This article is a preview from the Summer 2018 edition of New Humanist

Biology – Lydia Leon

Around three times as many bacterial as human cells inhabit our bodies. These diverse communities, the “microbiome”, are crucially important. Disruption of the microbiome’s delicate balance may modify risk for a range of diseases, from obesity to cancer. One path to such disruption is through antibiotics. The intention may be to kill the “bad bacteria” underlying an infection, but our “good bacteria” can also be affected. This effect is particularly pronounced in the gut, where bacteria are crucial to basic biological processes from immunity to metabolism.

The impact of non-antibiotic pharmaceuticals – not explicitly designed to fight infection – on our gut microbiome has received little attention. That was until a study published in March in the journal Nature documented work carried out in Germany at the world-famous European Molecular Biology Laboratory. The group monitored the impact that exposure to over 1000 medications across the spectrum of drug classes had on the growth of 40 gut bacterial species. Of the drugs tested, 78 per cent of antibiotics had a negative impact on at least one of the species, in line with previous research. But most interestingly, 24 per cent of the non-antibiotic drugs, from chemotherapy agents to anti-psychotics, also demonstrated this disruptive capacity.

The next step is to check if these petri dish observations are replicated in human studies. These preliminary results raise unexplored questions about the role of microbiome disruption in negative side-effects, as well as the intended activity of a wide range of non-antibiotic drugs. If these drugs can affect the growth of “bad” as well as “good” bacteria they could potentially be repurposed as antibiotics – a class of drug we desperately need to expand.

Another troubling observation was a strong correlation between the bugs screened that had known antibiotic resistance and those also unresponsive to non-antibiotic drugs. This potentially implicates the widespread use of non-antibiotic pharmaceuticals in the rise in antimicrobial resistance – one of the biggest threats to human health worldwide.

Lydia Leon is a research associate in women’s health at Kings College London and University College London

Physics – Ceri Brenner

There’s a group working downstairs from me who are right now trying to transform light into matter by directing two extreme bursts of x-rays at each other inside a chamber full of nothing. The team, led by Imperial College London, are testing the 84-year-old quantum physics theory postulated by Breit-Wheeler that the outcome of two particles of light (photons) colliding is an electron and its antimatter equivalent – same mass but opposite charge state – a positron. They’re doing this using two of the world’s most intense lasers. The first one is used to drive a burst of electrons that stream through gold and emit a burst of x-rays that are billion times more energetic than sunlight. The second is used to heat the inside of a tiny gold can so that it also emits x-ray photons. The two beams are aligned so that the first one goes through the tiny can where they then collide. The signature of the light-into-matter transformation being the positrons that are flung out of the quantum cauldron.

Working at a national laboratory I’ve become used to the novelty of sitting in the same postcode as world-changing discoveries. But this latest experiment is an amazing moment for any physicist. It is testing one of the core quantum predictions of how, on an absolute fundamental level, energy is interchangeable between light and particles – it’s one of the important processes behind the creation of matter from light during the first 100 seconds of the universe. Plus, for want of a better phrase, it’s just really cool to make particles appear out of thin air. The opposite process – an electron and positron colliding to emit a photon – is also physically possible and actually much more easily demonstrated. It’s the basis behind positron emission tomography scanners used to trace blood flow in hospitals.

So, did they manage to do it? We’ll have to wait and see. There’s a whole heap of analysis and critical thinking needed before you can assert the first demonstration of a decades-old theory. Are you a little bit excited? Intrigued? On the edge of your seat? Welcome to science.

Ceri Brenner is a physicist who works for the Science and Technology Facilities Council

Chemistry – Mark Lorch

From the naturally lithium-laced “crazy waters” of Texas to the origins of the soft drink 7-Up (which originally went by the slightly less catchy name of “Bib-Label Lithiated Lemon-Lime Soda”), lithium salts have long been known to have a significant effect on mood. By the 1940s this knowledge was being applied to clinical practice, and to this day it is the most commonly prescribed treatment for bipolar disorder. But despite its long history, it isn’t entirely clear how lithium actually works.

Most pharmaceutical compounds are complex chemicals, which, through design or chance, lodge in a particular protein in a cell, stop that protein functioning and in turn change the way the cell behaves. By using them, we are in effect altering the way our body reacts to other chemical stimuli.

Lithium salts, however, are different. They are no more complex than sodium chloride – common table salt. When these salts are consumed, the metal takes the form of charged ions, circulating freely around the body and interacting with a huge variety of proteins and other molecules. Sodium is a particularly important ion in the body; many proteins require interactions with it to function. Sodium and lithium are chemically very similar. This means that lithium can end up interacting with many of the same proteins as sodium. That interaction then alters the way the protein functions. As a consequence, lithium interferes with a huge number of biochemical systems, leading to many side-effects.

New research, led by Carmay Lim of Academia Sinica in Taiwan, has looked into the competition between lithium and sodium as they bind to a number of proteins known to be implicated in bipolar disorders. The scientists found that lithium binds more strongly to these particular proteins, and actually forces them “on”. This work provides valuable insights into the little understood mechanisms by which lithium affects our mental state. By understanding how lithium acts on these proteins the hope is for much more specific drugs that work on the proteins involved in the disorders, but without the numerous nasty side-effects.

Mark Lorch lectures in chemistry at Hull University