Leading neuroscientist Matthew Walker on why sleep deprivation is increasing our risk of cancer, heart attack and Alzheimers and what you can do about it
Matthew Walker has learned to dread the question What do you do? At parties, it signals the end of his evening; thereafter, his new acquaintance will inevitably cling to him like ivy. On an aeroplane, it usually means that while everyone else watches movies or reads a thriller, he will find himself running an hours-long salon for the benefit of passengers and crew alike. Ive begun to lie, he says. Seriously. I just tell people Im a dolphin trainer. Its better for everyone.
Walker is a sleep scientist. To be specific, he is the director of the Center for Human Sleep Science at the University of California, Berkeley, a research institute whose goal possibly unachievable is to understand everything about sleeps impact on us, from birth to death, in sickness and health. No wonder, then, that people long for his counsel. As the line between work and leisure grows ever more blurred, rare is the person who doesnt worry about their sleep. But even as we contemplate the shadows beneath our eyes, most of us dont know the half of it and perhaps this is the real reason he has stopped telling strangers how he makes his living. When Walker talks about sleep he cant, in all conscience, limit himself to whispering comforting nothings about camomile tea and warm baths. Its his conviction that we are in the midst of a catastrophic sleep-loss epidemic, the consequences of which are far graver than any of us could imagine. This situation, he believes, is only likely to change if government gets involved.
Walker has spent the last four and a half years writing Why We Sleep, a complex but urgent book that examines the effects of this epidemic close up, the idea being that once people know of the powerful links between sleep loss and, among other things, Alzheimers disease, cancer, diabetes, obesity and poor mental health, they will try harder to get the recommended eight hours a night (sleep deprivation, amazing as this may sound to Donald Trump types, constitutes anything less than seven hours). But, in the end, the individual can achieve only so much. Walker wants major institutions and law-makers to take up his ideas, too. No aspect of our biology is left unscathed by sleep deprivation, he says. It sinks down into every possible nook and cranny. And yet no one is doing anything about it. Things have to change: in the workplace and our communities, our homes and families. But when did you ever see an NHS poster urging sleep on people? When did a doctor prescribe, not sleeping pills, but sleep itself? It needs to be prioritised, even incentivised. Sleep loss costs the UK economy over 30bn a year in lost revenue, or 2% of GDP. I could double the NHS budget if only they would institute policies to mandate or powerfully encourage sleep.
Why, exactly, are we so sleep-deprived? What has happened over the course of the last 75 years? In 1942, less than 8% of the population was trying to survive on six hours or less sleep a night; in 2017, almost one in two people is. The reasons are seemingly obvious. First, we electrified the night, Walker says. Light is a profound degrader of our sleep. Second, there is the issue of work: not only the porous borders between when you start and finish, but longer commuter times, too. No one wants to give up time with their family or entertainment, so they give up sleep instead. And anxiety plays a part. Were a lonelier, more depressed society. Alcohol and caffeine are more widely available. All these are the enemies of sleep.
But Walker believes, too, that in the developed world sleep is strongly associated with weakness, even shame. We have stigmatised sleep with the label of laziness. We want to seem busy, and one way we express that is by proclaiming how little sleep were getting. Its a badge of honour. When I give lectures, people will wait behind until there is no one around and then tell me quietly: I seem to be one of those people who need eight or nine hours sleep. Its embarrassing to say it in public. They would rather wait 45 minutes for the confessional. Theyre convinced that theyre abnormal, and why wouldnt they be? We chastise people for sleeping what are, after all, only sufficient amounts. We think of them as slothful. No one would look at an infant baby asleep, and say What a lazy baby! We know sleeping is non-negotiable for a baby. But that notion is quickly abandoned [as we grow up]. Humans are the only species that deliberately deprive themselves of sleep for no apparent reason. In case youre wondering, the number of people who can survive on five hours of sleep or less without any impairment, expressed as a percent of the population and rounded to a whole number, is zero.
The world of sleep science is still relatively small. But it is growing exponentially, thanks both to demand (the multifarious and growing pressures caused by the epidemic) and to new technology (such as electrical and magnetic brain stimulators), which enables researchers to have what Walker describes as VIP access to the sleeping brain. Walker, who is 44 and was born in Liverpool, has been in the field for more than 20 years, having published his first research paper at the age of just 21. I would love to tell you that I was fascinated by conscious states from childhood, he says. But in truth, it was accidental. He started out studying for a medical degree in Nottingham. But having discovered that doctoring wasnt for him he was more enthralled by questions than by answers he switched to neuroscience, and after graduation, began a PhD in neurophysiology supported by the Medical Research Council. It was while working on this that he stumbled into the realm of sleep.
When you watch TV, you usually shut your brain off and just enjoy what’s in front of you. Watching television doesn’t require much thought or attention, and literally anyone can do it.
Luckily for the host of a show called Flip or Flop, one of the people watching was paying attention. A viewer noticed something odd about Tarek El Moussa’s neck, so she emailed the production company and told them that El Moussa needed to see a doctor immediately.
The lump on his neck was actually a malignant tumor. El Moussa has thyroid cancer.
Tarek had to undergo radioactive iodine therapy, which meant that he had to be isolated from his family for their protection. Thankfully, the cancer hasn’t spread any further, and he will find out in a week or so if he is cancer-free.
Extracted from foxgloves, digitalis was once used as a treatment for epilepsy. Could a side effect have triggered the artists yellow period?
It was recently the 127th anniversary of the tragic death of Vincent van Gogh. His short life came to an untimely end two days after he shot himself in the chest; he had experienced mental health issues through much of his life. In the absence of a definitive diagnosis, speculation as to the true nature of his illness fills volumes.
Although he came under the care of several doctors during his life time, knowledge of diseases of the mind was in its infancy in the late nineteenth century. As a result, many of the treatments used at the time would have been ineffective if not potentially dangerous. From our point of view, however, one drug that might have been given to Van Gogh is particularly interesting.
Towards the end of his life, under the care of Dr Gachet, it seems that Van Gogh may have been treated with digitalis for the epileptic fits he experienced. Digitalis, extracted from foxglove plants, is a powerful medicine still in use today as a treatment for certain heart conditions, but not epilepsy. In Van Goghs day, and for a long time before then, digitalis was known to be an effective treatment of dropsy, or accumulation of fluid in the body. Dropsy could have been caused by inefficient beating of the heart or because of liver disease. But with little understanding of the underlying causes of many diseases, almost anything shown to have an effect on the body even if that was simply to induce vomiting was considered a medical benefit. If the treatment for one disease was successful, it was often tried out on a host of others, just in case it proved to be a panacea. Extracts of foxglove really would have been effective in treating dropsy caused by heart failure, but would have done nothing for Van Goghs epilepsy. However, it is just possible it may have contributed to his artistic output.
Your internal chatter has a huge impact on the way you feel about yourself. Listen in, says Gary John Bishop
You stumble through the door into your morning coffee ritual. As you make your way through a maze of chairs, tables and outstretched legs you finally arrive at your space at the end of the queue, and the deliberation begins
Maybe Ill have something different this time, hmm, let me see Iced cranberry lemon tea? Nah, I need the jolt, Ill get my usual. Good, now what else What about one of those muffins? Nah, Im piling it on, theres about 6,000 calories in one of those Bagel? Ugh no, Ill stick to the coffee.
Your turn comes, the server asks: How can I help you? and you confidently declare: Vanilla latte with a shot of espresso please.
It all happens in seconds, this mass of deliberation, reasoning and decision making, and its never ending. While the coffee shop scenario might not be quite your thing, youll have your own version. This is how your mind works. Its how all of our minds work, going constantly back and forth, every moment of every day of our lives.
Sometimes its quiet, sometimes its loud, but its always there, that little voice in our head. We all know the one, the internal dialogue that filters life, categorises people and hears what it hears to give life that ever-so-familiar ring to it.
Studies show that we have more than 50,000 thoughts per day. While we have little or no say in those automatic and reactionary thoughts, we have a massive say in which of those thoughts we attach significance to.
Your emotional state, your moods, your ways of being and acting are in a dance with your internal dialogue. Your experience of yourself, of being you, is intricately woven into existence in the way that you speak to yourself and others. Its not only what you talk about but, more importantly, how you talk about it.
Most people believe that they have certain feelings first, followed by a thought to themselves about how they feel. Not quite. The language you use has a direct and powerful in-the-moment impact on your feelings. The German philosopher, Martin Heidegger, said: Language is the house of being, while his compatriot, Hans-Georg Gadamer, insisted: Without language nothing exists.
Look at your own life where you use terms like This is impossible, I cant, Im confused, This is too much or Im trying. Each of these (and a litany of others), gives rise to certain emotional states (anger, frustration, resentment, hopelessness, etc), all of which work against you in your endeavour. How does feeling hopeless help in that job search, or being frustrated help in healing your relationship, or feeling incompetent get you that promotion? It doesnt. It weighs you down and dampens your enthusiasm.
As a simple example, changing Its impossible to I havent worked it out yet has a remarkable impact on the way in which you deal with certain problems. Your emotional state shifts.
In very real terms, how you talk about what you are dealing with either works for or against you.
Next time youre feeling suppressed, frustrated or worn down, check yourself. Go over that internal chatter a few times and see if you can connect how youre describing it to yourself to how you feel. Ask yourself: Am I using the kind of language that is building something or destroying something? Is this in my favour or working against me?
Language really is that important. After all, you are what you speak.
Experts suggest patients should stop taking the drugs when they feel better rather than completing their prescription
Telling patients to stop taking antibiotics when they feel better may be preferable to instructing them to finish the course, according to a group of experts who argue that the rule long embedded in the minds of doctors and the public is wrong and should be overturned.
Patients have traditionally been told that they must complete courses of antibiotics, the theory being that taking too few tablets will allow the bacteria causing their disease to mutate and become resistant to the drug.
But Martin Llewelyn, a professor in infectious diseases at Brighton and Sussex medical school, and colleagues claim that this is not the case. In an analysis in the British Medical Journal, the experts say the idea that stopping antibiotic treatment early encourages antibiotic resistance is not supported by evidence, while taking antibiotics for longer than necessary increases the risk of resistance.
There are some diseases where the bug can become resistant if the drugs are not taken for long enough. The most obvious example is tuberculosis, they say. But most of the bacteria that cause people to become ill are found on everybodys hands in the community, causing no harm, such as E coli and Staphylococcus aureus. People fall ill only when the bug gets into the bloodstream or the gut. The longer such bacteria are exposed to antibiotics, the more likely it is that resistance will develop.
The experts say there has been too little research into the ideal length of a course of antibiotics, which also varies from one individual to the next, depending in part on what antibiotics they have taken in the past.
In hospital, patients can be tested to work out when to stop the drugs. Outside hospital, where repeated testing may not be feasible, patients might be best advised to stop treatment when they feel better, they say. That, they add, is in direct contravention of World Health Organisation advice.
Other experts in infectious diseases backed the group. I have always thought it to be illogical to say that stopping antibiotic treatment early promotes the emergence of drug-resistant organisms, said Peter Openshaw, president of the British Society for Immunology.
This brief but authoritative review supports the idea that antibiotics may be used more sparingly, pointing out that the evidence for a long duration of therapy is, at best, tenuous. Far from being irresponsible, shortening the duration of a course of antibiotics might make antibiotic resistance less likely.
Alison Holmes, a professor of infectious diseases at Imperial College London, said a great British authority, Prof Harold Lambert, had made the same point in a Lancet article entitled Dont keep taking the tablets as early as 1999. It remains astonishing that apart from some specific infections and conditions, we still do not know more about the optimum duration of courses or indeed doses in many conditions, yet this dogma has been pervasive and persistent.
Jodi Lindsay, a professor of microbial pathogenesis at St Georges, University of London, said it was sensible advice. The evidence for completing the course is poor, and the length of the course of antibiotics has been estimated based on a fear of under-treating rather than any studies, she said. The evidence for shorter courses of antibiotics being equal to longer courses, in terms of cure or outcome, is generally good, although more studies would help and there are a few exceptions when longer courses are better for example, TB.
But the Royal College of GPs expressed concerns. Recommended courses of antibiotics are not random, said its chair, Prof Helen Stokes-Lampard. They are tailored to individual conditions and in many cases, courses are quite short for urinary tract infections, for example, three days is often enough to cure the infection.
We are concerned about the concept of patients stopping taking their medication midway through a course once they feel better, because improvement in symptoms does not necessarily mean the infection has been completely eradicated. Its important that patients have clear messages and the mantra to always take the full course of antibiotics is well known. Changing this will simply confuse people.
The UKs chief medical officer, Prof Dame Sally Davies, said: The message to the public remains the same: people should always follow the advice of healthcare professionals. To update policies, we need further research to inform them.
[The National Institute for Health and Care Excellence] is currently developing guidance for managing common infections, which will look at all available evidence on appropriate prescribing of antibiotics.
The Department of Health will continue to review the evidence on prescribing and drug-resistant infections, as we aim to continue the great progress we have made at home and abroad on this issue.
From Alexander Fleming onwards, the lives of millions have been transformed and saved by treatments that scientists were not even looking for
When scientists in New Zealand discovered that a meningitis vaccine fortuitously protects against gonorrhoea, they were benefiting from an unpredictable force responsible for some of historys most striking medical breakthroughs: serendipity.
So many things have been discovered by chance. The German writer, scientist and all-round polymath Johann Wolfgang Goethe, a discoverer himself, wrote: Discovery needs luck, invention, intellect none can do without the other.
In pharmaceutical giant Pfizers laboratories in Kent, a failed treatment for angina accidentally became a billion-dollar erectile dysfunction blockbuster, and the worlds most famous blue pill.
During early clinical trials of sildenafil, now better known by its trade name Viagra, male volunteers taking the pills consistently reported unprovoked, long-lasting erections. After further investigation, it turned out that Viagra, designed to relax blood vessels around the heart to improve blood flow, was having the same effect on arteries within the penis. Since its commercial release in 1998, it has been used to improve the sex lives of millions of men worldwide.
Incidentally, the 2007 Ig Nobel Prize, awarded annually for that years most useless research, was awarded to three Argentinian scientists who discovered that Viagra helped hamsters recover faster from jet-lag.
Returning to work after a month-long Scottish vacation in 1928, pathologist Alexander Fleming made a discovery in a discarded culture dish, which he had unintentionally left open to the elements on a window sill in his laboratory at St Marys Hospital in London.
In Flemings absence, the dish, growing the dangerous bacteria staphylococcus aureus, had become contaminated with an air-borne mould a type of fungus. Fleming noticed that, near the blue-green strands of fungus, growth of the bacteria had been stopped in its tracks.
Fleming had inadvertently stumbled across the first antibiotic, which he called penicillin.
For his accidental discovery, he shared the Nobel prize for medicine in 1945 with Florey and Chain, Oxford chemists who perfected the process of penicillin mass production in time to treat infected battlefield injuries sustained in the second world war.
When I woke up just after dawn on 28 September, 1928, I certainly didnt plan to revolutionise all medicine by discovering the worlds first antibiotic, or bacteria killer, Fleming later recalled. But I suppose that was exactly what I did.
New York engineer Wilson Greatbatch invented the worlds first implantable heart pacemaker but he didnt mean to.
While trying to build a device to record heartbeats in 1956, he accidentally installed the wrong type of resistor into his prototype which promptly began to emit regular electrical pulses.
Realising these pulses were recapitulating the electrical activity of a normal heartbeat, Greatbatch immediately saw the potential of his device. After two years of refinements, his design for a pacemaker that could be implanted into the heart was patented in 1960 and soon went into production. Life-saving descendants of this first device now improve the lives of over half a million patients with slow heartbeats every year.
In the 1980s, two Australian doctors were ridiculed for suggesting that stomach ulcers were caused not by business lunches and stress, but by infection with a common bacteria. Barry Marshall, a gastroenterologist and his pathologist colleague in Perth, Robin Warren, noticed that stomach biopsies taken from their ulcer patients all contained the same spiral-shaped bacteria, called helicobacter pylori.
To prove their hunch, Marshall deliberately downed a pint of foaming helicobacter broth that hed grown in his lab after isolating it from the stomach of one of his patients. Within a week, he had rampant stomach inflammation which was then completely reversed by taking antibiotics.
Their discovery has also meant the virtual eradication of a type of stomach cancer caused by helicobacter infection.
For their work (and presumably Marshalls bravery), Marshall and Warren were awarded the 2005 Nobel prize for medicine.
Several classes of antidepressants owe their discovery to chance, from iproniazid, which was initially used to treat tuberculosis in the 1950s, to the tricyclics of the 1960s, which stemmed from an experimental treatment for schizophrenia and the more recent breakthrough involving the use of ketamine.
The entry-level benzodiazapine was developed in the 1950s by a Polish immigrant in the US, Leo Sternbach, from discarded chemical compounds he had synthesised 20 years earlier in Poland when he was working on experiments to create new dyes.
The dyes were a failure. The benzodiazapines quickly became the most popular prescription drugs in the US.
People who felt they had a strong purpose in life suffer from less insomnia and sleep disturbance, says neurologist
The secret to a good nights sleep later in life is having a good reason to get up in the morning, according to US researchers who surveyed people on their sleeping habits and sense of purpose.
People who felt they had a strong purpose in life suffered from less insomnia and sleep disturbances than others and claimed to rest better at night as a result, the study found.
Jason Ong, a neurologist who led the research at Northwestern University in Chicago, said that encouraging people to develop a sense of purpose could help them to keep insomnia at bay without the need for sleeping pills.
More than 800 people aged 60 to 100 took part in the study and answered questions on their sleep quality and motivations in life. To assess their sense of purpose, the participants were asked to rate statements such as: I feel good when I think of what Ive done in the past and what I hope to do in the future.
According to Ong, people who felt their lives had most meaning were less likely to have sleep apnea, a disorder that makes the breathing shallow or occasionally stop, or restless leg syndrome, a condition that compels people to move their legs and which is often worse at night. Those who reported the most purposeful lives had slightly better sleep quality overall, according to the study in the journal Sleep Science and Practice.
Insomnia and some other sleep disorders become more common in old age, but Ong said that the findings were likely to apply to the public more broadly. Helping people cultivate a purpose in life could be an effective drug-free strategy to improve sleep quality, particularly for a population that is facing more insomnia, he said.
Age UK, a charity, advises people who sleep badly to go to bed and rise at the same time every day; establish a bedtime routine; and cut out caffeine, alcohol and nicotine in the evening. Not eating a heavy meal late at night; avoiding exercise before bed; cutting out daytime naps and banning TVs and computers from the bedroom helps too, they add.
Research suggests people on proton pump inhibitors are more likely to die than those taking different antacid or none at all
Millions of people taking common heartburn and indigestion medications could be at an increased risk of death, research suggests.
The drugs, known as proton pump inhibitors (PPIs), neutralise the acid in the stomach and are widely prescribed, with low doses also available without prescription from pharmacies. In the UK, doctors issue more than 50m prescriptions for PPIs every year.
Now researchers say the drugs can increase risk of death, both compared with taking a different type of acid suppressant and not taking any at all.
We saw a small excess risk of dying that could be attributed to the PPI drug, and the risk increased the longer they took them, said Ziyad Al-Aly, an epidemiologist from the University of Washington and co-author of the study.
The team say the study suggests those who take the drugs without needing to could be most at risk. They urged people taking PPIs to check whether this was necessary.
Previous research has raised a range of concerns about PPIs, including links to kidney disease, pneumonia, more hip fractures and higher rates of infection with C difficile, a superbug that can cause life-threatening sepsis, particularly in elderly people in hospitals.
But the latest study is the first to show that PPIs can increase the chance of death. Published in the journal BMJ Open, it examined the medical records of 3.5 million middle-aged Americans covered by the US veterans healthcare system.
The researchers followed 350,000 participants for more than five years and compared those prescribed PPIs to a group receiving a different type of acid suppressant known as an H2 blocker. They also took into account factors such as the participants age, sex and conditions ranging from high blood pressure to HIV.
The results show that those who took PPIs could face a 25% higher risk of death than those who took the H2 blocker.
In patients on [H2 blocker] tablets, there were 3.3 deaths per 100 people over one year. In the PPI group, this figure was higher at 4.7 per 100 people per year, said Al-Aly.
The team also reported that the risk of death for those taking PPIs was 15% higher than those taking no PPIs, and 23% higher than for those taking no acid suppressants at all.
Similar levels of increased risk were seen among people who used PPIs but had no gastrointestinal conditions, a result which the authors speculated might be driving the higher risk seen overall.
Gareth Corbett, a gastroenterologist from Addenbrookes hospital in Cambridge who was not involved with the study, cautioned against panic, pointing out that in most cases the benefits of PPI far outweighed any risk. What was more, he said, while the increased risk sounded high, it was still very low for each person.
PPIs are very effective medicines, proven to save lives and reduce the need for surgery in patients with bleeding gastric and duodenal ulcers and several other conditions, he said.
The studys authors said it was important that PPIs were used only when necessary and stopped when no longer needed.
Corbett agreed that many people take PPIs unnecessarily. They could get rid of their heartburn by making lifestyle changes, such as losing weight and cutting back on alcohol, caffeine and spicy foods, he said.
The authors said the study was observational, meaning it did not show that PPIs were the cause of the increased risk of death, and that it was unclear how the drugs would act to affect mortality. They said the drugs could affect components within cells, known as lysosomes, that help break down waste material, or shortening protective regions at the end of chromosomes, known as telomeres.
Aly said people on PPIs should check with their GP whether the drugs were still needed, adding: In some cases we expect that PPIs can be safely stopped, particularly in patients who have been taking them for a long time.
Crispr inventor Jennifer Doudna talks about discovering the gene-editing tool, the split with her collaborator and the complex ethics of genetic manipulation
Jennifer Doudna, 53, is an American biochemist based at the University of California, Berkeley. Together with the French microbiologist Emmanuelle Charpentier, she led the discovery of the revolutionary gene-editing tool, Crispr. The technology has the potential to eradicate previously incurable diseases, but also poses ethical questions about the possible unintended consequences of overwriting the human genome.
Were you nerdy as a child? What got youhooked on science? Yes, I was nerdy. My father was a professor of American literature in Hawaii and he loved books. One day I came home from school and he haddropped a copy of The Double Helixon the bed, by Jim Watson. Onerainy afternoon I read it and Iwasjust stunned. I was blown awaythat you could do experiments about what a molecule looks like. I was probably 12 or 13. I think that wasthebeginning ofstarting to think,Wow, that could be an amazingthing to work on.
Youve spent most of your career uncovering the structure of RNA and never set out to create a tool to copy andpaste human genes. How did you endup working on Crispr? I think you can put scientists into two buckets. One is the type who dives very deeply into one topic for their whole career and they know it better than anybody else in the world. Then theresthe other bucket, where I wouldput myself, where its like youre at a buffet table and you see an interesting thing here and do it for a while, and that connects you to another interesting thing and you take a bit of that. Thats how I came to be working on Crispr it was a total side-project.
But when you first started your collaboration with Emmanuelle Charpentier, did you have a hunch youwere on to something special? We met at a conference in San Juan, Puerto Rico, and took a walk around the old town together. She was so passionate, her excitement was very infectious. I still remember walking down this street with her and she said: Well Im really glad you want to work with us on the mysterious [Cas9 the enzyme that snips DNA at the chosen location in the editing process]. It was this kind of electrifying moment. Even then I just had this gut feeling that this was something really interesting.
How important is personal chemistry inscience collaborations? Its essential. Working in a lab is analogous to being in a high-school play: youre rehearsing long hours, itscrowded, there are stressful things that come up. Its the same thing in science. Things never work as you think they will, experiments fail and so to have people around that really get along with each other is super important. Many collaborations dont work out, usually just because peoples interests arent aligned or people dont really like working together.
The real frenzy around your work started in 2012, when you showed that Crispr-Cas9 could be used to slice up DNA at any site [of the DNA molecule] you wanted. Did you realise this was abig deal gradually orimmediately? It wasnt a gradual realisation, it was one of those OMG moments where you look at each other and say holy moly. This was something we hadnt thought about before, but now we could see how it worked, we could see it would be such a fantastic way to do gene editing.
After you demonstrated Crispr could edit bacterial DNA, two rival labs (Harvard and the Broad Institute) got there first in human cells. How come they beat you to it? They were absolutely set up to do that kind of experiment. They had all the tools, the cells growing, everything was there. For us, they were hard experiments to do because its not thekind of science we do. What speaksto the ease of the system was that a lab like mine could even do it.
The Broad Institute won the latest round of an ongoing legal battle over patent rights they claim that it wasnt obvious that Crispr could be used to edit human cells too. Where do you stand? People have asked me over and over again: Did you know it was going to work? But until you do an experiment you dont know thats science. Ive been lambasted for this in the media, but I have to be true to who I am as a scientist. We certainly had a hypothesisand it certainly seemed likea very good guess that it would.
Theres the patent dispute and you and Emmanuelle Charpentier also ended up pursuing rival projects to commercialise the technology. Are you all still friends? If theres a sadness to me about all of this and a lot of its been wonderful and really exciting its that I wouldve loved to continue working with Emmanuelle, scientifically. For multiple reasons that wasnt desirable to her. Im not blaming her at all she had her reasons and I respect her a lot.
The media loves to drive wedges, but we are very cordial. I was just with her in Spain and she was telling me about the challenges [of building her new lab in Berlin]. I hope on her side, certainly on my side, we respect each others work and in the end were all init together.
In your book you describe a nightmare youhad involving Hitler wearing a pig mask, asking to learn more about your amazing technology. Do you still have anxiety dreams about where Crispr mightleave the human race? I had the Hitler dream and Ive had a couple of other very scary dreams, almost like nightmares, which is quite unusual for an adult. Not so much lately, but in the first couple of years after I published my work, the field was moving so fast. I had this incredible feeling that the science was getting out way ahead of any considerations about ethics, societal implications and whether we should be worrying about random people in various parts of the world using this for nefarious purposes.
In 2015, you called for a moratorium on the clinical use of gene editing. Where do you stand on using Crispr to edit embryos these days? It shouldnt be used clinically today, but in the future possibly. Thats a big change for me. At first, I just thought why would you ever do it? Then I started to hear from people with genetic diseases in their family this is now happening every day for me. Alot of them send me pictures of their children. There was one that Icant stop thinking about, just sent to me in the last 10 days or so. A mother who told me that her infant son was diagnosed with a neurodegenerative disease, caused by a sporadic rare mutation. She sent me a picture of thislittle boy. He was this adorable little baby, he was bald, in his little carrier and so cute. I have a son and myheart just broke.
What would you do as a mother? You see your child and hes beautiful, hes perfect and you know hes going to suffer from this horrible disease and theres nothing you can do about it. Its horrible. Getting exposed to that, getting to know some of these people, its not abstract any more, its very personal. And you think, if there were away to help these people, we should do it. It would be wrong not to.
What about the spectre of designerbabies? A lot of it will come down to whether the technology is safe and effective, are there alternatives that would be equally effective that we should consider, and what are the broader societal implications of allowing gene editing? Are people going to start saying I want a child thats 6ft 5in and has blue eyes and so on? Do we really want to go there? Would you do things that are not medically necessary but are just nice-to-haves, for some people?Its a hard question. There area lot of grey areas.
Are you worried about cuts to science funding, including to the National Institutes of Health (NIH) budget? I am very concerned. Science funding is not a political football but in fact a down payment on discovery, the seed money to fund a critical step toward ending Alzheimers or curing cancer.
Researchers currently working on projects aimed at improving numerous aspects of our agriculture, environment and health may be forced to abandon their work. The outcome is that people will not receive the medical treatments they need, our struggle to feed our exploding population will deepen, and our efforts to manage climate change will collapse.
Over the long term, the very role of fundamental science as a means to better our society may come into question. History and all evidence points to the fact that when we inspire and support our scientific community we advance our way of life and thrive.
Were you disturbed when Trump tweeted, If U.C. Berkeley does not allow free speech and practices violence on innocent people with a different point of view NO FEDERAL FUNDS? in response to a planned alt-right speaker being cancelled due to violent protests on campus? Yes. It was a confusing tweet since the university was clearly committed to ensuring that the event would proceed safely and first amendment rights were supported. Few expected the awful actions of a few to be met with a willingness from the highest office to deprive more than 38,000 students access to an education.
Youve spoken at Davos, shared the $3m2015 Breakthrough prize, been listedamong the 100 most influential people in the world by Time magazine. Areyou still motivated about heading intothe lab these days? Yesterday I was getting ready to go to a fancy dinner. I was in a cocktail gown and had my makeup on and my hair done, but I wanted to talk to a postdoc in my lab about an experiment he was doing, so I texted him saying can we Skype? It was 8am in California, I was over here [in the UK] in my full evening gown, talking abouttheexperiment.Thats how nerdy I am.
A Crack in Creation: The New Power to Control Evolution by Jennifer Doudna and Sam Sternberg is published by The Bodley Head (20). To order a copy for 17 go to bookshop.theguardian.com or call 0330 333 6846. Free UK p&p over 10, online orders only. Phone orders min p&p of 1.99