Day: 05/01/2015

The Likely Cause of Addiction Has Been Discovered, and It Is Not What You Think

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It is now one hundred years since drugs were first banned — and all through this long century of waging war on drugs, we have been told a story about addiction by our teachers and by our governments. This story is so deeply ingrained in our minds that we take it for granted. It seems obvious. It seems manifestly true. Until I set off three and a half years ago on a 30,000-mile journey for my new book, Chasing The Scream: The First And Last Days of the War on Drugs, to figure out what is really driving the drug war, I believed it too. But what I learned on the road is that almost everything we have been told about addiction is wrong — and there is a very different story waiting for us, if only we are ready to hear it.

If we truly absorb this new story, we will have to change a lot more than the drug war. We will have to change ourselves.

I learned it from an extraordinary mixture of people I met on my travels. From the surviving friends of Billie Holiday, who helped me to learn how the founder of the war on drugs stalked and helped to kill her. From a Jewish doctor who was smuggled out of the Budapest ghetto as a baby, only to unlock the secrets of addiction as a grown man. From a transsexual crack dealer in Brooklyn who was conceived when his mother, a crack-addict, was raped by his father, an NYPD officer. From a man who was kept at the bottom of a well for two years by a torturing dictatorship, only to emerge to be elected President of Uruguay and to begin the last days of the war on drugs.

I had a quite personal reason to set out for these answers. One of my earliest memories as a kid is trying to wake up one of my relatives, and not being able to. Ever since then, I have been turning over the essential mystery of addiction in my mind — what causes some people to become fixated on a drug or a behavior until they can’t stop? How do we help those people to come back to us? As I got older, another of my close relatives developed a cocaine addiction, and I fell into a relationship with a heroin addict. I guess addiction felt like home to me.

If you had asked me what causes drug addiction at the start, I would have looked at you as if you were an idiot, and said: “Drugs. Duh.” It’s not difficult to grasp. I thought I had seen it in my own life. We can all explain it. Imagine if you and I and the next twenty people to pass us on the street take a really potent drug for twenty days. There are strong chemical hooks in these drugs, so if we stopped on day twenty-one, our bodies would need the chemical. We would have a ferocious craving. We would be addicted. That’s what addiction means.

One of the ways this theory was first established is through rat experiments — ones that were injected into the American psyche in the 1980s, in a famous advert by the Partnership for a Drug-Free America. You may remember it. The experiment is simple. Put a rat in a cage, alone, with two water bottles. One is just water. The other is water laced with heroin or cocaine. Almost every time you run this experiment, the rat will become obsessed with the drugged water, and keep coming back for more and more, until it kills itself.

The advert explains: “Only one drug is so addictive, nine out of ten laboratory rats will use it. And use it. And use it. Until dead. It’s called cocaine. And it can do the same thing to you.”

But in the 1970s, a professor of Psychology in Vancouver called Bruce Alexandernoticed something odd about this experiment. The rat is put in the cage all alone. It has nothing to do but take the drugs. What would happen, he wondered, if we tried this differently? So Professor Alexander built Rat Park. It is a lush cage where the rats would have colored balls and the best rat-food and tunnels to scamper down and plenty of friends: everything a rat about town could want. What, Alexander wanted to know, will happen then?

In Rat Park, all the rats obviously tried both water bottles, because they didn’t know what was in them. But what happened next was startling.

The rats with good lives didn’t like the drugged water. They mostly shunned it, consuming less than a quarter of the drugs the isolated rats used. None of them died. While all the rats who were alone and unhappy became heavy users, none of the rats who had a happy environment did.

At first, I thought this was merely a quirk of rats, until I discovered that there was — at the same time as the Rat Park experiment — a helpful human equivalent taking place. It was called the Vietnam War. Time magazine reported using heroin was “as common as chewing gum” among U.S. soldiers, and there is solid evidence to back this up: some 20 percent of U.S. soldiers had become addicted to heroin there, according to a study published in the Archives of General Psychiatry. Many people were understandably terrified; they believed a huge number of addicts were about to head home when the war ended.

But in fact some 95 percent of the addicted soldiers — according to the same study — simply stopped. Very few had rehab. They shifted from a terrifying cage back to a pleasant one, so didn’t want the drug any more.

Professor Alexander argues this discovery is a profound challenge both to the right-wing view that addiction is a moral failing caused by too much hedonistic partying, and the liberal view that addiction is a disease taking place in a chemically hijacked brain. In fact, he argues, addiction is an adaptation. It’s not you. It’s your cage.

After the first phase of Rat Park, Professor Alexander then took this test further. He reran the early experiments, where the rats were left alone, and became compulsive users of the drug. He let them use for fifty-seven days — if anything can hook you, it’s that. Then he took them out of isolation, and placed them in Rat Park. He wanted to know, if you fall into that state of addiction, is your brain hijacked, so you can’t recover? Do the drugs take you over? What happened is — again — striking. The rats seemed to have a few twitches of withdrawal, but they soon stopped their heavy use, and went back to having a normal life. The good cage saved them. (The full references to all the studies I am discussing are in the book.)

When I first learned about this, I was puzzled. How can this be? This new theory is such a radical assault on what we have been told that it felt like it could not be true. But the more scientists I interviewed, and the more I looked at their studies, the more I discovered things that don’t seem to make sense — unless you take account of this new approach.

Here’s one example of an experiment that is happening all around you, and may well happen to you one day. If you get run over today and you break your hip, you will probably be given diamorphine, the medical name for heroin. In the hospital around you, there will be plenty of people also given heroin for long periods, for pain relief. The heroin you will get from the doctor will have a much higher purity and potency than the heroin being used by street-addicts, who have to buy from criminals who adulterate it. So if the old theory of addiction is right — it’s the drugs that cause it; they make your body need them — then it’s obvious what should happen. Loads of people should leave the hospital and try to score smack on the streets to meet their habit.

But here’s the strange thing: It virtually never happens. As the Canadian doctor Gabor Mate was the first to explain to me, medical users just stop, despite months of use. The same drug, used for the same length of time, turns street-users into desperate addicts and leaves medical patients unaffected.

If you still believe — as I used to — that addiction is caused by chemical hooks, this makes no sense. But if you believe Bruce Alexander’s theory, the picture falls into place. The street-addict is like the rats in the first cage, isolated, alone, with only one source of solace to turn to. The medical patient is like the rats in the second cage. She is going home to a life where she is surrounded by the people she loves. The drug is the same, but the environment is different.

This gives us an insight that goes much deeper than the need to understand addicts. Professor Peter Cohen argues that human beings have a deep need to bond and form connections. It’s how we get our satisfaction. If we can’t connect with each other, we will connect with anything we can find — the whirr of a roulette wheel or the prick of a syringe. He says we should stop talking about ‘addiction’ altogether, and instead call it ‘bonding.’ A heroin addict has bonded with heroin because she couldn’t bond as fully with anything else.

So the opposite of addiction is not sobriety. It is human connection.

When I learned all this, I found it slowly persuading me, but I still couldn’t shake off a nagging doubt. Are these scientists saying chemical hooks make no difference? It was explained to me — you can become addicted to gambling, and nobody thinks you inject a pack of cards into your veins. You can have all the addiction, and none of the chemical hooks. I went to a Gamblers’ Anonymous meeting in Las Vegas (with the permission of everyone present, who knew I was there to observe) and they were as plainly addicted as the cocaine and heroin addicts I have known in my life. Yet there are no chemical hooks on a craps table.

But still, surely, I asked, there is some role for the chemicals? It turns out there is an experiment which gives us the answer to this in quite precise terms, which I learned about in Richard DeGrandpre’s book The Cult of Pharmacology.

Everyone agrees cigarette smoking is one of the most addictive processes around. The chemical hooks in tobacco come from a drug inside it called nicotine. So when nicotine patches were developed in the early 1990s, there was a huge surge of optimism — cigarette smokers could get all of their chemical hooks, without the other filthy (and deadly) effects of cigarette smoking. They would be freed.

But the Office of the Surgeon General has found that just 17.7 percent of cigarette smokers are able to stop using nicotine patches. That’s not nothing. If the chemicals drive 17.7 percent of addiction, as this shows, that’s still millions of lives ruined globally. But what it reveals again is that the story we have been taught about The Cause of Addiction lying with chemical hooks is, in fact, real, but only a minor part of a much bigger picture.

This has huge implications for the one-hundred-year-old war on drugs. This massive war — which, as I saw, kills people from the malls of Mexico to the streets of Liverpool — is based on the claim that we need to physically eradicate a whole array of chemicals because they hijack people’s brains and cause addiction. But if drugs aren’t the driver of addiction — if, in fact, it is disconnection that drives addiction — then this makes no sense.

Ironically, the war on drugs actually increases all those larger drivers of addiction. For example, I went to a prison in Arizona — ‘Tent City’ — where inmates are detained in tiny stone isolation cages (‘The Hole’) for weeks and weeks on end to punish them for drug use. It is as close to a human recreation of the cages that guaranteed deadly addiction in rats as I can imagine. And when those prisoners get out, they will be unemployable because of their criminal record — guaranteeing they with be cut off even more. I watched this playing out in the human stories I met across the world.

There is an alternative. You can build a system that is designed to help drug addicts to reconnect with the world — and so leave behind their addictions.

This isn’t theoretical. It is happening. I have seen it. Nearly fifteen years ago, Portugal had one of the worst drug problems in Europe, with 1 percent of the population addicted to heroin. They had tried a drug war, and the problem just kept getting worse. So they decided to do something radically different. They resolved to decriminalize all drugs, and transfer all the money they used to spend on arresting and jailing drug addicts, and spend it instead on reconnecting them — to their own feelings, and to the wider society. The most crucial step is to get them secure housing, and subsidized jobs so they have a purpose in life, and something to get out of bed for. I watched as they are helped, in warm and welcoming clinics, to learn how to reconnect with their feelings, after years of trauma and stunning them into silence with drugs.

One example I learned about was a group of addicts who were given a loan to set up a removals firm. Suddenly, they were a group, all bonded to each other, and to the society, and responsible for each other’s care.

The results of all this are now in. An independent study by the British Journal of Criminology found that since total decriminalization, addiction has fallen, and injecting drug use is down by 50 percent. I’ll repeat that: injecting drug use is down by 50 percent. Decriminalization has been such a manifest success that very few people in Portugal want to go back to the old system. The main campaigner against the decriminalization back in 2000 was Joao Figueira, the country’s top drug cop. He offered all the dire warnings that we would expect from the Daily Mail or Fox News. But when we sat together in Lisbon, he told me that everything he predicted had not come to pass — and he now hopes the whole world will follow Portugal’s example.

This isn’t only relevant to the addicts I love. It is relevant to all of us, because it forces us to think differently about ourselves. Human beings are bonding animals. We need to connect and love. The wisest sentence of the twentieth century was E.M. Forster’s — “only connect.” But we have created an environment and a culture that cut us off from connection, or offer only the parody of it offered by the Internet. The rise of addiction is a symptom of a deeper sickness in the way we live — constantly directing our gaze towards the next shiny object we should buy, rather than the human beings all around us.

The writer George Monbiot has called this “the age of loneliness.” We have created human societies where it is easier for people to become cut off from all human connections than ever before. Bruce Alexander — the creator of Rat Park — told me that for too long, we have talked exclusively about individual recovery from addiction. We need now to talk about social recovery — how we all recover, together, from the sickness of isolation that is sinking on us like a thick fog.

But this new evidence isn’t just a challenge to us politically. It doesn’t just force us to change our minds. It forces us to change our hearts.

Loving an addict is really hard. When I looked at the addicts I love, it was always tempting to follow the tough love advice doled out by reality shows like Intervention — tell the addict to shape up, or cut them off. Their message is that an addict who won’t stop should be shunned. It’s the logic of the drug war, imported into our private lives. But in fact, I learned, that will only deepen their addiction — and you may lose them altogether. I came home determined to tie the addicts in my life closer to me than ever — to let them know I love them unconditionally, whether they stop, or whether they can’t.

When I returned from my long journey, I looked at my ex-boyfriend, in withdrawal, trembling on my spare bed, and I thought about him differently. For a century now, we have been singing war songs about addicts. It occurred to me as I wiped his brow, we should have been singing love songs to them all along.

Dog Infects Humans With Plague for First Time in US

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A plague-infected dog spread the dangerous disease to four Colorado residents, according to a new report from the U.S. Centers for Disease Control and Prevention.

Health officials told ABC News that this the first report of a dog infecting a human with the plague in the U.S.

The dog, a 2-year-old American pit bull terrier, became sick last summer with a fever and jaw rigidity, among other symptoms. The dog’s health declined so quickly that it was euthanized the following day at a local vet’s office, health officials said.

Four days later, the dog’s owner entered the hospital with a fever and a bloody cough that became worse over the next few hours, but an initial blood culture was misidentified, according to the CDC report.

As the patient’s symptoms grew worse, the test was redone and he was found to have been infected with pnumonic plague, according to the CDC report. The remains of the dog were also tested and were found to be positive for the plague bacteria.

“Frankly one of the biggest surprises of this outbreak is the source,” said John Douglas, of Tri-County Health Department in Colorado and one of the study authors. “Primarily … dogs don’t get sick at all or they get a minor illness,” after being infected with the plague.

Janine Runfola, of the Tri-County Health Department in Colorado and lead author of the report, explained that cats are more likely to infect humans with the disease than dogs because they exhibit more symptoms.

“For pneumonic plague a more likely scenario would be you have a cat [play] with prairie dogs and infected fleas get on the cat,” Runfola said. “The cat gets sick and sneezes and coughs on its owner.”

The dog’s owner remained hospitalized for 23 days as he recovered from the potentially deadly disease, the report said. In addition to the owner, a close contact of the owner and two veterinary employees who treated the dog or handled its body also became infected with the plague. All three were successfully treated with medication after exhibiting symptoms.

The plague is caused by the bacteria Yersinia pestis, and can infect the body in different ways. For example a flea bite can lead to infection of the glands, which is called bubonic plague — notorious for the epidemics it spawned during the Middle Ages in Europe. Because this plague was spread from dog to owner through coughing, it developed into pneumonic plague, according to Douglas.

The plague is known to be endemic to prairie dogs in the American Southwest, which can then lead to isolated outbreaks of the disease in domestic animals or humans.

“Pneumonic plague is the worst form,” said Douglas. “It’s the one that you least want to get. You get sick fast and the chances of getting a rocky or even fatal course” are increased.

The plague is incredibly rare in the U.S. with an estimated eight infections in the country reported every year. Douglas said pneumonic plague is even rarer and accounts for just 3 to 5 percent of plague cases.

Douglas said the case shows the importance of considering all the options when diagnosing a patient, even extremely rare options like the plague.

The dog’s owner remained hospitalized for 23 days as he recovered from the potentially deadly disease, the report said. In addition to the owner, a close contact of the owner and two veterinary employees who treated the dog or handled its body also became infected with the plague. All three were successfully treated with medication after exhibiting symptoms.

The plague is caused by the bacteria Yersinia pestis, and can infect the body in different ways. For example a flea bite can lead to infection of the glands, which is called bubonic plague — notorious for the epidemics it spawned during the Middle Ages in Europe. Because this plague was spread from dog to owner through coughing, it developed into pneumonic plague, according to Douglas.

The plague is known to be endemic to prairie dogs in the American Southwest, which can then lead to isolated outbreaks of the disease in domestic animals or humans.

“Pneumonic plague is the worst form,” said Douglas. “It’s the one that you least want to get. You get sick fast and the chances of getting a rocky or even fatal course” are increased.

The plague is incredibly rare in the U.S. with an estimated eight infections in the country reported every year. Douglas said pneumonic plague is even rarer and accounts for just 3 to 5 percent of plague cases.

Douglas said the case shows the importance of considering all the options when diagnosing a patient, even extremely rare options like the plague.

 

Deep-Space Radiation Could Damage Astronauts’ Brains .

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Cosmic rays could leave travelers to Mars confused, forgetful and slow to react

As NASA develops plans for a manned mission to Mars, scientists said Friday that cosmic rays during an interplanetary voyage could cause subtle brain damage, leaving astronauts confused, forgetful and slow to react to the unexpected.

In a NASA-funded study of radiation-exposed mice published Friday in Science Advances, researchers at the University of California, Irvine and the University of Nevada warned that prolonged bombardment by charged particles in deep space could affect the brain cells involved in decision-making and memory, with implications for possible manned forays into deep space.

“These sorts of cognitive changes could manifest during the mission and could be a real problem,” said Cary Zeitlin at the Southwest Research Institute in San Antonio, who wasn’t involved in the study. In 2013, Dr. Zeitlin reported radiation levels between Earth and Mars detected by the Mars Science Laboratory craft during its cruise to the red planet, and found that the exposure was the equivalent of getting “a whole-body CT scan once every 5 or 6 days.”

Deep-space radiation is a unique mix of gamma rays, high-energy protons and cosmic rays from newborn black holes, and radiation from exploding stars. Earth’s bulk, atmosphere and magnetic field blocks or deflects most deep-space cosmic rays. Shielding on spacecraft also helps.

In 54 years of human spaceflight, astronauts have rarely experienced a full dose. Apollo crews, who ventured furthest from Earth’s protective shield on their journeys to the Moon, reported seeing flashes of light when they closed their eyes, caused by galactic cosmic rays speeding through their retinas.

Researchers at the National Aeronautics and Space Administration have studied the potential health hazards of space radiation for decades, including the elevated risk of cancer. But it has been hard to simulate the behavioral effects of prolonged exposure to low levels of radiation that would be encountered by interplanetary travelers.

Although NASA funded the new experiment, the agency declined requests for interviews with its own radiation experts.

A NASA representative instead issued a written statement: “NASA recognizes the importance of understanding the effects of space radiation on humans during long-duration missions beyond Earth orbit, and these studies and future studies will continue to inform our understanding as we prepare for the journey to Mars.”

To test the neural effects of deep-space travel, a dozen researchers led by UC Irvine radiation oncologist Charles Limoli briefly exposed mice to charged particles in a radiation beam at the U.S. Department of Energy’s Brookhaven National Laboratory in Upton, N.Y. Six weeks later, they tested the irradiated mice and found the lab animals lacked normal curiosity, were less active, and became more easily confused, compared with a control group, the researchers said.

“Their curiosity is way down,” said Dr. Limoli. “They don’t want to explore novelties.”

The researchers found the mice had damaged neurons and synapses in areas associated with memory and decision-making, such as the hippocampus and prefrontal cortex.

“I don’t think our findings preclude future space missions,” Dr. Limoli said. “But they suggest we need to come up with some engineering solutions.”

Eye Stem Cell Therapy Moves Ahead

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Scientists in Korea have injected human embryonic stem cell (hESC)-derived retinal support cells into the eyes of four men with macular degeneration, according to a study published today (April 30) inStem Cell Reports. Three of the men experienced vision improvements in their treated eyes in the year following the procedure, while the fourth man’s vision remained largely the same. The trial adds to growing evidence that injecting hESC-derived cells is feasible, feeding hopes for their future therapeutic use.

This latest study follows on two papers published inThe Lancet in 2012 and 2014, which similarly demonstrated that hESC-derived cells could be safely injected into the space behind the retina in macular degeneration patients. These studies, sponsored by the Massachusetts-based company Advanced Cell Technology (now Ocata Therapeutics), were the first published accounts describing the application of hESC-based therapies in humans.

Korean company CHA Biotech carried out the new trial. Ocata provided the hESCs and some methodological instruction. “Together with the results here in the US, I think this bodes well for the future of stem cell therapies,” said study coauthor Robert Lanza, chief scientific officer at Ocata.

Jeanne Loring, a stem cell researcher at the Scripps Research Institute in La Jolla, California, agreed that the apparent safety of the therapy in the subjects tested is encouraging. However, she added, it would be difficult to draw firm conclusions about efficacy based on such a small study. “I think it’s still anecdotal that some people seem to improve,” said Loring.

“At least it shows safety,” said Magdalene Seiler, a project scientist at the University of California, Irvine. “Whether it works in the long term is up for debate.”

Like many other teams working to develop stem cell-based therapies, the Ocata-led team sought to treat a disease of the eyes in part because the organs are accessible. For the current study, the researchers treated two men with dry age-related macular degeneration, aged 65 and 79, as well as a 40-year-old man and a 45-year-old man, both with Stargardt macular dystrophy, an earlier-onset inherited disease. Both forms of macular degeneration lead to vision loss resulting from the destruction of retinal pigment epithelium (RPE) cells. RPE cells support retinal photoreceptor cells by nourishing them and cleaning up their waste. Without functional RPEs, retinal photoreceptors die.

The researchers differentiated hESCs into RPE cells and injected them into one eye of each patient, hoping that the transplanted RPE cells would take root and replace those that had been lost, preventing further loss of photoreceptors. Lanza explained that “the goal of the therapy was not to improve vision.”

Even so, the vision of three of the men improved by two to four lines of letters on a standard vision test. The vision of the fourth patient, the older man with age-related macular dystrophy, improved by just one letter —a negligible change.

Because of the study size, it is too early to conclude whether the treatment systematically improves vision in patients, said Lanza. However, he hypothesized that patients could have experienced vision improvements because the infusion of new RPE cells revived photoreceptors that had gone dormant but were not yet dead.

Lanza was also encouraged to see that the transplanted cells did not form tumors or differentiate into cells other than RPEs, a major concern among researchers in the field. Regulators “don’t really want to see a tooth in the eye or they don’t want to see beating heart cells in the wrong place,” Lanza said. By carefully screening all cells transplanted into patients, researchers were able to avoid transplanting cells that were not fully differentiated and could, therefore, have formed unwanted tissues.

The scientists were also relieved to see that the patients’ immune systems did not reject the transplanted cells. Like the brain, the eye is immune privileged, meaning that it is largely inaccessible to immune cells. To be safe, the researchers still gave the patients immunosuppressive drugs for a limited period before and following the surgery. It is unclear whether this was necessary.

Finally, by focusing on men of Asian descent, the study added to the diversity of the small group of patients who have received transplanted hESC-derived cells. The previous Lancet studies largely focused on Caucasian patients. Asian and Caucasian patients have different alleles that contribute to risk for age-related macular degeneration.

CHA Biotech is hopeful to get the go-ahead from Korean regulators to proceed with Phase 2 trials using hESC-derived cells to treat Stargardt macular dystrophy this year.

Ocata, meanwhile, will start Phase 2 trials for both Stargardt macular dystrophy and age-related macular degeneration in the “next several months,” according to Lanza. Meanwhile, researchers at the RIKEN Center for Developmental Biology in Japan last year began a trial to test induced pluripotent stem cell (iPSC)-derived RPE cells for the treatment of macular degeneration.

The new work adds to the climate of hope for stem cell therapies. “It’s inspiring other scientists,” said Loring, whose team is working to eventually treat people with Parkinson’s disease with iPSC-based therapies. “It makes us feel like we’ll be able to do similar things in whatever diseases we’re studying.”

W.K. Song et al., “Treatment of macular degeneration using embryonic stem cell-derived retinal pigment epithelium: preliminary results in Asian patients,” Stem Cell Reports,doi:10.1016/j.stemcr.2015.04.005, 2015.

Interview with 102 Year Old Doctor And Still Working

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The last surviving member of the Stanford class of 1933, Dr. Ephraim Engleman, is turning 102 in a few weeks. He serves as a shining example of healthy longevity — he continues to work part-time, filling his role as director of the Rosalind Russell Medical Research Center for Arthritis and occasionally seeing patients. Dr. Engleman told us he has no intentions of retiring. A violinist and music prodigy since the age of 6, he continues to play the violin regularly, hosting chamber music meetings at his home every Monday night. Dr. Engleman lives in San Mateo with his wife, Jean, who is 97. They have three children, whose achievements are as impressive as his, and six grandchildren.
It’s hard for us at Home Care Assistance to not be amazed by Dr. Engleman’s graceful aging, which he attributes in part to his work, music and successful family life. We want to thank Dr. Engleman for sitting down with us to share his secret to healthy longevity and living a happy life — we now have the honor to share his wisdom with you.

What do you think is the secret to aging well? Do you think continuing to work past the traditional retirement age has contributed to your healthy longevity?


I think that continuing to work past the traditional retirement age does indeed contribute — I think it’s contributed to my longevity. Now there are exceptions. But it’s obvious that some people can retire from what they’re doing and go on to other things that keep them mentally and physically active; in that case you’re sort of retiring from one thing and going on to something else. But if you don’t have [a new hobby or activity of interest], then I think one is making a terrible mistake.

We’ve read your 10 commandments for longevity in the San Francisco Gate from 2011. They gave us a good laugh. Would you modify these in any way today? Have any recent events made you feel differently about these tips? Which do you think is the most important?


Most of those are facetious. I think I did it simply to indicate that I really don’t know, but there are certain things that I do recommend. I would re-emphasize the importance of avoiding falls at all costs. That is terribly important. As we get older we tend to lose balance a little bit and falls can be very serious and cause all kinds of problems. Falls, particularly in the elderly, not only can cause serious fractures, but as a result, there can be serious effects on the heart and on blood pressure. I think hobbies can be helpful. In my case, music has been very helpful, emotionally.

What initially drew you towards rheumatology?

When I was a senior resident in medicine in Boston, I heard a man by the name of Walter Bauer, who was doing some pioneer research in arthritis, speak and I was very impressed by what he had to say. He was a professor at Harvard and worked at the Massachusetts General Hospital in Boston. He had a very limited number of fellowships available. Believing that I had nothing to lose, I applied for one of these fellowships without any real expectation I would get into the program. When I was visiting him at the hospital somebody came and interrupted us and said, “Ward rounds are about to start.” Dr. Bauer said, “Would you like to join us on these ward rounds?” and I said “Sure.”
We visited several patients, one of whom had a heart murmur that was a musical murmur. Heart murmurs generally are just a noise that one hears through the stethoscope but rarely does someone have a musical murmur — a murmur that really rings a note. I’m telling you all this because when they heard this note, they were ordering a test that would demonstrate the number of vibrations of this musical note. I said, as I wasn’t very shy, “I don’t need that test; I know how many vibrations it is.” What they didn’t know was that I had perfect pitch, so I knew exactly what note it was and how many vibrations there were. When I told Dr. Bauer this he said that I didn’t need an interview and awarded me the fellowship. I say all of this because that’s the way I became a rheumatologist — through my musical background and my perfect pitch.

What are some of your most cherished memories and why?

There are a lot of things that have happened over my lifetime that were very happy. I have three gold medals — they’re very flattering — one from my medical school, one from UCSF and one from the Professional Society of the United States, the American College of Rheumatology. These gold medals represent recognition, top quality. I’ve been, over the years, the leader in rheumatology as president of the American College of Rheumatology; president of the International League Against Rheumatism, which is in about 40 countries; and I was also chairman of a very important commission.
Rosalind Russell, a very beloved stage and screen actress, developed severe arthritis in her later years (during the 1950s). At that time, there weren’t many doctors who knew anything about arthritis and she was very frustrated. She was able to leverage her notoriety and successfully lobby Congress to pass legislation; the National Arthritis Act was signed by President Ford in 1970 to create a commission which would come up with recommendations on how to improve education and research around arthritis in the United States. I was appointed as the chairman of that commission and so that was a very happy event in my life. When Rosalind died, Congress decided there should be a center for arthritis research designated in her name. The center was developed at UCSF and I’ve been the director of it ever since. That was 1979.
Now there are some things that were very disappointing. When I was an intern at Mt. Zion hospital in San Francisco I had been promised to become a resident — you know, in medical training, a man or a woman starts as an intern in the hospital and then the next step up is you become a resident who is in charge of the interns. Well I had been promised to become a resident by everybody except the chief; the chief vetoed it and decided to give it to somebody else. That was a great disappointment to me. I thought, “Oh, there goes my career” and I was very, very depressed. I got another job there as a resident in pathology. During my year in pathology I did a study on patients who had cancer of the pancreas and I presented this at a meeting of doctors including the chief who had turned me down previously. He was so impressed by this paper that he got me the job here at UCSF as a resident.
I’ve had a couple of medical problems. One was a ruptured appendix, which can be fatal but it wasn’t, I was lucky. And then I had a minor cardiac problem three years ago resulting in a stent. But I think the greatest misfortunes that I have and I still have are related to my ability to play the violin or piano. I had carpal tunnel syndrome. My symptoms were progressing so I had surgery on [my] right hand and the result has been a disaster — I’ve lost all sensitivity in most of the hand. So it makes it difficult to bow.
More recently I’ve developed a slipping tendon in one finger of my left hand which I guess is the result of age, so it interferes with my ability to use my ring finger on my left hand. The results of these are very depressing — not earth-shaking, but it interferes seriously with my ability as a violinist. I am still playing; my colleagues know the problem and they tolerate me.

Who is/was your biggest inspiration and why?
Well, right now, I would say my wife, Jean.

How long have you and Jean been married?
Seventy-two years in March.

Do you have any advice for the secrets to a happy marriage?
Pick the right companion. It’s been a wonderful marriage and we have wonderful children who have been successful, I have been successful — all of which contributes to a happy marriage. I do feel that a happy marriage and a happy family are important factors that contribute to longevity.

Air Pollution in China Linked to Lower Birth Weights

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Oil refinery with vapor - petrochemical industry at night

Air pollution in China is linked to lower birth weights, as evidenced by a new study published in Environmental Health Perspectives.

In response to international scrutiny preceding the 2008 Olympic games, the Chinese government restricted automobile use, closed factories and imposed a moratorium on construction projects in an effort to reduce air pollution. University of Rochester researchers followed 80,000 women who were pregnant in Beijing in 2008 to track fetal growth and development.

The good news: the presence of certain air pollutants in Beijing decreased up to 60% during the Olympics, and babies born in 2008 were an average of 8 ounces heavier than those born in 2007.

The bad news: the restrictions were only temporary, and have since been rescinded. The birth weight of babies born in 2009 dropped back down to 2007 levels as air pollution rebounded.

Low birth weight is associated with a variety of conditions; babies born weighing less than 5 pounds, 8 ounces are at a higher risk of inhibited growth and cognitive development than babies born at a healthy weight.

Researchers believe that fetuses are especially vulnerable to air pollution during the later stages of pregnancy, a period of development for the central nervous, cardiovascular, and skeletal systems.

“While Beijing’s pollution is particularly noteworthy, many of the world’s other cities face similar air quality problems,” said study co-author Dr. Junfeng Zhang. “This study shows that pollution controls i even short-term ones i can have positive public health benefits.”

The ‘HemoLink’ Could Be How Blood Samples Are Taken In The Future

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Needle phobics of the world, rejoice! A Wisconsin start-up, Tasso Inc, has come up with a needle-free way of drawing blood for tests. Yup, you read that right… no needles! The clever little device would use a vacuum-like process, utilizing micro-fluid properties, to draw blood from below the skin without having to puncture it or use any kind of needle. It will only be able to draw 0.15 of a cubic centimeter of blood, but that is enough to test for blood sugar, cholesterol, cancer cells and infection. There would even be the option to post your blood sample to be tested, negating the need to attend a clinic at all, which is excellent news for those who dislike doctors almost as much as they dislike needles. The device is still being developed, but it could be available as soon as late 2016. Cool!

 

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The case for genetically engineered babies

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The first study to modify the genes of a human embryo, conducted at Sun Yat-sen University in China, has caused a furious backlash. Nature and Science, the world’s most prestigious scientific journals refused to publish the study, at least partly on ethical grounds. Instead they published commentaries calling for such research to be stopped. On Wednesday, the US government’s National Institutes of Health (NIH) restated their position that it will “not fund any use of gene-editing technologies in human embryos.” The NIH views such editing of the “germline” in human embryos as “a line that should not be crossed.” The stance will essentially stifle any research on gene editing in embryos in the US.

An illustration of a DNA strand. We know that some genes are bad in nearly every conceivable environment; do we lose anything by editing them out of the human lineage?

The ultimate goal of gene editing technologies is the capacity to make precise, controlled modifications to very specific areas of the genome. This would be a powerful ability. Gene editing unlocks access to an entirely novel way to fight disease which has been unreachable until now.
Scientists genetically modify human embryos in controversial world first

Around 7.9 million children each year are born with a serious birth defect that has a significant genetic contribution. If we could safely and easily correct these errors at the embryonic stage it would be possible to virtually eradicate this disease burden. In addition, 30% of all deaths worldwide are due to chronic diseases (such as heart disease, cancer, and diabetes) in those under 70. We all know of people who seem innately resistant to the perils of ageing and flourish well into their 80s and 90s. Gene editing could ensure we all have the best chance to live healthily into old age.

There are many challenges we must overcome to access the benefits of gene editing. The first and foremost is safety. Under agreed global research ethics standards, no experiments should be conducted where there is a high risk of harm to the participant, and a low chance of benefit. Gene editing is a long way from overcoming this barrier. Current techniques are imprecise, and lead to widespread damage to the genome. It would be highly unethical if a child was born whose genome was edited with current techniques.

Science Weekly Should we genetically engineer humans? – podcast
The team look at the rapid rise of genome editing procedures and the power scientists now have to tinker with human DNA. Where’s the technology going? And where should it stop?

However, we can still perform important research with current gene editing technologies in ways which harm no one. The pioneering Chinese study was performed entirely on abnormal, unviable IVF embryos that could never result in a live birth. Gene editing techniques could be greatly advanced by experiments conducted entirely in petri dishes, with embryos that would otherwise be destroyed and in accordance with existing regulations. The UK has a comprehensive and well-established regulatory framework for embryo research, including provisions that only embryos under 14 days old be used. This framework has successfully guided research involving embryos for over two decades.

Many fear that such research will lead us on a path to “designer babies”. People shudder at the thought of parents picking and choosing the genes of their children, just as they pick and choose the accessories for their nurseries. And we have good reasons to be concerned about this prospect. Widespread access to gene editing technologies could harm children and damage the gene pool. Genes fashionable in one generation may prove to be harmful in the next. In addition, parental control of the gene pool could reduce valuable forms of diversity. If every parent picks the same immunity genes for their children, it may make them collectively as vulnerable to pathogens as 19th century Irish potatoes.

But a fear of designer babies should not distract us from the goal of healthy babies. We know that some genes are bad in nearly every conceivable environment. There is no possible way that the gene which causes Tay-Sachs disease – a disease in which children develop normally for six months and then become progressively deaf, blind, unable to swallow, and paralytic, before dying at four – will benefit future generations. We lose nothing by editing this gene out of the human lineage.

There is no reason why we couldn’t restrict the use of gene editing technologies to removing valueless genes like this. For over two decades we have successfully used IVF and pre-implantation diagnosis (PGD) in this way. Regulations restrict the use of these technologies to the prevention of disease. Similar regulations could restrict gene editing technologies to therapeutic uses.

Some see unpredictable consequences, rather than designer babies, as the key risk in crossing the line to edited embryos. They see meddling with our genome as inherently dangerous – no matter which genes we target. Just dipping our toes in the gene pool will cause large ripples. These ripples will cause chaotic and uncontrollable consequences. According to this view it would be far wiser not to dip our toes in at all.

But the gene pool is a violent ocean rather than a peaceful pond. The human germline is in a constant state of flux. Every new birth adds new genetic variants, and each death removes some. Many permitted human activities, like delaying paternity, add to this chaos by increasing the number of random mutations in the germline. Any ripples caused by targeted therapeutic gene editing will likely be dwarfed by other factors.

No matter what is done in the UK, the line to edited embryos and intentional germline modifications will be crossed soon. In the US, work can go ahead with funding from foundations, charities, companies or private individuals. China will race ahead. Others will likely follow. If we want gene editing research to be done in a responsible way, we need countries with good regulatory systems leading the charge. The UK is one such country, where the Human Fertilisation and Embryology Authority can provide reassurance that no research or application proceeds without proper evaluation.

Whoever first crosses the line to edited embryos will find a powerful new resource in the fight against disease. Like many resources there are risks associated with its use. Indeed the risks are very high. However ignoring the resource is also risky. We may needlessly subject future generations to an endless cycle of suffering and disease.

What we ought to do is use this resource responsibly. We should harness its power to achieve good ends and restrict its use for purposes that are bad. This will not be achieved by simply withdrawing from research. It’s time to mount a responsible expedition across the line to edited embryos and the UK should lead the way.

Light — not pain-killing drugs — used to activate brain’s opioid receptors .

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Despite the abuse potential of opioid drugs, they have long been the best option for patients suffering from severe pain. The drugs interact with receptors on brain cells to tamp down the body’s pain response. But now, neuroscientists at Washington University School of Medicine in St. Louis have found a way to activate opioid receptors with light.

In a test tube, the scientists melded the light-sensing protein rhodopsin to key parts of opioid receptors to activate receptor pathways using light. They also influenced the behavior of mice by injecting the receptors into the brain, using light instead of drugs to stimulate a reward response.

Their findings are published online in the journal Neuron.

The eventual hope is to develop ways to use light to relieve pain, a line of discovery that also could lead to better pain-killing drugs with fewer side effects.

“It’s conceivable that with much more research we could develop ways to use light to relieve pain without a patient needing to take a pain-killing drug with side effects,” said first author Edward R. Siuda, a graduate student in the laboratory of Michael R. Bruchas, PhD, an assistant professor of anesthesiology and of neurobiology.

But before that’s possible, the researchers are attempting to learn the most effective ways to activate and deactivate the opioid receptor’s pathways in brain cells. Bruchas, the study’s principal investigator, explained that working with light rather than pain-killing drugs makes it much easier to understand how the receptors function within the complex array of cells and circuits in the brain and spinal cord.

“It’s been difficult to determine exactly how opioid receptors work because they have multiple functions in the body,” Bruchas explained. “These receptors interact with pain-killing drugs called opiates, but they also are involved in breathing, are found in the gastrointestinal tract and play a role in the reward response.”

So the researchers sought a way to limit opioid receptors to performing a single task at a time, and it turned out to be almost as easy as flipping on a light switch, according to Bruchas, Siuda and their collaborators, including co-first author Bryan A. Copits, PhD, a postdoctoral research scholar in the laboratory of Robert W. Gereau, IV, PhD, the Dr. Seymour and Rose T. Brown Professor of Anesthesiology.

By combining the rhodopsin protein, which senses light in the eye’s retina, with a specific type of opioid receptor called a Mu opioid receptor, the researchers were able to build a receptor that responds to light in exactly the same way that standard opioid receptors respond to pain-killing drugs.

When an opioid receptor is exposed to a pain-killing drug, it initiates activity in specific chemical pathways in the brain and spinal cord. And when the researchers shone light on the receptors that contained rhodopsin, the same cellular pathways were activated.

In a test tube and in cells, Siuda exposed the receptors to light and then watched as they released the same chemicals that standard opioid receptors release. Then, in mice, the researchers implanted a light-emitting diode (LED) device the size of a human hair into a brain region linked to the reward response. They injected the light-sensing receptors they had genetically manufactured into the same brain region. Neurons in that part of the brain release chemicals such as dopamine that create feelings of euphoria.

In decades of past opioid studies, researchers have observed mice and rats to press a lever to receive a dose of morphine, for example. The morphine would activate opioid receptors and the release of dopamine, and the animals would enjoy the response and press the lever again to continue feeling that reward sensation. This is one of the reasons opiates are so often abused in patients being treated for pain — people like the way the drugs make them feel as much as the pain relief  they provide — and rates of abuse have skyrocketed over the past ten years.

Working to deliver a similar reward sensation using light, the researchers put the mice into an enclosed chamber. In one part of the chamber, the lighted laser fiber-optic device stimulated the release of dopamine in the brain. When the animals left that part of the chamber, the light in the brain turned off. Soon after, the mice returned to the part of the chamber that activated the fiber-optic device so that the brain could receive more light stimulation.

“By activating the receptors with light, we are presumably causing the brain to release more dopamine,” Bruchas explained. “Rather than a drug such as morphine activating an opioid receptor, the light provides the reward.”

The researchers were able to vary the animals’ response depending on the amount and type of light emitted by the LED. Different colors of light, longer and shorter exposure to light, and whether the light pulsed or was constant all produced slightly different effects.

When a person takes an opioid drug such as Vicodin or OxyContin to relieve pain, such drugs interact with receptors in the brain to blunt pain sensations. But over time, patients develop tolerance and sometimes addiction. Opioids also can dramatically slow a person’s breathing, too, and typically cause constipation.

In theory, receptors tuned to light may not present the same danger. Siuda said it someday may be possible to activate, or deactivate, nerve cells without affecting any of the other receptors that pain-killing drugs trigger, although achieving that goal will be difficult.

Bruchas’ team is planning future studies that will use these receptors to test ways to control the brain cells that mediate pain and reward behavior with light rather than drugs.

– See more at: http://www.neuroscientistnews.com/research-news/light-not-pain-killing-drugs-used-activate-brain-s-opioid-receptors#sthash.x1aqXxOs.dpuf

From Foe to Friend: Viruses Show New Promise as Cancer Treatment .

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Almost as long as scientists have known of the existence of viruses, they’ve dreamed of using the tiny pathogens as a weapon against cancer. Now, as a result of advances in genetic engineering and insights into the workings of the immune system, science is giving substance to the dream.

A variety of studies over the past few years have demonstrated the ability of specially modified viruses to attack and kill cancer cells – in the laboratory and, very recently, in some patients. Techniques vary from study to study, but the basic approach is to inject the viruses directly into tumors – allowing the virus to infect and kill many of the cancer cells and, equally important, to stimulate the immune system to launch its own assault on the tumor.

One high-profile example of this approach, reported recently on CBS News’ “60 Minutes,” involved researchers at Duke University who treated patients with glioblastoma with a modified polio virus. In a small, early study, 11 of 22 patients showed substantial improvement from the regimen.

Other research attracting journalistic attention is a clinical trial at the Mayo Clinic that uses the measles virus to treat patients with multiple myeloma. Investigators found that after infecting cancer cells, the virus causes them to clump together and disintegrate. The wreckage may trigger an immune system response that can prevent the disease from returning for a long period of time, researchers have suggested.

At Dalhousie University in Halifax, Nova Scotia, scientists have shown that reoviruses – common, benign viruses often found in the respiratory tract – can be engineered to specifically infect melanoma cells. The infection appears to prompt an immune system attack that kills not only the infected cells but also the uninfected cancer cells nearby. In early-stage clinical trials, the treatment has been shown to be effective in some patients with melanoma and, when coupled with chemotherapy, in some patients with head and neck cancers.

“There have been efforts to use viruses in cancer therapy for more than 50 years, but we now have more of a grasp of what’s going on, and why some viruses work better than others,” says Harvey Cantor, MD, chair of Dana-Farber’s Department of Immunology and AIDS. A key component to this understanding, Cantor says, is that the impact of the virus should not only kill the tumor cells, but it should also initiate a T cell immune response that destroys the primary tumor as well as metastases.

Cantor says researchers are also looking at combining this treatment approach with immune-checkpoint inhibitors, which can help “take the brakes off” the immune system and enhance the patient’s anti-tumor response.

“It’s a treatment concept that is very interesting and certainly has a lot of promise,” Cantor says.