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How Social Networks Help Foster Genocide
Doing any networking this week? If you aren't, you probably feel you should. For a generation we've been hearing that rich social lives will find us jobs, get our chores done, preserve our sanity and even make us live longer and healthier lives. In policy jargon, these ties to other people create a major asset—our "social capital." This is why do-gooder organizations promote social capital from Afghanistan to Zimbabwe. Yet social networks have, as this paper puts it, a "dark side." During the Rwandan genocide in 1994, it reports, people with robust social networks were more likely to take part in the massacres. It was their less connected neighbors who abstained.
The paper, in this month's Journal of Conflict Resolution, is based on research conducted in Rwanda in 2009 by its aptonymically named author, Omar Shahabudin McDoom. (The published paper is paywalled, but you can get an earlier version of the entire paper here.) McDoom worked in Tare, a community in southwestern Rwanda, which had 647 households in 1994. In April 1994 its population was about 6 percent Tutsi. Then militant Hutus organized the mass slaughter of the Tutsi throughout the nation. By the time the genocide ended some three months later, slightly more than 6 in every 10 Tutsi in Tare were dead, and about a quarter of the community's adult Hutu men had participated involved in the killing. That made it a fairly typical Rwandan community.
McDoom surveyed 116 Hutu men in Tare about their social ties—37 who had participated in the genocide (which he defined as actually harming another human being, not simply manning a roadblock or passing on messages) and 79 who had refrained from joining the slaughter. (He also interviewed individuals at length about their experiences.) Each of the men who participated in genocide had, on average, 20 social ties. Men who did not kill had markedly smaller networks, with an average of 13 connections each.
This was a general effect—killers and mutilators had generally larger social networks, so they had more ties of all kinds, to both other participants in slaughter and to non-participants. However, we all know not all social ties are alike—connections to parents are different, for instance, than connections to fellow church-goers or co-workers. Did some kinds of connection have more influence?
The answer, McDoom writes of his statistical analysis, is yes: ties of kinship and neighborhood were influential in a way that other social connections weren't. Having relatives who were involved in the killing increased the odds that any given man would have participated himself. And close kin ties (parents, brothers, sisters, children) had more impact than more distant forms of family relation. On the other hand, for any given individual, having more neighbors in a social network increased the odds of his having participated—whether or not the neighbors did. McDoom thinks this might reflect the difference between types of ties—neighbors might simply be efficiently passing along information (the more neighbors, the more news you get about the massacres and your potential to join in) while family might influence each other with their actions (if my uncle took part, then why not me?). Other kinds of social connection had no particular influence on their own, though having more ties in general made a man more likely to join in the killing.
So what is it about social networks that makes them helpful to genocidal killers? McDoom thinks there are three traits that matter. First, networks spread information. Following the assassination of Rwanda's Hutu President Juvénal Habyarimana on April 6, 1994, hardline Hutus broadcast their anti-Tutsi call to arms via social ties. Almost all the Rwandans in McDoom's survey had received that message via word of mouth, not radio or other media. For example, several interviewees mentioned a local politician named Rekeraho, who'd been cooperative with Tutsi during the first days of the crisis. But after attending a political meeting in the nearby town of Butare, this man came back to Tare with the message that the Tutsi were the enemy. In other words, McDoom writes, Rekeraho acted as the node between one network, in a nearby large town, and the more peripheral network of Tare.
Secondly, social networks in Tare were tools for recruiting killers. The organizers of the genocide naturally used their social networks (friends, relatives neighbors, fellow churchgoers) to find men to take part in the killing.
Finally, social networks were an effective means of spreading the material rewards of the genocide to the killers, and (to a lesser extent) shaming and punishing those who did not join in. This mattered because money or some material gain was the most common motivation people ascribed to the killers in the interviews McDoom did to supplement his analysis. As one of his subjects put it: "In the first few days people went by force. But later they went willingly because they saw they could get property like roofing tiles and mattresses."
As ever in social science, the question of causality is not entirely settled. Perhaps McDoom got his results because people inclined to kill formed social ties to like-minded folk—in other words, their inclination to kill shaped their networks, rather than their networks shaping their inclination to kill.
For that to be true, though, then the perpetrators' social contacts should have been made up mostly of other perps. Instead, McDoom notes, the killers' social networks were full of both participants in mass killing and non-participants. Killers had larger social networks than non-killers, but the people in their networks were not like-minded. Moreover, as he writes, if each man's social network was created by "birds of a feather" flocking together, then the links people choose—friends, spouses, church, political ties—should have been most influential. It is in those voluntary links, after all, that the birds find one another. However, he found that social connections people don't choose — family, neighbors—had the most influence.
Now, it's not news that, as McDoom puts it "social networks and social ties, the sources of social capital, have a dark side." The mafia and al-Qaeda are both dense social networks, after all. Robert Putnam, whose Bowling Alone did so much to spread the idea that social capital matters, pointed out in that book that some social ties (the sort that bind people within their own group) do not promote harmony across ethnic or other boundaries, and in fact can do the opposite.
Still, while the influence of social networks has been invoked to explain the spread of good and bad habits, from voting to overeating, they haven't been much used to understand violence. In the field of genocide research, the debate still tends to focus on individuals. Some search for the key traits that make one person more prone to engage in genocidal acts. (Here is an example.) This hasn't gone so well; people with the supposedly crucial trait keep turning up as both killers and non-killers. This leads others to maintain that the killers are no different than anyone else, and so look for large-scale political, economic or ecological explanations. If we can't find some psychological indicator, the cause must be some force that effects everyone. (The Rwanda genocide has been blamed on the country's high population density and its farming methods, for example.) Yet these explanations also falter before the variety of people's responses: Why are some people affected by the general force and others immune?
A network approach, McDoom suggests, provides a new level of analysis—finer-grained than some nation-wide explanation but more realistic than a theory that looks at each person in isolation. Perhaps there, in the details of their relationships, we can find the reason one neighbor will take part in murder while another refuses. Such an understanding could provide tools for disrupting networks that are facilitating mass violence, or at least point to who is most vulnerable to the temptation to kill. And it would get us to stop thinking that social capital is inherently a good thing.
McDoom, O. (2013). Antisocial Capital: A Profile of Rwandan Genocide Perpetrators' Social Networks Journal of Conflict Resolution, 58 (5), 865-893 DOI: 10.1177/0022002713484282
Illustration: Skulls at the Genocide Memorial, Nyamata, Rwanda. Via Wikimedia.
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Innovation in manufacturing has crawled since the 1950s. That's about to speed up.
Health officials in China reported that a man was infected with bubonic plague, the infectious disease that caused the Black Death.
- The case was reported in the city of Bayannur, which has issued a level-three plague prevention warning.
- Modern antibiotics can effectively treat bubonic plague, which spreads mainly by fleas.
- Chinese health officials are also monitoring a newly discovered type of swine flu that has the potential to develop into a pandemic virus.
Bacteria under microscope
needpix.com<p>Today, bubonic plague can be treated effectively with antibiotics.</p><p style="margin-left: 20px;">"Unlike in the 14th century, we now have an understanding of how this disease is transmitted," Dr. Shanthi Kappagoda, an infectious disease physician at Stanford Health Care, told <a href="https://www.healthline.com/health-news/seriously-dont-worry-about-the-plague#Heres-how-the-plague-spreads" target="_blank">Healthline</a>. "We know how to prevent it — avoid handling sick or dead animals in areas where there is transmission. We are also able to treat patients who are infected with effective antibiotics, and can give antibiotics to people who may have been exposed to the bacteria [and] prevent them [from] getting sick."</p>
This plague patient is displaying a swollen, ruptured inguinal lymph node, or buboe.
Centers for Disease Control and Prevention<p>Still, hundreds of people develop bubonic plague every year. In the U.S., a handful of cases occur annually, particularly in New Mexico, Arizona and Colorado, <a href="https://www.cdc.gov/plague/faq/index.html" target="_blank">where habitats allow the bacteria to spread more easily among wild rodent populations</a>. But these cases are very rare, mainly because you need to be in close contact with rodents in order to get infected. And though plague can spread from human to human, this <a href="https://www.healthline.com/health-news/seriously-dont-worry-about-the-plague#Heres-how-the-plague-spreads" target="_blank">only occurs with pneumonic plague</a>, and transmission is also rare.</p>
A new swine flu in China<p>Last week, researchers in China also reported another public health concern: a new virus that has "all the essential hallmarks" of a pandemic virus.<br></p><p>In a paper published in the <a href="https://www.pnas.org/content/early/2020/06/23/1921186117" target="_blank">Proceedings of the National Academy of Sciences</a>, researchers say the virus was discovered in pigs in China, and it descended from the H1N1 virus, commonly called "swine flu." That virus was able to transmit from human to human, and it killed an estimated 151,700 to 575,400 people worldwide from 2009 to 2010, according to the Centers for Disease Control and Prevention.</p>There's no evidence showing that the new virus can spread from person to person. But the researchers did find that 10 percent of swine workers had been infected by the virus, called G4 reassortant EA H1N1. This level of infectivity raises concerns, because it "greatly enhances the opportunity for virus adaptation in humans and raises concerns for the possible generation of pandemic viruses," the researchers wrote.
So far, 30 student teams have entered the Indy Autonomous Challenge, scheduled for October 2021.
- The Indy Autonomous Challenge will task student teams with developing self-driving software for race cars.
- The competition requires cars to complete 20 laps within 25 minutes, meaning cars would need to average about 110 mph.
- The organizers say they hope to advance the field of driverless cars and "inspire the next generation of STEM talent."
Indy Autonomous Challenge<p>Completing the race in 25 minutes means the cars will need to average about 110 miles per hour. So, while the race may end up being a bit slower than a typical Indy 500 competition, in which winners average speeds of over 160 mph, it's still set to be the fastest autonomous race featuring full-size cars.</p><p style="margin-left: 20px;">"There is no human redundancy there," Matt Peak, managing director for Energy Systems Network, a nonprofit that develops technology for the automation and energy sectors, told the <a href="https://www.post-gazette.com/business/tech-news/2020/06/01/Indy-Autonomous-Challenge-Indy-500-Indianapolis-Motor-Speedway-Ansys-Aptiv-self-driving-cars/stories/202005280137" target="_blank">Pittsburgh Post-Gazette</a>. "Either your car makes this happen or smash into the wall you go."</p>
Illustration of the Indy Autonomous Challenge
Indy Autonomous Challenge<p>The Indy Autonomous Challenge <a href="https://www.indyautonomouschallenge.com/rules" target="_blank">describes</a> itself as a "past-the-post" competition, which "refers to a binary, objective, measurable performance rather than a subjective evaluation, judgement, or recognition."</p><p>This competition design was inspired by the 2004 DARPA Grand Challenge, which tasked teams with developing driverless cars and sending them along a 150-mile route in Southern California for a chance to win $1 million. But that prize went unclaimed, because within a few hours after starting, all the vehicles had suffered some kind of critical failure.</p>
Indianapolis Motor Speedway
Indy Autonomous Challenge<p>One factor that could prevent a similar outcome in the upcoming race is the ability to test-run cars on a virtual racetrack. The simulation software company Ansys Inc. has already developed a model of the Indianapolis Motor Speedway on which teams will test their algorithms as part of a series of qualifying rounds.</p><p style="margin-left: 20px;">"We can create, with physics, multiple real-life scenarios that are reflective of the real world," Ansys President Ajei Gopal told <a href="https://www.wsj.com/articles/autonomous-vehicles-to-race-at-indianapolis-motor-speedway-11595237401?mod=e2tw" target="_blank">The Wall Street Journal</a>. "We can use that to train the AI, so it starts to come up to speed."</p><p>Still, the race could reveal that self-driving cars aren't quite ready to race at speeds of over 110 mph. After all, regular self-driving cars already face enough logistical and technical roadblocks, including <a href="https://www.bbc.com/news/technology-53349313#:~:text=Tesla%20will%20be%20able%20to,no%20driver%20input%2C%20he%20said." target="_blank">crumbling infrastructure, communication issues</a> and the <a href="https://bigthink.com/paul-ratner/would-you-ride-in-a-car-thats-programmed-to-kill-you" target="_self">fateful moral decisions driverless cars will have to make in split seconds</a>.</p>But the Indy Autonomous Challenge <a href="https://static1.squarespace.com/static/5da73021d0636f4ec706fa0a/t/5dc0680c41954d4ef41ec2b2/1572890638793/Indy+Autonomous+Challenge+Ruleset+-+v5NOV2019+%282%29.pdf" target="_blank">says</a> its main goal is to advance the industry, by challenging "students around the world to imagine, invent, and prove a new generation of automated vehicle (AV) software and inspire the next generation of STEM talent."
A new Harvard study finds that the language you use affects patient outcome.
- A study at Harvard's McLean Hospital claims that using the language of chemical imbalances worsens patient outcomes.
- Though psychiatry has largely abandoned DSM categories, professor Joseph E Davis writes that the field continues to strive for a "brain-based diagnostic system."
- Chemical explanations of mental health appear to benefit pharmaceutical companies far more than patients.
Challenging the Chemical Imbalance Theory of Mental Disorders: Robert Whitaker, Journalist<span style="display:block;position:relative;padding-top:56.25%;" class="rm-shortcode" data-rm-shortcode-id="41699c8c2cb2aee9271a36646e0bee7d"><iframe type="lazy-iframe" data-runner-src="https://www.youtube.com/embed/-8BDC7i8Yyw?rel=0" width="100%" height="auto" frameborder="0" scrolling="no" style="position:absolute;top:0;left:0;width:100%;height:100%;"></iframe></span><p>This is a far cry from Howard Rusk's 1947 NY Times editorial calling for mental healt</p><p>h disorders to be treated similarly to physical disease (such as diabetes and cancer). This mindset—not attributable to Rusk alone; he was merely relaying the psychiatric currency of the time—has dominated the field for decades: mental anguish is a genetic and/or chemical-deficiency disorder that must be treated pharmacologically.</p><p>Even as psychiatry untethered from DSM categories, the field still used chemistry to validate its existence. Psychotherapy, arguably the most efficient means for managing much of our anxiety and depression, is time- and labor-intensive. Counseling requires an empathetic and wizened ear to guide the patient to do the work. Ingesting a pill to do that work for you is more seductive, and easier. As Davis writes, even though the industry abandoned the DSM, it continues to strive for a "brain-based diagnostic system." </p><p>That language has infiltrated public consciousness. The team at McLean surveyed 279 patients seeking acute treatment for depression. As they note, the causes of psychological distress have constantly shifted over the millennia: humoral imbalance in the ancient world; spiritual possession in medieval times; early childhood experiences around the time of Freud; maladaptive thought patterns dominant in the latter half of last century. While the team found that psychosocial explanations remain popular, biogenetic explanations (such as the chemical imbalance theory) are becoming more prominent. </p><p>Interestingly, the 80 people Davis interviewed for his book predominantly relied on biogenetic explanations. Instead of doctors diagnosing patients, as you might expect, they increasingly serve to confirm what patients come in suspecting. Patients arrive at medical offices confident in their self-diagnoses. They believe a pill is the best course of treatment, largely because they saw an advertisement or listened to a friend. Doctors too often oblige without further curiosity as to the reasons for their distress. </p>
Image: Illustration Forest / Shutterstock<p>While medicalizing mental health softens the stigma of depression—if a disorder is inheritable, it was never really your fault—it also disempowers the patient. The team at McLean writes,</p><p style="margin-left: 20px;">"More recent studies indicate that participants who are told that their depression is caused by a chemical imbalance or genetic abnormality expect to have depression for a longer period, report more depressive symptoms, and feel they have less control over their negative emotions."</p><p>Davis points out the language used by direct-to-consumer advertising prevalent in America. Doctors, media, and advertising agencies converge around common messages, such as everyday blues is a "real medical condition," everyone is susceptible to clinical depression, and drugs correct underlying somatic conditions that you never consciously control. He continues,</p><p style="margin-left: 20px;">"Your inner life and evaluative stance are of marginal, if any, relevance; counseling or psychotherapy aimed at self-insight would serve little purpose." </p><p>The McLean team discovered a similar phenomenon: patients expect little from psychotherapy and a lot from pills. When depression is treated as the result of an internal and immutable essence instead of environmental conditions, behavioral changes are not expected to make much difference. Chemistry rules the popular imagination.</p>