Chapter 3. The Chemistry of Behavior: Neurotransmitters and Neuropharmacology

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Researchers are now able to wirelessly record the directly measured brain activity of patients living with Parkinson’s disease and to then use that information to adjust the stimulation delivered by an implanted device. Direct recording of deep and surface brain activity offers a unique look into the underlying causes of many brain disorders; however, technological challenges up to this point have limited direct human brain recordings to relatively short periods of time in controlled clinical settings. This project, published in the journal Nature Biotechnology, was funded by the National Institutes of Health’s Brain Research Through Advancing Innovative Neurotechnologies (BRAIN) Initiative. “This is really the first example of wirelessly recording deep and surface human brain activity for an extended period of time in the participants’ home environment,” said Kari Ashmont, Ph.D., project manager for the NIH BRAIN Initiative. “It is also the first demonstration of adaptive deep brain stimulation at home.” Deep brain stimulation (DBS) devices are approved by the U. S. Food and Drug Administration for the management of Parkinson’s disease symptoms by implanting a thin wire, or electrode, that sends electrical signals into the brain. In 2018, the laboratory of Philip Starr, M.D., Ph.D. at the University of California, San Francisco, developed an adaptive version of DBS that adapts its stimulation only when needed based on recorded brain activity. In this study, Dr. Starr and his colleagues made several additional improvements to the implanted technology.

Keyword: Brain imaging
Link ID: 27800 - Posted: 05.05.2021

By Christine Kenneally The first thing that Rita Leggett saw when she regained consciousness was a pair of piercing blue eyes peering curiously into hers. “I know you, don’t I?” she said. The man with the blue eyes replied, “Yes, you do.” But he didn’t say anything else, and for a while Leggett just wondered and stared. Then it came to her: “You’re my surgeon!” It was November, 2010, and Leggett had just undergone neurosurgery at the Royal Melbourne Hospital. She recalled a surge of loneliness as she waited alone in a hotel room the night before the operation and the fear she felt when she entered the operating room. She’d worried about the surgeon cutting off her waist-length hair. What am I doing in here? she’d thought. But just before the anesthetic took hold, she recalled, she had said to herself, “I deserve this.” Leggett was forty-nine years old and had suffered from epilepsy since she was born. During the operation, her surgeon, Andrew Morokoff, had placed an experimental device inside her skull, part of a brain-computer interface that, it was hoped, would be able to predict when she was about to have a seizure. The device, developed by a Seattle company called NeuroVista, had entered a trial stage known in medical research as “first in human.” A research team drawn from three prominent epilepsy centers based in Melbourne had selected fifteen patients to test the device. Leggett was Patient 14. © 2021 Condé Nast.

Keyword: Robotics; Epilepsy
Link ID: 27791 - Posted: 04.28.2021

By Kim Tingley The brain is an electrical organ. Everything that goes on in there is a result of millivolts zipping from one neuron to another in particular patterns. This raises the tantalizing possibility that, should we ever decode those patterns, we could electrically adjust them to treat neurological dysfunction — from Alzheimer’s to schizophrenia — or even optimize desirable qualities like intelligence and resilience. Of course, the brain is so complex, and so difficult to access, that this is much easier to imagine than to do. A pair of studies published in January in the journal Nature Medicine, however, demonstrate that electrical stimulation can address obsessive-compulsive urges and symptoms of depression with surprising speed and precision. Mapping participants’ brain activity when they experienced certain sensations allowed researchers to personalize the stimulation and modify moods and habits far more directly than is possible through therapy or medication. The results also showed the degree to which symptoms that we tend to categorize as a single disorder — depression, for example — may involve electrical processes that are unique to each person. In the first study, a team from the University of California, San Francisco, surgically implanted electrodes in the brain of a woman whose severe depression had proved resistant to other treatments. For 10 days, they delivered pulses through the electrodes to different areas of the brain at various frequencies and had the patient record her level of depression, anxiety and energy on an iPad. The impact of certain pulses was significant and nuanced. “Within a minute, she would say, ‘I feel like I’m reading a good book,’” says Katherine W. Scangos, a psychiatrist and the study’s lead author. The patient described the effect of another pulse as “less cobwebs and cotton.” © 2021 The New York Times Company

Keyword: Depression
Link ID: 27712 - Posted: 02.28.2021

By Leslie Nemo Ironically, this tangle of brain cells is helping scientists tease apart a larger problem: how to help people with Alzheimer’s disease. Matheus Victor, a researcher at the Massachusetts Institute of Technology, photographed these neurons after coaxing them to life in a petri dish in the hope that the rudimentary brain tissue will reveal why a new therapy might alleviate Alzheimer’s symptoms. In humans and mice, a healthy memory is associated with a high level of synced neurons that turn on and off simultaneously. Those with neurological conditions such as Alzheimer’s and Parkinson’s disease often have fewer brain cells blinking unanimously. A couple of years ago Victor’s lab leader Li-Huei Tsai and her team at M.I.T. found that when they surrounded mice genetically predisposed to Alzheimer’s with sound pulses beating 40 times a second, the rodents performed better on memory-related tasks. The animals also lost some amyloid plaques, protein deposits in the brain that are characteristic of the disease. The researchers had previously performed a similar study with light flickering at the same rate, and the mice were found to experience additional improvements when the sound and light pulses were combined. Astoundingly, the mouse neurons synced up to the 40-beats-per-second rhythm of the audio pulses, though the mechanism behind this result and the reason the shift improves symptoms remain a mystery. To help solve it, the researchers want to watch how brain tissue responds to the stimulants at the cellular level. The goal is to one day understand how this exposure treatment might work for people, so the team is growing human brain cells in the lab and engineering them to respond to sound and light without eyes and ears. “We are trying to mimic the sensory stimulation in mice but missing a lot of the hardware that makes it possible. So this is a bit of a hack,” Victor says. © 2021 Scientific American

Keyword: Alzheimers; Brain imaging
Link ID: 27690 - Posted: 02.15.2021

By Diana Kwon Obsessive-compulsive disorder (OCD) is marked by repetitive, anxiety-inducing thoughts, urges and compulsions, such as excessive cleaning, counting and checking. These behaviors are also prevalent in the general population: one study in a large sample of U.S. adults found more than a quarter had experienced obsessions or compulsions at some point in their life. Although most of these individuals do not develop full-blown OCD, such symptoms can still interfere with daily life. A new study, published on January 18 in Nature Medicine, hints that these behaviors may be alleviated by stimulating the brain with an electrical current—without the need to insert electrodes under the skull. Robert Reinhart, a neuroscientist at Boston University, and his group drew on two parallel lines of research for this study. First, evidence suggests that obsessive-compulsive behaviors may arise as a result of overlearning habits—leading to their excessive repetition—and abnormalities in brain circuits involved in learning from rewards. Separately, studies point to the importance of high-frequency rhythms in the so-called high-beta/low-gamma range (also referred to as simply beta-gamma) in decision-making and learning from positive feedback. Drawing on these prior observations, Shrey Grover, a doctoral student in Reinhart’s lab, hypothesized with others in the team that manipulating beta-gamma rhythms in the orbitofrontal cortex (OFC)—a key region in the reward network located in the front of the brain—might disrupt the ability to repetitively pursue rewarding choices. In doing so, the researchers thought, the intervention could reduce obsessive-compulsive behaviors associated with maladaptive habits. To test this hypothesis, Grover and his colleagues carried out a two-part study. The first segment was aimed at identifying whether the high-frequency brain activity influenced how well people were able to learn from rewards. The team recruited 60 volunteers and first used electroencephalography to pinpoint the unique frequencies of beta-gamma rhythms in the OFC that were active in a given individual while that person took part in a task that involved associating symbols with monetary wins or losses. Previous work had shown that applying stimulation based on the particular patterns of rhythms in a person’s brain may enhance the effectiveness of the procedure. © 2021 Scientific American

Keyword: OCD - Obsessive Compulsive Disorder
Link ID: 27657 - Posted: 01.20.2021

By Diana Kwon Seizures are like storms in the brain—sudden bursts of abnormal electrical activity that can cause disturbances in movement, behavior, feelings and awareness. For people with epilepsy, not knowing when their next seizure will hit can be psychologically debilitating. Clinicians have no way of telling people with epilepsy whether a seizure will likely happen five minutes from now, five weeks from now or five months from now, says Vikram Rao, a neurologist at the University of California, San Francisco. “That leaves people in a state of looming uncertainty.” Despite the apparent unpredictability of seizures, they may not actually be random events. Hints of cyclical patterns associated with epilepsy date back to ancient times, when people believed seizures were tied to the waxing and waning of the moon. While this particular link has yet to be definitively proven, scientists have pinpointed patterns in seizure-associated brain activity. Studies have shown that seizures are more likely during specific periods in the day, indicating an association with sleep–wake cycles, or circadian rhythms. In 2018, Rao and his colleagues reported the discovery of long-term seizure-associated brain rhythms—most commonly in the 20- to 30-day range—which they dubbed as “multidien” (multiday) rhythms. By examining these rhythms in brain activity, the group has now demonstrated that seizures can be forecast 24 hours in advance—and in some patients, up to three days prior. Their findings, published December 17 in Lancet Neurology, raise the possibility of eventually providing epilepsy patients with seizure forecasts that could predict the likelihood that a seizure will occur days in advance. © 2020 Scientific American,

Keyword: Epilepsy
Link ID: 27631 - Posted: 12.19.2020

By Matt Richtel VALLEJO, Calif. — The adolescent patient turned sullen and withdrawn. He hadn’t eaten in 13 days. Treatment with steroids, phenobarbital and Valium failed to curb the symptoms of his epilepsy. Then, on Sept. 18, he had a terrible seizure — violently jerking his flippers and turning unconscious in the water. Cronutt, a 7-year-old sea lion, had to be rescued so he didn’t drown. His veterinarian and the caretakers at Six Flags Discovery Kingdom began discussing whether it was time for palliative care. “We’d tried everything,” said Dr. Claire Simeone, Cronutt’s longtime vet. “We needed more extreme measures.” On Tuesday morning, Cronutt underwent groundbreaking brain surgery aimed at reversing the epilepsy. If successful, the treatment could save increasing numbers of sea lions and sea otters from succumbing to a new plague of epilepsy. The cause is climate change. As oceans warm, algae blooms have become more widespread, creating toxins that get ingested by sardines and anchovies, which in turn get ingested by sea lions, causing damage to the brain that results in epilepsy. Sea otters also face risk when they consume toxin-laden shellfish. The animals who get stranded on land have been given supportive care, but often die. Cronutt may change that. “If this works, it’s going to be big,” said Mariana Casalia, a neuroscientist at the University of California, San Francisco, who helped pioneer the techniques that led to a procedure that took place a vet surgery center in Redwood City, Ca. © 2020 The New York Times Company

Keyword: Epilepsy; Neurotoxins
Link ID: 27516 - Posted: 10.10.2020

R. Stanley Williams For the first time, my colleagues and I have built a single electronic device that is capable of copying the functions of neuron cells in a brain. We then connected 20 of them together to perform a complicated calculation. This work shows that it is scientifically possible to make an advanced computer that does not rely on transistors to calculate and that uses much less electrical power than today’s data centers. Our research, which I began in 2004, was motivated by two questions. Can we build a single electronic element – the equivalent of a transistor or switch – that performs most of the known functions of neurons in a brain? If so, can we use it as a building block to build useful computers? Neurons are very finely tuned, and so are electronic elements that emulate them. I co-authored a research paper in 2013 that laid out in principle what needed to be done. It took my colleague Suhas Kumar and others five years of careful exploration to get exactly the right material composition and structure to produce the necessary property predicted from theory. Kumar then went a major step further and built a circuit with 20 of these elements connected to one another through a network of devices that can be programmed to have particular capacitances, or abilities to store electric charge. He then mapped a mathematical problem to the capacitances in the network, which allowed him to use the device to find the solution to a small version of a problem that is important in a wide range of modern analytics. © 2010–2020, The Conversation US, Inc.

Keyword: Learning & Memory; Robotics
Link ID: 27512 - Posted: 10.07.2020

Ian Sample Science editor Doctors believe they are closer to a treatment for multiple sclerosis after discovering a drug that repairs the coatings around nerves that are damaged by the disease. A clinical trial of the cancer drug bexarotene showed that it repaired the protective myelin sheaths that MS destroys. The loss of myelin causes a range of neurological problems including balance, vision and muscle disorders, and ultimately, disability. While bexarotene cannot be used as a treatment, because the side-effects are too serious, doctors behind the trial said the results showed “remyelination” was possible in humans, suggesting other drugs or drug combinations will halt MS. Advertisement “It’s disappointing that this is not the drug we’ll use, but it’s exciting that repair is achievable and it gives us great hope for another trial we hope to start this year,” said Prof Alasdair Coles, who led the research at the University of Cambridge. MS arises when the immune system mistakenly attacks the fatty myelin coating that wraps around nerves in the brain and spinal cord. Without the lipid-rich substance, signals travel more slowly along nerves, are disrupted, or fail to get through at all. About 100,000 people in the UK live with the condition. Funded by the MS Society, bexarotene was assessed in a phase 2a trial that used brain scans to monitor changes to damaged neurons in patients with relapsing MS. This is an early stage of the condition that precedes secondary progressive disease, where neurons die off and cause permanent disability. © 2020 Guardian News & Media Limited

Keyword: Multiple Sclerosis; Neuroimmunology
Link ID: 27496 - Posted: 09.28.2020

By Gunjan Sinha Light therapy can help lift moods, heal wounds, and boost the immune system. Can it improve symptoms of Parkinson’s disease, too? A first-of-its-kind trial scheduled to launch this fall in France aims to find out. In seven patients, a fiber optic cable implanted in their brain will deliver pulses of near-infrared (NIR) light directly to the substantia nigra, a region deep in the brain that degenerates in Parkinson’s disease. The team, led by neurosurgeon Alim- Louis Benabid of the Clinatec Institute—a partnership between several government-funded research institutes and industry—hopes the light will protect cells there from dying. The study is one of several set to explore how Parkinson’s patients might benefit from light. “I am so excited,” says neuropsychologist Dawn Bowers of the University of Florida College of Medicine, who is recruiting patients for a trial in which NIR will be beamed into the skull instead of delivered with an implant. Small tests in people with Parkinson’s and animal models of the disease have already suggested benefits, but some mainstream Parkinson’s researchers are skeptical. No one has shown exactly how light might protect the key neurons—or why it should have any effect at all on cells buried deep in the brain that never see the light of day. Much or all of the encouraging hints seen so far in people may be the result of the placebo effect, skeptics say. Because there are no biomarkers that correlate well with changes in Parkinson’s symptoms, “we are reliant on observing behavior,” says neurobiologist David Sulzer of Columbia University Irving Medical Center, an editor of the journal npj Parkinson’s Disease. “It’s not easy to guard against placebo effects.” © 2020 American Association for the Advancement of Science

Keyword: Parkinsons
Link ID: 27482 - Posted: 09.19.2020

Ken Solt & Oluwaseun Akeju The state of dissociation is commonly described as feeling detached from reality or having an ‘out of body’ experience. This altered state of consciousness is often reported by people who have psychiatric disorders arising from devastating trauma or abuse. It is also evoked by a class of anaesthetic drug, and can occur in epilepsy. The neurological basis of dissociation has been a mystery, but writing in Nature, Vesuna et al.1 describe a localized brain rhythm that underlies this state. Their findings will have far-reaching implications for neuroscience. The authors first recorded brain-wide neuronal activity in mice using a technique called widefield calcium imaging. They studied changes in these brain rhythms in response to a range of drugs that have sedative, anaesthetic or hallucinogenic properties, including three that induce dissociation — ketamine, phencyclidine (PCP) and dizocilpine (MK801). Only the dissociative drugs produced robust oscillations in neuronal activity in a brain region called the retrosplenial cortex. This region is essential for various cognitive functions, including episodic memory and navigation2. The oscillations occurred at a low frequency, of about 1–3 hertz. By contrast, non-dissociative drugs such as the anaesthetic propofol and the hallucinogen lysergic acid diethylamide (LSD) did not trigger this rhythmic retrosplenial activity. Vesuna et al. examined the active cells in more detail using a high-resolution approach called two-photon imaging. This analysis revealed that the oscillations were restricted to cells in layer 5 of the retrosplenial cortex. The authors then recorded neuronal activity across multiple brain regions. Normally, other parts of the cortex and subcortex are functionally connected to neuronal activity in the retrosplenial cortex; however, ketamine caused a disconnect, such that many of these brain regions no longer communicated with the retrosplenial cortex. © 2020 Springer Nature Limited

Keyword: Drug Abuse; Consciousness
Link ID: 27481 - Posted: 09.19.2020

Jon Hamilton Scientists used light to control the firing of specific cells to artificially create a rhythm in the brain that acted like the drug ketamine enjoynz/Getty Images Out-of-body experiences are all about rhythm, a team reported Wednesday in the journal Nature. In mice and one person, scientists were able to reproduce the altered state often associated with ketamine by inducing certain brain cells to fire together in a slow, rhythmic fashion. "There was a rhythm that appeared, and it was an oscillation that appeared only when the patient was dissociating," says Dr. Karl Deisseroth, a psychiatrist and neuroscientist at Stanford University. Dissociation is a brain state in which a person feels separated from their own thoughts, feelings and body. It is common in people who have some mental illnesses or who have experienced a traumatic event. It can also be induced by certain drugs, including ketamine and PCP (angel dust). The study linking dissociation to brain rhythms represents "a big leap forward in understanding how these drugs produce this unique state," says Dr. Ken Solt, an anesthesiologist at Harvard Medical School and Massachusetts General Hospital. Solt is the co-author of an article that accompanied the study but was not involved in the research. The finding also could be a step toward finding non-drug methods to control states of consciousness, Solt says. Deisseroth's lab made the discovery while studying the brains of mice that had been given ketamine or other drugs that cause dissociation. The team was using technology that allowed them to monitor the activity of cells throughout the brain. © 2020 npr

Keyword: Drug Abuse; Consciousness
Link ID: 27480 - Posted: 09.19.2020

Jon Hamilton The Food and Drug Administration has approved a variant of the anesthetic and party drug ketamine for suicidal patients with major depression. The drug is a nasal spray called Spravato and it contains esketamine, a chemical cousin of ketamine. In 2019, the FDA approved Spravato for patients with major depressive disorder who hadn't responded to other treatments. Now, the agency is adding patients who are having suicidal thoughts or have recently attempted to harm themselves or take their own lives. "Spravato is the first approved antidepressant medication that's been able to demonstrate a reduction in symptoms of major depressive disorder within 24 hours after the first dose," says Dr. Michelle Kramer, a psychiatrist and vice president of U.S. neuroscience, medical affairs at Janssen Pharmaceuticals, which makes the drug. Janssen is part of Johnson & Johnson. The drug's quick action is potentially important for suicidal patients because "existing drugs typically can take weeks or longer before you really get noticeable clinical benefit," says Dr. Gerard Sanacora, a professor of psychiatry at Yale University and director of Yale's depression research program. He was involved in the studies leading to the FDA approval and has consulted for Janssen. So a dose of esketamine "could potentially get a person out of a difficult, horrible situation when they're feeling so overwhelmed," says Dr. Charles Conway, a professor of psychiatry at Washington University School of Medicine in St. Louis who wasn't involved in the study. "This could be a significant improvement in how we can help people who have intense suicidal thinking." © 2020 npr

Keyword: Depression; Drug Abuse
Link ID: 27416 - Posted: 08.12.2020

Viviana Gradinaru Despite the wealth and quality of basic neuroscience research, there is still little we can do to treat or prevent most brain disorders. Industry efforts, meanwhile, have shied away from this field, particularly after a series of major drug candidates for the treatment of Alzheimer's disease failed to meet expectations (1). My previous research, which entailed developing and using optogenetics (2, 3) to understand how deep brain stimulation works in Parkinson's disease (PD) (4, 5), resulted in two key insights: We need to look and intervene earlier in brain disease progression, and we need to be able to access relevant cell populations with noninvasive yet precise tools to investigate, prevent, contain, or even reverse the course of disease. Accumulating evidence has highlighted a third insight: We may need to look beyond the brain to fully understand brain disorders (6, 7). My goal has been to develop an effective toolkit for neuromodulation so we can start to bridge the gap between what we know and what we can do to treat the brain. To achieve minimally invasive optogenetic-mediated modulation, we need to be able to penetrate the blood–brain barrier (BBB) so that vectors can be delivered systemically rather than through intracranial injections and address the poor reach of visible light through tissue so that large tissue volumes can be recruited without implantation of optical fibers. For early intervention, we need to get past the neuronal and brain-centric view of neurological disease. © 2020 American Association for the Advancement of Science

Keyword: Schizophrenia; Depression
Link ID: 27407 - Posted: 08.08.2020

By Nicholas Bakalar The incidence of hip fracture has decreased steadily over the past 40 years, but a new analysis suggests that new osteoporosis drugs have made only a small contribution to the trend. The report, published in JAMA Internal Medicine, included 10,552 men and women and their offspring followed since 1970. Every five years through 2010, the researchers recorded the number of hip fractures in people over 60. They found that the incidence of hip fractures decreased by 67 percent over those years, and rates were lower in people born later. The bone-strengthening bisphosphonates, like Fosamax (introduced in 1995) and Boniva (introduced in 2003), cut the fracture incidence by about 4.8 percent, the researchers estimate. But smoking decreased to 15 percent of participants in 2010, from 38 percent in 1970, and heavy drinking declined to 4.5 percent, from 7 percent. Both are significant risk factors for fracture. Other risk factors, like being underweight and early menopause, were stable over the years. “Smoking cessation accounts for about 90 percent of the decline in the age-adjusted decrease,” said the lead author, Dr. Timothy Bhattacharyya, an orthopedic surgeon with the National Institutes of Health. Other factors that may have played a role included estrogens, which were approved for osteoporosis treatment in 1988, and bone mineral density testing, which first became available in the 1990s. But “we didn’t observe any effect from estrogens or bone mineral density testing,” Dr. Bhattacharyya said. © 2020 The New York Times Company

Keyword: Drug Abuse
Link ID: 27406 - Posted: 08.08.2020

Craig W. Stevens Even as the COVID-19 pandemic cripples the economy and kills hundreds of people each day, there is another epidemic that continues to kill tens of thousands of people each year through opioid drug overdose. Opioid analgesic drugs, like morphine and oxycodone, are the classic double-edged swords. They are the very best drugs to stop severe pain but also the class of drugs most likely to kill the person taking them. In a recent journal article, I outlined how a combination of state-of-the-art molecular techniques, such as CRISPR gene editing and brain microinjection methods, could be used to blunt one edge of the sword and make opioid drugs safer. I am a pharmacologist interested in the way opioid drugs such as morphine and fentanyl can blunt pain. I became fascinated in biology at the time when endorphins – natural opioids made by our bodies – were discovered. I have been intrigued by the way opioid drugs work and their targets in the brain, the opioid receptors, for the last 30 years. In my paper, I propose a way to prevent opioid overdoses by modifying an opioid user’s brain cells using advanced technology. Opioid receptors stop breathing Opioids kill by stopping a person from breathing (respiratory depression). They do so by acting on a specific set of respiratory nerves, or neurons, found in the lower part of the brain that contain opioid receptors. Opioid receptors are proteins that bind morphine, heroin and other opioid drugs. The binding of an opioid to its receptor triggers a reaction in neurons that reduces their activity. Opioid receptors on pain neurons mediate the pain-killing, or analgesic, effects of opioids. When opioids bind to opioid receptors on respiratory neurons, they slow breathing or, in the case of an opioid overdose, stop it entirely. © 2010–2020, The Conversation US, Inc.

Keyword: Drug Abuse
Link ID: 27401 - Posted: 08.06.2020

By Aimee Cunningham Heavy drinking is robbing Americans of decades of life. From 2011 to 2015, an average of 93,296 deaths annually could be tied to excessive alcohol use, or 255 deaths per day. Excessive drinking brought death early, typically 29 years sooner than would have been expected. All told, the United States saw 2.7 million years of potential life lost each year, researchers report in the July 31 Mortality and Morbidity Weekly Report. The researchers used a program developed by the U.S. Centers for Disease Control and Prevention that estimates annual deaths and years of potential life lost due to an individual’s own or another’s excessive drinking. The tool takes into account whether the cause of death is fully attributable to alcohol, such as alcoholic liver cirrhosis, or whether excessive drinking can partially contribute to a condition, such as breast cancer. Annually, about 51,000 of the deaths were from chronic conditions. The rest were sudden demises such as poisonings that involved another substance along with alcohol or alcohol-related car crashes. The CDC defines excessive alcohol use as binging — drinking five or more drinks at a time for men, four or more for women — or drinking heavily over the course of the week. Men qualify at 15 or more drinks per week; for women, it’s eight or more. The numbers of deaths and years of life extinguished due to excessive drinking have gone up since the last report. That assessment covered 2006 to 2010 and reported close to 88,000 deaths and 2.5 million lost years annually. Recommendations from the Community Preventive Services Task Force, made up of public health and prevention experts, to stem excessive drinking include raising taxes on alcohol and regulating the number of places that sell alcoholic beverages (SN: 8/9/17). © Society for Science & the Public 2000–2020.

Keyword: Drug Abuse
Link ID: 27398 - Posted: 08.03.2020

Justin Rowlatt Chief environment correspondent If you have ever doubted whether solar power can be a transformative technology, read on. This is a story about how it has proved its worth in the toughest environment possible. The market I'm talking about is perhaps the purest example of capitalism on the planet. There are no subsidies here. Nobody is thinking about climate change - or any other ethical consideration, for that matter. This is about small-scale entrepreneurs trying to make a profit. It is the story of how Afghan opium growers have switched to solar power, and significantly increased the world supply of heroin. I was in a military helicopter thundering over the lush poppy fields of the Helmand valley in Afghanistan when I spotted the first solar panel. You've heard of Helmand. It is the most dangerous province in Afghanistan. Of the 454 British soldiers who died in the recent conflict in Afghanistan, all but five lost their lives in Helmand. The province is also at the heart of by far the most productive opium growing region on the planet. Most opium will be refined into heroin, one of the most addictive drugs there is. According to the UN body responsible for tracking and tackling illegal drug production, the UNODC, almost 80% of all Afghan opium now comes from the south-west of the country, including Helmand. That means pretty much two-thirds of global supply. So, not the kind of place you would expect to be at the forefront of efforts to decarbonise the economy. But, once I had seen that first solar panel, I saw more. In fact there seemed to be a small array of solar panels in the corner of most farm compounds, and that was back in 2016. It is only now that the scale of the revolution in heroin production I was unwittingly witnessing has been quantified. Because I wasn't the only person to notice that Afghan farmers were taking an interest in low-carbon technologies. © 2020 BBC.

Keyword: Drug Abuse
Link ID: 27386 - Posted: 07.27.2020

By Erica Rex In 2012, I had my first psychedelic experiences, as a subject in a clinical trial at Johns Hopkins University School of Medicine’s Behavioral Pharmacology Research Unit. I was given two doses of psilocybin spaced a month apart to treat my cancer-related depression. During one session, deep within the world the drug evoked, I found myself inside a steel industrial space. Women were bent over long tables, working. I became aware of my animosity towards my two living siblings. A woman seated at the end of a table wearing a net cap and white clothes, turned and handed me a tall Dixie cup. “You can put that in here,” she said. The cup filled itself with my bilious, sibling-directed feelings. “We’ll put it over there.” She turned and placed the cup matter-of-factly on a table at the back of the room. Then she went back to her tasks. Whenever I speak with her, Mary Cosimano, the director of guide/facilitator services at Johns Hopkins Center for Psychedelic and Consciousness Research, mentions the women in the chamber and the cup. My experience struck a chord. For me, the women in the chamber have become a transcendent metaphor for emotional healing. “I’ve thought about having a necklace made, with the cup, as a momento,” she said the last time I saw her at a conference. “Have you thought about it?” Prior to their 1971 prohibition, psilocybin and LSD were administered to approximately 40,000 patients, among them people with terminal cancer, alcoholics and those suffering from depression and obsessive-compulsive disorder. The results of the early clinical studies were promising, and more recent research has been as well. The treatment certainly helped me. Eight years after my sessions, researchers continue to prove the same point again and again in an ongoing effort to turn psychedelic drug therapy into FDA-sanctioned medical treatment. This can’t happen soon enough. © 2020 Scientific American,

Keyword: Depression; Drug Abuse
Link ID: 27361 - Posted: 07.14.2020

By Rachel Nuwer In the years leading up to the roaring 2020s, young people were once again dropping acid. Onetime Harvard psychologist Timothy Leary died almost 25 years ago, after which some of his ashes were launched into space. But from 2015 to 2018, the rate of “turning on and tuning in” with LSD, to paraphrase Leary, increased by more than 50 percent in the U.S.—a rise perhaps fueled by a need for chemical escapism. Those results were published in the July issue of Drug and Alcohol Dependence. The authors of the study suspect that many users may be self-medicating with the illegal substance to find relief from depression, anxiety and general stress over the state of the world. “LSD is used primarily to escape. And given that the world’s on fire, people might be using it as a therapeutic mechanism,” says Andrew Yockey, a doctoral candidate in health education at the University of Cincinnati and lead author of the paper. “Now that COVID’s hit, I’d guess that use has probably tripled.” To arrive at their findings, Yockey and his colleagues turned to data collected from more than 168,000 American adults by the National Survey on Drug Use and Health, an annual, nationally representative questionnaire. They analyzed trends since 2015, partly because of the timing of the 2016 presidential election. The researchers found that past-year LSD use increased by 56 percent over three years. The rise was especially pronounced in certain user groups, including people with college degrees (who saw a 70 percent increase) and people aged 26 to 34 (59 percent), 35 to 49 (223 percent) and 50 or older (45 percent). Younger people aged 18 to 25, on the other hand, decreased their use by 24 percent. © 2020 Scientific American

Keyword: Drug Abuse; Stress
Link ID: 27356 - Posted: 07.11.2020