Wheat belly 23. July 2007 William Davis (31) You've heard of "beer bellies," the protuberant, sagging abdomen of someone who drinks excessive quantities of beer. How about "wheat belly"? That's the same protuberant, sagging abdomen that develops when you overindulge in processed wheat products like pretzels, crackers, breads, waffles, pancakes, breakfast cereals and pasta. (By the way, this image, borrowed from the wonderful people at Wikipedia, is that of a teenager, who supplied a photo of himself.) It represents the excessive visceral fat that laces the intestines and triggers a drop in HDL, rise in triglycerides, inflames small LDL particles, C-reactive protein, raises blood sugar, raises blood pressure, creates poor insulin responsiveness, etc. How common is it? Just look around you and you'll quickly recognize it in dozens or hundreds of people in the next few minutes. It's everywhere. Wheat bellies are created and propagated by the sea of mis-information that is delivered to your door every day by food manufacturers. It's the same campaign of mis-information that caused the wife of a patient of mine who was in the hospital (one of my rare hospitalizations) to balk in disbelief when I told her that her husband's 18 lb weight gain over the past 6 months was due to the Shredded Wheat Cereal for breakfast, turkey sandwiches for lunch, and whole wheat pasta for dinner. "But that's what they told us to eat after Dan left the hospital after his last stent!"Dan, at 260 lbs with a typical wheat belly, had small LDL, low HDL, high triglycerides, etc. I hold the food companies responsible for this state of affairs, selling foods that are clearly causing enormous weight gain nationwide. Unfortunately, the idiocy that emits from Nabisco, Kraft, and Post (AKA Philip Morris); General Mills; Kelloggs; and their kind is aided and abetted by organizations like the American Heart Association, with the AHA stamp of approval on Cocoa Puffs, Cookie Crisp Cereal, and Berry Kix; and the American Diabetes Association, whose number one corporate sponsor is Cadbury Schweppes, the biggest soft drink and candy manufacturer in the world. As I've said many times before, if you don't believe it, try this experiment: Eliminate all forms of wheat for a 4 week period--no breakfast cereals, no breads of any sort, no pasta, no crackers, no pretzels, etc. Instead, increase your vegetables, healthy oils, lean proteins (raw nuts, seeds, lean red meats, chicken, fish, turkey, eggs, Egg Beaters, low-fat yogurt and cottage cheese), fruits. Of course, avoid fruit drinks, candy, and other garbage foods, even if they're wheat-free.Most people will report that a cloud has been lifted from their brains. Thinking is clearer, you have more energy, you don't poop out in the afternoon, you sleep more deeply, some rashes disappear. You will also notice that hunger ratchets down substantially. Most people lose the insatiable hunger pangs that occur 2-3 hours after a wheat-containing meal. Instead, hunger is a soft signal that gently prods you that it's time to consider eating again.You will also make considerable gains towards gaining control over your risk for heart disease and your heart scan score, a crucial step in the Track Your Plaque program.
If health won't motivate them, maybe money will 23. July 2007 William Davis (0) As part of our ongoing effort to educate everyone about the value of heart scans and how they can serve to start a program of heart disease prevention (or elimination), we occasionally distribute press releases on one facet of this discussion or another. Here's the one we released on our Cost Calculator, the one we developed that showed that $20 billion would be saved annually just by applying the program to men, ages 40-59. Accurate Detection and Prevention of Heart Disease Can Reduce Healthcare Costs, According to New Cost AnalysisA new cost analysis developed by cardiologist Dr. William Davis and his colleagues suggests that healthcare costs can be reduced by billions of dollars with the application of a simple program for heart disease detection and prevention.Milwaukee, WI (PRWEB) July 23, 2007 -- Billions of dollars in healthcare could be saved every year by applying a simple program of heart disease detection and prevention on a wide scale in the U.S., suggests a new cost analysis developed by cardiologist Dr. William Davis and colleagues. Davis and his colleagues are the developers of the Track Your Plaque program for heart disease detection and prevention.In the next 24 hours, 10,000 major heart procedures will be performed in hospitals across the U.S. The tab for this bill will top $400 billion in 2007 alone, nearly twice the sum spent on the war on cancer.As costs escalate at an alarming rate, tools for prevention of disease are also advancing. While drugs like Lipitor® make headlines and dominate direct-to-consumer TV ads, a quiet revolution is taking place among physicians and the public eager to find better answers, some of which also pose opportunities for stretching the healthcare dollar.“We’re essentially throwing away billions of dollars each and every year by ignoring the savings power of preventive strategies for heart disease,” proclaims Davis, a Milwaukee cardiologist. Davis is author of several books on heart disease detection and prevention, has been a vocal advocate for preventive strategies and is founder of www.cureality.com.Davis and his colleagues developed a cost model to predict how much money could be saved by the adoption of new preventive strategies on a broad scale in the U.S. “The cost savings are startling. If males in the 40–59-year-old age group, for instance, were to undergo a simple CT heart scan for early detection of coronary heart disease, followed by a purposeful yet focused program of prevention using widely available tools, our cost model shows that we would save the American public over $20 billion annually. Extending this calculation to the broader population would multiply savings several-fold.”Heart care is already the single largest healthcare category in the U.S. As costs go up by double-digit percentages, fewer people can afford healthcare. Those who can afford it spend an increasingly greater portion of their disposable income to maintain it. The Agency for Healthcare Research and Quality predicts that, at the current rate of growth, healthcare costs will balloon to absorb 20 percent of American Gross Domestic Product (GDP), about $4 trillion, in the next 10 years.Davis points out that reducing the annual U.S. expenditure for heart disease by 20 to 30 percent could save between $80 and $120 billion each year. That marginal savings exceeds the sum the U.S. spends on the domestic war on terror.Davis and his group have dubbed the conventional procedure-based approach to heart disease management the “crash and repair model” because of its focus on urgent procedural intervention that takes place in hospitals.The crash and repair model is costly. According to the American Heart Association, a heart catheterization (performed 3,553 times per day, seven days a week) costs an average of $24,893; a coronary bypass operation (performed 1,170 times every day, seven days a week) costs an average of $67,823 (hospital costs, 2004, the latest year for which data are available). These figures don’t incorporate long-term costs incurred in the years following the procedure or time lost from work.The relatively high payment to physicians and hospitals for performing high-tech heart procedures provides a disincentive to redirect patients to a less costly prevention model. The exceptional costs of high-tech, high-ticket heart procedures would become increasingly unnecessary if better heart disease preventive practices were delivered on a broad scale. “Like seatbelts, preventive measures for heart disease are more cost effective and extract a far lower toll in human suffering than the ‘crash and repair’ approach. Our cost calculations bear out the enormous savings possible. In fact, all of the tools necessary to deliver a method of early heart disease detection and prevention are already available throughout the U.S. We’ve just got to encourage physicians and the public to take advantage of them.”The cost calculator program can be found at http://cureality.com/library/fl_hh005bankrupt.asp on the cureality.com Web site.Track Your Plaque is an informational and educational Web site devoted to showing people how CT heart scans can be used as a starting point for a program of heart disease prevention and reversal.
What role calcium supplements? 22. July 2007 William Davis (8) A frequent question in the Track Your Plaque program is whether taking calcium supplements to reduce risk for osteoporosis adds to calcium in arteries and raises CT heart scan scores. No, calcium supplementation does not add to coronary calcium. Thankfully, there is some wisdom to calcium metabolism. Calcium deposition or resorption is under independent local control in bone, as it is in the artery wall. Taking calcium has no effect on calcium deposition in your coronary arteries. However, there's a lot more to it. Taking calcium has only a modest effect on bone health. Most women can only hope to slow or stop calcium loss from bone by taking calcium supplements. Calcium supplements do not increase bone calcium. The reason why calcium supplementation works at all is, when calcium is absorbed into the blood, it provides a feedback signal to the parathyroid gland to shut down parathyroid hormone production, the hormone responsible for extracting calcium from bone. But the calcium itself does not end up deposited in bone. Likewise, calcium supplements have essentially no effect on the artery wall. But vitamin D controls calcium absorption and, curiously, appears to exert a dramatic effect on calcium depostion in coronary arteries. In fact, I would credit vitamin D as among the most important factors in regulating arterial health that I've encountered in a long time. Thus, bone health and arterial health do indeed intersect via calcium, but not through calcium supplements. Instead, the control exerted by vitamin D connects the seemingly unconnected processes. Vitamin K2 provides another unexpected juxtaposition of the two processes. Deficiency of K2, which is proving to be a lot more common than previously thought, permits an enzyme in bone to exert unrestrained calcium extraction. Deficiency of K2 in artery walls allow another enzyme to deposit calcium and grow plaque without restraint. Yet another intersection between bone health and coronary health that involves calcium, but as a passive participant. Stay tuned for a comprehensive Track Your Plaque Special Report on these topics coming in the next couple of weeks. I'm very excited about the emerging appreciation of calcium as an active ingredient in plaque, not a dumb, passive marker as previously thought. Vitamins D3 and K2 are among the keys to this phenomenon.
"Heart scans" are not always heart scans 18. July 2007 William Davis (6) Beware of the media reports now being issued that warn that "CT heart scans" pose a risk for cancer.One report can be viewed at http://www.webmd.com/cancer/news/20070717/ct-heart-scan-radiation-cancer-risk. This was triggered by a Columbia University study of risk for cancer based on the dose of radiation used in CT coronary angiograms. Theoretically, exposure to the radiation dose of CT coronary angiography can raise risk for cancer by 1 in 143 women if radiated in their 20s just from that single exposure.If you've been following the Track Your Plaque discussion, as well as my diatribes in the Heart Scan Blog, you know that the media got it all wrong. The "heart scans" they are referring to are not the same as the heart scans that we discuss for the Track Your Plaque program. A conventional heart scan (of the sort we refer to) exposes the recipient to 4 chest x-rays of radiation if an EBT device is used, around 8-10 chest x-rays of radiation if a 64-slice CT scanner is used. For the quality of information we obtain from these screening heart scans, we feel that it's an acceptable exposure. The "heart scan" this study and subsequent reports refer to is not truly a screening heart scan, but a CT coronary angiogram, or CTA. CTAs are performed on the same CT or EBT devices, but involve far more radiation. CTA exposes the recipient to about 100 chest x-rays of radiation on a 64-slice device (more or less, depending on the way it is performed.) Just a couple of years ago, some centers were performing CTA on 16-slice devices, a practice I and the Track Your Plaque program vocally opposed, since up to 400 chest-rays of radiation were required! I even called a number of centers advising them that they were putting the public in jeopardy. CTAs also require injection of x-ray dye, just like any conventional angiogram. CTA on 64-slice CT scanners require the same radiation exposure as a conventional heart catheterization, an issue glossed over in most conversations. In other words, the test that many of my colleageus so casually recommend poses a similar risk.The message: the test I advocate for screening for coronary heart disease is a CT or EBT heart scan, not a CT coronary angiogram. CTA is a useful test and will get better and better as the engineers discover ways to reduce radiation exposure. But, in 2007, CTA is a diagnostic device, not a screening device. If you require an abdominal CT scan because your doctor suspects pancreatic cancer, or a CT scan of the brain because you might have a life-threatening aneurysm causing double-vision or seizures, it would be silly to not undergo the scan because of long-term and theoretical cancer risk. But undergoing a CT coronary angiogram for screening purposes is ridiculous with present technology. I've said it before and I will say it--shout it--again:CT coronary angiograms are not screening procedures; they are diagnostic procedures that should be taken seriously and do indeed pose measurable risk for cancer, a risk that is presently unacceptable for a screening test. You wouldn't undergo a mammogram to screen for breast cancer if it exposed you to 100 chest x-rays of radiation, would you? Screening tests should be safe, reliable, accurate, and inexpensive. CT coronary angiography is none of these things. Genuine heart scans--the kind the Track Your Plaque program talks about and relies on--is all of those things.
Toggle navigation Home Blog Home Archive Join Now Log in Kitchen sink approach for Lp(a) 29. August 2008 William Davis (12) Lipoprotein(a), Lp(a), can be a tough nut to crack. Having struggled and wrestled with this genetic pattern for the last 12 years or so in hundreds of patients, I have gained great respect for this difficult to control pattern. I regard lipoprotein(a) as the number one most aggressive cause for heart disease and coronary plaque known. It can account for heart attacks in men in their 40s, women in their 50s. It can cause heart disease and heart attacks in even the ultra-fit like marathon runners. It accounts for both excessive coronary risk and misleading cholesterol values in slender, healthy-appearing people. Niacin is the number one treatment choice for Lp(a), followed by testosterone for men, estrogens (preferably human, not horse or other non-human mammal) for women. I then often resort to DHEA, along with adjunctive nutritional agents like raw almonds, ground flaxseed, and others. Our most recent addition to the Lp(a) treatment list is high-dose fish oil, which appears to exert a significant effect in about 40% of people with Lp(a). Even with this multi-agent approach, not everybody gains control over Lp(a).That makes me wonder if someone has Lp(a) at a substantial level of, say, 200 nmol/L or 70 mg/dl (values can differ tremendously, depending on the method of measurement), should we throw everything but the kitchen sink at Lp(a) from the start? Right now, by adding an agent one at a time, it often takes two years to gain control over Lp(a) (if we are going to get it at all).While many people might find this unpalatable and overwhelming from the starting gate of their program, I do believe it may be a strategy we should consider adopting for full and more immediate plaque control in the Track Your Plaque program. Something to chew on. Clearly, we need better answers for Lp(a). A "kitchen sink," full-frontal assault might be a way to gain faster control, though not necessarily a superior approach with regards to efficacy and potency. There are a number of unique, potentially effective therapies for Lp(a) that are worth examining. Given the difficulty of performing clinical trials with non-drug agents (largely a lack of financial support, since nobody gets a financial return with non-patent-protectable agents), I am anxious to put these potential treatments to a test in the Track Your Plaque program Virtual Clinical Trail (VCT). The VCT gives us a quick and relatively easy method to test various potential treatments, with feedback generated in months, rather than years. Any suggestions on promising agents to test? Of course, they must be widely available nutritional agents, not drugs. Making Dr. Friedewald an honest man 28. August 2008 William Davis (3) Colleen started with the usual discrepancy between conventional calculated LDL cholesterol of 121 mg/dl and the far more accurate LDL particle number (NMR) of 1927 nmol/L. Those of you following this conversation or our many conversations on the Track Your Plaque Forum know that a useful and highly reliable rule-of-thumb for converting NMR LDL particle number to LDL is to drop the last digit: 1927 nmol/L becomes 192 mg/dl. (This is, admitttedly, arrived at empirically, not by design. However, it has held up through thousands of NMR analyses and plays out reasonably when you compare distributions of Friedewald LDL and LDL particle number on a population basis.)In other words, by this simple manipulation, Colleen's Friedewald calculated LDL is off by 58%. This is very common, a phenomenon I witness several times every day. By LDL particle size, 75% of all Colleen's LDL particle were abnormally small (small LDL particle number 1440 nmol/L). This is a moderately severe small LDL tendency.So we took all the steps for reduction of small LDL/LDL, including elimination of wheat and cornstarch, exercise, weight loss (which happens inevitably when wheat and cornstarch are eliminated), fish oil, vitamin D, etc. Another NMR lipoprotein panel showed an LDL particle number of 882 nmol/L and a Friedewald calculated LDL of 87 mg/dl. Using our rule-of-thumb, LDL by particle number is virtually the same as the calculated LDL. This time, small LDL numbered only 237 nmol/L, or 26.8% of the total, a marked reduction. Isn't that interesting? As small LDL is corrected, the crude Friedwald calculated LDL approximates the more accurate LDL particle number. It assumes that accuracy of the Friedewald calculation may be more likely to occur as LDL size approaches normal. However, when LDL size is abnormally small--a condition shared by at least 70% of people with coronary heart disease--then the Friedewald LDL becomes increasingly inaccurate.The opposite can also happen: When all or nearly all LDL particles are large, Friedewald calculated LDL can markedly overestimate LDL particle number. Yesterday, for instance, a patient had a Friedewald calculated LDL of 183 mg/dl, but an NMR particle number of 1110 nmol/L--drop the zero . . . LDL 110 mg/dl. This woman was advised to take a statin drug by her primary care physician, based on the Friedewald LDL. Instead, she proved to have a far lower LDL. She would not have benefitted from taking a statin drug. As I've warned many times before: Beware the Friedewald calculated LDL. Some basic vitamin D issues 24. August 2008 William Davis (7) The last post on vitamin D raised a number of basic questions among readers. So let me discuss some of these questions one by one. All of them raise important issues surrounding the practical aspects of managing vitamin D in your health. Anne said:I think it is important to stress that vitamin D supplementation needs to be continued long term. I have met too many people who have been prescribed 50,000 IU of D2 for 8-12 weeks and then told to stop because their 23(OH)D went over 30ng/ml. I know one person who's doctor stopped and started the D2 3 times. Thanks for pointing that out, Anne. Excellent point. I also see doctors do this with statin drugs: start it, check a LDL level which is lower, then think that you're done and stop the drug. What the heck are they thinking? If vitamin D is not being produced by sun exposure and not obtainable through diet, continued supplementation is necessary, essentially for life. Twinb asked:How often you think Vit. D levels should be tested after the initial test is done, especially if the levels are drastically low?We have used every 6 months in the office. Ideally, levels are in mid-summer and mid- to-late winter in order to gauge the extremes of your seasonal fluctuations. While most adults over 40 fail to fluctuate more than 10 ng/ml in the Wisconsin climate (and this summer, after an initial rainy season early, has been flawlessly bright and sunny, in the high-70s and 80s every single day for months), an occasional person fluctuates more widely. The only way to judge is to check a blood level. Rich said:Vitamin D dosage effects appear to be quite idiosyncratic.Yes, indeed it is. Despite using crude rules-of-thumb, like taking 1000 units of vitamin D per 10 ng/ml desired (a rule I learned from Dr. John Cannell, which he offered fully aware of its inaccuracy), many people will surprise you and have levels that make no sense. Testing is crucial to know your vitamin D level. Richard asked: Where do we get enough vitamin D wihout worring about laboratory tests? Well, the entire point of the post was that you absolutely, positively cannot just take vitamin D blindly at any dose and hope that your level is ideal, no more than you can blindly take a dose of thyroid and know you have achieved normal thyroid levels. In my view, vitamin D blood levels are an absolute. Another simple issue: Don't be afraid of vitamin D. It is, in all practicality, no more dangerous than getting a dark tan. (But, as many of you realize, getting a tan is no assurance of raising vitamin D if you are over 40 years old.)Wouldn't it be great if someone developed a do-it-yourself-at-home skin test for vitamin D? I know of no effort to develop this, but it would be a huge advantage for all of us. “How much vitamin D should I take?” 22. August 2008 William Davis (17) It’s probably the number one most common question I get today: “How much vitamin D should I take?”Like asking for investing advice, there are no shortage of people willing to provide answers, most of them plain wrong. The media are quick to offer advice like “Take the recommended daily allowance of 400 units per day,” or “Some experts say that intake of vitamin D should be higher, as high as 2000 units per day.” Or “Be sure to get your 15 minutes of midday sun.”Utter nonsense. The Food and Nutrition Board of the Institute of Medicine has been struggling with this question, also. They have an impossible job: Draft broad pronouncements on requirements for various nutrients by recommending Recommended Daily Allowances (RDA) for all Americans. The Food and Nutrition Board has tried to factor in individual variation by breaking vitamin D requirements down by age and sex, but what amounts to a one-size-fits-nearly-all approach. Much of the uncertainty over dosing stems from the fact that vitamin D should not be called a “vitamin.” Vitamins are nutrients obtained from foods. But, outside of oily fish, you'll find very little naturally-occurring vitamin D in food. (Even in fish, there is generally no more than 400 units per 4 oz. serving.) Sure, there’s 20 units in an egg yolk and you can activate the vitamin D in a shiitake mushroom by exposing it to ultraviolet radiation. Dairy products like milk (usually) contain vitamin D because the USDA mandates it. But food sources hardly help at all unless you’re an infant or small child. It all makes sense when vitamin D is viewed as a hormone, a steroid hormone, not a vitamin. Vitamin-no, steroid hormone-D exerts potent effects in tiny quantities with hormone-like action in cells, including activation of nuclear receptors. It is the only hormone that is meant to be activated by sun exposure of the skin, not obtained through diet. But the ability to activate D is lost by the majority of us by age 40 and even a dark tan is no assurance that sufficient skin prohormone D activation has taken place. As with any other hormone, such as thyroid, parathyroid, or growth hormones, dose needs to be individualized. Imagine you developed a severely low thyroid condition that resulted in 30 lbs of weight gain, lose your hair, legs swell, and heart disease explodes. Would you accept that you should take the same dose of thyroid hormone as every other man or woman your age, regardless of your body size, proportion of body fat, metabolism, genetics, race, dietary habits, and other factors that influence thyroid hormone levels? Of course you wouldn’t. Then why would anyone insist that vitamin D be applied in a one-size-fits-all fashion? (There’s another world in which a one-size-fits-all approach to hormone replacement has been widely applied, that of female estrogen replacement. In conventional practice, there’s no effort to identify need, estrogen-progesterone interactions, nor assess the adequacy of dose, not to mention the perverse non-human preparation used.) With thyroid hormone, ideal replacement dose of hormone ranges widely from one person to another. Some people require 25 mcg per day of T4; others require 800% greater doses. Many require T3, but not everybody. Likewise, vitamin D requirements can range widely. I have used anywhere from 1000 units per day, all the way up to 16,000 units per day before desirable blood levels were achieved. Vitamin D dose needs to be individualized. Factors that influence vitamin D need include body size and percent body fat (both of which increase need substantially); sex (males require, on average, 1000 units per day more than females); age (older need more); skin color (darker-skinned races require more, fairer-skinned races less); and other factors that remain ill-defined. But these are “rules” often broken. My office experience with vitamin D now numbers nearly 1000 patients. The average female dose is 4000-5000 units per day, average male dose 6000 units per day to achieve a blood level of 60-70 ng/ml, though there are frequent exceptions. I’ve had 98 lb women who require 12,000 units, 300 lb men who require 1000 units, 21-year olds who require 10,000 units. (Of course, this is a Wisconsin experience. However, regional differences in dosing needs diminish as we age, since less and less vitamin D activation occurs.)Let me reiterate: Steroid hormone-vitamin D dose needs to be individualized. There’s only one way to individualize your need for vitamin D and thereby determine your dose: Measure a blood level. Nobody can gauge your vitamin D need by looking at you, by your skin color, size, or other simple measurement like weight or body fat. A vitamin D blood level needs to be measured specifically-period. Unfortunately, many people balk at this, claiming either that it’s too much bother or that their doctor refused to measure it. I would rank normalizing steroid hormone-vitamin D as among the most important things you can do for your health. It should never be too much bother. And if your doctor refuses to at least discuss why he/she won’t measure it, then it’s time for a new doctor. If you’re worried about adding to rising healthcare costs by adding yet another blood test, think of the money saved by sparing you from a future of cancer, heart disease, osteoporosis, diabetes, etc. The cost of a vitamin D blood test is relatively trivial (around $40-50, a fraction of the cost of a one month supply of a drug for diabetes.) So how much vitamin D should you take? Enough to raise your blood level of 25-hydroxy vitamin D to normal. (We aim for a normal level of 60-70 ng/ml.) You probably don't take enough fish oil 20. August 2008 William Davis (17) The results of the recent Heart Scan Blog survey in response to the question: MY DAILY DOSE OF EPA + DHA FROM FISH OIL IS revealed:Zero--I don't take any 17 (7%) of respondents Less than 1000 mg per day 24 (10%) of respondents 1000-2000 mg per day 91 (38%) of respondents 2000-3000 mg per day 44 (18%) of respondents 3000-4000 mg per day 40 (16%) of respondents More than 4000 mg per day 20 (8%) of respondentsBased on the above results, I would say that only a minority of respondents are taking an ideal dose of omega-3 fatty acids. Nearly all of us should consider taking more. Benefits of omega-3 fatty acids (EPA + DHA) from fish oil begin around a dose of 840 mg per day, according to the GISSI Prevenzione Trial of 1999, an 11,000-participant trial. This dose also corresponds to a quantity of omega-3s that have been shown to raise EPA + DHA blood levels and thereby reduce the notoriously high AA:EPA ratio of Americans. But what dose is sufficient? What dose is ideal? Well, the answer to a great degree depends on what you are taking the fish oil for. If being taken to reduce triglycerides and triglyceride-containing lipoproteins, like VLDL and the after-eating (postprandial) IDL, then a higher dose will be necessary. (Triglyceride reduction for the genetically-determined very high triglyceride level of familial hypertriglyceridemia is the FDA-approved indication for prescription Lovaza.) If you are taking fish oil for treatment of ADHD, depression, or bipolar illness, very high doses are often necessary. But how about maximal reduction of cardiovascular risk and for control or reversal of atherosclerotic plaque? This conversation is still evolving. But we can learn some important lessons from three populations of the world that are vigorous consumers of fish:--The Inuits (aka Eskimos) of Greenland and northern Canada--The Japanese--The Bantus of Tanzania who live along Nyasa LakeAll three indigenous populations have several-fold greater intakes of fish and omega-3 fatty acids, have higher blood levels of omega-3 fatty acids, and have enjoyed reduced cardiovascular events, reduced atherosclerotic plaque, or improvement in various surrogates of cardiovascular risk (e.g., Lp(a)). The most recent addition to this conversation is the ERA JUMP Study, discussed in a previous Heart Scan Blog post. In ERA JUMP, despite being heavy smokers and having other markers for greater risk for heart disease, Japanese men living in Japan had markedly less carotid and coronary plaque, as compared to Caucasian men living in PIttsburgh or Hawaiian men of Japanese descent. The difference appeared to be attributable to serum levels of omega-3 fatty acids. I believe that the trend is here is to increase the amount of omega-3 fatty acids that most of us take. In the Track Your Plaque program, we have been advocating a rock-bottom starting dose of EPA + DHA of 1200 mg per day. However, I believe that this is due for a change. We will be increasing the minimum dose for plaque regression and control. Please attend our Webinar this evening for a full, in-depth discussion of the rationale behind this important change. As always, let me remind you that I am not selling, nor ever have sold, fish oil supplements. If I advocate a specific dose, a higher dose, I do so based on my interpretation of the data and experience with patients, not because I am interested in selling brand X of fish oil. Vitamin D and HDL 19. August 2008 William Davis (23) Despite the paucity of scientific documentation of this phenomenon, I am continuing to witness extraordinary increases in HDL cholesterol levels with vitamin D supplementation. I've touched on the interaction of vitamin D supplementation with HDL in The Heart Scan Blog previously:Vitamin D: Treatment for metabolic syndrome?HDL for DummiesAt first, I thought it was attributable to other factors. In real life, most people don't modify one factor at a time. They reduceprocessed carbohydrates/eliminate wheat and cornstarch, lose weight, add or increase omega-3 fatty acids from fish oil, begin niacin, increase exercise and physical activity. All these efforts also impact on HDL. Among the many things I do, I consult on complex lipid (cholesterol) disorders (complex hyperlipidemias) in my office. A substantial number of these people carry a diagnosis of hypoalphalipoproteinemia, a mouthful that simply means these people are unable to manufacture much apoprotein A1, the principal protein of HDL cholesterol particles. As a result, people with hypoalphalipoproteinemia have HDL cholesterol levels in the neighborhood of 20-30 mg/dl--very low. They are also at high risk for heart disease and stroke. Encourage these people to exercise, attain ideal weight, eliminate wheat and cornstarch: HDL increases 5 mg/dl or so. Add niacin, HDL increases another 5-10 mg/dl. Perhaps we're now sitting somewhere around an HDL of 35-40 mg/dl--better, but hardly great. Add vitamin D to achieve our target serum level . . . HDL jumps to 50, 60, 70, even 90 mg/dl. The first few times this occurred, I thought it was an error or fluke. But now that I've witnessed this effect many dozens of time, I am convinced that it is real. Just today, I saw a 40-year old man whose starting HDL was 25 mg/dl increase to 87 mg/dl. Responses like this are supposed to be impossible. Before vitamin D, I had never witnessed increases of this magnitude. Not all therapies for raising HDL raise the important large (also known as HDL2b) fraction. With lipoprotein analyses, it appears that is principally the large fraction of HDL that rises with vitamin D supplementation. Why? How? That I can't tell you. But for those of you struggling with low HDL cholesterols despite your best efforts, vitamin D can make a world of difference.An interesting corollary: If super-high HDL cholesterols are associated with extreme longevity, as they are with centenarians, does raising HDL to extraordinary levels with vitamin D lead to longer, healthier life, all the way up to age 110 years? Again, no answers, but an interesting thought. And one I'd bet on. (And I'm not selling vitamin D.) Weight loss and blood pressure 15. August 2008 William Davis (6) Here's another thought with regards to time issues with weight loss: reductions in blood pressure (BP). The previous post talked about how triglycerides initially go up, sometimes way up, when weight drops, only to be followed months later by substantial drops. HDL initially drops in response to the triglyceride fluctuations, only to be followed by a rise. Blood pressure also shows a curious pattern that is largely dependent on age. Say someone in their 20s or 30s, for instance, loses 30 lbs (through elimination of wheat and cornstarch, say). BP usually drops within a few weeks, perhaps a month or two at most. How about someone in their 70s? Say a substantial amount of weight is lost, say 50 lbs over 6 months. BP does indeed drop, but it may require 6 months or longer after weight plateaus for the full effects of BP-reduction to be fully expressed. But it will eventually drop. Why the age-dependent difference? It relates to the capacity of arteries to remain flexible and distensible. Over the years, cross-linking of collagen (a structural protein), glycation (glucose molecules attaching to proteins), loss of endothelial responsiveness to generate artery-dilating substances like nitric oxide, and arterial atherosclerotic plaque all all up to making older arteries less able to "relax" and BP to drop. But given time and the proper effort, BP will eventually drop. Awareness of this time effect can help most people decide better when medications are necessary or if weight loss alone is sufficient to reach BP goals. "I lost 30 lbs and my triglycerides went . . . up?" 13. August 2008 William Davis (6) Brad needed to lose weight. At 6 ft tall, he began the program at 291 lbs, easily 80 lbs overweight. He wore virtually all of it in his belly. He had laboratory numbers to match: HDL 33 mg/dl, triglycerides 225 mg/dl, LDL (calculated) 144 mg/dl, blood sugar 122 mg/dl (fasting--clearly "pre-diabetic"), c-reactive protein 3.0 mg/dl. Among his lipoprotein abnormalities: small LDL representing 80% of all LDL (no surprise). Readers of The Heart Scan Blog know that these are the patterns of the carbohydrate-indulgent. I asked Brad to eliminate all wheat flour products, all foods made with cornstarch, and follow a diet rich in healthy oils, raw nuts, vegetables, and lean meats. Brad returned for a discussion about follow-up basic lipids (cholesterol) values four months later--31 lbs lighter, most of it clearly lost from his abdomen. He claimed he felt more energetic and clear-headed than he had in years. His lipid panel: HDL 34 mg/dl, LDL 122 mg/dl, triglycerides 295 mg/dl. Brad's smile dissolved. "How could that happen? You said losing weight would make my HDL go up and my triglycerides go down!"Yes, I had said that. But I was oversimplifying. The truth is that, when there is weight loss, especially profound weight loss like Brad experienced eliminating wheat and cornstarch products, there is mobilization of fat stores. Fat is stored energy. Energy is stored as . . . triglycerides. So when there is substantial weight loss, there is a flood of triglycerides in the blood, and triglyceride levels in the midst of weight loss can commonly jump up, not uncommonly to the 200-300+ mg/dl range. When triglycerides go up, there is also a drop in HDL (triglycerides interact with HDL particles, modify their structure and make them more readily destroyed, thereby dropping blood levels). Occasionally, substantial weight loss like Brad experienced will drop HDL really low, as low as the 20's. Once weight stabilizes, this effect can last up to 2 months before correcting. Only then will triglycerides drop and HDL rise. The rise in HDL occurs even more slowly, requiring several more months to plateau. In other words, weight loss like Brad's causes triglycerides to increase and HDL to decrease, to be followed later by a drop in triglycerides and a rise in HDL. I know of no way to block this phenomenon. And perhaps we shouldn't, since this is how fat stores are mobilized and "burned off." Fish oil does blunt the triglyceride rise (perhaps through activation of lipoprotein lipase, an enzyme responsible for clearance of triglycerides), but doesn't eliminate it. I call these changes "transitional" changes in lipids. Patience pays. A few more months from now, Brad's numbers will be much happier, as will Brad. Divorce court for the doctor-patient relationship? 10. August 2008 William Davis (4) The doctor-patient relationship has gone sour. This probably comes as no surprise to most of you, particularly if you've been following conversations here in The Heart Scan Blog:Who is your doctor? discussing the emergence of the physician-as-hospital-employee phenomenon that causes your doctor to become the de facto portal (seller?) of hospital services to you, a model fraught with conflicts of interest.
Kitchen sink approach for Lp(a) 29. August 2008 William Davis (12) Lipoprotein(a), Lp(a), can be a tough nut to crack. Having struggled and wrestled with this genetic pattern for the last 12 years or so in hundreds of patients, I have gained great respect for this difficult to control pattern. I regard lipoprotein(a) as the number one most aggressive cause for heart disease and coronary plaque known. It can account for heart attacks in men in their 40s, women in their 50s. It can cause heart disease and heart attacks in even the ultra-fit like marathon runners. It accounts for both excessive coronary risk and misleading cholesterol values in slender, healthy-appearing people. Niacin is the number one treatment choice for Lp(a), followed by testosterone for men, estrogens (preferably human, not horse or other non-human mammal) for women. I then often resort to DHEA, along with adjunctive nutritional agents like raw almonds, ground flaxseed, and others. Our most recent addition to the Lp(a) treatment list is high-dose fish oil, which appears to exert a significant effect in about 40% of people with Lp(a). Even with this multi-agent approach, not everybody gains control over Lp(a).That makes me wonder if someone has Lp(a) at a substantial level of, say, 200 nmol/L or 70 mg/dl (values can differ tremendously, depending on the method of measurement), should we throw everything but the kitchen sink at Lp(a) from the start? Right now, by adding an agent one at a time, it often takes two years to gain control over Lp(a) (if we are going to get it at all).While many people might find this unpalatable and overwhelming from the starting gate of their program, I do believe it may be a strategy we should consider adopting for full and more immediate plaque control in the Track Your Plaque program. Something to chew on. Clearly, we need better answers for Lp(a). A "kitchen sink," full-frontal assault might be a way to gain faster control, though not necessarily a superior approach with regards to efficacy and potency. There are a number of unique, potentially effective therapies for Lp(a) that are worth examining. Given the difficulty of performing clinical trials with non-drug agents (largely a lack of financial support, since nobody gets a financial return with non-patent-protectable agents), I am anxious to put these potential treatments to a test in the Track Your Plaque program Virtual Clinical Trail (VCT). The VCT gives us a quick and relatively easy method to test various potential treatments, with feedback generated in months, rather than years. Any suggestions on promising agents to test? Of course, they must be widely available nutritional agents, not drugs.
Making Dr. Friedewald an honest man 28. August 2008 William Davis (3) Colleen started with the usual discrepancy between conventional calculated LDL cholesterol of 121 mg/dl and the far more accurate LDL particle number (NMR) of 1927 nmol/L. Those of you following this conversation or our many conversations on the Track Your Plaque Forum know that a useful and highly reliable rule-of-thumb for converting NMR LDL particle number to LDL is to drop the last digit: 1927 nmol/L becomes 192 mg/dl. (This is, admitttedly, arrived at empirically, not by design. However, it has held up through thousands of NMR analyses and plays out reasonably when you compare distributions of Friedewald LDL and LDL particle number on a population basis.)In other words, by this simple manipulation, Colleen's Friedewald calculated LDL is off by 58%. This is very common, a phenomenon I witness several times every day. By LDL particle size, 75% of all Colleen's LDL particle were abnormally small (small LDL particle number 1440 nmol/L). This is a moderately severe small LDL tendency.So we took all the steps for reduction of small LDL/LDL, including elimination of wheat and cornstarch, exercise, weight loss (which happens inevitably when wheat and cornstarch are eliminated), fish oil, vitamin D, etc. Another NMR lipoprotein panel showed an LDL particle number of 882 nmol/L and a Friedewald calculated LDL of 87 mg/dl. Using our rule-of-thumb, LDL by particle number is virtually the same as the calculated LDL. This time, small LDL numbered only 237 nmol/L, or 26.8% of the total, a marked reduction. Isn't that interesting? As small LDL is corrected, the crude Friedwald calculated LDL approximates the more accurate LDL particle number. It assumes that accuracy of the Friedewald calculation may be more likely to occur as LDL size approaches normal. However, when LDL size is abnormally small--a condition shared by at least 70% of people with coronary heart disease--then the Friedewald LDL becomes increasingly inaccurate.The opposite can also happen: When all or nearly all LDL particles are large, Friedewald calculated LDL can markedly overestimate LDL particle number. Yesterday, for instance, a patient had a Friedewald calculated LDL of 183 mg/dl, but an NMR particle number of 1110 nmol/L--drop the zero . . . LDL 110 mg/dl. This woman was advised to take a statin drug by her primary care physician, based on the Friedewald LDL. Instead, she proved to have a far lower LDL. She would not have benefitted from taking a statin drug. As I've warned many times before: Beware the Friedewald calculated LDL.
Some basic vitamin D issues 24. August 2008 William Davis (7) The last post on vitamin D raised a number of basic questions among readers. So let me discuss some of these questions one by one. All of them raise important issues surrounding the practical aspects of managing vitamin D in your health. Anne said:I think it is important to stress that vitamin D supplementation needs to be continued long term. I have met too many people who have been prescribed 50,000 IU of D2 for 8-12 weeks and then told to stop because their 23(OH)D went over 30ng/ml. I know one person who's doctor stopped and started the D2 3 times. Thanks for pointing that out, Anne. Excellent point. I also see doctors do this with statin drugs: start it, check a LDL level which is lower, then think that you're done and stop the drug. What the heck are they thinking? If vitamin D is not being produced by sun exposure and not obtainable through diet, continued supplementation is necessary, essentially for life. Twinb asked:How often you think Vit. D levels should be tested after the initial test is done, especially if the levels are drastically low?We have used every 6 months in the office. Ideally, levels are in mid-summer and mid- to-late winter in order to gauge the extremes of your seasonal fluctuations. While most adults over 40 fail to fluctuate more than 10 ng/ml in the Wisconsin climate (and this summer, after an initial rainy season early, has been flawlessly bright and sunny, in the high-70s and 80s every single day for months), an occasional person fluctuates more widely. The only way to judge is to check a blood level. Rich said:Vitamin D dosage effects appear to be quite idiosyncratic.Yes, indeed it is. Despite using crude rules-of-thumb, like taking 1000 units of vitamin D per 10 ng/ml desired (a rule I learned from Dr. John Cannell, which he offered fully aware of its inaccuracy), many people will surprise you and have levels that make no sense. Testing is crucial to know your vitamin D level. Richard asked: Where do we get enough vitamin D wihout worring about laboratory tests? Well, the entire point of the post was that you absolutely, positively cannot just take vitamin D blindly at any dose and hope that your level is ideal, no more than you can blindly take a dose of thyroid and know you have achieved normal thyroid levels. In my view, vitamin D blood levels are an absolute. Another simple issue: Don't be afraid of vitamin D. It is, in all practicality, no more dangerous than getting a dark tan. (But, as many of you realize, getting a tan is no assurance of raising vitamin D if you are over 40 years old.)Wouldn't it be great if someone developed a do-it-yourself-at-home skin test for vitamin D? I know of no effort to develop this, but it would be a huge advantage for all of us.
“How much vitamin D should I take?” 22. August 2008 William Davis (17) It’s probably the number one most common question I get today: “How much vitamin D should I take?”Like asking for investing advice, there are no shortage of people willing to provide answers, most of them plain wrong. The media are quick to offer advice like “Take the recommended daily allowance of 400 units per day,” or “Some experts say that intake of vitamin D should be higher, as high as 2000 units per day.” Or “Be sure to get your 15 minutes of midday sun.”Utter nonsense. The Food and Nutrition Board of the Institute of Medicine has been struggling with this question, also. They have an impossible job: Draft broad pronouncements on requirements for various nutrients by recommending Recommended Daily Allowances (RDA) for all Americans. The Food and Nutrition Board has tried to factor in individual variation by breaking vitamin D requirements down by age and sex, but what amounts to a one-size-fits-nearly-all approach. Much of the uncertainty over dosing stems from the fact that vitamin D should not be called a “vitamin.” Vitamins are nutrients obtained from foods. But, outside of oily fish, you'll find very little naturally-occurring vitamin D in food. (Even in fish, there is generally no more than 400 units per 4 oz. serving.) Sure, there’s 20 units in an egg yolk and you can activate the vitamin D in a shiitake mushroom by exposing it to ultraviolet radiation. Dairy products like milk (usually) contain vitamin D because the USDA mandates it. But food sources hardly help at all unless you’re an infant or small child. It all makes sense when vitamin D is viewed as a hormone, a steroid hormone, not a vitamin. Vitamin-no, steroid hormone-D exerts potent effects in tiny quantities with hormone-like action in cells, including activation of nuclear receptors. It is the only hormone that is meant to be activated by sun exposure of the skin, not obtained through diet. But the ability to activate D is lost by the majority of us by age 40 and even a dark tan is no assurance that sufficient skin prohormone D activation has taken place. As with any other hormone, such as thyroid, parathyroid, or growth hormones, dose needs to be individualized. Imagine you developed a severely low thyroid condition that resulted in 30 lbs of weight gain, lose your hair, legs swell, and heart disease explodes. Would you accept that you should take the same dose of thyroid hormone as every other man or woman your age, regardless of your body size, proportion of body fat, metabolism, genetics, race, dietary habits, and other factors that influence thyroid hormone levels? Of course you wouldn’t. Then why would anyone insist that vitamin D be applied in a one-size-fits-all fashion? (There’s another world in which a one-size-fits-all approach to hormone replacement has been widely applied, that of female estrogen replacement. In conventional practice, there’s no effort to identify need, estrogen-progesterone interactions, nor assess the adequacy of dose, not to mention the perverse non-human preparation used.) With thyroid hormone, ideal replacement dose of hormone ranges widely from one person to another. Some people require 25 mcg per day of T4; others require 800% greater doses. Many require T3, but not everybody. Likewise, vitamin D requirements can range widely. I have used anywhere from 1000 units per day, all the way up to 16,000 units per day before desirable blood levels were achieved. Vitamin D dose needs to be individualized. Factors that influence vitamin D need include body size and percent body fat (both of which increase need substantially); sex (males require, on average, 1000 units per day more than females); age (older need more); skin color (darker-skinned races require more, fairer-skinned races less); and other factors that remain ill-defined. But these are “rules” often broken. My office experience with vitamin D now numbers nearly 1000 patients. The average female dose is 4000-5000 units per day, average male dose 6000 units per day to achieve a blood level of 60-70 ng/ml, though there are frequent exceptions. I’ve had 98 lb women who require 12,000 units, 300 lb men who require 1000 units, 21-year olds who require 10,000 units. (Of course, this is a Wisconsin experience. However, regional differences in dosing needs diminish as we age, since less and less vitamin D activation occurs.)Let me reiterate: Steroid hormone-vitamin D dose needs to be individualized. There’s only one way to individualize your need for vitamin D and thereby determine your dose: Measure a blood level. Nobody can gauge your vitamin D need by looking at you, by your skin color, size, or other simple measurement like weight or body fat. A vitamin D blood level needs to be measured specifically-period. Unfortunately, many people balk at this, claiming either that it’s too much bother or that their doctor refused to measure it. I would rank normalizing steroid hormone-vitamin D as among the most important things you can do for your health. It should never be too much bother. And if your doctor refuses to at least discuss why he/she won’t measure it, then it’s time for a new doctor. If you’re worried about adding to rising healthcare costs by adding yet another blood test, think of the money saved by sparing you from a future of cancer, heart disease, osteoporosis, diabetes, etc. The cost of a vitamin D blood test is relatively trivial (around $40-50, a fraction of the cost of a one month supply of a drug for diabetes.) So how much vitamin D should you take? Enough to raise your blood level of 25-hydroxy vitamin D to normal. (We aim for a normal level of 60-70 ng/ml.)
You probably don't take enough fish oil 20. August 2008 William Davis (17) The results of the recent Heart Scan Blog survey in response to the question: MY DAILY DOSE OF EPA + DHA FROM FISH OIL IS revealed:Zero--I don't take any 17 (7%) of respondents Less than 1000 mg per day 24 (10%) of respondents 1000-2000 mg per day 91 (38%) of respondents 2000-3000 mg per day 44 (18%) of respondents 3000-4000 mg per day 40 (16%) of respondents More than 4000 mg per day 20 (8%) of respondentsBased on the above results, I would say that only a minority of respondents are taking an ideal dose of omega-3 fatty acids. Nearly all of us should consider taking more. Benefits of omega-3 fatty acids (EPA + DHA) from fish oil begin around a dose of 840 mg per day, according to the GISSI Prevenzione Trial of 1999, an 11,000-participant trial. This dose also corresponds to a quantity of omega-3s that have been shown to raise EPA + DHA blood levels and thereby reduce the notoriously high AA:EPA ratio of Americans. But what dose is sufficient? What dose is ideal? Well, the answer to a great degree depends on what you are taking the fish oil for. If being taken to reduce triglycerides and triglyceride-containing lipoproteins, like VLDL and the after-eating (postprandial) IDL, then a higher dose will be necessary. (Triglyceride reduction for the genetically-determined very high triglyceride level of familial hypertriglyceridemia is the FDA-approved indication for prescription Lovaza.) If you are taking fish oil for treatment of ADHD, depression, or bipolar illness, very high doses are often necessary. But how about maximal reduction of cardiovascular risk and for control or reversal of atherosclerotic plaque? This conversation is still evolving. But we can learn some important lessons from three populations of the world that are vigorous consumers of fish:--The Inuits (aka Eskimos) of Greenland and northern Canada--The Japanese--The Bantus of Tanzania who live along Nyasa LakeAll three indigenous populations have several-fold greater intakes of fish and omega-3 fatty acids, have higher blood levels of omega-3 fatty acids, and have enjoyed reduced cardiovascular events, reduced atherosclerotic plaque, or improvement in various surrogates of cardiovascular risk (e.g., Lp(a)). The most recent addition to this conversation is the ERA JUMP Study, discussed in a previous Heart Scan Blog post. In ERA JUMP, despite being heavy smokers and having other markers for greater risk for heart disease, Japanese men living in Japan had markedly less carotid and coronary plaque, as compared to Caucasian men living in PIttsburgh or Hawaiian men of Japanese descent. The difference appeared to be attributable to serum levels of omega-3 fatty acids. I believe that the trend is here is to increase the amount of omega-3 fatty acids that most of us take. In the Track Your Plaque program, we have been advocating a rock-bottom starting dose of EPA + DHA of 1200 mg per day. However, I believe that this is due for a change. We will be increasing the minimum dose for plaque regression and control. Please attend our Webinar this evening for a full, in-depth discussion of the rationale behind this important change. As always, let me remind you that I am not selling, nor ever have sold, fish oil supplements. If I advocate a specific dose, a higher dose, I do so based on my interpretation of the data and experience with patients, not because I am interested in selling brand X of fish oil.
Vitamin D and HDL 19. August 2008 William Davis (23) Despite the paucity of scientific documentation of this phenomenon, I am continuing to witness extraordinary increases in HDL cholesterol levels with vitamin D supplementation. I've touched on the interaction of vitamin D supplementation with HDL in The Heart Scan Blog previously:Vitamin D: Treatment for metabolic syndrome?HDL for DummiesAt first, I thought it was attributable to other factors. In real life, most people don't modify one factor at a time. They reduceprocessed carbohydrates/eliminate wheat and cornstarch, lose weight, add or increase omega-3 fatty acids from fish oil, begin niacin, increase exercise and physical activity. All these efforts also impact on HDL. Among the many things I do, I consult on complex lipid (cholesterol) disorders (complex hyperlipidemias) in my office. A substantial number of these people carry a diagnosis of hypoalphalipoproteinemia, a mouthful that simply means these people are unable to manufacture much apoprotein A1, the principal protein of HDL cholesterol particles. As a result, people with hypoalphalipoproteinemia have HDL cholesterol levels in the neighborhood of 20-30 mg/dl--very low. They are also at high risk for heart disease and stroke. Encourage these people to exercise, attain ideal weight, eliminate wheat and cornstarch: HDL increases 5 mg/dl or so. Add niacin, HDL increases another 5-10 mg/dl. Perhaps we're now sitting somewhere around an HDL of 35-40 mg/dl--better, but hardly great. Add vitamin D to achieve our target serum level . . . HDL jumps to 50, 60, 70, even 90 mg/dl. The first few times this occurred, I thought it was an error or fluke. But now that I've witnessed this effect many dozens of time, I am convinced that it is real. Just today, I saw a 40-year old man whose starting HDL was 25 mg/dl increase to 87 mg/dl. Responses like this are supposed to be impossible. Before vitamin D, I had never witnessed increases of this magnitude. Not all therapies for raising HDL raise the important large (also known as HDL2b) fraction. With lipoprotein analyses, it appears that is principally the large fraction of HDL that rises with vitamin D supplementation. Why? How? That I can't tell you. But for those of you struggling with low HDL cholesterols despite your best efforts, vitamin D can make a world of difference.An interesting corollary: If super-high HDL cholesterols are associated with extreme longevity, as they are with centenarians, does raising HDL to extraordinary levels with vitamin D lead to longer, healthier life, all the way up to age 110 years? Again, no answers, but an interesting thought. And one I'd bet on. (And I'm not selling vitamin D.)
Weight loss and blood pressure 15. August 2008 William Davis (6) Here's another thought with regards to time issues with weight loss: reductions in blood pressure (BP). The previous post talked about how triglycerides initially go up, sometimes way up, when weight drops, only to be followed months later by substantial drops. HDL initially drops in response to the triglyceride fluctuations, only to be followed by a rise. Blood pressure also shows a curious pattern that is largely dependent on age. Say someone in their 20s or 30s, for instance, loses 30 lbs (through elimination of wheat and cornstarch, say). BP usually drops within a few weeks, perhaps a month or two at most. How about someone in their 70s? Say a substantial amount of weight is lost, say 50 lbs over 6 months. BP does indeed drop, but it may require 6 months or longer after weight plateaus for the full effects of BP-reduction to be fully expressed. But it will eventually drop. Why the age-dependent difference? It relates to the capacity of arteries to remain flexible and distensible. Over the years, cross-linking of collagen (a structural protein), glycation (glucose molecules attaching to proteins), loss of endothelial responsiveness to generate artery-dilating substances like nitric oxide, and arterial atherosclerotic plaque all all up to making older arteries less able to "relax" and BP to drop. But given time and the proper effort, BP will eventually drop. Awareness of this time effect can help most people decide better when medications are necessary or if weight loss alone is sufficient to reach BP goals.
"I lost 30 lbs and my triglycerides went . . . up?" 13. August 2008 William Davis (6) Brad needed to lose weight. At 6 ft tall, he began the program at 291 lbs, easily 80 lbs overweight. He wore virtually all of it in his belly. He had laboratory numbers to match: HDL 33 mg/dl, triglycerides 225 mg/dl, LDL (calculated) 144 mg/dl, blood sugar 122 mg/dl (fasting--clearly "pre-diabetic"), c-reactive protein 3.0 mg/dl. Among his lipoprotein abnormalities: small LDL representing 80% of all LDL (no surprise). Readers of The Heart Scan Blog know that these are the patterns of the carbohydrate-indulgent. I asked Brad to eliminate all wheat flour products, all foods made with cornstarch, and follow a diet rich in healthy oils, raw nuts, vegetables, and lean meats. Brad returned for a discussion about follow-up basic lipids (cholesterol) values four months later--31 lbs lighter, most of it clearly lost from his abdomen. He claimed he felt more energetic and clear-headed than he had in years. His lipid panel: HDL 34 mg/dl, LDL 122 mg/dl, triglycerides 295 mg/dl. Brad's smile dissolved. "How could that happen? You said losing weight would make my HDL go up and my triglycerides go down!"Yes, I had said that. But I was oversimplifying. The truth is that, when there is weight loss, especially profound weight loss like Brad experienced eliminating wheat and cornstarch products, there is mobilization of fat stores. Fat is stored energy. Energy is stored as . . . triglycerides. So when there is substantial weight loss, there is a flood of triglycerides in the blood, and triglyceride levels in the midst of weight loss can commonly jump up, not uncommonly to the 200-300+ mg/dl range. When triglycerides go up, there is also a drop in HDL (triglycerides interact with HDL particles, modify their structure and make them more readily destroyed, thereby dropping blood levels). Occasionally, substantial weight loss like Brad experienced will drop HDL really low, as low as the 20's. Once weight stabilizes, this effect can last up to 2 months before correcting. Only then will triglycerides drop and HDL rise. The rise in HDL occurs even more slowly, requiring several more months to plateau. In other words, weight loss like Brad's causes triglycerides to increase and HDL to decrease, to be followed later by a drop in triglycerides and a rise in HDL. I know of no way to block this phenomenon. And perhaps we shouldn't, since this is how fat stores are mobilized and "burned off." Fish oil does blunt the triglyceride rise (perhaps through activation of lipoprotein lipase, an enzyme responsible for clearance of triglycerides), but doesn't eliminate it. I call these changes "transitional" changes in lipids. Patience pays. A few more months from now, Brad's numbers will be much happier, as will Brad.
Divorce court for the doctor-patient relationship? 10. August 2008 William Davis (4) The doctor-patient relationship has gone sour. This probably comes as no surprise to most of you, particularly if you've been following conversations here in The Heart Scan Blog:Who is your doctor? discussing the emergence of the physician-as-hospital-employee phenomenon that causes your doctor to become the de facto portal (seller?) of hospital services to you, a model fraught with conflicts of interest.