People of Northwest Public Radio
Fri August 17, 2012
Some Docs Doubt Blood Type, Heart Disease Link
Originally published on Fri August 17, 2012 10:22 am
FLORA LICHTMAN, HOST:
This is SCIENCE FRIDAY. I'm Flora Lichtman, filling in for Ira Flatow today. Do you know your blood type? You may have wondered about it this week if you heard news linking blood type to your risk of heart disease. In that study, researchers determined that those with blood type O had the lowest risk of heart disease and those with AB the highest.
But what does blood type have to do with heart disease? And you're born with it; you can't do much about it. Is blood type really something you should be worried about? Joining me now to talk more about that is Dr. Eric Topol. He's a practicing cardiologist and the author of "The Creative Destruction of Medicine." He's also director of the Scripps Translational Science Institute in La Jolla, California, and he joins us by phone. Welcome back to SCIENCE FRIDAY, Dr. Topol.
ERIC TOPOL: Well, thanks, great to be back with you.
LICHTMAN: OK, so give us your take on the study that came out this week.
TOPOL: Well, this study is concerning, because although it purports to have about a 10 percent lower risk for type O blood versus the other types of blood, the data are very soft. There are significant issues here. You know, these studies, which they looked into these large patient cohorts of almost 89,000 patients cumulatively, they were - this was not the purpose of the study.
So they were basically dredging the data, and this is the same type of problem we ran into with hormone replacement therapy and Vitamin E, and it's why a classic paper back in 2005 by John Ioannidis was why most published research findings are false. And I actually think that's what this is.
LICHTMAN: So they did find a correlation there. Is there another explanation?
TOPOL: Well, it's about a 10 percent effect of the, you know, so-called or putative protective effect of blood type O.
LICHTMAN: So small.
TOPOL: Very small effect. And they actually go back and look at the six other studies, cumulatively, and only half of them had any level of significance but very small effect. Beyond that, there's a problem of why. There's no real mechanism. There's no real science behind this.
And so you have very weak effect, which is inconsistent, that is many studies showed no significant effect. And then you have basically this data dredging affair, where they had to look at a very large number of patients to find - eke out this tiny effect.
LICHTMAN: What should people really be thinking about in terms of the drivers of heart disease?
TOPOL: Well, you know, the things that we know so well, like obesity and diabetes and smoking, high cholesterol, high blood pressure and sedentary - lack of exercise, those are the biggies. They're not going to go away. They are so much more overshadowing this tiny and questionable effect of blood group.
And of course if there was a blood group effect, which is quite questionable, as you already pointed out, we don't have a whole lot of control about that, but we do about much of our lifestyle.
LICHTMAN: Are these things, do they work in concert together, or is there sort of one big driver?
TOPOL: Well, you know, it really is kind of a multiple hit phenomena. First there's your genome, which, you know, we have particular variants in our sequence and other parts of our genome that put us at some risk. Some of that you find out through family history. Some of that is just the way parents' genomes blend together. It might not be in the family history.
So you have this genome story. Then you have these risk factors, some of which are gene encoded, like your cholesterol, in part, but also influenced by diet. So of course your weight, your blood pressure is influenced both by diet and genomics. So there's this complex interaction between one's DNA and then these multiple factors.
LICHTMAN: Do we understand this pretty well? I mean, you know, are there other sort of mystery factors that people are still looking for?
TOPOL: Oh, there's quite a bit still on the hunt. When we looked at the common variations in people's DNA, we found some markers, which - a couple of which are pretty important but not anything overriding, that is, you know, a 20, 30 percent risk if you have one of these alleles. But now with a lot more sequencing, with it become so high throughput, so inexpensive, the hunt is on for the low frequency or more rare variants, which cumulatively will probably explain a large part of the risk, that is, at least, the genomic risk for heart disease.
So in the next few years there should be a lot more progress along these lines.
LICHTMAN: When someone has a heart attack, can you give us a run-up of what happens in advance of that?
TOPOL: Yeah, that's really a very poorly understood event, which fortunately in recent times, we're getting a much better handle. That is there's a crack of the artery wall, usually when there's just a mild, a minimal amount of cholesterol buildup, not a tight buildup or blockage of cholesterol.
So there's a crack in the wall where there's some cholesterol buildup, and that crack proceeds over several days or a couple of weeks, and then ultimately a blood clot forms. And when the blood clot forms, which is trying to seal up the artery, it backfires because it cuts off the blood supply through the artery, and that's when the person has the chest pain and presents to the emergency room with all the symptoms of a heart attack.
LICHTMAN: And you've done some work on looking at the sort of early signs, right, trying to understand what happens when that crack occurs. Tell us about that.
TOPOL: Right, that's really exciting work, and we're really pleased that we can find the cells that are coming off from that artery that's starting to crack, that would be days or a couple of weeks before the event.
LICHTMAN: Wow, weeks.
TOPOL: Yeah, so this is something that we've never been able to do, to predict, temporally, when a heart attack is imminent, you know. And that is something that - it's a big problem today because so many people, about three million people go to an emergency room each year in the United States with chest heaviness and pain. And so many of them are sent home without any blood tests that show heart damage or a cardiogram that shows heart damage.
And then they have a heart attack the next day or within a week. So we hope that a blood test that shows these cells, the genomic signature of these cells, a rapid blood test, will be able to sort out those people who are basically harboring an impending or imminent heart attack.
LICHTMAN: So you only see these cells when the arteries are cracking. Is that right?
TOPOL: Right, right, they're shed from the artery wall, and they shouldn't be in the blood, and they are not only distinct from the very rare cell that you might see in a healthy person, but they're very sick, very abnormal-looking cells with a very specific gene signature.
LICHTMAN: So they're easy to identify, too.
TOPOL: I wish they were even easier...
TOPOL: But at least we can, and that's I think going to be really good. And that leads to this, you know, kind of futuristic way where you could put a little nanochip in the blood for people who are at risk of heart attacks, and then it could constantly have the blood under surveillance of these cells and then send a signal to one's cell phone, a heart attack app, which you would get the alert that, you know, something's brewing over the next several days.
LICHTMAN: Yeah, maybe a Facebook update, too.
TOPOL: Right, right.
LICHTMAN: Yeah, that's - I mean, that - I heard you talking about this in a video online, and I thought this is just an amazing idea. How far away do you think we are from something like that?
TOPOL: We're hoping the blood test will be in the next year, year and a half because we're pretty far along. We're working intensely in San Diego with multiple hospitals throughout the region to nail this down, the work that we already have to basically set up a blood test. So that hopefully won't be so far off.
The sensor, the nano-sensor, tiny grain of sand in the blood, that one's going to be at least a few years away.
LICHTMAN: And would this nano-sensor just float around your blood stream, or do you have to sort of put it in the heart or on an artery wall?
TOPOL: Oh anywhere in the blood stream would be fine. The only question would be is it better if it's just floating, as you say, or would it be better to put in a very tiny micro drug-coated stent and keep it somewhere, you know, like in the wrist or someplace that's accessible. So that is another - which one of those paths is better is still not clear.
LICHTMAN: Are there any dangers associated, that we know of, of putting a sensor like that in our body?
TOPOL: Well, multiple centers are doing it, and there's already, you know, models being done in animal studies, and there doesn't appear to be any danger, and it goes even beyond heart attack. You could pick up antibodies before diabetes is struck in auto-immune diabetes or cancer cells. So there's a lot of things that it has potential for if we can get these nano chips to last a long time, powered by the blood, the movement of the blood, so there's no other power need, which is also a big advance.
LICHTMAN: For people with heart disease, do you have a sense of how much is sort of genetics, the stuff you're born with, and how much are environmental effects?
TOPOL: Well, I always tell my patients it's 100 percent of both.
TOPOL: And that is because, you know, you can't change your genes, and that's probably not going to happen in any way for quite a long time, but you can work on all the other risk factors, and control if it's high blood pressure or diabetes, certainly smoking and being overweight. So it's really this very important interdependency of one's DNA and all these other conditions and lifestyle.
And so in any one individual, it could be emphasizing more genomics, because they do everything right, and they still have heart disease, or of course in people who don't, have a very poor lifestyle, an only relatively small DNA risk.
LICHTMAN: Is there any work on a heart disease vaccine or something like that? Is that even possible?
TOPOL: A heart...
LICHTMAN: A heart disease vaccine.
TOPOL: Oh, vaccine. Oh, actually it's funny you brought that up. This week, the group at La Jolla Immunology Institute published a paper in the Journal of Clinical Investigation on that very topic. And they identify an ideal target that could potentially be used for a heart disease vaccine.
Now, that's been talked about for some time, but the right target to make the vaccine against had not really been isolated. And so this looks promising. Now, that's many years off, but that would be extraordinary. That would be a great way to take people who are at risk for heart disease and get them vaccinated young in life so they never really had to worry about it.
LICHTMAN: What are you vaccinating against?
TOPOL: Well, here it's about the immune system that revs up this plaque process that leads to the cracks in the artery walls. So it's basically a component of the immune system that appears to be the real trigger, you know, kind of a master regulator of that whole process.
LICHTMAN: Oh wow, so that's what is actually creating that plaque?
TOPOL: Right, so if you can knock out its activity without - of course that's the other question is, what's the downside of it? These are the things we don't know and will take years of testing. But that would be a truly extraordinary way of being able to prevent heart disease.
But you know what? It's never going to be that you have to - that you can't take care of yourself, and you rely on a vaccine or take a medicine. There's always going to be, you know, some interplay between these things.
LICHTMAN: Thank you, Dr. Topol, for joining us today.
TOPOL: Thanks very much for having me.
LICHTMAN: Dr. Eric Topol is a practicing cardiologist and the author of "The Creative Destruction of Medicine: How the Digital Revolution Will Create Better Health Care." He's also the director of Scripps Translational Science Institute. This is NPR SCIENCE FRIDAY. Transcript provided by NPR, Copyright National Public Radio.