AGE OF AUTISM

Tics and Toxins: Similar Case in County Near LeRoy May Point to Environment

By Dan Olmsted and Mark Blaxill

BATH, N.Y., February 3 – “I’ve always been a fighter,” Bryan Tremblay says, and that’s not just a metaphor. Now 35 but still a slight 112 pounds at 5 foot 1, he was a bully magnet as a child and learned early to defend himself. That was an advantage when he wrestled for his high school team.

But now Tremblay, who lives in the Steuben County village of Bath in the Finger Lakes region, is battling a demon he can’t control. Since September, he’s suffered from a major tic disorder. It goes on, unpredictably, for hours a day. Even on three heavy-duty medicines, he has seizure-like episodes that leave him sitting dazed for half an hour.

 

The disorder keeps him at home. It makes it hard to study for his online degree in graphic design from the Art Institute of Pittsburgh – and well-nigh impossible to look for work after being laid off early last year from his job at a furniture factory. It creates inevitable fears for his health, his wife, his future.

“It’s so frustrating,” he says. “I just want an answer to what I’ve got.”

Whatever Bryan Tremblay’s got is remarkably similar to the tic-like illnesses that have afflicted 15 students at LeRoy Junior/Senior High School about 70 miles away. Many of the LeRoy students, all but one a girl, came down with the disorder about the same time Tremblay did (he didn’t hear about that until much later). Most were diagnosed with “conversion disorder,” and since so many cases were involved, medical experts have declared it a “mass psychogenic event,” in which stress or trauma is supposedly converted unconsciously into physical symptoms and spreads among affinity groups. School and state health officials say they’ve ruled out environmental or infectious causes and insisted again on Wednesday that the school the girls attend “is safe.”

No one is suggesting conversion disorder in Tremblay’s illness. No one he knows has anything like it. Extensive neurological workups have turned up nothing. He’s due for another follow-up in a couple of weeks at the University of Rochester Medical Center. Tremblay doesn’t drink or use prescription or recreational drugs, nor has he been to LeRoy.

He is no publicity seeker. His sister mentioned his situation in a comment on a story we wrote about LeRoy. She gave us his contact information when we asked, and we reached out to Tremblay.

In an e-mail, he responded: “The symptoms seemed to appear almost out of thin air. It started with uncontrollable body spasms and convulsions in my mid to upper body area. These convulsions lasted from approximately 15 minutes to a 30 minute span.

“Soon the spasms started moving to my head and neck area and the movement was similar to a strong neck-whip similar to that of whiplash, sharp and strong and completely random. I did seem to notice that the amount of stress was a factor in the strength of the tics. The problem is the stress level increases once it starts and the tics become stronger and increase as well.

“I noticed that after five months the tics have become vocal, more yelling and humming with points of time where I repeat noises over and over. I find myself spacing out for large amounts of time and daydreaming with difficulty recovering.

“I have also started hand and arm movements.”

In almost every way, Tremblay’s life circumstances could not be more different from the LeRoy cases. But one common factor was evident during a visit – water. Water everywhere. Tremblay lives in a low-lying area. His house backs up to a levee less than a football field’s length behind his house.

Tics and Toxins: Leroy Put Student Playing Fields on FEMA Flood Hazard Land

By Dan Olmsted and Mark Blaxill

LEROY, N.Y., February 2 – School officials who say environmental factors can’t be responsible for the outbreak of tics at the Junior/Senior High School might want to check last year’s record rainfalls – and the flood-prone ground right under their feet.

The tics broke out after an unusual pattern of heavy rain, followed by a mild winter that has kept the ground from freezing and left lots of standing water at Leroy Junior/Senior High School.

That should be no surprise. Part of the school grounds -- including athletic fields -- are right on top of a federally designated FEMA Flood Hazard Area. While a county official told us that the school itself sits on a slope just above the hazard area, the zone cuts right across the girls’ softball diamond, as well as the football/track field and another, larger baseball field.

The land in the flood hazard area generally correlates with other mapping that shows less optimal and more flood prone Canandaigua soil covering the site.

In fact, we’ve been told by local residents that some fields, including the girls’ softball field just built in 2009, had to be dug up and rebuilt within the last year because the ground was so wet. The building itself has not escaped water and structural woes – the gym could not be used when the school was first opened a few years back because the floor buckled and sank, and the opening of school was delayed one year for a week by flooding, according to a former student.

School officials won’t comment, but Superintendent Kim M. Cox issued a new statement Wednesday, mostly blasting national press attention and the involvement of famed advocate Erin Brockovich, who has cited a train derailment of hazardous material a few miles from town in 1970 as a likely cause. Cox said new tests have shown drinking water inside the school – which comes from neighboring Monroe County – is safe.

Citing state and federal experts, she said: “All of these agencies and professionals from these agencies have assured us that our school is safe. There is no evidence of an environmental or infectious cause. Environmental causes would not discriminate. We would see a wide range of people affected.”

But no one seems to be looking up at the sky or down at the ground. LeRoy, like other New York state and Northeastern U.S. locations, has seen an epic amount of rain during the past 12 months. We put this chart together to show 2011 rainfall versus normal amounts in Buffalo and Rochester. LeRoy is located between them.

An Elaborate Fraud, Part 10: In Which the BMJ Suppresses the Truth About a Child’s Treatment and Recovery From Autism

One of the 12 children on a doctor visit not long after the BMJ articles were published in January.

By Dan Olmsted

The British Medical Journal began its attack on Dr. Andrew Wakefield last January by telling the story of Child 11, one of the case histories Wakefield allegedly altered to manufacture "the appearance of a link" between the MMR shot and autism.

Contrary to Wakefield's claims, Child 11’s autism symptoms began before he got the shot, author Brian Deer wrote. The father, he said, was outraged by Wakefield’s "fraud.” Even the child’s autism diagnosis was questionable, Deer wrote, because it was solely based on parental “recall.” 

As we’ve shown in earlier articles, the BMJ was dead wrong on both counts – the shot did come before the symptoms, and the autistic regression that followed was all too real. Both facts were described and documented multiple times by outside doctors before the family got anywhere near Wakefield or the Royal Free Hospital in London, where he worked. They do not provide any basis to allege fraud or question Wakefield’s version of the child’s medical history.

There are three more critical facts about Child 11 – facts that contradict this “fraud” scenario -- that the BMJ suppressed:

The father did believe the MMR shot caused his son’s regression.

The child was treated accordingly.

And, according to the father, the child recovered.

“Our dedicated effort to save our son's life has been fruitful,” the father wrote Wakefield on January 7, 1997, when he first sought to have him evaluated at the Royal Free. “As a small child unable to communicate, he has now entered a normal kindergarten class with assistance of a tutor. He is quite intelligent and continues to progress, but is still fighting the [bowel] disease which we believe is viral, from the vaccine.”

Yes, from the vaccine. After the father saw how he had been portrayed in the BMJ, he said: "Mr. Deer’s article makes me appear irrational for continuing to believe that the MMR caused difficulties which predated its administration."

And how, exactly, did the child recover from what the father believed was a vaccine injury? The letter reports: “In March of 1994, we met with Dr. [name omitted] and his immunological panel of tests indicated an underlying immunodeficiency as you can see by his report. His suspicions of the MMR vaccine in my son's case are mentioned in his letter. He was immediately put on 400 mg/kg of IVIG every four weeks at [clinic name omitted], and he responded quite well to the treatment.”

IVIG is intravenous immunoglobulin, administered to boost antibody levels in immune deficient patients and, at high doses, to regulate autoimmune conditions.

The father took his son to another leading immunologist, who reported that his measles virus titer was above measurable limits. Workups by a third doctor revealed his son “was suffering from indeterminant inflammatory bowel disease.”

This was the apparent new syndrome the Royal Free doctors were treating and that Wakefield was investigating – indeterminate or non-specific inflammatory bowel disease and autistic regression, in most instances associated in time by parents or  doctors with the MMR shot. The father learned of the work at the Royal Free from his American doctors and was the first to fly his child across the Atlantic because he believed his son was showing the same pattern. The first case series, on 12 such children including Child 11, was published in The Lancet in 1998.

But this clear sequence – vaccination, illness, regression, chronic bowel inflammation, treatment, recovery – is nowhere to be found in the BMJ account of Child 11, even though Deer met with the father twice, in California and London, and also communicated with him via e-mail.

Absent, too, is the fact that Child 11 is now in college in California after graduating from high school with a 3.75 academic average.

The treatment the father cited, and the rationale for it, has been described in detail by the U.S. doctor who administered it. “A number of immunological abnormalities have been observed in patients with autism,” according to the text of comments he subsequently made at a meeting of an autism group. He said all the children he treated, which included child 11, had regressed after the MMR shot.

“Natural killer cells … that appear to play an important role in defense against virus infected cells and tumor cells are decreased both in numbers and functions in patients with autism. This deficiency may play a role in increased susceptibility to various infections that may in turn play a role in the pathogenesis of autism.”

He goes on to describe the use of IVIG in this context, at the 400 mg/kg dose the father cited. “IVIG has been used in a number of primiary immunodeficiency syndromes, and autoimmune and immunoinflammatory disorders including demyelinating polyneuropathy, multiple sclerosis, Guillain-Barre syndrome."

In his autistic patients, "The results of IVIG treatment show that a noticeable improvement, although to a variable degree, was observed in reciprocal social interaction, verbal and non-verbal communication, and repertoire of activity and interest in all children. One of these patients has been 'completely cured' and is attending regular school."

Deer had every opportunity to gather and report these crucial facts yet chose not to. Why? This more complete narrative would have contradicted his claims of fraud in the BMJ. You simply can’t have a child being treated for a presumed vaccine injury, and according to the father, recovering, if you’re trying to make the case that the shot came after the onset of regressive autism, that the sequence was manipulated by Wakefield, and that the father is outraged about the deception.

Instead, Deer spun a story using only fragments of the truth and, exploiting a typographical error in a discharge document, claimed that Wakefield faked the data on autistic regression and bowel disease.

Amazingly, multiplied by 12, such sleight-of-hand lies behind the entirety of the BMJ’s fraud claim. Speaking at the U.S. National Institutes of Health, BMJ Editor Fiona Godlee cited “multiple discrepancies” by Wakefield in the description of "inflammatory bowel problems, regressive autism, and the parental claim that MMR was the underlying cause. What these articles [in the BMJ] also say [is] that when those three things didn't come up trumps on the twelve children included, and the subsequent series of children, Andrew Wakefield altered the data to make those three things emerge."

Actually, in its treatment of Case 11, it was the BMJ that “altered the data to make those three things” disappear.

An Elaborate Fraud, Part 9: in Which the BMJ's Fraud Claim Collapses -- and No One Hears It Fall

One of the 12 children on a doctor visit not long after the BMJ articles were published in January.

Read parts 1 - 8 of An Elaborate Fraud in Age of Autism Exclusives.

By Dan Olmsted

In 37 years in the news business, I’ve never seen anything like it.

The stunning collapse of the British Medical Journal's allegation of fraud against Dr. Andrew Wakefield, less than a year after it was made with so much fanfare, raises an inevitable question: when is the mainstream media going to realize they've been had, and what are they going to do about it?

When will they notice that not only were the allegations recycled from a two-year-old account produced by the Murdoch media empire's disavowed methods, but that the whole tangled mess has landed right on the doorstep of the BMJ in Trafalgar Square?

NOW would be a good time to notice -- now that the central premise of the paper has been shown by the BMJ itself to be a "matter of interpretation" -- not an elaborate fraud perpetrated by Wakefield in plain sight of his 12 well-respected co-authors at one of the top medical clinics in the world. And now that "multiple discrepancies" claimed as the remaining evidence are turning out to be the journal’s, not Wakefield’s.

"A syndrome necessarily requires at least some consistency," author Brian Deer wrote in January in  "How the Case Against the MMR Was Fixed," attacking the Wakefield paper's claim that a consecutive series of children arrived at the Royal Free Hospital in the late 1990s with signs of regressive autism and bowel disease, and that some of the parents blamed the MMR. "But, as the records were laid out, Wakefield's crumbled."

What's crumbling now is the credibility of the British Medical Journal.

--

Like Gaul, the allegation of fraud is divided into three parts. According to BMJ Editor Fiona Godlee, speaking at the U.S. National Institutes of Health, the fraud was constituted of Wakefield’s statements about "inflammatory bowel problems, regressive autism, and the parental claim that MMR was the underlying cause. What these articles [by Brian Deer] also say [is] that when those three things didn't come up trumps on the twelve children included, and the subsequent series of children, Andrew Wakefield altered the data to make those three things emerge."

Altered the data on those three things? That seems clear enough. A sidebar titled "How the linked was fixed" – fixed as in faked as in fraudulent --  makes the same claims:

"--Three of nine children reported with regressive autism did not have autism diagnoses at all. Only one child clearly had regressive autism.

-- Despite the paper claiming that all 12 children were 'previously normal,' five had documented pre-existing developmental concerns.

-- In nine cases, unremarkable colonic histopathology results -- noting no or minimal fluctuations in inflammatory cell populations -- were changed after a medical school research review to 'non-specific' colitis."

And who made these fraudulent changes? "It had to be Wakefield," Godlee wrote. He was the one who "altered the data to make those three things happen."

But hold on. Godlee is now taking that back without saying so. In fact, she says she never said it. The reason she's slithering away from those clear assertions is that this month, an independent microbiologist named David Lewis presented the BMJ with the actual gut pathology "grading sheets" created by another member of the research team, Dr. Amar Dhillon. Godlee rustled up experts to claim that the pathology did not appear to be as problematic as the paper claimed, but also quoted an outside expert saying there was no evidence of fraud!

The Age of Polio: How an Old Virus and New Toxins Triggered a Man-Made Epidemic

(Managing Editor's Note: Below is the 7 part series in full for you to share, FB, Tweet. Thank you.)

By Dan Olmsted and Mark Blaxill

1. The Wrong Narrative.

Polio is the iconic epidemic, its conquest one of medicine’s heroic dramas. The narrative is by now familiar: Random, inexplicable outbreaks paralyzed and killed thousands of infants and children and struck raw terror into 20^th century parents, triggering a worldwide race to identify the virus and develop a vaccine. Success ushered in the triumphant era of mass vaccination. Now polio’s last hideouts amid the poorest of the poor in Asia and Africa are under relentless siege by, among others, the Bill & Melinda Gates Foundation. Eradication is just a matter of time, and many more illnesses will soon meet the same fate.

But based on our research over the past two years, we believe this narrative is wrong – and wrong for reasons that go beyond mere historical interest. The misunderstanding of polio has warped the public health response to modern illnesses in ways that actually make them harder to prevent, control, and treat.

The reality, we believe, is that the virus itself was just half the epidemic equation -- necessary but not sufficient to create The Age of Polio. Outbreaks were not caused solely by poliovirus – the microbe was an ancient and heretofore harmless intestinal bug -- but by its interaction with a new toxin, most often innovative pesticides used to treat fruits and vegetables.

This alternative narrative makes better sense of the natural history of polio, and it resolves a number of anomalies that remain to this day. It suggests why poliomyelitis outbreaks emerged, evolved, and exploded the way they did; it probably solves, for the first time, the enduring riddle of why Franklin D. Roosevelt was afflicted 90 years ago this summer on Campobello Island; and it may mean today’s billion-dollar-a-year eradication effort is misguided, if not downright quixotic.

These are large claims. Let us explain.

--

Polio was a strange illness, never fully understood even by those who devoted their lives to studying and subduing it. It was a summer plague, coming on in late spring and all but vanishing in the fall. Many thought contagion had something to do with water, and Americans kept their children away from swimming pools in droves.

There is a profound distinction between poliovirus – an enterovirus, one that enters through the mouth and takes up residence in the GI tract and bloodstream – and poliomyelitis, the paralytic form of the illness. In the vast majority of cases, the virus causes either a minor illness or an inapparent infection.

But in 1 or 2 in 100 cases, the virus somehow gets past multiple defenses and into the nervous system, where it finds its way to the anterior horn cells at the top front of the spinal column. There, it preferentially attacks the gray-colored motor neurons (polio means gray in Greek) and causes inflammation of the protective myelin sheath (myelitis). This interferes with nerve signals to the muscles and can lead to temporary or permanent paralysis of the limbs and the respiratory system. A small number of people who contract poliomyelitis -- on the order of 1 percent -- die.

The first recorded U.S. outbreak was in 1841 in West Feliciana, Louisiana (10 cases, no deaths). There was a half-century gap until the next cluster, in 1893 in Boston (26 cases, no deaths). Then, in 1894, came what is widely regarded as the first major epidemic, in Rutland and Proctor, Vermont (132 cases, 18 deaths). Thirty more outbreaks – from such seemingly disparate locations as Oceana County, Michigan, and California’s Napa Valley -- were reported in the United States through 1909. The worst by far was New York in 1907, with 2,500 cases and a five percent mortality rate, a harbinger of the 1916 epidemic in the Northeast that killed 2,000 in New York City alone.[i]

What is most remarkable about this list is that so few outbreaks of paralytic polio were recorded anywhere in the world before the latter 19^th century. Poliomyelitis is considered an ancient scourge, but the evidence supporting that belief is quite threadbare. An oft-cited Egyptian drawing depicts a priest with a withered leg that could have stemmed from paralytic polio, but for most of recorded history there were few observations of the sudden-onset fever and paralysis in infants that characterizes the disease. The earliest well-documented case of infantile paralysis in an individual is widely considered to be Sir Walter Scott, afflicted as an infant in 1773.[ii]

There is little question that the poliovirus was endemic in humans for millennia; there may even have been isolated cases of poliomyelitis for much of that period. Yet the poliovirus did not trigger widespread outbreaks of poliomyelitis. Setting aside for now the 1841 Louisiana outbreak, reported retrospectively, something seems to have happened around 1890 to launch The Age of Polio in the United States. And something else must have changed around the end of World War II to create the large modern epidemics seared into the minds of older Americans, thousands of whom are poliomyelitis survivors and almost all of whom know someone who was afflicted.

While we have not written about polio, we have seen this pattern before. In our book, The Age of Autism – Mercury, Medicine, and a Man-made Epidemic, we argued that something happened in the 1930s to launch The Age of Autism.[iii] We proposed it was the commercialization of ethyl mercury compounds for use in pesticides – seed disinfectants and lumber preservatives – and in vaccinations; we offered evidence of those inventions in the family backgrounds of the first autism cases identified in the medical literature, in 1943. Similarly, we proposed that the sharp rise in autism cases beginning around 1990 tracks with the federal government recommending several more mercury-containing shots.

Our attention was drawn to polio during our autism research when a virologist mentioned, in passing, that poliomyelitis could be triggered in some instances by injections. Called “provocation poliomyelitis,”[iv] this can happen when a needle stick punctures a nerve in the peripheral nervous system. An active poliovirus infection – typically, in a child exposed to the virus for the first time and not yet immune -- can gain access to the nervous system through a process called “retrograde axonal transport,” traveling back to the spinal column and triggering the dreaded paralytic form, poliomyelitis.

Such cases of provocation paralysis, we learned, occurred in Eastern Europe when antibiotics were excessively administered by injection; this practice led to multiple cases of poliomyelitis.[v] Bulbar polio – of the throat and respiratory system – was recognized as more common after tonsillectomies, again because nerve endings had been exposed.[vi] Outbreaks, then, can unquestionably occur as a result of an environmental injury, in these instances either excessive injection or surgery that led to peripheral nerve damage, in the presence of poliovirus infection.

We began to look at the poliomyelitis literature and found that another and much more comprehensive environmental theory of the disease had been put forward almost immediately after the early outbreaks, although it never gained mainstream attention. This theory proposed that what is called “polio” is not caused by a virus at all, but by poisoning from pesticides. In this theory, lead arsenate triggered the early clusters, and DDT kicked off the large outbreaks after World War II. (The pesticide theory has been championed in recent years by Jim West[vii] and by Janine Roberts[viii].)

That really got our attention. In our research for The Age of Autism, we investigated a paralytic illness we believe resulted from an unrecognized interaction between a toxin and a microbe. Called general paralysis of the insane, or GPI, it was a gruesome and universally fatal outcome in a percentage of people infected years earlier with the syphilis bacteria. We proposed that a manmade mercury compound -- ironically used to “treat” syphilis -- allowed syphilis to gain entrance to the brain. When penicillin was developed in the 1940s and actually killed syphilis infections, GPI disappeared because one of the two requirements for the illness – the microbe – was destroyed.

We suggested that a number of other illnesses may follow a similar pattern in which microbes and metals interact, including, in some instances, autism. So the idea that an environmental insult – whether a needle stick or surgery or a toxic metals exposure – could be at work in outbreaks of poliomyelitis intrigued us.

But we did not find the claim that polio was simply poisoning by pesticides alone to be persuasive. The strong versions of both the virus theory and the pesticide theory – that it was entirely one or the other – are too simple to explain the pattern of evidence. The strong viral theory can’t explain the sudden emergence of poliomyelitis; the strong pesticide theory can’t explain the sudden protective effect of poliovirus vaccinations. Rather, we propose that poliomyelitis outbreaks are man-made events that result from the synergy of microbe and toxin.

The Age of Polio: How an Old Virus and New Toxins Created a Man-made Epidemic -- Part 7, “Where was God?” Lessons learned and lost.

Read Part 6, Part 5, Part 4, Part 3, Part 2 and Part 1.

By Dan Olmsted and Mark Blaxill

What, then, is the natural history of polio telling us? Beyond the lessons for containing polio outbreaks themselves, we suggest that a single-minded focus on germs – and an unwillingness to explore novel and potentially uncomfortable ideas from outside medical orthodoxy – is an inadequate strategy when it comes to modern diseases.

It’s hard to overstate the impact the polio experience has had on our modern medical culture, starting with the doctors who watched helplessly as its victims fell. J.R. Paul, in his definitive A History of Poliomyelitis, wrote how “the flowering of scientific medicine brought a new point of view, an era of sudden and incredible hope that something might be done after all.”

For a generation of medical professionals born in the heart of this period, the heroic conquest of poliomyelitis was among the most influential narratives that shaped their beliefs about medicine. These beliefs go far beyond science, as Paul suggests. “As the crusade heightened, the world looked on expectantly. … Much as our grandparents had contributed during the nineteenth century to missionary societies, our dimes and dollars went to another ‘religious’ cause, signalized by efforts to stamp out this pestilence and to alleviate the suffering and tragedy it inflicted.”

Paul leaves no doubt as to the hero of this new religious crusade. “[I]n due time, the disease was abruptly scotched by means of vaccination. It was to all intents and purposes finished. The crusade has been described as one of the greatest technical and humanistic triumphs of the age. It was one of those rare achievements which the world greeted as an example of what could be done when science and technology were directed to good use for mankind.”[i]

--

But the victory over the epidemics of poliomyelitis means our understanding of polio is essentially frozen in amber, circa 1955. Few diseases have been so completely conquered, at least at home, while being so incompletely understood, and that is not a good outcome. In leaving so many important topics on the table – why outbreaks occurred, why the pattern of contagion was so atypical for an infectious disease – scientists allowed some weak ideas to become conventional wisdom and some important ones to be missed.

The prevailing current explanation for the rise of poliomyelitis outbreaks is the “hygiene hypothesis,” which posits that such simple steps as clean underwear, better sanitation and good housekeeping, along with less exposure to germs like polio in early infancy, meant the effects of disease became much worse when children were finally exposed. This is not a satisfactory explanation, and it never has been – the epicenter of the 1916 epidemic was placed in possibly the filthiest place in The Bronx, an Italian immigrant community evocatively called Pigtown. And hygiene certainly doesn’t work very well to explain polio’s persistence among the world’s poorest, where sanitation is bad and public health infrastructure is close to nonexistent.  (“One injection stops smallpox, The Times noted in its article of Gates’ polio drive, “but in countries with open sewers, children need 10 polio (vaccine) drops up to 10 times.”)

The Age of Polio: How an Old Virus and New Toxins Triggered a Man-made Epidemic -- Part 6, After: The Persistence of Polio

Read Part 5, Part 4, Part 3, Part 2 and Part 1.

By Dan Olmsted and Mark Blaxill

To summarize our theory: Polio is a virus, contagious like other viruses, and generally a harmless enterovirus. When it is introduced into the human body, it has the capacity to enter the nervous system when nerves are damaged. Damage can occur many ways: mechanically through needle puncture or surgery, or, we propose, biochemically via pesticidal or other toxic exposure. Once the virus enters the nervous system, it becomes dangerous in a way nature never allowed before. It spreads through the nervous system via "retrograde axonal transport." The resulting damage can lead to paralysis or death.  

Two regions of the world continue to experience polio outbreaks, despite hopes the virus would be eradicated by 2000. This persistence has surprised and confused the experts.

“The eradication campaign has been stalled from about 2002 to 2007 … Why is it so difficult to complete the global eradication of wild poliovirus?” asked Neal Nathanson of the University of Pennsylvania School of Medicine in a 2008 medical review, “The Pathogenesis of Poliomyelitis: What We Don’t Know.”[i] (What we don’t know turns out to be a lot – the paper runs to 50 pages.)

“Currently, there are two epicenters that have resisted virus elimination, one in South Asia (Afghanistan, Pakistan, northern India) and one in West Africa (centered in Nigeria). What explains the persistence of wild polioviruses in these two foci?”

Nathanson cites three possibilities: those are warm climates, so poliovirus doesn’t go dormant in the winter as it theoretically did in other countries; the prevalence of other enteroviruses means that the live-virus polio vaccine is not as effective because the other viruses interfere with it; and poor public health infrastructure couple with fears about vaccination made the achievement of “herd immunity” harder than expected.

If one considers the toxin idea, however, another explanation jumps out, especially in South Asia. Erase national borders for a moment. While outbreaks are small and have waxed and waned over the past decade, the primary sites have been directly south of the Himalayan range in a smiley-face arc that runs west from Nepal and Bangladesh, through the Northern India districts of West Bengal, Bihar and Uttar Pradesh, into Pakistan and Afghanistan.

(Photo: The Ganga-Meghna-Bramhaputra River Basins: An arsenic hotbed below the Himalayas)

This also happens to be the area with the worst mass poisoning from arsenic in human history. This is not ancient history – it didn’t even begin until the 1980s. It is a story of the single-minded war against microbes gone badly wrong. What happened is beautifully outlined in an American Scientist article, “No one checked: Natural Arsenic in Wells.”[ii]

The Age of Polio: How an Old Virus and New Toxins Triggered a Man-made Epidemic -- Part 5, Before

By Dan Olmsted and Mark Blaxill

Our research on the natural history of autism convinced us that while there may have been a few scattered cases throughout history, the disorder first occurred in appreciable numbers – as clusters and ultimately as an epidemic -- only after 1930. Observations at that time about the rarity and novelty of the disorder are far more persuasive than retrospective efforts to claim significant numbers of cases before then.

The same holds true for poliovirus. Nowhere is that clearer than in the 1917 book “Poliomyelitis In All Its Aspects,”[i] by John Ruhrah and Erwin E. Mayer. “It seems to be a disease of comparatively recent origin,” they wrote. “In the history of most diseases there is a gradual shading off into the older writers until the disease is lost in confusion of inaccurate descriptions. Not so with polio.”

They continued: “The disease is so striking in its symptomatology, so devastating in its results, and produces such a deep impression on the popular mind that it does not seem possible that any very considerable epidemics could have happened in the countries in which there were physicians making records of what occurred.”

The same point is driven home by John R. Paul in his standard 1971 text on the disease, A History of Poliomyelitis [ii]. “There was no idea in the eighteenth and early nineteenth centuries that poliomyelitis was contagious,” wrote Paul, a professor of preventive medicine and epidemiology at Yale who conducted important polio research himself. A half a dozen cases within a half-mile of each other might have escaped notice, but “had there been larger outbreaks in the early or mid-19^th century it seems highly unlikely that they would have gone unnoticed.”

But just as arsenic and lead caused instances of paralysis before the invention of lead arsenate, there was also an emerging medical literature of poliomyelitis before recurring outbreaks began in 1893. Beginning just before 1800, there’s a history of doctors who took a reasonable cut at identifying the disease. These include, in 1789, Michael Underwood, who used the term “debility of the lower extremities”[iii]; and in 1840, Jacob Heine, who is sometimes credited as the first to diagnose poliomyelitis.

Several doctors later used the word “paralysis” in describing a similar condition in infants: West in 1843; Rillet in 1851; Duchesne in 1864. By 1860, Heine had pinpointed the spinal cord as the source of the paralysis, and in 1872, the great French neurologist Jean-Martin Charcot called it “tephromyelitis anterior acuta parenchymatose.” This was a pretty modern description, but his precise nomenclature didn’t quite catch hold. In 1874, German doctor Adolph Kussmaul coined the term “poliomyelitis anterior acuta,” later shortened to poliomyelitis.

Going further back, plausible descriptions grow sparse but include the crippled Egyptian priest in a stele dated from 1580-1350 B.C. In 460 B.C., Hippocrates wrote about clubfoot, which may have included some cases of infantile paralysis. And in 200, Galen also discussed clubfoot.

But those were vanishingly rare, and when Underwood described “debility of the lower extremities” in 1789, he clearly thought he was reporting a new phenomenon, just as Ruhrah and Paul asserted with the benefit of much greater epidemiological sophistication. “This disorder either is not noticed by any medical writer within the compass of my reading, or is not so described as to ascertain the disease here intended,” Underwood wrote. “It is not a common disorder anywhere, I believe.”

--

Outbreaks of more than one case, then, were a distinctly 19^th-century phenomenon, and until the 1890s worldwide episodes can be counted on two hands[iv]:

-- In 1835, John Badham’s description of 4 cases in Worksop, England.

-- In 1830-36, Charles Bell’s discussion of multiple cases in St. Helena.

The Age of Polio: How an Old Virus and New Toxins Created a Man-made Epidemic -- Part 4, Post-War Epidemics and the Triumph of Vaccination

Read Part 3, Making Sense of Campobello; Part 2, A Gypsy Moth Flaps its Wings and Part 1, The Wrong Narrative.

By Dan Olmsted and Mark Blaxill

Life magazine for August 15, 1949, reflected the booming exuberance of the times. The cover, “How to Dress for Hollywood,” featured a buxom starlet in suitably sultry attire. There were ads for DeSotos and Nashes and Chevys to mobilize families and their growing broods of children; cigarettes like Pall Mall, whose “greater length of traditionally fine, mellow tobaccos serves as a longer, natural filter to screen and cool the smoke on the way to your throat”; toothpastes to brush away smoker’s breath and shine stained teeth, and articles on everything from a new sailboat called the Sunfish to a town in Louisiana that cut its taxes in half by installing slot machines.[i]

But twin specters of death and destruction hung over this bright baby-boomer world – the anxiety over atomic annihilation if the Cold War turned hot, and every parents’ most proximate fear for their children, polio.

There were two articles on polio in this August issue. One was titled “Summer season brings epidemics of this uncontrollable disease” and noted that “throughout the nation last week the threat of polio was growing. Starting with some spotty outbreaks during May and June the disease had reached near-epidemic proportions during the sultry drought-ridden month of July. By Aug. 1, 8,300 cases had been reported, a 43% increase over last year. Polio seemed more uncontrollable than ever.”

The peak was still ahead – 1952 would bring 58,000 cases -- but the path to prevention had already accelerated faster than any of the cars on display in Life’s pages in 1949. The year before, John Enders’ research group in Boston had cultivated the poliovirus in human tissue, a Nobel-winning breakthrough that cleared a path for Jonas Salk’s vaccine, which followed in 1955. Successful field trials among several hundred thousand children known as Polio Pioneers were announced on April 12, 1955 – the tenth anniversary of FDR’s death. Church bells rang out across the nation.

The jubilation was justified in terms of the vaccine’s effect on the poliovirus – by 1961, only 161 cases of poliomyeltis were confirmed in the United States, just 29 more than the first epidemic year of 1894. But with the outbreaks ending, basic research withered. As Life noted, “how polio is spread, how the virus enters the body, they do not know.”

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In 1949, the same year as the Life article, Drs. Morton S. Biskind and Irving Bieber published “DDT Poisoning – A New Symptom With Neuropsychiatric Manifestations” in the American Journal of Psychotherapy. “By far the most disturbing of all the manifestations are the subjective reactions and the extreme muscular weakness,” they reported.[ii]

The Age of Polio: How an Old Virus and New Toxins Triggered a Man-made Epidemic -- Part 3, Making Sense of Campobello

Read Part 2, A Gypsy Moth Flaps its Wings and Part 1, The Wrong Narrative.

By Dan Olmsted and Mark Blaxill

Despite its name, the town of Cherryfield in Washington County, Maine, calls itself the Blueberry Capital of the World, and there is no disputing the claim. More than 90 percent of the world’s commercial blueberries are grown in Washington County, and Cherryfield is a major processing and shipping center. Machias, the county seat, hosts the annual Blueberry Festival every August. The festival puts on a musical, this year titled “Blueberry Fields Forever,” and a pie-eating contest – blueberry, of course.

The area has a couple of other claims to fame. Washington County hugs the Atlantic Coast where the United States meets Canada, the easternmost point in the United States; the city of Eastport is the first to see the sunrise. The region is known as Down East.

[A Map of Washington County Maine, also known as Sunrise County, with Cherryfield and Campobello circled. Click photo to enlarge.]

Two miles offshore is the island of Campobello, part of New Brunswick, Canada, where Franklin D. Roosevelt and his family spent summers. It was on his “beloved island” in August, 1921 – ninety years ago – that Roosevelt was afflicted with a paralytic illness diagnosed as poliomyelitis.

But this remote and lightly populated area already had a significant history with polio – one of the first clusters in the United States occurred in Cherryfield a quarter-century earlier, in 1896 (we cited it in our list of pre-1910 outbreaks with links to fruits and vegetables). Seven children were affected, and one died. In all the discussion and theorizing about Roosevelt’s illness over the intervening decades, this convergence has been overlooked.

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Roosevelt arrived at Campobello on Sunday afternoon, August 7, on the yacht of a friend who sailed him up from New York City. The previous week, Roosevelt had visited a Boy Scout camporee on Bear Mountain, N.Y., not far from the family’s Hudson River home in Hyde Park.[i]

At the dock, his family was waiting. His children played on the yacht through the adults’ cocktail hour, then were taken home while Franklin and Eleanor stayed for an elegant dinner on the fantailed aft deck, served by uniformed stewards.

Three days later, on Wednesday, August 10, Roosevelt went to bed early in the cranberry-red cottage on Campobello Island, unusually tired and suspecting “a slight case of lumbago” (lower back pain). He had chills during the night, and in the morning one of his legs was weak; the paralysis had begun. By the next night, both legs were paralyzed.

Because of the defining role it played in his life and, inevitably, world history, the days leading up to the attack have been dissected in detail by Roosevelt’s multiple biographers. Most historians believe he contracted the poliovirus on his visit to the Boy Scouts, which would have multiplied the chances of exposure to a youth with an active infection. Alternatively, he could have come down with the virus sometime between the Bear Mountain trip and his departure for Campobello.

After his arrival at Campobello, much has been made of a fall overboard while sailing in the Bay of Fundy; of his typically energetic activities on the day he first felt ill, which included putting out a small forest fire on a nearby island and going for a dip with his children in a freshwater pond near his house. The “paralyzingly cold” water of the Bay of Fundy became an ominous metaphor for what was about to happen, but was never a serious biological argument.