Chapter 4. The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
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Some people may have a get-out clause when it comes to giving up cigarettes. A third of white people who smoke have gene variations that make it harder for them to kick the habit. A gene called ANKK1 regulates the release of dopamine – a chemical involved in the brain’s reward centres. Ming Li and colleagues at the Zhejiang University School of Medicine in Hangzhou, China, wondered whether variations of this gene might affect people’s ability to give up cigarettes. So his team analysed 23 studies that have linked ANKK1 to smoking, involving more than 11,000 participants in total. Across the board, there was no significant link between successful quitting and the gene variants. But when they looked at just the studies that analysed white people, the results were striking. About two-thirds of white smokers carried a variation of the gene called A2/A2. These people were about 22 per cent more likely to be able to quit smoking than those who carried an alternative version of the gene, either A1/A1 or A1/A2. The A1/A1 and A1/A2 gene variations have previously been linked to obesity and drug addiction, which suggests they may predispose people to addictive behaviours. People carrying these versions of ANKK1 may need more aggressive strategies to fight their addiction to cigarettes, says Li. It is not clear whether the gene has the same effect for non-white people, he says. More studies that involve non-white people will be necessary to investigate this. © Copyright Reed Business Information Ltd.
Ian Sample Science editor High-strength cannabis may damage nerve fibres that handle the flow of messages across the two halves of the brain, scientists claim. Brain scans of people who regularly smoked strong skunk-like cannabis revealed subtle differences in the white matter that connects the left and right hemispheres and carries signals from one side of the brain to the other. The changes were not seen in those who never used cannabis or smoked only the less potent forms of the drug, the researchers found. The study is thought to be the first to look at the effects of cannabis potency on brain structure, and suggests that greater use of skunk may cause more damage to the corpus callosum, making communications across the brain’s hemispheres less efficient. Paola Dazzan, a neurobiologist at the Institute of Psychiatry at King’s College London, said the effects appeared to be linked to the level of active ingredient, tetrahydrocannabinol (THC), in cannabis. While traditional forms of cannabis contain 2 to 4 % THC, the more potent varieties (of which there are about 100), can contain 10 to 14% THC, according to the DrugScope charity. “If you look at the corpus callosum, what we’re seeing is a significant difference in the white matter between those who use high potency cannabis and those who never use the drug, or use the low-potency drug,” said Dazzan. The corpus callosum is rich in cannabinoid receptors, on which the THC chemical acts. © 2015 Guardian News and Media Limited
By Lenny Bernstein BALTIMORE — Deep into a three-day heroin binge at a local hotel, Samantha told the newbie he was shooting too much. He wasn’t accustomed to heroin, she said, and hadn’t waited long enough since his last injection. “But he didn’t listen,” she said. Sure enough, he emerged from a visit to the bathroom, eyes glazed, and collapsed from an overdose. Samantha, who declined to give her last name to avoid trouble with her bosses at a nearby strip club, said she grabbed her naloxone, the fast-acting antidote to opioid overdoses. She was too panicked to place the atomizer on the end of the syringe, but her boyfriend wasn’t. He sprayed the mist into the nose of the unconscious drug user, who awoke minutes later. “I always have it because I’m scared to death,” said Samantha, who said she has been shooting heroin for 22 years. “I don’t want to be helpless.” As the opioid epidemic has exploded in small towns and suburbs in recent years, officials have scrambled to put naloxone in the hands of drug users’ families and friends, and to make it more widely available by equipping police officers with the drug. At the same time, thousands of lives are being saved by giving the antidote to drug users. More than 80 percent of overdose victims revived by “laypeople” were rescued by other users, most of them in the past few years, according to one national survey published in June.
Keyword: Drug Abuse
Link ID: 21654 - Posted: 11.24.2015
by Bethany Brookshire Many people perceive cocaine as one of the most intense stimulant drugs available: It’s illegal, highly addictive and dangerous. Caffeine, in contrast, is the kinder, cuddlier stimulant. It’s legal, has mild effects and in forms such as coffee, it might even be good for your health. But caffeine in combination with cocaine is another story. In South America, drug distributors have started “cutting” their cocaine with caffeine. This cheaper substitute might, at first glance, seem to make the cocaine less potent. After all, there’s less of the drug there. But new data shows that when combined, cocaine and caffeine make a heck of a drug. Coca paste is a popular form of cocaine in South American countries. A smoked form of cocaine, coca paste is the intermediate product in the extraction process used to get pure cocaine out of coca leaves. Because it is smoked, the cocaine in the coca paste hits the brain very quickly, making the drug highly addictive, explains Jose Prieto, a neurochemist at the Biological Research Institute Clemente Stable in Montevideo, Uruguay. Much of the time, Coca paste isn’t acting alone, however. In a 2011 study published in Behavioral Brain Research, Prieto and his colleagues examined the contents of coca paste from police seizures. “Nearly 80 percent of the coca paste samples” were adulterated, Prieto says, “most with caffeine.” Caffeine adulteration ranged from 1 to 15 percent of the drug volume. © Society for Science & the Public 2000 - 2015.
Keyword: Drug Abuse
Link ID: 21643 - Posted: 11.18.2015
by Teresa Shipley Feldhausen The benefits of drinking coffee continue to filter in. An analysis of more than 200,000 medical professionals followed for nearly 30 years finds that drinking up to five cups of coffee a day is associated with reduced risk of dying early from heart and brain diseases as well as suicide. The study’s results were adjusted for factors like smoking, weight and diet. Benefits were more pronounced for those who had never smoked, an international team of researchers report November 16 in Circulation. Both caffeinated and decaf java had positive effects, leading the researchers to speculate that coffee’s potency as a health elixir may stem from chemical compounds in the bean such as diterpenes and chlorogenic acids. © Society for Science & the Public 2000 - 2015.
Keyword: Drug Abuse
Link ID: 21634 - Posted: 11.17.2015
For the first time, the barrier that protects the brain has been opened without damaging it, to deliver chemotherapy drugs to a tumour. The breakthrough could be used to treat pernicious brain diseases such as cancer, Parkinson’s and Alzheimer’s, by allowing drugs to pass into the brain. The blood-brain barrier keeps toxins in the bloodstream away from the brain. It consists of a tightly packed layer of endothelial cells that wrap around every blood vessel throughout the brain. It prevents the passage of viruses, bacteria and other toxins, while ushering in vital molecules such as glucose via specialised transport mechanisms. The downside of this is that the blood-brain barrier also blocks the vast majority of drugs. There are a few exceptions, but those drugs that are able to sneak through can also penetrate every cell in the body, which makes for major side effects. Now researchers at Sunnybrook Health Sciences Centre in Toronto, Canada, say they have successfully used ultrasound to temporarily open the blood-brain barrier, with the ultimate aim of treating a brain tumour. The procedure took place on 4 November. Ultrasound prises open brain's protective barrier for first time The team, led by neurosurgeon Todd Mainprize and physicist Kullervo Hynynen, injected the chemotherapy drug doxorubicin along with tiny gas-filled microbubbles, into the blood of a patient with a brain tumour. The microbubbles and the drug spread throughout their body, including into the blood vessels that serve the brain. © Copyright Reed Business Information Ltd.
by Bethany Brookshire Cheese is a delicious invention. But if you saw the news last week, you might think it’s on its way to being classified as a Schedule II drug. Headlines proclaimed “Say cheese? All the time? Maybe you have an addiction,” “Cheese really is crack” and “Your cheese addiction is real.” Under the headlines, the stories referred to a study examining the addictive properties of various foods. Pizza was at the top. The reason? The addictive properties of cheese, which the articles claim contains “dangerous” opiate-like chemicals called casomorphins. But you can’t explain away your affinity for cheese by saying you’re addicted. The study in those stories, published earlier this year in PLOS ONE, did investigate which foods are most associated with addictive-like eating behaviors. Pizza did come out on top in one experiment. But the scientists who did the research say this has little to do with the delicious dairy products involved. Instead, they argue, the foods we crave the most are those processed to have high levels of sugars and fat, and it’s these ingredients that leave us coming back for another slice. The cheese? “I was horrified by the misstatements and the oversimplifications … and the statements about how it’s an excuse to overeat,” says Ashley Gearhardt of the University of Michigan in Ann Arbor, who led the study. “Liking is not the same as addiction. We like lots of things. I like hip-hop music and sunshine and my wiener dog, but I’m not addicted to her. I eat cheese every day. That’s doesn’t mean you’re addicted or it has addictive potential.” © Society for Science & the Public 2000 - 2015
Keyword: Drug Abuse
Link ID: 21592 - Posted: 11.02.2015
By KATHARINE Q. SEELYE NEWTON, N.H. — When Courtney Griffin was using heroin, she lied, disappeared, and stole from her parents to support her $400-a-day habit. Her family paid her debts, never filed a police report and kept her addiction secret — until she was found dead last year of an overdose. At Courtney’s funeral, they decided to acknowledge the reality that redefined their lives: Their bright, beautiful daughter, just 20, who played the French horn in high school and dreamed of living in Hawaii, had been kicked out of the Marines for drugs. Eventually, she overdosed at her boyfriend’s grandmother’s house, where she died alone. “When I was a kid, junkies were the worst,” Doug Griffin, 63, Courtney’s father, recalled in their comfortable home here in southeastern New Hampshire. “I used to have an office in New York City. I saw them.” When the nation’s long-running war against drugs was defined by the crack epidemic and based in poor, predominantly black urban areas, the public response was defined by zero tolerance and stiff prison sentences. But today’s heroin crisis is different. While heroin use has climbed among all demographic groups, it has skyrocketed among whites; nearly 90 percent of those who tried heroin for the first time in the last decade were white. And the growing army of families of those lost to heroin — many of them in the suburbs and small towns — are now using their influence, anger and grief to cushion the country’s approach to drugs, from altering the language around addiction to prodding government to treat it not as a crime, but as a disease. © 2015 The New York Times Company
Keyword: Drug Abuse
Link ID: 21583 - Posted: 10.31.2015
By Dina Fine Maron When powerful street drugs collectively known as synthetic pot are smoked, the resulting high mimics the effects of marijuana. Yet these man-made cannabinoids are not marijuana at all. The drugs, more commonly called spice, fake weed or K2, are made up of any number of dried, shredded plants sprayed with chemicals that live in a murky legality zone. They are highly dangerous—and their use is on the rise. Synthetic pot, which first hit the market in the early 2000s, has especially caught the attention of public health officials in the past couple of years, stemming from a surge in hospitalizations and violent episodes. Although the drugs act on the same brain pathway as weed's active ingredient, they can trigger harsher reactions, including heart attacks, strokes, kidney damage and delusions. Between June and early August usage of these drugs led to roughly 2,300 emergency room visits in New York State alone. Nationwide more than 6,000 incidents involving spice have been reported to U.S. poison-control centers this year—about double the number of calls in 2013. Ever changing recipes make it possible for spice sellers to elude the authorities. Each time an ingredient is banned, producers swap in another compound. The drugs are then sold on the Internet or at gas stations and convenience stores at prices lower than genuine marijuana. The changing formulations also pose a challenge for researchers trying to match the chemicals with their side effects or to develop tests to identify them in a user's system. “The drugs are present in blood for only a short period, so it's very difficult to detect them,” says Marilyn Huestis, chief of the Chemistry and Drug Metabolism Section at the National Institute on Drug Abuse. © 2015 Scientific American
Keyword: Drug Abuse
Link ID: 21570 - Posted: 10.27.2015
By R. Douglas Fields “Why can’t you stop drinking?” This week at the Annual Meeting of the Society for Neuroscience in Chicago, researchers from the University of Chicago announced a new finding that provides a fresh answer to this persistent question that plagues people addicted to alcohol. The discovery offers an entirely new approach to treatment. Neuroscientist, Amy Lasek, at the Department of Psychiatry at the University of Illinois, Chicago, and colleagues, report that after binge drinking, neurons in brain circuits responsible for alcohol addiction become encased in a protein material, called a perineuronal net. The impenetrable coating cements neurons involved in alcohol addiction into a circuit that is extremely difficult to break. Current drugs for treating alcohol dependence work by modifying neurotransmitter signaling between neurons, but for many people these treatments cannot break the overwhelming compulsion to drink. Drugs that can break down the glue-like cement in perineuronal nets could offer a new approach to treatment. Lasek’s unusual approach into addiction research stems from her background as a molecular and cell biologist working in the field of cancer research. The root of cancer is changes in specific genes. Small molecules designed to target these aberrant genes is the approach used in cancer therapy. Lasek’s background made her think of finding molecularly targeted therapies for psychiatric disorders. Lasek and her colleagues began by studying fruit flies to search for gene variations that altered the fly’s behavior toward alcohol. She found several genes that had this effect, including an obscure one called ALK (anaplastic lymphoma kinase). Then she suppressed these genes in mice to see if the animal’s response to alcohol was altered. “I got hooked,” she says, “because to me the fact that you can manipulate a single gene in a single brain region and change behavior—like drinking or cocaine reward—was fascinating from a biological point of view!” © 2015 Scientific America
Keyword: Drug Abuse
Link ID: 21561 - Posted: 10.24.2015
Olivia Maynard It has been described as a ‘disruptive technology’ potentially capable of breaking our fatal relationship with tobacco. So the setting for a public debate on e-cigarettes - a museum part-funded by the tobacco industry, in a city home to the global headquarters of one of the largest tobacco manufacturers - was perhaps ironic. Yet on Wednesday evening, I found myself at the M-Shed in Bristol, watching just that: a debate about whether e-cigarettes could be part of the solution to the tobacco epidemic. To mark the launch of a new Integrative Cancer Epidemiology Programme, linked to the Medical Research Centre Integrative Epidemiology Unit at the University of Bristol, Professor Marcus Munafò (Professor of Biological Psychology at the University of Bristol) and Professor Linda Bauld (Professor of Health Policy at the University of Stirling), both collaborators of mine, discussed e-cigarettes. Professor Gabriel Scally (Public Health Doctor and former Regional Director of Public Health for the South West of England) chaired the discussion. Billed as a debate about whether e-cigarettes might be ‘the key to reducing smoking’, some in the audience may have expected a heated discussion. However, with this line-up of academics, influential in the fields of public health, tobacco and addiction, the discussion was evidence-based and measured. As for the motion of the debate, the panel was unanimous: e-cigarettes may not be the key to reducing smoking, but they are certainly an important part of the solution. © 2015 Guardian News and Media Limited
Keyword: Drug Abuse
Link ID: 21556 - Posted: 10.24.2015
Mark Easton Home editor An attempt by UN officials to get countries to decriminalise the possession and use of all drugs has been foiled, the BBC can reveal. A paper from the UN Office on Drugs and Crime (UNODC) has been withdrawn after pressure from at least one country. The document, which was leaked, recommends that UN members consider "decriminalising drug and possession for personal consumption". It argued "arrest and incarceration are disproportionate measures". The document was drawn up by Dr Monica Beg, chief of the HIV/AIDs section of the UNODC in Vienna. It was prepared for an international harm reduction conference currently being held in Kuala Lumpur. The UNODC oversees international drugs conventions and offers guidance on compliance. Sources within the UNODC have told the BBC the document was never sanctioned by the organisation as policy. One senior figure within the agency described Dr Beg as "a middle-ranking official" who was offering a professional viewpoint. The document, on headed agency notepaper, claims it "clarifies the position of UNODC to inform country responses to promote a health and human-rights approach to drug policy". "Treating drug use for non-medical purposes and possession for personal consumption as criminal offences has contributed to public health problems and induced negative consequences for safety, security, and human rights," the document states. © 2015 BBC.
Keyword: Drug Abuse
Link ID: 21535 - Posted: 10.21.2015
by Helen Thompson It's no secret that some plants lace their nectar with caffeine in an effort to attract more pollinators, and that buzz sticks around in a bee's memory. These caffeinated flowers lure naive honeybees to return over and over again — and bring their friends, researchers report October 15 in Current Biology. When feeding off caffeinated nectar (versus noncaffeinated nectar), honeybees increased their foraging activity and performed four times as many waggle dances to alert other workers to food sources. Though bees might be more persistent foragers while under the influence of caffeine, they focused mainly on caffeinated sources instead casting a broad search. Plants may also substitute caffeine for sugar, the researchers note, duping bees into gathering nectar that's less valuable for honey production. © Society for Science & the Public 2000 - 2015.
By CATHERINE SAINT LOUIS Ever since the Food and Drug Administration approved the use of the narcotic painkiller OxyContin for certain children in August, it has faced unabated criticism from lawmakers and public officials who are wrestling with devastating rates of prescription opioid abuse in their communities. Last week, Hillary Rodham Clinton brought the issue to the presidential race, calling the agency’s action “absolutely incomprehensible.” The crux of the issue is whether the agency’s approval will lead to more prescriptions for OxyContin in young patients. For years, the powerful long-acting drug has been prescribed off-label to very sick children in severe pain from cancer or spinal-fusion surgery. (Doctors can prescribe an approved drug to anyone and for any use they see fit regardless of specifications on the label.) The agency’s approval means those doctors will finally have “information about how to do it appropriately,” like dosage recommendations, said Dr. Stephen Ostroff, the agency’s acting commissioner, in an interview. “We recognize this is a very nuanced issue,” said Dr. Ostroff, when asked about Mrs. Clinton’s recent comments. “It needs to be understood in the context of why this was done.” Dr. Kathleen A. Neville, a pediatric oncologist at Arkansas Children’s Hospital, routinely treats children with unremitting pain caused by cancer or sickle cell anemia. Her patients are the kind the F.D.A. envisioned would benefit from OxyContin, despite its “risks of addictions, abuse and misuse” as a warning on the new label says. Dr. Neville, who said she had no financial ties to makers of painkillers, applauded the agency’s approval. “Just because OxyContin has been abused or prescribed inappropriately doesn’t mean we should deprive the children who need the drug,” she said, adding it is “our obligation to have the best level of evidence for its use in children.” © 2015 The New York Times Company
By Gretchen Reynolds We’ve probably all heard someone exclaim, “Ah, my endorphins are kicking in!” at the end of a good run. Endorphins are famous for supposedly producing “runner’s high,” that fleeting sense of calm and euphoria that engulfs many of us after a satisfying workout. But in fact, endorphins may be unfairly hogging the credit for making workouts enjoyable, according to an enlightening new experiment with animals. The findings suggest that endorphins have little to do with runner’s high. Instead, that euphoric feeling may be the product of a completely different but oddly familiar substance — the body’s own endocannabinoids, the chemicals that, like the cannabinoids in marijuana, lighten mood. Endorphins first became a household word in the 1980s, when researchers found that blood levels increased after prolonged exercise. This finding made sense. Exercise can cause discomfort or pain, and endorphins are the body’s self-produced opiates, with pain-relieving properties much like morphine. From that discovery, it was a short step to believing that endorphins must also produce the pleasurable mental sensations that many people feel after exercise. But there is a substantial problem with that idea, and it involves the substantial-ness of endorphins. They are large molecules, too big to pass through the blood-brain barrier. They might staunch pain in the muscles, but they wouldn’t have effects directly inside the brain, where any high would originate. So for the past decade or so, scientists have been looking for other substances that might be involved in making exercisers feel high, which led them, perhaps unsurprisingly, to endocannabinoids. © 2015 The New York Times Company
Keyword: Drug Abuse
Link ID: 21488 - Posted: 10.08.2015
By Jessica Schmerler Many studies trumpet the positive effects of oxytocin. The hormone facilitates bonding, increases trust and promotes altruism. Such findings earned oxytocin its famous nickname, the “love hormone.” But more recent research has shown oxytocin has a darker side, too: it can increase aggression, risk taking and prejudice. A new analysis of this large body of work reveals that oxytocin's effects on our brain and behavior actually look a lot like another substance that can cut both ways: alcohol. As such, the hormone might point to new treatments for addiction. Researchers led by Ian Mitchell, a psychologist at the University of Birmingham in England, conducted the meta-analysis, which reveals that both oxytocin and alcohol reduce fear, anxiety and stress while increasing trust, generosity and altruism. Yet both also increase aggression, risk taking and “in-group” bias—favoring people similar to ourselves at the expense of others, according to the paper published in August in Neuroscience and Biobehavioral Reviews. The scientists posit that these similarities probably exist because oxytocin and alcohol act at different points in the same chemical pathway in the brain. Oxytocin stimulates release of the neurotransmitter GABA, which tends to reduce neural activity. Alcohol binds to GABA receptors and ramps up GABA activity. Oxytocin and alcohol therefore both have the general effect of tamping down brain activity—perhaps explaining why they both lower inhibitions. © 2015 Scientific American
by Bethany Brookshire Last weekend, I ran the Navy-Air Force half-marathon. After pounding pavement for an hour or so, my legs began to feel light. Slightly numb. I felt fantastic. I had to remind myself to run, not to stop and dance, and that singing along to my candy-pop workout music — even at mile 10 — is not socially acceptable. It’s the hope of this euphoria — this runner’s high — that keeps me running. We’re not totally sure what’s responsible for this incredible high. Some studies call out our body’s endorphins. Others point to cannabinoids — chemicals related to the active compound in marijuana. A new study suggests that the appetite hormone leptin may play a role in getting us going. And from an evolutionary perspective, it makes good sense. When our dinner might make a quick getaway, it’s important to link our drive to run with our need to feed. But it’s probably not the whole story. Like many other neurobiological events, the exact recipe for runner’s high is complex and hazy. It takes a whole suite of chemicals to help us get started and to make sure we want to go the distance. Those who get runner’s high know it when they feel it. But a clinical definition is a little more slippery. “I remember someone saying the runner’s high was the moment when the body was disconnected from the brain,” says Francis Chaouloff, who studies running and motivation in mice at the French Institute of Health and Medical Research in Bordeaux. This sense of extreme euphoria, he says, is generally limited to people running or exercising for long periods of time, over many miles or hours. © Society for Science & the Public 2000 - 2015.
Jon Hamilton A mind-altering drug called ketamine is changing the way some doctors treat depression. Encouraged by research showing that ketamine can relieve even the worst depression in a matter of hours, these doctors are giving the drug to some of their toughest patients. And they're doing this even though ketamine lacks approval from the Food and Drug Administration for treating depression. "It became clear to me that the future of psychiatry was going to include ketamine or derivatives of ketamine," says David Feifel, a professor of psychiatry at the University of California, San Diego, who began administering the drug to patients in 2010. Ketamine was developed as an anesthetic and received FDA approval for this use in 1970. Decades later, it became popular as a psychedelic club drug. And in 2006, a team from the National Institute of Mental Health published a landmark study showing that a single intravenous dose of ketamine produced "robust and rapid antidepressant effects" within a couple of hours. Since then, thousands of depressed patients have received "off-label" treatment with ketamine. One of those patients is Paul, 36, who lives in San Diego and is a patient of Dr. Feifel. We're not using his last name to protect his medical privacy. © 2015 NPR
By Karen Weintraub Depression makes people more vulnerable to alcoholism and vice versa, said Dr. Shelly Greenfield, a professor of psychiatry at Harvard Medical School and director of McLean Hospital’s Alcohol and Drug Abuse Clinical and Health Services Research Program. About a third of depressed people also have a problem with alcohol, she said, adding that the depression usually comes first. Genetics makes some people more vulnerable to each — and perhaps the combination, Dr. Greenfield said, “but it’s not the whole story.” Social environment, particularly in childhood, also plays a key role. People who are the victims of physical or sexual abuse, for example, are at higher risk for both alcoholism and depression later in life, she said. Depressed people who drink will most likely see their depression worsen, because alcohol is a depressant, tamping down the nervous system, said Dr. Kathleen Brady, a distinguished university professor at the Medical University of South Carolina. Abstinence will be harder for alcoholics who are depressed, because of the hopelessness that comes with depression. Getting help promptly may make recovery from alcoholism easier, Dr. Greenfield said. Needing help to quit drinking or to resolve depression is not a sign of weakness or personal failure, she noted. In families with a history of either depression or alcoholism, it is important to be vigilant about drinking, particularly in adolescence. © 2015 The New York Times Company
Nathan Seppa For a historically mistrusted drink, coffee is proving to be a healthy addiction. Scientific findings in support of coffee’s nutritional attributes have been arriving at a steady drip since the 1980s, when Norwegian researchers reported that coffee seemed to fend off liver disease. Since then, the dark brown beverage has shown value against liver cancer, too, as well as type 2 diabetes, heart disease and stroke. Coffee even appears to protect against depression, Parkinson’s and Alzheimer’s diseases. Taken as a whole, these results might explain the most astonishing finding of all. People who drink two or more cups of coffee a day live longer than those who don’t, after accounting for behavioral differences, U.S. researchers reported in 2012. Studies in Japan, Scotland and Finland agree. Talk about a twofer. Coffee not only picks you up, it might put off the day they lower you down. Yet coffee has had trouble shaking its bad-for-you reputation. It may be one of the most widely consumed drinks in the world, but people have long assumed that, at least in its energizing caffeinated version, coffee comes with a catch. “People notice the caffeine,” says cardiologist Arthur Klatsky, who has researched coffee for decades at the Kaiser Permanente Northern California Division of Research in Oakland. “And there is this general feeling that anything that has some effect on the nervous system has to have something bad about it.” It doesn’t help that caffeine is mildly addictive.