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 High LDL cholesterol--only Toggle navigation Home Blog Home Archive Join Now Log in High LDL cholesterol--only 11. May 2007 William Davis (3) As a sequel to my last post, just how often can we blame an isolated high LDL cholesterol as the cause of coronary plaque and a heart scan score?In other words, how often does someone prove to have only LDL cholesterol as the cause of a heart scan score . . . and nothing else? No low HDL, small LDL, lipoprotein(a), a post-prandial (after-eating) intermediate-density lipoprotein, inflammatory responses, phospholipase A2, high triglycerides, vitamin D deficiency, etc.Rarely. In fact, I can truly count the number of people who have only LDL cholesterol as their sole cause of coronary atherosclerotic plaque on one hand. It is really an infrequent situation. Far more commonly, people have 5, 6, 7 or more reasons for coronary plaque. Thus, the idea that a statin drug to reduce LDL will cure heart disease is completely folly. It does happen--but rarely. I think I've seen it happen twice. Much more commonly, a program that addresses all the causes of coronary plaque yields far superior benefits. In my view, an effort to identify all the causes is relatively easy, makes far better sense, and provides you much greater assurance that you will succeed in conquering heart disease and removing its evil influence from your life. Related posts High LDL cholesterol--only As a sequel to my last post, just how often can we blame an isolated high LDL cholesterol as the cau... When is LDL cholesterol NOT LDL cholesterol? Darlene had a high LDL cholesterol, at times as high as 200 mg/dl. Her primary care doctor first tri... I don’t have high blood pressure! Art undeniably had high blood pressure.At age 53, he had all the “footprints” of high blood pressure... Comments (3) - Anonymous 5/11/2007 7:21:00 PM | Dr. Davis, two things check out this web site http://www.traceminerals.com/research/synx.html it appears to have some good data on Metabolic Syndrome-X: I would like to share some good data that I have had by following the TYP program, I was diagnosed with type 2 diabetes Feb. 15 and after that I got my second heart scan, over 600 (my age 57) a 43% increase in 18 Mo. Not good needless to say, than I found TYP in march of this year I started slowly following and implementing a TYP plan, BackgroundIn February I did not feel well and I went to the doctor(2/15) I had lost 12 lbs my % body fat was going up the muscles in my stomach were sore at times I was so thirsty I could not stand it and my eye site was changing. Needless to say I was diagnosed as a type II diabetic glucose 344 A1C 11.2, was prescribed new medications for both the diabetic condition( Januvia 100mg 1X per day actoPlus Met 2X per day 15mg 850mg) along with cholesterol ( Advicor 20/1000 ). I started a life style changing program.Life style changesModified eating program- went to a low GI high Vegetable protein including soy no or almost no Fats, eat as much as I want .(needless to say I have changed this plan)Quit smoking Increased exercise- walking on treadmill 7%grade 3.75mph from 30 min. to 30 min twice a dayMy Medications were changed Advicor 20/1000; Lisinopril-hydrochlorothiazide tablets 10-12.5 mg and a 325mg aspirinApril started on the TYP plan, my Glucose average was way up, my total cholesterol number was 100 but my LDL-P was 1015 and my small LDL-P was 913 along with a HDL-C of 30 went on the TYP programHad my Vitamin D checked -it was low , had my DHEA checked it was low, had my Magnesium checked it was low, after my discussion with you came off Lisinopril , ( we are seeing were this settles out to pick the right med's) stopped talking all diabetic med's added two other supplements R-ALA , PGX Fiber Blend (instead of oatmeal too many carbs) along with Vit D, Magnesium, DHEA , 15 grams of soy protein Fish oil, healthy Fats, no wheat products, Dark chocolates L-Arginine. I have had a additional blood test for these items (Vit D magnesium, DHEA) adjusted supplements body fat down to less than 14% WHAT A DIFFERENCE, in the last 11 days my fasting glucose numbers are between 84 and 103 that’s normal, before they were above 125 solidly Diabetic (since Feb even with diabetic medications) my doctor has never seen this much improvement without medication, on someone that had a 12 week ave of over 340.I do not know who is more anxious to see my next lipid profile me or my doctor . I'am scheduled in three weeks. Needless to say i also beleive that very few people can just take one pill and be cured. I hope i'am alive when they do find the magic cure (and i think they will) but right now the TYP plan is the best game in town. Eugene buy jeans 11/3/2010 3:12:33 PM | Thus, the idea that a statin drug to reduce LDL will cure heart disease is completely folly. It does happen--but rarely. I think I've seen it happen twice. Much more commonly, a program that addresses all the causes of coronary plaque yields far superior benefits. viagra online 4/19/2011 8:16:49 PM | I knoe a lot about the Cholesterol!LDL particles vary in size and density, and studies have shown that a pattern that has more small dense LDL particles, called Pattern B, equates to a higher risk factor for coronary heart disease!!My grandpa died for this reason, I think that it was terrible!! Add comment Comment Preview Name * E-mail * Comment * Preview Notify me when new comments are added The captcha text was not valid. Please try again.
High LDL cholesterol--only 11. May 2007 William Davis (3) As a sequel to my last post, just how often can we blame an isolated high LDL cholesterol as the cause of coronary plaque and a heart scan score?In other words, how often does someone prove to have only LDL cholesterol as the cause of a heart scan score . . . and nothing else? No low HDL, small LDL, lipoprotein(a), a post-prandial (after-eating) intermediate-density lipoprotein, inflammatory responses, phospholipase A2, high triglycerides, vitamin D deficiency, etc.Rarely. In fact, I can truly count the number of people who have only LDL cholesterol as their sole cause of coronary atherosclerotic plaque on one hand. It is really an infrequent situation. Far more commonly, people have 5, 6, 7 or more reasons for coronary plaque. Thus, the idea that a statin drug to reduce LDL will cure heart disease is completely folly. It does happen--but rarely. I think I've seen it happen twice. Much more commonly, a program that addresses all the causes of coronary plaque yields far superior benefits. In my view, an effort to identify all the causes is relatively easy, makes far better sense, and provides you much greater assurance that you will succeed in conquering heart disease and removing its evil influence from your life.