“…like the ENTIRE SOCIETY was a 16 YEAR OLD GIRL…” [AUDIO]
by Ellen Horne / 2007
When Laughter (Almost) Kills
by Jim Cofer / February 17th, 2008
“Laughter is the best medicine, or so the old saying goes. But what if laughter wasn’t the best medicine? What if laughter was the disease? It all started in a boarding school in Tanganyika in January of 1962. These were heady times for the nation on Africa’s east coast: the country had only received its independence from Britain a few weeks previously, and it had yet to merge with Zanzibar to form the modern nation of Tanzania. Perhaps the joy of independence or the stress of what the future might hold was just too much. No one, it seems, will ever know for sure what the root cause of the epidemic was. All that’s known for sure is that someone told someone else a joke at an all-girls boarding school at Kashasha village on the morning of January 30, 1962. The three students involved in the joke became subject to uncontrollable fits of laughter, sometimes lasting only a few minutes, other times lasting as long as 16 hours. Since laughter is, in some sense, contagious, the laughter fits quickly spread to 95 of the school’s 159 students. The attacks left no permanent injuries, but the laughter fits did mean that few students could learn anything, so the school was shut down on March 18th.
As soon as the Kashasha school closed, all of the students went home… and the laughter epidemic spread across the region, almost exactly as it would in one of those [contagion] maps in a Hollywood movie. Within 10 days of the school’s closure, 217 of the 10,000 people in the village of Nshamba, home to several of the boarding school girls, came down with the “laughing disease”. Several girls that attended a school in Ramashenye but lived near some of the girls from Kashasha infected their own school; within a couple of weeks, 48 of the 154 students there became “infected” and the school was shut down in mid-June. One of the girls that attended the Ramashenye school went back to her home in Kanyangereka when the school closed and promptly “infected” several members of her own family, who in turn “infected” other villagers, who in turn “infected” people from other villages, causing two more schools to close. The “infection” would prove to be tough to eradicate at Kashasha school: after re-opening on May 21st, 57 additional students rapidly became “infected” and the school was shut down again in June.
By the time the “disease” finally ran its course in June 1964, the laughter epidemic had “infected” around 1,000 people and caused the closure of 14 schools in the area. Just like a “real” epidemic, the only effective preventative measure seemed to be quarantining villages yet to be touched by the disease. Scientists, both then and now, have been able to conclusively rule out any biological or environmental cause of the “disease”. Whatever it was, the epidemic was not caused by a virus or bacteria, or some chemical in the food supply or environment. There is no historical mention of a similar disease in the area, nor is there any word for it in any of the indigenous languages. In fact, scientists were completely puzzled by the initial spread of the “disease” at the Kashasha school. The girls lived in a dormitory-style arrangement there, yet the “disease” didn’t seem to follow any of the known rules of modern pathology. Girls that shared rooms with “infected” students didn’t necessarily become infected themselves. The disease didn’t follow any known pattern of friendship or location.
Once the disease left the school, however, a pattern became clear: adolescent females at mission-run schools were first to be infected. They would then take the disease home to infect their mothers and other female relatives. Young boys appeared to be somewhat susceptible to the disease, however adult men appeared to be completely immune to the epidemic. There is also not a single instance of a “person of stature” in the community – policemen, doctors or schoolteachers, either male or female – becoming infected. Europeans and other Westerners seemed to have immunity, too. In fact, the disease seemed to follow a strict path along tribal and familial lines. If a female relative, a male relative, and a complete stranger of either gender were locked in a room with an “infected” person, the disease would probably infect the female relative, possibly infect the male, and would almost never infect the stranger.”
from the CENTRAL AFRICAN MEDICAL JOURNAL, 1963
Posted by Ellen Horne / May 31, 2007
An Epidemic of Laughing in the Bukoba District of Tanganyika
by A. M. Rankin (Department of Medicine, Maskerere University College)
and P.J. Philip (Medical Officer, Bukoba, Tanganyika)
An epidemic disease is defined as one that “is prevalent among a people or a community at a special time and produce by some special causes not generally present in the affected community” (MacNaulty, 1961). As the commoner epidemics are caused by the spread of viruses, bacteria, or parasites, there is a tendency to forget that abnormal emotional behaviour may spread from person to person and so take on an epidemic form. It is purpose of this communication to report and epidemic in the Bukoba district of north-west Tanganyika. The epidemic was characterized by episodes of laughing and crying. It is not only of interest from the sociological aspect but as it has disrupted the normal life of the community for six months, it is of considerable public health importance.
The disease commenced on 30th January, 1962 at a mission-run girls’ middle school at Kashasha village, 25 miles from Bukoba (see map). From that date until the 18th March, 1962, when the school was forced to close down, 95 of the 159 pupils had been affected. Fifty-seven pupils were involved from the 21st May, when the school was re-opened, until it was again shut at the end of June. The spread of the disease to other areas is described below. Kashasha school is a barding school for girls between the ages of 12 and 18 years of age. The pupils sleep in dormitories where their ages are evenly distributed. The disease spread in a haphazard manner and did not involve the majority of the pupils in one dormitory at any one time. On the 30th January, three pupils commenced to act in an abnormal manner, and the disease rapidly spread through the school. None of the teaching staff which consists of two Europeans and three Africans was affected.
The clinical picture has varied slightly from place to place, but it is basically the same. Most of the victims have been adolescent school girls and school boys, though adult males and females have also been involved. No literate and relatively sophisticated members of society have been attacked. The patient has had some very recent contact with someone suffering from the disease. The incubation period is from a few hours to a few days. The onset is sudden, with attacks of laughing and crying lasting for a few minutes to a few hours, followed by a respite and then a recurrence. The attack is accompanied by restlessness and on occasions violence when restraint is attempted. The patient may say that things are moving around in the head and that she fears that someone is running after her. The examination is notable for the absence of abnormal physical signs. No fever was detected, although some reported that they had had fever after a few days. The only abnormalities found were in the central nervous system. The pupils were frequently more dilated than controls, but always reacted to light. The tendon reflexes in the lower limbs were frequently exaggerated. There were no tremors or fits or losses of consciousness. The neck was not stiff.
Course Of The Disease
No fatal cases have been reported. Symptoms have lasted from several hours in a few cases up to a maximum of 16 days. During this time the patient is unable to perform her normal duties and is difficult to control. The majority of those affected have had more than one attack separated by a period of normality. The maximum number of attacks was four. No serious sequelae have been reported. However school teachers state that for several weeks after the recovery the girls are unable to attend well to their lessons.
Subsequent Spread Of The Disease
About 10 days after the Kashasha school was closed for the first time and pupils sent home, the disease broke out at Nshamba village complex, 55 miles west of Bukoba. Several of the sick girls from Kashasha came from this village. During April and May, 217 people out of a total 10,000 were attacked. The majority of these were young adults of both sexes and the remainder school children. All the patients recovered and the disease has apparently died out in this area. Ramashenye girls’ middle school is situated on the outskirts of Bukoba. Between 10th and 18th June, when the school was forced to close, 48 girls were attacked out of a total of 154. Girls from Kashasha suffering from the disease had recently been sent to their homes in the vicinity of the Ramashenye school. A further outbreak occurred in the village of Kanyangereka, 20 miles from Bukoba on the 18th June. A pupil from Ramashenye school had been sent home to this village on the 17th, as she was impossible to control at the school. The outbreak in her village occurred in her immediate family, with involvement of the sister (16), brother (9) and mother-in-law, (18). The sister-in-law of the father walked 10 miles to see how the sick school girl was and within a few hours was also laughing and violent. Other people in the village soon became affected and the two boys’ schools 10 miles away were forced to close down. No case involving village headman, policemen, school teachers, or people of similar educational background was found. At the time of writing this paper the disease is spreading to other villages, the education of the children is being seriously interfered with and there is considerable fear among the village communities.
Investigations were carried out to determine if the disease had an infections, toxic, or psychological aetiology. Lumbar puncture was carried out in 17 cases and biochemical, bacteriological and microscopic examination showed no abnormality. Virus studies were done with the help of the Virus Research Institute at Entebbe. Blood taken from 15 active cases failed to grow and virus and no viral antibodies were found either in those who had recovered from the disease or in the people who had not been affected. An attempt was made to find a common food factor that might contain a toxic substance capable of producing the clinical picture. The water supplies varied from rainwater collected in sealed tanks at the Kashasha school to local wells and streams at smaller villages. Kashasha school obtained their Matoke bananas, beans and meat from nearby villages, where no cases of the disease had been reported. Maize flour for Kashasha and Ramashenye schools is purchased in Bukoba but is manufactured in the area south of Lake Victoria. Bukoba hospital and several schools that have not been attacked by the disease are supplied with the same flour. This applies to ground nuts. Sample of maize flour and ground nuts were examined macroscopically for evidence of contamination with extraneous seeds but none could be detected.
Evidence was sought that this was a manifestation of hysteria in an epidemic form. There is no record of a similar epidemic occurring in the area before and thus there is no traditional name for it. The Bahaya, who form the bulk of the population, are calling it either “Enwara Yokusheka” (the illness of laughing) or “Akajanja” which means madness. No relevant information could be obtained from the pupils at Kashasha school who were originally affected, despite the fact that these investigations were done by a Muhaya education officer. In Bukoba township, where the disease has aroused great interest, there is a belief that the atmosphere has been poisoned as a result of the atom bomb explosions. Others believe that someone has poisoned the maize flour. (Maize is not eater to any extent by the villages, who eat a basic diet of matoke. Most schools and hospitals, however, provide a basic diet of maize flour, as it is a much cheaper commodity.) Many of the patients say that they are frightened of something, but do not give any further information. They appear to fear that someone is chasing them. There is a definite belief that this is a contagious condition of some kind. One villager described it as a spreading madness. A milder outbreak with similar symptoms occurred near Mbarara, in Uganda, about 100 miles north of Bukoba. It started in February and involved about 60 pupils in a primary school. The disease has since ceased there.
The mode of spread of this disease would seem to be from person to person. In most instances it was possible to trace recent contact with someone exhibiting the same symptoms. This might suggest a virus disease spread by droplet infection. The results of the laboratory examination, the lack of abnormal signs on the physical examination and the fact that the majority of the patients had more than one attack of the disease are against an infectious aetiology. Contamination of food by toxic substances is possible explanation. Seeds of Datura Stramonium contaminating wheat and maize flour have been responsible for epidemics of food poisoning in East Africa (Anderson et al, 1944; Raymond 1944). This disease begins soon after eating posho made from the flour contaminated with the seeds and bears a superficial resemblance to the present syndrome. However, the dry mouth, fixed and dilated pupils and the muscular inco-ordination found in datura poisoning were not seen in Bukoba. Also symptoms only last a few hours as opposed to the average of seven days with the illness under discussion. No food factor which was peculiar to the people attacked has been found. No foreign seeds were found in the maize samples taken. A toxic food factor could not explain the spread of the disease from one person to another.
The third possibility of mass hysteria seems the most likely explanation. We are at a loss to explain why the disease first started. Close questioning of the girls involved has failed to produce any reasons for the initial attack. Once started, this mass hysteria could spread without the original precipitating factors being present. The middle ages in Europe produced several epidemics of mass hysteria, of which the dancing manias of Germany and Italy are the best known (Major, 1954.) These followed on the Black Death and are assumed to be a product of the dislocation of normal life caused by the plague.
Hecker (1844) describes the following example of how the tendency to sympathy and imitation increases under excitement: “In a Lancashire cotton shop in 1787 a woman worker put a mouse down the neck of a companion who had a dread of mice; the fit which she immediately threw continued with violent convulsions for 24 hours. On the next day three other women had fits and by the fourth no less than 24 people had been affected; among these was a male factory worker so exhausted by restraining the hysterical women that he had caught the illness himself. The disease spread to neighbouring factories because of the fear aroused by a theory that the illness was due to some sort of cotton poisoning.”
In Tanganyika, in the village of Kanyangereka, where most of one family were attacked, a man of 52 years of age living nearby saw these people during their attacks. He was very upset at the sight of their suffering, and soon after returning to his hut, where he lived along, he felt something telling him to laugh and cry and shout. This he continued to do for most of the night.
The type of mental disorder that affects a community is influenced by the culture of this particular community. Examples of this are Amok and Latah in Malaya, Koro in China and Arctic Hysteria in Siberia (Leighton and Hughes, 1961). These authors describe a religious revival in Kentucky, U.S.A. in 1800 where the population became so fearful of their future after death that many began to exhibit jerky movements and to fall down in an apparent state of unconsciousness. Others took to barking like dogs, and this spread from person to person.
This epidemic in Tanganyika of laughing and crying requires further study. In order to interpret this behavior as normal or pathological, a study of the culture context should be made. The Kentucky outbreak followed a pattern similar to the emotional release of the New England revival a few years before. We can find no written or verbal record of this present epidemic having occurred in the Bukoba district previously.
An epidemic of laughing, crying and restlessness in the Bukoba district of Northern Tanganyika is described. The disease commenced in a girls’ school and has since spread to other schools and to villages in the area. No significant abnormal physical signs were found and all laboratory tests were normal. There have been no fatalities. No toxic factor in the food supply was found. It is suggested that this is mass hysteria in a susceptible population. This is probably a culturally determined disease.
MASS PSYCHOGENIC ILLNESS (MPI)
The laughter of the 1962 Tanganyika ‘laughter epidemic’ / Christian
“The present article discusses the role of laughter in the much cited ‘laughter epidemic’ that occurred in Tanganyika in 1962. Despite its extraordinary nature, the veracity of the event is confirmed, crucially on the basis of similar reports. But most current representations are flawed by their exaggeration and misinterpretation of the role of laughter in the event, relating it to a humorous stimulus, a virus or environmental contaminant, or identifying it as contagious laughter. It is argued that the event is a motor-variant case of mass psychogenic illness of which laughter is one common symptom. Therefore it cannot serve as support for other arguments in humor research.”
email : hempelma [at] mac [dot] com
TANGANYIKA INDEPENDENCE TIMELINE
1945-1952: With the end of World War II, the newly formed United Nations changes the legal status of Tanganyika to a “trust territory,” to be steered toward self-governance and independence. In 1946 the colonial administration launches a 10-year development plan that stresses African involvement in the cash economy, education, and the establishment of elected local councils.
1953-1960: British-educated Julius K. Nyerere dominates local politics and advocates independence and egalitarianism. He becomes president of TAA in 1953 and forms the multiracial Tanganyika African National Union (TANU) in 1954. By 1959 TANU-backed candidates win seats in Legislative Council elections, and Britain agrees to internal self-rule with Nyerere as chief minister.
1961-1962: Tanganyika gains independence on December 9, 1961. Nyerere
installs Rashidi Kawawa as prime minister. Kawawa fills his cabinet with TANU loyalists, enacts broad “Africanization” policies throughout the civil service, and centralizes the administration. Nyerere sweeps the 1962 general elections, introduces a republican constitution, and names Kawawa vice president.
FACING the NEW
“The Tanganyika Laughter Epidemic of 1962 was an outbreak of mass psychogenic illness in the vicinity of the village of Kashasha on the western coast of Lake Victoria in the modern nation of Tanzania. Due to its nature the incident has been confused with positive humorous and/or infectious laughter as seen in phenomena like the Holy Laughter movement. The nature of MPI, however, is quite dissimilar to these more purely euphoric experiences.
No-one knows what sparked this incident, but scientists can make reasonable guesses as to why mass psychogenic illness may have affected this part of the world. Independence from Great Britain had been achieved recently, on December 9, 1961, and Kashasha was now part of the nation of Tanganyika (Tanganyika would merge with Zanzibar in 1964, creating the modern nation of Tanzania). Students felt that expectations from their teachers and parents had risen markedly, and said they felt stressed as a result. This could explain the epidemic’s genesis in a boarding school; one cure for MPI is removing sufferers from their current surroundings, impossible without shutting the school down, something which the administrators were surely reluctant to do. The spread of the epidemic, laughter, crying, rashes, and all, among the adult population may signify widespread uncertainty about the future among Tanganyikans. Situated in the northwestern corner of Tanganyika, the region may have been too isolated and insular to allow for a change of location, which allowed the epidemic to spread and last for a great amount of time. The unique characteristics of the Kashasha area, namely its isolation, a significant population, stress among the entire population and especially the boarding school component, combined perhaps with pure chance, probably best explain why the epidemic occurred and how it lasted so long.”
ONGOING RESEARCH : HAPPINESS TRANSMISSIBLE through SOCIAL NETWORKS
How your friends’ friends can affect your mood
BY Michael Bond / 30 December 2008
If you live in the northern hemisphere, this is probably not your favourite month. January tends to dispirit people more than any other. We all know why: foul weather, post-Christmas debt, the long wait before your next holiday, quarterly bills, dark evenings and dark mornings. At least, that is the way it seems. For while all these things might contribute to the way you feel, there is one crucial factor you probably have not accounted for: the state of mind of your friends and relatives. Recent research shows that our moods are far more strongly influenced by those around us than we tend to think. Not only that, we are also beholden to the moods of friends of friends, and of friends of friends of friends – people three degrees of separation away from us who we have never met, but whose disposition can pass through our social network like a virus.
Indeed, it is becoming clear that a whole range of phenomena are transmitted through networks of friends in ways that are not entirely understood: happiness and depression, obesity, drinking and smoking habits, ill-health, the inclination to turn out and vote in elections, a taste for certain music or food, a preference for online privacy, even the tendency to attempt or think about suicide. They ripple through networks “like pebbles thrown into a pond”, says Nicholas Christakis, a medical sociologist at Harvard Medical School in Boston, who has pioneered much of the new work.
At first sight, the idea that we can catch the moods, habits and state of health not only of those around us, but also those we do not even know seems alarming. It implies that rather than being in charge of where we are going in life, we are little more than back-seat drivers, since most social influence operates at a subconscious level. But we need not be alarmed, says Duncan Watts, a sociologist at Columbia University, New York. “Social influence is mostly a good thing. We should embrace the fact that we’re inherently social creatures and that much of who we are and what we do is determined by forces that are outside the little circle we draw around ourselves.” What’s more, by being aware of the effects of social contagion we may be able to find ways to counter it, or use it to our own benefit. “There’s no doubt people can have some control over their networks and that this in turn can affect their lives,” says Christakis.
To get an idea of what is going on, take Christakis’s findings on the spread of happiness, which were published last month. His team looked at a network of several thousand friends, relatives, neighbours and work colleagues who form part of the Framingham Heart Study, an ongoing multi-generational epidemiological survey that has tracked risk factors in cardiovascular disease among residents of Framingham, Massachusetts, since 1948. They found that happy people tend to be clustered together, not because they naturally orientate towards each other, but because of the way happiness spreads through social contact over time, regardless of people’s conscious choice of friends (BMJ,DOI: 10.1136/bmj.a2338). Christakis also found that a person’s happiness is dependent not only on the happiness of an immediate friend but – to a lesser degree – on the happiness of their friend’s friend, and their friend’s friend’s friend. Furthermore, someone’s chances of being happy increase the better connected they are to happy people, and for that matter the better connected their friends and family. “Most people will not be surprised that people with more friends are happier, but what really matters is whether those friends are happy,” says Christakis.
Happiness is near
They also discovered that the effect is not the same with everyone you know. How susceptible you are to someone else’s happiness depends on the nature of your relationship with them. For example, if a good friend who lives within a couple of kilometres of you suddenly becomes happy, that increases the chances of you becoming happy by more than 60 per cent. In contrast, for a next-door neighbour the figure drops to about half that, and for a nearby sibling about half again. Surprisingly, a cohabiting partner makes a difference of less than 10 per cent, which coincides with another peculiar observation about some social epidemics: that they spread far more effectively via friends of the same gender.
All this poses a key question: how can something like happiness be contagious? Some researchers think one of the most likely mechanisms is empathetic mimicry. Psychologists have shown that people unconsciously copy the facial expressions, manner of speech, posture, body language and other behaviours of those around them, often with remarkable speed and accuracy. This then causes them, through a kind of neural feedback, to actually experience the emotions associated with the particular behaviour they are mimicking.
Actions and feelings can be as contagious as a virus
Barbara Wild and her colleagues at the University of Tübingen, Germany, have found that the stronger the facial expression, the stronger the emotion experienced by the person observing it (Psychiatry Research, vol 102, p 109). She believes this process is hard-wired, since it acts so rapidly and automatically.
Others have suggested it works through the action of mirror neurons, a type of brain cell thought to fire both when we perform an action and when we watch someone else doing it, though it is not clear whether the mimicking would cause the neurons to fire or whether their firing would trigger the mimicry. What is clear is that unconscious imitation allows people to “feel a pale reflection of their companions’ actual emotions” and even “feel themselves into the emotional lives of others”, says Elaine Hatfield at the University of Hawaii, Honolulu, whose review of the latest research will appear next April in The Social Neuroscience of Empathy.
There is plenty of evidence for emotional contagion outside the lab. In 2000, Peter Totterdell at the University of Sheffield, UK, found a significant association between the happiness of professional cricketers during a match and the average happiness of their teammates, regardless of other factors such as whether the match was going in the team’s favour (Journal of Applied Psychology, vol 85, p 848). He found a similar effect among nurses and office workers. It has also been shown that if a college student suffers from mild depression their roommate will become progressively more depressed the longer they live with them, and that emotional displays by bank employees have a direct impact on the moods of their customers.
We can see, then, how a phenomenon such as happiness might pass quickly through a social network and infect clusters of friends and relatives. What none of these studies explains, however, is why the strength of the infection varies according to who is passing it to whom. Why are we so much more strongly affected by the happiness of a nearby friend than a nearby sibling? Why does a next-door neighbour have a significant impact, yet someone living a few tens of metres away on the same block have none?
The power of strangers
Two factors appear crucial: the frequency of social contact, and the strength of the relationship. This is not too surprising: we know that emotional contagion requires physical proximity. It is also likely that the closer we feel to someone, the more empathetic we are towards them, and the more likely we are to catch their emotional state. However, how these two factors play out in day-to-day interactions is uncertain. What is also unclear – because it has never been properly tested – is the extent to which emotions can propagate through virtual networks, where the opportunity for physiological mimicry is much reduced.
So much for emotions – what about other phenomena that we unwittingly pick up, and pass on, through our social networks? In 2007, Christakis’s team, again tracking members of the Framingham Heart Study, found that obesity is transmitted in a similar way to happiness. Your risk of gaining weight increases significantly when your friends gain weight, and it is also affected by the weight of people beyond your social horizon. “Obesity appears to spread through social ties,” Christakis says. Again, how likely you are to catch it depends on who you are interacting with: after controlling for factors such as difference in socioeconomic status, the researchers found that an individual’s chances of becoming obese increased by 57 per cent if one of their friends became obese, 40 per cent if a sibling did and 37 per cent if their spouse did, irrespective of age (The New England Journal of Medicine, vol 357, p 370).
However, neighbours have no influence, and how far away you live from a friend counts for little, which implies that obesity spreads via a different mechanism to happiness. Rather than behavioural mimicry, the key appears to be the adoption of social norms. In other words, as I see my friends gain weight, this changes my idea of what an acceptable weight is. One similarity with happiness is that friends and relatives have a far greater influence if they are of the same gender. While it is not evident why that should matter for emotional contagion, norms of body size are clearly gender-specific: “Women look at other women, men look at other men,” says Christakis. This could also help explain the epidemics of eating disorders reported among groups of schoolgirls in recent decades.
The spread of a social norm appears to account for another of Christakis’s findings: that when people stop smoking, they usually do so along with whole clusters of friends, relatives and social contacts. As more people quit, it becomes the socially acceptable thing to do, and those who choose to continue smoking are pushed to the periphery of the network. In this case, people are most strongly influenced by those closest to them – if your spouse quits, it is 67 per cent more likely that you will too. Your work colleagues can also have an effect, particularly if you are in a small, close-knit workplace; and more highly educated friends influence one another more than less educated (The New England Journal of Medicine, vol 358, p 2249).
Happiness, obesity, smoking habits – activities that we traditionally think of as shaped by individual circumstances, turn out to be ruled to a large degree by social forces. Many other day-to-day phenomena fit a similar pattern, often counter-intuitively. Take autism: Peter Bearman at the Institute for Social and Economic Research and Policy at Columbia University who in 2004 uncovered a link between suicidal behaviour and certain friendship patterns (American Journal of Public Health, vol 94, p 89), is looking at whether the recent rise in the diagnosis of autism is in any way socially determined. His study is ongoing, but he says his findings could be “explosive”. “It is likely that if you have an autistic child in your community the probability of your child being diagnosed with autism is significantly higher.” Happiness, obesity, smoking habits – all turn out to be ruled to a large degree by social forces.
Why three degrees?
While the mechanism of social contagion varies depending on the phenomenon being spread, in many cases the dynamics are very similar. For example, Christakis has found that with happiness, obesity and smoking habits, the effect of other people’s behaviour carries to three degrees of separation and no further. He speculates that this could be the case with most or perhaps all transmissible traits. Why three degrees? One theory is that friendship networks are inherently unstable because peripheral friends tend to drop away. “While your friends are likely to be the same a year from now, your friends of friends of friends of friends are likely to be entirely different people,” says Christakis.
This poses the question: what shapes the architecture of our social networks and our position in them? Clearly, many factors contribute: where we live, where we work, family size, education, religion, income, our interests, and our tendency to gravitate towards people similar to us. New research by Christakis’s team, due to be published in the next few weeks, suggests there is also a strong genetic component. The study compared the social networks of identical and fraternal twins, and found that identical twins had significantly more similar social networks than fraternal twins, suggesting the structure of your social network is influenced by your genes. That may not sound remarkable, since personality traits such as gregariousness and shyness clearly play a role in determining how connected we are. But there is much more to it, says Christakis. “It’s not just about having a genetic predilection to be friends with a lot of people, it’s about having a genetic predilection to be friends with a lot of popular people. That’s mysterious: how could our genes determine our actual location in this socio-topological space?”
Answering that should help us understand more about the “collective intelligence” of social networks, which some researchers liken to the flocking of birds – the decision to quit smoking, for example, is no more an isolated move than the decision by a bird in a flock to fly to the left.
Sociologists and others are using mathematical models to test these dynamics to try to understand better what triggers the spread of behaviours. Duncan Watts at Columbia University has shown that seeding localised social groups with certain ideas or behaviours can lead to the ideas cascading across entire global networks. This contradicts the notion – promoted by the author Malcolm Gladwell in The Tipping Point and others – that social epidemics depend on a few key influential individuals from whom everyone else takes their cue. It doesn’t ring true, argues Watts, because such “influentials” typically interact with only a few people. The key for the spread of anything, he says, from happiness to the preference for a particular song, is a critical mass of interconnected individuals who influence one another.
Is there any way to mitigate the effects of such powerful and pervasive social forces? It is unlikely we can ever escape social influence entirely, even if we wanted to. “Even when you’re aware of it, you’re probably susceptible,” says Watts. Still, being aware can help, especially when we are seeking to avoid undesirable behaviours or adopt positive habits. We can be choosy about new friends, seeking out people whose lifestyles we aspire to: if you want to lose weight, for example, join a running club and – most importantly – socialise with its members.
Actually cutting ties with old friends might be a bit drastic, though perhaps spending less time with those whose traits we do not wish to share would be a good idea – lazy people, perhaps, or those inclined to negative thinking. And beware those who hang out with such people even if they do not display their views or behaviours – remember the three degrees of contagion rule. Finally, if you really cannot avoid spending time with certain people whose behaviours or emotional state you would rather not take on board (certain relatives at family gatherings, perhaps), you could always try repressing your natural inclination to mimic their body language and facial expressions, and so limit the contagion effect – though be prepared for them to instinctively cool towards you as a result.
What this game plan amounts to is a kind of subtle social reorientation. We will always be vulnerable to what those around us are doing, so as far as possible make sure you are with the right people. Remember the new adage: we are who we hang out with.
Five tips for a healthier social network
1. Choose your friends carefully.
2. Choose which of your existing friends you spend the most time with. For example, hang out with people who are upbeat, or avoid couch potatoes.
3. Join a club whose members you would like to emulate (running, healthy cooking), and socialise with them.
4. If you are with people whose emotional state or behaviours you could do without, try to avoid the natural inclination to mimic their facial expressions and postures.
5. Be aware at all times of your susceptibility to social influence – and remember that being a social animal is mostly a good thing.
email : christak [at] hcp.med.harvard [dot] edu
email : djw24 [at] columbia [dot] edu
email : provine [at] umbc [dot] edu
The study of laughter provides a novel approach to the mechanisms and evolution of vocal production, perception and social behavior
by Robert Provine / January-February 1996
Consider the bizarre events of the 1962 outbreak of contagious laughter in Tanganyika. What began as an isolated fit of laughter (and sometimes crying) in a group of 12- to 18-year-old schoolgirls rapidly rose to epidemic proportions. Contagious laughter propagated from one individual to the next, eventually infecting adjacent communities. The epidemic was so severe that it required the closing of schools. It lasted for six months.
The Tanganyikan laughter epidemic is a dramatic example of the infectious power of laughter–something that many of us may have experienced in our own lives. Many readers will be familiar with the laugh tracks of television situation comedies—attempts to stimulate contagious laughter in viewers—and the difficulty of extinguishing their own “laugh jags,” fits of nearly uncontrollable laughter. Have you ever been overcome by a comparable urge to chant “hello-hello-hello?” Rather than dismissing contagious laughter as a behavioral curiosity, we should recognize it and other laugh-related phenomena as clues to broader and deeper issues.
Clearly, laughter is a powerful and pervasive part of our lives—an important component of that biobehavioral bedrock of our species known as human nature. Laughter’s significance has been recognized at various times and in various ways by such scientific and philosophical dignitaries as Aristotle, Kant, Darwin, Bergson and Freud. Yet aside from a general appreciation that laughter is good for us—”the best medicine”—and is somehow associated with humor, we know little about laughter itself.
My approach to understanding laughter is one that a visiting extraterrestrial might take were it to encounter a group of laughing human beings. What would the visitor make of the large bipedal animals emitting paroxysms of sound from a toothy vent in their faces? A reasonable approach would be to describe the simplest and most obvious aspects of the noisy behavior: its physical characteristics, the rules that govern its expression, characteristics of the animals emitting the sounds (such as gender), the mechanism of sound production, and whether similar sounds are made by related species. To Earthlings this naturalistic approach is known as ethology—a biologically oriented scientific discipline devoted to understanding what animals do and how and why they do it. Ethologists treat behavior as an evolutionary adaptation. The species-wide distribution of laughter and its stereotypical (and simple) structure suggests that the behavior has strong genetic and neurophysiological bases—qualities attractive to those who wish to understand the mechanisms and natural history of behavior.
During the past eight years I have been observing human laughter in various natural habitats—shopping malls, classrooms, sidewalks, offices and cocktail parties—with the investigative spirit of our hypothetical alien. Observing everyday behavior in these settings has provided an opportunity to appreciate laughter as a social vocalization of the human animal. These studies have produced some unexpected insights into the phenomenon of human laughter—its social nature, the lawful relationship between laughter and speech, gender differences and the biological basis of contagion.
One of my first goals was to describe the sonic structure of human laughter. This proved to be more difficult than I expected. Like other spontaneous acts, laughter often disappears when one attempts to observe it, especially in the laboratory. Some unconventional approaches were called for. Although I could occasionally elicit laughter from friends and colleagues during playful conversations, I was often forced to engage in shameless hamming (something that graduate school did not prepare me for). One of the most productive approaches was to encounter people in public places and simply ask them to laugh. The request was usually answered with a burst of laughter. About half of the laughing subjects reported that they could not laugh on command. Indeed, we have much less conscious control over laughter than over speech. It is easy to say “ha-ha-ha,” but difficult to laugh on cue. We do not “speak” laughter.
In collaboration with an undergraduate assistant, Yvonne Yong, I took the recordings to the Sound Laboratory of the National Zoo in Washington, D.C. Here the laughs were analyzed with a sound spectrograph, a device that translates a sound into an image that reveals the changes in frequency and intensity of the sound over time. Giggles, shrieks and belly laughs replaced the laboratory’s usual sonic fare of indigo bunting songs and the calls of golden lion tamarins. Laboratory workers gave us quizzical looks but politely refrained from asking about the origins of the sounds.
The sound spectra revealed the distinct signature of laughter. A laugh is characterized by a series of short vowel-like notes (syllables), each about 75 milliseconds long, that are repeated at regular intervals about 210 milliseconds apart. A specific vowel sound does not define laughter, but similar vowel sounds are typically used for the notes of a given laugh. For example, laughs have the structure of “ha-ha-ha” or “ho-ho-ho,” but not “ha-ho-ha-ho.” There are intrinsic constraints against producing such laughs. Try to simulate a “ha-ho-ha-ho” laugh—it should feel quite unnatural. When there are variations in the notes, they most often involve the first or last note in a sequence. Thus, “cha-ha-ha” or “ha-ha-ho” laughs are possible variants.
The explosively voiced blasts of a laugh have a strong harmonic structure, with each harmonic being a multiple of a low (fundamental) frequency. The harmonic structure is revealed in a sound spectrogram by the evenly spaced stacks of short horizontal lines in the spectrum, the lowest of which is the fundamental frequency. Given their higher-pitched voices, it is not surprising that the laughter of females has a higher fundamental frequency (about 502 hertz) than male laughter (about 276 hertz). Whether it is a deep belly laugh or a high-pitched titter, however, all human laughter is a variation of this basic form. It is this structure that allows us to recognize laughter in spite of individual differences.
The notes and internote intervals carry most of the information that allows us to identify a sound as laughter. If the sounds between laugh notes are edited out of a tape recording—leaving the notes separated by intervals of silence—a laugh still sounds normal. The internote time interval carries information, but the internote expiratory sounds do not. If the notes are removed from a recording and the gaps between
intervals are closed, all that remains of laughter is a long, breathy sigh.
The stereotypic structure of a laugh is, at least in part, a result of the limitations of our vocal apparatus. It is difficult to laugh with abnormally long note durations, such as “haaa-haaa-haaa,” or abnormally short durations (much less than 75 milliseconds in length). Likewise, normal note durations with abnormally long or short internote intervals do not occur. Try to produce a natural laugh with a long internote interval, such as “ha——————ha——————ha.” As with the natural rhythms of walking or running, there are only so many ways to laugh.
The structural simplicity of a laugh is also suggested by its reversibility. A short segment of laughter—”ha-ha-ha”—played backward on a tape recorder still sounds rather like “ha-ha-ha.” Indeed the sound spectrum of a laugh is similar whether scanned from left to right or from right to left—a laugh note has a high degree of temporal symmetry. Yet one aspect of a laugh that is not symmetrical is its loudness. Laughter is characterized by a decrescendo in which the laugh notes that are late in a sequence are usually lower in amplitude than earlier notes (presumably because we run out of air). Recordings of laughter played backward produce a bizarre-sounding crescendo.
There is a common misperception that laughter is exclusive to human beings. From at least the time of Darwin, however, it has been known that chimpanzees and other great apes perform a laugh-like vocalization when tickled or during play. To pursue the details of this primate laughter, I teamed up with Kim Bard, who is nursery director and caregiver for young chimpanzees at the Yerkes Regional Primate Center in Atlanta. It is a pleasure to be able to play with young chimpanzees in the pursuit of one’s science.
Chimpanzee (Pan troglodytes) laughter differs in many ways from its human counterpart. The vowel-like notes of human laughter are performed by chopping a single expiration, whereas chimpanzee laughter is a breathy panting vocalization that is produced during each brief expiration and inspiration. Unlike human laughter, the laughter of a chimpanzee lacks discrete, vowel-like notes that have sharp leading and trailing edges on sound spectra. Chimpanzee laughter has the sound and cadence of a handsaw cutting wood. The sounds of chimpanzee and human laughter are sufficiently different that without viewing the characteristic “play face” and source of stimulation (such as play and tickle), naive human beings may be unable to identify the chimpanzee
vocalization as laughter. You can experience the difference in production between the two forms of laughter by placing a hand on your abdomen and comparing the abdominal pulsations of chimpanzee-like panting with the smoother act of speaking “ha-ha-ha” during a single expiration.
People laugh as we speak. If chimpanzees laugh as they speak, by producing one laugh sound per expiration and inspiration, we have identified an important and previously unrecognized constraint on the evolution of speech and language in chimpanzees and presumably other great apes. The close coupling of laughter to breathing in chimpanzees may be evidence of a more general limitation on these animals to speak. (In contrast to the success of teaching hundreds of signs to chimpanzees, efforts to teach them to speak English have produced meager results.) Indeed, the inability to modulate expiratory airflow may be at least as limiting to speech as the structure of the vocal tracts of nonhuman primates.
Breathy, panting laughter is probably the primal form that dates back to the common ancestor of all great apes and people. Human beings evolved their characteristic laughter after branching from an ancestor in common with chimpanzees (estimated to be around six million years ago, according to DNA hybridization data).
It is noteworthy that chimpanzee laughter occurs almost exclusively during physical contact, or during the threat of such contact, during chasing games, wrestling or tickling. (The individual being chased laughs the most.) Although people laugh when tickled, most adult human laughter occurs during conversation, typically in the absence of physical contact.
Social and Linguistic Context
Laughter is a decidedly social signal, not an egocentric expression of emotion. In the absence of stimulating media (television, radio or books), people are about 30 times more likely to laugh when they are in a social situation than when they are alone. Indeed people are more likely to smile or talk to themselves than they are to laugh when they are alone. Aside from the obvious implication that sociality can enhance laughter and perhaps one’s mood, these observations indicate that laughter has a social function. What can we say about laughter as communication?
In an attempt to gather some clues, my colleagues and I have collected observations on 1,200 instances of naturally occurring human laughter. Three undergraduate assistants (Lisa Greisman, Tina Runyan, Michelle Bowers) and I wandered various public gathering places where we eavesdropped on groups of laughing people. We carefully took note of the principals engaged in the behavior—the gender of the speaker and the audience, whether the speaker or the audience laughed and what was said immediately before the laughter.
Contrary to our expectations we found that most conversational laughter is not a response to structured attempts at humor, such as jokes or stories. Less than 20 percent of the laughter in our sample was a response to anything resembling a formal effort at humor. Most of the laughter seemed to follow rather banal remarks, such as “Look, it’s Andre,” “Are you sure?” and “It was nice meeting you too.” Even our “greatest hits,” the funniest of the 1,200 pre-laugh comments were not necessarily howlers: “You don’t have to drink, just buy us drinks,” “She’s got a sex disorder—she doesn’t like sex,” and “Do you date within your species?” Mutual playfulness, in-group feeling and positive emotional tone—not comedy—mark the social settings of most naturally occurring laughter. Research that focuses only on the response of an audience to jokes (a common laboratory scenario) targets only a small subset of laughter.
One of the key features of natural laughter is its placement in speech. Laughter is not randomly scattered throughout the speech stream. The speaker and the audience seldom interrupt the phrase structure of speech with laughter. In our sample of 1,200 laughs there were only eight interruptions of speech by laughter, all of them by the speaker. Thus a speaker may say “You are going where?… ha-ha,” but rarely “You are going… ha-ha… where?” The occurrence of laughter during pauses at the end of phrases suggests that a lawful and probably neurologically based process governs the placement of laughter in speech—a process in which speech has priority access to the single vocalization channel. The strong and orderly relationship between laughter and speech is akin to punctuation in written communication (and is called the punctuation effect).
Our field study revealed other clues about laughter in human communication. A counterintuitive finding was that the average speaker laughs about 46 percent more often than the audience. This finding reveals the limits of analyses that report only audience behavior—the typical approach of humor research—and neglect the social nature of the laughing relationship.
The gender of the principals involved plays a large role in determining the amount of speaker laughter. Whether they are speakers or audiences (in mixed-sex groups), females laugh more often than males. Female speakers laugh 127 percent more than their male audience. In contrast, male speakers laugh about 7 percent less than
their female audience. Neither males nor females laugh as much to female speakers as they do to male speakers. (The lot of the female comedian is not an easy one—whether her audience is male or female.)
These gender differences in the pattern of laughter are at least as strong as those noted for speech by the linguist Deborah Tannen of Georgetown University. The limited cross-cultural evidence suggests that males are the leading humor producers and that females are the leading laughers. These differences are already present by the time that joking first appears around six years of age.
What message is being conveyed by a laughing speaker or a laughing audience? In some respects laughter may be a signal of dominance/ submission or acceptance/ rejection. Consider the distinction between laughing with and laughing at someone. Valuable insights about laughter’s social function will come from studies of laughter in groups of people who differ in social rank and gender.
A response of laughter by the audience may affirm or negate the spirit of the speaker’s message. “Polite” laughter, for example, may be a forced effort on the part of the audience to signal their accord with the speaker, quite the opposite of the indignant “ha!” A speaker, in other cases, may buffer an aggressive comment with laughter or deliver a remark using “laugh-speak,” a consciously controlled hybrid of laughter and speech. Talk-show hosts, who are experts at shaping the course of a conversation, commonly use laugh-speak. In this sense laughter may modify the behavior of others by shaping the emotional tone of a conversation.
Laugh Tracks and Contagion
The use of laughter to evoke laughter or a positive mood is familiar to viewers of situation comedy shows on television. “Laugh tracks” (dubbed-in sounds of laughter) have accompanied most “sitcoms” since 7:00 p.m. (Eastern Standard Time) on September 9, 1950. On that evening the Hank McCune Show—a comedy about “a likeable blunderer, a devilish fellow who tries to cut corners only to find himself the sucker”—first used a laugh track to compensate for the absence of a live audience. Despite the fact that the show was short-lived, the television industry discovered the power of laughter to evoke audience laughter. The recording industry recognized the seductive power of laughter shortly after World War I with the distribution of the OKeh Laugh Record, which consisted of trumpet playing that was intermittently interrupted by laughter. It remains one of the most successful novelty records of all time. Acknowledging the commercial potential of this novelty market, Louis Armstrong, Sidney Bechet, Woody Herman and Spike Jones all attempted to cash in with laugh records of their own.
In the intervening years social scientists have confirmed that laugh tracks do indeed increase audience laughter and the audience’s rating of the humorousness of the comedy material. However, scientists did not consider that, in the absence of a joke or a remark, laughter by itself can evoke laughter. This is a key element in the propagation of contagious laughter. I recently performed some investigations of the phenomenon of contagious laughter in an undergraduate psychology classroom. The stimulus was a “laugh box”—a small battery-operated record player from a novelty store—that emitted an 18-second span of laughter. The “canned” laughter was played 10 times, with the beginning of each segment separated by a one-minute interval.
On the first stimulus nearly half of the students reported that they responded with laughter themselves. (More than 90 percent reported smiling on the first stimulus.) However, the effectiveness of the stimulus declined with each repetition until only 3 of the 128 students laughed on the tenth trial. By that point about 75 percent of the students rated the laugh stimulus as “obnoxious.”
The negative effect of the repeated stimulus seems to go beyond the response expected from the recurrent exposure to a generic auditory stimulus, such as “Hello, my name is George.” The reaction may reflect the deep biological significance of laughter, which in this case may be perceived as jeering or ridicule. (Colleagues whose offices adjoin my own can attest to the aversiveness of periodic canned laughter. Personally, I find myself wincing every time one of the laugh boxes in my office is accidently activated.) Certainly it is pleasurable to laugh at or with people, but it is quite unpleasant to be laughed at, or to be the recipient of a scornful “ha.” Court fools and presidential aides learn early in their careers that it is safer to laugh with the boss than at him or her.
The efficacy of laughter alone to elicit laughter raises the intriguing possibility that human beings have auditory “feature detectors”—neural circuits that respond exclusively to this species-typical vocalization. In turn, the feature detector triggers the neural circuits that generate the stereotyped action pattern of laughter. This mechanism, involving a laugh detector that drives a laugh generator, may be the foundation of contagious laughter. (Contagious yawning appears to involve a similar process in the visual domain.) Those who attempt to explain away their laugh-evoked (contagious) laughter as nothing more than a response to a “funny” stimulus are saying that they laughed in response to a stimulus that made them laugh, a circular argument.
The structural simplicity and species-typical character of laughter makes it a prime candidate for the evolution of such a laugh detection and releasing process. Future psychophysical studies must determine which of laughter’s parameters—note structure, note duration, internote interval and amplitude dynamics—are necessary for the perception of laughter and the activation of the hypothetical laugh detector or releasing mechanism. Similar detectors may have evolved for universal phonemic features of speech but the variability and complexity of language and the absence of a contagious response to assay the activation of the detectors will make their discovery more difficult.
Now that the critical dimensions of laughter as a social stimulus and motor act have been identified, we can pursue a variety of promising issues. Consider “pathological laughter,” a frequent and often vaguely described medical symptom. Damage to a wide variety of brain regions produces abnormal laughter, a result consistent with the diverse emotional, respiratory, motor, cognitive and communicative aspects of the act. The most common cases of pathological laughter are found in pseudobulbar palsy, gelastic epilepsy and psychiatric illness. However, pathological laughter has also been reported in multiple sclerosis, amyotrophic lateral sclerosis (Lou Gehrig’s disease), and cases of tumors and lesions (especially in the limbic system and the brain stem). Particularly mystifying to both patient and clinician are sudden bursts of laughter that are not associated with a feeling of mirth or an environmental stimulus. Here we have a segregation of the emotional, cognitive and motor mechanisms of laughter. Other cases are more subtle. Some people with forebrain damage have their readjustment to society impeded by a tendency to laugh at almost anything—breaches in laugh etiquette have more serious consequences than one might think. Using our improved descriptive tools, we can now specify more precisely what is “abnormal,” “pathological” or “inappropriate” about these cases (whether it is sonic structure, placement in speech, social context, contagion sensitivity, perception or relation to humor). We may even discover new laugh-related syndromes.
The next time that you or a friend have one beer too many, you may research the age-old question of alcohol effects—while taking careful notes on a cocktail napkin, of course. Do alcohol, “laughing gas” and other drugs known to increase laughter simply lower the threshold for laughter, or do they alter its pattern or quality? In aphasia (a disorder of language production or perception) is there sparing of laughter and, if so, which of laughter’s several dimensions are spared? Does vocal laughter punctuate the signed speech of the congenitally deaf, in whom there is not a shared organ of expression? The left cerebral hemisphere has a specialized role in language—is this also true of the production or perception of laughter?
Many developmental issues remain open. Laughter typically appears in human babies around 3-1/2 to 4 months of age, but we know little about the details of the developmental process. Must babies hear their own laughter or the laughter of others for laughter to mature? If so, is there a critical period during which such laughter must be experienced? The report of laughter in a few congenitally deaf-blind children suggests that at least some features of laughter develop without benefit of auditory and visual stimulation, evidence of a strong maturational and genetic basis. For a more satisfying account of laugh acquisition, we must conduct high-resolution studies that contrast the development of normal and hearing-impaired children.
All of us have encountered people with bizarre-sounding laughter. What is different about such laughter and what does this tell us about the mechanism of normal laugh production? Do these odd types of laughter run in families? If so, what is the nature of its development and heritability? In my otherwise forgettable high-school physics class there was a kid who brayed like a donkey when he laughed. Where is Roger now that I need him?
Comparative studies may provide clues about both the evolution and social function of laughter. Does the low level of conscious control that we have over our own laughter reflect the typical level of control that non-human animals have over their own species-typical vocalizations? Do the great apes show the sexually dimorphic or contagious laughter described in human beings? Does the pattern of laughter vary with rank within a troop? Aside from the great apes, do other animals produce laugh-like vocalizations? How do the neurobehavioral mechanisms of laugh production vary between species? Tickle may be a kind of Rosetta Stone for such comparative laugh research because it triggers laugh-like vocalizations in all of the great apes and perhaps other species. Can you tickle your pet dog or cat? How can you tell? Is a laugh-evoking stimulus that works equally well in a variety of species the ultimate example of “low” humor? Laughter research is still in its infancy, an exciting time when the frontiers are near at hand and accessible with modest resources. Certainly much of the research described in this article can be replicated or extended by almost anyone, making it suitable for college or even high school research projects. Laughter research is a reminder that not all science concerns arcane or narrow problems. We should resist neglecting or trivializing the commonplace. There are rewards for approaching nature with a naive curiosity and attempting to see the familiar in new ways.
It happened. In 1518, People “danced themselves to death” for no obvious reason in Strasbourg, France. One woman started it, and others joined her. Within a month, there were 400 people involved. Many died from pure exhaustion. If 490 years sounds like a long time to wait for an explanation, it’s hardly a simple case. Discovery History’s introduction to the subject is hardly encouraging:
In July of 1518, a woman referred to as Frau Troffea stepped into a narrow street in Strasbourg, France and began a fervent dancing vigil that lasted between four and six days. By the end of the week, 34 others had joined her and, within a month, the crowd of dancing, hopping and leaping individuals had swelled to 400. Authorities prescribed “more dancing” to cure the tormented movers but, by summer’s end, dozens in the Alsatian city had died of heart attacks, strokes and sheer exhaustion due to nonstop dancing.
If that sounds weird, Frau Troffea should have been dead through dehydration after three days, max. Six days, and she was already dead, just still dancing, according to theory. That sort of physical exertion isn’t naturally maintainable. Even marathon runners wouldn’t be able to do it. Some historical corroboration from the profoundly qualified author of a new book doesn’t necessarily help:
Historian John Waller, author of the forthcoming book, “A Time to Dance, A Time to Die: The Extraordinary Story of the Dancing Plague of 1518,” studied the illness at length and has solved the mystery. “That the event took place is undisputed,” said Waller, a Michigan State University professor who has also authored a paper on the topic, which has been accepted for publication in the journal Endeavour. Waller explained that historical records documenting the dancing deaths, such as physician notes, cathedral sermons, local and regional chronicles, and even notes issued by the Strasbourg city council during the height of the boogying rage, all “are unambiguous on the fact that (victims) danced. These people were not just trembling, shaking or convulsing; although they were entranced, their arms and legs were moving as if they were purposefully dancing,” he said.
Possible reason? Stress-induced psychosis. Having suffered severely from famine, and in many cases wiped out and reduced to begging, the region was in an ongoing crisis. Many had died of starvation. The area was riddled with diseases, including smallpox and syphilis. Waller believes the stress was intolerable, and hence a mass psychological illness resulted. It was a superstitious time. From the sound of it, these people didn’t have much left in their lives but superstition.
“Anxiety and false fears gripped the region,” Waller said. One of these fears, originating from a Christian church legend, was that if anyone provoked the wrath of Saint Vitus, a Sicilian martyred in 303 A.D., he would send down plagues of compulsive dancing.
Waller’s theory is interesting, and quite a bit more plausible than other theories, including one that it was caused by ergot fungus, the organic version of LSD. Ergot is extremely poisonous, and it’s far more likely to kill people than start an impromptu dance party among starving people. The fact they were starving, or something like it, makes the dancing even more extraordinary. Where did they get the kilojoules? Perfectly healthy people can be exhausted by a few hours’ dancing, let alone days. There were many other strange plagues which are pretty good supports for the psychological elements of Waller’s idea, including a “laughing epidemic” that went on for 18 months in Tanzania. After all, why should social diseases be purely physical? Just to make the dancing plague a bit more bizarre, there were at least seven other cases of it in the same region during the medieval period, and one in Madagascar in 1840. They’ve even come up with a few ideas for therapy:
According to medical epidemiologist Timothy Jones, an assistant clinical professor of preventative medicine at the Vanderbilt University School of Medicine, who also reported an incident of hysteria in Belgium following soft-drink consumption, “Outbreaks of psychogenic illness are likely to be more common than is currently appreciated, and many go unrecognized.” Jones recommends that physicians treating such problems “attempt to separate persons with illness associated with the outbreak,” conduct tests to rule out other causes, monitor and provide oxygen for hyperventilation, attempt to minimize the individual’s anxiety, notify public health authorities and seek to assure patients that, while their symptoms “are real…rumors and reports of suspected causes are not equivalent to confirmed results.”
DANCING EPIDEMIC of 1518
Dancing Plague’ and Other Odd Afflictions Explained
by Jennifer Viegas
In July of 1518, a woman referred to as Frau Troffea stepped into a narrow street in Strasbourg, France and began a fervent dancing vigil that lasted between four and six days. By the end of the week, 34 others had joined her and, within a month, the crowd of dancing, hopping and leaping individuals had swelled to 400. Authorities prescribed “more dancing” to cure the tormented movers but, by summer’s end, dozens in the Alsatian city had died of heart attacks, strokes and sheer exhaustion due to nonstop dancing. For centuries this bizarre event, known variously as the dancing plague or epidemic of 1518, has stumped scientists attempting to find a cause for the mindless, intense and ultimately deadly dance. Historian John Waller, author of the forthcoming book, “A Time to Dance, A Time to Die: The Extraordinary Story of the Dancing Plague of 1518,” studied the illness at length and has solved the mystery. “That the event took place is undisputed,” said Waller, a Michigan State University professor who has also authored a paper on the topic, which has been accepted for publication in the journal Endeavour. Waller explained that historical records documenting the dancing deaths, such as physician notes, cathedral sermons, local and regional chronicles, and even notes issued by the Strasbourg city council during the height of the boogying rage, all “are unambiguous on the fact that (victims) danced. These people were not just trembling, shaking or convulsing; although they were entranced, their arms and legs were moving as if they were purposefully dancing,” he said.
Eugene Backman, author of the 1952 book “Religious Dances in the Christian Church and in Popular Medicine,” sought a biological or chemical origin for the dancing mania. Backman and other experts at the time believed the most likely explanation was ergot, a mold that grows on the stalks of damp rye. When consumed unknowingly in bread, the mold can trigger violent convulsion and delusions but not, Waller says, “coordinated movements that last for days.” While at Australia’s James Cook University, sociologist Robert Bartholomew proposed a theory that the dancers were performing an ecstatic ritual of a heretical sect, but Waller counters, “there is no evidence that the dancers wanted to dance. On the contrary,” he added, “they expressed fear and desperation,” according to the written accounts.
Praying to St. Vitus
Unusual Events Preceded the Epidemic
A series of famines, resulting from bitter cold winters, scorching summers, sudden crop frosts and terrifying hailstorms, preceded the maniacal dancing, Waller said. Waves of deaths followed from malnutrition. People who survived were often forced to slaughter all of their farm animals, secure loans and finally, take to the streets begging. Smallpox, syphilis, leprosy and even a new disease known as “the English sweat” swept through the area. “Anxiety and false fears gripped the region,” Waller said. One of these fears, originating from a Christian church legend, was that if anyone provoked the wrath of Saint Vitus, a Sicilian martyred in 303 A.D., he would send down plagues of compulsive dancing. Waller therefore believes a phenomenon known as “mass psychogenic illness,” a form of mass hysteria usually preceded by intolerable levels of psychological distress, caused the dancing epidemic.
Ivan Crozier, a lecturer in the Science Studies Unit at the University of Edinburgh, told Discovery News that he “agrees completely” with Waller’s conclusion. “His cultural explanation, combined with a contextualized view of the conditions in which people lived at the time on the Rhine and Mosel, is very convincing and is superior to the arguments about ergot, which is a compound like LSD,” Crozier said. “Ergot gave people visions, not energy to dance,” he added. Crozier is a world authority on yet another mass hysteria epidemic: koro. Since at least 300 B.C., plagues of koro — an irrational male fear that one’s genitals have been stolen or are fatally shrinking into the body — have swept through various parts of the world, particularly throughout Africa and Asia. Most recently, a 1967 outbreak, documented in the Singapore Medical Journal, caused over 1,000 men to use pegs and clamps in hopes of protecting themselves from the gripping fear. “In both cases we see cultural issues impacting on collective behavior,” Crozier said, explaining that preexisting superstitions, fears and beliefs surrounding both koro and the dancing epidemic led to group beliefs turning into “collective action.” Waller explained that victims often go into an involuntary trance state, fueled by psychological stress and the expectation of succumbing to an altered state. “Thus, in groups subject to severe social and economic hardship, trance can be highly contagious,” he said.
More Deadly Dancing, And Laughing
At least seven other outbreaks of the dancing epidemic occurred in medieval Europe, mostly in the areas surrounding Strasbourg. In more recent history, a major outbreak occurred in Madagascar in the 1840’s, according to medical reports that described “people dancing wildly, in a state of trance, convinced that they were possessed by spirits.” Perhaps the most unusual documented case of mass psychogenic illness was the Tanganyika Laughter Epidemic of 1962. A paper published the following year in the Central African Journal of Medicine described what happened. Triggered by a joke among students at a Tanzania boarding school, young girls began to laugh uncontrollably. At first there were spurts of laughter, which extended to hours and then days. The victims, virtually all female, suffered pain, fainting, respiratory problems, rashes and crying attacks, all related to the hysterical laughter. Proving the old adage that laughter can be contagious, the epidemic spread to the parents of the students as well as to other schools and surrounding villages. Eighteen months passed before the laughter epidemic ended.
Curing the Mind
According to medical epidemiologist Timothy Jones, an assistant clinical professor of preventative medicine at the Vanderbilt University School of Medicine, who also reported an incident of hysteria in Belgium following soft-drink consumption, “Outbreaks of psychogenic illness are likely to be more common than is currently appreciated, and many go unrecognized.” Jones recommends that physicians treating such problems “attempt to separate persons with illness associated with the outbreak,” conduct tests to rule out other causes, monitor and provide oxygen for hyperventilation, attempt to minimize the individual’s anxiety, notify public health authorities and seek to assure patients that, while their symptoms “are real…rumors and reports of suspected causes are not equivalent to confirmed results.” Aside from their medical interest, Waller believes such epidemics, particularly those from past centuries, are “of immense historical value.” He said the dancing plague “tells us much about the extraordinary supernaturalism of late medieval people, but it also reveals the extremes to which fear and irrationality can lead us.” He added, “Few events in my view so clearly show the extraordinary potentials of the human mind.”