The Poison Cause of Poliomyelitis And Obstructions To Its Investigation
Posted: Fri May 26, 2006 7:54 pm
The Poison Cause of Poliomyelitis And Obstructions To Its Investigation
From 1952
http://www.geocities.com/harpub/scobpois.htm
Images Of Poliomyelitis
From Archive Of Pediatrics (April, 1952)
The Poison Cause of Poliomyelitis
And Obstructions
To Its Investigation
Statement prepared for the Select Committee
to Investigate the Use of Chemicals in Food Products,
United States House of Representatives, Washington, D.C.
Ralph R. Scobey, M.D.
Syracuse, N.Y.
The disease that we now know as poliomyelitis was not designated as
such until about the middle of the 19th Century. Prior to that, it was
designated by many different names at various times and in different
localities.1,2 The simple designations, paralysis, palsy and apoplexy, were
some of the earliest names applied to what is now called poliomyelitis.
Paralysis, resulting from poisoning, has probably been known since the
time of Hippocrates (460-437 B.C.), Boerhaave,3 Germany, (1765) stated: "We
frequently find persons rendered paralytic by exposing themselves
imprudently to quicksilver, dispersed into vapors by the fire, as gilders,
chemists, miners, etc., and perhaps there are other poisons, which may
produce the same disease, even externally applied." In 1824, Cooke,4
England, stated: "Among the exciting causes of the partial palsies we may
reckon the poison of certain mineral substances, particularly of quick
silver, arsenic, and lead. The fumes of these metals or the receptance of
them in solution into the stomach, have often causes paralysis."
Colton5 (1850) mentions the case of a patient who swallowed some
arsenic accidentally and was admitted to the hospital. The primary effects
of the poison had been successfully combated with proper remedies, but
seven days afterward he became paralyzed. It is significant to note that
there was a latent period of several days before the paralysis appeared
since this delayed reaction is comparable to the incubation period in
infectious diseases.
Vulpian6 (1879) experimentally produced paralysis of the extensor
muscles of a dog by lead poisoning. The lesions, consisting in colloid
degeneration and cell atrophy of the anterior horn cells of the spinal cord
were pronounced by Vulpian as poliomyelitis. Adamkiewitz7 (1879) reported
two parallel cases, one of poliomyelitis and one of lead poisoning.
In 1881, Popow8 of St. Petersburg, published an essay upon the
pathological anatomy of arsenical paralysis as produced artificially in
animals. The work of Popow was carried out under the guidance of the
distinguished neurologist and microscopist, Professor Mierzeyeski. Popow
concluded that arsenic, even in a few hours after its ingestion, may cause
acute central myelitis or acute poliomyelitis.
During an epidemic of poliomyelitis in Australia in 1897, Altman9
pointed out that phosphorus had been widely used by farmers for fertilizing
that year. This observation may be of significance since in recent years
organic phosphorus insecticides, such as parathion, have been suspected as
possible causes of poliomyelitis.
Onuff10 (1900) reported a case of a painter with flaccid paralysis of
both legs, in whom the autopsy showed lesions characteristic of poliomyelitis.
Obsrastoff11 (1902) reported a case of acute poliomyelitis resulting
from arsenic poisoning. Phillippe and Gauthard12 (1903) reported a case of
anterior poliomyelitis from lead poisoning.
Gossage13 (1902), writing on infantile paralysis, says: "The nerve
cells or fiber may be acutely disabled by the action of some poison
circulating in the blood, and it is possible that such poison would only
temporarily impair their functions or so seriously affect them that
recovery would be impossible."
Dr. David E. Edsall14 (1907), writing on the pathology of carbon
monoxide poisoning in Osler's System of Medicine, states: "Peripheral
neuritis had repeatedly been described and poliomyelitis and disseminated
encephalitis have been seen."
Collins and Martland15 (1908) reported a case of poliomyelitis in a
man, 38 years of age, which resulted from the use of cyanide as a silver
polish. The illness began with diarrhea, followed by headache and pain and
stiffness in the back of the neck. About eight days after the onset of the
illness, he became paralyzed. In discussing Collins and Martland's paper,
Larkin stated that he had seen one instance of this disease following
potassium cyanide poisoning.
In the spring of 1930, there occurred in Ohio, Kentucky, Alabama,
Mississippi and other states an epidemic of paralysis.16,17 The patients
gave a history of drinking commercial extract of ginger. It is estimated
that at the height of the epidemic there were 500 cases in Cincinnati
district alone. The cause of the paralysis was subsequently shown to be
triorthocresyl phosphate in a spurious Jamaica ginger. Death resulted not
infrequently from respiratory paralysis similar to the bulbar paralysis
deaths in poliomyelitis. On pathological examination, the anterior horn
cells of the spinal cord in these cases showed lesions similar to those of
poliomyelitis.
These incidents show that epidemics of poisoning occur and furthermore,
that epidemic diseases do not always indicate that they are caused by
infectious agents. Moreover, following the ingestion of the spurious
Jamaica ginger, the symptoms appeared two to ten days later. In some cases
a longer time elapsed. This latent period is comparable to the incubation
period of infections diseases. As a matter of fact, the incubation period
of poliomyelitis is commonly stated to be seven to 10 days on the average
with considerable variation in either direction. The so-called incubation
period in poliomyelitis and the latent period in these cases of poisoning,
therefore, are strikingly similar in length.
Leenhardt et al.18 (1951) described acrodynia in the course of three
cases of acute poliomyelitis. Some authorities have considered acrodynia to
be caused by a poison. Elmore19 (1948) reported two cases of this disease
following the ingestion of mercury and Warkany and Hubbard20 (1951) found
mercury in the urines of 38 (92.7 per cent) of 40 acrodynia patients.
Meyerhofer21 (1939) reported that infantile acrodynia may immediately
follow certain forms at atypical poliomyelitis, especially
encephalomyelitis. Mercury is used as an insecticide and a fungicide and
the above clinical observations indicate that it might be a factor in
producing some cases of poliomyelitis.
Gougerot22 (1935) reported that during arsenical therapy for syphilis,
poliomyelitis developed in two patients, and lethargic encephalitis
followed by Parkinson's disease in one.
In 1936, during a campaign to eliminate yaws in Western Samoa by the
injection of arsenicals, an epidemic of poliomyelitis appeared
simultaneously.23 In one community all of the patients developed paralysis
in the same lower limbs and buttocks in which they had received the
injections and this pattern was repeated in 37 other villages, whereas
there was no paralysis in uninoculated districts. The natives accused the
injections as the cause of the epidemic of poliomyelitis. Most of the cases
of paralysis occurred one to tow weeks after the injection of the arsenic.
The foregoing reports indicate that poisons can cause poliomyelitis. It
would appear that not any one poison in particular would be responsible for
all cases of poliomyelitis but the effect of any one of several could
produce the same ultimate result. When a disease is known to be caused by a
poison, it is obvious that a search for a germ or virus in relation to it
would not be made. Conversely, if a so-called virus is believed to be
associated with the disease, then the possibility of poisoning as the cause
of the disease would not be considered. It will be shown, moreover, that
some so-called virus diseases and virus inclusions can be caused by poisons.
Dr. Robert W. Lovett24 of the Massachusetts State Board of health
(1908), describing the epidemic of poliomyelitis in Massachusetts in 1907,
and after reviewing the medical literature on experimental poliomyelitis,
states: "The injection experiments prove that certain metallic poisons,
bacteria and toxins have a selective action on the motor cells of the
anterior cornua when present in the general circulation; that the paralysis
of this type may be largely unilateral; that the posterior limbs are always
more affected than the anterior; and that the lesions in the cord in such
cases do not differ from those in anterior poliomyelitis." It appears to be
of great importance that various poisons, lead, arsenic, mercury, cyanide,
etc., found capable of causing paralysis are employed in relation to
articles of food that are used for human consumption.
There are two abnormal findings in cases of poliomyelitis that point
strongly to poisoning as the cause of this disease. One consists in the
appearance of increased amounts of porphyrin in the urine; the other is the
presence of increased amounts of guanidine in the blood. It is a well-known
fact that porphyria can follow poisoning by a number of chemicals.
Guanidine has been found in increased amounts in the blood in arsenic,
chloroform, and carbon tetrachloride poisonings.
The fact that ascorbic acid has been effective in the treatment of
poliomyelitis appears justly to imply that this disease has a poison cause.
Ascorbic acid has been used as a reducing agent in the treatment of
poisoning resulting from a number of toxic agents, including coal tar
antipyretics, nitro compounds, aniline, cyanide, benzene, lead, arsenic,
etc.32-40 Paralleling these modern scientific investigations is the
observation over a century ago that lime juice and lemon juice were
protective against the poisoning by fish which sometimes resulted in
paralysis,41,42. This early observation is perhaps the principle reason why
lemon juice is customarily served today when fish are eaten.
The fact that methylene blue,43 another reducing agent, is effective in
the treatment of poliomyelitis also points to the poison cause of this
disease. Methylene blue has been used as an antidote in the treatment of
nitrite, cyanide, carbon monoxide and other poisonings.
Another fact that strongly implies that human poliomyelitis is caused
by a poison is found in the recent report (1951) by Dr. Irwin S. Eskwith44
of Bridgeport, Conn., that BAL (dimercaprol) was effective in bringing
about complete recovery in a moribund 4 1/2 year-old girl with bulbar
poliomyelitis. BAL counteracts the effects of poisons; it has been shown
not to be effective in infectious diseases.
RELATIONSHIP OF HARVEST TO POLIOMYELITIS
[...]
In 1907, Dr. H. C. Emerson54, Massachusetts State Inspector of Health,
District 14, investigating an epidemic of poliomyelitis in that state, made
a careful inquiry regarding the diet. No infant who was fed exclusively on
the breast developed poliomyelitis. He found in six cases that fruit and
berries had been a large item of the diet. In the cases of two infants,
bananas and berries had been given in the diet in addition to breast milk.
In three cases of poliomyelitis, the illness was attributed to the eating
of large amounts of blackberries and blueberries. In one case the illness
was credited to eating heartily of English mulberries. In 39 instances it
was stated that food supplied were bought from fruit and vegetable peddlers
in their localities.
[...]
Dingman55 (1916) reported a milk-borne epidemic of poliomyelitis and
several similar outbreaks have been reported since then that were traceable
to milk.
[...]
Chapman58, raised the question of food poisoning to explain the
epidemic of poliomyelitis in England in 1947, when he stated: "Is it not
possible that the present prevalence of infantile paralysis may, in part at
any rate, be due to some article in our restricted and modified dietary?"
[...]
Toomey and August59 (1932) pointed out that some authors thought that
poliomyelitis is a disease of gastrointestinal origin which might follow
the ingestion of foodstuffs. In 193360, they noted that the epidemic peak
of poliomyelitis corresponds with the harvest peak of perishable fruits and
vegetables. They called attention to the fact that the disease occurs only
in those countries which raise the same type of agricultural products. Dr.
C.W. Burhans60, one of the colleagues of the authors, thought that green
apples might be a factor in the etiology of poliomyelitis. Toomey et al61.
(1943) points out that there is frequently a history of dietary
indiscretions previous to an attack of poliomyelitis. They suspected that a
virus could be found on or in unwashed fruit or in well water during
epidemics of poliomyelitis. Every year for eight years, therefore, grapes,
apples, peaches, and pears were collected from the vineyards and trees in
Northern Ohio at the time of the ripening. In none of their studies was the
so-called virus of poliomyelitis demonstrated when the washings of the
fruit or the well water were injected into experimental animals. However,
no chemical tests were made to determine whether or not a chemical
substance on or within the fruit or in the well water, acting by oral
ingestion top produce poliomyelitis, was present.
Draper62 (1935) recorded a series of cases of poliomyelitis which he
postulated originated from a Greek fruiterer. All of the cases were in
contact with the Greek as business associates, relatives or customers, and
there was nothing in the evidence to point to infection being carried by
the Greek himself other than the fruit he supplied.
[...]
Barber64 (1939) reported four cases of poliomyelitis that developed
simultaneously on the same day from the eating of strawberries in a single
house of a boarding school. He says that the simultaneous onset of these
cases resembled food poisoning. The seasonal and climatic incidence of
poliomyelitis, he points out, agree closely with the seasonal increase in
the consumption of fresh garden production. He says that the
epidemiological distribution of poliomyelitis resembles food poisoning.
Chenault65 (1941) noted that the history of poliomyelitis points to a
"suggested parallelism between a number of epidemics and the appearance of
fresh fruits and vegetables." [With regard to these numerous statements
regarding fruit and milk, note the high production of pesticides in the
form of lead and arsenic compounds during this pre-DDT period, graphed]
Goldstein et al66 (1946) reported an epidemic of polioencephalitis at a
naval training school among the cadets. The epidemic was explosive in
character and involved over 100 persons. Epidemiological evidence suggested
that some food served in the mess hall was the cause of the disease.
[...]
Gebhardt and McKay68 (1946) found during an epidemic of poliomyelitis
in Utah that of a total of 206 persons surveyed, 192 persons, or 93.2 per
cent, had one to two weeks prior to the onset of the disease eaten fresh
fruits. The authors found in Utah, New York and California, during 1943,
that the cases of poliomyelitis paralleled the harvest peaks. Most of the
multiple cases in families were found to have developed at the same time,
suggesting means other than contact as the mode of spread. Among the fruits
more commonly eaten were apples, peaches and pears; tomatoes headed the
list of vegetables. The authors stated that the data appeared to fit into
the jigsaw puzzle of epidemic poliomyelitis.
[...]
Abbott71 (1948), of Auckland, New Zealand, stated: "The public has
always been fully convinced that they caught poliomyelitis from one another
by direct infection. The 'germ' idea is indeed deeply ingrained in both the
profession and the public. It will be many years before our prolific
writers of medical textbooks attain the degree of sophistication that would
enable them to understand how and why poliomyelitis would be more likely to
be contacted from the flour-bag, or some homely article of food, rather
than from their neighbors."
[...]
Barondes72 (1949) points out that a study of the epidemiology of
poliomyelitis shows a definite correlation with the harvesting of fruit and
vegetable crops and to changes in climate, weather and humidity. The
harvesting of such fruits as cherries, grapes, berries, apricots, etc. and
the edible vegetables, as lettuce, radish, cucumbers, etc. usually from
June to September, corresponds with the period of poliomyelitis epidemics,
Barondes points out.
Toomey et al74 (1949) made some important experimental observations
that appear to show a correlation of the poison and virus theories of
poliomyelitis. They considered it possible that a food (fruit) which enters
the gastrointestinal tract could in some way act as a precursor of
catalytic enzyme on a normal constituent of the tract and accelerate the
production of poliomyelitis. Various materials, together with fruit
extracts, were tested.
When supernates of peach skin mash were injected intracerebrally into
cotton rats, followed at intervals with intracerebral injections of the
so-called poliomyelitis virus, accelerated production of paralysis
occurred. Because of the presence of cyanophore glucosides in peach skins,
a synthetic preparation, succinotrile, was injected intracerebrally into
the experimental animals. This chemical accelerated the production of the
disease similar to that produced with the peach supernates. Toomey et al.
emphasize that the injections of fruit supernates were made in a manner
that does not occur under natural circumstances.
Sabin75 (1951), although insisting on the virus etiology of
poliomyelitis, implicates food and drink as important factors in the cause
of this disease. He points out that measures which are often advocated to
combat poliomyelitis epidemics are not warranted, such as (a) avoidance of
crowds, large gatherings or sports events, (b) exclusion of children under
16 years of age from movies, churches, or schools, and (c) exclusion of
poliomyelitis patients and suspects from general hospital wards.
[...]
The implications [of the foregoing] should be obvious that
investigations of foods eaten by the poliomyelitis victim prior to his or
her illness should be carefully considered.
THE PRODUCTION OF SO-CALLED VIRUS DISEASES
AND "VIRUS" INCLUSIONS BY POISONS
much more at webpage
From 1952
http://www.geocities.com/harpub/scobpois.htm
Images Of Poliomyelitis
From Archive Of Pediatrics (April, 1952)
The Poison Cause of Poliomyelitis
And Obstructions
To Its Investigation
Statement prepared for the Select Committee
to Investigate the Use of Chemicals in Food Products,
United States House of Representatives, Washington, D.C.
Ralph R. Scobey, M.D.
Syracuse, N.Y.
The disease that we now know as poliomyelitis was not designated as
such until about the middle of the 19th Century. Prior to that, it was
designated by many different names at various times and in different
localities.1,2 The simple designations, paralysis, palsy and apoplexy, were
some of the earliest names applied to what is now called poliomyelitis.
Paralysis, resulting from poisoning, has probably been known since the
time of Hippocrates (460-437 B.C.), Boerhaave,3 Germany, (1765) stated: "We
frequently find persons rendered paralytic by exposing themselves
imprudently to quicksilver, dispersed into vapors by the fire, as gilders,
chemists, miners, etc., and perhaps there are other poisons, which may
produce the same disease, even externally applied." In 1824, Cooke,4
England, stated: "Among the exciting causes of the partial palsies we may
reckon the poison of certain mineral substances, particularly of quick
silver, arsenic, and lead. The fumes of these metals or the receptance of
them in solution into the stomach, have often causes paralysis."
Colton5 (1850) mentions the case of a patient who swallowed some
arsenic accidentally and was admitted to the hospital. The primary effects
of the poison had been successfully combated with proper remedies, but
seven days afterward he became paralyzed. It is significant to note that
there was a latent period of several days before the paralysis appeared
since this delayed reaction is comparable to the incubation period in
infectious diseases.
Vulpian6 (1879) experimentally produced paralysis of the extensor
muscles of a dog by lead poisoning. The lesions, consisting in colloid
degeneration and cell atrophy of the anterior horn cells of the spinal cord
were pronounced by Vulpian as poliomyelitis. Adamkiewitz7 (1879) reported
two parallel cases, one of poliomyelitis and one of lead poisoning.
In 1881, Popow8 of St. Petersburg, published an essay upon the
pathological anatomy of arsenical paralysis as produced artificially in
animals. The work of Popow was carried out under the guidance of the
distinguished neurologist and microscopist, Professor Mierzeyeski. Popow
concluded that arsenic, even in a few hours after its ingestion, may cause
acute central myelitis or acute poliomyelitis.
During an epidemic of poliomyelitis in Australia in 1897, Altman9
pointed out that phosphorus had been widely used by farmers for fertilizing
that year. This observation may be of significance since in recent years
organic phosphorus insecticides, such as parathion, have been suspected as
possible causes of poliomyelitis.
Onuff10 (1900) reported a case of a painter with flaccid paralysis of
both legs, in whom the autopsy showed lesions characteristic of poliomyelitis.
Obsrastoff11 (1902) reported a case of acute poliomyelitis resulting
from arsenic poisoning. Phillippe and Gauthard12 (1903) reported a case of
anterior poliomyelitis from lead poisoning.
Gossage13 (1902), writing on infantile paralysis, says: "The nerve
cells or fiber may be acutely disabled by the action of some poison
circulating in the blood, and it is possible that such poison would only
temporarily impair their functions or so seriously affect them that
recovery would be impossible."
Dr. David E. Edsall14 (1907), writing on the pathology of carbon
monoxide poisoning in Osler's System of Medicine, states: "Peripheral
neuritis had repeatedly been described and poliomyelitis and disseminated
encephalitis have been seen."
Collins and Martland15 (1908) reported a case of poliomyelitis in a
man, 38 years of age, which resulted from the use of cyanide as a silver
polish. The illness began with diarrhea, followed by headache and pain and
stiffness in the back of the neck. About eight days after the onset of the
illness, he became paralyzed. In discussing Collins and Martland's paper,
Larkin stated that he had seen one instance of this disease following
potassium cyanide poisoning.
In the spring of 1930, there occurred in Ohio, Kentucky, Alabama,
Mississippi and other states an epidemic of paralysis.16,17 The patients
gave a history of drinking commercial extract of ginger. It is estimated
that at the height of the epidemic there were 500 cases in Cincinnati
district alone. The cause of the paralysis was subsequently shown to be
triorthocresyl phosphate in a spurious Jamaica ginger. Death resulted not
infrequently from respiratory paralysis similar to the bulbar paralysis
deaths in poliomyelitis. On pathological examination, the anterior horn
cells of the spinal cord in these cases showed lesions similar to those of
poliomyelitis.
These incidents show that epidemics of poisoning occur and furthermore,
that epidemic diseases do not always indicate that they are caused by
infectious agents. Moreover, following the ingestion of the spurious
Jamaica ginger, the symptoms appeared two to ten days later. In some cases
a longer time elapsed. This latent period is comparable to the incubation
period of infections diseases. As a matter of fact, the incubation period
of poliomyelitis is commonly stated to be seven to 10 days on the average
with considerable variation in either direction. The so-called incubation
period in poliomyelitis and the latent period in these cases of poisoning,
therefore, are strikingly similar in length.
Leenhardt et al.18 (1951) described acrodynia in the course of three
cases of acute poliomyelitis. Some authorities have considered acrodynia to
be caused by a poison. Elmore19 (1948) reported two cases of this disease
following the ingestion of mercury and Warkany and Hubbard20 (1951) found
mercury in the urines of 38 (92.7 per cent) of 40 acrodynia patients.
Meyerhofer21 (1939) reported that infantile acrodynia may immediately
follow certain forms at atypical poliomyelitis, especially
encephalomyelitis. Mercury is used as an insecticide and a fungicide and
the above clinical observations indicate that it might be a factor in
producing some cases of poliomyelitis.
Gougerot22 (1935) reported that during arsenical therapy for syphilis,
poliomyelitis developed in two patients, and lethargic encephalitis
followed by Parkinson's disease in one.
In 1936, during a campaign to eliminate yaws in Western Samoa by the
injection of arsenicals, an epidemic of poliomyelitis appeared
simultaneously.23 In one community all of the patients developed paralysis
in the same lower limbs and buttocks in which they had received the
injections and this pattern was repeated in 37 other villages, whereas
there was no paralysis in uninoculated districts. The natives accused the
injections as the cause of the epidemic of poliomyelitis. Most of the cases
of paralysis occurred one to tow weeks after the injection of the arsenic.
The foregoing reports indicate that poisons can cause poliomyelitis. It
would appear that not any one poison in particular would be responsible for
all cases of poliomyelitis but the effect of any one of several could
produce the same ultimate result. When a disease is known to be caused by a
poison, it is obvious that a search for a germ or virus in relation to it
would not be made. Conversely, if a so-called virus is believed to be
associated with the disease, then the possibility of poisoning as the cause
of the disease would not be considered. It will be shown, moreover, that
some so-called virus diseases and virus inclusions can be caused by poisons.
Dr. Robert W. Lovett24 of the Massachusetts State Board of health
(1908), describing the epidemic of poliomyelitis in Massachusetts in 1907,
and after reviewing the medical literature on experimental poliomyelitis,
states: "The injection experiments prove that certain metallic poisons,
bacteria and toxins have a selective action on the motor cells of the
anterior cornua when present in the general circulation; that the paralysis
of this type may be largely unilateral; that the posterior limbs are always
more affected than the anterior; and that the lesions in the cord in such
cases do not differ from those in anterior poliomyelitis." It appears to be
of great importance that various poisons, lead, arsenic, mercury, cyanide,
etc., found capable of causing paralysis are employed in relation to
articles of food that are used for human consumption.
There are two abnormal findings in cases of poliomyelitis that point
strongly to poisoning as the cause of this disease. One consists in the
appearance of increased amounts of porphyrin in the urine; the other is the
presence of increased amounts of guanidine in the blood. It is a well-known
fact that porphyria can follow poisoning by a number of chemicals.
Guanidine has been found in increased amounts in the blood in arsenic,
chloroform, and carbon tetrachloride poisonings.
The fact that ascorbic acid has been effective in the treatment of
poliomyelitis appears justly to imply that this disease has a poison cause.
Ascorbic acid has been used as a reducing agent in the treatment of
poisoning resulting from a number of toxic agents, including coal tar
antipyretics, nitro compounds, aniline, cyanide, benzene, lead, arsenic,
etc.32-40 Paralleling these modern scientific investigations is the
observation over a century ago that lime juice and lemon juice were
protective against the poisoning by fish which sometimes resulted in
paralysis,41,42. This early observation is perhaps the principle reason why
lemon juice is customarily served today when fish are eaten.
The fact that methylene blue,43 another reducing agent, is effective in
the treatment of poliomyelitis also points to the poison cause of this
disease. Methylene blue has been used as an antidote in the treatment of
nitrite, cyanide, carbon monoxide and other poisonings.
Another fact that strongly implies that human poliomyelitis is caused
by a poison is found in the recent report (1951) by Dr. Irwin S. Eskwith44
of Bridgeport, Conn., that BAL (dimercaprol) was effective in bringing
about complete recovery in a moribund 4 1/2 year-old girl with bulbar
poliomyelitis. BAL counteracts the effects of poisons; it has been shown
not to be effective in infectious diseases.
RELATIONSHIP OF HARVEST TO POLIOMYELITIS
[...]
In 1907, Dr. H. C. Emerson54, Massachusetts State Inspector of Health,
District 14, investigating an epidemic of poliomyelitis in that state, made
a careful inquiry regarding the diet. No infant who was fed exclusively on
the breast developed poliomyelitis. He found in six cases that fruit and
berries had been a large item of the diet. In the cases of two infants,
bananas and berries had been given in the diet in addition to breast milk.
In three cases of poliomyelitis, the illness was attributed to the eating
of large amounts of blackberries and blueberries. In one case the illness
was credited to eating heartily of English mulberries. In 39 instances it
was stated that food supplied were bought from fruit and vegetable peddlers
in their localities.
[...]
Dingman55 (1916) reported a milk-borne epidemic of poliomyelitis and
several similar outbreaks have been reported since then that were traceable
to milk.
[...]
Chapman58, raised the question of food poisoning to explain the
epidemic of poliomyelitis in England in 1947, when he stated: "Is it not
possible that the present prevalence of infantile paralysis may, in part at
any rate, be due to some article in our restricted and modified dietary?"
[...]
Toomey and August59 (1932) pointed out that some authors thought that
poliomyelitis is a disease of gastrointestinal origin which might follow
the ingestion of foodstuffs. In 193360, they noted that the epidemic peak
of poliomyelitis corresponds with the harvest peak of perishable fruits and
vegetables. They called attention to the fact that the disease occurs only
in those countries which raise the same type of agricultural products. Dr.
C.W. Burhans60, one of the colleagues of the authors, thought that green
apples might be a factor in the etiology of poliomyelitis. Toomey et al61.
(1943) points out that there is frequently a history of dietary
indiscretions previous to an attack of poliomyelitis. They suspected that a
virus could be found on or in unwashed fruit or in well water during
epidemics of poliomyelitis. Every year for eight years, therefore, grapes,
apples, peaches, and pears were collected from the vineyards and trees in
Northern Ohio at the time of the ripening. In none of their studies was the
so-called virus of poliomyelitis demonstrated when the washings of the
fruit or the well water were injected into experimental animals. However,
no chemical tests were made to determine whether or not a chemical
substance on or within the fruit or in the well water, acting by oral
ingestion top produce poliomyelitis, was present.
Draper62 (1935) recorded a series of cases of poliomyelitis which he
postulated originated from a Greek fruiterer. All of the cases were in
contact with the Greek as business associates, relatives or customers, and
there was nothing in the evidence to point to infection being carried by
the Greek himself other than the fruit he supplied.
[...]
Barber64 (1939) reported four cases of poliomyelitis that developed
simultaneously on the same day from the eating of strawberries in a single
house of a boarding school. He says that the simultaneous onset of these
cases resembled food poisoning. The seasonal and climatic incidence of
poliomyelitis, he points out, agree closely with the seasonal increase in
the consumption of fresh garden production. He says that the
epidemiological distribution of poliomyelitis resembles food poisoning.
Chenault65 (1941) noted that the history of poliomyelitis points to a
"suggested parallelism between a number of epidemics and the appearance of
fresh fruits and vegetables." [With regard to these numerous statements
regarding fruit and milk, note the high production of pesticides in the
form of lead and arsenic compounds during this pre-DDT period, graphed]
Goldstein et al66 (1946) reported an epidemic of polioencephalitis at a
naval training school among the cadets. The epidemic was explosive in
character and involved over 100 persons. Epidemiological evidence suggested
that some food served in the mess hall was the cause of the disease.
[...]
Gebhardt and McKay68 (1946) found during an epidemic of poliomyelitis
in Utah that of a total of 206 persons surveyed, 192 persons, or 93.2 per
cent, had one to two weeks prior to the onset of the disease eaten fresh
fruits. The authors found in Utah, New York and California, during 1943,
that the cases of poliomyelitis paralleled the harvest peaks. Most of the
multiple cases in families were found to have developed at the same time,
suggesting means other than contact as the mode of spread. Among the fruits
more commonly eaten were apples, peaches and pears; tomatoes headed the
list of vegetables. The authors stated that the data appeared to fit into
the jigsaw puzzle of epidemic poliomyelitis.
[...]
Abbott71 (1948), of Auckland, New Zealand, stated: "The public has
always been fully convinced that they caught poliomyelitis from one another
by direct infection. The 'germ' idea is indeed deeply ingrained in both the
profession and the public. It will be many years before our prolific
writers of medical textbooks attain the degree of sophistication that would
enable them to understand how and why poliomyelitis would be more likely to
be contacted from the flour-bag, or some homely article of food, rather
than from their neighbors."
[...]
Barondes72 (1949) points out that a study of the epidemiology of
poliomyelitis shows a definite correlation with the harvesting of fruit and
vegetable crops and to changes in climate, weather and humidity. The
harvesting of such fruits as cherries, grapes, berries, apricots, etc. and
the edible vegetables, as lettuce, radish, cucumbers, etc. usually from
June to September, corresponds with the period of poliomyelitis epidemics,
Barondes points out.
Toomey et al74 (1949) made some important experimental observations
that appear to show a correlation of the poison and virus theories of
poliomyelitis. They considered it possible that a food (fruit) which enters
the gastrointestinal tract could in some way act as a precursor of
catalytic enzyme on a normal constituent of the tract and accelerate the
production of poliomyelitis. Various materials, together with fruit
extracts, were tested.
When supernates of peach skin mash were injected intracerebrally into
cotton rats, followed at intervals with intracerebral injections of the
so-called poliomyelitis virus, accelerated production of paralysis
occurred. Because of the presence of cyanophore glucosides in peach skins,
a synthetic preparation, succinotrile, was injected intracerebrally into
the experimental animals. This chemical accelerated the production of the
disease similar to that produced with the peach supernates. Toomey et al.
emphasize that the injections of fruit supernates were made in a manner
that does not occur under natural circumstances.
Sabin75 (1951), although insisting on the virus etiology of
poliomyelitis, implicates food and drink as important factors in the cause
of this disease. He points out that measures which are often advocated to
combat poliomyelitis epidemics are not warranted, such as (a) avoidance of
crowds, large gatherings or sports events, (b) exclusion of children under
16 years of age from movies, churches, or schools, and (c) exclusion of
poliomyelitis patients and suspects from general hospital wards.
[...]
The implications [of the foregoing] should be obvious that
investigations of foods eaten by the poliomyelitis victim prior to his or
her illness should be carefully considered.
THE PRODUCTION OF SO-CALLED VIRUS DISEASES
AND "VIRUS" INCLUSIONS BY POISONS
much more at webpage