Chapter 4. The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
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By Brady Dennis In one city after another, the tests showed startling numbers of children with unsafe blood lead levels: Poughkeepsie and Syracuse and Buffalo. Erie and Reading. Cleveland and Cincinnati. In those cities and others around the country, 14 percent of kids — and in some cases more — have troubling amounts of the toxic metal in their blood, according to new research published Wednesday. The findings underscore how despite long-running public health efforts to reduce lead exposure, many U.S. children still live in environments where they're likely to encounter a substance that can lead to lasting behavioral, mental and physical problems. "We've been making progress for decades, but we have a ways to go," said Harvey Kaufman, senior medical director at Quest Diagnostics and a co-author of the study, which was published in the Journal of Pediatrics. "With blood [lead] levels in kids, there is no safe level." Kaufman and two colleagues at Quest, the nation's largest lab testing provider, examined more than 5.2 million blood tests for infants and children under age 6 that were taken between 2009 and 2015. The results spanned every state and the District of Columbia. The researchers found that while blood lead levels declined nationally overall during that period, roughly 3 percent of children across the country had levels that exceed five micrograms per deciliter — the threshold that the Centers for Disease Control and Prevention considers cause for concern. But in some places and among particular demographics, those figures are much higher.
By Brian Platzer It started in 2010 when I smoked pot for the first time since college. It was cheap, gristly weed I’d had in my freezer for nearly six years, but four hours after taking one hit I was still so dizzy I couldn’t stand up without holding on to the furniture. The next day I was still dizzy, and the next, and the next, but it tapered off gradually until about a month later I was mostly fine. Over the following year I got married, started teaching seventh and eighth grade, and began work on a novel. Every week or so the disequilibrium sneaked up on me. The feeling was one of disorientation as much as dizziness, with some cloudy vision, light nausea and the sensation of being overwhelmed by my surroundings. During one eighth-grade English class, when I turned around to write on the blackboard, I stumbled and couldn’t stabilize myself. I fell in front of my students and was too disoriented to stand. My students stared at me slumped on the floor until I mustered enough focus to climb up to a chair and did my best to laugh it off. I was only 29, but my father had had a benign brain tumor around the same age, so I had a brain scan. My brain appeared to be fine. A neurologist recommended I see an ear, nose and throat specialist. A technician flooded my ear canal with water to see if my acoustic nerve reacted properly. The doctor suspected either benign positional vertigo (dizziness caused by a small piece of bonelike calcium stuck in the inner ear) or Ménière’s disease (which leads to dizziness from pressure). Unfortunately, the test showed my inner ear was most likely fine. But just as the marijuana had triggered the dizziness the year before, the test itself catalyzed the dizziness now. In spite of the negative results, doctors still believed I had an inner ear problem. They prescribed exercises to unblock crystals, and salt pills and then prednisone to fight Ménière’s disease. All this took months, and I continued to be dizzy, all day, every day. It felt as though I woke up every morning having already drunk a dozen beers — some days, depending on how active and stressful my day was, it felt like much more. Most days ended with me in tears. © 2016 The New York Times Company
[Agata Blaszczak-Boxe, Contributing Writer] People who use marijuana for many years respond differently to natural rewards than people who don't use the drug, according to a new study. Researchers found that people who had used marijuana for 12 years, on average, showed greater activity in the brain's reward system when they looked at pictures of objects used for smoking marijuana than when they looked at pictures of a natural reward — their favorite fruits. "This study shows that marijuana disrupts the natural reward circuitry of the brain, making marijuana highly salient to those who use it heavily," study author Dr. Francesca Filbey, an associate professor of behavioral and brain science at the University of Texas at Dallas, said in a statement. "In essence, these brain alterations could be a marker of transition from recreational marijuana use to problematic use." [11 Odd Facts About Marijuana] In the study, researchers looked at 59 marijuana users who had used marijuana daily for the past 60 days, and had used the drug on at least 5,000 occasions during their lives. The researchers wanted to see whether the brains of these long-term marijuana users would respond differently to picures of objects related to marijuana use than they did to natural rewards, such as their favorite fruits, compared with people who did not use marijuana.
Keyword: Drug Abuse
Link ID: 22317 - Posted: 06.14.2016
By Monique Brouillette The brain presents a unique challenge for medical treatment: it is locked away behind an impenetrable layer of tightly packed cells. Although the blood-brain barrier prevents harmful chemicals and bacteria from reaching our control center, it also blocks roughly 95 percent of medicine delivered orally or intravenously. As a result, doctors who treat patients with neurodegenerative diseases, such as Parkinson's, often have to inject drugs directly into the brain, an invasive approach that requires drilling into the skull. Some scientists have had minor successes getting intravenous drugs past the barrier with the help of ultrasound or in the form of nanoparticles, but those methods can target only small areas. Now neuroscientist Viviana Gradinaru and her colleagues at the California Institute of Technology show that a harmless virus can pass through the barricade and deliver treatment throughout the brain. Gradinaru's team turned to viruses because the infective agents are small and adept at entering cells and hijacking the DNA within. They also have protein shells that can hold beneficial deliveries, such as drugs or genetic therapies. To find a suitable virus to enter the brain, the researchers engineered a strain of an adeno-associated virus into millions of variants with slightly different shell structures. They then injected these variants into a mouse and, after a week, recovered the strains that made it into the brain. A virus named AAV-PHP.B most reliably crossed the barrier. © 2016 Scientific American,
Link ID: 22313 - Posted: 06.13.2016
By JOHN ELIGON and SERGE F. KOVALESKI Prince, the music icon who struggled with debilitating hip pain during his career, died from an accidental overdose of self-administered fentanyl, a type of synthetic opiate, officials in Minnesota said Thursday. The news ended weeks of speculation about the sudden death of the musician, who had a reputation for clean living but who appears to have developed a dependency on medications to treat his pain. Authorities have yet to discuss how he came to be in possession of the fentanyl and whether it had been prescribed by a doctor. Officials had waited several weeks for the results of a toxicology test undertaken as part of an autopsy performed after he was found dead April 21 in an elevator at his estate. He was preparing to enroll in an opioid treatment program when he died at 57, according to the lawyer for a doctor who was planning to treat him. The Midwest Medical Examiner’s Office, which conducted the autopsy, declined to comment beyond releasing a copy of its findings. The Carver County Sheriff’s Office is continuing to investigate the death with help from the federal Drug Enforcement Administration. The sheriff’s office had said it was looking into whether opioid abuse was a factor, and a law enforcement official had said that painkillers were found on Prince when investigators arrived. “The M.E. report is one piece of the whole thing,” said Jason Kamerud, the county’s chief deputy sheriff. Fentanyl is a potent but dangerous painkiller, estimated to be more than 50 times more powerful than heroin, according to the Centers for Disease Control and Prevention. The report did not list how much fentanyl was found in Prince’s blood. Last year, federal officials issued an alert that said incidents and overdoses with fentanyl were “occurring at an alarming rate throughout the United States.” © 2016 The New York Times Company
By Mark Gollom, Anti-smoking advocates who support the Liberal government's proposal to require plain packaging on tobacco products argue that Australia's implementation of similar regulations has had a significant effect on smoking rates in that country. "Australia has seen the biggest decline in smoking prevalence that they've ever recorded after plain packing [was introduced]," said David Hammond, an associate professor of public health and health systems at the University of Waterloo. "All the data we have suggest that plain packing has reduced smoking in Australia." Rob Cunningham, senior policy analyst for the Canadian Cancer Society, agrees and says research supports the effectiveness of plain packaging. "If it wasn't effective, the tobacco companies wouldn't be so strongly opposed," he said. "And it's precisely because it's going to have an effect on sales that they are going to lobby hard against it, threaten legal cases." But not everyone believes that Australia's policy of imposing bland tobacco branding has done much to deter smoking, which has been steadily declining for decades, according to Julian Morris, vice-president of research at the libertarian think tank the Reason Foundation. "The decline in smoking seems to have been continuous and not dramatically effected, one way or the other, by the introduction of plain packaging," he said. ©2016 CBC/Radio-Canada.
Keyword: Drug Abuse
Link ID: 22274 - Posted: 06.02.2016
By Kelly Servick There’s an unfortunate irony for people who rely on morphine, oxycodone, and other opioid painkillers: The drug that’s supposed to offer you relief can actually make you more sensitive to pain over time. That effect, known as hyperalgesia, could render these medications gradually less effective for chronic pain, leading people to rely on higher and higher doses. A new study in rats—the first to look at the interaction between opioids and nerve injury for months after the pain-killing treatment was stopped—paints an especially grim picture. An opioid sets off a chain of immune signals in the spinal cord that amplifies pain rather than dulling it, even after the drug leaves the body, the researchers found. Yet drugs already under development might be able to reverse the effect. It’s no secret that powerful painkillers have a dark side. Overdose deaths from prescription opioids have roughly quadrupled over 2 decades, in near lockstep with increased prescribing. And many researchers see hyperalgesia as a part of that equation—a force that compels people to take more and more medication, while prolonging exposure to sometimes addictive drugs known to dangerously slow breathing at high doses. Separate from their pain-blocking interaction with receptors in the brain, opioids seem to reshape the nervous system to amplify pain signals, even after the original illness or injury subsides. Animals given opioids become more sensitive to pain, and people already taking opioids before a surgery tend to report more pain afterward. © 2016 American Association for the Advancement of Scienc
Martha Bebinger Labels for the first long-acting opioid addiction treatment device are rolling off printing machines Friday. Trainings begin Saturday for doctors who want to learn to insert four matchstick-size rods under the skin. They contain the drug buprenorphine, which staves off opioid cravings. The implant, called Probuphine, was approved by the Food and Drug Administration on Thursday, and is expected to be available to patients by the end of June. "This is just the starting point for us to continue to fight for the cause of patients with opioid addiction," said Behshad Sheldon, CEO of Braeburn Pharmaceuticals, which manufactures Probuphine. But debate continues about how effective the implant will be and whether insurers will cover it. Nora Volkow, head of the National Institute on Drug Abuse, calls Probuphine a game changer, saying it will help addiction patients stay on their meds while their brain circuits recover from the ravages of drug use. And addiction experts say it will be much harder for patients prescribed the implant to sell their medication on the street, which can be a problem with addiction patients prescribed pills. "I think it's fantastic news," said Dr. Sarah Wakeman, medical director of the Substance Use Disorder Initiative at Massachusetts General Hospital. "We need as many tools in the toolbox as possible to deal with the opioid epidemic." © 2016 npr
Keyword: Drug Abuse
Link ID: 22256 - Posted: 05.28.2016
Ronald Crystal The goal of antiaddiction vaccines is to prevent addictive molecules from reaching the brain, where they produce their effects and can create chemical dependencies. Vaccines can accomplish this task, in theory, by generating antibodies—proteins produced by the immune system—that bind to addictive particles and essentially stop them in their tracks. But challenges remain. Among them, addictive molecules are often too small to be spotted by the human immune system. Thus, they can circulate in the body undetected. Researchers have developed two basic strategies for overcoming this problem. One invokes so-called active immunity by tethering an addictive molecule to a larger molecule, such as the proteins that encase a common cold virus. This viral shell does not make people sick but does prompt the immune system to produce high levels of antibodies against it and whatever is attached to it. In our laboratory, we have tested this method in animal models and successfully blocked chemical forms of cocaine or nicotine from reaching the brain. Another approach researchers are testing generates what is known as passive immunity against addictive molecules in the body. They have cultured monoclonal antibodies that can bind selectively to addictive molecules. The hurdle with this particular method is that monoclonal antibodies are expensive to produce and need to be administrated frequently to be effective. © 2016 Scientific American
By Lucas Powers, CBC News You're standing on the side of the road, with traffic whizzing past. The police officer who pulled you over suspects you may have smoked the reefer before departing for McDonald's. But she's in a bit of a quagmire, because, really, there's no reliable way to know for sure. Are you high? If you are high, how high are you, really? Or really did you just want those little cheeseburgers (no ketchup and extra pickles)? So she does the most logical thing: a field sobriety test. Tried and true. Walk the line. Touch the tip your nose. Can't do it? That's... suspicious. Maybe a night in the clink? Some Canadian cops also have roadside saliva swabs that can be used to test for the presence of drugs, but they are useless, legally speaking (for now.) Now, had you been quaffing ales before the drive, a breathalyzer — controversial as they can be in terms of accuracy and reliability — would have cleared up the situation pretty quickly. Of course, no such roadside device exists for cannabis and its psychotropic ingredient THC. There's growing evidence that cannabis can impair driving by slowing reaction times and encouraging perplexing moves by drivers, like slowing way down and being reluctant to change lanes. Doctors at Toronto's Centre for Addiction and Mental Health are doing the world's biggest-ever clinical study, asking exactly what causes this behaviour, and how dangerous it is. Either way, an innovation war worth billions to the victor has been declared over developing a cannabis breathalyzer. ©2016 CBC/Radio-Canada.
Keyword: Drug Abuse
Link ID: 22236 - Posted: 05.23.2016
Andrea Hsu Scientists and doctors say the case is clear: The best way to tackle the country's opioid epidemic is to get more people on medications that have been proven in studies to reduce relapses and, ultimately, overdoses. Yet, only a fraction of the more than 4 million people believed to abuse prescription painkillers or heroin in the U.S. are being given what's called medication-assisted treatment. One reason is the limited availability of the treatment. But it's also the case that stigma around the addiction drugs has inhibited their use. Methadone and buprenorphine, two of the drugs used for treatment, are themselves opioids. A phrase you often hear about medication-assisted treatment is that it's merely replacing one drug with another. While doctors and scientists strongly disagree with that characterization, it's a view that's widespread in recovery circles. Now, the White House is pushing to change the landscape for people seeking help. In his 2017 budget, President Obama has asked Congress for $1.1 billion in new funding to address the opioid epidemic, with almost all of it geared toward expanding access to medication-assisted treatment. The White House is also highlighting success stories. At the National Prescription Drug Abuse and Heroin Summit held in Atlanta in March, President Obama appeared on stage with Crystal Oertle, a 35-year-old mother of two from Ohio. Oertle spoke of her spiral into addiction, which began with prescription painkillers and progressed to heroin. She tried unsuccessfully to quit on her own several times, before being prescribed buprenorphine a year ago. © 2016 npr
Keyword: Drug Abuse
Link ID: 22226 - Posted: 05.18.2016
Zoe Cormier A hallucinogenic drug derived from magic mushrooms could be useful in treating depression, the first safety study of this approach has concluded. Researchers from Imperial College London gave 12 people psilocybin, the active component in magic mushrooms. All had been clinically depressed for a significant amount of time — on average 17.8 years. None of the patients had responded to standard medications, such as selective serotonin re-uptake inhibitors (SSRIs), or had electroconvulsive therapy. One week after receiving an oral dose of psilocybin, all patients experienced a marked improvement in their symptoms. Three months on, five patients were in complete remission. “That is pretty remarkable in the context of currently available treatments,” says Robin Carhart-Harris, a neuropsychopharmacologist at Imperial College London and first author of the latest study, which is published in The Lancet Psychiatry1. The equivalent remission rate for SSRIs is around 20%. The study's authors are not suggesting that psilocybin should be a treatment of last resort for depressed patients. “Our conclusion is more sober than that — we are simply saying that this is doable,” says Carhart-Harris. “We can give psilocybin to depressed patients, they can tolerate it, and it is safe. This gives us an initial impression of the effectiveness of the treatment.” © 2016 Nature Publishing Group
By CLYDE HABERMAN At respected research centers in the United States and other countries, scientists have spent much of their professional lives in drug rehabilitation. It is not because they themselves struggle with addiction. What they are trying to rehabilitate are the drugs. Their focus is on mind-altering compounds that fell far from grace nearly half a century ago, LSD prominent among them. Along with other psychedelics, it was outlawed by the federal government, damned as bearing a high potential for abuse and offering no accepted medical benefit. But in recent years, researchers have sought to rescue hallucinogens from exile by examining their efficacy in treating certain disorders of the mind, and perhaps even in understanding the nature of consciousness and spirituality. The work of these scientists now draws the attention of Retro Report, a series of video documentaries that examine major news stories of the past and their enduring significance. Psychoactive substances, often derived from mushrooms, have been part of human cultures from Central and South America to the Sahara for thousands of years. But there is no need to look that far back; 1938 will do. That was when Albert Hofmann, a Swiss chemist searching for a drug to combat circulatory ailments, happened to synthesize lysergic acid diethylamide: LSD or, more familiarly, acid. Five years later, Dr. Hofmann, who died in 2008 at age 102, accidentally ingested a small dose of his creation and discovered its mind-blowing potential as he embarked on the first known acid trip. Many more such journeys would follow, for him and for countless others. © 2016 The New York Times Company
By JONAH BROMWICH It’s relatively easy to determine when someone is too drunk to drive. If a driver’s blood-alcohol level is 0.08 percent or higher, that person is considered legally impaired. But a study says that measuring the effects of marijuana on drivers is far trickier, and that blood tests are an unreliable indication of impairment by cannabis. As more states consider legalizing the substance, that presents a challenge to legislators seeking to create laws on driving while impaired by marijuana. The study, commissioned by the AAA Foundation for Traffic Safety, found that laws in six states that legally assess impairment by measuring how much THC (the active ingredient in marijuana) is in a person’s blood are not supported by science. “There is no concentration of the drug that allows us to reliably predict that someone is impaired behind the wheel in the way that we can with alcohol,” said Jake Nelson, AAA’s director of traffic safety advocacy and research. Lawmakers in those states looked to policies on drunken driving for cues on how to legislate against driving while high. But the body absorbs alcohol and cannabis in different ways, the study said. While drunkenness directly correlates to alcohol in the bloodstream, cannabis impairment takes place only when THC makes its way into the fatty tissue of the brain. Regular marijuana users, including those who take the drug medicinally, often show no signs of impairment after using, according to Jolene Forman, a staff lawyer for the Drug Policy Alliance, a drug-reform advocacy group. She also said that marijuana can stay in the blood for hours, days and even weeks after its effects wear off. © 2016 The New York Times Company
Keyword: Drug Abuse
Link ID: 22214 - Posted: 05.14.2016
By Nicholas Bakalar Exposure to pesticides may increase the risk for amyotrophic lateral sclerosis, also known as Lou Gehrig’s disease, a new study has found. The study, in JAMA Neurology, included 156 patients with A.L.S. and 128 controls. All participants completed questionnaires providing information on age, sex, ethnicity, education, marital status, residential history, occupational history, smoking and military service. The researchers used the information on residence and occupation to estimate long-term exposure to pesticides, and then took blood samples to determine serum levels of 122 persistent environmental pollutants. The scientists divided exposure into four time periods: ever exposed, exposed in the last 10 years, exposed 10 to 30 years ago, and exposed more than 30 years ago. Exposure to pesticides at any time was associated with a fivefold increased relative risk for A.L.S. compared to no exposure. Even exposure more than 30 years ago tripled the risk. Military service was associated with double the risk, confirming findings of previous studies. “This is an association, not causality,” cautioned the senior author, Dr. Eva L. Feldman, a professor of neurology at the University of Michigan. “We found that people with A.L.S. were five times more likely to have been exposed to pesticides, but we don’t want people to conclude that pesticides cause A.L.S.” © 2016 The New York Times Company
By Lisa Damour Parents of teenagers face a confounding crosscurrent. While the legalization of marijuana in several American states now bolsters the common belief among adolescents that the drug is safe for recreational use, research documenting marijuana’s diffuse and possibly permanent harm to the teenage brain continues to pile up. Normally developing teenagers question authority and are likely to be skeptical of adults bearing bad news about a widely used party drug. So how do we have successful conversations about the hazards of marijuana use? An open-ended exchange that credits the adolescent’s own observations may do more good than a single sit-down or lecture. Beyond that, we might consider how the facts are often received by adolescents. With all the talk about cannabis legalization, parents may feel compelled to remind their teenagers that recreational marijuana is still banned for most American adults and for anyone under 21. Adolescents who use marijuana risk immediate legal consequences and, in districts with zero-tolerance policies, may be barred from organized school activities, suspended or expelled. They may also face long-term penalties affecting some jobs, internships, colleges and travel visas. But the repercussions of being caught with marijuana don’t faze all teenagers. Most adolescents can name celebrities, famous athletes and classmates who use marijuana regularly, even flagrantly, without running into trouble. Teenagers tend to bristle at rules that seem arbitrary, such as the state-by-state regulations for marijuana and the fact that alcohol, which has a lot in common with pot, is legal. Further, adolescents can be understandably cynical about laws that aren’t applied evenly to everyone: While African-Americans and whites use the drug at similar rates, African-Americans are nearly four times as likely to be arrested for marijuana possession. However real and lasting the penalties for pot use may be, parents often run into resistance when trying to make this case to teenagers. © 2016 The New York Times Company
By Maia Szalavitz Both the FDA and the CDC have recently taken steps to address an epidemic of opioid overdose and addiction, which is now killing some 29,000 Americans each year. But these regulatory efforts will fail unless we acknowledge that the problem is actually driven by illicit—not medical—drug use. You’ve probably read that 80 percent of heroin users started with prescription medications—and you may have seen billboards that compare giving pain medication to children to giving them heroin. You have probably also heard and seen media stories of people with addiction who blame their problem on medical use. But the simple reality is this: According to the large, annually repeated and representative National Survey on Drug Use and Health, 75 percent of all opioid misuse starts with people using medication that wasn’t prescribed for them—obtained from a friend, family member or dealer. And 90 percent of all addictions—no matter what the drug—start in the adolescent and young adult years. Typically, young people who misuse prescription opioids are heavy users of alcohol and other drugs. This type of drug use, not medical treatment with opioids, is by far the greatest risk factor for opioid addiction, according to a study by Richard Miech of the University of Michigan and his colleagues. For this research, the authors analyzed data from the nationally representative Monitoring the Future survey, which includes thousands of students. While medical use of opioids among students who were strongly opposed to alcohol and other drugs did raise later risk for misuse, the overall risk for this group remained small and their actual misuse occurred less than five times a year. In other words, it wasn’t actually addiction. Given that these teens had generally rejected experimenting with drugs, an increased risk of misuse associated with medical care makes sense since they’d otherwise have no source of exposure. © 2016 Scientific American
Keyword: Drug Abuse
Link ID: 22202 - Posted: 05.11.2016
Aaron E. Carroll People get hooked on cigarettes, and enjoy them for that matter, because of the nicotine buzz. The nicotine doesn’t give them cancer and lung disease, though. It’s the tar and other chemicals that do the real harm. A robust debate is going on among public health officials over whether electronic cigarettes, or e-cigarettes, can alleviate the harms of smoking tobacco, or whether they should be treated as negatively as conventional cigarettes. In other countries, such as Britain, officials are more in favor of e-cigarettes, encouraging smokers to switch from conventional to electronic. Last week, the Food and Drug Administration issued new rules on e-cigarettes, banning their sale to anyone under 18 and requiring that adults under the age of 26 show a photo identification to buy them. Electronic cigarettes carry the promise of delivering the nicotine without the dangerous additives. The use of e-cigarettes by youth has increased sharply in recent years. In 2011, about 1.5 percent of high school students reported using them in the last month. In 2014, more than 12 percent of students did. That means that nearly 2.5 million American middle and high school students used them in the past month. The problem is that nicotine is generally considered less safe for children and adolescents than for adults. Poisoning is possible. It’s thought that nicotine may interfere with brain development. Most worrisome, it’s believed that becoming addicted to nicotine in any form makes smoking more likely later in life. E-cigarettes are perceived to be less harmful than conventional cigarettes, and they are thought to be useful aids to quitting. These perceptions, however, are not always fully grounded in evidence. © 2016 The New York Times Company
Keyword: Drug Abuse
Link ID: 22201 - Posted: 05.11.2016
By JAN HOFFMAN The pop superstar Prince may have lived an outsize life, but emerging details about his long struggle with pain and reliance on opioids will resonate with thousands of patients who have stumbled down that well-trod path. It is a remarkably common narrative in the unfolding story of the nation’s opioid epidemic. Many details have yet to be confirmed about Prince’s case, but a typical trajectory can go something like this. A patient undergoes a procedure to address a medical issue — extracted wisdom teeth for example, or, as Prince did, orthopedic surgery. To help the patient get through recovery, a dentist or surgeon writes a prescription for opioid painkillers, like Percocet or Vicodin. Procedure over, problem addressed. But that prescription may not be written judiciously. “Opioids may be required after a procedure for a few days, but sometimes, physicians practice sloppy prescribing habits and they give patients much more than they need,” said Dr. Patrick G. O’Connor, a professor of medicine at Yale School of Medicine and a past president of the American Board of Addiction Medicine. “And the more patients take, the more likely they are to become dependent.” After a follow-up visit or two, the specialist who did the procedure has no reason to continue seeing the patient. (That doctor could also be an emergency room physician who treated kidney stones, sciatica or any number of other conditions involving stabbing pain.) Yet the patient’s pain may persist, demanding to be tamed. The patient, who now knows just how effective these drugs are, wants to refill the prescription. “The default approach is you go to your primary care provider, and they’ll take care of it,” said Dr. Jonathan H. Chen, an instructor at the Stanford University School of Medicine, who has researched the distribution of opioid prescriptions. As he spoke during a break in his shift in a same-day urgent care clinic, he had just attended to a patient who had recently had shoulder surgery but said she was still in pain. © 2016 The New York Times Company
Laura Sanders Ketamine, a drug that has shown promise in quickly easing depression, doesn’t actually do the job itself. Instead, depression relief comes from one of the drug’s breakdown products, a new study in mice suggests. The results, published May 4 in Nature, identify a potential depression-fighting drug that works quickly but without ketamine’s serious side effects or potential for abuse. The discovery “could be a major turning point,” says neuroscientist Roberto Malinow of the University of California, San Diego. “I’m sure that drug companies will look at this very closely.” Depression is a pernicious problem with few good treatments. Traditional antidepressants don’t work for everyone, and when the drugs do work, they can take weeks to kick in. Ketamine, developed in the 1960s as a sedative for people and now used commonly by veterinarians to knock out animals, can ease depression in minutes, not weeks, small studies show. But the new study suggests that a metabolite of ketamine — not the drug itself — fights depression. Inside the body, ketamine gets converted into a slew of related molecules. One of these breakdown molecules, a chemical called (2R,6R)-hydroxynorketamine, is behind the benefits, neuropharmacologist Todd Gould of the University of Maryland School of Medicine in Baltimore and colleagues found. On its own, a single dose of (2R,6R)-HNK reduced signs of depression in mice, restoring their drive to search for a hidden platform in water, to try to escape a shock and to choose sweet water over plain. A type of ketamine that couldn’t be broken down easily into HNKs didn’t ease signs of depression in mice. Finding that a breakdown product, and not ketamine itself, was behind the results was a big surprise, Gould says. © Society for Science & the Public 2000 - 2016