There are some circumstances in which new human friendships randomly form all at once, for example when recruits are assigned to military squadrons or students are allocated to university halls.[35] Unfortunately for researchers, these are rare examples. In most real-life situations, scientists can’t meddle with behaviour or friendship dynamics to see what might happen. Instead, they must try and gain insights from what they can observe naturally. ‘Though a lot of the best strategies involve randomisation or some plausible source of randomness, for many things we really care about as social scientists and citizens, we’re not going to be able to randomise,’ said Dean Eckles, a social scientist at MIT.[36] ‘So we should do the best job we can with purely observational research.’
Much of epidemiology relies on observational analysis: in general, reseachers can’t deliberately start outbreaks or give people severe illnesses to understand how they work. This has led to some suggestions that epidemiology is closer to journalism than science, because it just reports on the situation as it happens, instead of running experiments.[37] But such claims ignore the huge improvements in health that have come from observational studies.
Take smoking. In the 1950s, researchers started to investigate the massive rise in lung cancer deaths that had occurred during the preceding decades.[38] There seemed to be a clear link with the popularity of cigarettes: people who smoked were nine times more likely to die of the disease than non-smokers. The problem was how to show that smoking was actually causing cancer. Ronald Fisher, a prominent statistician (and heavy pipe smoker) argued that just because the two things were correlated, it didn’t mean one was causing the other. Perhaps smokers had very different lifestyles to non-smokers, and it was one of these differences, rather than smoking, that was causing the deaths? Or maybe there was some genetic trait – as yet unidentified – that happened to make people both more likely to develop lung cancer and more likely to smoke? The issue divided the scientific community. Some, like Fisher, argued that the patterns linking smoking and cancer were just a coincidence. Others, like epidemiologist Austin Bradford Hill, thought that smoking was to blame for the rising deaths.
Of course, there was an experiment that would have given a definitive answer, but as we’ve already seen, it wouldn’t have been ethical to run it. Just as modern social scientists can’t make people take up smoking to see if the habit spreads, researchers in the 1950s couldn’t ask people to smoke to find out if it caused cancer. To solve the puzzle, epidemiologists had to find a way to work out whether one thing causes another without running an experiment.
Ronald ross spent august 1898 waiting to announce his discovery that mosquitoes transmitted malaria. While he battled to get government permission to publish the work in a scientific journal, he feared others would pounce on his research and take the credit. ‘Pirates lay in the offing ready to board me,’ as he put it.[39]
The pirate he feared most was a German biologist named Robert Koch. Stories were circulating that Koch had travelled to Italy to study malaria. If he managed to infect a person with the parasite, it could overshadow Ross’s work, which had used only birds. Relief came a few weeks later, in the form of a letter from Patrick Manson. ‘I hear Koch has failed with the mosquito in Italy,’ Manson wrote, ‘so you have time to grab the discovery for England.’
Eventually Koch did publish a series of malaria studies, which fully credited Ross’s work. In particular, Koch suggested that children in malarial areas acted as reservoirs of infection, because older adults had often developed immunity to the parasite. Malaria was the latest in a line of new pathogens for Koch. During the 1870s and 1880s, he had shown that bacteria were behind diseases like anthrax in cattle and tuberculosis in humans. In the process, he’d come up with a set of rules – or ‘postulates’ – to identify whether a particular germ is responsible for a disease. To start with, he thought that it should always be possible to find the germ inside someone who has the disease. Then, if a healthy host – like a laboratory animal – was exposed to this germ, it should develop the disease too. Finally, it should be possible to extract a sample of the germ from the new host once they fall ill; this germ should be the same as the one they were originally exposed to.[40]
Koch’s postulates were useful for the emerging science of ‘germ theory’, but he soon realised they had limitations. The biggest problem was that some pathogens don’t always cause disease. Sometimes people would get infected but not have noticeable symptoms. Researchers therefore needed a more general set of principles to work out what might be behind a disease.
For Austin Bradford Hill, the disease of interest was lung cancer. To show that smoking was responsible, he and his collaborators would eventually compile several types of evidence. He’d later summarise these as a set of ‘viewpoints’, which he hoped would help researchers decide whether one thing causes another. First on his list was the strength of correlation between the proposed cause and effect. For example, smokers were much more likely to get lung cancer than non-smokers. Bradford Hill said this pattern should be consistent, cropping up in different places across multiple studies. Then there was timing: did the cause come before the effect? Another indicator was whether the disease was specific to a certain type of behaviour (although this isn’t always helpful because non-smokers can get lung cancer too).
