Bullying by Childhood Peers Leaves a Trace That Can Change the Expression of a Gene Linked to Mood

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A recent study by a researcher at the Centre for Studies on Human Stress (CSHS) at the Hôpital Louis-H. Lafontaine and professor at the Université de Montréal suggests that bullying by peers changes the structure surrounding a gene involved in regulating mood, making victims more vulnerable to mental health problems as they age.

The study published in the journal Psychological Medicine seeks to better understand the mechanisms that explain how difficult experiences disrupt our response to stressful situations. “Many people think that our genes are immutable; however this study suggests that environment, even the social environment, can affect their functioning. This is particularly the case for victimization experiences in childhood, which change not only our stress response but also the functioning of genes involved in mood regulation,” says Isabelle Ouellet-Morin, lead author of the study.

A previous study by Ouellet-Morin, conducted at the Institute of Psychiatry in London (UK), showed that bullied children secrete less cortisol — the stress hormone — but had more problems with social interaction and aggressive behaviour. The present study indicates that the reduction of cortisol, which occurs around the age of 12, is preceded two years earlier by a change in the structure surrounding a gene (SERT) that regulates serotonin, a neurotransmitter involved in mood regulation and depression.

To achieve these results, 28 pairs of identical twins with a mean age of 10 years were analyzed separately according to their experiences of bullying by peers: one twin had been bullied at school while the other had not. “Since they were identical twins living in the same conditions, changes in the chemical structure surrounding the gene cannot be explained by genetics or family environment. Our results suggest that victimization experiences are the source of these changes,” says Ouellet-Morin. According to the author, it would now be worthwhile to evaluate the possibility of reversing these psychological effects, in particular, through interventions at school and support for victims.

Journal Reference:

1.I. Ouellet-Morin, C. C. Y. Wong, A. Danese, C. M. Pariante, A. S. Papadopoulos, J. Mill, L. Arseneault. Increased serotonin transporter gene (SERT) DNA methylation is associated with bullying victimization and blunted cortisol response to stress in childhood: a longitudinal study of discordant monozygotic twins. Psychological Medicine, 2012; DOI: 10.1017/S0033291712002784

http://www.sciencedaily.com/releases/2012/12/121218081615.htm

The brain’s natural valium

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Hitting the wall in the middle of a busy work day is nothing unusual, and a caffeine jolt is all it takes to snap most of us back into action. But people with certain sleep disorders battle a powerful urge to doze throughout the day, even after sleeping 10 hours or more at night. For them, caffeine doesn’t touch the problem, and more potent prescription stimulants aren’t much better. Now, a study with a small group of patients suggests that their condition may have a surprising source: a naturally occurring compound that works on the brain much like the key ingredients in chill pills such as Valium and Xanax.

The condition is known as primary hypersomnia, and it differs from the better known sleep disorder narcolepsy in that patients tend to have more persistent daytime sleepiness instead of sudden “sleep attacks.” The unknown cause and lack of treatment for primary hypersomnia has long frustrated David Rye, a neurologist at Emory University in Atlanta. “A third of our patients are on disability,” he says, “and these are 20- and 30-year-old people.”

Rye and colleagues began the new study with a hunch about what was going on. Several drugs used to treat insomnia promote sleep by targeting receptors for GABA, a neurotransmitter that dampens neural activity. Rye hypothesized that his hypersomnia patients might have some unknown compound in their brains that does something similar, enhancing the activity of so-called GABAA receptors. To try to find this mystery compound, he and his colleagues performed spinal taps on 32 hypersomnia patients and collected cerebrospinal fluid (CSF), the liquid that bathes and insulates the brain and spinal cord. Then they added the patients’ CSF to cells genetically engineered to produce GABAA receptors, and looked for tiny electric currents that would indicate that the receptors had been activated.

In that first pass, nothing happened. However, when the researchers added the CSF and a bit of GABA to the cells, they saw an electrical response that was nearly twice as big as that caused by GABA alone. All of this suggests that the patients’ CSF doesn’t activate GABAA receptors directly, but it does make the receptors almost twice as sensitive to GABA, the researchers report today in Science Translational Medicine. This effect is similar to that of drugs called benzodiazepines, the active ingredients in antianxiety drugs such as Valium. It did not occur when the researchers treated the cells with CSF from people with normal sleep patterns.

Follow-up experiments suggested that the soporific compound in the patients’ CSF is a peptide or small protein, presumably made by the brain, but otherwise its identity remains a mystery.

The idea that endogenous benzodiazepinelike compounds could cause hypersomnia was proposed in the early 1990s by Elio Lugaresi, a pioneering Italian sleep clinician, says Clifford Saper, a neuroscientist at Harvard Medical School in Boston. But several of Lugaresi’s patients later turned out to be taking benzodiazepines, which undermined his argument, and the idea fell out of favor. Saper says the new work makes a “pretty strong case.”

Based on these results, Rye and his colleagues designed a pilot study with seven patients using a drug called flumazenil, which counteracts benzodiazepines and is often used to treat people who overdose on those drugs. After an injection of flumazenil, the patients improved to near-normal levels on several measures of alertness and vigilance, the researchers report. Rye says these effects lasted up to a couple hours.

In hopes of longer-lasting benefits, the researchers persuaded the pharmaceutical company Hoffmann-La Roche, which makes the drug, to donate a powdered form that can be incorporated into dissolvable tablets taken under the tongue and a cream applied to the skin. One 30-something patient has been taking these formulations for 4 years and has improved dramatically, the researchers report in the paper. She has resumed her career as an attorney, from which her hypersomnia had forced her to take a leave of absence.

The findings are “certainly provocative,” Saper says, although they’ll have to be replicated in a larger, double-blind trial to be truly convincing.

Even so, says Phyllis Zee, a neurologist at Northwestern University in Evanston, Illinois: “This gives us a new window into thinking about treatments” for primary hypersomnia. “These patients don’t respond well to stimulants,” Zee says, so a better strategy may be to inhibit the sleep-promoting effects of GABA—or as Rye puts it, releasing the parking brake instead of pressing the accelerator.

The next steps are clear, Rye says: Identify the mystery compound, figure out a faster way to detect it, and conduct a larger clinical trial to test the benefits of flumazenil. However, the researchers first need someone to fund such a study. So far, Rye says, they’ve gotten no takers.

http://news.sciencemag.org/sciencenow/2012/11/putting-themselves-to-sleep.html

How gender stereotypes warp our view of depression

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Stereotypes about male and female roles may influence the way we perceive depressed people.

It’s a well-known fact that men and women who behave the same way in the exact same situation—whether it’s a job interview, a cocktail party, or a traffic stop—are sometimes perceived and treated differently based on their gender.

Something similar, it seems, may happen when men and women start to show signs of depression. A new study, published this week in the journal PLoS ONE, suggests that people of both sexes are less likely to view men as being depressed and in need of professional help—even if a man’s symptoms are identical to a woman’s.

“A lot of attention has been paid to depression in women, and with good reason: Depression is twice as common in women,” says Dr. James B. Potash, the editor of the study and a professor of psychiatry at the University of Iowa, in Iowa City. “There has been relatively little focus on education about depression in men. This [study] emphasizes the importance of figuring out how to get through to men that depression can be disabling and treatment is important.”

Health.com: 12 Signs of Depression in Men

In the study, researchers in the U.K. asked a group of about 600 adults to read a short description of a hypothetical depressed person. This vignette, which was designed to illustrate the diagnostic criteria for clinical depression (also known as major depression), read in part:

For the past two weeks, Kate has been feeling really down. She wakes up in the morning with a flat, heavy feeling that sticks with her all day. She isn’t enjoying things the way she normally would. In fact, nothing gives her pleasure. Even when good things happen, they don’t seem to make Kate happy.

Fifty-seven percent of the study participants recognized Kate’s symptoms—which also included difficulty concentrating, fatigue, and insomnia—as indications of a mental health disorder, and more than three-quarters of those people correctly identified the disorder as depression. Only 10% of the respondents said Kate did not have a problem.

The researchers presented the same vignette to another group of 600 people. This time, however, every mention of “Kate” was replaced by “Jack,” and all the pronouns were switched from female to male. Those minor changes had a noticeable effect: Though nearly as many people recognized Jack as having a mental health problem (52%), more than twice as many as in the Kate scenario said he did not (21%).

In addition, men themselves were less likely than women to label Jack depressed—a pattern that was not seen with Kate.

Health.com: How to Help Someone Who’s Depressed

Why the difference? Male stereotypes that emphasize traits such as toughness and strength may dissuade both women and men, and especially the latter, from identifying or acknowledging the signs of depression in men, says study author Viren Swami.

“Men are expected to be strong, deny pain and vulnerability, and conceal any emotional fragility,” says Swami, a psychologist at the University of Westminster, in London. “Because of these societal expectations, men appear to have poorer understanding of mental health and aren’t as good at detecting symptoms of depression compared with women.”

Potash says the findings also may reflect the fact that women are generally more attuned to emotions and better at articulating them. Some men might have all the outward signs of depression, and yet when asked about their mood they “may not be able to say much more than ‘I don’t know,’” he says. “A substantial minority of men just don’t describe depression.”

Health.com: 10 Careers With High Rates of Depression

On a deeper level, men’s failure to recognize the symptoms of depression in a fellow male may represent a kind of defense mechanism prompted by an “unconscious identification” with that man, says Dr. Radu Saveanu, a professor of psychiatry at the University of Miami Miller School of Medicine.

“They may think, ‘If this guy is having trouble and may need treatment, I may be in the same position someday,’” says Saveanu, who was not involved in the study. “That anxiety distorts the ability to be more objective.”

All of these dynamics may affect the likelihood of seeking or recommending treatment. In the study, men were more likely than women to recommend that Kate seek professional help, but this gap disappeared in the Jack scenario. Men also expressed less sympathy for Jack than women did.

The reluctance to seek treatment isn’t unique to men, but it does reflect an independent-minded streak that is more common among males, Potash says. Men tend to think that pulling themselves out of depression is “something they ought to be able to do,” he says. “It’s the stereotype of men who never ask for directions. They won’t admit that they can’t take care of it themselves.”

Health.com: Depressed? 12 Mental Tricks to Turn It Around

Gender, of course, isn’t the only factor that shapes how we view depression symptoms. Swami also found that respondents of either sex who held negative attitudes towards psychiatry and science felt that both Kate and Jack’s symptoms were less distressing, more difficult to treat, and less worthy of sympathy or professional help.

Swami took these trends into account, but he can’t rule out that other factors might have influenced the gender differences seen in the study. The participants’ own mental health history was unknown, for instance, though Swami says previous diagnoses do not tend to impact “mental health literacy,” or how well people understand mental health issues.

Future research will need to address these limitations, he says.

Read more: http://healthland.time.com/2012/11/15/how-gender-stereotypes-warp-our-view-of-depression/#ixzz2Es26tBvB

 

Controversial surgical treatment for addiction burns away the brain’s pleasure center

 

How far should doctors go in attempting to cure addiction? In China, some physicians are taking the most extreme measures. By destroying parts of the brain’s “pleasure centers” in heroin addicts and alcoholics, these neurosurgeons hope to stop drug cravings. But damaging the brain region involved in addictive desires risks permanently ending the entire spectrum of natural longings and emotions, including the ability to feel joy.

In 2004, the Ministry of Health in China banned this procedure due to lack of data on long term outcomes and growing outrage in Western media over ethical issues about whether the patients were fully aware of the risks.

However, some doctors were allowed to continue to perform it for research purposes—and recently, a Western medical journal even published a new study of the results. In 2007, The Wall Street Journal detailed the practice of a physician who claimed he performed 1000 such procedures to treat mental illnesses such as depression, schizophrenia and epilepsy, after the ban in 2004; the surgery for addiction has also since been done on at least that many people.

The November publication has generated a passionate debate in the scientific community over whether such research should be published or kept outside the pages of reputable scientific journals, where it may find undeserved legitimacy and only encourage further questionable science to flourish.

The latest study is the third published since 2003 in Stereotactic and Functional Neurosurgery, which isn’t the only journal chronicling results from the procedure, which is known as ablation of the nucleus accumbens. In October, the journal World Neurosurgery also published results from the same researchers, who are based at Tangdu Hospital in Xi’an.

The authors, led by Guodong Gao, claim that the surgery is “a feasible method for alleviating psychological dependence on opiate drugs.” At the same time, they report that more than half of the 60 patients had lasting side effects, including memory problems and loss of motivation. Within five years, 53% had relapsed and were addicted again to opiates, leaving 47% drug free.

(MORE: Addicted: Why We Get Hooked)

Conventional treatment only results in significant recovery in about 30-40% of cases, so the procedure apparently improves on that, but experts do not believe that such a small increase in benefit is worth the tremendous risk the surgery poses.  Even the most successful brain surgeries carry risk of infection, disability and death since opening the skull and cutting brain tissue for any reason is both dangerous and unpredictable. And the Chinese researchers report that 21% of the patients they studied experienced memory deficits after the surgery and 18% had “weakened motivation,” including at least one report of lack of sexual desire. The authors claim, however, that “all of these patients reported that their [adverse results] were tolerable.” In addition, 53% of patients had a change in personality, but the authors describe the majority of these changes as “mildness oriented,” presumably meaning that they became more compliant. Around 7%, however, became more impulsive.

The surgery is actually performed while patients are awake in order to minimize the chances of destroying regions necessary for sensation, consciousness or movement.  Surgeons use heat to kill cells in small sections of both sides of the brain’s nucleus accumbens.  That region is saturated with neurons containing dopamine and endogenous opioids, which are involved in pleasure and desire related both to drugs and to ordinary experiences like eating, love and sex.

(MORE: A Drug to End Drug Addiction)

In the U.S. and the U.K., reports the Wall Street Journal, around two dozen stereotactic ablations are performed each year, but only in the most intractable cases of depression and obsessive-compulsive disorder and after extensive review by institutional review boards and intensive discussions with the patient, who must acknowledge the risks. Often, a different brain region is targeted, not the nucleus accumbens. Given the unpredictable and potentially harmful consequences of the procedure, experts are united in their condemnation of using the technique to treat addictions. “To lesion this region that is thought to be involved in all types of motivation and pleasure risks crippling a human being,” says Dr. Charles O’Brien, head of the Center for Studies of Addiction at the University of Pennsylvania.

David Linden, professor of neuroscience at Johns Hopkins and author of a recent book about the brain’s pleasure systems calls the surgery “horribly misguided.”  He says “This treatment will almost certainly render the subjects unable to feel pleasure from a wide range of experiences, not just drugs of abuse.”

But some neurosurgeons see it differently. Dr. John Adler, professor emeritus of neurosurgery at Stanford University, collaborated with the Chinese researchers on the publication and is listed as a co-author.  While he does not advocate the surgery and did not perform it, he believes it can provide valuable information about how the nucleus accumbens works, and how best to attempt to manipulate it. “I do think it’s worth learning from,” he says. ” As far as I’m concerned, ablation of the nucleus accumbens makes no sense for anyone.  There’s a very high complication rate. [But] reporting it doesn’t mean endorsing it. While we should have legitimate ethical concerns about anything like this, it is a bigger travesty to put our heads in the sand and not be willing to publish it,” he says.

(MORE: Anesthesia Study Opens Window Into Consciousness)

Dr. Casey Halpern, a neurosurgery resident at the University of Pennsylvania makes a similar case. He notes that German surgeons have performed experimental surgery involving placing electrodes in the same region to treat the extreme lack of pleasure and motivation associated with otherwise intractable depression.  “That had a 60% success rate, much better than [drugs like Prozac],” he says. Along with colleagues from the University of Magdeburg in Germany, Halpern has just published a paper in the Proceedings of the New York Academy of Sciences calling for careful experimental use of DBS in the nucleus accumbens to treat addictions, which have failed repeatedly to respond to other approaches. The paper cites the Chinese surgery data and notes that addiction itself carries a high mortality risk.

DBS, however, is quite different from ablation.  Although it involves the risk of any brain surgery, the stimulation itself can be turned off if there are negative side effects, while surgical destruction of brain tissue is irreversible. That permanence—along with several other major concerns — has ethicists and addiction researchers calling for a stop to the ablation surgeries, and for journals to refuse to publish related studies.

Harriet Washington, author of Medical Apartheid:  The Dark History of Medical Experimentation on Black Americans from Colonial Times to the Present, argues that by publishing the results of unethical studies, scientists are condoning the questionable conditions under which the trials are conducted. “When medical journals publish research that violates the profession’sethical guidelines, this serves not only to sanction such abuses, but to encourage them,” she says. “In doing so, this practice encourages a relaxing of moral standards that threatens all patients and subjects, but especially  the medically vulnerable.”

(MORE: Real-Time Video: First Look at a Brain Losing Consciousness Under Anesthesia)

Shi-Min Fang, a Chinese biochemist who became a freelance journalist and recently won the journal Nature‘s Maddox prize for his exposes of widespread fraud in Chinese research, has revealed some of the subpar scientific practices behind research conducted in China, facing death threats and, as the New York Times reported, a beating with a hammer. He agrees that publishing such research only perpetuates the unethical practices. Asked by TIME to comment on the addiction surgery studies, Fang writes that publishing the research, particularly in western journals, “would encourage further unethical research, particularly in China where rewards for publication in international journals are high.”

While he doesn’t have the expertise to comment specifically on the ablation data, he says “the results of clinical research in China are very often fabricated. I suspect that the approvals by Ethics Committee mentioned in these papers were made up to meet publication requirement. I also doubt if the patients were really informed in detail about the nature of the study.” Fang also notes that two of the co-authors of the paper are advertising on the internet in Chinese, offering the surgery at a cost of 35,000 renminbi, about $5,600.  That’s more than the average annual income in China, which is about $5,000.

Given the available evidence, in fact, it’s hard to find a scientific justification for even studying the technique in people at all. Carl Hart, associate professor of psychology at Columbia University and author of the leading college textbook on psychoactive drugs, says animal studies suggest the approach may ultimately fail as an effective treatment for addiction; a 1984 experiment, for example, showed that destroying the nucleus accumbens in rats does not permanently stop them from taking opioids like heroin and later research found that it similarly doesn’t work for curbing cocaine cravings. Those results alone should discourage further work in humans. “These data are clear,” he says, “If you are going to take this drastic step, you damn well better know all of the animal literature.” [Disclosure:  Hart and I have worked on a book project together].

(MORE: Top 10 Medical Breakthroughs of 2012)

Moreover, in China, where addiction is so demonized that execution has been seen as an appropriate punishment and where the most effective known treatment for heroin addiction— methadone or buprenorphine maintenance— is illegal, it’s highly unlikely that addicted people could give genuinely informed consent for any brain surgery, let alone one that risks losing the ability to feel pleasure. And even if all of the relevant research suggested that ablating the nucleus accumbens prevented animals from seeking drugs, it would be hard to tell from rats or even primates whether the change was due to an overall reduction in motivation and pleasure or to a beneficial reduction in desiring just the drug itself.

There is no question that addiction can be difficult to treat, and in the most severe cases, where patients have suffered decades of relapses and failed all available treatments multiple times, it may make sense to consider treatments that carry significant risks, just as such dangers are accepted in fighting suicidal depression or cancer.  But in the ablation surgery studies, some of the participants were reportedly as young as 19 years old and had only been addicted for three years.  Addiction research strongly suggests that such patients are likely to recover even without treatment, making the risk-benefit ratio clearly unacceptable.

The controversy highlights the tension between the push for innovation and the reality of risk. Rules on informed consent didn’t arise from fears about theoretical abuses:  they were a response to the real scientific horrors of the Holocaust. And ethical considerations become especially important when treating a condition like addiction, which is still seen by many not as an illness but as a moral problem to be solved by punishment.  Scientific innovation is the goal, but at what price?
Read more: http://healthland.time.com/2012/12/13/controversial-surgery-for-addiction-burns-away-brains-pleasure-center/#ixzz2ExzobWQq

Thanks to Dr. Lutter for bringing this to the attention of the It’s Interesting community.

 

Former Beatle Paul McCartney will fill in for Kurt Cobain in Nirvana reunion

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70 year old Sir Paul McCartney filled in for Kurt Cobain as the surviving members of Nirvana reunited at the Superstorm Sandy benefit in New York on Wednesday.

Grunge stars Dave Grohl and bassist Krist Novoselic have reportedly enlisted the Beatle to play onstage with them at the Madison Square Garden charity gig.

The Fab Four legend reveals Grohl invited him to “jam with some mates”, but admits he had no idea he was filling in for tragic rocker Cobain, who committed suicide in 1994.

Sir Paul tells Britain’s The Sun, “I didn’t really know who they were. They are saying how good it is to be back together. I said, ‘Whoa? You guys haven’t played together for all that time? And somebody whispered to me, ‘That’s Nirvana. You’re Kurt.’ I couldn’t believe it.”

The Rolling Stones, Bruce Springsteen, The Who, and Eric Clapton were also on the bill for the 12-12-12 Concert for Sandy Relief.

http://www.torontosun.com/2012/12/12/paul-mccartney-to-fill-in-for-kurt-cobain-in-nirvana-reunion-gig

Hoarders horror: Woman has nearly 100 dead cats in refrigerator

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After so many tragic tales of waste-filled homes, animal deaths and human suffering on A&E’s “Hoarders,” it’s hard to imagine finding anything on the show truly shocking anymore. Well, it was hard to imagine that before Monday night’s episode, which featured a woman whose cat obsession went beyond anything viewers of the docu-series had seen before.

As the episode opened, hoarder Terry explained what inspired her feline fascination.

“I really feel like the reason I collect cats is that I have this feeling in me that I’m helping save something,” she said.

A glance around her living space soon proved that Terry wasn’t saving cats or herself the way she was living. Floors and counters were covered in excrement and sick animals crawled over the scene.

“The complete number is probably about 50 cats,” she guessed.

But that low-estimate only included the living cats, and the dead ones outnumbered them by far.

“I probably have, in frozen and refrigerated cats, between 75 and 100 — if not more,” Terry said.

Terry had hoped to have them all cremated, but finances didn’t allow for that, so over time, she “saved” them all in the appliance, which wasn’t up to the task of preserving the cats. In fact, once the cleanup was underway, the “Hoarders” crew discovered that many of the cats had liquefied.

The removal process was difficult for Terry who broke down many times and finally seemed to see her hoarding problem as others viewed it.

“I can’t even say anymore that I love animals ’cause I treated them so horrible,” she said through tears.

By the end of the show, most of the mess and all of the cats were out of the home.

If you want to see the episode for yourself — and be forewarned, the feline footage gets far more graphic than the photos above — it’s available to view online at the A&E website.

http://theclicker.today.com/_news/2012/12/04/15676370-hoarders-horror-woman-has-nearly-100-dead-cats-in-refrigerator?lite

Chinese scientists turn human urine into brain cells

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Chinese researchers have developed a new technique for isolating kidney cells from urine and turning them into neural progenitors — –immature brain cells that can develop into various types of glial cells and neurons. Reprogramming cells has been done before, of course, but not with cells gleaned from urine and not via a method this direct. The technique could prove extremely helpful to those pursuing treatments for neurodegenerative disorders like Parkinson’s and Alzheimer’s.

The innovation here is in the source and the method. We know that embryonic stem cells offer potential treatments for neurodegenerative disorders. And we know that we can turn adult human cells–that is, non-embryonic cells gathered from adult humans–into pluripotent cells (those that can become a different type of cell) by reprogramming them, usually with genetically engineered viruses that tamper with the cells’ genetic codes.

But embryonic stem cell treatments are fraught with ethical issues and non-embryonic methods are complicated–and complexity introduces a greater chance of something going wrong (in this case that means mutations and genetic defects). The new method, which taps skin-like cells from the linings of the kidney tubes that are present in urine, converts its source cells into neurons and glia cells via a more direct route, making the process more efficient while narrowing the margin of error.

In their study, the researchers harvested kidney cells from the urine samples of three human donors and converted the cells directly to neural progenitors. Rather than using a genetically engineered virus to reprogram the cells, they used a small piece of bacterial DNA that can replicate in the cellular cytoplasm, a technique that eliminates the need to tamper directly with the chromosome (in theory, at least, this should reduce mutations) while also speeding up the entire process. After growing their progenitors into mature neurons and glial cells, the researchers transplanted the progenitors into the brains of newborn rats. A month later, the cells were still alive in the rats’ brains, though it is not yet clear that they can survive for extended periods or mesh with the brain’s wiring to become functioning parts of the neural machine.

There’s still a lot of research to be done on this method of course, but the researchers think it may provide a way to take cells gathered non-invasively and quickly and efficiently convert them into neural cells while reducing the likelihood of genetic mutations.

http://www.guardian.co.uk/science/neurophilosophy/2012/dec/09/turning-urine-into-brain-cells

 

Diuretic Drug Offers Latest Hope for Autism Treatment

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A drug used for decades to treat high blood pressure and other conditions has shown promise in a small clinical trial for autism. The drug, bumetanide, reduced the overall severity of behavioral symptoms after 3 months of daily treatment. The researchers say that many parents of children who received the drug reported that their children were more “present” and engaged in social interactions after taking it. The new findings are among several recent signs that treatments to address the social deficits at the core of autism may be on the horizon.

Several lines of evidence suggest that autism interferes with the neurotransmitter GABA, which typically puts a damper on neural activity. Bumetanide may enhance the inhibitory effects of GABA, and the drug has been used safely as a diuretic to treat a wide range of heart, lung, and kidney conditions. In the new study, researchers led by Yehezkel Ben-Ari at the Mediterranean Institute of Neurobiology in Marseille, France, recruited 60 autistic children between the ages of 3 and 11 and randomly assigned them to receive either a daily pill of bumetanide or a placebo. (Neither the children’s parents nor the researchers who assessed the children knew who received the actual drug.)

As a group, those who got bumetanide improved by 5.6 points on a 60-point scale that’s often used to assess behaviors related to autism, the researchers report today in Translational Psychiatry. That was enough to nudge the group average just under the cutoff for severe autism and into the mild to medium category. The study did not look directly at whether the drug improved all symptoms equally or some more than others. “We have some indications that the symptoms particularly ameliorated with bumetanide are the genuine core symptoms of autism, namely communication and social interactions,” Ben-Ari says. More work will be needed to verify that impression. Ben-Ari says his team is now preparing for a larger, multicenter trial in Europe.

The current study already looks interesting to some. “It’s enough to make me think about trying it in a few of my autism patients who haven’t responded to other interventions,” says Randi Hagerman, a pediatrician who studies neurodevelopmental disorders at the University of California, Davis. Social interactions tend to be reinforcing, Hagerman adds, so getting an autistic child to start interacting more can have a positive effect on subsequent brain development.

Other drugs have recently shown promise for autism. In September, Hagerman and colleagues reported that arbaclofen, a drug that stimulates a type of GABA receptor, reduced social avoidance in people with fragile X syndrome, a genetic disorder that shares many features with autism. Many researchers are also hopeful about clinical trials under way with drugs that block certain receptors for glutamate, the main neurotransmitter in the brain that excites neural activity. Results from those trials should come out next year.

All of this work, including the new study, suggests that drugs that reduce neural excitation by blocking glutamate or enhance inhibition by boosting GABA may be helpful for treating autism, says Elizabeth Berry-Kravis, a pediatric neurologist at Rush University in Chicago, Illinois, and a collaborator on the recent arbaclofen study. “There seems to be this imbalance between excitation and inhibition in people with autism.”

That’s a potentially game-changing insight. Now doctors can only prescribe drugs that treat individual symptoms of autism rather than the underlying cause of the disorder, Berry-Kravis says. Doctors often prescribe antipsychotic drugs to reduce irritability, for example, but those drugs don’t address the social and communication problems at the heart of the disorder. “It’s exciting that now we’re thinking about the underlying mechanisms and treating those.”

http://news.sciencemag.org/sciencenow/2012/12/diuretic-drug-offers-latest-hope.html

Oregon’s ‘The Faces of Meth’ Add Campaign

Eight years ago, the Multnomah County Sheriff’s Office launched a campaign called “the Faces of Meth” to address Oregon’s methamphetamine problem. The images showed the jarring effects of meth on addicts’ faces through before-and-after pictures from their arrest records.

Rehabs.com recently followed suit with this infographic. Warning: these images are disturbing.

 

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Rehabs.com

 

 

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Read more: http://www.businessinsider.com/new-faces-of-meth-ads-are-utterly-harrowing-2012-12#ixzz2E7zSezR1