Science Talk

Life Goes on within You and without You: Health and the Environment

In this episode, we'll hear parts of three talks from the recent symposium, Exploring the Dynamic Relationship Between Health and the Environment, organized by the American Museum of Natural History's Center for Biodiversity and Conservation. Speakers include Penn State's Peter Hudson, who talks about disease transmission; Oxford's Oliver Pybus, on how genome analysis exonerated health care workers accused of infecting children with HIV; and N.Y.U.'s Martin Blaser on our disappearing stomach flora. Plus, we'll test your knowlege of some recent science in the news. Web sites related to this episode include

Podcast Transcription

Steve: Welcome to Science Talk, the weekly podcast of Scientific American, posted on April 17th, 2009. I am Steve Mirsky. This week on the podcast, we'll hear three speakers from a recent conference on human health and the environment—the environment both outside you and inside you. And we'll test your knowledge about some recent science in the news. Back on April 3rd I was at the American Museum of Natural History here in New York City for a conference called Exploring the Dynamic Relationship Between Health and the Environment which was put on by the museum's Center for Biodiversity and Convservation. I'm going to play for you parts of three talks from just one of the sessions dealing with pathogens. We will hear the session moderator George Amato introduce Penn State's Peter Hudson who talks about disease transmission, then a short clip from Oxford's Oliver Pybus on how studying pathogens can save lives in unexpected ways, and then N.Y.U.'s Martin Blaser on the case of the disappearing stomach flora. Here's George Amato.

Amato: I would say in the field of human health for the last five or six years, the dominant news stories have been about emerging diseases, whether it was SARS or avian influenza or novel diseases like Nipah virus or other ones. It seems every couple of years where the public [of course] is just a[ware] of this; it seems like a new and unusual phenomenon. If it is not [a] new and unusual phenomenon, it is something that people are much more aware of and we have the tools to better understand. Our first speaker as well as anyone has added to our knowledge and information about these kinds of things. Peter Hudson is the director of the Huck Institutes of Life Sciences and the Willaman Chair of Biology at the Center for Infectious Disease Dynamics at Penn State University, and it's my distinct pleasure to welcome him to give our first talk.

Hudson: You know the scenario. There you are, just walking down the street, minding your own business, when suddenly somebody comes up behind you and "Acchoo!"; they spray you, they cover you and within just a short period of time, within 24 hours, you are starting to feel the symptoms; you are starting to feel rather groggy, you're starting to feel the virus, the fight that's going on inside you. Within 48 hours, your limbs are starting to ache, you are stuck in bed; you feel terrible. All you really want to do is actually die. You feel awful. Yes, you have just experienced a transmission event. Transmission is the very key to disease biology. That is what the pathogen wants to do, and that's how we must understand epidemiology—it's looking at transmission. And yet we can't record it. You've probably been exposed several times coming on the metro here today, but actually recording a transmission event is very, very difficult. And if you lie there in bed, you think to yourself, "What on earth is going on? Where did that disease come from? Who was that wretched person who caused this infection? Who is responsible? Was it them or was it some relative of theirs? Where did that come from? I've had just about every bug that is going around, I've had every bug that my kid has brought back from nursery school. Who is responsible for this and why is it so virulent? Why was that person who sneezed on me not stuck in bed? Why weren't they suffering like I'm suffering now? Why is it hurting me more than it's hurting them?" Important, interesting and difficult questions to sort of address, and I'm going to try and illustrate those by reaching from an ecological understanding towards the evolutionary understanding. Where did they come from? Well, there is some 1,400 different known human infections. Most of those are microparasites, the viruses, bacteria, fungi and protozoa. But even amongst those, by far and [a]way the majority were originally synoptic. Many of the infections we have were derived from wildlife or from domestic animals. Even diseases like measles are not a human specialist. They originated from something that we assume is [unclear] and at one stage during our history, as we were milking cows, we became infected and there was a spillover event and measles became a human specialized infection. What about vaccines? Haven't we got vaccines to everything? My mother always says, "We have solved the whole problem with infectious disease, darling, you can go home and retire, because we have vaccines and antibiotics." In reality, Mum, we have only got about, in the U.S. we've only got about 55 vaccines against something like 23 diseases; that's only about 2 percent. And then those cause significant problems at times because they generate a selective pressure that can result in rapid evolution away from the selective pressures that vaccines may give us. What about the emerging diseases, what about these new diseases we haven't heard of before, that seem to be coming, where are they all coming from? Well about 70 percent of those are also zoonotic—zoonotic meaning, derived from wildlife, derived from animals and spilling over towards us. You only have to think about the major epidemics we've had during the period of history: Bubonic plague, of course, came from rats. It devastated Europe; countries like Italy took 400 years just to recover their population size after the Bubonic plague spread through. We've had Spanish influenza, just nearly a 100 years ago that devastated population, of course‚Äëthere was more people died during that than died during the first world war and there's somebody who've had 11 uncles die in one day in the Great War, I think that's astonishing. Then of course, there is HIV, this new infection that emerges that we think has infected more than 50 million people, six million people a year. Where did that come from, why was that taking place? Well, once again that was an infection that came from primates. We believe from—the work of Beatrice Hahn indicates—that it came probably from chimpanzees, and we know that there have been a series of spillover events. With HIV-1, at least three, HIV-2 at least four spillover events. And most of them seem to be derived from a simian immunodeficiency virus, SIV, from different places such as the DRC, the Cameroon and places. We know that there are different subspecies of chimpanzees with different virus strains that link closely to the M, O and N strains that we see circulating. So what's the process? Well, the process is very much a dynamical process. We see a disease circulating in a reservoir host, it then spills over into a human population; got to realize this is very dynamical. Those wild animals are infecting each other and then something happens which results in an exposure to an individual that is both susceptible in the human population, and so they become infected. Now by far the way the majority of those diseases just stop at that point. So infections like rabies, it's very rare for one human with rabies to run around biting everybody else and it is very rare for a human to infect another human once they have rabies infection. But there are some infections that do start a stuttering chain of transmission. So individuals, for example, have monkey pox and they might transmit that to one or two other individuals, and so on to a couple of more individuals and then after sometime, the infection just fades out; there is no onward sustained transmission. Whereas other infections, we do see sustained transmission events taking place; the classic ones being HIV, dengue and to some extent SARS as well. But these are relatively rare in the recent history; they do occur but they are relatively rare, but when they do occur, we get extremely worried about them. We have got to start understanding what this dynamical situation really is like. There is a huge gap in our research and I'm arguing because of that gap, we really don't have the insights that we really need to start understanding what's happening with emerging diseases. And the real point is we need a lot more research and we need a lot more effort to look at the spillover situation. What is spillover? Spillover, I like to think of, as the interspecific force of infection. This is the force of that infection that is coming towards the human beings. It depends on what the prevalenc is in the reservoir, the contact rate between the reservoir and the human, and then the likelihood of that infection taking off, given some sort of contact taking place. Well, what sort of research has been done on this? Well, one of the classic studies is one by Nathan Wolfe. When Nathan went out into the Cameroon and he went and looked for the simian foamy virus in bushmeat hunters. he argued cogently and correctly [that] bushmeat hunters were the people who should be exposed to these infections. And he was wise enough to look for simian foamy virus because that is an asymptomatic retrovirus, not too far from HIV, but it is not one that's going to cause mortality and problems but it's one you should pick up the serum, you should be able to do the serology and identify that those individuals were infected. He found that there was just 1 percent of the 1,100 people that he sampled [who] had actually previously been infected and those were from three primate strains, one from a Cercopithecus, one from a mandrill and another from a gorilla. So, three different species of primate causing spillover to humans. We've also been doing some work on interspecific transmission and looking at it in chipmunks and mice just to see what the process is like, and once again we get sort of 1 percent spillover, even though the contact rate between those animals, we think, is much higher than the intraspecific contact rate. So chipmunks and mice will share territories that will come into contact more than mice were[will] with mice and a consequence of that is we see spillover at the sort of rate of 1 percent. This whole process is very much similar to an area in ecology where we've seen a great deal of research done, and that is in the bioinvasion research. So we've seen a lot of research done on insects and on plants and I think we can learn something from what has happened there. So you get a native plant, that's circulating its own habitat, it then gets an introduction, perhaps through an aeroplane flight into the U.S., there is an accidental release, then some lag goes on and then the weed or the insect becomes established, very similar to that process that I've devised here and the propagule pressure is a determinant of this, just as we think now the force of infection is very important for the invasion of these diseases into the human population. I think it is a good way to actually start thinking about it.

Steve: Oxford University's Oliver Pybus

Pybus: The next example I'd give is really unusual analysis we did because it kind of got us wrapped up into an international diplomatic scene, somewhat. And let me just set the background to the story. It was that in 1998, there was a large outbreak of HIV infections amongst children in a hospital in Libya, the Al-Fateh Hospital in Benghazi, and many of these children were referred to European hospitals, and many of them were found also be coinfected with hepatitis B and hepatitis C. And in an issue, World Health Organization report suggested that there was hospital-based or a nosocomial infection, and a lack of the required equipment for safe medical practice in the hospital. That didn't stop the Libyans accusing five Bulgarian nurses and a Palestinian doctor who actually started work, perhaps unfortunately, around the same time. They were accused of deliberately infecting the children in this hospital with HIV. After many years, they were actually convicted and sentenced to death for this alleged crime. On the 26th of October in 2006, we were e-mailed some virus sequences from the infected children and then told on the 19th of December the final judgment [was] due on a death sentence. I don't know if you've ever tried to do an entire analysis and write a paper in two weeks and get it submitted and reviewed and published, but we did make it. We didn't get much sleep, and our wives and girlfriends didn't see us too much, but we've managed to perform the analysis in around, kind of, 10 to 12 days. And the results were very clear. For the HIV infections it was a single infection that was closely related to strains from Ghana and Cameroon, and there were three separate clusters of hepatitis C infections in these children, and they were either closely related to hepatitis C strains in Egypt, which I've already mentioned, and also other strains from West Africa. You may be wondering, "Where is the epidemiological link between West Africa and Libya?" It turns out that Benghazi is the main stopping off point from economic migrants from West Africa trying to get into the European Union to try and find jobs. So they go across the Mediterranean into Sicily and southern Italy. And the Libyan government had actually written to the EU a few years ago and said, we are getting a bit worried about all these HIV and hepatitis C infections coming into Benghazi as a result of economic migration. [And we used our]the molecular clock and by trying to date the common ancestor, trying to date the origin of each of these clusters, we found that, again being really nerdy about our 95 percent confidence limits, that even under every scenario we tried to look at, the common ancestors of each of these outbreaks predated the arrival of the medical staff in Libya. So they weren't in Libya when these outbreaks started. Our report was then roundly ignored, and they were sentenced to death again and then there was a period of diplomatic behind-the-scenes wrangling and then suddenly six months later, they were released.

Steve: New York University's Martin Blaser.

Blaser: Animals have had residential organisms as long as we've been animals and several principles have emerged. The microbes that we carry are ancient, they are need specific, they live in particular locations in our bodies or all animal bodies. Certain of the organisms are persistent, lasting from months to [the] lifespan of the host; many of them are conserved and some of them are host specific. One of the things that we have learned about Helicobacter pylori is that it has been around for a long time, and it's now clear that there was an early African population and then populations that are present in Africa and then that have spread through the world in Europe, Asia and then across out of Asia to the New World. And these kind of data indicate that Helicobacter pylori has been in humans, at least since out of Africa 58,000 years ago and presumably much longer in relation to this ancestral root. We know that Helicobacter has been the dominant organism in the human stomach. It has been found in all populations of humans that have been looked at; it is essentially universal, especially in developing countries. It is acquired early in life and most people who have Helicobacter die with it in their stomach. We know that this one species numerically dominates the stomach with more than 70 percent of the count. So by all of these criteria, Helicobacter has been very successful persisting in the human stomach. People who are born early in the 20th century were frequently Helicobacter positive and people born later in the 20th century are most often Helicobacter negative. In fact, from near universality at the late 19th century/early 20th century, now only 5 percent of our children carry Helicobacter pylori. This organism has been disappearing extraordinarily fast. Several years ago, I've developed a hypothesis, which I've called the disappearing microbiota hypothesis, and it was stimulated by the work on Helicobacter; and the concept is that with changing human ecology, beginning in the late 19th century, there have been dramatic changes affecting the transmission and maintenance of the indigenous microbiota. These chain circumstances have affected the composition of our indigenous microbiota—I point to Helicobacter as an example of this—and the change composition affects human physiology and thus disease risk. If Helicobacter is disappearing and Helicobacter is a major factor for stomach cancer, which it is, then stomach cancer should be disappearing as well, and in fact it is—it's happening all over the developed world. On the other hand, new cancers are arising. And in particular, I want to focus on adenocarcinoma of the esophagus: It is the most rapidly rising cancer in the United States and in all developed countries in which it has been looked for. In the U.S. it is going up about 9 percent a year; in Sweden, Austria, Australia it is going up between 11 and 16 percent a year. Where are these cancers coming from? Why are these cancers going up, when stomach cancer is going down and Helicobacter is going down? So with colleagues at the National Cancer Institute and colleagues in Finland, we examined the relationship between Helicobacter and common stomach cancers, the cancers of the distal stomach—what's called noncardia—and the cancer is right up at the top of the stomach, next to the esophagus. This is from a cohort study of 29,000 men followed for a number of years, and we ascertained their Helicobacter status at the beginning of the study. And the bottom line is this, this odds ratio. For cancers, the typical cancers of the lower stomach, men who had Helicobacter were eight times more likely to develop these cancers over the study period, as expected; but those who had the cancers up against their esophagus, they were 0.3 times more likely. They had about 70 percent smaller risk of having, developing these cancers than men who had Helicobacter. So in the same study, we can see that there is a divergent trend between these two forms of cancer. That is one of a number of studies that all show the same phenomenon. This suggests a proposed reciprocal relationship between adenocarcinomas of the lower stomach and adenocarcinomas of the esophagus and upper stomach. And so the model is that people who have Helicobacter have increased risk over their lifetime of developing stomach cancer, phenomenon that takes multiple decades. In contrast, people who don't have Helicobacter appeared to be at increased risk for developing reflux which is going up dramatically, and its consequences also taking many years. Life is unfair, but not everyone who has Helicobacter gets stomach cancer, not everyone who doesn't have Helicobacter gets esophageal cancer; we're trying to understand why. Another disease that has been going up dramatically is asthma, as all of you know, and in particular, childhood asthma. And we've now conducted three large, independent blinded studies that have shown the same phenomenon. If we look at adult-onset asthma, there is no relationship between Helicobacter and adult-onset asthma, odds ratio is about 1. But if we look at childhood-onset asthma, we seen an inverse correlation odds ratio 0.63, about a 40 percent less childhood asthma. And this is one of three studies that show almost identical findings. We can look at it in another way from our study done here in New York and as part of that analysis we have a life table analysis of almost 300 people who have asthma. So they were born without asthma, and they all developed asthma by definition; and now we are asking, "How old were they when they developed asthma?" So in those who had Helicobacter, the median age that they developed asthma was 21, but in those without Helicobacter the median age is 10, and that is a huge difference. One final topic, and that is that the stomach also makes hormones; it makes hormones that are related to energy homeostasis. This slide shows that the hormone leptin is made in the stomach, and the stomach has leptin receptor. Leptin tells the brain "Don't eat" among its many other functions. There is a second hormone called the ghrelin which is the antagonist of leptin, and the stomach produces 60 to 80 percent of the body's ghrelin. So in very recent studies, my colleague, [Fritz Francois] and our group had been studying what happens when you eradicate Helicobacter, what happens to ghrelin. And to make a long story short, we look at ghrelin before a test meal and then after a test meal. in people in their baseline state and after Helicobacter is eradicated. What we find is that after we eradicate Helicobacter, ghrelin goes up dramatically. This has been confirmed by other investigators. as well. So what I can say at the least is that the presence of Helicobacter is involved in the regulation of this hormone that is involved in energy homeostasis. So, to summarize the evidence is now becoming clear that in addition to the late-in-life costs of having Helicobacter such as ulcer disease and gastric cancer, there is new evidence that Helicobacter may actually have some benefit to humans, especially early in life. Regardless, Helicobacter pylori is disappearing. And it's disappearing at a remarkably rapid rate. What's an alternative view of the future? Maybe we should start giving Helicobacter back to people, possibly early in life and perhaps eradicating it later before the harm comes. Finally, what I've told you about Helicobacter is specific to the stomach, but we have the tools that we can detect Helicobacter and we could measure the effects. If an organism disappeared in the colon, the vagina and the skin, right now, we don't have the capability of determining that. But it could be that as Helicobacter is disappearing other organisms are as well, and perhaps the human Human Microbiome Project will help us.

Steve: All the talks from the two-day conference, called the Exploring the Dynamic Relationship Between Health and the Environment, are now posted at the American Museum of Natural History's Center for Biodiversity and Conservation Web site. So you can check out the full roster of speakers and listen to any or all of the talks in their entirety. Just go to

Now it's time to play TOTALL....... Y BOGUS. Here are four science stories; only three are true. See if you know which story is TOTALL....... Y BOGUS.

Story number 1: A recently discovered type of lichen has been named for President Obama.

Story number 2: Just rinsing your mouth with sugar water can improve athletic performance.

Story number 3: A device called the Peepoo bag turns human waste into fertilizer.

And story number 4: In a small study, Naltrexone, a drug used to overcome heroin addiction, was found to increase the rate of bone healing after a fracture.

Time is up

Story number 1 is true. The lichen, which is an algae and fungus living together, is now officially Caloplaca obamae. Kerri Knudsen of the University of California, Riverside named it after the president to show his "appreciation for the president's support of science and science education" according to our friends at In 2005, a beetle in the genus Agathidium was named for then-President Bush.

Story number 2 is true. A sugar or carbohydrate rinse and spit improved athletic performance up to 3 percent in a study published in the Journal of Physiology. No need to actually swallow and put the calories to work. Might have something to do with the brain's pleasure pathways. For more check out the April 16th edition of the daily SciAm podcast, 60-Second Science.

And story number 3 is true. The Peepoo bag is designed for the developing world, where it could help two problems, sewage disposal and crop fertilization. The bag is lined with urea, which helps break down the feces and urine; then you just plant the entire bag.

All of which means that story number 4, about naltrexone helping bone healing ins TOTALL....... Y BOGUS. But what is true is that a study at Stanford found that naltrexone could decrease symptoms of fibromyalgia, a syndrome of muscle pain, depression and anxiety. The study was published in the journal Pain Medicine, one of the authors is Sean Mackey. To hear an interview [with] Mackey, check out the December 3rd, 2008 episode of Science Talk.


Well that's it for this edition of Scientific American's Science Talk. Check out for the latest science news and an article on learning how to think better featuring Daniel Tammet, who has publicly recited the first 22,514 digits of pi. That's right, he can run circles around us. For Science Talk, I'm Steve Mirsky. Thanks for clicking on us.

In this episode, we'll hear parts of three talks at the recent symposium, Exploring the Dynamic Relationship Between Health and the Environment, organized by the American Museum of Natural History’s Center for Biodiversity and Conservation. Speakers include Penn State’s Peter Hudson, who talks about disease transmission; Oxford’s Oliver Pybus, on how genome analysis exonerated health care workers accused of infecting children with HIV; and N.Y.U.’s Martin Blaser on our disappearing stomach flora. Plus, we'll test your knowlege of some recent science in the news. Web sites related to this episode include 

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