The SMON Fiasco (similar to poliomyelitis situation)

[Guest guest]

The SMON Fiasco

This shows one example of how something that was caused by toxicity was

assumed to be infectious to begin with - SAME AS WITH POLIOO)

Sheri

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

The SMON Fiasco

Ellison & 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 " sackie " 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.

--------------------------------------------------------

Sheri Nakken, former R.N., MA, Hahnemannian Homeopath

Vaccination Information & Choice Network, Nevada City CA & Wales UK

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