by Brian Deer
Two groups of five kids were proposed at this time. The first had Crohn’s disease, Wakefield said. That was still his primary focus. The rest would take him into a new field of inquiry, central to Barr’s ambitions. As in the DTP trials, the lawyer’s target was the brain, and particularly involving children with autistic spectrum disorders: an increasingly common group of developmental diagnoses, inevitably appearing in Fletcher’s client lists.
These patients, said the protocol, formed part of a “new syndrome”—Stuart-Smith’s checklist item 1. This married bowel inflammation and “symptoms akin to autism.” And (addressing the checklist item 2) the evidence, the document said, was “undeniably in favour of a specific vaccine-induced pathology.”
It is of course not possible to anticipate the conclusions that will be reached, but the indicators are that it should be possible to establish a clear causative link between the vaccines and the two sets of conditions.
In other words, they decided what the research ought to find, before they set out to find it.
Barr mailed the documents to a legal board office on Thursday, June 6, 1996. But, despite the offer of a vaccine-damage test (for a bargain price of less than sixty grand) they weren’t greeted with any dancing on desks. Class actions against drug companies had always failed in Britain. And after the collapse, not only of the DTP cases but also a massive suit over benzodiazepine tranquilizers (in which hundreds of claims from “victims” were found to be bogus), the board’s managers had begged the government for reform, complaining of litigants “giving it a go.”
“There is no incentive on the solicitor to act as a responsible filter for dubious cases,” the board said in a thirty-six page report. “This problem seems to be exacerbated by the fact that the applicant is not funding the case him or herself and that the claim may only arise due to the publicity.”
Following a guarded response, however, the board caved in after Barr pressed the argument that Ullstein’s opinion showed that a “prima facie case” existed. So, on Thursday, August 22, 1996, a twenty-nine-year-old board lawyer named Joanne Cowie signed her name to a two-page “authority to do contract work,” ordering a “preliminary report from Dr Andrew Wakefield,” and approving the following grant:
To facilitate the setting up of the clinical and scientific study proposed by Dr A J Wakefield in respect of 10 assisted persons at a maximum cost of £55,000.
“If the tests are positive, then I am reasonably confident that the Legal Aid Office will allow us to have further children tested,” Barr wrote to Wakefield later, setting out the doctor’s duties. “I have mentioned to you before that the prime objective is to produce unassailable evidence in court so as to convince a court that these vaccines are dangerous.”
Barr was delighted. He’d tell anyone who asked that he’d got a hospital testing his clients. But, although Wakefield’s personal fees were confidential between them, a month after Cowie’s approval of the deal a check came through as a first installment, which set off a crisis in the Royal Free medical school that would rumble on, in secret, for months.
The dean, Arie Zuckerman, spotted straight off that the payment raised issues of propriety. In more than thirty years in academic research, he’d never encountered such a source of finance. In principle, it wasn’t far from a lung disease study sponsored by a tobacco manufacturer. To him, the idea of Barr’s role in the science was deeply, and obviously, contentious.
“The dilemma which the School faces is whether it is ethical for lawyers to fund a particular piece of research where a specific action in law is contemplated,” he wrote to Michael Pegg, a burly consultant in anesthesia and chair of the hospital’s ethics committee, in a “strictly private and confidential” exchange.
Pegg’s reply did nothing to calm nerves. The ethicist knew something was wrong. “I have reviewed all submissions made by Mr Wakefield to the ethics committee in the last two years,” he wrote back. “None of the stated sources of funding include the legal aid board.”
If you have evidence that Mr Wakefield has made a false statement to the ethics committee then I would be obliged if you would formally lay that evidence before this committee.
But Zuckerman blinked. He later said he was overworked. Personally, I think he was spellbound. Either way, two days later, he wrote back to Pegg, with underlining, saying his inquiry had been “misunderstood.”
There is absolutely no suggestion of any misconduct by Dr Andrew Wakefield.
So, instead of the school taking the money, the dean suggested it be transferred to a “special trustees” fund, managed by the hospital’s chief executive, Martin Else. And all Else said he wanted, in a “private and confidential” request, was “written confirmation that there is no conflict of interest”—a Get Out of Jail Free card in the event of controversy—which Wakefield was glad to supply.
I am writing to confirm that there is no conflict of interest in relation to the Legal Aid funding for our clinical study . . . which has been sponsored by the Legal Aid Board.
So what happened was this: the money from Barr for the clinical and scientific study was paid to the medical school, diverted to the hospital’s special trustees fund, where, rinsed of its origins, it was then laundered back to pay for Wakefield’s research, carried out in the medical school.
Who would know? Not the Lancet’s editors, peer reviewers, or readers. And not the millions embroiled in what would become a global alarm over the safety of vaccination. Who would guess at the deal—or the money-go-round—any more than they would guess about the rest I would reveal behind that history-making twelve-child study?
“I remember noting at the time that the funding acknowledgment wasn’t there,” Barr tells me of the paper, before refusing further comment. “But it didn’t seem to be a big deal.”
TEN
Trouble in the Labs
On the last Monday morning of February 1997, a taxi pulled away from the Royal Free Hospital. It turned onto Pond Street, in front of the building, dense with patient transport and visitors looking to park, turned again, and gathered speed, heading south. It was a mild, rainy day, the wettest since November, and a grimy ceiling of sky shrouded the capital like a duvet abandoned to a dog.
The sole passenger was male. He was well built, with black hair, pricey clothing, and a somber expression. White, aged forty, from the Bay Area of California, he was an engineer and entrepreneur, owning an electropolishing business, specializing in stainless steel and aluminum. He was wealthy, shrewd, with an engineer’s precision. I’ll call him “Mr. Eleven.”
His destination was the renowned Chester Beatty Laboratories: a unit of the Institute of Cancer Research, rated, in partnership with its neighboring hospital, the Marsden, as one of the top four such centers in the world. Once endowed by a New Yorker, whom they called “the King of Copper,” and based in a narrow, brick building on Fulham Road, Chelsea, it was a place where puzzles of biology had been solved: as blue chip a center of scientific inquiry as the Hampstead medical school was gray.
Mr. Eleven’s fingers gripped a plastic pot. He nursed it like it bottled his life. As the taxi negotiated six miles of central London, through Paddington, Hyde Park, and South Kensington, he sensed a gentle movement of liquid within the vessel, rocking as the car turned or braked.
Meanwhile, back at Hampstead, his son, Child Eleven, had returned to Malcolm Ward after undergoing ileocolonoscopy. He was five years old, and labeled autistic. But like many children with evidence of developmental issues, a more precise diagnosis seemed elusive. Unlike Child Two, or Child Four, he was smart. And one day, when I meet him, he’d just seem like a shy, geeky teenager, if somewhat socially gauche.
“My son can be quite rude,” his father tells me, when we meet at a restaurant south of Los Angeles, when Child Eleven had turned sixteen. “He reads technical journals, and will lob off an email to a professor, and talk down to them in a condesce
nding manner. And he is right.”
For reasons unknown—his father suspected vaccines—his early years had been more worrying. He hadn’t started speaking by the age of two, suffered from apparent malabsorption and immunity issues, experienced delays in cognitive development, and his behavior was obsessive and repetitive. “Everything was off,” Mr. Eleven tells me. Then he corrects himself. “Twenty percent of everything was off.”
Unusually, it was the father who led the family quest for reasons and remedies for the issues. Mr. Eleven believed there could be “two hundred different types of autism,” blaming vaccines, heavy metals, pesticides, fluoridation, and viruses. “You name it,” he says. The trip to London was but the latest of countless initiatives by which he sought to diagnose and adjust his son, like a technician at a panel of dials.
Early on, he learned about “oxidative stress,” read countless books and papers on causes and treatment, and spent huge sums on blood tests and supplements, such as B12, folic acid, and glutathione. “I can tell you one thing: my son’s brain is healing,” he says. “I’ve got specific tests, very specific tests, that I’m targeting on him, looking for what I would consider his dysregulation, or his deficiency.”
Mr. Eleven knew nothing of the Lancet paper, which would be published twelve months after his journey across London. He’d simply heard from an immunologist in South Carolina—a pipe-smoking eccentric named Hugh Fudenberg—that the Royal Free had a test for vaccine damage.
“We would greatly appreciate the opportunity to bring our child to London as soon as possible to undergo testing at your facilities,” Mr. Eleven had written to Wakefield as the twelve-child study neared completion. “We are convinced that his medical condition can be successfully treated and he will recover from this ordeal if identification of the virus and the extent to which the infection has spread is better understood.”
Six weeks later, he was riding in the taxi, clutching the pot—inside which, drifting in formalin preservative, lay bowel tissue snipped from his son.
“I was in the room with my wife,” he tells me. “They took the biopsy material, cut it in half, put the piece in a jar, in a special container. I ran out the hospital, hopped in a cab I had waiting. I was down this place within a half hour.”
The mission, he explains, was the immunologist’s idea. Fudenberg, sixty-nine, recommended a second opinion. For all Wakefield’s confidence that measles virus persisted to cause inflammatory bowel disease, any literature search on the US National Library of Medicine’s PubMed database yielded a less hopeful consensus. Notwithstanding Wakefield’s optimistic submission to the Legal Aid Board, study after study had tried to replicate his virology. But time and again, they failed.
The trail had begun nearly four years before, after the paper in J Med Virol. As the Holy Grail of gastroenterology, the cause of Crohn’s disease couldn’t be left to one institution. So, from April 1993, the race was on to reproduce the Royal Free’s results.
First to hit the track was a Japanese group, led by Masahiro Iizuka, at Akita University, six hundred miles north of Tokyo. In a letter to The Lancet in January 1995 (three months before Wakefield’s question-marked paper), they reported on tissues from fifteen Crohn’s patients, using a different method to those reported from Hampstead. Deploying the molecular amplification technology of the polymerase chain reaction (the famed “PCR” genetic fingerprinting that catches rapists and serial killers who licked postage stamps years before), they hunted for sequences from four of six genes that code the virus’s nucleus, capsule, and protrusions.
The researchers told the journal, “We found none.”
Then a US group at the University of Connecticut broke cover. In the same month that Ms. Two phoned Wakefield at his desk, the journal Gastroenterology printed a nine-page study—Ying Liu et al.—that, as part of a bigger project, had tried to replicate a Wakefield method. In tissues from sixteen patients, they looked for measles proteins using immunohistochemistry (one of the three techniques in J Med Virol) with which Wakefield had reported thirteen of fifteen samples positive.
The immunohistochemistry was a staining technique. It was microscopic, not molecular. Specially made antibodies were meant to stick to their target protein, and a fluorescence, usually brown, signaled a match. Liu’s people got their antibody from the Royal Free lab. But, where Wakefield reported success, the Connecticut team failed, concluding that the antibody seemed to locate, and latch onto, normal components of human cells.
“Therefore our results,” they wrote, “do not confirm the data of Wakefield et al. regarding the presence of measles virus.”
Fudenberg could easily access this stuff. To any immunologist, the implication from Connecticut was that results from the Royal Free may have arisen from a cross-reaction: where an antibody mistakes “self” for “other.” It was no big surprise. In biology, shit happens. Targets aren’t always unique.
But Wakefield, as ever, remained cool under fire. Shrugging off his critics’ work as “flawed” and “ill considered,” he suggested they’d looked in the wrong place for the virus, or that it was present in tissues in such miniscule quantities that their methods—but not his—couldn’t find it. He’d seen the bug himself, under a microscope, he insisted. Measles infection was both “persistent” and “confirmed.”
Notwithstanding his rejoinders, the literature didn’t lighten. In February 1996—the month he formally signed up to his deal with Richard Barr, and a year before Child Eleven was brought to London for scoping—Yoichi Haga and others at Japan’s Hirosaki University published a six-page study in Gut. Claiming remarkably sensitive PCR amplification—which they reckoned could detect a single measles virion—they targeted the same gene sequence as in Wakefield’s in situ hybridization, as he described it in J Med Virol. But where he reported success in ten out of ten, they failed in all of fifteen.
“The aetiology of Crohn’s disease remains unknown,” they noted, “although evidence for a viral cause has long been sought.”
It was Fudenberg’s idea to check all this out before getting in any deeper with Wakefield. Hence the taxi ride with gut tissue in a pot to test for the presence of the virus.
Mr. Eleven had gone to London, not to validate a hypothesis, or join a lawsuit. And San Francisco had better hospitals than Hampstead. “I just wanted a simple little blurb, positive or negative,” he tells me. “I didn’t ask for a big report.”
Child Eleven had been admitted to Malcolm Ward the day before, after arriving at the airport with his parents. Like the rest of the twelve, he was bowel prepped overnight and trolleyed to the endoscopy suite Monday morning. His mother and father had watched on the video monitor as the instrument pressed forward: rectum; sigmoid colon; descending, transverse, and ascending colon; cecum; valve; ileum . . .
And behold.
Amid glistening pink mucosa, the parents saw the patches: the protruding pale nodules, the ugly swollen glands, the ileal lymphoid nodular hyperplasia.
Was this confirmation of the measles hypothesis, which, unknown to Mr. Eleven, had been proposed to the legal board in the scientific side of the study? The glands, he was told, were reacting to an infection, which Wakefield felt confident was the virus. This would be the topic of the second—scientific—paper to be submitted to The Lancet (and rejected).
But even as Child Eleven was wheeled back to the ward, more controversy brewed over the measles idea—and not thousands of miles from Hampstead. As the American father headed for the Chelsea lab, Nick Chadwick, the “coordinating investigator–molecular studies,” worked on PCR tests on gut, blood, and spinal fluid from the Lancet twelve, and others.
Chadwick—a quiet, waifish young scientist—had himself been diagnosed with Crohn’s disease. He’d come to the Royal Free as a Wakefield disciple, and for a year had toiled as a lowly lab technician before enrolling in a PhD program. At first he investigated, and tried to replicate, the go
od news of J Med Virol.
He was a well-regarded, dogged, and meticulous investigator, able to handle the endless hours of repeating the same assays and the interpersonals of laboratory life. One joy of the hospital was seeing research in context: the patients, like Child Eleven, for whom it mattered. In Chadwick’s case, he was a patient himself, receiving care from Wakefield’s mentor, Roy Pounder.
Working in room 324 on the hospital’s tenth floor, Chadwick was one of a team of usually four researchers, lab-coated at a pair of parallel, double-sided benches, split by bottle- and box-cluttered shelves. At right angles to the workstations were plate glass windows, with stunning views across a slice of north London.
His project had started with evaluating techniques for amplifying measles RNA. This led to a twelve-page paper, with Wakefield the last author, in a cousin publication to J Med Virol, the Journal of Virological Methods. Then he applied the most sensitive and specific to Crohn’s tissues—and, whoaah, his working life soured.
The tests were negative, like those from Japan and Connecticut. He could find the virus—but only in spiked control tissues, plus occasional rogue contaminants. And when he reported his findings to his PhD joint supervisor—Wakefield—that supervisor was none too thrilled.
“He tended to believe, you know, positive data that fitted in with his hypothesis,” Chadwick tells me, “and then disregard negative data.”
Here was the downside of research in the hospital: direction by medics, not scientists. “Andy never actually did any of the techniques himself, from scratch,” Chadwick remembers. “He would spend a lot of time looking at tissue sections, and looking at the results. And, like most lab leaders’ jobs are, to raise money for the group, and to try to interpret results, and write up papers. But in terms of hands-on stuff, he never put a lab coat on really, as far as I can remember.”