the body all the vitamin D metabolites it craves. So Hollis asked, Is vitamin D's metabolism different in populations in the upper end of 25(OH)D levels (a population of sun-exposed people and a group of women prescribed 7,000 IU per day)? Note, the Hollis study is free on Medline, you can download the entire paper on the right hand of the PubMed page below. Hollis BW, et al. 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):631-634.If you look at the two graphs, Figures 1 and 2 of Hollis' paper, you find vitamin D's kinetics can be normalized, made just like all other steroid hormones in the body, but you have to get enough sunshine or take enough vitamin D to get your 25(OH)D level above 50 ng/ml, and 60 ng/ml would be better. Then your body starts to store cholecalciferol in the body without much further increase in 25(OH)D levels. The reaction becomes saturable. This is a remarkable discovery and it implies levels of 30 and 40 ng/ml are usually not sufficient. It also implies actual vitamin D levels (cholecalciferol levels), not just 25(OH)D levels, may be useful in diagnosing and treating deficiency. Note, that not all of the sun-exposed individuals or women prescribed 7,000 IU/day achieved such levels. That's because the sun-exposed individuals were tested after an Hawaiian winter and because prescribing and taking are two different things.In answer to the question, "How much vitamin D should someone with cancer take?," Dr. Cannell advises:"Take enough to get your 25(OH)D level above 60 ng/ml, summer and winter." In doing so, you will have normalized the kinetics of vitamin D and stored the parent compound, cholecalciferol, in your tissues. In the absence of sunshine, you need to take about 1,000 IU/day per 30 pounds of body weight to do this. A 150 pound cancer patient may need to take 5,000 IU per day, a 210 pound cancer patient about 7,000 IU per day, all this in the absence of sunlight. Dr. Cannell, no stranger to the resisitance among many practicing physicians unaware of the expanding and robust literature on vitamin D, advises people with cancer that: In the end, if you have cancer and your physician won't do a risk/benefit analysis, do it yourself. The risk side of that equation is easy. Both Quest Diagnostics and Lab-Corp, the two largest reference labs in the USA, report the upper limit of 25(OH)D normal is 100 ng/ml and toxic is above 150 ng/ml, so 60 ng/ml is well below both. The reason levels up to 100 ng/ml are published normals is because there is no credible evidence in the literature that levels of 100 ng/ml do any harm and because sun worshipers often have such levels. (If you don't believe me, go to the beach in the summer for one month, sunbath every day for 30 minutes on each side in your bathing suit, and go home and have a 25(OH)D level.) By getting your level above 60 ng/ml, all you are doing is getting your levels into the mid to upper range of laboratory reference normals. Little or no risk.For readers wishing to read the entire text of Dr. Cannell's newsletter, it is reprinted below:The Vitamin D NewsletterJanuary, 2008 The January newsletter is coming early as I will be out of touch for awhile. If you remember, the last newsletter was on preventing cancer, not treating it. Below is a sampling of the tragic emails the last newsletter generated: "Dr. Cannell, I was just diagnosed with breast cancer, how much vitamin D should I take?""My mother has colon cancer, how much vitamin D should she take?" "I've had prostate cancer for four years, is there any reason to think vitamin D would help?" "Dr. Cannell, my son has leukemia, should I give him vitamin D?"It's one thing to talk about evidence vitamin D may prevent cancer but something quite different to discuss evidence vitamin D might help treat cancer. I used to think the answers to all the above questions were the same. Like anyone else, people with cancer should be screened for vitamin D deficiency and be treated if deficiency is present. Simple. However, it's not that simple. The real questions are, What are reasonable 25-hydroxy-vitamin D [25(OH)D] levels for someone with a life-threatening cancer? How much vitamin D do they need to take to obtain such levels? Is there any evidence, of any kind, that vitamin D will help treat cancer? The risk/benefit analysis of taking vitamin D is quite different if you are in perfect health than if your life, or your child's life, is on the line. Remember, unlike cancer prevention, not one human randomized controlled trial exists showing vitamin D has a treatment effect on cancer. By treatment effect, I mean prolongs the lives of cancer patients. However, as I cited in my last newsletter, Dr. Philippe Autier of the International Agency for Research on Cancer, and Dr. Sara Gandini of the European Institute of Oncology, performed a meta-analysis of 14 randomized controlled trials showing even low doses of vitamin D extend life but they looked at all-cause mortality, not just cancer (Arch Intern Med. 2007;167(16):1730-1737). However, some epidemiological studies indirectly address the treatment issue and are quite remarkable. The first are a series of discoveries by Professor Johan Moan, Department of Physics at the University of Oslo, with Dr. Alina Porojnicu as the lead author on most of the papers.Moan J, et al. Colon cancer: Prognosis for different latitudes, age groups and seasons in Norway. J Photochem Photobiol B. 2007 Sep 19Lagunova Z, et al. Prostate cancer survival is dependent on season of diagnosis. Prostate. 2007 Sep 1;67(12):1362-70.Porojnicu AC, et al. Changes in risk of death from breast cancer with season and latitude: sun exposure and breast cancer survival in Norway. Breast Cancer Res Treat. 2007 May;102(3):323-8. Porojnicu A, et al. Season of diagnosis is a predictor of cancer survival. Sun-induced vitamin D may be involved: a possible role of sun-induced Vitamin D. J Steroid Biochem Mol Biol. 2007 Mar;103(3-5):675-8. Porojnicu AC, et al. Season of diagnosis is a prognostic factor in Hodgkin's lymphoma: a possible role of sun-induced vitamin D. Br J Cancer. 2005 Sep 5;93(5):571-4. Porojnicu AC, et al. Seasonal and geographical variations in lung cancer prognosis in Norway. Does Vitamin D from the sun play a role? Lung Cancer. 2007 Mar;55(3):263-70. What Professor Moan's group discovered, repeatedly, is quite simple, whether it be cancer of the breast, colon, prostate, lung, or a lymphoma. You live longer if your cancer is diagnosed in the summer. And it is not just Moan's group who has found this. A huge English study recently confirmed Moan's discovery.Lim HS, et al. Cancer survival is dependent on season of diagnosis and sunlight exposure. Int J Cancer. 2006 Oct 1;119(7):1530-6. What do these studies mean? Something about summer has a treatment effect on cancer. Whatever it is, you live longer if you are
Niacin vs. low-carb weight loss 10. December 2007 William Davis (28) Niacin:--Raises HDL and shifts HDL towards the healthier large (HDL2b) subclass.--Reduces total LDL.--Reduces small LDL particles.--Reduces triglycerides and triglyceride-containing particles like VLDL and IDL (intermediate-density lipoprotein). --Reduces fibrinogen.--Reduces inflammatory responses. Weight loss achieved through a low-carbohydrate (read "wheat-free") diet: --Raises HDL and shifts HDL towards the healthier large (HDL2b) subclass.--Reduces total LDL.--Reduces small LDL particles.--Reduces triglycerides and triglyceride-containing particles like VLDL and IDL (intermediate-density lipoprotein). --Reduces fibrinogen.--Reduces inflammatory responses.Curious, isn't it? Niacin achieves virtually the same effect as weight loss achieved through a low-carbohydrate diet, particularly if free of wheat products. The only major difference is that niacin also reduces lipoprotein(a), though even that distinction shrinks if monounsaturated fat sources like almonds are included in a low-carbohydrate program. So which should you do first if you have any of the above patterns? Well, it's a question of 1) severity, 2) how carbohydrate-rich your starting diet is, 3) how much weight you could stand to lose, and 4) how urgent your program is (determined largely by your heart scan score). Niacin can also be very helpful if you've taken full advantage of weight loss through a carbohydrate-restricted program, yet still retain some of the abnormal lipoprotein patterns that could continue to grow coronary plaque. For instance, if HDL cholesterol rises from 28 to 40 mg/dl by eliminating wheat and reducing carbohydrates and losing weight, niacin could raise HDL to 50 mg/dl or higher. As much as I love and use niacin for its broad array of plaque-controlling effects, a low-carbohydrate, wheat-free diet can achieve many of the same effects. Use this strategy to full advantage.
Explosive plaque growth 10. December 2007 William Davis (3) Every once in a while, we will see someone experience more-than-expected rate of coronary plaque growth, a sudden jump in heart scan scores. I'm talking about increases in score of 50%, even 100%, sometimes despite favorable lipid and lipoprotein patterns.It's not always easy to pin this phenomenon down, since we often detect it after a year or more on a repeat heart scan. It would be wonderfully insightful to perform heart scans more frequently and track plaque growth more precisely, but of course, radiation exposure is the most important limiting factor, as is cost.So this list is, admittedly, speculative. It is based on observation, on presumptive associations between events and heart scan scores. But, judging from what we do confidently know about coronary atherosclerotic plaque, I think these observations make physiologic sense.These are the sorts of increases in heart scan score that can scare the heck out of you, silent yet explosive growth of coronary atherosclerotic plaque that can grow with no warning whatsoever.Image courtesy Wikipedia and the United States Geological Survey.Factors which I have observed to possibly be responsible for explosive plaque growth include:--Overwhelming tragedy such as death of a loved one, financial ruin, divorce. One of my early and catastrophic failures was a young man in his early 40s who, in the space of just a few months, suffered the loss of his mother, a brother, and his mother-in-law, while working a high-stress job. His heart scan score doubled from around 100 to 200 in one year, despite perfect lipoproteins. He had a heart attack shortly after the second score, despite a normal stress test just months earlier. (Pessimism is tragedy's weak cousin, but one that still holds power to corrupt our otherwise best efforts at plaque reversal.) --Substantial weight gain. In the early years of the Track Your Plaque program, before it was even called "Track Your Plaque," I witnessed a man more than double his score from 1100 to 2400 in 18 months just by allowing himself to gain 40 lbs. (I don't know what became of him. His life apparently suffered other disasters, as well, and we lost track of him.)--Poorly-controlled diabetes. High blood sugars out of control have yielded explosive growth.--Kidney disease--However, I am uncertain of how much this overlaps with a deficiency of vitamin D's active form, 1,25-OH-vitamin D3, the form that is often deficient in people with dysfunctional kidneys.--An inflammatory disease that is out of control, e.g., rheumatoid arthritis.--This is very speculative, but I've witnessed explosive growth after vaccine administration that yielded strange viral-like symptoms. In this one instance, the man was getting heart scans (on his own) every three to six months and described a severe illness following a vaccine administered in preparation for travel out of the U.S.--Unrecognized low thyroid function--i.e., hypothyroidism. This is easily corrected with thyroid hormone replacement. These factors can also be relative and they can be overcome. Look at our current Track Your Plaque reversal record-holder: a 53-year old woman who dropped her heart scan score an amazing 63% despite the loss of a loved one during the 15 months of her program. Despite an overwhelming tragedy, she overcame the potential adverse effects and set a record, probably a record for the entire world.
Dr. Cannell on "How much vitamin D?" 6. December 2007 William Davis (14) In his most recent Vitamin D Council Newsletter (reprinted in its entirety below, minus clickable links, as Dr. Cannell apparently lost his webmaster and this issue of the newsletter is therefore not posted on the Vitamin D Council website; if you would like to either donate money to the Vitamin D Council or pitch in with help with his website, go to www.vitamindcouncil.com), Dr. John Cannell once again enlightens us with some new insights into vitamin D and its enormous role in health. In this issue, he discusses the role of vitamin D in people diagnosed with cancer (treatment, not prevention). While cancer is not our focus on the Heart Scan Blog, Dr. Cannell's always insightful comments provide some helpful thoughts for our management of vitamin D doses and blood levels. Dr. Cannell cites a recent study from vitamin D research expert, Dr. Bruce Hollis:In the first study of its kind, Professor Bruce Hollis of the Medical University of South Carolina gave all of us something to think about. He asked and answered a simple question: How much vitamin D do you have to take to normalize the metabolism of vitamin D? Remember, unlike other steroid hormones, vitamin D has very unusual metabolism in most modern humans, called first-order, mass action, kinetics. All this means is that the more vitamin D you take, the higher the 25(OH)D level in your blood, and the higher the 25(OH)D level in your blood, the higher the levels of activated vitamin D in your tissues. No other steroid hormone in the body behaves like this. Think about it: would you like your estrogen level to be dependent on how much cholesterol you ate? Or your cortisol level? (I'd ask the same about testosterone levels but I know men well enough not to ask.) No, the body must tightly regulate powerful steroid hormones through substrate inhibition, that is, if an enzyme turns A into B, when the body has enough B, B inhibits the enzyme and so limits its own production. Not so with vitamin D, at least at modern human vitamin D levels. Professor Reinhold Vieth was the first to write about this and Vieth's Chapter 61 in Feldman, Pike, and Glorieux's wonderful textbook, Vitamin D (Elsevier, 2005, second edition), is a great reason to buy the textbook or have your library do so. (I'm glad to see Amazon is out of stock of the new ones (someone must be reading about vitamin D) but you can still buy used editions.) Why would the kinetics of vitamin D be different from all other steroids? Maybe they are not, Hollis reasoned, like Vieth before him. Maybe vitamin D levels are so low in modern humans that its metabolic system is on full blast all the time in an attempt to give the body all the vitamin D metabolites it craves. So Hollis asked, Is vitamin D's metabolism different in populations in the upper end of 25(OH)D levels (a population of sun-exposed people and a group of women prescribed 7,000 IU per day)? Note, the Hollis study is free on Medline, you can download the entire paper on the right hand of the PubMed page below. Hollis BW, et al. 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):631-634.If you look at the two graphs, Figures 1 and 2 of Hollis' paper, you find vitamin D's kinetics can be normalized, made just like all other steroid hormones in the body, but you have to get enough sunshine or take enough vitamin D to get your 25(OH)D level above 50 ng/ml, and 60 ng/ml would be better. Then your body starts to store cholecalciferol in the body without much further increase in 25(OH)D levels. The reaction becomes saturable. This is a remarkable discovery and it implies levels of 30 and 40 ng/ml are usually not sufficient. It also implies actual vitamin D levels (cholecalciferol levels), not just 25(OH)D levels, may be useful in diagnosing and treating deficiency. Note, that not all of the sun-exposed individuals or women prescribed 7,000 IU/day achieved such levels. That's because the sun-exposed individuals were tested after an Hawaiian winter and because prescribing and taking are two different things.In answer to the question, "How much vitamin D should someone with cancer take?," Dr. Cannell advises:"Take enough to get your 25(OH)D level above 60 ng/ml, summer and winter." In doing so, you will have normalized the kinetics of vitamin D and stored the parent compound, cholecalciferol, in your tissues. In the absence of sunshine, you need to take about 1,000 IU/day per 30 pounds of body weight to do this. A 150 pound cancer patient may need to take 5,000 IU per day, a 210 pound cancer patient about 7,000 IU per day, all this in the absence of sunlight. Dr. Cannell, no stranger to the resisitance among many practicing physicians unaware of the expanding and robust literature on vitamin D, advises people with cancer that: In the end, if you have cancer and your physician won't do a risk/benefit analysis, do it yourself. The risk side of that equation is easy. Both Quest Diagnostics and Lab-Corp, the two largest reference labs in the USA, report the upper limit of 25(OH)D normal is 100 ng/ml and toxic is above 150 ng/ml, so 60 ng/ml is well below both. The reason levels up to 100 ng/ml are published normals is because there is no credible evidence in the literature that levels of 100 ng/ml do any harm and because sun worshipers often have such levels. (If you don't believe me, go to the beach in the summer for one month, sunbath every day for 30 minutes on each side in your bathing suit, and go home and have a 25(OH)D level.) By getting your level above 60 ng/ml, all you are doing is getting your levels into the mid to upper range of laboratory reference normals. Little or no risk.For readers wishing to read the entire text of Dr. Cannell's newsletter, it is reprinted below:The Vitamin D NewsletterJanuary, 2008 The January newsletter is coming early as I will be out of touch for awhile. If you remember, the last newsletter was on preventing cancer, not treating it. Below is a sampling of the tragic emails the last newsletter generated: "Dr. Cannell, I was just diagnosed with breast cancer, how much vitamin D should I take?""My mother has colon cancer, how much vitamin D should she take?" "I've had prostate cancer for four years, is there any reason to think vitamin D would help?" "Dr. Cannell, my son has leukemia, should I give him vitamin D?"It's one thing to talk about evidence vitamin D may prevent cancer but something quite different to discuss evidence vitamin D might help treat cancer. I used to think the answers to all the above questions were the same. Like anyone else, people with cancer should be screened for vitamin D deficiency and be treated if deficiency is present. Simple. However, it's not that simple. The real questions are, What are reasonable 25-hydroxy-vitamin D [25(OH)D] levels for someone with a life-threatening cancer? How much vitamin D do they need to take to obtain such levels? Is there any evidence, of any kind, that vitamin D will help treat cancer? The risk/benefit analysis of taking vitamin D is quite different if you are in perfect health than if your life, or your child's life, is on the line. Remember, unlike cancer prevention, not one human randomized controlled trial exists showing vitamin D has a treatment effect on cancer. By treatment effect, I mean prolongs the lives of cancer patients. However, as I cited in my last newsletter, Dr. Philippe Autier of the International Agency for Research on Cancer, and Dr. Sara Gandini of the European Institute of Oncology, performed a meta-analysis of 14 randomized controlled trials showing even low doses of vitamin D extend life but they looked at all-cause mortality, not just cancer (Arch Intern Med. 2007;167(16):1730-1737). However, some epidemiological studies indirectly address the treatment issue and are quite remarkable. The first are a series of discoveries by Professor Johan Moan, Department of Physics at the University of Oslo, with Dr. Alina Porojnicu as the lead author on most of the papers.Moan J, et al. Colon cancer: Prognosis for different latitudes, age groups and seasons in Norway. J Photochem Photobiol B. 2007 Sep 19Lagunova Z, et al. Prostate cancer survival is dependent on season of diagnosis. Prostate. 2007 Sep 1;67(12):1362-70.Porojnicu AC, et al. Changes in risk of death from breast cancer with season and latitude: sun exposure and breast cancer survival in Norway. Breast Cancer Res Treat. 2007 May;102(3):323-8. Porojnicu A, et al. Season of diagnosis is a predictor of cancer survival. Sun-induced vitamin D may be involved: a possible role of sun-induced Vitamin D. J Steroid Biochem Mol Biol. 2007 Mar;103(3-5):675-8. Porojnicu AC, et al. Season of diagnosis is a prognostic factor in Hodgkin's lymphoma: a possible role of sun-induced vitamin D. Br J Cancer. 2005 Sep 5;93(5):571-4. Porojnicu AC, et al. Seasonal and geographical variations in lung cancer prognosis in Norway. Does Vitamin D from the sun play a role? Lung Cancer. 2007 Mar;55(3):263-70. What Professor Moan's group discovered, repeatedly, is quite simple, whether it be cancer of the breast, colon, prostate, lung, or a lymphoma. You live longer if your cancer is diagnosed in the summer. And it is not just Moan's group who has found this. A huge English study recently confirmed Moan's discovery.Lim HS, et al. Cancer survival is dependent on season of diagnosis and sunlight exposure. Int J Cancer. 2006 Oct 1;119(7):1530-6. What do these studies mean? Something about summer has a treatment effect on cancer. Whatever it is, you live longer if you are