Kitchen sink approach for Lp(a) 29. August 2008 William Davis (12) Lipoprotein(a), Lp(a), can be a tough nut to crack. Having struggled and wrestled with this genetic pattern for the last 12 years or so in hundreds of patients, I have gained great respect for this difficult to control pattern. I regard lipoprotein(a) as the number one most aggressive cause for heart disease and coronary plaque known. It can account for heart attacks in men in their 40s, women in their 50s. It can cause heart disease and heart attacks in even the ultra-fit like marathon runners. It accounts for both excessive coronary risk and misleading cholesterol values in slender, healthy-appearing people. Niacin is the number one treatment choice for Lp(a), followed by testosterone for men, estrogens (preferably human, not horse or other non-human mammal) for women. I then often resort to DHEA, along with adjunctive nutritional agents like raw almonds, ground flaxseed, and others. Our most recent addition to the Lp(a) treatment list is high-dose fish oil, which appears to exert a significant effect in about 40% of people with Lp(a). Even with this multi-agent approach, not everybody gains control over Lp(a).That makes me wonder if someone has Lp(a) at a substantial level of, say, 200 nmol/L or 70 mg/dl (values can differ tremendously, depending on the method of measurement), should we throw everything but the kitchen sink at Lp(a) from the start? Right now, by adding an agent one at a time, it often takes two years to gain control over Lp(a) (if we are going to get it at all).While many people might find this unpalatable and overwhelming from the starting gate of their program, I do believe it may be a strategy we should consider adopting for full and more immediate plaque control in the Track Your Plaque program. Something to chew on. Clearly, we need better answers for Lp(a). A "kitchen sink," full-frontal assault might be a way to gain faster control, though not necessarily a superior approach with regards to efficacy and potency. There are a number of unique, potentially effective therapies for Lp(a) that are worth examining. Given the difficulty of performing clinical trials with non-drug agents (largely a lack of financial support, since nobody gets a financial return with non-patent-protectable agents), I am anxious to put these potential treatments to a test in the Track Your Plaque program Virtual Clinical Trail (VCT). The VCT gives us a quick and relatively easy method to test various potential treatments, with feedback generated in months, rather than years. Any suggestions on promising agents to test? Of course, they must be widely available nutritional agents, not drugs.
Making Dr. Friedewald an honest man 28. August 2008 William Davis (3) Colleen started with the usual discrepancy between conventional calculated LDL cholesterol of 121 mg/dl and the far more accurate LDL particle number (NMR) of 1927 nmol/L. Those of you following this conversation or our many conversations on the Track Your Plaque Forum know that a useful and highly reliable rule-of-thumb for converting NMR LDL particle number to LDL is to drop the last digit: 1927 nmol/L becomes 192 mg/dl. (This is, admitttedly, arrived at empirically, not by design. However, it has held up through thousands of NMR analyses and plays out reasonably when you compare distributions of Friedewald LDL and LDL particle number on a population basis.)In other words, by this simple manipulation, Colleen's Friedewald calculated LDL is off by 58%. This is very common, a phenomenon I witness several times every day. By LDL particle size, 75% of all Colleen's LDL particle were abnormally small (small LDL particle number 1440 nmol/L). This is a moderately severe small LDL tendency.So we took all the steps for reduction of small LDL/LDL, including elimination of wheat and cornstarch, exercise, weight loss (which happens inevitably when wheat and cornstarch are eliminated), fish oil, vitamin D, etc. Another NMR lipoprotein panel showed an LDL particle number of 882 nmol/L and a Friedewald calculated LDL of 87 mg/dl. Using our rule-of-thumb, LDL by particle number is virtually the same as the calculated LDL. This time, small LDL numbered only 237 nmol/L, or 26.8% of the total, a marked reduction. Isn't that interesting? As small LDL is corrected, the crude Friedwald calculated LDL approximates the more accurate LDL particle number. It assumes that accuracy of the Friedewald calculation may be more likely to occur as LDL size approaches normal. However, when LDL size is abnormally small--a condition shared by at least 70% of people with coronary heart disease--then the Friedewald LDL becomes increasingly inaccurate.The opposite can also happen: When all or nearly all LDL particles are large, Friedewald calculated LDL can markedly overestimate LDL particle number. Yesterday, for instance, a patient had a Friedewald calculated LDL of 183 mg/dl, but an NMR particle number of 1110 nmol/L--drop the zero . . . LDL 110 mg/dl. This woman was advised to take a statin drug by her primary care physician, based on the Friedewald LDL. Instead, she proved to have a far lower LDL. She would not have benefitted from taking a statin drug. As I've warned many times before: Beware the Friedewald calculated LDL.
Some basic vitamin D issues 24. August 2008 William Davis (7) The last post on vitamin D raised a number of basic questions among readers. So let me discuss some of these questions one by one. All of them raise important issues surrounding the practical aspects of managing vitamin D in your health. Anne said:I think it is important to stress that vitamin D supplementation needs to be continued long term. I have met too many people who have been prescribed 50,000 IU of D2 for 8-12 weeks and then told to stop because their 23(OH)D went over 30ng/ml. I know one person who's doctor stopped and started the D2 3 times. Thanks for pointing that out, Anne. Excellent point. I also see doctors do this with statin drugs: start it, check a LDL level which is lower, then think that you're done and stop the drug. What the heck are they thinking? If vitamin D is not being produced by sun exposure and not obtainable through diet, continued supplementation is necessary, essentially for life. Twinb asked:How often you think Vit. D levels should be tested after the initial test is done, especially if the levels are drastically low?We have used every 6 months in the office. Ideally, levels are in mid-summer and mid- to-late winter in order to gauge the extremes of your seasonal fluctuations. While most adults over 40 fail to fluctuate more than 10 ng/ml in the Wisconsin climate (and this summer, after an initial rainy season early, has been flawlessly bright and sunny, in the high-70s and 80s every single day for months), an occasional person fluctuates more widely. The only way to judge is to check a blood level. Rich said:Vitamin D dosage effects appear to be quite idiosyncratic.Yes, indeed it is. Despite using crude rules-of-thumb, like taking 1000 units of vitamin D per 10 ng/ml desired (a rule I learned from Dr. John Cannell, which he offered fully aware of its inaccuracy), many people will surprise you and have levels that make no sense. Testing is crucial to know your vitamin D level. Richard asked: Where do we get enough vitamin D wihout worring about laboratory tests? Well, the entire point of the post was that you absolutely, positively cannot just take vitamin D blindly at any dose and hope that your level is ideal, no more than you can blindly take a dose of thyroid and know you have achieved normal thyroid levels. In my view, vitamin D blood levels are an absolute. Another simple issue: Don't be afraid of vitamin D. It is, in all practicality, no more dangerous than getting a dark tan. (But, as many of you realize, getting a tan is no assurance of raising vitamin D if you are over 40 years old.)Wouldn't it be great if someone developed a do-it-yourself-at-home skin test for vitamin D? I know of no effort to develop this, but it would be a huge advantage for all of us.
“How much vitamin D should I take?” 22. August 2008 William Davis (17) It’s probably the number one most common question I get today: “How much vitamin D should I take?”Like asking for investing advice, there are no shortage of people willing to provide answers, most of them plain wrong. The media are quick to offer advice like “Take the recommended daily allowance of 400 units per day,” or “Some experts say that intake of vitamin D should be higher, as high as 2000 units per day.” Or “Be sure to get your 15 minutes of midday sun.”Utter nonsense. The Food and Nutrition Board of the Institute of Medicine has been struggling with this question, also. They have an impossible job: Draft broad pronouncements on requirements for various nutrients by recommending Recommended Daily Allowances (RDA) for all Americans. The Food and Nutrition Board has tried to factor in individual variation by breaking vitamin D requirements down by age and sex, but what amounts to a one-size-fits-nearly-all approach. Much of the uncertainty over dosing stems from the fact that vitamin D should not be called a “vitamin.” Vitamins are nutrients obtained from foods. But, outside of oily fish, you'll find very little naturally-occurring vitamin D in food. (Even in fish, there is generally no more than 400 units per 4 oz. serving.) Sure, there’s 20 units in an egg yolk and you can activate the vitamin D in a shiitake mushroom by exposing it to ultraviolet radiation. Dairy products like milk (usually) contain vitamin D because the USDA mandates it. But food sources hardly help at all unless you’re an infant or small child. It all makes sense when vitamin D is viewed as a hormone, a steroid hormone, not a vitamin. Vitamin-no, steroid hormone-D exerts potent effects in tiny quantities with hormone-like action in cells, including activation of nuclear receptors. It is the only hormone that is meant to be activated by sun exposure of the skin, not obtained through diet. But the ability to activate D is lost by the majority of us by age 40 and even a dark tan is no assurance that sufficient skin prohormone D activation has taken place. As with any other hormone, such as thyroid, parathyroid, or growth hormones, dose needs to be individualized. Imagine you developed a severely low thyroid condition that resulted in 30 lbs of weight gain, lose your hair, legs swell, and heart disease explodes. Would you accept that you should take the same dose of thyroid hormone as every other man or woman your age, regardless of your body size, proportion of body fat, metabolism, genetics, race, dietary habits, and other factors that influence thyroid hormone levels? Of course you wouldn’t. Then why would anyone insist that vitamin D be applied in a one-size-fits-all fashion? (There’s another world in which a one-size-fits-all approach to hormone replacement has been widely applied, that of female estrogen replacement. In conventional practice, there’s no effort to identify need, estrogen-progesterone interactions, nor assess the adequacy of dose, not to mention the perverse non-human preparation used.) With thyroid hormone, ideal replacement dose of hormone ranges widely from one person to another. Some people require 25 mcg per day of T4; others require 800% greater doses. Many require T3, but not everybody. Likewise, vitamin D requirements can range widely. I have used anywhere from 1000 units per day, all the way up to 16,000 units per day before desirable blood levels were achieved. Vitamin D dose needs to be individualized. Factors that influence vitamin D need include body size and percent body fat (both of which increase need substantially); sex (males require, on average, 1000 units per day more than females); age (older need more); skin color (darker-skinned races require more, fairer-skinned races less); and other factors that remain ill-defined. But these are “rules” often broken. My office experience with vitamin D now numbers nearly 1000 patients. The average female dose is 4000-5000 units per day, average male dose 6000 units per day to achieve a blood level of 60-70 ng/ml, though there are frequent exceptions. I’ve had 98 lb women who require 12,000 units, 300 lb men who require 1000 units, 21-year olds who require 10,000 units. (Of course, this is a Wisconsin experience. However, regional differences in dosing needs diminish as we age, since less and less vitamin D activation occurs.)Let me reiterate: Steroid hormone-vitamin D dose needs to be individualized. There’s only one way to individualize your need for vitamin D and thereby determine your dose: Measure a blood level. Nobody can gauge your vitamin D need by looking at you, by your skin color, size, or other simple measurement like weight or body fat. A vitamin D blood level needs to be measured specifically-period. Unfortunately, many people balk at this, claiming either that it’s too much bother or that their doctor refused to measure it. I would rank normalizing steroid hormone-vitamin D as among the most important things you can do for your health. It should never be too much bother. And if your doctor refuses to at least discuss why he/she won’t measure it, then it’s time for a new doctor. If you’re worried about adding to rising healthcare costs by adding yet another blood test, think of the money saved by sparing you from a future of cancer, heart disease, osteoporosis, diabetes, etc. The cost of a vitamin D blood test is relatively trivial (around $40-50, a fraction of the cost of a one month supply of a drug for diabetes.) So how much vitamin D should you take? Enough to raise your blood level of 25-hydroxy vitamin D to normal. (We aim for a normal level of 60-70 ng/ml.)
You probably don't take enough fish oil 20. August 2008 William Davis (17) The results of the recent Heart Scan Blog survey in response to the question: MY DAILY DOSE OF EPA + DHA FROM FISH OIL IS revealed:Zero--I don't take any 17 (7%) of respondents Less than 1000 mg per day 24 (10%) of respondents 1000-2000 mg per day 91 (38%) of respondents 2000-3000 mg per day 44 (18%) of respondents 3000-4000 mg per day 40 (16%) of respondents More than 4000 mg per day 20 (8%) of respondentsBased on the above results, I would say that only a minority of respondents are taking an ideal dose of omega-3 fatty acids. Nearly all of us should consider taking more. Benefits of omega-3 fatty acids (EPA + DHA) from fish oil begin around a dose of 840 mg per day, according to the GISSI Prevenzione Trial of 1999, an 11,000-participant trial. This dose also corresponds to a quantity of omega-3s that have been shown to raise EPA + DHA blood levels and thereby reduce the notoriously high AA:EPA ratio of Americans. But what dose is sufficient? What dose is ideal? Well, the answer to a great degree depends on what you are taking the fish oil for. If being taken to reduce triglycerides and triglyceride-containing lipoproteins, like VLDL and the after-eating (postprandial) IDL, then a higher dose will be necessary. (Triglyceride reduction for the genetically-determined very high triglyceride level of familial hypertriglyceridemia is the FDA-approved indication for prescription Lovaza.) If you are taking fish oil for treatment of ADHD, depression, or bipolar illness, very high doses are often necessary. But how about maximal reduction of cardiovascular risk and for control or reversal of atherosclerotic plaque? This conversation is still evolving. But we can learn some important lessons from three populations of the world that are vigorous consumers of fish:--The Inuits (aka Eskimos) of Greenland and northern Canada--The Japanese--The Bantus of Tanzania who live along Nyasa LakeAll three indigenous populations have several-fold greater intakes of fish and omega-3 fatty acids, have higher blood levels of omega-3 fatty acids, and have enjoyed reduced cardiovascular events, reduced atherosclerotic plaque, or improvement in various surrogates of cardiovascular risk (e.g., Lp(a)). The most recent addition to this conversation is the ERA JUMP Study, discussed in a previous Heart Scan Blog post. In ERA JUMP, despite being heavy smokers and having other markers for greater risk for heart disease, Japanese men living in Japan had markedly less carotid and coronary plaque, as compared to Caucasian men living in PIttsburgh or Hawaiian men of Japanese descent. The difference appeared to be attributable to serum levels of omega-3 fatty acids. I believe that the trend is here is to increase the amount of omega-3 fatty acids that most of us take. In the Track Your Plaque program, we have been advocating a rock-bottom starting dose of EPA + DHA of 1200 mg per day. However, I believe that this is due for a change. We will be increasing the minimum dose for plaque regression and control. Please attend our Webinar this evening for a full, in-depth discussion of the rationale behind this important change. As always, let me remind you that I am not selling, nor ever have sold, fish oil supplements. If I advocate a specific dose, a higher dose, I do so based on my interpretation of the data and experience with patients, not because I am interested in selling brand X of fish oil.
Vitamin D and HDL 19. August 2008 William Davis (23) Despite the paucity of scientific documentation of this phenomenon, I am continuing to witness extraordinary increases in HDL cholesterol levels with vitamin D supplementation. I've touched on the interaction of vitamin D supplementation with HDL in The Heart Scan Blog previously:Vitamin D: Treatment for metabolic syndrome?HDL for DummiesAt first, I thought it was attributable to other factors. In real life, most people don't modify one factor at a time. They reduceprocessed carbohydrates/eliminate wheat and cornstarch, lose weight, add or increase omega-3 fatty acids from fish oil, begin niacin, increase exercise and physical activity. All these efforts also impact on HDL. Among the many things I do, I consult on complex lipid (cholesterol) disorders (complex hyperlipidemias) in my office. A substantial number of these people carry a diagnosis of hypoalphalipoproteinemia, a mouthful that simply means these people are unable to manufacture much apoprotein A1, the principal protein of HDL cholesterol particles. As a result, people with hypoalphalipoproteinemia have HDL cholesterol levels in the neighborhood of 20-30 mg/dl--very low. They are also at high risk for heart disease and stroke. Encourage these people to exercise, attain ideal weight, eliminate wheat and cornstarch: HDL increases 5 mg/dl or so. Add niacin, HDL increases another 5-10 mg/dl. Perhaps we're now sitting somewhere around an HDL of 35-40 mg/dl--better, but hardly great. Add vitamin D to achieve our target serum level . . . HDL jumps to 50, 60, 70, even 90 mg/dl. The first few times this occurred, I thought it was an error or fluke. But now that I've witnessed this effect many dozens of time, I am convinced that it is real. Just today, I saw a 40-year old man whose starting HDL was 25 mg/dl increase to 87 mg/dl. Responses like this are supposed to be impossible. Before vitamin D, I had never witnessed increases of this magnitude. Not all therapies for raising HDL raise the important large (also known as HDL2b) fraction. With lipoprotein analyses, it appears that is principally the large fraction of HDL that rises with vitamin D supplementation. Why? How? That I can't tell you. But for those of you struggling with low HDL cholesterols despite your best efforts, vitamin D can make a world of difference.An interesting corollary: If super-high HDL cholesterols are associated with extreme longevity, as they are with centenarians, does raising HDL to extraordinary levels with vitamin D lead to longer, healthier life, all the way up to age 110 years? Again, no answers, but an interesting thought. And one I'd bet on. (And I'm not selling vitamin D.)
Weight loss and blood pressure 15. August 2008 William Davis (6) Here's another thought with regards to time issues with weight loss: reductions in blood pressure (BP). The previous post talked about how triglycerides initially go up, sometimes way up, when weight drops, only to be followed months later by substantial drops. HDL initially drops in response to the triglyceride fluctuations, only to be followed by a rise. Blood pressure also shows a curious pattern that is largely dependent on age. Say someone in their 20s or 30s, for instance, loses 30 lbs (through elimination of wheat and cornstarch, say). BP usually drops within a few weeks, perhaps a month or two at most. How about someone in their 70s? Say a substantial amount of weight is lost, say 50 lbs over 6 months. BP does indeed drop, but it may require 6 months or longer after weight plateaus for the full effects of BP-reduction to be fully expressed. But it will eventually drop. Why the age-dependent difference? It relates to the capacity of arteries to remain flexible and distensible. Over the years, cross-linking of collagen (a structural protein), glycation (glucose molecules attaching to proteins), loss of endothelial responsiveness to generate artery-dilating substances like nitric oxide, and arterial atherosclerotic plaque all all up to making older arteries less able to "relax" and BP to drop. But given time and the proper effort, BP will eventually drop. Awareness of this time effect can help most people decide better when medications are necessary or if weight loss alone is sufficient to reach BP goals.
"I lost 30 lbs and my triglycerides went . . . up?" 13. August 2008 William Davis (6) Brad needed to lose weight. At 6 ft tall, he began the program at 291 lbs, easily 80 lbs overweight. He wore virtually all of it in his belly. He had laboratory numbers to match: HDL 33 mg/dl, triglycerides 225 mg/dl, LDL (calculated) 144 mg/dl, blood sugar 122 mg/dl (fasting--clearly "pre-diabetic"), c-reactive protein 3.0 mg/dl. Among his lipoprotein abnormalities: small LDL representing 80% of all LDL (no surprise). Readers of The Heart Scan Blog know that these are the patterns of the carbohydrate-indulgent. I asked Brad to eliminate all wheat flour products, all foods made with cornstarch, and follow a diet rich in healthy oils, raw nuts, vegetables, and lean meats. Brad returned for a discussion about follow-up basic lipids (cholesterol) values four months later--31 lbs lighter, most of it clearly lost from his abdomen. He claimed he felt more energetic and clear-headed than he had in years. His lipid panel: HDL 34 mg/dl, LDL 122 mg/dl, triglycerides 295 mg/dl. Brad's smile dissolved. "How could that happen? You said losing weight would make my HDL go up and my triglycerides go down!"Yes, I had said that. But I was oversimplifying. The truth is that, when there is weight loss, especially profound weight loss like Brad experienced eliminating wheat and cornstarch products, there is mobilization of fat stores. Fat is stored energy. Energy is stored as . . . triglycerides. So when there is substantial weight loss, there is a flood of triglycerides in the blood, and triglyceride levels in the midst of weight loss can commonly jump up, not uncommonly to the 200-300+ mg/dl range. When triglycerides go up, there is also a drop in HDL (triglycerides interact with HDL particles, modify their structure and make them more readily destroyed, thereby dropping blood levels). Occasionally, substantial weight loss like Brad experienced will drop HDL really low, as low as the 20's. Once weight stabilizes, this effect can last up to 2 months before correcting. Only then will triglycerides drop and HDL rise. The rise in HDL occurs even more slowly, requiring several more months to plateau. In other words, weight loss like Brad's causes triglycerides to increase and HDL to decrease, to be followed later by a drop in triglycerides and a rise in HDL. I know of no way to block this phenomenon. And perhaps we shouldn't, since this is how fat stores are mobilized and "burned off." Fish oil does blunt the triglyceride rise (perhaps through activation of lipoprotein lipase, an enzyme responsible for clearance of triglycerides), but doesn't eliminate it. I call these changes "transitional" changes in lipids. Patience pays. A few more months from now, Brad's numbers will be much happier, as will Brad.
Divorce court for the doctor-patient relationship? 10. August 2008 William Davis (4) The doctor-patient relationship has gone sour. This probably comes as no surprise to most of you, particularly if you've been following conversations here in The Heart Scan Blog:Who is your doctor? discussing the emergence of the physician-as-hospital-employee phenomenon that causes your doctor to become the de facto portal (seller?) of hospital services to you, a model fraught with conflicts of interest.(0)
Value of a zero heart scan score 27. March 2007 William Davis (1) Margaret is 73. She's a very good 73. She loves children and works full-time in a daycare. She manages her own household, goes to dinner at least once each week with one or more of her adult children. She is slender and has never been in the hospital--until she developed an abnormal heart rhythm called atrial fibrillation. Most people who develop atrial fibrillation do so with no immediate identifiable cause. However, Margaret has been a widow since her husband died 15 years ago of a heart attack. She was therefore especially frightened of any heart issues in her own health. Her doctor also raised the question of whether atrial fibrillation might represent the first hint of future heart attack. So we advised a CT heart scan. Score: zero, or no detectable plaque whatsoever. This put Margaret's risk for heart attack as close to zero as humanly possible. (Nobody is truly at zero risk for heart attack for a number of reasons. One reason is that people do irrational things like take cocaine or amphetamines, or they take too much decongestant medication, all of which can trigger heart attack.)The heart scan settled it. Margaret has the sort of atrial fibrillation which likely simply develops as a result of "wear and tear" on the heart's electrical impulse conducting system and it has nothing to do with coronary heart disease or heart attack. As that MasterCard commercial goes: Cost of a heart scan: About $200. Peace of mind: priceless.
You're at the cutting edge 26. March 2007 William Davis (3) If you're a participant in the Track Your Plaque program for atherosclerotic plaque regression, you are at the cutting edge of health. Few physicians give this issue any thought. Chances are, for instance, that if you were to bring up the subject of reversal of heart disease to your primary care physician, you'd get a dismissive "it's not possible," or " Yeah, it's possible but it's rare." Ask a cardiologist and you might make a little more progress. He/she might tell you that Lipitor 80 mg per day or Crestor 40 mg per day might achieve a halt in plaque growth or a modest reduction of up to 5-6%. If they've tried this strategy, they would likely also tell you that hardly anybody can tolerate these doses for long due to muscle aches. I'd estimate that 1 of 10 of my colleagues would even be aware of these studies. Both groups are, however, reasonably adept at diagnosing chest pain, an everyday occurrence in hospitals and offices. Chest pain, for them, is a whole lot more interesting. It holds the promise of acute catastrophe and all its excitement. It also holds the key to lots of hospital revenues. Did you know that 80% of all internal medicine physicians are now employees of hospitals? They're also commonly paid on an incentive basis. More revenues, more money. Ask Drs. Dean Ornish or Caldwell Esselstyn about reversal of heart disease and they will tell you that a very low-fat diet (<10% of calories)can do it. That's true if you use a flawed test of coronary disease like heart catheterization (angiograms) or nuclear stress tests (Ornish calls them "SPECT"). It would be like judging the health of the plumbing in your house by the volume of water flowing out the spigot. It flows even when the pipes are loaded with rust. In the Track Your Plaque experience, extreme low-fat diets (i.e., high wheat, corn, and rice diets) grotesquely exagerrate the small LDL particle size pattern, among the most potent triggers for coronary plaque growth. This approach also makes your abdomen get fatter and fatter and inches you closer to diabetes. Triglycerides go up, inflammation increases. If you were able to measure the rust in the pipes, that would be a superior test. You can measure the "rust" in your "pipes," the atherosclerotic plaque in your coronary arteries, using two methods: CT heart scans or intracoronary ultrasound. Take your pick. I'd choose a heart scan. It's safe, accurate, inexpensive. I've performed many intracoronary ultrasounds for people in the midst of heart attacks or some other reason to go to the catheterization laboratory. But for well people, without symptoms, who are interested in identifying and tracking plaque? That's the place for heart scans. In our program, 18-30% reductions in heart scan scores are common.
A stent--just in case 26. March 2007 William Davis (3) Burt came to me last week. He'd received a stent a few months earlier. He'd been feeling fine except for some fatigue. A nuclear stress test proved equivocal, with the question of an abnormal area of blood flow in the bottom (inferior wall) of the heart. "The doctor said I had a 50% blockage. Even though it wasn't really severe, he said I'd be better off with a stent, just in case."Just in case what? What justification could there be for implanting a stent "just in case"? (The artery that was stented did not correspond to the area of questionable poor blood flow on the nuclear stress test.)Just in case of heart attack? If that's the case, what about the several 20 and 30% blockages Burt showed in other arteries? The cardiologist was apparently trying to prevent the plaque "rupture" that results in heart attack by covering it with a stent. Why stent just one when there were at least 7 other plaques with potential for rupture?That's the problem. And that's why stents do not prevent heart attack (unless the stent is implanted in the midst of heart attack, when the rupturing plaque declares itself.) Of course, when no plaque is in the midst of rupturing, as with Burt, there's no way to predict which plaque will do so in future. Since only one plaque was stented, there is a 7 out of 8 chance (87.5%) that the wrong plaque was chosen. And that's assuming that there aren't plaques not detected by catheterization angiogram; there commonly are. The odds that the right plaque was chosen would be even lower. In other words, stenting one blockage that is slightly more "severely blocked" in the hopes of preventing heart attack is folly. If it's not resulting in symptoms and blood flow is not clearly reduced, a stent can not be used to prevent plaque rupture. A stent is not a device to be used prophylactically. It is especially silly when an approach like ours is followed, since plague progession is a stoppable process.Note: This issue is distinct from the one in which symptoms and/or an abnormal stress test show clearly reduced blood flow and flow is restored by implantation of a stent. While some controversies exist here, as well, a stent implanted under these circumstances may indeed provide some benefit.
How will you know your score dropped? 25. March 2007 William Davis (0) This issue came up twice this week. Bill is a busy accountant. Two years ago, just after the tumult of the 2005 tax season was over, he got a CT heart scan. His score: 398. At age 53, this was a significant score. His internist did the usual: prescribed a statin (Zocor), told him to cut the fat in his diet, and be sure to exercise. (Yawn.)Since then, Bill quit preparing tax returns and migrated to a less harried job in corporate accounting. It took two years since his heart scan for Bill to start thinking that perhaps his doctor's advice wasn't enough. If it was, he realized, everyone on a statin drug who made these minimal lifestyle changes would be cured of heart attack risk. Clearly not the case. So Bill enrolled in the Track Your Plaque program. Our first step: Get another heart scan. Bill was surprised. "Why another scan? I already had one!"I explained to Bill that atherosclerotic plaque is like money: it grows in percentages, just like money in a bank account or in a mutual fund. If, for instance, you deposit $500 in a mutual fund and it yields 5% return, then after one year you will have $550. One year later, you will have 5% x $550, or $605. Another year: $665. In other words, growth is not 10% of the original amount you deposited. Growth is compounded, year over year. That's why money, when compounded, can grow so quickly. Atherosclerotic plaque and your CT heart scan score do the same thing: they grow by a percentage of the current plaque quantity. In fact, we use the compound interest equation to calculate the annualized rate of plaque growth. But plaque grows at the extraordinary rate of 30% per year, on average. Imagine that was the rate of return on your money. You'd be the richest man or woman on earth. Back to Bill. Now Bill, in his defense, was on a statin drug and did make modest efforts towards a (mis-guided) low-fat diet and walking four days per week. If, on a second CT heart scan, his score was:398--No change. That's a success, since the expected rate of increase of 30% has been stopped. However, on his current program, this is highly unlikely. (I've seen it happen just once ever out of about 2000 people.) 250--Pop the cork on your champagne, because Bill needs to celebrate. He has substantially reversed his plaque. Highly unlikely on the current effort.525 --The score is higher by 30%, so it has slowed, but it surely hasn't stopped. This is the most typical result on the sort of program Bill is following. The message: Don't delay after your first heart scan score. It plaque grows like money with a huge return, there's no time like the present to take the steps to regain control.
Firefighters Face Added Risk of Fatal Heart Attack 22. March 2007 William Davis (1) Firefighters are twice as likely to die from a heart attack in the line of duty than are policemen, and three times more likely than EMTs. That's among the headlines run today because of a report in the New England Journal of Medicine documenting a dramatically higher risk for heart attack for fire fighters putting out fires. The above headline is from an excellent report run on NPR radio. You can listen to the webcast at http://www.npr.org/templates/story/story.php?storyId=9047656.The story sparked comments from experts insisting that all fire fighters should have physicals, should be in better physical condition, should be covered by health insurance (the NPR report said that 1 out of 4 fire fighters lack health insurance). Judging from the indisputable risk firefighters encounter, these are all good ideas. But if you've been following my blog or the Track Your Plaque program, you know that physicals alone are hopeless exercises for identifying hidden heart disease. Among the solutions: identify whether or not heart disease is present in the first place--do a CT heart scan. In fact, several local fire companies in my area have done just that: insisting that all firefighters undergo a heart scan. When groups of people like firefighters arrange for heart scans, they gain the advantage of doing so en masse, thereby allowing many scan centers to offer a dramatically reduced price to the city, town, or village that is paying for them. I've even seen many firefighters scanned at no cost. It would also help to have health insurance, be physically fit, and have a stress test (an exception to my view that stress tests are also useless to screen asymptomatic people for heart disease). But a CT heart scan would settle the question quickly, easily, undeniably, and inexpensively.
Prophylactic bypass surgery? 20. March 2007 William Davis (0) This question comes up around once a week:My CT heart scan score is ____. Wouldn't I be better off just getting a bypass (or stent, etc.) and getting it over with? If I know that heart attack is in my future, why not just get it over with?The most recent source of this question was the wife of a patient. Jack had a heart scan score of 92 in 2005. He made very little effort to correct his causes, permitting pre-diabetic patterns to persist, failed to correct vitamin D, etc. and a repeat heart scan score showed a dramatic rise to 264. Jack's wife asked whether he should just have a bypass. There are several problems with this line of reasoning:1) Bypass surgery does not reduce the long term risk for heart attack. 2) The risk of bypass surgery often outweighs the risk of an asymptomatic heart scan score. 3) Bypass surgery is a temporary "fix," a fancy Band Aid for a disease that progresses after the procedure. One bypass typically prompts another, and another...4) Bypassing arteries that have vigorous blood flow often causes the bypass graft to not "take" and close within the first few days. Thankfully, nobody in his right mind has proposed that we perform prophylactic bypass operations. Of course, hospitals and surgeons would jump at the chance to perform procedures in anybody with some threshhold heart scan score. It would double or triple their business overnight. At $70,000 or more per procedure, they would dance in glee. Of course, you and I would pay for their new burst of wealth by a sharp increase in our health insurance premiums. Not only that, the people who underwent the procedure would not benefit.
Lipitor 80 mg 20. March 2007 William Davis (4) I'm seeing more and more people taking 80 mg of Lipitor per day. For the most part, these are people who come in for another opinion after a stent or heart attack and are prescribed the drug during their hospitalization. This practice is based on the results of the PROVE IT-TIMI 22 (PRavastatin Or atorVastatin Evaluation and Infection Therapy-Thrombolysis In Myocardial Infarction) trial, and the Reversal of Atherosclerosis with Aggressive Lipid Lowering (REVERSAL) trial, both reported in 2005. In the PROVE IT Trial, 4,000 people experiencing heart attacks were treated with Lipitor (atorvastatin), 80 mg, or Pravachol (pravastatin), 40 mg. There was a reduction in events like recurrent heart attack from 13.1% in the Pravachol group to 9.6% in the Lipitor group. In the REVERSAL Trial, the Lipitor group also showed no plaque growth compared to the Pravachol group, which did progress, with disease tracked by intracoronary ultrasound.I believe that many of my colleagues took the bait. In a half-hearted effort to reduce events and trend towards better coronary plaque control, writing a prescription for 80 mg rather than a lower dose has become increasingly popular. Some problems: Despite the favorable tolerance to high dose Lipitor in these trials, I don't know anybody who can tolerate 80 mg per day for more than a few months in real life. In my experience, people inevitably end up with intolerable muscle aches. Also, I believe it is folly to believe that we can regress coronary plaque on a broad scale by just using one drug that addresses only a single cause (i.e., LDL cholesterol). Yes, drug companies would argue that the statin drugs are so wonderful because of their so-called "pleiotropic", or non-lipid, effects like reducing inflammation. I have seen regression of plaque once using Lipitor alone. We struggle to reduce coronary plaque using a multi-faceted approach. It is highly unlikely that Lipitor alone at a 80 mg dose will be sufficient in most people to regress plaque. How about lipoprotein(a)? Or vitamin D deficiency? Lipitor has no effect on these patterns and people do not regress just by taking statin agents.
Orlistat for weight loss 19. March 2007 William Davis (3) In early February, the FDA approved orlistat, formerly known as prescription Xenical, for over-the-counter sale. Orlistat is a blocker of fat absorption. The new OTC version will be called "Alli" (pronounced like "ally") and will come at a dose of 60 mg to be taken three times a day with meals. Prescription Xenical came as a 120 mg tablet. However, the company claims that the reduced dose sacrifices only 5% in reduced fat absorption, dropping from 30% with Xenical to 25% with Alli. It will cost in the neighborhood of $1 to $2 per day, or $30-60 per month, far less expensive than the $110-150 for the prescription form. Does it work? Is it worth the money? Clinical trials document around 5-10 lbs lost over a 3 to 6 month period, 50% greater than using diet and exercise alone. Our experience is that it works, though inconsistently. Results depend heavily on how reliant you are on fat calories. If you were to follow a low-fat diet while on the drug, you likely will lose little or no weight, since there's little fat absorption to block. However, I have witnessed more substantial weight loss of 10-20 lbs. in people who follow a higher fat intake in their diet, e.g., a traditional American diet. However, these people gain the weight back immediately because they've made no effort to modify food choices. It is messy. Even though the clinical trials claims modest inconvenient effects like gas and greasy stools, I have found that it is, without fail, a very annoying product that results in crampiness and frequent messy stools in nearly everybody.The company has created a glitzy website that you can view at www.myalli.com and promises to provide a personalized program and support for registrants when it is up and running by summer 2007. I think that's a good idea, since the drug itself is no more than a temporary fix unless it's combined with long-term diet changes. However, the website, I believe, oversells the value of the drug with a drug company's usual over-the-top hints and innuendoes without actually coming out with straight pitches of the truth. Beware of the vitamin D-blocking effect of Orlistat. The period of time you take it may be a time to resort to some modest sun exposure (10-15 minutes; be careful not to burn), rather than than oil-based vitamin D capsules, in order to avoid the inevitable vitamin D plunge in blood level. I am not a fan of orlistat, having seen it tried many times with minimal success. However, it is another option for those who are really struggling. Personally, I would try fasting or some of the other strategies we've detailed on the www.cureality.com website before I resorted to orlistat.