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 caus Toggle navigation Home Blog Home Archive Join Now Log in Self-empowerment is coming! 11. June 2006 William Davis (0) I've discussed this before: The coming wave of self-empowerment in health. Health that is driven by you, not a hospital, not a doctor, not by procedures, but by information and access to tools that are powerful and effective. The seeds are being planted right now and won't take full root for many years or decades. But it's going to happen. I previously cited several broad trends that are examples of this emerging wave:--The nutritional supplement movement. Contrary to the media's ill-informed bashing, nutritional supplements are getting better: improved quality, better substantiation of when/how to use them, new agents that appear rapidly, since introduction is not slowed by the molasses of the FDA.--Medications moving to over-the-counter status. Health insurers are driving this one. OTC means not paid for by insurance. That also means access to you. --What I call "retail imaging", i.e. screening ultrasound, heart scans, full body scans, etc. that are available in most states without a doctor's order.--The Internet. The mind-boggling rapidity and depth of information available on the Internet today is fueling the self-empowerment movement by providing sophisticated information to health care consumers. Information here is uneven at present. But, as consumer sophistication increases and the system of checks and balances evolves, internet-driven information will be often superior to what you get from a doctor or other health professional.--High-deductible health insurance plans. If health care consumers bear more and more of the costs of health care, they will seize greater responsibility for early identification and prevention and minimize long-term costs.This trend does not mean treating your own infection, taking out your own gall bladder, repairing your own broken leg. It means that conventional routes of health delivery will recede into providing only catastrophic care. It means that you and your family will take a larger role in learning how to eat and exercise properly, use foods to maintain and promote health (the "designer food" and "nutraceutical" movement), take supplements that have real benefits, use medications for treatment of many everyday ailments. It also means seizing control of diseases that previously were only treated in hospitals, like coronary heart disease. This, of course, is where our program, Track Your Plaque, is an example of how you can have a powerful and effective role in your heart health. Track Your Plaque goes so far beyond the "eat low-fat, exercise, and know your numbers" media mantra that it's like comparing a brand-new Mercedes to a rusted, run-down '87 Ford Escort. There truly is no comparison. (Sorry if you're an Escort driver!) But you get the idea. Another option for lipoprotein testing 9. June 2006 William Davis (0) For those of you who have been frustrated in trying to get your lipoprotein analysis performed, here's another option. The Life Extension Foundation at www.lef.org provides access to the VAP test, or Vertical Auto Profiler. This is the lipoprotein test run by the Atherotech company in Birmingham, Alabama. The name refers to the method used, a form of centrifugation, or high-speed spinning of your blood (plasma) to separate the various components by density. This is a fine technique that works well. Though our preferred method is NMR (www.Lipoprofile.com, Liposcience Inc.), the Atherotech VAP is a reasonable alternative. If you go through the Life Extension process, they will direct you to blood draw sites in your area. They charge $185 for Life Extension members, $247 for non-members. (Membership in Life Extension costs $75.) Drawback: No billing for health insurance reimbursement. A full description of the significance of lipoproteins can also be found in my article posted on-line at the www.lef.org website at http://www.lef.org/magazine/mag2006/may2006_report_heart_01.htm Weight and lipoproteins 8. June 2006 William Davis (0) Tom, an accountant, came into the office eager to know what his 2nd heart scan score showed. A year ago, Tom's view of himself as a healthy, middle-aged man was shattered when he found out his heart scan score: 1236. Tom had severe coronary plaque with a heart attack risk of 25% per year (without intensive preventive action). In the way of lipoprotein abnormalities, he had several: low HDL, deficient large HDL, small LDL, high triglycerides, IDL (the after-eating inability to clear dietary fats), and a high blood sugar in the pre-diabetic range. In addition, Tom was hypertensive, with blood pressure so high it even landed him in the emergency room last winter. In addition to our approach to correct all these patterns, Tom was urged to lose a significant quantity of weight. Starting at 225 lb., at 5 ft 7 inches, Tom was clearly at least 40 lbs over his ideal weight. I stressed to Tom that the entire spectrum of causes of coronary plaque were weight-related. I likened his patterns to throwing gasoline on a fire: As weight increased, his lipoprotein and other abnormalties flared dramatically. But each time Tom came back to the office over the ensuing year, he'd gained another 3 to 6 lbs. And each time he had an explanation. "My daughter just got married. I couldn't turn down wedding cake, now could I?" Or, I just survived another tax season. I was working day and night--no time for exercise!" "It's getting too hot to walk anymore." Well, despite multiple treatments, Tom's repeat heart scan showed a score of 1677, a 35% increase. That's a dangerous rate of growth that virtually guarantees that plaque is building up momentum to "rupture", which results in heart attack. I therefore stressed to Tom that weight loss was crucial. Control of coronary plaque was simply not going to occur without weight loss to our target. Alternatively, we could add several new prescription medicines and hope that they could achieve the same effect, though at a price (side-effects, expense). I tell Tom's story to highlight again just how important weight loss can be for a number of lipoprotein abnormalities. What measures specifically are sensitive to weight? They are:--HDL cholesterol--Triglycerides--Small LDL--VLDL--Blood pressure--Blood sugar and insulin--C-reactive protein--LDLWeight exerts profound influence on these patterns. In Tom and people like him, weight can be a "make it or break it" issue. If you, like Tom, have any of the above patterns, consider weight loss as a potent tool you can use to gain control of coronary plaque. Variation in vitamin D requirements 7. June 2006 William Davis (0) For Track Your Plaque followers, you know we are very concerned about vitamin D blood levels. My prediction is that, in 10 years, vitamin D will be regarded as an important item on the list of coronary artery disease risk factors. In our experience of trying to stop or reverse heart scan scores, restoration of vitamin D to a blood level of 50 ng/ml appears to have increased our success rate dramatically. As we've talked about before, on the bell curve of vitamin D dosing in a northern climate, the majority of women require 2000 units per day, men require 3000 units per day to achieve a level of 50 ng. However, there are "outliers" on this bell curve, i.e., people who require much more or much less.This week, I saw two people who were very instructive cases of extreme requirements on the high end of vitamin D dosing. Both started with unmeasurable blood levels, i.e., essentially zero ng/ml. On 5000 units of vitamin D per day, both raised their blood levels to around 17-18 ng/ml--in the range of severe deficiency (defined as <20 ng/ml). I advised both to increase their oral dose of vitamin D to 8000 units per day. Notably, both people avoided sunlight and lived in Wisconsin, a terribly sun-deprived locale 10 months a year. Both were also substantially overweight (around 300 lbs each). The vitamin D issue continues to be endlessly fascinating in all its nuances and twists. Heart attacks in your own backyard 7. June 2006 William Davis (0) Two men from my community just died of heart attacks. Both were in their 40s. What bothers me most about these all too frequent stories is that it is so preventable. You can bet that both had little or no symptoms prior to their deaths. You can also bet that they've had cholesterol panels taken by their doctors. Followers of the Track Your Plaque program know that these are sure-fire paths to failure. The absence of heart disease symptoms should provide no reassurance whatsoever. High cholesterol, in-between cholesterol, low cholesterol--none are confident indicators in a specific individual.Stress test? How about the patient I saw today who, until I met him, had been undergoing stress test after stress test, every year--all while the quantity of coronary plaque tripled. False reassurances provided by his cardiologist led him to believe that all was well--while this stack of oily rags was just waiting for the spark to ignite. Too little time, too much money, too far away--there's a hundred excuses for not getting a heart scan. Or, you've had a heart scan and no one can tell you what to do about it. If you're reading this, however, you've found the most intensive source of information available on how your heart scan can serve as the start of a program of heart attack prevention for a life free of dangers. It's not that tough. But it won't just go away on its own. I just have to look around me in my own community, watch the local news, talk to friends, and I'll heart about all the people just in my neighborhood who should be learning these lessons. I rant and rave about this but some people need to hear it from a friend, colleague, neighbor, rather than some crazy doctor bucking the standard line. You, too, should be telling anyone who will listen about how heart disease can be identified and controlled. Pilot lands safely after heart attack, then dies 6. June 2006 William Davis (1) That was the disturbing headline on a report from MSNBC, also reported nationally on all the major news networks. The story goes on:"A pilot suffering a heart attack made an emergency landing on a highway, saving his three passengers shortly before he died...He landed the single-engine Cessna 185 on Utah 30 near Park Valley and was taken to Bear River Hospital in Tremonton, where he died."We track these sorts of stories and it's frightening just how common they are. A school bus driver recently had a heart attack while driving 30 children; the bus crashed but no one was hurt. A 52-year old commercial bus driver suffered a heart attack while transporting 49 conference attendees; the bus plunged 400 feet down a ravine. Remarkably, 17 passengers suffered only minor injuries and there were no deaths. There have even been incidents where the pilot of a jet liner suffered a heart attack in-flight. In 2000, the 53-year old pilot of a Northwest Airlines DC-10 died while in-flight from a heart attack while landing in Minneapolis. The 290 passengers were landed safely by co-pilot. Most incidents where the driver or pilot has been incapacitated or died resulted in the deaths of only a handful of people. No major catastrophe has yet occured. But--mark my words--it will. These incidents just happen too frequently. Virtually all of these and similar incidents could have been prevented. If the FAA, for instance, would insist that all pilots have a simple CT heart scan, it would become immediately obvious which pilots should be grounded and who should fly. Similar requirements could easily be applied to persons in charge of the welfare of many people, most notably school bus drivers. It's not that tough! The FAA currently requires stress testing and cholesterol testing. Well, guess what? Followers of the Track Your Plaque program know that these tests do not effectively identify the person at risk for heart attack in the majority of individuals. Just ask former President Bill Clinton how helpful his stress tests (five in a row!) were. Or how valuable his cholesterol monitoring was--all prior to his emergency bypass surgery. Large new clinical study launched to study. . .niacin 5. June 2006 William Davis (3) Oxford University has issued a press release announcing plans for a new clinical trial to raise HDL cholesterol and reduce heart attack risk. 20,000 participants will be enrolled in this substantial effort. The agent? Niacin.How is that new? Well, this time niacin comes with a new spin. Dr. Jane Armitage, formerly with the Heart Protection Study that showed that simvastatin (Zocor) reduced heart attack risk regardless of starting LDL, is lead investigator. She hopes to prove that niacin raises HDL cholesterol and thereby reduces heart attack risk. But, this time, niacin will be combined with an inhibitor of prostaglandins that blocks the notorious "flushing" effect of niacin. The majority of Track Your Plaque participants hoping to control or reverse coronary plaque take niacin. Recall that niacin (vitamin B3)is an extremely effect agent that raises HDL, dramatically reduces small LDL, shifts HDL particles into the effective large fraction, reduces triglycerides and triglyceride-containing particles like IDL and VLDL. Several studies have shown that niacin dramatically reduces heart attack. The HATS Study showed that niacin combined with Zocor yielded an 85-90% reduction in heart attack risk and achieved regression of coronary plaque in many participants.In our experience, approximately 1 in 20 people will really struggle using niacin. Flushes for these occasional people will be difficult or even intolerable. Should Dr. Armitage's study demonstrate that this new combination agent does provide advantages in minimizing the hot flush effect, that will be a boon for the occasional Track Your Plaque participant who finds conventional niacin intolerable. But you already have access to niacin, an agent with an impressive track record even without this new study. And you have a reasonably effective prostaglandin inhibitor, as well: aspirin. Good old aspirin is very useful, particularly in the first few months of your niacin initiation to blunt the flush. Although this study is likely to further popularize niacin and allow its broader use, it's also a method for the drug companies to profit from an agent they know works but is cheap and available. You don't have to wait. You already have niacin and aspirin available to you. The dark side of CT heart scans 4. June 2006 William Davis (0) "I just got a heart scan!" declared Eric to his doctor. He handed the report to him."Oh my. Your score is 154." The doctor paused, then looked at Eric with a serious look on his face. "If we're going to understand whether or not you're in danger, you'll need a heart catheterization."I've seen this happen countless times. How can I say this diplomatically? THIS IS WRONG!! In my view, it's absolutely criminal for this to happen. Physician ignorance, profiteering, whatever--it is wrong. There's very few reasons why someone who has no symptoms should go directly to the cath lab for a procedure. (A rare exception might be an exceptional quantity of plaque in the left mainstem artery, e.g., >100. This is highly unusual.)Even a nuclear stress test (e.g., thallium) at this level of scoring is only 10-15% likely to be abnormal. That means 85-90% likelihood of being normal. There's rare reasons to perform a heart catheterization in a person with no symptoms and an entirely normal stress test. The vast majority of people like Eric do not need a heart catheterization to discern risk. If Eric's doctor had been up-to-date on the published literature on the prognostic value of heart scans, he could have advised Eric what the risks were--without a catheterization. Many doctors simply don't want to be bothered. Or, they opt for the more profitable method--a hospital procedure.Always discuss your heart scan with your doctor--but be armed with information in case your doctor is uninformed or unscrupulous. Unfortunately, that's not uncommon. The Track Your Plaque program is your advocate, a source for unbiased information. The dirty little secret about aneurysms 2. June 2006 William Davis (1) Jake had an abdominal aneurysm identified--by accident. While getting a CT scan of his abdomen for unexplained abdominal pain, a 4.4 cm aneurysm was discovered. Jake's abdominal pain eventually passed without explanation, but he was left with this aneurysm.Jake's primary care doctor referred him to a surgeon. "It's too small to require surgery right now. Wait a few years and it'll probably get bigger. When it gets to around 5.5 cm, that'll be the time to operate. Let's schedule an abdominal ultrasound or CT scan every 6 months."Jake then got himself a heart scan. His high score of 879 then led him to my office. Lipoprotein testing, a stress test, correction of his lipoprotein patterns, changes in lifestyle followed. One year later, Jake's heart scan score was unchanged. How about his abdominal aneurysm? 4.2 cm--a modest quantity of regression. When Jake's surgeon learned of the change, he just shrugged. "Okay, we'll just watch it from here."Shockingly, the conversation surrounding aneurysms is just like the one Jake received: Let's just watch it grow until you need surgery. If you've every seen anyone have abdominal aneurysm surgery, you know it is an awful, painful, barbaric process with high risk for major complications like kidney failure and loss of the legs. Waiting for an aneurysm to grow is a lousy solution. Surgeons point out that, although surgery is imperfect, it's better than the alternative: rupture, which is catastrophic with a 50% chance of dying. But what about stopping the growth of the aneurysm? Or even reversing, or shrinking, it? Surgeons say it can't be done. Yet we've done it--many times. And it's not that difficult. The steps to take are very similar to that in the Track Your Plaque program for coronary plaque regression, with a few different strategies. Suppression of inflammation, for instance, plays a more important role and blood pressure must be abolutely normal, even during exercise. More to come on this important topic in the future, including an upcoming Special Report on the www.cureality.com membership website. Heart scan scores dropping like stones!! 1. June 2006 William Davis (0) I saw two instances of dramatic coronary plaque regression today. John, a 53-years old mechanical lift operator, dropped his heart scan score from 479 to 323--a 32% regression of coronary plaque volume! Eric, a 50-year consulting engineer, dropped his heart scan score from 668 to 580--a 13% reduction. Both men did nothing special beyond the principles advocated in the Track Your Plaque program. Recall that, without preventive efforts, your heart scan score is expected to increase by 30% per year. Both men are well on their way to freedom from risk of coronary "events". Two less people to feed the revenue-hungry hospital procedure system! We need many more like them. << Older posts Newer posts >> Newer posts12...113114115116117118119120121...123124Older posts All posts by william-davis Toggle navigation Home Blog Home Archive Join Now Log in Optimal medical therapy 9. April 2007 William Davis (6) I was re-reading some of the details behind the recently announced COURAGE Trial comparing angioplasty/stent in 1100 people compared to "optimal" medical therapy in another 1100. You'll recall that no difference was found. In particular, over approximately 5 years, 20% of participants in each group died, experienced heart attacks, or strokes. Of those treated with "timal" medical therapy, 32% ended up getting a procedure like stents or bypass anyway due to deteriorating symptoms. What is "optimal" medical therapy? I bring this up again because the study investigators in COURAGE, as well as in similar trials, say this with a straight face. Optimal medical therapy means aspirin and/or Plavix (the anti-platelet, aspirin-like blood thinner); "aggressive" statin drug therapy to reduce LDL cholesterol to 60-85 mg/dl; and "anti-ischemic" therapy (that reduces angina and the phenomena of poor coronary blood flow) using nitroglycerin preparations, beta blockers, and other drugs. I do give credit to the investigators for having the courage to perform this trial in a world hell bent on doing procedures and still reporting the neutral outcome. But the notion of "optimal" medical therapy begs for comment. Indeed, this is regarded as optimal by most practitioners. Some would even argue excessive, based on the low LDL target achieved. Would you be satisfied with a 20% likelihood of heart attack, stroke, or death or 5 years, a 1 in 5 roll of the dice? I would not. Recall that we aim for near-total elimination of risk. What could have been further "optimized"? Plenty. For instance:--What is the real LDL, not the fabricated, calculated LDL? The two can be commonly 100 mg/dl different. --How about raising HDL to 60 mgd/? --What about reducing the proportion of small LDL particles? After all, small LDL is the number one cause of heart disease in the U.S., not high LDL.--What is Lp(a)? If you treat LDL with a statin drug, Lp(a) is unaffected and continues to trigger huge plaque growth. You will fail if this is not identified and corrected. --What is vitamin D3? One of the most powerful facilitators of plaque reversal I know of. --What are triglycerides? Triglycerides create hidden particles in the blood like intermediate-density lipoprotein, potent triggers for coronary plaque growth. Speaking of intermediate-density lipoprotein, that's another very important pattern to identify, the after-eating persistence of dietary fats. --Why aren't they taking fish oil? With a 28% reduction in heart attack and 45% reduction in sudden death from heart attack, this alone would have halved the number of "events" in the "optimal" medical treatment group. Of course, there's more. But the idea that aspirin, statins, and anti-ischemic therapy is somehow optimal is silly and sad at the same time. But that's the bias. The COURAGE Trial does represent a step forward, a step away from the "stent everyone and everything" mentality that motivates my colleagues, aided and abetted by their co-conspirators, the hospitals. But you and I know better. "Optimal" medical therapy, in truth, can mean a far better approach that can dramatically reduce, perhaps eliminate, risks for events like heart attack. The conventional "optimal" medical therapy will suffice only if you're content with a 20% likelihood of heart attack, death or stroke, or a 32% likelihood of an urgent procedure in your future. Niacin, postprandial patterns 9. April 2007 William Davis (0) For a detailed report on the very important postprandial (after eating) patterns that contribute hugely to heart disease risk, read my recent article in Life Extension Magazine, available (no cost) at: Uncovering a Hidden Source of Cardiovascular Disease Risk at http://www.lef.org/magazine/mag2007/mar2007_report_heart_01.htmFor a report on using niacin to reduce risk of heart disease, see another report in the same issue of Life Extension:Ask the Doctor: Using Niacin to Improve Cardiovascular Health at http://www.lef.org/magazine/mag2007/mar2007_atd_01.htm.Also, keep your eyes open for a lengthy report focused exclusively on the Track Your Plaque program in an upcoming issue of Life Extension. I'll provide links in this Blog when it comes out. What's better than fish oil? 9. April 2007 William Davis (1) One of the recent questions on our Track Your Plaque Forum related to what to do about a triglyceride level of 101 mg/dl while on fish oil.Recall that, contary to conventional thinking like that articulated in the ATP-III cholesterol treatment guidelines, we aim to reduce triglycerides to 60 mg/dl or less. This is important to suppress the formation of abnormal triglyceride-containing lipoprotein particles, especially small LDL, reduced HDL, lack of healthy large HDL, VLDL. ATP-III advises a level of 150 mg/dl or less. Unfortunately, triglyceride levels this high guarantee appearance of all these undesirable particles and an increasing heart scan score. What's better than 4000 mg of fish oil for its 1200 mg of EPA and DHA (omega-3 fatty acids)? More fish oil. In other words, the 4000 mg fish oil providing 1200 mg EPA + DHA is our minimum. A simple increase to 6000 mg to provide 1800 mg EPA + DHA is usually all that is necessary to reduce triglycerides and put a halt to the cascade of abnormal lipoprotein particles that trigger plaque growth. Occasionally, a somewhat higher dose may be required. Doses are best divided into two, with meals (e.g., three capsules twice a day).Another important issue: An over-reliance on wheat products can also increase triglycerides. This includes any flour product like breads (regardless of whether it's white, whole wheat, or whole grain--they all raise triglycerides), pretzels, bagels, breakfast cereals, and pasta. A dramatic reduction in wheat-containing products will reduce triglycerides substantially, help you reduce your abdominal fat, reduce blood pressure, raise HDL and reduce small LDL, clear your mind, provide more energy, avoid afternoon "fogginess" . . . Huge benefits. Valve disease and vitamin D 8. April 2007 William Davis (1) There are two common forms of heart valve disease: aortic valve stenosis (stiffness) and insufficiency (leakiness), and mitral anular calcification. Both valve issues are regarded as evidence of senescence, or aging--the older you are, the more likely you will have one or both. Both conditions involve progressive calcium deposition and, to some degree, cholesterol deposition. They might be regarded as phenomena of "wear and tear" just like hip arthritis. There are no known therapies to stall or stop the development of mitral anular calcification. However, several attempts have been made over the years to identify treatments that can slow or stop the progression of aortic valve disease, which is becoming increasingly common and is addressed by surgical valve replacement when severe. The most recent trials have examined whether high-dose Lipitor (80 mg) has any effect (it did not) and high dose Crestor (40 mg), which slowed but did not stop the deterioration of stiff valves. It's been my suspicion that vitamins D and K2 may play a crucial factor in valve health. After all, vitamin D is the master controller of calcium deposition. Preliminary data also suggest that people who are intentionally made vitamin K deficient with the drug, Coumadin, develop twice the calcium deposition on aortic valves that non-Coumadin takers develop.I saw a patient Friday, Marianne. In addition to a moderate heart scan score of 379 at age 71, Marianne had a leaky (insufficient) aortic valve. By an echocardiogram 18 months ago, the valve was moderately leaky. I put Marianne on vitamin D, 4000 units, to raise her blood level to 50 ng/ml. Last week, I asked Marianne to have another echocardiogram. This time, no leakiness whatsoever--none. I have never seen this happen before. Although Marianne is only one example and we don't want to extrapolate too far from the experience of one person, it's hard not to attribute this phenomenal response to vitamin D supplementation. I wonder what would have happened if we had added vitamin K2, as well?Anyway, just another potential wonderful effect of vitamin D restoration. Homocysteine and coronary plaque 8. April 2007 William Davis (4) If you’ve watched the news over the past year, you know that doubt has been cast over the idea that reducing homocysteine blood levels with high doses of B vitamins (B6, B12, and folic acid, or B9) results in reduced risk for heart attack. Is the homocysteine concept dead? Shall we empty our bottles of costly B vitamins into the trash and move on?I don’t think so. As detailed in one of our Track Your Plaque Special Reports from a few months ago, I think the homocysteine issue still deserves lots of respect and further investigation. After all, hundreds of clinical studies have connected higher homocysteine levels with greater risk for heart disease, stroke, and aneurysm. Numerous studies, for example, have repeatedly and consistently demonstrated a tripling of heart attack risk when homocysteine levels exceed 14 ?mol/l. Can we dismiss this association because several more recent studies—NORVIT, HOPE, and VISP—suggested that, when starting homocysteine levels are 12.5, that B vitamin supplementation does not reduce heart attack risk?I think there’s lots more to know about the homocysteine connection. That said, I have never seen a patient who I thought had heart disease strictly because homocysteine was increased.I believe that we can at least use homocysteine as an index of lifestyle: the higher the homocysteine, the poorer the diet, or the less effective the absorption of B vitamins (especially vitamins B12 and folic acid). Homocysteine levels of <9 micromol/l suggest both adequate intake and absorption of these B vitamins. If homocysteine is tightly connected with risk for heart disease, yet supplementation of B vitamins fails to reduce risk, might there be another means of connection? Or, could both homocysteine and heart disease be connected in some way that has nothing to do with B vitamins? Don’t close the book on homocysteine. Just because conventional experience fails to draw connection does not necessarily mean that none exists. If it’s any consolation, taking B vitamins has been correlated with better memory, concentration, and other health benefits, even if no reduction in heart disease develops. Big heart scan scores drop 6. April 2007 William Davis (0) High heart scan scores of, say, greater than 1000 are more difficult to reduce than lower scores. I learned this lesson early in the experience of trying to drop scores. In the first few years of trying to drop scores, I saw relatively modest scores of 20, 50, or 100 drop readily, even when the usual targets were not fully achieved, and even before the incorporation of some of the more exciting recent additions to the Track Your Plaque program, like vitamin D.But big scores of 1000, 2000, or 3000 are a tougher nut to crack. In the first few years, what I usually saw was a slowing , or "deceleration," of growth from the expected rate of annual score increase of 30% that would continue for a year or two, followed by zero change. In the first year of effort, for example, a score increase of 18% was common. 10% was common in year two, then finally zero change in year three. Somehow, the more plaque you begin with, the more "momentum" in growth is present and the longer it takes to stop it. Kind of like stopping a compact car versus stopping a freight train. But more recently, I'm seeing faster drops. Today, Charlie came to the office to discuss his second heart scan. 18 months earlier, Charlie's first scan showed a score of 3,112, high by anybody's standard.His repeat score: 3,048. While the drop is relatively small on a percentage basis and may even fall within the expected rate of error for heart scans (which tends to be <2% at this high a score), I told Charlie that it still represented a huge success. Not only did he not increase his score by the expected 30% per year, he also brought a charging locomotive to a rapid stop. Next year, Charlie is targeting a big drop. Given the tools he now has available, I'm optimistic that he will succeed. Watch for the Track Your Plaque May, 2007 Newsletter in which we will detail Charlie's story further. Does the American Heart Association diet reduce heart disease? 5. April 2007 William Davis (0) If you have a heart attack and land in the hospital where, invariably, you will have a heart procedure. Or, if you get a stent or coronary bypass operation, sometime before your discharge from the hospital, a well-meaning hospital staff dietitian will provide instruction in the American Heart Association (AHA) diet. Does this diet reduce the risk of heart disease?The answer depends on where you start. If you begin with a conventional American diet that is enormously influenced by convenience, food manufacturers like Nabisco, General Mills, Quaker Oats, ADM, and Cargill, or food distributors like McDonald’s, Pizza Hut, and Taco Bell, then the American Heart Association diet is indeed an improvement. But just a small one. If LDL cholesterol is the yardstick, the average reduction in LDL is between 10 and 15 mg/dl. This is the same amount of change you’d experience by adding 1 tablespoon of oat bran to your diet. Hardly worth boasting about. HDL, triglycerides, blood glucose, and body weight do not change. The diet could be substantially better. After all, it’s become common knowledge that other diets, such as the so-called Mediterranean diet, the South Beach Diet, and similar broad projects result in far greater changes than the AHA diet dispensed by your hospital and cardiologist. These diets more effectively reduce LDL, raise HDL, reduce triglycerides, reduce C-reactive protein, reduce blood pressure. Diets like South Beach also yield substantial weight loss and reversal of diabetic tendencies, with the magnitude of benefit dependent on the amount of weight lost. Why this stubborn adherence to the outdated concepts articulated in the AHA diet? Cardiologists would argue that insufficient data has been generated to permit widespread application of these diets. They also differ on whether they really work. Of course, the majority remain ignorant and dismiss them as fad diets. A little digging into the financial disclosures of the AHA suggests another, more malignant influence: who is paying the bills? Until recently, drug manufacturers were major contributors to the AHA. However, more recently AHA administrators have become sensitive to the public perception that they might be nothing more than a voice box for the drug industry. They have since limited contributions from the drug companies to 8% of annual charitable revenues. The drug manufacturers have been replaced by the food industry. In addition to food manufacturers that make the cereals on your grocery shelf, it includes the multi-national conglomerates that produce unimaginable revenues and carry enormous political clout, like ADM and Cargill. Ever wonder how it is that Honey Nut Cheerios received a “Heart Healthy” endorsement from the AHA? The AHA diet does not provide the answers we’re looking for, not even close. It is a perversion from an organization that has its strings pulled by industry. The answers to health will not come from the AHA, AMA, the American College of Cardiology, the American Hospital Association, and it won’t come from your doctor. It won’t come from a titillating report on the evening news or Good Morning America. It will come from collective and expanding wisdom placed directly into the hands of the public. It will be untainted by the temptation of drug industry dollars. It will not be dirtied by million dollar contributions, or the multi-million dollar behind-closed-doors lobbying of the food manufacturers. It will come from the truth relayed to the healthcare-consuming public. I hope you recognize it when you see it. If you want a healthy diet for your heart, throw away the pamphlets from the AHA unless you are partial to bread, breakfast cereals, corn, and the supporters of their misguided nutritional advice. Vitamin K2 and coronary plaque 4. April 2007 William Davis (1) The vitamin K2 story, though still preliminary, is becoming increasingly interesting from the perspective of CT heart score reduction. The origin of this concept came from some unexpected observations. One, the observation that osteoporosis (lack of bone calcium that leads to fractures) arises from deficiency of vitamin K2. Two, deficiency of K2 leads to unrestrained calcium deposition in animal models, leading to heart attack in just weeks. Vitamin K2 has been largely ignored for years, since the more widely understood K1 is rarely deficient. K1 deficiency can occur from prolonged antibiotic use, or from severe malnutrition. But deficiency in otherwise well people is very uncommon. Vitamin K2, however, may be a different story. Deficiency may be common.The Rotterdam Heart Study of cheese-eating Dutch showed that greater K2 intakes resulted in a halving of heart attacks. Cheese (traditional varieties, not Velveeta or other make-believe cheese products) is a modest source of K2, as is the Japanese native food, natto. (If you've ever seen natto, I dare you to eat it. I have a pretty strong stomach and curiousity for food, but natto is the one thing I could not eat--it is truly horrible.)The weight of evidence suggests that vitamin K2 supplementation may prove to be a useful addition to your coronary plaque control program. Clearly, more data are needed, particulary therapeutic obserations, i.e., observing people who take dose X of a K2 prepartion and tracking some feedback measure, e.g., bone density, CT heart scan score, "events" like heart attack, etc. Nonetheless, the K2 story is clearly worth reading about, perhaps even considering supplementation. Please watch for the Special Report on the www.cureality.com website in the coming days. Exercise and blood pressure 4. April 2007 William Davis (5) The media has gotten a hold of a case report from the University of Maryland describing a 51-year old physician who, despite being a long distance runner, had a high heart scan score. An example of the report can be found at Heart Disease In A Marathon Runner: Is Too Much Exercise A Bad Thing?http://www.sciencedaily.com/releases/2007/03/070315091100.htm in Science Daily."The mystery was all the more intriguing because his resting blood pressure and fasting cholesterol levels, the usual measures of cardiovascular health, were in the normal range."When this man was put on a treadmill for a stress test, his blood pressure skyrocketed from a normal 118/78 to 230/78--extremely high, even for exercise. The physicians reporting the case raised the question of whether long-distance running represents a risk for heart disease and if the high blood pressure with exercise is a contributor or cause of the high heart scan score. These are phenomena we are very familiar with. We have stressed the importance of exercise blood pressure as a trigger for coronary plaque for years. While 230/78 is clearly too high, we find that any blood pressure over 170/80 with exercise adds to the fire and can trigger plaque growth. However, I think it is absurd to suggest that marathon running itself is a trigger of coronary plaque. I think it is far more likely that the person described in the report had lipoprotein(a), a potent trigger for both exercise-induced hypertension and high CT heart scan scores in seemingly well people. He likely also suffered from a deficiency of vitamin D deficiency, another contributor. There's no need to indict exercise. If you are in the Track Your Plaque program, you know that stress tests are of questionable helpfulness for the detection of hidden heart disease. But they are useful for assessment of blood pressure responses during exercise. If BP exceeds 170/80 at 10 mets (a measure of exercise effort achieved by walking 3.4 mph at a 14% grade for 3 minutes), then blood pressure may be a contributor to your heart scan score. "Fish oil is stupid" 3. April 2007 William Davis (13) "Fish oil is a waste of time and money. It's stupid. Just stop it."So a patient of mine was advised by another physician when he complained that he occasionally experienced a fishy aftertaste. This attitude perplexes me. After all the confirmatory data that support the enormous health benefits of omega-3 fatty acid supplementation, including the 11,000 participant GISSI-Prevenzione Trial, you'd think this attitude would be history. What's a little fish aftertaste when heart attack risk is slashed 28%? Perhaps the tendency to pooh-pooh fish oil is because it's available as a nutritional supplement. This shouldn't make fish oil appear inconsequential. Far from it. If you witness the extraordinary power for fish oil to reduce triglycerides, you will be immediately convinced of its effectiveness. The ability of omega-3 fatty acids from fish to eliminate intermediate-density lipoprotein (IDL), the persistent abnormal lipoprotein which signals an inability to clear dietary fats from the blood, can also convince you. More than 90% of people with excessive IDL have it completely eliminated by 4000-6000 mg of fish oil (providing 1200-1800 mg EPA + DHA) per day. The fact that fish oil is available as a prescription "medication," as well as an over-the-counter supplement, causes some physicians to dismiss the power of the supplemental form. This is nonsense. The over-the-counter form is every bit as effective as the prescription form. The makers of prescription Omacor also make the claim that their preparation is safer and purer. That may be true, but I'd like to see independent verification from the FDA, USDA, or an unbiased organization like Consumer Reports before I accept their marketing as fact--particularly at $120 to $240 per month! If Omacor proves to contain substantially less mercury and pesticide residues, then that will need to be factored in. (Please note that both Consumer Reports and Consumer Labs measured no substantial mercury or pesticide residues in their analyses of 16 and 41 brands, respectively.) I try to persuade my colleagues that the idea of taking supplements is a wonderful trend that allows people to express ownership of their own health. What people need is guidance, not salesmanship for a more expensive version, nor dismissal of nutritional preparations that actually possess considerable benefits. << Older posts Newer posts >> Newer posts12...878889909192939495...121122Older posts
Self-empowerment is coming! 11. June 2006 William Davis (0) I've discussed this before: The coming wave of self-empowerment in health. Health that is driven by you, not a hospital, not a doctor, not by procedures, but by information and access to tools that are powerful and effective. The seeds are being planted right now and won't take full root for many years or decades. But it's going to happen. I previously cited several broad trends that are examples of this emerging wave:--The nutritional supplement movement. Contrary to the media's ill-informed bashing, nutritional supplements are getting better: improved quality, better substantiation of when/how to use them, new agents that appear rapidly, since introduction is not slowed by the molasses of the FDA.--Medications moving to over-the-counter status. Health insurers are driving this one. OTC means not paid for by insurance. That also means access to you. --What I call "retail imaging", i.e. screening ultrasound, heart scans, full body scans, etc. that are available in most states without a doctor's order.--The Internet. The mind-boggling rapidity and depth of information available on the Internet today is fueling the self-empowerment movement by providing sophisticated information to health care consumers. Information here is uneven at present. But, as consumer sophistication increases and the system of checks and balances evolves, internet-driven information will be often superior to what you get from a doctor or other health professional.--High-deductible health insurance plans. If health care consumers bear more and more of the costs of health care, they will seize greater responsibility for early identification and prevention and minimize long-term costs.This trend does not mean treating your own infection, taking out your own gall bladder, repairing your own broken leg. It means that conventional routes of health delivery will recede into providing only catastrophic care. It means that you and your family will take a larger role in learning how to eat and exercise properly, use foods to maintain and promote health (the "designer food" and "nutraceutical" movement), take supplements that have real benefits, use medications for treatment of many everyday ailments. It also means seizing control of diseases that previously were only treated in hospitals, like coronary heart disease. This, of course, is where our program, Track Your Plaque, is an example of how you can have a powerful and effective role in your heart health. Track Your Plaque goes so far beyond the "eat low-fat, exercise, and know your numbers" media mantra that it's like comparing a brand-new Mercedes to a rusted, run-down '87 Ford Escort. There truly is no comparison. (Sorry if you're an Escort driver!) But you get the idea.
Another option for lipoprotein testing 9. June 2006 William Davis (0) For those of you who have been frustrated in trying to get your lipoprotein analysis performed, here's another option. The Life Extension Foundation at www.lef.org provides access to the VAP test, or Vertical Auto Profiler. This is the lipoprotein test run by the Atherotech company in Birmingham, Alabama. The name refers to the method used, a form of centrifugation, or high-speed spinning of your blood (plasma) to separate the various components by density. This is a fine technique that works well. Though our preferred method is NMR (www.Lipoprofile.com, Liposcience Inc.), the Atherotech VAP is a reasonable alternative. If you go through the Life Extension process, they will direct you to blood draw sites in your area. They charge $185 for Life Extension members, $247 for non-members. (Membership in Life Extension costs $75.) Drawback: No billing for health insurance reimbursement. A full description of the significance of lipoproteins can also be found in my article posted on-line at the www.lef.org website at http://www.lef.org/magazine/mag2006/may2006_report_heart_01.htm
Weight and lipoproteins 8. June 2006 William Davis (0) Tom, an accountant, came into the office eager to know what his 2nd heart scan score showed. A year ago, Tom's view of himself as a healthy, middle-aged man was shattered when he found out his heart scan score: 1236. Tom had severe coronary plaque with a heart attack risk of 25% per year (without intensive preventive action). In the way of lipoprotein abnormalities, he had several: low HDL, deficient large HDL, small LDL, high triglycerides, IDL (the after-eating inability to clear dietary fats), and a high blood sugar in the pre-diabetic range. In addition, Tom was hypertensive, with blood pressure so high it even landed him in the emergency room last winter. In addition to our approach to correct all these patterns, Tom was urged to lose a significant quantity of weight. Starting at 225 lb., at 5 ft 7 inches, Tom was clearly at least 40 lbs over his ideal weight. I stressed to Tom that the entire spectrum of causes of coronary plaque were weight-related. I likened his patterns to throwing gasoline on a fire: As weight increased, his lipoprotein and other abnormalties flared dramatically. But each time Tom came back to the office over the ensuing year, he'd gained another 3 to 6 lbs. And each time he had an explanation. "My daughter just got married. I couldn't turn down wedding cake, now could I?" Or, I just survived another tax season. I was working day and night--no time for exercise!" "It's getting too hot to walk anymore." Well, despite multiple treatments, Tom's repeat heart scan showed a score of 1677, a 35% increase. That's a dangerous rate of growth that virtually guarantees that plaque is building up momentum to "rupture", which results in heart attack. I therefore stressed to Tom that weight loss was crucial. Control of coronary plaque was simply not going to occur without weight loss to our target. Alternatively, we could add several new prescription medicines and hope that they could achieve the same effect, though at a price (side-effects, expense). I tell Tom's story to highlight again just how important weight loss can be for a number of lipoprotein abnormalities. What measures specifically are sensitive to weight? They are:--HDL cholesterol--Triglycerides--Small LDL--VLDL--Blood pressure--Blood sugar and insulin--C-reactive protein--LDLWeight exerts profound influence on these patterns. In Tom and people like him, weight can be a "make it or break it" issue. If you, like Tom, have any of the above patterns, consider weight loss as a potent tool you can use to gain control of coronary plaque.
Variation in vitamin D requirements 7. June 2006 William Davis (0) For Track Your Plaque followers, you know we are very concerned about vitamin D blood levels. My prediction is that, in 10 years, vitamin D will be regarded as an important item on the list of coronary artery disease risk factors. In our experience of trying to stop or reverse heart scan scores, restoration of vitamin D to a blood level of 50 ng/ml appears to have increased our success rate dramatically. As we've talked about before, on the bell curve of vitamin D dosing in a northern climate, the majority of women require 2000 units per day, men require 3000 units per day to achieve a level of 50 ng. However, there are "outliers" on this bell curve, i.e., people who require much more or much less.This week, I saw two people who were very instructive cases of extreme requirements on the high end of vitamin D dosing. Both started with unmeasurable blood levels, i.e., essentially zero ng/ml. On 5000 units of vitamin D per day, both raised their blood levels to around 17-18 ng/ml--in the range of severe deficiency (defined as <20 ng/ml). I advised both to increase their oral dose of vitamin D to 8000 units per day. Notably, both people avoided sunlight and lived in Wisconsin, a terribly sun-deprived locale 10 months a year. Both were also substantially overweight (around 300 lbs each). The vitamin D issue continues to be endlessly fascinating in all its nuances and twists.
Heart attacks in your own backyard 7. June 2006 William Davis (0) Two men from my community just died of heart attacks. Both were in their 40s. What bothers me most about these all too frequent stories is that it is so preventable. You can bet that both had little or no symptoms prior to their deaths. You can also bet that they've had cholesterol panels taken by their doctors. Followers of the Track Your Plaque program know that these are sure-fire paths to failure. The absence of heart disease symptoms should provide no reassurance whatsoever. High cholesterol, in-between cholesterol, low cholesterol--none are confident indicators in a specific individual.Stress test? How about the patient I saw today who, until I met him, had been undergoing stress test after stress test, every year--all while the quantity of coronary plaque tripled. False reassurances provided by his cardiologist led him to believe that all was well--while this stack of oily rags was just waiting for the spark to ignite. Too little time, too much money, too far away--there's a hundred excuses for not getting a heart scan. Or, you've had a heart scan and no one can tell you what to do about it. If you're reading this, however, you've found the most intensive source of information available on how your heart scan can serve as the start of a program of heart attack prevention for a life free of dangers. It's not that tough. But it won't just go away on its own. I just have to look around me in my own community, watch the local news, talk to friends, and I'll heart about all the people just in my neighborhood who should be learning these lessons. I rant and rave about this but some people need to hear it from a friend, colleague, neighbor, rather than some crazy doctor bucking the standard line. You, too, should be telling anyone who will listen about how heart disease can be identified and controlled.
Pilot lands safely after heart attack, then dies 6. June 2006 William Davis (1) That was the disturbing headline on a report from MSNBC, also reported nationally on all the major news networks. The story goes on:"A pilot suffering a heart attack made an emergency landing on a highway, saving his three passengers shortly before he died...He landed the single-engine Cessna 185 on Utah 30 near Park Valley and was taken to Bear River Hospital in Tremonton, where he died."We track these sorts of stories and it's frightening just how common they are. A school bus driver recently had a heart attack while driving 30 children; the bus crashed but no one was hurt. A 52-year old commercial bus driver suffered a heart attack while transporting 49 conference attendees; the bus plunged 400 feet down a ravine. Remarkably, 17 passengers suffered only minor injuries and there were no deaths. There have even been incidents where the pilot of a jet liner suffered a heart attack in-flight. In 2000, the 53-year old pilot of a Northwest Airlines DC-10 died while in-flight from a heart attack while landing in Minneapolis. The 290 passengers were landed safely by co-pilot. Most incidents where the driver or pilot has been incapacitated or died resulted in the deaths of only a handful of people. No major catastrophe has yet occured. But--mark my words--it will. These incidents just happen too frequently. Virtually all of these and similar incidents could have been prevented. If the FAA, for instance, would insist that all pilots have a simple CT heart scan, it would become immediately obvious which pilots should be grounded and who should fly. Similar requirements could easily be applied to persons in charge of the welfare of many people, most notably school bus drivers. It's not that tough! The FAA currently requires stress testing and cholesterol testing. Well, guess what? Followers of the Track Your Plaque program know that these tests do not effectively identify the person at risk for heart attack in the majority of individuals. Just ask former President Bill Clinton how helpful his stress tests (five in a row!) were. Or how valuable his cholesterol monitoring was--all prior to his emergency bypass surgery.
Large new clinical study launched to study. . .niacin 5. June 2006 William Davis (3) Oxford University has issued a press release announcing plans for a new clinical trial to raise HDL cholesterol and reduce heart attack risk. 20,000 participants will be enrolled in this substantial effort. The agent? Niacin.How is that new? Well, this time niacin comes with a new spin. Dr. Jane Armitage, formerly with the Heart Protection Study that showed that simvastatin (Zocor) reduced heart attack risk regardless of starting LDL, is lead investigator. She hopes to prove that niacin raises HDL cholesterol and thereby reduces heart attack risk. But, this time, niacin will be combined with an inhibitor of prostaglandins that blocks the notorious "flushing" effect of niacin. The majority of Track Your Plaque participants hoping to control or reverse coronary plaque take niacin. Recall that niacin (vitamin B3)is an extremely effect agent that raises HDL, dramatically reduces small LDL, shifts HDL particles into the effective large fraction, reduces triglycerides and triglyceride-containing particles like IDL and VLDL. Several studies have shown that niacin dramatically reduces heart attack. The HATS Study showed that niacin combined with Zocor yielded an 85-90% reduction in heart attack risk and achieved regression of coronary plaque in many participants.In our experience, approximately 1 in 20 people will really struggle using niacin. Flushes for these occasional people will be difficult or even intolerable. Should Dr. Armitage's study demonstrate that this new combination agent does provide advantages in minimizing the hot flush effect, that will be a boon for the occasional Track Your Plaque participant who finds conventional niacin intolerable. But you already have access to niacin, an agent with an impressive track record even without this new study. And you have a reasonably effective prostaglandin inhibitor, as well: aspirin. Good old aspirin is very useful, particularly in the first few months of your niacin initiation to blunt the flush. Although this study is likely to further popularize niacin and allow its broader use, it's also a method for the drug companies to profit from an agent they know works but is cheap and available. You don't have to wait. You already have niacin and aspirin available to you.
The dark side of CT heart scans 4. June 2006 William Davis (0) "I just got a heart scan!" declared Eric to his doctor. He handed the report to him."Oh my. Your score is 154." The doctor paused, then looked at Eric with a serious look on his face. "If we're going to understand whether or not you're in danger, you'll need a heart catheterization."I've seen this happen countless times. How can I say this diplomatically? THIS IS WRONG!! In my view, it's absolutely criminal for this to happen. Physician ignorance, profiteering, whatever--it is wrong. There's very few reasons why someone who has no symptoms should go directly to the cath lab for a procedure. (A rare exception might be an exceptional quantity of plaque in the left mainstem artery, e.g., >100. This is highly unusual.)Even a nuclear stress test (e.g., thallium) at this level of scoring is only 10-15% likely to be abnormal. That means 85-90% likelihood of being normal. There's rare reasons to perform a heart catheterization in a person with no symptoms and an entirely normal stress test. The vast majority of people like Eric do not need a heart catheterization to discern risk. If Eric's doctor had been up-to-date on the published literature on the prognostic value of heart scans, he could have advised Eric what the risks were--without a catheterization. Many doctors simply don't want to be bothered. Or, they opt for the more profitable method--a hospital procedure.Always discuss your heart scan with your doctor--but be armed with information in case your doctor is uninformed or unscrupulous. Unfortunately, that's not uncommon. The Track Your Plaque program is your advocate, a source for unbiased information.
The dirty little secret about aneurysms 2. June 2006 William Davis (1) Jake had an abdominal aneurysm identified--by accident. While getting a CT scan of his abdomen for unexplained abdominal pain, a 4.4 cm aneurysm was discovered. Jake's abdominal pain eventually passed without explanation, but he was left with this aneurysm.Jake's primary care doctor referred him to a surgeon. "It's too small to require surgery right now. Wait a few years and it'll probably get bigger. When it gets to around 5.5 cm, that'll be the time to operate. Let's schedule an abdominal ultrasound or CT scan every 6 months."Jake then got himself a heart scan. His high score of 879 then led him to my office. Lipoprotein testing, a stress test, correction of his lipoprotein patterns, changes in lifestyle followed. One year later, Jake's heart scan score was unchanged. How about his abdominal aneurysm? 4.2 cm--a modest quantity of regression. When Jake's surgeon learned of the change, he just shrugged. "Okay, we'll just watch it from here."Shockingly, the conversation surrounding aneurysms is just like the one Jake received: Let's just watch it grow until you need surgery. If you've every seen anyone have abdominal aneurysm surgery, you know it is an awful, painful, barbaric process with high risk for major complications like kidney failure and loss of the legs. Waiting for an aneurysm to grow is a lousy solution. Surgeons point out that, although surgery is imperfect, it's better than the alternative: rupture, which is catastrophic with a 50% chance of dying. But what about stopping the growth of the aneurysm? Or even reversing, or shrinking, it? Surgeons say it can't be done. Yet we've done it--many times. And it's not that difficult. The steps to take are very similar to that in the Track Your Plaque program for coronary plaque regression, with a few different strategies. Suppression of inflammation, for instance, plays a more important role and blood pressure must be abolutely normal, even during exercise. More to come on this important topic in the future, including an upcoming Special Report on the www.cureality.com membership website.
Heart scan scores dropping like stones!! 1. June 2006 William Davis (0) I saw two instances of dramatic coronary plaque regression today. John, a 53-years old mechanical lift operator, dropped his heart scan score from 479 to 323--a 32% regression of coronary plaque volume! Eric, a 50-year consulting engineer, dropped his heart scan score from 668 to 580--a 13% reduction. Both men did nothing special beyond the principles advocated in the Track Your Plaque program. Recall that, without preventive efforts, your heart scan score is expected to increase by 30% per year. Both men are well on their way to freedom from risk of coronary "events". Two less people to feed the revenue-hungry hospital procedure system! We need many more like them.
Optimal medical therapy 9. April 2007 William Davis (6) I was re-reading some of the details behind the recently announced COURAGE Trial comparing angioplasty/stent in 1100 people compared to "optimal" medical therapy in another 1100. You'll recall that no difference was found. In particular, over approximately 5 years, 20% of participants in each group died, experienced heart attacks, or strokes. Of those treated with "timal" medical therapy, 32% ended up getting a procedure like stents or bypass anyway due to deteriorating symptoms. What is "optimal" medical therapy? I bring this up again because the study investigators in COURAGE, as well as in similar trials, say this with a straight face. Optimal medical therapy means aspirin and/or Plavix (the anti-platelet, aspirin-like blood thinner); "aggressive" statin drug therapy to reduce LDL cholesterol to 60-85 mg/dl; and "anti-ischemic" therapy (that reduces angina and the phenomena of poor coronary blood flow) using nitroglycerin preparations, beta blockers, and other drugs. I do give credit to the investigators for having the courage to perform this trial in a world hell bent on doing procedures and still reporting the neutral outcome. But the notion of "optimal" medical therapy begs for comment. Indeed, this is regarded as optimal by most practitioners. Some would even argue excessive, based on the low LDL target achieved. Would you be satisfied with a 20% likelihood of heart attack, stroke, or death or 5 years, a 1 in 5 roll of the dice? I would not. Recall that we aim for near-total elimination of risk. What could have been further "optimized"? Plenty. For instance:--What is the real LDL, not the fabricated, calculated LDL? The two can be commonly 100 mg/dl different. --How about raising HDL to 60 mgd/? --What about reducing the proportion of small LDL particles? After all, small LDL is the number one cause of heart disease in the U.S., not high LDL.--What is Lp(a)? If you treat LDL with a statin drug, Lp(a) is unaffected and continues to trigger huge plaque growth. You will fail if this is not identified and corrected. --What is vitamin D3? One of the most powerful facilitators of plaque reversal I know of. --What are triglycerides? Triglycerides create hidden particles in the blood like intermediate-density lipoprotein, potent triggers for coronary plaque growth. Speaking of intermediate-density lipoprotein, that's another very important pattern to identify, the after-eating persistence of dietary fats. --Why aren't they taking fish oil? With a 28% reduction in heart attack and 45% reduction in sudden death from heart attack, this alone would have halved the number of "events" in the "optimal" medical treatment group. Of course, there's more. But the idea that aspirin, statins, and anti-ischemic therapy is somehow optimal is silly and sad at the same time. But that's the bias. The COURAGE Trial does represent a step forward, a step away from the "stent everyone and everything" mentality that motivates my colleagues, aided and abetted by their co-conspirators, the hospitals. But you and I know better. "Optimal" medical therapy, in truth, can mean a far better approach that can dramatically reduce, perhaps eliminate, risks for events like heart attack. The conventional "optimal" medical therapy will suffice only if you're content with a 20% likelihood of heart attack, death or stroke, or a 32% likelihood of an urgent procedure in your future.
Niacin, postprandial patterns 9. April 2007 William Davis (0) For a detailed report on the very important postprandial (after eating) patterns that contribute hugely to heart disease risk, read my recent article in Life Extension Magazine, available (no cost) at: Uncovering a Hidden Source of Cardiovascular Disease Risk at http://www.lef.org/magazine/mag2007/mar2007_report_heart_01.htmFor a report on using niacin to reduce risk of heart disease, see another report in the same issue of Life Extension:Ask the Doctor: Using Niacin to Improve Cardiovascular Health at http://www.lef.org/magazine/mag2007/mar2007_atd_01.htm.Also, keep your eyes open for a lengthy report focused exclusively on the Track Your Plaque program in an upcoming issue of Life Extension. I'll provide links in this Blog when it comes out.
What's better than fish oil? 9. April 2007 William Davis (1) One of the recent questions on our Track Your Plaque Forum related to what to do about a triglyceride level of 101 mg/dl while on fish oil.Recall that, contary to conventional thinking like that articulated in the ATP-III cholesterol treatment guidelines, we aim to reduce triglycerides to 60 mg/dl or less. This is important to suppress the formation of abnormal triglyceride-containing lipoprotein particles, especially small LDL, reduced HDL, lack of healthy large HDL, VLDL. ATP-III advises a level of 150 mg/dl or less. Unfortunately, triglyceride levels this high guarantee appearance of all these undesirable particles and an increasing heart scan score. What's better than 4000 mg of fish oil for its 1200 mg of EPA and DHA (omega-3 fatty acids)? More fish oil. In other words, the 4000 mg fish oil providing 1200 mg EPA + DHA is our minimum. A simple increase to 6000 mg to provide 1800 mg EPA + DHA is usually all that is necessary to reduce triglycerides and put a halt to the cascade of abnormal lipoprotein particles that trigger plaque growth. Occasionally, a somewhat higher dose may be required. Doses are best divided into two, with meals (e.g., three capsules twice a day).Another important issue: An over-reliance on wheat products can also increase triglycerides. This includes any flour product like breads (regardless of whether it's white, whole wheat, or whole grain--they all raise triglycerides), pretzels, bagels, breakfast cereals, and pasta. A dramatic reduction in wheat-containing products will reduce triglycerides substantially, help you reduce your abdominal fat, reduce blood pressure, raise HDL and reduce small LDL, clear your mind, provide more energy, avoid afternoon "fogginess" . . . Huge benefits.
Valve disease and vitamin D 8. April 2007 William Davis (1) There are two common forms of heart valve disease: aortic valve stenosis (stiffness) and insufficiency (leakiness), and mitral anular calcification. Both valve issues are regarded as evidence of senescence, or aging--the older you are, the more likely you will have one or both. Both conditions involve progressive calcium deposition and, to some degree, cholesterol deposition. They might be regarded as phenomena of "wear and tear" just like hip arthritis. There are no known therapies to stall or stop the development of mitral anular calcification. However, several attempts have been made over the years to identify treatments that can slow or stop the progression of aortic valve disease, which is becoming increasingly common and is addressed by surgical valve replacement when severe. The most recent trials have examined whether high-dose Lipitor (80 mg) has any effect (it did not) and high dose Crestor (40 mg), which slowed but did not stop the deterioration of stiff valves. It's been my suspicion that vitamins D and K2 may play a crucial factor in valve health. After all, vitamin D is the master controller of calcium deposition. Preliminary data also suggest that people who are intentionally made vitamin K deficient with the drug, Coumadin, develop twice the calcium deposition on aortic valves that non-Coumadin takers develop.I saw a patient Friday, Marianne. In addition to a moderate heart scan score of 379 at age 71, Marianne had a leaky (insufficient) aortic valve. By an echocardiogram 18 months ago, the valve was moderately leaky. I put Marianne on vitamin D, 4000 units, to raise her blood level to 50 ng/ml. Last week, I asked Marianne to have another echocardiogram. This time, no leakiness whatsoever--none. I have never seen this happen before. Although Marianne is only one example and we don't want to extrapolate too far from the experience of one person, it's hard not to attribute this phenomenal response to vitamin D supplementation. I wonder what would have happened if we had added vitamin K2, as well?Anyway, just another potential wonderful effect of vitamin D restoration.
Homocysteine and coronary plaque 8. April 2007 William Davis (4) If you’ve watched the news over the past year, you know that doubt has been cast over the idea that reducing homocysteine blood levels with high doses of B vitamins (B6, B12, and folic acid, or B9) results in reduced risk for heart attack. Is the homocysteine concept dead? Shall we empty our bottles of costly B vitamins into the trash and move on?I don’t think so. As detailed in one of our Track Your Plaque Special Reports from a few months ago, I think the homocysteine issue still deserves lots of respect and further investigation. After all, hundreds of clinical studies have connected higher homocysteine levels with greater risk for heart disease, stroke, and aneurysm. Numerous studies, for example, have repeatedly and consistently demonstrated a tripling of heart attack risk when homocysteine levels exceed 14 ?mol/l. Can we dismiss this association because several more recent studies—NORVIT, HOPE, and VISP—suggested that, when starting homocysteine levels are 12.5, that B vitamin supplementation does not reduce heart attack risk?I think there’s lots more to know about the homocysteine connection. That said, I have never seen a patient who I thought had heart disease strictly because homocysteine was increased.I believe that we can at least use homocysteine as an index of lifestyle: the higher the homocysteine, the poorer the diet, or the less effective the absorption of B vitamins (especially vitamins B12 and folic acid). Homocysteine levels of <9 micromol/l suggest both adequate intake and absorption of these B vitamins. If homocysteine is tightly connected with risk for heart disease, yet supplementation of B vitamins fails to reduce risk, might there be another means of connection? Or, could both homocysteine and heart disease be connected in some way that has nothing to do with B vitamins? Don’t close the book on homocysteine. Just because conventional experience fails to draw connection does not necessarily mean that none exists. If it’s any consolation, taking B vitamins has been correlated with better memory, concentration, and other health benefits, even if no reduction in heart disease develops.
Big heart scan scores drop 6. April 2007 William Davis (0) High heart scan scores of, say, greater than 1000 are more difficult to reduce than lower scores. I learned this lesson early in the experience of trying to drop scores. In the first few years of trying to drop scores, I saw relatively modest scores of 20, 50, or 100 drop readily, even when the usual targets were not fully achieved, and even before the incorporation of some of the more exciting recent additions to the Track Your Plaque program, like vitamin D.But big scores of 1000, 2000, or 3000 are a tougher nut to crack. In the first few years, what I usually saw was a slowing , or "deceleration," of growth from the expected rate of annual score increase of 30% that would continue for a year or two, followed by zero change. In the first year of effort, for example, a score increase of 18% was common. 10% was common in year two, then finally zero change in year three. Somehow, the more plaque you begin with, the more "momentum" in growth is present and the longer it takes to stop it. Kind of like stopping a compact car versus stopping a freight train. But more recently, I'm seeing faster drops. Today, Charlie came to the office to discuss his second heart scan. 18 months earlier, Charlie's first scan showed a score of 3,112, high by anybody's standard.His repeat score: 3,048. While the drop is relatively small on a percentage basis and may even fall within the expected rate of error for heart scans (which tends to be <2% at this high a score), I told Charlie that it still represented a huge success. Not only did he not increase his score by the expected 30% per year, he also brought a charging locomotive to a rapid stop. Next year, Charlie is targeting a big drop. Given the tools he now has available, I'm optimistic that he will succeed. Watch for the Track Your Plaque May, 2007 Newsletter in which we will detail Charlie's story further.
Does the American Heart Association diet reduce heart disease? 5. April 2007 William Davis (0) If you have a heart attack and land in the hospital where, invariably, you will have a heart procedure. Or, if you get a stent or coronary bypass operation, sometime before your discharge from the hospital, a well-meaning hospital staff dietitian will provide instruction in the American Heart Association (AHA) diet. Does this diet reduce the risk of heart disease?The answer depends on where you start. If you begin with a conventional American diet that is enormously influenced by convenience, food manufacturers like Nabisco, General Mills, Quaker Oats, ADM, and Cargill, or food distributors like McDonald’s, Pizza Hut, and Taco Bell, then the American Heart Association diet is indeed an improvement. But just a small one. If LDL cholesterol is the yardstick, the average reduction in LDL is between 10 and 15 mg/dl. This is the same amount of change you’d experience by adding 1 tablespoon of oat bran to your diet. Hardly worth boasting about. HDL, triglycerides, blood glucose, and body weight do not change. The diet could be substantially better. After all, it’s become common knowledge that other diets, such as the so-called Mediterranean diet, the South Beach Diet, and similar broad projects result in far greater changes than the AHA diet dispensed by your hospital and cardiologist. These diets more effectively reduce LDL, raise HDL, reduce triglycerides, reduce C-reactive protein, reduce blood pressure. Diets like South Beach also yield substantial weight loss and reversal of diabetic tendencies, with the magnitude of benefit dependent on the amount of weight lost. Why this stubborn adherence to the outdated concepts articulated in the AHA diet? Cardiologists would argue that insufficient data has been generated to permit widespread application of these diets. They also differ on whether they really work. Of course, the majority remain ignorant and dismiss them as fad diets. A little digging into the financial disclosures of the AHA suggests another, more malignant influence: who is paying the bills? Until recently, drug manufacturers were major contributors to the AHA. However, more recently AHA administrators have become sensitive to the public perception that they might be nothing more than a voice box for the drug industry. They have since limited contributions from the drug companies to 8% of annual charitable revenues. The drug manufacturers have been replaced by the food industry. In addition to food manufacturers that make the cereals on your grocery shelf, it includes the multi-national conglomerates that produce unimaginable revenues and carry enormous political clout, like ADM and Cargill. Ever wonder how it is that Honey Nut Cheerios received a “Heart Healthy” endorsement from the AHA? The AHA diet does not provide the answers we’re looking for, not even close. It is a perversion from an organization that has its strings pulled by industry. The answers to health will not come from the AHA, AMA, the American College of Cardiology, the American Hospital Association, and it won’t come from your doctor. It won’t come from a titillating report on the evening news or Good Morning America. It will come from collective and expanding wisdom placed directly into the hands of the public. It will be untainted by the temptation of drug industry dollars. It will not be dirtied by million dollar contributions, or the multi-million dollar behind-closed-doors lobbying of the food manufacturers. It will come from the truth relayed to the healthcare-consuming public. I hope you recognize it when you see it. If you want a healthy diet for your heart, throw away the pamphlets from the AHA unless you are partial to bread, breakfast cereals, corn, and the supporters of their misguided nutritional advice.
Vitamin K2 and coronary plaque 4. April 2007 William Davis (1) The vitamin K2 story, though still preliminary, is becoming increasingly interesting from the perspective of CT heart score reduction. The origin of this concept came from some unexpected observations. One, the observation that osteoporosis (lack of bone calcium that leads to fractures) arises from deficiency of vitamin K2. Two, deficiency of K2 leads to unrestrained calcium deposition in animal models, leading to heart attack in just weeks. Vitamin K2 has been largely ignored for years, since the more widely understood K1 is rarely deficient. K1 deficiency can occur from prolonged antibiotic use, or from severe malnutrition. But deficiency in otherwise well people is very uncommon. Vitamin K2, however, may be a different story. Deficiency may be common.The Rotterdam Heart Study of cheese-eating Dutch showed that greater K2 intakes resulted in a halving of heart attacks. Cheese (traditional varieties, not Velveeta or other make-believe cheese products) is a modest source of K2, as is the Japanese native food, natto. (If you've ever seen natto, I dare you to eat it. I have a pretty strong stomach and curiousity for food, but natto is the one thing I could not eat--it is truly horrible.)The weight of evidence suggests that vitamin K2 supplementation may prove to be a useful addition to your coronary plaque control program. Clearly, more data are needed, particulary therapeutic obserations, i.e., observing people who take dose X of a K2 prepartion and tracking some feedback measure, e.g., bone density, CT heart scan score, "events" like heart attack, etc. Nonetheless, the K2 story is clearly worth reading about, perhaps even considering supplementation. Please watch for the Special Report on the www.cureality.com website in the coming days.
Exercise and blood pressure 4. April 2007 William Davis (5) The media has gotten a hold of a case report from the University of Maryland describing a 51-year old physician who, despite being a long distance runner, had a high heart scan score. An example of the report can be found at Heart Disease In A Marathon Runner: Is Too Much Exercise A Bad Thing?http://www.sciencedaily.com/releases/2007/03/070315091100.htm in Science Daily."The mystery was all the more intriguing because his resting blood pressure and fasting cholesterol levels, the usual measures of cardiovascular health, were in the normal range."When this man was put on a treadmill for a stress test, his blood pressure skyrocketed from a normal 118/78 to 230/78--extremely high, even for exercise. The physicians reporting the case raised the question of whether long-distance running represents a risk for heart disease and if the high blood pressure with exercise is a contributor or cause of the high heart scan score. These are phenomena we are very familiar with. We have stressed the importance of exercise blood pressure as a trigger for coronary plaque for years. While 230/78 is clearly too high, we find that any blood pressure over 170/80 with exercise adds to the fire and can trigger plaque growth. However, I think it is absurd to suggest that marathon running itself is a trigger of coronary plaque. I think it is far more likely that the person described in the report had lipoprotein(a), a potent trigger for both exercise-induced hypertension and high CT heart scan scores in seemingly well people. He likely also suffered from a deficiency of vitamin D deficiency, another contributor. There's no need to indict exercise. If you are in the Track Your Plaque program, you know that stress tests are of questionable helpfulness for the detection of hidden heart disease. But they are useful for assessment of blood pressure responses during exercise. If BP exceeds 170/80 at 10 mets (a measure of exercise effort achieved by walking 3.4 mph at a 14% grade for 3 minutes), then blood pressure may be a contributor to your heart scan score.
"Fish oil is stupid" 3. April 2007 William Davis (13) "Fish oil is a waste of time and money. It's stupid. Just stop it."So a patient of mine was advised by another physician when he complained that he occasionally experienced a fishy aftertaste. This attitude perplexes me. After all the confirmatory data that support the enormous health benefits of omega-3 fatty acid supplementation, including the 11,000 participant GISSI-Prevenzione Trial, you'd think this attitude would be history. What's a little fish aftertaste when heart attack risk is slashed 28%? Perhaps the tendency to pooh-pooh fish oil is because it's available as a nutritional supplement. This shouldn't make fish oil appear inconsequential. Far from it. If you witness the extraordinary power for fish oil to reduce triglycerides, you will be immediately convinced of its effectiveness. The ability of omega-3 fatty acids from fish to eliminate intermediate-density lipoprotein (IDL), the persistent abnormal lipoprotein which signals an inability to clear dietary fats from the blood, can also convince you. More than 90% of people with excessive IDL have it completely eliminated by 4000-6000 mg of fish oil (providing 1200-1800 mg EPA + DHA) per day. The fact that fish oil is available as a prescription "medication," as well as an over-the-counter supplement, causes some physicians to dismiss the power of the supplemental form. This is nonsense. The over-the-counter form is every bit as effective as the prescription form. The makers of prescription Omacor also make the claim that their preparation is safer and purer. That may be true, but I'd like to see independent verification from the FDA, USDA, or an unbiased organization like Consumer Reports before I accept their marketing as fact--particularly at $120 to $240 per month! If Omacor proves to contain substantially less mercury and pesticide residues, then that will need to be factored in. (Please note that both Consumer Reports and Consumer Labs measured no substantial mercury or pesticide residues in their analyses of 16 and 41 brands, respectively.) I try to persuade my colleagues that the idea of taking supplements is a wonderful trend that allows people to express ownership of their own health. What people need is guidance, not salesmanship for a more expensive version, nor dismissal of nutritional preparations that actually possess considerable benefits.