A new uncertainty principle holds that quantum objects can be at two temperatures at once, which is similar to the famous Schrödinger’s cat thought experiment, in which a cat in a box with a radioactive element can be both alive and dead.

By Meredith Fore

The famous thought experiment known as Schrödinger’s cat implies that a cat in a box can be both dead and alive at the same time — a bizarre phenomenon that is a consequence of quantum mechanics.

Now, physicists at the University of Exeter in England have found that a similar state of limbo may exist for temperatures: Objects can be two temperatures at the same time at the quantum level. This weird quantum paradox is the first completely new quantum uncertainty relation to be formulated in decades.

Heisenberg’s other principle
In 1927, German physicist Werner Heisenberg postulated that the more precisely you measure a quantum particle’s position, the less precisely you can know its momentum, and vice versa — a rule that would become the now-famous Heisenberg uncertainty principle.

The new quantum uncertainty, which states that the more precisely you know temperature, the less you can say about energy, and vice versa, has big implications for nanoscience, which studies incredibly tiny objects smaller than a nanometer. This principle will change how scientists measure the temperature of extremely small things such as quantum dots, small semiconductors or single cells, the researchers said in the new study, which was published in June in the journal Nature Communications.

In the 1930s, Heisenberg and Danish physicist Niels Bohr established an uncertainty relation between energy and temperature on the nonquantum scale. The idea was that, if you wanted to know the exact temperature of an object, the best and most precise scientific way to do that would be to immerse it in a “reservoir” — say, a tub of water, or a fridge full of cold air — with a known temperature, and allow the object to slowly become that temperature. This is called thermal equilibrium.

However, that thermal equilibrium is maintained by the object and the reservoir constantly exchanging energy. The energy in your object therefore goes up and down by infinitesimal amounts, making it impossible to define precisely. On the flip side, if you wanted to know the precise energy in your object, you would have to isolate it so that it could not come into contact with, and exchange energy with, anything. But if you isolated it, you would not be able to precisely measure its temperature using a reservoir. This limitation makes the temperature uncertain.

Things get weirder when you go to the quantum scale.

A new uncertainty relation
Even if a typical thermometer has an energy that goes up and down slightly, that energy can still be known to within a small range. This is not true at all on the quantum level, the new research showed, and it’s all due to Schrödinger’s cat. That thought experiment proposed a theoretical cat in a box with a poison that could be activated by the decay of a radioactive particle. According to the laws of quantum mechanics, the particle could have decayed and not decayed at the same time, meaning that until the box was opened, the cat would be both dead and alive at the same time — a phenomenon known as superposition.

The researchers used math and theory to predict exactly how such superposition affects the measurement of the temperature of quantum objects.

“In the quantum case, a quantum thermometer … will be in a superposition of energy states simultaneously,”Harry Miller, one of the physicists at the University of Exeter who developed the new principle, told Live Science. “What we find is that because the thermometer no longer has a well-defined energy and is actually in a combination of different states at once, that this actually contributes to the uncertainty in the temperature that we can measure.”

In our world, a thermometer may tell us an object is between 31 and 32 degrees Fahrenheit (minus 0.5 and zero degrees Celsius). In the quantum world, a thermometer may tell us an object is both those temperatures at the same time. The new uncertainty principle accounts for that quantum weirdness.

Interactions between objects at the quantum scale can create superpositions, and also create energy. The old uncertainty relation ignored these effects, because it doesn’t matter for nonquantum objects. But it matters a lot when you’re trying to measure the temperature of a quantum dot, and this new uncertainty relation makes up a theoretical framework to take these interactions into account.

The new paper could help anyone who’s designing an experiment to measure temperature changes in objects below the nanometer scale, Miller said. “Our result is going to tell them exactly how to accurately design their probes and tell them how to account for the additional quantum uncertainty that you get.”





Medical training exercises are getting more and more realistic. Recently, companies have developed robots that medical students can practise on.

The idea is that these pretend people can lead us a little way into the uncanny valley, so we have to deal with the emotional response as well as the methodology behind a procedure.

One of the latest medical robots is called HAL. It takes the form of a five-year-old boy which can respond to certain questions, follow a finger with its eyes, bleed, and convulse.

It even has a pulse.

HAL was built by Gaumard Scientific, a company that produced the first synthetic human skeleton for medical schools.

The company’s technology has come a long way since then, having developed a synthetic boy who can simulate many medical problems, cry tears, and shout for its mother.

Using HAL is supposed to help students retain their knowledge better, because it is as close to treating a real person without actually using a human volunteer.

HAL’s other functions include going into cardiac arrest, anaphylactic shock, and the ability to have its blood sugar, blood oxygen level, and carbon dioxide levels measured.

Also, its pupils dilate when a light is shined into its eyes.

In a promotional video, a doctor asks HAL about how much its head hurts, and it responds “an eight”.

To prepare for the really bad injuries and problems, HAL can be hooked up to real hospital machines and shocked with a defibrillator.

When it’s awake it can be set to several different emotional states, including lethargic, angry, amazed, quizzical, and anxious.

The idea is to make HAL just realistic enough to help students with their studies, but not so realistic that it’s too traumatic to deal with when they have to slit its throat to insert a trachael tube.

HAL is one of a few medical robots currently in use. On the Gaumard website there is also a premature baby simulator, and a scarily realistic robot that gives birth.

These pretend people are very different from the lifeless dummies medical professionals have used for decades.

“I’ve seen several nurses be like, ‘Whoa it moves!'” Marc Berg, the medical director at the Revive Initiative for Resuscitation Excellence at Stanford, told Wired in a chilling article.

“I think that’s kind of similar to the idea that if you’ve driven a car for 20 years and then you got a brand new car, you’re kind of amazed initially.”

Watch the video explaining all of HAL’s functions here:



The NIHR and King’s College London are calling for 40,000 people diagnosed with depression or anxiety to enrol online for the Genetic Links to Anxiety and Depression (GLAD) Study and join the NIHR Mental Health Bioresource.

Researchers hope to establish the largest ever database of volunteers who can be called up to take part in research exploring the genetic factors behind the two most common mental health conditions – anxiety and depression.


The GLAD study will make important strides towards better understanding of these disorders and provide a pool of potential participants for future studies, reducing the time-consuming process of recruiting patients for research.

Research has shown 30-40% of the risk for both depression and anxiety is genetic and 60-70% due to environmental factors. Only by having a large, diverse group of people available for studies will researchers be able to determine how genetic and environmental triggers interact to cause anxiety and depression.

Leader of the GLAD study and the NIHR Mental Health BioResource, Dr Gerome Breen of King’s College London, said: “It’s a really exciting time to become involved in mental health research, particularly genetic research which has made incredible strides in recent years – we have so far identified 46 genetic links for depression and anxiety.

“By recruiting 40,000 volunteers willing to be re-contacted for research, the GLAD Study will take us further than ever before. It will allow researchers to solve the big unanswered questions, address how genes and environment act together and help develop new treatment options.”

The GLAD Study, a collaboration between the NIHR BioResource and King’s College London, has been designed to be particularly accessible, with a view to motivating more people to take part in mental health research.

Research psychologist and study lead Professor Thalia Eley, King’s College London, said: “We want to hear from all different backgrounds, cultures, ethnic groups and genders, and we are especially keen to hear from young adults. By including people from all parts of the population, what we learn will be relevant to everyone. This is a unique opportunity to participate in pioneering medical science.”




Dr. Leslie Norins is willing to hand over $1 million of his own money to anyone who can clarify something: Is Alzheimer’s disease, the most common form of dementia worldwide, caused by a germ?

By “germ” he means microbes like bacteria, viruses, fungi and parasites. In other words, Norins, a physician turned publisher, wants to know if Alzheimer’s is infectious.

It’s an idea that just a few years ago would’ve seemed to many an easy way to drain your research budget on bunk science. Money has poured into Alzheimer’s research for years, but until very recently not much of it went toward investigating infection in causing dementia.

But this “germ theory” of Alzheimer’s, as Norins calls it, has been fermenting in the literature for decades. Even early 20th century Czech physician Oskar Fischer — who, along with his German contemporary Dr. Alois Alzheimer, was integral in first describing the condition — noted a possible connection between the newly identified dementia and tuberculosis.

If the germ theory gets traction, even in some Alzheimer’s patients, it could trigger a seismic shift in how doctors understand and treat the disease.

For instance, would we see a day when dementia is prevented with a vaccine, or treated with antibiotics and antiviral medications? Norins thinks it’s worth looking into.

Norins received his medical degree from Duke in the early 1960s, and after a stint at the Centers for Disease Control and Prevention he fell into a lucrative career in medical publishing. He eventually settled in an admittedly aged community in Naples, Fla., where he took an interest in dementia and began reading up on the condition.

After scouring the medical literature he noticed a pattern.

“It appeared that many of the reported characteristics of Alzheimer’s disease were compatible with an infectious process,” Norins tells NPR. “I thought for sure this must have already been investigated, because millions and millions of dollars have been spent on Alzheimer’s research.”

But aside from scattered interest through the decades, this wasn’t the case.

In 2017, Norins launched Alzheimer’s Germ Quest Inc., a public benefit corporation he hopes will drive interest into the germ theory of Alzheimer’s, and through which his prize will be distributed. A white paper he penned for the site reads: “From a two-year review of the scientific literature, I believe it’s now clear that just one germ — identity not yet specified, and possibly not yet discovered — causes most AD. I’m calling it the ‘Alzheimer’s Germ.’ ”

Norins is quick to cite sources and studies supporting his claim, among them a 2010 study published in the Journal of Neurosurgery showing that neurosurgeons die from Alzheimer’s at a nearly 2 1/2 times higher rate than they do from other disorders.

Another study from that same year, published in The Journal of the American Geriatric Society, found that people whose spouses have dementia are at a 1.6 times greater risk for the condition themselves.

Contagion does come to mind. And Norins isn’t alone in his thinking.

In 2016, 32 researchers from universities around the world signed an editorial in the Journal of Alzheimer’s Disease calling for “further research on the role of infectious agents in [Alzheimer’s] causation.” Based on much of the same evidence Norins encountered, the authors concluded that clinical trials with antimicrobial drugs in Alzheimer’s are now justified.

NPR reported on an intriguing study published in Neuron in June that suggested that viral infection can influence the progression of Alzheimer’s. Led by Mount Sinai genetics professor Joel Dudley, the work was intended to compare the genomes of healthy brain tissue with that affected by dementia.

But something kept getting in the way: herpes.

Dudley’s team noticed an unexpectedly high level of viral DNA from two human herpes viruses, HHV-6 and HHV-7. The viruses are common and cause a rash called roseola in young children (not the sexually transmitted disease caused by other strains).

Some viruses have the ability to lie dormant in our neurons for decades by incorporating their genomes into our own. The classic example is chickenpox: A childhood viral infection resolves and lurks silently, returning years later as shingles, an excruciating rash. Like it or not, nearly all of us are chimeras with viral DNA speckling our genomes.

But having the herpes viruses alone doesn’t mean inevitable brain decline. After all, up to 75 percent of us may harbor HHV-6 .

But Dudley also noticed that herpes appeared to interact with human genes known to increase Alzheimer’s risk. Perhaps, he says, there is some toxic combination of genetic and infectious influence that results in the disease; a combination that sparks what some feel is the main contributor to the disease, an overactive immune system.

The hallmark pathology of Alzheimer’s is accumulation of a protein called amyloid in the brain. Many researchers have assumed these aggregates, or plaques, are simply a byproduct of some other process at the core of the disease. Other scientists posit that the protein itself contributes to the condition in some way.

The theory that amyloid is the root cause of Alzheimer’s is losing steam. But the protein may still contribute to the disease, even if it winds up being deemed infectious.

Work by Harvard neuroscientist Rudolph Tanzi suggests it might be a bit of both. Along with colleague Robert Moir, Tanzi has shown that amyloid is lethal to viruses and bacteria in the test tube, and also in mice. He now believes the protein is part of our ancient immune system that like antibodies, ramps up its activity to help fend off unwanted bugs.

So does that mean that the microbe is the cause of Alzheimer’s, and amyloid a harmless reaction to it? According to Tanzi it’s not that simple.

Tanzi believes that in many cases of Alzheimer’s, microbes are probably the initial seed that sets off a toxic tumble of molecular dominoes. Early in the disease amyloid protein builds up to fight infection, yet too much of the protein begins to impair function of neurons in the brain. The excess amyloid then causes another protein, called tau, to form tangles, which further harm brain cells.

But as Tanzi explains, the ultimate neurological insult in Alzheimer’s is the body’s reaction to this neurotoxic mess. All the excess protein revs up the immune system, causing inflammation — and it’s this inflammation that does the most damage to the Alzheimer’s-afflicted brain.

So what does this say about the future of treatment? Possibly a lot. Tanzi envisions a day when people are screened at, say, 50 years old. “If their brains are riddled with too much amyloid,” he says, “we knock it down a bit with antiviral medications. It’s just like how you are prescribed preventative drugs if your cholesterol is too high.”

Tanzi feels that microbes are just one possible seed for the complex pathology behind Alzheimer’s. Genetics may also play a role, as certain genes produce a type of amyloid more prone to clumping up. He also feels environmental factors like pollution might contribute.

Dr. James Burke, professor of medicine and psychiatry at Duke University’s Alzheimer’s Disease Research Center, isn’t willing to abandon the amyloid theory altogether, but agrees it’s time for the field to move on. “There may be many roads to developing Alzheimer’s disease and it would be shortsighted to focus just on amyloid and tau,” he says. “A million-dollar prize is attention- getting, but the reward for identifying a treatable target to delay or prevent Alzheimer’s disease is invaluable.”

Any treatment that disrupts the cascade leading to amyloid, tau and inflammation could theoretically benefit an at-risk brain. The vast majority of Alzheimer’s treatment trials have failed, including many targeting amyloid. But it could be that the patients included were too far along in their disease to reap any therapeutic benefit.

If a microbe is responsible for all or some cases of Alzheimer’s, perhaps future treatments or preventive approaches will prevent toxin protein buildup in the first place. Both Tanzi and Norins believe Alzheimer’s vaccines against viruses like herpes might one day become common practice.

In July of this year, in collaboration with Norins, the Infectious Diseases Society of America announced that they plan to offer two $50,000 grants supporting research into a microbial association with Alzheimer’s. According to Norins, this is the first acknowledgement by a leading infectious disease group that Alzheimer’s may be microbial in nature – or at least that it’s worth exploring.

“The important thing is not the amount of the money, which is a pittance compared with the $2 billion NIH spends on amyloid and tau research,” says Norins, “but rather the respectability and more mainstream status the grants confer on investigating of the infectious possibility. Remember when we thought ulcers were caused by stress?”

Ulcers, we now know, are caused by a germ.


Walter Mischel in 2004. “If we have the skills to allow us to make discriminations about when we do or don’t do something,” Dr. Mischel said, “we are no longer victims of our desires.” (David Dini/Columbia University)

By Emily Langer

The experiment was “simplicity itself,” its creator, psychologist Walter Mischel, would later recall. The principal ingredient was a cookie or a pretzel stick or — most intriguingly to the popular imagination — a marshmallow.

In what became known as “the marshmallow test,” a child was placed in a room with a treat and presented with a choice. She could eat the treat right away. Or she could wait unaccompanied in the room, for up to 20 minutes, and then receive two treats in reward for her forbearance.

Conducting their work at a nursery school on the campus of Stanford University in the 1960s, Dr. Mischel and his colleagues observed responses that were as enlightening as they are enduringly adorable. Some children distracted themselves by putting their fingers in their ears or nose. At least one child caressed the marshmallow as he hungered for it. Only about 30 percent of the children managed to wait for the double reward.

Dr. Mischel, who continued his career at Columbia University and died Sept. 12 at 88, followed a cohort of the children for decades and presented his findings to mainstream readers in his 2014 book “The Marshmallow Test: Why Self-Control is the Engine of Success.”

His observations, widely noted and hotly debated, were striking: Children who had found ways to delay gratification, he found, had greater success in school, made more money and were less prone to obesity and drug addiction.

“What emerged from those studies is a different view of self-control, one that sees it as a matter of skill” and not a matter of “gritting your teeth,” said Yuichi Shoda, a professor of psychology at the University of Washington who worked with Dr. Mischel as a graduate student.

As worried parents conducted marshmallow tests at home, policymakers, educators and motivational speakers found a compelling catchphrase: “Don’t eat the marshmallow!” Even the ravenous Cookie Monster, a mainstay of the children’s TV show “Sesame Street,” was coaxed to resist a cookie.

Meanwhile, some psychologists challenged Dr. Mischel’s findings, arguing that a study group drawn from the privileged environs of Stanford could hardly yield reliable results. Skeptics noted that while affluent families might teach their children to delay gratification, in an effort to encourage financial and other forms of responsibility, children from disadvantaged homes learn that waiting to eat might mean not eating at all.

Dr. Mischel defended his research, emphasizing that in no way did he wish to suggest a laboratory performance — particularly by a preschooler — was destiny. The question, he said, is “how can you regulate yourself and control yourself in ways that make your life better?”

Walter Mischel was born Feb. 22, 1930, to a Jewish family in Vienna. His home was not far from that of Sigmund Freud, the founder of psychoanalysis. “Even as a young child I was aware of his presence,” Dr. Mischel once told the British Psychological Society, “and I suspect at some level I became quite interested in what makes people tick.”

Dr. Mischel’s family enjoyed a comfortable life until the rise of Nazism. His father, a businessman who had suffered from polio, was made to limp through the streets without his cane. Dr. Mischel recalled being humiliated by members of the Hitler Youth who tread on his new shoes. The experience, he told the Guardian, planted in him a desire to understand “the enabling conditions that allow people to go from being victims to being victors.”

After the Nazi annexation of Austria in 1938, the family fled the country and settled eventually in New York City, where they ran a five-and-dime store. Dr. Mischel, who became a U.S. citizen in the 1950s, helped support the family by working in an umbrella factory and as an elevator operator.

He was a 1951 psychology graduate of New York University and received a master’s degree from the City College of New York in 1953 and a PhD from Ohio State University in 1956, both in clinical psychology. He taught at Harvard University before settling at Stanford.

He said he became fascinated by the development of self-control in children by watching his daughters emerge from infancy into toddler-hood and girlhood.

“I began with a truly burning question,” he told the Guardian. “I wanted to know how my three young daughters developed, in a remarkably short period of time, from being howling, screaming, often impossible kids to people who were actually able to sit and do something that required them to concentrate. I wanted to understand this miraculous transformation.”

The subjects of the Stanford nursery-school tests were his daughters’ classmates. As the children grew up and he noticed correlations between their childhood self-control and future success, he decided to pursue the question more rigorously, through longitudinal study.

He conceded the limitations of his study group at Stanford. “It was an unbelievably elitist subset of the human race, which was one of the concerns that motivated me to study children in the South Bronx — kids in high-stress, poverty conditions,” he told the Atlantic in 2014, “and yet we saw many of the same phenomena as the marshmallow studies were revealing.”

Dr. Mischel proposed strategies for delaying gratification, such as putting the object at physical distance, by removing it from view, or at symbolic distance by imagining it to be something else. A marshmallow is not a sugary treat, for example, but rather a cotton ball.

In his own life, he reported success at resisting chocolate mousse by imagining the dessert to be covered in roaches. A self-described “three-packs-a-day smoker, supplemented by a pipe . . . supplemented by a cigar,” he said he conquered his addiction by recalling the image of a lung-cancer patient he had seen at Stanford, branded with X’s where he would be treated by radiation.

In addition to “The Marshmallow Test,” Dr. Mischel wrote and co-authored numerous texts on personality, child development and other fields of psychological research. He retired last year after more than three decades at Columbia.

His marriages to Frances Henry and Harriet Nerlove ended in divorce. Survivors include his partner of nearly two decades, Michele Myers of New York; three daughters from his second marriage, Judy Mischel of Chicago, Rebecca Mischel of Portland, Ore., and Linda Mischel Eisner of New York City; and six grandchildren.

Linda Mischel Eisner confirmed the death and said her father died at his home of pancreatic cancer.

Dr. Mischel professed to have found hope in his life’s work. “If we have the skills to allow us to make discriminations about when we do or don’t do something,” he told the New Yorker magazine, “we are no longer victims of our desires.”

“It’s not,” he said, “just about marshmallows.”




When somebody mentions anaesthetics, we probably think straight away of pain relief, but there’s a lot more going on in these complex chemical compounds than the simple negation of discomfort.

While there’s a range of chemicals that can induce anaesthesia in humans, just how these unrelated compounds trigger a lack of consciousness remains somewhat unclear.

And the mystery deepens when you consider it isn’t only animals that are affected by anaesthetics – plants are, too.

Humans in ancient societies were using things like herbs for various sedative purposes thousands of years ago, but the roots of modern anaesthesia began around the mid-19th century, when physicians began administering diethyl ether to patients during surgical procedures.

It was only a few decades later that scientists realised plants were similarly affected by ether, leading French physiologist Claude Bernard to conclude plants and animals shared a common biological essence that could be disrupted by anaesthetics.


A century and a half later, scientists are still investigating this strange commonality – basically by slipping plants the mickey and seeing what it does to them.

In a new study by Japanese and European researchers, the team filmed a number of plants that exhibit the phenomenon of rapid plant movement to see what kinds of anaesthetic chemicals affected them.

The sensitive plant (Mimosa pudica) usually closes its leaves in response to touch stimuli; but when exposed to diethyl ether, the dosed-up plants completely lost this response, becoming motionless, with the movement response only returning to normal after 7 hours.

In a separate experiment with the sensitive plants, a lidocaine solution also immobilised the leaves.

Similarly, the Venus flytrap (Dionaea muscipula) lost its ability to close its trap when exposed to diethyl ether – despite repeated prongings by the researchers – but the mechanism recovered in just 15 minutes.

Another carnivorous plant, Cape sundew (Drosera capensis), captures prey via sticky tentacles on its leaves, but experiments showed they lost the ability to bend their leaves and tentacles when exposed to the ether.

As for why plants are incapacitated by these chemicals, the researchers hypothesise it is to do with the inhibition of action potentials, preventing electrical impulses that help plants’ biological systems function.

“[B]ioelectricity and action potentials animate not only humans and animals but also plants,” the researchers explain.

“That animals/humans and also plants are animated via action potentials is of great importance for our ultimate understanding of the elusive nature of plant movements and plant-specific cognition/intelligence based plant behaviour.”

Ultimately, the team thinks these similarities between plant and animal reactions to anaesthetic compounds could lead to future research where plants might function as a substitute model or test system to explore human anaesthesia – something scientists are still pretty uncertain about.

It’s not easy being green, perhaps, but at least they shouldn’t feel any pain.

The findings are reported in Annals of Botany.




Why is it sometimes so hard to convince someone that the world is indeed a globe, or that climate change is actually caused by human activity, despite the overwhelming evidence?

Scientists think they might have the answer, and it’s less to do with lack of understanding, and more to do with the feedback they’re getting.

Getting positive or negative reactions to something you do or say is a greater influence on your thinking than logic and reasoning, the new research suggests – so if you’re in a group of like-minded people, that’s going to reinforce your thinking.

Receiving good feedback also encourages us to think we know more than we actually do.

In other words, the more sure we become that our current position is right, the less likely we are to take into account other opinions or even cold, hard scientific data.

“If you think you know a lot about something, even though you don’t, you’re less likely to be curious enough to explore the topic further, and will fail to learn how little you know,” says one of the team members behind the new study, Louis Marti from the University of California, Berkeley.

For the research, more than 500 participants were recruited and shown a series of colored shapes. As each shape appeared, the participants got asked if it was a “Daxxy” – a word made up for these experiments.

The test takers had no clues as to what a Daxxy was or wasn’t, but they did get feedback after guessing one way or the other – the system would tell them if the shape they were looking at qualified as a Daxxy or not. At the same time they were also asked how sure they were about what a Daxxy actually was.

In this way the researchers were able to measure certainty in relation to feedback. Results showed the confidence of the participants was largely based on the results of their last four or five guesses, not their performance overall.

You can see the researchers explain the experiment in the video below:

The team behind the tests says this plays into something we already know about learning – that for it to happen, learners need to recognise that there is a gap between what they currently know and what they could know. If they don’t think that gap is there, they won’t take on board new information.

“What we found interesting is that they could get the first 19 guesses in a row wrong, but if they got the last five right, they felt very confident,” says Marti. “It’s not that they weren’t paying attention, they were learning what a Daxxy was, but they weren’t using most of what they learned to inform their certainty.”

This recent feedback is having more of an effect than hard evidence, the experiments showed, and that might apply in a broader sense too. It could apply to learning something new or trying to differentiate between right and wrong.

And while in this case the study participants were trying to identify a made-up shape, the same cognitive processes could be at work when it comes to echo chambers on social media or on news channels – where views are constantly reinforced.

“If you use a crazy theory to make a correct prediction a couple of times, you can get stuck in that belief and may not be as interested in gathering more information,” says one of the team, psychologist Celeste Kidd from UC Berkeley.

So if you think vaccinations are harmful, for example, the new study suggests you might be basing that on the most recent feedback you’ve had on your views, rather than the overall evidence one way or the other.

Ideally, the researchers say, learning should be based on more considered observations over time – even if that’s not quite how the brain works sometimes.

“If your goal is to arrive at the truth, the strategy of using your most recent feedback, rather than all of the data you’ve accumulated, is not a great tactic,” says Marti.

The research has been published in Open Mind.