We need to stop worrying and trust our robot researchers

The work of Francis Crick and James Watson gives us a vision of what's to come.

It’s now 60 years since the publication of the structure of DNA. As we celebrate the past, the work of Francis Crick and James Watson also gives us a vision of what’s to come. Their paper was not subjected to peer review, today’s gold standard for the validation of scientific research. Instead, it was discussed briefly over a lunch at the Athenaeum Club. In an editorial celebrating the anniversary, the journal Nature, which originally published the research, points out that this is “unthinkable now”.

However, peer review has always been somewhat patchy and it is becoming ever more difficult. This is the age of “big data”, in which scientists make their claims based on analysis of enormous amounts of information, often carried out by custom-written software. The peer review process, done on an unpaid, voluntary basis in researchers’ spare time, doesn’t have the capacity to go through all the data-analysis techniques. Reviewers have to rely on their intuition.

There are many instances of this leading science up the garden path but recently we were treated to a spectacular example in economics. In 2010, Harvard professors published what quickly became one of the most cited papers of the year. Simply put, it said that if your gross public debt is more than 90 per cent of your national income, you are going to struggle to achieve any economic growth.

Dozens of newspapers quoted the research, the Republican Party built its budget proposal on it and no small number of national leaders used it to justify their preferred policies. Which makes it all the more depressing that it has been unmasked as completely wrong.

The problem lay in poor data-handling. The researchers left out certain data points, gave questionable weight to parts of the data set and – most shocking of all – made a mistake in the programming of their Excel spreadsheet.

The Harvard paper was not peer-reviewed before publication. It was only when the researchers shared software and raw data with peers sceptical of the research that the errors came to light.

The era of big data in science will stand or fall on such openness and collaboration. It used to be that collaboration arose from the need to create data. Crick and Watson collaborated with Maurice Wilkins to gather the data they needed – from Rosalind Franklin’s desk drawer, without her knowledge or permission. That was what gave them their pivotal insight. However, as Mark R Abbott of Oregon State University puts it, “We are no longer data-limited but insight-limited.”

Gaining insights from the data flood will require a different kind of science from Crick’s and Watson’s and it may turn out to be one to which computers and laboratorybased robots are better suited than human beings. In another 60 years, we may well be looking back at an era when silicon scientists made the most significant discoveries.

A robot working in a lab at Aberystwyth University made the first useful computergenerated scientific contribution in 2009, in the field of yeast genomics. It came up with a hypothesis, performed experiments and reached a conclusion, then had its work published in the journal Science. Since then, computers have made further inroads. So far, most (not all) have been checked by human beings but that won’t be possible for long. Eventually, we’ll be taking their insights on trust and intuition stretched almost to breaking point – just as we did with Crick and Watson.

President Obama inspects a robot built in Virginia. Photograph: Getty Images.

Michael Brooks holds a PhD in quantum physics. He writes a weekly science column for the New Statesman, and his most recent book is At the Edge of Uncertainty: 11 Discoveries Taking Science by Surprise.

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Autism and gut bacteria – the surprising link between the mind and the stomach

A recent paper has found that autistic-related social patterns can be reversed when one species of gut bacteria is present in the microbiome of mice. 

Autism – a developmental disorder that causes impediments to social interactions and behaviour – is usually linked by scientists to abnormalities in brain structure and function, caused by a mix of genetic and environmental factors. Scientists have almost always attempted to understand the way autistic people process the world around them by looking to the mind.

According to the National Autistic Society, “There is strong evidence to suggest that autism can be caused by a variety of physical factors, all of which affect brain development; it is not due to emotional deprivation or the way a person has been brought up.”

Recently, however, a lesser-known link to autism has gained traction. This time, the link is not found in the brain but in the gut.

Reporting their findings in the journal Cell, researchers from the Baylor College of Medicine, Texas, found that the presence of a single species of gut bacteria in mice could reverse many behavioural characteristics related to autism.

In the digestive tracts of humans and other animals, there exists a complex, symbiotically integrated network of trillions of microorganisms known as the “gut flora” or “microflora”. The idea that all these bacteria and microorganisms have taken up a home in our gut may initially seem startling, but they serve a number of beneficial purposes, such as aiding digestion and offering immunity from infection.

The potential link between gut flora and autism arose as researchers identified the increased risk of neurodevelopmental disorders, such as autism, among children born from mothers who were obese during pregnancy. The microflora of obese people is demonstrably different from those who are not obese, and as a result, connections have been made to the gut issues often reported in autistic people.

The senior author of the study and neuroscientist Mauro Costa-Mattioli said: “Other research groups are trying to use drugs or electrical brain stimulation as a way to reverse some of the behavioural symptoms associated with neurodevelopmental disorders – but here we have, perhaps, a new approach.”

To determine what the differences in gut bacteria were, the researchers fed 60 female mice a high-fat diet, with the aim of replicating the type of gut flora that would be found among people consuming a high-fat diet which would contribute to obesity. A control group of mice was fed a normal diet to serve as comparison. The mice in each group then mated, and their eventual offspring then spent three weeks with their mothers while being observed to see how behaviour and microflora was affected.

It was found that the offspring from the mice laden with high-fat foods exhibited social impairments, including very little engagement with peers. Meanwhile, a test called ribosomal RNA gene sequencing found that the offspring of the mice that were fed a high-fat diet housed a very different bacterial gut environment to the offspring of mice fed a normal diet.

Discussing the result, co-author Shelly Buffington was keen to stress just how significant the findings were: “By looking at the microbiome of an individual mouse we could predict whether its behaviour would be impaired.”

In an effort to understand whether the variation in microbiome was the reason for differences in social behaviour, the researchers paired up control group mice with high-fat diet mice. Peculiarly, mice eat each other’s faeces, which is why researchers kept them together for four weeks. The high-fat diet mice would eat the faeces of the normal mice and gain any microflora they held. Astonishingly, the high-fat diet mice showed improvements in behaviour and changes to the microbiome, hinting that there may be a species of bacteria making all the difference.

After careful examination using a technique called whole-genome shotgun sequencing, it was found that one type of bacteria – Lactobacillus reuteri – was far less prevalent in the offspring of high-fat diet mice than the offspring of normal-diet mice.

Discussing the method and finding, Buffington said: “We culture a strain of Lactobacillus reuteri originally isolated from human breast milk and introduced it into the water of the high-fat diet offspring. We found that treatment with this single bacterial strain was able to rescue their social behaviour.”

What the Lactobacillus reuteri seemed to be doing was increasing production of oxytocin, a hormone which is known by various other names such as the “trust hormone”, or the “love hormone”, because of its role in social interactions.

The results of the experiment showing that Lactobacillus reuteri can influence social behaviour are profound findings. Though the work would need to be transferred from mice studies to full human clinical trials to see if this could be applied to autistic people, the impact of adding Lactobacillus reuteri to the gut flora of mice can’t be underestimated. It seems then, for now, that research will go with the gut.