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.

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The Second Coming of Ultrasound

Before Pierre Curie met the chemist Marie Sklodowska; before they married and she took his name; before he abandoned his physics work and moved into her laboratory on Rue Lhomond where they would discover the radioactive elements polonium and radium, Curie discovered something called piezoelectricity. Some materials, he found—like quartz and certain kinds of salts and ceramics—build up an electric charge when you squeeze them. Sure, it’s no nuclear power. But thanks to piezoelectricity, US troops could locate enemy submarines during World War I. Thousands of expectant parents could see their baby’s face for the first time. And one day soon, it may be how doctors cure disease.

Ultrasound, as you may have figured out by now, runs on piezoelectricity. Applying voltage to a piezoelectric crystal makes it vibrate, sending out a sound wave. When the echo that bounces back is converted into electrical signals, you get an image of, say, a fetus, or a submarine. But in the last few years, the lo-fi tech has reinvented itself in some weird new ways.

Researchers are fitting people’s heads with ultrasound-emitting helmets to treat tremors and Alzheimer’s. They’re using it to remotely activate cancer-fighting immune cells. Startups are designing swallowable capsules and ultrasonically vibrating enemas to shoot drugs into the bloodstream. One company is even using the shockwaves to heal wounds—stuff Curie never could have even imagined.

So how did this 100-year-old technology learn some new tricks? With the help of modern-day medical imaging, and lots and lots of bubbles.

Bubbles are what brought Tao Sun from Nanjing, China to California as an exchange student in 2011, and eventually to the Focused Ultrasound Lab at Brigham and Women’s Hospital and Harvard Medical School. The 27-year-old electrical engineering grad student studies a particular kind of bubble—the gas-filled microbubbles that technicians use to bump up contrast in grainy ultrasound images. Passing ultrasonic waves compress the bubbles’ gas cores, resulting in a stronger echo that pops out against tissue. “We’re starting to realize they can be much more versatile,” says Sun. “We can chemically design their shells to alter their physical properties, load them with tissue-seeking markers, even attach drugs to them.”

Nearly two decades ago, scientists discovered that those microbubbles could do something else: They could shake loose the blood-brain barrier. This impassable membrane is why neurological conditions like epilepsy, Alzheimer’s, and Parkinson’s are so hard to treat: 98 percent of drugs simply can’t get to the brain. But if you station a battalion of microbubbles at the barrier and hit them with a focused beam of ultrasound, the tiny orbs begin to oscillate. They grow and grow until they reach the critical size of 8 microns, and then, like some Grey Wizard magic, the blood-brain barrier opens—and for a few hours, any drugs that happen to be in the bloodstream can also slip in. Things like chemo drugs, or anti-seizure medications.

This is both super cool and not a little bit scary. Too much pressure and those bubbles can implode violently, irreversibly damaging the barrier.

That’s where Sun comes in. Last year he developed a device that could listen in on the bubbles and tell how stable they were. If he eavesdropped while playing with the ultrasound input, he could find a sweet spot where the barrier opens and the bubbles don’t burst. In November, Sun’s team successfully tested the approach in rats and mice, publishing their results in Proceedings in the National Academy of Sciences.

“In the longer term we want to make this into something that doesn’t require a super complicated device, something idiot-proof that can be used in any doctor’s office,” says Nathan McDannold, co-author on Sun’s paper and director of the Focused Ultrasound Lab. He discovered ultrasonic blood-brain barrier disruption, along with biomedical physicist Kullervo Hynynen, who is leading the world’s first clinical trial evaluating its usefulness for Alzheimer’s patients at the Sunnybrook Research Institute in Toronto. Current technology requires patients to don special ultrasound helmets and hop in an MRI machine, to ensure the sonic beams go to the right place. For the treatment to gain any widespread traction, it’ll have to become as portable as the ultrasound carts wheeled around hospitals today.

More recently, scientists have realized that the blood-brain barrier isn’t the only tissue that could benefit from ultrasound and microbubbles. The colon, for instance, is pretty terrible at absorbing the most common drugs for treating Crohn’s disease, ulcerative colitis, and other inflammatory bowel diseases. So they’re often delivered via enemas—which, inconveniently, need to be left in for hours.

But if you send ultrasound waves waves through the colon, you could shorten that process to minutes. In 2015, pioneering MIT engineer Robert Langer and then-PhD student Carl Schoellhammer showed that mice treated with mesalamine and one second of ultrasound every day for two weeks were cured of their colitis symptoms. The method also worked to deliver insulin, a far larger molecule, into pigs.

Since then, the duo has continued to develop the technology within a start-up called Suono Bio, which is supported by MIT’s tech accelerator, The Engine. The company intends to submit its tech for FDA approval in humans sometime later this year.

Ultrasound sends pressure waves through liquid in the body, creating bubble-filled jets that can propel microscopic drug droplets like these into surrounding tissues.
Suono Bio

Instead of injecting manufactured microbubbles, Suono Bio uses ultrasound to make them in the wilds of the gut. They act like jets, propelling whatever is in the liquid into nearby tissues. In addition to its backdoor approach, Suono is also working on an ultrasound-emitting capsule that could work in the stomach for things like insulin, which is too fragile to be orally administered (hence all the needle sticks). But Schoellhammer says they have yet to find a limit on the kinds of molecules they can force into the bloodstream using ultrasound.

“We’ve done small molecules, we’ve done biologics, we’ve tried DNA, naked RNA, we’ve even tried Crispr,” he says. “As superficial as it may sound, it all just works.”

Earlier this year, Schoellhammer and his colleagues used ultrasound to deliver a scrap of RNA that was designed to silence production of a protein called tumor necrosis factor in mice with colitis. (And yes, this involved designing 20mm-long ultrasound wands to fit in their rectums). Seven days later, levels of the inflammatory protein had decreased sevenfold and symptoms had dissipated.

Now, without human data, it’s a little premature to say that ultrasound is a cure-all for the delivery problems facing gene therapies using Crispr and RNA silencing. But these early animal studies do offer some insights into how the tech might be used to treat genetic conditions in specific tissues.

Even more intriguing though, is the possibility of using ultrasound to remotely control genetically-engineered cells. That’s what new research led by Peter Yingxiao Wang, a bioengineer at UC San Diego, promises to do. The latest craze in oncology is designing the T-cells of your immune system to better target and kill cancer cells. But so far no one has found a way to go after solid tumors without having the T-cells also attack healthy tissue. Being able to turn on T-cells near a tumor but nowhere else would solve that.

Wang’s team took a big step in that direction last week, publishing a paper that showed how you could convert an ultrasonic signal into a genetic one. The secret? More microbubbles.

This time, they coupled the bubbles to proteins on the surface of a specially designed T-cell. Every time an ultrasonic wave passed by, the bubble would expand and shrink, opening and closing the protein, letting calcium ions flow into the cell. The calcium would eventually trigger the T-cell to make a set of genetically encoded receptors, directing it it to attack the tumor.

“Now we’re working on figuring out the detection piece,” says Wang. “Adding another receptor so that we’ll known when they’ve accumulated at the tumor site, then we’ll use ultrasound to turn them on.”

In his death, Pierre Curie was quickly eclipsed by Marie; she went on to win another Nobel, this time in chemistry. The discovery for which she had become so famous—radiation—would eventually take her life, though it would save the lives of so many cancer patients in the decades to follow. As ultrasound’s second act unfolds, perhaps her husband’s first great discovery will do the same.

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Photographer Reveals The Addicted Side Of The Streets Of Philadelphia, And Its Terrifying

Kensington Avenue in North Philadelphia is infamous for drug abuse and prostitution. The Avenue runs 3 miles through what is now a dangerous and crime-ridden neighborhood. Kensington Blues is a photography series by Jeffrey Stockbridge, 36, that documented the struggles and the dark reality of local residents.

Between 2008 and 2014, the photographer took a series of intimate portraits of people capturing a side of Philadelphia that is rarely seen or talked about. The residents shared their stories, talking about drugs, prostitution and other struggles of their lives.

“The goal of my work is to enable people to relate to one another in a fundamentally human way, despite any commonly perceived differences”- Jeffrey shared on his website. “I rely on the trust and sincerity of those I photograph to help me in this process.”

Take a look at the powerful images below.

“We out here so we can get money so we has somewhere to rest our heads. We look out for each other. If I can’t get money, she gets it, and whatever money we get we share…We need quick money cause we need somewhere to sleep every day. I mean, trust me, we don’t want to be out here doing this. This is the last thing I want to do….

“We out here so we can get money so we has somewhere to rest our heads. We look out for each other. If I can’t get money, she gets it, and whatever money we get we share…We need quick money cause we need somewhere to sleep every day. I mean, trust me, we don’t want to be out here doing this. This is the last thing I want to do. But I do what I have to do to take care of my sister. Cause she’s all I got and I’m all she’s got.”

Al lives in a house off Kensington Avenue without electricity or running water. He sometimes rents his upstairs bedroom to prostitutes in need of a private location for engaging in sex and drug use.

“I’m 55 years old, I have a master’s degree in psychology, but after my husband, mother and father, died in a car accident two years ago, I lost my whole family, my career, one, my health, all in one go.”

She told that she often sleeps on the streets during the day to protect herself at night.

They still have children, whom they gave away to a special agency for their protection. “We gave the kids away, people say it’s a selfish act, but I think it’s the best I could do for their better future,” Rachel said.

She is 25 years old, working in the sex industry since she was 18.

“I’ve been raped, and, you know, almost killed really”

A local resident, at the time she was 41. Carol told the photographer that she had been doing heroin for 21 years and it became “the love of her life”.

The veins in Sarah’s arms were no good for injection, so she asked Dennis for the drug to be injected to her neck.

“I don’t just do this for drugs. I do this because I wanna eat, because I like to buy clothes, because I like the small things, you know. I did have a normal life once but…I really believe, like if my, if my family say like, “Mary come, come home stay with us” like, if I could I would…”

He struggled with drug addiction after being released from prison. Sepsis developed in his left leg. Because of his addiction, he failed to meet the treatment regimen and eventually the doctors had to amputate part of the leg.

Matt shoots Brian in the neck in front of the McPherson Square Library on Kensington Avenue. It’s 10 AM on Sunday morning.

Maria: “I’ve been here almost 8 years and I see a lot of bad stuff going around. They say when you go between it, you gonna do it too.” Robert: “You don’t need no cable, you don’t have to watch TV. You just gotta sit out here. You see drama, you see soap opera, you see violence and crime.” Maria: “You even see sex.”

“I don’t really ask people for a lot, I get my money, like I don’t like to, cause a lot of times to get people to take care of you, you have to lie to them. And then lead them on and make them think that you’re gonna get clean. And then, and then it ends up getting to be too much, where they’re trying to control what you do….

“I don’t really ask people for a lot, I get my money, like I don’t like to, cause a lot of times to get people to take care of you, you have to lie to them. And then lead them on and make them think that you’re gonna get clean. And then, and then it ends up getting to be too much, where they’re trying to control what you do. And I’d rather just get the money and end it at that with no strings attached cause I don’t need someone following me around, trying to track me down like, trying to drop me off at rehabs and shit.”

“I went into rehab, for, like, snorting cocaine, taking oxies, perks, and I met people that did dope and smoked crack, and, you know, like, one thing led to another, and I was just, I was, I wanted to try it, and I did.”

“I sold a lot of drugs and was involved with a lot of like, stuff that had to do with shooting guns and all. Most of it was uh selling drugs and collecting money that was owed to me and it caused me getting into a lot of trouble.”

“What I’m doing I really don’t particularly care to be doing, but I do it anyway, and I’m not ashamed of it ’cause if I was ashamed of it, I wouldn’t do it….Until I decide to change it’s what I’m gonna do. Hopefully, like, the will of God…will make me strong enough and give me the determination to stop and get some help.”

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Spinal-Cord Implants to Numb Pain Emerge as Alternative to Pills

For millions of Americans suffering from debilitating nerve pain, a once-overlooked option has emerged as an alternative to high doses of opioids: implanted medical devices using electricity to counteract pain signals the same way noise-canceling headphones work against sound. 

The approach, called neuromodulation, has been a godsend for Linda Landy, who was a 42-year-old runner when a foot surgery went awry in 2008. She was diagnosed with complex regional pain syndrome, a condition dubbed the suicide disease by doctors: The pain is so unrelenting that many people take their own lives.

Linda Landy and family

Last November, Landy underwent surgery to get an Abbott Laboratories device that stimulates the dorsal root ganglion, a spot in the spine that was the pain conduit for her damaged nerves. A year after getting her implant, called DRG, she’s cut back drastically on pain pills.

“The DRG doesn’t take the pain completely away, but it changes it into something I can live with,” said Landy, a mother of three in Fort Worth, Texas. She’s now now able to walk again and travel by plane without using a wheelchair. “It sounds minor, but it’s really huge.”

Crackdown on Opioids

Recent innovations from global device makers like Abbott to smaller specialists such as Nevro Corp. made the implants more powerful and effective. Combined with a national crackdown on narcotics and wanton pain pill prescriptions, they are spurring demand for implants.

The market may double to $4 billion in 10 years, up from about $1.8 billion in the U.S. and $500 million in Europe today, according to health-care research firm Decisions Resources Group.

“There was a big stigma around this when it first came out,” said Paul Desormeaux, a Decisions Resources analyst in Toronto. “The idea of sending an electrical signal through your nervous system was a little daunting, but as clinical data has come out and physicians have been able to prove its safety, there has been a big change in the general attitude.”

Read More: Millions Face Pain, Withdrawal as Opioid Prescriptions Plummet

At least 50 million adults in the U.S. suffer from chronic pain, according to the Centers for Disease Control and Prevention. Only a fraction of them would benefit from spinal-cord stimulation — about 3.6 million, according to Decisions Resources — but those are patients who are often given the highest doses of narcotics. They include people with nerve damage stemming from conditions like diabetic neuropathy and shingles, as well as surgeries.

“There is no question we are reducing the risk of opioid dependence by implanting these devices,” said Timothy Deer, president of the Spine and Nerve Centers of the Virginias in Charleston, West Virginia, a hotbed of the opioid epidemic. “If we get someone before they are placed on opioids, 95 percent of the time we can reduce their need to ever go on them.”

Studies show spinal-cord stimulators can reduce use of powerful pain drugs by 60 percent or more, said Deer, a clinical professor of anesthesiology.

Read More: Tangled Incentives Push Drugmakers Away From an Opioid Solution

Technology breakthroughs that are just now reaching patients came from a better understanding of how pain signals are transmitted within the spinal cord, the main thoroughfare between the command center in the brain and the body.

For some chronic pain patients, the spinal cord runs too efficiently, speeding signs of distress. Stimulators send their own pulses of electrical activity to offset or interrupt the pain zinging along the nerve fibers. They have been available for more than three decades, but until recently their invasive nature, potential safety risks and cost limited demand.

Market Leader Abbott

Illinois-based Abbott, with its $29 billion acquisition of St. Jude Medical this year, took the market lead with advances that allow it to target specific nerves and tailor the treatment. Nevro, of Redwood City, California, has rolled out improvement to its Senza system, a best-in-class approach that is safe while getting an MRI and operates without the tingling that often accompanies spinal-cord stimulation.

In the latest devices, which cost $30,000 or more, codes that are running the electrical pulses are more sophisticated. The frequency, rate and amplitude can be adjusted, often by the patients, which allows personalized therapy. 

The new implants are also smaller: The surgery is generally an outpatient procedure with minimal post-operative pain and a short recovery. They have longer battery life, reducing the need for replacement. And patients can try out a non-invasive version of the equipment before getting a permanent implant.

“This is really a defining moment in what we can do to impact the lives of people who suffer from chronic pain,” said Allen Burton, Abbott’s medical director of neuromodulation. “We can dampen the chronic pain signal and give patients their lives back.”

Medtronic Plc, which pioneered the technique but ceded the lead in recent years, is now working on next-generation devices. The company recently gained approval for the smallest pain-management implant, Intellis. In development are devices that can detect pain waves and adjust automatically, said Geoff Martha, executive vice president of Medtronic’s restorative therapies group.

“A self-correcting central nervous system — that’s the panacea. That’s the ultimate goal,” Martha said. “It could take a huge bite out of the opioid problem.”

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    The Most Promising Cancer Treatments In a Century Have ArrivedBut Not For Everyone

    In 1891, a New York doctor named William B. Coley injected a mixture of beef broth and Streptococcus bacteria into the arm of a 40-year-old Italian man with an inoperable neck tumor. The patient got terribly sick—developing a fever, chills, and vomiting. But a month later, his cancer had shrunk drastically. Coley would go on to repeat the procedure in more than a thousand patients, with wildly varying degrees of success, before the US Food and Drug Administration shut him down.

    Coley’s experiments were the first forays into a field of cancer research known today as immunotherapy. Since his first experiments, the oncology world has mostly moved on to radiation and chemo treatments. But for more than a century, immunotherapy—which encompasses a range of treatments designed to supercharge or reprogram a patient’s immune system to kill cancer cells—has persisted, mostly around the margins of medicine. In the last few years, though, an explosion of tantalizing clinical results have reinvigorated the field and plunged investors and pharma execs into a spending spree.

    Though he didn’t have the molecular tools to understand why it worked, Coley’s forced infections put the body’s immune system into overdrive, allowing it to take out cancer cells along the way. While the FDA doesn’t have a formal definition for more modern immunotherapies, in the last few years it has approved at least eight drugs that fit the bill, unleashing a flood of money to finance new clinical trials. (Patients had better come with floods of money too—prices can now routinely top six figures.)

    But while the drugs are dramatically improving the odds of survival for some patients, much of the basic science is still poorly understood. And a growing number of researchers worry that the sprint to the clinic offers cancer patients more hype than hope.

    When immunotherapy works, it really works. But not for every kind of cancer, and not for every patient—not even, it turns out, for the majority of them. “The reality is immunotherapy is incredibly valuable for the people who can actually benefit from it, but there are far more people out there who don’t benefit at all,” says Vinay Prasad, an Oregon Health and Science University oncologist.

    Prasad has come to be regarded as a professional cancer care critic, thanks to his bellicose Twitter style and John Arnold Foundation-backed crusade against medical practices he says are based on belief, not scientific evidence. Using national cancer statistics and FDA approval records, Prasad recently estimated the portion of all patients dying from all types of cancer in America this year who might actually benefit from immunotherapy. The results were disappointing: not even 10 percent.

    Now, that’s probably a bit of an understatement. Prasad was only looking at the most widely used class of immunotherapy drugs in a field that is rapidly expanding. Called checkpoint inhibitors, they work by disrupting the immune system’s natural mechanism for reining in T cells, blood-borne sentinels that bind and kill diseased cells throughout the body. The immune cells are turned off most of the time, thanks to proteins that latch on to a handful of receptors on their surface. But scientists designed antibodies to bind to those same receptors, knocking out the regulatory protein and keeping the cells permanently switched to attack mode.

    The first checkpoint inhibitors just turned T cells on. But some of the newer ones can work more selectively, using the same principle to jam a signal that tumors use to evade T cells. So far, checkpoint inhibitors have shown near-miraculous results for a few rare, previously incurable cancers like Hodgkin’s lymphoma, renal cell carcinoma, and non-small cell lung cancer. The drugs are only approved to treat those conditions, leaving about two-thirds of terminal cancer patients without an approved immunotherapy option.

    But Prasad says that isn’t stopping physicians from prescribing the drugs anyway.

    “Hype has encouraged rampant off-label use of checkpoint inhibitors as a last-ditch effort,” he says—even for patients with tumors that show no evidence they’ll respond to the drugs. The antibodies are available off the shelf, but at a list price near $150,000 per year, it’s an investment Prasad says doctors shouldn’t encourage lightly. Especially when there’s no reliable way of predicting who will respond and who won’t. “This thwarts one of the goals of cancer care," says Prasad. "When you run out of helpful responses, how do you help a patient navigate what it means to die well?”

    Merck and Bristol-Myers Squibb have dominated this first wave of immunotherapy, selling almost $9 billion worth of checkpoint inhibitors since they went on sale in 2015. Roche, AstraZeneca, Novartis, Eli Lilly, Abbvie, and Regeneron have all since jumped in the game, spending billions on acquiring biotech startups and beefing up in-house pipelines. And 800 clinical trials involving a checkpoint inhibitor are currently underway in the US, compared with about 200 in 2015. “This is not sustainable,” Genentech VP of cancer immunology Ira Mellman told the audience at last year’s annual meeting of the Society for Immunotherapy of Cancer. With so many trials, he said, the industry was throwing every checkpoint inhibitor combination at the wall just to see what would stick.

    After more than a decade stretching out the promise of checkpoint inhibitors, patients—and businesses—were ready for something new. And this year, they got it: CAR T cell therapy. The immunotherapy involves extracting a patient’s T cells and genetically rewiring them so they can more efficiently home in on tumors in the body—training a foot soldier as an assassin that can slip behind enemy lines.

    In September, the FDA cleared the first CAR-T therapy—a treatment for children with advanced leukemia, developed by Novartis—which made history as the first-ever gene therapy approved for market. A month later the agency approved another live cell treatment, developed by Kite Pharma, for a form of adult lymphoma. In trials for the lymphoma drug, 50 percent of patients saw their cancer disappear completely, and stay gone.

    Kite’s ascendance in particular is a stunning indicator of how much money CAR-T therapy has attracted, and how fast. The company staged a $128 million IPO in 2014—when it had only a single late-phase clinical trial to its name—and sold to Gilead Science in August for $11.9 billion. For some context, consider that when Pfizer bought cancer drugmaker Medivation for $14 billion last year—one of the biggest pharma deals of 2016—the company already had an FDA-approved blockbuster tumor-fighter on the market with $2 billion in annual sales, plus two late-stage candidates in the pipeline.

    While Kite and Novartis were the only companies to actually launch products in 2017, more than 40 other pharma firms and startups are currently building pipelines. Chief rival Juno Therapeutics went public with a massive $265 million initial offering—the largest biotech IPO of 2014—before forming a $1 billion partnership with Celgene in 2015. In the last few years, at least half a dozen other companies have made similar up-front deals worth hundreds of millions.

    These treatments will make up just a tiny slice of the $107 billion cancer drug market. Only about 600 people a year, for example, could benefit from Novartis’ flagship CAR-T therapy. But the company set the price for a full course of treatment at a whopping $475,000. So despite the small clientele, the potential payoff is huge—and the technology is attracting a lot of investor interest. “CAR-T venture financing is still a small piece of total venture funding in oncology, but given that these therapies are curative for a majority of patients that have received them in clinical trials, the investment would appear to be justified,” says Mandy Jackson, a managing editor for research firm Informa Pharma Intelligence.

    CAR-T, with its combination of gene and cell therapies, may be the most radical anticancer treatment ever to arrive in clinics. But the bleeding edge of biology can be a dangerous place for patients.

    Sometimes, the modified T cells go overboard, excreting huge quantities of molecules called cytokines that lead to severe fevers, low blood pressure, and difficulty breathing. In some patients it gets even worse. Sometimes the blood-brain barrier inexplicably breaks down—and the T cells and their cytokines get inside patients’ skulls. Last year, Juno pulled the plug on its lead clinical trial after five leukemia patients died from massive brain swelling. Other patients have died in CAR-T trials at the National Cancer Institute and the University of Pennsylvania.

    Scientists don’t fully understand why some CAR-T patients experience cytokine storms and neurotoxicity and others come out cured. “It’s kind of like the equivalent of getting on a Wright Brother’s airplane as opposed to walking on a 747 today,” says Wendell Lim, a biophysical chemist and director of the UC San Francisco Center for Systems and Synthetic Biology. To go from bumping along at a few hundred feet to cruise control at Mach 0.85 will mean equipping T cells with cancer-sensing receptors that are more specific than the current offerings.

    Take the two FDA-approved CAR-T cell therapies, he says. They both treat blood cancers in which immune responders called B cells become malignant and spread throughout the body. Doctors reprogram patients’ T cells to seek out a B cell receptor called CD-19. When they find it, they latch on and shoot it full of toxins. Thing is, the reprogrammed T cells can’t really tell the difference between cancerous B cells and normal ones. The therapy just takes them all out. Now, you can live without B cells if you receive antibody injections to compensate—so the treatment works out fine most of the time.

    But solid tumors are trickier—they’re made up of a mix of cells with different genetic profiles. Scientists have to figure out which tumor cells matter to the growth of the cancer and which ones don’t. Then they have to design T cells with antigens that can target just those ones and nothing else. An ideal signature would involve two to three antigens that your assassin T cells can use to pinpoint the target with a bullet instead of a grenade.

    Last year Lim launched a startup called Cell Design Labs to try to do just that, as well as creating a molecular on-off-switch to make treatments more controlled. Only if researchers can gain this type of precise command, says Lim, will CAR-T treatments become as safe and predictable as commercial airline flight.

    The field has matured considerably since Coley first shot his dying patient full of a dangerous bacteria, crossed his fingers, and hoped for the best. Sure, the guy lived, even making a miraculous full recovery. But many after him didn’t. And that “fingers crossed” approach still lingers over immunotherapy today.

    All these years later, the immune system remains a fickle ally in the war on cancer. Keeping the good guys from going double-agent is going to take a lot more science. But at least the revolution will be well-financed.

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    Amazon Threat Causes Shakeout in the Health-Care Industry Inc. is casting a long shadow over the health-care industry.

    The prospect of the giant Internet retailer entering the business is beginning to cause far-reaching reverberations for a range of companies, roiling the shares of drugstore chains, drug distributors and pharmacy-benefit managers, and potentially precipitating one of the biggest corporate merger deals this year.

    On Thursday, the pressure was plain to see. A report that Amazon had received pharmacy-wholesaler licenses in a dozen states triggered a fast and steep selloff that wounded the likes of McKesson Corp., AmerisourceBergen Corp. and Cardinal Health Inc. And late in the day, shares of Aetna Inc. surged after a report that it was in talks to be taken over by CVS Health Corp.

    Executives in the drug industry say that Amazon could use its expansive online reach and its logistical muscle to threaten companies that ship and sell medicines to consumers and cut pricing deals with drug makers.

    “Size and scale-wise, they can disrupt anywhere they want to disrupt,” said Chip Davis, president of the Association for Accessible Medicines, a trade group for generic medication, in an interview Thursday.

    Competitive Squeeze

    A deal for Aetna could conceivably move CVS further away from the business of brick-and-mortar retail drugstores and deeper in health services such as pharmacy benefits, where it already has a sizable presence.

    Combining Aetna and CVS would create a health-services giant and a bigger competitor for UnitedHealth Group Inc., which is the largest U.S. health insurer and has its own own clinics and a pharmacy-benefits unit.

    The presence of Amazon is already being felt by retailers and companies that sell drugs over the counter. The head of of Bayer AG’s consumer-health business said on a conference call with analysts Thursday that the wider shift to online shopping by U.S. consumers was hurting its business. Erica Mann, the division’s chief, dubbed it the “Amazon effect,” saying buyers are looking for value.

    At the same time, the pecking order in the health-supply chain is beginning to shift.

    Earlier this month, insurance giant Anthem Inc. said it was cutting ties with Express Scripts Holding Co. after a long dispute over pricing and starting its own pharmacy-benefits manager in 2020. A bulked-up CVS and Anthem’s new venture could raise the pressure on Express Scripts, which has touted its independence.

    Any tie-up of Aetna and CVS would follow a pair of failed mergers among health insurers. The deals would have reduced the ranks of big U.S. health insurers from five to three, a prospect that led the Justice Department to oppose both prospective tie-ups.

    If the Aetna deal happened, “CVS would have a dominant position” in the drug-benefits business, said Michael Rea, founder of Rx Savings Solutions, which has an app that helps patients find low cost drugs.

    Pharmacy Threat

    Analysts have speculated that Amazon could soon enter the business of selling prescription drugs, threatening to disrupt retail drugstores, drug wholesalers, and the pharmacy-benefits management business. While Amazon has never publicly commented on what its plans may be, CNBC reported this month that the Internet giant could make a decision about selling drugs online by Thanksgiving. The network didn’t name its sources.

    McKesson slid 5.2 percent at 4 p.m. in New York, while AmerisourceBergen shares fell 4.2 percent and Express Scripts sank 3.7 percent following the report on Amazon’s state licenses by the St. Louis Post-Dispatch.

    Bloomberg News confirmed that Amazon had obtained wholesale-pharmacy licenses in at least 13 states, including Nevada, Idaho, Arizona, North Dakota, Oregon, Alabama, Louisiana, New Jersey, Michigan, Connecticut, New Hampshire, Utah and Iowa. An application is pending in Maine. Some of the licenses were obtained late last year and some this year.

    Amazon declined to comment.

    The licenses could be part of Amazon’s business-to-business sales effort, which would include sales to hospitals, doctor’s offices and dentists. Amazon on Tuesday announced “Business Prime Shipping,” which brings the quick delivery associated with Amazon household orders to workplaces. 

    The Seattle company launched Amazon Business in 2015, offering tractor parts, latex gloves, file folders and millions of other products needed in factories, hospitals, schools and offices. Businesses are shifting their supply shopping online from less-efficient methods such as browsing print catalogs, faxing orders and telephoning sales representatives.

    Online business-to-business sales – a broad category that includes pens and paper for the office as well as lab equipment and parts used in factories — will grow to $1.2 trillion in 2021 from $889 billion this year, according to Forrester Research Inc.

    On a conference call Thursday with analysts, McKesson CEO John H. Hammergren said the wholesaler doesn’t “take the entry of any competitor lightly,” but said the company already has a large online order operation and similar to what Amazon does logistically. “To some extent, we were Amazon before it was cool to be Amazon.”

      Read more:

      Trump Officials Dispute the Benefits of Birth Control to Justify Rules

      When the Trump administration elected to stop requiring many employers to offer birth-control coverage in their health plans, it devoted nine of its new rule’s 163 pages to questioning the links between contraception and preventing unplanned pregnancies.

      In the rule released Friday, officials attacked a 2011 report that recommended mandatory birth-control coverage to help women avoid unintended pregnancies. That report, requested by the Department of Health and Human Services, was done by the National Academies of Sciences, Engineering and Medicine — then the Institute of Medicine — an expert group that serves as the nation’s scientific adviser.

      “The rates of, and reasons for, unintended pregnancy are notoriously difficult to measure,” according to the Trump administration’s interim final rule. “In particular, association and causality can be hard to disentangle.”

      Multiple studies have found that access or use of contraception reduced unintended pregnancies. 

      Claims in the report that link increased contraceptive use by unmarried women and teens to decreases in unintended pregnancies “rely on association rather than causation,” according to the rule. The rule references another study that found increased access to contraception decreased teen pregnancies short-term but led to an increase in the long run.

      “We know that safe contraception — and contraception is incredibly safe — leads to a reduction in pregnancies,” said Michele Bratcher Goodwin, director of the Center for Biotechnology and Global Health Policy at the University of California, Irvine, School of Law. “This has been data that we’ve had for decades.”

      Riskier Behavior

      The rules were released as part of a broader package of protections for religious freedom that the administration announced Friday.

      The government also said imposing a coverage mandate could “affect risky sexual behavior in a negative way” though it didn’t point to any particular studies to support its point. A 2014 study by the Washington University School of Medicine in St. Louis found providing no-cost contraception did not lead to riskier sexual behavior.

      The rule asserts that positive health effects associated with birth control “might also be partially offset by an association with negative health effects.” The rule connects the claim of negative health effects to a call by the National Institutes of Health in 2013 for the development of new contraceptives that stated current options can have “many undesirable side effects.” 

      The rule also describes an Agency for Healthcare Research and Quality review that found oral contraceptives increased users’ risk of breast cancer and vascular events, making the drugs’ use in preventing ovarian cancer uncertain.

      Federal officials used all of these assertions to determine the government “need not take a position on these empirical questions.”

      “Our review is sufficient to lead us to conclude that significantly more uncertainty and ambiguity exists in the record than the Departments previously acknowledged.”

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        It was all yellow: did digitalis affect the way Van Gogh saw the world?

        Extracted from foxgloves, digitalis was once used as a treatment for epilepsy. Could a side effect have triggered the artists yellow period?

        It was recently the 127th anniversary of the tragic death of Vincent van Gogh. His short life came to an untimely end two days after he shot himself in the chest; he had experienced mental health issues through much of his life. In the absence of a definitive diagnosis, speculation as to the true nature of his illness fills volumes.

        Although he came under the care of several doctors during his life time, knowledge of diseases of the mind was in its infancy in the late nineteenth century. As a result, many of the treatments used at the time would have been ineffective if not potentially dangerous. From our point of view, however, one drug that might have been given to Van Gogh is particularly interesting.

        Towards the end of his life, under the care of Dr Gachet, it seems that Van Gogh may have been treated with digitalis for the epileptic fits he experienced. Digitalis, extracted from foxglove plants, is a powerful medicine still in use today as a treatment for certain heart conditions, but not epilepsy. In Van Goghs day, and for a long time before then, digitalis was known to be an effective treatment of dropsy, or accumulation of fluid in the body. Dropsy could have been caused by inefficient beating of the heart or because of liver disease. But with little understanding of the underlying causes of many diseases, almost anything shown to have an effect on the body even if that was simply to induce vomiting was considered a medical benefit. If the treatment for one disease was successful, it was often tried out on a host of others, just in case it proved to be a panacea. Extracts of foxglove really would have been effective in treating dropsy caused by heart failure, but would have done nothing for Van Goghs epilepsy. However, it is just possible it may have contributed to his artistic output.

        Portrait of Dr Gachet, by Vincent van Gogh. Gachet holds a foxglove, seen by some to suggest that he treated Van Gogh with digitalis. Photograph: DEA / G. DAGLI ORTI/De Agostini/Getty Images

        Digitalis is, in fact, a mixture of several different compounds that today are separated and used individually to treat heart conditions. One of the compounds, digoxin, is listed by the World Health Organisation as an essential medicine because of its huge benefit in the treatment of abnormal heart rhythms such as atrial fibrillation. Digoxin has two effects on the heart. Firstly, it helps to control the electrical signals that are sent across the heart to trigger the cells to beat in a coordinated way producing a heartbeat. Secondly, it makes the individual heart cells contract more slowly and strongly, improving the efficiency of the pumping action to move blood round the body.

        To achieve these effects on the heart, digoxin and related compounds interact with the enzyme Na+/K+ ATPase. Digoxin is a very potent drug, the therapeutic dose is miniscule, and it is very close to the level that can also produce digitalis intoxication. Such a narrow gap between a therapeutic and potentially harmful dose would simply not be tolerated in a new drug being brought to market. However, the undoubted benefit of digoxin and its long history of use means it is a vital part of modern medicine. Because the drug has been in use for so long over 200 years, since the physician William Withering advocated its use in 1775 we have had plenty of time to understand how the drug works and the potential side-effects. Patients taking digoxin are carefully monitored and a number of antidotes have been developed to treat overdoses.

        The problem, as with all drugs, is side-effects. To achieve its effects on the heart, digoxin and related compounds interact with the enzyme Na+/K+ ATPase.Digoxins strong interaction with the enzyme means it is very potent, but Na+/K+ ATPase is distributed throughout the body. It is therefore the interaction between the drug and the enzymes located elsewhere in the body that is the cause of side-effects. The most common problems associated with digoxin are nausea and loss of appetite, but its other effects are more intriguing.

        Particularly high concentrations of digoxins target enzyme are found in the cone cells in retina of the eye. These are the cells that give us our colour perception. It is very rare, but some people taking digoxin and related drugs can experience haziness to their vision, or a yellow tinge to everything they see, known as xanthopsia. Occasionally, points of light may appear to have coloured halos around them. Rarer still are effects on pupil size, such as dilation, constriction or even unequal-sized pupils.

        The effects of digitalis intoxication have been suggested as the cause of Van Goghs yellow period and the spectacular sky he painted in The Starry Night. More circumstantial evidence comes from the two portraits Van Gogh produced of his doctor, Paul Gachet, showing him holding a foxglove flower. One of Van Goghs self portraits also shows uneven pupils.

        All of this is very interesting but it is pure speculation. Van Gogh may not have taken digitalis, and perhaps simply liked the colour yellow and the effect of swirling colours around the stars he painted. Unequal pupil size in his self-portrait may have been the result of a simple slip of the paintbrush.

        There are also many other factors to consider. Van Gogh was known to drink large quantities of absinthe (though not enough to produce yellow colour perception) as well as turpentine (which can affect vision but not colour perception). Whatever the reason for Van Goghs particular artistic choices, we can still appreciate his remarkable output from such a tragically short life.

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        Rule that patients must finish antibiotics course is wrong, study says

        Experts suggest patients should stop taking the drugs when they feel better rather than completing their prescription

        Telling patients to stop taking antibiotics when they feel better may be preferable to instructing them to finish the course, according to a group of experts who argue that the rule long embedded in the minds of doctors and the public is wrong and should be overturned.

        Patients have traditionally been told that they must complete courses of antibiotics, the theory being that taking too few tablets will allow the bacteria causing their disease to mutate and become resistant to the drug.

        But Martin Llewelyn, a professor in infectious diseases at Brighton and Sussex medical school, and colleagues claim that this is not the case. In an analysis in the British Medical Journal, the experts say the idea that stopping antibiotic treatment early encourages antibiotic resistance is not supported by evidence, while taking antibiotics for longer than necessary increases the risk of resistance.

        There are some diseases where the bug can become resistant if the drugs are not taken for long enough. The most obvious example is tuberculosis, they say. But most of the bacteria that cause people to become ill are found on everybodys hands in the community, causing no harm, such as E coli and Staphylococcus aureus. People fall ill only when the bug gets into the bloodstream or the gut. The longer such bacteria are exposed to antibiotics, the more likely it is that resistance will develop.

        The experts say there has been too little research into the ideal length of a course of antibiotics, which also varies from one individual to the next, depending in part on what antibiotics they have taken in the past.

        In hospital, patients can be tested to work out when to stop the drugs. Outside hospital, where repeated testing may not be feasible, patients might be best advised to stop treatment when they feel better, they say. That, they add, is in direct contravention of World Health Organisation advice.

        Other experts in infectious diseases backed the group. I have always thought it to be illogical to say that stopping antibiotic treatment early promotes the emergence of drug-resistant organisms, said Peter Openshaw, president of the British Society for Immunology.

        This brief but authoritative review supports the idea that antibiotics may be used more sparingly, pointing out that the evidence for a long duration of therapy is, at best, tenuous. Far from being irresponsible, shortening the duration of a course of antibiotics might make antibiotic resistance less likely.

        Alison Holmes, a professor of infectious diseases at Imperial College London, said a great British authority, Prof Harold Lambert, had made the same point in a Lancet article entitled Dont keep taking the tablets as early as 1999. It remains astonishing that apart from some specific infections and conditions, we still do not know more about the optimum duration of courses or indeed doses in many conditions, yet this dogma has been pervasive and persistent.

        Jodi Lindsay, a professor of microbial pathogenesis at St Georges, University of London, said it was sensible advice. The evidence for completing the course is poor, and the length of the course of antibiotics has been estimated based on a fear of under-treating rather than any studies, she said. The evidence for shorter courses of antibiotics being equal to longer courses, in terms of cure or outcome, is generally good, although more studies would help and there are a few exceptions when longer courses are better for example, TB.

        But the Royal College of GPs expressed concerns. Recommended courses of antibiotics are not random, said its chair, Prof Helen Stokes-Lampard. They are tailored to individual conditions and in many cases, courses are quite short for urinary tract infections, for example, three days is often enough to cure the infection.

        We are concerned about the concept of patients stopping taking their medication midway through a course once they feel better, because improvement in symptoms does not necessarily mean the infection has been completely eradicated. Its important that patients have clear messages and the mantra to always take the full course of antibiotics is well known. Changing this will simply confuse people.

        The UKs chief medical officer, Prof Dame Sally Davies, said: The message to the public remains the same: people should always follow the advice of healthcare professionals. To update policies, we need further research to inform them.

        [The National Institute for Health and Care Excellence] is currently developing guidance for managing common infections, which will look at all available evidence on appropriate prescribing of antibiotics.

        The Department of Health will continue to review the evidence on prescribing and drug-resistant infections, as we aim to continue the great progress we have made at home and abroad on this issue.

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        People taking heartburn drugs could have higher risk of death, study claims

        Research suggests people on proton pump inhibitors are more likely to die than those taking different antacid or none at all

        Millions of people taking common heartburn and indigestion medications could be at an increased risk of death, research suggests.

        The drugs, known as proton pump inhibitors (PPIs), neutralise the acid in the stomach and are widely prescribed, with low doses also available without prescription from pharmacies. In the UK, doctors issue more than 50m prescriptions for PPIs every year.

        Now researchers say the drugs can increase risk of death, both compared with taking a different type of acid suppressant and not taking any at all.

        We saw a small excess risk of dying that could be attributed to the PPI drug, and the risk increased the longer they took them, said Ziyad Al-Aly, an epidemiologist from the University of Washington and co-author of the study.

        The team say the study suggests those who take the drugs without needing to could be most at risk. They urged people taking PPIs to check whether this was necessary.

        Previous research has raised a range of concerns about PPIs, including links to kidney disease, pneumonia, more hip fractures and higher rates of infection with C difficile, a superbug that can cause life-threatening sepsis, particularly in elderly people in hospitals.

        But the latest study is the first to show that PPIs can increase the chance of death. Published in the journal BMJ Open, it examined the medical records of 3.5 million middle-aged Americans covered by the US veterans healthcare system.

        The researchers followed 350,000 participants for more than five years and compared those prescribed PPIs to a group receiving a different type of acid suppressant known as an H2 blocker. They also took into account factors such as the participants age, sex and conditions ranging from high blood pressure to HIV.

        The results show that those who took PPIs could face a 25% higher risk of death than those who took the H2 blocker.

        In patients on [H2 blocker] tablets, there were 3.3 deaths per 100 people over one year. In the PPI group, this figure was higher at 4.7 per 100 people per year, said Al-Aly.

        The team also reported that the risk of death for those taking PPIs was 15% higher than those taking no PPIs, and 23% higher than for those taking no acid suppressants at all.

        Similar levels of increased risk were seen among people who used PPIs but had no gastrointestinal conditions, a result which the authors speculated might be driving the higher risk seen overall.

        Gareth Corbett, a gastroenterologist from Addenbrookes hospital in Cambridge who was not involved with the study, cautioned against panic, pointing out that in most cases the benefits of PPI far outweighed any risk. What was more, he said, while the increased risk sounded high, it was still very low for each person.

        PPIs are very effective medicines, proven to save lives and reduce the need for surgery in patients with bleeding gastric and duodenal ulcers and several other conditions, he said.

        The studys authors said it was important that PPIs were used only when necessary and stopped when no longer needed.

        Corbett agreed that many people take PPIs unnecessarily. They could get rid of their heartburn by making lifestyle changes, such as losing weight and cutting back on alcohol, caffeine and spicy foods, he said.

        The authors said the study was observational, meaning it did not show that PPIs were the cause of the increased risk of death, and that it was unclear how the drugs would act to affect mortality. They said the drugs could affect components within cells, known as lysosomes, that help break down waste material, or shortening protective regions at the end of chromosomes, known as telomeres.

        Aly said people on PPIs should check with their GP whether the drugs were still needed, adding: In some cases we expect that PPIs can be safely stopped, particularly in patients who have been taking them for a long time.

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