From AI to Russia, Heres How Estonias President Is Planning for the Future

At 48 years old, Kersti Kaljulaid is Estonia’s youngest president ever, and its first female president. A marathon runner with degrees in genetics and an MBA, she spent a career behind the scenes—mostly as a European government auditor—before being elected by Estonia’s legislature in 2016. Two years later, she’s continuing Estonia’s push for global digital security while deflecting military and cyber threats from Russia, which occupied Estonia for 50 years until its liberation in 1991.

Known for its digital government, tax, and medical systems, Estonia is planning for the future. The country’s “e-resident” program—which allows global citizens to obtain a government-issued ID card and set up remotely-operated businesses in Estonia—has attracted 35,000 people since 2014. Now the government is discussing a proposal to grant some rights to artificially intelligent systems. The law could make it easier to regulate decision-making by autonomous systems, robots, or driverless cars.

This week, Kaljulaid visited the White House along with the leaders of Latvia and Lithuania, to meet with President Donald Trump about issues including security along the Russian border. The visit coincided with the 100th anniversary of Baltic independence after World War I, and Trump took the opportunity to reaffirm the US's commitment to protecting the Baltic States in accordance with the NATO Treaty. After attending the US-Baltic Trade Summit and laying a wreath at Arlington National Cemetery on Wednesday, Kaljulaid sat down with WIRED’s Eric Niiler for an interview at the Estonian Embassy in Washington.

EN: With various efforts over the past decade, Estonia is moving from a traditional state to a digital society in many ways. Where does that effort stand now and what do you hope to see happen during your next few years in office?

KK: Digital society is born when your people refuse to use paper. And in our country we know that our people refuse to use paper. If you arrive at such a point in your development, you have to make your digital state always secure. You need several alternatives if something goes wrong. All the time you need to worry about security; it doesn’t differ much from your paper archives.

We have already a society which is digitally disrupted. We also see that it changes how people think about technology and work and what possibilities the internet can offer for new types of careers. For example, people don’t need enterprises to work; they can sell their skills online independently.

In our case, also the government is within in the digital sphere. We recognize that there is the need to think about tax systems if people work in five different companies in five different countries at the same time. This needs to be sorted out. We cannot sort it alone, we need to sort it globally.

Estonian citizens seem to trust their government when it comes to sharing digital information. Here in the US, we trust Facebook and Amazon to a point, but with the government, it’s quite the opposite. How have you done this?

The way we have created our trust is because our people are not anonymous on the internet. It has always been secure. If you try to transact with someone online, you would not do it with an email and pay with a credit card. What we do instead is create an encrypted channel and sign a contract that is time stamped. Estonians are much more used to internet banking rather than an online credit card. You can create trust, but you have to create tools and the legal space that supports the security for these tools. The state has to promise people to keep them safe on the internet. I find it astonishing that globally businesses are on the internet. Very few states have followed them.

What about external threats? What other sort of steps might be needed to prevent Russian aggression in places like Ukraine, or the kind of cyber-attacks and hacking that have occurred in the United States during the 2016 presidential election?

With conventional aggression, since we got the sanctions in place, Russia has not made any further advances in any other region. In cyber, we must not get narrowly concentrated on Russia only. Cyber attacks rain down on us from many places. You have to make your systems secure and safe and teach your people cyber hygiene. If you are able to attribute some attacks, it's good to be open about it as the United States has been. We need to have an understanding globally about how international rules apply in the internet sphere. Right now, that is massively missing.

What do you mean, global rules?

There’s lot of academic work on this, for example the Tallinn Manual 1 and 2. For example, we don’t attack each other’s sovereignty. Could attacking some vital electronic systems be considered an attack? What are the rights of the defender in that case? What are the rights where you fall under attack from a country you can identify, but not from the government? And if this government cannot go after the attacker because it is too weak—what are your rights then?

Speaking of rights, Estonia is looking to become perhaps the first nation to grant legal rights to artificial intelligence agents, such as fully autonomous robots or vehicles. How will it affect ordinary Estonians?

The discussion centers on whether we need to create a special legal entity for autonomous systems. If you regulate for AI, you also regulate for machine learning, self-acting and autonomous systems. We want our state to be proactive to offer services to people. You need to carefully think how to make this offer safe to our people and their private data. We want AI to be safely grown in Estonia.

Was this pushed by the advent of driverless cars?

No, it's pushed by the Estonian people's demand to get more proactive state services. For example, if a couple has a child, they are entitled to universal child support. In the Estonian people’s minds, it is unnecessary to apply for this. They say, “I had my baby, just pay me." For that, this is proactive. People demand efficiency from an automated system that is making decisions. We have to regulate. Once you go digital, you are constantly pushed by your people to provide better services.

You’ve just launched a new genetic testing program for 100,000 Estonian citizens adding to the 52,000 who have already been tested. How will this information be used to improve public health? And what kind of safeguards are there to prevent possible genetic discrimination by employers, for example?

This information belongs to those people whose genome has been analyzed. This information does not belong to the Estonian Genome Bank or the government, and it's not shared with other individuals. People’s genetic data is in an anonymous form. The aim of this program is so people will know their diabetes risk, or their heart attack risk. They can share this information with their family doctor, but they are not obliged to. They can keep it to themselves, but most people will probably share it with their doctor.

Are there any other big things on the horizon in Estonia that we should be looking for?

I wouldn’t tell you if I had. The genome bank and the digital society are the projects that have flied. I am sure there are others that have not. Our people are willing to work with the government on new technologies. Now it’s a habit; every Estonian looks at it as part of our national identity. We understand that this allows us to provide better services to our people than our money would allow.

Read more: https://www.wired.com/story/from-ai-to-russia-heres-how-estonias-president-is-planning-for-the-future/

Empty half the Earth of its humans. It’s the only way to save the planet | Kim Stanley Robinson

There are now twice as many people as 50 years ago. But, as EO Wilson has argued, they can all survive in cities

Discussing cities is like talking about the knots in a net: theyre crucial, but theyre only one part of the larger story of the net and what its supposed to do. It makes little sense to talk about knots in isolation when its the net that matters.

Cities are part of the system weve invented to keep people alive on Earth. People tend to like cities, and have been congregating in them ever since the invention of agriculture, 10,000 or so years ago. Thats why we call it civilisation. This origin story underlines how agriculture made cities possible, by providing enough food to feed a settled crowd on a regular basis. Cities cant work without farms, nor without watersheds that provide their water. So as central as cities are to modern civilisation, they are only one aspect of a system.

There are nearly eight billion humans alive on the planet now, and thats a big number: more than twice as many as were alive 50 years ago. Its an accidental experiment with enormous stakes, as it isnt clear that the Earths biosphere can supply that many peoples needs or absorb that many wastes and poisons on a renewable and sustainable basis over the long haul. Well only find out by trying it.

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Right now we are not succeeding an aerial view of houses in Florida. Photograph: Alamy

Right now we are not succeeding. The Global Footprint Network estimates that we use up our annual supply of renewable resources by August every year, after which we are cutting into non-renewable supplies in effect stealing from future generations. Eating the seed corn, they used to call it. At the same time were pumping carbon dioxide into the atmosphere at a rate that is changing the climate in dangerous ways and will certainly damage agriculture.

This situation cant endure for long years, perhaps, but not decades. The future is radically unknowable: it could hold anything from an age of peaceful prosperity to a horrific mass-extinction event. The sheer breadth of possibility is disorienting and even stunning. But one thing can be said for sure: what cant happen wont happen. Since the current situation is unsustainable, things are certain to change.

Cities emerge from the confusion of possibilities as beacons of hope. By definition they house a lot of people on small patches of land, which makes them hugely better than suburbia. In ecological terms, suburbs are disastrous, while cities can perhaps work.

The tendency of people to move to cities, either out of desire or perceived necessity, creates a great opportunity. If we managed urbanisation properly, we could nearly remove ourselves from a considerable percentage of the the planets surface. That would be good for many of the threatened species we share this planet with, which in turn would be good for us, because we are completely enmeshed in Earths web of life.

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A farmer at work near the village of Lok Ma Chau, outside Shenzhen, Hong Kong. Photograph: Jerome Favre/EPA

Here Im referring to the plan EO Wilson has named Half Earth. His book of the same title is provocative in all the best ways, and I think it has been under-discussed because the central idea seems so extreme. But since people are leaving the land anyway and streaming into cities, the Half Earth concept can help us to orient that process, and dodge the sixth great mass extinction event that we are now starting, and which will hammer humans too.

The idea is right there in the name: leave about half the Earths surface mostly free of humans, so wild plants and animals can live there unimpeded as they did for so long before humans arrived. Same with the oceans, by the way; about a third of our food comes from the sea, so the seas have to be healthy too.

At a time when there are far more people alive than ever before, this plan might sound strange, even impossible. But it isnt. With people already leaving countrysides all over the world to move to the cities, big regions are emptier of humans than they were a century ago, and getting emptier still. Many villages now have populations of under a thousand, and continue to shrink as most of the young people leave. If these places were redefined (and repriced) as becoming usefully empty, there would be caretaker work for some, gamekeeper work for others, and the rest could go to the cities and get into the main swing of things.

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The seas have to be healthy too vessels set sail after a four-month fishing ban on Chinas Yellow Sea and Bohai Sea. Photograph: Fang Yi/China News Service/VCG

So emptying half the Earth of its humans wouldnt have to be imposed: its happening anyway. It would be more a matter of managing how we made the move, and what kind of arrangement we left behind. One important factor here would be to avoid extremes and absolutes of definition and practice, and any sense of idealistic purity. We are mongrel creatures on a mongrel planet, and we have to be flexible to survive. So these emptied landscapes should not be called wilderness. Wilderness is a good idea in certain contexts, but these emptied lands would be working landscapes, commons perhaps, where pasturage and agriculture might still have a place. All those people in cities still need to eat, and food production requires land. Even if we start growing food in vats, the feedstocks for those vats will come from the land. These mostly depopulated landscapes would be given over to new kinds of agriculture and pasturage, kinds that include habitat corridors where our fellow creatures can get around without being stopped by fences or killed by trains.

This vision is one possible format for our survival on this planet. They will have to be green cities, sure. We will have to have decarbonised transport and energy production, white roofs, gardens in every empty lot, full-capture recycling, and all the rest of the technologies of sustainability we are already developing. That includes technologies we call law and justice the system software, so to speak. Yes, justice: robust womens rights stabilise families and population. Income adequacy and progressive taxation keep the poorest and richest from damaging the biosphere in the ways that extreme poverty or wealth do. Peace, justice, equality and the rule of law are all necessary survival strategies.

Homes
Homes in Palm Springs, where the average daily water usage per person is 201 gallons more than double the California average. Photograph: Lucy Nicholson/Reuters

Meanwhile, cities will always rely on landscapes much vaster than their own footprints. Agriculture will have to be made carbon neutral; indeed, it will be important to create some carbon-negative flows, drawing carbon out of the atmosphere and fixing it into the land, either permanently or temporarily; we cant afford to be too picky about that now, because we will be safest if we can get the CO2 level in the atmosphere back down to 350 parts per million. All these working landscapes should exist alongside that so-called empty land (though really its only almost empty empty of people most of the time). Those areas will be working for us in their own way, as part of the health-giving context of any sustainable civilisation. And all the land has to be surrounded by oceans that, similarly, are left partly unfished

All this can be done. All this needs to be done if we are to make it through the emergency centuries we face and create a civilised permaculture, something we can pass along to the future generations as a good home. There is no alternative way; there is no planet B. We have only this planet, and have to fit our species into the energy flows of its biosphere. Thats our project now. Thats the meaning of life, in case you were looking for a meaning.

This week, the Overstretched Cities series examines the impact of the rush to urbanisation, which has seen cities around the world explode in size. Follow Guardian Cities on Twitter, Facebook and Instagram to join the discussion, and explore our archive here

Read more: https://www.theguardian.com/cities/2018/mar/20/save-the-planet-half-earth-kim-stanley-robinson

To Stay Healthy On Your Next Flight, Avoid Aisles and Stay Put

If you want to avoid getting sick on a plane, the worst place to sit, according to Charles Gerba, is along the aisle. The issue is exposure—not just to other passengers, but anything they touch. That means obvious hot spots (arm rests, tray tables, in-flight magazines) and less-obvious ones like aisle seats, which people use to steady themselves as they move about the cabin, frequently on their way to and from a lavatory.

Oh right, lavatories. Don't get Gerba started on those. Overtrafficked and underserviced, many are swarming with E. coli. "Your typical flight will have one for every 50 people," he says. "Sometimes it's more like one per 75."

Gerba is an environmental microbiologist at the University of Arizona, where he studies how diseases spread through indoor spaces. Planes. Kitchens. Casinos. Cruise ships. He's an internationally renowned expert on fomites (i.e. objects and surfaces that are liable to carry infectious matter), a bottomless cesspit of stomach-turning stories (one of his go-tos involves someone projectile-vomiting into a spinning roulette wheel), and, this probably goes without saying, one of my favorite people to talk with about infectious diseases.

So when I caught wind of an impressive study about virus-transmission aboard airplanes in this week's Proceedings of the National Academy of Sciences, Gerba was the third person I called. Calls one and two were to the study's lead authors, Emory University biostatistician Vicki Hertzberg and Georgia Tech biomathematician Howard Weiss. However neither was allowed to give interviews without official approval from Boeing, the study's sponsor, which the researchers had yet to receive.

Which is a shame! Because, as I said, their study was impressive: To investigate how an infection might spread aboard an aircraft, Hertzberg and Weiss conducted observations of passenger behavior on actual flights. Which, well, nobody had ever done before. "It's one of the most sophisticated studies I've seen," Gerba told me. And their in-situ observations of passengers could improve our understanding of the role that air transportation plays in the spread of illnesses and epidemics.

That's because most of what we know about disease transmission aboard airplanes is based on indirect evidence. Gerba, for instance, studies planes by swabbing their surfaces for microbes. Computational models of disease-spread do exist, but most account only for the displacement of an infected person from one geographic location to another—not how that person might transmit their infection en route. The upshot: Many risks of disease transmission aboard airplanes remain largely unknown.

Consider, for example, the "two-row-rule," popular among public health agencies like the CDC and WHO, which states that an infected passenger poses the greatest risk of transmission to those sitting within two rows of them. That guideline is based on case studies which, despite being empirically based, tend not to account for how people move about an airplane. Oversights like these could explain why case reports of disease transmission aboard airplanes have also seen infections spread to passengers well outside the two-row vicinity of the primary infection.

Things like passenger movement are important to include in epidemiological models. The main transmission vehicle for viral infections like flu are the droplets of saliva and mucous that an infected person ejects, which are usually at least five micrometers in diameter. That’s pretty big, biologically speaking, which means they rarely make it more than a meter before landing on something. But people often move around during a flight, expanding their area of transmission beyond their assigned seat. At least in theory.

To test that theory, Hertzberg, Weiss, and a team of researchers took to the skies. Dividing into teams of two, they sat at five-row intervals throughout the economy cabins of single-aisle aircraft, where they proceeded to log detailed notes on the behavior of everyone aboard. On 10 transcontinental US flights, the researchers kept tabs on 1,540 passengers and 41 crew members, logging things like whether, how often, and for how long a person left her seat. How many visits she made to the bathroom. How long she waited to use the bathroom. How much time she spent in contact with other passengers. And so on.

Their observations are probably the most detailed account of in-flight behavior ever compiled, and are loaded with fascinating tidbits about the risks that people take aboard an airplane every time they leave their seats—and how where you sit hurts or helps your chances of becoming sick.

For instance: Thirty-eight percent of passengers didn't leave their seats during their flight, and 38 percent left once (the rest left more frequently). Perhaps unsurprisingly, the proportion of people who got up during the flight varied by seat assignment: People sitting in the aisle were most likely to move beyond their seating area, then middle seats, then windows. Aisle sitters also came into contact with other passengers more than five times as often as people in window seats.

I could go on. OK, I'll go on. Of the 1,296 passengers who had close contact with passengers outside their one-meter radius, the median duration of contact was 47 person-minutes (the average crew member spent a staggering 1,149 person-minutes in contact), presenting ample opportunity to spread germs throughout the plane.

All that behavioral data in hand, Hertzberg and Weiss used it to simulate two scenarios of in-flight transmission of an infectious, respiratory disease—the first involving a passenger seated in a midcabin aisle seat, the second involving an infectious crew member.

Their findings were surprising: Despite all the potential for contact with other passengers, their model indicated that a respiratory infection was unlikely to be directly transmitted more than one meter beyond a vector's assigned seat—probably because the average contact time between individuals was so low, averaging well under a minute. That meant transmission risk was effectively limited to passengers within just one row of the index passenger—even smaller than the area allotted by the two-row-rule. The infected person's 11 nearest neighbors faced a greater than 80 percent chance of infection. All the remaining passengers, however, had a lower than 3 percent risk.

On average, the researchers write, "this manifests as 0.7 additional infected passengers per flight." Because they spend so much more time in contact with passengers, the model predicts an infected crew member stands to infect an average of 4.6 passengers.

So why have past case studies reported transmissions well beyond two rows? A likely explanation is that some of these transmissions didn't occur in flight. "There are so many possible ways for travelers to move and interact, and the way they do so on a plane, in the air, is just one of them," says Embry Riddle aerospace engineer Sirish Namilae, an expert in the computational modeling of active particles. "Transmission could also occur while boarding, deplaning, while waiting at your departure gate, or while making your way through security."

Namilae says he's developing models to simulate transmission at each of these choke points, to see how different layouts and boarding strategies might affect disease spread. He adds that while Hertzberg and Weiss' study is impressive and valuable, it also highlights the limitations of observational work. "They struggle to account for the multitude of potential real life cases. You can sit aboard 10 flights, but with computation models you can simulate hundreds of thousands of scenarios across various environments."

Hertzberg and Weiss cop to their study's limitations, too. In their paper, they advise not to extrapolate their findings to double-aisle cabins, or to local or international flights, with different lengths that could lead to different passenger behaviors.

Asked why Boeing would keep Hertzberg and Weiss from talking about their findings until after their study was published, Gerba gives a shrug. “Aerospace companies often work with researchers to see what they can do to alleviate real and perceived risks of disease transmission aboard planes,” he says, but the fact that Boeing had restricted access to the researchers in this case was surprising—especially since their findings suggest the area of risk is smaller than current guidelines indicate.

As for how to avoid getting sick on your next flight, stick with Gerba's advice and avoid the center of the plane. The data backs him up: In Hertzberg and Weiss's simulations, passengers in window seats faced the smallest risk of infection, whether the carrier was a crewmember or a fellow passenger. "The aisle," as Gerba says, "is where they get ya."

More Plane Science

Read more: https://www.wired.com/story/to-stay-healthy-on-your-next-flight-avoid-aisles-and-stay-put/

WHO launches health review after microplastics found in 90% of bottled water

Researchers find levels of plastic fibres in popular bottled water brands could be twice as high as those found in tap water

The World Health Organisation (WHO) has announced a review into the potential risks of plastic in drinking water after a new analysis of some of the worlds most popular bottled water brands found that more than 90% contained tiny pieces of plastic. A previous study also found high levels of microplastics in tap water.

In the new study, analysis of 259 bottles from 19 locations in nine countries across 11 different brands found an average of 325 plastic particles for every litre of water being sold.

In one bottle of Nestl Pure Life, concentrations were as high as 10,000 plastic pieces per litre of water. Of the 259 bottles tested, only 17 were free of plastics, according to the study.

Scientists based at the State University of New York in Fredonia were commissioned by journalism project Orb Media to analyse the bottled water.

The scientists wrote they had found roughly twice as many plastic particles within bottled water compared with their previous study of tap water, reported by the Guardian.

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A colourful microfibre of plastic found in bottled water. Photograph: Abigail Barrows

According to the new study, the most common type of plastic fragment found was polypropylene the same type of plastic used to make bottle caps. The bottles analysed were bought in the US, China, Brazil, India, Indonesia, Mexico, Lebanon, Kenya and Thailand.

Scientists used Nile red dye to fluoresce particles in the water the dye tends to stick to the surface of plastics but not most natural materials.

The study has not been published in a journal and has not been through scientific peer review. Dr Andrew Mayes, a University of East Anglia scientist who developed the Nile red technique, told Orb Media he was satisfied that it has been applied carefully and appropriately, in a way that I would have done it in my lab.

The brands Orb Media said it had tested were: Aqua (Danone), Aquafina (PepsiCo), Bisleri (Bisleri International), Dasani (Coca-Cola), Epura (PepsiCo), Evian (Danone), Gerolsteiner (Gerolsteiner Brunnen), Minalba (Grupo Edson Queiroz), Nestle Pure Life (Nestle), San Pellegrino (Nestle) and Wahaha (Hangzhou Wahaha Group).

A World Health Organisation spokesman told the Guardian that although there was not yet any evidence on impacts on human health, it was aware it was an emerging area of concern. The spokesman said the WHO would review the very scarce available evidence with the objective of identifying evidence gaps, and establishing a research agenda to inform a more thorough risk assessment.

A second unrelated analysis, also just released, was commissioned by campaign group Story of Stuff and examined 19 consumer bottled water brands in the US.It also found plastic microfibres were widespread.

The brand Boxed Water contained an average of 58.6 plastic fibres per litre. Ozarka and Ice Mountain, both owned by Nestle, had concentrations at 15 and 11 pieces per litre, respectively. Fiji Water had 12 plastic fibres per litre.

Abigail Barrows, who carried out the research for Story of Stuff in her laboratory in Maine, said there were several possible routes for the plastics to be entering the bottles.

Plastic microfibres are easily airborne. Clearly thats occurring not just outside but inside factories. It could come in from fans or the clothing being worn, she said.

Stiv Wilson, campaign coordinator at Story of Stuff, said finding plastic contamination in bottled water was problematic because people are paying a premium for these products.

Jacqueline Savitz, of campaign group Oceana, said: We know plastics are building up in marine animals and this means we too are being exposed, some of us every day. Between the microplastics in water, the toxic chemicals in plastics and the end-of-life exposure to marine animals, its a triple whammy.

Nestle criticised the methodology of the Orb Media study, claiming in a statement to CBC that the technique using Nile red dye could generate false positives.

Coca-Cola told the BBC it had strict filtration methods, but acknowledged the ubiquity of plastics in the environment meant plastic fibres may be found at minute levels even in highly treated products.

A Gerolsteiner spokesperson said the company, too, could not rule out plastics getting into bottled water from airborne sources or from packing processes. The spokesperson said concentrations of plastics in water from their own analyses were lower than those allowed in pharmaceutical products.

Danone claimed the Orb Media study used a methodology that was unclear. The American Beverage Association said it stood by the safety of its bottled water, adding that the science around microplastics was only just emerging.

The Guardian contacted Nestle and Boxed Water for comment on the Story of Stuff study, but had not received a response at the time of publication.

Read more: https://www.theguardian.com/environment/2018/mar/15/microplastics-found-in-more-than-90-of-bottled-water-study-says

The CDC Can’t Fund Gun Research. What if that Changed?

America doesn't have good data on guns. Blame the Dickey amendment. First introduced in 1996, the legislation didn't ban gun investigations explicitly (it forbade the use of federal dollars in the advocacy or promotion of gun control), but Congress that year also cut the budget for the Centers for Disease Control and Prevention by the exact amount it had previously devoted to firearm research. It's had a chilling effect on the field ever since. (While some states and private foundations are conducting peer reviewed studies on gun violence, the federal government has been AWOL.) That means policymakers in Washington have little information about what causes gun violence, how it can be prevented or reduced, and who is most at risk.

But that could change. The February 14 killings in Parkland, Florida led a bipartisan group of lawmakers to consider repealing the Dickey amendment and resuming government-backed gun-research. Which raises a pressing question: If the CDC were to resume funding studies on the epidemiology of firearm violence, what questions would they want to answer right now?

"We don't know enough about the risk factors, for either the perpetrators or victims of gun violence," says Garen Wintemute, an ER physician and director of the UC Davis Violence Prevention Research Program.

Wintemute says that one of the big predictors of future gun violence is a history of other forms of violence, like domestic abuse. But connecting the dots between prior behavior and future threat is difficult—especially on an individual basis. That said, researchers think that by identifying early signals and studying them more closely, they could help police and social service agents make better decisions about when to intervene.

He also wants to study the psychological impact that high rates of gun violence can have on communities. Does living in place where gunfire or gun violence is common make someone more or less likely to use a gun in the future? Social scientists say they don't know the answer yet.

As for preventing the next mass shooting, experts say they don't know enough about the effectiveness of proposed interventions. Take, for instance, the "gun restraining order" laws recently enacted in California, Oregon and Washington. Such regulations allow family members as well as law enforcement to ask a judge to confiscate guns from people deemed to pose "a serious risk of harm." (In San Diego County, ten gun owners recently received court orders to surrender their weapons under the new law.) It sounds like a good idea in theory, but to expand such laws to other states, or the federal level, policymakers would need to make a case for their effectiveness. And at least for now, the data on whether the laws have a measurable impact on either suicides or murders just doesn't exist.

“There isn’t any information other than anecdotal,” says Shannon Frattaroli, associate professor of health policy at the Johns Hopkins University Center for Gun Policy and Research.

Frattaroli says a key factor, when it comes to studying the effectiveness of firearm policies, is being able to follow weapons. One way to track how violence spreads is by tracing implicated weapons to their source. In big cities plagued by gun violence, these weapons are often bought and sold illegally. "We need to understand where guns are coming from, how they get from the legal market to the hands of people who are prohibited to purchase them," Frattaroli says. "That’s important to know if we want to get a handle on the flow of guns."

Doing so will require a lot more money, time, and resources than researchers currently possess. That’s where the CDC might serve as both a deep-pocketed grant-making agency, as well as a clearinghouse for various databases on gun violence and gun ownership. A boost in funding would also attract more and better scientists to the field, whose numbers have dwindled since the Dickey amendment went into effect. “As I recruit new investigators, it has been a critical question for applicants: 'Will I have a job in a couple years, or will I have to look for a job in another field because there’s no funding,'" Wintemute says.

Social scientist and ER docs like Frattaroli and Wintemute are encouraged by the possibility that Congress might direct the CDC to renew gun research. President Trump’s Secretary of Health and Human Resources, Alex Azar, said the day after the Florida shootings that he backs such efforts. But this shift might take a while. The agency has been without a leader since January, when director Brenda Fitzgerald resigned after news reports that she purchased tobacco stocks after taking office. Any big change in the status quo of the amendment—and more money for gun violence research—will probably have to wait for a change in control of Congress.

Gun Shy

  • The United States has never funded a research center to study gun violence—so last year, California started one on its own.

  • If the CDC's commitment to gun violence research expands, it could be a surprise to these researchers, who raced to protect the little data they had from the Trump administration.

  • If it doesn't, though, researchers will continue to find novel ways to work around their utter lack of data, like this group that rifled through old gun magazines for information.

Read more: https://www.wired.com/story/what-if-the-cdc-could-fund-gun-research/

When WhatsApp’s Fake News Problem Threatens Public Health

In remote areas of Brazil’s Amazon basin, yellow fever used to be a rare, if regular visitor. Every six to ten years, during the hot season, mosquitoes would pick it up from infected monkeys and spread it to a few loggers, hunters, and farmers at the forests’ edges in the northwestern part of the country. But in 2016, perhaps driven by climate change or deforestation or both, the deadly virus broke its pattern.

Yellow fever began expanding south, even through the winter months, infecting more than 1,500 people and killing nearly 500. The mosquito-borne virus attacks the liver, causing its signature jaundice and internal hemorrhaging (the Mayans called it xekik, or “blood vomit”). Today, that pestilence is racing toward Rio de Janeiro and Sao Paulo at the rate of more than a mile a day, turning Brazil’s coastal megacities into mega-ticking-timebombs. The only thing spreading faster is misinformation about the dangers of a yellow fever vaccine—the very thing that could halt the virus’s advance. And nowhere is it happening faster than on WhatsApp.

In recent weeks, rumors of fatal vaccine reactions, mercury preservatives, and government conspiracies have surfaced with alarming speed on the Facebook-owned encrypted messaging service, which is used by 120 million of Brazil’s roughly 200 million residents. The platform has long incubated and proliferated fake news, in Brazil in particular. With its modest data requirements, WhatsApp is especially popular among middle and lower income individuals there, many of whom rely on it as their primary news consumption platform. But as the country’s health authorities scramble to contain the worst outbreak in decades, WhatsApp’s misinformation trade threatens to go from destabilizing to deadly.

On January 25, Brazilian health officials launched a mass campaign to vaccinate 95 percent of residents in the 69 municipalities directly in the disease’s path—a total of 23 million people. A yellow fever vaccine has been mandatory since 2002 for any Brazilian born in regions where the virus is endemic. But in the last two years the disease has pushed beyond its normal range into territories where fewer than a quarter of people are immune, including the urban areas of Rio and Sao Paulo.

By the time of the announcement, the fake news cycle was already underway. Earlier in the month an audio message from a woman claiming to be a doctor at a well-known research institute began circulating on WhatsApp, warning that the vaccine is dangerous. (The institute denied that the recording came from any of its employees). A few weeks later it was a story linking the death of a university student to the vaccine. (That too proved to be a false report). In February, Igor Sacramento’s mother-in-law messaged him a pair of videos suggesting that the yellow fever vaccine was actually a scam aimed at reducing the world population. A health communication researcher at Fiocruz, one of Brazil’s largest scientific institutions, Sacramento recognized a scam when he saw one. And no, it wasn’t a global illuminati plot to kill off his countrymen. But he could understand why people would be taken in by it.

“These videos are very sophisticated, with good editing, testimonials from experts, and personal experiences,” Sacramento says. It's the same journalistic format people see on TV, so it bears the shape of truth. And when people share these videos or news stories within their social networks as personal messages, it changes the calculus of trust. “We are transitioning from a society that experienced truth based on facts to a society based on its experience of truth in intimacy, in emotion, in closeness."

People are more likely to believe rumours from family and friends. There’s no algorithm mediating the experience. And when that misinformation comes in the form of forwarded texts and videos—which look the same as personal messages in WhatsApp—they’re lent another layer of legitimacy. Then you get the network compounding effect; if you’re in multiple group chats that all receive the fake news, the repetition makes them more believable still.

Of course, these are all just theories. Because of WhatsApp’s end-to-end encryption and the closed nature of its networks, it’s nearly impossible to study how misinformation moves through it. For users in countries with a history of state-sponsored violence, like Brazil, that secrecy is a feature. But it’s a bug for anyone trying to study them. “I think WhatsApp hoaxes and disinformation campaigns are a bit more pernicious [than Facebook] because their diffusion cannot be monitored,” says Pablo Ortellado, a fake news researcher and professor of public policy at the University of Sao Paulo. Misinformation on WhatsApp can only be identified when it jumps to other social media sites or bleeds into the real world.

In Brazil, it’s starting to do both. One of the videos Sacramento received from his mother-in-law is still up on YouTube, where it’s been viewed over a million times. Other stories circulated on WhatsApp are now being shared in Facebook groups with thousands of users, mostly worried mothers exchanging stories and fears. And in the streets of Rio and Sao Paulo, some people are staying away from the health workers in white coats. As of February 27, only 5.5 million people had received the shot, though it’s difficult to say how much of the slow start is due to fake news as opposed to logistical delays. A spokeswoman for the Brazilian Ministry of Health said in an email that the agency has seen an uptick in concern from residents regarding post-vaccination adverse events since the start of the year and acknowledged that the spread of false news through social media can interfere with vaccination coverage, but did not comment on its specific impact on this latest campaign.

A spokesperson for WhatsApp pointed out the public health benefits of making communications cheaper and more reliable for millions of people, while recognizing that some of them have unfortunately found ways to abuse the platform. "We encourage people to think twice before forwarding suspicious messages," the spokesperson wrote in an email. "People can always report problematic content to WhatsApp so we can be aware and help take action.”1

While the Ministry of Health has engaged in a very active pro-vaccine education operation—publishing weekly newsletters, posting on social media, and getting people on the ground at churches, temples, trade unions, and clinics—health communication researchers like Sacramento say health officials made one glaring mistake. They didn’t pay close enough attention to language.

You see, on top of all this, there’s a global yellow fever vaccine shortage going on at the moment. The vaccine is available at a limited number of clinics in the US, but it’s only used here as a travel shot. So far this year, the Centers for Disease Control and Prevention has registered no cases of the virus within US borders, though in light of the outbreak it did issue a Level 2 travel notice in January, urging all Americans traveling to the affected states in Brazil to get vaccinated first.

Because it’s endemic in the country, Brazil makes its own vaccine, and is currently ramping up production from 5 million to 10 million doses per month by June. But in the interim, authorities are administering smaller doses of what they have on hand, known as a “fractional dose.” It’s a well-demonstrated emergency maneuver, which staved off a yellow fever outbreak in the Democratic Republic of the Congo in 2016. According to the WHO, it’s “the best way to stretch vaccine supplies and protect against as many people as possible.” But a partial dose, one that’s guaranteed for only 12 months, has been met by mistrust in Brazil, where a single vaccination had always been good for a lifetime of protection.

“The population in general understood the wording of ‘fractionated’ to mean weak,” says Sacramento. Although technically correct, the word took on a more sinister meaning as it spread through social media circles. Some videos even claimed the fractionated vaccine could cause renal failure. And while they may be unscientific, they’re not completely wrong.

Like any medicine, the yellow fever vaccine can cause side effects. Between 2 and 4 percent of people experience mild headaches, low-grade fevers, or pain at the site of injection. But there have also been rare reports of life-threatening allergic reactions and damage to the nervous system and other internal organs. According to the Health Ministry, six people died in 2017 on account of an adverse reaction to the vaccine. The agency estimates that one in 76,000 will have an anaphylactic reaction, one in 125,000 will experience a severe nervous system reaction, and one in 250,000 will suffer a life-threatening illness with organ failure. Which means that if 5 million people get vaccinated, you’ll wind up with about 20 organ failures, 50 nervous system issues, and 70 allergic shocks. Of course, if yellow fever infected 5 million people, 333,000 people could die.

Not every fake news story is 100 percent false. But they are out of proportion with reality. That’s the thing about social media. It can amplify real but statistically unlikely things just as much as it spreads totally made up stuff. What you wind up with is a murky mix of information that has just enough truth to be credible.

And that makes it a whole lot harder to fight. You can’t just start by shouting it all down. Sacramento says too often health officials opt to frame these rumors as a dichotomy: “Is this true or is this a myth?” That alienates people from the science. Instead, the institution where he works has begun to produce social media-specific videos that start a dialogue about the importance of vaccines, while remaining open to people’s fears. “Brazil is a country full of social inequalities and contradictions,” he says. “The only way to understand what is happening is to talk to people who are different from you.” Unfortunately, that’s the one thing WhatsApp is designed not to let you do.

1 Update 03/10/18 7:29pm EST This story has been updated to include comment from WhatsApp.

Viral Falsehoods

Read more: https://www.wired.com/story/when-whatsapps-fake-news-problem-threatens-public-health/

E-cig vapor tested positive for arsenic, lead, and other toxic metals

E-cigarette vapor has tested positive for lead and arsenic.
Image: Getty Images/EyeEm

Bad news, vapers. Your e-cigs might not be the healthier alternative to cigarettes you think they are.

A new study has found that vaping may be exposing e-cigarette users to harmful toxins and carcinogens, like lead, chromium, and even arsenic.

The study, published Wednesday in the scientific journal Environmental Health Perspectives by researchers from Johns Hopkins University’s Bloomberg School of Public Health, sampled 56 vape devices. They gathered these e-cigs from actual vapers who they recruited for the study at smoke shops and vape conventions. Prior studies have only looked at newly purchased e-cigs, and the authors of this study wanted to test devices that people actually use for a more representative sample, since they often contain modifications and wear-and-tear.

The study’s authors tested three elements of the e-cigs: the liquid itself, the liquid inside of the vape pen’s chamber, and the aerosol (or vapor). They were specifically interested in whether the metal coil that vape pens use to heat the liquid in order to turn it into vapor was leeching or generating toxic metals. 

And it turns out, their hypothesis was right. There was not a significant amount of toxic metals in the e-cig liquid itself. But in over half of the e-cigs, the liquid inside the dispenser and the aerosol contained significant levels of chromium, nickel, and lead. According to the study’s authors, chromium and nickel have been linked to respiratory disease and lung cancer. And lead can cause neurotoxicity and cardiovascular disease — there is also no safe amount of lead exposure.

“It’s important for the FDA, the e-cigarette companies and vapers themselves to know that these heating coils, as currently made, seem to be leaking toxic metals—which then get into the aerosols that vapers inhale,” study senior author Ana María Rule, PhD, MHS, an assistant scientist in the Bloomberg School’s Department of Environmental Health and Engineering, said in a statement.

Troublingly, the authors also found arsenic in over 10 percent of the sampled e-cigs. Unlike the metals, arsenic was present in the liquid, liquid in the dispenser, and aerosol alike. While the study’s authors hypothesize that the metals appear in the e-cig vapor thanks to the metal coils, they do not know how arsenic apparently finds it way into the e-cig refill liquid itself.

I asked some acquaintances who vape what they thought of these findings. These vapers, who preferred not to be named, used to be daily smokers. But they almost entirely vape now; vaping, they have said, is what allowed them to quit cigarettes. 

“I’m not really surprised to be honest,” one vaper said. “I never expected them to be good for me.”

“My question is why is arsenic a necessary ingredient,” said another. “I would love to understand why these toxins are remotely necessary.”

Cigarettes, of course, also contain toxins including lead and arsenic — with the hugely unhealthy bonus of inhaling burnt tobacco, which itself is damaging to the lungs. And several studies have shown that vaping is far healthier than smoking. One showed that vapers have far fewer toxic substances in their bodies than smokers; another suggested that the cancer risk of vaping is one percent of smoking’s cancer risk. However, a study that claimed vaping was 95 percent healthier than smoking was widely criticized. And study author Dr. Ana María Rule sees a comparable risk in terms of metal exposure between e-cigs and cigarettes.

“We found the emission rates were similar between cigarettes and e-cigarettes for elements like chromium, nickel, zinc, lead and silver (all toxic to the lung),” Dr. Rule told Mashble over email. “We found lower concentrations in e-cigarettes for cadmium and arsenic.”

Plus, comparing e-cigs to cigarettes is complicated. Dr. Rule said cigarette risk is easier to quantify, because they can measure risk by cigarette. With e-cigs, risk is studied by a designated amount of puffs, which may or may not represent an accurate unit for any given user. 

Furthermore, comparing vaping to cigarettes was not the study’s authors’ primary aim. 

“We know there are many young vapers that have never smoked,” Dr. Rule said. “A better comparison for them is to breathing ambient air, so for them this represents an increase in risk.”

The study’s authors hope that their findings will prompt the FDA to regulate e-cigs for the presence of these toxic chemicals, as evidence mounts that vaping is not a risk-free endeavor.

“Our results add to the existing evidence that e-cigarettes are a relevant source of exposure to a wide variety of toxic metals,” the study’s authors write. “Due to potential toxicity resulting from chronic exposure to metals in e-cigarette aerosols, additional research is needed to more precisely quantify metal exposures resulting from e-cigarette use and their implications for human health, and to support regulatory standards to protect public health.”

Read more: https://mashable.com/2018/02/23/e-cigarettes-toxic-metals-lead-arsenic/

Inside the Mind of Amanda Feilding, Countess of Psychedelic Science

Amanda Feilding, Countess of Wemyss and March, also known as Lady Neidpath, sits cross-legged on a bench on a tiny island at the center of an artificial pond in her English country estate, a 15-minute drive outside of Oxford. At her feet is a tiny pure-white cloud of a dog, which traipses around chewing on the grass, only occasionally coughing it up.

Feilding is 75 years old. She wears a black skirt and knee-high boots and grips a tan shawl around her shoulders, on account of this being a gray November morning. From her ears hang jewelry that looks like green rock candy. Her light brown hair is frizzy but not altogether unkempt.

In the distance, peeking over a towering hedge, is her castle, built in the 1520s. “In the ’60s we called it Brainblood Hall,” she says in a posh accent that periodically turns sing-songy and high, à la Julia Child. “We always saw it as the masthead from where this change would happen.”

Feilding now lives in the castle in the English countryside where she was raised.

Ren Rox for WIRED

This change being the de-villainization of lysergic acid diethylamide, more commonly known as LSD. Feilding believes LSD has tremendous potential to treat maladies like anxiety and depression and addiction. The theory goes that the drug can manipulate blood flow in the brain to “reset” what you might consider to be the ego, allowing patients to reconceptualize their issues. Hence Brainblood Hall.

If LSD is having its renaissance, Feilding is its Michelangelo. She works 15 hours a day, seven days a week, to coordinate—and contribute to—research on one of the most highly controlled substances on Earth. And not with any old dumpy university she can find—we’re talking big names, like Imperial College London. Study by study, each following rigorous research standards, Feilding is building a case for making LSD a standard weapon in the clinical fight against mental illness. It's a path, though, that's fraught with scientific pitfalls—researchers are just beginning to understand how the human brain works, much less the mechanisms behind psychedelics.

The fact that psychedelics ended up as pariah drugs “is an example, in a way, of man's madness,” she says, toying with the edges of her shawl. “There are these incredible compounds that synergize amazingly well with the human body and can be used to have incredibly positive results. And what do we do? We criminalize it.”

To change that, she won’t just have to upend decades of draconian drug policies. She’ll have to convince a public that has, for a half-century, been told that LSD is a great evil, a drug that makes people put flowers in their hair and jump out of windows. And Feilding will have to use science to convince policymakers that her hunch is right, that LSD and other psychedelics can be a force for good.

Which would be hard for anyone to pull off, but Feilding faces the extra hurdle of not being a classically trained scientist. “Immediately if you say you left school at 16 and self-educated thereafter, people don’t believe you can do anything,” she says. “It's a funny thing.”

Typical 12th-Century Stuff

Feilding is a descendant of the Hapsburg family, a dynasty that rose to great power in the 12th century. I ask her how—typical 12th-century stuff? “Typical 12th-century stuff,” she laughs. “Duffing over someone”—a Britishism for giving a beating—“and, funny enough, someone did a family tree and the number of people, I keep meaning to underline them and put a little red star on the ones who had their heads cut off. There was really quite a lot of people having their heads cut off.”

Feilding’s branch of the Hapsburg family tree wasn’t so much the let’s-rule-the-world-and-make-lots-of-money kind of royalty. More of a stick-it-to-the-man vibe. “One was going to be executed around the Gunpowder Plot, and then his wife went to visit him and they swapped clothes,” she says. “He got out the day before his execution. I mean, they were all rather nice antiestablishment personalities.”

But they were not particularly doers, Feilding adds. And, generally speaking, to maintain a dynasty you have to at least care about cash flow. “If you spend 500 years kind of reading and doing interesting things and not making money, it tends to run out,” she says.

Accordingly, Feilding grew up in a manor her parents couldn’t afford to heat. Her father liked painting during the day, which meant he needed to do farming and chores around the castle at night. “Cutting all those wretched hedges, he had to do himself,” she says. “And he was diabetic and he’d always do them just before meal time and pass out. He was always passing out.”

Feilding adored her father and scrambled everywhere after him. “He never went by what an authority said. He always went with his own thoughts,” she says. “In a way he was quite a big guru to me. He was my main intellectual influence.”

It was a loving yet isolated family that lived in difficult postwar times. Few visitors made the trek over bumpy roads to the edge of a marshland to appreciate the castle’s wall-to-wall artworks and exquisite furniture and precariously low door frames—at least by modern standards of human height. So Feilding immersed herself in reading and, as always, chasing after her father. She had mystical experiences, like imagining she was flying down the castle’s spiral staircase. But with no hot water or heating in the mansion, winters were brutal. “I suppose we were vaguely called impoverished aristocracy,” she says.

Feilding grew up in a manor her parents couldn’t afford to heat.

Ren Rox for WIRED

At 16, Feilding was studying in a convent and wanted to pursue her interest in mysticism. The nuns declined her request and instead gave her books on art. She wouldn’t stand for this. So with her parents’ blessing, Feilding dropped out of high school and set off abroad to find her godfather, Bertie Moore, whom she had never met. She figured he could teach her about mysticism: He had been a spy catcher during the war, but at this point was a Buddhist monk living in Sri Lanka.

Feilding headed toward Sri Lanka and ended up in Syria. Stuck at the border without a passport, a group of drunk, big-deal Bedouins came to her rescue. “We got into this Cadillac and all the people were completely drunk,” she says. “They asked me if I could drive it”—indeed she could—“and we drove out into the desert and then we went to encampments and they all brought out their cushions and feasts.”

Feilding—photographed in 1970 with her pet pigeon, Birdie—began experimenting with LSD in the mid-1960s.

Amanda Feilding, Countess of Wemyss

She never made it to Sri Lanka to find Bertie, and after half a year abroad Feilding returned to the UK to study mysticism with Robert Charles Zaehner, the famous scholar, at All Souls College in Oxford. Before long she made her way to the swinging London of the Beatles, the Kinks, the mods, and the miniskirt. In 1965, Allen Ginsberg and Lawrence Ferlinghetti crashed on the floor of her flat after the Wholly Communion poetry happening at Royal Albert Hall.

Later that year, someone spiked the 22-year-old Feilding’s coffee with a massive dose of LSD. It nearly broke her. She retreated to the castle in the country to recuperate but returned to London a month later at the insistence of a friend.

This is when Feilding met the man who would shape her thinking on LSD and consciousness and mental health: the Dutch natural scientist Bart Huges. The two fell in love and began experimenting with LSD, leading them to think about it in a fundamentally different way. The counterculture at the time had embraced the drug as a way to expand consciousness. All well and good. But Feilding and Huges wanted to go deeper, to explore the use of LSD as a kind of medicine for the brain. Even after the spiked coffee incident, Feilding grew fascinated with the physiological underpinnings of the drug, as well as its potential.

“I thought that LSD had the power to change the world,” she says. “That was our work, understanding the ego and the deficiencies of humans and how one might heal and treat them with altered states of consciousness.” And not just with LSD, mind you, but also yoga and fasting, anything that would (in theory) manipulate blood flow in the brain. Including the ancient practice of drilling a hole in your skull.

Blood Oath

By the time Feilding discovered LSD, it had been around for decades—the Swiss chemist Albert Hofmann synthesized the drug in 1938. It wasn’t until five years later, though, that he would accidentally dose himself—he reckoned he absorbed the drug through his skin—and discover its profound effects on the mind. “In a dreamlike state,” he wrote to a colleague at the time, “with eyes closed (I found the daylight to be unpleasantly glaring), I perceived an uninterrupted stream of fantastic pictures, extraordinary shapes with intense, kaleidoscopic play of colors.”

Hofmann wrote in his autobiography that he recognized both the drug’s dangers and its potential in psychiatry—very, very well-supervised psychiatry. But because LSD produced “unfathomably uncanny, profound effects, so unlike the character of a recreational drug,” he never fathomed that it would turn into the phenomenon that it did. “The more its use as an inebriant was disseminated, bringing an upsurge in the number of untoward incidents caused by careless, medically unsupervised use,” he wrote, “the more LSD became a problem child for me.”

It also became a problem for the United States government. Even though early studies on LSD in the 1940s and ’50s hinted at its therapeutic potential—and, indeed, psychiatrists were already treating patients with it—the feds branded it a schedule 1 drug, the most tightly controlled category, and the world followed in its prohibition.

“LSD getting out put the research back 50 years,” Feilding says. “I think there was misuse of it, and there were accidents, but, my goodness me, there weren’t many.”

The drug’s dark ages, though, are now giving way to a new era of psychedelics research, thanks in large part to the efforts of the Beckley Foundation, a think tank that Feilding runs here in the Oxford countryside, as well as California’s Multidisciplinary Association for Psychedelic Studies, or MAPS. Both groups are not only pursuing the scientific research of psychedelics, but political action as well. That is, they advocate the worldwide relaxation of what they see as an unnecessarily restrictive grip on the use of potentially therapeutic drugs.

Potentially. The problem with a psychedelic like LSD is you can show what it does to people—namely, it makes them trip, sometimes very hard—but science knows little about how these drugs produce those effects. One recent study found that an LSD trip can last a good long while because when the drug binds to serotonin receptors, a lid closes over it, trapping the molecules. All well and good, but the bigger picture is still a mystery: What does LSD do to the brain to induce something users call ego dissolution, a sort of breaking down of the self?

Feilding advocates the worldwide relaxation of what she sees as an unnecessarily restrictive grip on the use of potentially therapeutic drugs.

Ren Rox for WIRED

Feilding believes the secret is the blood flow in what’s known as the default mode network, an interconnected group of structures in the brain. The thinking is that the DMN is what governs the ego, or the sense of self. “That’s where psychedelics come in and shake it up,” Feilding says, “reducing the blood supply to the default mode network,” thus releasing the ego’s grip on the brain.

In 2016 Feilding coauthored a paper with scientists at Imperial College London showing the first images of the brain on LSD. And indeed, it seems the drug dampens communication between the components of the DMN, in turn dampening the ego to produce that feeling of “oneness with the universe” that LSD is so famous for. Or so the theory goes.

But Feilding’s coauthor differs with her on the mechanism responsible for the effect. “I think blood flow is a little bit of a sideshow,” says Robin Carhart-Harris, a neuropsychopharmacologist at the Imperial College. “The brain doesn't fundamentally work through flowing blood. That’s part of it, but we know that the function is electrical, and so why don’t we measure the electrical signals?”

Which is not to say blood flow isn’t a piece of the puzzle. In that study, the measurement of blood flow worked as a complement to measurement of electrical signals, the bit that Carhart-Harris is really after. “In our forthcoming studies we've decided to drop the blood flow because of this concern that I have that it can take you off the scent,” Carhart-Harris says. “I think it’s a primitive view of how the brain works.”

But Feilding remains convinced that blood flow is the key to psychedelics. (Not that the electrical signals aren’t important. “I love neural patterns,” she says.) Recall that she works out of what in the ’60s she called Brainblood Hall. And blood is what drove her to undergo a bizarre and controversial procedure called a trepanation, in which you drill a hole in your skull to theoretically increase cerebral circulation. It’s an ancient practice that’s popped up across world cultures, usually for the treatment of headaches or head trauma. This, as you can imagine, is not backed by science.

Most people, though, wouldn’t perform the procedure on themselves. But in 1970, Feilding sat in front of a camera and drilled into the top of her forehead. “I share the film now,” she narrates in the film of the process, “in the hope that it may attract the attention of some doctor able and willing to start the essential research into the subject, without which it will not become an accepted practice, available in the national health to anyone who wants it.” (Feilding implores people to never perform their own trepanation.)

Five decades later, that research has yet to emerge, and trepanation is both unproven and dangerous, very much not a recommended practice among medical professionals. “I don't think it's a mad, scary thing,” Feilding says. “I think it's very likely to have a physiological base, which I'm going to research.”

Why now and not decades ago? “Trepanation is more taboo even than LSD, so I'm going from the base to the top of the taboo ranking,” she says with a laugh.

Three decades after her self-trenapation, a brain surgeon in Mexico performed another trepanation on Feilding. She admits the supposed effects it produces are subtle—a boost in energy, for example. “It could obviously be placebo,” she says. “How does one know? Placebo is so strong. But I noticed things like my dreams became less anxious.”

The decor of Feilding’s cavernous mansion includes a human skull drilled through with six holes.

Ren Rox for WIRED

Really, trepanation is her sidequest, another way to approach the manipulation of blood flow in the brain. LSD is Feilding’s calling. LSD unleashed—not in the acid-in-every-liquor-store kind of way but, rather, as part of a new era of psychedelic therapy.

Bad Brains

This is the future of therapy as Feilding sees it: You enter a clinic with your mind in a certain unwanted setting. Perhaps you’re ruminating over some kind of trauma. You meet with a therapist and do a relatively large dose of LSD, followed by smaller doses down the line, known as microdosing. (This has come into vogue of late, especially among Silicon Valley types who believe a minute dose of LSD makes them more creative without all the pesky hallucinations.)

“You need the peak experience to break through and change the setting,” Feilding says. “And then the microdose experience can give a little booster along the way and make it more energetic and vital and a bit more lively.”

Which sounds like something the authorities wouldn’t be so keen on. But medical officials in the UK and the US and elsewhere have actually been giving permission to study psychedelics of late. Still, the red tape is a nightmare, as are the costs. “There are three institutions in England which have a safe that can store psychoactive controlled substances,” Feilding says. “And then you’re meant to weigh them every week and have two people guarding the door. It's insane. But I think it's breaking down a little bit, and the more good results we can bring in, the better.”

In the States, too, research on psychedelics is humming along. The MAPS organization, for instance, is entering phase three of clinical trials—tests on humans comparing the drug to a placebo—using MDMA to treat PTSD.

What’s happening is the authorities in the US and UK seem to be coming around to the potential of psychedelics, probably because it’s too politically stupid not to. If MDMA does turn out to help treat PTSD, and indeed MAPS’ research so far suggests it does, opposing its use in therapy would be tantamount to opposing the mental well-being of veterans and active duty troops. (The thinking goes that MDMA lowers the fear response, allowing patients to reconceptualize their traumatizing memories under the supervision of a therapist.)

Again, doing this research is still a tremendous pain, but at least scientists can do it. “Before I was limited by not being able to get ethical approvals,” Feilding says. “But now theoretically it’s possible—with great trouble and vastly extra costs. I mean, they are more carefully controlled than nuclear weapons. It is mad.”

The Countess of Psychedelics

In the cavernous living room of Feilding’s mansion—near the giant fireplace, on top of a beautiful cabinet, next to a still-more-beautiful cabinet of tiny drawers atop the main cabinet—is a human skull drilled through with six holes. It’s the remains of an ancient human who for whatever reason went through multiple trepanations.

Feilding sits on a couch in front of the fireplace. An assistant comes in and asks if she wants hummus, and indeed she does, so the assistant returns with hummus. Feilding’s cook periodically pops in with updates on the imminence of dinner.

In the early days of Beckley, Feilding’s husband, the historian and earl Jamie Wemyss, who belongs to a wealthy Scottish family, helped pay the Beckley Foundation's bills until Feilding got better at fund-raising. But all the while Feilding has worried about money for the foundation. Governments aren’t exactly lining up to fund research into psychedelics. Neither are pharmaceutical companies. So she relies on private donors, but that’s never enough for the scope of what Feilding wants to do—studies, studies, more studies, to convince the scientific community and the public that there’s promise in psychedelics. “I can put up 10, 20, 30 thousand, but I can't put up hundreds of thousands,” she says.

Feilding has 50 years of experience using psychedelics. But she also thinks like a classically trained scientist.

Ren Rox for WIRED

Feilding occupies a strange niche as both a fund-raiser with specific policy goals and doer of science. She’s a co-author on all these papers that study psychedelics like psilocybin (the active ingredient in magic mushrooms) and LSD, but she sticks out. She's not a trained scientist. She doesn't have an undergraduate degree, much less a PhD. It’s not that she doesn’t belong, but she’s just not like everyone else.

And yet: People have this conception of science as being 100 percent objective and sober. It’s not. Any scientist, whether studying psychedelics or global warming, comes to the table with opinions and preconceived notions. Does Feilding have a more pronounced political agenda than most? She sure does—that’s what sets her apart from other researchers in the field, who’d rather focus all their attention on mechanisms of action and the like.

Feilding has 50 years of experience using psychedelics. But she also thinks like any of the classically trained scientists she authors papers with. “The real focus is not who is doing the study,” says Doblin of MAPS, “but how the study is being designed, and how sincere are the efforts to follow the gold standard scientific methodology.”

And Feilding’s studies are great, he adds. “They're the epitome of neuroscience research these days.”

Feilding comes from a long line of people who didn’t give a damn about societal norms. She sits next to the fireplace in a home her father tended at night, driving a tractor around in the darkness. Her ancestors plotted against the government. And now Feilding plots to upend not only the way humanity views psychedelics but how humanity treats mental disorders.

“We’re depriving millions of people of a better life by not making use cleverly of what has been known throughout history,” she says. “These are tools to heal, to treat, to get to another level.”

Maybe, though, the powers that be are willing to at least reconsider psychedelics. Maybe the hippies were on to something, and acid can change the world, but they just went about it all wrong. And maybe the breakthrough will one day come from a 16th-century mansion in the Oxford countryside, where the Countess of Wemyss and March toils.

Read more: https://www.wired.com/story/inside-the-mind-of-amanda-feilding-countess-of-psychedelic-science/

A Familys Race to Cure a Daughters Genetic Disease

One July afternoon last summer, Matt Wilsey distributed small plastic tubes to 60 people gathered in a Palo Alto, California, hotel. Most of them had traveled thousands of miles to be here; now, each popped the top off a barcoded tube, spat in about half a teaspoon of saliva, and closed the tube. Some massaged their cheeks to produce enough spit to fill the tubes. Others couldn’t spit, so a technician rolled individual cotton swabs along the insides of their cheeks, harvesting their skin cells—and the valuable DNA inside.

One of the donors was Asger Vigeholm, a Danish business developer who had traveled from Copenhagen to be here, in a nondescript lobby at the Palo Alto Hilton. Wilsey is not a doctor, and Vigeholm is not his patient. But they are united in a unique medical pursuit.

Wilsey’s daughter, Grace, was one of the first children ever diagnosed with NGLY1 deficiency. It’s a genetic illness defined by a huge range of physical and mental disabilities: muscle weakness, liver problems, speech deficiencies, seizures. In 2016, Vigeholm’s son, Bertram, became the first child known to die from complications of the disease. Early one morning, as Bertram, age four, slept nestled between his parents, a respiratory infection claimed his life, leaving Vigeholm and his wife, Henriette, to mourn with their first son, Viktor. He, too, has NGLY1 deficiency.

Grace and her mother, Kristen Wilsey.

BLAKE FARRINGTON

The night before the spit party, Vigeholm and Wilsey had gathered with members of 16 other families, eating pizza and drinking beer on the hotel patio as they got to know each other. All of them were related to one of the fewer than 50 children living in the world with NGLY1 deficiency. And all of them had been invited by the Wilseys—Matt and his wife Kristen, who in 2014 launched the Grace Science Foundation to study the disease.

These families had met through an online support group, but this was the first time they had all come together in real life. Over the next few days in California, every family member would contribute his or her DNA and other biological samples to scientists researching the disease. On Friday and Saturday, 15 of these scientists described their contributions to the foundation; some studied the NGLY1 gene in tiny worms or flies, while others were copying NGLY1 deficient patients’ cells to examine how they behaved in the lab. Nobody knows what makes a single genetic mutation morph into all the symptoms Grace experiences. But the families and scientists were there to find out—and maybe even find a treatment for the disease.

That search has been elusive. When scientists sequenced the first human genome in 2000, geneticist Francis Collins, a leader of the Human Genome Project that accomplished the feat, declared that it would lead to a “complete transformation in therapeutic medicine” by 2020. But the human genome turned out to be far more complex than scientists had anticipated. Most disorders, it’s now clear, are caused by a complicated mix of genetic faults and environmental factors.

And even when a disease is caused by a defect in just one gene, like NGLY1 deficiency, fixing that defect is anything but simple. Scientists have tried for 30 years to perfect gene therapy, a method for replacing defective copies of genes with corrected ones. The first attempts used modified viruses to insert corrected genes into patients’ genomes. The idea appeared elegant on paper, but the first US gene therapy to treat an inherited disease—for blindness—was approved just last year. Now scientists are testing methods such as Crispr, which offers a far more precise way to edit DNA, to replace flawed genes with error-free ones.

Certainly, the genetics revolution has made single-mutation diseases easier to identify; there are roughly 7,000, with dozens of new ones discovered each year. But if it’s hard to find a treatment for common genetic diseases, it’s all but impossible for the very rare ones. There’s no incentive for established companies to study them; the potential market is so small that a cure will never be profitable.

Which is where the Wilseys—and the rest of the NGLY1 families—come in. Like a growing number of groups affected by rare genetic diseases, they’re leapfrogging pharmaceutical companies’ incentive structures, funding and organizing their own research in search of a cure. And they’re trying many of the same approaches that Silicon Valley entrepreneurs have used for decades.

At 10:30 on a recent Monday morning, Grace is in Spanish class. The delicate 8-year-old with wavy brown hair twisted back into a ponytail sits in her activity chair—a maneuverable kid-sized wheelchair. Her teacher passes out rectangular pieces of paper, instructing the students to make name tags.

Grace grabs her paper and chews it. Her aide gently takes the paper from Grace’s mouth and puts it on Grace’s desk. The aide produces a plastic baggie of giant-sized crayons shaped like cylindrical blocks; they’re easier for Grace to hold than the standard Crayolas that her public school classmates are using.

Grace’s NGLY1 deficiency keeps her from speaking.

BLAKE FARRINGTON

At her school, a therapist helps her communicate.

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The other kids have written their names and are now decorating their name tags.

“Are we allowed to draw zombies for the decorations?” one boy asks, as Grace mouths her crayons through the baggie.

Grace’s aide selects a blue crayon, puts it in Grace’s hand, and closes her hand over Grace’s. She guides Grace’s hand, drawing letters on the paper: “G-R-A-C-E.”

Grace lives with profound mental and physical disabilities. After she was born in 2009, her bewildering list of symptoms—weak muscles, difficulty eating, failure to thrive, liver damage, dry eyes, poor sleep—confounded every doctor she encountered. Grace didn’t toddle until she was three and still needs help using the toilet. She doesn’t speak and, like an infant, still grabs anything within arm’s reach and chews on it.

Her father wants to help her. The grandson of a prominent San Francisco philanthropist and a successful technology executive, Matt Wilsey graduated from Stanford, where he became friends with a fellow undergraduate who would one day be Grace’s godmother: Chelsea Clinton. Wilsey went on to work in the Clinton White House, on George W. Bush’s presidential campaign, and in the Pentagon.

But it was his return to Silicon Valley that really prepared Wilsey for the challenge of his life. He worked in business development for startups, where he built small companies into multimillion-dollar firms. He negotiated a key deal between online retailer Zazzle and Disney, and later cofounded the online payments company Cardspring, where he brokered a pivotal deal with First Data, the largest payment processor in the world. He was chief revenue officer at Cardspring when four-year-old Grace was diagnosed as one of the first patients with NGLY1 deficiency in 2013—and when he learned there was no cure.

At the time, scientists knew that the NGLY1 gene makes a protein called N-glycanase. But they had no idea how mistakes in the NGLY1 gene caused the bewildering array of symptoms seen in Grace and other kids with NGLY1 deficiency.

Wilsey’s experience solving technology problems spurred him to ask scientists, doctors, venture capitalists, and other families what he could do to help Grace. Most advised him to start a foundation—a place to collect money for research that might lead to a cure for NGLY1 deficiency.

As many as 30 percent of families who turn to genetic sequencing receive a diagnosis. But most rare diseases are new to science and medicine, and therefore largely untreatable. More than 250 small foundations are trying to fill this gap by sponsoring rare disease research. They’re funding scientists to make animals with the same genetic defects as their children so they can test potential cures. They’re getting patients’ genomes sequenced and sharing the results with hackers, crowdsourcing analysis of their data from global geeks. They’re making bespoke cancer treatments and starting for-profit businesses to work on finding cures for the diseases that affect them.

“Start a foundation for NGLY1 research, get it up and running, and then move on with your life,” a friend told Wilsey.

Wilsey heeded part of that advice but turned the rest of it on its head.

In 2014, Wilsey left Cardspring just before it was acquired by Twitter and started the Grace Science Foundation to fund research into NGLY1 deficiency. The foundation has committed $7 million to research since then, most of it raised from the Wilseys’ personal network.

Many other families with sick loved ones have started foundations, and some have succeeded. In 1991, for instance, a Texas boy named Ryan Dant was diagnosed with a fatal muscle-wasting disease called mucopolysaccharidosis type 1. His parents raised money to support an academic researcher who was working on a cure for MPS1; a company agreed to develop the drug, which became the first approved treatment for the disease in 2003.

But unlike Dant, Grace had a completely new disease. Nobody was researching it. So Wilsey began cold-calling dozens of scientists, hoping to convince them to take a look at NGLY1 deficiency; if they agreed to meet, Wilsey read up on how their research might help his daughter. Eventually he recruited more than 100 leading scientists, including Nobel Prize-winning biologist Shinya Yamanaka and Carolyn Bertozzi, to figure out what was so important about N-glycanase. He knew that science was unpredictable and so distributed Grace Science’s funding through about 30 grants worth an average of $135,000 apiece.

Two years later, one line of his massively parallel attack paid off.

Matt Wilsey, Grace’s father.

BLAKE FARRINGTON

Bertozzi, a world-leading chemist, studies enzymes that add and remove sugars from other proteins, fine-tuning their activity. N-glycanase does just that, ripping sugars off from other proteins. Our cells are not packed with the white, sweet stuff that you add to your coffee. But the tiny building blocks of molecules similar to table sugar can also attach themselves to proteins inside cells, acting like labels that tell the cell what to do with these proteins.

Scientists thought that N-glycanase’s main role was to help recycle defective proteins, but many other enzymes are also involved in this process. Nobody understood why the loss of N-glycanase had such drastic impacts on NGLY1 kids.

In 2016, Bertozzi had an idea. She thought N-glycanase might be more than just a bit player in the cell’s waste management system, so she decided to check whether it interacts with another protein that turns on the proteasomethe recycling machine within each of our cells.

This protein is nicknamed Nerf, after its abbreviation, Nrf1. But fresh-made Nerf comes with a sugar attached to its end, and as long as that sugar sticks, Nerf doesn’t work. Some other protein has to chop the sugar off to turn on Nerf and activate the cellular recycling service.

Think of Nerf’s sugar like the pin in a grenade: You have to remove the pin—or in this case, the sugar—to explode the grenade and break down faulty proteins.

But nobody knew what protein was pulling the pin out of Nerf. Bertozzi wondered if N-glycanase might be doing that job.

To find out, she first tested cells from mice and humans with and without working copies of the NGLY1 gene. The cells without NGLY1 weren’t able to remove Nerf’s sugar, but those with the enzyme did so easily. If Bertozzi added N-glycanase enzymes to cells without NGLY1, the cells began chopping off Nerf’s sugar just as they were supposed to: solid evidence, she thought, that N-glycanase and Nerf work together. N-glycanase pulls the pin (the sugar) out of the grenade (the Nerf protein) to trigger the explosion (boom).

The finding opened new doors for NGLY1 disease research. It gave scientists the first real clue about how NGLY1 deficiency affects patients’ bodies: by profoundly disabling their ability to degrade cellular junk via the proteasome.

As it turns out, the proteasome is also involved in a whole host of other diseases, such as cancer and brain disorders, that are far more common than NGLY1 deficiency. Wilsey immediately grasped the business implications: He had taken a moon shot, but he’d discovered something that could get him to Mars. Pharmaceutical companies had declined to work on NGLY1 deficiency because they couldn’t make money from a drug for such a rare disease. But Bertozzi had now linked NGLY1 deficiency to cancer and maladies such as Parkinson’s disease, through the proteasome—and cancer drugs are among the most profitable medicines.

Suddenly, Wilsey realized that he could invent a new business model for rare diseases. Work on rare diseases, he could argue, could also enable therapies for more common—and therefore profitable—conditions.

In early 2017, Wilsey put together a slide deck—the same kind he’d used to convince investors to fund his tech startups. Only this time, he wanted to start a biotechnology company focused on curing diseases linked to NGLY1. Others had done this before, such as John Crowley, who started a small biotechnology company that developed the first treatment for Pompe disease, which two of his children have. But few have been able to link their rare diseases to broader medical interests in the way that Wilsey hoped to.

He decided to build a company that makes treatments for both rare and common diseases involving NGLY1. Curing NGLY1 disease would be to this company as search is to Google—the big problem it was trying to solve, its reason for existence. Treating cancer would be like Google’s targeted advertising—the revenue stream that would help the company get there.

But his idea had its skeptics, Wilsey’s friends among them.

One, a biotechnology investor named Kush Parmar, told Wilsey about some major obstacles to developing a treatment for NGLY1 deficiency. Wilsey was thinking of using approaches such as gene therapy to deliver corrected NGLY1 genes into kids, or enzyme replacement therapy, to infuse kids with the N-glycanase enzyme they couldn’t make on their own.

But NGLY1 deficiency seems particularly damaging to cells in the brain and central nervous system, Parmar pointed out—places that are notoriously inaccessible to drugs. It’s hard to cure a disease if you can’t deliver the treatment to the right place.

Other friends warned Wilsey that most biotech startups fail. And even if his did succeed as a company, it might not achieve the goals that he wanted it to. Ken Drazan, president of the cancer diagnostics company Grail, is on the board of directors of Wilsey’s foundation. Drazan warned Wilsey that his company might be pulled away from NGLY1 deficiency. “If you take people’s capital, then you have to be open to wherever that product development takes you,” Drazan said.

But Wilsey did have some things going for him. Biotechnology companies have become interested of late in studying rare diseases—ones like the type of blindness for which the gene therapy was approved last year. If these treatments represent true cures, they can command a very high price.

Still, the newly approved gene therapy for blindness may be used in 6,000 people, 100 times more than could be helped by an NGLY1 deficiency cure. Wilsey asked dozens of biotechnology and pharmaceutical companies if they would work on NGLY1 deficiency. Only one, Takeda, Japan’s largest drug company, agreed to conduct substantial early-stage research on the illness. Others turned him down flat.

If no one else was going to develop a drug to treat NGLY1 deficiency, Wilsey, decided, he might as well try. “We have one shot at this,” he says. “Especially if your science is good enough, why not go for it?”

“Matt was showing classic entrepreneurial tendencies,” says Dan Levy, the vice president for small business at Facebook, who has known Wilsey since they rushed the same Stanford fraternity in the 1990s. “You have to suspend a little bit of disbelief, because everything is stacked against you.”

At 11 am, Grace sits in a classroom with a speech therapist. Though Grace doesn’t speak, she’s learning to use her “talker,” a tablet-sized device with icons that help her communicate. Grace grabs her talker and presses the icons for “play” and “music,” then presses a button to make her talker read the words out loud.

The "talker" used for Grace’s therapy.

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“OK, play music,” her therapist says, starting up a nearby iPad.

Grace watches an Elmo video on the iPad for a few moments, her forehead crinkled in concentration, her huge brown eyes a carbon copy of her dad’s. Then Grace stops the video and searches for another song.

Suddenly, her therapist slides the iPad out of Grace’s reach.

“You want ‘Slippery Fish,’” her therapist says. “I want you to tell me that.”

Grace turns to her talker: “Play music,” she types again.

The therapist attempts one more time to help Grace say more clearly which particular song she wants. Instead, Grace selects the symbols for two new words.

“Feel mad,” Grace’s talker declares.

Grace working with a therapist in one of their therapy rooms.

BLAKE FARRINGTON

There’s no denying how frustrating it can be for Grace to rely on other people to do everything for her, and how hard her family works to meet her constant needs.

Matt and Kristen can provide the therapy, equipment, medicines, and around-the-clock supervision that Grace needs to have a stable life. But that is not enough—not for Grace, who wants "Slippery Fish," nor for her parents, who want a cure.

So last summer, Wilsey raised money to bring the Vigeholms and the other NGLY1 families to Palo Alto, where they met with Grace’s doctors and the Grace Science Foundation researchers. One Japanese scientist, Takayuki Kamei, was overjoyed to meet two of the NGLY1 deficiency patients: “I say hello to their cells every morning,” he told their parents.

And because all of these families also want a cure, each also donated blood, skin, spit, stool, and urine to the world’s first NGLY1 deficiency biobank. In four days, scientists collected more NGLY1 deficiency data than had been collected in the entire five years since the disease was discovered. These patient samples, now stored at Stanford University and at Rutgers University, have been divvied up into more than 5,000 individual samples that will be distributed to academic and company researchers who wish to work on NGLY1 deficiency.

That same month, Wilsey closed a seed round of $7 million to start Grace Science LLC. His main backer, a veteran private equity investor, prefers not to be named. Like many in Silicon Valley, he’s recently become attracted to health care by the promise of a so-called “double bottom line”: the potential to both to make money and to do good by saving lives.

Wilsey is chief executive of the company and heavily involved in its scientific strategy. He’s looking for a head scientist with experience in gene therapy and in enzyme replacement therapy, which Mark Dant and John Crowley used to treat their sick children. Gene therapy now seems poised to take off after years of false starts; candidate cures for blood and nervous system disorders are speeding through clinical trials, and companies that use Crispr have raised more than $1 billion.

Wilsey doesn’t know which of these strategies, if any, will save Grace. But he hopes his company will find an NGLY1 deficiency cure within five years. The oldest known NGLY1 deficient patient is in her 20s, but since nobody has been looking for these patients until now, it’s impossible to know how many others—like Bertram—didn’t make it that long.

“We don’t know what Grace’s lifespan is,” Wilsey says. “We’re always waiting for the other shoe to drop.”

But at 3 pm on this one November day, that doesn’t seem to matter.

School’s out, and Grace is seated atop a light chestnut horse named Ned. Five staff members lead Grace through a session of equine therapy. Holding herself upright on Ned’s back helps Grace develop better core strength and coordination.

Grace on her horse.

BLAKE FARRINGTON

Grace and Ned walk under a canopy of oak trees. Her face is serene, her usually restless legs still as Ned paces through late-afternoon sunshine. But for a little grace, there may be a cure for her yet.

Read more: https://www.wired.com/story/a-familys-race-to-cure-a-daughters-genetic-disease/

Why No Gadget Can Prove How Stoned You Are

If you’ve spent time with marijuana—any time at all, really—you know that the high can be rather unpredictable. It depends on the strain, its level of THC and hundreds of other compounds, and the interaction between all these elements. Oh, and how much you ate that day. And how you took the cannabis. And the position of the North Star at the moment of ingestion.

OK, maybe not that last one. But as medical and recreational marijuana use spreads across the United States, how on Earth can law enforcement tell if someone they’ve pulled over is too high to be driving, given all these factors? Marijuana is such a confounding drug that scientists and law enforcement are struggling to create an objective standard for marijuana intoxication. (Also, I’ll say this early and only once: For the love of Pete, do not under any circumstances drive stoned.)

Sure, the cops can take you back to the station and draw a blood sample and determine exactly how much THC is in your system. “It's not a problem of accurately measuring it,” says Marilyn Huestis, coauthor of a new review paper in Trends in Molecular Medicine about cannabis intoxication. “We can accurately measure cannabinoids in blood and urine and sweat and oral fluid. It's interpretation that is the more difficult problem.”

You see, different people handle marijuana differently. It depends on your genetics, for one. And how often you consume cannabis, because if you take it enough, you can develop a tolerance to it. A dose of cannabis that may knock amateurs on their butts could have zero effect on seasoned users—patients who use marijuana consistently to treat pain, for instance.

The issue is that THC—what’s thought to be the primary psychoactive compound in marijuana—interacts with the human body in a fundamentally different way than alcohol. “Alcohol is a water-loving, hydrophilic compound,” says Huestis, who sits on the advisory board for Cannabix, a company developing a THC breathalyzer.1 “Whereas THC is a very fat-loving compound. It's a hydrophobic compound. It goes and stays in the tissues.” The molecule can linger for up to a month, while alcohol clears out right quick.

But while THC may hang around in tissues, it starts diminishing in the blood quickly—really quickly. “It's 74 percent in the first 30 minutes, and 90 percent by 1.4 hours,” says Huestis. “And the reason that's important is because in the US, the average time to get blood drawn [after arrest] is between 1.4 and 4 hours.” By the time you get to the station to get your blood taken, there may not be much THC left to find. (THC tends to linger longer in the brain because it’s fatty in there. That’s why the effects of marijuana can last longer than THC is detectable in breath or blood.)

So law enforcement can measure THC, sure enough, but not always immediately. And they’re fully aware that marijuana intoxication is an entirely different beast than drunk driving. “How a drug affects someone might depend on the person, how they used the drug, the type of drug (e.g., for cannabis, you can have varying levels of THC between different products), and how often they use the drug,” California Highway Patrol spokesperson Mike Martis writes in an email to WIRED.

Accordingly, in California, where recreational marijuana just became legal, the CHP relies on other observable measurements of intoxication. If an officer does field sobriety tests like the classic walk-and-turn maneuver, and suspects someone may be under the influence of drugs, they can request a specialist called a drug recognition evaluator. The DRE administers additional field sobriety tests—analyzing the suspect’s eyes and blood pressure to try to figure out what drug may be in play.

The CHP says it’s also evaluating the use of oral fluid screening gadgets to assist in these drug investigations. (Which devices exactly, the CHP declines to say.) “However, we want to ensure any technology we use is reliable and accurate before using it out in the field and as evidence in a criminal proceeding,” says Martis.

Another option would be to test a suspect’s breath with a breathalyzer for THC, which startups like Hound Labs are chasing. While THC sticks around in tissues, it’s no longer present in your breath after about two or three hours. So if a breathalyzer picks up THC, that would suggest the stuff isn’t lingering from a joint smoked last night, but one smoked before the driver got in a car.

This could be an objective measurement of the presence of THC, but not much more. “We are not measuring impairment, and I want to be really clear about that,” says Mike Lynn, CEO of Hound Labs. “Our breathalyzer is going to provide objective data that potentially confirms what the officer already thinks.” That is, if the driver was doing 25 in a 40 zone and they blow positive for THC, evidence points to them being stoned.

But you might argue that even using THC to confirm inebriation goes too far. The root of the problem isn’t really about measuring THC, it’s about understanding the galaxy of active compounds in cannabis and their effects on the human body. “If you want to gauge intoxication, pull the driver out and have him drive a simulator on an iPad,” says Kevin McKernan, chief scientific officer at Medicinal Genomics, which does genetic testing of cannabis. “That'll tell ya. The chemistry is too fraught with problems in terms of people's individual genetics and their tolerance levels.”

Scientists are just beginning to understand the dozens of other compounds in cannabis. CBD, for instance, may dampen the psychoactive effects of THC. So what happens if you get dragged into court after testing positive for THC, but the marijuana you consumed was also a high-CBD strain?

“It significantly compounds your argument in court with that one,” says Jeff Raber, CEO of the Werc Shop, a cannabis lab. “I saw this much THC, you're intoxicated. Really, well I also had twice as much CBD, doesn't that cancel it out? I don't know, when did you take that CBD? Did you take it afterwards, did you take it before?

“If you go through all this effort and spend all the time and money and drag people through court and spend taxpayer dollars, we shouldn't be in there with tons of question marks,” Raber says.

But maybe one day marijuana roadside testing won’t really matter. “I really think we're probably going to see automated cars before we're going to see this problem solved in a scientific sense,” says Raber. Don’t hold your breath, then, for a magical device that tells you you’re stoned.

1 UPDATE: 1/29/18, 2:15 pm ET: This story has been updated to disclose Huestis' affiliation with Cannabix.

Read more: https://www.wired.com/story/why-no-gadget-can-prove-how-stoned-you-are/