This essay is dedicated to the memory of Dan Olmsted, who died in January 2017 before he could complete the arc he had begun. Olmsted was a Yale-trained investigative journalist and founding writer at United Press International, where his “Age of Autism” series posed the question that would define the second half of his career: why don’t Amish children have autism? His fifteen-part “Age of Polio” series, published on Age of Autism in 2016, forms this essay’s forensic spine. He spent years reconstructing the 1916 New York epidemic from the health department’s contact-tracing files at the American Philosophical Society library in Philadelphia. His evidence chain is the single most granular piece of investigative work on this subject in print. In the last installment he wrote that he was taking a break to complete another project and would return “with a vengeance.” He did not return. This essay carries the work one step forward.
Forrest Maready’s 2018 book The Moth in the Iron Lung covers adjacent ground with a wider historical sweep, and at two junctures reaches conclusions that differ from Olmsted’s. Those junctures are noted where they arise. Both writers hold onto an infectious co-factor, viral in Olmsted’s case, bacterial in Maready’s. This essay does not. No exogenous infectious agent has ever been demonstrated as necessary to produce the paralysis called poliomyelitis. The evidence Olmsted assembled is toxin evidence. The paralysis was the poisoning.
Where establishment vocabulary appears (poliovirus, immune system, epidemic in its contagion sense), it appears in quotation, in attribution to named sources, or in reference titles. The author’s own analytical voice operates within the terrain paradigm, in which disease arises from toxic exposure, nutritional depletion, electromagnetic burden, and psychological strain, and in which microorganisms respond to terrain conditions rather than cause disease by invasion.
On June 19, 1916, Mrs. G.H. Franklin, fifty-six years old, was working behind the counter of her ice cream parlor at 1295 Gates Avenue, Brooklyn, when she collapsed. When she came to, she was paralyzed.¹
The building above her shop was an Italian tenement. Six weeks earlier, on May 1, a family had moved into the apartment adjacent to the parlor. Their thirteen-month-old daughter, Lettie Caruso, took ill on May 9 and died on May 23. On the top floor of the same building, a baby named Peter Pinchero died on May 24 after a four-day illness. Eight days before he was taken ill, a cousin living at the same address had also died. Two more Pinchero cousins and an aunt fell ill in May and recovered. Mrs. Franklin, according to the health department’s later reconstruction, had attempted to bathe one of the children who subsequently died.²
She kept the store open through all of it. The children in the building, in the words of the health department report, “naturally frequented” the parlor. She waited on them herself. In early June she began to feel pain in her neck, arms, and legs. She continued to work. On June 19 she went down.
She was taken to St. Mary’s Hospital. Nine different physicians examined her over the next ten weeks. None of them could agree on what she had. The final diagnosis was “a light case of meningitis.” She recovered enough to walk. On September 20 she was taken to Jamaica Hospital, and on October 1 she died. A health department card noted, quietly, that hers was the oldest case on record in the paralytic wave that killed 2,343 people in New York City that summer, most of them children under the age of six.³
The record of what happened at 1295 Gates Avenue in the spring and summer of 1916 is one address in one contact-tracing file among thousands preserved in Philadelphia. The address matters because the standard account of what happened that summer collapses in front of it. A common respiratory illness, transmitted from child to child in a tenement, does not paralyze a fifty-six-year-old woman who has worked around children all her life. Something else was in that building. Something else was on Gates Avenue. Something else was in the ice cream she was serving.
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The Brooklyn Wave
Before Mrs. Franklin collapsed, before the Brooklyn Daily Eagle carried its front-page notice on June 17 that “the officials of the board of health are somewhat worried and are taking measures to stamp out the disease,”⁴ twenty-nine cases of paralytic illness had already been recorded in Brooklyn for the month of May. The health department was slow to notice. Commissioner Haven Emerson later insisted that “there was nothing to excite suspicion” before the first eight days of June. The May cases were quietly omitted from his official chart.⁵
When workers finally went door to door and plotted the early cases on a map, a pattern emerged. The plurality clustered around the Gowanus Canal, in an Italian neighborhood the department would eventually identify as the epicenter. This became the standard story: an Italian neighborhood, filth, immigrants, dockworkers, a virus. The neighborhood was blamed for a century afterward, on the theory that the poliovirus had traveled from the canal outward.
The map, read carefully, tells a different story. By July 15, Brooklyn had recorded 1,403 cases of death or paralysis. One hundred nineteen sat close to the waterfront. Ninety-one of those clustered on six streets: 3rd, 4th, and 5th Avenues, and 17th, 20th, and 21st Streets. The dots do not converge on the Gowanus Canal. They converge on the streets leading to and from the docks at Bush Terminal, on the western edge of Brooklyn.⁶
Bush Terminal was one of the largest shipping complexes in the world. Pier 7, at the southern end, belonged to the American-Hawaiian Steamship Company. It was the largest sugar dock in the world. It received raw sugar shipped from Hawaii for delivery to the East Coast refineries. The paralysis cases were clustered on the streets a dockworker would walk to get to and from work.
The pattern then moved. From Brooklyn it reached Queens, where Queens recorded the highest polio rate of any borough. The National Sugar Refining Company operated a plant in Long Island City, on the Queens waterfront, that had at one point been the largest sugar refinery in the world. It sat where the East River meets Newtown Creek, bounded by rail tracks.⁷ The health department noted a “compact block of houses” on the Queens shore of the East River, directly opposite the refinery, in which multiple cases appeared. From Queens the pattern reached Yonkers, home to another National Sugar refinery. Yonkers had the highest polio rate of any American city with a population between 50,000 and 100,000.⁸
Forrest Maready, working the same territory two years after Olmsted, looked at the 1916 New York outbreak and reached a different conclusion. He wrote: “Lead arsenate poisoning alone could not explain the way the outbreak had started in Brooklyn and radiated outwardly.”⁹ Maready concluded that some additional infectious element was needed, and turned to Edward Rosenow’s work on pleomorphic bacterial forms to supply it.
The objection would be devastating if Olmsted’s account rested on ambient lead arsenate residues on fruit. It does not. Olmsted’s account rests on a specific delivery point (the American-Hawaiian dock at Bush Terminal), two specific refineries in the neighborhoods with the highest case rates in the outbreak (Long Island City and Yonkers), and a specific distribution chain reaching the ice cream parlors, candy shops, and bakeries where the ordinary observers repeatedly identified the case clusters. The radiating pattern is not mysterious. It follows the sugar. Maready did not consider the sugar chain, and reached for a bacterial explanation to solve a problem that the geography had already solved.
None of this was the story Emerson’s department was investigating. His workers were tracking stables, flies, rats, and secondary human contacts. The map was already telling a different story. The paralysis was following the sugar.
Olaa
The Olaa plantation sat on the windward side of Hawaii’s Big Island, on the volcanic slope where the westerly ocean winds crash into the mountain spine and dump up to two hundred inches of rain a year. Sugarcane grew well in the wet climate. So did everything else. Weeds ran wild over the two-year growing season, and the labor cost of pulling them by hand was breaking the plantation’s books.
In 1913 the owners hired a new manager, Charles F. Eckart, the former head of the Hawaii Sugar Planters Association’s experiment station. His salary was reported at $12,000 a year, roughly $290,000 in today’s money. He was hired to solve the weed problem, and he had a solution ready. He had been working on it at the experiment station with a colleague named H.P. Agee.¹⁰
The solution was arsenic.
In June 1915 the industry journal Sugar reported the method. Weeds were sprayed with sodium arsenite dissolved in water at a ratio of five pounds of arsenite to one hundred gallons. Two special spraying rigs had been invented, a sled sprayer and a knapsack sprayer. The journal noted that this appeared to be the first time arsenic had been applied at scale to sugarcane fields anywhere in the world. “It may be said that this method of weed control already has passed the experimental stage,” the article stated, “as it has been adopted as a part of the normal field work in the extensive plantation at Olaa.”¹¹
The article addressed two concerns. Would the arsenic damage the cane itself? Experiments had shown that even at five pounds per acre per week for six months, arsenic had no injurious effect on cane growth. Would the arsenic harm consumers of the eventual sugar? The article did not raise the question. The killed weeds were left in place to decompose back into the soil. The arsenic accumulated in the ground beneath the cane.
The question had been answered in 1900. The industrial districts of Manchester, England had experienced a mass poisoning event that affected roughly six thousand people. The source was sugar contaminated with arsenic. The sugar had gone into beer. The symptoms included nerve damage, paralysis, and skin eruptions. The mechanism was investigated and documented in the British medical literature at the time. The 1915 Sugar journal did not mention Manchester. Neither would the New York City Department of Health a year later.²⁷
By early 1916 the numbers looked spectacular. In February, Eckart reported that the 1915 crop had produced 283,116 tons of cane, yielding 32,308 tons of sugar. Grinding had started early because the yield was so high. The Honolulu Star-Bulletin ran a headline: “Cost of Producing Ton of Olaa Cane Cut Almost 50 Percent.” The plantation’s directors approved a $150,000 expansion. In May 1916 they declared their first dividend.¹²
By October 1916 the wheels had come off. The Louisiana Planter and Sugar Manufacturer reported that Olaa’s crop estimates for the coming year had collapsed. “Olaa Plantation, whose varying fortunes have been often the subject of comment by sugar statisticians and publicists, has further reduced its 1916 crop estimates. The disappointment of the investors and of the stock market players is keen over Olaa’s showing this year.” Nobody explained the reversal. Something had gone wrong with the crop, or with the sugar, or with what came out the other end of the refining process. In 2003 the Honolulu Star-Bulletin would report that health officials had found high levels of arsenic in the soil at community gardens in Keaau, the modern name for Olaa, and were offering free medical tests. The article traced the source to the herbicides sprayed on the local sugar plantation from 1915 to 1950.¹³
An environmental toxicologist Olmsted worked with on the series explained the chemistry. Sodium arsenite is highly water-soluble. On the volcanic Hawaiian slope, with two hundred inches of rain a year, it would have washed into the porous soil, migrated downhill, been available to the roots of any plant nearby, and been taken up into the cane tissue. Brazilian research she cited confirmed that sugarcane does take up arsenic and that more of it ends up in the stalk than in the leaves. The decomposing sprayed weeds served as a secondary source, cycling the arsenic back through the soil.
At the refinery, arsenite in solution behaves almost exactly like sugar. Both dissolve readily in water. Passive filtration systems of the era, designed to catch large particulates like crushed plant matter and stones, could not separate them. Arsenite runs through the filters. It travels with the sugar all the way to crystallization. Roughly eighty tons of cane produce one ton of sugar, meaning the refining process concentrates any dissolved impurity present in the cane. The final white crystals give no visual indication of what came with them.¹⁴
The 1915 crop, grown under the full arsenic treatment, was loaded onto American-Hawaiian Steamship Company freighters and arrived at Bush Terminal in Brooklyn in the early months of 1916.
What Arrived at the Refineries
The refineries noticed something was wrong. In 1917 the Hawaiian Sugar Planters Association sent a representative named R.S. Norris to the East Coast to investigate mounting complaints. His report was picked up and reprinted in three parts by the Louisiana Planter and Sugar Manufacturer in February 1918.
Hawaiian sugar, and only Hawaiian sugar, was giving the refineries fits. The grains were uneven and too small. Scale on the vacuum pan coils had to be boiled out with corroded lead every two weeks. The cotton bags tore. There was cloudiness and sediment in the barrel syrups, the golden syrup product sold as a sweetener for cooking. Even after repeat washing and flocculation with phosphate, the final product remained a dull gray. Something in the grain, in Norris’s phrase, “caused the trouble.”¹⁵
Norris tried to isolate what the sediment was. He reported that he “found it difficult to separate out, and for that reason have not had sufficient time to isolate the substance in a pure form.” The analyzed sediment showed potash, soda, lime, magnesia, sulfuric anhydride, and chlorine. Norris allowed that the sediment “may be an organic compound.” The Hawaiian syrup sold at a steep discount. In Philadelphia, Hawaiian barrel syrup went for nine to ten cents a gallon; Cuban syrup went for fifteen to seventeen. Nobody was buying Hawaiian syrup at full price because there was visibly something wrong with it, and nobody could say exactly what.
The consumers, of course, could not see what was in the crystals they bought at the store, or in the ice cream, the candy, the baked goods, the condensed milk, the soft drinks, and the summer fruits that were preserved with sugar.
What the Ordinary Observers Saw
Emerson’s health department received 230 written suggestions from the public about the cause of the paralysis. Eighty of them, the largest single category, blamed food. “Ice cream, soft drinks, candy and summer fruits were generally accused,” Emerson wrote in his 1917 official monograph. “Cereals and canned foods coming second in favor.” Emerson found this hilarious. “One hardly knows whether to laugh at the fantasies or weep over the ignorance and superstition exhibited,” he wrote.¹⁶
A few pages later in the same document, Emerson recorded that his own investigators, whom he called “unbiased minds,” had noticed the same thing:
There seems to be a well-marked tendency for cases in Manhattan to appear in the immediate vicinity of stables, groceries, meat or poultry markets, lunch rooms, delicatessen shops and bakeries or macaroni factories. It is surprising with what regularity one or the other is found in the building next door to a house in which poliomyelitis has occurred. Others who have also examined the same districts with an unbiased mind, seem always to believe that cases range themselves with a definite relation to shops of this type.¹⁷
His own chart, published on the facing page, tallied the associations from two neighborhoods in Manhattan and the Bronx: Candy. Grocery. Bakery. Ice cream. Candy. Grocery. Bakery. Ice cream. Candy. Grocery. Delicatessen. Grocery. Lunch Room. Grocery.¹⁸ The list overlapped substantially with the one Emerson had mocked when it came from the letter writers. Places that sold food heavy in sugar, and the sugary syrup that flavored soda water and ice cream, appeared with regularity next to buildings where children had been paralyzed. Emerson elevated the stables and meat markets in his written discussion and quietly buried the ice cream and candy.
The Coney Island and Rockaway Beach resort strips, which drew huge summer crowds to boardwalks lined with candy, ice cream, hot dogs, and soft drinks, suffered heavy case tolls that summer. Nathan’s Hot Dogs opened its first stand at Coney Island in 1916.¹⁹ A Brooklyn boy named Frederick Chapin, whose Brooklyn Daily Eagle obituary noted a kindergarten Eagle Honor Roll medal he was “the only one ever to receive,” went to Coney Island on June 20, developed paralytic illness, and died. His family remembered the Coney Island visit as the exposure. He was one of many. Several health department files describe families going to Coney Island over the July 4 holiday and children falling ill within days of the visit.
The pattern reached Baltimore. On October 15, 1916, the New York Times ran a story: “Germ of Paralysis Carried by Food. Theory of Baltimore Health Official. Seat of Disease is Large Intestine.” Dr. J.F. Hempel of the Baltimore Health Department and Dr. H.T. Burrows of Johns Hopkins had proposed that “candy, ice cream, fruit, and other uncooked foods that children eat, are primarily responsible for bringing the germ into the system.” They were preparing transmission experiments to test the theory.²⁰
Twenty-four hours later, the Times ran a follow-up: “Denies Hopkins Rumors: Stories of Startling Discoveries in Paralysis Untrue, Dr. Welch Says.” Dr. William H. Welch, head of the Johns Hopkins medical faculty and perhaps the most powerful medical authority of his day, told the paper that Hopkins had discovered nothing that would change the established view of the disease. “The statement that the disease may be transmitted through candy,” Welch said, “is entirely gratuitous.”²¹ Welch could have said “unfounded” or “incorrect.” He said “gratuitous.” The experiments were not conducted. The theory disappeared. Hempel and Burrows did not publish on the subject again.
The pattern that “unbiased minds” saw with regularity, that eighty of 230 letter writers described from their own neighborhoods, and that two respected physicians proposed to test experimentally, was closed down inside a day. Emerson had, in the same document, published a chart showing the pattern and then written a paragraph mocking the people who saw it. The Hopkins researchers had a testable hypothesis. Their institution’s most powerful figure publicly killed it inside a day.
The record of the summer of 1916 does not show a health department that pursued and rejected the food-supply hypothesis. It shows a health department that documented the food-supply hypothesis in its own charts and then refused to name what its charts showed.
Mrs. Franklin’s Death
After her collapse in the ice cream parlor on June 19, Mrs. Franklin’s decline was slow and confused. She spent weeks at St. Mary’s Hospital, where the doctors could not settle on a diagnosis. In early July she was released to her son’s home at 1250 Curtis Avenue in Woodhaven, Queens. On July 15 she moved again, to 4559 Metropolis Avenue in Queens. Nine days after she arrived at Metropolis Avenue, her grandson Willy fell ill. So did Edith Smith, the daughter of another tenant in the building. On July 30, at the Woodhaven home she had left two weeks earlier, her grandsons Herbert and Calvin fell suddenly ill. Herbert was diagnosed with poliomyelitis.²²
The nurse who tracked the family through the summer wrote that Franklin was “able to be up and around and shows no sign of paralysis although she is still very weak.” The nurse added: “There can be no doubt that Mrs. Franklin had poliomyelitis and as far as our records go this is the oldest case on record.”
The final card in the file, dated October 6, is three lines:
Name of patient: Mrs. G.W. Franklin. Patient was taken to Jamaica Hospital about September 20 and died October 1. She never entirely regained use of her limbs.
The health department, which had spent months tracking her movements and building files on the illnesses of her grandsons and the tenants who lived near her, never asked what she had been eating or what she had been serving the children. She died in October and the paperwork went into an envelope, and a century later Olmsted opened the envelope and read what was there.
Broadstairs
The pattern was not confined to New York in 1916. In October 1926 a cluster of paralytic illness struck the Broadstairs area of Kent, England. The British Medical Journal reported it in January 1927. Sixty-seven cases, four deaths. The features were peculiar. The illness was “limited mainly to the children attending private schools in the district, particularly boarding schools.” The schools had “very little communication with each other.” The illness started simultaneously in all the schools affected and ceased almost entirely at the end of a fortnight. It did not appear in the adjoining districts. It did not appear in the elementary schools.²³
Alongside the schoolchildren, adults fell ill: a mistress and two members of the domestic staff at the private schools. In one convalescent home, two children and three staff members. A twenty-two-year-old waiter at a Broadstairs hotel, who left the town on October 6, developed the illness on October 16, and died on the 21st. A twenty-nine-year-old woman who visited Broadstairs from October 2 to 9 died on the 22nd. The brother-in-law of one headmaster, who had been staying in Broadstairs for three weeks, visited the school for lunch on October 10 and fell ill on the 16th, six days after the boys at the school had.
Boarding pupils took all their meals at school. Day pupils went home in the evening. Elementary students went home for lunch. The waiter ate at the hotel. The lunch guest ate at the school. The visitor from London ate somewhere in Broadstairs for a week. What the affected shared was not proximity to one another but a food supply. Something contaminated came into the private-school and hotel kitchens of Broadstairs in early October 1926, was served over roughly two weeks, and stopped being served. Nobody at the British Medical Journal pursued the question. The report attributed the cases to the accepted viral agent and moved on.
The pattern from Brooklyn a decade earlier appeared again. Institutional food supply as the shared exposure. Ages skewed older than usual because the exposure was where people ate together, not where children played together. Adjacent populations spared because the supply route did not reach them. Two weeks of illness and then a stop when the tainted batch was consumed.
What Was Documented and What Was Assumed
Olmsted spent fifteen articles assembling a chain of documented facts. Arsenic was sprayed for the first time at scale on a Hawaiian sugar plantation in 1915. The first crop grown under the full arsenic treatment arrived at Bush Terminal in Brooklyn in early 1916. The earliest cases of paralytic illness in Brooklyn clustered around the streets leading to and from the sugar docks. The two boroughs whose refineries processed the sugar had the highest per capita rates in the outbreak. The Hawaiian sugar carried a visible impurity the refineries could not remove and could not identify, and it sold at a steep discount for that reason. Ordinary observers, health department investigators, and two named physicians all independently identified sugar-heavy foods and the shops that sold them as the pattern’s center. The commissioner of the New York Health Department mocked the food theory in one section of his own report and documented food-shop clustering in the next. A researcher at Johns Hopkins who proposed to test the food-transmission theory was silenced by the head of the medical faculty within twenty-four hours. Ten years later in Kent, England, a cluster of paralysis with the same shared-food-supply signature appeared, ran for two weeks, and stopped.
That is the record. Every piece of it points at a toxic exposure delivered through the food supply, most heavily through sugar.
Olmsted assumed something else was also present. He assumed the poliovirus, circulating quietly in the population, whose harm was “amplified” by the arsenic. He never demonstrated the virus. Nobody had demonstrated it in a single one of the cases he examined. The department’s contact-tracing files record symptoms, exposures, movements, and deaths. They do not record a virus. The virus was the frame within which the paralysis had been named. Once the illness was called poliomyelitis, the poliovirus was assumed to be present in every case, and the investigative work at the time proceeded from that assumption backward.
Maready looked at the same 1916 outbreak and reached a different conclusion about what accompanied the arsenic. He turned to Edward Rosenow, head of experimental bacteriology at the Mayo Foundation, who obtained tissue samples from 1916 victims and reported finding a form of streptococcus. Rosenow cultured the organism under conditions that shifted its form, worked with Royal Rife on microscopes that could visualize what standard equipment could not, and reported that his organism reliably produced poliomyelitis when injected into test animals. He conducted the work on over 2,000 experimental animals and considered it definitive.²⁴
Rosenow’s work is a real finding and deserves to be taken seriously. What he observed under Rife’s microscope was pleomorphism, the capacity of microorganisms to shift form in response to the conditions of their environment. Antoine Béchamp documented this in the nineteenth century. Günther Enderlein extended it. Rife visualized it. Lida Mattman, whose Nobel-nominated work on cell wall-deficient bacterial forms confirmed the same phenomenon under a different name, demonstrated it repeatedly in the mid-twentieth century. Pleomorphism is not a fringe claim. It is what happens when you look at bacteria closely enough and under conditions that let them show what they can do.
The question is what pleomorphism means. Maready reads Rosenow’s finding as an infectious agent, the polio-causing microbe medicine was looking for, only in bacterial rather than viral form. This keeps the germ-theory frame intact and swaps one microorganism for another. Through the terrain paradigm, the same finding reads differently. Compromised tissue, poisoned by arsenic, hosts microbial forms that would not appear in healthy tissue. Bacteria change shape in response to the terrain they occupy. What Rosenow visualized was the microbial signature of tissue that had already been damaged. The bacteria arrived because the tissue was compromised, not the other way around. They are the flies at the garbage heap. They are not the garbage.
Under the virus reading or the bacterial reading, an infectious agent has to be posited alongside the toxin, though nobody in 1916 or since has demonstrated one in the cases where the paralysis actually happened. Under the terrain reading, the toxin is sufficient. The paralysis is what arsenic does to nerve tissue. Popov demonstrated this in the nineteenth century, poisoning animals with arsenic and finding in their spinal cords the anterior horn cell damage that pathologists identify as poliomyelitis. Erlicki and Rybalken documented the same damage in human cases of arsenical paralysis.²⁵ The lesions are the same because the cause is the same.
The evidence Olmsted assembled requires only the toxin. The virus and the bacterium are inference from unexamined premises.
What actually declined between 1916 and the 1960s was the exposure. American-Hawaiian Steamship’s East Coast sugar runs stopped after the United States entered the war in 1917; the freighters were leased to the Navy, and Hawaiian sugar redirected west, staying at the Crockett, California refinery instead of crossing the country. Lead arsenate, invented in 1892 for the Boston gypsy moth infestation, dominated American orchards through the 1940s and was suspected as a paralysis trigger in medical journals as early as Putnam’s 1893 Boston paper, Caverly’s 1894 Vermont documentation, and a 1914 report from New Zealand. Lead arsenate was replaced after the Second World War by DDT, which the physician Morton Biskind identified in 1949 as producing symptoms nearly identical to what was then being diagnosed as polio, and which he testified to Congress about in 1950. Ralph Scobey followed with a 1952 statement to the same committee, arguing that poliomyelitis was a poisoning, not an infection.²⁶ DDT was restricted in the United States beginning in the late 1960s. Lead arsenate residues in soil declined over decades.
The Salk vaccine was introduced in 1955. Church bells rang across America. The paralysis outbreaks receded. The credit went to a vaccine acting on a virus that had never been demonstrated to cause the paralysis in the cases where the paralysis had actually happened. The exposures whose removal corresponds in time to the disappearance of the outbreaks were phased out for other reasons, under other names. Nobody in a position of authority was permitted to say what they had done.
Mrs. Franklin sold ice cream on Gates Avenue in Brooklyn in the spring of 1916. In the same weeks, the first commercial shipment of Hawaiian sugar grown under sodium arsenite was arriving at Bush Terminal, on the western edge of the borough. Two children in the building above her died. She served ice cream to their siblings and cousins. She collapsed in June and died in October. Nine doctors could not agree on what she had. Her card in the health department file records the oldest case in the outbreak.
The address is there. The date is there. The sugar chain is there. The refinery data is there. The letter writers are there. Emerson’s own contradictory chart is there. The Baltimore physicians silenced in a day are there. The Broadstairs cluster is there. The pesticide phase-out timeline is there.
What is not there, in any of it, is the virus.
How to Explain It to a Six-Year-Old
A hundred years ago there was a lady named Mrs. Franklin who sold ice cream in a shop in Brooklyn. Children in the building where she lived came into her shop every day. She scooped ice cream for them and gave them the cones.
Far away, on an island in the middle of the ocean called Hawaii, farmers were trying to grow sugar. Weeds kept eating their plants. So the farmers sprayed poison on the weeds. The poison killed the weeds. But some of the poison also went into the ground and into the sugarcane plants that grew there. When the sugar was cut and cleaned and turned into white sugar in a big factory, the poison was still inside it. Nobody could see it. The sugar looked just like normal sugar.
The poisoned sugar was put on big ships and sent to New York. It came to a dock near Mrs. Franklin’s shop. The bakers and candy makers and ice cream makers of Brooklyn bought the sugar and used it in everything they made. Mrs. Franklin used it in her ice cream.
Children ate the ice cream and the candy and the cake and drank the sugary drinks. Some of them got very sick. They could not move their legs. Some of them died. Two of the children in Mrs. Franklin’s building died. Mrs. Franklin got sick too and died a few months later.
The grown-ups called the sickness “polio” and said it was caused by a tiny germ that nobody could see. They spent fifty years blaming the germ. They made a shot to fight the germ and when the sickness went away they said the shot had saved everyone.
But the sickness went away because the farmers had stopped using the poison. The shot did not save the children. Stopping the poison did.
Nobody said so, because nobody wanted to say the sugar had been poisoned all along.
In Print
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References
Dan Olmsted, “The Age of Polio, Part 2,” Age of Autism, 2016.
Olmsted, “The Age of Polio, Part 1,” Age of Autism, 2016, from New York City Health Department contact-tracing files archived at the American Philosophical Society library, Philadelphia.
Olmsted, “The Age of Polio, Part 12,” Age of Autism, 2016; Haven Emerson, A Monograph on the Epidemic of Poliomyelitis (Infantile Paralysis) in New York City in 1916 (New York City Department of Health, 1917).
Brooklyn Daily Eagle, June 17, 1916, cited in Olmsted, “The Age of Polio, Part 3.”
Emerson, Monograph, cited in Olmsted, “The Age of Polio, Part 3.”
Olmsted, “The Age of Polio, Part 5,” Age of Autism, 2016.
Olmsted, “The Age of Polio, Part 11,” Age of Autism, 2016.
Olmsted, “The Age of Polio, Part 12,” Age of Autism, 2016.
Forrest Maready, The Moth in the Iron Lung: A Biography of Polio (Feels Like Fire, 2018), chapter “August, 1916.”
Masayo Umezawa Duus (1987), cited in Olmsted, “The Age of Polio, Part 7.”
Sugar journal, June 1915, quoted in Olmsted, “The Age of Polio, Part 7.”
Hawaiian Gazette, February 9 and May 19, 1916; Honolulu Star-Bulletin, February 25, 1916; Louisiana Planter and Sugar Manufacturer, September 1915 and October 1916, cited in Olmsted, “The Age of Polio, Part 9.”
Honolulu Star-Bulletin, 2003, quoted in Olmsted, “The Age of Polio, Part 9.”
Environmental toxicologist consultation reported in Olmsted, “The Age of Polio, Parts 8 and 11.”
R.S. Norris, report reprinted in Louisiana Planter and Sugar Manufacturer, February 1918, quoted in Olmsted, “The Age of Polio, Part 11.”
Emerson, Monograph, cited in Olmsted, “The Age of Polio, Part 3.”
Emerson, Monograph, quoted in Olmsted, “The Age of Polio, Part 3.”
Emerson, Monograph, food-cluster chart reproduced in Olmsted, “The Age of Polio, Part 3.”
Olmsted, “The Age of Polio, Part 3,” Age of Autism, 2016.
New York Times, October 15, 1916, quoted in Olmsted, “The Age of Polio, Part 4.”
New York Times, October 16, 1916, quoted in Olmsted, “The Age of Polio, Part 4.”
Olmsted, “The Age of Polio, Part 12,” Age of Autism, 2016, from health department contact-tracing files.
British Medical Journal, January 15, 1927, quoted in Olmsted, “The Age of Polio, Part 14.”
Maready, The Moth in the Iron Lung, chapters “Rosenow” and “The City of Dreams.”
James Ross and Judson S. Bury, On Peripheral Neuritis: A Treatise (1893), cited in Maready, The Moth in the Iron Lung, chapter “Boston, 1893.”
Morton S. Biskind and Irving Bieber, “DDT Poisoning: A New Symptom with Neuropsychiatric Manifestations,” American Journal of Psychotherapy, 1949; Biskind, statement to the Select Committee to Investigate the Use of Chemicals in Food Products, U.S. House of Representatives, December 12, 1950; Ralph R. Scobey, statement to the same committee, 1952. All cited in Olmsted, “The Age of Polio, Part 10.”
Liam Scheff, Official Stories (2012), chapter on polio. The 1900 Manchester arsenic-in-beer epidemic is further documented in the report of the Royal Commission on Arsenical Poisoning (1903) and contemporaneous articles in The Lancet.
As an RN educated in the late '60's in Central California I have had an interest in a book used in my education titled THE MERCK MANUAL. Interestingly, the "Manual" changed completely from the years 1899 to 1900. The 1899 manual is a homeopathic outline of all "conditions" and the different treatments available. The 1900 manual switches to fake germ-based "medicine" and pharma and calls the "virus" the "tiniest parasite "...fyi
Beyond interesting; it’s enlightening! There are two causal chains here; one imaginary and one causal, and along those twin rails runs a bullet train that takes us all the way to where we are today with SV40 promoters and enhancers. Underneath it all are two paradigms; ignorance hiding behind a narrative we call germ theory and enlightenment that leads us to the promised land of terrain theory! These two twin tracks give us our freedom if we know how to use them, and gives a whole new meaning to the phrase;” just follow the science.”