Something thought to be infectious turns out to be toxicity - The SMON Fiasco

[Sheri Nakken]

REMINDER of something thought to be contagious/infectious, later
found to be something caused by toxicity

"As the race to find a SMON virus was capturing all the attention,
other scientists were turning up some important clues to the
mysterious syndrome. One pharmacologist, Dr. H. Beppu, visited the
hard-hit Okayama province in 1969 to investigate the increasing
outbreak and independently discovered the same coincidence the
Mackawa group had years earlier - that SMON victims had taken certain
drugs to treat diarrhea. Unlike the Maekawa group, Beppu investigated
and found that Entero-vioform and Emaform - the diarrhea-fighting
drugs found present in an earlier SMON study - turned out to be
different brand names for a substance known as clioquinol,"

The SMON Fiasco

Sheri

http://www.primitivism.com/smon.htm

The SMON Fiasco

Bryan Ellison & Peter Duesberg

(Excerpt from Inventing the AIDS Virus)

Blaming non-infectious diseases on infectious microbes has occurred
many times before. Hidden in foreign-language materials and the
footnotes of obscure sources lies the story of SMON, a frightening
disease epidemic that struck Japan while the war on polio was
accelerating in the 1950s. In many ways, SMON anticipated the later
AIDS epidemic. For fifteen years the syndrome was mismanaged by the
Japanese science establishment, where virtually all research efforts
were controlled by virus hunters. Ignoring strong evidence to the
contrary, researchers continued to assume the syndrome was contagious
and searched for one virus after another. Year after year the
epidemic grew, despite public health measures to prevent the spread
of an infectious agent. And in the end, medical doctors were forced
to admit that their treatment had actually caused SMON in the first
place. Once the truth about SMON could no longer be ignored, the
episode dissolved into lawsuits for the thousands of remaining
victims. This story has remained untold outside of Japan, ignored as
being too embarrassing for the virus hunters. It deserves to be told
in full here.

The patient was middle aged, suffering from a mysterious nerve
disorder that had already paralyzed both her legs. Reisaku Kono was
there to observe the victim because of his work studying poliovirus,
which in a few infected individuals would break into the central
nervous system, causing progressive paralysis and sometimes a slow,
miserable, death. While the condition he examined that day in 1959
was not polio, it bore a certain resemblance to it. And the suspicion
was growing that this, too, could be the result of some undiscovered
virus, perhaps one similar to poliovirus.

Kono was visiting the patient at the hospital affiliated with Mie
University's medical school. Hiroshi Takasaki, a professor of
medicine at the university, told Kono about a number of these cases
he had recently seen at the hospital. They now realized they were
facing an outbreak of something new, not just a minor mystery that
doctors would catalog and forget. Just the previous year, medical
Professor Kenzo Kusui had published a report of another such case in
central Japan: The patient had suffered a similarly strange
combination of intestinal problems, manifesting as internal bleeding
and diarrhea, with symptoms of nerve degeneration. This illness,
stomach pains or diarrhea followed by nerve damage, had been noticed
in a few isolated cases as early as 1955, but was now turning into a
local epidemic.

More published reports began accumulating after Kono's visit to the
hospital. The next five years saw seven major regional epidemics of
the new polio-like syndrome, with the annual number of new cases
increasing from several dozen in 1959 to 161 victims by 1964 - an
alarming rate for those small areas. Scientists jumped to
conclusions, believing they had every reason to assume the disease
was infectious. Just its sudden appearance was enough evidence to
convince them. The disease also broke out in clusters around specific
towns or cities, and clusters were seen within families. The first
person to develop the condition in each of these families was
followed by a relative within several weeks. Many outbreaks were
centered around hospitals, places notorious for spreading disease.
The annual peak of new patients occurred in late summer, hinting at
possible spread of the disease through insects. Those scientists who
first thought the disease might be related to some noncontagious
occupational hazard were quickly dissuaded once the data showed that
the disease lacked the expected preferences. Farmers, for example,
who would be more easily exposed to pesticides, had a
lower-than-average incidence. Medical workers, on the other hand, had
a rather high rate of this condition - further suggesting it was contagious.

However, the scientists investigating the epidemic did notice some
important contradictions. For instance, the disease had an odd,
amazingly consistent bias for striking middle-aged women, but was
less common among men and could hardly be found among children, who
normally transmit virtually any infectious disease. Careful medical
inspection showed that the symptoms did not coincide with those
typically expected for an infection. Blood and other bodily fluids,
which usually circulate a virus throughout the body, showed no
abnormalities, nor did the patients manifest any fevers, rashes, or
other signs of fighting off some invading germ. These important
pieces of evidence should have raised doubts about the viral hypothesis.

The virus hunt pressed onward. Scientists were expecting to find a
virus that primarily induced diarrhea, as was the case in polio.
Looking back on this period, Kono has since become admirably frank
about his early biases, shared at the time by his fellow virologists:
"I was at that time engaged in poliovirus research, so I suspected
such a virus to be the cause."(1) Despite years spent searching for
the elusive virus, he never could isolate a single one from any
patient. Kono patiently reported his null results as he plodded forward.

Meanwhile the epidemic was growing and the 1964 Olympic Games were
approaching. Ninety-six new cases had been diagnosed the previous
year, and the increased number of cases was being accompanied by new
symptoms. Some victims, for example, were now suffering debilitating
blindness. Preparing to host tourists from around the world for the
1964 Olympics, Japan could ill afford to have an uncontrolled plague.
To make matters worse, forty-six new patients suddenly appeared
around the city of Toda, one of the locations for Olympic events.
Embarrassingly dubbed the "Toda disease," this outbreak directly
threatened Japan's reputation and tourist industry while focusing
public fear on the epidemic. Etsuro Totsuka, later to become a lawyer
for victims of the disease, summarized the public mood at the time:
"Even I was quite worried at the time, as a university student
studying physics. The general public, including me, was extremely
worried; we didn't know how to prevent it, and there was no cure."(2)

In May of 1964, at the 61st General Meeting of the Japanese Society
of Internal Medicine, the disease was raised as a formal topic. Kenzo
Kusui, one of the first doctors to report patients stricken with this
condition, chaired that session. The participating researchers gave
the disease a formal name, Subacute Myelo-Optico-Neuropathy (SMON),
and they agreed on a standardized clinical diagnosis. The Japanese
Ministry of Health and Welfare quickly provided a research grant and
launched a formal commission to investigate the epidemic under the
leadership of Magojiro Maekawa, a medical professor at Kyoto
University. Kono was one of several virologists named to the
commission, thereby establishing its mandate as a formal search for a virus.

The same year brought the first sign of a possible breakthrough.
Masahisa Shingu, a virologist at Kurume University and a fellow
member of the commission, announced his discovery of a virus in
excretions from SMON patients. The virus was classified as an
echovirus - an acronym for enteric cytopathogenic human orphan virus.
The viruses were called orphans because they had been discovered
accidentally during polio research but caused no disease. Echoviruses
were known for infecting the stomach or intestines, and Shingu found
evidence of infection in various SMON sufferers. He excitedly drew
the conclusion that this orphan virus had finally been matched with a
disease. Perhaps, he speculated, this virus could also occasionally
break into the nervous system, much like poliovirus. He published the
finding in 1965, unabashedly boasting he had isolated the syndrome's cause.

But Kono, knowing the potentially disastrous results of blaming the
wrong microbe for the disease, took a more cautious attitude. In
1967, after three years of research trying to confirm Shingu's
claims, Kono could only report to a SMON symposium that he had not
isolated the virus from patients, nor could he find even indirect
evidence that the patients had previously been infected. Kono's
better judgment saved Japanese science from stampeding in the wrong
direction. He was fully vindicated four years later when other
researchers announced the same lack of evidence to suggest any danger
from Shingu's virus.

In the midst of this fruitless investigation, the Maekawa team made a
surprising observation that was tragically brushed aside. According
to surveys of hospitals, about half the SMON patients had previously
been prescribed a diarrhea-fighting drug known by the brand name
Entero-vioform, and the other half had received a compound marketed
under the name Emaform. Both drugs were prescribed for problems of
the digestive tract - the early symptom of SMON. The suspicion
naturally arose that these drugs might play some role in the
syndrome, but the commission, intent on the viral hypothesis, bowed
to the consensus view of SMON as contagious and quickly dismissed
this, noting that two different drugs should not cause the same new
disease. Had the commission researchers checked further, however,
they would have discovered that the two drugs were merely different
brand names applied to the same drug, a fact that did not surface for
several years.

The SMON commission dissolved in 1967, a failure. The cumulative
total of reported SMON cases had meanwhile reached nearly two
thousand by the end of 1966, a significant but not terrifying number.
If not for the quiet growth of the disease epidemic, the floundering
virus hunt might have killed public interest in SMON research altogether.

Almost immediately after the official commission was dissolved, two
rural areas in the Okayama province began reeling from a new
explosive outbreak of the syndrome. Dozens of elderly women, and some
men in their thirties, began filling the nearby hospitals, totaling
almost 3 percent of the local population by 197I. Scientific
attention was again focused on SMON, with the specter of a resurgent
epidemic recharging the virus hunt.

Two researchers issued reports in 1968 describing a new virus found
in tissues of SMON patients, stirring a wave of excitement. The agent
fell under the classification of "Coxsackie" viruses, a type of
passenger virus known to infect the digestive tract and originally
discovered as a by-product of polio research. It was another false
alarm: The virus proved to be an accidental laboratory contamination.

In 1969 the Japanese Ministry of Health and Welfare, anxious about
the expanding epidemic, again decided to form an official
investigating body. With more than ten times the funding of the old
1964 commission, the SMON Research Commission became the largest
Japanese research program ever devoted to a single disease. Its first
meeting was held in the heavily affected Okayama province in early
September. The consensus view among Japanese scientists had
completely focused on some unknown virus as the probable cause of the
disease. The naming of Kono, Japan's most respected virologist, as
chairman symbolically established the new commission's priorities.

So far, after more than a decade of persistent research, the
virologists had come up painfully empty-handed. Kono, though himself
a virologist, now saw the need to explore alternative hypotheses.
Kono divided the commission's work into four sections, each led by
top Japanese medical officials. An epidemiologist was put in charge
of a group conducting nationwide surveys on the extent, distribution,
and associated risk factors of the disease. Kono himself headed the
virology group. A pathologist headed a group focused on analyzing
autopsy results, and a neurologist led a group classifying
neurological and intestinal SMON symptoms. Altogether, forty top
scientists participated in the commission during 1969.

Although Kono had opened the door for alternative research
directions, the virus hunt accelerated - for just at this time, some
key scientific claims by English and American virologists were
beginning to have a profound impact on virus research worldwide, and
particularly on SMON research in Japan. The first came in the early
1960s from virologist Carleton Gajdusek of the American National
Institutes of Health, who reported finding evidence of the first
"slow virus" in humans. (A slow virus is a virus alleged to produce a
disease long after the original infection, that is, after a long
"latent period.") He believed it to be the cause of kuru disease
among New Guinea natives. Kuru was a slowly progressing neurological
disease that led to the debilitation of motor skills. The patients
presented with symptoms of tremor and paralysis similar to
Parkinson's disease. Gajdusek claimed to have found the kuru virus,
but his methods were highly unusual by any scientific standards. He
had never actually isolated a virus but instead had ground up the
diseased brains of dead kuru victims and injected these unpurified
mixtures into the brains of living monkeys. When some of the monkeys
showed deficits in motor skills, Gajdusek published his findings in
the world's oldest scientific journal, Nature, and was lauded by his
fellow virologists. The second alleged discovery came from London's
Middlesex Hospital in 1964, directly inspired by Gajdusek's claims.
Two researchers found a virus that was believed to cause the
childhood cancer, Burkitt's lymphoma. It was the first virus ever
claimed to cause human cancer and the first known human virus thought
to have an incubation time between infection and disease measured in
years, rather than days or weeks.

These claims were made by very large and respected research
establishments; therefore, Kono could not afford to ignore them.
Other medical experts on the SMON commission warned him that the SMON
symptoms did not resemble those of standard virus infections,
suggesting the condition was not contagious. Kono, however, brushed
aside this advice, arguing that if scientists were unwilling to
consider the possible existence of nonclassic viruses then "Dr.
Gajdusek could not have established a slow virus etiology for
kuru."(3) Imitating Gajdusek's methods, he injected unpurified fluids
from SMON patients into the brains of experimental mice and monkeys,
hoping to cause the disease and isolate the guilty virus. Frustrated,
but not willing to give up, he decided the American researchers were
better equipped to find such a virus. He mailed the same fluid
samples directly to Gajdusek, who repeated the inoculations into the
brains of his own chimpanzees; after three years, they, too, remained
perfectly normal. With that, Kono finally abandoned the search for a
"slow virus."

With their virus research faltering, a few of the investigators began
looking for bacteria. One lab found that SMON patients had imbalanced
levels of the beneficial bacteria normally growing in everyone's
intestines, but it could not isolate any new invading microbe. Kono's
own lab, as well as two other researchers, did notice unusually large
amounts of a mycoplasma, one type of bacterial parasite, in disease
victims. However, since mycoplasma are found in a large percentage of
human populations and are usually known for being either relatively
harmless or causing some pneumonias, Kono and his fellow researchers
decided against pursuing this further.

By 1970, one fact stood out more agonizingly than any other: Twelve
years of microbe research into the SMON epidemic had yielded nothing
but dead ends. Yet the pressure continued to mount as the death toll
rose. The year 1969 alone claimed almost two thousand new SMON
victims, the worst toll ever. Kono and his commission were running
out of options.
Fortunately for the Japanese people, several researchers on the
commission were not virus hunters, and these scientists actually
rediscovered the evidence for a toxin-SMON hypothesis.

The Drug Connection

As the race to find a SMON virus was capturing all the attention,
other scientists were turning up some important clues to the
mysterious syndrome. One pharmacologist, Dr. H. Beppu, visited the
hard-hit Okayama province in 1969 to investigate the increasing
outbreak and independently discovered the same coincidence the
Mackawa group had years earlier - that SMON victims had taken certain
drugs to treat diarrhea. Unlike the Maekawa group, Beppu investigated
and found that Entero-vioform and Emaform - the diarrhea-fighting
drugs found present in an earlier SMON study - turned out to be
different brand names for a substance known as clioquinol, a freely
available medical drug used against some types of diarrhea and
dysentery. Beppu fed the chemical to experimental mice, hoping to see
nerve damage like that in SMON, but was disappointed when the mice
merely died. He missed the significance of his own results.
Clioquinol was sold because it was believed not to be absorbed into
the body, instead remaining in the intestines to kill invading germs.
The death of Beppu's animals, however, proved that the drug not only
entered the body, but could kill many essential tissues in the
animal. His experiment led the SMON commission to rediscover this
clioquinol connection the following year. "He later confessed to
feeling stupid, because he gave up the experiment when the animals
died," Totsuka explained of Beppu. "He wanted to prove a neurological
disorder, but only proved the drug's severe toxicity."(4)

Meanwhile the SMON commission's first priority lay in conducting a
nationwide survey of SMON cases reported since 1967, gathered by
sending questionnaires to doctors and hospitals throughout Japan. In
the fall of 1969, shortly after the commission began analyzing survey
data, the head of the clinical symptoms section came across several
SMON patients with a strange green coating on their tongues, a
symptom unnoticed before nationwide data were gathered. At first
other researchers on the commission suggested that this new symptom
might be caused by Pseudomonas bacteria, which can release colorful
blue and green pigments. One of the investigators did isolate such a
bacterium from some patients but not from others, and the
inexplicable symptom merely became a part of the revised SMON
definition. The green tongue observation achieved new importance in
May of 1970, when one group of doctors encountered two SMON patients
with greenish urine. Enough of the pigment could be extracted to
perform chemical tests. Within a short time the substance was
determined to be an altered form of clioquinol, the same drug
previously found by the Maekawa commission and by Beppu.
This raised two very troubling questions. Clioquinol had been
marketed for years on the assumptions that it only killed amoeba in
the intestinal tract and could not be absorbed into the body; its
appearance on the tongue and in the urine now proved this belief
wrong. Could the medicine therefore have unexpected side effects? And
why would SMON patients manifest the drug by-products so much more
obviously than the rest of the population? This latter question
particularly bothered one neurology professor at Niigata University,
Tadao Tsubaki. Making an educated guess, he openly formulated the
hypothesis abandoned by earlier investigators - that SMON might be
the result of clioquinol consumption, not of a virus.

As expected, the interpretation of SMON as a noncontagious syndrome
did not become popular among the virus hunters. And the suggestion
that clioquinol might be guilty met even stronger resistance, for the
drug was being used to treat the very abdominal symptoms found in
SMON. Doctors, naturally, were reluctant to believe they were
exacerbating these abdominal pains and thus adding the severe insult
of nerve damage to the injury. Totsuka recalled that "doctors and
scientists wanted to believe in a virus, because they prescribed
clioquinol. One of the drug's main side effects was constipation and
abdominal pain. Now because the drug caused pain, doctors again
prescribed the drug."(5) Doctors, ignorant of clioquinol's side
effects, assumed the stomach pains resulted from the primary sickness
and kept increasing the dose in a vicious cycle.
Tsubaki knew he had to gather strong evidence before they could shoot
down the virus-SMON hypothesis. Pulling together several associates,
Tsubaki arranged for a small study of SMON patients at seven
hospitals. By July of 1970 he had already compiled enough data to
draw several important conclusions: 96 percent of SMON victims had
definitely taken clioquinol before the disease appeared, and those
with the most severe symptoms had taken the highest doses of the
medication. The number of SMON cases throughout Japan, moreover, had
risen and fallen with the sales of clioquinol.

This clioquinol hypothesis explained all the strangest features of
the SMON syndrome, such as its preference for striking middleaged
women, its absence in children (who received fewer and smaller doses
of the drug), and its symptomatic differences from typical viral
infections. It also shed new light on the supposed evidence that SMON
was infectious: its tendency to appear in hospital patients, to
cluster in families, to afflict medical workers, and to break out
more heavily in the summer - all of these reflected the patterns of
clioquinol use. The epidemic itself had begun shortly after approval
for pharmaceutical companies to begin manufacturing the drug in Japan.
In 1970 there were thirty-seven SMON cases in January and nearly
sixty more cases during the month of July. The Japanese Ministry of
Health and Welfare decided not to wait any longer, and promptly
released the information about clioquinol to the press. The news of
Tsubaki's research reached the public in early August, and the number
of new SMON cases for that month dropped to under fifty, presumably
because some doctors stopped prescribing clioquinol to their
patients. On September 8 the Japanese government banned all sales of
the drug, and the total new caseload for that month sank below
twenty. The following year, 1971, saw only thirty-six cases. Three
more cases were reported in 1972, and one in 1973. The epidemic was over.

For the next few years, the commission's research focused on
confirming the role of clioquinol. In 1975 it released a
comprehensive report. Systematic epidemiological surveys matched use
of the drug with outbreaks of the syndrome, and experiments were
performed on animals ranging from mice to chimpanzees. As it turned
out, the drug induced SMON-like symptoms most perfectly in dogs and
cats. Meanwhile, the investigators began uncovering individual case
reports of SMON symptoms from around the world, wherever clioquinol
had been marketed. Totaling roughly one hundred cases, the published
reports ranged from Argentina in the 1930S to Great Britain, Sweden,
and Australia in more recent times, often with the doctor
specifically pointing out the association with the use of clioquinol
or similar compounds. Ciba-Geigy, the international producer of the
drug, had received warnings of these incidents years before the
Japanese epidemic, a fact that later became the basis of a successful
lawsuit against the pharmaceutical company.

Clioquinol, often marketed under the brand name Enterovioform, has
been available for decades throughout many countries in the world.
But while doctors outside Japan have published a few reports of
SMON-like conditions, no real epidemic of the disease has ever broken
out in Europe, India, or other countries with widespread use of the
drug. Much of the difference lies in the heavier consumption of
clioquinol in Japan, where the stomach, rather than the heart, is
considered the seat of the emotions. The general over-prescription of
drugs in that country further worsens the problem, such that many
SMON victims had histories of using not only clioquinol but also
multiple other medications, often at the same time. Government health
insurance policies have encouraged this over-medication, paying
doctors for every drug prescribed to the patient. As a result, the
proportion of the Japanese health insurance budget spent on
pharmaceutical drugs grew from 26 percent in 1961 to 40 percent in
1971, a level many times higher than in other nations. By the time
the Japanese government decided to ban clioquinol, many of the
hardest-hit SMON patients had each consumed hundreds of grams over
the course of several months. And whereas the outside world mostly
used clioquinol to prevent diarrhea when traveling abroad, the
Japanese usually received the drug as hospital patients, having an
already weakened condition.
Years later, at a 1979 conference, Reisaku Kono asked, "Why had
research on the etiology of SMON not hit upon clioquinol until 1970?"
The question has two answers; both pointed out by Kono himself:

There were at least two occasions when physicians suspected that
clioquinol might have something to do with SMON. I know of a certain
professor rebuking one of his staff physicians for connecting
clioquinol with SMON. In 1967 the study group of the National
Hospitals on SMON reported as follows: Entero-vioform (clioquinol's
brand name), mesaphylin, Emaform (home producer of clioquinol),
chloromycetin and llosone were often prescribed to SMON patients, but
no link was found between Entero-vioform and SMON. This report
referred to Entero-vioform in particular so that clioquinol must have
been suspected by someone in the study group. Dr. Tsugane, who was
responsible for the survey, said that the survey was not thorough
enough to unearth clioquinol as a causative agent. One of the reasons
could have been that clioquinol had been used as a drug for the
intestinal disorders of SMON, and it was hard to believe that
clioquinol was toxic rather than a remedy. (6)

Referring here to the tentative fingering of clioquinol by the
Maekawa group, Kono observed that too many medical doctors refused to
recognize the possibility of an iatrogenic disease (one caused by the
doctor's treatment). They understandably disliked the idea that a
drug might cause some of the very symptoms for which it was
prescribed in the first place.

Another, more fundamental, reason for overlooking clioquinol lay in
the prevailing attitude of the virologists. As expressed by Kono, "We
were still within grasp of the ghosts of Pasteur and Koch!"(7) SMON,
a vaguely polio-like syndrome, had first appeared in the midst of a
war against polio. The polio virologists, Kono included, were
naturally inclined to search for a new virus as the cause of the new
disease. The Japanese government, having funded poliovirus research,
simply kept up the momentum by funding the same virologists to study
SMON. Thus, the virus hunters received the lion's share of research
moneys and attention, and with that the power to direct the SMON
research program. Had it not been for Kono's foresight in also
appointing nonvirologists to the commission, the epidemic might have
lasted much longer.
At least the epidemic had ended, with the truth universally
recognized. The virologists had learned their lesson, and the search
for SMON viruses was over.

Or was it? Incredibly, against all evidence, the SMON virus hunt
suddenly came back to life within weeks of the epidemic's end. The
fight over the cause of the syndrome was to drag on for several more
years, with the virus hunters simply ignoring the fact that SMON
itself had disappeared after the ban on clioquinol.

The Virus Hunt Revived

In February of 1970, while the SMON Research Commission was still
scrambling to find the cause of the epidemic and a few researchers
were just beginning to notice the greenish pigments in some patients,
Assistant Professor Shigeyuki Inoue at Kyoto University's Institute
for Virus Research claimed discovery of a virus in the spinal fluid
and excretions of SMON patients. He added the extracts to laboratory
culture dishes of hamster tumor cells and found that the new agent
killed the cells. With more experimentation, Inoue classified the
microbe as a new herpes virus. He was able to isolate this particular
virus from nearly all SMON patients he tested, more than forty in
all, and found antibodies against the virus in other victims.

Reisaku Kono moved promptly to test these new observations. He used
Inoue's own virus isolate and cell cultures, and within three months
of Inoue's first report found that the virus could kill some cells.
These particular cells, however, were extremely sensitive, prone to
spontaneous death even in the uninfected cultures. Kono began to
suspect the virus was harmless. He also could not isolate the virus
from any SMON patients, unlike Inoue's lab. Perhaps, he openly
wondered, the alleged virus might not exist at all.

A number of scientists sided with Kono, insisting they could neither
find the virus in SMON victims nor cause cell death in culture dishes
by adding virus samples from Inoue's lab. Nor could Inoue's extracts
induce symptoms when injected into mice. Indeed, Kono and some of
these other investigators could never even find the virus at all,
reinforcing the growing question of whether it truly existed. The
virus could not even be detected in the samples sent them from Inoue.
An occasional mouse injected with Inoue's supposed virus would become
sick, but the symptoms did not resemble those of SMON. Kono won
allies among his peers when many of them could not reproduce Inoue's
observations. a troubling problem for any scientific claim.
Nevertheless, Inoue had meanwhile rapidly achieved celebrity status
for his "SMON virus" during 1970, before the clioquinol announcement
that August. The Japanese news media had prematurely publicized his
results, creating the widespread impression that the cause of SMON
had been determined. Hysteria over the contagious plague swept
through much of the country, causing frightened family members of
SMON patients to avoid contact with their "infected" relatives, and
leading many of the victims to commit suicide. "Patients were
isolated, many committed suicide, and there was national panic,"
reflected Totsuka on the horror he witnessed. "I met families who
lost relatives. I heard from most or all of my goo clients; most of
the patients said they very much feared and dreaded the disease.
Everybody told me about that, about those sufferings. Once they found
out about the drug, they were somewhat relieved, because it was not
infectious."(8)

The new virus-SMON hypothesis had indeed achieved a life of its own,
causing a few scientists to Jump on the Inoue bandwagon; months after
clioquinol had been banned and the epidemic had virtually
disappeared, several labs excitedly issued reports claiming they
could reproduce Inoue's findings. Inoue himself further insisted he
had caused SMON-like symptoms in mice - including weight loss,
paralysis, and nerve damage - either by injecting the virus into
their brains or feeding the virus to other immune-suppressed mice
unable to fight off the infection. Inoue and a collaborating
scientist also both claimed to have photographed the virus directly
with electron microscopes, although Inoue's colleague eventually
retracted his own report as having been mistaken.

A meeting of the SMON Research Commission was finally held in July of
1972 to resolve the controversy. Until that time, Inoue's results had
received attention and concern equal to the ciioquinol research. But
based on the inability of many scientists to produce the same
results, which must be done for any scientific hypothesis to be
accepted, the members at the meeting decided not to focus any more
research efforts on the Inoue virus. Samples were frozen for future
study, and the group thereafter devoted its resources to studying clioquinol.

Despite the absence of confirming evidence, and despite the
disappearance of SMON following the ban on clioquinol, Inoue and his
supporting colleagues continued to publish reports of evidence for
the virus hypothesis. This publicity carried the Inoue hypothesis
overseas, leading the 1974 edition of the Review of Medical
Microbiology, an American textbook, to incorporate the Inoue virus
hypothesis of SMON.

Shocked and angered by the favorable publicity surrounding Inoue's
hypothesis, Kono wrote a letter to the British medical journal
Lancet; the letter was published in August of 1975. The international
popularity of virus research had whetted scientists' appetite for
Inoue's hypothesis, but Kono also knew he was battling a nearly
complete ignorance of the SMON episode outside Japan:

Inoue et al. published several papers on SMON virus, and a standard
textbook adopted Inoue's virus theory as confirmed. However, research
in the laboratories of the SMON Research Commission in Japan failed
to confirm Inoue's results. Unfortunately, this negative information
has not been published in English.(9)

The epidemic's toll had officially ended in 1973 with 11,007 victims,
including thousands of fatalities. Angered upon learning of
Ciba-Geigy's disregard of previously reported clioquinol toxicity,
many of these patients filed a lawsuit in May of 197I against the
Japanese government, Ciba-Geigy of Japan, fifteen other distributors
of the drug, and twenty-three doctors and hospitals. The ranks of the
plaintiffs soon swelled to some forty-five hundred, with legal action
initiated in twenty-three Japanese district courts. The largest group
of SMON victims sued jointly in the Tokyo District Court. When
frustrations mounted over the slow and indecisive actions of their
lawyers, nine hundred of the plaintiffs broke away to form a second
group. The aggressive investigations conducted by this new legal team
reinvigorated the case, bolstering the positions of the plaintiffs in
parallel lawsuits. Etsuro Totsuka, one of the thirty members of this
legal team, has described the fight:

We were the only team gathering information outside Japan, inviting
foreign experts to testify in Japanese courts, discovering the United
States FDA had restricted clioquinol ten years before Japan, and
waging an international campaign against Ciba-Geigy...

We found many foreign doctors who had reported clioquinol side
effects before. They were contacted by Ciba-Geigy, and except in one
or two instances were persuaded not to help us. By the time I saw the
doctors, they had already been contacted by the other side. They had
been invited on trips, some to Ciba-Geigy's headquarters... We felt
they were already compensated, under the condition not to tell us anything.(10)

The two sides slugged it out for several years, but the testimony by
members of Kono's SMON Research Commission proved devastating, and a
string of legal victories followed in the courts.

Today most scientists and laymen outside Japan have never heard of
the virus-SMON controversy, even in the face of the lawsuit against
the distributors of clioquinol, television documentaries in Germany
and England on clioquinol, and two conferences during the 1970s on
iatrogenic (medically caused) disease. The story that SMON research
had ignored the evidence of a toxic cause for fifteen years and had
sacrificed thousands of human lives to a flawed virus hypothesis is
too embarrassing to the virus-hunting establishment to record. *

References:
1. R. Kono, "The SMON Virus Theory," Lancet, ii (1975): 370-371; I.
Shigematsu, H. Yanagawa, S.I. Yamamoto, and K. Nake, "Epidemiological
Approach to SMON (Subacute Myelo-Optico-Neuropathy)," Japanese
Journal of Medicine, Science, and Biology, 28 Supplement (1975): 23-33
2. E. Totsuka, personal communication, 1 May 1992.
3. T. E. Soda, Drug-lnduced Sufferings: Medical, Pharmaceutical, and
Legal Aspects (Amsterdam: Excerpta Medica, 1980).
4. Totsuka, personal communication, 1 May 1992.
5. Ibid.
6. Soda, Drug-lnduced Sufferings.
7. Ibid.
8. Totsuka, personal communication, 1 May 1992.
9. Kono, "SMON Virus Theory," 370-371.
10. Totsuka, personal communication, 1 May 1992.
11. Soda, Drug-lnduced Sufferings.

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Sheri Nakken, R.N., MA, Hahnemannian Homeopath
http://www.wellwithin1.com/vaccine.htm & http://www.wellwithin1.com/homeo.htm
ONLINE/Email classes in Homeopathy; Vaccine Dangers; Childhood Diseases Reality
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