If you get your science and health news from the New Scientist, July 27 was an ‘unprecedented’ day: scientists announced they had made a tremendous leap forward in treating Alzheimer’s disease.
If you rely on STAT, it was just another frustrating day in a losing fight against the most common form of dementia.
The twist? Both STAT and the New Scientist were reporting on the same exact phase III trial of the same exact Alzheimer’s drug.
New Scientist‘s headline: Unprecedented Alzheimer’s drug slows disease by 80 per cent
STAT’s headline: Promising Alzheimer’s treatment flops in new trial, crushing hopes
These weren’t the only two sites to carry stories on the new drug:
- Daily Mail, as might be expected, was the most sensational: Revolutionary twice-daily pill can slow the progress of Alzheimer’s and even trigger ‘extraordinary recoveries’
- New York Times was more critical: Alzheimer’s Drug LMTX Falters in Final Stage of Trials
- BBC News struck a more even tone: Drug ‘may slow’ Alzheimer’s brain death
So why does this happen? How do widely-circulated and respected news outlets interpret news developments, in this case a controversial study, in such starkly different ways? The answers strike at the heart of a problem that has long plagued science communication and journalism.
Story within a story
The study in question was a phase 3 clinical trial of a drug, LMTX, that inhibits the aggregation and tangling of a protein called tau that some believe is the cause of Alzheimer’s disease. The results were presented at the Alzheimer’s Association International Conference in Toronto by scientists working with TauRX, which owns the drugs. The trial consisted of 890 subjects who had mild or moderate forms of the disease, many of whom were taking other drugs for the condition.
The results were complicated, even confusing. Overall, as even TauRx said, the trial failed to achieve its primary goal. However, there was another story embedded in the data: those who only took LMTX and no other Alzheimer’s drug experienced an 80 percent reduction in the progression of the disease. This statistically significant finding though disappeared when the whole cohort of those taking LMTX was considered and compared to those taking a placebo.
The key to most well reported science stories are quotes from a scientist, which are intended to give a piece weight and a sense of expertise. Veteran science writer Andy Coghlan, who wrote the New Scientist piece, used quotes from Claude Wischik, a professor of gerontology and the co-founder of TauRx:
On the whole, [the drug] slowed progression by about 80 per cent,” says Wischik.
Those taking LMTX were more engaged with their families, and one couple said it had allowed their lives to re-start again, says Wischik. “A wife of a patient told me her husband suddenly got up and fixed the garden fence, which he’d needed to do for years,” he says.
Coghlan also included comments from Serge Gauthier, a researcher at McGill University, who worked with the drug in the clinic and presented the results in Toronto. “In a study of this size, it is encouraging to see improvements of this magnitude in tests, and reassuring to see supporting brain scan evidence,” he is quoted as saying. Overall, Coghlan’s story followed the TauRx narrative that the drug was successful because it worked for those people only taking LMTX.
In contrast, the STAT piece, written by biotech industry reporter Damian Garde, quoted neither Gauthier nor Wischik. Garde’s expert analysis comes from David Knopman, a Mayo Clinic neurologist, who was not involved with the study. “I must say I’m disappointed by the results,” Knopman said. The quote was also widely circulated by other reporters who covered the story. Another one bites the dust is probably the best way to describe Garde’s take on LMTX and its status as a breakthrough drug:
The results are yet another blow to Alzheimer’s research. Academics, startups, and pharmaceutical giants have poured decades of work, and billions of dollars, into finding treatments. One therapy after another has looked promising in the lab — only to crumble when tested in large patient populations.
Indeed, 99.6 percent of Alzheimer’s treatments tested in the decade between 2002 and 2012 failed in clinical trials, according to an analysis by the Cleveland Clinic.
At first glance, it may be tempting to see Coghlan’s experts as being too vested in the results to trust their opinions. Another reporter, Matthew Herper, writing for Forbes, accused the company of trying to spin its failed study: “The study failed, with patients on LMTX faring no better than those on placebo, but TauRX may use the data to try to get its medicine approved anyway.”
That very well may be, but that doesn’t mean Coghlan was necessarily wrong to include comments from Gauthier and Wischik—or anyone else tied to the drug. They have first-hand experience with it. And their views were not a total whitewash; Wischik noted some of the drug’s shortcomings in the company press release (emphasis added):
The results we see in those patients not taking Alzheimer’s disease medications show the considerable potential of LMTX® as a monotherapy for both mild and moderate Alzheimer’s disease…However, the reason for the observed loss of efficacy of LMTX® when taken in combination with currently available treatments for Alzheimer’s disease is not as yet understood.
Furthermore, conflict of interest wasn’t limited in this case to those who worked for and with TauRX. LMTX’s target is highly controversial. Many people believe the protein tau tangles are the main driver of Alzheimer’s disease—STAT refers to Wischik as an evangelist for this belief. But there’s another camp that believes that the buildup of plaque consisting of a protein called beta-amyloid in the brain are what cause Alzheimer’s disease. Right now, the lion’s share of funding (and media attention) goes to researching amyloid beta plaques. From STAT:
Meanwhile, the biggest wheels of industry have largely placed their bets on amyloid. Pharma giant Eli Lilly is in the midst of a final-stage study on an amyloid antibody. It’s failed in two prior trials, but the company is trying once more in patients with milder forms of Alzheimer’s. Data from that study are expected next year.
Biogen is pursuing the same path, staking more than $1 billion on a huge amyloid trial that Wall Street analysts say could make or break the company’s future.
Who can we trust?
So this is the problem confronting both the public and journalists: when almost everyone has a potential conflict of interest, who can we trust for reliable science information?
In an ideal world, the answer is: trust the data. Unfortunately, not every science controversy has enough conclusive data to resolve the questions. And it isn’t just Alzheimer’s research in which two camps have a vested interest. Most areas of science have similar ambiguities, particularly in cases in which data is limited or research is difficult or is expensive (like, for example, researching the human brain). That’s why the phrase scientific consensus, areas where an abundance of conclusive data on a topic exists, is reserved for but a few topics—like vaccine and GMO food safety.
The data from TauRx is still just preliminary and other studies could provide a deeper understanding of why the effect is lost when other drugs are being taken. The drug may yet turn out to not work very well. But calling it “a flop” or an “unprecedented success” right now is the type of hype journalist should avoid in their reporting if we ever do want to see the day when all the headlines read: Alzheimer’s disease cured.
Nicholas Staropoli is the associate director of GLP and director of the Epigenetics Literacy Project. He has an M.A. in biology from DePaul University and a B.S. in biomedical sciences from Marist College. Follow him on twitter @NickfrmBoston.