IRA FLATOW, host:

I'm Ira Flatow. This is TALK OF THE NATION: SCIENCE FRIDAY from NPR News.

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FLATOW: You're listening to TALK OF THE NATION: SCIENCE FRIDAY. I'm Ira Flatow and for the rest of the hour, a new way of looking at many of our most common diseases. Let's say you're chopping vegetables and preparing your holiday meal this season, and you slip with the knife, you cut your finger, and almost instantly your body mounts an immune response. White blood cells rush to the site. You know, it becomes red, maybe swollen. But pain aside, your body's reaction is really a good thing. It's inflammation and it's a sign of a healthy immune response - your body is attacking those foreigners. Inflammation is your body's way of fighting off disease, but sometimes inflammation can go into overdrive, and the response doesn't turn off. And when that happens your tissues and your organs can be damaged.

Now doctors think that in some cases, inflammation can even lead to heart attacks. And if inflammation can damage your heart, what about the other organs in your body? Might inflammation be damaging them too? Joining us now to talk more about this are my guests. Gary L. Wenk is a professor of the Department of Psychology and Neuroscience as well as molecular virology, immunology and medical genetics at Ohio State University. He joins us from WOSU in Columbus. Hi, welcome to SCIENCE FRIDAY.

Professor GARY WENK (Psychology and Neuroscience, Ohio State University): Good afternoon, Ira.

FLATOW: Good afternoon to you. Excuse me. Ann Marie Schmidt is Chief of the Department of Surgery, a division of Surgical Science. She is also the Gerald and Janet Carrus Professor of Surgical Science at Columbia University Medical Center. She joins us here in our New York Bureau. Welcome to SCIENCE FRIDAY.

Dr. ANN MARIE SCHMIDT (Columbia University Medical Center): Thank you very much.

FLATOW: You're welcome. Peter Libby is Chief of Cardiovascular Medicine at Brigham and Women's Hospital and the Mallinckrodt Professor of Medicine at Harvard Medical School. Welcome to SCIENCE FRIDAY, Dr. Libby.

Dr. PETER LIBBY (Harvard Medical School): Happy to be here, Ira.

FLATOW: Thank you. Let's talk about inflammation. What is inflammation, Dr. Wenk?

Dr. WENK: Well, you described inflammation pretty well. It's the attempt of some specialized cells in the body - and also the brain, as we'll talk about later - whose purpose is to defend self from non-self. This system, in us, exists in all organisms and it's there to protect us from invasive, you know, bacteria, viruses - all the things that would happen after you cut your finger, as you described - and it's there to protect us.

FLATOW: Dr. Libby, can this immune response lead to sort of a runaway inflammation that just doesn't stop?

Dr. LIBBY: That's right. The immune and inflammatory response is very important in our usual defenses against invaders and repair of injury, but it can get turned against us when it's deployed inappropriately or when it is, as you implied in your opening comments, fails to turn off.

FLATOW: Ann Marie Schmidt, you're looking at a gene that is part of the immune response in many different diseases. Tell us about this RAGE gene.

Dr. SCHMIDT: The RAGE gene is a gene that interacts with distinct molecules that our laboratory and others have shown - these molecules appear to be increased in chronic inflammatory settings. And it's our hypothesis, that when these molecules specifically interact with this receptor, that they form a part of the mechanism that amplifies inflammation and basically leads to chronic types of diseases. And what's interesting about this gene, is that it is up-regulated in settings where inflammation is present, such as in diabetes, in Neurodegenerative disorders, and also in classical immune inflammatory settings as well.

FLATOW: So might this sort of be a master switch for inflammation?

Dr. SCHMIDT: That is our hypothesis, and certainly the biology of this receptor is really driven by the specificity of the specific molecules that interact with it. But what we and others have shown is that this family of binding molecules that interact with RAGE appear to have one of their common facets being up regulation relief in inflammatory settings.

FLATOW: How then would inflammation be a factor in a disease like diabetes?

Dr. SCHMIDT: Well, in diabetes - that's a very good point. Because certainly, as you know, subjects that have diabetes are affected, not only in their large blood vessels - that is a vulnerability, increased susceptibility to heart attacks and strokes - but also they have diseases of what we call their micro vessels, and this is, for example, in the eye, in the kidney, in the peripheral nervous system. And many researchers now have shown, that at least one component of these complications that occurs in these individuals, is due to an increased inflammatory response. So our laboratory has focused on studying animals with diabetes, observing and studying the molecular pathways linked to inflammation, and then showing how the RAGE molecule - and specifically its antagonism or genetic modification might modulate the course of inflammation -and interestingly thus, the course of complications.

FLATOW: Dr. Libby, we're talking about, in passing, inflammation playing a role in heart disease. I always thought that, you know, it was the plaques and the cholesterol and all that kind of stuff that caused heart disease. Where does inflammation come in here?

Dr. LIBBY: Well, we used to think of the atherosclerotic plaque as a fatty deposit of cholesterol on the wall of the artery that we formerly envisaged as a lifeless tube. And we now understand that it's really quite different from that, that the lipids - the fatty material that accumulates in the artery wall when we have too high a cholesterol or when or good cholesterol isn't high enough - actually can incite this inflammatory response call in the blood cells, just like the knife wound that you discussed in your introductory comments, and set up a spiraling signaling cascade that sustains and amplifies the damage that's done to the artery. And eventually, sometimes after decades of brewing silently, can express itself as a blood clot that can cause a heart attack or a stroke or gangrene of a limb.

FLATOW: Dr. Wenk, would we then say that inflammation can play a role in all kinds of different diseases? Would it be fair to say that?

Dr. WENK: Well, I think it's very fair to say that. We're beginning to think that it plays a role in many different neurological diseases, especially those that occur with aging. And I think Dr. Libby has touched on it. Just similar to what you see in the periphery, in the brain, time seems to be the key factor. In our studies here at OSU, you know, we've discovered that acute inflammation isn't as damaging to the brain as long-term chronic inflammation. So I think time is our greatest enemy when it comes to inflammation, because it always seems to be in the background, just working away. It's got good features, it has bad features, and we're trying to identify how to augment the good and somehow attenuate the bad.

FLATOW: Let me ask all of you, if inflammation is suspect and the criminal in this case, why don't we just take an anti-inflammatory drug - pop an aspirin, an Advil or something every day - and combat it that way. Who wants to jump in on that one? Go ahead, Dr. Libby, you can go first.

Dr. LIBBY: Okay, well, you know, the kinds of doses which are anti-inflammatory really are the kinds that cause significant side effects, such as ringing in the ears and problems with increased stomach problems with bleeding. And the doses of aspirin which actually work to reduce heart attacks - which it certainly does in certain populations - are doses that can interfere with the blood element that causes blood clotting, that is the platelet in our blood, but doesn't really have a direct anti-inflammatory effect. So the problem with your concept of putting everyone on anti-inflammatory drugs is that we don't have a safe enough anti-inflammatory drug for widespread use.

And a lot of where we're going in medicine in general, and in this area in particular, is personalized - where we want to be able to learn more about an individual so that we can get exactly the right recipe of interventions - both in lifestyle, and occasionally we need to use drugs to try to improve their outcomes, and decrease their risk of having events in the particular disease that we're interested in.

FLATOW: Dr. Wenk, you wanted to jump in there.

Dr. WENK: Yeah, I did. With regard to the brain, aspirin doesn't cross into the brain very well. It doesn't get across the blood-brain barrier hardly at all, and it doesn't need to to treat a headache or, you know, a bruised limb of some kind. So when you look at the epidemiology of people who've taken aspirin and asked the question, are they less likely to get Alzheimer's disease, and the answer is then no. The data correlates much better with drugs like ibuprofen, what we know as Advil, which does seem to cross the blood-brain barrier, and other anti-inflammatories that can get in. So with the brain, because it's protected, there's another barrier to get across when people are taking these things. So as Dr. Libby mentions, dose becomes critical, and you want to find something that's safe but also gets in at a dose that actually has some impact on the brain.

FLATOW: We've heard stories about - medical reports and research about the statins. The statins is fighting off cholesterol, but also helping in heart disease because it's an anti-inflammatory drug. Is there reason to believe that this might also be an effective way of reducing inflammation?

Dr. LIBBY: Yes, this is Peter Libby. We have definite evidence that the statins can be anti-inflammatory, and maybe by combination effect lowering the bad cholesterol so that we remove one of the stimuli to the inflammation - one of the triggers - and also because the pathway which leads to the makeup of cholesterol by the body has more than 20 steps. And along that long complicated biochemical pathway, there are little side roads that lead to modification of some of the signaling molecules that we think are crucial in regulating - in modulating the immune and inflammatory response. And there's very good biochemical and molecular, as well as clinical evidence, that we may activate those side roads of the cholesterol synthesis pathway in a way that actually will put a break on inflammation.

And I think you can't just think of inflammation as the flame that burns ever brighter, because there's actually a tug of war going on in these chronic diseases, between our body's own anti-inflammatory mechanisms, these counter regulatory measures and the inflammation. So it's really a complex tug-of-war that's going on in the brain that's affected by chronic inflammatory diseases, as well as the blood vessel, as well as many other organs.

FLATOW: 1-800-989-8255 is our number. We're talking about inflammation. Are you saying that we might go too far in the other direction, you know, that inflammation may be good for us?

Dr. Schmidt, we might go too far in fighting the body's own defense mechanism?

Dr. SCHMIDT: Exactly. The body, basically, is designed into, in terms of inflammation, the innate inflammatory response, which is really a very ancient and critical response to, for example, bacterial infections. And then, along the line of how the immune response evolved, we have the adaptive immune response, which is the type of immune reactions that can lead to, for example, the types of things we're talking about, as well as autoimmune diseases, in general.

So it surely is a fine line in terms of being able to retain the ability to react rapidly and acutely to pathogenic settings such as infection and wounding, and the ability to know how to modulate this properly in order to not shutdown affective responses that are critical for our survival in complex environments in which we live.

FLATOW: Let's go to Bonnie(ph) in Salt Lake City. Hi Bonnie. Welcome to Science Friday.

BONNIE (Caller): Thank you.

FLATOW: Go ahead.

BONNIE: Hey, I was calling because I had taken a community college course, and we have been talking about inflammation some years ago. And one of the things that the doctor that was teaching the course had said was that stress and processed sugars actually increase inflammation in the body. So I was wondering if you reduce those that you would actually reduce these chronic diseases associated with inflammation?

FLATOW: Good question. Dr. Libby, can you tackle that one?

Dr. LIBBY: Yeah. Well, unrefined carbohydrates are generally easier for the body to deal with, metabolically, than the highly refined carbohydrates such as granulated sugar or white bread, which causes a real burst of insulin. And over the years, that can put a stress on the pancreas, which is where insulin comes from the body. And it really can stress out the cells that pump out insulin because if you have these big spikes in your blood sugar because you've had these quickly broken down carbohydrates, then the cell of the pancreas that makes the insulin - we call the beta cell - can get tired.

And that's one of the reasons that we think people can develop diabetes, because they get stress on their beta cells.

FLATOW: 1-800-989-8255. We're talking about inflammation, this hour, on TALK OF THE NATION Science Friday from NPR News.

Thank you for calling.

FLATOW: I hope that answers your question. So is the Holy Grail, Dr. Schmidt, I know that Columbia's working on a patent that - for the RAGE gene, correct? Is the Holy Grail, then, defines one of these master controllers of inflation, or a simple drug that might keep inflation in check and then ward off a lot of diseases?

Dr. SCHMIDT: Well, you know, obviously, this is something that's been tested by we and others in cell culture systems and also in animals. And certainly, the real test of this concept that this family of molecules that is linked to inflammation that interact with this receptor, that the blockade of those pathways might be beneficial, is certainly one of the things - as physicians - that drove us may years ago to try to reach that point.

There are early stage clinical trials in progress, now, with patients who have diabetes, and also, patients with Alzheimer's disease, really testing that concept that blocking this receptor might actually afford benefiting this chronic settings.

So certainly, that is open to clinical trial testing and this is a work that's very aggressively being pursued at this time.

FLATOW: Dr. Libby, there is a marker of inflammation that can be correlated with coronary artery disease, and some people have - we've heard about the C-reactive protein - had sort of had its up and downs. Is it still considered a good and reliable marker?

Dr. LIBBY: Well, it is a controversial matter, and one that the experts can debate for days, and have, in the last year. The C-reactive protein is a simple blood test that is sort of an overall gauge of the inflammation that's taking in your body. And it turns out to be a very good predictor of your cardiovascular risk in the future that adds to what we can figure out from the usual, traditional risk factors that everyone knows about that is age, and sex, and smoking, and blood pressure, and good cholesterol, bad cholesterol.

And what those of us who are working in this field are becoming convinced of is that when we measure the C-reactive protein in addition to all those traditional risk factors, which still hold up very, very well - we can sharpen our ability to predict who might be at risk, at a higher risk for a cardiovascular event in the future. And that can be very important in trying to select people who need special attention in terms of their diet, in terms of physical activity and people are now testing whether or not we can guide therapy with drugs based on this C-reactive protein measurement, in addition to the traditional risk factors.

FLATOW: Well, we also look toward this new age of individualized medicine where we look at the genetic makeup of each individual and decide what might work for them?

Dr. LIBBY: Yeah. That's exactly right. That's the goal, is to try to find markers, which look at different pathways that leads to disease, and can each give us additional information. So we think that the C-reactive protein, bringing out information, is giving us a view of the disease that we don't get from the traditional risk factors, and that's why it's not just gilding the lily, it's actually added value.

FLATOW: We're going to take a short break and come back, take your questions about inflammation, talk lots more with Gary Wenk, Ann Marie Schmidt, Peter Libby, about inflammation and about what role inflammation may play in some of the many diseases we have. Our number is 1-800-989-8255, 1-800-989-TALK. We'd be very happy to take your questions. Stay with us. We'll be right back after this short break.

You're listening to TALK OF THE NATION Science Friday. I'm Ira Flatow.

We're talking this hour about inflammation with my guests. Gary Wenk is professor in the Department of Psychology and Neuroscience as well as Molecular Virology, Immunology and Medical Genetics at Ohio State University; Ann Marie Schmidt is chief of the Department of Surgery's Division of Surgical Science. She's also the Gerald and Janet Carrus Professor of Surgical Science at Columbia University Medical Center right here in New York. And Peter Libby, Chief of Cardiovascular Medicine at Brigham and Women's Hospital and the Mallinckrodt Professor of Medicine at Harvard Med School. All taking about inflammation. Our number 1-800-989-8255.

Let's go to Mike in Lansing, Michigan. Hi, Mike.

MIKE (Caller): Good morning or afternoon. Great show. On the marijuana situation, with the recent research that show the prophylactic effect for lab animals, mice and rats, as far as Alzheimer's, and it also showed that it slowed the progression once these animals had contracted the disease. Is that due to anti-inflammation? And if so, does that anti-inflammatory characteristic carry through to any other organs on issues of inflammation?

FLATOW: Good question. Dr. Wenk?

Dr. WENK: Well, I think he's referring to our last time we spoke, Ira. Actually, yes, indeed it does. The mechanisms of action of cannabinoids, you know, the active ingredient in marijuana, has not been fully worked out, but we're making some progress of that.

In fact, since the last time we spoke, there's been a real landmark study by Marshall Lanch(ph), showing that aged animals and therefore, by extension, we hope aged people - may be able to benefit from cannabinoids. You know, the stimulation of the brain's own endogenous marijuana receptors might be able to reduce inflammation in an aged brain.

And before the break, we heard that aging plays a huge role in inflammation in the periphery, and that's especially true in the brain. So it's been difficult to find ways to reduce inflammation in brain. And I think that's why this recent research on, you know, these marijuana-like compounds is so exciting. For the first time, we may be able to help people out when inflammation develops as they age.

And given what we've heard about inflammation of the periphery from other two guests, there is every reason to believe that if an anti-inflammatory works in the brain, it's likely to work by the similar mechanisms in the rest of the body. So I think it's very exciting.

The epidemiologists suggest that it should work. Animal studies suggest that it should work. So I think if we can just find a nice, safe, effective drug that gets into the brain and doesn't, you know, produce the psychoactive high, which would simply make, you know, the symptoms of dementia worse, then I think there's a lot of hope for what might lie down in the future for the treatment of a number of different degenerative diseases of the brain.

FLATOW: But that's such a hot button political issue?

Dr. WENK: Oh, it certainly has been. I've heard from people all over the - actually, all over the world, since our last conversation, who feel very strongly on both sides of this issue. We're not going to be giving marijuana to Alzheimer's patients. That's not what we're talking about.

But what we're saying is that the epidemiology has led to some, I think, some awareness, recognition, that there's something in this plant that when it gets in the human body, has some very positive, sort of controlling influences over the runaway inflammation that we've been talking about.

We can see that inflammation is a double-edged sword. It is good for us. It is bad for us. Sometimes, there is bystander injury. And you know, cells of the body will suffer due to the presence of these inflammatory proteins and genes such as RAGE and the things that it controls.

So what we've seen - because so many people over the past few thousand years have been using this plant, you know, recreationally and obviously illegally - they've indicated something to us that we can see now is beneficial. So hopefully, we can isolate, you know, the beneficial aspects of this plant and take advantage of it. We've done this in the past. The pharmaceutical industry has shown themselves to be very creative at finding ways to extract things out of plants and to use them effectively as treatment for diseases.

You know, this is the history of pharmacotherapy. Well, this is the future of it as well.

Dr. LIBBY: So Ira, they're actually - it cuts two ways, with marijuana and also our body's own endogenous kind of marijuana, we call them endocannabinoids. It turns out that there are two kinds of receptors that are molecules on the surface of cells that engage these molecules, the cannabinoids, the marijuana-like molecules - and cause changes in the biology of the cells.

One of them, the first kind, actually causes the munchies, and it is the target of a drug, which will probably be approved in the U.S. shortly, which is quite effective in controlling weight because it sort of combats your endogenous munchies.

The other receptor, the second kind of receptor, is one that regulates the immune and inflammatory system. And in experimental preparations, where we can make mice atherosclerotic, if you stimulate the second kind of receptor, you can actually attenuate the atherosclerotic lesion.

So I would underscore what Gary's saying, is that with creative chemistry, we may be able to block one of these receptors that seems to be a bad guy and causes us to gain weight and stimulate the other in a modulated way, which may ratchet down the immune and inflammatory response and really have a very nice menu of biological consequences.

FLATOW: Phyllis(ph) in New Albany, Indiana - is it in Indiana, Phyllis?

PHYLLIS (Caller): That's correct.

FLATOW: Hi, go ahead.

PHYLLIS: My question has to do with omega-3 fish oil. What role does this play in the anti-inflammatory process, and does this cross the blood-brain barrier, say, to help with preventing Alzheimer's?

FLATOW: Dr. Libby?

Dr. LIBBY: Well, Gary can answer about the central nervous system, but certainly we have a very large body of clinical trial evidence that consumption of fish and that fish oil supplementation can benefit cardiovascular outcomes. And we think we have some insight into how that's working at this cellular and molecular level.

The fatty acids do get incorporated by the cell, and the fatty acids that are found - the fatty substances that are found in fish and in fish oil - have some particular anti-inflammatory effects because they may engage some receptors inside the cells - we call them nuclear receptors - that again can have beneficial effects in terms of increasing the synthesis of good cholesterol and decreasing the synthesis of bad cholesterol.

And in addition, we may have some effects that stabilize the heart rhythm that protect us against sudden death if we have predisposition to it because it's a sick heart.

So there's both good clinical observations and epidemiologic observations, as well as basic science - which is getting more solid by the year - that gives us a very important link between dietary variables, such as fish and fish oils, and improvement in outcomes. That's why lifestyle is so important in combating the development of these chronic diseases associated with aging.

FLATOW: But what about the antioxidants, and the antioxidant supplements like Vitamin E, Vitamin C. The really - research has shown there really is no beneficial effect of taking these supplements on heart disease, is there?

Dr. LIBBY: No. For the cardiovascular end points that have been studied, Vitamin E, Vitamin C, alpha-tocopherol, have really crashed and burned as useful therapeutics. Now, that doesn't mean that the antioxidant hypothesis, or the oxidation hypothesis, is not tenable. What it means is that these vitamins are not good kinds of anti-inflammatories to get in the right place at the right time to quell the inflammation.

So there are targeted agents that we think may be better, and that's being tested in clinical trials. And even in the coming year, we'll have some of those trials that will be becoming available and will give us more information about this possibility of antioxidants - not vitamin antioxidants, but different kinds of antioxidants - as therapeutics in the cardiovascular area.

FLATOW: Dr. Schmidt, I know that one of your colleagues is working on the link between obesity and inflammation. Can you fill us in on why fat causes inflammation?

Dr. SCHMIDT: Yes. These are very exciting studies from Tony Ferrante and Rudy Leibel at Columbia, in which they hypothesized that in the setting of adipose tissue increases - this is the fat tissue - that part of the mechanism involved in the development towards insulin resistance or hyperglycemia, might be related to inflammation.

And what they showed for the first time was that in the adipose tissue, the fat tissue of mice that were fed very high-fat diets, that there was an increased accumulation of macrophages, which are very critical inflammatory cells in the body. And these macrophages were shown to be producing a number of different inflammatory mediators. And indeed their work focused on the idea that this inflammatory mechanism might contribute and be along the parallel lines of development of insulin resistance and ultimate hyperglycemia.

So indeed, our laboratory, in fact, is collaborating with Dr. Ferrante in that very context as well, because it may be a vicious cycle of events in which inflammation may lead to insulin resistance, and then once individuals develop insulin resistance and perhaps (unintelligible) diabetes, this in turn sets up additional inflammatory mechanisms, as I mentioned before - in the large and small blood vessels - which then contribute to complications.

So inflammation is becoming a hypothesized important, critical link to not only the pathogenesis of complications in diabetes but, perhaps, be very importantly involved in the development of Type 2 diabetes itself. And Dr. Ferrante and colleagues - Dr. Leibel, Ferrante and colleagues - showed this very clearly in animal models, in which they showed the critical importance of inflammation in the setting of high-fat diet fed to the animals, to the mouse model.

FLATOW: Are there any symptoms in your body that inflammation is overrunning? Like, I'm going to give out one, for example. Let's say your gums are inflamed. Does that say to you that the rest of your body is inflamed, and maybe your other organs or your arteries, Dr. Libby, might be inflamed also?

Dr. LIBBY: Right. Well, what the - in chronic infections in various places - it could be the gums, it could be bronchitis, it could be prostatitis, it could be a bladder infection - those are all fairly localized but could have systemic effects.

I think that one of the kinds of inflammation that we're measuring with the C-reactive protein that isn't read out by the usual risk factors are these inflammatory conditions in other tissues than the blood vessel.

What we do know, at least experimentally, is that when we have systemic inflammation, that it can first of all change the blood in a way which makes it more likely that we're going to have a blood clot, because it ratchets up some of the pro-coagulant chemicals in our blood and inhibits some of the anti-coagulant and clot-busting molecules that we have.

And in addition, within the atherosclerotic plaque itself, we think that when we have systemic inflammation, that it can augment the inflammation within the plaque. So there's sort of an echo of systemic inflammation within the artery wall, and we think that that really is one of the ways that we can link some of these remote infections in peripheral tissues such as the gums and the cardiovascular events.

Now in terms of symptoms, it's been known since the ancients, the first century A.D., there was a physician named Celsus, and in his book "De Re Medica" told us that heat, swelling, and redness, and pain are the cardinal signs of inflammation, and we teach that to our medical schools today.

But those are more the obvious kind of acute inflammation, and as Gary said earlier, these chronic diseases that are associated with aging are a smoldering kind of tug-of-war inflammation that goes on for many decades, often.

FLATOW: Talking about inflammation this hour on TALK OF THE NATION Science Friday from NPR News. Our number is 1-800-989-8255. Let's see if we might get a phone call or two before we have to go. Let's go to Bob in Mansfield, Ohio. Hi, Bob.

BOB (Caller): Hi. In recent hours, they announced on the radio that elders taking Viagra may have their immune system stimulated so much that they're going to start a several-year program to see how many forms of cancer this might treat.

And a second one, when you talked about an unhappy overreaction, after years of nano-debris occurring in your arteries - when your body finally recognizes this, its response makes it far worse. It takes a little bit of debris in the system and fills it with clots, and suddenly you have a heart attack. Thank you.

FLATOW: You're welcome. Any - well, let's talk about the Viagra. Any connection there, anybody know of? Anybody see any connection? No. Okay, and the debris. Might this inflammation be from years of just debris floating around your arteries?

Dr. LIBBY: Well, I think the listener has really got it right, and that is that the hardening of the arteries, or arthrosclerosis, sort of smolders on for decades and can be totally asymptomatic, without producing any symptoms whatsoever. Yet one day, it seems like a lightning bolt, someone will get a heart attack. But in fact, that's only the end process of what's been smoldering under the hood of the plaque for decades.

And we think we have a very good understanding of why that happens. And it turns out that inflammation is critical in changes in the biology of the plaque that make it likely to pop open like a boil that bursts and cause a heart attack.

You can imagine if a boil bursts inside your artery, that it could cause a blood clot, and that's indeed what we think happens, and inflammation is critical to that transition from…

FLATOW: But could it be a chronic inflammation from a disease, or exercise, or something that suddenly turns that on?

Dr. LIBBY: The inflammation has probably been going on for a long time, but it manifests itself suddenly, seemingly suddenly, because the - just like a boil will be there for days and not burst - when we have inflammation that is peaking, it can burst, and when the plaque bursts, then it can cause a blood clot that we see as a heart attack.

Dr. WENK: This is Gary Wenk. Actually, I should point out that with regards to the brain, it's quite different. You don't tend to see that kind of a burst of, you know, a change in terms of pathology or symptomotology. We believe strongly that inflammation underlies the changes that lead ultimately to Parkinson's Disease, but yet the symptoms come on very, very slowly. And so, you know, it's quite different in different organs, and I think that we've seen that clearly here from our comments.

FLATOW: All right. We've run out of time, but this is quite fascinating, and we'll be following the progress you all make on inflammation.

Gary L. Wenk is professor of the departments of psychology and neuroscience as well as molecular virology, immunology and medical genetics at Ohio State University. Ann Marie Schmidt, chief of the department of surgery's division of surgical science. She's also the Gerald and Janet Carrus professor of surgical science at Columbia University Medical Center. Peter Libby is chief of cardiovascular medicine at Brigham and Women's Hospital and the Mallinckrodt Professor of Medicine at Harvard Medical School. Thank you all for joining us today.

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