2011-09-08 Peter H. Langsjoen, MD Congestive Heart Failure and the Clinical Use of Coenzyme Q10
of Coenzyme Q10
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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 Be and Stay 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 "Congestive Heart Failure and the Clinical Use of Coenzyme Q10." Our guest today is Dr. Peter Langsjoen, a practicing cardiologist since 1985, and expert in the clinical uses and bioavailable forms of coenzyme 10.
Welcome, Dr. Langsjoen. Thank you for taking time out of your busy day to be on the show.
DR. PETER H. LANGSJOEN: Oh it's my pleasure.
KIRK HAMILTON: So tell me first a little bit about your educational background, just the medical part, and how you got to where you are.
DR. PETER H. LANGSJOEN: Oh, I guess standard training. You know medical school in San Antonio, internal medicine was actually in Fargo, North Dakota, and then cardiology fellowship was back in Texas at Scott and White Hospital that's in Temple, Texas. And that's where I began working under my father who was a staff cardiologist there at the time. And right around that time, around 1983 and actually a little before, my father had just begun the first of clinical research trials using supplemental coenzyme Q in heart failure in the United States. So that was my introduction to Q (coenzyme Q10) and heart failure.
KIRK HAMILTON: Was your dad a biochemist? Why did he choose to look at a biochemical agent or nutraceutical versus a drug?
DR. PETER H. LANGSJOEN: He was not a biochemist, but he was a remarkably open-minded physician. He was a pioneer in other nonconventional things such as the use of dextran, which is a long polysaccharide that decreases blood viscosity in patients with acute infarction. So, and then he met a biochemist by the name of Karl Folkers who was hugely important in coenzyme Q research. And those two became rapid and very close friends. And he was just an open-minded wonderful genius of a physician and it was his nature to look into anything new that might be helpful particularly for patients with critical heart disease.
KIRK HAMILTON: Well let's talk a little bit about the pathophysiology I guess of congestive heart failure. Why would he think using this agent ubiquinone or ubiquinol or coenzyme Q10 in a heart failure patient?
DR. PETER H. LANGSJOEN: Yeah, we can just refer to it as Q for brevity.
KIRK HAMILTON: Good.
DR. PETER H. LANGSJOEN: Well if you put in historical content, congestive heart failure of any cause is traditionally a terrifically difficult disease. We have many drugs that palliate it. We have diuretics that may decrease edema. You can use oxygen that may help shortness of breath, but and then as a last-ditch effort you can try dramatic things like transplant, but the prognosis in advanced heart failure was quite poor despite, you know, the best medical efforts. And when CoQ10 came along, you know it was discovered in 1957. And then there was a decade or so of basic animal work and biochemical work. And then another decade or so of early Japanese work. All of which was favorable. And it showed very simply that CoQ10, which is the cofactor essential for the great majority of cell energy production, was very low in animals and then later in human studies in the failing heart. And it was low if you measured it in the blood and it was even more accurately low if you took a biopsy of the heart. So even before my father's first studies, it was pretty clear that you could measure CoQ10. It was low in patients with heart failure. And the worse the heart failure, the lower the level, and we knew even in those early years that it was essential for the production of cell energy. And heart muscle was the obvious organ to study because it uses a huge amount of energy and therefore requires an adequate and very high concentration of Q.
KIRK HAMILTON: Well let me then ask you, is heart failure then an energy deficit disorder, or are there - well there's obviously other risk factors, but is it primarily an energy deficit disorder in the heart muscle or is it a combination of things?
DR. PETER H. LANGSJOEN: Well that is certainly a major factor in it. And the reason you can say that is because when you replenish Q, you can bring about just beautiful changes in heart muscle function that can't be explained in any other way. In other words, you're not changing the -- say the anatomy of valves in the heart, you're not changing the blood flow or the coronary circulation. So I think you could safely say that the majority of patients with failing hearts have as one of the fundamental problems an energy deficit or a weakening of heart muscle function.
KIRK HAMILTON: Well does then the heart failure continue to make the heart weaker? Is it kind of a self-fulfilling prophesy, so to speak?
DR. PETER H. LANGSJOEN: Oh, yeah, they do tend to have a gradual downhill course. It can be sort of stuttering. You know, you can have good days and bad days and that sort of thing, but the natural history of heart failure is one of a gradual downhill course.
KIRK HAMILTON: Well tell me then, why do you think there is so much heart failure?
DR. PETER H. LANGSJOEN: Oh, I don't pretend to know for sure. There's so many things that can affect heart function, but one of them I might just mention in passing. People don't think too much about it, but you always have to be worried in any common illness and as you're probably aware, heart failure is the number one diagnosis in hospitalization over the age of 65. So it's certainly a huge and common problem. You always have to be careful that as a profession we are not in some way contributing to it and one convenient villain that comes to my mind is the very aggressive use of statins. Statins dramatically deplete both cholesterol and the coenzyme Q. Because they block the common pathway for the biosynthesis of both. And our current research right now is looking at the sort of the natural history if you will of statin cardiomyopathies. And just in the past 12 months we have a little less than 100 cases of, which is a lot, you know, and we're excluding anyone who might have a weak heart for any other cause. So these are not - these are people who have never had a heart attack, who do not have a bad heart valve, who haven't had chemotherapy or some other insult to the heart. So statins come to mind as a possible aggravating factor. It's not recognized by the general cardiology community, but I think it's - it's worthy of further work for sure.
KIRK HAMILTON: Well let me bring this up. So I'm at a conference at UCSF and the physician is talking actually about heart failure - well, nutraceuticals, and she's kind of giving her overview from the establishment medical point of view. And she brings up CoQ10. And so she says, yeah, there's some reports of CoQ10 being used to treat the side effects of, you know, heart failure because of what you've said, but here's the thing. When I listened, I'm sitting there listening and I do CoQ10 levels all the time and I shoot to get my patients above 3.5. And I know that if she's giving 100, 200 mg, she not's getting close to the - that level and you talk about in your article, because that's one of the things is bioavailability. So a lot of these people might say that the biochemistry is there, but because they're using inadequate dosages to get blood levels up, they're not gonna get any therapeutic benefit or reduce the side effect that much.
DR. PETER H. LANGSJOEN: Yes, that's absolutely right. There's a threshold effect and it's interesting, you know. It took a long time to figure that out. When we first viewed this, we thought, okay if heart failure patients, let's say on average had a blood Q level of 0.5 micrograms per milliliter, and if normal people were around 1. In other words the failing hearts had about half normal blood levels of Q. If we supplemented with Q and we attained a blood level of 1 or a little higher, that should be sufficient if we're - if what we're doing is just correcting a deficiency state.
KIRK HAMILTON: Correct.
DR. PETER H. LANGSJOEN: Much like you would with let's say beriberi with thiamine deficiency. But what happened was that wasn't the case at all. We didn't see much improvement in patients unless these levels in the early studies were above 2.5. And then later when we, especially as we started to treat more and more really sick class 4 heart failure patients. We didn't really turn them around or get our best effect until we had blood levels greater than 3.5. But you know that took a good 15 or more years to figure that out.
KIRK HAMILTON: And what dose range would your average say your patient was on then?
DR. PETER H. LANGSJOEN: Early on we used 100 mg. We used, it was an odd dosage but we used 33 1/3 mg three times a day. Later, I'd say an average amount of Q, we had some 60 mg tablets that we had people chew with peanut butter, and we had them take two twice a day. So 240 mg was an average dose for a good six or eight years. Later forms of Q that were better absorbed came along and there was several formulations that would, you know, were better than what we had before. And so I would say the average dose is now in the 3 to 400 mg range, but it varies quite a bit because we can follow levels now much more easily than we could originally. You know at first the only lab in the United States doing Q levels was in Austin, fairly slow turnaround and it was - it wasn't that easy to get them done. Whereas now we do Q levels here in our office. We have a wonderful research lab and so we don't have to guess as much as we used to. Some people absorb Q very well and so on a dose of 100 mg twice a day they may have a Q level of 5.8 and you don't have to change a thing. And then another patient on the same dose may have a much lower level so, you know, you have to increase them.
KIRK HAMILTON: Well let's assume then that CoQ10 is good for a failing heart, and you're trying to get levels up to - and I don't want to put words in your mouth, above 3.5 if we're measuring. I measure at Quest Laboratories and I can get it there with varying amounts. But for the average person out there, or actually if a physician is listening, there are different forms, and that was the nature of your article that I actually called you about. Supplemental ubiquinol in patients with advanced congestive heart failure and that was in Biofactors and then you have a newer one also in Biofactors. But what I wanted to get across is when do you choose the different forms, because you know in the nutraceutical world when something new comes out they sell it like anything else, you know?
DR. PETER H. LANGSJOEN: Right. Right. Well, one way to look at it is the standard Q which is its oxidized state, it's called ubiquinone, that's what we have over 40 years experience with. It has some advantages. It's very stable so it has a long shelf life. And if you're not in a big hurry, you know, if you're not treating someone who's in active or obvious heart failure. There would be nothing wrong with using any form of Q including the standard ubiquinone formulations. Wait a few weeks or so and check a level and see if it's adequate. In my particular situation patients are referred into my cardiology clinic usually because they're pretty sick, and so I don't have a lot of time to fool around with possibly an inadequate blood level. So currently in people who are presenting in heart failure I'm using ubiquinol pretty much exclusively because it's more predictable. It's always better absorbed. It's anywhere from 2 to 4 times better absorbed. And then like I said, some of these people are so sick you need to get them better as soon as you can, you know.
KIRK HAMILTON: Which one of the agents is better for, as an antioxidant and which form is better for energy production?
DR. PETER H. LANGSJOEN: Well the way to look at that is they're identical because when you absorb either form of Q, if you take ubiquinone, the oxidized form, it is very rapidly, what we call reduced or changed into ubiquinol even within the intestinal lining cells. So let's say that if you gave someone 1000 mg a day of ubiquinone and you measure their blood levels 98% at least of what you measure is going to be in its reduced state, ubiquinol state. So you need to look at the ubiquinol and ubiquinone, they're essentially identical except for that very first transit across the intestinal wall. So the absorption is better with ubiquinol. After that they're identical. There's no difference, and they're in a constant cycle. You know, when we use Q as a coenzyme, it's converted to its reduced or ubiquinol state. And it's in a setting where it's in the presence of a great deal of free radicals in the mitochondria with which it reacts and it goes back to its ubiquinone state so it's a cycle.
KIRK HAMILTON: So that would make it - one of the things I never realized was, you know, I realized that the mitochondria was this organelle in the cell that's responsible for any energy production, but what I didn't realize is that it was a major oxidative stress producer, free radical producer, so it kind of destroyed itself in away.
DR. PETER H. LANGSJOEN: It's huge. You can think of it as a slow-burning fire. You know, you have carbon fuel, you have oxygen, and you burn it essentially and what you do is you produce heat which is handy if you're cold. You produce a high concentration of ATP, which is handy if, that's sort of the currency of cell energy. And you always have a certain amount of free radical production and one of the problems with it is those free radicals are being produced in the vicinity of mitochondrial DNA which is, as you probably know, is - it's a single strand circular DNA that's not protected by protein, and mitochondria are dividing all the time even if the cell itself isn't. And so if your Q is inadequate, not only are you not producing cell energy at an optimal level, you're not providing a defense for your mitochondrial DNA. So all these offspring, all these future generations are more defective than there, you know, with each step. So one of the theories of aging has to do with this progressive mitochondrial DNA damage and you can get to a point where it's irreversible. If you have a population of mitochondria that are really screwed up you can't undo that. So, at any rate it's quite important and you're right, mitochondria are the major source of free radical production in our cells.
KIRK HAMILTON: So let's talk about side effects. How safe is it? If I was going to tell my cardiac - cardiology colleague across the way to give it a trial. Give somebody 200 mg twice a day of ubiquinol with food. He would say, "Well what drug is it going to interact with, and, is my patient going to get an adverse effect?"
DR. PETER H. LANGSJOEN: Yeah, there's - the thing to tell him, no there's no side effects from Q and there's no drug interactions including no interaction with Coumadin. But there is something they need to be aware of and that is if you have someone with heart failure, they're going to be on a variety of medications. And at least a couple of those drugs are going to have some blood pressure lowering effect on them. They'll either be on an ACE inhibitor or a beta blocker or both. And when you improve heart muscle function, let's say you have an ejection fraction of 20% and you put them on Q, and three or four months later it's 40%. Well when heart function improves your need for some of these other drugs decreases. They don't need as high a dose of diuretics, for instance. And there tends to be a little lower blood pressure, so, you know, they should anticipate that they may have to decrease some of these other drugs as heart function improves.
KIRK HAMILTON: Do you -
DR. PETER H. LANGSJOEN: Makes sense.
KIRK HAMILTON: Yeah, it makes perfect sense. If you adequately gave heart failure patients coenzyme Q10, or for that matter statin users, let me stay with statin users because it's, you know, used like candy. Do you think you could pretty much eliminate the myalgias and things like that occur? And also if you were taking - you know the average statin person was taking a couple hundred milligrams of CoQ10 and we got the blood levels up, also reduce the risk of increasing the likelihood of failure since we might be keeping people alive longer?
DR. PETER H. LANGSJOEN: We don't know for sure, but I think so. I think that - you know statins are more complicated than just the reduction of Q and cholesterol. And - but it makes sense to me that if we routinely gave let's say 2 or 300 mg a day of Q to patients on statins, we could expect to decrease the symptoms of fatigue and also the symptoms of either muscle pain or weakness, and you can have either or both. There's some side effects that you probably won't influence those too much and those would be the central nervous system problems. When you - you know, the brain requires a huge amount of cholesterol and when it's decreased it doesn't work as well. So many people on statins have an insidious deficit in their mental capacity and it can be subtle at first, but almost all of them will eventually have a noticeable impairment in short-term memory. Sometimes it's noticed more by family members than by the patient, but I don't think Q would prevent that.
KIRK HAMILTON: Well wouldn't it be - it's almost like a two-edged sword though, because coenzyme Q10 is used to treat Parkinson's disease and I think the rationale is to help prevent the mitochondria from degradating itself and improving energy production in the neuron.
DR. PETER H. LANGSJOEN: Yes. Yeah, you know, I'm sort of an unusual cardiologist in that I'm not convinced that the benefits of statins come close to outweighing their harm and so I don't tend to be a big advocate of them in the first place. But if you're just looking at the big general way medicine is practiced, 99.9% of physicians use statins aggressively and they believe that the side effects are minimal. I think they're just not seeing it and that they're not minimal and they're certainly not uncommon, so - but whether you could prevent most of that with Q we don't know. My guess is you could prevent most of the muscle trouble. But I'm not so sure about memory.
KIRK HAMILTON: We are talking to cardiologist Dr. Peter Langsjoen. He is from the East Texas Medical Center and Trinity Mother Frances Hospital in Tyler, Texas. I wanted to kind of wrap up here, so if you had your ideal study how you would like to really show the world, I guess, and your colleagues, the cardiologists that coenzyme Q10 probably has some significant benefit in heart failure?
DR. PETER H. LANGSJOEN: Well, the ideal thing to do would be to do another randomized placebo controlled trial in heart failure patients on all the moderate current medicines and use - probably use ubiquinol so you get the best possible absorption, and use a dose that would assure a good therapeutic level and that would be I'd say at least 200 mg twice day if not three times a day. I mean there's no harm to going higher. So to use a good Q at a big dose and do it at some big center with a big name so that you would get more coverage and more attention. There have been nice controlled studies with Q that show benefit, but most of them are relatively small, many are published in relatively obscure journals. So it would be nice, for instance, to get let's say the Mayo Clinic in Rochester interested in it, or even just have them very skeptical about it. But if they did a study like that using a good dose of a very well absorbed Q, I don't think they could - you could lose, and it would show benefit and that would translate into an expansion of the use of Q in all heart failure patients.
KIRK HAMILTON: So before I close if I just review if somebody off the street had a family member with heart failure and they just want to try it. Ubiquinol 200 mg twice a day split with food. Trying to get somebody to do a blood level, get it above 3.5, that would be a reasonable thing to do, and watch out for your medicines if your blood pressure improves and other things improve.
DR. PETER H. LANGSJOEN: Yeah, right. Right. And those things happen gradually so you know even if you were checking things like blood pressure once a week, you know, you'd pick it up. But no, that would be accurate.
KIRK HAMILTON: And lastly, you know, everybody sees the science in CoQ10, so everybody and their "mother" makes a CoQ10 product, and, got any pearls on picking a good one?
DR. PETER H. LANGSJOEN: Oh, a good product on Q? Well I've managed to stay with no conflict of interest with Q companies. So we just check them as they come and we advise people to use whatever is the best at the time. And most of the time, you know, these products are really pretty good. If they say they have 100 mg most of them do. It - I think you mentioned earlier, the available or the ability to check blood levels is a really big deal because regardless of what type of Q you're taking, if your level's good then it's good. It's being absorbed and it'll do what it's supposed to do so.
KIRK HAMILTON: Okay, so you don't have - you wouldn't have to - I've heard some people say that the serum's one thing, but we don't know really what's happening in the cell, but you see -
DR. PETER H. LANGSJOEN: Oh, that was 10 or 15 years ago. That was sort of a common argument tossed around at meetings. It's become much more clear that, these higher plasma levels to translate into higher tissue levels and most of this is animal data, but it's quite good and so now when we see a good level, you know, it means a lot.
KIRK HAMILTON: Okay. Alright, Dr. Langsjoen, thank you so much for going over that with me. And I'm sure it will help clinicians and lay people listening to the interview. So thanks so much for being on the show.
DR. PETER H. LANGSJOEN: Well you're very welcome. My pleasure.
KIRK HAMILTON: And I want to thank you, the audience, for listening to this edition of Staying Health Today Radio. And until next time, Stay and Be Well.
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