Big Think Interview With Gregory Hannon
Dr. Gregory Hannon is a molecular biologist and a Professor at Cold Spring Harbor Laboratory in New York, as well as an Investigator at the Howard Hughes Medical Institute. His research focuses on growth control in mammalian cells and post-transcriptional gene silencing. Dr. Hannon received his PhD from Case Western Reserve University in 1992.
Gregory Hannon: Greg Hannon and I’m a Professor at Cold Spring Harbor Lab.\r\n
Question: How does your lab typically operate?\r\n
Gregory Hannon: Sure. The lab is sort of organized chaos. There are about 35 or 40 people in it. Graduate students, post-doctoral fellows, technicians, support staff, etc. We have probably an unusually broad research program. We focus in on three major areas. We work on the biology of small RNAs, we work on cancer biology, usually with the roles of the small RNAs in cancer and ways in which we can use small RNAs to understand cancer. And then we have a third area, which is technology development and genomics and mostly making use of some new generation sequencing technologies to try to understand everything from the evolution of cancer to human evolution.\r\n
Question: What is RNA interference?\r\n
Gregory Hannon: Well, RNA interference actually now describes a fairly broad range of biological phenomena. The notion is that RNA has a sequence just like DNA does. So then that sequence can be used to recognize complementary RNAs that share the sort of inverse of that sequence, the image of that sequence if you want to think of it that way. And through that recognition, a lot of jobs can be done. The RNAs recognized can be destroyed, they can be taken to different places in the cell, or they can even guide processes as strange as taking pieces out of the genome, depending on what organism you are talking about.\r\n
Question: How can RNA interference be used to “silence” genes in living cells?\r\n
Gregory Hannon: The evolutionarily deepest role of RNAi is as a genome defense. It’s a way that plants, for example, recognize and fight viruses. It’s a way that animals recognize parasitic pieces of DNA within their genomes, called transposons, and shut those off. It’s also a way that the cell uses RNA to program the regulation of its own genes, and we can exploit any one of these responses, essentially tricking the RNAi machinery into silencing any gene that we want just by fooling the machinery into recognizing it as, in essence, one of these foreign elements. And we can use that for a number of purposes. The one we mainly use it for is for trying to understand the biology of those genes. And again, in our case, mostly trying to understand what different sets of genes do in tumor development.\r\n
Question: What experiments have you performed to investigate the role of the RNAi pathway in animals?\r\n
Gregory Hannon: We’ve done a number of experiments in mice to try to figure out really, what RNAi does in animals, and I can give you a couple of examples. One is, we’ve looked at the small RNAs that the cell makes in order to regulate its own genes and compared the spectrum of those small RNAs in normal cells versus tumor cells.\r\n
In one of the first cases that we did this was in a tumor type called D-cell lymphoma. And by making that comparison, we discovered that there were a set of micro-RNAs, which is what these endogenous small RNAs are called. They’re different between the normal cells and the tumor cells. It turns out that that locust, that gene which encodes those micro-RNAs is often amplified in that specific tumor type. And if we reproduce that event, adding extra copies of that micro-RNA gene, we actually accelerate the development of that particular tumor in mice.\r\n
Another way we approach this problem is by taking all of the components of the RNAi machinery, all the proteins that actually bind to the small RNAs and that the small RNAs programmed to do these regulatory events and delete them from the genome and ask what the consequences are. And it was in part those experiments that led us to the realization that RNAi in animals placed this sort of genome defensive role, protecting the DNA of germ cells from the ravages of these mobile genetic elements called transposons.\r\n
Question: What are the potential applications of your RNAi studies in the field of cancer research?\r\n
Gregory Hannon: Well, for a long time, we’ve been interested in using RNAi as a tool to silence genes of interest, whatever genes we want. And in fact, my lab has built large collections of RNAi inducing agents, in fact, collections that can be used to turn off every gene in the human **** genome. Now, the way that we use these to investigate cancer biology is essentially to take a set of cancer cells, engineer them so that each cell has a different gene turned off, and then we ask how those cells react under stress. What genes do cancer cells require that normal cells don’t? These are potential targets for therapy. What genes modify the responsive cancer cells to chemotherapeutic agents, or targeted therapies? What genes modify the ability of cancer cells to engrafted host to metastasize, etc.?\r\n
Question: What new cancer therapies might be drawn from this research?\r\n
Gregory Hannon: Well there are really two ways that one would move from the work that we’re doing to something that would be applicable in the clinic. One is a process that is being repeated in many pharmaceutical companies. Many labs really built on the foundation of understanding this basic piece of biology, which is searching for unique vulnerabilities in tumor cells. Now, once one finds a cell upon which a particular subtype of breast cancer, for example, depends that the normal epithelial cells don’t depend on, then one can find targeted agents using standard pharmaceutical chemistry that could inhibit the activity of that particular target. And there you have a potentially selective therapy in a way that things like Gleevec are selective for specific gene rearrangement upon with the tumor cells carrying that arrangement uniquely depend.\r\n
Another promise of RNAi is that it can be used as a therapy itself. And there is a tremendous interest in this, both in the academic and in the industrial communities. The notion that pharmaceutical chemistry can only access only about 20% of the genes encoded in the genome being as we have a limited ability to regulate chemically, the activity of the proteins encoded by the other 80%. RNAI doesn’t have such a limitation. All it needs to be able to do is to specifically recognize the sequence of that gene in order to shut it off. And so it is essentially, in some ways, a potentially universal pharmaceutical approach. The difficulty is, and I think this is where many of us are focusing a lot of effort, is trying to figure out how to take this relatively large molecule compared to a normal pharmaceutical and get it efficiently delivered to the cells in which the therapy needs to operate.\r\n
And so really, that is one of the major barriers to taking this basic science discovery and really exploiting it as a tool for improving human health.\r\n
Question: How do you foresee this molecular delivery barrier being overcome?\r\n
Gregory Hannon: Well, I think that the way this barrier to delivery will be overcome is chemistry. So, it’s clear that we’ve pushed the biology of RNAI as a silencing tool sufficiently far that, given an inability to deliver this, we could shut off any gene that we wanted to and in fact, we could probably dial the activity of these inhibitors to the point that we could even figure out exactly how far down we have to turn a gene. Maybe you don’t want to shut it off because maybe it’s essential. Maybe you want to inhibit its activity 50% or 80%, and the tools **** in the biology is sufficient that we can achieve that with the tools that we have.\r\n
I think we will see advances in delivery come from is in changing the chemistry of the small RNA itself sufficiently that it can pass through cell membranes without the aid of a specific delivery agent. Delivery agents are the other arm of research into RNAI delivery encapsulating RNAs and lipids and polymers, and that’s another strategy for getting small RNAs into cells.\r\n
But my own feeling is that the unformulated molecules probably have the best potential to be a future therapy, the simpler formulation in something where you’re mixing an RNA agent and a series, for example, of polymers, to try to get them across the cell.\r\n
Question: What insights did your research reveal into the origins of the facial cancer wiping out Tasmanian devils?\r\n
Gregory Hannon: Well, this is, I think, an interesting story about the social aspects of science in a way. The realization that this transmissible cancer even existed came from a graduate student in my lab who happened to be Tasmanian. She did her PhD on basic aspects of RNA biology, and when she finished her degree before she moved on to a position as a post doctoral fellow, she was looking for a transition project. And she explained to me that this transmissible cancer existed that, in the last 10 years, it had wiped out roughly half of the Devil population and that it was estimated to actually drive the Devils to extinction sometime in the next 30 or so years if nothing were to be done. So, she was very passionate about his and convinced me that we had the tools to try to understand at least something about the biology of this disease.\r\n
Now, there are only two transmissible cancers that I know about where the cancer itself, the cancer cells themselves move from one individual to another. There’s this Tasmanian Devil facial tumor and there is also a tumor that does this in dogs. In dogs, the tumor isn’t as aggressive. It often spontaneously goes into remission and doesn’t often kill the animals that are, in essence, infected with this. In Tasmanian Devils the tumor is extremely aggressive, often kills affected animals in roughly six months with these horrific facial tumors that ultimately kill the animal often because they grow so large that the animal can no longer eat. But it’s a very aggressive disease also in the sense that it metastasizes to many sites in the body, but the animals are killed so quickly that it’s usually not the metastases that cause them to succumb as happens in many instances of human cancer.\r\n
So, our basic question was really to try to understand the origins of this transmissible tumor to try to understand what cell type the tumor was derived from so that we could maybe gain some insight into to why this tumor has such an unusual etiology. And also to try to understand why it is that this tumor can spread from individual to individual, you know, is that such an unusual property?\r\n
We came at it from a number of different perspectives. First, really founded upon our work on small RNAs, each cell type expresses a specific repertoire of small RNAs that it uses to regulate genes, but that repertoire is also kind of a signature of the cell type that the small RNAs is expressed in. So you can use a small RNA signature to tell a mammary cell from a germ cell. You can tell a nerve cell from a muscle cell. And so we started off by asking what spectrum of small RNAs these Devil facial tumors expressed. And that pointed us, in addition to looking at the messenger RNAs, these RNAs that encode the proteins within that cell by looking at the small RNA profiles and the messenger profiles. That really led us to a specific cell type, which in this case happens to be a Schwann cell.\r\n
What Schwann cells are is essentially like the insulation on a wire. They wrap nerve cells and act essentially as an insulator to make their conductance of signals more efficient.\r\n
Question: What course of treatment or action does this research suggest?\r\n
Gregory Hannon: Well, I mean, I think the two things that really come out of the work that we’ve done looking both at the tumor and the host animals are that the host animals themselves are remarkably genetically homogeneous. And so, one insight that emerged from the study is that the notion that the tumors may be able to spread from animal to animal essentially like a metastasis, but within a population rather than within an organism, in part because the animals can’t recognize these cells as foreign.\r\n
Now, in terms of a treatment, it’s difficult to envision wild animals undergoing cancer therapy. You can’t really imagine a mobile ICU in the Tasmanian bush. But one thing that one can consider is a prophylactic therapy. And so cancer vaccines have kind of a bad rap in part because they haven’t worked particularly well for humans, but the unusual nature of the Tasmanian Devil tumor and the fact that every tumor is identical, is a very different situation than one has with human cancers where every cancer is different. It is individual not only to the person, but in its genetic composition. And so, in some cases the difficulties in developing cancer vaccines in humans might be related to the heterogeneity of the tumors, whereas when it is precisely the opposite of the situation in Tasmanian Devils.\r\n
So, one can really envision two approaches; one is the approach which is being taken, which is to take a set of Devils and set them aside as an insurance population. And so you essentially sequester disease-free Devils with the idea that should the population actually go extinct in the wild, you have animals to reintroduce. Now in that case, we can use the work that we’ve done, which in essence led to a diagnostic marker for this disease, to ensure that any tumors that that insurance population might develop aren’t DFTD.\r\n
In the second instance one might imagine trying to develop a vaccine against this particular unusual tumor cell that could potentially be used on wild populations, although you can imagine the challenges that one would face in doing that.\r\n
Question: What obstacles does the unique genetic composition of human cancers pose to treatment, and how can they be overcome?\r\n
Gregory Hannon: Although each cancer is unique, there are certain core pathways, biological modules in essence, that are altered in nearly every cancer cell. And the number of those modules expands as one gets more specific to a particular subtype; let’s say estrogen receptor positive breast cancer. So, the notion, and this is one of the ways in which RNAi is being deployed very powerfully, is to try to correlate the vulnerabilities that are created by the inactivation in those individual biological models and then exploit that vulnerability for therapy. The way that you can think about this is that cells are designed or evolve to be robust. And every time you take away one of these biological modules, these pathways, it affects the robustness of cells. Think about a Jenga tower, and you’re pulling blocks out of a Jenga tower. The more blocks that you pull out, the easier it is to make that tower fall. And what people are doing with RNAi is trying to figure out precisely what additional block to pull out to make that tower fall. Where the tower wouldn’t fall if one had a normal cell which essentially has homeostatic mechanisms to be robust, to resist the biological difficulties that would be created by the loss of the pathway that would represent that key therapeutic target. So, the idea is to exploit common aspects of the genetics to create therapies that overcome the individuality of the disease.\r\n
Question: What kinds of bioethical issues arise in your work, and how do you address them?\r\n
Gregory Hannon: In our own work, I think we encounter bioethical issues in a few different ways. One is anytime we are dealing with experiments with living animals. There are certain standards that we have to maintain about the treatment of those animals. And we also try to plan using statistical tests to make sure that we use enough animals to get a definitive answer, but no more than we actually need to do an experiment.\r\n
From the standpoint of using human materials, we encounter issues of bioethics in two different ways. They are in some ways related and I think this goes to the development of a lot of these new high-capacity technologies that are being deployed in biology at the moment. So, on one hand, anytime we use human’s samples, there are a set of rules that are in place to maintain the anonymity of patients. And so, for example, when tumor samples are collected, they are anonymized and we have no way of tracing back the material that we are analyzing to the patient that was its source.\r\n
The difficulty comes as we are more and more able to sequence people’s complete genomes for reasonable cost and in a very short time. If you think about how long the human genome project took and what its cost, I mean it was astronomical, compared to today when we could conceivably sequence an entire human genome in probably a week, maybe two weeks and presently for a cost of $40,000 to $50,000. And that time it’s taking to resequence a genome and the cost of doing so is dropping continuously to the point where, really by the end of this year, it will be down to $10,000 and maybe one week. And who knows where we will be in another year or so.\r\n
Essentially, once you have determined that genomic sequence, there is a unique identifier, an identifier unique to that person in whom the sample was derived. Now, if we go to publish data derived from that sequence, we are obligated to put the primary – the raw data to make it available to the community. So that means that a sample has turned into a sequence which is unique to that individual, which then essentially, in some ways, public. Now for other investigators to access that, they need to have specific bioethics training, etc., but that information is out there. And although it’s not immediately connected to that person from which that sample is derived, it is in some ways eventually connectable.\r\n
And so I think that one of the places that we really struggle now is using the power of these new sequencing tools to try to understand biology and how we can do that in a way that doesn’t necessarily put the sequence of many people’s genomes essentially freely accessible on the Web. And I think this is something that a lot of people are struggling with at the moment as the sequencing technologies that I’ve mentioned become more and more widely available within the academic community. We need to establish ways to, I think at least, anonymize the information that we provide to the community without degrading the quality of the science that we do and without hampering the ability of others to analyze that data and reproduce our work, or at least verify our conclusions.\r\n
Question: Are you optimistic that patients’ genetic information can be successfully anonymized?\r\n
Gregory Hannon: I think it will happen. A lot of it is driven – there is a sort of tug of war between maximizing people’s access to your raw information because essentially you’ve spent the money, you’ve spent the time, you’ve produced this resource, you’ve analyzed it in one way. But it could probably be analyzed in an infinite variety of ways by others. And so, you want to have people maximally be able to make use of the data you generate. And also able to, as I said, verify your conclusions. On the other hand, there is this drive to maintain privacy and in the end, what’s going to have to happen is that the community will have to establish a set of procedures that are universally acceptable to allow a sequence to remain private and anonymous without destroying the value of the data that we publish. And scientists can take a lead in this, scientific journals can take the lead in this, but it is something that we are going to face remarkably soon.\r\n
Question: What opportunities in your science education were you most grateful for?\r\n
Gregory Hannon: Well, I came from a very small town. I had very good and very dedicated science teachers in high school who really went far beyond the call, in a way, to make additional science available after school hours, etc., doing things like science competitions that were held at local colleges, things like this and even making available some very basic college science courses during our later years of high school. Going on to undergraduate, I went to Case Western Reserve, a private university in Cleveland, with the idea that I was probably going to do medicine. The first semester I was there, I needed a job and talked to my undergraduate advisor who said, “Hey, why don’t you come to work in my lab.” And it took about a week to decide that that’s what I really wanted to do. So, for me, and I think for many, the turning point comes as an undergraduate student when you become exposed to the world of scientific research. It’s not something that a lot of people are intimately familiar with, it’s not a job that people see or encounter.\r\n
And so, I think the key opportunity is to give undergraduates the chance to come into the lab, to provide them exposure to what a life in academic sciences is really like. Graduate education is something that at Cold Spring Harbor, we’ve spent a lot of time thinking about. And really, Jim Watson pushed very hard about a decade ago to encourage us to fight against the length of graduate training, which was increasing to what he felt were ridiculous timeframes. So, a seven-year PhD of a student essentially not becoming an independent scientist until well into their 30’s was something that he thought completely inappropriate.\r\n
And so we’ve really tried to essentially reinvent graduate education in a way that allows biologists to get a PhD degree in a short amount of time; four years is our goal. We tend to meet it by and large over the ten years that our graduate program has been running; our average is about four years and three months. And in fact, I graduated a student yesterday in 3 ½ years. And so the notion of bringing people into research early and then giving them an opportunity to do independent work while they’re young and full of fire is, I think, a really critical issue that the community is trying to address.\r\n
Question: How can science improve its outreach to the general public?\r\n
Gregory Hannon: Well, I mean, we work for the public, if you want to think about where the funding comes for our research. It comes from the National Institutes of Health, which his supported by taxpayers. And I think consequently, we have a real obligation to communicate science to the public. Outreach, I think, should happen at every level. I think that working scientists should be interfacing with high schools, for example, going into high school biology classrooms, and communicating the excitement of their work to the student. Cold Spring Harbor Lab has a very strong community outreach program, something they call the DNA Learning Center, and it’s designed to bring middle school students and high school students into laboratories and expose them to laboratory science. I think it’s our obligation as scientists to reach out to the public in the form of public lecture series. We also have a strong public lecture program at the laboratory. I participate in it and I know that many of the other investigators at the lab participate in it. And I think that the public has to understand science. Not only because they pay for it, but because science is increasingly a part of their everyday life. And to go back to the discussion of sequencing and bioethics, a time will come in the not too distant future when you walk into a doctor’s office and they sequence at least part of your genome and without a basic understanding of biology, how is the general public going to react to this. How are they going to understand what’s being communicated to them about their risk of disease and about how their own genetics affect their response to treatments?\r\n
Question: What research being conducted at Cold Spring Harbor Lab excites you the most?\r\n
Gregory Hannon: Well, personally to me, what’s exciting about research is the moment of discovery. I think for most scientists it’s what addicts you to this; the idea that for just a few minutes you know something that nobody else in the world knows. And it doesn’t happen often because science is really a sort of an exercise in banging your head against the wall over and over again. Scientists need a very high tolerance for failure and frustration because most experiments do fail. But when something really works, and you really learn something fundamentally new, it’s something that I think I’ve never experienced in any other way.\r\nRecorded on February 9, 2010
A conversation with the molecular biologist at Cold Spring Harbor Laboratory.
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Fear that new technologies are addictive isn't a modern phenomenon.
This article was originally published on our sister site, Freethink, which has partnered with the Build for Tomorrow podcast to go inside new episodes each month. Subscribe here to learn more about the crazy, curious things from history that shaped us, and how we can shape the future.
In many ways, technology has made our lives better. Through smartphones, apps, and social media platforms we can now work more efficiently and connect in ways that would have been unimaginable just decades ago.
But as we've grown to rely on technology for a lot of our professional and personal needs, most of us are asking tough questions about the role technology plays in our own lives. Are we becoming too dependent on technology to the point that it's actually harming us?
In the latest episode of Build for Tomorrow, host and Entrepreneur Editor-in-Chief Jason Feifer takes on the thorny question: is technology addictive?
Popularizing medical language
What makes something addictive rather than just engaging? It's a meaningful distinction because if technology is addictive, the next question could be: are the creators of popular digital technologies, like smartphones and social media apps, intentionally creating things that are addictive? If so, should they be held responsible?
To answer those questions, we've first got to agree on a definition of "addiction." As it turns out, that's not quite as easy as it sounds.
If we don't have a good definition of what we're talking about, then we can't properly help people.
LIAM SATCHELL UNIVERSITY OF WINCHESTER
"Over the past few decades, a lot of effort has gone into destigmatizing conversations about mental health, which of course is a very good thing," Feifer explains. It also means that medical language has entered into our vernacular —we're now more comfortable using clinical words outside of a specific diagnosis.
"We've all got that one friend who says, 'Oh, I'm a little bit OCD' or that friend who says, 'Oh, this is my big PTSD moment,'" Liam Satchell, a lecturer in psychology at the University of Winchester and guest on the podcast, says. He's concerned about how the word "addiction" gets tossed around by people with no background in mental health. An increased concern surrounding "tech addiction" isn't actually being driven by concern among psychiatric professionals, he says.
"These sorts of concerns about things like internet use or social media use haven't come from the psychiatric community as much," Satchell says. "They've come from people who are interested in technology first."
The casual use of medical language can lead to confusion about what is actually a mental health concern. We need a reliable standard for recognizing, discussing, and ultimately treating psychological conditions.
"If we don't have a good definition of what we're talking about, then we can't properly help people," Satchell says. That's why, according to Satchell, the psychiatric definition of addiction being based around experiencing distress or significant family, social, or occupational disruption needs to be included in any definition of addiction we may use.
Too much reading causes... heat rashes?
But as Feifer points out in his podcast, both popularizing medical language and the fear that new technologies are addictive aren't totally modern phenomena.
Take, for instance, the concept of "reading mania."
In the 18th Century, an author named J. G. Heinzmann claimed that people who read too many novels could experience something called "reading mania." This condition, Heinzmann explained, could cause many symptoms, including: "weakening of the eyes, heat rashes, gout, arthritis, hemorrhoids, asthma, apoplexy, pulmonary disease, indigestion, blocking of the bowels, nervous disorder, migraines, epilepsy, hypochondria, and melancholy."
"That is all very specific! But really, even the term 'reading mania' is medical," Feifer says.
"Manic episodes are not a joke, folks. But this didn't stop people a century later from applying the same term to wristwatches."
Indeed, an 1889 piece in the Newcastle Weekly Courant declared: "The watch mania, as it is called, is certainly excessive; indeed it becomes rabid."
Similar concerns have echoed throughout history about the radio, telephone, TV, and video games.
"It may sound comical in our modern context, but back then, when those new technologies were the latest distraction, they were probably really engaging. People spent too much time doing them," Feifer says. "And what can we say about that now, having seen it play out over and over and over again? We can say it's common. It's a common behavior. Doesn't mean it's the healthiest one. It's just not a medical problem."
Few today would argue that novels are in-and-of-themselves addictive — regardless of how voraciously you may have consumed your last favorite novel. So, what happened? Were these things ever addictive — and if not, what was happening in these moments of concern?
People are complicated, our relationship with new technology is complicated, and addiction is complicated — and our efforts to simplify very complex things, and make generalizations across broad portions of the population, can lead to real harm.
JASON FEIFER HOST OF BUILD FOR TOMORROW
There's a risk of pathologizing normal behavior, says Joel Billieux, professor of clinical psychology and psychological assessment at the University of Lausanne in Switzerland, and guest on the podcast. He's on a mission to understand how we can suss out what is truly addictive behavior versus what is normal behavior that we're calling addictive.
For Billieux and other professionals, this isn't just a rhetorical game. He uses the example of gaming addiction, which has come under increased scrutiny over the past half-decade. The language used around the subject of gaming addiction will determine how behaviors of potential patients are analyzed — and ultimately what treatment is recommended.
"For a lot of people you can realize that the gaming is actually a coping (mechanism for) social anxiety or trauma or depression," says Billieux.
"Those cases, of course, you will not necessarily target gaming per se. You will target what caused depression. And then as a result, If you succeed, gaming will diminish."
In some instances, a person might legitimately be addicted to gaming or technology, and require the corresponding treatment — but that treatment might be the wrong answer for another person.
"None of this is to discount that for some people, technology is a factor in a mental health problem," says Feifer.
"I am also not discounting that individual people can use technology such as smartphones or social media to a degree where it has a genuine negative impact on their lives. But the point here to understand is that people are complicated, our relationship with new technology is complicated, and addiction is complicated — and our efforts to simplify very complex things, and make generalizations across broad portions of the population, can lead to real harm."
Behavioral addiction is a notoriously complex thing for professionals to diagnose — even more so since the latest edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5), the book professionals use to classify mental disorders, introduced a new idea about addiction in 2013.
"The DSM-5 grouped substance addiction with gambling addiction — this is the first time that substance addiction was directly categorized with any kind of behavioral addiction," Feifer says.
"And then, the DSM-5 went a tiny bit further — and proposed that other potentially addictive behaviors require further study."
This might not sound like that big of a deal to laypeople, but its effect was massive in medicine.
"Researchers started launching studies — not to see if a behavior like social media use can be addictive, but rather, to start with the assumption that social media use is addictive, and then to see how many people have the addiction," says Feifer.
The assumption that a lot of us are addicted to technology may itself be harming us by undermining our autonomy and belief that we have agency to create change in our own lives. That's what Nir Eyal, author of the books Hooked and Indistractable, calls 'learned helplessness.'
"The price of living in a world with so many good things in it is that sometimes we have to learn these new skills, these new behaviors to moderate our use," Eyal says. "One surefire way to not do anything is to believe you are powerless. That's what learned helplessness is all about."
So if it's not an addiction that most of us are experiencing when we check our phones 90 times a day or are wondering about what our followers are saying on Twitter — then what is it?
"A choice, a willful choice, and perhaps some people would not agree or would criticize your choices. But I think we cannot consider that as something that is pathological in the clinical sense," says Billieux.
Of course, for some people technology can be addictive.
"If something is genuinely interfering with your social or occupational life, and you have no ability to control it, then please seek help," says Feifer.
But for the vast majority of people, thinking about our use of technology as a choice — albeit not always a healthy one — can be the first step to overcoming unwanted habits.
For more, be sure to check out the Build for Tomorrow episode here.
The Inglehart-Welzel World Cultural map replaces geographic accuracy with closeness in terms of values.
- This map replaces geography with another type of closeness: cultural values.
- Although the groups it depicts have familiar names, their shapes are not.
- The map makes for strange bedfellows: Brazil next to South Africa and Belgium neighboring the U.S.
Some countries value self-expression more than others.Credit: Robyn Beck / AFP via Getty Images
Question: On what map is Lithuania a neighbor of China, Poland lies next to Brazil, and Morocco and Yemen touch?
Answer: The Inglehart-Welzel World Cultural Map. To be precise, the 2017 map. Because on the 2020 version, each of those pairs has drifted apart significantly.
These are not, strictly speaking, maps but rather scatterplot diagrams. Each dot represents a country, the position of which is based on how it ranks on two different values (discussed below). The dots are corralled together into geo-cultural groups:
- Catholic Europe, which comprises countries as diverse and far apart as Hungary and Andorra■ Protestant Europe, taking in both Iceland and Germany
- The Orthodox world, from Belarus all the way to Armenia
- The three Baltic states
- The English-speaking world, including both the U.S. and Northern Ireland
- The huge African-Islamic world, ranging from Azerbaijan to South Africa
- Latin America, which goes from Mexico to Argentina
- South Asia, which comprises both India and Cyprus
- The Confucian world, encompassing China and Japan.
The placement of the dots indicates cultural proximity or distance. Some countries from different groups can be more similar than other countries in the same group.
See the examples indicated above: cultural neighbors China and Lithuania belong to the Confucian and Baltic groups, respectively. Poland is part of Catholic Europe; its 2017 neighbor Brazil is in Latin America. Morocco and Yemen are closer culturally to Armenia, in the Orthodox group, than they are to Qatar, despite all belonging to the African-Islamic group.
The 2017 version of the map places Malta deep inside South America and lets Vietnam, Portugal, and Macedonia meet.Credit: World Values Survey, public domain.
Creating a culture map
So, what exactly are the criteria used for plotting these dots in the first place?
These maps are part of the World Values Survey, first conducted by political scientist Ronald Inglehart in the late 1990s. With his colleague Christian Welzel, he produced an update in 2005. The WVS has been revised several times since, most recently in 2020.
The WVS asserts that there are two fundamental dimensions to cross-cultural variation across the world. These are used as the axes to plot the various countries on the diagram.
- The X-axis measures survival versus self-expression values.
Survival values focus on economic and physical security. There is not much room for trust and tolerance of "others." Self-expression values prioritize well-being, quality of life, and self-expression. There is more room for tolerating ethnic, religious, and sexual minorities.
- The Y-axis measures traditional versus secular-rational values.
Traditional values include deference to religion and parental authority as well as traditional social and family values. Societies that score high on traditions typically also are highly nationalistic. In more secular-rational societies, science and bureaucracy replace faith as the basis for authority. Secular-rational values include high tolerance of things like divorce, abortion, euthanasia, and suicide.
As indicated by the significant changes on the 2020 map, the cultural values of nations are not static:
- Countries that move up on the map are shifting from traditional to more secular-rational values.
- Countries that move to the right on the map are shifting from survival values to self-expression values.
- And, of course, vice versa in both cases.
According to the authors of the map, changes in cultural outlook can be the result of socioeconomic changes — increasing levels of wealth, for example. But the religious and cultural heritage of each country also plays a part.
The world's cultural landscape is dynamic — you could even say promiscuous, producing new bedfellows every few years.Credit: World Values Survey, public domain.
Some notable features of the 2020 map:
- The Baltic group has been dissolved; Lithuania is now part of Catholic Europe, Estonia a lone Protestant island in a Catholic sea. More worryingly, Latvia seems to have dissolved completely.
- In general, survival values are strongest in African-Islamic countries, self-expression values in Protestant Europe.
- Traditional values are strongest in African-Islamic countries and Latin America, while secular values dominate in Confucian countries and Protestant Europe.
- The United States is an atypical member of the English-speaking group, scoring much lower on both scales (that is to say, lower and more to the left). In other words, the U.S. is more into traditional and survival values than the group's other members.
- Shifting attitudes don't just separate; they also unite. Belgium and the U.S. are now culture buddies, as are New Zealand and Iceland. Kazakhstan is virtually indistinguishable from Bosnia.
The Inglehart-Welzel map is not without its critics. It has been decried as Eurocentric, simplistic, and culturally essentialist (that is, the assumption that certain cultural characteristics are essential and fixed, and that some are superior to others). Which is, of course, a very self-expressive thing to say.
For more on these maps, on the WVS surveys, and on the methodology used, visit the World Values Survey.
Strange Maps #1098
Got a strange map? Let me know at firstname.lastname@example.org.
Evolution proves to be just about as ingenious as Nikola Tesla
- For the first time, scientists developed 3D scans of shark intestines to learn how they digest what they eat.
- The scans reveal an intestinal structure that looks awfully familiar — it looks like a Tesla valve.
- The structure may allow sharks to better survive long breaks between feasts.
Considering how much sharks are feared by humans, it is a bit of a surprise that scientists don't know much about the predators. For example, until recently, sharks were thought to be solitary creatures searching the seas for food on their own. Now it appears that some sharks are quite social.
Another mystery is how these prehistoric swimming and eating machines digest food. Although scientists have made 2D sketches of captured sharks' digestive systems based on dissections, there is a limit to what can be learned in this way. Professor Adam Summers at University of Washington's Friday Harbor Labs says:
"Intestines are so complex, with so many overlapping layers, that dissection destroys the context and connectivity of the tissue. It would be like trying to understand what was reported in a newspaper by taking scissors to a rolled-up copy. The story just won't hang together."
Summers is co-author of a new study that has produced the first 3D scans of a shark's intestines, which turns out to have a strange, corkscrew structure. What's even more bizarre is that it resembles the amazing one-way valve designed by inventor Nikola Tesla in 1920. The research is published in the journal Proceedings of the Royal Society B.
What a 3D model reveals
Video: Pacific spiny dogfish intestine youtu.be
According to the study's lead author Samantha Leigh, "It's high time that some modern technology was used to look at these really amazing spiral intestines of sharks. We developed a new method to digitally scan these tissues and now can look at the soft tissues in such great detail without having to slice into them."
"CT scanning is one of the only ways to understand the shape of shark intestines in three dimensions," adds Summers. The researchers scanned the intestines of nearly three dozen different shark species.
It is believed that sharks go for extended periods — days or even weeks — between big meals. The scans reveal that food passes slowly through the intestine, affording sharks' digestive system the time to fully extract its nutrient value. The researchers hypothesize that such a slow digestive process may also require less energy.
It could be that this slow digestion is more susceptible to back flow given that the momentum of digested food through the tract must be minimal. Perhaps that is why sharks evolved something so similar to a Tesla valve.
What is Tesla's valve doing there?
Above, a Tesla valve. Below, a shark intestine.Credit: Samantha Leigh / California State University, Domi
Tesla's "valvular conduit," or what the world now calls a "Tesla valve," is a one-way valve with no moving parts. Its brilliance is based in fluid dynamics and only now coming to be fully appreciated. Essentially, a series of teardrop-shaped loops arranged along the length of the valve allow water to flow easily in one direction but not in the other. Modern tests reveal that at low flow rates, water can travel through the valve either way, but at high flow rates, the design kicks in. According to mathematician Leif Ristroph:
"Crucially, this turn-on comes with the generation of turbulent flows in the reverse direction, which 'plug' the pipe with vortices and disrupting currents. Moreover, the turbulence appears at far lower flow rates than have ever previously been observed for pipes of more standard shapes — up to 20 times lower speed than conventional turbulence in a cylindrical pipe or tube. This shows the power it has to control flows, which could be used in many applications."
A deeper dive
Summers suggests the scans are just the beginning. "The vast majority of shark species, and the majority of their physiology, are completely unknown," says Summers, adding that "every single natural history observation, internal visualization, and anatomical investigation shows us things we could not have guessed at."
To this end, the researchers plan to use 3D printing to produce models through which they can observe the behavior of different substances passing through them — after all, sharks typically eat fish, invertebrates, mammals, and seagrass. They also plan to explore with engineers ways in which the shark intestine design could be used industrially, perhaps for the treatment of wastewater or for filtering microplastics.
It could fairly be said, though, that Nikola Tesla was 100 years ahead of them.
A study finds that baby mammals dream about the world they are about to experience to prepare their senses.
- Researchers find that babies of mammals dream about the world they are entering.
- The study focused on neonatal waves in mice before they first opened their eyes.
- Scientists believe human babies also prime their visual motion detection before birth.
Imagine opening your eyes for the first time as a brand new baby. The world is so mysterious, full of obstacles and strange shapes. And yet it does not take babies all that long to get their bearings, to latch on to their parents, and to start interacting. How do they do this so quickly? A new study published in Science proposes that babies of mammals dream about the world they are about to enter before being born, developing important skills.
The team, led by professor Michael Crair, who specializes in neuroscience, ophthalmology, and visual science, wanted to understand why when mammals are born, they are already somewhat prepared to interact with the world.
"At eye opening, mammals are capable of pretty sophisticated behavior," said Craig, "But how do the circuits form that allow us to perceive motion and navigate the world? It turns out we are born capable of many of these behaviors, at least in rudimentary form."
Unusual retinal activity
The scientists observed waves of activity radiating from the retinas of newborn mice before their eyes first open. Imaging shows that soon after birth, this activity disappears. In its place matures a network of neural transmissions that carries visual stimuli to the brain, as explained by a Yale press release. Once it reaches the brain, the information is encoded for storage.
What's particularly unusual about this neonatal activity is that it demonstrates a pattern that would happen if the animal was moving forward somewhere. As the researchers write in the study, "Spontaneous waves of retinal activity flow in the same pattern as would be produced days later by actual movement through the environment."
Crair explained that this "dream-like activity" makes sense from an evolutionary standpoint, as it helps the mouse get ready for what will happen to it after it opens its eyes. It allows the animal to "respond immediately to environmental threats," Crair shared.
Retinal waves in a newborn mouse prepare it for vision www.youtube.com
What is creating the waves?
The scientists also probed what is responsible for creating the retinal waves that mimic the forward motion. They turned on and off the functionality of starburst amacrine cells — retinal cells that release neurotransmitters — and discovered that blocking them stopped the retinal waves from flowing, which hindered the mouse from developing the ability to react to visual motion upon birth. These cells are also important to an adult mouse, affecting how it reacts to environmental stimuli.
Graphic showing the origin and functionality of directional retinal waves.Michael C. Crair et al, Science, 2021.
What about human babies?
While the study focused on mice, human babies also seem to be able to identify objects and motion right after birth. This suggests the presence of a similar phenomenon in babies before they are born.
"These brain circuits are self-organized at birth and some of the early teaching is already done," Crair stated. "It's like dreaming about what you are going to see before you even open your eyes."