Posts Tagged ‘science’

cientific studies on the cleaning power of spit, a lone fruit fly’s ability to spoil wine, and cannibals’ caloric intake garnered top honors at the 28th Ig Nobel Prize ceremony. The seriously silly citations, which “honor achievements that first make people laugh, and then think,” were awarded on Sept. 13 at Harvard University’s Sanders Theatre. Entertaining emcee Marc Abrahams and the savvy satirists of the Annals of Improbable Research produced the ceremony.

The coveted Chemistry Prize went to Portuguese researchers who quantified the cleaning power of human saliva. Nearly 30 years ago, conservators Paula Romão and Adília Alarcão teamed up with late University of Lisbon chemist César Viana to find out why conservators preferred their own saliva to any other solvent for cleaning certain objects—with the goal of finding a more hygienic substitute. Compared with popular solvents, saliva was the superior cleaning agent, particularly for gilded surfaces. The researchers attributed the polishing power to the enzyme α-amylase and suggested solutions of this hydrolase might achieve a spit shine similar to spit (Stud. Conserv. 1990, DOI: 10.1179/sic.1990.35.3.153).

A fruit fly in a glass of wine is always an unwelcome guest. But it turns out that as little as 1 ng of Drosophila melanogaster’s pheromone (Z)-4-undecenal can spoil a glass of pinot blanc. That discovery, from researchers led by Swedish University of Agricultural Sciences’ Peter Witzgall, received the Ig Nobel’s Biology Prize. Only female fruit flies carry the pheromone, so males can swim in spirits without delivering the offending flavor, but the Newscripts gang still prefers to drink wine without flies (J. Chem. Ecol. 2018, DOI: 10.1007/s10886-018-0950-4).

Putting the paleo diet in a new perspective, University of Brighton archaeologist James Cole took home the Nutrition Prize for calculating that Paleolithic people consumed fewer calories from a human-cannibalism diet than from a traditional meat diet. Thus, Cole concludes, Paleolithic cannibals may have dined on their companions for reasons unrelated to their nutritional needs (Sci. Rep. 2017, DOI: 10.1038/srep44707).

A team led by Wilfrid Laurier University psychologist Lindie H. Liang won the Economics Prize “for investigating whether it is effective for employees to use voodoo dolls to retaliate against abusive bosses.” Push in some pins: The findings indicate voodoo doll retaliations make employees feel better (Leadership Q. 2018, DOI: 10.1016/j.leaqua.2018.01.004).

The Newscripts gang previously reported about this year’s winners of the Ig Nobel for medicine, physicians Marc Mitchell and David Wartinger, who found that riding roller coasters can help people pass kidney stones (J. Am. Osteopath. Assoc.2016, DOI: 10.7556/jaoa.2016.128).

The Reproductive Medicine Prize went to urologists John Barry, Bruce Blank, and Michel Boileau, who, in 1980, used postage stamps t
o test nocturnal erections, described in their study “Nocturnal Penile Tumescence Monitoring with Stamps” (Urol. 1980, DOI: 10.1016/0090-4295(80)90414-8).

The Ig Nobel committee also gave out a Medical Education Prize this year, to gastroenterologist Akira Horiuchi for the report “Colonoscopy in the Sitting Position: Lessons Learned from Self-Colonoscopy” (Gastrointest. Endoscopy 2006, DOI: 10.1016/j.gie.2005.10.014).

Lund University cognitive scientists Gabriela-Alina Sauciuc and coworkers claimed the Anthropology Prize “for collecting evidence, in a zoo, that chimpanzees imitate humans about as often, and about as well, as humans imitate chimpanzees” (Primates 2017, DOI: 10.1007/s10329-017-0624-9).

For a landmark paper documenting that most people don’t read the instruction manual when using complicated products, a Queensland University of Technology team led by Alethea L. Blackler garnered the Literature Prize (Interact. Comp. 2014, DOI: 10.1093/iwc/iwu023).

And finally, the Ig Nobel Peace Prize was awarded to a team from the University of Valencia’s University Research Institute on Traffic & Road Safety “for measuring the frequency, motivation, and effects of shouting and cursing while driving an automobile” (J. Sociol. Anthropol. 2016, DOI: 10.12691/jsa-1-1-1).

The Ig Nobel ceremony can be viewed in its entirety at youtube.com/improbableresearch, and National Public Radio’s “Science Friday” will air an edited recording of the ceremony on the day after U.S. Thanksgiving.

https://cen.acs.org/people/awards/2018-Ig-Nobel-Prizes/96/i37

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The detailed, all-sky picture of the infant universe created from nine years of WMAP data. The image reveals 13.77 billion year old temperature fluctuations (shown as color differences) that correspond to the seeds that grew to become the galaxies. The signal from our galaxy was subtracted using the multi-frequency data. This image shows a temperature range of ± 200 microKelvin.CREDIT: NASA/WMAP SCIENCE TEAM

by Jesse Shanahan

In a study published earlier this month, a team of theoretical physicists is claiming to have discovered the remnants of previous universes hidden within the leftover radiation from the Big Bang. Our universe is a vast collection of observable matter, like gas, dust, stars, etc., in addition to the ever-elusive dark matter and dark energy. In some sense, this universe is all we know, and even then, we can only directly study about 5% of it, leaving 95% a mystery that scientists are actively working to solve. However, this group of physicists is arguing that our universe isn’t alone; it’s just one in a long line of universes that are born, grow, and die. Among these scientists is mathematical physicist Roger Penrose, who worked closely with Stephen Hawking and currently is the Emeritus Rouse Ball Professor of Mathematics at Oxford University. Penrose and his collaborators follow a cosmological theory called conformal cyclic cosmology (CCC) in which universes, much like human beings, come into existence, expand, and then perish.

As a universe ages, it expands, and the constituent parts grow farther and farther apart from each other. Consequently, the interactions between galaxies that drive star formation and evolution become rarer. Eventually, the stars die out, and the remaining gas and dust is captured by black holes. In one of his most famous theories, Stephen Hawking proposed that this isn’t the end; black holes might have a way to slowly lose mass and energy by radiating certain particles. So, after many eons, the remaining black holes in the universe would disappear, leaving only disparate particles. Seemingly a wasteland, this end-state eventually mirrors the environment of our universe’s birth, and so, the cycle starts anew.

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Artist’s logarithmic scale conception of the observable universe with the Solar System at the center, inner and outer planets, Kuiper belt, Oort cloud, Alpha Centauri, Perseus Arm, Milky Way galaxy, Andromeda galaxy, nearby galaxies, Cosmic Web, Cosmic microwave radiation and Big Bang’s invisible plasma on the edge.CREDIT: WIKIPEDIA/PABLO CARLOS BUDASSI

When our universe was very young, before any recognizable components like stars, planets, or galaxies formed, it was filled with a dense, hot soup of plasma. As the universe expanded, it cooled, and eventually, particles could combine to form atoms. Eventually, the interaction and fusion of these atoms resulted in all of the matter that we observe today. However, we can still observe the leftover radiation from that initial, dense period in our universe’s history. This leftover glow, called the Cosmic Microwave Background (CMB), is the oldest electromagnetic radiation, and it fills the entirety of our universe. If the CCC theory were true, then there would be hints of previous universes in our universe’s CMB.

At the end of a universe, when those final black holes dissolve, CCC theory states they should leave behind a signature that would survive the death of that universe and persist into the next. Although not definitive proof of previous universes, detecting that signature would be strong evidence in support of CCC theory. In searching for these “Hawking points”, cosmologists face a difficult obstacle as the CMB is faint and varies randomly. However, Penrose is claiming that a comparison between a model CMB with Hawking points and actual data from our CMB has proven that Hawking points actually exist. If true, this would be the first-ever detection of evidence from another universe.

Unfortunately, as groundbreaking as this discovery seems, the scientific community has largely dismissed it. One of the fundamental characteristics of the CMB is that, although it has patterns, the variations are entirely statistically random. In fact, Penrose’s former collaborator, Stephen Hawking, spotted his own initials in the CMB while others have found a deer, a parrot, and numerous other recognizable shapes in the noise. Similarly, the Wilkinson Anisotropy Microscope Probe that mapped the CMB released an interactive image where you can search for familiar shapes and patterns. An avoidable result of both these random fluctuations and the sheer size of the CMB is that if scientists look hard enough, they can find whatever pattern they need, like the existence of Hawking points, perhaps. Another criticism of Penrose’s claim is that if CCC theory holds true, our universe should have tens of thousands of Hawking points in the CMB. Regrettably, Penrose could find only about 20.

Still, the possibility of alternate universes, whether long-dead or existing in parallel to our own, is tantalizing. Many other theories also claim to find traces of other universes hiding in the patterns of the CMB as well. Although it sounds like science fiction, we are left to wonder: is this just the cosmological equivalent of seeing shapes in random clouds or will scientists one day discover that we are one among many infinite universes?

Jesse Shanahan is an astrophysicist, EMT, and science communicator. For more space and language news, follow her on Twitter here.

https://www.forbes.com/sites/jesseshanahan/2018/08/24/did-scientists-actually-spot-evidence-of-another-universe/#2278663f1425

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Diagram of the brain of a person with Alzheimer’s Disease.

In recent years, researchers have largely converged on the role of inflammation in the development and progression of Alzheimer’s disease (AD). Studies over the past decade have revealed unexpected interactions between the brain and the immune system, and metabolic conditions such as obesity and diabetes may activate inflammatory responses that contribute to the development and progression of AD.

The activation of the inflammatory response is controlled by the inflammasome, a multi-protein oligomer that promotes the release of several pro-inflammatory cytokines including interleukin 1β (IL-1β) and interleukin 18 (IL-18). In an earlier study, a group of researchers with the University of Massachusetts Medical School, the University of Tokyo and the University of Bonn reported that mice with a cognate of Alzheimer’s disease that were additionally bred to knock out the NLRP3 gene encoding the inflammasome were completely protected from neurodegenerative effects of the disease. The researchers presumed that this was the result of their inability to produce IL-1β and IL-18.

This finding was quite promising, suggesting that targeting components of the inflammasome might be a path to Alzheimer’s treatments. In their new study, they sought to determine the effect of IL-18 by breeding IL-18 knockout mice. The researchers considered IL-18 to be a promising target, because levels are elevated in the cerebrospinal fluid of AD patients with mild cognitive impairment. Additionally, it is known to increase the production of amyloid peptide.

But the result of the new mouse study was startling, and completely unprecedented in Alzheimer’s research. The IL-18 knockout mice developed a lethal seizure disorder that the researchers attribute to an increase in neuronal network transmission. The authors write, “… the effects of IL-18 deletion were so dramatic that we were unable to identify previous evidence to help understand the phenomena.”

The finding that a proinflammatory cytokine might in some way ameliorate seizure-inducing neural activity seems counterintuitive, since inflammation is theorized to promote neurodegenerative symptoms in AD. The researchers believe that epilepsy is understudied in AD patients, even though it is a common complication; they point out that two-thirds of AD patients experience both motor and non-motor seizures. Additionally, AD patients with epilepsy are more likely to develop memory loss and other cognitive symptoms, and experience a more widespread loss of brain cells than AD patients without epilepsy, according to the researchers.

They theorize that IL-18 may be counteracting seizure-promoting effects of IL-1β, and suppressing IL-18 thus induced seizures in the test mice. “In fact,” they write, “the countereffect of IL-18 and IL-1β has been documented in a mouse model of cerebellar ataxia. Importantly, we found that the acute application of IL-18 protein reduced excitatory synaptic transmission in the hippocampus, providing evidence that IL-18 has a protective function in neuronal excitability. Thus, we speculate that IL-18 directly suppresses these proepileptogenic effects of IL-1β in APP/PS1 mice.”

However, the most important implication of the study may be that, while the inflammasome is a promising therapeutic target for Alzheimer’s, inhibiting specific cytokines could negatively affect people with the disease.

More information: Inflammasome-derived cytokine IL18 suppresses amyloid-induced seizures in Alzheimer-prone mice. Proceedings of the National Academy of Sciences (2018). doi.org/10.1073/pnas.1801802115

Abstract
Alzheimer’s disease (AD) is characterized by the progressive destruction and dysfunction of central neurons. AD patients commonly have unprovoked seizures compared with age-matched controls. Amyloid peptide-related inflammation is thought to be an important aspect of AD pathogenesis. We previously reported that NLRP3 inflammasome KO mice, when bred into APPswe/PS1ΔE9 (APP/PS1) mice, are completely protected from amyloid-induced AD-like disease, presumably because they cannot produce mature IL1β or IL18. To test the role of IL18, we bred IL18KO mice with APP/PS1 mice. Surprisingly, IL18KO/APP/PS1 mice developed a lethal seizure disorder that was completely reversed by the anticonvulsant levetiracetam. IL18-deficient AD mice showed a lower threshold in chemically induced seizures and a selective increase in gene expression related to increased neuronal activity. IL18-deficient AD mice exhibited increased excitatory synaptic proteins, spine density, and basal excitatory synaptic transmission that contributed to seizure activity. This study identifies a role for IL18 in suppressing aberrant neuronal transmission in AD.
Journal reference: Proceedings of the National Academy of Sciences

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A 3-D rendering of the serotonin system in the left hemisphere of the mouse brain reveals two groups of serotonin neurons in the dorsal raphe that project to either cortical regions (blue) or subcortical regions (green) while rarely crossing into the other’s domain.

As Liqun Luo was writing his introductory textbook on neuroscience in 2012, he found himself in a quandary. He needed to include a section about a vital system in the brain controlled by the chemical messenger serotonin, which has been implicated in everything from mood to movement regulation. But the research was still far from clear on what effect serotonin has on the mammalian brain.

“Scientists were reporting divergent findings,” said Luo, who is the Ann and Bill Swindells Professor in the School of Humanities and Sciences at Stanford University. “Some found that serotonin promotes pleasure. Another group said that it increases anxiety while suppressing locomotion, while others argued the opposite.”

Fast forward six years, and Luo’s team thinks it has reconciled those earlier confounding results. Using neuroanatomical methods that they invented, his group showed that the serotonin system is actually composed of at least two, and likely more, parallel subsystems that work in concert to affect the brain in different, and sometimes opposing, ways. For instance, one subsystem promotes anxiety, whereas the other promotes active coping in the face of challenges.

“The field’s understanding of the serotonin system was like the story of the blind men touching the elephant,” Luo said. “Scientists were discovering distinct functions of serotonin in the brain and attributing them to a monolithic serotonin system, which at least partly accounts for the controversy about what serotonin actually does. This study allows us to see different parts of the elephant at the same time.”

The findings, published online on August 23 in the journal Cell, could have implications for the treatment of depression and anxiety, which involves prescribing drugs such as Prozac that target the serotonin system – so-called SSRIs (selective serotonin reuptake inhibitors). However, these drugs often trigger a host of side effects, some of which are so intolerable that patients stop taking them.

“If we can target the relevant pathways of the serotonin system individually, then we may be able to eliminate the unwanted side effects and treat only the disorder,” said study first author Jing Ren, a postdoctoral fellow in Luo’s lab.

Organized projections of neurons

The Stanford scientists focused on a region of the brainstem known as the dorsal raphe, which contains the largest single concentration in the mammalian brain of neurons that all transmit signals by releasing serotonin (about 9,000).

The nerve fibers, or axons, of these dorsal raphe neurons send out a sprawling network of connections to many critical forebrain areas that carry out a host of functions, including thinking, memory, and the regulation of moods and bodily functions. By injecting viruses that infect serotonin axons in these regions, Ren and her colleagues were able to trace the connections back to their origin neurons in the dorsal raphe.

This allowed them to create a visual map of projections between the dense concentration of serotonin-releasing neurons in the brainstem to the various regions of the forebrain that they influence. The map revealed two distinct groups of serotonin-releasing neurons in the dorsal raphe, which connected to cortical and subcortical regions in the brain.

“Serotonin neurons in the dorsal raphe project to a bunch of places throughout the brain, but those bunches of places are organized,” Luo said. “That wasn’t known before.”

Two parts of the elephant

In a series of behavioral tests, the scientists also showed that serotonin neurons from the two groups can respond differently to stimuli. For example, neurons in both groups fired in response to mice receiving rewards like sips of sugar water but they showed opposite responses to punishments like mild foot shocks.

“We now understand why some scientists thought serotonin neurons are activated by punishment, while others thought it was inhibited by punishment. Both are correct – it just depends on which subtype you’re looking at,” Luo said.

What’s more, the group found that the serotonin neurons themselves were more complex than originally thought. Rather than just transmitting messages with serotonin, the cortical-projecting neurons also released a chemical messenger called glutamate – making them one of the few known examples of neurons in the brain that release two different chemicals.

“It raises the question of whether we should even be calling these serotonin neurons because neurons are named after the neurotransmitters they release,” Ren said.

Taken together, these findings indicate that the brain’s serotonin system is not made up of a homogenous population of neurons but rather many subpopulations acting in concert. Luo’s team has identified two groups, but there could be many others.

In fact, Robert Malenka, a professor and associate chair of psychiatry and behavioral sciences at Stanford’s School of Medicine, and his team recently discovered a group of serotonin neurons in the dorsal raphe that project to the nucleus accumbens, the part of the brain that promotes social behaviors.

“The two groups that we found don’t send axons to the nucleus accumbens, so this is clearly a third group,” Luo said. “We identified two parts of the elephant, but there are more parts to discover.”

https://medicalxpress.com/news/2018-08-brain-serotonin.html

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Researchers have identified a brand new ‘micro-organ’ inside the immune system of mice and humans – the first discovery of its kind for decades – and it could put scientists on the path to developing more effective vaccines in the future.

Vaccines are based on centuries of research showing that once the body has encountered a specific type of infection, it’s better able to defend against it next time. And this new research suggests this new micro-organ could be key to how our body ‘remembers’ immunity.

The researchers from the Garvan Institute of Medical Research in Australia spotted thin, flat structures on top of the immune system’s lymph nodes in mice, which they’ve dubbed “subcapsular proliferative foci” (or SPFs for short).

These SPFs appear to work like biological headquarters for planning a counter-attack to infection.

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Immune cells gathering at the SPF, with the purple band showing the SPF surface.

These SPFs only appear when the mice immune systems are fighting off infections that have been encountered before.

What’s more, the researchers detected SPFs in human lymph nodes too, suggesting our bodies react in the same way.

“When you’re fighting bacteria that can double in number every 20 to 30 minutes, every moment matters,” says senior researcher Tri Phan. “To put it bluntly, if your immune system takes too long to assemble the tools to fight the infection, you die.”

“This is why vaccines are so important. Vaccination trains the immune system, so that it can make antibodies very rapidly when an infection reappears. Until now we didn’t know how and where this happened.”

Traditional microscopy approaches analyse thin 2D slices of tissue, and the researchers think that’s why SPFs haven’t been spotted before – they themselves are very thin, and they only appear temporarily.

In this case the team made the equivalent of a 3D movie of the immune system in action, which revealed the collection of many different types of immune cell in these SPFs. The researchers describe them as a “one-stop shop” for fighting off remembered infections, and fighting them quickly.

Crucially, the collection of immune cells spotted by the researchers included Memory B type cells – cells which tell the immune system how to fight off a particular infection. Memory B cells then turn into plasma cells to produce antibodies and do the actual work of tackling the threat.

“It was exciting to see the memory B cells being activated and clustering in this new structure that had never been seen before,” says one of the team, Imogen Moran.

“We could see them moving around, interacting with all these other immune cells and turning into plasma cells before our eyes.”

According to the researchers, the positioning of the SPF structures on top of lymph nodes makes them perfectly positioned for fighting off infections – and fast.

They’re strategically placed at points where bacteria would invade, and contain all the ingredients required to keep the infection at bay.

Now we know how the body does it, we might be able to improve vaccine techniques – vaccines currently focus on making memory B cells, but this study suggests the process could be made more efficient by also looking at how they transform into plasma cells through the inner workings of an SPF.

“So this is a structure that’s been there all along, but no one’s actually seen it yet, because they haven’t had the right tools,” says Phan.

“It’s a remarkable reminder that there are still mysteries hidden within the body – even though we scientists have been looking at the body’s tissues through the microscope for over 300 years.”

The research has been published in Nature Communications.

https://www.sciencealert.com/researchers-identify-new-lymph-node-structures-powering-immunity

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The Milky Way is a zombie. No, not really, it doesn’t go around eating other galaxies’ brains. But it did “die” once, before flaring back to life. That’s what a Japanese scientist has ascertained after peering into the chemical compositions of our galaxy’s stars.

In a large section of the Milky Way, the stars can be divided into two distinct populations based on their chemical compositions. The first group is more abundant in what is known as α elements – oxygen, magnesium, silicon, sulphur, calcium and titanium. The second is less abundant in α elements, and markedly more abundant in iron.

The existence of these two distinct populations implies that something different is happening during the formation stages. But the precise mechanism behind it was unclear.

Astronomer Masafumi Noguchi of Tohoku University believes his modelling shows the answer. The two different populations represent two different periods of star formation, with a quiescent, or “dormant” period in between, with no star formation.

Based on the theory of cold flow galactic accretion proposed back in 2006, Noguchi has modelled the evolution of the Milky Way over a 10 billion-year period.

Originally, the cold flow model was suggested for much larger galaxies, proposing that massive galaxies form stars in two stages. Because of the chemical composition dichotomy of its stars, Noguchi believes this also applies to the Milky Way.

That’s because the chemical composition of stars is dependent on the gases from which they are formed. And, in the early Universe, certain elements – such as the heavier metals – hadn’t yet arrived on the scene, since they were created in stars, and only propagated once those stars had gone supernova.

In the first stage, according to Noguchi’s model, the galaxy is accreting cold gas from outside. This gas coalesces to form the first generation of stars.

After about 10 million years, which is a relatively short timescale in cosmic terms, some of these stars died in Type II supernovae. This propagated the α elements throughout the galaxy, which were incorporated into new stars.

But, according to the model, it all went a bit belly-up after about 3 billion years.

“When shock waves appeared and heated the gas to high temperatures 7 billion years ago, the gas stopped flowing into the galaxy and stars ceased to form,” a release from Tohoku University says.

During a hiatus of about 2 billion years, a second round of supernovae took place – the much longer scale Type Ia supernova, which typically occur after a stellar lifespan of about 1 billion years.

It’s in these supernovae that iron is forged, and spewed out into the interstellar medium. When the gas cooled enough to start forming stars again – about 5 billion years ago – those stars had a much higher percentage of iron than the earlier generation. That second generation includes our Sun, which is about 4.6 billion years old.

Noguchi’s model is consistent with recent research on our closest galactic neighbour, Andromeda, which is thought to be in the same size class as the Milky Way. In 2017, a team of researchers published a paper that found Andromeda’s star formation also occurred in two stages, with a relatively quiescent period in between.

If the model holds up, it may mean that the evolution models of galaxies need to be revised – that, while smaller dwarf galaxies experience continuous star formation, perhaps a “dead” period is the norm for massive ones.

If future observations confirm, who’s up for renaming our galaxy Frankenstein?

Noguchi’s paper has been published in the journal Nature.

https://www.sciencealert.com/milky-way-star-formation-two-generations-cold-flow-accretion-model-noguchi

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Even the occasional drink is harmful to health, according to the largest and most detailed research carried out on the effects of alcohol, which suggests governments should think of advising people to abstain completely.

The uncompromising message comes from the authors of the Global Burden of Diseases study, a rolling project based at the University of Washington, in Seattle, which produces the most comprehensive data on the causes of illness and death in the world.

Alcohol, says their report published in the Lancet medical journal, led to 2.8 million deaths in 2016. It was the leading risk factor for premature mortality and disability in the 15 to 49 age group, accounting for 20% of deaths.

Current alcohol drinking habits pose “dire ramifications for future population health in the absence of policy action today”, says the paper. “Alcohol use contributes to health loss from many causes and exacts its toll across the lifespan, particularly among men.”

Most national guidelines suggest there are health benefits to one or two glasses of wine or beer a day, they say. “Our results show that the safest level of drinking is none.”

The study was carried out by researchers at the Institute of Health Metrics and Evaluation (IHME), who investigated levels of alcohol consumption and health effects in 195 countries between 1990 to 2016. They used data from 694 studies to work out how common drinking was and from 592 studies including 28 million people worldwide to work out the health risks.

Moderate drinking has been condoned for years on the assumption that there are some health benefits. A glass of red wine a day has long been said to be good for the heart. But although the researchers did find low levels of drinking offered some protection from heart disease, and possibly from diabetes and stroke, the benefits were far outweighed by alcohol’s harmful effects, they said.

Drinking alcohol was a big cause of cancer in the over-50s, particularly in women. Previous research has shown that one in 13 breast cancers in the UK were alcohol-related. The study found that globally, 27.1% of cancer deaths in women and 18.9% in men over 50 were linked to their drinking habits.

In younger people globally the biggest causes of death linked to alcohol were tuberculosis (1.4% of deaths), road injuries (1.2%), and self-harm (1.1%).

In the UK, the chief medical officer Sally Davies has said there is no safe level of drinking, but the guidance suggests that drinkers consume no more than 14 units a week to keep the risks low. Half a pint of average-strength lager contains one unit and a 125ml glass of wine contains around 1.5 units.

While the study shows that the increased risk of alcohol-related harm in younger people who have one drink a day is small (0.5%), it goes up incrementally with heavier drinking: to 7% among those who have two drinks a day (in line with UK guidance) and 37% for those who have five.

One in three, or 2.4 billion people around the world, drink alcohol, the study shows. A quarter of women and 39% of men drink. Denmark has the most drinkers (95.3% of women, and 97.1% of men). Pakistan has the fewest male drinkers (0.8%) and Bangladesh the fewest women (0.3%). Men in Romania and women in Ukraine drink the most (8.2 and 4.2 drinks a day respectively), while women in the UK take the eighth highest place in the female drinking league, with an average of three drinks a day.

“Alcohol poses dire ramifications for future population health in the absence of policy action today. Our results indicate that alcohol use and its harmful effects on health could become a growing challenge as countries become more developed, and enacting or maintaining strong alcohol control policies will be vital,” said the report’s senior author, Prof Emmanuela Gakidou.

“Worldwide we need to revisit alcohol control policies and health programmes, and to consider recommendations for abstaining from alcohol. These include excise taxes on alcohol, controlling the physical availability of alcohol and the hours of sale, and controlling alcohol advertising. Any of these policy actions would contribute to reductions in population-level consumption, a vital step toward decreasing the health loss associated with alcohol use.”

Dr Robyn Burton, of King’s College London, said in a commentary in the Lancet that the conclusions of the study were clear and unambiguous. “Alcohol is a colossal global health issue and small reductions in health-related harms at low levels of alcohol intake are outweighed by the increased risk of other health-related harms, including cancer,” she wrote.

“There is strong support here for the guideline published by the Chief Medical Officer of the UK who found that there is ‘no safe level of alcohol consumption’.”

Public health policy should be to prioritise measures to reduce the numbers who drink through price increases, taxation, or setting the price according to the strength of the drink (minimum unit pricing), followed by curbs on marketing and restricting the places where people can buy alcohol.

“These approaches should come as no surprise because these are also the most effective measures for curbing tobacco-related harms, another commercially mediated disease, with an increasing body of evidence showing that controlling obesity will require the same measures,” she wrote.

Ben Butler, a Drinkaware spokesperson, said: “This new study supports existing evidence about the harms associated with alcohol. Our research shows that over a quarter of UK adults typically exceed the low risk drinking guidelines and are running the risk of serious long term illnesses.”

But David Spiegelhalter, Winton professor for the public understanding of risk at the University of Cambridge, said the data showed only a very low level of harm in moderate drinkers and suggested UK guidelines were very low risk.

“Given the pleasure presumably associated with moderate drinking, claiming there is no ‘safe’ level does not seem an argument for abstention,” he said. “There is no safe level of driving, but government do not recommend that people avoid driving. Come to think of it, there is no safe level of living, but nobody would recommend abstention.”

https://www.theguardian.com/society/2018/aug/23/no-healthy-level-of-alcohol-consumption-says-major-study