TANGANYIKA LAUGHTER EPIDEMIC, 1962-64

[spectre]

"...LIKE THE ENTIRE SOCIETY WAS A 16 YEAR OLD GIRL..."
http://www.wnyc.org/shows/radiolab/episodes/2008/02/22 [AUDIO]
BY Ellen Horne / February 22, 2008 [segment starts @ 39:30]

NOT JUST HAPPINESS
http://jimcofer.com/personal/?p=591
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
http://rltz.blogspot.com/2007/05/from-central-african-medical-journal.html
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.

Clinical Picture
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
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 explo9sions. 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.

Discussion
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.

Summary
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)
http://familydoctor.org/online/famdocen/home/articles/648.html
http://www.reference-global.com/doi/abs/10.1515/HUMOR.2007.003
The laughter of the 1962 Tanganyika ‘laughter epidemic’ / Christian
F. Hempelmann
"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."

CONTACT
Christian Hempelmann
www.kikihempelmann.com
email : hempelma [at] mac [dot] com

TANGANYIKA INDEPENDENCE TIMELINE
http://www.pbs.org/wgbh/commandingheights/lo/countries/tz/tz_overview.html
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
http://www.nationmaster.com/encyclopedia/Tanganyika-Laughter-Epidemic
"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.

Explanations
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
http://www.newscientist.com/article/mg20126881.600-how-your-friends-friends-can-affect-your-mood.html
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.

CONTACT
Nicholas Christakis
http://christakis.med.harvard.edu/pages/research/social_networks.html
email : christak [at] hcp.med.harvard [dot] edu

Duncan Watts
http://www.sociology.columbia.edu/fac-bios/watts/faculty.html
http://smallworld.columbia.edu/watts.html
email : djw24 [at] columbia [dot] edu

Robert Provine
http://www.umbc.edu/psyc/faculty/provine/research.html
email : provine [at] umbc [dot] edu

CONTAGIOUS LAUGHTER
http://www.americanscientist.org/issues/id.880,y.0,no.,content.true,page.1,css.print/issue.aspx
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.

Laugh Structure
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.

Chimpanzee Laughter
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.

Future Directions
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.