The following information is used for educational purposes only.
Filmed February 2016 at TED2016
Trevor Timm: How free is our freedom of the press?
In the US, the press has a right to publish secret information the public needs to know, protected by the First Amendment. Government surveillance has made it increasingly more dangerous for whistleblowers, the source of virtually every important story about national security since 9/11, to share information. In this concise, informative talk, Freedom of the Press Foundation co-founder and TED Fellow Trevor Timm traces the recent history of government action against individuals who expose crime and injustice and advocates for technology that can help them do it safely and anonymously.
Transcript:
So this is James Risen. You may know him as the Pulitzer Prize-winning reporter for The New York Times. Long before anybody knew Edward Snowden's name, Risen wrote a book in which he famously exposed that the NSA was illegally wiretapping the phone calls of Americans. But it's another chapter in that book that may have an even more lasting impact. In it, he describes a catastrophic US intelligence operation in which the CIA quite literally handed over blueprints of a nuclear bomb to Iran. If that sounds crazy, go read it. It's an incredible story.
But you know who didn't like that chapter? The US government. For nearly a decade afterwards, Risen was the subject of a US government investigation in which prosecutors demanded that he testify against one of his alleged sources. And along the way, he became the face for the US government's recent pattern of prosecuting whistleblowers and spying on journalists.
You see, under the First Amendment, the press has the right to publish secret information in the public interest. But it's impossible to exercise that right if the media can't also gather that news and protect the identities of the brave men and women who get it to them. So when the government came knocking, Risen did what many brave reporters have done before him: he refused and said he'd rather go to jail. So from 2007 to 2015, Risen lived under the specter of going to federal prison.
That is, until just days before the trial, when a curious thing happened. Suddenly, after years of claiming it was vital to their case, the government dropped their demands to Risen altogether. It turns out, in the age of electronic surveillance, there are very few places reporters and sources can hide. And instead of trying and failing to have Risen testify, they could have his digital trail testify against him instead. So completely in secret and without his consent, prosecutors got Risen's phone records. They got his email records, his financial and banking information, his credit reports, even travel records with a list of flights he had taken. And it was among this information that they used to convict Jeffrey Sterling, Risen's alleged source and CIA whistleblower.
Sadly, this is only one case of many. President Obama ran on a promise to protect whistleblowers, and instead, his Justice Department has prosecuted more than all other administrations combined. Now, you can see how this could be a problem, especially because the government considers so much of what it does secret. Since 9/11, virtually every important story about national security has been the result of a whistleblower coming to a journalist. So we risk seeing the press unable to do their job that the First Amendment is supposed to protect because of the government's expanded ability to spy on everyone.
But just as technology has allowed the government to circumvent reporters' rights, the press can also use technology to protect their sources even better than before. And they can start from the moment they begin speaking with them, rather than on the witness stand after the fact. Communications software now exists that wasn't available when Risen was writing his book, and is much more surveillance-resistant than regular emails or phone calls. For example, one such tool is SecureDrop, an open-source whistleblower submission system that was originally created by the late Internet luminary Aaron Swartz, and is now developed at the non-profit where I work, Freedom of the Press Foundation. Instead of sending an email, you go to a news organization's website, like this one here on The Washington Post. From there, you can upload a document or send information much like you would on any other contact form. It'll then be encrypted and stored on a server that only the news organization has access to. So the government can no longer secretly demand the information, and much of the information they would demand wouldn't be available in the first place.
SecureDrop, though, is really only a small part of the puzzle for protecting press freedom in the 21st century. Unfortunately, governments all over the world are constantly developing new spying techniques that put us all at risk. And it's up to us going forward to make sure that it's not just the tech-savvy whistleblowers, like Edward Snowden, who have an avenue for exposing wrongdoing. It's just as vital that we protect the next veteran's health care whistleblower alerting us to overcrowded hospitals, or the next environmental worker sounding the alarm about Flint's dirty water, or a Wall Street insider warning us of the next financial crisis. After all, these tools weren't just built to help the brave men and women who expose crimes, but are meant to protect all of our rights under the Constitution.
Thank you.
(Applause)
In this blog, teachers, students and all those who have some kind of interest in the English language will find useful, interesting, curious and funny things to be used in their classes or for their personal enjoyment.
Sunday, May 22, 2016
GralInt-Why video games shouldn’t freak parents out
The following information is used for educational purposes only.
Why video games shouldn’t freak parents out
May 17, 2016 / Ali Carr-Chellman
An advocate for educational video games realizes that our kids might actually learn more from Civilization, Minecraft, Call of Duty and World of Warcraft.
Everything changed at a lunch with the legendary game designer Sid Meier.
For years, I’d been making the case that we should borrow from the games kids love to create new kinds of educational games. But after that one memorable lunch, I realized that we didn’t need to co-opt the mechanics of gaming at all. We could — and should — use the games that kids were already playing, the immersive, sometimes violent games that hold boys and girls enraptured for hours in a state of flow and focus.
Sid, the mind behind games like Civilization and Pirates, is a bold thinker. In our long chat, he gently suggested that my approach — basically, to ask companies like Blizzard and Rockstar to contribute to educational game design — was off base. He convinced me that kids really do not like educational games; in fact, they hate them. And as I watched more kids play video games, I realized Sid was 100% correct. If given a choice between a game designed with a learning goal or a commercial game designed for fun, kids’ll choose fun every time.
This was a true turning point in my work. I spoke to more game designers, particularly educational game designers. Some of them said that designing educational games was crucial because even though kids hate them, they’re “better than what they get in the classroom.” This seemed deplorable. No matter the media, the one thing that research shows most impacts learning is a caring teacher. Replacing a human being with a video game that kids hate, simply because the teacher, constrained in his or her own ways, cannot create an engaging experience … that didn’t seem a good swap to me — and I learned that it wasn’t a swap most teachers wanted either.
Games are surprisingly powerful learning tools on their own. How can they be applied to classroom learning?
Inspired by my observations of kids playing games like Civilization, Minecraft, Call of Duty and World of Warcraft, I decided to try to figure out if they were learning anything inside these games that might translate to a traditional classroom. I wasn’t the only one looking at the connections between gaming and real-world success. As I read widely, I discovered things like:
kids who gamed were less likely to re-offend if they’d been in trouble with the law.
companies were hiring kids off leaderboards from major games because they believed them to have certain 21st-century skills like communication, grit, teamwork, leadership, followership and perseverance.
Something was happening here, and it wasn’t thanks to educational games.
Now I’m in the middle of a larger four-year research project, still ongoing, that focuses on boys, and what they learn when they game. And one major thing I’ve learned already is that when we reject the games that boys play, the games are merely a proxy for the boys themselves.We reject games because they’re violent, individualistic, competitive, engrossing and largely foreign to us as teachers, parents, leaders, adults. And these are the precise characteristics of boys that we reject when we enforce zero tolerance policies.
Instead, bringing these commercial games into schools will communicate to boys (and girls) that they are indeed valued, that their culture is welcome here, that the teachers, parents and adults in their lives respect who they are and want to learn from and with them as well as teach them.
Competitive, violent fantasy games contribute to the development of strong future leaders and citizens.
So far, this series of studies, led by the work of Jason Engerman, has resulted in some amazing findings. We heard boys describe failure in school as taboo, and failure in a game as desirable. We heard boys describe facile ways of dividing up leadership and recognizing one another’s expertise in the most collaborative and generative of ways — which also happens to be the key to a diverse workplace. We learned about boys and girls who had learned so much about a topic from a game that they realized, as author Kurt Squire learned in his own youth, that games are surprisingly powerful learning tools on their own. How can they be applied to classroom learning?
There are several things that we can do now. First, we can encourage our schools, teachers, boards, policy makers and other parents to value the gaming that our kids are engaged in. At least ten times a month, the parent of a young boy (usually) asks me: “Is it bad for my son to game? What limits do you place on gaming?” Myself, I strive for balance; we need to guard against addictive behaviors in all our life activities. My own sons play games, but they are also active in music, sports and scouting. We don’t have specific limits, because their lives are full of other things that are equally as fun and engaging for them. So, yes, it’s OK for your child to game, as long as they do it in a careful, balanced and sustained way (yes, sustained: deep engagement, grit, perseverance and other good skills are not built by grazing). Valuing their gaming activities amounts to respecting them and their culture.
Second, I’d very much like to gather stories of incidents where parents, teachers, and other adults were surprised by the kinds of learning that they realized their children (or even they) were engaging within games. Tell me your stories. I would love to compile a book of examples of ways that commercial gaming is contributing to real learning out in the world.
Third, I’d love to see more gaming. Like Jane McGonigal, I believe that gaming can make the world a better place. I feel that competitive, violent fantasy games contribute to the development of strong future leaders and citizens. Therefore, I’d challenge all readers to pick up a game their kids or their neighbors’ kids are playing, and play for at least one full hour in sincere and earnest game play. You’ll be amazed at what you learn about yourself, about the game, about your preconceptions about games and gamers, and likely about that kid.
ABOUT THE AUTHOR
Ali Carr-Chellman is an instructional designer and author who studies the most effective ways to teach kids and to make changes at school.
Source: http://ideas.ted.com/why-video-games-shouldnt-freak-parents-out/
Why video games shouldn’t freak parents out
May 17, 2016 / Ali Carr-Chellman
An advocate for educational video games realizes that our kids might actually learn more from Civilization, Minecraft, Call of Duty and World of Warcraft.
Everything changed at a lunch with the legendary game designer Sid Meier.
For years, I’d been making the case that we should borrow from the games kids love to create new kinds of educational games. But after that one memorable lunch, I realized that we didn’t need to co-opt the mechanics of gaming at all. We could — and should — use the games that kids were already playing, the immersive, sometimes violent games that hold boys and girls enraptured for hours in a state of flow and focus.
Sid, the mind behind games like Civilization and Pirates, is a bold thinker. In our long chat, he gently suggested that my approach — basically, to ask companies like Blizzard and Rockstar to contribute to educational game design — was off base. He convinced me that kids really do not like educational games; in fact, they hate them. And as I watched more kids play video games, I realized Sid was 100% correct. If given a choice between a game designed with a learning goal or a commercial game designed for fun, kids’ll choose fun every time.
This was a true turning point in my work. I spoke to more game designers, particularly educational game designers. Some of them said that designing educational games was crucial because even though kids hate them, they’re “better than what they get in the classroom.” This seemed deplorable. No matter the media, the one thing that research shows most impacts learning is a caring teacher. Replacing a human being with a video game that kids hate, simply because the teacher, constrained in his or her own ways, cannot create an engaging experience … that didn’t seem a good swap to me — and I learned that it wasn’t a swap most teachers wanted either.
Games are surprisingly powerful learning tools on their own. How can they be applied to classroom learning?
Inspired by my observations of kids playing games like Civilization, Minecraft, Call of Duty and World of Warcraft, I decided to try to figure out if they were learning anything inside these games that might translate to a traditional classroom. I wasn’t the only one looking at the connections between gaming and real-world success. As I read widely, I discovered things like:
kids who gamed were less likely to re-offend if they’d been in trouble with the law.
companies were hiring kids off leaderboards from major games because they believed them to have certain 21st-century skills like communication, grit, teamwork, leadership, followership and perseverance.
Something was happening here, and it wasn’t thanks to educational games.
Now I’m in the middle of a larger four-year research project, still ongoing, that focuses on boys, and what they learn when they game. And one major thing I’ve learned already is that when we reject the games that boys play, the games are merely a proxy for the boys themselves.We reject games because they’re violent, individualistic, competitive, engrossing and largely foreign to us as teachers, parents, leaders, adults. And these are the precise characteristics of boys that we reject when we enforce zero tolerance policies.
Instead, bringing these commercial games into schools will communicate to boys (and girls) that they are indeed valued, that their culture is welcome here, that the teachers, parents and adults in their lives respect who they are and want to learn from and with them as well as teach them.
Competitive, violent fantasy games contribute to the development of strong future leaders and citizens.
So far, this series of studies, led by the work of Jason Engerman, has resulted in some amazing findings. We heard boys describe failure in school as taboo, and failure in a game as desirable. We heard boys describe facile ways of dividing up leadership and recognizing one another’s expertise in the most collaborative and generative of ways — which also happens to be the key to a diverse workplace. We learned about boys and girls who had learned so much about a topic from a game that they realized, as author Kurt Squire learned in his own youth, that games are surprisingly powerful learning tools on their own. How can they be applied to classroom learning?
There are several things that we can do now. First, we can encourage our schools, teachers, boards, policy makers and other parents to value the gaming that our kids are engaged in. At least ten times a month, the parent of a young boy (usually) asks me: “Is it bad for my son to game? What limits do you place on gaming?” Myself, I strive for balance; we need to guard against addictive behaviors in all our life activities. My own sons play games, but they are also active in music, sports and scouting. We don’t have specific limits, because their lives are full of other things that are equally as fun and engaging for them. So, yes, it’s OK for your child to game, as long as they do it in a careful, balanced and sustained way (yes, sustained: deep engagement, grit, perseverance and other good skills are not built by grazing). Valuing their gaming activities amounts to respecting them and their culture.
Second, I’d very much like to gather stories of incidents where parents, teachers, and other adults were surprised by the kinds of learning that they realized their children (or even they) were engaging within games. Tell me your stories. I would love to compile a book of examples of ways that commercial gaming is contributing to real learning out in the world.
Third, I’d love to see more gaming. Like Jane McGonigal, I believe that gaming can make the world a better place. I feel that competitive, violent fantasy games contribute to the development of strong future leaders and citizens. Therefore, I’d challenge all readers to pick up a game their kids or their neighbors’ kids are playing, and play for at least one full hour in sincere and earnest game play. You’ll be amazed at what you learn about yourself, about the game, about your preconceptions about games and gamers, and likely about that kid.
ABOUT THE AUTHOR
Ali Carr-Chellman is an instructional designer and author who studies the most effective ways to teach kids and to make changes at school.
Source: http://ideas.ted.com/why-video-games-shouldnt-freak-parents-out/
Sunday, May 15, 2016
HEALTH/GEN/GralInt-TED Talks-Jennifer Kahn: Gene editing can now change an entire species -- forever
The following information is used for educational purposes only.
Filmed February 2016 at TED2016
Jennifer Kahn: Gene editing can now change an entire species -- forever
CRISPR gene drives allow scientists to change sequences of DNA and guarantee that the resulting edited genetic trait is inherited by future generations, opening up the possibility of altering entire species forever. More than anything, the technology has led to questions: How will this new power affect humanity? What are we going to use it to change? Are we gods now? Join journalist Jennifer Kahn as she ponders these questions and shares a potentially powerful application of gene drives: the development of disease-resistant mosquitoes that could knock out malaria and Zika.
Transcript:
So this is a talk about gene drives, but I'm going to start by telling you a brief story. 20 years ago, a biologist named Anthony James got obsessed with the idea of making mosquitos that didn't transmit malaria.
It was a great idea, and pretty much a complete failure. For one thing, it turned out to be really hard to make a malaria-resistant mosquito. James managed it, finally, just a few years ago, by adding some genes that make it impossible for the malaria parasite to survive inside the mosquito.
But that just created another problem. Now that you've got a malaria-resistant mosquito, how do you get it to replace all the malaria-carrying mosquitos? There are a couple options, but plan A was basically to breed up a bunch of the new genetically-engineered mosquitos release them into the wild and hope that they pass on their genes. The problem was that you'd have to release literally 10 times the number of native mosquitos to work. So in a village with 10,000 mosquitos, you release an extra 100,000. As you might guess, this was not a very popular strategy with the villagers.
(Laughter)
Then, last January, Anthony James got an email from a biologist named Ethan Bier. Bier said that he and his grad student Valentino Gantz had stumbled on a tool that could not only guarantee that a particular genetic trait would be inherited, but that it would spread incredibly quickly. If they were right, it would basically solve the problem that he and James had been working on for 20 years.
As a test, they engineered two mosquitos to carry the anti-malaria gene and also this new tool, a gene drive, which I'll explain in a minute. Finally, they set it up so that any mosquitos that had inherited the anti-malaria gene wouldn't have the usual white eyes, but would instead have red eyes. That was pretty much just for convenience so they could tell just at a glance which was which.
So they took their two anti-malarial, red-eyed mosquitos and put them in a box with 30 ordinary white-eyed ones, and let them breed. In two generations, those had produced 3,800 grandchildren. That is not the surprising part. This is the surprising part: given that you started with just two red-eyed mosquitos and 30 white-eyed ones, you expect mostly white-eyed descendants. Instead, when James opened the box, all 3,800 mosquitos had red eyes.
When I asked Ethan Bier about this moment, he became so excited that he was literally shouting into the phone. That's because getting only red-eyed mosquitos violates a rule that is the absolute cornerstone of biology, Mendelian genetics. I'll keep this quick, but Mendelian genetics says when a male and a female mate, their baby inherits half of its DNA from each parent. So if our original mosquito was aa and our new mosquito is aB, where B is the anti-malarial gene, the babies should come out in four permutations: aa, aB, aa, Ba. Instead, with the new gene drive, they all came out aB. Biologically, that shouldn't even be possible.
So what happened? The first thing that happened was the arrival of a gene-editing tool known as CRISPR in 2012. Many of you have probably heard about CRISPR, so I'll just say briefly that CRISPR is a tool that allows researchers to edit genes very precisely, easily and quickly. It does this by harnessing a mechanism that already existed in bacteria. Basically, there's a protein that acts like a scissors and cuts the DNA, and there's an RNA molecule that directs the scissors to any point on the genome you want. The result is basically a word processor for genes. You can take an entire gene out, put one in, or even edit just a single letter within a gene. And you can do it in nearly any species.
OK, remember how I said that gene drives originally had two problems? The first was that it was hard to engineer a mosquito to be malaria-resistant. That's basically gone now, thanks to CRISPR. But the other problem was logistical. How do you get your trait to spread? This is where it gets clever.
A couple years ago, a biologist at Harvard named Kevin Esvelt wondered what would happen if you made it so that CRISPR inserted not only your new gene but also the machinery that does the cutting and pasting. In other words, what if CRISPR also copied and pasted itself. You'd end up with a perpetual motion machine for gene editing. And that's exactly what happened. This CRISPR gene drive that Esvelt created not only guarantees that a trait will get passed on, but if it's used in the germline cells, it will automatically copy and paste your new gene into both chromosomes of every single individual. It's like a global search and replace, or in science terms, it makes a heterozygous trait homozygous.
So, what does this mean? For one thing, it means we have a very powerful, but also somewhat alarming new tool. Up until now, the fact that gene drives didn't work very well was actually kind of a relief. Normally when we mess around with an organism's genes, we make that thing less evolutionarily fit. So biologists can make all the mutant fruit flies they want without worrying about it. If some escape, natural selection just takes care of them.
What's remarkable and powerful and frightening about gene drives is that that will no longer be true. Assuming that your trait does not have a big evolutionary handicap, like a mosquito that can't fly, the CRISPR-based gene drive will spread the change relentlessly until it is in every single individual in the population. Now, it isn't easy to make a gene drive that works that well, but James and Esvelt think that we can.
The good news is that this opens the door to some remarkable things. If you put an anti-malarial gene drive in just 1 percent of Anopheles mosquitoes, the species that transmits malaria, researchers estimate that it would spread to the entire population in a year. So in a year, you could virtually eliminate malaria. In practice, we're still a few years out from being able to do that, but still, a 1,000 children a day die of malaria. In a year, that number could be almost zero. The same goes for dengue fever, chikungunya, yellow fever.
And it gets better. Say you want to get rid of an invasive species, like get Asian carp out of the Great Lakes. All you have to do is release a gene drive that makes the fish produce only male offspring. In a few generations, there'll be no females left, no more carp. In theory, this means we could restore hundreds of native species that have been pushed to the brink.
OK, that's the good news, this is the bad news. Gene drives are so effective that even an accidental release could change an entire species, and often very quickly. Anthony James took good precautions. He bred his mosquitos in a bio-containment lab and he also used a species that's not native to the US so that even if some did escape, they'd just die off, there'd be nothing for them to mate with. But it's also true that if a dozen Asian carp with the all-male gene drive accidentally got carried from the Great Lakes back to Asia, they could potentially wipe out the native Asian carp population. And that's not so unlikely, given how connected our world is. In fact, it's why we have an invasive species problem. And that's fish. Things like mosquitos and fruit flies, there's literally no way to contain them. They cross borders and oceans all the time.
OK, the other piece of bad news is that a gene drive might not stay confined to what we call the target species. That's because of gene flow, which is a fancy way of saying that neighboring species sometimes interbreed. If that happens, it's possible a gene drive could cross over, like Asian carp could infect some other kind of carp. That's not so bad if your drive just promotes a trait, like eye color. In fact, there's a decent chance that we'll see a wave of very weird fruit flies in the near future. But it could be a disaster if your drive is deigned to eliminate the species entirely.
The last worrisome thing is that the technology to do this, to genetically engineer an organism and include a gene drive, is something that basically any lab in the world can do. An undergraduate can do it. A talented high schooler with some equipment can do it.
Now, I'm guessing that this sounds terrifying.
(Laughter)
Interestingly though, nearly every scientist I talk to seemed to think that gene drives were not actually that frightening or dangerous. Partly because they believe that scientists will be very cautious and responsible about using them.
(Laughter)
So far, that's been true. But gene drives also have some actual limitations. So for one thing, they work only in sexually reproducing species. So thank goodness, they can't be used to engineer viruses or bacteria. Also, the trait spreads only with each successive generation. So changing or eliminating a population is practical only if that species has a fast reproductive cycle, like insects or maybe small vertebrates like mice or fish. In elephants or people, it would take centuries for a trait to spread widely enough to matter.
Also, even with CRISPR, it's not that easy to engineer a truly devastating trait. Say you wanted to make a fruit fly that feeds on ordinary fruit instead of rotting fruit, with the aim of sabotaging American agriculture. First, you'd have to figure out which genes control what the fly wants to eat, which is already a very long and complicated project. Then you'd have to alter those genes to change the fly's behavior to whatever you'd want it to be, which is an even longer and more complicated project. And it might not even work, because the genes that control behavior are complex. So if you're a terrorist and have to choose between starting a grueling basic research program that will require years of meticulous lab work and still might not pan out, or just blowing stuff up? You'll probably choose the later.
This is especially true because at least in theory, it should be pretty easy to build what's called a reversal drive. That's one that basically overwrites the change made by the first gene drive. So if you don't like the effects of a change, you can just release a second drive that will cancel it out, at least in theory.
OK, so where does this leave us? We now have the ability to change entire species at will. Should we? Are we gods now? I'm not sure I'd say that. But I would say this: first, some very smart people are even now debating how to regulate gene drives. At the same time, some other very smart people are working hard to create safeguards, like gene drives that self-regulate or peter out after a few generations. That's great. But this technology still requires a conversation. And given the nature of gene drives, that conversation has to be global. What if Kenya wants to use a drive but Tanzania doesn't? Who decides whether to release a gene drive that can fly?
I don't have the answer to that question. All we can do going forward, I think, is talk honestly about the risks and benefits and take responsibility for our choices. By that I mean, not just the choice to use a gene drive, but also the choice not to use one. Humans have a tendency to assume that the safest option is to preserve the status quo. But that's not always the case. Gene drives have risks, and those need to be discussed, but malaria exists now and kills 1,000 people a day. To combat it, we spray pesticides that do grave damage to other species, including amphibians and birds.
So when you hear about gene drives in the coming months, and trust me, you will be hearing about them, remember that. It can be frightening to act, but sometimes, not acting is worse.
(Applause)
Filmed February 2016 at TED2016
Jennifer Kahn: Gene editing can now change an entire species -- forever
CRISPR gene drives allow scientists to change sequences of DNA and guarantee that the resulting edited genetic trait is inherited by future generations, opening up the possibility of altering entire species forever. More than anything, the technology has led to questions: How will this new power affect humanity? What are we going to use it to change? Are we gods now? Join journalist Jennifer Kahn as she ponders these questions and shares a potentially powerful application of gene drives: the development of disease-resistant mosquitoes that could knock out malaria and Zika.
Transcript:
So this is a talk about gene drives, but I'm going to start by telling you a brief story. 20 years ago, a biologist named Anthony James got obsessed with the idea of making mosquitos that didn't transmit malaria.
It was a great idea, and pretty much a complete failure. For one thing, it turned out to be really hard to make a malaria-resistant mosquito. James managed it, finally, just a few years ago, by adding some genes that make it impossible for the malaria parasite to survive inside the mosquito.
But that just created another problem. Now that you've got a malaria-resistant mosquito, how do you get it to replace all the malaria-carrying mosquitos? There are a couple options, but plan A was basically to breed up a bunch of the new genetically-engineered mosquitos release them into the wild and hope that they pass on their genes. The problem was that you'd have to release literally 10 times the number of native mosquitos to work. So in a village with 10,000 mosquitos, you release an extra 100,000. As you might guess, this was not a very popular strategy with the villagers.
(Laughter)
Then, last January, Anthony James got an email from a biologist named Ethan Bier. Bier said that he and his grad student Valentino Gantz had stumbled on a tool that could not only guarantee that a particular genetic trait would be inherited, but that it would spread incredibly quickly. If they were right, it would basically solve the problem that he and James had been working on for 20 years.
As a test, they engineered two mosquitos to carry the anti-malaria gene and also this new tool, a gene drive, which I'll explain in a minute. Finally, they set it up so that any mosquitos that had inherited the anti-malaria gene wouldn't have the usual white eyes, but would instead have red eyes. That was pretty much just for convenience so they could tell just at a glance which was which.
So they took their two anti-malarial, red-eyed mosquitos and put them in a box with 30 ordinary white-eyed ones, and let them breed. In two generations, those had produced 3,800 grandchildren. That is not the surprising part. This is the surprising part: given that you started with just two red-eyed mosquitos and 30 white-eyed ones, you expect mostly white-eyed descendants. Instead, when James opened the box, all 3,800 mosquitos had red eyes.
When I asked Ethan Bier about this moment, he became so excited that he was literally shouting into the phone. That's because getting only red-eyed mosquitos violates a rule that is the absolute cornerstone of biology, Mendelian genetics. I'll keep this quick, but Mendelian genetics says when a male and a female mate, their baby inherits half of its DNA from each parent. So if our original mosquito was aa and our new mosquito is aB, where B is the anti-malarial gene, the babies should come out in four permutations: aa, aB, aa, Ba. Instead, with the new gene drive, they all came out aB. Biologically, that shouldn't even be possible.
So what happened? The first thing that happened was the arrival of a gene-editing tool known as CRISPR in 2012. Many of you have probably heard about CRISPR, so I'll just say briefly that CRISPR is a tool that allows researchers to edit genes very precisely, easily and quickly. It does this by harnessing a mechanism that already existed in bacteria. Basically, there's a protein that acts like a scissors and cuts the DNA, and there's an RNA molecule that directs the scissors to any point on the genome you want. The result is basically a word processor for genes. You can take an entire gene out, put one in, or even edit just a single letter within a gene. And you can do it in nearly any species.
OK, remember how I said that gene drives originally had two problems? The first was that it was hard to engineer a mosquito to be malaria-resistant. That's basically gone now, thanks to CRISPR. But the other problem was logistical. How do you get your trait to spread? This is where it gets clever.
A couple years ago, a biologist at Harvard named Kevin Esvelt wondered what would happen if you made it so that CRISPR inserted not only your new gene but also the machinery that does the cutting and pasting. In other words, what if CRISPR also copied and pasted itself. You'd end up with a perpetual motion machine for gene editing. And that's exactly what happened. This CRISPR gene drive that Esvelt created not only guarantees that a trait will get passed on, but if it's used in the germline cells, it will automatically copy and paste your new gene into both chromosomes of every single individual. It's like a global search and replace, or in science terms, it makes a heterozygous trait homozygous.
So, what does this mean? For one thing, it means we have a very powerful, but also somewhat alarming new tool. Up until now, the fact that gene drives didn't work very well was actually kind of a relief. Normally when we mess around with an organism's genes, we make that thing less evolutionarily fit. So biologists can make all the mutant fruit flies they want without worrying about it. If some escape, natural selection just takes care of them.
What's remarkable and powerful and frightening about gene drives is that that will no longer be true. Assuming that your trait does not have a big evolutionary handicap, like a mosquito that can't fly, the CRISPR-based gene drive will spread the change relentlessly until it is in every single individual in the population. Now, it isn't easy to make a gene drive that works that well, but James and Esvelt think that we can.
The good news is that this opens the door to some remarkable things. If you put an anti-malarial gene drive in just 1 percent of Anopheles mosquitoes, the species that transmits malaria, researchers estimate that it would spread to the entire population in a year. So in a year, you could virtually eliminate malaria. In practice, we're still a few years out from being able to do that, but still, a 1,000 children a day die of malaria. In a year, that number could be almost zero. The same goes for dengue fever, chikungunya, yellow fever.
And it gets better. Say you want to get rid of an invasive species, like get Asian carp out of the Great Lakes. All you have to do is release a gene drive that makes the fish produce only male offspring. In a few generations, there'll be no females left, no more carp. In theory, this means we could restore hundreds of native species that have been pushed to the brink.
OK, that's the good news, this is the bad news. Gene drives are so effective that even an accidental release could change an entire species, and often very quickly. Anthony James took good precautions. He bred his mosquitos in a bio-containment lab and he also used a species that's not native to the US so that even if some did escape, they'd just die off, there'd be nothing for them to mate with. But it's also true that if a dozen Asian carp with the all-male gene drive accidentally got carried from the Great Lakes back to Asia, they could potentially wipe out the native Asian carp population. And that's not so unlikely, given how connected our world is. In fact, it's why we have an invasive species problem. And that's fish. Things like mosquitos and fruit flies, there's literally no way to contain them. They cross borders and oceans all the time.
OK, the other piece of bad news is that a gene drive might not stay confined to what we call the target species. That's because of gene flow, which is a fancy way of saying that neighboring species sometimes interbreed. If that happens, it's possible a gene drive could cross over, like Asian carp could infect some other kind of carp. That's not so bad if your drive just promotes a trait, like eye color. In fact, there's a decent chance that we'll see a wave of very weird fruit flies in the near future. But it could be a disaster if your drive is deigned to eliminate the species entirely.
The last worrisome thing is that the technology to do this, to genetically engineer an organism and include a gene drive, is something that basically any lab in the world can do. An undergraduate can do it. A talented high schooler with some equipment can do it.
Now, I'm guessing that this sounds terrifying.
(Laughter)
Interestingly though, nearly every scientist I talk to seemed to think that gene drives were not actually that frightening or dangerous. Partly because they believe that scientists will be very cautious and responsible about using them.
(Laughter)
So far, that's been true. But gene drives also have some actual limitations. So for one thing, they work only in sexually reproducing species. So thank goodness, they can't be used to engineer viruses or bacteria. Also, the trait spreads only with each successive generation. So changing or eliminating a population is practical only if that species has a fast reproductive cycle, like insects or maybe small vertebrates like mice or fish. In elephants or people, it would take centuries for a trait to spread widely enough to matter.
Also, even with CRISPR, it's not that easy to engineer a truly devastating trait. Say you wanted to make a fruit fly that feeds on ordinary fruit instead of rotting fruit, with the aim of sabotaging American agriculture. First, you'd have to figure out which genes control what the fly wants to eat, which is already a very long and complicated project. Then you'd have to alter those genes to change the fly's behavior to whatever you'd want it to be, which is an even longer and more complicated project. And it might not even work, because the genes that control behavior are complex. So if you're a terrorist and have to choose between starting a grueling basic research program that will require years of meticulous lab work and still might not pan out, or just blowing stuff up? You'll probably choose the later.
This is especially true because at least in theory, it should be pretty easy to build what's called a reversal drive. That's one that basically overwrites the change made by the first gene drive. So if you don't like the effects of a change, you can just release a second drive that will cancel it out, at least in theory.
OK, so where does this leave us? We now have the ability to change entire species at will. Should we? Are we gods now? I'm not sure I'd say that. But I would say this: first, some very smart people are even now debating how to regulate gene drives. At the same time, some other very smart people are working hard to create safeguards, like gene drives that self-regulate or peter out after a few generations. That's great. But this technology still requires a conversation. And given the nature of gene drives, that conversation has to be global. What if Kenya wants to use a drive but Tanzania doesn't? Who decides whether to release a gene drive that can fly?
I don't have the answer to that question. All we can do going forward, I think, is talk honestly about the risks and benefits and take responsibility for our choices. By that I mean, not just the choice to use a gene drive, but also the choice not to use one. Humans have a tendency to assume that the safest option is to preserve the status quo. But that's not always the case. Gene drives have risks, and those need to be discussed, but malaria exists now and kills 1,000 people a day. To combat it, we spray pesticides that do grave damage to other species, including amphibians and birds.
So when you hear about gene drives in the coming months, and trust me, you will be hearing about them, remember that. It can be frightening to act, but sometimes, not acting is worse.
(Applause)
HEALTH/GralInt-TED Talks-Tal Danino: Programming bacteria to detect cancer (and maybe treat it)
The following information is used for educational purposes only.
Filmed March 2015 at TED2015
Tal Danino: Programming bacteria to detect cancer (and maybe treat it)
Liver cancer is one of the most difficult cancers to detect, but synthetic biologist Tal Danino had a left-field thought: What if we could create a probiotic, edible bacteria that was "programmed" to find liver tumors? His insight exploits something we're just beginning to understand about bacteria: their power of quorum sensing, or doing something together once they reach critical mass. Danino, a TED Fellow, explains how quorum sensing works — and how clever bacteria working together could someday change cancer treatment.
Transcript:
You may not realize this, but there are more bacteria in your body than stars in our entire galaxy. This fascinating universe of bacteria inside of us is an integral part of our health, and our technology is evolving so rapidly that today we can program these bacteria like we program computers.
Now, the diagram that you see here, I know it looks like some kind of sports play, but it is actually a blueprint of the first bacterial program I developed. And like writing software, we can print and write DNA into different algorithms and programs inside of bacteria. What this program does is produces fluorescent proteins in a rhythmic fashion and generates a small molecule that allows bacteria to communicate and synchronize, as you're seeing in this movie. The growing colony of bacteria that you see here is about the width of a human hair. Now, what you can't see is that our genetic program instructs these bacteria to each produce small molecules, and these molecules travel between the thousands of individual bacteria telling them when to turn on and off. And the bacteria synchronize quite well at this scale, but because the molecule that synchronizes them together can only travel so fast, in larger colonies of bacteria, this results in traveling waves between bacteria that are far away from each other, and you can see these waves going from right to left across the screen.
Now, our genetic program relies on a natural phenomenon called quorum sensing, in which bacteria trigger coordinated and sometimes virulent behaviors once they reach a critical density. You can observe quorum sensing in action in this movie, where a growing colony of bacteria only begins to glow once it reaches a high or critical density. Our genetic program continues producing these rhythmic patterns of fluorescent proteins as the colony grows outwards. This particular movie and experiment we call The Supernova, because it looks like an exploding star.
Now, besides programming these beautiful patterns, I wondered, what else can we get these bacteria to do? And I decided to explore how we can program bacteria to detect and treat diseases in our bodies like cancer. One of the surprising facts about bacteria is that they can naturally grow inside of tumors. This happens because typically tumors are areas where the immune system has no access, and so bacteria find these tumors and use them as a safe haven to grow and thrive. We started using probiotic bacteria which are safe bacteria that have a health benefit, and found that when orally delivered to mice, these probiotics would selectively grow inside of liver tumors. We realized that the most convenient way to highlight the presence of the probiotics, and hence, the presence of the tumors, was to get these bacteria to produce a signal that would be detectable in the urine, and so we specifically programmed these probiotics to make a molecule that would change the color of your urine to indicate the presence of cancer. We went on to show that this technology could sensitively and specifically detect liver cancer, one that is challenging to detect otherwise.
Now, since these bacteria specifically localize to tumors, we've been programming them to not only detect cancer but also to treat cancer by producing therapeutic molecules from within the tumor environment that shrink the existing tumors, and we've been doing this using quorum sensing programs like you saw in the previous movies.
Altogether, imagine in the future taking a programmed probiotic that could detect and treat cancer, or even other diseases. Our ability to program bacteria and program life opens up new horizons in cancer research, and to share this vision, I worked with artist Vik Muniz to create the symbol of the universe, made entirely out of bacteria or cancer cells. Ultimately, my hope is that the beauty and purpose of this microscopic universe can inspire new and creative approaches for the future of cancer research.
Thank you.
(Applause)
Filmed March 2015 at TED2015
Tal Danino: Programming bacteria to detect cancer (and maybe treat it)
Liver cancer is one of the most difficult cancers to detect, but synthetic biologist Tal Danino had a left-field thought: What if we could create a probiotic, edible bacteria that was "programmed" to find liver tumors? His insight exploits something we're just beginning to understand about bacteria: their power of quorum sensing, or doing something together once they reach critical mass. Danino, a TED Fellow, explains how quorum sensing works — and how clever bacteria working together could someday change cancer treatment.
Transcript:
You may not realize this, but there are more bacteria in your body than stars in our entire galaxy. This fascinating universe of bacteria inside of us is an integral part of our health, and our technology is evolving so rapidly that today we can program these bacteria like we program computers.
Now, the diagram that you see here, I know it looks like some kind of sports play, but it is actually a blueprint of the first bacterial program I developed. And like writing software, we can print and write DNA into different algorithms and programs inside of bacteria. What this program does is produces fluorescent proteins in a rhythmic fashion and generates a small molecule that allows bacteria to communicate and synchronize, as you're seeing in this movie. The growing colony of bacteria that you see here is about the width of a human hair. Now, what you can't see is that our genetic program instructs these bacteria to each produce small molecules, and these molecules travel between the thousands of individual bacteria telling them when to turn on and off. And the bacteria synchronize quite well at this scale, but because the molecule that synchronizes them together can only travel so fast, in larger colonies of bacteria, this results in traveling waves between bacteria that are far away from each other, and you can see these waves going from right to left across the screen.
Now, our genetic program relies on a natural phenomenon called quorum sensing, in which bacteria trigger coordinated and sometimes virulent behaviors once they reach a critical density. You can observe quorum sensing in action in this movie, where a growing colony of bacteria only begins to glow once it reaches a high or critical density. Our genetic program continues producing these rhythmic patterns of fluorescent proteins as the colony grows outwards. This particular movie and experiment we call The Supernova, because it looks like an exploding star.
Now, besides programming these beautiful patterns, I wondered, what else can we get these bacteria to do? And I decided to explore how we can program bacteria to detect and treat diseases in our bodies like cancer. One of the surprising facts about bacteria is that they can naturally grow inside of tumors. This happens because typically tumors are areas where the immune system has no access, and so bacteria find these tumors and use them as a safe haven to grow and thrive. We started using probiotic bacteria which are safe bacteria that have a health benefit, and found that when orally delivered to mice, these probiotics would selectively grow inside of liver tumors. We realized that the most convenient way to highlight the presence of the probiotics, and hence, the presence of the tumors, was to get these bacteria to produce a signal that would be detectable in the urine, and so we specifically programmed these probiotics to make a molecule that would change the color of your urine to indicate the presence of cancer. We went on to show that this technology could sensitively and specifically detect liver cancer, one that is challenging to detect otherwise.
Now, since these bacteria specifically localize to tumors, we've been programming them to not only detect cancer but also to treat cancer by producing therapeutic molecules from within the tumor environment that shrink the existing tumors, and we've been doing this using quorum sensing programs like you saw in the previous movies.
Altogether, imagine in the future taking a programmed probiotic that could detect and treat cancer, or even other diseases. Our ability to program bacteria and program life opens up new horizons in cancer research, and to share this vision, I worked with artist Vik Muniz to create the symbol of the universe, made entirely out of bacteria or cancer cells. Ultimately, my hope is that the beauty and purpose of this microscopic universe can inspire new and creative approaches for the future of cancer research.
Thank you.
(Applause)
HEALTH/GralInt-TED Talks-Sangeeta Bhatia: This tiny particle could roam your body to find tumors
The following information is used for educational purposes only.
Filmed November 2015 at TED Talks Live
Sangeeta Bhatia: This tiny particle could roam your body to find tumors
What if we could find cancerous tumors years before they can harm us — without expensive screening facilities or even steady electricity? Physician, bioengineer and entrepreneur Sangeeta Bhatia leads a multidisciplinary lab that searches for novel ways to understand, diagnose and treat human disease. Her target: the two-thirds of deaths due to cancer that she says are fully preventable. With remarkable clarity, she breaks down complex nanoparticle science and shares her dream for a radical new cancer test that could save millions of lives.
Transcript:
In the space that used to house one transistor, we can now fit one billion. That made it so that a computer the size of an entire room now fits in your pocket. You might say the future is small.
As an engineer, I'm inspired by this miniaturization revolution in computers. As a physician, I wonder whether we could use it to reduce the number of lives lost due to one of the fastest-growing diseases on Earth: cancer. Now when I say that, what most people hear me say is that we're working on curing cancer. And we are. But it turns out that there's an incredible opportunity to save lives through the early detection and prevention of cancer.
Worldwide, over two-thirds of deaths due to cancer are fully preventable using methods that we already have in hand today. Things like vaccination, timely screening and of course, stopping smoking. But even with the best tools and technologies that we have today, some tumors can't be detected until 10 years after they've started growing, when they are 50 million cancer cells strong. What if we had better technologies to detect some of these more deadly cancers sooner, when they could be removed, when they were just getting started?
Let me tell you about how miniaturization might get us there. This is a microscope in a typical lab that a pathologist would use for looking at a tissue specimen, like a biopsy or a pap smear. This $7,000 microscope would be used by somebody with years of specialized training to spot cancer cells. This is an image from a colleague of mine at Rice University, Rebecca Richards-Kortum. What she and her team have done is miniaturize that whole microscope into this $10 part, and it fits on the end of an optical fiber. Now what that means is instead of taking a sample from a patient and sending it to the microscope, you can bring the microscope to the patient. And then, instead of requiring a specialist to look at the images, you can train the computer to score normal versus cancerous cells.
Now this is important, because what they found working in rural communities, is that even when they have a mobile screening van that can go out into the community and perform exams and collect samples and send them to the central hospital for analysis, that days later, women get a call with an abnormal test result and they're asked to come in. Fully half of them don't turn up because they can't afford the trip. With the integrated microscope and computer analysis, Rebecca and her colleagues have been able to create a van that has both a diagnostic setup and a treatment setup. And what that means is that they can do a diagnosis and perform therapy on the spot, so no one is lost to follow up.
That's just one example of how miniaturization can save lives. Now as engineers, we think of this as straight-up miniaturization. You took a big thing and you made it little. But what I told you before about computers was that they transformed our lives when they became small enough for us to take them everywhere. So what is the transformational equivalent like that in medicine? Well, what if you had a detector that was so small that it could circulate in your body, find the tumor all by itself and send a signal to the outside world? It sounds a little bit like science fiction. But actually, nanotechnology allows us to do just that. Nanotechnology allows us to shrink the parts that make up the detector from the width of a human hair, which is 100 microns, to a thousand times smaller, which is 100 nanometers. And that has profound implications.
It turns out that materials actually change their properties at the nanoscale. You take a common material like gold, and you grind it into dust, into gold nanoparticles, and it changes from looking gold to looking red. If you take a more exotic material like cadmium selenide -- forms a big, black crystal -- if you make nanocrystals out of this material and you put it in a liquid, and you shine light on it, they glow. And they glow blue, green, yellow, orange, red, depending only on their size. It's wild! Can you imagine an object like that in the macro world? It would be like all the denim jeans in your closet are all made of cotton, but they are different colors depending only on their size.
(Laughter)
So as a physician, what's just as interesting to me is that it's not just the color of materials that changes at the nanoscale; the way they travel in your body also changes. And this is the kind of observation that we're going to use to make a better cancer detector.
So let me show you what I mean. This is a blood vessel in the body. Surrounding the blood vessel is a tumor. We're going to inject nanoparticles into the blood vessel and watch how they travel from the bloodstream into the tumor. Now it turns out that the blood vessels of many tumors are leaky, and so nanoparticles can leak out from the bloodstream into the tumor. Whether they leak out depends on their size. So in this image, the smaller, hundred-nanometer, blue nanoparticles are leaking out, and the larger, 500-nanometer, red nanoparticles are stuck in the bloodstream. So that means as an engineer, depending on how big or small I make a material, I can change where it goes in your body.
In my lab, we recently made a cancer nanodetector that is so small that it could travel into the body and look for tumors. We designed it to listen for tumor invasion: the orchestra of chemical signals that tumors need to make to spread. For a tumor to break out of the tissue that it's born in, it has to make chemicals called enzymes to chew through the scaffolding of tissues. We designed these nanoparticles to be activated by these enzymes. One enzyme can activate a thousand of these chemical reactions in an hour. Now in engineering, we call that one-to-a-thousand ratio a form of amplification, and it makes something ultrasensitive. So we've made an ultrasensitive cancer detector.
OK, but how do I get this activated signal to the outside world, where I can act on it? For this, we're going to use one more piece of nanoscale biology, and that has to do with the kidney. The kidney is a filter. Its job is to filter out the blood and put waste into the urine. It turns out that what the kidney filters is also dependent on size. So in this image, what you can see is that everything smaller than five nanometers is going from the blood, through the kidney, into the urine, and everything else that's bigger is retained. OK, so if I make a 100-nanometer cancer detector, I inject it in the bloodstream, it can leak into the tumor where it's activated by tumor enzymes to release a small signal that is small enough to be filtered out of the kidney and put into the urine, I have a signal in the outside world that I can detect.
OK, but there's one more problem. This is a tiny little signal, so how do I detect it? Well, the signal is just a molecule. They're molecules that we designed as engineers. They're completely synthetic, and we can design them so they are compatible with our tool of choice. If we want to use a really sensitive, fancy instrument called a mass spectrometer, then we make a molecule with a unique mass. Or maybe we want make something that's more inexpensive and portable. Then we make molecules that we can trap on paper, like a pregnancy test. In fact, there's a whole world of paper tests that are becoming available in a field called paper diagnostics.
Alright, where are we going with this? What I'm going to tell you next, as a lifelong researcher, represents a dream of mine. I can't say that's it's a promise; it's a dream. But I think we all have to have dreams to keep us pushing forward, even -- and maybe especially -- cancer researchers.
I'm going to tell you what I hope will happen with my technology, that my team and I will put our hearts and souls into making a reality. OK, here goes. I dream that one day, instead of going into an expensive screening facility to get a colonoscopy, or a mammogram, or a pap smear, that you could get a shot, wait an hour, and do a urine test on a paper strip. I imagine that this could even happen without the need for steady electricity, or a medical professional in the room. Maybe they could be far away and connected only by the image on a smartphone.
Now I know this sounds like a dream, but in the lab we already have this working in mice, where it works better than existing methods for the detection of lung, colon and ovarian cancer. And I hope that what this means is that one day we can detect tumors in patients sooner than 10 years after they've started growing, in all walks of life, all around the globe, and that this would lead to earlier treatments, and that we could save more lives than we can today, with early detection.
Thank you.
(Applause)
Filmed November 2015 at TED Talks Live
Sangeeta Bhatia: This tiny particle could roam your body to find tumors
What if we could find cancerous tumors years before they can harm us — without expensive screening facilities or even steady electricity? Physician, bioengineer and entrepreneur Sangeeta Bhatia leads a multidisciplinary lab that searches for novel ways to understand, diagnose and treat human disease. Her target: the two-thirds of deaths due to cancer that she says are fully preventable. With remarkable clarity, she breaks down complex nanoparticle science and shares her dream for a radical new cancer test that could save millions of lives.
Transcript:
In the space that used to house one transistor, we can now fit one billion. That made it so that a computer the size of an entire room now fits in your pocket. You might say the future is small.
As an engineer, I'm inspired by this miniaturization revolution in computers. As a physician, I wonder whether we could use it to reduce the number of lives lost due to one of the fastest-growing diseases on Earth: cancer. Now when I say that, what most people hear me say is that we're working on curing cancer. And we are. But it turns out that there's an incredible opportunity to save lives through the early detection and prevention of cancer.
Worldwide, over two-thirds of deaths due to cancer are fully preventable using methods that we already have in hand today. Things like vaccination, timely screening and of course, stopping smoking. But even with the best tools and technologies that we have today, some tumors can't be detected until 10 years after they've started growing, when they are 50 million cancer cells strong. What if we had better technologies to detect some of these more deadly cancers sooner, when they could be removed, when they were just getting started?
Let me tell you about how miniaturization might get us there. This is a microscope in a typical lab that a pathologist would use for looking at a tissue specimen, like a biopsy or a pap smear. This $7,000 microscope would be used by somebody with years of specialized training to spot cancer cells. This is an image from a colleague of mine at Rice University, Rebecca Richards-Kortum. What she and her team have done is miniaturize that whole microscope into this $10 part, and it fits on the end of an optical fiber. Now what that means is instead of taking a sample from a patient and sending it to the microscope, you can bring the microscope to the patient. And then, instead of requiring a specialist to look at the images, you can train the computer to score normal versus cancerous cells.
Now this is important, because what they found working in rural communities, is that even when they have a mobile screening van that can go out into the community and perform exams and collect samples and send them to the central hospital for analysis, that days later, women get a call with an abnormal test result and they're asked to come in. Fully half of them don't turn up because they can't afford the trip. With the integrated microscope and computer analysis, Rebecca and her colleagues have been able to create a van that has both a diagnostic setup and a treatment setup. And what that means is that they can do a diagnosis and perform therapy on the spot, so no one is lost to follow up.
That's just one example of how miniaturization can save lives. Now as engineers, we think of this as straight-up miniaturization. You took a big thing and you made it little. But what I told you before about computers was that they transformed our lives when they became small enough for us to take them everywhere. So what is the transformational equivalent like that in medicine? Well, what if you had a detector that was so small that it could circulate in your body, find the tumor all by itself and send a signal to the outside world? It sounds a little bit like science fiction. But actually, nanotechnology allows us to do just that. Nanotechnology allows us to shrink the parts that make up the detector from the width of a human hair, which is 100 microns, to a thousand times smaller, which is 100 nanometers. And that has profound implications.
It turns out that materials actually change their properties at the nanoscale. You take a common material like gold, and you grind it into dust, into gold nanoparticles, and it changes from looking gold to looking red. If you take a more exotic material like cadmium selenide -- forms a big, black crystal -- if you make nanocrystals out of this material and you put it in a liquid, and you shine light on it, they glow. And they glow blue, green, yellow, orange, red, depending only on their size. It's wild! Can you imagine an object like that in the macro world? It would be like all the denim jeans in your closet are all made of cotton, but they are different colors depending only on their size.
(Laughter)
So as a physician, what's just as interesting to me is that it's not just the color of materials that changes at the nanoscale; the way they travel in your body also changes. And this is the kind of observation that we're going to use to make a better cancer detector.
So let me show you what I mean. This is a blood vessel in the body. Surrounding the blood vessel is a tumor. We're going to inject nanoparticles into the blood vessel and watch how they travel from the bloodstream into the tumor. Now it turns out that the blood vessels of many tumors are leaky, and so nanoparticles can leak out from the bloodstream into the tumor. Whether they leak out depends on their size. So in this image, the smaller, hundred-nanometer, blue nanoparticles are leaking out, and the larger, 500-nanometer, red nanoparticles are stuck in the bloodstream. So that means as an engineer, depending on how big or small I make a material, I can change where it goes in your body.
In my lab, we recently made a cancer nanodetector that is so small that it could travel into the body and look for tumors. We designed it to listen for tumor invasion: the orchestra of chemical signals that tumors need to make to spread. For a tumor to break out of the tissue that it's born in, it has to make chemicals called enzymes to chew through the scaffolding of tissues. We designed these nanoparticles to be activated by these enzymes. One enzyme can activate a thousand of these chemical reactions in an hour. Now in engineering, we call that one-to-a-thousand ratio a form of amplification, and it makes something ultrasensitive. So we've made an ultrasensitive cancer detector.
OK, but how do I get this activated signal to the outside world, where I can act on it? For this, we're going to use one more piece of nanoscale biology, and that has to do with the kidney. The kidney is a filter. Its job is to filter out the blood and put waste into the urine. It turns out that what the kidney filters is also dependent on size. So in this image, what you can see is that everything smaller than five nanometers is going from the blood, through the kidney, into the urine, and everything else that's bigger is retained. OK, so if I make a 100-nanometer cancer detector, I inject it in the bloodstream, it can leak into the tumor where it's activated by tumor enzymes to release a small signal that is small enough to be filtered out of the kidney and put into the urine, I have a signal in the outside world that I can detect.
OK, but there's one more problem. This is a tiny little signal, so how do I detect it? Well, the signal is just a molecule. They're molecules that we designed as engineers. They're completely synthetic, and we can design them so they are compatible with our tool of choice. If we want to use a really sensitive, fancy instrument called a mass spectrometer, then we make a molecule with a unique mass. Or maybe we want make something that's more inexpensive and portable. Then we make molecules that we can trap on paper, like a pregnancy test. In fact, there's a whole world of paper tests that are becoming available in a field called paper diagnostics.
Alright, where are we going with this? What I'm going to tell you next, as a lifelong researcher, represents a dream of mine. I can't say that's it's a promise; it's a dream. But I think we all have to have dreams to keep us pushing forward, even -- and maybe especially -- cancer researchers.
I'm going to tell you what I hope will happen with my technology, that my team and I will put our hearts and souls into making a reality. OK, here goes. I dream that one day, instead of going into an expensive screening facility to get a colonoscopy, or a mammogram, or a pap smear, that you could get a shot, wait an hour, and do a urine test on a paper strip. I imagine that this could even happen without the need for steady electricity, or a medical professional in the room. Maybe they could be far away and connected only by the image on a smartphone.
Now I know this sounds like a dream, but in the lab we already have this working in mice, where it works better than existing methods for the detection of lung, colon and ovarian cancer. And I hope that what this means is that one day we can detect tumors in patients sooner than 10 years after they've started growing, in all walks of life, all around the globe, and that this would lead to earlier treatments, and that we could save more lives than we can today, with early detection.
Thank you.
(Applause)
HEALTH/BRAIN/GralInt-TED Talks-Sandrine Thuret: You can grow new brain cells. Here's how
The following information is used for educational purposes only.
Filmed June 2015 at TED@BCG London
Sandrine Thuret: You can grow new brain cells. Here's how
Can we, as adults, grow new neurons? Neuroscientist Sandrine Thuret says that we can, and she offers research and practical advice on how we can help our brains better perform neurogenesis—improving mood, increasing memory formation and preventing the decline associated with aging along the way.
Transcript:
Can we, as adults, grow new nerve cells? There's still some confusion about that question, as this is a fairly new field of research. For example, I was talking to one of my colleagues, Robert, who is an oncologist, and he was telling me, "Sandrine, this is puzzling. Some of my patients that have been told they are cured of their cancer still develop symptoms of depression." And I responded to him, "Well, from my point of view that makes sense. The drug you give to your patients that stops the cancer cells multiplying also stops the newborn neurons being generated in their brain." And then Robert looked at me like I was crazy and said, "But Sandrine, these are adult patients -- adults do not grow new nerve cells." And much to his surprise, I said, "Well actually, we do." And this is a phenomenon that we call neurogenesis.
[Neurogenesis]
Now Robert is not a neuroscientist, and when he went to medical school he was not taught what we know now -- that the adult brain can generate new nerve cells. So Robert, you know, being the good doctor that he is, wanted to come to my lab to understand the topic a little bit better. And I took him for a tour of one of the most exciting parts of the brain when it comes to neurogenesis -- and this is the hippocampus. So this is this gray structure in the center of the brain. And what we've known already for very long, is that this is important for learning, memory, mood and emotion. However, what we have learned more recently is that this is one of the unique structures of the adult brain where new neurons can be generated. And if we slice through the hippocampus and zoom in, what you actually see here in blue is a newborn neuron in an adult mouse brain. So when it comes to the human brain -- my colleague Jonas Frisén from the Karolinska Institutet, has estimated that we produce 700 new neurons per day in the hippocampus. You might think this is not much, compared to the billions of neurons we have. But by the time we turn 50, we will have all exchanged the neurons we were born with in that structure with adult-born neurons.
So why are these new neurons important and what are their functions? First, we know that they're important for learning and memory. And in the lab we have shown that if we block the ability of the adult brain to produce new neurons in the hippocampus, then we block certain memory abilities. And this is especially new and true for spatial recognition -- so like, how you navigate your way in the city.
We are still learning a lot, and neurons are not only important for memory capacity, but also for the quality of the memory. And they will have been helpful to add time to our memory and they will help differentiate very similar memories, like: how do you find your bike that you park at the station every day in the same area, but in a slightly different position?
And more interesting to my colleague Robert is the research we have been doing on neurogenesis and depression. So in an animal model of depression, we have seen that we have a lower level of neurogenesis. And if we give antidepressants, then we increase the production of these newborn neurons, and we decrease the symptoms of depression, establishing a clear link between neurogenesis and depression. But moreover, if you just block neurogenesis, then you block the efficacy of the antidepressant. So by then, Robert had understood that very likely his patients were suffering from depression even after being cured of their cancer, because the cancer drug had stopped newborn neurons from being generated. And it will take time to generate new neurons that reach normal functions.
So, collectively, now we think we have enough evidence to say that neurogenesis is a target of choice if we want to improve memory formation or mood, or even prevent the decline associated with aging, or associated with stress.
So the next question is: can we control neurogenesis? The answer is yes. And we are now going to do a little quiz. I'm going to give you a set of behaviors and activities, and you tell me if you think they will increase neurogenesis or if they will decrease neurogenesis. Are we ready? OK, let's go.
So what about learning? Increasing? Yes. Learning will increase the production of these new neurons.
How about stress? Yes, stress will decrease the production of new neurons in the hippocampus.
How about sleep deprivation? Indeed, it will decrease neurogenesis.
How about sex? Oh, wow!
(Laughter)
Yes, you are right, it will increase the production of new neurons. However, it's all about balance here. We don't want to fall in a situation --
(Laughter)
about too much sex leading to sleep deprivation.
(Laughter)
How about getting older? So the neurogenesis rate will decrease as we get older, but it is still occurring.
And then finally, how about running? I will let you judge that one by yourself.
So this is one of the first studies that was carried out by one of my mentors, Rusty Gage from the Salk Institute, showing that the environment can have an impact on the production of new neurons. And here you see a section of the hippocampus of a mouse that had no running wheel in its cage. And the little black dots you see are actually newborn neurons-to-be. And now, you see a section of the hippocampus of a mouse that had a running wheel in its cage. So you see the massive increase of the black dots representing the new neurons-to-be.
So activity impacts neurogenesis, but that's not all. What you eat will have an effect on the production of new neurons in the hippocampus. So here we have a sample of diet -- of nutrients that have been shown to have efficacy. And I'm just going to point a few out to you: Calorie restriction of 20 to 30 percent will increase neurogenesis. Intermittent fasting -- spacing the time between your meals -- will increase neurogenesis. Intake of flavonoids, which are contained in dark chocolate or blueberries, will increase neurogenesis. Omega-3 fatty acids, present in fatty fish, like salmon, will increase the production of these new neurons. Conversely, a diet rich in high saturated fat will have a negative impact on neurogenesis. Ethanol -- intake of alcohol -- will decrease neurogenesis. However, not everything is lost; resveratrol, which is contained in red wine, has been shown to promote the survival of these new neurons. So next time you are at a dinner party, you might want to reach for this possibly "neurogenesis-neutral" drink.
(Laughter)
And then finally, let me point out the last one -- a quirky one. So Japanese groups are fascinated with food textures, and they have shown that actually soft diet impairs neurogenesis, as opposed to food that requires mastication -- chewing -- or crunchy food.
So all of this data, where we need to look at the cellular level, has been generated using animal models. But this diet has also been given to human participants, and what we could see is that the diet modulates memory and mood in the same direction as it modulates neurogenesis, such as: calorie restriction will improve memory capacity, whereas a high-fat diet will exacerbate symptoms of depression -- as opposed to omega-3 fatty acids, which increase neurogenesis, and also help to decrease the symptoms of depression. So we think that the effect of diet on mental health, on memory and mood, is actually mediated by the production of the new neurons in the hippocampus. And it's not only what you eat, but it's also the texture of the food, when you eat it and how much of it you eat.
On our side -- neuroscientists interested in neurogenesis -- we need to understand better the function of these new neurons, and how we can control their survival and their production. We also need to find a way to protect the neurogenesis of Robert's patients. And on your side -- I leave you in charge of your neurogenesis.
Thank you.
(Applause)
Margaret Heffernan: Fantastic research, Sandrine. Now, I told you you changed my life -- I now eat a lot of blueberries.
Sandrine Thuret: Very good.
MH: I'm really interested in the running thing. Do I have to run? Or is it really just about aerobic exercise, getting oxygen to the brain? Could it be any kind of vigorous exercise?
ST: So for the moment, we can't really say if it's just the running itself, but we think that anything that indeed will increase the production -- or moving the blood flow to the brain, should be beneficial.
MH: So I don't have to get a running wheel in my office?
ST: No, you don't!
MH: Oh, what a relief! That's wonderful. Sandrine Thuret, thank you so much.
ST: Thank you, Margaret.
(Applause)
Filmed June 2015 at TED@BCG London
Sandrine Thuret: You can grow new brain cells. Here's how
Can we, as adults, grow new neurons? Neuroscientist Sandrine Thuret says that we can, and she offers research and practical advice on how we can help our brains better perform neurogenesis—improving mood, increasing memory formation and preventing the decline associated with aging along the way.
Transcript:
Can we, as adults, grow new nerve cells? There's still some confusion about that question, as this is a fairly new field of research. For example, I was talking to one of my colleagues, Robert, who is an oncologist, and he was telling me, "Sandrine, this is puzzling. Some of my patients that have been told they are cured of their cancer still develop symptoms of depression." And I responded to him, "Well, from my point of view that makes sense. The drug you give to your patients that stops the cancer cells multiplying also stops the newborn neurons being generated in their brain." And then Robert looked at me like I was crazy and said, "But Sandrine, these are adult patients -- adults do not grow new nerve cells." And much to his surprise, I said, "Well actually, we do." And this is a phenomenon that we call neurogenesis.
[Neurogenesis]
Now Robert is not a neuroscientist, and when he went to medical school he was not taught what we know now -- that the adult brain can generate new nerve cells. So Robert, you know, being the good doctor that he is, wanted to come to my lab to understand the topic a little bit better. And I took him for a tour of one of the most exciting parts of the brain when it comes to neurogenesis -- and this is the hippocampus. So this is this gray structure in the center of the brain. And what we've known already for very long, is that this is important for learning, memory, mood and emotion. However, what we have learned more recently is that this is one of the unique structures of the adult brain where new neurons can be generated. And if we slice through the hippocampus and zoom in, what you actually see here in blue is a newborn neuron in an adult mouse brain. So when it comes to the human brain -- my colleague Jonas Frisén from the Karolinska Institutet, has estimated that we produce 700 new neurons per day in the hippocampus. You might think this is not much, compared to the billions of neurons we have. But by the time we turn 50, we will have all exchanged the neurons we were born with in that structure with adult-born neurons.
So why are these new neurons important and what are their functions? First, we know that they're important for learning and memory. And in the lab we have shown that if we block the ability of the adult brain to produce new neurons in the hippocampus, then we block certain memory abilities. And this is especially new and true for spatial recognition -- so like, how you navigate your way in the city.
We are still learning a lot, and neurons are not only important for memory capacity, but also for the quality of the memory. And they will have been helpful to add time to our memory and they will help differentiate very similar memories, like: how do you find your bike that you park at the station every day in the same area, but in a slightly different position?
And more interesting to my colleague Robert is the research we have been doing on neurogenesis and depression. So in an animal model of depression, we have seen that we have a lower level of neurogenesis. And if we give antidepressants, then we increase the production of these newborn neurons, and we decrease the symptoms of depression, establishing a clear link between neurogenesis and depression. But moreover, if you just block neurogenesis, then you block the efficacy of the antidepressant. So by then, Robert had understood that very likely his patients were suffering from depression even after being cured of their cancer, because the cancer drug had stopped newborn neurons from being generated. And it will take time to generate new neurons that reach normal functions.
So, collectively, now we think we have enough evidence to say that neurogenesis is a target of choice if we want to improve memory formation or mood, or even prevent the decline associated with aging, or associated with stress.
So the next question is: can we control neurogenesis? The answer is yes. And we are now going to do a little quiz. I'm going to give you a set of behaviors and activities, and you tell me if you think they will increase neurogenesis or if they will decrease neurogenesis. Are we ready? OK, let's go.
So what about learning? Increasing? Yes. Learning will increase the production of these new neurons.
How about stress? Yes, stress will decrease the production of new neurons in the hippocampus.
How about sleep deprivation? Indeed, it will decrease neurogenesis.
How about sex? Oh, wow!
(Laughter)
Yes, you are right, it will increase the production of new neurons. However, it's all about balance here. We don't want to fall in a situation --
(Laughter)
about too much sex leading to sleep deprivation.
(Laughter)
How about getting older? So the neurogenesis rate will decrease as we get older, but it is still occurring.
And then finally, how about running? I will let you judge that one by yourself.
So this is one of the first studies that was carried out by one of my mentors, Rusty Gage from the Salk Institute, showing that the environment can have an impact on the production of new neurons. And here you see a section of the hippocampus of a mouse that had no running wheel in its cage. And the little black dots you see are actually newborn neurons-to-be. And now, you see a section of the hippocampus of a mouse that had a running wheel in its cage. So you see the massive increase of the black dots representing the new neurons-to-be.
So activity impacts neurogenesis, but that's not all. What you eat will have an effect on the production of new neurons in the hippocampus. So here we have a sample of diet -- of nutrients that have been shown to have efficacy. And I'm just going to point a few out to you: Calorie restriction of 20 to 30 percent will increase neurogenesis. Intermittent fasting -- spacing the time between your meals -- will increase neurogenesis. Intake of flavonoids, which are contained in dark chocolate or blueberries, will increase neurogenesis. Omega-3 fatty acids, present in fatty fish, like salmon, will increase the production of these new neurons. Conversely, a diet rich in high saturated fat will have a negative impact on neurogenesis. Ethanol -- intake of alcohol -- will decrease neurogenesis. However, not everything is lost; resveratrol, which is contained in red wine, has been shown to promote the survival of these new neurons. So next time you are at a dinner party, you might want to reach for this possibly "neurogenesis-neutral" drink.
(Laughter)
And then finally, let me point out the last one -- a quirky one. So Japanese groups are fascinated with food textures, and they have shown that actually soft diet impairs neurogenesis, as opposed to food that requires mastication -- chewing -- or crunchy food.
So all of this data, where we need to look at the cellular level, has been generated using animal models. But this diet has also been given to human participants, and what we could see is that the diet modulates memory and mood in the same direction as it modulates neurogenesis, such as: calorie restriction will improve memory capacity, whereas a high-fat diet will exacerbate symptoms of depression -- as opposed to omega-3 fatty acids, which increase neurogenesis, and also help to decrease the symptoms of depression. So we think that the effect of diet on mental health, on memory and mood, is actually mediated by the production of the new neurons in the hippocampus. And it's not only what you eat, but it's also the texture of the food, when you eat it and how much of it you eat.
On our side -- neuroscientists interested in neurogenesis -- we need to understand better the function of these new neurons, and how we can control their survival and their production. We also need to find a way to protect the neurogenesis of Robert's patients. And on your side -- I leave you in charge of your neurogenesis.
Thank you.
(Applause)
Margaret Heffernan: Fantastic research, Sandrine. Now, I told you you changed my life -- I now eat a lot of blueberries.
Sandrine Thuret: Very good.
MH: I'm really interested in the running thing. Do I have to run? Or is it really just about aerobic exercise, getting oxygen to the brain? Could it be any kind of vigorous exercise?
ST: So for the moment, we can't really say if it's just the running itself, but we think that anything that indeed will increase the production -- or moving the blood flow to the brain, should be beneficial.
MH: So I don't have to get a running wheel in my office?
ST: No, you don't!
MH: Oh, what a relief! That's wonderful. Sandrine Thuret, thank you so much.
ST: Thank you, Margaret.
(Applause)
Sunday, May 8, 2016
GralInt-Parejas desparejas: cuando el deseo no es de los dos
The following information is used for educational purposes only.
Parejas desparejas: cuando el deseo no es de los dos
Cinco de cada diez argentinos lidian con la discordancia sexual
Soledad Vallejos, DOMINGO 08 DE MAYO DE 2016
Foto: LA NACION
Uno quiere y el otro no. Y viceversa. ¿Te pasó que vos quieras tener relaciones y tu pareja no? fue la pregunta disparadora de una encuesta diseñada por la Universidad Abierta Interamericana (UAI) sobre Deseo Sexual Desincronizado o SDD, por sus siglas en inglés.
Según los expertos, esa conducta es un motivo de consulta cada vez más frecuente. El tema suele provocar malestar en la pareja y puede llegar a desembocar en malentendidos y falsas interpretaciones. Sobre todo del estilo "no le atraigo como antes", "quizá piense en otra persona" o "ya no le gusto".
A esa pregunta de la encuesta, cinco de cada diez entrevistados (todos en pareja) respondieron sí. Y la misma proporción aceptó luego que "de vez en cuando" tiene relaciones sexuales aun sin tener deseos en ese momento.
Para Adrián Helien, psiquiatra y sexólogo del hospital Durand, hay que comenzar por reconocer que "así como tenemos distintos gustos, inclinaciones y necesidades, nuestros mapas del deseo también son diferentes y pretender coincidir siempre es un idilio que nos lleva directo a la desilusión".
¿Cuál es la razón de la discordancia? ¿Hay factores ajenos a la pareja? "Las circunstancias de mayor peso son las de la cotidianidad, ya que el trabajo, la familia, las cuestiones de la casa y la crianza de los niños, si los hay, ocupan un enorme tiempo y energía -dice Helien-. Si la pareja no administra bien estas actividades, la sexualidad queda relegada al último puesto. Y así como la regla general dice que el sexo trae más sexo, creo que aplicada en el sentido contrario es aún más contundente: cuanto menos sexo tengas, menos sexo vas a tener."
Según la encuesta de la UAI, realizada entre mujeres y hombres mayores de 18 años de la Ciudad Autónoma de Buenos Aires y del conurbano bonaerense, la circunstancia ajena a la relación que más afecta el deseo sexual es el cansancio, respuesta por la que se inclinó el 41,1%. En segundo lugar, con el 21,8% quedaron el estrés y los problemas laborales, seguidos por la rutina (14,1%), las demandas de los hijos (12,4%), la falta de atracción sexual (5,5%) y la baja autoestima (5,2%).
Olga Tallone es psicóloga, sexóloga clínica y especialista en sexualidad tántrica. Dirige Tantra Club, lugar adonde acuden parejas que buscan mejorar o recuperar sus encuentros sexuales reconectándose desde lo afectivo.
"Vienen parejas con hijos chicos, es decir, con edades muy demandantes, que consultan porque sienten que están perdiendo frecuencia -cuenta Tallone-. Pero también hay parejas veinteañeras que llegan por el mismo motivo. Pero ojo, porque las circunstancias ajenas nunca son tan «ajenas». El deseo sexual está muy afectado por una comunicación pobre, falta de unión entre lo erótico y lo afectivo, y la lucha por el poder que, desde el inicio o en alguna fase del vínculo, se manifiesta inevitablemente."
La psicóloga, sexóloga y coach sexual Celia Laniado aconseja, ante todo, la conversación franca y abierta, ya que muchas veces el solo hecho de plantearlo mejora el panorama. "Hay que acostumbrarse a hablar de sexo con naturalidad, indagar sobre lo que le gusta a nuestra pareja. Atreverse a preguntar y abrir el diálogo abre también las posibilidades de mejorar los encuentros y evitar la discordancia", dice.
Y agrega: "Hay que estar alerta a que la discrepancia no se instale. Alguno de los dos tiene que dar el primer paso".
Disfunciones sexuales y SDD
Desde su experiencia clínica, tanto el sexólogo León Roberto Gindin, profesor de Sexualidad y Salud de la UAI, como la psicóloga y sexóloga Andrea Gómez, autora del libro Sexualidad, pareja y embarazo: mitos y verdades, de Lugar Editorial, sostienen que este fenómeno de discrepancia puede surgir también en el contexto de una terapia donde se revisa algún tipo de disfunción concreta, ya sea en el hombre o en la mujer.
"Suele aparecer, especialmente, cuando se necesita aumentar la frecuencia para corregir algún trastorno más específico con técnicas congnitivo-conductuales", señala Gindin.
Por su parte, Gómez dice: "Cuando hay problemas de erección, control eyaculatorio o dispareunia en la mujer [coito vaginal doloroso], por mencionar algunos ejemplos, y uno como terapeuta interviene con un trabajo en función de aumentar la frecuencia sexual para corregirlo, entonces, aparece el SDD... Que uno está motivado y el otro no, que cuando uno quiere el otro ya no tiene ganas".
"Hay que ir entonces más profundo -agrega-, revisar si existe alguna fobia o algún reclamo escondido. Y en el caso de diagnosticar un SDD como tal, hay que ahondar desde la psicoterapia para abordar esa situación porque, en realidad, para entender la sexualidad en la historia de una pareja hay que empezar por la historia individual de cada uno. Es decir, las propias experiencias, el inicio sexual, la educación y los propios permisos para el placer y el encuentro sexual sin tabúes".
Como dice Helien, "el sexo en piloto automático no existe, no funciona solo, y si uno quiere coincidir con el otro en tener relaciones sexuales, también hay que hacerse cargo y ocuparse de que eso suceda sin hacer conjeturas".
"Hay una creencia milenaria de que el sexo siempre es espontáneo y natural, y no es siempre así -asegura Laniado-. La idea de programar un encuentro sexual, acordado entre ambos, suele resultar muy placentero, y además permite la posibilidad de innovar. Darse el permiso para disfrutar alienta el acercamiento en la pareja y aleja la discordancia."
Fuente: www.lanacion.com.ar
Parejas desparejas: cuando el deseo no es de los dos
Cinco de cada diez argentinos lidian con la discordancia sexual
Soledad Vallejos, DOMINGO 08 DE MAYO DE 2016
Foto: LA NACION
Uno quiere y el otro no. Y viceversa. ¿Te pasó que vos quieras tener relaciones y tu pareja no? fue la pregunta disparadora de una encuesta diseñada por la Universidad Abierta Interamericana (UAI) sobre Deseo Sexual Desincronizado o SDD, por sus siglas en inglés.
Según los expertos, esa conducta es un motivo de consulta cada vez más frecuente. El tema suele provocar malestar en la pareja y puede llegar a desembocar en malentendidos y falsas interpretaciones. Sobre todo del estilo "no le atraigo como antes", "quizá piense en otra persona" o "ya no le gusto".
A esa pregunta de la encuesta, cinco de cada diez entrevistados (todos en pareja) respondieron sí. Y la misma proporción aceptó luego que "de vez en cuando" tiene relaciones sexuales aun sin tener deseos en ese momento.
Para Adrián Helien, psiquiatra y sexólogo del hospital Durand, hay que comenzar por reconocer que "así como tenemos distintos gustos, inclinaciones y necesidades, nuestros mapas del deseo también son diferentes y pretender coincidir siempre es un idilio que nos lleva directo a la desilusión".
¿Cuál es la razón de la discordancia? ¿Hay factores ajenos a la pareja? "Las circunstancias de mayor peso son las de la cotidianidad, ya que el trabajo, la familia, las cuestiones de la casa y la crianza de los niños, si los hay, ocupan un enorme tiempo y energía -dice Helien-. Si la pareja no administra bien estas actividades, la sexualidad queda relegada al último puesto. Y así como la regla general dice que el sexo trae más sexo, creo que aplicada en el sentido contrario es aún más contundente: cuanto menos sexo tengas, menos sexo vas a tener."
Según la encuesta de la UAI, realizada entre mujeres y hombres mayores de 18 años de la Ciudad Autónoma de Buenos Aires y del conurbano bonaerense, la circunstancia ajena a la relación que más afecta el deseo sexual es el cansancio, respuesta por la que se inclinó el 41,1%. En segundo lugar, con el 21,8% quedaron el estrés y los problemas laborales, seguidos por la rutina (14,1%), las demandas de los hijos (12,4%), la falta de atracción sexual (5,5%) y la baja autoestima (5,2%).
Olga Tallone es psicóloga, sexóloga clínica y especialista en sexualidad tántrica. Dirige Tantra Club, lugar adonde acuden parejas que buscan mejorar o recuperar sus encuentros sexuales reconectándose desde lo afectivo.
"Vienen parejas con hijos chicos, es decir, con edades muy demandantes, que consultan porque sienten que están perdiendo frecuencia -cuenta Tallone-. Pero también hay parejas veinteañeras que llegan por el mismo motivo. Pero ojo, porque las circunstancias ajenas nunca son tan «ajenas». El deseo sexual está muy afectado por una comunicación pobre, falta de unión entre lo erótico y lo afectivo, y la lucha por el poder que, desde el inicio o en alguna fase del vínculo, se manifiesta inevitablemente."
La psicóloga, sexóloga y coach sexual Celia Laniado aconseja, ante todo, la conversación franca y abierta, ya que muchas veces el solo hecho de plantearlo mejora el panorama. "Hay que acostumbrarse a hablar de sexo con naturalidad, indagar sobre lo que le gusta a nuestra pareja. Atreverse a preguntar y abrir el diálogo abre también las posibilidades de mejorar los encuentros y evitar la discordancia", dice.
Y agrega: "Hay que estar alerta a que la discrepancia no se instale. Alguno de los dos tiene que dar el primer paso".
Disfunciones sexuales y SDD
Desde su experiencia clínica, tanto el sexólogo León Roberto Gindin, profesor de Sexualidad y Salud de la UAI, como la psicóloga y sexóloga Andrea Gómez, autora del libro Sexualidad, pareja y embarazo: mitos y verdades, de Lugar Editorial, sostienen que este fenómeno de discrepancia puede surgir también en el contexto de una terapia donde se revisa algún tipo de disfunción concreta, ya sea en el hombre o en la mujer.
"Suele aparecer, especialmente, cuando se necesita aumentar la frecuencia para corregir algún trastorno más específico con técnicas congnitivo-conductuales", señala Gindin.
Por su parte, Gómez dice: "Cuando hay problemas de erección, control eyaculatorio o dispareunia en la mujer [coito vaginal doloroso], por mencionar algunos ejemplos, y uno como terapeuta interviene con un trabajo en función de aumentar la frecuencia sexual para corregirlo, entonces, aparece el SDD... Que uno está motivado y el otro no, que cuando uno quiere el otro ya no tiene ganas".
"Hay que ir entonces más profundo -agrega-, revisar si existe alguna fobia o algún reclamo escondido. Y en el caso de diagnosticar un SDD como tal, hay que ahondar desde la psicoterapia para abordar esa situación porque, en realidad, para entender la sexualidad en la historia de una pareja hay que empezar por la historia individual de cada uno. Es decir, las propias experiencias, el inicio sexual, la educación y los propios permisos para el placer y el encuentro sexual sin tabúes".
Como dice Helien, "el sexo en piloto automático no existe, no funciona solo, y si uno quiere coincidir con el otro en tener relaciones sexuales, también hay que hacerse cargo y ocuparse de que eso suceda sin hacer conjeturas".
"Hay una creencia milenaria de que el sexo siempre es espontáneo y natural, y no es siempre así -asegura Laniado-. La idea de programar un encuentro sexual, acordado entre ambos, suele resultar muy placentero, y además permite la posibilidad de innovar. Darse el permiso para disfrutar alienta el acercamiento en la pareja y aleja la discordancia."
Fuente: www.lanacion.com.ar
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