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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The answer to the antibiotics crisis might be inside your nose

The medical weapons we have equipped ourselves with are losing their power. But scientists scent an answer. 

They say there’s a hero in everyone. It turns out that actually, it resides within only about ten percent of us. Staphylococcus lugdunensis may be the species of bacteria that we arguably don’t deserve, but it is the one that we need.

Recently, experts have cautioned that we may be on the cusp of a post-antibiotic era. In fact, less than a month ago, the US Centres for Disease Control and Prevention released a report on a woman who died from a "pan-resistant" disease – one that survived the use of all available antibiotics. Back in 1945, the discoverer of penicillin, Alexander Fleming, warned during his Nobel Prize acceptance speech against the misuse of antibiotics. More recently, Britain's Chief Medical Officer Professor Dame Sally Davies has referred to anti-microbial resistance as “the greatest future threat to our civilisation”.

However, hope has appeared in the form of "lugdunin", a compound secreted by a species of bacteria found in a rather unlikely location – the human nose.

Governments and health campaigners alike may be assisted by a discovery by researchers at the University of Tubingen in Germany. According to a study published in Nature, the researchers had been studying Staphylococcus aureus. This is the bacteria which is responsible for so-called "superbug": MRSA. A strain of MRSA bacteria is not particularly virulent, but crucially, it is not susceptible to common antibiotics. This means that MRSA spreads quickly from crowded locations where residents have weaker immune systems, such as hospitals, before becoming endemic in the wider local community. In the UK, MRSA is a factor in hundreds of deaths a year. 

The researchers in question were investigating why S. aureus is not present in the noses of some people. They discovered that another bacteria, S. lugdunensis, was especially effective at wiping out its opposition, even MRSA. The researchers named the compound created and released by the S. lugdunensis "lugdunin".

In the animal testing stage, the researchers observed that the presence of lugdunin was successful in radically reducing and sometimes purging the infection. The researchers subsequently collected nasal swabs from 187 hospital patients, and found S. aureus on roughly a third of the swabs, and S. lugdunensis on up to 10 per cent of them. In accordance with previous results, samples that contained both species saw an 80 per cent decrease of the S. aureus population, in comparison to those without lugdunin.

Most notably, the in vitro (laboratory) testing phase provided evidence that the new discovery is also useful in eliminating other kinds of superbugs, none of which seemed to develop resistance to the new compound. The authors of the study hypothesised that lugdunin had evolved  “for the purpose of bacterial elimination in the human organism, implying that it is optimised for efficacy and tolerance at its physiological site of action". How it works, though, is not fully understood. 

The discovery of lugdunin as a potential new treatment is a breakthrough on its own. But that is not the end of the story. It holds implications for “a new concept of finding antibiotics”, according to Andreas Peschel, one of the bacteriologists behind the discovery.

The development of antibiotics has drastically slowed in recent years. In the last 50 years, only two new classes of this category of medication have been released to the market. This is due to the fact almost all antibiotics in use are derived from soil bacteria. By contrast, the new findings record the first occurrence of a strain of bacteria that exists within human bodies. Some researchers now suggest that the more hostile the environment to bacterial growth, the more likely it may be for novel antibiotics to be found. This could open up a new list of potential areas in which antibiotic research may be carried out.

When it comes to beating MRSA, there is hope that lugdunin will be our next great weapon. Peschel and his fellow collaborators are in talks with various companies about developing a medical treatment that uses lugdunin.

Meanwhile, in September 2016, the United Nations committed itself to opposing the spread of antibiotic resistance. Of the many points to which the UN signatories have agreed, possibly the most significant is their commitment to “encourage innovative ways to develop new antibiotics”. 

The initiative has the scope to achieve a lot, or dissolve into box ticking exercise. The discovery of lugdunin may well be the spark that drives it forward. Nothing to sniff about that. 

Anjuli R. K. Shere is a 2016/17 Wellcome Scholar and science intern at the New Statesman