sábado, 1 de novembro de 2014

Humanity’s Ticking Time Bomb: How the Chemical Age Spun Evolution Out of Control

By Lindsay Abrams

Human activity is influencing the genetic world in unexpected and dangerous ways, Emily Monosson tells Salon.

Photo Credit: Wichy / Shutterstock.com
And despite the opinions of those who don’t like to think that human activity can have a significant, detrimental effect on our planet, they’re proof of just the opposite. We may temporarily gain the upper hand over pests and diseases through our use of chemicals, but eventually they’re all but guaranteed to bounce back, stronger than before. Less intentional still, says Monosson, are the impacts we’re having on larger species: where industrial pollution meets wildlife, frogs, fish and salamanders evolve to survive in their newly toxic environments.
In “Unnatural Selection,” Monosson discusses the myriad ways in which the chemical age is changing life, and, most importantly, what we can do to slow things down. Part of the challenge, she told Salon, is just understanding that this is evolution we’re seeing — something that not everyone seems to grasp. ”Maybe if we did,” she mused, “we’d realize how important it is to reduce our chemical influence on life.”
This interview has been lightly edited for length and clarity, and to incorporate some follow-up points made later over email.

Just to start off, I was hoping we could talk about how evolution, as you write about it, is defined — how is it different from what we’re typically taught?

Well, just to clarify, I’m not sure I’m defining it any differently from what we’re normally taught. By definition, evolution is a change in gene or trait frequency in a population — so a trait like hair or eye color becomes more common in a population over time. The difference is probably that we’re often taught that evolution is something that happens over very long time frames, and we tend to think of evolution in terms of the evolution of different species or very large traits. That’s called macroevolution: big changes. So what I’m writing about here is called microevolution: it’s very small changes. These are changes that normally would probably be difficult to see or that we might not notice — a change in an enzyme or protein, something like that — but because we’re looking at things like resistances, they become very noticeable.
There are a couple of evolutionary biologists who are working on popularizing the idea that evolution can happen very rapidly, and in contemporary time. And that the more we look, the more we see it — so it’s probably more of the norm than the oddball thing. Probably everybody learned about the peppered moths that evolved during the Industrial Revolution, and that was the oddball situation, but what these guys are saying now is that this is kind of more the norm; that these things can happen pretty rapidly.

And that’s something that we’re still working on understanding — how prevalent it is?

Yes, that’s right.

How much time passed between the time when humans began to have this outsized effect on other organisms, and when we began to really understand the implications of that, or even that it was happening?

That is a great question, which I’d best leave to the evolutionary biologists. If people were mining a thousand years ago or something like that, and putting their mine tailings in the soil next to the mine, they might have been influencing the microbes and the worms that were living there. And I guess somebody could say that when people were hunting they were probably influencing evolution, because there’s evidence with fisheries that if you take the biggest fish, you can influence the growth rate of fish populations. If I had to say when we began, I’d say it’s probably when we started becoming dominant and messing with nature.

That said, my focus has been how our use of industrial-age chemicals has influenced evolution; and that influence probably began whenever humans started using, discarding and producing chemicals, but really took off with the industrial age and the chemical revolution. Ever since we started killing things either intentionally or not with chemicals, turning up the pressure, those species that could evolve rapidly probably did so. (In the case of the moths the soot was a more indirect influence — it wasn’t killing the moths, only making them more visible.) We are just now learning the scope of who can and in many cases cannot evolve rapidly in response to our chemicals.

As far as when we really started to understand the effects that we have with the chemicals we’re using, that would probably go back to thinking about antibiotic resistance. That was becoming known back in the 1940s, at least, and maybe even sooner — that if you use too much of the chemical you can influence evolution and cause resistance. I write about Alexander Fleming, who discovered penicillin, and it was being proposed that penicillin be put in all sorts of consumer products — things from vaginal creams to toothpastes. Just like people use antimicrobials now. And back then, he warned in his Nobel Prize speech that if you’re going to do this, you’re going to lose the efficacy of penicillin. The sensitive bacteria are going to become resistant. And that was already happening: during World War II there was evidence of bacteria resistant to penicillin.

One of the things you write about is this idea of “consequences of denial”: We’ve known this has been happening for a long time, but haven’t always changed our ways in recognition of that knowledge. Would you characterize most of the problems we’re facing now, like antibiotic resistance or the emergence of superweeds, as arising in large part from our unwillingness to admit these things could even happen?

Even though evolution or resistance was known in the medical world in response to antibiotics early on — the fact that resistance could be shared among different pathogens, or that pathogens could become resistant to multiple antibiotics — took a while to catch on. Those things were first reported in the late ’50s and ’60s but the studies were received with disbelief. That just couldn’t happen. Similarly farmers have been dealing with resistance to pesticides. They see it. But they use more or use the next pesticide. So in some odd way we seem to accept it as an inevitability, but don’t think about changing how we do things. Maybe because we never thought about it explicitly as evolution; or more profoundly that we have changed that population of insects or weeds or whatever. Maybe if we did, we’d realize how important it is to reduce our chemical influence on life.

I think a lot of it is also this attitude of “technology will save us.” It’s always that thinking that the next best thing is just around the corner — and that did happen right away in the early days when penicillin was becoming less effective: they tweaked it a little and made methicillin, and that worked for awhile, until bacteria became resistant to that. So I think that pesticides, herbicides, antibiotics, antivirals — we tend to think there’s a new one around the corner. We just think we’re so great, we’ll come up with something else.

And I can’t speak for everyone, but I’d guess some might not believe that evolution can happen that quickly, let alone at all. (One of my favorite Gary Trudeau comics is a doctor who is treating a creationist who has TB.)

Contemporary evolution and our understanding of it I guess really blossomed in the late 1980s through the 1990s with work by scientists like Peter and Rosemary Grant with Darwin’s finches and articles by Andrew Hendry and Mike Kinnison. Their work helped popularize the idea. But well before that, rapid evolution in bacteria and plants and other prolific species was well known. It just wasn’t known how pervasive it was across all types of organisms, including vertebrates. And in how few generations it can happen.

You know, sometimes when some of these things are really effective and not that toxic, they’re kind of precious, and they should be treated that way. When we lose those, then it’s difficult to discover something else like them. I think we can’t always be saved by technology. The other thing is that we keep developing newer and newer chemicals — we want another antibiotic, we want a different kind of herbicide — but we’re just going to keep having the same problem, that those are going to become ineffective. And so we really need to change our ways. Which is what’s starting to happen with antibiotics.

I’ve been thinking about what you wrote in the context of factory farms — we’re saying we want to take on antibiotic resistance, but the U.S. government still hasn’t done anything about the 80 percent of antibiotics that go to livestock. Is that another example of our just not understanding the enormity of the problem?

Well, I’m not sure it’s not understanding the enormity of the problem, because I just don’t get how anybody could not understand that at this point. So my guess is it’s more different kinds of forces of inertia, not wanting to change, maybe not having good substitutes… I image that just using that much antibiotics in an industrial situation — it’s hard to get an industry to change its ways. I don’t know if there’s a disconnect.

So, one of the things that I was thinking about is that when we’re thinking about antibiotics, and we think about the human side of it — you know, how we can change our behavior — part of it is that it’s kind of an issue of the commons. So antibiotics affect us all, and I might cut back on using them, or be less demanding of a doctor, because I want them to work in my kids, when my kids are sick, or I want them to work in me. But when you’re talking about farming, that’s a different kind of approach. If the industry or whatever loses the use of an antibiotic, that’s not going to affect them personally.

One of the other lessons that you focus on in the book is that evolution is inevitable, which seems like another really obvious thing that we keep failing to think through. The most egregious example, I thought, was Monsanto coming out with Roundup and calling it “evolution-proof.” Is that a fallacy that we still struggle with?

I think now it’s becoming less so. So they said it was nearly evolution-proof, and I’m guessing the thought was that it was probably evolution-proof. I think that there still is probably a little bit of the thinking that through technology, we’ll figure out something that is evolution-proof, and people certainly strive for that. And it would be great — I was just listening to a webinar on resistance in chemotherapy, and what you strive for is to come up with something, whether it’s a chemical or a combination of chemicals or a series of treatments, that is evolution-proof — but it just seems like no matter what we do, even those things that people think are evolution-proof… evolution happens. So I think it’d be surprising if a chemical, whether an antibiotic or herbicide or whatever, came out that’s truly evolution-proof.

This is the story of presumably unexpected resistance — no matter how one feels about GMO, even if you are okay with it, this shows just how innovative nature can be and how little we know.

Some of the examples you give in the book sound more like science fiction — are there any that you’ve found people have a particularly hard time believing are happening?

Of all of these, probably the more surprising one is evolution in vertebrates, because when we’re talking about leaves or bacteria or something like that, we’re talking about very prolific species that have high reproductive rates. So we tend not to think like that when it comes to animals like fish or salamanders or even mice and rats, even though they do have high reproductive rates (but not like bacteria). Those are the ones where I think it’s more surprising when people hear that they evolve, and especially that they evolve in response to pollutants. The difference is that when you have pesticides or antibiotics, those things have a specific target site: insects or bacteria that you’re trying to get at. And it almost makes sense that they’d evolve resistance to those. But when you’re talking about something like PCBs or dioxins, those weren’t designed to kill. And so when you think of selective pressures, you don’t always think that they’re imposing that strong or that big of a selective pressure on those organisms.

The really interesting thing, at least in Ike Wirgin’s work — he’s the one who discovered that tomcods were developing resistance to PCBs and dioxides — is that a lot of these resistances come from selective pressures, but a lot of time there’s something called standing genetic variation. That’s just the variation that’s in a population: you know, every population has lots of genetic variation for any particular gene. So what he thinks is that the reason that resistance is happening so quickly in the populations he’s studying, which is probably within the timeframe of 50 years, is that they already had a gene for resistance somewhere in the population, and that gene was just getting selected for. It’s not like there were necessarily new mutations within that timeframe that arose. And that actually is really important with antibiotics and with cancers — the thinking now is that a lot of times, cancers aren’t just any one clone of an aberrant cell, that they have their own evolutionary course and there are lots of different variants within a particular cancer, and some of those might be resistant to drugs right off the bat. So when you’re treating with that drug, then you’re selecting for that resistant population, that’s a problem. And that’s something that I think now they can do a lot of genetics to see what the mutations are in any cell population, and then try to think about how they can treat it better from the start.

What other solutions can we be looking for, aside from just creating new chemicals? Is the key to try to direct evolution — if that’s even possible — or maybe just to scale back as much as possible?

So, yes, the most obvious is that these chemicals cause evolution because they’re an incredibly powerful selective pressure, so by removing that pressure you’ll reduce or at least change the pace of evolution or the outcome. So using less is a big deal. Using things differently: a lot of these chemicals attack a single target, so some alternatives are to use combinations of antibiotics, or chemotherapy drugs, or herbicides at the same time, because you’re attacking multiple targets, and so it becomes more difficult, through the process of evolution, to become resistant in that way. When you do back off, there are strategies: with agriculture, there’s integrated pest management; with antibiotics, there’s just being better at prevention. The other big thing is using identification — using the right antibiotic for the right pathogen. That’s a really big deal. This year’s Longitude Prize, this $16 million prize awarded through the U.K., will go to someone who develops a quick test to identify pathogens that you can use bedside. There are also some innovative ways, when you’re talking about drugs, of using evolution to your advantage. If you can understand how an organism will evolve, or what mechanisms it will evolve, you could push it in one direction so that it becomes more susceptible to a different kind of treatment, or another drug.

Which of those seem most realistic, the most doable to you?

The pathogen test is actually one realistic thing that we can do, and it’s probably something that could be developed pretty quickly. I wouldn’t be surprised if somebody figures that one out soon. Another is backing off; they’ve definitely cut back with antibiotic use in hospitals. And I think another one is prevention; I think there’s some evidence that they’ve been much more aware of resistant diseases and pathogens in general being spread around hospitals, that if they really work to improve the hygiene in the hospitals, they see a reduction in hospital-borne infections.

There’s also hope for developing new things, too, especially in antibiotics. But realistically, I think reining in the use of these chemicals is something we can do. Because I think we’ve gotten very cavalier about how we use them. You know, I wrote about how, when my kids were little, we just showed up at the doctor with an ear infection, and we’d get antibiotics. Nobody knew whether they had a virus or a bacterial infection, and the antibiotics wouldn’t help against a viral infection. But we got the stuff anyway. And I’d be surprised if that happens now. And I don’t know that anybody would really complain now — you know, part of the problem was pushy parents saying “we’re not going to leave until we get something to treat our kids.” I’m not sure that would happen anymore, because I think people are so much more aware. So I think there’s been a good job of getting people aware that we need to conserve these, and that we don’t need to take them all the time.

Lindsay Abrams is an assistant editor at Salon and a former writer and producer for The Atlantic's Health Channel.
http://www.alternet.org/drugs/humanitys-ticking-time-bomb-how-chemical-age-spun-evolution-out-control?paging=off&current_page=1#bookmark



Human-induced evolution caused by unnatural selection through harvest of wild animals

Fred W. Allendorf and Jeffrey J. Hard


Human harvest of phenotypically desirable animals from wild pop-
ulations imposes selection that can reduce the frequencies of those
desirable phenotypes. Hunting and fishing contrast with agricultural
and aquacultural practices in which the most desirable animals are
typically bred with the specific goal of increasing the frequency of
desirable phenotypes. We consider the potential effects of harvest on
the genetics and sustainability of wild populations. We also consider
how harvesting could affect the mating system and thereby modify
sexual selection in a way that might affect recruitment. Determining
whether phenotypic changes in harvested populations are due to
evolution, rather than phenotypic plasticity or environmental varia-
tion, has been problematic. Nevertheless, it is likely that some unde-
sirable changes observed over time in exploited populations (e.g.,
reduced body size, earlier sexual maturity, reduced antler size, etc.)
are due to selection against desirable phenotypes—a process we call
‘‘unnatural’’ selection. Evolution brought about by human harvest
might greatly increase the time required for over-harvested popula-
tions to recover once harvest is curtailed because harvesting often
creates strong selection differentials, whereas curtailing harvest will
often result in less intense selection in the opposing direction. We
strongly encourage those responsible for managing harvested wild
populations to take into account possible selective effects of harvest
management and to implement monitoring programs to detect ex-
ploitation-induced selection before it seriously impacts viability.

artigo completo: PNAS, vol. 106, 2009.

http://www.pnas.org/content/106/Supplement_1/9987.full.pdf



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