In science, no work is completed until it has been picked to pieces

Dangerous dithering.

What does a scientist have to do to convince you? The answer used to be “wait until his critics die” – hence the physicist Max Planck’s assertion that science advances one funeral at a time.

But sometimes even that is not enough. Late last month, the smell researcher Luca Turin published striking new evidence supporting an idea first put forward by Sir Malcolm Dyson in 1938. Dyson presented his “vibrational” theory of how our sense of smell works to universal apathy. Three generations later, scientists are still saying “meh”.

That year, 1938, was also when it was first argued that pumping carbon dioxide into the atmosphere would raise global temperatures. The idea came from the steam engineer Guy Stewart Callendar; the broad response was “implausible”. Today, in 2013, scientists have shifted: they generally agree that Callendar was right. Yet there remains a dangerous level of disagreement about the detail.

At least Turin’s scientific peers have presented him with a clear path to follow. Dyson’s idea was that when a molecule gets up our nose, its characteristic smell is created by the way the bonds within that molecule vibrate. In a clever piece of experimental work, Turin has shown that human beings can distinguish between two molecules that differ only in the way they vibrate. The two molecules tested were both cyclopentadecanone, but while one contained normal hydrogen atoms the other contained “deuterated” hydrogen, which has an added neutron in its atomic nucleus. The additional particle creates a difference in the way the molecules vibrate. And that is why, according to Turin, they smell different to us.

The experiment punches a hole in the accepted theory of smell, which says that smell experiences are triggered by differently shaped molecules fitting different receptors in the nose. This “lock and key” idea can’t explain why two identically shaped molecules smell different. But Turin’s critics said last month that before they will even consider accepting his theory, they want him to show exactly what goes on in human smell receptors.

They are right to make such demands. This is science, where no work is finished until it has been picked to pieces. But that is exactly why it has been so easy to do so little about climate change since 1938. Later this year, the Intergovernmental Panel on Climate Change will make some highly equivocal, backtracking announcements. In a report due for release in December, the IPCC will concede that we can’t be sure tropical cyclones will become more frequent, or that droughts will get worse. Worries that the Gulf Stream will collapse, tentatively raised in the 2007 IPCC report, are allayed: such an event is “unlikely” to occur in the foreseeable future.

Concern over details can have an unhelpful effect, masking the big picture on climate change – the one that Nicholas Stern, who wrote the UK government’s 2006 review on the science, said at Davos last month is “far, far worse” than we were led to believe originally. Until that, rather than the detail, becomes the focus, we can continue to dither over whether to do anything, let alone deciding what course we might take.

It does not matter a great deal that no one is willing to risk his career by backing Luca Turin – but to wait for absolute certainty over the details of climate change before we do anything about it will spell life or death for many. If science continues to advance one funeral at a time, its acceleration is assured; and there will be no shortage of funerals in a world that’s 4° warmer.

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.

This article first appeared in the 11 February 2013 issue of the New Statesman, Assange Alone

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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.