60-year old man dies of high cholesterol 1. February 2012 William Davis (12) Never saw a headline like this? Neither have I. That's because it doesn't happen.Cholesterol doesn't harm, maim, or kill. It is simply used as a crude--very crude--marker. It is, in reality, a component of the body, of the cell wall, of lipoproteins (lipid-carrying proteins) in the bloodstream. It is used a an indirect gauge, a "dipstick," for lipoproteins in the blood to those who don't understand how to identify, characterize, and quantify actual lipoproteins in the blood.Cholesterol itself never killed anybody, any more than a bad paint job on your car could cause a fatal car accident.What kills people is rupture of atherosclerotic plaque in the coronary arteries. For all practical purposes, you must have atherosclerotic plaque in order for it to rupture (much like a volcano erupts and spews lava). It's not about cholesterol; it's about atherosclerotic plaque. Plaque might contain cholesterol, but cholesterol is not the thing itself that causes heart attack and death.So why do most people obsess about cholesterol? Good question. It is, at best, a statistical marker for the possibility of having atherosclerotic plaque that ruptures. High cholesterol = higher risk for heart attack, low cholesterol = lower risk for heart attack. But the association is weak and flawed, such that people with high cholesterol can live a lifetime without heart attack, people with low cholesterol can die at age 43.The same holds true for LDL cholesterol, you know, the calculated value based on flawed assumptions about LDL's relationship to total cholesterol, HDL cholesterol, and VLDL cholesterol.A crucial oversight in the world of cholesterol: There are many other factors that cause atherosclerotic plaque and its rupture, such as inflammatory phenomena, calcium deposition, artery spasm, hemorrhage within the plaque itself, degradative enzymes, etc., none of which are suggested by cholesterol measures.But one observation has held up, time and again, over the past 40 years of observations on coronary disease: The greater the quantity of coronary atherosclerotic plaque, the greater the risk of atherosclerotic plaque rupture. An increasing burden of atherosclerotic plaque along the limited confines of coronary arteries, just a few millimeters in diameter and a few centimeters in length, is like a house of cards: It's bound to topple sooner or later, and the bigger it gets, the less stable it becomes.If you are concerned about future potential for heart disease and heart attack, don't get a cholesterol panel. Get a measure of coronary atherosclerotic plaque.
Back to basics: Coronary calcium 30. January 2012 William Davis (42) After having my attentions pulled a thousand different directions these past 6 months, with the release of Wheat Belly and all the wonderful media attention it has attracted, I've decided to pick up here with a series of discussions about the fundamental issues important to the Track Your Plaque program and prevention and reversal of coronary atherosclerotic plaque.I fear the discussions at times have drifted off into the exotic. This is great because this is how we learn new lessons, but we can never lose sight of the basics, else we risk losing control over this disease.Imagine you've got a beautiful new car. You wax it, gap the spark plugs, rotate the tires, etc. and it looks brand-new, just like it came off the dealer's lot. 50,000 miles pass, however, and you realize you've forgotten to change the oil. Ooops! In other words, no matter how meticulous the attention to transmission, tires, and paint job, neglect of the most basic responsibility can ruin the whole thing. We can't let that happen with heart health.If we propose to reverse coronary atherosclerotic plaque, we've got to have something to measure. First, it tells us whether we have atherosclerotic plaque in the first place, the stuff that accumulates and blocks flow and causes anginal chest pains, and ruptures like a little volcano and causes heart attacks. Second, it gives us something to track over the years to know whether plaque has grown, stopped growing, or been reduced. Without such a measure, you will be driving without a speedometer or odometer, just guessing whether or not you've gotten to your destination.Of course, the conventional approach to heart disease and heart attack is not to track atherosclerotic plaque in your coronary arteries, but to track some distant "risk factor" for atherosclerotic plaque, especially LDL cholesterol. But LDL cholesterol is flawed at several levels. First, it is calculated, not measured. The nearly 50-year old Friedewald equation used to calculate LDL cholesterol is based on several flawed assumptions, yielding a value that can be 20, 30, or 50% inaccurate as a rule, only occasionally generating a value close to the real value. (No point in publicizing this problem, of course: Why compromise a $27 billion annual cash cow?) It also ignores the effect of diet. (No, cutting fat does not reduce LDL for real, only the calculated value. Cutting carbohydrates, especially wheat--"healthy whole grains"--slashes measured LDL values like NMR LDL particle number and apoprotein B.)But all risk factors are, at best, snapshots of the situation at that moment in time. They change from day to day, week to week, month to month, year to year. If you do something dramatic in health, like lose 50 pounds, you can substantially change your risk factors values, like LDL cholesterol and HDL cholesterol. But you may not modify the amount of atherosclerotic plaque in your heart's arteries.Measuring the amount of atherosclerotic plaque in your heart's arteries is, in effect, a cumulative expression of the effects of risk factors up until the moment of measurement.There are several stumbling blocks, however, in the concept of measuring coronary atherosclerotic plaque. We cannot measure all the unique components of plaque, such as fibrous tissue like collagen, or degradative enzymes like collagenases, or inflammatory proteins like matrix metalloproteinase, or the debris of hemorrhage and inflammation. We struggle to contemporaneously mix in measures of bloodborne inflammation, coagulation and viscosity, and physiological phenomena of the artery itself, like endothelial dysfunction, medial (muscle) tone, and adventitial fat.So we are left with semi-static measures of total coronary atherosclerotic plaque like coronary calcium, obtainable via CT heart scans as a calcium "score." No, it is not perfect. It does not reflect that moment's blood viscosity, it does not reflect the inflammatory status of the one nasty plaque in the mid-left anterior descending, nor does it reflect the irritating sheer effects of a blood pressure of 150/95.But it's the best we've got.If anyone has something better, I invite you to speak up. Carotid ultrasound, c-reactive protein, ankle-brachial index, stress nuclear studies, myoglobin, skin cholesterol, KIF6 genotype . . . none of them approach the value, the insight, the trackability of actually measuring coronary atherosclerotic plaque. And the only method we've got to gauge coronary atherosclerotic plaque that is non-invasive and available in 2012? Yup, a good old CT heart scan calcium score.
Myocardial infraction 15. January 2012 William Davis (45) I've seen a few heart attacks this past year . . . but none in the people who follow this program. I saw a heart attack in a priest, a wonderful man who was unable to say "no" to his parishioners who insisted on bringing pies, cakes, and cookies every day. I saw an impending heart attack in a 74-year old man, a football coach who thought the whole wheat-free, low-carb thing was some wacko trend. Four stents later, he's changed his mind. A 69-year old woman had to be hospitalized for heart failure due to partial closure of an artery. She repeatedly told me that she simply could not follow the diet because it was "too restrictive." There were a few others. Interestingly, all felt they were eating healthy, minimizing junk foods and avoiding fatty foods. None were wheat-free nor restricted carbohydrates. In other words, in the people who follow the basic advice of the Track Your Plaque program to do such simple things as eliminate wheat, don't indulge in junk carbohydrates, normalize vitamin D status, supplement omega-3 fatty acids, supplement iodine and correct any thyroid dysfunction . . . well, they have no heart attacks.
Diet is superior to drugs 7. January 2012 William Davis (27) Might-o’chondri-AL left this wonderful record of his lipoprotein experience in the comments to the last Heart Scan Blog post. It is a great example of what is achievable with diet and a few supplements . . . without drugs. (A) Jan. 2011 1st ever NMR lipo-protein analysis was done after 4 months of consistent home food prep of pretty low fat (only olive oil and 1 tablespoon coconut oil daily) but plenty of whole wheat and half potatoes:* LDL # of particles (P) = 1,676 in nmol/L————being a LDL cholesterol (C) reading of 139 mg/dL* small LDL # P = 1,021 nmol/L —————yikes! you advise smLDL be less than 117 nmol/L* HDL # of particles = 28.8 umol/L ————–being a HDL C reading of 45 mg/dL* Triglycerides = 90 mg/dL ————– true, I never struggled with my weight(B) May 2011 2nd NMR after another 4 months but added in more fat (1 teaspoon highly concentrated fish oil daily, 90% chocolate, handfulls of nuts, more olive oil and kept coconut oil at 1 tablespoon daily for a controlled experiment), added 500 mg Niacin 3 times a day (in stages up to1,500 mg. total daily), 6000 IU daily vitamin D, deliberately cut out all grains except for social politeness and substituted in daily Koji fermented brown rice (rustic Amazake):** LDL # P……………= 976 nmol/L ——————————– being LDL C of 100 mg/dL** small LDL # P …. = 96 nmol/L ——————————– nice surprise** HDL # P ………… = 27.3 umol/L ——————————being an increase to HDL C of 64 mg/dL** Triglycerides …… = 42 mg/dL ——————————– despite daily carbs over 150 gr. daily(C) Dec. 2011 3rd NMR after another 7 more months thinking Doc’s advice is worthwhile I added in yet more fat (mainly daily 2 tablespoons of coconut oil, more 90% chocolate), bumped Niacin up to 1,000 mg twice a day (2,000 mg. total daily), cut out the Amazake, kept up the vitamin D adding daily vitamin K & daily ate main mid-day meal out as lunch on spicy Thai & Chinese fish/shrimp/soup/rice meals (my next control):*** LDL # P ………. = 764 nmol/L ————— being LDL C of 107 mg/dL ( 2x coconut’s saturated fat)***small LDL # P… = less than 90 nmol/L ——–surprised me NMR can’t count lower***HDL # P ……… = 41.4 umol/L ——————– being an increase to HDL C of 88 mg/dL*** Triglycerides ….= 43 mg/dL ——————- daily carbs below ~ 120 gr. & lost too much weightIsn't that great? Spectacular job, Might!MIght achieved values that are superior to that achievable with, say, a high-dose statin strategy. Statins only reduce total LDL particles, reducing small LDL in a non-selective way. And, of course, this diet does not cause muscle aches, memory loss, nor liver problems. Something to consider: As the diet has become so effective, we can reduce our reliance on niacin. In fact, the benefits of niacin diminish substantially, as small LDL is reduced, HDL increased, triglycerides decreased, and postprandial lipoproteins subdued with the diet only.
Low-carb is heart healthy 4. January 2012 William Davis (88) Anybody following the discussions in these pages know that: Limiting carbohydrate intake reduces risk for coronary heart disease and heart attack.First of all, why do conventional diets advocate restricting saturated and total fat? From the standpoint of surrogate markers of cardiovascular risk, cutting saturated and total fat reduces total cholesterol; reduces calculated LDL cholesterol; and may reduce c-reactive protein modestly (an index of inflammation). It also increases blood sugar and HbA1c (reflecting the prior 60 days blood sugars), increases glycation of the proteins of the body leading to cataracts, arthritis, and hypertension. Problem: Total cholesterol is a combination of HDL cholesterol, an estimate of VLDL cholesterol (triglycerides), and LDL cholesterol. It is a composite of both "good" things (HDL) and "bad" things (LDL and VLDL). Cutting saturated and total fat results in reduced HDL, increased VLDL/triglycerides, and a reduction in calculated LDL. Pretty weak stuff. The last item, i.e., reduction in calculated LDL, is not even a real phenomenon. In fact, the net effect in most genotypes (genetic types) may be negative: increased heart disease risk. In contrast, what is the effect of reducing carbohydrate without restricting fat? (In the approach I use, we start with elimination of the most destructive of carbohydrates, wheat, followed by reducing exposure to other carbohydrates, especially cornstarch and corn products, sugar, and oats.) If, say, we cut carbohydrate intake into the range of a truly low-carbohydrate diet of 10-15 grams per meal ("net" carbs, or total carbohydrates minus fiber), then we witness a number of metabolic transformations:Reduced fasting triglycerides and VLDLReduced postprandial (after-eating) triglycerides, chylomicrons, and chylomicron remnantsIncreased HDL and shift towards large HDL particles (presumably more protective)Reduced small LDL particlesReduced glycation and oxidation of small LDL particlesReduced hemoglobin A1cReduced c-reactive protein and other inflammatory markersReduced blood pressureBy slashing carbohydrates, we also witness weight loss from visceral fat, reversal of pre-diabetes and diabetes, and reduced phenomena of glycation. And, if the wheat-free part of low-carb is maintained, you can also see marked improvement in gastrointestinal health, relief from joint pains, relief from leg edema, relief from migraine headaches, improved behavior and ability to concentrate in children with impaired learning, ADHD, and autism, better mood, deeper sleep. You will see multiple inflammatory and autoimmune diseases improve or completely relieved, such as rheumatoid arthritis and ulcerative colitis. Having personally gone down the diabetic path and back by cutting the fat in my diet, now maintaining a HbA1c of 4.8% with fasting glucose 84 mg/d; (without medications), there should be no remaining doubt: Low-carb diets, especially if wheat-free, dramatically reduce the factors leading to heart disease; low-fat diets worsen the factors leading to heart disease.
All posts by william-davis Toggle navigation Home Blog Home Archive Join Now Log in Firefighters Face Added Risk of Fatal Heart Attack 22. March 2007 William Davis (1) Firefighters are twice as likely to die from a heart attack in the line of duty than are policemen, and three times more likely than EMTs. That's among the headlines run today because of a report in the New England Journal of Medicine documenting a dramatically higher risk for heart attack for fire fighters putting out fires. The above headline is from an excellent report run on NPR radio. You can listen to the webcast at http://www.npr.org/templates/story/story.php?storyId=9047656.The story sparked comments from experts insisting that all fire fighters should have physicals, should be in better physical condition, should be covered by health insurance (the NPR report said that 1 out of 4 fire fighters lack health insurance). Judging from the indisputable risk firefighters encounter, these are all good ideas. But if you've been following my blog or the Track Your Plaque program, you know that physicals alone are hopeless exercises for identifying hidden heart disease. Among the solutions: identify whether or not heart disease is present in the first place--do a CT heart scan. In fact, several local fire companies in my area have done just that: insisting that all firefighters undergo a heart scan. When groups of people like firefighters arrange for heart scans, they gain the advantage of doing so en masse, thereby allowing many scan centers to offer a dramatically reduced price to the city, town, or village that is paying for them. I've even seen many firefighters scanned at no cost. It would also help to have health insurance, be physically fit, and have a stress test (an exception to my view that stress tests are also useless to screen asymptomatic people for heart disease). But a CT heart scan would settle the question quickly, easily, undeniably, and inexpensively. Prophylactic bypass surgery? 20. March 2007 William Davis (0) This question comes up around once a week:My CT heart scan score is ____. Wouldn't I be better off just getting a bypass (or stent, etc.) and getting it over with? If I know that heart attack is in my future, why not just get it over with?The most recent source of this question was the wife of a patient. Jack had a heart scan score of 92 in 2005. He made very little effort to correct his causes, permitting pre-diabetic patterns to persist, failed to correct vitamin D, etc. and a repeat heart scan score showed a dramatic rise to 264. Jack's wife asked whether he should just have a bypass. There are several problems with this line of reasoning:1) Bypass surgery does not reduce the long term risk for heart attack. 2) The risk of bypass surgery often outweighs the risk of an asymptomatic heart scan score. 3) Bypass surgery is a temporary "fix," a fancy Band Aid for a disease that progresses after the procedure. One bypass typically prompts another, and another...4) Bypassing arteries that have vigorous blood flow often causes the bypass graft to not "take" and close within the first few days. Thankfully, nobody in his right mind has proposed that we perform prophylactic bypass operations. Of course, hospitals and surgeons would jump at the chance to perform procedures in anybody with some threshhold heart scan score. It would double or triple their business overnight. At $70,000 or more per procedure, they would dance in glee. Of course, you and I would pay for their new burst of wealth by a sharp increase in our health insurance premiums. Not only that, the people who underwent the procedure would not benefit. Lipitor 80 mg 20. March 2007 William Davis (4) I'm seeing more and more people taking 80 mg of Lipitor per day. For the most part, these are people who come in for another opinion after a stent or heart attack and are prescribed the drug during their hospitalization. This practice is based on the results of the PROVE IT-TIMI 22 (PRavastatin Or atorVastatin Evaluation and Infection Therapy-Thrombolysis In Myocardial Infarction) trial, and the Reversal of Atherosclerosis with Aggressive Lipid Lowering (REVERSAL) trial, both reported in 2005. In the PROVE IT Trial, 4,000 people experiencing heart attacks were treated with Lipitor (atorvastatin), 80 mg, or Pravachol (pravastatin), 40 mg. There was a reduction in events like recurrent heart attack from 13.1% in the Pravachol group to 9.6% in the Lipitor group. In the REVERSAL Trial, the Lipitor group also showed no plaque growth compared to the Pravachol group, which did progress, with disease tracked by intracoronary ultrasound.I believe that many of my colleagues took the bait. In a half-hearted effort to reduce events and trend towards better coronary plaque control, writing a prescription for 80 mg rather than a lower dose has become increasingly popular. Some problems: Despite the favorable tolerance to high dose Lipitor in these trials, I don't know anybody who can tolerate 80 mg per day for more than a few months in real life. In my experience, people inevitably end up with intolerable muscle aches. Also, I believe it is folly to believe that we can regress coronary plaque on a broad scale by just using one drug that addresses only a single cause (i.e., LDL cholesterol). Yes, drug companies would argue that the statin drugs are so wonderful because of their so-called "pleiotropic", or non-lipid, effects like reducing inflammation. I have seen regression of plaque once using Lipitor alone. We struggle to reduce coronary plaque using a multi-faceted approach. It is highly unlikely that Lipitor alone at a 80 mg dose will be sufficient in most people to regress plaque. How about lipoprotein(a)? Or vitamin D deficiency? Lipitor has no effect on these patterns and people do not regress just by taking statin agents. Orlistat for weight loss 19. March 2007 William Davis (3) In early February, the FDA approved orlistat, formerly known as prescription Xenical, for over-the-counter sale. Orlistat is a blocker of fat absorption. The new OTC version will be called "Alli" (pronounced like "ally") and will come at a dose of 60 mg to be taken three times a day with meals. Prescription Xenical came as a 120 mg tablet. However, the company claims that the reduced dose sacrifices only 5% in reduced fat absorption, dropping from 30% with Xenical to 25% with Alli. It will cost in the neighborhood of $1 to $2 per day, or $30-60 per month, far less expensive than the $110-150 for the prescription form. Does it work? Is it worth the money? Clinical trials document around 5-10 lbs lost over a 3 to 6 month period, 50% greater than using diet and exercise alone. Our experience is that it works, though inconsistently. Results depend heavily on how reliant you are on fat calories. If you were to follow a low-fat diet while on the drug, you likely will lose little or no weight, since there's little fat absorption to block. However, I have witnessed more substantial weight loss of 10-20 lbs. in people who follow a higher fat intake in their diet, e.g., a traditional American diet. However, these people gain the weight back immediately because they've made no effort to modify food choices. It is messy. Even though the clinical trials claims modest inconvenient effects like gas and greasy stools, I have found that it is, without fail, a very annoying product that results in crampiness and frequent messy stools in nearly everybody.The company has created a glitzy website that you can view at www.myalli.com and promises to provide a personalized program and support for registrants when it is up and running by summer 2007. I think that's a good idea, since the drug itself is no more than a temporary fix unless it's combined with long-term diet changes. However, the website, I believe, oversells the value of the drug with a drug company's usual over-the-top hints and innuendoes without actually coming out with straight pitches of the truth. Beware of the vitamin D-blocking effect of Orlistat. The period of time you take it may be a time to resort to some modest sun exposure (10-15 minutes; be careful not to burn), rather than than oil-based vitamin D capsules, in order to avoid the inevitable vitamin D plunge in blood level. I am not a fan of orlistat, having seen it tried many times with minimal success. However, it is another option for those who are really struggling. Personally, I would try fasting or some of the other strategies we've detailed on the www.cureality.com website before I resorted to orlistat. Low HDL makes Dr. Friedewald a liar 17. March 2007 William Davis (5) There's a $22 billion industry based on treating LDL cholesterol, a fictitious number. LDL cholesterol is calculated from the following equation:LDL cholesterol = Total cholesterol - HDL cholesterol - triglycerides/5So when your doctor tells you that your LDL cholesterol is X, 99% of the time it has been calculated. This is based on the empiric calculation developed by Dr. Friedwald in the 1960s. Back then, it was a reasonable solution, just like bacon and eggs was a reasonable breakfast and a '62 Rambler was a reasonable automobile.One of the problems with Dr. Friedewald's calculation is that the lower HDL cholesterol, the less accurate LDL cholesterol becomes. If it were just a few points, so what? But what if it were commonly 50 to 100 mg/dl inaccurate? In other words, your doctor tells you that your LDL is 120 mg/dl, but the real number is somewhere between 170 and 220 mg/dl. Does this happen?You bet it does. In my experience, it is an everyday event. In fact, I'm actually surprised when the Friedewald calculated LDL closely approximates true LDL--it's the exception. Dr. Friedewald would likely have explained that, when applied to a large population of, say, 10,000 people, calculated LDL is a good representation of true LDL. However, just like saying that the average weight for an American woman is 176 lbs (that's true, by the way), does that mean if you weigh 125 lbs that you are "off" by 41 lbs? No, but it shows how you cannot apply the statistical observations made in large populations to a single individual. The lower HDL goes, the more inaccurate LDL becomes. This would be acceptable if most HDLs still permitted reasonable estimation of LDL--but it does not. LDL begins to become significantly inaccurate with HDL below 60 mg/dl. How to get around this antiquated formula? In order of most accurate to least accurate:--LDL particle number (NMR)--the most accurate by far.--Apoprotein B--available in most laboratories.--"Direct" LDL--Non-HDL--i.e., the calculation of total cholesterol minus HDL. But it's still a calculated with built-in flaws. --LDL by Friedewald calculation. My personal view: you need to get an NMR if you want to know what your LDL truly is. A month of Lipitor costs around $80-120. A basic NMR costs less than $90. It's a relative bargain. Menopause unleashes lipoprotein(a) 16. March 2007 William Davis (0) Faye was clearly frustrated. At age 52, she was having chest pains every day. A CT heart scan showed a score of zero. A CT coronary angiogram showed no plaque whatsoever. "Everything went downhill when my menopause started. I gained weight, I started to have chest pains, my blood pressure went up, my cholesterol shot up."She saw three physicians, none of whom shed much light on the situation. They ran through the predictable sequence of (horse, not human) estrogens, anti-depressants, suggestions for psychological counseling. But we checked Faye for lipoprotein(a), which she proved to have at a high level of 182 nmol/l. This explained a lot.A curious and predictable set of phenomenon occur to females with Lp(a) proceeding through the menopause. As estrogen recedes:--Lp(a) levels rise dramatically.--Blood pressure goes up, sometimes creating severe hypertension by mid- to late-50s. --Chest pain can develop, presumably due to "endothelial dysfunction" or "microvascular angina", both representing abnormal coronary artery constriction facilitated by worsening expression of Lp(a). All too often, these phenomena get dismissed as simply part of the menopausal package, when they are, in fact, important facets of this very important genetic pattern that confers high risk for heart disease. If any of this rings familiar for you or a loved one, think Lp(a). Though Faye hadn't yet developed any measurable coronary plaque by her CT heart scan score, it was likely on its way, given the surge in Lp(a) expression as menopause unfolded--unless its recognized and appropriate preventive action taken. Vitamin D must be oil-based 15. March 2007 William Davis (0) I've ta
Firefighters Face Added Risk of Fatal Heart Attack 22. March 2007 William Davis (1) Firefighters are twice as likely to die from a heart attack in the line of duty than are policemen, and three times more likely than EMTs. That's among the headlines run today because of a report in the New England Journal of Medicine documenting a dramatically higher risk for heart attack for fire fighters putting out fires. The above headline is from an excellent report run on NPR radio. You can listen to the webcast at http://www.npr.org/templates/story/story.php?storyId=9047656.The story sparked comments from experts insisting that all fire fighters should have physicals, should be in better physical condition, should be covered by health insurance (the NPR report said that 1 out of 4 fire fighters lack health insurance). Judging from the indisputable risk firefighters encounter, these are all good ideas. But if you've been following my blog or the Track Your Plaque program, you know that physicals alone are hopeless exercises for identifying hidden heart disease. Among the solutions: identify whether or not heart disease is present in the first place--do a CT heart scan. In fact, several local fire companies in my area have done just that: insisting that all firefighters undergo a heart scan. When groups of people like firefighters arrange for heart scans, they gain the advantage of doing so en masse, thereby allowing many scan centers to offer a dramatically reduced price to the city, town, or village that is paying for them. I've even seen many firefighters scanned at no cost. It would also help to have health insurance, be physically fit, and have a stress test (an exception to my view that stress tests are also useless to screen asymptomatic people for heart disease). But a CT heart scan would settle the question quickly, easily, undeniably, and inexpensively.
Prophylactic bypass surgery? 20. March 2007 William Davis (0) This question comes up around once a week:My CT heart scan score is ____. Wouldn't I be better off just getting a bypass (or stent, etc.) and getting it over with? If I know that heart attack is in my future, why not just get it over with?The most recent source of this question was the wife of a patient. Jack had a heart scan score of 92 in 2005. He made very little effort to correct his causes, permitting pre-diabetic patterns to persist, failed to correct vitamin D, etc. and a repeat heart scan score showed a dramatic rise to 264. Jack's wife asked whether he should just have a bypass. There are several problems with this line of reasoning:1) Bypass surgery does not reduce the long term risk for heart attack. 2) The risk of bypass surgery often outweighs the risk of an asymptomatic heart scan score. 3) Bypass surgery is a temporary "fix," a fancy Band Aid for a disease that progresses after the procedure. One bypass typically prompts another, and another...4) Bypassing arteries that have vigorous blood flow often causes the bypass graft to not "take" and close within the first few days. Thankfully, nobody in his right mind has proposed that we perform prophylactic bypass operations. Of course, hospitals and surgeons would jump at the chance to perform procedures in anybody with some threshhold heart scan score. It would double or triple their business overnight. At $70,000 or more per procedure, they would dance in glee. Of course, you and I would pay for their new burst of wealth by a sharp increase in our health insurance premiums. Not only that, the people who underwent the procedure would not benefit.
Lipitor 80 mg 20. March 2007 William Davis (4) I'm seeing more and more people taking 80 mg of Lipitor per day. For the most part, these are people who come in for another opinion after a stent or heart attack and are prescribed the drug during their hospitalization. This practice is based on the results of the PROVE IT-TIMI 22 (PRavastatin Or atorVastatin Evaluation and Infection Therapy-Thrombolysis In Myocardial Infarction) trial, and the Reversal of Atherosclerosis with Aggressive Lipid Lowering (REVERSAL) trial, both reported in 2005. In the PROVE IT Trial, 4,000 people experiencing heart attacks were treated with Lipitor (atorvastatin), 80 mg, or Pravachol (pravastatin), 40 mg. There was a reduction in events like recurrent heart attack from 13.1% in the Pravachol group to 9.6% in the Lipitor group. In the REVERSAL Trial, the Lipitor group also showed no plaque growth compared to the Pravachol group, which did progress, with disease tracked by intracoronary ultrasound.I believe that many of my colleagues took the bait. In a half-hearted effort to reduce events and trend towards better coronary plaque control, writing a prescription for 80 mg rather than a lower dose has become increasingly popular. Some problems: Despite the favorable tolerance to high dose Lipitor in these trials, I don't know anybody who can tolerate 80 mg per day for more than a few months in real life. In my experience, people inevitably end up with intolerable muscle aches. Also, I believe it is folly to believe that we can regress coronary plaque on a broad scale by just using one drug that addresses only a single cause (i.e., LDL cholesterol). Yes, drug companies would argue that the statin drugs are so wonderful because of their so-called "pleiotropic", or non-lipid, effects like reducing inflammation. I have seen regression of plaque once using Lipitor alone. We struggle to reduce coronary plaque using a multi-faceted approach. It is highly unlikely that Lipitor alone at a 80 mg dose will be sufficient in most people to regress plaque. How about lipoprotein(a)? Or vitamin D deficiency? Lipitor has no effect on these patterns and people do not regress just by taking statin agents.
Orlistat for weight loss 19. March 2007 William Davis (3) In early February, the FDA approved orlistat, formerly known as prescription Xenical, for over-the-counter sale. Orlistat is a blocker of fat absorption. The new OTC version will be called "Alli" (pronounced like "ally") and will come at a dose of 60 mg to be taken three times a day with meals. Prescription Xenical came as a 120 mg tablet. However, the company claims that the reduced dose sacrifices only 5% in reduced fat absorption, dropping from 30% with Xenical to 25% with Alli. It will cost in the neighborhood of $1 to $2 per day, or $30-60 per month, far less expensive than the $110-150 for the prescription form. Does it work? Is it worth the money? Clinical trials document around 5-10 lbs lost over a 3 to 6 month period, 50% greater than using diet and exercise alone. Our experience is that it works, though inconsistently. Results depend heavily on how reliant you are on fat calories. If you were to follow a low-fat diet while on the drug, you likely will lose little or no weight, since there's little fat absorption to block. However, I have witnessed more substantial weight loss of 10-20 lbs. in people who follow a higher fat intake in their diet, e.g., a traditional American diet. However, these people gain the weight back immediately because they've made no effort to modify food choices. It is messy. Even though the clinical trials claims modest inconvenient effects like gas and greasy stools, I have found that it is, without fail, a very annoying product that results in crampiness and frequent messy stools in nearly everybody.The company has created a glitzy website that you can view at www.myalli.com and promises to provide a personalized program and support for registrants when it is up and running by summer 2007. I think that's a good idea, since the drug itself is no more than a temporary fix unless it's combined with long-term diet changes. However, the website, I believe, oversells the value of the drug with a drug company's usual over-the-top hints and innuendoes without actually coming out with straight pitches of the truth. Beware of the vitamin D-blocking effect of Orlistat. The period of time you take it may be a time to resort to some modest sun exposure (10-15 minutes; be careful not to burn), rather than than oil-based vitamin D capsules, in order to avoid the inevitable vitamin D plunge in blood level. I am not a fan of orlistat, having seen it tried many times with minimal success. However, it is another option for those who are really struggling. Personally, I would try fasting or some of the other strategies we've detailed on the www.cureality.com website before I resorted to orlistat.
Low HDL makes Dr. Friedewald a liar 17. March 2007 William Davis (5) There's a $22 billion industry based on treating LDL cholesterol, a fictitious number. LDL cholesterol is calculated from the following equation:LDL cholesterol = Total cholesterol - HDL cholesterol - triglycerides/5So when your doctor tells you that your LDL cholesterol is X, 99% of the time it has been calculated. This is based on the empiric calculation developed by Dr. Friedwald in the 1960s. Back then, it was a reasonable solution, just like bacon and eggs was a reasonable breakfast and a '62 Rambler was a reasonable automobile.One of the problems with Dr. Friedewald's calculation is that the lower HDL cholesterol, the less accurate LDL cholesterol becomes. If it were just a few points, so what? But what if it were commonly 50 to 100 mg/dl inaccurate? In other words, your doctor tells you that your LDL is 120 mg/dl, but the real number is somewhere between 170 and 220 mg/dl. Does this happen?You bet it does. In my experience, it is an everyday event. In fact, I'm actually surprised when the Friedewald calculated LDL closely approximates true LDL--it's the exception. Dr. Friedewald would likely have explained that, when applied to a large population of, say, 10,000 people, calculated LDL is a good representation of true LDL. However, just like saying that the average weight for an American woman is 176 lbs (that's true, by the way), does that mean if you weigh 125 lbs that you are "off" by 41 lbs? No, but it shows how you cannot apply the statistical observations made in large populations to a single individual. The lower HDL goes, the more inaccurate LDL becomes. This would be acceptable if most HDLs still permitted reasonable estimation of LDL--but it does not. LDL begins to become significantly inaccurate with HDL below 60 mg/dl. How to get around this antiquated formula? In order of most accurate to least accurate:--LDL particle number (NMR)--the most accurate by far.--Apoprotein B--available in most laboratories.--"Direct" LDL--Non-HDL--i.e., the calculation of total cholesterol minus HDL. But it's still a calculated with built-in flaws. --LDL by Friedewald calculation. My personal view: you need to get an NMR if you want to know what your LDL truly is. A month of Lipitor costs around $80-120. A basic NMR costs less than $90. It's a relative bargain.
Menopause unleashes lipoprotein(a) 16. March 2007 William Davis (0) Faye was clearly frustrated. At age 52, she was having chest pains every day. A CT heart scan showed a score of zero. A CT coronary angiogram showed no plaque whatsoever. "Everything went downhill when my menopause started. I gained weight, I started to have chest pains, my blood pressure went up, my cholesterol shot up."She saw three physicians, none of whom shed much light on the situation. They ran through the predictable sequence of (horse, not human) estrogens, anti-depressants, suggestions for psychological counseling. But we checked Faye for lipoprotein(a), which she proved to have at a high level of 182 nmol/l. This explained a lot.A curious and predictable set of phenomenon occur to females with Lp(a) proceeding through the menopause. As estrogen recedes:--Lp(a) levels rise dramatically.--Blood pressure goes up, sometimes creating severe hypertension by mid- to late-50s. --Chest pain can develop, presumably due to "endothelial dysfunction" or "microvascular angina", both representing abnormal coronary artery constriction facilitated by worsening expression of Lp(a). All too often, these phenomena get dismissed as simply part of the menopausal package, when they are, in fact, important facets of this very important genetic pattern that confers high risk for heart disease. If any of this rings familiar for you or a loved one, think Lp(a). Though Faye hadn't yet developed any measurable coronary plaque by her CT heart scan score, it was likely on its way, given the surge in Lp(a) expression as menopause unfolded--unless its recognized and appropriate preventive action taken.