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2011-02-18 William Castelli MD Heart Disease Risk, Cholesterol and Lipids in 2011: What Do We Really Know?

Heart Disease Risk: Cholesterol and Lipids in 2011
What Do We Really Know?

An Interview with William Castelli, M.D.

February 18, 2011, By Kirkham R. Hamilton, PA-C
©copyright 2011, Prescription 2000, Inc.
www.prescription2000.com

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KIRK HAMILTON: Hi, my name is Kirk Hamilton, your host of Staying Healthy Today. Our message is simple: To provide you credible usable health information from interviews and our educational resources to help you Stay and Be Well in the busy modern world. Please take a few moments before or after listening to this interview to browse through the Prescription2000.com website, the home of Staying Healthy Today Radio, for our free educational services.

Today's show topic is "Heart Disease Risk: Cholesterol and Lipids in 2011. What Do We Really Know?"
Our guest today is Dr. William Castelli, former director of the Framingham Heart Study and currently a staff physician at the Heart Center of MetroWest in Framingham, Massachusetts.

Welcome Dr. Castelli. It's an honor to have you on the show today.

DR. WILLIAM CASTELLI: Well thank you.

KIRK HAMILTON: Tell me. You know, I've heard your name for so many years with regards to the Framingham Heart Study and lipids. How long have you been practicing medicine and how did your career take twists and turns to lead you to do the Framingham Study and then get into really being known as, I guess of somewhat of the cholesterol man, so to speak?

DR. WILLIAM CASTELLI: Well, I started my internships probably in 1959 and then residencies in the early 60s. But then I went over to the Harvard Medical School to start growing cells that lined people's arteries in dishes and we fed them fat and carbohydrate. And then '65 I went out to Framingham to spin the bloods in the ultracentrifuge to separate the total into HDL and LDL and IDL and VLDL and chylos and Lp(a)s and some of the triglycerides. And you know it took us about 10 years after we measured something in Framingham to find out how it played out, and that's when we learned in the 70s that the higher the HDL went the lower the heart attack rate and the higher the LDL went the higher the heart attack rate. We also learned the higher the triglycerides went the higher the heart attack rate. But unfortunately the triglycerides have been ignored until very recently in medicine because in the 60s when lots of us were separating these totals into all these different kinds we ended up with the Fredrickson-Levy-Lees typing system based on essentially bell-shaped curves on LDL and bell-shaped curves on triglycerides. But you had to be in the upper end of those bell-shaped curves to have what they call the type. It was a Type II if you're in the upper end of the bell-shaped curved on LDL and a Type IV if you're on the upper end of the triglyceride curve and those were the two major types. But our lipid experts in America were attracted only to the upper end of the bell-shaped curve on LDL. And the reason for that is that if you are there in that upper end of that curve you have one of these really very dangerous genes for what we call familial hypercholesterolemia. And those people who get that gene get a very high LDL cholesterol, such that if you look in the clinics taking care of them after their heart attack, you learn that 5% of their patients have gotten their heart attack by age 30, 20% by age 40, half of them by age 50, 85% by the age of 65. And because they mostly did end up with a 300 cholesterol we learned in the Framingham Study that if you had a 300 cholesterol, 90 out of 100 of those people got a heart attack in the first 26 years. So that was a very dangerous place to be and those people wanted to find those genes and they found dozens and dozens and dozens. But unfortunately they were also the people who were advising the guidelines about what should be measured. And that's why the focus just went over to LDL for a long time, and then they made some very, very dangerous mistakes. See they were the ones who called a total cholesterol under 200 desirable. Now in Framingham when you had a cholesterol between 150 and 200 in the first 26 years, 20 out of 100 of those people went on and got a heart attack. Well these people of course were treating way up at the upper end of the cholesterol scale, up around 300 where the rate was 90 out of 100. So I guess when you've been treating 90 out of 100 and it falls to 20 out of 100 you call that desirable. But what is it they didn't understand? Well they didn't have a good statistical background, these people, so they didn't realize that this was 20 out of 100 of 45% of the population. And in the first 26 years of Framingham it produced 35% of all the heart attacks. Now that was twice as many heart attacks as that in 90 out of 100 at 5 to 10% of the population but they didn't get it as young as those people up there at the upper end, but they did get it and you can't call that desirable.

KIRK HAMILTON: So is the Framingham Study still going on, correct? It's fourth generation?

DR. WILLIAM CASTELLI: Yes it is. And you know I joined in '65 and in '70 I was instrumental in starting the second generation. And then when I retired in '95 and started a wellness clinic to get into how do you treat these risks, these lipid risks and blood pressure risk and all the risk factors. The guy that replaced me, Dan Levy, started the head of the third generation (Framingham Study). So we actually have three full generations under study in Framingham. The first is practically all passed away, but still you know we're going to get into someday all these genes as well and B but the dilemma in this whole issue about where we were in lipids. See if you were down there between 150 and 200 (cholesterol), how do I find the 20 that would need to be treated, but not - wouldn't want to have to treat perhaps the 80? Or if you had an average cholesterol with someone who gets a heart attack in America which would be in the low 220s, the rate is 40 out of 100. Well see, LDL is not going to help you identify those people the best. In fact, you're going to have to go to this ratio of the total (cholesterol) divided by the HDL, which is the best predictor. And see in the early, in the mid '70s when we finally did get outcome data on what we had measured starting in the mid '60s in Framingham, we had the best statisticians from the National Heart, Lung and Blood Institute. And one of them, Tavia Gordon, of course, went and looked at all these different measures - LDL and total cholesterol and HDL and triglycerides and that ratio - to find out which one would predict the best. Well, see it wasn't LDL like our guidelines would have you believe. And HDL way out-predicted LDL. But it was actually that total (cholesterol):HDL ratio. And you know not everyone wanted to accept that. And Ernie Schaefer's group at Tufts once took the 44,000 people that had been in all the most recent trials lowering cholesterol and lipids and changing the lipids and so on, and asked the question, "Which lipid change explained the fall in the heart attack rate the best?" Was it the total cholesterol, the fall in total cholesterol? Well, no, but it helped. Was it the fall in the LDL like the majority of our lipid experts would say? No, and it wasn't quite as good as the fall in total (cholesterol). The fall in triglycerides helped, but it wasn't the best. The rise in HDL out-predicted the fall in LDL by a lot, and now they're into what's called the non-HDL cholesterol. Now non-HDL is simply adding to LDL the VLDL of the triglycerides, because 70 to 75% of your fasting triglycerides are in the beta VLDL. But Dr. Goldstein who got the Nobel prize with Dr. Brown in Dallas in '85 are teaching us about these receptors on cells. How fat particles outside a cell get into a cell showed went into their macrophages at a faster rate than their beloved LDL. As a matter of fact, it took a while before we learned you had to oxidize the LDL to make it go in as fast, and these macrophages are the cells in your artery wall where the first fat deposits take place. And the latest in that came out of some work I guess out of California, where they found a compound in the skin of red grapes called resveratrol, that was going to be a very powerful antioxidant and they postulated it would slow the entry of LDL into your artery wall and speed up the removal of the oxidized LDL. The focus had largely been in American medicine on LDL and of course they wanted good therapies for LDL. Now the diet therapies for LDL is the intake of saturated fat and cholesterol in your diet and that was found by these folks like Ancel Keys up in Minneapolis and Dr. Hegsted out of Harvard teaching us the role of saturated fat and cholesterol and then we went and did all these trials. Lowering the saturated fat and cholesterol in people's diets and lowering their heart attacks and strokes and all that sort of stuff. You know, in our clinic we learned very early on that it's very hard to convince an American to give up the American diet. Now the American diet is the worst diet you could possibly eat anywhere in the world. No one else in the world can eat as much as we can and that is one of our enormous problems in America. Getting people to give up all that stuff. Lowering the LDL business if you didn't make it on the diet and exercise, the best drugs turned out eventually to be the statins. And then we went and did statin-only trials. You know if you look at the results of these statin-only trials if it was a weak statin you used, you get a 25% fall in the heart attack rate. If it was the best statins, right around 50%, maybe not even quite 50%. Well, when are you going to get rid of the other 50%? And in a way it all began on the West Coast of the United States and the first big piece of evidence we had in that regard came out of L.A. by Dr. Blankenhorn, I must say the late Blankenhorn, where he added - he gave people 4000 mg of niacin and he added that to 10 Colestid® tablets three times a day. Now 10 Colestid® - I had trouble getting people to take 10 Colestid® tablets once a day.

KIRK HAMILTON: What is Colestid®?

DR. WILLIAM CASTELLI: Colestid® is a resin and it's like eating a million little sponges. They go in one end and they come out the other. They never go inside your body and they drag out the bile acids and lower your cholesterol that way. And then the 4000 of the niacin, this was not the no-flush niacin, this was the sustained release niacin over-the-counter and you know you flush and itch on the niacin. And you know within two years he starts to shrink the deposits in the coronary arteries and that, in a way, was one of the first trials to show us in a trial that you could do this.

KIRK HAMILTON: And this is without diet? Just by the two agents?

DR. WILLIAM CASTELLI: Just by those two agents. And you know some of us knew you could shrink these deposits - I mean I learned you could shrink the deposits in people's arteries when I was a medical student in Belgium working for a pathologist in the '50s. When he did an autopsy he would call us over and say "Look at this coming back to Belgium at autopsy all these fat deposits in their arteries." We said, "Well wait a minute if it's coming back where did it go?" He said, "I don't know where it went. Disappeared by 1942." Well what happened in Belgium in the early '40s, an army came and well right behind the army came the German trucks. They backed them up to all the farms in Belgium, northern France, Holland, Poland, all the countries the Germans invaded, the trucks showed up. All the meat and livestock went back to Germany and by 1942 in Belgium at autopsy all the fat deposits in the arteries had disappeared.

KIRK HAMILTON: Well let me interject there and ask you this question then. First of all is cholesterol just something that goes along with atherosclerosis or is it in your mind a cause of atherosclerosis, or if we had non-oxidized LDL or cholesterol going around it wouldn't cause atherosclerosis? So are we talking about cholesterol as a marker or as an agent that causes the disease?

DR. WILLIAM CASTELLI: Well it's part of the disease because when you look in the arteries that fill up with these fat deposits what is that deposit it's cholesterol. And some of it is other kinds of fats as well, and then when we lower the cholesterol we lower the heart attack rate. So it's a very important player. You know, we know that if I can get your total cholesterol down around let's say 100 to 130 or so, and I have maybe not quite a billion people on the earth like that, and those people cannot get atherosclerosis. You know in the China Study, for example, when Chou En-lai was dying of cancer he started a study in China just like the Framingham Study. The only difference was it was in 880,000,000 people so it was a little larger than the Framingham Study. But you know they found these villages in China where you couldn't get a heart attack or you couldn't get diabetes and the women couldn't get breast cancer and you know their total cholesterol were 127, but the chances we could ever get Americans down that low with diet and exercise are not good.

KIRK HAMILTON: Well let me ask you. Let's talk about then - here's the controversy that I always get from different doctors and cardiovascular specialists. We look at atherosclerosis as an inflammatory condition. Some say for example they do the new VAP panels now and if it's a large LDL, some doctors I've heard say, "I'm not worried about their cholesterol level." Now can you comment on that?

DR. WILLIAM CASTELLI: The larger LDLs go in your artery wall slower than the small ones that go in at three times the rate. But the best study, you know, and all of that was from Quebec by Lamarck, and he had people who had high LDL or low LDL and then small LDL and larger LDL. Well let's say you had the large sized LDL but you had a high amount. You ran twice the heart attack rate of people with the large LDLs who had a small amount. But if you had the small dense LDL and a large amount you ran six times the heart attack rate of people with the low amount of the small, but it was three times worse based on the size, and the sizes of your LDLs are related to your triglycerides. And we learned that by a very old study by Ron Krauss, and this was the Berkeley Study. Where he actually took people who had either large or small LDLs according to their triglycerides. Now when your triglycerides in his data went up and hit 150 and this unfortunately - the American guidelines says 150 is the goal of therapy which is so stupid. Why? Because in Ron Krauss's data if you are at 150 I wouldn't have to get the VAP test or the Berkeley Lab or the Lipomed Labs and look at these particles because you'd have a 99% chance of having this small dense LDL. On the other hand if I were to get your triglycerides all the way down to 60 I wouldn't have to measure them either because you'd have the large size 99% chance. Nothing is ever 100%. And we lately have shown in Framingham that it's the number of LDL particles per level of LDL is related to your triglycerides. So as your triglycerides go up, and once you get over 100 on the triglycerides in Framingham, you put out more LDL particles per level of LDL. And if I get you below, let's say I take you down to a triglyceride of 50, you'd have half as many particles. And we showed in Framingham now recently that you know it's the number of LDL particles out-predicts the level of LDL. So the VAP things, and things like while the larger particles are safer, they are not entirely safe even if you have the larger types of LDL compared to people who have the lower types of LDL. But see this is all we're talking about now is LDL and you need to know that there are in the better labs 7 LDLs and 12 HDLs and I wouldn't have to measure those in two instances if, and those are if your trigs (triglycerides) are up at 150 I'd know you have the wrong kinds of LDL and probably not the best mix of the HDLs either. Just like if I lower your triglycerides I change the nature of your LDLs and I change the nature of your HDLs, the better protective kinds and the bigger kinds of LDL that are less likely to go into your wall and cause a blockage.

KIRK HAMILTON: Well then let's talk about triglycerides because you made a point about those as something that can -

DR. WILLIAM CASTELLI: And there are these three issues on triglycerides. One that 70 to 75% of your triglycerides are in those beta VLDL that go into your artery wall as rapidly as LDL. And that is why when you add those beta VLDL to LDL in the so-called non-HDL cholesterol, that out-predicts the LDL by a large amount. You have to go after these triglycerides. Now diet-wise, they (triglycerides) are more or less related to the refined carbohydrate in your diet, the white flour, the sugar, the candies, the cookies, the cakes, the ice creams. If you can get them to get away from a lot of that refined carbohydrate stuff you can lower those triglycerides. But then the drugs that are good for lowering a triglyceride are drugs like niacin and the fibrates and the fish oils. You know where we first learned about the fish oils in all of this was in the people with the one, two, three, four, five, six thousand triglycerides. Where they get acute pancreatitis and die from the acute pancreatitis. And I, you know way back in the Framingham we didn't treat anyone but I was out lecturing initially on those types of hyperlipoproteinemias and doctors would call me every once in a while to get help to treat some of these patients. Well one of them sent me a lady who had a 5000 triglyceride and she was getting acute pancreatitis every three to four months. And back in 1970 we had five drugs in the American pharmacopeia and I put her on all five and nothing happened. I mean I used to treat these people in the lab because we didn't want them in the clinic where we weren't treating anyone.

KIRK HAMILTON: What is the level or your goal for triglycerides for prevention?

DR. WILLIAM CASTELLI: Well the most ideal triglycerides would be under 60 because then you'd have the best particle sizes, and you'd have a very low amount of these beta VLDL as atherogenic as LDL.

KIRK HAMILTON: How important is C-reactive protein as an inflammatory marker related to cholesterol or triglycerides as a risk factor?

DR. WILLIAM CASTELLI: Well you see those inflammatory particles, inflammation speeds up the entry of these cholesterol particles into your artery wall and that's where it plays a role. If I get your Framingham Risk Calculator score down to 5 or below, then the inflammation doesn't count any more.

KIRK HAMILTON: So do you use C-reactive protein levels?

DR. WILLIAM CASTELLI: I don't really bother with them because we're driving your risk down to where you don't need to go. And then when I first started in medicine I was going to be a rheumatologist. And I worked for Marion Ropes at the Mass General. And you know she measured the C-reactive protein in those days. And then would take, you up the dose of aspirin until it fell. And when it fell their arthritis got better. Now some people have this high sensitivity C-reactive protein that they relate to the coronary risk and it does count when your risk factors are very high. But if I get your standard risk factors low, then it doesn't count so much.

KIRK HAMILTON: So tell me your ideal for the standard risk factors. Let's say we didn't do a VAP panel, we just did the basic cholesterol, LDL, HDL B

DR. WILLIAM CASTELLI: Well I would want your total (cholesterol) to HDL ratio down under 3.5. And that came out of these intravascular ultrasound studies from the Cleveland Clinic where they go in and look with ultrasound so they can see all the lesions in an artery. Not just ones that grow in, but the ones that stay in the wall and grow out. They can see them all. Unlike our cardiologists who use an x-ray technology, they can only see the deposits that grow in. Well, they're interested in the ones that grow in because if they grow in enough they block the blood flow. And if they block the blood flow enough to your heart, your heart will "squawk" and we call that angina. And you get sent to one of those folks and they do that little opacify the blood to x-ray, click a picture of the left coronary, the right, they can see all the blockages. You got a blockage, they got a balloon and they bust them open and then overnight you lose your angina, but along the way these deposits can rupture.

KIRK HAMILTON: So if you have - your goal is to get the cholesterol to HDL ratio below 3.5, and would you at the same time look to get your triglycerides below 50? Is that a goal?

DR. WILLIAM CASTELLI: Below 60, that's right. So I'd have the right kind of HDL making up that ratio.

KIRK HAMILTON: Now how about if somebody let's say was on a very strict no-fat, let=s say vegan diet. And let's say for example the Tarahumara Indians have very low cholesterols but they have very low HDLs as well and so they have a high cholesterol/HDL ratio but they don't have atherosclerosis. Does it get less-

DR. WILLIAM CASTELLI: Well if they have a low enough LDL, see I get sent people that have a 10 HDL and a 4 HDL and you'll never be able to get their ratios down. But then I take your LDLs under 70 and your triglycerides under 60 and now you don't need HDL. It was actually Michael Brown of Dallas there with Goldstein, one of the Nobel laureate folks, he used to say if your LDL was under 90 or 80 you didn't need HDL. Well I don't think that's true but if you're a lot lower than that, you probably don't need HDL. The idea was your cells were not making more cholesterol than they could use, so you didn't need HDL to take away the excess because if they make more than they can use, they make a fat deposit in the cell of cholesterol and if it's a cell that's in your artery wall you get the atherosclerosis. We need to get those triglycerides down to get rid of the atherogenicity of these particles and at the same time improve the nature of the LDLs and the HDLs.

KIRK HAMILTON: Let's say you had no medication and you could get everybody behaviorally to do everything you exactly wanted them to do by diet, the average American. How would you reverse the heart disease epidemic by diet?

DR. WILLIAM CASTELLI: I would. I would do it and it would work better than the drugs. And I can show you all of the reversibility trials and they were mostly drug trials.

KIRK HAMILTON: But what would the diet be if you didn't have drugs and you could get everybody to do exactly what you wanted diet-wise in the United States? How would you reverse the heart disease?

DR. WILLIAM CASTELLI: Well you'd have them on a pure vegetarian diet and not getting fat on the vegetarian diet. And in these reversibility trials there were these two diet trials. One was the St. Thomas Hospital study in London and the other was the Dean Ornish study. And for the same fall in cholesterol, if you get there with diet you get twice the shrinkage of the lesions than if you do it with drugs. In any event, what we've learned is that in these reversibility trials, that the two diet trials, for the same fall in cholesterol if you get there with diet you did get twice the shrinkage of the deposits than trying to do it with drugs alone. And you see we have these patients, you know, they want the golden bullet. Doctor, give me that magic bullet so I can go out and eat anything I want. Well we don't have a therapy like that. And we need to get our B it's much better if you can get people to go on a diet. Now if I would have put everyone on a vegetarian diet and drive their numbers down by diet, we would get rid of all the atherosclerosis in America. Now I have as I said a billion people out there somewhere around the world where they're on that kind of a diet and they can't get this disease. But you know some of them are close to starvation, too, so - they're a step away, but you know you could do this with diet and exercise eventually but it's hard. You know, we, when I first started the clinic had a nurse manager and a dietician. The nurse manager would get you in an exercise program and the dietician a better diet. But then the HMOs would not pay for that so I got - I was stuck by myself trying to do a little diet and exercise, I went over and made their score cards and got them to show where we wanted their numbers to go to for them to shrink their deposits. Now we do shrink the deposits in the people's arteries in my clinic, and we keep getting, you know, repeat angiography done on their coronary arteries and their deposits start to shrink. And you can do this, but it's not easy for them to do it with diet and exercise.

KIRK HAMILTON: Well let me ask you, because you can say vegetarian diet and that can mean anything from a white flour vegetarian diet to you know a very -

DR. WILLIAM CASTELLI: It would have to be a whole grain -

KIRK HAMILTON: Right.

DR. WILLIAM CASTELLI: Vegetarian diet and you know you start your breakfast with oatmeal and soy milk.

KIRK HAMILTON: Correct. So in your regression vegetarian diet, your ideal one, would it have any fat in at all? In other words, would it have nuts and seeds in it at all, or added oils or -

DR. WILLIAM CASTELLI: It can have some nuts and seeds. It wouldn't have a lot of fat, and we've had a lot of these new diets come along to teach you how to get rid of all the refined carbohydrate. One of them, like in the recent Reader's Digest said eat sirloin. Well that would be a mistake because when you eat fat it goes into your blood, as chylomicrons. Well they're not atherogenic, but they're quickly converted to two of the most atherogenic things we know of, chylomicron remnants and the free fatty acids. And they shower down on your artery wall after a high fat meal and make fat deposits. And show me a country that eats that kind of fat and all that stuff that is free of atherosclerosis, there isn't one.

KIRK HAMILTON: I recently had Loren Cordain on, who's the author of the Paleo Diet, and you know went around and studied hunter-gatherer populations, and his thing is that they eat 50 to 60% animal products and the rest is just fruits, vegetables, and it's unrefined. I mean it's fruits, vegetables, maybe some nuts or seeds and wild game, let's say. One, we have to have access to that, but two, do you think if everybody did that that we would have as much heart disease or would it be less?

DR. WILLIAM CASTELLI: Well, we'd have less because this more recent thing about what's in these animals that are on the range and fed. And this came about with the study of these calcium trials where the ladies in New Zealand and in Finland put on the calcium supplements ran a higher heart attack rate and the ones on the placebo did not get that and the calcium was going into their arteries instead of their bones. And then this revived this old WHO trial where they went around the world, country by country, measuring hip fracture and came up with the WHO paradox. That the countries that eat the most calcium have the most osteoporosis and the highest hip fracture rate, and these poor countries, they eat hardly any calcium, have hardly any osteoporosis and no hip fracture hardly. Well, they said this demands an explanation. Well it took a while before we learned from our molecular friends who started studying the entry and exit of calcium into your artery wall. And let's face it, you live in a country where 70% of us have calcifications in our major arteries. They found these proteins that control the entry and exit of calcium into your artery wall and then they stimulated these proteins and the thing that worked the best was vitamin K2. And where would you get vitamin K2 in your diet? Well, this is not K1 by the way, it's K2. Well you actually would have to go out on the range and eat all these plants by the gazillions to get enough K2, or you had to live in one of those poor countries where the meats they eat are from animals raised on the range and their meats are loaded with K2 and their milks and their cheeses. And then you know we'd already done the animal experiments now, putting the animals on K2 and shrinking the calcium. And then there's the Rotterdam study which in a way is the Framingham Study of Holland. And the higher the K2 in the blood of the people of Rotterdam, the lower their aortic calcium. And then what about heart attack? Aren't you gonna clot on K? You know, K stood for coagulation but spelled with a K the way they do in some of the European languages and won't you clot if you take K2? No. Well, if you're gonna clot, you'd run a higher heart attack rate, but in Rotterdam, the higher the K2, the lower the heart attack rate and the total death. Not K1, by the way. K1 did not lower the heart attack death rate, but K2 is associated with lowering. You'd have to eat animals that would be raised on the range or you know in Holland there is a particular type of cheese that they have to use animals that were range fed to make that. They think that's where they're getting their K2 some of these people.

KIRK HAMILTON: Last question. And you probably already answered it, but if you control blood sugar levels and insulin levels, people describe insulin as an inflammatory hormone. So if you're on any diet that controls blood sugar levels or keeps them low will that not help control the atherosclerotic process?

DR. WILLIAM CASTELLI: Of course. Well, diabetes, and let's face it I would get rid of 80% of the diabetes if I got rid of the obesity in America. We want to get the weights down but we're losing that game. The CDC, you know, showed in '85 that true obesity, a BMI of 30 where your tummy gets there a foot or two before you do, we only had states with less than 10% of that obesity or 10 to 14. Every year since '85 in every state they look at, and eventually they had all the states in survey - the weights have gone up. In '09, for example, where they have the latest data, there are no states left with less than 10% or 10 to 14. Only one state in the union is 15 to 19% obese. Most of the states are 25 to 29% of the population now have that obesity, then 20 to 24% and in '09 nine states made it for the first time, 30 to 34% of that obesity. And I would get rid of the diabetes for the most part. But you know we want the blood pressures under 120 and under 80, we want people to get out and do the exercise and lose their weight and keep their tummies flat. And you know we're going in the wrong direction in most of these risks.

KIRK HAMILTON: Well let me ask you this then. Obviously, I think I know the answer, but the same regression diet that you talked about for vascular disease, would that not wipe out obesity and diabetes at the same time?

DR. WILLIAM CASTELLI: It would. Yes, it would because they'd lose weight and the total calories would be lower and you know the portion size in America is out of site. And when you look at the exercise, you know we used to tell people that if you did a mile it's 100 calories which made an American candy bar two and a half miles to work it off and a Big Mac or - so it would have been five miles to work it off. But if, there's a new paper out saying that if you're 5'5" or less it's 50 calories a mile. Well now that may, if you're short then, a candy bar is five miles to work it off and one of those double-decker triple hamburger things is gonna be like 10 miles or more. Most Americans cannot run as far as they'd like to eat. And we've got to do a better job controlling the amount of food we eat. It's too much.

KIRK HAMILTON: Well I've got to wrap this up, but I'd like to ask two more questions. One is did you not have a significant risk factor with elevated cholesterol and what have you done to lower yours?

DR. WILLIAM CASTELLI: Well I started by, my grandfather on my mother's side, and old Scotsman from Nova Scotia drops dead at 57 working for the Canadian Railroad in Brownville Junction, Maine, in 1924. And all, not all the McNeils, but most of us, you know, got that gene. My brother had coronary disease in his 30s because he smoked and I beat it by running five miles a day for 43 years and I took my HDL from 40 to 70. But then my knee went and I have to go on the niacins now to drive my HDLs back up and I've got my HDL up to 93.

KIRK HAMILTON: Do you use a Slow Niacin or Niaspan?

DR. WILLIAM CASTELLI: I actually wanted to - I've used the crystalline niacin because I wanted to study this flushing and itching on the niacin. And you know it comes on the first day big time and usually half as much the second day, and by the third day it's down to a quarter and then by the fourth or fifth day it's almost gone. A little bit. But you know if you skip a day, the five days of flushing and itching start all over again and that's called a pharmacological first pass effect. So I wondered whether there was a metabolic first pass effect so when my knee had gone and I couldn't get as much biking done as I needed to, my HDL started down. So I went and got this crystalline niacin over-the-counter where you flush and itch the most. And you cut that in half by using sustained release over-the-counter, and then you cut that in half by going to the prescription niacin, the Niaspan, and those are the real good niacins, not the over-the-counter no-flush stuff. That doesn't work as well. In any event I went and got the crystalline kind and I took it 1000 mg every day and it took my HDL up to 77, then I took it every other day to maximize the flushing and itching. I wanted to see if that would have a special effect. Now I'm on half the dose so I should have a fall in my HDL but it went up to 93.

KIRK HAMILTON: Doesn't niacin do almost everything - drive up HDL, drive down lipoprotein (a) and triglycerides, or am I -

DR. WILLIAM CASTELLI: Yeah, it does just about everything and if you get to 2000 of the niacin, you'll get the same fall in LDL that you would get with Zetia. But Zetia, you know has not shown that even though it lowered the cholesterol it doesn't lower the lesions as yet. So in fact in a couple of studies the lesions got worse, even though the thing fell, whereas in - and you know you have Welchol®, one of the better resins now, and that lowers the LDL by about 20 points, but you know 2000 niacin in one of the studies lowered the LDL the same 20 points. So and then you get this big fall in the trigs (triglycerides) and a big rise in the HDLs, so you get this better ratio which out-predicts everything.

KIRK HAMILTON: And tell me about the Castelli heart prevention diet that you're on. What do you do?

DR. WILLIAM CASTELLI: Well I have my oatmeal with soy milk in the morning and then I usually have, if I have lunch, it's a salad, with it could be herring snacks with it. I eat a lot of sardines. The fish you know we're getting into these fish oil things because of a big study in California where they found over-the-counter fish oils had PCBs. These are carcinogenic things that are found in the fish oil coming from the larger fishes and they found that - you know they suspect that a lot of the fish oil in California was made in some place in Texas where they were using the big fishes. Well the big fishes are loaded with all these different things like mercury and lead and PCBs and all these toxins from the ocean and there's a lesson about what size fish you should eat. And we had two folks in the EPI Counsel, Ancel Keys and Jerry Stamler showed up at the meetings all the time eating a can of sardines. Well Ancel Keys died about five years ago at 100 years of age eating sardines. And so I'm a big sardine guy. And then at dinner my wife will make fish or chicken and we rarely have beef or pork or lamb or any of those.

KIRK HAMILTON: And do you have vegetables in the evening obviously, or no?

DR. WILLIAM CASTELLI: Lots of vegetables, yeah.

KIRK HAMILTON: Okay.

DR. WILLIAM CASTELLI: And salads. Yeah.

KIRK HAMILTON: Well this is what I think I got. I appreciate your time. If I could summarize and correct me if I'm wrong. If we were really gonna jump after reducing cardiovascular disease, you'd go on this very low fat vegetarian diet that's totally unrefined, you would shoot for an LDL of less than 70, triglycerides less than 60, and a cholesterol:HDL ratio 3.5 or less and maybe a total somewhere around, I don't know, maybe between 130, 150, something like that? Those are all good -

DR. WILLIAM CASTELLI: Well if you could, yeah. I mean, we have had about a half a dozen people get eventually a heart attack with a total cholesterol under 150 in Framingham. One of them did have this high triglyceride/low HDL syndrome. The other four or five, we don't know what they had.

KIRK HAMILTON: So that's a half dozen in how many years?

DR. WILLIAM CASTELLI: A long time, 30, 40 years almost. Yeah.

KIRK HAMILTON: Okay. Well, Dr. Castelli, I want to thank you so much for taking time to explain and go through all that history and I wish you the best of luck. Are you actively practicing, or are you doing the wellness thing?

DR. WILLIAM CASTELLI: I still do. I run this clinic two days a week and these are more than 12 hour days. But you know the rest of the week I've been out doing the lecture circuit because it's thanks to the people of Framingham you can go into any town in the world, measure a few simple numbers on people's bodies, identify most of the people who get a heart attack or stroke and better than that, you can treat those numbers and prevent it.

KIRK HAMILTON: And that's the calculator. I went to your website and at the bottom it said calculate your risk and it has age, gender, total cholesterol, HDL, smoker, blood pressure and are you treated for blood pressure. Is that what you're talking about?

DR. WILLIAM CASTELLI: Yeah. You gotta treat everything.

KIRK HAMILTON: That little questionnaire there.

DR. WILLIAM CASTELLI: Don't leave any doors open, you know.

KIRK HAMILTON: Okay. Thank's Dr. Castelli, for being on the show today. I appreciate it.

DR. WILLIAM CASTELLI: Okay. You're welcome.
KIRK HAMILTON: And I want to thank you, the audience for being on this edition of Staying Health Today Radio. And until next time, Stay and Be Well.


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