by Matthew Herper

A Harvard scientist thinks he’s reached a new milestone: a genetic test that helps identify people who are at high risk of having a heart attack. Can he convince doctors to use it?

“I think–in a few years, I think everybody will know this number, similar to the way we know our cholesterol right now,” muses Sekar Kathiresan, director of the Cardiovascular Disease Initiative at the Broad institute and a professor at Harvard Medical School.

Not everyone else is so sure. “I think it’s a brilliant approach,” says Harlan Krumholz, the Harold H. Hines Jr. professor of cardiology at Yale University and one of Kathiresan’s collaborators. But he worries about whether Kathiresan’s tests are ready to compete with the plethora of diagnostic tests, from AI-boosted CT scans to new types of “bad” cholesterol proteins, that are on offer. And he worries about cost. There is no commercial version of the gene test. But the very idea that such a test is not only available, but also near, is the result of a cresting wave of new genetic science, the result of large efforts to gather genetic information from millions of volunteers.

The number in question is what is called a polygenic risk score. Instead of looking for one miswritten gene that causes heart attacks, or, for that matter, other health problems, geneticists are increasingly looking at thousands of genetic alterations without even being sure what each does. In the case of Kathiresan’s polygenic score, the test looks for 6.6 million single-letter genetic changes that are more prevalent in people who have had early heart attacks.

Our genetic inheritances, the current thinking goes, are not so much a set of declarative orders as a cacophony of noise. There are big genetic changes that can have a big effect, but most diseases are the result of lots of tiny changes that add up. In Kathiresan’s words, it’s mostly a gemish (Yiddish for “a mixture”). And it’s not clear which changes are biologically important – Kathiresan says only 6,000 or so of the 6.6 million genetic changes are probably actually causing heart attacks. But finding those specific changes will take a long time. The risk score could be used now.

The effect of this genetic cacophony can be huge. The most common single mutation that increases the risk of heart disease is a gene that causes a disease called heterozygous familial hypercholesterolemia (literally: inherited high cholesterol) that occurs in one person in 250 and triple’s a person’s risk of having a heart attack. But today, in a paper in Nature Genetics, Kathiresan and his colleagues present data that 5% to 8% have a polygenic score that also at least triples their risk of having a heart attack. That’s about 20 times as many people, Kathiresan says.

“These patients are currently unaware of their risk because the polygenic patients don’t have higher levels of the usual risk factors,” Kathiresan says. “Their cholesterol is not high. Their blood pressure is not that high. They are hidden from the current risk assessment tools.”

In the Nature Genetics paper, Kathiresan’s team tested the 6-million-variant polygenic score in two groups of patients numbering, respectively, 120,280 and 288,978 people, from the U.K. BioBank, a government-backed effort in the United Kingdom to collect genetic data. For some patients, the risk was even higher, with the genetic changes predicting a fivefold increase in heart attack risk. The paper also argues that polygenic risk scores could be used to predict risk of conditions such as type 2 diabetes and breast cancer.

Another study, yet to be published, looked at the prevalence of both familial hypercholesterolemia and the polygenic score in a population of people who had heart attacks in their 40s and 50s, Katherisan says. Only 2% had familial hypercholesterolemia, but 20% had a high polygenic risk score. Knowing one’s polygenic risk score might matter. A 2016 paper in the New England Journal of Medicine showed that people with high polygenic scores had fewer heart attacks if they had healthier lifestyles, and a 2017 paper in the medical journal Circulation showed that patients with high polygenic risk scores got an outsize benefit from cholesterol-lowering statin drugs. Those papers, both by Kathiresan’s group, used a score that included only a few dozen gene variants.

Doctors should be skeptical of such a test. There’s a long history of tests in medicine that have done more harm than good by leading to people to take drugs they do not need. Cardiologists have gotten used to even higher standards for data. For instance, many might want to see if the test can show a benefit in a large study in which people are tested at random. Many will want more evidence that the test can identify people at high risk they’d otherwise miss, as Kathiresan says, and that it doesn’t lead to treatment in those who don’t need it. Kathiresan says he hopes to do a study in the highest-risk individuals to prove that statin drugs can lower their risk. If the test becomes a commercial prospect, more studies will drive up the eventual cost.

Kathiresan is hoping to follow a less expensive path. He notes that 17 million people have already used genotyping services like 23andMe and Ancestry. He hopes that people who use those services (23andMe costs $99, Ancestry $59) will submit their data to a portal he’ll build for free. He also says he’s in discussions with commercial providers, but he’s hoping that people will be able to get their polygenic scores for about as much as the cost of a cholesterol test. For the people at the highest risk, he argues, this is information that could be important. For others, he argues, why deny people information that has been scientifically validated?

Whether Kathiresan can really pull off a low-cost version in a medical system that is optimized to make money is as big a question as whether the test is ready for prime time. Krumholz worried about the cost of the test until a reporter told him of Kathiresan’s planned website. “If you say it’s free, I’m going, ‘Why not?'” Krumholz says. “It’s a better family history,” he says, comparing the test to asking whether a relative has had a heart attack. But that may be the biggest ‘if’. If anything is more puzzling than genetics, it is the economics of healthcare in the U.S.A.


Crohn’s disease is a long-term condition that causes inflammation of the lining of the digestive system, and results in diarrhoea, abdominal pain, extreme tiredness and other symptoms that significantly affect quality of life.

Current treatments include drugs to reduce inflammation but these have varying results, and surgery is often needed to remove the affected part of the bowel. In extreme cases, after multiple operations over the years, patients may require a final operation to divert the bowel from the anus to an opening in the stomach, called a stoma, where stools are collected in a pouch.

Chief investigator Professor James Lindsay from Queen Mary’s Blizard Institute and a consultant at Barts Health NHS Trust said: “Despite the introduction of new drugs, there are still many patients who don’t respond, or gradually lose response, to all available treatments. Although surgery with the formation of a stoma may be an option that allows patients to return to normal daily activities, it is not suitable in some and others may not want to consider this approach.

“We’re hoping that by completely resetting the patient’s immune system through a stem cell transplant, we might be able to radically alter the course of the disease. While it may not be a cure, it may allow some patients to finally respond to drugs which previously did not work.”

Helen Bartlett, a Crohn’s disease patient who had stem cell therapy at John Radcliffe Hospital, Oxford, said: “Living with Crohn’s is a daily struggle. You go to the toilet so often, you bleed a lot and it’s incredibly tiring. You also always need to be careful about where you go. I’ve had to get off trains before because there’s been no toilet, and I needed to go there and then.

“I’ve been in and out of hospital for the last twenty years, operation after operation, drug after drug, to try to beat this disease. It’s frustrating, it’s depressing and you just feel so low.

“When offered the stem cell transplant, it was a complete no brainer as I didn’t want to go through yet more failed operations. I cannot describe how much better I feel since the treatment. I still have problems and I’m always going to have problems, but I’m not in that constant pain.”

The use of stem cell transplants to wipe out and replace patients’ immune systems has recently been found to be successful in treating multiple sclerosis. This new trial will investigate whether a similar treatment could reduce gut inflammation and offer hope to people with Crohn’s disease.

In the trial, patients undergo chemotherapy and hormone treatment to mobilise their stem cells, which are then harvested from their blood. Further chemotherapy is then used to wipe out their faulty immune system. When the stem cells are re-introduced back into the body, they develop into new immune cells which give the patient a fresh immune system.

In theory, the new immune system will then no longer react adversely to the patient’s own gut to cause inflammation, and it will also not act on drug compounds to remove them from their gut before they have had a chance to work.

Professor Tom Walley, Director of the NIHR Evaluation, Trials and Studies programmes, which funded the trial, said: “Stem cell therapies are an important, active and growing area of research with great potential. There are early findings showing a role for stem cells in replacing damaged tissue. In Crohn’s disease this approach could offer real benefits for the clinical care and long term health of patients.”

The current clinical trial, called ‘ASTIClite’, is a follow up to the team’s 2015 ‘ASTIC’ trial, which investigated a similar stem cell therapy. Although the therapy in the original trial did not cure the disease, the team found that many patients did see benefit from the treatment, justifying a further clinical trial. There were also some serious side effects from the doses of drugs used, so this follow-up trial will be using a lower dose of the treatment to minimise risks due to toxicity.

Patients will be recruited to the trial through Barts Health NHS Trust, Cambridge University Hospitals NHS Foundation Trust, Guy’s & St Thomas’ NHS Foundation Trust, NHS Lothian, Nottingham University Hospitals NHS Trust, Oxford University Hospitals NHS Foundation Trust, Royal Liverpool and Broadgreen University Hospital NHS Trust and Sheffield Teaching Hospitals NHS Foundation Trust.

The trial will involve academics from the University of Manchester, University of Nottingham, University of Sheffield, Nottingham Trent University, University of Edinburgh, University of Oxford, King’s College London, as well as Queen Mary University of London.

The study was funded by a Medical Research Council and NIHR partnership created to support the evaluation of interventions with potential to make a step-change in the promotion of health, treatment of disease and improvement of rehabilitation or long-term care.



A specific part of the brain called the caudate nucleus could control pessimistic responses, according to animal tests, a finding which might help us unlock better treatments for mental disorders like anxiety and depression.

These disorders often come with negative moods triggered by a pessimistic reaction, and if scientists can figure out how to control that reaction, we might stand a better chance of dealing with the neuropsychiatric problems that affect millions of people worldwide – and maybe discover the difference between glass half full and glass half empty people along the way.

The research team from MIT found that when the caudate nucleus was artificially stimulated in macaques, the animals were more likely to make negative decisions, and consider the potential drawback of a decision rather than the potential benefit.

This pessimistic decision-making continued right through the day after the original stimulation, the researchers found.

“We feel we were seeing a proxy for anxiety, or depression, or some mix of the two,” says lead researcher Ann Graybiel. “These psychiatric problems are still so very difficult to treat for many individuals suffering from them.”

The caudate nucleus has previously been linked to emotional decision-making, and the scientists stimulated it with a small electrical current while the monkeys were offered a reward (juice) and an unpleasant experience (a puff of air to the face) at the same time.

In each run through the amount of juice and the strength of the air blast varied, and the animals could choose whether or not to accept the reward – essentially measuring their ability to weigh up the costs of an action against the benefits.

When the caudate nucleus was stimulated, this decision-making got skewed, so the macaques started rejecting juice/air ratios they would have previously accepted. The negative aspects apparently began to seem greater, while the the rewards became devalued.

“This state we’ve mimicked has an overestimation of cost relative to benefit,” says Graybiel. After a day or so, the effects gradually disappeared.

The researchers also found brainwave activity in the caudate nucleus, part of the basal ganglia, changed when decision-making patterns changed. This might give doctors a marker to indicate whether someone would be responsive to treatment targeting this part of the brain or not.

The next stage is to see whether the same effect can be noticed in human beings – scientists have previously linked abnormal brain activity in people with mood disorders to regions connected to the caudate nucleus, but there’s a lot more work to be done to confirm these neural connections.

Making progress isn’t easy because of the incredibly complexity of the brain, but the researchers think their results show the caudate nucleus could be disrupting dopamine activity in the brain, controlling mood and our sense of reward and pleasure.

“There must be many circuits involved,” says Gabriel. “But apparently we are so delicately balanced that just throwing the system off a little bit can rapidly change behaviour.”

The research has been published in Neuron.

Paul McCartney and John Lennon wrote songs for The Beatles under Lennon-McCartney, but a new statistical model can be used to tell who actually took the lead.

Lennon-McCartney is likely one of the most famous songwriting credits in music. John Lennon and Paul McCartney wrote lyrics and music for almost 200 songs and The Beatles have sold hundreds of millions of albums. The story goes that the two Beatles agreed as teenagers to the joint credit for all songs they wrote, no matter the divide in work.

Over the years, Lennon and McCartney have revealed who really wrote what, but some songs are still up for debate. The two even debate between themselves — their memories seem to differ when it comes to who wrote the music for 1965’s “In My Life.”

If the songwriters’ memories (perhaps tainted by the mind-altering era they were writing in) have failed, how can this mystery ever be solved? Well, we can get by with a little help from math.

Mathematics professor Jason Brown spent 10 years working with statistics to solve the magical mystery. Brown’s the findings were presented on Aug. 1 at the Joint Statistical Meeting in a presentation called “Assessing Authorship of Beatles Songs from Musical Content: Bayesian Classification Modeling from Bags-Of-Words Representations.”

Stanford University mathematician Keith Devlin breaks down how Brown figured it out. Read Devlin’s edited conversation with NPR’s Scott Simon below and listen at the audio link.

Scott Simon: I don’t understand “bags-of-words representations,” although, I’ve sometimes been called a bag of words by some.

Keith Devlin: We’ll get to that. First of all, just to say that this is really serious stuff in terms of what was done. The three co-authors of this paper — there was someone called Mark Glickman who was a statistician at Harvard. He’s also a classical pianist. Another person, another Harvard professor of engineering, called Ryan Song. And the third person was a Dalhousie University mathematician called Jason Brown. And you may recall back to 2008, you and I talked about him. He figured out how The Beatles created that striking opening chord in “Hard Day’s Night.” And when we did that piece, I actually said he was working on who wrote the music for “In My Life.” And 10 years later, here we are talking about the discovery. It took him a long time, but he’s now got it.

“Bags of words”? What are they?

It actually goes back to the 1950s. It’s used by the computer scientists who created spam filters. What you do is you take a piece of text, and you ignore the grammar, you ignore the word order, and you just regard it as a collection of words. And once you’ve done that, you can count the frequencies of the different words in the bag of words. To do it for music, you had to get little snippets, and the way they did that was the team analyzed, I think, about 70 songs from Lennon and McCartney, and they found there were 149 very distinct transitions between notes and chords that are present in almost all Beatles songs. And those transitions will be unique to one person or the other person.

So they’d be bags of notes and chords.

Bags of notes and chords, pairs of notes and chords. Those are the little items, and you just count them.

Part of the confusion is that Paul McCartney said he wrote the music. John Lennon said Paul McCartney wrote a section of music. So what did this trio of mathematicians detect?

Cutting to the chase, it turns out Lennon wrote the whole thing. When you do the math by counting the little bits that are unique to the people, the probability that McCartney wrote it was .018 — that’s essentially zero. In other words, this is pretty well definitive. Lennon wrote the music. And in situations like this, you’d better believe the math because it’s much more reliable than people’s recollections, especially given they collaborated writing it in the ’60s with an incredibly altered mental state due to all the stuff they were ingesting.

I know what you are saying.

I would go with mathematics.

Keith, alright, I ask you — what about the artistic process of collaboration? Isn’t it possible they were such close and accomplished collaborators that they inhaled a little bit of each other’s technique and Lennon could write like McCartney and McCartney like John Lennon?

For sure. And that’s why it’s hard for the human ear to tell the thing apart. It’s also hard for them to realize who did it and this is why actually the only reliable answer is the mathematics because no matter how much people collaborate, they’re still the same people, and they have their preferences without realizing it. Lennon would use certain kinds of things over and over again. So would McCartney. It was the collaboration. Those two things come together that works, but they were still separate little bits. The mathematics isolates those little bits that are unique to the two people.

Angela Saini

With Inferior, Angela Saini counters long-held beliefs that biology stands in the way of parity between the sexes. Now her message is set to reach thousands of schools.

When young men and women come up against sexist stereotypes masquerading as science, Angela Saini wants them to be armed with the facts. “I call my book ammunition,” she says of her 288-page prize-winning work Inferior: The True Power of Women and the Science that Shows It. “There are people out there who insist that somehow the inequalities we see in society are not just because of historic discrimination, but also because of biology – the idea that there are factors within us that will cause men or women to be better at some things than others.”

She wrote Inferior to demonstrate that “actually, science doesn’t support that point of view. I think it’s important we understand these scientific facts. We need that ammunition to counter the weird mistruths that are circulating within and outside science about sex difference”.

To female scientists fed up with being treated as though their brains are the odd exceptions among their sex, Inferior is more than just a book. It’s a battle cry – and right now, it is having a galvanising effect on its core fanbase. On 31 July a crowdfunding campaign to send a copy of Inferior to every mixed secondary school in England with more than 1,000 pupils was launched by Dr Jessica Wade, a British physicist who writes 270 Wikipedia pages a year to raise the profile of female scientists. Within two days the campaign had raised £2,000. Yesterday it reached its original £15,000 target and was powering its way towards £20,000 – a figure which would allow the book to be sent to every state school in the country.

“There’s nothing you want more than for people to be inspired by your work,” says Saini, 37, a multiple award-winning science journalist, who first became intrigued by sex difference research when she wrote about the menopause for the Observer. “What Jess is doing means such a lot to me. I hope if my book can empower her, it can empower other young women, and men, too.”

The key message she hopes her readers will take away is that nothing in science suggests equality is not possible. “We are not as different as the inequalities in our society makes us believe we are. Even now, there are people saying we shouldn’t be pushing for gender equality because we’re never going to see it for biological reasons.” For example, many people think there are large psychological differences in spatial awareness, mathematical reasoning or verbal skills between men and women. “Actually, those differences are tiny, a fraction of a standard deviation,” says Saini. “Psychologically, the differences between the sexes are not enough to account for the inequalities we see in our society today.”

Inferior is not a children’s book by any stretch of the imagination. It includes a firsthand account of female genital mutilation and deliberately examines a large number of academic studies in painstaking detail. But, like recent bestselling children’s books Goodnight Stories for Rebel Girls and Fantastically Great Women Who Changed the World, it could play a valuable role in breaking down gender stereotypes for the next generation of would-be scientists and mathematicians, and Saini is confident many teenagers will engage with it. “Girls and boys aged 13 or 14 upwards have really responded to the message, and the earlier we can get this message to them, the better.” She was the only girl in science and maths classes at school. “Even if it’s not overtly stated to you, just being in a minority – especially a minority of one – makes you think maybe there are some differences between the sexes.”

Researching and writing the book has totally changed how she feels about herself, destroying her own “subconscious stereotypes” about women. “It made me look at the world differently. That’s the power of science.”

In one of the most shocking chapters, Saini relays a letter written by Charles Darwin in which he argues that women are intellectually inferior to men. “He was looking at society. He saw women weren’t achieving as much and he treated us almost the way you would treat observations of lions or peacocks in the wild. He thought: this reflects the biological facts.”

Even at the time, contemporary female intellectuals pointed out that this theory ignored a lot of obvious historical and cultural factors, but Darwin failed to take on board their arguments. “It was quite lazy of him, which is surprising, because he wasn’t a lazy scientist. He was usually so painstaking and thorough.”

But she still admires him for everything he got right. “Even the best scientists can fall into this trap of looking at the world around them and thinking: things are the way they are because of nature.” After all, she points out, assuming 19th-century scientists could be biased but 21st-century scientists never are makes no sense. “That’s why, in the book, I look not just at the science, but at the scientists.”

These range from Kristen Hawkes, whose research suggesting postmenopausal women played a vital role in increasing the human lifespan has been met with dogged resistance from some male scientists, to Robert Trivers who, Saini shows, used evidence from a flawed 1948 experiment on fruit flies when he famously argued that men are more naturally promiscuous than women. “A lot of people – especially scientists – view science as perfectly objective and rational. But the questions researchers choose to ask, and the answers they come up with, are heavily affected by their prior assumptions.” At times, the book shows a staggering lack of respect from male scientists towards the work of their female contemporaries. “Science won’t improve unless we understand that we all have biases and those biases affect research,” says Saini.

Since it was published in 2017, her book has sold 20,000 copies, won Physics World Book of the Year and triggered a worldwide “STEMinist” book club movement among feminist scientists, technologists, engineers and mathematicians. Saini says she has even had positive feedback about it from James Damore, a Google software engineer who made headlines last year when he wrote an internal memo arguing biological differences were the reason behind the low number of women in tech. “We need scientific arguments to counter those politically motivated statements,” she says. “These arguments matter personally, in terms of how we think about ourselves, but also politically. We cannot afford to be complacent. There are movements around the world that are trying to take back the rights of women – rights our mothers and grandmothers fought so hard for. We can take anything for granted.”

Wade says the book gave her “all this power. You read it and you have evidence. You can debate it”. She set up the crowdfunding campaign because she suspected private girls’ schools would be buying it for their libraries, and wanted state school students to have the same access. “Reading this book when doing your GCSEs or A levels is the perfect time, because you’re making decisions that will impact your entire career. I want girls to recognise they can do anything.”

The actor Daniel Radcliffe, a childhood friend of Wade, is planning to release a video in support of the crowdfunding campaign this week. He describes Inferior as “a truly mind-blowing book”, which has made him completely reevaluate his understanding of the world.“As many people as possible should have access to this book, and I am certain Jessie – who has always been the smartest person I know – is going to make that happen,” he says.

Saini, a Londoner with Indian parentage, is working on her next book on the science of race. “Race science is more taboo, but the way prejudice plays out within the research illuminates similar issues as those of Inferior.”

Despite the sexism and racism she has documented in science, she feels positive about the future. “If we catch children early, we can achieve enormous change. I don’t think anyone is born with prejudices. I’m optimistic.” She points out that, historically, male scientists gained their power by excluding women from clubs, societies and institutes. “Now women are forming their own networks. And there’s no limit to what we can achieve.”

By Timothy Roberts

Being able to recall memories, whether short-term or long-term is something that we all need in life. It comes in handy when we are studying at school or when we are trying to remember where we left our keys. We also tend to use our memory at work and remembering somebody’s name is certainly a good thing.

Although many of us may consider ourselves to have a good memory, we are all going to forget things from time to time. When it happens, we might feel as if we are slipping but there may be more behind it than you realize.

Imagine this scenario; you go to the grocery store to pick up 3 items and suddenly, you forget why you were there. Even worse, you may walk from one room to another and forget why you got up in the first place!

If you often struggle with these types of problems, you will be happy to learn that there is probably nothing wrong with you. In fact, a study that was done by the Neuron Journal and it has some rather good news. It says that forgetting is part of the brain process that might actually make you smarter by the time the day is over.

Professors took part in a study at the University of Toronto and they discovered that the perfect memory actually doesn’t necessarily reflect your level of intelligence.

You might even be surprised to learn that when you forget details on occasion, it can make you smarter.

Most people would go by the general thought that remembering more means that you are smarter.

According to the study, however, when you forget a detail on occasion, it’s perfectly normal. It has to do with remembering the big picture compared to remembering little details. Remembering the big picture is better for the brain and for our safety.

Our brains are perhaps more of a computer than many of us think. The hippocampus, which is the part of the brain where memories are stored, tends to filter out the unnecessary details.

In other words, it helps us to “optimize intelligent decision making by holding onto what’s important and letting go of what’s not.”

Think about it this way; is it easier to remember somebody’s face or their name? Which is the most important?

In a social setting, it is typically better to remember both but if we were part of the animal kingdom, remembering somebody as being a threat would mean our very lives. Remembering their name would be inconsequential.

The brain doesn’t automatically decide what we should remember and what we shouldn’t. It holds new memories but it sometimes overwrites old memories.

When the brain becomes cluttered with memories, they tend to conflict with each other and that can make it difficult to make important decisions.

That is why the brain tends to hold on to those big picture memories but they are becoming less important with the advent of technology.

As an example, at one time, we would have learned how to spell words but now, we just use Google if we don’t know how to spell them. We also tend to look everything up online, from how to change a showerhead to how to cook meatloaf for dinner.

If you forget everything, you may want to consider having a checkup but if you forget things on occasion, it’s perfectly okay.

The moral of the story is, the next time you forget something, just think of it as your brain doing what it was designed to do.

Blue light’s rap sheet is growing ever longer. Researchers have connected the high-energy visible light, which emanates from both the sun and your cell phone (and just about every other digital device in our hands and on our bedside tables), to disruptions in the body’s circadian rhythms. And physicians have drawn attention to the relationship between our favorite devices and eye problems, ranging from everyday eye strain to glaucoma to macular degeneration.

Humans can see a thin spectrum of light, ranging from red to violet. Shorter wavelengths appear blue, while the longer ones appear red. What appears as white light, whether it’s from sunlight or screen time, actually includes almost every color in the spectrum. In a recent paper published in the journal Scientific Reports, researchers at the University of Toledo have begun to parse the process by which close or prolonged exposure to the 445 nanometer shortwave called “blue light” can trigger damage irreversible damage in eye cells. The results could have profound consequences for consumer technology.

“Photoreceptors are like the vehicle. Retinal is the gas,” says study author and chemistry professor Ajith Karunarathne. In the lab, when cells from the eye were exposed to blue light directly—in theory, mimicking what happens when we stare at our phone or computer screens—the high-intensity waves trigger a chemical reaction in the retinal molecules in the eye. The blue light causes the retinal to oxidize, creating “toxic chemical species,” according to Karunarathne. The retinal, energized by this particular band of light, kills the photoreceptor cells, which do not grow back once they are damaged. If retinal is the gas, Karunarathne says, then blue light is a dangerous spark.

Catastrophic damage to your vision is hardly guaranteed. But the experiment shows that blue light can kill photoreceptor cells. Murdering enough of them can lead to macular degeneration, an incurable disease that blurs or even eliminates vision.

Blue light occurs naturally in sunlight, which also contains other forms of visible light and ultraviolet and infrared rays. But, Karunarathne points out, we don’t spend that much time staring at the sun. As kids, most of us were taught it would fry our eyes. Digital devices, however, pose a bigger threat. The average American spends almost 11 hours a day in front of some type of screen, according to a 2016 Nielsen poll. Right now, reading this, you’re probably mainlining blue light.

When we stare straight at our screens—especially in the dark—we channel the light into a very small area inside our eyeball. “That can actually intensify the light emitted from the device many many fold,” Karunarathne says. “When you take a magnifying glass and hold it to the sun, you can see how intense the light at the focal point gets. You can burn something.”

Some user experience designers have been criticizing our reliance on blue light, including Amber Case, author of the book Calm Technology. On her Medium blog she documented the way blue light has become “the color of the future,” thanks in part to films like 1982’s Blade Runner. The environmentally-motivated switch from incandescent light bulbs to high-efficiency (and high-wattage) LED bulbs further pushed us into blue light’s path. But, Case writes, “[i]f pop culture has helped lead us into a blue-lit reality that’s hurting us so much, it can help lead us toward a new design aesthetic bathed in orange.”

The military, she notes, still uses red or orange light for many of its interfaces, including those in control rooms and cockpits. “They’re low-impact colors that are great for nighttime shifts,” she writes. They also eliminate blue light-induced “visual artifacts”—the sensation of being blinded by a bright screen in the dark—that often accompany blue light and can be hazardous in some scenarios.

Apple offers a “night shift” setting on its phones, which allow users to blot out the blue and filter their screens through a sunset hue. Aftermarket products designed to control the influx of blue light into our irises are also available, including desktop screen protectors. There are even blue light-filtering sunglasses marketed to specifically to gamers. But as the damage done by blue light becomes clearer—just as our vision is getting blurrier—consumers may demand bigger changes.

Going forward, Karunarathne plans to stay in data-collection mode. “This is a new trend of looking at our devices,” he says. “It will take some time to see if and how much damage these devices can cause over time. When this new generation gets older, the question is, by that time, is the damage done?” But now that he appears to have identified a biochemical pathway for blue light damage, he’s also looking for new interventions. “Who knows. One day we might be able to develop eye drops, that if you know you are going to be exposed to intense light, you could use some of those… to reduce damage.”