Big Think Interview With Carol Greider
Carol W. Greider is the Daniel Nathans Professor & Director of Molecular Biology & Genetics at Johns Hopkins University. Her research on telomerase (an enzyme she helped discover) and telomere function won her a 2009 Nobel Prize in Medicine. Prior to joining the Johns Hopkins faculty, she obtained a Ph.D. in Molecular Biology from the University of California, Berkeley, in 1997, and was a faculty member at the Cold Spring Harbor Laboratory. She is a member of the National Academy of Sciences and a recipient of the 1998 Gairdner Foundation International Award.
Question: Have you encountered any gender-specific obstacles as a scientist?\r\n
Carol Greider: I think that that's a very complicated kind of question, because although I really feel like I never had a particular obstacle that I had to overcome as a female scientist—I never felt that I was singled out or had anything done against me—I do see that when one looks at where women are in science that there is a very large discrepancy, and that there does seem to be an inability for women to get to higher echelons in the scientific hierarchy or in academia. So I think that although I didn't feel like I had anything done personally to me, I think that there may be more subtle social interactions at play in the scientific world that does have a little bit of a negative effect on women advancing in their careers.\r\n
Question: What can be done to remove these obstacles?\r\n
Carol Greider: I think that as more women get into higher levels of science, and as it's very clear to younger women coming into the field that yes, it is possible to get to the higher ranks, that will help. And also I think that the way that women run meetings, and when the power structure is such that you have a larger representation of women at higher levels, that the conversation may change somewhat. And so that could also be helpful moving forward.\r\n
Question: What is your advice to female scientists starting out today?\r\n
Carol Greider: Just follow what you're excited about. I would say the same thing to female scientists as to male scientists, to all young people, really: the fun thing is to be able to do something that excites you. A lot of times what we do is a lot of hard work, but hard work is actually okay if you really are engaged in it. And so that really, I think, is the main thing, is find something that you're passionate about and be able to follow that.\r\n
Question: How did it feel to win the Nobel Prize?\r\n
Carol Greider: That was very exciting. It was a tremendous honor to get a phone call from Stockholm and to share it with Elizabeth Blackburn, who I've worked with for many years, as well as Jack Szostak. So I was very excited, and I was very happy that I got to share the day with my children. I was able to wake them up at five o'clock in the morning after I got this phone call and to have them there with me to share and to celebrate.\r\n
Question: What role did you and your co-winners each play in the prizewinning research?\r\n
Carol Greider: Yeah, Liz Blackburn and Jack Szostak had a collaboration in the early 1980s where they were interested in trying to understand the function of telomeres. And they had a collaboration which was a cross-country collaboration with one in Berkeley and the other one in Boston. And they would call each other up on the phone and explain experiments and send materials back and forth. And that collaboration resulted in this idea that there may be some way that the cells have of maintaining their chromosome ends. It was known that chromosome ends would shorten every time a cell divided, and in doing a collaboration to try and understand the functional components that make up the telomeres they proposed that there may be an enzyme that lengthens telomeres. And so then when I went to graduate school at U.C. Berkeley and I met Liz Blackburn, that was the project—after I had worked on a smaller project in her lab—that was the project that I thought was the most exciting to follow up on and find out, is there really going to be this hypothesized enzyme which can lengthen telomeres? So that's when I started to work with Liz Blackburn, and it was together in her laboratory that we discovered the enzyme telomerase.\r\n
Question: How do you think the prize will affect your work?\r\n
Carol Greider: I don't think I can anticipate the kinds of changes. Again, I never have been one to sort of think 10, 15 years out. I really just sort of try to follow what's exciting at the time. And it certainly is an honor, not just to me, but really to everybody working in the field of telomeres, because of course the prize is given to a person for a particular discovery, but the prize wouldn't be given unless there were many, many, many different people working in various laboratories that made it clear that that discovery was going to be important and has implications to it. So I really think that I'm sort of sharing this with the telomere field in general and many of my colleagues.\r\n
Question: Is your research highly targeted or guided by curiosity?\r\n
Carol Greider: Well, I've always been somebody that likes to follow interesting questions, and that initial work in Liz's lab was really a curiosity-driven question: how can the cell maintain its chromosome ends when we know that they should be getting shorter? So it was a puzzle that we needed to solve. But it was an important puzzle because all cells need to solve this problem of replicating the chromosome ends. But I feel like I've been really fortunate because at every step then along the way I've been able to follow my curiosity and see where the next step led. So, for instance, I started off working on this enzyme telomerase and trying to understand how the enzyme actually functions. What are the different components? Can we find out the mechanism by which this enzyme operates? And then the question came up about cells, and if the telomeres are shortening every time, what would happen to cells? And I got then into this field of cellular senescence, which is that cells can divide a certain number of times and then they stop dividing. And it turns out that the short telomeres play a role in that. So that was a very interesting discovery, and that then led to the next question, which is: if the cells normally stop dividing, why don't cancer cells stop dividing? That's a cell type that has to divide many times. So then our interest went into the area of cancer research, and I was able to follow that because it's very nice to be able to be in this kind of environment where you can just do science, and as long as you're learning something interesting and you can get funded—and I've been funded continuously by the National Institutes of Health, and so that's been very nice—to then be able to follow the next steps along the way in terms of what the most interesting question was to me.\r\n
Question: Did you ever doubt that you were on the right track with your telomere hypothesis?\r\n
Carol Greider: Well, at the time there were really two main hypotheses for how telomeres may be elongated: that there could be a recombination-based model or this hypothetical enzyme. And I just thought it was like an exciting puzzle to see which might be true. And so I chose one because I was working with Liz, which was to look for an enzyme which might lengthen telomeres. And it was really just fun to be part of solving that puzzle.\r\n
Question: Do scientists fear chasing false hypotheses?\r\n
Carol Greider: Of course it could have been possible that there was another mechanism that lengthened telomeres, and it's not clear how long one would then keep looking for something without any success. Luckily, in my case it was about nine months of trying various things, and then I had some success. But yes, there are a number of dead ends in science, and you may be doing experiments along one track, and either technically the experiments don't work, or you get something slightly wrong. And that's what's really important about the whole scientific process, is that it's really about what the results are. And either you or somebody else will be able to determine whether or not the result of your research are correct. And so being able to let go of ideas and move forward I think is just as important as having good new ideas.\r\n
Question: What was the telomere problem and how did you solve it?\r\n
Carol Greider: Well, at the basic level it has to do with how cells can divide many times. What was known in the late 1970s was that when you copy a chromosome, the way that the mechanism copies a chromosome, every time a cell divides, the very, very end bit can't be completely copied. And so then the idea was that the chromosomes, or the telomeres, which are the chromosome ends, would get shorter and shorter and shorter every time a cell divides. And that can't happen indefinitely; there has to be some mechanism which will balance that shortening. And that's where the discovery of telomerase comes in. And so for any cell that has to divide many times, they need to have a way to balance so that there's some shortening and some lengthening and some shortening and some lengthening, and an equilibrium is then maintained so that the cells can then go on and divide.\r\n
Question: What was your methodology in making the discovery?\r\n
Carol Greider: We were very interested in, as I said, telomeres and chromosomes and how they functioned. And so we really went to the source where there are a lot of telomeres. And this was something that Liz Blackburn had done a number of years before, when she had discovered the DNA sequence that telomeres is made up of. And it's a very, very simple repeated DNA sequence that is sort of a monotonous many, many, many repeats. And she had discovered the telomere DNA sequence in this organism called tetrahymena; it's a single-celled organism very much like the paramecium that high school students might go out to a pond and bring back some pond water and see the paramecium floating around. The thing about tetrahymena is that they have 40,000 chromosomes. And so it was a very good source to be able to understand what the ends of the chromosomes were. So when we set out to ask, is there an enzyme that can lengthen the chromosomes to balance the shortening, we went again to tetrahymena, and you can just get these organisms and grow them up in the laboratory. So we would grow up a large batch of the cells, and then you spin the cells down in a centrifuge so you make a very compact collection of them, and then break them open to get the insides of the cells out so that you can understand what is going on inside the cells.\r\n
Question: Was the 25-year delay in recognizing your discovery unusual?\r\n
Carol Greider: I think it's more that the discovery was made in 1984, and it was clear that it was important at the time. But it was important as a very basic cellular mechanism. And there wasn't a lot of questions; I didn't get a lot of people doubting what the conclusion was. But instead, it wasn't clear what the implications were. In the 25 years that have intervened, my lab and Liz's lab and a number of other labs throughout the world have contributed all kinds of different ideas from different avenues that have made it very clear now what the medical implications are. And so there are clear medical implications that we didn't know at all at the beginning. We were just solving a puzzle because we were curious about how cells worked, although we knew that it was a fundamental mechanism. We weren't just doing experiments just to find out anything, but rather to really understand how a cell works. And the 25 years in between really has allowed it to be clear what the implications of that discovery were.\r\n
Question: What are some practical applications of your telomere discovery?\r\n
Carol Greider: Well, it turns out that there are really two different areas in which the ability of cells to divide have medical implications. And one is in cancer, where a cancer cell has to divide many, many more times than any of the normal tissue surrounding it. And so the cancer cells have to solve this telomere problem, or the telomeres will shorten and the cells won't divide. And the other area is normal cells in the body which have to do with tissue renewal. So tissue-specific stem cells where—for instance, in your blood the cells need to be able to divide every day to provide new blood cells, because the blood cells only have a very short lifespan. And so it turns out that there are a number of degenerative diseases that are typically associated with aging because the cells have gone through so many rounds of cell division. If they have short telomeres, then there are problems with tissue renewal. So the degenerative diseases of aging and cancer really are the same kind of question of how many times cells can divide.\r\n
Question: Will the discovery have anti-aging applications even for healthy patients?\r\n
Carol Greider: Yeah, I think that the interest in this age-related disease isn't just limited to certain families where they have short telomeres due to mutations in telomerase. That's where they have been studied, as well as we've studied them in mice which we create that have short telomeres. But the implication is that all individuals, when the telomeres get short, will have a certain risk associated of these age-related degenerative diseases. And it's not limited to just a subset of patients with particular mutations, but rather pointing out a general risk of these degenerative diseases in the whole population.\r\n
Question: What other medical mysteries might your research illuminate?\r\n
Carol Greider: Well, I think that we're just really trying to understand the role of telomeres in these diseases, and the spectrum of the different kinds of diseases that short telomeres may play a role in, and down the road whether or not there would be some way to have a therapeutic intervention in these diseases. They're really devastating diseases: bone marrow failure and lung diseases. And so if there were some way to intervene and change the process so that the telomeres don't shorten progressively or don't shorten as rapidly, then perhaps there would be therapeutic approaches for these diseases. So going in that direction in terms of the therapeutics, but also I think the work that has been done has opened up many more questions than it really has answered. The number of questions that have to do with how telomere length equilibrium is maintained is greater today than when we started back in the 1980s. What we discovered was the enzyme telomerase that has to provide the raw material to make telomeres longer. But how is that process regulated? There is a very, very tight equilibrium of shortening and lengthening and shortening and lengthening, and it's maintained at a very precise spot in the cell. And we would like to know, what are the molecular details that go into that? Because those molecular details will then tell us about any potential diseases in the future where the changes might lie that have to do with telomere length.\r\n
Question: How do you suspect telomere length equilibrium is maintained?\r\n
Carol Greider: I think that there are going to be multiple different layers of regulation. When the cell really cares about a process, there are always multiple different inputs and several backup mechanisms. So people are working now on the actual proteins that bind along the length of the telomere, and how those proteins then tell telomerase to elongate the telomere, and how those proteins are modified by other proteins, and I think that it's going to be a fairly complex interactive network that will take some time to tease out. But it's exciting to find out even a few of the little pieces of the puzzle.\r\n
Question: Are we on the cusp of a genetics revolution?\r\n
Carol Greider: I think that we're in the middle of the age of genetics; I don't think that we're on the cusp of a revolution. I mean, I think with the sequencing of the human genome and now sequencing of many, many different genomes from a variety of organisms have given researchers such powerful tools to find out new associations. Being able to compare whole genome sequences from many, many different organisms, one can see what is conserved and therefore what is very important. So I think that the tools that we've been given just in the last 10 years are tremendous, and people are just now learning to be able to take advantage of those. And yes, there are of course ethical implications in terms of issues having to do with insurance and genetic privacy issues. If whole genomes are going to be sequenced, who will have that information? And I think that there are a lot of processes going on. There's a bill that was passed a number of years ago, the Genetic Information Privacy Act, which will limit the use that can be made of some of this. But I think it's an ongoing process that people need to be discussing more widely, that the more people in general in the population understand about genetics, the more they'll be able to have an informed discussion about these issues when they come up. So I think that scientific literacy is going to be really important as these things are disseminated more into the public in terms of the possibility of people having their own DNA sequenced, and what does it mean? And what does it mean to them, and what does it mean to family members who might not want to know that? Those are privacy issues. And the only way to move forward with that is to really have an informed discussion and to talk about it. So that's why I think that general education in terms of genetics is really essential.\r\n
Question: Are you worried or excited about the changes genetics research will bring?\r\n
Carol Greider: I'm excited about what's to come, but I think that along with the actual scientific changes there's a certain responsibility of scientists and educated people in general to talk about these things, because I think that with knowledge comes power. And so the more that the lay public understands about what we're learning in genetics, the more they can then understand how it would be useful to them. So I think it's a very, very exciting time, but I think that there's also a responsibility to be able to discuss things in a very open way that makes clear what the implications are and what the implications aren't.\r\n
Question: What will be the technical and ethical limits to genetic manipulation?\r\n
Carol Greider: It depends on what you mean by genetic manipulation, in the sense that we do genetic manipulation in the laboratory all the time to try and test ideas about how genes work. So we will take cells and we will change the genes in those cells and then be able to ask what is the consequence of that change. That's basically doing an experiment. We do that with mice as well. If we want to understand—for instance, we wanted to understand what would happen if a cancer cell didn't have telomerase. Could it still grow? So we generated a mouse, and the whole mouse doesn't have telomerase. So that's a genetic manipulation of the mice, but it was an important question to know the answer what would happen if you could completely get rid of telomerase. So I think that in that sense, those kinds of genetic manipulations are very powerful tools that scientists have. Now, if you're talking about things like human genetic engineering and those kinds of things, there are certainly ideas about gene therapy that people have put out there to solve various diseases, and some of the ones that people have been looking at are diseases that are in the blood, because blood cells are very accessible to changes. And those kinds of things don't worry me so much except for the technical aspects of—in some cases when you try and put genes back into cells, people have found that then those genes can cause other changes, which in some cases can lead to cancer. So there are clear technical hurdles which have to be overcome in that realm. And in terms of germline gene therapy, where you may change something permanently in the human germline, I think that basically that is something that's out of the question and shouldn't really be on the table. I don't think that anybody's really discussing changing the human genetic germline.\r\n
[Question: For technical or ethical reasons?]\r\n
Carol Greider: For ethical reasons. Technical as well, if we can't even get it right right now. If the science today—we can't do a bone marrow transplant; that is, take some bone marrow cells and correct a defect of a single gene in the blood, put that back in and know that the correction is going to happen. And instead, these children developed tumors because of unknown consequences in doing that. So if we can't even do this to blood cells, we are very, very far technically from being able to do anything without having many unintended consequences in the germline. So for technical reasons I would say it should be completely out of bounds, and then there are the ethical issues, which again would need to be discussed in a broader context. And I don't know of anyone that seriously thinks that that is something that one should be changing.\r\n
Question: What has been your biggest mistake as a scientist?\r\n
Carol Greider: Well, I've made a number of mistakes along the way. When you make—I feel like if there's a scientific mistake—so when I publish something and it turns out that the conclusion that was drawn wasn't completely correct, then it's the responsibility of the scientist to then do the experiments and publish the correct answer. But in that sense, science is very self-correcting, because if something is published and it's important, and it's wrong, then a number of other people will find out that it's wrong, although that may take a number of years, and some people may be led astray. So I think that the real importance is to not be necessarily attached to a particular idea, with the idea that telomere shortening plays some role in cell death, say. The thing that we would like to do is to test that idea. And one thing that I think creeps into people's thinking sometimes is that they want to prove a hypothesis. And I never think about proving a hypothesis, but rather think about different ways to test the hypothesis. And this was something that I think I learned very early on in Liz Blackburn's lab when we first had discovered something that looked like it was elongating telomeres. And then a period of about nine months went by where we set up to ask ourselves, is it really true that we've discovered a new enzyme? And we came up with a variety of methods to shoot down our own hypothesis. Maybe we're being fooled because it's a normal DNA polymerase that's just making this, and it looks like it's something new. Or maybe we're being fooled in a different direction. And then after the discovery withstood the test of nine months of attacks from our own standpoint about how could we shoot ourselves down, then I started to really believe that it was true. And so that really taught me that it's most important to be critical of your own hypothesis rather than to be a cheerleader for it. And I have a little bit of a fear against people just cheerleading for ideas, rather—I think it's more important to test them because that's how you then move forward, because many ideas are going to be wrong. And if you test an idea and find out it's wrong, you can go in another direction. But if you're a cheerleader for an idea, it may last for a longer period of time even if it's not correct.\r\n
Question: What was your opinion of President Obama’s Nobel win?\r\n
Carol Greider: Oh, I was very excited when I heard that he had won the Nobel Peace Prize, and I really saw it as a promise of something for the future. And he's been such a supporter of science, and science in the public eye, that I really felt like that was a very good thing. And I do see it as a hope for the future for the direction that he is going in terms of world peace.\r\n
Question: Can science promote peace?\r\n
Carol Greider: Science can promote an understanding between people at a really fundamental level. So yes, I think that science can promote peace by bringing people together to work on problems and to realize that there are problems that everybody faces that can be best approached by people working together in different directions.
Recorded November 10th, 2009
Interviewed by Austin Allen
A conversation with the Johns Hopkins University molecular biologist and co-winner of the 2009 Nobel Prize in Medicine.
The team caught a glimpse of a process that takes 18,000,000,000,000,000,000,000 years.
- In Italy, a team of scientists is using a highly sophisticated detector to hunt for dark matter.
An innovation may lead to lifelike evolving machines.
- Scientists at Cornell University devise a material with 3 key traits of life.
- The goal for the researchers is not to create life but lifelike machines.
- The researchers were able to program metabolism into the material's DNA.
One victim can break our hearts. Remember the image of the young Syrian boy discovered dead on a beach in Turkey in 2015? Donations to relief agencies soared after that image went viral. However, we feel less compassion as the number of victims grows. Are we incapable of feeling compassion for large groups of people who suffer a tragedy, such as an earthquake or the recent Sri Lanka Easter bombings? Of course not, but the truth is we aren't as compassionate as we'd like to believe, because of a paradox of large numbers. Why is this?
Compassion is a product of our sociality as primates. In his book, The Expanding Circle: Ethics, Evolution, and Moral Progress, Peter Singer states, "Human beings are social animals. We were social before we were human." Mr. Singer goes on to say, "We can be sure that we restrained our behavior toward our fellows before we were rational human beings. Social life requires some degree of restraint. A social grouping cannot stay together if its members make frequent and unrestrained attacks on one another."
Attacks on ingroups can come from forces of nature as well. In this light, compassion is a form of expressed empathy to demonstrate camaraderie.
Yet even after hundreds of centuries of evolution, when tragedy strikes beyond our community, our compassion wanes as the number of displaced, injured, and dead mounts.
The drop-off in commiseration has been termed the collapse of compassion. The term has also been defined in The Oxford Handbook of Compassion Science: ". . . people tend to feel and act less compassionately for multiple suffering victims than for a single suffering victim."
That the drop-off happens has been widely documented, but at what point this phenomenon happens remains unclear. One paper, written by Paul Slovic and Daniel Västfjäll, sets out a simple formula, ". . . where the emotion or affective feeling is greatest at N =1 but begins to fade at N = 2 and collapses at some higher value of N that becomes simply 'a statistic.'"
The ambiguity of "some higher value" is curious. That value may relate to Dunbar's Number, a theory developed by British anthropologist, Robin Dunbar. His research centers on communal groups of primates that evolved to support and care for larger and larger groups as their brains (our brains) expanded in capacity. Dunbar's is the number of people with whom we can maintain a stable relationship — approximately 150.
Some back story
Professor Robin Dunbar of the University of Oxford has published considerable research on anthropology and evolutionary psychology. His work is informed by anthropology, sociology and psychology. Dunbar's Number is a cognitive boundary, one we are likely incapable of breaching. The number is based around two notions; that brain size in primates correlates with the size of the social groups they live among and that these groups in human primates are relative to communal numbers set deep in our evolutionary past. In simpler terms, 150 is about the maximum number of people with whom we can identify with, interact with, care about, and work to protect. Dunbar's Number falls along a logorithmic continuum, beginning with the smallest, most emotionally connected group of five, then expanding outward in multiples of three: 5, 15, 50, 150. The numbers in these concentric circles are affected by multiple variables, including the closeness and size of immediate and extended families, along with the greater cognitive capacity of some individuals to maintain stable relationships with larger than normal group sizes. In other words, folks with more cerebral candlepower can engage with larger groups. Those with lesser cognitive powers, smaller groups.
The number that triggers "compassion collapse" might be different for individuals, but I think it may begin to unravel along the continuum of Dunbar's relatable 150. We can commiserate with 5 to 15 to 150 people because upon those numbers, we can overlay names and faces of people we know: our families, friends and coworkers, the members of our clan. In addition, from an evolutionary perspective, that number is important. We needed to care if bands of our clan were being harmed by raids, disaster, or disease, because our survival depended on the group staying intact. Our brains developed the capacity to care for the entirety of the group but not beyond it. Beyond our ingroup was an outgroup that may have competed with us for food and safety and it served us no practical purpose to feel sad that something awful had happened to them, only to learn the lessons so as to apply them for our own survival, e.g., don't swim with hippos.
Imagine losing 10 family members in a house fire. Now instead, lose 10 neighbors, 10 from a nearby town, 10 from Belgium, 10 from Vietnam 10 years ago. One could almost feel the emotion ebbing as the sentence drew to a close.
There are two other important factors which contribute to the softening of our compassion: proximity and time. While enjoying lunch in Santa Fe, we can discuss the death toll in the French revolution with no emotional response but might be nauseated to discuss three children lost in a recent car crash around the corner. Conflict journalists attempt to bridge these geotemporal lapses but have long struggled to ignite compassion in their home audience for far-flung tragedies, Being a witness to carnage is an immense stressor, but the impact diminishes across the airwaves as the kilometers pile up.
A Dunbar Correlation
Where is the inflection point at which people become statistics? Can we find that number? In what way might that inflection point be influenced by the Dunbar 150?
"Yes, the Dunbar number seems relevant here," said Gad Saad, PhD., the evolutionary behavioral scientist from the John Molson School of Business at Concordia University, Montreal, in an email correspondence. Saad also recommended Singer's work.
I also went to the wellspring. I asked Professor Dunbar by email if he thought 150 was a reasonable inflection point for moving from compassion into statistics. He graciously responded, lightly edited for space.
Professor Dunbar's response:
"The short answer is that I have no idea, but what you suggest is perfect sense. . . . One-hundred and fifty is the inflection point between the individuals we can empathize with because we have personal relationships with them and those with whom we don't have personalized relationships. There is, however, also another inflection point at 1,500 (the typical size of tribes in hunter-gatherer societies) which defines the limit set by the number of faces we can put names to. After 1,500, they are all completely anonymous."
I asked Dunbar if he knows of or suspects a neurophysiological aspect to the point where we simply lose the capacity to manage our compassion:
"These limits are underpinned by the size of key bits of the brain (mainly the frontal lobes, but not wholly). There are a number of studies showing this, both across primate species and within humans."
In his literature, Professor Dunbar presents two reasons why his number stands at 150, despite the ubiquity of social networking: the first is time — investing our time in a relationship is limited by the number of hours we have available to us in a given week. The second is our brain capacity measured in primates by our brain volume.
Friendship, kinship and limitations
"We devote around 40 percent of our available social time to our 5 most intimate friends and relations," Dunbar has written, "(the subset of individuals on whom we rely the most) and the remaining 60 percent in progressively decreasing amounts to the other 145."
These brain functions are costly, in terms of time, energy and emotion. Dunbar states, "There is extensive evidence, for example, to suggest that network size has significant effects on health and well-being, including morbidity and mortality, recovery from illness, cognitive function, and even willingness to adopt healthy lifestyles." This suggests that we devote so much energy to our own network that caring about a larger number may be too demanding.
"These differences in functionality may well reflect the role of mentalizing competencies. The optimal group size for a task may depend on the extent to which the group members have to be able to empathize with the beliefs and intentions of other members so as to coordinate closely…" This neocortical-to-community model carries over to compassion for others, whether in or out of our social network. Time constrains all human activity, including time to feel.
As Dunbar writes in The Anatomy of Friendship, "Friendship is the single most important factor influencing our health, well-being, and happiness. Creating and maintaining friendships is, however, extremely costly, in terms of both the time that has to be invested and the cognitive mechanisms that underpin them. Nonetheless, personal social networks exhibit many constancies, notably in their size and their hierarchical structuring." Our mental capacity may be the primary reason we feel less empathy and compassion for larger groups; we simply don't have the cerebral apparatus to manage their plights. "Part of friendship is the act of mentalizing, or mentally envisioning the landscape of another's mind. Cognitively, this process is extraordinarily taxing, and as such, intimate conversations seem to be capped at about four people before they break down and form smaller conversational groups. If the conversation involves speculating about an absent person's mental state (e.g., gossiping), then the cap is three — which is also a number that Shakespeare's plays respect."
We cannot mentalize what is going on in the minds of people in our groups much beyond our inner circle, so it stands to reason we cannot do it for large groups separated from us by geotemporal lapses.
In a paper, C. Daryl Cameron and Keith B. Payne state, "Some researchers have suggested that [compassion collapse] happens because emotions are not triggered by aggregates. We provide evidence for an alternative account. People expect the needs of large groups to be potentially overwhelming, and, as a result, they engage in emotion regulation to prevent themselves from experiencing overwhelming levels of emotion. Because groups are more likely than individuals to elicit emotion regulation, people feel less for groups than for individuals."
This argument seems to imply that we have more control over diminishing compassion than not. To say, "people expect the needs of large groups to be potentially overwhelming" suggests we consciously consider what that caring could entail and back away from it, or that we become aware that we are reaching and an endpoint of compassion and begin to purposely shift the framing of the incident from one that is personal to one that is statistical. The authors offer an alternative hypothesis to the notion that emotions are not triggered by aggregates, by attempting to show that we regulate our emotional response as the number of victims becomes perceived to be overwhelming. However, in the real world, for example, large death tolls are not brought to us one victim at a time. We are told, about a devastating event, then react viscerally.
If we don't begin to express our emotions consciously, then the process must be subconscious, and that number could have evolved to where it is now innate.
Gray matter matters
One of Dunbar's most salient points is that brain capacity influences social networks. In his paper, The Social Brain, he writes: "Path analysis suggests that there is a specific causal relationship in which the volume of a key prefrontal cortex subregion (or subregions) determines an individual's mentalizing skills, and these skills in turn determine the size of his or her social network."
It's not only the size of the brain but in fact, mentalizing recruits different regions for ingroup empathy. The Stanford Center for Compassion and Altruism Research and Education published a study of the brain regions activated when showing empathy for strangers in which the authors stated, "Interestingly, in brain imaging studies of mentalizing, participants recruit more dorsal portions of the medial prefrontal cortex (dMPFC; BA 8/9) when mentalizing about strangers, whereas they recruit more ventral regions of the medial prefrontal cortex (BA 10), similar to the MPFC activation reported in the current study, when mentalizing about close others with whom participants experience self-other overlap."⁷
It's possible the region of the brain that activates to help an ingroup member evolved for good reason, survival of the group. Other regions may have begun to expand as those smaller tribal groups expanded into larger societies.
There is an eclectic list of reasons why compassion may collapse, irrespective of sheer numbers:
(1) Manner: How the news is presented affects viewer framing. In her book, European Foreign Conflict Reporting: A Comparative Analysis of Public News, Emma Heywood explores how tragedies and war are offered to the viewers, which can elicit greater or lesser compassionate responses. "Techniques, which could raise compassion amongst the viewers, and which prevail on New at Ten, are disregarded, allowing the victims to remain unfamiliar and dissociated from the viewer. This approach does not encourage viewers to engage with the sufferers, rather releases them from any responsibility to participate emotionally. Instead compassion values are sidelined and potential opportunities to dwell on victim coverage are replaced by images of fighting and violence."
(2) Ethnicity. How relatable are the victims? Although it can be argued that people in western countries would feel a lesser degree of compassion for victims of a bombing in Karachi, that doesn't mean people in countries near Pakistan wouldn't feel compassion for the Karachi victims at a level comparable to what westerners might feel about a bombing in Toronto. Distance has a role to play in this dynamic as much as in the sound evolutionary data that demonstrate a need for us to both recognize and empathize with people who look like our communal entity. It's not racism; it's tribalism. We are simply not evolved from massive heterogeneous cultures. As evolving humans, we're still working it all out. It's a survival mechanism that developed over millennia that we now struggle with as we fine tune our trust for others.
In the end
Think of compassion collapse on a grid, with compassion represented in the Y axis and the number of victims running along the X. As the number of victims increases beyond one, our level of compassion is expected to rise. Setting aside other variables that may raise compassion (proximity, familiarity etc.), the level continues to rise until, for some reason, it begins to fall precipitously.
Is it because we've become aware of being overwhelmed or because we have reached max-capacity neuron load? Dunbar's Number seems a reasonable place to look for a tipping point.
Professor Dunbar has referred to the limits of friendship as a "budgeting problem." We simply don't have the time to manage a bigger group of friends. Our compassion for the plight of strangers may drop of at a number equivalent to the number of people with who we can be friends, a number to which we unconsciously relate. Whether or not we solve this intellectual question, it remains a curious fact that the larger a tragedy is, the more likely human faces are to become faceless numbers.
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