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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An antibiotic-resistant superbug is silently spreading through UK hospitals

There have already been outbreaks in Manchester, London, Edinburgh, and Birmingham, but deaths are not centrally recorded. 

Lying in a hospital bed, four months pregnant, Emily Morris felt only terror. She had caught a urinary tract infection and it was resistant to common antibiotics. Doctors needed to treat it as it could harm the baby, but the only drugs that could work hadn’t been tested on pregnant women before; the risks were unknown. Overwhelmed, Emily and her husband were asked to make a decision. A few hours later, gripping each other’s arms, they decided she should be given the drugs.

In Emily’s case, the medicine worked and her son Emerson (pictured below with Emily) was born healthy. But rising antibiotic resistance means people are now suffering infections for which there is no cure. Doctors have long warned that decades of reliance on these drugs will lead to a "post-antibiotic era"– a return to time where a scratch could kill and common operations are too risky.

It sounds like hyperbole – but this is already a reality in the UK. In the last four years 25 patients have suffered infections immune to all the antibiotics Public Health England tests for in its central lab, the Bureau of Investigative Journalism has discovered.

While these cases are rare, reports of a highly resistant superbug are rising, and infection control doctors are worried. Carbapenem resistant enterobacteriaceae (CRE) are not only difficult to pronounce, but deadly. These are bugs that live in the human gut but can cause an infection if they get into the wrong place, like the urinary tract or a wound. They have evolved to become immune to most classes of antibiotics – so if someone does become infected, there are only a few drugs that will still work. If CRE bacteria get into the bloodstream, studies show between 40 per cent and 50 per cent of people die.

These bugs are causing huge problems in India, certain parts of Asia, the Middle East and some countries in southern Europe. Until recently, most infections were seen in people who had travelled abroad, had family members who had, or had been in a foreign hospital. The boom in cheap cosmetic surgery in India was blamed for a spate of infections in Britain.

Now, doctors are finding people who have never boarded a plane are carrying the bug. There have already been outbreaks in Manchester, London, Liverpool, Leeds, Edinburgh, Birmingham, Nottingham, Belfast, Dublin and Limerick among other areas. Patients found with CRE have to be treated in side rooms in hospital so the bacteria does not spread and harm other vulnerable patients. But in many of Britain’s Victorian-built hospitals, single rooms are in sparse supply. Deaths from CRE aren’t centrally recorded by the government - but it is thought hundreds have already died. 

Across the country, doctors are being forced to reach for older, more toxic drugs to treat these infections. The amount of colistin – called the "last hope" antibiotic as it is one of few options still effective against CRE infections - rose dramatically in English hospitals between 2014 and 2015, the Bureau has revealed. Colistin was taken off the shelves soon after it was introduced, as it can harm the kidneys and nervous system in high doses, but was reintroduced when infections became immune to standard treatment. The more we use colistin the more bacteria develop resistance to it. It’s only a matter of time before it stops working too, leaving doctors’ arsenal near-empty when it comes to the most dangerous superbug infections.

Due to a kidney problem, Emily Morris suffers repeat urinary tract infections and has to be hospitalised most months. Her son Emerson comes to visit her, understanding his mummy is ill. If she catches a superbug infection, she can still be given intravenous antibiotics to stem it. But she worries about her son. By the time he is an adult, if he gets ill, there may be no drugs left that work.

Madlen Davies is a health and science reporter for the Bureau of Investigative Journalism